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Summary Hemodynamic Disorders

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The document summarizes the histologic descriptions for the hemodynamic disorders as well as some thromboembolic disease

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  • Chapter 4
  • October 6, 2024
  • 3
  • 2024/2025
  • Summary
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• Reduced plasma albumin
EDEMA • Pathologic diseases:
o Nephrotic
• Accumulation of
Syndrome/Protein-
INTERSTITIAL FLUID Within
Losing
the tissue
Glomerulopathy
• Increased movement
o Liver
Definition OUT of the vessel.
disease/Cirrhosis
• Increased vascular
o Protein malnutrition
hydrostatic pressure
o Protein-losing
• Decrease plasma
gastroenteropathy
protein
Reduced plasma • FACTORS:
• Accumulation of o Increased
Effusion extravascular fluid within osmotic/oncotic pressure
glomerular
adjacent body cavity permeability
• Severe generalized o Reduced protein
edema synthesis
• Profound swelling of • RESULTS
Anasarca subcutaneous tissues o Reduced
manifested as intravascular
accumulation of fluid in volume
body cavities o Renal
hypoperfusion
EXUDATES VS TRANSUDATES
o Secondary
EXUDATES TRANSUDATES hyperaldosteronism
• Protein-RICH • Protein-POOR • Compromises resorption of
• High SG • Low SG fluid from interstitial space
• Increase vascular • Non-inflammatory • Pathologic diseases
permeability= involvement (Edema (inflammatory or neoplastic
inflammatory and effusion) condition):
involvement o Lymphatic
Lymphatic Obstruction
filariasis—
CAUSES OF EDEMA elephantiasis
o Breast cancer
• Impairment of venous o Neoplasm,
return Postsurgical, and
• Deep vein thrombosis Post-irradiation
(lower extremity) • Excessive retention of salt
• CHF (generalized (and water)
increase in venous • Wherever sodium goes,
pressure)— leads to water follows
pulmonary or general • Pathologic diseases
edema o Poststreptococcal
o Left-sided HF glomerulonephritis
(incomplete Sodium and Water Retention o Acute Renal Failure
emptying of left (excessive salt
ventricle): intake with renal
retrogrades to the insufficiency)
pulmonary • FACTORS:
interstitium. o Renal hypoperfusion
o Right-sided HF o Increased
(incomplete filling activation of RAAS
Increased hydrostatic of right ventricle): • Acute and chronic
pressure retrogrades to Inflammation inflammation
systemic • Angiogenesis
circulation— lower
extremities, liver, GI MORPHOLOGY OF EDEMA
tract • Influenced by gravity (legs)
• Constrictive pericarditis Subcutaneous Edema • Associated with cardiac or
(fibrotic pericardial renal disease
sac/defect in diastolic • Leaves a depression/finger
filling) pressure over markedly
• Ascites (Liver cirrhosis) Dependent/Pitting Edema edematous subcutaneous
• Venous insufficiency tissue
(obstruction or • Secondary to nephropathy
compression)— related • Results from renal
to varicose veins dysfunction or nephrotic
• FACTORS: syndrome
o Reduced cardiac Peri-orbital Edema • Manifest in loose CT
output • Graves’ disease/
o Systemic venous Thyrotoxicosis
congestion
• Frequently seen in left
Pulmonary Edema
ventricular failure

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