lec 1 Atectectasis

Question 1

Pathogenisis: Atelectasis

(lung collapse)

Answer 1

inadequate expansion of airspace in lung
leading to hypoxia (collapse)
reversible if cause is removed EXCEPT in CONTRACTION

Question 2

Resorptive(obstructive atelactasis)

mediastinal shift, cause, notes

Answer 2

-Same side
-foreign body, IB tumor and plug, post-surgery
-air is resorbed from distal alveoli (collapse distally)

mucus plug seen in asthma and chronic bronchitis

Question 3

Compression atelectasis

mediastinal shift, cause , notes

Answer 3

-Opposite side
-Significant fluids,pneumothorax, elevated diaphragm
-Air of fluid accumilates within pleural cavity

pleural effusion occurs here

Question 4

Contraction atelectasis:

med shift, cause

Answer 4

-no shift
-Fibrosis: post inflammatory scarring

Question 5

Morphology and outcomes of atelectasis:

gross and microscopic

Answer 5

-Gross: shrunken, purple, nodular lung
-microscopic: slit like alveoli, congested septae, fluid in spaces
-hyaline membranes in microatelectasis

outcomes: depend on cause, size of area, time until treatment

significant atelectasis reduces oxygenation causes infection, except in fibrosis cases

Question 5

Micro atelectasis:

Answer 5

-no shift
- surfactant loss (generalized) acute or neonatal respiratory distress syndrome

Question 5

Clinical manifestastions of ARDS:

5 causes

Answer 5

-develops within 72hrs
-sudden and acute onset of severe dyspnea
-hypoxemia(rapid) , hypercapnia, cyanosis
-diffuse bilateral pulmonary infiltrates
-secondary infection and DIC

all should happen in abscence af LHF

hypercapnia: inc in CO2 partial pressure

Question 6

ARDS caused by:

Answer 6

-rapid onset and life threatening condition
-epithelial or endothelial alveolar damage
-cascade of reactions

Question 7

Etiology: Direct injury common causes

Answer 7

-Pneumonia 35-45%
-aspiration of gastric contents

Question 8

also among pathogenisis

Diffuse alveolar damage(DAD):

Answer 8

Increased permeability in vascular endothelium—severe edema
Decreased Surfactant in alveolar epithelium— microatelectasis

Later on, fibroblasts recruited— fibrogenisis

Question 8

Etiology: Indirect injury common causes:

S and S

Answer 8

Sepsis 30%-35%
Severe trauma with shock

Question 9

Pathogenisis Of ARDS:

Answer 9

-imbalance in anti and proinflammatory mediators:
nuclear factor NF-kB proinflam
-activated macrophages: IL-8, IL-1, TNF
-polymorphonuclear neutrophils(PMN) releasing oxidants, PAF etc… cause tissue damage.

Question 10

Pathogenisis signs can be counteracted by:

Answer 10

Antiprotreases
Antioxidants
Anti-inflammatory cytokines (IL-10)

Question 11

Acute Phase of ARDS:

Answer 11

-neutrophil inflitration
-plasma protein in spaces, dysfunctional surfactant= hyaline membranes
-Vascular injury— microthrombi and fibrocellular proliferation— **pulmonary HTN

protien rich fluid accumulates in dependant areas and interstitium

Question 12

Organizing phase:

histology included too:

Answer 12

patients may recover rapidly, but dyspnea and hypoxemia may be present

Histology:
-Lymphocyte predominant inflitrate
-proliferation of type II pneumocytes

Question 13

Fibrosis phase:

histology included:

Answer 13

-Some recover in 6-12 months
-Some enter fibrotic phase: long term mechanical ventilation or O2 supply

Histology:
-extensive fibrosis— emphysema-like
-proliferation in microcirculation— Vascular occlusion+ P.HTN
-HONEYCOMB LUNG

Question 14

Cytology:

Answer 14

Proper cough.
-Adequate sample shows macrophages.
-High macrophages or PMN indicate pathology
-hemosiderin macrophages sometimes seen

Question 15

Hyaline membrane composed of:

Answer 15

transduate and amniotic fluid (dead cells)