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USMLE Step 1 Random Facts > Respiratory > Flashcards

Respiratory Flashcards

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USMLE® Step 1 flashcards
1
Q

area of lung w/ largest physiologic dead space

A

apex

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2
Q

IC =

A

IRV + TV

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3
Q

FRC =

A

RV + ERV

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4
Q

VC =

A

IRV + TV + ERV

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5
Q

TLC =

A

IRV + TV + ERV + RV

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6
Q

Vd (physiologic dead space) =

A

Vt x [(PaCO2 - PECO2)]/PaCO2

Vt = tidal vol
PECO2 = expired air CO2
PaCO2 = arterial CO2

=anatomic dead space + functional dead space (ex. in apex of lung)

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7
Q

equilibration of O2 in NORMAL individual @ rest is what-limited?

A

perfusion-limited

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8
Q

what causes equilibration to become diffusion-limited?

A

emphysema, pulmonary fibrosis, increased exercise

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9
Q

what does it mean to be diffusion-limited?

A

gas doesn’t equilibrate by the time blood reaches end of capillary

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10
Q

what does it mean to be perfusion-limited?

A

diffusion only increased IF blood flow increases

equilibration normally occurs along first 1/3 of capillary

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11
Q

primary TB likes to be where?

A

lower lung fields

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12
Q

2ndary TB likes to be where?

A

upper lobes

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13
Q

A-a gradient =

A

PAO2 - PaO2
should be 10-15mmHg
increased in right to left shunt, diffusion limitation, V/Q mismatch

PAO2 = alveolar PO2
PaO2 = arterial PO2
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14
Q

PAO2 equation

A

= 150 - (PaCO2)/0.8

or

= PIO2 - (PaCO2)/R

PIO2 = PO2 in inspired air

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15
Q

causes of hypoxemia w/ normal A-a gradient?

A

high altitude

hypoventilation

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16
Q

causes of hypoxemia w/ increased A-a gradient?

A

V/Q mismatch (pneumonia, COPD, pulm embolism)
R–>L shunt (EIsenmenger synd)
pulmonary fibrosis (diffusion limited)

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17
Q

minute ventilation =

A

TV x breaths/min

ALL air!

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18
Q

alveolar ventilation =

A

(TV - dead space) x breaths/min

ONLY AIR participating in gas exchange

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19
Q

diffusion of gas (Vgas) =

A

A/T x Dk (P1 - P2)

A = area (decreased in emphysema)
T = thickness (increased in pulmonary fibrosis)
Dk (P1 - P2) = diff in partial pressure

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20
Q

in diffusion limited states what’s the main physiologic change

A

increased partial pressure difference b/w alveolar air + pulm capillary blood

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21
Q

cause of primary pulm HTN

A

BMPR2 inactivating mut (inhib vasc SM prolif normally)

TGF-beta!!!

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22
Q

causes of 2ndary pulm HTN

A

COPD
mitral stenosis
recurrent thromboemboli (decreases cross-sectional area of pulm bed)
autoimmune disease
L –> R shunt
sleep apnea
living @ high altitudes (hypoxic vasoconstriction)

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23
Q

PVR =

A

[P(pulm artery) - P(pulm wedge pressure)]/cardiac output

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24
Q

pulm wedge pressure is the same as what?

A

LA pressure

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25
Q

Resistance (R) =

A

(change in P)/Q

Q = flow

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26
Q

as viscosity increases, R –>

A

increases

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27
Q

as vessel length increases, R –>

A

increases

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28
Q

as vessel RADIUS increases, R –>

A

decreases (prop to the 4th power)

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29
Q

O2 content of blood =

A

(O2 binding capacity x %sat) + dissolved O2

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30
Q

1g of Hb can normally bind how much O2

A

1.34mL O2

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31
Q

as Hb falls, what changes happen in blood O2

A

O2 content decreases

O2 sat and arterial pO2 DON’T change!!

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32
Q

PAO2 =

A

150 - PaCO2/0.8

33
Q

if PaO2/FiO2 =

A

300-500 (normal)

<200 (severe hypoxia)

34
Q

increased A-a gradient usually seen in what state

A

hypoxemia

35
Q

O2 changes in anemia

A

decreased TOTAL O2 content

no change in PaO2, O2 sat

36
Q

O2 changes in COPD

A

decreased PaO2
physio shunt –> decreased O2 extraction ratio
decreased blood O2 content

37
Q

O2 changes in exercise

A

decreased venous PO2 (bc increased demand)
right shift of curve
PaO2 doesn’t change

38
Q

as V/Q –> 0, what happens?

A

airway obstruction, aka SHUNT!

100% O2 doesn’t improve condition bc air can’t REACH alveoli

39
Q

as V/Q –> infinity, what happens?

A

blood flow obstruction aka PHYSIOLOGIC DEAD SPACE

100% O2 DOES improve if <100% dead space bc blood rerouted to other areas of lung w/ better O2 content

40
Q

physio @ zone 1 (apex) of lung

A 
PA > Pa > Pv
physiologic dead space
V/Q > 1
pulmonary capillaries collapsed
decreased perfusion
41
Q

physio @ zone 2 of lung

A

Pa > PA > Pv

pulsatile blood flow (increases as BP increases)

42
Q

physio @ zone 3 (base) of lung

A

Pa > Pv > PA
decreased ventilation
V/Q < 1
SHUNTING

43
Q

ventilation and perfusion are BOTH greatest @

A

base of lung than at apex

44
Q

majority of CO2 transported in blood as

A

bicarb

45
Q

cabaminohemoglobin (aka CO2 bound to Hb) is bound to Hb at what position?

A

@ N-terminus of GLOBIN not heme

46
Q

Haldane effect?

A

lungs –> oxyg of Hb promotes dissociation of H+ from Hb –> leads to CO2 formation –> CO2 released from RBC

47
Q

Bohr effect?

A

periph tissue –> increased H+ from tissue (from increased pCO2) –> shifts curve right –> unloads O2 (due to histidine side chains found on alpha + beta Hb subunits)

48
Q

RBC exports bicarb out cell by exchanging for

A

plasma Cl-

49
Q

body response to high altitude

A

decreased PAO2 –> decreased PO2
increased ventilation –> decreased PCO2
increased erythropoietin –> increased Hct, Hb
increased 2,3-BPG (unload more O2)
increased mitochondria
increased renal excretion of bicarb (to comp for resp alkalosis)
chronic hypoxic vasoconstriction –> RVH

50
Q

body response to exercise

A

increased O2 consumpt + increased CO2 prod
increased ventilation rate
V/Q ratio uniform throughout lung (bc capillaries dilated in apices to lessen O2 wasting)
increased pulm BF bc of increased cardiac output
decreased pH (2ndary to lactic acidosis)
increased venous CO2, decreased venous O2, decreased venous pH; NO change in PaO2, PaCO2

51
Q

Homan’s sign?

A

dorsiflexion –> calf pain

for DVT!

52
Q

triad for fat embolus

A

hypoxemia
neuro abnorm
petechial rash
(TCP - from platelets coating fat microglobules)

53
Q

amniotic fluid emboli can cause?

A

DIC

54
Q

2 histo findings in asthma

A 
Curshmann spirals (shed epith forming mucus plugs)
Charcot-Leyden crystals (from breakdown of eosinophils in sputum)
55
Q

anthracosis

A

coal mines
black lung, but asympt
no increased risk of lung cancer
UPPER lobes

56
Q

silicosis

A

foundries, sandblasting
macrophages –> release fibrogenic factors –> fibrosis
silica can disrupt phagolysosome –> impair macrophages –> increased risk of TB
increased risk of bronchogenic carcinoma
UPPER lobes
“eggshell” calcifications in hilar LN

57
Q

all pneumoconioses increase risk of?

A

cor pulmonale

Caplan’s synd (pneumoconiosis w/ rheumatoid arthritis - present w/ intrapulm nodule)

58
Q

asbestosis

A

shipbuilding, roofing, plumbing
calcified parietal pleural plaques (not precancerous)
increased of bronchogenic carcinoma (1), mesothelioma (2)
LOWER lobes
asbestos bodies - golden-brown rods (“dumbbell shaped”) [aka ferruginous bodies - bc contain Fe]

59
Q

Berylliosis

A

aerospace manufacturing
non-caseating granulomas (from CMI)
increased risk of lung cancer

60
Q

RF for neonatal RDS

A

maternal diabetes, pre-maturity

61
Q

therapeutic supplemental O2 in neonatal RDS can lead to?

A

retinopathy
bronchopulmonary dysplasia

due to ROS!!

62
Q

low compliance is when

A

stiff lung and means extra work is required to bring in a normal volume of air (ex. pulm fibrosis)

63
Q

high compliance is when

A

due to the poor elastic recoil –> no problem inflating the lungs but have extreme difficulty exhaling air
**extra work is required to get air out of the lungs.

Compliance also increases with increasing age

64
Q

2 lung cancers not ass w/ smoking

A

BRonchial carcinoid

BRonchoalveolar carcinoma

65
Q

tumors located peripherally

A

adenocarcinoma

large cell carcinoma

66
Q

tumors located centrally

A

small cell

squamous cell

67
Q

bronchoalveolar subtype carcinoma from what cells?

A

Clara cells

68
Q

adenocarcinoma ass w/ what mutation

A

activating k-ras

69
Q

squamous cell carcinoma of lung arises from?

A

hilar mass from bronchus

70
Q

mesothelioma features?

A

hemorrhagic pleural effusions + pleural thickening
can arise in tunica vaginalis (sac around testes) as well
psammoma bodies

71
Q

SVC synd signs

A

facial plethora
JVD
edema of UE

72
Q

pneumonia caused by exacerbation of COPD =

A

H.influenza

73
Q

granulomatous rxn w/ eosinophils

A

hypersensitivity pneumonitis

74
Q

chlyothorax findings

A

milky fluid

increased TG content (from chylomicrons)

75
Q

one cause of spontaneous pneumothorax

A

rupture of apical blebs (ass w/ paraseptal [distal acinar] emphysema)

76
Q

straddle embolus occludes what

A

bifurcation of pulm arteries

77
Q

EKG changes/lab changes seen in PE

A

wide S in lead I
large Q, inverted T in lead III
“SIQ3T3”

elevated D-dimer

78
Q

when in pulmonary vascular resistance lowest?

A

@ FRC

USMLE Step 1 Random Facts (35 decks)

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