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Pathology > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

components of a thrombus

A
  • fibrin

- platelets

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2
Q

definition of a thrombus

A

a solid mass, formed in the circulation from the constituents of the blood during life

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3
Q

where do atheromas tend to develop?

A

areas of turbulent blood flow

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4
Q

how are white thrombi formed?

A

Platelets adhere to the damaged vascular

endothelium and aggregate in response to ADP and TXA2

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5
Q

what limits the growth of thrombi?

A
  • PGI2

- NO

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6
Q

how does plaque rupture lead to thrombus formation?

A

Plaque rupture leads to the exposure of blood containing factor VIIa to tissue factor within
the plaque, which may trigger blood coagulation and lead to thrombus formation.

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7
Q

main component of a white thrombus

A

platelet

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8
Q

what are red thrombi?

A

these are also known as venous thrombi and contains more fibrin

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9
Q

management of venous thrombi

A

antifibrin like heparin or warfarin

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10
Q

management of arterial thrombi

A

antiplatelet like aspirin

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11
Q

major causes of venous thrombi

A
  • stasis

- hypercoagulability

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12
Q

what is postphlebetic syndrome?

A

Chronic venous
obstruction following thrombosis in the deep veins of the leg frequently results in a
permanently swollen limb and may lead to ulceration

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13
Q

patient factors that are risk factors for VTE

A
  • age
  • high BMI
  • varicose veins
  • frequent/recent continuous travel
  • immobility
  • pregnancy and puerperium
  • thrombophilia
  • oestrogen therapy
  • dysfibrinogenaemia
  • plasminogen deficiency
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14
Q

diseased stated that are risk factors for VTE

A
  • trauma/surgery
  • cardiac/resp failure
  • malignancy
  • recent MI/CVA
  • acute medical illness/severe infection
  • inflammatory bowel disease
  • behcet’s disease
  • nephrotic syndrome
  • myeloproliferative disorders
  • paroxysmal noctural haemoglobinuria
  • paraproteinaemia
  • sickle cell anaemia
  • central venous catheter
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15
Q

who has problems with blood stagnation?

A
  • long distance flights
  • bedridden patients
  • sedentary occupations
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16
Q

problems with coagulability

A
  • clotting factors and natural anticoagulants
  • pregnancy
  • oestrogen therapy/hormone
  • post-inflammation/surgery
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17
Q

what causes endothelial damage?

A
  • trauma
  • fractures
  • cannulation
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18
Q

what’s Virchow’s triad?

A
  • circulatory stasis
  • vascular wall injury
  • hypercoaguable state
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19
Q

risk factors for arterial thrombosis

A
  • HTN
  • DM
  • hypercholesterolaemia
  • smoking
  • hyperlipidaemia
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20
Q

what are the 3 systems involved in clot formation?

A
  • platelets
  • clotting factors
  • endothelium
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21
Q

what are steps does the platelet go through in clotting?

A
  • platelet activation
  • platelet adhesion
  • platelet aggregation
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22
Q

what substances mediate platelet adhesion?

A
  • vWF

- GPIb

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23
Q

what substances change the shape of the platelet?

A
  • ADP
  • Ca
  • serotonin
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24
Q

which substances mediate platelet aggregation?

A
  • GPIIb/IIIa
  • fibrinogen
  • prostacyclin
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25
Q

how many pathways does the clotting cascade have?

A

2; intrinsic and extrinsic

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26
Q

what is the result of the clotting cascade?

A

conversion of fibrinogen into fibrin

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27
Q

what is PT?

A

prothrombin time

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28
Q

another name for PT

A

INR

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29
Q

which pathways does the INR monitor?

A
  • extrinsic

- common

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30
Q

which clotting factors are monitored through the INR?

A
  • 5
  • 7
  • 10
  • prothrombin
  • fibrinogen
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31
Q

normal INR

A

1.0

32
Q

INR for people on warfarin

A

2.0-3.0

33
Q

what does a high INR indicate?

A

bleeding risk

34
Q

what dose a low INR indicate?

A

thrombosis risk

35
Q

which medication can be monitored using APTT?

A

heparin

36
Q

what is APTT?

A

activated prothrombin clotting time

37
Q

which pathways are monitored through APTT?

A
  • intrinsic

- common

38
Q

which factors are monitored through the APTT?

A
  • 5
  • 8
  • 9
  • 10
  • 11
  • 12
  • prothrombin
  • fibrinogen
39
Q

causes of a prolonged APTT

A
  • heparin use
  • antiphospholipid antibody
  • coagulation factor deficiency
  • sepsis
  • presence of antibodies against coagulation factors
40
Q

what is the principle enzyme for haemostasis?

A

thrombin

41
Q

what does thrombin do?

A
  • fibrinogen to fibrin
  • activates V, VIII, XI and XIII
  • activates Protein C, when bound to thrombomodulin
  • activates platelets
  • plasminogen to plasmin (this breaks the clot)
42
Q

what do we use to break down clots?

A

thrombolytics

43
Q

what do protein C and S collectively inhibit?

A

factor V

44
Q

what are people deficient in protein C or S prone to?

A

thrombosis

45
Q

prevention and treatment of arterial thrombosis

A
  • minimise risk factors for thrombosis
  • antiplatelet drugs
  • thrombolytic therapy
46
Q

what are the main antiplatelet drugs?

A
  • aspirin

- clopidogrel

47
Q

what does aspirin bind to?

A

cyclooxygenase, which reduces the platelet production of TXA2

48
Q

what does clopidogrel inhibit?

A

ADP receptor on platelet cell membranes

49
Q

types of thrombolytics

A
  • streptokinase

- plasminogen activators

50
Q

what does streptokinase do?

A
  • binds to plasminogen, activating it to produce more plasmin
  • risk of haemorrhage as indiscriminate of the clots it breaks down
51
Q

example of a plasminogen activator

A

alteplase i.e. TPA

52
Q

which of the thrombolytic drugs are antigenic and thus, can cause allergic reasons?

A

streptokinase

53
Q

what are the 2 types of oral anticoagulants?

A
  • coumarins

- indanediones

54
Q

the most common coumarin used

A

warfarin

55
Q

what does warfarin inhibit?

A

the reductase enzyme which activates Vitamin K, making it impossible to produce factors 2, 7, 9, 10

56
Q

what will be prolonged as warfarin is used?

A
  • PTT (factor 7, 10)

- APTT (factor 9, 10)

57
Q

in which situation should the INR be between 3 and 4?

A
  • recurrent VTE
  • antiphospholipid syndrome
  • mechanical prosthetic heart valve
  • coronary artery graft thrombosis
  • stroke prevention
58
Q

in which situations should the INR be between 2 and 3?

A
  • PE
  • proximal and calf DVT
  • recurrent VTE wo warfarin therapy
  • symptomatic inherited thrombophilia
  • atrial fibrillation
  • cardioversion
  • mural thrombus
  • cardiomyopathy
59
Q

how long should you give warfarin in situations of VTE?

A
  • at least 6w-3m if the cause goes away
  • at least 6m if no cause is found
  • indefinite if no cause is found or if this is persistent
60
Q

contraindications to anticoagulants

A
  • severe uncontrolled hypertension
  • non-thromboembolic strokes
  • peptic ulceration
  • severe liver and renal disease
  • pre-existing haemostatic defects
  • non-compliance
  • pregnancy
61
Q

what happens if the INR is too high?

A
  • depending on the INR level, reduce or stop the warfarin, until the INR is lower than 5
  • if above 8 and the patient is not bleeding, administer Vitamin K
  • if there is a major bleed, stop the warfarin and give a prothrombin complex concentrate
62
Q

what enhances warfarin action?

A
  • alcohol
  • aspirin
  • NSAIDs
63
Q

what decreases warfarin action?

A
  • contraceptive steroids

- vitamin K

64
Q

example of an anti-Xa inhibitor

A
  • rivaroxaban (xarelto) (you do not need monitoring with this)
65
Q

example of an active direct thrombin

A

dabigatran

66
Q

what does heparin bind to?

A

anti-thrombin

67
Q

actions of heparin

A
  • activates anti-thrombin
  • inhibits factor 10
  • mild inhibitor of all factor except 7
68
Q

which clotting screen tests are altered due to heparin?

A
  • PT (prolonged)

- APTT (more prolonged)

69
Q

what is the target ratio for heparin patients?

A

1.5-2.0

70
Q

which drug can be used as an antidote in high dose heparin situations?

A

protamine sulfate

71
Q

why are LMWH heparins used instead of UFH?

A
  • higher bioavailability
  • more potent against factor Xa than IIa (lower risk of bleeding)
  • longer half-life than normal heparin
  • have little effect on the clotting screen
  • less likely to cause HIT
72
Q

what eliminates the LMWH?

A

kidneys

73
Q

administration method of LMWH

A

subcutaneous

74
Q

administration method of UFH

A

IV

75
Q

what complication can happen with heparin?

A
  • bleeding
  • heparin-induced thrombocytopenia
  • osteoporosis
  • hyperkalaemia
76
Q

when does heparin-induced thrombocytopenia happen?

A

5-14 days

77
Q

contraindications of heparin

A
  • bleeding disorders
  • low platelet count
  • HIT
  • peptic ulcer
  • cerebral haemorrhage
  • severe hypertension
  • neurosurgery

Pathology (21 decks)

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