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72 Cards in this Set

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Typical antipsychotics
reduce positive symptoms
little effect on negative symptoms
extrapyramidal side effects (EPS)
Atypical antipsychotics
reduce positive symptoms
reduce negative symptoms
fewer EPS
different types of side effects
Clinical Effects of Antipsychotic Drugs
some sedation acutely
decrease in psychotic symptoms
slow onset of improvement variability in responses
relapses during chronic therapy
high therapeutic index when used alone
antiemetic actions
side effects to some extent dependent on particular drug
Psychiatric indications for antipsychotics
schizophrenia
schizoaffective disorder
delusional disorder (paranoid)
manic episodes in bipolar disorder
Tourette’s syndrome
disturbed behavior in Alzheimer's disease
Nonpsychiatric indications for antipsychotics
emesis- prochlorperazine (compazine)
pruritis
preoperative anesthesia
Proposed Mechanism of Action of typical antipsychotics
block D2 receptors
what are the three dopamine pathways and the effect of the antipsychotic?
Mesolimbic-mesocortical pathway (antipsychotic action)

Nigrostriatal pathway (extrapyramidal side effects)

Tuberoinfundibular pathway (hyperprolactinemia)
Hypothetic Model for Atypical Antipsychotics
Atypical antipsychotics block both D2 and 5-HT2 receptors.

Clozapine blocks D4 and 5-HT2 receptors.

Aripiprazole is a partial agonist at D2 and 5-HT1A
receptors and is an antagonist at 5-HT2A receptors.
Side Effects of antipsychotics
alpha1-adrenergic antagonism
-orhtostatic hypotension
-dizziness
Antihistamine
-sedation
-wt gain
Antimuscarinic
-blurred vision, dry mouth, confusion,urinary retention, constipation
Extrapyramidal Side Effects
acute dystonia
akathisia(motor restlessness)
parkinsonism
perioral tremor
tardive dyskinesia
Tardive Dyskinesia (TD)
late onset
oral-facial dyskinesia
widespread choreoathetosis or dystonia
debilitating and sometimes irreversible
worse on withdrawal
due to dopamine receptor supersensitivity
Tx of TD
no approved drugs for treatment of TD
early recognition is important
reduce or stop use of antipsychotic
lower incidence of TD with clozapine
Neuroleptic Malignant Syndrome (NMS)
malignant hyperthermic syndrome
rare but potentially life-threatening
SX-muscle rigidity, impaired sweating, fever, autonomic instability, leukocytosis, inc serum CPK
due to excessively rapid blockade of postsynaptic dopamine receptors
Tx of NMS
Stop antipsychotic!!!!
treat symptoms
Endocrine Side Effects of antipsychotics
women-amenorrhea, galactorrhea, infertility

men-impotence, infertility, gynecomastia
Side Effects of Clozapine
agranulocytosis (potentially fatal)
seizures (1% to 4%)
weight gain
diabetes
Side Effects of Olanzapine
weight gain
diabetes
Side Effects of Risperidone
extrapyramidal side effects
hyperprolactinemia
Side Effects of Aripiprazole
akathisia
insomnia
excess sedation
Indications for opoids
Relief of intense pain
Relief of cough
Treatment of diarrhea
Treatment of acute pulmonary edema
Mechanism of Action
Produce analgesia by interacting with endogenous receptors called opioid receptors.

Receptors are activated by endogenous opioid peptides, and localized primarily to brain and spinal cord regions that are involved in the
transmission and modulation of pain.
Endogenous Opioid Peptides
Enkephalins
Endorphins
Dynorphins
Endogenous Opioid Peptides-properties
Peptide neurotransmitters
or neuromodulators
- Released during stress
- Modulation of pain, stress,
dependence, eating
Mu Receptors
high affinity for enkephalins, beta-endophin, and morphine

mediate opioid-induced analgesia and positive reinforcement, respiratory depression, miosis, decreased GI motility, and neuroendocrine effects
Delta Receptors
high affinity for enkephalins and beta-endophin

antinociception, motor integration, and cognitive function
Kappa Receptors
high affinity for dynorphin

regulation of food intake, temperature control, GI motility, pain perception, and neuroendocrine function
Which fibers carry tonic and phase pain in the ascending pathway?
phasic-alpha gamma
tonic-C
Action of Opioid on Ascending Pain Transmission Pathways
Decreases calcium entry into presynaptic terminal preventing release of glutamine.

Increase conductance of potassium at post-synaptic neuron to hyperpolarize it.
Action of Opioid on Descending Pain Modulatory Pathways
decrease the amount of GABA to disinhibit the pain inhibitory interneurons.
Effects of Opioids on the CNS
Analgesia
Euphoria or dysphoria
Sedation
Resp depression
cough suppression
miosis (constriction)
emesis
Effects of Opioids on Other Body Systems
CV, GI, GU, uterus, neuroendocrine, skin
CV-hypotension and vasodilation
GI-constipation
GU-urinary retention
Uterus-decreased contraction
Neuroendocrine-+ADH and prolactin, -LH
Skin-flush, pruritis, urticaria
Tolerance in opoids
Tolerance to the analgesic, sedative, euphoric, emetic, and respiratory depressant effects

No tolerance to the miotic and constipating actions

Cross-tolerance among opioid analgesics
Dependence in opoids
withdrawal syndrome--
-Strong Flu-like symptoms
- Goose flesh
- Muscle tremor and twitches
- Abdominal cramps and diarrhea
- Increased heart rate, blood pressure
- Hyperventilation
- Anxiety and hostility
Strong Opioid Agonists
Morphine,Heroin (acetylmorphine)

- high affinity for mu receptors
- treatment of severe pain
Morphine
major active ingredient (10%) in opium

4-6 hr duration of action

active metabolite: morphine-6-glucuronide

treatment of severe pain associated with trauma, myocardial infarction, and cancer
Heroin (acetylmorphine)
Acetylation makes it more lipid soluble and fast acting

A Schedule I Controlled Substance
Methadone (Dolophine®)
orally effective

longer duration of action (15-20 hrs)

used for detoxication and controlled withdrawal from heroin and morphine
Meperidine (Demerol®)
less potent than morphine

shorter duration of action (2-4 hrs)

an obstetric or postsurgical analgesic
Fentanyl (Sublimaze®)
80 times more potent than morphine

rapid onset (< 5 min)

very short duration (15-30 min)

an adjunct to general anesthesia
Moderate Opioid Agonists
less potent than strong agonists

lower abuse potential

used with non-opioid analgesics for treating moderate pain
Codeine
0.5% concentration in opium

metabolized to morphine for
analgesic activity

used with aspirin and acetaminophen for moderate pain

included in many cough syrups for relief of cough
Mixed Opioid Agonist-Antagonists
drugs that exhibit partial agonist or antagonist activity at mu receptors and show agonist or antagonist activity at k receptors
Mixed Opioid Agonist-Antagonists

Advantages and Disadvantages
A:ceiling to resp depression
lower abuse potential

D:dysphoric at high doses
difficult to antagonize
Pentazocine (Talwin®)
a K-receptor agonist with weak mu-receptor antagonist activity

orally administered for treating moderate to severe pain

parenteral formulation as a preanesthetic medication

precipitates a withdrawal syndrome in a morphine abuser
Buprenorphine (Buprenex®)
a partial agonist at MU-receptors and an antagonist at K-receptors

resistant to Naloxone reversal

treatment for cocaine addiction and heroin abusers
Opioid Antagonists
competitive antagonist that compete for agonist binding sites
Naloxone (Narcan®)
a competitive antagonist (t1/2 ~ 1-2 hrs)

no effects in normal people

antagonist-precipitated withdrawal

Intravenous injection for treating opioid overdose
Naltrexone (Re Via®)
a competitive antagonist (t1/2 ~ 10 hrs)

antagonist-precipitated withdrawal

a “maintenance” drug for addicts

also used in treatment of alcoholics
Stimulants
CONVULSANTS-Strychnine, Picrotoxin,Pentylenetetrazol

ANALEPTICS-Doxapram

XANTHINES-caffeine, theophylline, theobromine
Stimulant mechanism
Adenosine receptor antagonists
Phosphodiesterase inhibitors
Mobilize intracellular calcium
PHARMACOLOGICAL EFFECTS of Stimulants
CNS stimulation
Smooth muscle relaxation
Diuresis
Mild sympathomimetic
Tolerance
Dependence
THERAPEUTIC USES
Stimulant / antifatigue
Apnea in preterm infants
Asthma
Analgesic adjuvant (OTC)
PSYCHOMOTOR STIMULANTS
Amphetamine
Methylphenidate (Ritalin)
Cocaine
PHARMACOLOGICAL EFFECTS OF PSYCHOMOTOR STIMULANTS
Increased wakefulness / activity
Elevation of mood
Increased ability to concentrate
Improved physical performance
Sympathomimetic
Toxic psychosis
THERAPEUTIC USES OF PSYCHOMOTOR STIMULANTS
Narcolepsy
Attention Deficit Disorder
(ADD / ADHD)
Weight control
ACUTE TOXIC REACTIONS(CNS)
Anxiety / agitation
Paranoia / delirium
Seizures
Hyperthermia
Treatment is supportive; diazepam for seizures
ACUTE TOXIC REACTIONS (CARDIOVASCULAR)
Tachycardia
Ventricular arrhythmias
Severe hypertension
Cerebral hemorrhage
Myocardial ischemia / infarction
LYSERGIC ACID DIETHYLAMINE (LSD) GROUP
Indolealkylamines (5HT)
LSD, psilocybin
Phenylethylamines (DA, NE)
mescaline
PHYSIOLOGICAL EFFECTS of LSD group
Dilated pupils
Increased muscle tone / tremors
Ataxia / incoordination
Dizziness / drowsiness
Tolerance / cross-tolerance
AMPHETAMINE DERIVATIVES
3,4-methylenedioxyamphetamine (MDA, love)
3,4-methylenedioxymethamphetamine (MDMA, ecstasy)
PERCEPTUAL EFFECTS of AMPHETAMINE DERIVATIVES
Sense of well-being
Heightened insight
Disturbed sense of time
Paranoid psychosis
PHYSIOLOGICAL EFFECTS of AMPHETAMINE DERIVATIVES
Similar to LSD
Prominent sympathomimetic
Neurotoxicity (5HT)
ACUTE TOXIC REACTIONS of AMPHETAMINE DERIVATIVES
Amphetamine-like effects (hypertension/ hyperthermia)

Seizures most common reason for emergency services

Treatment of hyperthermia mainly symptomatic
LONG-TERM EFFECTS OF ECSTASY
Brain chemistry changes
serotonin reduced
serotonin metabolites reduced

Brain structure changes
serotonin transporters reduced
serotonin terminals degenerate
Brain areas affected by ectasy
neocortex
basal ganglia
amygdala
hippocampus
hypothalamus
ARYLCYCLOHEXYLAMINES
Phencyclidine (PCP)
Ketamine
PERCEPTUAL EFFECTS OF ARYLCYCLOHEXYLAMINES
Closely resemble schizophrenia
Sensory deprivation
Inability to integrate sensory input
Distortions of body image
Psychotic symptoms
PHYSIOLOGICAL EFFECTS OF ARYLCYCLOHEXYLAMINES
Hypertension
Nystagmus
Sweating
Salivation
Ataxia
Analgesia
THERAPEUTIC USES OF ARYLCYCLOHEXYLAMINES
Intravenous anesthetic
Veterinary anesthetic
Neuroprotective effects
MARIHUANA
Most commonly used illegal drug
True hallucinations only at high doses
Primarily alters thought processes and mood
9-Tetrahydrocannabinol (THC) psychoactive constituent
PHYSIOLOGICAL EFFECTS OF MARIHUANA
Tachycardia
Dry mouth
Conjunctival reddening
Increased appetite
Decreased attention span
Memory impairment
THERAPEUTIC USES OF MARIHUANA
Anti-emetic
Appetite stimulant
Glaucoma