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Pathology > Thrombosis, Embolism and Infarction > Flashcards

Thrombosis, Embolism and Infarction Flashcards

1
Q

what is thrombosis

A

pathologic formation of intravascular blood clot

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2
Q

where can thrombi occur

A

in veins or arteries

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3
Q

most commonly thrombi are found in and originate from

A

deep veins of lower extremities (leg)

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4
Q

characteristics of thrombi

A
  • Lines of Zahn (alternating layers of platelets, fibrin and red blood cells)
  • attached to vessel walls
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5
Q

what is Virchow’s Triad of formation

A
  1. Endothelial damage
  2. Alterations in normal blood flow
  3. Hypercoagulability
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6
Q

Normally, thrombosis is prevented bc

A
  • Intact endothelium limits exposure to subendothelial collagen and tissue factor
  • Endothelial cells produce prostacyclin and nitric oxide- inhibit vasodilation and platelet aggregation
  • Endothelial cells produce substances which inhibit thrombin and coagulation factors
  • Secrete tissue plasminogen activator
  • Secrete thrombomodulin
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7
Q

endothelial damage can be defined as

A

any disturbance in dynamic balance of endothelium can lead to thrombosis

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8
Q

physical loss of endothelium leads to

A
  • exposure of subendithelial ECM
  • aggregation of platelets
  • release of TF
  • local depletion of prostaglandins and plasminogen activators
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9
Q

how does endothelial cell dysfunction disturb balance

A

convert procoagulant factors to anticoagulant effectors

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10
Q

name 3 causes of endothelial cell damage

A
  1. atherosclerosis
  2. increased homocysteine levels
  3. vasculitis
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11
Q

normal blood flow is

A

laminar - platelets flow centrally in vessel lumen, separated from endothelium by slower moving plasma

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12
Q

what can cause alteration in blood flow

A
  1. turbulence

2. stasis

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13
Q

what is turbulence

A

countercurrents and pockets of stasis contribute to arterial and cardiac thrombi

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14
Q

what is stasis

A

contributes to venous thrombi (slow moving blood)

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15
Q

ulcerated atherosclerotic plaques cause

A

turbulence and exposure to ECM

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16
Q

aneurysms cause

A

local stasis

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17
Q

myocardial infarctions cause

A

stasis and flow abnormalities

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18
Q

mitral valve stenosis cause

A

left atrial dilation

arterial fibrillation and stasis

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19
Q

hyperviscosity causes

A
  1. polycythemia

2. sickle cell anemia

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20
Q

what is polycythemia

A

small vessel stasis and increased resistance to blood flow

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21
Q

what is sickle cell anemia

A

vascular occlusion

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22
Q

other clinical settings for thrombosis

A
  • arterial aneurysms in myocardial infarction
  • immobilization (causes DVT)
  • trauma, surgery, burns associated with reduced physical activity
  • cardiac failure
  • malignancies associated with tumour-associated tissue thromboplastic release (called migratory trombophlebitis)
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23
Q

hypercoagulability/thrombophilia due to increased

A

procoagulation or defective anticoagulation

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24
Q

inherited forms of hypercoagulability/thrombophilia

A
  • patients present with deep venous thrombosis at young age

- usually veins of leg are involved

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25
Q

name 4 inherited hypergoaulable diseases

A
  1. Factor V Mutation/Leiden mutation
  2. Prothrombin 20210A
  3. Protein C/S deficiency
  4. Antithrombin III deficiency
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26
Q

Factor V Leiden has a mutated form of factor

A

V therefore lack cleave site for deactivation by protein C and S

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27
Q

Factor V Mutation presents in –% of Caucasians

A

2-15%

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28
Q

Factor V mutation is one of the most common reasons for inherited

A

hypercoagulation

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29
Q

do homozygous and heterozygous pts have an increase risk of thrombosis with a factor V mutation

A

homozygous

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30
Q

what happens in pts with heterozygous genes for factor V mutation

A

propensity for thrombosis with other acquired risk factors:

  • pregnancy
  • prolonged best rest
  • long airplane flights
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31
Q

prothrombin 20210A is what type of mutation

A

point mutation in prothrombin - increased gene expression

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32
Q

prothrombin 20210A increases

A

thrombin increases chance of thrombosis

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33
Q

Protein C/S deficiency decreases

A

negative feedback on coagulation cascade

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34
Q

describe Warfarin skin necrosis

A

Protein C/S deficiency causes skin thrombosis at onset of warfrin therapy (normally, warfarin causes temporary deficiency of protein C and S in normal individuals)

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35
Q

the drug warfarin is given to patients with

A

thrombosis

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36
Q

what is heparin

A

an anticoagulant

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37
Q

mechanism of action of heparin

A
  • given to patients to prevent thrombosis

- acts by binding and activating antithrombin III

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38
Q

what happens to patients with antithrombin III deficiency

A

heparin is unable to find to antithrombin III and anticoagulation is not achieved

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39
Q

pts with antithrombin III deficiency is given —- insntead

A

Coumadin

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40
Q

Name 2 acquired hypercoaulable states

A
  1. Heparin induced thrombocytopenia

2. antiphospholipid antibody syndrome/ lupus anticoagulant syndrome

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41
Q

when does heparin induced thrombocytopenia occur

A

following administration of unfractionated heparin

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42
Q

what happens in heparin induced thrombocytopenia

A

induces antibodies which recognize complexes of heparin and platelet factor 4 on the surface of platelets

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43
Q

heparin induced thrombocytopenia can lead to

A

thrombocytopenia

prothrombotic state

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44
Q

what is used instead of unfractionated heparin

A

newer low molecular weight fractionated heparins - less incidence of HIT

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45
Q

see slide 25

A

see slide 25

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46
Q

clinical presentation of Antiphopholipid Antibody Syndrome/ Lupus Anticoagulant syndrome

A
  • recurrent thrombosis
  • repeated miscarriages
  • cardiac valve vegetations
  • thromboytopenia
  • pulmonary embolism
  • bowel infarction
  • renovascular hypertension
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47
Q

mechanism of antiphospholipid antibody syndrome/ lupus anticoagulant syndrome

A
  • auto-antibodies induce a hypercoaguable state mediated by binding to epitopes on prothrombin
  • activating platelets and endothelial injury
48
Q

primary form of antiphospholipid antibody syndrome/ lupus anticoagulant syndrome

A

no autoimmune disorders associated with certain drugs/infections

49
Q

secondary form of antiphospholipid antibody syndrome/ lupus anticoagulant syndrome

A

associated with lupus

50
Q

aggressive form of antiphospholipid antibody syndrome/ lupus anticoagulant syndrome causes

A

widespread small vessel thrombi and multiorgan failure

51
Q

antiphospholipid antibody syndrome/ lupus anticoagulant syndrome causes a false positive for

A

serologic test fr syphillis

52
Q

what are the types of thrombi

A
  1. mural - occur on endocardium; not occlusive
  2. arterial
  3. venous
  4. cardiac
53
Q

arterial and cardiac thrombi develop at sites of

A

turbulence or endothelial injury

54
Q

venous thrombi develop at sites of

A

stasis

55
Q

arterial and venous thrombi can both propagate towards

A

heart - can detach and become emboli

56
Q

DVT occur in what veins

A
  • popliteal
  • femoral
  • iliac
57
Q

LE DVTs associated with

A

stasis and hypercoagulable states

58
Q

predisposing factors of DVT

A

immobilization, congestive heart failure, pregnancy, tumors

59
Q

DVTs can emobolize to

A

lungs and cause pulmonary infarction

60
Q

pulmonary infarction are asymptomatic in –% cases

A

50% (develop collateral channels)

61
Q

arterial thrombi may send fragments (emboli) in

A

systemic circulation

62
Q

which organs are more prone to emboli

A

organs that get more % of cardiac output

ex. brain, kidneys, spleen

63
Q

what is disseminated intravascular coagulation (DIC)

A

-fibrin thrombi in small vessels that cause circulatory insufficiency

64
Q

DIC is a consumptove coagulopathy, meaning

A

there is reduced platelets, fibrinogen, F-VIII and other consumable clotting factors

65
Q

in what patient type is DIC seen in

A
  • obstetric complications
  • advanced malignancy
  • shock
66
Q

DIC is caused by

A

widespread activation of thrombin

67
Q

what organs are affected by DIC

A

brain, heart, kidneys

68
Q

DIC is initially

A

thrombotic, then bleeding (after clotting factors used up)

69
Q

what is an embolus

A

intravascular mass carried away by blood stream to a site remote from its origin

70
Q

emboli may consist of

A
  • blood clots (thromboembolism- most common),
  • atherosclerotic plaques (cholesterol clefts seen)
  • gas / air
  • amniotic fluid
  • fat
  • bone marrow fragments
  • microorganisms
  • tumor cells
71
Q

pulmonary embolism due to

A

thromboemboli

72
Q

name 4 sources of pulmonary thrombi

A
  • Deep saphenous veins
  • Periprostatic venous plexus
  • Uterine venous plexus
  • Right atrium
73
Q

risk factors for pulmonary embolism

A
  • immobility due to recent surgery, injury or obesity
  • hereditary states eg. factor V leiden
  • oral contracepties
  • neoplasms
74
Q

complications of pulmonary embolism

A
  • sudden death (saddle embolus)
  • pulmonary infarct
  • pulmonary hypertenstion
75
Q

pulmonary infarct

A

occlusion of large or medium artery obstructed in compromised lung (eg. pneumonia, congestive heart disease)

76
Q

pulmonary hypertension

A

> 60% obstruction by thrombus and with chronic emboli, increases work of R ventricle

77
Q

systemic thromboembolism usually — emboli

A

arterial

78
Q

systemic thromboembolism cause

A

infarction and gangrene

79
Q

80% of systemic thromboembolism arise from — heart

A

left heart

80
Q

paradoxical emobli

A

-emboli gaining access to systemic circulation through heart defects

81
Q

how does air embolisms form

A

air enters venous circulation

81
Q

how does air embolisms form

A

air enters venous circulation

82
Q

air enters venous circulation through

A
  • neck wounds
  • thoracocentesis
  • puncture of major veins during surgical procedures
  • hemodialysis
82
Q

air enters venous circulation through

A
  • neck wounds
  • thoracocentesis
  • puncture of major veins during surgical procedures
  • hemodialysis
83
Q

gas bubbles within circulation can coalesce to form

A

frothy masses obstructing blood flow

83
Q

gas bubbles within circulation can coalesce to form

A

frothy masses obstructing blood flow

84
Q

decompression sickness affects

A

deep sea scuba divers

84
Q

decompression sickness affects

A

deep sea scuba divers

85
Q

how do you treat acute decompression sickness

A

placing individual in high pressure chamber

85
Q

how do you treat acute decompression sickness

A

placing individual in high pressure chamber

86
Q

mechanisms of fat embolism

A

mechanical obstruction of circulation and endothelial damage caused by fatty acids release from embolizing fat globules

86
Q

what is caissons disease

A

chronic form of decompression sickness

-persistence of gas emboli in skeletal system causing ischemic necrosis of bone

87
Q

clinical symptoms of amniotic emboli

A 
severe dyspnea
cyanosis
hypotensive shock
seizures
coma
88
Q

most common risk factors for fat embolism

A

long bone fracture after accidents or orthopedic procedures

89
Q

clinical consequences of fat embolism

A
  • respiratory failure (tachypnea, dyspnea, tachcardia, petechie)
  • neurologic findings (delirium, coma)
90
Q

when do clinical symptoms of fat embolism appear

A

1-3 days after injury

91
Q

mechanisms of fat embolism

A

mechanical obstruction of circulation and endothelial damage caused by fatty acids release from embolizing fat globules

92
Q

amniotic fluid emboli

A

amniotic fluid enters venous circulation through torn veins in pts having difficult labor or immediate postpartum period

93
Q

clinical symptoms of amniotic emboli

A 
severe dyspnea
cyanosis
hypotensive shock
seizures
coma
94
Q

infarct

A

localized area of dead cells within an organ

95
Q

white infarcts occur in

A

arterial occlusions in solid organs with end-arterial circulation (heart, spleen, kidney)

96
Q

which is more damaging: hypoxia or ischemia

A

ischemia - bc decreased oxygen, nutrients and decreased removal of toxic metabolites

97
Q

causes on infarcts

A
  1. obstruction of vessel

2. hyptension

98
Q

septic infarctions

A

an infarct is converted into an abscess by superimposed infection

99
Q

red (hemorrhagic) infarcts seen with

A
  1. venous occlusions (ovary)
  2. loose tissue (lung)
  3. dual circulations (lung and small intestine) - blood flows form an unobstructed parallel supply into a necrotic zone
  4. sluggish venous outflow
  5. blood flow re-established to site of previous arterial occlusion and necrosis (e.g., following angioplasty of an arterial obstruction)
100
Q

white (anemic) infarcts occur in organs with – blood supply

A

single (ie. heart, spleen)

101
Q

white infarcts occur in

A

arterial occlusions in solid organs with end-arterial circulation (heart, spleen, kidney)

102
Q

most infarcts morphologically show

A

ischemic coagulative necrosis

103
Q

Brain and CNS show what type of infarct

A

liquefactive necrosis

104
Q

septic infarctions

A

an infarct is converted into an abscess by superimposed infection

105
Q

— blood supply helps against infarction

A

alternate (ex. liver, lung)

106
Q

— arterial vascular obstruction causes infarction

A

end (ex. spleen)

107
Q

— developing occlusions less likely to cause infarction

A

slow

108
Q

neurons have irreversible damage in – minutes

A

3-4

109
Q

myocardial cells damage in – minutes

A

20-30

Pathology (18 decks)

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