Pharmacology

Review
2012

Mrunal M. Koche
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Table of Contents

Basic Pharmacology Page 3

Autonomic Nervous System Page 10

Parasympathetic System Page 13
Sympathetic System Page 17

Central Nervous System Page 19

Anti-Seizure Drugs Page 23
Anesthetics Page 26
Anti-Parkinson’s Drugs Page 28
Alzheimer’s Drugs Page 30
Opiates Page 30

Cardiovascular Pharmacology Page 32

Anti-Hypertensives Page 34
Anti-Arrhythmics Page 39
Anti-Anginal Page 42
Anti-Hyperlipidemics Page 45

Endocrine Pharmacology Page 47

Anti-Psychotics Page 56
Typical (conventional) anti-psychotics Page 58
Atypical Anti-psychotics Page 58
Anti-Mania & Anti-Anxiety Page 59

Hematology Page 60
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Gastroenterology – Anti-ulcers Page 63

Anti-emetics Page 64
Emetics Page 65
Anti-Diarrheal Page 65

Antibiotics Page 66

Antifungals Page 73

Antivirals Page 74
Anti-TB Page 77
Anti-Protozoals Page 79
Anti-Malarial Page 80

Anti-Inflammatory Page 81
Migraine drugs Page 84
Asthma drugs Page 84
Osteoarthritis Page 87
Rheumatoid Arthritis Page 88
Gout Page 89

Antineoplastic Page 90
Cancer Antibiotics Page 91

Miscellaneous drugs Page 92

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Basics and ANS

New Drugs approved 2011 

 Dificid (Fidaxomicin)  An Antibiotic used to treat C. Difficile Diarrhea.
 Tocilizumab  Antirheumatic used to treat Arthritis.
 Romidepsin  Antineoplastic, used in treatment for Cutaneous T-Cell Lymphoma.
 Desirudin  Anticoagulant, used to treat DVT

Therapeutic Index (TI)  Is the Lethal Dosage of a drug in 50% over the Effective Dosage in 50%.
The Higher the TI the Safer the drug will be. ( LD50 ), The TI is determined via Animal Studies.
ED50
 So if a drug has an LD of 6 and an ED of 5 the total TI = 1.2. Whereas, as drug with LD of 25 and
an ED of 5 the TI = 5.
o This is important to know b/c then it gives a “leeway” if you make a mistake in the
dosage of a certain drug, such as overdosing slightly.
o Drug with low TI means you can only take it in such small mg’s and any slight overdose
can be deadly.
Human Studies & 4-Phases 

 Phase – 1: This is where the beginning / initial pharmacological evaluation is done, using normal
volunteers to determine the SAFETY for Humans.
 Phase – 2: Here Patients are used in the Limited controlled evaluation to see if the Drug Works.
 Phase – 3: Is an Extended Clinical Trial in which Patients are used to test for How Well the Drug
works & the Common side effects.
 Phase – 4: This is where the FDA does surveillance of the new approved drug. They have
Volunteers report any adverse-side effects.

Pregnancy Safety Categories

Categories Animal Studies Human Studies Drugs

A - ve - ve Folic Acid
B - ve Not done Zidovudine (AZT)
+ ve - ve
C + ve Not done Aspirin
Not done Not done
D + ve + ve ACE-Inhibitors
X + ve + ve Isotretenoin
Both Category D and X are bad, But category X-drugs are worse due to the Risks being higher than the
Benefits, whereas in category D the even though it is bad the Benefits are higher than the Risks.
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Pharmacodynamics & Pharmacokinetics 

 Pharmacodynamics is how the drug works
 Pharmacokinetics is how the body will react to the drug.
- Absorption
- Distribution, Metabolism and Excretion
Pharmacokinetics:
 Absorption – When giving drugs via Orally, IM, or Subcutaneously there is a
possibility to lose the drug.
 When given in an IV-line absorption will not take place thus there is NO
possibility of losing the drug.
 Most drugs are Lipid soluble b/c they have to cross the Lipid Bilayer.
 The Free uncharged (Unionized) drugs contribute to the concentration
gradient. The Unionized& Lipid soluble are the only drugs that can cross
the lipid bilayer membrane. The Ionized drugs are excreted.
 The Greater the surface area and vascularity the better the absorption.

Henderson-Hasselbalch Equation 

 Nonionized = Lipid soluble

 Ionized = water soluble (thus excreted)
i. pH – pKa = log Ionized .
Unionized
ii. When the pH – pKa = a negative # it’s an Acidic media
iii. When the pH – pKa = a Positive # it’s an Basic media
1. Acid in an Acidic media is nonionized.
2. Acid in Basic media is Ionized.
**Same goes for basic drugs. **

 First know if the drug is an Acid or a Base, and then calculate to see what the media is using pH –
pKa.
 Once you determine the number, such as -1, -2 or +1, +2 then use that value to figure out the %
ionization or nonionization.
o For example if the media is acidic and the drug is acidic then it will be nonionized thus
the % of nonionized will be greater than the ionized %.

% of Free (unionized) drug in relation to pH.

pH – pKa -3 -2 -1 0 +1 +2 +3
Weak acid 99.9% 99% 90% 50% 10% 1% 0.1%%
Weak base 0.1% 1% 10% 50% 90% 99% 99.9%
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Plasma Level curve 

 Drugs MUST reach the MEC (minimum effective concentration) in order

to work.
 Cmax = is the maximum / peak drug level
 Tmax = is the time at which it reaches the Cmax
 Duration of action = is the time of plasma concentration usually > MEC

Bioavailability (f) 
 This is the measure of the dose fraction that gets into the systemic circulation.
 IV doses have 100% bioavailability (f = 1). F = AUC-po / AUC-iv
Bioequivalence 
 The 2 cmpds must have the 
 The same Bioavailability
 And same Rate of Absorption
 The Faster the rate of absorption  the smaller the Tmax and The Faster we will
reach Cmax.

First-Pass Effect 
 This occurs ONLY with Oral drugs basically explains that drugs that are taken orally -
 Pass through the liver  where they lose some of their dosage before reaching
the circulation.

Distribution  correlates the dose with the plasma level at time Zero (0).
Vd = Dose .
C0 (conc time at zero)

**** Some Normal Lab Values 

 Plasma Volume – 3L, Blood Volume – 5L, ECF – 12-14L & Total body water – 40-42L

Biotransformation (metabolism)  This is the process in which water solubility is increased, basically to
undergo elimination.
 Phase 1: Modification of the drug molecule by  Oxidation, Reduction and Hydrolysis
 Phase 2: Conjugation occurs by the enzymes Transferases.
i. Glucuronidation  Reduces the activity of the drug in Neonates.
ii. Acetylation  Drug induced SLE such as  Hydralazine (used for anti-HTN),
Procainamide (used for anti-arrhythmia) & Isoniazid (used for TB).
iii. GSH (glutathione) conjugation  Decrease in the GSH is associated w/
Tylenol (acetaminophen) hepatotoxicity.
 Acetylation basically gets rid of the drug, so if the Pt is a
Poor acetylator then they won’t get rid of the drug as easily.
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Cytochrome P450 

 Has a major role in Phase 1 of the drug metabolism process.

 Localized in the liver cells, which REQUIRES O2 & NADPH.

Drugs that INDUCE CP450:

 Anticonvulsants such as  Barb, Phenytoin, & Carbamazepine.
 Antibiotics such as  Rifampin
 Chronic alcohol and Glucocorticoids, Quinidine, Griseofulvin & St. John’s Wart
** This is Necessary to know b/c they increase the metabolism of drugs via inducing CyP450
which in-turn reduce their effectiveness. ***

Drugs that INHIBIT CyP450:

 Anti-ulcer Medicines such as  Cimetidine & Omeprazole
 Antibiotics such as  Chloramphenicol, Macrolides, Ritonavir & Ketoconazole
 Acute Alcohol, Amiodarone, Ciprofloxacin, Sulfonamides, & Isoniazid
*** These drugs and products Decrease the metabolism of drugs that are metabolized by
CyP450 thus Increase the toxicity level.
 Ex  Theophylline is an Asthma medication, when toxicity occurs it can
cause Seizures and Arrhythmia.
 Grapefruit Juice  Also INHIBITS CyP450.
 The Furanocoumarins in the grapefruit juice inhibits the
metabolism of  Alprazolam (panic attack) , Atorvastatin,
Cisapride (GI motility) , Cyclosporine (immunosuppressant)
& Midazolam (pre-anesthetic).
Elimination (Half-life t1/2) 

 This occurs via the Kidney, but excretion can also occur via the Bile ducts, lungs and Sweat.
 Half-Life (t1/2) is the time it takes to eliminate half of the given amount of the drug, or decrease
the amount in the plasma by 50%.

Zero-Order elimination: constant Amount of the drug is eliminated

 These are independent of the plasma concentration; the Half-Life is variable
such as seen in  Ethanol, toxic dosage of Aspirin, and High doses of Phenytoin.

First-Order elimination:
 Constant Fraction (t1/2) of the drug is eliminated.
 Most drugs fall into this category.
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Clearance (Cl) 
 Is defined as the volume of blood cleared of a drug per unit time.
 The rate of Elimination = GFR + active secretion – reabsorption.
 Inulin is used to estimate GFR (b/c it is neither secreted nor is it reabsorbed), OR CK levels in the
blood.
 Normal GFR is around 120ml/min

****Must know equations. ***

Vol distribution (VD) = Dose / C0 Half life (t1/2) = .7/k Clearance (Cl) = K x Vd or
Cl= rate of elimination / plasma concen.

Infusion rate (Ko) = Cl x Css Loading dose (LD) = Vd x Csss Maintenance dose (MD) = Cl x Css
Css = dosing rate/Cl
K = Elimination constant Css = Steady state Conc = Dosing interval

Steady state 
 Describes the Rate going IN = Rate going OUT
 Plateau principle – Is the time that it takes to reach the steady state.

EX  when administering (IV) a 100units of a drug at (dose interval) equal to the original amount
every half-life of 4hrs. When will it reach the steady state? At 7 half-life’s.

 So at 100 the half-life is 50 BUT it says you administer another 100units at every half-life, so
it goes to 150 and etc… you do this until the steady state is reached which is equivalent to
the original administration of 100 (at 7 half-life’s in this case).

Pharmacodynamics  How the drug works.

 This is describes the drugs ability to bind to the desired receptor in order to produce a response.
 The drug MUST have affinity for the receptor as well as must have efficacy.

Potency  Is a comparative measure b/w 2 drugs that produce the Same Effect.

This graph shows that the 2 drugs are parallel, meaning they work on the
same receptor. The difference is that Drug A is more Potent than Drug B, but,
since both drugs reach the 100% that tells they are both produce an equal
response (same efficacy).
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These 2 drugs are NOT parallel stating that they work/bind on 2 different
receptors. Thus you are unable to compare their affinity since they bind to 2-
different receptors.
Only thing we can conclude is that Drug X is more potent than Drug Z as well as
has Higher Efficacy.

Agonist  Must have affinity and efficacy in order to work.

Antagonist  Must have affinity with Zero efficacy. Does this via  binding to the receptors and
blocking them, But the agonist must be present for the prevention.

This is showing Full & Partial agonist (B & AC).

All 3 drugs bind to the same receptor, BUT drug B has the maximum efficacy (full
agonist) whereas, drugs A & C show partial efficacy.
Drug A is more potent than B & C, but it is more potent only up to 50%
compared to B.

Antagonist  This graph is displaying the effects when an Antagonist is put

with an Agonist. The graph Shifts to the Right the lines are parallel thus
stating that both Compete for the same receptor. Thus it is Competitive
Antagonism.
When the slopes are shifted to the right but are NOT parallel then it is non-
competitive antagonist (not competing for the same receptor).

Potentiation  During potentiation the graph Shifts to the Left, stating that
there is an Agonist added which will Increase the potency bringing it closer to
the Y-axis.
EX: Benzo’s potentiate GABA….. Amphetamine potentiate NE.

Ceiling Effect 
 This describes the effects of the Partial Agonist when used alone
VS. when used with a Full agonist (agonist with an agonist).
 So when using the Partial agonist the ceiling effect is only 50%.
 Whereas, using the Partial agonist with a Full agonist with 100%
efficacy brings the effect down to 50% (displaces the effects of
the full agonist).
 It is NOT an Antagonist but it has Zero efficacy.
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Receptors 
 When an agonist binds to a receptor an effector is activated thus initiating the Signaling
Mechanism.
 Most Receptors are coupled via the G-Protein, thus binding to the G-protein will stimulate
Adenylate Cyclase which will convert ATP  cAMP.
 cAMP is a SECOND MESSANGER that activated Protein Kinase A  pk.A
Phosphorylates tissue-specific substrate enzymes that produce an
effect.

GS Proteins (Stimulatory) 
 GS protein example are  β-adrenergic (affects the heart, decreases BP), and
D1-Dopamniergic (stimulates heart and Kidneys).
 When drugs bind to the GS proteins it leads to activation of Adenylyl Cyclase 
which causes an INCREASE in the production of the SECOND MESSANGER cAMP 
Which ACTIVATES Protein Kinase A.
 Activation of Protein Kinase A  Activates Phospholipase A 
which Phosphorylates enzyme proteins

GI Protein (Inhibitory) 
o GI-protein receptor examples are  α-2 adrenergic (Inhibits NE) and M2-
Muscurinic (cholinergic slowing down the heart).
 When drugs bind to the GI proteins it leads to Inhibition of Adenylyl Cyclase 
which causes a DECREASE in the production of the SECOND MESSANGER cAMP 
Which DEACTIVATES Protein Kinase A.
 Deactivation of Protein Kinase A  Deactivates Phospholipase A 
which Dephosphorylates enzyme proteins.

Gq Proteins (Stimulatory) 
 The Gq protein is a stimulatory protein which activates Phospholipase C, once a drug
has bound to it.
 Upon activation of Phospholipase C  it INCREASES the production of the SECONDARY
MESSANGERS IP3 and DAG.
 IP3  causes the release of Ca2+.
 The Ca2+ combines with DAG and activates Protein Kinase C which
Phosphorylates enzyme proteins.
 Gq receptor example are  M1 & M3-muscurinic and α-1 adrenergic (in blood vessels
causing constriction).
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Cyclic GMP (cGMP) & NO-signaling  cGMP is a SECOND MESSENGER in Vascular SMs.
 Once a drug binds to the endothelial cells it Activates NO  which INCREASES production of
cGMP  this now will Dephosphorylate Myosin light chains, preventing them from interacting
with Actin thus Vasodilate.
o Examples of cGMP and NO signaling are  H1-histaminic (causes
hyperemia/vasodilation), M3-muscurinic, Nitroglycerine (activates cAMP and
vasodilates) and Sodium-Nitroprusside (drug of choice in emergency HTN Pts).

Receptors functioning as Transmembrane Enzymes 

o Insulin & GFs such as – Epidermal GF (EGF), and PDGF

Receptors for Cytokines 

 ERP, Somatotrophin, and IFNs.
 When these receptors are activated they stimulate JAKs  which phosphorylate signal
transducers and activators of transcription molecules such as STAT.

Autonomic Nervous System (ANS):

ANS consists of the Parasympathetics and Sympathetics.

 Parasympathetic 
 Is like “pressing on a brake” via Acetylcholine.
 Slows down the HR, Bradycardia, Maintains Resting body functions, Digestion
and save energy.
 Parasympathetic works via the cholinergic system remember ACETYLCHOLINE.

 Sympathetic 
o Is “accelerating, pressing on the pedal” also called as adrenaline rush, Fast and causes
tachycardia. It is the Flight or Fight response.
o Also called as the Adrenergic System remember NOREPINEPHRINE.

***All preganglionic neurons release Ach  that bind to the nicotinic receptors. ***

Postganglionic PARASYMPATHETIC 
 There is a release of Ach  binds to the muscarinic receptors.

Postganglionic SYMPATHETIC 
 Release NE
Adrenal Medulla 
 Has no postganglion thus its releases Preganglionic Acetylcholine  binds to nicotinic receptors
and causes the release of hormone (epinephrine).
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Response to Parasympathetic Stimulation:

 This is the Cholinergic system due to the Ach.
Drugs that stimulate parasympathetic 
 Cholinergic Agonist, Parasympathetic drugs, Parasympathomimetics, ACE-I, and
Anticholinesterase.
Drugs that Inhibit parasympathetics 
 Anticholinergics, Cholinergic Antagonists, and Parasympatholytics.

Response to Sympathetics Stimulation:

 Also called as the Adrenergic System due to release of adrenaline NE and Epinephrine.
Drugs that Stimulate the Sympathetic 
o These are called as Adrenergic Agonist, Sympathetics drugs, and Sympathomimetics.

Drugs that Inhibit the Sympathetic 

o These are called as Adrenergic Antagonist (blockers), Sympatholytics OR Beta Blockers.

Control of Blood Pressure BP = TPR x CO and CO = HR x SV

 Increased BP will result in  Increase in the baroreceptor pressure, this will cause the
Parasympathetic response to be stimulated thus  Decreasing the HR, and Inhibit the
Sympathetics response  Decrease in Force of contraction, vasoconstriction and Decrease TPR.
 Increase TPR by α-1 stimulation (vasoconstriction) this leads to  Reflex bradycardia via
increasing the M2.
 Decrease the TPR by β-2 stimulation (vasodilation) leading to  Reflex Tachycardia via
increasing B1.

*** When there is a DECREASE in BP it lead to  Decrease renal blood flow, this stimulates Release of
Renin thus  increasing Angiotensin  Angiotensin 1 is converted to Angiotensin 2 (vasoconstrictor)
thus  Increasing the TPR.
While Renin increases angiotensin, it also simulates the release of aldosterone causing  Salt & Water
retention. ****

Parasympathetic Effect on the Eye  (pupil & Lens)

 Parasympathetic stimulation on the eye causes  Miosis (constriction) & Accomodation.
 It does this via the Muscarinic receptor on the Sphincter muscles of the eye &
the Ciliary Muscle.
 If there is a Muscarinic Antagonist it will lead  Mydriasis & Cycloplegia (paralysis of
accommodation).
Sympathetic Effects on the Eye  (Only the Pupil)
 When there is an Adrenergic Stimulation to the eyes it affects the  Radial muscles of the eye
via (α-1 stimulation).
 Sympathetic stimulation causes the PUPIL to  Dilate (Mydriasis).
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Glaucoma 
 Glaucoma is an abnormal increase in the intraocular pressure which damages the Optic nerve.
o The pressure comes from the increased production of Aqueous humor OR decrease in
the drainage (outflow) through the Canal of Schlemm.

Subtypes of Glaucoma 
1. Primary:
 Angle-closure Glaucoma  more serious type caused due to drugs or
surgery.
 Open-Angle Glaucoma  MOST COMMON can be controlled by drugs.
2. Secondary:
 Occurs usually after Lens (Cataract) extraction.
3. Congenital:
 Requires surgical treatment.

Drugs to treat Glaucoma 

o Direct Acting Cholinomimetics (parasympathetics) :
 Carbachol & Pilocarpine (more popular)
o These drugs activate the M receptor  contraction of the ciliary
muscle and  increase the drainage through the Canal.

o Indirect Acting: AchE-Inhibitors

 Ecothiophate  Increases the outflow through the Canal of Schlemm.

o β-blockers: think of suffix “olol”

 Betaxolol and Timolol
o These drugs block NE at the Ciliary Epithelium thus  decreasing
the production of aqueous humor.
o Sympathomimetic:
 Apraclonidine (α-2 agonist)  this decreases the NE release at the
prejunction leading  decrease in the aqueous humor.
 Epinephrine Increases the outflow through the Canal of Schlemm.

o Carbonic Anhydrase Inhibitors:

 Acetazolamide and Dorzolamide
o These Decrease the HCO3 leading to  decrease in AH.

o Prostaglandin PGF2 (α-analog):

 Latanoprost
o Increases the drainage (outflow) through the canal & meshwork
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Parasympathetic System:

 Ach is synthesized via 

o Choline + Acetyl CoA Choline acetyl transferase (ChAT)  Ach
 Ach is released via 
 Due to influx of Ca2+ causing the release of Ach from the nerve endings at the
NMJ to the its corresponding receptors  leading to muscle contraction.

Ach Release is INHIBITED by 

 Botulinum Toxin:
 Botulism causes Food Poisoning  leads to Muscle Weakness and
paralysis.
Ach Metabolism 
 Ach is metabolized by the enzyme AchEsterase.
o The inhibition of AchE is done by indirect acting Cholinomimetics.
Ach Receptors  ****
 Cholinomimetic drugs (direct acting)
o Nicotinic = Nicotine
o Muscarinic = Bethanechol, Methacholine, & Pilocarpine.

 Cholinoreceptor Blockers
o Nicotinic Neuron (NN) = Hexamethonium & Mecamylamine (these are
Ganglionic blockers)
o Nicotinic Muscular (NM) = Tubocurarine, Atracurium, & Succinylcholine
(These work at the NMJ, they are skeletal muscle relaxants).
o Muscarinic = Atropine, Benzatropine, Glycopyrrolate, Scopolamine,
Toldterodine & Oxybutynin (these 2 are commonly used for
urinary incontinence & urgency)

Muscarinic Receptor Activation  Most drugs works here

 The M1 receptor is for the GI glands, M2 receptor for the Heart & M3 everything else.
 M1 & M3 work via Gq – Increase Phospholipase C leading to increase in IP3, DAG & Ca2+.
 M2 works via Gi – decrease adenylate Cyclase leading to decrease in cAMP.
1. EYE –
o M3 on the Sphincter muscle causes Contraction (Miosis)
o M3 on the Ciliary muscle causes Accommodation.

2. HEART –
o M2 on the SA node leads to Bradycardia.
o M2 on the AV node leads to decrease in conduction velocity.
o NO Effect on the Ventricular system (parasympathetic doesn’t effect it).
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3. LUNGS –
o M3 in the bronchioles leads to Constriction (bronchospasm).
4. GI –
o M1 on the Glands causes Acid Secretion.
o M3 in the stomach causes increase in motility.
o M3 in the intestines causes contractions (Diarrhea).
5. URINIARY BLADDER –
o M3 on the Detrusor Muscle causes contraction with relaxation of the sphincter
leading to  Urinary incontinence. (Give these Pts tolterodine, oxybutynin or
Detrazole).
6. GLANDS –
o M3 Causes secretion leading to  Sweating, Salivating, & Lacrimation.
7. BLOOD –
o M3 Causes Vasodilation via NO.

Muscarinic Agonist 
 Bethanechol: Is used in treatment for Ileus (no bowel movement) & Urinary
Retention.
 Methacholine: Is used for Diagnostic Bronchial Hyperactivity. Methacholine
Challenge test for asthma. *****
 Pilocarpine: Used for Glaucoma & Xerostomia.

Indirect Acting Agonists 

 AchE-Inhibitors:
o Endrophonium: Used for Myasthenia Gravis Diagnosis.
o Physostigmine: It is a tertiary amine that ENTERS the CNS. Antidote for OD of
atropine.
 Neostigmine & Pyridostigmine: These are quaternary amines and DO NOT enter CNS.
o Used to treat Myasthenia Gravis, Ileus, and Urinary retention.
 Alzheimer’s drugs 
 Tacrine, Donepezil, Gallantamine, & Rivastigmine.

Insecticide Toxicity 
 Malathion & Parathion:
 These are transformed by insect CypP450 into AchE-Inhibitors thus
causes accumulation of Ach. Leading to 
 Bradycardia, Bronchospasm (constriction), Diarrhea,
Miosis, Urinary Incontinence, increase in sweating,
salivation and lacrimation.
 Treat with  Atropine (anticholinergic) + Pralidoxime (2PAM). Ex:
Kid in a farm ****.
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Parasympatholytics (anticholinergics) anticholinergic are used to treat Asthma.

 ATROPINE –
o This is a Muscarinic Receptor antagonist leads to 
 Tachycardia, Constipation, Urinary Retention, Cycloplegia & Mydriasis,
Decrease in sweating, salivation, & lacrimation, Hyperthermia and
Bronchodilation.
 Atropine is CONTRAINDICATED for glaucoma Pts (so look for Pts
presenting with eye pain before trying to treat hypotension, nausea
perspiration etc...
 Drugs that have anticholinergic side effects 
 Antihistamines, Cold Meds, Antidepressants, and Antipsychotics.
 Pts who OD to these give them  Physostigmine (AchE-inhibitor).

Clinical Anticholinergics 
 ATROPINE: Antispasmodic, Antidiarrheal, & treatment for Cholinergic toxicity.
 Used during anesthesia to block bradycardia (in normal low HR Pts).
 TROPICAMIDE: Causes quick 2hr  Mydriasis and Cycloplegia.
 IPRATROPIUM: Treatment for Asthma & COPD, doesn’t affect the mucus.
 SCOPOLAMINE: Treatment for Motion Sickness. Can also block Angiotensin 2-receptors.
 GLYCOPYRROLATE: Used to treat Peptic Ulcers and Antispasmodic.

Nicotinic Blocking Agents  These are Ganglion blockers

 These are competitive inhibitors they block BOTH parasympathetic and sympathetic effects.

Parasympathetic is Dominant in  Heart, GI, GU, Pupil & the Sphincters.

o Thus blocking the Parasympathetic ganglion leads to 
 Tachycardia, Mydriasis, Decrease in GI motility (constipation), Urinary
retention, and Xerostomia (dry mouth).

Sympathetics are Dominant in  Blood Vessels, & Sweat glands.

o Blocking the sympathetic ganglion leads to 
 Vasodilation, Dilation and decrease venous return, and Anhydrosis (cant
sweat).

Ganglion Blockers  Only blocks reflex

 Hexamethonium and Mecamylamine Ganglion blockers block autonomic reflexes

How do you identify if the action of a drug on the heart is Direct or due to Autonomic reflex
response?
 Ganglion blockers will block ONLY Bradycardia caused by α-1 agonist causing
vasoconstriction. Due to Reflex Bradycardia.
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Neuromuscular blockers  Skeletal Muscle Relaxant

 These block Ach at the nicotinic receptors of the skeletal muscles.
 Used as muscle relaxants during Anesthesia, and for endotracheal intubation.

2-types of neuromuscular blockers 

1. Non-depolarizing (Competitive):
a. These are Nicotinic Receptor Antagonists.
b. Competitive  means that the affect can be reversed by increasing Ach.
c. MOA  These block Ach causing paralysis of the eyes & face which
progresses to the limbs and respiratory muscles.
o MOAs DO NOT affect the cardiac or SMs or consciousness.
Competitive drugs 
 D-tubocurarine, Pancuronium, and Atracurium.

2. Depolarized (non-competitive):
a. These are Nicotinic Receptor Agonist.
b. Such as Succinylcholine.
c. Non-competitive  Means that it cannot be reversed by giving Ach.
d. When adding succinylcholine the membrane gets desensitized thus 
becoming unresponsive to Ach.
i. Succinylcholine is metabolized by pseudocholine esterase and has a
short duration of action.
ii. Hyperkalemia is a life-threatnining side effect – presents as tall-
peaked t-waves, prolonged PR-intervals, & Wide QTS complex.

Malignant Hyperthermia 
 There is a life-threatening increase in body temperature, about 1.80F every 5min.
 Can be caused due to drugs such as 
o Succinylcholine and or D-tubocurarine also with inhalation of anesthetics.
 Treatment 
 Dantrolene

Spasmolytics 
 These are skeletal muscle relaxants that act in the CNS, Spinal Cord or directly on the muscle
itself. Such drugs as 
 Benzodiazepines – used to calm people down. Benzos potentiate GABAa
receptors thus reducing the tone of spinal motor neurons.
 Baclofen – Is a Direct Agonist works on GABAb receptors in the Spinal Cord and
is less sedative than benzos.
 Dantrolene – Acts directly on the skeletal muscles to decrease contraction. Does
this by Blocking Ca2+ release from the SR. Used to treat Malignant Hyperthermia.
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Sympathetic System: Adrenergic System

Norepinephrine (NE) is synthesized from Tyrosine.

 Tyrosine  (tyrosine hydroxylase)  DOPA  (DOPA decarboxylase)  Dopamine  (dopamine β-
hydroxylase)  NE.
o NE is metabolized MAO which gets rid of the NE from the mobile pool, but NOT the ones
that are stored in granules.
o 2 types of MAOIs 
 MAOI type A – for Tx of depression these include Phenelzine &
Tranylcypromine.
 MAO type B – Tx for Parkinson Selegilline which metabolizes dopamine.

Adrenergic Receptors 
 α-1 – found in the blood vessels causing vasoconstriction thus leading to INCREASE in TPR
leading to  Reflex bradycardia.
 α-2 – Decreases the sympathetic outflow (like a blocker).
 β-1 – Works on the heart leading to  Increase force of contraction, Increase conduction
velocity and Increase in HR.
 β-2 – Found in the bronchioles and uterus. Causes vasodilation leading to  Decrease in TPR 
leading to Reflex tachycardia.
 D-1 (dopaminergic) – Found in the renal leading to Vasodilation leading to increase in the GFR.

α-1 Agonists  vasoconstrictors

 Phenylephrine – decongestant, mydriasis without cycloplegia & reflex bradycardia.
 Methoxamine – Used to Tx PAT.

α-2 Agonists  decrease sympathetic

 Apraclonidine – used to treat glaucoma.
 Clonidine & α-Methyldopa

β-Agonists  (β-1 increases HR, SV & CO…. β-2 vasodilates & decreases TPR)
 Dobutamine – has β-1 greater than β-2.
 Used for Acute CHF
 Isoproterenol – has β-1 = β-2 and is used to Tx Bronchospasm (asthma).
β-2 agonists 
 Albuterol, Metaproterenol, Salmeterol (all these are used in treating Asthma).
 Terbutaline – is a bronchodilator and a Tocolytic (used to prevent premature labor).
 Ritodrine – is a Tocolytic (commonly used to prevent premature labor).
*** Salmeterol is a longer acting β-agonist than albuterol***
***Ex:  α-1 agonist contraction of uterus …. β-2 agonist relaxation of uterus***
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NE and Epi are both α & β agonists.

 NE contains α-1, 2 & β-1 (β-1 increases cardiac contractility).
 Epinephrine has all 4 of the receptors properties.
o In low doses of epinephrine β is more sensitive
 Since β is more sensitive  increase HR & contractility and Vasodilation leading
to decrease in TPR.
o In high doses of epinephrine α-dominates  reflex bradycardia.
 Epi-reversal 
 When a high dose of epinephrine is given the α-receptors dominate – thus it
leads to increase vasoconstriction by α-1  leading to HTN.
 Epi-reversal is when you give α-blocker (Phentolamine) which in turn
causes β-2 to activate which causes vasodilation - leading to HypoTN.
o Clinically Epinephrine is used for  Cardiac Arrest &
Anaphylactic Shock.
Indirect acting Agonists 
 Tyramine – is usually broken down / inhibited by MAO’s. Its function is to cause HTN, thus
when MAOI’s are given tyramine cannot be broken down leading to  HTN crisis.
 Amphetamines – Causes release of NE & DA in the CNS. Clinically used for ADHD, Narcolepsy.
 Ephedrine – Decongestant

α-Blockers 
 Phentolamine has both α-1 & α-2 properties. And b/c α-1 is blocked It can lead to Reflex
tachycardia.
 Phenoxybenzaime has α-1 & α2 properties. Used for short period to Tx pheochromocytoma.
(Miosis & reflex tachycardia).

α-1 blockers 
o The “”zocin”” drugs – Terazocin, Doxazocin, & Prazocin
 These 3 drugs are used to Tx Pts with HTN & BPH
 Can produce Syncope in the elderly.
o Tamsulosin – used for Tx BPH only.

α-2 blockers 
o Yohimbine – Used for Postural HypoTN & Impotence.
o Mirtazapine – Tx for Depression.

β-blockers (ββ)  “”Olol”” drugs

 Propranolol (non-selective blocker). β-1 blockers Acebutolol, Metaprolol, & Atenolol
 (SE –increases LDL & TGs / dyslipidemia).
 Carvedolol & Labetolol (these have both α1 & β1-blocking properties).
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Central Nervous System Drugs:

 Anticonvulants antiarrythmic of the brain irregularity of the brain

 Antiparkinson lot of new drugs are in the market to manage the symptoms of Parkinson’s
 Opioid analgesics (to relieve pain without losing consciousness)
 Anesthetic, Antipsychotic and Antidepressant

CNS stimulants:
 Amphetamine  Increase NE & DA in the CNS
o ADHD Rx: methylphenidate (ridaline) and Pemoline, Atomoxitine
why are we giving a stimulant for a kid with hyperactivity, the brain is super
active, so when u give a drug that stimulates the brain, the brain will think it is
stimulated, so it’ll calm down.
o NARCOLEPSY attack of sleep during daytime sudden attack of sleep that
is accompanied by cataplexy loss of muscle tone
 Treat with Dextroamphetamine
 Modofinil Used in sleep disorders such as (SWSD) Shift work
sleep disorder.
 Doxapram Treatment as a respiratory stimulant after anesthesia.
Toxicity of Amphetamines which can occur if someone is taking them to stay
awake all night...such as students studying all night etc…treated with  Ammonium
Chloride (acidifies the urine to increase Renal Excretion).
 Stimulants are controlled substances b/c of their risk of dependence & abuse.
 Avoid Coffee with stimulant b/c of its further action as a stimulant
 Last dose should be 6 hours before bedtime.

CNS Depressants (Sedatives & Hypnotics) 

 Sedative dosage increase & its effects 
 Sedation & decrease anxiety
 Hypnosis, Anesthesia, Respiratory & vasomotor depression and Coma.

o Benzodiazepines and Barbiturates, & GABA

 Activate GABAa receptors
 inhibitory NT, calm down, decrease the firing in the brain
 Activation of GABAa receptors leads to increase in Cl ions 
hyperpolarization (relaxation).
o GABA receptors has 5 receptors, a, b, y, and we don’t care on the other 2
o GABA binds to the receptor, benzos binds to y (BZ receptor), barbiturates bind to
beta receptor.
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o BACLOFEN binds to GABAb receptors

 GABAb decreases potassium hyperpolarization (phase III)
 Benzos bind to its own receptors (BZ receptors) Y site
 BZ1 these drugs are for sleep
 BZ2 memory, sensory-motor, cognitive like anxiety
 Barbiturates bind to B-stie
 These increase the duration Cl channels that are open.
o So at high doses Barbs open Cl channels but block Na+ channels.

Barbiturates 
 Phenobarbital:
o Long-acting drug for Seizures.
 Amobarbitol, Secobarbitol, Pentobarbitol
o These are Intermediate Acting drugs.
 Thiopental
o Ultrashort acting used for IV Anesthesia.

Indications
 seizures
 Insomnia barbs aren’t prescribed anymore don’t want to become
addictive, reduced the REM sleep.
Contraindications
o Hypersensitivity, Pregnancy
o IF YOUR TAKING BARB, DON’T BE DRINKING CAN LEAD TO 
ADDITIVE CNS DEPRESSION.

o Barbiturates INDUCE CYP450 in the liver thus leading to  increase in liver metabolism
of other drugs leading to  Reduced effect of other drugs.

Side effects of Barbiturates 

 Tolerance (need to increase the dose to get some effect) & Dependence (Cant’
live without it).
 Respiratory Distress & Withdrawal syndrome after chronic use
 Intermitted porphyria  due deficiency of Porphobilinogen Deaminase.
 EFFECTS THE NUERONS NEUROLOGICAL PAIN HOW DO WE
MANAGE, NEED TO GIVE THEM IV HEME
o PT GONNA COME IN WITH BARBS AND HAVING ABD PAIN
INTERMITTEND PORHYRIA.
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Benzodiazepines  Increase the Frequency of the GABAa / Cl- channel opening.

o All the Drugs ending in ‘“pam”’
o Alprazolam – Treatment for Panic Attacks
o Clonazepam – Anticonvulsant
o Diazepam – Long-acting anticonvulsant (statis epileptics)
o Flurazepam – It’s a Prodrug with no REM suppression, Forms an Active metabolite
o Midazolam – Treatment for Insomnia (& IV anesthetic).
o Lorazepam, Oxazepam, Temazepam (LOT) – Are NOT metabolized in the liver, can be
given to Alcoholics.
Side Effects 
 Sedation, Disinhibition leading to  Aggressive behavior
 Anterograde memory amnesia (Bad with Alcohol usage)
 Rebound withdrawal -- Anxiety & Insomnia.

Overdosing Benzodiazepines in ER 
 Give IV Flumezanil

New Sleep Disorder Drugs 

o Zolpidem, & Zaleplon
o These are NOT Benzos, but they do bind to BZ1 receptors these
induce sleep (used only for sleep).
 Effects can be reversed by Flumezanil.

Non-Benzodiazepine Anxiolytics 
 Buspirone – Used to treat Generalized Anxiety disorder
 Pts will be always worried about everything, more common
in women; symptoms must be for at least 6 months.
o Does NOT affect the GABA receptors, and takes about 1 -2 weeks to
work.
o Possible 5HT-1a Agonist, and has NO withdrawal symptoms or
addiction.

Alcohols:
 Ethylene Glycol, Methanol & Ethanol  All are metabolized by the enzyme Alcohol
Dehydrogenase.
 Ethylene Glycol (antifreeze)  Glycoaldehyde Oxalic acid
o This can lead to Toxicity  CNS Depression, Metabolic Acidosis
and Renal Toxicity.
o Treat with Fomepizole (Inhibits alcohol dehydrogenase)
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 Methanol (ex: wood alcohol) Formaldehyde  Formic Acid

o Formic Acid Toxicity leads to  Blindness, Respiratory distress
and Metabolic Acidosis with anion gap.
o Treat toxicity with Ethanol.

 Ethanol  Acetaldehyde  Acetic acid

o Ethanol follows zero order kinetics greater than 25mg/dl.
o Acetaldehyde side effects: throbbing headache, hypotension,
nausea, vomiting, sweating and confusion.
o Disulfiram inhibits acetaldehyde dehydrogenase leading to 
accumulation of acetaldehyde.

Acute Alcoholism 
 Leads to increase sociability, Gait Disturbances, & Ataxia
 Increase in rxn time  get slower and more accidents
 Affects motor and mental skills, Impaired memory, Coma and death

Chronic alcoholism
 Hypoglycemia, fatty liver, muscle wasting, Gout, Increased lactate & malate levels.

Drugs Causing Disulfiram-like actions 

o Metronidazole antibiotic
o Cephalosporins
 Avoid drinking while taking these drugs
o Chlorproproamide (Sulfonylurea)
o Naltrexone antidote to morphine, and helps the craving, OPIOD ANTAGONIST,
but it can be used for Drug addicts to resist their craving, as well as for boozers.
o Topiramate anticonvulsant, NMDA receptor blocker.

ER management of Acute Alcoholism 

 Don’t want the pt to reach the respiratory depression and have aspiration of
vomitus.
o Need to give IV glucose to prevent hypoglycemia can trigger seizures
o IV thiamine to prevent Wernicke encephalopathy
 Korsakoff, amnesia, confabulation, ophthalmoplegia, encephalopathy & ataxia
o Need to give K+ if Pt starts throwing up, and give Phosphate.
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Alcoholism Withdrawal 
 Alcoholic comes in for surgery and eventually starts going crazy, is paranoid,
seizures what is going? He’s an alcoholic he has Delirium Tremens (DT) b/c of
booze withdrawal.
 B/c alcohol inhibits GABA receptor too much inhibition the GABA will say the
person is no good, so its starts to down regulate and NE, Epi, 5HT, Dopamine the
excitatory NTs are increased and start working more 3-4 days after stopping, GABA
is no longer affected too much sympathetic and Hormones get the shakes and
hallucinations
 Visual Hallucinations begin about 1-2 days after stoppage od
drinking. Delirium begins usually anywhere from 2-5 days after last
drink.
 Treat these Pts with 
 IV Diazepam or IV Chlordiazepoxide
 IV Thiamine, K+, Phosphate & Mg+

Seizures:
Epilepsy 
 These are recurrent spontaneous seizures associated with PROLONGED Depolarization with
PROLONGED Hyperpolarization.
o SHFRF (sustained High Frequency Rate of Firing)
 Status Epilepticus 
 Is an Emergency, it is when there is a CONTINUOUS seizure for more than
30min.
o DOC is IV Diazepam (Pam’s)
Types of Seizures:
1. Generalized Seizure 
i. Involves the ENTIRE Brain
ii. It is Convulsive, Tonic (Grand Mal)
a. Pts will lose consciousness; bite their tongue, and
alternation in contraction & relaxation of muscles.
iii. Petit Mal (non-convulsive) occurs in Kids.
a. Kid is just staring into space, can’t get his attention,
he is ‘absent’, just not there.
2. Partial Seizure 
i. Occurs at a portion of the Brain
ii. There is NO loss of Consciousness and is aware of it
a. Pts say they can see it coming “Aura” Had funny
feelings about it.
iii. In complex form – Pt is unaware of it
 P a g e | 24

Causes for Seizures 

 Metabolic defects, Perinatal Injury, Infection, Brain Tumor &/or Fever (M/C cause).

Diagnosis of Seizures 
 Complete Neuro exam, EEG, CT-scan or MRI, PET-scan (position Emission Tomography).
 Hypoglycemia can lead to seizures  which can cause further glucose to be used up
leading to  COMA.

Treatment for Seizures 

 The Goal of the treatment is to Decrease Firing.
o If the Pt is seizing in front you  give them IV Diazepam and Phenobarbitol.
 Decrease the Spread of electrical activity
 Do this via Increasing the Threshold by giving them  Phenytoin or
Carbamazepine.
Drugs 
1. Na+ channel blockers:
a. Phenytoin – Inhibits the spread of seizures by  Interfering with Na+
currents.
Side Effects –
 Gingival Hyperplasia, Hypertrichosis, Hirsutism,
Megalobalstic anemia, Granulocytopenia, Osteomalacia,
INDUCES CYP450.
 Has a narrow Therapeutic Index.

b. Carbamezepine – DOC for Trigeminal Neuralgia and 2nd to lithium in

treatment for Bipolar disorder.
Side Effects –
 Agranulocytosis, Aplastic anemia, Enhances ADH secretion
thus leading to Hyponatremia.
 Teratogenic  Craniofacial abnormalities and Spina Bifida.

2. GABA activity drugs:

a. Barbiturates (Phenobarbitol) – Decreases the firing of seizures, suppresses
the seizure focus (like diazepam), give to a pt seizing right there, Rx of
insomnia, (long acting Rx of seizures).
Side Effects –
 Sedation, Osteomalacia, Megaloblastic anemia (like phenytoin),
Induces CYP450.
 CONTRAINDICATED in Intermittent porphyria (Barbs).
b. IV Diazepam (Benzo) – DOC for Status Epileptics and for DT (delirium
tremens).
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3. Ethosuximide –
i. Decreases the Ca2+ ions, used to treat Absence Seizures

4. Valproic Acid – lowers Ca++ ions

i. Activates GABA & Inhibits Na+ channels
ii. Used as a second option for Migraines and Bipolar disorder.
Side Effects 
 Pancreatitis, hepatotoxicity, SLE-like symptoms, and Spina bifida
o Pts with pancreatitis will present with Abdominal Pain, and
elevated Amylase (or Lipase).

5. Drugs that Inhibit Glutamate (NMDA antagonist) 

a. Lamotrigine – for migraines, but can cause Steven-Johnson Syndrome (skin
issues).
b. Topimarate – Stops craving in addicts
i. Side effects include  Kidney stones
c. Felbamate – NMDA blocker that can cause Aplastic anemia as a side effect.

6. New Seizure Drugs 

a. Zonisamide, Gabapentin (stimulates GABA), Primidone (barb),
Vigabatrin, Levetiracetam (used in Bipolar).

Status Epilepticus 
 Seizing Give IV diazepam, not responding for more than 20mins, seizure is eating glucose it
can result in brain damage (coma).
o Give IV diazepam first + load of IV phenytoin not with regular seizure (Only for Pts
with history of status epileptics).
 If this is not effective, then give Pt IV Phenobarbiturate, if this doesn’t work YOU NEED TO
CALL A NUEROLOGIST.
o The neurologist will induce coma by giving Thiopental (ultra-short acting anesthetic),
to stop eating glucose, till the glucose is normal, then wake the Pt up.
***Recurrent Seizures can be prevented by  Diazepam/Loarazepam + Phenytoin.***
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Anesthetics:
 General Anesthesia  Is the complete absence and consciousness induced by inhalation
and/or IV.
 Stage I: less pain or no pain
 Stage II: excitement
 Stage III: surgical anesthesia (want to keep Pt in this stage)
o most surgeries are plane 2 or upper 3, want the Pts to breathe on their own
 Stage IV: Medullary Paralysis, Toxic Stage (anesthesiologist are the first to blame).

Inhalational Anesthetics 
 These are gasses or liquids than can be administered by inhalation via mixing them with oxygen.
 Move through inhaled air  Lungs  Blood  Brain
 All volatile agents have the tendency to cause malignant hyperthermia  Treat with Dantrolene
(blocks Ca2+ release from SR).
 PRECAUTION with the Elderly they require less anesthesia so give it in smaller doses, otherwise
they will have longer recovery, hypotension and prolonged respiratory depression.
 MAC- is a measure of potency, meaning how much of the anesthetic is needed. So the lower the
MAC the higher the potency of that drug.
 Higher solubility into blood and tissues and the greater the gradient = slow onset of action.

Volatile Agents –
o Halothane  has slow onset  can cause Hepatotoxicity (usually occurs when
halothane used again) and also causes Malignant hyperthermia.
o Enflurane  Causes occasional seizures.
o Isoflruane  Causes Reflex Bronchospasm
o Desflurane  This is Most Potent; Poor inducing agent causes Airway Irritation.
o Sevoflurane  USED IN CHILDREN can cause Bradycardia & Hypotension.
o Methoxyflurane  Not used anymore b/c causes Nephrotoxicity.

Nitrous Oxide Gas

 It’s an incomplete anesthetic, but provides good analgesia.
 Used in Dental or Minor surgeries.
Side Effects 
o Causes Diffusional Hypoxia (lowers O2 in the blood)
 Treat with Hyperbaric Oxygen (mainly used for CO poisoning).

***All anesthesiologists must keep Atropine to reverse any possible bradycardia, they must Monitor
the Pts temperature b/c hypothermia is common with Inhaled anesthetics.
Shivering is normal during recovery and keep the Pts in a warm blanket or heat. ***
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Intravenous General Anesthetics 

 Thiopental Ultrashort acting anesthetic that puts Pts into coma, & causes pain at injection
site. (equilibrates in the brain very fast, & rapidly is distributed to skeletal & adipose tissue )
 Midazolam Fast acting that treats insomnia, but causes Respiratory depression.
 Lorazepam dizziness
 Diazepam paradoxical excitation
o Midazolam, Lorazepam & Diazepam are used a Pre-medications before surgery.
 Sufentanil Confusion
 Alfentanil 1000x more potent than morphine
 Fentanyl  causes Bradycardia
o These drugs are Opioids that are used Post-Opp.

IV Agents 
 Etomidate  This is the preferred anesthetic for the Elderly with decreased Cardiac Reserve.
 Causes Muscle & Eye movements with Pain at the injection site.
 Can also Increase HR & BP
 Propofol  Used for outpatient (daycare) surgeries and does NOT cause Post-Opp vomiting or
Nausea.
Side Effects  Apnea and Severe fall in BP.
***IV is used to start anesthesia and is maintained with inhalational. ***

Dissociative Anesthesia 
 It is Separation from reality  Amnesia, Catatonia (state of immobility) and Analgesia
 Ketamine – Causes dissociative anesthesia
Side Effects 
 Cardiac stimulation and Hallucinations (emergence phenomenon)
 Pts can become aggressive and wild.

Neuroleptanalgesia 
 Is a state of Intense analgesia
o Neuroleptics (tranquilizing) + Analgesic
o Droperidol (neuroleptic) + Fentanyl (opioid causes bradycardia IV general anesthetic)

Neuroleptanesthesia 
 Caused by –
o Droperidol + Fentanyl + Nitrous Oxide
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Local Anesthetics 
 These are administered directly to induce absence of sensation in a portion of the body
WITHOUT losing consciousness.
 Does this via blocking the conduction of nerve impulses and Decreasing Na+
permeability.
 2 types of local anesthetics  Esters & Amides.
o Esters – Are metabolized by pseudocholinesterase. These include 
 Procaine, Tetracaine, & Benzocaine, Cocaine
o Amides – These are metabolized in the liver (DO NOT give to liver Disease Pts)
 Lidocaine, Etidocaine, Bupivacaine & Mepivacaine
Antiparkinson’s Drugs 
 “Dopamine Agonists”
o Basal Ganglia & Substantia Nigra (for movement) decrease dopamine here can cause 
Parkinson’s disease.
o Mesolimbic System (drug abuse) Increased dopamine leads to  Euphoria
o Mesocortical area (schizophrenia) increased dopamine leads  Psychosis
o Dopamine inhibits  prolactin
o Chemoreceptor trigger zone (CTZ)  increased dopamine leads to Emesis (vomiting)
o Hypothalamus, increased dopamine  loss of appetite, hyperthermia (temp regulation).
Dopamine Receptors 
o D1A (Gs)  increases cAMP
o D1B (Gs)  increases cAMP
 These are present in the kidney stimulating it will
increase GFR.
o D2A (Gi)  Decreases cAMP
o This is the one we need to know the most (D2A) it’s the site
of Typical Antipsychotics (such as Haloperidol).
o D2B (Gi)  Decreases cAMP
o D2C (Gi)  Decreases cAMP
 This is blocked by Atypical Antipsychotics (such as
Clozapiem).

**A patient with Parkinson’s, has an is an imbalance, dopamine goes down, Ach goes up
o To decrease Ach in PD pts give (Muscarinic antagonist)
 Trihexphnydylol and Benzatropine are used in Parkinson’s
 SEs – constipation, urinary retention, dry mucus membranes, blurred
vision, skin flushing and disorientation.
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Clinical Presentation of Parkinson’s Pts  decreased DA & increased Ach

 Hand Tremors (pill rolling), Cog wheel Rigidity, Bradykinesia (difficulty rising
from chair)
 Masked face (no expressions) and Impaired Gait (shuffling/festinating) &
Coordination.

Drugs to Increase Dopamine 

 Give dopamine precursors
o Levodopa, but can’t give levodopa alone need to give Carbidopa (combo is Sinimet)
 Levodopa is metabolized in circulation by AAAD (aromatic amino acid
decarboxylase) to give  Dopamine.
 Since dopamine cannot cross BBB, so we need a way to get it across, so
levodopa can cross and get metabolized in the brain just make a drug to
inhibit AAAD (carbidopa) this can’t cross the BBB.
o VITAMIN B6 IS A COFACTOR OF AAAD, SO PYRIDOXINE POTENTIATES AAAD, IF U GIVE
B6, TOO MUCH LEVODOPA IS CONVERTED TO DOPAMINE.
 SEs  Anxiety, agitation, insomnia, HypoTN, confusion and delusional.

 Dopamine Reuptake Inhibitors : “enhance the effects of endogenous dopamine”

o Amantadine antiviral drug as well
 Side Effects  Livedo reticularis (bluish mottling of the skin).

 Dopamine Agonists
o Ergot Agonists –
 Bromocriptine, Pergolidethese inhibit prolactin, thus are treatment for
hyperprolactemia. ****
o Non Ergot Dopamine Agonist
 Pramipexole and Ropinirole

 MAO-I Type B
o These inhibit the enzyme MAO that metabolizes dopamine.
 Selegiline – Preserves dopamine in the brain.

 COMPT-I these can act like Carvidopa by increasing levodopa levels available to cross BBB.
o These are inhibitors for COMPT which metabolizes dopamine normally.
 Entacapone and Talcapone
o These can cause Hepatotoxicity, BUT work great when given in
combination with Carbidopa + Levodopa/Entacapone.
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Alzheimer’s disease 
 Most common type of Dementia in the Elderly with slow gradual symptoms 
 Loss of Recent memory first then later Remote memory
 Difficulty with speech and writing
 Most common type is due to ApoE protein (cholesterol transport protein), this is elevated in AD.
 Loss of the Tau Protein  leads to Neurofibrillary Tangle formation.
 Amyloid plaque buildup as well.

Drugs Approved for AD -

 Rivastagime, Donepezil, Gallantamine, Tacrine, Memantine.
o Gallantamine and Rivastagmine used more these days
o NMDA receptor blockers Memantine

Opioid Analgesic 

 Morphine: Binds to opioid receptors in CNS

o Used as an adjuvant in anesthesia
 Cough relief, for Chest pain due to MI and Refractory pain (if other non-opioid drugs don’t work)

Opioid Neurotransmitters ****

 µ β-Endorphin
 K Dynorphin
 δ Enkephalin
 Pro-Opiomelanocortin β-Endorphin
 Pro-Enkephalin met & leu enkephalin
 Pro-Dynorphin dynorphin and Leu-enkephalin

 μ: Receptors (β-endorphin)
o Analgesia Supraspinal, Respiratory depression, Sedation, Euphoria, Miosis,
Dependence and Constipation
 K: Receptors (Dynorphin)
o Analgesia Spinal and Dysphoria

Morphine Effects 
1. Acts an Analgesic
2. Sedation
3. Decreased Respiration via decreasing the sensitivity of respiration to pCO2.
a. DO NOT give O2 to Pts with morphine sedative they will stop breathing.
4. Miosis by activating M receptors.
 P a g e | 31

5. Cough suppression (codeine), as well as Oxycodone and Hydrocodone

6. Emesis & Nausea by stimulating CTZ (D2 receptors)
7. Constipation
8. Liver – Increases biliary pressure and Spasms.
i. Contraindicated in biliary colic (spasm of gallbladder)all opioids are
contraindicated except meperidine (Demoral) not metabolized by the liver.

9. Histamine – Urticaria (Hives is frequently caused by allergic reactions, rashes on skin).

10. CV system – Hypotension due to histamine release.

Morphine OD 
 Pts will present with 
 Pinpoint Pupils, Respiratory Depression and Coma.
 Treat this with IV Naloxone – This ONLY blocks the Opioid receptor, it doesn’t
block the Ach (pupil) or Dopamine (nausea & vomiting). So also give Chlorpromazine
for Vomiting and Anticholinergics for pupils.
Methadone – Has a long half-life thus long duration of action.
Morphine (t1/2) = 2-4hrs Naloxone (t1/2) = 1 – 1.5hrs
Nalbuphene  analgesic during LABOR.
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Cardiovascular Pharmacology:

Antihypertensives 
Diuretics (Thiazides) ****
ACEI (Angiotensin converting enzyme inhibitor) ***
ARB (Angiotensin Receptor blocker) such as Losartan
β-blocker (BB - the “olols”) *** mainly post-MI
CCB (Ca2+ channel blocker)
α-2 agonist (Apraclonidine, Clonidine, & methyldopa)
Adrenergic neuronal blockers
α-blockers (α-1 – Terazocin, doxazocin, & prazocin)
Direct acting vasodilators (β-2 agonist SMART)
Renin Inhibitors

** The class of Antihypertensive drugs that have proven to decrease the mortality in heart diseases are
the  β-B, ACEI, & Thiazide Diuretics. ****

ACEI (fluid overload) heart failure, decrease preload, decrease afterload, the heart is pumping no
blood, so the ACE inhibitor decreases the amount of blood in the LV and the afterload (not going to have
the aorta work too, reduce the resistance so the heart doesn’t pump against resistance).

Hypertension 
Described as having Systolic, Diastolic or both pressures greater than 120/80bpm.
Normal BP is less than >120/80.
Prehypertension:
Having BP of – 120-139
80-89
In these Pts you want to recommend Life-style changes such as, Weight reduction, cut
down on alcohol, regular exercises, less smoking and less Na+ intake.

Stage 1-HTN:
These Pts have a BP of – 140-159
90-99
Recommend these Pts on drugs such as Thiazide Diuretics, but be careful with Pts that
have gout, b/c thiazides increase uric acid levels.
You can also give these Pts ACEI, ARB, BB, or CCBs.

Stage 2 HTN:
Having a BP of – >160 .
>100
Give these Pts combination of  Thiazide diuretic + ACEI (or CCB + ARB +Bb)
 P a g e | 33

*** Pt comes complaining of food poisoning, has diarrhea 145/95 is the BP, is that HTN?
-no its not, you never seen the guy before, cannot diagnosis HTN off that, need to let
him calm down, then take BP again 142/92 now no its not HTN, to diagnosis HTN u need 3
consecutive readings on 3 different occasions
-do not give HTN drug on the first visit, tell him to come back next week, first you try a
life style modification.
-common symptom of high BP is headache & dizziness. ***

What to do in a HTN + Medical condition Pt 

Hypertension in a Pts with Angina pectoris.

Give BB, CCB
HTN in Pts with BPH
α-blockers such as – “zocins” – terazocin, doxazocin & prazocin.
Or if just BPH give tamsulosin.
HTN in diabetic Pts
Give ACEI (drug of choice) this can delay/prevent kidney damage in diabetics & ARB.
HTN in Heart Failure Pts
ACEI, ARB & BB (widely used).
HTN after MI
BB
HTN in a Pt with hyperlipidemia
α-blocker & CCB

*** For a Pt with refractory HTN which combination of classes of drugs will reduce the systolic BP the
most?
K sparing and thiazide diuretics are the best for reducing the systolic by 5-15 pts**** Thiazide have
the side effects of causing hypokalemia so in combination with a K sparing drug like
spironolactone (causes hyperkalemia), there is a balance.****

*** Which of the following activities can have the greatest effect on BP-reading?
Consume 3 alcohol dirnks 12hrs before the reading
Drinking coffee 1hr before measurement
Smoking 15min before measurement – This will raise by 5-25 mmHg systolic BP, need to ask your pt
if they smoked a cigarette in the parking lot.
 P a g e | 34

Diuretics:

Thiazide Diuretics  these are most commonly used for HTN. Work on the DCTs.
Chlorothiazide, Hydrochlorothiazide (HCTZ) #1 prescribed, Chlorthalidone,
Indapamide and Metolazone (these 2 do not have thiazide but are diuretics).
Function of the drugs:
These drugs inhibit the Na+/Cl- cotransport
They increase the excretion of – Na+, K+, Cl-, Mg3+ & HCO3.
Also decrease excretion of – Ca2+, Uric acid
Side Effects:
Hyponatremia, Hypokalemia, Hypomagnesia, Metabolic Alkalosis, Hypercalcemia,
Hyperuricemia, and increased aldosterone.
They also increase the plasma cholesterol and TGs EXCEPT for Indapamide.

Loop Diuretics Work on the Thick Ascending limb

Furosemide, Bumetanide, Torsemide and Ethacrynic acid.

Mode of action:
The loop diuretics inhibit the Na+/K+ dichloride cotransport system.
They Increase excretion of – Na+, K+, Cl-, Mg3+, HCO3, Ca2+ , decreases medullary osmolarity.
Side Effects:
Hyponatremia, Hypokalemia, Hypomagnesia, Metabolic Alkalosis and Hypocalcaemia.
Causes Ototoxicity  Is damage to the ear (Tinnitus), specifically the cochlea or
auditory nerve and sometimes the vestibular system. The risk is increased if taken in
combination with antibiotic such as aminoglycosides.

****Hydrochlorothiazide and Loop diuretics are Sulfa derived so they are contraindicated for sulfa
allergy Pts, except for ethacrynic acid. ***
**Thiazide Diuretics have a (GFR)aka Creatinine Clearance (CrCl) of 40ml/min, whereas Loop Diuretics
are effective down to 10ml/min. Potassium Sparing Diuretics are not recommended for Pts with
increased CrCl.***

Osmotic Diuretics these push everything in all the tubules, mainly through the PCTs.
Mannitol.
Mode of Action:
Osmotic diuretics increase the osmotic pressure in the PCTs thus  Inhibit reabsorption of
water & Electrolytes. (Increases Plasma osmolality & ADH)
Used during 
Increase intracranial pressure, intraocular pressure and Acute Renal failure
(forces urine production thus helping kidney from shutting down).
 P a g e | 35

Carbonic Anhydrase Inhibitors  Acts on the PCTs.

Acetazolamide and Dorzolamide
Mode of Action:
Increases the excretion of – Na+, K+, and HCO3 (in greater amount).
Used for 
Treating Glaucoma & Overdose of acidic drugs (does this via alkalizes
the urine) Acetazolamide is used for Altitude sickness as well.

K+-Sparing diuretics Works on the Collecting Ducts (these drugs Spare Potassium).
Spironolactone is an aldosterone antagonist  thus it will block testosterone and
glucocorticoids (anti-androgenic SEs) and can start developing Gynecomastia. ****
Amiloride & Triamterene block Na+ reabsorption.

Used to treat:
Spironolactone + ACEI increase the survival rate in Heart Failure Pts.
Spironolactone has an antiandrogenic effect – Treatment for hirsutism.
Triamterene Nephrolithiasis (kidney stones)
Amiloride is used to treat Nephrogenic Diabetes Insipidus caused by Lithium.
What drugs are used to Treat Nephrogenic DI in general?? Thiazides Diuretics (resets the
kidney receptors).
Nephrogenic DI kidney is not responsive
Diagnosis by giving ADH, if fixed then its Central DM  need to give
vasopressin, desmopressin
If unresponsive to ADH then its nephrogenic DI give amiloride only when
caused by lithium, in general Tx with thiazide diuretics.
Side Effects:
Hyperkalemia, Metabolic Acidosis, Decrease Libido (via spironolactone), and dry
mucus membranes.

A 38 year old man under treatment with Lithium for a bipolar mood disorder comes into your office
complaining of nocturia of increasing frequency.
Serum: Na+ 164 mEq/L (hypernatremia), K+ 5.0 mEq/L, Cl- 126 mEq/L, total CO2 25 mEq/L, creatinine 1.1
mg/dl (normal 0.7-1.5), blood urea nitrogen 10 mg/dl (normal 10-20). BP 116/74 mmHg lying, 88/60
standing. (Orthostatic HTN)
Urine: Na+ 2 mEq/L, osmolality 140 mOsm/kg water.
One hour after injection of 5 units of ADH his urine osmolality was 138 mOsm/kg water, unresponsive to
ADH and kidney problem. Nephrogenic Diabetes Insipidus
 P a g e | 36

ACE-Inhibitors: angiotensin converting enzyme

These are the drugs that end in the suffix “pril”. These are good for preventing cardiac remodeling.
Captopril, Enalapril (give IV for emergency HTN), Lisinopril and Fosinopril.
ACE-I Decrease Phospholipase C levels.
Bradykinin is converted to an inactive compound, so keep bradykinin around which produces
vasodilation Endothelial Derived Releasing Factor (EDRF)results in dry cough most common
complaint about ACE inhibitor.

ACEI side effects:

Hyperkalemia metabolic acidosis
Angioedema  Swelling of the upper airways, face, lips, and tongue etc…
ACE inhibitors are contraindicated in pregnancy. First trimester  CNS & Cardiac issues. ACEI’s are
contraindicated in the 2nd and 3rd trimester b/c it can lead to  Fetopathy. ***
Intrauterine growth retardation
Hypocalvaria small skull cap small head or skeletal head
Oligohydramnios less amniotic fluid
Amniotic fluid in baby urine kid is not ok something is wrong

***ACEI’s are the best for HTN in DM Pts  B/c DM Pts tend to get nephropathy and ACEI will help by
slowing down the renal damage.

Congenital malformation of which systems are the most frequent among children exposed to ACEI’s
during the first trimester? Cardiac & CNS

Angiotensin II Receptor Blockers (ARB)

Drugs ending in the suffix “Sartan”.
Losartan, Valsartan, Candesartan and Irbesartan
CAUSES NO DRY COUGH
These drugs block angiotensin II (type I recept.) leading to  Vasoconstriction via AT-1 receptor.
ARB’s are also contraindicated during pregnancy b/c it can lead to  Acute Renal failure and to
proteinuria.
 P a g e | 37

β-Blockers (BB)  These drugs end in the suffix “Olol”.

Pts who have a history of chronic smoking AVOID prescribing non-selective ββ, b/c they may have
underlying lung pathologies. If you are prescribing ββ give them β-1 blockers.
β-1 & β-2 blockers  Propranolol & Pindolol β-1 blocker  Atenolol
Labetalol & Carvedilol – These block both α-1 & β-1 activities.
Labetalol – Is also used in HTN crisis
Carvedilol – Used in Acute CHF
Indications 
CAD, Tachyarrhythmia
Migraine headaches (used as prophylaxis)
Anxiety FOR STAGE FRIGHT, NERVOUS DUE TO RELEASE OF NE, SO JUST TAKE A BB AND
CALM THEM DOWN
Just give beta-blocker excellent for anxiety.
IT IS CONTRAINDICATED FOR ASTHMA AND HEART BLOCK.
Causes bronchospasm (constriction), fatigue, & glucose intolerance.
Also Metoprolol is a selective B-1 thus decrease bronchospasm.**

Ca2+-Channel Blockers (CCBs) 

Drugs that end in “Dipine”.
Amlodipine – (norvaz) most commonly prescribed.
Nifedipine & Isradipine
These 3 drugs work peripherally
Dihydropyridines (vascular tissue)  Reflex Tachycardia, ankle edema & flushing.

Diltiazem & Verapamil – These work DIRECTLY on the (heart) coronary arteries & a little on the
periphery and also decrease conduction.
Produces no Reflex tachycardia but may produce bradycardia.
Nonhydropyrinides (heart)  decrease cardiac contractility.
CCBs Indicated for 
Angina Pectoris, PVDs and Tachyarrhythmia’s
Nimodipine – approved for subarachnoid hemg, thus prevents hemgic vasospasms;
“worst headache of my life”.
EXAMPLE:
Patient is taking Nifedipine and they ask about coronary vasodilation, peripheral vasodilation, and AV
conduction – what are the effects on each?
- ↑, ↑, -no effect-
55 yrs old male, w/ a 160/96 bp, was given Amlodipine, peripheral vasodilation (increase), coronary
vasodilation (increase), AV conduction (no effect)
Amlodipine works on blood vessels, not heart
 P a g e | 38

Alpha 2 Agonist  Decrease NE (sympathetic)

Clonidine
Used to treat Mild to moderate Hypertension (patches cause less side effects)
Side effects: Edema, rebound hypertension after sudden withdrawal
α-Methyldopa
Used to treat Mild-Moderate HTN
Side Effects: + Coombs test (for hemolytic anemia)
Safe in pregnancy & Renal dysfunction
Methoxamine
This is a α-1 agonist used for PAT (paroxysmal atrial tachycardia).

Adrenergic Neuronal Blockers 

Guanethidine
Binds to storage vesicles and inhibits NE release.
Can cause Fluid Retention.
Also CONTRAINDICATED with Antidepressants (TCAs).
Reserpine
Blocks the transportation of of NE, 5HT and Dopamine into vesicles in the neurons.
Has been banned due to its severe side effects such as  Psychotic depression & suicide

Alpha Blockers  “Zocin” drugs

Prazocin, Doxazocin & Terazocin
Used to treat Low BP and BPH
Side Effects: first dose Syncope and orthostatic HTN. Also Incontinence in women when
coughing, sneezing or trying to lift weights.
Prazocin has an effect on the sphincter of the bladder. α-1 maintains the control.

Direct Acting Vasodilators 

Hydralazine
Relaxes the arteriole smooth muscle
Side effects: Reflex Tachycardia and Palpitations (use BB for this), SLE-like syndrome
and hemolytic anemia.
Sodium Nitroprusside
DOC for HTN crisis via IV.
Side effects: long term accumulation of Cyanide and Thiocyanate.

Minoxidil
Prodrug that activates K+ channels after sulfation. Used to treat baldness (ROGAINE) topically.
Side effects: Hypertrichosis (abnormal hair growth)
 P a g e | 39

Diazoxide
Activates the K+ channels leading to relaxation of SM.
Treatment for Insulinoma
(Sulfonylurea) oral hypoglycemic for DM-2 blocks K+ channels
Side effects: Hyperglycemia and Hypertrichosis

*** HTN Crisis IV drugs – Enalapril (ACE-I), Labetalol (BB), Diazoxide & Na+-nitroprusside (DOC). **

Antiarrhythmic Drugs:
Class 1: Na+ Channel Blockers
Class 2: β-blockers
Class 3: K+ Channel blockers
Class 4: CCBs
1 & 3 are used in more severe life threatening situations

Action Potential
More negative = more relaxed phase
More positive = more Na channels are open (depolarization) thus more contraction
Calcium contributes by making it more positive = calcium overshoot (phase 1)
Resting membrane potential around -90, when the heart starts contraction
Na channels are open phase 0 depolarization due to increase in Na current
Calcium contributes by making it more positive = calcium overshoot (phase 1)
Phase II still due to increase Ca and decrease K efflux. Cell becomes more (-)
Sustained effect of increase in Ca from phase 1, and decrease K in phase 3
Phase III repolarization, decreased potassium
Phase IV Na/K ATPase Pump

Refractoriness – Is the inability to respond to a stimulus.

Effective Refractory period  Is the period in which no stimulus will produce a
response.
RRP  Period in which a Strong Impulse may elicit s response.
ERP/APD (action potential duration)
 P a g e | 40

Class 1—Na+ channel blockers 

ACTIVATED Na+ channels – it causes decrease in the Vmax and prolonged APD.
Such drugs as 
Quinidine, Procainamide, & Disopyramide.
Quinidine 
Increases ADP & ERP in the Atria, Ventricles and the Purkinje fibers.
Has a Anticholinergic effect thus – Increases the HR & conduction
Also has α-blocking effect leading to Vasodilation & Reflex tachycardia.
Side Effects –
Nausea, vomiting and diarrhea
Increases QT-interval (Torsades De Ponte)
Thrombocytopenia
Cinchonism  Tinnitus, loss of hearing, GI upset and Diplopia.

Procainamide  Class 1A
It is a lesser anticholinergic with NO α-blocking activity
Side Effects –
Agranulocytosis & SLE-like syndrome

Disopyramide  Class 1A
MOST ANTICHOLINERGIC
Can causes dry mouth & Urinary retention

CLASS 1B Inactivated Na+ channel – Have NO effect on Vmax but do Decrease APD.
Such Drugs as 
Lidocaine, Tocainide, & Mexiletine.

Lidocaine 
It is a local anesthetic
Treatment for VTac via IV, after an MI or Digitalis toxicity
Works best on ischemic area of the heart
LEAST Cardiotoxic.

Tocainide & Mexiletine 

Given ORALLY.

Class 1C – Both Na+ channel  IT IS NOT USED CLINICALLY such as 

Flecainide & Moricizine.
 P a g e | 41

Class 2 – β-Blockers 
Only 3 are used for antiarrhythmic
Propranolol, Acebutolol, & Esmolol.
Blocks B1 receptor decrease contraction of the heart and slow down the conduction
Slows down the SA and AV nodal conduction
Decreases the slope of phase 4 depolarization, longer time to initiate phase zero
Used as prophylaxis Post MI and to Rx SVT (supraventricular tachycardia) Atrial contraction (not
life threatening)
Don’t use a beta blocker in an emergency room
Esmolol works very fast – It is given IV for emergency treatment or SVT.

Class 3 – K+ Channel blockers 

These INCREASE the APD & ERP – leading to Prolonged repolarization and lengthened Phase 2
(increases Ca++ and decreases K+ efflux).
Bretylium, Amiodarone, & Sotalol.

Bretylium ***
This is the DOC after Lidocaine for the treatment for Ventricular arrhythmias
not controlled by drugs 1A or 1B.
It causes the release of Catecholamines and may worsen or cause
arrhythmia.
Side Effects 
Causes Orthostatic HypoTN and Reflex tachycardia.
Amiodarone 
This mimics all 4 classes.
DOC for Wolf-Parkinson-White (WPW)
Also Blocks the K+ & Ca2+ channel as well as it is a non-comp inhibitor of β-receptor.
Side Effects 
Pulmonary fibrosis, Hepatotoxicity, Smurf skin, Hypothyroidism 5% may
cause Torsade De Ponte (increase QT-interval), Ataxia & Neuropathy
Sotalol 
Works like β-blocker & K+ channel blocker
Treatment for Life threatening V-arrhythmia
Side Effects 
Headache, depression, & Impotence
CARFEUL when giving to asthmatics.
New drug -- Dronaderone – like amiodarone
New drug – Ibutilide – for pharmacological cardioversion? Only given IV.
Dofetilide – can be given as tablets (like Ibutilide).
 P a g e | 42

Class 4 – Ca2+ channel blockers 

These decrease the SA & AV nodal conduction thus decreasing the slope in Phase 4.
Verapamil & Diltiazem.
Treatment for PSVT due to AV-nodal reentry
CONTRAINDICATED in Atrial Tachy due to WPW (tissue problems).
Adenosine 
Causes vasodilation leading to Bradycardia  Reflex tachycardia
DOC for PSVTs

Coronary Artery Diseases:

Risk factors include 
HTN, High cholesterol, DM, Cigarette smoking and Obesity (BMI >30).

Angina Pectoris 
Pts will present with burning, squeezing or crushing chest pain which radiates to the left arm,
shoulder or jaw.
Mostly after physical activities/exertion
ST-segment depression.

Types of Angina’s 
Stable Angina 
There is chest pain which occurs with exercise or stress that is Relieved
by Rest.
Unstable Angina 
Chest pain that occurs during rest or during exertion which can progress to an
MI.
Vasospastic (Prinzmetal) Angina 
Occurs to due Coronary artery vasospasm  ST-segment elevation & T-wave Inversion.

Antianginal Drugs 
Nitrates, β-B, & CCBs

Nitrates  Nitroglycerine, Isosorbide

Activate NO, which enhances the activity of Guanylyl Cyclase converting GTP
cGMP  leading to relaxation (vasodilation).
Cause dilation of large veins  decreased preload and decrease Oxygen
demand.
At high doses nitrates cause arteriolar dilation (Aorta)  decrease afterload
&increase oxygen supply.
Inhibit platelet aggregation and decrease coronary vasospasm.
 P a g e | 43

Side effects of Nitrates 

Headache, flushing, Syncope, Reflex tachycardia, and edema
Tachyphylaxis (decrease in the response to a drug due to previous
exposure to that drug), requires rest of more than 12hrs.

Cyanide Poisoning Antidote  Na+ thiosulfate

Amyl Nitrate
Methmoglobinemia treat with methylene blue.
This forms methmoglobin that binds to CN-ions to form
cyanomethmoglobin.
Cyanomethmoglobin  is reconverted into methmoglobin
 via Treatment by Na+ Thiosulfate.
β-Blockers for anginas
Atenolol
β-1 blocker -- Acts directly on the heart
Decreases the force of contraction, HR and CO thus  overall
decreasing the oxygen demand.
Be careful w/ Pts that have Prinzmetal (Vasospastic) angina,
b/c Atenolol keeps α-1 open causing vasospasm.
Carvedilol
The ONLY βB that has shown to have similar effect as nitrates, b/c it is
both α & β blocker.

Ca2+ Channel Blockers for anginas

Dihydroperidine: Amlodipine
Non-dihydroperidine: Verapamil & Diltiazem
Bepridil 
This is an FDA approved drug for Angina; it dilates the Coronary Arteries
via blocking Na+ and K+ channels
Thus it can produce symptoms of Torsade’s De Ponte
via increasing the QT-interval.
Managing a Pt in the ER with an MI 
First give O2  Morphine for pain  Nitroglycerine sublingually  Aspirin to chew on (prevents
platelet aggregation)  βB to lower cardiac load  ACE-I to reduce preload & afterload 
thrombolytics to dissolve the clots.

How a Pt with Heart failure presents 

Left heart failure Pts present with  Dyspnea, Orthopnea, & PND
They can also be Diaphoretic (cool extremities) and a pathologic S3-Gallop.
Right Heart failure  Edema, Acites, JVD, Hepatomegaly and Epistaxis (bleed from nose).
 P a g e | 44

Drugs that INCREASE Cardiac Contractility 

Digitalis (aka cardiac glycoside)
Inhibits Na+/K+ ATPase Pump leading to increase intracellular Na+  increase in Ca2+ 
increase in the force of contraction.
Digoxin decreases the AV node conduction as well.

Indirect Effect of Digitalis:

Cholinergic effect through vagal stimulation
Causes decreases in the SA node rate
AV node it increases ERP and decreases velocity of conduction.
NO EFFECT ON THE PERKINJE OR VENTRICLES
Side Effects of Digoxin 
If there is Digoxin Toxicity  EKG changes will show PVCs (AV-nodal block w/
ventricular escape), Hypersalivation, fatigue, and NV.
Treat Digoxin toxicity with Digifab (digibind) type of Immunological
strategy.
*** Hypokalemia exacerbates digoxin toxicity so avoid drugs that decrease K+ such as thiazides & loop
diuretics. ***
CONTRACINDICATED IN WOLF PARKINSON W (WPW).

New Inotropic Drugs 

End in the suffix “rinone”
Amrinone, Inamrinone, & Milirinone.
These drugs inhibit PDE causing increase in cAMP  leading to positive inotropy, inhibition
of PDE also leads to  increase cGMP thus leading to  vasodilation.
These drugs provide short term treatment for HFs
Side effects 
HypoTN
Inamrinone – Thrombocytopenia
Milirinone – Decrease survival in HF.

ER treatment for HF Pts 

Dobutamine (sympathomimetic)  For HF to increase contractility.
Diuretics (loop / thiazides)  reduces congestion and edema.
Spironolactone Reduces mortality when combined with ACE-I.
ACEI (Lisinopril)
CCBs (amlodipine, Verapamil)
βB (Carvedilol has proven to decrease mortality)
Metoprolol survival benefits used in AP & MI.
Nesiritide (type of BNP increases cGMP leading to SM relaxation  relieves dyspnea
at rest in severe CHF).
 P a g e | 45

Antihyperlipidemic Drugs:
Normal levels of cholesterol = 200mg/dl
Borderline = up to 239mg/dl
Elevated = > 240mg/dl

Statin Drugs 
Look for the suffix “Statin” these are HMG-CoA reductase inhibitors  Increases LDL receptors.
Atorvastatin, Simvastatin, & Pravastatin.
These drugs inhibit HMG-CoA reductase thus inhibiting the rate limiting step in
cholesterol synthesis.
Used to treat 
Hyperlipidemia, Hypercholesterolemia, HyperTGemia
They Increase HDL (good cholesterol).
New Studies reveal that Statins are used secondarily to prevent Heart Disease.
They increase NO and decrease mRNA for Endothelin-1  vasodilation.
Side Effects of Statin drugs
Myopathy, muscle aches, myalgia, myositis to rhabdomyolysis (breakdown of skeletal
muscle which goes into the blood stream and can lead to  Renal failure).

Bile Acid Sequestrants 

These drugs include – Cholestyramine and Cholestipol.
Cholesterol is used to make more bile acid thus LOWERING LDLs.
Causes formation of insoluble complexes that is excreted in the feces.
These drugs enhance that, BUT they are not used in Pts with HyperTGemia b/c it the drugs
cause an increase in VLDL & TGs.
Cholestyramine
Also used to treat Pruritis due to biliary obstruction, thus liver is
unable to excrete bile.
Side Effects 
Constipation, Malabsorption of Fat soluble vitamins (KADE)
Malabsorption of Digoxin, thiazides and Warfarin.

Nicotinic Acid (Niacin) Best drug to Increase HDL levels.

Inhibits VLDL synthesis by activating Lipoprotein Lipase.
Can cause Flushing, Pruritis, Hyperkalemia and Hyperuricemia. These two drugs are the
First line Tx for Increased
levels of TGs. They increase
Gemfibrozil & Clofibrate 
the activity of PPAR-α.
Also activates Lipoprotein Lipase thus -> reducing VLDL, LDL & TGs.
Can cause flu-like muscle aches, Gallstones and Inhibits CYP450.
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Probucol
Increases levels of cholesterol ester transport protein.
Can cause Torsade De Ponte via increasing the QT-interval and Arthralgia.

Ezetimibe 
New drug that Inhibits cholesterol absorption in the small intestines. Highly effective when used in
combination with Statin drugs.
Can cause Sinusitis, and pharyngitis.
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Endocrine Pharmacology:

Treatments for Hyper-Prolactinoma 

Normal levels are about less than (<) 20ng/ml
Moderate elevation is about 30-300ng/ml (pregnancy).
Increase in prolactin will produce  Galactorrhea & Irregular menses.
Tx include  Dopamine agonist such as  Bromocriptine, Pergolide and Cabergoline.

Drugs for Acromegaly 

Best treatment is Surgery BUT second best choice is Octreotide – a somatostatin analogue.
Somatostatin – Affects the Anterior pituitary and INHIBITS GH release. Also
Decreases the GI motility (so it can be given as a Tx for Carcinoid tumors).
Bromocriptine – A dopamine agonist (used to Tx hyperprolactinoma).
Pegvisomant  New approved drug for acromegaly. It is a GH-receptor Antagonist.

Dwarfism  occurs due to Decrease GH

Somatrem & Somatropin – These are GH-Agonists which are also used in Osteoporosis.

Hypopituitarism 
Look for Tired, Quiet people that will also show sign of Hypothyroidism due to lack of TSH
(fatigue, cold intolerance and no goiter).
Due to ACTH deficiency – the young female post-partum who is UNABLE to Lactate (Sheehan’s
Syndrome).
To diagnose ACTH deficiency do the Metyrapone test  this inhibits the cortisol
formation thus  stimulating ACTH release.
If there is NO release of ACTH then there is a problem in the pituitary or
hypothalamus.
Posterior Pituitary Disease diagnosis 
Arginine Vasopressor Receptors – Aka V1-V3, now called as AVPR1A, AVPR1B & AVPR2
AVPR1A – is a G-coupled receptor protein that activates the IP3 & DAG system.
Found mainly in the Blood Vessels.
Once it is activated it leads to  Vasoconstriction

AVPR2 – Also a G-coupled protein that activated the adenylate Cyclase pathway.
Found mainly in the Kidney tubules, fetal lung and lung cancer.
AVPR2 responds to vasopressin to concentrate the urine and maintain
homeostasis.
Blockade to the AVPR2 will result in  NDI.
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Diabetes Insipidus 
Occurs due to ADH (vasopressin) deficiency.
Pts will present with  Polyuria, Polydipsia & Excessive thirst
The Na+ levels increase resulting in  Hypernatremia.
Treatment 
Central DI – give Vasopressin or Desmopressin SQ
NDI – Thiazide diuretic (HCTZ), Indomethacin, & Amiloride.
SIADH 
Demeclocycline which causes fluid restriction.
Conivaptan – ADH receptor antagonist which blocks AVPR1 & AVPR2.
It also approved to Tx Hyponatremia.
Lithium can also be used b/c of its effects on the V2 receptors on the kidneys.

Parathyroid Gland 
Controls secretes PTH which controls the levels of Phosphate and Calcium (PTH increases the levels
of Ca2+).
Primary hyperparathyroidism  Occurs due to Adenoma to the parathyroids – which
causes an increase in the levels of PTH and Calcium.
Secondary hyperparathyroidism  Occurs due to problems in the hypothalamus or
other areas, but not a direct problem to the parathyroid. In secondary there is a
decrease level of Ca2+ which leads to an increase in PTH.
Findings in Hypercalcemia 
There is an Increase in Ca2+ levels greater than 10.2mg/dL with an elevated PTH.
Remember the phrase – Stones, Bones, Moans & Groans
Also it affects the Renal, Musculoskeletal, GI & Neruo functions.
Treatment of Hyperparathyroidism
Calcitonin – decreases the blood levels of Ca2+ via  inhibiting Ca2+ absorption in the
intestines, Inhibits osteoclast activity in the bones and inhibits renal tubular absorption
of Ca2+.
IV Bisphosphonates (IV “dronate” drugs) 
Etidronate & Pamidronate
Zoledronic acid  used to Tx multiple myeloma.

Oral Bisphosphonates  These are used to Tx Osteoporosis.

Alendronate, Ibandronate, & Risedronate
In case of an Emergency in treatment of severe hypercalcemia do the following 
IV normal saline  Furosemide ONLY for CHF Pts  IV Pamidronate  Calcium
gallium nitrate (this inhibits Ca2+ reabsorption from bones).
SE of “dronates” 
GERD-like symptoms, Osteonecrosis of jaw, Ulcers and rare rashes.
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Thyroid Gland 
Secretes T3 and T4 which influence many metabolic processes.
Hyperthyroidism  “Graves’ Disease”
Most commonly occurs in Females ages 30-40yrs.
There are Autoantibodies against TSH (Thyroid Stimulating Ig’s).
There is a decrease in TSH levels  b/c of Increase in the levels of T3 & T4.

Findings in Grave’s Disease  “thyrotoxicosis”

Tachycardia, Exophthalmos, Pretibial Myxedema, Emotional instability,
Inability to sleep, Tremors, Diarrhea, Heat Intolerance, and Weight loss
(despite increase in appetite).
Treatment for Hyperthyroidism 
Thioamides 
Propylthiouracil (PTU) & Methimazole
Inhibits Oxidation of Iodide into active Iodine.
Inhibits rxn of Iodine with Tyrosine to form T1 & T2.
Inhibits coupling of T1 & T2 to form T3 & T4.
Can Cross placenta thus used during pregnancies.
Side Effects 
Agranulocytosis – sore throat, fever, arthalgia
Tx – granulocyte-colony stimulating factor (G-CSF)
Drugs that affect Iodide Transporters  Thiocynate & Perchlorate.
Radiation & Thyroid 
High risk of developing cancer
Treat with 
Potassium Iodide.
Toxic multinodular goiter (Plummer’s Disease) 
Arrhythmias and Congestive Heart Failure (NOT autoimmune).
Treat with Radioactive Iodide – which will destroy thyroid cells.
CONTRAINDICATED during pregnancy.

Hypothyroidism”Hashimoto’s Disease” or “Adult Myxedema”.

Occurs primarily due to  Antimicrosomal and Anti-thyroglobulin Antibodies.

Findings in Hashimoto’s 
Lethargy, Constipation, Cold Intolerance, Weight gain, Myxedema, Cool Skin,
and Expressionless face.

Treatment of Hypothyroidism 
Levothyroxine & Liothyronine (Long-term excessive use of these drugs can
cause Palpitations, headaches, myalgia, nervousness & HTN)
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Adrenal Glands 
The Adrenal Cortex secretes the hormones – Mineralocorticoids (Aldosterone), Glucocorticoids
(Cortisol), Androgens (Testosterone).

Cushing’s syndrome 
These Pts have an INCREASE in Cortisol levels. Can occur due Primarily due to Adrenal
Neoplasia, or Secondarily due to Pituitary issues (too much secretion ACTH) **** It’s
called cushing’s ONLY when it is due to pituitary adenoma.

Clinical Presentation 
Moon face, Amenorrhea, Diabetes, and Osteoporosis.
Diagnostic testing 
Dexamethasone Suppression Test, if it is ABNORMAL  then do a
Low dose dexamethasone test if this is ABNORMAL  it is
Cushing’s syndrome.
Treatment of Cushing’s Syndrome 
Aminoglutethimide – Inhibits the conversion of
Cholesterol to Pregnenolone.
Metyrapone – Inhibits 11-β-hydroxylase.
Trilostane – Inhibits 3β-dehydrogenase.
Addison’s disease ”adrenocortical deficiency”
This is due to DECREASE in cortisol levels.

Clinical Presentation 
HypoTN, Hyperpigmented Skin (tan/bronze darkening of the exposed and
unexposed area).
Lab Findings 
Plasma cortisol, blood glucose and Urinary free Cortisol levels are DECREASED.

Treatment for Addison’s 

FIRST – Glucocorticoids
Hydrocortizone (short-acting)
Prednisone, Prednisolone, & Methylprednisolone
Dexamethazone

Adrenal Crisis 
Pts will present with  Fever, Abdominal Pain, Altered mental status and Vascular
Collapse.
Treatment  IV Fluid and IV Glucocorticoids.
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Diabetes Mellitus 
Type 1 DM (IDDM) 
This occurs to Pts less than 30yrs, or it is from birth.
There is NO Insulin, due to autoantibodies against the β-cells in the islet of Langerhans.
Pts will have Ketoacidosis and are lean. MUST give them Insulin.
Type 2 DM (NIDDM) 
These Pts have Insulin resistance for the receptors.
Usually occurs in adults commonly greater than 40yrs.
Pts present as Obese, NO autoantibodies, Hyperosmolar coma (HHNS) in few Pts.
Give them Oral hypoglycemic.

Diagnosis of DM 
Polyphagia, Polydipsia & Polyuria.
Ketonuria (only in DM-1), and plasma glucose levels above 200mg/dl.
Values 
Fasting plasma glucose < 115mg/dL
2 readings of fasting plasma glucose Above 125mg/dL are asymptomatic DM Pts.
Hemoglobin A1C levels not diagnostic but are done as a Follow up for DM Pts.
Increase in A1C levels indicated an Increase in blood glucose.
Normal A1C levels are 6-7%.

Diabetic Ketoacidosis (DKA)  Type 1 DM

Can be due to precipitation factors such as Insufficient Insulin Therapy,
Infection, Emotional stress and or Excessive alcohol intake.
When there is NO Insulin  leads to INCREASE in Lipolysis  Leads
to INCREASE in free fatty acids  Ketone Bodies.
Clinical Finding in DKA 
Fruity breath odor of acetone
Give these Pts acetone drips until acetone disappears.
Give IV fluids and IV insulin.
When there are High levels of Glucose  Insulin will be released to lower the hyperglycemic state.
When there are Low levels of Glucose  Regulatory hormones such as Glucagon, GH, Cortisol &
Epinephrine will kick in the increase the levels.
Hypoglycemia 
Pts will present with 
Sweating, Tremors, Tachycardia, Anxiety and Hunger
This occurs b/c of DECREASE in the blood glucose levels which triggers epinephrine
Just give these Pts sweets, candies etc.. anything with sugar.
Insulinoma 
Occurs due to a benign tumor which produces abnormal amounts of insulin.
Whereas, Factitious Hyperinsulinoma  occurs due to self-ingestion of insulin.
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Differentiating b/w Insulinoma & Factitious  Tx Insulinoma with “Diazoxide”

There is an elevation of BOTH Insulin & Insulin/glucose ratio.
So look for peptide C & proinsulin – these are ONLY INCREASED in Insulinoma.
Same thing can be found if taking the drug Glipizide.
For Factitious look for – antibodies against insulin, ONLY if you are taking insulin

Type 2 DM (NIDDM) Therapy 

Oral Hypoglycemics 
1. Sulfonylureas, 2. Biguanides, 3. α-glucosidase inhibitors, 4. Meglitinide and 5.
Thiazolidinedione.
Sulfonylureas – These block the ATP-dependent K+ channels acting on the β-cells of
the pancreas. Don’t give these to pts with “Sulfa” drug allergies.
1st generation sulfonylureas
Acetohexamide, Chlorpropamide (has longest ½ life & disulfiram
action), Tolbutamide (Used in Renal dysfunction, b/c it’s not excreted),
2nd generation sulfonylureas 
Glipizide (increases the release of insulin from the β-cells),
Glyburide (accumulates in renal impairment).
Biguanides 
Metformin – Inhibits Hepatic gluconeogenesis, thus increasing tissue sensitivity
to insulin (by increasing methylation), but has a major side effect of Lactic
Acidosis.
α-glucosidase inhibitors 
Acarbose & Miglitol These drugs decrease Carb absorption
(SEs causes abdominal pain, Gas/flatulence & diarrhea).
Meglitinide 
Nateglinide & Repaglinide
Thiazolidinedione (Glitazone) -> weight gain is a common SE of these drugs.
Pioglitazone & Rosiglitazone
Thiazolidinediones – Increase the sensitivity of tissues to insulin via Release of
Adipokines (adiponectin) and by stimulating the transcription of insulin gene
by binding to Peroxisome Proliferator Activating Receptor (PPARs) a
nuclear/DNA enhancer element.
Both Metformin and Thiazolidinediones DECREASE Hepatic
gluconeogenesis.

Non-insulin Polypeptide Analogues  GLP-1 antagonists.

Pramlintide – for Type 1 DM taken with Insulin.
Exenatide – for Type 2 DM.
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Sex Hormones 
How can you diagnose Hypogonadism 
This basically means the Ovaries or the Testes are not
producing decrease levels of Estrogen or Progesterone and or
Testosterone.
Test this by giving the Pts Gonadorelin (synthetic
GnRH).
If the levels of the hormones come back to
normal then the problem is b/c of hypothalamus or pituitary.
If the levels do not come to normal then the
problem is with the ovary or testes.

Precocious Puberty 
Is having puberty at an earlier age than it should have been. Anywhere from age 7-
11yrs.
When diagnosing the cause if all CT scans are negative – then the cause is said to be
Idiopathic so we must treat.
Give them GnRH Agonists such as  (eventually decrease FSH & LH levels)
Nafarelin & Leuprolide
SEs  low self-esteem, hirsutism, hot flashes,
osteoporosis, body odor and changes in
menstruations.

Clomiphene  “SERM” selective estrogen receptor modulator.

This drug is used to Treat Anovulation which causes infertility in females.
Blocks the estrogen receptors in the hypothalamus  increase in GnRH  increase in FSH & LH
Ovarian Stimulation.

Urofollitropin  This is taken from the urine of postmenopausal women containing FSH. It is used in
combination with hCG to aid with ovulation and fertility.

Estrogens & Progestin 

Estrogens 
Primarin, Ethinyl estradiol, Mestranol & DES (diethylstilbestrol).
These are used for 
Contraception, Menstrual irregularities, Menopausal hot
flashes, Atrophic Vaginitis and Postmenopausal
Osteoporosis.
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Side Effects of Estrogens 

NVD, increase risk of thromboembolism (via inhibiting
antithrombin 3), and gall stone formation.
DES side effects 
Clear Cell Adenocarcinoma & incompetent Cervix.
Progestin 
Progesterone, Medroxypregesterone, Norethindrone & Norgesterol.
These are used for Contraception depot, basically opposing the actions of
estrogen.
Mifepristone  This is Progesterone Antagonist
Used to terminate pregnancy through day 49.
Causes vaginal bleeding and cramps.

Selective Estrogen Receptors Modulators (SERM) 

Fulvestrant, Tamoxifen & Raloxifene 
Tamoxifen – Used for breast cancer in premenopause
Functions as Antiestrogenic in breast receptors & Estrogenic in
bones and uterus.
SEs Intermittent vaginal bleeding from the uterine endometrium.
Raloxifen – Used for prevention of Osteoporosis in postmenopause.
Fulvestrant  It is an estrogen receptor antagonist with no agonist effects, which works both by
down-regulating and by degrading the estrogen receptor.
Tx of hormone receptor-positive metastatic breast cancer in postmenopausal.
Oxytocin  Induces labor and controls postpartum hemorrhage.
It contracts the pregnant uterus leading to rapid birth.

Ergonovine Increases uterine contractions.

It is a Partial Agonist of α-adrenergic & 5HT receptors.
Used for Postpartum hemorrhage.
Dinoprostone  This drug Promotes Cervical Ripening. It is PGE2 analogue.

Tocolytics  3 of them
These are drugs that Inhibit premature labor.
Ritodrine 
β-2 agonist, that relaxes the uterine muscle via inhibiting uterine contractions.
Terbutaline & MgSO4 (magnesium sulfate).

Oxandrolone  Is a synthetic anabolic steroid derived from DHT. It is a type of androgen used to
gain weight.
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BPH drugs 
Flutamide – Blocks the androgen receptors (anti-androgenic) – inhibits ligand-receptor interaction.
Finasteride –
Is a 5α-reductase inhibitor
Stops the conversion of Testosterone  DHT (grows the prostate gland).

Prazocin, Doxazocin & Terazocin – These are α1-blockers that are used for BPH w/ HTN Pts.
Tamsulosin – used for BPH only.

Erectile Dysfunction Drugs 

Sildenafil (Viagra), Tadalafil (Cialis) & Vardenafil (Levitra).
These Inhibit Phosphodiesterase enzyme (PDE5) – thus stopping the metabolism of
cGMP in the corpus cavernosum.

Side Effects 
Headache, Facial Flushing and Back Pain. Decreases basal vascular smooth muscle tone
DO NOT use PDE5 inhibitors on Pts taking nitroglycerine as will cause severe HypoTN.
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Psychopharmacology, Hematology & GI:

Decreased levels of NE & 5HT  Depression

Increased levels of NE & 5HT  Bipolar (mania)
Increased levels of DA  Psychosis / hallucinations
Decreased levels of GABA  Anxiety

Antipsychotic Drugs:
These drugs are Antidopaminergics, they block the D2A receptors, and they are also given the
name Neuroleptics.

Schizophrenia
Positive Symptoms Negative Symptoms
Hallucination – False perception Flat Affect
Delusions- False Beliefs Social Withdrawal
Agitation Poor Speech
Antidopaminergics work ONLY on the Positive symptoms.

Conventional (Typical) Antipsychotics 

Phenothiazines – “Blocks the DA-receptors in the CTZ”.
Chlorpromazine: Used as an Antiemetic
Fluphenazine: it is short acting, But when given IM it is long acting.
Mesoridazine: Causes Prolonged QT-intervals (torsade’s de ponte)
Thioridazine: Causes Prolonged QT-intervals (torsade’s de ponte), Retinal deposits (giving a
brownish discoloration to vision).
Perphenazine: Has Low Cardiac Risks.
All of the Phenothiazines are WEAK antipsychotics EXCEPT for Fluphenazine.

Butyrophenones –
These are the MOST POTENT
Haloperidol: Used to treat Psychosis, Tourette’s and Hyperactivity in children.

Other antipsychotics –
Loxapine: Has Low Cardiac Risk
Molindone: Has Low Cardiac Risk.
Pimozide: Causes Prolonged QT-interval just like (mesoridazine & Thioridazine).
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Side Effects of Typical Antipsychotics 

All Typical (conventional) Antipsychotics have adverse side effects such as Extrapyramidal
symptoms (EPS).
EPS 
PD symptoms – Tremors
Akathisia – Inability to stand still, always moving around.
Dystonia – Muscle Spasms
Tardive Dyskinesia – It’s a Late Onset, involving Painless Involuntary movement of
the face, such as protruding of the tongue.
NMS (neuroleptic malignant syndrome) – This similar to malignant hyperthermia
which includes Hyperpyrexia, Muscle rigidity, fever, muscle stiffness and
Tachycardia.
Tx – Dantrolene

Anticholinergic  Dry mouth and Constipation

Orthostatic HypoTN – b/c of the α-blockade.
Pts also complain of Reflex Tachycardia leading to impaired ejaculation.
Photosensitivity and Rashes – Caused by Chlorpromazine.
Increased appetite & Weight gain (all except Molindone cause this).

Antipsychotics are Antidopaminergics, they block the D2A receptors.

The More Potent the antipsychotic the more EPS and the less anticholinergic effects.
Such as – Haloperidol & Fluphenazine.

The Less Potent the antipsychotic the less EPS and the more anticholinergic effects.
Such as – Chlorpromazine & Thioridazine.

How to manage Pts on Antipsychotics 

Tell Pt that Phenothiazine may discolor urine to pink or reddish-brown.
Avoid OTC or herbal medications
Monitor the QT-interval when giving Thioridazine or mesoridazine.
Avoid Alcohol in conjunction with other CNS depressants.
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Atypical Antipsychotics:
These work on both the Positive and negative symptoms of schizophrenia.
Drugs 
Clozapine – used for Refractory schizophrenia (when other drugs don’t work). Causes
Agranulocytosis.
Olanzapine  causes weight gain and DM
Quetiapine  Treatment for Autism in children
Risperidone  Causes EPS with high doses
Ziprasidone  Blocks dopamine and 5HT
Aripiprazole  Partial agonist on dopamine receptor as well as has antagonist activity.

Major affective Depression 

Unipolar – occurs due to Decrease in the levels of NE & 5HT
Bipolar – Occurs due to Increase in NE & 5HT.

Antidepressants 
Tricyclics  These inhibit the reuptake of NE & 5-HT at presynaptic membrane.
Amitriptyline & Nortriptyline  both used to treat chronic pain.
SEs Comatose, intermittent seizures, prolonged QT (heart block), confusion,
vomiting, Flushing dilated pupils and tachycardia.
Clomipramine  Used for OCD.
Imipramine  Used for Enuresis (bedwetting normal in children up to age 6).
Trimipramine  Same as Imipramine, except gives No GI upset.
Desipramine  Causes sudden cardiac death in children.
Doxepin  Used for anxiety.
Tetracyclics
Amoxapine  Is a dopamine blocker.
Maprotiline  may produce Seizures.
Mirtazapine  Used for Seizures & Agranulocytosis.

2nd generation tetracyclics 

Nefazadone  Causes Hepatotoxicity
Trazodone  Priapism
Bupropion  Smoking cessation and Seizures.
Venlafaxine  dose dependent. Small doses increases NE only,
under 75mg. And at high doses it increases Serotonin and NE,
over 75mg.
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MAOI (monoamine Oxidase inhibitors) 

Phenelzine & Tranylcypromine  Can cause HTN crisis with consumption of foods
containing tyramine such as Cheese and Wine.

SSRIs 
Fluoxetine, Paroxetine, Sertraline, Fluvoxamine, & Citalopram
ALL SSRIs are safe during pregnancy and they have fewer side effects.
Sertraline is also used for menstrual pain.
Duloxetine  same family of fluoxetine. It is an SSRI and NE reuptake inhibitor
but used for pain cause by diabetic neuropathy, can Rx the nerve damage, but
somehow relieves the pain.
**Paroxetine Hydrochloride – Can be used to Tx Premature Ejaculation. ***
Managing Pts on Antidepressants 
Tricyclics take 30 days to work, whereas SSRIs take about 1-4 weeks.
Fluoxetine interferes with sleep so should be taken early in the day.
DON’T MIX SSRIs with MAOIs  cause Serotonin Syndrome, fever, HTN, Hyperthermia & Seizures.
Tx for Serotonin Syndrome  Cyproheptadine

Antimania Drugs  Bipolar disorder

Lithium a “mood stabilizer”. (AVOID thiazides, NSAIDs & ACEI when giving lithium)
Mania is  hyperactivity, reduced sleep, excessive spending with poor judgment and
aggressiveness.
Lithium 
Has a narrow TI
Causes NDI (nephrogenic DI) leading to Hyponatremia due to vomiting and diarrhea.
May also cause Hypothyroidism and suicidal tendencies, as well as Tremors.
Carbamezepine  Agranulocytosis
Valproic Acid (pancreatitis & hepatotoxicity) & Levetiracetam
Antianxiety Drugs 
Alprazolam  DOC for panic disorder
For Phobia’s give SSRIs.
OCD Pts give  Clomipramine, Paroxetine & Fluvoxamine (this newly approved FDA drug).
Generalized Anxiety Disorder (GAD)
Buspirone  it is a 5HT-agonist
Zolpidem  is a Non-Benzo
Hydroxyzine  Antihistamine
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Hematology:
Antiplatelets that Inhibit TxA2 
Aspirin 
Given as prophylaxis in MI & Stroke Pts.
Irreversibly inhibits COX1 & COX 2 receptors. Used as Antiplatelet and Antiinflammatory
Side Effects – Gastric Ulcers, Bleeding, and Tinnitus (ringing in the ear).

Dipyridamole 
Inhibits Platelet aggregation and in high doses also inhibits Phosphodiesterase.
Used to prevent embolization on prosthetics valves.

Antiplatelets that Inhibit ADP-receptors 

Clopidogrel and Ticlopidine 
Used as alternatives for aspirin in MI and Stroke.
Side effects  Hemorrhage, leukopenia and TTP (thrombgenic Thrombocytopenic
Purpura).
With Ticlopidine some reports of Agranulocytosis has been reported.
Cilostazol 
Is a Selective PDE3 inhibitor
Approved for treatment of Intermittent Claudication (PAD).

Antiplatelets that Inhibit GpIIb/IIIa receptors 

IV Abciximab, Eptifibatide & Tirofiban.
Prevents platelet aggregation by inhibiting fibrinogen from binding with GpIIb/IIIa receptors.
Used to Treat ACD (acute coronary Disease) and Angioplasty.

Anticoagulants 
Heparin IV and Warfarin Orally.
LMWH heparin 
Has less hemorrhagic complications and drugs include 
Dalteparin and Enoxaparin (MC prescribed, not as strong).
Danaparoid – safer in hypersensitivity to heparin
Thrombin Inhibitors
Argatroban
Bivalirudin best for unstable angina undergoing PTCA (now use PTI,
percutaous transluminal intervention). Treatment for Heparin-Induced
thrombocytopenia.
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Heparin
Activates antithrombin III by enhances serine protease activity
This will cause the inactivation of activated factors – 2, 9, 10, 11 & 12
Effective both In-Vivo and In-Vitro. Safe in Pregnancy b/c doesn’t cross the Placenta
It only affects the PTT (measures intrinsic pathway of coagulation)

SE  Heparin-induced thrombocytopenia – Tx with “”rudin”” drugs

Warfarin is contraindicated in pregnancy
Pregnant female with history of DVT, give her heparin, labor is bloody and
messy.
Works on the liver stops vit K needed for 2, 7, 9, 10
Increase in PT (measures extrinsic pathway)
Blocks gamma carboxylation of clotting factors, only effective in liver (warfarin
works on blood).
Sulfa drugs, & Azoles and other drugs that inhibit CYP450 increase warfarin toxicity.
Side Effects 
Skin necrosis (painless demarcated rashes & purpura), purple toe syndrome
(Occurs in 3-8wks) and Teratogenic bone defects.
Enoxaparin  LMWH
Has high activity against factor X compared to factor 2 with longer t1/2 than
heparin.
DOESN’T affect PT or PTT and is FDA Approved for Tx of DVTs
Side Effects – Hemorrhage, thrombocytopenia and local irritation.
Contraindicated in Prosthetic Heart Valves (b/c of high risk of
thromboembolism.

Antidote to Heparin  Protamine Sulfate

Antidote to Warfarin  Vit K (phytonadione) or Fresh-frozen plasma

Fibrinolytics  Thrombolytics
These activate the conversion of plasminogen to plasmin  leading to lysis of fibrin clot to
degradation products.
Plasmin is a serine protease thus it is Inhibited by α-2-antiplasmin.
tPA 
Alteplase and Reteplase  these are clot specific and have NO allergies or
hypersensitivities.
Streptokinase  Nonspecific they decrease the circulating fibrinogen and factors 5 & 8
Can cause allergies and hypersensitivities.
What if there is too much bleeding with Fibrinolytics?
Antidote – Aminocaproic Acid (systemic hemostatics).
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Topical Hemostatics 
Surgeons use this to limit blood loss.
Absorbable gelatin sponge, Absorbable gelatin powder, Microfibrillar collagen hemostat and
Thrombin.

Blood & Blood Components 

Whole Blood –
Used for hemorrhages and hypovolemic shock
Packed RBCs –
Transfused when whole blood results in overload.
Fresh Frozen plasma –
Used in Clotting deficiencies.
Plasma exchange (Plasmapheresis) –
Immune disorders
Cryoprecipitate
Hemophilia and vWF (desmopressin)
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Gastroenterology:
Drugs used in gastric Ulcers 
Antacids 
Mylanta & Tums
Aluminum hydroxide (SEs – Constipation, muscle weakness & decrease P+)
Mg hydroxide (SEs – Diarrhea, HypoTN, & Cardiac arrest)
Ca2+ carbonate (SEs – hypercalcemia – metabolic alkalosis)
These neutralize the gastric acid. Used to treat indigestion, reflux esophagitis and peptic
ulcers.
Side Effects 
Aluminum hydroxide – can cause Hypophosphatemia and Osteodystrophy.
Mg Hydroxide – causes Hypermagnesemia and loss of deep tendon reflexes.
Ca2+ Carbonate – Hypercalcemia

H2 Antagonists 
Histamine – found in the lungs, skin and GI
Released by the mast cells via type 1 hypersensitivity
H1 activation 
Causes Hypotention via NO, Edema b/c of increase in capillary permeability and
Bronchospasm, increased pain and pruritis.

H1 receptor Antagonist  Produces Sedation

Used to treat allergic rxns, N&V, sleep aids and cold meds.
Causes Sedation EXCEPT Loratadine, Cetirizine and Fexofenadine.
Diphenhydramine  OTC (SEs --anticholinergic, antiserotogenic).
Promethazine  α-blocker
Meclizine  Treatment for Motion Sickness
Hydroxyzine & Chlorpheniramine

H2 Activation 
Causes an Increase in HCL secretion, increase SA nodal rate and contractility.
H2 Receptor Antagonist 
Blocks HCL secretion and the secretory response to food stimuli.
Cimetidine, Famotidine & Ranitidine
These are Tx for indigestion, heart burn, duodenal ulcers and Zollinger-
Ellison syndrome.
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Side Effects of H2-Antagonist –

Cimetidine inhibits CYP450  increases toxicity of Theophylline,
Warfarin, Phenytoin and Diazepam.
Cimetidine Decreases androgen leading to gynecomastia and
decrease libido.
Also Acid Inhibitors will decrease the action of Sucralfate.
Famotidine causes blood dyscrasias

Proton Pump Inhibitors (PPI)  “prazole” drugs

Omeprazole, Lansoprazole & Esomeprazole
These drugs block gastric acid secretion by inhibiting H+/K+ ATPase pump.
These are BETTER than H2 Antagonists.
CONTRAINDICATED in Pregnancy, Breast-feeding and hypersensitivity

Sucralfate  Forms a protective acid resistant shield in the ulcer.

SE – Constipation.
Misoprostol  Prostaglandin analog (PGs suppress gastric secretion). That is why Aspirin and
NSAIDs cause Ulcers.
So it is used to Tx Ulcers caused by NSAIDs. Can cause Early Abortion.

H. Pylori Treatment Plan 

Triple Therapy  2 antibiotics + 1 PPI (proton pump inhibitor).
Amoxicillin + Clarithromycin + Omeprazole

Antiemetics 
Metoclopramide –
Centrally It inhibits DA in the CTZ
Peripherally Reverse the mobility of vomiting reflex.
Used to Tx  Nausea & Vomiting with Cancer therapy, Promotes gastric emptying
and reduces gastric regurgitation during surgery.
SEs Diarrhea & HypoTN.

Chlorpromazine, Promethazine & Haloperidol –

These are Antipsychotic drugs that can also be used to Tx Nausea & Vomiting b/c they block
the DA-receptors in the CTZ. They also have EPS side effects.

Scopolamine – It is an Anticholinergic indicated to prevent Nausea & vomiting via blocking the
Labyrinthine vestibular system.
Used to Tx  MOTION SICKNESS
SEs  anticholinergic such as – constipation, Urinary retention & dry mouth.
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Aprepitant – Antiemetic that belongs to a class of drugs called substance P antagonists (SPA). It
mediates its effect by blocking the neurokinin 1 (NK1) receptor.

Ondasetron & Dolasetron (“setron” drugs)  Work as a 5HT3 receptor antagonist, at the CTZ
(area Postrema) and the GI tract.
Used to Tx  N & V caused by cancer chemotherapy.

Dronabinol  Cannabinoids a Schedule 3 substance.

2ndline of Tx for N & V caused by chemotherapy
MOA = decreases the emesis by activating the receptors that block pain receptors in the GIT.
Used to Treat  Appetite stimulant in Anorexia and Weight loss in AIDS Pts.

Emetic Drugs 
Activated Charcoal It filters the poison from the GIT, thus this is given for poisoning and OD
after oral injection.
CONTRAINDICATED in Acid, Alkali or Petroleum ingestion.
SEs  Pulmonary Aspiration.

Ipecac  Stimulates the CTZ to induce vomiting and can cause Lethargy as a SE.

Antidiarrheals 
Loperamide – It is a Opioid receptor Agonist that decreases the activity of the Myenteric plexus.
Bismuth subsalicylate
Diphenoxylate + Atropine (Opioid + Anticholinergic)
These are CONTRAINDICATED in Abdominal pain of unknown cause with fever.
Loperamide & Diphenoxylate work on the Mu-receptors.
Laxatives 
Psyllium (bulky-forming laxative)
Lactulose – this is a hyperosmotic laxative used to Decrease the ammonia (Increase excretion of
NH4) in Pts with hepatic encephalopathy.
Docusate Ca2+ -- Stool softener.
GoLYTEL – is used for bowel cleansing before colonoscopy.

Inflammatory Bowel Disease (IBD) 

Sulfasalazine (specifically for Ulcerative Colitis)
Mesalamine (Salicylic acid) and Infliximab (blocks TNF-α)
These drugs are indicated for Ulcerative Colitis & Crohn’s disease.
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Antibiotics, Antifungals & Antiviral:

Antibiotics 
Inhibit the cell wall synthesis via 
They bind to the (PBPs) cytoplasmic-protein-binding proteins  Inhibit
transpeptidation  and inhibit cross-linking of bacterial cell wall.
Drugs that inhibit Cell wall synthesis 
Penicillins, Cephalosporins, Imipenem, Meropenem & Aztreonam.
Vancomycin: Inhibits Peptidoglycan synthase via binding to D-alanine.
Drugs that Inhibit Protein Synthesis 
Drugs interfering with Initiation complex:
Aminoglycosides – Works on the 30S,
Linezolid – works on the 50S
These are also Bactericidal (kills the bacteria)

Drugs interfering with incorporation of next AA:

Tetracyclines – work on 30S
Dalfopristin & Quinupristin – they both work on 50S
Bacteriostatic (b/c interferes w/ insertion of aminoacyl-tRNA into A-site.

Drugs interfering w/ formation of peptide bond:

Chloramphenicol – DOC for pregnant woman with tick infections.
SE includes gray baby syndrome (Aplastic Anemia)

Drugs interfering with Translocation:

Macrolides – for 50S; Clindamycin – 50S
Inhibits the translocation of Peptidyl-tRNA from accepting the donor site.

Drugs that Inhibit Folic Acid Synthesis 

Sulfonamide – Inhibits Dihydropteroate synthetase.
Trimethoprim & Pyrimethamine – These inhibit Dihydrofolate
Reductase.
Drugs that Inhibit Nucleic Acid Synthesis 
Fluoroquinolones – Inhibits DNA-gyrase (Topo II).
Rifampin – Inhibits DNA-dependent RNA-polymerase.
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Mechanisms of Resistance  bacteria that produce

β-Lactamase (Penicillinase) cleavage of drugs with β-lactam ring which include 
Penicillins and Cephalosporins
Production of conjugation enzymes that increase the drug clearance 
Aminoglycosides
Formation of Acetylating enzymes that inactivate drugs 
Chloramphenicol
Methylation of base in RNA that alters the drugs binding
Macrolides
Production of active transport system that pushes the drugs out of the cell
Tetracyclines
Formation of PABA, increases the resistance to inhibition of Dihydropteroate synthase 
Sulfonamides

Antibiotic Combination 
Additive Effect: 1+1= 2
Synergistic Effect: 1+1= 3 (drugs like Penicillin + Aminoglycosides) give for PID pts.
Antagonist Effect: 1+1= 0 (Penicillin + Tetracyclines in pneumococcal meningitis).

Bacteria’s 
Gram + (purple) Gram – (red)
Staphylococcus E. Coli
Streptococcus Neisseria
Clostridium H. Influenza, Pseudomonas, Bacterioides & Klebsiella

Staph Aureus 
Nonpenicillinase producing, Penicillinase producing, MRSA and VRSA.
Penicillinase Resistant Penicillins include  for Penicillinase producing Staph aureus.
Put these for STAPH INFECTIONS….
Oxacillin (IV), Cloxacillin (PO), Dicioxacillin (PO) & Nafcillin (IV).
These are Methicillin Group of drugs (only used in labs).
Tx for MRSA is Vancomycin

Amoxacillin and Ampicillin – These are Broad Spectrum antibiotics used to Treat Strep
species and G (-) bacteria, NOT Staph.

Extended Spectrum penicillins (Antipseudomonads)  not good for Staph aureus.

Piperacillin, Ticarcillin, Carbenicillin
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β-Lactamase inhibitors 
Clavulanate & Sulbucatam
These drugs are combined with broad spectrum and extended
spectrum to cover everything including Staph aureus.
Amoxacillin + Clavulanate
Ampicillin + Sulbucatam
Piperacillin + Tazobactam
Ticarcillin + Clavulanate
These are good for G (+) & G (-) except MRSA.
Antibiotic Do’s & Don’ts 
Check for allergies, b/c if they are allergic to Penicillin then they are also allergic to Cephalosporins.
Can get a Superinfection if the normal body flora is disrupted.
Occurs due to microorganisms that are resistant to the antibiotic therapy.
Pts will present with 
Black, furry overgrowth on the Tongue, Loose/Foul smelling stools. Women
will have vaginal itching or discharge.
Don’t drink acidic juices with Oral Penicillin b/c it reduces the drug absorption.

Cephalosporins  DOC for gonorrhea

First Generation Cephalosporins:

These are good against G (+) bacteria.
Cefazolin (surgical prophylaxis)
Cephalothin (Renal Tubular necrosis)
NO CNS entry with these drugs
Second Generation of Cephalosporins:
Cefotetan – Treatment for Bacteroid fragilis infection & has Disulfiram activity.
Cefaclor – Causes Some Serum Sickness
Cefuroxime – Can do CNS entry.

Third Generation of Cephalosporins:

These enter the CNS EXCEPT for Cefoperazone
Ceftriaxone – IV single dose for Tx of Gonorrhea also give Doxycycline for 10 days
for chlamydia.
Cefixime (PO)
Ceftriaxone & Cefoperazone – Biliary sludge w/ cholecystitis like illness.
Side Effects 
Pseudomembranous Colitis
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Fourth Generation of Cephalosporins:

Good as third generation, they are also good against G (+) bacteria
Cefepime IV

If the Pt is allergic to Penicillin don’t give Cephalosporins.

If the bacteria is G (+) give them Macrolides.
If it is G (-) rods use Aztreonam.
Cephalosporins are NOT effective against 
Chlamydia, MRSA, Mycoplasma, Listeria & Enterococci.

New β-Lactams 
Monobactams –
Aztreonam – Binds to the PBPs 1a & 3 and inhibits transpeptidation.
It is given IV for G (-) bacteria and has NO cross sensitivity to penicillin.
Synergistic to aminoglycosides and DOC for Pseudomonas infections.
Carbapenem –
Imipenem / Cilastatin – ***
Imipenem is rapidly metabolized by renal dipeptidase.
Cilastatin is inhibitor of dipeptidase  thus increases the duration
of action of Imipenem.
Meropenem –
Treatment for Serious Infections
Carbapenems are given IV for G (+), G (-) and Anaerobes.
Side Effects 
Seizures with renal dysfunction (caused by Imipenem).

Vancomycin 
Non-penicillin or Cephalosporin
Used for G (+) bacteria ONLY. It Inhibits the Cell wall, inhibits elongation of peptidoglycan chains
and is Bactericidal.
When Given IV it is effective against MRSA
Orally it is effective against Clostridium difficile (G +) (pseudomembranous colitis).
Vancomycin NOT effective in G (-) bacteria.
Side Effects 
“Red man Syndrome” – Chills, fever, rash, red face & neck all due to Histamine
release.
Ototoxicity, Hypersensitivity & Nephrotoxicity.
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Macrolides  binds to 50s and Inhibits Translocation of tRNA

Erythromycin, Azithromycin & Clarithromycin
Macrolides are the DOC for  CAP caused by mycoplasma pneumoniae.
NOT effective for MRSA
Erythromycin Estolate – Causes cholestatic jaundice via binding to motilin receptors  causing
diarrhea.
Erythromycin  DOC for infections during pregnancy.
This is good against Staph, Strep, Mycoplasma and Legionella.
Side Effects – Diarrhea, Vomiting, and in High Doses causes Increase QT-interval, inhibits
CYP450.
Azithromycin most commonly Rx (ZPAC)
Just as good as erythromycin but also helps with Chlamydia urethritis, and has LESS Side
Effects.
Clarithromycin 
Just as effective as erythromycin but also takes care of H. Influenza & H. Pylori, and is
also good against MAC (mycobacterium avium complex- causes pneumonia in AIDS
Pts).

Ketolides 
These are new class of drugs related to the macrolides.
Telithromycin – Similar to azithromycin
Side Effects 
Prolonged QT-interval and Inhibits CYP450.

Bacterioides Anaerobic infections

Clindamycin Metronidazole
For Oral Infections caused by Bacterioides Intraabdominal infections caused by Bacterioides
Risk of causing AAPMC (antibiotic associated Treats AAPMC (pseudomembranous colitis)
pseudomembranous colitis).

Metronidazole 
It is Bactericidal and is the DOC for 
Protozoa – Giardia Lamblia, Trichomonas Vaginalis &
Entamoeba histolytica.
Bacterial – AAPMC, Bacterioides & G. Vaginalis
Side Effects 
Furry Tongue, Glossitis, Peripheral Neuropathy & Disulfiram action.
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Tetracyclines  “Cycline” drugs

Tetracycline, Doxycycline, Minocycline & Demeclocycline
These drugs are good for chlamydia, rickettsia, Mycoplasma, Brucella, Yersinia and Vibrio Cholera.
Used in Pts those are allergic to penicillin.
AVOID Dairy products b/c it acts as a chelators thus it will reduce the absorption of tetracyclines,
EXCEPT for doxycycline & Minocycline.
Demeclocycline  Used to treat SIADH b/c it inhibits ADH.
Doxycycline  Penetrates the prostate and used to in Prostatitis.
Minocycline  can cause drug induced hepatitis and SLE-like syndrome.
Doxycycline & Minocycline – out of all the tetracyclines these can be given to Pts with Renal Failure
Side Effects of Tetracyclines 
CONTRAINDICATED in children younger than 8yrs old b/c it causes permanent discoloration of
the teeth.
Use sunscreen when outdoors while taking the drugs b/c of Phototoxicity risk.
Expired tetracyclines causes – Fanconi-like syndrome
Hepatotoxicity (pregnant women), Nephrogenic DI (caused by Demeclocycline), Vestibular
ototoxicity (caused by Minocycline).

Fluoroquinolones  “Floxacin” drugs – inhibit insertion of negative supercoils in DNA

Ciprofloxacin, Norfloxacin, Ofloxacin, Enoxacin, Sparfloxacin & Trovafloxacin.
These are Analogues of Nalidixic Acid ..commonly used to treat UTIs.
DOC for – Anthrax 2ndary choice is penicillins or tetracyclines.
Good against G (-)’s
Ciprofloxacin & Ofloxacin given in single dose for gonorrhea.
CONTRAINDICATED in Pregnancy. Be CAREFUL in adults younger than 18yrs of age b/c it these drugs
inhibit chondrocytes – causing tendon ruptures or arthropathy’s.

Aminoglycosides  These are used for G(-) organisms

Gentamycin, Tobramycin & Paramomycin
Amikacin, Neomycin, Kanamycin & Streptomycin
Has MOA of active transport of O2 dependent system.
Used in combination with
Endometritis – Triple antibiotic therapy via gentamycin + ampicillin + Metronidazole.
Enterococcus infections – Used synergistically with Ampicillin.
Pseudomonas infections – Used synergistically with extended spectrum penicillin’s.
Side Effects 
Ototoxicity in about 2% of the Pts
Nephrotoxicity in 7% -- Proteinuria, Hypokalemia and Acute Tubular Necrosis.
Neuromuscular blockade – Decreases prejunctional release of ACH.
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Spectinomycin 
This is NOT an aminoglycoside
Used in Tx of Gonorrhea.
Inhibits protein synthesis by binding to 30S doesn’t cause the misreading of the genetic
code.
Sulfonamides  “Sulfa” drugs
Sulfisoxazole – Used in Tx of UTI & Nocardial infections.
Sulfasalazine – Tx of Ulcerative Colitis.
Sulfacetamide  Tx for Trachoma (topically)
Silver Sulfadiazine  Tx for Burns (topically)
Sulfadiazine & Pyrimethamine – Tx for Toxoplasmosis
TMZ-SMX – Tx for PCP
Side Effects 
Rash to Steven Johnson Syndrome, Hemolysis in G6PD Pts, Photosensitivity and Crystalluria.
CONTRAINDICATED in 3rd trimester of pregnancy b/c it crosses the BBB  leading to
kernicterus.
Warfarin & Phenytoin activity are increased when taken with Sulfas.

TMZ-SMX (trimethorprin-sulfamethoxazole) 
DOC for Prohylaxis and Tx for PCP
2nd choice for treatment of Salmonella, Chancroids and MRSA
Side Effects 
Thrombocytopenia, Leukopenia, GI Distress in AIDS Pts and Hemolysis.
Urinary Tract Antiseptics 
Methanamine mandalate and Nitrofurantoin
Urinary Tract Analgesics 
Phenazopyridine
May produce Orange to Red urine that stains clothing.

Methicillin Resistant Staph Aureus (MRSA) 

Treatment via Vancomycin

VRE & VRSA 

Treatment via – Linezolid (Quinupristin/Dalfopristin).
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Antifungal Drugs:
Polyene Antifungal
Amphotericin B – used IV for life threatening infections.
Also used for Aspergillus, Candida, Cryptococcus and Histoplasmosis.
The drug binds to Ergosterol and inhibits it.
Side Effects 
Dose dependent 
Nephrotoxic, Hypokalemia & Normochromic Normocytic anemia.
Infusion Dependent 
Flu-like symptoms, low distribution into the CSF
Drug interaction  Synergistic with fluocytosine.

Nystatin –
Used topically for Treatment of Candidiasis (oral thrush). Should not be used
systemically b/c it is too toxic.
Azole Antifungals
Ketoconazole, Fluconazole, Itraconazole, Clotrimazole & Miconazole
This drugs block synthesis of Ergosterol by inhibiting 14-α-demethylase in the fungal P450
complex.
They are Given PO for – Candidiasis & Coccidiomycosis.
Also used for Paracoccidiomycosis, Blastomycosis & Histoplasmosis.

Clotrimazole & Miconazole – Given topically to Tx Candida and Dermatophytic infections.

Side Effects  Inhibit CYP450

Ketoconazole causes Gynecomastia & decrease libido
Menstrual irregularities
Fluconazole penetrates CSF, Itraconazole NO CSF,
Absorption of these drugs is increased by food.

Limited Indication Antibiotics 

Griseofulvin – Causes disruption of mitotic spindle at M-phase by interfering with α/β tubulin
dimers of the Microtubules.
Used to Tx Tinea Cruis (Jock Itch)
Side Effects  Increases the effects of alcohol, CONTRAINDICATED in intermittent
porphyria, Inhibits CYP450.
Terbinafine – Inhibits Squalene epoxidase.
Tx for Onychomycosis (nail fungal infection)
Side Effects  Elevated liver function tests.
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Flucytosine – Inhibits Thymidylate Synthetase which decreases the Thymine levels.

Used with Amphotericin B in severe candidiasis.
Side Effects 
Decrease bone marrow, Leukopenia, Thrombocytopenia
Severe enterocolitis and hepatitis.

Antiviral Drugs:
Mechanism of Action 
Drugs that inhibit the viral Penetration and Uncoating are –
Amantadine & Rimantadine
Drugs that inhibit Viral DNA Polymerase
Acyclovir, Gancyclovir, Famcyclovir and Valacyclovir (Valtrex).
Drugs that inhibit DNA & RNA Polymerase
Foscarnet
Drugs that Inhibit Viral RNA Polymerase
Ribavirin
Drugs that inhibit Viral Reverse Transcriptase
Zidovudine, Didanosine, Zalcitabine, Stavudine, Lamivudine and
Nevirapine.
Drugs that inhibit Viral Aspartate Protease
Indinavir, Ritonavir, Saquinavir and Nelfinavir.
Drugs that inhibit Viral Neuraminidase
Zanamivir (Relenza) and Oseltamivir (Tamiflu)

Amantadine 
Interferes with the attachment, penetration and Uncoating of the viral particles.
Used to treat Influenza A and now recently used for Parkinson’s disease.
Side Effects 
Livedo Reticularis (only seen with amantadine) and Anticholinergic effects.

Ribavirin 
Inhibits RNA polymerase & also Inhibits end capping of viral mRNA.
Used for RSV infections in children less than 2years old.
Side Effects  Teratogenic, non-immune hemolytic anemia (decreased Hb & increased
indirect bilirubin).
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Acyclovir 
Inhibits viral DNA polymerase. Needs viral Thymidylate kinase in order to work.
Used to Tx  Herpes simplex, VZV (shingles) and is NOT effective for CMV infections.

Side Effects 
Nephropathy if give IV only
Neurotoxicity and Crystalluria.

Famcyclovir & Valacyclovir 

Newly approved for Herpes Simplex, with MOA similar to acyclovir.

Gancyclovir 
Used to treat CMV infections ****
Has same MOA as acyclovir  Needs Viral Thymidylate kinase for herpes and Phosphotransferase in
CMV.
Side Effects 
Leukopenia, Thrombocytopenia, Seizures in OD, & Crystalluria.
Pts can also develop Retinal Detachment.

Foscarnet 
Inhibits DNA Polymerase
Can be used as prophylaxis for Retinal Detachment.
Also newly approved for treatment for CMV. Tx for CMV retinitis in AIDS Pts.
When given along with IV-Pentamidine + Foscarnet  Severe Hypocalcemia.
Side Effects Nephrotoxicity

Zanamivir & Oseltamivir 

Inhibits neuraminidases of Influenza A & B.
Used as prophylaxis to reduce Flu-symptoms.
Side Effects 
Inhaled Zanamivir causes Throat Irritation
Nausea & Vomiting.
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4 Classes of Drugs used to treat AIDS 

Nucleoside Reverse transcriptase Inhibitors
Non-nucleoside Reverse transcriptase inhibitors
Protease Inhibitors
Fusion Inhibitors

Nucleoside Reverse Transcriptase Inhibitors (NRTIs) 

These drugs are phosphorylated to triphosphate which inhibits the Reverse Transcriptase.
Zidovudine (AZT)  Can cause as a side effect Bone Marrow Suppression leading to
Neutropenia, Can also cause Peripheral Neuropathy and Lactic Acidosis.
Didanosine (DDI)  Can cause Pancreatitis and Hyperuricemia.
Zalcitabine (DDC)  Causes Peripheral Neuropathy.
Stavudine (D4T) Causes Peripheral Neuropathy.
Lamivudine (3TC) This is the First oral drug for Hep B which removes the sAg form
blood. As a side effect it can cause GI-Distress.
Adifovir  FDA approved for HBV, but NOT for HIV.

Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) 

NO BM Suppression, But does cause Rashes.
Delavirdine, Nevirapine and Efavirenz.

Protease Inhibitors  “navir” drugs

These inhibit the Aspartate protease via binding to Dipeptides.
Protease inhibitors can cause
Abnormal lipid and Carb metabolism
Can also cause Central Adiposity (accumulation of fat) & Insulin resistance.
Indinavir  Side Effects include  Nephrolithiasis, Hyperbilirubinemia and Inhibition
of CYP450.
Ritonavir  Side Effects are GI-distress and Inhibition of CYP450.
Nelfinavir  SE  GI-distress
Saquinavir  SE GI-distress

Fusion Inhibitors 
Inhibits the Fusion of HIV to CD4 cells.
Enfuvirtide
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AIDS 
CD4-cells count drop to less than 500.
Recommended treatment is combination of 2 + 1  so Any 2 nucleoside inhibitors + 1 Protease
Inhibitor.
AZT, DDI, 3TC, D4T + Indinavir/ Ritonavir etc..
CD4 count is < 200  Pneumocystis Carini Pneumonia (PNP) prophylaxis
Dapsone, Trimethoprim (sulfa) and Pentamidine
CD4 count < 100  Toxoplasmosis Prophylaxis
Trimethoprim (sulfa)
CD4 count < 75  Mycobacterium Avium Complex (MAC) prophylaxis
Azithromycin and Clarithromycin
CD4 count < 50  CMV Prophylaxis
Gancyclovir

HIV Transmission 
Needle stick – 1:300, Anal Receptive – 1:50 – 100 & Vaginal – M-to-F 1:1000 , F-to-M 1:2-3000
Pregnant mom to baby – 25% and pregnant taking AZT 8%.

Cases 
If stuck by a needle from a Pt who’s HIV (+) 
2 (nucleoside inhibitor) + 1 (protease inhibitor) for 4 weeks.
If Pt had sex ONE time with HIV (+) person 
2 + 1 therapy for 4 weeks
Pregnant women with CD4 > 500 and PCR <200 
Give AZT to reduce the transmission from mom to baby to 25-8%.
Pregnant female with CD4 1 and PCR 700,000 
2+1
PCP, MAC & CMV Prophylaxis

Anti-Tuberculosis Drugs 

Isoniazid (INH)
Inhibits the Mycolic Acid Synthesis (cell wall synthesis)
Low Resistance – Deletion in INHA gene (encodes for acyl carrier protein)
High Resistance – Deletion in katG gene (encodes catalase needed for INH bioactivation)
Use Pyridoxine (vit B6) with INH b/c it prevents numbness & tingling.
Side Effects 
Hepatitis, Neuritis, Hemolysis in G6PD deficiency and SLE in Slow acetylators.
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Rifampin:
Inhibits DNA-dependent RNA polymerase
Side Effects 
Red-orange discoloration of the urine, Sweat and Tears
Proteinuria, Flu-like symptoms, Thrombocytopenia and INDUCES CYP450.

Ethambutol:
Inhibits synthesis of Arabinogalactan (part of the cell wall)
Side Effects 
Loss of red-green acuity & Retrobulbar Neuritis.

Pyrazinamide (PZA): Unknown MOA.

Side Effects  Arthralgia due to Hyperuricemia, Hepatotoxicity & Increased porphyrin synthesis.

Aminoglycosides:
Inhibits Protein synthesis
Side Effects 
Streptomycin – Hearing loss, Ataxia & nephrotoxicity
Amikacin – Nystagmus
Kanamycin – Electrolyte abnormalities
Capreomycin:
NOT an Aminoglycoside. Used as second-line Tx for resistant TB with aminosalicylin acid and
Cycloserine.
Side Effects  Hearing loss and Ataxia.

Clinical TB 
PPD (purified Protein Derived)  screens the Asymptomatic people
(+) test is anything > 10mm of induration
High Risk > 5mm with HIV (+) or close contact.
Pts with (+) PPD
Do Chest X-ray
If (-) then just give INH alone for 6 months
If (+) sputum culture
If Sputum culture is (-) INH for 6months
If (+) 4 drugs treatment
With a BCG immunization the PPD will be 3-4mm induration for 5 years. BUT if it has been 10 years
after BCG and the PPD was >10mm then do the protocol steps.
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How long to treat TB 

4 drugs (INH + PZA + Rif + Ethambutol) x 2months + 2 drugs (INH + Rif) x 4month = 6
months.
If the Pts are HIV (+) with TB 
4 drugs (INH + PZA + Rif + Ethambutol) x 2months + 2 drugs (INH + Rif) x 7month = 9 months.
So if the Pts who present with TB symptoms and are also confirmed via AFB (+) test then DO  4 drugs
(INH + PZA + Rif + Ethambutol) x 2months + 2 drugs (INH + Rif) x 4month = 6 months.
Pregnant Pt with (+) PPD 
Chest X-ray with Lead Apron at 2nd Trimester
If (-) x-ray wait until delivery then do INH alone
If (+) Sputum Culture  (-) do INH alone, or if (+) 4 drugs.

Antiprotozoal
Giardia Lamblia 
One of the MOST COMMON Water Born Diseases causes Giardiasis (also called as “Back
Packers Diarrhea”).  Treatment Metronidazole

Entamoeba Histolytica 
Causes Amoebiasis  Treated by Metronidazole.
Non-Invasive Intestinal amoebiasis is treated via  Diloxanide

Trichomonas Vaginalis 
Causes Trichomoniasis  Treated by Metronidazole; the partner MUST be treated as well.

Leishmania Brasiliensis 
American Mucocutaneous Leishmaniasis  Treated by Stibogluconate.

Trypanosoma Cruzi 
Chaga’s Disease (American Trypanosomiasis)  Tx by Nifurtimox.
Sleeping Sickness (African Trypanosomiasis)  Tx by combination of Suramin + Melarsoprol.

Toxoplasma Gondii 
Causes Toxoplasmosis  Tx by combination of Pyrimethamine + Sulfadiazine.

Pneumocystis Carinii 
Causes Pneumocystosis Tx by  TMZ-SMX, IV Pentamide and Atovaquone.
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Malaria Drugs 
Plasmodium Falciparum and Plasmodium Malariae  Tx by Chloroquine.
Plasmodium Vivax and Plasmodium OvaleTx by combination of Chloroquine + Primaquine.
Prophylaxis for Chloroquine RESISTANT malaria 
First choice – Mefloquine, Second choice – Atovaquone-Proquanil
and Doxycycline.
Treatment for Chloroquine Resistant Malaria Quinine / Doxycycline

Side Effects of Malarial Drugs 

Chloroquine – Can cause Pruritis, Ocular dysfunction, Hemolysis and AVOID in Psoriasis
Pts.
Mefloquine – Can Cause Syncope & Extrasystole. AVOID in cardiac arrhythmias &
Seizure Pts.
Primaquine – Can cause Neutropenia, Hemolysis. AVOID in Pregnancy & G6PDD Pts.
Quinine – Cinchonism, CNS defects, & Hemolysis; AVOID in Pregnancy.

Intestinal Nematodes (Worms) 

Tx with Mebendazole – Decreases the glucose uptake & microtubular structure. Pyrantel
Pamoate.

Tissue Nematodes 
Ivermectin
Cestodes (Tapeworms) & Trematodes (Flukes)  Tx with Praziquantel.
MOA – Increases Ca2+ influx

Leprostatic Drugs 
Dapsone – Treatment for Leprosy & Dermatitis Herpetiformis.
Thalidomide – Approved to treat Erythema Nodosum Leprosum. It is a CATEGORY
X drug in pregnancy.
RISK of Developing Phocomelia (absent arms & Legs).
Thiabendazole – Inhibits Fumurate Reductase.
Dibucaine – Inhibits Na+ Permeability
Piperazine – Inhibits Ach leading to Muscle Paralysis.
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Anti-Inflammatory
Prostaglandins (PGs) 
PGE1 – Protective on the GI mucosa
Misoprostol – Tx for Ulcers caused by NSAIDs. (can cause Early Abortion)
Alprostadil – Maintains PDA.
Abortificient – CONTRAINDICATED in Pregnancy.
PGE2 – Uterine Contractions
Dinoprostone – for Cervical Ripening / softening.

PGF2-α – Uterine & Bladder Contractions

Dinoprost & Carboprost (Abortificient)
Latanoprost – Tx for Glaucoma
PGE2 & PGF2-α are increased in dysmenorrhea.
PGI2 (prostacyclin) – Inhibits platelet aggregation and is a Vasodilator
Activates cAMP  causing increase in Internal Ca2+ pumps  leading to decrease in
Free Ca2+  platelet stabilization.
Epoprostenol used in Pulmonary HTN.

Thromboxane’s (TXA2) 
Promote Platelet aggregation, Bronchoconstrict and Vasoconstrict.
Activates Phospholipase C  Increase in IP3  Increase in Free Ca2+  platelet
aggregation.
Leukotriene’s (LTs) 
LTB4 – Mediates inflammation  chemotaxis  increases free radicals  Cell Injury
LTA4-LTC4-LTD4 – Causes bronchoconstriction and Vasoconstriction

Drugs Affecting Leukotrines Pathways 

Corticosteroids – Inhibit Phospholipase A2 enzyme.
Block cyclooxygenase – Antiinflammatory effects.
Block Lipoxygenase – Immunosuppressant effects.
Zileuton – Lipoxygenase Inhibitors. (SE – causes increases in liver enzymes)
Montelukast & Zafirlukast – Leukotriene Inhibitors.
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NSAIDs 
These block cyclooxygenase pathways via COX1 & COX2 thus  decreasing the levels of PGs &TXA2.
Aspirin (acetyl salicylic acid)

Pharmacological Effects of Aspirin 

Analgesic – Inhibits PGs leading to  inhibition of sensitization of pain receptors
via mediators as Bradykinin and Histamine.
Antiseptic – Presence of Pyrogens  increase production of IL-1 leading to 
increase in PGE2.
Antiinflammatory Effects – Does this via Inhibiting COX2.
Aspirin affects the signal transduction proteins. Aspirin also interferes with
cell surface selectins and integrins leading to  Decrease neutrophil
adhesion.
Antiplatelet Aggregation – By inhibiting TXA2
Uricosuric Effects – At low doses causes Hyperuricemia via  decreases tubular
secretion. At High doses cause Uricosuric, b/c it decreases tubular reabsorption.
Aspirin Dosage 
1 to 2 tablet for occasional headaches.
High doses – 3 to 5g/day for inflammatory conditions.

High Dose Aspirin Effects 

Respiratory Alkalosis, Metabolic Acidosis, Gastritis (b/c inhibits PGE2)
Increase Bleeding Time (b/c decreases platelet aggregation)
Increase Prothrombin time (b/c inhibits synthesis of Vit K factors).
Salycylism – in chronic dosing Pts present with  Tinnitus, Vertigo and Decrease Hearing.

Acute Aspirin Toxicity 

Hypokalemia, Fever, Metabolic and Respiratory Acidosis.

Drug Interactions w/ Aspirin 

Ethanol – Increases GI bleeding.
Uricosurics – Aspirin blocks their activity.
Oral hypoglycemic – Aspirin increases their activity.
Warfarin – aspirin increase its activity.

Emergency Tx for Aspirin OD 

Adults severe toxicity in about 30 pills, whereas children it’s about 4-6 tablets.
Do a Gastric Lavage, Activated Charcoal and or Alkalinization of urine.
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Acetaminophen 
This NOT Antiinflammatory. Inhibits only CNS cyclooxygenases, NO effect peripherally.
Similar MOA as Aspirin, BUT has NO GI bleeding, NOT anti-inflammatory and NO effect on blood.

Acetaminophen Toxicity 
Hepatotoxicity
In normal dosage acetaminophen metabolite N-acetylbenzoquinoneimine is produced
by liver P450 and gets conjugated with reduced glutathione (GSH).
OD of acetaminophen  there is decreased levels of GSH leading to  reactive
metabolites which react with liver hepatocytes  hepatotoxicity.
OD antidote  Acetylcysteine – give SH-groups to inactivate metabolites.

Reversible Inhibitors of COX1 & COX2 

Ibuprofen  200mg is available OTC and is #1 for Pain Relief.
Decreases the PGE2 & PGF2-α.
Naproxen  Used to Treat Gout
Indomethacin  SE’s are – Thrombocytopenia & Agranulocytosis.
Etodolac, Ketorolac & Nabumetone
Sulindac  Cramps & Rashes and has NO renal effects.
SE’s – Pancreatitis
Tolmetin  Doesn’t affect oral hypoglycemic activity.
Diclofenac  SE – Hepatotoxicity

***NSAIDs  Decrease the activity of Antihypertensives  Loop Diuretics, ACE-I & βB. ***

Selective COX2 Inhibitors  “Coxib” drugs

Rofecoxib (VIOXX), Celecoxib & Valdecoxib
COX1 receptors are found in the Blood Vessels causing platelet aggregation and are also found in the
Stomach thus are protective against ulcers.
COX2 receptors are activated by Inflammation.

Rofecoxib (VIOXX)  Selective CO2 inhibitor used for Inflammation (Arthritis), But
activates COX1 receptors.
So it is good for the stomach BUT bad for the heart b/c of platelet
aggregation leading to blood clot and  MI.
Celecoxib  Cross allergy with sulfonamides.
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Drugs used to treat Migraines 

Drugs ending in “triptan”.
Sumatriptan, Zolmitriptan and Frovatriptan
These drugs are AGONISTs at the 5HT1D/1B receptors in the cerebral Blood vessels.
SEs Asthenia and Throat pressure.
Ergotamine and Methysergide
These are Partial Agonists at α-1 & 5HT2 in the BVs.
Analgesics  ASA, Acetaminophen, Oral/IM Opioid analgesic and Butrophanol (spray).

Drugs used to treat Asthma 

Bronchodilators
β2 Agonists – use in Bronchospasms
Short-acting β-2 agonists  Albuterol (DOC), Metaproterenol & Terbutaline
Long-acting β-2 agonists  Salmeterol (monitor heart when giving this drug).
β-1 & β-2 agonist  Isoproterenol
α-1, β-1 & β-2 agonist  Epinephrine
β-2 agonists – bind to the β-2 receptors on the lungs and stimulate Adenylate Cyclase 
producing cAMP and leading to  Bronchodilation (relaxation of SMs).
CONTRAINDICATED in Uncontrolled arrhythmias
Side Effects  Anxiety, Tremors, Headaches, Palpitations, Tachycardia, HTN & Arrhythmias
(just give βB to treat the SEs).

Xanthine Bronchodilators
Theophylline and Aminophylline
These drugs Competitively Inhibit Phosphodiesterase (metabolizes cAMP) b/c it is
inhibited it leads to  Increase in the cAMP levels leading to  Relaxation of
bronchial muscles.
Theophylline – has a narrow TI. Macrolides (erythromycin) & Quinolones (ciprofloxacin)
increase theophylline elimination.
Phenobarbitol, Carbamezepine, Tobacco & Marijuana – Decrease
theophylline effects.

Anticholinergic Bronchodilators
M-Blockers 
Ipratropium (antimuscirinic) – causes local broncodilation after inhalation
SEs – Dry mount, constipation, tachycardia, urinary retention and
Mydriasis (like atropine).
The anticholinergic Bronchodilators are INDICATED for 
DOC for bronchospasm caused by βBs.
Used as adjuncts inhalers in asthma and COPD.
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Corticosteroids
Inhaled Steroids
Beclomethasone, Fluticasone and Triamcinolone

Oral corticosteroid
Prednisone
These drugs Inhibit the release of inflammatory mediators such as
– Kinins, Histamine (these causes airway constriction).
They also inhibit the synthesis of leukotriene’s.
INDICATED for
Chronic Bronchitis, Allergic Rhinitis and Bronchial Asthma
CONTRACINDICATED in Acute bronchospasm.

Side Effects 
Abdominal distress, anorexia, unpleasant taste, oral fungal infections or
Candidiasis.
Leukotriene Antagonists 
Montelukast and Zafirlukast – These drugs are Antagonist at the LTD4 receptor.

Lipoxygenase Antagonist 
Zileuton – Works as an Antagonist on all LTs.

Both types are indicated for 

Prophylaxis for seasonal allergic rhinitis and chronic Tx of Asthma.
Side Effects  Headache, Dental Pain, GI-distress and Rash.

Mast Cell Stabilizers 

Cromolyn & Nedocromil – These prevent degranulation of the pulmonary mast cells and inhibit
the release of histamine and LTs. NO bronchodilation affect.

*** Omalizumab – New drug that binds to IgE receptor on the mast cell. ***
Given in Moderate to severe asthma ONLY.

Management of Asthma 
Infants & Young Children (5yrs or younger)
Quick Relief  Short-acting β-2 agonist (Inhaled Albuterol).
Mildly persistent asthma lasting either >2 days/wk or >2 nights/month give 
1 drug – Low dose Beclomethasone OR inhaled Cromolyn
OR Montelukast orally.
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Asthma for >1night/wk give  2 drugs

Low dose Beclomethasone + Salmeterol OR Montelukast + medium
dose Beclomethasone.
Daily / Nightly Asthma  3 drugs
High dose Beclomethasone + Salmeterol + Oral Prednisone.
Adults & Children (older than 5yrs)
Quick Relief  Short-acting β-2 agonist & Inhaled Albuterol.
Mildly persistent asthma lasting either >2 days/wk or >2 nights/month give 
1 drug – Low dose Beclomethasone OR inhaled Cromolyn
OR Montelukast/Cromolyn OR Theophylline.
Asthma for >1night/wk give  2 drugs
Low-medium dose Beclomethasone + Salmeterol or Montelukast.
Daily / Nightly Asthma  3 drugs
High dose Beclomethasone + Salmeterol + Oral Prednisone.

Status Asthmaticus in Children 

ER management 
Supplemental O2, Inhaled Albuterol, IV Methylprednisone & Nebulized Ipratropium.
In severe attack if inhaled drugs don’t work use  IV or SC Epinephrine.
Antitussives 
Codeine (opioid)
Non-opioid antitussives – Dextromethorphan (Robitussin) & Benzonatate.
These drugs are used to treat nonproductive cough and cough that interferes with sleep or
daily activities. Has the same effect as codeine but NO addictive potential.

Expectorants 
Guaifenesin – Decreases the viscosity of the secretions.
Used to treat cough associated with common cold and URTIs
DON’T give for Pts having cough due to smoking, asthma or emphysema.

Diluents 
Water / Normal Saline – to dilute the respiratory secretions, administered via Ultrasonic nebulizers.
Mucolytics 
Acetylcysteine (Mucomyst)  breaks down the mucoprotein molecules.
Used to treat Thick abnormal mucus in CF or Atelectasis.
Also is an ANTIDOTE for Acetaminophen OD.
Decongestants 
Pseudoephedrine (Sudafed) & Phenylephrine (α-1 agonist)
These stimulate the α-1 receptors leading  vasoconstriction.
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Osteoarthritis 
M/C form of arthritis affecting M & F equally.
There is Cartilage disruption and New Bone Formation = Osteophytes.
Incidence increases with age.
Morning stiffness lasting less than 30min.

Diagnosis of osteoarthritis 
X-ray, UNEQUAL Loss of Joint space.
Treatment by  Exercise, Weight loss
Medication include 
Acetaminophen (Tylenol), Ibuprofen, COX2 inhibitors
(Celecoxib).

Osteomyelitis 
It is NOT an inflammatory disease it occurs due to Bacterial Infection  Staph Aureus.
Causes Acute infection in children and Chronic in Adults.
52 yr male with DM presents with Ulcer on the tibia for past 4 wks, draining tract with no
fever?  DO X-ray first, NOT blood culture.
If the X-ray is (+) do a biopsy and Rx Antibiotics.
If the X-ray is (-) do bone scan/MRI  If there is No osteomyelitis then Tx
for Ulcer.
Tx for Staph Aureus  Ox, Clox, Diclox and Naf drugs.

Fibromyalgia 
Widespread aching and stiffness for more than 3 months.
Lab values are NORMAL  so look for Tender points such as  Short sleeve shirt parts, Shoulders,
Trapezius and Hip girdle.
Tx with  Analgesics & Antidepressants.

Polymyalgia Rheumatica 
Same presentation as Fibromyalgia but common in the ELDERLY.
Increased ESR
Commonly seen in Pts with Giant Cell Temporal Arteritis.
Give Steroids 15mg/day and taper  If the Pts come back with severe headaches
Increase the dosage to 40mg/day
If you don’t increase the dosage after they come with severe headache they go
blind.
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Rheumatoid Arthritis 
Rheumatoid Factor is (+), affects the Synovium, bones get thinner and symmetrical arthritis.
Extra-articular involvement (Joints, Eye, Heart & Lungs).

Diagnosis of RA 
Early morning stiffness for about 1 hour or longer with swelling of 3 or more joints
for 6 weeks or more.
Do Joint X-ray for elbow, wrist, ankle and knee.
Rheumatoid Nodules and ESR elevated.
Treatments for RA 
ALWAYS answer NSAIDs / Or COX2 inhibitors FIRST.
If the Pt is not okay within 3 months, then give them DMARDS (disease modifying
Antirheumatic drugs). Such as 
Methotrexate – Inhibits dihydrofolate reductase.
SEs Hair loss and mucositis (mouth ulcers, jaundice &
Glossitis). Tx toxicity w/  Leucovorin (Folinic acid)
Hydroxychloroquine (antimalarial) – Stabilizes lysosomes and decreases
chemotaxis.
Can cause Cinchonism (GI distress & visual dysfunction).
Hemolysis in G6PD deficiency Pts.
Sulfasalazine – ASA inhibits COX2, Sulfapyridine – Decreases B-cell
functions.
SEs – GI-distress and Sulfapyridine – Rash, Hemolysis & SLE-
like syndrome.
Corticosteroids – Decrease LTs, IL-2 and PAF
SEs – ACTH depression, susceptibility to infections and can
induce Diabetes.
Gold Salts – Decreases the lysosomal & macrophages functions.
SEs – Stomatitis, rash, bone marrow depression, Proteinuria
& Nephrotic syndrome.
D-Penicillamine – DOC for Wilson’s disease.
Suppresses T-cells & decreases the Rheumatoid factor.
SEs – Aplastic anemia, myasthenia gravis & SLE-like syndrome.
Cyclophosphamide – Alkylating agent used in severe cases
SEs – hemorrhagic cystitis (Tx w/ Mensa or N-acetylcystein)
Azathioprine – Immunosuppressive in autoimmune disease.
Inhibits purine synthesis
SEs – Bone marrow suppression
Infliximab – Decreases TNF by binding and neutralizing it.
SEs – Infusion rxns & infections.
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Etanercept – recombinant of TNF receptor which binds to TNF

SEs – Hypersensitivity & infections.
Leflunomide – Pyrimidine synthesis inhibitor  Inhibits dihydro-orotic acid
dehydrogenase leading to  decrease in UMP and decrease in RNA
synthesis.
SEs – Alopecia, Rash & hepatotoxicity.
Anakinra – IL-1 receptor antagonist.
SEs – Rxn at injection site and infections.
Adalimumab (humera) – Recombinant MAb binds to TNF-α & blocks
interaction with TNF-receptors.

Gout
Also called as Crystal Induced Arthritis.
Occurs most commonly in Males affecting the  Big Toe
Increased levels of Serum Uric Acid
Negative birefringence with polarized light.
Drugs to Tx Gout 
DOC are NSAIDs first such as  Indomethacin, Naproxen & Sulindac
For Acute Gout  Colchicine
Binds to Tubulin thus decreasing microtubular
polymerization.
Decreases the LTB4 and Inhibits Leukocyte &
granulocyte migration.
SEs  Diarrhea & GI pain
Long term – Mylosuppression, peripheral neuropathy,
hematuria and alopecia.
Chronic Gouty Arthritis 
Allopurinol – Inhibits Xanthine Oxidase leading to  decrease purine
metabolism  Decreased uric acid levels.
SEs Peripheral neuropathy, stones, Rash and Vasculitis.
DECREASE the Dosage of 6-MP with allopurinol b/c it can lead
to Severe Liver Toxicity.

Probenicid  Inhibits PCT reabsorption of Urate and Also Inhibits Secretion of Acidic
drugs such as penicillins.
SEs  high excreter of urate leading to  urate crystals in the kidneys.
Sulfinpyrazone  Similar to Probenicid.
Inhibits platelet aggregation if the GFR is below 30ml/min.
SEs  Gi-distress, Rash & nephrotic syndrome.
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Antineoplastic

Cancer 
 Is uncontrolled growth or spread of abnormal cells, with an imbalance b/w cell renewal and
replacement.
o 2-types of drugs are used in cancer treatment.
 Cell-cycle specific that act on the cells when dividing.
 Cell-cycle non-specific that act on any phase of the cell.
Cell-Cycle Drugs 
 G0-phase: Non-specific
o Alkylating Agents 
 Antitumor antibiotics, Nitrosourea, Dacarbazine & Cisplatin.
 G1-phase: synthesis of cells components needed for DNA synthesis.
 L-asparaginase & Mitomycin

 S-phase: cell-cycle specific, period of DNA synthesis.

 Cytarabine, 6-MP, 6-Thiguanine, Methotrexate, Hydroxyurea &
Etoposide.
 G2-phase: Preparation for Mitosis.
 Bleomycin
 M-phase: Mitosis.
 Vinblastine, Vincristine & Paclitaxel.
Alkylating Agents 
 Nitrogen Mustard –
o Cyclophosphamide & Ifosfamide.
 These drugs affect guanine N7 leading to  non-functional DNA.
 SEs  Hmgic Cystitis
 Prevent it by giving Mesna or N-acetylcystein.
 Nitrosourea –
o Lomustine – Crosses the BBB

 Platinum Agents –
o Cisplastin
 SEs  Nephrotoxicity Toxicity (treat with Amifostine), ototoxicity, N & V.

 Procarbazine – Depolymerizes DNA

 Dacarbazine (MM) and Altretamine (OC)
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Antimetabolites 
 Purine Analogs –
o 6-MP – inactivated by Xanthine Oxidase (Reduce the dosage if given w/ allopurinol).
o 6-Thioguanine – No dose modifications with allopurinol.

 Pyrimidine Antagonists –
o 5-Fluorouracil – Inhibits thymidine synthase
 Flucytosine – Fungal cells… Fluorouracil – Cancer cells.

 Folate Antagonists –
o Methotrexate – Inhibits the dihydrofolate reductase thus inhibiting DNA & RNA
synthesis.
 Toxicity causes, Mouth ulcers, jaundice, Glossitis and NVD 
Leucovorin (Folinic acid) rescue for Tx of Methotrexate toxicity.
 Hydroxyurea – Inhibits Ribonucleotide reductase.
 USED to Treat CML, BUT in low doses can be used for sickle cell anemia.
Antibiotics  for cancer patients
 Doxorubicin (anthracycline) & Daunorubicin.
 These drugs inhibit Topoisomerase, and forms free radicals.
 SEs  Cardiotoxicity (dilated cardiomegaly)
o Dexrazoxane  Antidote for the SE.
 Bleomycin
o Causes DNA strand scission.
 SEs  pulmonary toxicity.
Mitotic Inhibitors  M-Phase blockers
 Vinca Alkaloid – Binds to tubulin and blocks microtubular polymerization.
oVinblastine – Causes bone marrow suppression as a SE.
o Vincristine – Causes neurotoxicity and peripheral neuropathy as a SE.
 Taxanes
o Paclitaxel (taxol) – Prescribed for Breast, Lung and Ovarian Cancers works in
Metaphase arrested cells.
 SEs – Alopecia and Arthralgia.
o Docetaxel – Tx for advanced breast cancer.
 Both of these drugs are metabolized by CYP450.
 Miscellaneous 
o Topoisomerase Inhibitors –
 Etoposide – for Lung Cancer
 Irinotecan – For Colorectal Cancer.
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o Enzymes
 L-asparaginase – Catalyzes the hydrolysis of L-asparagine to aspartic
acid. SEs  Pancreatitis.

o Busulphan – Used for CML

o SEs: skin pigmentation, pulmonary fibrosis

Tyrosine Kinase Inhibitors 

 Imatinib (Gleevac) – Inhibits the tyrosine kinase domain Bcr-Abl oncoprotein.
 Prevents phosphorylation of kinase substrate by ATP
 First line of therapy for CML chronic phase & Blast crisis.
 Gefitinib (Iressa) and Erlotinib (Tarceva) – Small molecule inhibitor of tyrosine kinase
associated with EGFR.
 Used to treat Non-small cell lung cancer.
GROWTH FACTOR RECEPTOR INHIBITORS
• Cetuximab (ERBITUX) : epidermal growth factor receptor (EGFR)
•metastatic colorectal cancer
• Bevacizumab (AVASTIN): vascular endothelial growth factor (VEGF)
• Metastatic colorectal cancer
• Rituximab (RITUXAN): CD20
• B cell lymphoma
• Trastuzumab (HERCEPTIN): HER2/neu (ErbB-2) member of the epidermal growth factor family
of cellular receptors
• breast cancer

Few Missing Drugs 

Cyclosporine – Binds to Cyclophillin and inhibits Calceinurin thus  Inhibits IL-2 & γ-IFN from T-cells.

Tacrolimus – Similar to cyclosporine, It inhibits FK-binding protein  inhibiting Calceinurin – inhibiting

IL-2, TNF & IFN-γ.

Bosentan – Endothelin receptor antagonist  stopping the action of Endothelin.

Used to treat Pulmonary HTN.

Drugs with Disulfiram action 

Metronidazole, Chlorpropamide, Topimarate (NMDA-blockers), Cephalosporin’s, Naltrexone,
Tolbutamine, and Griseofulvin.