HEPATO-BILIARY

SYSTEM
DR.SRINATH.CHANDRAMANI

HEPATOBILIARY SYSTEM
ANATOMY
PHYSIOLOGY
SYMPTOMATOLOGY
INVESTIGATIONS
INDIVIDUAL

DISEASES

INDIVIDUAL DISEASES
VIRAL

HEPATITIS
AUTOIMMUNE HEPATITIS
DRUG INDUCED HEPATITIS
ALCOHOLIC HEPATITIS
CIRRHOSIS + COMPLICATIONS
LIVER TRANSPLANTATION
GALLSTONES + PANCRAETITIS

Anatomy

The right and the Left lobe are independent with regard to :
1. Portal blood supply
2. Arterial blood supply
3. Bile drainage.

Basic liver architecture :

Hepatocytes, which constitute two-thirds of the mass of the
liver.
Kupffer cells (members of the reticuloendothelial system),
Stellate (Ito or fat-storing) cells,
endothelial cells and blood vessels,
bile ductular cells, and
supporting structures.

Functional classification
Based

on drainage by major hepatic vein, Liver is

Functionally divided into 4 Sectors / 8 Segments

Caudate

lobe is anatomically distinct having no

drainage by either of the 3 major hepatic veins. By
segment classification, It is classified as Segment 1.

Significance

of above classification :

Interpretation

of Radiological data
Planning of liver resection procedures.

PHYSIOLOGY
Organ with a high metabolic rate and rich blood supply.
Dual Blood supply :
1. Hepatic artery
2. Portal Vein

20% supply
80% supply

Oxygen rich
Nutrition rich

Portal Zones :
Blood flows from zone 1 to zone 3 of the acinus and drains
into the hepatic veins (central veins).
Secreted bile flows in the opposite direction, in a counter
current pattern from zone 2 to zone 1.
The sinusoids are lined by unique endothelial cells that have
prominent fenestrae of variable size, allowing the free flow
of plasma but not cellular elements.
The plasma is thus in direct contact with hepatocytes in the
subendothelial space of Disse.

Functions

Hepatocytes perform numerous and vital roles in maintaining

homeostasis and health. These include :

synthesis of most essential serum proteins viz. albumin, carrier

proteins, coagulation factors, many hormonal and growth
factors.

production of bile and its carriers (bile acids, cholesterol,

lecithin, phospholipids),

regulation of nutrients (glucose, glycogen, lipids, cholesterol,

amino acids),

metabolism and conjugation of lipophilic compounds

(bilirubin, anions, cations, drugs) for excretion in the bile or
urine.

Symptomatology
Jaundice
Parotid

enlargement
Fetor hepaticus
Spider naevi
Gynaecomastia
Abdominal pain
Ascitis
Caput medusa

Dupeytrens

contracture
Paper money skin
Pruritis
Testicular atrophy
High coloured urine
Pedal edema
Altered
sensorium/convulsion
Peticheia/ echymosis

Etiology & Approach

Acute ( < 6 months )

Infective
Trauma
Vascular
Toxin/Drug induced
Autoimmune
Physical obstruction

Chronic ( > 6 months )

Infective
Toxin/Drug induced
Genetic/enzyme deficiency
Glycogen storage disorders
Neoplasms
Obstruction

Recurrent Jaundice
Hemolysis
Intermittent obstruction
Autoimmune hepatitis
Drug induced hepatitis
BRIC benign recurrent intrahepatic cholestasis

Liver Function Test

S.Bilurubin
Transaminases

AST / ALT
Alkaline phosphatase / GGTP
S.Proteins / A:G ratio
Prothrombin time
Alpha-fetoprotein

TEST 1
1.

Nucleotidase activity is increased in

(A)
Bone disease
(B)
Prostate cancer
(C)
Chronic renal failure
(D)
Cholestatic disorders

2.

Which does not contribute to serum alkaline

phosphatase
(A)
Liver
(B)
Osteoblasts
(C)
Renal tubular cells
(D)
Neutrophils

3.

Ratio of AST/ALT>1 present in

(A)
Non-alcoholic steatohepatitis
(B)
Alcoholic hepatitis
(C)
Wilson's disease
(D)
All of the above

TEST 1
4.

5.

6.

7.

A 50 year old lady presented with history of pain upper abdomen, nausea and
decreased
appetite for 5 days. She had undergone cholecystectomy 2
year ago. Her bilirubin
was
10 mg/dl, SGOT 900 IU SGPT 700 IU/I and
serum alkaline phosphatase was 280
IU/I.
What is the most likely
diagnosis?
(A)
Acute pancreatitis
(B)
Acute cholangitis
(C)
Acute viral hepatitis
(D)
Posterior penetration of peptic ulcer
Patients with coagulation abnormality due To liver disease Are likely to have
(A)
Prolonged bleeding time
(B)
Prolonged prothrombin time
(C)
Thrombocytosis
(D)
Short partial thromboplastin time
All are haemoglobin except
(A)
Bilirubin
(B)
Biliverdin
(C)
Hemosiderin
(D)
Lipofuscin
Chances of developing kernicterus appears to be significant when serum level of
unconjugated bilirubin reaches
(A)
50 mg%
(B)
20 mg%
(C)
10 mg%
(D)
5 mg%

TEST 1
8.

Gilbert's syndrome all are true, except

(A)
Conjugated hyperbilirubinemia
(B)
Fasting hypoglycaemia
(C)
Normal liver histology
(D)
Liver enzymes normal

9.

Conjugated hyperbilirubinemia is seen in

(A)
Gilberts syndrome
(B)
Criggler Najjar type-I
(C)
Criggler Najjar type-II
(D)
Dubin Johnsons syndrome

10.

The test used to diagnose Dubin Johnson syndrome is

(A)
Serum transminases
(B)
Bromsulphalein test (BSP)
(C)
Hippurate test peptidase
(D)
Gamma glutamyl transferase level

Viral Hepatitis
Hepatotrophic

virus.
Classification based on Route of
transmission.
Clinical Features :
- Prodromal phase
- Clinical phase
- Recovery phase
Extraintestinal manifestations.

General info
All

viruses are RNA viruses except Hepatitis B which

is a DNA virus.

Pathological

injury occurs due to :

Direct injury
Immune mediated

Incubation
Start

period :

with B(+D) , C, E and A and substract 10 from

60 days.
B(+D) 60 days , C 50 days, E 40 days and A 30
days.

General Info

The typical morphologic lesions of all types of viral hepatitis

consist of :
panlobular infiltration with mononuclear cells,
hepatic cell necrosis,
hyperplasia of Kupffer cells,
variable degrees of cholestasis.
Hepatic cell regeneration is present, as evidenced by
numerous mitotic figures, Multinucleated cells, and rosetteor
pseudoacinar formation.
Liver cell damage consists of hepatic cell degeneration and
necrosis, cell dropout, ballooning of cells, and acidophilic
degeneration of hepatocytes (forming so-called Councilman
or apoptotic bodies).
Lipofuschin is a wear and tear pigment.

Waterborne Hepatitis
Parameter
Epidemiology
Mode of transmission
Incubation period
Clinical peculiarity
Diagnosis
Treatment
Prognosis

Hepatitis A

Hepatitis E

Blood borne Hepatitis

Parameter
Epidemiology
Mode of
transmission
Mother to child
Needle stick injury
Incubation period
Clinical peculiarity
Diagnosis
Treatment
Prognosis

Hepatitis B

Hepatits C

Serum markers for Hepatitis B

HBsAg
Anti-HBs

antibody

HBcAg
Anti-

HBcAb
HBeAg
Anti Hbe antibody
HBV DNA by PCR

Hepatitis B Plus D
Co-Infection

Superinfection

Both together

IgM HBc positive

No change in chronicity

No change in cirrhosis

Increase risk of HCC

HBV precedes
HDV infection
IgM HBc negative
6 fold increase in
chronicity
Hastened progression
to cirrhosis
Greater risk of HCC

Autoimmune hepatitis
Autoimmune hepatitis is characterised by :
Female predominance 2nd decade / post menopausal.
Hyperglobulinemia
Positive circulating auto anti-bodies
Association with HLA-DR3 and HLA-DR4.
Prominence of extrahepatic features of autoimmunity
Secondary conditions have to be excluded viz.
virus,drugs,alcohol,etc.
Good response to immunosuppressive therapy. In general,
responders have :
Florid clinical picture
High antibody titer/ hyper globulinemia
Higher SGPT
Active Liver histology.
Classification is based on circulating antibody type.
may have a 6-month mortality of as high as 40%.

AUTOIMMUNE HEPATITIS
ANTIBODY

TYPE 1

TYPE 2

TYPE 3

ANA

ANTI-LKM

ANTI-LsAg

4-5TH DECADE
F>M

5-6TH DECADE
M>F

EPIDEMIOLOG 2-3RD DECADE

Y
F >> M
CLINICAL
COURSE

ACUTE,
FLORID

CHRONIC,
INDOLENT

UNDERLYING
MALIGNANCY

TREATMENT

IV STEROIDS,
PLASMAPHERE
SIS

ORAL
STEROIDS

UNDERLYING
MALIGNANCY

PROGNOSIS

GOOD

MODERATE

POOR

Drug induced Hepatitis

Mode of Hepatic Injury
In

general, two major types of chemical

hepatotoxicity have been recognized :
(1) direct toxic type and
(2) idiosyncratic type.

Drug induced Hepatitis is classified based

on the clinical and labaratory pattern.

Patterns of hepatotoxicity
Hepatitis
Anesthetic : Halothane
Anticonvulsant : Phenytoin, carbamazepine
Antihypertensive : Methyldopa, captopril, enalapril
Antibiotic : Isoniazid, rifampin, nitrofurantoin
Diuretic : Chlorothiazide
Antidepressant : Iproniazid, amitriptyline, imipramine, trazodone,
venlafaxine
Anti-inflammatory : Ibuprofen, indomethacin, diclofenac
Antifungal : Ketoconazole, fluconazole, itraconazole
Antiviral : Zidovudine, didanosine, nevirapine
Calcium channel blocker :Nifedipine, verapamil, diltiazem
Mixed hepatitis/cholestatic
Immunosuppressive : Azathioprine
Lipid lowering : Nicotinic acid, lovastatin and other statins
Antibiotic : Amoxclav, trimethoprim-sulfamethoxazole
Antifungal : Terbinafine

Patterns of Hepatotoxicity

Cholestasis
Anabolic steroid : Methyl testosterone
Antibiotic : Erythromycin, nitrofurantoin, rifampin, amox
clav, oxacillin
Oral contraceptive : Norethynodrel with mestranol
Anticonvulsant : Carbamazepine
Calcium channel blocker : Nifedipine, verapamil

Fatty liver
Antibiotic : Tetracycline
Anticonvulsant : Sodium valproate
Antiarrhythmic : Amiodarone
Antiviral : NRTI, Protease inhibitors.
Oncotherapeutic : methotrexate

Patterns of hepatotoxicity

Toxic (necrosis)

Hydrocarbon Carbon tetrachloride

Metal : Yellow phosphorus
Mushroom : Amanita phalloides
Analgesic : Acetaminophen

Granulomas

Anti-inflammatory : Phenylbutazone
Antibiotic : Sulfonamides
Xanthine oxidase inhibitor : Allopurinol
Antiarrhythmic : Quinidine, diltiazem
Anticonvulsant : Carbamazepine

Vascular injury

Veno-occlusive/Portal vein thrombosis : Cytotoxic / Irradiation

Sex hormones

Neoplastic

Focal adenoma : sex hormones

Hepatocellular carcinoma : Danazol, Anobolic hormones

Management

Diagnosis : is mainly based on history. Correlation with clinical

manifestation and above mentioned clinical picture helps.
Anti-Histone Antibody is important marker.

Treatment : is largely supportive, except in acetaminophen

hepatotoxicity.
Withdrawal of the suspected agent is indicated at the first
sign of an adverse reaction.
Liver transplantation maybe curative in fulminant cases.
Glucocorticoids for drug hepatotoxicity with allergic features,
silibinin for hepatotoxic mushroom poisoning, and
ursodeoxycholic acid for cholestatic drug hepatotoxicity
have never been shown to be effective and are not
recommended.

Misc Hepatitis
Reyes

syndrome
Characterised by vacuolisation of liver
and renal tubules.
Increases Transaminases, Prothrombin
time and ammonia
hypoglycaemia and metabolic alkalosis.
Characterised by lack of jaundice.

Misc Hepatitis
Budd-Chiari

syndrome : Extremely rare disorder.

Thrombosis of Hepatic vein.
Etiology : Hypercoagulable states , Malignancy,
Myeloproliferative state.
Clinical features depend on extent and rate of
venous obstruction.
Hepatomegaly and Ascitis present in nearly 100%.
Varices in >50%.
Angiography diagnostic. CT preferred mode. Search
for underlying cause.
Medically lifelong anticoagulation . Surgical stenting.
SOS Liver transplant.
Prognosis is poor. Death wihin 3 years if untreated.

Misc Hepatitis
Liver

abscesses : Most common Amoeba

vs Pyogenic.
Intense RHypochondriac pain,
septicaemia. Intercostal tenderness.
USG, FNAC,CT is diagnostic.
Multiple sites is Pyogenic, Single lesion is
amoebic.
Metronidazole for 2 weeks. Antibiotics SOS.
Drainage SOS.
Prognosis excellent. Rupture and sub
phrenic abscess are complication.

Summary of chronic hepatitis

Etiology

Age/gender

Association

Diagnosis

All/males

Orient, African,
Drug users,
Homosexuals,
Immunosupressed

HEP C

All/equal

Blood transfusion
Drug users,
Hemodialysis

Autoimmune

14-25 yrs/
Females

Multisystem
involvement

Drug induced

3rd-5th decade
females

Drug history

Anti histone,
drug levels

Family history,
Hemolysis

KF ring,biopsy
Neurological
symptom.
Cu,Cerupl. level

Hep B & D

Wilson

10-30 yrs/
equal

HBsAg,HBVDNA
Anti-HCV Ab
HCV RNA by PCR
ANA, ASMA,
Anti-LKM, LsAg

TEST 2
11.

True about hepatitis A include

(A) Spreads by faco-oral route
(B) Incubation period is 45-180 days
(C) Predisposes to cirrhosis
(D) lgG anti-HIV antibodied used for diagnosis

12.

The marker of Hepatitis B in the window

period is
(A)
HBsAG
(B)
Anti HBsAG
(C) Anti HBC
(D)
HBcAg

TEST 2
13.

Two laboratory technicians from a District hospital were tested

Australia Antigen positive. True about the further steps is.....
(A) Discard all the blood samples collected by them.
(B) Do not allow them to work in the laboratory.
(C) test the if they are Anti-HBC (IgM) positive
(D) Retest them for Australia antigen after 6 months

14.

Antigen which does not appear in blood in Hepatitis B is....

(A)
HBc Ag
(B)
HBe Ag
(C)
HBs Ag
(D)
None of the above

15.

Acute liver injury associated with hepatitis B virus is due to

(A)
Direct cytopathic effect of the virus
(B)
Sensitized cytotoxic T-cells
(C)
Immune-complex mediated tissue damage
(D)
Vasculitis

TEST 2
16.

Extrahepatic manifestation of Hepatitis-B are

(A) Aplastic anemia
(B) Cryoglobulinemia
(C) Peptic ulcer
(D) Gallstones

17.
after

The likelihood of becoming an HbsAg carrier

acute HBV infection is high in....
(A) Neonates
(B) Chronic hemodialysis patients
(C) Persons with Down's syndrome
(D) Persons with HIV infection
(E) All of the above

TEST 2
18.
A person screened for blood donation, which of the following
serology
is safe for blood donation?
(A)
Anti HBsAg positive
(B)
HBsAg positive
(C)
Anti HBc positive and anti HBSAg positive
(D)
HBeAg positive
19.

The disease associated with hepatitis C virus is...

(A)
Leprosy
(B)
Lichen planus
(C)
Psoriasis
(D)
Vitiligo

20.
liver?

Which of the following drugs is known to cause granuloma in the

(A) Allopurinol
(B) Nifedipine
(C) Tetracycline
(D) Methyl testosterone

Alcoholic Liver Disease

Cirrhosis
Etiological

classification of cirrhosis :
(1) alcoholic;
(2) cryptogenic and posthepatitic;
(3) biliary;
(4) cardiac; and
(5) metabolic, inherited, and drugrelated.
(6) NAFLD / NASH

Biliary Cirrhosis
Primary

biliary cirrhosis :
auto- immune
AMA, Lipoprotein X
CREST syndrome,
Ursodeoxycholic acid
Cholestyramine
Liver transplant with excellent results.
Secondary biliary cirrhosis
Better prognosis
6-12 months
surgical correction is the cure.

NAFD/NASH/NON-ALCOHOLIC
CIRRHOSIS
MORE

IN FEMALES
ASSOCIATION WITH PANCREATIC
INSUFFICIENCY / DM/OBESITY
HAS BECOME THE COMMONEST
CAUSE OF CRYPTOGENIC CIRRHOSIS

Complications of Cirrhosis
Variceal

bleeding
Hepatic Encephalopathy
Spontaneous Bacterial Peritonitis
Coagulopathy
Hepato-renal syndrome
Hepato-Pulmonary syndrome
CHILD PUGH Grading of Liver disease

PORTAL CIRCULATION

Adult portal circulation

Portal blood flow : 1000 1200ml/min

Portal pressure : normally 7mm of Hg.
Various sites of porto-systemic shunts/collaterals exist in the body.
Normally 100% of portal venous blood can be recovered from the
hepatic veins.
Collateral circulation comes into play in 2 situations :

1. INTRA HEPATIC PORTAL VEIN OBSTRUCTION :

The site of obstruction is within the liver. Commonest example being
cirrhosis.
Both physical as well as myo-proliferative factors are involved in portal
vein obstruction.
In such cases barely 13% blood flows through the hepatic vein, rest is
shunted.
Blood ultimately reaches Superior vena cava through the Azygous
system.
Typically the collaterals are abdominal shunts as discussed below.
Few collaterals to pulmonary veins described but rare.

 2.

EXTRA HEPATIC PORTAL VEIN

OBSTRUCTION :

The

block lies outside the liver and hence

collaterals develop to bypass the block
and enter the liver as close to the porta
hepatis as possible.
Lumbar collaterals may be large.
The volume of shunt may be smaller than
intra hepatic obstruction.

SITES OF PORTO-SYSTEMIC ANASTOMOSIS : (Refer Figure)

SITE

PORTAL VEIN

1. Cardia Stomach

2. Anus

CLINICAL OUTCOME

a. Left Gastric

Esophageal

Gastro-esophageal

c. Short Gastric

Intercostal/Azygous

b. Posterior Gastric Diagphramatic & Fundic varices

Sup. Hemorrhoidal
Vein

3. Falciform ligament
4. Abdominal organ
5. Renal

SYSTEMIC VEIN

Paraumbilical
Vein
Veins of Sappey
Splenic vein

Middle & Inferior

Hemorrhoidal Vein

Rectal varices

Umbilical circulatn
of fetus

Caput Medusa

Diapragmatic
Lumbar vein

Prominent veins

Left Renal vein

Not known

Porto-systemic Anastomosis

Hepatic Encephalopathy
Cause
Precipitating

Factors

Daignosis
Clinical

Grading
Management

Spontaneous Bacterial Peritonitis

Difference

from secondary
bacterial peritonitis
Mixed anaerobic flora
Presentation
Diagnosis
Treatment
Prophylaxis

Hepato-renal Syndrome
Diagnostic

criteria
S.Creatinine > 1.5 mg/dl / GFR < 40ml/min
Failure to improve with volume expansion
Avid Sodium retention < 20mmol
Hyponatremia
Rule out Volume loss/Nephrotoxic Drugs
Anatomically normal kidneys.
No Hematuria/Proteinuria
Vasopressin.
Liver transplant.

Hepato-pulmonary syndrome
Orthodeoxia
Concept
Prognosis

of Pa-aO2 gap.

Orthoptic Liver transplant

Indications for liver transplantation are :

In children Biliary atresia, Neonatal hepatitis, Antitrypsin

deficiency , Inherited disorders of metabolism, Wilsons
disease, Glycogen storage disorders.

In adults, Primary biliary cirrhosis, Viral hepatitis, drug/toxin

induced hepatitis and end stage liver disease.

Contraindications for liver transplantation :

Absolute : HIV, Malignancy

Relative : Age > 70, Renal failure, immunosuppression

Types of donor organ

Cadaver donor transplant : demand >>> supply.
Unpredictable. Hence always done in emergency.
Transport issues.
Can be split into potential 2 (1 adult + 1 child) rarely.

Living-donor transplantation : can reduce waiting time

and cold-ischemia time.
done under elective, rather than emergency,
circumstances;
and may be lifesaving in recipients who cannot afford to
wait for a cadaver donor.

Success measured as 1-year survival has improved

from_30% to_85% today.

Pancreatitis

Pancreatitis is the inflammation of the pancreas.

Phyiology : Pancreas is a exocrine gland as well as an endocrine

gland.
Pancreas have a large functional reserve so as to maintain normal
function till >90% is destroyed. Even sensitive tests (Secretin stimulation)
detect only when >60% damage has occurred. Moreover the
symptoms of disease are very vague and non-specific.

Epidemiology : Pancreatic insufficiency is found in 0.4-5% of autopsy

studies.
However true incidence and prevalence is very difficult due to above
mentioned reasons.
Incidence increases with age i.e. > 15% have some problem > 65
years.
Common in the male gender, however this is changing and closely
matches alco

 Pancreatitis

is of two types depending on

the duration viz.

Acute

pancreatitis

Chronic

pancreatitis

<

2 weeks

>
6 weeks
more often months

Etiology : remember the following acronym:

A

D
E
Others -

Alcohol
Anatomic pancreatic division, Annular pancreas
Auto-immune Sjogrens syndrome
Bile stones / Gallstones
Biliary duct strictures
Carcinoma
Cholestrol - Hypertriglyceridemia
Connective tissue disorder - TTP
Drugs Anti-HIV , Valproate, Sulfonamides
ERCP
Post surgery
Trauma
Renal failure
Infections Coxsackie, Mumps

Hyperamylasemia

Test 3
21.

Most common presenting symptom in primary biliary cirrhosis is...

(A) Jaundice
(B) Pruritis
(C)Splenomegaly
(D)Gastrointestinal bleeding

22.

Which of the following statements are Correct of cirrhosis EXCEPT

(A) Antimitochondrial antibodies positive in primary biliary cirrhosis.
(B) In late stage of PSC treatment is liver transplantation.
(C) In advanced stages major blood supply is through hepatic vein.
(D) Elevated lipoprotein-X in PBC.

23.
Which one of the following is not a feature of liver histology in noncirrhotic portal
fibrosis (NCPF)?
(A) Fibrosis in and around the portal tracts.
(B) Thrombosis of the medium and small portal vein branches.
(C) Non-specific inflammatory cell infiltrates in the portal tracts.
(D) Bridging fibrosis

Test 3
24.

A 20 year old boy presented with severe hematemesis. On

examination there was no hepatomegaly, mild splenomegaly
present. On endoscopy esophageal varices were
seen. What is the most probable diagnosis?
(A) Cirrhosis liver
(B) Budd Chiari syndrome
(C) Non cirhotic portal fibrosis
(D) Veno occlusive disease

25.

Which of the following statements is incorrect with regard to

heptorenal syndrome in a patient with wlicirrosis?
(A) The creatinine clearance is > 40 ml/min
(B) The urinary sodium is less than 10 mol/L
(C) The urine osmolality is lower than the plasmaosmolality.
(D) There is poor response to volume expansion.

Test 3
27..
All of the following drugs are used in hepatic encephalopathy,
except....
(A)
Mannitol
(B)
Metronidazole
(C)
Lactulose
(D)
Phenoharbitone
28.

Which of the following is false regarding non-alcoholic fatty liver

(A) Seen in diabetic
(B) Clofibrate is used in treatment.
(C)Commonest cause of cryptogenic cirrhosis
(D) Associated with transaminitis

29.

Reye's syndrome is characterized by all except ....

(A) Viral infection is seen.
(B) Present as deep jaundice
(C) Cerebral edema
(D) Microvesicular fatty infiltration

Test 3
30.
What is the line of management of a case of moderate to severe
hepatic insufficiency with portal hypertension, according to the modified
Pugh's classification?
(A) Sclerotherapy
(B) Orthotopic liver transplantation
(C) Shunt Surgery
(D) Conservative
31.

32.
except

In hereditary spherocytosis, the gall bladder shows....

(A)Mixed stones
(B)Cholesterol stones
(C)Pigment stones
(D)All of the above
Acalculous cholecystitis can be seen in all the following conditions
(A) Enteric fever
(B) Dengue haemorrhagic fever
(C) Leptospirosis
(D) Malaria

Test 3
33.
A patient presents with jaundice, right upper quadrant pain
chills with
high fever, hypotension and mental confusion. The
most likely diagnosis
is...
(A)
Gallstone pancreatitis
(B)
Hepatitis
(C)
Acute suppurative cholangitis
(D)
Amoebic liver abscess
34.

Hemoblia is characterised by all except

(A)
Jaundice
(B)
Biliary colic
(C)
Malena
(D)
Fever

35.
Serum amylase usually becomes elevated in acute
pancreatitis after
(A)
1/2 hrs.
(B)
4-6 hrs.
(C)
24-48 hrs.
(D)
48-72 hrs.

Test 3
36.

Serum amylase level is raised in all except

(A) Acute pancreatitis
(B) Perforation of stomach
(C) Strangulated small intestine
(D) Acute appendicitis

37.

Serum amylase is raised in

(A)
Rubella
(B)
(C)
Mumps
(D)

Measles
Chicken pox

38..
The following can be associated with acute pancreatitis
EXCEPT
(A)
Hyperparathyroidism
(B)
Hyperthyroidism
(C)
Hypercalcemia
(D)
Hypertriglceridemia

Test 3
39.

Which one of the following types of pancreatitis

has the best prognosis?
(A) Gall stone pancreatitis
(B) Alcoholic pancreatitis
(C) Idiopathic pancreatitis
(D) Traumatic pancreatitis

40. How much of the acinar pancreas must be destroyed to

result in steatorrhoea
(A)
10%
(B)
30%
(C)
60%
(D)
90%