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19 Cards in this Set

  • Front
  • Back
What is hemodynamic edema?
Pulm cap hydrostatic pressure increases secondary to elevated EDP in LV, fluid is directed into interstitium.
Acute vs Chronic Pulmonary Edema:
Pathologic Features
Acute: noninflammatory, no fibrosis; distended alveolar capillaries, ephilic

Chronic: thick alveolar walls with fibrosis, HEMOSIDERIN-laden macs in alveoli (brown)--bc macs have engulfed RBCs
How do the pathologic features of edema due to microvascular injury differ from hemodynamic edema?
Leakage from capillaries includes proteins and inflammatory cells

Exudation vs transudation

Fibrosis!
Acute Lung Injury:
AKA
Cause
Presentation
Noncardiogenic Pulmonary Edema

Caused by alveolar epithelial and endothelial damage; inc'd vasc perm and inflammn

Rapid onset of severe respiratory insufficiency with cyanosis
ARDS vs Acute Lung Injury:
General
Specific causes of ARDS
ARDS is a more severe form of ALI

Can result from direct/indirect lung injury (multi-system organ failure)

Direct causes: pneumonia, aspiration (gastric contents), contusion, fat embolus

Indirect:
Sepsis, trauma with shock, cardiac bypass, transfusion of blood products
What is diffuse alveolar damage?
Effects?
DAD:
Compromised integrity of alveolar endothelium and epithelium

Effects:
Inc'd vasc perm, exudate in interstitium and alveoli

Loss of surfactant due to damage of Type II pneumocytes

microthrombi

Loss of diffusion capacity
Pathologic features of diffuse alveolar damage.
Gross: heavy, dark, red, no air

Micro: congestion, necrosis, edema, hemorrhage, nphils
Hyaline membranes
When are hyaline membranes present in alveoli?
When there's lack of surfactant; occurs in DAD and premature birth
When would a newborn carried to term display hyaline membranes in the alveoli?
Newborns carried at or near term can develop Diffuse Alveolar Damage (ARDS) on the basis of sepsis, meconium aspiration, or prolonged shock
Transfusion Related Acute Lung Injury:
What is it?
Cause
Acute resp failure within 6 hours of transfusion (must rule out circulatory overload before diagnosis!)
Due to preformed Abs in donor plasma against pt's WBCs in plasma-rich products

Most common in plasma in multiparous women!
Pulmonary Embolism:
Source of thrombus
Likelihood of infarct
Symptoms (large vs small emboli)
Mostly from fragmented DVT in leg, occluding according to size

Rarely benign or malignant tumor emboli

Bc of bronchial circuln, chance of infarct is 10%; when do occur, they are hemorrhagic

Large embolus-->acute cor pulmonale and sudden death

Repeated small emboli-->pulm HTN and chronic cor pulmonale
Pulmonary Embolism:
Nonthrombotic sources
Bone marrow, fat (can go to peripheral organs, especially brain!), amniotic fluid, air, foreign bodies
Fat Embolism:
Source of fat
Effects
Fat from BM with long bone fractures

Some fat globules go through lung to peripheral organs (like brain)

Chemical (acts as irritant) and obstructive effects, results in thrombocytopenia, hemolytic anemia
Air Embolism:
Sources
Air entering circulation during delivery, CV catheterization, surgery, injection in arteries, veins, body cavities

Air will airlock in RV and won't enter circulation
Pulmonary Hypertension:
General Causes (2)
Specific Causes
Dec'd cross-SA of pulm vasc OR inc'd flow

Specific:
Congenital/acd'q heart dz (Eisenmenger syndrome, Mitral Stenosis)

Thromboembolism

Pulm obstructive and interstitial dz; hyphoscoliosis

Drugs: appetite suppressant meds; aminorex, fenfluramine, phentermine
Cocaine
Collagen vasc dz (scleroderma)
Viruses (HIV, HHV-8)
What is primary pulmonary HTN?
Pulmonary HTN when no secondary cause can be established, i.e., idiopathic.
Mutations in bone morphogenetic protein receptor 2 (BMPR2) signaling pathway can result in _______.
Primary Pulm HTN
Microscopic changes of pulmonary hypertension.
Intimal and medial thickening

Plexogenic (plexiform) lesions--side branching off arteriole
What is a dilatation lesion?
More advanced form of plexiform lesion (side branches off the side branches)--severe pulm HTN