Atelectasis Flashcards

1
Q

what is atelectasis

A

loss of lung volume due to inadequate expansion

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2
Q

does atelectasis lead to ventilation perfusion imbalance (leading to hypoxia)

A

yes

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3
Q

it involves segment or …. or ….

A

lobe or lung

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4
Q

if cause is removed is it reversible

A

yes

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5
Q

types of atelectasis

A

resorption (obstructive), compression , contraction , microatelectasis

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6
Q

resorption atelectasis due to

A

foreign body, mucus plug due to bronchitis or asthma or cystic fibrosis , post surgery , tumor

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7
Q

mediastinal shift in each type of atelectasis

A

resorption same side
compression opposite side
contraction and microatelectasis no shift

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8
Q

compression atelectasis causes

A

air or fluid in pleural cavity

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9
Q

what happens to diaphragm in compression atelectasis

A

elevated

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10
Q

contraction atelectasis causes

A

post inflammatory scarring, fibrotic changes

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11
Q

is contraction atelectasis reversible

A

usually irreversible

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12
Q

microatelectasis cause

A

loss of surfactant

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13
Q

microatelectasis location

A

generalized

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14
Q

where is microatelectasis usually seen

A

acute or neonatal respiratory distress synd

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15
Q

grossly and microscope ate.

A

gross: shrunken purple sub crepiant nodular lung

micro,: slit like alveoli, congested septae and hyaline mem in micro

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16
Q

ARDS caused by many conditions

A

true

17
Q

clinical manifestation of ARDS

A

Hypoxemia hypercapnea
diffuse bilateral pulmonary infil
acute onset of severe dyspnea

18
Q

direct etiology of ARDS

A

Pneumonia
toxic inhalation
aspiration of gastric contents

19
Q

why do some ppl have gastric aspiration

A

ppl with disability or chronic alcoholics or coma (ma 3andhom gag reflex)

20
Q

indirect etiology of ARDS

A
sepsis 
pancreatitis 
multiple transfusion 
drug overdose 
multiple trauma
21
Q

risk factor of ards

A

multiple predispose conditions
old age
chronic alcoholics
metabolic acidosis

22
Q

what is pathognomic for ARDS

A

DAD diffuse alveolar damage

23
Q

pathogenisis of ards (start with imbalance)

A

imbalane in pro inflam and anti inflam mediators
nuclear factor kabba is pro inflam that activates macrophages
macrophages release IL 1 IL8 and TNF
these select isolate and activate neutrophils
neutrophils release protease leukotriene oxidant and PAF
lead to endothelium and epithelium injury and DAD

24
Q

what later happens in ARDS pathogenisis

A

macrophage derived fibrogenic factors released ( IL-1 IL8 TGF and PDGF )
Recruit fibroblasts
clotting cascade

25
Q

how pathogenisis of ARDS counteracted

A

by anti protease anti oxidant and anti inflammatory (IL-10)

26
Q

acute phase of ARDS

A
Exaudate in alveoli 
altered diffusion 
atelectasis 
neutrophil infiltration 
hyaline membrane ( cellular debris dysfunction surfactant and exaudate 
pulmonary HTN
27
Q

organizing phase of ARDS

A

Organize exaudate
pneumocyte type 2 prolif
lymphocyte infiltrate

28
Q

fibrosis phase of ARDS

A

loss of lung architecture emphysema like
extensive fibrosis
intimal prlif in microcirculation leading to vascular occlusion and pulmonary HTN
honey comb apperance

29
Q

which phase of ARDS has lymphocyte

A

organizing

30
Q

which phase of ARDS has neutrophils

A

acute

31
Q

clinical picture of ARDS first 72 hours

A

severe dyspnea nd hypoxemia and cyanosis

32
Q

clinical picture of ARDS after 72 hours

A

bilateral severe pneumonia and bilateral pulmonary infiltrate , multisystem failure , DIC