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PHARMACOLOGY - Heme > Drugs Used For Coagulation Disorders > Flashcards

Drugs Used For Coagulation Disorders Flashcards

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1
Q

What anticlotting drugs are classified as Anticoagulants?

A

Heparins
Direct Thrombin Inhibitors
Direct Factor Xa inhibitors
Warfarin

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2
Q

What anticlotting drugs are classified as thrombolytics?

A

t-PA Derivatives

Aminocaproic Acid

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3
Q

What anticlotting drugs are classified as antiplatelet drugs?

A

Asprin
Gp IIb/IIIa inhibitors
ADP inhibitors (clopidogrel)
PDE/adenosine uptake inhibitors

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4
Q

What drugs are COX inhibitors?
• Drug Sub-Class of Clotting Drug
• MOA

A

Antiplatelet Drugs
• ASPRIN (irreversible)
• Ibuprofen (reversible)

MOA:
• Asprin inhibits COX-1 and prevents TXA2 from being formed

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5
Q

What drugs are ADP P2Y212 inhibitors?
• Drug Sub-Class of Clotting Drug
• MOA

A

Antiplatelet Drugs
• CLOPIDOGREL (preferred agent)
• TICLOPIDINE
• Prasugrel

MOA:
• Block the effects of ADP by blocking its receptor (P2Y212)

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6
Q

What drugs are Phosphodiesterase inhibitors
• Drug Sub-Class of Clotting Drug
• MOA

A

Antiplatelet Drugs
• Dipyridamole

MOA:
• Blocks hydrolysis of cyclic nucleotides like cAMP and cGMP

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7
Q

What drugs are GpIIb/IIIa inhibitors
• Drug Sub-Class of Clotting Drug
• MOA

A

Antiplatelet Drugs
• ABCIXIMAB
• EFTIBATIDE
• Tirofiban

MOA:
• Blocks binding of fibrinogen to the GpIIb/IIIa receptor, thus preventing platelet AGGREGATION

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8
Q

What drugs are PAR-1 inhibitors
• Drug Sub-Class of Clotting Drug
•MOA

A

Antiplatelet Drugs
• Vorapaxar

MOA:
• Blocks TXA2 RECEPTOR (PAR-1)

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9
Q

What happens when GPIIb/IIIa binds to fibrinogen?

• What is the GPIIb/IIIa conformational change dependent on?

A
  • Conformational Change to HIGH AFF. Depends on Ca2+
  • GPIIb/IIIa binds Fibrinogen - sends signal to platelets
  • Platelet then Binds harder in an IRREVERSIBLE manner
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10
Q

Who shouldn’t use platelet inhibiting drugs?

A

• Anyone at a high risk of bleeding or that may undergo elective surgery soon

***Make sure you give a sufficient amount of time when you discontinue the drug for its effects to dissipate

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11
Q

Asprin***
• Why is it so specific for platelets?
• Is increased dosing ever necessary?

A

Asprin:
• Blocks COX-1 which is present in many cells and produces PGI2 (a platelet inhibitor) and TXA2 (a platelet aggregant)

  • At low doses ENDOTHELIAL cells which make mostly PGI2 can compensate and upreulate COX-1 activity
  • Platelets have NO NUCLEUS so no upregulation of COX-1 can happen and TXA2 ceases to be produced

Increased Dose:
• NOT NECESSARY, it will start to inhibit COX2

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12
Q

Asprin***
• Organs typically affected by dose-related toxicity
• Weird Adverse Effects

A

Organs
• GI tract causing potential for Bleeding and Perforation
• Hepatic and Renal function affected in OD

Weird Effects:
• In some ppl. Asprin induces bronchospasm

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13
Q

Clopidogrel***

• MOA

A

FIRST LINE therapy in hearth attack and stroke

MOA
• Binds to ADP Receptor (P2Y212) and prevents the GPCR associated Adenylyl Cyclase from getting deactivated

• High levels of cAMP PREVENT platelet conformational changes

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14
Q

Ticlopidine***

• MOA

A

SECOND LINE therapy in heart attack and stroke

MOA
• Binds to ADP Receptor (P2Y212) and prevents the GPCR associated Adenylyl Cyclase from getting deactivated

• High levels of cAMP PREVENT platelet conformational changes

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15
Q

Dipyridamole

A

used in heart attack and stroke

MOA
• Binds to ADP Receptor (P2Y212) and prevents the GPCR associated Adenylyl Cyclase from getting deactivated

• High levels of cAMP PREVENT platelet conformational changes

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16
Q

Between the 3 drugs (clopidogrel, Ticlopidinek and Prasugrel) which are pro-drugs?
• How are these drugs given?
• Which shows the greatest variability in metabolism?

A

Pro-Drugs:
• Clopidogrel**
• Prasugrel

Active Drug:
• Ticlopidinek**- still gets activated to an even more active form.

Administration:
Oral

Variability:
Clopidogrel shows the greastest variability because of CYP2C19 polymorphisms

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17
Q

**Of the P2Y212 inhibitors, which has the most side effects?
• What are these effects?
• Name all of the inhibitors

A

Ticlopidinek** - SEVERE HEMATOLOGIC SIDE EFFECTS
• Agraulocytosis, Neutropenia
• **THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP)
• Anemia, Thrombocytopenia

All: Clopdigrel, Ticlopidinek, Prasugrel

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18
Q

Dipyridamole
• Use
• MOA
• Adverse Effects

A

Use:
• Prevention of Thrombosis in ppl. with prosthetic heart valves

MOA:
• Blocks Phosphodiesterase and causes elevated cAMP which has 2 effects
1. High cAMP prevents Arachiodonic Acid release
2. High cAMP prevents changes in platelet conformation

Adverse Effects:
• Not Remarkable

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19
Q

Abciximab***

MOA

A

MOA
Bind GPIIa/IIIb and prevent fibrogen from binding
**Abciximab is a MONOCLONAL Ab. and binds the to Arg-Gly-Asp sequence

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20
Q

Eftibatide***

A

MOA
Bind GPIIa/IIIb and prevent fibrogen from binding
**Derived from snake venom and binds Lys-Gly-Asp but is NOT an Ab.

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21
Q

Tirofiban

A

MOA
Bind GPIIa/IIIb and prevent fibrogen from binding
**IS NOT an Ab. but binds the to Arg-Gly-Asp sequence

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22
Q

Explain the descrepancy in duration of action between the 3 drugs that bind GPIIa/IIIb.
• Name all of the drugs

A

Abciximab** is a MONOCLONAL Ab. so its action last for WEEKS (2 wks)

• Effects of Eptifibatide** and Tirofiban cease after only 4 hrs

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23
Q

What are some adverse effects (other than increased bleeding) that may result from the 3 GpIIa/IIIb inhibitors?
• Name these drugs

Study These Flashcards
A

Abciximab, Eptifibatide, Tirofiban

*Low risk of Anaphylaxis (all 3)
• ABCIXIMAB –> Thrombocytopenia

24
Q

Vorapaxar
MOA
Major Adverse Effects

Study These Flashcards
A

MOA:
PAR-1 (protease activated receptor) antagonis

Major Adverse Effects:
VERY LONG HALF LIFE so it acts as though its irreversible and puts you at a VERY HIGH RISK OF BLEEDING

25
What herbals should you ask patients about before giving them an antiplatelet drug?
Ginko Biloba Garlic Ginger (inhibits thromboxane synthetase)
26
What drug acts as an indirect thrombin inhibitor? | • what is its antidote?
Indirect Thrombin Inhibitors: • Heparin*** Antidote: • Protamine Sulfate***
27
What drug acts as an inhibitor of clotting factor synthesis? • Antidote?
Prevention of Clotting factor synthesis: • Warfarin*** Antidotes: • Prothrombin Complex** • Phytonadione Vit. K1**
28
What drugs act directly on thrombin to inhibit?
* Dabigatran** * Bivalirudin * Lepirudin
29
What drugs act directly or indirectly on factor Xa to inhibit?
* Aprixiban** * Rivaroxaban*** * Enoxaparin*** (LMWH) * Fondaparinux (indirectly) *****NOTICE ALL THESE HAVE AN X in their name*****
30
What could be the problem with giving someone who has renal problems heparin?
Heparin is eliminated Renally and Renal dysfunction with increase the half life of the drug
31
How does heparin work? • what biochemical differences are there in heparin and Low MW heparin? • What clinical Differences are there?
MOA • Heparin binds Antithrombin which binds and inactivates thrombin **LOW MW Heparin inactivates factor Xa by catalyzing Antithrombin inactivation of Xa, this comes at the cost of NOT being long enough to from the Thrombin:Heparin:Antithrombin complex that regular heparin does Differences Clinically: NONE
32
What are some adverse effects of Heparin (other than bleeding)? • Explain the mechanism of adverse rxn • Name the LWM heparin we need to know
May Trigger Allergic/Anaphylatic Rxns • B/c it is obtained from an animal source Thrombocytopenia MOAR - Heparin binds to Factor 4 from platelet and causes immune reaction 30% of the time and can Venous and Arterial THROMBOSIS Enoxaparin low-molecular weight (indirect factor Xa inhibition)
33
How do you monitor the adverse effects of heparin in pts.? • what about LMWH? • How do you counteract the effects if you gave too much?
Heparin: Measure PTT - its should be 1.5 - 2.5x as long NOTE: a prolonged PTT does NOT happen with LMWH because it inhibits Xa not IIa LMWH: Measure with Factor Xa assay or Chromogenic test Antidote: • Protamine Sulfate*** • Whole blood plasma
34
What is given to counteract the effects of Heparin? • MOA • Risks
Protamine*** is a highly positively charged peptide (derived from fish sperm) - very BASIC MOA: • Combines with negatively charged (ACIDIC) heparin to pull it out of blood stream Risks: • Excess protamine may have anticoagulant effect • PROTAMINE REACTION
35
Explain the adverse effects of Protamine***. • What may predispose you to these reactions? • How can these be prevented?
Prevent by not giving too much * Shaking, Flushing, Chills, Back, Chest, or Flank pain * can be Anaphylactic Predisoposition: • Diabetes • Fish Allergy • Vasectomy
36
Warfarin • MOA • Drug-Drug interactions?
MOA: • Inhibits Vit. K epoxide Reductase and possibly Vit. K Reductase and prevents formation of Reduced Vit. K • Synthesis of Factors II, VII, IX, and X, and Protein C and S is inhibited CYP2C9 metabolized - causing drug-drug interactions
37
In the 1st 2-5 days of warfarin treatment what factor is most depressed? • after that?
Factor VII, then Factors II (thrombin) and X
38
``` Compare the following for Heparin and Warfarin. • Adminstration • Site of Action • Onset of Action • Duration ```
Heparin: • Given IV and acts In Blood • Quick to act, Quick to leave Warfarin: • Given Orally and acts in Liver • Slow to act, Slow to leave
39
Compare the following for Heparin and Warfarin. • Teratogenicity • Monitoring • Revseral Agents
Heparin: • Monitor with PTT • not teratogenic • Protamine** (antidote) Warfarin: • Monitor PT • TERATOGENIC • Prothrombin Complex, Vit. K.
40
Drug-Drug Interactions and Food are a big deal with Heparin | **See if he gives specifics in lecture
Drug-Drug Interactions and Food are a big deal with Heparin | **See if he gives specifics in lecture
41
What is a major Risk Warfarin and its effects on LIVER proteins? • Why does it occur? • Who is this adverse affect typically seen in? • How is this effect attenuated?
Risk: • Hyerpcoagulable state on initial dosing that can even lead to Skin Necrosis • Occurs because Prot. C and S have a shorter turnover time and their levels are decreased before factor VII Who: • Fat Middle-aged women typically have this reaction Attenuation: • Given it with Heparin then ween off the heparin
42
What drug causes Cholesterol Emoblism? | • How does this present?
Warfarin • Typically starts with Cyanosis in the feet and proceed to necrosis • Typcally presents as cyanosis in the feet, or pain in the feet
43
``` What is the MOA of both of the Direct Factor Xa Inhibitors? • Name them • Administration • Metabolism • Toxicity? ```
Drugs: Apixaban***, Rivaroxaban*** MOA: • Bind Directly to Factor Xa and inhibit it Administration: • Oral Metabolism: CYP3A4** drug-drug ints Toxicity: • Bleeding and we have no reversal agents available
44
``` What is the MOA of the Indirect Factor X inhibitor? • Name it • Administration • Metabolism • Toxicity? ```
Drugs: Fondaparinux • Bind to ATIII causing it to bind and inhibit Factor Xa Administration: • IV or SC Metabolism: • Unchanged Toxicity: • Bleeding and we don't have any reversal agents
45
``` What is the MOA of the direct Thrombin Inhibitors? • Name it. • Administration • Reversal? • Metabolism? ```
Drug: Dabigatran*** MOA: • Binds Directly and Inhibits BOTH free and clot-bound thrombin ``` Administration: • ORAL (all other drugs in this class are IV) ``` Metabolism: Plasma Esterases -- but Induces P-gp Bleeding reversal is possible with Idarucizumab
46
Why would you give someone Phynadione or Vitamin K1? • how long would these take to work? • Administration method?
You can give them anyway you like * Given to reduce Warfarin Toxicity * Take 3-8 hours to work after given IV
47
If you want to treat Warfarin Toxicity in faster than 3-8 hours what should you use? • what's in it?
Prothrombin Complex Concentrate (prepared from human blood) Contains (all liver coag. prots.): • Factor II, VII, IX, X • proteins C and S ***Better than Fresh Frozen plasm
48
Alteplase*** • MOA • Elimination • Risks
MOA: • This is just t-PA, it breaks up fibrin by hydrolyzing the arginine-valine bond in FIBRIN BOUND Plasminogen converting it into plasmin *Remember you run the risk of shooting small broken up clots everywhere when using this Elmination: • Hepatic Risk: • ANAPHYLAXIS
49
What drug has the opposite effect of Alteplase***?
Aminocaproic Acid
50
How does the MOA of streptokinase differ from Alteplase? | • other risks of streptokinase?
* Steptokinase activates BOTH fibrin and non-fibrin bound Plasminogen * Activating so much to plasmin can overwhelm alpha2-antiplasmin * This causes a LYTIC STATE Risk: • ANAPHYLAXIS
51
What drugs should you not use with thombolytics? | • Name the thombolytic we need to know.
Alteplase** Contradindications: • Other anti-coags. and anti-platelet drugs (seems to be okay with asprin and heparin) * Antineoplastic Agents * AntiFibrinolytics * Antibiotics (cephalosporins)
52
Aminocaproic Acid • Indication? • MOA • Risks
Used in hemorrhage or hyperfibrinolysis MOA: • Binds lysine-binding sites in Plasminogen and plasmin Risks: • Don't use in DIC without also using Heparin • Hypotension and Bradycardia
53
What drug should not be given to poor CYP2C19 metabolizers?
Clopdigrel
54
Aprixiban | MOA
MOA | • binds directly to factor Xa to inhibit it
55
Enoxaparin | • MOA
MOA • binds to Antithrombin inducing it to inhibit factor Xa and not as much IIa because its not long enough to form the complex necessary to inhibit IIa.
56
Idarucuzimab | MOA
Drugs used for reversal of Dabigatran action in case of too much bleeding.

PHARMACOLOGY - Heme (4 decks)

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