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Pulmonology > Pulmonary Infection Pathology > Flashcards

Pulmonary Infection Pathology Flashcards

A lot of this we saw back in micro... but that feels like a lifetime ago.

0
Q

4 routes for pathogens to get to the lungs?

A

Inhalation.
Aspiration. (implies liquid from stomach/mouth)
Hematogenous.
Direct extension (corrected from inspection… too much ICM)

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1
Q

6 respiratory defenses that can be impaired / problems that can increase susceptibility to infection?

A
  1. Cough reflex.
  2. Mucociliary function.
  3. Phagocytosis / bacterial killing.
  4. Pulmonary edema.
  5. Altered secretion.
  6. Immunosuppression.
    (Immunosuppression is perhaps the most obvious, but the infections people get from 1-5 illustrate their importance.)
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2
Q

You guys know what acute, chronic, and granulomatous inflammation look like.

A

Sure do.

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3
Q

What does alveolar damage from “atypical” pneumonia / ARDS look like on histology?

A

Alveolar destruction with hyaline membranes, which is made of debris from Type I & II epithelial cells + leaked capillary proteins.

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4
Q

A “typical” bacterial pneumonia can either have a lobar pattern or a…

A

lobular pattern (bronchopneumonia)

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5
Q

How do auscultation findings change when a pneumonia becomes “consolidated”?

A

When mucus in the alveoli dries out, sounds go from wet rales to “tubular breath sounds.”

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6
Q

4 classic stages of untreated lobar pneumonia?

A

Congestion (with edema, wet rales).
Red hepatization (lobe solidified with dense PMN infiltrate, RBCs, and fibrin, tubular breath sounds).
Grey hepatization (fibrin and macs present, RBCs and PMNs going away).
Resolution.

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7
Q

Grossly, and on CXR, bronchopneumonia appears more patchy.

A

Okay.

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8
Q

4 complications of bacterial pneumonia?

A
  1. Organization (i.e. scarring).
  2. Abscess.
  3. Empyema (pus in the pleural space).
  4. Hematogenous dissemination.
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9
Q

What are Masson bodies?

A

Markers of a prior, organized pneumonia.

Fibroblasts make a collagen plug that can fill alveoli /block airways.

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10
Q

What’s BOOP?

A

Bronchiolitis obliterans with organizing pneumonia.

Fibroblasts grow into the exudate of a bronchopneumonia… and gum things up.

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11
Q

2 clinical signs of lung abscess? (1 is by imaging)

A

On CXR, can see a mass with an air-fluid level.

Foul-smelling sputum.

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12
Q

3 ways that abscess can happen?

A

Aspiration.
Infection with virulent organism (eg. Staph, Kleb).
Bacteria post-obstruction. (if you see a smoker with a lung abscess, look for cancer).

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13
Q

Why might a abscess caused by aspiration be associated with hemorrhage?

A

Damage from gastric acid.

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14
Q

What kind of bugs will you see on a sputum gram stain in aspiration pneumonia?

A

A polymicrobial infection - lots of different things.

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15
Q

3 types of organisms that cause an “atypical” pneumonia?

A

Viruses
Mycoplasma
Chlamydia.

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16
Q

Where’s the inflammation happens in viral pneumonia?

A

Interstitial space.

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17
Q

General rule about the location of inclusions caused by DNA vs. RNA viruses?

A

DNA viruses - nuclear inclusions, usually (eg. CMV, Herpes)
RNA viruses - cytoplasmic inclusions, usually (eg. RSV, adeno)
Both can cause syncytia to form, though.

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18
Q

Measles can cause pneumonia?

A

Yeah, that’s the part that kills kids.

19
Q

Review: Stain for MTB (and other mycobacteria)?

A

Acid-fast stain.

Mycobacteria are stained with carbol fuschin because of the mycolic acid in their cell wall.

20
Q

What remnant does a controlled, primary TB infection leave?

A

Calcifications in the lung and its draining lymph nodes.

A Ghon complex.

21
Q

When does the “consumption” part of TB happen? (i.e. the fevers, night-sweats, weight loss, hemoptysis, etc.)

A

Secondary TB infection.

22
Q

Is secondary TB infection from re-infection with a new strain, or from reactivation?

A

Unclear. In the US, it’s probably reactivation, because there’s not much TB around.
Elsewhere, could be reinfection.

23
Q

Why does TB like the lung apices?

A

The pO2 there is higher, due to the higher V/Q.

TB is aerobic.

24
Q

Why is secondary TB so much more contagious?

A

There’s just a much higher load of TB organisms…

25
Q

What causes milliary TB?

A

Hematogenous spread

26
Q

What happens when TB spreads through airways?

A

Tuberculous bronchopneumonia.

27
Q

How is TB diagnosis made?

A

Culture (can be done more quickly when DNA probes are used).

Acid fast stain (fast, but a lot less sensitive).

28
Q

Atypical mycobacteria… how are they different from MTB?

A

Acquired from environment, usually.
More antibiotic resistance.
Higher bacterial load seen on acid-fast stain…

29
Q

4 systemic mycoses? (of importance in the US.)

Do these affect healthy people?

A 
Histoplasmosis.
Cryptococcosis.
Coccidiomycosis.
Blastomycosis.
Yes, these can cause disease in non-compromised people. (but they're worse when immunocompromised)
30
Q

3 examples of opportunistic fungal infections?

A

Candida, aspergillus, mucor… (there are others).

32
Q

Which lung fungus is yeast only? (the rest are dimorphic: yeast in tissue, mold in culture)

A

Cryptococcus is yeast-only.

33
Q

Which of the systemic mycoses have animal vectors?

A

Histoplasma - birds and bats (spelunkers!)

Cryptoccus - birds

34
Q

A lot of the fungal infections look like TB with granulomatous inflammation.

A

Indeed… which might even have something to do with why it’s called mycobacteria.

35
Q

Key histological feature of histoplasmosis?

A

Narrow-necked budding yeast.

36
Q

Key histological feature of cryptococcus?

A

Capsule stained by mucicarmine, or its halo on H&E.

37
Q

Key histological feature of blastomycosis?

A

Large budding yeast.

38
Q

Key histological feature of coccidiodes?

A

Spherules.

39
Q

Key histological features of candida?

A

Football-shape yeast, sometimes with pseudohyphae.

40
Q

4 fungi that cause opportunistic infections?

A

Candida.
Aspergillus.
Mucor. (and absidia and rhizopus…)
Pneumocystis jiroveci.

41
Q

How does aspergillus appear different from mucor? (3 things)

A

Aspergillus…

  • branches at acute angles (45ish degrees)/
  • has septate hyphae.
  • has consistent width, because hyphae are cyclindrical. (in contrast, mucor is ribbon-shaped)
42
Q

How does mucor/absidia/rhizopus get to the brain?

A

It tends to invade sinuses… then go to brain.

43
Q

What pathological pattern do candida lung infections have?

A

Purulent bronchopneumonia.

44
Q

What pathological pattern do pneumocystic jiroveci lung infections have?

A

Foamy fluid accumulation in alveoli (not intensely inflammatory).

45
Q

What pathological pattern do aspergillus and muco lung infections have?

A

Vasoinvasive infarcts.

and fungus balls formed in old cavitary lesions

46
Q

Key histological feature of pneumocystis?

A

“crushed ping pong balls” on silver stain

Pulmonology (42 decks)

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