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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
Four mechanism can create drop in Mean arterial pressure
Cardiogenic Shock Obstructive Shock Hypovolemic Shock Distributive Shock
26
What is Cardiogenic shock
Reduced force of cardiac contraction and stroke volume. | Result in Cool, clammy peripheries due to compensatory systemic vasorestriciton
27
Treatment for Myocardial infarction if it's within 90 minutes
Percutaneous cardiac intervention (PCI)
28
What is Obstructive shock
Obstruction to cardiac outflow, not caused by cardiac failure. Evidence of raised JVP and distended neck veins may be seen
29
Examples of causes of Obstructive shock
Cardiac tamponade Tension pneumothorax Pulmonary embolous
30
What is Hypovolemic shock
Reduced blood volume Lower venous return Reduced force of cadiac contraction and CO (Frank-Starling law)
31
What is Distributive shock
Reduced systemic vascular resistance due to Vasodilation with warm, red peripheries Compensatory increase in Cardiac output
32
Explain Intrinsic pathway
Clotting factor VIIIa+IXa activates X into Xa
33
Explain Extrinsic pathway
Tissue Factor and Clotting factor VIIa together activates Clotting factor X to Xa
34
Explain the common pathway
Clotting factor Xa and Va together converts Prothrombin into Thrombin. Thrombin then activates Fibrinogen into Fibrin
35
What is Henoch-Schonlein Purpura
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.
36
Causes of peripheral platelet destruction
Coagulopathy (Disseminated intravascular coagulation) Autoimmune (Immune thrombocytopenic purpura, ITP) Hypersplenism
37
von Willenbran Factor deficiency cause
Autosomal dominant Common Variable severity, generally mild
38
Commonest cause of primary hemostatic failure
Thrombocytopenia
39
Multiple clotting factor deficiency is causes
Liver failure VitK deficiency/Warfarin therapy Complex coagulopathy
40
Lab results in Multiple clotting factor deficiency
Prolonged Prothrombin time (PT) and Activated partial thromboplastin time (APTT)
41
Vitamin K act on which clotting factors and how
Factors 2, 7, 9 and 10. | VitK carboxylates them
42
Why does liver failure cause clotting factor deficiency
Because all coagulation factors are synthesized in hepatocytes
43
How and where is VitK absorbed
Absorbed in upper intestine | Requires bile salts for absorption
44
Causes of VitK deficiency
``` Poor diet intake Malabsorption Obstructive jaundice VitK antagonists (Warfarin) Hemorhagic disease of the newborn ```
45
Disseminated Intravascular coagulation is what
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
What test is done for the Extrinsic pathway
Prothrombin time
47
What test is done for the intrinsic pathway
Activated partial thromboplastin time
48
Causes of Disseminated Intravascular Coagulopathy
Sepsis Obstetric emergencies Malignancy Hypovolemic shock
49
Treatment of Disseminated Intravascular coagulopathy
``` Treat underlying cause Replacement therapy (Platelet, Plasma Fibrinogen transfusions and replacement) ```
50
Genetics of Hemophilia
X-linked
51
Types of hemophilia and what it effects, most common
Hemophilia A - Factor 8 deficiency Hemophilia B - Factor 9 deficiency Hemophilia A is more common
52
Features of Hemophilia bleeds
No abnormality of primary hemostasis Bleeding from medium to large blood vessels Severity ranges
53
Clinical features of severe hemophilia
Recurrent Hemarthroses Bleeding into joints Recurrent soft tissue bleeds (bruising in toddlers) Prolonged bleeding after dental extractions, surgery or invasive procedures
54
Types of Venous thrombotic events
DVT | PE
55
Features of Arterial thrombosis
High pressure system Atherosclerosis Platelet rich thrombus
56
Features of Venous thrombosis
Low pressure system Platelets not activated Activated coagulation cascade - rich in fibrin clot
57
Treatment for Venous thrombosis
Heparin Warfarin New oral anticoagulants
58
Features of DVT
Limbs feel hot, swollen, tender | Pitting edmea
59
Categorize of causes of thrombosis
Virchow's triad Stasis Vessel wall (injury) Hypercoagulability
60
What is Thrombophilia
Familial or acquired disorders of the hemostatic mechanism which are likely to predispose to thrombosis
61
Mechanisms of Thrombophilia
Increased coagulation activity Decreased fibrinolytic activity Decreased anticoagulant activity
62
Types of Hereditary thrombophili
``` Factor V Leiden Prothrombin 20210 mutation Antithrombin deficiency Protein C deficiency Protein S deficiency ```
63
When should you consider hereditary thrombophilia screening
Venous thrombosis
64
Management of Hereditary Thrombophilia
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
Acquired Thrombophilia can occur in
Antiphospholipid antibody syndrome
66
Features of Antiphospholipid syndrome
Recurrent thromboses (Arterial and Venous) Recurrent Fetal loss Mild thrombocytopenia
67
Treatment of Anti-phospholipid syndrome
Aspirin | Warfarin
68
Indictions for anticoagulant drugs
Venous thrombosis | Atrial fibillation
69
What is the target of anticoagulant drugs
secondary hemostasis
70
What is the action of Heparin
Potentiates antithrombin
71
What are the two forms of Heparin
Unfractionated | Low Molecular weight (LMWH)
72
How is Heparin given, how fast does it act
Parentral (IV or SC) | Immediated effect
73
Types of Heparin has a slightly different affinity to the same two targets, what are they?
Unfractioned - Thrombin | LMWH - Factor Xa
74
How is heparin monitored
Unfractionated - Activated partial thromboplastin time (APTT) LMWH - Anti-Xa assay but usually does not need monitoring
75
Complications of Heparin
Bleeding Heparin induced thrombocytopenia (w/thrombosis) Osteoperosis in long term
76
Heparin used in pregnancy
LMWH
77
Antidot for heparin
Protamine sulphate Unfractionated - complete reverse LMWH - partial reverse
78
Is antidot for heparin needed
Only in severe bleed | Otherwise short half-life
79
What are Coumarin
Vit K antagonists
80
Types of Coumarin anticoagulants
Warfarin Phenindione Acenocoumarin Phenprocoumon
81
MOA of Coumarin
Inhibits VitK to carboxylase Factors 2, 7, 9 and 10. Add a -COOH group
82
What is VitK
Fat soluble vitamin absorbed in upper intestine
83
What factors need VitK
``` Factors 2 (prothrombin) 7,9 and 10. Protein C and protein S ```
84
Issues with Warfarin
Narrow therapeutic window Needs monitoring Needs regular dose taking at same time every day
85
How is Warfarin monitored
INR | International Normalized Ratio
86
How is INR calculated
(Patient's PT in seconds/Mean normal PT in seconds)^ISI International sensitivity index Target between 2-3
87
What are mild bleeding complications on Warfarin
Skin bruising Epistaxis Hematuria
88
Warfarin reversal and how fast drug acts
``` Administer VitK (6 hours) If more is needed Administer clotting factors (immediate) ```
89
Name a Thrombin inhibitor
Dabigatran
90
Name a Xa inhibitor
Rivaroxaban | Apixaban
91
Pro's and Con's about new anticoagulants such as Dabigatran, Rivaroxaban, Apixaban
Pro- Oral and no monitoring needed, less drug interactions | Con- No specific antidote for reversal
92
What type of drug is given in arterial vs venous thrombosis
Arterial - Anti-platelet | Venous - Anticoagulants
93
What is Atherosclerosis
Damage to endothelium and recruitment of foamy macrophages rich in cholesterol Forms plaques rich in cholestrol
94
Features of Stable Atherosclerotic plaques
Hyalinised and calcified
95
When are stable atherosclerotic plaques seen
Stable angina | intermittent claudication
96
Prevention of arterial thrombosis
Stop smoking Treat hypertension and diabetes Lower cholesterol Anti-platelet drugs
97
How does Aspirin act as an antiplatelet
Inhibits Cyclo-oxygenase (COX) which is necessary to produce Thromboxane A2 (a platelet agonist released from granules on activation)
98
Side effects of Aspirin
Also blocks prostaglandin, this may cause GI ulceration, bronchospasm
99
MOA of Clopidogrel, prasugrel
ADP receptor antagonist | platelet activation/recruiting agent
100
MOA of Dipyridamole
Phosphodiesterase inhibitor | Reduces cAMP production which is a second messenger in platelet activation
101
MOA of Abciximab
GP IIb/IIIa inhibitor | Inhibits aggregation of platelets, molecule needed for platelet to aggregate to each other
102
How long before elective surgery should anti-platelet drugs be stopped
7 days
103
What is immune thrombocytopenic purpura
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
Signs of shock
Pale, clammy Tachycardia Hypotension Hypoxia
105
Symptoms and signs of Pulmonary embolism
Shortness of breath Pleuretic chest pain Rub Hypoxia
106
What is a blood test to look for in DVT or PE
D-dimer | May also occur in many other conditions
107
What are D-dimers
Cross linked product of fibrin degradation Produced whenever fibrin is generated Produced when coagulation has been activated
108
Relationship between D-dimer and Venous thromboembolism
Elevated D-dimer is not always VTE | Normal D-dimer is most likely not VTE
109
DVT prophyaxis and treatment
TED stockins Physio - Early mobilisation Heparin -- Warfarin
110
Week 3 lectures done
Yes

Mattias - Hemotology (3 decks)

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