Download Pathopharmacology of Thought, Mood and Anxiety Disorders

PATHOPHARMACOLOGY OF
THOUGHT, MOOD AND ANXIETY
DISORDERS
WANDA LOVITZ, APRN
LEARNING OUTCOMES:
THOUGHT, MOOD AND ANXIETY
Upon completing this presentation, the student should be able to:
 Define neurotransmitter.
 Explain how neurotransmitters work.
 Identify the relationship of neurotransmitter imbalance and
various mental illnesses.
 Describe the indications, MOA, and common and serious side
effect of selected medications from the classifications of drugs
used to treat thought and mood disorders:
Antidepressants
Barbiturates
Benzodiazepines
Hypnotics
Antipsychotics
DRUGS TO KNOW
ANTIDEPRESSANTS
ANXIOLYTICS
BARBITURATES/NON-BENZOS
First Generation
Benzodiazepines
Luminal/phenobarbital –
*Tofranil/imipramine -TCA
Elavil/amitriptyline
*Valium/diazepam
- TCA
antiseizure
Nembutal/pentobarbital –
Nardil/phenelzine - MAOI
Ativan/lorazepam
Second Generation
Xanax/alprazolam
Dalmane/flurazapam –
*Prozac/fluoxetine -SSRI
Versed/ midazolam
sedative/hypnotic
Romazicon/flumazenil -
Ambien/zolpidem -
ANTIDOTE
sedative/hypnotic
Zoloft/sertraline-SSRI
Lexapro/escitapram -SSRI
Cymbalta/duloxetine -SNRI
* = Prototype
sedative/sedative/hypnotic
DRUGS TO KNOW
MOOD STABILIZERS/
MOOD STABILIZERS
ANTIPSYCOTICS
ANTISEIZURE
Lithobid/lithium
Haldol/haloperidol
Depakote/valproic acid
Neurontin/gabapentin –
Thorazine/chlorpromazine
Tgegretol/carbamazepine
adjuvant tx
Olanzapine/Zyprexa
Lamitctal/lamotrigine
Risperdal/risperidone
Seroquel/quetiapine
NEUROTRANSMITTER
• A substance released when axon terminal of PREsynaptic
neuron is EXCITED
• acts by INHIBITING or EXCITING a target cell
• Disorders of NEUROTRANSMITTERS
• Too MUCH or too LITTLE
Neurological and mental illnesses
• Pharmacologic treatment of mental illness derived
from this basic premise
FOUR STEPS OF NEUROTRANSMITTER
TRANSMISSION:
1. Synthesis of a transmitter substance
2. Storage/release of the transmitter@
PREsynapse
3. Binding of the transmitter to receptors on
POSTsynaptic membrane
4. Removal of the transmitter from the synaptic
cleft
(Summarized in handout)
1= Synthesize
2=Storage & release
@ presynapse
3=Binding @
postsynapse
4= Reuptake & Deactivation:
removal and degradation
1
2
4
2
3
4
Neurotransmission
2
Deactivation
of
Neurotransmission:
1. Reuptake into
presynaptic terminal
2. Enzymatic degradation
1
Neurotransmission
MAJOR NEUROTRANSMITTERS
IMPLICATED IN MENTAL ILLNESS
• Dopamine (also impt in Parkinson’s)
• Norepinephrine
• Serotonin (5-HT) hydroxytryptamine
• GABA gamma aminobutyric acid
(Also addressed in handout)
EFFECT OF NEUROTRANSMITTERS
DEPRESSION
ANTIDEPRESSANTS
• Used to treat:
• Major depression
• Anxiety conditions
•
•
•
•
•
GAD
OCD
Panic
Social phobia
PTSD
PHARMACOLOGICAL TREATMENT OF DEPRESSION AND
ANXIETY
Benzodiazipines
Depression/Anxiety
Antidepressants
Selective Serotonin
Reuptake
Inhibitors
(SSRIs & SNRIs)
Monamine
Oxidase Inhbitors
(MAOIs)
Tricylic
Antidepressants
Atypical
Antidepressants
Antidepressants
(TCAs)
MOOD DISORDERS:
PHARMACOLOGIC TREATMENT
Depression 
First Generation ANTIDEPRESSANTS
1. (TCA) Tricyclic antidepressants
2. (MAOI) Monoamine oxidase inhibitors
Second-Generation ANTIDEPRESSANTS
1. SSRI
Selective Serotonin Reuptake Inhibit
2. SNRI
Serotonin Norepinephrine Reuptake Inhibitors
(* 2-4 WKS)
TRICYCLIC ANTIDEPRESSANTS
•
MOA:
• Block REUPTAKE of neurotransmitters NE and serotonin (5-HT)
• causing ↑ ACCUMULATION at nerve endings
•
Indications:
• Depression, bipolar disorder ,neuropathic pain, panic disorder, OCD, chronic pain,
anxiety
Adverse Effects:
• Anticholinergic effects (dry mouth, constipation, blurred vision, and sedation)
• Sedation/orthostatic hypotension
• Sexual dysfunction
• Common Drugs:
• amitriptyline (Elavil)
• imipramine (Tofranil)* PROTOTYPE
TRICYCLIC ANTIDEPRESSANTS
(TCA)
• Treat depression for over 40 years (1950’s)
• ↑ efficacy
• Less expensive than newer agents
• Side effect profiles well established
•
annoying anticholinergic effects: dry mouth, blurred vision, urine retention and
hypertension SLUG
•
not recommended for patients with heart problems
• OVERDOSES → NOTORIOUSLY LETHAL
•
•
NO ANTIDOTE!
FYI: also given for neuropathic pain, fibromyalgia, and management of nocturnal enuresis
MONOAMINE OXIDASE INHIBITORS
(MAOI)
• SECOND-LINE AGENTS for treatment of depression
NOT responsive to
other pharmacologic agents – “treatment resistive depression”
• Especially useful for ATYPICAL depressions
• Prototype  phenelzine (Nardil)
• Serious disadvantage → potential for HYPERTENSIVE CRISIS
when taken WITH tyramine (an amino acid)
WHAT ARE MONOAMINE
OXIDASE INHIBITORS?
• MOA:
• INHIBIT THE ENZYME MAO
•
MAO widely distributed in body, particularly in nerves, liver &
lung
•
MAO is responsible for INACTIVATING many important
neurotransmitters in nervous system
(particularly dopamine,
epinephrine, norepinephrine & serotonin)
• Inhibit MAO → then less INACTIVATION and
therefore……
• ↑ NEUROTRANSMITTERS AT NERVE ENDINGS!
MONOAMINE OXIDASE
INHIBITORS
• Adverse Effects/Interactions
• CNS stimulation – anxiety, insomnia, agitation and elevated mood
• Weight gain, diarrhea, orthostatic hypotension and sexual dysfunction
• Seizures and liver toxicity
• Drug-food interaction
•
Tyramine (amino acid) + MAOI = HYPERTENSIVE CRISIS!
•
Tyramine displaces presynaptic NOREPINEPHRINE = ↑↑↑ BP
•
•
↑ BP abruptly/dramatically
May cause cerebral hemorrhage, stroke, coma or death
WHAT FOODS CONTAIN
TYRAMINE?
• Tyramine-rich foods
•
Aged cheese (swiss, blue, cheddar)
•
Smoked meats (pepperoni, salami)
•
Yeast
•
Red wines
•
Italian broad beans
SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIs)
•
NEWER classification of antidepressants (1980’s)
• INDICATION: FIRST LINE ANTIDEPRRESSANT AND ANTXIOLYTIC
•
Some SSRIs are also used for GAD, diabetic neuropathy chronic pain, OCD, PTSD, social anxiety disorder,
and premenstrual dysphoric disorder
• Advantages over TCAs/MAOIs:
•
•
LESS SEVERE/FEWER side effects (especially with elderly)
Few drug-drug/drug-food interactions
• Takes approx 4 weeks to reach maximum clinical effectiveness!!
• Should be tapered when discontinuing to avoid withdrawal sx
•
Serious Drug- Drug Interaction
•
Do not give WITH MAOIs (possibly fatal serotonin syndrome!)
SELECTIVE SEROTONIN REUPTAKE
INHIBITORS
 Common Drugs: fluoxetine/Prozac *prototype
◦
Other commonly rx SSRIs
◦ sertraline/Zoloft
◦ citalopram/Celexa
◦ escitalapram/Lexapro
◦ MOA: inhibits serotonin reuptake
SELECTIVE SEROTONIN REUPTAKE
INHIBITORS
• MOA:
• Specific/potent INHIBITORS of presynaptic
serotonin reuptake
•
thus ↑ levels at nerve endings
• Adverse Effects:
• Generally well tolerated
• GI disturbances
•
N/V/D, constipation, dry mouth
• CNS disturbances
•
H/A, nervousness, insomnia
• Sexual dysfunction
• Suicidality (esp in children), seizures
• Serotonin Syndrome
WHAT IS SEROTONIN SYNDROME?
• A DRUG REACTION caused by
body having too much serotonin
accumulating in the brain stem and
spinal cord
•
• SX: altered mental status and
•
•
coordination
•
•
•
•
•
•
Agitation and restlessness
Hallucinations
Diarrhea
Diaphoresis and Fever
Overactive reflexes
Confusion
Often occurs when 2 drugs
that affect serotonin are taken
together
•
SSRI with an MAOI
Migraine meds with SSRI
Treatment
•
•
•
Benzo
Withdrawal of meds
Drug called Periactin that
blocks serotonin
production
INHIBITION OF REUPTAKE OF
SEROTONIN
SEROTONIN-NOREPINEPHRINE REUPTAKE
INHIBITOR SNRI
• Adverse Effects:
• Cymbalta/duloxetine
•
MOA: prevents the reuptake of
serotonin AND norepinephrine
•
Indications:
•
•
•
•
Depression
Anxiety
Peripheral Neuropathy
Chronic musculoskeletal pain
•
•
Similar to the SSRIs
Important to note
the increased risk
of SUICIDE with
both SSRIs and
SNRIs
SUMMARY: DRUGS TO TREAT DEPRESSION
TCAs and MAOIs (older drugs with more SE)
SSRIs (selective SEROTONIN reuptake inhibitors)
SNRIs (Serotonin-NOREPINEPHRINE reuptake inhibitors)
ANXIETY DISORDERS
ANXIETY DISORDERS: 5 SUBTYPES
ANXIETY MAY COEXIST WITH DEPRESSION, EATING DISORDERS, AND
SUBSTANCE ABUSE

PANIC disorder


intense feelings of immediate apprehension, terror, or impending doom
Post-traumatic stress disorder (PTSD)

type of extreme situational anxiety that develops in response to a previous
life event


Generalized ANXIETY disorder

excessive anxiety lasting 6 months or more

very common
SOCIAL ANXIETY disorder


fear of crowds
Obsessive-compulsive disorder (OCD)

recurrent, intrusive thought or repetitive behaviors that interfere with
ANXIETY/SLEEP DISORDERS:
PHARMACOLOGY
Anxiolytics  relieve anxiety
Sedatives  cause relaxation
Hypnotics  produce sleep
Low dose – High dose = anxiolytic or hypnotic
-------------------------
Sedatives
Hypnotics
Anxiolytics
 Anxiety
 Nervousness/
excitability without
causing sleep
Cause sleep
Two major classes of
ANXIOLYTICS:SEDATIVES/HYPNOTICS
1. BENOZODIAZEPINES
2. BARBITURATES (NON-BENZOS)
BENZODIZEPINES
• Indications:
• treatment of anxiety
and insomnia
• to augment SSRI/SNRIs
•
do NOT affect serotonin so
no risk for Serotonin
Syndrome
• also used to treat:
•
•
•
seizure disorder
•
induction agents for
anesthesia
ETOH withdrawal
for central muscle relaxation
(muscle cramps)
• Commonly rx benzos:
• For insomnia:
•
flurazepam/Dalmane
• For anxiety:
•
•
•
•
diazepam/Valium
lorazepam/Ativan
alprazolam/Xanax
midazolam/Versed
•
also used to induce
anesthesia
BENZODIAZEPINES
• MOA:
• Bind to gammaaminobutyric acid
(GABA) receptor
• Intensify the effect of
GABA
• GABA is a natural
INHIBITORY
neurotransmitter found
in the brain
•
•
•
•
Most given orally and IV
diazepam/Valium
lorazepam/Ativan
midazolam/Versed (IV only)
• Advantage of Benzos over
Barbiturates:
•
they do not produce life-threatening
resp depression or coma (if taken in excessive
amounts)
•
MUCH SAFER THAN BARBITURATES
•
antidote is available for overdoses:
•
flumazenil/
Romazicon
BENZODIAZEPINES/BENZO LIKE
DRUGS
•
Benzodiazepines work by
enhancing response to GABA
Anxiolytics
•
Onset of action is IMMEDIATE
•
Main SE are sedation, psychomotor
slowing, and amnesia
•
Physical dependence can occur with
long term use – Schedule IV drugs
•
Benzodiazepines can be classified
as EITHER
•
•
SEDATIVE/HYPNOTICS
ANXIOLYTICS
Sedatives/
Hypnotics
Benzodiazepines
COMMON
BENZODIAZEPINES/ANXIOLYTICS
Valium/
*Ativan/
diazepam
lorazepam
Benzos/Anxiolytics
rapid relief of anxiety
Xanax/
Versed/
alpraxolam
midazolam –given
to induce anesthesia
EXAMPLES OF BENZO/BENZO-LIKE AGENTS
Anxiolytics
Sedative/Hypnotics
*Ativan/lorazepam
*Ambien/zolpidem
Valium/diazepam
Dalmane/flurazapam
newer agent/less SE
Romazicon/flumazenil is the ANTIDOTE for all of the benzodiapine and benzo like drugs
Benzos/non-benzos
INDICATIONS: BENZOS AND NONBENZOS
Decrease anxiety –First line
tx for anxiety
To promote drowsiness and
relaxation prior to procedures
Inhibit seizure activity
Promote sleep
Induce anesthesia
BARBITURATES
•
Barbiturates (also known as “nonbenzos”) are drugs derived from barbituric acid
• Cause very powerful CNS depression
• Prescribed for:
•
•
SEDATIVE EFECT
HYPNOTIC EFFECT
• ANTI-SEIZURE EFFECT- most common indication
• Not commonly prescribed today for sedation because of:
•
High risk of psychological and physical dependence.. several are Schedule II drugs
• WITHDRAWAL FROM THESE DRUGS CAN BE SEVERE AND EVEN FATAL!
• Overdose causes profound resp depression, hypotension and shock
BARBITURATES FOR SLEEP: HYPNOTICS
• Rarely used today d/t habit forming nature of this class of drugs
 tolerance/dependence
• Examples of barbiturates:
• pentobarbital/Nembutal – sedative
• phenobarbital/ Luminal – anti-seizure
OTHER AGENTS USED FOR ANXIETY
AND INSOMNIA
• propranolol/Inderal – a beta •
blocker used for social anxiety
symptoms including ‘test anxiety’
zolpidem/Ambien for insomnia
•
Ambien NOT chemically r/t benzos but
does interact with GABA receptors
• Considered a “non-benzo”
• Ambien generally preserves all
sleep stages with little effect on
REM sleep
• Should only be used for short-term
tx of insomnia (7-10 days)
MOOD DISORDERS
MOOD DISORDERS
• MAJOR (unipolar) DEPRESSION
• MOST COMMON MOOD DISORDER
•
•
•
8-20% of population
Unable to experience pleasure
Show loss of outside interest
• Bipolar disorder (Manic-depression)
• Recurrent patterns of depression & mania
• cyclic episodes of energized mania and deep depression
• episodes can last months or even years
Bipolar is less common than unipolar
•
• Usually emerges in young adulthood
MANIA DIAGNOSIS
•
Genetic component
• Manic episode of at least one weeks duration that leads to hospitalization or
other significant impairment
•
Grandiosity
• Diminished need to sleep
•
Excessive talking or pressured speech
• Increased level of goal focused activities
PATHOPHYSIOLOGY OF BIPOLAR
DISORDER
• NOT ENTIRELY KNOWN
• Genetic, neurochemical and environmental factors
• Current thinking: a predominantly biological disorder d/t
malfunction of neurotransmitters
• Malfunctioning neurotransmitters: Serotonin, dopamaine and norepinephrine
•
May lie dormant and be activated spontaneously or triggered by stressors in life
Mania episodes – high levels of norepinephrine cause an exhilarating high, euphoric, hypersexual, spending sprees,
aggressive
Depressive episodes – low levels of serotonin cause the person to experience a plummeting fall from the
euphoric manic stage, sad, unable to cope
Psychotic Symptoms – too much dopamine affects emotions and perceptions is linked to psychotic sx such as
hallucinations
PATHO OF MANIA
•
Poorly understood
• Imaging studies show changes in brain structure
• Seem to be associated with imbalance in
neurotransmitters
• Diagnosis:
• Manic sx must be present for at least one week
DRUGS TO TREAT MANIA
• Mood Stabilizers
*Lithium
*Valproic
acid
• Relieve sx during manic and depressive episodes
• Anti-seizure
• Antidepressants
SSRIs
• With Bipolar, antidepressants ALWAYS combined with a mood stabilizer to avoid
elevating the mood so much that a manic episode may be triggered
• Antipsychotics and/or benzodiazepines
Risperdal
• Given to help control severe manic episodes
• Ativan alone may be enough.
DRUGS FOR MANIA: MOOD
STABILIZERS
•
Mania  “mood stabilizers”
•
Lithium salts
•
•
Atypical Antipsychotics
•
•
•
•
as monotherapy or in combination with other drugs
olanzapine/Zyprexa
risperdal/Risperdal*
quetiapine/Seroquel
Antiseizure drugs
•
•
•
sometimes used to tx mood disorders
valproic acid/Depakote
carbamazepine/Tegretol
lamotrigine/Lamictal
TREATING MANIA
LITHIUM (1970)
•
- MOOD STABILIZERS:
Norepinephrine & serotonin play role in development of mania
•
( NE & serotonin =  mania)
• Lithium
•
Mainstay treatment of bipolar disorder (mania)
• MOA:
•
•
How Lithium works is still not fully understood
More effective in controlling mania than depression
• Alters SODIUM ion transport in nerve cells →
•
•
↓ NE & 5HT (serotonin) metabolism and synthesis
SE: common = dazed feeling and hand tremors
• polyuria (up to 3 Liters a day), excessive thirst
•
Imbalance in ELECTROLYTES
• Acts like sodium in the body
• Inhibits ADH and ability for body to concentrate
urine
TREATING MANIA:
{LITHIUM}
•
MOOD STABILIZERS
Lithium
• NOT metabolized in liver
•
•
98% excreted unchanged in kidney
NARROW THERAPEUTIC INDEX:
•
0.5 – 1.5 meq/dl
• Monitor serum levels q 1 – 3 days initially
• also monitor sodium levels
• Monitor q 2 – 3 months thereafter
• Dehydration/excessive sweating can increase lithium toxicity
•
Requires one week of treatment before see results
TREATING MANIA: LITHIUM
MOOD STABILIZERS
• Lithium - adverse effect:
• ‘Lithium toxicity’
• Diarrhea** (classic early symptom)
•
•
•
•
•
Tremors (fine or gross)
1.5 – 2 mEq/L
Slurred speech
Drowsiness/somnolence
2 – 2.5 mEq/L
Seizures
Cardiac dysrhythmias
• Death
> 2.5 mEq/L
DEPAKOTE/VALPROIC ACID: MOOD
STABLIZER
• First line treatment for bipolar manic episodes
•
Is an anti-seizure med
•
Works faster and less SE than Lithium
•
Known teratogen
•
Side Effects:
•
Well tolerated generally but CAN cause
•
•
•
•
WEIGHT GAIN - frequent
Thrombocytopenia - rare
Pancreatitis -rare
Liver Failure- rare
THOUGHT DISORDERS
(PSYCHOSIS)
SCHIZOPHRENIA
•
1% of world population
•
30% homeless have schizophrenia
•
Thought disorder that involves a loss of touch with reality

delusions, grandiose delusions, paranoid delusions, mood disturbances, behavior
disturbances, purposeless aimless mannerisms, disorganized speech
• Strong genetic predisposition
• Onset typically occurs between 20 & 35 years of age
SCHIZOPHRENIA: PATHOGENESIS
• Not sure, several theories
• Neurotransmitter alteration theory
• DOPAMINE HYPOTHESIS of schizophrenia
• Abnormal ↑ in dopaminergic transmission
contributes to the onset of schizophrenia
SCHIZOPHRENIA:
A TYPE OF PSYCHOSIS
•
NEGATIVE SYMPTOMS
◦ SUBTRACT from the normal
behavior
◦
lack of
motivation/interest/drive
◦
◦
◦
indifferent personality
Poor self care, judgement
Flattened affect
◦
**sometimes mistaken for
depression or laziness
• POSITIVE SYMPTOMS
•
ADD on the normal
behavior
•
•
•
•
•
hallucinations
delusions
disorganized thoughts
or speech patterns
Combativeness
“VOICES”
SCHIZOPHRENIA:
PHARMACOLOGIC TREATMENT
•
Antipsychotics
• sometimes referred to as ‘neuroleptics’ because of the
NEUROLOGICAL side effects
•
1. Typical
•
•
Conventional, first-generation agents (FGA)
Help with controlling the positive sx –
auditory and visual hallucinations and
delusions
•
Less effective for negative sx
– emotional and social withdrawal and blunted
affect
2. Atypical
•
•
•
Second-generation agents (SGA)
Effective for both positive and negative symptoms
Can be used to tx acute mania and bipolar depression
ANTI-PSYHCOTICS: SE
Thorazine
Haldol
chlorpramazine
Haloperidol
Very High EPS
Low EPS
Low potency FGA
Risperdal
risperidone
High potency FGA
Zyprexa
Mod EPS
olanzapine
Low EPS
SGA
SGA
ANTIPSYCHOTICS
• Indications
• Schizophrenia
• Bipolar
• OCD
• Severe depression
• Mechanism of Action
• Typicals – block D2
receptor (dopamine)
• Common extrapyramidal
SE
• Atypicals – block D2
AND 5HT (dopamine and
serontonin)
•
produce fewer
extrapyramidal SE
because they are loosely
bound to D2 receptors
•
Weight gain, DM, and
dyslipidemia common
ANTIPSYCHOTICS
• Conventional/Typical
Antipsychotic
• chlorpromazine/Thorazine
• haloperidol/Haldol*
• Atypical Antipsychotics
• olanzapine/Zyprexa
• risperidone/Risperdal
• quetiapine/Seroquel
ANTIPSYCHOTICS: MOA
• All antipsychotics have a COMMON MOA
• Block dopamine receptors in the
brain
• thus ↓ dopamine concentration in CNS
• Atypical antipsychotics block specific
DOPAMINE receptors
•
as well as specific SEROTONIN
receptors in the brain (5HT)
SIDE EFFECTS OF ANTIPSYCHOTICS
ANTICHOLINERGIC METABOLIC
EXTRAPYRAMIDAL
SYMPTOMS (EPS)
Movement disorders
Acute dystonia-
dry mouth
Weight gain
blurred vision
Dyslipidemia
photophobia
Heart disease
urinary retention
Diabetes
Parkinsonism - bradykinesia, masklike facies, drooling, tremor rigidity,
shuffling gait, stopped posture, cogwheeling – occurs early in t
Akathsia - uncontrollable urge to
be in motion (pacing and squirming)
– occurs early in tx
constipation
tachycardia
severe spasms of
neck, tongue, face, or back – occurs early
in tx (hours/days)
* Seen more with the NEWER
antipsychoitcs
Tardive Dyskinesia
MOST TROUBLING SE- OCCURS LATE
IN THERAPY
occurs in 15-20% of pts
thought to be r/t over activation of
dopamine receptors making them
super sensitive
no good management or treatment
NEUROLOGICAL SIDE EFFECTS OF
ANTIPSYCHOTICS
Acute
Akathisa
Dystonia
Parkinsonism
Tardive
Late/chronic
Tardive Dyskinesia
“Chronic”
Perioral Movements
AKATHISIA
• Means “inability to sit still”
• Subjective distress
• Akathisia can be confused with agitation
• Frequently occurs 5-30 days after therapy begins
• Can occur with not only FGA but also with
•
the 2nd generation atypicals
ACUTE DYSTONIA
• Intermittent and sustained contractions of muscles
of the tongue, face, neck and back
• Typically occurs during the first 5 -30 days of
treatment
• Responds rapidly to anti-parkinsonism agents and Botox
PARKINSONSIM
• Antipsychotics can induce symptoms similar to
parkinson’s disease
• Generally happens 5-30 days after starting tx
•
•
•
•
tremor
muscle rigidity
stooped posture
shuffling gait
TARDIVE DYSKINESIA
 Tardive dyskinesia (TD)
Involuntary contractions of oral and face
muscles
 choreoathetosis
(wave-like movements of extremities)
 Starts as slow, worm-like movements
of the tongue
 Can interfere with chewing, swallowing, speaking
 Malnutrition and weight loss can occur
 Over time involuntary movements of the limbs, toes, fingers,
and trunk occur
SUMMARY SE OF ANTIPSYCHOTICS
Conventional/
Typical (FGA)
Atypical
Drugs
haloperidol/Haldol
chlorpromazine/Thorazine
quetipaine/Seroquel
aripiprazole/Abilify
olanzapine/Zyprexa
Common
Side
Effects
Extrapyramidal
Weight gain
Anticholinergic effects
Type 2 DM
Anti-cholinergic SE
(dry mouth, blurred vision, photophobia,
(SGA)
Cardiac Disease
urinary retention/hesitancy, tachycardia)
Sedation