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Pulmonary > Nichols: PE, Acute Lung Injury, ILD, Cryptogenic organizing pneumonia, Pneumothorax > Flashcards

Nichols: PE, Acute Lung Injury, ILD, Cryptogenic organizing pneumonia, Pneumothorax Flashcards

1
Q

What are the common sources of PE?

A

DVT and thrombi around long term catheters

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2
Q

What are risk factors from developing a PE?

A 
smoking 
immobilization
malignancy
surgery
central venous instrumentation
thrombophilia, 
obesity
oral contraceptives
pregnancy
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3
Q

Virchow’s triangle

A

endothelial injury
abnormal blood flow
hypercoagulable

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4
Q

Do small emboli cause infarction in the lung? Why or why not?

A

no bc the lung has dual blood supply

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5
Q

Saddle embolus

A

large PE that obstructs the pulm trunk

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6
Q

consequences of a saddle embolus

A

acute cor pulmonale or sudden death

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7
Q

What happens to the small emboli that make it to the lung but are not big enough to cause an infarction?

A

become organized into vessel wall (may leave a fibrous band)

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8
Q

describe the gross appearance of a pulmonary infarct

A

subpleural, wedge-shaped and hemorrhagic

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9
Q

CXR finding of peripheral wedge-shaped opacity that is suggestive o PE

A

hampton hump

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10
Q

focal oligemia that is suggestive of PE

A

Westermark sign

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11
Q

most common symptom of PE

A

dyspnea

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12
Q

PE Tx

A

anti-coagulation

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13
Q

most specific and sensitive Dx test for PE

A

spiral CT with IV contrast

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14
Q

hypoxemia, neurological impairment and petechial rash 1-3 days after trauma

A

fat embolism

**petechia in <50%

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15
Q

3 etiologies of a fat embolism

A

long bone fractures
orthopedic surgery
sickle cell disease
(also liposuction, burns, pancreatitis, osteomyelitis – in his word doc)

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16
Q

describe the clinal syndrome assc with a fat embolus

A

acute onset of dyspnea, confusion, tachypnea, tachycardia, irritability, restlelssness, anemia and thrombocytopenia

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17
Q

How long after trauma will a fat embolus present? Why?

A

1-3 days

*due to metabolism of fat creating toxic intermediates –> inflammation –> CRP agglutinates lipids

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18
Q

Where do the petechia form that may present with a fat embolus (pulm)

A

head, neck, and anterior chest

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19
Q

How is a fat embolus differentiated from air bubbles microscopically?

A

oil-red-O stain of fresh tissue or freshly frozen tissue
or
electron microscopy with osmium tetroxide of fixed tissue

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20
Q

Tx for fat embolus

A

supportive care

21
Q

What is the pathogenesis of an air embolus?

A

hole in blood vessel open to air at higher pressure than the blood (or formation of gas within the blood)

22
Q

What are the 4 etiologies of air embolus?

A
  1. vascular catheterization: breakage of vascular catheter connections, failure to occule catheter during insertion or removal
  2. sugery: brain in sitting postion, back in prone)
  3. chest wall injury
  4. barotrauma: MV at high press with blood vessel rupture in lungs, rapis ascent during underwater trauma)
23
Q

signs of air embolism

A

dyspnea, gasp, cough, millwheel heart murmur, tachypena, rales, shock

24
Q

Generally, more than ____ ml needed to have a clinical effect, but ____ ml introduced at a rate of _____ ml/second is fatal

A

100 ml = clinical effect

300-500 ml at a rate of 100ml/s = fatal

25
Q

How is air embolus Dx?

A

Dx of exclusion

26
Q

Tx of air embolus

A

left lateral decubitus positioning (Durant’s maneuver)

27
Q

non-cardiogenic pulmonary damage manifested by edema with an inflammatory and fibrosing response

A

acute lung injury

28
Q

ALI starts with edema. Where in the lung does this edema start?

A

interstitial –> alveolar and sometimes with hemorrhaging

29
Q

What causes ALI to be hemorrhagic?

A

when the injury kills capillary endothelial cells and pneumocytes

30
Q

What are the stages of ALI?

A

Exudative –> transition –> proliferative –> fibrotic

31
Q

Describe the pathogenesis of ALI.

A

binding of microbial products or cell injury activates innate immune response –>
dysregulated inflammation (macrophage production of IL1, 8, TNF) –>
inc permeability of endothelium and epithelium (disruption of cadherins and adherens) –>
edema –>
TGF-B and PDGF released –> fibrosis

32
Q

How does the gross appearance of ALI change as the disease progresses?

A

red, edematous –> white and fibrous

33
Q

Describe the microscopic changes assc with ALI

A

exudative phase: hyaline membranes, congestion, lymphocytes, macrophages

proliferative: less hyaline, intersitial infitration by lymphocytes, macrophages, and proliferating fibroblasts
* *type 2 pneumoplasia and fibroplasia

fibrosis: interstitial and progressive

34
Q

lipid laiden macrophages

A

amiodarone toxicity

35
Q

How does ALI commonly present?

A

rapidly progressive dyspnea and bilateral pulmonary infiltrates superimposed on the manifestations of the cause of injury
=ARDS

36
Q

Tx of ALI

A

MV but with low TV to protect lungs from further injury/inflammation, conservative fluid resuscitation

37
Q

How long after radiation exposure will radiation pneumonitis present? How does it present?

A

1 -2 mos after exposure

with dyspnea, cough, pleuritic chest pain, fever, CXR infilrates

38
Q

What are the microscopic findings specific to radiation pneumonitis?

A

atypical type 2 pneumocyte hyperplasia and blood vessel injury

LATE: hemosiderin and interstitial fibrosis

39
Q

IPF/UIP is (acute or chronic) fibrosis of what part of the lung?

A

chronic, septa btwn airspaces

40
Q

How does a pt with IPF/UIP present

A

In a late-middle aged (male) smoker with…

insidious onset of dyspna and dry cough
inspiratory velcro crackles

CXR: asymmetric subpleural peripheral reticular opacities in the lower lobes

41
Q

What it is the radiologic finding with advanced IPF/UIP?

A

honeycombing

42
Q

What is the hallmark microscopic finding of UIP/IPF

A

fibroblast foci of immature fibroblasts bulging into the alveoli from the interstitium

43
Q

Tc for IPF/UIP

A

transplantation

Corticosteriods + immunosuppressive drugs + INF-gamma

44
Q

necrotizing infection –> organizing pneumonia is known as

A

cryptogenic organizing pneumonia

45
Q

How doe COP preset

A

in late middle age non-smoker with…

dyspnea and cough with ground glass opacities that are less dense than acute bacterial pneumonia

46
Q

It is different to distinguish COP from IPF/UIP. WHy?

A

COP responds to corticosteriod treatment while UIP usually does not

47
Q

Masson bodies

A

seen in COP = fibrosing granulation tissue in the alveoli

48
Q

All of Nichols pneumothorax stuff was covered in that other lecture

A

so check that out

Pulmonary (31 decks)

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