NBME CBSE (USMLE Step 1) 2026-2027
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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
Goodpasture
HS II
Auto-Ab against BM destroys lung alveoli (restrictive) and renal
glomeruli
Obstructive Lung Disease
DECREASED FEV1, Decreased FVC
increased RV, FRC, TLC
**different shape
COPD
PMN, mo, CD8
Newest Update / Premium Questions
Bank and Accurate Responses / 100%
Solved / Already Graded A+
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
Goodpasture
HS II
Auto-Ab against BM destroys lung alveoli (restrictive) and renal
glomeruli
Obstructive Lung Disease
DECREASED FEV1, Decreased FVC
increased RV, FRC, TLC
**different shape
COPD
PMN, mo, CD8
