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Questions and Answers
What determines whether the occlusion of a blood vessel will cause significant damage to an organ?
Which tissue is most vulnerable to irreversible damage when deprived of its blood supply?
What physiological response occurs during the initial stage of compensation in shock?
What is a common consequence of prolonged excessive vasoconstriction during the progressive stage of shock?
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What morphological change is most prominently associated with hypoxic injury during shock?
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Which type of shock is characterized by initially warm and flushed skin in patients?
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What are the 'lines of Zahn' characterized by in a true thrombus?
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Which of the following best describes disseminated intravascular coagulation (DIC)?
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What is the most common source of pulmonary thromboemboli?
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Which clinical feature is associated with fat embolism?
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What is the key feature of red (hemorrhagic) infarcts?
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What event leads to gas embolism during obstetric procedures?
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Which type of embolism results from the infusion of amniotic fluid into the maternal circulation?
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What effect can poor collateral circulation have in the case of ischemia?
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Which of these conditions is NOT a common cause of ischemia?
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What is the primary consequence of endothelial injury in thrombosis?
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Which of the following is NOT a component of Virchow’s triad?
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What type of thrombosis is associated with turbulent blood flow?
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Which of the following is a primary genetic cause of blood hypercoagulability?
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What is a common characteristic of arterial thrombi compared to venous thrombi?
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How do post mortem clots differ from thrombi?
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What is the fate of a thrombus that undergoes dissolution?
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What is the role of stasis in thrombus formation?
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Which feature is characteristic of all forms of thrombi?
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Study Notes
Thrombosis
- Formation of a solid or semi-solid mass from blood constituents within the vascular system during life, due to inappropriate activation of hemostasis.
- This mass is called a thrombus.
- Three predisposing factors for thrombus formation (Virchow's triad):
- Endothelial injury
- Stasis or turbulence of blood flow
- Blood hypercoagulability (changes in composition of blood)
Endothelial Injury
- Mechanical injury: pressure, rupture, or torsion of the vessel.
- Degeneration: atherosclerosis, aneurysm, endothelium covering a myocardial infarction.
- Inflammatory processes: phlebitis, arteries, and inflammation of heart valves.
- Endothelial injury leads to exposure of subendothelial ECM, causing platelet adhesion.
Alteration in Normal Blood Flow
- Turbulence: leads to arterial and cardiac thrombosis.
- Stasis: leads to venous thrombosis.
- Stasis and turbulence lead to thrombus formation by:
- Endothelial injury
- Disrupting laminar flow and bringing platelets into contact with endothelium
- Preventing dilution of activated clotting factors by fresh blood
- Retarding the inflow of clotting factors inhibitors, permitting thrombus build-up
- Promoting endothelial cell activation, leading to local thrombosis, leukocyte adhesion, etc.
Blood Hypercoagulability
- Primary causes (genetic): antithrombin III deficiency, protein C deficiency
- Secondary causes (acquired): immobilization, MI, HF, tissue damage, burns, OCCP, sickle cell anemia, leukemia, smoking
Fate of Thrombus
- Propagation: thrombus grows larger
- Embolization: thrombus breaks off and travels to another location
- Dissolution: thrombus dissolves
- Organization and recanalization: thrombus is replaced by connective tissue and new channels form within it
- Calcification: thrombus hardens
Morphology of Thrombus
- Grossly and microscopically: have apparent laminations (lines of Zahn), produced by alternating pale layers of platelets admixed with some fibrin and darker layers of red cells.
- Arterial thrombi: usually occlusive, firmly attached to the wall, gray-white, and friable.
- Venous thrombi: almost invariably occlusive, less firmly attached to the wall, and red.
- Post mortem clots: gelatinous, dark red, usually not attached to the wall, and lack lines of Zahn.
- Mural thrombi: attached to the wall of heart chambers or in the aortic lumen.
- Vegetations: thrombi formed on heart valves.
Disseminated Intravascular Coagulation (DIC)
- Sudden or insidious onsets of widespread fibrin thrombi formation in the microcirculation.
- Associated with rapid consumption of platelets and coagulation proteins (consumption coagulopathy).
- Leads to activation of fibrinolytic mechanisms and serious bleeding disorders.
- DIC is not a primary disease, but a potential complication of various conditions that share widespread activation of thrombin (obstetrical complications, infections, massive tissue injury).
Embolism
- Detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin.
Types of Emboli
- Thrombo-emboli
- Fat and bone marrow
- Gas (air, nitrogen)
- Atero-emboli
- Tumor fragments
- Foreign body (bullet)
Pulmonary Thrombo-embolism
- Deep leg vein thrombi are the most common source.
- Depending on the size of the embolus, it can:
- Occlude the main pulmonary artery
- Impact across the bifurcation (saddle embolus)
- Pass into smaller arterioles
- Enter the systemic circulation (paradoxical embolism)
Clinical Consequences of Pulmonary Embolism
- Most pulmonary emboli are silent
- Sudden death (acute cor pulmonale)
- Obstruction of medium-size arteries: pulmonary hemorrhage
- Obstruction of small endarterioles: infarction
- Multiple emboli over time: chronic cor pulmonale
Systemic Thrombo-Emboli
- Can originate from:
- Intra-cardiac mural thrombi (89% of emboli)
- Aortic aneurysm
- Thrombi on ulcerated atherosclerotic plaques
- Fragmentation of valvular vegetations
- Paradoxical emboli
- 15% are of unknown origin
- Main sites involved in embolism:
- Lower extremities (75%)
- Brain (10%)
- Intestines
- Kidneys
- Spleen
- Upper extremities
Fat Embolism
- May result from:
- Fractures of long bones (most common)
- Soft tissue trauma and burns (rare)
- Clinical features:
- Pulmonary insufficiency
- Neurologic symptoms
- Anemia
- Thrombocytopenia
- Symptoms appear within 1 to 3 days.
Gas Embolism
- Air may enter the circulation during:
- Obstetric procedures
- Chest wall injury
- More than 100 cc is required to have a clinical effect.
- Bubbles produce physical obstruction to vessels, causing infarction.
Decompression Sickness
- Type of gas embolism in people exposed to sudden changes in atmospheric pressure (deep-sea divers)
- If air is breathed at high pressure, a high amount of gas (nitrogen) dissolves in the blood and tissues.
- If the diver ascends (depressurizes) too rapidly, nitrogen expands in tissues and bubbles out of solution in the blood to form gas emboli.
- Clinically, the diver suffers from:
- Muscle and joint pain
- Respiratory distress
- Infarctions in various tissues
Amniotic Fluid Embolism
- Grave but uncommon complication of labor.
- Cause: infusion of amniotic fluid or fetal tissue into maternal circulation via a tear in placental membranes or rupture of uterine veins.
- Clinically: sudden severe dyspnea, cyanosis, hypotensive shock, seizure, and coma.
- If the patient survives, pulmonary edema and DIC develop.
Ischemia:
- Inadequate blood supply to an area of tissue.
- Causes:
- 99% result from a thrombotic or embolic mechanism
- Complicated atheroma (i.e. atheroma with subsequent hemorrhage)
- Twisting of blood vessel
- Compression from outside by tumor or by entrapment in a hernial sac
- Venous obstruction can occur in a varicose vein
Effect of Ischemia
- Variable depending on the adequacy of collateral circulation.
- If good collateral circulation is present, it will produce little or no effect.
- If collateral circulation is poor, it will lead to functional disturbances or even cell death.
- Ischemia in the heart can lead to chest pain (angina), while in the lower limb, it can cause intermittent claudication (pain in the calf muscle during exercise).
Infarction
- Definition: Ischemic necrosis due to occlusion of either an artery or vein.
- Causes:
- Thrombosis or embolism (99%)
- Local vasospasm
- Expansion of an atheroma
- Extrinsic compression of a vessel (tumor, twisting, edema, hernia)
- Traumatic rupture of vessel
Morphology of Infarction
- Infarction has a wedge shape, the apex at the site of the occluded blood vessel & the periphery of the organ forming the base which is poorly defined.
- The dominant histological characteristic of infarcts is ischemic coagulative necrosis.
- With time, the edge becomes more defined by a narrow zone of hyperemia due to inflammation and pale infarction becomes more paler & sharply defined while red infarction becomes more firm and brown.
- Septic infarcts: abscess is formed.
Red Infarcts (hemorrhagic)
- Occur in the following situations:
- Venous occlusion (testis, ovaries)
- Loose tissue
- Tissue with dual circulation
- Previously congested tissue
- Re-established blood flow
White Infarcts (anemic)
- Occur following arterial occlusion in solid organs with end-arterial circulation and, by time, change into scar tissue.
Factors that Influence Infarct Development:
- Anatomy of the vascular supply: presence or absence of alternative blood supply, can determine whether the occlusion of a blood vessel can cause damage. e.g., lungs have dual blood supply from the pulmonary and bronchial arteries, so obstruction of the pulmonary artery will not cause severe damage until the bronchial artery is also blocked. While kidneys and spleen have end-arterial circulation, so any arterial obstruction will lead to infarction of these tissues.
- Rate of development of occlusion: Slowly developing occlusion will allow time for collateral circulation to open, e.g., in coronary arteries anastomosis.
- Vulnerability to Hypoxia: neurons undergo irreversible damage when deprived of their blood supply for 3-4 min. Myocardial cells can withstand ischemia for 20-30 min only. In contrast to the fibroblast within the myocardium, which can remain viable for hours after ischemia.
- Oxygen content of blood: Low blood O2 --> increase extent and vulnerability of infarction.
Shock
- Pathological state of life-threatening hypoperfusion of vital organs and cellular hypoxia, due to diminished cardiac output or reduced effective circulating blood volume.
- Leads to: hypotension, impaired tissue perfusion, cellular hypoxia.
- Initially, cellular injury is reversible, but if shock is sustained, cell death occurs.
Causes of Shock
- Hypovolemic (loss of fluid volume)
- Cardiogenic (heart failure)
- Septic (infection)
- Neurogenic (damage to nervous system)
- Anaphylactic (allergic reaction)
Stages of Shock
- Stage of Compensation (initial nonprogressive stage): - Decreased cardiac output causes reflexive sympathetic stimulation. - Reflexive sympathetic stimulation increases the heart rate (tachycardia) and causes peripheral vasoconstriction. - Vasoconstriction maintains blood pressure in vital organs (brain and myocardium). - Vasoconstriction in renal arterioles decreases pressure and the rate of glomerular filtration. - Decreased glomerular filtration results in decreased urine output (oliguria).
- Stage of Impaired Tissue Perfusion (progressive stage):
- Prolonged excessive vasoconstriction impairs tissue perfusion and oxygenation.
- Impaired tissue perfusion promotes anaerobic glycolysis, leading to the production of lactic acid and lactic acidosis.
- Cell necrosis occurs, which is most apparent in the kidney. - Cell necrosis in the kidney causes acute renal tubular necrosis and acute renal failure. - In the lungs, hypoxia causes acute alveolar damage with intraalveolar edema, hemorrhage, and formation of hyaline fibrin membranes (shock lung, or adult respiratory distress syndrome [ARDS]) - In the liver, anoxic necrosis of the central region of hepatic lobules may occur. - Ischemic necrosis of the intestine is important because it is frequently associated with hemorrhage or release of bacterial endotoxins that further aggravate the shock state. - Stage of Decompensation: - As shock progresses, decompensation occurs. - Widespread vasodilation and stasis result in a progressive fall in blood pressure to a critical level. - Cerebral hypoxia causes brain dysfunction (loss of consciousness). - Myocardial hypoxia leads to further diminution of cardiac output, and death may occur rapidly.
Morphological Changes in Shock
- Those of hypoxic injury, especially in the organs (brain, heart, lungs, kidneys, adrenals, gastrointestinal tract)
Clinical Features:
- Hypovolemic and cardiogenic shock:
- Hypotension
- Weak rapid pulse
- Cool, clammy, and cyanotic skin
- Septic shock:
- Skin initially warm and flushed
Prognosis:
- Varies with the cause of shock and its duration, and the age of the patient.
- Best prognosis: young with hypovolemic shock.
- Worst prognosis: an old person with cardiogenic shock or with septic shock.
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Description
This quiz explores the formation of thrombosis, focusing on the mechanisms behind thrombus formation and the critical factors that contribute to it. It delves into topics such as endothelial injury and alterations in normal blood flow, providing a comprehensive understanding of this crucial medical condition.
