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Hemodynamic Disorders Overview, Study notes of Pathology

This document contains histologic characteristics and brief overview of different hemodynamic disorders such as edema, hemorrhage, congestion, hyperemia, and hemostasis

Typology: Study notes

2023/2024

Available from 09/28/2024

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Pulmonary Edema
Frequently seen in left
ventricular failure
EDEMA
Definition
Accumulation of
INTERSTITIAL FLUID Within
the tissue
Increased movement
OUT of the vessel.
Increased vascular
hydrostatic pressure
Decrease plasma
protein
Effusion
Accumulation of
extravascular fluid within
adjacent body cavity
Anasarca
Severe generalized
edema
Profound swelling of
subcutaneous tissues
manifested as
accumulation of fluid in
body cavities
EXUDATES VS TRANSUDATES
EXUDATES
Protein-RICH
High SG
Increase vascular
permeability=
inflammatory
involvement
TRANSUDATES
Protein-POOR
Low SG
Non-inflammatory
involvement (Edema
and effusion)
CAUSES OF EDEMA
Increased hydrostatic
pressure
Impairment of venous
return
Deep vein thrombosis
(lower extremity)
CHF (generalized
increase in venous
pressure)— leads to
pulmonary or general
edema
o Left-sided HF
(incomplete
emptying of left
ventricle):
retrogrades t o the
pulmonary
interstitium.
o Right-sided HF
(incomplete filling
of righ t ventricle):
retrogrades to
systemic
circulation— lower
extremities, liver, GI
tract
Constrictive pericarditis
(fibrotic pericardial
sac/defect in diastolic
filling)
Ascites (Liver cirrhosis)
Venous insufficiency
(obstruction or
compression)— related
to varicose veins
FACTORS:
o Reduced cardiac
output
o Systemic venous
congestion
Reduced plasma
osmotic/oncotic pressure
Reduced plasma albumin
Pathologic diseases:
o Nephrotic
Syndrome/Protein-
Losing
Glomerulopathy
o Liver
disease/Cirrhosis
o Protein malnutrition
o Protein-losing
gastroenteropathy
FACTORS:
o Increased
glomerular
permeability
o Reduced protein
synthesis
RESULTS
o Reduced
intravascular
volume
o Renal
hypoperfusion
o Secondary
hyperaldosteronism
Lymphatic Obstruction
Compromises resorption of
fluid from interstitial space
Pathologic diseases
(inflammatory or neoplastic
condition):
o Lymphatic
filariasis—
elephantiasis
o Breast cancer
o Neoplasm,
Postsurgical, and
Post-irradiation
Sodium and Water Retention
Excessive retention of salt
(and water)
Wherever sodium goe s,
water follows
Pathologic diseases
o Poststreptococcal
glomerulonephritis
o Acute Renal Failure
(excessive salt
intake with renal
insufficiency)
FACTORS:
o Renal hypoperfusion
o Increased
activation of RAAS
Inflammation
Acute and chronic
inflammation
Angiogenesis
MORPHOLOGY OF EDEMA
Subcutaneous Edema
Influenced by gravity (legs)
Associated w ith cardiac or
renal disease
Dependent/Pitting Edema
Leaves a de pression/finger
pressure over markedly
edematous subcutaneous
tissue
Secondary to nephropathy
Peri-orbital Edema
Results from renal
dysfunction or nephrotic
syndrome
Manifest in loose CT
Graves’ disease/
Thyrotoxicosis
EDEMA
Definition
Accumulation of
INTERSTITIAL FLUID Within
the tissue
Increased movement
OUT of the vessel.
Increased vascular
hydrostatic pressure
Decrease plasma
protein
Effusion
Accumulation of
extravascular fluid within
adjacent body cavity
Anasarca
Severe generalized
edema
Profound swelling of
subcutaneous tissues
manifested as
accumulation of fluid in
body cavities
EXUDATES VS TRANSUDATES
EXUDATES
Protein-RICH
High SG
Increase vascular
permeability=
inflammatory
involvement
TRANSUDATES
Protein-POOR
Low SG
Non-inflammatory
involvement (Edema
and effusion)
CAUSES OF EDEMA
Increased hydrostatic
pressure
Impairment of venous
return
Deep vein thrombosis
(lower extremity)
CHF (generalized
increase in venous
pressure)— leads to
pulmonary or general
edema
o Left-sided HF
(incomplete
emptying of left
ventricle):
retrogrades t o the
pulmonary
interstitium.
o Right-sided HF
(incomplete filling
of righ t ventricle):
retrogrades to
systemic
circulation— lower
extremities, liver, GI
tract
Constrictive pericarditis
(fibrotic pericardial
sac/defect in diastolic
filling)
Ascites (Liver cirrhosis)
Venous insufficiency
(obstruction or
compression)— related
to varicose veins
FACTORS:
o Reduced cardiac
output
o Systemic venous
congestion
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Pulmonary Edema •^ Frequently seen in ventricular failure^ left

EDEMA

Definition

  • Accumulation of INTERSTITIAL FLUID Within the tissue
  • Increased movement OUT of the vessel.
  • Increased vascular hydrostatic pressure
  • Decrease plasma protein Effusion
  • Accumulation of extravascular fluid within adjacent body cavity Anasarca
  • Severe generalized edema
  • Profound swelling of subcutaneous tissues manifested as accumulation of fluid in body cavities EXUDATES VS TRANSUDATES EXUDATES
  • Protein-RICH
  • High SG
  • Increase vascular permeability= inflammatory involvement

TRANSUDATES

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

EDEMA

Definition

  • Accumulation of INTERSTITIAL FLUID Within the tissue
  • Increased movement OUT of the vessel.
  • Increased vascular hydrostatic pressure
  • Decrease plasma protein Effusion
  • Accumulation of extravascular fluid within adjacent body cavity Anasarca
  • Severe generalized edema
  • Profound swelling of subcutaneous tissues manifested as accumulation of fluid in body cavities EXUDATES VS TRANSUDATES EXUDATES
  • Protein-RICH
  • High SG
  • Increase vascular permeability= inflammatory involvement

TRANSUDATES

  • Protein-POOR
  • Low SG
  • Non-inflammatory involvement (Edema and effusion) CAUSES OF EDEMA Increased hydrostatic pressure
  • Impairment of venous return
  • Deep vein thrombosis (lower extremity)
  • CHF (generalized increase in venous pressure)— leads to pulmonary or general edema o Left-sided HF (incomplete emptying of left ventricle) : retrogrades to the pulmonary interstitium. o Right-sided HF (incomplete filling of right ventricle) : retrogrades to systemic circulation— lower extremities, liver, GI tract
  • Constrictive pericarditis (fibrotic pericardial sac/defect in diastolic filling)
  • Ascites (Liver cirrhosis)
  • Venous insufficiency (obstruction or compression)— related to varicose veins
  • FACTORS: o Reduced cardiac output o Systemic venous congestion
  • May also occur in renal failure, ARDS, inflammatory, and infectious disorders.
  • Sectioning: frothy, blood-tinged fluid (autopsy) Brain Edema
  • Narrowed sulci, distended gyri, flattened against the skull
  • Compresses vascular supplies and medullary centers
  • Severe swelling can cause the brain to herniate through the foramen magnum Dermal Edema
  • Separation of collagen fibers (increased spaces of collagen type I fibers) GROSS
  • Heavier and have a reddish hue HISTOLOGY
  • Cell swelling and widening of ECM
  • Distended alveoli with edematous fluid
  • Presence of hyaline membrane
  • Some cases may present focal areas of hemorrhage/ septal hemorrhage in interstitium HYPEREMIA AND CONGESTION
  • Increased blood volume within tissues.
  • REVERSIBLE HYPEREMIA CONGESTION
  • ACTIVE
  • Arteriolar dilation
  • Affected tissue is erythematous
  • Increased blood flow— delivery of O2 blood

• PASSIVE

  • Reduced venous blood flow
  • Affected tissue is cyanotic— RBC stasis
  • Decreased blood flow (O2 blood) MORPHOLOGY OF CONGESTION ACUTE PULMONARY CHRONIC PULMONARY
  • Edema
  • Alveolar septal thickening (fluid distended alveoli) + edema
  • Blood-engorged alveolar capillaries
  • Evident hemorrhage (focal intra-alveolar hemorrhage)
  • Fibrosis
  • Alveolar septal thickening + fibrosis
  • Numerous hemosiderin laden macrophages/heart failure cells within alveolar spaces
  • Hemorrhagic foci (extra-alveolar) ACUTE HEPATIC CHRONIC HEPATIC
  • Distended central vein and sinusoids filled with RBCs
  • Centrilobular necrosis
  • Periportal hepatocytes (better oxygenation) : reversible fatty change
  • Nutmeg liver (uncongested)
  • Gross: centrilobular area is red-brown and slightly depressed
  • Microscopic: hemosiderin-laden macrophages, centrilobular hemorrhage, hepatocyte dropout and necrosis HEMORRHAGE Definition Ex vessel travasation of blood^ from the Reasons for Hemorrhage
  • Damage and defective clot formation
  • Trauma
  • Atherosclerosis
  • Inflammatory and neoplastic erosion of a vessel wall
  • Inherited or acquired defects in vessel wall, platelets, or coagulation factors Manifestations
  • Hematoma: external or accumulation within tissue
  • Hemothorax
  • Hemopericardium
  • Hemoperitoneum
  • Hemarthrosis
  • Jaundice: extensive hemorrhages Principles of Hemorrhagic Disorders
  • Defects in Primary Hemostasis: platelets and vWD— petechiae, purpura, epistaxis, GI bleeding, menorrhagia, intracerebral hemorrhage
  • Defects in Secondary Hemostasis: Coagulation factor— hemarthrosis, intracranial hemorrhage
  • Defects involving microvasculature: systemic disorders that disrupt small blood vessels and make them more fragile— palpable purpura, ecchymoses Patterns of Tissue Hemorrhage Petechiae
  • 1 - 2mm
  • Skin, mucous membranes
  • Thrombocytopenia, Vit. C deficiency Purpura
  • 3 - 5mm
  • Trauma, vasculitis— increased vascular fragility Ecchymoses
  • Subcutaneous hemorrhage (bruises)
  • Hemoglobin— Bilirubin— Hemosiderin Hematoma
  • Palpable mass of blood that is clotted Clinical Significance
  • Depends on the: o Volume of bleed o Rate at which it occurs o Location
  • Hemorrhagic/hypovolemic shock: >20% blood loss