Pharmacology Class Upd

9/11/18
Reference
•  Board Review Series, Pharmacology!
•  Crush Step 1 !
•  First Aid Step 1 2017!
•  Up to Date !
KISSPharm.com!
•  USMLE Road map, Pharmacology. !
Pharmacokinetics
ANS
Oncology
Dr. Bismarck Bisonó
Pharmacology
Pharmacokinetics
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ACID
•  PKA less than 7

•  Dissociates early
•  Likes to give up hydrogen ions (protons)
•  Gains a negative charge
•  Gains solubility: charge, polar, water sol.
•  Loses bioavailability: neutral, fat sol.
•  COOH àCOO- + H+
•  Strong acid: PKA 1-3
•  Weak acid: 4-7
BASE
•  PKA greater than 7
•  Dissociates later
•  Likes to accept hydrogen ions
•  Loses a positive charge
•  Loses solubility: charge, polar, water sol.
•  Gains bioavailability: neutral, fat sol.
•  NH3+à NH2 + H+
•  Weak base: 7-9
•  Strong base: >10
Acid vs Base
Henderson Hasselbalch Equation
PH = PK – Log B / A
Acid Dissociates Bioavailable Base Bioavailable Dissociates

Water sol. Fat sol. Fat sol. Water sol.
+2 99% 1% +2 99% 1%
+1 90% 10% +1 90% 10%
PH= PK–log B/A 50% 50% PH= PK–log B/A 50% 50%
-1 10% 90% -1 10% 90%
-2 1% 99% -2 1% 99%
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Take Notes!
Weak acids! Weak basis!
ASA, TCA! PCP!
Ketoconazole! Amphetamines!
Digoxin! Morphine!
Iron (anion GAP metabolic Quinidine!
acidosis). !
Erythromycin!
Treat: bicarbonate. Active
charcoal. ! Atropine!
! Treat: ammonium chloride,
Cranberry juice. Vit C.!
If you want to absorbs more
acid: add acid! !
If you don’t want to absorbs If you want to absorbs more
more acid: add base! base: add base!
! If you don’t want to absorbs
more base: add acid!
!
!
!
Enzyme kinetics
Michaelis-Menten kinetics
•  S: Substrate
•  V: Velocity
•  Km: Substrate concentration at 50% of Vmax.
•  Vmax: is the maximal effect of the enzyme
Competitive inhibition VS Non Competitive

inhibition
•  Inhibits by similar substance

•  Competing for active site
•  Affinity decrease
•  Km Increases
•  Reversible by increase in substrate
•  Vmax not change
•  Not similar substance

•  Competing for regulatory site
•  Turning the enzyme off
•  Km not change
•  IRReversible
•  Vmax decrease
•  Efficacy decrease
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inhibition

inhibition
FORMULAS
•  Bioavilability (F): Fraction of the drug that get to

systemic circulation unchanged.
•  IV = 100%
•  Volume of distribution: Amount of drug in the body
related to the plasma concentration.
•  Vd = Amount of drug in body
Plasma concentration
•  LOW: Intravascular space (<5L). ALBUMIN BOUND
•  MEDIUM: Extracellular space (<20).
•  HIGH: all tissue including fat. TISSUE PROTEIN BOUND
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Tips !
Protein Binding: Competition between drugs> WARFARIN
and SULFONAMIDES. !
!
DIGOXIN:!
•  High Vol of distrubution due to tissue deposit. !
•  QUINIDINE and VERAPAMIL displaces digoxin from
tissue sites. DIGOXIN TOXICITY.!
!
REDISTRIBUTION: !
Lipid soluble drugs resitribute into fat tissue prior
elimination (Thipental, IV anesthesia) INCREASE T1/2.!
!
** If cross BBB CROSS PLACENTA. Ex. Phenobarbital.!
FORMULAS
• Clearance: volume of plasma cleared of drug per unit

time
CL= rate of elimination of drug
plasma drug concentration

• Half life: time required to eliminate 50% of the drug
concentration of the body
t½= 0.693 (0.7) x Vd
Cl

Half Live
#of t1/2 1! 2! 3! 4! 5!
% remain! 50%! 25%! 12.5%! 6.25%! 3.125%!
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FORMULAS
•  Loading dose: fill the volume of distribution (Vd) to

achieve the target plasma concentration (Cp).
Load dose = Vd x Cp
F

•  Maintenance dose: replace the drug that is being
eliminated over time to maintain the target plasma
concentration. **Modify if CKD
Maintenance dose = Cl x Cp
F
Type of Drug
interaction
•  Additive
•  Effect of substance A and B together is equal to the
sum of their individual effects!
•  ASA + Acetaminophen!
•  Permissive
•  Substance A is required for the full effect of
substance B!
•  Cortisol on NE!
Type of Drug
interaction
•  Synergistic
–  Effect of substance A and B together is greater than
the sum of each individual
–  Clopidogrel + ASA

•  Tachyphylactic
–  Acute decrease to a drug after initial or repeated use
–  MDMA and LSD. Nitrates.
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Administration road
High FIRST PASS
effect: !
- Lidocaine!
- Nitrates!
Elimination of drugs
•  Metabolize drugs:
•  Hepatic: C. P-450!
•  Phase I: Reduction, oxidation, hydrolysis – Active metabolite
and water soluble.!
•  Phase II: Glucuronidation, Acetylation, Sulfation – Renal
excreted!
• Renal: PCT. Dehydropeptidase !
•  ACTIVE TRANSPORT: Penicillin and diuretics. May
precipitate gout. !
***GRAY BABY SYNDROME: ASEN COLOR!
**DU-SLE> ACETYLATORS!
•  Zero order:
•  Eliminate the same amount of the drug!
•  Phenytoin, Ethanol, Aspirin “ ZERO PEA FOR YOU” !
•  First order:
•  Eliminate the same fraction of the drug !
P-450
P-450 Isoenzyme Drug Substrate Inhibitirs Inducers
Theophiline, Fluorquinolones,
Acetaminophen, Macrolides
CYP1A2! Clozapine, Imipramine, Cimetidine, Omeprazole, Tobacco!
Mexiletine, Naproxen, Fluvoxamine,
Tacrine, Setraline Ticlopidine!
Phenytoin, Warfarine,
Diclofenac, Glipizide,
CYP2C9! Ibuprofen, Losartan, Amiodarone, Rifampin!
Naproxen, Piroxicam, Fluconazole, Isoniazid!
Tamoxifen, Tolbutaline
Amitriptiline, Fluoxetine,
Clomipramine, Fluvocamine,
CYP2C19! Cyclophosphamide, Ketoconazole, Rifampin!
Diazepam, Omeprazole, Omeprazole,
Phenytoin, Progesterone! Ticlopidine!
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P-450
P-450 Drug Substrate Inhibitirs Inducers
Isoenzyme
Metoprolol,
Propanolol, Timolol.! Haloperidol,
Mexiletine! Quinidine,
Amitriptyline, Amiodarone,
Clomipramine, Bupropion,
Codeine, Chlorpheniramine,
CYP2D6! Desipramine, Cimetidine,
Imipramine, Clomipramine,
Dextromethorphan, Fluoxetine,
Haloperidol, Methadone,
Paroxetine, Paroxetine, Ritonavir

Risperidone,
Thioridazine !
P-450 Drug Substrate Inhibitirs Inducers

Isoenzyme
Verapamil, Diltiazem,
Felodipine, Nifedipine!
Atorvastatine,
Lovastatine,
Sinvastatine! Amiodarone,
Alprazolam, Cimetidine,
Diazepam,Midazolam Diltiazem,
, Triazolam, Erythromicin,
Buspirone,Methadone! Fluvoxamine, Carbamazepine,
Clarithromycin, Grapefruit, Phenobarbital,
CYP3A4,5,7! Phenytoin,
Indinavir, Imatinib, Rifampin,
Erythromycin! St. John’s
Cyclophosphamide, Isoniazid, wort, Troglitazone!
Tamoxifen, Itraconazole,
Vinblastine, Nefazodone,
Vincristine! Nelfinavir, Ritonavir,
Indinavir, Ritonavir, Verapamil!
Saquinavir!
Chlorpheniramine,
Cycloporine,
Quinidine, Tacrolimus!
P-450
Induce P450 Inhibit P450 P450 Dependent
INH !
Dapsone !
Barbiturates ! Sulfa Drugs !
Alcohol chronic use! Macrolides ! Warfarin !
Griseofulvin ! Amiodarone ! Estrogen !
Carbamazepine ! Cimetidine ! Phenytoin !
Rifampin ! Ketoconazole ! Theophylline !
Tetracycline ! Fluoroquinolones! Digoxin !
Spironolactone ! Quinidine! !
! !
Azythro<Claritro<Erythro!
!
COKE + Grape fruit with your PI!

**Furanocoumarin!
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Transformation!
Drug-> active Prodrug-> toxic

o Enalapril-> enalaprilat!
Benzos get converted to Nordiazepam
o Methyldopa-> Methyl
(active)!
Fluoxetine -> norfluoxetine (accumulates and norepinephrine!
o Procarbazine ->
active for weeks)!
Sulindac -> sulfide metabolite azoxy metabolite!
o Acetaminophen->
NAPQI
Elimination!
Probenecid competes with WEAK ACIDS.

Increase Penicillin and cephalosporin levels. !
Metformin 100% excreted by the kidney. NOT
metabolized not used on patient with less than
80% of renal function. !
!
•  Efficacy:
•  Maximal effect a drug can produce!
•  Vmax!
•  CLINICALLY MORE IMPORTANT!!!
!
•  Potency:
•  Amount of drug needed for a given effect.!
•  Km!
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Competitive Antagonist VS Non Competitive

Antagonist
•  Shift curve to the right •  Shift the curve down
•  Decrease potency •  Decrease efficacy
•  No change in efficacy •  Cannot be overcome by
•  Can be overcome by increase agonist
increase agonist •  NE Vs Phenoxybenzamine
•  Diazepam Vs Flumazenil !
Partial
Agonist
•  Acts as a full agonist
•  Decrease efficacy
•  Increase or decrease potency
•  Morphine Vs Buprenorphine
•  Pindolol (less lipids effect)
Chemical antagonist (Antacids)

Physiological antagonist (M3 on bronchi Vs B2)
Therapeutic index
•  Measure drug safety
TI = TD50 - median toxic dose
ED50 - median effective dose
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Beers criteria!
l  Widely used criteria developed to reduce

potentially inappropriate prescribing and harmful
polypharmacy in the geriatric population.
Includes > 50 medications that should be
avoided in elderly patients due to reduce efficacy
and/or high risk of adverse events. !
l  Examples include: !
l  Anticholinergics, antihistamines,
antidepressants, benzodiazepines, opioids

(q risk of delirium, sedation, falls, constipation,
urinary retention) !
l  α-blockers (q risk of hypotension) !
l  PPIs (q risk of C difficile infection)!

l  NSAIDs (q risk of GI bleeding, especially with
concomitant anticoagulation)!
Autonomic Nervous
System
Pharmacology
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Nervous system
Anatomy:
•  Central:
•  Brain
•  Spinal Cord

•  Peripheral:
•  Cranial nerves
•  Peripheral nerves
•  Somatic: voluntary muscle
•  Autonomic: involuntary body functions
ANS
•  Controls involuntary body functions.
•  Have Afferent-Sensory and Efferent- Motor.
•  Innervates organs, smooth muscle and glands.
•  Have ganglionic synapses.
•  Divided in:
•  SYMPATHETIC SYSTEM
•  PARASYMPATHETIC SYSTEM
Sympathetic, Parasympathetic,
Somatic
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PARASYMPATHETIC SYSTEM
•  Craneal-sacral
•  Use Acetylcholine in the ganglionic and
postganglionic synapses!
•  All ganglionic receptor are Nicotinic!
•  Ligand-gated Na/K channels!
•  Nn: Autonomic ganglia!
•  Nm: Neuromuscular junction!
!
•  Muscarinic: Cardiac, smooth muscle, ganglia,
nerve terminal
•  G protein, M1, M2, M3, M4, M5!
SYMPATHETIC SYSTEM
•  Thoraco-lumbar
•  Use Acetylcholine and Nicotinic receptor in the
ganglionic synapses
•  Most are Noradrenergic with Alpha and Beta receptor.
•  Except sweet glands that use Acetylcholine and
Muscarinic receptor
•  Renal vasculature that uses Dopamine receptor.
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Second
Messengers
•  cAMP
•  cGMP
•  IP3 / DAG
•  Ca / Calmodulin
•  Calcium
•  Tyrosine Kinase
•  NO
Muscarinic
Receptor G protein Function
M1 Gq ↑ CNS, PNS
Gastric parietal cell
M2 GI ↓ Heart rate, contractility
↑ Exocrine gland secretion

↑ Gut motility
Miosis- pupilari sphinter
M3 Gq Accomodation - ciliary muscle
Broncoconstriction
Bladder contraction
M 4! G I! CNS Unclear !
M 5! G q! Unclear!
Noradrenergic
↑ Smooth muscle contraction!
Alpha 1! G q! Mydriasis (papillary dilator contraction)!
↑ Sphincter contraction!
↓ NE, Epi release!

↓ Insulin!
Alpha 2! G i! ↓lipolysis!
↓ Aqueous humor production!
↑ platelets aggregation!
↑ HR, contractility!
Beta 1! G s! ↑ Renin release!
↑ Lipolysis!
↓ Vasoconstriction!
↓ Bronchoconstriction!
↓ Uterine contraction!
Beta 2! G s! ↑ Lipolysis!
↑ insulin release,!
↑ Aqueous humor production!
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Dopamine / Histamine /
Vasopressin
D1 Gs Relax renal vascular
D2! G i! Modulate neurotransmitter release!
↑ nasal bronchial mucus production

H1 Gq ↑ vascular permeability
Bronchioles contraction
Pruritus, Pain
H2 Gs ↑ Gastric acid production
V1! G q! ↑ Vascular contraction!
V2! G s! ↑ H2O reabsorption on CT!
Cholinomimetic
Agents
Direct
•  Bethanecol
•  Carbacol
•  Methacholine
•  Pilocapine
Cholinesterase regenerator
•  Pralidoxime (2-PAM)
Indirect Cholinesterase inhibitor
•  Donepezil
•  Galantamine
•  Rivastigmine
•  Edrophonium
•  Neostigmine
•  Physostigmine
•  Echothiophate
•  Pyridostigmine
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Direct Cholinomimetic
Agents
•  MOA: Direct agonist of Ach receptors
•  USE:
•  Bethanecol: Post operative ileus, neurogenic ileus,
urinary retention
•  Carbacol: Glaucoma (pupil contriction)
•  Methacholine: Asthma challenge test
•  Pilocapine: Stimulate sweat, tears, saliva, Cystic
fibrosis test, Glaucoma
•  SE: Exacerbation of COPD, Asthma, PUD.
Indirect Cholinomimetic
Agents
!
•  MOA: Cholinesterase inhibitors. NOT EFFECT ON

NON INNERVATED RECEPTOR.
•  SE: Exacerbation of COPD, Asthma, PUD, nausea,

Dizziness, insomnia.
Indirect Cholinomimetic
Agents
•  USE:!
•  Donepezil, Galantamine, Rivastigmine:
Alzheimer
•  Edrophonium: Diagnosis of Myasthenia gravis
•  Neostigmine: Treatment of MG, Post operative
ileus, neurogenic ileus, urinary retention.
•  No CNS penetration!
•  Physostigmine, Echothiophate: CNS
penetration, Anticholinergic toxicity
•  Pyridostigmine: MG
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Organophosphates
•  MOA: Irriversable inhibitors of Achetilcholinestarase
•  USE: insecticides
•  Sings & Symptoms!
•  Diarrhea
•  Urination
•  Miosis
•  Bronchospasm
•  Bradicardia
•  Excitation of Skeletal muscle and CNS
•  Lacrimation
•  Sweeting
•  Salivation
•  Treatment: Atropine + Pralidoxime (2-PAM)
Cholinesterase
Regenerator
•  Pralidoxime (2-PAM)
•  MOA: Break the bond between the

organophosphate and the enzyme.
•  Regenerate free enzyme
•  USE: Organophosphate poison

•  SE: Muscle weakness
Toxins
•  Tetrodotoxin
•  Pufferfish, FUGU!
•  Binds fast voltage gated Na channels. BLOCK
IT !
•  Nauseas, diarrhea, paresthesia, weakness.
Dizziness, lost of reflexes.!
•  Treatment: supportive!
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Toxins
•  Ciguatoxin
•  Barracuda, snapper!
•  Binds open Na channels causing
depolarization. OPEN IT !
•  Temperature related dysesthesia (hot like
cold, cold like hot). Diarrhea, Vomit.!
•  Treatment: supportive!
Toxins
•  Scombroid poisoning “ Acute Fish ALLERGY”
•  Deep sea fish!
•  Burning in the mouth, flushing of face,
erythema, urticaria, pruritus, headache,
anaphylaxis like symptoms.!
•  Treatment: antihistaminic.!
•  Antimuscarinic Sympathomimetic
•  Atropine
•  Phenylephrine
•  Homatropine
•  Nor-Epinephrine
•  Tropicamide
•  Epinephrine
•  Benztropine
•  Isoproterenol
•  Glycopyrolate
•  Dobutamine
•  Hyoscyamine
•  Albuterol
•  Dicyclomine
•  Salmeterol
•  Tiotropium
•  Dopamine
•  Ipratropium
•  Cocaine
•  Oxibutynin
•  Ephedrine
•  Solifenacin
•  Pseudoephedrine
•  Tolterodine
•  Scopolamine
!
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Anti-muscarinic
Atropine
•  MOA: Block muscarinic receptor
•  USE: Bradycardia, Organophosphate toxicity
•  SE: Cycloplegia – worse glaucoma; ↓ sweat - ↑

temperature, dry skin; flushing, constipation,
disorientation
Anti-muscarinic
•  Atropine, Homatropine, Tropicamide: Eyes-
Mydriasis
•  Benztropine: Parkinson’s disease
•  Glycopyrolate: GI, Respiratory surgeries
•  Hyoscyamine, Dicyclomine: IBS
•  Tiotropium, Ipratropium: COPD, Asthma
•  Oxibutynin, Solifenacin, Tolterodine: Urgency
incontinence
•  Scopolamine: Motion sickness
Sympathomimetics
•  MOA: Direct agonist of Alpha, Beta, Dopamine
receptors
•  MOA: Alpha 1 > 2
•  USE: Hypotension, Rhinitis

•  MOA: Alpha 1 > 2 > Beta
•  USE: Hypotension

•  Epinephrine
•  MOA: Beta > Alpha
•  USE: Anaphylaxis shock, asthma, open angle
glaucoma **AVOID closed angle glaucoma

•  MOA: Beta 1 = 2
•  Rarely use
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Sympathomimetics
•  Dobutamine:
•  MOA: Beta 1 > Beta 2 =Alpha
•  USE: Heart failure (inotropic >chronotropic), cardiac
stress test
•  Albuterol (short ½ life), Salmeterol
•  MOA: Beta 2 > B1
•  USE: Asthma, COPD
•  Dopamine:
•  MOA: D > Beta > Alpha
•  USE: Bradycardia, HF, Shock.
•  **Fenoldopam: D1 partial agonist.
Sympathomimetics
•  Cocaine
•  MOA: inhibits reuptake
•  SE: Coronary vasospasm, local anesthetic

•  Ephedrine, Pseudoephedrine, Phenylephrine
•  MOA: inhibits reuptake, Alpha agonist
•  USE: Nasal decongestion, Urinary incontinence,
hypotension.
•  SE: Hypertension
•  Pseudoephedrine: anxiety
Amphetamine
•  Methylphenidate- ritilan
•  Dexadrine- dexatrim
•  Adderal
•  LSD
•  PCP
•  ECSTACY
•  Pemoline
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Amphetamine
•  MOA: Indirect agonist, Inhibits re-uptake, release
stored catecholamine
•  SE: Vertical nystagmus, Nauseas, Vomiting (DA
stimulant), Tics (basal ganglia)
•  Methylphenidate- ritalin
•  USE: Narcolepsy, ADHD in kids, gain weight
•  SE: Hypnogogic hallucinations as you fall asleep
•  USE: Weight loss + exercise and diet; OTC
•  Adderal
•  MOA: Dexadrine + racimic amp
Amphetamine
•  LSD
•  SE: Hallucinations from Serotonin (slow, lazy) + Amp
•  PCP *NMDA antagonist.
•  SE: Hallucinations from Serotonin (violent,
aggressive) + ↑↑↑Amp violent; Vertical nystagmus.
•  ECSTACY
•  SE: Hallucinations from Serotonin (stimulate thirst) +
Amp
•  Pemoline
•  SE: Hepatic necrosis (hepatitis)- off the market 2005
•  Alpha Agonist •  Beta blockers

•  Clonidine •  Propranolol
•  Brimonidine •  Esmolol
•  Carvedilol
•  Alpha Methyldopa
•  Labetalol
•  Alpha Blocker
•  Pindolol
•  Phentolamine
•  Acebutolol
•  Phenoxybenzamine •  Metoprolol
•  Prazosin •  Nadalol
•  Terazosin •  Timolol
•  Doxazosin •  Butexalol
•  Tamzosin •  Carteolol
•  Mirtazapine •  Sotalol
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Alpha 2 Agonist
•  Clonidine
•  USE: Hypertensive urgency, ADHD, Tourette
syndrome
•  SE: CNS depression, respiratory depression,
bradycardia, hypotension, miosis. **decrease REFLEX
tachycardia.

•  Brimonidine
•  MOA: Alpha 2 agonist
•  USE: open angle glaucoma

•  USE: Hypertension in pregnancy. DOC.
•  SE: Hemolysis, Drug induce SLE. + Direct Coombs test
Autoimmune Hemolytic
Anemia
•  PTU!
•  Cephalosporins !
•  α-methyldopa !
•  Sulfa drugs !
•  Anti-malarials !
•  Penicillin !
•  Penicillamine !
•  Dapsone !
•  Aspirin !
•  Heparin !
•  Quinidine !
•  Quinine!
Alpha Blockers
•  MOA: Nonspecific alpha inhibitors
•  SE: Orthostatic hypotension, reflex tachycardia
•  Phentolamine
•  Reversible
•  Use: Diagnosing Pheochromocytoma, MAO Inh.
With tyramine.
•  Phenoxybenzamine
•  Irreversible
•  USE: treat Pheochromocytoma
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Alpha 1 blocker
•  MOA: Block alpha 1 receptor
•  USE: BPH, HTN
•  SE: Hypotension, Dizziness, Headache
•  Prazosin:
•  PTSD, 1st dose syncope
•  Terazosin
•  Doxazosin
•  Tamsulosin
•  Less SE. More specific to prostate. Retrograde
ejaculation.
Mirtazapine
•  MOA: Alpha 2 blocker (also 5HT)
•  USE: Depression, insomnia.
•  SE: sedation, ↑ cholesterol and appetite. WEIGHT
GAIN (useful in elderly anorexic patient)
Beta blockers
•  A-M à Beta 1; except C-L
•  N-Z à Beta 1-2
•  C-L à Alpha + Beta

•  USE: Angina, MI, Hypertension, HF, Glaucoma, SVT,
Ventricular rate in A-fib, Aflutter
•  Decrease mortality in MI.

•  SE: Impotence, Exacerbation of COPD, Asthma, AV
block, bradycardia
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Beta blockers
•  Propranolol
•  Long ½ life
•  Thyroid storm: Block 5’-deiodinase : prevent conversion of
T4 to T3
•  Migraine prophylaxis
•  Esophageal bleeding

•  Esmolol
•  Short ½ life
•  Anesthesiology, A-fib.

•  Carvedilol, Labetalol
•  Alpha + Beta antagonist
•  HTN emergency
Beta blockers
•  Pindolol, Acebutolol
•  Partial agonist
•  Metoprolol, Carvedilol
•  DECRASE MORTALITY MI.
•  Nadolol
•  Liver failure
•  ↓ esophageal bleeding

•  Timolol, Betaxolol, Carteolol
•  Open angle glaucoma
Oncology
Pharmacology
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Antimetabolites
•  Azathioprine
•  6-Mercaptopurine (6MP)
•  6-Thioguanine (6-TG)
•  Cladribine
•  Cytarabine
•  5-Fluorouracil (5-FU)
•  Methotrexate (MTX)
•  Hydroxyurea
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Purine Analogs
•  Azathioprine
•  Metabolize into 6MP!
!
•  6-Mercaptopurine (6MP), 6-Thioguanine (6-

TG)
•  MOA: Block the novo purine synthesis (A, G). PRPP
amidotransferase.
•  Activated by HGPRT!
•  USE: preventing organ rejection, Rheumatoid arthritis,
IBD, SLE. Steroids stop.
•  SE: Myelosuppression, GI, Liver, Gout
Purine Analogs
•  Cladribine
•  MOA: Purine analog, Inhibits DNA polymerase,

DNA strand breaks
•  USE: Hairy cell leukemia
•  SE: Myelosuppression,
Pyrimidine Analog
•  Cytarabine
•  MOA: Pyrimidine analog, inhibits of DNA

polymerase
•  USE: AML, Lymphoma. ** AML M3 is the
exception, ATRA.
•  SE: Pancytopenia
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5-Fluorouracil (5-FU)
•  MOA: Inhibits thymidylate synthase, ↓ dTMP, ↓
DNA synthesis
•  USE: Colon cancer, Pancreatic cancer, Basal cell

carcinoma
•  SE: Myelosuppression, Photosensitivity
Methotrexate (MTX)
•  MOA: Folic acid analog that inhibits
dihydrofolate reductase, ↓ dTMP, ↓ DNA
synthesis
•  USE: ALL, Lymphomas, Choriocarcinoma,

Sarcomas, Ectopic pregnancy, medical abortion,
Rheumatoid arthritis, Psoriasis, IBD, vasculitis
!
•  SE: Myelosuppression (Tx: Leucovorin),
Hepatotoxicity, Mucositis, Pulmonary fibrosis
Hydroxyurea
•  MOA: Inhibits ribonucleotide reductase, ↓ DNA
synthesis
•  USE: Melanoma, CML, Sickle cell disease (↑ HbF)
•  SE: myelosuppression, GI upset
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Antitumor Antibiotics
•  Bleomycin
•  Dactinomycin
•  Actinomycin D
•  Doxorubicin
•  Daunorubicin
Bleomycin
•  MOA: Induce free radical formation and breaks DNA
strains
•  USE: Testicular cancer, Hodgkin lymphoma
•  SE: Pulmonary fibrosis, Skin hyperpigmentation,

mucositis.

TIPS!
Pulmonary fibrosis!
•  Bleomycin !
•  Bisulfan !
•  MTX!
•  Amiodarone !
•  Nitrofurantoin!
28
9/11/18
Dactinomycin,
Actinomycin D
•  MOA: Intercalates in DNA
•  USE: Wilms tumor, Ewing sarcoma,

Rhabdomyosarcoma
•  SE: Myelosuppression
Doxorubicin, Daunorubicin,
Adriamycin
•  MOA: Generate free radicals, Intercalates in DNA,
break in DNA, ↓ replication
•  USE: Solid tumors, leukemias, lymphomas

!
•  SE: Cardiac fibrosis, Dilated cardiomyopathy,
myelosuppression, alopecia.
•  Antidote: Dexrazoxane
•  Iron chelator that prevent cardiotoxicity
Alkylating agents
•  Busulfan!
•  Cyclophosphamide!
•  Ifosfamide!
•  Cisplatin!
•  Carboplatin!
!
•  Nitrosoureas!
•  Carmustine!
•  Iomustine!
•  Semustine!
•  Streptozocin!
29
9/11/18
Busulfan
•  MOA: Cross links DNA
•  USE: CML, Bone marrow ablation for

transplantation
•  SE: Severe myelosuppression, Pulmonary fibrosis,

hyperpigmentation
Cyclophosphamide,
Ifosfamide
•  MOA: Cross link DNA at guanine
•  Requires activation by the liver!
•  USE: solid tumors, leukemia, lymphomas
•  SE: Myelosuppression, Hemorrhagic cystitis
•  Prevented by MESNA. Binds to toxic

metabolite(acrolein) and N-acetylcysteine!
Nitrosoureas
•  Carmustine
•  Lomustine
•  Semustine
•  Streptozocin
•  USE: Brain tumors

•  MOA: Cross link DNA, require bioactivation, Crosss
Blood Brain Barrier
•  SE: Convulsions, dizziness, ataxia
30
9/11/18
Cisplatin, Carboplatin
•  MOA: Cross link DNA
•  USE: Testicular, bladder, ovary, lung carcinomas
•  SE: Nephrotoxicity, Ototoxicity,
•  Amifostine prevents nephrotoxicity
Microtubule inhibitors
•  Paclitaxel
•  Vincristine
•  Vinblastine
Paclitaxel/Docetaxel
•  MOA: Stabilize microtubules in M phase, stops
mitotic division
•  USE: ovarian, Breast cancer
•  SE: Myelosuppression, Alopecia, Hypersensitivity
31
9/11/18
Vincristine, Vinblastin
•  MOA: bind to tubulin and inhibits microtubules, M
phase arrest.
•  USE: Solid tumors, Leukemias, Hodgkin

(Vinblastine), non-Hodgkin (Vincristine), Lymphomas
•  SE: Neurotoxicity (Vincristine), Blast bone marrow

(Vinblastine)
Topoisomerase
Inhibitors
•  Etoposide
•  Teniposide
•  Irinotecan
•  Topotecan
Etoposide, Teniposide
•  MOA: Inhibits topoisomerase II, ↑ DNA degradation
•  USE: Solid tumors, Leukemia, Lymphomas. Small

cell Ca.
•  SE: Myelosuppression, GI upset, Alopecia
32
9/11/18
Irinotecan, Topotecan
•  MOA: Inhibits topoisomerase I and prevent DNA
unwinding and replication
•  USE: Colon cancer (Irinotecan), Ovarian and small

cell lung cancer (Topotecan)
•  SE: Myelosuppression, diarrhea
Hydroxyurea !
MOA: Inh. Ribonucleotide Reductase. Decrease
dUDP synthesis. S-phase inhibitor. !
!
Use: SCD, Melanoma, CML. !
!
SE: Myelosuppression, GI . !
!
Antibodies
•  Bevacizumab
•  Rituximab
•  Cetuximab
•  Erlotinib
•  Trastuzumab
•  Vemurafenib
•  Imatinib
•  Bortezomib, carfilzomib
33
9/11/18
Antibodies
•  Bevacizumab
!
•  MOA: inhibits vascular endothelial growth factor A
(VEGF-A)
•  Inhibits angiogenesis!
•  USE: Neovascular age-related macular degeneration
•  Solid tumors, Colorectal cancer, Renal cell carcinoma!
•  SE: Hemorrhage, blood clots, impaired wound healing
Antibodies
•  Rituximab
•  MOA: block CD20
•  USE: B-cell non-hodgkin lymphoma, CLL,
Rheumatoid arthritis, IBD.
•  SE: risk of multifocal leukoencephalopathy
Antibodies
•  Cetuximab
•  MOA: block Epidermal growth factor receptor

•  USE: Stage IV colorectal cancer, Head and neck cancer
•  SE: acute reaction (fever, rash, headaches), serum sickness (Type III
HSR). Treat steroids.
•  MUST confirm KRAS mutation before use it *act on KRAS mutated

colon cancer.

•  Erlotinib
–  MOA: EGFR tyrosine kinase inhibitor
–  USE: non Small cell lung carcinoma
–  SE: Rash
34
9/11/18
Antibodies
•  Trastuzumab
•  MOA: bind to Human Epidermal growth factor
receptor 2 (HER2/neu), a tyrosine kinase receptor
•  USE: Breast cancer (HER2+), gastric.
•  SE: Cardiotoxicity
Vemurafenib
•  MOA: Small molecule inhibitor of BRAF oncogene.
•  VEmuRAF-enib (V600E mutated, BRAF inhibitor.
•  USE: Metastatic melanoma
Imatinib
•  MOA: Tyrosine kinase inhibitor of BCR-ABL gen,
Philadelphia chromosome, t (9;22) and c-kit (Stroma
tumors
•  USE: CML, GI stromal tumors
•  SE: Fluid retention. Ankle and periorbital edema.
35
9/11/18
Bortezomib, carfilzomib!
l  MECHANISM OF ACTION!
-  Proteasome inhibitors, induce arrest at G2-M
phase and apoptosis. !
l  CLINICAL USE !
-  Multiple myeloma, mantle cell lymphoma !

l  ADVERSE EFFECTS !
-  Peripheral neuropathy, herpes zoster

reactivation.!
Tumor lysis syndrome!
l  Oncologic emergency triggered by massive

tumor cell lysis, most often in lymphomas/
leukemias. Release of K+ hyperkalemia, release
of PHOSPHATE– hyperphosphatemia,
hypocalcemia due to Ca2+ sequestration by
PO4. nucleic acid breakdown
hyperuricemia, acute kidney injury. !
l  Treatments include aggressive hydration,
allopurinol, rasburicase!
Rasburicase !
l  MECHANISM !
-  Recombinant uricase that catalyzes metabolism
of uric acid to allantoin. !
l  CLINICAL USE !
-  Prevention and treatment of tumor lysis

syndrome.!
36
9/11/18
Selective Estrogen Receptor

Mod.
•  Tamoxifen
•  MOA: Antagonist on the breast, partial agonist on
endometrium.
•  USE: estrogen receptor breast cancer
•  SE: Endometrial cancer, hot flashes.
•  Raloxifene
•  MOA: agonist on bone, reduce reabsorption of
the bone
•  USE: osteoporosis
•  SE: BOTH THROMBOSIS RISK
Steroids
•  MOA: Anti-inflammatory Actions
•  Inhibit PLP-A2!
•  Kills T-cells and eosinophils!
•  Inhibits macrophages migration!
•  Stabilizes endothelium!
•  Stabilizes mast cells!
•  Physiologic actions
•  Proteolysis!
•  Gluconeogenesis!
Steroids
•  USE: Addison’s, Inflammation, Immune
suppression, Asthma, COPD
•  SE: Cushing’s, Osteoporosis, Adrenocortical atrophy,

Adrenal insufficiency if stop chronic use, PUD,
Diabetes, weight gain, fat redistribution, psychosis,
hypertension, cataracts, acne
•  Prophylaxis: H2 blocker or PPI, Ca2+, Vit. D,

Bisphosphonate, Nystatin/Fluconazole. MOUTH
WASH!
37
9/11/18
•  Prednisone, Prednisolone: CLL, non-Hodgkin lymphoma

•  Methylprednisolone: Main IV
•  Triamcinolone: Main Inhale, next Budesonide,
Cyclosenide (kids)
•  Beclamethasone, Betamethasone: preterm fetus for
increase surfactant production
•  Hydrocortisone: Main Topical, injective
•  Dexamethasone: CNS penetration **Decrease EDEMA
•  Fludrocortisone: take the place of aldosterone
•  Cypropterone: only that block DHT receptor in prostate CA
•  Megestrol: strong anabolic effect, in cancer patient **
INCREASE APPETITE
•  Fluticasone, Mometasone: nasal allergies
•  Danazol: Endometriosis
38
9/11/18
Cardiology!
Renal!
Pulmonary!
Gastroenterology!
Antibiotics!
Cardiology
Pharmacology
Antihypertensive
•  Essential Hypertension
•  Thiazides diuretics
•  ACE inhibitors
•  Angiotensin II receptor blocker
•  Calcium channel blockers

•  HTN with Diabetes Mellitus
•  CCB
•  Thiazides diuretics
•  Beta blockers
1
9/11/18
Antihypertensive
•  HTN with Heart Failure
•  Diuretics
•  Beta Blockers
•  Aldosterone antagonist
•  HTN in Pregnancy
•  Hydralazine
•  Labetalol
•  Nifedipine
Calcium channel
Blocker
Non dihydropyridines - HEART
•  Verapamil, Diltiazem:

•  USE: Atrial Arrhythmias, class IV anti-arrhythmic

•  SE: Constipation. AV block, Bradycardia,
Hyperprolactinemia (verapamil).
Calcium channel
Blocker
Dyhydropyridines – Systemic
• Nimodipine:
USE: Stops vasospasm after subarachnoid hemorrhage;
• 
↓ Mortality
• Nifedipine, Amlodipine, Nimodipine
•  USE: HTA, Angina, Prinzmetal angina, Raynaud
phenomenon.
• Felodipine, Nicardipine, Clevidipine
•  USE: HTN Emergency
•  SE: Peripheral edema, flushing, dizziness, constipation,
gingival hyperplasia
2
9/11/18
Hydralazine
•  MOA: ↑ cGMP in the smooth muscle causing
relaxation.
•  Arterioles > veins à ↓ Afterload

•  USE: HTN, Heart Failure, Pregnancy

•  SE: Drug induce SLE, Reflex tachycardia, angina, fluid
retention, headache

•  CI: Angina, Coronary artery disease
Drug Induce Lupus

Anti - Histone Ab

HIPPPE
•  Hydralazine
•  INH
•  Procainamide
•  Penicillamine
•  Phenytoin
•  Ethosuximide
HTN Emergency
•  Nitroprusside
•  MOA: ↑ cGMP by ↑ NO
•  SE: Cyanide poison

•  Fenoldopam
•  MOA: Dopamine D1 agonist cause dilation of
coronary, renal, peripheral, splanchnic arteries
•  ↓BP, ↑ diuresis

•  Labetalol, Clevidipine, Nicardipine
3
9/11/18
TIPS!
HTN emergency: !
Clevidipine, fenoldopam, labetalol, nicardipine,
nitroprusside *DOC* !
Vasodilation!
Arteriolar: hydralazine, minoxidil, diazoxide!
Venous: Nitrates!
Both: ALL others!
Nitrates
•  Nitroglycerin, Isosorbide Dinitrate, Isosorbide
Mononitrate

•  MOA: ↑ NO à ↑ cGMP in the smooth muscle vessels
•  Veins > Arteries
•  ↓ Preload

•  USE: Angina, Acute Coronary syndrome, Pulmonary
edema

•  SE: Tachycardia, hypotension, flushing, headache,
Ranolazine
•  MOA: Inhibits the late phase of Na current, reducing
diastolic wall tension and oxygen consumption. Reduce
Ca2+ entry.
•  Not affect HR or contractility

•  USE: Angina refractory

•  SE: Constipation, dizziness, headache, QT prolongation
4
9/11/18
Cardiac glycoside
Digoxin
• MOA: Direct inhibitor of Na/K ATPase, switch the Na/Ca
exchange.
•  ↑ Ca, inotropic positive.
•  ↑ parasympathetic output (CN X), ↓ HR

• USE: HF, Atrial fibrillation

• Antidote: Digibind (digoxin Fab), Mg2+. Normalize K+.
• SULFA DECREASE Digoxin ABSORPTION.
• Drugs increase digoxin levels
–  Aminodarone, Verapamil, Diltiazen, Erythromycin,
Tetracyclins, Quinidine, hypomagnesemia, hypokalemia.
• SE: Nauseas, Vomiting, Diarrhea, Yellow vision, arrhythmias,

AV block, hypo- / hyper-kalemia., Vtach, Vfib.
PDE 3 inhibitors!
Inamrinone, Milrinone!
MOA: inh PDE3, raise levels of cAMP decrease
phase 4 of AP on slow fibers. !
Use: HF!
AE: thrombocytopenia!
TIPS!
Angina: Beta-blockers, CCB !

**Don’t use Beta-blocker for vasospastic angina. !
Diabetes: ACEI, ARBS. Avoid BB!
HF: BB, ACEI, ARBS!
Post MI: BB!
BPH: Alpha blockers!
Dyslipidemia: avoid BB!
5
9/11/18
TIPS !
HF Goals: !
-  Decrease O2 consumption *BB!
-  Decrease preload **Diuretics, venous dilators,
ARB’s/ACEI!
-  Increase contraction: Digoxin and beta agonist!
-  Decrease remodeling **INCREASE SURVIVAL!
-  BB, ACEI, ARB’s, Spironolactone *Vasodilators
in black people.!
Cellular physiology… TO LEARN!
Anti-Arrhythmics
•  Class I: Na+ ch. blocker
•  Class II: Beta blocker
•  Class III: K+ ch. blocker
•  Class IV: Ca2+ ch. Blocker
•  Others:
•  Adenosine
•  Mg2+
•  Ivabradine
6
9/11/18
Class I: Na+ ch. Blocker 1A

•  MOA: Block intermediate Na Channels. OPEN channel.
•  BLOCK K+ Channels
•  USE: Atrial and Ventricular Arrhythmias
AE: thrombocytopenia, LONG QTc and TORSADES
•  Quinidine
•  Block M2 and alpha receptors
–  SE: Cinchonism (HA, ↓ Hearing, Tinnitus),
High anticholinergic. TOXIC with ANTACIDS
•  Procainamide
–  MAO: Block Na Channels, Metabolize to NAPA
–  SE: Neuropathy, Drug induce Lupus
•  Disopyramide *Same effect as quinidine
–  SE: Mild anti-cholinergic, HF
Class I: Na+ ch. Blocker 1B

•  MOA: Block Fast Na Channels. RESTING *Inactive*
•  USE: Ventricular Arrhythmias, digitalis induce
arrhythmias

•  Lidocaine
–  USE: post MI like Ischemic Tissue
–  SE: Neuropathy
•  Tocainide
–  SE: Neuropathy, Pulmonary Fibrosis
•  Mexiletine ONLY ONE ORAL
–  SE: GI upset
Class I: Na+ ch. Blocker 1C

•  MOA: Block 90% of Na Channels (Slow). OPEN +
RESTING
•  USE: SVT, A-fib. Last resort V-tach
•  SE: Proarrhythmic. SUDDEN DEATH
•  CI: Ischemic Heart Disease.
•  Flecainide
•  Propafenone
–  Block β receptor
7
9/11/18
Clase II: Beta blockers

•  A-M: beta 1; except C-L
•  N-Z: Beta 1-2
•  C-L: Alpha + Beta
PROLONG PHASE 4. Decrease mortality, decrease renin release
•  USE: Angina, MI, Hypertension, HF, Glaucoma, SVT, Ventricular rate in
A-fib, A-flutter
•  SE: Impotence, Exacerbation of COPD, Asthma, AV block, bradycardia
•  Propranolol
–  Long ½ life
–  Thyroid storm
–  Migraine prophylaxis
–  Esophageal bleeding
•  Esmolol
–  Short ½ life
–  Anesthesiology to reduce hemodynamic changes induced by
laryngoscopy
Clase II: Beta blockers

•  Pindolol, Acebutolol
•  Partial agonist
•  Metoprolol, Carvedilol
•  DECRASE MORTALITY MI
•  Carvedilol, Labetalol
•  Alpha + Beta antagonist
•  HTN emergency
•  Nadolol
–  Liver failure
–  ↓ esophageal bleeding
•  Timolol, Betaxolol
–  Open angle glaucoma
Class III: K+ ch.

• 
blocker
MOA: Block K channels
•  USE: A-fib, Aflutter, V-tach
•  Napa
•  Metabolite of Procainamide
•  Sotalol
•  MOA: Block Beta receptor,
Block K channels
•  SE: Torsade de pointes
•  Ibutilide, Bretylium,
Dofetilide
8
9/11/18
Class III: K+ ch.

blocker
•  Amiodarone, dromedarone
•  MOA: Block everything (Na+, K+, Ca2+)
•  Large Vd, long T1/2 *80 days*
•  SE: Pulmonary fibrosis, hyper or
hypothyroidism, hepatotoxicity,
photosensitivity, neuropathy, constipation,
bradycardia, heart block, HF, corneal deposits.
Less QT prolongation. Gray discoloration skin.
Pulmonary fibrosis
•  Bleomycin
•  Busulfan
•  Amiodarone
•  Tocainide
•  Methotrexate
•  Nitrofurantoin
Class IV: Ca2+ ch.

blocker
Non-dihydropyridines – HEART
• Verapamil, Diltiazem
• Prolong phase 4 and 0
•  USE: Atrial Arrhythmias (SVT,

A-fib)

•  SE: Constipation, AV block,
Bradycardia, flushing,
Hyperprolactinemia
9
9/11/18
Others
Antiarrhythmics
Adenosine
• MOA: Hyper-polarizing all the cells by ↑ K out of the cell.
(Gi mechanism, decrease cAMP)
• Short ½ life (15 sec)
• USE: SVT (dx and tx) first line.

• SE: Flushing, Hypotension, Chest pain, bronchospasm
• Interact: caffeine and theophylline
Others
Mg2+
Antiarrhythmics
•  MOA: Block all the Channels

•  USE: Torsades de points, Digoxin toxicity, atropine
intox.
Ivabradine!
l  MECHANISM !
-  Selective inhibition of funny sodium channels
(If), prolonging slow depolarization phase
(phase 4). Reduce SA node firing; negative
chronotropic effect without inotropy. Reduces
cardiac O2 requirement. !
l  CLINICAL USE !
-  Chronic stable angina in patients who cannot

take β-blockers. Chronic HF with reduced
ejection fraction. !
l  ADVERSE EFFECTS!
-  Luminous phenomena/visual brightness,

hypertension, bradycardia.!
10
9/11/18
Proarrhythmic !
A antiArrhythmic!
B antiBiotics *macrolides!
C antiCicotic *atypical, typical!
D antiDepressant *TCA!
E antiEmetics *Ondansetron!
Renal Pharmacology
11
9/11/18
Diuretics
•  Acetazolamide
•  Mannitol
•  Loops
•  Furosemide, Bumetanide, Torsemide,
Ethacrynic acid
•  Thiazide
•  Hydrochlorothiazide, Chlorthalidone,
Methyclothiazide, Metolazone
•  Potassium sparing diuretics
•  Spironolactone, Eplerenone
•  Triamterene, Amiloride
Acetazolamide, Dorzolamide
•  MOA: Carbonic anhydrase
inhibitors in the Proximal
convoluted tubule, decrease
bicarbonate

•  USE: Glaucoma, Altitude
sickness, reduce metabolic
alkalosis, decrease CSF
•  SE: Paresthesia,
Hyperchloremic metabolic
acidosis, sulfa allergy. Stones!!
•  MOA: Osmotic diuretic, increase

Mannitol
tubular osmolality and pulls
water, decrease intracranial and
intraocular pressure. ONLY ONE
that excretes more water than
solutes.

•  USE: Drug overdose, elevated
intracranial and intraocular
pressure.

•  SE: Pulmonary edema,
dehydration, hypotension
•  CI: Anuria, Heart
12
9/11/18
Loops Diuretics
•  Furosemide,
Bumetanide,
Torsemide
•  Ethacrynic acid (no
sulfa).

•  MOA: Block Na/K/Cl
symporter in the
ascending limp of the
loop of Henle.
Prevent
concentration of
urine. Release PGE.

Loops Diuretics
•  USE: Heart failure, Cirrhosis, Nephrotic syndromes,
Pulmonary edema, Hypertension, Hypercalcemia
•  SE: Ototoxicity, Hypokalemia, Dehydration, Sulfa allergy,

Nephritis, Gout. Metabolic Alkalosis.
•  Most ototoxic: Ethacrynic Acid.
•  Interaction:
•  Aminoglycosides: early hearing loss.
•  Digoxin: increase toxicity. Loss K+
•  Lithium: increase Li2+ toxicity.
•  Hydrochlorothiazide,
Thiazide
Chlorthalidone,
Methyclothiazide,
Metolazone
•  MOA: Inhibits NCC

reabsorption in early
Distal Convoluted Tubule,
decrease excretion of Ca.

13
9/11/18
Thiazide

•  USE: Hypertension, HF, Hypercalciuria, Nephrogenic
Diabetes insipidus, Osteoporosis.
•  Metolazone: used in refractory to furosemide edematous
states.
•  SE: Hyperglycemia, Hyperlipidemia, Hyperuricemia,

Hypercalcemia, Hyponatremia, Hypokalemic metabolic
alkalosis, Sulfa allergy.
Potassium sparing
Potassium sparing
•  Spirinolactone, Eplerenone
•  MOA: Competitive inhibitor of aldosterone

receptor in the collecting tubule.
•  USE: HF. Hyperaldosteronism. Hypokalemia.
•  SE: Spironolactone cause gynecomastia,

androgenic effect.
•  Interactions:
•  Diabetes: increase glycaemia due to keep open
Katp
•  Digoxin: reduced K+. Toxicity.
14
9/11/18
Potassium sparing
diuretics
•  Triamterene, Amiloride
•  MOA: Block eNaC channels in the collecting tubule.

•  Use: Lithium toxicity
•  SE: All causes Hyperkalemia, arrhythmias.
•  USE: hyperaldosteronism, Conn syndrome, K

depletion, HF.
Renin-Angiotensin-
Aldosterone
Renin-Angiotensin-
•  ACEI:
Aldosterone
•  Captopril,
Enalapril,
Lisinopril,
Ramipril
•  ARBS:
•  Losartan,
Candesartan,
Valsartan
•  Renin Inhibitor:
•  Aliskiren
15
9/11/18
Angiotensin Converting Enzyme

Inhibitor
•  Captopril, Enalapril, Lisinopril, Ramipril
•  MOA: inhibits ACE, decrease Angiotensin II. Decrease

GFR and FF.
•  USE: Hypertension (prevent heart remodeling), HF,

Proteinuria, DM Nephropathy.
•  Decrease mortality in CHF
ACEI
•  SE: Cough (Bradykinin), Angioedema (C1 sterase def),
Teratogen (Renal malformation), Increase Cr (decrease
GFR), Hyperkalemia, Hyponatremia

•  CI: Pregnancy (Cat D), Renal artery stenosis
•  **Can cause 1st DOSE HYPOTENSION when combined

with diuretics.
Angiotensin II receptor
blocker
•  Losartan, Candesartan, Valsartan
•  MOA: Block Angiotensin II receptor, don’t increase
bradykinin

•  USE: Hypertension (prevent heart remodeling), HF,
Proteinuria, DM Nephropathy, all patients with
intolerance to ACE Inhibitors.
•  SE: Hypotension, Teratogen (Renal malformation),

Increase Cr (decrease GFR), Hyperkalemia,
Hyponatremia
16
9/11/18
Aliskiren
•  MOA: Direct renin inhibitor

•  USE: Hypertension
•  SE: Increase Cr (decrease GFR), Hyperkalemia,

Hyponatremia, Hypotension
•  CI: DM taking ACEI
•  Which other can block Renin release?
Pulmonary
Pharmacology
AntiHistaminic
•  MOA: reversible inhibitors histamine 1 receptor

• 1st gen
Dephenhydramine, Dimenhydrinate,
• 
Chlorpheniramine, Meclizine
•  USE: Allergy, motion sickness, sleep aid. Acute
parkinsns symptoms.
•  SE: Sedation, Antimuscarinic, anti α adrenergic
• 2nd gen
•  Loratadine, Fexofenadine, Desloratadine,
Cetirizine
•  USE: Allergy, less sedation. No CNS entry, NO
Muscarinic.
17
9/11/18
Expectoran
•  Guaifenesin
•  MOA: remove excess sputum, not cough suppress.
•  USE: Cold
•  N-acetylcysteine
•  MOA: mucolytics, loosen mucus plug, decrease free
radical
•  USE: Cystic Fibrosis, Acetamenophen overdose
(replenish glutathione), Prevent kidney injury with IV
contract, Hemorrhagic cystitis with Cyclophosphamide
Cough suppressant
•  Dextromethorphan
•  MOA: antagonizes NMDA glutamate receptors,
codeine analog, mild opioid.

•  USE: Cough suppressant
•  SE: abuse potential. Naloxone for overdose.
Pulmonary
Hypertension
•  Bosentan
•  MOA: Endothelin-1 receptor blocker, and decrease
pulmonary vascular resistance
•  SE: Hepatotoxic. NOT GIVE IN PREGNANCY
•  Sildenafil, Vardenafil, Tadalafil
•  MOA: inhibits cGMP phosphodiesterase-5, increase
cGMP, cause smooth muscle relaxation in the corpus
cavernosum, cause erection
•  USE: ED, Pulmonary hypertension
•  SE: Hypotension, Headache, flushing, dyspepsia,
vision impaired, caution with Nitrates.
18
9/11/18
l  Epoprostenol!
l  PGI2 (prostacyclin) with direct vasodilator effects
on pulmonary and systemic arterial vascular
beds. Inhibits platelet aggregation.!
l  Side effects: flushing, jaw pain.!
Asthma drugs
Symptoms - Attacks Treatment
Attacks < 2 / week!
Mild Intermittent Nocturnal awakening < 2 a PNR short acting B2 agonist!
month!
Daily inhale low dose

> 2 / week but not every day!
corticosteroid or !
Mild Persistent Nocturnal awakening > 2 a
Anti-Leukotriene!
month!
PNR short acting B2 agonist!
Daily Attacks but get better Daily inhale high dose

with Tx! corticosteroid!
Moderate Persistent
Nocturnal awakening > 1 a Long acting B2 agonist!
week! PNR short acting B2 agonist!
Daily oral corticosteroid high

Continuous attacks!
inhale dose corticosteroid!
Severe Persistent Nocturnal awakening 4-7
Long acting B2 agonist!
nights per week!
PNR short acting B2 agonist!
Asthma
drugs
19
9/11/18
Cholinomimetic
Agents
•  MOA: Direct agonist of Ach receptors
•  USE:
•  Bethanecol: Post operative ileus, neurogenic ileus,
urinary retention
•  Carbacol: Glaucoma (pupil contriction)
•  Methacholine: Asthma challenge test
•  Pilocapine: Stimulate sweat, tears, saliva, Cystic
fibrosis test, Glaucoma
Antimuscarinic
Atropine
• MOA: Block muscarinic receptor
• USE: Bradicardia, Organophosphate toxicity
• SE: Cycloplegia – worse glaucoma; ↓ sweat - ↑
temperature, dry skin; flushing, constipation,
disorientation
Anti-muscarinic
•  Atropine, Homatropine, Tropicamide: Eyes
•  Benztropine: Parkinson’s disease
•  Glycopyrolate: GI, Respiratory surgeries
•  Hyoscyamine, Dicyclomine: IBS
•  Tiotropium, Ipratropium: COPD, Asthma
•  Oxibutynin, Solifenacin, Tolterodine: Urgency
incontinence
•  Scopolamine: Motion sickness
20
9/11/18
Sympathomimetics
•  MOA: Direct agonist of Alpha, Beta, Dopamine receptors
•  MOA: Alpha 1 > Alpha 2
•  USE: Hypotension, Rinitis
•  MOA: Alpha 1 > Alpha 2 > Beta
•  USE: Hypotension
•  Epinephrine
•  MOA: Beta > Alpha
•  USE: Anaphilaxis shock, asthma, open angle glaucoma
•  MOA: Beta 1 = Beta 2
•  USE: Rarely use
Sympathomimetics
•  Dobutamine:
•  MOA: Beta 1 > Beta 2 > Alpha
•  USE: Heart failure (inotropic >chronotropic), cardiac
stress test
•  Albuterol (short ½ life), Salmeterol:
•  MOA: Beta 2
•  USE: Asthma, COPD
•  Dopamine:
•  MOA: D > Beta > Alpha
•  USE: Bradicardia, HF, Shock.
Sympathomimetics
•  Cocaine
•  MOA: inhibits reuptake
•  SE: Coronary vasospasm, local anesthetic

•  Ephedrine, Pseudoephedrine, Phenylephrine
•  MOA: inhibits reuptake, Alpha agonist
•  USE: Nasal decongestion, Urinary incontinence,
hypotension.
•  SE: Hypertension
•  Pseudoephedrine: anxiety
21
9/11/18
Steroids
•  Inhibit PLP-A
•  Kills T-cells and eosinophilis
•  Inhibits macrophages migration
•  Stabilizes endothelium
•  Stabilizes mast cells
•  Proteolysis
•  Gluconeogenesis
•  USE: Addison’s, Inflammation, Immune suppression,
Asthma, COPD
•  SE: Cushing’s, Osteoporosis, Adrenocortical atrophy, PUD,
Diabetes, Adrenal insufficiency if stop chronic use.
•  Prednisone: Mc oral form

•  Methylprednisalone: Main IV
•  Triamcinalone: Main Inhale, next Budesonide,
Cyclosenide (kids)
•  Beclamethasone, Betamethasone: preterm
fetus for increase surfactant production
•  Dexamethasone: CNS penetration
•  Cypropterone: only that block DHT receptor in
prostate CA
•  Megestrol: strong anabolic effect, in cancer patient
•  Danozol: Endometriosis
Methylxanthines
•  Theophylline
•  MOA: Inhibits phosphodiesterase, increase cAMP,
and cause bronco dilation
•  Adenosine receptor antagonist
•  USE: Asthma
•  SE: narrow therapeutic index, cardiotoxicity,
neurotoxicity.
•  Metabolize by P-450.
•  Toxicity: agitation, tachycardia, arrhythmia,
tremor, seizures. TREAT: Beta-B, Benzo’s Charcoal.
22
9/11/18
P-450 dependent
•  Theophiline
•  Estrogen
•  Digoxin
•  Warfarine
•  Phenitoin
Cromolyn / Nedocromil
•  MOA: Inhibits mast cells release of leukotrienes,
cytokines, histamine

•  USE: Prevent asthma, ocular, nasal, gastrointestinal
allergies. USED IN CHILDREN
•  AE: sore throat
Antileukotrienes
•  Zafirlukast, Montelukast
•  MOA: Block leukotrienes receptor
•  USE: Aspirine induce asthma. Mild-persistent
asthma
•  Zileuton
•  MOA: Lipoxygenase inhibitor, can’t produce
leukotrienes.
•  AE: hepatotoxicity
23
9/11/18
Anti-IgE monoclonal
therapy
•  Omalizumab
•  MOA: binds to unbound serum IgE and block binding
to FceRI

•  USE: Allergic asthma with High IgE, resistant to
steroid
ANTIBIOTICS
24
9/11/18
Penincillins
•  Penicillin G •  Nafcillin
•  Penicillin V •  Dicloxacillin
•  Penicillin Benzathine •  Methicillin
•  Oxacillin •  Ampicillin
•  Amoxicillin
!
Penicillins
•  MOA: !
•  Inhibits the last step of cell wall synthesis!
•  Uses penicillin binding proteins.!
•  Bactericidal!
•  Block transpeptidation!
!
•  USE: !
•  Gram Positive (Strep. Pneumonia, Strep.
Pyogenes, Actinomyces)!
•  Spirochetes.!
Penicillins
•  Side Effects: !
• Hypersensitivity!
•  Hemolytic anemia, interstitial nephritis!
•  Mechanism of Resistance:
•  Produce penicillinase (Beta-lactamase)!
•  Change Penicillin binding protein!
•  Porins Structure inhibits access to
cytoplasmic membrane **PSEUDOMONES!
25
9/11/18
Penicillin types.
•  Penicillin G: IV
•  Penicillin V: Oral
•  Penicillin Benzathine: IM, 14 days ½ life
Penicillinase Resistance
Penicillin
•  Cloxacillin Oxacillin Nafcillin: High Sodium load
•  Dicloxacillin Methicillin. SE: Interstitial nephritis
•  CONDoM
•  USE: !
•  STAPH AUREUS, except MRSA!
•  Gram Positive producing Penicillinase (Beta

lactase)!
Aminopenicillins
•  Ampicillin. SE. Rash
•  Amoxicillin. Oral

•  USE: H. influenza, E. Coli, Listeria, Proteus

Mirabilis, Salmonella, Shigella, Enterococci.!
•  SE: Pseudomembranous colitis!
26
9/11/18
Anti-Pseudomonals
•  USE: Psuedomonas, G neg rods!

!
•  Carbenicillin: High Sodium load
•  Ticarcillin
•  Meziocillin
•  Aclocillin
•  Piperacillin

•  CiTy MAP
Beta Lactamase Inhibitors

•  MOA:
•  Inhibits destruction by Beta lactamase - penicillinase!
•  USE:
•  Add to penicillin!
•  Clavulanic Acid!
•  Sulbactam!
•  Tazobactam!
•  Avibactam!
•  SE:
•  Same
•  Amoxicillin / Clavulanic acid!
•  Ticarcillin / Sulbactam!
•  Piperacillin / Tazobactam!
**Synergy with aminoglycosides: PSEUDOMONES AND
ENTEROCOCCUS
Cephalosporins
•  1st gen! •  3rd gen!
•  Cefazolin! •  Cefotaxime !
•  Ceftriaxone!
•  Cephalexin!
•  Ceftazidime!
•  Cefadroxin!
•  Cefpodoxime!
•  Cefalopin!
•  4th gen!
•  2nd gen! •  Cefepime !
•  Cefaclor! !
•  Cefoxitin! •  5th gen !
•  Cefotetan! •  Ceftaroline !
!
27
9/11/18
Cephalosporins
•  MOA:
•  Inhibits the last step of cell wall synthesis, uses
penicillin binding proteins.!
•  Block transpeptidation!
!
•  SE:
•  Hypersensitivity reactions (10% cross with
penicillin), Rash, Nephritis, Disulfiram like
reactions, Autoimmune Hemolytic Anemia !
Disulfiram Like Reaction

• Chlorpropamide !
• Cephalosporins !
• Antabuse !
• Metronidazole !
• Procarbazinie !
!
Autoimmune Hemolytic Anemia
• PTU!
• Cephalosporins !
• α-methyldopa
• Sulfa drugs !
• Anti-malarials !
• Penicillin !
• Penicillamine !
• Dapsone !
• Aspirin !
• Heparin !
• Quinidine !
• Quinine!
1st. Gen.
Cephalosporin
•  USE: Gram Positive and PEcK!
•  Proteus Mirabilis
•  E. coli
•  Klebsiella Pneumoniae
•  Gram Positive!
•  Cefazolin. Parenteral!
•  Cephalexin!
•  Cefadroxin!
•  Cefalopin. Interstital nephritis!
•  Cephalothin!
•  Cephapitin!
•  Cephradine!
•  Cefadroxil!
28
9/11/18
2nd. Gen. Cephalosporin
USE: G. Pos. and ! •  Cefotetan!

• 
HEN PEcK! –  Anaerobe, Block
H. Influenza
•  Potassium!
Enterobacter Aerogenes
•  •  Cefomandole!
•  Neissera Spp.
•  Proteus Mirabilis
–  Block Potassium!
•  E. coli •  Cefuroxime!
•  Klebsiella Pneumonia •  Cefmetazole!
•  Cefaclor! •  Cefprozil!
•  Cefoxitin!
–  Anaerobe!
•  Loracardef!
•  Cefdinir!
!
3rd. Gen. Cephalosporin

•  USE: Severe Gram Negative infections !
•  Resistance to β-lactams!
•  Cefotaxime (Kids): less hepatic metabolism!
•  Ceftriaxone (Adults)!
–  Cross BBB!
•  Ceftazidime: Pseudomonas!
•  Cefoperazone!
–  Pseudomonas!
•  Ceftizoxime!
•  Cefixime!
•  Cefpodoxime!
•  Ceftibuten!
4th. Gen. Cephalosporin !

!
•  USE: G. Neg. and Pseudomonas!
!
•  Cefepime!
•  Cefozopram!
•  Cefpirome!
!
5th. Gen. Cephalosporin !
!
•  USE: G. Neg. and MRSA. NOT COVER
PSEUDOMONA!
Ceftaroline!
•  Ceftobiprole!
29
9/11/18
-  Hypersensitivity reactions, autoimmune
hemolytic anemia, disulfiram-like reaction,
vitamin K deficiency. Low rate of
crossreactivity even in penicillin-allergic
patients. increase nephrotoxicity of
aminoglycosides. !
l  MECHANISM OF RESISTANCE!
-  Structural change in penicillin-binding proteins

(transpeptidases).!
Vancomycin
•  MOA:
•  Inhibits the cell wall synthesis:

transglycosylation.
•  Inhibits glycosylation reaction by binding
D-Ala-D-Ala terminal of the peptidoglycan
•  Resistance by change of the peptidoglycan

terminal to D-Ala-D-Lac.
Vancomycin
•  USE: G. Pos, Methicillin resistant

Staphylococcus Aureus, Pseudomembranous
colitis (C. difficile-PO)
SE: Flushing (Red Man Syndrome)(largely

preventable by pretreatment with antihistamines
and slow infusion rate), Nephrotoxic, Ototoxic,
Thrombophlebitis.
30
9/11/18
Carbapenems
•  MOA: Inhibits cell wall synthesis, highly resistant to β

lactamase!
•  Cilastatian: Block Renal tubular dihydropeptidases I!
!
•  USE: Gram Pos. cocci, Gram Neg. rods, Anaerobes.
Pseudomones?!
!
•  Imipenem/Cilastatin, Meropenem, Ertapenem, Doripenem!
g!
•  SE: Seizures (CNS Toxicity), GI Distress, Skin rash!
•  Ertapenem not cover P. Aeruginosa!
•  Resistance Carbapenemases induced by plasmids!
•  Metallo -B- Lactamase - NDM-1!
•  Meropenem: less seizures!
Aztreonam
MOA: Binds to PBP3, Preventing Peptidoglycan

Crosslinking, Synergistic with aminoglycosides. No
cross-allergenicity with penicillins.
Use: G neg rods, For penicillin-allergic patients and

those with renal insufficiency who cannot tolerate
aminoglycosides.
ADVERSE EFFECTS: Usually nontoxic; occasional GI

upset.
DNA
•  DNA Topoisomerases
Fluorquinolones!
• 
•  Norfloxacin!
•  Ciprofloxacin!
•  Levofloxacin!
•  Free radicals
–  Metronidazol!
–  Tanidazol!
31
9/11/18
Fluorquinolones
MOA: Inhibit prokaryotic enzymes topoisomerase II (DNA
gyrase) and topoisomerase IV. Bactericidal. !
!
Must not be taken with antacids (decrease efficacy)!
Resistance: Chromosome-encoded mutation in DNA gyrase, plasmid-
mediated resistance, efflux pumps.

•  USE: Gram neg. rods Urinary and GI track. Travelers

diarrhea
•  Norfloxacin: UTI!
•  Ciprofloxacin!
–  Pseudomonas
•  Levofloxacin!
–  Pseudomonas!
•  Ofloxacin!
•  Sparfloxacin!
•  Moxifloxacin!
•  Gatifloxacin!
•  Enoxacin!
•  Nalididicxic Acid. (Quinolone)!
!
Fluorquinolones
ADVERSE EFFECTS!
GI upset, superinfections, skin rashes, headache,
dizziness. Less commonly, can cause leg cramps
and myalgia. !
!
Contraindicated: !
pregnant women !
nursing mothers!
children < 18 years possible damage to cartilage.
Prolong QT interval. !
Tendonitis or tendon rupture in people > 60 years old
and in patients taking prednisone. !
Inhibits cytochrome P-450.!
32
9/11/18
Metronidazol / Tanidazol
MOA: Forms toxic free radical metabolites in the bacterial
cell that damage DNA. Bactericidal, antiprotozoal.

• USE: Anaerobes below the diaphragm
Giardia, Entamoeba, Trichomonas, Gardenerella,
Can be used in place of amoxicillin in H pylori “triple
therapy” in case of penicillin allergy.!

, Methemoglobinemia, Disulfiram like reaction,
• SE:
Hemolytic anemia, metallic taste
Daptomycin!
l  MOA !
-  Lipopeptide that disrupts cell membranes of
gram ⊕ cocci by creating transmembrane
channels. !
l  CLINICAL USE !
-  S aureus skin infections (especially MRSA),

bacteremia, endocarditis, VRE.!
l  ADVERSE EFFECTS:!
-  Myopathy, rhabdomyolysis.!
-  Not used for pneumonia (is inactivated by
surfactant).!
!
Disulfiram Like Reaction

•  Chlorpropamide !
•  Cephalosporin!
•  Antabuse !
•  Metronidazole !
•  Procarbazine !
!
Dysgeusia **altered taste
•  Metronidazole!
•  Clarithromycin !
•  Zinc def. !
•  Li !
33
9/11/18
Protein Synthesis
Inhibitors at 30s
•  Aminoglycosides!
•  Gentamicin!
•  Tobramacin!
•  Amikacin!
•  Streptomycin!
•  Neomycin!
•  Tetracyclines!
•  Tetracycloine!
•  Doxicycline!
•  Demecocycline!
•  Tigacycline!
•  Minocycline!
Aminoglycosides
•  MOA:
•  Bacteriocidal
•  Inhibits protein
synthesis at 30s!
•  Inhibits formation of
Initiation complex,
prevent translocation
and miss read of
mRNA.!
•  Require O2 for uptake;
therefore ineffective
against anaerobes!

Aminoglycosides
•  USE: !
•  Gram neg. rod
•  Synergistic to β lactams. Streptomycin DOC
bubonic plague. !
•  SE:
•  Nephrotoxic
•  Ototoxic!
•  Teratogenic!
•  Neuromuscular blockade!
!
•  Amikacin: Hepatic excreted!
•  Streptomycin: TB, Tularemia!
•  Neomycin: bowel surgery. Cause contact
dermatitis!
34
9/11/18
MECHANISM OF RESISTANCE!
l  Bacterial transferase enzymes inactivate the drug

by acetylation, phosphorylation, or adenylation.!
•  MOA: !
Tetracyclines
-  Bacteriostatic; bind to 30S and
prevent attachment of aminoacyl-
tRNA; limited CNS penetration.
-  Doxycycline is fecally eliminated and
can be used in patients with renal
failure.
-  Do not take tetracyclines with milk
(Ca2+), antacids (Ca2+ or Mg2+), or
iron-containing preparations because
divalent cations inhibit drugs’
absorption in the gut
!
!
-  GI distress, discoloration of teeth and inhibition
of bone growth in children, photosensitivity.
Contraindicated in pregnancy. !
l  MECHANISM OF RESISTANCE !
-  decrease uptake or increase efflux out of

bacterial cells by plasmid-encoded transport
pumps.!
!
35
9/11/18
Tetracyclines
•  Tetracycline
•  Doxycycline: Hepatic excreted
•  Demeclocycline: Block ADH. Use SIADH
•  Tigecycline: MRSA
•  Minocycline: Use in acne
Tetracyclines
•  USE:
Borrelia burgdorferi, M pneumoniae. Drugs’ ability to
accumulate intracellularly makes them very effective
against Rickettsia and Chlamydia.
Glycylcyclines (Tigecycline)!
l  MOA: !
-  Tetracycline derivative. Binds to 30S, inhibiting
protein synthesis. Generally bacteriostatic !
l  USE:!
Broad-spectrum anaerobic, gram ⊝, and gram

- 
⊕ coverage. Multidrug-resistant (MRSA, VRE)
organisms or infections requiring deep tissue
penetration.!
-  GI symptoms: nausea, vomiting!
36
9/11/18
Protein Synthesis
Inhibitors at 50s
•  Cloramphenicol

•  Macrolides
•  Eritromycin
•  Claritromycin!
•  Daptomycin!
•  Azitromycin!
•  Lincomycin
–  Clindamycin!
!
•  Linezolid
Chloramphenicol
•  MOA:
•  Blocks peptide bond
formation at 50s!
•  Block
peptidyltransferase!
•  Block complex IV of the
ETC.!
!
Resistance : Plasmid-
encoded acetyltransferase
inactivates the drug.!
Chloramphenicol
•  USE:
-  Meningitis (Haemophilus influenzae, Neisseria
meningitidis, Streptococcus pneumoniae) and
Rocky Mountain spotted fever (Rickettsia
rickettsii). !
-  Limited
use owing to toxicities but often still used
in developing countries because of low cost. !
!
!
37
9/11/18
-  Anemia (dose dependent), aplastic anemia
(dose independent),!
-  gray baby syndrome (in premature infants
because they lack liver UDP-
glucuronyltransferase).!
Clindamycin
•  MOA:
•  Blocks peptide bond formation at 50s!
•  Translocation!
•  Bacteriostatic!
!
•  USE:
•  Anaerobes above the diaphragm!
•  Gram Pos., Neg.!
!
•  SE: !
•  Pseudomembranous colitis, fever, diarrhea. !
!
•  Resistance:
•  Methylation of 23S rRNA, Ribosomal structural alteration,
inactivating enzyme, poor permeability in G neg!
Macrolides
MOA: Inhibit protein synthesis by
blocking translocation ; bind to the
23S rRNA of the 50S ribosomal
subunit. Bacteriostatic.!
!
•  USE: Gram Pos., Neg., Atypical
(1st line)!
!
•  MOR: Methylation of 23s rRNA
binging site, inactivating enzyme,
drug efflux pump!
38
9/11/18
-  MACRO: Gastrointestinal Motility issues,
Arrhythmia caused by prolonged QT interval,
acute Cholestatic hepatitis, Rash, eOsinophilia. !
-  Increases serum concentration of theophylline,
oral anticoagulants.!
-  Clarithromycin and erythromycin inhibit
cytochrome P-450.!
Macrolides
•  Erythromycin: Gastroparesis
•  Clarithromycin: Dysgeusia
•  Azithromycin: Longest ½ life

•  1 dose: Chlamydia!
•  3 doses: Lung Dz!
•  5 doses: all else!
Oxazolidinones Linezolid.
MOA: Inhibit protein synthesis by
binding to 50S subunit and preventing
formation of the initiation complex !
!
•  USE: Vancomycin
resistance bugs!
!
SE: Bone marrow
suppression (especially
thrombocytopenia), peripheral
neuropathy, serotonin
syndrome.!
!
•  Resistance: Point mutation
in 23s rRNA, Efflux pumps!
39
9/11/18
Polymyxins!
Colistin, polymyxin B!
MOA: cation binds to phospholipids on Gram –
bacteria.. Cell death.!
Use: salvage therapy for MDR. !
Superficial skin infection in triple abx ointment. !
AE: nephrotoxic!!! Neurotoxic, resp. failure. !
DNA Synthesis inhibitor

•  Sulfonamides!
•  Sulfamethoxazole (SMX)
•  Sulfisoxazole
•  Sulfadiazine
•  Sulfazalazine
•  Trimethoprim (TMP)
Sulfonamides
•  Sulfamethoxazole (SMX)!
•  Sulfisoxazole, Sulfadiazine!
•  Sulfazalazine: 1st line IBD
!
MOA: Inhibit dihydropteroate synthase, thus
inhibiting folate synthesis. Bacteriostatic!
(bactericidal when combined with trimethoprim). !
!
•  Resistance: altered enzyme, Decrease uptake,
Increase PABA synthesis!
40
9/11/18
Sulfonamides
•  USE: Gram Pos, Neg, Nocadria, Chlamidia,
Simple UTI!
!
SE: Hypersensitivity reactions, hemolysis if G6PD
deficient, nephrotoxicity (tubulointerstitial nephritis),
photosensitivity, Stevens-Johnson syndrome,
kernicterus in infants, displace other drugs from
albumin (eg, warfarin). !
!
•  CI: Sulfa allergies!
Dapsone!
l  MOA: !
-  Similar to sulfonamides, but structurally distinct
agent. !
l  USE :!
-  Leprosy (lepromatous and tuberculoid),

Pneumocystis jirovecii prophylaxis. !
-  Hemolysis if G6PD deficient.!

!
Trimethoprim (TMP)
•  MOA: Inhibits Dihydrofolate reductase,
bacteriostatic !
!
USE: Used in combination with sulfonamides
(trimethoprim-sulfamethoxazole [TMPSMX]),
causing sequential block of folate synthesis.
Combination used for UTIs, Shigella, Salmonella,
Pneumocystis jirovecii pneumonia treatment and
prophylaxis, toxoplasmosis prophylaxis.!
!
•  SE: Megaloblastic anemia, Leukopenia,
Granulocytopenia, Allergies!
41
9/11/18
Sulfa drugs
•  Sulfonamides !
•  Sulfonilureas !
•  Sulfasalazine!
•  Probenecid!
•  Celecoxib !
•  Furosemide!
•  Tiazides!
TB drugs - RESPI
42
9/11/18
Isoniazid
•  MOA: !
-  decrease synthesis of mycolic acids. Bacterial
catalase-peroxidase (encoded by KatG) needed
to convert INH to active metabolite. !
•  USE
•  Mycobacterium tuberculosis. !
•  The only agent used as solo prophylaxis against
TB. !
•  Also used as monotherapy for latent TB!
!
-  Hepatotoxicity, P-450 inhibition, drug-induced
SLE, anion gap metabolic acidosis, vitamin B6
deficiency (peripheral neuropathy,
sideroblastic anemia). Administer with
pyridoxine (B6)!
l  MOR:!
-  Mutations leading to underexpression of KatG!
Rifampin / Rifabutin
•  MOA
•  Inhibits DNA dependent RNA polymerase!
•  Metabolize by P450!
!
• USE
Mycobacterium tuberculosis; delay resistance to dapsone
when used for leprosy. Used for meningococcal
prophylaxis and chemoprophylaxis in contacts of children
with Haemophilus influenzae type B.!
!
43
9/11/18
l ADVERSE EFFECTS !
-  Minor hepatotoxicity and drug interactions
(increase cytochrome P-450); orange body
fluids (nonhazardous side effect). Rifabutin
favored over rifampin in patients with HIV
infection due to less cytochrome P-450
stimulation.!
l  MECHANISM OF RESISTANCE!
-  Mutations reduce drug binding to RNA

polymerase. Monotherapy rapidly leads to
resistance.!
Ethambutol
•  MOA
-  Decrease carbohydrate polymerization of
mycobacterium cell wall by blocking
arabinosyltransferase. !
•  USE
•  TB!
•  Atypical mycobacteria Avium!
•  SE
•  Optic neuropathy, red/ green color blindness,
central scotoma!
•  MOR
•  Arabinosyl transferase over-expression!
Pyrazinamide
MOA!
• 
-  Mechanism uncertain. !
-  Pyrazinamide is a prodrug that is converted to
the active compound pyrazinoic acid. Works
best at acidic pH (eg, in host phagolysosomes). !
USE!
•  TB!
SE!
•  Hepatitis, Hiperuricemia!
•  MOR!
•  Mutation of pyrazinamidase!
•  CI!
•  Pregnancy!
44
9/11/18
Streptomycin!
l  MOA!
-  Interferes with 30S component of ribosome. !
l  CLINICAL USE!
-  Mycobacterium tuberculosis (2nd line).!

-  Tinnitus, vertigo, ataxia, nephrotoxicity!
Prophylaxis in HIV patients!

!
l  CD4 < 200 cells/mm3 -->TMP-SMX

Pneumocystis pneumonia !
!
l  CD4 < 100 cells/mm3 -->TMP-SMX
Pneumocystis pneumonia and toxoplasmosis!
!
l  CD4 < 50 cells/mm3 --> Azithromycin or
clarithromycin Mycobacterium avium complex!
!
Clinical escenario!
l  High risk for endocarditis and undergoing

surgical or dental procedures !
-  Amoxicillin!
l  Exposure to gonorrhea!
-  Ceftriaxone + azithromycin!
l  Exposure to meningococcal infection!
-  Ceftriaxone, ciprofloxacin, or rifampin !
l  Pregnant woman carrying group B strep!
-  Intrapartum penicillin G or ampicillin !

!
45
9/11/18
l  Prevention of gonococcal conjunctivitis in newborn!

-  Erythromycin ointment on eyes!
l  Prevention of postsurgical infection due to S aureus!
-  Cefazolin!
l  Prophylaxis of strep pharyngitis in child with prior
rheumatic fever!
-  Benzathine penicillin G or oral penicillin V!
l  Exposure to syphilis !
-  Benzathine penicillin G!
!
46
9/11/18
Gastrointestinal!
Endocrinology!
Reproductive!
Neurology!
Antifungal!
Antiparasites!
Gastrointestinal
Pharmacology
Acid suppression therapy
1
9/11/18
H2 blockers
•  Cimetidine, Ranitidine, Famotidine, Nizatidine
MOA: Reversible block of histamine H2-receptors ->
decrease H+ secretion by parietal cells.
•  USE: PUD, Gastritis, GERD
•  SE: !
–  Cimetidine
•  Cross BBB!
•  Inhibits P-450!
•  antiandrogen effects (prolactin release,
gynecomastia, impotence, decrease libido in
males)!
–  Cimetidine and Ranitidine
•  Decrease renal creatinine excretion!
P-450 Inhibitors
•  INH!
•  Dapsone!
•  Sulfa drugs!
•  Macrolides!
•  Amiodarone!
•  Ketoconazole!
•  Quinolones!
•  Grape fruit!
•  Ritonavir!
•  Cimetidine!
Proton Pump Inhibitors

•  Omeprazole, Lansoprazole, Esomeprazole,
Pantoprazole, Dexlansoprazole
•  MOA: Irreversibly inhibit H+/K+ ATPase in

stomach parietal cells

•  USE: PUD, Gastritis, GERD, Zollinger-Ellison S.,
combine with ATB for H. Pylori. Stress ulcer
prophylaxis
•  SE: increase risk of C difficile infection,

pneumonia. decrease serum Mg2+ with long-term
use
2
9/11/18
Bismuth, Sucralfate
•  MOA: Bind to ulcer base, providing physical
protection and allowing HCO3– secretion to
reestablish pH gradient in the mucous layer. Require
acidic environment; usually not given with PPIs/H2
blockers
•  USE: PUD, Traveler’s diarrhea (bismuth)
•  SE: Constipation
Misoprostol
•  MOA: PGE-1 analog
•  Stimulates mucus production!
•  Decrease acid production!
•  USE: Prevention of NSAID-induced peptic ulcers
(NSAIDs block PGE1 production). Also used off-
label for induction of labor (ripens cervix).
•  SE: Diarrhea
•  CI: Pregnancy or may become pregnant
Antacids
•  MOA: Can affect absorption, bioavailability, or urinary
excretion of other drugs by altering gastric and urinary
pH or by delaying gastric emptying. All can cause
hypokalemia.
•  USE: Gastritis
•  Aluminum OH
-  SE: Constipation and hypophosphatemia; proximal
muscle weakness, osteodystrophy, seizures!
•  Magnesium OH
-  SE: Diarrhea, hyporreflexia, hypotension, cardiac arrest!
•  Calcium carbonate
-  SE: Hypercalcemia (milk-alkali syndrome), rebound acid
increase.!
!
3
9/11/18
Octreotide
•  MOA: Long-acting somatostatin analog; inhibits
secretion of various splanchnic vasodilatory
hormones.
•  USE: Slow down the progression of Acromegaly,

carcinoid, gastrinoma, glucagoma, VIPoma, Acute
varices Bleeding
•  SE: Nausea, cramps, steatorrhea. increase risk of

cholelithiasis due to CCK inhibition.
Laxatives
Indicated for constipation or patients on opiates requiring
a bowel regimen
•  Bulk-forming laxatives:
-  Psyllium,methylcellulose
•  MECHANISM: !
-  Soluble fibers; draw water into gut lumen, forming
a viscous liquid that promotes peristalsis. !
•  ADVERSE EFFECTS:!
-  Bloating !
Osmotic laxatives!
l  Magnesium hydroxide, magnesium citrate,

polyethylene glycol, lactulose !
l  MOA:!
-  Provide osmotic load to draw water into GI
lumen.!
-  Lactulose also treats hepatic encephalopathy
because gut flora degrade it into metabolites
(lactic acid, acetic acid) that promote nitrogen
excretion as NH4+!
l  ADVERSE EFFECTS: !
l  Diarrhea, dehydration; may be abused by

bulimics !
4
9/11/18
Stimulants (Senna)!
l MOA: !
-  Enteric nerve stimulation increase colonic
contraction!
-  Diarrhea, melanosis coli !

l  Emollients Docusate !
l  MOA!
-  Osmotic draw into lumen -> increase water
absorption by stool !
-  Diarrhea!
!
!
Sulfasalazine
•  MOA: A combination of sulfapyridine (antibacterial)
and 5-aminosalicylic acid (anti-inflammatory).
Activated by colonic bacteria
•  USE: Inflammatory bowl disease (IBD), Crohn
•  SE: Malaise, Nausea, Sulfonamide poisoning,

Reversible oligospermia
5
9/11/18
Antiemetics
Ondasentron
•  MOA: 5-HT3 antagonist; decrease vagal stimulation.

Powerful central-acting antiemetic.
•  USE: Control vomiting postoperatively and in

patients undergoing cancer chemotherapy.
•  SE: Headache, constipation, QT interval

prolongation, serotonin syndrome.
Aprepitant !
l  MOA: !
-  Substance P antagonist. Blocks NK1 receptors
in brain. !
l  USE:!
-  Antiemetic for chemotherapy-induced nausea

and vomiting.!
Metoclopramide/Prochlorperazine!
l  MOA:!
-  D2 receptor antagonist. increase resting tone, contractility, LES tone,
motility, promotes gastric emptying. Does not influence colon
transport time. !
l  USE:!
-  Diabetic and postsurgery gastroparesis, antiemetic, persistent
GERD. !
-  increase parkinsonian effects, tardive dyskinesia. Restlessness,
drowsiness, fatigue, depression, diarrhea. Drug interaction with
digoxin and diabetic agents. !
l  Contraindicated in patients with small bowel obstruction or Parkinson
disease (due to D2-receptor blockade).!
!
6
9/11/18
Antiemetics
!
•  Prochlorperazine
!
•  MOA: D2 receptor antagonist

•  USE: Antiemetic

•  SE: Parkinson like effects, Depression

•  CI: Parkinson’s and GI obstruction
Orlistat
MOA: Inhibits gastric and pancreatic lipase →
decrease breakdown and absorption of dietary fats.
• USE: Weight loss
• SE: Steatorrhea, Fat soluble vitamin deficiency
Ursodiol
•  Ursodeoxycholic acid
•  MOA: nontoxic bile acid, increase bile secretion,

decrease cholesterol secretion and reabsortion
•  USE: PBC, PSC, Gallstone prevention or dissolution
7
9/11/18
Loperamide!
l  MOA: !
-  Agonist at μ-opioid receptors; slows gut
motility. Poor CNS penetration (low addictive
potential). !
l  USE Diarrhea. !
l  ADVERSE EFFECTS: Constipation, nausea.!
Lipid lowering drugs

•  STAINS!
•  Lovastatin!
•  Pravastatin!
•  Simvastatin!
•  Atorvastatin!
•  Rosuvastatin!
•  Niacin!
!
•  Ezetimidea!
!
•  Cholestyramine, Colestipol, Colesevelam!
•  Fibrates!
–  Gemfibrozil!
–  Clofibrate!
–  Bezafibrate!
–  Fenofibrate!
8
9/11/18

STATINS (HMG-CoA reductase inhibitors)!
• Lovastatin
• Pravastatin
• Simvastatin
• Atorvastatin
• Rosuvastatin
!
• MOA: Inhibits conversion of HMGCoA to mevalonate, a
cholesterol precursor; decrease mortality in CAD patient
!
• USE: very decrease LDL, and slight Triglycerides,
Increase HDL
SE: Hepatotoxicity, Rhabdomyolysis, myopathy (esp.
when used with fibrates or niacin)
Myositis
•  Rifampin !
•  INH !
•  Prednisone !
•  Statins !
•  Fibrates!

•  Niacin
l  MOA: Inhibits lipolysis (hormone sensitive lipase) in
adipose tissue; reduces hepatic VLDL synthesis
•  USE: medium Decrease LDL and slight
Triglycerides, Increase by 45% HDL

l  SE: Red, flushed face, which is r by NSAIDs or long-
term use Hyperglycemia Hyperuricemia.

9
9/11/18

•  Cholestyramine, Colestipol, Colesevelam
•  MOA: inhibits intestinal reabsorption of bile salts,

liver need to make more bile salts
•  USE: Decrease LDL, slightly Increase HDL and
Triglycerides
•  SE: GI upset, decrease absorption of other drugs
and fat-soluble vitamins

•  Ezetimide
•  MOA: Block reabsorption of cholesterol in the

intestinal brush border.
•  USE: medium decrease LDL and slight decrease

triglycerides
•  SE: Rare increase LFTs, diarrhea

•  Fibrates
•  Gemfibrozil, Clofibrate, Bezafibrate,
Fenofibrate
•  MOA: Upregulate LPL --> increase TG clearance Activates

PPAR-α to induce HDL synthesis
•  USE: very decrease triglycerides
•  SE: Rhabdomyolysis ( in combination with statins),

diarrhea. cholesterol gallstones
10
9/11/18
PCSK9 inhibitors (Alirocumab, evolocumab)!

!
l  MOA: Inactivation of LDL-receptor degradation,

increasing amount of LDL removed from
bloodstream!
!
l  USE: Very decrease LDL , slight decrease
Triglyceride!
!
l  SE: myalgia, delrium, dementia, other
neurocognitive effects !
Endocrine
Pharmacology
l  Diabetes mellitus management!
strategies:
l  Type 1 DM—dietary modifications, insulin replacement
l  Type 2 DM—dietary modifications and exercise for weight loss; oral
agents, non-insulin injectables, insulin replacement

l  Gestational DM (GDM)—dietary modifications, exercise, insulin
replacement if lifestyle modification fails
11
9/11/18
Insulin Preparation
•  MOA: Binds insulin receptor (tyrosine kinase
activity).
-  Liver: increase glucose stored as glycogen.
-  Muscle: increase glycogen, protein synthesis;
increase K+ uptake.
-  Fat: increase TG storage.

•  USE: DM type 1, 2, Gestational diabetes
•  SE: Hypoglycemia, lipodystrophy, rare
hypersensitivity reactions

l  Rapid acting
Peak in ½ hour!
USE: postprandial glucose control!
Lispro, Aspart, Glulisine
• Short acting
Use: Type 1 DM, type 2 DM, GDM, DKA (IV), hyperkalemia (+ glucose),
stress hyperglycemia.!
Regular
!
12
9/11/18
Intermediate acting
l 
Peak in 4-12 hrs, last 18-24!

Use: Type 1 DM, type 2 DM, GDM.!
NPH
Long acting
l 
Last >24 hrs!

USE: Type 1 DM, type 2 DM, GDM (basal glucose control).!
Glargine, Detemir
•  Somoji effect
•  Actually caused by Hypoglycemia that
occurred in the early morning (2-3 am) leading
to reactive Hyperglycemia in the late morning
(6-7 am)!
•  Tx: decrease evening NPH insulin!
!
•  Dawn effect
•  Increase in blood sugar each morning caused
by the normal increase in epinephrine,
glucagon and cortisol that occurs each
morning!
•  Tx: increase morning regular insulin!
Oral Hypoglycemics
•  Biguanides- Metformin
l  MOA: Inhibit hepatic gluconeogenesis and the action
of glucagon. decrease gluconeogenesis,
increase glycolysis, increase peripheral glucose
uptake (increase insulin sensitivity).!
l  USE: Oral. First-line therapy in type 2 DM, causes
modest weight loss. !
-  Can be used in patients without islet function!
•  SE: GI upset, Lactic acidosis, B12 deficiency.

Weight loss!
•  CI: Renal Failure!
13
9/11/18
Oral Hypoglycemics
•  Sulfonylurea
l  MOA: Close K+ channel in β cell membrane -> cell depolarizes -
> insulin release via increase Ca2+ influx.!
l  USE: Stimulate release of endogenous insulin in type 2 DM.
Require some islet function, so useless in type 1 DM.!
l  SE: Risk of hypoglycemia increase in renal failure, weight gain. !
-  First generation: disulfiram-like effects. !
-  Second generation: hypoglycemia.!
•  1st generation:!
•  Chlorpropamide, Tolbutamide
•  2nd generation:!
•  Glimepiride, Glipizide *decrease dose in hepatic imp.,
Glyburide** decrease dose renal imp.
Oral Hypoglycemics
•  Meglitinides derivatives, Nateglinide,
Repaglinide
l  MOA: Stimulate postprandial insulin release by
binding to K+ channels on β cell membranes (site
differs from sulfonylureas).
l  USE: used in monotherapy in type 2 DM or
combined with metformin
•  SE: Hypoglycemia (increase risk with renal failure),
weight gain.

Oral Hypoglycemics
•  Thiazolidinediones
l  MOA: increase insulin sensitivity in peripheral
tissue. Binds to PPAR-γ nuclear transcription
regulator.!
l  USE: Used as monotherapy in type 2 DM or
combined with above agents. Safe to use in
renal impairment!
•  SE: Hypoglycemia, weight gain,
hepatotoxicity, Heart failure, increase risk of
fracture.!
•  Pioglitazone, Rosiglitazone
14
9/11/18
Oral Hypoglycemics
•  Glucagon Like Peptide (GLP-1) analogs
•  MOA: increase insulin release, decrease
glucagon and delay gastric emptying,
increase satiety !
•  USE: DM 2!
•  SE: Nauseas, vomiting, pancreatitis. Modest
weight loss, no hypoglycemia. !
•  Exenatide, Liraglutide (sc inject)
Oral Hypoglycemics
•  DPP-4 inhibitors
l  MOA: Inhibit DPP-4 enzyme that deactivates
GLP-1, thereby increase glucose-dependent
insulin release, decrease glucagon release,
decrease gastric emptying, increase satiety!
• USE: DM 2!
l  SE: anaphylaxis, nauseas, mild urinary or
respiratory infection!
•  Sitagliptin, Vidagliptin, Saxagliptin,

Linagliptin, Alogliptin
Oral Hypoglycemics
•  Amylinomimetics
•  Pramlintide
•  MOA: decrease gastric emptying/saciety and
glucagon. AMP kinase!
•  USE: DM 1, 2, postprandial hyperglycemia
(decrease by ½ the insulin with meal!
•  SE: nauseas, diarrhea, hypoglycemia!
15
9/11/18
Oral Hypoglycemics
•  SGLT-2 Inhibitors
Selective sodium-glucose transporter-2
• 
•  Canagliflozin
•  MOA: Block reabsorption of glucose in PCT!
•  USE: DM 2!
l  SE: Glucosuria, UTIs, vaginal yeast infections,
hyperkalemia, dehydration (orthostatic

hypotension), weight loss.!
!
Oral Hypoglycemics
•  α- glucosidase inhibitors
•  Acarbose, Miglitol
MOA: Inhibits α- glucosidase at the brush border

of the intestine, Delayed carbohydrate
hydrolysis and glucose absorption -> decrease
postprandial hyperglycemia!
•  USE: DM 2!
•  SE: Osmotic Diarrhea!
Hypothalamic / Pituitary
drugs
•  ADH antagonist
•  Conivaptan, Tolvaptan
•  MOA: Block ADH at the V2 receptor!
•  USE: SIADH!
•  SE: Diabetes Insipidus nephrogenic!
•  Demiclocycline
•  MOA: ADH antagonist (member of tetracycline family).
•  USE SIADH.
•  ADVERSE EFFECTS: Nephrogenic DI, photosensitivity,
abnormalities of bone and teeth.
•  Desmopressin, Vasopressin, DDAVP
• MOA: ADH agonist!
l  USE: Diabetes Insipidus central, von Willebrand disease, sleep
enuresis. !
16
9/11/18
drugs
•  Oxytocin
MOA: Stimulates contraction of the smooth
• 
muscle of the uterus and ducts of breast

•  USE: Stimulates labor, Uterine contraction,
Dysfunctional uterine bleeding, milk let-down
drugs
•  Growth hormone: Somatotropin
•  MOA: Stimulate linear growth, muscle growth,
increase glucose.!
•  USE: GH def., Turner’s syndrome!
!
!
•  Somatostatin / Octreotide
•  MOA: Inhibits GH release.!
•  USE: Slow down the progression of Acromegaly,
carcinoid syndrome, gastrinoma, glucagoma,
esophageal varices!
•  SE: Nauseas, cramps, steatorrhea!
drugs
•  Thyroid Stimulating Hormone
•  USE: diagnosis of thyroid disorder!
!
•  Thyroid hormone
•  Levothyroxine (T4)
•  Triiodothyronine (T3)
!
•  MOA: agonist of the thyroid hormone receptor!
•  USE: hypothyroidism, mixedema. !
•  SE: weight lost, tachycardia, tremors, arrhythmias!
17
9/11/18
Thioamides
•  MOA: Block thyroid peroxidase, inhibiting the oxidation of
iodide and the organification and coupling of iodine ->
inhibition of thyroid hormone synthesis.
  Propylthiouracil also blocks 5ʹ-deiodinase -
> decrease peripheral conversion of T4 to T3.
•  USE: Hyperthyroidism. PTU blocks Peripheral conversion. PTU
used in first trimester of pregnancy (due to methimazole
teratogenicity); methimazole used in second and third
trimesters of pregnancy (due to risk of PTU-induced
hepatotoxicity).
•  SE: Skin rash, agranulocytosis (rare), aplastic anemia,
hepatotoxicity. Methimazole is a possible teratogen (can cause
aplasia cutis).
Iodine
•  I131: radioactive iodine
•  MOA: uptake by the gland and the radiation destroy
most of the gland!
•  USE: thyrotoxicosis!
•  SE: Hypothyroidism!
!
•  Iodine salt:
•  MOA: inhibits the uptake of iodine by the gland and
inhibits the release of the hormone!
•  USE: Radiation poison!
18
9/11/18
•  Agranulocytosis
•  Carbamazepine !
•  Clozapine!
•  Ticlopidine !
•  PTU !
•  Methimazole!
!
!
!
!
!
!
!
•  Hemolytic Anemia
•  PTU!
•  Penicillin !
•  Dapsone !
•  Aspirin ! drugs
•  Heparin !
•  Adrenocortropic hormone
•  Quinidine !
•  MOA:
•  stimulate fasciculate layer of the
Quinine!
adrenal gland and increase cortisol release!
•  USE: Allergies, inflammatory conditions,
Diagnosis of adrenal disorder !
Fludrocortisone !
l  MOA: Synthetic analog of aldosterone with little

glucocorticoid effects. !
l  USE: Mineralocorticoid replacement in 1° adrenal
insufficiency. !
l  ADVERSE EFFECTS: Similar to glucocorticoids;
also edema, exacerbation of heart failure,

hyperpigmentation.!
!
19
9/11/18
Cinacalcet
•  MOA: Sensitizes Ca2+-sensing receptor (CaSR) in
parathyroid gland to circulating Ca2+, decrease PTH.
•  USE: Hyperparathyroidism
•  SE: Hypocalcemia
Reproductive
Pharmacology
20
9/11/18
HORMONES
•  FSH, LH, hCG
•  MOA: natural peptides
•  USE: infertility
Leuprolide
•  MOA: GnRH analog with agonist properties when
used in pulsatile fashion; antagonist properties
when used in continuous fashion (downregulates
GnRH receptor in pituitary -> Decrease FSH/LH).
USE: Pulsatil for infertility

•  Continuous for prostate cancer (Add
Flutamide), Uterine fibroids, Precocious
puberty, Endometriosis!
•  SE: Antiandrogen, nauseas, vomiting
Testosterone /
Methyltestosterone
•  MOA: Agonist at androgenic receptor
•  USE: Hypogonadism, promotes development of

sexual characters, stimulates anabolism
•  SE: Masculinization in female, gonadal atrophy,

premature closer of growth plate, Increase LDL,
Decrease HDL, hypercoagulable state.
21
9/11/18
Antiandrogenic
•  Finasteride
l  MOA: 5α-reductase inhibitor(decrease conversion of testosterone
to DHT).
•  USE: BPH, Male pattern baldness
!
•  Flutamide
–  MOA: Non competitive inhibitor of androgens at the
testosterone receptor
–  USE: Prostate carcinoma
–  SE: Gynecomastia, amenorrhea.
!
Antiandrogenic
l  Ketoconazole: Inhibits steroid synthesis (inhibits 17,20
desmolase/17α-hydroxylase). !
!
l  Spironolactone: Inhibits steroid binding ( 17,20
desmolase/17αhydroxylase.!
!
l  Used in PCOS to reduce androgenic symptoms. Both
can cause gynecomastia and amenorrhea!
22
9/11/18
Estrogens
•  Ethinyl estradiol, DES (diethylstilbestrol),
Mestranol
•  MOA: Bind estrogen receptor

•  USE: Hypogonadism, ovarion failure, menstrual
adnormalities, Hormone replacement therapy, androgenic
dependent prostate cancer

•  SE: Endometrial cancer, bleeding in postmenopausal
woman, hypercoagulable state
•  DES: Clear cell carcinoma in baby of women that used it.

•  CI: estrogen receptor breast cancer, DVT.
Selective Estrogen
Receptor Mod.
•  Clomiphene
•  MOA: Partial agonist at the hypothalamus, increase in LH, FSH
•  USE: Infertility, PCOS
•  SE: hot flashes, ovarian enlargement, multiple pregnancy,
visual disturbances
•  Tamoxifen
l  MOA: Antagonist at breast; agonist at bone, uterus
•  USE: estrogen receptor breast cancer
•  SE: Endometrial cancer
•  Raloxifen
l  MOA: Antagonist at breast, uterus; agonist at bone
•  USE: osteoporosis
l  SE: increase risk of thromboembolic
Hormone Replacement
therapy
•  USE: Used for relief or prevention of menopausal
symptoms (eg, hot flashes, vaginal atrophy),
osteoporosis (increaseestrogen, decrease osteoclast
activity).
•  SE: endometrial cancer, increase CV risk!
23
9/11/18
Anastrozole,
Exemestane, Letrozole
MOA: Aromatase inhibitors, Inhibit peripheral
conversion of androgens to estrogen
•  USE: post menopausal woman with breast cancer
Progestins
•  MOA: Binds progesterone receptor, reduce growth,
increase vascularization of endometrium
•  USE: Contraception (forms include pill, intrauterine

device, implant, depot injection), endometrial
cancer, abnormal uterine bleeding.
-  Progestin challenge: presence of withdrawal
bleeding excludes anatomic defects (eg, Asherman
syndrome) and chronic anovulation without
estrogen.
Mifepristone/Ulipristal
•  MOA: competitive inhibitor of progestins.
•  USE: termination of pregnancy, emergency

contraception pill
•  SE: heavy bleeding, GI effects, abdominal pain
24
9/11/18
Oral Contraception
•  MOA: estrogen and progesterone blocks LH and
FSH, no ovulation

•  USE: pregnancy prevention

•  SE: Hyper-coagulable state.

•  CI: smokers > 35 y/o., tromboembolism, stroke,
estrogen dependent tumors.
Ritodrine / Terbutaline
•  MOA: Beta agonist that relax uterus, reduce
premature uterine contractions.
•  USE: Premature uterine contration.
Sildenafil, Vardenafil,
Tadalafil
•  MOA: inhibits cGMP phosphodiesterase, increase
cGMP, cause smooth muscle relaxation in the
corpus cavernosum, cause eraction

•  USE: ED, Pulmonary hypertension

•  SE: Hypotension, Headache, flushing, dyspepsia,
vision impaired, caution with Nitrates.
25
9/11/18
Danazol
•  MOA: partial agonist at androgen receptor
•  USE: endometriosis, hereditary angioedema
•  SE: weight gain, edema, acne, hirsutism,

masculanization, decrease HDL.
Minoxidil
•  MOA: Direct arteriolar vasodilator
•  USE: Androgenetic alopecia, severe refractory

hypertension
Neurology
Pharmacology
26
9/11/18
Noradrenergic
↑ Smooth muscle contraction!
Alpha 1! G q! Mydriasys (papillary dilator contraction)!
↑ Sphincter contraction!
↓ NE, Epi release!
↓ Insuline!
Alpha 2! G i! ↓lipolisys!
↓ Aqueous humor production!
↑ platelets aggregation!
↑ HR, contractility!
Beta 1! G s! ↑ Renin release!
↑ Lipolisis!
↓ Vasodilation!
↓ Broncodilation!
↓ Uterine contraction!
Beta 2! G s!
↑ Lipolisis!
↑ insuline release,!
↑ Aqueous humor production!
Glaucoma
•  Alpha agonist
•  Epinephrine
•  MOA: Beta > Alpha!
•  USE: Anaphylaxis shock, asthma, open angle glaucoma!
•  SE: Mydriasis!
•  CI: Closed angle glaucoma!

•  Beta blocker !
•  Timolol, Butexalol, Carteolol
•  USE: Open angle glaucoma!
•  Decrease aqueous humor synthesis!
Muscarinic
Receptor! G protein! Function!
↑ CNS, PNS!
M 1! G q!
Gastric parietal cell!
M 2! G I! ↓ Heart rate, contractility!
↑ Exocrine gland secretion!
↑ Gut motility!
Miosis- pupilari sphinter
M 3! G q!
Accomodation - ciliary muscle
Broncoconstriction!
Bladder contraction!
M 4! G I! CNS Unclear !
M 5! G q! Unclear!
27
9/11/18
Glaucoma
•  Cholinomimetic Agents
•  Carbacol
•  Pilocapine
•  Emergency!
•  MOA: Direct agonist of Ach receptors!
•  USE: Glaucoma!
•  SE: Miosis, Cyclospasm!

•  Increase outflow to the Schlernm canal!
•  Indirect Cholinomimetic Agents
–  Physostigmine
–  Echothiophate
–  MOA: Cholinesterase inhibitors!

–  USE: Glaucoma!
–  SE: Miosis, Cyclospasm!
Glaucoma
•  Diuretic
•  Acetazolamide
•  MOA: Carbonic anhydrase inhibitors in the Proximal
convoluted tubule, decrease biocarbonate
•  USE: Glaucoma, Altitude sickness, reduce metabolic
acidosis, decrease CSF
•  SE: Parestesia, Hyperchloremic metabolic acidosis, sulfa
allergy.
•  Prostaglandin
•  Latanoprost
•  MOA: PGF-2α, increase outflow of aqueous humor!
•  USE: Glaucoma!
•  SE: iris color change!
Opioid analgesics
•  MOA: κappa: dynorphin,spinal cord, Analgesia;
mu: morphine; delta: enkephalin
•  Open K channels, close Ca channels, causing a
decrease in synaptic transmission, including
substance P!
•  Muscle Relaxation, Analgesia, CNS Depressant!
!
•  SE: Addiction, Respiration depression; Weakness/
SOB; Hypotension; Lightheadedness, Tolerance but
not with Miosis and Constipation

•  Overdose: Antidote Naloxone, Naltrexone
•  MOA: Opioid receptor antagonist
28
9/11/18
Opioid analgesics
•  USE:
•  Heroine
•  Abused; Pinpoint pupils → overdose sign!
•  Methadone
•  ↑ t ½; Used instead for heroine withdrawal; Social intervention!
•  Morphine
•  Used of severe pain;!
•  CI: head injury b/c of ↑ ICP
•  Meperidine
•  GI pain; No sphincter of oddi spasms!
•  Mc abused by physicians block DO, NE, no pinpoint pupil!
•  Codone, Oxycodone, Hydrocodiene
•  for moderate pain!

Tincture of Opium
Infants, diarrhea!
Codiene
Anti-tussive, mild pain; !
Dextroamethorphan
OTC anti-Tussive!
Loperamide
Diarrhea!
Diphenoxylade
Diarrhea!
Fentanyl
Potent used in anesthesia!
Pentazocin
Only opiate that antagonizes it’s own receptor; !
Never use with an opiate addict; Use Ketorolac!
Butorphanol
•  MOA: κ receptor agonist, mu receptor partial
agonist, produce analgesia
•  USE: Severe pain
•  SE: less respiratory depression, and withdrawal

symptoms if use with opioid agonist.
29
9/11/18
Tramadol
•  MOA: Weak opioid agonist, Inhibits 5-HT and NE
reuptake.
•  USE: Chronic Pain
•  SE: same as opioid, decrease seizure threshold,

Serotonin syndrome.
Chronic pain
•  Amitriptyline:
•  Tricyclic antidepressants
•  MOA: Block reuptake of NE, and serotonin
•  USE: Mayor depression, fibromyalgia, Chronic pain
•  SE:
•  Sedation, alpha block, anticholinergic.!
•  Convulsions, Coma, Cardiotoxicity, respiratory
depression, hyperpyrexia.!
•  Tx. CV NaHCO3!
Barbitures
•  MOA: Facilitate GABA by increasing duration of Cl channel
opening and decrease firing

•  USE: Sedative, Seizures, Insomnia

•  Phenobarbital, Pentobarbital, Secobarbital,
Thiopental (induction of anesthesia)
•  SE: Respiratory and Cardiovascular depression, CNS

depression, dependence, P-450 inducer

•  CI: Porphyries
30
9/11/18
Benzodiazepine
•  MOA: Facilitate GABA by Increasing frequency of Cl
channel opening. Decrease REM

•  USE: Anxiety, Status epilepticus, alcohol detoxification,
night terrors, sleepwalking, general anesthetic, insomnia

•  SE: CNS depression, dependence, less respiratory
depression that barbiturates

•  Overdose: Flumazenil
•  MOA: Competitive antagonist of benzodiazepine receptor !
Benzodiazepine
•  Flourezapam Long action
•  Alprazolam, Oxazepam, Triazelam, Short action.
•  Alprazolam: Panic attack
•  Triazelam: Tray to sleep
•  Tamazepam: Mateing sleep
•  Diazepam: status epilecticus; Lorazepam
(Suppository)
•  Clonazepam: Apzon seizures
•  Clordazeponide (alcohol withdraw seizures)
•  Midazolam (45min anterograde amnesia)
NON Benzodiazepine
Hypnotic
•  Zolpidem, Zaleplon, Eszopiclone
•  MOA: Activate the BZ1 subtype of GABA receptor
•  USE: Insomnia
•  SE: Ataxia, Headache, Confusion
31
9/11/18
Insomnia treatment !
l  Suvorexant!
l  MOA: Orexin (hypocretin) receptor antagonist. !
-  USE Insomnia.!
-  ADVERSE EFFECTS CNS depression,
headache, dizziness, abnormal dreams, upper
respiratory tract infection. Contraindicated in
patients with narcolepsy. Not recommended in
patients with liver disease. No or low physical
dependence. Contraindicated with strong
CYP3A4 inhibitors.!
!
Insomnia treatment!
l  Ramelteon !
-  MOA: Melatonin receptor agonist, binds MT1
and MT2 in suprachiasmatic nucleus. !
-  USE Insomnia. !
-  ADVERSE EFFECTS Dizziness, nausea, fatigue,
headache. No dependence (not a controlled
substance).!
!
Epilepsy drugs !
32
9/11/18
Agranulocytosis
•  Clozapine !
•  PTU !
•  Methimazole!
•  Ethosuximide !
•  Phenytoin !
•  Lamotrigine !
33
9/11/18
Parkinson’s disease drugs
Strategy treatment of parkinson !

l  Dopamine agonists :!
-  Ergot—Bromocriptine !
-  Non-ergot (preferred)—pramipexole, ropinirole!
l  Increse dopamine availability!
-  Amantadine (increase dopamine release and
decrease dopamine reuptake); toxicity = ataxia, livedo
reticularis. !
!
l  Increase L-DOPA availability !

-  Agents prevent peripheral (pre-BBB) l-DOPA
degradation ->increase l-DOPA entering CNS -
> increase central l-DOPA available for conversion to
dopamine. !
-  Levodopa (l-DOPA)/carbidopa—carbidopa blocks
peripheral conversion of l-DOPA to dopamine by
inhibiting DOPA decarboxylase. Also reduces side
effects of peripheral l-DOPA conversion into dopamine
(eg, nausea, vomiting). !
-  Entacapone, tolcapone—prevent peripheral l-DOPA
degradation to 3-O-methyldopa (3-OMD) by inhibiting
COMT.!
34
9/11/18
l  Prevent dopamine breakdown!

-  Agents act centrally (post-BBB) to inhibit breakdown of
dopamine. !
-  Selegiline—blocks conversion of dopamine into DOPAC by
selectively inhibiting MAO-B. !
-  Tolcapone—blocks conversion of dopamine to 3-
methoxytyramine (3-MT) by inhibiting central COMT.!
l  Curb excess cholinergic activity!
-  Benztropine, trihexyphenidyl (Antimuscarinic; improves
tremor and rigidity but has little effect on bradykinesia in
Parkinson disease)!
•  Bromocriptine-Ergot
•  USE: hyperprolactinamia, Parkinson
•  Pramipexole, Ropinirole-Non Ergot

•  MOA: Dopamine Agonist in the striatum
•  SE: Hallucinations, GI Distress, dyskinesias,
hypotension
•  Amantadine
•  MOA: Prevent viral fusion and uncapping
•  Increase dopamine availability, block
muscarinic receptor
•  USE: Influenza A, parkinson’s disease
•  SE: GI distress, dizziness, behavioral effects,
dermatotoxicity
35
9/11/18
•  Levodopa
•  MOA: increase availability of L-DOPA in the periphery
and entering to CNS for conversion to Dopamine

•  Carbidopa
•  MOA: Block peripheral DOPA decarboxylase
•  USE: Parkinson’s
•  SE: Arrhythmias, dyskinesia, behavioral effect, On/OFF
phenomenon,
•  Selegiline
•  MOA: Inhibits MonoAmine Oxidase type B, which
break down Dopamine
•  USE: Adjunctive agent to L-DOPA for parkinson
•  SE: enhance L-DOPA SE

•  Entacapone, Tolcapone
•  MOA: Inhibits Catechol-O-Methyltransferase
(COMT).
•  USE: Adjunctive agent to L-DOPA for parkinson
•  SE: Tolcapone hepatotoxic
Alzheimer’s Drugs
•  Memantine
•  MOA: NMDA receptor antagonist
•  SE: Dizziness, confusion, hallucinations

•  Donepezil, Galantamine, Rivastigmine
•  MOA: Cholinesterase inhibitors
•  SE: Exacerbation of COPD, Asthma, PUD, nausea,
Dizzines, insomnia.
36
9/11/18
Triptans
•  Sumatriptan, Naratriptan, Zolmitriptan
•  MOA: 5-HT agonist, inhibits trigeminal nerve
action, prevent vasoactive peptide release causing
vasoconstriction
•  USE: Migraine, Cluster headache
•  SE: Paresthesia
•  CI: Prinzmetal angina, Coronary Artery disease
Huntington Drugs
•  Neurotransmiter: decrease GABA, Ach;
increase Dopamine!
•  Tetrabenzine, Reserpine
•  MOA: Inhibits vesicular monoamine transporter
(VMAT), decrease Dopamine release

•  Haloperidol

General Anesthesia
•  Unconsciousness, analgesia, amnesia, muscle
relaxation, lost of reflexes.!
•  Protocols involve Inhaled, Intravenous, skeletal

muscle relaxants, local anesthetics.!
•  Must be lipid soluble or actively transported!
37
9/11/18
General Anesthesia
•  Drugs with DECREASE solubility in Blood and
Gas ratio have rapid induction and recovery.
Eg. Nitrous oxide, desflurance.!
!
•  Drugs with INCREASE solubility in Lipids
have High potency = 1 /MAC!
!
•  Minimal Alveolar Concentration –MAC–, at
50% of the population is anesthetized, varies
with age.!
•  Is Inversely related to potency!
Inhaled Anesthesia
•  MOA: Block Na channels or activate GABA mediated Cl
ion flux.
•  Increase cerebral blood flow!
•  Uterine smooth muscle relaxation!
•  Decrease respiratory respond to hypoxia!
•  Myocardial depression!
•  Decrease cerebral metabolic demand!
Inhaled Anesthesia
•  SE:
•  Halothane: Hepatotoxicity
•  Methoxyflurane: Nephrotoxicity
•  Enflurane: Proconvulsant
•  Sevoflurane
•  Isoflurane
•  Nitrous Oxide
38
9/11/18
IV Anesthesia
•  Thiopental
•  MOA: Facilitate GABA by increasing duration of Cl
channel opening and decrease firing
•  High potency, High lipid solubility, Rapid entry
into the brain. Decrease cerebral blood flow!
•  Short time due to rapid redistribution into
tissues. Rapid recovery!
•  USE: Induction and short procedures
IV Anesthesia
•  Ketamine (Arylcyclohexylamine)
•  MOA: Block NMDA receptor, PCP analog, Cardiovascualr
stimulants
•  USE: Short procedures. Major depression ?
•  SE: Disorientation, Hallucination, Bad dreams, dissociative
anesthesia. Increase ICP!
•  Propofol
•  MOA: Potentiates GABA. Rapid anesthesia induction.
•  USE: Short procedures
•  SE: Less Post operative nauseas
IV Anesthesia
•  Midazolam
•  MOA: Benzodiazepine with amnestic effect

•  Fentanyl
•  MOA: Opioid, Less cardiovascular effect

39
9/11/18
Local Anesthesia
•  Esters
•  Procaine, Cocaine, Tetrecaine
•  Amide: have 2 I on the name

•  Lidocaine, Mepivacaine, Bupivacaine
•  MOA: Block Na channels on the inner portion
•  Bind to the activated Na channels!
•  Can be given with vasocontrictors (epinephrine)
to enhance local action!
Local Anesthesia
•  USE: Minor surgery, spinal block, Class 1B
antiarrhythmic.
•  SE: CNS excitation
•  Severe cardiotoxicity (Bupivacaine)
•  HTN, Hypotension
•  Arrhythmias (Cocaine)
Neuromuscular Blocking
drugs
Depolarizing
•  Succinylcholine
•  MOA:
•  Phase 1: Prolong depolarization causing fasciculation,
•  Potentiated by AChE inhibitors!
•  Phase 2: Block repolarization of the end plate

•  USE: Surgery, assist mechanical ventilation

•  SE: Hypercalcemia, Hyperkalemia, malignant
hyperthermia
40
9/11/18
Neuromuscular Blocking
drugs
Nondepolarizing
•  Tubocurarine, Atracurium, Mivacurium,
Pancuronium, Vecuronium, Rocuronium
•  MOA:
•  Competitive antagonist of Ach in the muscle end
plate.!
•  USE: Surgery, assist mechanical ventilation
•  SE: respiratory paralisis
•  Reversed with ACHE inhibitors!
Spasmolytics
•  Dantrolene
•  MOA: Block Ca release from the sarcoplasmic reticulum
of skeletal muscle
•  USE: Malignant hyperthermia, Neuroleptic malignant
syndrome
•  Baclofen
•  MOA: Inhibits GABA-B receptor in the spinal cord
•  USE: Muscle spasms
•  Cyclobenzaprine
•  MOA: Centrally acting skeletal muscle relaxing.
•  USE: Muscle spasms
•  SE: Anticholinergic
ANTIFUNGAL
ANTIPARASITIC
41
9/11/18
Cell Membrane
•  Form Pores!
•  Amphotericin B!
•  Nystatin!
•  Synthesis!
–  Azoles!
•  Clotrimazole!
•  Fluconazole!
•  Itraconazol!
•  Ketoconazolle!
•  Miconazole!
•  Voriconazole!
Amphotericin B
•  MOA: !
•  Binds to ERGOSTEROL
•  Forms artificial pores to increase permeability of the
membrane
•  Resistance: !
•  Change in the structure of the ergosterol
•  Liposomal, less SE
42
9/11/18
Amphotericin B
•  USE: Severe fungal inf.

•  Cryptococcus!
•  Blastomyces!
•  Coccidoides!
•  Histoplasmosis!
•  Candida!
•  Mucor!
•  SE:
•  Optic neuritis!
•  Hypotension!
•  Nephrotoxicity, hypokalemia, hypomagnesemia!
•  Arrhythmias!
•  IV phlebitis!
Nystatin
•  MOA: Bind to Ergosterol
•  USE: Oral Candidiasis

•  Diaper rash!
•  Vaginal Candidiasis!
•  SE: Toxic for systemic use
AZOLES
•  MOA:
•  Inhibit fungal sterol synthesis by inhibiting P450!
•  Lanosterol to ergosterol!

•  USE:
•  Cryptococcal meningitis in AIDS
•  Blastomyces!
•  Coccidoides!
•  Histoplasmosis!
•  Candida!
43
9/11/18
AZOLES
•  Fluconazole. CNS penetration, Renal excreted

•  Systemic
•  Itraconazole!
•  Ketoconazole!
•  Voriconazole!
•  Topical
•  Clotrimazole!
•  Miconazole!
•  SE:
•  Gynecomastia!
•  Inhibits P450!
Others Anti-fungal
•  DNA!
•  Flucytosine!
•  Cell Wall!
•  Caspofungin!
•  Micafingin!
•  Block Ergosterol!
•  Terbinafine!
!
•  Block Microtubules!
•  Griseofulvin!
Flucytosine
•  MOA:
•  Transform to 5-FU by Cytosine deaminase!
•  Inhibits DNA and RNA biosynthesis!
•  USE:
•  Cryptococcal meningitis in combination with
Amphotericin B!
•  SE:
•  Bone marrow suppression !
44
9/11/18
Echinocandins
•  Anidulafungin, Caspofungin, Micafungin!
•  MOA:
•  Inhibits Synthesis of cell wall (β glycan)
•  USE:
•  Aspergillosis
•  Candida!
•  SE:
•  GI upset
•  Flushing!
•  Headache!
Griseofulvin
•  MOA:
•  Deposits in Skin, binds to Keratin.
•  Disrupts microtubules function on mitosis

•  USE: Dermatophytoses

•  SE:
•  GI irritation, P450 Inducer ,Serum Sickness, Hepatitis,
Headache, Confusion, Teratogenic, Carcinogenic
Terbinafine
•  MOA:
•  Inhibits Squalene Epoxidase
•  Increase Squalene that block Ergosterol
•  USE:
•  Dermatophytoses
•  Onychomycosis
•  SE:
•  Hepatotoxic
•  GI upset
•  Taste disturbances!
•  Headaches !
45
9/11/18
Antiparasitic
Antimalarial
•  Chloroquine!
•  Quinine !
•  Mefloquine !
•  Primaquine !
•  Atovaquone + proguanil!
Antiprotozoal
•  Metronidazole!
•  Pyrimethamine!
•  Pyrimethamine!
•  Suramin
•  Melarsoprol!
•  Nifurtimox!
•  Sodium Stibogluconate!
Antimalarial
MOA USE SE
Plasmodial infection: Retinopathy!
Block detoxification of
Chloroquine Heme in to Hemozoin!
Except P. Falciparum! Pruritus!
Prophylaxis! GI distress!
Cinchonism,
Quinine, Block DNA replication, Chloroquine resistance Cardiotoxicity!
Quinidine transcription! P. Falciparum! !
CI: G6PD, Pregnancy!
GI distress, rash,
Chloroquine resistance headache!
Mefloquine Same as Chloroquine! malaria! !
Avoid Seizure!
GI disttress, Pruritus,
Forms redox methemoglobinemia!
Primaquine compounds that cause P. Vivax, Ovale! !
cellular oxidation!
CI: G6PD!
GI disttress!
Inhibits mitochondrial
Atovaquone electron transport and Chloroquine resistance !
+ proguanil malaria! CI: Pregnancy, Renal
folate metabolism!
dysfuntion!
Antiprotozoal
•  Metronidazole
MOA: Forms free radical and damage the DNA
• 
•  Antiprotozoa!
•  USE: Giardia, Entamoeba, Trichomonas,
Gardenerella, Anaerobes, H. Pylori
•  SE: Disulfiram-like reaction, Disgusia,
thrombophlebitis
46
9/11/18
Antiprotozoal
•  Pyrimethamine + sulfa
Toxoplasmosis!
• 
•  Suramin and Melarsoprol

Trypanosoma Brucei!
• 
•  Nifurtimox
• Trypanosoma Cruzi!
•  Stibogluconate
• Leishmaniasis!
Antihelmitic
•  Mebendazole
•  Albendazol
•  Ivermectin
•  Piperazine
•  Diethylcarbamazine
•  Praziquantel
•  Thiabendazole
•  Pyrantel pamoate
Antihelmitic
•  Albendazol
•  MOA: inhibits microtubule assembly in worms
•  USE: Most common nematodes, Cysticercosis,
hydatid disease

•  Mebendazole
USE: Whipworm, Hookworm, Pinworm,
• 
Roundworm
47
9/11/18
Antihelmitic
•  Ivermectin
•  MOA: GABA receptor activation leading to
paralysis and expulsion of worms
•  USE: Threadworm

•  Piperazine
• USE: roundworm
Antihelmitic
•  Dimethylcarbamazine
•  USE: Filariasis
•  SE: Reaction to parasite proteins include fever, rash,
joint pain, ocular dysfunction

•  Praziquiantel
•  MOA: increase Ca influx causing contraction then
relaxation.
•  USE: flukes, tapeworm
•  SE: Headache, dizziness, malaise, GI distress
Antihelmitic
•  Thiabendazole
•  USE: Larva migrans
•  SE: GI distress, cholestasis, leukopenia, CNS effects,
reactions to dying parasites

•  Pyrantel pamoate
•  MOA: Nicotinic receptor activator cause paralysis
•  USE: hookworm, roundworm
48
9/11/18
Antihelmitic
•  Bithionol
•  USE: liver fluke
•  SE: tinitus, headache, GI distress, Leukopenia

•  Metrifonate
•  MOA: Inhibits acetylcholinesterase of parasite
•  USE: Bilharziasis

•  Niclosamide
•  USE: tapeworm
•  MOA: Uncouple oxidative phosphorylation
•  SE: Headache, GI distress, rash, fever
Anti-mite/ louse
therapy
•  USE: Scabies and Lice

•  Permethrin
•  MOA: Block Na channels
•  SE: Neurotoxicity
•  Malathion
•  MOA: Acetylcholinesterase inhibitor
•  Lindane
•  MOA: Block GABA
•  SE: Neurotoxicity
49
9/11/18
MSK!
Psychiatry!
Hematology!
Immunology!
Antiviral!
Musculoskeletal
Pharmacology
1
9/11/18
Prostaglandins
•  Alprostadil
•  Misoprostol
•  Latanoprost
•  Dinoprostone
•  Carboprost
Prostaglandins
•  PGE1:
•  MOA: Vaso dilated, afferent artery of kidney
•  USE:
•  Alprostadil: PDA open, alternative to –fil in Erectile
dysfunction.
•  Misoprostol: prevent NSAID gastric ulcers
!
•  SE: Pregnancy cause abortion do to
vasoconstriction
Prostaglandins
•  PGE2:
•  MOA: Vase constriction, found on semen,
dysmenorrhea
•  USE:
•  Latanoprost (PGF2): Glaucoma, grow out
eyelashes
•  Dinoprostone, Carboprost: separate placenta
•  SE: Pregnancy cause abortion do to
vasoconstriction, Pigmentation of the iris
2
9/11/18
NSAIDS
•  Aspirin!
•  Indomethacin!
•  Phenylbutazone!
•  Ibuprofen!
•  Naproxen!
•  Baclofen!
•  Ketorolac!
•  Diclofenac!
•  Ketoprofen!
•  Sulindac!
•  Cyclobenzaprine!
•  Acetaminophen!
Aspirin (ASA)
•  MOA: NSAID that irreversibly inhibits cyclooxygenase
(both COX-1 and COX-2) by covalent acetylation -
> decrease synthesis of TXA2 and prostaglandins.
increase bleeding time. No effect on PT, PTT. Effect lasts
until new platelets are produced
•  USE:
  Low dose (< 300 mg/day): decrease platelet aggregation.
  Intermediate dose (300–2400 mg/day): antipyretic and
analgesic.
  High dose (2400–4000 mg/day): anti-inflammatory.
l  SE: Gastric ulceration, tinnitus (CN VIII). Chronic use

can lead to acute renal failure, interstitial nephritis, GI
bleeding.!
l  Risk of Reye syndrome in children treated with aspirin
for viral infection. !

l  Toxic doses cause respiratory alkalosis early, but
transitions to mixed metabolic acidosis-respiratory

alkalosis!
3
9/11/18
Aspirin (ASA)
Time CO2 HCO3 PH

Initially Respiratory!
↓! No change! ↑!
increase RR! Alkalosis!
Respiratory!
! ! Alkalosis
! !
After 12 hr! Close to with
↓! ↓!
ASA- Acid! normal! Metabolic
Acidosis!
Respiratory!
>24 h Late!
Acidosis!
↑ GABA
↑! ↓! ↓! with
Respiratory
Metabolic
depression!
Acidosis!
NSAIDs
•  MOA: reversible COX 1 and COX 2 Inhibitors by
covalent acetylation
•  USE: anti-inflammatory, antipyretic, analgesic
•  SE: Gastric ulcers, GI bleeding, insterstitial nephritis
NSAIDs
•  Indomethacin: •  Ibuprofen
•  1st line Gout, Close PDA! •  Ketorolac
•  Phenylbutazone: •  Diclofenac:
•  2nd most potent!
•  IM, Topical!
•  Naproxen
•  Ketoprofen:
•  Dysmenorrhea!
•  Topical!
•  High sodium don’t in heart
failure, renal failure, •  Sulindac
seizures! •  Sulfa.Steven-J!
•  Cyclobenzaprine
•  Anticholinergic effect!
!
4
9/11/18
Acetaminophen
•  MOA: Inhibits COX 1 and 2, mostly in the CNS.
•  Stimulate Anterior, inhibits Posterior nucleus in
thalamus
•  USE: Antipyretic, analgesic. No Reye’s syndrome
•  SE: Overdose produces hepatic necrosis;
acetaminophen metabolite (NAPQI) depletes
glutathione and forms toxic tissue byproducts in liver.
N-acetylcysteine is antidote—regenerates glutathione.
Microsteatosis Causes
•  Acetaminophen !
•  Reye Syndrome !
•  Pregnancy !
•  Macrosteatosis Causes
•  Alcohol !
COX 2 Inhibitor
•  Celecoxib
•  MOA: Reversibly inhibits specifically the

Cyclooxygenase 2, mediates pain and
inflammation. No effect on TXA2 (COX1
dependent).
•  USE: Rheumatoid arthritis, Osteoarthritis,
Patients with Gastritis
•  SE: Thrombosis, Osteoarthritis , Sulfa allergy. CV
risk
5
9/11/18
Leflunomide
MOA: Reversible inhibits Dihydroorotate
dehydrogenase
•  Prevent pyrimidine synthesis, suppresses
T cell
•  USE: RA, Psoriatic arthritis
•  SE: Diarrhea, Hypertension, Hepatotoxicity,

Teratogenicity, alopecia.
Bisphosphonates !
Alendronate, ibandronate, risedronate, zoledronate. !
l  MAO: Pyrophosphate analogs; bind

hydroxyapatite in bone, inhibiting osteoclast
activity. !
l  USE: Osteoporosis, hypercalcemia, Paget
disease of bone, metastatic bone disease,

osteogenesis imperfecta. !
l  SE: Esophagitis (if taken orally, patients are
advised to take with water and remain upright for

30 minutes), osteonecrosis of jaw, atypical stress
fractures.!
Teriparatide
•  MOA: PTH analog, ↑ osteoblastic activity (Pulsatile)
and continuous cause decrease bone mass. 3rd line
•  USE: Osteoporosis
•  SE: increase risk of osteosarcoma after 2 years

(avoid use in patients with Paget disease of the bone
or unexplained elevation of alkaline phosphatase).
•  Avoid in patients who have had prior cancers or

radiation therapy. Transient hypercalcemia.
•  Give bisphosphonate after to maintain bone mass
6
9/11/18
Gout
treatment
•  Acute:!
•  Indometacin
•  Glucocorticoids
•  Colchicine
•  Chronic:!
•  Allopurinol
•  Probenecid
•  Febuxostat
•  Pegloticase
•  Rasburicase
Steroids
•  Inhibit PLP-A!
•  Kills T-cells and eosinophilis!
•  Inhibits macrophages migration!
•  Stabilizes endothelium!
•  Stabilizes mast cells!
•  Proteolysis!
•  Gluconeogenesis!
7
9/11/18
Steroids
•  USE: Addison’s, Inflammation, Immune
suppression, Asthma, COPD, Gout
•  SE: Cushing’s, Osteoporosis, Adrenocortical

atrophy, Adrenal insufficiency if stop chronic use,
PUD, Diabetes, weight gain, fat redistribution,
phychosis, hypertension, cataracts, acne
Steroids
•  Prednisone, Prednisolone: CLL, non-Hodgkin
lymphoma
•  Methylprednisalone: Main IV
•  Triamcinalone: Main Inhale, next Budesonide,
Cyclosenide (kids)
•  Beclamethasone, Betamethasone: preterm fetus
for increase surfactant production
Steroids
•  Dexamethasone: CNS penetration
•  Cypropterone: only that block DHT receptor in
prostate CA
•  Megestrol: strong anabolic effect, in cancer patient
•  Danozol: Endometriosis
8
9/11/18
Colchicine
•  MOA: Binds and stabilizes tubulin to inhibit
microtubule polymerization, impairing neutrophil
chemotaxis and degranulation.
•  USE: Acute Gout and prophylactic value
•  SE: GI side effects, myelosuppression
Xanthine oxidase
inhibithors
Allopurinol
•  MOA: Competitive inhibitor of xanthine oxidase.

decrease conversion of hypoxanthine and xanthine to urate.
•  USE: Gout, hyperuricemia, used in lymphoma and leukemia to

prevent tumor lysis–associated urate nephropathy
•  SE: Increase concentration of Azathioprine and 6-MP, rash
•  Febuxostat: Inhibits xanthine oxidase.
Probenecid
•  MOA: Inhibits reabsorption of uric acid in proximal
convoluted tubule (also inhibits secretion of
penicillin)
•  USE: Gout
•  SE: Kidney stone (urate)
•  CI: renal failure
9
9/11/18
Pegloticase, Rasburicase
•  MOA: Recombinant uricase that catalyzes

metabolism of uric acid to allantoin (a more water-
soluble product).
•  USE: Gout
•  AE: Rash, urticarial
Gout!
ACUTE!
1- NSAIDS (naproxen, indomethacin)!
2- Steroids!
3- Colchicine !
CHRONIC!
- XO inhibitors !
Inh Microtubules!
-  Colchicine!
-  Vincristine/vinblastine!
-  Paclitaxel!
-  Griseofulvin !
-  Albendazol !
10
9/11/18
TNF-α Inhibitor
Adalimumab, Infliximab , certolizumab,
golimumab
•  MOA: TNF-α inhibitor
USE: IBD, Rheumatoid arthritis, Ankylosing

• 
spondylitis, Psoriasis
• Etanercept
–  MOA: Inhibits the fusion receptor
!
–  USE: Rheumatoid arthritis, Ankylosing spondylitis,
Psoriasis
Psychiatry
Pharmacology
Amphetamin
•  Methylphenidate- ritilan!
•  Dexadrine- dexatrim!
•  Adderal!
•  LSD!
•  PCP!
•  ECSTACY!
•  Pemoline!
11
9/11/18
CNS Stimulants /
Amphetamin
•  MOA: Indirect agonist, Inhibits reuptake, release stored
catecholamine!
•  SE: Vertical nystagmus, Nauseas, Vomiting (DA stimulat), Tics
(basal ganglia)!
•  Methylphenidate- ritilan
•  USE: Narcolepsy, ADHD in kids, gain weight!
•  SE: Hypnogogic hallucinations as you fall asleep!
•  USE: Weight loss + exercise and diet; OTC!
•  Adderal
•  MOA: Dexadrine + racemic amp!
Amphetamin
•  LSD
•  SE: Hallucinations from Seratonin (slow, lazy) + Amp!
•  PCP
•  SE: Hallucinations from Seratonin (violent, aggressive) +
↑↑↑Amp violent; Vertical nigtasmo!
•  ECSTACY
•  SE: Hallucinations from Seratonin (stimulate thirst) + Amp!
•  Pemoline
•  SE: Hepatic necrosis (hepatitis)- off the market 2005!
Neuroleptics /
Antipsychotics
•  Haloperidol!
•  Fluphenazine!
•  Trifluoperazine!
•  Prochlorperazine!
•  Chlorpromazine!
•  Thioridazine!
•  Atypical
–  Olanzapine !
–  Clozapine !
–  Quetiapine!
–  Risperidone!
–  Aripiprazole!
–  Ziprasidone!
12
9/11/18
Neuroleptics /
Antipsychotics
•  MOA: Block D2 receptors
•  High potency: !
•  Haloperidol (butyrophenones)
•  Fluphenazine, Trifluoperazine (Phenothiazines)
•  Low potency: !
•  Prochlorperazine
•  Chlorpromazine (Coneal deposits)
•  Thioridazine (Retinal deposits)
!
•  USE: Schizophrenia (positive symptoms),
psychosis, bipolar disorder, delirium, Tourette
syndrome, Huntington disease, OCD.
Neuroleptics /
Antipsychotics
•  SE:
-  Lipid soluble -> stored in body fat -> slow to be removed from
body. !
-  Endocrine: dopamine receptor antagonism -
> hyperprolactinemia → galactorrhea, oligomenorrhea,
gynecomastia. !
-  Metabolic: dyslipidemia, weight gain, hyperglycemia. !
-  Antimuscarinic: dry mouth, constipation. !
-  Antihistamine: sedation. !
-  α1-blockade: orthostatic hypotension. !
-  Cardiac: QT prolongation. !
-  Ophthalmologic: Chlorpromazine—Corneal deposits;
Thioridazine—reTinal deposits.!
l  Neuroleptic malignant syndrome (NMS):

Myoglobinuria, Fever, Encephalopathy, unstable
Vitals, increase Enzymes, muscle Rigidity. !
-  Treatment: dantrolene, D2 agonist (eg,
bromocriptine).!
!
13
9/11/18
Extrapyramidal side effects (High)

ADAPT
•  Acute Dystonia, akinesia
•  1 week – 2 weeks
•  Muscle spasm, stiffness
•  Tx. Diphendramine or benztropine
•  Parkinsonism, Bradykinesia
•  3 weeks
•  Parkinson’s like symptoms
•  Akinesia
•  Tx: benztropine or Trihexylphenidyl
•  Akathisia
–  10 weeks
–  Restless legs
–  Tx. Benzodiazepine or beta blockers
•  Tardive dyskinesia
–  18 weeks
–  Oral – facial movement
–  Tx. discontinue offend agent and start on clozapine
Atypical antipsychotics
Olanzapine, Clozapine, Quetiapine, Aripiprazole,
Asenapine, Iloperidone, Lurasidone, Paliperidone,
Ziprasidone
• MOA: Not completely understood. Most are D2 antagonists;

aripiprazole is D2 partial agonist. Varied effects on 5-HT2,
dopamine, and α- and H1-receptors.
• USE: Schizophrenia (positive and negative), Also used for

bipolar disorder, OCD, anxiety disorder, depression, mania,
Tourette syndrome.
  Use clozapine for treatment-resistant schizophrenia or
schizoaffective disorder and for suicidality in schizophrenia.
!
l  SE: All—prolonged QT interval, fewer EPS and

anticholinergic side effects than typical
antipsychotics. !
-  “-pines”—metabolic syndrome (weight gain,
diabetes, hyperlipidemia). !
-  Clozapine—agranulocytosis (monitor WBCs
frequently) and seizures (dose related). !
-  Risperidone—hyperprolactinemia (amenorrhea,
galactorrhea, gynecomastia).!
-  Lurasidone – safe in pregnancy. !
-  Ziprasidone – QTc prolong!
14
9/11/18
Agranulocytosis
•  Clozapine !
•  PTU !
•  Methimazole !
Mood Stabilizer
•  Lithium
•  Valproic Acid
•  Carbamazepine
Mood Stabilizer
•  Lithium
•  MOA: Inhibits recycling of phosphatidylinositol bisphosphate (PIP)
• USE: Bipolar disorder

l  SE: Tremor, hypothyroidism, polyuria (causes nephrogenic
diabetes insipidus), teratogenesis. Causes Ebstein anomaly in
newborn if taken by pregnant mother. Narrow therapeutic window
requires close monitoring of serum levels. Almost exclusively
excreted by kidneys; most is reabsorbed at PCT with Na+.
Thiazides (and other nephrotoxic agents) are implicated in lithium
toxicity.!
l  Withdrawal symptoms: flu—like symptoms !

!
15
9/11/18
Mood Stabilizer
•  Valproic Acid
•  MOA: Block Na and Ca channels, Increase GABA
concentration
•  USE: 1st line Tonic clonic seizure, 2nd line rest, Bipolar.
•  SE: GI distress, hepatotoxicity, tremor, weight gain
•  CI: Pregnancy – neural tube defect

Mood Stabilizer
•  Carbamazepine
•  MOA: Block Na channels
•  USE: 1st line for Partial, and tonic clonic seizure,
Trigeminal neuralgia, Bipolar
•  SE: Agranulocytosis, Diplopia, Ataxia, liver toxic,
teratogenic, SIADH, Stevens Johnson syndrome
•  CI: pregnancy
Buspirone!
MOA: stimulates 5HT1A!

Use: GAD!
Doesn’t interact with alcohol, no dependence, no
sedative.!
1-2 weeks to effect. Use BZD’s !
16
9/11/18
Antidepressants
•  Tricyclic antidepressants!
•  Amitriptiline
•  Nortriptiline
•  Imipramine
•  Desipramine
•  Clomipramine
•  Doxepin
•  Amoxapine
Antidepressants
•  SSRI
•  Fluoxetine •  MAO I
•  Paroxetine –  Tranylcypromine
•  Sertraline –  Phenelzine
•  Citalopram –  Isocarboxazid
–  Selegiline
•  SNRI •  Atypical
•  Venlafaxine –  Bupropion
•  Duloxetine –  Maprotiline
•  Desvenlafaxine –  Mirtazapine
•  Levomilnacipran –  Trazodone
•  Milnacipran –  Buspirone
Antidepressants
•  Tricyclic antidepressants
•  MOA: Block reuptake of NE, and serotonin
•  USE: Mayor depression, fibromyalgia
•  Amitriptiline: Chronic pain
•  Nortriptiline
•  Imipramine (bedwetting) 3erd choice (behave,
ADH)
•  Desipramine
•  Clomipramine (OCD) after SSRI
•  Doxepin
•  Amoxapine
17
9/11/18
Tricyclic antidepressants -
TCA
•  SE:
•  Sedation, alpha block, anticholinergic.!
!
•  Convulsions, Coma, Cardiotoxicity, respiratory
depression, hyperpyrexia. Serotonin Sx. St.
John’s wort. Orthostatic hypotension. MCC of
death cardiac arrhythmia. !
•  Tx. CV NaHCO3!
Antidepressants
•  SSRI:
•  Fluoxetine, paroxetine, Sertraline,
Citalopram
•  MOA: Serotonin specific reuptake inhibitors
•  USE: 1st line Depression, OCD, Bulimia, Social
phobias, PTSD
•  Take 4-8 weeks to stabilize effect!
•  SE: GI distress, Anorgasmia
•  Serotinin syndrome (IMOA): hyperthermia,
myoclonus, cardiovascular collapse, flushing, diarrhea,
seizure.
•  Tx. Cyproheptadine !
•  Serotinin syndrome
•  Hyperthermia, myoclonus, cardiovascular collapse,
flushing, diarrhea, seizure.
•  Cause: SSRT+SNRI, TCA’s, St. Jonh’s wort, MAOI.
•  Tx. Cyproheptadine *5HT2 antag!
18
9/11/18
Antidepressants
•  SNRI
•  MOA: Serotonin and NE reuptake inhibitor
!
•  USE: Depression,
•  Venlafaxine: Generalized anxiety disorder
•  Duloxetine: Diabetic neuropathy
•  Desvenlafaxine
•  Levomilnacipran
•  Milnacipran
!
•  SE: HNT, sedation, nauseas
•  MAO I
Antidepressants
•  Tranylcypromine, Phenelzine, Isocarboxazid
•  Selegiline (MAO B) – Parkinson’s
•  MOA: Nonselective Monoamina Oxidase Inhibitor in the
post synamptic membrane, cause an increase in NE,
Serotonine, Dopamine
!
•  USE: Atypical depression, anxiety, hypochondriasis
increased appetite or weight gain, sleepiness or
excessive sleep, marked fatigue or weakness,
moods that are strongly reactive to
environmental circumstances, and feeling
extremely sensitive to rejection.!
•  SE: Hypertensive crisis (with tyramine), CNS stimulation
•  CI: SSRI, Meperidine
Antidepressants
•  Atypical
•  Bupropion
l  MOA: Inhibits reuptake of NE and dopamine
•  USE: Smoking cessation, Depression **NOT SEXUAL
ISSUES
•  SE: tachycardia, insomnia, headache
•  CI: bulimic patients cause seizure
•  Maprotiline
•  MOA: block reuptake NE
•  SE: Sedation, orthostatic hypotension
19
9/11/18
Atypical
Antidepressants
•  Mirtazapine
  MOA: α2-antagonist (q release of NE and 5-HT), potent 5-
HT2 and 5-HT3 receptor antagonist and H1 antagonist.
•  USE: Depression
•  SE: Sedation, ↑ cholesterol, appetite and weight gain, dry
mouth
•  Trazodone
l  MOA: Primarily blocks 5-HT2, α1-adrenergic, and H1
receptors; also weakly inhibits 5-HT reuptake
•  USE: insomnia, depression in men
•  SE: sedation, priapism, postural hypotension
l  Varenicline!
-  MOA: Nicotinic ACh receptor partial agonist. !
-  Use: smoking cessation. !
-  Toxicity: sleep disturbance, may depress mood. !
l  Vilazodone!
-  MOA: Inhibits 5-HT reuptake; 5-HT1A receptor
partial agonist.!
-  Use: major depressive disorder and generalized
anxiety disorder (off-label).!
-  Toxicity: headache, diarrhea, nausea, q weight,
anticholinergic effects. !
-  May cause serotonin syndrome if taken with other
serotonergic agents. !
l  Vortioxetine!
-  MOA: Inhibits 5-HT reuptake; 5-HT1A receptor
agonist and 5-HT3 receptor antagonist.!
-  Use: major depressive disorder. !
-  Toxicity: nausea, sexual dysfunction, sleep
disturbances (abnormal dreams),
anticholinergic effects. !
l  May cause serotonin syndrome if taken with
other serotonergic agents.!
20
9/11/18
l  Serotonin syndrome!
l  Occur with any drug that increase 5-HT (eg, MAOIs,

SSRIs, SNRIs, TCAs, tramadol, ondansetron, triptans,
linezolid, MDMA, dextromethorphan). !
l  Characterized by 3 A’s: !
-  neuromuscular hyperActivity (clonus, hyperreflexia,
hypertonia, tremor, seizure), !
-  Autonomic stimulation (hyperthermia, diaphoresis,
diarrhea), !
-  Agitation. !
-  Treatment: cyproheptadine (5-HT2 receptor antagonist).!
Hematology
Pharmacology
21
9/11/18
Anti-platelets
•  NSAID!
Aspirin
• 
•  ADP Receptor Inhibitors!

Clopidogrel, Prasugrel, Ticagrelor, Ticlopidine
• 
•  Phosphodiesterase III inhibitor !

Cilostazol, Dipyridamole
• 
•  GP IIb/IIIa inhibitors!
Abciximab, Eptifibatide, Tirofiban
• 
Anti-platelets
Aspirin (ASA)
•  MOA: Irreversible COX 1 and COX 2 Inhibitors by
covalent acetylation
•  USE: Antiplatelets (81mg), anti-inflammatory,

antipyretic, analgesic, 1st line MI, 2nd Stroke
•  Decrease mortality in MI
•  SE: Gastric ulcers, GI bleeding, drug induce asthma,

instertitial nephritis, hypersensitivity
•  Reye’s syndrome (Liver failure)!
•  Cinchonism (Tinnitus, Low plateles, Decrease hearing;
Quinidine, Quinine) !
22
9/11/18
Aspirin (ASA)
Time CO2 HCO3 PH
Initially Respiratory!
↓! No change! ↑!
increase RR! Alkalosis!
Respiratory!
! !
! ! Alkalosis with
30 min – 1 hr! Close to
↓! ↓! Metabolic
ASA- Acid! normal!
Acidosis!
Late! Respiratory!
↑ GABA Acidosis!
↑! ↓! ↓!
Respiratory with Metabolic
depression! Acidosis!
Autoimmune Hemolytic
Anemia
•  PTU !
•  Penicillin !
•  Dapsone !
•  Aspirin !
•  Heparin !
•  Quinidine !
•  Quinine !
ADP Receptor Inhibitors

•  MOA: Inhibit platelet aggregation by
irreversibly blocking ADP (P2Y12) receptor. !
-  Prevent expression of glycoproteins IIb/IIIa on
platelet surface!
•  USE: Acute coronary syndrome, Coronary stents,

Decrease chance of thrombotic stroke
•  SE: TTP, Neutropenia (ticlopidine)
23
9/11/18
ADP Receptor Inhibitors

•  Clopidogrel
•  Prasugrel
•  Ticagrelor
•  Reversible!
•  Ticlopidine
•  SE: Neutropenia
Agranulocytosis !
•  Clozapine!
•  PTU !
•  Methimazole !
Cilostazol, Dipyridamole
•  MOA: Phosphodiesterase III inhibitor,
•  Increase cAMP in plateles!
•  Inhibits platelets aggregation!
!
•  USE: Intermitent claudication, Coronary
vasodilation, Prevent stroke (With ASA), Angina
prophylaxis
!
•  SE: Nausea, Headache, Flushing, Hypotension,
Abdominal pain
24
9/11/18
GP IIb/IIIa inhibitors
•  Abciximab, Eptifibatide, Tirofiban
•  MOA: Bing to the Glycoprotein IIb/IIIa receptor

on the activated platelets
•  Abciximab: Monoclonal antibody Fab fragment
•  USE: unstable angina, Percutaneous

transluminal coronary angioplasty
•  SE: Bleeding, Thrombocitopenia
Anticoagulants
•  Heparin
•  Low molecular weight heparin!

• Enoxaparin, Dalteparin, Fondaparinux
•  Warfarine
•  Thrombin inhibitors!
• Argatroban, Bivalirudin, Dabigatran
•  Direct factor Xa inhibitor!

• Apixaban, Rivaroxaban
Anticoagulants
25
9/11/18
Heparin
MOA: activates antithrombin. Lowers the activity of thrombin
and factor Xa. Short half-life. Increase PTT.
• USE: DVT, PE, Acute coronary syndrome, MI, Pregnancy
• SE: Bleeding, Heparin induce thrombocytopenia, osteoporosis.

• Heparin-induced thrombocytopenia (HIT)—development of IgG
antibodies against heparin bound platelet factor 4 (PF4). Antibody-
heparin-PF4 complex activates platelets increase thrombosis and
thrombocytopenia.
• Antidote Protamine sulfate!
Low molecular weight

• 
heparin
Enoxaparin, Dalteparin, Fondaparinux
•  MOA: Inhibits factor Xa, longer half life, SQ,

no need monitoring
Fondaparinux acts only on factor Xa. Have

better bioavailability and 2–4× longer half
life than unfractionated heparin; can have
better bioavailability, and 2–4 times longer
half life; can be administered
subcutaneously and without laboratory
monitoring
Thrombin inhibitors
•  Argatroban, Bivalirudin, Dabigatran
•  MOA: Direct thrombin inhibitor
•  USE: Patient with Heparin Induce Thrombocytopenia

• Cause by IgG antibodies against heparin bound
platelets factor 4.!
l  Bleeding; can reverse dabigatran with idarucizumab.
Consider PCC and/or antifibrinolytics (eg, tranexamic
acid) if no reversal agent available!
l  Argatroban, Lepirudin: HIT!
l  Dabigatran: alternative to warfa. Not monitor PT!
l  Bivalirudin: alternative to ASA !
26
9/11/18
Warfarin / Coumadin
•  MOA: inhibits Gamma carboxylation of vitamin K dependent
clotting factors 2, 7, 9, 10 and protein C, S. ↑ PT, ↑ INR.
•  USE: Chronic anticoagulation
•  SE: Bleeding, teratogenic, skin necrosis, initialy cause

Transient hypercoagulability due to short half life of protein C,
S.
•  CI: Pregnancy
!
•  Overdose treatment with Vitamin K, or Fresh Frozen
Plasma.!
Direct factor Xa
inhibitor
•  Apixaban, Rivaroxaban
•  MOA: Bind to and inhibits factor Xa
•  USE: Profilaxis for DVT, PE, Stroke (afib).
•  SE: Bleeding
Thrombolytics
•  Alteplase (tPA)
•  Reteplase (rPA)
•  Tenecteplase (TNK-tPA)
•  Anistreplase
•  Streptokinase
•  Urokinase
27
9/11/18
Thrombolytics
•  MOA: Stimulate the convertion of plasminogen to
plasmin, that breack fibrin and thrombin
•  ↑PT, ↑PTT!
!
•  USE: early MI and stroke, PE.
!
•  Decrease mortality in MI (<12 hours)!
!
•  SE: Bleeding, anaphylaxis (Streptokinase,
Anistreplase)
!
•  Antidote: Aminocaproic acid
Thrombolytics
•  Absolute CI
•  Active bleeding!
•  Active internal bleeding!
•  Prior intracranial bleeding!
•  Cerebral neoplasia!
•  CVA with in 1 year!
•  Relative CI
–  BP >180/100 at presentation!
–  Recent trauma or surgery <2-3 weeks!
–  Active PUD!
–  Prolong CRP!
–  Pregnancy!
–  Pericarditis!
–  Use of anticoagulant!
–  Diabetic hemorrhagic retinopathy !
Immunology
Pharmacology
28
9/11/18
Immunosuppresor
IMMUNOSUPPRESSANTS
•  Steroids
–  Beclamethasone
•  Calcineurin inhibitor –  Betamethasone
•  Cyclosporine, Tacrolimus –  Budesonide

–  Cyclosenide
•  mTOR inhibitors –  Cypropterone
• Sirolimus, Rapamycin –  Dexamethasone
–  Fludrocortisone
•  Monoclonal Antibodies –  Fluticasone
• Daclizumab, Basiliximab –  Hydrocortisone
–  Megestrol
•  Antimetabolite –  Methylprednisalone
–  Mometasone
• Azathioprime –  Prednisolone
–  Prednisone
•  Mycophenolate Mofetill –  Triamcinalone
–  Danozol
!
Calcineurin inhibitor
•  Cyclosporine
•  MOA: Calcineurin inhibitor; binds cyclophilin.
-  Blocks T-cell activation by preventing IL-2 transcription.
USE: Transplant rejection prophylaxis, Psoriasis, Rheumatoid arthritis
•  SE: Nephrotoxicity, hyperlipidemia, neurotoxicity, gingival

hyperplasia, hisutism.
•  Tacrolimus
•  MOA: Calcineurin inhibitor, bind to FK506 binding protein
Blocks T-cell activation by preventing IL-2 transcription.
USE: Transplant rejection prophylaxis

•  SE: Diabetes, Nephrotoxicity, hyperlipidemia, neurotoxicity
29
9/11/18
Sirolimus, Rapamycin
•  MOA: mTOR inhibitor; binds FKBP.!
-  Blocks T-cell activation and B-cell
differentiation by preventing response to IL-2.!
USE: Renal transplant prophylaxis
•  SE: Anemia, Thrombocytopenia, Leukopenia,

(pancytopenia) Insulin resistance, Hyperlipidemia.
•  Not nephrotoxic
Thrombocytopenia
•  Sirolimus !
•  Rapamycin !
•  Azathioprine !
Basiliximab
•  MOA: Monoclonal antibody; blocks IL-2R
•  USE: Renal transplant prophylaxis
•  SE: Edema, hypertension, tremor
30
9/11/18
Azathioprine
•  MOA: Antimetabolite precursor of 6-
mercaptopurine.
  Inhibits lymphocyte proliferation by blocking
nucleotide synthesis.
•  USE: Transplant prophylaxis, Rheumatoid arthritis,

chohn’s disease, Glomerulonephritis
SE: Leukopenia, anemia, Thrombocytopenia
Comment: 6-MP degraded by xanthine oxidase; toxicity

increase by allopurinol.
Mycophenolate
Mofetill
•  MOA: Reversibly inhibits IMP dehydrogenase,
preventing purine synthesis of B and T cells.!
•  USE: Transplant rejection, Lupus nephritis
•  SE: GI upset, pancytopenia, hypertension,

hyperglycemia. Less nephrotoxic and neurotoxic.
•  Associated with invasive CMV infection
Corticosteroids!
l  MOA: Inhibit NF-κB. Suppress both B- and T-cell

function by r transcription of many cytokines.
Induce T cell apoptosis.!
l  USE: Many autoimmune and inflammatory
disorders, adrenal insufficiency, asthma, CLL,

non-Hodgkin lymphoma.!
l  SE: Cushing syndrome, osteoporosis,
hyperglycemia, diabetes, amenorrhea,

adrenocortical atrophy, peptic ulcers, psychosis,
cataracts, avascular necrosis (femoral head).!
31
9/11/18
Recombinant
Cytokines
•  Aldesleukin IL-2
•  Epoetin Alpha
•  Colony stimulating factors!
•  Filgrastim G-CSF
•  Sargramostim GM-CSF
•  INF-α, β, γ
•  Platelets Stimulating factors!
•  Romiplostim, Eltrombopag
•  Oprelvekin IL-11
Recombinant
Cytokines
•  Aldesleukin
•  MOA: IL-2 analog
!
•  USE: Renal cell carcinoma, Metastatic melanoma
!
•  Epoetin Alpha
–  MOA: Erythropoietin
–  USE: Anemia, Renal cell carcinoma
–  SE: Hypertension, Thrombotic events
Colony stimulating factors
•  Filgrastim
•  MOA: Granulocyte colony stimulating factor (G-CSF)
•  USE: recovery of Bone marrow specially neutrophil
•  SE: Bone pain

•  Sargramostim
–  MOA: Granulocyte macrophage colony stimulating factor (GM-CSF)
–  USE: recovery of Bone marrow.
–  SE: Fever, headache, dizziness
32
9/11/18
Interferon
•  INF-α
•  USE: Chronic hepatitis B and C, Kaposi sarcoma,
Malignant melanoma
•  INF-β
•  Multiple sclerosis!
!
•  INF-γ
•  Chronic granulomatous disease!
Platelets stimulating
factors
•  Romiplostim, Eltrombopag, Oprelvekin
•  MOA: Stimulate IL-11
•  USE: Thrombocytopenia
•  SE: Fatigue, headache, dizziness
Cancer Antibodies
•  Alemtuzumab
•  Bevacizumab
•  Cetuximab
•  Rituximab
•  Tratuzumab
33
9/11/18
Cancer Antibodies
•  Alemtuzumab

•  MOA: Target CD52
•  USE: Chronic Lymphocytic leukemia

•  Bevacizumab
•  MOA: Binds to Vascular Endothelial growth factor
VEGF
•  USE: Colonrectal cancer, Renal cell carcinoma
Cancer Antibodies
•  Cetuximab
•  MOA: block Epidermal growth factor receptor
!
•  USE: Stage IV colorectal cancer, Head and neck cancer

•  Rituximab
•  MOA: block CD20
!
•  USE: B-cell non-hodgkin lymphoma, CLL, Rheumatoid
arthritis, ITP, IBD.
•  SE: risk of multifocal leukoencephalopathy
Cancer Antibodies
•  Trastuzumab
•  MOA: bind to Human Epidermal growth factor
receptor 2 (HER2/neu), a tyrosin kinase receptor
•  USE: Breast cancer (HER2+)
•  SE: Cardiotoxicity
34
9/11/18
Antibodies - Autoimmune
disease
•  Adalimumab, Infliximab, Certolizumab
•  Daclizumab
•  Eculizumab
•  Natalizumab
•  Ustekinumab
disease
Adalimumab, Infliximab, Certolizumab,
golimumab
•  MOA: TNF-α inhibitor
USE: IBD, Rheumatoid arthritis, Ankylosing

• 
spondylitis, Psoriasis
Etanercept is a decoy TNF-α receptor and not a
monoclonal antibody

disease
•  Eculizumab
•  MOA: Binds to Complement protein C5
USE: Paroxysmal nocturnal hemoglobinuria

• 

•  Natalizumab
–  MOA: bind to α integrin
–  USE: Multiple sclerosis, Crohns disease
l  α4-integrin: WBC adhesion Risk of PML in patients with
JC virus

35
9/11/18
disease
l  Daclizumab!
-  MOA: CD25 (part of IL-2 receptor)!
-  USE: Relapsing multiple sclerosis !
!
l  Ustekinumab!
-  MOA: IL-12/IL-23 !
-  USE: Psoriasis, psoriatic arthritis!
**Calcipotriol !
Others antibodies
•  Abciximab
•  Denosumab
•  Digoxin immune Fab
•  Omalizumab
•  Palivizumab
•  Ranibizumab, Bevacizumab
Antibodies
•  Abciximab
•  MOA: Bind to platelet glycoprotien IIb/IIIa
USE: Patients undergoing percutaneous coronary

• 
intervention
•  Denosumab
–  MOA: inhibitor of RANKL (receptor activator of
nuclear factor kappa-B ligand)
–  Inhibits osteoclast
–  USE: Osteoporosis
36
9/11/18
Others antibodies
•  Digoxin immune Fab
•  MOA: bind to digoxin
•  USE: Digoxin toxicity

•  Omalizumab
–  MOA: prevents IgE binding
  USE: Refractory allergic asthma; prevents IgE binding
to FcεRI
Others antibodies
•  Palivizumab
•  MOA: bind to the fusion protein of RSV

!
•  USE: high risk infants
Others antibodies
•  Ranibizumab, Bevacizumab
!
•  MOA: inhibits vascular endothelial growth factor A (VEGF-
A)
•  Inhibits angiogenesis!
•  USE: Neovascular age-related macular degeneration

•  Bevacizumad: Solid tumors, Colorectal cancer, Renal cell
carcinoma
•  SE: Hemorrhage, blood clots, impaired wound healing
37
9/11/18
Antivirals
Antivirals
•  H. Influenza A, B!
Amantadine
• 
•  Oseltamivir
•  Zanamivir
•  HCV!
–  Ribavirin
–  Simeprevir
–  Sofosbuvir
–  Interferons
•  Herpes virus!
•  Acyclovir
•  Valacyclovir
•  Famciclovir
•  Ganciclovir
•  Valganciclovir
•  Foscarnet
•  Cidofovir
38
9/11/18
Amantadine
•  MOA: Prevent viral fusion and uncapping
•  Increase dopamine availability, block
muscarinic receptor!
•  USE: Influenza A, parkinson’s disease
•  SE: GI distress, dizziness, behavioral effects,

dermatotoxicity
Oseltamivir, Zanamivir
•  MOA: Inhibits Neuraminidases
•  Decrease viral release!
•  USE: Influenza A, B
•  Only in the 1st 48 hrs after onset of symptoms!
•  SE: Retinopathy, throught erythema
Acyclovir, Valacyclovir,
Famciclovir
•  MOA: Guanosine analogs. Monophosphorylated by HSV/VZV
thymidine kinase and not phosphorylated in uninfected cells -> few
adverse effects. #1 viral kinase, #2, #3 by host kinases. !
-  Triphosphate formed by cellular enzymes. Preferentially inhibit viral
DNA polymerase by chain termination.!
Resistance: Mutated viral thymidine kinase.
•  USE: HSV and VZV. Weak activity against EBV. No activity against CMV.
Used for HSV-induced mucocutaneous and genital lesions as well as for
encephalitis.
•  Prophylaxis in immunocompromised patients. No effect on latent forms of
HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral
bioavailability.
•  For herpes zoster, use famciclovir
l  SE: Obstructive crystalline nephropathy and acute renal failure if not
adequately hydrated

39
9/11/18
Ganciclovir,
Valganciclovir
•  MOA: Phosporilated by CMV kinase
•  Inhibits viral DNA polymerase by chain
termination!
•  Guanosine analog!
•  USE: CMV, especially in immunocompromised

patients. Valganciclovir, a prodrug of ganciclovir, has
better oral bioavailability
•  SE: Leukepenia, Neutropenia, Thrombocytopenia,

Nephrotoxicity
•  MOR: Mutated viral kinase.
Foscarnet
•  MOA: Viral DNA/RNA polymerase inhibitor and HIV reverse
transcriptase inhibitor. Binds to pyrophosphate-binding site of
enzyme.
-  Does not require any kinase activation.

USE: CMV retinitis in immunocompromised patients when
ganciclovir fails; acyclovir-resistant HSV.

SE: Nephrotoxicity, electrolyte abnormalities (hypo- or
hypercalcemia, hypo- or hyperphosphatemia, hypokalemia,
hypomagnesemia) can lead to seizures

•  MOR: Mutated DNA polymerase.

Cidofovir
MOA: Preferentially inhibits viral DNA polymerase.
Does not require phosphorylation by viral kinase.!
USE: CMV retinitis in immunocompromised patients;

acyclovir-resistant HSV. Long half-life.
SE: Nephrotoxicity (co-administer with probenecid

and IV saline to reduce toxicity).
40
9/11/18
Ribavirin
•  MOA: Inhibits synthesis of guanine nucleotides by
competitively inhibiting inosine monophosphate
dehydrogenase
•  USE: also used in RSV (palivizumab preferred in

children), Chronic Hepatitis C
•  SE: Hemolitic Anemia, Teratogenic
Simeprevir
• MOA: Protease inhibitor, prevents viral replication!
• USE: Chronic HCV in combination with ledipasvir (NS5A

inhibitor).!
• SE: rash, photosensitivity!

!
Sofosbuvir (Harvoni= Ledipasvir + Sofosbuvir)
• MOA: Inhibits HCV RNA dependent RNA polymerase
acting as a chain terminator!
• USE: Chronic HCV in combination with ribavirin,

simeprevir, ledipasvir (NS5A inhibitor), +/– peginterferon
alfa.!
• SE: Fatigue, headache, nausea.!
Interferons
•  MOA: Block replication of both RNA and DNA
•  USE:!
•  IFN α: Hepatitis A, B, Kaposi’s sarcoma!
•  IFN β: MS!
•  IFN ϒ: NADPH oxidase def.!
•  SE: Neutropenia, myopathy
41
9/11/18
HIV drugs
•  NRTI!
•  Abacavir!
•  Tenofovir!
•  Stavudine!
•  Didanosine!
•  Lamivudine!
•  Zidovudine!
•  Zalcitadine!
•  Emtrictadine!
•  NNRTI!
•  Nevirapine!
•  Efavirenz!
•  Delavirdine!
•  Protease Inhibitors!
•  Liponavir!
•  Atzanavir!
•  Fosamprenavir!
•  Saquinavir!
•  Ritonavir!
•  Darunavir!
•  Indinavir!
•  Integrase Inhibior!
•  Raltegravir!
•  Fusion Inhibitor!
•  Enfurvitide!
NRTI
•  MOA: Competitively inhibit nucleotide binding to
reverse transcriptase and terminate the DNA
chain (lack a 3′ OH group). !
-  Tenofovir is a nucleoTide; the others are
nucleosides. !
-  All need to be phosphorylated to be active. !
-  ZDV can be used for general prophylaxis and
during pregnancy to r risk of fetal
transmission. !
l  SE: Bone marrow suppression (can be reversed

with granulocyte colony-stimulating factor [G-CSF]
and erythropoietin), peripheral neuropathy, lactic
acidosis (nucleosides), anemia (ZDV), pancreatitis
(didanosine). !
l  Abacavir contraindicated if patient has HLA-
B*5701 mutation due to increase risk of

hypersensitivity!
42
9/11/18
NRTI
•  Abacavir **hypersens
•  Tenofovir. no need phosphorylation
•  Stavudine
•  Didanosine. SE: Pancreatitis, Neuropathy
•  Lamivudine **HBV
•  Zidovudine. SE: Aplastic anemia

• USE: Pregnancy
•  Zalcitadine
•  Emtrictadine
NNRTI
•  MOA: Bind to reverse transcriptase at site
different from NRTIs.
-  Do not require phosphorylation to be active or
compete with nucleotides.
-  No need thymidine kinase to be activated!
•  SE: Rash and hepatotoxicity are common to all

NNRTIs.
•  Vivid dreams and CNS symptoms are common with
efavirenz.
•  Delavirdine and efavirenz are contraindicated in
pregnancy.
Protease Inhibitors
•  MOA: Assembly of virions depends on HIV-1
protease (pol gene), which cleaves the
polypeptide products of HIV mRNA into their
functional parts. !
-  Thus, protease inhibitors prevent maturation of
new viruses. !
-  Resist: mutation of Pol gene!
43
9/11/18
l  SE:
l  Hyperglycemia, GI intolerance (nausea,
diarrhea), lipodystrophy (Cushing-like

syndrome). !
l  Nephropathy, hematuria, thrombocytopenia
(indinavir). !
l  Rifampin (potent CYP/UGT inducer) reduces
protease inhibitor concentrations; use rifabutin

instead.!
l  Ritonavir used to inh P450.!
Protease Inhibitors
•  All end in NAVIR!
•  Lopinavir
•  Atazanavir *less ins resistance, also
nephrolithiasis
•  Fosamprenavir
•  Saquinavir: Neutropenia
•  Ritonavir
•  Darunavir
•  Indinavir: Nephrotoxicity (crystaluria),
Hematotoxicity
Integrase Inhibior
•  MOA: Inhibits HIV genome integration into host cell
chromosome by reversibly inhibiting HIV integrase.
Raltegravir Elvitegravir Dolutegravir
•  SE: Hypercolesterolemia, Increase CK
44
9/11/18
Fusion Inhibitor
•  Enfurvitide
-  MOA: Binds to the PG41 subunit of the HIV
envelop protein, blocking the fusion.
-  SE: Skin reaction at injection sites.
•  Maraviroc
-  MOA: Binds CCR-5 on surface of T cells/monocytes,
inhibiting interaction with gp120
Disinfection and sterilization!

!
Goals include the reduction of pathogenic organism counts to safe levels
(disinfection) and the inactivation of self-propagating biological entities
(sterilization). !
Autoclave: Pressurized steam at > 120°C. May be sporicidal. !
l 
Alcohol: Denature proteins and disrupt cell membranes. Not sporicidal. !

l 
Chlorhexidine: Denatures proteins and disrupts cell membranes. Not sporicidal. !

l 
Hydrogen peroxide: Free radical oxidation. Sporicidal.!

l 
Iodine and iodophors: Halogenation of DNA, RNA, and proteins. May be

l 
sporicidal.!
Thanks for share this journey!
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9/11/18

• First Aid Step 1 2017!

• USMLE Road map, Pharmacology. !

• PKA less than 7

Acid Dissociates Bioavailable Base Bioavailable Dissociates

Competitive inhibition VS Non Competitive

• Inhibits by similar substance

• Not similar substance

Competitive inhibition VS Non Competitive

Competitive inhibition VS Non Competitive

• Bioavilability (F): Fraction of the drug that get to

• Clearance: volume of plasma cleared of drug per unit

• Loading dose: fill the volume of distribution (Vd) to

P-450 Drug Substrate Inhibitirs Inducers

COKE + Grape fruit with your PI!

Drug-> active Prodrug-> toxic

Probenecid competes with WEAK ACIDS.

Competitive Antagonist VS Non Competitive

Chemical antagonist (Antacids)

l Widely used criteria developed to reduce

antidepressants, benzodiazepines, opioids

l PPIs (q risk of C difficile infection)!

M2 GI ↓ Heart rate, contractility

↑ Exocrine gland secretion

↓ NE, Epi release!

D1 Gs Relax renal vascular

D2! G i! Modulate neurotransmitter release!

↑ nasal bronchial mucus production

H2 Gs ↑ Gastric acid production

V1! G q! ↑ Vascular contraction!

V2! G s! ↑ H2O reabsorption on CT!

• MOA: Cholinesterase inhibitors. NOT EFFECT ON

• SE: Exacerbation of COPD, Asthma, PUD, nausea,

• MOA: Break the bond between the

• USE: Organophosphate poison

• MOA: Block muscarinic receptor

• USE: Bradycardia, Organophosphate toxicity

• SE: Cycloplegia – worse glaucoma; ↓ sweat - ↑

• **Fenoldopam: D1 partial agonist.

• Alpha Agonist • Beta blockers

• 6-Mercaptopurine (6MP), 6-Thioguanine (6-

• MOA: Purine analog, Inhibits DNA polymerase,

• MOA: Pyrimidine analog, inhibits of DNA

• USE: Colon cancer, Pancreatic cancer, Basal cell

• SE: Myelosuppression, Photosensitivity

• USE: ALL, Lymphomas, Choriocarcinoma,

• USE: Melanoma, CML, Sickle cell disease (↑ HbF)

• SE: myelosuppression, GI upset

• USE: Testicular cancer, Hodgkin lymphoma

• SE: Pulmonary fibrosis, Skin hyperpigmentation,

• USE: Wilms tumor, Ewing sarcoma,

• USE: Solid tumors, leukemias, lymphomas

• USE: CML, Bone marrow ablation for

• SE: Severe myelosuppression, Pulmonary fibrosis,

• USE: solid tumors, leukemia, lymphomas

• SE: Myelosuppression, Hemorrhagic cystitis

• Prevented by MESNA. Binds to toxic

• USE: Brain tumors

• SE: Convulsions, dizziness, ataxia

• USE: Testicular, bladder, ovary, lung carcinomas

• SE: Nephrotoxicity, Ototoxicity,

• Amifostine prevents nephrotoxicity

• USE: ovarian, Breast cancer

•  First Aid Step 1 2017!

•  USMLE Road map, Pharmacology. !

•  PKA less than 7

•  Inhibits by similar substance

•  Not similar substance

•  Bioavilability (F): Fraction of the drug that get to

• Clearance: volume of plasma cleared of drug per unit

•  Loading dose: fill the volume of distribution (Vd) to

l  Widely used criteria developed to reduce

l  PPIs (q risk of C difficile infection)!

•  MOA: Cholinesterase inhibitors. NOT EFFECT ON

•  SE: Exacerbation of COPD, Asthma, PUD, nausea,

•  MOA: Break the bond between the

•  USE: Organophosphate poison

•  MOA: Block muscarinic receptor

•  USE: Bradycardia, Organophosphate toxicity

•  SE: Cycloplegia – worse glaucoma; ↓ sweat - ↑

•  **Fenoldopam: D1 partial agonist.

•  Alpha Agonist •  Beta blockers

•  6-Mercaptopurine (6MP), 6-Thioguanine (6-

•  MOA: Purine analog, Inhibits DNA polymerase,

•  MOA: Pyrimidine analog, inhibits of DNA

•  USE: Colon cancer, Pancreatic cancer, Basal cell

•  SE: Myelosuppression, Photosensitivity

•  USE: ALL, Lymphomas, Choriocarcinoma,

•  USE: Melanoma, CML, Sickle cell disease (↑ HbF)

•  SE: myelosuppression, GI upset

•  USE: Testicular cancer, Hodgkin lymphoma

•  SE: Pulmonary fibrosis, Skin hyperpigmentation,

•  USE: Wilms tumor, Ewing sarcoma,

•  USE: Solid tumors, leukemias, lymphomas

•  USE: CML, Bone marrow ablation for

•  SE: Severe myelosuppression, Pulmonary fibrosis,

•  USE: solid tumors, leukemia, lymphomas

•  SE: Myelosuppression, Hemorrhagic cystitis

•  Prevented by MESNA. Binds to toxic

•  USE: Brain tumors

•  SE: Convulsions, dizziness, ataxia

•  USE: Testicular, bladder, ovary, lung carcinomas

•  SE: Nephrotoxicity, Ototoxicity,

•  Amifostine prevents nephrotoxicity

•  USE: ovarian, Breast cancer

•  SE: Myelosuppression, Alopecia, Hypersensitivity

•  USE: Solid tumors, Leukemias, Hodgkin

•  SE: Neurotoxicity (Vincristine), Blast bone marrow

•  USE: Solid tumors, Leukemia, Lymphomas. Small

•  SE: Myelosuppression, GI upset, Alopecia

•  USE: Colon cancer (Irinotecan), Ovarian and small

•  SE: Myelosuppression, diarrhea

•  MUST confirm KRAS mutation before use it *act on KRAS mutated

–  USE: non Small cell lung carcinoma

•  VEmuRAF-enib (V600E mutated, BRAF inhibitor.

•  USE: Metastatic melanoma

•  USE: CML, GI stromal tumors

•  SE: Fluid retention. Ankle and periorbital edema.

-  Multiple myeloma, mantle cell lymphoma !

-  Peripheral neuropathy, herpes zoster

l  Oncologic emergency triggered by massive

-  Prevention and treatment of tumor lysis

•  SE: Cushing’s, Osteoporosis, Adrenocortical atrophy,

•  Prophylaxis: H2 blocker or PPI, Ca2+, Vit. D,

•  Prednisone, Prednisolone: CLL, non-Hodgkin lymphoma

• SE: Nauseas, Vomiting, Diarrhea, Yellow vision, arrhythmias,

•  USE: Atrial Arrhythmias (SVT,

• USE: SVT (dx and tx) first line.

-  Chronic stable angina in patients who cannot

-  Luminous phenomena/visual brightness,

•  MOA: Osmotic diuretic, increase

•  SE: Ototoxicity, Hypokalemia, Dehydration, Sulfa allergy,

•  MOA: Inhibits NCC

•  SE: Hyperglycemia, Hyperlipidemia, Hyperuricemia,

•  MOA: Competitive inhibitor of aldosterone

•  SE: Spironolactone cause gynecomastia,

•  MOA: Block eNaC channels in the collecting tubule.

•  SE: All causes Hyperkalemia, arrhythmias.

•  USE: hyperaldosteronism, Conn syndrome, K

•  MOA: inhibits ACE, decrease Angiotensin II. Decrease

•  USE: Hypertension (prevent heart remodeling), HF,

•  Decrease mortality in CHF

•  **Can cause 1st DOSE HYPOTENSION when combined