drugs used for PAD and DVT Flashcards

(50 cards)

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
Pharmacokinetics and toxicites of enoxaprin?
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
what are the characteristics of delteparin, and tinazeparin?
similar to enoxaparin with similar indications
27
MOA, effects, Clinical applications of Fondaparinux
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
Pharmacokinetics and toxicites of fondaparinux
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
MOA, effects, CLinical applications of Bivalirudin
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
Pharmacokinetics and Toxicites of Bivalirudin
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
what is desirudin?
recombinant form of Hirudin and is no longer available in U.S.
32
MOA, effects, and clinical applications of argatroban?
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
Pharmacokinetics and toxicites of argatroban
Pharmaco: given IV and has a short half life Toxicities: -risk for hemorrhage
34
MOA, effects, and clinical applications of warfarin
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
Pharmacokinetics, toxicites and contraindications of warfarin?
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
two proteins that are first seen lost in the administration of warfarin
Factor VII | Protein C
37
what is Cutaneous Necrosis?
Protein c has a shorter half life than several other clotting factors that warfarin administration can initially cause a pro coagulant state
38
MOA, Effects, and Clinical applications of rivaroxban?
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
Pharmacokinetics and toxicites of rivaroxban
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
what are other drugs similar to rivaroxaban?
apixaban, and edoxaban
41
MOA, effects, and clinical applications of dabigatran
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
Pharmacokinetics and toxicities of dabigatran:
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
how to monitor Heparins?
aPTT, anti-Xa
44
how to monitor warfarin
PT-based (INR)
45
how to monitor DOAC-factor Xa inhibitors
anti-Xa
46
how to monitor DOAC- direct thrombin inhibitor
Diluted thrombin time (TT)
47
Non fractionated and LMW heparin antidote?
Protamine sulfate due to high + charge
48
Warfarin antidote?
Vitamin K, prothrombin complex concentrate
49
DOAC factor Xa inhibitors antidote
andexanet alfa
50
DOAC direct thrombin inhibitors antidote
idarucizumab