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

(74 cards)

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
Common ways in which patient can develop edema due to microvascular injury?
infections, inhaled smoke and other gases, shock
26
Microscopic appearance of pulmonary edema?
engorged alveolar capillaries and intraalveolar granules and precipitate
27
Chronic pulmonary edema microscopic apperance?
alveolar microhemorrhages and resulting hemosiderin–laden macrophages (“heart failure cells”) may be seen
28
ARDS (acute respiratory distress syndrome) characterized by ? (referring to alveolar capillaries)
diffuse alveolar capillary damage
29
Onset of ARDS?
rapid
30
ARDS manifests histologically as ?
diffuse alveolar damage (DAD)
31
ARDS histologic findings are similar to __?
preterm infants with deficient surfactant (neonatal RDS)
32
Pathophysiology of Acute lung injury?
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
Fibrin+necrotic epithelial cells leads to production of what in acute lung injury?
hyaline membrane within alveolar walls
34
During organizing stage of acute lung injury, what happens to the hyaline membrane?
resorbed and replaced with plugs of intraalveolar organizing fibroconnective tissue
35
Pneumonia most likely to occur in what subset of patients (think general)?
those with chronic disease, immunologic deficiency, on immunosuppressants
36
Three patterns of pneumonia? Which are more likely bacterial vs viral
More likely bacterial: bronchopneumonia, lobar pneumonia | More likely viral: interstitial (atypical) pneumonia
37
CAP (community acquired pneumonia) most common bacteria?
streptococcus pneumoniae
38
Gross geographic feature of bronchopneumonia?
patchy distribution in lungs
39
Gross geographic feature of lobar pneumonia?
entire lobe or large portion of lobe
40
Stages of inflammatory response in pneumonia?
Congestion ⇒ Red Hepatization ⇒ Gray Hepatization ⇒ Resolution
41
Stages of inflammatory response. Congestion features?
Numerous bacteria, few neutrophils, vascular engorgement and edema
42
Stages of inflammatory response. Red Hepatization features?
Massive congestion, lots of neutrophils
43
Stages of inflammatory response. Gray Hepatization features?
Disintegration of RBCs, macrophages. Fibronopurulent exudate
44
Stages of inflammatory response. Resolution features?
Enzymatic digestion, resorption by macrophages
45
Pneumonia. Elderly with acute COPD exacerbation. What bug?
Moraxella catarrhalis
46
Pneumonia. IV drug abusers. What bug?
Staph aureus
47
Pneumonia. debilitated, malnourished, alcoholics. What bug?
Klebsiella pneumoniae
48
Pneumonia. CF patients. What bug?
Pseudomonas aeruginosa
49
Pneumonia. Water towers and smokers. What bug?
Legionella pneumophila
50
Main complications of pneumonia?
abscess, empyema (spread to pleural cavity), dissemination to other organs (meningitis)
51
Necrotizing pneumonia (abscess) are most likely due to what bugs?
streptococcus, klebsiella
52
Atypical pneumonia main distinguishing feature?
lack of neutrophil infiltration, predominantly lymphocytes instead
53
Microscopic appearance of atypical pneumonia?
lymphocytic inflammation of the interstitium. Type II Pneumocyte hyperplasia
54
Primary TB occurs in previously ___?
unexposed patients
55
T/F. Over 10% of newly infected patients (TB) develop clinical disease.
False, only 5% of newly infected actually develop TB disease
56
Secondary (reactivation) of TB typically occurs in what part of lung?
Apex
57
Gross appearance of primary TB. What complex is seen? What is the definition of this complex?
Ghon complex = calcified parenchymal focus + caseous hilar lymph nodes
58
Microscopic appearance of TB?
granulomatous inflammation w/ central necrosis, surrounded by rim of macrophages
59
Secondary TB gross appearance?
Confluent areas of caseous necrosis and cavitation, found primarily in upper lobes (site of highest O2 tension)
60
Gross appearance of miliary TB?
Lymphohematogenous dissemination of mycobacteria results in multiple 2-4 mm foci (look like millet seeds, hence the name) of granulomatous inflammation.
61
Fungal pneumonia primarily due to what fungus?
histoplasma capsulatum
62
Classic cause of fungal pneumonia? (Histoplasmosis common with exposure to what?)
inhalation of dust contaminated with bird/bat droppings that contain spores
63
Fungal pneumonia microscopic appearance?
granulomatous inflammation, typically necrotizing
64
Besides histoplasma capsulatum, what other 3 fungi can cause fungal pneumonia?
Blastomyces dermatidis, cryptococcus neoformans, coccidioides immitis
65
BIG, broad-based buds. Name that fungus.
Blastomyces. Think alliteration. BIGGG, broad-based buds. Gupta thinks they look like snowmen...or snow-women #genderequality #allmysingleladies
66
Pigeon droppings. What fungus most likely?
Cryptococcus neoformans
67
Coccidioides immitis endemic to what geographic region in US?
Southwest and western U.S. (San Joaquin Valley)
68
Main staining feature seen with cryptococcus?
large anti-phagocytic capsule is easily stained
69
Main microscopic feature of coccidioidomycosis?
Thick walled, nonbudding large sphere, filled with small endospores
70
Pneumonia in immunocompromised host usually due to what bugs?
CMV, pneumocystis jiroveci, mycobacterium avium-intracellulare, invasive aspergillosis, mucormycosis, candidiasis
71
CMV pneumonia microscopic appearance?
enlarged cell w/ cytoplasmic and intranuclear (OWL EYES) viral inclusion
72
Granular alveolar exudate with central umbilications. Seen in what form of immunocompromised pneumonia?
Pneumocystis pneumonia
73
Pulmonary aspergillosis pneumonia characterized by what feature?
angioinvasion of regular septate hyphae with progressive acute-angle branching
74
Main dif between aspergillosis and mucormycosis.
Also angioinvasive, however produces wide angle "ribbons" with non-septate hyphae