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

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

Flashcards in Nichols: PE, Acute Lung Injury, ILD, Cryptogenic organizing pneumonia, Pneumothorax Deck (48):
1

What are the common sources of PE?

DVT and thrombi around long term catheters

2

What are risk factors from developing a PE?

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

3

Virchow's triangle

endothelial injury
abnormal blood flow
hypercoagulable

4

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

no bc the lung has dual blood supply

5

Saddle embolus

large PE that obstructs the pulm trunk

6

consequences of a saddle embolus

acute cor pulmonale or sudden death

7

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

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

8

describe the gross appearance of a pulmonary infarct

subpleural, wedge-shaped and hemorrhagic

9

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

hampton hump

10

focal oligemia that is suggestive of PE

Westermark sign

11

most common symptom of PE

dyspnea

12

PE Tx

anti-coagulation

13

most specific and sensitive Dx test for PE

spiral CT with IV contrast

14

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

fat embolism
**petechia in <50%

15

3 etiologies of a fat embolism

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

16

describe the clinal syndrome assc with a fat embolus

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

17

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

1-3 days
*due to metabolism of fat creating toxic intermediates --> inflammation --> CRP agglutinates lipids

18

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

head, neck, and anterior chest

19

How is a fat embolus differentiated from air bubbles microscopically?

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

20

Tx for fat embolus

supportive care

21

What is the pathogenesis of an air embolus?

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

22

What are the 4 etiologies of air embolus?

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

signs of air embolism

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

24

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

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