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
How is air embolus Dx?
Dx of exclusion
26
Tx of air embolus
left lateral decubitus positioning (Durant's maneuver)
27
non-cardiogenic pulmonary damage manifested by edema with an inflammatory and fibrosing response
acute lung injury
28
ALI starts with edema. Where in the lung does this edema start?
interstitial --> alveolar and sometimes with hemorrhaging
29
What causes ALI to be hemorrhagic?
when the injury kills capillary endothelial cells and pneumocytes
30
What are the stages of ALI?
Exudative --> transition --> proliferative --> fibrotic
31
Describe the pathogenesis of ALI.
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
How does the gross appearance of ALI change as the disease progresses?
red, edematous --> white and fibrous
33
Describe the microscopic changes assc with ALI
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
lipid laiden macrophages
amiodarone toxicity
35
How does ALI commonly present?
rapidly progressive dyspnea and bilateral pulmonary infiltrates superimposed on the manifestations of the cause of injury =ARDS
36
Tx of ALI
MV but with low TV to protect lungs from further injury/inflammation, conservative fluid resuscitation
37
How long after radiation exposure will radiation pneumonitis present? How does it present?
1 -2 mos after exposure | with dyspnea, cough, pleuritic chest pain, fever, CXR infilrates
38
What are the microscopic findings specific to radiation pneumonitis?
atypical type 2 pneumocyte hyperplasia and blood vessel injury LATE: hemosiderin and interstitial fibrosis
39
IPF/UIP is (acute or chronic) fibrosis of what part of the lung?
chronic, septa btwn airspaces
40
How does a pt with IPF/UIP present
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
What it is the radiologic finding with advanced IPF/UIP?
honeycombing
42
What is the hallmark microscopic finding of UIP/IPF
fibroblast foci of immature fibroblasts bulging into the alveoli from the interstitium
43
Tc for IPF/UIP
transplantation | Corticosteriods + immunosuppressive drugs + INF-gamma
44
necrotizing infection --> organizing pneumonia is known as
cryptogenic organizing pneumonia
45
How doe COP preset
in late middle age non-smoker with... | dyspnea and cough with ground glass opacities that are less dense than acute bacterial pneumonia
46
It is different to distinguish COP from IPF/UIP. WHy?
COP responds to corticosteriod treatment while UIP usually does not
47
Masson bodies
seen in COP = fibrosing granulation tissue in the alveoli
48
All of Nichols pneumothorax stuff was covered in that other lecture
so check that out