Pulmonary Exam II Flashcards

1
Q

Pneumonia is the ____th leading cause of death

A

7th

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2
Q

Last part of the upper respiratory tract

A

larynx

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3
Q

Smallest respirable particle

A

less than 10 um

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4
Q

Intrinsic defenses that serve as barriers against inhaled particles or microorganisms

A

surfactant

iron-containing proteins (transferrin, IgG)

complement pathway activation

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5
Q

principle phagocytic cells in the distal air spaces

A

alveolar macrophages

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6
Q

results of cytokind production

A

increases alveolar capillary permeability

decreases lung compliance

increases work of breathing

V/Q mismatch

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7
Q

Infection and proliferation of microorganisms within the alveolar space cause ___, ___, and ___

A

acute inflammatory response

cytokine production

hypoxia

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8
Q

two types of bacterial pneumonia

A

bronchopneumonia and lobar

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9
Q

why may giving oxygen widen V/Q ratios in lobar pneumonia?

A

decreases HPV and activates inflammatory mediators

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10
Q

Types of eartly onset bacterial pneumonia

A

strep, influenza, staph, and e.coli

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11
Q

types of late onset bacterial pneumonia

A

pseudomonas, MRSA

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12
Q

Abx should begin within ____ of presentation to ER with pneumonia

A

4 hours

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13
Q

anti-microbial therapy for patients under 65 y.o for pneumonia

A

oral marcolide or oral doxycycline

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14
Q

which patients have the greatest risk of viral pneunomia?

A

infants and children

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15
Q

most common viruses in adults

A

influenza, adenovirus, and hanta

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16
Q

Diagnosis of viral pneumonia

A

obtain viral cultures or via nasal swabs

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17
Q

Overview of Tuberculosis

A
  • between 1-5 um
  • thrive in high O2 lung zones (zone 1)
  • settle beyond terminal bronchioles
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18
Q

Ghon Complex

A

lesion in the lung caused by tuberculosis that involves a lymph node

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19
Q

Drug treatment for Tuberculosis

A

isoniazid, Rifapentine, and rifampin

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20
Q
A

Tuberculosis

left (cavilary lesion)

right (ghon complex)

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21
Q
A

fungal infection

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22
Q

reflection coefficient of pulmonary capillary endothelium

A

0.5

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23
Q

Stages of Pulmonary Edema

A
  1. Interstitial pulmonary edema
  2. crescentric filing of alveoli
  3. alveolar flooding
  4. froth in air passages
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24
Q

at what stage of pulmonary edema will you have dyspnea at rest?

A

stage II

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25
Q

normal mean pulmonary arterial pressures (mPAP)

A

12-14 mmHg

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26
Q

SVR equation

A

(MAP - CVP) / CO

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27
Q

PVR equation

A

(PAP - PCWP) / CO

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28
Q

Normal PCWP

(pulmonary capillary wedege pressure)

OR

left atrial pressure

A

6-8 mmHg

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29
Q

determinants of mPAP

A

left atrial pressure, pulmonary blood flow, and PVR

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30
Q

normal albumin levels

A

3.5 - 5.5 g/dL

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31
Q

How does albumin affect the oncotic pressure?

A

increases

allows the fluid to not leak into interstital space

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32
Q

Interstital pressure equation

A

(HPinterstital - HPcapillary) - omega(piin - picap)

HP - hydrostatic pressure

pi - protein osmotic pressure

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33
Q

Increased capillary hydrostatic pressure may imply ____

A

transudate

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34
Q

Elevated pulmonary capillary pressure is caused by what 4 things?

A
  • hypervolemia
  • redistribution of circulating blood volume
    • T-berg, vasopressors
  • increased pulmonary vensou pressure
    • left heart failure, cardiogenic pulmonary edema
  • increased pulmonary blood flow
    • left-to-right shunt
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35
Q

what may cause pulmonary edema?

A

increased permeability of alveolar/capillary membrane

  • stress failiure
  • inflammation
  • aspiration
  • drowning
  • TRALI
  • exudate
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36
Q

NPE

A

neurogenic pulmonary edema

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37
Q

Neurogenic Pulmonary Edema

A

acute pulmonary edema following a CNS insult

  • large surge of catecholamines resulting in ventricular dysfunction
  • increase in pulmonary venous pressure
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38
Q

Etiology of Pulmonary Edema

A
  • neurogenic pulmonary edema
  • re-expansion pulmonary edema
  • osmotic pressure
  • lymphatic obstruction or reduced drainage
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39
Q

Treatment for cardiogenic pulmonary edema

A
  • decrease left atrial pressure (Pc)
    • decrease preload
    • increase inotropy
  • volume overload
    • vasodilators or diuretics
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40
Q

Permeability treatment for pulmonary edema

A

increase plasma albumin

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41
Q

NPPE

A

negative pressure pulmonary edema

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42
Q

Type I NPPE

A

occurs immediately after onset of airway obstruction

(hanging, chocking, croup)

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43
Q

Type II NPPE

A

occurs after relief of airway obstruction

(removal of tonsils)

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44
Q

under what pressures may cause NPPE

A

-50 to -100 cmH2O

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45
Q

Treatment of NPPE

A
  • relieve obstruction
  • diuretics
  • artifical ventilation
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46
Q

Dyspnea in pulmonary edema

A

stimulaiton of J receptors

minimizes low compliance of lungs

hypoxemia

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47
Q

where should you see the end of an ETT on chest x-ray?

A

clavicle

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48
Q
A

Pulmonary Edema

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49
Q

acute sigs of PE

A

increases dead space and right heart failure

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50
Q

early signs of pulmonary air embolism

A

reduction in EtCO2 and decrease in PaO2

an increase in EtN2 is most sensitive

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51
Q

late signs of pulmonary air embolism

A

hypotension, tachycardia, dysrhythmias, and cyanosis

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52
Q

most sensitive sign of a PE

A

increase in EtN2

must have a mass spec

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53
Q

anatomical variation with increased risk of PE

A

patent foramen ovale

54
Q

causes of pulmonary venous HTN

A

LV failure and mitral insufficiency

55
Q

Drugs for Treatment in PHTN

A
  • phosphodiesterase III inhibitors
  • B-Type Natriuretic Peptide
  • PGI2
    • prostacyclin
  • PGE1
    • alprostadil
56
Q

Isoproterenol

A
  • non-selective Beta agonist
  • positive chronotropy and inotropy
  • pulmonary and systemic vasodilator
57
Q

Dobutamine

A
  • Beta agonist with minimal alpha
  • positive chronotropy and inotropy
  • pulmonary and systemic vasodilator
58
Q

Epinephrine

A
  • alpha and beta agonist
  • pulmonary vasodilator
  • potent right ventricular inotrope
59
Q

distance between pleural of lung

A

10-20 um

60
Q

how much fluid is contained within the pleural space?

A

0.1 - 0.2 mL/kg

61
Q

which pleura is painful when inflammed?

A

pleuritic

no innervation of the visceral pleura

62
Q

physical exam for pleural effusions

A

diminised breath sounds

dullness on percussion

pleuritic chest pain

63
Q
A

left sided effusion

64
Q

Transudate

A

systemic process

  • favors fluid accumulation
  • imbalance between hydrostatic and oncotic pressures
  • premeability is not changed
65
Q

Exudate

A

local process

  • alters permeability
  • formation of fluid
  • high protein content
66
Q

Light’s Critera

A

determines wheter exudative or transudate

  • pleural:protein ratio > 0.5
  • pleural:LDH ratio > 0.6
  • pleural LDH > 2/3

if more than one are present, >95% sensitivity of the lfuid being exudative

67
Q

causes of exudate

A
  • infectious
    • bacterial pneumonia, parasitic, viral
  • autoimmune
    • lupus, RA
  • neoplastic malignancies
68
Q

causes of transudate

A
  • heart failure, nephrotic syndrome, dialysis
  • autoimmune
    • sarcoidosis
  • thyroid
    • myoxedema
  • ovarian
    • megis syndrome
69
Q

Myxoedema

A

swellin gof the skin and underlying tissues giving a waxy appearance

  • due to an underactive thyroid gland
70
Q

Meigs Syndrome

A

triad of ascites, pleural effusions, and benign ovarian tumor

71
Q

In “trapped lung” the _____ pleural forms a fibrous peel overlying the tissue

A

visceral

72
Q

Fibrothorax

A

visceral pleura is covered by a dense, thick, fibrous layer of connective tissue

results in a restrictie lung disease and chronic hypoventilation

73
Q

causes of fibrothorax

A
  • hemothorax
  • tuberculosus
  • pancreatitis
  • uremia
74
Q
A

Fibrothorax

  • “pleural peel” surrounding the lungs
75
Q

Chylothorax

A

chyle leak into the pleural cavity

  • due to disruption of toracic duct
76
Q

Pleurodesis

A

procedure where the pleural space is obliterated

77
Q

primary spontaneous pneumothorax

A

results from rupture of apical subpleural bullae

78
Q

secondary causes of sponatenous pneumothorax

A
  • COPD
  • pulmonary fibrosis
  • asthma
  • CF
  • pulmonary tissue necrosis
79
Q

gold standard in diagnosing a pneumothorax

A

chest radiograph

80
Q

small pneumo that will resolve on its own is under ____ cm

A

2

81
Q

signs of stage II sleep

A

sleep spindles and K-complexes

breathing can be irregular due to fluctuations in respiratory drive

82
Q

Dyssomias

A

initiating and maintaining sleep that produces excessive sleepiness

83
Q

Parasomias

A

Rhythmic body movements or rocking that occur exclusively during sleep and are manifestations of nervous system activity

84
Q

Medicopsychiatric Sleep Disorders

A

disturbed sleep and wakefullness

85
Q

VT decreases _____ during sleep

A

15-25%

86
Q

VE decreases _____ during sleep

A

0.5 - 1.5 L/min

87
Q

PaCO2 increases _____ during sleep

A

2-3 mmHg

88
Q

PaO2 decreass _____ during sleep

A

3-10 mmHg

89
Q

decrease in MAP in stage I vs stage 3 of sleep

A

I = 5-9%

III = 4-8%

90
Q

change in heart rate during sleep

A

in NREM, HR decreases 5-8%

increases to waking levels during REM sleep

91
Q

Hypopnea

A

incomplete or absence of airflow resultin gin arousal from sleep

92
Q

central apnea

A

cessation in oronasal airflow which coincides with the lack of effort detected in muscles of inspriation

  • due to absence of CNS respiratory drive
93
Q

Apnea-Hypopea Index (AHI)

A

refers to number of A-H that occurs in 1 hour of sleep

  • <5 normal
  • > 30 severe
94
Q

desaturation during apnea does not begin until PaO2 falls below _____ mmHg

A

60

(90% saturation)

95
Q

carotid and aortic chemoreceptors detect _____

A

low PaO2

high PaCO2

low arterial pH

96
Q

Pickwickian Syndrome

A

obestiy hypoventilaiton syndrome

  • everely overweight people fail to breathe rapidly enough or deeply enough, resulting in low blood oxygen levels and high blood carbon dioxide
97
Q

Cheyne-Stokes Respiration

A

starts off with huge breaths which get more and more shallow until eventually releasing apnea. Catecholamines will then cause a giant increase in breathing, and the cycle repeats.

98
Q

Cheyne-Stokes respiration is often associated with _____

A

severe CHF

99
Q

Kussmaul breathing

A

fast, deep breaths

100
Q

major site of upper airway obstruction in OSA

A

pharynx

101
Q

cardinal symptom of OSA

A

daytime hypersomnia

102
Q

oral appliances are affective if ___, ___, and ____

A

person is not over 125% of normal body weight

apnec episodes are not over 30 per hour

oxygen saturation is not less than 80%

103
Q

GGA

A

Genio-Glossus-Advancement

opens the upper breathing passageway by tightening the front tongue tendon

104
Q

STOP

A

snoring

tiredness

observed apnea

high blood pressure

105
Q

2 types of respiratory failure

A

hypoxic respiratory failure

hypercapnic-hypoxic respiratory failure

106
Q

acute hypoxic respiratory failure

A

severe arterial hypoxemia that cannot be correct by increased FiO2 > 0.5

  • A-a gradient increases
  • PaO2/FiO2 ratio decreases
107
Q

Acute Respiratory Distress Syndrome

A

ALI that causes acute and persistent lung inflammation with increased capillary permeability

108
Q

hypercapnia-Hypoxic Respiratory Failure

A

ventillatory insufficiency resulting from a reduciton in VE, or increased VD, that is associated with a direct reduction in VA

109
Q

PCO2 and PO2 in hypoventilation

A

80mmHg pCO2

40 mmHg pO2

110
Q

PCO2 and PO2 in hyperventilation

A

PCO2 20 mmHg

PO2 115 mmHg

111
Q

clinical presentation of HHRF

A

papilledema

112
Q

early complications of O2 therapy in COPD

A

abolishes HPV response

worsening of V/Q ratio

increased Vd/Vt

113
Q

when should you start mechanical ventilation

A

PaO2 < 70 mmHg on FiO2 > 0.5

RR > 30

A-a gradient > 400 mmHg on FiO2 1.0

VC < 15 mL/kg

114
Q

two mechanisms of fluid accumulation

A

cardiogenic or hydrostatic

115
Q

increased HP in the pulmonary capillaries leading to fluid accumulation may be cuased by ____ or ____

A

LV failure (CHF) or mitral stenosis

116
Q

major cause of non-cardiogenic pulmonary edema

A

ARDS

117
Q

PCP in cardiogenic pulmonary edema

A

increased

118
Q

PCP in non-cardiogenic pulmonary edema

A

normal

119
Q

PC permeability in non-cardiogenic pulmonary edema

A

increased

120
Q

protein content in cardiogenic pulmonary edema

A

low

121
Q

protein content in non-cardiogenic pulmonary edema

A

high

122
Q

most common precipitant for ARDS

A

sepsis

123
Q
A

ARDS

diffuse, patchy infiltrates

124
Q

3 treatments in ARDS

A
  • treat precipitating disorder
  • interrupt pathogenic event
  • support gas exchange
125
Q

mechanical ventilation in ARDS/ALI

A

6-6 mL/kg Tv

limit alveolar pressure to < 35 cmH2O

inverse I:E ratios

126
Q

limit FiO2 to _____ in ALI/ARDS

A

< 0.65

127
Q

symptoms of TRALI

A
  • hypoxemia
  • hypotension
  • fever
  • severe bilateral pulmonary edema
128
Q

TRALI is treated the same as ALI without using ____

A

diuretics

129
Q

Acute Phase of ALI

A

“exudative”

  • damaged alveolar membrane
  • neutrophils
  • type I epithelial cells are destroyed
  • interstitial edema
  • increased permeability
130
Q

Chronic Phase of ALI

A

chronic/fibroproliferative stage

  • thickening of endothelium and epithelium
  • Type II cells replace Type I
  • extracellular fibrin deposition and remodeling
131
Q
A