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Hemodynamic Disorders
Dr.Abhinav Golla
MBBS .MD Pathology
Assistant Proffessor.
Lab Director
Aadhya Medicure Pathlabs .
EDEMA
• Disorders that upset
• Cardiovasular
• Renal
• Hepatic .
• Are often Marked by accumulation of fluid in Tissues ( EDEMA)
• In body cavities are called as (EFFUSSIONS)
EDEMA & EFFUSIONS
• May be:
•INFLAMMATORY
•NON INFLAMMATORY
INFLAMMATORY EDEMA
• Caused by Inflammatory Mediators.
• These fluids are PROTEIN RICH (EXUDATES).
• Accumulates due to INCREASE IN VASULAR
PERMEABILITY.
• Usually Inflammatory Associated edema is localized to one or few
tissues.
NON INFLAMMATORY EDEMA
• Common in many diseases
• Seen in severe Nutritional disorders
• PROTEIN POOR FLUIDS (TRANSUDATES)
CAUSES
• Increased HYDROSTATIC PRESSURE. Caused by disorders that IMPAIR
VENOUS RETURN.
Ex. Congestive Cardiac Failure
• Reduced PLASMA ONCOTIC PESSURE. Because
• ALBUMIN accounts half of the total PLASMA PROTEIN.( Increased
loss or Inadequate synthesis of albumin from circulation )
Ex. Nephrotic Syndrome.
Causes
• SODIUM & WATER RETENTION.
• Increased Hydrostatic pressure ( Intravascular fluid volume expansion)
• Diminished vascular colloid osmotic pressure( Due to dilution)
• LYMPHATIC OBSTRUCTION
• Trauma , Infection , Parasitic , Invasive Tumours ( IMPAIR THE
CLEARENCE OF LYMPHATIC FLUID ) resulting LYMPHEDEMA.
MORPHOLOGY
• GROSSLY
• Subcutaneous Edema (Dependent edema) : In region
with high hydrostatic Pressure.(leg & Sacrum). Causes
PITTING EDEMA.
• Periorbital edema :
• Pulmonary edema : (Frothy & Blood tinged).
• Brain Edema
EFFUSIONS
•HYDROTHORAX
•HYDROPERITONIUM
•HYDROPERICARDIUM
HYPEREMIA & CONGESTION.
•INCREASED BLOOD
VOLUME WITHIN
THE TISSUES , BUT
HAVING DIFFERENT
UNDERLYING
MECHAMISM &
CONSEQUENCES.
HYPEREMIA
•Active process.
•( site of
inflammation or in
skeletal muscle
during exercise.)
increase blood flow.
CONGESTION
•PASSIVE PROCESS. Results
from REDUCED OUTFLOW OF
BLOOD FROM TISSUES.
•COMMOMLY LEADS TO EDEMA.
• IN CHRONIC CASES capillary
rupture can also produce
small hemorrhagic foci ,
subsequent catabolism of
extravasated red
cells forms (HEMOSIDERIN
LADEN MACROPHAGES)
MORPHOLOGY
•GROSSLY
• Congested tissue take on a dusky reddish blue colour (Cyanosis) due
to red cell stasis and presence of deoxygenated hemoglobin .
•MICROSCOPICALLY
• ACUTE PULMONARY CONGESTION .
• Exhibits engorged alveolar capillaries
• Alveolar septal edema.
• Focal intraalveolar hemorrhage .
• In CHRONIC PULMONARY
CONGESTION .
•Caused by congestive heart failure
•Septa are thickned & fibrotic.
•Alveoli contains numerous
hemosiderin -
laden macrophages.( Heart Failure
Cells).
HEPATIC CONGESTION
•ACUTE HEPATIC CONGESTION.
• CENTRAL VEIN & SINUSOIDS ARE DISTENDED.
• Distal end of the hepatic blood supply (centrilobular area)
hepatocytes in this area undergo ischemic necrosis.
• Periportal hepatocytes may develop fatty change due
to oxygenation from hepatic arterioles.
CHRONIC HEPATIC CONGESTION
• GROSS
• Centrilobular are red brown and slightly depressed. Because of cell
death . More prominent against the surrounding zones of
uncongested tan liver .
•NUTMEG LIVER
NUTMEG LIVER
• Microscopically
• Centrilobular hemorrhage .
• Hemosiderin laden macrophages
• Variable degree of hepatocytes
dropout & necrosis.
EDEMA HYPEREMIA CONGESTION.pptx
EDEMA HYPEREMIA CONGESTION.pptx
EDEMA HYPEREMIA CONGESTION.pptx

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EDEMA HYPEREMIA CONGESTION.pptx

  • 1. Hemodynamic Disorders Dr.Abhinav Golla MBBS .MD Pathology Assistant Proffessor. Lab Director Aadhya Medicure Pathlabs .
  • 2. EDEMA • Disorders that upset • Cardiovasular • Renal • Hepatic . • Are often Marked by accumulation of fluid in Tissues ( EDEMA) • In body cavities are called as (EFFUSSIONS)
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  • 5. EDEMA & EFFUSIONS • May be: •INFLAMMATORY •NON INFLAMMATORY
  • 6. INFLAMMATORY EDEMA • Caused by Inflammatory Mediators. • These fluids are PROTEIN RICH (EXUDATES). • Accumulates due to INCREASE IN VASULAR PERMEABILITY. • Usually Inflammatory Associated edema is localized to one or few tissues.
  • 7. NON INFLAMMATORY EDEMA • Common in many diseases • Seen in severe Nutritional disorders • PROTEIN POOR FLUIDS (TRANSUDATES)
  • 8. CAUSES • Increased HYDROSTATIC PRESSURE. Caused by disorders that IMPAIR VENOUS RETURN. Ex. Congestive Cardiac Failure • Reduced PLASMA ONCOTIC PESSURE. Because • ALBUMIN accounts half of the total PLASMA PROTEIN.( Increased loss or Inadequate synthesis of albumin from circulation ) Ex. Nephrotic Syndrome.
  • 9. Causes • SODIUM & WATER RETENTION. • Increased Hydrostatic pressure ( Intravascular fluid volume expansion) • Diminished vascular colloid osmotic pressure( Due to dilution) • LYMPHATIC OBSTRUCTION • Trauma , Infection , Parasitic , Invasive Tumours ( IMPAIR THE CLEARENCE OF LYMPHATIC FLUID ) resulting LYMPHEDEMA.
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  • 11. MORPHOLOGY • GROSSLY • Subcutaneous Edema (Dependent edema) : In region with high hydrostatic Pressure.(leg & Sacrum). Causes PITTING EDEMA. • Periorbital edema : • Pulmonary edema : (Frothy & Blood tinged). • Brain Edema
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  • 14. HYPEREMIA & CONGESTION. •INCREASED BLOOD VOLUME WITHIN THE TISSUES , BUT HAVING DIFFERENT UNDERLYING MECHAMISM & CONSEQUENCES.
  • 15. HYPEREMIA •Active process. •( site of inflammation or in skeletal muscle during exercise.) increase blood flow.
  • 16. CONGESTION •PASSIVE PROCESS. Results from REDUCED OUTFLOW OF BLOOD FROM TISSUES. •COMMOMLY LEADS TO EDEMA.
  • 17. • IN CHRONIC CASES capillary rupture can also produce small hemorrhagic foci , subsequent catabolism of extravasated red cells forms (HEMOSIDERIN LADEN MACROPHAGES)
  • 18. MORPHOLOGY •GROSSLY • Congested tissue take on a dusky reddish blue colour (Cyanosis) due to red cell stasis and presence of deoxygenated hemoglobin . •MICROSCOPICALLY • ACUTE PULMONARY CONGESTION . • Exhibits engorged alveolar capillaries • Alveolar septal edema. • Focal intraalveolar hemorrhage .
  • 19. • In CHRONIC PULMONARY CONGESTION . •Caused by congestive heart failure •Septa are thickned & fibrotic. •Alveoli contains numerous hemosiderin - laden macrophages.( Heart Failure Cells).
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  • 21. HEPATIC CONGESTION •ACUTE HEPATIC CONGESTION. • CENTRAL VEIN & SINUSOIDS ARE DISTENDED. • Distal end of the hepatic blood supply (centrilobular area) hepatocytes in this area undergo ischemic necrosis. • Periportal hepatocytes may develop fatty change due to oxygenation from hepatic arterioles.
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  • 23. CHRONIC HEPATIC CONGESTION • GROSS • Centrilobular are red brown and slightly depressed. Because of cell death . More prominent against the surrounding zones of uncongested tan liver . •NUTMEG LIVER
  • 24. NUTMEG LIVER • Microscopically • Centrilobular hemorrhage . • Hemosiderin laden macrophages • Variable degree of hepatocytes dropout & necrosis.