Exam 2 Flashcards

1
Q

lamberts canals

A

terminal and respiratory airways to alveoli

allows 1 alveolus to help open another

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2
Q

volatile vs. fixed acids

A

volatile: from CO2, can be eliminated by respiration (12,000-20,000 mEq/day)
fixed: from protein catabolism, eliminated by kidneys (50-100 mEq/day)

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3
Q

basal cells

A

adult stem cells of respiratory epithelium; at the base of epithelium above the basement membrane

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4
Q

AMP Kinase

A

activated with AMP:ATP ratio is low (ATP used up) that activates PGC-1alpha to go to nucleus for mitochondrial biogenesis and energy production

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5
Q

how is the epithelium in the larynx

A

false vocal cords: typical respiratory epithelium

true vocal cords: squamous epithelium

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6
Q

body’s 3 methods of preserving pH

A
  1. extracellular and intracellular buffering (sponge) - immediate
  2. respiratory adjustments - few seconds
  3. renal adjustments - hours to days
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7
Q

where are intrapleural pressures less negative? what are the implications of this?

A

the dependent portion of the lung

means that in the apex of the lung there is higher transpulmonary pressure/are already distended and less compliant

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8
Q

pink puffer

A

emphysema

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9
Q

pneumotaxic center

A

(pons) can inhibit inspiration

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10
Q

cromolyn sodium

A

asthma treatment

targets mast cells

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11
Q

mesothelioma

A

malignant tumor of the pleura assoc. with asbestos exposure

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12
Q

where is the central chemoreceptor located and what does it sense

A

brainstem (ventral surface of medulla), senses changes in CSF pH when CO2 diffuses out of cerebral capillaries

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13
Q

what is wedge a surrogate marker of?

A

left arterial pressure

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14
Q

fowler method

A

anatomic dead space

breathing in 100% O2 and wait to detect nitrogen

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15
Q

haldane effect

A

when Hb is bound to less O2 it has more affinity for CO2

H dissoc. from Hb shifts equilibrium to CO2 formation so it can leave the RBC

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16
Q

what is the A-a gradient?

A

by the time blood exits to the left heart there is a gradient between O2 in the alveolus and O2 in arterial system that creates the venous admixture (due to intrapulmonary and anatomical shunts)

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17
Q

irritant receptors

A

located between airway epithelial cells, rsponse is to constrict (from noxious gases, cigarette smoke, inhaled dust/cold air

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18
Q

J receptors

A

juxtacapillary receptors
located in alveolar walls close to capillaries, activated by engorgement of pulm caps and inc. in interstitial lung volume. result in increased breathing rate

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19
Q

what is the optimal position of a swan ganz catheter

A

zone 3 because Pa>Pv>PA

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20
Q

expiratory time constant

A

describes lung emptying

Exp TC = C x R

(in emphysema higher because higher compliance and increased resistance)

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21
Q

glutaminase

A

stimulated by low pH to make glutamate –> alpha KG –> bicarb (reabsorbed) and also make NH4 which becomes NH3 (diffuses out) and H pumped out to excrete NH4

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22
Q

cortex controls

A

voluntary ventilation (hyper/hypoventilation)

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23
Q

what happens to fixed acid?

A

100% gets excreted!
40% excreted as titratable acid and is excreted with urinary buffers
60% excreted as NH4+

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24
Q

pleurisy

A

inflammation of the pleura, secondary infection and exudate cause restriction of lung movement

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25
Q

Dalton’s law

A

Px=(PB-PH2O) x F

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26
Q

ventral respiratory group

A

(medulla) assoc with expiration

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27
Q

seromucous glands found in

A

extrapulmonary bronchi

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28
Q

main immune cells activated in asthma

A

eosinophils and mast cells

mast cells = bronchoconstriction
dendritic cells = release TH2 which causes B cell and Ab production which makes more mast cells and eosinophils that lead to inflammation

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29
Q

chloride shift

A

trade bicarb for chloride in RBC to continue driving reaction forward

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30
Q

why is nitrogen washout used?

A

to assess anatomic dead space - underestimate lung volumes in COPD, use C1V1=C2V2

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31
Q

where are peripheral chemoreceptors? what do they repsond to?

A

carotid and aortic bodies

respond to dec. PO2, inc. PCO2, dec. pH

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32
Q

inflammatory cell population differences between COPD and bronchial asthma

A

COPD: neutrophila, macrophages, CD8 T lymphocytes, eosinophils (exacerbations)

Asthma: eosinophils, mast cells, CD4 T lymphocytes, macrophages and neutrophils

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33
Q

alpha 1 antitrypsin deficiency

A

increases neutrophil elastase with no antiprotease activtity

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34
Q

impaction occurs in the

A

nasopharynx (largest particles)

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35
Q

what does macrophage recruitment in COPD do?

A

Th1 and Tc1 cells –> alveolar wall destruction
neutrophils (proteases like n elastase and MMP9) –> destruction and mucous hypersecretion
monocytes

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36
Q

normal arterial plasma H

A

40 nM (means pH = 7.4)

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37
Q

sedimentation occurs in the

A

smaller airways (medium particles; mucocilliary transport)

38
Q

normal values for K

A

3.5-5.5 mEq/L

39
Q

hysteresis

A

PV curves are different for inspiration and expiration - we measure compliance on expiratory limb

40
Q

VILI

A

ventilator induced lung injury (in ARDS)
barotrauma, volutrauma, atalectrauma (low lung vol), biotrauma (inflammation from mediators recruited by mechanotransduction)

41
Q

normal intrapulmonary shunt

A

V/Q mismatch

42
Q

dorsal respiratory group

A

(medulla) assoc with inspiration

43
Q

what is the only way to decrease mortality in ARDS

A

lung protective ventilation (with lower tidal volumes and airway pressures)

44
Q

when is arterial bicarb considered saturated?

A

if it is over 40 mEq/L, excess gets excreted

45
Q

triacylglycerol lipase

A

activated by PKA, cuts FA so they are released to make ATP

46
Q

bowmans glands

A
secrete serous (watery/proteins) not mucous to wash away ligands/no odor fatigue
in nasopharynx
47
Q

DLCO

A

used to see lung’s ability to absorb O2 - CO mean cap pressure is zero and doesn’t reach equilibrium –> depends on characteristic of membrane, bf and Hb

48
Q

hering breuer reflex

A

due to pulmonary stretch receptors in the lung - mechanoreceptors in SM of airways sense stretch to see if tidal volume goes higher than it should

49
Q

where do club cells appeal

A

bronchioles

50
Q

low K means…

A

NH3 synthesis/H excretion (low K = low H = high pH)

51
Q

pre-botzinger complex

A

(medulla) pattern generator, also ventral

52
Q

what do PAMPs and DAMPs do?

A

activate innate immune response which causes SIRS (systemic inflammation response syndrome) in ARDS

53
Q

PaCo2 < expected

A

respiratory alkalosis

54
Q

if a structure is above its stressed volume it wants to:

A

collapse/shrink

think of lungs by themselves at their unstressed volume of 150 mL

55
Q

is deoxyHb or oxyHb a better intracellular buffer?

A

deoxyHb (pK is 7.9 versus oxyHb Pk is 6.7)

56
Q

diffusion occurs in the

A

alveoli (smallest particles; alveolar macrophages engulf particles)

57
Q

pores of kohn

A

between alveoli/cell traffiking

58
Q

heliox is useful because

A

changes turbulent flow to laminar flow, result is decreased work of breathing (in asthma, COPD, tracheal mass)

59
Q

normal albumin levels in plasma

A

3.5-5.5 g/dL

60
Q

abnormal anatomical shunts

A

patent ductus arteriosus, VSD, pulmonary A-V anastamosis

61
Q

PaCo2 > expected

A

respiratory acidosis

62
Q

abnormal intrapulmonary shunt

A

decreases ventilation due to atalectesis/low compliance/high resistance/inactivated surfactant

63
Q

albumin and alkalemia

A

in alkalemia, less H is bound to albumin so more Ca is bound (=less free in blood –> hypocalcemia)

symptoms of hypocalcemia are respiratory alkalosis, tingling, numbness and tetany

64
Q

Henry’s law

A

Cx = Px x solubility

65
Q

what do epithelial cells do in COPD?

A

secrete TGF beta for fibroblast proliferation/fibrosis of small airways

66
Q

O2 content equation

A

O2 content = (1.32 x Hb x SaO2) + (0.0031 x PaO2)

67
Q

delta AG < delta bicarb

A

non gap metabolic acidosis

68
Q

how does epitheiulm change in the bronchioles

A

low pseudostratified –> ciliated columnar –> simple cuboidal

69
Q

alveolar gas equation

A

PACO2 = (PIO2 - PACO2) / R

70
Q

bronchial C fibers

A

response to stimulation are shallow breathing, bronchoconstriction, mucous secretion

71
Q

total resistance of an airway is determined by:

A

radius of airway, length of airway, viscosity of gas

72
Q

kartageners syndrome

A

immotile cilia - microtubules lack dyenin arms of ciliary anexomes

73
Q

anti leukotrienes

A

asthma treatment

targets histamine, PGD2 (lead to bronchoconstriction)

74
Q

blue bloater

A

chronic bronchitis

75
Q

alveolar ventilation equation

A

VA=(VCO2 x K) / PACO2

76
Q

normal anatomical shunts

A

thebesian veins (drains LV), bronchial veins (drain lungs right into pulmonary vein)

77
Q

mean end pulmonary capillary gas content equation

A

the contribution of each area is weighted based on the amount of blood flow leaving each area, not the average of contents from all areas

Ccgas = sum (%QT) (CcGas)

78
Q

2 main extracellular buffers

A

CO2/HCO3 (pk=6.1) and H2PO4/HPO42- (pk=6.8)

79
Q

at what pH does urinary H secretion stop

A

under 4.4 urinary pH

80
Q

apneustic center

A

(pons) excitatory funciton

81
Q

delta AG = delta bicarb

A

inc gap metbaolic acidosis

82
Q

squamous metaplasia

A

epithelium changes from pseudostratified ciliated columnar epithelium to squamous epithelium

excessive drying of the mucosa leading to change in epithelium –> severe infections

83
Q

is the response faster in central or peripheral chemoreceptors?

A

peripheral! but most of the stimulus comes from central

84
Q

limbic system and hypothalamus control

A

alternations in breathing patterns from emotional states

85
Q

autophagy

A

process of getting rid of damaged mitochondria. phagophore engulfs mito and fuses with lysosme

86
Q

normal values for Na

A

135-145 mEq/L

87
Q

delta AG > delta bicarb

A

metabolic alkalosis

88
Q

refractory hypoxemia

A

unresponsive to giving O2

seen in ARDS

89
Q

high K means…

A

inhibits NH3 synthesis/H excretion (high K = high H = low pH)

90
Q

what happens to K when H concentration inside the cell increases

A

K decreases to try to maintain H concentration