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162 Cards in this Set
- Front
- Back
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What does DSM-IV stand for?
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Diagnostic and Statistical Manual of Mental Disorders, fourth edition
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What are the 5 axes of DSM-IV diagnosis?
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I--psychiatric diagnosis
II--Personality disorders/mental retardation III--medical diagnosis IV--Psychosocial and environmental problems V--Global assessment of functioning |
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What are the six parts of a mental status exam, and what acronym is used to memorize each part?
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JOIMAT
Judgement: or insight to disease Orientation: alert and oriented to time, place, or person Intellectual functioning: helps determine cognitive status Memory/Mood: both distant and recent events Appearance/Affect: how they physically present Thought: content of thinking, auditory hallucinations, thought blocking, bizarre delusions, loose associations |
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What is the difference between mood and affect?
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Mood is the patient's description of how they are feeling while affect is their physical appearance.
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What are the five parts of DSM-IV criteria for depression diagnosis?
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1. >5 symptoms present for 2 weeks most of the day nearly every day
2. Symptoms cause clinically significant distress or impairment in social, occupational, or other areas of functioning 3. Symptoms are not due to a medical condition or drug use 4. Symptoms are not due to bereavement 5. Symptoms are not due to another mental illness |
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List the nine symptoms DSM-IV lists as basis for depression diagnosis. Which two do you need at least one of?
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**Depressed Mood
**Loss of interest or pleasure Appetite or weight change Sleep disturbance Psychomotor agitation/retardation Fatigue/Loss of Energy Feelings of worthlessness/guilt Decreased concentration/indecisiveness Suicidal Ideation |
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What are the five types of depression?
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Major Depression (typical, atypical, psychotic)
Dysthimia Organic Causes Substance Induced Medication Induced |
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List five risk factors for depression:
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Family History
Female Previous Depressive Episode Chronic Medical Illness Substance Abuse |
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Explain two pathophysiological mechanisms hypothesized as the cause of depression:
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Monoamine Hypothesis (MAO creates a state of decreased NTs, MAOI blocks MAO and allows more NTs to reach receptors)
NT Receptor Hypothesis (Decreased NT amounts due to upregulation of receptors; AD blocks the reuptake pump causing more NT to remain in synapse; increase in NT causes receptors to down regulate over 4-6 weeks; gradually increasing amount of NTs available and gradually decreasing side effects of med as receptors downregulate) |
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Explain D-SIG-E-CAPS:
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D--depressed mood
S--sleep I--interest G--guilt E--energy C--concentration A--appetite P--psychomotor S--suicide |
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Why is it necessary to check lab values before diagnosing depression?
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Thyroid levels can indicate hypothyroidism; depression is a symptom of hypothyroidism.
Urine Drug Screen will be indicate whether patient is currently using illicit drugs which may cause depression. |
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List five TCAs
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Amitriptyline (Elavil)
Nortriptyline (Pamelor) Imipramine (Tofranil) Desipramine (Norpramin) Clomipramine (Anafranil) |
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What is the MOA of TCAs? What is the difference between secondary and tertiary molecules? Which molecules have less side effects?
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Primarily 5-HT and NE reuptake block.
Tertiary amines have a greater ability to block 5-HT reuptake while secondary amines block NE more effectively. Secondary amines have less side effects. |
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List five types of side effects associated with TCAs:
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Cardiovascular (slowing of H-V conduction, 1st degree AV block, Delirium, Grand Mal Seizures, Coma, Cardiac Arrhythmia, Cardiac Arrest)
Anticholinergic Sedation Weight gain Sexual Dysfunction |
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Do TCAs have many or few interactions?
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many, many, many
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List two MOAIs (brand and generic)
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Phenelzine (Nardil)
Tranylcypromine (Parnate) |
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Explain the MOA of MAOIs:
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irreversible inhibition of MAO A and B, resulting in increased levels of 5HT, NE, and DA
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List the side effects of MAOIs:
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hypotension
dizziness weight gain insomnia cardiac effects constipation sexual dysfunction |
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What is the main risk with MAOIs?
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hypertensive crisis
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What are two ways MAOIs can cause hypertensive crisis?
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Food-Drug Interactions (tyramine containing foods: aged cheese, cured meats, banana peels, sauerkraut, soy sauce, tap beer, *red or white wine, *bottled or canned beer)
Drug-Drug Interactions: (SSRIs, TCAs, Stimulants, Levodopa) |
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What is selegiline?
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MAOI that has action on both MAO-A and MAO-B (transdermal patch)
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List six SSRIs:
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Citalopram (Celexa)
Escitalopram (Lexapro) Fluoxetine (Prozac) Fluvoxamine (Luvox) Paroxetine (Paxil) Sertraline (Zoloft) |
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List the unique characteristics of the six SSRIs we are responsible for:
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Fluoxetine: long t1/2, active metabolite (OK if pt misses a dose), CYP2D6, 3A4, 2C inhibition)
Sertraline: active metabolite Fluvoxamine: CYP1A2, 3A4, 2C inhibitor Paroxetine: Anticholinergic, shortest t1/2, no active metabolite, CYP2D6 inhibition Citalopram: only 5-HT activity Escitalopram: S-enantiomer of citalopram |
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List short term and chronic side effects of SSRIs:
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Short term: nausea, diarrhea, sedation, insomnia, anxiety
Chronic: headache, sexual dysfunction, night sweats, nightmares |
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List common symptoms of Serotonin Syndrome:
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hyperthermia
excitement rigidity hypotension diaphoresis tachycardia |
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List four AD categories besides TCAs, SSRIs, and MAOIs:
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SNRI
NDRI S2 Antagonists alpha-2 Antagonists |
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Name two SNRIs used to treat depression:
(describe) |
Venlafaxine (Effexor)
--SNRI effects at doses >150 mg daily, otherwise SSRI --active metabolite Duloxetine (Cymbalta) --5HT and NE reuptake inhibitor --CYP2D6 and 1A2 substrate |
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List side effects of venlafaxine and duloxetine:
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venlafaxine:
nausea/diarrhea headache HTN sexual dysfunction nervousness insomnia (using the XR formulation can reduce the side effect profile) duloxetine: nausea, insomnia, headache |
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What is Desvenlafaxine?
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major active metabolite of venlafaxine (SSRI and SNRI)
XR tablet intended for once daily dosing |
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Name an NDRI and three contraindications:
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Bupropion (Wellbutrin, SR, XL)
--seizure disorders --eating disorders --patients on Zyban for smoking cessation |
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List side effects of bupropion:
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GI upset
restlessness insomnia seizures headache NO SEXUAL DYSFUNCTION |
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Name an S2 antagonist and describe:
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Nefazodone (Serzone)
--MOA: SRI and S2 antagonist, some NE activity at high doses (prevents reuptake and increases production of NE and 5HT) --Potent 3A4 inhibitor --brand was pulled because of liver damage |
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List side effects of nefazodone:
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dry mouth
sedation nausea dizziness constipation liver failure: monitor LFT's NO SEXUAL DYSFUNCTION |
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List an alpha-2 antagonist and common side effects:
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Mirtazapine (Remeron)
--results in increased NE and 5HT --dosed at bedtime --WEIGHT GAIN --SEDATION --dry mouth --constipation --NO SEXUAL DYSFUNCTION |
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Explain Trazodone:
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--potent antihistamine
--large doses needed for AD effect so used mostly as a sleeper |
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Explain St. John's Wort:
(interactions?) |
Herbal OTC
Active ingredient: hypericum MOA: similar to SSRI interacts with OCP |
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Explain the therapeutic trial with ADs:
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--titrate to effective dose
--6-8 weeks at effective dose (4-6 weeks needed for effect typically) --do not change medication quickly (leads to more side effects, decreased effectiveness, decreased patient satisfaction) |
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Explain options for refractory depression:
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--assure adequate trial of initial agent
--assess for unrecognized drug and medical causes for depression --combination ADs (use drugs from different classes) --augment AD therapy with lithium, APs, stimulants, thyroid --ECT |
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List six factors that may play into selecting an AD:
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personal history
family history medical history cost convenience side effects |
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When is suicide risk the greatest?
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Once patient has started AD therapy and has more energy to carry out plan
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What are the goals of AD therapy?
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--eliminate/reduce signs and symptoms
--restore occupation and social functioning --reduce risk of relapse and recurrence |
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Explain the three stages of AD symptom remission:
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1-2 Weeks (decreased anxiety, improvement in sleep, improvement in appetite)
2-4 weeks (increased activity, sex drive, self-care, and memory, thinking and movements normalize, sleeping and eating patterns normalize) 4-6 weeks (relief of depressed mood, less hopeless/helpless, thoughts of suicide subside) |
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List the criteria for medicinal management of depression:
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1. Goal is preventing new episodes of depression
2. Potential candidates: --three or more episodes of major depressive disorder --two episodes and: ---family history of bipolar disorder in 1st degree relative ---history of recurrence within 1yr after d/c of effective PcTx, or poor symptom control in continuation ---family history or recurrent major depression in a first degree relative ---onset prior to age 20, or after age 60 ---both episodes were severe, sudden or life threatening in the past 3 years ---concurrent depression and dysthymia |
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B/G: amitriptyline
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Elavil
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B/G: nortriptyline
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Pamelor
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B/G: imipramine
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Tofranil
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B/G: desipramine
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Norpramin
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B/G: clomipramine
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Anafranil
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B/G: phenelzine
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Nardil
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B/G: tranylcypromine
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Parnate
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B/G: selegiline
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Eldepryl
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B/G: citalopram
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Celexa
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B/G: escitalopram
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Lexapro
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B/G: fluoxetine
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Prozac
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B/G: fluvoxamine
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Luvox
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B/G: paroxetine
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Paxil
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B/G: sertraline
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Zoloft
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B/G: venlafaxine
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Effexor
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B/G: duloxetine
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Cymbalta
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B/G: desvenlafaxine
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Prystiq
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B/G: bupropion
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Wellbutrin
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B/G: nefazodone
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Serzone
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B/G: mirtazapine
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Remeron
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Define: existential mood changes
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normal fluctuations in mood
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Define: euthymia
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Describes a mood state in which the person is neither depressed and nor euphoric; this is the baseline condition around which existential mood fluctuations occur.
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Define: pathological mood changes
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A mood becomes pathologic when it produces significant psychic distress and/or significant interference with social, occupational, or other important areas of functioning
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List the four types of mood episodes:
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major depressive episodes
manic episodes hypomanic episodes mixed episodes |
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Briefly explain major depressive disorders:
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--depressed mood
--markedly diminished interest or pleasure --change in apetite --insomnia or hypersomnia -psychomotor agitation or retardation --fatigue or loss of energy --feelings of inferiority, inappropriate guilt --decreased ability to think, concentrate, or make decisions --recurrent suicidal thoughts or a suicide attempt |
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Briefly explain manic episodes:
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--inflated self-esteem or grandiosity
--decreased need for sleep --excessive or pressured speech --flight of ideas or racing thoughts --distractability --increase in goal directed activity --excessive involvement in pleasurable activities which have a high potential for negative consequences |
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Briefly explain mixed mood episodes:
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--defined as a week in which both major depressive episodes and manic episodes occur
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Briefly explain hypomanic episodes:
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--basically a mild form of a manic episode
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List the seven types of mood disorders:
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major depressive disorder
dysthymic disorder bipolar 1 disorder bipolar 2 disorder cyclothymic disorder mood disorders due to a general medical condition substance induced mood disorder |
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Briefly explain Major Depressive Disorder:
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defined by one or more major depressive episodes with no history of manic, hypomanic, or mixed episodes
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Briefly explain dysthymic disorder:
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defined by the presence of what might be characterized as an incomplete depressive episode which persists for at least two years
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Briefly explain Bipolar 1 Disorder:
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characterized as major depressive disorder with at least one instance of mania or of a mixed episode (can actually have this without major depressive order too, as long as you have one period of mania)
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define: rapid cycling
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present when there have been 4 or more individual mood episodes in the previous 12 months
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Briefly explain Bipolar 2 Disorder:
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characterized by one or more major depressive episodes and at least one hypomanic episode (no full manic episodes)
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Briefly explain Cyclothymic Disorder:
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chronic, fluctuating mood disturbance lasting at least 2 years and involving numerous periods of hypomanic symptoms and numerous incomplete depressive episodes
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Briefly explain Mood Disorders due to a general medical condition:
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a direct physiological consequence of a medical condition
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Briefly explain Substance Induced Mood Disorder:
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a direct physiological consequence of a substance (intoxication with alcohol, amphetamines, hallucinogens, etc...)
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Are mood disorders biologically based or environmentally based?
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Both!
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List five pieces of evidence supporting a biological basis of mood disorders:
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1. strong genetic linkage
2. respond well to drug treatment 3. drugs can produce mood disorders 4. episodes occur at regular intervals 5. evidence of CNS aminergic dysfunction |
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Classically, which two NTs were included in the aminergic hypothesis?
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NE, 5-HT
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Name two currently used MAOIs for AD:
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Phenelzine
Tranylcypromine |
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At what concentration (high, medium, low) is seleligine effective for treating depression?
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high
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Where is MAO located?
What does it do? How many isoforms are there? |
--mitochondria
--oxidatively deaminates monoamines --two isoforms, MAO-A and MAO-B |
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List 5 preferred substrates for MAO-A:
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dopamine
5-HT NE E tyramine |
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List 2 preferred substrates for MAO-B:
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dopamine
tyramine |
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Identify three locations and functions of MAO in the body:
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-GI tract mucosa--destroys ingested monoamines in food
-Liver--destroys circulating monoamines such as E and NE released by the adrenals, NE released from adrenergic nerve terminals and any ingested monoamines that survived GI MAO -Peripheral Aminergic Nerve Terminals--keeps cytoplasmic concentration of the monoaminergic NT low (NE, DA, 5-HT) |
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Are MAO inhibitors reversible or irreversible?
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both
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List several MAOIs which bind irreversibly, explain how function of MAO is regained, and state how long this can take.
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--Phenezine, tranylcypromine, isocarboxazid, deprenyl
--new MAOs are synthesized --can take up to two weeks (must wait two weeks to start interacting drug) |
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Name a reversible MAOI, explain how it is effective, and state the abbreviation for reversible inhibitors.
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--Meclobamide
--drug concentration must always be high enough to fill all MAOs present --Reversible Inhibitor of Monoamine oxidase A (RIMA) |
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List three non-specific inhibitors of MAO
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phenelzine
tranylcypromine isocarboxazid |
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Name one MAO-B specific inhibitor
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Deprenyl (seleligine)
--specific for MAO-B at normal dosage range, above normal dosages it becomes non-specific |
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Name one MAO-A specific inhibitor
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Meclobamide
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Explain the antidepressant effect of MAO inhibition:
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MAO inhibition results in decreased cytosolic breakdown of NT in aminergic regions. This leads to increased cytosolic concentrations of NT and maximum filling of storage vesicles. This also leads to non-exocytotic efflux of NT into the synapse and release of maximally filled vesicles with each action potential. Eventually, this leads to enhanced neurotransmission at hypofunctional CNS NE and/or 5HT synapses.
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Explain non-exocytotic release of NT
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reverse of the membrane transporters that pump it in (in PNS, similar to uptake1; in CNS, similar to NETransporter and SERitoninTransport)
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Why is MAO-A inhibition necessary for an antidepressive effect?
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MAO-A specifically breaks down 5-HT and NE
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Do MAOIs have a hypotensive or hypertensive effect? Does this make sense?
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hypotensive.
nope. |
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List TWELVE adverse effects of MAOI therapy:
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1. psychostimulant effects (insomnia, agitation)
2. switch to mania or rapid cycling 3. activation or exacerbation of psychotic symptoms 4. increased suicidality 5. postural hypotension 6. sexual dysfunction 7. weight gain 8. muscarinic blocking-like effects (mydriasis, dry mouth, constipation, blurred vision, urinary problems) 9. hypertension and hypertensive crisis 10. serotonin syndrome 11. acute overdose toxicity 12. abuse and dependence factors |
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Explain the production of hypertensive crises with MAOIs: (two methods)
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1. tyramine from foods reaches NE terminals causing the release of large amounts of NE into the circulation
2. use of other drugs which increase NE concentration at vascular alpha-1 and cardiac beta-1 receptors (ephedrine, pseudoephedrine, amphetamines, E, NE, PE, SNRIs, TCAs, maprotiline, amoxapine, nefazodone, cocaine, methylphenidate, buspirone) |
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Explain what causes serotonin syndrome and list accompanying symtpoms:
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excessive CNS 5-HT activity (confusion, agitation, myoclonus, rigidity, rhabdomyolysis, tremor, hyperreflexia, sweating autonomic instability, coma, fatality)
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--How fast is the onset of action for MAOIs used to treat depression?
--What is the last symptom to respond? |
--1-3 weeks (usually go with 4-6 weeks for patient to feel effect)
--mood elevation is the last symptom to respond |
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define: acute treatment
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treatment of depression symptoms, and not the depressive episode
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define: continuation treatment
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continued use of an AD for a minimum of 6 months after complete remission of therapy to prevent relapse
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define: prophylactic/preventative treatment
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continued use for 3-5 years to prevent relapse
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What is the risk of using ADs in bipolar patients?
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ADs may cause the patient to experience manic episodes.
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Explain the use of MAOIs in the treatment of chronic pain syndromes (especially neuropathic pain):
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MAOIs inhibit neurotransmission of pain signals by increasing the amount of NTs available????
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Explain the effect of SNRIs on NT reuptake and receptor/channel blockade:
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--inhibits both 5HT and NE reuptake (stronger 5HT reuptake blockade than NE reuptake blockade)
--minimal blockade of M, H-1, and a-1 receptors and sodium channels |
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Explain the similarities and differences between the side effect profile and clinical uses of SSRIs and SNRIs:
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similar side effects except SNRIs can cause moderate hypertension
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Describe venlaxafine and what is unique about its effect on reuptake:
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--blocks both NE and 5HT but NE block is only at high doses
--metabolized by 2D6 |
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How does desvenlaxafine relate to venlaxafine?
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--desvenlaxafine is an active metabolite of venlaxafine
--des. is much more potent and blocks NE better throughout its dosing range --not necessarily more effective than venlaxafine however |
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Describe the difference between duloxetine and venlaxafine/desvenlaxafine:
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blocks NE and 5HT better throughout its dosing range
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Explain the MOA of SSRIs:
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Selectively blocks presynaptic reuptake of 5-HT. SSRIs do not block M, H-1, or a-1 receptors or sodium channels so the side effect profile is much better than TCAs.
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List side effects that occur in TCAs that do not occur with SSRIs:
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--sedation
--anticholinergic effects --postural hypotension --weight gain --cardiac effects --seizures |
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List the most common side effects of SSRIs:
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nausea
nervousness insomnia headache sexual dysfunction initial weight loss (due to action on 5HT receptors) |
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What two classes of drugs can interact with SSRIs to cause serotonin syndrome?
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MAOIs
triptans |
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Which SSRI(s) affect(s) the metabolism of CYP1A2? What other drug plasma levels are affected?
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--fluvoxamine inhibits CYP1A2
--large increases in plasma levels of duloxetine, caffeine, and theophylline |
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Which SSRI(s) affect(s) the metabolism of CYP3A4? What other drug plasma levels are affected?
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--fluvoxamine and fluoxetine inhibit CYP3A4
--large increases in plasma levels of carbamazepine, triazolam, and alprazolam |
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Which SSRI(s) affect(s) the metabolism of CYP2D6? What other drug plasma levels are affected?
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--fluoxetine, fluvoxamine, and paroxetine inhibit 2D6
--major increases in plasma levels of TCAs and atomoxetine |
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Relate the overdose toxicity of SSRIs to TCAs:
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SSRIs have a much lower toxicity, much less cardiac effects, and less seizures
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Describe abuse and dependence factors of SSRIs:
Additionally, which SSRIs have the longest and shortest half-lives? |
-There is no psychological or physical dependence associated with SSRIs; however doses must still be tapered to prevent withdrawal symptoms.
--Fluoxetine has a long half-life and is self tapering (takes 5 weeks to wash out) --Paroxetine has a much shorter half-life and in addition is a substrate and inhibitor of 2D6 so dose reductions have a very large impact. |
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Explain the effect of SSRIs on bone strength:
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SSRI use can result in decreased bone density due to increased stimulation of 5HT receptors in the bones. At-risk patients, should have regular bone density tests.
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Relate the effectiveness of SSRIs in treating depression to other ADs:
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--Equally effective, no difference within SSRIs
--slow onset of action --mood may be last to respond |
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Relate the effectiveness of SSRIs in treated anxiety disorders relative to other ADs:
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SSRIs are sometimes first line for anxiety, certainly over MAOIs and TCAs due to side effects, toxicity, and efficacy
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Which SSRIs are appropriate for treating OCD?
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all of them
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Relate the effectiveness of SSRIs to TCAs in the treatment of chronic pain:
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SSRIs are less effective because they have an unbalanced block reuptake, favoring 5HT to NE
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Which drug can be used for treating PMS and PMDD?
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fluoxetine
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What is the half-life of fluoxetine?
Which enzymes does it inhibit? |
--4-6 days (advantage: self tapering, disadvantage: long time for effect)
--2D6 and 3A4 |
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Which enzyme does paroxetine inhibit?
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2D6
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Explain how sertraline differs from other SSRIs:
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also blocks DA reuptake
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What is fluvoxamine specifically approved for, and what enzymes does it strongly inhibit?
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--OCD
--1A2, 2D6, 3A4 |
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Explain the difference between citalopram and escitalopram:
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Citalopram is a racemate. Lexapro is only the S enantiomer. The S enantiomer has a higher specificity for 5HT reuptake block. The effectiveness of one over the other is disputed.
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Why is it important to know whether a TCA is secondary or tertiary?
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structure will help us determine the side effect profile of the drug
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Explain the MOA of TCAs:
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TCAs bind non-competitively/(competitively) with reuptake transporters in presynaptic nerve terminals and inhibit the reuptake of NE (NET) and 5HT (SERT). This increases the amount of NT available for post-synaptic neurons to take up.
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Clarify whether TCAs block NE or 5HT uptake more effectively:
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TCAs block NE uptake more effectively, and secondary amines have the highest NE preference
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Do tertiary or secondary amines block muscarinic receptors more effectively?
Alpha-1 receptors? H-1 receptors? |
tertiary
tertiary tertiary |
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What effect does TCA blocking of H-1 receptors have? VSSC?
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Blocking H-1 receptors has a highly sedative effect and ma also cause weight gain.
Blocking VSSC can cause seizures or be used as a local anesthetic. |
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What effect do TCAs have on the seizure threshold?
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lower
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Explain the adverse effects of TCAs, specifically in relation to:
stimulant effects mania suicidality sedation |
--psychostimulant effects can include insomnia, drowsiness, excitation, agitation
--switch from depression to mania, rapid cycling --increased suicidality --tertiary amines cause worse sedation than secondary amines |
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Explain the adverse effects of TCAs, specifically in relation to:
confusion/disorientation blood pressure cholinergic effects cardiac effects |
--tertiary amines cause more disorientation than secondary amines
--tertiary amines cause more postural hypotension than secondary amines --peripheral anticholinergic effects (including dry mouth, blurred vision, constipation); tertiary are worse than secondary --cardiac effects: tachycardia due to muscarinic blockade, baroreflex tachycardia (those without cardiac risk factors are OK to take drug) |
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Explain the adverse effects of TCAs, specifically in relation to:
extrapyramidal reactions seizures weight gain sexual disturbances |
--D-2 block (hand tremor)
--seizures may be seen with high doses --weight gain (5HT receptors) is a major cause of non-adherence --low libido, impotence, delayed or absent ejaculation/orgasm |
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Explain the adverse effects of TCAs, specifically in relation to:
Body temperature Overdoses Abuse and Dependence Factors |
--hyperthermia in hot environments and exercise (TCA blocks sweating)
--highly toxic in overdosage --abuse and dependence (can have withdrawal symptoms but they are not abused because they do not create euphoria) |
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Explain possible interactions of TCAs with other drugs and food:
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--no interaction with food
--Serotonin syndrome with MAOIs --additive sedation with other depressants --additive anticholinergic effect with muscarinic blockers --potentiation of NE and E --antagonism of indirectly acting sympathomimetic amines --antagonism of antihypertensive effect of clonidine and guanethidine |
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--Describe the acute overdosage toxicity of TCAs:
--Describe the potential for abuse of TCAs |
--highly toxic in overdosage; a week's worth of pills can kill you
--typical symptoms include coma, respiratory depression, seizures, cardiac effects (arrhythmia, arrest) --no potential of abuse; no euphoria |
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Describe the use of TCAs for depression:
--onset --symptom response --efficacy --clinical utility |
--1-3 weeks for onset
--mood may be the last symptom to respond --equally effective as MAOIs, certain drugs within class may be more effective than others --second line because of side effects (orthostatic hypotension, sedation, antiCh effects, weight gain, sexual dysfunction) |
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Describe the use of TCAs in anxiety disorders:
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--panic disorder: second or third line because of side effects
--OCD: clomipramine is the only effective TCA for OCD; it has a numerical preference for 5-HT over NE reuptake block |
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Describe the use of TCAs in narcolepsy:
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--cataplexy is blocked (sudden loss of motor tone, weakness, collapse triggered by a motor stimuli such as a laugh)
--does not relieve other symptoms |
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Can TCAs be used for ADHD?
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Yes, but they are second line behind stimulants.
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Explain the proposed mechanism for relief from neuropathic pain facilitated by TCAs:
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--Same MOA as MAOIs
--Reuptake is blocked, enhances neurotransmission, blocks throughput of pain signals --non-specific reuptake blockade is more effective than specific blockade because both NE and 5-HT have an effect on the throughput. |
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Explain the two-headed approach to bulimia treatment with TCAs:
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TCAs have an antibinging effect and an antidepressant effect.
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Decide whether the following are secondary or tertiary amines.
desipramine imipramine clomipramine nortriptyline amitriptyline Additionally, which TCAs are the most and least sedative? |
desipramine--secondary
imipramine--tertiary clomipramine--tertiary nortriptyline--secondary amitriptyline--tertiary protryptiline is not sedative doxepin is highly sedative |
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List key general (non-drug) counseling points for antidepressants
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-DSIGECAPS (assess at baseline and w/ refills)
-takes 1-2 weeks for energy and appetite improvement -takes 4-6 weeks for mood improvement -do not take SJW -alcohol is a depressant -don't stop w/o talking to MD (important to taper some) -duration usually 9-12 months -suggest support groups and counseling |
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DSIGECAPS
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depressed mood
sleep interests guilt energy concentration appetite psychomotor sx suicide |
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TCA counseling points
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-NE/5HT reuptake inhibition
-common SE: dry mouth, dizy, sedation, weight gain, sexual dysfunction -serious SE: hallucinations, fainting, irregular heartbeat, skin rash/hives, CV death in overdose -DDI (incr TCA levels): cimetidine, SSRIs, OCs, graprefruit -DDI (decr TCA levels): CBZ, PHT -other DDI (incr warf, incr drowsiness, MAOIs, hypoglycemics) -take at bedtime due to sedation -may increase appetite and sweet cravings -take w/ or w/o food -EtOH incr sedation |
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MAOI counseling points
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-inhibits MAO-A/B
-common SE: hypotension, dizziness, weight gain, insomnia, cardiac effects, constipation, sexual dysfunction -serious SE: hypertensive crisis, tachycardia, muscle twitching, seizures -DDI: SSRIs, TCAs, stimulants, levodopa, tyramine foods, insulin (low blood sugar) -Avoid alcohol to prevent HTN response -2 week washout between SSRIs and TCAs -wait 5 t1/2 after previous SSRIs |
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SSRI counseling points
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-blocks reuptake of 5HT
-common SE: sexual dysfunction, N/D, HA, insomnia, sedation -serious SE: 5HT syndrome (hypothermia, excitement, rigidity, hypotension, tachycardia) -DDI: MAOIs, NSAIDS incr fluox levels -take with food to prevent nausea -avoid sedatives (incr sedation)_ -avoid alcohol (incr sedation/depression) -take in AM to avoid insomnia (fluoxetine) -take in PM to prevent drowsiness (paroxetine) |
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SNRI counseling points
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-inhibits 5HT/NE reuptake
-common SE: N/D, headache, HTN, sex dysfunction, nervousness, insomnia -serious SE: rash, blurred vision, chest pain, trouble breathing -DDI: MAOI, SSRI, TCA, haloperidol, CBZ, PB, PHT -do not crush or chew -XR has less S/Es -do not take late in the day (stimulant effect) -take w/ food to prevent N |
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NDRI counseling points
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-inhibits NE/DE reuptake
-common SE: GI upset, nausea, restlessness, insomnia, headache, dizzy, dry mouth serious SE: seizure, rash, itching, chest pain -DDI: MAOI, cimetidine, grapefruit -CI: seizures, eating disorders -NO sexual dysfunction -do not crush or chew -do not take after dinner to avoid insomnia |
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Clinical presentation of SSRI overdose
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Common signs and symptoms include nausea, vomiting, CNS depression, drowsiness, dizziness, sinus tachycardia, tremor, and blurred vision. Major outcomes following intoxication were noted in only ~0.1% of children <6 years old (Nelson, 2007). Rare, but potentially life-threatening effects may occur with larger ingestions (>50 times the daily dose; Barbey, 1998) and/or coingestions and may include seizures, QTc prolongation, decreased consciousness, and serotonin syndrome. Cardiotoxicity is most commonly associated with citalopram and escitalopram intoxications; however, seizures are more commonly associated with citalopram intoxication as compared to escitalopram intoxication (8% vs 0.2%, respectively [p<0.001] in one study) (Hayes, 2010). Symptom onset is typically gradual, occurring over several hours. Expected duration of toxicity is <24 hours.
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Decontamination treatment of SSRI overdose
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-single dose activated charcoal if able to protect airways
-ipecac and cathartics not recommended |
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Supportive treatment of SSRI overdose
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-agitation (benzos)
-autonomic instability (benzos, short acting agents for BP: nitroprusside, esmolol) (not propranolol b/c longer acting and harder to evaluate toxicity) -hyperthermia (benzos, NDMBs if >41.1 C) -muscle rigidity (benzos) -excessive serotonin (cyproheptadine) -seizures (diazepam, lorazepam, phenobarbital, midazolam) -impaired conduction (QT prolongation): sodium bicarbonate to maintain pH 7.45-7.55; replace Mg and K |
