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Block 9 Week 4 > Infectious Disease of Lung- Parks and Baker > Flashcards

Infectious Disease of Lung- Parks and Baker Flashcards

1
Q

What is this:
inflammation of the large airways of the lung
What is it characterized by?
How do you treat it?

A

Acute bronchitis
Cough without pneumonia (pneumonia =consolidations)
Self-limited inflammation

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2
Q

Is acute bronchitis common?

A

very common

(Acute upper respiratory symptoms are 4th leading reason for office visits_

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3
Q 
What class of pathogen typically causes acute bronchitis?
What specific bugs of this class cause it?
A

typically viral

  • Influenza A and B
  • Parainfluzenza
  • RSV
  • Coronavirus
  • Adenovirus
  • Rhinovirus
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4
Q

What does acute bronchitis due to the bronchial epithelium?

A

inflammation of the large airways

-desquamation and denudation of the airways-> sputum

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5
Q

Do adults get fevers with viral infections?

Do children?

A 
not really (cept for influenza)
yes always!
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6
Q

What are the clinical features of acute bronchitis?

A

“chest cold”

  • cough> 5 days= acute bronchitis
  • usually no fever or constitutional symptoms
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7
Q

How can you distinguish mild URI from acute bronchitis in the first few days?

A

you cant!

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8
Q

How long does an acute bronchitis cough last?

A

cough typically lasts 10-20 days but some > 4 weeks

may or may not have sputum production

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9
Q

What does the pulmonary exam look like on acute bronchitis?

A

normal (possible wheezing from bronchospasm)

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10
Q

What can acute bronchitis exacerbate?

A

chronic lung conditions (COPD and Asthma)

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11
Q

Should you give a suspected acute bronchitis pnt a CXR?

A

no, because it is usually normal (may be some non-specific bronchial wall thickening)

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12
Q

How do you treat acute bronchitis?

A

with steroids or codeine NO ANTIBIOTICS!

DO NOT SMOKE

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13
Q

What causes pneumonia?

Is the morbidity or mortality significant?

A

bacteria, viral, myocplasmal. fungal infections

YES!

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14
Q

Pneumonia is the (blank) leading cause of death in US

Pneumonia is the (blank) leading cause of death in NV

A

9th

7th

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15
Q

Viral syndrome (influenza) can lead to (blank)

A

secondary bacterial infxn

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16
Q

What causes community acquired pnuemonia?

A

bacterial or viral or both

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17
Q

How do you get consolidation of the lung in CAP?

A

inflammation of lung parenchyma-> exudates in alveoli-> consolidation of lung

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18
Q

What is the presentation, clinical cours and pathology of CAP dependent on?

A

organism, host reaction, extent of involvement

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19
Q

What are predisposing conditions of CAP?

A
  • Extremes of age
  • Presence of chronic conditions (DM, pulm dz, CV dz)
  • Immune deficiencies
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20
Q

What does the histology of CAP look like?

A

alveoli full of neutrophils and bacteria and you have congested BVs

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21
Q

What are the two types of CAP?
How are they different?
How are they similiar?

A

lobar pneumonia and bronchopneumonia

  • differ by their degree and pattern of consolidation
  • overlap in morphology and in microbiology
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22
Q

What is this:
Large portions of a lobe or a whole lobe consolidation.
What typically causes this?

A

Loba

Strep Pneumo

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23
Q

What does bronchopneumonia look like?

What parts of the lung does it affet?

A

patchy consolidation

often mulitlobar
sometimes bilateral
lower lobe predominance

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24
Q

What are the four stages of CAP?

A

Four Stages

  • Congestion
  • Red Hepatization (feels like liver tissue)
  • Gray Hepatization (lose blood low)
  • Resolution
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25
Q

CAP make cause (blank) dut to consolidation extending to pleura and causing inflammation

A

pleuritis

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26
Q

Does resolution of CAP mean complete healing?

A

their may be complete clearance of pathogen but fibrin may organize leaving permanent scarring

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27
Q

What is the mechanism behind bronchopneumonia?

A

-suppurative, neutrophil rich exudate in bronchi, bronchioles and alevolar spaces

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28
Q

What are the clinical features of CAP?

A
  • abrupt onset of high fever, chills
  • cough with mucopurulent sputum
  • +/-pleuritic chest pain
  • crackles on auscultation
  • dullness to percussion
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29
Q

What are the complications of CAP?

A

Pulmonary abscess
Infected pleural effusion (empyema)
Bacteremic dissemination

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30
Q

What is the tx for CAP?

A
  • antibiotics
  • thoracentesis for peural effusion/empyema
  • vaccinate
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31
Q

What does the pneumonia vaccine do?

A

prevents you from dying of pneumonia but doesnt prevent you from getting it

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32
Q

What is atypical pneumonia?

A

Atypical pneumonia= walking pnuemonia
-acute, febrile respratory condition with patchy inflammatory changes in the lungs THAT is confined to the alveolar septa and pumonary interstitium

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33
Q

What are the bacterial and viral etiologies of atypical pneumonia (walking pneumonia)?

A
  • Mycoplasma pneumoniae (most common)
  • Chlamydia pneumoniae
  • Influenza A and B, RSV, Human metapneumovirus, adenovirus, rhinovirus, rubeola, varicella
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34
Q

Who gets mycoplasma pneumoniae?

A

children/young adults; sporadic in closed communities (school)

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35
Q

How do you treat atypical pneumoniae?

A

azithromycin and fluoroquinolone

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36
Q

What is “atypical” about atypical pneumoniae as compared to community acquired pneumonia?

A
  • moderate amount of sputum
  • no physical findings of consolidation
  • only moderately elevated WBC
  • lack of alveolar exudate
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37
Q

How is atypical pneumonia distinguished from acute bronchitis?

A

site of infection

alveolar septum and interstitum vs. bronchial wall

38
Q

When looking at a histology slide, how can you tell that you are looking at atypical pneumonia rather than typical?

A

atypical-> interstitial infiltrate of lymphocytes and monotyctes
typical-> intra-alveolar neutrophils

39
Q

What is the clinical course of atypical pneumonia like?

A

bad chest cold to severe illness with secondary infection

  • fever, headache, muscle aches
  • maybe cough
40
Q

Who is hospital-acquired pneumonia common in?

A

Common in patients with

  • Severe underlying disease
  • Immunosuppression
  • Prolonged antibiotic therapy (resistance)
  • Invasive intravascular access
  • Mechanical ventilation – VERY high risk
41
Q

Is HAP life theatening?

A

yes

42
Q

What causes hosptial-acquired pneumonia (HAP)?

A

gm neg rods (pseudomonal, enterobacteriaceae)

Staph aureus

43
Q

What is apsiration pneumonia?

What causes aspiration pneumonia?

A

inhalation of gastric contents

-debilitated patients (stroke, intoxication or other causes of altered mental status)

44
Q

Aspiration pneumonia occurs while unconscious or during (blank)

A

vomiting

45
Q

How can you tell the difference between aspiration pneumonia vs asp. (chemical) pneumonitis?

A
  • multiple organisms (oral flora)
  • fulminant clinical course (get very sick, very quickly)
  • possibly lung abscess and ARDS
46
Q

Alcoholics frequently get aspiration pneumonia, why?

A

they frequently go on binges and pass out. THey stay passed out for hours and aspirate. -> so they often get lung abscesses.

47
Q

What is this:

suppurative process in the lung with tissue necrosis

A

lung abscess

48
Q

How does a lung abscess get there?

A
  • aspiration
  • post-pneumonic (S. aureus, K. pneumoniae)
  • Septic emboli from distant infections
  • Obstructive (neoplastic conditions)
  • Trauma, infected adjacent organs, hematogenous seeding (bacteremia)
49
Q

What is this:

Suppurative (liquiefactive necrosis) destruction of the lung parenchyma within a central area of cavitation

A

lung abscess

50
Q

What are the clinical features of a lung abscess?

A
  • cough, fever, copious foul smeling purulent sputum
  • clubbing
  • radiologic diagnosis
  • rule out underlying cancer in older people
51
Q

What is this:
Localized lesion
Granulomatous inflammatory reaction

Whats it caused by?

A

Chronic Pneumonia

Mycobacterium TB
Fungi 
-Histoplasma capsulatum
-Blastomyces dermatitidis
-Coccidioides immitis
52
Q

A patient with (bank) has a clinical presentation and morphology very similiar to TB

A

histoplasmosis

53
Q

What is histoplasmosis?
Is histoplasmosis self limited?
What is the secondary infection like?

A

an intracellular parasite of macrophages
It is self-limited and has a latent primary infection.
-chronic progressive 2ndary disease (fever, night sweats, cough)

54
Q

(blank) causes a localized extrapulmonary involvement

A

Histoplasmosis

55
Q

Who is histoplasmosis common in?

A

immunocompromised patients

56
Q

Histoplasmosis causes (blank) formation with (blank) necrosis (like TB)

A

granuloma

caseation

57
Q

How is histoplasmosis resolved?

What does the body look like afte the resolution?

A

spontaneous or with antifungals

-fibrosis of granuloma and concentric calcification

58
Q

How cna you distinguish histoplasmosis from TB?

A
  • yeast on tissue exam
  • culture
  • antibody testing
59
Q

Unlike Histoplasmosis, (blank) have limited ability to ingest and kill blastomycosis.

A

macrophages

60
Q

What kind of granulomas does blastomycosis cause and why?

A

suppurative granulomas, neutrophil recruitment

61
Q

Blastomycosis can be mistaken for squamos cell cancer due to epithelial hyperplasia. BUT the actually pathological skin change are due to direct incoulation of (blank) to the skin.

A

fungus

62
Q

What causes the San Joaquin Valley Fever?

A

Coccidioidomycosis

63
Q

What are they primary infections of cocciodiomycosis like?

A

most primary infections are asymptomatic

64
Q

(blank) percent of coccidiomycosis patints have lung lesions.

A

10%

65
Q

What are the clinical signs of coccidiomycosis?

A

fever, cough, pleuritic chest pain, erythea nodosum, or erythema multiformae

66
Q

Is Coccidiomycosis granulomatous or pyogenic (suppurative)? What does it depend on?

A

can be either or both

  • depends on if spherules remain intact
  • ruppture and release of endospores results in a pyogenic reaction
67
Q

In coccidiomycosis, less than (blank) percent disseminate. BUT if they do, where can it go? What will it look like if it has disseminated?

A

1%

  • meninges, skin, bones, adrenals, lymph nodes, spleen, liver
  • more purulent than granulomatous in disseminated disease
68
Q

Where will you find coccidiodomycosis?

A

San Joaquin Valley Fever

69
Q

Aspergillus fumigatus is a ubiquitous mold that presents three different ways?

A
  • allergies (acute bronchopulmonary aspergillosis in health people)
  • invasive aspergillosis in immunosuppressed hosts
  • pulmonary lesions
70
Q

Invasive aspergillosis will present where in immunosupressed hosts?

A

primarily in lungs, but common to have hematogenous dissemination

71
Q

What do the lesions look like in Aspergillus fumigatus?

A

it is a necrotizing pneumonia with sharp delineated, rounded lesions wth hemorrhagic borders (looks like a nipple)

72
Q

Mycobacterium TB infects more than 1.7 billion people. What are the risk factors for it?

A

Poverty, crowing, chronic disease (DM, Lymphoma, Chronic Lung Dz, Immunosuppression, HIV/AIDS)

73
Q

If you get mycobacterium TB, are you destined to get the disease?
How is it transmitted?
How does primary TB present? Can it reactivate?

A

no
person to person. airborne
primary TB is asymptomatic
Organism can remain dormant, then reactive when immunity is down

74
Q

A Mycobacterium infection will cause activation of (Blank). What kind of sensitivity reaction does this cause and when?

A

cell-mediated immunity

Delayed type IV hypersensitivity reaction 2-4 weeks after exposure.

75
Q

How does the PPD test work?

A

injected SQ, then 48-72 hours, the type IV reaction peaks and a PALPABLE induration is noted

76
Q

TB can cause what three things from the primary infection?

A 
Ghon complex (pulmonary parenchymal tubercle in LN)
Ghon focus (pulmonar parenchyma tubercle)
77
Q

TB has what kind of necrosis?

A

caseating

78
Q

What happens within the first 3 weeks of primary TB?

A

mycobacteria enters macrophage and manipulates endosome so that you cannot form a phagolysosome. You get a NRAMP1 polymorphism and unchecked proliferation-> bacteremia w/ seeding of multiple sites

79
Q

For a granuloma to develop. Patients with Chron’s disease or RA use anti-TNF agents (such as infliximab) which can cause what?

A
  • TNF-alpha (i.e. granuloma formation is a defense against TB dissemination)
  • causes reactivation of latent TB in patients so TNF is important in controlling TB
80
Q

(blank) heps to activate macrophages in TB. SOOO (blank) are used to detect latent TB infections.

A

IFN-gamma

IGRAs

81
Q

(blank) amplify effector memory T cells.

A

IGRAs

82
Q

What happens 3 weeks after a primary pulmonary TB infection?

A

Infected alveolar macrophage wth TB causes a T cell mediate response. IFN-gamma is released from T cell asn causes the activate macrophage to relase TNF and chemockines which recruit monocytes and creates a granuloma due to caseous necrosis

83
Q

Primary TB is caused from an exogenous source. (blank) percent develop clinically signif response initially.
Cell Mediated Immunity wanes over time, so possible to get a (blank) primary TB infection.

A

5%

2nd

84
Q

What can primary mycobacterium TB progress to?

A
  • acute bacterial pneumonia
  • TB meningitis, Miliary TP
  • Cavitary lesions (rare)
85
Q

Reactivation TB is typically secondary TB and it when does it usually occur and why? Where is the classic location of TB lesions in the lung?

Why is caseous necrosis protective in TB?

A

years after primary infection when host resistance is down
-At the apex of the lung

-pre-existin hypersensitivity activates and walls off the infection (caseous necrosis)

86
Q

Why o you have coughing up of sputum and blood in TB?

A

due to erosion of airways and blood vessels

87
Q

What is the clinical presentation of mycobacterium TB?

A 
Malaise, anorexia, wt. loss -> consumption
Fever
Night Sweats
Hemoptysis
Pleuritic chest pain
88
Q

How do you diagnose mycobacterium TB?

A

must identify TB with a culture, acid fast stain, BAL fluid, or PCR with M. TB DNA.

89
Q

HIV + TB= bad news.
If you have a CD4 >300 it is usually (blank) TB
If you have a CD4 < 200 it presents more like (blank) TB.

A

2ndary TB

primary progressive

90
Q

Patients with HIV and TB usually have what kind of TB tests?

A

false negatives

91
Q

HIV and TB results in decreased erosion?

A

decreased T cell activity-> decreased cavitation-> decrease erosion

Block 9 Week 4 (9 decks)

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