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Pharmacology > Blood & Cardiology > Flashcards

Blood & Cardiology Flashcards

1
Q

Unfractionated heparin

A

Anticoagulant

MOA: Binds to and activates antithrombin. Activated antithrombin inactivates Xa and IIa.

Indications:

  • Treatment and prophylaxis of DVT or PE (post-op patient who is obese who has to stay in bed)
  • Drug of choice during pregnancy (does not cross placenta)

Toxicities:

1) Severe bleeding
- Discontinue
- Give protamine sulfate (binds heparin and prevents its antithrombin interaction)
- “HElP me, PlS”!
2) Thrombocytopenia OR
3) Thrombosis:
- UFH binds platelet factor 4 and can initiate immune response OR promote platelet aggregation
4) Osteoporosis
- Chronic use only

  • Must monitor therapy (because of variability between patients and bleeding risk)
  • Only used parenterally (IV or SC)
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2
Q

Low Molecular Weight Heparin (LMWH)

A

Anticoagulant

MOA: Binds to and activates antithrombin. Inhibits factor Xa BUT NOT IIa (lacks thrombin binding site).

Indications:

  • Similar to UFH, but is the DRUG OF CHOICE for:
  • Prophylaxis and treatment of DVT and PE
  • Management of acute coronary syndrome

Toxicities:

1) Bleeding
2) Lower incidence of thrombocytopenia than UFH

  • Advantage over UFH: Less binding to plasma and EC proteins
  • More predictable response
  • Less patient-patient variations
  • Less need for monitoring

*Given IV or SC

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3
Q

Warfarin (Coumadin)

A

Anticoagulant

MOA: Inhibits epoxide reductase so that vitamin K cannot gamma carboxylate clotting factors 2, 7, 9, 10.
Note: Protein C also decreased

Indications:

  • For prolonged anticoagulant action
  • Prevent recurrence of DVT and PE (often following heparin)
  • Prophylaxis of thrombotic complication re atrial fibrillation, post MI

Toxicities:

1) Bleeding
- Interacts with everything so monitor after you begin a new drug, new diet, or new disease
2) Skin lesions/Tissue necrosis
- Due to thrombus formation from protein C inhibition.
3) DO NOT USE IN PREGNANCY
- Abortion, birth defects, etc.
- UFH or LMWH alternatives

*Given orally

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4
Q

Fondaparinaux

A

New Anticoagulant

MOA: Factor 10a inhibitor

Indications:

  • Prophylactic DVT and PE treatments (patient undergoing hip replacement)
  • Treats acute DVT and PE
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5
Q

Dabigatran

A

New Anticoagulant

MOA: Factor 2a inhibitor

Indications:

  • Warfarin alternative. Since warfarin has tons of drug-drug interactions, 50% of atrial fib patients do not receive it.
  • Give this to prevent stroke in AF patients who cannot take Warfarin.
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6
Q

Rivaroxaban

A

New Anticoagulant

MOA: Factor 10a inhibitor

Indications:

  • Prophylactic DVT and PE treatments (patient undergoing hip replacement)
  • Treats acute DVT and PE
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7
Q

Aspirin

A

Antiplatelet Drug

MOA: Irreversible inhibition of COX-1 (AA –> Thromboxane A2)

Indications:

  • Primary prevention for those at HIGH risk for ischemic disease
  • Secondary prevention of recurrent MI or stroke

Toxicities:
- Bleeding

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8
Q

Clopidogrel

A

Antiplatelet Drug

MOA: Irreversible inhibition of P2Y-12 ADP receptor

Indications:
- Secondary prevention of recurrent MI or stroke

Toxicities:
- Bleeding

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9
Q

Abciximab

A

Antiplatelet Drug

MOA: Blocks GP 2b-3a

Indications:

  • Stent placement
  • Used with heparin and aspirin

Toxicities:

  • Bleeding
  • Thrombocytopenia
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10
Q

Streptokinase

A

Thrombolytic Drug (Clot Buster)

MOA: Promote plasminogen conversion to plasmin.

  • No intrinsic enzymatic activity.
  • Instead, binds to plasminogen, exposes active site, and promotes conversion.
  • Give bolus to overwhelm antibody response
  • Can cause anaphylaxis

Indications:

  • Rapid lysis of occlusive thrombi
  • For MI, PE, and ischemic stroke, give within 3 hours of onset!

Toxicities:

  • Life threatening bleeding by lysing “physiologic” thrombi
  • Aminocaproic acid can treat bleeding (binds plasminogen and plasmin –> blocks access to fibrin)
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11
Q

Tissue plasminogen activator (t-PA)

A

Thrombolytic Drug (Clot Buster)

MOA: Promote plasminogen conversion to plasmin

  • Naturally occurring serine protease
  • Give as bolus followed by constant infusion

Indications:

  • Rapid lysis of occlusive thrombi
  • For MI, PE, and ischemic stroke, give within 3 hours of onset!

Toxicities:

  • Life threatening bleeding by lysing “physiologic” thrombi
  • Aminocaproic acid can treat toxic bleeding (binds plasminogen and plasmin –> blocks access to fibrin)
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12
Q

Tenecteplase

A

Thrombolytic Drug (Clot Buster)

MOA: Promote plasminogen conversion to plasmin

  • Genetically engineered t-PA
  • 3 point mutations introduced to increase half-life and increase activity
  • Only have to give as one bolus (as opposed to t-PA)

Indications:

  • Rapid lysis of occlusive thrombi
  • For MI, PE, and ischemic stroke, give within 3 hours of onset!

Toxicities:

  • Life threatening bleeding by lysing “physiologic” thrombi
  • Aminocaproic acid can treat bleeding (binds plasminogen and plasmin –> blocks access to fibrin)
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13
Q

Dipyridamole

A

Antiplatelet Drug

MOA:

  • Adenosine Reuptake inhibitor (ADP and ATP).
  • Inhibits thromboxane synthase
  • Results in less ADP and TxA2 release.
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14
Q

NovoSeven

A

Recombinant factor 7a

Treats Glanzman’s Thrombasthenia

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15
Q

Cytarabine

A

Antineoplastic
Subclass: Antimetabolite

MOA: Pyrimidine antagonist

  • Converted to ara-CMP, which is converted to ara-CDP and ara-CTP.
  • The triphosphate (CTP) is the main cytotoxic metabolite.
  • Ara-CTP competitively inhibits DNA polymerases and is incorporated into RNA and DNA.

Toxicity:

  • Myelosuppression
  • Arthralgia
  • Cerebellar neurotoxicity
  • Ocular toxicity

*S-phase specific

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16
Q

Fludarabine

A

Antineoplastic
Subclass: Antimetabolite

MOA: Purine antagonist

*S-phase specific

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17
Q

5-Fluorouracil

A

Antineoplastic
Subclass: Antimetabolite

MOA:

  • Incorporates into RNA + DNA
  • Covalently binds and inhibits thymidylate synthase

Toxicity:

  • Mucositis
  • Myelosuppression
  • Hand-foot syndrome
  • S-phase specific
  • Leucovorin enhances activity
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18
Q

Irinotecan

A

Antineoplastic

MOA: Inhibits Topoisomerase I, a key enzyme responsible for DNA replication.

Toxicity:

  • Myelosuppression
  • Transaminitis
  • Explosive diarrhea (fix acute diarrhea with atropine; fix delayed with loperamide)

*S-phase specific

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19
Q

Methotrexate

A

Antineoplastic
Subclass: Antimetabolite

MOA: Inhibits DHF reductase
- DHF reductase reduces DHF to THF. THF helps create thymidylate. Thymidylate involved in DNA and RNA synthesis.

Toxicity:
- Renal (do not use if patient has kidney problem or is on another nephrotoxic)

  • S-phase specific
  • Leucovorin prevents harmful effects of methotrexate
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20
Q

Paclitaxel

A

Antineoplastic
Subclass: Microtubule Inhibitor

MOA: Stabilize MT so they cannot disassemble

Toxicity:
- Hypersensitivity reactions (premedicate with steroids)

*M-phase specific

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21
Q

Vincristine

A

Antineoplastic
Subclass: Microtubule Inhibitor

MOA: Inhibits MT polymerization (disrupts assembly)
*Lagaan. PacliTAXel does one thing. We “vin”!!!!! does the opposite. Taxing vs. Vinning in cricket lol.

Toxicity:
- ***Neuropathy & Constipation

*M-phase specific

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22
Q

Bleomycin

A

Antineoplastic
Subclass: Antibiotic

MOA:

  • Has DNA and Iron binding domains at opposite ends.
  • Oxidizes iron atom and sends off electrons to nip at the local DNA.
  • **Toxicity:
  • Pulmonary toxicity
  • Hypersensitivity
  • Mucositis

*S/G2-Phase specific

23
Q

Carmustine

A

Antineoplastic
Subclass: Alkylating agent

Toxicity:
- Bone marrow suppression (administer every 6-8 weeks)

24
Q

Cyclophosphamide

A

Antineoplastic
Subclass: Alkylating agent

Toxicity:

  • Bone marrow suppression
  • Cystitis
  • Cardiac (high doses)
  • Immunosuppression

*Acrolein, a byproduct, causes severe hemorrhagic cystitis. MESNA is used to protect against this.

25
Q

Nitrogen Mustard (Mechlorethamine)

A

Antineoplastic

Subclass: Alkylating agent

26
Q

Carboplatin

A

Antineoplastic
Subclass: Alkylating agent
*Forms platinum coordination complexes

Toxicity:

  • Myelosuppression
  • Nausea/Vomiting
27
Q

Cisplatin

A

Antineoplastic
Subclass: Alkylating agent
*Forms platinum coordination complexes

Toxicity:

  • Nephrotoxic
  • Nausea/Vomiting
  • Neuropathy
28
Q

Leucovorin

A

Modulant

Folic acid analog:
- THF derivative (reduced folic acid)

Uses:

  • Prevents harmful effects of methotrexate while allowing methotrexate to kill cancer
  • Enhances 5-FU activity
29
Q

Docetaxel

A

Antineoplastic
Subclass: Microtubule Inhibitor

MOA: Stabilizes MT and prevents so they cannot disassemble
*Taxes the disassembly of MT’s (“You can’t just assemble to disassemble. There is a tax on your actions.”)

Toxicity:

  • Hypersensitivity
  • Myelosuppression
  • Fluid retention (leg edema)
  • M-phase specific
  • Can give if resistant to Paclitaxel (different binding sites on MTs)
30
Q

Vinblastine

A

Antineoplastic
Subclass: Microtubule Inhibitor

MOA: Inhibits MT polymerization (disrupts assembly)

31
Q

Doxorubicin

A

Antineoplastic
Subclass: Antibiotic

  • **MOA:
  • Intercalates between DNA base pairs during uncoiling.
  • Generates free radicals that damage DNA

Toxicity:
- Lifetime dose of 550 mg/m^2 due to cardiotoxicity

32
Q

Hydroxyurea

A

Antineoplastic
Subclass: Miscellaneous

MOA: Inhibits ribonucleotide reductase (which reduces a ribonucleotide to a deoxyribonucleotide).

*Treats Acute Myelocytic Leukemia

33
Q

ATRA (all-trans-retinoic acid)

A

Treats promyelocytic leukemia

MOA: Binds to mutated vitamin A receptor from t(15:17) and induces differentiation.

Toxicity:

  • Can induce DIFFERENTIATION SYNDROME, a potentially fatal complication of giving chemotherapy in APL.
  • Symptoms = fever, dyspnea, pulmonary infiltrates, hypotension
34
Q

Imatinib

A

Antineoplastic
Subclass: Tyrosine kinase inhibitor

MOA: Inhibits tyrosine kinases, which normally alter gene expression to promote cell cycle.

*Treats CML (Chronic Myelogenous Leukemia)

35
Q

Erlotinib

A

Antineoplastic
Subclass: Tyrosine kinase inhibitor

MOA: Inhibits tyrosine kinases, which normally alter gene expression to promote cell cycle.

Toxicity:

  • Diarrhea
  • Rash
  • Gastric perforation (rare but very serious)
  • Interstitial pneumonitis (rare but very serious)
36
Q

Rituximab

A

Antineoplastic
Subclass: Monoclonal antibody

MOA: Targets CD20 on B cells

*Treats non-Hodgkin’s lymphoma

37
Q

Trastuzumab

A

Antineoplastic
Subclass: Monoclonal antibody

MOA: Targets HER2 receptor

*TrASS and Titties, TrASS n’ Titties.

38
Q

Thalidomide

A

Antineoplastic
Subclass: Anti-angiogenic

Toxicity:

  • Teratogenic
  • Neurotoxic

*Treats Multiple Myeloma

39
Q

Bortezomib

A

Antineoplastic
Subclass: Proteosome inhibitor

MOA:

  • Decreases NF kappa B (decreases IL-6 production)
  • Inhibits proteosome, which causes accumulation of poly-ubiquitinated proteins, which causes autophagy

*Treats Multiple Myeloma

40
Q

Desmopressin

A

Treats von Willebrand’s disease (and mild-moderate Hemophilia A)

MOA: Induces vWF release from Weibel-Palade bodies of endothelial cells

*Does not treat Hemophilia B or severe hemophilia A

41
Q

Allopurinol

A

Treats Tumor Lysis Syndrome

MOA:

  • Hypoxanthine analog that competitively binds xanthine oxidase
  • Blocks metabolism of hypoxanthine and xanthine –> uric acid
  • Inhibits more uric acid production
42
Q

Rasburicase

A

Treats Tumor Lysis Syndrome

MOA:

  • Uricolytic (breaks down existing uric acid)
  • Use if current uric acid levels too high
43
Q

Eculizumab

A

Treats aHUS and Paroxysmal nocturnal hemoglobinuria

MOA: Monoclonal antibody against complement factor C5 (convertase). This prevents formation of C5b + C6-C9 (MAC).

44
Q

Dobutamine

Indications?
Side effects?
MOA?

A

Positive Inotrope
Subclass - Sympathomimetics
*Beta-adrenergic agonist

Use: For acute improvement of heart function in decompensated HF

Side effects:

  • Worsens arrhythmias (can cause sudden cardiac death)
  • Do not use in patients with myocardial ischemia (overworking an ischemic heart)
  • Tolerance may result due to beta-receptor down regulation

Beta receptor tickling on cardiac cells causes + isotropy (enhanced contraction) AND + lusitropy (enhanced relaxation)

+ isotropy pathway:

  • Dobutamine tickles Beta 1 which make cAMP
  • cAMP activates PKA
  • PKA phosphorylates and activates L-type Calcium channels
  • Influx of extracellular calcium binds to Ryanodine receptor and triggers more calcium release from SR (Ca-induced Ca release)
  • Increased contraction

+ lusitropy pathway:

  • cAMP activates PKA
  • PKA (also) phosphorylates Phospholamban
  • Phospholamban stimulates calcium reuptake into SR via SERCA
  • Increased relaxation
45
Q

Metoprolol

Indications?
Effects?
Adverse Effects?

A

Beta-adrenergic receptor antagonist
- Selectively block beta 1 receptors over beta 2

Uses:

  • Hypertension
  • CHF

Effects:

  • Bradycardia (decrease heart stress)
  • Prevent catecholamine myocyte toxicity
  • Upregulate beta receptors to enhance beta adrenergic signaling
  • Inhibit the renin-angiotensin system to reduce vasoconstriction and prevent cardiac remodeling

Adverse effects:

  • Bronchospasm (worsens COPD and asthma)
  • Cardiac (heart block and severe bradycardia)
  • Neuro (depression and insomnia)
  • Sexual dysfunction/Impotence
46
Q

Carvedilol

Indications?
Effects?
Adverse effects?

A

Beta-adrenergic receptor antagonist
- Selectively block beta 1 receptors over beta 2 AND block alpha receptors for vasodilatory effects

Uses:

  • Hypertension
  • CHF

Effects:

  • Bradycardia (decrease heart stress)
  • Prevent catecholamine myocyte toxicity
  • Upregulate beta receptors to enhance beta adrenergic signaling
  • Inhibit the renin-angiotensin system to reduce vasoconstriction and prevent cardiac remodeling

Adverse effects:

  • Bronchospasm (worsens COPD and asthma)
  • Cardiac (heart block and severe bradycardia)
  • CNS (depression and insomnia)
  • Sexual dysfunction/Impotence
47
Q

Digoxin

Subclass?
Indications?
Effects?
MOA?
Toxicity?
Contraindications?
A

Positive Inotrope
Subclass - Cardiac Glycosides

Uses:

  • Chronic CHF
  • Atrial Fibrillation

Effects:

  • Increases contractility of heart
  • Enhances parasympathetic (vagal) tone of heart to control HR
MOA:
\+ inotropy pathway
- Inhibits Na/K ATPase
- Sodium levels rise in cell
- This enhances the sodium/calcium exchanger (which pumps sodium out and calcium in)
- Increase in intracellular calcium
- Increased contractility

Parasympathetic pathway
- Slows AV conduction via ACh release

Toxicity (too much):
Cardiac
- Arrhythmias (due to too much sodium and calcium moving the myocyte closer to threshold)
- Heart block
- HF exacerbation

Extracardiac

  • GI
  • Neuro (depression)
  • Visual (blurry yellow vision)
  • Hyperestrogenism (inhibits metabolism of E2)

Contraindications:

  • Renal failure (decreased excretion)
  • Verapamil (displaces Digoxin from plasma protein binding)
  • Hypokalemia (nothing to displace Digoxin from potassium binding site)
48
Q

Milrinone

Subclass?
Indication?
Effect?

A

Positive Inotrope
Subclass - Phosphodiesterase III Inhibitor

Use: Acute decompensated HF

Effect:
+ inotropy and + lusitropy:
- Phosphodiesterase III breaks down cAMP and cGMP.
- Inhibiting PDE III increases cAMP –> + inotropy pathway and + lusitropy pathways engaged

Vasodilation
- Increases cGMP in vascular smooth muscle

49
Q

Aliskiren

Contraindications?

A

Renin Inhibitor

Contraindications:

  • Pregnancy (teratogenic)
  • Diabetics (hyperkalemia occurs)
  • Impaired renal function
50
Q

Lisinopril

  • MOA?
  • Indications?
  • Adverse Effects & Contraindications?
A

ACE Inhibitor

MOA:

  • Inhibits conversion of Ang I to Ang II.
  • Inhibits ACE’s usual breakdown of Bradykinin (a vasodilator).

Indications:

  • Hypertension
  • Heart Failure
  • MI
  • Diabetic nephropathy and Chronic renal failure (used even in absence of hypertension)

Adverse Effects:

  • Decreased efficacy in African Americans
  • Angioedema (swelling of tongue, throat, mouth)
  • Dry cough
  • Hyperkalemia (aldosterone impaired)
  • Contraindicated in 2nd-3rd trimesters (teratogenic)
  • Temporarily discontinue in patients with chronic renal failure who develop volume depletion like vomiting or diarrhea (since ACEIs interfere with GFR)
51
Q

Losartan

Effects?
Indications?
Contraindications?

A

Angiotensin II receptor blocker (ARB)

Effects:

  • Dilates arteries and veins (reduces arterial afterload and venous preload)
  • Natriuretic and Diuretic effects (sodium and water excretion because of aldosterone block)
  • Inhibits cardiac and vascular remodeling

Indications:

  • Hypertension
  • Heart Failure
  • Diabetic nephropathy
  • Chronic renal failure

Contraindications:

  • Decreased efficacy in African Americans
  • Angioedema
  • Dry cough (much less common than ACEIs)
  • Hyperkalemia
  • Contraindicated in 2nd and 3rd trimesters (teratogenic)
  • Temporarily discontinue in patients with chronic renal failure who develop volume depletion like vomiting or diarrhea (since ARBs interfere with GFR)
52
Q

Bosentan

Indications?
Contraindications?

A

Endothelin Receptor Antagonist
- Nonselective (blocks ET a and b receptors)

Indications:
- Pulmonary Arterial Hypertension

Contraindications:

  • Hepatotoxic
  • Pregnancy (teratogenic)
  • Oral contraceptives (may cause unplanned pregnancy)
53
Q

Ambrisentan

Indications?
Contraindications?

A

Endothelin Receptor Antagonist
- Selective (only blocks ET a receptors)

Indications:
- Pulmonary Arterial Hypertension

Contraindications:

  • Hepatotoxic
  • Pregnancy (teratogenic)
  • Oral contraceptives (may cause unplanned pregnancy)
54
Q

Nesiritide

Indications?
Effects?
MOA?
Adverse Effects?

A

Natriuretic Peptide Agonist
- BNP mimetic (a natural vasodilator that is released when myocytes are overstretched - indicator of HF)

Indications:

  • Acute HF
  • Does not treat hypertension

Effects:

  • Vasodilation
  • Natriuresis/Diuresis
  • Inhibit renin-angiotensin system

MOA:

  • Activates guanylyl cyclase
  • cGMP made
  • cGMP activates phosphatase
  • Phosphatase cleaves phosphate group on myosin to allow smooth muscle relaxation

Adverse Effects:
- Excessive hypotension

*No tolerance developed

Pharmacology (5 decks)

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