Cardiovascular Disease

Chest pain
M.I.
Heart failure
AF
HTN
ARF

Q. Name some common cardiac emergencies you have seen in our ward.
Ans.
MI
Acute left ventricular failure
Acute coronary syndrome

Q. Name some cardiac disease you have seen in our ward.

Ans.
Coronary artery disease M I, angina
Heart failure
HTN
Acute rheumatic fever
Valvular heart disease MS
Arrhythmia AF

Q. Name some coronary artery disease.

Ans.
Stable angina
Unstable angina
MI
Heart failure

Q. Name some causes of chest pain.

Ans.
Cardiac or central causes Peripheral or non cardiac
Myocardial ischemia / Angina Lung
Myocardial infarction Pneumonia (pleuritis)
Pericarditis Pneumothorax
Myocarditis Pulmonary embolism/ infarction
Aortic dissetion Malignancy
Aortic aneurysm Musculoskeletal pain
Osteoarthritis
Rib fracture
Muscle pain
Herpes zoster

1
Q. How will you differentiate between cardiac chest pain from non cardiac chest pain?
Ans:
Trait Cardiac chest pain Non cardiac chest pain
1) Site Central Peripheral
2) Character Choking, tighting, squeezing Sharp, stabbing
3) Aggravating factor Exertion, heavy meal, cold Not so
exposure
4) Relieving factor Rest , Nitrate Not so
5) Radiate to Left shoulder blade, arm, jaw Not so

Q. How will you differentiate between pain of MI and angina?

Ans.
Pain of MI Pain of angina
Sudden, more severe Less severe
Not relieved by rest or nitrate Relieved by rest or nitrate
Associated with Not so
Sweating
Vomiting
Cold calmy skin
Hypotension

Q. Define acute coronary syndrome.

Ans. Prolonged and sever chest pain may be due to unstable angina , STE MI or non-STE MI
(non
Q wave MI) are collectively called acute coronary syndrome.
Pain ECG Toponin I Diagnosis
Cardiac chest pain ST elevation +++ STE MI
Cardiac chest pain ST depression ++ Non STE MI or non Q
T inversion wave MI
Cardiac chest pain Transient ECG change or - Unstable angina
normal ECG

Q. Define unstable angina.

Ans. Unstable angina is characterized by newly onset of rapidly worsening angina or angina on
minimal exertion or angina on rest in absence of myocardial damage.

Q. A 40 years old male came to you with severe chest pain with sweating, cold calmy skin,
vomiting and BP 90/62 mm of Hg. What is your diagnosis?
Ans. Acute myocardial infarction.

Q. In which ward you will suggest to admit the patient?

Ans. CCU [ some of you mistakenly answer ICU. So be careful]

2
Q. Assume, you are in CCU. What will you do to manage the patient?
Ans. First I shall give high flow o2. Then I shall do ECG.

Q. What do you expect in ECG?

Ans. ST-elevation, then `Q inversion then `T inversion

Q. What other investigation you will do?/ Do we measure any enzyme level?
Ans. Toponin I.

Q. What treatment you will do?

Ans.
O2 inhalation
For pain: Inj. Morphin [ I.V. ,5-10 mg]
Injectable anti-emetic [Metochlorpromide]
Tab. Aspirin,300mg (crush the tablet and give it )
Tab. Clopidogrel, 300mg
Glycerine trinitrate spray- 2 puff stat ,sublingually.

Q. In which condition Morphin cannot be given?

Ans. Bronchial asthma, COPD.

Q. Then what will you do?

Ans. Then I shall institute reperfusion therapy: Inj. Streptokinase.

Q. When you will administer streptokinase?

Ans. If the patient comes with ST elevation and within 12 hours of chest pain.

Q. How streptokinase is administered?

Ans. 1.5 million unit in 100ml of NS: 60 drops/min or over one hour.

Q. In which route streptokinase is administered: I.V. or I.M.?

Ans. I.V. in drip.

Q. What are the complications of streptokinase?

Ans. a) hypotension b) bleeding manifestation

Q. What are the follow up you will give after administration of streptokinase?
ans. I shall regularly measure the B.P. to see hypotension.

3
Q. What are the contraindications of thrombolytic therapy or streptokinase?
Ans.
Active internal bleeding
Previous sub-arachnoid haemorrhage/ Intracerebral haemorrhage.
Uncontrolled hypertension
Recent surgery
Active peptic ulcer disease
Pregnancy

Q. How will you understand that streptokinase is working?

Ans. By seeing the ECG- reperfusion arrhythmia.

Q. A patient was administered streptokinase 2 years back. Now he developed M I. Can he take
streptokinase again?
Ans. No. Because, as he took streptokinase before, there is developed antibody against
streptokinase.

Q. Then what drug he will take now?

Ans. Now he will take Alteplase [tissue plasminogen activator].

Q. For how long the antibody persist?

Ans. Up to 5 years.

Q. If this patient of MI goes to higher center, what could be done?/ What are the interventions in
MI?
Ans. In higher center, we can do:
PCI [primary percutaneus coronary intervention]
CABG [ coronary artery bypass grafting]

Q. In CABG which artery is used?

Ans. Internal mammary artery or great saphenous vein

Q. What will you give if a patient comes 12 hours later of MI or have no ST elevation or non Q
wave MI?
Ans. Here we give low molecular weight heparin. Name Enoxaparin (1unit/kg), [trade name
claxene].

Q. How it is given?
Ans. It is given subcutaneously, 12 hourly for 5-7 days.

Q. What is the most dangerous complication of MI?

Ans. Ventricular fibrillation (VF).

Q. What are the immediate causes of death after MI?

Ans. VF, Cardiac arrest/ asystole.

4
Q. Mention the complications of MI.
Ans.
1) Arrhythmia (tell the names of every arrhythmia)
VF
Ventricular tachycardia
Ventricular ectopic
AF
Atrial flutter
SVT
A-V block
Complete heart block
2) Cardiogenic shock
3) Heart failure
4) Pericarditis
5) Late complications:
Rupture of papillary muscles
Rupture of interventricular septum
Ventricular aneurysm

Q. What do you mean by Dresslers syndrome?

Ans. Persistent fever, pericarditis, pleurisy occur few week after MI.

Q. Mention the secondary prophylaxis of MI.

Ans.
Aspirin 75mg daily
Clopedogrel 75mg daily
- blocker
ACE inhibitor
Management of hyperlipidaemia statin Atorvastin
Stop smoking.

Q. Which MI is worse- anterior MI or inferior MI?

Ans. Anterior MI is worse. Because it causes arrhythmia. Inferior MI causes only bradycardia.

Heart failure

Q. A patient came to you with sudden, sever respiratiory distress. What are the differential
diagnosis?
Ans. First say,
Acute LVF with pulmonary edema
Tension pneumothorax
Next you may say,
Acute severe asthma
Acute exaggerations of COPD

5
Q. What are the causes of left ventricular failure?
Ans.
1st cause- Systemic hypertension
MI -2nd cause
AS (aortic stenosis )
Q. What are the cardinals sings of LVF?
Ans.
Pulsus alternus/ Tachycardia
Gallop rhythm
Bilateral basal creps
Q. What will be the management?
Ans. Frist say the following three:
Propped up position
High flow O2 inhalation
Diuretic: Inj. Frusemide ,I.V. up to 160mg (1 amp Lasix= 20mg, Tab. Lasix=40mg)
If sir wants to know more, then say the followings
Glycerinetrinitrate
ACE inhibitor
In some cases, opiate or morphin.
Q. What are the causes of right heart failure/ CCF?
Ans.
PHTN
Cor pulmonale
VSD/ASD
Anaemia
MS
Q. What are the cardinal features of CCF/ right heart failure?
Ans.
Raised JVP
Tender hapatomegaly
Dependent edema
Q. What is the management of right heart failure?
Ans.
Propped up position
Low flow O2
Injectable diuretic
Q. What are the complications of heart failure?
Ans. To remember (RATE )
R-Renal failure
A-Arrhythmia
T-Thromboembolism
E--Electrolyte imbalance: hyponatramia, hypokalaemia, hyperkalaemia.
Impaired liver function

6
Q. What is systolic heart failure and what is diastolic heart failure?
Ans.
systolic heart failure diastolic heart failure
When heart fails in systole, that means reduced When heart fails to dilate
contractility Or poor diastolic filling
e.g.- M I, cardiomyopathy e.g. constrictive pericarditis,
restrictive cardiomyopahty.

To remember the causes of heart failure, you may see the chart, but do not write in the exam
paper.
Pressure overload Volume Muscle,
Type of heart failure overload Usually biventricular
Visible Invisible
pressure pressure due to
Due to valve HTN
stenosis
LV AS Sys. HTN MR, AR Cardiomyopathy
MI /IHD
RV PS P. HTN PR, TR Cardiomyopathy
(uncommon) MI /IHD
VSD, ASD,
anaemia,
pregnancy,
thyrotoxicosis

Volume overload occurs to that chamber of the heart which is weaker. LH is stronger than RH
due to more pressure. So in case of VSD, ASD, anaemia, pregnancy- there is right heart failure.
Q. In systemic hypertension, which type of heart failure occurs?
Ans. LHF

Q. In aortic stenosis, which type of heart failure occurs?

Ans. LHF

Q. In VSD, ASD, anaemia which type of heart failure occurs?

Ans. RHF

Q. In mitral stenosis, which type of heart failure occurs?

Ans. RHF (you will fail if you tell LHF in MS).

Q. Define dyspnea.
Ans. Dyspnoea can be defined as an unpleasant subjective awareness of sensation of breathing.

7
Q. Define orthopnea.
Ans. Dyspnea in lying position

Q. Define PND.
Ans. It is a sudden severe breathlessness which wakes the patient form sleep.

Q. What are the causes of sudden death?

Ans.
MI
AS
Hypertrophic cardiomyopathy
DCM

Atrial fibrillation
Q. What are the causes of atrial fibrillation?
Ans. Mnemonic: MITHA
M- mitral stenosis
I- IHD
T- thyrotoxicosis
H- hypertension
A- alone (lone atrial fibrillation)
Q. What are the causes of irregularly irregular pulse?
Ans.
AF
Atrial flutter with variable block
Multiple ventricular ectopics
Then sir may ask question from AF
Q. What are the treatment of AF?
Ans.
Rate control
Rhythm control
Restoration sinus rhythm
Q. What are the drugs used in AF?
ans. Mnemonic: ABCD
A- amidarone
B- -blocker
C- calcium channel blocker: verapamil, diltiazem.
D- digoxin
Q. which drug commonly used?
Ans. -blocker
Q. which drug used in a patient with MS?
Ans. Digoxin

Q. which drug used in a patient with bronchial asthma ?

Ans. Diltiazem (Ca- channel blocker).

8
Q. What are the complications of AF?
Ans. 1.Thromboembolism
2.Heart failure/ acute pulmonary edema

Q. A patient with AF came to you with unconsciousness or right sided hemiparesis. What is your
diagnosis?
Ans. AF with stroke due to thromboembolism.

Q. A patient with AF came to you with dyspnoea. What is your diagnosis?

Ans. acute pulmonary edema.

Q. What is pulsus deficit?

Ans. In atrial fibrillation, heart rate is more than pulse rate. This is called pulsus deficit.
Q how will u see it ?
Ans. Simultaneously you have to see pulse and heart rate

Q. What will be your approach to a patient of AF?

Ans. A patient with AF , following things must be seen:
Pulse: irregular/ pulsus deficit
BP: HTN- cause of AF
Look for: thyroid gland and features of thyrotoxicosis
Auscultate: For murmur- MS & variable heart sound
Chest pain- IHD

Hypertension
Q. In your chamber, you found a patient with BP 190/95 mm of Hg. What will be the approach
to this patient?
Ans. Sir, I shall take some history, do some clinical examination and suggest some investigations
to find out etiology, co-morbid conditions and to see complications (target organ damage).

History: Age, family history, Drug- steroid, in female- OCP

Appearance: Cushing syndrome (to exclude 2ndaries)
Anaemia: present in CRF
Xanthalesma:
Pulse: radio-femoral delay coarcation of aorta
Apex beat: heaving due to HTN
Heart sound: loud 2nd heart sound, murmur
Gallop rhythm and basal crep: LVF
Abdomen: Palpable kidney PKD, Renal bruit renal artery stenosis
Oedema: Renal failure
Funduscopy: to see retinopathy
Investigations: given below.

9
Q. A patient of 15 years age came to you and you found his BP 150/100 mm of Hg. What will be
the cause?
Ans. Here answers will be the secondary causes: AGN and other causes.

Q. A newly married female patient came to you and you found her BP 160/90 mm of Hg. What
may be the causes?
Ans. May be due to OCP.

Q. Classify HTN.
Ans.
1) Primary or essential: 95%
2) Secondary: 5%

Q. Name some secondary causes of hypertension.

Ans.
Renal Drug Endocrine (all the endocrine disease other
except Addisons disease)
AGN Steroid Cushing syndrome Renal artery
Polycystic kidney OPC Conns disease stenosis
disease Acromegaly
Renal artery stenosis Thyrotoxicosis
Phaeochromocytoma
Hypothyroidism

Q. Mention the grading of BP.

Ans.
Category Systolic Blood pressure Diastolic Blood pressure
( mm of Hg) ( mm of Hg)
Normal <140 <90
Hypertension
Grade 1 140-159 (to remember: add 20) 90-99 (to remember: add 10)
Grade 2 160-179 100-109
Grade 3 180 110

Q. What do you mean by isolated systolic hypertension?

Ans. When systolic BP >140 mm of Hg, but diastolic BP <90 mm of Hg.
Category Systolic Blood pressure Diastolic Blood pressure
( mm of Hg) ( mm of Hg)
Grade 1 140-159 <90
Grade 2 160 <90

10
Q. What do you mean by White coat hypertension?
Ans. When a patients BP becomes elevated when he goes to the doctor, but otherwise, his BP is
normal, this incident is called White coat hypertension.

Q. Mention the grading of hypertensive retinopathy.

Ans. Mnemonic: SAC in Prem (prem means --love)
Grade 1 [S] Silver wiring
Grade 2 [A] Arteriovenus nipping
Grade 3 [C] Cotton wool exudates + flamed / blot haemorrhage
Grade 4 [Prem] Papilloedema

Q. How will you differentiate between diabetic and hypertensive retinopathy?

Ans.
Diabetic retinopathy Hypertensive retinopathy
Dot haemorrhage Arteriovenus nipping
Hard exudates Cotton wool exudates + flamed / blot
Neovasculization haemorrhage
Papilloedema

Q. what are the target organs of hypertension?

Ans.
Brain
Retina
Heart
Kidney
Blood vessel
Q. What are the complications of hypertension?
ans.
Brain: stroke
Retina: Retinopathy
Heart: Coronary artery disease, AF, LVH
Kidney: Renal failure
Blood vessel: atherosclerosis

Q. What investigations you want to do?

Ans. To see complications:
ECG: Left ventricular hypertrophy
Echocardiography: Left ventricular hypertrophy / LVF
CXR: Left ventricular type cardiomegaly
Urine RME Protein, to see nephropathy
Serum creatinine , to see nephropathy
Others:
Urinary catecholamine pheochromocytoma

11
 Renal USG: to diagnose PKD
RBS and lipid profile

Some 1st choice of antihypertensive drugs in following conditions:

DM: ACE inhibitor/ receptor blocker
CRF: ACE inhibitor + then calcium channel blocker+ vasodialator
MI, Stroke: ACE inhibitor
Heart failure: ACE inhibitor + diuretic
IHD: - blocker.

Antihypertensive drug

A- ACE inhibitor-
Ramipril
Captopril
A-Angiotensive receptor blocker
losartan
valsartan

B-Beta blocker
Cardioselective
Metoprolol
Atenolol
Combined - and -adrenoceptor antagonists .
Carvedilol
Nonselective
propranolol used in anxiety, palpitatinon and portal HTN

C-Ca channel bIocker-

dihydropyridines
Amlodipine (vasa-selective)
Rate-limiting calcium antagonists
Diltiazem (intermediate)-
Verapamil ( cardioselective ) -use in SVT

D- Diuretic
Thiazide -Indepamide

D- Vasodilator
-blocker Prazosin

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Commonly asked questions

Which ant HTN drug given in DM? ACE I/ ANG.BLOCKER

Which ant HTN drug given in HEART FAILURE? ACE I/ ANG. BLOCKER Ramipril
plus
DIURETIC
Which ant HTN drug given in IHD? BETA BLOCKER
Which ant HTN drug given in CRF? ACE I/ ANG.BLOCKER next
Ca CHANNEL BLOCKER next
Alpha BLOCKER next
WITH DIURETIC
AT LAST BETA BLOCKER
Which ant HTN drug given in STROKE I CVD ACE I/ ANG.BLOCKER Ramipril
Which ant HTN drug given in isolated systolic HTN Ca CHANNEL BLOCKER Amlodipine
DIURETIC
which ant HTN drug given in COPD Ca CHANNEL BLOCKER

ACE inhibitor I Angiotensin receptor blocker

indication contraindication
DM Hyperkalaemia
CKD Oligouria or ARF
CVD In hypovolaemic patient
HEART FAILURE Pregnancy and Renal artery stenosis
LV dysfunction / hypertrophy /DCM CLD
POST MI COPD
SIDE EFFECT
Dry cough
Postural hyopotension- to avoid it, give first dose at night

BETA BLOCKER
Indications Contraindications
Myocardial infarction Bronchial asthma/ COPD
Angina Heart block /if pulse less than 60
Heart failure stable--only carvedilol DM
Atrial fibrillation Psoriasis
PVD
Heart failure (can be used in Carvedilol
compensated heart failure)
Why beta blocker is not used In DM:
it will mask the sign +symptoms hypoglycaemia (tremor I tachycardia I sweating )

13
Before giving beta blocker see following:
H/O DM, COPD. asthma, heart failure, Auscultate lung for spasm and pulse for bradycardia

Ca channel blocker
Indications Contraindications
Amlodipin- Heart block
Any patient/Elderly patient without Heart failure
heart failure
Isolated systolic HTN Complications
CRF Amlodipin
COPD/ Bronchial asthma Flushing of face, headache
Verapamil (240 mg daily) Palpitation
Can be useful when hypertension Fluid retention
coexists with angina Verapamil
Verapamil used in SVT Constipation
Diltiazem
Bradycardia

Hypertensive crisis
Hypertensive emergency
Hypertensive urgency

Hypertensive emergency
Severe elevation of BP > 180 /120 mm of Hg complicated by evidence impending or
progressive target organ damage.
They require immediate reduction of BP ( not necessarily to normal )

Example of hypertensive emergency

HTN Encephalopathy
Intracerebral haemorrhage
Acute MI
Acute LVF
Acute pulmonary edema
Unstable angina
Eclampsia

Management of hypertensive emergency

Treatment in ICU with monitor
Parental administration of Anti- HTN drugs.
Goal of therapy is to BP not more than 25 % in 1st hour.
Then target BP 160/110 mm Hg in next 6 hrs
Sudden fall may cause
Cerebral ischemia

14
 Renal ischemia
Coronary ischemia
Then reduction of BP to normal in next 24-48 hours.

Hypertensive urgency
Severe elevation of BP with target organ damage
Upper level of stage ii with
Severe headache
Epistaxis
Dyspnea
Severe anxiety

Acute rheumatic fever

Q: scenario: A 13years old boy comes with fever & multiple joint pain & swelling
(polyarthritis). What is your diagnosis?
A: Acute rheumatic fever.

Q: Mention the diagnostic criteria.

A:
Major criteria:
Migratory polyarthritis(75%)
Carditis
Sydenhams chorea
Subcutaneous nodule
Erythema marginatum

Minor criteria:
Fever
Arthralgia
Elevated acute phase reactants (e.g. high ESR,CRP)
Prolonged P-R interval

Evidence of group A streptococcal infection

Raised ASO titre
Positive throat swab culture
Recent scarlet fever
The diagnosis of acute rheumatic fever is made when there is
2 major criteria or,
1 major +2 minor +
Supporting evidence of group A streptococcal infection

15
Q: Which organism is responsible for RF?
A: Group A haemolyticus streptococcus (S.pyogens)

Q: How many days are required for development of RF?

A: 2-3weeks (pt. has a H/O of sore throat i.e; pharyngitis)

Q: Why 2-3weeks are required after sore throat?

A: For antibody formation.

Q: What type of hypersensitivity reaction is it?

A: Type -2.

Q: What do you mean by migratory polyarthritis?

A: It means a joint is involved, when it resolved another joint is involved.

Q: What type of carditis is it?

A: pancarditis (all the 3layers is involved)

Q: What are the features of pancarditis?

A:
Endocarditis: murmur due to valvular involvement
Myocarditis : conduction defect, cardiomegaly (HF), tachycardia
Pericarditis: pericardial effusion & rub , pain
Q. how will understand pericarditis ? pain & rub
Q. How will understand myocarditis ? Feature of heart failure and tachycardia
Q. How will understand endocarditis ? feature of changing murmur
Q: What is Carey Coombs murmur?
A: It is a soft mid-diastolic murmur due to vulvulitis.
Q: What is the common age of RF?
A: 5-15years.

Q: Causes of HF in ARF?
A:
o Myocarditis
o Vulvular causes (MR, AR)

16
Q: Rx of ARF?
A:
Bed-rest (Next Q: How many days? > The duration should be guided by symptoms
along with temperature, leucocyte count & ESR. It should be continued until these have
settled)
Aspirin 60-100mg/kg BW/day in 6 divided dose. Continue until ESR falls and then taper
gradually.
Steroid (If severe arthritis or carditis): Tab. Prednisolone 1-2mg/kg BW/day
Antibiotic (to eliminate residual streptococcal infection)
Inj. Benzathine pencillin 1.2million unit 1ampule I/M stat. or,
Tab. Phenoxymethyle penicillin 250mg, 6hourly for 10days

Q: Which should be done before administration of Benzathine penicillin?

A: skin sensitivity test should be performed to prevent Hypersensitivity/anaphylactic reaction.

Q: Complications of Aspirin.
A: Nausea, vomiting, tinnitus, deafness and metabolic acidosis*.

NB: if pain is not subsided within 24hours, then it suggests that it is not due to RF.

Q: What should be done for secondary prevention?

A:
Inj. Benzathine penicillin 1.2million U 1amp I/M monthly.
Or,
Phenoxymethyl penicillin 250mg 1+0+1.

Next Q: How many days?

A:
If RF without residual heart disease upto 5years last attack or until 21 years
whichever is longer.
If RF with residual heart disease continue upto 10years of last attack or until
40years or lifelong.

NB: If there is penicillin allergy, erythromycin can be used.

Q: What are the complications of RF?

A:
Acute: HF
Chronic: MS, MR or aortic Valvular disease.

17
Q: What is the mechanism of development of MS?
A: Repeated RF cause progressive fibrosis & thereby cause MS.
Q. scenario : 15 yr old male comes to u with fever and increased ASO titer will u start anti-
rheumatic fever treatment or prophylaxis ?
Ans. No I will not started anti-Rheumatic drug . I look for major criteria and minor criteria if it
fulfilled then only start drug .
Q: What is the pathognomic feature of RF?
A: Aschoff nodules (multinucleated Giant cell surrounded by macrophage & T-lymphocytes)

Important

Name of Pulse Apex Heart sound Murmur

murmur beat
MS Normal /as Tapping Loud 1st HS , Mid-diastolic in mitral area, which
like AF opening snap is low-pitched, localized, rough,
rumbling (LLRR), best heard with
bell of stethoscope, if left lateral
position breath hold after
expiration, with presystolic
accentuation.
MR Normal Thursting Soft 1st HS Low blowing pansystolic murmur
best heard at apex & radiate to left
axilla
AS Slow rising Heaving Soft 2nd HS Harsh high pitched ejection
systolic murmur best heard in
aortic area sitting & leaning
forward with breath hold
expiration & radiate to right side
of neck.
AR Collapsing Thursting High pitch blowing ejection
systolic murmur best heard at left
parasternal area sitting & leaning
forward with breath hold
expiration.

18
 Infective endocarditis
Q: Scenario: A pt. comes to you with fever for 2weeks. On examination there is clubbing, rash,
splinter haemorrhage, there is also changing murmur & splenomegaly. What is your diagnosis?
A: Infective endocarditis.
Rx: according to culture report.

Q: What investigation you want to do?

A: Blood culture & echocardiography.

Q: Name some organisms that cause infective endocarditis?

A:
Staphylococcus aureus
Streptococcus viridians
Streptococcus epidermidis
HACEK ( Haemophilus, Actinobacillus, Actinomycosis, Cardiobacterium hominis,
Eikenella spp. , Kingella kingae)

Complete heart block

Q: Cause of complete heart block?

A:
Acute MI (inferior)
Drug ( mnemonic- BAD: -blocker, amiodarone, digoxin)
Cardiomyopathy

Q: Clinical feature:
A: Symptom: Blackout, Syncope and Dizziness
Pulse: Regular but bradycardia
JVP: Cannon wave
Complications: Stoke Adams attack

Rx: -If Bradycardia - Inj.Atropin

-Temporary pacing followed by permanent pacing

Q: Scenario:A pt. comes to you with sudden loss of consciousness & fall. On examination
pulse is 30-35beats/minutes. What is your Diagnosis?
A: Complete heart block with Stoke Adams attack.

19
Q: What is the Rx of 1 & 2 heart block?
A:
1 HB & 2 HB Type-1 No need of Rx
2 HB Type-2
o If due to Inferior MI:
-Asymptomatic: No Rx
-Symptomatic: Inj. Atropine

o If due to Acute Anterior MI: Temporary pacing followed by permanent pacing.

Q: Sequele of 2 HB.
A: mnemonic--HSC
a. C-Complete HB
b. S-Stoke Adams attack
c. H-Heart failure

Q: Name some cyanotic heart diseases?

A: Tetrology of Fallot, transposition of great vessel, tricuspid atresia with pulmonary atresia,
Ebstein anomaly.

Q: What are the components of tetrology of Fallot?

A: mnemonic: PROVed
Pulmonary stenosis
Right ventricular hypertrophy
Over riding of aorta
Ventricular septal defect.
Q: What is the presentation of TOF?
A:
Clubbing
Cyanotic spell /Fallots spell (pt. becomes cyanosed after crying or feeding and may
become apnoeic or unconscious & relief by squatting position)

Q: VSD/ASD- cyanotic / acyanotic heart disease?

A: acyanotic.

NEXT Q: Can they be cyanotic??

A: Yes, they may develop cyanotic heart disease if associated with reverse shunt (Rt
Lt) [Eissenmenger Syndrome]

Please see the following topics from short case

MS
Tachycardia & bradycardia
Heart sound
Venous & arterial pulsation

20
Q: What are the causes of acute pericarditis?
A: In our country: TB
Foreign: Viral
Then: MI, Uraemia, Malignancy, Connective tissue

Q: Clinical features of Pericarditis.

A: Pain & pericardial rub

If there is effusion:
o Apex beat non palpable
o Area of cardiac dullness
o Heart sound-muffle
o JVP

Q: What is the X-ray finding of pericardial effusion?

A: Globular / Pear shaped heart with oligaemic lung field

ECG : low voltage ECG

Echo : confirmatory

Q: What do you mean by Cardiac tamponade?

A: It is a term used to describe acute heart failure due to compression of heart by large or rapidly
developing pericardial effusion.
Rx: Pericardial aspiration.

Q: What Rx should be given for the following cases?

A:
Pericardial effusion with TB : - Anti TB
- Steroid ( 3 months)
Pericardial effusion with uraemia: dialysis.
Q: What is the indication of use Steroid in pericardial effusion?
A: Pericardial effusion due to TB.
(Advantage of use:
1) Early absoption
2) Prevent adhesion)

Q: What is constrictive pericarditis?

A: It is the condition where pericardium became progressively thickened, fibrosed & calcified.
So the heart encased in a solid shell & cant fill properly.
C/F of constrictive pericarditis /Cardiac tamponade:
o Low volume pulse
o Raised JVP
o Kussmaul sign ( Paradoxic raised of JVP in inspiration )
o Hepatomegaly

21
 o Ascites
o Pulsus paradoxus ( excessive fall of BP during inspiration)
o Oedema

Q: Scenario: A pt. comes to you & on examination you get early diastolic murmur in left lower
sterna area with high volume pulse, what is your diagnosis?
A: AR

Q: Scenario: A pt. comes to you & on examination you get ejection systolic / a systolic murmur
murmur in aortic area with radiation to neck and low volume pulse, what is your diagnosis?
A: As

Q: Scenario: A pt. comes to you & on examination you get diastolic murmur in mitral area with
loud first heart sound , what is your diagnosis?
A: MS

Q: Scenario: A pt. comes to you & on examination you get systolic murmur in mitral area with
radiation to axilla , what is your diagnosis?
A: MR

22
 GIT and Pancreatic Disease
Q: 30 years old man come to you with haematomesis and malaena. How will you approach?

A:

First, I will resuscitated the patient.

See- Pulse, B.P, Urine output.
Then open I.V. Channel,
Blood grouping and cross matching and give one unit of fresh blood ,
inj. P.P.I,
Tab.Sucralfate(1+1+1+1)

Q: What are the causes of upper GIT Bleeding / Haematomesis?

A:

1.Peptic ulcer disease

2.gastric erosion
3.Carcinoma of stomach
4. esophageal varies
5.esophagytis

Q: what is the most important one investigation for Upper GIT Bleeding?

A: Upper GIT endoscopy

Q:What is the Definition of malaenae?

A: Black tarry offensive stool.

Q: what are the causes of haematocrazia?

A:

hemorrhoids
Anal fissure
Diverticulitis
Cancinoma rectum
Polyps

23
Q: a patient with CLD comes with haematomesis and melaena. What wiil you do?

A:

Initial Rx- resuscitation, see pulse , blood pressure , urine output

-I.V. fluid

-Blood grouping and Cross matching

-Give one unit of blood

-Do emergency endoscopy

. sclerosis therapy
.band and ligation
.balloon tamponade

Medical Rx

Vesopress- such as terlipressin

-give antibiotic to prevent SBP

What is the definite treatment ?

TiPSS- Transjugular intrahepatic Protosystemic Slent Shunnting

Q. 30 years old female comes to you with epigestric pain . what will be the diffential;
diagnosis?\

A: Acute exaggeration od PUD

Acute cholecyctitis

Acute pancreatitis

Q: how will you approach the patient?

PUD- epigestric pain, recurrent episodic pain; if relief by food-in duodenum, if increase by food-
in Gastric

Duodenal point is tender

Acute cholecystitis- in epigastric and right hypochondrium region, Murphys sign present

Acute pancreatitis- severe pain, pain radiate to back, patient in knee-elbow position.

24
Q What Investigation for patients:

1st USG of whole abdomen- acute cholecystitis or acute pancreatitis.

Q. If normal then,

Do upper GIT endoscopy

Q .If u suspect perforation or intestinal obstruction ,

Do plain X-ray of abdomen in erect position

Q. If u suspect pancreatitis , do Serum amylase with in 24 hours(24 to 48 hours)

Q.If patient comes after 24 hours, do urinary amylase

Other investigation- USG of whole abdomen,

Q. if can not be diagnosed by that or for more specific test- CT scan

And to see complication-RBC,CBC, S.calcium, S.Creatinin

Q: how will you see the prognosis or severity of this patien?

A: By CRP

Q. what will be the treatment?

A. diet-nothing per oral

-NG Feeding

-I.V. fluid (3 liter in adult)

-injection. Broad spectrum antibiotic (ceftriaxon/cefuroxime/imipenem)

-Analgesic (inj.pathedin/ opiate analgesic)

-Inj. PPI

-I/O chart

Q. what are the causes of pancreatitis

A G-. gall-stone
I-idiopathic
A-alcohol
ERCP--post ERCP
(to remember:GIA-ERCP)

25
Q. Complication of acute pancreatitis?

a. 1.Systemic Inflammatory Response Syndrome(Sirs)

2. Hypoxia

3. hypo-albominia

4. hypo-calcaemia

5. hyperglycemia

Local- N-Necrosis,A-- Abscess, P--pseudocyst, A--ascitis(NAPA)

(For remember: Sirs, 3 hypos, 1 hyper, NAPA)

GIT complication-

V--Variceal bleeding

E-Erosion of colon

D--Duodenal obstruction

I--Upper GIT Bleeding

O-Obstructive jaundice

(For remember: VEDIO)

Q. what are the non-abdominal causes of that patient?

A. MI

Right lower lob pneumonia

Q. What are the causes of hyperglycaemia with abdominal pain?

A.Pencreatitis

DKA

Q. When Pencreatic Pseudocyst need surgical removal?

A. If it become more than 6 cm

Rx- Drainage in stomach , duodenum, after 6 weeks(because pseudo capsule takes 6 week to be
matured)

26
Q. when ERCP is needed?

A. if pancreatitis is associated with jaundice

Q. who many days after pancreatitis, cholecystitis can be done?

A. 2 weeks later

q. A patient comes to you with recurrent upper bdominal pain with diarrhea specially after falts
good. And the patien is cachectic. What will be you diagnosis?

A. chronic pancreatitis

Q. what are the causes of chronic pancreatitis?

A.

C-Hypercalcemia

O-Obstruction/ obstructive(ductal adenocarcinoma or pancrease division or spheiler oddislener)

C-CRF

A-Alcoholism

(to remember: COCA)

Q. what are the clinical features?

A.

-Patient is cachectic and lean &thin

-recurrent upper abdominal pain
-Malabsorption- Stealorrhoea(bulks of pale and offensive stool, which float in the toilet,
due to fat malabsorption)
-Patient may have DM
Pain relief by Alcohol consumption.

Write down the treatment ?

Fat free diet and stop alcohol

Enzyme supplementation(pancreatic enzyme)
Pain killer: NSAIDs, Antispasmodic
PPI(because it optimizes duodenal pH for pancreatic enzyme)

27
Q. what are the investigations for the diagnosis of chronic pancreatitis?

A.
USG
CT
Plain X-ray of abdomen to see stone
MRCP

Q. a patient comes to you with different lump in region. What are the causes?

A. if epigastric region-

Carcinoma stomach
Ca- left lobe of liver
Pancreatic pseudocyst
Ca transverse colon

If hypochondrium region-

Right lobe of liver

Palpable gall bladder

If right iliac fossa-

Appebdicullar lump
Ileo-caecal TB
Caecal carcinoma

If left iliac fossa-

Ca sigmoid colon
Viverticular mass
Stool/ impaoted stool

Q. what are the most common types of Peptic ulcer disease?

A.

duodenal ulcer
gastric ulcer

28
Q. what is the difference between ulcer and erosion?

A. Ulcer involved the muscularis mucosa but erosion not involves

Q.Causes of PUD?

A.

H.Pylori
NSAID
Smoking

Q. causes of erosion?

A. NSAID

Q.Difference between gastric ulcer and duodenal ulcer

A.

Gastric ulcer Duodenal ulcer

Usually single multiple
Turns into melignancy Not so
Pain increases after food taking Pain relives after food taking

Q. which one is worse?

A. Gastric ulcer, because there is a chance of malignancy.

Q. when we need to take biopsy during endoscopy?

A. Gastric ulcer

Q. what are the investigation?

A.Upper GIT Endoscopy

Q.what is h. pylori?

A. gram negative bacteria

Q. h.pylori is responsible for which malignancy?

A. MALToma, Gastric lymphoma

29
Q. what are the complication of PUD?

A.

Haemorrhage(Haematomesis , malaena)
Gastric ulcer(Carcinoma)
Perforation
Gastric outlet obstruction

Q. what are the treatment?

A. Eradication of H. pylori

Triple therapy one strip on the morning and one strip at night

One strip contains the following (Tab. Amoxicillin 1 gm, Cap. Clarithrimycin 500mg,
Cap. PPI 20 mg)

Q Duration of triple therapy ?

For 7 days

Q Then what will u give after 7 days , ?

Cap.PPI for 2 months

Q. what are the complication of h. pylori therapy?

A.

D-Diarrhoea
R-Rash
C-Clostrideum difficle associate colitis
A-Abdominal pain/cramp
N-Nausea, vomiting

(to remember- DR.CAN)

Q. Name some indication of h.pylori treatment ?

A.

PUD
H.pylori paritive dyspepsia
MALToma

30
Q. What are the investigations for diagnosis?

A. non-invensive

Urea breath test

Serology test

Invasive

Rapid urease test

Histology
Microbiological culture

Q. What is Zolliger-Ellison syndrome?

A. it is a disorder characterized by severe peptic ulcer, gastric acid hyper secretion ann non-beta
cell eslet tumour of the pancrease(gastrioma)

Q. name some functional bowel disorder?\

A.

IBS
Pshychogenia dysphagia
Volumia nervosa
Anorexia nervosa

Q. what are the causes of chronic diarrhea?

A.

IBD
IBS
Chronic pancreatitis
Celiac disease
Malsbsorption
Colonic neoplasm

A 20 years female comes to you with history of frequent loose stool proceed by abdominal pain
without nocturnal symptom? What is your diagnosis?

A. IBS

31
Q. what are the clinical features of IBS?

A.

Abdominal pain/cramp/colic
Pain relief by Defecation
Alternation of bowel habit
More on day and nocturnal symptom free.

What are the Alarming sign?

Age>50 years
Weight loss
Fever
Anaemia
Rectal bleeding

D/D- IBD,Neoplasm of colon, Malabsorption

Q. what will be the investigation?

A. no investigation is needed .do only exclude malignancy

ESR---normal
Colonoscopynormal

Q. what will be the treatment?

A. treatment

Diarrohoea predominant Constipation predominant

Reassurance
Diet: Avoid fiber diet, wheat free, milk and
milk product
For pain: anti-spasmodic-mebeverine
For diarrohea loperamid 2-8 mg daily
TCA-tab. Amitriptyline(10 mg) at night
Reassurance
Diet: increase fibers and increase water taking
Anti-spasmodic-mebeverine
For constipation- lactilose, ispaghula
TCA-tab. Amitriptyline(10 mg) at night

Q. name of IBD?

A. Inflammatory bowel disease-1.ulaerative colitis, 2.chronns disease

Q. how will you differentiate ulaerative colitis and chronns disease?

32
A. Difference between ulaerative colitis and chronns disease

traits ulaerative colitis chronns disease

1. involvment Only colon From mouth to anus(mainly
recto-segmoid junctiom)
2.nature of lesion continuous Skip lesion
3.Ulcer Superficial ulcer Deep ulcer , crypt abscess
4. smoking relation Non smoker smoker
5. treatment Masalazin. corticosteroid MTx, steroid, Azathioprine
Q. What is the skin manifestation of IBD?

A. Erythama nodusum

Q. how will you differentiate the colonic carcinoma left side to right side?

A.

in case of right sided colon: anaemia due to malaena , alternation of bowel habit
In case of left sided colon: obstruction and fresh blood

Q. how will you approach to a patient with dysphagia? How will you differentiate these?

A.

traits Neurological dysphagia Mechanical dysphagia

Type of food Initially liquid Initially solid
onset Acute Gradual
timing Difficulties in initiating Food sticking at a specific sit /
swallowing certain point
Association Associated with chocking or Not so
nasal regurgitation

Q. what are the causes of neurological dysphagia?

A.

Bulbar pulsy
Pseudobalbar pulsy
Myasthenia graves

33
Q. Name some causes of mechanical dysphagia?

A.

Inside lumen

Ca. aesophagus
Stricture aesophagus

External: enlarge thymus, enlarge thyroid

Q. what is GERD?

A. Gastro esophageal reflex disease

Factors responsible for GERD:

Increased extra abdominal pressure

Decreased tone of lower esophageal sphincter
Diet-choclate, coffee, alcohol
Hiatus hernia
Obesity
Delayed emptying of gastric content
Pregnancy

Q .How will u diagnose this?

Diagnosis by-

1. Upper GIT endoscopy

Othe investigation
2. 24 hour intraluminal pH monitoring of the esophagus.
3. Esophageal manometry.

What are the complication ?

Esophagitis
Barretts esophagus

34
Treatment of GERD:

Avoid precipitating factor

Cessation of smoking,
loss of weight
Avoid alcohol, fatty meals & drugs e.g. nitrates.
Avoid heavy meals especially before sleep.
Raising the head of the bed at night.
should not go to bed within 2 hours of taking foods
Avoid any other precipitating factor.

Drugs-PPI 20 mg (1+0+1)

Domperidone 10 mg(2+2+2)

Endoscopy. to confirm the presence of esophagitis.

Q. write down the difference between Hematemesis & Hemoptysis:

Hematemesis Hemoptysis
Def Hematemesis is the vomiting of blood Hemoptysis means coughing out of
blood
Source GIT tract stomach and duodenum From respiratory tract
Color dark red or brown or coffee ground Bright red
due to action of gastric acid
pH Acidic pH Alkaline pH
Mixed Mixed with food Mixed with mucous
Associated Abdominal pain , nausea Cough , chest pain , resp. distress
Investigation Upper GIT endoscopy Bronchoscopy

35
 Hepato billiary
Define jaundice?

Jaundice refers to the yellow appearance of the skin, sclerae and mucous membranes
resulting from an increased bilirubin concentration in the body fluids.

Normal bilirubin level ?

When will jaundice detectable clinically?

it is usually detectable clinically when the plasma bilirubin l > 3 mg/dl) or 50 mol/

Classify jaundice?

Prehepatic or Haemolytic jaundice

Hepatocellular
Post Hepatic or Obstructive jaundice

Mention the cause of haemolytic jaundice?

Haemolysis.
Gilbert's disease.
Dubin-Johnson syndrome.
Rotor syndrome.

Mention the cause of hepatocellular jaundice?

Acute viral hepatitis,

Alcoholic,
Autoimmune,
Drug-induced
Cirrhosis
Mention the cause of obstructive jaundice?

Causes of cholestatic jaundice

Extrahepatic

Choledocholithiasis
Carcinoma
Ampullary
Pancreatic
Bile duct (cholangiocarcinoma)
Secondary
Parasitic infection

36
 Intrahepatic

Viral hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Alcohol
Drugs
Autoimmune hepatitis
Pregnancy

How will u differentiate these three types of jaundice?

Haemolytic Hepatocellular obstructive

jaundice less moderate to severe severe
anemia more marked absent absent
hepatospleno present absent absent
megaly
stool pale normal color normal color
itching absent usually not present
viral prodome absent present absent
nausea , Malaise
investigation
Bilirubin unconjugated mixed conjugated
SGPT/ ALT >6 times
Alk.phosphatate > 2.5 times

Name some causes of viral hepatitis?

Common causes:

Hepatitis A
Hepatitis B hepatitis D
Hepatitis C
Hepatitis E
Uncommon causes:

Cytomegalovirus
Epstein-Barr virus
Herpes simplex
Yellow fever

37
Route of transfusion?

Oro-faecal route ---A & E

parental route ----B & C

D-virus how transmit?

IF only B infected patient

How does hepatitis D spread along ?

The hepatitis D virus (HDV) is an RNA-defective virus which has no independent

existence; it requires HBV for replication . it infected people only in presence of HBV
infection
which virus is more spread via IV drugs User ?

HCV mainly spread between IV drugs user

which one is DNA virus ?

Hepatitis B
which virus have chronic form ?

Hepatitis B & hepatitis C

What investigation you want of do?

Liver function test

SGPT (ALT)
Alkaline phosphatase
S. Blirubin
Prothrobin time
Viral marker

HBs Ag
Anti HAV
Anti HEV
Anti HCV
USG of hepato billiary system

What will be the finding of liver function test in viral hepatitis?

SGPT/ ALT >6 times

Alk.phosphatate < 2.5 times

38
What are the complications of viral hepatitis?

Acute liver failure.

Cholestatic hepatitis.
Aplastic anaemia.
Chronic liver disease and cirrhosis (hepatitis B and C).
Relapsing hepatitis .

What is fate of viral hepatitis ?

In Most of viral hepatitis the fate is complete resolution.

Plus above complication.
What is the most dangerous complications of viral hepatitis ?

Acute liver failure

Which one has more chance of turn in to chronic viral hepatitis between B @C?

or which form of viral hepatic needs treatment ?

Acute B viral hepatitis no needs of treatment --- 95 % resolve spontaneously

Acute C viral hepatitis needs of treatment ----- 95 % turn into chronic

What is the mechanism of jaundice viral hepatitis A, B, E ?

HAV , HBV cause viral hepatitis by immunological mechanism

HEV ---Here jaundice occur due to direct cell destruction that why it is cytopathic

Why jaundice is more severe / deep acute viral hepatitis than CLD ?

In CLD jaundice less because here hepatocyte are fibrosed

Mention the route of transfusion of HBV?

parental

Transfusion of blood and blood product

Sexual exposure
IV drug user
Vertically from mother to child

39
A patient comes to you with deep jaundice for 1 month what may be the cause?

It may be due to hepatitis E virus

Which viral hepatitis is dangerous in pregnancy and at which trimester ?

hepatitis E and at last trimester

Classification of acute hepatic failure

Hyperacute < 7 days

Acute 8-28 days

Subacute 29 days-12 weeks

What do u mean by Non-A, non-B, non-C (NANBNC) or non-A-E hepatitis ?

Non-A-E hepatitis is the term used to describe hepatitis thought to be due to a virus that is not
HAV, HBV, HCV or HEV.

Mention the anti viral therapy in hepatitis B virus ?

acute ---no antiviral therapy

chronic carrier -- no antiviral therapy and observe only
chronic active hepatitis anti viral therapy

Mention the criteria of and will be the treatment of carrier ?

Criteria for carrier

1. HBs Ag positive > 6months

2. ALT normal
3. HBV-DNA level undetectable
4. Biopsy: minimal hepatitis ( Knodal score )
5. anti- HBc ( + )
if all these are positive than it is carrier

What treat u will give the patient?

No treatment is needed
Do the following

Patient will do normal activity

Stop smoking and alcohol consumption as it aggravate CLD
Do not donate blood

40
 Sexual partner should be vaccinated
Breast feeding allowed
When will u tell chronic active hepatitis?

Chronic active hepatitis

1. HBs Ag positive > 6months

2. ALT > 2 times (persistent / intermittent )
3. HBe Ag +
4. HBV-DNA level > 10 5 copies
5. Biopsy: moderate / bridging hepatitis ( Knodal score )

A single test to diagnosed chronic viral hepatitis?

Anti-HBC Ig G

Name some anti-viral drug use in chronic hepatitis B virus?

Dug use in HBV

Interferons/ Pegylated interferons

Adefovir
Lamivudine

What will u do A patient comes to u with HBs Ag positive and wants to go foreign?

Or patient with HBs Ag positive and want to make it negative?

No , He cannot go to foreign as there is no chance of spontaneous Removal of HBs Ag(

chance of spontaneous recovery 0.5% year )
Interferon can clear the virus 10 % per year , no role of oral anti viral therapy
Come to 6 month later and Repeat HBs Ag if positive then look for whether it carrier and
chronic Active hepatitis

If doctors get needle is stick injury what Will u do?

First see he is vaccinated or not

If not
o give immunoglobulin ( Ig G )
o Followed by active immunization
If doctors is immunized then see triter Do accordingly level of triter

41
what advise u will give to wife of HBsAg positive husband

Wife of HBs Ag + husband

Do HBs Ag of wife
Immunized her if negative
Until developing immunization ( 36 mon) pl. use barrier contraceptic method
If she become positive do not immunized her.

What will u do A HBs Ag + mother give birth a child?

Within 24 hr s of Delivery give Ig G

Both active and passive immunization should be done after delivery

What is cirrhosis?

Cirrhosis is defined pathologically as a diffuse liver abnormality characterized by fibrosis and

abnormal regenerating nodules

Micronodular cirrhosis ---nodules about 1 mm in diameter (seen in alcoholic cirrhosis.)

Macronodular cirrhosis nodules is about > 1 mm in diameter

Mixed --- Both micro and macro nodular

What are causes of cirrhosis or CLD?

CAUSES OF CIRRHOSIS

TO remember ---ABCDEFGHI

A--- Alcohol
B---
o Biliary
o Primary biliary cirrhosis
C--- Chronic viral hepatitis (B or C)
D---Drug
E--- Endocrine - Wilson's disease
F--- Non-alcoholic fatty liver disease
Ggenetic- 1-antitrypsin deficiency
H--- Haemochromatosis
I---
o Autoimmune liver disease/hepatitis
o Primary sclerosing cholangitis

42
Mention the Complication of CLD?

1. Hepatic encephalopathy.
2. Ascites
3. Spontaneous bacterial peritonitis.
4. Hepatorenal syndrome.
5. Hepatopulmonary syndrome
6. Hepatocellular carcinoma
7. Portal hypertension.
o Variceal haemorrhages.
o Portal gastropathy
8. Coagulopathy and feature of hypersplenism

Mention The Factor Predisposing Hepatic Encephalopathy ?

To remember it BCDEF minus TOP

BBleeding from GIT haematemesis @ malaena

C--- Constipation
D---drug sedative, hypnotic, NSAID,
E---electrolyte imbalance, hypokalaemia
FFever indicate infection
Minus top

T--- Trauma , Ooperation , Pparacentasis

What follow u will give in a patient with CLD in ur ward ?

Level of consciousness orientation & alternation sleep rhythm and

Jaundice
Dehydration
Flapping tremor
Pulse , BP, Cyanosis
Abdomen
o Abdominal pain
o Percussion distension
o Bowel sound
o Fever / Temp.
o Constipation / bowel pass
o Bladder (urine out put )
o Rebound tenderness
Abdominal girth
Planter extensor
Daily weight

43
What investigation u want to done in case of CLD ?

Liver function test

SGPT------N /
S.Bilirubin --- N /
Prothrombin time N /
s.ablumin----
AG ratio---- alter
Viral marker

HBs Ag
Anti-HBc Ig G
Anti-HCV
Imaging

USG of HBS and pancreasescoarse echo structure ,

o splenomegaly , ascites
Ascitic fluid study Transudative and SAAG > 1 .1
urine copper (Wilson's disease),
Serum ferritin in case of haemochromatosis
Endoscopy of upper GIT --- to see varcies

Write down the Treatment decompensate CLD?

Diet
o Salt restriction
o No fluid restriction until Na< 120 m mol / l
Diuretic
o spirolactone
o or Combination spirolactone and frusemide
Paracentesis
o Aspiration of 2-5 L/ d ascitic fluid is safe
o If more than 5 L is done in one day then need 6-8 gm albumin for each litre
Syp. Lactulose is given for bowel movement
Treatment of complication such as
SBP
Hepato-renal syndrome
Specific Rx -- liver transplantation
what is the definite treatment of CLD ?

liver transplantation

44
what is refractory ascites ?

failure to decrease wt loss 0.5 kg/d after 1 wk of max dose of combin diuretic (frusemide 160
,spirolactone-400 )

How will u differentiate between acute and chronic viral hepatitis?

Acute viral hepatitis Chronic viral hepatitis

Clinical

Prodrome present (nausea / vomiting No prodome

/anorexia )

Short HO < 1 month Jaundice present Usually absent if present duration is > 3
month

No stigmata of CLD Stigmata CLD present Ascites ,

splenomegaly , spider and gynaecomastia ,
testicular atrophy

Bio-chemical

Prothrombin time increased Prothrombin time increased in Acute on

chronic

Albumin and A:G ratio normal hypoAlbuminia and A:G ratio alter

Viral marker HBs Ag + < 6 months Viral marker HBs Ag + > 6 months

Anti-HBC Ig G negative Anti-HBC Ig G positive

Imaging ( USG )

Shows liver Hypo echoic Coarse echo structure

Inflammation of gall bladder (Chloe cystitis ) Ascites @ or Spleno-megaly

Normal

45
What the clinical signs are of decompensate CLD?

To remember JEA

Jjaundice
EEncephalopathy
A---Ascites
What is management hepatic encephalopathy? Or A patient with CLD suddenly become
unconscious

What is ur diagnosis?

Hepatic encephalopathy

Treatment of hepatic encephalopathy?

A, B, C
NGfeeding
Based on carbohydrate diet and protein restricted
IV fluid
o glucose containing fluid
injectable antibiotic
o ceftriaxone
H 2 blocker
syp . lactulose What is 1st neurological sign in encephalopathy?
enema simplex
inj. Vitamin K Constructional apraxia (ask to draw star )

If the patient of CLD develop fever and abdominal pain? what is your diagnosis ?

Spontaneous bacterial peritonitis (SBP)

How many organism is responsible for SBP and what is the organism?

Usually by single organism mostly Escherichia coli

46
 Clinical feature is to remember -- BAFAR

BAbsence of bowel sound,

A- ascites,

Ffever,

A abdominal pain,

Rrebound tenderness

What is the treatment Treatment ?

o Broad spectrum antibiotic

o Injectable Cefotaxime or ceftriaxon

what is used for prophylacting

For Prophylactic antibiotic

o Norfloxacin (400 mg daily) or Ciprofloxacin (250 mg daily)

A patient with CLD suddenly comes to u recently appearing lump in the right upper
abdomen .what is ur diagnosis ?

Hepatocellular carcinoma

What are sign of hepatic insufficiency? What are the signs of portal hypertension?
Hepatic faces (sunken eye, Malar To remember it keep mind SEA
prominent) SSlepnomegaly
Jaundice EEngorged vein
Flapping tremor o Abdomen
Gynaecomastia o Esophageal varices
In case of female breast atrophy AAscites
Spider nevi Other
Loss of body and pubic hair o Fetor hepaticus ,
In hand o Hepatic encephalopathy
leukonychia.
Dupuytren's contracture
Palmar erythema
Testicular atrophy

47
How the portal vein is formed

It is formed by combination superior mesenteric vein and splenic vein

What is the normal portal pressure?

Normally 2-5 mmHg

Clinical features Developed when portal venous pressures above 12 mmHg
What are blood supplies of liver

Liver has dual blood supply

2/3 is supplied by portal vein rich in nutrients

1/3 is supplied by hepatic artery rich in O2
Oxygen supply of liver

Half of the oxygen supply is met by the portal vein and rest half by the hepatic artery

Complications of portal hypertension

to remember portal HTN HAV HCR

H- Hypersplenism
A- Ascites
V--Variceal bleeding (Oesophageal)
H-- Hepatic encephalopathy
C--Congestive gastropathy
R--Renal failure

Write down the causes of ascites

Exudative cause Transudative

infection and malignancy all causes of edema u look at ward
Infection Nephrotic syndrome
o Tuberculosis CLD
o Spontaneous bacterial Peritonitis CCF
Malignancy Malnutrition
Budd-Chiari syndrome Protein-losing enteropathy
hepatic venous obstruction
Pancreatitis
Lymphatic obstruction
Hypothyroidism

48
CAUSE of HEPATOMEGALY:

Tender hepatomegaly Non tender hepatomegaly

o Viral hepatitis o Secondary in the liver

o Liver abscess o Kala-azar
o HCC o Malaria
o Congestive cardiac failure o Lymphoma
o Leukemia
o Myelofibrosis
o Polycythemia

Common cause spleenomegaly

What are the cause common hepato-splenmegaly
KamaL-3 my Thal ?

Ka-Kala-azar KamaL-3 my Thal

Ma-Malaria Ka-Kala-azar

Lchronic liver disease with portal HTN Ma-Malaria

Llymphoma Lchronic liver disease with portal HTN

Lluekemia (CML) Llymphoma

MYMylofibrosis Lluekemia (CML)

MYMylofibrosis
ThaThalassaemia
o Lymphoma
o leukaemia
What are causes of just palpable spleen? o Dessiminated TB
ThaThalassaemia
Enteric fever
Malaria
Subacute bacterial endocarditis
SLE
Other cause of spelnomegaly
o Lymphoma
o Leukemia
o CLD with Portal HTN
o Disseminated TB

49
A patient with hepatomegaly with ascitis A patient with splenomegaly with ascites
CCF o CLD
Hepatoma with secondary in the peritoneum o Lymphoma
Lymphoma o leukaemia
Dessiminated TB o Dessiminated TB
Chirrohsis of liver with portal HTN
mention the causes of Fever with ascites ? mention the causes of Fever with
splenomegaly ?
o Abdominal TB o Kala-azar
o Lymphoma o Malaria
o leukaemia o Enteric fever
o SBE
o Lymphoma
o leukaemia
o Dessiminated TB

How will u differentiate from primary HCC from 2nd HCC

HCC 2nd in the liver

Tenderness Tender hepatomegaly Non tender hepatomegaly

Number Single lesion Multiple lesion

Umbilication Present Absent

Bruit Present Absent

Bio chemical marker Alpha feto protein + (60%) CEA +

Clinically how how will u differentiate between HCC @ 2nd in liver?

Primary case sing of hepatic insufficiency present such as ascites, splenmegaly , spider ,
jaundice
Palmer erythema , leuconychia , gynaecomastia testicular atrophy

Patient is more toxic in primary case & it is more pain ful

Secondary only hepatomegaly which hard and non tender , left supraclavicular gland
Plus ---see the difference between HCC @ 2ndaries in the liver

50
What may the primary site?

To remember PUBLIC-T

C-Colon, I-intestine-- gastric, P--prostate and pancreas, B--breast and T--thyroid , L--Lung , U
uterus

51
 Connective Tissue Disease
Q.What do you mean by arthritis & arthralgia?

Arthralgia: only pain in the joint Arthritis: Pain & swelling of joint.

Q.What do you mean by monoarthritis?

When single joint involved then it is called monoarthritis.

Causes monoarthritis:

Septic arthritis

Tubercular arthritis

Trauma

Gout

Pseudogout

Haemophila

Q.What do you mean by oligoarthritis?

Involved of 2-4 joint or <5 joint

Seronegative arthritis is the oligoarthritis.

gb ivLvi Rb( RAPE) R: Reactive arthritis

A: Ankylosing spondylitis

P: Psoriatic arthritis

E: Enteropathic arthritis

Causes of enteropathic arthritis:

Ulcerative colitis

Chronns diseases

Q.What do you mean by polyarthritis?

Involvement of 5 or more joint.

52
 Causes polyarthritis:

Viral arthritis

Rheumatoid arthritis

SLE

Osteoarthritis

JIA

Causes of non-inflammatory arthritis:

Osteoarthritis

Haemochomalasis

Acromegaly

Q.How will you differentiate from mechanical low back pain from inflammatory back pain?

point mechanical inflammatory

Onset Acute insideires
Exercise pain pain
Rest pain pain
Morning stiffness Absent Present
Systemic feature (-) (+)
Swell/warm joint (-) (+)
ESR Normal Raised
mvi Connective Tissue GB Chapter XyKe by following Questions:

Qj`i ewk nq Ggb KqwU arthritis Gi bvg ej?

Seronegative arthritis

R: Reactive arthritis

A: Ankylosing spondylitis

P: Psoriatic arthritis

E: Enteropathic arthritis

G: Gout

gq`i ewk nq Ggb KqwU arthritis Gi bvg ej?

SLE

RA
53
Causes of seronegative arthritis:

R: Reactive arthritis

A: Ankylosing spondylitis

P: Psoriatic arthritis

E: Enteropathic arthritis

Q: A pt of 5-15 yrs old with fever,joint pain & swelling.what is your diagnosis?

1st say Rheumatic fever

AviI hw` RvbZ Pvq, Zvnj eje : JIA

Q: A 30 yrs old pt comes to you with H/O lose motion 3-4 wks ago.Now, he develops pain
& swell at rt knee.Left ankle & rt wrist joint?

Pt developed seronegative arthritis probable reactive arthritis

Q: A female pt comes to you with pain & swell of hand joint with morning stiffness.What is
your diagnosis?

RA D/D SLE

Q: 40 yrs old male comes to you pain,red ,tender swell of Rt MTP(metatarsophalangeal

joint). What is your diagnosis?

Gout

Q: A male Pt comes to you H/O recurrent joint swell due fall during playing. What is your
diagnosis?

Haemophilic arthritis

Q: A female old pt(60) yrs complained of knee joint pain during sitting from standing
position. What is your diagnosis?

Osteoarthritis

Q: A 40 yrs old lady comes to you with pain & swell of both hand joint & also Rt knee
joint.She gave H/O morning stiffness. What is your diagnosis?

RA arthritis

Q: A Pt comes to you with H/O hand joint arthritis with rt sided pleural effusion. What is
your diagnosis?

SLE, RA

54
Q: Mention the diagnostic criteria for RA?

A RA( American Rheumatism association criteria)

Morning stiffness> 1hr

Arthritis 3 or more joint area

Arthritis hand joint & wrist

Symmetrical arthritis

Rheumatoid nodule

RA factor positive

Radiological change

Duration more than 6 wks

Q: KLb eje RA?

If 4 or more criteria present

Q: mention the Specificity & sensitive ARA criteria

93% Specific , 90% sensitive

Q. RA Kv`i ewk nq?

Female

Q . Zzwg GKUv ARcvov Mvq AvQ,hLvb Kvb investigationGi myweav bvB|mLvb Zzwg wK RA Dx KiZ
cvie?

Yes,I can do this and how?

By seeing the ARA diagnostic criteria .If I find 4 or more, without investigation doing.

Q . hw` Dx Ki RA Zvnj wK mv_ DMARD hvM Kie bv Acv Kie??

h w`b Dx Kie mB w`b nZ DMARD hvM Kie

Q . Kb 1g w`b nZ DMARD hvM Kie?

Because this is Deforming arthritis.It causes deforming the joint and pt will be disable if

not treat with DMARD

55
Q.Name common DMARD we use in RA?

Methotrexate ( MTX)

Sulphasalazin

Q. DMARD KvR KiZ KZ w`b mgq jvM?

4-12 mvn

Q. 4-12 wks Gi ga symptoms subside Kivi Rb wK w`e?

Oral prednirolone (Dose: 7-10 mg daily for 3 months)

Q. MTx wK dose `B?

MTx (7.5 mg) _K i Ki max 25 mg `B day MTx weekly `B

Zvicii w`b Folic acid `B

Q. Common side effect of MTx :

GIT upset

Nausea & vomiting

Q. Others side effect of MTx

Bone marrow suppression

Hepatic fibrosis

Interstitial lung disease

Q. Follow up due to MTx

1st monthly CBC , liver function & renal function test .

Then 3 monthly should be done.

Q. Dose of Sulphasalazin:

Sulphasalazin(500mg)

+0+ for 1 week

1+0+1 for 1 week

2+0+2 continue

56
Q. Complication of Salazin:

Common:

Agranulocytosis

Stevens Johnsons Syndrome

Others:

GIT upset

Reversible sterility

Haemolytic anaemia

Q. A pt on salazin complaint of sore throat.what is your Dx?

Agranulocytosis

Q. Male pt with salazin.what complication he may develop?

Sterility

Q. Is it reversible or irreversible?

It is reversible & sterility will be disappear if pt stop the drug.

Q.what are the other DMARD use in RA?

Reflunomide (100 mg daily for 3 days). then maintance dose ( 10 to 20 mg daily)

Hydroxychloroquine ( 200 to 400 mg)

[ Trade name: Reconil]

Q.Name some biological agent use in RA? Mention the remission criteria in RA

Infleximab 5 or more of the following condition for at least 2

Etanercept
Adalimumab
Q.What is side effect?
serious infection
reactivation of latent TB
consecutive months
To remember Morn. STEP
Morn --Morning stiffness less than 15 min
S--No soft tissue swelling in joint or tendon sheath
T--No tenderness or no pain with motion
E--ESRin female < 30 & male < 20 mm
P--No joint pain
No fatigue

Lymphoma

57
Q.If sir directly ask Rx?

* Suppertive Rx

Rest

Pain killer NSAID

* Specific Rx

DMARD

* To prevent deformity or restoration of function Physiotherapy

Q. what investigation you will done?

usually clinical Dx by Dx criteria

we do CBC - ESR

CRP

RA factor

X-ray of hand,wrist joint

Q.what is x-ray finding?

Perearticular osteopenia , joint space narrow

Q.Early Dx Kivi Rb / Dx criteria/CF Avmvi AvM Dx Kivi Rb wK cixv KiZ cvi?

Anti CCP antibody

Q. what is anti CCP antibody?

Anti Cyclic Citrullinated Peptide

Q.How will follow up the pt with RA or assess respond?

[to remember: PGT in Med(medicine) ]

P - Pain

G Grip strength

T Joint tenderness

Med Morning stiffness

58
 *Laboratory:

ESR

CRP

Plasma viscosity

Q. RA pt died suddenly. what may be the cause?

Sudden death due sublaxation Atlanto-axial joint, which compress on vital centre of brain

stem

Q.Name some extra articular manifestation of RA?

EYE

Piscleritis

Scleritis

Kerato conjunctiva sicca

RESPIRATION

Pleurosy

Pleural effusion

Fibrosing Alveolitis

CVS

Pericarditis

Pericardial effusion

Chronic constrictive pericarditis

Neurological

Peripheral neuropathy

Cervical cord compression

Entrapment neuropathy

Menneuritis multiplex

59
 Vasculitis

Raynaud Phenomennon

Ulcer

Degital arthritis

Q.What do you mean by Felty syndrome?

RA with splenomegaly with neutropenia.

Q. what do you mean by palindromic RA?

Recurrent ( relapsing & remitting) episode of joint pain and stiffness and swelling which
last only for few hours or days..

Q. A pt with rheumatoid arthritis presented with pain,swell of rt culf muscle?what is Dx?

Rupur Baker cyst

Q. what are the deformity of hand?

Swan neck

Boutinniere

Z sorm deformity

Triggering of fingers

Q. Difference between RA & RF ?

Rheumatoid arthritis Rheumatoid fever

Age 20-40 <15

Joint small & hand large

Type of arthritis bilateral symmetrical migratory

Morning stiffness (+) (-)

RA factor (+) (-)

Diagnostic criteria ARA jones

60
 Q. what do you mean by Rheumatoid factor?

RA factor is an antibody directed against Fc portion of IgG. It is IgG/ IgM

In RA KZ % gq positive nq? 70%

Q.Name the disease where RA positive?

RA - 70%

Jorgen syndrome 90%

SLE

Primary billiary cirrosis

Mixed connective tissue disease

Q. what do you mean by seronegative RA?

30% of RA with typical clinical feature . if RA factor negative this called seronegative
RA

Q. Difference between RA with psoriatric arthritis?

Rheumatoid arthritis psoriatric arthritis

Joint PIP DGP

Skin lesion Absent Present

gb ivLe: Rheumatoid arthritis DIP involved nq bv, Ab arthritis nq

Q.30 yrs old female comes to you with complaints of fever,arthralgia/arthritis with H/O
Alopecia or photosensitivity [ mvi GLvb ejZ cvi iv` Mj cyo hvq/rash nq/Burning

sensation]

Dx - SLE

Avi wK question aks the pt Alopecia

Oral ulcer

H/O repeated Abortion

Q. 30 yrs old women comes to you with complaints of fever & joint pain with rash.She also
give H/O recurrent abortion for 6 years. what Dx?

SLE with antiphospholipid syndrome

61
Q.Name some connective tissue disease?

SLE

Systemic sclerosis

Mixed connective tissue disease

Polymyosilis & dermatomyosilis

Jorgen syndrome

Q. Mention the diagnostic criteria of SLE?

[To remember: DOPAMIN RASH]

D- Discoid rash

O- Oral ulcers: oral or nasopharyngeal ulceration,which may be painless

P- Photosensitivity

A- Arthritis: non-erosive,involving 2 or more ppripheral joints

M- Malar rash: fixed erythema,flat or raised,sparing the nasolabial fold

I- Immunological disorder: Anti-DNA antibiotics in abnormal titre or

Presence of antibody to Sm antigen or

Positive antiphospholipid antibiotics

N Neurological disorder: Seizures or psychosis

R- Renal disorder: Persistent proteinuria> 0.5g/day or

Cellular casts (red cell,granular or tubular)

A- ANA

S- Serositis: Pleuritis,pleural effusion, pericarditis,pericardial effusion

H- Haematological disorder: Haemolytic anaemia or

Leucopenia2 ( < 4X109/l) or

Lymphopenia2 (< 1X109/l) or

Thrombocytopenia2 (< 100X109/l)

62
Q.what investigation you want to do?

CBC - ESR

PBF Anaemia, pancytopenia,some times only thrombocytopenia

Urine proteinuria/RBC/RBC cast

24 hr total urinary protein

CRP normal

ANA positive in 90% case

Anti-ds DNA positive in 30-50% case

Anti sm (simth) 10-20% case positive

Serum anti phospholipid syndrome

Complement C3,C4 (decrease in active disease)

X-ray joint- normal

Q. GKUv investigation Kij wK Kie? ANA

Q.ANA positive, wK Kie? Anti ds- DNA

Q.what is ANA? Anti Neuclear Antibody

Q. In SLE KZ% sensitive? 100%

Q. In SLE KZ% specific? 10-40%

Q. In Anti-ds-DNA KZ% sensitive? 95%

Q. In Anti-ds-DNA KZ% specific? 30%

Q. ANA positive all connective tissue

SLE

Systemic sclerosis

Mixed connective tissue disease

Polymyosilis & dermatomyosilis

Jorgen syndrome
63
Q.what is Rx of SLE?

Mild disease:( fever/arthralgia/arthritis)+cutaneous involvement

explanation of the disease

avoid survey

NSAID

TAB: Hydroxychloroquine ( 200 to 400 mg)

Moderate disease: (serosilis/pleuropericarditis)

oral steroid/tab: prednisolen

In life threatening SLE:

lupus nephritis or CNS involvement

o I.V. methylprednisolone plus

o I.V. cyclophosphamide

Q. what is the cause of death in SLE?

Renal failure

Q.SLE pt comes to you with convulsion.what is your Dx?

Lupus cerebrilitis

Q.SLE pt comes to you with renal failure/ s.creatinin /oligourea. what is your Dx?

Lupus nephritis

Q. GB Zzwg wK Rx w`e?

I.V. pulse therapy

Q.what is pulse therapy?

I.V. methylprednisolone ( 1gm IV in 500 ml DA/DNS pulse)

plus

I.V. cyclophosphamide ( 2g/kg Bwt I>V in 5oo mlda/DNS)

64
Q. KZ w`b w`e? 3-5 days. Repeat: 3 wks interval on 6-8 occasion

Q.What is the complication of I.V. cyclophosphamide?

Haemorrhagic cystitis

Q.Rx of haemorrhagic cystitis:

Inj. mensa on 0,4,8 hourly

Q.SLE pt with back pain. what is your Dx?

Avasacular necrosis due to steroid therapy

Q.Difference between SLE & RA arthritis?

SLE is non-erosive arthritis but deforming arthritis & erosive arthritis in RA.

Q. what do you mean by Jaccoud arthropathy?

When in SLE arthritis cause deformity is called Jaccoud arthropathy.

Q. A pt with SLE & pregnancy.what will be Rx?

Usually SLE causes abortion or still birth, (IUGR)

Rxo.SLE in pregnancy is prednisolene in low dose.

Q.SLE pt evPv wK complication nZ cvi?

Complete Heart Block

Q.GUv Zvi evPvi ne wKbv --- Zvi Rb gvi wK cixv Kie?

Anti-Ro-Antibody

Q.Drug induced SLE Rb wK `wL?

Anti-histone-antibody

Q.Causes of anaemia? Haemolytic anaemia

Q.Classification of SLE?

Classical SLE ---- many criteria

Definite SLE ---- when 4 or more

Probable SLE ---- when 3 or more

Possible SLE ----- when 2 or more

65
Q.Describe rash of SLE------

Butterfly rash this erythematous raised up painful,itchy over cheeks with spare the

naso-labial fold.

Q.20 yrs old boy H/O low back pain & morning stiffness with pain & swell of rt knee,left
ankle, rt elbow joint.What is your Dx?

Ankylosing Spondylitis

Q. GKUv jvK bvgvh covi mgq iKzZ Mj mgmv nq.wK Dx? / Qj`i ewk nq Ggb wKQy arthritis

Gi bvg ej / or name some seronegative arthritis?

GLvb nZ AKS Pj hve|

Seronegative arthritis causes --- RAPE

R: Reactive arthritis

A: Ankylosing spondylitis

P: Psoriatic arthritis

E: Enteropathic arthritis

Q.what are the common features of seronegative arthritis or AKS?

[ to rememberSALFER-27]

S- sacroilites & inflammation spondyloarthritis

A- asymmetrical oligoarthritis

L- Lower is more affect than upper limb

F- familiar

E- inflammation enthesitis

R- Ra factor negative

27- genetic association with HLA-B-27

Q. Kv`i AKS ewk nq? ratio KZ?

Qj`i 3:1

66
Q. Kvb eqm ewk nq? - 2nd & 3rd decade

Q.Clinical features of AKS?

low back pain

stiffness

other feature of seronegative arthritis

examination

- restricted spine movement ( mainly lumber)

- obliteration lumber lordosis

schober test --- negative & feature of extra articular manifestation

Q. Name of feature of extra articular manifestation?

[to remember- C.P.U of CAM Puter]

C---- conjunctivitis

P---- prostatitis

U---- Ant. uveitis

C---- conduction defect

A---- aortic regurgitation

M---- mitral regurgitation

Puter---- pulmonary fibrosis in upper lobe

Q. what do you mean by enthesitis?

Inflammation of the legamental attachment with erosion of adjacent bone is called

enthesitis.

Q.What do you mean by syndesmophyte?what is the hallmark of AKS?

Syndesmophyte is the hallmark of AKS.

Q.How does syndesmophute form?

It is formed by healing of enthesitis at function of intervertebral bodies cause new

formation.It is called syndesmophyte

67
Q.X-ray of lumber spine/ s-g joint?

X-ray S.I joint:

irregularity, marginal sclerosis, later on fusion at S.I joint from below to upward

L-S spine:

- squaring of vertebra

- fusion of ant.longitudinal ligament

- bridging syndesmophyte

- bamboo spine

Q.what Rx you will give in pt with AKS?

General measure:

- educate the pt about disease nature

- exercise & physiotherapy

Swimming, cycling

Regular daily back extension exercise

Avoid poor & bad chair posture

Avoid prolong period inactivity

For pain: NSAID

Q.What are the indication of DMARD?

Only axial involvement No DMARD

When peripheral joint involved- then we give DMARD

Q. What DMARD use?

1st choice: Sulpha-salazin

2nd choice: MTx

Q. Which is an ideal exercise? ----- swimming

68
Q.Newer drugs/ biological agent/ Anti TNF Therapy?

Infleximab

Etanercept

Q. A 30 yrs old man comes to you H/O pain & swelling rt knee joint,left ankle, rt wrist joint.
Pt have diarrhoea 3 wks/1 month ago.what is your Dx?

Reactive arthritis

Q. A 30 yrs old man comes to you with the complaints of conjunctivitis, urethritis , arthritis.

what is your Dx?

Reiters disease

Q.what is reactive arthritis?

Arthritis after 3 ek at fever or diarrhoea or sexual exposure is called reactive arthritis.

Q. Diarrhoea/Fever Gi 3 mvn ci Kb arthritis?

As because infection nIqvi ci antibody Zix nZ 3 mvn mgq jvM|GB antibody cross react
with joint/eye cause arthritis & conjunctivitis.

Q.which organism is responsible for reactive arthritis?(to remember SSC)

Diarrhoea:S--Shigella, S--Salmonella, C--Chompylobacteria

Urethritis: C--Chlamyda

Q.Feature of reactive arthritis?

Arthritis: oligoarthritis, lower>ujpper limb+ other feature of spondyloarthritis,

male>female, asymmetrical

Other extra articular manifestation

Q. Name some extra-articular manifestation of reactive/ Reiters disease?

[to remember- CKD]

C--- cercinate balanitis

K--- keratoderma blnnorrhagica

D--- Nail dystrophy

69
Q. what is triad Reiter disease?

- non specific urithritis

- conjunctivitis

- reactive artyhritis

Q.Is conjunctivitis infective or not?

It is not infectious. It is inflammatory conjunctivitis

Q.which investigation you will do?

- CBC--- ESR

- Urine--- pus cell

- RA--- negative

- X-ray--- sacro-iliac joint

Q. Rx:

- Rest

- NSAID

- Antibiotic

cap: tetracycline ( 500 mg) 1+1+1+1

Q. why we use tetracycline?

To remove residual chlamydal infection

Q.when we use DMARD?

- recurrent arthritis

- severe persistent syndrome

- keratoderma blennorrhagia

Q.Which DMARD we use?

Sulpha- salazin

70
Q.A pt with AKS. Avi wK examination Kie?

LUNG--- apical fibrosis

PHTN

Type 11 failure

HEART--- AIR/MR

Q.what type respiration failure occure? why type 11 res. failure?

Due to ankylosis of costochondral or costovertebral joint cause restriction of respiratory .

movement & thus causes type 11 res. failure

Q. Difference between syndesmophyte with osteophyte?

syndesmophyte osteophyte

Hallmark of AKS Hallmark osteoarthritis

Inflammatory Degenerative

Grows longitudinally Grows horizontally/outward

Due to calcification of ligamental attachment New bone formation at corners vertebra

Q.A 30 yrs old man comes to you with complaint of red,hot,tender & painful rt
metatersophalangeal joint.What is Dx?

Acute gout

Q.Acute gout G red, hot ,tender MTP nq,ZvK wK ej?----- Podagra

Q.Name criystal related arthritis or

Gout wK crystal Rgv nq? & Pseudo-gout wK crystal Rgv nq?

Goutdue to monosodium urate monohydrate

Pseudogout--- due to calcium pyrophosphate dihydrate

Q. Why gout occur?

Due to disorder of purin metabolism

Q. who are suffer for primary gout? ----- common in male> 40 yrs

Q. who are suffer for secondary gout?------ common in female> 50 yrs

71
Q. where we found trophy?

In chronic gout.. It is nodular,hard,irregular swelling due to deposition of urate.

Acute gout---- Podagra

Q.How you will confirm it?

Aspiration from joint ,bursa, to see( monosodium urate monohydral MSUM)

Q. Avi wK investigation :

S. uric acid

S. creatinine

Urine RME

RBS

CBC

Q. wK wK Rx w`e acute gout?

For pain: Bed rest

NSAID

if not pain subside --- colchicine use

Long term Rx:

Dietary restriction purine contained food

o red meat,kidney,liver,brain

o cabbage,cauliflower

avoid alcohol& starvation

precipiating drugs.

Q.Are we use hypouricaemic drug in acute gout?------- NO

Q.Indication of uricosuric drug such as Allopurinol? (to remember RTX)

R--recurrent attack

T--presence of tophi

X (x-ray)--radiological evidence of joint damage

72
Q.X-ray finding of gout?

Para-articular punchout lesion with well delineated border & normal bone density

Q.Causes of pseudogout?

Deposotion CPPD

Osteoarthritis

Haemochromatosis

Hyperparthyroidism

Q.Difference between MSUM & CCPD ?

MSUM CCPD

Monosodium urate monohydrate Calcium pyrophosphate

Needle shape Rhomboid shape

Negatively birefringence Positively birefringence

Q.Causes of Hyperuricaemia?

Decrease renal excretion:

Renal failure

Drugs: Diuretic----

Thiazide

Aspirine

Pyrazimamid

low dose aspirin

Increased production:

Idiopathic( primary)

Myeloproliferative disease

Lympho proliferative disease

Psoriasis

73
Q.What are the disease responsible for enteropathic arthritis?

Ulcerative colitis

Chronns disease

Q. A pt comes to you with skin lesion with arthritis.what is your Dx?

Psoriatic arthritis

Q. How will you differenciate RA from Psoriatic arthritis?

RA Psoriatic arthritis

Hand joint PIP DIP

Skin lesion/nail change Absent Present

Symmetry Symmetrical Asymmetrical

Q. Name other arthritis involved?

DIP, Gout, Osteoarthritis

Q. Rx of Psoriatic arthritis:

NSAID

DMARD--- MTx

Salazin

Q.Can we use biological agent?

yes, Infleximab

entararcept

Q.Rx of Psoriasis/ skin lesion?

Local--- coal tar

Retenoid

PUV-A

Q. A 65 yrs old female complaint of pain in rt knee joint from sitting to standing position on
exam.The joint not warm/tender/swell.Passive movement produce crepitus.what is your Dx?

Osteoarthritis
74
Q. GUv wK aibi arthritis?-------- Degenerative arthritis

Q.which is the common arthritis of world?--------- osteoarthritis

Q.which joint is more involved?-------- Hip & knee joint

Q. Kvb eqm nq?------ > 65 yrs

Q. Clinical feature of OA?

Old age

Insidion onset

related to movementpain relief in rest

Morning stiffness less 15 min

good days & bad days

Sign:

restricted movement

on movement of joint palpable course crepitus---- present

no feature of red,warm over joint

.Q. what is the X-ray finding of OA?

[to rememberJOS]

J---Narrowing joint space

S---Subchondral sclerosis

O----Marginal osteophyte

Cyst

Q. Rx of OA?

explanation reassurance

Exercise: both strengthening & aerobic

wt reduction & abscess

Drugs----

Paracetamol
75
 NSAID

Local/topical oinment--- NSAID

Capsalcin

Surgery----

Hip replacement

Knee replacement

Q.what will be the ESR in OA?----------- normal

Q.Which gender is affect more?---------- female

Q.What do you mean by osteoporis?

It is a condition characterized by reduced bone mineral density(BMD),micro-architecural

deterioration of bone tissue & an increased risk of fracture.

Q.Who are the common sufferer of osteoporosis?

Postmenopausal women

Q.Why?

After the menopause oestrogen deficiency causes uncoupling of bone resorption & bone
formation that means the amount of bone removed by osteoclast exceeds the rate of new bone
formation by osteoblast.

Q.What is the clinical presentation of osteoporosis?

Usually is asymptomatic until fracture happen

Back pain,height loss & kyphosis

Q.What is the most common site of fracture in osteoporosis?

The forearm ( colles fracture)

Spine ( vertebral fracture)

Femur (hip fracture)

76
Q.What can you do in diagnosis of osteoporosis?/Name a single test to diagnose the
osteoporosis?

BMD or Bone Mineral Density---when it is told osteoporosis/osteopenia

Condition T-score in BMD

Osteoporosis T-score value falls to -2.5 or below

Osteopenic T-score value that lie between -1.0 and -2.5

Normal T-score value lies above -1.0

Q.Treatment of osteoporosis?

Whereas pts with osteopenia should be given advice

Lifestyle factors such as--------

Stop smoking on

Alcohol(limit to <20 U/week)

Dietary calcium (aim for 1500 mg daily) and

Exercise

Adv the pt to repeat BMD measurement in 2-3 years

Anti-osteoporosis treatment is given in pts with BMD values in the osteoporotic

These drugs ate

Main drug is Bisphosphonates

Alendronate (10 mg daily,or 70 mg once weekly) and

Risedronate(5 mg daily or 35mg once weekly)

Calcium & vitamin D supplements

Hormone replacement therapy(HRT)

HRT with oestrogen & progestagens prevents post- menopausal bone loss

Calcitonin

Q.Write down the mechanism of action of Bisphosphonates?

77
 Bisphosphonates inhibit bone resorption by binding to hydroxyapatite crystal on the bone
surfacewhen osteoclasts resorb bone that contains bisphosphonate, the drug is released
within the cell,where it inhibits signaling pathways that are essential for osteoclast function.

Q.What adv you will give during taking Bisphosphonates?

Should be taken in empty stomach

In morning

Remaining sitting for hours

Name some endocrine disease that cause osteoporosis ?

Endocrine Disease others

Hypogonadism Inflammatory bowel disease

Hyperparathyroidism Corticosteroids
Cushings Syndrome Malabsorption
Hyperthyroidism Chronic liver disease
Myeloma
immobilisation

The red Flag sign

History

Age-presentation under age 20 or over age 50

Character- constant, progressive pain unrelieved by rest
Location- thoracic pain
Past medical history- carcinoma, tuberculosis, human immunodeficiency virus(HIV),
Systemic corticosteroid use
Constitutional- sweats, malaise, weight loss
Major trauma
Examination

Painful spinal deformity

Severe/symmetrical spinal deformity
Saddle anesthesia
Progressive neurological signs/muscle-wasting
Multiple levels of root signs

78
Low back pain classified in 4 category

Mechanical pain Inflammatory pain Non mechanical Specific/spinal cause

pain

Ankylosing Malignancy Spondylolysis &

spondylitis osteoporosis spondylolisthesis

Frature Spinal stenosis

Prolapsed
intervertebral
dise

spondylysis

Spondylosis: degenerative change in the spine

Spondylolysis : defect in the pars interarticularis of a vertebral arch

Spondylolisthesis: the anterior slip of one vertebra of an inferior vertebra

Spondylitis: inflammation of spine

79
 Neurological disease and Stroke
Q: What neurological disease you have seen in your ward?
A: CVD, epilepsy , GBS , paraparesis

Q: Name some neurological emergencies?

A: status epilepticus, stroke.

Q: Define status epilepticus?

A: Status epilepticus is defined as a seizure or a series of seizure lasting 30minutes without

regaining consciousness between attacks.

Next Q: how will you manage it?

A:

First ensure whether airway is patent.

Inj. Diazepam 10mg (1vial I/V stat & if control give another ampule I/V 15minutes later)
If not control, give I/V infusion of anyone of the followings:
Inj. Phenytoin 15mg/kg, 50mg/min
Inj. Fosphenytoin 15mg/kg, 100mg/min
Inj. Phenobarbitone 10mg/kg, 100mg/min

*practically we use : Fosphenytoin

*dose memorizing is not obligatory here
If not control yet, then send the pt. to ICU for Thiopental-Na through intubation.

Q: How will you differentiate true seizure from pseudo-seizure?

A:
Traits True seizure Pseudo-seizure
1.Tongue bite Present Absent
2.Urinary incontinence Present Absent
3.Post ictal amnesia Present Absent

Some essential definitions:

Seizure: It is a clinical condition characterized by abnormal hypersynchronous discharge
of cerebral neuron which may be sensory, motor or autonomic.
Convulsion: motor component of seizure is called convulsion.
Epilepsy: tendency to have recurrent seizure.

80
Q: classify the epilepsy?
A:
According to seizure type: (mnemonic: TATA MP3)
i. P--Partial seizure ( simple & complex)
ii. P--Partial seizure secondarily generalized
iii. P-Primary generalized seizure
iv. T-Tonic-clonic seizure
v. A-Absence seizure
vi. T--Tonic seizure
vii. A--Atonic seizure
viii. M--Myoclonic seizure

*first tell the above ,if the examiner ask more..then tell following:

According to EEG or physiology:

Focal & Generalized

According to aetiology: (mnemonic: GTV MIT DDD)

Genetic
Tumour
Vascular
Metabolic
Infectious
Trauma
Developmental
Drug & alcohol
Degenative

(remember:
Major seizure: fall occur
Minor seizure: no fall
Simple seizure : pt conscious
Complex seizure: pt become unconscious

Q: Indications of imaging in epilepsy?

A: mnemonic: CAF

A--Epilepsy started after the age of 20.

F--Seizure having focal neurological deficit

81
 E--EEG shows focal seizure.
C--Difficult to control seizure.

Q: which one is superior- CT/MRI?

A: MRI

Q: name some anti-epileptic drugs?

A: carbamazepin, Na-valproate, ethosuximide, phenytoin, gabapentin

Q: name some new generation anti-epileptic drugs?

A: lamotrigine, topiramate. (nice to know: side effects of them)

Q: how will you start & stop anti-epileptic drugs?

A:
Start first line drug
Start at low dose & gradually increase until effective control of seizure/side effects
appear.
If first drug fail, then start second drug with gradual tapering the first drug.
If second drug fail, start a second line drug +preferred first-line drug.
Never use more than 2 drugs in combination.

Q: what advise you will give an epileptic pt?

A:

Explain the disease & also say that it is a natural ,it is not related with curse/stigma.
Avoid exposure to :
Height
Dangerous machinery
Open fire and
Water
Only take shallow bath ( dont take bath or dive in the pond)
Bathroom door should be unlocked
Avoid driving
Keeping card regarding information about the pt &the disease.

Q: what is the treatment of epilepsy?

A:
Immediate care
life style modification (see previous answer)

82
 Anti-convulsant therapy:
Partial /secondary GTCS carbamazepine
Primary GTCS /myoclonic seizure Na-valproate
Absence seizure ethosuximide

Q: what advice will you give a pt. taking anti-epileptic drug about contraception?
A:
[all anti epileptic drugs are enzyme inducer so, cause enhanced metabolism of estrogen as
result there will be:
o Contraceptive failure
o Breakthrough bleeding]

Advice- alternative contraception containing high dose estrogen

Or,
Na-valporate can be used as it doesnt interact with OCP.

Q: An epileptic pt. become pregnant ,what will you do?

A:
Before conception anti-epileptic drug should be withdrawn ( as these may cause cleft
palate,spina bifida etc)
Folic acid should be given 2weeks before conception
At last month ,to prevent haemorrhagic disease give inj. Vitamin-K ,20mg daily orally
At birth, give the child inj. Vitamin-K 1amp i/m stat.

Q: safe drug in pregnancy?

A: Gabapentin

Q: what do you mean by Dejavu, Jamais Vu, Todds palsy, Jacksonian seizure?
A:
Deja vu : undue familiarity temporal lobe lesion,,
Jamis Vu: undue reality. complex partial seizure
Todds palsy: in case of some partial motor seizure ,pt may develop paresis of involved limb
lasting for several hours after the seizure ceases.

Jacksonian seizure: in case of partial motor seizure, some attacks begin in one part of the body
(e.g. mouth ,thumb,great toe) and spread (march) gradually to other parts of the body, this is
known as Jacksonian seizure.

83
Q: what do you mean by Absence seizure (petit mal)?
A:

Q: Scenario- a 20years old lady comes with fever for 3days followed by unconsciousness. What
is your diagnosis?
A: Encephalitis, Cerebral malaria, Meningoencephalitis
(then sir will ask you about the treatment of cerebral malaria or meningitis..here we discuss
the treatment of meningitis onlyl)

Next : what will you do?

History taking about endemic zone of malaria or H/O rash
Examination: neck rigidity, kernigs sign

What investigation will you do?

CBC: TC neutrophilic leucocytosis in case of Bacterial meningitis.
Thick & thin film: for malarial parasite
ICT for malaria
CSF study

What will be the treatment?

[ in the ward combination of anti-bacterial+anti-viral+anti-malarial are usually practiced]
NG-feeding 200ml ,2hourly
I/V fluid (normal saline)
Inj. Ceftiaxone (2mg) 1vial I/V ,12hourly
Anti-malarial
Tab.Virux (400mg)- 2+2+2+2+2
Catheterization
Eye & mouth care
Changing posture 2hourly

{NB: conditions where inj. Ceftriaxone(2mg) I/V ,b.d usually practice

Meningitis
Enteric fever
Aspiration pneumonia}

Q: Questions regarding CSF.

Normal CSF amount 150ml

Normal CSF pressure 50-250mm of water
Site of production choroid plexus of lateral , 3rd &4th ventricle
84
 Absorption occur in arachnoid villi
Pathway of CSF see from anatomy
Normal cell in CSF <5/HPF
Normal glucose in CSF >60% of blood level[40-80mg/dl]
Normal protein in CSF 20-40mg/dl

What are the CSF findings of meningitis due to bacteria, virus, TB?
A:
Traits Bacterial meningitis Tubercular Viral meningitis
meningitis
1.cell count neutrophil (1000- lymphocyte(50- lymphocyte(10-
(WBC) 5000) 5000) 2000)
2.glucose
3.protein

Q: Indications of lumbar puncture?

A: diagnostic purpose:
Meningitis/encephalitis
Subarachnoid haemorrhage
Multiple sclerosis*
BIH (benign intracranial hypertension)
*multiple sclerosis oligoclonal band

Q: what will you see before doing lumbar puncture?

A: Fundoscopy to see whether there is papilloedema (to exclude ICSOL). If LP is done in
presence of ICSOL, there will be herniation of cerebral contents downwards, towards & into the
spinal cord ( this process is known as coning).

Q: what are the differences between viral & bacterial meningitis?

A:
Viral meningitis Bacterial meningitis
1.headache is main feature- self limiting & less 1.neck rigidity ,high fever, drowsiness,
sever unconsciousness are predominant.
2.CBC: lecopenia or normal 2.neutrophilic leucocytosis
3.no focal neurological sign 3.focal neurological signs are present
4.CSF: lymphocyte count, protein & glucose 4.CSF finding: neutophil count, protein,
leves are normal glucose

85
Q: Name the organism causing meningitis according to age?
A:
NEONATE: E.coli, proteus, group-B streptococci (mnemonic- EPS)
PRE-SCHOOL: Haemophilus influenza, Neisseria meningitides, Streptococcus pneumonia
(mnemonic- HNS)
OLDER CHILDREN: NS (above)

Q: Other common virus causes meningitis?

A: Echovirus.

Q: In which route meningococcus enter into the body?

A: nasopharynx ( *it is the commensal of upper respiratory tract)

Q: scenario: a pt comes to you with H/O splenectomy 3years back. Now he develops fever, rash,
neck rigidity & hypotension, what is your diagnosis?
A: meningococcal septicaemia.

Q: which organisms are responsible for meningitis after otitis media?

A: pneumococcus & haemophilus.

Q: which organism cause meningitis after skull fracture?

A: staphylococcus aureus.

Q: which organism cause brainstem encephalitis?

A: listeria monocytogens.
(treatment: inj. Ampicillin 2gm I/V 4hourly + inj. Gentamycin 1amp. I/V 8hourly)

Q: which is used in associated with antibiotic?

A: steroid ( inj. Dexamethasone)

Q: which antibiotic should be used in ward?

A: commonly Ceftriaxone 2gm ,b.d
In case of meningococci, inj. Benzylpenicillin 2.4gm I/V , 4hourly for 7days

Q: what preventive measures should be taken in case of close contact with meningococcal pt?
A:
In case of adult: Tab.ciprofloxacin (500mg) single dose
In case of child: Tab. Rifampicin( <1yr 5mg/kg, >1yr 100mg/kg)

86
Q: scenario: A pt came to you with a fever for 15days.The Fever is intermittent for few months,
on examination :pt is drowy, neck rigidity (+ve), kernigs sign (+ve), 6th nerve palsy with
fundoscopy reveals papilloedema

Diagnosis: tubercular meningitis

Cause: primary TB in childhood or military TB.

CSF findings: glucose, protein, lymphocyte.

Q: What is the physical finding if CSF fluid is allowed to stand?

A: There is formation of spider-web

Treatment: antitubercular chemotherapy for 12 month + steroid.

Complications: hydrocephalus, tuberculoma, cranial nerve palsy.

C/F of tubercular meningitis:

Symptoms:
Headache
Low grade fever
Vomiting
Confusion
Sign:
Meningism
Cranial nerve palsy
Papilloedema
Focal neurological sign

Q: What is meningism?
A: It consist of headache, photophobia & stiffness of neck often accompanied kernigs sign.
Cause: meningitis, subarachoid haemorrage.

Q: What is sterile meningitis & cause of it?

A: meningitis due to non-infective cause.

Cause:
Malignancies: breast cancer, leukaemia, bronchogenic carcinoma
Connective tissue: SLE, Bechet disease.

87
Q: mortality rate of Rabies?
A: 100%

Q: what is the treatment of dog bite?

A: Human diploid cell vaccine (I/M), dose schedule 0,3,7,14,28 (days)

Q: what type virus is polio?

A: Enterovirus (route: feco-oral)

Q: target site of polio virus?

A: anterior horn of lumbar spinal segment.

Guillain-barre syndrome
Q: Scenario-A pt comes to you with progressive lower motor neuron type or faccid type
paraparesis, on examination there is no sensory or bowel-bladder involvement. He has a H/O of
fever or diarrhoea 3weeks back. What is your diagnosis?
A: GBS

Q: C/F of GBS?
A:

Faccid (LMN) type of paralysis

Lower limb more involve than upper limb
Ascending type
Reflex absent
No sensory or autonomic involvement

Q: Why not it is spinal cord compression?

A: If pt. has spinal cord compression then pt will have UMN lesion, exaggerated jerk, definitive
sensory level& bowel-bladder involvement.

Q: What type of lesion (GBS)?

A: acute inflammatory demyelinating polyneuropathy.

It is immune reaction where antibody is formed against gangliosides in the Schwann cell

Q: Site of the lesion?

A: nerve root/ radical lesion

88
Q: What type of lesion?
A: Autoimmune

Q: which organism is responsible?

A: Campylobacter jejuni.

Q: what investigation will you do?

A: CSF study.

Finding: albumino-cytologic dissociation that means protein increase but cell count doesnt
increase. If lymphocyte >50x106 suggest alternative diagnosis.

** CSF examination should be done after 10days.

Q: Definitive test / confirmatory diagnosis of GBS?

A: nerve conduction test & elecromyogram.

Q: What is the dangerous complication of GBS?

A: respiratory muscle paralysis.
Q: what will you do then?
A: Send the pt to ICU for ventilatory support.

Q: Tell the prognosis.

A:
80% achieve full recovery within 3-6 months.
04% die &
Remainder suffer from severe neurological disability

Q: What is Miller Fisher?

A: It comprises the triad of
Ophthalmoplegia
Ataxia
Areflexia

Q: What is the treatment of GBS?

A: symptomatic, supportive & specific.

Q: What is the specific trearment?

A: I/V Immunoglobulin or plasmapheresis within 14 days.

89
Q: What is the mechanism of GBS?
A:
Infection by Campylobacter jejuni

Antibody formation against it

Due to molecular mimicry it crosses reacts with ganglioside in Schwann cell

Destruction of myelin sheath

Blockade of nerve conduction

Myasthenia gravis

Q: Scenario: a 40years lady comes to you with complaints of easy fatigability with dropping of
both upper eyelids which is more marked on the evening. She had recurrent type of attack of this
type of disesase. What is your diagnosis?
A: myasthenia gravis

Q: what is the lesion?

A: auto-immune disease.

Q: where is the lesion (site)?

A: Neuro-muscular junction

Q: why is the lesion?

A: due to antibody formation against acetylcholine receptor.

Q: Who are commonly affected?

A: females.

Q: C/F of myasthenia gravis.

A:
Relapsing & remission
Bilateral ptosis with muscle fatigability which is more marked at the end of the day
Difficulty in swallowing
No sensory involvement
Higher psychic function normal

90
Q: what investigation will you do?
A:
Tensilon test ( by I/V inj. Of endrophonium bromide.
Electromyogram
Detection of antibody against acetylcholine receptor.

Q: To which malignancy myasthenia gravis is related?

A: thymoma
Q: what is the treatment?
A: anticholinesterase drug such as pyridostigmine.

Q: A pt comes with the complaints of inability to move Rt side of the body & deviation of the
mouth to the Lt side. What is your diagnosis?
A: stroke with Rt sided hemiparesis

NEXT: what is the site of lesion in this pt?

A: left cerebral cortex.

Q: If your pt. has hemiparesis or hemiplegia, what will be the site of lesion?
A: Anterior 2/3rd of posterior limb of internal capsule.

NEXT: which vessel is involved?

A: lenticulo-striate branch of middle cerebral artery (end artery & here lacunar infarction
happen)

NEXT: what is the cause of lesion?

A: may be thrombosis or embolism.

NEXT: what is the source of embolism?

A: cardic to artery (thrombus in heart it dislodge go to cerebral artery) and artery to artery
(thrombus in carotid a. it dislodge goes to cerebral artery )

NEXT: why hemiparesis occur?

A: Because all the compact fibre of pyramidal cell pass through this narrow area.

91
 Stroke
Q: Define stroke,TIA & completed stoke
A:
Acute stroke: acute stroke is characterized by the rapid appearance (usually over minutes) of a
focal deficit of brain function, most commonly a hemiplegia with/without signs of focal higher
cerebral dysfunction (such as aphasia) ,hemi-sensory loss & visual field defect or brainstem
deficit.

Classification of stroke:
TIA: when symptoms resolve within 24hours of onset.
Stroke: when neurological symptoms lasts >24hours
Progressive stroke/stroke in evaluation: the stroke in which the focal neurological deficit
worsen after the pt. first present. Such worsening may be due to increasing volume of infarction,
haemorrhage or related oedema.
Completed stroke: The stroke in which the focal deficit persists & is not progressing.

Q: Classification of stroke. Which one is more common?

A:
According to aetiology:
a) Ischaemic stroke (85%)
b) Heamorrhagic stroke (15%)

Q: How will you differentiate haemorrhagic stroke from ischaemic stroke?

A:
Haemorrhagic stroke Ischaemic stroke
Occur during activity ,excitement Occur in normal activity , even in sleep
Headache & vomiting followed by Associated with risk factors such as
unconsciousness HTN, hyperlipidemia
Pt has HTN with irregular anti- Carotid bruit & murmur & atrial
hypertensive therapy. fibrillation
Feature of raised ICP BP incr &
bradycardia

Q: What are the features of brainstem involvement?

A: Features of brainstem stroke (mnemonic ABCD)
A- Ataxia(loss of balance)
B- vertigo and/or Bilateral weakness
C- Crossed hemiplegia
D- Disarthria ( difficulty in articulation)

92
 Dysphagia
Dysphonia(tone)
Diplopia

Q: what do you mean by cross hemiplegia?

A: it means LMN type of cranial nerve lesion in one side & hemiperesis in the opposite side.

Where it is found?
A: In brainstem lesion.

Q: Mention the risk factors of stroke?

A: Unmodifiable (mnemonic GRAPH):
G-Gender (male>female, except in very young & very old)
R- Race ( Afro-Caribbean>Asian> European)
A- Age
P- Previous vascular event e.g. MI, stroke or peripheral embolism
H- Heredity

Modifiable (mnemonic ABCD-SHOP):

A- excess Alcohol consumption
B- high Blood pressure
C- Cardiac disease (atrial fibrillation, HF, endocarditis)
D- DM

S- Smoking
H- Hyperlipidaemia
O- OCP
P- Polycythaemia

Q: What will you do if you get pt with stroke?

A: history +examination+investigation

What examination will you do?

GCS- if unconscious
Neck rigidity, kernigs sign
Pupil- unequal-herniation
Pinpoint- pontine haemorrhage
Non-reacting- brainstem

93
 Cranial nerve palsy- 3rd, 6th, 7th nerve
Pulse- irregular- AF
Bradycardia- haemorrhage or ICSOL
BP- high BP- haemorrhagic stroke
Carotid bruit- if + , indicating atherosclerosis , source of embolus
Fundus- papilloedema- ICSOL, haemorrhage
Heart rhythm- (atrial fibrillation)
Murmurs- (source of embolism)
Apex beat- shifted or not
Peripheral pulses (generalized arteriopathy) & bruits(carotid)

Q: A pt comes with severe thunderclap headache, vomiting followed by unconsciousness. On

examination neck rigidity & kernigs sign is positive. What is your Dx?

A: Sub-arachnoid hemorrhage

Cause- ruptures of Barry aneurysm

Definitive Rx- Clipping of aneurysm vessel

Q: What do you mean by UMN?

A: Pyramidal cell & their axon up to anterior horn cell & up to motor neuclei of brain stem.

Q: What do you mean by LMN?

A: Ant horn cell & their homologous neuron in the brain stem with their axon upto effector
organ are called LMN.

Q: Write down difference between UMNL & LMNL.

A:
Traits UMNL LMNL
Fasciculation & wasting Absent Present
Tone Hypertonic Hypotonic
Reflex Deep reflex exaggerated Both superficial & deep reflex
are lost
Planter reflex Extensor Flexor
Clonus Present Absent
Paralysis Spastic flaccid

94
Q: Write down the causes of UMNL?
A:
Stroke
ICSOL
Cerebral abscess
Multiple sclerosis
Spinal cord compression:
3T: trauma, TB, tumor (2ndary & multiple myeloma)

Q: Write down the causes of LMNL?

A:
GBS
Poliomyelitis
Motor neuron disease
Diabetic amyotrophy

Q: What are the causes of stroke in old & young pt?

A:
Old pt with stroke Young pt with stroke
Causes are: Causes are:
HTN valvular heart disease
DM HTN
IHD Vasculitis
atherosclerosis AVM
Rupture Barry aneurysm
Hyperlidaemia

Q:

Cause of haemorrhagic stroke Cause of stroke in young pt.

Mnemonic-ABCD CAT HAS vasculitis
A Arteriovenous malformation C- Cardiac embolism(MS)
Amyloid angiopathy A- premature Atherosclerosis
B- BP- hypertension T- Thrombophilia
C-Coagulopathy Protein C
Anticoagulant therapy Protein S
Blood dyscrasia Antithrombin III
Thrombolytic therapy H- homocystinuria
D- Drugs: A- Antiphospholipid Ab syndrome
Alcohol S- Systemic lupus erythematosus
Amphetamine Vasculitis
Cocaine

95
Q: What investigation will you do in a pt with stroke?
A:
For Diagnosis: Imaging- CT Scan of brain
To detect cause & risk factor:
I. ECG
II. RBS
III. S. Creatinine
IV. Echocardiography
V. Fasting lipid profile

In CT- scan of brain:

Hemorrhage-hyperdense (white)
Infarction hypodense (black)

Q: What is the Rx of stroke?

A:
If unconscious If CT- scan show ischemic Haemorrhagic stroke
stroke
A Please add : If subarachnoid/ ventricular
B extension:
C Antiplatelet : Tab. Nimodipine 30
Diet- NG feeding Tab. Aspirin 75 mg mg 2+2+2+2+2+2 for
200 ml 2 hourly 0+1+0 21 days
Inj. Ceftriaxone 1 Tab. Clopidegrol Tab. Phenytoin 100 mg
gm 1vial iv bd 0+1+0 1+0+2 for 1 month
Inf. NS 1 L iv @20
drops/min If HTN: If midline shift:
Inj. Oradexon 1amp ACE inhibitor Inj. Manisol
iv stat & 8 hrly Anti-lipid
Inj. Ranitidine 50 If HTN:
mg 1 amp iv stat & If dyslipidaemia: ACE inhibitor
8 hrly Tab. Atorvastin 20 mg
Posture change 2 0+0+1
hrly
Continuous
catheterization
Eye care & mouth
care

96
Q: What are the causes of episodic loss of consciousness?
A:
TIA
Seizure
Syncope

Q: What do you mean by lacunars infarction?

A: occlusion of deep penetrating arteries produces sub cortical infarction characterized by
preservation of cortical function- language, other cognitive & visual functions.

Size of infarction- 0.5-1.5 cm in diameter

Site -
Periventricular white matter & basal ganglia 80%
Cerebellum & brainstem 20%

Q: A young pt comes with lt sided hemiparesis & examination reveals irregular pulse & diastolic
murmur. What is your diagnosis?
A: Mitral stenosis with AF & infarctive stroke (due to thromboembolism that arise from the
left atrium & goes to cerebral vessel.)

Q: In which condition jerk is absent with planter extensor?

A:
SCD
MND
Tabes dorsalis
Fredrich ataxia
DM with stroke

Q: A pt comes with absent rt knee jerk & exaggerated rt ankle jerk. What is the cause?
A:
It happens if lesion is in L3 & L4 level of spinal cord
Knee jerk absent as there is LMNL at the level of L3 & L4 & ankle jerk is exaggerated as
there is UMNL below it.

Q: 26 yrs old woman came to you with the complaints of unilateral headache with nausea,
vomiting & photophobia? What is the Diagnosis?
A: Migraine headache

97
 next you try to differentiate tension type headache and migraine headache:
points Tension type headache migraine headache
Site Bilateral, occipital, vertex Usually unilateral
character Dull ,diffuse, band like Throbbing pain
pressure
Duration & frequency Many hours to days, even Last for 24 hour to 72 hour
months
Severity Mild to moderate severe
Prodrome/aura Absent Visual aura ,tingling
sensation, numbness over
affected area , nausea
vomiting
Photophobia& Absent Present
phonophobia
Aggravating factor Workload, depression, anxiety Cheese, chocolate, red wine,
OCP, bright light, loud noise,
menstruation, changing
weather, citrus food, travel
Frequency Infrequently daily, episodic, Sub acute, acute, weekly,
chronic monthly, before menstruation

Q: Write down the characters of headache of ICP.

A:
Worse in morning, improves through the day
Associated with morning vomiting
Worse bending forward
Worse with cough and straining
Relieved by analgesic
Dull ache, often mild
Transient loss of vision

Q: A pt comes with chronic mild headache with hypertension and bradycardia with
papilloedema. What is the Dx?
A: ICSOL

98
Q: Give the treatment of migraine and tension type headache.
A:
Rx of migraine Rx of tension headache
Life style modification Drugs:
Regular exercise During acute attack:
Regular sleep patterns Tab. Paracetamol
Avoidance of excess caffeine and Anxiolytic
alcohol
Avoidance of acute changes in stress Prophylaxis:
level Low dose Amitriptyline 10 mg
Drugs: 0+0+1
A. During acute attack: NSAID,
Paracetamol
B. Prophylaxis:
Tab. Pizotifen 1.5-3.0 mg/day
0+0+1..continue

Q: What do you mean by Bells palsy?

A: It is the lower motor type of facial palsy.

Q: What are the causes of Bells palsy?

A:
Idiopathic
Viral infection-Herpes simplex

Q: Tell the pathophysiology of Bells palsy.

A: Bells palsy is an acute condition caused by swelling of he facial nerve in the facial canal
resulting in LMNL of 7th CN.

Q: Give the Rx of Bells palsy.

A:
i. Oral corticosteroid- Tab. Prednisolone 1mg/kg/day as single morning dose
ii. Acyclovir 2+2+2+2+2
iii. Use eye glass(eye shield) all the time
iv. Use eye pad(made of cotton or gauze) during sleep
v. Physiotherapy of upper eyelid muscle
vi. Physiotherapy of muscle of angle of mouth.

99
Q: What are the causes of unilateral & bilateral facial nerve palsy?
A:
Unilateral Bilateral
Bells palsy (idiopathic) GBS
Herpes zoster Sarcoidosis
Cerebellopontine angle tumours Lyme
Parotid tumour
Skull fracture

Q: what is Bells phenomenon?

A: When you close your eyes, your eyeball will roll upward. This is normal phenomenon. This
phenomenon seen in Bells palsy is called Bells phenomenon.

What will you see in ear?

After doing examination of 7th nerve forgets to see the ear & soft palate to see vesicle-
due to Ramsay Hunt Syndrome.

Herpes zoster

Q: A pt comes to you with unilateral vesicular rash in any part of the body, which does not cross
the midline. What is the Diagnosis?
A: SHINGLES (HERPES ZOSTER)

Q: Which organism is responsible for shingles?

A: Vericella zoster

Q: Where virus remains latent?

A: In dorsal root ganglia.

Q: How it enters into the body?

A: It enters into the body in early life as chickenpox & then remains dormant in dorsal root
ganglia.

100
Q: When/why it becomes reactivated?
A:
Spontaneous reactivation or
Due to immunosuppression (as in DM, malignant disease or AIDS)

Q: If this pt comes to you 1yr later with severe pain of affected areas, what is your diagnosis?
A: Post herpetic neuralgia.

Q: What is the Rx of Herpes zoster?

A:
Diet normal
Tab. Virux 400mg
2+2+2+2+2..7days
Topical Virux ointment
Over the affected area tds
Tab. Tryptin 25mg
0+0+1
Tab. Gabapen or Pregabalin 300 mg
+0+ or 1+0+1
Cap. Omeprazole
1+0+1, 45 min before meal

Parkinsonism

Q: A pt comes to you with resting tremor & difficulty in walking mainly starting, stoping &
turning with expressionless face. What is the Dx?
A: Parkinsonism (PD)

Q: What type of disease it is?

A: degenerative disease.

Q: What is the cardinal feature of PD?

A: mnemonic RBT
R- Rigidity
T- resting Tremor
B- Bradykinesia
Q: Where is the lesion?
A: Substantia nigra of midbrain.

101
Q: Why is the lesion?
A: Due to dopamine secretion.

Q: Tell the pathogenesis of PD.

A:
dopamine secretion from substantia nigra

Loss of balance between inhibitory Dopamine & excitatory acetylcholine

Relative in cholinergic transmission in caudate nucleus & Putamen

Tremor

Q: Tell about the C/F of Parkinsonian disease.

A:
Mask face
Hand writing (micrographia)
Resting tremor
Rigidity
I. Cogwheel
II. Lead pipe
Bradykinesia

Q: what are the disturbances of gait in PD?

A:
Slow to start & stop
Reduce arm swing
Difficulty in turning
Festinate gait

Q: What is the Rx of PD?

A:
Medical:
Dopamine supplementation
o Dopa-agonist: levodopa + carbidopa
Anticholinergic procyclidine

Surgery: not done

Options are: stereotactic thalamotomy
Fetal midbrain/adrenal gland implantation in basal ganglia

102
Q: Why Carbidopa is used?
A: it is a peripherally acting (does not cross BBB) dopa-decarboxylase inhibitor which prevent
peripheral (in GIT, blood vessel) conversion of levodopa.

Q: What are the causes of PD?

A: mnemonic PID (common) PG Hospital
I- Idiopathic (paralysis agitan)
P- Post encephalitis
D- Drug
P- Poisoning
Hospital - Herbicide
G- Genetic ( Wilson disease, Huntingtons disease)

Q: What do you mean by Parkinson plus? (not for all )

A:
When Parkinsons disease is present with one of the following disease:
Shy-Dragyer syndrome
Progressive supranuclear palsy
Olivo- ponto- cerebellar degeneration
Alzheimers disease,
Then it is called Parkinsons plus

Q: Name some involuntary movement.

A: mnemonic ABCD-MT
A- Athetosis
B- hemi Ballismus
C- Chorea
D- Dystonia
M- Myoclonus
T Tremor
Q: What are the causes of tremor?
A:
Exaggerated physiological tremor:
Anxiety
Thyrotoxicosis
Senile tremor
Drugs: e.g. salbutamol, theophylin

103
 Resting tremor:
PD/ extrapyramidal
Action tremor:
Flapping tremor
Respiratory failure
Renal failure
Hepatic failure
Intention tremor: cerebellar lesion

Q: A pt comes to you with bending of neck following after taking drug. What is the Dx?
A: Extrapyramidal syndrome (due to drug probably stemetil / anti-psychotic drug).

Delirium & Dementia

Q: Define delirium & dementia.
A:
Delirium: Acute confusional state in which pt is unaware of himself & surrounding.
Dementia: It is a clinical syndrome characterized by loss of previously acquired intellectual
function without impairment of arousal.

Q: Name two common cause of dementia?

A:
Alzheimers disease
Vascular dementia

Q: Name some common cause of dementia.

A: mnemonic VITAMIN D3
V- Vascularmultiple stroke
I- Infective syphilis, HIV, post encephalitis
T- Trauma chronic sub dural haematoma
A- Autoimmuneabsent here
M- Metabolic
I- Inflammatory- absent here
N- Neoplastic 2ndary, paraneoplastic
D- Degenerative Alzheimers, Wilsons, Huntingtons, Lewy body disease.
Deficiency B1 , B12
Drug & toxic material Alcohol, CO poisoning

104
Q: What is the treatable cause of dementia?
A:
Chronic sub dural haematoma
Cerebral tumour
Hydrocephalus
Deficiency

Q: A pt comes to you with the complaints that he forgets telephone no. address, can not
recognize known people. He goes out for market but eventually reaches the school. What is your
Dx?
A: Dementia
What may be the cause?
A: Alzheimers disease

Which drug is used?

A: Donepezil or rivastigmine or galamine.

Q: What do you mean by Wernicks encephalopathy? Give the Rx.

A: It is an acute confusional state presented with brainstem abnormality such as confusion,
opthalmoplegia, nystagmus, ataxia (mnenomics CONA). It is caused by thiamine deficiency &
often associated with alcoholism.

Treatment: -Thiamine 2 vial I/V 8hourly for 48 hour

-Followed by Tab. Thiamine 100 mg 8 hourly
-Rx of the cause.

Q: What is Wernick-korsakoff syndrome?

A: It is an organic brain disorder resulting from damage to mamillary body & dorsomedial nuclei
of thalamus adjacent & adjacent areas of periventricular grey matter due to thiamine deficiency
often associated with chronic alcohol misuse.

Feature: mnemonic SmC

Sm- short term memory loss
C- Confabulation
If Wernick-korsakoff syndrome is left untreated it turns to Irreversible Wernick-
korsakoff syndrome.

105
Q: What are the differences between Wernick-korsakoff syndrome & Wernick encephalopathy?
A:
Wernick encephalopathy Wernick-korsakoff syndrome
Acute Chronic
Reversible Irreversible
Remission if treated No Rx available

Q: What do you mean by Delirium tremens?

A: It is a form of delirium associated with severe alcohol withdrawal.

Feature: mnemonic I HAD

I- Illusion
H- Hallucination
A- Agitation
D- Delusion
Q: A pt comes to you with lower motor type of (flaccid) paraparesis & unable to pass urine. On
examination there is definite sensory level at T10. What is the Dx?
A: Dorsal myelopathy with spinal shock. It is upper motor type of lesion here jerk and planter
flexor due to spinal shock

[ Myelopathy- lesion in the spinal cord

Radiculopathy- lesion in the nerve root]

Q: why this is not a case of GBS?

A: As sensory & bladder, bowel is involved (not involved in GBS).

Q: What are the causes of dorsal myelopathy/ spinal cord pathology?

A: 4T
Non-compressive:
Acute Transverse myelitis
Compressive: 3T
Trauma
TB- potts
Tumour

Q: What history you have to take in case of acute transverse myelitis?

A: H/O fever & diarrhea 3/4 wks back.

Q: What is the inv in case of acute transverse myelitis?

A: MRI of dorsal spine.

106
Q: What is the Rx in case of acute transverse myelitis?
A: Inj. Methyl prednisolone.
Q: A pt comes with inability to see with rt eye, lt sided hemiparesis & cerebral sign. He has H/O
similar type of attack 2 years back. . What is the Dx?
A: Multiple sclerosis

Q: What is the presentation of MS? What r the site of lesion

A: eye optic neuritis
Cerebral cortex upper motor lesion hemiparesis , aphasia
Cerebellum cerebellar sign
Spinal cord ---paraparesis
Sensory loss
Q. what type of disease it is ?
A. demyelinating disease
Q. what investigation u have to do ?
A. CSF---oligoconal band
MRI--
Q.Treatment ?
1. Treatment of acute exacerbations:
Pulse IV methyl prednisolone0.5-1 gm/D for 3 to 5 days.
2. Prevention of relapse:
Azathioprine.
3. Symptomatic treatment:
Spasticity: give muscle relaxant.
Bladder: give anticholinestrase

Q: When a pt. smokes, he burns his hand.. What is your Dx?

A: Syringomyelia (due to dissociated sensory loss in which there is loss of sensation of pain &
temperature but dorsal column is intact)

Q: A pt. when splashes his face with water, he fall down. Why?
A: Due to sensory ataxia.
Q define Ataxias
A. It is an Incoordination of voluntary movement in absence of motor weakness

107
 Environmental and Nutritional Factor Diseases
NAME SOME ENVIRONMENTAL DISEASES

Cold injury

Frostbite
Non-freezing cold injury (trench or immersion foot

Heat related disease

Heat syncope
Heat exhaustion
Heat stroke
Heat cramp

High altitude--Acute mountain sickness (AMS

Drowning and near-drowning

Name some disease of hot environment?

Heat syncope
Heat exhaustion
Heat stroke
Heat cramp
Q. What do you mean by heat exhaustion and its treatment?
Heat exhaustion is condition which occur due to prolonged exertion in hot and humid weather
with profuse sweating and inadequate salt and water replacement
It occur when core temp: 37-400
Treatment
Nonpharmacological
removal of the patient from the heat, and
Cooling using tepid sponging and fanning (strip-spray-fan).
Pharmacological :
Hydration with
oral rehydration mixtures or (up to 5 L in 24 hr)
Intravenous isotonic saline.
What is complication of heat exhaustion
, heat exhaustion may progress to heat stroke
what do you mean by heat stroke and write down its treatment
Heat injury (heat stroke) is an acute life-threatening situation occurs when the core body
temperature rises above 40 C.
Clinical feature:

108
 Headache, nausea, vomiting and weakness,
Neurological: confusion, coma and death.
The skin feels very hot to the touch.
Sweating is often absent
Treatment
Resuscitated the patient with rapid cooling by
spraying with water,
fanning and
ice packs in the axillae and groins.
IV fluid
o Cold crystalloid intravenous fluids are given(but potassium fluid containing should
be avoided)
Manage in intensive care
Q a patient becomes unconscious during working at field in very hot humid day. What is
your diagnosis and what how you manage it?
The patient is suffering from heat stroke :
Management : like heat stroke
What is the causes of heat cramp
It is Painful muscle cramps, usually in the legs, often occur when people exercise
excessively in hot weather
Cramps are probably due to low extracellular sodium caused by excess intake of water
without salt .

Cramps can be prevented by increasing dietary sal

What do you mean by drowning and near drowning ?

Drowning is defined as death due to asphyxiation following immersion in a fluid.
Near-drowning is defined as survival for longer than 24 hours after suffocation by
immersion
What do you mean by dry drowning ?
Between 10% and 15% of drownings occur without water aspiration into the lungs.
Laryngeal spasm develops acutely, followed by apnoea and cardiac arrest.
How will manage a case of near drowning?
At the spot
CPR should be started immediately
It is important to clear the airway of foreign bodies and protect the cervical spine.
At hospital
administration of oxygen and maintenance of the circulation
give Continuous positive airways pressure (CPAP) if oxygen saturations below 94%

109
 give Prophylactic antibiotics if it occur in contaminated contaminated water
correction of electrolyte imbalance and metabolic acidosis
What happened in drowning ?
Hypoxaemia
Metabolic acidosis
electrolyte imbalance
Acute lung injury
complication
o dehydration,
o hypotension,
o haemoptysis,
o rhabdomyolysis,
o renal failure and cardiac dysrhythmias.

What metabolic and electrolyte imbalance occur in sea water and fresh water
drowning
Fresh water hypotonic haemolysis of RBC Sea water as hypertonic
Metabolic acidosis Metabolic acidosis
Hyponatraemia Hypernatraemia and hypercalcaemia
Alveolar collapse Alveolar edema

110
Write down the consequence of drowning or near-drowning :
inhalation of water inhalation of water

Fresh water is hypotonic Fresh water is hypotonic

rapidly absorbed across alveolar membranes Salt water is hypertonic

which leads to alveolar collapse and impairs So fluid comes into alveoli from vessel
surfactant function

Imbalance of ventilation-perfusion provokes alveolar oedema

hypoxaemia

diffuse pulmonary oedema

What r the problem u may face if u go to high altitude?

To remember: MRCP

M--Acute mountain sickness (AMS)

R-- Retinal haemorrhage
C--- Cerebral oedema
P-- pulmonary oedema

What r the feature of acute mountain sickness?

Headache , lassitude , anorexia ,nausea and vomiting

What do you mean by decompression illness?

When we go under water partial pressure of gass is increase so more gass (nitrogen) is dissolved
.when driver descend more nitrogen is dissolved in blood . the amount dissolved depends on the
depth/pressure and on the duration of the dive.

On ascent, the tissues become supersaturated with nitrogen and other gass as partial pressure is
decrease.These extra nitrogen that was desolved released as gas bubbles in tissues if the ascent
is too fast.produce following symptoms in different part of the body .

111
 Pain: often large joints, e.g. shoulder ('the bends')
Neurological: any deficit is possible
Ear : vertigo, tinnitus, nystagmus; may mimic inner ear barotrauma
Pulmonary: chest pain, cough, haemoptysis, dyspnoea; may be due to arterial gas
embolism
Cutaneous: itching, erythematous rash
Lymphatic: tender lymph nodes, oedema

Name one common environment disease occurs in Bangladesh?

Arsinocosis

What normal arsenic level in drinking water ?

The World Health Organization (WHO) guideline value for arsenic content in tube well water is
10 g/L
Clinical feature of chronic arsenocosis ?
Clinical features of chronic arsenic poisoning
GI tract
Anorexia, vomiting, weight loss, diarrhoea, increased salivation, metallic taste
Neurological
Peripheral neuropathy
Skin
Hyperpigmentation,
palmar and plantar keratosis,
alopecia
Bone marrow
Aplastic anaemia
Increased risk of malignancy
Lung, liver, bladder, kidney, larynx and lymphoid system

What is normal fluride level in water?

Normal fluorides at levels of 1 part per million (ppm)
What do you mean by Fluorosis ?
the presence of excessive quantities of fluoride (> 10 ppm)
it cause pigmentation of teeth

112
What are the complications of obesity

Coronary heart disease

'Metabolic syndrome'
Sleep Apnoea
Osteoarthritis
Fatty liver
Gallstones
Exertion dyspnoea
Type 2 diabetes
Psychological morbidity
Stroke
Poly cystic ovaries syndrome

Name some reversible cause for weight gain

Hypothyroidism
Cushing's syndrome
Insulinoma
Drug
Name some causes of drug that causes weight gain
Drug treatments
Tricyclic antidepressants
Estrogen-containing contraceptive pill
Corticosteroids
Sodium valproate

What do you mean by BMI?

BMI is calculated as the person's weight in kilograms divided by the square of his or her height
in metres (kg/m2). For example, an adult weighing 70 kg with a height of 1.75 metres has a BMI
of 70/1.752 = 22.9
<18= under weight
18.5----24.9= normal
25----29.9 = over weight
>30= Obesity
How will manage a case of obesity?

113
 Vitamin
Name some fat soluble and water soluble?
Fat soluble : ADEK
Water soluble : BC

Name of vitamin Source Disease due to deficiency

Vitamin A Liver, milk, butter, cheese, fish oils Xerophthalmia,
night blindness,
keratomalacia,
follicular hyperkeratosis
Vitamin D Sunlight Rickets, osteomalacia
Vitamin E Vegetables, seed oils Haemolyticanaemia, ataxia
Vitamin K Green vegetables, dairy products Coagulation disorder
B
Thiamin Cereals, grains, bean, Beri-beri, Wernicke-Korsakoff
(Vitamin B1) Meat, fish syndrome
Riboflavin glossitis, angular stomatitis
(Vitamin B2) and cheilosis
Niacin Pellagra
Vitamin B6 Polyneuropathy
(Pyridoxine)
Vitamin B12 Animal products MegaloblasticAnaemia,
(Cobalamin) neurological degeneration
Folate Vegetable s MegaloblasticAnaemia

Vitamin C Fresh fruit and Scurvy

(Ascorbic acid) vegetables

What is effect of hyper vitaminosis of Vit-A?

Acute overdose leads to nausea and headache, increased intracranial pressure and skin
desquamation.
Chronic overdose :liver damage, hyperostosis and teratogenicity

114
What are human source of Vit-K?
Vegetables source : leafy vegetables and liver
In human :synthesised by bacteria in the colon
Name Vit- k depend coagulating factor ?
II, VII, IX and X
Mention 3 clinical uses of vitamin K?
To prevent haemorrhagic disease of the newborn.
In obstructive jaundice
Warfarin induced bleeding

What are the feature of vitamin B1 deficiency?

Dry ( neurological) beri-beri
Wet (cardiac) beri-beri
Feature of dry beri-beri
peripheral neuropathy, and wrist and/or foot drop,
Korsakoff's psychosis
Wernicke's encephalopathy
Wet (or cardiac) beri-beri feature :
generalisedoedema
biventricular heart failure
pulmonary congestion

Treatment of wet beriberi?

Wernicke's encephalopathy and wet beri-beri should be treated without delay with i.v. thiamin
A patient come to you with complain diarrhea , skin lesion what is your diagnosis ?
Pellagra
What is pellagra ?mention it treatment ?
It is occur due to Vit-B(niacin )deficiency .
It is characterized by 3 D
Dermatitis: especially on the neck (Casal's necklace)
Diarrhoea.:
Dementia :
Treatment is with nicotinamide, given in a dose of 100 mg 8-hourly by mouth
What is the feature of vitamin B-12 deficiency ?
Optic atrophy
Peripheral neurophathy (dorsal column)
Dementia
NAM E SOME ANTI-OXIDANT
C, E, and beta-carotene, and the antioxidant mineral zinc,

115
 Geneitic

How many chromosomes human have?

Human have 23 pair of chromosome of then 22 are autosome and 1 is sex chromosome .

What do mean by gene?

Genes are functional units of the chromosome. It produce messenger mRNA from DNA. this
mRNA is responsible for protein synthesis .

What do u mean by transcription and translation?

Transcription is the formation of mRNA from DNA
Translation is process of formation of protein by mRNA

What do you mean by haploid and diploid chromosome? Which cell contain haploid and
diploid chromosome?
When chromosome number is 23 is called haploid present germ cell like sperm and ovum karyo
typing 23X or 23Y
When chromosome number is 46 is called diploid present somatic cell 46, XY

In human chromosome have each has two copies one come from mother and one from father
Homozygote state : when both the copy of the gene is defected
Heterozygote state when one of copy of the gene is defected / abnormal and other is normal
Autosomal dominance: disease express in Heterozygote state
Autosomal recessive: disease express in Homozygote state
When will trait / carrier : it found in autosomal recessive when one chromosome have defected
gene and other chrosome is normal . it will not manifest disease .

Write down the feature of Autosomal dominance:

Autosomal dominance Autosomal recessive

Disease only manifested in Heterozygote
state
No carrier sate
run from generation to generation
In each pregnancy
o 50% of his offspring have chance to
have / transmit the disease
Disease only manifested in Homozygote
state (both chromosome is affected )
Have carrier sate / trait (when only one
chromosome is affect )
run from generation to generation
In each pregnancy
o 25% of his offspring have chance to

116
 o 50% of his offspring have chance to have / transmit the disease
be normal o 25% of his offspring wil be normal
One of his parent is have affected o 50% of his offspring have chance to
chromosome be carrier or trait
Both of the parent carry the affect
chromosome

Name some AD and AR Disease

Autosomal dominance(AD) Autosomal recessive (AR)

MnemonicMAN PH CSF , WHAT
M---Marfan's syndrome W--Wilson's disease
A---Familial Alzheimer's disease H---Haemochromatosis
N---Neurofibromatosis A--1-antitrypsin deficiency
P----Polycystic kidney disease T--- thalassaemia (Alpha- and beta)
H---Huntington's disease C--Cystic fibrosis
S--Sickle-cell disease
F--Friedreich's ataxia

What r the characteristic of SEX link disease

X-link recessive Female are carrier

Male are sufferer
50% of his male child is sufferer and 50
% of his male child will be normal
50% of his female child is carrier and 50
% of his female child will be normal

Can female become sufferer Yes if in following way

Due to lionization theory

If female carrier married diseased male
Turner

Give example mnemonic HAD H---Haemophilia A and B

A--Alport's syndrome
D--Duchenne muscular dystrophy
Name one sex linked dominant disease Hypophosphataemic rickets

117
What do you mean by lionization theory Random inactivation of one of the two X
chromosome is called lionization theory

Mitochondrial DNA comes from mother So both male and female are affect but
affect female transmit the disease . But
affected male does not transmit diseases

Frequent question will be ask about the syndrome must read karyotype and some
important

Phenotype

Down's syndrome (trisomy 21)

Write the karyotype 47,XY,+21 or 47,XX+21
Why it is called trisomy 21 We know that normal human contain diploid
number of cell that mean 46XY OR 46 XX. In
down syndrome pt have one extra chromosome
that is 21. So he / she has three 21
chromosome. that why called Trisomy 21
Phenotype or clinical feature Characteristic facies
o Epicanthic folds (picture 1)
o Flat nasal bridge
o Low-set small ears
o Open mouth
o Large Protruding tongue
o Short neck
o Transverse palmar (Simian) crease
IQ Less
Heart Congenital heat disease (VSD)
Clinical scenarios a boy come your chamber he Down syndrome
begin to dance when some start music what is
ur diagnosis

118
 Klinefelter's syndrome Turner's syndrome
Phenotype Male Female
Karyotype 47,XXY 45,X
Stature Tall stature Short stature
Clinical feature Phenotypic male, Phenotypic female,
Tall stature short stature,
infertility, webbed neck,
Gynaecomastia, coarctation of the aorta,
small testes primary amenorrhoea
fish mouth appearance

Name disease of old age

FALL
DEMENTIA
CATARACT
BEP
HYPERTENSION
STROKE
HEARING LOSS
OSTEOARHTRITIS
OSTEOPOROSIS

Cause of fall in old age

Postural hypotension
Visual disturbance
Accidental
Osteoarthritis
Drug
Perkinson disease
Muscle weakness
Gait or balance abnormality
Use of a walking aid

119
 Define postural hypotension
If postural hypotension defined as a drop in blood pressure of > 20 mmHg systolic or > 10
mmHg diastolic pressure on standing from supine
Cause
Autonomic neuropathy DM
Addison disease
Drugs vasodilator
Management of postural hypotension
Correction of dehydration
Head-up tilt of the bed
Support stockings
NSAIDs
Fludrocortisone (causes salt and water retention)

Critical care illness

What are feature of shock?

Rapid, shallow respiration

Cold, clammy skin
Tachycardia (> 100/min)
Drowsiness, confusion, irritability (usually occurs late)
Oliguria
Multi-organ failure

How will differentiate between septic shock and hypovolaemic shock ?

hypovolaemic shock septic shock

HO fluid or blood loss Ho of infection or septic focus
Cold, clammy skin Warm periphery
Thread pulse Bounding pulse
Hypotension (systolic BP < 100 mmHg) Hypotension (systolic BP < 100 mmHg and
disproportionately low diastolic BP-early

Name the following definition

Bacteraemia Viable bacteria in the blood
Systemic Defined by the presence of two or more of:
inflammatory Respiratory rate > 20/min
response Heart rate > 90/min
syndrome (SIRS) White blood count > 12 109/L or < 4 109/L
Temperature > 38.0C or < 36.0C

120
 PaCO2 < 4.3 kPa (< 32 mmHg) or ventilated
Sepsis Systemic inflammatory response caused by documented infection

Severe sepsis Sepsis/SIRS with evidence of early organ dysfunction or hypotension

Septic/SIRS Sepsis associated with organ failure and hypotension (systolic BP < 90
shock mmHg or > 40 mmHg fall from baseline) unresponsive to fluid therapy

Admission criteria for intensive care units (ICU)

Patient needs intubation and mechanical ventilator support
Patients need support of 2 or more organ (e.g. inotropes and haemofiltration)
Patients with chronic impairment of one or more organ systems (e.g. COPD or severe
ischaemic heart disease) who also require support for acute reversible failure of another
organ system

high-dependency units (HDU

Patients who require more detailed observation or monitoring than can be safely provided on
a general ward:

o Direct arterial BP monitoring

o CVP monitoring
o Fluid balance
o Neurological observations, regular GCS recording

Patients requiring support for a single failing organ system, excluding invasive ventilatory
support:

o CPAP or non-invasive (mask) ventilation (NIV)

o Moderate inotropic or vasopressor support
o Renal replacement therapy in an otherwise stable patient

Patients no longer requiring intensive care but who cannot be safely managed on a general
ward

121
A very cachetic or emaciated patient admitted in your ward? You give NG feeding and
patient died after NG feeding what may the cause ?
Due to refeeding syndrome
Because patient was feed carbohydrate rich food and which causes hypokalaemia
and pt died due to arrhythmia
What may another causes
Patient was in B1 deficiency . giving only glucose causes wernicks encephalopathy

What is the name of your book ?

Davidsons principles and practice of medicine , 21 edition
Part of the book ?
Part one principle of medicine
Part two practice of medicine

122
 Respiratory Disease
Q.Name some respiratory emergency?
Tension pneuumothorax
Acute severe asthma
Acute exacerbation COPD
Q.Name disease of respiration you have seen in ward?
COPD
Bronchial asthma
Pneumothorax
Pleural effusion
Pulmonary TB
Bronchogenic carcinoma

Q.GKUv Pt. Zvgvi KvQ Avmj sudden severe respiratory distress with chest pain.What is
your DX?
Tension pneuumothorax
Acute LVF

Q.Have you seen any Pt. of pneuumothorax?

Yes,How they come to hospital ? sitting or lying sitting position

Q.what is the finding of tension pneuumothorax?

GE cyanosis
Pulse: feeble
BP:hypotension & sweaty ,cold hand
On exam
trachea shifted to opposite site
percussion hyper-resonance on affected side
breath sound diminish on affected side

Q.what is the definite sign of pneuumothorax?

percussion: hyper-resonance
breatth sound : deminish

Q.what will you do in that pt?

O2 inhalation
Immediately insertion of wide bore needle at 2nd intercostal space at
level of mid-clavicular line
Then intercostal drain followed by water sealed drainage

QIntercostal drain tube Kvb space G `Iqv nq?

GUv 4th ,5th , 6th intercostal space G mid-axillary line `Iqv nq|Tube direction _vK
upwards

Q.GB drain Tube KLb remove Kiv nq ?

24 hr after full inhlation lung or,
24 hr after stop bubbling

123
Q KLb Thoracotomy KiZ ne?
If bubbling continue after 5-7 days of IT tube insertion
QCauses of pneuumothorax?
According to etiology [ to remember SIT]
S spontaneous
primary 1) rupture apical subplural bleb
2) emphysematous bullae
secondary 1) COPD
2) TB
3) Lung abscess
4) Bronchial asthma

I Iatrogenic [aspiration pleural fluid]

T Traumatic chest injury

Q.Type of pneuumothorax anatomical

[to remember COT]
C closed communication between the lung & pleural space sealed off
O open - communication between the lung & pleural space persist
T tension/valvular pneumothorax one way valve, air can enter inspiration
cannt escap during expiration
QKv_vq hydropneuumothorax common?
Open type of spontaneous pneuumothorax

Q RX of pneuumothorax?
Primary pneuumothorax
Closed type mild< 20% , moderate 20-50 %,large > 50%
Mild < 20% of lung volume or lung edge is less than 2 cm from the
chest wall are normally absorb
Moderate to large percutaneous aspiration with wide bore needle
Open type & Tension pneuumothorax IT(intercostal) insertion
Secondary pneuumothorax
COPD IT tube
Q. percutaneous aspiration KLb e Kie?
Aspiration> 2.5
Pt cough excessive
Felt resistance during aspiration

Q Kvb space nZ aspiration Kiv nq?
2nd intercostal space at mid-clavicular line

QHow will you manage a Pt with IT tube?

Observe that bubbling present or not
if bubbling ceased-then do a x-ray 24 hrs later
if lung fully expand then remove it
if bubbling persist after 5-7 days do thoracotomy
if bubbling caesed then check the tube for any obstruction

124
Q.Name some causes of recurrent pneumothorax?
{To remember- CASE]
S- Subpleural bullae
E- Emphysematous bullae
C- Cystic febrosis
A-alpha anti trypsin deficiency

Q.RX of recurrent pneumothorax?

Chemical pleurodosisby give Inj. Tetracycline, Kaolin or Talc via IT tube
Surgical pleurodosis--- by pleural abrasion or parietal pleurectomy

Q.Indication of thoracotomy?
persistent air leak or unexpanded lung after 5-7 days of giving IT tube
3rd recurrence

Q. wK Dc`k w`e pneumothorax Gici?

wegvb DVZ bv Kie 1-2 mvn ch after full inflation of lung

Q. 45 yrs old man comes to you with haemoptysis.what will you do?
At first I will do resuscitation of this Pt
See pulse, BP & urine output
Give immediate open a I.V. channel (Inj. Hartsol 1000 I.V 20dl/min)
Do blood grouping & cross matching
Give one unit of blood
After resuscitation try to find out the cause
For this I take H/O,do clinical exam and some investigation when the Pt is salt led

Q. Common cause
TB
Bronchongeinc Ca
Bronchiectasis
Acute/chronic bronchictis
Acute pulmonary edema due to acute LVF

Q.What H/O,exam or investigation after resuscitation?

H/O low grade fever cough: TB

Voice change+smooker,Wt loss: Br. carcinoma
H/O breatlessness & cough: Bronchitis
Fever & cough with productive,foul smell sputum: Bronchiectasis
HTN,chest pain& H/O heart disease,orthropnea: Acute LVF

Examination
Clubbing,lymphadenopathy or SVO & horners :Gas fever Br. carcinoma
Cyanosis,clubbing,coarse geps: Bronchiectasis
Vesicular breath soundwith prolong expiration with cough: Bronchitis
Cyanosis,tachycardia,bilateral basel gep,murmur,gallop rhythm: Acute LVF
125
Next I do investigation:
TC,DC,ESR ESR- in TB,BR. ca
Sputum for AFB: TB
Sputum for malignant cell: Bronchogenic carcinoma
MT: positive TB
CxR PA: TB, Br. Ca, Bronchiectasis,Bronchitis,LVF
Bronchiectasis: honey comb, ring like,tram line
Bronchitis: COPD feature
LVF: Perihilor hoziness,Bat wings, Kerlys B.line,Cardiomegaly, upper lobe
diversion
If lymph node palpable: FNAC, Biopsy
if suspect Br.carcinoma:
PeripheralCT biopsy
Central lession: Bronchoscopy & Biopsy,Bronchial cleavage
ECG- to LVF

Pneumonia
Q.A 30 yrs old man comes to you with fever,chest pain,cough for 5 day.On xm, you
find increase breath sound,Bronchial or increase & percussion is not dull.What is
your diagnosis?
Pneumonia/ pheumonic consolidation/CAP

Q.What is Pneumonia?
Pneumonia define as acute respiratory illness with recently developed
radiological pulmonary shadows which be lober,segmental or multilober.

Lober pneumonia:It is radiological or pathological term referring to homogenous

consolidation of one or more lobe of lung often associated with pleural inflammation.

Bronchopneumonea: Refer to patchy alveolar consolidation associated with bronchial

& bronchiolar inflammation affected both lower lobes.

Q.Name the common organism in CAP?

[to remember MSC in low]
3. M- Mycoplasma pneumoniae
1. S- Streptococcus pneumoniae
4. C- Chlamydia pneumoniae
Low- legionella pneumoniae
Less common [to remember- HSC]
2.H- Haemophilus influenzae
S- Staphylococcus aureus
C- Chlamydia prittaci

Common: 1,2,3,4

QGKUv Pt Zvgvi KvQ Avmj Breath sound increase & vocal resonance increase. 2 w`b

126
 ci `Lj Breath sound deminesh & percussion note dull/ stony dull.what is Dx?

A. This case of pneumonic consolidation.now,turn into para pneumonia effusion or

Empyema

Q.Pneumonia pt Gi wK investigation Kie?

CBC--- Neutrophelic leucocytosis
MT
Sputum for AFB
CXR PA---- consolidation

Q.Ligeonella Gi Rb wK investigation Kie?

Ligeonella Gi Rb Antigen `wL urine G

Q.Radiological shadow AvmZ KZY mgq jvM?

12-18 hr

Q.A pt with pneumonic consolidation & but get crep+ on auscultation .what Dx?
Pt is in resolution phase

Q.Pneumonia pt Gi wK Rx?
Specefic:
Uncomplicated: Cap: Amoxycillin(500 mg) 1+1+1----------7-10 days
Severe:
Inj. co-amoxyclav 1.2 1ampI.V.8hrs
Inj. clarithromycin 500 mg 1 amp I.V. B.d
Surpportive:
O2 inhalation of need
Pain killer----NSAID( but if not control/severe nj opiate `B)
Fluid balance

Q.What are the complication of pneumonia?

parapneumonia effusion
empyema
Lung abscess
ARDS
Pneumothorax
All itishepatitis, pericarditis, myocarditis, meningoencephalitis

Q.A pt of pneumonia not responding to Rx.Dx?

Diagnosis wrong(TB)
developed complication like empyema
atypical organism/inappropriate or vinadequate drugs

Q.Nosocromial/Hospital acquired pneumonia?

Pneumonia that occur at least 2 days after admission into hospital

Q.Gi organism bvg wK?------[to remember: KEP]

EE.coli

127
 K-- Klebsiella
Ppseudomonas

Q.Gi Rx wK?
Injectable 3rd generation cephalosporin [ cefotaxin/ceftriaxin with
aminoglycosides- gentamycen]
Q.what do you mean by CURB-65?
C- confusion
U- urea> 7 mmol
R- respiratory rate> 30/min
B- Blood pressure[ systolic<90,Diastolic<60]
65- Age>65
each pointscore-1
0/1- home Rx, 2- hospital supervised 3 or more- ICU treatment

Q.How will you differentiate between viral & bactereal pneumonia?

viral pneumonia Bacterial pneumonia

Onset less abrup,H/O RTI acute or abrup onset
cough Dry Productive
pain uncommon common
CXR normal feature of consolidation
CBC Leucopenia leucocytosis

Q.A pt comes to you clubbing. What are the causes?

Respiratory causes----
Bronchogenica
Suporrative lung disease
Bronchiectasis
Lung abscess
Empyema

Q.what do you mean by empyema?

Collection of pus in plural space

Q.A pt comes to you with foulsmelling & clubbing & fever.what is your Dx?
or
Zzwg IqvW ivMx `LQ|Ggb mgq GKUv jvK Gm Kvwk w`q Kd ei nj `~M mviv IqvW fi Mj|
Dx wK?
Bronchiectasis
Lung abscess

Q.GKUv ivMx Zvgvi KvQ clubbing & bilateral coarse Gep(+) wbq Avmj|what is your Dx?
Bronchiectasis
Fibrosing Alveolitis(ILD)

Q.How will difference between ILD& Bronchiectasis?

ILD& Bronchiectasis both have clubbing & Gep(++). But coughing Gep in
Bronchiectasis is disappear or alter.But in case of fibrosing alveolitis Gep does not
alter after coughing.
128
Q.Define Bronchiectasis?
Permanent destructive dilatation of Bronchi proximal to terminal Bronchiole.

Q.Causes of Bronchiectasis?
Congenital causes----[to rememberCKD]
C- cystic fibrosis
K- Karteyener syndrome
D- primary celliary dyskenesea
Acquired causes-----[to remember---PTB]
P- pneumonia
T-T.B.
B- Bronchogenic carcinoma {in case of children----foreign bodies}

Q.which investigation is more sensitive in Dx Bronchiectasis?

CT is most sensitive

Q.Complication of Bronchiectasis?
recurrent infection
abscess formation
empyema
pulmonary HTN
corpulmonale
Res. failuretype 11
amylodosis

Q.A pt of Bronchiectasis comes to you with generalized oedema.what is your Dx?

amylodosis

Q.Rx of Bronchiectasis?
[to remember PAST]
Ppostural drainage chest physiotherapy
A- antibiotic ( during acute infection)
S- Surgery( if young pt & confined, unilateral & localized single lobe)
T- Heart-Lung transplantation( Done in bilateral extensive Bronchiectasis)

Q.Clinical presentation?
Coughchronic productive foul smelling spudum,that increase in change posture
& more marked in murmer.
Clubbing
Haemoptysis
Coarse Gep that changed after coughing

Q.what are X-ray finding of Bronchiectasis?

ring like shadow( ring with clear centre)
honey comb appearance
lenear streak or termline
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Q.Common site of Bronchiectasis?----- lower lobe of left lung
Q.what do you mean by dry Bronchiectasis / Bronchiectasis Sicca?
When Bronchiectasis with dry cough thin called it dry Bronchiectasis.It present
with haemoptysis.

Q.Rx of lung abscess?

Injectable antibiotic
Inj. Amoxycillin, Inj. Gentamycin, Inj. Metronidazol
Q. how long you will give the antibiotic (must remember)
(6-8 weeks)
Q. what will do if not respond by medical treatment ?
medical Rx G respond bv Kij percutaneous aspiration eighter CT/uSG guidal

Q. Causes of lung abscess?

[to remember---SHIBA]
A- aspiration
B- bronchial obstruction
I- Specific infection
H- haemotogenesis
S- spread from local structure such as sei phraeg & lung abscess

Q.Complication of lung abscess?

pleurisy
empyema
Bronchiectasis
metastasis abscess
amylodaures

Q.Investigation for lung abscess?

CBC
MT
Sputum for AFB
Sputum for maleynon cell
Sputum for gm stain & CS
CXR

Q.Classify Bronchogenic carcinoma?

Small cell20% Non small cell-- [SAL]
Squamous cell- 35%
Adeno carcinoma- 30%
Large cell carcinoma- 15%

Q.which is most dangerous and why?

Small cell carcinoma as early wide spread metastasis

130
 Bronchogenic carcinoma
Q.Which is peripheral bronchogenic carcinoma?
Squamous cell carcinoma
Periphery carcinoma grow largely without producing symptoms. Central lesion
small but produce early symptom

Q.Clinical feature of Br. carcinoma?

cough
haemoptysis
bronchial obstruction---- collapse/ consolidation
superior venacava obstruction
breathlessness & hoarsness of voice
pain
Q. examination Kij wK cve?
clubbing
cervical lymphadenopathy
SVO
Horners syndrome

Q.Name some non metastatic extra pulmonary menifestation of bronchial carcinoma?

Small cell carcinoma -SIADH---hyponatraemia

endocrine
-ACTH---cushing
-carcinoid tumour

Squamous cell carcinoma -hypercalcaemia

Large cell carcinoma -gynaecomastia
Any type of carcinoma
Neurological---
polyneuropathy
myelopathy
MND
Nyasthenia Clum bert-eatim Syndrome
Musculoskeletal
polymyositis & dermatomyositis
Nephrotic syndrome
Clubbing & hypertrophy pulmonary(no small cell) osteoarthropathy

Q.Where is clubbing?-------non small cell

Q.Where is hypercalcaemia?-------Squamous cell

Q.where is gynaecomastia?----------large cell

Q. Endocrine(SIADH,ACTH,Carcinoid)?----------- small cell

Q.what do you mean by hypertropic pulmonary osteoarthropathy(HPDA)?

It is tender& painful swelling of distal end of tibia,febula,radius & ulnaa
131
 Due toperiostitis & subperiosteal new bone formation
Kv_vq _vK clubbing Gi mv_-------non small cell carcinoma

Q.what investigation you will do?

CBC--ESR
sputum for malignant cell
If lymphnode palpable----FNAC/Biopsy
CXR
If lesion is peripheral ---CT/USG guided FNAC
if lesion is central-------
Bronchoscopy & biopsy
Bronchial brushing for malignant cell
Q.Mention the Rx of Bronchogenic ca?
Surgery ( only stage 1)
radio therapy
chemotherapy

Q.Which is chemo sensitive? ------small cell carcinoma

Q.Which is radio sensitive?-------- Squamous cell

Q.Name the chemotherapeutic agent use in Br.Ca?

[to remember---CVD or CE]
C- cyclophosphamide C- Cisplalin
V- Veingistine E- Etoposide
D- Doxorubicin
3to 6 cycle after every 3 weeks interval.
non small cell carcinoma is chemo sensitive

Q.Indication of Radiotherapy?
squamous cell ca.
SVO
reecurrent haemoptysis
chest pain/skeletal metastasis
bronchial obstruction

Q.what are the radiological finding in bronchogenic ca.?

peripheral opacity
collapse
pleural effusion
hilar lymph adenopath & paratracheal lymph
rib destruction
elevation of hemidiaphragm
lung abscess

Q.What do you mean by pancoast tumour?

the apical tumour involve the brachial plexus causes pain in inner aspect of arm &
shoulder

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Q.Why Horner syndrome occur?
due to involvement of cervical sympathetic ganglia

Q. What is Horner syndrome?

[to remember---PEMA]
P- Ptosis E- Enoplhalmus M- Meosis
A- Ankydosis

Q.Write down the management of acute bronchial asthma or status asthmaticus?

1. High flow O2 inhalation (6 l/min)
2. Nebulization stat and sos or 4/6 hrly (sulbutamol .sol 1ml+1ml ipratropium
.sol +2 ml normal sal.)
3. Inj. Hydrocortisone ( 2amp I.V sat and 1 amp I.V 6 hrly)
4. Salbutamol inhaler (2 puff qds)
5. Beclomethason inhaler ( 2 puff tds)
6. Tab. Montelukas 10 mg

Q. If not control then what will you do?

I.V aminophylline drip

Q. If not control then what will you do?

I.V magnesium sulphate

Q. If not control then what will you do?

If still not control refer the pt ICU

COPD
Q.Write down the management of acute exaggerated of COPD?
1. low flow O2 inhalation (2-4 l/min)
2. Nebulization stat and sos or 4/6 hrly (sulbutamol .sol 1ml+1ml ipratropium
.sol +2 ml normal sal.)
3. Inj. Hydrocortisone ( 2amp I.V sat and 1 amp I.V 6 hrly)
4. Antibiotics
5. Salbutamol inhaler ( 2 puff qds)
6. Ipratropium inhaler (2 puff tds)
7. Beclomethason inhaler (2 puff tds)
8. Tab. Theophyline

Q.Why low flow O2 is given in COPD?

To preserve the hypoxic drive for respiration
We know res. centre is stimulated by CO2 and hypoxia (O2) & H2. CO2 play
main role in stimulating the respiratory centre, but in coped there is hypoxia and
hypercapnea. so, due to elevated CO2 for long time respiratory centre become
insensitive to CO2 .so, hypoxia is the only drive that maintain the respiration by
stimulating the respiratory centre.so, if hypoxia is totally corrected then respiratory
centre loss the drive and there will be respiratory arrest.

133
Q. How will you differentiate bronchial asthma & COPD?

Bronchial asthma COPD

Age- young Old ,usually after 40 / smoker
Family history,atopy,HO of triggering Usually not, but respiratory tract infection
factor such as tree and grass pollen, cat aggravate the symptoms
and dog dander, cold air exposure, drugs
NAID,viral RTI may provoke the
symptoms
Episodic cough usually non productive or Chronic cough, productive and persistent
mucoid sputum,more marked at morning
Have diurnal variation more marked in Not so
the morning
GE: tachycardia and tachypnea in severe Usually feature of type 11resp. failure
case * Eyecongested
* Tonguecyanosed
* Palmwarm
* Pulsebounding pulse
* flapping tremor may present
Respiratory exam
Not so Lip pursing, prominence accessory
muscle of neck, engorge neck vein
Apex beat palpable In emphysema not palpable
Upper border of liver dullness is normal Upper border of liver dullness is lower in
emphysema
Crepitating absent May present
Feature of pulmonale HTN and corpulmonale
Not so * palpable- P2
* left para sterna heave
*epigastric pulsation
*loud P2
*tender hepatomegaly
*raised JVP
*depended edema
Investigation:
The diagnosis is certain if:
*20% diurnal PEF variation on> 3 days *reduced REV1 to <80% predicted
per week, in a week of peak flow diary *FEV1/FVC <0.7
measures. *CxRhyper inflated lung fields with
*FEV1 > 15% decrease after 6 minutes low flat diaphragm with tubular heart
exercise *ECGPpulmonale, RVH and poor
*FEV1 >15% (and 200ml) increase after 2 progression of R wave
week trial of oral steroid (30 mg *Echo cardiogram
prednisolone od)
*bronchodilator reversibility testing
FEV1> 15%
*CxR and ECG normal

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Q. What test you will do to establish diagnosis of bronchial asthma?
What investigation you want to do?
Pulmonary function test with spirometry
The diagnosis is certain if:
*20% diurnal PEF variation on> 3 days per week, in a week of peak flow diary
measures.
*FEV1 > 15% decrease after 6 minutes exercise
*FEV1 >15% (and 200ml) increase after 2 week trial of oral steroid
(30 mg prednisolone od)
*bronchodilator reversibility testing FEV1> 15% ( or 200ml) increase after
short- acting beta agonist therapy

Q. Which immunoglobin is responsible for asthma and what type of hypersensitivity

Reaction it is?
IgE
Type one hypersensitivity reaction
Q.What is the immunological mechanisms of asthma?
A subgroup of asthmatics are atopic and therefore inhalation of an allergen
producing specific IgE from B lymphocytes.This leads to the formation of
IgE depended antigen complexes that bind to mast cells, basophils, macrophages,
release of mediators such as histamine and eosinophil chemotactic factor. These
factors cause bronchoconstriction and airway oedema

Q. Write down the step wise management of bronchial asthma?

Step:1 Occasional use of inhaled short acting 2- agonist bronchodilators

Step:2 Regular preventer therapy (inhaled corticosteroids- ICS)
(start Beclomethasone BDP at 400 ug/day in a twice daily dose)
Step:3 Add on therapy
* low to moderate dose of inhaled corticosteroids plus
* long acting 2- agonist (LABAs), such as salmeterol
Step:4 Addition of fourth drug
* leukotriene receptor antagonist
* Theophylline
Step:5 Continuous or frequent use of oral steroids

Q. What new drug / biological agent use in bronchial asthma today?

It is Omalizamub
It is monoclonal antibody against IgE

Q. What do you mean by brittle asthma?

Most of acute attack of bronchial asthma are characterized by gradual
deterioration over several hour to days ,but some are appear with little or no warming
which is called brittle asthma

135
Q. Write down the feature of severe asthma?
[to rememberHIP Replacement]
HHR> 110/min
Iinability to complete sentence in one breath
PPEFR 3350% predicted or best (<200 l/ min)
ReplacementRR>25/min

Q. What do you mean by rescues therapy?

To prevent frequent exacerbation and control symptoms short courses of oral
Corticosteroids are therefore often required and this is called rescues therapy.
Indications for rescue courses include:
Symptoms and PEF progressively worsening day by day
Fall of PEF below 60% of the patients personal best recording
Sleep disturbance
Persistence of morning symptoms until midday
Progressively diminishing response to an inhaled bronchodilator
Symptoms severe enough to require treatment with nebulised or
Injected bronchodilators
Q patient developed cough after returning home from occupation and he remain
cough or symptom free in holiday ? what Dx ?
A . occupational asthma
Q. Some definitions:

Asthma Asthma is characterized by chronic airway inflammation and

increased airway hyper-responsiveness leading to symptoms of
wheeze, cough, chest tightness and dyspnoea. it is characterized
functionally by the presence of airflow obstruction which is variable
over short periods of time or reversible with treatment
Chronic Chronic bronchitis is the condition where patient suffer from cough
bronchitis with most of the day at least 3 consecutive months for at least 2
successive year
Emphysema Emphysema is abnormal permanent destructive enlargement of air
space distal to terminal bronchiole due loss of elastic recoil
Bronchiectasis Bronchiectasis is abnormal permanent dilation of bonchi proximal to
terminal bronchiole
COPD COPD is chronic obstructive pulmonary disease characterized by---
* fixed airflow obstruction
* minimal or no reversibility with bronchodilators
* minimal variability in day- to- day symptoms
* slowly progressive and irreversible deterioration in lung function,
leading to progressively worsening symptoms

Q. What diseases are with in COPD?

Chronic bronchitis
Emphysema
Chronic bronchiolitis /chronic asthma

136
Q. Types of Emphysema?
Panacinar Emphysemaall the alveoli and alveolar ducts in acinus are
involved
Centriacinarinvolve proximal part of acini
Periacinar or paraseptal Emphysema along the septa, blood vessels and pleura
Scar and irregular Emphysema

Q. What investigation for definite diagnosis of Emphysema?

High resolution of CT- scans

Q. What is the definite treatment of Emphysema?

Heart lung transplantation

Q. What type of disease is COPD and bronchial asthma?

Both are obstructive disease

Q. How will you differentiate it from restrictive type of disease?

restrictive obstructive
FEV1 & FVC decreased Markedly decrease
FEV1 / VC normal decreased

Q.What investigation you want to do in pt with COPD?

To Dx
Spirometry
Reduced FEV1 to <80% predicted ( FEV1 is the measurement of choice to
assess progression of COPD)
FEV1/FVC < o.7
Minimal bronchodilator reversibility (< 15%,usually <10%)
To see the etiology
Young pt: serum Alfa anti-trypsin
High resolution CT scan to see emphysema
To see complication
Arterial blood gas analysis: low Pco2 and low Po2
CxR PA
Hyperinflated lung fields with attenuation of peripheral vasculaturea
Low and flat diaphragms
More horizontal ribs & tubular heart
May see bullae
Loss vascular marker and prominent pulmonary vessel at both hilum
ECG
Ppulmonale, RVH and poor progression of R wave
ECHO CARDIOGRAPHY

Q. Complications of COPD?
Pulmonary hypertension
Corpulmonale

137
 Type 11 respiratory failure
Pneumothorax
Polycythaemia
Secondary infection

Q. Mention the treat of stable COPD?

NONPHARMACOLOGICAL:
Smoking cessation
Pulmonary rehabilitation
Diet: wt loss is recommended if the pt is obese
PHARMACOLOGICAL:
1. Bronchodilator:
1st short acting 2-adrenoreceptor agonist ( sulbutamol inhaler)
If not control then add a short acting anti-cholinergic
( Ipratropium inhaler)
If still symptomatic,regular long acting bronchodilator with
anti-cholinergic
2. Cortico steroid
3. Theophyllines
4. O2 therapy:
Long term domiciliary oxygen therapy (LTOT)
Low flow O2 2-4 l/min for a minimum of 15 hours/day
5. Vaccination: influenza vaccine annually and pneumococcal vaccine
6. Antibiotics
7. Surgery: bullectomy if largr bulla
8. Lung transplantation in young pt if emphysema

Q.How will you differentiate between pink puffer & blue puffer?

pink puffer blue puffer

Cause Emphysema Chronic bronchitis
Clinical feature Dyspnea is more than Cough with sputum is
cough and lips pursing more than dyspnea
Lean and thin Yes no
Cyanosis and edema Absent present
Arterial gas analysis Pco2 and Po2 are normal Pco2 and low Po2
corpulmonalae Absent present

When will u discharge a pt with asthma ?

The patient should be stable on discharge medication
Nebulized should be discontinued before 24 hrs of discharge
PEF > 75% of predicted or personal best record

What do u mean by cough variant asthma?

Cough sometimes in some asthma pt cough is the predominate feature and have
no wheez or breathlessness . this is called cough variant asthma

138
Q.What will you get if pt have pulmonary hypertension and corpulmonalae?

In GE:
Eyecongested
Tonguecyanosis
Oedema(+)
Sign of rt heart failure
Raised JVP
Tender hepatomegally
Sign of pulmonary hypertension:
Palpable P2 and loud P2
Left para sterna heave
Epigastric pulsation

TB

Q. names the organism responsible for TB?

A. Mycobacterium tuberculosis (MTB)

Q. what do u mean by pulmonary TB and extra pulmonary TB?

Pulmonary TB where lung parenchyma involved
Extrapulmonary ----other then lung parenchyma such as pleural effusion

Q. . . mention the site of extra pulmonary TB ?

Ans:
Intestine
Bone
Braine and meninges
Skin
Lymph node & Pleura
Q what do u mean by primary TB
A. Primary TB refers to the infection of a previously uninfected person.

Q. what do u mean by post pulmonary TB?

Post pulmonary TB refer to infection in a person who has been sensitized by early
exposure

Q . what u mean by miliary TB ?

A . Miliary TB is a disseminated TB with radiological evidence of miliary millet
throughout the both lung field . all miliary TB is disseminated TB but all disseminated
TB is not miliary TB .

Q. what is fate of primary TB?

(1)Spread from the primary focus to hilar and mediastinal lymph glands to form the
'primary complex', which in most cases heals spontaneously.
(2) Direct extension of the primary focus-'progressive pulmonary tuberculosis'.
(3) Spread to the pleura-tuberculous pleurisy and pleural effusion.
(4) Blood-borne spread

139
Q. what do u mean by 'Ghon focus?
A. Ghon focus is the aggregation of numerous granuloma at site of lesion it is the
primary lesion in the lung. Usually situated in periphery of lung.

Q what do u mean by primary complex of rankle?

A. Ghon focus and regional lymphnode combinedly called primary complex of rankle

Q . What use in MT test and where it given ?

purified protein derivative (ppd) is used in TB , 10 tubercular unit or 0.1ml is given
intradermly over forearm.
Q . when will u told that it is positive ? if induration more than > 10m m

Q. what indicate MT positive ?

A. It is not diagnostic test but supportive investigation
Positive of the test indicate that pt have one of the three:
TB infection
TB disease
BCG vaccination

Q. where false positive?

A. Atypical mycobacterium

Q names the condition where MT is false negative?

A. False negatives
Severe TB (25% of cases negative)
Newborn and elderly
HIV (if CD4 count < 200 cells/ml)
Recent infection (e.g. measles) or Immunisation
Malnutrition
Immunosuppressive drugs
Malignancy
Sarcoidosis
Q What investigation u want to do in patient with TB
Investigation for Diagnosis pleural effusion ?
CBC -- Normal CBC with persistent high ESR
MT
Sputum for AFB and
CXR PA
If lymphadenopathy FNAC and biopsy
Pleural fluid aspiration if associate with pleural effusion
Q. what are the Radiological finding of TB in CXR
A. Radiological finding of TB in CXR
Patchy opacity
Pleural effusion
Hilar lymphadenopathy- unilateral, paratracheal or mediastinal)
Collapse
Consolidation
Cavitation / lung abscess

140
 Pleural effusion

What clinical feature of active TB?

A. Fever , night sweating , weight loss are the clinical feature of active TB

Q . what do u mean by smear positive and smear negative TB ?

Smear positive case Smear negative pulmonary TB

A patient with A patient with symptoms suggestive of

At least 2 sputum positive specimens TB with
Or 3 sputum specimens negative for
One sputum positive specimens for AFB and
AFB plus Persisting symptoms after a course
CXR abnormality consistent with antibiotics and
active TB Again 3 sputum specimens negative
Or for AFB and
One sputum positive specimens for CXR abnormality consistent with
AFB plus Active TB and
culture positive for Mycobacterium Decision by a medical officer
TB

Some definition :
New case who have never received anti- TB drugs or received less than one
months
Relapse ----- A patient who previously received treatment and was cured or treatment
completed .And again developed Smear positive pulmonary TB.
Treatment A patient who while treatment ,remain smear positive or became
failure smear Positive again at 5 month or more after the start of treatment
Or
Patient was initially sputum negative but again become sputum at the
end of 2 months
Q. What do u mean by cryptic TB?
A . In some specially in old patient TB present with only wt loss and low grade fever
without radiological change in , MT and sputum negative . Diagnosis only done by
biopsy of the bone marrow . This called cryptic TB.

Q. What are the radiological feature of active TB

A. Pleural effusion
Cavitation
Serial Xray show progressive extension of lesion

141
Q . How will u make difference from active TB to inactive TB?

ActiveTB Inactive TB
Clinical Fever , wt loss, night Absent
feature sweat usually present

Sputum Positive Negative

Creps Marked Less Marked
Radiology Soft shadows Feature of fibrosis
Pleural effusion Calcification
Cavitation Fibrous band
Serial Xray show Tracheal shift
progressive extension Hilar elevation
of lesion Diaphragm tenting
Change of fissure

Name the stain and cultur media for MTB?

AFB stain Ziehl-Neelsen
Auramine fluorescence
Culture Solid Lwenstein-Jensen 4 to 6 weeks need for
Middlebrook growth
Liquid BACTEC 1-3weeks need for growth

Q. Indication of category I and Category II

Indication of CAT-1 Indication of CAT 2
New smear-positive patient Should be given
New smear negative PTB Relapse
Extra pulmonary TB Treatment after interruption / default
Meningeal Miliary Treatment failure
Pericardial , Pleural effusion
Spinal , Intestinal TB, dessiminiated
TB

Q when will u tell this is a open case ?

When sputum for AFB is positive

Q How many sample is given?

Three samples 1sr sample at spot
2nd over night morning sample
3rd 0n the spot next day

142
Q Mention the categoryI treatment
Intensive phase Continuation phase
4FDC drugs for ---- 2 month 2FDC drugs -------------4 month

RIEZ -- RI
Rifampicin Rifampicin
Isoniazid Isoniazid
Ethambutol
Pyrazinamide

Q Mention the categoryI I treatment

Intensive phase Continuation phase
For 5 months

RIEZ -- 3 months RI
Rifampicin Rifampicin
Isoniazid Isoniazid
Ethambutol Ethambutol
Pyrazinamide

Inj. Streptomycin IM daily 2 months

Mention the dose of anti TB drugs

Drugs Daily doses Maximum doses
INH 5 mg/kg max 300 mg
Rifampicin 10 mg/kg, max 600 mg
Ethambutol 15 mg/kg,(1520 mg/kg)
Pyrazinamide 20 mg/kg, 2025 mg/kg), max 2 g
Streptomycin 15 mg/kg daily max 750 mg

Mention one important side effect of anti TB drug s ?

Isoniazid Rifampicin Pyrazinamide Streptomycin Ethambutol

Peripheral Hepatitis Gout 8th nerve Retrobulbar
neuropathy1 damage neuritis

Q. A patient came to u with the compliant

of dimness of vision after taking anti TB ? Ethambutol

of burning sensation after taking anti TB ? Isoniazid

of joint pain after taking ant-TB ? Pyrazinamide

Q A patient developed jaundice after taking Anti TB drug? what will u do ?

143
Do the following
Stop the drugs immediately
Do liver function test ( SGPT and s.bilirubin )
When test become normal or near to normal
Strar anti TB drug in challenging dose
Start with low dose single less hepato toxic drug
Goes its optimum dose gradually and
Start one by one drug and
Finally give combination drug
Due to unknown mechanism jaundice does not develop

Q. mention the name of 2nd line anti TB drugs ?

2nd line Anti TB
1. The injectable aminoglycosides, kanamycin, and amikacin
2. the injectable e capreomycin;
3. The oral agents ethionamide, cycloserine,
4. the fluoroquinolone antibiotics. third-generation agents are preferred:
levofloxacin, gatifloxacin , and moxifloxaci
5. Amithiozone (thiacetazone).

Q. If you give the Rx of TB but no cured what r the cause ?

Patient compliance
Multi-drug resistance TB
Wrong diagnosis ( bronchogenic ca)
Q. If TB patient does not take drug what will be the complication ?
He develop complication like fibrosis
Q. what do u mean by Multi drug resistant TB. ?
When TB is resistant to both INH and Rifampicine
Q What do u mean by X-DRTB ?
Extreme drug resistant TB means resistance to INH and Rifampicine , fluroquinolone
and at least one injectable drug

Q . What adv. U will give a patient with on Anti-TB drugs

Do not miss any does and take drugs regularly
Ur urine ,saliva will turn into orange colour so do not affarid.
Stop the drugs if patient develop Jaundice
and seek for medical advice if patient develop
visual disturbance

Q Now read the pleural effusion effusion from long case sheet
Q. finding consolidation , pneumothorax , collapse and fibrosis , other question from
shortcase sheet

144
Define dyspnea ?
Breathlessness or dyspnoea can be defined as the feeling of an uncomfortable need to
breathe.

Acute dyspnoea at rest Chronic exertional dyspnoea

Acute pulmonary oedema Chronic heart failure
Acute severe asthma COPD
Acute exacerbation of COPD Chronic asthma
Pneumothorax Bronchial carcinoma
Pneumonia Interstitial lung disease
Pulmonary embolus Severe anaemia
Acute respiratory distress syndrome
Metabolic acidosis

Q .What do you mean by type I and type II respiratory failure?

Type I respiratory failure Type II respiratory failure

Hypoxia and Normal CO2 level Hypoxia & hypercapnia
Occur due to disease of lung parenchyma It occur due to obstruction of air way or
chest wall , muscle , neurological disorder
where hypo
Acute asthma Acute exacerbation COPD
Pulmonary oedema Acute severe asthma
Pneumonia Neuropathies/paralysis
Lobar collapse Myopathies
Pneumothorax Kyphoscoliosis
ARDS Narcotic drugs
Lung fibrosis Ankylosing spondylitis
Flail chest injury
PaO2 < 8.0 kPa (60 mmHg)) Hypoxia (PaO2 < 8.0 kPa (60 mmHg))
PaCO2 (< 6.6 kPa (50 mmHg)) RaisedPaCO2 (> 6.6 kPa (50 mmHg))
High-flow oxygen (35-60%) Lower concentrations of oxygen (24-28%)

145
 Blood
Q. Define Anaemia.
Ans. Anaemia is a clinical condition characterized by both qualitative and quantitative decrease
in Hb below the normal level irrespective to age and sex of a person.

Q. Where we look anemia?

Ans.

Lower palpebral conjunctiva.

Dorsal surface of tongue.
Palm and sole of feet.

Q. Tell me the normal values of blood parameter.

Ans.
RBC:
WBC:4,000-11,000/cu mm
Platelet: 1,50,000-4,00,000/mm3
Hb- male: 13-18 gm/dl
Female: 11.5-16.5 gm/dl

Q. In which condition Hb level is 100% and ESR `0?

Ans. Polycythaemia.

Q. Infusion of 1 unit of blood causes how much increase in Hb level?

Ans. Infusion of 1bag blood causes 1gm/dl increment of Hb level.

Q. Classify anaemia.
Ans.
Etiological
a) Central cause Marrow failure aplastic anaemia, anemia of chronic disease.
b) Peripheral cause blood loss, heamolysis
Morphological classification
a) Microcytic hypochromic anaemia
b) Macrocytic anaemia
c) Normocytic normochromic anaemia

Q. Name the causes of microcytic and hypocromic anaemia.

Ans. Iron deficiency anaemia, Thalassaemia, Sideroblastic anaemia.

146
Q. What are the causes of macrocytic anaemia?
Ans. Vitamin B and folic acid deficiency.

Q. what are the causes of normocytic normochromic anaemia?

Ans. Aplastic anaemia, anaemia of chronic disease, anaemia due to blood loss.

Q. what are the causes of iron deficiency anaemia?

Ans.
In both male & female In female- Other-
PUD Pregnancy Coeliac disease
Hook worm Menorrheagia
Carcinoma stomach
Drug- NSAID
haemorrhoid

Q. What are the investigations you will do to diagnose Iron deficiency anaemia?
Ans.
TC, DC, Hb%, ESR
PBF- Microcytic hypochromic anaemia
Iron profile: Serum ferritin
Total iron binding capacity
To find etiology:
Upper GI endoscopy
Colonoscopy
Stool for ova of helminthes

Q. What are the PBF findings in iron deficiency anaemia?

Ans. Microcytic hypochromic anaemia, anisocytosis, pencil cell, target cell, nucleated RBC.

Q. How will you differentiate PBF of iron deficiency anaemia and Thalassaemia.
Ans.

Iron deficiency anaemia Thalassaemia

Few target cell Plenty of target cell
No features of heamolysis Features of heamolysis present
eg. Fragment cell
Pencil cell

Q. Tell me the one investigation to diagnose iron deficiency anaemia.

Ans. Serum Ferritin

147
Q. Mention the treatment of iron deficiency anaemia.
Ans. Tab. Ferus Sulphate (200mg), tds, for 3-6 months.

Follow up: Hb will increase 1gm/dl in every 7-10 days. Reticulocyte count will increase after
1 week.

Q. What are the indications of blood transfusion in anaemia?

Ans.

Angina
Heart failure
Evidence of cerebral hypoxia.

Q. what are the complications of oral iron therapy?

Ans. Dyspepsia, Altered bowl habit.

Q. What is the indication of Parenteral iron therapy?

Ans. Malabsorption.

Q. Name the sites of iron and Vitamin B absorption.

Ans. Iron absorbed in jejunam.
Vitamin B absorbed in ileum.

Q. What are the causes of megaloblastic anaemia?

Ans. Deficiency of Vitamin B and Folic acid.

Q. Vitamin B and Folic acid deficiency- which one is more common? Why?
Ans. Folic acid deficiency is more common than vitamin B12 deficiency.
For following reasons:
Point Vitamin B Folic acid
Store 3years 3 months
Sources Animal plant
Effect of cooking Not destroyed Destroyed during cooking

Q. in which anaemia causes neurological manifestation ?

Ans. Megaloblastic anaemia due to Vitamin B deficiency

Q. What are the neurological feature of Vitamin B deficiency?

Ans. Neurological features:
Eye: optic atrophy
Loss of memory : dementia
Sensation: gloves and stock sensory loss, loss of vibration and joint sense position.

148
Q. Name causes of Vitamin B and Folic acid deficiency.
Ans. causes of Vitamin B and Folic acid deficiency:
Vitamin B Folic acid
Diet: vegan Increased demand, poor intake of
Stomach: pernicious anaemia, partial/ vegetables
total gastrectomy Intestine: malabsorption, coeliac
Intestinal: tropical sprue, coeliac disease
disease, crohns disease Drug: phenytoin, MTX
Other: haemolysis,

Q. Name the investigations for diagnosis of megaloblastic anaemia.

Ans.
Hb%
PBF- macrocytic RBC
Bone marrow- megaloblast
Vitamin B level
To see cause:
Schilling test
Anti-parietal cell antibody

Q. What are the PBF findings of Vitamin B and Folic acid deficiency?
Ans. Pancytopenia with Macrocytosis with hypersegmented neutrophil. Megaloblast & Howel-
jolly body may present.

Q. Bone marrow findings of Vitamin B deficiency?

Ans. Megaloblastic change in erythoid series .

Q. what are the other causes of macrocytosis?

Ans.
Alcohol
Liver disease
Hyperlipidaemia
Hypothyroidism.

Q. How Vitamin B absorbed in GIT?

Ans. Vitamin B+food stomach acid causes release of Vitamin B from food
Vitamin B + intrinsic factor(secrete from parietal cell) absorption at terminal ileum.

149
Q. What is pernicious anaemia?
Ans. It is an autoimmune disease in which antibody is formed against parietal cell (which secrete
intrinsic factor).

Q. what is the treatment of Vitamin B deficiency anaemia?

Ans. Vitamin B supplementation:
Inj. Hydroxycobalamine 1000 gm , 1 ampule, I.M. every 2 day for 5 days.
Maintenance: 1 amp, I.M. 3 monthly for lifelong.

Q. what is the treatment of folic acid deficiency?

Ans. Tab. Folic acid 5 mg, (1+0+0) for 3 weeks, than lifelong.

Q. What is the importance of folic acid in pregnancy?

Ans. Deficiency of folic acid during pregnancy causes neural tube defect in fetus.

Q. To prevent neural tube defect in fetus, when folic acid supplementation should be started?
Ans. Folic acid supplementation should be started before conception, because, neural tube
development occur within 1-3 weeks of conception.

Q. In witch conditions folic acid is used prophylactically?

Ans.
Haemolytic anaemia
Pregnancy
With MTX therapy

Q. If a patient with Vitamin B deficiency is given folic acid without giving Vitamin B,
what will happen?
Ans. It will cause subacute combined degeneration of spinal cord.

Q. . What are the neurological feature of subacute combined degeneration of spinal cord?

Ans. Jerks absent but planter extensor .

Q. what is the daily requirement of Vitamin B?

Ans. 1gm/ day

Q. what are the sources of Vitamin B?

Ans. Animal source.

Q. What are the causes of anaemia of chronic disease?

Ans.
Renal failure
Connective tissue disease
150
Q. What are the PBF findings of anaemia of chronic disease?
Ans. Normocytic normochromic RBC.

Q. what is the mechanism of anaemia of chronic disease?

Ans. IL suppresses the bone marrow.

Q. What biochemical abnormality occurs in heamolytic anaemia?

Ans. Mnemonic: BDR- Head- quarter
B- billirubin
D- LDH
R-Reticulocyte
Head-heptoglobin
Quarter-urobillinogen

Aplastic anaemia
Q. A patient comes to you with gum bleeding, petechiae, purpuric spot. What will be the
differential diagnosis?
Ans.
Acute leukaemia
Aplastic anaemia
I.T.P
(*If fever present, Dengue will be added to the D/D)

Q. How will you differentiate these three conditions?

Ans.
Topic Acute leukaemia Aplastic anaemiaIdiopathic
throbocytopanic
purpura
Clinical features Fever, bleeding spot, Fever,bleeding spot, No fever, only
patient is toxic Patient is not toxic bleeding spot
Anemia Mild to moderate Severe , it is the main Usually absent
manifestation
Bony tenderness present absent absent
hepatosplenomegaly May be present absent Absent
PBF Leukocytosis with pancytopania Thromocytopenia
blast cell
Bone marrow Blast cell Hypoplasia or dry tap megakaryocytosis

151
Q. what is the treatment of aplastic anaemia?
Ans. Supportive treatment
For anaemia Blood transfusion
For infection Antibiotic
Granulocyte stimulating factor/ colony stimulating factor.
Specific treatment
Allogenic bone marrow transplantation
Anabolic steroid
Cytotoxic drug- cyclosporine

Q. What are the causes of aplastic anaemia?

Ans.
Primary- Idiopathic.
Secondary-
Drug
Radiation
Hepatitis (viral)
Pregnancy

Q. What are the presentations of aplastic anaemia?

Ans.
Pallor, weakness , palpitation - anaemia
Fever- leucopenia
Bleeding spot- thrombocytopenia.

Purpura
Q. What are the causes of purpuric spot?
Ans.
I.T.P.
Aplastic anaemia
Leukaemia
DIC
Henoch- schonlein purpura
Dengue

152
Q. What are the differences between purpura and spider neavi?
Ans.
purpura spider neavi
Due to extravasation of blood Due to arteriolar dialation
No blanch on pressure blanch on pressure
Due to platelet Due to estrogen

Q. What are the characters of pupura of vasculitis?

Ans. Painful and tender & palpable

Q. Who are mostly affected?

Ans. Female.

Q. What type of disease it is?

Ans. Autoimmune disease.

Q. Which antibody is formed and against whom it works?

Ans. Antibody IgG
It is against platelet membrane glycoprotein IIb, IIIa.

Q. When I.T.P is called acute and chronic?

Ans. Acute I.T.P when duration <6 weeks
Chronic I.T.P when duration >6 weeks.

Q. What is the treatment of I.T.P. in case of children?

Ans. In case on children, I.T.P. is self limiting. So no drug is needed.
If given, then, Tab. Prednisolone 2mg/kg/day

Q. What is the treatment of I.T.P. in case of adult?

Ans. Tab. Prednisolone, 1 mg/kg/day for 6 weeks, then taper.

Q. What are the indications for I.V. IgG?

Ans.
Persistent epistaxis
GIT bleeding
Intra cranial haemorrhage

Q. What are the treatments of relapse?

Ans. Relapse for the first time again steroid
Relapse more than 2 times Splenectomy.

153
Q. What is the cause of I.T.P. in splenectomized patient?
Ans. Probably patient has ectopic spleen.

Q. What is the treatment in this case?

Ans. Cytotoxic drug- Cyclosporin.

Q. A patient comes to you with bloody diarrhoea, abdominal pain, purpuric spot in the buttock,
leg. What is your diagnosis?
Ans. Henoch-Scheonlein purpura.

Q. What are the indications of splenectomy?

Ans.
I.T.P.
Thalassaemia
Features of hypersplenism

Q. What prophylactic measures should be taken before splenectomy?

Ans. Vaccination should be done against capsulated organisms;
Meningococcus
Pneumococcus- (Streptococcus pneumonae)
Haemophilus influenza

Q. When these vaccines should be administered?

Ans. Three weeks before splenectomy.

Q. What measures should be taken after splenectomy?

Ans.
Vaccination against Meningococcus- 5yearly
For Streptococcus pneumonae Tab. Pen v 250 mg, 1+0+1, lifelong
Vaccination against Haemophylus influenza-yearly

Q. Name some haematological malignancies.

Ans.
Multiple myeloma
Lymphoma
Leukaemia

Q. Name some myeloproliferative disorder.

Ans.
Chronic myeloid leukaemia (CML)
Polycythaemia rubra vera
Myelofibrosis
Essential thrombocythemia
154
Q. Name some lymphoproliferative disorders.
Ans.
Lymphoma
Chronic lymphocytic leukaemia
Multiple myeloma

Multiple myeloma
Q. What are the diagnostic criteria of multiple myeloma?
Ans. 2 of the following 3:
Skeletal lesion (lytic lesion)
Bone marrow plasma cell >30%
Serum and urinary paraprotein

Q. A 60 years old man comes to you with generalized bony ache. What are the differential
diagnoses?
Ans.
multiple myeloma
chronic renal failure
osteoporosis
malignancy with bony metastasis

Q. What are the investigations you will do to diagnose multiple myeloma?

Ans.
CBC Hb, ESR- highly raised
PBF- Normocytic normochromic RBC with increased roleuax formation
X- ray skullmultiple punch out lytic lesion
Plasma protein electrophoresis
S. creatinine and urine RME & urine for bones-jones protein

Q. What do you expect in X-ray skull in MM pt?

Ans. Lytic lesion.

Q. what are the complications of multiple myeloma?

Ans. Mnemonic- CRPV
C- Hypercalcaemia
R-Renal failure
P- paraplegia due to fracture
V- hyperviscocity

155
Q. Mention the treatment of multiple myeloma?
Ans.
Specific treatment: Melphalan and prednisolone
Supportive treatment:
For hypercalcemia- fluid intake, I.V. fluid, Bisphosphonate
For pain- analgesic
Correction of anaemia
Antibiotic- if infection

Q. What are the drugs used in chemotherapy?

Ans. Malphalan and Prednisolone (1mg/kg) For 4 days, then at 4-6 weeks interval, then
repeat this cycle until paraprotein reach the plateu stage.

Q. the patient of multiple myeloma comes to with paraparesis . what is your diagnosis ?

Ans. Cord compression

Leukaemia
Q. What are the difference between acute lymphoblastic leukaemia and acute myeloblastic
leukaemia? Some ques will ask from this such as common luekaemia in child , which leukaemia
is better ?
Ans.
Topic Acute lymphoblastic Acute myeloblastic leukaemia
leukaemia (AML)
(ALL)
Common age group Children (1-5) years Adult
Lymph node enlargement Present absent
PBF and bone marrow Lymphoblast Myeloblast
Prognosis Good/ better Not so

Q. Tell me the clinical presentation of acute leukaemia.

Ans. clinical presentation of acute leukaemia:
Fever
Bleeding manifestation
Anaemia and weakness
Lymphadenopathy and organomegaly

156
Q. What are the investigations you will suggest?
Ans. TC-, DC, Hb%, ESR
PBF- Blast cell- only test for diagnosis of leukaemia
Bone marrow- done for typing of leukaemia
Ultrasonography and chest-X ray- for staging

Q. What is the treatment of acute leukaemia?

Ans.
Supportive:
For correction of anaemia- blood transfusion
For thrombocytopenia- platelet transfusion
For prevention of infection- antibiotic
For hyperuacemia- allopurinol
Specific treatment- Chemotherapy.

Q. Which leukaemia may involve CNS, what measures taken for it?
Ans. In ALL, there is chance of CNS involvement. For this reason, intrathecal MTX is
administered.
Q. What is the definite treatment?
Ans. Allogenic bone marrow transplantation.

Q. What are the signs of remission?

Ans.
Improved clinical features
In bone marrow, blast cell less than 5%
No blast cell in PBF

Q. Name some indications of bone marrow transplantation.

Ans.
Leukaemia
Aplastic anaemia
Thalassaemia
Inborn error of metabolism

Q. What do you mean by allogenic and autologus?

Ans. Allogenic- Donor stem cell
Autologous- Own bone marrow.

157
Q. What are the complications of bone marrow transplantation?
Ans.
A) Mucositis, B) Acute graft versus host C) Chronic graft versus
Infection disease with 100 days host disease.
Bleeding after transplantation
Pneumonitis Skin rash
Liver- jaundice
GUT- diarrhoea

Q. What is neutropenic fever? What is its treatment?

Ans. Fever >38 C over 1 hour if the patients neutrophil count < 1x109

Treatment: Aminoglycoside, penicillin. Continue at least 3 days after fever subside.

Q. What are the newer agent used in acute leukaemia?

Ans.
BCG
Interleukin -2
Mono Ab

Q. Tell me the prognosis of acute leukaemia if not treated.

Ans. Without treatment, survival is about 5 weeks.

CML
Q. A 65 years old patient comes to you with the complaints of fatigue and weakness. On
examination, you find that, the patient is anaemic and there is huge splenomegaly. What is your
diagnosis?
Ans. CML

Q. Which is the common age group for CML?

Ans. Old age, >60 years.

Q. What are the investigations you will suggest?

Ans. CBC- Hb , ESR , TC-more than one lakh (1,00,000-5,00,000),
DC- Precursor cell of granulocyte series such as myelocyte, promyelocyte ,
metamyelocyte
PBF- leucocytosis with myelocyte >20% & myeloblast more <10%, platelet-normal or ,
nucleated RBC may present.
Bone marrow- Chromosome study.

158
Q. Minimum which investigation can diagnose CML?
Ans. Only CBC by seeing precursor of granulocyte series.

Q What is the blast cell count in CML?

Ans. Less than 10%

Q. What are the phases of CML?

Ans. A-accelerate phase
B- blast crisis
C- chronic phase

Q. Which chromosome has the relation with CML?

Ans. Philadelphia Chromosome.

Q. What do you mean by Philadelphia Chromosome?

Ans. It is the shortened 22 chromosome resulting from reciprocal translocation of genetic
material with 9 chromosome.

Q. Which gene involved in this situation?

Ans. BCR Abl gene.

Q. What does it do?

Ans. It secrete tyrosine which stimulate granulocyte.

Q. Name the newer drug for this condition.

Ans. Imatinib (400 mg)- for 18 months.

Q. How Imatinib works?

Ans. It inhibit Tyrosine kinase.

Q. What are the other drugs used?

Ans. Hydroxyurea.

Q. Which follow up is done during treatment with Hydroxyurea? For how long Hydroxyurea is
given?
Ans. Regular CBC is done. Target WBC count <20,000.
Stop drug if WBC <10,000
Duration- upto when the WBC count becomes 20,000.

159
 Lymphoma
Q. What are the causes of generalized lymphadenopathy?
Ans.
Lymphoma
Leukaemia
Disseminated TB

Q. What investigations are done on a lymphoma patient?

Ans.
CBC- normal or eosinophil and lymphopenia
PBF
FNAC and biopsy from lymph node
CXR- Hilar and paratracheal lymhadenopahy
USG- Intra-abdominal lymphadenopathy
CT scan

Q. Name some lymphatic structures.

Ans.
Lymph node
Spleen
Thymus
Payers patches
Appendix
Waldeyers ring

Q. What are B symptoms?

Ans. Fever, weakness, drenching sweating- all these are collectively called B symptoms.

Q. What is Pel- ebstin fever?

Ans. Period of pyrexia followed by apyrexia and repeatation of the cycle.

Q. What are the difference between Hodgkin and Non-Hodgkin lymphoma?

Ans. Mnemonic HCC is Pale and Red
That means,
H- Hodgkin
C- Central
C- contiguous
I- Itching
S- Systemic features and fever
Pale- Pel-ebsin fever

160
 Red- Reed sternburg cell
All these features are present in Hodgkin lymphoma and absent in Non-Hodgkin lymphoma.

Q. Which investigation is done to see prognosis?

Ans. Serum LDH level.

Q. Which investigation is done prior to FNAC/Biopsy of lymph node?

Ans. PBF- to exclude leukaemia.

Q. What are the treatments of lymphoma?

Ans. Hodgkin-stage I, IIA Radiotherapy
In other stage chemotherapy
Mnemonic: Chl VPP
Chl- Chlorambucil
V- Venblastin
P-Procarbazin
P- Prednisolone

Other therapy
COPP MOPP ABCD
C- Cyclophosphamide M- Mustin A- Adriamycen
O- vincrestin O- Onchovesin B- Bleomycen
P- Procarbazin P- Procarbazin V- Vencrestin
P- Prednisolone P- Prednisolone D- Decurbazin

Q. What is the staging & treatment of NHL?

A:
1. Low variety:
Asymptomatic no treatment
Symptomatic : chemo : chlorambucil & rituximab(R)
2. High variety: R-CHOP
Q. which type of lymphoma occur in HIV patient ?
Ans. NHL
Q. what are the bad prognostic criteria in lymphoma?
Ans . Age , male gender , lymphopenia , lymphnode > 10 cm

161
Q. Name cause of lymphadenopathy , (infective , non-infective )

Infective Non-infective causes

Bacterial Neoplastic
Streptococcal, tuberculosis, brucellosis Primary
Viral Lymphomas,
Epstein-Barr, HIV leukaemias
Protozoal Secondary
Toxoplasmosis Lung, breast, thyroid, stomach
Fungal Connective tissue disorders
Histoplasmosis Rheumatoid arthritis,
systemic lupus erythematosus (SLE

Q. Name a drug that cause lymphadenopathy ?

Ans. Phenytoin

Haemophilia A
Q. A patient came to you with recurrent swelling of right knee joint after fall, during playing.
What is your diagnosis?
Ans. Haemophilia.

Q. What type of disease it is?

Ans. X- linked disease.

Q. Who are affected?

Ans. Males are affected, females are carrier.

Q. Which factor responsible for haemophilia?

Ans. Factor VIII.

Q. Is any other factor responsible?

Ans. Factor IX, Which other name Haemophilia B or Christmas disease.

Q. Can female be affected?

Ans. Yes. Female can be affected in following conditions:
Lyonisation theory
If affected father marry carrier female
Turners syndrome.

Q. What are the investigations you will suggest?

162
Ans. BT- normal, CT- prolonged. [ In ITP, BT- normal, CT- normal]
Ideally PT, APTT should be done. PT- normal, APTT- increased.

Q. What is the half life of Factor VIII?

Ans. 12 hours.

Q. What do you mean by Lyonisation theory?

Ans. Females have 2 X chromosomes. Random inactivation of one `X chromosome is called
Lyonisation theory.

Q. What are the clinical features of haemophilia?

Ans.
Haemathrosis
Muscle haematoma.

Q. What are the complications of joint?

Ans. Recurrent bleeding, Synovial hypertrophy, destruction of cartilage and secondary
osteoarthritis.

Q. Tell something about pedigree of Haemophilia?

Ans. If father is affected all daughters will be carrier, all sons will be spared.
If mother is carrier 50% of daughters will be carrier, 50% sons will be affected.

Q. What is the treatment of Haemophilia?

Ans. In acute condition:
Resting of bleeding site either by bed rest or by using a splint
Factor VIII concentrate in I.V. route. If not available- then fresh frozen plasma.

Q. In Haemophilia, which pathway of coagulation is involved?

Ans. Intrinsic pathway.

Q. What complication may develop after Factor VIII infusion?

Ans. In 20% cases after giving Factor VIII, there is development of anti-factor VIII antibodies,
which causes neutralization of Factor VIII.

Q. What thing is done in this condition?

Ans. Then we shall give activate Factor VIIa or FEIBA.

Q. What is the hallmark of haemophilia?

Ans. Haemarthrosis.

163
Q. A patient continued to bleed, even after 24 hours of circumcision. What is the diagnosis?
Ans. Haemophilia.

Q. Why it is called maternal disease?

Ans. Because, affected boys maternal uncles are also gives history of haemophilia.

Q. Name 2 congenital bleeding disorder.

Ans. X linked: Haemophilia A and B
Autosomal: Von-Willebrand disease.

Q. Name some acquired coagulation disorder.

Ans.
a) Due to synthesis of clotting factors: liver failure
b) Due to consumption of clotting factors: DIC
c) Drug: Heparin, Warfarin

Q. Have you heard the name of Von-Willebrand disease?

Ans. Yes. It is an autosomal dominant coagulation disorder due to impaired function of Von-
Willebrand factor.

Q. What is the source of Von-Willebrand factor?

Ans. It is produced by: Endothelial cell, platelet.

Q. What is the function of Von-Willebrand factor?

Ans.
It is a carrier protein of factor VIII.
It also form bridges between platelet and sub-endothelial component.

Q. Von-Willebrand factor present in which blood group?

Ans. Blood group A and B.

Q. Gene of Von-Willebrand factor present in which chromosome?

Ans. Chromosome no 12.

Q. Name the coagulation factors that are produced in the liver with the help of
vitamin k ?
Ans. These are- factor II, VII, IX, X.

Q. Where vitamin k is produced?

Ans. It is produced by intestinal flora.

164
Q. A patient of 65 years age came to you and you found anaemia on examination. Investigations
showed no cause of blood loss, PBF was normal, no history of chronic disease. 6 months later
the patient developed blast cell 20% in PBF. Now what is your diagnosis?
Ans. Myelodysplastic syndrome.

Q. Name some causes of high ESR.

Ans.
Multiple myeloma
Tuberculosis
Kala-azar
Malignancy
Connective tissue disease

Q. Name a disease where ESR is `0?

Ans. Polycythaemia Rubra vera.

Q. Name some causes of pancytopenia.

Ans. Central cause: Mnemonic: ALL of MMC
A- aplastic anaemia
L- leukaemia
L- lymphoma
M-multiple myeloma
M- myelofibrosis
C- carcinoma metastasis in bone marrow

Peripheral cause: Kala-azar, CLD.

Q. Name common causes of lymphadenopathy.

Ans. Common causes of lymphadenopahy:
Lymphoma
Leukaemia
Disseminated TB
Causes of lymphadenopathy as a whole:
Infective:
Bacterial: streptococcal, TB, brucellosis
Viral: EBV, HIV, CMV
Protozoal: toxoplasmosis
Fungal: histoplasmosis, coccidiomycosis.

Neoplastic:

165
 Primary: lymphoma, leukaemia(ALL (child),CLL (old))
Secondary: lung, breast, thyroid, stomach

Connective tissue disease: RA, SLE

Sarcoidosis
Amylodosis
Drugs: Phenytoin

Q. Name some causes of thrombocytopenia.

Ans.
1) Due to production 2) Due to increased consumption:
All causes of pancytopenia ITP
Mnemonic: ALL of MMC DIC
A- aplastic anaemia Dengue
L- leukaemia Hypersplenism
L- lymphoma CLD
M-multiple myeloma Haemolytic uraemic syndrome
M- myelofibrosis
C- carcinoma metastasis in bone
marrow

166
 Endocrine Disease
Q.Name some endocrine disease you have seen in ward?

DM
Thyroid--- hypo & hyper
Cushing
Acromegaly

Q.Name some endocrine emergency?

1st tell------- DM-Hypoglycemic coma
-DKA
-HONKC
Then thyroid---thyrotoxicosis crisis
Myxedema coma
Addisonian crisis
Q.Name some endocrine condition where wt gain occur?

Hypothyroidis
Cushing

Q. Name some endocrine condition where wt loss occur?

Thyrotoxicosis
Adrenal insufficiency ( Addison)
DM

Thyroid
Q.Name thyroid hormone?

T4 thyroxin T3 tri-iodothyronine TSH Thyroid stimulating hormone

Q.Which hormone is more active?--------------- T3

Q.Classification of thyroidisis? [to remember-- T3, T4 1/ TSH]

Primary thyrotoxicosis T3, T4 TSH [or undectable]

Sub. thyrotoxicosis T3, T4 upper part of TSH [ or undetectable]
normal level
Primary hypothyroidism T3, T4 TSH [ ,>20 mu/l]
Sub. Clinical hypothyroidism T3, T4 lower part of TSH [ <20 mu/l]
normal level
Secondary hypothyroidism T3, T4 TSH

167
Q.Name the investigation you will do in pt with thyroid disease?

Thyroid hormone----- T3, T4 ,TSH

Thyroid scan & radio-iodine uptake
USG of thyroid gland
Antibody

* Graves Gi Rb wK `wL ----- TSH receptor antibodyTRAb

* Hashimoto thyroidis Gi Rb wK `wL----- Anti thyroglobin antibody

Q.What information you get from thyroid scan?

Hyperthyroid Hypothyroid
Temp Heat intolerance Cold intolerance
Hand Warm but sweaty hand
Fine tremor
Palmer erythma
Wt & appetite Loss of Wt Weight gain
But increased appetite
Face Irritability, staring look Moon/puffy face, baggy eye,
q. what is face finding of pt Agitated, eye sign periorbitaledema, loss of
with hypo & hyper thyroid Lid log, lied retraction lateral eye brow
exophthalmus
GIT Loss motion Constipation
ascitis
CVS Sinus tachycardia Bradycardia
What is the CVS finding of AF HTN
Hypothyroid or hyperthyroid Systolic BP/HTN IHD
Palpitation Pericardial effusion
Heart failure astherosclerosis
Angina
Menstruation Amenorrhea menorrhea
What is the mens finding ind
Hypothyroid pt ?
Neurological Hyper refiexia Delay relaxation ankle jerk
Periodic paralysis Hoarsness of voice
Proximal myopathy Depression
Carpal tunel syndrome
deafness
Q.30 yrs old cachexic lady comes to you polyphagia & diarrhea with increased appetite.What
is your Dx?

Hyperthyroidism
DM

Q.30 yrs obes female comes to you H/O constipation, depression & hoarsness of voice &
easily fatigue. What is your Dx?-----------Hypothyroidis

168
Q.Clinically/ bed side wK exam Ki hypothyroid cgvY Kiv hve ?

By examination of delay relaxation ankle jerk.

Q.Telephone G Dx Kiv hvq Ggb GKwU disease Gi bvg ej?-------Hypothyroidism

Q. GKUv investigation Kij KvbUv Kie?-----------TSH

Q.Name some cause of hyperthyroidis or thyrotoxicosis?

[to remember---GAMSa]

G- graves disease
Name three sign u look in a pt with hypothyroid ?
A- Toxic adenoma Speech husky voice
Pulse brady cardia
M- Toxic multinodular goiter Jerk delayed relaxation of ankle jerk
Sa- Sub-acute thyroiditis

Q. Name some cause of hypothyroidism?

[to remember---DR. TISHa]

D- drug

R- radio-iodine

T- thyroidectomy

I- Iodine deficiency

S- spontaneous atrophic thyroiditis

Ha- hashimotos thyroiditis

Q. Name some cause of goitrious hyperthyroidism?

Causes are same of thyrotoxicosis.

Q. Name some cause of goitrious hypothyroidism?

Hashimotos thyroiditis
Spontaneous atrophic thyroiditis
Iodine deficiency

169
Q.Name some cause of goiter?

Simple goiter
Multinodular goiter
Graves
Toxic ademona
Hashimotos thyroiditis
Spontaneous atrophic thyroiditis

Q.Name some auto-immune disease?

Graves
Hashimotos thyroiditis
Spontaneous atrophic thyroiditis

Q.Rx of hyperthyroidis?

3 modalits Rx ------- Antithyroid drug

-------Radio-iodine

-------Surgery

Q.Name the anti-thyroid drug used?

Tab. Carbimazol (45-60 mg/day-in developed dose)-------18 to 24 month who are in

< 40 yrs

Q.Complication of Carbimazol?

Rash
Agronulocytosis

Q.A pt with hyperthyroidism on Carbimazole comes to you with sore throat?What Dx?

Pt develop agronulocytosis
Stop drug,give antibiotics

Q.Contraindication of Carbimazole?-------Pregnancy & lactation

Q.What will happen if pregnant women take Carbimazole?------Aplasia cutis

Q.What is Rx if pt is pregnant?---propylthiouracil (400-600 daily)

* 4 week before EDD ea KiZ nq to prevent neonatal hypothyroidis

170
Q.mv_ Avi wK `Iqv nq?----Tachycardia Gi Rb -blocker w`Z nq

Tab. Propanolol up 160 mg/day

Q.What are the indication of radio-iodine?

If age >40 years

Recurrent after surgery
Toxic adenoma or multinodular goiter

Q.Contraindication of radio-iodine?

Pregnancy or planned pregnancy with 6 month of Rx

Lactation

Q.Indication of surgery?

[to remember---MRCP]

M- large multinodular goiter

R- recurrent after one course anti thyroid drug

C- Cosmetic purpose

P- pressure affect

Q.Complication of surgery?

Hypothyroidism
Hypo parathyroidism
Transient hypocalcaemia
Recurrent laryngeal nerve palsy

Q.What is the Rx of toxic adenoma & toxic multinodular goiter?

Radio-iodine thrrapy

Q.Rx of graves disease?

Same as thyrotoxicosis

Q.What are the cardinal feature of graves?

Exophthalmus
Goiter
Dermopathy pre-tibial myxoedema

Q.What type disease it is?------Auto immune

Q.Name the antibody & whats against it is?

171
 The antibody is IgG & it is against TSH receptor [TRAb]

Q. Graves wK iKg Hypo bv Hyperthyroidis ?

Graves may ------- Hyper thyroid if antibody stimulate TSH receptor

------- Hypo thyroid if antibody inhibit TSH receptor

------- Eu thyroid neight stimulal nor inhibit

Q.Kv`i ewk nq?-------cigarate smoker

Q.What will exam in pt with graves?

Goiter will diffuse soft & bruit present

Eye ------lid lay eye lid log behind the eye ball

------lid retractionupper sclera is visible above cornia

------ Exophthalmus

172
A patient come to you with pain in the throat and have HO of fever 7 days ago? On
examination pt have tenderness over thyroid gland ? What is your diagnonsis ?
My diagnosis is subacute thryroiditis or Dequervain s syndrome
What will be the treatment?
NSAID
blocker if symptomatic
may need oral steroid prednisolone
careful monitoring of thyroid function
if patient become hypothyroid may need temporary thyroxin therapy
What is feature of subacute thryroidistis ?
HO FEVER
Pain in thyroid
Pain worse on chewing or swallowing and movement of neck
On exam ---diffuse tender thyromegaly
Age : female , 20 -40 yr
Thyroid scan
Low uptake
ESR---increased
What is the nature history of subacute thryroiditis ?
Hyperthyroid (4-6wks) ----then hypothyroid(4-6 month)----then euthyroid

What is biochemical feature sub acute What is biochemical feature sub acute
hyperthuroidism ? hyperthuroidism
TSH---is undetectable TSH---is increased
T4 and T3 --upper limit of normal T4 and T3 --lower limit of normal
Is treatment need in this condition? Is treatment is needed ?
.
Yes Usually not needed
why Mention the indication of treatment in
subclinical hypoth?
Because chance of Treatment is needed only in following
AF condition ?
Osteoporosis THS>10
TPO is more
Pregnancy
Infertility
Goiter

173
Suppose a patient of graves disease if you give treat become hypo / if not then become
hyper what will you dc?
We will give both carbimazole and thyroxin.
What are the clinical features of hypothyroid?

What are investigations you will do in hypothyroid patient?

Thyroid hormone T4 and T3 decrease and THS increase
Antibody Antiperoxidase antibody
Anti thyroglobin antibody
ECG Low voltage ECG, sinus bradycardia , T-inverseon
CXR Cardiomegaly
Lipid profile Dyslipidaemia
PBF Macrocytic anaemia

Q.What is the treatment of Hypothyroid ?

Thyroxin ---therapy
Q. How long u will give ?
Life long
Write down the dose of thyroxin ?
Initially ---50mg for 3 wk
Then do it 100mg for 3 wk
Then increase it to 150mg
What is half life of thyroxin?
7days
What will be treatment in a patient with IHD?
Thyroxin precipitated angina
So patient with IHD started low doses 25mg and gradually under supervision
What will be treatment of hypothyroid in pregnancy?
Have to increase the dose of thyroxin . usually 50mg extra is needed with usual dose .
Because increase thyroglobulin and increase total thyroid but decrease FT3 & FT4 .and also
increase thyroxin metabolism in placenta ?

174
Name two thryroid emergency

Thyrotoxicosis crisis Myxoedema coma

Fever or infection / illness Elderly patient ,HO hypothyroid
Restlessness , confusion , drowsy Cold and hypothermia < 25 0c
Irritable and agitated Unconscious , convulsion
Diarrhea , vomiting , atrial fibrillation Hyponatraemia
Treatment ICU Main treatment :
IV fluid NS Rewarming
Antibiotic IV T3 / triiodothyronine
O2 therapy If not available give
Carbimazole 40/60 mg o Oral thyroxin
IV propanolol General Mx
Na-iopodate IV fluid NS
Steroid / hydrocortisone Antibiotic
O2 therapy
Inj. Hydrocortisone 100 mg * hr

Mortality 10 % 50 %

Describe different types of nodule

Hot nodule Only functioning nodule take uptake Radio-iodine
and rest of the gland dosent take Surgery
Local ethanol injection
Warm nodule Only Functioning nodule and surround Local ethanol injection
area take the uptake
Iso- functioning Both nodule and rest of the gland take
uptake equally
Cold nodule Nodule dosent take uptake FNAC

What is dangerous of cold nodule? What will u do ?

Chance of malignancy
FNAC should be done

175
Name thyroid malignancy
Papillary carcinoma
Follicular carcinoma
Medullary cell carcinoma
Anaplastic carcinoma
Lymphoma

This chapter you read in surgery

POLY---Po-papillary Llymphatic metastasis Y--young

Papillary carcinoma 2040yr Total thyroidectomy

Young followed by radio-iodine
Lymphatic metastatic therapy and life long
thyroxin therapy
Follicular carcinoma 4060yr do
Old
Blood borne metastatic

Medulary carcinoma Middle age and elderly

From parafolicular C cell
How will follow up?
By seeing serum thyroglobulin / if increased then think recurrence or metastasis

Acromegaly

Scenario : A patient comes to you with history head ache and when he go out through the door
he stuck with the door right or left side of body

Or Scenario :pt complain of head ach and he also notice that he has to change hat and shoe size
day to day

Ans. My diagnosis is acromegaly

What is the cause of acromegaly?

Pituitary macroadenoma causing excess growth hormone (GH) secretion,

176
What are feature of acromegaly ?
Large hand and feet
Large face with with prominent supraorbital ridge
Teeth show malocclusion and widely apart
prognathisin (protrusion of lower jaw forward,)
Large tongue (macroglossia).
Eyes: bitemporal hemianopia
Skin: thick, greasy and sweaty

Why it occur ?
Acromegaly is due to excess growth hormone secretion from pituitar, macroadenoma (>10mm)
after union of epiphysis. As long bone fused pt does not in height rather peripheral part grow

If occurs before the union of epiphysis it is called ?

if occurs before the union of epiphysis, it is called gigantism.

Can acrome-aly and gigantism exist together?

Yes, if excess growth hormone starts in adolescence and persists in adult life, the two conditions
may be present together

Mention some causes of macroglossia.?

To remember DATA
D--Down's syndrome.
A--Acromegaly.
T--Hypothyroidism.
A--Amyloidosis.

What investigation you want to do?

Skull x-ray: enlarged Sella turcica
GH assay
CT and MRI of brain

What is the treatment?

1. Surgery:
Trans-sphenoidal removal of adenoma
Post-operative radiotherapy s
2. Drugs: given if surgery is not possible
Somatostatin analogue: octreotide

177
ADDISON :
Cachetic and emaciated Patient comes to with with nausea vomiting and diarrhea , dizziness on
examination you find postural hypotension . and (marked pigmentation )

What is your diagnosis?

Addison disease / addisionial crisis

What else do you want to see? And where?

I will Examine the patient for pigmentation for pigmentation
In mouth
o Mucous membrane
o Soft plate
o Gums and lip
Skin crease (palmar crease), knuckles and nipples.
Pressure points (elbow and knee).
Recent scar.

What will be the BP?

BP will be low
May present postural hypotensison

What are the diagnostic criteria in Addison's disease? A: Triad of:

Weakness or emaciation (100% cases).
Pigmentation (90% cases).
Hypotension

What is common of Addison in our country?

1st say .TB
Other causes
Idiopathic / autoimmune
HIV
Metastasis
Sarcoidosis , haemochromatois

What is heart size in addision ?

Small heart

178
What are the other causes of small heart ?
COPD
Addison
Constrictive pericarditis
If you do plain X-ray of abdomen what you expect?
Calcification of adrenal gland
What will b the electrolyte finding of Addison and cushing ?
Addison Hyper kalaemia and hyponatraemia
Cushing Hypo kalaemia

What investigation you will do

CBC ESRincreased
Blood glucose low or lower limit,
Electrolytes (hyponatraemia and hyperkalaemia,
Hormone
Serum ACTH high
cortisol low
Tests to find out causes:
o Chest x-ray (TB).
o Plain x-ray abdomen (to see adrenal calcification in TB),
o USG or CT scan of adrenals.
How will confirm diagnosis ?(just remember the name only )

Synacthen test: short and long synacthen test

Not need for all who want more marks (75%)

Short synacthen Basic principal if you give ACTH then it normally increase cortisol level
test and if it dose not occur then it is adrenal insufficiency . may be primary
(addison)or secondary
250 mg ACTH (synacthen) IM or IV is givevn
Serum cortisol at 0 and 30 minutes is measured.
If cortisol raises> 460nmoVL, rule out Addison's disease.
Failure to raise may indicate partial adrenal insufficiency or secondary
adrenocorrical insufficiency

179
long synacthen Basic principle if u give ACTH injection for 3 three day
test If secondary insufficiency ---cortisol increased
In case primary / addison not increased
I mg- ACTH IM daily for 3 days.
Measure serum cortisol at 0, 4, 8 and 24 hours (each day).
Progressive raise of cortisol indicates secondary adrenocortical
insufficiency.( >700ninol/1- at 8 hours after last injection.)
fallure to raise indicates Addison'sdisease cortisol remains < 700ninol/1- at 8
hours after last injection

Why pigmentation
Due to increase ACTH secretion.
Primary Secondary
Pigmentation No , pallor
Increased ACTH level Undetectable

What is the treatment of addision crisis

Immediately (3Ssaline , sugar ,steroid)
Open IV channel with normal saline
Give hydrocortisone 100 mg IV 8 hrly
Iv glucose therapy
Fludrocortisones for postural hypotension
Treatment of etiology?
. If TB, start antituberrular therapy.

What advice you will give the patient ?

I will told him to keep steroid card every time with him
In which his name, address, name of the disease, what to do when he become ill .
Following advise
Take steroid regularly
Dont stop it
If vomiting or unable to take orally , take it injectable form
If fever or other illness increase the doses
If patient become unconscious take him immediate to hospital and show the doctor
steroid card or bracelet

180
Name some autoimmune endocrine disease?
Graves
Hashimotos thyroiditis
Addison
Name some endocrine emergency?

Scenarios a patient come to you with complaint of nausea , vomiting , diarrhea ,weakness with
history of long time oral steroid which he suddenly stop 7 days ago ?
Dx :
Secondary adreno-cortical insufficiency
Rx continue stroid

Cushing syndrome

Remember this picture to your mind:

You will give answer two frequent question from this picture?

181
What are the feature of cushing syndrome?
What are the feature of steroid over doses?

What are common feature of cushing syndrome

Face
Moon face and plethoric

Neck
Buffalo hump
Supraclavicular fat deposition

HTN
DM
Central obesity
Striae
Osteoporosis
Fracture of vertraeba / bone
Skin thin
Bruising
Proximal myopathy
Cant stand up from sitting position

Peptic ulcer disease

What is the common cause of cushing syndrome? have you seen any patient of cushing in ward
what was the causes ?
Iatrogenic chronic glucocorticoid therapy which given in
bronchial asthma ,
nephrotic syndrome ,
Rheumatoid arthritis
SLE
What are cause of cushing diseases ?
Classification of Cushing's syndrome
ACTH-dependent
Pituitary adenoma secreting ACTH (Cushing's disease)
Ectopic ACTH syndrome (bronchial carcinoid, small-cell lung carcinoma, other neuro-
endocrine tumour)

Non-ACTH-dependent
Iatrogenic (chronic glucocorticoid therapy)

182
 Adrenal adenoma
Adrenal carcinoma

What is cause of cushing diseases ?

Pituitary micro-adenoma . is less than <10 mm

What do you mean by cushing disease and cushing syndrome?

Cushing syndrome due to Pituitary micro-adenoma is called cushing disease
Cushing syndrome is due to excessive steroid of any causes

What investigation you want to do in Cushing syndrome ?

Just remember the name not interpretation

Step --1 To establish Urine free cortisol

diagnosis Diurnal rhythm of plasma Evening sample is more than
cortisol 75 % of morning

Low-dose dexamethasone Not suppress in cushing

suppression test

Step --2 To detect ACTH Undetectable adrenal

etiology causes
Detectable ---ACTH
depended
Step --3 To pituitary or High -dose dexamethasone Suppressed in pituitary
Ectopic ACTH suppression test origin
Depended Not suppressed in ectopic
ACTH

MRI of brain
CT or MRI of adrenal gland
What is the electrolyte in cushing ?
Hypokalaemia
How will differentiate cushing from pseudocushing ?
Cortisol excess due to other illness is called pseudoCushing's syndrome. May occur in chronic
alcoholics, severe depression and in simple obesity
Biochemical parameter :

183
 There is increased urinary excretion of steroid,
absent diurnal variation of cortisol and
Failure of suppression by dexamethasone.
All revert to normal after removal of the cause
How will differentiate from cushing :
By insulin stimulation test
In Cushing's syndrome almost no response,
but in pseudo-Cushing's syndrome, insulin-induced hypoglycaemia due to s excess
cortisol secretion.
Treatment of cushing ?
ACTH dependent pituitary Cushing :
Surgery :
Transphenoidal removal of microadenoma
Radiotherapy :
Pituitary irradiation
Is there any drug use in
Ketoconazole
Adrenal causes :
Surgery
Adrenalectomy
Radiotherapy
Patient of cushing comes to with back pain ?
Osteioporosis

When growth hormone secrete?

At night
When cortisol secrete ?
At morning
What do you know about Nelson's syndrome?

It is a syndrome that occurs after bilateral adrenalectomy and is characterized by a

rapidly growing pituitary adenoma,

very high ACTH levels and
hyperpigmentation.
It is occur in patients with Cushing's disease who have undergone adrenalectomy .

184
Causes of tall stature
Marfan Constitutional
Klinefelter Turnners
Kallman Achondroplasia
Gigantism Cretinism
Constitutional Hypopituitarism
Chronic systemic disease in child hood
Heart failure
Asthma
Renal failure

Anatomy of adrenal gland

Cortex Zona Aldosterone
glomerulosa
Zona fasciculate Glucocorticoid hormone
Zona reticularis Androgen
Medulla Epinephrine / norepinephrine

Scenario :
A patient come to you hypertension , oedma and proximal muscle weakness (ubable to getting
up from sitting position )
My diagnosis is conn diseas
What are the feature
Hypertension due Na retention
muscle weaknessdue to hypokalaemia
polyuria---due to DI
tetany ----metabolic alkalosis
oedema
Biochemical
Hypo K
Metabolic alkalosis
Hypernatraemia
CT--/ MRI adrenal adenoma

A patient comes to you with paroxysmal head ache, sweating, palpitation and hypertension what
is your diagnosis .
My diagnosis is phaeochromocytoma

185
Clinical features of phaeochromocytoma
Hypertension (usually paroxysmal; often postural drop of blood
pressure)
Paroxysms of:
o Pallor (occasionally flushing)
o Palpitations
o Sweating
o Headache
o Anxiety (fear of death-)
Abdominal pain, vomiting

186
 Diabetis Mellitus
Define Diabetes mellitus?

Diabetic is a clinical syndrome characterized by hyperglycaemia caused by absolute or relative

deficiency of insulin.

Write down the difference between types I and Type II diabetes mellitus?

Type 1 Type 2
age of onset young less than 4o yrs more than 50 yrs
Body weight low / underweight Obese
Diabetic complications at absent usually present in 25 %
diagnosis
ketonuria present absent
Autoantibodies & usually present absent
autoimmune disease
family history absent present

What r the causes of type I?

Immune-mediated
Idiopathic

What r the causes of type II?

Genetic defects
Pancreatic disease
Excess endogenous production of hormonal antagonists to insulin
Drug-induced
Associated with genetic syndromes
Name some pancreatic causes of DM?

The pancreatic disease that causes

Pancreatitis acute and chronic

Pancreatectomy,
Neoplastic disease,
Cystic fibrosis,
Haemochromatosis,
Fibrocalculous pancreatopathy

187
Name some diabetogenic hormone or hormonal antagonists to insulin? or

Endocrine disease that causes DM ?

to remember all the excess fun

Diabetogenic hormone endocrine disease

Growth hormone Acromegaly;
Glucocorticoids Cushing's syndrome;
Glucagon- Glucagonoma
Catecholamines- Phaeochromocytoma;
Thyroid hormones Thyrotoxicosis

Drugs that causes diabetes?

Drug-induced diabetes

Corticosteroids,
Thiazide diuretics,
Phenytoin

Name some genetic diseases that cause Diabetes?

Down's syndrome;
Klinefelter's syndrome;
Turner's syndrome;

DIDMOAD (Wolfram's syndrome)-

Diabetes insipidus, Diabetes mellitus,optic atrophy, nerve deafness; Friedreich's ataxia; myotonic
dystrophy

What do you mean by metabolic syndrome?

Following are collective called metabolic syndrome:

Type-2 diabetes mellitus

HTN
Central obesity
Hypertriglyceridaemia

188
When u told that the patient is suffering from diabetes?

Diagnosis confirmed by*:

Fasting plasma glucose 7.0 mmol/l (126 mg/dl)
Random plasma glucose 11.1 mmol/l (200 mg/dl)

Some teacher want hear 2HABF or 2 hr after 75 gm glucose 11.1 mmol/l ( in case of
chandan sir )

Or what will u do if you want to get accurate result of 2 hrs after breakfast result?

I will tell the patient to do blood glucose 2 hrs after 75gm glucose

What examination will you do if u want to know the glycaemic status of previous 2/ 3
months?

Glycated haemoglobin (HbA1c)

Normal value 7
1% HbA1c = 2 mmol / L

Indication of OGTT

Indications for oral glucose tolerance test

o Fasting plasma glucose 6.1-6.9 0 mmol/l (110-126 mg/dl)

o Random plasma glucose 7.8-11.0 mmol/l (140-199 mg/dl)

step the procedure of ORAL GLUCOSE TOLERANCE TEST (OGTT)

o Unrestricted carbohydrate diet for 3 days before test

o Fasted overnight (for at least 8 hrs)
o Rest before test (30 mins); no smoking; seated for duration of test
o Plasma glucose measured before, and 2 hrs after, 75 g glucose load

when will u called impair fasting glucose ?

Mention the complication of DM ?

189
What do you mean by micro vascular and macro vascular complication ?

Ans :

chronic complication of DM are two types

Microvascular

Retinopathy,
Nephropathy
Neuropathic
Peripheral neuropathy or somatic
Autonomic neuropathy
Foot disease
o Ulceration
o Arthropathy

Macrovascular

Coronary circulation
Myocardial ischaemia/infarction
Cerebral circulation
Transient ischaemic attack
Stroke
Peripheral vascular disease
Claudication
Ischaemia

A diabetic patient comes to you with complaint unconsciousness or semi consciousness?

What will b ur diagnosis?

o Hypolgycaemia
o DKA
o Hyper osmolar nonketotic coma, (HONK)
From here sir will ask what will be the management of any one of these three ?

190
How will u differentiated from hypoglycemic coma from hyperglycemic coma?

hypoglycemic coma hyperglycemic coma

Sweating with cold periphery Not so
Pulse bounding pulse Low volume pulse or tachycardia
BP normal Bp- hypotension
No sign of dehydration Sign of dehydration

If u fail to differentiate the between hypoglycemic coma from hyperglycemic coma then what
will do ?

I will treat the patient as hypoglycaemia coma

Why ?

Because hypoglycaemic coma is more dangerous than hyperglycemic coma . it causes

irreversible brain damage .

What are the feature of hypoglycemia ?

The feature of hypoglycemia

Autonomic symptoms CNS: /

Sweating Confusion
Pounding heart Convulsion
Hunger Drowsy
Tachycardia Inability to concentrate
Tremor Slurring speech
Suppose u r an intern doctor in ward suddenly a pt attendant come and told u that my patient is
diabetic and he become unconscious after taking insulin or take OHA and on examination pt is
drowsy with cold sweaty hand. What is ur diagnosis and what is the management or tell the
management of hypoglycemia?

My diagnosis is hypoglycaemic coma ?

I will manage the pt in following ways :

If look at the patient is unconsciousness or not

Or he is able to take food orally or not

If the patient is able to take food orally then give

191
Oral carbohydrate as form of

Orange juice / glucose

Sugar (4 6 tsf sugar in a glass of water)

Whatever carbohydrate u gets near ur hand

IV fluid:

Inj. 25 % glucose 100 ml (in text book ---50 ml of 50 % glucose if any one ask to know the
text book )

-----------------------------------------------------------

IV @ 20 D / min

(if u do not get 25 % then 1st give 5%DA and ask the pt bring immediately )

Followed by

Inj. 10 % DA 1000 ml

--------------------------------

IV @ 20 D/ min

Stop insulin or other oral Hypoglycemic drug immediately

Do FBS and 2 hr ABF next day @
20to 30 % reduction of dose of insulin and oral hypoglycemia drug .

What will u do if a patient with hypoglycemia come to u with unconsciousness but 25% or 5%
DA is not available?

Give him NG tube and give glucose / orange juice/ sugar via it

What may the causes of hypoglycaemia in this pt ? or what history u will ask the pt ?

Pt usually present With following HO

o HO insulin or oral hypoglycaemic drug intake followed by

o Missed, delayed or inadequate meal
o Unexpected or unusual exercise
o Vomiting
o
HYPOGLYCAEMIA When hypoglycaemia (blood glucose < 3.5 mmol/l (63 mg/dl)) occurs in
a person with diabetes it is a result of treatment and not a manifestation of the disease itself.

192
SPONTANEOUS HYPOGLYCAEMIA When hypoglycaemia develops in non-diabetic
people,(if < 3 mmol/L) it is called 'spontaneous' hypoglycemia

Write down the management of DKA?

Basic principal of DKA Mx (all have to memorized these four line if u want to pass )

1. correction of dehydration with appropriated fluid .

2. short acting soluble insulin
3. broad septum antibiotic
4. correction electrolyte imbalance hypokalaemia
(then sir will ask you how will correct dehydration , ETC )

Correction of dehydration

we have to give 6L Fluid (4L NS + 2 L 5%DA) in 24 hrs

1st L NS in hr To remember simply

nd
2 L NS in 1 hr doubling
rd
3 L NS in 2 hr
4th L NS in 4 hr
Then when RBS < 15 mmol
1st L 5 %DA in 8 hr
nd
2 L 5 %DA in 8 hr
Correction of hypeglyceamia

50 units soluble insulin in 50 ml 0.9% saline i.v. via infusion pump

o 6 units/hr initially
o 3 units/hr when blood glucose < 15 mmol/l
o 2 units/hr if blood glucose declines < 10 mmol/l
Check blood glucose hourly initially- Aim for fall in blood glucose of 3-6 mmol/l per
hour

Have u the infusiong pump in the ward ? answer no

Then how will u manage it ?

10 to 20 unit IM stat and

then

6 units IM hrly initially

3 units IM hrly when blood glucose < 15 mmol/l
2 units IM hrly if blood glucose declines < 10 mmol/l

193
What antibiotic we use?

Parental 3rd generation antibiotic such as ceftriaxone

How will u correct the hypokalaemia? (Not for all to memorized it)

In following way

plasma K is > 5.0 mmol/l no

plasma K is 3.5-5.0 mmol/l inj. KT or kcl 1 amp or 2 0 mmol
plasma K is < 3.5 mmol/l, inj. KT or kcl 2 amp or 40 mmol
How will give the potassium

Give in 1 litre of fluid

Avoid infusion rate of > 20 mmol/hr

What are the Complication of DKA

To remember it D--CAT

o D-- Disseminated intravascular coagulation

o C---Cerebral oedema
o A--Acute respiratory distress syndrome
o T---Thromboembolism
How the patient is present to u

The pt is usually present to us with

Sign symptom of DKA

Confusion, drowsiness, coma (10%)

Abdominal pain
On examination we will get following

Air hunger (Kussmaul breathing)

Dehydration
Hypotension (postural or supine)
Tachycardia
Smell of acetone

194
Usually not asked but some time sir wants to know the following information about HONK

In which age it common Elderly

In type of DM it is common Type--II
what is blood glucose level > 50 mmol/ L
Mortality 40 %
What is most common complication of it Thrombo-embolism

What will be the management of HONK

(To remember of the keto-acidosis management:)

Thats means

Fluid ---1/2 strength normal saline or 0.45 % normal saline

Short acting soluble insulin 3 unit / hr
For prevention of thromboembolism

subcutaneous low molecular weight heparin is recommended.

Write down the treat DM ?

Treatment of DM is combination of 3D

1. Discipline
2. Diet
3. Drug
In discipline

Educate the pt about the disease and life style modification

it is the disorder of glucose metabolism

it cant be cured and only pt have maintain normal blood sugar by dietary and drug
control
he has to maintain a discipline life with daily regular exercise with calculated food and
timely food intake
avoid sugar and sugar containing food
counseling the pt about or educate about complication of the disease
teach the pt about foot care
Teach he sign symptom of hypoglycemia and what will do when these appear .

195
Here sir may ask u what exercise and how long u do Tell the Contraindication of exercise?
it? a. Coronary heart disease,
Methods of exercise: b. Proliferative retinopathy,
Stretching Exercise c. Severe neuropathy,
Free hand exercise Duration 10 minutes d. Osteoarthritis,
Aerobic Exercise e. Neprhopathy,
(Minutes i.e., brisk walking, swimming, cycling, f. Ketonuria.
jogging.
Treadmill, static
cycling)
Duration at least 30 min at least 3 times a week.

Diet

Depend on patient body weight or BMI

If patient is obese than ---low calorie diet
If patient is non obese or underweight ----weight maintaining diet

Carbohydrate 45-60%

Fat (total) < 35%, Polyunsaturated

Protein 10-15% (do not exceed 1 g/kg body weight)

Drugs

In type one -----insulin

In type II OHA (oral hypoglycemic agent:)

If patient is obese

First add --- Metformin (Monotherapy )

If not control Add ----Sulphonylurea ((combination therapy ))
If not control add insulin or give only insulin
If patient is non-obese

First add --- Sulphonylurea(Monotherapy )

If not control Add ---- Metformin ((combination therapy ))
If not control add insulin or give only insulin

196
Now sir will ask about metformin

What type of drug it is Sensitizer

Why it is use in obese It reduce weight also
What invest. U do before prescribe it and S.creatinine and SGPT
why Because if S. Creatinine > 1.5 mg/dl in male
and 1.4 mg/dl in female metformin cant
given
Mention one complication of metformin Lactic acidosis
Name another disease where it use ? Polycystic ovarian syndrome

Now sir some scenario and ask u to give treatment

A 40 years obese leady newly diagnosed DM Diet ---Diabetic diet (low calorie diet )
.BMI 30 Exercise : 30 min each day
or wt -60 kg FBS13 mmol/l and 2HABF Drug ----OHA----Metformin 500 mg
18 mmol/ l
A 40 years non-obese leady newly diagnosed Diet ---Diabetic diet (weight maintaining
DM diet)
.BMI 22 or wt -50 kg FBS13 mmol/l and Exercise : 30 min each day
2HABF 18 mmol/ l Drug ----OHA----Sulphonylurea
A 20 years obese leady newly diagnosed Diet ---Diabetic diet (weight maintaining
DM .BMI 22 diet)
or wt -30 kg FBS13 mmol/l and 2HABF Exercise : 30 min each day
18 mmol/ l Drug ----insulin

Diabetic patient with MI , stroke , severe insulin

infection TB, CLD , jaundice ,
pregnancy

Approach to patient with DM

I will take some history, do some clinical examination to find out the etiology , and
complication of DM and

1st history

o Age of the pt to type I and Type-II

o History of wt loss (type I) and wt gain (Type-II)
o Difficulty in vision retinopathy or cataract
o Family history
o Drug HO steroid
o Chest pain
197
 o Palpitation
o Intermittent claudication (PAD)
o Buring and Parasthesia , Numbness /Cold periphery---neuropathy
o urinary incontinence , gastroparesis , erectile disfunction
o abdominal pain and diarrhea

examination

general examination

eye -- anaemia ---CRF and

cataract
Xanthelasmahyperlipidaemia
Appearance (2ndary cause Cushing , acromegaly , hypothyroid
)
Mouth Candidacies
Hand Pulse resting tachycardia
Fixed heart rate
Postural hypotension
Oedema CRF and autonomic neuropathy
Skin change Dry , fungal infection

Examination of foot Ulceration ,Callous formation, Infection, Evidence of injury,

Hair loss, Fissures in the feet
Examination of hand Muscle wasting , Payer sign ,Dupytren contracture, trigger
finger
Neurological examination Sensory ---joint sense position and vibration ,Touch and
pain sensation
Motor jerk , muscle power
Cranial nerve examination ---light reflex & opthalmoplegia
Peripheral pulse Lower limb
Cardiac Apex beat shift IHD
Fundoscopy

What other investigation will u do in pt with diabetes milieus

Urine RME---proteinuria ----nephropathy

s.creatinine
fasting lipid profile
ECG
CXR
HbA1c

198
What is the target BP in DM ?

130/ 80 mm of hg if proteinuria is more than > 1 gm per 24 125/75

Which ant-HTN u will use in a pt with DM ?

ACEinhibitor or angiotensin receptor blocker

Classify neuropathy

Somatic neuropathy
Sensory --- Motor jerk , muscle power
loss joint sense position and vibration Diabetic amyotrophy
loss of Touch and pain sensation
Buring and Parasthesia ,
Numbness

Autonomic neuropathy
Cardiac Resting tachycardia
Fixed heart rate
Postural hypotension
Gastro-intestinal Gastro-paresis
Dyphagia
Diarrhea (nocturnal )
Constipation
Gentio-urinary Urinary incontinence
Erectile disfucntion
Retrograde ejaculation
SUDOMOTOR Gustatory sweating
Anhidrosis;
Vasomotor Cold Feet
Dependent oedema
Cranial nerve Pupillary reflex
Opthalmoplagia
Name of oral hypoglycemic agent

1. Insulin Secretagogues:
A. SULPHONYLUREA
Glibenclamide ,

Glimepride ,

Gliclazide

B GLINIDES

Rapaglinide.

199
Nateglinide

2. INSULIN SENSITIZERS

A. BIGUANIDES
Metformin 500 mg /850 mg
B. THIAZOLIDINEDIONES

Rosiglitazone 4 mg / 8 mg
Pioglitazone 15 mg / 30 mg
3. OTHERS : The -glucosidase inhibitors

Acarbose 50 mg

Name drug there mechanism of action

SULPHONYLUREA stimulate the release of insulin from the pancreatic cell

INSULIN Increase insulin sensitivity and peripheral glucose uptake in muscle and
SENSITIZERS impairs glucose absorption by the gut and
inhibits hepatic gluconeogenesis
The -glucosidase delay carbohydrate absorption in the gut by selectively inhibiting
inhibitors disaccharidases

Indication of insulin in DM patient:

Insulin therapy is indicated in those who meet the following criteria:

1. Type 1 DM patients

2. Type 2 DM patients

1. Who remain persistently symptomatic hyperglycaemic on maximum dose of oral

agents and diet (primary/secondary failure).
2. Acute stress, such as
*severe Infection

* Myocardial infarction

* Stroke

DKA and HONK

3. Diabetes with complication

* Eye disease: Prolifertive retinopathy

200
 * Kidney disease: nephropathy Serum Creatinine >2.5 mg/dl.

* Acute metabolic neuropathy

4. Prior to surgery;
5. pregnancy

Classify insulin:

Type Generic name

Ultra short acting insulin analogues-
lispro,
aspart,
Short acting / rapid Soluble
regular
Intermediate acting Basal
Lente
Isophane (NPH-Neutral
protamin hagedorn )

Long acting Insulin analogues-

Glargine,
Detemir

Tell the side affect of insulin?

Hypoglycaemia
Weight gain
Peripheral oedema (insulin treatment causes salt and water retention in the short term)
Local allergy (rare)
o Lipodystrophy at injection site

How insulin is given and what are the sites?

Insulin is given subcutaneously

Site of insulin:

Outer aspect of thighs, upper arms and

Abdomen below the umbilicus
Buttocks,

201
How will u differentiated between HTN & Diabetic retinopathy?

HTN retinopathy Diabetic retinopathy

Artery venous nipping Dot and blot hemorrhage
Slivery wiring Micro-aneurysm
Flamed shape is hemorrhage Hard exudates

Treatment of retinopathy

prevention and management

tight glycemic control with insulin

photocoagulation (eliminates neovascularization)

vitrectomy

frequent follow-up visits with an ophthalmologist (immediate

referral after diagnosis of type 2 DM; in type 1, only after 5 years of DM)

Treatment of nephropathy

tight glucose control

tight blood pressure control ACE inhibitors
limit use of nephrotoxic drugs

When and what do u mean by gestation dm?

Gestational diabetes is defined as diabetes with first onset during pregnancy

Gestation diabetes fasting plasma glucose > 5.5 mmol/l or

2 hours after a glucose > 9.0 mmol/l
Treatment

Pregnancy should be planned

Folic acid supplementation begins before conception
Maintain strict glycaemic control, with short acting soluble insulin .

202
 Kidney and Urinary Tract Disease
Q: Mention 3 important functions of kidneys?
A:
Excretory function: it excretes many metabolic breakdown of products ( including
ammonia, urea & creatinine from protein & uric acid from nucleic acids) ,drugs &
toxins.
Metabolic function: in vitamin-D metabolism, the kidneys hydroxylate 25-
hydroxycholecalciferol to the active form 1,25,-dihydroxycholecalciferol(failure of this
process contributes to the hypocalcemia & bone disease of chronic kidney disease)
Endocrine function: the kidneys secrete
Erythropoietin- from interstitial peritubular cells in response to hypoxia
Renin- from the juxtaglomerular apparatus in response to reduced afferent
arteriolar pressure, stimulation of sympathetic nerves & changes in sodium
content of fluid in the distal convoluted tubule at the macula densa.
Q: Define haematuria. Causes of painless & painful haematuria.
A:
Heamaturia: passes of blood in the urine.
Causes of painful haematuria: stone ,UTI, loin pain haematuria syndrome
Causes of painless haematuria: glomerulonephritis ,tumour, TB, polycystic kidney
disease, vascular malformation

Q: Causes of dark urine?

A: haemoglobiuria, myoglobinuria, food dyes, drug- rifampicin; bilirubinuria, porphyria,
alkaptouria etc.

Q: Define anuria & oliguria. polyuria with their causes.

A:
Anuria: complete absence of urine (<50ml/day). Causes-ARF, AGN
Oliguria: when urine output <300ml/day
Polyuria: when urine output >3litres /day.
Causes of polyuria:
Excess fluid intake
DM
Hypercalcemia
DI (cranial & nephrogenic DI)

Q: What are the causes of cranial DI?

A: due to ADH secretion [causes- idiopathic (50%), mass lesion, trauma, infection]

203
Q: What are the causes of nephrogenic DI?
A: Due to tubular dysfunction ( By- drugs:lithium ,diuretics, interstitial renal disease,
hypokalemia, hypercalcemia, genetic)

Q: What is the amount of normal protein in urine?

A: 150mg/day (name of this protein is Tamm Horsfall protein secreted by tubules)

Q: What is micro-albuminuria? Cause of it ?

A: when urinary excretion of albumin is 30-300mg/day.
Cause diabetic nephropathy
(glomerular proteinuria :when excretion of protein is >2.5g/day
Nephroteic range of proteinuria : >3g/day )

Q: Name the condition of proteinuria other than glomerular disease

A: after vigorous exercise, during fever or UTI and in heart failure

Q. what do mean by 'orthostatic proteinuria' ?

a. proteinuria that occurs only during the day without renal disease and the first morning sample
is negative is called 'orthostatic proteinuria'.

Q: Name the presentation of UTI.

A:
Asymptomatic baceteriuria
Lower UTI
Upper UTI
Prostatitis

Q: Define asymptomatic bacteriuria?

A: Presence of >105 organism per ml in the urine at apparently asymptomatic pt. is called
asymptomatic bacteriuria

Next Q: what treatment will you give?

A: no treatment is required (but in case of DM & pregnancy treatment is required)

Q: Mention the feature of lower UTI.

A: dysuria, frequency, urgency.

204
Q: What is the triad of pyelonephritis?
A:
Fever with chills & rigor.
Abdominal pain or loin pain
Renal angle tenderness

Q: Investigation of UTI pt?

A:
Urine RME: pus cell >105 in HPF
Urine for c/s
Others: USG

Q: Treatment of UTI?
A:
Uncomplicated UTI Tab. Ciprofloxacin (500mg)-1+0+1 3days
Complicated UTI Same 10days
In pyelonephritis Inj. Cefuroxime (750mg)-1+1+1+1 14days
In acute prostatitis Tab. Ciprofloxacin (500mg)-1+0+1 28days

Q: What advice will you give in a pt. coming with recurrent UTI?
A:
Fluid intake at least 2litres/day
Regular complete emptying of bladder
Maintenance of good personal hygiene
Emptying of bladder before & after sexual intercourse

Q: Name the common organism cause UTI.

A: mnemotic-KEP
E.coli
Klebsiella
Proteus & pseudomonas
Staphylococcus epidermidis

Q: What is sterile pyuria?

A: when neutrophil present in urine but urine culture negative. Found in renal TB.

Q: What do you mean by urethral syndrome?

A: Some patients, usually female, have symptoms suggestive of urethritis & cystitis but no
bacteria cultured from the urine is called urethral syndrome.

205
Possible explanation includes:
Infection with organisms not readily cultured by ordinary methods (Chlamydia, certain
anaerobes)
Intermittent or low-count bacteriuria
Reaction to toiletries or disinfectants
Post-menopausal atrophic vaginitis
Symptoms related to sexual intercourse

Q: Define ARF ( acute renal failure)

A: ARF ,also referred to as Acute Kidney Injury , describes a sudden & usually reversible
loss of renal function, which develops over days or weeks and usually accompanied by a
reduction of urine volume.

Q: Causes of ARF.
A:
Pre-renal Volume loss:
-blood loss (hemorrhage)
-fluid loss (diarrhea, vomiting, pancreatitis)
-3rd space loss (peritonitis, intestinal obstruction)
cardiac output ( heart failure, CCF)
Renal arterial stenosis/occlusion/diseases affecting
arterioles
renal Mnemonic- TIA
Acute tubular necrosis/toxins-85%
[toxins: endogenous-drug(gentamycin), exogenous-
bacteria(malaria)]
Interstitial disease -10%
AGN -5%
Post-renal Prostatic enlargement, stone ,tumour

Q: Treatment of ARF.
A:
Diet: -protein restriction
-fluid restriction (fluid =previous day output +500ml)
Diuretics: Inj. Frusemide
Treatment of complications: e.g. if hyperkalaemia then treat it.
For acidosis: Inj. Sodium-bicarbonate
If infection: antibiotic
Other : -avoid nephrotoxic medication, maintain intake-output chart
If urinary output not increase then go for dialysis

206
Q: Name the causes of CRF (now it is called chronic kidney disease).
A: mnemonic-DGHS
DM
Glomerulonephritis
Hypertension
SLE & connective tissue diseases
Others polycystic kidney disease

Q: Indications of dialysis in ARF.

A: mnemonic- KFC of UA
K --Hyperkaemia >6mmol/litre not responding to medical therapy(C=)
F--Fluid overload & pulmonary oedema
C--Serum creatinine 600 mmole/L (6.8mg/dl)
U--Serum urea 30 mmol/L (180mg/dl)
U--Uraemic pericarditis & uraemic encephalitis
A--Metabolic acidosis

Q: Name renal replacement therapies.

A: -haemodialysis
-peritoneal dialysis
-transplantation

Q: what are the features of CRF?

A: -anaemia
- HTN
-bone pain & renal osteodystrophy
- edema, if volume overload
-GIT: nausea, anorexia & hiccough
-muscle cramps & peripheral neuropathy

To remember it-
A=anaemia
B=bony change
C=HTN, uraemic pericarditis, pulmonary edema (c for cvs features)
D=dermopathy, pruritus
E= endocrine: hyperparathyroidism, hyperprolactenemia
F=fluid overload: edema
G=GIT: anorexia, nausea, vomiting, hiccough
H=haematological: bleeding manifestation

207
I=evidence of Infection
K=kidney: polyuria & nocturia
M= myopathy
N=neurological : sensory-polyneuropathy ; motor-foot drop

Q: Causes of anaemia in CRF?

A:
Relative deficiency of erythropoietin
erythropoiesis due to toxic effects of uraemia on marrow precursor cells
Reduced red cell survival
blood loss due to capillary fragility & poor platelet function
Reduced dietary intake & absorption & utilization of iron

Q: What is the target BP in CRF ?

A: 130/80 mmHg
If proteinuria >1gm/day then 125/75 mmHg

Q: What are the bony changes in Renal failure? Or, a pt. with CRF complaint of bone pain, what
is your diagnosis??
A: Renal osteodytrophy which contain- osteomalacia, osteoporosis, osteosclerosis,
hyperparathyroid bone disease (osteitis fibrosa)

Q: Treatment of CRF.
A:
Diet & fluid: plenty of fluid intake 3L/day
Correction of anaemia: -blood transfusion
-erythropoietin supplementation
- iron

Q: how will correct anaemia in CRF?

Control of HTN
For hypocalcemia: Tab. vitamin-D/Dicaltrol (2.5microgram) - 0+0+1
For binding of dietary phosphate: Tab.Calcium (300mg) after meal - 1+1+1
Diuretics
Pantoprazole
Treatment of infection

208
Q: Name some anti-hypertensive drug in CRF.
A:
ACEi / Angiotensin Receptor blocker
Diuretics
Calcium channel blocker
vasodilator

Q: How will you differentiate ARF from CRF?

A:
Traits ARF CRF
History Sudden onset, predisposing factors, Insidious onset, may have H/O: HTN,
H/O hypovolemia, drug, obstruction glomerulonephritis, anorexia ,vomiting
& infection
C/F Sign of hypovolemia, BP, oliguria Anaemia, HTN +/-edema, proteinuria
Investigations: Normal except AGN proteinuria
Urine RME
S. electrolyte Calcium & phosphate-normal calcium ,phosphate
USG normal kidney size (<9cm) & echogenic
cortex
*** In short:
In CRF: -pt. have anaemia + HTN,
-investigation : calcium, phosphate ; USG- kidney size <9cm, echogenic
cortex( cant be differentiate the cortex & medulla)
Above features are absent in ARF.

Q:When CRF with normal size kidney present?

A: DM

Q: CRF with large kidney?

A: polycystic kidney disease (PKD), amyloidosis, hydronephrosis.
Q: CRF without anaemia?
A: PKD

Q: what are the features present in PKD?

A:
Multiple cyst in both kidney
Palpable kidney
HTN
Haematuria
Recurrent UTI etc

209
Q: Staging of CKD (chronic kidney disease).
A:
Stage-1 Kidney damage with normal GFR ( >90 ml/min)
Stage-2 Kidney damage with mild decrease of GFR 60-89
Stage-3 Kidney damage with moderate decrease of GFR 30-59
Stage-4 Kidney damage with severe decrease of GFR 15-29
Stage-5 Kidney damage with GFR <15

Q: Have you heard the name of AIN?

Or, what is the cause of non-oliguric ARF??
A: yes , AIN is the acute interstitial nephritis/renal failure due to drug

Q: Clinical features of AIN.

A:
Fever, rash & eosinophilia (due to drug hypersensitivity reaction)
Non-oliguric ARF features
Urine RME: leucocyturia & eosinophiluria

Q: How can you confirm AIN?

A: renal biopsy

Q: What is the treatment?

A: Oral Prednisolone 1gm/kg BW .

SOME DEFINITIONS:

RENAL FAILURE/ CKD: irreversible deterioration in renal function which classically

develops over a period of years.
URAEMIA: when loss of excretory, metabolic & endocrine function of kidney produce
clinical sign and symptoms of renal failure is called uraemia.
ESRD (end-stage renal disease): when life become impossible without renal replacement
therapy is called ESRD.

Q .What do mean by Nephritic and Nephrotic Syndrome

A.
Nephritic syndrome1
Haematuria (brown urine)
Oedema and generalised fluid retention
Hypertension
Oliguria

210
Nephrotic syndrome2
Massive proteinuria-usually > 3.5 g/24 hrs (urine may be frothy)
Hypoalbuminaemia (< 30 g/l)
Oedema and generalised fluid retention
Hyper lipideamia

Q write down the Difference between

AGN NS

1. Onset acute 1. Onset insidious

2. Older children 2. Younger children
3. Preceding throat or skin infection 3. no such infection
4. Oliguria at onset 4. Oliguria later
5. Edema mild to moderate 5. Edema marked, ascites, genital edema,
6. Hypertension and hematuria pleural effusion
7. Urine ---protein ++ , RBC and RBC 6. Hypertension 30 %
cast + 7. Urine ---protein ++ , RBC and RBC
8. UTP < 3 gm / 24 hr cast -
8. UTP > 3 gm / 24 hr

211
Mention the causes of nepphrotic and nephritic syndrome
Cause of nephrotic syndrome Cause of nephritic syndrome

Primary cause Post streptococcus glomerulonephritis

Minimal change disease Ig A nephropathy
Membranous glomerulo nephritis RPGN
Focal segmental glomerulo sclerosis God posture syndrome

secondary cause of nephrotic syndrome

DM
Amyloidosis
SLE
Infection
HBV HCV
Malaria palsmodium Malarae
HIV
DRUG NSAID ,
AEI captopril
Gold and penicilinamide
Malignancy
Hodge king lymphoma

212
 Electrolyte and Acid base Balance
Q. Name some electrolyte imbalance/ what type of electrolyte imbalance you have seen in
ward?
Ans. Hyponatraemia
Hypernatraemia
Hypokalaemia
Hyperkalaemia

Q. Name some extracellular and intracellular electrolytes.

Ans.

Intracellular Extracellular
K Na
PO3- Cl-
Mg+ HCO-
Q. What is the normal level of Na and K in extracellular fluid?
Ans. Na 135-145 mmol/L
K 3.5-5.5 mmol/L

Q. Which electrolyte imbalance causes unconsciousness?

Ans. Na (Hyponatraemia and Hypernatraemia )
(if Sir asks for more answers, then tell- Ca and Mg)

Q. Which electrolyte imbalance causes muscle weakness?

Ans. Hypokalaemia.

Q. What are the common causes of Hyponatraemia?

Ans. Mnemonic: DVD
D- Diarrhoea
V- Vomiting
D- Diuretic- Frusemide.

Q. Which Diuretic causes Hyperkalaemia?

Ans. Spironolactone

Q. Tell me the management of Hyponatraemia.

Ans. Management of Hyponatraemia depends on serum level of Na

Type of Hyponatraemia Serum level of Na Management by

Mild 135-125 mmol/L Oral table salt
Moderate 115-125 mmol/L 0.9% NaCl (inj.)
Severe <115 mmol/L 3% NaCl (inj.)
or <110 mmol/L

213
Q. what is the target of daily correction of Hyponatraemia?
Ans. 10 mmol/day.

Q. How will you correct Hyponatraemia in the following cases where serum Na level is 128
mmol/L, 120 mmol/L and 102 mmol/L?
Ans.
Na level Method of correction
128 mmol/L ORS / Oral table salt
120 mmol/L Inj. 0.9% NaCl
102 mmol/L Inj. 3% NaCl

Q. In which condition 3% NaCl is used?

Ans.
If the patient is unconscious/ in coma/ convulsion.
When Na level is <115mmol/L or <110mmol/L.
Q. What is the consequence of Hyponatraemia?
Ans. Hyponatraemia osmotic pressure fluid goes in the cell from extracellular
space cerebral edema.

Q. what is the method of injection of 3% NaCl?

Ans. It is given very slowly in micro-burette set.

Q. what may happen if Hyponatraemia is corrected rapidly? / or complication of 3% NaCl

Ans. Myelinolysis may occur.

Q. What is Myelinolysis?
Ans.
Rapid correction of Hyponatraemia

Abrupt increase in extracellular osmolarity

Water shift out of the cerebral neuron

Abrupt reduction of cell volume of cerebral neuron and detachment from their myelin
sheath (Myelinolysis)

Permanent structural and functional damage of midbrain structures.

214
Q. What are the causes of Hyponatraemia? (not for all )
Ans. Causes of Hyponatraemia
Hypovolumic Hyponatraemia Euvolumic Hyponatraemia Hypovolumic
Hyponatraemia
Na loss > water loss Only water re-absorption, To remember- causes of
To remember- all loss Dilutional hyponatraemia edema

D- Diarrhoea SIADH (Syndrome of CCF

V- Vomiting inappropriate ADH NS
D- Diuretic secretion) CLD

Q. What are the causes of SIADH (Syndrome of inappropriate ADH secretion)?

Ans. mnemonic CLD
C---CNS- Stroke, Trauma, Infection
L--Lung- Carcinoma, Pneumonia
D--Drug- Phenytoin, Carbamazepine, Amitriptyline.

Q. what is the treatment of SIADH (Syndrome of inappropriate ADH secretion)?

Ans.
Water restriction.
Withdrawal of the drug responsible for SIADH.
Demeclocycline.

Q. Name some causes of dilutional Hyponatraemia.

Ans. Same as the causes of SIADH.

Q. Name some causes of Hypernatraemia.

Ans.
Hypovolumic Euvolumic Hypervolumic
Water loss>Na loss Only water loss
Osmotic diuretic Diabates incipidus I.V. salaine
Glycosuria (HONK)
Colonic Diarrhoea

Q. What fluid you shall use to correct Hypernatraemia?

Ans.
5% DA
0.45% NaCl

Q. An unconscious patient is brought to you with a history of vomiting 2/3 times. What is the
probable diagnosis?
Ans. Hyponatraemia.

215
 Potassium
Q: What is the normal level of k+?
A: 3.5-5.5 mmol/L

Q: What are the signs of hypokalaemia?

A: sign:
skeletal muscle: proximal myopathy
smooth muscle: paralytic ileus
cardiac muscle: arrhythmia

Q: What is the site of action of potassium?

A: potassium acts on muscle.

Q: What is the cause of dangerous complication and death in hypokalaemia?

A: Cardiac Arrhythmia.

Q: What is the cause of death in hyperkalaemia?

A: Cardiac arrest in diastole.

N.B: Hypokalaemia is associated with alkalosis

Hyperkalaemia is associated with acidosis.

Q: What are the ECG changes in hypo and hyperkalaemia?

A:

Hypokalaemia: Hyperkalaemia:

Tall & tent shape T

Flat T
Inverted T
Appearance of U wave Wide QRS complex
Sine wave

216
Q: Name the causes of hypokalaemia?
A: Common causes mnemonics DVD
D= Diarrhoea
V=Vomiting
D=Diuretic

Q: Give the management of hypokalaemia?

A: if K+ > 2.5 mmol/L = oral correction by
green coconut water
fruit and fruit juice
Oral KCl supplementation (syp. KT/Electro k 3-4 TSF in half glass water TDS; 1TSF=
15 mmol/L)

If K+ <2.5 mmol/L
Oral correction +
Parenteral correction( in drip)
Inj. NS 1000ml+ inj. K+ 2 amp iv. @ 30 drops/ min

NB: 1 amp KT contain 20 mmol/L K+

Q: what is the maximum correction rate of K+?

A: not more than 10mmo/L per hour

Q: A hospital admitted pt complains about inability to stand from squatting position. What is the
diagnosis?
A: Hypokalaemia (cause- probably pt gets I/V glucose containing saline)
Q: A pt comes with the complaints of inability to move the 4 limbs after awakening from sleep
in morning. There may also be history of heavy exercise or heavy CHO meal in the previous
night. What is the diagnosis?
A: Hypokalaemic periodic paralysis.

Q: What is the cause of lesion?

A: disturb in Ca2+ channel

217
Q: What are the predisposing factors?
A:
heavy exercise
heavy CHO meal or glucose intake

Q: What is the treatment?

A: syp. KT
Spironolactone diuretic

Q: What advise will you give to this pt?

A:
Reduce intake of sugar rich diet
Avoid heavy meal
Avoid heavy exercise
If there is weakness of limbs, take Syp. KT or fruit juice

Q: Name another endocrine disease where periodic paralysis occurs.

A: Thyrotoxic periodic paralysis.

Q: In ward a cachetic malnourished pt died after NG feeding. What is the diagnosis?

A: Refeeding syndrome (Malnourished pt is hypokalaemic. CHO based NG feeding causes
further hypokalaemia which in turn causes cardiac arrhythmia & death)

Q: If that pt becomes unconscious what will be the diagnosis?

A: Wernicks encephalopathy (due to thiamine deficiency).

Q: What are the causes of hyperkalaemia?

A: Renal failure- ARF & CRF
Drugs ACEi
Diuretics-spironolactone

Q: Tell the step of management of hyperkalaemia.

A: First: stabilize cell membrane potential with I/V Ca-gluconate (10% 10 ml Inj. over 10min)
NEXT: (to shift K+ into cells)
Glucose with insulin: 50 ml of 50% glucose with 5U Actrapid
(in our ward inj. 25% glucose 100ml+inj. Actrapid 10 U @ 10 drops/min)
Nebulization with 2 agonist (salbutamol)
Correction of acidosis by inj. Sodium bicarbonate (sodibicarb)

218
 THEN: (to remove K+ from body)
I/V Frusemide & NS
Ion exchange resin (eg Ca-resonium)
Dialysis

Q: What type of electrolyte imbalance occurs in Cushings syndrome & Addisons

Disease?
A: Cushings syndrome- hypokalaemia
Addisons Disease- Hyperkalaemia & Hyponatraemia.
Q: What are the causes of hypokalaemia & hyperkalaemia? (For more marks)
Trait Hypokalaemia Hyperkalaemia
Intake IV glucose containing saline, Drugs-ACEi, Spironolactone;
excess glucose/ CHO IV K+ infusion; Haemolysis;
containing food Rhabdomyolysis.
Shift into/out of cells Shift into cell: due to Shift outside the cells: due to
Alkalosis Acidosis
Insulin excess Insulin deficiency
2 agonist 2 antagonist
Hypokalaemic periodic hyperkalaemic
paralysis periodic paralysis
Renal loss With HTN: Renal retention:
Conns syndrome S. cretinine > 500mol/L:
Cushings syndrome ARF
Liddles syndrome CRF
Normal BP: S. creatinine <500mol/L:
Alkalosis: With aldosterone low
Loop diuretics Addisons disease
Bartters syndrome With normal aldosterone/:
Gitelmans syndrome Tubular transport
Acidosis: defect
RTA( type 1 & 2) Tubulointerstitial
disease
Drugs- spironolactone
GIT loss With acidosis
Diarrhoea
Laxative 00000
Villous adenoma
With alkalosis
Vomiting

219
Q: tell about electrolyte imbalance after vomiting.
A:
Hyponatraemia
Hypokalaemia
Metabolic alkalosis
Paradoxic aciduria

Q: which fluid is given following vomiting?

A: IV NS

Q: what are the electrolyte imbalance in diarrhoea?

A:
Hypokalaemia
Hyponatraemia
Metabolic acidosis
Q: which fluid is given following diarrhoea?
A: Cholera saline

Q: what are the metabolic abnormalities following diarrhoea & vomiting?

A: diarrhoea metabolic acidosis
vomiting metabolic alkalosis
Q: What are the causes of hyper calcaemia?
A:
Hyperparathyroidism (primary & tertiary)
Malignancy (Br. Ca, RCC, MM)
Milk alkali syndrome
Vitamin D intoxication
Pagets disease

Hypocalcaemia
Q: name some cause of hypocalcaemia.
A:
CRF
Hypoalbuminaemia
Alkalosis
Acute pancreatitis
Hypoparathyroidism
Hypo-Mg

220
Q: A pt comes to you with hyperventilation followed by spasm of hand. What is the diagnosis?
A: Tetany

Q: What is the mechanism of tetany?

A:
Hyperventilation

Loss of CO2

Alkalosis

OH-

+
Need H to neutralize it

Albumin bind H is released to neutralize OH-
+

Then albumin binds with positive ion Ca2+

in ionized serum calcium

Tetany

Q: What treatment is given in tetany?

A: 10% 10 ml inj. Calcium gluconate slowly over 10min & amp I/M in each buttock

Q: If not corrected by Calcium gluconate then what will you do?

A: I will give Mg.

Q: What is the triad of tetany?

A:
Carpopedal spasm
Stridor
Convulsion

Q: What is the cause of stridor?

A: Laryngeal spasm.

221
Q: What is the characteristic position of hand in carpopedal syndrome?
A:
Flexion of Metacarpophalangeal (MP) joint
Extension of Interphalangeal (IP) joint
Opponens of thumb
Like PV Hand (Position of hand during pervaginal examination )

Q: What are Trousseaus sign & Chvosteks sign?

A:
Trousseaus sign: Inflation of a sphygmomanometer calf on upper arm to more than systolic BP
is followed by carpal spasm within 3 minutes in hypocalcaemic (latent tetany also) pt.

Chvosteks sign: tapering over the branch of facial nerve as they emerge from parotid gland
causes ipsilateral contraction of facial muscle in hypocalcaemic pt. It is less specific.

Q: What is the ECG change in hypocalcaemia?

A: Prolongation of QT interval.

Q: What are the other features of chronic hypocalcaemia?

A:
Papilloedema
Basal ganglia calcification
Grand mal epilepsy

Metabolic Acidosis

Q: Define Acidosis.
A: Accumulation of acid rather than H2SO4

Q: A 13 years old school girl comes to you with respiratory distress. But examination reveals
lung is clear. What is your diagnosis?
A:
Metabolic Acidosis
Psychogenic hyperventilation

Q: What may be the cause of Metabolic Acidosis in this pt?

A: Common:
Diabetic ketoacidosis(DKA)
Renal failure

222
 Others: mnemonics KUSsMaL
K- DKA
U- Uraemia
Ss- Salicylic acid
Ma- Methanol
L- lactic acid

For more marks not for all

Q: Define anion gap?
A:

Q: tell the causes of metabolic acidosis.

A:
A. Normal anion gap:
Acid addition(inorganic)- NH4Cl, HCl
GIT loss- diarrhoea (HCO3 loss)
Renal loss:
Proximal RTA- HCO3 loss
Distal RTA- tubular acid secretion
B. Increased anion gap:
KUSsMaL- see above

Lactic Acidosis (for more mark)

Q: What is the level of lactic acid?

A: normal lactate level is 2mmol/L

Q: What are the types of lactic acidosis?

A: Two types of lactic acidosis have been defined, these are:
Type-1: due to tissue hypoxia & peripheral generation of lactate, as in patients with
circulatory failure and shock.
Type-2: due to impaired metabolism of lactate as in liver disease. A number of drugs
& toxins also impair lactate metabolism including metformin.

Q: Name the drug responsible for lactic acidosis?

A: Metformin.

223
 OTHERS

Q: Cause of metabolic alkalosis? (2 causes must be said)

A: mnemonic-CV
-C--Conns syndrome & Cushings syndrome
- V--Vomiting.

Q: Cause & Complications of respiratory acidosis.

A: due to hypoventilation, such as
o COPD
o Chest wall injury
o Respiratory muscle paralysis/respiratory center depression.

Complication:
o Type-2 respiratory failure.

Q: Cause & complication of respiratory alkalosis.

A: due to hyperventilation, such as-
o Anxiety
o Psychogenic hyperventilation.

Complication:
o Tetany.

Q: scenario: A 30years old man comes to you with H/O diarrhoea for 3days, now he complains
of respiratory distress. What is your diagnosis?
A: metabolic acidosis due to ARF followed by diarrhoea.

224
 Infectious Disease

Malaria
Q.A 40 yrs old man comes to you with H/O fever for 3 days followed by
Unconsciousness. Write the provisional Dx?
Encephalitis
Cerebral malaria
Meningo-encephalitis

Q.What will you do?

Take H/O endemic zone of malaria nZ GmQ wKbv
Examination: Neck regidity
Kerning sign

Q.what investigation?
CSF study
MP
ICT for malaria
CBCNeutrophilic leukocytosis--- Bacterial meningitis

Q.what Rx you will be prefer?

A,B,C
NG feeding 200ml 2 hrly
I.V. channelInj.normal saline
Antibiotic- Inj.Ceftriaxon 2 gm 1 vial I.V. B.d.
Inj. anti-malarial drug
Tab. virux 400 mg 2+2+2+2+2
continuous catheterization
eye care & mouth care
change postural 2 hrly

Q. Severe malaria/Cerebral malaria Z anti-malarial therapy wKfve w`e?

Quinine Sulphate
Bolus dose- 20 mg/kg in 500ml 5% DA/DNS over 4 hrly
then - 10mg/kg in 500ml 5% DA/DNS over 8 hrly

Q.I.V. quinine KZY w`e?---- until the pt is able to take food orally

Q.What are the complication I.V. quinine?

Arrhythmia with prolongation of QT interval
Hypoglycemia
Circulatory collapse

Q.What type of disease it is?-------- Protozoal disease

Q.Name the types of malaria with their causative organism?
Plasmodium vivax
Plasmodium ovale

225
 Plasmodium malariae
Plasmodium falciparum
Q.Describe the life cycle of malaria?
Vector--- the female anophelis mosquito
h form G gvbyli kixi XyK------------ sporozite
gvbyl nZ gkvq h form G XyK-------- Gametocytes
In mosquito--- sexual cycle ; In man--- Asexual cycle

Q.Why fever occur?--- As merozoites release due to breakdown schizont

Q Kvb `yB type G Hypnozyte/Dorment _vK or Kv`i Relapse nq?

Plasmodium vivax
Plasmodium ovale

Q. Kb Relapse nq?----- KviY GB `yUv Liver Dorment wnme _vKZ cvi

Q KvbUv Kvb Blood cell G cvIqv hvq?

[to rememberOver Man]
falciparum all type cell
Overovalae in reticular cell (oveovalae, R--reticulocyte)
MaNmalaria in normoblast (MaMalaria, N--normoblast)

Q.What are the cause of jaundice?

Haemolysis
Hepatic dysfunction

Q.Kvb Hb disease falciparum malaria nq bv?----- Hbs,Hbc,HbF

Q.Mechanism of cerebral malaria?

Red cell contain schizont so RBC become adhere & stick to capillary & caused
anoxic injury brain, icidrug,lung,liver

Q.Type of fever in malaria?

Ovalae---Tertian (48 hr)
Malarae--- Quordien (72 hr)

Q.which plasmodium is responsible for GN & NS?------- Plasmodium malariae

Q. Investigation:
Blood film
thick film
thin film
ICT for malaria

Q.What we see in thick film?

Parasite (as more blood chance tobe seen parasite even in low parasitaence)

Q.What we see in thin film?

Species of parasite

226
Q.Rx of malaria:
In case vivax
Tab. chloroquine 150mg (4,4,2)
1st day4 Tab 2nd day4 Tab 3rd day2 Tab
Plus
Tab. primaquine 15mg (0+0+1-----------for 14 days)

In case of falciparum
complicated---Rx of cerebral malaria
uncomplicated--- Tab. coartem
1st day4 Tab Zvi 8 NUv ci 4 Tab
2nd day4+o+4
3rd day4+o+4
nd
2 line: Quinine sulphate 300 mg (2+2+2------------7 days)

Q.Vivax G Kb premaquine `q?-------- to prevent releapse

Q.What are the complication of quinine therapy?

Hypoglycemia
Tinnitus
Headache
Psychosis

Q.Pregnant with malaria.what Rx?

Quinine sulphate or
Chloroquinine

Q.Malaria with shock.what is Dx?------------ Algid malaria

Q.Complication of cerebral malaria?

A- Acidosis/ARD/ARF
B- Behavior change
C- coma,convulsion
D- Drowsy
E- Pulmonary edema
Hypoglycemia

Q. Chemoprophylaxis?
Choroquine 150mg 2Tab wkly
proguanil 100mg daily
stinted 1 wk before 4 wk after travel
If Choroquine resist---
Doxycyclin 100mg daily
stinted 1 wk before 4 wk after travel

227
 Enteric Fever
Q.A pt comes to you fever for for 10 days.what are the D/D?
Enteric fever
Malaria

Q.Route of transmission?----------oro-faecal route

Q.which organism is responsible for enteric fever?-------Salmonella Typhi

Q.Incubation period?-------10-14 days

Q.How organis enter in the body & where multiply?

After enter into the bloof bacilli localize,mainly in the lymphoid tissue of small
intestine the peyer patches.

Q.Clinical feature of enteric fever?

1st week [to remember--- My FRCH]
My- Myalgia
F- Fever
R- Relative Bradycardia
C- Constipation
H- Headache
2nd week[ to rememberRCDAS]
R- Ras
C- Cough
D- Diarrhoea
A- Abdominal distension
S- Splenomegaly
3rd week------
Delerium,coma

Q.when occur constipation?-------- 1st week

Q.When occur Diarrhoea?---------- 2nd week
Q.When occur rash & spleen?------ 2nd week

Q.What is relation with pulse & fever in enteric fever?

we know 10C increased temperature will increased 10 pulse/min
but in case of enteric fever this does not follow.This cause relative bradycardia

Q.Complication of enteric fever?

Haemorrhage from GIT
Perforation ilium
Minengitis
Pneumonitis
Myocarditis
Cholis-cystitis
Nepfritis
Osteomylitis & Hepatitis
228
Q.What investigation you will do in this pt?
CBCLeucopenia
1st weekBlood culture
2nd weekWidal test stool culture

Q. How will confirm the disease?-------By blood culture

Q.Is widal test specific?------No,it is non-specific test raising titre is significant

Q. Describe the fever of enteric fever?

It is step ladder pattern that temp progressively increased day by day.

Q.What is your Rx?------Tab.Ciprofloxacin(500mg) 1+0+1---------14days

In ward----- Inj. ceftriaxon(2 gm) 1 vial I.V. B.d for 7 days

Q.Ri KgZ KZw`b mgq jvM?--- Antibiotic i Kivi ci 5 w`b mgq jvM Ri KgZ

Q. A pt enteric fever Rx Kij fvj nq|Avevi wKQyw`b ci Ri nq?

As pt developed carriers state

Q.Where present the carrier organism?-----------Gallbladder

Q.what Rx?------- Tab.Ciprofloxacin(500mg) 1+0+1---------4 weeks

Q.What is surgical Rx?---------Cholecystectomy

Q . classify fever with definition and example ?

Type of fever
Continued
Remittent
Intermittent -
o a.Quotidian
o b.Tetrtian
o C.Quartan

1. Continued fever : When fever does not fluctuate more than about 1` C
(1.5' F) during 24 hours but never touches the base line is called
continued fever.
Causes :-
I. I .Typhoid fever
II. 2- Millar,y tuberculosis
III. Lobar pneumonia
2.Remmittent fever
When daily fluctuations exceed 2 0 C called remittent fever.

229
 Causes
I. I Amoebic liver abscess
II. Luna abscess
III. Collection of pus in the tissues

3.Intermittent fever
When the fever is present only, for several hours during the day it is called
intermittent-fever.
a) Quotidian: When a paroxysm of intermittent fever occurs daily. the
type is quotidian.
Cause - Kala-azar (double quotidian)
b) Tertian
When fever comes on alternate days, it is tertian. Causes: P. Vivax and P
.Ovale Malaria.
C) Quartan
W h e n t h e r e i s T w o d a y s i n t e r v a l b e t w e e n t w o consecutive
attacks. Then it is call quartan.
Cause- P. Malariae infection.

Q.Name some parasite in blood or intestine or both ?

1) Protozoa
* In blood----------
Plasmodium--- malaria
Leishmenia---- kala-azar
*In intestine--------
Entamoeba histolytica Amobiasis
Liver abscess
Giardia lamblia------ Giardeasis
Cryptosporideum

Q.Name protozoa both intestine & tissue?------- Entamoeba histolytica

2)Helminth (name som helminth that remain in tissue or intestine )

* In intestine----------
Hook worm--- Ankylostoma duodenal
Round worm--- Ascaris lumbricoidis
Pin worm------ Enterobius vermicularis
Tap worm------ Taenia solium/ Taenia sagenata
*In tissue-----------
Tissue nematodes---
Wuchereria bancrofti
Loa loa
Tapes worm/cestodes-----
Echinococcus granulosus
Q.Name the organism of Hydatid disease/cyst?------------Echinococcus granulosus

230
Q.Who is the definitive host? -----Dog

Q.Life cycle:
worm with in dog gut----- ova comes with defecation it usually enter into
sheep or other animal
Q.How it comes to man?
By handling dog or drinking contaminated water

it enter (egg) in human intestine ( small intestine)

Enter into liver

Form hydatid cyst

Q.Where it is involved? ----------- Mainly rt lobe of liver(75%), lung

Q. Rx:
Medical Rx-------- Tab. Albendazol (400mg) 1+0+1-------------3 months
Others---------
Surgery excision
PAIR ( percutaneous puncture,aspiration , injection of scolicidalayent &
respiration)

wK w`q gviv nq?---------- 0.5% silver nitrate & 2.7% sodium

Q.Which oganism responsible for anaemia?----Ancylostoma duodenale

Daily blood loss: 0.15ml/day

Q.what does round worm? ------------intestinal obstruction

Q.Rx:
A single dose of albendazol 400mg or
Tab. mebendazol 100mg-------1+0+1--------3 days

Q.Name the worm which is responsible for pruritis Ani?

Enterobius vermicularis
Female worm lay ova around anus--- cause enters itching at night---- through
finger nail it enters at mouth---- intestine
it is human to human transferred

Q.Rx:
Mebendazol 100mg ----- 1+0+1----------- 3 days

231
Q. Name some causes of acute watery diarrhoea?

viral causes Rotavirus

Bacterial causes V. cholera
Bacillus cereus
Staphylococcus aureus
Enterotoxigenic E.coli
Protozoal causes G- Giardiasis
A- Amoebic dystotry
C- Cryptosporidium
Q.Name some infectious cause of diarrhoea?
Above all plus
Bloody diarrhoae

Q.Name some causes of bloody diarrhoea?

[to remember---SSC Z E+ cqQ]
S- Salmonella
S- Shigella
C- Compylo bactor jejuri
E+ - Enteroenvasive e.coli
Entamebea histolytica
There are four main groups: Sh. dysenteriae, flexneri, boydii and sonnei.
Q.Name some non infectious causes of diarrhoea?
[to remember---BID,TID]
I- Inflammatory bowel disease
I- Irritable bowel syndrome
T- thyrotoxicosis
D- Diabetis melitis
B- Bowel malignancy
D- Drugs-------- NSAID,Cytotoxid drug,Antibiotic,PPI

Q.Antibiotic LvIqvi h Diarrhoea nq Zvi Rb Kvb organism `vqx?

Clostridium dissicile
Q.Rx:
Metronidazol
STI
Q.Name some STI related organism?name some viral STI?Name disease of STI with
causative organism?

Name of the organism Causative organism

VIRAL
Herpes simplex virus(HSV-2) Genital herpes
HIV AIDs
Human papilloma virus Genital wart
Hepatitis B-virus Hepatitis
BACTERIAL
Nisseria gonorrhoeae Gonorrhoeae
Chlamydia trachomatis Non gonococcul urethritis
Treponema pallidum Syphylis

232
Q. What are causes of urethral discharge?
Gonorrhea
Chlamydia trachomatis
Trichomonus vaginitis
Q.Name some cause of genital ulcer?

Genital herpes multiple

Caused by Herpes simplex virus painful ulcer
over glans penis
Chancre single
Caused by: Traponema pallidium painless
indurated
Chancroid single/multiple
Caused by: Haemophilus ducreyi painful ulcer
ulcer is undermined& rage
Lymphogranuloma venerum Small transit
Caused by: Chlamydia trachomalis painless ulcer
inguinal involve( inguinal lymph node)

Q.Difference between Chancre & Chancroid?

Chancre Chancroid
single single/multiple

painless painful
Organism: Traponema pallidium Organism: Haemophilus ducreyi

Q.Name the organism of syphilis?----- Traponema pallidium

Q.Classify syphilis?
*early--------
primary
secondary
*Late---------
Benign tertiary
Cardiovascular
Neuro syphilis

Q.Feature of primary syphilis?

Chancre

Q.Feature of secondary syphilis?

Rash(75%)
Condylomata lata
On tender generalized lymph node(50%)
Snail Track ulcer

Q.Describe the rasth----It maculopopular lesion involved trunk & limb

233
Q.Tertiary syphilis?
3-10 yrs after primary syphilis
muscle, skin,bone,viscera

Q. Change in CVS?
Aortitis
Aortic aneurysm
Aortic incompetence

Q.Neuro syphilis?
Meningovascular disease
Tabes dorsalis
General paralysis of insane constitute
Argyl Roberson pupil
Q.what investigation you will do?
*Non-treponemal/non specific
VDRL ( venereal disease research laboratory test)
RPR (Rapid plasma reugin)
*Treponal Antibody test (specific)
TPHA ( Treponema pallideum haemo agglutination assay)
TPPA ( Treponema pallideum particle agglutination assay)

Non specific-------positive within 4 eks

Specific test--------positive within 2 wks

Q.VDRL negative nq KZ w`b?

6 month mgq jvM primary
12-18 month mgq jvM secondary

234
Q. Organism of gonorrhea?--------- Nisseria gonorrhoeae

Q. what type of organism it is?------It is gm negative deplococci

Q.Site of involvement?-----genital tract ,rectum ,pharynx, eye

Q. what is the clinical presentation?

In male: urethral purulent discharge
Dysuria
In female: 80% asymptomatic

Q. Investigation?
Gm stain Kij gm(-) ve deplococci cvIqv hvq
Q.Rx:
Cap: cefixime (400mg) 1 tab stat
Tab.Ceprofloxacin (500mg) stat
or
Inj. Ceftreaxon (250mg) 1 amp IM stat

Q. Complication of gonorrhea?
*In male:
Acute prostatitis
Epididymo-orchitis
Stricture urethra
*In female:
Salphingo-ophoritis
PID
Barthrolin abscess
Ectopic pregnancy
Sterility
*In children:
opthalmia neonalum

Q. Chlamydial infection?

In case of male In case of female

Non-gonococcal urethritis(NGU) Cervical vaginal discharge
Conjunctivitis PID
Reactive arthritis Cervicitis
Eyididymo-orchitis NGU

Q.Rx?
Tab. azethromycin 1 gm orally single dose or
Tab. Doxycyclin (100mg) 1+0+1------------7 days

235
Q.Name condition where fever with rash?
Dengue
Rikettsia
Typhoid
Measless
Meningo coccal seplis
viral hemorrhagic fever

Q.Name some Herpes virus?

Herpes simplex virus-1 Herpes labialis

Herpes simplex virus-2 genital ulcer
Varicelloa zoster virus chicken pox
herpes zoster
Cytomegalo virus(CMV)
Epsteen Barrvirus Burkit lymphoma
infectious mononucleosis
Human herpes virus-8(HHV-8) kaprosi sarcoma

Q.name the causes of fever with chill and rigor and anemia

Fever with chill rigor Fever with jaundice Fever with anaemia
Malaria viral hepatitis aplastic anaemia
UTI(pylonephritis) leptospirosis leukomia
Cholangitis lymphomea kala-azar
Pneumonia leukaemia lymphoma
Abscess dessiminalei TB Malaria`

Q.Name some infective /infectious causes of fever?--------all infective cause

Q. Name some non-infective causes of fever?

Drug fever
vasculities
connective tissue disease
neoplasm
graft versus host disease

Q.Name some immune supression condition?

HIV
DM
Transplantation
Pt on immune supresion therapy-------- steroid
cytotoxic drugs

236
Q. Define PUO?(332)
PUO is defined as a temperature persistently above 38.00C for more then 3 wks
without diagnosis despite initial investigation during 3 days of inpatient care or after
more then 2 out patient visit.
Causes:
Malignancy---- lymphoma, leukamia, myeloma renal,liver,colon
Infection-------Abscess, infective endocarditis
Connective tissue disease

Q. Pt comes to you hypo pigment patch with loss of sensation over that area. What is
your Dx?
Leprosy

Q. What is the organism is responsible for leprosy?

Mycobacterium leprae

Q.Classify leprosy?
Mainly 2 types:
Tuberculoid leprosy / paucibacillary
Lepromatous leprosy/multibacillary

If sir want more then tell the chart

Tuberculoid leprosy
Boderline tuberculoid
Boderline lepromatous leprosy
Lepromatous leprosy
High level CMI(cell mediated immunity) with
elimination of bacilli cause paucibacillary
Moderate CMI
A few CMI
Absent of CMI causes multibacillary

Q.When will you say paucibacillary & multibacillary?

Paucibacillary (2-5 skin lesions)
Multibacillary (more than 5 skin lesions)

Q.What is the cardinal feature of leprosy?

Skin lesions,typically anaesthetic at tuberculoid end of spectrum
Thickened peripheral nerves
Acid-fast bacilli on skin smears or biopsy

Q.How will you diagnose a case of leprosy?

The diagnosis is clinical having a cardinal sign of leprosy
Slit skin smears----- to see acid fast bacilli

Q. Treatment of leprosy?

Type of leprosy Monthly single Daily Duration

dose
Paucibacillary Rifampicin 600 mg Dapsone 100 mg 6 months
Multibacillary Rifampicin 600 mg clofazimine 50 mg 12 months
clofazimine 300mg Dapsone 100 mg

237
Leperomatous leprosy skin will less and late and tuberculoid all marked nd early
Lepromatous Tuberculoid
Bacilli (bacterial index) Multibacillary Paucibacillary
many ( 5 or 6+) Absent (0)
Distribution Widely disseminated One or a few sites,
asymmetrical
Natural outcome Progression Healing
Reactions Immune complexes Cell-mediated
Nerve enlargement & Late Early and marked
damage

Description of skin lesion

Colour Dark skin- slight Dark skin- marked
hypopigmentation hypopigmentation
Light skin- slight Light skin- coppery or red
erythema
Surface Smooth,shiny Dry,scaly
Central healing None Common
Loss of sensation Late Early and marked
Other tissue involvement
such as-----
Upper respiratory mucosa,
eye, testes, bones, muscle

Reactions on leprosy
Lepra reaction Lepra reaction type 11 (erythema nodosum
type 1 (reversal) leprosum)
Mechanism Cell- mediated Immune complexes
hypersensitivity
Clinical Painful tender Tender papules and nodules;may ulcerate
feature nerves Painful tender nerves
Loss of function Loss of function
Swollen skin Iritis,orchitis,myositis,lymphadenitis,fever,oedema
lesions
New skin lesion
Management Prednisolone Moderate: Prednisolone 40mg daily
40mg Severe:Thalidomide2 or Prednisolone 40-80mg
Reducing over 3- Reducing over 1-6 month;local if eye involved3
6 months1

Q.A patient comes to you hypo-pigmentation path.What is your Dx?

Leprosy
Ptyriasis versicolor
Teniasis

238
Q.How will differentiate it leprosy?
By seeing sensation with pink

Q.What will you see now?

Nerve thickening present or not

Dengue
Q . a 30 yr old boy comes to you with the complaint of multiple purpuric rash whole
over the body mostly on the trunk . He give history fever with headache 7 days ago.
The pt live in Dhaka .

Q What is your diagnosis?

Dengue hemorrhagic fever

QWhat do u mean by dengue syndrome?

Following three conditions is collectively called dengue syndrome :
1. Dengue Fever (DF)
2. Dengue Hemorrhagic Fever (DHF)
3. Dengue Shock Syndrome (DSS)

Write down the diagnostic criteria of Dengue Fever, Dengue Hemorrhagic Fever,
Dengue Shock Syndrome? (No all student need to memorized it )

Dengue Fever (if u want more mark )

Dengue fever is an acute febrile illness of 2 -7 days duration sometimes with two
peaks having the
following manifestations:
1. Sudden onset continuous fever
And
2. Two or more of the following features:
a. Severe headache
b. Retro-orbital pain
c. Severe myalgia / arthralgia / back pain
d. Hemorrhagic manifestations
e. Nausea/vomiting/abdominal pain
f. Leucopenia
g. Rash
And
3. High index of suspicion based on Period, Population & Place
And
4. Absence of convincing evidence of any other febrile illness

239
Dengue Hemorrhagic Fever (if u want more mark )
Dengue Hemorrhagic Fever is a probable manifestation of dengue syndrome with
hemorrhagic manifestations having the following features:

1. Features of dengue fever at initial stage

And
2. Hemorrhagic manifestations evidenced through one or more of the following:
a. Positive tourniquet test
b. Petechiae / ecchymosis / purpura
c. Mucosal bleeding: Epistaxis, gum bleeding
d. Bleeding from injection or other site
e. Hematemesis, melena, hematuria, PV bleeding
f. Thrombocytopenia with platelets 100,000 / m3 or less
And
3. Any evidence of plasma leakage due to increased capillary permeability
manifested by one or more of the following:
a. A > 20% rise in hematocrit for age or sex
b. A < 20% drop in hematocrit following treatment with fluids as compared to base
line
c. Pleural effusion / ascitis / hypoproteinemia

Dengue Shock Syndrome ((if u want more mark ))

Dengue Shock Syndrome is a presentation of Dengue Syndrome when a case of DHF
manifests
circulatory failure with one or more of the following features:

1. Hypotension for age

2. Cold clammy skin, restlessness, rapid weak pulse
3. Narrow pulse pressure (<20 mm of Hg)
4. Profound shock

But u have to learn this question?

QWhat is the clinical feature of Dengue fever ?

Degue present with an acute febrile illness of 2 -7 days duration with Severe headache
with Retro-orbital pain , myalgia / arthralgia / back pain Hemorrhagic
manifestations ,Rash .

QDescribe the rash of dengue fever?

A. Rash usually appear between 2-5 days after onset of fever

Nature of the rash is macular or macula-papular

How many sero type the dengue virus have ?

There are four sero types of dengue virus, Den-1, Den-2, Den-3 and Den-4

240
Q Name the vector of dengue fever?
A. Female aedes aegypti mosquito

Q. When it bites?
A It bites in the day times?

Q Who developed DHF?

A. Who have pre-existing anti-dengue antibody. That means who previously attack by
dengue fever if second type attack by another dengue sero type more prone to develop
DHF

What investigation you will do in pt with dengue fever?

CBC leucopenia, thrombocytopenia

PCV> increased or 40%
Anti-IgM for dengue
Platelet count thrombocytopenia

Q .When will u do the this investigation?

Usually before 3 days no change in the lab tests is expected in febrile phase. So no
tests should be done before 3 days.

Q. when will u do Anti-IgM for dengue?

Not before 5to 7 days

Q Indication of hospitalization in dengue patient?

DHF Grades II, III & IV.

DHF Grade I where nutrition and oral fluid electrolytes therapy, monitoring and
observation cannot be ensured,
DHF Grade I and or presence of concomitant illness or in special situations eg
Diabetes, IHD, Pregnancy, etc.

Q Treatment of dengue fever?

DF and DHF are not distinguishable in febrile phase and treatment is essentially same.
Treatment is symptomatic and supportive. These are:

Rest
Antipyretic therapy for fever above 39 C.
Sponging: With tepid water at room temperature.
Paracetamol (not more than 4 times in 24 hours)
Do not give Aspirin or any other NSAID
Do not give antibiotics
Oral Rehydration Salt (ORS) is recommended for patients with moderate dehydration
If patient is in shock then give management of sock
If platelet transfusion is given when platelet count is 10000 or less

241
Write down the Severity Grading of Dengue Syndrome?

Syndromes Grade Clinical features Laboratory features

DF Features of DF as per case Leucopenia

definition Thrombocytopenia
No change in hematocrit
DHF I Features / History of features of DF Thrombocytopenia
+ < 100,000 /mm3
Positive Tourniquet Test Hematocrit rise 20%
DHF II Features / History of features of DF Thrombocytopenia
+ < 100,000/mm3
Spontaneous bleeding Hematocrit rise 20%
DHF III Features / History of features of DF Thrombocytopenia
(DSS) + < 100,000/mm3
Features of circulatory failure Hematocrit rise 20%
DHF IV Features / History of features ofDF Thrombocytopenia
(DSS) + < 100,000 /mm3
Profound shock Hematocrit rise 20%
DHF Grade III & IV are also called Dengue Shock Syndrome (DSS)

What are the sign of recovery?

Signs of Recovery
Stable pulse, blood pressure and breathing rate
Normal temperature
No evidence of external or internal bleeding
Return of appetite
Good urinary output
Stable hematocrit
Convalescent stable petechial rash

Mention the discharge criteria of dengue patient ?

Criteria for Discharging Patients

Absence of fever for at least 24 hours without the use of anti-fever therapy
Return of appetite
Visible clinical improvement
Good urine output
Minimum three days after recovery from shock
No respiratory distress from pleural effusion and no ascitis
Platelet count of more than 50,000/mm3

242
What follow up you will give in patient with dengue?
Daily vital sign of circulation
Pulse
BP
Urine out put
Evidence of external or internal bleeding
Hematocrit
platelet count

Name some no in dengue ?

Don'ts
Do not give aspirin or NSAID for the treatment of fever.
Avoid giving intravenous therapy before there is evidence of hemorrhage or
bleeding.
Avoid giving blood transfusion unless indicated, reduction in hematocrit or severe
bleeding.
Avoid giving steroid.
Do not use antibiotics.

243
 Skin
Q . Define itch or pruritus ?

A. unpleasant sensation that provoke the desire to scratch .

Q. Mention the causes of pruritis ?

A.

generalised pruritus localised pruritus

Eczema Eczema
Scabies Lichen planus
Urticaria Dermatitis herpetiformis
Pediculosis

Q . name some systemic disease that cause ithching ?

Liver disease Obstructive jaundice

Primary biliary cirrhosis
CRF
Blood Lymphoma
Leukaemia
Polycythemia rubra vera
Myeloma
Anemia (iron deficiency )
Endocrine Diabetes
Thyrotoxicosis
Hypothyroidism
Q .Name the organism of scabes ?

A . Female gravid Sarcoptes scabiei

Q. sites of scabes

A. finger , interdigital area , anticubital fossa , axilla ,around the umbilicus , genitalia , buttock ,
dorsum of the foot

Q what are the diagnostic sign of scabes ?

A . Scabetic furrow

Q. What is scabetic furrow ?

A .These are short, wavy, dirty appearing line found in the edge of fingers , toes or side of hand
or foot . burrow contain . female mites and egg .

244
Q. what are complication of scabies ?

A.
secondary infection / impetigo
Eczema
Lichenification
AGN
Urticaria
Exfoliative dermatitis

Q. write down the treatment of scabies ?

A . general measure :
Maintain personal hygiene
Wash bed sheet and clothes with hot water
Simultaneous treatment of all family member
Drug treatment
Permethrin 5 % cream (donot forgot to remember % )
Apply from neck to toe and keep it for 24 hrs and take bath and repeat after
week
Benzyl benzoate 25^% lotion
Apply 3 consecutive day

Q I . IS there any oral medication ?

A . Yes . Name is Ivermectin (200 mg / kg )
Single dose

Q .What is the dangerous complication of scabies?

A . AGN

Q . Which organism is responsible for AGN?

A . Group A -hemolytic streptococci

Tell the mechanism AGN from scabies

Following scabies scratching due to itching --- Breach the continuity of skin and secondary
infection with streptococcus infection --- immunity develop against strep--- that cross react with
glomerular basement membrane ( antibody +antigen + complement C 3 )

245
Why kidney affect in after strep. Infection

1. AGN develop only when skin or sore throat infection by nephritogenic strain of
streptococci
2. kidney is involved due antigenic mimicry between the bacteria and GBM of kidney

what type reaction it is ?

Type -3 hypersensitivity reaction

Q. This question is frequently asked by dr. CN sarker ----4 boys with scabies were playing in
field but suddenly Develop head ache followed by convulsion and unconsciousness what is ur
diagnosis?
A. diagnosis is hypertensive encephalopathy

Acne
Q.Female patient is frequently usually the teen ager are suffer from a skin disease usually
affect the face ?
A. this is acne

Q what is the mechanism of acne ?

A.
Increase sebum formation
And occlusion of pilosebaceous duct

Q which hormone is responsible acne?

A. Mainly androgen
And also progesterone

Q. Which hormone decrease ace or protect from acne ?

A . estrogen

Q. Name a bacteria responsible for acne ?

A. Propionibacterium acnes

Q how it is causes acne?

A. it colonies in the pilosebaceous duct and occlude it

Q mention the Sit of acne ?

A. Acne presents in areas rich in sebaceous glands such as
The face, back and sterna area.

246
Q Mention the treatment of acne ?

A non pharmacological
Maintain personal hygiene
Was face with soap or antiseptic cream

pharmacological

First-line therapy
topical agent
keratolytics
o benzoyl peroxide
o azelaic acid
topical retinoids
o tretinoin
o isotretinoin
retinoid-like agents
adapalene
Topical antibiotics,
erythromycin or
clindamycin

Second line therapy

Oral antibiotic
Erythromycin
AZithromycin
Oxytetracyclin or tetracycline

Tenia
Name some superficial fungal infection? Name of tenia or Dermatophyte infection according to
site of body

Site
scalp Tinea capitis
Body surface or trunk Tinea corporis
Groin Tinea cruis
Between two figner cleft Tinea pedis
In nail Tinea ungium

247
Q. What do you mean by ring worm or dermatophytosis ?

A. These are the superficial fungal infection causes by dermatophyte known as ring worm or
dermatophytosis

Q. What is the characteristic of ring worm?

A. the Central of the lesion is smooth and peripheral border or margin is elevated. Itchy and
sensation intact

Q . How will you differentiate from leprosy?

leprosy ring worm

Pain sensation Lost Intact

Q Name the organism responsible for tenia infection ?

Microsporum
Trichophyton
Epidermophyton

Q. Treatment of Tinea
Topical
clotrimazole,
miconazole,
terbinafne
systemic
Fluconazole
itraconazole
terbinafine

Q how long we give it?

A 2 weeks but increase Tinea unguium 6 months

Q. What investigation you want to do?

A. Diagnosis should be confirmed by skin scraping or nail clippings

Q A patient comes to u with area of hypo pigmentation or alter pigmentation area over trunk what is ur
diagnosis ?

A. it is called Pityriasis versicolor

248
Q. name the organism responsible form Pityriasis versicolor ?
A. Malassezia furfur

Q. How will you differentiate it from tinea ?

A.
tinea Pityriasis versicolor
Character of lesion Centre is smooth and border is Scaly macules or alter
elevated pigmentation
Itching Itchy No itchy

Q. Treatment of it?
Topical
Selenium sulphide or
2% ketoconazole hampoo
Apply to body and remove after 3060 minutes and repeat daily for 1 week
Systemic
itraconazole
terbinafine

Psoriasis

Q. A patient comes to you with multiple erythematous plaques with silvery scales ? what is your
diagnosis ?

A. psoriasis
Q. Describe the lesion of psoriasis ?
A.these are well circumscribed erythematous plaque with silvery scales .

Q. site of psoriasis ?
Extensor surface of elbow , knee wrist
Extensor surface of limb
Nail , scalp , hair line , cleft and flexures

Q. what do u mean by psoriasis?

A. Psoriasis is a non-infectious, chronic inflammatory disease of the skin, characterised by well-defined
erythematous plaques with silvery scale, with a predilection for the extensor surfaces and scalp, and a
chronic fluctuating course.

249
Q. what is the basic pathology of this disease ,
Hyper proliferation of keratinocyte with a grossly increased mitotic index leading to retention of
nuclei in the statum corneum which not normally present
In single word ----It is the diseases of rapid turn over . cellproliferation is more than turn over so
nucleus deposit in the epidermis .

Q . mention the treatment of psoriasis ?

General :
Explanation and reassurance of that this is not a contagious disease.
Disease have remission and relapse
Avoid precipitating factor
Specific
Local / topical
Tar
Dithranol
Vitamin D agonist
Calcipotriol
Topical steroid

Ultra violate therapy

PUVA ---Psoralen oral + ultravioletA
SYSTEMIC
MTX

Q. Complication of psoriasis?
A.
Psoriasis
Exfoliative dermatitis
Secondary infection
Hyper uricaemia and gout

Q. if the patient develop joint pain then what is ur diagnosis ?
Psoriatic arthropathy or seronegative arthritis
Q. Name two important sign of psoriasis?
A.
Auspitz sign
koebners phenomeno

Q. what is Auspitz sign

A. attempt to removal of scales forcefully causes capillary bleeding
250
Q. koebners phenomeno
A. if you make a scratch or following injury of normal skin of psoriatic patient causes psoriatic
lesion in that site.

Q. name the factor predispose to psoriasis

to remember BATA ASS
B -blocker
A Anti-malarial , ACE-inhibitor
T Trauma
A Alcohol
A Anxity
S Streptococcal infection
S Steroid withdrawal

Q.Name skin emergency ?

Stevens johnsons syndrome (SJS)

Q. why its happen ?

Usually drug reaction
Q. Name the drugs responsible for SJS ?
Co-trimoxazole /sulphonamides,
Carbamazepine
Thiacetazone
Phenytoin
penicillins and
barbiturates
Q What is the another name of SJS ?
Erythema multiform . SJS is the severe form of Erythema multiform.

Q. Define Erythema multiform ?

Acute inflammatory reaction in the skin and mucous membrane characterized by multiple
erythematous skin lesion such as macules , papules , vesicle , bullae

Q . what is the target lesion in Erythema multiform ?

Bull eyes lesion characterized by central pallor with oedema and peripheral redness .

251
Q. What are the causes of Erythema multiform ?
Infection Herpes simplex , streptococcus
Drugs Sulfonamide , carbamazepin
Idiopathic
Maligjnancy

Q who will understand SJS ?

By looking or find out muco-cutaneous involvement . Mucosal involvement around the
mouth or lip .

Q. treatment of SJS ?
Stop offending drugs
IV fluid
Antibiotic
Steroid
Mouth and eye care

Q. when you told SJS or TEN?

Name of the disease % of body surface area
Steven Johnsons syndrome < 10 % of body surface area
SJS-TEN 10-30% of body surface area
Toxic epidermal necrolysis > 30% of body surface area

Name some skin manifestation of systemic disease ?

Erythema nodosum Sarcoidosis, ulcerative colitis and Crohn's disease
Erythema multiform Herpes simplex , mycoplasma
Acanthosis nigrican CA-stomach
Pyoderma gangrenosum
necrobiosis lipoidica DM
Dermatitis herpetiformis Celiac disease
XANTHOMAS Hyperlipidaemia

QWhat do u mean by Erythema nodosum?

These are Painful, palpable, dusky blue-red nodules are most commonly seen on the lower legs due to a
vasculitis in the deep dermis and subcutaneous fat .

252
Q Cause of erythema nodosum ?
Bacteria M Mycobacterium tuberculosis , leprosy , mycoplasma

R rickettsia,

c Chlamydia

s Streptococci

Drugs Sulphonamides and

Oral contraceptives
Systemic disease Sarcoidosis,
ulcerative colitis and
Crohn's disease

Q . Name some skin cancer?

Basal cell carcinoma (rodent ulcer)
Squamous cell carcinoma
Malignant melanoma

Q Name some bacterial infection that involved skin or soft tissue ?

Impetigo
Furuncle /boil
Carbuncle
Staphylococcal scalded skin syndrome
Cellulitis
Erysipelus

Urticaria

Q. A patient give history of localized swelling of skin which is itchy and disappear after 15
hr what is your diagnosis?
A. Acute urticaria

Define urticaria ?

Urticaria refers to an area of focal dermal oedema secondary to a transient increase in

capillary permeability
urticaria how long persist ?
the swelling lasts less than 24 hours

253
How long does the individual lesion last'

< 24 hours (urticaria)I

> 24 hours (urticaria) vasculitis)

When will u say it is acute or chronic urticaria:'

It depends on how long the condition has been present for;

Acute urticaria: if the condition is persist < 6 weeks then called acute urticaria
Chronic urticaria : if the condition is persist > 6 weeks then called chronic urticaria

What type of hypersensitivity reaction it is?

Type one hypersensitivity
" i e in production of antibodies that cross link with the 1-gF. Receptor on mast cells)

What are the causes of the urticaria?

Autoinimunc
Allergens (in foods, inhalants and injections)
Drugs

Treatment of urticaria?

Antihistamin
H
2 Mocker
in some case mastcell stabilizer or leukotriene inhibitors

Q. Name some bolus lesion in the skin?

Pemphigus vulgaris
Bullous pemphigoid
Dermatitis herpetiformis
Stevens-Johnson syndrome
Epidermolysis buiiosa acquisita

254
 Q. which disease u may find Dermatitis herpetiformis as skin manifestation?
In celiac diseases.
Disease Pemphigus vulgaris Bullous pemphigoid
Age
40-60 yrs 60s and over
Site of blisters Torso, h e a d Trunk a n d l i m b s
Nature blisters Flaccid and fragile Tense
Mucous membrane involvement 1 0 0 % Occasionally
level of blister intra-epidermal(superficial) subepidermal

Name some causes of hypo pigmentation and hyper pigmentation?

hypo pigmentation hyper pigmentation

Albinism Haemochromatosis
Vitiligo Addison
ptyriasis versicolor Nelson's syndrome
increase ACTH secretion
chloasma

Name the causes of drug induce pigmentation?

A Amiodarone
Arsenic
B Bleomycin
Busulfan
C Chloroquine
Clofazimine
M Minocycline
P Phenothiazines

Q. defines eczema?
The terms 'eczema' and 'dermatitis' are synonymous. Here The skin can become so acutely
inflamedthat fluid weeps out or vesicles appear.

Classify eczema?
Classification of eczema
Endogenous Exogenous

Atopic eczema Contact eczema irritant

Discoid eczema Contact eczema allergic
Seborrhoeic eczema Photosensitive eczema
Venous (gravitational) eczema Lichen simplex
Asteatotic eczema

255
Define Atopy?
Atopy is a genetic predisposition to form excessive IgE which leads to a generalised and
prolonged hypersensitivity to common environmental antigens

Write down the diagnostic criteria for atopic eczema?

Itchy skin and at least three of the following:

History of itch in skin creases (or cheeks if < 4 years)

History of asthma/hay fever (or in a first-degree relative if < 4 years)
Dry skin (xeroderma)
Visible flexural eczema (cheeks, forehead, outer limbs if < 4 years)
Onset in first 2 years of life

Management of eczema
General management
Education Explanation, reassurance and encouragement
Avoidance of irritants/allergens
Regular use of greasy Emollients
Bath oils/soap substitutes
Topical therapies:
Appropriate use of topical corticosteroids
Adjunct therapies:
oral antibiotics
sedating antihistamines

Classification of topical steroids by potency

Potency Name of steroid
Very potent clobetasol propionate
Potent betamethasone valerate
Moderately clobetasone butyrate
Mild hydrocortisone

Remember following as question may ask where u will use what type of steroid
The face should be treated only with mild steroids.
In adults the body should be treated with either mild, moderately potent or diluted potent
steroids.
In young children the body should be treated with mild and moderately potent steroids.
Potent steroids are used for short courses (710 days).
Treatment of the palms and soles (but not the dorsal surfaces) may require potent or very
potent steroids as the skin is much thicker.
Regular use of emollients may lessen the need forsteroid use.
Name the treatment of following eczema:
General management is common in all types

256
Seborrhoeic eczema ketoconazole shampoo and
ketoconazole creams
Irritant eczema avoidance of irritants
protective clothing, e.g. gloves, and
regular use of emollients
Appropriate use of topical corticosteroids
Contact allergic eczema Avoidance of the culprit allergen
lifestyle changes such as
a new job or
giving up hobbies.
Appropriate use of topical corticosteroids

With which organism seborrhoeic dermatitis is associate with ?

Overgrowth of Malassezia furfur

What are investigation we can do in eczema ?

Patch tests Done in cases of contact allergic dermatitis

IgE and specific IgE to support the diagnosis of atopic eczema and
to determine specific environmental allergens, e.g. pet dander, horse
hair, house dust mite, pollens and foods.

Prick tests The indications are that of specific IgE

Write down the complication of eczema ?

257
Read the following definition which is frequently asked ?

Macule : A flat, colored lesion, <2 cm in diameter, not raised above the surface of the
surrounding skin.
Patch : A large (>2 cm) flat lesion with a color different from the surrounding skin. This
differs from a macule only in size.
Papule : A small, solid lesion, <0.5 cm in diameter, raised above the surface of the surrounding
skin and hence palpable
Nodule : A larger (0.55.0 cm), firm lesion raised above the surface of the surrounding skin.
This differs from a papule only in size
Tumor : A solid, raised growth >5 cm in diameter.
Plaque : A large (>1 cm), flat-topped, raised lesion; edges may either be distinct (e.g., in
psoriasis) or gradually blend with surrounding skin (e.g., in eczematous dermatitis).
Vesicle : A small, fluid-filled lesion raised above the surface, <0.5 cm in diameter,
Pustule : A vesicle filled with pus .
Bulla : A fluid-filled lesion raised above the surface >0.5 cm in diameter.
Erosion : Loss of epidermis without an associated loss of dermis.
Ulcer: Loss of epidermis and at least a portion of the underlying dermis.
Petechiae, Petechiae are pinhead-sized macules of extravascular blood in the dermis.
purpura These are larger than petechiea (>2mm )
ecchymosis Large confluent area of purpura (bruise)
Telangiectasia The visible dilatation of small cutaneous blood vessels

258
 Psychiatric disorder

Name and classify psychiatric disorder

Stress-related disorders to remember APA

A---Acute stress disorder
P---Post-traumatic stress disorder
A---Adjustment disorder

Anxiety disorders to remember POP-Gun

P-- Phobic anxiety
O --Obsessive-compulsive disorder
P- Panic disorder
Gun-- Generalised anxiety
Affective (mood) disorders
Depressive disorder
Mania and bipolar disorder
Schizophrenia and delusional disorders
Substance misuse
Alcohol
Drugs
Organic
Acute, e.g. delirium
Chronic, e.g. dementia
Disorders of adult personality and behavior
Personality disorder
Factitious disorder
Eating disorders
Anorexia nervosa

259
Bulimia nervosa
Somatoform disorders to remember To remember ADH , FCPS
A----Somatoform autonomic dysfunction
D--Body dysmorphic disorder
H--Hypochondriasis

F--- chronic Fatigue syndrome /Neurasthenia

C--Dissociative (Conversion) disorder
P--Pain disorder
S--Somatisation disorder
Puerperal mental disorders

Mention the feature of anxiety

SYMPTOMS OF ANXIETY DISORDER
Psychological to remember FIPA-world cup
F---------- Fear of impending disaster
I---------- Irritability
P----------Depersonalisation
A-------- -Apprehension
World--- Worry
Cup-- -----Poor concentration

Somatic to remember do PBF TDS In ICU

P-----Palpitations
B--- Breathlessness
F--- Fatigue

T--- Tremor
D--- Diarrhoea
S--- Sweating
In
I---Initial insomnia
C--- Chest pain
U--- Frequent desire to pass urine

260
What are the features of depression?
Psychological Somatic
Depressed mood Reduced appetite
Reduced self-esteem Weight change
Suicidal thinking Disturbed sleep
Pessimism Fatigue
Guilt Loss of libido
Loss of interest Bowel disturbance
Loss of enjoyment (anhedonia) Motor retardation (slowing of activity)

Story I

It is the manic phase of Bi-polar affective disorder

What is treatment?
anti-psychotic drugs . such as chlorpromazine and haloperidol
What will u give for prophylaxis?
Lithium carbonate

261
story 2

what is your diagnosis ?

the patient was patient of depression
What is the treatment
Usually Antidepressant drugs
Tricyclic antidepressants
Classify mood disorder
Mood or affective disorders include:
unipolar depression: the patient suffers one or more episodes of lowered mood
bipolar disorder: the patient also experiences episodes of elevated mood, usually (but not
always) interspersed with episodes of depression
dysthymia: describes a particularly chronic low-grade depression

Treatment of depression treatment of mania

Usually Antidepressant drugs Manic episodes treated with antipsychotic drugs
Tricyclic antidepressants (TCAs)
Selective serotonin re-uptake inhibitors (SSRIs)
Escitalopram to prevent recurrent episodes
Fluoxetine Lithium carbonate
Newer antidepressants what are other drugs also use ?
venlafaxine, carbamazepine and
mirtazapine, sodium valproate
reboxetine and duloxetine

262
Anti depressant therapy how long given?
Treatment should be continue 6-12 months after recovery

what complication of lithium ?

Short term:
Nausea,
vomiting
Tremor and
Convulsions
Long-term:
weight gain,
hypothyroidism,
nephrogenic diabetes insipidus
Renal failure can occur.
what investigation you will do to follow-up ?
Thyroid and renal function should be checked before treatment is started and every 6 months
thereafter.

263
Name some anti depressant drug with their complication.
Anti- depressant drug:
Group Drug Usual dose side effect
Tricyclics 75-150 mg daily Anticholinergic effects,
Amitriptyline
Postural hypotension,
Cardiotoxicity.
Imipramine 75-150 mg daily Deteriorate Glaucoma and
prostatism.
SSRIs 10-20 mg daily Headache,
Escitalopram
Nausea, anorexia and
20 mg daily Sexual dysfunction
Fluoxetine

50-100 mg daily
Sertraline

Newer agent 75-375 mg daily

Venlafaxine

8-12 mg daily
Reboxetine

15-45 mg daily
Mirtazapine

Mentions some antipsychotic drugs:

Group Drug Usual dose
Phenothiazines Chlorpromazine 100-1500 mg daily

Butyrophenones Haloperidol 5-30 mg daily

Atypical antipsychotics Clozapine 25-900 mg daily

Risperidone 2-16 mg daily
Olanzapine 5-20 mg daily
264
Name some side effect of antipsychotic drugs ?
Weight gain due to increased appetite What do you mean by tardive dyskinesia ?
Effects due to dopamine blockade*
Tardive dyskinesia is abnormal movements commonly of
Parkinsonism the face, over which the patient has no voluntary control.
Akathisia (motor restlessness)
Acute dystonia
Tardive dyskinesia
Gynaecomastia
Galactorrhoea
Effects due to cholinergic blockade
Dry mouth
Blurred vision
Constipation
Urinary retention
Impotence
Hypersensitivity reactions
Cholestatic jaundice
Photosensitive dermatitis
Blood dyscrasias (neutropenia with clozapine)
Ocular complications (long-term use)
Corneal and lens opacities
Story : 3

What is your diagnosis?

SCHIZOPHRENIA
What is treatment?
Anti-psychotic drugs. such as chlorpromazine and haloperidol

265
Define schizophrenia?
Schizophrenia is a psychosis characterized by delusions, hallucinations and lack of insight
Mention the sign of Define schizophrenia?
Schizophrenia is a psychosis characterized by delusions, hallucinations and lack of insight
First-rank symptoms of acute schizophrenia Symptoms of chronic schizophrenia
(negative symptoms)
To remember A,B,C,D To remember it ASP BP

A = Auditory hallucinations-second or third person

A--Apathy and loss of drive (avolition)
B = Broadcasting, insertion/withdrawal of thoughts
S---Social isolation
C = Controlled feelings, impulses or acts
P---Poverty of speech
D = Delusional perception (a particular experience is
B--Blunted/ Flattened affect
bizarrely interpreted)
P---Poor self-care

Where you will give treatment of acute schizophrenia?

Acute schizophrenia usually requires admission to hospital because patients lack insight that
they are ill and are unwilling to accept drug treatment. In some cases, they may be at risk of harming
themselves or others.
Where you will give treatment of chronic schizophrenia?
commonly managed in the community
Story 4:

What is your diagnosis?

My diagnosis is OBSESSIVE-COMPULSIVE DISORDER

266
What will be the Rx?
Dugs
Antidepressant drugs such as clomipramine
CBT (cognitive behavior therapy) which
Name some eating disorder?
Anorexia nervosa
Bulimia nervosa
Diagnostic criteria:
Anorexia nervosa Bulimia nervosa
A Amenorrhoea for at least 3 months 1. Recurrent bouts of binge eating
B--- Body mass index 17.5 / Bwt loss at least 15 2. Lack of self-control over eating during binges
% of total body wt 3. Self-induced vomiting, or dieting after binges
C-- Avoidance of high-calorie foods 4. Weight maintained within normal limits
D--- Distortion of body image so that patients
regard themselves as fat even when grossly
underweight

what do you mean by somatoform disorders? Name the somatoform disorders?

The clinical feature of these disorders is somatic symptoms which are not explained by a medical
condition and not better diagnosed as part of a depressive or anxiety disorder.

Somatoform disorders to remember To remember ADH , FCPS

A----Somatoform autonomic dysfunction
D--Body dysmorphic disorder
H--Hypochondriasis

F--- chronic Fatigue syndrome /Neurasthenia

C--Dissociative (Conversion) disorder
P--Pain disorder
S--Somatisation disorder
267
Story:

What is your diagnosis?

DISSOCIATIVE (CONVERSION) DISORDER / previous name was hysteria'
what do you mean by DISSOCIATIVE (CONVERSION) DISORDER?
It is characterised by a loss of neurological function not fully explained by organic disease
What treatment you will give?
CBT or antidepressant drugs
What the common presentations of dissociative (conversion) disorder?
TO remember it GBS and ALS (amyotrophic lateral sclerosis)

G--Gait disturbance
B--Blindness
S---Sensory loss
A--Aphonia
L---Loss of function in limbs
S---Non-epileptic seizures

268
Not for all who want get more marks:

Somatoform Where r symptoms related that organ of body Antidepressant drugs

autonomic which is control by autonomic nerves system. CBT
dysfunction
Body dysmorphic Here patient thought that his body s
disorder configuration is disfigured. patient Dislike of
body parts.
Hypochondriasis Here patient belief that he has serious or CBT
fatal, disease that persists despite appropriate
medical reassurance
chronic Fatigue it is characterised by excessive fatigue after Antipsychotic drugs
syndrome minimal physical or mental exertion, poor CBT
concentration, dizziness, muscular aches and
sleep disturbance
Pain disorder This describes severe, persistent pain which Antidepressantdrugs
cannot be explained by a medical condition. Tricyclics and
duloxetine and
mirtazapine
CBT
Somatisation disorder It is characterized by occurrence of chronic
multiple somatic symptoms for which no
physical cause is found.

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SOMATIC SYNDROMES of deferent system:

Gastroenterology Irritable bowel syndrome, non-ulcer dyspepsia

Gynaecology Premenstrual syndrome, chronic pelvic pain
Rheumatology Fibromyalgia
Cardiology Atypical or non-cardiac chest pain
Respiratory medicine Hyperventilation syndrome
Infectious diseases Chronic (post-viral) fatigue syndrome
Neurology Tension headache, non-epileptic attacks
Dentistry Temporomandibular joint dysfunction, atypical facial pain
Ear, nose and throat Globus syndrome

Phobic anxiety Panic disorder Generalised anxiety

disorder disorder
definition A phobia is an these are attacks of This is chronic anxiety
abnormal or excessive severe anxiety, which associated with
fear of an object or are not restricted to any uncontrollable worry
situation, which he particular situation or
want to circumstances and are
therefore unpredictable

Occurrence of anxiety Situational Paroxysmal Persistent

Associated behaviour Avoidance Escape Agitation
Associated cognitions Fear of situation Fear of symptoms Worry
Somatic symptoms On exposure Episodic Persistent
examples phobia of going out hyperventilation symptoms of
alone phobia of chest pain and muscle tension and
venepuncture. palpitations bowel disturbance
phobia of crowded
places

270
management of anxiety :
Psychological treatment
Explanation and reassurance
Graded exposure (desensitisation) to feared situations for phobic disorders, and
CBT for panic.
Drug treatment
Antidepressants are the drugs of choice
Benzodiazepines are useful in the short term
A -blocker ( propranolol) can help when peripheral somatic symptoms are prominent

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Name some anxiolytic drugs ?
Benzodiazepines
Action Main groups Clinical use
Antipsychotic Phenothiazines

Butyrophenones
Schizophrenia
Mania
atypical Acute confusion

Antidepressant Tricyclics and related drugs Depressive illness

Obsessive-compulsive disorder

SSRIs (selective serotonin re-uptake inhibitors) Depressive illness

Mood-stabilising Lithium Prophylaxis of manic depression

Acute mania
Carbamazepine Prophylaxis of manic depression
Sodium valproate Prophylaxis of manic depression
Anti-anxiety Benzodiazepines Anxiety disorders

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 Insomnia
Alcohol withdrawal
-adrenoceptor antagonists Anxiety (somatic symptoms)

273
 Poisoning
What type poisoning case you have seen in the word?

OPC
Sedative
Kerosene
Herpic and savlone
Corrosive poisoning
Dhutura poisoning
Snake bite

OPC

POISONING

OPC may be accidental an suicidal

Q. Name some example of accidental OPC poisoning ?

Farmer who spray OPC in field.

Q what are the sign symptom of OPC poisoning?

Following sing symptom you will find

MUSCARINIC

Smell of OPC

Salivation

Constricted pupil

Bradycardia

Other hypotension and sweating, lacrimation

Lung : creps ++++++

NICOTINIC

Fasciculation and muscle twitching and

weakness of muscle

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CNS

Coma, confusion ,

Convulsion, respiratory depression

Write down the manage ment of OPC poisoning

1st give stomach wash

Take off the cloth and give a bath with soap
Open IV channel
Keep NPO
Give bolus dose
Inj .Atropin

10- 20amp iv stat

Then
Inj. Atropin , 5- 15 amp 5 to 15 min interval untill sign of atropinisaion appear
Inj. PAM / Pralidoxime
2 amp iv over 10 min stat and

Give another 2 amp. In drip inj . DNS/ normal saline

Inj. Cefriaxon 1 gm or any antibiotic

Inj . H 2 blocker or inj. PPI
Catheter must be done immediately after atropine started
Maintain atropine chart
Input and output chart
When sign of atropinisation appear tapering the dose

Q. What is the amount atropine in one ampoule?

In one ampoule contain 0.6 mg atropine

Q What is the specific anti-dot of OPC?

Pralidoxime

Q write down the dose of pralidoxime ?

Dose : 30 mg /kg BWT over 10 minutes

We give Inj. PAM 2 amp iv over 10 mins
The maintenance dose is
8- 10 mg / kg / hr in infusion drip
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Q. what are the sign of Atropinization ?

Pupil dilated
Tachycardia
Increased temperature / dry axilla
Clear lungs or no creps
Increased blood pressure

Q. What are the causes of death in OPC poisoning?

Immediate cause of ---ventricular arrhythmia

Then / mainly ----respiratory failure due paralysis of the respiratory muscle
Q. A patient come to u with no clear cut HO and Sign symptoms of OPC poisoning then
how will U exclude the OPC poisoning ?

Give test dose of Atropine ( inj. Atropine 2 amp iv stat)

Look for the dilation of pupil after 5 mins if pupil become full dilated after 5 min
then
It was not a case of OPC poisoning

Q A patient of opc poisoning suddenly become restless and agitated ?

Then think and about over atropinisation

Do the following
Give inj. Sedil 1 amp slow IV stat and
Reduce the current dose of atropine
Q. A patient was responding to treatment and u r tapering the atropine but suddenly u
noticed that the patient is become disoriented and drowsy with generalized weakness
and respiratory distress?

This is a case of intermediated syndrome

Do re-atropinisation, give inj. Atropin 20 amp iv stat and give it iv every 5 min
interval until patient Lung become crep. Free .and patient condition improved.
If not improved and give CALL TO ICU otherwise pt will die from respiratory
failure

Q . Write down Treatment of atropine intoxication / over atropinisation?

If patient become over atropinisation do following

Stop inj. Atropine for 30 min
Give inj.sedil depending on the situation
Observe after 30 min and if the patient settled then
Restart atropine at 70 80 % of previous rate

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 Benzo-diazepam poisoning
Do not be worried
Lethal dose is more then 40 / 50 tab.
Dangerous complication is
o Respiratory distress or respiratory arrest , -- main complication
What treatment you will give in patient with diazepam poisoning?

First see the patient is conscious or not

Supportive and symptomatic
Stomach was given if come within one hour
Open an IV channel

What follow up?

I will monitor the pulse and BP

Specially respiratory distress

What is the specific antidote of Benzo-diazepam?

The specific antidote is Flumazenil

A PATIENT WITH TRICYCLIC ANTI DEPRSSION POISONING

It is more dangerous than diazepam poisoning

What is do I patient of TCA poisoning comes to you?

First look that the patient is unconscious / or not

Immediate look for the

Pulse ----arrhythmia / tachycardia

BP - hypotension
Respiration rate / rhythm and any res. distress
Q what are complication of TCA?

Severe intoxication causes

Cardiac arrhythmia , ischaemia hypoxia,

Deep coma with respiratory depression
A metabolic acidosis.

277
What treatment you will give?

Give stomach wash if come within 1 hours

Supportive and symptomatic
Open an IV channel

What is lethal dose of TCA?

Death may follow ingestion of as little as 1000mg of a tricyclic

What investigation you want to do?

I want of do ECG first

First ECG to see

Tachycardia. ,
ST depression ,
QT prolongation ,
Arrhythmia
Do s.creatinin

S. electrolytes ---to see hypokalaemia

Q. Clinical feature of TCA

Anti-cholinergic features are

o Dry mouth,
o Dilated pupils, Blurred vision,
o Sinus tachycardia, Urinary retention,
o Agitation and even hallucinations.
Cardiac arrhythmic

DHATURA POISONING / STUPEFY POISONING

Scenario: An unconscious patient come to u without attendants by police or unknown

people and the patient was found unconscious in bus / rail station or lunch station.

Or patient may comes to u with his attendance with HO that he ate something in bus and
followed he cannot remember anything and lost all his money.

278
What is your diagnosis?

So do not be worried this is a case of Dutra poisoning or stupefy poisoning

Patient will be ok with in 24- 48 hr give only supportive care

Rx of Dutra poisoning?

A ..clear away with suction if secretion

B . O2 inhalation if respiratory distress C . Circulation
Diet NG feeding
200 ml 2 hrly

Inj. Normal saline 1000 ml

I V @ v 20 drop / min

Inj. Antibiotics
Inj. Ranison 50 mg
Continuous catheterization
Maintain input output chart

How will monitor this patient?

Pulse
BP
Respiration
Heart
GCS
Neurological exam
Fundoscopy
Evidence of external injury

A PATIENT WITH CORROSIVE POISONING / CHEMICAL POISONING THIS

INCLUDE

Acid , alkali , Bleaching powder ,

Harpic , savelon , Shampoo and kerosin

Name some condition where stomach wash is contraindicated

Acid , alkali ,
Bleaching powder ,
kerosin

279
 Harpic , savelon , Shampoo and

Why stomach wash is contraindicated ?

Chance of aspiration pneumonia

In case of korosin poisoning chance of Chemical pneumonitis

TREATMENT OF CORROSIVE

Do not give stomach wash / NG suction

Do not try to do induce vomiting ( because of aspiration pneumonia )
Keep the patient NPO for 6 hrs
Inj. DNS 1000 or 2000 ml
Iv @ 20 D / min

Inj.ceftriaxone 1 gm
1 vial IV BD

Inj. Pantonix 40 mg
1 vial IV stat and daily

If patient complaint pain

Inj. Anadol 100mg / inj. Toradolin or nalbun 2
1 amp im stat and TDS

If patient ingest chemical other than Acid and alkali

Patient may give liquid paraffin

Syp. Entacid plus 2 TSF TDS
Which one is more dangerous acid or alkali? Why?

Alkali burn is more dangerous than acid

When ingested acid produce coagulation necrosis of gut mucosa and formation of
escher limits the damage up to superficial layer
While alkali causes liquifactive necrosis of the mucosa with saponification and
continued deeper Penetration into the underlying tissues causing extensive damages.
Which group of people are affect by kerosin poisoning?

Usually child
Write down the treatment of kerosin poisoning

Like that of corrosive poisoning bur here dexamethason(oradexon) is added to prevent

chemical pneumonitis

Do not give stomach wash / NG suction

280
 Do not try to do induce vomiting ( because of aspiration pneumonia )
Keep the patient NPO for 6 hrs
Inj. DNS 1000 or 2000 ml
Iv @ 20 D / min

Inj.ceftriaxone 1 gm
1 vial IV BD

inj. Dexamethason
I amp iv 6 hrly

Inj. Pantonix 40 mg
1 vial IV stat and daily

A patient with HO kerosin poisoning comes to 3 days later with complaint of fever and
respiratory distress what is your diagnosis ?

Chemical pneumonitis

What treatment you have to give?

Antibiotic and steroid

Snake Bite Poisoning

Have you seen snake bite patient in ward?

Yes sir
What type of snake bite it was?

Most of them are non-poisonous

Remember the following ?

Most of the snake of our country are nonpoisonous

Poisonous snake are Cobra @ krait in all area
Green pit viper found only in chittagonj
What will u do if a patient comes to an unknown snake bite ?

Frist take HO snake bite / bite marks / is it snake or other animal

Release the tourniquet

First loose the tourniquets to maintain circulation

Then remove all tourniquet keeping only one
Then gradually remove last one
Warn the patient attendants that removing of this tourniquet may produced sign of
poisoning

281
 Bed rest
Inj. Normal saline 1000 ml
IV @ 10 D / min

Cap .Moxin / Cephradine 500 mg (if local wound )

1+ 1 + 1

Cap . Omeprazole 20 mg
1+ 0 + 1

Inj. TT / Tetanus Toxoid ( if local wound )

1 amp IM stat

Inj. TIG ( if local wound contaminated )

1 amp IM stat (in separate hand )

If patient complaint pain

Tab. Paracetamol 500mg 1 + 0 + 1

Never give the following

Inj. Oradexon
Inj Avil
And NSAID
Observe the patient at least for 24 hours

If no sign symptom appear with in this period

Then discharge the patient

Name poisonous snake found in Bangladesh ?

Cobra @ krait

Can you difference the bite mark of cobra from krait

Cobra Krait

Usually bite in limb Bite anywhere in the body

Bite mark present May have no bite mark
Produce local envenoming (blister and No local envenoming
necrosis and rapid extension of swelling Produce neurological feature
bitten limb ) Usually bite at night
Produce neurological feature No haematological feature
No haematological feature May bite in home
Usually bite in jungle and fluid

282
What are the sign of poisonous snake bit ?

Look for following neurological sign

Nasal voice
Ptosis
Opthalmoplegia
Dysphagia
Broken neck sign
Dyspnea
Difficult in opening mouth and
protruding tongue

Unconscious
Hematological (not in our country )

Gum bleeding , epistaxis ,

Bruise and echymosis
Other sign

Dark color urine / oliguria

Vomiting
Collapses

What the nature toxin release by out poisonous snake in our country?
Neurotoxin
How Will u diffrentites the poisonous snake bit from non poisonous ?

Poisonous snake bite Non poisonous

Two frank mark in equal distance apart Multiple marks

Look for local envenoming Absent

Rapid swelling or extension of swelling
Blister and necrosis

neurological sign present neurological sign absent

TREATMENT OF POISONOUS SNAKE BITE

Before start polyvalent antivenom do the following

Take written informed consent from patient attendant

Informed the patient may has 50% chance to die due to reaction of antivenom and

283
100 % chance to die with out antivenom .

Dose of antivenom Dose is the same irrespective to age n sex

Total vial = 10 vial , each vial dilute with 10 ml distilled water (if vials are not in dilute
form ) Mix this 10 vial(100 ml) with 100 ml NS saline and give in 1 hour via micro
burette set
Inj. Normal saline 100
+
Inj . Antivenom 10 vial
IV @ 60 D/ min

Some want to Give following before starting anti-venom to prevent anaphylactic reaction

Inj. Cotson 100 mg 1 vial IV stat

Inj .avil 1 vial IV stat
Additional treatment indicated for neurotoxic feature
Atropine Neostigmine regimen
1st Inj. Atropin
15 gm / kg body weight IV stat then

Inj. Neostigmine
50-100 gm / kg body weight SC stat and repeat every 4 hrly until neuro .sign
improved

Give call to ICU as patient may need assisted ventilation for respiratory paralysis

WHAT WILL U DO IF PATIENT DEVELOP ANAPHYLITIC REACTION

Inj. Adrenaline 1:1000

For adult = 0.5ml IM (500 gm)
Sign and symptom of anaphylactic reaction
For child = 0.o1 mg / kg
Intense itching
6-11 yr. = 0.25 ml IM
Urticaria
1-5 yr. = 0.125 ml IM
Angio-edema
Inj. Avil ( in case of child 0.2mg /kg)
1 amp slow iv after dilution Dyspnea due to Bronchospasm

Inj. Cotson
1 vial iv stat @ 8 hrly

284
 Paracetamol poisoning

What is complication of paracetamol poisoning ?

Acute liver failure most common

Renal failure (25%)

Q .What is the specific antidote ?

Intravenous N-acetylcysteine
Q Management?

If patient comes within one hours then

Give stomach wash
Activated charcoal
Open and IV channel with dextrose
Intravenous N-acetylcysteine
Q. what investigation will you do ?

ALT
Prothrombin time
S.creatinine
Blood paracetamol level

Wasp bite
Some time a patient may comes to you with history wasp bite or

Swelling of different part of the body after eating Chinese soap / thi soap

Q. what will you look for ?

I will see feature of anaphylactic shock

characterized by

Bp ---hypotension
Stridor laryngeal spasm
Lung wheeze
Kidney oligouria

285
What follow-up you will give the patient

Exam .

Pulse
BP
Auscultation of lung
I/O chart
Do

ECG
S.Creatinine

What treatment you will give the patient?

Treatment depends on according to severity:

In severe case:

Inj. Ranisone
1 amp IV stat

Inj. Oradexon / inj.Cotson

I amp IV stat and 8 hrly

Inj. Avil
1 amp IM / IV stat

In mild to moderate

ANTIBIOTICS (Cap . amoxycilline or cephradine 500 mg)---In case of wasp bites

1+1+1

ANTI-HISTAMIN (Tab . deslor 10 mg )

0 + 0+ 1

H 2 BLOCKER ( tab. Ranitidine 150 mg )

1+ 0 + 1

286