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CVPR > Pulmonary Exam: Clinical > Flashcards

Pulmonary Exam: Clinical Flashcards

1
Q

normal heart size on chest x-ray

A

smaller than half the width of the midline to the outside of the ribs

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2
Q

pulmonary edema on CXR

A

bilateral fluffy infiltrates, kerley B lines +/- cardiomegaly

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3
Q

pleural effusion on CXR

A

blunting of costophrenic angle (where diaphragm meets ribcage)

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4
Q

pneumothorax on CXR

A

absence of pulmonary markings on affected side with visibly deflated lung

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5
Q

lobar pneumonia on CXR

A

infiltrate in lobar pattern

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6
Q

interstitial lung disease on CXR

A

diffuse honeycombing

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7
Q

Normal FVC

A

5L

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8
Q

Normal FEV1

A

4L

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9
Q

normal FEV1/FVC

A

0.8

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10
Q

obstructive lung disease on CXR

A

hyperinflation with flattened diaphragms

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11
Q

obstructive lung disease on spirometry

A

reduced FEV1 and reduced FEV1/FVC ratio

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12
Q

restrictive lung disease on spirometry

A

Reduced FEV1 and FVC with normal ratio

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13
Q

chronic bronchitis criteria

A

productive cough 3 months per year for at least 2 years

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14
Q

chronic bronchitis pathophys

A

mucosal hypertrophy, inflammation, increased mucus leading to smaller airway diameter. Shunting from mucus plugs causes cyanosis

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15
Q

emphysema pathophys

A

smoke recruits macrophages and neutrophils into alveolar space; subsequent protease production destroys alveolar walls. Increased compliance and loss of elastic recoil

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16
Q

why use CO for DLCO

A

it’s diffusion-limited so it’s a good indicator of ability for gas exchange

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17
Q

decreased DLCO in COPD indicates

A

emphysema

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18
Q

emphysema characteristics

A

high respiratory rate can diminish cyanosis

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19
Q

pathophys of alpha-1 antitrypsin deficiency

A

deficiency of protease inhibitor leads to too much elastase that destroys alveoli. Misfolded proteins can occur in liver to cause cirrhosis

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20
Q

alpha-1 antitrypsan deficiency emphysema pattern

A

panacinar emphysema that is lower lobe predominant

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21
Q

smoking-associated emphysema pattern

A

centriacinar involvement that is upper lobe predominant

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22
Q

what is bronchiectasis

A

dilated and thickened airways due to repeated episodes of inflammation/infection

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23
Q

causes of bronchiectasis

A

cystic fibrosis, chronic infection, reflux, primary ciliary dyskinesia

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24
Q

primary ciliary dyskinesia

A

autosomal recessive, leads to cilia not being able to beat, coexists with infertility and situs inversus

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25
Q

2 categories of restrictive lung disease causes

A

poor breathing mechanics (neuromuscular, structural problems), interstitial lung disease

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26
Q

2 hallmarks of restrictive lung disease

A

low volumes and decreased DLCO

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27
Q

general pathophys of interstitial lung disease

A

inflammation in interstitium and alveoli

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28
Q

causes of interstitial lung disease

A

idiopathic pulmonary fibrosis, systemic autoimmune disease, pneumoconioses, drug toxicities

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29
Q

common presentation of ILD

A

insidious dyspnea, dry cough, fine “velcro” crackles in all lung fields, digital clubbing

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30
Q

ILD on CXR

A

diffuse, bilateral, small irregular opacities

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31
Q

idiopathic pulmonary fibrosis pathophys

A

repetitive epithelial injury with disordered repair leading to increased type II pneumocytes and fibroblasts and decreased type I pneumocytes

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32
Q

idiopathic pulmonary fibrosis presentation

A

insidious onset dry cough, dyspnea, ILD crackles, clubbing

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33
Q

idiopathic pulmonary fibrosis prognosis

A

average survival of 4 years (death due to pulmonary HTN, respiratory failure, lung cancer, arrhythmia)

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34
Q

idiopathic pulmonary fibrosis CXR/CT

A

honeycombing pattern

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35
Q

systemic diseases that can cause pulmonary fibrosis

A

scleroderma, RA, granulomatosis with polyangiitis, sarcoidosis

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36
Q

Sarcoidosis pathophys

A

activated macrophages cause widespread non-caseating granulomas

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37
Q

sarcoidosis lab findings

A

high serum ACE levels, hypercalcemia with elevated vitamin D activation

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38
Q

sarcoidosis clinical presentation

A

cough, dyspnea, fatigue, skin lesions, uveitis

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39
Q

sarcoidosis imaging

A

coarse reticular opacities with bilateral hilar adenopathy

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40
Q

sarcoidosis treatment

A

steroids

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41
Q

types of pneumoconioses

A

coal miner’s lung, silicosis, asbestosis, berylliosis, hypersensitivity pneumonitis

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42
Q

drug toxicities that can cause ILD

A

bleomycin, busulfan, amiodarone, methotrexate

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43
Q

tidal volume

A

amount of air moved in a quiet breath

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44
Q

inspiratory reserve volume

A

amount that can be inhaled after quiet inhalation

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45
Q

vital capacity

A

tidal volume plus expiratory reserve plus inspiratory reserve (total lung capacity minus residual volume)

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46
Q

functional residual capacity

A

expiratory reserve volume plus residual capacity (amount of air in lungs at the end of quiet exhalation)

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47
Q

total lung capacity

A

quantity of air in lungs at maximum inspiration

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48
Q

inspiratory capacity

A

tidal volume plus inspiratory reserve volume

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49
Q

forced vital capacity

A

total amount of air exhaled from total lung capacity down to residual volume in a forced maneuver

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50
Q

flow-volume loop for obstructive lung disease

A

wider than normal

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51
Q

flow-volume loop for restrictive lung disease

A

narrower than normal

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52
Q

bronchodilator response

A

increase in FEV1 of 12% and greater than 0.2L

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53
Q

main lung volumes measured

A

TLC and RV

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54
Q

definition of restrictive lung disease in lung volumes

A

TLC below lower limit of normal with reduced FEV1 and FVC but normal ratio

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55
Q

a decreased vital capacity in the presence of a normal FEV1/FVC ratio suggests

A

restriction

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56
Q

what might need to be corrected for when measuring DLCO

A

blood hemoglobin level

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57
Q

causes of decreased DLCO

A

emphysema, interstitial lung disease, lung damage from radiation or drugs, pulmonary embolism, pulmonary HTN

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58
Q

basic definition of pneumonia

A

infection of alveoli

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59
Q

basic def of pneumonitis

A

immune-mediated inflammation of alveoli

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60
Q

what is an empyema

A

purulent exudate in pleural cavity

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61
Q

what is a lung abscess

A

circumscribed collection of pus within the parenchyma

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62
Q

pulmonary physiology of pneumonia

A

impaired alveolar ventilation causes V/Q mismatch with shunting and causes hypoxia due to increased A-a gradient

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63
Q

pneumonia risk factors

A

old age, immobility, immunosuppression, impaired airway protection, chronic diseases, environmental factors (crowded conditions, toxins)

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64
Q

which pathogen is associated with ETOH abuse in pneumonia

A

klebsiella

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65
Q

foul-smelling sputum in pneumonia is associated with

A

aspiration pneumonia

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66
Q

most common pathogens in typical community-acquired pneumonia

A

strep pneumoniae, haemophilus influenzae, moraxella

67
Q

what pathogen is usually responsible for bacterial superinfection in pneumonia

A

staph aureus

68
Q

CXR CAP (typical)

A

lobar poorly defined patchy infiltrates with or without effusion

69
Q

definition of community-acquired pneumonia

A

occurs outside of healthcare setting

70
Q

atypical bacteria causing pneumonia

A

chlamydophila, mycoplasma, legionella

71
Q

atypical pneumonia viruses

A

influenza, RSV, adenovirus, COVID

72
Q

atypical pneumonia chest xray

A

diffuse reticular pattern concentrated in perihilar region

73
Q

pathogens in hospital acquired pneumonia

A

pseudomonas, enterobacteriaceae, acinetobacter, staph aureus, strep pneumoniae

74
Q

definition of hospital acquired pneumonia

A

onset >48 hours after admission

75
Q

aspiration pneumonia pathogens

A

anaerobes and gram negeatives

76
Q

ssx of aspiration pneumonia

A

immediate: bronchospasms, crackles. Late (24 hours): fever, dyspnea, cough with foul-smelling sputum

77
Q

aspiration pneumonia CXR

A

depends on position on aspiration

78
Q

bronchopneumonia on CXR

A

patchy areas spread throughout

79
Q

cryptogenic organizing pneumonia definition

A

a non-infectious pneumonia of unknown etiology characterized by involvement of the bronchioles, alveoli, and surrounding tissue without response to abx. Supportive treatment only

80
Q

outpatient pneumonia treatment

A

amoxicillin+azithromycin/clarithromycin or doxycycline

81
Q

inpatient pneumonia treatment

A

ceftriaxone + azithromycin or doxycycline OR levofloxacin

82
Q

hospital-acquired pneumonia treatment if gram negative

A

pip-taz or cefepime or ceftazidime+levofloxacin

83
Q

hospital-acquired pneumonia treatment if gram-positive

A

add vancomycin to gram negative treatment

84
Q

aspiration pneumonia treatment

A

ampicillin sulbactam or clindamycin

85
Q

etiologies of syncope

A

vasovagal (psychogenic, stimulation of visceral organs/carotid bodies), orthostatics (dehydration, ANS dysfunction), cardiac valve dysfunction, arrhythmia, neurogenic

86
Q

most common dvt location

A

popliteal

87
Q

Homans sign

A

calf pain on dorsiflexion

88
Q

superficial thrombophlebitis

A

pain ,tenderness, induration and erythema overlying a superficial vein with palpable cord (maybe)

89
Q

superficial thrombophlebitis treatment

A

hot compress, nsaids, remove offending agent

90
Q

superficial thrombophlebitis risk factors

A

same as DVT

91
Q

when is indefinite anticoagulation

A

high-risk patients and those with 2 or more VTE events

92
Q

what anticoagulant to give in case of renal insufficiency

A

unfractionated heparin

93
Q

what anticoagulant to use in pregnancy

A

LMWH

94
Q

anticoagulant duration for provoked VTE

A

3-6 months

95
Q

anticoagulant duration for unprovoked VTE

A

6+ months and search for underlying cause such as cancer screening

96
Q

part of coagulation cascade affected by enoxaparin

A

activates antithrombin III

97
Q

part of coagulation cascade affected by heparin

A

inactivates thrombin and factor Xa

98
Q

Large vessel vasculitis

A

giant cell, takayasu

99
Q

Giant cell arteritis aka

A

temporal arteritis

100
Q

Giant cell arteritis summary

A

involves branches of carotid artery, unilateral headache, associated polymyalgia rheumatica, can involve ophthalmic artery

101
Q

Takayasu arteritis summary

A

commonly affects Asian women<40, involves aortic arch and proximal great vessels, fever, night sweats, skin nodules, arthritis, vision disturbances, weak upper extremity pulses

102
Q

treatment for large vessel vasculitis

A

steroids

103
Q

medium cell vasculitis

A

Buerger disease, Kawasaki disease, Polyarteritis nodosa

104
Q

Buerger disease affects

A

young adult men, smokers

105
Q

Buerger disease ssx

A

intermittent claudication of extremities leading to gangrene

106
Q

Buerger disease treatment

A

smoking cessation

107
Q

Kawasaki disease affects

A

Asian children <4 y/o

108
Q

Kawasaki disease ssx

A

conjunctival injection, rash, adenopathy, strawberry tongue, hand/foot edema, fever, coronary artery aneurysms

109
Q

Kawasaki disease treatment

A

IVIG, ASA

110
Q

Polyarteritis nodosa affects

A

middle aged men who may be HepB positive

111
Q

polyarteritis nodosa ssx

A

fever, weight loss, malaise, headache, abd pain, melena, HTN, kidney damage

112
Q

polyarteritis nodosa treatment

A

steroids, cyclophosphomide

113
Q

polyarterteritis nodosa affects what arteries

A

mesenteric, renal

114
Q

Small vessel vasculitis - immune mediated

A

Behcet disease, immunoglobolin A, cutaneous small vessel, mixed cryoglobulinemia

115
Q

Behcet disease is associated with what gene

A

HLA-B51

116
Q

Behcet disease ssx

A

aphthous/genital ulcers, uveitis, erythema nodosum

117
Q

Behcet disease precipitated by

A

HSV or parvo

118
Q

Behcet disease treatment

A

none, self-resolving in 1-4 weeks

119
Q

immunoglobulin A aka

A

HSP

120
Q

immunoglobulin A follows

A

URI, IgA immune complex deposition

121
Q

immunoglobulin A ssx

A

purpura of LE, arthralgia, GI pain

122
Q

immunoglobulin A treatment

A

supportive, steroids

123
Q

cutaneous small vessel vasculitis due to

A

response to certain meds or infections

124
Q

cutaneous small vessel vasculitis ssx

A

palpable purpura

125
Q

mixed cryoglobulinemia due to

A

viral infections (especially hep C), B cell malignancies

126
Q

mixed cryoglobulinemia ssx

A

palpable purpura, weakness, arthralgias due to IgG and IgM immune complex deposition

127
Q

small cell vasculitis ANCAs

A

Churg-strauss, Wegeners, microscopic polyangitis

128
Q

Churg-strauss aka

A

eosinophilic granulomatosis with polyangiitis

129
Q

Churg-strauss ssx

A

asthma, sinusitis, skin manifestations

130
Q

Wegeners aka

A

Granulomatosis with polyangiitis

131
Q

Wegeners ssx

A

upper respiratory, lower respiratory, renal

132
Q

microscopic polyangiitis

A

like Wegeners but without nasopharyngeal involvement or granulomas

133
Q

treatment for microscopic polyangiitis and Wegeners

A

cyclophosphamide, steroids

134
Q

what is an ANCA

A

an IgG autoimmune reaction to neutrophils

135
Q

other causes of vasculitis

A

infective endocarditis, syphilis, connective tissue diseases (SLE, RA), fungus

136
Q

pediatric SBP should be

A

70+age*2

137
Q

definition of shock

A

inability to remain aerobic metabolism

138
Q

4 kinds of shock

A

hypovolemic, distributive, cardiogenic, obstructive

139
Q

hallmark of hypovolemic shock

A

decreased preload

140
Q

hallmark of distributive shock

A

decreased afterload

141
Q

most common cause of distributive shock

A

septic shock

142
Q

CO in shock means what kind

A

distributive

143
Q

hallmark of cardiogenic shock

A

decreased CO

144
Q

cardiogenic shock treatment

A

inotropes

145
Q

hallmark of obstructive shock

A

normal contractility with decreased CO

146
Q

distributive shock treatment

A

volume with or without pressors

147
Q

low cardiac output and low filling pressures means

A

hypovolemic shock

148
Q

low cardiac output and high filling pressures means

A

cardiogenic or obstructive shock

149
Q

shock with low SVR means

A

distributive shock

150
Q

neurogenic shock

A

vasodilation due to loss of sympathetic tone above T6 leading to bradycardia, hypotension, decreased SVR

151
Q

neurogenic shock treatment

A

pressors

152
Q

first sign of hypovolemic shock

A

narrowed pulse pressure with or without tachycardia

153
Q

distributive shock skin findings

A

warm, moist

154
Q

signs of obstructive shock

A

distended neck veins, muffled heart tones, possible tracheal deviation

155
Q

what does a vasopressor do

A

increase SVR

156
Q

what does an inotrope do

A

increase cardiac contractility

157
Q

important principle of starting pressors

A

fill tank before starting pressors

158
Q

goal MAP for septic shock

A

> 65

159
Q

mainstay for inotropes

A

dobumatine (primarily B1 but also some B2, helps with decreasing SVR)

160
Q

pure vasopressors

A

vasopressin and phenylephrine

161
Q

when to use pure vasopressors

A

distributive shock

162
Q

agents with both inotropic and vasopressor activity

A

norepi, epi, dopamine

163
Q

norepi is primarily

A

vasopressor (alpha)

164
Q

epi is primarily

A

inotrope (beta)

CVPR (5 decks)

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