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Block 9 Week 4 > Baker/Parks > Infectious Lung Diseases > Flashcards

Baker/Parks > Infectious Lung Diseases Flashcards

1
Q

define acute bronchitis

A

self-limited inflammation of the LARGE airways of the lung, characterized by cough W/O PNEUMONIA

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2
Q

T/F: acute upper respiratory infections are v common

A

TRUE

4th leading reason for office visits

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3
Q

T/F: acute bronchitis is typically bacterial

A

FALSE

it’s typically VIRAL

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4
Q

which viruses cause acute bronchitis?

A 
influenza A & B
parainfluenza
RSV
coronavirus
adenovirus
rhinovirus
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5
Q

what do viruses infect in acute bronchitis?

A

bronchial epithelium

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6
Q

what gets inflamed in acute bronchitis?

A

large airways

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7
Q

what causes sputum in acute bronchitis?

A

desquamation & denudation of the airway

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8
Q

what is acute bronchitis indistinguishable from for the first few days?

A

mild URI

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9
Q

how long do you need a cough to have acute bronchitis?

A

> 5 days

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10
Q

how long does the cough usually last in acute bronchitis?

A

10-20 days, but sometimes >4 wks

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11
Q

what do you usually NOT have in acute bronchitis?

A

NO fever
NO constitutional sx
+/- sputum

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12
Q

what does the pulmonary exam of acute bronchitis look like?

A

usu normal, sometimes wheezing d/t bronchospasm

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13
Q

T/F: acute bronchitis can exacerbate chronic lung conditions

A

TRUE

COPD & asthma

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14
Q

should you do an x-ray if you suspect acute bronchitis?

A

usu no
bc CXR is usu normal in these pts
possibly some non-specific bronchial wall thickening

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15
Q

what is the treatment for acute bronchitis?

A

STOP SMOKING

DON’T FUCKING GIVE ABX BC IT’S NOT FUCKING BACTERIAL!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

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16
Q

what are the 4 general types of infection that can cause pneumonia?

A

bacterial
viral
mycoplasmal
fungal

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17
Q

T/F: various types of pneumonia can “gang up”

A 
true
viral syndrome (influenza) can lead to secondary bacterial infxn
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18
Q

what are the 7 main types of pneumonia?

A
  1. community-acquired acute
  2. community-acquired atypical
  3. hospital acquired
  4. chronic
  5. aspiration
  6. necrotizing + lung abscess
  7. in immunocompromised host
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19
Q

what is the etiology of CAP?

A

bacterial or viral or BOTH

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20
Q

what is the pathophysiology of CAP?

A

invasion of lung parenchyma > inflammatory exudates in alveoli > lung consolidation

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21
Q

T/F: the presentation, clinical course, and pathology of pneumonia are always the same in every pt

A

FALSE

variable depending on organism, host rxn, & extent of infxn

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22
Q

what are the 3 predisposing conditions for CAP?

A
  1. age extremes
  2. chronic conditions
  3. immune deficiencies
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23
Q

where in the lung is the inflammatory infiltrate in CAP?

A

in the ALVEOLI

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24
Q

what are the 2 types of CAP?

A

lobar & bronchopneumonia

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25
Q

how are lobar & broncho CAP different?

A

degree & pattern of consolidation

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26
Q

how are lobar & broncho CAP the same?

A

morphology & microbiology

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27
Q

what are the 4 stages of lobar CAP?

A
  1. congestion
  2. red hepatization
  3. gray hepatization
  4. resolution
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28
Q

what can happen if the consolidation of CAP extends to the pleura?

A

pleuritis (rxn to inflammation)

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29
Q

what happens in the “resolution” phase of lobar CAP?

A

complete clearance, but there may be organized fibrin which leaves permanent scarring

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30
Q

what parts of the lung does broncho CAP affect?

A

PATCHY, multilobar, sometimes bilateral

LOWER LOBE PREDOMINANCE

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31
Q

what is the exudate in broncho CAP & where does it go?

A

suppurative, neutrophil-rich exudate

in bronchi, bronchioles, & alveolar SPACES

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32
Q

what are the clinical sx of CAP?

A
  1. abrupt onset of high fever & chills
  2. cough w/ mucopurulent sputum
  3. crackles on ausc, dullness to percussion
  4. maybe pleuritic chest pain, maybe not
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33
Q

what are 3 possible complications of CAP?

A
  1. pulmonary abscess
  2. empyema
  3. bacteremic dissemination
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34
Q

what is the treatment for CAP?

A
  1. ABX
  2. thoracentesis
  3. VAX!!
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35
Q

how does atypical pneumonia present?

A

acute, febrile condition w/ patchy inflammatory changes in lungs

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36
Q

where is atypical pneumonia confined to in the lung?

A

alveolar SEPTA & pulmonary INTERSTITIUM

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37
Q

what are the 2 possible (generally) etiologies of atypical pneumonia?

A

bacterial & viral

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38
Q

what is the most common cause of atypical pneumonia?

A

mycoplasma pneumoniae

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39
Q

who gets atypical pneumonia typically?

A

children & young adults in closed communities sporadically

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40
Q

what is the other bacterial cause of atypical pneumonia?

A

chlamydia pneumoniae

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41
Q

what viruses can cause atypical pneumonia?

A 
influenza A & B
RSV
human metapneumovirus
adenovirus
rhinovirus
rubeola
varicella
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42
Q

what are the 4 “atypical” things about atypical pneumonia?

A
  1. moderate sputum
  2. no consolidation on physical
  3. moderately high WBC
  4. no alveolar exudate
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43
Q

how can you distinguish atypical pneumonia from acute bronchitis?

A

SITE OF INFXN

alveolar septum & interstitium (atypical pneumonia) vs. bronchial wall (bronchitis)

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44
Q

what is the main clinical feature of atypical pneumonia?

A

sx out of proportion to minimal physical exam findings

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45
Q

T/F: the clinical course of atypical pneumonia is variable

A

TRUE

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46
Q

what is the range of sx for atypical pneumonia?

A

bad “chest cold” to severe illness w/ secondary infxn
fever, HA, myalgias
maybe cough, maybe not

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47
Q

how does atypical pneumonia look on CXR?

A

patchy d/t interstitial lymphocyte/monocyte infiltrate

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48
Q

what cells are involved in atypical pneumonia vs CAP?

A 
CAP = neutrophils
atypical = lymphs & monos
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49
Q

what pts are at risk for getting HAP?

A

pts w/…

  1. severe underlying dz
  2. immunosuppression
  3. prolonged abx tx (resistance)
  4. invasive intravascular access
  5. MECHANICAL VENTILATION
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50
Q

what pt population is at the HIGHEST risk for HAP?

A

pts on MECHANICAL VENTILATION!!! (that’s what Kuhls’ whole lecture was about)

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51
Q

T/F: HAP is potentially life-threatening

A

TRUE

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52
Q

what types of organisms cause HAP?

A

gram negative rods (Pseudomonas & Enterobacter)
&
S. aureus (MRSA)

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53
Q

how do you get aspiration pneumonia?

A

inhalation of gastric contents

54
Q

what pts get aspiration pneumonia?

A

debilitated pts

d/t stroke, intoxication, or other AMS cause

55
Q

when does the aspiration of aspiration pneumonia occur?

A

while unconscious or during vomiting

56
Q

how can you tell the diff btwn aspiration pneumonia vs. aspiration/chemical pneumonitis?

A

aspiration pneumonia has…

  1. multiple organisms (oral flora)
  2. fulminant course (v sick v fast)
  3. possibly lung abscess & ARDS
57
Q

what is a lung abscess?

A

suppurative process in the lung w/ tissue necrosis

58
Q

what are 5 possible ways you can get

A
  1. aspiration
  2. post-pneumonic
  3. septic emboli d/t distant infection
  4. obstructive (cancer)
  5. bacteremia (hematogenous seeding)
59
Q

what 2 organisms can cause a post-pneumonic lung abscess?

A

s. aureus

k. pneumoniae

60
Q

what does a lung abscess look like?

A

suppurative destruction of lung PARENCHYMA w/ central area of CAVITATION

61
Q

what is another name for “suppurative destruction”?

A

liquefactive necrosis

62
Q

what are the clinical sx of lung abscess?

A

cough
fever
COPIOUS foul-smelling purulent sputum (yuck)
clubbing

63
Q

how do you dx lung abscess?

A

radiology

64
Q

what do you have to rule out in old people if you suspect lung abscess?

A

cancer

65
Q

what are the 2 etiologies of chronic pneumonia?

A

mycobacterium TB

fungi

66
Q

T/F: chronic pneumonia typically presents as a localized lesion

A

TRUE

67
Q

what fungi can cause chronic pneumonia?

A
  1. histoplasma capsulatum
  2. blastomyces dermatidis
  3. coccidioides immitis
68
Q

what type of rxn is involved in chronic pneumonia?

A

granulomatous inflammatory rxn

69
Q

which 2 etiologies of chronic pneumonia are very similar?

A

histoplasmosis & TB

similar clinical presentation & morphology

70
Q

which cells does histoplasmosis infect?

A

MACROPHAGES

intracellular parasite

71
Q

T/F: you can have primary or secondary histoplasmosis

A

TRUE

72
Q

what is primary histoplasmosis?

A

self-limited & latent

73
Q

what is secondary histoplasmosis?

A

chronic progressive

74
Q

what are the sx of secondary histoplasmosis?

A

fever
night sweats
cough

75
Q

T/F: you can have localized extrapulmonary involvement w/ histoplasmosis

A

TRUE

76
Q

what happens to immunocompromised pts if they get histoplasmosis?

A

wide dissemination

77
Q

what forms in the lung w/ histoplasmosis?

A

granuloma w/ caseation necrosis (just like TB)

78
Q

how does a histoplasmosis granuloma resolve?

A

spontaneously or w/ antifungals
fibrosis of the granuloma
concentric calcification

79
Q

how can you distinguish histoplasma from TB?

A
  1. yeast on tissue exam
  2. culture
  3. ab testing
80
Q

what is the MAIN way that blastomycosis is different from histoplasmosis?

A

macrophages have limited ability to ingest & kill blastomycosis!

81
Q

what types of cells are recruited in blastomycosis?

A

neutrophils

82
Q

what do neutrophils lead to in blastomycosis?

A

main gross morphology of suppurative granulomas

83
Q

what are the 3 types of blastomycosis?

A

pulmonary
disseminated
primary cutaneous

84
Q

how can you get primary cutaneous blastomycosis?

A

direct inoculation of fungus to the skin

85
Q

what can be hard to distinguish from cutaneous blastomycosis?

A

squamous cell cancer

d/t epithelial hyperplasia

86
Q

what is another name for coccidioidomycosis?

A

San Joaquin Valley Fever (Joaquin Phoenix’s cocc [SORRY])

87
Q

T/F: most people in endemic areas are not infected w/ coccidioidomycosis

A

FALSE

they HAVE BEEN infected

88
Q

how do primary coccidioidomycosis infections present?

A

asymptomatic

89
Q

10% of coccidioidomycosis pts have WHAT?

A

lung lesions

90
Q

what are the sx of San Joaquin Valley Fever?

A

fever
cough
pleuritic chest pain
erythema nodosum or multiformae

91
Q

what are the 3 main types of coccidioidomycosis?

A
  1. granulomatous
  2. pyogenic (suppurative)
  3. disseminated (RARE)

(can be 1 & 2 simultaneously)

92
Q

what is the main diff btwn granulomatous & pyogenic coccidioidomycosis?

A

it depends on if the spherules remain intact
intact = granulomatous
ruptured (endospores released) = pyogenic

93
Q

what organs can be affected d/t disseminated coccidioidomycosis?

A 
meninges
skin
bones
adrenals
lymph nodes
spleen
liver
94
Q

is disseminated coccidioidomycosis more like granulomatous or pyogenic?

A

more purulent/pyogenic

95
Q

where is the San Joaquin Valley?

A

Cali

96
Q

how does aspergillus affect healthy people vs immunosuppressed ppl?

A

healthy ppl get allergies (acute bronchopulmonary aspergillosis)
immunosuppressed ppl get invasive aspergillosis

97
Q

what is affected in invasive aspergillosis in immunocompromised hosts?

A

lungs + hematogenous dissemination is common

98
Q

what do the pulmonary lesions of aspergillosis look like?

A

necrotizing pneumonia w/ sharply delineated round lesions w/ HEMORRHAGIC BORDERS

99
Q

what are the risk factors of mycobacterium TB infection?

A
  1. poverty
  2. crowding
  3. chronic dz (DM, lymphoma, chronic lung dz, immunosuppression, HIV/AIDS)
100
Q

T/F: mycobacterium TB infection equates to dz

A

FALSE

infection does NOT equal disease!!!!!

101
Q

how is mycobacterium TB spread?

A

person-to-person

airborne

102
Q

how does primary TB present?

A

asymptomatic

103
Q

what does the mycobacterium TB do in your body?

A

remains dormant

reactivates when your immunity is down

104
Q

what type of immunity is activated in mycobacterium TB infection?

A

cell-mediated

105
Q

what type of allergic rxn is involved w/ mycobacterium TB infection?

A

delayed (type IV) sensitivity rxn

106
Q

WHEN does the allergic rxn to mycobacterium TB occur?

A

2-4 weeks after exposure

107
Q

how does the PPD test work?

A

inject PPD subQ
type IV rxn peaks 48-72 hours later
PALPABLE INDURATION is noted

108
Q

what are Ghon foci & complexes assoc w/?

A

TB

109
Q

what % of TB pts progress from primary complex to progressive primary TB?

A

5%

110
Q

what is a Ghon complex?

A

focal CASEATING necrosis in the lower lobe
AND
hilar lymph nodes undergo fibrosis & calcification

111
Q

what is a Ghon FOCUS?

A

the “focus” of infection, i.e. the caseating necrosis

112
Q

what is very important in order for a granuloma to develop?

A

TNF

113
Q

what pts are susceptible to reactivation of latent TB infxn?

A

Crohn’s dz & RA pts bc they are on anti-TNF agents (infliximab)

114
Q

what can be used to detect latent TB infxn?

A

IGRAs (interferon gamma releasing assays)

115
Q

what activates macrophages?

A

IFN gamma

116
Q

generally, how do you get primary TB?

A

exogenous source

117
Q

what % of primary TB pts develop a clinically significant response?

A

5%

118
Q

cell-mediated immunity wanes over time, so what is possible w/ TB?

A

a 2nd primary TB infxn

119
Q

what can primary progressive TB result in?

A

TB meningitis

miliary TB

120
Q

primary progressive TB is less likely to develop WHAT?

A

cavitary lesions

121
Q

when does secondary reactivation TB usu occur?

A

years after primary infxn when host resistance is down

122
Q

where are lesions of secondary reactivation TB classically located?

A

apex of lung

123
Q

how do you get caseous necrosis in secondary reactivation TB?

A

pre-existing hypersensitivity activates & walls off the infection

124
Q

why do secondary TB pts have TB-laced sputum?

A

erosion in airways

125
Q

why do secondary TB pts have hemoptysis?

A

erosion into BVs

126
Q

what are the sx of secondary TB?

A
  1. CONSUMPTION (malaise, anorexia, weight loss)
  2. fever > low grade & remittant
  3. night sweats
  4. maybe hemoptysis
  5. maybe pleuritic chest pain
127
Q

how do you diagnose secondary TB?

A

IDENTIFICATION OF TUBERCLE BACILLI via ACID FAST STAIN of sputum or PCR

128
Q

TB + ? = bad news

A

HIV

129
Q

how do CD4 counts affect TB presentation?

A

CD4 > 300 = secondary TB presentation

CD4 <200 = primary progressive TB presentation

130
Q

how does HIV + TB cause false negative sputum?

A

higher bacterial loads, but LOWER T CELL ACTIVITY > less cavitation > less erosion

131
Q

what 2 things can be false negative w/ HIV + TB?

A

sputum

PPD

Block 9 Week 4 (5 decks)

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