Lecture 2: Mood and Affect PDF

LECTURE 2: MOOD AND AFFECT Type Lecture Reviewed Mood and Affect Mood is the sustained emotion experience reported by your patient part of every mental status assessment Affect is the emotiona...

LECTURE 2: MOOD AND AFFECT Type Lecture Reviewed Mood and Affect Mood is the sustained emotion experience reported by your patient part of every mental status assessment Affect is the emotional tone we observe. For examples: a blunted affect, constricted affect, flat affect, inappropriate affect or labile affect. Depression Major depressive disorder (MDD) most common psychiatric disorders. Women experience depression approx. 2x more often than men and apprx. 1/8th in adults have identified symptoms that met the criteria for a mood disorder at some point during their lifetime. leading cause of disability worldwide characterized by a persistently depressed mood lasting for a minimum of 2 weeks. Length of depressive episode may vary. Most people experience recurrent episodes. Diagnostic specifiers to describe most recent episode of depression 1. Psychotic features a. indicates the presence of disorganized thinking, delusions (e.g., delusions of guilt or of being punished fro sins, somatic delusions of horrible disease or body rotting, delusions of poverty or going bankrupt) or hallucinations (usually auditory voices berating persons for sins) 2. Melancholic Features a. severe form of endogenous depression b. characteristics: severe apathy, weight loss, profound guilt, symptoms worse in the morning, early morning awakening, suicidal ideation c. no environmental factors at all, purely biological depression 3. Atypical Features a. dominant vegetative symptoms - overeating, oversleeping b. onset younger c. psychomotor activities slow + anxiety 4. Catatonic features a. non-responsiveness b. extreme psychomotor retardation (may seem paralyzed???) c. withdrawal LECTURE 2: MOOD AND AFFECT 1  d. negativity 5. Postpartum Onset a. onset within 4 wks after childbirth. b. common for pyschotic features to accompany this depression c. severe ruminations d. delusional thoughts about infant signifying increased risk of harm 6. Seasonal Features (seasonal affective disorder) a. indicates episodes mostly begin in fall or winter and remit in spring b. have reduced cerebral metabolic activity c. characterized by anergia (lack of energy/passivity), and hypersomnia (excessive daytime sleep), overeating, weight gain, craving carbohydrates, responds to light therapy Different types of depressive disorders Disruptive mood dysregulation disorder severe and recurrent temper outbursts that are inconsistent with developmental level. introduced in 2013 in response to an alarming number of children and adolescents being diagnosed with bipolar disorder symptoms: constant and severe irritability and anger in individuals between ages 6 and 18. Onset before age 10. Temper tantrums with verbal or behavioural outbursts out of proportion occurring at least 3x/ wk. to be dx: need to exhibit irritability, anger, and temper tantrums in at least two of these settings: home, school, and with peers. Persistent Depressive disorder (dysthymia) dx when feelings of depression occur most of the day, for the majority of days. low-level depressive feelings last at least 2 years in adults and 1 year in children and adolescents. in addition to depressed mood, individuals with this disorder have at least two of the ff: decreased appetite or overeating, insomnia or hypersomnia, low energy, poor self-esteem, difficulty thinking, and hopelessness. patients often express that they have “always felt this way” and that being depressed seems like a normal way of functioning. not uncommon for people with this low-level depression to also have periods of full-blown major depressive episodes Premenstrual Dysphoric disorder relatively new addition to the dx system for psychiatry. refers to cluster of symptoms that occur in the last week before the onset of a menstrual period. causes problems severe enough to interfere with the ability to work or interact with others symptoms: mood swings, irritability, depression, anxiety, feeling overwhelmed, difficulty concentrating symptoms decrease significantly or disappear with the onset of menstruation. Substance/ Medication induced depressive disorder result of a prolonged use of or withdrawal from drugs and alcohol last longer than the expected length of physiological effects, intoxication, or withdrawal of the substance. Symptoms appear within 1 month of use. Once the substance is removed, depressive symptoms usually remit within a few days to several weeks Depressive disorder due to another medical condition LECTURE 2: MOOD AND AFFECT 2  CVAs Parkinson’s Huntington’s Alzheimer’s TBI Cushing’s Hypothyroidism high association in BPD - TSH levels Arthritis, back pain Vitamin B12 deficiency HIV diabetes infections cancer autoimmune problems Depression Etiology Depression Etiology p. 249-251(2nd edition) and p. 224-226 (3rd edition) 1. Biochemical Neurotransmitter abnormalities (two main are serotonin (sleep disturbances, decreased appetite, poor sex drive, impulse control and irritability) and norepinephrine (attention and behaviour). Genetic or environmental factors or medical conditions (Parkinson’s; AIDS)(related to serotonin transport, dopamine receptors, and stress response) Substance usage Results from a dysregulation of a number of neurotransmitters systems beyond norepinephrine and serotonin (others include glutamate, acetylcholine, GABA) Stress is associated with decreased neurogenesis 2. Biological (Genetic) If one twin is affected the second has a 50% chance of being affected as well There is a genetic marker but not a direct gene related Certain genetic markers are related to depression when accompanied by childhood maltreatment or history of stressful life events Understanding genetic involvement in the role of transport of neurotransmitters is necessary for effective pharmacological treatment of depression 3. Biological (Hormonal): Cause: hyperactivity of the hypothalamic pituitary adrenal axis Tests: elevated corticotropin releasing hormone & increased urine cortisol levels decreased estrogen and progesterone lifetime rate of depression is 2x greater in women with child-bearing potential than in men (p.224) Biological (Inflammation) Inflammation may result from psychological injury as well as physical injury LECTURE 2: MOOD AND AFFECT 3  Research indicates that while inflammation does not cause depression, it does play a role. One third of people with major depression have elevated inflammatory biomarkers in the absence of a physical illness. People with inflammatory diseases have increased risk for major depression. Inflammation may interfere with typical antidepressants which decrease their effectiveness to treat depression Chronic inflammation may trigger or worsen depression Can worsen symptoms such as fatigue, decreased appetite, and altered sleep patterns. 4. Psychological (Cognitive Theory) May acquire a psychological predisposition to depression due to early life experiences Assumption that a person’s thoughts will result in emotions. The way a person looks at their life (positive or negative) can influence weather they feel positive emotions or negative ones (sorrow, anger)- Thought than an individual can learn depressive cognitions socially through observation (perception, memory, and problem-solving) Three thoughts becks cognitive triad negative view of self Pessimistic view of the world Belief that negative reinforcement will continue in the future 5. Psychological (Learned Helplessness) Learned helplessness is believing that one is unable to control or change a stressful situation or that highly desired outcomes are unachievable so they do not try to change the will or outcome This can lead to increased stress and depression 6. Diathesis Stress Model combination of Biology + life events + early life trauma can result into long-term hyperactivity of CNS corticotropin-releasing factors (CRF) = releasing cortisol and Norepinephrine = stress goes up = neurotoxic effect on the hippocampus = sensitization of CRF circuits = exaggerated stress response in adulthood some people also have predisposition toward depression when triggered by very stressful life events = altering neuro connections in the brain = recurrent depressive disorder. Early treatment therapy is needed to help find a solution towards care Epidemiology Children and Adolescents children as young as 3 have been diagnosed with depression - prevalence is relatively low, little difference between boys and girls depression higher among girls than boys in teens youth onset carries a high recurrence rate which sets the stage to lifelong periods of depression Disruptive mood dysregulation disorder was added too represent the presentation of irritability and frequent episodes of uncontrolled behaviour in an attempt to deal with the potential of children being misdiagnosed with schizophrenia, a personality disorder, or bipolar disorder. Older persons although depression in older persons is common - it is not normal result of aging. The risk for depression in the elderly increases as health deteriorates. 1%-5% of older persons who live in the community have depression and it rises to 11.5% for hospitalizations and 13.5% for those requiring home care. LECTURE 2: MOOD AND AFFECT 4  subsyndromal depression - experience many, but not all, of the symptoms of a major depressive episode. Elderly individuals that experience this have an increased risk of eventually developing major depression. Sometimes the psychomotor slowing and cognitive effects of depression lead others to believe that the older person is developing a neurocognitive disorder such as Alzheimer’s disease. this condition is refereed to as pseudodementia, a problem that can be reversed when the underlying depression is treated and eliminated. Comorbidity a depressive syndrome frequently accompanies other psychiatric disorders such as anxiety disorders, schizophrenia, substance use, eating disorders, and schizoaffective disorder people with anxiety disorders such as panic disorder, GAD, OCD commonly present with depression, as do people with personality disorders, particularly borderline personality disorder, adjustment disorder, and brief depressive reactions. A combination of anxiety and depression is perhaps one of the most common psychiatric presentations Symptoms of anxiety occur in an average of 70% of cases of major depression. Medical Conditions and substances or medications associated with major depressive disorder Substances or Medication CNS depressants Alcohol, barbiturates, benzodiazepines, clonidine CNS medications Amantadine, bromocriptine, levodopa, phenothiazines, phenytoin Psychostimulants Amphetamines Systemic Corticosteroids, digoxin, diltiazem, enalapril, ethionamide, isotretinoin, mefloquine, methyldopa, metoclopramide, quinolones, reserpine, Medications statins, thiazides, vincristine Medical Conditions epilepsy, Parkinson’s disease, multiple sclerosis, Alzheimer’s disease, Huntington’s disease. traumatic brain injury, cerebrovascular Neurological accident Infectious or Neurosyphilis, HIV inflammatory Cardiac disorders Ischemic heart disease, cardiac failure, cardiomyopathies Endocrine Hypothyroidism, diabetes mellitus, vitamin deficiencies, parathyroid disorders Inflammatory disorders collagen vascular diseases. irritable bowel syndrome, chronic liver disorders Neoplastic disorders central nervous system tumours, paraneoplastic syndromes Assessment 1. Suicide Assessment daily 2. Screening tools - Beck’s depression inventory, hamilton depression rating scale, patient health questionnaire-9, columbia what to watch out for: Loss of interest Loss of ability to feel pleasure (anhedonia) Appetite changes: Weight loss/gain (vegetative) Sleep is disturbed (vegetative) Restless or extremely slowed down (vegetative) No energy Excessive/inappropriate guilt feelings LECTURE 2: MOOD AND AFFECT 5  Unable to think clear, indecisive Thoughts of death or suicide Changes in bowel habits (vegetative) Sexual dysfunction/menstruation changes (vegetative) Vegetative = alterations in activities necessary to support physical life. Physical s/s of depression. All this = severe impairment in functioning (social, occupational, relationships) Nursing dx: risk for suicide hopelessness or powerlessness ineffective coping social isolation or impaired social interaction spiritual distress self-care deficit (bathing, dressing, feeding) chronic low self-esteem Outcomes identification 1. tenants of recovery model a. focus is on pt’s strengths and goals b. pt needs and values central Recovery is individualized phases: 1. Acute Phase (6-12 wks) a. After diagnosis focus is on symptom management. Medication started or adjusted, sometimes hospitalization required. 2. Continuation phase (4-9 months) a. Stabilized and preventative measures are implemented (follow up). Counselling, medication, education. 3. Maintenance (1 year) a. Considered recovered and individualized plans of prevention are implemented. Treatment: 1. medication 2. complementary and integrative therapies 3. psychotherapy and group therapy 4. ECT 5. transcranial magnetic stimulation - “increasing neurons” 6. vagus nerve stimulation - surgical treatment approved for treatment-resistant depression. Goal is to increase neurotransmitters via vagus nerve stimulation. costs $25k Bio-psychiatry LECTURE 2: MOOD AND AFFECT 6  psychiatric symptoms primarily due to neurotransmitters changing the way they produce and respond to chemical messages this approach is not “purely” medical. it recognizes the influence of genetics, drugs, infections, and psychosocial experiences. rarely, perhaps never, is a mental illness simply an imbalance of brain chemistry Psychotropic medications - restore balance, and in the bio psychiatry approach are the primary source of treatment Brain Function review Works to maintain homeostasis: internally and externally Regulates our Autonomic System (sympathetic and parasympathetic) Controls our Biological Drives and Behaviour (sex, hunger, sleep) Our conscious self (thoughts) Memory Social skills (not clear links here but our social behaviour is believed to be influenced by genetics and our experiences) …when we think about psychiatric symptoms many of the above functions are affected… Our limbic system (emotional nervous system) and endocrine system significant in mental health. Neuron Functions 1. RESPOND TO STIMULI 2. CONDUCT ELECTRICAL IMPULSES 3. RELEASE CHEMICALS CALLED NEUROTRANSMITTERS The presynaptic neuron releases the neurotransmitter into the synaptic cleft. The neurotransmitter binds to the targeted receptor then the action must be TERMINATED. 4. Terminated in synaptic cleft by enzymes, other processes 5. Reuptake process back into presynaptic neuron. For the monamine neurotransmitters, there is an enzyme called MAO (monamine oxidase) awaiting them in presynaptic neuron to terminate the action. LECTURE 2: MOOD AND AFFECT 7  Pharmacology Agonist: drugs that bind to and activate response from the targeted receptor Antagonist: drugs that bind to, BUT DO NOT activate targeted response. No effect. They kind of act like a bully “I’m here so you can’t be” to other drugs. DRUGS Anti-depressants Generally Drugs used to treat depression increase synaptic levels of norepinephrine and/or serotonin target symptoms include: sleep disturbance appetite disturbance (decreased or increased) fatigue decreased sex drive psychomotor retardation or agitation diurnal variations in mood (often worse in the morning) impaired concentration or forgetfulness anhedonia drawback: improvement in mood may take 1-3 weeks or longer. goal: complete remission of symptoms. 4 main classes: Tricyclic antidepressants (old ones) Selective Serotonin Reuptake Inhibitors (SSRI’s) Serotonin-Norepinephrine Reuptake Inhibitors (SNRI’s) Monoamine Oxidase Inhibitors (MAOI’s) Drug treatment of patients with major depression SSRIs - Selective Serotonin Reuptake Inhibitors blocks reuptake of serotonin LECTURE 2: MOOD AND AFFECT 8  first line treatment for major depression some SSRIs activate and others sedate → choice depends on patient symptoms Effective in depression with anxiety features and in depression with psychomotor agitation. INDICATIONS: broad. In addition it can be used in anxiety disorder treatment such as OCD and panic disorder. have relatively low adverse-effect profile compared to older antidepressants, blurred vision, or urinary retention which makes it easier to take. risk of lethal overdose minimized with SSRIs adherence is necessart toward remission of symptoms. Discontinuation syndrome - dizziness, insomnia, nervousness, irritability, nausea and agitation → abrupt withdrawal. taper slowly Side effects- agitation, insomnia, headache, nausea and vomiting, sexual dysfunction, hyponatremia Drug Name Action Notes Adverse Effects Warnings - first line treatment for major discontinuation syndrome - insomnia, depression, some SSRIs activate and nervousness, irritability, nausea, and Citalopram (Celexa), others sedate; choice depends on agitation, insomnia, agitation—may occur with abrupt Fluoxetine (Prozac), patient symptoms, Risk of lethal headache, nausea and withdrawal (depending on half-life); taper Fluvoxamine (Luvox), Blocks serotonin overdose minimized with SSRIs. vomiting, sexual slowly. Contraindicated in people taking Paroxetine (Paxil), reuptake Fluoxetine found tp be effective for dysfunction, MAOIs. Serotonin syndrome is a Sertraline (Zoloft), women who suffer from late luteal hyponatremia lifethreatening event associated with Escitalopram (Cipralex) phase dysphoric disorder and SSRIs. Pt needs to d/c all SSRIs for 2-5 bulimia nervosa. wks before starting a MAOI. Patient teaching for SSRIs may cause sexual dysfunction or lack of sex drive may cause insomnia, anxiety, and nervousness. may interact with other medications such as digoxin or warfarin. SSRIs should not be taken within 14 days of the last dose of MAOI no OTC drug should be taken without first notifying primary care provider common adverse effect include: nausea, fatigue, diarrhea, dry mouth, dizziness, tremor, and sexual dysfunction or lack of sex drive. because of the potential for drowsiness and dizzines,s patient should not drive or operate machinery until these adverse effects are rules alcohol should be avoided liver and renal function tests should be performed and blood counts checked periodically medication should not be discontinued abruptly. If adverse effects become bothersome, pt should ask pcp about changing to a different drug. Abrupt cessation canlead to serotonin withdrawal. any of the following symptoms shold be reported immediately to primary care provider: increase in suicidal thoughts or depression, rash or hives, rapid heartbeat, sore throat, difficulty urinating, fever, malaise, anorexia and weight loss, unusual bleeding, initiation of hyperactive behaviour, severe headache SNRI’s Inhibit reuptake of both serotonin and norepinephrine and to a lesser degree inhibit dopamine mostly indicated for MDD. Venlafaxine (Effexor) in low doses acts as an SSRI (often tried after no response with SSRI) Duloxetine (Cymbalta): indicated in maintenance treatment of depression, generalized anxiety, fibromyalgia, neuropathic pain side effects Hypertension (Effexor), nausea, insomnia, dry mouth, sweating, agitation, headache, sexual dysfuntion LECTURE 2: MOOD AND AFFECT 9  These are often prescribed for major depression Serotonin syndrome Drug Name Action Notes Adverse Effects Warnings monitor BP with effexor, especially at higher Effexor is a popular next-step Hypertension (venlafaxine), doseas and with a history of HTN. HTN may Venlafaxine Blocks serotonin and strategy after trying SSRIs. nausea, insomnia, dry mouth, be particularly noted in the diastolic (Effexor), Duloxetine norepinephrine Cymbalta has the advantage of sweating, agitation, headache, measurement. Discontinuation syndrome (see (Cymbalta) reuptake decreasing neuropathic pain sexual dysfunction SSRIs above). Contraindicated in people taking MAOIs. Norepinephrine Reuptake Inhibitors (NRIs) Drug Name Action Notes Adverse Effects Warnings Antidepressent effects similar to Insomnia, sweating, dizziness, dry Venlafaxine (Effexor Blocks the reuptake of SSRIs and TCAs. Useful with severe mouth, constipation, urinary contraindicated in XR), Duloxetine norepinephrine and enhances depression and impaired social hesitancy, tachycardia, decreased people taking MAOIs (Cymbalta) its transmission functioning libido Norepinephrine-dopamine reuptake inhibitors (NDRIs) Drug Name Action Notes Adverse Effects Warnings Blocks the reuptake of Stimulant action may reduce Contraindicated in people taking agitation, insomnia, Bupropion norepinephrine and dopamine. appetite; may increase sexual MAOIs. High doses increase seizure headache, nausea and (Wellbutrin) Not indicated for patients under desire; used as an aid to quit risk, especially in people who are vomiting, seizures (0.4%) 18 years of age. smoking predisposed to seizures. Serotonin-Norepinephrine disinhibitors (SNDIs) Drug Name Action Notes Adverse Effects Warnings drug-induced somnolence exaggerated by Blocks alpha1-adrenergic Antidepressant effects Weight gain, sedation, Mirtazapine alcohol, benzodiazepines, and other CNS receptors that normally inhibit equal SSRIs and may dizziness, headache, sexual (Remeron) depressants. Contraindicated in people nirepinephrone and serotonin occur faster dysfunction is rare taking MAOIs Tricyclic Antidepressants Inhibits the reuptake of serotonin and norepinephrine antagonizes adrenergic, histaminergic, and muscarinic receptors Sedating effect, best to take at night Therapeutic effect may take 10-14 days or longer. Full effects may nnot be seen for 4-8 weeks but an effect on some symptoms of depression, such as insomnia and anorecia can be earlier. Cardiovascular risks: ensure there has been a cardiac work-up prior to treatment Teach about symptom relief: could be up to two months. Teach to avoid alcohol as it blocks the effects of the antidepressant Do not stop abruptly: likely to cause nausea, altered heartbeat, nightmares and cold sweats. Will occur within 2-4 days. Advise to take one dose of med again and see physician. Side effects: dry mouth, constipation, urinary retention, blurred vision, orthostatic hypotension, cardiac toxicity, sedation, will make you fat Drug Name Action Notes Adverse Effects Warnings Interactions Amitriptyline Inhibits the reuptake of Therapeutic effects similar Anticholinergic effetcs: lethal in overdose. Use MAOIs, phenothiazines, (Elavil), serotonin and to SSRIs, but adverse Dry mouth, constipation, cautiously in older persons barbiturates, disulfram, Clomipramine norepinephrine. effects are more urinary retention, blurred and those with cardiac oral contraceptives (or LECTURE 2: MOOD AND AFFECT 10  (Anafranil), Antagonizes prominent. May work vision, tachycardia, disorders, elevated other estrogen Nortriptyline adrenergic, better in melancholic esophageal reflux; intraocular pressure, preparations), (Aventyl), histaminergic, and depression. TCAs can orthostatic hypotension, urinary retention, anticoagulants, some Desipramine muscarinic receptors worsen many cardiac and sedation; weight gain; hyperthyroidism, seizure antihypertensives, (Desipramine), other medical conditions. cardiac toxicities: disorders, or lover or bezodiazepines, and Doxepin (Sinequan) Desipramine dysrhythmias, MI, and kidney dysfucntion. alcohol. (Desipramine) may be best heart block. Contraindicated in people for a patient who is taking MAOIs. Initial lethargic and fatigued. dose should always be Amitriptyline (Elavil) and low and increased Doxepin (Sinequan) may gradually. be more appropriate if sedating effect is needded for agitation or restlessness. Patient Teaching mood elevation may take from 7-28 days. Up to 6-8 weeks may be required for full effect to be reached and for major deprrssive symptoms to subside other family members should relay and reinforce this information frequently to the family member with depression, who may have trouble remembering and may respond to ongoing reassurance pt should be reassured that drowsiness, dizziness, and hypotension usually subside after the first few weeks pt should be cautioned to be careful when working around machines, driving cars, and crossing streets because of possible altered reflexes, drowsiness, or dizziness alcohol can block the effects of antidepressants. The patient should be told to refrain from drinking pt should take the full dose at bedtime to reduce the experience of adverse effects during the day if the bedtime dose (or once-a-day dose) is missed, the patient should take the dose within 3 hoursl otherwise the patient should wait until the usual medication time on the next day. The patient should not double the dose suddenly stopping TCAs can cause nausea, altered heartbeat, nightmares, and cold sweates within 2-4 days. The patient should call the primary care provider or take one dose of the TCA until the primary care provider can be contacted. Monoamine Oxidase Inhibitors (MAOI’s) Inhibits monoamine oxidase which would normally break down serotonin and norepinephrine Indications: effective for people with atypical depression (characterized by mood reactivity, oversleepinng, and overeating), panic disorder, social phobia, GAD, OCD, PTSD, bulimia. Cannot be given with any other anti-depressant Often used when all else has failed (for atypical depression, phobias, anxiety, OCD, PTSD, bulimia) Side effects: Insomnia, nausea, agitation, confusion, hypotension, weight gain, cardiac rhythm changes, sexual impotence, constipation * Hypertensive crisis - usually occur within 15-90 mins of ingestion of CI products (tyramine-containing foods or other antidepressants). early symptoms irritability anxiety flushing sweating severe headache later symptoms: very severe fever LECTURE 2: MOOD AND AFFECT 11  seizures coma death if ingestion is recent: gastric lavage and charcoal pyrexia = treated with hypothermic blankets or icepacks fluid therapy essential with hyperthermia Short acting antihypertensive such as nitroprusside, nitroglycerin, or phentolamine IV benzodiazepines are useful for agitation and seizure control * Serotonin Syndrome if used with other anti-depressants Special dietary restrictions: No tyramine p. 264 in 2nd edition text and p. 239 3rd edition(!) - tyramine containing foods: no cheeses, avocadoes, fermented bean curd, soybeans, figs, banana, fermented/smoked/aged/spoiled meats, yeast, beers, chianti wine, protein dietary supplements, soups, shrimp paste, soy sauce Potential toxic Drug Name Action Notes Adverse Effects Warnings Interactions Contraindic effects OTC medications for Insomnia, nausea, colds, allergies, or agitation, congestion (any confusion. cereebrovas product containing Potential for disease, ephedrine or hypertensive crisis hyperension phenylpropanolamine), or serotonin congestive Inhibits the tricyclic Efficacy similar to syndrome with Contraindicated in failure, live enzyme antidepressants increased BP with other concurrent use of poeple taking disease, monoamine (imipramine, possible antidepressents, other other consumptio Phenelzine oxidase, which amitriptyline), development of but dietary antidepressants; antidepressants. foods conta (Nardil), normally breaks narcotics, intercranial restrictions and changes in cardiac tyramine-rich tyramine, Tranylcypromine down antihypertensives hemmorhage, potential drug rate and rhythm, foods could bring tryptoophan (parnate) neurotransmitters, (methyldopa, hyperpyrexia, interactions make constipation, a hypertensive dopamine; including spironolactone), amine convulsions, tgis drug type less urinary hesitancy, crisis. Many other recurrent or serotonin and precursors (levodopa, coma, and deat desirable sexual drug interactions headaches, norepinephrine L-tryptophan), dysfunction, surgery in t sedatives (alcohol, vertigo, previous 10 barbiturates, overactivity, days; age y benzodiazepines), muscle twitching, than 16 yea general anesthetics, hypomanic and stimulants manic behaviour (amphetimes, cocaine) Contraindicated if Acts on serotonin, Moclobemide MDD and social nausea and known norepinephrine, (Manerix) anxiety dizziness hypersensitivity to and dopamine moclobemide. Serotonin syndrome Serotonin Syndrome - too much serotonin in the body via very high doses or interactions with other drugs, including non-precription medication like St. John’s Wort. Life-threatening situation. Risk is very high when an SSRI is administered in combination with a second serotonin-enhancing agent such as MAOIs. Symptoms: hyperactivity or restlessness Tachycardia → cardiovascular shock LECTURE 2: MOOD AND AFFECT 12  Fever → hyperpyrexia Elevated BP Altered mental status (delirium) irrationality, mood swings, hostility seizures → status epilepticus myoclonus, incoordination, tonic rigidity abdominal pain, diarrhea, bloating apnea → death WHAT TO DO: Hold SSRI, MAOIs. Remove any offending agents Call for orders (anticipate serotonin receptor blocker: cyproheptadine, methysergide or propranolol) Cooling blankets Dantrolene or valium for muscle rigidity Anticonvulsants Artificial ventilation Paralysis F.L.U.S.H. Electroconvulsive Therapy (ECT) procedures where electrical currents are passed through the brain, intentionally triggering a brief seizure. “seems” to cause changes in brain chemistry that can quickly reverse symptoms of mental illnesses. often works when other treatments are unsuccesful Procedure: for patients with depression: 2-3 treatments per week to a total of 6-12 treatments Pt is given general anaesthetic to induce sleep and a muscle-paralyzing agent to prevent muscle distress and fractures. EEG measures brain waves, ECG montors cardiac responses Brief seizures (30-60s) are induced by an electrical current (as brief as 1s) transmitted through electrodes attached to one or both sides of the head to ensure that seizure is on entire brain: BP cuff is inflated on the lower arm or leg before admin of paralytic agent this is so the convulsion can be visualized in the unparalyzed extremity After the procedure, pt wake about 15 mins after PRE-ECT assessment: CXR ECG Urinalysis CBC BUN Electrolyte panel LECTURE 2: MOOD AND AFFECT 13  benzodiazepines should be d/c small dose of caffeine may be administered to combat effects of benzodiazepines Indications Risk Factors Adverse Reactions NOT EFFECTIVE IN: 1. the heart can be sressed at the onset 1. confusion and disorientation for 1. non-responsive depression of seizure during ECT and for up to 10 1. people with dysthymia several hours after the procedure minutes after 2. retrograde amnesia - loss of memory 2.psychotic illnesses 2. hypertension of events leading up to and including the 2. atypical depression treatment itself 3.drug-resistant psychosis 3. congestive heart failure 3. paradoxical reactions 3. personality disorders 4. depression associated with bipolar 4. cardiac arrhythmias 4. drug dependence disorder 5. when a pt is experiencing intense suicidal 5. stresses the brain as a result of 5. depression secondary to ideation, and there is a need for a rapid cerebral oxygen, blood flow, and situational or social definitive response intracranial pressure difficulties 6. when a pt is severely malnourished, exhausted, and dehydrated due to lengthy 6. brain tumours depression (after rehydration) 7. if previous medication trials have not 7. subdural hematoma successfully treated the illness if the pt chooses when there is a marked agitation, marked vegetative symptoms, or catatonia for major depression with psychotic features in pregnant people fopr people with rapid cycling mood swings (4 or more in one year) Transcranial Magnetic Stimulation (TMS) non-invasive tx modality that uses MRI strength magnetic pulses to stimulate focal areas of the cerebral cortex. Indications: pts who have been unresponsive to at least one antidepressant. used to enhance cognitive funstion in healthy, non-depressed individuals risk factors: presence of metal in the area of stimulation ex: cochlear implants, brain stimulators, medication pumps Procedure: outpatient: TMS takes about 30 minutes and is typically ordered for 5 days a week for 4-6 weeks pts are awake and alert during procedure An electromagnet is placed on the pt’s scalp short, magnetic pulses pass into the prefrontal cortex of the brain. pulses are similar to those used by MRI scanners but are more focused. the pulses cause electrical charges to flow and induce neurons to fire or become active. During TMS, pts may feel a slight tapping or knocking in the head, contraction of the scalp, and tightening of the jaw. Potential Adverse Rx: LECTURE 2: MOOD AND AFFECT 14  after procedure, pts may experience headache or lightheadedness no neuro deficits or memory problems have been noted seizures - rare complication mild scalp tingling and discomfort at the administration site. Emerging Tx: Ketamine: A dissociative anesthetic originally used in 1970’s to treat wounded soldiers in Vietnam War. Short acting. An opiate Started to be used in emergencies to calm agitated patients. Found depressive, suicidal ideations rapidly decreased and it lasted. Causes a dissociative experience, popular as a club drug : Special K”, “Super k”, “Vitamin K”. inject, drink, snort or smoke. Can induce hallucinations and delirium. Today ketamine is used to treat depression/suicidal ideation: IV, nasally and sometimes used as the anesthetic for ECT. Duration of treatment varies. Glutamate is the neurotransmitter involved, may improve communication between neurons. Opioid receptors also involved. Not enough research done yet but there is optimism. However, concerns around dissociation, hallucinations and cognitive effects (attention, judgment, thinking) have been raised. Potential for addiction and abuse. Long term safety unknown. Important Points: Depression Safety is top priority. Treatment options include counselling, alternative measures and medication. Effects of medication take 3 weeks + depending on what medication. This is an important teaching point. Hypertensive Crisis Serotonin Syndrome Bipolar Disorder once commonly known as manic depression. chronic, recurrent illness that must be carefully managed throughout a person’s life. Bipolar I disorder Bipolar II disorder Cyclothymic disorder Causes Biological factors genetics neurotransmitter involvement brain structure (prefrontal cortical dysfunction, hippocampus) hypothalamic-pituitary-thyroid-adrenal axis Psychological factors no longer considered a cause. However part of assessment Environmental factors increased prevalence among upper socioeconomic class stardom LECTURE 2: MOOD AND AFFECT 15  Bipolar I Disorder - hypermania marked by severe shifts in mood, energy, and inability to function. Periods of normal functioning may alternate with periods of illness (highs, lows, or a combination of both). continue to experience chronic interpersonal or occupational difficulties even during remission Manic Episode - delusions of grandeur initially feel euphoric and energized, don’t sleep or eat, and they are in perpetual motion. Often take significant risks and engage in hazardous activities. If intensified, individuals may become psychotic and experience hallucinations (tend to be auditory— sometimes the voice of “God”), delusions, and dramatically disturbed thoughts and behaviour after euphoria, it becomes agitation and irritability, then will go into exhaustion, then ultimately collapse into depression. Depression + agitated mania = can lead into a dangerous combination that can lead to extreme behaviours such as violence or suicide. Individuals may even develop MDD and GAD after a manic episode These individuals need SLEEP Bipolar II Disorder - hypomania individuals have experienced at least one hypomanic episode and at least one major depressive episode. Hypomania - refers to a lower-level and less dramatic mania. Accompanied by excessive activity and energy for at least 4 days and involves at least three of the behaviours listed in criterion B in DSM-5. 1. Inflated self-esteem or grandiosity. 2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep). 3. More talkative than usual or pressure to keep talking. 4. Flight of ideas or subjective experience that thoughts are racing. 5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed. 6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation (i.e., purposeless non–goal-directed activity). 7. Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments). psychosis is never present with hypomania psychotic symptoms may accompany the depressive side of the disorder = high risk of suicide BPD II patients are often underdiagnosed and is often mistaken for major depression or personality disorders Cyclothymic Disorder has symptoms of hypomania alternating with symptoms of mild to moderate depression for at least 2 years in adults and 1 year in children. Hypomanic and depressive symptoms do not meet the criteria for either bpd2 or major depression, yet symptoms are disturbing enough to cause social and occupational impairment. Some people experience rapid cycling and may have at least changes in mood episodes in a 12 month period. Can also occur within the course of a month or 24h period. Outcomes Acute Phase LECTURE 2: MOOD AND AFFECT 16  occurs during an intense manic, hypomanic or depressive episodes injury prevention be well hydrated maintain stable cardiac status maintain and obtain tissue integrity get sufficient sleep and rest demonstrate thought self-control make no attempt at self-harm Continuation Phase - presenting symptoms are being controlled but the individual’s mental health is still quite fragile. Lasts for 4-9 months Relapse prevention psychoeducational classes for the patient and family related to knowledge of disease process knowledge of medication consequences of substance addictions for predicting future relapse knowledge of early signs and symptoms of relapse Support groups or therapy (cognitive behavioural, interpersonal) Communication and problem-solving skills training Maintenance Phase continue to focus n prevention of relapse and limitation of the severity and duration of future episodes participation in learning interpersonal strategies related to work, interpersonal, and family problems participation in psychotherapy, group, or other ongoing supportive therapy modality. Epidemiology men and women have nearly equal rates of bipolar disorders but respond differently with their conitions men: more likely to have legal problems and commit acts of violence women: more likely to abuse alcohol, commit suicide, develop thyroid disease. women who experience severe postpartum psychosis within two weeks of giving birth have 4x greater chance of subsequent conversion to bipoolar disorder. Children and Adolescents: prevalence rate of bipolar disorder in late adolescents is same in adults 1 in 5 young people with mania + depression will attempt suicide. experience nearly 2 months per year of role impairment poses significant implications for individuals who are positioning themselves for a lifetime and a career, as well as developing relationship patterns. Cyclothymic disorder: usually begins in adolescence or early adulthood. 15-50% chance of risk of developing bipolar I or II with individuals having this disorder LECTURE 2: MOOD AND AFFECT 17  major risk factor: having first-degree relative, parent, sibling, or child, with bipolar I disorder. Comorbidities Bipolar I 75% of people dx w/ this condition also experience an anxiety disorder. may experience panic attacks, social anxiety disorder, and specific phobias Disorders that can complicate clinical presentation and management of bipolar I: attention-deficit/hyperactivity disorder all of the disruptive, impulse control, or conduct disorders disorders that may lead to pre-mature death due to heart dis3ease, stroke and diabetes: migraines metabolic syndromes hypertension high blood glucose excess body fat around the waist abnormal cholesterol levels Substance use disorder are often present in more than hald of individuals with Bipolar I, perhaps in an attempt to self-medicate or as a symptom related to increased risk-taking. alcohol-use disorder: more than 50% of the individuals which elevates suicide risk. Bipolar II disorder 75% of individuals dx with this disease also have a comorbid anxiety disorder. anxiety disorders come before the hypomania and depressive symptoms 37% of individuals are affected by a Substance use disorder rise along with hypomanic symptoms Anxiety and eating disorders are also associated with the depressive side of bipolar II 14% of people are affected with eating disorders, particularly binge eating disorder. Cyclothymic disorder substance use disordes are common self-medication subduing bipolar symptoms Sleep disorders where people have difficulty falling asleep or staying asleep are often present Attention-deficit/hyperactivity disorder is more common in childeen with cyclothymic disorder vs. those with other mental health conditions Etiology Genetic bipolar illnesses tend to run in families those with pts who have bipolar disorders have 15-30% greater chance for a lifetime risk LECTURE 2: MOOD AND AFFECT 18  there may be an overlap between rare genetic variations linked to bipolar disorder and those implicated in schizophrenia and autism concordance rate in twins - 70% The disease is polygenic - a lot of genes contribute to its expression some evidence suggest that bipolar disorders are more prevalent in adults who had high IQs and who were particularly verbal as children. they appear to have higher levels of education and higher occupational status vs individuals with unipolar depression the proportion of pts with bipolar disorders among creative writers, artists, highly educated men and women and professionals is higher than those in the general population. Pharmacology Lithium Exact mechanism of action not known. But we know it mimics the role of sodium in neurons and thus alters electrical conductivity so body functions regulated by electrical currents are potential problems. Cardiac contraction , which with therapeutic doses can induce sinus bradycardia and in overdose cerebral conductivity leads to convulsions. Nerve and muscle conduction changes so may see a tremor at therapeutic doses and extreme motor dysfunction with overdose. Note this and observe if it worsens. Blood Levels are VERY IMPORTANT due to the low therapeutic index (fine line between therapeutic and toxic). We want to see levels at 0.6 - 1.2 mEq/L. 1.4 - 1.5 = start of toxicity. Monitored regularly. Polyuria common: consequence of decreasing effectiveness of vasopression on renal function. So we must monitor RENAL FUNCTIONS. **Hyponatremia can increase risk of toxicity because increased kidney reabsorption of sodium leads to increased reabsorption of lithium as well*** THYROID FUNCTION monitored (long term use possible enlargement and possible hypothyroidism) Onset of action 10 to 21 days and it usually takes 7 to 14 days to reach therapeutic levels. Often an antipsychotic (i.e. olanzapine or accuphase as brings mania under rapid control) or antianxiety used in acute phase of mania. Seroquel (quetiapine), olanzapine, clopixol - used to treat BPD during the time the lithium does its thing Indications: reducing Elation, grandiosity, and expansiveness Flight of ideas Irritability and manipulation Anxiety To a lesser extent, lithium controls: Insomnia Psychomotor agitation threatening or assaultive behaviour distractibility hypersexuality paranoia Side Effects and Toxicity: Common to have patient report polyuria. Encourage normal salt intake as low salt intake will increase lithium retention and possible toxicity. Mild tremor normal. TOXIC SIGNS LECTURE 2: MOOD AND AFFECT 19  Patients may have diarrhea, sweating and some vomiting. If persistent and patient becomes dehydrated this is worrying and physician needs to be notified as high risk for toxicity. Extreme motor dysfunction (ataxia), confusion, convulsions, dehydrated, arrhythmias, polyuria, polydipsia, edema, goiter, hypothyroidism. No specific antidote. Symptom management. Hemodialysis in extreme cases. Anticonvulsant drugs Valproate - Divalproex Sodium (Epival) Carbamazepine Lamotrigine Antianxiety drugs diazepam (valium) clonazepam (rivotril) lorazepam (ativan) Atypical Antipsychotics olanzapine risperidone Treatments 1. ECT 2. Milieu management 3. support groups 4. health teaching and health promotion 5. psychotherapy 6. Advanced-Practice Interventions Personality Disorders Cluster A - weird individuals with these disorders share characteristics of eccentric behaviours, such as social isolation and detachment. may also display perception distortions, unusual levels of suspiciousness, magical thinking, and cognitive impairment Paranoid Personality disorder - longstanding distrust and suspiciousness of others based on the belief, which is unsupported by evidence, that others want to exploit, harm, or deceive the person Schizoid Personality Disorder - exhibit lifelong pattern of social withdrawal, somewhat expressionless and operate with a restricted range of emotional expression. Emotional detachment. Schizotypal Personality Disorder - do not blend in with the crowd. Magical thinking, odd beliefs, strange speech patterns, and inappropriate affect are hallmarks of this disorder. Experience extreme anxiety. Cluster B - wild LECTURE 2: MOOD AND AFFECT 20  show patterns of responding to life demands with dramatic, emotional, or erratic behaviour. Problems with impulse control, emotion processing and regulation, and interpersonal difficulties characterize this cluster of disorders. Insight into these issues is generally limited. To get their needs met, individuals with cluster B personality disorders may resort to behaviours that are considered desperate or entitled, including acting out, committing anti-social acts, or manipulating people and circumstances BPD most well known and dramatic of the personality disorders. patterns of marked instability in emotion regulation, unstable interpersonal relationships, identity or self-image distortions, and unstable mood. Result in severe functional impairments, a high mortality rate and excessive use of health care services. Very impulsive. Emotional lability (rapid and extreme mood changes), ineffective and harmful self-soothing habits (cutting, multiple sexual partners, chronic suicidal ideation). Splitting - primary defense or coping style which is the inability to incorporate positive and negative aspects of oneself or others into a whole image (Black and white thinking, no in-betweens) treatment: Often present with a myriad of symptoms. Antidepressants, mood stabilizers, antipsychotics, Recently an opioid receptor antagonist (Naltrexone) being tried as found to decrease self harm behaviours, anti anxiety meds common. Psychotherapy, Dialectical Behavioural Therapy (DBT) Intervention: Assess and monitor for suicide Do not assume all complaints are manipulation (i.e. physical) Give support for direct communication and for fulfilling responsibilities If possible, have one staff member work with* Focus on self responsibility (obtaining resources) Help patient ID own role in lead up to hospitalization Teach problem solving process Help ID strengths and successful coping and teach other coping Observe how functions in different situations and give feedback Discuss discharge planning frequently and positively Narcissistic personality disorder histrionic personality disorder anti-social personality disorder - a pattern of disregard for, and violation of, the rights of others. Dx reserved for adults. People with this dx may be commonly referred to as sociopaths. Cluster C - worried an individual with these types of personality disorders will demonstrate a consistent patterns of anxious and fearful behaviours, rigid patterns of social shyness, hypersensitivity, need for orderliness, and relationship dependence avoidant personality disorder dependent personality disorder obsessive-compulsive personality disorder LECTURE 2: MOOD AND AFFECT 21