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PHARMACOLOGY - Heme > Drugs Used For Coagulation Disorders > Flashcards

Drugs Used For Coagulation Disorders Flashcards

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

A

Abciximab, Eptifibatide, Tirofiban

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

24
Q

Vorapaxar
MOA
Major Adverse Effects

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
Q

What herbals should you ask patients about before giving them an antiplatelet drug?

A

Ginko Biloba
Garlic
Ginger (inhibits thromboxane synthetase)

26
Q

What drug acts as an indirect thrombin inhibitor?

• what is its antidote?

A

Indirect Thrombin Inhibitors:
• Heparin***

Antidote:
• Protamine Sulfate***

27
Q

What drug acts as an inhibitor of clotting factor synthesis?
• Antidote?

A

Prevention of Clotting factor synthesis:
• Warfarin***

Antidotes:
• Prothrombin Complex**
• Phytonadione Vit. K1**

28
Q

What drugs act directly on thrombin to inhibit?

A
  • Dabigatran**
  • Bivalirudin
  • Lepirudin
29
Q

What drugs act directly or indirectly on factor Xa to inhibit?

A
  • Aprixiban**
  • Rivaroxaban***
  • Enoxaparin*** (LMWH)
  • Fondaparinux (indirectly)

NOTICE ALL THESE HAVE AN X in their name

30
Q

What could be the problem with giving someone who has renal problems heparin?

A

Heparin is eliminated Renally and Renal dysfunction with increase the half life of the drug

31
Q

How does heparin work?
• what biochemical differences are there in heparin and Low MW heparin?
• What clinical Differences are there?

A

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
Q

What are some adverse effects of Heparin (other than bleeding)?
• Explain the mechanism of adverse rxn
• Name the LWM heparin we need to know

A

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
Q

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?

A

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
Q

What is given to counteract the effects of Heparin?
• MOA
• Risks

A

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
Q

Explain the adverse effects of Protamine***.
• What may predispose you to these reactions?
• How can these be prevented?

A

Prevent by not giving too much

  • Shaking, Flushing, Chills, Back, Chest, or Flank pain
  • can be Anaphylactic

Predisoposition:
• Diabetes
• Fish Allergy
• Vasectomy

36
Q

Warfarin
• MOA
• Drug-Drug interactions?

A

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
Q

In the 1st 2-5 days of warfarin treatment what factor is most depressed?
• after that?

A

Factor VII, then Factors II (thrombin) and X

38
Q 
Compare the following for Heparin and Warfarin. 
• Adminstration
• Site of Action
• Onset of Action
• Duration
A

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
Q

Compare the following for Heparin and Warfarin.
• Teratogenicity
• Monitoring
• Revseral Agents

A

Heparin:
• Monitor with PTT
• not teratogenic
• Protamine** (antidote)

Warfarin:
• Monitor PT
• TERATOGENIC
• Prothrombin Complex, Vit. K.

40
Q

Drug-Drug Interactions and Food are a big deal with Heparin

**See if he gives specifics in lecture

A

Drug-Drug Interactions and Food are a big deal with Heparin

**See if he gives specifics in lecture

41
Q

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?

A

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
Q

What drug causes Cholesterol Emoblism?

• How does this present?

A

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
Q 
What is the MOA of both of the Direct Factor Xa Inhibitors? 
• Name them 
• Administration 
• Metabolism
• Toxicity?
A

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
Q 
What is the MOA of the Indirect Factor X inhibitor? 
• Name it
• Administration
• Metabolism
• Toxicity?
A

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
Q 
What is the MOA of the direct Thrombin Inhibitors? 
• Name it. 
• Administration
• Reversal?
• Metabolism?
A

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
Q

Why would you give someone Phynadione or Vitamin K1?
• how long would these take to work?
• Administration method?

A

You can give them anyway you like

  • Given to reduce Warfarin Toxicity
  • Take 3-8 hours to work after given IV
47
Q

If you want to treat Warfarin Toxicity in faster than 3-8 hours what should you use?
• what’s in it?

A

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
Q

Alteplase***
• MOA
• Elimination
• Risks

A

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
Q

What drug has the opposite effect of Alteplase***?

A

Aminocaproic Acid

50
Q

How does the MOA of streptokinase differ from Alteplase?

• other risks of streptokinase?

A
  • 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
Q

What drugs should you not use with thombolytics?

• Name the thombolytic we need to know.

A

Alteplase**

Contradindications:
• Other anti-coags. and anti-platelet drugs
(seems to be okay with asprin and heparin)

  • Antineoplastic Agents
  • AntiFibrinolytics
  • Antibiotics (cephalosporins)
52
Q

Aminocaproic Acid
• Indication?
• MOA
• Risks

A

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
Q

What drug should not be given to poor CYP2C19 metabolizers?

A

Clopdigrel

54
Q

Aprixiban

MOA

A

MOA

• binds directly to factor Xa to inhibit it

55
Q

Enoxaparin

• MOA

A

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
Q

Idarucuzimab

MOA

A

Drugs used for reversal of Dabigatran action in case of too much bleeding.

PHARMACOLOGY - Heme (4 decks)

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