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Brain Power: Neuropharmacology > Blood Drugs > Flashcards

Blood Drugs Flashcards

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1
Q

How do Thromboxane A2 (TXA2) ADP and Serotonin (5-HT) affect platelets and vessel walls?

A

PLT activator/aggregator and vasoconstrictor

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2
Q

Which is responsible? Platelet problem or coagulation problem:

  1. Bleeding gingiva, skin, heavy menses
  2. Bleed in joints, muscle, retroperitoneum
A
  1. PLT

2. Coagulation

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3
Q

What do antithrombin 3, protein C and protein S have in common?

A

They are anticoagulants
AT for 10a, 1a, 9a, 11a, 12a
C and S for 5a and 8a

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4
Q

What is the most common defect in the natural anticoagulant system?

A

Mutation in Factor 5 which results in resistance to inactivation by protein c and s

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5
Q

What remodels the thrombus and limits its extension by proteolytic digestion of fibrin?

A

PLASMIN that is converted form plasminogen by Tissue plasminogen activator t-PA

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6
Q

How does the MOA of heparin and enoxaparin differ?

A

UF Heparin and LMW heparin binds to Antithrombin III and increases the catalytic action of antithrombin by 1000 fold– while UFH affects both 10a and thrombin LMWH only affects factor 10a

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7
Q

What is a feared complication with more than 7 days of heparin and decreasing PLT count?

A

A HYPERcoaguable state– HIT Heparin induced thrombocytopenia occuring in 1-4% of individuals

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8
Q

How does fondaparinux work?

A

Avidly binds to antithrombin III resulting in efficient inactivation of factor 10a– DOES NOT AFFECT THROMBIN

Compare with heparin that affects both 10a and thrombin

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9
Q

Differentiate the MOA of Dabigatran, Apixaban, Rivaroxaban

A

Dabigatran: inhibits thrombin

Apixaban and Rivaroxaban: inhibits factor 10a directly

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10
Q

How is bivalirudin different from dabigatran?

A

Both are direct thrombin inhibitors BUT B is IV while D is oral.

Bivalirudin also inhibits platelet activation.

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11
Q

What is an antidote to dabigatran toxicity?

A

Idracizumab

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12
Q

What molecules are inhibited by warfarin by block of the carboxylation process?

A

10 9 7 2
BUT ALSO PROTEIN C AND S WHICH ARE ANTICOAGULANTS

Reduction in protein C may cause warfarin induced skin necrosis due to a hypercoaguable state.

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13
Q

How does warfarin prevent the carboxylation process of the clotting factors?

A

It does so by preventing the reductive metabolism of inactive vitamin K epoxide back to its hydroquinine form which is needed for protein carboxylation of the factors 10 9 7 2

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14
Q

How does warfarin cause cutaneous necrosis and venous thrombosis?

A

By depression of protein C

Skin necrosis usually occurs shortly after initiating warfarin therapy with a large loading dose or without concomitant heparin. Warfarin inactivates vitamin K-dependent clotting factors II, VII, IX, and X. At the same time, vitamin K-dependent proteins C and S are inactivated. This may cause a paradoxical hypercoagulable milieu in which microthrombi develop in cutaneous and subcutaneous venules, as the concentration of anticoagulant protein C falls more rapidly than other vitamin K-dependent precoagulant factors, which have longer half-lives

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15
Q

How is rt-PA different from streptokinase or urokinase

A

t-pa selectively activates plasminogen that is bout to fibrin which in theory confines fibrinolysis to the formed thrombus

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16
Q

What is the MOA of aspirin?

A

Irreversible inhibition of COX1 and COX2 resultin in low thromboxane A2 (responsible for causing platelets to change shape, release granules and aggregate)

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17
Q

What is the MOA of clopidogrel, ticlodipine and prasugrel?

A

Inhibit the ADP pathway of platelets by blocking the ADP receptor on platelets– ADP promotes aggregation of platelets

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18
Q

Why should omeprazole not be used with clopidogrel?

A

Omeprazole inhibits CYP2C19 which is responsible for converting clopidogrel into its active form

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19
Q

What is the final common pathway for platelet aggregation?

A

IIb/IIIa complex activation that acts as a receptor for fibrinogen, fibronectin, von Willebrand factor

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20
Q

What are blockers of the IIb/IIIa complex on platelets?

A

Abciximab, Eptifibatide, Tirofiban

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21
Q

How do dipyridamole and cilostazol act?

A
  1. Vasodilator that inhibits platelet function by inhibiting adenosine uptake by endothelial cells thereby increasing adenosine levels and by extension cAMP levels that function to inhibit platelet aggregation.
  2. Furthermore they inhibit phosphodiesterase activity that degrade cAMP and cGMP, a vasodilator.
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22
Q

What type of vitamin K is in food?

A

K1: Phytonadione

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23
Q

What is missing in hemophilia A and B

A

A Factor 8

B Factor 9

24
Q

What are the 3 chemicals secreted from platelets that all stimulate plate let aggregation?

A
  1. Thromboxane A2
  2. Adenosine diphosphate ADP
  3. Serotonin 5HT
25
Q

The activation of what receptor allows platelets to bind to fibrinogen?

A

alpha IIB and beta IIIA

26
Q

The intrinsic and extrinsic pathways of clotting converge in the activation of which factor? (First factor activated)

A

Factor X to Xa that catalyzes Prothrombin (2) to thrombin (2a)

But Xa needs to be with 5a the PROTHROMBINASE complex to accomplish this task

27
Q

What are the primary components of white and red thrombi?

A

White: Platelet
Red: Fibrin

28
Q

How does thrombin exert anticoagulant effects?

A

Activation of Protein C

29
Q

Factor 8 and 9, involved in the hemophilia conditions are involved in the activation of which co-factor?

A

10

30
Q

What complex heralds the start of the extrinsic pathway?

What protein keeps this complex in check to prevent excessive clotting?

A

Tissue Factor + Factor 7a

Tissue factor pathway inihibitor

31
Q

Identify which endogenous anticoagulant affects these group of factors:

  1. 2a 9a 10a 11a 12a
  2. 5a 8a
  3. Tissue factor and 7a complex
A
  1. Antithrombin– also inhibited by heparin
  2. Protein C and Protein S
  3. TFPI (Tissue factor pathway inhibitor)
32
Q

Whereas, tissue plasminogen activator tpa facilitates activation of plasminogen what drug antagonizes this process?

A

Aminocaproic acid and tranexamic acid

33
Q

Besides enoxaparin what other 2 LMWH can you name?

A

Tinzaparin

Dalteparin

34
Q

Bleeding from heparin or enoxaparin can be treated with? At what dose?

A

Protamine sulfate
100u heparin 1mg PS
1u enoxaparin 1mg PS

35
Q

What two medications that are direct thrombin inhibitors are from leech saliva?

A

Hirudin

Lepirudin

36
Q

What is the half life of dabigatran? how about warfarin?

A

D: 12-17 hours
W: 36 hours

37
Q

What critical renal clearance value requires the reduction in the standard dose of dabigatran?

A

30ml/min or less

38
Q

What does warfarin stand for?

A

Wisconsin Alumni Research Foundation

39
Q

Which warfarin is more potent? L or R?

A

L. 4x more

40
Q

How does warfarin work exactly?

A

It inhibits vitamin K epoxide reductase. It prevents the Vitamin K epoxide to go back to the hydroquinone form thereby preventing it from activating the gamma carboxylation of the Vit K dependent factors: 10, 9, 7, 2 (As well as protein C–> Pathophysiology behind HIT)

41
Q

Which vitamin K dependent clotting factor has the longest half life?

A

2

60 hours

42
Q

Which among these decrease PT time?

  1. Hyperthyroidism
  2. Hypothyroidism
  3. Metronidazole
  4. Rifampin
  5. Fluconazole
  6. Amiodarone
  7. Barbiturates
  8. Diuretics
  9. Cholestyramine
A 
Barbiturates
Hypothyroidism
Rifampin
Diuretics
Cholestyramine
43
Q

Warfarin resistance is most commonly seen in

patients with advanced cancers, typically of _________ origin

A

gastrointestinal

Trousseau’s syndrome

44
Q

The mechanisms
for their hypoprothrombinemic interaction are a stereoselective
inhibition of oxidative metabolic transformation of S-warfarin (the more potent isomer) and displacement of albumin- bound warfarin, increasing the free fraction: This is true of which drugs?

  1. Hyperthyroidism
  2. Hypothyroidism
  3. Metronidazole
  4. Rifampin
  5. Fluconazole
  6. Amiodarone
  7. Barbiturates
  8. Diuretics
  9. Cholestyramine
A

Metronidazole

Fluconazole

45
Q

How do 3rd generation cephalosporins augment the effect of warfarin?

A

The third-generation cephalosporins
eliminate the bacteria in the intestinal tract that produce vitamin K and, like warfarin, also directly inhibit vitamin K epoxide reductase.

46
Q

How does rTPA (tenecteplase and alteplase) differ from sterptokinase and urokinase in its selection of plasmin activation?

A

These activators preferentially
activate plasminogen that is bound to fibrin, which (in theory) confines fibrinolysis to the formed thrombus and avoids systemic activation.

47
Q

What is exact MOA of ASA?

A

Aspirin inhibits the synthesis of
thromboxane A 2 by irreversible acetylation of the enzyme cyclooxygenase.

Thromboxane
A 2 (TXA 2 ) is synthesized from arachidonic acid within platelets and is a platelet activator and potent vasoconstrictor.
48
Q

What is the exact MOA of TICLOPIDINE, CLOPIDOGREL, & PRASUGREL?

A

These drugs
irreversibly block the ADP receptor on platelets.

Products secreted from platelet granules include adenosine diphosphate (ADP), a powerful inducer of platelet aggregation, and serotonin (5-HT), which stimulates aggregation and vasoconstriction.

49
Q

What is the moa of abciximab, tirofiban and eptifibatide?

A

Blockade of platelet glycoprotein receptors 2b 3a

Activation of platelets results in a conformational change in the αIIbβIII integrin (IIb/IIIa) receptor, enabling it to bind fibrinogen, which cross-links adjacent platelets, resulting in aggregation and formation of a platelet plug

50
Q

Depending on the single nucleotide polymorphism inheritance pattern in
_______, some individuals may be poor metabolizers (activators) of clopidogrel

A

CYP2C19

51
Q

What is the disease related to those without 2b3a receptors on platelets?

A

Glanzmann Thrombasthenia

52
Q

What are the 2 MOA of cilostazol and dipyridamole?

A

Dipyridamole and the newer cilostazol appear to have a dual mechanism of action. They prolong the platelet-inhibiting action of intracellular cAMP by inhibiting phosphodiesterase enzymes that degrade cyclic nucleotides, including cAMP, an inhibitor of platelet aggregation, and cyclic guanosine monophosphate (cGMP), a vasodilator (see Chapter 19). They also inhibit the uptake of adenosine by endothelial cells and erythrocytes and thereby increase the plasma concentration of adenosine. Adenosine acts through platelet adenosine A2 receptors to increase platelet cAMP and inhibit aggregation.

53
Q

How many hours does IV vitamin K take before initial effect? Complete effect?

A

6 hours

24 hours

54
Q

Which anticoagulant can be used in pregnancy, heparin or warfarin?

A

Heparin

55
Q

What is the MOA of heparin and how is it monitored?

A

The heparin–ATIII complex combines with and irreversibly inactivates thrombin and several other factors, particularly factor Xa (Figure 34–1). In the presence of heparin, ATIII proteolyzes thrombin and factor Xa approximately 1000-fold faster than in its absence. Because it acts on preformed blood components, heparin provides anticoagulation immediately after administration. The action of heparin is monitored with the activated partial thromboplastin time (aPTT) laboratory test.

Brain Power: Neuropharmacology (5 decks)

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