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01. Cardiopulm Renal > Pulmonary Pathology 1/2 > Flashcards

Pulmonary Pathology 1/2 Flashcards

(52 cards)

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1
Q

alveolar pores (of Kahn)

A

allow aeration but also bacteria/cells/exudate to travel between alveoli

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2
Q

type 2 pneumocytes

A

produce surfactant and replace type 1 pneumocytes

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3
Q

resorption atelectasis

A

airway obstruction with gradual resorption of air reduces lung expansion

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4
Q

compression atelectasis

A

accumulated material in pleural cavity compresses the lung parenchyma

*pleural effusion

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5
Q

contraction atelectasis

A

fibrotic or other innate restrictive process in the pleura or peripheral lung restricts lung expansion

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6
Q

hemodynamic “pushing out” causes of pulmonary edema

A
  • left sided heart failure
  • volume overload
  • pulmonary vein obstruction
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7
Q

hemodynamic “leaking out” pulmonary edema

A
  • hypoalbuminemia
  • nephrotic syndrome
  • liver disease
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8
Q

injury to alveolar wall causes of pulmonary edema

A
  • bacterial pneumonia
  • sepsis
  • smoke inhalation
  • aspiration
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9
Q

What will show pink proteinaceous material in the alveolar spaces histologically?

A

pulmonary edema

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10
Q

acute lung injury

A

acute onset, hypoxemia, bilateral infiltrates, NO evidence of cardiac failure

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11
Q

Acute respiratory distress syndrome

A
  • worsening hypoxemia
  • PaO2/FiO2 < 200
  • bilateral infiltrates
  • abrupt onset of Sx
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12
Q

Diffuse alveolar damage

A

histologic manifestation of ARDS

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13
Q

DAD formula

A

Edema + fibrin + cell debris = HYALINE MEMBRANES

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14
Q

What is the difference between ARDS and Acute interstitial pneumonia?

A

acute interstitial pneumonia cannot be attributed to a specific etiology
(same clinical presentation and histology as ARDS)

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15
Q

stages of ARDS

A

1) exudative
2) proliferative
3) fibrotic

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16
Q

What happens after the fibroproliferative phase of ARDS?

A

Either
Resolution- restoration of normal cellular structure and function
-OR-
Fibrosis- destruction and distortion of normal cellular structure (irreversible)

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17
Q

Pathogenesis of neonatal respiratory distress syndrome

A

immature lungs with limited pulmonary surfactant lead to development of RDS at birth

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18
Q

Restrictive lung disease characteristics

A
  • volume restriction
  • FEV1/FVC normal
  • FVC reduced
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19
Q

Obstructive lung disease characteristics

A
  • decreased flow

- low FEV1/FVC ratio

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20
Q

Dx criteria for chronic bronchitis

A

persistent cough with sputum production for 3 months out of 2 consecutive years

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21
Q

lung sounds chronic bronchitis

Study These Flashcards
A

rhonchi and wheezing

22
Q

lung sounds emphysema

23
Q

airway remodeling

Study These Flashcards
A
  • occurs with asthma
  • progressive structural changes to airways (fibrosis, smooth muscle hyperplasia, increased goblet cells)
  • may be irreversible
  • decreased response to therapeutic agents
24
Q

status asthmaticus

Study These Flashcards
A
  • potentially fatal asthma attack
  • bronchial occlusion by thick mucus
  • eosinophils and breakdown product (charot leyden crystals)
25
Curschmann spirals
coiled mucus plugs found in status asthmaticus
26
Kartagener's syndrome
or primary ciliary dyskinesia; dysfunction of dynein arm of microtubules
27
What is cause of death with a saddle pulmonary embolism?
Acute cor pulmonale (no pulmonary infarct)
28
who have Talc embolisms?
IV drug users
29
pulmonary HTN Dx criteria
pulmonary artery pressure (PAP) greater than 25 mmHg
30
pulmonary HTN subgroups
1) pulmonary arterial HTN (primary vascular Dz) 2) secondary to left heart failure 3) secondary to chronic pulmonary parenchymal Dz or hypoxia 4) secondary to thromboembolic pulmonary Dz 5) multifactorial
31
pathology pulmonary HTN
1) plexiform lesion | 2) medial hypertrophy
32
Three pulmonary hemorrhage syndromes
1) goodpasture syndrome 2) granulomatosis with polyangiitis 3) idiopathic pulmonary hemosiderosis
33
immunofluorescence showing linear pattern of deposition is related to..
Good pasture syndrome (due to anti-basement membrane antibodies)
34
goodpasture syndrome is what type of hypersensitivity reaction?
type II
35
Who does good pasture syndrome affect?
male patients in their 2nd or 3rd decade
36
Goodpasture syndrome pathophys
Abs against a noncollagenous subunit of collagen IV
37
Cause of clinical Sx of goodpasture syndrome
Ab-mediated damage to basement membranes in lung and kidneys
38
Stages of lobar PNA
1) congestion 2) red hepatization 3) grey hepatization 4) resolution
39
complications of lobar PNA
- abscess - empyema - bacteremia
40
typical pneumonia features
- abrupt onset - respiratory Sx - consolidation on chest x-ray - in older adults or children
41
atypical/walking pneumonia features
- slower onset - systemic symptoms - patchy infiltrates on chest x-ray - in young adults/teens/older children
42
antigenic drift
- causes epidemics - minor changes to antigens on virus, allowing for increased spread - similar enough to original virus to allow for some immunity in many individual
43
antigenic shift
- causes pandemics - genomic alterations with major resulting changes to protein structure - Naive immunity for almost all people
44
where does bacterial PNA show infiltrates on histology?
in the alveolar spaces
45
where does viral PNA show infiltrates on histology?
in the interstitium
46
general presentation bacterial PNA
- abrupt onset - high grade fever - crackles on lung exam - lobar or consolidated appearance - may involve pleura
47
general presentation viral PNA
- gradual onset - epidemics are common - no or low grade fever - wheezes on lung exam - diffuse infiltrates on CXR
48
lung abscess causes
1) complication on PNA | 2) aspiration
49
what histological finding is highly associated with TB?
caseating granuloma
50
ghon complex
- radiological/histo finding with TB | - lesion has a ghon focus (primary lesion) and pulmonary lymphadenopathy
51
chronic pneumonia
pneumonic process lasting for months in an immunocompetent patient
52
what does histo of lung transplant rejection look like?
mononuclear infiltrates around vessel

01. Cardiopulm Renal (9 decks)

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