Haemostasis Flashcards

1
Q

Platelet based pathways

A

Platelets form a primary haemostatic plug - platelet adhesion, activation and aggregation.
Coagulation makes a meshwork on the clot - enzyme cascade.
Vasoconstriction slows blood flow - vasoconstrictors and prothrombotic agents.
Virchows triad - risk factors for all 3

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2
Q

Haemostatic Plug

A

Adhesion to exposed collagen.
Activation: excytose dense granules, change shape and increase respiratory rate.
Aggregation: stimulated by ADP - blocked by prasugrel via fibrinogen.

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3
Q

Platelet Activation

A

Extracellular ADP -> activation by P2Y receptor -> cation flow.
Platelets release Thromboxane A2
ADP -> positive feedback on platelets

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4
Q

Coagulation

A

Initial activation factor is segregated.
Tissue factor is hidden behind endothelial cells.
If the basement membrane is exposed, tissue factor starts cascade
Extrinsic (tissue factor pathway - initiation of coagulation) OR Intrinsic (contact activation - positive feedback) Pathway -> common pathway -> clot

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5
Q

Prothrombin Group

A
Factors II, VII, IX, X
enzymes
need vitamin K for synthesis
require Ca2+ for activation
stable
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6
Q

Thrombin Group

A
Factors I, V, VIII
activated by trhombin
V and VIII are co-factors
Factor I = fibrinogen
Increased with inflammation, pregnancy and oral contraceptives
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7
Q

Coagulation info

A

based on a positive feedback loop
where thrombin activates clotting factors
clotting factors made by the liver - liver dysfunctions lead to clotting deficiency

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8
Q

Vitamin K

A

Fat soluble vitamins, required to synthesise enzyme coagulation factors.
made by bacteria of large intestine.
Essential for gamma carboxylating of clotting enzymes.
Deficiency: results in clotting insufficiency. caused by GI disease/no fat absorption. warfarin prevents recycling of vit K

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9
Q

Plasmin

A

Lyses fibrin - stops/destroys clots
Starts as inactive plasminogen - made by liver
Requires tissue plasminogen activator (tPA) to mature
tPA found on surface of endothelial cells

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10
Q

Protein C

A

Coagulation inhibitor
Starts as inactive enzyme made by liver
Activated on surface of endothelial cells
Works with Protein S to inactivate Factor Va & VIIIa

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11
Q

Antithrombin III

A

Peptide in the blood, made by liver
Blocks activity of thrombin, Xa and IXa
Heparin -> greater ATIII activity
Recombinant ATIII form used for thrombotic diseases
Lack of ATIII -> risk of thrombotic disease

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12
Q

Pharmacological Disease - Anti-platelet agents

A

prevents clots in arteries
Used in acute coronary syndromes
Aspirin - CoX inhibitor - blocks formation of thromboxane A2, lengthens bleeding time, doesn’t increase coagulation time, used for MI.
ADP receptor inhibitors - prasugrel/clopidogrel

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13
Q

Pharmacological Disease - Anti-coagulants

A

Prevents clotting in veins
Prophylactic for DVT and PE
Heparins inhibit coagulation by inhibiting factor Xa
DOACs - dabigatran/rivaroxaban
Warfarin - vit K antagonist - slow onset/requires monitoring

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14
Q

Pharmacological Disease - Fibrinolytics

A
Clot busting
Thrombolytic drugs
Prevents clots in arteries
Used in acute coronary syndromes - AMI
tPA
Streptokinase
Urokinase
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15
Q

Fibrinolysis and Inhibition of Coagulation

A

Imbalance of fibrinolysis -> leads to BV accumulating damage/haemorrhage.
Imbalance of clot formation -> leads to clot obstructing vessel lumen

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16
Q

Haemophilia A

A

Affects larger BVs, joints & muscles
Lack of factor VIII
X linked - only in males

17
Q

Christmas disease

A

Haemophilia B
Lack of factor IX
Same symptoms as haemophilia A

18
Q

Atherogenesis - A disease of inflammation

A
monocytes enter lesion and become macrophages
- consume cholesterol esters
- can become foam cells
- which can die and release contents
- attracts more leukocytes 
- inflammation  haemostasis
synergistic effects on atherogenesis
19
Q

Atherogenesis - A disease of Lipids

A

LDL deposits lipids in lesion
cholesterol esters are non-aqueous, making them solid
cholesterol esters are oxidised - oxygen radicals
- this makes them immunogenic
oxidised lipids are consumed by macrophages
which become foam cells which explode

20
Q

Atherogenesis - A disease of Endothelium

A

endothelium expresses chemo-attractants for monocytes to find and enter lesion
when endothelium is lost, collagen stimulates coagulation
endothelium normally covers collagen and basement membrane
endothelium lost -> vessel can’t control dilation
endothelium usually releases NO