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Advanced Pharmacology > Exam 4 - Coagulation Disorders > Flashcards

Exam 4 - Coagulation Disorders Flashcards

1
Q

What are the phases of platelet formation?

A
  1. Adhesion
  2. Aggregation
  3. Secretion
  4. Cross-linking of adjacent platelets
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2
Q

What are red and white thrombi?

A

Red: contain RBC and occur in slow moving vessels, can detach and lead to PE
White: contain only fibrin and platelets in fast moving vessels, causes downstream ischemia

White thrombi
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3
Q

Describe the role PGI2 in thrombogenesis?
What drugs are noted here?

A

“Prostacyclin” - sits in endothelial cell wall and normally inhibits platelet aggregation
NSAIDS, except aspirin,inhibit formation of PGI2 and are therefore “pro-clot”

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4
Q

What is collagen and vWF role in thrombogenesis?

A

Collagen: Exposed during endothelial cell injury and binds to GP Ia in platelets
vWF: Exposed during endothelial cell injury and binds to GP Ib in platelets
Both of these binding lead to release of soluble mediators from platelets

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5
Q

What is the role of ADP, TXA2, and 5-HT during thrombogenesis?

A

5-HT: causes vasoconstriction of smooth muscle and binds to other platelets, activating them
ADP, TXA-2: Bind to receptors on other platelets activating them
* Activation of other platelets causes release of more of these mediators in a positve feedback system

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6
Q

How does aspirin effect platelet aggregation?

A

Inhibits COX-1, inhibiting production of TXA2, preventing platelet activation

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7
Q

What is fibrins role in platelet aggregation?

A

Creates a web-like structure that holds the platelets together, allowing them to aggregate

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8
Q

Describe what the common pathway does?

A

Activates thrombin which leads to fibrin formation

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9
Q

Describe the extrinsic pathway?

A
  1. Tissue damage exposes tissue factor (TF)
  2. TF activates factor VII
  3. TF facilitates conversion of factor VII to factor X
  4. Factor X converts prothrombin to thrombin
  5. Thrombin converts fibrinogen to fibrin
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10
Q

Describe the common pathway?

A
  1. Factor X is activated by the extrinsic and intrinsic pathway
  2. Factor X converts prothrombin to thrombin with the help of factor V
  3. Thrombin converts fibrinogen to fibrin
  4. Fibrin becomes cross linked with the help of factor XIII
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11
Q

Describe the intrinsic pathway?

A
  1. Damage to endothelial cells activates factor XII
  2. Activating factor XI
  3. Activating factor IX
  4. Activating factor X

Factor VIII aids in activation of factor X

12, 11, 9, 10, common pathway

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12
Q

What does thrombin activate?

A

Activates: factors V, VIII, XI, XIII, and protein C

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13
Q

What are the inhibitors in the coagulation cascade and their effects?

A
  • Protein C - inhibits factors VIII and V
  • Antithrombin - inhibts factor X and thrombin
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14
Q

Draw the coagulation cascade.

A
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15
Q

What 3 factors can lead to DVT + what is the name of this group of symptoms?

A

Virchow’s Triad
* Stasis
* Endothelial injury
* Hypercoagulability

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16
Q

What are the risk factors for DVT?

A
  • Can be inherited like coagulation factor deficency
  • Acquired like being bedridden, trauma, obesity, estrogen use, cancer, venous insufficiency
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17
Q

What is DIC?

A
  • Overstimulation of the blood clotting mechanism resulting in excessive consumption of factors and platelets leading to spontaneous bleeding
18
Q

What are the causes and treatments for DIC?

A
  • Causes: massive tissue injury, malignancy, bacterial sepsis, placental abruption
  • Treatments: Plasma transfusion, correct the underlying cause

Has a high mortality rate

19
Q

Define TTP and HIT?
Causes and treatments?

A

Heparin Induced Thrombocytopenia (HIT) is caused by HMWH use. The body creates antibodies against platelets and destroys them.
Can be treated with protamine, platelet transfusions, and stopping heparin use.

20
Q

Draw the fibrinolysis pathway, including mediators involved.

A
  • t-PA, urokinase, and streptokinase activates plasminogen to plasmin
  • Plasmin will induce breakdown of fibrinogen and fibrin
21
Q

What are the 4 classes of coagulation modifiers?

A
  • Anticoagulants
  • Antiplatelets
  • Thrombolytics
  • Hemostatics/Antifibrinolytics
22
Q

What drugs are anticoagulants?

A

Heparin, Fondaparinux, Hirudin, Warfarin, Rivaroxaban, Apixaban, Dabigatran, Argotroban

23
Q

What drugs are antiplatelets?

A

Aspirin, clopidogrel, abciximab

24
Q

What drugs are thrombolytics?

A

Streptokinase and t-PA

25
Q

What drugs are hemostatics/antifibrinolytics?

A
26
Q

What are the indirect thrombin inhibitors and their MOA?

A
  • Unfractionated heparin: Enhances the activity of antithrombin by 1000X which irreversibly binds thrombin AND factor Xa - most effective
  • LMWH: Enhances antithrombin specifically to factor X, not effecting thrombin - less effective
  • Fondaparinux: Specific for only enhancing antithrombin- least effective.
27
Q

What are the direct thrombin inhibitors and their MOA?

A
  • Hirudin: bind to both the active and substrate sites on thrombin, derived from leech saliva
  • Argatroban, dabigatran: bind only to the thrombin active sites
28
Q

What are the toxicities and contraindications for HMWH?
Treatments?

A
  • Bleeding, HIT (heparin induced thrombocytopenia, 7-10 days after exposure)
  • Any state with increased bleeding risk: active bleeding, hemophilia, thrombocytopenia, severe HTN, intracranial hemorrhage, infective endocarditis, active TB, GI ulcers, advanced hepatic disease
  • Treatment: Protamine sulfate. Its positive charge binds to heparin’s negative charge to inactivate it.
29
Q

Describe the lab tests used for coagulation and their normal values?

A
  • Prothrombin Time (PT) Time to clot. Assesses function of extrinsic system and common pathway of coag cascade.
  • INR = (PT test / PT normal)
    -Normal = 0.8 - 1.2
    -Warfarin Target = 2 – 3
  • Activated Partial Thromboplastin Time (aPTT): Assess function of intrinsic system and common pathway.
    -Normal = 35 – 45 sec
30
Q

What is the MOA of Warfarin?

A
  • MOA: blocks gamma-carboxylation of glutamate residues via inhibition of vitamin K reductase, inhibiting production of factors II, VII, IX, X.
  • Blocks REDOX cycle of vitamin K
31
Q

Treatment considerations and pharmokinetics of Warfarin?

A
  • 100% bioavailibility, 99% protein bound
  • Can cause birth defects and fetal hemorrhage
  • Metabolism depends on genetic based enzyme induction or inhibition
  • Vitamin K levels can alter function
32
Q

Reversal for Warfarin?

A
  • Large dose of Vitamin K
  • FFP
  • Stop drug
  • Factor IX concentrates
33
Q

What are the non-warfarin oral anticoagulant drugs and their targets?

A
  • Apixaban, rivaroxaban- inhibit factor Xa
  • Dabigatran, argatroban - inhibts thrombin
34
Q

What are the fibrinolytic drugs?

A

t-PA, urokinase, streptokinase

35
Q

List the antiplatelet drugs and their MOA?

A
  • Aspirin: COX-1 inhibitor preventing formation of TXA2 preventing platelet aggregation
  • Clopidogrel: Irreversably inhibits ADP receptors on platelets
  • Abcixamab: inhibits receptors IIb/IIIa preventing cross linking by fibrin
36
Q

Describe the use and mechanism of vitamin K?

A
  • Found in leafy green vegetables
  • Reverses warfarin by increasing the clotting factors that warfarin inhibits (II, VII, IX, X)
37
Q

Describe the use of plasma fractions?

A
  • Used for deficiencies in plasma clotting factors
  • Can be derived from plasma or recombinant
38
Q

Describe the uses and MOA of desmopressin?

A
  • Increases factor VIII activity
  • Used in mild hemphilia A and von Willebrand disease
39
Q

Desctibe the uses and MOA of aminocaproic acid?

A
  • Competitvely inhibts plasminogen activation
  • Used for hemophila treatment, bleeding from fibrinolytic therapy, intracranial aneurysms, post surgical bleeding
40
Q

Describe the uses and MOA of transexamic acid (TXA)?

A
  • Decreases the risk of death in major bleeding
  • It is an antifibrinolytic that inhibits conversion of plasminogen to plasmin

Advanced Pharmacology (17 decks)

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