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MED4 ACP > Bleeding, thrombosis, and transfusion > Flashcards

Bleeding, thrombosis, and transfusion Flashcards

1
Q

Life span of platelets

A

7 to 10 days

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2
Q

Normal platelet count

A

150 to 400 ⨉ 10^9 /L

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3
Q

Receptors on platelets for adhesion to collagen and platelet aggregation

A

glycoprotein (GP) receptors

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4
Q

3 Steps in primary haemostasis

A

platelet adhesion, platelet activation, platelet aggregation

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5
Q

How do platelets adhere to endothelium?

A

direct adhesion / indirect adhesion through von Willebrand factors (vWF)

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6
Q

Coagulation pathway

A

Extrinsic pathway: TF + 7 –> + 10. Intrinsic pathway: 2 –> + 5, 8, 11; 11 –> + 9; 9 + 8 –> + 10; 10 + 5 –> + 2; Common pathway: 2 –> + 1; 13 –> stabilise 1

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7
Q

What is TFPI?

A

Tissue factor pathway inhibitor, which inhibits TF-VIIa complex in extrinsic pathway

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8
Q

Which clotting factors are vitamin K dependent?

A

2,7,9,10

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9
Q

4 natural anticoagulants and their actions

A

TFPI –> inhibit TF-VIIa complex in extrinsic pathway; Protein C –> degrade factors 5a, 8a; Protein S –> enhance protein C activity; antithrombin –> suicidal inhibitor of thrombin and factor 10a

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10
Q

Fibrinolysis pathway

A

plasmin digests fibrin polymers, TPA activates plasminogen, PAI inhibits TPA

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11
Q

What is spurious thrombocytopenia?

A

falsely low platelet count due to platelet clumps by EDTA / automated blood analyser

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12
Q

Coagulation profile and the respective pathway being assessed

A

PT (extrinsic pathway), APTT (intrinsic pathway), TT (fibrinogen)

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13
Q

INR formula

A

(PT(test) / PT(normal))^ISI

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14
Q

Reason for increased PT only

A

deficiency / inhibitor of factor 7

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15
Q

Reasons for increased APTT only (3)

A
  • deficiency / inhibitor of 8,9,11
  • lupus anticoagulant
  • heparin
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16
Q

Reasons for increased PT and APTT (4)

A
  • deficiency / inhibitor of 2,5,10
  • multiple factor deficiency
  • fibrinogen deficiency / disorder
  • heparin
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17
Q

Reasons for increased PT, APTT, TT but decreased PLT

A

DIC, acute liver failure

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18
Q

Method and interpretations of mixing test

A

Method: mixing patient sample with normal plasma –> measure clotting time
Results: reduced time –> factor deficiency; unchanged time –> factor inhibitors

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19
Q

Differentiate petechiae, purpura and ecchymosis

A

petechiae (<3mm), purpura (3~10mm), ecchymosis (>10mm)

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20
Q

Differentiate presentations between platelet disorders and coagulopathy

A

Site, presence of petechiae (platelet), presence of ecchymosis / purpura (coagulopathy), bleeding after cuts (platelet), bleeding after surgery (immediate vs delayed)

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21
Q

Indications for platelet transfusion

A

PLT <10

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22
Q

Contraindications of platelet transfusion (4)

A

ITP, SLE, TTP, HUS

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23
Q

Indications for FFP transfusion (2)

A

TTP, reversal of warfarin overdose

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24
Q

Indications for cryoprecipitate transfusion (3)

A

vWD, fibrinogen deficiency, factor 13 deficiency

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25
Q

Mechanism of DDAVP

A

increase release of vWF from endothelium

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26
Q

Haematological indications (2) and side effects (3) of DDAVP

A

indications: vWD, mild haemophilia A; side effects: water retension, flushing, headache

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27
Q

What is Novoseven and its indications?

A

recombinant FVIIa. Indications: haemophilia, factor 7 deficiency

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28
Q

Mechanism of action of Tranexamic acid

A

inhibit conversion of plasminogen to plasmin to reduce fibrinolysis

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29
Q

MC cause of isolated thrombocytopenia

A

ITP

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30
Q

Pathogenesis of ITP

A

autoAb coats platelets –> destroyed in spleen; autoAb coats megakaryotes –> destroyed prematurely in BM

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31
Q

Diagnosis of ITP

A

exclusion of secondary causes

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32
Q

Treatment of ITP: first line (2) and second line (2)

A

First line: steroid, IVIG; Second line: TPO mimetics, splenectomy

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33
Q

TPO mimetics (2)

A

Eltrombopag, Romiplostim

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34
Q

Pathogenesis of drug-induced thrombocytopenia purpura

A

drugs bind to GP-R of platelets –> recognised by IgG

(For heparin, IC is formed, and platelets could be activated and cause thrombosis)

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35
Q

Treatment of drug-induced thrombocytopenia purpura

A

stop offending drugs, platelets

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36
Q

Aetiology of DIC (5)

A

Obstetrics, Malignancy, Infection, Trauma, HSR

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37
Q

Pathogenesis of DIC

A

pathologically increase thrombin –> widespread intravascular consumption of platelets, clotting factors, fibrin –> bleeding

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38
Q

Blood test results in DIC (6)

A

↑ PT, APTT, TT; ↓ Plt; ↑ D-dimer, ↓ fibrinogen

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39
Q

What is D-dimer?

A

degradation products of cross-linked fibrin plugs

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40
Q

Management of DIC

A

treat underlying cause, supportive: platelets, FFP, cryoprecipitate

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41
Q

Pathogenesis of TTP

A

lack of ADAMTS13 –> ↑ vWF –> thrombi formation

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42
Q

Presentations in TTP (5)

A

(FAT RN) Fever, MAHA, Thrombocytopenia, Renal impairment, Neurological symptoms

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43
Q

Management of TTP

A

FFP

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44
Q

Pathogenesis of HUS

A

E. coli O157:H7 –> produce verotoxin that destroy endothelial wall –> platelet aggregation [esp. renal vessels]

45
Q

vWD screening tests (3)

A

vWD antigen, vWD:RCo (ristocetin cofactor), Factor VIII activity

46
Q

Management of vWD

A

cryoprecipitate, DDAVP

47
Q

Haemophilia hereditary pattern

A

XR

48
Q

Types of haemophilia

A

A (factor VIII deficiency), B (factor IX deficiency)

49
Q

Severity levels of haemophilia (3)

A

6~30%: mild (bleeding after surgery / trauma), 1~5%: moderate (bleeding with mild injury), <1%: severe (spontaneous bleeding)

50
Q

Management of haemophilia (3)

A

factor concentrates replacement, Novoseven, DDAVP (type A only)

51
Q

Virchow’s triad (3+6+3)

A

(1) Stasis (immobility, venous insufficiency, obesity); (2) Hypercoagulability (malignancy, pregnancy, oestrogen, dehydration, myeloproliferative diseases, APS) ; (3) Endothelial injury (surgery, trauma, indwelling catheter)

52
Q

What is antiphospholipid syndrome (APS)?

A

autoimmune hypercoagulable state caused by antiphospholipid antibodies

53
Q

Presentations of APS

A

recurrent arterial / venous thrombosis, recurrent miscarriage

54
Q

Antiphospholipid antibodies (3)

A

lupus anticoagulant, anti-Cardiolipin Ab, anti-β2-glycoprotein-1 Ab

55
Q

Management of APS

A

warfarin (INR: 2.5~3.5)

56
Q

Homan sign

A

pain illicited by forceful leg dorsiflexion –> indicate DVT

57
Q

Presentations of DVT

A

LL swellling and tenderness, pitting oedema, superfical vein dilatation, Homan sign

58
Q

Diagnosis of DVT (3)

A

Doppler USG, Contrast venogram, D-dimer

59
Q

What will be observed in Doppler USG of a DVT patient?

A

no phasic pattern

60
Q

PE aetiology

A

venous thromboembolism (MC), right ventricular thrombus, paradoxical embolism, septic emboli…

61
Q

Presentations of PE (3)

A

acute breathlessness, haemoptypsis, chest pain

62
Q

Risk stratification system for PE to determine the need for CT pulmonary angiogram

A

Wells score

63
Q

Investigations for PE (3)

A

D-dimer, CT pulmonary angiogram, ventilation perfusion scan (obsolete)

64
Q

Compare UFH and LMWH

A

UFH: anti-platelet effect, IV, monitor by APTT, ok for pregnancy, renal impaired patients; LMWH: more anti-Xa effect, SC, monitor by FXa assay, fewer side effects

65
Q

Mechanism of Warfarin

A

inhibit of vitamin K epoxide reductase –> ↓ reduced vitamin K –> - γ-glutamyl carboxylase —> cannot activate clotting factors 2,7,9,10 —> - clotting factors 2,7,9,10

66
Q

Target INR for Warfarin intake in (1) DVT, PE, AF; (2) Mechanical heart valves; (3) recurrent VTE

A

(1) 2.5; (2) 2.5~3.5; (3) 3.5

67
Q

DDI of Warfarin (3)

A

99% albumin binding; NSAIDs, aspirin –> ↑ bleeding risk; antibiotics –> ↑ efficacy

68
Q

Warfarin overdose management (4)

A

withhold warfarin, vitamin K, FFP, prothrombin complex concentrate (PCC)

69
Q

Reversal agent for dabigatran

A

Idarucizumab (“DA”bigatran) 依達露茲

70
Q

Fibrinolytic agents (2)

A

r-TPA, streptokinase

71
Q

Transfusion triangle for correct patient identification

A

Patient wristbnad, Request form, Sample tube

72
Q

Type of variance of blood group antigens and examples (3)

A

whole molecule (RhD); single monosaccharide (ABO); single AA

73
Q

2 types of blood group antigens (class, examples)

A

naturally occurring (IgM, anti-A anti-B) v.s. immune-related (IgG, anti-D, develop after exposure)

74
Q

Pathogenesis of haemolytic disease of newborn (HDN)

A

in a RhD- mother, labour / prenatal bleeding for a RhD+ fetus will sensitise the mother to produce anti-D IgM –> on subsequent pregnancy, exposure to fetal RhD+ will produce anti-D IgG, which attacks red cells in fetus

75
Q

Pre-transfusion compatibility testing (3)

A

Blood typing (forward / cell –> reverse / serum) –> Antibody screening –> Cross-matching

76
Q

Which blood product requires continuous agitation during storage?

A

Platelets

77
Q

Storage temperature and shelf life of blood products (6)

A

Storage temperature: whole blood & red cells 2~6°C, platelets & leukocytes 20~24°C, FFP & cryoprecipitate -30°C
Shelf life: whole blood 35 days, red cells 42 days, leukocytes 1 day, platelets 5 days, FFP & cryoprecipitate 1 year

78
Q

Which blood product should be given for children to replenish blood loss?

A

Plasma methylene blue treated

79
Q

Transfusion: adverse event definition

A

an undesirable and unintended occurrence

80
Q

Transfusion: error definition

A

deviation from standard procedure

81
Q

Transfusion: near miss definition

A

error that is discovered before the start of transfusion

82
Q

Transfusion: incident definition

A

error that leads to mis-transfusion

83
Q

Transfusion: adverse reaction definition

A

undesirable response in a patient

84
Q

Adverse transfusion reaction: Severity versus Imputability

A

4 grades (non-severe to death) to 5 levels (excluded to definite)

85
Q

Acute transfusion reactions definition

A

adverse reactions within 24 hours of transfusion

86
Q

Acute management before blood results come back in acute transfusion reaction (5)

A
  1. Stop transfusion immediately –> save the blood units & blood giving set for investigation
  2. Use a new giving set and keep vein open with normal saline
  3. Clerical check for compatibility between recipient and blood units given
  4. Maintain blood pressure with IV colloid solutions
  5. Monitor urine output, give diuretics to maintain adequate urine output
87
Q

Aetiology of acute transverse reactions (6)

A
  1. Allergic transfusion reaction
  2. NFHTR
  3. Septic reaction
  4. AHTR
  5. TRALI
  6. TACO
88
Q

Management of allergic transfusion reaction (2)

A

IV chlorpheniramine, IV steroids

89
Q

Pathogenesis and management of FNHTR

A

(Febrile non-haemolytic transfusion reaction)
Pathogenesis: recipient Ab –> + donor leukocytes –> release cytokines
Management: paracetamol (restrat infusion of the same unit if mild)

90
Q

MC blood product that causes septic reaction

A

platelets

91
Q

Management of septic reaction

A

septic workup, IV Tazocin, report to blood bank

92
Q

Major vs minor blood group incompatibility

A

Major: recipient Ab attack donor RBCs
Minor: Donor Ab attack recipient RBCs

93
Q

Pathogenesis of AHTR

A

IgM recognise foreign blood group Ags –> complement activation that forms MAC –> intravascular haemolysis

complement –> endothelial damage –> DIC

94
Q

Management of AHTR

A

fluid resuscitation + monitor electrolytes

95
Q

Pathogenesis and presentations (2) of TRALI

A

Pathogenesis: donor Abs –> attack recipient’s lungs
Presentations: respiratory distress, fever

96
Q

Presentations of TACO (2)

A

volume overload, respiratory distress

97
Q

Aetiology of delayed transfusion reactions (5)

A
  1. Delayed haemolytic transfusion reactions
  2. Post-transfusion pupura
  3. Transfusion-associated graft-versus-host disease
  4. Transfusion-transmitted infection
  5. Transfusion-related haemosiderosis
98
Q

Pathogenesis and presentations of delayed haemolytic transfusion reactions

A

patient Abs destroy donor RBCs
failure to respond adequately to transfusion

99
Q

Pathogenesis of post-transfusion purpura

A

patient Abs –> destroy donor platelets –> destroy own platelets via collateral damages

100
Q

Pathogenesis of transfusion-associated graft-versus-host disease

A

donor T cells –> attack recipient BM

101
Q

Alternatives to transfusion (3+3)

A

Pharmacological: oral iron, EPO, anti-fibrinolytics
Autologous blood transfusion: predeposit autologous blood, intraoperative cell salvage, postoperative cell slavage

102
Q

3 pillars of patient blood management

A
  1. Optimise red cell mass
  2. Minimise blood loss
  3. Manage tolerance to anaemia
103
Q

2 Aims of patient blood management

A
  1. Improve patient outcomes
  2. Reduce demands for blood products
104
Q

Restrictive transfusion strategies definition

A

transfusion of the right number of units of blood to the right patient at the right time, in the right conditions, and according to appropriate guidelines

105
Q

What is Evans syndrome?

A

autoimmune thrombocytopenia (ITP + AIHA)

106
Q

Difficulties in compatibility testing in patients with AIHA

A
  • recipient autoAb may react with normal RBCs —> FP
  • recipient autoAb may mask RBC alloAb
107
Q

Mechanism of action of heparin

A

+ anti-thrombin III –> - factor IIa, Xa

108
Q

Antidote for heparin

A

Protamine

109
Q

How does PE lead to death?

A

obstructive shock –> Right heart failure
hypoxia / respiratory failure

MED4 ACP (13 decks)

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