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Pharm 1 > Hematopoietics, Anticoag, Antiplatelets and Thrombolytic Drugs > Flashcards

Hematopoietics, Anticoag, Antiplatelets and Thrombolytic Drugs Flashcards

1
Q

HEMATOPOIETICS

A

Recombinant growth factors

3 types:

  1. Erythropoietin Stimulating Agent
    - increase RBC production (Epoetin)
  2. Granulocyte Stimulating Agents
    - increase myeloblast cells (G-CSF, GM-CSF)
  3. Platelet Stimulating Agents
    - increases platelet production (thrombocytes)
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2
Q

ESAs

A

Epoetin, Procrit, Darbepoetin given IV or SQ

Uses: Anemia: renal disease

Onset of Action

  • 2 to 6 weeks (take a while to work)
  • 8-26 days to actually increase RBC numbers

Monitoring

  • hemoglobin
  • iron levels
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3
Q

G-CSF

A

Increases WBCS-neutrophils

Filgrastim, Pegfilgrastrim
IV, SQ or patch

Uses:
-treats neutropenia complications in cancer pt.

Pegfilgrastim needs to be given once
Filgrastrim is daily

Monitoring: absolute neutrophil count (ANC)

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4
Q

GM-CSF

A

Increases WBC production (neutrophils, eosinophils, basophils and mast cells) and RBCs

Sargramostin

Uses:

  • acute myelogenous leukemia
  • bone marrow transplant

Monitoring: CBC with differential

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5
Q

TPO Receptors

A

Increase platelet production

Romipolstim(outside of receptor) Eltrombopag (inside of receptor)

MOA:
-binds to and activates human thrombopoetin receptor

OOA:
-increased platelet production in a week

Uses: chronic immune thrombocytopenia

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6
Q

Drugs to combat CLOT FORMATION

A

1: ANTICOAGULANTS
2: ANTI-PLATELETS
3: THROMBOLYTICS

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7
Q

ANTICOAGULANTS

A
  • prevent further propagation of clots
  • disrupt clotting cascade
  • best for treatment of arterial and venous clots
  • inhibit activity of clotting factors
  • inhibit synthesis of clotting factors

HEPARIN, LMWH, FONDAPARINUX, WARFARIN, DIRECT THROMBIN AND DIRECT Xa INHIBITORS

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8
Q

Heparin UNFRACTIONATED MOA

A

MOA: enhance the activity of antithrombin

  • inhibit factor Xa and thrombin equally
  • inhibits the change of fibrinogen to fibrin

A mixture of long polysaccharide chains
Active section is a pentassaccharide sequence found randomly along the chain
Metabolized by the LIVER
Bolus dose

Indications: treatment and prevention of thrombosis

Bodies own way of responding to clot is ENHANCED by heparin

  1. First binds with Antithrombin + causes a conformational change
  2. Then binds to factor 10 (Xa) and thrombin EQUALLY
  3. THIS DISRUPTS FINAL STEP OF FIBRINOGEN TO FIBRIN
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9
Q

UPH Monitoring

A

Monitoring efficacy

  • aPTT (more common) or anti-Xa
  • checked usually every 4-6 hours until stable

APPT and ANTI XA SHOULD BE HIGHER WITH HEPARIN

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10
Q

APTT test

A

Activated partial thromboplastin

  • measures the time it takes for the blood to clot
  • higher aPTT=more anticoagulation effects

We want high aPPT when on heparin
-but not too high or too low

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11
Q

Anti-Xa

A

Measures the amount of Xa not bound by heparin

Higher the level=more anticoagulation effects

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12
Q

UPH Adverse Effects

A

BLEEDING (10%)

  • must monitor for:
  • blood loss
  • decreased BP
  • increased HR
  • black tarry stools
  • red colored urine
  • headache
  • somnolence
  • abdominal pain
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13
Q

UFH Side Effects

A

Spinal epidural hematoma

Heparin-Induced Thrombocytopenia (HIT)
-DECREASE IN PLATELETS
-Type 1: usually 1-2 days after exposure
(transient drop in platelets, will recover)
-Type 2: 4-7 days after exposure WORSE
(>50% drop in platelets over time, worry about thrombosis)
(COULD cause a secondary clot)

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14
Q

HIT

A

Body develops antibodies to heparin-PF4 (platelet factor 4) complex
-results in new thrombosis development

Confirm by ordering HIT antibody test with SRA assay

Treatment

  • discontinue heparin
  • initiate ARGATROBAN (antidote) - different drug that causes clot formation
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15
Q

Reversing bleeding with UFH

A

Antidote: PROTAMINE(+)
-Binds with Heparin(-)—>no longer able to bind to anti-thrombin—>CAUSES CLOTS, prevents heparin from working

  • neutralization occurs immediately and last for 2 hours
  • little roll for protamine if the heparin infusion was discontinued over 4 hours agin
  • give plasma or blood (if Hg<7 or hypotension) in addition to protamine if necessary
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16
Q

PROTAMINE

A

First isolated from fish sperm

Highly positive charged molecule (binds with heparin-negatively charged)

Sequesters heparin so it cannot bind with antithrombin

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17
Q

Low-molecular weight heparins

LMWH

A

Smaller pieces of polysaccharides -cannot hug thrombin

MOA:
-bind to antithrombin and inactivate Factor Xa (only)

Indications: treatment and prevention of thrombosis

Onset: 1-2 hours QUICKER; SQ (Patient can be treated outpatient!

Formulations: Enoxaparin, Tinzaparin, and Dalteparin

Monitoring: anti Xa (level)
-rental cleared (cannot use in patients with acute kidney injury or hemodialysis

PREFERRED OVER UFH to treat and prevent venous thrombosis
-quicker, no hospital stay, can self administer, don’t have to monitor, rare to cause HIT

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18
Q

LMWH Adverse Events

A

Bleeding (less common that UFH)

Spinal /epidural hematoma

Thrombocytopenia (similar to HIT)

  • antibody mediated, less likely with LMWH
  • discontinue medication, treat with Argatroban
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19
Q

LMWH Reversal of Bleeding

A

Antidote: PROTAMINE can be used, not as effective

  • binds 80% of LMWH
  • can give within 12-24 hours after last done of LMWH
  • give plasma or blood (if Hg<7 or hypotension) in addition to PROTAMINE if necessary
  • protamine cannot bind to LMWH, less of a negatively charged tail present for protamine to bind to
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20
Q

Fondaparinux MOA

A

-inhibits Factor Xa by binding to antithrombin

Only contains the essential pentasaccharide

DVT/PE treatment and prevention

Administration: SQ -once a day

Renally eliminated, cannot use in acute kidney injury or hemodialysis

Can be used in patients with a history of HIT

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21
Q

Fondaparinux Adverse Events and Reversal

A

Adverse events:

  • bleeding
  • similar to UFH and LMWH

Antidote: None

  • give plasma or blood (if Hg<7 or hypotensive)
  • cannot give PROTAMINE, drug is too small and will not bind to protamine
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22
Q

Vitamin K Antagonist

A

WARFARIN

Treats and prevents thrombosis

MOA: inhibits clotting factor synthesis that require vitamin K

  • inhibits vitamin K epoxide reductase complex 1 and vitamin k reductase
  • inhibit production of: Prothrombin (Factor II), VII, IX, X, Protein C and S (FACTORS 2, 7, 9, 10 and PROTEIN C and S)
  • conversion of fibrinogen to fibrin will not occur
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23
Q

Warfarin (cont.)

A

Extensively bound to albumin

Metabolized by the liver CYP2C9

OOA: DELAYED! takes approx 2 days to start decreasing clotting factors
-usually takes several days to achieve full therapeutic effect
(Half life of factor II=90hours)
-if drug is stopped, effects linger

  • Must BRIDGE with another anticoagulant to treat the clot in the meantime!
  • bridge while receiving SQ or IV anticoagulants for active clots
24
Q

Warfarin Monitoring and Goals

A

Monitoring:

  • International Normalized Ratio (INR)
  • prothrombin time (PT)

INR measures decrease in clotting factor caused by warfarin

INR=higher=more anticoagulation with warfarin

  • want it around 2-3
  • INR>3-4=HIGH RISK OF BLEEDING
25
Q

Warfarin Adverse Effects and Reversal

A

BLEEDING

Reversal of uncontrolled bleeding:

  • antidote: Phytonadione (Vitamin K) -takes a while
  • takes at least 2-6 hours to start reversing effects
  • total effect within 24 hours
  • MUST give plasma or prothrombin complex concentrate (PCC) or factor VII (novoseven) in the meantime to treat the bleeding right away-gives you all the factors that warfarin inhibits (2, 7, 9, 10) quicker
  • can give blood in addition based on HgB
26
Q

Warfarin Interactions

INCREASED

A 
Bactrim
Amidarone 
Cimetidine 
Acetaminophen 
Metronidazole 
Anole Antifungals

Example: Give warfarin while a patient is on bactrim treating a UTI

  • bactrim will inhibit metabolization of warfarin
  • warfarin will accumulate in the blood
  • INR=too higher, depleted too many clotting factors =HIGH BLEEDING RISK
  • more warfarin, inhibits anticoagulant factors, not metabolized=toxic effects
27
Q

Warfarin Interactions

DECREASED

A

Phenobarbital
Rifampin
Phenytoin
Carbamazepine

*Anticoagulants and antiplatelets can have an added pharmacodynamic effect to increase rates of bleeding

28
Q

Direct Thromin Inhibitors

A

MOA:

  • inhibit thrombin (IIa) to prevent conversion of fibrinogen to fibrin
  • binds directly to thrombin and inhibit conversion of

Oral and IV available

  • Diabigatran (PO)
  • Argatroban (IV)
  • Bivalirudin (IV)
29
Q

Dabigatran (Pradaxa)

A

Indications:

  • prophylaxis for non-valvular afib
  • Treatment of DVT/PE

Rapid onset, prodrug converted by blood esterases

Renally eliminated and dose adjusted for CKD
(Cannot use in hemodialysis patients)

Treat life threatening bleed with PRAXBIND (can remove drug with hemodialysis)
-sequesters Dabigatran

-give plasma or blood in addition if needed

30
Q

Argatroban

A

Indications:
-HIT treatment

Metabolized by liver
-dose adjustment needed for chronic liver disease

Monitoring: aPTT
Will artificially increase INR

Adverse events: BLEEDING

  • no antidote
  • give plasma plus or minus blood if necessary
31
Q

Bivalirudin

A

For patients going to the cath lab

Eliminated by the kidneys
-dose adjustment needed for renal dysfunction

Monitoring: aPTT

Adverse events: BLEEDING

  • no antidote
  • give plasma plus or minus blood if needed
32
Q

Direct Xa Inhibitors

A

Bind directly to Xa and inhibit conversion of fibrinogen to fibrin

No monitoring values

Rapid onset

Oral agents only

  • Rivaroxaban
  • Apixaban
  • Edoxaban
  • Betrixaban

Antidote: Andexxa IF BLEEDING OCCURS

HD does not remove drug

Can give blood with or without plasma as needed

33
Q

Apixaban (Eliquis)

A

Indications:

  • DVT/PE treatment
  • stroke prophylaxis in non-value afib
  • post op DVT prophylaxis

Dose Adjustments
-for afib, if 2 or 3 are met: Age>80, Scr>1.5, or Wt. <60kg

Drug Interactions

  • strong CYP 3A4
  • PGP inhibitors or inducers
34
Q

Rivaroxaban (Xarelto)

A

Indications:

  • DVT/PE treatment
  • stoke prophylaxis in non-valve afib
  • post op DVT prophylaxis

Dose Adjustments:
-renal insufficiency

Drug Interactions:

  • strong CYP 3A4
  • PGP inhibitors or inducers
35
Q

Edoxaban (Savaysa)

A

Indications:

  • DVT/PE treatment
  • stroke prophylaxis in non-valve afib

Dose adjustments:
-renal insufficiency

Drug Interactions:

  • strong CYP3A4
  • PGP inhibitors or inducers
36
Q

Betrixaban (Bevyxxa)

A

Indications:
-prophylaxis for VTE

Dose adjustments:
-renal insufficiency

Drug Interactions:
-strong PGP inhibitors

37
Q

ANTIPLATELETS

A

Used to prevent arterial thrombosis by

  • cox inhibition
  • increased plasma adenosine
  • phosphodiesterase-3 (PDE-3) inhibition
  • P2Y12 ADP inhibition
  • glycoproteins IIb/IIIa inhibition

*used to treat arterial clots rather than venous clots

38
Q

COX Inhibitors

A

Cause irreversible inhibition cyclooxygenase 1 and 3
-enzyme responsible for making Throboxane A2 (TXA2) which causes platelets to aggregate

Aspirin only medication in this class

Effects last for duration of platelet (7-10 days)

IRREVERSIBLE: Inhibits enzyme cyclooxygenase for its whole life
-Aspirin (a cox inhibitor) binds to cycooxygenase 1 and 2 and prevents formation of thromboxane, platelets won’t clot=PREVENTS CLOTS

39
Q

P2Y12 Inhibitors

A

Prevent platelet activation by inhibiting ADP binding to P2Y12 receptor

Monitoring: platelet assay tests

Irreversible and reversible

REVERSIBLE: patient cannot stop taking the medication

  • decreases platelet stickiness and coagulation but has the reverse if the drug is not taken
  • beneficial for those who need to undergo heart/emergency surgery because the drug will wear off, if the bleeding occurs during surgery normal clotting will occur
40
Q

Clopidogrel (Plavix)

A

Type of Inhibition:
IRREVERSIBLE

Prodrugs: Metabolized to active drug by CYP2C19 (genetic variance)

41
Q

Clopidogrel Adverse Effects and Reversal

A

Bleeding
Thrombocytopenia (TTP)

No antidote to reverse
-give platelets

Many drug interactions with CYP2C19
-Genetic factors: poor metabolizes

Hold 5 days prior to major surgery/procedure

42
Q

Prasugrel (Effient)

A

Type of Inhibition:
IRREVERSIBLE

Prodrug converted by the liver

No antidote

Hold 5 days prior to surgery

Avoid use in patients who are over 75, or have a history of stroke or TIA

Dose adjust if patients weighs over 60

43
Q

Prasugrel (Effient) Adverse effects and reversals

A

Bleeding, angioedma (rare)

  • avoid using in patients who are over 75 with a history of stroke or TIA
  • dose adjust if patient weights less than 60kg

No antidote
-give platelets or blood

Hold 5 days prior to surgery

44
Q

Tricagrelor (Brilinta)

A

Type of Inhibition:
REVERSIBLE

Significant drug interactions: aspirin, Digoxin, CYP3A4 inhibitors

Don’t used if concerned about medication adherence

Hold 1 day prior to surgery

45
Q

Tricagrelor (Brilinta) Adverse Effects and Reversal

A

Adverse effects:

  • bleeding
  • dyspnea
  • ventricular pauses

Sig. Drug Interactions:

  • aspirin dose >100mg/day , make the drug less effective
  • CYP3A4 inhibitors/inducers
  • do not exceed over 40mg a day of simvastatin or lovastatin
  • Digoxin levels may increase (PGP inhibitor)

No antidote available
-give platelets, wears off fathers

Don’t use if concerned about medication adherence

Hold 1 day prior to surgery

46
Q

Cangrelor (Kengreal)

A

Type of inhibition:
REVERSIBLE

Adverse events: bleeding
-treat with platelets or blood

Same thing as Ticagrelor but IV form
-only in IV formulation

47
Q

GP IIB/IIIA Inhibitors

A

Block the final receptors where fibrinogen should bind to

IV only

Cause reversible blockade

Available agents: Abciximab, Eptifbatide and Tirofiban

Adverse events: bleeding

  • no antidote available
  • give platelets or blood
48
Q

Dipyridamole

A

MOA: Inhibits platelets by increasing plasma levels of adenosine

Always given in combo with aspirin (Aggrenox)

Adverse effects: bleeding, dyspepsia

No antidote available
-give platelets or blood

49
Q

Cilostazol (Pletal)

A

MOA: PDE-3 Inhibitor

Full onset of action: 12 weeks -takes a while!

Adverse effects: horrible headache

Contraindication to use: patients with heart failure

Drug interactions: Inhibitors of CYP3A4

No antidote
-give platelets of blood

Good for people with intermittent clot risks

50
Q

Pentoxyifylline (Trental)

A

MOA: Increases cAMP in RBCs, leading to increased RBC flexibility and decreased Viscosity-less likely to clot

Adverse Events:

  • nausea, vomiting, leukopenia
  • no sig. bleeding risk
51
Q

THROMBOLYTICS

A

Given to remove thrombi that have already formed

CLOT BUSTERS

  • these drugs augment plasminogen conversion to plasmin
  • plasmin degrades fibrin, breaks up the clot

Used emergency

Contraindications to using (relative and absolute)

3 formulations:

  • Alteplase (tPA)
  • Tenecteplase
  • Reteplase

Example: have an MI, but don’t have access to a catheter lab, you would give a thrombolytic to break up the clot
-used in rural areas

52
Q

Alteplase (Activase or tPA)

A

MOA: binds with plasminogen to form an active complex

  • complex catalyze the conversion of other plasminogen molecules into plasminogen
  • digests the fibrin meshwork
53
Q

Alteplase

A

Drug binds with plasminogen to form an active complex

Ischemic stroke, MI, acute massive PE (cant get to cath lab in time)

Adverse events: bleeding, angioedema (swelling of lips/tongue

Reversal:
-no antidote, give plasma or blood

54
Q

Tenecteplase (TNkase)

A

Only indicated to treat a heart attack (AMI)
-rural area, no access to cath lab

Single dose

Longer half life

Adverse events:
-bleeding

Reversal:
-no antidote, give plasma or blood

55
Q

Reteplase (Retavase)

A

Only indicated to treat AMI

Short half life -give 2 intermittent injections

Complex dosing schedule, not as favorable as others

Adverse events:
-bleeding

Reversal:
-no antidote, give plasma or blood

Pharm 1 (4 decks)

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