NBME CBSE USMLE-Questions with Correct Answers/ Verified/
Latest (2024/2025)
Type II pneumocytes - ✔✔surfactant (*lecithin*)
Proliferate after injury
Type I progenitors
*Neonatal Respiratory Distress Syndrome*
Polio live v killed vaccine - ✔✔Killed = Salk = IgG
Live = Sabin = IgG + IgA
- can be shed in feces
Neonatal Respiratory Distress:
Etiology + Tx - ✔✔Maternal DM (*high insulin*)
or C-section (*low cortisol*)
TX: *dexamethasone* before birth
Lung maturity determined with - ✔✔Amniocentesis of Phospholipids (*type II pneumocytes)
L >> S
Type I pneumocytes - ✔✔Squamous gas diffusion
Elastase in lungs - ✔✔macrophage: *lysosomes*
PMN: *azuronphilic granules*
Elastin stretches and recoils due to - ✔✔Lysine interchain crosslinks
air pressure and
intrapleural pressure at FRC - ✔✔Air pressure = 0
,Intrapleural pressure = -5
Pulm Vasc Resistance is lowest during - ✔✔Exhale of Tidal Volume
Lung Compliance is decreased by - ✔✔LHF, pulmonary edema,
pulmonary fibrosis
Lung Compliance is increased by - ✔✔emphysema, age
Obesity affects ERV and FRC - ✔✔DECREASE
ERV & FRC
Blood flow/min (pulmonary v systemic) - ✔✔pulmonary = systemic
Anatomic pulmonary shunting - ✔✔Bronchial circulation causes
*decreased PO2 in LA/LV*
than in pulmonary capillaries
More ventilation is at the - ✔✔BASE
O2-Hgb dissociation LEFT shift - ✔✔basic, cold, low 2,3 BPG
low pO2 (compensatory erythrocytosis)
O2-Hgb dissociation RIGHT shift - ✔✔low pH, high 2,3BPG, high T
HOT, ACIDIC
CO2 transport to lungs - ✔✔*carbonic anhydrase*
Cl shift
*Haldane*: CO2 released to lung
,(*Bohr*: O2 release to tissue)
CO poisoning causes - ✔✔carboxyhemoglobin
no affect on PaO2
Cyanide poisoning causes - ✔✔lactic acidosis
How to treat cyanide poisoning - ✔✔*Amyl nitrite* --> Methemoglobin
THEN *Thiosulfate* (hydroxycobalamin)
Normal A-a gradient - ✔✔5-15
Hypoventilation: Heroin OD or high altitude
Increased A-a gradient - ✔✔*Diffusion impairment* (fibrosis)
*R-L shunt* (aspiration, ARDS)
*V/Q mismatch* (pulmonary edema
AT --> AT II
where and how - ✔✔ACE
(- high in sarcoidosis)
In small pulmonary bV
C5a induces what - ✔✔PMN influx (ie: in lungs)
Korotkoff sound - ✔✔BP cuff - appear and disappear
in inflation/deflation
Pulsus Paradoxus - ✔✔10mmHg difference in
, Korotkoff sound
Pulsus Paradoxus occurs in - ✔✔Cardiac Tamponade
Kussmaul sign - ✔✔JVP rises *during inspiration*
Constrictive Pericardiditis
Restrictive/Interstitial Lung Disease:
A-a, FVC, FEV1, EFR - ✔✔Airway widening due to *radial traction* from fibrosis
*increase Aa*
decreased FVC & FEV1
*Increased EFR*
Sarcoidosis - ✔✔*Th1 *noncaseating granulmona
bilateral hilar adenopathy
increased *ACE*
increased IL2, IFNg
1-a-hydroxylase in macrophages: vit D --> *HyperCa*
Hyper Ca causes - ✔✔stones, thrones, groans, psych overtones
1-a-hydroxylase in macrophages - ✔✔PTH independent conversion of
Calcifediol to *calcitriol* (bioactive Vit D)
Vit D --> Hyper Ca
Idiopathic pulmonary fibrosis - ✔✔*Honeycomb* pattern
loss of Type 1 pneumocytes
*hyperplasia Type II* pneumocytes
Latest (2024/2025)
Type II pneumocytes - ✔✔surfactant (*lecithin*)
Proliferate after injury
Type I progenitors
*Neonatal Respiratory Distress Syndrome*
Polio live v killed vaccine - ✔✔Killed = Salk = IgG
Live = Sabin = IgG + IgA
- can be shed in feces
Neonatal Respiratory Distress:
Etiology + Tx - ✔✔Maternal DM (*high insulin*)
or C-section (*low cortisol*)
TX: *dexamethasone* before birth
Lung maturity determined with - ✔✔Amniocentesis of Phospholipids (*type II pneumocytes)
L >> S
Type I pneumocytes - ✔✔Squamous gas diffusion
Elastase in lungs - ✔✔macrophage: *lysosomes*
PMN: *azuronphilic granules*
Elastin stretches and recoils due to - ✔✔Lysine interchain crosslinks
air pressure and
intrapleural pressure at FRC - ✔✔Air pressure = 0
,Intrapleural pressure = -5
Pulm Vasc Resistance is lowest during - ✔✔Exhale of Tidal Volume
Lung Compliance is decreased by - ✔✔LHF, pulmonary edema,
pulmonary fibrosis
Lung Compliance is increased by - ✔✔emphysema, age
Obesity affects ERV and FRC - ✔✔DECREASE
ERV & FRC
Blood flow/min (pulmonary v systemic) - ✔✔pulmonary = systemic
Anatomic pulmonary shunting - ✔✔Bronchial circulation causes
*decreased PO2 in LA/LV*
than in pulmonary capillaries
More ventilation is at the - ✔✔BASE
O2-Hgb dissociation LEFT shift - ✔✔basic, cold, low 2,3 BPG
low pO2 (compensatory erythrocytosis)
O2-Hgb dissociation RIGHT shift - ✔✔low pH, high 2,3BPG, high T
HOT, ACIDIC
CO2 transport to lungs - ✔✔*carbonic anhydrase*
Cl shift
*Haldane*: CO2 released to lung
,(*Bohr*: O2 release to tissue)
CO poisoning causes - ✔✔carboxyhemoglobin
no affect on PaO2
Cyanide poisoning causes - ✔✔lactic acidosis
How to treat cyanide poisoning - ✔✔*Amyl nitrite* --> Methemoglobin
THEN *Thiosulfate* (hydroxycobalamin)
Normal A-a gradient - ✔✔5-15
Hypoventilation: Heroin OD or high altitude
Increased A-a gradient - ✔✔*Diffusion impairment* (fibrosis)
*R-L shunt* (aspiration, ARDS)
*V/Q mismatch* (pulmonary edema
AT --> AT II
where and how - ✔✔ACE
(- high in sarcoidosis)
In small pulmonary bV
C5a induces what - ✔✔PMN influx (ie: in lungs)
Korotkoff sound - ✔✔BP cuff - appear and disappear
in inflation/deflation
Pulsus Paradoxus - ✔✔10mmHg difference in
, Korotkoff sound
Pulsus Paradoxus occurs in - ✔✔Cardiac Tamponade
Kussmaul sign - ✔✔JVP rises *during inspiration*
Constrictive Pericardiditis
Restrictive/Interstitial Lung Disease:
A-a, FVC, FEV1, EFR - ✔✔Airway widening due to *radial traction* from fibrosis
*increase Aa*
decreased FVC & FEV1
*Increased EFR*
Sarcoidosis - ✔✔*Th1 *noncaseating granulmona
bilateral hilar adenopathy
increased *ACE*
increased IL2, IFNg
1-a-hydroxylase in macrophages: vit D --> *HyperCa*
Hyper Ca causes - ✔✔stones, thrones, groans, psych overtones
1-a-hydroxylase in macrophages - ✔✔PTH independent conversion of
Calcifediol to *calcitriol* (bioactive Vit D)
Vit D --> Hyper Ca
Idiopathic pulmonary fibrosis - ✔✔*Honeycomb* pattern
loss of Type 1 pneumocytes
*hyperplasia Type II* pneumocytes
