Secondary Hemostasis Quiz

Hemodynamic Disorders

• Hemodynamic disorders involve thrombosis and shock.
• 60% of body weight is water.
• 2/3 of the water is intracellular.
• 1/3 is extracellular, mostly as interstitial fluid.
• 5% of extracellular fluid is in the vascular compartment.
• Edema is increased fluid in the interstitial tissue spaces.
• Fluid collections in body cavities are named according to location (e.g., hydrothorax, hydropericardium, hydroperitoneum).
• Anasarca is severe, generalized edema with profound subcutaneous tissue swelling.
• The balance between vascular hydrostatic pressure and plasma colloid osmotic pressure drives fluid movement between vascular and interstitial spaces.
• Normally, fluid outflow from arteriolar ends is balanced by inflow at venular ends.
• A small amount of fluid remains in the interstitium due to slightly higher hydrostatic pressure.
• This excess fluid is drained by the lymphatic system.
• Normal hydrostatic pressure is 32 mm Hg at the arteriolar end of a capillary bed and 12 mm Hg at the venous end.
• The mean colloid osmotic pressure of tissue is approximately 25 mmHg.
• In inflammation, arteriolar pressure increases to 50 mmHg due to dilation, and venous pressure increases to approximately 30 mmHg.
• Osmotic pressure averages 20 mmHg due to protein leakage across the venules.
• The net result is excess extravasated fluid.

Sodium Retention

• Excessive sodium intake with renal insufficiency increases sodium reabsorption.
• Renal hypoperfusion and increased renin-angiotensin-aldosterone secretion cause increased tubular sodium absorption.

Inflammation

• Acute inflammation and chronic inflammation can cause edema.
• Angiogenesis can also cause edema.

Reduced Plasma Osmotic Pressure

• Protein-losing glomerulopathies (nephrotic syndrome), liver cirrhosis, malnutrition, and protein-losing gastroenteropathy can reduce plasma osmotic pressure.
• This reduction results in edema.
• Lymphatic obstruction can cause edema, which occurs due to inflammatory, neoplastic, postsurgical, or postirradiation etiologies.

Hyperemia and Congestion

• Hyperemia is an active process of increased blood flow caused by arteriolar dilation.
• Tissues appear redder due to increased oxygenated blood flow.
• Congestion is a passive process of impaired venous return.
• Tissues appear bluish/cyanotic due to increased deoxygenated blood.
• Chronic passive congestion of the liver can cause pooling of poorly oxygenated blood, hypoxia, parenchymal cell death, capillary rupture, and foci of hemorrhage.
• Red blood cell fragments are phagocytosed, leading to the formation of hemosiderin-laden macrophages.
• Chronic congestion can cause fibrosis.

Hemorrhage

• Hemorrhage means bleeding.
• It can occur due to clotting disorders or trauma.
• Capillary bleeding can occur from congestion, tissue injury, or inflammation.
• Hematoma is the collection of blood within a tissue.

Significance of Bleeding

• Bleeding significance depends on volume and location.
• Small amounts of bleeding may be fatal if in the cranial cavity.

Petechiae

• Small (1-2mm) hemorrhages on the skin or mucous membranes.
• These are caused by increased intravascular pressure, low platelet counts, defective platelet function, or clotting factor deficiency.

Ecchymosis

• Subcutaneous hematomas (bruises) that are larger (1-2cm).
• The red-blue hemoglobin in the clot is broken down to bilirubin and then to hemosiderin.
• Changes in color reflect these conversions (starting red-blue and progressively changing to greenish, then yellow, and finally golden-brown).

Hematoma

• Blood collection within tissues.
• Large hematomas can be fatal.
• Bruises are a type of insignificant hematoma.

Larger Blood Accumulations

• Hemothorax: blood in the pleural cavity
• Hemopericardium: blood in the pericardial cavity
• Hemarthrosis: blood in joint spaces
• Hemoperitoneum: blood in peritoneal cavity.

Thrombosis/Hemostasis

• Hemostasis: the process of maintaining blood in fluid state within vessels.
• Thrombosis: the pathological formation of a blood clot within intact vessels.

Normal Hemostasis (Sequence)

• Vasoconstriction: immediate response after injury, reducing blood flow to the damaged area. It's triggered by endothelin release from endothelial cells.
• Primary hemostasis: platelets stick to the damaged area (adhesion) and change shape to become "sticky" (shape change). Platelets release granules (secretion) containing factors that attract more platelets (and other components), and platelets aggregate. This forms the primary hemostatic plug—it's reversible.
• Secondary hemostasis: a cascade of enzymatic reactions, converting inactive plasma proteins into active proteins that activates thrombin.
• Thrombin converts fibrinogen to fibrin—insoluble fibrin meshwork forms stable clot.

Antithrombotic Counter Regulation

• Tissue Plasminogen Activator (tPA) is activated to limit clot expansion following formation of permanent clot.
• tPA converts plasminogen to plasmin—plasmin breaks down fibrin.
• This process prevents further clot formation.

Fate of thrombus

• Propagation: More fibrin and platelets accumulate on the clot.
• Embolization: The clot breaks off and travels through the circulation, potentially lodging in another area, causing embolism.
• Dissolution: The clot dissolves.
• Organization and canalization: The clot is reorganized and remodeled into healthy vessel tissue.

Venous Thrombosis (Phlebothrombosis)

• Most venous thrombi occur in the deep veins, especially in the lower extremities.
• Superficial thrombi occur in the saphenous system, especially in varicose veins.
• Deep thrombi, especially those above the knee, are more serious.
• They are often asymptomatic in 50% of cases.

Pulmonary Thromboembolism

• Often arise from deep vein thrombi (DVTs) in the lower extremities.
• Emboli travel to the right side of the heart and into the pulmonary arteries.
• Saddle emboli can block the main pulmonary artery.
• Smaller emboli may lodge in the smaller branches.

Systemic Thromboembolism

• These emboli travel through the arterial circulation.
• In 80% of cases, the source is mural thrombi in the cardiac walls.
• Atherosclerotic plaques in the aorta or aortic aneurysms can also be sources.
• Paradoxical emboli can travel through abnormal openings between atria or ventricles.

Fat Embolism

• Fat emboli arise from fractures of long bones, releasing fat from bone marrow following sinusoid rupture.
• Symptoms appear three days post-injury, including respiratory distress, neurological symptoms, thrombocytopenia, petechiae, and anemia.

Air Embolism

• Air emboli result from surgical procedures, scuba diving, or underwater work.
• Nitrogen, dissolved in the blood at high pressure, forms bubbles during ascent.
• These bubbles can cause focal ischemia in the brain, heart, or bones and respiratory distress.

Caisson Disease

• Chronic form of decompression sickness.
• Results from persistent gas emboli in bones, causing ischemic necrosis primarily in the heads of femur, tibia, and humerus.

Amniotic Fluid Embolism

• Occurs during or shortly after labor.
• Amniotic fluid enters the circulation, damaging lungs.
• Symptoms include sudden respiratory distress, hypotension, seizures, and coma.

Infarction

• Area of ischemic necrosis due to arterial occlusion.
• Obstruction to venous drainage can also cause infarction.
• Types include myocardial, pulmonary, and bowel infarction.
• Infarcts can be red (hemorrhagic) or white (ischemic), depending on blood flow.

Rare Causes of Infarction

• Vasospasm (e.g., Prinzmetal angina)
• Vessel compression (tumors)
• Vessel twisting (testis or intestinal torsion)
• Vessel entrapment (strangulated hernia)

Types of Infarcts

• Red infarcts are hemorrhagic, occurring in tissues with a dual blood supply or venous obstruction.
• White infarcts are not hemorrhagic, occurring in organs with a single arterial blood supply, and no reperfusion.

Factors Affecting Infarct Development

• Impaired blood supply
• Tissue's susceptibility to hypoxia
• Oxygen content of blood
• Rate of occlusion development (slow occlusion allows collateral blood supply),

Shock

• Systemic hypoperfusion due to reduced cardiac output or blood volume.
• Cardiogenic shock: failure of the cardiac pump due to myocardial damage.
• Hypovolemic shock: inadequate blood volume due to bleeding, vomiting, diarrhea, or burns.
• Neurogenic shock: loss of vasomotor tone from spinal cord injury or trauma.
• Septic shock: overwhelming bacterial infection that causes widespread inflammation.
• Stages of shock: initial (nonprogressive), progressive, and irreversible.