Glossary of Pathology-Hemodynamic Changes

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An abnormal accumulation of fluid in the intercellular spaces or body cavities.
Anasarca (dropsy)
generalized edema especially evident in subcutaneous tissues (pitting edema).
collection of edema in the peritoneal cavity.
edema in the pleural cavity
Pericardial infusion
or hydropericardium - edema of the pericardium
Causes of Edema
Lowered plasma colloid oncotic pressure.
Elevated hydrostatic pressure.
Increased permeability of the endothelium.
Lymphatic blockage.
Generalized Edema found primarily in:
Congestive heart failure (CHF) - edema most severe in lower extremities.

Renal disease - nephrotic syndrome with proteinuria, hypoproteinemia, edema - edema generalized throughout body, greater than CHF edema, and identified by edema of the face especially of eyelids.

Cirrhosis of the liver - results particularly in ascites.

Other causes: starvation, malabsorption syndromes, toxemia, hypothyroidism, estrogen (sodium retention).
Localized edema found primarily in:
-Impaired venous drainage
-Localized increase in vascular permeability
-Lymphatic obstruction
Gross Pathological changes of edema
Pitting edema

Organs are enlarged, pale, heavier than normal.

Tense capsules which upon sectioning have a glistening appearance

In brain, edema results in flattened, swollen gyri with compressed ventricles.

In lung, edema generally found in lower lobes - sectioning results in the escape of a frothy, sanguineous fluid.
Microscopic Pathological changes of edema
Granular acidophilic interstitial precipitate.

Separation of cellular and fribillar elements

In brain, swelling of intercellular and perivascular spaces.

In lung, widening of septal walls and presence of a granular pink precipitate within the alveoli.
Increased volume of blood in an affected tissue or part.
Active hyperemia
Results from an increased flow of blood into capillary beds because of arteriolar dilation. This occurs by:

-Increase in functional activity of a tissue.
-Neurogenic mechanisms
-Hormones and other vasodilators
Escape of blood from the cardiovascular system
Types of hemorrhage
Hematoma - localized collection of blood.

Petechiae - minute capillary hemorrhages.

Purpura - up to 1 cm.

Ecchymoses - large, blotchy hemorrhages.
Passive hyperemia (congestion)
Results from decreased venous drainage. This occurs in:

-Heart failure
-Venous obstruction
Gross Patholoogical Changes in hyperemia
Most obvious in lungs, liver, and spleen.

-Organs excessively bloody.
In liver, results in “nutmeg liver”; in spleen, splenomegaly.
Microscopic Patholoogical Changes in hyperemia
-Lungs have enlarged and engorged capillaries with “heat failure” cells.
-Liver has central hemorrhagic necrosis.
-Spleen has enlarged and engorged sinusoids with hemosiderin deposits.
blood in urine
blood in stools
vomiting of blood
expectoration of blood
nose bleed
Formation of a solid mass from constituents of the blood within the vascular system.
Factors involved in thrombogenesis: Endothelial injury
Decreases sulfated mucopolysaccharides, plasminogen activator, PGI2, and other substances to degrade platelet-aggregating agents.
Promotes platelet adhesion and activates clotting factors by exposing circulation to subendothelial collagen.
Factors involved in thrombogenesis: Alteration in normal blood flow
-occurs with stasis or turbulence.
-Bring platelets in contact with endothelium.
-Prevent liver from clearing activated coagulation factors.
-Damage endothelial cells.
-Loss of normal velocity prevents thrombi from being washed away.
Factors involved in thrombogenesis: Hypercoagulability
in prolonged rest, CA, serious illness, estrogens
-Endothelial injury.
-Platelet adherence and activation of plasma clotting system.
-Granule release and prostaglandin release by platelets.
-Platelet aggregation and vasoconstriction from primary hemostatic plug.
-Formation of secondary hemostatic plug (viscous metamorphosis) from thrombin, fibrin, and rbc’s.
-Plasminogen activator and antithrombin reduce rapid clotting.
-Clot retraction and fibrinolysis reduce size of clot.
-Endothelial regeneration.
Primary Hemostasis ( clot forming)
1)Platelet adhesion
2)Shape change
3)Granule release (ADP, TXA2)
5)Aggregation (hemostatic plug)
1) Tissue Factor
2) Phospholipid complex expression
3) Thrombin activation
4) Fibrin polymerization
Vichow’s triad in thrombosis:
Endothelial injury, hypercoagulability, and abnormal blood flow, all lead to thrombosis
Appearance of arterial thrombi
“white or conglutination thrombi” - composed primarily of platelets and fibrin with mixed layer of rbc’s (lines of Zahn) -
Appearance of venus (phlebothromboses) thrombi
“stasis or red coagulation thrombi” - origin attached to endothelium and appears gelatinous yet friable - contains fibrin - swells vein - related to cancer as Trousseau’s sign (migratory thrombophlebitis).
Appearance of post-mortem thrombi
Postmortem clots - rubbery, gelatinous coagulum, moist homogenous - not attached to underlying wall - forms perfect cast of vessel and its branches.
“currant jelly” - cyanotic dark red.
“chicken fat” - coagulated clear plasma over darker red cell settled area.
Types of Thrombus--Mural
do not occlude lumen
Types of Thrombus--Occlusive
- fill lumen

Arterial - in frequency, coronary, cerebral, iliac, femoral

Venous - in frequency, deep calf, femoral, popliteal, iliac
Types of Thrombus--Vegetations
thrombi on valves of heart
Septic - contain bacterial infection
Bland - non-bacterial
Types of Thrombus--Disseminated intravascular coagulations (DICs)
microcirculatory thromboses
Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.
Pulmonary Embolism
-Most common and most lethal.

-95% arise from veins of the leg.

-Large emboli cause sudden death by occluding the pulmonary artery or by blocking its bifurcation (saddle embolus).

-Smaller emboli may cause infarction, cardiac, or circulating insufficiency with inadequate bronchial circulation.
Systemic Embolism
-Emboli in arterial circulation.

-Arises from left side of the heart or thrombi in the aorta or major arteries.

-Most often affects the brain, lower extremities, spleen, and kidneys.

-Causes infarction of the affected organ.
Air or Gas Embolism (Caisson Disease)
Formed by air or gasses.

Decompression sickness (Caisson Disease) occurs from nitrogen coming out of solution and forming bubble or gas emboli.

“Bends” - patient doubles up with pain because of gas emboli in joints and skeletal muscles.

“Chokes” - respiratory distress from emboli in the lungs.
Fat Emboli
Trauma to fat-laden tissue, e.g. bone fracture ( bone marrow embolus )

Non-traumatic by emulsion instability of chylomicrons of fat.
Amniotic Embolism (amniotic fluid infusion).
Originally believed to be caused by debris in amniotic fluid.

Now known to be a cause of disseminated intravascular coagulation (DIC) because of thromboplastin-like substances in amniotic fluid.
Localized area of ischemic necrosis in an organ or tissue resulting from occlusion of either its arterial supply or venous drainage.
Types of Infarcts: Anemic (white)
occur with arterial occlusions and in solid tissues - occurs in heart, spleen, and kidneys.
Types of Infarcts: Hemorrhagic (red)
occur with venous occlusions and in loose tissues with double circulation or previously congested - occurs in lung, intestine, brain, liver.
Types of Infarcts : Septic
presence of bacterial inflammation in area of necrosis.
Types of Infarcts : Bland
absence of bacterial inflammation
Morphology of Infarcts: Gross
Are wedge-shaped, apex toward focus of occlusion, external part of the organ forms the base.
Factors Affecting Infarction Damage
General status of the blood and cardiovascular system.

Anatomic patterns of arterial supply.

Rate of development of occlusion - collateral circulation.

Vulnerability of tissue to ischemia.
A constellation of syndromes, all characterized by low profusion circulatory insufficiency leading to imbalance between the metabolic needs of vital organs and the available blood flow.
Hypovolemic Shock
Reduction in blood volume from external loss of blood plasma or water.
Reduction in blood volume from internal loss; e.g., massive exudation or internal hemorrhage.
Cardiogenic Shock
Intrinsic myocardial damage from infarction or diffuse myocardial disease.

Extrinsic embarrassment of cardiac function from pulmonary embolus or cardiac tamponade.
Septic Shock
Overwhelming gram-negative infections with endotoxemia (endotoxic shock).

Overwhelming gram-positive infections.
Morphology of Shock
Results in generalized cellular damage.

Organs most affected are brain, heart, lungs, kidneys, also adrenal, GI tract, and liver.
Neurogenic Shock
Clinical examples are anesthesia & spinal cord injury

principle mechanism is peripheral vasodialation with pooling of blood
In shock you get a cascade of cytokine mediators. Give some examples.
LPS – TNF – IL1 – IL6/IL8 – NO, PAF (platelet activating factor)
In low quantities these cytokine mediators lead to (what is the end result)
monocyte/macrophage activation– endothelial cell activation – complement activation – then LOCAL INFLAMMATION
In moderate quantities these cytokine mediators lead to (what is the end result)
Moderate quantities result in fever—acute-phase reactants (fibrinogen; C-reactive protein; complement proteins B, C3, C4; alpha 2-acid glycoprotein, serum amyloid A, proteinase inhibitors, etc) leading to SYSTEMIC EFFECTS
In high quantities these cytokine mediators lead to (what is the end result)
High quantities you get low cardiac output, low peripheral resistance, blood, vessel injury, thrombosis, disseminated intravascular coagulation, adult respiratory distress syndrome and SEPTIC SHOCK

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