NBME CBSE STUDY GUIDE/ TEST BANK
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:
...
nbme cbse study guide test bank type ii pneumocytes surfactant lecithin proliferate after injury type i progenitors neonatal respiratory distress syndrome polio live v killed vaccine killed salk
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NBME CBSE STUDY GUIDE/ TEST BANK
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
V/Q mismatch: O2 induced hypercapnia;
physio dead space
Myeloperoxidase causes
Green sputum/pus
Do not give O2 supplement to
COPD patient
Decreased stimulation of
carotid bodies = decreased RR
TX COPD with
LIVER
LUNG: inc PMN elastase --> emphysema
Asthma dx
Methacholine (maCh) challenge
= induce bronchoconstriction
to reduce FEV1
+ test = Airways ARE reactive
B2 agonist MOA
B2 (Gs) --> AC --> increase cAMP
Corticosteroid MOA
inhibit cytokine synthesis
suppress T lymphocyte
mACh Antagonist ("tropium") MOA
inhibit Vagal via ACh
--> decreased Ca
OSA causes
pulmonary HTN and RHF
increases EPO which worsens HTN
EPO can do what
on Cardiovascular
worsen HTN
Pulmonary Arterial HTN
BMPR2
High endothelin, Low NO
SMC hypertophy, fibrosis, narrow lumen
P2 louder than A2
When is P2 louder than A2
Pulmonary Artherial Hypertension
TX pulmonary arterial hypertension
Endothelin-R antagonist:
- Bosentan, Ambisentan
PGEi (inc cGMP):
- Sildenafil
Pulmonary Embolism
perfusion defect (V/Q mismatch)
sudden SOB + calf swelling
Hypoxemia --> Hyperventilate
--> Respiratory Alkalosis
--> Metabolic compensation in 2 days
dx pulmonary embolism
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