Hemodynamic Disorders Flashcards
(46 cards)
Accumulation of fluid in tissues or body cavities
EDEMA - tissues
EFFUSIONS - body cavities
Increased blood volume w/n tissues
hyperemia
congestion
Pathologic counterpart of hemostasis
Thrombosis
A detached intravascular solid, liquid or gaseous mass that is carried by the blood from its point of origin to a distant site where it often causes tissue dysfunction or infarction
Embolus
Area of ischemic necrosis caused by occlusion of either arterial supply or venous drainage
Infarct
State in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion — cellular hypoxia
Shock
4 main mechanisms of edema formation
- INCREASED hydrostatic pressure
- DECREASED oncotic pressure
- INCREASED vascular permeability
- Lymphatic OBSTRUCTION
General morphologic appearance of edema
- Clearing and separation of ECM
- Subtle cell swelling
58/M w/ hx of MI presented w/ paroxysmal noctunal dyspnea (PND)
CXR - bilateral pleural effusion
diagnosis, mechanism of edema, kind of effusion
Congestive Heart Failure
Increased Hydrostatic Pressure
Transudate
32/M, hx of remittent fever and productive cough, developed dyspnea
CXR -R pleural effusion w/ L parenchymal infiltrates
diagnosis, mechanism of edema, kind of effusion
Parapneumonic effusion; CAP MR
Increased vascular permeability
Exudate
57/M chronic alcoholic, increase in abdominal girth. Chem showed low serum albumin and elevated ALT and AST. Abdominal UTZ showed moderate ascites
diagnosis, mechanism of edema, kind of effusion
Decreased oncotic pressure
34/F, known case of breast cancer stage 2 (T2N0M0), s/p MRM, developed left arm swelling
mechanism of edema
Lymphatic obstruction
Transudate
abnormalities in Starling forces
normal vascular permeability
absent plasma protein leak
low protein content of fluid
<1.012
absent fibrin
absent inflammatory cells
Exudative
increased vascular permeability
presence of plasma protein leak
high protein content in fluid
>1.012
present fibrin
present inflammatory cells
It is an ACTIVE process d.t. augmented blood flow from ARTERIOLAR DILATION of increased O2 demand; affected tissue is REDDER than normal because of engorgement w/ OXYGENATED blood
Hyperemia
It is a PASSIVE process d.t. IMPAIRED VENOUS RETURN out of a tissue, has BLUE-RED color d.t. accumulation of DEOXYGENATED blood in the affected tissue
Congestion
24/F w/ large left atrial myxoma that obstructed flow of blood into the left atrium. Autopsy of the lung showed engorged alveolar capillaries, alveolar septal edema and focal intraalveolar hemorrhage.
Diagnosis
Acute pulmonary congestion
34/F died from acute R sided HF sec to saddle embolus. Autopsy of the liver showed distended central vein and sinusoids, centrilobular ischemic necrosis and periportal fatty change
Diagnosis
Acute Hepatic Congestion
55/M died of complications from congestive heart failue. Autopsy of the lung showed thickened and fibrotic alveolar septa and hemosiderin laden macrophases.
Diagnosis
Chronic Passive Congestion, Lung
60/M died of complications from HF. On autopsy, liver is heavier than normal and has nutmeg like appearance. Sections show centrilobular hemorrhage, hemosiderin laden macrophages and hepatocyte loss of variable degrees.
Diagnosis
Chronic Passive Congestion, liver
Components of Virchow Triad
Endothelial Injury
Stasis
Hypercoagulability
Major contributor to the development of ARTERIAL thrombi
Turbulence or Endothelial injury
Major contributor to the development of VENOUS thrombi
Stasis
Any alteration of the COAGULATION pathway that predisposes to thrombosis
Can be primary (Factor V Leiden, Protein C and S deficiency), or secondary (cancer, atrial fibrillation and prolonged immobilization)
Hypercoagulability
