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Case 20 > Theme 3: Haematology > Flashcards

Theme 3: Haematology Flashcards

1
Q

what are the 5 stages of haemostats?

A
  1. vasoconstriction
  2. primary haemostasis
  3. secondary haemostasis
  4. clot retraction and repair
  5. fibrinolysis
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2
Q

what happens when NO production is disrupted by injury to the endothelium?

A

vasoconstriction

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3
Q

what does ADP released from damaged endothelial cells do?

A

ADP acts on platelet P2Y1 and P2Y12 receptors causing platelet activation- they form pseudopodia and release the contents of their granules

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4
Q

where is von willebrand factor found and what does it bind to in primary heamostasis?

A

vWF is found on exposed collagen and binds to glycoprotein 1b on platelets

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5
Q

what platelet glycoprotein does collagen bind directly to?

A

GPVI

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6
Q

what does cyclooxyrgenase-1 (cox-1) released by activated platelets do?

A

converts arachidonic acid to thromboxane A2 which activates more platelets

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7
Q

how do platelets bind to each other?

A

the GPIIb/ GPIIIa molecules on platelets bind to each other via a molecule of fibrin

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8
Q

what is the trigger for the extrinsic pathway of the coagulation cascade?

A

tissue factor

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9
Q

which coagulation factor is involved in the extrinsic pathway?

A

factor VII which then activates factor x in the common pathway

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10
Q

what is the trigger for the intrinsic pathway of the coagulation cascade?

A

negatively charged collagen in the sub-endothelium of blood vessels

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11
Q

which coagulation factors are involved in the intrinsic pathway?

A

twelve, eleven, nine, eight then ten in the common pathway

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12
Q

what activates factor XIII and what is its function?

A

thrombin (factor IIa) activates factor XIII which then stabilises the clot by cross linking fibrin

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13
Q

what is the function of fibrin?

A

fibrin forms a sticky mesh which traps platelets and RBCS into the plug stabilising it

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14
Q

how is plasminogen activated and what does it do?

A

plasminogen is activated to plasmin by tissue plasminogen activator (tPA) and urokinase.
plasmin degrades fibrin into fibrin degradation products (FDP) such as D dimer

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15
Q

how does sodium citrate act as an anticoagulant?

A

sodium citrate binds to calcium which stops the coagulation cascade. its effects can be reversed by adding calcium

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16
Q

which pathway does the prothrombin time measure?

A

the extrinsic pathway

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17
Q

which pathway does the activated partial thromboplastin time measure?

A

the intrinsic pathway

18
Q

what is the INR?

A

the international normalised ratio is a measure derived from PT which allows standardisation of PT so it can be compared between different labs- used to measure the affects of warfarin

19
Q

what is a D dimer test used for?

A

it is used to detect the presence of fibrin clots e.g DVT or PE

20
Q

what are the different categories of platelet disorders?

A

quantitative- to do with platelet number e.g thrombocytopenia/ thombocytosis
qualitative- to do with platelet function. can be hereditary or aquired ( drugs, liver/renal failure)

21
Q

what can cause thrombocytopenia?

A

decreased synthesis- BM failure, aplastic anaemia, leukaemia
increased consumption- infection, disseminated intravascular coagulation
increased destruction- idiopathic thrombocytopenia purpura (ITP), splenomegaly

22
Q

how does glazmans thrombasthenia cause abnormal platelet function?

A

abnormality in GPIIb/IIIa (fibrinogen receptor)- platelets can’t bind to one another

23
Q

how does Bernard-soulier syndrome cause abnormal platelet function?

A

abnormality in GPIb (vWF receptor)- platelets do not bind to the injury site

24
Q

what is the pathogenesis of haemophilia A/B?

A

there is a genetic variant in factor VIII (A) or factor IX (B)

25
Q

what is the pathogenesis of acquired haemophilia?

A

autoantibodies against a coagulation factor (usually factor VIII) are formed
is either idiopathic or associates with malignancy, autoimmune disease or drugs

26
Q

what are the favourable conditions for coagulation?

A

virchows triad:

  • stasis of blood flow- venous stasis, AF
  • endothelial injury- e.g atheroma
  • hypercoagulability
27
Q

what are the symptoms of DVT?

A

pain, swelling, warmth, erythema, shiny skin

28
Q

where is a venous thromboembolism usually lodge?

A

a pulmonary artery- pulmonary embolism

29
Q

what are the signs and symptoms of pulmonary embolism

A

symptoms- breathlessness, chest pain, haemoptysis, syncope

signs- tachycardia, tachypnoea, signs of pleural effusion, signs of right heart strain

30
Q

what can cause hyper coagulability?

A

cancer- especially pancreas, lung, brain, gastric
antiphospholipid syndrome
oestrogen- post-partum, COCP
hereditary thrombophilia
factor V leiden mutation
antithrombin III deficiency
protein C/S deficiency (normally degrade coagulation factors)

31
Q

what can arterial thrombosis cause?

A

myocardial infarction
actue limb ischamia
acute mesenteric (gut) ischaemia
stroke

32
Q

what is the mechanism of action of heparin and low molecular weight heparin?

A

heparin- activates antithrombin III which inhibits thrombin clotting factors IX, Xa and XIII
LMWH- inactivates factor Xa via action of antibrombin III. cannot inactivate thrombin as it is not large enough to bind to ATIII and thrombin at the same time

33
Q

what are the side effects of heparin?

A

bleeding
hypersensitivity
heparin- induced thrombocytopenia

34
Q

what is the clinical use of heparin?

A

treatment of established VTE
prevention of post-operative VTE
used to initiate coagulation therapy until an oral anticoagulant takes effect

35
Q

what is the mechanism of action of warfarin?

A

vitamin K antagonist

inhibits the activation of vitamin K dependant clotting factors (VII, IX, X, II)

36
Q

what is the clinical use of wrafarin?

A

prevent the recurrence or progression of venous thrombosis or PE
prevent arterial thromboembolism in patients with AF or cardiac disease (mechanical heart valves)

37
Q

what is the mechanism of action of rivaroxaban?

A

selective factor Xa inhibitor- binds to and inhibits both free and bound Xa

38
Q

what is the mechanism of action of dibigatran?

A

direct thrombin inhibitor- competitive reversible inhibitor of thrombin

39
Q

what is the mechanism of action of aspirin as an anti-platelet drug?

A

aspirin irreversible inhibits COX-1 and therefore inhibits the synthesis of thromboxane A2 (which promotes platelet aggregation)

40
Q

what is the mechanism of action of altepase?

A

recombinant tissue plasminogen activator- activates the conversion of plasminogen to plasmin which breaks down fibrin and degrades clots

Case 20 (5 decks)

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