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01/11 pulm

Friday, January 11, 2019

12:31 PM
Q 2145
 Postoperative massive PE complicated by cardiogenic shock
o Massive PE = PE w/ hypotension and or acute R. heart strain
o Syncope occurs only in massive PE, segmental PE can have pleuritic CP
o Jugular venous distension on physical and RBBB on ECG are signs of acute R. heart strain
o R. heart strain can progress rapidly to RV dysfunction, decreased return to L heart,
decreased CO, left heart pump failure, and resultant bradycardia ---> cardiogenic
shock and causes CNS effects = dilated pupils and death
o Poor survival
o If time permits, massive PE can be confirmed with CT pulmonary angiography
o Echo has poor sensitivity for segmental PE, massive PE are visible, that allow for rapid
beside diagnosis
o In conjunction with respiratory and hemodynamic support, fibrinolysis is indicated as
treatment, but its contraindicated if surgery within preceding 10 days
o Hypoxemia from PE can cause slurred speech and confusion

Q 4116
Differential diagnosis based on carbon monoxide diffusing capacity of the lung
Obstructive Restrictive pattern Normal
pattern (FEV1/FVC >70% spirometry
(FEV1/FVC predicted, FVC <80%
<70% predicted)

Low DLCO Emphysema  Interstitial lung  Anemia

disease  Pulmonary
 Sarcoidosis embolism
 Asbestosis  Pulmonary
 Heart failure HTN

Normal  Chronic  Musculoskeletal

DLCO bronchitis deformity
 Asthma  Neuromuscular

Increased  Asthma  Morbid obesity  Pulmonary

DLCO hemorrhage
 Polycythemia

 COPD = progressive airflow limitation = chronic bronchitis + emphysema
 Presentations with predominant chronic bronchitis: chronic smoking (≥1pp for at least 20
years), productive cough, dyspnea on exertion, and PFT = obstructive pattern [decreased
FEV1/FVC ratio, decreased FEV1, normal FVC) with normal diffusion capacity of lung for
carbon monoxide
 Chronic bronchitis= productive cough for ≥ 3 months over 2 consecutive years
 Chronic bronchitis has no alveolar and capillary destructions so DCLO normal, CXR shows
prominent bronchovesicular marking and mildly flattening diaphragm, more pronounced
 Emphysema has destruction of interalveolar walls = decreased DLCO, CXR reveals decreased
vascular markings and hyperinflated lungs
Q 4628
If you suspect patient has PE but WELL criteria is 0 / for highly unlikely then do D-dimer assay, if
its ≤500 ng/mL then its not PE = normal, if its greater than 500 then do CT pulmonary
If PE is likely in patient then directly do CT pulmonary angiography, if positive PE confirmed
Q 4617
Asthma severity of patients not on controller medication
Asthma Symptoms Nighttime Indicated
severity frequency/ awakenings therapy
SABA use initiation

Intermittent ≤2 days a ≤2 times a Step 1 SABA prn

week month

Mild >2 days a 3-4 times a Step 2 SABA prn + low-dose

persistent week but not month ICS

Moderate Daily >1 time a Step 3

Persistent week but not Low-dose ICS + LABA
nightly or
Medium dose ICS

Severe Throughout 4-7 times a Step 4 or 5  4 = medium-dose

persistent the day week ICS + LABA
 5 = high-dose ICS +
LABA and consider
omalizumab for
patients with
 6 = high-dose ICS +
LABA + oral
corticosteroids and
omalizumab for
patients with

 condition well controlled on same therapy for 3 months can considered step down
 If very poorly controlled then step up by 1 or 2 steps and a short course of oral prednisone
should be considered

Q 12135
Clinical features of pulmonary hypertension
Classification  Pulmonary arterial hypertension
(WHO group 1)
 Due to left-sided heart disease
(group 2)
 Due to chronic lung disease (eg.
COPD, ILD) (group 3)
 Due to chronic thromboembolic
disease (group 4)
 Due to other causes (eg. Sarcoidosis)
(group 5)

Symptoms  Dyspnea, fatigue/weakness

 Exertional angina, syncope
 Abdominal distension/ pain

Signs  Left parasternal lift, right ventricular

 Loud P2, right-sided S3
 Pan systolic murmur of tricuspid
 JVD, ascites, peripheral edema,

Q 12136
 Right heart catheterization is the most accurate method of measuring pulmonary arterial
pressure, echo is non-invasive provide a reliable estimate and pulmonary HTN if > 30 mm Hg
 Systemic sclerosis = pulmonary HTN --> hyperplasia of the intimal smooth muscle layer -->
increase pulmonary vascular resistance, lung parenchyma not affected then normal FEV1
and FEV1/FVC ratio on PFT

Q 4864
Causes of hemoptysis
Pulmonary  Bronchitis
 Lung cancer
 Bronchiectasis

Cardiac  Mitral stenosis/ acute pulmonary


Infectious  TB
 Lung abscess
 Bacterial pneumonia
 Aspergillosis

Hematologic  Coagulopathy

Vascular  PE
 Arteriovenous malformation

Systemic  Granulomatosis with polyangiitis

disease  Goodpasture syndrome

Other  Trauma
 Cocaine use (inhalation)

 Longstanding smoking and chronic productive cough with recent hemoptysis- is consistent
with chronic bronchitis

Q 10982
Evaluation of subacute (3-8 weeks) or chronic (>8 weeks) cough
 The most common etiology of chronic cough include upper airway cough syndrome
(postnasal drip), GERD, and asthma
 Other cause drugs (ACE), airway disease (non-asthmatic eosinophilic bronchitis, chronic
bronchitis, bronchiectasis, malignancy) and pulmonary parenchymal disease (lung abscess,
interstitial lung disease)
 Chronic cough that worsens overnight and did not improve with antihistamines therapy =
suspect asthma and do spirometry to asses bronchodilator response, if no response to
bronchodilators then methacholine challenge test
 Nocturnal or early morning peak expiratory flow rate measurements can be used to
diagnose patients with only nocturnal symptoms
 An alternate approach to treat empirically with 2-4 weeks of inhaled glucocorticoids, if
cough improves then diagnosis of asthma
Q 4753
 Pleural effusion = Transudates and exudates
 Transudates = imbalance between hydrostatic and oncotic pressure = increases fluid
movement across the capillaries, no further intervention except for treatment directed at
underlying disease
 Exudate = due to pleural and lung inflammation = increased capillary and pleural membrane
permeability, require more extensive diagnostic investigations

o Light criteria defined an exudate as having at least one of the following
 Pleural fluid protein/serum protein ratio > 0.5
 Pleural fluid lactate dehydrogenase (LDH)/ serum LDH ratio > 0.6
 Pleural fluid LDH >2/3 of the upper limit of normal for serum LDH
o Pleural fluid LDH of 252 U/L is > 2/3 of the upper limit of normal for serum LSH (2/3* 90
= 60 60 U/L)
o Low pleural glucose= exudative pleural effusion, <60 mg/dL is usually d/t Rheumatoid
pleurisy, complicated parapneumonic effusion or empyema, malignant effusion,
tuberculous pleurisy, lupid pleurisy, or esophageal rupture
o Gluc < 30 mg/dL in particular suggest an empyema or rheumatic effusion
o Glucose concentration in empyema is decreased due to high metabolic activity of
leukocytes (and or bacteria) in fluid

Q 3859
 Early, effective anticoagulation decreases the mortality risk of acute PE and should be
considered in patients without absolute contraindication (hemorrhagic stroke, massive GI
 Peptic ulcer disease is not absolute contraindication to anticoagulation
 Diagnosis of PE confirmed with CT angiography

Q 4613
 Sudden-onset dyspnea, chest pain, and tachycardia with no consolidation on chest imaging
suggests PE, it can cause pleural effusion (typically small ,exudative and bloody), and pain
due to pleural irritation

Q 3776
Clinical presentation of Pancoast tumors
 Shoulder pain (most common)
 Horner syndrome (ipsilateral ptosis, miosis, exophthalmos & anhidrosis) from involvement
of paravertebral sympathetic chain & inferior cervical ganglion
 C8-T2 neurological involvement
o Weakness &/or atrophy of intrinsic hand muscles
o Pain & paranesthesia's of 4th & 5th digits, medial arm & forearm
 Supraclavicular lymph node enlargement
 Weight loss
 MCC of Pancoast tumors are squamous cell lung carcinoma and adenocarcinoma
o Strongest risk factor is smoking

Q 12459
Pulmonary function tests in chronic lung disease
Asthma COPD Interstitial lung PA HTN Restrictive
disease chest wall

TLC Normal/↑ ↑ ↓ Normal ↓

FEV1/FVC ↓ ↓ Normal Normal Normal

DLCO Normal/ ↑ ↓ ↓ ↓ Normal

 Slowly progressive dyspnea, dry cough, and fine crackles in the absence of smoking history =
interstitial lung disease d/t idiopathic pulmonary fibrosis
 Commonly presents at ag 50-70, most patients have h/o smoking
 In addition to fine bibasilar crackles, patients in advanced disease may develop end-
inspiratory squeaks, digital clubbing, and an abnormal S2 (loud P2, fixed, splits S2) due to
pulmonary HTN
 Evaluated history ; autoimmune disease, use of associated medications (amiodarone),
occupational exposures, and therapeutic radiation
 CXR = nonspecific reticular infiltrates, chest CT finding peripheral or basilar reticular
infiltrates and honeycombing
 If imaging is non diagnostic or the clinical picture is atypical a biopsy can confirm the

Q 4631
Parapneumonic effusions
Uncomplicated Complicated

Etiology Sterile exudate in Bacterial invasion

pleural space of pleural space

Pleural fluid  pH≥7.2  pH<7.2

analysis  Glucose ≥60  Glucose <60
mg/dL mg/dL
≤50,000/mm3 >50,000/mm3

Pleural fluid Negative Negative

gram stain &

Treatment Antibiotics Antibiotics +


Q 4114
 Histoplasma capsulatum is the mc endemic mycosis in USA
 Exposure occurs primarily in the mid-west (particularly the Ohio and Mississippi river valleys)
and, to a lesser extend, the northeast
 Soil contaminated with bat or bird droppings
 Symptoms usually present 2-4 weeks after exposure with subacute fever, chills, malaise,
HA, myalgias, and dry cough
 CXR mediastinal or hilar lymphadenopathy with focal, reticulonodular, or milliary infiltrates
 Diagnosis is usually made with histoplasma antigen testing of the urine or blood, plus
 Tissue diagnosis often reveals granulomas with narrow-based budding yeasts
 Most cases resolved over weeks without intervention, if severe give oral itraconazole or IV
liposomal amphotericin B
Q 4663
OSA can exist alone or combo with obesity hypoventilation syndrome (OHS)
 Patients with OSA in the absence of OHS experience hypoventilation only at night with
transient hypoxia and hypercapnia that resolve while awake
 Those with OHS, physical restriction of the thoracic cavity caused by excess thoracic tissue
continues throughout the day, = chronic hypoxia and hypercapnia
o In an effort to maintain normal pH, the kidneys increase bicarbonate retention and
decrease chloride reabsorption (in intercalated cell of distal nephron) to create
compensatory metabolic alkalosis
o Can develop HTN with eventual co pulmonale (R heart failure), which can cause
peripheral edema
o OHS can have increase erythropoietin secretion and a compensatory erythrocytosis =
 Systemic HTN is common in both isolated OSA and comorbid OSA/OHS, possibly due to
hypoxic triggering of the sympathetic nervous system and increased levels of circulating

Q 4569
 An acute exacerbation of COPD, characterized by a change in ≥1 of the following:
 Cough severity or frequency
 Volume or character of sputum production
 Level of dyspnea
 Physical examination: wheezing, tachypnea, prolonged expiration, and use of accessory
respiratory muscles
 JVD maybe observed, especially during expiration, due to increase intrathoracic pressure
 Hyperinflation can be seen in CXR
 URI is the MC trigger of COPD exacerbation

Q 4689
 Hodgkin lymphoma is curable lymphoma that tend to affect young patients, those treated before
age 30 can develop secondary malignancies from chemo/radiation
 18.5 fold increased risk of developing a second cancer in HL
 The MC secondary solid tumor malignancies are lung (especially in smokers), breast, thyroid,
bone and GI (colorectal, esophageal, gastric tumors)
 Have increased risk of developing subsequent acute leukemia or non-HL

Q 4566
Acute bronchitis
Etiology  Preceding respiratory illness (90%

Clinical  Cough for >5 days to 3 weeks (+/-

presentations purulent sputum)
 Absent systemic findings (eg.
Fever, chills)
 Wheezing or rhonchi, chest wall

Diagnosis &  Clinical diagnosis, CXR only when

treatment pneumonia suspected
 Symptomatic treatment (NSAID's
& or bronchodilators)
 Antibiotics not recommended

Q 4166
 Elderly patient with fever, cough, tachypnea, leukocytosis, and CXR evidence of lobar infiltrates =
 Pneumonia classification
 Community-acquired- develops in non hospitalized setting
 Hospital-acquired- develops ≥48 hrs of admission to the hospital
 Ventilatory-acquired- develops ≥ 48 hrs after endotracheal intubation
 MCC of community acquired = S. pneumoniae

Q 3026
 Beta-2 agonists like albuterol reduce serum potassium levels by driving potassium into cells
 Clinically significant hypokalemia can result, causing muscle weakness, arrhythmias, and ECG
 Other common SE of beta-2 agonists include tremor, headache, and palpitations
 Obtaining a serum electrolyte panel would be helpful here to confirm and assess the severity of
this patient's hypokalemia

Q 4568
 Approximately 40% of pneumonias are associated with pleural effusions
 Most a small, free-flowing, sterile and resolve with Abx
 If bacteria is persistently crossing from infection pulmonary parenchyma to pleural space, a
complicated parapneumonic effusion or an empyema can develop
 Both empyema and complicated parapneumonic effusions are marked by large, often loculated
effusion and typical thoracentesis abnormalities (low pH, low glucose); unlike complicated
parapneumonic effusions, empyema's also have frank pus or bacteria (GM stain) in pleural space
 The risk of this increases in immunocompromised patients

Q 4536
 Acute pancreatitis can be complicated by acute respiratory distress syndrome (ARDS) in ~15%
 IN ARDS, mechanical ventilation improves oxygenation by providing an increased fraction of
inspired oxygen (FiO2) and positive end-expiratory pressure (PEEP) to prevent alveolar collapse
 The goal is to maintain arterial partial pressure of oxygen (PaO2) at 55-80 mm Hg, = >88%-95%
 Immediately following intubation, a high FiO2 ≥60% is usually provided and then adjusted
according to first ABG analysis
 The PaO2, an important measure of oxygenation, is influenced mainly by FiO2 and PEEP
 The arterial partial pressure of CO (PaCO2) a measure of pulmonary minute ventilation, is
affected mainly by the respiratory rate and tidal volume
 Prolonged, high FiO2 can cause oxygen toxicity as it can lead to formation of proinflammatory
oxygen free radicals and predispose to atelectasis and alveolar nitrogen is displaced, resulting in
worsened oxygenation
 There is not strict cut-off but FiO2 <60% is considered generally safe

Q 4575
Symptoms/signs of ankylosing spondylitis
 Low back pain (onset age <40, insidious onset, improves with exercise but not with rest, pain at
 Hip & buttock pain
 Limited chest expansion & spinal mobility
 Enthesitis (inflammation at the site of insertion of a tendon to the bone)
 Systemic symptoms (fever, chills, fatigue, weight loss)
 Acute anterior uveitis (unilateral pain, photophobia, blurry vision)

 Ankylosing spondylitis is chronic inflammatory disease of the axial skeleton characterized by

progressive stiffness of the spine, sacroiliitis on radiographs, and positive serology of HLA-B27 in
the majority of patients
 Some patients also develop extraarticular features, such as anterior uveitis, IBD, and cardiac
involvement with aortic regurgitation
 They develop limitations in lung expansion due to diminished chest wall and spinal mobility
 PFT may reveal a mildly restrictive pattern with reduced vital capacity and total lung capacity
but normal FEV1/FVC ratio
 Functional residual capacity and residual volume are normal or increased due to fixation of the
rib cage in an inspiratory position

Q 4596
 Solitary pulmonary nodule = round opacity up to 3 cm in diameter with surrounded paranchyma
 By convention there must be no associated pleural effusion, adenopathy, or atelectasis
 First step is to compare previous x-rays or scans
 If is stable size and appearance for 2 to 3 years has low malignancy risk and the patient may be
given reassurance without further workup
 Ground-glass lesions have a higher malignancy risk and likely require yearly assessment, even with
stable appearance and size
 Unstable or new lesions require further testing for malignancy
 Nodules <0.8 cm with smooth margins are less likely to be malignancy; nodules ≥2 cm with
irregular or speculated margins are more likely to be malignant
 Other factors are age and smoking status

 Patients age >60 have higher risk, current smokers have increasing malignancy risk
 CT scan is more sensitive than CXR, also can detect other smaller nodules that may present
 If CT scan findings are suspicious for malignancy, biopsy followed by likely surgical excision
should be performed
 Lesions that appear less likely to be malignant on CT scans can be followed with serial CT scans for
2-3 years to monitor for growth

Q 4036
 Glucocorticoid use causes a leukocytosis due to the following:
 Mobilization of marinated neutrophils into the bloodstream (predominant mechanism):
marinated neutrophils are attached to the endothelium of blood vessels; glucocorticoid-
induced mobilization of these neutrophils leads to higher number of circulating neutrophils
 Stimulation of release of immature neutrophils from the bone marrow (as evidenced by
the 3% band forms in this patient)
 Inhibition of neutrophil apoptosis
 In contrast, glucocorticoids decrease the number of circulating lymphocytes and eosinophils
through a combination of increased apoptosis, increased emigration into the tissues and
decreased production

Q 4087
 Diagnostic thoracentesis is the preliminary investigation of choice in the management of pleural
effusion, except in patients with classic signs and symptoms of CHF, where a trial of the diuretic
is warranted
 Diagnostic thoracentesis is beside, minimally invasive procedure that permits fluid to be rapidly
sampled, visualized and examined microscopically and quantified
 Lung carcinoma, breast carcinoma, and lymphoma are the three tumors that cause
approximately 75% of all malignant pleural effusion

Q 4119
 Aspiration pneumonia typically develops over the course of days and causes low grade fever,
dyspnea, and productive, foul-smelling cough, it may be complicated by necrosis and abscess
 The location of the infiltrate is gravity dependent and differs according to the patients position at
the time of aspiration
 In supine patients, the posterior segments of the upper lobes and superior segments of the
lower lobes are most affected
 Broad-spectrum Abx with good anaerobic coverage (clindamycin, amoxicillin-clavulanate) are
mainstay of treatment

Q 4065
 Aspirin-exacerbated respiratory disease is a non-IgE mediated reaction that results from aspirin-
induced prostaglandin/leukotriene misbalance
 It is most often seen in patients with a history of asthma or chronic rhinosinusitis with nasal
 It is characterized by bronchospasm and nasal congestion following aspirin ingestion
 Treatments includes avoidance of NSAIDs, desensitization if NSAIDs are required, and the use of
leukotriene receptor antagonists (Montelukast)

Q 3474
Signs &  Cough with daily mucopurulent
symptoms sputum production
 Rhinosinusitis, dyspnea,
 Crackles, wheezing

Pathophysiology  Infectious insult with impaired


Etiology's  Airway obstruction (eg. Cancer)

 Rheumatic disease (eg. RA,
Sjogren), toxic inhalation
 Chronic or prior infections (eg.
Aspergillosis, mycobacteria)
 Immunodeficiency
 Congenital (CF, alpha-1-
antitrypsin deficiency)

Evaluation  HRCT scan of the chest (needed

for initial diagnosis)
 Immunoglobulin quantification
 CF testing, sputum culture
(bacteria, fungi & mycobacteria)
 Pulmonary function testing

 Impaired immune defense contributes to the development of bronchiectasis. Impaired muco-

ciliary clearance in CF typically leads to bronchiectasis located predominantly in the upper lobes
 The diagnosis is made using high resolution CT scan of the chest

Q 4052
 Diagnosis of mediastinal tumors is based on CXR and CT scans
 A bronchogenic cyst maybe seen on AP CXR
 The diagnosis is best made with CT scan
 Bronchogenic cysts are located in the middle mediastinum and are benign entities
 Other middle mediastinal masses include: tracheal tumors, pericardial cysts, lymphoma, lymph
node enlargement, and aortic aneurysms of the arch

 Thymoma is usually found in the anterior mediastinum

 All neurogenic tumors are located posterior mediastinum

Q 4489
Obesity hypoventilation syndrome OHS
Diagnostic  Obesity with BMI ≥30
criteria  Awake daytime hypercapnia
(PaCO2>45 mm Hg)
 No alternate cause of

Workup  ABG on room air (hypercapnia,

normal A-a gradient)
 No intrinsic pulmonary disease on
 Restrictive pattern on PFTs
 Normal TSH
 Polysomnography

Treatment  Nocturnal positive-pressure

ventilation as first line therapy
 Weight loss (bariatric surgery)
 Avoidance of sedative medication
 Respiratory stimulants
(acetazolamide) as last resort

Q 3031
 Chronic shortness of breath, productive cough, and evidence of destruction of lower lung lobes
likely has alpha-1 antitrypsin (AAT) deficiency = pan-acinar emphysema
 Smoking-induced centri-acinar (centrilobular) emphysema most commonly causes disease in the
upper lobes of the lungs, whereas the pan-acinar emphysema of AAT deficiency classically results
in greater destruction of the lower lobes
 Smokers presents in their 30s and non-smokers presents in the 40s
 AAT deficiency is frequently associated with liver disease, most commonly resulting in neonatal
hepatitis, cirrhosis, or hepatocellular carcinoma
 AAT deficiency should be considered in 1) COPD at a young age (≤45), 2) COPD with minimal or
no smoking history, 3) basilar-predominant COPD, or 4) a history of unexplained liver disease
 Confirmed by measuring serum AAT levels, and PFT
 Treatment IV supplementation with pooled human AAT

Q 11669
Aspiration syndromes
Pneumonia Pneumonitis

Pathophysiology  Lung  Lung parenchyma

parenchyma inflammation
infection  Aspiration of gastric acid
 Aspiration of with direct tissue injury
upper airway
or stomach

Clinical features  Present days  Present hours after

after aspiration event
aspiration  Range from no
event symptoms to non-
 Fever, cough, productive cough,
increase decrease O2, respiratory
sputum distress
 CXR infiltrate  CXR infiltrates (one or
in dependent both lower lobes)
lung segment resolve without Abx
 Can progress
to abscess

Management  Abx:  Supportive (no Abx)

clindamycin or
beta-lactam &

Q 3400
Triggers  Food (nuts, shellfish)
 Medical (b-lactam antibiotics)
 Insect stings

Clinical  Cardiovascular
manifestation  Vasodilation -->
hypotension & tissue
 Tachycardia
 Respiratory
 Upper airway edema -->
stridor & hoarseness
 Bronchospasm --> wheezing
 Cutaneous
 Urticarial rash, pruritus,
 Gastrointestinal
 Nausea, vomiting,
abdominal pain

Treatment  Intermuscular epinephrine

 Airway management & volume
 Adjunctive therapy
(antihistamines, glucocorticoids)

 Patients usually have a prior exposure to the offending substance resulting in preformed IgE
antibodies that create a widespread type-1 hypersensitivity reaction on repeat exposure
 Patients with history of atopy (asthma, eczema) are at higher risk
 The alpha-1 receptor stimulation of epinephrine causes vasoconstriction resulting in decreased
tissue edema as well as increased blood pressure and improved organ perfusion

Q 3045
Clinical features of interstitial lung disease
Common etiology  Sarcoidosis, amyloidosis, alveolar proteinosis
 Vasculitis (granulomatosis with polyangiitis)
 Infections (fungal, tuberculosis, viral
 Occupational & environmental agents (eg.
Silicosis, hypersensitivity pneumonitis)
 Connective tissues disease (eg. SLE,
 Idiopathic pulmonary fibrosis, interstitial
 Cryptogenic organizing pneumonia

Clinical  Progressive exertional dyspnea or persistent

presentations dry cough
 Pulmonary finding due to other underlying
conditions (eg. Silicosis, connective tissue
 >50% of patients with significant smoking
 Lung examination with fine crackles during
mid-late inspiration, possible digital clubbing

Laboratory/imaging  CXR can show reticular or nodular opacities

 High resolution chest computed tomography
HRCT usually show fibrosis, honeycombing, or
traction bronchiectasis
 PFT: Normal or ↑FEV1/FVC ratio, ↓DLCO,
 Resting arterial blood gas can be normal or
show mild hypoxemia
 Exertion usually causes significant hypoxemia
due to V/Q mismatch

 In idiopathic pulmonary fibrosis there is excessive collagen deposition in ECM around the alveoli,
leading to scarring reducing the TLC, FRC, RV, FEV1 decreased, FVC decreased but ratio normal or

Q 8818
Pulmonary auscultation examination findings
Condition Breath sounds Tactile Percussion Mediastinal
fremitus shift

Normal lung Bronchovesicular Normal Resonance None

(hilar), vesicular

Consolidation Increased Increased Dullness None

(lobar (crackles &
Pneumonia) egophony

Pleural effusion Decreased or Decreased Dullness Away from

absent effusion (if

Pneumothorax Decreased or Decreased Hyper resonant Away from

absent tension

Emphysema Decreased Decreased Hyper resonant None

Atelectasis Decreased or Decreased Dullness Toward

(mucus absent atelectasis (if
Plugging) large)

 Pleural effusion insulate sounds originating from the lung tissues. Physical examination of patients
with a pleural effusion typically shows decreased breath sounds, decreased tactile fremitus, and
dullness to percussion over the effusion.

Q 4053
 Common cause of pleural effusion
 Transudate
o Cirrhosis
o Nephrotic syndrome
o Peritoneal dialysis
 Exudate
o Infections
o Malignancy
o Connective tissue disease
o Inflammatory disorder
o Movement of fluid from abdomen to pleural space
o Coronary artery bypass surgery
o Pulmonary embolism (usually)
 CHF= transudate effusion = bilateral (61%), unilateral R>L

 The elevated pressure from left ventricular end diastole and the left atrium transmits back to the
alveolar capillaries to increase hydrostatic pressure
 Normal pleural fluid pH = 7.60, transudate gives ph of 7.4-7.55, and exudate gives ph of 7.30-7.45
 Pleural fluid pH <7.30 (with normal arterial pH and low pleural glucose) is usually due to increased
acid production by pleural fluid cells and bacteria (empyema) or decreased hydrogen ion efflux
from the plueral space (pleuritis, tumor, pleural fibrosis)

Q 4017
 The most efficient test to differentiate asthma and COPD is spirometry before and after
administration of a bronchodilator (usually albuterol).
 Patients with asthma should show significant reversal (>15% increased in forced expiratory
volume in 1 second) is airway obstruction after administration of bronchodilator
 Patients with COPD may have partial reversibility with bronchodilators, but restoration of normal
airflow after administration of bronchodilator effectively rules out COPD

Q 4562
 Fever, respiratory distress, hypoxemia, and bilateral opacities = ARDS
 It is an inflammatory condition associated with infections, trauma, or other conditions (massive
transfusion, pancreatitis)
 Lung injury causes release of proteins, inflammatory cytokines and neutrophils into the alveolar
space., leads to leakage of bloody and proteinaceous fluid into the alveoli, alveolar collapse due to
loss of surfactant, and diffuse alveolar damage, which results in alveolar collapse and impaired gas
exchange due to physiologic shunting and increased physiologic dead space
 Arterial blood gas results show hypoxemia O2 <60 mm Hg, reflecting inadequate oxygenations
 In general, oxygenation may be improved by increasing either the fraction of inspired oxygen
FiO2 or PEEP proved by mechanical ventilatory
 PEEP prevents alveolar collapse during respiratory cycles and may also reopen some alveoli
that have already collapsed, reducing shunting. High PEEP approaches may improve
mortality in patients with sever ARDS
 FiO2 is already high in the patients , FiO2 s usually weaned to <60% as quickly as possible
because prolonged high FiO2 increases the risk of pulmonary oxygen toxicity (O2 radicles)
 Therefore, in patients requiring high levels of FiO2, PEEP levels should be increased to
allow for reduction in the FiO2 as oxygenation improves

Q 3050
 Short-acting beta-adrenergic agonists administered 10-20 minutes before exercise are the first-
line treatment for exercise-induced bronchoconstriction if required only a few times a weeks
(less than daily)
 Inhaled corticosteroids or anti-leukotriene agents can be used in patients who exercise daily

Q 2298
 Patients presenting with an extensive smoking history and evidence of COPD and digital clubbing
on physical exams.
 Hypertrophic osteoarthropathy (HOA) is a condition where digital clubbing is accompanied by
sudden-onset arthropathy, commonly affecting the wrist and hand joints
 Hypertrophic pulmonary osteoarthropathy (HPOA) is a subset of HOA where the clubbing and
arthropathy are attributable to underlying lung disease like lung cancer, TB, bronchiectasis, or

 Given this patient's smoking history, lung cancer should be of particular concerns
 CXR is appropriate initial study if suspecting HPOA

Q 4105
 Patients with an acute asthma exacerbation usually have respiratory alkalosis with a low PaCO2
due to hyperventilation
 A normal or elevated PaCO2 is an alarming and extremely important finding that suggests
impeding respiratory failure

Q 4643
 Pulmonary pathology may lead to the SIADH, which is characterized by hypotonic hyponatremia in
an euvolemic patients.
 Infusion of normal saline may worsen hyponatremia in patients with SIADH

Q 2997
Invasive aspergillosis Chronic pulmonary

Risk factors  Immunocompromised  Lung disease/damage

(neutropenia, (cavitary tuberculosis)
glucocorticoids, HIV)

Finding  Triad of fever, chest  >3months: weight loss

pain, hemoptysis (>90%), cough,
 Pulmonary nodules hemoptysis, fatigue
with halo sign  Cavitary lesion +/- fungus
 Positive cultures ball
 Positive cell wall  Positive Aspergillus IgG
biomarkers serology
(galactomannan, beta-

Management  Voriconazole +/-  Resect aspergilloma (if

caspofungin possible)
 Azole medication
 Embolization (if severe

 Invasive aspergillosis primarily affects immunocompromised patients and typically cause the triad
of fever, pleuritis chest pain, an hemoptysis.
 CT scan often reveals pulmonary nodules with surrounding ground-glass opacities (halo sign)
 Treatment usually requires a combination of voriconazole and an echinocandin (caspofungin)

Q 4297
Characteristic finding of co pulmonale
Common  COPD (most common)
etiology's  Interstitial lung disease
 Pulmonary vascular disease

Symptoms  Dyspnea on exertion, fatigue,

 Exertional syncope (due to ↓ CO)
 Exertional angina (due to ↑
myocardial demand)

Examination  Peripheral edema

 ↑ Jugular venous pressure with
prominent a wave
 Loud S2
 Right-sided heave
 Pulsatile liver from congestion
 Tricuspid regurgitation murmur

Imaging  ECG: partial or complete RBBB, right

axis deviation, RVH, right atrial
 Echo: pulmonary HTN, dilated right
ventricle, tricuspid regurgitation
 Right heart catheterization: Gold
standard for diagnosis showing
right ventricular dysfunction,
pulmonary HTN, & no left heart
 CXR: enlarged central pulmonary
arteries and loss of retrosternal air
space due to right ventricular

 End-stage cor pulmonale may present with Hypotension, tachycardia and other signs of
cardiogenic shock due to decreased stroke volume
 Cor pulmonale refers to isolated Right-sided heart failure from pulmonary hypertension, most
commonly due to COPD
 Sighs of RHF include JVD, increased intensity of P2 (pulmonic components of the 2nd heart sound),
right ventricular heave, hepatomegaly, dependent pitting edema, and possible ascites.

Q 2632
 SCC of lung = anorexia, constipation increased thirst, and easy fatigability, and lab studies are
consistent with hypercalcemia
 A hilar mass on CXR film of a smoker is most probably a lung caner

 Hypercalcemia usually results from the effects of parathyroid hormone-related protein (PTHrP),
which is similar in nature to PTH in the receptor binding area
 Binding to PTH receptor results in increased calcium resorption from the bones and increased
renal calcium resorption in the distal tubule
 Hypercalcemia in such a setting may result from metastatic involvement of the bone and usually
develops as a late complication of the cancer
 Small cell carcinoma of the lung usually causes other paraneoplastic syndromes such as ACTH
production and SIADH

Q 3433
 The management of ARDS involves avoiding complication of mechanical ventilation by using lung
protective strategies such as low tidal volume ventilation (LTVV)
 LTVV results in lower pulmonary pressure, decreasing the likelihood of over distending alveoli
 In addition, it improves mortality in patients with ARDS

Q 3958
 Hypovolemia is a common cause of orthostatic hypotension and orthostatic syncope, especially in
elderly patients
 Due to decreased renal perfusion and activation of renin-angiotensin-aldosterone system,
decreased urine sodium is usually present in patients with hypovolemia

Q 3579
 Renal and pulmonary finding together suggest a diagnosis of Goodpasture's disease, a condition
most common in young adult males.
 Renal findings in Goodpasture's disease include nephritic-range proteinuria (<1.5 g/day), acute
renal failure, and urinary sediment with dysmorphic red cell and red cell casts
 Pulmonary findings include SOB, cough, hemoptysis caused by pulmonary hemorrhage.
 Systemic symptoms (fever, weight loss, arthralgias) are uncommon
 The underlying cause is formation of antibodies to the alpha-3 chain of type IV collagen, a protein
expressed most strongly in the glomerular and alveolar basement membranes.
 Renal biopsy demonstrating linear IgG deposition along the glomerular basement membrane on
immunofluorescence is diagnostic

Q 4716
 Underlying malignancy (prothrombotic state) and acute presentation of dyspnea, chest pain,
tachycardia, hypoxia and clear lung are high suggestive of PE
 Acute massive PE can present with syncope and hemodynamic collapse
 Examination can show an accentuated (loud) pulmonic component of the second heart sound
and elevated central venous pressure (high JVP)
 Acute massive PE results in abrupt increases in pulmonary vascular resistance and subsequently,
right ventricular pressures
 Elevated RV pressure can increase RV wall tension, cardiac muscle stretching, and RV dilation
 This increases RV myocardial O2 demand and decreases coronary artery perfusion, which causes
supply/demand mismatch and RV ischemia
 Consequent RV dysfunction can lead to an inability to pump blood through the pulmonary
circulation, decreased venous return to the left atrium, decreased CO, and potential
hemodynamic collapse

 Bedside echo can show bowing of the septum into the left ventricle (due to RV pressure
exceeding left ventricular diastolic pressure) and RV free-wall hypokinesis with sparing of the apex
 The presence of RV dysfunction, along with elevated BNP and troponin levels, is associated with
increased mortality risk

Q 4665
 Decreased alveolar elasticity in COPD disease causes lung hyperinflation, which results in
increase TLC, FRC, and RV, as well as diaphragmatic flattening
 The flattened diaphragm has more difficulty contracting to expand the thoracic cavity, resulting in
increased work of breathing

 Fever, pleuritic chest pain, hypoxemia, and dullness to percussion with bronchial breath sounds in
the left lung field are consistent with acute pneumonia
 Alveolar consolidation in pneumonia causes markedly impaired alveolar ventilation in the affected
portion of the lung
 This results in hypoxemia due to right to left intrapulmonary shunting of blood and extreme
ventilation (V)/perfusion (Q) mismatch (V~0)
 In the normal lung of an upright patients, V and Q are highest in the bases of the lung as gravity
creates hydrostatic pressure acting on both air and blood
 When this patient is lying on the left side, gravity induces an increase blood flow to the left lung,
where there is markedly reduced V due to alveolar consolidation
 The result is more profound V/Q mismatch (V remains approximately zero, but Q increase),
increased right-to-left intrapulmonary shunting, and worsening hypoxemia
 The opposite occurs when the patients is lying on his right side (decrease in the Q to the are of
alveolar consolidation), leading to more favorable V/Q mismatch and improvement in hypoxemia

Q 4200
Manifestation of sarcoidosis
Pulmonary  Bilateral hilar adenopathy
 Interstitial infiltrates

Cutaneous  Papule, nodular, or plaque-like-

 Erythema nodosum

Ophthalmologic  Anterior uveitis (iridocyclitis or

 Posterior uveitis
 Keratoconjunctivitis sicca

Reticuloendothelial  Peripheral lymphadenopathy

 Hepatomegaly
 Splenomegaly

MSK  Acute polyarthritis (especially

 Chronic arthritis

Cardiovascular  Atrioventricular block
 Dilated or restrictive

CNS/endocrine  Facial nerve palsy

 Central diabetic insipidus
 Hypercalcemia

Lofgren syndrome  Erythema nodosum

 Hilar adenopathy
 Migratory polyarthralgia
 Fever

 Sarcoidosis is frequently detected incidentally on chest x-ray, and bilateral hilar adenopathy is the
first manifestation of disease in 50% of patients
 It can also present with symptoms of cough, dyspnea, fever, fatigue, and weight loss
 Definitive diagnosis requires consistent radiographic and clinical findings, and a biopsy
demonstrating noncaseating granulomas
 Bronchoscopy with transbronchial biopsy is often performed to obtain tissue diagnosis
 If there is evidence of systemic involvement, more accessible sites such as peripheral lymph nodes
or cutaneous lesions can be biopsied,
 Patients with incidental bilateral hilar adenopathy are typically monitored without biopsy unless
symptoms develop

Q 4772
 An acute massive pulmonary embolism can present initially with syncope and shock.
 Right heart catheterization will show elevated right atrial and pulmonary artery pressure along
with normal pulmonary capillary wedge pressure

Q 3874
 Mitral stenosis is most commonly due to rheumatic heart disease and presents with gradual and
progressively worsening dyspnea or orthopnea
 A.Fib is a common complication and can cause rapid decompensation in previously asymptomatic
 Longstanding mitral stenosis can cause severe left atrial enlargement leading to an elevation of
the left main bronchus or chest radiography

Q 3016
 Hypersensitivity pneumonitis (HP) is inflammation of the lung parenchyma caused by antigen
 Acute episodes present with cough, breathlessness, fever, and malaise that occur within 4-6 hrs of
antigenic exposure
 Chronic exposure may cause weight loss, clubbing, and honeycombing of the lung
 The cornerstone of HP management is avoidance of responsible antigen

Q 4667
 The only therapies proven to prolong survival in patients with COPD are smoking cessation,
supplemental O2, and lung reduction surgery in certain patients

 The mainstays of treatment are inhaled bronchodilators, especially anti-cholinergic medication
like ipratropium and tiotropium
 Anti-muscarinic agents maybe combined with short-acting beta agonists like albuterol
 Inhaled steroids and long-acting beta agonists maybe used for patients with more severe COPD

Q 4131
 Progressive hypoxemia is common in patients with advanced COPD, and studies have shown
survival benefit of long-term home oxygen therapy LTOT in those with significant chronic
 The criteria for initiating LTOT in patients with COPD include:
1. Resting arterial oxygen tension (PaO2) ≤55 mm Hg or pulse oxygen saturation (SaO2) ≤88%
on room air
2. PaO2 ≤59 mm Hg or SaO2 ≤89% in patients with cor pulmonale, evidence of right heart
failure, or hematocrit >55%
 The dose of supplemental oxygen should be titrated so that SO2 is maintained at >90% during
sleep, normal walking and at rest
 Survival benefits of home oxygen therapy are significant when it is used for ≥15 hrs a day

Q 2919
 Young patient with chronic dyspnea on exertion, decreased breath sounds, slight liver function
test (LFT) abnormalities, and a family history of cirrhosis likely has alpha-1 antitrypsin (AAT)
 AAT deficiency, a codominant genetic disease, presents similarly to other forms of COPD with
chronic productive cough, dyspnea, wheezing, and recurrent respiratory infections.
 AAT deficiency can also affect the livers (neonatal hepatitis, HCC) and skin (panniculitis)
 Patients with liver disease maybe asymptomatic up until the point of end-stage disease, and
cirrhosis is the 2nd most common cause of death in these patients
 AAT deficiency should be considered in a number of situations, including patients with COPD at a
young age (<45), COPD with minimal or no history of smoking, or a family history of emphysema
or liver disease
 Diagnosis is confirmed with measurement of serum AAT levels and should also include PFT
 Treatment includes IV supplementation with human AAT in addition to bronchodilators and

Q 4730
 Systemic glucocorticoids decrease inflammation associated with COPD exacerbation, improve
lung function and hypoxemia, and have been shown to decrease risk of relapse, treatment
failure, and length of hospital stay
 They usually administered for 5 days as oral prednisone or intravenous methylprednisolone

Q 2300
Classic findings of PE on ECG (prominent S in lead I, Q in lead III, and inverted T in lead III [S1Q3T3)
or CXR (Hampton hump, westermark sign)

Q 4718
 Supplemental oxygen in patients with advanced COPD can worsen hypercapnia due to
combination Of increased dead space perfusion causing ventilation perfusion mismatch,
decreased affinity of oxyhemoglobin for CO2, and reduced alveolar ventilation.

 The goal oxyhemoglobin saturation in the patients is 90%-93%

Conditions commonly associated with digital clubbing
Intrathoracic  Bronchogenic carcinoma
neoplasms  Metastatic cancers
 Malignant mesothelioma
 Lymphoma

Intrathoracic  Lung abscess

suppurative disease  Empyema
 Bronchiectasis
 Cystic fibrosis
 Chronic cavitary infections
(eg. Fungal, mycobacterial)

Lung disease  Idiopathic pulmonary fibrosis

 Asbestosis
 Pulmonary arterio-venous

Cardiovascular  Cyanotic congenital heart

disease disease

 Pathophysiology involves megakaryocytes that skip the normal route of fragmentation within
pulmonary circulation (due to circulatory disruption from tumors, chronic lung inflammation) to
enter systemic circulation
 Megakaryocytes becomes entrapped in the distal fingertips due to their large size and release
platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF)
 These promote connective tissue hypertrophy and capillary permeablity and vascularity,
ultimately leading to clubbing

Q 4629
 Low-molecular weight heparin (enoxaparin), fondaparinux (injection factor Xa inhibitor), and
rivaroxaban (oral factor Xa inhibitor) cannot be used in patients with severe renal insufficiency
(estimated GFR <30) as reduced renal clearance increases anti-Xa activity levels and bleeding risk
 Unfractionated heparin is recommended in patients with decreased eGFR, as it is more
convenient to monitor its therapeutic level in activated PTT, once goal is archived PTT>1.5-2 times
normal, warfarin is initiated
 Warfarin can take up to 5-7 days to reach therapeutic levels, it also inhibits protein C and S (anti-
thrombogenic proteins) and can be thrombogenic without a second anticoagulant (heparin) bridge

Q 4048
 Theophylline toxicity can manifest as CNS stimulation (HA, insomnia, seizures), GI disturbances
(N/V), and cardiac toxicity (arrhythmia)
 Inhibition of the cytochrome oxidase system by other medication, diet, or underlying disease can
alter its narrow therapeutic window

Q 4118
 Aspiration pneumonia treatment; clindamycin, amoxicillin-clavulanate

Q 4024
Empiric treatment of CAP(community acquired pneumonia)
Outpatient  Macrolide or doxycycline (healthy)
 Fluoroquinolone* or beta-lactam +
macrolide (comorbidities)

Inpatient  Fluoroquinolone* (IV)

(non-ICU)  Beta-lactam + macrolide (IV)

Inpatients  Beta-lactam + macrolide (IV)

(ICU)  Beta-lactam + fluoroquinolone* (IV)

*Respiratory fluoroquinolones (levofloxacin, moxifloxacin) are required

 Patients with CAP are often risk stratified using the pneumonia severity index or CURB-65 criteria
to help guide treatment and treatment locations (home, medical floor, intensive care unit)
decisions. This patients with a score of 3 on the CURB-65 criteria (age>65, confusion, BUN
>20mg/dL), likely needs hospitalization on the medical floor and treatment with fluoroquinolone
moxifloxacin or beta-lactam plus macrolide (ceftriaxone plus azithromycin). These medications
treat the most common bacteria CAP organism - strep pneumonia, H. influenza, legionella, and
mycoplasma pneumoniae

CURB-65 determine hospitalization

1 point for each of the following:
 Confusion
 Urea >20 mg/dL
 Respiration ≥30/min
 Blood pressure (systolic blood pressure <90 mm Hg or diastolic <60 mm Hg)
 Age ≥65
1. Low mortality- outpatient treatment
2. 2 -- intermediate mortality -- likely inpatient treatment
3. 4 --- high mortality --- urgent inpatient admission; possibly ICU if score >4

Q 4201
Nonallergic rhinitis Allergic rhinitis

Clinical  Nasal  Water rhinorrhea,

features congestion, sneezing, eye
rhinorrhea, symptoms
sneezing,  Earlier age of onset
postnasal  Identifiable
drainage allergen or
 Later onset seasonal pattern
common  Pale/bluish nasal
(age>20) mucosa
 No obvious  Associated with
allergic trigger other allergic
 Perennial disorders (eczema,
symptoms (may asthma, eustachian
worsen with dysfunction)
season changes)
 Erythematous
nasal mucosa

Treatment  Mild-intranasal  Intranasal

antihistamine or glucocorticoids
glucocorticoids  Antihistamines
 Moderate to

 NAR- Those with prominent rhinorrhea and/or postnasal drip sometimes respond to first-
generation oral H1 antihistamines (chlorpheniramine) but rarely ever to antihistamines without
anticholinergic properties (loratadine)
 These patients are best managed with either a topical intranasal antihistamine spray (azelastine,
olopatadine) or intranasal glucocorticoids. Moderate to severe symptoms usually require both
intranasal antihistamine and intranasal glucocorticoids

Q 3580
Granulomatosis with polyangiitis
Clinical  Upper respiratory: sinusitis/otitis,
manifestations saddle-nose deformity
 Lower respiratory: Lung
 Renal: Rapidly progressive GN
 Skin: Livedo reticularis,
nonhealing ulcers

Diagnosis  ANCA: PR3 (~70%), MPO (~20%)

 Biopsy:
 Skin (leukocytoclastic
 Kidney (pauci-immune GN)
 Lung (granulomatous

Management  Corticosteroids &

 (MTX, cyclophosphamide)

 Granulomatosis with polyangiitis is a vasculitis affecting small and medium size blood vessels and
is characterized by upper and lower respiratory tract disease and glomerulonephritis. Diagnosis
is made by antineutrophil cytoplasmic antibody positivity and tissue biopsy

Q 2297
Clinical features:
 Hyper-resonance to percussion
 Diminished breath sounds
 Decreased tactile vocal fremitus
 Hypotension: decreased venous return

 Positive pressure mechanical ventilation can cause numerous complications including alveolar
damage, pneumothorax, and hypotension. Patients with underlying lung disease such as ARDS,
pneumonia, or obstructive airway disease are especially predisposed to barotrauma due to the
already compromised lung tissue
 In ARDS, lung injury causes inflammation and edema, leading to alveolar collapse and poor
oxygenation. PEEP maintains airways pressure above atmospheric pressure at the end of
expiration, preventing alveolar collapse, increasing the functional residual capacity, and
decreasing the work of breathing. Unfortunately, delivery of positive pressure ventilation to such
patients can rupture the fragile lung parenchyma, resulting in air leakage into the pleural space.
Pneumothorax may result, which can cause absent parenchyma, resulting in air leakage into
pleural space.
 Pneumothorax may result, which can cause absent breath sounds on the affected side and lead to
compression of structures in the mediastinum and impaired right ventricular filling, resulting in
hypotension and tachycardia

 As the intrapleural space fills with air, intrathoracic pressure increases and results in decreased
venous compliance. When the central veins lose their ability to stretch and expand (increased
venous stiffness), the central venous pressure also rises

Q 8815
 Subacute (3-8 weeks) and chronic (>8 weeks) cough is seen frequently in adults. Postnasal drip
(upper-airway cough syndrome), GERD, and asthma cause >90% of chronic cough in non-smokers
without pulmonary disease
 A thorough history and examination can identify the important causes
 Patients with clear history of upper airway cough syndrome, asthma, or Gerd should be treated
accordingly; those taking ACE inhibitors should discontinue the drug
 In some patients, postnasal drip can be silent without clinical presentation
 The best diagnostic approach is to treat empirically with an oral first generation antihistamine
(chlorpheniramine) or combined antihistamine-decongestant (brompheniramine and
 Patients who do not response after 2-3 weeks may require further investigations (sinus imaging,
PFT, high resolution CT scan of chest) or empiric sequential therapy for GERD, cough variant
asthma, chronic sinusitis, and non-asthmatic eosinophilic bronchitis

Q 8905
Normal Obstructive Restrictive
lung disease lung

FEV1 >80% Decreased Decreased

(of predicted)

FEV1/FVC >70% Decreased Normal to


FVC >80% Normal to Decreased

(of predicted) decreased

 Adult-onset asthma tends to be more severe and less likely to go into remission
 It is difficult to clinically distinguish asthma from COPD in adults, particularly in smokers. So PFT is
 Both disease may show airflow obstruction but only asthma shows complete reversibility of the
obstruction with bronchodilators
 The diffusion capacity of DLCO may also be useful as a differentiating feature. DCLO in asthma is
usually normal or increased (severe asthma). It is never increased in patients with COPD

Q 4210 - repeat chart

 Aspergillus is a ubiquitous fungus that most people encounter daily. Conidia are inhaled into the
lungs and convert to potentially pathogenic hyphae. Patients with immunocompetency rapidly
clear the organism and rarely develop infection: however, a subset of immunocompetent patients

with a history of pulmonary disease (cavitary tuberculosis) may develop chronic pulmonary
aspergillosis (CPA) at sites of lung damage.
 Diagnosis is made by the presence of all 3 of the following:
 >3 months of symptoms - fever, weight loss, fatigue, cough, hemoptysis, and/or dyspnea
 Cavitary lesions containing debris, fluid, or an aspergilloma (fungal ball)
 Positive aspergillus IgG serology
 Therapy depends on symptoms and severity of disease; antifungal medications
(itraconazole, voriconazole), surgery (to prevent hemoptysis), and bronchial artery
embolization (for hemoptysis with extensive disease) may be used together or separately.
 A simple aspergilloma is sometimes categorized as CPA but is typically quiescent (aside from
occasional mild cough or hemoptysis) with no systemic symptoms

Q 4387
 Patient with SOB, cough, and dullness to percussion with increased breath sounds over the right
lower lung field likely has lobar pneumonia causing focal lung consolidation.
 A normal lung is resonant to percussion, and auscultation at the periphery demonstrates vesicular
breath sounds that consists of a quiet inspiratory phase and an almost inaudible expiratory phase.
 When a portion of the lung is consolidated (lobar pneumonia), the density of tissue/fluid increases
and dullness to percussion is detected. In addition, sound conducts more rapidly through the
consolidated lung, resulting in increased intensity of breath sound and a more prominent
expiratory component. More rapid sound conduction also results in increased tactile fremitus as
well as egophony (sound like the letter "A" when the patients says the letter "E") in areas of lung
consolidation. Crackles are also often heard. With pneumonia, fever is most often present but not
always present.

Q 3027
 The pharmacologic management of asthma is guided by a stepwise approach. In patients with
newly diagnosed asthma or intermittent asthma managed with only an as needed short acting
beta-2 agonist (SABA) (albuterol), the need for controller medications (and level of controller
therapy) is assessed by categorizing symptoms into 1 to 4 levels of asthma severity: intermittent,
mild persistent, moderate persistent, and severe persistent. The factors that define severity are
frequency of daytime symptoms ( can be assessed as frequency of SABA use if already prescribed)
and frequency of nighttime awakenings. Spirometry also plays a role as decreases in FEV1 and
FEV1/FVC ratio correlates with asthma severity and lack of symptom control.
 In intermittent asthma, daytime symptoms occur ≤2 days per week, nighttime awakenings occur
≤2 times per month, FEV1 and FEV1/FVC are normal, and no limitation exists on daily activity.

Q 4039
Acute exacerbation of chronic obstructive pulmonary disease
Cardinal  Increased dyspnea
symptoms  Increased cough (more frequent
or sever)
 Sputum production (change in
color or volume)

Diagnostic  Chest X-ray: hyperinflation

testing  ABG: Hypoxia, CO2 retention
(chronic &/or acute)

Management  Oxygen (target SpO2 of 88%-92%)

 Inhaled bronchodilators
 Systemic glucocorticoids
 Antibiotics if ≥2 cardinal
 Oseltamivir if evidence of
 NPPV if ventilatory failure
 Tracheal intubation if NPPV failed
or contraindicated

 All patients with acute COPD exacerbation should receive bronchodilators and systemic
glucocorticoids. In addition, antibiotics are indicated for patients with the following:
 Moderate to severe COPD exacerbation (defined as ≥2 cardinal symptoms), especially with
increased sputum purulence or
 Mechanical ventilation requirement (endotracheal intubation or non-invasive positive
 In such patients, antibiotic therapy has demonstrated increased likelihood of clinical
improvement, reduced risk of subsequent exacerbation, and decreased in-hospital mortality in
cases requiring mechanical ventilation
 Up to 50% of COPD exacerbations are likely caused by acquisition of a bacterial respiratory
pathogen, but identifying such a trigger can be clinically challenging. Collection of sputum cultures
is not recommended (except in patients with risk factors for pseudomonas aeruginosa infection)
due to difficulty in isolating a single bacterial pathogen. Therefore, empiric antibiotic therapy is
directed at common upper respiratory bacterial pathogens (H. Influ, Moraxella catarrhalis, and
strep pneumoniae) and includes macrolides (azithromycin), respiratory fluoroquinolones
(levofloxacin, moxifloxacin), or penicillin/beta-lactamase inhibitors (amoxicillin-clavulanate).
Typical duration of antibiotic therapy is 3-7 days.

Q 2788
 Hypoxemia can be caused by reduced inspired oxygen tension, hypoventilation, diffusion
limitation, shunt, and V/Q mismatch. Hypoventilation is associated with a normal A-a gradient and
respiratory acidosis

Q 4040
Non-invasive positive-pressure ventilation
Indications  COPD (severe exacerbation,
(strongest prevent extubating failure)
evidence)  Cardiogenic pulmonary edema
 Acute respiratory failure
 Postoperative hypoxemic
respiratory failure
 Immunosuppressed patients
 Facilitate early extubating

Contraindications Medical instability

 Cardiac or respiratory arrest (or
impending arrest)
 Severe acidosis. (pH<7.10)
 Non-respiratory organ failure
o Unstable cardiac
o Encephalopathy (Glasgow
coma score <10)
o GI bleed
Inability to protect airway
 Uncooperative or agitated
 Inability to clear secretions/high
aspiration risk
Mechanical issues
 Recent esophageal anastomosis
 Facial or neurological surgery,
deformity, or trauma
 Upper airway obstruction
 Initial management of acute exacerbation of COPD includes inhaled short acting bronchodilators,
glucocorticoids, and antibiotics. Patients with continued symptoms despite medical management
should be considered for non-invasive ventilatory support.
 Non-invasive positive-pressure ventilation NPPV is ventilatory support delivered by facemask
rather than endotracheal tube; it can be delivered in several different modes, including
continuous positive airway pressure and bilevel positive airway pressure. NPPV decreases work of
breathing, improves alveolar ventilation, and is the preferred method of respiratory support in
patients with AE COPD.
 Physiologic benefits include a decrease in respiratory rate and arterial carbon dioxide tension
(PaCO2), with an increase in tidal volume, minute ventilation, and arterial oxygen tension (PaO2).
NPPV in patients with AE COPD is associated with a decrease in mortality, intubation rate,
treatment failure, length of hospital stay, and incidence of nosocomial infection.
 Endotracheal intubation with mechanical ventilation is recommended for patients who fail a trial
of NPPV.

Q 4097
 CAP is a pulmonary parenchymal infection that may be caused by bacterial (majority), viral (30%),
of fungal pathogens. Symptoms often develop acutely and frequently include fever, cough, pleuritic
chest pain, and dyspnea. Tachycardia, tachypnea, and pulmonary auscultation abnormalities (focal
crackles) may be present. Clinical and physical findings are notorious poor at predicting the
presence of pneumonia <50% sensitivity)
 The diagnosis of CAP requires the presence of a lobar, interstitial, or cavitary infiltrate on chest
imaging (usually CXR)
 Sputum and blood cultures are typically not required in the outpatient setting as empiric oral
antibiotics are almost always curative.

Q 4519
 The 3 most common causes of chronic cough (lasting >8 weeks) are upper-airway cough
syndrome (postnasal drip), asthma, and GERD. Upper-airway cough syndrome is caused by rhino
sinus condition including allergic, perennial nonallergic, and vasomotor rhinitis; acute
nasopharyngitis; and sinusitis. Cough is caused by mechanical stimulation of the afferent limb of
the cough reflex in the upper airways in these conditions
 The diagnosis is confirmed by the improvement of nasal discharge and cough with the used of the
first-generation antihistamines. Chlorpheniramine is a specific H1 antihistaminic receptor blocker
that reduces the action of histamine on H1 receptors, decreasing the allergic response
 In addition to block H1 histamine receptors, chlorpheniramine exhibits anti-inflammatory effects
by blocking histamine release from mast cells and limiting the secretory response to inflammatory

Q 3042
 COPD is a progressive condition of limited airflow during expiration that is not entirely reversible.
COPD encompasses chronic bronchitis and emphysema and is one of the leading causes of death
worldwide. Smoking is the most important risk factor for COPD. Signs and symptoms include
progressive dyspnea, cough with sputum production, decreased breath sounds, and a prolonged
expiratory phase. Patient may have a barrel-shaped chest, which is due to air trapping and
hyperinflation of the lungs.
 Chronic hypoxemia is often present in advanced disease, and consequent secondary polycythemia
may occur
 Long-term supplemental oxygen therapy LTOT has demonstrated prolonged survival and improved
quality of life in patients with COPD with significant chronic hypoxemia. The criteria for initiating
LTOT in such patients include:
1. Resting arterial oxygen tension (PaO2)≤55 mm Hg or pulse oxygen saturation (SaO2) ≤88%
on room air
2. PaO2 ≤59 mm Hg or SaO2 ≤89% in patients with co pulmonale, evidence of right heart
failure, or hematocrit >55%
 In addition to continued abstinence from smoking, initiation of LTOT will have the greatest benefit
to this patient's survival

Q 4645
 COPD is characterized by progressive expiratory airflow limitation which causes air trapping,
decreased VC and increased total lung capacity. FEV1 is disproportionately decreased as compared
to VC

Q 4570
 On pulmonary examination, patients with worsening CHF will commonly have bibasilar crackles.
Decreased breath sounds at the bases could be due to pleural effusion from CHF. Wheezing can
occasionally be present in heart failure (cardiac asthma)
 Congestive heart failure exacerbation can cause tachypnea as left ventricular dysfunction allows
fluid to pool in the lungs, causing a pleural effusion and hypoxemia due to reduced ventilation,
tachypnea causes hypocapnia and respiratory alkalosis. Examination typically shows signs of fluid
over load, S3 and S4 gallops, cardiomegaly, and bibasilar crackles in the lungs.

Q 3021
 Occupations associated with asbestosis include plumbers, electricians, carpenters, pipefitters,
and insulation workers. Other industries associated with asbestosis include construction,
shipbuilding, and plastic or rubber manufacturing. Asbestos exposure alone (without smoking)
increases the risk of lung cancer by almost 6 fold. Smoking adds a synergistic effect, and smokers
with asbestos exposure have an almost 59 fold increased risk of bronchogenic carcinoma.
 Asbestosis and bronchogenic carcinoma can present similarly, with most patients developing
progressive dyspnea. However, patients with asbestosis can be asymptomatic for up to 20-30
years after asbestos exposure
 Cough, sputum production, and wheezing are not typically present (unless there is concurrent
chronic obstructive pulmonary disease)
 PE frequently shows bibasilar, end-inspiratory crackles and fingernail clubbing as the disease
progresses. CXR can show bibasilar reticulonodular infiltrates, honeycombing (cystic area
surrounded by interstitial infiltrates) and bilateral pleural thickening. High-resolution chest CT
typically shows subpleural linear densities and parenchymal fibrosis. Almost 50% of patients
have pleural plaques, which can help differentiae asbestosis from other pulmonary fibrosis.
Imaging studies may show signs of bronchogenic carcinoma

Clinical features of asbestosis

Clinical  Prolonged asbestos exposure
presentation (shipyard, mining)
 Symptoms develop ≥20 years after
initial exposure
 Progressive dyspnea, basilar fine
crackles, clubbing
 Increases risk for lung cancer &

Diagnostic  Pleural plaques on chest imaging

evaluation  Imaging, PFT & histology
consistent with pulmonary fibrosis

Q 3029
Causes of recurrent pneumonia
Involving same Local airway obstruction
region of lung  Extrinsic bronchial
compression (neoplasm,
 Intrinsic bronchial
obstruction (bronchiectasis,
foreign body)
Recurrent aspiration (region may
vary depending on body position)
 Seizures
 Alcohol or drug use
 GERD, dysphagia

Involving different  Immunodeficiency (HIV,

regions of lungs leukemia, CVID)
 Sinopulmonary disease (CF,
immotile cilia)
 Non-infectious (vasculitis,
BOOP bronchiolitis obliterans
with organizing pneumonia

 Smoking is the strongest risk factor for the development of primary lung malignancy, it is essential
to evaluate for lung malignancy using a CT of chest

Q 2615
Type of tumor Incidence Location Clinical associations

Adenocarcinoma 40%-50%  Periphery  Clubbing

 Hypertrophic

SCC 20%-25%  Central  Hypercalcemia

 Necrosis &

Small cell 10%-15%  Central  Cushing

carcinoma syndrome
 Lambert-Eaton

Large cell 5%-10%  Peripheral  Gynecomastia

carcinoma  Galactorrhea

 Of the main cell types of lung cancer, adenocarcinoma is the most common in both smokers and
non-smokers. It accounts for most of the primary lung cancers in non-smokers. It usually located

peripherally and may present as a solitary nodule, with or without symptoms. Stage at diagnosis is
the most important prognostic factor, with survival determined primarily by respectability.

Q 2602
Clinical presentation of Pancoast tumors
 Shoulder pain (most common)
 Horner syndrome (ipsilateral ptosis, miosis, exophthalmos & anhidrosis) from involvement of
paravertebral sympathetic chain & inferior cervical ganglion
 C8-T2 neurological involvement
 Weakness &/or atrophy of intrinsic hand muscles
 Pain & paresthesia's of 4h 5th digits, medial arm & forearm
 Supraclavicular lymph node enlargement
 Weight loss

 Superior pulmonary sulcus tumors are usually malignant lung neoplasms and most commonly
present with referred shoulder pain. Other common findings include Horner syndrome and
radicular pain, paresthesia's, or weakness of ipsilateral arm due to invasion of the brachial plexus.

Q 3020
Risk factors  Infection, trauma, massive
transfusion, acute pancreatitis

Pathophysiology  Lung injury--> fluid/cytokine

leakage into alveoli
 Impaired gas exchange,
decreased lung compliance,

Diagnosis  New/worsening respiratory

distress within 1 week of insult
 Bilateral lung opacities
(pulmonary edema) not due to
CHF/fluid overload
 Hypoxemia with PaO2/FiO2
ratio ≤300 mm Hg

Management  Mechanical ventilation (low TV,

high PEEP, permissive

 ARDS, an inflammatory condition that can develop in the setting of infection (sepsis, pneumonia)
trauma, or other conditions (massive transfusion, pancreatitis). Lung injury causes the release of
proteins, inflammatory cytokines, and neutrophils into the alveolar space. This leads to leakage of
bloody and proteinaceous fluid into alveoli, alveolar collapse due to loss of surfactant, and diffuse
alveolar damage.
 As a result:
 Gas exchange is impaired due to ventilation-perfusion mismatch

 Lung compliance (ability to expand) is decreased (stiff lung) due to both loss of surfactant
and increased elastic recoil of edematous lungs
 Pulmonary arterial pressure is increased (pulmonary hypertension) due to hypoxic
vasoconstriction, destruction of lung parenchyma, and compression of vascular structures
from positive airway pressure in mechanically ventilated patients
 Findings suggestive of ARDS include respiratory distress, diffused crackles on lung examination,
severe hypoxemia, and bilateral alveolar infiltrates on chest imaging, which occur within a week of
an insult. The partial pressure of arterial oxygen PaO2 decreases and leads to an increased fraction
of inspired oxygen FiO2 requirement. As a result, PaO2/FiO2 (P/F) is decreased (≤300 mm Hg) with
lower P/F ratios indicating more severe degrees of ARDS

Q 4177
 Pulmonary HTN is defined as a mean pulmonary arterial pressure ≥25 mm Hg at rest. It is seen
following the narrowing of the precapillary vessels, the loss of the pulmonary capillary bed, or
passive backpressure from the post capillary vessels from any cause. It can be classified as follows:
 Group1 - pulmonary arterial hypertension PAH, which can be idiopathic (primary PAH) or
due to drugs, HIV, or connective tissue disease
 Group 2- pulmonary HTN due to left heart disease
 Group 3- pulmonary HTN due to COPD or hypoxemia
 Group 4- pulmonary HTN due to chronic thromboembolic disease
 Group 5 - pulmonary HTN due to other causes (hematologic, systemic disorders)
 The clinical features of pulmonary HTN remain the same regardless of the underlying cause
 Dyspnea, weakness, and fatigue are early complaints, which may be followed by chest pain,
hemoptysis, syncope, or hoarseness (due to compression of the recurrent laryngeal nerve)/
 RV failure develops last in the disease and manifests with right ventricular heave, jugular venous
distension, tender hepatomegaly, ascites, edema, stc. CXR would show enlargement of pulmonary
arteries and rapid tapering of the distal vessels (pruning) and enlargement of the right ventricles
 An ECG may show right axis deviation, which is doe to right ventricular streaning and hypertrophy
due to pulmonary HTN.
 Untreated pulmonary HTN eventual lead to COR pulmonale

Q 4863
Interstitial lung disease ILD is a collective term referring to multiple aetiologies of progressive
fibrosis affecting the pulmonary interstitium, alveoli, and conducting airways. Aetiologies of ILD
include chronic inhalation or organic/inorganic dust (asbestos, beryllium, silicon dioxide), drug
toxicity (amiodaraone, bleomycin, nitrofurantoin) radiation, and systemic connective tissues
disease (RA, scleroderma)
Pleural plaques on CXR is consistent with asbestos exposure, mostly from work, like working in
ship yard.
 ILD is a disease of progressive pulmonary fibrosis characterized by restrictive physiology on
pulmonary function testing (decreased FEV1 and FVC with a normal or an increased FEV1/FVC
ratio. The diffusion capacity of the lung for carbon monoxide is decreased in ILD but remains
normal in extrinsic causes of restrictive pulmonary phyisology.

Q 3453
 A solitary pulmonary nodule (SPN) is defined by the features of round opacity, up to 3 cm in
diameter and surrounded by pulmonary parenchyma

 By convention, there must be no associated pleural effusion, adenopathy, or atelectasis. Most
incidentally discovered SPNs are benign (infectious granuloma, hamartoma).
 However, it is important to differentiate benign from malignant nodules (bronchogenic carcinoma.
Metastatic). The first step in evaluating an SPN is comparison with previous x-rays. If a solid lesion
reveal on prior imaging is stable in a size for >2 years, malignancy is effectively ruled out and no
further testing is necessary. Malignant nodules tend to double in size over the course of a month
to a year.
 If no previous radiographs are available for comparison, a CT scan should be performed to further
characterize the lesion. CT provides greater details of a lesion's size, borders, and density.
 Large nodule size, low density, speculated borders, and eccentric calcification favor carcinoma.
 Other clinical characteristic suggesting malignancy include age >40, history of smoking, weight
loss, and previous malignancy
 Nodules with high overall risk for malignancy should be excised. Those with low malignant
potential should be followed with serial CT scans. The exact interval of imaging depends on
patient and nodeul characteristic
 18-flurodeoxyglucose positron emission tomography FDG-PET or tissue biopsy is warranted when
clinical and radiographic data indicate an intermediate probability of malignancy
 Bronchoscopy is best for biopsy of centrally located lesions, and CT-guided percutaneous biopsy
is best for peripheral lesions

Q 4630
 A fixed upper-airway obstruction will decreased the airflow rate during inspiration and expiration,
flattening both the top and bottom of the flow-volume loop.
 Laryngeal edema secondary to food allergy is likely in sudden setting, and pt will require
treatment with epi pen, systemic corticosteroids and antihistamine
 Asthma causes intrapulmonary airway obstruction via bronchoconstriction, this decreases airflow
during the effort- independent phase of exhalation, causing flow-volume loop to have a scooped
out pattern during exhalation

Q 4677
 The first step in determining whether patient has a respiratory or metabolic acidosis is to evaluate
the pCO2. An elevated pCO2 is consistent with a respiratory acidosis due to hypoventilation.
This is supported by hypoventilation-induced hypoxia. A low bicarbonate concentration, on the
other hand, would argue for a metabolic acidosis. Post ictal state- hypoventilation- it can be
explained by apnea/hypopnea during prolonged seizures or an aspiration event

Q 4467
 Transudative effusion are commonly caused by decreased intrapleural or plasma oncotic
pressures or elevated hydrostatic pressure. Exudative effusion are often the results of increased
capillary or pleural membrane permeability or disruption to lymphatic outflow

Q 3944
 The chronic non-productive cough in patient with heart failure is likely an adverse effect of ACE
inhibitor therapy. ACE inhibitors (lisinopril) cause cough in up to 20% of patients, and onset of the
cough is typically within a week of drug initiation or dosage increase (although onset may be
delayed for months) the pathogenesis of the cough is likely related to an increased in the
circulating levels of inflammatory mediators (bradykinin, substance P, thromboxane,
prostaglandins) that results in bronchoconstriction and bronchial irritation

Q 4717
 Immunosuppressed patients are susceptible to pneumonia due to typical organism (strep,
pneumo) as well as opportunistic organism (PCJ)
 In consolidative pneumonia, the alveoli become filled with inflammatory exudate, leading to
marked impairment of alveolar ventilation in that portion of the lung. The result is right-to-left
intrapulmonary shunting, which describes perfusion of lung tissues in the absence of alveolar
ventilation, as extreme form of ventilation/perfusion (V/Q) mismatch (~0). A characteristic of
intrapulmonary shunting is inability to correct hypoxemia with increased concentration of inspired
oxygen (FiO2). Other causes of V/Q mismatch (emphysema, interstitial lung disease, pulmonary
embolism) allow for correction of hypoxemia with an increased in fiO2 because V>o. In particle,
increased FiO2 typically leads to some improvement in hypoxemia in patients with pneumonia
because only a portion of the lung is being affected by intrapulmonary shunting

Q 3717
 The first step in managing patients with suspected PE is supportive care (O2, IV fluids for
hypotension). The next step is assessing absolute contraindications to anticoagulation (active
bleeding, hemorrhagic stroke) patients with contraindication should undergo diagnostic testing for
PE, with appropriate treatment (IVC filter) if positive. Patients without contraindication can be
assessed with modified Wells criteria for PE pretest probability. In patients in whom PE is unlikely
based on these criteria, diagnostic testing is performed before anticoagulation is considered.
However anticoagulation (low-molecular weight heparin or unfractionated heparin) should be
given prior to diagnostic testing patients with likely PE, especially when patients are in moderate
to sever distress
 Anticoagulation can be safely started with 6-12 hrs of a caesarean delivery
 Early and effective anticoagulation decreases mortality risk of acute PE from 30% to ~2%-8%

Q 4208
 Obesity and malignancy are important risk factors for DVT and PE. Wheezing can occur in acute
PE. An elevated alveolar-arterial oxygen gradient is commonly seen in patients with PE

Q 3033
Obstructive sleep apnea OSA
Pathophysiology  Relaxation of pharyngeal
muscles lead to closure of
 Loud snoring with periods of

Symptoms  Daytime somnolence

 Non-restorative sleep with
frequent awakenings
 Morning headaches
 Affective & cognitive

Sequelae  System hypertension

 Pulmonary hypertension &
right heart failure

 OSA is more common in men, and the incidence increases with age until approximately age 65
 Obesity is the strongest risk factor anatomical characteristic such as tonsillar hypertrophy,
excessive soft tissue, or a short mandible are also risk factors.
 Consequences of untreated OSA can included pression, systemic hypertension, impotence, and
accidents related to daytime somnolence
 Nocturnal polysomnography is the gold standard for diagnosis. Polysomnography determines the
frequency of abnormal ventilation events that occur during sleep
 There are 2 types of abnormal ventilation during sleep; apnea (cessation of breathing for >10 sec)
or hypopnea (reduced airflow causing SaO2 to creased by >4%)
 In symptomatic patients, experiencing >5 obstructive respiratory events (apneas or hypopnea) per
hour is diagnostic of OSA

Q 4520
 Patient with COPD and acute onset of SOB, hypoxia, and unilaterally decreased breath sounds
likely has a secondary pneumothorax SSP
 SSP occurs in patients with known lung disease (COPD, CF). Other common manifestations include
cheat pain and hyper-resonance on percussion
 Cigarette smoking markedly increases the risk of pneumothorax. Chronic destruction of alveolar
sacs leads to the formation of large alveolar blebs, which can eventually rupture and leak air into
pleural space
 Diagnosis of pneumothorax is made by CXR, which demonstrates a visceral plural line beyond
which no pulmonary markings are apparent. Tracheal deviation can occur but is rare
 Management depends on the size of the lesion and clinical status of the patient, and ranges from
observation with supplemental oxygen to emergency tube thoracotomy

Q 4632
 The ideal location of the distal tip of the endotracheal tube ETT is 2-6 cm above the carina.
Because the right mainstem bronchus diverges from the trachea at a relatively non-acute angle,
an ETT advanced too far will preferentially enter into the right main bronchus. This results in over
inflation of the right lung, underventilation of the left lung, and asymmetric chest expansion
 Auscultation with show markedly decreased or absent breath sounds. CXR confirms the diagnosis.
Repositioning the ETT by pulling back slightly will move the tip between the carina and vocal cords
and solve the problem.

Q 3022
 Asbestosis is a type of pneumoconiosis with an increased incidence in occupations such as mining,
shipbuilding, insulation, and pipe work. There is usually a latency period of ≥20 years between
initial asbestos exposure and disease presentations.
 Progressive dyspnea over a period of months is typical for asbestosis
 Cough, sputum production, and wheezing ae uncommon.PE can show digital clubbing and
bibasilar end-inspiratory crackles; each is seen in approximately 50% of affected individuals
 Co pulmonale can eventually develop with peripheral edema, hepatojugular reflux, jugular venous
distension, and/or a right ventricular heave.
 Typical CXR findings include interstitial abnormalities of the lower lung fields and pleural
plaques (the hallmark of the disease)
 As in other forms of interstitial lung disease, pulmonary function tests show a restrictive pattern
(decreased lung volumes with normal or elevated forced expiratory volume in 1 second/forced
vital capacity [FEV1/FVC] ratio) accompanied by reduction in diffusion lung capacity and
pulmonary compliance.

Q 4344
 Pleuritic chest pain in the setting of a long-distance flight, hemoptysis, dyspnea, tachypnea,
tachycardia, and oral contraceptive pill use- is concerning for PE
 Approximately 10% of patients with PE have occlusion of a peripheral pulmonary artery by
thrombus, causing pulmonary infarction. These small peripheral thrombi are more likely to cause
pleuritic chest pain and hemoptysis, due to inflammation and irritation of the lung parenchyma
and adjacent visceral and parietal pleura
 CT pulmonary angiopgraphy is typically used for diagnossi in most patietns

Q 4252
Solitary pulmonary nodules
Factors increasing  Large size *
malignant probability  Advanced patients age
 Female sex
 Active or previous
 Family or personal history
of lung cancer
 Upper lobe location
 Speculated radiographic

*size >2 cm independently correlates with >50% malignant probability
 A solitary pulmonary nodule SPN is defined by the following features:
 Rounded opacity
 ≤3 cm in diameter (>3 cm is considered a "mass")
 Surrounded by pulmonary parenchyma
 No associated lymph node enlargement
 The size of an SPN strongly correlates with the chances of it being malignant. Nodules <0.6 cm are
unlikely to be malignant and generally do not require follow-up; however, nodules >0.8 cm require
additional management or surveillance
 In addition to size, other factors that influence the probability of an SPN being malignant include
patient age, sex, smoking history, family history, location of the nodule in the lung, and
radiographic appearance of the nodule (regular versus irregular borders)
 Nodules >0.8 cm that are intermediate or high probability for malignancy (≥5% risk) based on
these factors require tissue diagnosis with biopsy or surgical excision
 This relatively large SPN with irregular borders in the 65 year old patient with a significant smoking
history has high malignant probability and should biopsied or surgical excised.
 For patients in who the need for tissue diagnosis in unclear, PET scan be helpful. Nodules
demonstrating high metabolic activity on PET scan are more likely malignant than benign and
warrant biopsy or surgical excision

1) Stepwise management is now putting less emphasis on ICS. These are indicated but typically in
more moderate to severe cases. One potential step-up regimen is as follows:

-SABA + SAMA (both together are better than either one separately)

-Add LAMA (+/- LABA) to SABA (LAMA + LABA together appear to be have better outcomes)


-Can add theophylline, PDE4 inhibitor, or long-term macrolide therapy

Side notes - theophylline does potentially have a role in stable COPD. However, it should
probably be used after the above therapies have been optimized. Oral steroids are felt to have
less and less of a role in the chronic maintenance of COPD. This does go against some of what the
notes and lecture state. We are currently working to provide the best balance of most recent
literature vs what the test will ask and will update as we go to improve consistency.

(2) Are antibiotics always needed for COPD exacerbations? Hell no. A lot of people still follow the
major/minor symptoms to determine the appropriateness of antibiotics. This is a reasonable way
to proceed. However, there is well-established literature showing that using procalcitonin to
trigger antibiotic administration decreases antibiotic usage without increasing adverse outcomes.

(3) Why is excessive oxygen bad in COPD? Good question. A lot of us are taught that the chronic
CO2 retention pushes the respiratory drive into a more "hypoxic-driven" state. Excess oxygen
blunts this drive, leading to decreased respirations (and therefore hypoventilation). However, this

is no longer felt to be true. Oxygen is a potent pulmonary vasodilator and excessive
administration can override the appropriate shunting that the body is doing to move blood flow
away from poorly ventilated alveoli. Decrease excessive oxygen = allow appropriate shunting
away from poorly ventilated areas = improved ventilation.

(4) Classification of COPD has changed. It is no longer based solely on FEV1. One needs to take
into consideration symptom burden and stabillity. The new staging has a number (grade 1-4,
based off FEV1) and a letter (group A-D, based off exacerbations/symptom burden). For example,
a patient with a FEV1 <30%, 2 hospitalizations in the past year, and a heavy symptom burden
would be a GOLD Grade 4, Group D. Same patient but without symptoms or exacerbations?
GOLD Grade 4, Group A. These two groups have very different trajectories pertaining to disease

Bottom line - there is more than airflow restriction to consider when determining the severity of
one's COPD.