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Physiology And Pharmacology Of Systems > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

Definition of haemostasis

A

Arrest of blood loss from damaged vessels

Vital to life

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2
Q

Definition of thrombosis

A

Local coagulation or clotting of blood

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3
Q

Definition of embolism

A

Lodging of a blockage causing material in a blood vessel

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4
Q

Definition of thrombocytopenia

A

Decreased no of platelets in the blood

Can lead to bruising and bleeding

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5
Q

Definition of thrombolytics

A

Used for rapid removal of thrombus in coronary and cerebral artery thrombosis

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6
Q

Definition of anticoagulants

A

Used for venous thrombosis and sometimes in arterial thrombosis

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7
Q

Definition of anti platelet drugs

A

Used to reduce thrombosis risk short and long term

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8
Q

Name the receptors on the platelets and what they attach to

  • GPIb
  • GPVI
  • Integrin a2b1
A

GPIb = vWF binding

GPVI = collagen binding
Integrin = collagen and vWF binding
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9
Q

Describe the steps in primary haemostasis

A

Platelets exposed to collagen and vWF in ECM

Endothelin release, NO and prostaglandin inhibition => VC

GPIb binds to vWF from endothelium, binds to collagen => activation, binds to other platelets

Activated COX => thromboxane formation => platelet activated VC

Seretonin => VC

ADP => fibrinogen receptor (GPIIbIIIa) exposure, activate

Fibrinogen cross links via GPIIbIIIa => platelet plug

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10
Q

What initiates the extrinsic pathway

A

Tissue factor (TF) present on the cell surface of tissues is normally not in contact with blood

If there is endothelial damage, F7 in blood comes into contact with TF

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11
Q

Describe the extrinsic pathway (initiation)

A 
TF + F7 => F7aTF
F10 => F10a
F5 => F5a + Ca
F2 (prothrombin) => F2a (thrombin)
F1 (fibrinogen) => F1a (fibrin) => provides rigidity and strength to repair

F2a (thrombin) activates F13
F13 => F13a => provides rigidity and strength to repair

Some steps need Ca2+ and phospholipids

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12
Q

What initiates the intrinsic pathway

A

F12 is a plasma protein, activated when in contact with an injured blood vessel

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13
Q

Describe the intrinsic pathway

A 
F12 => F12a
F11 => F11a
F9 => F9a
F8 => F8a
F10 => F10a
F5 => F5a + Ca
F2 (prothrombin) => F2a (thrombin)
F1 (fibrinogen) => F1a (fibrin) => stable fibrin clot

F2a (thrombin) activates F13

F13 => F13a activates F1a to form a stable fibrin clot

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14
Q

What factors are activated by F2a (thrombin)

Importance of the cascade and thrombin

A 
Thrombin initiates amplification and propagation by activating
F8
F5
F13
F10
F11
F9

Cascade accelerates clotting to reduce excess blood loss

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15
Q

How do the 2 extrinsic and intrinsic pathways relate to each other

A

Conversion of 10 => 10a onwards

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16
Q

Differences in different types of thrombosis in arterial and venous

  • when and where
  • components
  • prophalactic drug
  • causes what conditions
  • clot color
A

Arterial

  • Atherosclerosis at vascular injury/disturbed flow
  • platelets
  • antiplatelets
  • MI, strokes
  • white
Venous
-Stasis, vascular injury after trauma
-RBC, fibrin, some platelets
Anticoagulants
-Cardiovascular associated death
-red
17
Q

Name the 3 components of Virchow’s triad

A

Vascular damage
Low flow/stasis
Hypercoagulability

18
Q

What are the consequences when the fibrous cap of the plaque is disrupted

  • 2 possible outcomes
  • clot builds up
  • clot breaks down
A

Fibrous cap disrupted

Coagulation cascade activated as lipid contents are released

Clot builds up => thrombosis
Clot breaks down => embolism downstream

19
Q

When to use anti platelet drugs

What are the risks

A

Prevent secondary atherothrombotic/VC events

Increased hemorrhage risk

20
Q

What is the mechanism of aspirin (anti platelet drugs)

What are the AEs

A

COX 1 inhibition
COX 2 unaffected => prostacyclin production, stops haemostasis

GI harmorrhage

21
Q

What is the mechanism of P2Y12 antagonists (anti platelet drugs)
What are the AEs

Name the 2 irreversible drugs and the genetic effects on use
Name the 2 reversible drugs

A

Prevents ADP P2Y12 binding => decreased activation and aggregation

Irreversible

  • clopidogrel (2 reactions, CYP450)
  • prasugrel (1 reaction, unaffected by CYP)

Reversible

  • ticagrelor
  • cangrelor

Hemorrhage

22
Q

What is the mechanism of GPIIbIIIa (anti platelet drugs)
What are the AEs

Name the 2 types of drugs used and some examples

A

Prevents fibrinogen binding

Haemorrhage, thrombocytopenia

Fab fragments
-Tirofiban, Abcimiximab
Small molecule inhibitors
-Eptifibatide

23
Q

What are the problems with current anti platelet therapy

A

Incomplete efficacy due to multiple activation pathways

Variable responses

Bleed risk, but outweigh cardiac event risk

Genetics

Side effects

24
Q

What is the mechanism of heparin (anticoagulant)

What are the 2 types
What are the pros and cons of both

A

Inhibits F2, 9, 10, 11, 12 directly/indirectly via antithrombin 3

Unfractionated

  • cheap, short T1/2
  • protamine antidote
  • continuous infusion, monitoring needed
  • variable bioavailability
  • increased HIT risk

Low weight (Enoxaparin)

  • increased bioavailability
  • decreased HIT risk
  • expensive
  • partial protamine reversal
25
Q

What is the mechanism behind warfarin (anticoagulant)

What are the pros and cons

A

Modifies liver synthesized factors (F2, 7, 9, 10)

  • long term oral treatment
  • vitamin K/factor replacement antidote
  • frequent monitoring needed
  • affected by diet, genes, drugs
26
Q

What is the mechanism behind F10a inhibitors (anticoagulant)

What are the pros

What are the 3 examples of direct oral inhibitors
What are the 2 examples of indirect IV inhibitors

A

DIrect F10a inhibition
Indirect antithrombin 3

  • predictable PK
  • HIT rare

Direct

  • Rivaroxaban
  • Apixaban
  • Edoxaban

IV

  • Fondaparinux
  • Idraparinux
27
Q

What is the mechanism behind thrombin inhibitors

What are the 3 examples of IV thrombin inhibitors
What is an example of a direct thrombin inhibitor. What is this used to treat

A

Binds to factor binding site

IV

  • hirudin
  • desirudin
  • lepirudin

Direct
-dagabitran for AF, DVT

28
Q

How does the management of traditional anticoagulants vary from DOACs

A

Anticoagulants

  • regular blood tests
  • dietary consideration

DOACs

  • less INP monotiroing
  • decreased risk of uncontrolled bleeds
  • faster acting
29
Q

How do the antidotes differ between anticoagulants and DOACs

A

Anticoagulants

  • warfarin => vit K
  • heaprin => protamine

DOACs
-only dagabitran has an AD

30
Q

Describe how HIT can arise

  • 1st exposure
  • 2nd exposure
A

1st exposure
-platelet F4 binds to heparin => AB prod

2nd exposure
-AB binds to Fc on platelet => thrombocytopenia, thrombus formation

31
Q

When would you use anticoagulants

-2 situations

A

Inhibit coagulation cascade

Prophylaxis

32
Q

Describe the fibrinolytic system

A

F2a + Thrombomodulin => APC
F5a, F8a => F5, 8

Plasminogen =(TPA)=> Plasmin
Fibrin =(Plasmin)=> Fibrinogen

33
Q

What is the mechanism behind streptokinase (fibrinolytic)

What are the pros and cons

What is the AD

A

Binds, activates plasminogen

Lyse arterial thumb

Allergenic
High haemorrhage risk

Tranexaemic acid

34
Q

What is the mechanism behind alteplase (fibrinolytic)

What are the pros and cons

A

Binds, activates plasminogen bound fibrin

Non allergenic
Lyse arterial thrombin

High hemorrhage risk

Physiology And Pharmacology Of Systems (22 decks)

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