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SBM > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Which airways have cartilage and which airways do not?

A

large airways- cartilage

small airways- non-cartilage

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2
Q

What decreases and increases surface tension in lungs?

A

decreased- saline filled lungs

increased - surfactant deficiency

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3
Q

Flow limitation

A

point where any increase in effort makes no increase in flow because airway can collapse

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4
Q

Pcritical is a marker of

A

tendency of airways to collapse

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5
Q

Three Factors that contribute to maximum flow rate

A

decreased Elastic recoil
Increase in Pcritical
Increase in R upstream

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6
Q

decreased expiratory flow rates seen in (3)

A

1- increased airway resistance
2- decreased elastic recoil
3- decrease in lung volume

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7
Q

RV is increased most in

A

obstructive airway disease (air trapping)

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8
Q

5 general categories of restrictive lung disease

A 
neuromuscular disease
chest wall problems
pleural disease 
loss of lung
interstitial lung disease
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9
Q

Efferent impulses in respiratory control from Cranial nerves

A

9,10,11,12

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10
Q

Length tension, a short muscle is a

A

weak muscle

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11
Q

energy consumption is via 2 factors in muscles

A

tension produced by muscle

velocity of shortening in muscle

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12
Q

two reasons resp muscles require more energy

A
  • asked to do more

- at a mechanical disadvantage

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13
Q

Centriacinar Emph

A

enlarged resp bronchioles and normal distal ascini

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14
Q

panacinar emph

A

resp–>distal ascini all affected

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15
Q

Paraseptal emph

A

distal ascinus only

associated with bullae and pneumothroax

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16
Q

charcot-leyden crystals

A

degranulated eosinophil membranes found in asthma

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17
Q

curschmann spirals

A

whorls of shed epithelium in asthma

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18
Q

acute vs late phase asthma

A

acute- mast cell mediated

late phase- leukocyte mediated, tissue destruction

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19
Q

3 types of medications for COPD

A

B-agonists, Anticholinergic, Methylxanthines

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20
Q

when are glucocorticoids appropriate for COPD patients?

A

<50% FEV1 and freq exaccerbations

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21
Q

airway remodeling

A

increase in ECM

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22
Q

pulmonary arterial hypertension

A

pH when fundamental abnormality arises in pulmonary vasculature

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23
Q

2 ways that pulmonary arterioles dilate

A

passive- thin-walled and contain little muscle (so due to CO2)
active- release of EDRF/NO

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24
Q

ihibitors vs constrictors in PVR

A

inhibitors- prostacyclin, NO

vasoconstriction- thrmboxane A2, endothelin-1, 5HT

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25
Q

Pressure left atrium best estimated by

A

pulmonary wedge pressure

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26
Q

pulmonary artery pressure equation

A

Ppa= (CO x PVR) + PLa

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27
Q

two types of granulomatous ILD

A

sarcoidosis

hypersensitivity pneumonia

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28
Q

smoking related ILD

A

respiratory bronchiolitis ILD

desquamative interstitial pneumonia

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29
Q

first thing that happens in ILD

A

type 2 pneumocyte hyperplasia

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30
Q

3 ways lung can get fibrotic

A

fibroblast can get activated –>interstitum thicker

epithelial gets injured–>fibrin leaks out and fibroblasts pass through

granulomas

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31
Q

caplan syndrome

A

rheumatoid arthritis + pneumoconiosis

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32
Q

2 forms silicosis

A

crystalline- most fibrogenic, 100x smaller than sand

amorphous (talc)-more clearance, less firbogenic

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33
Q

two fiber types in asbestosis

A

serpentine-curly and flexibile- more widely used in industry

amphibole- straight and rigid- more pathogenic

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34
Q

smoking + asbestos

A

55 fold increase in lung cancer–>synergistic!

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35
Q

three examples of hypersensitivity pneumonitis

A

1) farmers lungs
2) pigeon breeders lungs
3) humidifier lung

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36
Q

patient profile of sarcoidosis

A

cytokines- IL2
CD4+ lymphs
activated macrophages
class II HLA expression

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37
Q

why does ILD have decreased compliance and diffusion impairment?

A

deposition of collagen

thickening of interstitum

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38
Q

ILD breath patterns

A

rapid and shallow

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39
Q

treatments in IPF

A

Pirenidone-inhibits TGFB1- slows progression IPF

Nitendanib- inhibits multiple tyrosine kinases and a variety of growth factor receptors–>slows decline in lung function

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40
Q

inertial impaction increases with

A

large particle size
high inspiratory flow rates
tortuous pathways
interceptors

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41
Q

sedimentation increases with

A

lower airflow
smaller airway lumen
optimal particle size

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42
Q

three variations of disease in mucociliary disease

A

cystic fibrosis: sol phase
chronic bronchitis: gel phase
kartagener syndrome: cilia

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43
Q

varenicline

A

smoking pharmaceutic–partial agonist of A4B2 nicotinic acetylcholine receptor which may play a role in addiction

44
Q

pleurodesis

A

process or intervention where inject something or do something to pleural surface to make it inflamed and when body has inflammation, responds by forming adhesions

45
Q

opiate antidote

A

naloxone

46
Q

central alveolar hypoventlation

A

due to altered function of brainstem resp neurons, resulting in hypoventilation

47
Q

Obestiy-Hypoventilation/Pickwickian Syndrome

A

R heart failure due to plum vasoconstriction from hypoxemia

48
Q

no hypercapnia in

A

asthma

49
Q

where is periodic breathing seen

A

bilateral cerebral dysfunction
congestive heart failure
hypoxia

50
Q

paraneoplastic syndrome

A

signs and symptoms caused by factors produced by cancer cells that act a distance from both primary cancer site and its metastases

51
Q

ectopic ACTH secretion

A

small cell lung carcinoma with poor prognosis

52
Q

inappropriate secretion of ADH

A

small cell lung carcinoma that does not effect prognosis

53
Q

pancoast tumor

A

tumor at lung apex where pleural reflex is

horner’s syndrome
pancoast syndrome
recurrent laryngeal nerve–>hoarseness

54
Q

squamous cell carcinoma

A

central lesion, may cavitate

55
Q

adenocarcinoma

A

peripheral lesion

56
Q

Erlotinib

A

EGFR-TK1 tyrosine kinase inhibitor

57
Q

Class 1 mutation

A

defective protein product

58
Q

class 2 mutation

A

defective protein processing

59
Q

class III

A

defective protein regulation- diminished ATP binding and hydrolysis

60
Q

class IV

A

defective protein conductance- defective chloride conductance or channel gating

61
Q

class V

A

promoter or splicing abnormality-reduced number of CFTR transcripts due to promoter or splicing abnormality

62
Q

class VI

A

accelerated turnover-accelerated turnover from cell surface

63
Q

fetal vasoconstriction

A

physical lung fluid
dec O2 and pH
leukotrienes
thrmboxane A2

64
Q

fetal vasodilation

A

NO
increase O2 and pH
PGI2 prostacyclin

65
Q

major constrictor ductus arteriosus

A

ET1

66
Q

major dilator ductus arteriosus

A

PGE2

67
Q

4 things that cause DA constriction

A

increase PaO2
decrease PVR from O2–>decrease in BP in DA
decrease PGE2 (loss of placenta and increased PG removal from lung)
decrease in PGE2 receptors in DA wall

68
Q

indomethacin

A

prostaglandin synthetase inhibitors

complications-renal failure, GI perforations, necrotizing enter colitis

69
Q

what age are alveoli close enough to caps to transmit o2?

A

24 weeks

70
Q

bronchial tree developed by

A

16th week of intrauterine life

71
Q

alveoli continue to grow

A

through life

72
Q

preacinar blood vessels follow

A

airways

73
Q

intra-acinar vessels

A

follow alveoli

74
Q

aberrant subclavian artery only compresses

A

esophagus

75
Q

anomalous innominate artery only compresses

A

trachea

76
Q

extrathoracic obstruction produces

A

inspiratory stridor

77
Q

intrathoracic obstruction

A

exp wheeze

78
Q

single point of obstruction

A

one wheeze

79
Q

mutiple pts of obstruction

A

lots of little wheezes

80
Q

in situ means

A

hasn’t invaded through the basement membrane yet

81
Q

cytokeratin

A

intermediate filament in the cytoplasm of epithelial cells

82
Q

vimentin

A

intermediate filament in the cytoplasm of tissue derived from mesoderm

83
Q

TTF1

A

nuclear transcription factor expressed in lung epithelium and thyroid epithelium

84
Q

synaptophysin

A

neuroendocrine marker

85
Q

Met vs Primary

A

Met has sharp demarcation of metastasis

86
Q

carcinoid tumor

A

ribbons of cells

87
Q

positive synaptophysin stain

A

small cell carcinoma

88
Q

virchow’s triad

A

endothelial injury
abnormal blood flow
hypercoag

89
Q

saddle embolus

A

thromboembolus that lodges at bifurcation of right and left plum arteries

associated with sudden death

90
Q

pulmonary infarcts early

A

deep red color
ischemic necrosis
diffuse RBC
exudate

91
Q

infarcts greater than 48 hrs

A

RBC lysis
hemosiderin laden
macrophages
lung appears paler

92
Q

days

A

fibrosis (from margins inward)

gray-white color

93
Q

compliance

A

deltaV/deltaP

94
Q

Pmax=

A

Pelastic-Pcrit/R upstream

95
Q

Pcrit=

A

> 0 tendency to collapse
<0 tendency to stay rigid

Pcrit=Pcollapse-Ppleural

96
Q

PIO2

A

(Pb-47)(.21)

97
Q

sol phase

A

water and solute that lines resp tract

98
Q

gel phase

A

glyoprotiens

99
Q

pleurodesis

A

chemical irritant put to increase inflammation and remove what is bothering

100
Q

zone 1 conditions

A

Palv>Ppa>Ppv

no cap perfusion; in normal conditions no zone 1

101
Q

zone 2 conditions

A

Ppa>Palv>Ppv
driving pressure is difference between Ppa and Palv
as you move down the lung, driving pressure and blood flow increases

102
Q

zone 3

A

Ppa>Ppv>Palv

traditional flow relationship

103
Q

pvr=

A

ppa-pla/co

usually < 2

104
Q

hemoglobin does not affect

A

po2 or O2sat

105
Q

oxygen content but not saturation shift based on

A

polycythemia vs anemia

106
Q

extrathoracic obstruction causes

A

collapse on inspiration (decrease flow on inspiration)

107
Q

intrathoracic obstruction causes

A

a collapse on expiration (decrease flow on expiration)

SBM (18 decks)

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