Pharmacology Review Sheets: Neuro Drugs, p.

1
Antidepressants
General comments:
- All drugs involve phosphorylation in their mechanism of action (resulting in changes in release, cytoskeleton, gene expression) thus
clinical improvement may take several weeks
- All drugs have immediate pharmacological actions
Class

Drugs in that Class Mechs of Action/Effects

Pharmacokinetics/Uses
Adverse
Effects/Toxicities/Drug Interactions
Tricyclic
Tertiary amines:
Block norepinephrine uptake
Distribution: Large Vd (15-20L/kg)
Adverse effects:
antidepressants
- Imipramine
Antimuscarinic (see side effects)
- Highly protein-bound
Dry
mouth, blurred vision, urinary retention, constipation
(TCAs)
- Amitryptiline
Antihistaminergic (see side effects) Duration of action: Long t
Sedation
Secondary amines:
-adrenergic blocker (see side-effects)
- Imipramine (3 amine): 12 hrs
Orthostatic
hypotension
- Desimipramine
Sedation (amitryptiline has the most)
- Nortryptiline (2 amine): 31 hrs
Weight
gain
- Nortryptiline
- Effect from antimusc. and antihist.
Metabolism: Many active metabolites, also w/long t
Excessive sweating
Note: Do not elevate mood
Uses:
Sexual dysfunction
- Depression
Acute toxicity: Can lead to death; give
small prescriptions!
- Panic disorder
Cardiac conduction defects: m/c
cause of death from this
- Enuresis (bedwetting)
Coma with shock, metabolic
acidosis (can also cause death)
- Chronic pain (mechanism unknown)
Respiratory depression
(can also cause death)
Agitation/delirium
Neuromuscular irritability/seizures
Hyperpyrexia/hypothermia
Bowel and bladder paralysizs
Drug Interactions:

 Additive with alcohol and other

sedatives

Antagonizes guanethidine (uptake

blockade)
Reversal of methyldopa, clonidine
activity

Phenytoin, aspirin, etc. can displace

TCAs from binding sites

Antipsychotics, methylphenidate,
steroids inhibit metabolism
Serotonin-selective Fluoxetine (Prozac)
effects:
reuptake inhibitors Sertraline
Nausea, anorexia, imsomnia
(SSRIs)
dysfunction

Selectively block reuptake of 5-HT Distribution: Vd >> that of the TCAs

- Results in 5-HT release, but 5-HT
output overall

Adverse

- Fluoxetine 35 L/kg; sertraline 76 L/kg

- Highly protein bound

- Fluoxetine 94%; sertraline 99%
Duration of action: Long t

Sexual
Weight loss
Seizures (fluoxetine only) due

to seizure threshold
- Fluoxetine 76 hrs; sertraline 23 hrs
Acute toxicity: < than TCAs
or MAOIs
Uses:
Drug Interactions:
- Depression
MAOIs: Serotonin syndrome tremor, hyperthermia,
- Obsessive-compulsive disorder (OCD)

CV collapse.

- Panic disorder (more often than TCAs)

- Wait 2 wks after

(Obviously) life-threatening
MAOI use before starting SSRIs
- Bulemia
Fluoxetine inhibits cytP-450 (CYP2D6)
- Not used for enuresis or pain
Inhibits dopamine and norepinephrine
Duration: t = 11-14 hrs

Atypical
Bupropion
Adverse effects:
antidepressants
(Welbutrin, Zyban)
reuptake (better at blocking dopamine)
Reduces nicotine craving
toxicities (not antimuscarinic)
Not antimuscarinic or sedating

Seizures
NO hypotension/cardiac
Drug Interactions:

Nefazodone
Blocks serotonin reuptake (5HT2A and
mild orthostatic hypotension, impotence
5HT2C receptors)
Mirtazapine
2-adrenergic antagonist
Duration: t= 20-40 hrs
mild orthostatic hypotension

Carbamazepine metabolism
Adverse effects: sedation,

Adverse effects: Sedation,

Pharmacology Review Sheets: Neuro Drugs, p.2

Antidepressants, continued
Class

Drugs in that Class Mechs of Action/Effects/Uses

Pharmacokinetics/Uses
Effects/Toxicities/Drug Interactions
Monoamine oxidase Hydrazines:
Inhibits monoamine oxidase (MAO)
(Not discussed)
effects: Seen before benefits; severely limits use
inhibitors (MAOIs) - Phenelzine
- MAO-A has preference for serotonin
hypersensitivity (aged cheese, Chianti wine,
- Iproniazid
and is located peripherally
results in acute severe HTN,
Proparylamines:
- MAO-B has perference of dopamine
agitation.
- Pargyline (suicide inhibitor)
and is located in the CNS
hypotension
- Selegiline (MAO-B select.)
- Result: in 5-HT, NE, DA in
effects (dry mouth, blurred vision, etc.)
Cyclopropylamines:
CNS and periphery
convulsions due to excess CNS stimulation
- Tranylcypromine (suicide)
Except for meclobemide and selegiline,
(contraindicated in epileptics)
Reversible inhibitors:
MAOIs are irreversible and nonselective
(hydrazine): 1:10,000
- Meclobemide (MAO-A sel.)
for MAO-A and MAO-B

Adverse
Adverse
Tyramine
pickled herring, sardines)
headache,
Orthostatic
Atropine-like
Tremors, insomnia,

Hepatotoxicity
Drug Interactions:

 Elevate mood

OTC nasal drugs too.

Lithium
Lithium
Adverse effects:

Interferes with monoaminergic

transmitter release

diarrhea

Serotonin syndrome with SSRIs

Meperidine (Demerol) MAOIs
potentiate depressant effects
of all narcotics and may result in death!
Duration: t = 20 hrs

Excretion: Renal

Decreases IP3 formation by blocking

Nausea, vomiting,

Note: Narrow therapeutic window (0.5-1.25 mEq/L)

Tremor (especially in hands)

recycling of IP (inhibits myoinositol
Uses:
Renal: Polyuria from
+
inhibition of ADH action; Na retention
phosphatase). Important acute effect.
Drug of choice for the manic phase of bipolar
due to
increased aldosterone secretion. Pt. feels bone dry
Replaces Na+ in action potentials
disorder
Thyroid enlargement;
intereference with iodination of tyrosine
Edema
Acute toxicity: Confusion, convulsions,
arrhythmias
Drug interactions: Diuretics plasma
concentration
Alcohol
Blood alcohol concentration Effects
10 mg% (0.010%)
Subtle differences in visual acuity
50 mg% (0.050%)
Motor/mental impairment
100-150 mg% (0.1%-0.15%) Legal standard for prima facie intoxication (Breathalyzer)
200 mg% (0.2%)
Mild/moderate intoxication
300 mg% (0.3%)
Marked intoxication (> 300 mg% = medical and legal definition of drunk)
400 mg% (0.4%)
Deaths can occur here (due to respiratory depression)
500 mg% (0.5%)
Lethal dose for most individuals
Pharamacodynamics of alcohol
Fetal Alcohol Syndrome
CNS: Depressant (slows EEG), slows heart rate, mild analgesic. Respiratory/vasomotor depression at > 400 mg% Miscarriage, stillbirth
CV: Vasodilation
Low birth weight, slow postnatal growth

 GI: Gastric acid release

Renal: Diuresis (due to ADH)

Birth defects: Microcephaly, mental retardation, etc.

Pharmacokinetics of alcohol
Absorption/Distribution: Lipid soluble; absorbed through oral/GI mucosa and widely distributed
Metabolism

Excretion

Primary pathway: Alcohol dehydrogenase/aldehyde dehydrogenase (elimination by zero-order kinetics)

Zero-order kinetics the average
person eliminates 0.018%/hr
Secondary pathway: Mixed ethanol oxidizing system (MEOS). Stimulatable!
Widmarks equation (for calculating BAC)
Note: MEOS is responsible for metabolizing other drugs.
= (Amt EtOH ingested in oz /body weight in oz) (100/r),
where r = 0.55 (female), 0.68 (male) on average
- When a person has recently drank drugs metabolize more slowly
- 10-12 hrs after drinking, drugs will metabolize faster

Pharmacology Review Sheets: Neuro Drugs, p.3

Psychomotor Stimulants
Biogenic amine actions in the CNS
Dopamine: Involved with reward systems (frontal cortex, mesolimbic regions), motor systems, attention span (orbitofrontal cortex)
Norepinephrine: Sympathetic activation in the hypothalamus, euphoria (frontal cortex)
Serotonin: Sleep-wake cycles, appetite (hypothalamus), behavior, euphoria (frontal cortex)
Class

Drugs in that Class Mechs of Action/Effects/Uses

Pharmacokinetics
Adverse
Effects/Toxicities/Drug Interactions
Nicotine
Mechanism: Stimulates nicotinic ACh
Absorption: Well-absorbed (oral mucosa, GI tract)
Highly addictive
receptor
Distribution: Lipid-soluble; gets in breast milk, lungs
Cigarette
smoke adds health hazards
Effects:
Metabolism: Liver, lung
Irritability, tremors

 Cortical activation: Arousal, euphoria, Excretion: Renal

anxiety, nervousness, lethargy, fatigue, etc.
relaxation; improves attention
Methylxanthines
Caffeine
Mechanism: Blocks adenosine receptors
(phosphodiesterase, PDE, at higher doses)
Theophylline

Mechanism: Blocks adenosine receptors

Absorption: Well absorbed

Withdrawal

Narrow therapeutic

window
(phosphodiesterase, PDE, at higher doses) Distribution: Tissues, crosses placenta
CNS:
Seizures, insomnia, motor impairment, tremors
Metabolism: Liver
Cardiac arrhythmias
Theobromine

Mechanism: Blocks adenosine receptors

(phosphodiesterase, PDE, at higher doses)

Amphetamines
Dextramphetamine
Mechanism: DA in synaptic cleft Admin/Absorption: Oral; well-absorbed in GI

Highly addictive/abused; amphetamine psychosis w/chronic use

Competitively inhibits DA/NE transp. Metabolism: Liver
Tolerance with
chronic use
Ca2+-independent release of NE Excretion: Renal
Drug interactions: MAO
inhibitors, drugs affecting DA/NE
Competitive inhibition of MAO Duration of action: t (Ritalin) < t (Cylert)
Methylphenidate (Ritalin) Mechanism: DA in synaptic cleft Admin/Absorption: Oral; well-absorbed in GI
appetite

Pemoline (Cylert )
Competitively inhibits DA/NE transp. Metabolism: Liver
Insomnia
2+
Ca -independent release of NE Excretion: Renal
GI upset
Competitive inhibition of MAO Duration of action: t (Ritalin) < t (Cylert)
Headaches
Uses: Ritalin/Cylert: ADHD
Drug interactions: MAO
inhibitors, drugs affecting DA/NE
Cocaine
Action: Blocks Na+-activated ATPase, and
Potentiates
adrenergic agonists
thus reuptake of NE into the adrenergic
Tonic-clonic seizures (high
doses)
nerve terminal; NE stays around longer,
Cardiac arrhythmias
causing sympathetic stimulation
Respiratory depression (high
doses)

 If taken with alcohol metabolites

Effects:
conjugate to form

Anorexiants
pressure

Sibutramine

CNS: Stimulation; body temp. by

psychoactive compound with a long
effects on hypothalamus (pyrogenic)
Local anesthetic: best available in terms
of absorption through membranes and
numbing effects. Not used clinically!
Cardiovascular: Vasoconstriction
Action: Blocks 5HT and NE reuptake
Absorption: GI

cocaethylene, a very toxic

t .

Increased blood

Use: Obesity (recently approved by FDA) Distribution: Placenta (but minimal)

Headaches
Metabolism: Liver
Insomnia
Excretion: Renal
Constipation
Dry mouth
Contraindicated with anorexia, MAO
inhibitors, CV/renal
disease, pregnancy, lactation
Dexfenfluramine
Fenfluramine
Phentermine
inhibition of 5-HT clearance

Action: Releases 5-HT & inhibits reuptake

Action: Releases 5-HT & inhibits reuptake
Action: Inhibits NE reuptake
Inhibits 5-HT clearance in lung

Fen/Phen (now illegal) because of

in lung

Pharmacology Review Sheets: Neuro Drugs, p.4

Antipsychotic Drugs (Neuroleptics)
General Characteristics/Effects
Reduces hallucinations, delusions, fear/panic, aggressive behavior
Produces an indifference to surroundings w/out stupor or ataxia
Takes time for drug to work (weeks); treatment is palliative, not curative
Typical neuroleptics treat mainly positive symptoms (delusions, hallucinations); atypical neuroleptics can help with negative symptoms (emotional
bluting, cognitive deficits) which affect the patients function

Clinical Uses
Schizophrenia
Tourettes syndrome (tics, curses)
Acute psychotic disorders
Anesthetic adjunct
Drug (amphetamine, LSD)-induced psychoses
Antiemetic
of choice!)

Antipruritic
Intractable hiccups
Initial Rx for bipolar disorder (remember, lithium is drug

Pharmacokinetics
Absorption/Distribution: Lipid soluble; well-absorbed in GI tract. Distributes to CNS; large volume of distribution
Metabolism: Extensive 1st pass metabolism, to active metabolites!
Class

Drugs in that Class Mechanism of action

Drug-specific Adverse Effects

Typical neuroleptics Chlorpromazine (Thorazine) Low D2 blockade

1-receptor blockade: postural hypotension, impotence,
failure to ejaculate (> than haloperidol)
High 1, H1, M1 blockade
Muscarinic receptor blockade: dry mouth, constipation, urinary
retention, visual problems (> than haloperidol)
Histaminic receptor blockade: Sedation, weight gain (> than haloperidol)
DA prolactin gynecomastia, infertility, galactorrhea-amenorrhea
syndrome
Extrapyramidal side-effects (< than haloperidol)
Cardiac arrhythmias

Haloperidol (Haldol )
High D2 blockade
Extrapyramidal side-effects (> than chlorpromazine)
Low 1, H1, M1 blockade
- Dystonias spastic reactions (1 week)
- Akathesias (restlessness) (3 weeks)
- Parkinson-like symptoms (tremors, rigidity, etc).(1-2 months)
- Tardive dyskinesia (irreversible!) (12-16 months)
Neuroleptic malignant syndrome: severe musuclar rigidity, body temp,
impaired sweating. Seen more in patients
experiencing Parkinsons symptoms.
DA prolactin gynecomastia, infertility, galactorrhea-amenorrhea
syndrome
1-receptor blockade: postural hypotension, impotence, failure to ejaculate (<
than chlorpromazine)
Muscarinic receptor blockade: dry mouth, constipation, urinary retention,
visual problems (< than chlorpromazine)

 Histaminic receptor blockade: Sedation, weight gain (< than chlorpromazine)

Atypical neuroleptics Clozapine (Clozaril )
Very low D2 blockade
Extrapyramidal side-effects: < than typicals
High 1, H1, M1 blockade
No increase in prolactin
D1, D3, D4 blockade
1, histaminic, muscarinic blockade
5-HT2 blockade
Agranulocytosis
Seizures

Risperidone (Risperidal )
Very low D2 blockade
Extrapyramidal side-effects: < than typicals
Low 1, H1, M1 blockade
1, histaminic, muscarinic blockade low to moderate side-effects
5-HT2 blockade

Pharmacology Review Sheets: Neuro Drugs, p.5

Drugs affecting the Basal Ganglia (Drugs for Parkinson Disease)
Drug

Mechs of Action/Effects

Drug-specific Uses

Anticholinergic (helps with tremor, but

not bradykinesia)
Levodopa
Crosses BBB, then converted to dopamine
of drug required lead to nausea, vomiting, postural
in the CNS

Pharmacokinetics

Adverse Effects

Atropine

Metabolism: Extensively by:

- Aromatic amino acid decarboxylase (AADC)
- Catechol-O-methyltransferase (COMT)

High levels
hypotension, CV effects
Effects as disease

progresses (wearing-off phenomenon)

- Monoamine oxidase (MAO)

(this takes about 3-5 years)

Carbidopa
Tolcapone
toxicity

AADC inhibitor peripherally

COMT inhibitor peripherally

Combo w/Levodopa (Sinemet)

Can be combined w/Sinemet;

useful in stopping wearingoff phenomenon

Bromocriptine Non-specific D1, D2 agonist (ergot alk.)
side effects
Pergolide
D2-specific agonist (ergot alkaloid)
Autonomic side effects
Pramipexole D2-specific agonist (non-ergot)
Only effective for about 1 year of Rx
Ropinirole
D2-specific agonist (non-ergot)
Selegiline
MAO-B selective inhibitor (CNS) Used in young patients to delay

(Eldepryl ) Neuroprotective!!
use of dopa (neuroprotective)
Amantadine synthesis, release, re-uptake of DA
Also an antiviral drug
agitation; psychosis with high doses

Liver

Bromocriptine: D1-related
Ergot alkaloids:
All dopamine agonists:

Restlesslessness,
Orthostatic hypotension, urinary retention,

dry mouth
Baclofen

Acts at GABA receptors in CNS

Antianxiety drugs/Sleep drugs

Class

Mechanism of action/Effects

Drugs in that Class Duration

Uses

Adverse Effects

Benzodiazepines
Binds to benzodiazepine receptor adjacent Chlordiazepoxide (Librium) Long-acting Anti-anxiety (but not OCD)
Sedation
to the GABAA receptor, increasing the
Insomnia

frequency of opening of the Cl channel

Muscular disorders
Suppression of stage 4 sleep
Diazepam (Valium)
Long-acting Anti-anxiety (but not OCD) Sedation
No effect on REM sleep/no rebound effect
Insomnia, sleep terrors
No induction of CYP-450 (cp. barbitur.)
Anticonvulsant (drug of choice
Lower potential for addiction, cp.
for status epilepticus)
barbiturates
Muscular disorders

 Insomnia

Sedation; metabolites are

Flurazepam (Dalmane)

Long-acting

Alprazolam (Xanax)

Temazepam (Restoril)

Intermediate-acting Anti-anxiety (but not OCD)

Panic disorders
Insomnia
Intermediate-acting Insomnia

Lorazepam (Ativan)

Intermediate-acting

Insomnia

Triazolam (Halcion)

Very short-acting

Insomnia

active; may cause falls as a result

(behavioral problems)

Bizarre behavior

Rebound insomnia (more trouble falling

asleep afterwards)
Anterograde amnesia (blocks process of
recent learning)
Oxazepam
Midazolam

Short-acting
Short-acting

Insomnia

Insomnia
Date-rape drug formulation

Flunitrazepam (Rohypnol) Short-acting

now changes color w/EtOH

(Non-benzodiazepine) Binds to Benzodiazepine-1 receptor
Zolpidem (Ambien)
Short-acting Insomnia
No effect on Stage 4/rebound insomnia
Azapirones Blocks 5-HT1A receptor
Buspirone (BuSpar)
Anti-anxiety (but not OCD Minimal sedation
No muscle-relaxant properties
or panic disorders)
Slow onset of action
Benzodiazepine
Flumazenil
Short (1 hr) Rapid antagonism of
Antagonists
benzodiazepine effects
Pharmacology Review Sheets: Neuro Drugs, p.6
Antianxiety drugs/Sleep drugs, continued
Class

Mechanism of action/Effects

Drugs in that Class Duration

Barbiturates

Binds to GABAA receptor and increasing Pentobarbital

Uses
Insomnia

Adverse Effects (in general)

Addiction potential

duration of opening of the Cl channel Phenobarbital

Longer-acting than Insomnia
Tolerance
develops over time ( metabolism, cellular adaptation)
General depressants no antidote (only
pentobarbital
Anticonvulsant
- Induction
of CYP-450!
supportive care)
Thiopental
Rapid onset/offset
Anesthetic (IV)
Rebound
effect one must make up REM sleep after use
Suppression of REM sleep
Insomnia
Contraindicated in
patients with porphyrias
Sedative-hypnotics Reduced to trichloroethanol (active Chloral hydrate
Sedation in pediatrics
GI upset
ingredient)
Synergism with alcohol (Mickey Finn)
Antihistamines
(More later)
Diphenhydramine
Mild/moderate insomnia
CNS stimulants
Stimulates hypothalamus
Modafinil (Provigil)
Narcolepsy
dopamine in synaptic cleft
Amphetamines
dopamine in synaptic cleft
Methylphenidate (Ritalin)
MAO inhibitors
Eliminate REM sleep
Phenelzine
Narcolepsy
TCA antidepressants Block NE reuptake
Imipramine
Cataplexy assoc. w/narcolepsy
Anticonvulsants
Drug

Mechs of Action/Effects

Uses

Pharmacokinetics

Adverse Effects

Phenytoin
Inhibits voltage-gated Na+ channel Focal seizures
Admin/Absorption: Oral, variable absorption
CNS:
Nystagmus, diplopia, ataxia, sedation/seizures (high dose)
Tonic-clonic seizures
Distribution: > 90% protein-bound (displaceable) GI: Nausea,
vomiting
Metabolism: Not first order, but hydroxylated to Endocrine: Increased
metabolism of Vitamin D, interference of
inactive metabolite
Ca2+ absorption (can lead to
osteomalacia)
Altered tissue growth: Hirsutism,
thickened facial features,
gingival hyperplasia
Megaloblastic anemia (due to increase of
folate metabolism)

 Skin allergy (possible Stevens-Johnson

reaction)

Teratogen (cleft palate)

Inducer of CYP-450
Metabolism: Epoxide metabolite is active

Carbamazepine
Inhibits voltage-gated Na+ channel Focal seizures
Diplopia, ataxia, sedation (less serious than phenytoin)
(rare)
Ethosuximide Inhibits T-type Ca2+ channel
at high doses

Aplastic anemia, other blood dyscrasias

Absence seizures

CNS: Drowsiness, lethargy

GI: Nausea, vomiting, epigastric

(drug of choice)
pain

Hiccups
Metabolism: Hydroxylation (metabolite is active)

Valproic acid Blocks T-type Ca channel

Absence seizures
Hepatotoxicity (especially in kids)
GABA/ glutamate transmission (Some tonic-clonic seizures)
(associated with spina bifida)
Non-sedating
carbamazepine, ethosuximide
Phenobarbital Binds to GABAA receptor and increasing Tonic-clonic seizures
window
duration of opening of the Cl channel
2+

Diazepam

Clonazepam
develop

CNS:

Binds to benzodiazepine receptor adjacent Status epilepticus

to the GABAA receptor, increasing the
(drug of choice)

frequency of opening of the Cl channel

Binds to benzodiazepine receptor adjacent Status epilepticus

to the GABAA receptor, increasing the

frequency of opening of the Cl channel
Vigabatrin
Inhibits GABA transaminase ( GABA) Absence seizures
Lomotrigine Inhibits voltage-gated Na+ channel Partial & generalized seizures
(not used in kids less than 16)

Teratogenic
Affects clearance of phenytoin,
Narrow therapeutic
Sedation, ataxia
Inducer of CYP450
Contraindicated with porphyrias

Tolerance can
Narrow therapeutic window

Severe skin allergy

Felbamate
Hepatotoxicity

Enhances GABA transmission

Antagonizes glutamate transmission

Generalized seizures in pts.

Aplastic

with severe mental retardation

anemia
(Lenox-Gestalt Syndrome)
Pharmacology Review Sheets: Neuro Drugs, p.7
Antihistamines
Type

General mechs/General effects

Drugs

Duration

Uses

Adverse Effects (in general)

1st generation Competitive, reversible inhibition of the Diphenhydramine (Benadryl )

Anti-motion sickness

Sedation
Antihistamines
H1 receptor
Antitussive
Antimuscarinic effects: dry mouth,
blurry vision, constipation
(H1 blockade)
Muscarinic cholinergic blockade
OTC sleep aid
Convulsions (esp. in
kids)
-adrenergic blockade
Dimenhydrinate (Dramamine)
Anti-motion sickness
Excitation
(elderly) Sundown condition
5-HT receptor blockade
Meclizine (Antivert)
Long (12-24 h)
Anti-motion sickness
Postural
hypotension (-blockade)
Local anesthetic
Chlorpheniramine
OTC cold remedy
Drug allergy
(topical use)
(ChlorTrimeton)
Promethazine (Phenergan)
Anti-emetic
nd
2 generation More selective H1-receptor blockade
Citeridine (Zyrtec)
Allergic rhinitis/urticaria Minimal
sedation
Antihistamines
No anesthetic effects
Loratidine (Claritin)
Allergic rhinitis/urticaria No
anticholinergic effects
(H1 blockade)
Longer acting
Fexofenadine (Allegra)
Allergic rhinitis/urticaria No
antisertoninergic effects
CV: QT prolongaion, arrhythmias
H2 - specific Block gastric acid secretion by blocking Cimetidine (Tagamet)
Peptic duodenal, gastric ulcers
CNS:
delirium, confusion (elderly); dizziness, headache

Antagonists histamine, gastrin, vagal stimulation,

androgenic effects: gynecomastia, galactorrhea, impotence
Cholinomimetics

Ranitidine (Zantac)

Zollinger-Ellison syndrome,

Anti-

Erosive esophagitis
Blood dyscrasias
Inhibits CYP-450
GI: Hepatotoxicity, diarrhea
Skin: Rash
Peptic duodenal, gastric ulcers
CNS: Diziness,

headache
Zollinger-Ellison syndrome GI: Hepatotoxicity, diarrhea
Erosive esophagitis
Skin: rash
Famotidine (Pepcid)
headache

Peptic duodenal, gastric ulcers

CNS: Diziness,

Zollinger-Ellison syndrome GI: Hepatotoxicity, diarrhea

Erosive esophagitis
Skin: rash
Nizatidine (Axid)

Peptic duodenal, gastric ulcers

CNS: Diziness,

headache
Zollinger-Ellison syndrome GI: Hepatotoxicity, diarrhea
Erosive esophagitis
Skin: rash