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Pharmacology > Test 2 Drugs > Flashcards

Test 2 Drugs Flashcards

1
Q

Atorvastatin, Rosuvastatin, Simvastatin

A
  • Statins/HMB-CoA Reductase Inhibitors
  • MOA: 1) Inhibition of HMG-CoA results in decreased LDL production 2) Decreased LDL production results in an increase in LDL receptor production, resulting in more LDL being pulled from the blood
  • Pharmacokinetics: Taken orally at bed time and hepatically metabolized
  • Uses: Hyperlipidemia. Lower LDL, promote plaque stability, reduced inflammation at site of plaque, enhance blood vessel dilation, reduce coagulation and platelet aggregation
  • Side effects: Few side effects. Hepatotoxicity and rhabdomyolysis (muscle breakdown)
  • Adverse effects (rare): Hepatotoxicity and myopathy
  • Nursing considerations: Monitor hepatic function
  • Who gets statins: 20-75y/o with LDL >190, 40-75 y/o w T2DM (regardless of LDL levels), >75 y/o, 40-75 with LDL 70-190
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2
Q

Niacin

A

-Nicotinic Acid
-Uses: Hyperlipidemia. Reduce LDL and TG levels. Also increases HDL
Side effects: Intense flushing, GI upset, liver injury

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3
Q

Cholestyramine/Colesevelam

A
  • Bile-Acid Sequestrant
  • MOA: Binds to bile acids (derivatives of cholesterol) and prevents their reabsorption in the small intestine
  • Uses: Hyperlipidemia
  • Used alongside with statins
  • Dosing: Oral. Due to interactions with diuretics, antibiotics, and blood thinners, bile-acid sequestrants should be give an hour after or 4 hours before
  • Side effects: GI issues, such as bloating
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4
Q

Gemfibrozil (Lopid) /Fenofibrate (Tricor)

A

-Fibrates
-MOA: Interact with receptors on the liver to accelerate clearance of TG
-Uses: Hyperlipidemia. Lowers TG but no effect on LDL
Side effects: Increased risk of bleeding for those taking Coumadin. Well tolerated. Some GI issues (bloating), rash, increased risk of gallstones, myopathy
-Dosing: Oral. Hepatically metabolized
-Nursing considerations: Monitor patients taking fibrates and Coumadin due to risk of increased bleeding

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5
Q

Nitroglycerine, Imdur, and Isordil

A
  • Nitrate
  • Antianginal drugs
  • Vasodilator
  • MOA: Converted into active nitric oxide, which is a vasodilator, thereby decreasing oxygen demand of the heart (works less hard). Decreases preload
  • Uses: Angina
  • Dosing: PO, SL, IV, transdermal. Begins working very quickly
  • Side effects: Headache, orthostatic hypotension, tachycardia
  • Nursing considerations: Do not abruptly stop due to risk of vasospasm. Can increase effects of other hypotensive drugs
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6
Q

Metoprolol and Propranolol

A
  • Beta Blockers
  • Antianginal
  • MOA: Block beta receptors, thereby decreasing cardiac oxygen demand. Additionally, B1 block decreases renin release which decrease afterload
  • Dosing: PO and IV, hepatically metabolized
  • Uses: MI, HF, hypertension
  • Side effects: Bradycardia, decreased AV conduction (dromotropic) , reduction of contractility, bronchoconstriction (B2), masking hypoglycemia
  • Nursing considerations: Do not stop abruptly (can cause vasospasm) and monitor for signs of hypoglycemia
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7
Q

Verapamil, Diltiazem, and Nifedipine

A
  • Calcium Channel Blockers
  • Antianginal
  • MOA: Slow movement of calcium into cells of heart and blood vessels resulting in decreased afterload, HR, and contractility
  • Dosing: PO and IV. Hepatically metabolized (effected by first pass effect)
  • Uses: MI, HF, hypertension
  • Side effects: Constipation due to reduced flow of calcium into intestinal smooth muscle, and bradycardia
  • Interacts with grapefruit (grapefruit inhibits drug metabolism) and digoxin (increased risk of heart block)
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8
Q

Morphine

A
  • Opioid
  • Treatment of choice for STEMI-associated pain
  • MOA: CNS depressant that decreases anxiety, thereby lowering SNS response, thereby decreasing CO
  • Also decrease preload and afterload
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9
Q

Warfarin (Coumadin)

A

-Vitamin K Antagonist
-Anticoagulant
-MOA: Decreases production of vitamin K dependent clotting factors (VII, IX, X, prothrombin). Additionally, inhibits the vitamin K epoxide reductase complex 1 (VKORC1) which prevents vitamin K from being converted into its active from
-Dosing: Oral, 99% binds to albumin. Amount is variable based on genetics
-Uses: Prevention of DVT and PE
-Interactions: Many fucking drugs, some increase and some decrease the effects. Important ones
-ASA (aspirin): Increased
risk of bleeding and
gastric ulcers
-Other NSAIDS:
Increased risk of ulcers
-Acetaminophen:
Inhibition of warfarin
(coumadin) degradation
-Antidote: Vitamin K (foods or supplements)
-Nursing considerations: Must monitor pt’s prothrombin time (PT) and International Normalized Ration (INR). INR is super important to monitor
-Contraindicated for people who are pregnant or lactating

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10
Q

Dabigatran (Pradaxa)

A
  • Direct Thrombin Inhibitor
  • Anticoagulant
  • MOA: Binds to the activation site of thrombin, inhibiting its activation thereby preventing clotting
  • Uses: Prevention of DVT and PE
  • Advantages over warfarin: Rapid onset, few drug interaction, same dose for all patients, lower risk for bleeding
  • Disadvantages over warfarin: Short duration of action (must be taken at the prescribed time), limited clinical experience
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11
Q

Rivaroxaban (xarelto)/ Abixiban

A
  • Direct Factor Xa inhibitor
  • Anticoagulant
  • MOA: Binds directly to the active center of factor Xa, which inhibits activation of thrombin
  • Uses: Prevent blood clots
  • Dosing: Oral
  • Advantages over warfarin: Rapid onset, few drug interactions, same dose for all patients, lower risk of bleeding
  • Disadvantages over warfarin: short duration of action meaning it must be taken at the prescribed time, and limited clinical experience
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12
Q

Aspirin

A
  • NSAID/COX inhibitor
  • MOA: Inhibition of cyclooxygenase results in decrease TXA2 availability, which results in decreased activation of GP IIb/IIIa receptor, which leads to decreased platelet aggregation. Lasts for the life of the platelet
  • Dosing: Oral 81 mg/day
  • Uses: Prevent of stroke and MI
  • Not to be given to anyone under 18 (Reye’s syndrome)
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13
Q

Clopidogrel

A
  • P2Y12 ADP Receptor Antagonist
  • Antiplatelet aggregation
  • MOA: Irreversible blockage of P2Y12 ADP receptors on platelets results in less activation of GP IIb/IIIa, which results in decreased platelet aggregation. Lasts for the life of the platelet
  • Dosing: Oral
  • Uses: Prevention of atherosclerotic events in patients with unstable angina and MI
  • Side effects: Similar to aspirin (bleeding). Small risk of TTP (thrombotic thrombocytopenic purpura)
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14
Q

Abciximab

A
  • Glycoprotein IIb/IIIa Receptor Antagonist
  • Antiplatelet
  • Super Aspirin
  • MOA: Blocks GP IIb/IIIa receptor, which inhibits receptor binding to fibrinogen
  • Dosing: IV (short term use)
  • Uses: Short term for patient undergoing cardiac angiography or stentings, or in acute coronary syndrome
  • Nursing consideration: Bleeding
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15
Q

Alteplase (tPA)

A
  • Thrombolytic
  • MOA: Catalyzes conversion of plasminogen to plasmin, an enzyme that digests fibrin meshwork of clots
  • Uses: Acute MI, acute ischemic stroke, acute pulmonary embolus
  • Side effects: Greatly increases risk of bleeding
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16
Q

Unfractionated Heparin

A

-Anticoagulant
-MOA: Inactivated factor Xa and thrombin
Molecular weight range: 3000-30,000
-Molecular weight mean: 12,000-15,000
-Dosing: SubQ and IV. Adjusted based on aPTT (partial thromboplastin clotting time)
-Cheaper than LMW Heparin but must be taken in the hospital, meaning costs for treatment are higher
-Uses: DVT/PE prevention
-Preferred during pregnancy
-Side effects: Heparin Induced Thrombocytopenia
-Antidote: Protamine

17
Q

Low molecular weight Heparin

A
  • Anticoagulant
  • MOA: Inactivation of factor Xa, some inactivation of thrombin
  • Molecular weight range:1000-9000
  • Molecular weight mean: 4000-5000
  • Dosing: Only subQ. Amount often based on body weight
  • Uses: Prevention of DVT/PE
  • More expensive than unfractionated heparin, but can be taken at home meaning no costs from the hospital
  • Side effects: Heparin Induced Thrombocytopenia
  • Antidote: Protamine
18
Q

Fondaparinux

A
  • Anticoagulant
  • MOA: Selective inactivation of Xa
  • Molecular wieght: 1728
  • Dosing: Sub Q only (like LMW heparin)
  • Dosage: Fixed (not based on pt’s weight or PTT levels)
  • Uses: DVT/PE prevention
  • More expensive than u.f heparin and LMW heparin, but not lab or hospital costs
19
Q

Furosemide (Lasix) and Bumetanide (Bumex)

A
  • Loop diuretics
  • Antihypertensive
  • MOA: Blocks reabsorption of sodium and chloride in the thick segment of the ascending loop of Henle
  • Dosing: PO, IV
  • Uses: Lower BP/hypertension
  • Side effects: Hypokalemia, hyponatremia, hypochloremia, dehydration, hypotension, ototoxicity (hearing loss related to medication)
  • Drug interactions: Digoxin (becomes more toxic if patient is hyponatremic), oxotoxic drugs, potassium sparing drugs (given with loop diuretics to counteract potassium wasting)
  • Metabolized via renal
20
Q

Hydrochlorothiazide and Metolazone

A
  • Thiazide diuretics
  • Antihypertensive
  • MOA: Blocks reabsorption of sodium and chloride in the early segment of the distal convoluted tubule. Since only 10% of sodium and chloride is reabsorbed at the distant convoluted tubule, the maximum diuresis of thiazide loop diuretics is less than that of loop diuretics
  • Dosing: PO
  • Side effects: Same as loop diuretics but less sever and no ototoxicity
  • Nursing considerations: Monitor electrolytes
21
Q

Spironolactone (aldactone)

A
  • Potassium-sparing diuretics
  • Antihypertensive
  • MOA: Blocks actions of aldosterone in the distal nephron, resulting in retention of potassium and increased excretion of sodium. Minimal diuresis (diuresis = kidney’s filtering too much bodily fluid)
  • Uses: Hypertension and edema (used alongside a loop or thiazide), heart failure (reduces mortality and hospital admission via protective effects of blockade at heart and vessels), and HRT
  • Side effects: Hyperkalemia and endocrine effects owing to its similarity in structure to other hormones
  • Drug interactions: Frequently combined with thiazide and loop diuretics, interacts with other drugs that increase potassium levels (i.e renin inhibitors)
22
Q

Mannitol

A
  • Osmotic diuretic
  • Antihypertensive
  • Dosing: Must be IV
  • Has 4 ideal properties (freely filtered at the glomerulus, undergoes minimal tubular reabsorption, undergoes minimal metabolism, is pharmacologically inert
23
Q

Doxazosin and Terazosin

A
  • Sympatholytic Alpha 1 blockers
  • Antihypertensive
  • MOA: Prevents stimulation of alpha 1 receptors on arterioles and veins which prevents vasoconstriction
  • SE: Orthostatic hypotension
24
Q

Propranolol, metoprolol, atenolol, carvedilol

A

-Sympatholytic beta blockers

25
Q

Carvedilol

A
  • Sympatholytic alpha/beta blockers
  • MOA: Alpha 1 blockage (dilates arterioles and veins), beta 1 blockade (reduces HR and contractility, suppresses renin release)
  • Side effects: Bradycardia, heart block
26
Q

Clonidine

A
  • Sympatholytic central acting Alpha 2 agonist
  • MOA: Work within brainstem to supress sympathetic outflow to the heart and blood vessels resulting in vasodilation and reduced CO. In other words, reduces SNS activity and enhances PSNS activity
  • SE: Dry mouth, sedation, rebound hypertension
  • Comes in patch form
27
Q

Hydralazine, minoxidil, some Ace inhibitors, and nitrates

A
  • Vasodilators
  • Some dilate arterioles (reduce afterload)
  • Some dilate veins (reduced preload)
  • Uses: HTN, angina, HF
  • Decreases cardiac workload and cardiac output, increase tissue perfusion

Pharmacology (11 decks)

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