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Year 3 - Haematology (DP) > Haemostasis + Bleeding Disorders > Flashcards

Haemostasis + Bleeding Disorders Flashcards

1
Q

What are the results of hypoperfusion?

A 
Systemic acidosis (pH <7.35)
Microcapillary thrombus:
- Patchy tissue injury
- Large vessel thrombus -> Organ infarction
Eventual cellular necrosis
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2
Q

How might shock be recognised initially?

A 
Mottling
GCS <15:
- Confusion
- Agitation
Urine output <0.5ml/kg/hr
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3
Q

How is shock confirmed?

A

Lactate levels:

  • > 2mmol/L is arguably diagnostic
  • > 4mmol/L results in significant mortality
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4
Q

What is cardiogenic shock?

A

Reduced force of contraction and reduced stroke volume
Results in:
- Reduced CO
- Reduced MAP

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5
Q

How can compensation occur in cardiogenic shock?

A

Increased SVR:

- Cool, clammy peripheries

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6
Q

What are some causes of cardiogenic shock?

A 
Arrhythmia
Poisoning
MI
Cardiomyopathy
Valve failure
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7
Q

What clinical signs might be seen in obstructive shock?

A

Increased JVP

Distended neck veins

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8
Q

What are some causes of obstructive shock?

A

Cardiac tamponade
Tension pneumothorax
Pulmonary embolus

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9
Q

How does hypovolaemic shock come about?

A

Reduced blood volume
Reduced venous return (reduced EDV)
Reduced force of contraction and CO

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10
Q

What is Class I of blood volume loss?

A

<15% (<750ml)

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11
Q

What is Class II of blood volume loss?

A

<30% (<1500ml)

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12
Q

What is Class III of blood volume loss?

A

<40% (<2000ml)

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13
Q

What is Class IV of blood volume loss?

A

> 40% (>2000ml)

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14
Q

What is the pathogenesis of distributive shock?

A

Reduced SVR due to vasodilation:
- Warm, red peripheries
Reduced MAP
Compensatory increase in CO

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15
Q

What can cause distributive shock?

A 
Inflammation:
- Sepsis
- SIRS
- Anaphylaxis
Neurogenic:
- Spinal cord damage
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16
Q

What are the three categories of aetiologies for causes of platelet plug formation failure?

A 
Vascular abnormalities
Platelets:
- Thrombocytopaenia
- Reduced function
von Willebrand factor
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17
Q

What hereditary vascular abnormalities can cause a failure of platelet plug formation?

A 
Haemorrhagic telangiectasia (Osler-Weber-Rendu)
CTDs:
- Ehlers-Danlos
- Marfan's
- Osteogenesis imperfecta
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18
Q

What acquired vascular abnormalities can cause a failure of platelet plug formation?

A 
Vasculitis:
- HSP
- Rheumatic disorders
Severe infections (Meningococcus, Measles, Typhoid)
Drugs:
- Steroids
- Sulfonamides
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19
Q

What acquired disorders result in reduced platelet formation (thrombocytopaenia)?

A 
General bone marrow failure
MDS
Myeloma
Solid tumour infiltration
Aplastic anaemia
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20
Q

What acquired disorders result in increased platelet destruction/sequestration?

A

Coagulopathy (DIC)
Autoimmune (ITP)
Hypersplenism
TTP

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21
Q

What are some examples of acquired platelet function defects?

A 
MPDs
Renal and liver disease
Paraproteinaemias
Drugs:
- Aspirin
- NSAIDs
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22
Q

What is an acquired cause of vWF deficiency?

A

Thrombocythaemia:

- vWF sequestration

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23
Q

What are some hereditary causes of vWF deficiency?

A

Autosomal dominant:

  • Most common factor deficiency
  • Usually mild (but variable)
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24
Q

What causes failure of fibrin clot formation?

A

Multiple clotting factor deficiencies:
- Usually acquired (eg. DIC)
Single clotting factor deficiency:
- Usually hereditary (eg. Haemophilia)

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25
Q

What can cause multiple factor deficiencies?

A 
Liver failure
Vit. K deficiency/Warfarin therapy
Complex coagulopathy (DIC)
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26
Q

How do multiple factor deficiencies affect clotting assays?

A

Prolonged:

  • PT
  • APTT
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27
Q

Where are coagulation factors synthesised?

A

Hepatocytes

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28
Q

What factors are carboxylated by Vit. K?

A

II
VII
IX
X

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29
Q

Where is Vit. K absorbed?

A

Upper intestine

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30
Q

What does Vit. K require for absorption?

A

Bile salts

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31
Q

What can cause a Vit. K deficiency?

A 
Poor dietary intake
Malabsorption
Obstructive jaundice
Warfarin
Haemorrhagic Disease of the Newborn
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32
Q

What does clotting factor consumption in DIC cause?

A

Bruising
Purpura
Generalised bleeding

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33
Q

What can cause DIC?

A

Sepsis
Obstetric emergencies
Malignancy
Hypovolaemic shock

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34
Q

How is haemophilia inherited?

A

X-linked

35
Q

What is Haemophilia A?

A

Factor VIII deficiency

36
Q

What is Haemophilia B?

A

Factor IX deficiency

37
Q

What type of Haemophilia is more common?

A

A (by 5x)

38
Q

What vessels bleed in Haemophilia?

A

Medium-large

39
Q

What are the clinical features of Haemophilias?

A 
Recurrent haemarthrosis
Recurrent soft tissue bleeds (bruising in toddlers)
Prolonged bleeding after:
- Dental extractions
- Surgery
- Invasive procedures
40
Q

How does haemophilia affect clotting assays?

A

Isolated prolonged APTT

41
Q

What is an arterial thrombus rich in?

A

Platelets

42
Q

How is an arterial thrombus treated?

A

Aspirin (and other anti-platelets)

Modify risk factors for atherosclerosis

43
Q

What is a venous thrombus rich in?

A

Fibrin

44
Q

How is a venous thrombus treated?

A

Heparin
Warfarin
New oral anticoagulants

45
Q

What is the most common hereditary thrombophilia? What is its pathophysiology?

A

Factor V Leiden:

- Reduced activated protein C degradation of Factor V

46
Q

What are some other causes of hereditary thrombophilia?

A

Prothrombin 20210 mutation
Antithrombin deficiency
Protein C or S deficiency

47
Q

How does antiphospholipid syndrome affect clotting assays?

A

APTT prolonged

48
Q

When an atherosclerotic plaque ruptures, what do platelets adhere to?

A

Released vWF

Exposed endothelial collagem

49
Q

What do platelets release when activated?

A

ADP

Thromboxane A2

50
Q

How do platelets aggregate?

A

Attach to each other via:

  • GbIIb/IIIa
  • Fibrinogen
51
Q

Why do platelets alter shape on activation?

A

To expose more phospholipid

52
Q

Via what receptors do platelets become activated?

A

ADP

53
Q

How does aspirin work?

A

Inhibits cyclooxygenase:

  • Reduced Thromboxane A2 production
  • Reduced aggregation and activation
54
Q

What are the side effects of aspirin?

A

Bleeding
Blocks prostaglandin production:
- GI ulcers
- Bronchospasm

55
Q

How do ADP receptor antagonists work?

A

Bind irreversibly to P2Y12 subtype

56
Q

What are some examples of ADP receptor antagonists?

A

Clopidogrel

Prasugrel

57
Q

How does Dipyridamole work?

A

Phosphodiesterase inhibitor:

- Reduces cAMP production

58
Q

What type of drug is Abciximab? How does it work?

A

GPIIb/IIIA inhibitor:

- Inhibits aggregation

59
Q

When should anti-platelets be stopped before elective surgery and why?

A

7 days
They have a 7-10 day lifespan:
- Drug affects them for their entire lifespan

60
Q

How does heparin work?

A

Potentiates antithrombin (III):

  • Inhibits thrombin (IIa)
  • Inhibits Xa
61
Q

How is heparin administered?

A

IV

S/C

62
Q

Why do LMWHs only inhibit factor Xa?

A

To inhibit thrombin (IIa), heparin must bind to antithrombin (III) AND thrombin (IIa)
LMWHs are too small:
- Can only bind factor Xa
- Cannot bind both III and IIa

63
Q

How is unfractionated heparin monitored?

A

APTT

64
Q

How are LMWHs monitored?

A

Anti-Xa assay

65
Q

When may LMWH monitoring be used?

A

Renal failure

66
Q

What is heparin induced thrombocytopaenia/with thrombosis?

A

> 50% drop in platelets:

- Usually >=5 days of therapy

67
Q

What long term complication can arise with heparin therapy?

A

Osteoporosis

68
Q

How can heparin be reversed?

A 
STOP IT (short half-life)
Protamine sulphate IV:
- Reverses AT III
- Complete reversal for unfractionated heparin
- Partial reversal for LMWH
69
Q

When is phenindone used?

A

If resistant/intolerable of warfarin

70
Q

Where is warfarin absorbed?

A

Upper intestine (requires bile salts)

71
Q

Why is the carboxylation if factors II, VII, IX and X important?

A

Both -COOH groups are required for the factors binding, via calcium ions, to phospholipid
Without both groups:
- Bond too weak
- Inefficient coagulation

72
Q

When is initial dosing of warfarin slow?

A

AF
Liver disease
Malnourished
Elderly

73
Q

What is the first typical dose of warfarin?

A

10mg dose at 6pm on day 1

74
Q

How is warfarin maintained?

A

INR daily for first 5 days:

Take warfarin at same time every day

75
Q

What is the target INR?

A

2-3

  1. 5 (3-4) in recurrent VTE
  2. 5-3.5 if mechanical heart valves
76
Q

How is INR calculated?

A

(Patient’s PT in secs/Mean normal PT in secs)^ISI

77
Q

How can warfarin be reversed?

A 
Stop warfarin
Administer oral Vitamin K
Administer clotting factors:
- FFP or
- Factor concentrates
78
Q

How does Dabigatran work?

A

Oral direct thrombin inhibitor

79
Q

How can Dabigatran be reversed?

A

Idracizumab

80
Q

What drugs are examples of oral direct Factor Xa inhibitors?

A

Rivaroxaban

Apixaban

81
Q

When are newer oral anticoagulants used?

A

Prophylaxis in elective hip +/or knee replacements (instead of LMWH)
Stroke prevention in AF for some
Treatment of DVT/PE

82
Q

What is primary haemostasis?

A

Formation of platelet plug

83
Q

What is secondary haemostasis?

A

Formation of fibrin clot

84
Q

What are the consequences of the failure of platelet plug formation?

A 
Spontaneous bleeding and purpura
Mucosal bleeding:
- Epistaxis
- GI
- Conjunctival
- Menorrhagia
Intracranial haemorrhage
Retinal haemorrhage

Year 3 - Haematology (DP) (3 decks)

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