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STEP 1 > 10b: Resp > Flashcards

10b: Resp Flashcards

1
Q

Respiration is possible after which week of embryonic development?

A

Week 25 - end of canalicular stage

incompatible with life before that

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2
Q

Errors at (X) stage of lung development can lead to tracheoesophageal fistula

A

X = Embryonic (weeks 4-7)

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3
Q

By the end of the embryonic stage of lung development, the (X) (bronchi/bronchioles/alveoli) have formed

A

X = tertiary (segmental)

bronchi

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4
Q

By the end of the pseudoglandular stage of lung development, the (X) (bronchi/bronchioles/alveoli) have formed

A

X = terminal
bronchioles

(Weeks 5-17)

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5
Q

The respiratory bronchioles and alveolar ducts are formed by (X) stage of respiratory development.

A

X = Canalicular (Weeks 16-25)

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6
Q

Alveolar ducts form terminal sacs in which stage of lung development?

A

Saccular (Week 26-birth)

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7
Q

Pneumocytes develop in which stage of lung development?

A

Saccular (Week 26-birth) - mature levels not achieved until around week 35

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8
Q

The terminal sacs become adult alveoli in (X) stage of lung development. What is the key feature that distinguishes the two structures?

A

X = Alveolar (Week 36-8 years old)

Secondary septation (adult alveoli) versus primary septation (terminal sacs)

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9
Q

CXR of newborn shows discrete, round, sharply defined density in medial 1/3 of lungs. What is the likely congenital malformation?

A

Bronchogenic cyst (fluid-filled; air-filled if infected)

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10
Q

Pulmonary surfactant is a complex mix of (X). (Y) is the most important of these

A 
X = lecithins
Y = dipalmitoylphosphatidylcholine (DPPC)
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11
Q

List the potential complications of neonatal oxygen supplementation for respiratory distress

A

“RIB”

  1. Retinopathy of prematurity (hyperoxia, high VEGF/neovascularization, retinal detachment/blindness)
  2. Intraventricular hemorrhage
  3. Bronchopulmonary dysplasia
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12
Q

Screening test for fetal lung maturity:

A

Measure phospholipid content of amniotic fluid

Lecithin/Sphingomyelin ratio (L/S ratio) in amniotic fluid; greater than 2 is healthy, less than 1.5 predictive of NRDS

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13
Q

Anatomic dead space refers to air in which structure(s)?

A

Conducting zone of respiratory tree (no gas exchange) = nose up to terminal bronchioles

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14
Q

(X) structure(s) are lost when bronchi become bronchioles

A

X = cartilage and goblet cells

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15
Q

Transition from (X) epithelium to (Y) epithelium occurs at the (Z) bronchioles

A 
X = pseudostratified columnar (ciliated)
Y = cuboidal (ciliated; lose cilia in respiratory bronchioles)
Z = terminal
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16
Q

T/F: Mucociliary clearance remains the primary clearance mechanism throughout the entire conducting zone of lung

A

True (alveolar macrophages clear debris in resp zone)

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17
Q

Least resistance in airway/respiratory tree is seen at level of (X) (bronchi/bronchioles/alveoli). And highest resistance?

A

X = terminal
Bronchioles (large numbers in parallel)

Med-sized bronchioles (due to turbulent flow)

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18
Q

RALS (“right anterior, left superior”) refers to (X) relationship to (Y) in lungs

A 
X = pulmonary artery
Y = bronchus

In hilum

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19
Q

The carina is sandwiched between which two key structures in thorax?

A

(Carina is bifurcation of trachea into R and L bronchi)

Anterior: ascending aorta
Posterior/lateral: descending aorta

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20
Q

T/F: Aspirating peanut while upright or supine will both cause it to enter R lower lobe

A

False - if supine, R upper lobe probably

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21
Q

List the three main structures perforating the diaphragm and at which levels they do so

A
  1. IVC (T8)
  2. Esophagus (T10)
  3. Aortic hiatus (T12)

“I(VC) 8 10 eggs (esophagus) at (aorta) 12”

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22
Q

The IVC as well as (X) perforate diaphragm at T(8/10/12).

A

X = right phrenic n

T8

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23
Q

The Esophagus as well as (X) perforate diaphragm at T(8/10/12).

A

X = vagus n (CN 10)

T10

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24
Q

The Aorta as well as (X) perforate diaphragm at T(8/10/12).

A

X = azygos vein, thoracic duct
T12

“At T-1-2 is the red, white, and blue”

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25
Q

The trachea bifurcates at which SC level?

A

T4 (biFOURcates)

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26
Q

The common carotid bifurcates at which SC level?

A

C4 (biFOURcates)

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27
Q

Functional residual capacity calculation:

A

RV+ERV (volume of gas in lungs after normal expiration)

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28
Q

Vital capacity calculation:

A

IRV + TV + ERV (max volume of gas that can be expired after max inspiration; also equals TLC - RV)

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29
Q

Aging changes: (increased/decreased) chest wall compliance, (increased/decreased) lung compliance, and (increased/decreased) (RV/TLC).

A

Decreased (calcification/stiffening of ribs)
Increased (loss of elastic recoil)
Increased RV; no change in TLC

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30
Q

Physiologic dead space equation

A

VD = VT*((PaCO2-PeCO2)/PaCO2)

“Taco, Paco, Peco, Paco”
VT= Tidal V
PeCo2 = expired air PCO2

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31
Q

Physiologic dead space refers to air in:

A

Conducting zone (aka anatomical dead space) + alveolar dead space (primarily in apices of lungs)

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32
Q

T/F: Physiologic dead space is much greater than anatomical dead space in normal lungs

A

False - the two are approximately equal in healthy lungs (barely any physio dead space), but physiological dead space may be greater if V/Q defect

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33
Q

At (X) lung volume, airway/alveolar pressures are zero and intrapleural pressure is (pos/zero/neg).

A

X = FRC (note: inward pull of lung balanced by outward pull of chest wall at this volume)

Neg (about -5 cm H2O)

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34
Q

T/F: Alveolar transmural pressure is always positive, regardless of volume of air in lungs.

A

True - perpetual collapsing force on lungs

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35
Q

Deoxy Hgb has (high/low) oxygen affinity

A

Low (taut form;promotes release/unloading of O2)

Oxy Hgb is relaxed form and has high affinity for O2

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36
Q

Mutations that alter (X) in Hgb will cause lower 2,3-BPG affinity

A

X = 2,3-BPG binding pocket positive charge

2,3-BPG is negatively charged, so mutation in binding pocket that decreases positive charge will decrease affinity (ex: familial erythrocytosis)

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37
Q

The phrenic nerve carries pain fibers from which parts of (visceral/parietal) pleura?

A

Parietal (diaphragmatic and mediastinal; the rest is via intercostal nerves)

Visceral pleura does not have pain fibers

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38
Q

Oxidized form of Hgb is (X). It binds O2 (more/less) readily and patient presents with which unique features?

A

X = MetHgb (Fe3+ state)
O2 less readily (but high affinity for CO)

Cyanosis (dusky skin) and chocolate-colored blood

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39
Q

Carboxyhemoglobin, aka bound to (X), (increases/decreases) Hgb affinity for O2.

A

X = CO
Increases; curve shifts left (puts Hgb in relaxed, high affinity state)

BUT also binds Hgb competitively with 200x greater affinity (so both lower O2 binding capacity and lower O2 unloading in tissues)

40
Q

(X) Hgb modification Sx: headaches, dizziness, cherry red skin

A

X = carboxyHgb (CO poisoning)

41
Q

Altitude will (R/L)-shift Hgb curve

A

R

42
Q

T/F: Normal, healthy lungs are perfusion-limited

A

True (diffusion-limited examples: emphysema, fibrosis)

43
Q

Which parts of the diffusion equation are (increased/decreased) in emphysema? And in pulm fibrosis?

A

Equation: V = AD(P1-P2)/T

Emphysema: Decreased area (for diffusion)
Fibrosis: Increased thickness (T)

44
Q

Oxygenation (dips/rises) between alveolar capillary blood and systemic arterial blood. Why?

A

Dips slightly

Mix of pulmonary vein oxygenated blood with deoxy blood from bronchial and Thebesian veins

45
Q

Pulmonary vascular resistance is lowest at which lung volume?

A

FRC

46
Q

As lung volume increases, Pulm vasc resistance (increases/decreases) due to (alveolar/extra-alveolar) vessels

A

Increases;

Alveolar (lower diameter at higher volumes)

47
Q

As lung volume decreases, Pulm vasc resistance (increases/decreases) due to (alveolar/extra-alveolar) vessels

A

Increases

Extra-alveolar

48
Q

Alveolar gas equation:

A

PAO2 = PIO2 - (PaCO2/R)

PIO2 is PO2 of inspired air
R is respiratory quotient (CO2 produced/O2 consumed; normally 0.8)

49
Q

Normal A-a (PAO2-PaO2) gradient

A

10-12 mmHg

50
Q

Main two causes of hypoxemia with normal A-a gradient

A

Altitude and hypoventilation (ex: opioids, obesity hypovent syndrome)

51
Q

V/Q at base of lung is (0.6/3) and at apex is (0.6/3).

A

0.6 (wasted perfusion)

3 (wasted ventilation)

52
Q

T/F: Ventilation is greater at apex of lung and perfusion is greater and base of lung

A

False - both greater at base

53
Q

How does exercise alter the V/Q ratio?

A

Vasodilation of apical capillaries (causes V/Q to approach 1 instead of 3ish)

54
Q

Pulmonary embolus V/Q ratio:

A

Infinity (Q = 0); blood flow obstruction, physiologic dead space (an example of V/Q mismatch)

55
Q

Haldane effect seen in (periphery/lungs)

A

Lungs; O2 displaces H+ from Hgb, promoting CO2 formation/release from RBCs

56
Q

Bohr effect seen in (periphery/lungs)

A

Periphery; high H+ from metabolism causes R curve shift and promotes O2 unloading

57
Q

Major form of CO2 in blood is carried as:

A

HCO3-

58
Q

Renal excretion of (H/HCO3) occurs after (X) hours at high altitude. What would the pH, PCO2, PO2 be at that time?

A 
HCO3
X = 24-48
pH = mildly alkalotic
PCO2 = still low 
PO2 = super low (ex: 55 mmHg)
59
Q

T/F: Exercise increases PaO2 and decreases PaCO2

A

False - values don’t change; but venous CO2 increases and venous O2 decreases

60
Q

(X) sinus is most typically affected in rhinosinusitis. It drains into (Y)

A 
X = maxillary
Y = middle meatus
61
Q

Life-threatening nosebleeds can result from hemorrhage of (X) artery

A

X = sphenopalatine (branch of maxillary; in posterior segment of nostril)

62
Q

T/F: Both tobacco and alcohol are risk factors for H+N squamous cell carcinoma

A

True

63
Q

Pre- and post-mortem thrombi can be distinguished by which finding?

A

Lines of Zahn: inter-digitating areas of pink (platelets, fibrin) and red (RBCs) only in pre-mortem thrombi

64
Q

Clots in pulmonary vasculature staining black with osmium tetroxide

A

Fat emboli

65
Q

Imaging test of choice of PE:

A

CT pulm angiography

66
Q

(Proximal/distal) PEs are more likely to cause lung infarct

A

Distal (under 3 mm, in small aa) since they occlude areas distal to pulmonary and bronchial system anastamoses

67
Q

Curschmann spirals:

A

Asthma

Shed epithelium forming whorled mucous plugs

68
Q

Charcot-Leyden crystals

A

Asthma

Formed from eosinophil breakdown in sputum; eosinophilic, hexagonal, needle-like crystals

69
Q

Primary immune cells/response in asthma

A

Th2 (excess IgE; IL-4, 5, 13 and eosinophils)

70
Q

Primary cells increased/involved in pathogenesis of COPD

A

Neutrophils (and their elastase);

also macros, CD8 T cells

71
Q

Which (obstructive/restrictive) lung disease associated with Kartagener?

A

Bronchiectasis (poor ciliary motility); obstructive

72
Q

Asthma: key pathology is (X) (hypertrophy/atrophy)

A

X = smooth muscle
Hypertrophy and hyperplasia

(Mucous glands as well in chronic asthma)

73
Q

Sudden onset cough, wheezing, tachypnea in 6 yo child. Lungs appear vertically elongated on CXR and you hear pulsus paradoxus on exam.

A

Asthma

74
Q

Bronchiectasis pathophysiology

A

Chronic necrotizing infection of bronchi leading to permanently dilated airway

75
Q

Asbestos affects (upper/lower) lung lobes. What about Silica? Coal?

A

Asbestos: lower (“Asbestos from the roof, but affects base”)

Silica and coal: upper (“Silica and coal from base/earth, but affect roof”)

76
Q

Aerospace industry worker with restrictive lung disease

A

Berylliosis (non-caseating granulomas, usually upper lungs)

77
Q

Which restrictive lung disease increases susceptibility to TB?

A

Silicosis (impairs macrophages and disrupts phagolysosomes)

78
Q

Ferruginous bodies can be visualized using (X) stain

A

X = Prussian (since coated with iron)

79
Q

PCWP in ARDS

A

Normal (non-cardiogenic pulmonary edema)

80
Q

Distinguishing features between obstructive sleep apnea and Obesity hypoventilation syndrome

A

OHS/Pickwickian syndrome associated with hypoventilation and high PaCO2 during waking hours as well as during sleep;
OSA not necessarily only in obese patients and involves airways obstruction, snoring, etc.

81
Q

Heritable Pulm HT caused by mutation in (X), the product of which normally has what function?

A

X = BMPR2 gene (AD inheritance)

Inhibits smooth muscle proliferation

82
Q

Pulm HT Rx:

A

Bosentan (endothelin-R antagonist)

83
Q

Lungs: Decreased breath sounds, decreased fremitus with hyperresonance on percussion. Differential?

A

Either simple or tension pneumothorax

Check tracheal deviation (will be away from side of lesion in tension pneumothorax; no deviation in simple)

84
Q

Lungs: decreased breath sounds, dullness to percussion, decreased fremitus. Differential?

A

Either pleural effusion or atelectasis (bronchial obstruction)

Check tracheal deviation (will be toward side of lesion in atelectasis; no deviation or away from lesion in pleural effusion)

85
Q

(PaO2/PaCO2) is the significant drive for respiration in chronic COPD patients

A

PaO2 (unlike healthy individuals) due to decreased sensitivity of central chemoreceptors for PaCO2

So carotid bodies sensing increase in PaO2 are responsible for decreasing respiratory rate in these patients

86
Q

Aging: TLC (increases/decreases), RV (increases/decreases), forced VC (increases/decreases).

A

No change;
Increases
Decreases

87
Q

Obesity effect on lungs:

A

Obesity-related restrictive lung disease (decline in all lung volumes except minimal effect on RV)

88
Q

Air enters pleural space and can’t exit. Trachea deviated (toward/away from) affected lung

A

Away from

Tension pneumothorax

89
Q

H. flu and S. aureus cause which type of pneumonia?

A

Bronchopneumonia (patchy distribution involving 1+ lobes)

90
Q

Non-infectious pneumonia characterized by inflammation of bronchioles and surrounding structures. Negative sputum/blood cultures and non-responsive to antibiotics

A

COP (Cryptogenic organizing pneumonia); unknown etiology

91
Q

Most common causes of SVC syndrome

A
  1. Lung cancer (superior sulcus aka Pancoast tumor)

2. NHL

92
Q

“Innominate” vein

A

Brachiocephalic v

93
Q

Lung cancer staining positive for Chromogranin A and synaptophysin

A

Small cell (neuroendocrine tumor)

94
Q

EML4-ALK Fusion protein codes for (X) and usually seen in (Y) cancer

A 
X = constitutively active Tyr Kinase (like Bcr-Abl)
Y = adenocarcinoma of lung
95
Q

Pseudoephedrine belongs to which class of drugs?

A

Alpha 1 agonists (like phenylephrine) - used as nasal decongestant

…Also illicitly used to make meth

96
Q

Methylxanthines can be used to treat (X) via which MOA?

A

X = asthma

Inhibit PDE and thus increase cAMP (by decreasing its hydrolysis)

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