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.
- 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
- 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.
- HYPEREMIA & CONGESTION
- 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.
-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:
- 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.
- Primary Hemostasis ( clot forming)
- 1)Platelet adhesion
3)Granule release (ADP, TXA2)
5)Aggregation (hemostatic plug)
- SECONDARY HEMOSTASIS
- 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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