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Steve IHO week 6 > Regal- Thursday Drugs and stuff > Flashcards

Regal- Thursday Drugs and stuff Flashcards

1
Q

Generally speaking: Phase 1 of hemostasis

A

Phase 1: Vascular constriction limits the flow of blood to the area of injury

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2
Q

Generally speaking: Phase 2 of hemostasis

A

Phase 2: Platelets become activated and aggregate at the site of injury, forming a temporary, loose platelet plug (Primary Hemostasis)

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3
Q

Generally speaking: Phase 3 of hemostasis

A

Phase 3: A fibrin mesh (also called the clot) forms and entraps the plug (Secondary Hemostasis)

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4
Q

Generally speaking: Phase 4 of hemostasis

A

Phase 4: The clot is dissolved in order for normal blood flow to resume following tissue repair.

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5
Q

Aspirin

A 
Acetylsalicylate
Irreversible inhibitor of COX
decreasing the expression of gpIIb/IIIa
Platelets do not have COX2
Antipyretic, analgesic and anti-inflammatory
Adverse effects: Bleeding, GI disturbances, Tinnitus
Low dose (platelet effect) vs high dose (anti-inflammatory)
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6
Q

Clopidogrel

A

Irreversible ADP receptor antagonist that prevents activation of ADP receptor
Oral
lasts days
Used during stenting
recommended for patients that don’t tolerate aspirin

Adverse effects include:
BLEEDING, nausea, diarrhea, rash (10-50% of patients)
severe leukopenia (1% of patients)
thrombotic thrombocytopenic purpura (TTP) – very rare (usually with ticlopidine)

requires activation via CYP2C19 so drugs that impair this isoform (e.g. omeprazole) should be used with caution

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7
Q

Prasugrel

A

Irreversible ADP receptor antagonist that prevents activation of ADP receptor
Oral
lasts days
Used during stenting
recommended for patients that don’t tolerate aspirin

Adverse effects include:
BLEEDING, nausea, diarrhea, rash (10-50% of patients)
severe leukopenia (1% of patients)
thrombotic thrombocytopenic purpura (TTP) – very rare (usually with ticlopidine)

have fewer side effects than Ticlopidine

Prasugrel has fewer side effects than Ticlopidine

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8
Q

Ticlopidine

A

Irreversible ADP receptor antagonist that prevents activation of ADP receptor
Oral
lasts days
Used during stenting
recommended for patients that don’t tolerate aspirin

Adverse effects include:
BLEEDING, nausea, diarrhea, rash (10-50% of patients)
severe leukopenia (1% of patients)
thrombotic thrombocytopenic purpura (TTP) – very rare (but more likely to happen with ticlopidine)

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9
Q

ADP Receptor Antagonists Class: names

A

Clopidogrel, Prasugrel, Ticlopidine

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10
Q

GPIIb/IIIa Receptor Inhibitors Class: names

A

Tirofiban, Abciximab, Eptifibatide

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11
Q

Abciximab

A

humanized MAB against GPIIb/IIIa

GPIIb/IIIa Receptor Inhibitor

Prevent binding of adhesive glycoproteins such as fibrinogen and vWF to activated platelets

Inhibits the final common pathway for platelet aggregation

Given IV: with aspirin and heparin during angioplasty for acute coronary syndromes
Adverse effects include: Bleeding, Thrombocytopenia (chronic use)

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12
Q

Eptifibatide

A

fibrinogen analogue

GPIIb/IIIa Receptor Inhibitor

Prevent binding of adhesive glycoproteins such as fibrinogen and vWF to activated platelets

Inhibits the final common pathway for platelet aggregation

Given IV: with aspirin and heparin during angioplasty for acute coronary syndromes
Adverse effects include: Bleeding, Thrombocytopenia (chronic use)

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13
Q

Tirofiban

A

GPIIb/IIIa Receptor Inhibitor

non-peptide competitive inhibitor

Prevent binding of adhesive glycoproteins such as fibrinogen and vWF to activated platelets

Inhibits the final common pathway for platelet aggregation

Given IV: with aspirin and heparin during angioplasty for acute coronary syndromes
Adverse effects include: Bleeding, Thrombocytopenia (chronic use)

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14
Q

Dipyridamole

A

Increases cAMP and inhibits platelet activation

Phosphodiesterase 3 inhibitor (increases cAMP by preventing it’s breakdown to 5’AMP by phosphodiesterase)

Inhibits platelet uptake of adenosine and thus increases adenosine interaction with Adenosine A2 receptor-> increased cAMP.

Also a vasodilator –> adverse effect is headache

Little or no beneficial effect by itself

Used in combination with aspirin or warfarin

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15
Q

Indirect thrombin inhibitors: names

A

Unfractionated heparin
Low molecular weight heparin
Fondaparinux

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16
Q

direct thrombin inhibitors: names

A

Bivalirudin
Argatroban
Dabigatran etexylate

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17
Q

Unfractionated heparin (UFH) is the same thing as

A

high molecular weight (HMW) heparin, often just called heparin

18
Q

Indirect thrombin inhibitors: mechanism

A

Bind to antithrombin to have their effect

Antithrombin inactivates both thrombin and Factor Xa

Heparin’s activity against thrombin is size dependent

Heparin is mainly obtained from porcine intestine

Also binds to plasma proteins, platelet (platelet factor 4), macrophages, and endothelial cells limiting its bioavailability and and gives highly variable anticoagulant response

Inactivates several coagulation enzymes, including Factors IIa (thrombin), Xa, IXa, XIa, and XIIa, by binding to the cofactor AT

Heparin’s activity against thrombin is size dependent

can cause thrombocytopenia

19
Q

Patients on Unfractionated heparin (UFH) or High molecular weight heparin (HMW heparin) require what

A

Requires close monitoring of activated partial thromboplastin time (aPTT or PTT)

Less predictable pharmacokinetics (large ranges of molecular weights in this treatment)

20
Q

Do patients on Low molecular weight heparin = LMW heparin require monitoring?

A

No monitoring required in most patients

More predictable pharmacokinetics
Fewer non-hemorrhagic side effects

21
Q

Clotting time: aPTT test

A

aPTT tests intrinsic pathway

If you add negatively charged PL and particulates, Factor XII is activated and it clots faster –> activated partial thromboplastin time

If the aPTT is prolonged (and PT normal), then the person is considered to have a defect in the intrinsic pathway

Normal PTT times require the presence of the following coagulation factors: I, II, V, VIII, IX, X, XI, & XII

22
Q

Clotting times: PT and derived INR test

A

PT and derived INR tests extrinsic pathway

Recalcified plasma clots in 12-14 sec if you add thromboplastin (TF + phospholipids)

If PT is prolonged (and aPTT normal), then the person has a defect in the extrinsic pathway

PT measures factors I (fibrinogen), II (prothrombin), V, VII, and X

23
Q

Heparin-induced thrombocytopenia

A

Thrombotic complications may precede the drop in platelets

Twice as likely in women than men

Probably due to development of IgG antibodies against complexes of heparin with platelet factor 4

24
Q

Protamine

A

Highly basic positively charged peptide that combines with negatively charged heparin to form a stable complex that lacks anticoagulant activity

Only binds long heparin molecules
HMW heparin has a short half life.
Incompletely reverses activity of LMWH
Will not reverse the activity of fondaparinux.

25
Q

Bivalirudin

A

Bind directly to thrombin and inhibits the enzyme

26
Q

Argatroban

A

Bind directly to thrombin and inhibits the enzyme

27
Q

Dabigatran etexylate

A

oral, new (don’t know why it’s age is important)

Binds directly to thrombin

28
Q

Warfarin

A

inhibits conversion of oxidized vitamin K epoxide into its reduced form, vitamin K hydroquinone

(blocks Vitamin K dependent epoxide reductase)

This inhibits vitamin K-dependent gamma-carboxylation of factors II, VII, IX, and X and Protein C

29
Q

Warfarin Dosing Varies Widely, Why?

A

Polymorphisms in the C1 subunit of vitamin K reductase (VKORC1) can affect the susceptibility of the enzyme to warfarin-induced inhibition

Common genetic polymorphisms in CYP2C9 can influence warfarin metabolism – 30% are slow metabolizers

30
Q

which form of Warfarin is more active

A

S is more active than R

31
Q

Direct Factor Xa inhibitors: names

A

Rivaroxaban, apixaban, exodaban

32
Q

Rivaroxaban

A

Inhibit Factor Xa
Rapid onset of action and shorter half lives than warfarin
Don’t require monitoring
No antidote
Newer drugs so their place in treatment and as a replacement for warfarin is being determined

33
Q

apixaban

A

Inhibit Factor Xa
Rapid onset of action and shorter half lives than warfarin
Don’t require monitoring
No antidote
Newer drugs so their place in treatment and as a replacement for warfarin is being determined

34
Q

exodaban

A

Inhibit Factor Xa
Rapid onset of action and shorter half lives than warfarin
Don’t require monitoring
No antidote
Newer drugs so their place in treatment and as a replacement for warfarin is being determined

35
Q

Pharmacokinetics: what is it

A

Think of Absorption, distribution, metabolism and elimination (ADME)

For oral anticoagulants pharmacokinetic drug interactions are primarily due to:
enzyme induction
enzyme inhibition
reduced plasma protein binding

36
Q

Pharmacodynamics: what is it

A

Biochemical and physiological effects of drugs and their mechanism of action
Individuals vary in the magnitude of their response to the same concentration of a drug
For oral anticoagulants pharmacodynamic drug interactions are primarily due to:
reduced clotting factor synthesis
competitive antagonism with Vitamin K
hereditary resistance to oral anticoagulant

37
Q

Phytonadione

A

vitamin K1

good for warfarin overdoes

38
Q

Streptokinase

A

Fibrinolytic Drug

Streptokinase – from Strep
rarely used clinically
Complexes with plasminogen wherever it is and facilitates formation of plasmin

39
Q

Urokinase

A

Fibrinolytic Drug

Kidney enzyme that directly converts plasminogen to plasmin
Occurs primarily in response to inflammatory stimuli
Promotes extravascular fibrinolysis

40
Q

tPAs: names

A

= tissue plasminogen activators

Alteplase
Reteplase
Tenecteplase

41
Q

tPAs: mechanism

A

Preferentially activate plasminogen that is bound to fibrin which confines it to the thrombus rather than systemic activation.
Dissolve EXISTING life-threatening thrombi
Activate plasminogen
Given IV
Narrow spectrum of use
BLEEDING
Costly

42
Q

Aminocaproic acid

A

Potent inhibitor of fibrinolysis
Blocks the interaction of plasmin with fibrin
Very minor uses

Steve IHO week 6 (3 decks)

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