FIRST AND SECOND SHIFT PHARMACOLOGY REVIEWER

PHARMACOKINETICS 1.Desired response and toxicity is a function of drug concentration.

ABSORPTION

2.Cmax and Tmax affect RATE of absorption; AUC reflects the EXTENT of absorption.

DISTRIBUTION

3.pH partition hypothesis: Only unionized non polar drug penetrates the membrane!

METABOLISM

4.PHASE I reaction involves conversion of parent drug to a more polar metabolite by UNMASKING A FUNCTIONAL GROUP while PHASE II reaction is a CONJUGATION REACTION.

EXCRETION

5.Glomerular filtration is affected by protein binding; Renal tubular secretion is NOT.

6.T affects the TIME to STEADY STATE (time to Css) while rate of infusion affects STEADY STATE CONCENTRATION (Css).

so if t is short, time to Css is reached RAPIDLY; no effects on Css

7.The sole factor controlling the time to plateau is t . Plateau is reached in 4-5 t .

ANSWER: After 5 days

SQ: Drug G has a half-life of 24 hours. When will Drug G attain a steady state concentration?

a. After 24 hours

b. After a week

c. After 5 days

d. After a month

PHARMACODYNAMICS 1. Competitive inhibitors bind REVERSIBLY to CATALYTIC SITE while

Noncompetitive inhibitors bind IRREVERSIBLY to the ADJACENT SITE. 2. 4 main types of receptors: Ligand-gated ion channel (ionotropic), GPCRs

(metabotropic), Enzyme/kinase linked receptors, Nuclear receptors. 3. LAW OF MASS ACTION states that the rate of chemical reaction is

proportional to the product of the concentrations of the reactants. 4. Ka is the conc of the drug required to occupy 50% of sites at equilibrium;

a measure of affinitythe higher the affinity, the lower the Ka. Kd measures the drugs tendency to BIND to a receptor.

5. EFFICACY (intrinsic activity) is the tendency of a drug to ACTIVATE a receptor; measured by Emax

6. Potency is the amount of drug required to produce a response; measured by EC50

7. RECEPTOR OCCUPANCY THEORY states that the magnitude of response is proportional to the fraction of total receptor sites occupied. EC50=Ka

8. SPARE receptors allow maximal response WITHOUT full receptor occupancy.

9. AGONISTS: a FULL agonist has maximal response while PARTIAL agonist has submaximal response even with full receptor occupancy.

10. MEDIAN THERAPEUTIC INDEX is a measure of the quantification of drug safety; TI50=LD50/ED50=TD50/ED50

ANSWER: Kd

SQ: A drugs tendency to bind to the receptor is measured by which of the following?

a. ED50

b. Kd

c. EC50

d. Emax

AUTONOMICS 1. CHOLINERGIC RECEPTORS release Ach.

a. ALL preganglionic neurons (SNS & PNS) and all parasympathetic postganglionic neurons are NICOTINIC.

b. Sympathetic postganglionic neurons that innervate sweat glands, piloerector muscles, and peripheral blood vessels are MUSCARINIC.

2. ADRENERGIC RECEPTORS release norepinephrine. They include the sympathetic postganglionic neurons except the ones that innervate sweat glands, piloerector muscles, and peripheral blood vessels

BENZENE RING (#3-6)

3. Substitution of OH groups @ C3 & C4 converts it to CATECHOLmaximal alpha and beta effects

4. Absence of substituents @ C3 causes diminution in potency.

5. Substitution of OH groups at C3 & C5 imparts B2 selectivity.

6. Loss of 2 OH enhances oral effectiveness and duration of action.

7. Substitution at the alpha carbon causes LONGER DURATION of action: EPHEDRINE & AMPHETAMINE

8. Substitution at the amine side chain increases B2-selectivity: EPI, ISOPROTENEROL, TERBUTALINE.

AUTONOMICS

Alpha 1 stimulation cause CONTRACTION of vascular and GU smooth muscle; cause RELAXATION of intestinal smooth muscle. Phenylephrine is a selective alpha 1 agonist that is used as

decongestantto contract vascular smooth muscle. Prazosin is a selective alpha 1 antagonist used in HTNto allow

relaxation of smooth muscle.

Alpha 2 stimulation cause decreased insulin secretion of islets, aggregation of platelets, and contraction of vascular smooth muscle Clonidine is a selective alpha2 agonist used in treatment of HTN.

Beta 1 stimulation cause increased force and rate of contraction of the heart and increased renin secretion in juxtaglomerular cells Metoprolol is a selective B1 antagonist used as anti-HTN.

Beta 2 stimulation causes RELAXATION of vascular, bronchial, GI and GU smooth muscle, GLYCOGENOLYSIS and K uptake in skeletal muscle and GLYCOGENOLYSIS & GLUCONEOGENESIS in liver. Terbutaline is a selective B2 agonist used as BRONCHODILATOR &

TOCOLYTIC.

ANSWER: Beta-blocker Hypoglycemia can present with palpitations &

shakiness. Betablockers can reverse hypoglycemic symptoms by decreasing heart rate.

SQ: In a diabetic patient who is on antihypertensive drug, choose the drug that is most likely responsible for not being able to recognize hypoglycemic symptoms

a. Beta-blocker

b. CCB

c. ACEI

d. ARBs

AUTACOIDS 1. H1 blockers act as inverse agonist which has a

preferential affinity to inactive state. 2. Second generation H1 blockers are less sedating

because of their high MW, poor lipophilicity. 3. 5HT3 is the only ligand operated ion channel

among the serotonergic receptors. Ondansetron is a 5HT3 antagonist for p/v of nausea & vomiting.

4. CGPR is the most potent vasodilator. 5. Neurotensin Y is the most abundant neuropeptides

in the CNS and PNS. 6. Bromocriptine is a D2R agonist used to suppress

lactation but causes serious postpartum CV toxicity.

ANSWER: 5HT3 It is the only ligand operated ion channel

among the serotonergic receptors

SQ: All the serotonin receptors are G-protein coupled receptors except:

a. 5HT1A

b. 5HT1B/D

c. 5HT2

d. 5HT3

PSYCHOPHARMACOLOGIC AGENTS 1. SCHIZOPHRENIA HYPOTHESIS:

Mesolimbic pathwayPOSITIVE SYNDROMES Mesocortical pathway NEGATIVE SYNDROMES Nigrostriatal pathway EPS/ movement disorder Tuberoinfundibular pathway HYPERPROLACTINEMIA

2. Olanzapine has the greatest affinity to the 5HT2A system. 3. Aripirazole is the only partial agonist antipsychotic that has similar

efficacy with atypical antipsychotics and minimal to absent EPS. 4. MOST WEIGHT GAIN: Clozapine, Olanzapine 5. LEAST WEIGHT GAIN: Ziprasidone 6. MOST TARDIVE DYSKINESIA: Risperidone, praliperidone 7. LEAST TARDIVE DYSKINESIA: Clozapine & Quietiapine 8. OPTHALMOLOGIC EFFECTS: Chlorpromazine & Thioridazine 9. TRUE MEDICAL EMERGENCIES in CLOZAPINE: Agranulocytosis &

Myocarditis 10. PARKINSONISM: Haloperidol & Fluphenazine

ANSWER: Olanzapine Refer to #4 of previous slide

SQ: Which of the following atypical antipsychotic agents must be avoided in schizophrenics with hyperlipidemia nad borderline elevation of blood glucose?

a. Quetiapine

b. Risperidone

c. Olanzapine

d. Aripiprazole

ANTICONVULSANTS 1.Phenytoin is the oldest NON-sedative, antiseizure drug. TL:

10-20 mcg/mL 2.Carbamazepine is effective in the treatment of bipolar

disorder. Its only available in ORAL FORM! TL: 4-8 mcg/mL 3.Phenobarbital is the oldest of the currently available

antiseizure drug. TL: 10-40 mcg/mL 4.Valproic acid is used in treatment of bipolar disorder and

migrane headache. 5.Clonazepam is useful in myoclonic seizures, absence seizures,

and infantile spasms. 6.Mechanism of action of ANTIEPILEPTIC DRUGS include

REDUCTION of sodium conductace, REDUCTION of calcium current and ENHANCEMENT of GABA current.

7.Inhibition of excitatory amino acids: a) Felbamatethru NMDA receptor antagonism; b) Topiramatethru AMPA and kainate receptor antagonism; c) Leviteracetamthru modification of synaptic release of glutamate and GABA.

ANSWER: Carbamazepine used in bipolar disorder and trigeminal neuralgia

SQ: Medications that are used to control status epilepticus, EXCEPT:

a. Phenobarbital

b. Diazepam

c. Phenytoin

d. carbamazepine

PARKINSONS DISEASE 1.Parkinsons disease is due to loss of dopaminergic neurons in substantia nigra. In treating parkinsons, you want to INCREASE dopamine and DECREASE acetylcholine.

2.Levodopa is a metabolic precursor of dopamine. It is given with CARBIDOPA/BENSEZARIDE, a dopa decarboxylase inhibitor to reduce the peripheral conversion of levodopaMORE LEVODOPA in the brain!!! You want dopamine in the brain so dont give pyridoxine with it because it will only enhance EXTRACEREBRAL metabolism of levodopa.

3.Dopamine receptor agonists include Bromocriptine and Pramipexole; FIRST LINE THERAPY FOR PARKINSONS DISEASE!

4.Monoamine oxidase B inhibitors retards the breakdown of dopamine. They are the first line drug in MILD PD to delay introduction of levodopa.

5.Cathechol-O-Methyltransferase inhibitors prolong the action of levodopa by diminishing its peripheral metabolism to 3OMD. Ex: Tolcapone, Entecapone

6.Amantadine is an ANTIVIRAL AGENT that may potentiate dopaminergic function by influencing the SYNTHESIS, RELEASE, and REUPTAKE of Dopamine.

7.Acetylcholine Blocking Drugs (Biperidine and Benztropine mesylate) improve TREMOR and RIGIDITY but little effect on BRADYKINESIA.

ANSWER: D LEVODOPA

SQ: Mechanism of treating Parkinsons Disease:

a. Antagonism at dopamine receptor

b. Inhibition of release of dopamine from presynaptic neuron

c. Inhibition of monoamine oxidase A

d. Administration of dopamine precursor

ALZHEIMERS DISEASE

1. In Alzheimers disease, there is lack of Ach in the CNS (opposite of parkinsons). The goal of therapy is to INCREASE acetylcholine.

2. Acetylcholinesterase inhibitors (Donepezil, Galantamine, Rivastigmine) inhibit the breadown of acetylcholine in the brain.

3. MEMANTINE is an noncompetitive NMDA receptor antagonist that prevent excitotoxic damage. It is indicated in moderate to severe AD.

RESPIRATORY DRUGS RELIEVERS/ BRONCHODILATORS

CONTROLLERS/ ANTI-INFLAM AGENTS

B2 agonist Epinephrine Antimuscarinics Systemic Steroids

1. Glucocorticoids 2. Leukotriene Antagonist 5-LOX inhibitor (Zileuton) CYS-LT1R Antagonist (Montelukast & Zafirlukast) 4. Mast cell stabilizers Cromolyn Na & Nedocromil alters function of

delayed chloride channels Ketotifen H1 receptor antagonist 5. Anti-IgE (Omalizumab)binds to Fc portion of IgE 6. Long acting beta-agonist (salmeterol, formoterol)

Both: METHYLXANTHINES

MAGNESIUM SULFATE LAGUNDI

FORMOTEROL

RESPIRATORY DRUGS 1. Formoterol is the only LABA for quick relief of asthma exacerbations. It

is a reliever and controller

2. Methylxanthines (e.g. Theophylline) have narrow therapeutic index (5-20 mg/L).

3. Lagundi , herbal medicine endorsed by DOH, contains chrysophenol D which possess anti-histamine and muscle relaxant properties.

4. Omalizumab (Anti-IgE) is the first biological drug approved for treatment of asthma.

5. Fixed-dose combinations in ASTHMA!!!

-ADDITION: Salbutamol + Ipratropium

-SYNERGISM: Salmeterol + Fluticasone (Seretide); Formoterol + Budesonide (Symbicort)

6. Beractant is an artificial surfactant prepared from mammalian lungs.

7. Peripheral cough suppressants: Local Anesthetics, Benzonatate

8. Central Cough receptor suppressant: Opiate, Dextrometorphan, Butamirate

ANSWER: Omalizumab Its the only approved Anti-IgE!

SQ: This agent can dramatically lower free serum IgE concentration and Fc receptors for IgE on mast cells among highly allergic asthmatics.

a. Lagundi

b. MgSO4

c. Omalizumab

d. Systemic Steroids

ANSWER: SYNERGISM -Formoterol (LABA)+ Budesonide

(INHALED STEROIDS)

SQ: The fixed dose combination of LABA + Inhaled steroids exhibits this type of drug interaction

a. Addition

b. Synergism

c. Antagonism

d. Potentiation

GASTROINTESTINAL DRUGS

1. H2 receptor antagonist suppress nocturnal & meal-stimulated acid secretion while Proton Pump Inhibitors (IDEAL DRUGS) inhibit both fasting & meal-stimulated secretion.

2. Cimetidine has anti-androgenic effect due to CYP450 inhibition: cause gynecomastia, oligospermia, inpotence

3. CimetidineImidazole ring; Ranitidinefuran ring; Famotidine & NizatidineThiazole ring

4. Omeprazole & sucralfate need activation in the ACID environment.

PEPTIC ULCER DISEASE

1. Antacids traditional therapy 2. H2 receptor antagonist 3. Proton Pump Inhibitor IDEAL drugs 4. Mucosal Protective Agents (Sucralfate, Bismuth Compounds) 5. Antibiotics (Metronidazole, Amoxicillin, Clarithromycin) 6. Anticholinergics (Atropine, Dicycloverine)

Constipation 1. Bulk-forming agents (Psyllium seeds, methylcellulose) swell on contact with water

2. Emollient laxatives (Docusate Sodium or Calcium)increase water secretion in the intestine

3. Lubricants/Mineral oil productscoat bowel and decrease absorption of water

4. Stimulant laxatives (Anthraquinolones, Dimethyltthane/Bisacodyl)stimulates intestinal motility

Diarrhea 1. Oral salt solution 2. IVF 3. Antimotility Drug (Loperamide (opioid agonist but does not cross BBB);

Tsaang gubat)

Antiemetics 1. Antihistamines 2. Phenothiazines 3. Metoclopramide 4. Ondansetron

ANSWER: Ranitidine H2 receptor antagonists suppress nocturnal & meal-stimulated acid secretion while Proton Pump Inhibitors (IDEAL DRUGS) inhibit

both fasting & meal-stimulated secretion.

SQ: Which of the following effectively inhibits nocturnal acid secretion but has only modest impact on meal-stimulated acid secretion?

a. Ranitidine

b. Omeprazole

c. Misoprostol

d. Sucralfate

DIURETICS 1.CAI causes HYPERCHLOREMIC METABOLIC ACIDOSIS (Why? Chloride is secreted with

HCO3 reabsorption. But CAI inhibits reab or HCO3 so Cl stays in the body.) This can worsen hepatic encephalopathy. Use CAI only for 2-3 days unless you replace HC03 loss.

2.Loop diuretics and Thiazides cause HYPOKALEMIC METABOLIC ALKALOSIS.

3.Acutely, loop diuretics cause increased uric acid secretion but chronically, they decrease its excretion because of VOLUME depletion. Thiazides can also cause hyperuricemia. Watch out for GOUTY attack in THIAZIDES & LOOP.

4.Hypocalcemia and Hypomagnesemia may occur with loop diuretic administration because of the diminished lumen-positive potential that comes from K recycling.

5.Thiazides cause hyperglycemia and hyperlipidemia thus, their use in patients with DM is limited. Hyperglycemia can lead to hypokalemiaTORSADES de POINTES!

6.CAI, Loop (except ethacrynic acid), and Thiazides in general have sulfonamide moiety in their structure watch out for allergic reactions.

7.Ethacrynic acid, a loop diuretic and aminoglycoside, can cause ototoxicity.

8.Amiloride is the DOC for Liddle Syndrome (Pseudohyperaldosteronism)

9.Mannitol should not be continued unless there is increase in urine flow rate to >50 mL during the first 3 hours after parenteral administration.

DIURETICS MECHANISM OF ACTION/ LOCATION OF ACTIVITY

INDICATION

Carbonic anhydrase inhibitor (Acetazolamide)

PROXIMAL CONVOLUTED TUBULE decreases reabsorption of bicarbonate in the kidney & inhibits bicarbonate secretion in ciliary body

Open-angle Glaucoma Urinary Alkalinization Metabolic alkalosis Acute Mountain sickness

Loop Diuretics (Furosemide, Ethacryinic acid, Torsemide, Bumatanide)

THICK ASCENDING LIMB Inhibition of NKCC2 transporter Decrease NaCl reabsoprtion and increase Ca & Mg excretion HIGH-CEILING DIURETICS!!!

Acute PULMONARY EDEMA Hyperkalemia & Hypercalcemia ARF Anion overdose

Thiazides (Hydrocholorthiazide)

DISTAL COLLECTIING TUBULE Inhibit NCC transporter Inhibit NaCl reabsorption from luminal side of epithelial cells

Hypertension CHF Nephrolithiasis Edema

Potassium-sparing Diuretics

LATE DCT and CCT EDEMA/ HTN (seldom) HYPERALDOSTERONISM

Osmotic diuretic (Mannitol)

PROXIMAL TUBULE & DTAL

To increase urine volume & decrease ICP & IOP

ADH Antagonist (CONIVAPTAN)

COLLECTING DUCT SIADH

ANSWER: Furosemide Furosemide causes hypokalemia because it promotes

diuresis of Na & K. Hypokalemia facilitates the the enzyme inhibition of Digoxin.

SQ: A female patient, known case of RHD, MS in AF, develops frequent PVCs. Digitalis toxicity is highly entertained because of the use of which of the ff?

a. Spironolactone

b. Furosemide

c. Hydrochlorothiazide

d. Acetazolamide

ANTIARRHYTHMIC AGENTS CLASS DRUGS Location

of activity OTHERS

CLASS IA Ex. Procainamide A,V Ideal for treatment of paroxysmal tachyarrhythmia Has increased risk of Torsades de Pointes!!!

CLASS IB Ex. Lidocaine V Ideal for tx of VENTRICULAR ARRHYTHMIAS

CLASS IC Ex. Encainide A,V

CLASS II B-blockers AVN, V can prevent recurrent infarction & sudden death in pt recovering from MI

CLASS III K+-blocker (Amiodarone, Bretyllium, Sotalol, Ibutilide)

A,V Has increased risk of Torsades de Pointes!!!

CLASS IV Ca-channel blockers AVN For treatment of SUPRAVENTRICULAR ARRHYTHMIA

ANSWER: Beta-blocker Beta-blockers can prevent recurrent infarction &

sudden death in pt recovering from MI

SQ: What is given to a patient with premature ventricular contraction who had myocardial infarction a month ago?

a. Beta-blocker

b. CCB

c. ACEI

d. ARBs

DRUGS USED IN CHF WITH POSITIVE INOTROPIC

ACTION 1. Digitalisinhibits Na/K

ATPase 2. PDE inhibitors 3. Beta-adrenoceptor

Stimulants -Dobutamine, Dopamine

WITHOUT POSITIVE INOTROPIC ACTION

1. Diuretics 2. Aldosterone Antagonist

(Spironolactone) 3. ACEi 4. ARBS 5. Beta-blockers 6. Vasodilators Venousfurosemide Arteriolarhydralazine Bothnitrates, ACEi, ARBS,

alpha blockers, nitroprusside

DRUGS USED IN CHF 1. 2/3 of administered Digoxin is excreted unchanged in the kidneys

and less than 40% metabolized in the liver. Digitoxin is metabolized in the liver and excreted in the gut via the bile. So!!! In patients with liver cirrhosis, Digoxin is preferred over Digitoxin. While in patients with Chronic kidney failure, Digitoxin is given.

2. The therapeutic level of Digoxin is 0.5-2.5 ng/ml.

3. Hypokalemia facilitates enzyme inhibition of cardiac glycosides (Digoxin) greater toxicity!...Hypokalemia, Hypercalcemia, and Hypomagnesemiaincrease the risk of cardiac-induced ARRHYTHMIAS.

4. Cardiac glycosides are CONTRAINDICATED in patients with ATRIAL FIBRILLATION in WOLF-PARKINSONIAN-WHITE SYNDROME.

5. To reverse digitalis toxicity, give DIGITALIS ANTIBODIES (Digoxin Immune Fab or Digifab)

6. Dobutamine improves contractility and decreases afterload.

ANTIHYPERTENSIVE AGENTS 1.Beta-blockers (-OLOLs) are indicated for UNCOMPLICATED HYPERTENSION.

2.ACE inhibitors are the first-line drugs for hypertensive patients with DIABETES MELLITUS.

3.Hydralazine is used for hypertensive emergency in PREGNANT WOMEN; Methyldopa is mainly indicated in hypertension in pregnancy.

4.Guanadrel cause retrograde ejaculation.

5.Minoxidil is a K+ ATP channel opener antihypertensive thats used for correction of baldness (ROGAINE) bec of it side effect, hypertrichosis.

6.ACE inhibitors (-PRILS) have dry cough as a side effect because of the decrease in breakdown of bradykinin and substance P.

7.ACE inhibitors (-PRILS) cause hyperkalemia when given with K-sparing diuretics.

8.Aliskiren (SPP 100) is an oral renin inhibitor given once daily.

9.ACEI, ARBS, Spironolactone prevents VENTRICULAR REMODELLING.

10.CCBS: Dihydropyridines (Nifedipine, Nicardipine) have higher inhibitory effect on vascular smooth muscles than myocardial cells. Nondihydropyridines have greater inhibitory effect on myocardial cells than vascular smooth muscles.

ANSWER: Enalapril ACEI (-PRILS), ARBS (-ARTAN), Spironolactone

prevents VENTRICULAR REMODELLING.

SQ: This drug reduces ventricular remodelling in post-MI patients.

a. Enalapril

b. Amlodipine

c. Digoxin

d. Diltiazem

ANTIPLATELETS INHIBITION OF PG SYNTHESIS

INHIBITION OF ADP pathway

GP IIb/IIIa receptor blocker

PDE inhibitor

Aspirin Clopidogrel Ticlopidine

Abciximab Eptifibatide Tirobifan

Dipiridamole Cilostazol

SQ: Match the antiplatelets with the agonists to platelet activation that they antagonize:

1. Eptifibatide

2. Ticlopidine

3. Dipyridamole

4. ASA

A. Phosphodiesterase

B. Thromboxane A2

C. GP Iib/IIIa

D. ADP

ANSWER: 1) C ;2) D; 3) A; 4) B

FIBRINOLYTIC DRUGS

Streptokinase

Urokinase

Antistreplase

t-PA

Alteplase

Reteplase

Tenecteplase

Give to patient with chest pain suggestive of MI. The time to therapy should be less than 12 hours from onset of pain.

ANTICOAGULANTS A. INDIRECT THROMBIN

INHIBITORS Their effect is exerted by their

interaction with ANTITHROMBIN

1. Unfractionated heaprin 2. LMW heparin 3. Fondaparinux Monitoring: aPTT & PTT ANTIDOTE for HEPARIN:

Protamine Sulfate

B. DIRECT THROMBIN INHIBITORS exert their anticoagulant effect

by binding to the active site of THROMBIN

1. Parenteral: Hirudin, Lepirudin, Bivalirudin, Argatroban, Melagatran

2. Oral: Ximelagatram, Dabigatran, Rivaroxiban

C. WARFARIN blocks the gamma carboxulation of glutamate residues in Factors 2,7,9,10 & protein C&S.

Antidote: VITAMIN K!

ANTILIPIDEMIC DRUGS DRUGS MOA INDICATION

HMG-CoA reductase Inhibitors (-STATINS)

Most effective at reducing LDL Inhibits the FIRST COMMITTED STEP in sterol synthesis dec LDL & TG, inc HDL

Niacin Decreases VLDL and LDL Increase HDL

Fibric Acid derivatives -Clofibrate, Gemfibrozil, Fenofibrate, Bezafibrate

Dec VLDL, LDL, TG ligand for ppar alpha upregulates LPL, apo-AI, apo-AII and down-regulate apo-CII

Useful in hypertriglyceridemias in which VLDL predominate

Bile acid binding resins colestipol, cholestyramine,

dec LDL bind bile acid in the intestinal lumen and p/v reabsoprtion

For isolated increase in LDL

Sterol Absorption inhibitor (Ezetemibe)

decreases LDL ?selective inhibitor of intestinal absorption of cholesterol and phytosterols through the transport protein, NPC1L1

ANTILIPIDEMIC DRUGS 1. Rosuvastatin is the most efficacious agent for severe

hypercholesterolemia.

2. MYOPATHY can occur when HMGCoA reductase inhibitor is used with Amiodarone or Verapamil. If you have to use one with Verapamil, choose Pravastatin or Rosuvastatin.

3. Niacin is the most effective agent to increase HDL and the only agent that can reduce Lp(a). Flushing can be a harmless side effect. May also cause acanthosis nigricans.

4. There is increased risk of myopathy when fibrates are given with HMGCoA reductase inhibitors.

5. Ezetemibe is the FIRST MEMBER of a group of drugs that inhibit intestinal absorption of phytosterols and cholesterol.

ANSWER: Simvastatin -Refer to #2. MYOPATHY can occur when HMGCoA reductase

inhibitor is used with Amiodarone or Verapamil. If you have to use one with Verapamil, choose Pravastatin or Rosuvastatin.

SQ: A 70 y/o male farmer with chronic stable angina complains of more frequent claudication. Which of the following maintenance medication is he currently taking responsible for this?

a. ISMN

b. Trimetazidine

c. Metoprolol

d. Simvastatin