Pharmacotherapy of Depression and Anxiety

Pharmacotherapy of Depression and Anxiety
Vickie Corbett Ripley, PharmD, BCPP Clinical Pharmacist Practitioner Coastal Plain Hosptial Rocky Mount, NC

Pharmacotherapy for Major Depression
Etiology and Pathophysiology Diagnosis and clinical presentation Antidepressant efficacy and side effects Treating major depression Special Populations Other treatment options Drug interactions

Limbic System Dysfunction

Spectrum of Psychiatric Disorders
ANXIETY Panic disorder GAD OCD Agoraphobia AFFECTIVE Major Depression Bipolar Disorder Dysthymia PSYCHOSES Schizophrenia Schizoaffective

Neurotransmitters and Psychiatric Pharmacotherapy
Anti- Depressants Serotonin Anxiolytics Norepinephrine Anti-Psychotics Dopamine GABA, others

Phases of MDD Treatment
Severity Time

Recurrence After Recovery from Major Depression
n = 555 Unipolar Depressives ( ) Cumulative Probability of Recurrence, % Time to Recurrence, years The NIMH Collaborative Depression Study,

Diagnosis of mental illness
DSM IV (Diagnostic and Statistical Manual of Mental Disorders – 4th edition) Lists criteria necessary to meet diagnosis Useful for standardizing diagnoses To meet most diagnoses generally must Interfere with social or occupational functioning Must be interpreted in context of culture Psychiatry is somewhat different from other medical specialties in that for the most part, rather than relying on labs and objective measures, diagnoses is based on subject report DSM-I introduced in 1950’s was the first manual to contain a description of diagnostic categories Culture – 1) somebody involved in trance ceremony in native american culture in which they are hearing from deceased ancestors are not psychotic b/c it within culture; jimmy swagard hears from g-d, OK if within cultural context

Multiaxial Assessments
Axis I – Clinical Disorders Axis II – Personality disorders and mental retardation Axis III – General medical conditions Axis IV – Psychosocial and Environmental problems Axis V – Global assessment of functioning (GAF) Axis II – often in chart will see it say “deferred”, means that at the time of the evaluation there was insufficient information to make any diagnostic judgment about an axis II diagnosis Stressors are rated on a scale of 1 (none) to 6 (catastrophic) and can be acute (lasting less than 6 months) or enduring. Examples include difficulties with primary support group (i.e. death of a family member, divorce) , problems related to social environmetn (living alone, adjustment to life cycle transition such retirment), educational problems, occupational problems, housing probkems, economic problems, problems with access to health services or legal problems. GAF – rated on a scale of 1 (persistent danger to self or others) to 100 (superior functioning, life’s problems never seem to get out of hand).

Axis I disorders Mood disorders Anxiety disorders
Major depressive disorder Bipolar disorder Anxiety disorders Generalized anxiety disorders Panic disorder Social phobia Obsessive Compulsive Disorder Psychotic disorders - schizophrenia

DSM IV Classification of Major Depressive Episode
Depressed mood and/or loss of Interest present during a two week period Plus at least FOUR of the following symptoms: Weight change Sleep disturbance Psychomotor agitation or retardation Loss of energy Feelings of worthlessness/guilt Loss of ability to concentrate Suicidal ideations

Psychiatric Patient Presentation
Chief Complaint History of Present Illness Past Medical History Family and Social Histories Medications Allegies Review of Systems Physical Examination Mental Status Exam Appearance, behavior, and speech Mood and Affect Sensorium Intelligence Thought process Labs

Symptoms of Depression and Serotonin Function
Depressed or elated Mood Appetite changes Sleep changes Decreased libido Increased pain sensitivity Circadian rhythm disturbances Body temperature changes

Physical and Social Functioning in Depression and Chronic Illness
Wells, et al. J Amer Med Assoc 1989; 262:

Symptoms of Depression (Sig: E caps)
S Sleep I Interest G: Guilt E Energy C Concentration A Appetite P Psychomotor retardation S Suicidality

Treatment choices Psychotherapy Light Exercise Diet Medication
Medication and Psychotherapy Electroconvulsive therapy (ECT)

Psychotherapies Interpersonal therapy Cognitive therapy
Behavior therapy Group therapy Interpersonal – Dep resulting from pts relations with other people, work or marital problems Cognitive – dep resulting from self defeating thoughts, irrational beliefs Behavior therapy – social learning therapy, activity scheduling, problem solving Group therapy – bereavement, chronic illness, med maintenance support groups

Psychotherapy Less severe Less chronic Nonpsychotic
Previous positive response Medical contraindication to medication

Algorithm for Treatment of Uncomplicated Major Depression
1st line: Favorite SSRI or TCA Failed trial: switch to alternative Partial response - increase dose, switch or augment Fully remits (maintain at least 4 to 6 months or longer) 2nd line: Switch or Augment Switch to other favorite - TCA or SSRI Augment with Li or TCA plus the SSRI (consult with psychiatrist) 3rd line: Failed or Partial response to 2nd line Consult with psychiatrist Switch (nefazodone, mirtazepine, bupropion, venlafaxine) Augment with Li or TCA plus the SSRI Adapted from Kando JC et al: in Pharmacotherapy, 4th ed, Dipiro, eds., 1999, p 1156

Target Symptoms and Therapeutic Response Rates
Week One: anxiety insomnia decreased appetite Weeks two and three: increase in energy increase suicide risk increase in libido Up to 4 to 8 Weeks: Improvement in dysphoria or sadness improvement in pessimism improvement in anhedonia

Treatment strategies if no response
Confirm compliance Maximize dose Change drug Combine antidepressants Augmentation therapy

Augmentation medications
Lithium AED’s Stimulants Thyroid Estrogen Sleep aids Pain meds

Melancholic Depression
Clinical Presentation Subtype of severe depression Nearly complete absence of capacity for pleasure Diurnal mood swings (worse in the morning) Excessive guilt and weight loss Unclear if SSRI’s as effective as TCA’s in treatment Some data indicate that mirtazapine and venlafaxine more effective than SSRI’s

Atypical Depression Clinical Presentation
Weight gain or increased appetite Hypersomnia Heavy feeling in arms or legs (leaden paralysis) Interpersonal rejection sensitivity MAOI’s greater efficacy than TCA’s Efficacy of SSRI’s relative to MAOI’s unclear

MDD with psychotic features
Clinical Presentation: Delusions or hallucinations present during depressive episodes Usually need an antidepressant and an antipsychotic

Differentiation Between Depression and Dementia
Area Depression Dementia Depression history (self/family) Present Absent Depression symptoms precede cognitive deficit Present Absent Duration of Symptoms Weeks Months-Years Cognitive Deficit Complains Silent Concern Cognitive Function Test Performance deficits Inconsistent Consistent Response to MSE questions "I don't Know" Attempts to answer Effort on Testing Little Tries hard Baker FM. J National Med Assoc 1991; 83:

Psychiatric Pharmacotherapy
Anxiolytics Benzodiazepines Anti- Depressants Tricyclics MAO Inhibitors SSRIs Mood Stabilizers Anti-Psychotics Phenothiazines Butyrophenones Atypicals

Serotonin receptors 5-HT 2 agitation akathisia anxiety panic attacks
insomnia sexual dysfunction

Serotonin receptors 5-HT 3 nausea gastrointestinal distress diarrhea
headache

Dopamine receptors Stimulation can lead to agitation
aggravation of psychosis

Norepinephrine receptors
Stimulation can lead to activation hypertension panic

Alpha 1 adrenergic receptors
Blockade can lead to dizziness orthostatic hyotension reflex tachycardia

Histamine receptors (H1)
Blockade can lead to sedation weight gain

Muscarinic cholinergic receptors
Blockade can lead to blurred vision dry mouth sinus tachycardia constipation urinary retention memory impairment

Medications TCA MAOI SSRI SNRI (venlafaxine) NDRI (buproprion)
NaSSA (mirtazipine) SARI (nefazadone) SNRI – serotonin/norepi reuptake inhibitor NDRI – norepi/dopamine reuptake inhibitor NaSSA – noradreneric and specific serotonergic antidepressant SARI – serotonin antagonist/serotonin reuptake inhibitor

SSRI and New Antidepressants Metabolism

Antidepressant Side Effects
Drug Sedation Anticholinergic Orthostatic Amitriptyline Doxepin Nortriptyline Desipramine Trazodone Bupropion Fluoxetine -/ Sertraline -/ Paroxetine Venlafaxine +/ Nefazodone Mirtazapine Adapted from: MJ Dewan et al J Geriatr Psychiat Neurol 1992; 40-44

Single mechanism drugs
Mostly noreinephrine desirpramine buproprion Mostly serotonin SSRI’s nefazadone

Tricyclic Antidepressants
Serotonin reuptake Inhibition Norepinephrine reuptake inhibition Anticholinergic effects Alpha1 blockade Histamine blockade

Useful in the treatment of a number of conditions Depression Migraine prophylaxis Neuropathic pain Obsessive compulsive disorder (Clomipramine) Enuresis Panic disorder Sleep disorders Attention deficit / hyperactivity disorder

Clomipramine (Anafranil) mg Amitriptyline (Elavil) mg Doxepin (Sinequan) mg Imipramine (Tofranil) mg Desipramine (Norpramin) mg

Tricyclic Antidepressant
Secondary amine Desipramine (Norpramine) Nortriptyline (Pamelor) Protriptyline (Vivactil) Tertiary amine Amitriptyline (Elavil) Clomipramine (Anafranil) Imipramine (Tofranil) Doxepine (Sinequan) Trimipramine (Surmontil) Greater NE relative to 5HT activity Greater anticholinergic effects

Tricyclic Antidepressant
Secondary amine Desipramine to 300 mg Nortriptyline to 150 mg Protriptyline to 60 mg Tertiary amine Amitriptyline to 300 mg Clomipramine to 250 mg Imipramine to 300 mg Doxepin to 300 Trimipramine 100 to 300 With most TCA’s start with 50 mg and increase by 25 to 50 mg every 3 days (lower for nortriptyline or protriptyline)

TCA plasma concentrations
Nortriptyline - Curvilinear conc/response profile 50 to 150 ng/ml Desipramine 125 to 300 ng/ml Imipramine 200 – 300 ng/ml Not routinely performed but can be useful in certain situations Should be obtained at steady state (at least 1 week after initiating or dose change)

TCA Adverse Events Anticholinergic effects Antihistaminic effects
Alpha1 adrenergic blockade Sexual dysfunction Cardiac conduction delays Can result in arrhythmias in overdose Decreased seizure threshold Toxic in overdose Do not use in acutely suicidal patients

Preferred uses of TCA’s
Depression with Pain Fibromyalgia Migraine insomnia

Least preferred uses of TCA’s
Patients in whom anticholinergic effects would be problematic Overweight patients Suicidal patients Cardiac patients Patients with dementia

Selective Sertotonin Reuptake Inhibitors (SSRI’s)
Fluoxetine (Prozac) Paroxetine (Paxil) Sertraline (Zoloft) Fluvoxamine (Luvox) Citalopram (Celexa) Escitalopram (Lexapro)

Uses of SSRI’s Depression Social phobia Panic disorder
Obsessive compulsive disorder Bulimia Nervosa Post Traumatic Stress Disorder Pre Menstrual Dysphoric Disorder (Sarafem)

SSRI Dosing Dosing Relatively safe in overdose
Fluoxetine to 60 mg Paroxetine to 50 mg Sertraline to 200 mg Fluvoxamine to 300 mg Citalopram to 60 mg Escitalopram – 10 to 40 mg Relatively safe in overdose Relatively safe in patients with cardiovascular disease

SSRI Adverse Effects Gastrointestinal Sexual dysfunction Headache
Nausea, vomiting, diarrhea Sexual dysfunction Headache insomnia Fatigue Agitation Akathesia and dystonic reactions 5HT can reduce DA levels

Differences between SSRI’s
Most likely to cause sedation Paroxetine, fluvoxamine Paroxetine Mild anticholinergic effects Fluoxetine Higher rates of anxiety and nervousness Sertraline More diarrhea

When to use SSRI First line monotherapy Depression
Anxiety (start with low doses) OCD Panic

Least preferred use of SSRI
Patients with sexual dysfunction Patients with secondary refractoriness Patients with nocturnal myoclonus Patients with consistent agitation Patients with consistent insomnia

SSRI Withdrawal Syndromes
More likely to occur with short t1/2 agents (paroxetine warning) May affect up to 1/3 of patients and more likely to be reported with short half-life agents May be due to sudden decrease in available synaptic 5HT in face of down-regulated receptors Onset in 24 to 72 hours and last up to 7-14 days Symptoms: dizziness, nausea, lethargy, headache, flu-like symptoms, parasthesia (electrical “shock-like” sensations)

Discontinuation syndrome
Worse with short acting drugs Taper dose Flu-like symptoms Anxiety GI distress Mood, appetite, sleep changes

Serotonin Syndrome Symptoms
Altered mental status – confusion, agitation Autonomic dysfunction – diaphoresis, tachycardia, BP changes, fever Neuromusucular abnormalities – clonus Allow 2 weeks between MAOI and other antidepressant administration 5 weeks for fluoxetine

Serotonin Syndrome Occurs when several serotonergic drugs combined
Often involves MAOI’s as one of the drugs Other serotonergic drugs implicated SSRI’s TCA’s Serotonin releasing agents (i.e. MDMA or “ecstasy”) Dextromethorphan, meperidine, others

Nefazodone (Serzone, Bristol-Myers Squibb)
Potent 5HT2 receptor antagonist Relatively weak 5HT reuptake inhibition Alpha1 receptor blockade Metabolism: OH-Nefazodone = hours triazole-dione = 18 hours mCPP = 4-8 hours Usual Dosage: mg/day in 2 divided doses Preserves sleep architecture Potent CYP3A4 inhibitor

Therapeutic uses of nefazadone
depression in association with anxiety, agitation, sleep disturbances Prior SSRI induced sexual dysfunction Inability to tolerate SSRI’s Tolerance to SSRI’s

Lest preferred use of nefazadone
Patients with hypersomnia Non-compliance with BID dosing Retarded depression Patients with difficulty with dose titration

Dual-Action Drugs Norepinephrine and serotonin venlafaxine mirtizapine
clomipramine venlafaxine mirtizapine

NaSSA Noradrenergic and specific serotonergic antidepressant
mirtazipine (Remeron) 15-90mg

Mirtazapine (Remeron®, Organon)
Initial Dosing: Start with 15mg qd (hs) (supplied as 15 and 30 mg tablets) Average effective dose is 20-25mg qd Maximum dose=45mg qd Half life Women have longer half-life than men 37 vs 26 hours Half-life allows for qd dosing Dosage adjustments: Any dosage should be made after one to two weeks Adjust dose for hepatic disease Slow titration in the elderly

Mirtazapine (Remeron, Organon)
Receptors: -5HT2 and 5HT3 antagonist, histamine 1, minimal activity on alpha 1, muscarinic, and dopamine Common Side Effects: Somnolence, dry mouth, weight gain Cautions: Can precipitate mania, hepatotoxicity (dose adjust in hepatic disease) Drug Interactions: additive cognitive and motor CNS depression, Metabolized by CYP2D6, 1A2, 3A4,Wait 14 days after stopping MAOI Dosing: Start with Start with 15mg qd, usually mg qd, maximum dose = 45mg qd

Therapeutic uses of mirtazapine
Depression with anxiety or agitation Depression with insomnia Problems with SSRI’s Weight loss Severe depression Loss of response to SSRI’s

Least preferred uses of mirtazapine
Hypersomnia Motor retardation Cognitive slowing overweight

SNRI Serotonin/norepinephrine reuptake inhibitor
venlafaxine (Effexor) mg

Venlafaxine (Effexor, Wyeth-Ayerst)
Dose Serotonin reuptake inhibition Norepinephrine reuptake inhibition Dopamine reuptake inhibition Usual dose: 75 to 225 mg

Therapeutic uses of venlafaxine
At low doses, use as an SSRI At high doses has dual action Patients with hypersomnia Patients with GAD Patients with weight gain

Least preferred use of venlafaxine
Agitated patients Patients with sexual dysfunction Patients with insomnia Patients with labile HTN

Venlafaxine Adverse Effects
Nausea, constipation Headache Dizziness Nervousness Somnolence Dry mouth Sexual dysfunction Increased blood pressure (monitor closely)

NDRI Norepinephrine/dopamine reuptake inhibitor
buproprion (Wellbutrin) mg

Therapeutic uses of buproprion
Patients with retarded depression patients with hypersomnia Non-responders to SSRI’s Non-tolerators of SSRI’s Patients concerned about sexual dysfunction Patients concerned about weight gain Patient with cognitive slowing

Least preferred use of buproprion
Patients with seizure disorders Patients who are seizure prone Patients with head injury Patients non-compliant with multiple daily doses Patients with agitation Patients with insomnia

Comparative Safety and Tolerability Summary
Nausea Common with all Dose related, dissipates with use Diarrhea- higher incidence with Sertraline Dry Mouth- VEN, NEF > PAR, SER > FLU, FVX Anorexia- More likely with Fluoxitine, Venlafaxine Anxiety/nervousness- More common with Fluoxitine Sexual Dysfunction- all SSRIs, Ven > Nefazodone CL DeVane Human Psychopharmacology 1995; 10:S185-S193,

Monoamine Oxidase Inhibitors (MAOI’s)
Used in patients with atypical MDD/ anxiety Phenelzine (Nardil) Tranylcypromine (Parnate) Hypertensive crisis can occur when combined with high tyramine foods or sympathomimetics Aged cheeses, sour cream, wines, beer, canned or processed meats, fermented foods, coffee, chocolate Amphetamines, ephedrine, other decongestants Doses: Phenelzine – 15 to 90 mg Tranylcypromine – 20 to 60 mg

MAOI adverse effects All agents More likely with phenelzine
Sexual dysfunction Mild anticholinergic effects More likely with phenelzine Orthostatic hypotension Sedation More likely with tranylcypromine Insomnia

Drugs Metabolized by Human Liver Cytochromes P450s
Superfamily P-450 Families 3 1 2 Subfamilies A A C D 3A4 1A2 2C9/19 2D6 Members with narrow therapeutic index Theophylline Imipramine (S)-Warfarin Phenytoin Carbamazepine Tolbutamide Imipramine Desipramine Amitriptyline Nortriptyline Thioridazine Terfenadine Cyclosporine Triazolam Imipramine Carbamazepine D. Rodrigues Pharmacogenetics Conf, May 1996

Inhibition of Cytochromes P450

1A2 substrates/inhibitors
Antispychotics TCA’s Fluoroquinolones theophylline

Drug interactions 1A2 Fluvoxamine ++++

2D6 substrates/inhibitors
Antiarrhythmics Antipsychotics Beta blockers Opiates TCA’s

Drug interactions 2D6 Fluoxetine ++++ Sertraline + Paroxetine ++++
Venlafaxine +?

2C substrates/inducers/inhibitors
Barbiturates NSAIDS Warfarin Antifungals TCSA’a

Drug interactions 2C Sertraline Fluoxetine Fluvoxamine ++

3A4 substrates/inducers/inhibitors
Antiarrhythmics Antifungal Antihistamines Antipsychotics Barbiturates Benzodizepines Calcium channel blockers Grapefruit juice TCA’s

Drug interactions 3A4 Sertraline + Fluoxetine ++ Fluvoxamine +++
Nefazadone

Drug Interactions - Herbal Remedies
St. John’s Wort (Hypericum perforatum) Drugs that interact with MAOIs Ginko (Ginko biloba) Anticoagulants (2 cases), or ASA Kava (Piper methysticum) Benzodiazepines (1 alprazolam case), alcohol Ginseng (Siberian ginseng) potentiates MAOIs, stimulants (caffeine) and haloperidol Yohimbine (Pausinystalia yohimbine) a2 antagonist TCA, MAOIs, antimuscarinic agents potentiate yohimbine Wong AHC et al Archives Gen Psychiatry 1998; 55(11)

St. John’s Wort Reduces the AUC of the HIV-1 PI Indinavir
Open-label, Eight healthy volunteers (6M/2F) yo Indinavir 800 mg orally(q8h x4) Blood samples 0-8 hours (AUCss) Before and after SJW 300 mg tid x 14 d (Hypericum Buyers Club) AE’s: taste changes (50%), nausea (25%), circumoral paresthesias (25%) associated with indinavir. Reduced intensity and duration with SJW. Increased resistance and Tx failure? Piscetelli SC Burstein AH, Alfaro RM, The Lancet, 2000; 355(9203) 12 Feb

Basic algorithm Monotherapy Allow time for drug to work (4-6 weeks)
Symptoms will resolve gradually Maximize dose

Selection of Antidepressant
Presenting symptoms Previous response Family history Neurotransmitter profile Co-morbid conditions Human data Side effect profile Potential drug interactions Patient age Compliance Cost

Monitoring Antidepressant Therapy
Monitor antidepressant regimen Is the dosage appropriate? Response favorable and adequate? Side effects present? Review new chart entries New orders? New Diagnoses? Changes in life events? Review progress notes Physician, nursing, social service, psychiatric service Continue therapy 9-12 months if first episode. If multiple: chronic maintenance S.M. Feldman ASCP November 1995

Clinical Management of Treatment Emergent Adverse Effects
Continuation of current pharmacotherapy Dose Reduction Trial period of discontinuing medication Antidepressant substitution Adjunctive therapy (cases reported)

Combining other medications
Add augmentation therapy Consider drug interactions Monitor other medications - OTC’s and herbals - beta blockers - steroids

Combining medications
Use two drugs with different mechanisms SSRI plus venlafaxine mirtazipine buproprion nefazadone Or combinations of non SSRI’s

Depression Co-Morbidity
20% Diabetes mellitus Myocardial infarction 30% to 50% Parkinson's disease 11% to 30% Epilepsy 35% to >50% Chronic pain 15% Chronic medical illness 20% to 50% Stroke 25% to 38% Terminal solid tumors Depression Prevalence Medical Illness

Concurrent medical disorders
Asthma - avoid MAOI Cardiac disease - avoid TCA Dementia - avoid TCA and other anticholinergic drugs Seizures - avoid buproprion and TCA Glaucoma - avoid TCA HTN - watch orthostasis

Antidepressant Selection in the Cardiac Patient
Avoid concomitant Type IA antiarrhythmics (TCA with quinidine or procainamide) BUP, SSRIs, VFX, SRZ appear to be low risk for arrhythmias and orthostatic hypotension Venlafaxine is associated with increases in BP MAOIs, Trazodone, maprotiline, amoxapine, SSRIs, and venlafaxine have not been well studied in CHF APA Practice Guidelines, Am J Psychiatry

Comorbid MDD and Cardiac Disease
Tricyclic antidepressants complicate and/or are contraindicated in specific cardiac conditions Hx ventricular arrhythmia subclinical sinus node dysfunction conduction defects (including asymptomatic) prolonged QT intervals recent history of myocardial infarction Consider using bupropion, fluoxetine, sertraline, paroxetine, nefazodone, citalopram or ECT APA Practice Guidelines, Am J Psychiatry

Comorbid MDD and Cardiac Disease
MAO inhibitors may induce orthostatic hypotension and lead to drug-drug interactions Monitor patient for emergence of cardiac symptoms, ECG changes, or orthostatic BP decrements Major depression is a major risk factor for increased cardiac morbidity and mortality. APA Practice Guidelines, Am J Psychiatry

Depression and Coronary Artery Disease
Januzzi et al. Archives of Internal Med 2000;160(13):

Case of JC 30 year old, married female, 4 children
Feelings of helpless, hopeless, worthless, guilt Started with birth of last child 6 months ago Sleepy and tired all the time, no energy East too much Decreased libido No interest in much FH + depression No other medical problems

Case of BH 54 year old married female, 2 children grown 30 year hx MDD
Multiple medications have been tried Medical Dx – fibromyalgia, IBS, chronic sinusitis Meds – Remeron. Lortab, Bently, Allegra D, various OTC and herbals Previous Ads – Prozac, Paxil, AMI, Effexor, Zoloft, Serzone, Celexa, “everything else” c/o weight gain, still depressed

MDD Presentation in Late Life
Often lacks family history of depression Highest Suicide risk of all age groups twice the risk in elderly white males less in elderly black males same in females Often associated with medical illness Stroke (50% develop clinically significant depression) Parkinson’s disease (40 to 90% have associated depression) Typically seen by primary care physicians and may need referrals to mental health specialist for certain aspects of treatment

Diagnosis and Treatment of Depression in Late Life
Recognition may be more difficult in late life “normal aging” and overshadowed by physical illness Similar social and demographic risk factors: female sex, single (esp. widowed), stressful life events, lack of supportive social network Treatment with sufficient: doses (plasma concentrations) of antidepressants length of treatment (e.g. at least 6 to 12 weeks in the elderly) to maximize likelihood of recovery maintenance treatment for 6 to 12 or more months NIH Consensus Development Conference

MDD Symptomatology in Late Life
Symptoms: irritability, agitation, somatic delusions Somatic complaints: pain syndromes (general, headache, chest, GI), cardiac (palpitations, tightness), abdominal (constipation) Loss of interest or pleasure may appear as apathy

Symptomatology in Late Life (cont’d)
Difficulty in concentration may appear as inattentiveness Disorientation, memory loss, distractibility as “dementia” 10% of “senile or pseudo dementia” is actually depression (now called “dementia syndrome of depression”) depression can coexist with dementia Heterogeneity of geriatric depression (early Vs late onset) early onset has more recurrences, more (+) family history

Response to Effective Treatment of Depression in Late Life
Majority should expect partial or complete remission of depressive symptoms Amelioration of pain and suffering associate with physical illness Enhancement of general mental, physical and social functioning Minimization of cognitive disability NIH Consensus Development Conference

MDD Presentation in the Elderly
“R.M., a 71-year-old male, is brought for psychiatric evaluation by his daughter, C.M., with whom he has been living for the past 3 years. C.M. reports that R.M. had been in good health until 3 months ago when he was noted to keep to himself and began showing little interest in his usual activities. She reports that he used to be a happy, very outgoing personality He has lost weight over the past 4 months, has been noted to be irritable, anxious, and has trouble falling asleep. He also frequently becomes agitated over insignificant things. He has appeared on occasion to be confused and slow in understanding concepts. ....” LK Laird and WH Benefield, Jr. Applied Therapuetics, 1996, pp 76/15-18

MDD Presentation in the Elderly Cont’d
“...His recent physical examination is normal except for benign prostatic hypertrophy (BPH). Laboratory examinations are WLN except for a subnormal serum creatinine. He currently is on no medication except for a daily stool softener and a bulk laxative. Mental Status Examination reveals a thin, nervous, sad-appearing man. His responses to questions are slow. Affect is sad. He shows no signs of delusions or hallucinations. He shows mild impairments in his ability to think through problems and mathematical exercises. He denies suicidal ideation but feels hopeless at the present time.” LK Laird and WH Benefield, Jr. Applied Therapuetics, 1996, pp 76/15-18

MDD Presentation in the Elderly
“How does a depressive episode in late life, such as that in R.M., differ from a depressive episode earlier in life?” “What is R.M.’s differential diagnosis?” “Should R.M. be placed on antidepressant therapy?” What factors would influence drug selection? LK Laird and WH Benefield, Jr. Applied Therapuetics, 1996, pp 76/15-18

The Case of R.M., Cont’d How does the pharmacokinetic profile of the SSRI’s affect your choice? What are the significant drug interacts that should be considered with R.M.’s pharmacotherapy if treatment for other common disorders were added?

For a first episode of depression patients should be on medication for at least 12 months

For a second episode of depression, the patient should be on medication for 2 to 3 years

For a third episode of depression, most patients stay on medication for life

When deciding to take a patient off an antidepressant, the patient’s medical and psychosocial situations must be considered

Patient education Do not perpetuate the stigma of psychiatric illness
Treat the patient with the same empathy, respect and concern you would treat a patient with a medical disorder Explain depression as a medical disorder Do not be afraid to discuss the signs and symptoms of depression

Patient education Encourage compliance with medication
Help patients understand the medications and common side effects Help patients understand there is no magic bullet, but most people are successfully treated

Questions ?

Pharmacotherapy of Depression and Anxiety

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