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CPR II Drugs test 1 > drugs used for PAD and DVT > Flashcards

drugs used for PAD and DVT Flashcards

1
Q

What are the Parenteral anticoagulants that are indirect thrombin/Xa inhibitors

A

Unfractionated/high molecular heparin

low molecular weight heparins:
-enoxaparin, dalteparin, tinzaparin

synthetic pentasccharides:
-fondaparinux

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2
Q

what are the paraenteral anticoagulants that are direct thrombin inhibitors

A

Bivalirudin

argatroban

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3
Q

what are the oral anticoagulant?

A

Coumarin derivative

Warfarin

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4
Q

what are the direct oral anticoagulant factor Xa inhibitors

A

rivaroxaban
apixaban
endoxaban

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5
Q

what are the direct oral anticoagulant thrombin inhibitors

A

dabigatran

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6
Q

what are the oral antiplatelet phosphodiesterase inhibitor?

A

dipyridamole, cilostazol

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7
Q

difference between a red clot and white clot

A

red clot is fibrin rich with trapped RBC

  • atrial fibrillation to stroke
  • DVT
  • PE

White clot: platelet rich
-damaged endothelium ruptured atherosclerotic plaques that lead to unstable angina, myocardial infarction

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8
Q

what are some PAD complications?

A

Critical limb ischemia:

  • sores that dont heal that lead to infection, tissue death (gangrene)
  • may need amputation

Stroke and Heart attack

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9
Q

what is the best way for PAD prevention?

A

HEalthy lifestyle

  • quit smoking
  • keep diabetes under control
  • exercise
  • low cholesterol
  • heat healthy foods and maintain a healthy weight
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10
Q

Medications to treat PAD

A

•
Cholesterol-lowering medications… e.g., statins (see “Drugs to Treat Hyperlipidemia”)
–
goal is LDL < 100 mg/dL
•
High blood pressure medications, if needed… (see “Drugs to Treat Hypertension and HTN Urgency/Emergency”)
–
goal is < 130/80 mm Hg
•
Control blood sugar levels if diabetic…
–
e.g., metformin for T2DM (drugs will be discussed in EN RE II, Med 218)
•
Prevent arterial blood clots (see “Drugs to Treat Cardiac Arrhythmias/ACS/Stable Angina”)
–
antiplatelet drugs: e.g., aspirin, clopidogrel… avoid concurrent gingko biloba (↑bleeding risk)
–
locally-infused clot buster drugs if occlusion from clot due to plaque rupture
•
Symptom-relief medications.
–
cilostazol
–
pentoxifylline, well-tolerated but less efficacious alternative

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11
Q

cilostazol MOA, effects and Clinical applications

A

MOA: type 3 phosphodiesterase inhibitor that prolongs life of cAMP on platelets and cells

Effects: Platelet aggregation inhibitor
-vasodilator

Clinical applications:
-intermittent claudication

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12
Q

Pharmacokinetics, toxicities and BB warning ciostazol

A

Pharmacokinetics:

  • oral tablet 2x a day
  • metabolized by CYP3A4

toxicities:

  • headache
  • diarrhea
  • palpitations
  • dizziness
  • peripheral edema
BB warning:
-contraindicated in patients with heart failure, use is asssociated with decreased survival of class III and class IV patients
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13
Q

what are the surgical treatment of PAD

A

Balloon or laser angioplasty stent

atherectomy

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14
Q

symptoms of an affected leg with DVT

A

swelling
pain and cramping in the calf
-red/discolored skin
-warmth

lead to PE

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15
Q

DVT risk factors

A

•
genetic blood-clotting disorder –e.g., factor V Leiden, mutation ↑prothrombin
•
prolonged bed rest, such as during a long hospital stay, or paralysis –calf muscles don’t help blood circulate
•
injury or surgical damage to veins
•
pregnancy
•
overweight or obese
•
oral contraceptives or hormone replacement therapy –estrogen ↑synthesis of clotting factors
•
smoking affects blood clotting and circulation
•
cancer –
•
vein compression by tumor, unusual blood flow patterns in tumor
•
hypercoagulable state due to secretions –e.g., tissue factor, ADP, thrombin, thrombogenic tumor exosomesdue to surface expression of phosphatidylserine
•
heart failure–low cardiac output means sluggish flow
•
inflammatory bowel disease–2-3x higher risk due to hypercoagulable state from altered expression of various proteins, exact etiology uncertain
•
family history
•
age… risk increases if age > 60 yrs
•
sitting for long periods of time, such as when driving or flying

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16
Q

DVT prevention

A

Avoid sitting still
-dont cross legs

Make lifestyle changes:

  • lose weight if overweight
  • quit smoking

Exercise

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17
Q

Drug options for treatment of DVT

A

Anticoagulants

Clot busters

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18
Q

Non-pharmacologic treatment of DVT

A

Compression socks
Stents
Vena cava filter

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19
Q

what drugs block white clot formation

A

antiplatelet drugs

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20
Q

what drugs block red clots formation

A

Anticoagulant drugs block thrombin activation/fibrin formation

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21
Q

what drugs destroy formed clots?

A

thrombolytic drugs

22
Q

MOA effects and Clinical applications of heparin unfracetionated

A

MOA: made from lungs of cattle and pigs and lots can vary

  • long polysaccharide chain
  • pentasaccharide sequence found randomly that binds antithrombin III and inhibits factor Xa

effects:

  • blocks generation of thrombin
  • inactivates thrombin
  • prevents red clots

Clinical applications:
-rapid onset anticoagulant effects
(PE, stroke, DVT, DIC, acute MI)
-used in pregnancy and doesn’t cross placenta
-used in catheters extracorporeal circuits

antidote: Protamine (positive charges)

23
Q

Pharmacokinetics and toxicites

A

Pharma:

  • parenterally (IV or SC) since it is negatively charged
  • binds nonspecifically
  • variable plasma levels so must monitor aPTT assay (1.5-2)
  • half life 1.5 hrs can vary

Toxicities:

  • contraindicted in thrombocytopenia and uncontrolled bleeding
  • avoid in surgery
  • heparin induced thrombocytopenia (reduced platelet and thrombotic events)
24
Q

MOA, effects, and Clinical applications of Enoxaparin

A

MOA: LMW heparin
-cant form tertnary complex with antithrombin III and thrombin but factor Xa is inhibited

effects:

  • selectively blocks factor Xa
  • prevents red clots
  • little effect on thrombin

Clinical applications:

  • prevent DVT, after surgery
  • treatment of DVT +/- PE
  • prevent ischemic complications
  • safe in pregnancy
25
Q

Pharmacokinetics and toxicites of enoxaprin?

A

Pharm:

  • easier to use than unfrac hep since dosing is predictable
  • first choice treatment and prevention of DVT
  • longer half lives

Toxicites:

  • bleeding is a major adverse effect
  • protamine is the antidote
  • Heparin induced toxicity
  • can cause severe neurological injuries in spinal punctures
26
Q

what are the characteristics of delteparin, and tinazeparin?

A

similar to enoxaparin with similar indications

27
Q

MOA, effects, Clinical applications of Fondaparinux

A

MOA: synthetic pentasaccharide identical to antithrombin binding structure of heparin
-short length it is selectively inhibits factor Xa without affecting thrombin

Effects:

  • blocks coagulation by preventing conversion of prothrombin to thrombin
  • no effect on thrombin
  • more effective than enoxaparn but has increased risk for bleeding

Clinical applications:

  • prevents DVT
  • treatment of acute PE and DVT in conjunction of warfarin
28
Q

Pharmacokinetics and toxicites of fondaparinux

A

Pharm:

  • administer subQ as a fixed dose
  • predictable pharmacokinetics
  • long half life

Toxicities:

  • bleeding is biggest concern
  • not reversible with protamine
  • does not cause heparin induced thrombocytopenia
29
Q

MOA, effects, CLinical applications of Bivalirudin

A

MOA: synthetic 20 aa peptide similar to hirudin (anticoagulant of leeches)
directly blocks thrombin

effects:
-reversibly inhibits thrombin blocks both catalytic site and substrate binding site of thrombin

Clinical applications:
-can be given in combination with aspirin to patients undergoing coronary angioplasty

30
Q

Pharmacokinetics and Toxicites of Bivalirudin

A

Pharm:

  • must be given IV like heparin
  • expensive

TOxicites:

  • doesn’t require antithrombin and causes less bleeding
  • but no antidote
  • anaphylaxis with repeated use
31
Q

what is desirudin?

A

recombinant form of Hirudin and is no longer available in U.S.

32
Q

MOA, effects, and clinical applications of argatroban?

A

MOA: small molecular weight thrombin inhibitor that directly binds to catalytic site of thrombin similar to hirudin analogs
-does not bind to substrate binding site as well

effects:

  • reduces development of new thrombosis
  • permits restoration of platelet counts in those with HIT

Clinical applications:

  • Prophylaxis and treatment of thrombosis in patients with HIT
  • efficacy of treatment is monitored by aPTT
33
Q

Pharmacokinetics and toxicites of argatroban

A

Pharmaco: given IV and has a short half life

Toxicities:
-risk for hemorrhage

34
Q

MOA, effects, and clinical applications of warfarin

A

MOA: vitamin K antagonist
-oldest oral anticoagulant

effects:
-decreases production of biologically active forms of calcium dependant factors II, VII, IX, and X and protein C and S

Clinical applications:

  • used for long term prophylaxis of thrombosis
  • prevent DVT, PE, Thrombosis via afib
  • prevent thromboembolism of mechanical heart valves
  • not useful in emergencies since effects are delayed
35
Q

Pharmacokinetics, toxicites and contraindications of warfarin?

A

Pharm:

  • orally active
  • eliminated by liver in bile
  • slow onset
  • slow offset
  • monitored with prothrombin time (INR) (2-3)
  • Monitored frequently whenever a drug is added or subtracted

Contraindicted:
-patients with high risk of bleeding or surgery of the brain, eye, or spinal cord

Toxicites:

  • bleeding
  • reversed by administering vitamin K, FFP
  • liver disease is a risk

drugs can increase the effects

  • promote bleeding
  • decrease effects as well
36
Q

two proteins that are first seen lost in the administration of warfarin

A

Factor VII

Protein C

37
Q

what is Cutaneous Necrosis?

A

Protein c has a shorter half life than several other clotting factors that warfarin administration can initially cause a pro coagulant state

38
Q

MOA, Effects, and Clinical applications of rivaroxban?

A

MOA: direct inhibitor of activated factor X

Effects :

  • directly inhibits the production of thrombin
  • rapid onset
  • fixed dosage
  • lower bleeding risk
  • fewer drug interactions
  • no need for INR monitoring

Clinical applications:
-prevent DVT and PE, and stroke with a nonvalvular a fib

no antidote but maybe andexanet alfa

39
Q

Pharmacokinetics and toxicites of rivaroxban

A

Pharm:

  • administered orally as a high bioavailabillity
  • half life 5-9 hrs

Toxicites:

  • bleeding
  • epidural hematoma, intercranial, adrenal, GI bleeding
  • avoided in patients with significant renal or hepatic impairment
  • appears safe in pregnancy
  • not combined with other anticoagulants interacts with CYP34A
40
Q

what are other drugs similar to rivaroxaban?

A

apixaban, and edoxaban

41
Q

MOA, effects, and clinical applications of dabigatran

A

MOA: reversible direct thrombin inhibitor

Effects:

  • directly blocks thrombin
  • rapid onset
  • no need to monitor
  • few drug interactions
  • lower risk of bleeding
  • same dose is used for all patients

Clinical applications:

  • prevention of stroke and systemic embolism in patients with nonvalvular atrial fib
  • contraindication for therapy of those with mechanical heart valves
42
Q

Pharmacokinetics and toxicities of dabigatran:

A

Pharmacokinetics:

  • pills are unstable and must be kept in bottle
  • eliminated by kidney with half life of 13 hrs
  • given orally be taken with or without food

Toxicites:

  • Bleeding is the major concern
  • antidote recently approved (idarucizumb)
  • compete for p-GP transporter
43
Q

how to monitor Heparins?

A

aPTT, anti-Xa

44
Q

how to monitor warfarin

A

PT-based (INR)

45
Q

how to monitor DOAC-factor Xa inhibitors

A

anti-Xa

46
Q

how to monitor DOAC- direct thrombin inhibitor

A

Diluted thrombin time (TT)

47
Q

Non fractionated and LMW heparin antidote?

A

Protamine sulfate due to high + charge

48
Q

Warfarin antidote?

A

Vitamin K, prothrombin complex concentrate

49
Q

DOAC factor Xa inhibitors antidote

A

andexanet alfa

50
Q

DOAC direct thrombin inhibitors antidote

A

idarucizumab

CPR II Drugs test 1 (8 decks)

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