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Cardio > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

What is thrombosis

A

formation of an aggregate of coagulated blood containing platelets, fibrin and entraped cellular elements within the vascular lumen

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2
Q

Virchow’s triad of thrombosis

A

endothelial injury

abnormal blood flow

hypercoagulability

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3
Q

how does endothelial injury contribute to thrombosis

A
  • severe injury exposes vWF and tissue factor
  • inflammation downregulates protein C and tissue factor protein inhibitor
  • when cytokines activate injured cells, they downregulate the expression of thrombomodulin
  • injured endothelium secretes plasminogen activator inhibitors, which limits fibrinolysis and downregulates tPA
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4
Q

How does abnormal blood flow contribute to thrombosis

A

disrupted laminar flow brings platelets in contact with the epithelium and prevents the washout/ dilution of activated clotted factors/ inflow of factor inhibitors

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5
Q

main cause of arterial and cardiac thrombi

A

turbulence

endocardial injury

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6
Q

main cause of venous thrombi

A

stasis

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7
Q

causes of abnormal blood flow

A

mitral valve stenosis

hyperviscosity

MI

aortic and arterial dilation

ulcerated athersclerotic plaques

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8
Q

contrast the location, growth pattern and factors of formation in venous vs arterial thrombi

A

Arterial:

Location: coronary> cerebral> femoral arteries

Growth pattern: retrograde

Formation: ruptured atherosclerotic plaques and vascular injury

Venous:

Location: BLE> BUE> periprostatic/ovarian plexus/periuterine veins> dural sinus > hepatic veins

Growth pattern: in te direction of blood flow

Formation: stasis

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9
Q

compare and contrast the clinical features of arterial and venous thrombi

A

Arterial: MI, intestinal infarction, renal infarction, ischemic leg/ gangrene

BOTH: stroke, bowel infarction

Venous:positive homan sign, congestion, edma, cyanosis, induration, budd-chiari syndrome

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10
Q

Morphology of a thrombus

A

lines of zahn

microscopically apparent laminations

pale platelet and fibrin deposits alternating with darker red cell-rich layers

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11
Q

compare and contrast antemortem and postmortem thrombi

A
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12
Q

causes of mural thrombi

A

in heart chambers:

  • arrhythmias
  • dilated cardiomyopathy
  • myocarditis
  • catheter trauma
  • MI

aortic lumen:

  • ulcerated atherosclerotic plaques
  • aneurysmal dilation
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13
Q

causes of hypercoagulability

A
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14
Q

Factor V Leiden Deficiency

  • Pathology
  • Consequences
  • Clinical features
A
  • Pathology: DNA point mutation where guanine substitutes adenine, leading to glutamine replacing arginine at position 506
  • Consequences: Peptide cleavage site is is moved, making it resistant to Protein C
  • Clinical features: young caucasian person with no risk factors, but appear with thrombosis
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15
Q

Prothrombin mutation

Pathology

Consequences

A
  • Pathology: mutation of G20210A in the promoter region increases the expression of prothrombin by 30%
  • Consequences: more prothrombin can be converted to thrombin to form a clot
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16
Q

Antithrombin III Deficiency

Pathology

Consequences

Clinical features

A
  • Pathology: liver disease or nephrotic syndrome causes decreased serum concentration
  • Consequences: uninhibited thrombin, factors 9a-12a
  • Clinical features: heparin resistance
17
Q

Protein C Deficiency

Pathology

Consequences

Clinical features

A
  • Pathology: protein S deficiency, Vitamin deficiency, liver disorders, increased excretion
  • Consequences: uninhibited activity of Factor 5a and 8a
  • Clinical features: warfarin skin necrosis
18
Q

Explain the pathology of Heparin-induced thrombocytopenia

A
  1. Activated platelets release PF4, which binds to heparin
  2. IgG binds to the PF4-heparin complex, destroying them and causing thrombocytopenia
  3. compound that were in the platelet are now free to bind to other platelets in circulation
  4. cycle repeats with thrombocytopenia and clotting
19
Q

clinical presentation of HIT

A

thrombocytopenia following the administration of unfractioned heparin

Trousseau syndrome

THrombosis with chronic DIC

Nonbacterial thrombotic endocarditis

THrombosis with ALL treatment and estrogen-like drugs

20
Q

pathology of antiphospholipid syndrome

A

patient procoagulation antibodies target phospholipid-binding proteins that activate platelets and vascular endothelium

21
Q

clinical presentation of antiphospholipid syndrome

A

recurrent thromboses

repeated miscarriages

cardiac valve vegetations

thrombocytopenia

ulceration

pulmonary HTN

infarctions

renovascular HTN

22
Q

Diagnostics of Antiphospholipid Syndrome

A

Prolonged PTT that is not corrected with a mixing study

anticardiolipin antibodies

anti-Beta2 glycoprotein antibodies

lupus anticoagulants

false-positive RPR/VDRL

23
Q

Fates of a thrombus

A

Propagation= accumulation with additional platelets and thrombi

Dissolution= total disappearance via fibrinolysis

Organization and recanalization= ingrowth of endothelial cells, smooth muscle cells and fibroblasts to continue with the original lumen

Embolization= travel to other sites

24
Q

Tyes of emboli

A

systemic thromboemboli

pulmonary embolism

fat/ marrow embolism

air embolism

amniotic fluid emboism

25
Q

what causes systemic thromboemboli and what are the consequences

A

cause: displaced thrombi

intracardiac mural thrombi

aortic aneurysms

atherosclerotic plaques

valve vegetations

paradoxical emboli in the case o ASD/ VSD

26
Q

do systemic thromboemboli prefer the brain or lower extremities

A

lower extremities

27
Q

clinical features of pulmonary emboli

A

Sudden onset dyspnea

Pleuritic chest pain

Tachypnea

Tachycardia

Cough

Hemoptysis

Decreasing level of consciousness

Flank pain

Delirium (in elderly patients)

28
Q

cause of pulmonary emboli

A

DVT travels to right heart and into pulmonary vasculature

OR

paradoxical emboli travel through cardiac defects into systemic arteria circulation

29
Q

consequences of pulmonary emboli

A

cardiovascular collapse

cor pumonale

pulmonary hemorrhage

infarction

pulmonary HTN

sudden hypotension

30
Q

causes of fat/ marrow emboli

A

fractures of long ones

soft tissue trauma

burns

31
Q

pathology/consequences of fat/ marrow emboli

A
  1. ruptured vascular sinusoids in the marrow/ small venules
  2. marrow/ adipose tissue herniates into vascular space
  3. travel to the lunh
32
Q

clinical features of fat/ marrow emboli

A

sudden onset of tachypnea

dyspnea

tachycardia

irritability, restlessness

delirium or coma

diffuse petechial rash due to thrombocytopenia

anemia

Typically 1-3 days post injury

33
Q

pathogenesis of a fat embolism

A

fat globules release free fatty acids inducing local endothelial injury, platelet activation and granulocyte recruitment

34
Q

Air Embolism

  • Pathology
  • Etiology
  • Clinical Presentation
A
  • Pathology: gas bubbles within the circulation obstruct vascular flow, causing ischemic injury
  • Etiology: surgery, laparoscopic procedures, chest wall injury, decompression sickness
  • Clinical Presentation: the chokes and the bends
35
Q

consequences of chronic decompression sickness

A

multiple foci of ischemic necrosis in the femoral heads, tibia and humeri

36
Q

clinical features of amniotic fluid embolism

A

sudden severe dyspnea

cyanosis

Shock

headache to seizures and coma

Pulmonary edema

DIC

37
Q

pathology of amniotic fluid emboli

A

tears in the placental membranes or rupture of uterine veins🡪 infusion of amniotic fluid/fetal tissue into the maternal circulation

38
Q

morphology of amniotic fluid emboli

A
  • squamous cells shed from fetal skin
  • lanugo hair
  • fat from vernix caseosa
  • mucin (derived from the fetal respiratory or gastrointestinal tract in the maternal pulmonary micro­vasculature)

Cardio (10 decks)

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