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2A week 2 - coagulation and bone marrow disease > blood coagulation and anticoagulation > Flashcards

blood coagulation and anticoagulation Flashcards

1
Q

what is haemostasis

A

the mechanism that leads to cessation of bleeding from a blood vessel - blood coagulates to allow for healing of vessel

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2
Q

haemostasis process pathway

A

injury -> vasoconstriction to reduce blood loss from damaged vessel -> platelet plug forms -> fibrin mesh forms due to activation of clotting system on platelet surface ->clot dissolusion (via plasmin)

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3
Q

what keeps the blood in its non-coagulated form

A

the endothelium

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4
Q

what molecule is important in the make up of the subendothelium

A

collagen

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5
Q

what activates the coagulation system

A

damage to the endothelium which results in exposure of the subendothelium (incl, collagen and other CT proteins) which activated the coagulation cascase (hageman factor XII)

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6
Q

what changes happen to the platelets post vasoconstriction (during clot formation)

A

inactive -> active;
non-sticky -> sticky, resulting in aggregation to form a platelet mass which will plug the hole

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7
Q

what do active clotting factors act as (2)

A

as anchors between platelets and collagen, and between the platelets themselves

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8
Q

function of the Von Willebrand factor (pathway)

A

binds to collagen -> platelets can then bind to VWF though surface receptors -> platelet activation occurs -> platelet undergo shape change to maximise their SA:V ratio -> promotes aggregation -> amplified to a level which will fill the hole

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9
Q

what granules are found in the platelet (2)

A

dense granules - ADP (nucleotides), Ca2+, 5-HT (seratonin);
alpha granules - fibrinogen, FV, vWF

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10
Q

what does release of the the platelet granules cause

A
  1. promotes platelet activation + aggregation;
  2. recruits other clotting factors (e.g. Thromboxane A2, 5-HT, ADP) to the area of injury;
  3. activation of the clotting cascade + generation of fibrin to stabilise the plug;
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11
Q

what do aspirin and clopidogrel inhibit

A

aspirin - thromboxane A2;
clopi - ADP (via P2Y12)

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12
Q

what is the most common congenital inherited bleeding disorder

A

von Willebrand disease

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13
Q

presentation of vW disease

A

mucosal haemorrhage; bleeding at times of trauma/surgery; menorrhagia (heavy periods); nose bleeds

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14
Q

what is secondary haemostasis

A

stabilisation of the platelet plug

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15
Q

what causes inactive blood clotting factors to activate

A

phospholipid on the surface of the platelets

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16
Q

what is fibrin

A

an insoluble protein that is produced in response to bleeding and is the major component of the blood clot - long strands are generate and act like glue, giving the platelet mass strength

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17
Q

what is the purpose of fibrin generation

A

LOCALISED production to produce a stable haemostatic plug

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18
Q

what is the clotting cascade (draw out)

A

see osmosis/lecture

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19
Q

intrinsic system clotting pathway factors and why is it known as intrinsic

A

XII -> XI -> IX –(VIII)–> X (common)

all the factors circulate inside the blood vessels in their inactive form

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20
Q

extrinsic system pathway factors

A

VII + tissue factor (III) -> VIIa:TF -> X

TF comes from outside the blood vessels (=> extrinsic)

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21
Q

what kind of process is the coagulation cascade

A

amplification

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22
Q

where does the coagulation cascade take place

A

phospholipid surface generate by the platelets

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23
Q

congential disorders of secondary haemostasis

A

Haemophilia A (boys with low levels of factor VIII); Hameophilia B (boys with low levels of factor IX)

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24
Q

presentation of haemophliia A/B (4)

A

bleeding into joints + soft tissues; ‘target’ joint bleeds (due to weaking on that joint/muscle surrounding) ; bleed into retroperitoneum; bleeding at times of trauma/surgery

varying bleeding presentation which depends on levels of factor 8/9 present

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25
Q

acquired disorders of secondary haemophilia

A

warfarin side effects (2,7,9,10); liver disease (liver produces clotting factors)

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26
Q

what are the 3 endogenous anticoagulants circulating the blood

A

antithrombin; protein C; protein S

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27
Q

what does antithrombin inhibit (4)

A

factors Xa, IXa, XIa, thrombin

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28
Q

what do protein C/S inhibit

A

factor V

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29
Q

what does a deficiency in one of the endogenous anti-coagulating factors cause

A

shift in equilibrium towards clotting

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30
Q

what breaks down the clot flormed

A

plasmin (product of plasminogen)

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31
Q

fibrin degredagtion pathway

A

fibrin –(plasmin)–> fibrin degredation products, FDPs (D-dimers)

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32
Q

what does a test for D-dimer indicate

A

the likelihood someone has had a clot in the venous system

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33
Q

how is a blood sample kept in its anticoagulated state

A

put into a tube with an anticoagulant in it -> citrate

34
Q

serum vs plasma and what tests is serum used for

A

serum does not have coagulation proteins present as they been used to for the blood clot -> used for biochemitsry investigations (Na+, K+, creatine etc.)

35
Q

anticoagulant vs serum bottle colours in hospitals

A

blue - anticoag; yellow - serum

36
Q

what do the lab coagulation tests measure

A

the time it takes to generate a fibrin clot - activator must be added to cancel the anticoagulating effects of citrate, different activators target particular pathwyas (good for info about where the defect exists)

37
Q

3 commonly used lab coagulation tests

A
  1. prothrombin time;
  2. activated partial thrombooplstin time (APTT);
  3. thrombin time
38
Q

what does the prothrombin time assess

A

the extrinsic pathway (play tennis (PT) outside -> extrinsic)

39
Q

how is prothrombin time measured

A

thrmoboplastin + Ca2+ put into test tube as an activator -> clock started -> time taken to form clot measured (light detector used as in unclotted form the liquid is more transparent)

40
Q

lack of what factors can increase prothrombin time

A

2, 7, 9, 10 (i.e. what warfarin targets); usually factor 7

41
Q

what does the APTT measure

A

the intrinsic system (8, 9, 11, 12) - play table tennis (TT) inside -> intrinsic

42
Q

what activators are used in APTT

A

contact factor, Ca2+, phospholipid

43
Q

what conditions will result in prolonged APTT

A

Hameophilia A (>35s); vWF; DIC;

44
Q

what deficiency picked up by APTT is not associated with a bleeding phenotype

A

factor 12

45
Q

what can cause and artificially long APTT

A

proteins interfering with the reaction e.g antiphospholipid

46
Q

does a prolonged APTT always indicate an increased risk of bleeding

A

no - factor 12 deficiceny and interfering proteins can also cause prolonged APTT

47
Q

what does thrombin time measure

A

fibrinogen -> fibrin (thrombin is the activator)

48
Q

what is thrombin time abnormal in (5)

A

low fibrinogen states; heparin; trauma; factor 1 deficiency; dabigatran

49
Q

3 causes of hypercoagulability

A
  1. too many cells - increased platelets/rbcs;
  2. deficency of natural anticoagulants - e.g. due to drugs or congenital;
  3. coagulation of factor abnormalities - facto V leiden variant, prothrombin gene variant
50
Q

what occurs in factor V leiden variant

A

factor V becomes resisitant to inactivation by protein C

51
Q

4 causes for bleeding disorders

A
  1. vascular - inherited (haemorrhagic telangictasia, CTDs) or acquired (steroids, scurvy, amyloid, senile purpura);
  2. von willebran disease;
  3. platetles - low: inherited (rare), acquired (ITP, bone marrow failure, drugs); platelet abnormalities: inherited, acquired (drugs e.g. clopi, uraemia);
  4. coagulation cascade problems - inherited (haemophilia A/B), acquired (drugs, liver disease, DIC, massive blood loss)
52
Q

what is thrombotic thrumbocyotpenic purpura

A

a rare condition in which absent ADAMTS13 leads to ulta larger multimers of vWF which cause thrombosis in the the microcirculation -> leads to ischaemia in critical organs

53
Q

classic pentade of thrombotic thrumbocyotpenic purpura

A
  1. fever;
  2. microangiopathic haemolytic anaemia;
  3. renal impariment;
  4. fluctuation neurological signs (clots in brain microcirculation);
  5. thrombocytopenia (all the platelets are being consumed and so production can’t keep up)
54
Q

blood film of thrombotic thrumbocyotpenic purpura

A

“cheese-wired” RBCs (by fibrin strands inside the rbcs cutting them in half) - no longer round

55
Q

thrombotic thrumbocyotpenic purpura maagement

A

haematological EMERGENCY - ask for senior help, treatment to remove plasma which has the large multimers and replace it with plasma from the lab (plasma exchange)

56
Q

6 common indications for anticoag prescription

A
  1. prevention of stroke in AF;
  2. treatment of DVT/PE;
  3. prevention of recurrent venous thrombiembolis;
  4. preventio of valvular themobosis/embolism in metallic heart vavles;
  5. treatment of acute coronary syndrome;
  6. thromboprophylaxis
57
Q

what are the 3 types of anticoagulant drugs

A
  1. reduce clotting factors - prevent liver synthesis e.g warfarin;
  2. inhibit clotting factors indirectly e.g. heparins, fondaparinux;
  3. directly inhibit clotting factors - usually factor Xa e.g. apixaban, revaroxaban etc. or thrombin inhibitors e.g. dabigatran
58
Q

warfarin MOA

A

competitively antagonises vit K (necessary for production of factors 2,7,9,10) stops the conversion of vit K epoxide back into vit K and so further synthesis cannot take place

59
Q

vit K coagulation metabolism pathway

A

precursors for factors 2,7,9,10 –(vit K)–> completed factors 2,7,9,10 + Vit K epoxide (must be reduced back to vit K to allow for cycle to repeat)

60
Q

what is INR

A

PT patient/ PT control

61
Q

what is used for warfarin monitoring

A

yellow book which documents:
1. the pt’s target INR;
2. their last INR reading;
3. their current does of warfarin;
4. when their next INR test is due

62
Q

usual INR target

A

2.5

63
Q

when is a high INR target indicated

A

pts with a clotting tendacny?

64
Q

5 reasons why INR can fluctuate

A
  1. individual variation/genetic;
  2. drugs interacting w warfarin (incl alcohol);
  3. diet (vit K content);
  4. intercurrent illness;
  5. mistakes (elderly, visually impaired etc.)
65
Q

what are the 2 main types of heparin

A

unfractionated heparin (rarely used); LMWH

66
Q

why can heparins not be given orally

A

destroyed by gastric acid

67
Q

unfractionated heparin MOA

A

increased the anticoagulant effect of the endogenous anticoag - antithrombin

68
Q

when is unfractionated heparin used

A

when anticoag is required with a rapid onset and offset action (short half life)

69
Q

side effects of heparin

A

bleeding; heparin induced thrombocytopenia (HIIT) - immune reaction

70
Q

UH vs LMWH

A

LMWH - more targeted effect on coagulation system, mostly focuses on anti-Xa

71
Q

can APTT be used to assess heparin effects

A

yes for UH, no for LMWH

72
Q

2 main targets of DOACs

A

factor Xa inhibiton, thrombin inhibition

73
Q

what usually decide what anti-coagulation is given

A

time of onset - rapid (thrombosis treatment), slow onset (long term prevention)

74
Q

what is used to treat VTEs

A

LMWH and warfarin - both rapid and slow onset; DOACs may be used now

75
Q

durations of giving anticoag post VTE (4)

A

1st calf vein thrombosis - 6wks;
1st provoked VTE - 3 months;
1st unprovoked VTE - 3-6 months (may be indefinate);
2nd VTE - consider lifelong

76
Q

6 risk factors for bleeding on anticoagulants

A

minor skin brusing; epistaxis; GI haemorrahe; muscle haematoma; haemturia; intracranial haemorrage

77
Q

what can be given to reverse warfarin

A

vit K (slow) + prothrombin complec concentrate (PCC)

78
Q

what can be done to stop bleeding due to DOAC

A

stopping the drug - short half life so should be fine within 12hrs; tranexamic acid; idaracuzimab; PCC

79
Q

What are the clotting test results in DIC (PT,APTT etc)

A

Increased PT, APTT

80
Q

What does the presence of howl-jolly bodies indicate

A

Spleen not functioning - meant to remove them

2A week 2 - coagulation and bone marrow disease (8 decks)

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