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Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

what is haemostasis?

A

The arrest of bleeding and the maintenance of vascular patency

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2
Q

what are the components of a normal haemostatic system?

A

Primary Haemstasis - platelet plug
Secondary - fibrin clot
Fibrinolysis
Anticoagulant Defences

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3
Q

what are the three stages of primary haemostasis?

A

Adhesion
Aggregation
Activation

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4
Q

what occurs in the adhesion stage of primary haemostasis?

A

Platelets bind to subendothelial collagen via Glycoprotein 1b and Von Willebrand Factor

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5
Q

what occurs in the aggregation stage of primary haemostasis?

A

Platelets attach to each other via GPIIb/IIIa and fibrinogen.
Activation stage occurs at same time.

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6
Q

what occurs in the activation stage of primary haemostasis?

A

Aggregation stage occurs at the same time
Platelets alter shape to expose phospholipid for coagulation activation and fibrin production.
Granules further stimulate platelet activation/recruitment eg Thrombin,Thromboxane A2 and ADP via receptors. Positive feedback loop as more platelets stick.

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7
Q

what is the role of the additional chemicals in primary haemostasis?

A

ADP attracts more platelets, serotonin is a vasoconstrictor and thromboxane A2 assists in aggregation, vasoconstriction and degranulation.

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8
Q

what is the initial step of secondary hameostasis?

A

platelets release calcium on surface (+ve surface) attracts -ve blood clotting factors
Damage tissue releases TF

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9
Q

what is are the steps in coagulation

A

TF activates VIIa
TF/VIIa then activate V/Xa – which activates prothrombin (factor 2) into thrombin (2a)
2a then activates fibrinogen and also VIII/IXa (and XI/XII)
VIII/Ixa reactivates V/Xa increasing fibrinogen (amplification)

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10
Q

what are the different classifications of causes of primary haemostasis?

A

Vascular (vessel wall)
Platelets
Von Willebrand Factor

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11
Q

What are the causes of vascular related primary haemostasis failure?

A 
hereditary
acquired
	ageing (lose collagen)
	scurvy 
	steroid therapy 
	Vasculitis – Henoch-Schonlein Purpura syndrome
	marfaarns syndrome
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12
Q

What are the causes of platelets related primary haemostasis failure?

A

thrombocytopenia
• reduced production – pancytopenia
• increased destruction, DIC, Autoimmune - Immune thrombocytopenic purpura (ITP), Hypersplenism

Reduced Function - drugs, renal failure

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13
Q

what is the cause of Von Willebrand disease?

A

autosomal dominant

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14
Q

what are the clinical features of primary haemostasis failure?

A
  • Spontaneous Bruising and Purpura
  • Mucosal Bleeding - Epistaxes, GI (mouth), Conjunctival, Menorrhagia
  • Intracranial haemorrhage
  • Retinal haemorrhages
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15
Q

how is primary haemostasis failure diagnosed?

A

platelet counts

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16
Q

what are the different causes of secondary haemostasis failure?

A

single clotting factor deficiency
multiple clotting factor deficiency
increased fibrinolysis

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17
Q

what are the causes of single clotting factor deficiency?

A

Haemophilia

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18
Q

what are the causes of multiple clotting factor deficiency?

A

Usually acquired
Liver failure
Vitamin K Deficiency - poor dietary intake, malabsorption, obstructive jaundice, warfarin therapy, haemorrhagic disease of new-born
Complex coagulopathy
DIC - microthrombus (end organ failure), clotting factor consumption (bruising, purpura, bleeding)

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19
Q

what are the clinical features of Failure of Secondary Haemostasis?

A 
•	No characteristic clinical syndrome
•	May be combined primary/secondary haemostatic failure
•	Pattern of bleeding depends on
o	Single/multiple abnormalities
o	The clotting factors involved
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20
Q

what are the two tests for failure of secondary haemostasis?

A
  • prothrombin time (TF/VIIa) = measures initiation

* Activated partial Thromboplastin Time (VIII/IXa) = amplification

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21
Q

what is thrombophilia?

A

: Familial or acquired disorders of the haemostatic mechanism which are likely to predispose to thrombosis

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22
Q

what are the different mechanisms of thrombophilia?

A

Increased coagulation activity - Platelet plug or Fibrin clot formation
Decreased fibrinolytic activity
Decreased anticoagulant activity - decreased serine protease inhibitors, Protein C and Protein S

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23
Q

what are the clinical features of thrombophilia?

A
  • DVT and PE
  • Recurrent miscarriage
  • Complications of pregnancy
  • Purpura Fulminans (clotting disorder of newborn (give Vit K)
  • Skin necrosis
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24
Q

what are the hereditary causes of thrombophilia?

A
  • Factor V Leiden
  • Prothrombin 20210 mutation
  • Antithrombin deficiency
  • Protein C deficiency
  • Protein S deficiency
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25
Q

what are the features to consider hereditary thrombophilia screening?

A 
o	Venous thrombosis <45 years old
o	Recurrent venous thrombosis
o	Unusual venous thrombosis
o	Family history of venous thrombosis
o	Family history of thrombophilia
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26
Q

what is the management of hereditary thrombophilia?

A
  • Advice on avoiding risk
  • Short term prophylaxis - to prevent thrombotic events during periods of known risk
  • Short term anticoagulation -to treat thrombotic events
  • Long term anticoagulation - recurrent thrombotic events
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27
Q

what is acquired thrombophilia?

A

Antiphospholipid Syndrome

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28
Q

what are the causes of Antiphospholipid Syndrome?

A 
o	Autoimmune Disorders
o	Lymphoproliferative Disorders
o	Viral Infections
o	Drugs
o	Primary
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29
Q

what is the pathophysiology of APS?

A
  • Antibodies cause conformational change in β2 glycoprotein 1 - activates primary and secondary haemostasis and vessel wall abnormalities.
  • Autoantibodies have specificity for anionic phospholipids, can prolong phospholipid dependant coagulation tests in vitro
  • Also known as Lupus anticoagulants
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30
Q

what are the clinical features of APS?

A

Recurrent thromboses - Arterial, including TIAs, Venous
• Recurrent fetal loss
• Mild thrombocytopenia (using up thrombin making clots)

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31
Q

how can APS be diagnosed?

A
  • Prothrombin Time

* APTT

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32
Q

what is the management of APS?

A
  • Activation of both primary and secondary haemostasis
  • management of Arterial and venous thrombosis
  • Aspirin
  • Warfarin
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33
Q

what is the platelet level in TTP?

A

↓↓↓

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34
Q

what is the platelet level in ITP?

A

↓↓↓

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35
Q

what is the platelet level in HIT?

A

↓↓

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36
Q

what is the haemoglobin level in TTP?

A

↓↓

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37
Q

what is the haemoglobin level in ITP?

A

Normal

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38
Q

what is the haemoglobin level in HIT?

A

Normal

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39
Q

what is the LDH level in TTP?

A

↑↑↑

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40
Q

what is the LDH level in ITP?

A

Normal

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41
Q

what is the LDH level in HIT?

A

Normal

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42
Q

what is the indirect bilirubin level in TTP?

A

↑

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43
Q

what is the indirect bilirubin level in ITP?

A

Normal

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44
Q

what is the indirect bilirubin level in HIT?

A

Normal

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45
Q

what is the haptoglobin level in TTP?

A

↓

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46
Q

what is the haptoglobin level in ITP?

A

Normal

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47
Q

what is the haptoglobin level in HIT?

A

Normal

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48
Q

what is the reticulocyte level in TTP?

A

↑

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49
Q

what is the reticulocyte level in ITP?

A

Normal

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50
Q

what is the reticulocyte level in HIT?

A

Normal

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51
Q

what is the schistocyte level in TTP?

A

↑↑↑

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52
Q

what is the schistocyte level in ITP?

A

Normal

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53
Q

what is the schistocyte level in HIT?

A

↑

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54
Q

what is the underlying mechanism of Heparin-Induced Thrombocytopenia (HIT)?

A

Exposure to heparin/LMWH causes IgG autoantibodies to be formed against it

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55
Q

what i the pathophysiology of HIT?

A
  • Exposure to heparin/LMWH → IgG autoantibodies formed against heparin → platelet factor 4 (PF4) binds to heparin →antibody-heparin-PF4 complex →increased platelet activation → thrombosis formation in arteries, veins
  • Increased consumption of platelets for clotting + removal of antibody-heparin-PF4 complexes by macrophages of reticuloendothelial system →thrombocytopenia
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56
Q

what is the severity of Type 1 HIT?

A

Transient, mild, not clinically significant

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57
Q

what is the severity of Type 2 HIT?

A

Complications can be life-threatening

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58
Q

what is the onset of Type 1 HIT?

A

1-4 days after exposure

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59
Q

what is the onset of Type 2 HIT?

A

5-10 days after exposure

60
Q

how is Type 1 HIT mediated?

A

Not antibody mediated; may be caused by heparin-induced platelet aggregation

61
Q

how is Type 2 HIT mediated?

A

Antibody Mediated (IgG)

62
Q

what is the Nadir platelet count in Type 1 HIT?

A

100,000/microL:

63
Q

what is the Nadirplatelet count in Type 2 HIT?

A

60,000/microL

64
Q

what are the causes of HIT?

A

Heparin
- Unfractionated > LMWH
- Prophylactic dose > therapeutic doses > intermittent heparin flushes
Acquired platelet disorder - heparin-induced thrombocytopenia thrombosis (HITT)

65
Q

what are the clinical features of HIT?

A
  • Skin necrosis at injection site
  • Acute systemic reaction after IV heparin bolus = Fever with chills, tachycardia, hypertension, dyspnoea
  • Limb ischemia, organ infarction - kidney, MI, CNS insult,
  • VTE
66
Q

how is HIT diagnosed?

A

HIT antibody testing

67
Q

which antibodies are tested for in HIT?

A

o ELISA for anti-PF4
o Functional assay – Serotonin release assay
o HIPA – heparin induced platelet aggregation

68
Q

what is the management of HIT?

A

Medication - discontinuation of heparin, administration of non-heparin anticoagulant
Surgery – thromboembolectomy

69
Q

what is underlying mechanism of Idiopathic Thrombocytopenic Purpura (ITP)?

A

B cells produce IgG autoantibodies against platelet glycoproteins (e.g. IIb/IIIa, Ib/IX complexes)

70
Q

what is the pathophysiology of ITP?

A

B cells produce IgG autoantibodies against platelet glycoproteins → platelets coated with antibodies recognized as “non-self” by splenic macrophages → platelet destruction

71
Q

what are primary causes of ITP?

A

Idiopathic

72
Q

what are secondary causes of ITP?

A

o Viral infections – HIV, hepatitis C, cytomegalovirus

o SLE, lymphoid malignancy, chronic lymphocytic leukaemia

73
Q

what are drug induced causes of ITP?

A

Quinidine, phenytoin, valproic acid, rifampin, trimethoprim-sulfamethoxazole, sulfonamides

74
Q

what are risk factors of ITP?

A

age, genetic/acquired factors

75
Q

what are the clinical features of ITP?

A
  • Bruising easily after minor trauma
  • Mucocutaneous bleeding - Petechiae, purpura, epistaxis, gingival bleeding
  • severe ITP - <10,000-20,000/microL
  • Refractory - Severe ITP, fails to respond to/relapses after splenectomy
76
Q

how is ITP diagnosed?

A
  • Low Platelets
  • Blood smear – scarce platelets
  • Assays – drug dependent platelet antibodies
77
Q

what is the initial management of ITP?

A

raise platelet count – high dose glucocorticoid (dexamethasone, prednisolone), Immune globulin (IVIG)

78
Q

what are the complications of ITP?

A

Severe haemorrhage

o Intracranial bleeding, subarachnoid haemorrhage, gastrointestinal (GI) haemorrhage, haematuria, severe menorrhagia

79
Q

what is the further management of ITP?

A
  • Rituximab, thrombopoietin (TPO), immunosuppressive

* Surgery – splenectomy

80
Q

what is the underlying mechanism of THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP)?

A

caused by deficient activity of ADAMTS13 protease

81
Q

what is the function of ADAMTS13?

A

breaks vWF molecules into smaller multimers, prevents excessive accumulation on endothelial surfaces in microvasculature

82
Q

what is the pthophysiology vWF?

A

Excessive vWF on endothelial surfaces→ increased propensity for platelets to attach, accumulate (esp. in high pressure areas with shearing stress) + endothelial damage → platelet-rich thrombi in microcirculation

83
Q

what is the consequences of TTP?

A

tissue ischemia, organ dysfunction, microangiopathic haemolytic anaemia (MAHA - schistocytes), thrombocytopenia

84
Q

what organs are most affected in TTP?

A

Brain, heart, adrenal glands, pancreas, kidneys

85
Q

what are the causes of ADAMTS13 deficiency in TTP?

A

Acquired inhibitory autoantibody (IgG) to ADAMTS13; inherited mutation of ADAMTS13 gene (minority)

86
Q

what are the risk factors of TTP?

A

female, african descent, SLE

• Sepsis, liver disease, pancreatitis, cardiac surgery, pregnancy

87
Q

what are the 5 pentad features of TTP?

A 
o	Thrombocytopenia
o	MAHA
o	renal dysfunction
o	neurologic impairment (e.g. headache, confusion, seizures, coma)
o	fever
88
Q

what are the additional clinical features of TTP?

A
  • Mucocutaneous bleeding – petechiae, purpura, epitaxies, gingival bleeding
  • Intravascular haemolysis – dark urine
  • Light-headedness, abdo pain, easy bruising, nausea/vomiting
89
Q

what is the management of TTP?

A
  • glucocorticoids
  • monoclonal antibody
  • plasma exchange (PEX)
90
Q

how is TTP diagnosed?

A
  • FBC
  • Peripheral
  • Haemolysis
  • elevated Creatinine (renal)
  • ADAMTS13 assay, ADAMTS13 inhibiotr assay, genetic testing
91
Q

what are the features of FBC in TTP?

A

decreased platelet count, increased reticulocyte count, decreased haemglobin, hematocrit

92
Q

what are the features of peripheral blood smear in TTP?

A

schistocytes, spherocytes

93
Q

what are the features of haemolysis in TTP?

A

elevated LDG, elevated indirect bilirubin, reduced haptoglobin

94
Q

what is the function of Von Willebrand Factor?

A

o large glycoprotein
o promotes platelet adhesion to damaged endothelium
o carrier molecule for factor VIII

95
Q

What is Type 1 VWD?

A

partial reduction in vWF

96
Q

What is Type 2 VWD?

A

abnormal form of vWF

97
Q

What is Type 3 VWD?

A

total lack of vWF

98
Q

what is the cause of Type 2A VWD?

A

defective platelet adhesion due to decreased high molecular weight VWF multimers (i.e. the VWF protein is too small).

99
Q

what is the cause of Type 2B VWD?

A

characterised by a pathological increase of VWF-platelet interaction (increased affinity)

100
Q

what is the cause of Type 2M VWD?

A

decrease in VWF-platelet interaction (not related to loss of high molecular weight multimers).

101
Q

what is the cause of Type 2N VWD?

A

by abnormal binding of the VWF to Factor VIII.

102
Q

how is VWD inherited?

A
  • autosomal dominant

* type 3 inherited as autosomal recessive

103
Q

what are the clinical features of VWD?

A
  • positive family history
  • excessive or prolonged bleeding
  • postoperative bleeding
  • easy/excessive bruising
  • menorrhagia-
  • GI bleeding
  • epistaxis
104
Q

how is VWD diagnosed?

A
  • prolonged bleeding time
  • prolonged APTT
  • factor VIII levels reduced
  • defective platelet aggregation with ristocetin
105
Q

how is VWD managed?

A
  • tranexamic acid for mild bleeding
  • desmopressin (DDAVP)
  • factor VIII concentrate
106
Q

what are the causes of DIC?

A
  • Infection/ Sepsis
  • Malignancy
  • Trauma e.g. major surgery, burns, Hypovolemic shock, dissecting aortic aneurysm
  • Liver disease
  • Obstetric complications
107
Q

what are the clinical features of DIC?

A
  • oliguria, hypotension or tachycardia
  • purpura fulminans, gangrene, or acral cyanosis
  • delirium or comapetechiae, ecchymosis, oozing, haematuria
  • end organ damage
108
Q

what is the pathophysiology of DIC?

A
  • continuous generation of intravascular fibrin and consumption/depletion of procoagulants and platelets
  • impaired fibrinolytic system
  • Mutual potentiation between the inflammatory and coagulation pathways
  • microvascular thrombus formation
  • clotting factor consumption
109
Q

what causes an impaired fibrinolytic system in DIC?

A

decreased production of plasmin due to a sustained increase in plasma level of plasminogen activator inhibitor type I (PAI-I).

110
Q

what is the Mutual potentiation between the inflammatory and coagulation pathways?

A

o Interleukin-6 and tumour necrosis factor are cytokines that activate the coagulation pathway.
o products produced by coagulation, such as factor Xa, thrombin, and fibrin, activate endothelial cells to release pro-inflammatory cytokines.

111
Q

what leads to continued production of fibrin and depletion of platelets in DIC?

A

Without the functional counteraction from the anticoagulant pathways, increased thrombin continuously amplifies the coagulation cascade through its positive feedback and consumptive depletion of procoagulants and platelets, finally leading to widespread fibrin deposition, resulting in multi-organ failure.

112
Q

what are the diagnostic features of DIC?

A
  • prothrombin time prolonged
  • APTT prolonged
  • Bleeding time prolonged
  • Platelet Count low
113
Q

how is DIC managed?

A
  • Treat the underlying cause
  • Replacement therapy – cryoprecipitate (fibrinogen. factor VIII, thrombin)
  • Platelet, plasma transfusions
114
Q

haemophilia A is a deficiency of which factor?

A

Factor VIII

115
Q

haemophilia B is a deficiency of which factor?

A

Factor IX

116
Q

haemophilia affects which part of hemostasis?

A

Secondary haemostasis only

117
Q

what are the causes of hameophilia?

A

X linked, hereditary disorder

118
Q

what are the clinical features of haemophilia?

A
  • bleeding from medium to large blood vessels
  • Mild moderate and severely affected families depending on factor VIII/IX level
  • Recurrent Haemarthroses
  • Recurrent soft tissue bleeds
  • bruising in toddlers
  • Prolonged bleeding after dental extractions, surgery and invasive procedures
119
Q

how is haeophilia diagnosed?

A
  • FBC
  • aPTT – increase
  • Prothrombin time – no change
120
Q

how is haemophilia managed?

A
  • antifibrinolytic agent
  • supportive care
  • factor concentrate
121
Q

what is the pressure in the arterial system?

A

high

122
Q

what is the pressure in the venous system?

A

low

123
Q

what is the arterial clot made up of?

A

Platelet rich thrombus

124
Q

what is the venous clot made up of?

A

Fibrin clot

125
Q

what is the underlying mechanism of arterial thrombus?

A

atherosclerosis

126
Q

what is the underlying mechanism of venous thrombus?

A

Virchow’s triad

127
Q

what are the risk factors to venous thrombus?

A

Stasis – age, marked obesity, pregnancy, previous DVT/PE, trauma/surgery, malignancy, paralysis
Vessel Wall – age, previous DVT/PE
Hypercoagulability – age, pregnancy, puerperium, oestrogen therapy, trauma/surgery, malignancy, infection, thrombophilia

128
Q

what is Virchow’s Triad?

A

STASIS, VESSEL WALL, HYPERCOAGULABILITY

129
Q

where do venous thrombus commonly form?

A

valves of veins

130
Q

what is the pathophysiology of venous thrombus formation at valves?

A

Stasis exacerbates hypoxia, activates of hypoxia-inducible factor-1 (HIF-1) and early growth response 1 (EGR-1) = monocyte association with endothelial proteins, such as P-selectin, causes monocytes to release TF filled microvesicles, which initiate fibrin deposition

131
Q

what are two common examples of venous thrombus?

A

PE and DVT

132
Q

what is the pathophysiology of PE?

A

 with infarction, pleural gets stuck on infarcted lung

133
Q

what are the clinical features of PE?

A

chest pain: typically pleuritic, dyspnoea, haemoptysis, tachycardia, tachypnoea, CVS collapse/death, Hypoxia, RH strain

134
Q

how are PE diagnosed?

A 
Xray
computed tomography pulmonary angiogram (CTPA)
D Dimers
ECG
VQ Scan
Pulmonary angiography
135
Q

what is a key feature of PE on xray?

A

wedge shaped ossification

136
Q

what are the features of PE in ECG?

A

large S wave, large Q wave, inverted T wave, right bundle branch block, sinus tachycardia

137
Q

how is PE managed?

A

 LMWH
 continued warfarin for 3 months
 thrombolysis

138
Q

what is the pathophysiology of DVT?

A

Blood can’t get back to heart, leaks out into leg

139
Q

what are the clinical features of DVT?

A

pain, tenderness, swelling, warmth, redness or discolouration, distention of surface veins

140
Q

how is DVT diagnosed?

A

 clinical features
 D-Dimer
 Doppler Ultrasound
 Contrast Venography

141
Q

what is the management of DVT?

A

 anticoagulation (LMWH)

 Stockings

142
Q

what are the common causes of arterial thrombus?

A

Hypertension
Smoking
High cholesterol
Diabetes

143
Q

what is the management of arterial thrombus?

A
  • Stop smoking
  • Treat hypertension
  • Treat diabetes
  • Lower cholesterol
  • Anti-platelet drugs
144
Q

how do arterial thrombi form?

A

o Plaque ruptures
o Platelet adheres to it – exposed endothelium and release of Von Willebrand factor
o Platelets becomes activated - release granules that activate coagulation and recruit other platelets to developing platelet plug
o Platelet aggregation via membrane glycoproteins

145
Q

what is the disease progression in arterial thrombus?

A

atherosclerosis - stable atherosclerotic plaque - unstable atherosclerotic plaque - acute thrombus - acute organ ischaemia and infarction

Haematology (13 decks)

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