Atelectasis Flashcards
what is atelectasis
loss of lung volume due to inadequate expansion
does atelectasis lead to ventilation perfusion imbalance (leading to hypoxia)
yes
it involves segment or …. or ….
lobe or lung
if cause is removed is it reversible
yes
types of atelectasis
resorption (obstructive), compression , contraction , microatelectasis
resorption atelectasis due to
foreign body, mucus plug due to bronchitis or asthma or cystic fibrosis , post surgery , tumor
mediastinal shift in each type of atelectasis
resorption same side
compression opposite side
contraction and microatelectasis no shift
compression atelectasis causes
air or fluid in pleural cavity
what happens to diaphragm in compression atelectasis
elevated
contraction atelectasis causes
post inflammatory scarring, fibrotic changes
is contraction atelectasis reversible
usually irreversible
microatelectasis cause
loss of surfactant
microatelectasis location
generalized
where is microatelectasis usually seen
acute or neonatal respiratory distress synd
grossly and microscope ate.
gross: shrunken purple sub crepiant nodular lung
micro,: slit like alveoli, congested septae and hyaline mem in micro
ARDS caused by many conditions
true
clinical manifestation of ARDS
Hypoxemia hypercapnea
diffuse bilateral pulmonary infil
acute onset of severe dyspnea
direct etiology of ARDS
Pneumonia
toxic inhalation
aspiration of gastric contents
why do some ppl have gastric aspiration
ppl with disability or chronic alcoholics or coma (ma 3andhom gag reflex)
indirect etiology of ARDS
sepsis pancreatitis multiple transfusion drug overdose multiple trauma
risk factor of ards
multiple predispose conditions
old age
chronic alcoholics
metabolic acidosis
what is pathognomic for ARDS
DAD diffuse alveolar damage
pathogenisis of ards (start with imbalance)
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
what later happens in ARDS pathogenisis
macrophage derived fibrogenic factors released ( IL-1 IL8 TGF and PDGF )
Recruit fibroblasts
clotting cascade
how pathogenisis of ARDS counteracted
by anti protease anti oxidant and anti inflammatory (IL-10)
acute phase of ARDS
Exaudate in alveoli altered diffusion atelectasis neutrophil infiltration hyaline membrane ( cellular debris dysfunction surfactant and exaudate pulmonary HTN
organizing phase of ARDS
Organize exaudate
pneumocyte type 2 prolif
lymphocyte infiltrate
fibrosis phase of ARDS
loss of lung architecture emphysema like
extensive fibrosis
intimal prlif in microcirculation leading to vascular occlusion and pulmonary HTN
honey comb apperance
which phase of ARDS has lymphocyte
organizing
which phase of ARDS has neutrophils
acute
clinical picture of ARDS first 72 hours
severe dyspnea nd hypoxemia and cyanosis
clinical picture of ARDS after 72 hours
bilateral severe pneumonia and bilateral pulmonary infiltrate , multisystem failure , DIC
