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Theme 2 > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

Overview

A

Injury/rupture to blood vessel
Blood vessel around wound constricts - reduce flow to damaged areas
Activated platelets stick to injury site
Platelets become sticky and clump together to form platelets
Platelets and damaged tissue release or activate clotting factors
Clotting factor cascade -> coagulation leads to cross linked fibrin mesh to stop bleeding

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2
Q

Endothelial cells

A

Layer of cells lining inner surface of vascular system - huge SA

Controls blood fluidity
Controls size of blood vessel
Contributes to preventing clots

Signals inflammatory cells to areas needing defence/repair

Gate-keeper between blood and tissues
Nutrients, hormones, waste
Actively controls extravasation of fluid, cells & molecules

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3
Q

3 Platelet based pathways to repair blood vessels

A

Platelets form primary haemostatic plug

  - Platelet adhesion
   - Platelet activation
    - Platelet aggregation

Coagulation – meshwork on the clot
Enzyme cascade
Part of coagulation requires platelet’s membrane

Vasoconstriction slows down blood flow
Platelets releases vasoconstrictors and pro-thrombotic agents
Serotonin, ADP and Thromboxane A2

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4
Q

Megakaryocytes

A

Megakaryocytes in bone marrow

Thrombocyte = platelet
Thrombocytopaenia = low platelet count in blood

4000 platelets / megakaryocyte

In blood normally:
Platelet count is 50X < RBCs
Platelet size = 3 x 0.5 µm

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5
Q

Platelet activation for haemostasis

A 
Platelet Activation = exocytose +
change shape +  respiratory rate

Activation required for haemostasis: aggregation of platelets, some coagulation steps (phospholipid)

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6
Q

Haemostatic Plug

A

Adhesion
to exposed collagen

Activation
Exocytose dense granules
serotonin, ADP, calcium

Aggregation
Stimulated by ADP
Blocked by Clopidogrel
Via fibrinogen

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7
Q

Clotting factors

A

All circulate as inactive precursors *E
Most are enzymes, which cleave other factors to activate them
Factor V and Factor VIII are NOT enzymes, they necessary are co-factors allowing the enzymes to function

V and VIII also are inactive initially

Initial activating factor is segregated
“works like epoxy”
Example: tissue factor is behind endothelial cells, while clotting factor precursors are in the blood

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8
Q

Plasma & Serum definitions

A 
Plasma = fluid portion of blood
Serum = fluid left after clotting
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9
Q

Coagulation Overview

A

Goal: activate thrombin
Thrombin is normally inactive (prothrombin)

Extrinsic (Tissue Factor) Pathway
Requires tissue factor to “see” plasma
Initiation of coagulation

Intrinsic (Contact Activation) Pathway
All factors/proenzymes are already in place
Amplification of process through positive feedback

Fibrinogen (+ thrombin) -> Fibrin (+ XIII + Ca2+) -> Fribrin cross linked

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10
Q

Activating Thrombin

A

Activated by Factor Xa, but poorly
Factor Va is a co-factor for Factor Xa
Together they activate Thrombin well

Three pathways to activate Factor X —> Xa
Extrinsic Xase
Intrinsic Xase
Thrombin also activates it - +ve feedback

Extrinsic Xase = Tissue factor (under endothelium) + factor VIIa

Intrinsic Xase = Factor VIIIa + Factor IXa

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11
Q

Coagulation factors

A

Prothrombin group: Factors II VII IX X

They are Enzymes
Vitamin K needed for synthesis
Require Ca2+ for activation
Stable

Thrombin group: Factors I V VIII

Thrombin activates them
V & VIII are co-factors
Factor I is fibrinogen
Increased in inflammation, pregnancy & with oral contraceptives

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12
Q

Vitamin K

A

Clotting factors are made by the liver
- Liver dysfunction, cirrhosis or hepatitis can clotting deficiency

Vitamin K
Is required to synthesize enzyme coagulation factors:
Prothrombin (II), VII, IX, X (calcium dependent proteases)
Vit K essential for gamma carboxylation of clotting enzymes

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13
Q

Plasmin

A

Lyses fibrin – stops / destroys clots

Starts as inactive Plasminogen
Plasma protein made by liver

Requires tissue Plasminogen Activator (tPA) to mature
tPA is on the surface of endothelial cells

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14
Q

Protein C

A

Coagulation Inhibitor

Starts as an inactive enzyme
Activated on surface of endothelial cells
Made by liver

Inactivates Factor Va & Factor VIIIa
Works with a co-factor Protein S to inactivate Va

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15
Q

Antithrombin III (+ heparin)

A

Peptide in blood made by liver

Blocks activity of thrombin
Also of Xa, IXa

Heparin increases AT III activity

AT III deficiency risk thrombotic disease

Recombinant form of AT III used medically for thrombotic disorders

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16
Q

Vitamin K deficiency

A

Results in a clotting insufficiency

Rare b/c vitamin K is made by bacteria of large intestine
Also found in leafy green vegetables (e.g. broccoli)

Caused by GI disease or no fat absorption
Liver disease no bile salts  no absorption

Warfarin prevents recycling of vitamin K
Depletes active vitamin K after a few days

17
Q

Haemophilia A

A

Clotting disorder
Affects Larger blood vessels
Joints, muscles
Wounds that bleed for days

Due to Congenital lack of factor VIII

X-linked – only males have symptoms

Treat with injected purified Factor VIII

18
Q

Christmas disease

A

Defect is factor IX
Also called “Haemophilia B”
Symptoms as per Haemophilia A

19
Q

Pharmacological control of blood clotting

A

Anti-platelet agents
Block platelet activation
Good for treating arterial disease *E

Anti-coagulants
Block production or activity of clotting factors
Used to treat venous disease

Fibrinolytics
Primarily used to dissolve fibrin in arterial disease

20
Q

Anti-platelet Agents

A

Prevent clotting in arteries
Where anticoagulants have limited effects
Used in acute coronary syndromes

Aspirin
Blocks formation of thromboxane A2 in platelets
Lengthens bleeding time
Does NOT increase coagulation time
Prophylaxis for myocardial infarction

ADP receptor inhibitors
Prasugrel / Clopidogrel

21
Q

Anti-coagulants

A 
Prevent clotting in veins 
And in low pressure pulmonary circ
Prophylactic for: 
deep vein thrombosis
Pulmonary embolism
Heparins
Inhibit coagulation (with AT III) by inhibiting Factor Xa
Different types of heparins

Novel Oral Anti-Coagulants (NOACs)
Dabigatran (thrombin inhibitor)
Rivaroxaban (factor Xa inhibitor)

Warfarin
Vitamin K antagonist
Slow onset (days)
Requires monitoring

22
Q

Fibrinolytics (Clot busting)

A

Clotting in arteries (high pressure)
Also called thrombolytics

Tissue Plasminogen Activator
Streptokinase
Urokinase

Theme 2 (8 decks)

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