Mid-Ohio Psychological Services, Inc. Staff Training:
Psychopharmacology
Daniel DiSalvo, CNPFebruary 8, 2008
Outline Welcome, Introduction & Lunch Content
Pharmacodynamics/kinetics & Basic Principles Antidepressants
MAOIs, TCAs SSRIs SNRIs Other
Mood Stabilizers Antipsychotics
Discussion Question & Answer Conclusion
Psychopharmacology The study of the effects of drugs
on affect, mood, cognition and behavior and the use of drugs to treat disorders of the central nervous system where it is the expressed intent to alter mood, thought or behavior.
The Concept of Chemical Imbalance
NT in deficit in excess
acetylcholine memory impairment/delirium aggression/depression
dopamine dementia/depression psychosis/anxiety/ confusion/aggression
serotonin depression/impulsivity/anxiety anxiety
norepinephrine depression/anxiety/dementia anxiety/aggression
GABA anxiety/impulsivity cognitive/motor slowing
glutamate cognitive slowing/dementia seizures/neuronal
degeneration
The Basis of Psychopharmacology
Correcting the chemical imbalance – either increasing or decreasing activity of that
NT. For disorders associated with
hypofunctioning:1. Stimulate NT release2. Use chemical (drug) that mimics NT3. Block metabolic inactivation of NT4. Block reuptake For disorders associated with
hyperfunctioning:1. Inhibit or reduce NT release2. Block target receptors
Antidepressants >8 different pharmacological MOAs >2 dozen ADs Most block monoamine reuptake Some block alpha-2 receptors Others might work on the enzyme MAO Some have direct actions on only one
monoamine NT system, while others work on multiple monoamine NT systems
The immediate pharmacological actions of all ADs eventually have the effect of boosting the levels of monoamine NTs
Why Does It Take So Long?
Down Regulation: no matter what their initial actions on receptors and enzymes, ADs eventually cause a desensitization of key NT receptors in a time course consistent with the delayed onset of AD action of these drugs.
Delayed actions of ADs may not only explain the delay in onset of therapeutic action of ADs; they may also explain why some patients fail to respond to ADs, as…
It is possible that in such patients the initial pharmacological actions are not translated into the required delayed pharmacologic and genetic actions.
Function Pharmacokinetics: How the body acts on the drug. Pharmacodynamics: How the drug acts on the body,
especially the brain. Drug is absorbed and delivered through the gut wall to
the liver to be biotransformed so that it can be excreted.
CYP450: enzyme in the gut wall or liver converts the drug substrate into a biotransformed product in the bloodstream.
After the passing through the gut wall and liver, the drug will exist partly as unchanged drug and partly as biotransformed drug.
CYP450 Systems
1A2Substrates of this enzyme:clomipramineimipramine
Biggie for ADs
fluvoxamine inhibits
2D65-10% of Caucasians are poor metabolizers
Several SSRIs are inhibitors (paroxetine, fluoxetine – most)
2C920% of Japanese and Chinese persons
3-5% of Caucasians
2C19Inhibitors: bupropion, fluphenazine, sertraline
Inducers:carbamazepine, ethanol, phenytoin, St. Johns’ wort
3A4Some BDZs are substrates
Some ADs are inhibitors (nefazodone)
Mood stabilizers
Classical ADs: MAOIs & TCAs
MAOIs – the very first! 1950s, 1960s Anti-TB drug Great for panic and social phobia Used to stop ‘em…dead! Subtypes: A (depression – 5-HT, NE),
B (anti-neurodegenerative - Parkinson’s) Hypertensive crisis
MAOI Diet Cheese pizza, sour cream, yogurt, and all cheeses except
cream and cottage Beef and chicken livers, unrefrigerated fermented
sausage, summer sausage, bologna, salami, pepperoni, tofu, pickled fish/herring, lox caviar, dried salted herring/other smoked fish
Broad bean pods, fava beans, Italian green beans, snow pea pods, sauerkraut, avocados
Chocolate cake, cookies, ice cream, pudding, chocolate candy
Chianti, sherry, red, burgundy, ale, beer, vermouth, Reisling, liqueurs
Salad dressings with cheese or MSG Brewer’s yeast/yeast extract (e.g., some soups, sauces,
gravies), MSG, meat tenderizers , soy sauce.
MAOI Medication Interactions Sympathomimetics General anesthetics Local or spinal anesthetics w/ epi (e.g., Novocaine) OTC cough, cold and sinus w/ sympathos (e.g.,
Actifed, Sudafed, Contact, Dristan, Afrin, NyQuil, Dimetapp, Triaminic, etc.)
Demerol and other narcotics containing codeine, morphine, hydrocodone (e.g., Percocet, Percodan)
Cocaine Macrolantin Other ADs
MAOIs-ADrug Form Generic Daily
DoseMax Price
(qd dose)
Marplan
10mg tab
No 30mg 60mg $2.45
Nardil 15mgtab
No 60mg 90mg $2.64
Parnate
10mgtab
No 40mg 60mg $3.94
MAOIs-B & RIMAs Selegiline – parkinsonism…
Emsam (selegiline): greater affinity for B, but works on both at AD doses
6/9/12mg transdermal/qd – no restrictions at 6
RIMAs not available in US Manerix – few dietary restrictions
Pharmacological Actions - MAOIs
Readily absorbed through GI Peak plasma in 2hr. T ½ is 2-3hr. Irreversibly inactivate MAOs – i
dose can last for 2w.
Therapeutic Indications –MAOIs
Depression, esp. that associated with mood reactivity, extreme sensitivity to interpersonal loss or rejection, prominent anergia, hyperphagia, hypersomnia (atypical features)
Also great for panic, PTSD, AN, BN, SP and pain syndromes.
Refractory Panic (high) OCD (none) GAD (moderate) BDD (moderate)
Precautions & Adverse Reactions – MAOIs
Orthostasis, insomnia, weight gain, edema, sexual dysfunction
(divide dose, increase fluids/salt, support stockings, take in a.m., add sleep agent, or…switch)
HTN crisis w/o tyramine (Parnate) – avoid Taper and wait for >2w w/ a switch
Paresthesias, myoclonus, muscle pains Pyridoxine 50-150mg/d
Less cardiotoxic, epileptogenic compared to TCAs Caution, though, w/ renal, CV and hyperthyroidism May alter dosage of a hypoglycemic agent Associated w/ induction of mania in pts. in depressed
phase of BPAD I and triggering psychotic decompensation in scz
Contraindicated in pregnancy/nursing
Precautions & Adverse Reactions – MAOIs OD: agitation coma w/
hyperthermia, HTN, tachypnea, tachycardia, dilated pupils and hyperreflexia, involuntary movements (face, jaw) Asymptomatic 1-6hrs. acidify urine, dialyze Multi-drug (esp. 5-HT) – increase effects
Precautions & Adverse Reactions – MAOIs Labs:
DM meds (hypoglycemia) minimal, false elevation of TFTs Periodic LFTs
TCAs Wide range: MDD, Panic, GAD, PTSD, OCD, EDs, Pain
Syndrome Yet, very toxic and we have alternatives Significant FPE Peak plasma 2-8hrs T ½ 10-70hrs 2D6: (Is) quinidine, cimetidine, fluoxetine, sertraline,
paroxetine, phenothiazines, carbamazepine, some antiarrhymics (propafenone, flecainide)
Block reuptake of NE, 5-HT Competitive antagonists of muscarinic acetylcholine,
H1, alpha-1, -2 Use if cannot tolerate anxiety/GI upset (SSRIs)
TCAs – Approved / Off-Label Uses
MDD: induce mania in susceptible pts. (compared to bupropion, SSRIs)
Panic: imipramine, yet anxiogenic, so start low, go slow GAD: doxepin, imipramine OCD: clomipramine (2-4w…4-5m) and depressed pts.
w/ marked obsessive features EDs: imipramine, desipramine, clomipramine Pain: any Enuresis: imipramine Peptic ulcer: doxepin Others: narcolepsy, nightmare d/o, PTSD, sometimes
for ADHD, sleepwalking, separation anxiety, sleep terrors, premature ejaculation, movement d/os
Precautions & Adverse Reactions – TCAs
Anticholinergic, sedation, orthostasis, seizure, conduction abnormalities, weight gain
Can induce mania (over SSRIs, bupropion) May exacerbate psychotic d/os Confusion, delirium
Tachycardia, flattened T waves, prolonged QTc intervals, depressed ST segments
Don’t use w/ cardiac pts., unless other agents have failed (monitor)
Sore throat in initial stages – monitor Transient increase in LFTs vs. hepatitis
Drug Interactions – TCAs MAOIs Antihypertensives
Esimil, Ismelin (block reuptake) propranolol, clonidine (also block) Aldomet + TCA = agitation
DA blockers perphenazine = doubling of plasma [ ] of both products (add to anticholinergic SE
profile, too) Sympathomimetics
Serious CV effects CNS depressants
Opioids, EtOH, anxiolytics, hypnotics, OTC cold remedies Oral contraceptives
BCPs may decrease TCA plasma [ ] through the induction of hepatic enzymes Diamox, ASA, cimetidine, thiazide diuretics, fluoxetine, sodium bicarbonate =
increase, while ascorbic acid, ammonium chloride, barbiturates, cigarette smoking, carbamazepine, chloral hydrate, lithium decrease levels
TCA Dosages / Clinical Guidelines
DRUG TABLET (mg) CAPSULES PARENTERAL (mg/mL)
SOLUTION (mg/mL)
imipramine 10, 25, 50 75, 100, 125, 150
12.5
desipramine 10, 25, 50, 75, 100, 150
25, 50
trimipramine 25, 50, 100
amitriptyline 10, 25, 50, 75, 100, 150
10
nortriptyline 10, 25, 50, 75 10/5
protriptyline 5, 10
amoxapine 25, 50, 100, 150
doxepin 10, 25, 50, 75, 100, 150
10
maprotiline 25, 50, 75
clomipramine 25, 50, 75
Clinical Guidelines of TCAs Prior to tx: PE, CBC w/ diff, lytes, LFTs, EKG (esp. women >40,
men >30)
Contraindicated in pts. w/ a QTc >450msc
Consider using newer agents 1st, esp. if pt. has an interfering medical dx
In kids, elderly – avoid, but if need to use, EKG should be monitored frequently
Those w/ chronic pain might be sensitive to initial dosing, but may benefit later
Taper to avoid cholinergic rebound syndrome
Dosing & Levels – TCAsDrug Usual Adult Dosage Range
(mg/d)Therapeutic Plasma [ ](mcg/mL)
Tofranil 150-300 150-300
Norpramin 150-300 150-300
Surmontil 150-300 ?
Elavil 150-300 100-250
Pamelor 50-150 50-150
Vivactil 15-60 75-250
Asendin 150-400 ?
Sinequan 150-300 100-250
Ludiomil 150-230 150-300
Anafranil 130-250 ?
TCAs & OD Serious, can easily be fatal NRF, <1w quantity for those at risk amoxapine – most fatal OD Sx:
agitation, delirium, convulsions, hyperreflexia, bowel/bladder paralysis, dysregulation of BP, T and mydriasis…coma, respiratory depression
cardiac arrhythmias may not be correctable, and are at risk for up to 4d s/p OD d/t long T ½
SSRIS(the ones we know and love)
fluoxetine – 1987
Rapidly eclipsed the MAOIs/TCAs
Don’t necessarily work better, but are safer and have a less (different) SE profile
Subtle differences between compounds: T 1/2 , potency for reuptake inhibition and affinity for some other receptors
Overall, less effects on adrenergic, histaminergic and cholinergic
Pharmacologic Actions – SSRIs Selectively block the reuptake of 5-HT presynaptically Slightly different pharmacokinetic profiles, as each drug is
structurally different from the others Many are highly protein bound Varying T ½ - 24hr to several days
fluoxetine (active metabolite) = 7-15d citalopram = 1.5d sertraline / paroxetine = 1d
All are well absorbed and not generally affected by food administration except for sertraline (level may be increased w/ food)
No correlation between T ½ and time to onset All eliminated in urine as active metabolites citalopram / escitalopram – more selective for 5-HT receptor
blockade
Indications For / Off-Label Use
of SSRIs MDD – acute, single, recurrent, prevention, etc. DD, PD OCD (may need more, take longer) GAD, SP, PTSD AN, BN (APA recommends use for persistent depression after pt.’s gained wt.) BDD PMDD Children
Repetitive-type abnormalities, e.g., autism, ADHD (as adjunct), MR/DD, chronic enuresis
Other complex behavioral d/os Obesity (high dose fluoxetine) Binge eating (sertraline) Substance abuse Decrease aggressive behaviors – impulsivity / uncontrolled anger in all ages
Migraine / cluster HAs Diabetic neuropathy, facial pain, fibrositis, arthritis, RLS
Pharmacokinetic Profiles – SSRIs
Drug Time to Peak Plasma [ ]
T ½ T ½ metabolite
Time to Steady State (days)
Plasma-Protein Binding (%)
fluoxetine 6-8h 4-6d 4-16d 28-35 95
fluvoxamine
3-8h 15h -- 5-7 80
paroxetine 5-6h 21h -- 5-10 95
sertraline 4.5-8.5h 26h 62-104h 5-7 95
escitalopram
3-5h 30h 50-60h 10 90
citalopram 4h 35h 3h 7 80
Basics – SSRIs
Drug Generic/Supply Dose/Day Price Index ($ cost of dose/d)
Prozac Y/Soln, Tabs, Delayed Cap
60mg 1.10
Zoloft Y/Soln, Tabs 100mg 3.02 (brand)
Paxil Y/Soln, Tabs 40mg 2.97
Luvox Y/Tabs 200mg 5.25
Lexapro N/Soln, Tabs 20 2.65
Celexa Y/Soln, Tabs 40 2.65
Precautions & Adverse Reactions – SSRIs
¾ of pts. experience no SEs ¼ have SEs in first 2w, usually subside 10-15% are unable to tolerate
Sexual dysfunction: 50-80%, might not go away… Decrease dose; switch (bupropion, nefazodone); add
(bupropion) GI: sertraline, fluvoxamine, citalopram
N, V, D, anorexia, dyspepsia – transient? Weight gain: initially lose, but 1/3 will gain
(>20lbs.); paroxetine (d/t anticholinergic SE) HAs: 18-20% (fluoxetine – most); alternately,
SSRIs are wonderful for tension HAs/migraines
Precautions & Adverse Reactions – SSRIs
CNS Anxiety: fluoxetine (most), but then tx it Insomnia/sedation: ¼ have insomnia (fluoxetine – take in
a.m.); sertraline = fluvoxamine; citalopram/paroxetine – sedation
Tx w/ trazodone, BDZ, other off-labels Nightmares: small amount of pts. (resolves) Seizures: 0.1 - 0.2% of all pts. txd w/ SSRIs (comparable to
other ADs/placebo) EPS:
Tremor 5-10% TD (exceptionally rare) Pts. w/ well-controlled Parkinson’s – acute worsening of their motor
symptoms Bruxism (buspirone) Most common w/ fluoxetine
Precautions & Adverse Reactions – SSRIs
Anticholinergic: paroxetine (mild)
opposite of S.L.U.D. Dry mouth (up to 20%) Dose-dependent
Hematologic: Can decrease plt. function = bruisability paroxetine, fluoxetine (reversible neutropenia – rare, usually if concurrent
w/ clozapine)
Electrolyte / Glucose: Hypoglycemia (rare – DM pts. need to be careful) Hyponatremia/ADH release (also rare) – if diuresing/H2O deprived
Endocrine / Allergic: Decrease prolactin/galactorrhea (breast changes may take several months
to correct) Various rash types – 4% (d/c)
Precautions & Adverse Reactions – SSRIs
5-HT Syndrome: SSRI + MAOI or SSRI + L-tryptophan or SSRI + lithium = can raise 5-HT
concentrations to toxic levels, causing cascade of: D Restlessness Extreme agitation Hyperreflexia Autonomic instability Myoclonus Seizures Hyperthermia Uncontrollable shivering, rigidity Delirium Coma Status epilepticus CV collapse Death
Precautions & Adverse Reactions – SSRIs
5-HT Syndrome Tx: D/C offender Supportive care Nitro Cyproheptadine Methysergide Cooling blankets Chlorpromazine Dantrolene Benzodiazpines Anticonvulsants Mechanical vents Paralyzing agents
Precautions & Adverse Reactions – SSRIs
SSRI W/D: Abrupt discontinuation, esp. w/ a
shorter T ½ (paroxetine, fluvoxamine) After 6w; ends by 3w
dizziness, weakness, N, HA, rebound depression, anxiety, insomnia, poor concentration, UR Sx, paresthesias, migraine-like Sx
Tx: don’t abruptly stop; use fluoxetine
SNRIs “3rd Generation” ADs 5-HT, NE – equal affinity
duloxetine, venlafaxine, mirtazapine Differences among the three:
mirtazapine – antagonist of central presynaptic alpha2-adrenergic receptors; potent antagonist of H1
venlafaxine – a little faster onset w/ rapid dose increase; great for severe MDD w/ melancholy; 1st non-bdz drug (other than buspirone) to be approved for GAD
duloxetine – compared w/ venlafaxine, it has a greater effect on 5-HT reuptake in vitro; approved for diabetic neuropathic pain
Other ADs bupropion (DA, NE) – late 80’s
augmentation, SEs, off-label, etc. be careful w/ OD and EDs – sz d/o
trazodone structurally related to nefazodone, structurally unrelated to SSRIs,
TCAs, MAOIs active metabolite is mCPP (5-HT2c agonist), is especially sedating
(off-label use), blocking H1 priapism (1:6000; surgical intervention in 33%)
nefazodone mixed 5-HT antagonist/reuptake inhibitor great for anxiety less sedation, hypotension than TCAs, trazodone
atomoxetine (NOT approved for depression) – NRI; could use off-label
Special Considerations in the Selection of an AD
Gender: women have less gastric acid / slower
emptying = slower GI absorption volume distribution = more adiposity than
lean muscle H2O retention associated w/ menses =
affects volume distribution, too PO contraceptives can alter hepatic
metabolism (TCAs)
Special Considerations in the Selection of an AD
Ethnicity: AAs slow metabolizers compared to Europeans
d/t metabolic enzyme expression AAs have higher plasma levels per dose of AD
(demonstrated most w/ TCAs) Asians are slower to metabolize nortriptyline than
other groups Minorities were less likely than
nonminorities to be offered AD treatment, independent of dx (study of CMHCs’ prescribing practices in Westchester County, NY)
Special Considerations in the Selection of an AD
Age: Elderly? Steady-state [ ] are minimally affected by
age (except paroxetine) Remember: start low, go slow
Comorbidities: Renal – dose adjustment (except fluoxetine,
sertraline) Liver – can increase levels of TCAs (monitor); give
lower doses of SSRIs; don’t use nefazodone Pregnant Women and Nursing Mothers:
Risks vs. benefits Generally safe, but be careful of w/d for neonate
Mood Stabilizers Agents that are geared at affecting
one phase of illness w/o worsening any other phase(s)
3 families: lithium anticonvulsants atypicals
Lithium 1970 Used the longest, quite frequently and is excellent
for mania, maintenance – all phases Yet non-response rate can be as high as 40% Narrow TI Structurally simple = Li+ MOA: unclear if NTs are involved, like they are in
depression tx; occurs intracellularly w/ second-messenger systems
A monocovalent cation – a direct competitior of Mg+ @ regulatory enzyme, IMPase = reduces intracellular Ca+/protein kinase C activation
Lithium lithium carbonate, Lithobid, Eskalith CR =
immediate and extended (better tolerated, convenience)
Peak plasma 1-4h T ½ 18-36h Rapid, complete absorption Low protein binding No first-pass effect 95% drug excretion by kidneys Can remit mania in many cases, but clinically
an antiepileptic or atypical is also used
Lithium – Labs / Pre-Treatment Testing
CBC Lytes KFTs TFTs EKG Pregnancy
Check level q3-6mos, as well as associated labs/EKG
Normal range: 0.5-1.5mEq/L
Adverse Effects – Lithium Narrow TI
Prolonged exposure to >2.0mEq/L: CNS impairment, renal collapse, coma, permanent brain injury, death
Tox s/s: tremor, confusion, ataxia, N, V, D, tinnitus, blurred vision, HA, dizziness.
Common SEs: N, V, D, tremor, polydipsia, polyuria, weight gain, hypothyroidism (reversible), fatigue
Drug Interactions – Lithium Increase levels
ACE Is Alprazolam Antipsychotics Fluoxetine Ibuprofen Indomethacin Naprosyn NSAIDs Some antibiotics Aldactone Thiazide diuretics
Decrease levels Caffeine Carbonic
anhydrase Is Dilor Laxatives Osmotic diuretics Atenolol Theophylline
Lithium & Pregnancy No!…? 1st trimester = Ebstein’s anomaly (1:2000) However, discuss the risk and benefit Be very clear in initial interview about
risks, as a female pt. might be well into her 1st trimester…
Retrospective studies have shown to use aggressive pharmacotherapy in the immediate PPP (90% of bipolar I females are at risk for relapse in first 2mos of PP)
Depakote / Depakene Acts at Na channels, at steps in GABA
metabolism, and on the activity of histone deacetylase
-Kote “coats” Available in IR, ER Rapid absorption, reaching peak plasma in 2-4h Bioavailability unaffected by food, though
absorption may be delayed Rapid distribution and high (90%) plasma protein
binding T ½ 9-16h
Depakote / DepakeneUses / Indications
Bipolar I d/o Acute, maintenance, prophylaxis
SCZ (off-label) IED, kleptomania, other behavioral
dyscontrol syndromes Physical aggression, restlessness, agitation Also off-label for anxiety d/os such as panic,
PTSD, OCD, BN MDD EtOH, sedative/hypnotic w/d; cocaine detox Borderline PD
Depakote / Depakene – Pre-Treatment / Labs
CBC w/ diff., LFTs, check levels and associated labs q3-6mos
Level: 50-100mcg/mL, but be clinically-driven
Check for bleeding and bruisability
Depakote / DepakenePreparations
Depakene: 250mg caps, #100, $207.01
Depakote: 125mg tab, #180, $110.29; also available in 250mg and 500mg tabs, and in ER (which does not affect timing of lab, but affects timing of dose)
Depakote / Depakene Common SEs:
Alopecia GI upset Sedation Tremor Weight gain
Rare SEs: Acute pancreatitis Anemia Ataxia Bone marrow suppression Breast enlargement Dermatitis Diplopia, dizziness Edema Hepatotoxicity Irregular menses Leukopenia Nystagmus Parotid gland swelling Stevens-Johnson syndrome Thrombocytopenia
Depakote / DepakeneDrug Interactions
2D6 metabolism Can increase phenobarb, phenytoin,
TCAs, Retrovir, diazepam Can decrease lamotrigine,
carbamazepine DVP levels can be increased by ASA,
highly protein-bound drugs DVP levels can be decreased by
carbamazepine, Rifampin, mefloquine
Depakote / Depakene & Pregnancy / Nursing
Do not give to pregnant or nursing pts. Associated w/ neural tube defects
(e.g., spina bifida) in 1-2% of all women during 1st trimester
This risk can be reduced if FA (1-4mg/d) is taken 90d prior to and throughout gestation
Antipsychotics Rapidly expanding! Atypicals over conventionals, w/ birth of
clozapine Newer agents have less EPS, TD, cognitive
impairment, and improvement in negative Sx
Nonconventionals are used for other d/os, not just psychosis
Atypicals: Clozaril, Zyprexa, Seroquel, Risperdal, Geodon,
Abilify
Pharmacology – Atypicals All have affinity for DA, but vary in potency 5-HT2a > D2 (different SE profile compared to
conventionals) Attracted to alpha1/2-adrenergic, muscarinic
acetylcholine, H1 as well Antagonize DA, 5-HT2a Rapidly absorbed from GI tract w/ extensive FPM Highly lipophilic – cross BBB Primarily metabolized by 2D6, 1A2, 3A4 & 2C19 Average T ½ is 20-24h, except for aripiprazole: 95h Parenteral form: olanzapine, aripiprazole, ziprasidone
as IR and risperidone as decanoate
Indications for Use – Antipsychotics
SCZ, Schizoaffective d/o Acute manic/mixed episodes – bipolar MDD w/ psychosis Delusional d/o Delirium Dementia MR Developmental d/o (e.g., autism) Huntington’s Tourette’s Substance-induced psychotic d/o (stimulants, PCP,
levodopa, steroids)
Preparations / Dosage – Antipsychotic
Risperdal (mg tabs 0.25, 0.5, 1, 2, 3, 4; soln; M-tabs;
RisConsta): 2-8mg/d Geodon (mg caps 20, 40, 60, 80; soln): 80-200mg/d Clozaril (mg tabs 25, 100): 25-600mg/d Zyprexa (mg tabs 2.5, 5, 7.5, 10, 15, 20; Zydis; soln):
5-30mg/d Seroquel (mg tabs 25, 50, 100, 200, 300, 400): 150-
800mg/d Abilify (mg tabs 5, 10, 15, 20, 30; soln): 10-30mg/d
Drug Selection & Initiation of Treatment – Antipsychotics
Tests: height, weight, waist circum., BMI; interview about personal and family h/o diabetes or lipid dysregulation
Obtain FBS, lipid panel Is this psychotic episode consistent w/ SCZ? Have affective syndromes such as mania and depression with psychotic
features been ruled out? Is this the patient’s first episode? Previous AP exposure – efficacy and tolerability profiles? H/O EPS or TD? H/O NMS? What Sx are current predominant: + or -? H/O noncompliance/depot exposure? If AP trials have failed, were the doses/duration of tx adequate? Etc.
Side Effect Profile of SGAs
aripiprazole
clozapine risperidone
olanzapine
quetiapine ziprasidone
EPS + 0 ++ + 0 +
TD + 0 ++ + 0 +
NMS ? + + + ? +
Prolactin 0 - + 0 +++ 0 - + 0 0 - +
QTc 0 0 + 0 + ++
Hypotension + +++ + ++ ++ +
Anticholinergic 0 +++ 0 ++ + 0
Hepatic + +++ + ++ + +
Agranulocytosis 0 ++ 0 0 0 0
Sedation + +++ + ++ +++ +
Seizure 0 - + +++ 0 0 - + 0 - + 0 - +
Side Effect Profile of SGAs
S eroq ue lG e od on
R isp e rd a lA b ili fy
M on ito rfo r
M eta bo licS yn d ro m e!
W e ig h t G a inT ie rs
C lozar ilZ ypre xa
Case Study 32yo MWF who’s escorted to the clinic by her BF. Pt.’s been
c/o, and partner corroborates, that she’s been feeling quite sad lately, cannot get out of bed, has been w/ regular crying spells, is sleepless, has felt hopeless and believes she’d be better off dead. She adds that she has no health insurance and is 13w pregnant. You observe that she is nearly morbidly obese. She is not sure, but she’s been so sad that she thinks she’s been hearing her name being called and hears occasional, indecipherable whispers. She’s w/ severe GI discomfort, associated w/ her pregnancy, as well as sedation, probably within the context of both pregnancy and mood. The BF’s asking for a medication to help the pt., and the pt. is very willing to try a product.
What thoughts come to mind as far as a product for this pt.?
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