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Path - Haematology > Haemostasis and Bleeding Disorders > Flashcards

Haemostasis and Bleeding Disorders Flashcards

1
Q

What are procoaguolant factors in Primary and Secondary Haemostasis?

A

Primary: platelets, endothelium, vWF
Secondary: coagulation cascade

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2
Q

What are anticoagulant processes?

A

Fibrinolysis

Inhibition of thrombosis (antithrombin, Protein C/S, TFIP)

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3
Q

What are the THREE simultaneous responses to vessel injury?

A

VASOCONSTRICTION - to prevent excess blood loss
PLATELET ACTIVATION - primary haemostasis
COAG CASCADE - secondary haemostasis

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4
Q

What are the two key functions of endothelium?

A

BARRIER - prevent exposure of pro coag sub endothelial structures to blood

SYNTHESIS - of prostaglandins, vWF, plasminogen activators, thrombomodulin

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5
Q

What occurs following endothelial injury, when subendothelial factors are exposed?

A

Platelet aggregation at site of damage occurs

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6
Q

What cell do platelets derive from?

A

Megakaryocytes

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7
Q

How many platelets can each megakaryocyte produce?

A

4000

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8
Q

How long is the lifespan of a platelet?

A

10 days

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9
Q

How soon before surgery do you need to stop someone on aspirin?

A

7-10 days prior to surgery

This is because aspirin (anti-platelet drug) has effect for about 10 days, until platelets are able to regenerate

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10
Q

Explain the 5 stages of primary haemostasis

A
  1. Endothelial injury
  2. Exposure - damaged endothelial cells expose sub endothelial collagen and release vWF, which binds to the collagen
  3. Adhesion - platelets bind to vWF through GP1b protein
  4. Activation - platelet is activated, releases ADP and thromboxane A2, expresses GPIIb/IIIa to bind to other platelets
  5. Aggregation - GPiib/IIIa is used to bind to other platelets
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11
Q

What do damaged endothelial cells produce and release?

A

von Willenbrand Factor

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12
Q

What binds to vWF?

A

PLATELETS bind to vWF through GPIb protein

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13
Q

What surface glycoprotein to platelets use to aggregate?

A

GpIIb/IIIa

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14
Q

What is the function of the open canalicular system on platelets?

A

To massively expand platelet SA

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15
Q

What chemicals do platelets produce top attract more platelets?

A

Thromboxane A2

ADP

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16
Q

What molecule other than platelets binds to GlpIIb/IIIa?

A

Fibrinogen

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17
Q

How does ASPIRIN work?

A

It irreversibly inhibits COX enzyme

COX is necessary to convert Arachidonic Acid to Thromboxane A2 > platelet formation

Thereby aspirin inhibits platelet formation

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18
Q

What do NSAIDS do to COX?

A

REVERSIBLY inhibit COX

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19
Q

What is the rate limiting step in Secondary Haemostasis?

A

Fibrin formation

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20
Q

Explain the extrinsic pathway

A 
Factor 7a binds to Tissue Factor
This complex activates F10a
F10a activates F5a (COMMON PATHWAY)
F10a+F5a = prothrombinase complex 
They cleave prothrombin into thrombin (small amount)
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21
Q

What are the functions of thrombin?

A

(Platelets
Co-factors
Fibrin
FXIII)

Activates Platelets
Activates co-factors FV, FVIII (and FIX) > THROMBIN BURST
Converts fibrinogen to FIBRIN
Cleaves FXIII to FXIIIa (forms cross links between fibrin clot, strengthening it=

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22
Q

What occurs in the propagation stage of the clotting cascade?

A

F5,8,9 generate thrombin burst
High amount of thrombin converts fibrinogen to fibrin
This enables the formation of a fibrin clot

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23
Q

What is the intrinsic pathway? Explain

A 
Collagen + platelets activate FXIIa
FXIIa activates FXIa
FXIa activates FIX
FIXa + FVIIa activates F10
Then common pathway
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24
Q

Where are clotting factors produced in the body?

A

in the LIVER

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25
Q

What ion do some factors require?

A

CALCIUM

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26
Q

Which factors require Vitamin K for production?

A

F2, 7, 9, 10

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27
Q

Where / how do we make or find Vitamin K?

A

In green leafy vegetables

Produced by Gut Bacteria

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28
Q

What kind of medications can reduce Vitamin K?

A

Warfarin

Antibiotics (as they alter gut flora)

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29
Q

What is anticoagulation?

A

Process that occurs during primary/secondary haemostasis to regulate clot formation (keeps it from becoming too large/prevents emboli)

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30
Q

What is fibrinolysis?

A

Degradation of clot mesh once endothelial injury has resolved

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31
Q

Through which 3 processes does anticoagulation work?

A
  1. Thrombomodulin-ProteinC-ProteinS
  2. Antithrombin
  3. NO, prostacyclin
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32
Q

Explain Thrombomodulin-ProteinC-ProteinS action

A

Thrombomodulin is the protein found on healthy endothelial cells
Thrombomodulin binds to Protein C and Protein S to form Active Protein C complex

Active protein C breaks down F5/F8 to slow down coagulation

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33
Q

Explain Antithrombin action

A

Antithrombin binds to thrombin OR to F10 (prevents thrombin formation)

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34
Q

What drug augments antithrombin?

A

Heparin

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35
Q

Explain how NO and prostacyclin cause anticoagulation

A

They decrease thromboxane A2

Thereby there is less platelet aggregation

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36
Q

Explain fibrinolysis process

A

Endothelial cell is now healthy, and produces tPA
tPA converts plasminogen to plasmin
Plasmin cuts up the fibrin

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37
Q

Which other molecule can also convert plasminogen to plasmin?

A

UROKINASE

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38
Q

What occurs in mutated F5?

A

Factor 5 leiden
This means there is protein C resistance
So there is a prothrombotic state

39
Q

What does tissue factor pathway inhibition block?

A

TFPI blocks F7

40
Q

When does TFPI occur?

A

Physiologically, after the activation of F7

As F7 is only needed temporarily to activate the rest of the intrinsic pathway, then it can be switched off

41
Q

How can we split causes of excessive bleeding?

A

Genetic

Acquired

42
Q

What are genetic causes of excessive bleeding ?

A

Platelet abnormalities
Endothelial wall abnormalities
Clotting factor abnormalities
Excessive clot breakdown

43
Q

What are acquired causes of excessive bleeding?

A 
liver disease 
Vit K deficiency
AI disease 
Trauma 
Anticoagulant / anti platelet
44
Q

What are sites of bleeding in primary haemostasis disorders?

A 
Skin 
Mucous membranes (epistaxis, gum, vaginal, GI tract)
45
Q

What kind of bruising occurs in primary haemostasis disorders?

A

Petechiae, purpura

Small, superficial bleeding

46
Q

What is the timing of bleeding in primary haemostasis disorders?

A

Immediate

47
Q

What are the sites of bleeding in secondary haemostasis disorders?

A

Soft tissues
Joints
Muscles (deep)
e.g. haemoarthroses

48
Q

What is the timing of bleeding in secondary haemostasis disorders?

A

Slow, delayed

49
Q

What kind of bruising occurs in secondary haemostasis disorders?

A

deep

Large bleeds

50
Q

Below what platelet count is treatment required always?

A

Below 30 x10^9

51
Q

Why must we always perform microscopy in thrombocytopenia?

A

To confirm true thrombocytopenia
To exclude pseudothrombocytopoenia from ETPA
To investigate rare conditions eg Grey Platelet syndrome

52
Q

What does typical anti platelet therapy comprise of?

A

DUAL therapy

e.g. aspirin + clopidogrel

53
Q

How does clopidogrel work?

A

Block ADP binding
> no GLPIIb/IIIa activation
> no platelet aggregation

54
Q

How are causes of thrombocytopenia categorised?

A

Immune mediated

Non-immune mediated

55
Q

Immune mediated causes of thrombocytopoena

A 
Idiopathic 
Drug induced
Connective tissue disease (RA, SLE)
Lymphoprolif disease 
Sarcoidosis
56
Q

What are drugs that can cause thrombocytopenia?

A

Quinine (malaria)
Rifampicin (TB)
vancomycin

57
Q

What are non-immune mediated causes of thrombocytopoenia’

A

DIC

MAHA

58
Q

What is the pathogenesis of ITP^

A

Antiplatelet antibodies circulate in the blood
Platelets become sensitised to antibodies (as antibodies tag them)
Platelets get destroyed by macrophages

59
Q

What are the two types of ITP?

A

Acute vs chronic

60
Q

Who does acute ITP occur in? How long does it take to resolve?

A

Children

2-6 weeks

61
Q

Who does chronic ITP occur in? How long does it take to resol ve?

A

Adults

Never resolves, need treatment, indolent

62
Q

How do u stratify risk and thereby tx of ITP?

A

Based on platelet count

63
Q

How do u treat ITP if platelet count <20000

A

Steroids regardless of bleeding status

If bleeding, also IVIG

64
Q

What does IVIG do?

A

It competes with anti-platelet antibodies

65
Q

What is an important feature of petechiae in ITP?

A

They DO NOT blanche

66
Q

What does Vitamin B12 deficiency present as on blood film?

A

Megaloblastic anaemia

So large RBC, as DNA synthesis is impaired and cell cycle cannot progress

67
Q

What are examples of INHERITED coagulation factors disorders? (disorders of secondary haemostasis)

A

Haemophilia A, B
vWD
Other factor deficiencies

68
Q

What are examples of ACQUIRED coagulation factors disorders? (disorders of secondary haemostasis)

A

Liver disease
Vitamin K deficiency
Warfarin
DIC

69
Q

What is the cause of haemophilia?

A

congenital deficiency of F8,9

70
Q

How is haemophilia carried across generations?

A

X linked

71
Q

What clotting test will be prolonged for haemophilia?

A

APTT

72
Q

What are clinical features of haemophilia?

A

Haemarthroses
Soft tissue haematoma
Other sites of bleeding
Prolonged bleeding following surgery

73
Q

How is vWD carried across generations?

A

Autosomal DOMINANT

74
Q

What is the classical clinical feature of vWD?

A

mucocutaneous bleeding

75
Q

How do you classify vWD?

A

Type 1,2,3

76
Q

What is T1 vWD?

A

partial qualitative deficiency = LOW vWF

77
Q

What is T2 vWD?

A

qualitative deficiency = NON-FUNCTIONING vWF

78
Q

What is T3 vWD?

A

total qualitative deficiency = NO vWF

79
Q

What are sources of vitamin K?

A

Green vegetables

Synthesis by bacterial flora

80
Q

What is vitamin K soluble in?

A

FAT soluble

81
Q

What factors and proteins is vitamin K required to synthesise?

A

Factors 2,7,9,10

Proteins C, S, Z

82
Q

What are common causes of vitamin K deficiency?

A

Malnutrition
Biliary obstruction (reduces absorption of VitK)
Malabsorption
Antibiotic therapy (kills gut flora)

83
Q

How do you treat Vitamin K deficiency?

A

Vitamin K replacement

FFP

84
Q

What is DIC?

A

Activation of both coagulation and fibrinolysis

85
Q

What can trigger DIC?

A

TOM VIS

Trauma, toxins 
Obstetric complications 
Malignancy 
Vascular disorder 
Immune disorder (allergic reaction, incompatible blood transfusion, transplant rejection) 
Sepsis (common in children)
86
Q

What two simultaneous clinical occurrences occur in DIC?

A

Thrombosis

Bleeding

87
Q

What is tx for DIC?

A

TREAT UNDERLYING DISORDER
Anticoagulation with heparin
Platelet transfusion
FFP

88
Q

What ways does liver disease cause bleeding disorders?

A 
Decreased clotting factor synthesis 
Dietary Vitamin K deficiency 
Dysfibrinohenaemia 
Enhanced haemolysis 
DIC 
Thrombocutopoenia
89
Q

How do you treat low fibrinogen?

A

Cryoprecipitate

90
Q

How do you monitor warfarin?

A

INR

91
Q

What is the target INR values you want

A
  1. 5 if 1st episode of DVT/PE, AF

3. 5 if recurrent DVT/PE, mechanical prosthetic valve

92
Q

What do you do in the different cases of raised INR?

A

INR 5-8, no bleeding: withhold few doses, reduce maintainance, restart when INR<5

INR 5-8, minor bleeding: stop warfarin, vit K slow IV

INR > 8, no bleed/minor bleeding: stop warfarin, vit K

INF >8, bleeding: stop warfarin, give PCC (or FFP if PCC unavailable) + vit K

93
Q

What components in the blood drop in pregnancy?

A

Hb, Htc
Platelets
F11, Prot S

94
Q

what should you be offered if you. are OVER 60 YEARS OLD and have IDIOPATHIC THROMBOEMBOLIC DISEAASE?

A

Offer. Ct scan to look for underlying cause of clotting e.g. malignancy

Path - Haematology (17 decks)

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