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Mattias - Hemotology > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is Hemostasis

A

The arrest of bleeding and the maintenance of vascular patency

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2
Q

Components of Normal hemostatic system

A

Formation of platelet plug (Primary hemostasis)
Formation of fibrin clot (Secondary hemostasis)
Fibrinolysis
Anticoagulant Defences

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3
Q

What happens when the endothelial wall is damaged

A

Exposes collagen and releases von Willebrand Factor and other proteins which platelets have receptor -Platelet adhesion at the site of injury

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4
Q

What happens when the platelets adhere to a damaged vessel wall

A

Secretion of various chemicals from platelets - leads to aggregation of platelets at the site of injury

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5
Q

What is reduced number of plateles called

A

Thrombocytopenia

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6
Q

Consequences of failure of platelet plug formation

A

Spontaneous bruising and purpura
Mucosal bleeding
Intracranial hemorrhage
Retinal hemorrhage

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7
Q

What is the screening tests for primary hemostasis

A

Platelet count

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8
Q

Secondary hemostasis has what pathways

A

Extrinsic pathway
Intrinsic pathway
Common pathway

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9
Q

2nd hemo - The Extrinsic pathway involves what components

A

Tissue factor
Clotting factor VII
Clotting factor X

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10
Q

2nd hemo - The Intrinsic pathway involves what components

A

Clotting factor 8-12

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11
Q

2nd hemo - The Common pathway involves what components

A

Clotting factor X
Thrombin
Fibrin

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12
Q

Single clotting factor deficiency cause

A

Usually hereditary

ie Hemophilia

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13
Q

Multiple clotting factor deficiency cause

A

Usually acquired

ie Disseminated Intravascular Coagulation

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14
Q

How does Fibrinolysis pathway work

A

Plasminogen –(Tissue Plasminogen Activator, tPA)–>Plasmin

Fibrin–(Plasmin)–>Fibrin Degradation Products

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15
Q

Naturally occuring anticoagulants

A

Serine Protease Inhibitors (Anti-thrombin III)

Protein C and Protein S

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16
Q

What activates Protein C and Protein S. What do they block

A

Thrombin activates

Block Intrinsic and common pathway

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17
Q

What is Thrombophilia

A

Deficiency of naturally occuring anticoagulants, may be hereditary.
Increased tendency to develop enous thrombosis (Deep vein thrombosis/pulmonary embolism)

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18
Q

What is shock

A

Shock is the clinical syndrome of Tissue hypoperfusion due to Circulatory Failure

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19
Q

How to calculate Mean arterial pressure

A

(2x Diastolic+ systolic) /3

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20
Q

What is the Virchow’s triad

A

Stasis of blood flow
Endothelial injury
Hypercoagubility
Three things that lead to thrombis

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21
Q

Inadequate perfusion causes

A

Systemic acidosis
Microcapillary thrombus
Ischemia of organs

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22
Q

Signs of hypoperfusion

A

Mottling of skin, clammy

Kidney - Oliguria

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23
Q

Blood test to confirm hypoperfusion

A

Lactate levels
>2mmol/L diagnostic
>4mmol/L significant mortality

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24
Q

Mean arterial pressure is due to four physiological causes

A

1.Heart rate
2.Stroke Volume
3. Cardiac output
4. Systemic vascular resistance
1 and 2 makes up 3

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25
Q

Four mechanism can create drop in Mean arterial pressure

A

Cardiogenic Shock
Obstructive Shock
Hypovolemic Shock
Distributive Shock

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26
Q

What is Cardiogenic shock

A

Reduced force of cardiac contraction and stroke volume.

Result in Cool, clammy peripheries due to compensatory systemic vasorestriciton

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27
Q

Treatment for Myocardial infarction if it’s within 90 minutes

A

Percutaneous cardiac intervention (PCI)

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28
Q

What is Obstructive shock

A

Obstruction to cardiac outflow, not caused by cardiac failure. Evidence of raised JVP and distended neck veins may be seen

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29
Q

Examples of causes of Obstructive shock

A

Cardiac tamponade
Tension pneumothorax
Pulmonary embolous

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30
Q

What is Hypovolemic shock

A

Reduced blood volume
Lower venous return
Reduced force of cadiac contraction and CO (Frank-Starling law)

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31
Q

What is Distributive shock

A

Reduced systemic vascular resistance due to Vasodilation with warm, red peripheries
Compensatory increase in Cardiac output

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32
Q

Explain Intrinsic pathway

A

Clotting factor VIIIa+IXa activates X into Xa

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33
Q

Explain Extrinsic pathway

A

Tissue Factor and Clotting factor VIIa together activates Clotting factor X to Xa

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34
Q

Explain the common pathway

A

Clotting factor Xa and Va together converts Prothrombin into Thrombin.
Thrombin then activates Fibrinogen into Fibrin

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35
Q

What is Henoch-Schonlein Purpura

A

Small vessel vasculitis where IgA and complement 3 deposits in arterioles, capillaries and venolos. Present with palpable purpura and kidney problems, Affect kids. Similar to IgA nephropathy but it affect young adults.

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36
Q

Causes of peripheral platelet destruction

A

Coagulopathy (Disseminated intravascular coagulation)
Autoimmune (Immune thrombocytopenic purpura, ITP)
Hypersplenism

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37
Q

von Willenbran Factor deficiency cause

A

Autosomal dominant
Common
Variable severity, generally mild

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38
Q

Commonest cause of primary hemostatic failure

A

Thrombocytopenia

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39
Q

Multiple clotting factor deficiency is causes

A

Liver failure
VitK deficiency/Warfarin therapy
Complex coagulopathy

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40
Q

Lab results in Multiple clotting factor deficiency

A

Prolonged Prothrombin time (PT) and Activated partial thromboplastin time (APTT)

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41
Q

Vitamin K act on which clotting factors and how

A

Factors 2, 7, 9 and 10.

VitK carboxylates them

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42
Q

Why does liver failure cause clotting factor deficiency

A

Because all coagulation factors are synthesized in hepatocytes

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43
Q

How and where is VitK absorbed

A

Absorbed in upper intestine

Requires bile salts for absorption

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44
Q

Causes of VitK deficiency

A 
Poor diet intake
Malabsorption
Obstructive jaundice
VitK antagonists (Warfarin)
Hemorhagic disease of the newborn
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45
Q

Disseminated Intravascular coagulation is what

A

Innapropriate activation of coagulation cascade, causes microvascular thrombus and organ failure. Due to clotting factor consumption it also leads to bruising, purpura and generalised bleeding

46
Q

What test is done for the Extrinsic pathway

A

Prothrombin time

47
Q

What test is done for the intrinsic pathway

A

Activated partial thromboplastin time

48
Q

Causes of Disseminated Intravascular Coagulopathy

A

Sepsis
Obstetric emergencies
Malignancy
Hypovolemic shock

49
Q

Treatment of Disseminated Intravascular coagulopathy

A 
Treat underlying cause
Replacement therapy (Platelet, Plasma Fibrinogen transfusions and replacement)
50
Q

Genetics of Hemophilia

A

X-linked

51
Q

Types of hemophilia and what it effects, most common

A

Hemophilia A - Factor 8 deficiency
Hemophilia B - Factor 9 deficiency
Hemophilia A is more common

52
Q

Features of Hemophilia bleeds

A

No abnormality of primary hemostasis
Bleeding from medium to large blood vessels
Severity ranges

53
Q

Clinical features of severe hemophilia

A

Recurrent Hemarthroses
Bleeding into joints
Recurrent soft tissue bleeds (bruising in toddlers)
Prolonged bleeding after dental extractions, surgery or invasive procedures

54
Q

Types of Venous thrombotic events

A

DVT

PE

55
Q

Features of Arterial thrombosis

A

High pressure system
Atherosclerosis
Platelet rich thrombus

56
Q

Features of Venous thrombosis

A

Low pressure system
Platelets not activated
Activated coagulation cascade - rich in fibrin clot

57
Q

Treatment for Venous thrombosis

A

Heparin
Warfarin
New oral anticoagulants

58
Q

Features of DVT

A

Limbs feel hot, swollen, tender

Pitting edmea

59
Q

Categorize of causes of thrombosis

A

Virchow’s triad
Stasis
Vessel wall (injury)
Hypercoagulability

60
Q

What is Thrombophilia

A

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

61
Q

Mechanisms of Thrombophilia

A

Increased coagulation activity
Decreased fibrinolytic activity
Decreased anticoagulant activity

62
Q

Types of Hereditary thrombophili

A 
Factor V Leiden
Prothrombin 20210 mutation
Antithrombin deficiency
Protein C deficiency 
Protein S deficiency
63
Q

When should you consider hereditary thrombophilia screening

A

Venous thrombosis

64
Q

Management of Hereditary Thrombophilia

A

Advice avoiding risk
Short term prophylaxis (prior to known risk event)
Short term anticoagulation (to treat thrombotic events)
Long term anticoagulation (only if recurrent thrombotic events)

65
Q

Acquired Thrombophilia can occur in

A

Antiphospholipid antibody syndrome

66
Q

Features of Antiphospholipid syndrome

A

Recurrent thromboses (Arterial and Venous)
Recurrent Fetal loss
Mild thrombocytopenia

67
Q

Treatment of Anti-phospholipid syndrome

A

Aspirin

Warfarin

68
Q

Indictions for anticoagulant drugs

A

Venous thrombosis

Atrial fibillation

69
Q

What is the target of anticoagulant drugs

A

secondary hemostasis

70
Q

What is the action of Heparin

A

Potentiates antithrombin

71
Q

What are the two forms of Heparin

A

Unfractionated

Low Molecular weight (LMWH)

72
Q

How is Heparin given, how fast does it act

A

Parentral (IV or SC)

Immediated effect

73
Q

Types of Heparin has a slightly different affinity to the same two targets, what are they?

A

Unfractioned - Thrombin

LMWH - Factor Xa

74
Q

How is heparin monitored

A

Unfractionated - Activated partial thromboplastin time (APTT)
LMWH - Anti-Xa assay but usually does not need monitoring

75
Q

Complications of Heparin

A

Bleeding
Heparin induced thrombocytopenia (w/thrombosis)
Osteoperosis in long term

76
Q

Heparin used in pregnancy

A

LMWH

77
Q

Antidot for heparin

A

Protamine sulphate
Unfractionated - complete reverse
LMWH - partial reverse

78
Q

Is antidot for heparin needed

A

Only in severe bleed

Otherwise short half-life

79
Q

What are Coumarin

A

Vit K antagonists

80
Q

Types of Coumarin anticoagulants

A

Warfarin
Phenindione
Acenocoumarin
Phenprocoumon

81
Q

MOA of Coumarin

A

Inhibits VitK to carboxylase
Factors 2, 7, 9 and 10.
Add a -COOH group

82
Q

What is VitK

A

Fat soluble vitamin absorbed in upper intestine

83
Q

What factors need VitK

A 
Factors 2 (prothrombin) 7,9 and 10.
Protein C and protein S
84
Q

Issues with Warfarin

A

Narrow therapeutic window
Needs monitoring
Needs regular dose taking at same time every day

85
Q

How is Warfarin monitored

A

INR

International Normalized Ratio

86
Q

How is INR calculated

A

(Patient’s PT in seconds/Mean normal PT in seconds)^ISI
International sensitivity index
Target between 2-3

87
Q

What are mild bleeding complications on Warfarin

A

Skin bruising
Epistaxis
Hematuria

88
Q

Warfarin reversal and how fast drug acts

A 
Administer VitK (6 hours)
If more is needed Administer clotting factors (immediate)
89
Q

Name a Thrombin inhibitor

A

Dabigatran

90
Q

Name a Xa inhibitor

A

Rivaroxaban

Apixaban

91
Q

Pro’s and Con’s about new anticoagulants such as Dabigatran, Rivaroxaban, Apixaban

A

Pro- Oral and no monitoring needed, less drug interactions

Con- No specific antidote for reversal

92
Q

What type of drug is given in arterial vs venous thrombosis

A

Arterial - Anti-platelet

Venous - Anticoagulants

93
Q

What is Atherosclerosis

A

Damage to endothelium and recruitment of foamy macrophages rich in cholesterol
Forms plaques rich in cholestrol

94
Q

Features of Stable Atherosclerotic plaques

A

Hyalinised and calcified

95
Q

When are stable atherosclerotic plaques seen

A

Stable angina

intermittent claudication

96
Q

Prevention of arterial thrombosis

A

Stop smoking
Treat hypertension and diabetes
Lower cholesterol
Anti-platelet drugs

97
Q

How does Aspirin act as an antiplatelet

A

Inhibits Cyclo-oxygenase (COX) which is necessary to produce Thromboxane A2 (a platelet agonist released from granules on activation)

98
Q

Side effects of Aspirin

A

Also blocks prostaglandin, this may cause GI ulceration, bronchospasm

99
Q

MOA of Clopidogrel, prasugrel

A

ADP receptor antagonist

platelet activation/recruiting agent

100
Q

MOA of Dipyridamole

A

Phosphodiesterase inhibitor

Reduces cAMP production which is a second messenger in platelet activation

101
Q

MOA of Abciximab

A

GP IIb/IIIa inhibitor

Inhibits aggregation of platelets, molecule needed for platelet to aggregate to each other

102
Q

How long before elective surgery should anti-platelet drugs be stopped

A

7 days

103
Q

What is immune thrombocytopenic purpura

A

Low platelet with normal bone marrow. Present with purpuric rash and bleeding.
Acute version happens in kids post infection, however this is normally resolved within 2months

104
Q

Signs of shock

A

Pale, clammy
Tachycardia
Hypotension
Hypoxia

105
Q

Symptoms and signs of Pulmonary embolism

A

Shortness of breath
Pleuretic chest pain
Rub
Hypoxia

106
Q

What is a blood test to look for in DVT or PE

A

D-dimer

May also occur in many other conditions

107
Q

What are D-dimers

A

Cross linked product of fibrin degradation
Produced whenever fibrin is generated
Produced when coagulation has been activated

108
Q

Relationship between D-dimer and Venous thromboembolism

A

Elevated D-dimer is not always VTE

Normal D-dimer is most likely not VTE

109
Q

DVT prophyaxis and treatment

A

TED stockins
Physio - Early mobilisation
Heparin – Warfarin

110
Q

Week 3 lectures done

A

Yes

Mattias - Hemotology (3 decks)

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