-
Depression
- MAOI's
- Atypical
Antidepressants
- SSRI's
-
Tricyclic
Antidepressants
-
Potentiates actions of NE & S
By inhibiting reuptake transporter
- Topic
-
Alzheimer's
Disease
-
Ach inhibitors
-
Tacrin
- Hepatotoxic
- Donepezil
- Rivastigmine
-
N-methyl-D-aspartame
Receptor antagonist
-
Memantine
- Overexposure to NMDA
leads to cellular degeneration
-
Depression
-
SSRI
- Citalopram
- Escitalopram
- Paroxetine
- Sertraline
- Fluoxetine
-
Psychosis and
Agitation
-
Antipsychotics
- Risperidone
- Olanzapine
- Quetiapine
-
Parkinson's
Disease
-
Increase Dopamine
-
Levodopa
-
MOA: decarboxylated to
Dopamine in D neurons
In the striatum
- Early in Tx: N, V, OhTN, tachy, arrh.
Late in Tx: diskinesias, halluc.,
wild dreams and delusions
- Don't take pyridoxine (B6)
Increases peripheral break-
down of levodopa
- Most effective PD agent
-
Dopamine receptor
Agonists
-
Bromocriptine
-
May save D neurons from
Oxidative stress,
ERGOT LIKE
Fibrosis
(vasoconstrictor)
- MOA: agonist at D2 receptors
Partial antagonist at D1 receptors
- Dyskinesias, OhTN, <3 prob. in pt w/ MI
-
Pergolide
-
ERGOT LIKE
Fibrosis
(vasoconstrictor)
- MOA: agonist at both D1 & D2
MORE POTENT THAN
BROMOCRIPTINE
-
Pramipexole
-
First line, best in pt that
HAVE NOT received levodopa,
- MOA: NON ERGOT
dopamine agonist at
D2 & D3 receptors
- Daytime sedation, cause
Reward seeking compulsive
Behavior: drinking, shopping,
And gambling.
- CIMETIDINE inhibits
Renal secretion of
PRAMIPEXOLE
- Ropinrole
-
Dopamine release/
Uptake
-
Amantadine
-
MOA: alters D release
(if at max, no effect) or
Uptake.
- OhTN, dry mouth, hallucinations
-
Monoamine
Oxidase B
Inhibitor
-
Selegiline
-
MOA: enhances the
effect of levodopa
- High doses affect MAOI type A-->
Severe HTN
-
Antimuscarinic
Agents
-
MOA: blockage of cholinergic
Transmission to augment D.
- Same side Fx as high
Dose atropine.
-
COMT inhibitors
-
Tolcapone
-
Useful in on-off phenomenon
Long acting.
- MOA: inhibits COMT
catechol-o-methyl transf.-->
dec'd 3-O-methydopa,--> ind'd
Uptake of levodopa
- Hepatotoxic,
Cause blood dyscrasias
-
Entacapone
-
MOA: SEE TOLCAPONE
- NOT HEPATOTOXIC,
does cause blood, dyscrasias
-
Alcohol
-
Alcohol
Abuse
-
Disulfiram
-
MOA: inhibits ADH and ALDH
so aldehyde accumulates
- Face hot and flushed, throbbing
headache, hypotension, thirst, sweating
Chest pain, copious vomiting.
-
Naltrexone
- MOA: opiate antagonist
-
Acamprosate
Calcium
- MOA: not sure, but:
Has affinity for GABA A &B
-
Ethanol
-
MOA: competes
for ADH
- Methanol
Poisoning
- Ethylene glycol
Poisoning
- Isopropyl alcohol
Poisoning
-
Psychomotor
Stimulants
-
Methylxanthines
-
BENEFITS: increased alertness,
loss of fatigue, sustained attention
-
MOA: --| phophodiesterases,
raising cAMP;
Antagonizing adenosine
A1 and A2 receptors;
= enhanced neurotransmission
- Nausea/vomiting,
>200mg = nervousness,
restlessness and tremors
- Caffeine
- Theophylline
- Can cause seizures
at high doses.
-
Amphetamines
-
Large amounts excreted
in urine. (can "ion trap")
-
MOA: (oral) causes the release
Of biogenic amines (NE,S&D)
MAY interfere with re-uptake
- CNS: restlessness, tenseness, irritability
Weakness, insomnia, confusion, delirium
Paranoid hallucinations, suicidal
or homicidal tendencies.
CV: headache, palpitation, cardiac
arrhythmias, HTN, circulatory collapse.
EXCESSIVE SWEATING
- Dextroamphetamine
- Methamphetamine
- More central, less
peripheral effects
-
Amphetamine
Derivatives
-
Methylphenidate
- *SEE AMPHETAMINE
- *SEE AMPHETAMINE
- Narcolepsy
- ADHD
-
Phentermine
- Exogenous
Obesity
- C/I in pt with history
Of CV. problems;
HTN crisis with MAOI
-
Nicotine
-
Smoking
Cessation
-
BENEFITS: euphoria,
Arousal, improved attention,
Learning, problem solving
and reaction time
- MOA: stimulates nicotinic
Receptors in the CNS
- OBVIOUS
-
Cocaine
- MOA: --| reuptake
Of dopamine
-
Ephedrine
-
Stay awake preps,
Energy boosters and
Come asthma preps.
- MOA: [oral] α/β adrenergic
agonist, also enhances
Release of NE
-
NON-AMPHETAMINE
-
Modanifil
-
MOA: UNKNOWN
(may weakly block
Dopamine uptake)
- psychoactive and euphoric
Fx seen in CNS stimulants
- ADHD
- Narcolepsy
-
OTHERS
-
Narcolepsy
-
Sodium
Oxybate
- Take at bedtime
and 2.5-4 hours
After falling asleep
- MOA: Reduces cataplexy
(loss or muscle control/weakness)
- Depression, BEDWETTING,
Sleep walking and abuse potential.
-
Weightloss
-
Sibutramine
- MOA: weak inhibitor of the re-uptake
Of NE and S, also thought to interact
With the receptors causing hunger.
- HTN, cardiac Dz, stroke,
narrow angle glaucoma,
renal or hepatic Dz
POSSIBLE CARDIAC
VALVE DISORDERS
- DRUG INTERACTIONS:
MAOI
-
ADHD
-
Atomoxetine
- MOA: re-uptake
Inhibitor of NE and S
- Suicidal thoughts
and liver DZ
-
Guanfacine
- MOA: agonist at post synaptic
α2 adrenergic receptors
- Caution with
Cardiac problems
-
Sleep disorders
-
BDZ's
-
MOA: BZ1 receptor on GABA-
Chloride channel receptor
Complex --> hyperpolarization
-
DO NOT TAKE WITH:
OSA (obstructive sleep
apnea) dec. muscle tone
in upper airway worsen
Apnea episode
DON'T DRINK!
- Short Acting
(3-8 hours)
- Midazolam
- Triazolam
- Intermediate
(10-20 hours)
- Temazepam
- Estazolam
- Long Acting
(1-3 days)
- Quazepam
- Flurazepam
-
Barbiturates
-
Weak acid, can induce
P450 enzymes, can
Also increase ALA,
Therefore C/I in pt.s
With porphyria
-
MOA: bind to separate
Sight on the GABA Cl channel
Receptor complex increasing
The duration that the channel is open
- Tolerance, high
Abuse potential
SMALL THERAPEUTIC
INDEX
- DRUG INTERACTIONS!
Decreased serum Warfarin
Decreased serum digoxin
Decreased serum CCB's
- Ultra-short Acting
(20 min)
- Thiopental
- Methohexital
- Short Acting
(3-8 hours)
- Pentobarbital
- Secobarbital
- Amobarbital
- Long Acting
(1-2 days)
- Phenobarbital
-
Miscellaneous
-
Zolpidem
-
Increases sleep
Duration
- No effect on different Stages of sleep
Minimal rebound insomnia,
Little to no tolerance,
Great to avoid jet lag.
- MOA: binds to a
Sub-site of BZ1
- Can cause sleepwalking
Pt.s binge eat, shop and drive
With no memory
DO NOT DRINK!
(Increases sleepwalking)
-
Zaplelon
-
Increases sleep
Duration
- No effect on different Stages of sleep
Minimal rebound insomnia,
Little to no tolerance,
- MOA: binds to a
Sub-site of BZ1
-
Eszopiclone
-
Increases sleep
Duration
- No effect on different Stages of sleep
Minimal rebound insomnia,
Little to no tolerance,
APPROVED FOR LONG TERM.
- MOA: binds to a
Sub-site of BZ1
-
Ramelteon
-
MOA: MT1, MT2 receptor
Agonist (no affinity for BZ1
Or BZ2)
- DO NOT DRINK!
-
Choral Hydrate
- Sedation for Kids
Undergoing procedures
-
Panic Disorder
-
Symptoms:
1. Palpitations, pounding heart, inc. HR
2. Sweating. 3. Trembling or shaking
4. Sensations of SOB or smothering
5. Feeling dizzy, unsteady, lightheaded or faint
6. Fear of dying
-
BDZ
- Alprazolam
-
SSRI
- Sertraline
- Paroxetine
-
Anxiety
-
Antihistamines
-
MOA: antagonist
at H1 receptors
(excitatory)
-
SEDATION!
Do not drink!
- Hydroxyzine HCL
- Hydroxyzine pamoate
-
SSRI
-
MOA: --| reputake
Of serotonin at transporter
= more in synaptic cleft
-
[buspirone] + sexual dysfunction
AND insomnia, tremors; palpitations,
Postural HTN (paroxetine only)
Vasodilation; anorexia, NVD;
Loss of libido... Wah wah.
- DRUG INTERACTIONS!
MAOI's (14 day wait)
TCA's (inhibits metabolism)
TRYPTOPHAN
(add. serotonin Fx)
WARFARIN (inc. risk of bleeding)
- Paroxetine
- Sertraline
-
SNRI
-
MOA: blocks S & N
Reuptake transporters
-
See SSRI,
AND Hypertension
With withdrawal.
- Venlafaxine
- Also treats
Depression!
- Desvenlafaxine
- Duloxetine
-
Carbamates
-
Respiratory depression
Dangerous withdrawal
Geriatric problems
- Meprobamate
-
Azapirones
-
MOA: 5HT1a receptors -->
G proteins --> inc. opening of
K+ channels = hyperpolarization
= decreased firing
-
Headache and dizziness BUT!
NO impaired motor function
NO D.W.T.
NO cross tolerance with BDZ
NO problems drinking
NO muscle relaxation/
Anticonvulsant
- Buspirone
-
Benzodiazepines
-
MOA: enhances the affinity
for GABA receptors to its NT,
-> more frequent opening of Cl
channels, --| neuronal firing.
-
Drowsiness and confusion
Ataxia at high doses
Brain Drain-
(Recall and learning)
DON'T DRINK!
D.W.T.
- Short Acting
(3-8 hours)
- Oxazepam
- Choice in Aged
and Hepatic Dz
BECAUSE:
Bypasses oxidation
And n-dealkylation
- Intermediate
(10-20 hours)
- Lorazepam
- Alprazolam
- Long Acting
(1-3 days)
- Diazepam
- Clorazepate
- Prodrug
- Chlordiazepoxide
-
BDZ overdose,
Anesthesia
sedation reversal
-
BDZ Antagonist
- MOA: binds and
Completely antagonizes
binding and allosteric
Effects of BDZs
- Flumazenil
- Lipid soluble!