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Pathology - Exam 1 > Thrombosis/Embolism/Infarction/Shock > Flashcards

Thrombosis/Embolism/Infarction/Shock Flashcards

1
Q

Thrombus definition

A

Intravascular clot, often impeding or preventing blood flow

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2
Q

Thrombosis definition

A

Formation or presence of a thrombus
May result in infarction
Uncontrolled or pathologic stoppage of bleeding

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3
Q

What components make up Virchow’s triad?

A

Endothelial Injury
Alterations in blood flow
Hypercoagulability

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4
Q

Endothelial injury

A

Loss of endothelial cell barrier
Increased prothrombic activity caused by hemodynamic stress; hypertension, homocystinuria, hypercholesterolemia, radiation, cytokines, endotoxin

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5
Q

What types of alterations in blood flow can cause Thrombosis

A

Stasis

Turbulence

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6
Q

How does turbulence effect Thrombosis

A

Increases the chance for endothelial cell injury and activation
Can lead to a hypercoagulative state

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7
Q

How does stasis effect Thrombosis

A

Stasis disrupts laminar flow (platelets move to the periphery of the vessel) - this allows for a concentration of clotting factors and it activates endothelial cells

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8
Q

What are some inherited conditions that can increase Hypercoagulability?

A

Factor V Leiden mutation - favor Va cannot be degraded
ATIII deficiency
Prothrombin mutation

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9
Q

What are some acquired conditions that can increase Hypercoagulability?

A 
Prolonged bed rest
Extensive tissue injury
Pregnancy
Cancer
Anti-phospholipid antibody syndrome
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10
Q

Where do Arterial Thrombi tend to occur?

A

Sites of turbulence or endothelial injury and loss

Emboli lodge in smaller arteries, often causing infarction

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11
Q

What does an Arterial Thrombi look like?

A

Pale white appearance
They have distinct Lines of Zahn
May be occlusive or mural

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12
Q

Venous Thrombi

A

Have a dark maroon color (“red”) and indistinct Lines of Zahn
Often form in the deep veins of the legs

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13
Q

What are the different Fates of Thrombi

A

Propagation
Embolization
Dissolution
Organization

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14
Q

Propagation of Thrombi

A

Enlarge by additional fibrin/platelet deposition

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15
Q

Embolization of Thrombi

A

Entire thrombus dislodges or a piece breaks loose

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16
Q

Dissolution of Thrombi

A

Lysis by fibrolytic activity

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17
Q

Organization of Thrombi

A

Ingrowth of fibroblasts and smooth muscle cells, leads to deposition of collagen (replacing the fibrin) and recanalization, which may reestablish some flow through the thrombus

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18
Q

Disseminated Intravascular Coagulation

A

Widespread activation of the coagulation cascade and fibrinolytic system leading to depletion of coagulation factors and platelets and accumulation of fibrin split products
This can be associated with widespread formation of microthrombi and risk of hemorrhage

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19
Q

What conditions are associated with Disseminated Intravascular Coagulation

A 
Infection (especially gram-)
Obstetric complications (placental abruption, retained dead fetus)
Neoplasm
Shock
Massive Injury
Others
20
Q

Embolism definition

A

A solid, liquid, or gas carried from one point to another point in the vascular system

21
Q

What is the origin of a pulmonary embolism?

A

Usually they arise from deep veins in the legs

Less frequently, they can originate from pelvic veins, right heart chambers, and others

22
Q

What is the treatment for Disseminated Intravascular Coagulation?

A

Highly variable

Depends upon management of the underlying disorder

23
Q

What is the most common embolus?

A

Dislodged thrombus material (Thromboembolism)

24
Q

What are the clinical consequences of pulmonary thromboemboli?

A
  • No clinical manifestation - small emboli cause no ischemia due to the double blood supply, bronchial and pulmonary arteries in the lungs
  • Pulmonary hemorrhage and hematemesis due to ischemia injury without infarction
  • Pulmonary infarction
  • Sudden death - due to large emboli obstructing a large pulmonary artery or straddling the bifurcation of the pulmonary arterial trunk
  • Pulmonary hypertension - gradual obstruction of many small pulmonary arteries by repeated embolization over time can result in pulmonary hypertension
25
Q

Paradoxical embolus definition

A

Embolus that arises in a systemic vein and crosses a communication from the venous side to the arterial side of circulation

26
Q

Where is the communication that leads to a Paradoxical Embolus?

A

Usually in the heart through a patent foramen ovale, atrial septal defect, or other anomalous communication

27
Q

Systemic embolization

A

Origin usually the left atrium or left ventricle, or ulcerated atherosclerotic plaque
Can travel to any systemic artery

28
Q

What are some other types of emboli?

A

Fat
Air - chest wall injury, bends, etc
Amniotic fluid - rare complication of pregnancy associated with DIC
Atherosclerotic - debris form the central core of an atherosclerotic plaque

29
Q

Infarction definition

A

Ischemic necrosis involving all cell types in a segment of an organ or an entire organ - irreversible injury associated with hypoxia
Major contributor to mortality associated with cardiovascular disease

30
Q

What causes an infarction?

A

Usually due to arterial obstruction; and less often due to vessel twisting, venous obstruction, or slow flow from other cause such as shock

31
Q

What are the two major types of infarction

A

Red (hemorrhagic) infarcts

White (pale) infarcts

32
Q

When does red infarction occur?

A

It’s seen in areas where the venous side of blood flow is blocked off and the vein is impacted, but the artery is still pushing blood there

33
Q

White (pale) infarcts

A

Occur with arterial occlusions in solid organs

Where tissue density limits blood seepage from adjacent vascular beds

34
Q

What is the gross morphology of infarcts?

A

Tend to be wedge-shaped with the point of the wedge at the site of the arterial obstruction

35
Q

What is notable about the histology of infarctions?

A

The histologic changes of coagulation necrosis do not develop for several hours after the infarct has occurred
The infarct becomes more distinct over time

36
Q

What follows an infarction?

A

An acute inflammatory response that begins within several hours and peaks at 2 to 3 days

37
Q

How does healing of an infarction occur

A

Healing occurs by granulation tissue ingrowth, starting at the edge of the infarct, followed by scar formation

38
Q

What do infarcts in the brain result in?

A

Liquefactive necrosis and heal with the formation of a cystic space

39
Q

What factors influence infarct development?

A

Nature of vascular supply
Rate of development of occlusion - slow occlusion allows time for collateral vessels
Vulnerability to hypoxia - more vulnerable = more danger
Oxygen carrying capacity of the blood

40
Q

Shock definition

A

Systemic hypoperfusion of tissue

41
Q

What are the pathophysiologic categories

A

Cardiogenic - loss of pumping capacity of the heart
Hypovolemic - blood loss
Septic - bacterial infection
Anaphylactic - hypersensitive reaction mediated by IgE
Neurogenic - loss of vascular tone (anesthesia, spinal cord injury)

42
Q

What is the pathogenesis of septic shock?

A

Pathogen-associated molecular patterns (PAMPs; including LPS)
PAMPS bind to toll-like receptors (TLRs) on monocytes and neutrophils, mediating the release of IL-1 and TNF
Secondary release of other cytokines in response
Vasodilation, hypotension, endothelial cell activation and injury, reduced myocardial contractility occur in response to the release of the secondary cytokines

43
Q

What are the stages of Shock?

A

Nonprogressive
Progressive
Irreversible

44
Q

Nonprogressive stage of shock

A

Compensatory mechanisms maintain perfusion - maintains tissue perfusion by tachycardia, renal conservation of water, redistribution of blood to vital organs and away from skin by peripheral vasoconstriction

45
Q

Progressive stage of shock

A

Inadequate perfusion - we have metabolic imbalances such as acidosis and increased lactic acid. The acidosis reduces vasomotor responses to sympathetic stimulation leading to pooling of blood and reduced perfusion
Hypoxic injury to endothelium can lead to DIC

46
Q

Irreversible shock

A

Tissue injury that can not be reversed by reprofusion

47
Q

Clinical manefestations of shock

A 
Tachycardia
Tachypnea
Hypotension
Cool, clammy skin (may be warm, flushed with septic shock)
Decreased urinary output
Confusion
Low blood pH (acidosis)

Pathology - Exam 1 (9 decks)

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