Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Category: ANGINA PECTORIS

BETA BLOCKERS

Prophylaxis of angina Cardiac arrhythmias,

angina pectoris,
hypertension,
essential tremor,
myocardial infarction,
pheochromocytoma

Nonselective
competitive
antagonist
adrenoceptors

Decreased heart rate,

cardiac output, and
blood pressure,
decreases myocardial
oxygen demand

Oraland parenteral,
duration 4-6 h
*Toxicity: asthma,
atrioventricular block,
acute heart failure;
sedation*Interactions:
Additive with all
cardiac depressants

CALCIUM CHANNEL
BLOCKERS

Prophylaxis of
Vasospastic angina
angina, hypertension (Prinzmetal's variant
angina), chronic stable
angina, hypertension

Block vascular Ltype calcium

channels > cardiac
channels

Like verapamil and

Oral, duration 4-6 h
diltiazem; less cardiac *Toxicity: Excessive
effects
hypotension
*Interactions: Additive
with other vasodilators

Dizziness,
lightheadedness,
nervousness,
headache, nausea,
constipation,
peripheral edema,
asthenia, bradycardia,
atrioventricular block,
arrhythmias, flushing

Nifedipine,
Adalat,
procardia,
procardia XL,
dihydropyridine

CALCIUM CHANNEL
BLOCKERS

Prophylaxis of
Angina pectoris,
angina, hypertension arrhythmia, essential
hypertension, atrial
flutter/fibrillation

Nonselective block
of L-type calcium
channels in vessels
and heart

Reduce vascular
resistance, cardiac
rate, and cardiac
force results in
decreased oxygen
demand

Dizziness, light
headedness,
nervousness,
bradycardia, flushing,
rash

Verapamil
(Calan, isoptin,
verelan),
Diltiazem
(Cardizem,
dilacor XR)

Oral, IV, duartion 4-8 h

*toxicity:
Atrioventricular block,
acute heart failure;
constipation,edema
*Interactions: Additive
with other cardiac
depressants and
hypotension

Fatigue, weaknesses,
Inderal, inderal
nausea, vomiting,
LA, Propranolol,
depression,
Atenolol
bradycardia, dizziness,
vertigo, rash, decrease
libido, hypotension,
hyperglycemia,
decrease exercise
tolerance,
proarrhythmic effects

Page 1 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

MISCELLANEOUS
Ranolazine

for angina

Inhibit late Na+

current in heart, also
may modify fatty acid
oxidation, reduce
contractility

Reducescardiac
oxygen demand,
fatty oxidation
modification may
improve efficiency
of cardiac oxygen
utilization

Oral, duration 6-8 h * Prophylaxis of angina,

Toxicity: QT interval
hypertension
prolongation, nausea,
constipation,
dizziness
*Interactions:
Inhibitors of CYP3A
increase ranolazine
concentration and
duration of action

No significant
hemodynamic effects

ivabradine

NITRATES

Angina: Sublingual
dose form for acute
episodes *oral and
transdermal forms
for prophylaxis

Treatment and
prevention of angina
pectoris

Release nitrate
oxide in smooth
muscles, which
activate guanylyl
cyclase and
increased cGMP

Smooth muscle
relaxation especially,
in vessels, other
smooth muscle is
relaxed but not as
markedly,
vasodilation
decreases venous
return and heart size
, may increase
coronary flow in
some areas and in
variant angine

very high first pass

effect, so sublingual
dose is much smaller
than oral, high lipid
solubility ensures
rapid absorption *
Toxicity: Orthostatic
hypotension,
tachycardia, head
ache * Interaction:
Synergistic
hypotension with
phosphodiesterase
type 5 inhibitors
(Sildenafil, etc.)

headache,
hypotension,
dizziness, weakness,
flushing, restlessness

Nitroquick,
nitrostat,
nitrolingual,
isodril, dilatrate,
nitroglycerin,
isosorbide
dinitrate,
isosorbide
mononitrate

Ventricular arrhythmia Sodium channels

(INa) Blockade

Blocks activated and

inactivated channels
with fast kinetics
*does not prolong
and may shorten
action potential

IV *First-pass hepatic
metabolism *reduces
dose in patients with
heart failure or liver
disease *Toxicity:
Neurologic symptoms

Lightheadedness,
nervousness,
bradycardia,
hypotension,
drowsiness,
proarrhythmic effect

Lidocaine,
Mexiletine

Category: ANTIARRHYTHMIA

CLASS 1B

Terminate
ventricular
tachycardias and
prevent ventricular
fibrillation after
cardioversion

Page 2 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

CLASS 1B
Dofetilide

Maintenance or
restoration of sinus
rhythm in atrial
fibrillation

Conversion of atrial
fibrillation, flutter to
normal sinus rhythm,
maintenance of
normal sinus rhythm

Ikr Block

Prolongs actions
potential ,effective
refractory period

Oral *renal excretion

*Toxicity: Torsade de
pointes (initiate in
hospitals)
*Interactions: Additive
with other QTprolonging drugs

Headache, chest pain,

dizziness, respiratory
tract infection,
dyspnea, nausea, flu
like syndrome,
proarrhythmic effect

Sotalol, Ibutilide,
Dronedarone,
Vernakalant,
Dofetilide
(Tikosyn)

CLASS 1C

Supraventricular
arrhythmias in
patients with normal
heart *do not use in
ischemic conditions
(post-myocardial
infarction)

Paroxymal atrial
fibrillation, flutter and
supraventricular
tachycardia

Sodium channels
(INa) Blockade

Dissociates from
channels with slow
kinetics *No change
in action potential
duration

Oral *Hepatic, and

Kidney metabolism
*half life ~20 h
*Toxicity:Proarrhythmi
c

Dizziness, headache,
faintness, blurred
vision, headache,
nausea, dyspnea,
fatigue, palpitations,
proarrhythmic effect

Flecainide,
Propafenone,
Moricizine

CLASS 2

Atrial arrhythmias
and prevention of
recurrent infarction
and sudden death

Ventricualr
arrhythmia,
hypertension

- Adrenoceptors
blockade

Direct membrane
effects (Sodium
channel block) and
prolongation of
action potential
duration *slows SA
node automaticity
and AV nodal
conduction velocity

Oral, Parenteral
*duration 4-6 h
*Toxicity: Asthma, AV
blockade, acute heart
failure *Interactions:
With other cardiac
depressants and
hypotensive drugs

Hypotension,
proarrhythmic effect,
nausea, headache,
decreased exercise
tolerance

Propanolol
(Inderal),
Esmolol
(Breviloc)

Page 3 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

CLASS 3
Amiodarone

Serious ventricular
arrhythmias and
supraventricular
arrhythmias

Life threatening
Blocks IKr, INa, ICa-L Prolongs actions
ventricular arrhythmia channels,
potential duration
adrenoceptors
and QT interval
*slows heart rate and
AV node conduction
*low incidence of
torsade de pointes

Oral, IV, *Variable

absorption and tissue
accumulation *hepati
metabolism,
elimination complex
and slow *Toxicity:
Bradycardia and heart
block in diseased
heart, peripheral
vasodilation,
pulmonary and
hepatic toxicity
*Hyper -or
Hypothyroidism
*Interactions: Many
based on CYP
metabolism

Malaise, fatigue,
Cordarone,
tremor, proarrhythmic Pacerone
effect, nausea,
vomiting,
constipation,
photosensitivity

CLASS 4

Supraventricular
tachycardia

Supravwentricular
tachyarrhythmia,
temporary control of
rapid ventricular rate
in atrial
flutter/fibrillation,
angina, hypertension

Oral, IV, *hepatic

metabolism *caution
in patients with
hepatic dysfunction
*toxicity:
Atrioventricular block,
acute heart failure;
constipation, edema
*Interactions: Additive
with other cardiac
depressants and
hypotension

Constipation,
dizziness, headache,
mental depression,
proarrhythmic effect,
peripheral edema,
vomiting, nausea

Calcium channels
IKr, INa, ICa-L
blockade

Slows SA node
automaticity and AV
nodal conduction
velocity *decreases
cardiac contractility
*reduces blood
pressure

Verapamil
(Colan, Covera
HS, Isoptin,
Verelan),
Diltiazem

Page 4 of 41

Drugs

Clinical
Application

CLASS IA

Most atrial and

ventricular
arrhythmias *drug of
second choice for
most sustained
ventricular
arrhythmias
associated with
acute myocardial
infarction

MISCELLANEOUS
Adenosine

Paroxysmal
supraventricular
tachycardia

MISCELLANEOUS
Magnesium

Torsade de pointes
*digital-is-induced
arrhythmias

MISCELLANEOUS:
Potassium

Digitalis-induced
arrhythmias
*arrhythmias
associated with
hypokalemia

Uses

Mechanism
of Action

Procainamide - life
INa (primary) and
threatening
IKr (secondary)
ventricular arrhythmia blockade
Quinidine - premature
atrial and ventricular
contractions, atrial
tachycardia and
flutter, paroxysmal

Effects

Slows conduction
velocity and
pacemaker rate,
prolongs action
potential duration
and dissociates from
Ina channel with
intermediate kinetics
, direct depressant
effects on SA & AV
nodes

Pharmacokinetics,
Toxicities,
Interactions
Oral, IV, IM
*eliminated by
hepatic metabolism to
N-acetylprocainamide
(NAPA) and renal
elimination *NAPA
implicated in torsade
de pointes in atients
with renal failure
*Toxicity: Hypotension
*Long-term therapy
produces reversible
lupus-related

Adverse
Reaction

Trade
Name

Hypotension,
disturbances of
cardiac rhytthm,
proarrhythmic effect

Procainamide,
Disopyramide,
Quinidine

Activates inward
rectifier IK *Blocks
Ica

Very brief, usually

IV only *duration 10complete AV blockade 15 *Toxicity: Chest
tightness, dizziness
*Interactions: Additive
with other cardiac
depressants and
hypotension

Seizure associated
with eclampsia and
acute nephritis in
children

Poorly understood
*interacts with Na+,
K+ ATPase, K+, and
Ca2+ channels

Normalizes or
increases plasma
Mg2+

IV *duration
dependent on dosage
*Toxicity: Muscle
weakness in overdose

Flushing, sweating,
depressed reflexes,
hypotension, cardiac
and CNS depression

Magnesium
sulfate

Hypokalemia due to
arrhythmia

Increases K+
permeability, K+
currents

Slows ectopic
pacemakers *slows
conduction velocity in
heart

Oral, IV *Toxicity:
Reentrant
arrhythmias,
fibrillation or arrest in
overdose

Nausea, vomiting,
diarrhea, flatulence,
abdominal discomfort

K-tab, K lyte,
Slow-K

Page 5 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Category: ANTICHOLINERGIC

CHOLINERGIC
POISONING
Atropine

Mandatory antidote
for severe
cholinesterase
inhibitor poisoning

Pylorospasm,
reduction of bronchial
and oral secretion,
excessive vagalinduced bradycardia,
ureteral and biliary
colic

Nonselective
competitive
antagonist at all
muscarinic
receptors in CNS
and periphery

Blocks muscarinic
excess at exocrine
glands, heart, smooth
muscle

Intravenous infusion
until antimuscarinic
signs appear
*continue as long as
necessary *toxicity:
Insignificant as long as
AChE inhibition
continues

Drowsiness, blurred
vision, tachycardia,
dry mouth, urinary
hesitancy

CHOLINERGIC
POISONING
Pralidoxime

Usual antidote for

early stage (48
hours)
cholinesterase
inhibitor

Treat
organophosphorus
poisoning

Very high affinity for

phosphorus atom
but does not enter
CNS

Regenerates active
AChE; can relieve
skeletal muscle end
plate block

Intravenous every 4-6

hours *toxicity: Can
cause muscle
weakness and
overdose

Neuromuscular
weakness

GASTROINTESTINAL
DISORDERS

Reduces smooth
oral; peptic ulcer,
muscle and secretory parenteral;
activity of gut
inconjunction with
aneasthesia to reduce
bronchial and oral
secretion, to bloch
cardiac vagal
inhibitory reflexes
during induction of
anaesthesia and
intubation; protection
against the
pheripheral
muscuranic effects of
cholinergic agents

Competitive
antagonist at M3
receptors

Reduces smooth
muscle and secretory
activity of gut

Available in oral and

parenteral forms
*short t1/2 but action
last up to 6 hours
*Toxicity:Tachycardia,
confusion, urinary
retention, increased
intraocular pressure
*Interactions: With
other antimuscarinics

Blurred vision, dry

mouth, altered taste
perception, nausea,
vomiting, dysphagia,
urinary hesitancy and
retention

AtroPen

Rubinol,
Dicyclomine,
Hyoscyamine,
Glycopyrrolate

Page 6 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

MOTION SICKNESS
DRUGS

Prevention of motion Preanaesthetic

sicknessand
sedation, motion
postoperative
sickness
nausea and vomiting

Unknown
mechanism in CNS

Reduces vertigo,
Transdermal patch
postoperative nausea used for motion
sickness *IM injection
for postoperative use
*Toxicity:Tachycardia,
confusion, urinary
retention, increased
intraocular pressure
*Interactions: With
other antimuscarinics

Confusion, dry mouth, Scopolamine

constipation, urinary
hesitancy, urinary
retention, blurred
vision

OPHTHALMOLOGY
Atropine

Retinal examination:
prevention of
synechiae after
surgery

Competitive
antagonist at all M
receptors

Causes mydriasis and

cycloplegia

Used as drops * long

(5-6days) action *
Toxicity: Increased
intraocular pressure in
close angle glaucoma
* Interactions: With
other antimuscarinics

Drowsiness, blurr
vision, tachycardia,
dry mouth, urinary
hesitancy

RESPIRATORY
(ASTHMA, COPD)

Prevention and relief Bronchospasm

of acute episodes of associated with
bronchospasm
chronic obstructive
pulmonary disease,
chronic bronchitis,
emphysema and
rhinorrhea

Competitive,
nonselective
antagonist at M
receptors

Reduce or prevent
bronchospasm

Aerosol canister, up to
qid
* Toxicity:
Xerostomia,
cough
*
Interactions: With
other antimuscarinics

Dryness of the
Ipratropium,
oropharynx,
Tiotropium
nervousness, irritation
from aerosol,
dizziness, headache,
GI distress, dry mouth,
nausea, palpitation

URINARY
Oxybutynin

Urge incontinence;
Overactive bladder,
postoperative spasms neurogenic bladder

Nonselective
muscarinic
antagonist

Reduces detrusor
smooth muscle tone,
spasms

Oral, IV, patch

formulations *toxicity:
Tachycardia,
constipation,
increased intraocular
pressure, xerostomia
*Patch: Pruritus
*Interactions: With
other antimuscarinics

Dry mouth,
constipation, nausea,
headache, drowsiness,
urinary retention

Pylorospasm,
reduction of bronchial
and oral secretion,
excessive vagalinduced bradycardia,
ureteral and biliary
colic

Atropen,
Atropine,
Scopolamine,
Homatropine,
Cyclopentolate,
Tropicamide

Enablex,
Ditropan,
Oxybutynin,
Darifenacin,
solifenacin,
Tolterodine,
Trospium

Page 7 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Category: ANTI-DEPRESSANT

5-HT2 ANTAGONIST

Major
depression*sedation
and hypnosis
(trazodone)

Depression, alcohol
craving

Inhibition of 5HT2A
receptors
*Nefazodone also
blocks SERT weakly

Trazodone forms a
metabolite (m-cpp)
that blocks 5HT2A, 2C
receptors

Relatively short halflives *active

metabolites
*Toxicity:Modest and H1 -Receptor
blockade (trazodone)
*Interactions:Nefazodo
ne inhibits CYP3A4

Somnolence,
insomnia, dizziness,
nausea, dry mouth,
constipation,
headache, weakness,
drowsiness, priapism,
vomiting, fatigue,

Deseryl,
Trazodone,
Nefazodone

MONOAMINE
OXIDASE INHIBITORS
(MAOIs)

Major depression
unresponsive to the
other drugs

Depression, anxiety
associated with
depression,
neuropathic pain,
attention deficit
hyperactivity disorder
(ADHD), smoking
cessation (Zyban)

Blockade of MAO-A
and MAO-B
(Phenelzine,nonselec
tive) *MAO-B
irreversible selective
MAO-B inhibition
(low dose selegiline)

Transdermal
absorption of
selegiline achieves
levels that inhibit
MAO-A

Very slow elimination

*Toxicity:
Hypotension, insomnia
*Interactions:Hyperten
sie crisis with
tyramine, other
indirect
sympahtomimetics
*serotonin syndrome
with serotogenic
agents, meperidine

Orthostatic
hypotension, vertigo,
dizziness, nausea,
constipation, dry
mouth, diarrhea,
headache,
restlessness, blurred
vision, hypertensive
crisis

Nardil, Parnate,
Phenelzine,
Tranylcypromine,
Selegiline

SELECTIVE
SEROTONIN
REUPTAKE
INHIBITORS (SSRIs)

Major depression,
anxiety disorder *
Panic disorder *
Obsessivecompulsive disorder
* Post-traumatic
stress disorder *
Perimenopausal
vasomotor
symptoms * Eating
disorder (bulimia)

Depression, panic
disorder, post
traumatic stress
disorder (PTSD),
premenstrual
disorder, generalized
anxiety disorder,
bulimia

Highly selective
blockade of
serotonin
transporter (SERT) *
little effect in
norepinephrine
transporter (NET)

Acute increase of
serotonergic synaptic
activity * slower
changes in several
signaling pathways
and neurotrophic
activity

Half-lives from 15-75 h

* Oral-activity *
Toxicity: Well
tolerated but cause
sexual dysfunction *
Interaction: some CYP
inhibition or
fluoxetine 2D6, 3A4;
fluvoxamine 1A2;
paroxetine 2D6

Nausea, dry mouth,

sweating,
somnolence, insomia,
anorexia, diarrhea,
nervousness,
drowsiness, asthenia,
tremor, constipation,
dyspepsia, ejaculatory
disturbances,

Celexa, Lexapro,
Prozac, Prozac
weekly, sarafem,
Paxil, Zoloft,
Citalopram,
Escitalopram,
Fluoxetine,
Fluvoxamine

Page 8 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

SEROTONINNOREPINEPHRINE
REUPTAKE
INHIBITORS (SNRIs)

Major depression,
chronic pain
disorders *
fibromyalgia,
perimenopausal
symptoms

Depression, diabetic
Moderately
peripheral
selective blockade
neuropathy,
of NET and SERT
fibromyalgia, stress
incontinence, anxiety
disorder,
premenstrual disorder

Acute increase in
serotonergic and
adrenergic synaptic
activity * otherwise
like SSRIs

Toxicity:
Anticholinergic
sedation,
hypertension
(venlafaxine) *
Interaction: Some
CYP2D6 inhibition
(duloxetine,
desvenlafaxine)

Insomnia, dry mouth,

nausea, constipation,
headache, dizziness,
nervousness,
weakness, anorexia,
somnolence, sweating

Cymbalta,
Effexor,
Duloxetine,
Venlafaxine, and
Desvenlafaxine

TETRACYCLICS,
UNICYCLIC

Major depression
*smoking cessation
(bupropion)
*sedation
(mirtazapine)
*amoxapine and
maprotiline rarely
used

Depression, anxiety
associated with
depression,
neuropathic pain,
attention deficit
hyperactivity disorder
(ADHD), smoking
cessation (Zyban)

Increaed
norepinephrine and
dopamine activity
(bupropion)
*NET>SERT
inhibition
(amoxapine,
maprotiline)
*increased relaease
of norepinephrine 5HT (mirtazapine)

Presynaptic release
of catecholamines
but no effects on 5HT (bupropion)
*amoxapine and
maprotiline resemble
TCAs

Extensive metabolism
in liver
*Toxicity:Lower
seizure threshold
(amoxapine,
bupropion); sedation
and weight gain
(mirtazapine)
*Interactions: CYP2D6
inhibitor (bupropion)

Agitation, dizziness,
dry mouth, insomnia,
sedation, headache,
nausea, vomiting,
tremor, constipation,
weight loss, anorexia,
excess sweating

Wellbutrin,
Wellbutrin SR,
Zyban (smoking
cessation),
Remeron,
Buprupion,
Amoxapine,
Maprotiline,
Mirtazapine

TRICYCLIC
ANTIDEPRESSANT
(TCA)

Major depression
not responsive to
other drugs *chronic
pain disorder
*incontinence
*obsessivecompulsive disorder

Depression, enuresis,
eating disorders

Mixed and variable Like SNRIs plus

blockade of NET and significant blockade
SERT
of autonomic nervous
system and histamine
receptors

Long half-lives *CYP

substrates *active
metabolites
*Toxicity:Anticholinergi
c, -blocking effects,
sedation and weight
gain, arrhythmias, and
seizures in overdose
*Interactions:CYP
inducers and inhibitors

Sedation,
anticholinergic effects
(dry mouth, dry eyes,
urinary retention),
constipation

Tofranil, Tofranil
PM, Imipramine

Block AT1 angiotensin

receptors

Same as ACE
inhibitors but no
increase in
bradykinin

Oral *toxicity: Same as

ACE inhibitors but no
cough,

Category: ANTIHYPERTENSION
ANGIOTENSIN
Hypertension *heart
RECEPTOR BLOCKERS failure,

Losartan, many
others

Page 9 of 41

Drugs

Clinical
Application

ANGIOTENSINCONVERTING
ENZYMES (ACE)
INHIBITORS

Hypertension *heart
failure, diabetes

DIURETICS Loop
diuretics:
Furosemide

Uses

Hypertension HF, LVD,

after MI, diabetic
nephropathy

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Inhibit angiotensin
converting enzyme

Reduce angiotensin II Oral *toxicity: Cough,

levels *reduce
angioedema
vasoconstriction and *teratogenic
aldosterone secretion
*increase bradykinin

Tachycardia, gastric
Captopril,
irritation, peptic ulcer, Capoten
proteinuria, rash,
pruritus, cough

Severe hypertension, Edema due to CHF,

heart failure
cirrhosis of the liver,
renal disease, acute
pulmonary edema
plus hypertension

Block Na+, Cl-, K+

transporter in renal
loop of Henle

Like thiazides *
Greater efficacy

Oral * Duration: 8-12

h * Toxicity:
Hypokalemic
metabolic alkalosis
hyperuricemia,
hyperglycemia,
hyponatremia

Electrolyte and
hematologic
imbalances, anorexia,
nausea, vomiting,
dizziness, rash,
photosensivity,
ortostatic
hypotension,
glycosuria

DIURETICS Thiazides:
Hydrochlorothiazide

Hypertension, mild
heart failure

Block Na+ or Cltransporter in renal

distal convoluted
tubule

Reduce blood volume

plus poorly
understood vascular
effects

Oral * Duration: 8-12

h * Toxicity:
Hypokalemic
metabolic alkalosis,
hyperuricemia,
hyperglycemia,
hyponatremia

Orthostatic
HydroDIURIL,
hypotension,
esidrix,
dizziness, vertigo,
microzide, oretic
light-headedness,
weakness, anorexia,
gastri distress, nausea,
diarrhea, constipation,
hematologic changes,
rash, photosensitivity
reaction,
hyperglycemia, fluid
and electrolyte
imbalances, reduced
libido

DIURETICS
Spironolactone

Aldosteronism, heart hypertension, edema Blocks aldosterone

failure, hypertension due to CHF, cirrhosis,
receptor in a renal
renal disease,
collecting tubule
hypokalemia,
prophylaxis of
hypokalemia in at- risk
patients,
hyperaldosteronism

Increase Na+ and

decrease K+ * poorly
understood reduction
in heart failure
mortality

Oral * Duration: 8-12

h * Toxicity:
Hypokalemic
metabolic alkalosis
hyperuricemia,
hyperglycemia,
hyponatremia

Headache, diarrhea,
drowsiness, lethargy,
hyperkalemia,
cramping, gastritis,
erectile dysfunction,
gynecomastia

Hypertension, edema
due to CHF, cirrhosis,
corticosteroid and
estrogen therapy

Lasix

Aldactone,
Eplerenone

Page 10 of 41

Drugs

Clinical
Application

PARENTERAL AGENTS Hypertensive

Nitroprusside
emergencies

PARENTERAL
AGENTS:
Fenoldopam

Hypertensive
emergencies

PARENTERAL
AGENTS:
Diazoxide

Hypertensive
emergencies

RENIN INHIBITORS

Uses

Hypertensive crisis

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Releases nitric oxide Powerful vasodilation Parenteral *Short

duration *Toxicity:
Excessive hypotension,
shock

Adverse
Reaction

Trade
Name

Apprehension
headache,
restlessness, nausea,
vomiting, palpitation,
diaphoresis

Nitropress

Dizziness, weakness,
nausea, vomiting,
sodium and water
retention,
hypotension,
myocardial ischemia

Hyperstat IV

Activates D1
receptors

Powerful vasodilation Parenteral *Short

duration *Toxicity:
Excessive hypotension,
shock

Hypertensive
emergencies, or crisis

Opens K channels

Powerful vasodilation Parenteral *Short

duration *Toxicity:
Excessive hypotension,
shock

Hypertension

Inhibits enzyme
activity of renin

Reduce angiotensin
I and II and
aldosterone

SYMPATHATHIC
NERVE TERMINAL
BLOCKERS
Guanethidine

Hypertension but
rarely used

Hypertension

Interferes with
amine released and
replaces
norepinephrine in
vesicles

Reduces all
sympathetic effects,
especially
cardiovascular, and
reduce blood pressure

Guanethidine: Severe
orthostatic
hypotension *sexual
dysfunction

Dizziness, weakness,
lassitude, syncope,
postural or exertional
hypotension diarrhea
bradycardia, fluid
retention and edema,
CHF, inhibition of
ejaculation

Ismelin

SYMPATHOPLEGICS,
CENTRALLY ACTIVE:
Clonidine, Methyl
DOPA

Hypertension
*clonidine also used
in withdrawal from
abused drugs

Hypertension

Activates 2
adrenoceptor

Reduce central
sympathetic outflow
* reduce
norepinephrine
release from
noradrenergic nerve
endings

Oral *Clonidine also

patch *Toxicity:
sedation *methyldopa
hemolytic anemia

Drowsiness, sedation,
dizziness, headache,
fatigue that tends to
diminish within 4-6
weeks, dry mouth,
constipation,
impotence, decrease
sexual activity

Catapres,
clonidine

Oral
*toxicity:Hyperkalemia
, renal impairment
*potential teratogen

Aliskiren

Page 11 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

VASODILATORS
Hydralazine

Hypertension
*Minoxidil also used
to treat hair loss

Essential hypertension Causes nitric oxide

(oral), when needed
release
to lower blood
pressure (parenteral)

Vasodilation *reduce
vascular resistance
*arterioles more
sensitive than veins
*reflex tachycardia

Oral *Toxicity: Angina,

tachycardia
*Hydralazine: Lupuslike syndrome

Dizziness, palpitation, Apresoline

tachycardia, angina,
anorexia, nausea,
vomiting, headache,
hypotension, diarrhea,
rash, nasal congestion

VASODILATORS:
Minoxidil

Hypertension
*Minoxidil also used
to treat hair loss

Severe hypertension

Metabolite opens K
channels in vascular
smooth muscle

Vasodilation *reduce
vascular resistance
*arterioles more
sensitive than veins
*reflex tachycardia

Minoxidil:Hypertrichosi Headache,
s
hypotension,
electrocardiogram
changes, tachycardia,
rash, fatigue, sodium
and water retention,
nausea, hair growth,
changes in direction
and magnitude of T
waves

Loniten

VASODILATORS:
Nifedipine,
Amlodipine

Hypertension

Vasospastic angina
(Prinzmetal's variant
angina), chronic stable
angina, hypertension
(sustained release
only)

Block vascular
calcium channels >
cardiac calcium
channels

*reduce vascular
resistance

Oral, duration 4-6 h

*toxicity: Excessive
hypotension
*Interactions: Additive
with other vasodilators

Dizziness, light
headedness,
nervousness,
headache, nausea,
constipation,
peripheral edema,
asthenia, bradycardia,
atrioventricular block,
arrhythmias, flushing

Adalat,
procardia,
procardia XL

VASODILATORS:
Verapamil, Diltiazem

Hypertension,
angina, arrhythmias

Supraventricular
tachyarrhythmias,
temporary control of
rapid ventricular rate
in atrial flutter or
fribrillation, angina,
unstable angina,
hypertension

Nonselective block
of L-type calcium
channels

Reduce cardiac rate

and output *reduce
vascular resistance

Oral, IV, duration 4-8 h

*toxicity:
Atrioventricular block,
acute heart failure;
constipation, edema
*Interactions: Additive
with other cardiac
depressants and
hypotension

Constipation,
dizziness, light
headedness,
headache, asthenia,
nausea, vomiting,
peripheral edema,
hypotension, mental
depression,
aggranulocytosis,
proarrythmic effects

Calan, covera
HS, Isoptin,
verelan, verelan
PM

Page 12 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

BLOCKERS

hypertension
*benign prostatic
hyperplasia

Hypertension

Selectively block 1 Prevent sympathetic

adrenoceptors
vasoconstriction
*reduce prostatic
smooth muscle tone

Oral *toxicity:
Orthostatic
hypotension

Dizziness, headache,
Prazosin,
drowsiness, lack of
Terazosin,
energy, somnolence,
Doxazosin
nausea, palpitation,
edema, dyspnea, nasal
congestion, sinusitis

BLOCKERS

Hypertension, heart
failure

Hypertension, angina
pectoris, MI

Blocks 1 receptors:
carvedilol also
blocks receptor

Prevent sympathetic
cardiac stimulation *
reduce renin
secretion

Oral *Toxicity: Fatigue

Dizziness, vertigo,
fatigue, bradycardia,
CHF, arrhythmias,
tachycardia, sinuatrial
or atrioventricular
block, gastric pain,
flatulence,
constipation, diarrhea,
nausea, vomiting,
impotence, decrease
libido, decrease
exercise tolerance,
rash, eye irritation

Metoprolol,
Carvedilol,
Propranolol,
atenolol

Blockade of 5HT2A
receptors >
blockadeof D2
receptors

Some blockade
(clozapine,
risperidone,
ziprasidone) and Mreceptor blockade
(clozapine,
olanzapine) *variable
H1-receptor blockade
(all)

Toxicity:
Agranulocytosis
(clozapine), diabetes
(clozapine,
olanzapine),
hypercholesterolemia
(clozapine,
olanzapine),
hyperporlactinemia
(ziprasidone), QT
prolongation
(ziprasidone), weight
gain (clozapine,
olanzapine)

Agitation, anxiety,
headache,
constipation, dry
mpouth, nausea

aripiprazole,
clozapine,
olanzapine,
Quetiapine,
risperidone,
Ziprasidone

Category: ANTI-PSYCHOTIC
Atypical
Antipsychotics

Schizophrenia
Psychotic disorders
improve both positve
and negative
symptoms *bipolar
disorder (olanzapine
or risperidone
adjunctive with
lithium) *agitation in
Alzheimer's and
Parkinson's (low
doses) *major
depression
(aripiprazole)

Page 13 of 41

Drugs

Clinical
Application

Uses

Butyrophenone

Schizophrenia
(alleviates positve
symptoms), bipolar
disorder (manic
phase), Huntington's
chorea, Tourette's
syndrome

Psychotic disorders,
Tourette's syndrome,
hyperactivity

Lithium

Bipolar affective
Manic episodes of
disorder -bipolar disorder
prophylactic use can
prevent mood
swings between
mania and depression

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Blockade of D2
receptors >>5HT2A
receptors

Some blockade, but

minimal M receptor
blockade and much
less sedation than the
phenothiazines

Oral and parenteral

forms with
metabolism
elimination *Toxicity:
Extrapyramidal
dysfunction is the
major adverse effect

EPS, dystonia,
akathisia, drowsiness,
headache, orthostatic
hypotension

Haloperidol

Mechanism of
action uncertain
*Suppresses inositol
signaling and
inhibits glycogen
synthase kinase-3
(GSK-3), a
multifunctional
protein kinase

No significant
antagonistic actions
on autonomic
nervous system
receptors or specific
CNS receptors *no
sedative effects

Oral absorption, renal

elimination *half-life
20 h *narrow
therapeutic window
(monitor blood levels)
*Toxicity: Tremor,
edema,
hypothyroidism, renal
dysfunction,
dysrhythmias *
pregnancy category D
*Interactions:
Clearance decreased
by thiazides and some
NSAIDs

Headache,
drowsiness, tremor,
nausea, polyuria

Eskalith, Lithobid

Page 14 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Newer Agents for

Bipolar Disorder

Valproic acid is
increasingly used as
first choice in acute
illness *
carbamazepine and
lamotrigine are also
used both in acute
mania and for
prophylaxis in
depressive phase

Bipolar disorder

Mechanism of
action in bipolar
disorder is unclear.

Carbamazepine
causes dose-related
diplopia and ataxia *
lamotrigine causes
nausea, dizziness, and
headache * valproic
acid causes
gastrointestinal
distress, possible
weight gain, alopecia

Oral absorption *
once-daily dosing
carbamazepine forms
active metabolite *
lamotrigine and
valproic acid form
conjugates * Toxicity:
Hematotoxicity and
induction of P450 drug
metabolism
(carbamazepine), rash
(lamotrigine), tremor,
liver dysfunction,
weight gain, inhibition
of drug metabolism
(valproic acid)

Dizziness, nausea,
insomnia, headache,
lamotrigine StevensJohnsons Syndrome
rash

Carbamazepine
(Tegretol,
Epitol),
Lamotrigine
(Lamictal) and
Valproic acid
(Depakote.
Depakene)

Phenothiazines

Psychiatric:
Schizophrenia
(alleviate positive
symptoms), bipolar
disorder (manic
phase)
*nonpsychiatric:
antiemesis,
preoperative
sedation
(promethazine)
*Pruritus

Psychotic disorders,
intractable hiccups

Blockade of D2
receptors >>5HT2A
receptors

-Receptor blockade
(fluphenazine least)
*muscarinic (M)receptor blockade
(especially
chlorpromazine and
thioridazine) *H1receptor blockade
(chlorpromazine and
thioridazine) *Central
nervous system (CNS)
Depression (sedation)
*decreased seizure
threshold *QT
prolongation
(thioridazine)

Oral and parenteral

forms, long half-lives
with metabolismdependent elimination
*Toxicity: Extensions
of effects on - and
M- receptors
*blockade of
dopamine receptors
may result in
akathisia, dystonia,
Parkinsonian
symptoms, tardive,
dyskinesias, and
hyperprolactinemia

Hypotension,
drowsiness,
dyskinesia, dystonia,
behavioral changes,
photosensitivity

Chlorpromazine,
Fluphenazine
and Thioridazine

Page 15 of 41

Drugs

Thioxanthene

Clinical
Application
Psychiatric:
Schizophrenia
(alleviate positive
symptoms), bipolar
disorder (manic
phase)
*nopsychiatric:
antiemesis,
preoperative
sedation
(promethazine)
*Pruritus

Uses

Schizophrenia

Mechanism
of Action
Blockade of D2
receptors >>5HT2A
receptors

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

-Receptor blockade
(fluphenazine least)
*muscarinic (M)receptor blockade
(especially
chlorpromazine and
thioridazine) *H1receptor blockade
(chlorpromazine and
thioridazine) *Central
nervous system (CNS)
Depression (sedation)
*decreased seizure
threshold *QT
prolongation
(thioridazine)

Oral and parenteral

forms, long half-lives
with metabolismdependent elimination
*Toxicity: Extensions
of effects on - and
M- receptors
*blockade of
dopamine receptors
may result in
akathisia, dystonia,
parkinsonian
symptoms, tardive
dyskinesias, and
hyperprolactinemia

Extrapyramidal
syndrome (EPS),
drowsiness, nausea,
diarrhea

Thiothixene
(Navane)

Category: ANTI-SEIZURE
BENZODIAZEPINES
Clonazepam

Absence seizures,
myoclonic seizures,
infantile spasms

Seizure disorder, panic Potentiates GABA

disorder
responses

Documented efficacy
against absence
seizure

>80% bioavailabilty
*extensively
metabolized but no
active metabolites *t
1/2 20-50 h

Drowsiness,
depression, ataxia,
anorexia, diarrhea,
constipation, dry
mouth, palpitations,
visual disturbances,
rash

Klonopin

BENZODIAZEPINES
Diazepam

Status epilepticus,
seizures clusters

Status epilepticus,
seizures disorders (all
forms), anxiety
disorder, alcohol
withdrawal

Stops continuous
seizure

Well absorbed orally,

*rectal administration
gives peak
concentration in ~1 h
with 90%
bioavailability *IV for
status epilepticus
*highly protein-bound
*extensively
metabolized to several
active metabolites *t
1/2 ~2 d

Drowsiness,
depression, ataxia,
anorexia, diarrhea,
constipation, dry
mouth, palpitations,
visual disturbances,
rash

Valium, diastat

Potentiates GABA
responses

Page 16 of 41

Drugs

Uses

Clinical
Application

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

CYCLIC UREIDES
Ethosuximide

Absence seizures

Partial seizures

Reduces low
threshold Ca2+
currents (T-type)

effective against
pentylenetetrazol
seizures

Well absorbed orally,

with peak levels in 3-7
h *not protein-bound
*completely
metabolized to
inactive compounds *t
1/2 typically 40 h

Drowsiness, ataxia,
dizziness, nausea,
vomiting, urinary
frequency, pruritus,
urticaria, gingival
hyperplasia

Zarontin

CYCLIC UREIDES
Phenobarbital

generalized tonicclonic seizures,

partial seizure,
myoclonic seizures,
neonatal seizures,
status epilepticus

Status epilepticus,
cortical focal seizures,
tonic-clonic seizures

Enhances phasic
GABA receptor
responses *reduces
excitatory synaptic
responses

Decrease excitatory
response, selectively
suppress abnormal
neurons

nearly complete
absorption *not
significantly bound to
plasma proteins
*peak concentration
in 1/2 to 4 h *no
active metabolites *t
1/2 varies from 75 to
125 h

Somnolence,
agitation, confusion,
ataxia, CNS
depression,
nervousness, nausea,
vomiting,
constipation, diarrhea

Phenobarbital
sodium (Luminal
sodium)

CYCLIC UREIDES
Phenytoin,
fosphenytoin

generalized tonicclonic seizures,

partial seizure

Status epilepticus

Blocks high
Inhibit a variety of
frequency firing of
calcium induced
neurons through
secretory processes
action on voltagegated (VG) Na+
channels *
decrease of synaptic
release of glutamate

Absorption is
formulation
dependent, highly
bound plasma
proteins, no active
metabolites *dosedependent
elimination, t 12-36
hours *fosphenytoin
is IV, IM routes

Ataxia, CNS
depression,
hypotension, mental
confusion, slurred
speech, dizziness,
drowziness, gingival
hyperplasia, rash

Cerebyx, Dilantin

CYCLIC UREIDES
Primidone

generalized tonicclonic seizures,

partial seizure

Epilepsy

Similar to phenytoin Effective in

Well absorbed orally, Dizziness,
but converted to
controlling seizures in not highly bound to
somnolence, nausea,
phenobarbital
newborn infants
plasma proteins *peak vomiting
concentrations in 2-6
h * t 10-25 hours
*two active
metabolites
(phenobarbital and
phenylethymalonamid
e)

Mysoline

Page 17 of 41

Drugs

Clinical
Application

Uses

GABA DERIVATIVE
Pregabalin

Partial seizures

Partial seizure
(adults), postherpetic
neuralgia, neuropathic
pain

GABA
DERIVATIVES

Generalized tonicclonic seizures,

partial seizures,
generalized seizures

GABA DERIVATIVES
Vigabatrin

Mechanism
of Action

Effects

Adverse
Reaction

Trade
Name

Well absorbed orally * Dizziness and

not bound to plasma
somnolence
proteins * not
metabolized * t1/2 6-7
h

Lyrica

Partial seizure (adults) Decreases excitatory Act presynaptically to

postherpetic neuralgia transmission by
decrease the release
acting on VG Ca2+
of glutamate
channels
presynaptically (2
subunit)

Bioavailability 50%,
decreasing with
increasing doses * not
bound to plasma
proteins * not
metabolized * t 1/2 68h

Somnolence,
dizziness, ataxia

Neurontin

Partial seizures,
infantile spasms

Partial seizures and

West's syndrome

Irreversably inhibits
GABA-transaminase

Produces sustained
increase in the
intracellular
concentration of
GABA in the brain

70% bioavailable * not

bound to plasma
proteins *not
metabolized, *t 1/2 57 h (not relevant
because of mechanism
of action)

Irreversible visual field

defects, drowsiness,
dizziness and weight
gain

Levetiracetam

Generalized tonicclonic seizures,

partial seisures,
generalized seizures

Effective against
partial seizure in
adults and children,
ineffective when
caused by maximum
electric shock

Action on synaptic
protein SV2A

Modify the synaptic

release of glutamate
and GABA

Well absorbed orally * Somnolence, asthenia, Keppra

no significant protein ataxia and dizziness,
binding * extensively
agitation, anxiety
metabolized but no
active metabolite *
t1/2 6-11 h

MISCELLANEOUS

Generalized tonicclonic seizures,

partial seisures

pain syndrome and

partial seizure

Enhances slow
inactivation of Na+
channels * Blocks
effect of
neurotrophins (via
CRMP-2)

Adjunctive therapy in
partial onset seizure
with or without
secondary
generalizations in
patients with epilepsy
16 years and older

well absorbed
*minimal protein
binding *one major
nonactive metabolite
* t1/2 12-14 h

Gabapentin

Lacosamide

Decreases excitatory Act presynaptically to

transmission by
decrease glutamate
acting on VG Ca2+
channels
presynaptically (2
subunit)

Pharmacokinetics,
Toxicities,
Interactions

Dizziness, headache,
nausea and diplopia

Vimpat

Page 18 of 41

Drugs

MISCELLANEOUS

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Generalized tonicclonic seizures,

partial seisures,
generalized seizures,
absence seizures,
myoclonic seizures

Epilepsy, migraine,
headache, mania

Blocks highfrequency firing of

neurons * modifies
amino acid
metabolism

Inhibits GABA
transaminase in the
brain blocking its
degradation, potent
inhibitor of histone
deacetylase and
changes transcription
of many genes

Well absorbed from

several formulations *
highly bound to
plasma proteins *
extensively
metabolized * t 1/2 916 h

Headache,
Depakote,
somnolence, dizziness, depakene
tremor, nausea,
vomiting, diplopia

Partial seizure (used

with other
anticonvulsants),
bipolar disorder

Prolongs
inactivation of VGNa+ channels * acts
presynaptically on
VG-Ca+ channels,
decreasing
glutamate release

Decrease synaptic
release of glutamate

Lamotrigine

Generalized tonicclonic seizures,

generalized seizures,
partial seisures,
absence seizures

Well absorbed orally *

no significant protein
binding * extensively
metabolized, but no
active metabolites * t
1/2 25-35 h

Dizziness,
somnolence, insomia,
ataxia, nausea,
vomiting, diplopia,
headache, Steven'sJohnsons syndrome,
rash

Tiagabine

Partial seizures

Partial seizures

Blocks GABA
reuptake in
forebrain by
selective blockade
of GAT-1

Inhibit GABA uptake,

prolong inhibitory
action of synaptically
released GABA and
potentiate tonic
inhibition

Well absorbed *
Highly bound to
plasma protein *
Extensively
metabolized but no
active metabolite *
t1/2 4-8 h

Dizziness,
Gabitril
somnolence, asthenia,
nervousness, nausea

Topiramate

Generalized tonicclonic seizures,

partial seisures,
generalized seizures,
absence seizures,
migraine

Partial/ tonic-clonic
seizures, migraine,
headache

Multiple actions on
synaptic function,
primary action on
kinases altering the
phosphorylation of
voltage-gated and
ligand-gated ion
channels

Potentiate the
inhibitory effect of
GABA acting at site
different from
benzodiazepine,
depress the
excitatory action of
kainate on glutamate
receptor,

Well absorbed * not

Fatigue concentration
bound to plasma
problems,
protein * Extensively
somnolence, anorexia
metabolized but 40%
excreted unchanged in
the urine * no active
metabolite * t1/2 20
h, but decreases with
concomitant drugs

Valproate

MISCELLANEOUS

Lamictal

Topamax

Page 19 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

TRICYCLICS
Carbamazepine

generalized tonicclonic seizures,

partial seizure

Epilepsy, bipolar
Blocks highdisorder, trigeminal/
frequency firing of
postherpetic neuralgia neurons through the
action on VG Na+
cahnnels *decreases
synaptic release of
glutamate

Treats bipolar
depression,
trigeminal neuralgia
and epilepsy

Well absorbed orally,

with peak levels in 6-8
h *no significant
protein binding
*metabolized in part
to active 10-11epoxide
*t1/2 of
parent ranges from 812 h in treated
patients to 36 h in
normal subjects

Dizziness, nausea,
drowsiness, unsteady
gait, aplastic anemia
and blood cells
abnormality

Zonisamide

Generalized tonicclonic seizures,

partial seisures,
myoclonic seizures

Partial seizures of
epilepsy

Effect on sodium
channels, may also
act on voltage-gated
calcium channel

Approximately 70%
bioavailable orally *
minimally bound to
plasma proteins * >
50% metabolites *
t1/2 20 h

Somnolence, anorexia, Zonegran

headache, dizziness,
rash, heat stroke

Anaphylaxis, asthma, Asthma, bronchospasm Nonselective and

others *rarely used
agonist
for asthma (2selective agents
preferred)

Bronchodilation plus
all other
sympathomimetic
effects on
cardiovascular and
other organ systems

Aerosol, nebulizer, or
parenteral

palpitation,
tachycardia,
hypertension,
arrhythmias, dizziness,
vertigo, shakiness,
nervousness,
headache, insomnia,
nausea, vomitting,
anxiety, fear, pallor

Adrenaline,
Epinephrine
mist, primatene
mist

Asthma, chronic
obstructive
pulmonary disease
(COPD) *Drug of
choice in acute
asthmatic
bronchospasm

Prompt, efficacious
bronchodilation

Aerosol inhalation
*duration several
hours *also available
for nebulizer and
parenteral use
*Toxicity: Tremor,
tachycardia
*overdose:arrhythmias

palpitation,
tachycardia,
hypertension, tremor,
dizziness, shakiness,
nervousness, nausea,
vomiting

Proventil,
Ventulin, Volmax

Blocks highfrequency firing via

action on VG-Na+
channels

Tegretol, epitol

Category: ASTHMA
BETA
AGONISTS
Epinephrine

BETA AGONISTS
Albuterol

Bronchospasm,
prevention of EIB

Selective 2 agonist

Page 20 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

BETA AGONISTS
Isoproterenol

Asthma, but 2selective agents

preferred

Bronchospasm during
anaesthesia,
vasopressor during
shock

1 and 2 agonist

Bronchodilation plus Aerosol, nebulizer, or

powerful
parenteral
cardiovascular effects

Palpitation,
tachycardia, chest
tightness, angina,
shakiness,
nervousness,
weakness,
hyperactivity,
headache, nausea,
vomiting, flushing,
sweating

Isuprel

BETA AGONISTS
Salmeterol

Asthma prophylaxis

Asthma,
bronchospasm,
prevention of EIB

Selective 2 agonist

Slow onset, primarily

preventive action;
potentiates
corticosteroid effects

Aerosol inhalation
*duration several
hours *Toxicity:
Tremor, tachycardia
*overdose:arrhythmias

palpitation,
tachycardia, tremor,
nervousness,
headache, nausea,
vomitting, heartburn,
GI distress, diarrhea,
cough rhinitis

Serevent, diskus,
metaproterenol,
terbutaline,
formoterol

CORTICOSTEROIDS,
INHALED
Fluticasone

Asthma * adjunct in
COPD

Prophylactic
maintenance and
treatment of asthma

Alters gene
expression

Reduces mediators of
inflammation *
powerful prophylaxis
of exacerbations

Aerosol * duration
hours
* Toxicity:
limited by aerosol
application * candidal
infection, vocal cord
changes.

Oral laryngeal,
pharyngeal irritation,
fungal infection,
suppression of HPA
function

Flovent, flovent
rotadisk, flovent
diskus

CORTICOSTEROIDS,
SYSTEMIC
Prednisone

Asthma * adjunct in
COPD

Endocrine, rheumatic,
collagen,
dermatologic,
allergies, ophthalmic,
respiratory,
hematologic,
edematous,
gastrointestinal,
nervous system
diseases

Like fluticasone

Reduces mediators of Oral * duration hours

inflammation,
* Toxicity: Multiple
powerful prophylaxis
of exacerbations

Fluid and electrolyte,

masculoskeletal,
cardiovascular,
gastrointestinal,
dermatology,
neurology, endocrine,
ophthalmic, metabolic

Methylprednisol
one: Parenteral
agent like
prednisone

Page 21 of 41

Drugs

Clinical
Application

Uses

IGE ANTIBODY
Omalizumab

Severe asthma
inadequately
controlled by above
agents

Moderate to severe
persistent asthma

LEUKOTRIENE
ANTAGONISTS
Montelukast,
zafirlukast

Headache (usually
mild), flatulence,
abdominal pain,
cramps, constipation,
nausea, dyspepsia,
rhabdomyolysis with
acute renal failure

METHYLXANTHINES
Theophylline

STABILIZERS OF
MAST AND OTHER
CELLS
Cromolyn, nedocromil

Mechanism
of Action
Humanized IgE
antibody reduces
circulating IgE

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Reduces frequency of Parenteral * duration

asthma exacerbations 2-4 d *Toxicity:
Injection site reactions
(anaphylaxis
extremely rare)

Injection site reaction, Xolair

viral infection,
sinusitis, headache,
pharyngitis,
anaphylaxis,
malignant cyst

Prophylaxis and
Block leukotriene
treatment of chronic
D4 receptors
asthma in adults and
pediatric patients 12
months of age and
older, seasonal allergic
rhinitis in adults and
pediatric patients 2
years of age and older

Block airway
Oral * duration hours
response to exercise * Toxicity: Minimal
and antigen challenge

Headache, dizziness,
dyspepsia,
gastroenteritis,
influenza like
symptoms, cough,
abdominal pain,
fatigue

Singulair,
Zileuton (Zyflo):
Inhibits
lypoxygenase,
reduces
synthesis of
leukotrienes

Asthma, COPD

Symptomatic relief or
prevention of
bronchial asthma and
reversible
bronchospasm of
chronic bronchitis and
emphysema

Uncertain *
phosphodiesterase
inhibiton *
adenosine receptor
antagonist

Bronchodilation,
cardiac stimulation,
increased skeletal
muscle strength
(diaphragm)

Oral * duration 8-12 h

but extended-release
preparations often
used * Toxicity:
Multiple

Nausea, vomitting,
restlessness, vomiting,
tachycardia, tremor,
headache, palpitation,
hyperglycemia,
electrocardiographic
changes, cardiac
arrhythmias

Theo-24, TheoDUR,
elixophyllin, slophyllin, uniphyl

Asthma (other routes

used for ocular,
nasal, and
gastrointestinal
allergy)

Bronchial asthma,
prevention of
bronchospasm;
prevention of EIA,
nasal preparation:
prevention and
treatment of allergic
rhinitis

Alters function of
delayed chloride
channels * inhibits
inflammatory cell
activation

Prevents acute
bronchospasms

Aerosol * duration 6-8

h * Toxicity: Cough *
not absorbed so other
toxicities are minimal

Dizziness, headache,
Intal, nasalcrom,
nausea, dry and
gastrocrom
irritated throat, rash,
joint swelling and pain

Page 22 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Category: CHOLINOMIMETIC

DIRECT ACTING
CHOLINE ESTERS

Postoperative and
Urinary cholinergics,
Neurogenic ileus and acute non obstructive
urinary retention
urinary retention

Muscarinic agonist
Activate M1 through
*negligible effects
M3 receptors in all
at nicotinic receptors peripheral tissue ,
cause increased
secretion, smooth
muscle contraction
(except vascular
smooth muscle
relaxes,) and changes
in heart rate

Oral and parenteral,

duration ~30 mins
*does not enter
central nervous
system (CNS)
*Toxicity: Excessive
parasympathomimetic
effects especially
bronchospasm in
asthmatics *
Interactions: Additive
with other
parasympathomimetics

Abdominal
discomfort, headache,
diarrhea, nausea,
salivation, urgency

Bethanechol
(Duvoid,
urecholine),
Carbachol
(Miostat)

DIRECT ACTING
NICOTINIC AGONIST

*Medical use in
smoking cessation
*non medical use in
smoking and
insecticides

Agonist at both NN
and NM receptors

Oral gum, patch for

smoking cessation
*toxicity:Increased
gastrointestinal (GI)
activity, nausea,
vomiting, diarrhea
acutely, Increase in
blood pressure *high
dose causes seizures
*long-term GI and
cardiovascular risk
factor *Interactions:
Additive with CNS
stimulants varenicline
has long half life

Excess nicotine convulsion, coma,

respiratory arrest,
nausea and insomnia

Nicotine,
Varenicline

Varenicline - for
cessation of smoking

Activates autonomic
postganglionic
neurons (both
sympathetic and
parasympathetic) and
skeletal muscle
neuromuscular end
plates *Enters CNS
and activities NN
receptors

Page 23 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

DIRECT-ACTING
MUSCARINIC
ALKALOIDS OR
SYNTHETICS

Glaucoma:Sjgren's
syndrome

Glaucoma

Muscarinic agonist
*negligible effects
at nicotinic
receptors, partial
agonist

Activate M1 through
M3 receptors in all
peripheral tissue ,
cause increased
secretion, smooth
muscle contraction
(except vascular
smooth muscle
relaxes,) and changes
in heart rate

INTERMIDIATEACTING
CHOLINESTERASE
INHIBITORS

Myasthenia gravis
*Postoperative and
Neurogenic ileus and
urinary retention

Therapeutic uses in
myasthenia gravis,
physostigmine for
glaucoma

Forms covalent
Like edrophonium,
bond with AChE, but but longer-acting
hydrolyzed and
released

LONG-ACTING
CHOLINESTERASE
INHIBITORS

Obsolete *was used

in glaucoma

as insecticides

Like Neostigmine,
but released more
slowly

SHORT-ACTING
CHOLINESTERASE
INHIBITOR

Diagnosis and acute

treatment of
myasthenia gravis

Diagnosis of
myasthenia gravis

Alcohol, binds
briefly to active site
of
acetylcholinesterase
(AChE) and prevents
access of
acetylcholine (Ach)

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Oral lozenge and

topical *toxicity
&interactions: Like
Bethanechol

Temporary reduction
in visual acuity,
headache

Pilocarpine,
Cevimeline

Oral and parenteral

*quaternary amine,
does not enter CNS.
duration 2-4 h
*toxicity
&interactions:Like
Edrophonium

Prolonged duration of
effect

Neostigmine,
Pyridostigmine,
Physostigmine

Like Neostigmine, but Topical only

longer-acting
*Toxicity:Brow ache,
uveitis, blurred vision

Central nervous
system toxicity

Echothiophate,
Malathion,
Parathion, Sarin,

Amplifies all actions

of ACh *increases
parasympathetic
activity and somatic
neuromuscular
transmission

Increased bronchial
secretions, cardiac
arrhythmias, muscle
weakness, urinary
frequency

Edrophonium
(Enlon, Tensilon)

Parenteral
*quaternary amine
*does not enter CNS
*Toxicity:
Parasympathomimetic
excess *Interactions:
Additive with
parasympathomimetics

Page 24 of 41

Drugs

Pharmacokinetics,
Toxicities,
Interactions

Mechanism
of Action

Effects

Glaucoma, mountain Open angle glaucoma,

sickness, edema with secondary glaucoma,
alkalosis
drug-induced edema,
edema due to CHF

Inhibition of the
enzyme prevents of
dehydration of
H2CO3 and
hydration of CO2

Reduces reabsorption
of HCO3- in kidney ,
causing self-limited
diuresis
*Hyperchloremic
metabolic acidosis
reduces body pH,
reduces intraocular
pressure

Oral and topical

preparations available
*Duration of action~ 812 h *Toxicity:
Metabolic acidosis,
renal stones,
hyperammonemia in
cirrhotics

Weakness, fatigue,
anorexia, vomiting,
paresthesias,
photosensitivity

Brinzolamide,
dorzolamide

LOOP DIURETICS
Furosemide

Pulmonary edema,
peripheral edema,
Hypertension, acute
hypercalcemia or
hyperkalemia, acute
renal failure, anion
overdose

Edema due to CHF,

cirrhosis of the liver,
renal disease, acute
pulmonary edema

Inhibition of the
Na/K/2Cl
transporter in the
ascending limb of
Henle's loop

Marked increase in
NaCl excretion, some
K wasting
hypokalemic
metabolic alkalosis,
increased urine Ca
and Mg

Oral and parenteral

preparations
*Duration of action 24 hours *Toxicity:
Ototoxicity,
Hypovolemia, K
wasting,
Hyperuricemia,
hypomagnesemia

Electrolyte and
hematologic
imbalance, anorexia,
vomiting, dizziness,
photosensitivity,
glycosuria

Bumetanide,
Torsemide,
Ethacrynic acid

OSMOTIC DIURETICS
Mannitol

Renal failure due to

increased solute load
(rhabomyolysis,
chemotheraphy),
increased
intracranial pressure,
glaucoma

Promote diuresis in
acute renal failure,
reduce IOP, treatment
of cerebral edema

Physical osmotic
effect on tissue
water distribution
because it is
retained in the
vascular
compartment

Marked increase in
IV administration
urine flow, rduced
*Toxicity: Nausea,
brain volume,
vomiting, headache
decreased intraocular
pressure, initial
hyponatremia, then
hypernatremia

Edema, fluid and

Osmitrol
electrolyte imbalance,
headache, blurred
vision, nausea,
vomiting, urinary
retention

OTHER AGENTS
Conivaptan

Hyponatremia

reduce objective signs

of hyponatremia and
heart failure
associated with
elevated
concentration of
vasspressin

Antagonist at V1a
and V2 ADH
receptors

Reduces water
reabsorption,
increases plasma Na
concentration

Can not be
administered for
those with congestive
heart faiulure

Clinical
Application

Uses

Adverse
Reaction

Trade
Name

Category: DIURETICS

CARBONIC
ANHYDRASE
INHIBITORS
Acetazolamide

IV only *Toxicity:
Infusion site reactions

Page 25 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

POTASSIUM-SPARING Hypokalemia from

DIURETICS
other diuretics
Amiloride
*reduces lithiuminduced polyuria

CHF, hypertension,
prevention of
hypokalemia in atriskpatients, polyuria
prevention with
lithium use

Blocks epithelial
sodium channels in
collecting tubules

Reduces Na retention
and K wasting
*Increases lithium
clearance

Orally active *duration

24 h *Toxicity:
Hyperkalemic
metabolic acidosis

Headache, diarrhea,
dizziness, nausea,
fatigue, weakness,
hypotension

POTASSIUM-SPARING Aldosteronism from

DIURETICS
any cause
Spironolactone
*Hypokalemia due to
other diuretics
*postmyocardial
infarction

Edema due to CHF,

cirrhosis of the liver,
acute renal disease,
hypokalemia,
hyperaldosteronism

Pharmacologic
antagonist of
aldosterone *weak
antagonism of
androgen receptors

Reduces Na retention
and K wasting in
kidney *poorly
understood
antagonism of
aldosterone in heart
and vessels

Slow onset and offset

of effects *Duration
24-48 h *Toxicity:
Hyperkalemia,
gynecomastia
(spironolactone, not
eplerenone) *additive
interaction with other
K-retaining drugs

Headache, diarrhea,
lethargy,
hyperkalemia,
cramping, gastritis,
erectile dysfunction,
gynecomastia

THIAZIDES
Hydrochlorothiazides

Edema due to CHF,

cirrhosis of the liver,
acute renal
dysfunction

Inhibition of the
Na/Cl transported in
the distal
convoluted tubule

Modest increase in
NaCl excretion *some
K wasting
*Hypokalemic
metabolic alkadosis
*Decreases urine Ca

Oral *Duration 8-12 h

*Toxicity:
Hypokalemic
metabolic alkadosis,
hyperuricemia,
hyperglycemia,
hyponatremia

Electrolyte and
hematologic
imbalance, anorexia,
vomiting, dizziness,
photosensitivity,
glycosuria

Hypertension,mild
heart failure,
nephrolithiasis,
nephrogenic
diabetes insipidus

Trade
Name
Eplerenone,
Triamterene

Metolazone,
Chlorothiazide

Page 26 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Category: DYSLIPIDEMIA

BILE ACID
SEQUESTRANT
Colestipol

Elevated LDL,
digitalis toxicity,
pruritus

Hyperlipidemia

FIBRATES
Fenofibrate,
gemfibrozil

Hypertriglyceridemia, Hyperlipidemia,
Peroxisome
low HDL
hypertri- glyceridemia, proliferatorreduction of CAD risk
activated receptor
alpha (PPAR-)
agonists

Decrease secretion of Oral *duration 3-24 h

very-low-density
*Toxicity: Myopathy,
lipoproteins (VLDL)
hepatic dysfunction
*increase lipoprotein
lipase activity
*increase highdensity lipoproteins
(HDL)

Dyspepsia, abdominal Lopid

pain, diarrhea,
nausea, vomiting,
rash, vertigo,
headache,
cholecystitis,cholelithia
sis

NIACIN

Low HDL *elevated

VLDL, LDL, Lp(a)

Increases HDL
*decreases
lipoprotein a [Lp(a)],
LDL and triglycerides

Generalized flushing
sensation of warmth,
severe itching and
tingling, nausea,
vomiting, abdominal
pain

Adjunctive treatment
for hyperlipidemia

Binds bile acids in

gut, prevent
reabsorption,
increases
cholesterol
catabolism, upregulates LDL
receptor

Decreases
catabolism of apo
A1 *reduces VLDL
secretion from liver

Decreases LDL

oral, taken with meals,

not absorbed, toxicity:
constipation, bloating,
interferes with
absorption of some
drugs and vitamins

Oral *large doses

*Toxicity: Gastric
irritation, flushing, low
incidence of hepatic
toxicity *may reduce
glucose tolerance

Constipation (may
lead to fecal
impaction),
exacerbation of
hemorrhoids,
abdominal pain,
distention, cramping,
nausea, increase
bleeding related to
vitamin K,
malabsorption,
vitamin A and D
deficiency

colestid,
cholestryramine,
colesevalam

Niaspan, Niacor,
extended
release niacin

Page 27 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

STATINS
Atorvastatin,
simvastatin,
rosuvastatin

Atherosclerotic
vascular disease
(primary and
secondary
prevention) *acute
coronary syndrome

Primary
hyperlipidemia,
reduction of elevated
total and LDL
cholesterol levels and
serum triglycerides

Inhibit HMG-CoA
reductase

Reduce cholesterol
synthesis and upregulate low-density
lipoprotein (LDL)
receptors on
hepatocytes *
modest reduction in
triglycerides

Oral *duration 3-24 h

*Toxicity: Myopathy,
hepatic dysfunction
*Interactions:CYPdependent
metabolism (3A4, 2C9)
Interacts with CYP
inhibitors

Headache (usually
mild), flatulence,
abdominal pain,
cramps, constipation,
nausea, dyspepsia,
rhabdomyolysis with
acute renal failure

Lipitor,
fluvastatin,
pravastatin,
lovastatin

STEROL ABSORPTION
INHIBITOR
Ezetimibe

Elevated LDL,
phytosterolemia

Primary
hypercholesterolemia

Blocks sterol
transporter NPCL1L
in intestine brush
border

Inhibits reabsoption
of cholesterol
excreted in bile,
decreases LDL and
phytoesterols

Oral, duration 24 h,

Diarrhea, back pain,

sinusitis, dizziness,
abdominal pain,
arthralgia, cough,
fatigue

Zetia

Category: GASTROINTESTINAL CONDITIONS

ANTIDIARRHEAL
DRUGS
Loperamide

Nonspecific,
noninfectious
diarrhea

Nausea, diarrhea,
abdominal cramps, H.
pylori infection with
duodenal ulcer

Activates -opioid
receptors in enteric
nervous system

Slows motility in gut

with negligible CNS
effects

Mild cramping but

Dry skin and mucus
little or no CNS toxicity membranes, nausea,
constipation, light
headedness

Immodium,
kaopectate,
Maalox,
Diphenoxylate,

ANTIEMETIC DRUGS
Aprepitant

Effective in reducing
both early and
delayed emesis in
cancer
chemotheraphy

Prevent acute and

delayed nausea and
vomiting from highly
emetogenic
chemotherapeutic
regimens

NK1-receptors
blocker in CNS

Interferes with
vomiting reflex
*Noeffects on 5-HT,
dopamine or steroid
receptors

Given orally *IV

fosaprepitant
available *fatigue,
dizziness, diarrhea
*CYP interactions

Fatigue, dizziness and

diarrhea

Emend,
Corticosteroids,
Antimuscarinics
(scopolamine),
Antihistaminiccs,
Phenothiazines,

ANTIEMETIC DRUGS First-line agents in

Ondansetron, other 5 cancer
HT3 antagonists
chemotheraphy; also
useful for postop
emesis

Prevention of
chemotheraphy
induced and
postoperative nausea
vomitting, bulimia,
spinal analgesiainduced pruritus,
levodopa-induced
psychosis

5-HT3 blockade in
gut and CNS with
shorter duration of
binding than
alosetron

Extremely effective in Usually given

preventing
chemotheraphyinduced and postoperative nausea and
vomiting

Headache, fatigue,
drowsiness, sedation,
constipation, hypoxia

Zofran

Page 28 of 41

Drugs

Clinical
Application

BILE ACID THERAPHY

FOR GALLSTONES
Ursodiol

Gallstones in
patients refusing or
not eligible for
surgery

DRUG STIMULATING
MOTILITY
Metoclopramide

Uses

Dissolution of small
cholesterol gallstones
in patients with
asymptomatic
gallbladder disease
who refuse
cholecystectomy

Mechanism
of Action
Reduces cholesterol
secretion into bile

Effects

Dissolve gallstones

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

May cause diarrhea

Hepatotoxicity

Gastri paresis (eg, in Diabetic gastroparesis, D2-receptor blocker Increases gastric

diabetes) *antiemetic GERD, prevention of
* removes inhibition emptying and
nausea and vomiting
of acetylcholine
intestinal motility
neurons in enteric
nervous system

Parkinsonian
symptoms due to
block of central
nervous system (CNS)
D2 receptors

Restlessness,
Reglan,
dizziness, fatigue,
Domperidone,
extrapyramidal effects Cholinomimetics,
Macrolides

DRUGS FOR
IRRITABLE BOWEL
SYNDROME (IBS)
Alosetron

Approved for severe

diarrheapredominants IBS in
women

For severe IBS with

diarrhea

5-HT3 antagonist of
high potency and
duration of binding

Reduces smooth
muscle activity in gut

Rare but serious

Ischemic colitis,
constipation *ischemic serious complication
colitis *infarction
of constipation
requiring
hospitalization or
surgery

Lotronex

DRUGS USED IN ACIDPEPTIC DISEASES

Proton pump
inhibitors (PPIs)

Peptic ulcer,
gastroesophageal
reflux disease,
erosive gastritis

Errosive esophagitis,
GERD, H.pylori,
erradication, NSAIDassociated gastric
ulcer, hypersecretory
condition, heartburn,
reduce risk of upper
GI bleeding

Irreversible
blockade of H+, K+ATPase pump in
active parietal cells
of stomach

Long-lasting
reduction of
stimulated and
nocturnal acid
secretion

Half-lives much
Headache, nausea,
shorter than duration diarrhea
of action * low toxicity
*reduction of stomach
acid may reduce
absorption of some
drugs and increase
that of others

Prilosec,
zegerid,
omeprazole,
Iansoprazole

DRUGS USED IN
INFLAMMATORY
BOWEL DISEASE (IBD)
Anti-TNF antibodies,
eg, infliximab others,

Infliximab:
Moderately severe
to severe Crohn's
disease and
ulcerative colitis
*others approved in
Crohn' disease

Crohn's disease,
ulcerative colitis and
rheumatoid arthritis

Bind tumor necrosis

factor and prevent it
from binding to its
receptors

Suppression of
severalaspects of
immune function,
especially TH1

Infusion reactions
*reactivation of latent
tuberculosis
*Increased risk of
dangerous systemic
fungal and bacterial
infections

Remicade,
Corticosteroids

Sore throat, cough,

sinus infection, gastric
distress

Actigall, URSO

Page 29 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

DRUGS USED IN
INFLAMMATORY
BOWEL DISEASE (IBD)
Purine analogs and
antimetabolites, eg,
6-mercaptopurine,
methotrexate

Mild to moderately
severe Crohn's
disease and
ulcerative colitis

Chronic inflammatory
diseases, Crohn's
disease and
rheumatoid arthritis

Mechanism
Generalized
uncerain *may
suppression of
promote apoptosis
immune processes
of immune cells
*Methotrexate
blocks dihydrofolate
reductase

GI upset, mucositis
*myelosuppression
*purine analogs may
cause hepatotoxicity,
but rare with
methotrexate at low
doses used

Bone marrow
depression,
megaloblastic anemia,
alopecia, for patients
with psoriasis, hepatic
damage is common

DRUGS USED IN
INFLAMMATORY
BOWEL DISEASE (IBD)
5-Aminosalicylates,
eg, mesalamine in
many formulations

Mild to moderately
severe Crohn's
disease and
ulcerative colitis

Ulcerative colitis,
rheumatoid arthritis

Mechanism
uncerain *may be
inhibtion of
eicosanoid
inflammatory
mediators

Sulfasalazine causes
sulfonamide toxicity
and may cause GI
upset,
myalgias,arthralgias,
myelosuppression
*other
aminosalicylates much
less toxic

Headache, nausea,
anorexia, vomitting,
gastric distress,
reduced sperm count

DRUGS USED TO
TREAT VARICEAL
HEMORRHAGE
Octreotide

Patients with
bleeding varices or
at high risk of repeat
bleeding

Inhibit intestinal
Somatostatin analog May alter portal
secretion and ixhibit
*mechanism not
blood flow and
dose related effect on certain
variceal pressure
bowel motility,Inhibit
pancreatic secretion in
patients with
pancreatic fistula

Reduced endocrine
and exocrine
pancreatic activity
*other endocrine
abnormalities *GI
upset

Steatorrhea, nausea,
abdominal pain,
flatulence

LAXATIVES
Magnesium
hydroxide, and other
non-absorbable salts
and sugars

Simple constipation;
bowel prep for
endoscopy
(especially PEG
solutions)

Symptomatic relief of
peptic ulcer and
stomach hyperacidity,
constipation

Osmotic agents
increase water
content of stool

Usually causes
evacuation within 4-6
h, sooner in large
doses

Magnesium may be
absorbed and caused
toxicity in renal
impairment

Diarrhea, bone loss in

patients with chronic
renal failure

PANCREATIC
SUPPLEMENTS
Pancrelipase

Pancreatic
insufficiency due to
cystic fibrosis,
pancreatitis,
pancreatectomy

Treat pancreatic
enzyme insufficiency

Replacement
enzymes from
animal pancreatic
extracts

Improves digestion of Taken with every meal Oropharyngeal

dietary fat, protein,
*may increase
mucositis, diarrhea,
and carbohydrates
incidence of gout
abdominal pain, renal
stones, colonic
strictures

Topical therapeutic
action *systemic
absorption may cause
toxicity

Trade
Name

Azulfidine,
Sulfasalazine

Milk of
Magnesia, Bulk
forming
laxatives:
Methylcellulose,
Pancreatin

Page 30 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Category: MOVEMENT DISORDER

ANTUMUSCARINIC
AGENTS
Benztropine

Parkinson's disease

Parkinson's disease,
drug-induced EPS

Antagonist at M
receptors in basal
ganglia

Reduces tremor and

rigidity * little effect
on bradykinesia

Oral * Toxicity: Typical

antimuscarinic effects:
sedation, mydriasis,
urinary retention, dry
mouth

Dry mouth, blurred

vision, dizziness,
nausea, nervousness,
skin rash, urinary
retention, dysuria,
tachycardia, muscle
weakness,
disorientation,
confusion

Cogentin,
Biperiden
(Akineton),
orphenadrine,
procycline,
trihexyphenidyl

COMT INHIBITORS
Entacapone

Parkinson's disease

adjunct to
levodopa/carbidopa

Inhibits COMT in
periphery *does
not enter CNS

Reduces metabolism
of levodopa and
prolongs its action

Oral
*Toxicity:increased
levodopa toxicity
*nausea, dyskinesias,
confusion

Dyskinesis, nausea,
diarrhea, urine
discoloration

Tolcapone
(Tasmar),
Entacapone
(Comtan)

DOPAMINE AGONISTS Parkinson's disease: Parkinson's disease

Pramipexole
Can be used as initial
therapy, also
effective in on-off
phenomenon

Direct agonist at D3
receptor, nonergot

Reduces symptoms of
Parkinsonism *
smooths out
fluctuations in
levodopa reponse

Oral *~8 h effect

*Toxicity: Nausea and
vomiting, postural
hypotension,
dyskinesias

Dizziness,
hallucination,
dyspepsia, syncope,
confusion, insomnia

Ropinirole
(Requip),
Bromocriptine
(Parlodel, Snap
Tabs),

DRUGS USED
HUNTINGTON'S
DISEASE
Tetrabenazine

Huntington's disease

Deplete cerebral
dopamine

Deplete amine
transmitters,
especially
dopamine, from
nerve endings

Reduce chorea
severity

Oral * Toxicity:
Hypertension,
sedation, depression,
diarrhea *
Tetrabenazine
somewhat less toxic

Hypotension,
depression, sedation,
diarrhea, nasal
congestion

Haloperidol

DRUGS USED IN
TOURETTE'S
SYNDROME
Haloperidol

Tourette's syndrome

Deplete cerebral
dopamine

Blocks central D2
receptors

Reduces vocal and

motor frequency,
severity

Oral * Toxicity:
Parkinsonism, other
dyskinesias * sedation

Hypotension,
depression, sedation,
diarrhea, nasal
congestion

Clonidine,
Phenothiazines,
Benzodiazepines,
Carbamazepine

Page 31 of 41

Drugs

Clinical
Application

Uses

Pharmacokinetics,
Toxicities,
Interactions

Mechanism
of Action

Effects

Transported into the

central nervous
system (CNS) and
converted to
dopamine (which
does not enter he
CNS); also converted
to dopamine in the
periphery

Ameliorates all
symptoms of
Parkinson's disease
and causes significant
peripheral
dopaminergic effects

Oral *6-8 h effect

*Toxicities:
Gastrointestinal upset,
arrhythmias,
dyskinesias, on-off and
wearing-off
phenomena,
behavioral
disturbances
*Interactions: Use
with carbidopa greatly
diminishes required
dosage *use with
COMT or MAO-B
inhibitors prolong
duration of effects

Anorexia, vomiting,
abdominal pain,
mental changes,
headaches, dizziness,
increased hand
tremor dystonic
movements

Levodopa+Carbid
opa (SINEMET),
Levodopa+Carbid
opa+
Entacapone
(STALEVO)

Increases dopamine
stores in neurons;
may have
neuroprotective
effects

Oral *Toxicity &

interactions: may
casue serotonin
syndrome with
meperidine, and
theoretically also with
selective serotonin
reuptake inhibitors,
tricyclic anti
depressants

Nausea, dizziness

Selegiline
(Eldepryl)

LEVODOPA AND
COMBINATIONS
Levodopa

Parkinson's disease:
Most efficacious
therapy but not
always used as the
first drug due to
development of
disabling response
fluctuations over
time

Parkinson's disease

MONOAMINE
OXIDASE (MAO)
INHIBITORS
Rasagiline

Pakinson's disease;
adjunctive to
levodopa; smooths
levodopa response

Agonist for
Inhibits MAO-B
levodopa/carbidopa in selectively, higher
parkinson's disease
doses also inhibits
MAO-A

Adverse
Reaction

Trade
Name

Category: OPIOID
ANTITUSSIVE

Severe pain, adjunct Moderate to severe

in anesthesia
pain, antitussive,
(fentanyl, morphine), anesthetic adjunct
Pulmonary edema
(morphine only),
maintenance in
rehabilitation
programs
(methadone only)

Poorly understood
Reduces cough reflex
but strong and
partial and agonist
are also effective

30-60 mins. Duration * Respiratory

Toxicity: Minimal
depression, skeletal
when taken as directed muscle rigidity,
constipation, nausea,
vomiting,
lightheadedness,

Roxanol,
Dolophine,
Sublimaze,
Dilaudid,
Numorphan,
Demerol,
Sufenta,
Alfentha, Ultiva

Page 32 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

MIXED OPIOID
AGONISTANTAGONISTS
Buprenorphine

Moderate pain *
Some maintenance
rehabilitation
programs

Moderate to severe
pain, chronic pain,
treatment of opioid
dependence

Partial agonist *
antagonist

Like strong agonist

but can antagonize
their effects * also
reduces craving for
alcohol

Long duration of
action 4-8 h * May
precipitate abstinence
syndrome

light headedness,
sedation, dizziness,
respiratory
depression, nausea,
vomiting

Buprenex,
Suboxone,
Subutex

MIXED OPIOID
AGONISTANTAGONISTS
Nalbuphine

Moderate pain

Moderate to severe
pain, anesthetic
adjunct

agonist *
antagonist

Like strong agonist

but can antagonize
their effects * also
reduces craving for
alcohol

Long duration of
action 4-8 h * May
precipitate abstinence
syndrome

lightheadedness,
sedation, dizziness,
respiratory
depression,nausea,
vomiting,

Nubain

OPIOID ANTAGONIST

Opioid overdose

Moderate to severe
pain, anesthetic
adjunct

Antagonist at ,
and receptors

Rapidly antagonizes
all opioid effects

Duration 1-2 h (may

have to be repeated
when treating
overdose) * Toxicity:
Precipitates
abstinence syndrome
in dependent users

light headedness,
sedation, dizziness,
respiratory
depression, nausea,
vomiting

Naloxone,
naltroxone,
nalmefene,
alvimopan,
methylnatrexone
bromine

OTHERS ANALGESIC
USED IN MODERATE
PAIN

Moderate pain,
adjunct to opioid in
chronic pain
syndrome

Moderate to severe
pain, anesthetic
adjunct

Mixed effects: weak Analgesia

agonist, moderate
SERT inhibitor, weak
NET inhibitor

Duration: 4-6 h
Toxicity: seizures

Sedation, sweating,
headache, dizziness,
lethargy, confusion

Ultram,
Tramadol

PARTIAL AGONIST

Mild moderate pain

* cough (codeine)

Moderate to severe
pain, antitussive,
anesthetic adjunct

Less efficacious than Like strong agonist *

morphine * can
weaker effects
antagonize strong
agonists

Like strong agonists,

toxicity dependent on
genetic variation of
metabolism

Sedation, sweating,
headache, dizziness,
lethargy, confusion

STRONG OPIOID
AGONIST

Severe pain *adjunct

in anesthesia
(fentanyl, morphine)
*Pulmonary edema
(morphine only)
*maintenance in
rehabilitation
programs
(methadone only)

Anesthetic adjunct,
moderate to severe
pain, preoperative
sedation, obstetric
analgesia

Strong -receptor
agonists *variable
affinity for and
receptors

First-pass effect
*duration 1-4 h except
methadone, 4-6 h
*Toxicity:Respiratory
depression *severe
constipation
*addiction liability
*convulsion

Respiratory
depression, skeletal
muscle rigidity,
constipation, nausea,
vomiting,
lightheadedness,

Analgesia *relief of
anxiety *sedation
*slowed
gastrointestinal transit

Roxanol,
Dolophine,
Sublimaze,
Dilaudid,
Numorphan,
Demerol,
Sufenta,
Alfentha, Ultiva

Page 33 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Category: SKELETAL MUSCLE RELAXANT

CENTRALLY ACTING
SPASMOLYTIC DRUG
Tizanidine

Spasm due to
nultiple sclerosis,
stroke, amyotrophic
lateral sclerosis

Spasticity due to
spinal cord injury

2-Adrenoceptor
agonist in the spinal
cord

Presynaptic and
postsynaptic
inhibition of reflex
motor output

CENTRALLY ACTING
SPASMOLYTIC
DRUGS Baclofen

severe spasticity due

to cerebral palsy,
multiple sclerosis,
stroke

Spasticity due to
multiple sclerosis,
spinal cord injuries
(intrathecal
administration)

GABA agonist,
facilitates spinal
inhibition of motor
neurons

Pre- and postsynaptic Oral, intrathecal

inhibition of motor
*Toxicities: Sedation,
output
weakness,

CENTRALLY ACTING
Acute spasm due to
SPASMOLYTIC DRUGS muscle injury
Cyclobenzaprine
*inflammation

Relief of discomfort
due to acute, painful
musculoskeletal
conditions

Poorly understood
inhibition of muscle
stretch reflex in
spinal cord

CENTRALLY ACTING
Chronic spasm due
SPASMOLYTIC DRUGS to cerebral palsy,
Diazepam
stroke, spinal cord
injury *acute spasm
due to muscle injury

Relief of skeletal
muscle spasm,
spasticity due to
cerebral palsy,
epilepsy, paraplegia,
anxiety

DEPOLARIZING
NEUROMUSCULAR
BLOCKING AGENT
Succinylcholine

Placement of
Prototypical
tracheal tube at the depolarizing blocking
start of anesthetic
drug
procedure* Rarely
control of muscle
contractions in status
epilepticus

Renal and hepatic

Somnolence, fatigue, Zanaflex
elimination *Duration dizziness, dry mouth,
~3-6 h
urinary tract infections
*toxicities:Weakness,
sedation *hypotension
Drowsiness, dizziness,
tachycardia, nausea,
vomiting

Lioresal

Reduction in
hyperactive muscle
reflexes *
antimuscarinic effects

Hepatic metabolism
Drowsiness, dizziness,
*duration ~4-6 h
dry mouth, nausea,
*strong antimuscarinic constipation
effects

Flexeril

Facilitates
GABAergic
transmission in
central nervous
system

Increases interneuron
inhibition of primary
motor afferents in
spinal cord *Central
sedation

Hepatic metabolism
*Duration ~12-24 h
*toxicities: Strong
antimuscarinic effects

Drowsiness, sedation, Valium

sleepiness, lethargy,
constipation, diarrhea,
bradycardia,
tachycardia, rash

Agonist at nicotinic
acetylcholine (Ach)
receptors especially
at the
neuromuscular
junctions *
depolarizes * may
stimulate ganglionic
nicotinic Ach and
cardiac muscarinic
Ach receptors

Initial depolarization
causes transient
contractions,
followed by prolong
flaccid paralysis *
depolarization is then
followed by
repolarization that is
also accompanied by
paralysis

Rapid metabolism by
plasma
cholinesterase*
normal duration ~
5min * Toxicities:
Arrhythmias *
Hyperkalemia *
Transient increase
intraabdominal,
intraocular pressure *
postoperative muscle
pain

Can cause cardiac

arrhythmia when
administered during
halothane anesthesia,
may cause
bradycardia when
second dose is given
less than 5 minutes
after the initial dose

Anectine

Page 34 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

DIRECT-ACTING
MUSCLE RELAXANTS
Dantrolene

IV: Malignant
hyperthermia *Oral:
Spasm due to
cerebral palsy, spinal
cord injury, multiple
sclerosis

Spasticity due to
spinal cord injury,
stroke, cerebral palsy,
multiple sclerosis

Blocks RyR1 Ca2+release channels in

the sarcoplasmic
reticulum of skeletal
muscle

Reduces actin-myosin IV, oral *Duration 4-6

interaction *weakens h *Toxicities: Muscle
skeletal muscle
weakness
contraction

Drowsiness, diizziness, Dantrium

weakness,
constipation,
tachycardia, malaise

NON DEPOLARIZING
NEUROMUSCULAR
BLOCKING AGENT :
d-Tubocurarine

Prolongs relaxation
for surgical
procedures *
superseded by
newer non
depolarizing agents

Non depolarizing drug

Competitive
antagonist at nACh
as receptor,
especially at the
neuromuscular
junction

Prevents
depolarization by
ACh, causes flaccid
paralysis * can cause
histamine release
with hypotension *
weak block of
cardiacmuscarinic
ACh receptor

NON DEPOLARIZING
NEUROMUSCULAR
BLOCKING AGENT :
Rocuronium

Like cisatracurium *
Useful in patients
with renal
impairment

Neromuscular
blocking drug

Similar to
Cisatracurium

Like cisatracurium
Hepatic metabolism * Minimal, if any
but slight
Duration ~ 20-35 mins. cardiovascular effect
antimuscarinic effects Toxicities: Like
Cisatracurium

Zemuron

NON DEPOLARIZING
NEUROMUSCULAR
BLOCKING AGENT:
Cisatracurium

Prolongs relaxation
for surgical
procedures *
relaxation of
respiratory muscles
to facilitate
mechanical
ventilation in
intensive care unit

Neuromuscular
blocking drug

Similar to
tubocurarine

Light tubocurarine
but lacks histamine
release and
antimuscarinic effects

Non dependent on
renal or hepatic
function * Duration ~
25-45 mins. *
Toxicities: Prolonged
apnea but less toxic
than atracurium

Nimbex

Tamsulosin is
slightly selective for
1A

1A Blockade may
relax prostatic
smooth muscles
more than vascular
smooth muscles

Orthostatic
hypotension may be
less common with this
subtype

Renal excretion *
Initially cause muscle
Duration ~ 40-60 mins. weakness, hypotension
* Toxicities: Histamine
release * Hypotension
* Prolonged apnea

Minimal, if any
cardiovascular effect

Category: SYMPATHETIC
ALPHAADRENORECEPTOR
ANTAGONIST
TAMSULOSIN

Benign prostatic
hyperplasia

Page 35 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

ALPHAADRENORECEPTOR
ANTAGONIST

Hypertension *
Benign prostatic
hyperplasia

Blocks 1 but not 2 Lower BP

Larger depressor
effect with first dose
may cause orthostatic
hypotension

ALPHAADRENORECEPTOR
ANTAGONIST

Male erectile
dysfunction *
Hypotension

Blocks 2 * elicits
increased central
sympathetic activity
* Increase
norepinephrine
release

Raises BP and HR

May cause anxiety *

excess pressor effect if
norepinephrine
transporter is blocked

> 1 block

Lowers BP with
limited HR increase

Oral, parentheral *
Toxicity: Less
tachycardia than other
1 agents

Irreversibly block 1 lowers blood

and 2 * indirect
pressure (BP) * But
baroreflex activation heart rate (HR) rises
due to baroreflex
activation

Irreversible blocker *
half-life > than 1 day *
Toxicity: Orthostatic
hypotension *
Tachycardial *
Myocardial ischemia

1 > 2

Intravenous used *
Half-life ~ 10 mins.

Parentheral only *
Dizziness, headache,
Toxicity: Bradycardia * hypotension, nausea,
hypotension
cold, extremities,
bradycardia, urinary
retention,
proarrythmic effect

Blocks 2 > 1
receptors

Increases peripheral
resistance

Toxicity: Asthma
provocation

> 1 block

Long half-life

Oral * Toxicity: fatigue Bradycardia,

hypotension, cardiac
insufficiency, fatigue,
dizziness, diarrhea

YOHIMBINE
ALPHAADRENORECEPTOR
ANTAGONIST:
LABETALOL

Hypertension

Hypertension

ALPHAPheochromoADRENORECEPTOR
cytoma * high
ANTAGONIST:
catecholamine states
PHENOXYBENZAMINE

BETAADRENORECEPTOR
ANTAGONIST
ESMOLOL

Rapid control of BP
and arrhythmias,
thyrotoxicosis and
myocardial ischemia
intraoperatively

BETAADRENORECEPTOR

No clinical indication

BETAADRENORECEPTOR
ANTAGONIST
CARVEDILOL

Heart failure

Rapid, short term

treatment of
ventricular in
supraventricular
arrhythmia, sinus,
tachycardia

Hypertension, CHF,
left ventricular
dysfunction

Trade
Name
Doxazosin,
Terazosin

Fatigue, drowsiness,
insomnia,
hypotension,
impotence, diarrhea

Trandate

Brevibloc

Coreg,
Medroxalol,
Bucindolol

Page 36 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

BETAADRENORECEPTOR
ANTAGONIST
PINDOLOL

Hypertension,
Arrhythmias,
Migraine * May
avoid worsening of
bradycardia

Hypertension

1,2 with intrinsic

sympathomimetic
(partial agonist)
effects

Lowers BP *
Modestly lower HR

Oral * Toxicity: fatigue Bradycardia, dizziness, Acebutolol,

* vivid dreams * cold
hypotension, nausea, Carteolol,
hands
vomiting, diarrhea
Bopindol,
Penbutolol,
Oxprenolol,Viske

BETAADRENORECEPTOR
ANTAGONIST:
METOPROLOL

Angina pectoris *
Hypertension *
Arrhythmias

Hypertension, angina,
MI, CHF

Blocks 1 > 2
receptors

Lower HR and
BP
* Reduce
renin may safer than
asthma

Oral, 100-450 mg/d,

extended release
products are given
once daily

Bradycardia * fatigue
* vivid dreams * cold
hands

BETAADRENORECEPTOR
ANTAGONIST:
PROPRANOLOL

Hypertension *
Angina pectoris *
arrhythmias *
migraine,
hyperthyroidism

Cardiac arrhythmias,
angina pectoris,
hypertension,
essential tremor,
myocardial infarction,
migraine headache,
pheochromocytoma

Blocks 1 and 2
receptors

Lower HR and
BP
* Reduce
renin

Oral, parentheral *
Toxicity: bradycardia *
worsened asthma *
fatigue * vivid dreams
* cold hands

Dizziness, vertigo,
Inderal, inderal
fatigue, bradycardia,
LA, Nadolol,
CHF, arrhythmia,
timolol
tachycardia, sinoatrial
or atrioventricular
block,gastric pain,
flatulence,
constipation, diarrhea,
nausea, vomiting,
impotence, decreased
libido, decreased
exercise tolerance,
rash, eye irritation

TYROSINE
HYDROXYLASE
INHIBITOR

Pheochromocytoma

Blocks tyrosine
hydroxylase *
reduces synthesis of
dopamine,
norepinephrine and
epinephrine

Lowers BP * in the
central nervous
system may elicit
extrapyramidal
effects due to low
dopamine

Extrapyramidal
symptoms *
Orthostatic
hypotension *
Crystalluria

Metyrosine

Vascular smooth
muscle relaxation

Requires dose titration Headache, flushing,

to desired effect
reflex tachycardia

Fenoldopam

Atenolol,
alprenolol,
betaxolol,
nebivolol,

Category: SYMPATHOMIMETIC
DOPAMINE D1
AGONISTS

Hypertension

Peripheral arteriolar
Activates adenylyl
dilator for
cyclase
hypertensive
emergencies and post
operative hypertension

Page 37 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

DOPAMINE D2
AGONISTS

Parkinson's Disease,
Prolactinemia

for patients with

hyperprolactinemia to
suppress prolactin
release

Inhibits adenylyl
cyclase and
interacts with other
intracellular
pathways

Restores dopamine
actions in the central
nervous system

Oral * Toxicity:
Nausea, head ache,
hypotension,
orthostatic
hypotension

Nausea, headache,
light headedness,
fatigue

Bromocriptine

1 AGONIST

Orthostatic
hypotension

Orthostatic
hypotension, only
when patient is
considerably impaired

Activates
phospholipase C,
resulting in
increased
intracellular calcium
and vasoconstriction

Vascular smooth
muscle contraction
increasing blood
pressure (BP)

Oral *Prodrug
converted to active
drug with a 1-h peak
effect *Toxicity:
Produces supine
hypertension,
piloerection
(goosebumps), and
urinary retention

Nasal burning,
stinging, dryness,
rebound nasal
congestion

Pro Amantine,
Midodrine,
Phenylephrine

2 AGONIST

Hypertension

Hypertension, severe
pain in patients with
cancer

Inhibits adenylyl
cyclase and
interacts with other
intracellular
pathways

Vasoconstriction is
masked by central
sympatholytic effects,
which lowers (BP)

Oral *transdermal
*peak effect 1-3 h
*half-life of oral
drug~12 h *produces
dry mouth and
sedation

Drowsiness, dizziness,
sedatioin, dry mouth,
constipation, dreams,
rash, syncope

Clonidine, methyldopa,
guanfacine,
guanabenz,
Dexmedetomidin
e, tizanidine,

1 AGONIST

Cardiogenic shock,
acute heart failure

Cardiac
decompensation due
to depressed
contractility caused by
organic heart disease
or cardiac surgical
procedures

Activates adenylyl
cyclase, increase in
myocardial
contractility

Positive inotropic
effects

IV * requires dose
titration to desired
effect

Headache, nausea,
increased heart rate,
increase in systolic
blood pressure,
palpitations, anginal
and non specific chest
pain

Dobutamine

2 AGONIST

Asthma

Bronchospasm,
prevention of EIB

Activates adenylyl
cyclase

Bronchial smooth
muscle dilation

Inhalation * Duration:
4-6 h * Toxicity:
Tremor and
tachycardia

Palpitation,
tachycardia,
hypertension, tremor,
shakiness, dizziness,
nervousness, nausea,
vomiting

Albuterol

Page 38 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action

Effects

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Category: VASOACTIVE PEPTIDES

ANGIOTENSIN
RECEPTORS
ANTAGONISTS
Valsartan

Hypertension

Hypertension, CHF

CALCITONIN GENREALTED PEPTIDE

ANTAGONISTS
BIBN4096BS

Migraine

CONVERTING
ENZYME INHIBITORS
Enalapril

Hypertension *Heart
failure

Hypertension, CHF,
asympptomatic LVD

ENDOTHELIN
ANTAGONISTS
Bosentan

Pulmonary arterial
hypertension

NATRIURETIC
PEPTIDES
Nesiritide

heart failure

NEUROPEPTIDE
ANTAGONISTS
BIBP3226

None identified

NEUROTENSIN
AGONISTS PD149163

Potential treatment
of schizophrenia and
parkinson's disease

Selective
competitive
antagonist of
angiotensin AT1
receptors

Arteriolar dilation
Oral
*decreased
aldosterone secretion
*Increased sodium
and water excretion

Headache, dizziness,
diarrhea, abdominal
pain, nausea, URI
symptoms, cough

Eprosartan,
Irbesartan,
Candesartan,
Olmesartan,
telmisartan

Antagonist of
calcitonin generelated peptide

Blocks some central

and peripheral
(vasodilators) actions
of CGRP

Inhibits conversion
of angiotensin I to
angiotensin II

Arteriolar dilation
Oral as single dose or
*decreased
in 2 divided doses
aldosterone secretion
*Increased sodium
and water excretion

Headache, dizziness,
fatigue, nausea,
diarrhea, decreased
hematocrit and
hemoglobin, cough

Vasotec,
Eprosartan,
Irbesartan,
Candesartan,
Olmesartan,

Non selective receptor Nonselective

blocker
antagonist of
endothelin ETA and
ETB receptors

Vasodilation and
decrease arterial
pressure in humans

Intra-arterial
administration causes
slow onset of forearm
vasodilation

systemic hypotension Sitaxsentan,

facial flushing, edema, Ambrisentan
headaches

in patients with severe Agonist of

heart failure
natriuretic peptide
receptors

*Increased sodium
and water excretion
*vasodilation

IV infusion

Fatal renal damage

Selective antagonist
of neuropeptide Y1
receptors
Schizophrenia,
Agonist of central
parkinson's disease,
neurotensin
smoking cessation and receptors
weight loss

Blocks
vasoconstrictor
response to
neurotensin
interacts with central
dopamine systems

can cross the blood

brain barrier

Page 39 of 41

Drugs

Clinical
Application

NEUROTENSIN
ANTAGONISTS
Meclinertant

None identified

RENIN INHIBITORS
Aliskiren

Hypertension

RENIN INHIBITORS
Aliskiren

Uses

Mechanism
of Action

Effects

Antagonist of
central and
peripheral
neurotensin
receptors

Blocks some central

and peripheral
(vasodilators) actions
of neurotensin

Inhibits catalytic
activity of renin

Arteriolar dilation
*decreased
aldosterone secretion
*Increased sodium
and water excretion,
suppress plasma
renin activity and
reduction in blood
pressure

Potential use for

inflammatory pain
and inflammation

Selective antagonist
of kinin B2
receptors

Blocks effects of
kinins on pain,
hyperalgesia, and
inflammation

SUBSTANCE P
ANTAGONISTS
Aprepitant

Prevention of
chemotherphyinduced nausea and
vomiting

Selective antagonist
of tachykinin NK1
receptors

Blocks several central

nervous system
efffects of Substance
P

UROTENSIN
ANTAGONISTS
Palosuran

Diabetic renal failure

Peptide antagonist
of urotensin
receptors

Blocks potent
vasoconstrictor
response of
endothelin

VASOACTIVE
INTESTINAL PEPTIDE
AGONISTS

Type2 diabetes
*chronic obstructive
pulmonary disease

Selective and
nonselective
agonists of VPAC1
AND VPAC2
receptors

Vasodilation
*multiple metabolic,
endocrine, and other
effects

Hypertension

Therapeutic agent for

cardiovascular,
pulmonary,
gastrointestinal,
nervous system
diseases

Pharmacokinetics,
Toxicities,
Interactions

Adverse
Reaction

Trade
Name

Dose related
reduction in blood
pressure similar to
that of ACE inhibitors,
safety and tolerability
are comparable to
angiotensin antagonist
and placebo

poor oral availability,

rapid metabolism

Hypotension

Page 40 of 41

Drugs

Clinical
Application

Uses

Mechanism
of Action
Decreases
metabolism of
natriuretic peptides
and formation of
angiotensin II

Effects

Pharmacokinetics,
Toxicities,
Interactions

Trade
Name

VASOPEPTIDASE
INHIBITORS
Omapatrilat

Hypertension *heart
failure

Vasopeptidase
inhibitor, lowers blood
pressure
inhypertensive
patients and improves
cardiac function in
patients with heart
failure

VASOPRESSIN
AGONISTS
Arginine vasopressin

Vasodilatory shock

Antioxytoxic activity
Agonist of
but does not
vasopressin V1 and
antagonize the
V2 receptors
antidiuretic action of
vasopressin, Arg
vasopressin is used in
sytemic
vasoconstriction and
decreases pulmonary
hypertension.
Terlipressin is used for
fluid catecholamine
refractory septic
shock, V1 rceptor
agonist

Vasoconstriction

More selective for V1

receptor and has
longer half life

under study

Terlipressin

VASOPRESSIN
ANTAGONISTS
Conivaptan

Potential use in
hypertension and
heart failure
*hyponatremia

Dual antagonist of
arginine vasopressin

Vasoconstriction

non linear
pharmacokinetics
following intravenous
infusion and oral
adminstration, inter
action with CYP A34

safe if IV route, under

study

Relcovaptan

Antagonist of
vasopressin V1 and
V2 receptors

Vasodilation
*increased sodium
and water excretion

Adverse
Reaction
Angioedema, cough
and dizziness

Page 41 of 41