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Pulmonology > Pulm Vascular Disease, Acute Lung injury, & Infections - Gupta > Flashcards

Pulm Vascular Disease, Acute Lung injury, & Infections - Gupta Flashcards

1
Q

Usual source of PE (location?)

A

DVT from lower extremity

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2
Q

Virchows triad?

A

hypercoaguable state, stasis, endothelial injury

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3
Q

Consequence of PE depends on what 2 factors?

A

size of embolus, status of circulation (adequate vs inadequate)

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4
Q

Adequate circulation preventing severe consequence from PE refers to?

A

Bronchial arterial supply sufficient enough to sustain lung tissue distal to small peripheral emboli

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5
Q

Infarcted lung tissue distal to site of PE has what characteristic features?

A

alveolar hemorrhage, coagulative necrosis of alveolar septa

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6
Q

Resolving pulmonary infarction has what characteristic features?

A

After 48 hours, infarcted lung tissue begins to organizing and becomes a paler red–brown due to the conversion of hemorrhage into hemosiderin by macrophages and will eventually form a contracted scar

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7
Q

Examples of non-thrombotic emboli?

A

air, fat, amniotic fluid, foreign material (i.e. IV drug abuse)

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8
Q

Pulmonary circulation is (what fraction) of systemic pressure?

A

1/8

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9
Q

Primary pulmonary HTN: predominantly seen in what epidemiologic make up?

A

young female (3rd to 5th decade)

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10
Q

What inactivating mutation is seen in primary pulmonary HTN? cause of this mutation?

A

BMPR2 (bone morphogenetic protein receptor type 2, leads to proliferation of vascular smooth muscle

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11
Q

Primary pulmonary HTN genetics?

A

Autosomal dominant

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12
Q

Secondary causes of pulmonary HTN?

A
  • Chronic obstructive or interstitial lung diseases
  • Cardiac disease (congenital or acquired)
  • Recurrent thromboemboli
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13
Q

What cardiac disease can cause secondary pulmonary HTN? Mechanism?

A

Mitral stenosis

- elevated left atrial pressure causes increased pulmonary venous and arterial pressure

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14
Q

Regardless of etiology, all forms of pulmonary HTN are associated with what 3 outcomes?

A
  1. medial hypertrophy of the pulmonary muscular and elastic arteries
  2. pulmonary arterial atherosclerosis
  3. right ventricular hypertrophy
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15
Q

Microscopic appearance of pulmonary HTN?

A

plexogenic lesions

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16
Q

3 examples of diffuse pulmonary hemorrhage syndromes (pulmonary vascular diseases)

A
  • goodpasture
  • idiopathic pulmonary hemosiderosis
  • vasculitis - associated hemorrhage (SLE, Wegener’s)
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17
Q

Goodpasture = autoimmune disorder with circulating antibodies towards ___?

A

alpha-3 chain of collagen IV

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18
Q

Goodpasture is characterized by destruction of (what) in what organ(s)?

A

destruction of basement membrane in kidney glomeruli and lung alveoli

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19
Q

Good pasture epidemiology?

A

men in teens-20s, smokers

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20
Q

Microscopic appearance of goodpasture?

A

Alveolar basement membrane destruction evidenced by:

  • necrosis of alveolar walls
  • intra-alveolar hemorrhage
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21
Q

pulmonary edema due to what 2 primary factors?

A 
hemodynamic edema (increased hydrostatic pressure, decreased oncotic pressure)
edema due to microvascular injury
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22
Q

Increased hydrostatic pressure resulting in pulmonary edema most commonly associated with what disease?

A

left heart failure

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23
Q

Left heart failure resulting in pulmonary edema worst in what part of lungs? why?

A

at bases of lungs, hydrostatic pressure greatest here

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24
Q

Decreased oncotic pressure resulting in pulmonary edema due to what disease?

A

liver disease (hypoalbuminemia)

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25
Q

Common ways in which patient can develop edema due to microvascular injury?

A

infections, inhaled smoke and other gases, shock

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26
Q

Microscopic appearance of pulmonary edema?

A

engorged alveolar capillaries and intraalveolar granules and precipitate

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27
Q

Chronic pulmonary edema microscopic apperance?

A

alveolar microhemorrhages and resulting hemosiderin–laden macrophages (“heart failure cells”) may be seen

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28
Q

ARDS (acute respiratory distress syndrome) characterized by ? (referring to alveolar capillaries)

A

diffuse alveolar capillary damage

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29
Q

Onset of ARDS?

A

rapid

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30
Q

ARDS manifests histologically as ?

A

diffuse alveolar damage (DAD)

31
Q

ARDS histologic findings are similar to __?

A

preterm infants with deficient surfactant (neonatal RDS)

32
Q

Pathophysiology of Acute lung injury?

A

Capillary damage ⇒ Activates macrophages ⇒ Activates neutrophils ⇒ Neutrophils release PAF, leukotrienes, proteases ⇒ These attack and kill Type II (and Type I) pneumocytes. Type II are in charge of surfactant production and stem cells for production of further pneumocytes ⇒ TGF-beta moves in causing fibrosis. At the end of all this, protein rich fluid+necrotic epithelial cells will produce the hyaline membrane (BIG POINT)

33
Q

Fibrin+necrotic epithelial cells leads to production of what in acute lung injury?

A

hyaline membrane within alveolar walls

34
Q

During organizing stage of acute lung injury, what happens to the hyaline membrane?

A

resorbed and replaced with plugs of intraalveolar organizing fibroconnective tissue

35
Q

Pneumonia most likely to occur in what subset of patients (think general)?

A

those with chronic disease, immunologic deficiency, on immunosuppressants

36
Q

Three patterns of pneumonia? Which are more likely bacterial vs viral

A

More likely bacterial: bronchopneumonia, lobar pneumonia

More likely viral: interstitial (atypical) pneumonia

37
Q

CAP (community acquired pneumonia) most common bacteria?

A

streptococcus pneumoniae

38
Q

Gross geographic feature of bronchopneumonia?

A

patchy distribution in lungs

39
Q

Gross geographic feature of lobar pneumonia?

A

entire lobe or large portion of lobe

40
Q

Stages of inflammatory response in pneumonia?

A

Congestion ⇒ Red Hepatization ⇒ Gray Hepatization ⇒ Resolution

41
Q

Stages of inflammatory response. Congestion features?

A

Numerous bacteria, few neutrophils, vascular engorgement and edema

42
Q

Stages of inflammatory response. Red Hepatization features?

A

Massive congestion, lots of neutrophils

43
Q

Stages of inflammatory response. Gray Hepatization features?

A

Disintegration of RBCs, macrophages. Fibronopurulent exudate

44
Q

Stages of inflammatory response. Resolution features?

A

Enzymatic digestion, resorption by macrophages

45
Q

Pneumonia. Elderly with acute COPD exacerbation. What bug?

A

Moraxella catarrhalis

46
Q

Pneumonia. IV drug abusers. What bug?

A

Staph aureus

47
Q

Pneumonia. debilitated, malnourished, alcoholics. What bug?

A

Klebsiella pneumoniae

48
Q

Pneumonia. CF patients. What bug?

A

Pseudomonas aeruginosa

49
Q

Pneumonia. Water towers and smokers. What bug?

A

Legionella pneumophila

50
Q

Main complications of pneumonia?

A

abscess, empyema (spread to pleural cavity), dissemination to other organs (meningitis)

51
Q

Necrotizing pneumonia (abscess) are most likely due to what bugs?

A

streptococcus, klebsiella

52
Q

Atypical pneumonia main distinguishing feature?

A

lack of neutrophil infiltration, predominantly lymphocytes instead

53
Q

Microscopic appearance of atypical pneumonia?

A

lymphocytic inflammation of the interstitium. Type II Pneumocyte hyperplasia

54
Q

Primary TB occurs in previously ___?

A

unexposed patients

55
Q

T/F. Over 10% of newly infected patients (TB) develop clinical disease.

A

False, only 5% of newly infected actually develop TB disease

56
Q

Secondary (reactivation) of TB typically occurs in what part of lung?

A

Apex

57
Q

Gross appearance of primary TB. What complex is seen? What is the definition of this complex?

A

Ghon complex = calcified parenchymal focus + caseous hilar lymph nodes

58
Q

Microscopic appearance of TB?

A

granulomatous inflammation w/ central necrosis, surrounded by rim of macrophages

59
Q

Secondary TB gross appearance?

A

Confluent areas of caseous necrosis and cavitation, found primarily in upper lobes (site of highest O2 tension)

60
Q

Gross appearance of miliary TB?

A

Lymphohematogenous dissemination of mycobacteria results in multiple 2-4 mm foci (look like millet seeds, hence the name) of granulomatous inflammation.

61
Q

Fungal pneumonia primarily due to what fungus?

A

histoplasma capsulatum

62
Q

Classic cause of fungal pneumonia? (Histoplasmosis common with exposure to what?)

A

inhalation of dust contaminated with bird/bat droppings that contain spores

63
Q

Fungal pneumonia microscopic appearance?

A

granulomatous inflammation, typically necrotizing

64
Q

Besides histoplasma capsulatum, what other 3 fungi can cause fungal pneumonia?

A

Blastomyces dermatidis, cryptococcus neoformans, coccidioides immitis

65
Q

BIG, broad-based buds. Name that fungus.

A

Blastomyces. Think alliteration. BIGGG, broad-based buds. Gupta thinks they look like snowmen…or snow-women #genderequality #allmysingleladies

66
Q

Pigeon droppings. What fungus most likely?

A

Cryptococcus neoformans

67
Q

Coccidioides immitis endemic to what geographic region in US?

A

Southwest and western U.S. (San Joaquin Valley)

68
Q

Main staining feature seen with cryptococcus?

A

large anti-phagocytic capsule is easily stained

69
Q

Main microscopic feature of coccidioidomycosis?

A

Thick walled, nonbudding large sphere, filled with small endospores

70
Q

Pneumonia in immunocompromised host usually due to what bugs?

A

CMV, pneumocystis jiroveci, mycobacterium avium-intracellulare, invasive aspergillosis, mucormycosis, candidiasis

71
Q

CMV pneumonia microscopic appearance?

A

enlarged cell w/ cytoplasmic and intranuclear (OWL EYES) viral inclusion

72
Q

Granular alveolar exudate with central umbilications. Seen in what form of immunocompromised pneumonia?

A

Pneumocystis pneumonia

73
Q

Pulmonary aspergillosis pneumonia characterized by what feature?

A

angioinvasion of regular septate hyphae with progressive acute-angle branching

74
Q

Main dif between aspergillosis and mucormycosis.

A

Also angioinvasive, however produces wide angle “ribbons” with non-septate hyphae

Pulmonology (31 decks)

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