Thrombosis, Embolism and Infarction

Question 1

describe Virchow’s triad

Answer 1

Question 2

describe endothelial cell injury and causes of it

Answer 2

• important in arterial thrombi
• stress induced by HT
• bacterial toxins in shock
• hypercholesterolemia
• homocystinuria
• cigarette smoking (CO)
• all predispose to thrombus formation at the site of endothelial injury

Question 3

describe loss of laminar flow

Answer 3

• stasis
  
  • endothelial cell hypoxia/damage
  • allows platelets to come in contact with endothelium
  • allows local activation of coagulation factors
  • allows buildup of platelets/fibrin
  • prevents dilution of activated clotting factors
  • reduces flow of clotting inhibitors
  • stasis in aneurysms and leg veins

Question 4

____ is the commonest disease causing hypercoagulability of blood

Answer 4

Factor V Leiden is the commonest disease causing hypercoagulability of blood

Question 5

describe acquired syndromes leading to hypercoagulability

Answer 5

• terminal cancer
  
  • thrombogenic substances released from necrotic tumor cells (Trousseau syndrome)
• cardiac failure
  
  • anoxic damage to tissues, release of thrombogenic substances
• severe trauma, burns
• oral contraceptives (estrogen specifically) → increased production of clotting factors

Question 6

describe features of a thrombus

Answer 6

Question 7

describe a thrombus vs. a clot

Answer 7

Question 8

describe a venous thrombosis

Answer 8

• takes the shape of vessels in which it forms
• redder than arterial thrombus
• superficial veins of legs (varicosities) → rarely embolize
• deep veins of legs (90%)
  
  • deep calf veins (at or above the knee)
    
    • femoral, popliteal, iliac

Question 9

describe the morphology of thrombi

Answer 9

• gross
  
  • dark gray friable mass
  • arterial thrombi → pale
  • venous thrombi → red
• microscopy = lines of Zahn
  
  • alternate pale and dark lines
  • light = platelets and fibrin
  • dark = RBCs

Question 10

describe clinical features of venous thrombosis

Answer 10

• deep leg veins → edema of ankle and foot, pain, tenderness
• asymptomatic in 50% (due to collaterals)
• high risk of embolization
• Trousseau’s Syndrome: unexplained thrombophlebitis, recurrent → look for underlying abdominal malignancy like pancreatic cancer (release of procoagulants)

Question 11

describe the effect of arterial vs. venous thrombus on organs

Answer 11

Question 12

the commonest origin of an embolism is from ____ and reaches ____ but most are clinically silent

Answer 12

the commonest origin of an embolism is from the deep leg veins and reaches the lungs but most are clinically silent

Question 13

the commonest clinically significant thromboemboli arise ____ and embolize to ____ (75%) and ___ (10%)

Answer 13

the commonest clinically significant thromboemboli arise from the heart (80%) and embolize to the lower extremities (75%) and brain (10%)

Question 14

classify different types of pulmonary thromboembolisms

Answer 14

• massive
  
  • sudden obstruction of 60% of pulmonary vasculature; sudden death, no time to develop infarction → no morphological changes seen in lungs or heart
• major
  
  • multiple medium sized vessels occluded → dyspnea, pain
  • infarction only in 10% because of collateral circulation by bronchial arteries
• minor
  
  • small vessels obstructed, get lysed, remain asymptomatic

Question 15

describe systemic thromboembolism

Answer 15

• thrombi that travel in arterial circulation
• sites of origin:
  
  • heart: mural thrombus (80%)
  • aorta: ulcerated atherosclerotic plaques
  • venous circulation: paradoxical through ASD, VSD
• effect: embolize to the lower extremities (75%) and bain (10%)
  
  • they block an end artery leading to infarction

Question 16

describe fat emboli

Answer 16

• trauma to bone, subcutaneous tissue, burns
• fat globules enter the circulation by rupture of the marrow vascular sinusoids or rupture of venules
• pathogenesis:
  
  • mechanical blockage: globules enlarge in circulation, platelets adhere
  • biochemical injury: free fatty acids are released from adipose tissue in the circulation and are toxic to endothelial cells → DIC, clogged pulmonary and systemic capillaries

Question 17

describe fat embolism syndrome

Answer 17

• characterized by pulmonary insufficiency, neurologic symptoms, anemia and thrombocytopenia and is fatal in about 10% of cases
• typically, the symptoms appear 1-3 days after injury, with sudden onset of tachypnea, dyspnea and tachycardia and petechiae
• neurologic symptoms include irritability and restlessness, with progression to delirium or coma

Question 18

describe what is seen in the image

Answer 18

fat embolus

Question 19

describe the diagnosis of fat embolism

Answer 19

• diagnosis: fat globules in sputum, urine
• postmortem: frozen section of tissues since routine processing through alcohol will dissolve the fat

Question 20

describe an air embolism

Answer 20

• air may be introduced into the venous circulation through neck wounds, thoracocentesis, cut in IJV, hemodialysis
  
  • childbirth, abortion
• 150 mL of air causes death
• air bubbles tend to coalesce and physically obstruct the flow of blood in the right ventricle, lungs and the brain

Question 21

describe nitrogen embolism (aka the bends aka Caisson’s disease)

Answer 21

• O2, N2 dissolve in high amounts in blood and tissues when diving due to high pressure
• sudden resurfacing release N2, O2
  
  • O2 is reabsorbed…
  • but N2 bubbles out → ruptures tissues and in vessels it forms emboli
  • platelets adhere to N2 to form secondary thrombi and aggravate the ischemia
• brain death, muscles, joints (bends), lungs (chokes)

Question 22

describe Caisson’s disease and treatment for it

Answer 22

• more chronic form with persistent gas emboli in bones
  
  • necrosis in femur, tibia, humerus
• treatment:
  
  • pressure chamber → slow decompression

Question 23

describe an amniotic fluid embolism

Answer 23

• sudden event after labor
• squames, hair, meconium in pulmonary vessels
• usually fatal → DIC, pulmonary edema, diffuse alveolar damage

Question 24

describe what is seen in the image

Answer 24

amniotic fluid embolism

Question 25

describe red infarct vs. white infarct

Answer 25

• red infarcts
  
  • large amount of bleeding into the organ
  • soft organs with tissue spaces (lungs)
  • tissues with dual blood supply (lungs and small intestine) → bleeding from anastomosing vessels
  • venous infarcts (congestion followed by infarction) → testicular/ovarian torsion
  • when flow is reestablished after arterial occlusion and necrosis
• white infarcts (pale)
  
  • little bleeding into the organ affected
  • solid organs like kidney, spleen, heart
  • arterial occlusion

Question 26

describe the morphology of infarcts

Answer 26

• gross:
  
  • wedge-shaped, with the occluded vessel at the apex and the periphery of the organ forming the base
  • initially congested and ill-defined margins
  • well-defined, rim of hyperemia
  • later brown due to hemosiderin
• micro
  
  • ischemic coagulation necrosis
• septic
  
  • abscess formation

Question 27

describe how the nature of the blood supply can impact infarctions

Answer 27

• dual blood supply: less change of infarction
  
  • lungs, liver
  • Circle of Willis
  • hand (ulnar and radial arteries)
• collateral circulation
  
  • enlargement of anastomoses in the coronary circulation reduces the risk of infarction

Question 28

describe the etiology of a pulmonary infarction

Answer 28

Question 29

describe cerebral infarcts

Answer 29

• embolism is the most common cause → mostly from cardiac mural thrombi (MI, Afib), but emboli can originate in the carotids too
• thrombotic occlusions: caused by atherosclerosis

Question 30

describe the evolution of cerebral infarcts

Answer 30

• 12 hours:
  
  • starts as coagulation necrosis
  • softening, color changes
  • may have hemorrhage due to reperfusion
• 48 hours:
  
  • edema of the infarcted region, acts like a intracerebral mass causing raised intracranial pressure
  • microglial engulf necrotic material → ​Gitter cells
    
    • Gitter cells are the result of microglial cell’s phagocytosis of infectious material or cellular debris. Eventually, after engulfing a certain amount of material, the phagocytic microglia becomes unable to phagocytose any further materials.

Question 31

describe the later evolution of cerebral infarcts

Answer 31

• further breakdown of the tissue constituents, softening
• liquefaction necrosis
• cyst formation
• overlying meninges thickened
• surrounding regions of gliosis

Question 32

describe a myocardial infarction

Answer 32

• coronary atherosclerosis with superimposed thrombosis
  
  • LAD is the commonest involved
• coagulation necrosis
• initially blotchy, later pale scar tissue
• cardiac enzymes raised in serum
• presents with severe chest pain (angina)