Thrombosis, Thromboembolism, and Infarction Flashcards

1
Q

Define thrombosis

A

Thrombosis is the formation of a blood clot within a blood vessel that has been damaged

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2
Q

What are 3 major predisposing factors of thrombosis?

A
  • endothelial injury
  • altered blood flow
  • hypercoagulability

Virchow’s Triad

  • endothelial injury abnormal blood flow
  • endothelial injury –> hypercoagulability
  • abnormal blood flow –> hypercoagulability
  • all lead to thrombus
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3
Q

What features differentiate a true thrombus from a postmortem clot?

A

True thrombus:

  • has tissue-like quality
  • attached to the blood vessel wall
  • Lines of Zahn (alternating pale layers of platelets admixed with fibrin and darker layers of RBCs)

Post-mortem thrombus:

  • has gelatinous quality
  • not attached to vessel wall
  • no Lines of Zahn
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4
Q

What are the four potential fates of a thrombus?

A
  • dissolution
  • embolization
  • propagation
  • organization and recanalization
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5
Q

Describe dissolution of a thrombus and its clinical significance

A
  • thrombi are cleared by the fibrinolytic system

Clinical significance: none

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6
Q

Describe embolization of a thrombus and its clinical significance

A
  • portions of the thrombus break off and travel through the circulation
  • thrombi inevitably get stuck, causing partial or complete occlusion

Clinical significance: may cause ischemic necrosis of distal tissue

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7
Q

Describe propagation of a thrombus and its clinical significance

A
  • thrombus grows by accumulating more platelets and fibrin

Clinical significance: can lead to occlusion and ischemic necrosis if the larger clot then embolizes

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8
Q

Describe organization and recanalization of a thrombus and its clinical significance

A
  • thrombus undergoes fibrosis and blood flow may be reestablished

Clinical significance: blood flow may be reestablished

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9
Q

What is the general clinical significance of a thrombus?

A
  • can cause obstruction of arteries and veins with ischemia or necrosis of tissue supplied by the vessel
  • congestion and edema
  • can embolize another site
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10
Q

Where is endothelial injury typically found (leading to thrombus)?

A

mainly in arterial circulation

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11
Q

What does abnormal blood flow cause (leading to thrombus)?

A

turbulence –> pockets of stasis –> dilution of activated clotting factors –> prevents inflow of clotting inhibitors

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12
Q

What is hypercoagulability (leading to thrombus)?

A

any alteration of coagulation pathway

Causes:

  • acquired (secondary): high risk medical factors and low risk ones
  • inherent (primary): mutations, deficiencies
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13
Q

Describe the mechanism whereby factor V Leiden gene mutation leads to hypercoagulability

A
  • in Factor V Leiden, FV is mutated such that the Protein C system is unable to inactivate it
  • this prevents one of the inhibitory mechanisms of the coagulation cascade from working and causes hypercoagulability
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14
Q

Describe the mechanism whereby the prothrombin gene mutation leads to hypercoagulability

A
  • prothrombin helps with fibrin formation

- a mutation in prothrombin results in increased levels of prothrombin that result in increased fibrin formation

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15
Q

What are the general outcomes of pulmonary embolism?

A
  • most are small and clinically silent (60-80%)
  • SUDDEN DEATH, right heart failure or cardiovascular collapse (>60% of the pulmonary circulation is obstructed with emboli)
  • PULMONARY HEMORRHAGE but not infarction due to the dual blood flow (pulmonary and bronchial circulation)
  • small emobli of end-arteriolar small branches
  • PULMONARY HYPERTENSION (multiple episodes of small emboli)
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16
Q

Define infarction; describe the clinical significance

A
  • tissue death due to the obstruction of the tissue’s blood supply
  • results in ischemic necrosis
17
Q

What are the two types of infarcts?

A
  • red infarct

- white infarct

18
Q

What are the gross and microscopic features of white infarcts?

A
  • do not have hemorrhage
  • appear lighter in color than the surrounding tissue
  • occur with arterial occlusion in organs that do not have dual blood supplies:
    • heart
    • kidney
    • spleen
19
Q

What are the gross and microscopic features of red infarcts?

A
  • occur with venous occlusion (eg ovarian or testicular torsion)
  • in tissues with dual circulation (lung, small intestine) that allow blood flow from an unobstructed parallel supply into a necrotic zone
  • in loose tissues (lung) which allow blood to collect in the infarcted zone
  • when flow is reestablished to a previously infected area
20
Q

Why do white and red infarcts occur in different organs?

A
  • they occur in different areas due to the nature of the blood supply
  • dual blood supplies in some organs allow blood to flow to an area that may have a blockage; since the tissue may be necrotic, blood can flow out of the vessels and cause a hemorrhage (RED infarct)
21
Q

Where do white infarcts occur?

A

with arterial occlusion in organs that do not have dual blood supplies:

  • heart
  • kidney
  • spleen
22
Q

Where do red infarcts occur?

A
  • in tissues with dual circulation (lung, small intestine) that allow blood flow from an unobstructed parallel supply into a necrotic zone
  • in loose tissues (lung) which allow blood to collect in the infarcted zone
23
Q

What are the four factors that influence the development of an infarct?

A
  • nature of blood supply
  • rate of development of occlusion
  • vulnerability to hypoxia
  • oxygen content of blood
24
Q

How does nature of blood supply influence the development of an infarct?

A

if the organ has a dual blood supply, then it is relatively immune to small occlusions as long as the alternate blood supply is intact

25
Q

How does the rate of development of occlusion influence the development of an infarct?

A

if the development of the blockage is slow, then the body may have time to develop alternate sources of blood flow (other blood vessels may accommodate more flow) to the area to prevent infarct

26
Q

How does vulnerability of hypoxia influence the development of an infarct?

A

Tissues that are particularly sensitive to hypoxia are more likely to infarct

  • neurons undergo irreversible damage within 3-4 minutes
  • myocardial cells die after 20-30 minutes of ischemia
  • fibroblasts in myocardium can last several hours
27
Q

How does oxygen content of blood influence the development of an infarct?

A

patients with anemia are more susceptible to even partial occlusions causing infarct

28
Q

What enzyme is important fibrinolysis (the enzymatic breakdown of the fibrin in blood clots)?

A

Plasmin (an enzyme, formed in the blood in some circumstances, that destroys blood clots by attacking fibrin)

29
Q

What are two pathophysiologic consequences of a pulmonary embolism?

A
  • respiratory compromise (due to ventilation of non-perfused segment of lung)
  • hemodynamic compromize (due to increased resistance to pulmonary blood flow as result of vascular obstruction)
30
Q

What are microscopic features of infarct?

A
  • ischemic coagulative necrosis
  • karyolysis (outline of cells, no nuclei)
  • inflammation/inflammatory cells to clean up debris
  • most infarcts replaced by scar tissue