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Haematology > Blood coagulation + anticoagulants > Flashcards

Blood coagulation + anticoagulants Flashcards

1
Q

Define haemostasis

A

arrest of bleeding

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2
Q

What dies a hypercoagulable state lead to?

A

thrombosis

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3
Q

What does reduced coagulation lead to?

A

bleeding disorders

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4
Q

Describe the process of haemostasis

A

Tissue injury
vasoconstriction (limits blood flow to injured region)
formation of platelet plug
thrombus (clot) formation
formation of fibrin mesh to stabilise thrombus
clot dissolution –> through action of plasmin

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5
Q

What are the 3 main steps in formation of a platelet plug?

A

adhesion
activation
aggregation

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6
Q

Describe in detail the formation of a platelet plug

A

plasma proteins circulate in blood –> activated on exposure to collagen
von willebrand factor binds to collagen
platelets bind to von villebrand factor through surface receptors
platelets change shape –> increase SA:V ratio –> promotes aggregation to each other + von willebrand factor
platelet-platelet interaction via fibrinogen

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7
Q

Describe the presentation of von Willebrand disease

A

usual pattern = mucosal haemorrhage:
- bleeding at times of trauma/surgery
- menorrhagia
- nose bleeds

varies according to amount of vWF

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8
Q

What is secondary haemostasis?

A

stabilisation of platelet plug

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9
Q

Describe secondary haemostasis

A

fibrin acts like glue –> gives platelet mass strength
allows it to function as a secure patch + protects base to allow repair + healing

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10
Q

What is the purpose of blood coagulation?

A

produce stable haemostatic plug via localised fibrin clot formation at site of vessel injury

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11
Q

Describe the mechanism of blood coagulation

A

enzymatic cascade: series of coagulation proteins sequentially activated + amplified which results in a fibrin clot

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12
Q

What are congenital disorders of secondary haemostasis

A

decreased levels of clotting factors

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13
Q

What factor is deficient in Haemophilia A?

A

factor 8

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14
Q

What factor is deficient in Haemophilia B?

A

factor 9

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15
Q

Key symptoms of Haemophilia A/B

A

joint/soft tissue bleeding:
- bleeds into ‘target’ joints
- bleeds into retroperitoneum
- bleeding at times of trauma/surgery

varies according to amount of factor 8/9

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16
Q

What are 2 acquired disorders of secondary haemostasis

A

warfarin
liver disease

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17
Q

Warfarin mechanism of action

A

Vitamin K antagonists

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18
Q

What are the Vitamin K dependent clotting factors?

A

10
9
7
2
(1972)

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19
Q

What stops coagulation process from forming thrombi throughout circulation?

A

coagulation inhibitors:
- antithrombin
- protein C
- protein S

fibrinolysis:
- breakdown of fibrin clot by plasmin

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20
Q

Name 3 coagulation tests

A

prothrombin time
activated partial thromboplastin time
thrombin time

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21
Q

Describe prothrombin time

A

activators = thromboplastin (source of tissue factor) and calcium
INR derived from PT
time until fibrin formation occurs is measures
extrinsic ( + common) pathway

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22
Q

What does INR stand for?

A

International Normalised Ratio

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23
Q

Describe APTT

A

activated partial thromboplastin time
activators = contact factor, calcium + phospholipid
time until fibrin formation occurs is measured
antiphospholipid interferes with test
intrinsic (+common) pathway

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24
Q

Describe thrombin time

A

activator = thrombin
specifically measures conversion time of fibrinogen to fibrin

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25
Q

What can cause an abnormal PT?

A

liver disease
warfarin
DIC

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26
Q

What can cause abnormal APTT?

A

haemophilia A/B
DIC
lupus anticoagulant

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27
Q

What can cause abnormal TT?

A

low fibrinogen states

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28
Q

What can cause both PT and APTT to be prolonged?

A

DIC
DOAC treatment
warfarin overdose
severe vitamin K deficiency

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29
Q

3 key causes of thrombosis (too much coagulation)

A

too many cells:
- increased platelets/RBCs

deficiency of natural anticoagulants:
- protein C
- protein S
- Antithrombin

other coagulation factor abnormalities:
- Factor 5 Leiden variant
- prothrombin gene variant (elevated levels of prothrombin)

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30
Q

4 key causes of bleeding disorders

A

problems with blood vessel wall
problems with von Willebrand factor
problems with platelets
problems with coagulation factor cascade

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31
Q

Describe causes of low platelets

A

inherited (rare)
acquired:
- immune (ITP, TTP)
- bone marrow failure
- drugs

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32
Q

Acquired problems with the coagulation cascade

A

drugs eg. warfarin, heparin, DOACs
severe liver disease
disseminated intravascular coagulation (DIC)
massive blood loss

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33
Q

Describe TTP

A

thrombotic thrombocytopenic purpura
absent ADAMTS13 (due to an antibody), leads to large von willebrand factors multimers which bind platelets in the microcirculation
microthrombi and consumption of platelets
ischaemia in critical organs

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34
Q

What is the TTP classical pentad?

A

fever
microangiopathic haemolytic anaemia (MAHA)
renal impairment
fluctuating neurological signs
thrombocytopenia

(haematological emergency)

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35
Q

6 common indications for anticoagulant therapy

A

prevention of stroke in AF
treatment of DVT/PE (VTE)
prevention of recurrent (VTE)
prevention of valvular thrombosis/embolism in metallic heart valves
treatment of acute coronary syndrome
thromboprophylaxis

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36
Q

Which anticoagulant drugs work by reducing clotting factors?

A

Coumarins eg. warfarin, phenindione

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37
Q

Which anticoagulant drugs work by indirectly inhibiting clotting factors?

A

Heparins:
- unfractioned (UFH)
- low molecular weight heparin (LMWH)

Fondaparinux
Danaparoid

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38
Q

Which anticoagulant drugs work by directly inhibiting clotting factors?

A

Direct oral anticoagulants (DOACs):
- factor Xa inhibitors = apixaban, rivaroxaban, edoxaban
- thrombin inhibitors = dabigatran

  • parenteral thrombin inhibitors eg. argatroban, bivalirudin
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39
Q

INR calculation

A

INR = (PT patient/PT control)

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40
Q

How is warfarin monitored?

A

regular monitoring needed
yellow book (has target INR, last INR reading, date of last test, current dose, when next test due)
International normalised ratio (INR)
target = 2.5 (2-3) = standard
incidence of haemorrhage associated with INR but can occur in target range

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41
Q

What factors affect INR?

A

individual variation/genetic
drugs (including alcohol) can potentiate warfarin effects (check INR within 5 days of stopping/starting new drug)
diet (eg. vitamin K content)
intercurrent illness
mistake (dosage, eg. elderly, visually impaired - comes in 3 different coloured tablets of different strengths)

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42
Q

How are heparins administered and why are they administered this way?

A

IV or SC
destroyed by gastric acid so oral administration not possible

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43
Q

Describe unfractionated heparin

A

mixture of different weight heparin molecules
potentiates antithrombin
prolongs APTT
immediate onset of action
large variability between people
short half-life in plasma (30-120 mins)

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44
Q

What is the reversal agent of unfractionated heparin?

A

protamine

45
Q

Potential side effect of unfractionated heparin

A

heparin induced thrombocytopenia (HIT)

46
Q

Clinical uses of unfractionated heparin

A

when rapid onset/offset of action needed
examples:
- initial treatment VTE
- anticoagulant ‘bridging therapy’ to cover surgery in high thrombotic risk patients

47
Q

Describe low molecular weight heparin

A

low molecular weight fragments only
majority of effect is anti Xa (indirectly through antithrombin)
variable effect on APTT (may be normal - APTT cannot be used to assess LMWH effect)
immediate onset
monitoring not required
treatment dose based on weight
renally excreted
longer plasma half-life than UFH
lower risk of HIT
not easily reversed

48
Q

What monitoring is required for heparins?

A

LMWH = monitoring not needed unless severe renal failure or extremes of body weight (can use anti Xa level)

UFH = APTT ratio (target 2.0) every 6 hours until stable

49
Q

Describe fondaparinux

A

synthetic
effect mediated by antithrombin (only inhibits factor Xa, does not prolong APTT)
immediate onset of action + very long half-life
no monitoring required
renally excreted
SC injection
no reversal agent
infrequently used

50
Q

Clinical uses of Fondaparinux

A

treatment of VTE
treatment of acute coronary syndrome
thromboprophylaxis

51
Q

What are the 2 types of DOACs?

A

factor Xa inhibitors
thrombin inhibitors

52
Q

Describe DOACs

A

oral administration
rapid onset
no monitoring required
part renal, part hepatic metabolism

53
Q

DOACs clinical uses

A

prevention of stroke in AF
treatment of VTE (DVT + PE)
thromboprophylaxis

54
Q

Examples of bleeding on anticoagulants

A

minor skin bruising
epistaxis
GI haemorrhage
muscle haematoma
haematuria
intracranial haemorrhage

55
Q

What factors increase risk of major bleeding on anticoagulants?

A

elderly
renal failure
liver failure
recurrent falls
concurrent antiplatelet/NSAID use
alcoholism
cancer

56
Q

Management of warfarin overanticoagulation/bleeding

A

stop warfarin

If bleeding or INR>8 need to reverse:
- Vitamin K
- prothrombin complex concentrate if major bleeding

57
Q

How does prothrombin complex concentrate work?

A

immediately reverses warfarin effect by replacing clotting factors (give with vitamin K)

58
Q

Management of heparin overanticoagulation/bleeding

A

stop heparin (short half-life, may be sufficient)
local measures eg. apply pressure
consider tranexamic acid
if bleeding consider protamine sulphate

59
Q

Management of DOAC overanticoagulation/bleeding

A

stop DOAC (short half-life, may be sufficient)
local measures eg. apply pressure
consider tranexamic acid
Idarucixumab = reversal of dabigatran
antidote to Xa inhibitors not available, life threatening bleeding = consider prothrombin complex concentrate

60
Q

What anticoagulant would you give to a 72 year old man with hypertension + AF?

A

warfarin/DOAC

61
Q

What anticoagulant would you give to a 23 year old woman with a post-surgical DVT?

A

warfarin/DOAC/LMWH
warfarin/DOAC only if definitely not pregnant

62
Q

What anticoagulant would you give to a 74 year old man with peripheral arterial disease?

A

clopidogrel
needs an antiplatelet not an anticoagulant

63
Q

What anticoagulant would you give to a 43 year old woman with a mechanical heart valve?

A

warfarin

64
Q

What anticoagulant would you give to a woman in her 2nd pregnancy who had a postpartum PE with her 1st baby?

A

LMWH
do not give DOAC/warfarin in pregnancy

65
Q

Which anticoagulants cannot be given in pregnancy?

A

DOAC
Warfarin

66
Q

If a woman needs anticoagulating during pregnancy, which anticoagulant would be given the day before a C-section?

A

Unfractionated heparin (UFH)
shorter half-life so can still clot during C-section
given as a continuous drip so can be easily stopped before

67
Q

What drugs would be given to a 45 year old man who has had a coronary artery stent after a heart attack?

A

aspirin + clopidogrel
2 antiplatelets for 1st year then down to 1 for life

68
Q

Name the 4 vitamin K-dependent clotting factors

A

X
IX
VII
II

69
Q

Aspirin mechanism of action

A

inhibits cyclooxygenase enzyme (COX)
affects prostaglandin synthesis via arachidonic acid pathway

70
Q

What drug does clopidogrel interact with?

A

omeprazole

71
Q

Clopidogrel mechanism of action

A

binds to PTY12 receptors on platelets and prevents ADP binding preventing platelet aggregation

72
Q

What scoring system is used to asses for DVT?

A

Wells score

73
Q

Describe coagulation screen findings in DIC

A

prolonged APTT
prolonged PT
decreased fibrinogen

(clotting factors being used up)

74
Q

What does HUS stand for and what can cause it?

A

haemolytic uraemic syndrome
bacterial infection eg. E.Coli

75
Q

Which factors can affect APTT?

A

8, 9, 11, 12
(von Willebrand as associated with factor 8)

76
Q

What causes Haemophilia C?

A

factor XI (11) deficiency

77
Q

What can cause an isolated prolonged APTT?

A

von Willebrand’s disease
Haemophilia A/B/C
antiphospholipid syndrome (interferes with phospholipid in test –> patient actually has increased thrombosis risk)

78
Q

Mechanism of action of tranexamic acid

A

antifibrinolytic (prevents clot breakdown)

79
Q

Von Willebrand’s disease treatment

A

tranexamic acid
desmopressin
vWF concentrate if severe

80
Q

What medications are given in venous vs arterial thrombotic events?

A

venous = anticoagulation
arterial = antiplatelets

81
Q

State Virchow’s triad for DVT risk factors

A

stasis
hypercoagulability of blood
vessel wall damage

82
Q

How long does it take vitamin K to work?

A

6 hours

83
Q

Where are clotting factors made?

A

liver

84
Q

Inheritance patterns of rare factor deficiencies

A

autosomal recessive

(consanguinity increases risk)

85
Q

List some common medication errors

A

wrong patient
contraindicated medicines
wrong dose/frequency
wrong administration route
poor administration techniques
paediatric doses (age + size of child is important)

86
Q

Why do you need to be particularly careful with chemotherapy prescribing?

A

narrow therapeutic index
very toxic
patient specific dosage (BSA - body surface area)
complex multi-drug regimens
multiple day dosing
variable cycle lengths

87
Q

Why are multi-drug regimens used for chemotherapy?

A

reduce resistance
drugs have different mechanisms of action and so can target different stages of the cell cycle

88
Q

Common indications for anticoagulation

A

AF/stroke prevention
DVT/PE prevention and treatment
mural thrombus
mechanical aortic and mitral valve
arterial thrombosis
antiphospholipid syndrome
cardiomyopathy

89
Q

List 3 Vitamin K antagonists

A

warfarin
acenocoumarol
phenindione

90
Q

List 4 DOACs

A

rivaroxaban
apixaban
edoxaban
dabigatran

91
Q

List 3 parenteral anticoagulants

A

UFH
LMWH
Fondaparinux

92
Q

What is HAS-BLED score and what does each letter stand for?

A

score to guide the decision to start anticoagulation in patients with AF
1 point for each letter (each bleeding risk factor)

Hypertension
Abnormal renal/liver function
previous Stroke
Bleeding history/predisposition
Labile INRs
Elderly
Drugs/alcohol excess

> 3 = high risk of bleeding, caution and regular review of patient required

93
Q

When should INR be checked after starting warfarin?

A

after 4-7 days

94
Q

Which antibiotics are at high risk of interfering with warfarin?

A

trimethoprim
sulfamethoxazole
metronidazole
ciprofloxacin
levofloxacin
azithromycin
clarithromycin

95
Q

Drugs likely to increase INR

A

(increase bleeding risk)
allopurinol
ketoconazole
omeprazole
amiodarone
tamoxifen
metronidazole
erythromycin
alcohol
fluconazole

96
Q

Drugs likely to reduce INR

A

(increase clot risk)
oral contraceptives
rifampicin
phenytoin
St John’s Wort

97
Q

Can antiplatelets be taken with warfarin?

A

antiplatelet drugs or NSAIDs will increase bleeding risk
review indication for these drugs and stop if possible

98
Q

When should antiplatelet drugs not be stopped?

A

if patient has had a coronary/arterial stent unless advised by cardiologist/vascular surgeon

99
Q

When are heparins used?

A

treatment and prevention of VTE
whilst loading with warfarin
VTE in cancer patients
anticoagulation during pregnancy

100
Q

What monitoring is required on UFH?

A

APTT monitoring/dose adjustments

101
Q

When should LMWH dose be modified?

A

if impaired renal function
eGFR<20L/min

102
Q

When is Fondaparinux contraindicated?

A

eGFR<20L/min
use dalteparin instead

103
Q

2 benefits of DOACs

A

few drug interactions
no routine monitoring

104
Q

When should you avoid all DOACs?

A

if patient taking:
- azole anti-mycotics
- HIV protease inhibitors (eg. ritonavir)

105
Q

When should you avoid apixaban/dabigatran/rivaroxaban?

A

if patient taking ketoconazole or dronedarone

106
Q

When should you avoid dabigatran?

A

if patient taking cyclosporine or tacrolimus

107
Q

When should renal function be checked when a patient is on a DOAC?

A

annually if CrCl >60L/min
6 monthly if CrCl 30-60L/min
3 monthly if CrCl <30L/min

should also be checked during acute illness and DOAC dose may need to be modified

standard clotting screen is unreliable

108
Q

What is Virchow’s triad?

A

3 contributing factors to thrombus formation:
- venous stasis
- vascular injury
- hypercoagulability

Haematology (16 decks)

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