Pharmacology: Bipolar, Anxiety, Psychosis
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| What is the usual Tx of Bipolar before the long term Tx is administered? What are or is an example of each? | Atypical anti-psychotic usually started before lithium carbonate. Atypical: Haldol (haloperidol), quetiapine, risperidal, olanzapine)
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| Only know anti-suicidal Tx for bipolar? What reduction has been seen? | Lithium; Greater than 50% reduction
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| True MOA for lithium? | Unknown
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| How long for steady state and therapeutic level for Lithium? Elimination? | 5-7 day steady state to get therapeutic levels from 0.4-1.2 mEq/L. Elimination is 95% though kidneys
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| What is the connection between sodium and lithium? | They compete for reabsorption. EXCESS SODIUM intake can INCREASE lithium EXCRETION, reducing efficacy. INADEQUATE SODIUM intake can result in RETENTION of lithium and intoxicity.
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| What baseline labs should you get before Rx lithium? (2) | Thyroid and Renal function
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| What should a contract be signed for before giving lithium? Why? | Contract so they don't get pregnant...Ebstein's anomoly (fetal heart valve and septal defect) occurrence is doubled. Also, cannot breast feed during this time
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| Common adverse of lithium (4) | 1) Increased thirst and polyuria 2) wt gain 3) thyroid effects (goiter and hypothyroidism) 4) CNS including blurring of vision
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| Level of moderate lithium toxicity and a few Sx | 2.0-2.5 mEq/L: anorexia, blurred vision, motor impairment, delirium
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| Level of mild lithium toxicity and a few Sx | 1.5-2.0 mEq/L: abd pain, dry mouth, N/V, drowsiness, dizziness, lethargy or excitement
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| Level of severe lithium toxicity and a few Sx | Over 2.5 mEq/L: coma, decreased urine production, renal failiure
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| 3 main causes of lithium toxicity (one overarching theme) | 1) Decreased sodium intake (no competition for lithium) 2) Extreme exercise water and sodium loss through sweat. 3) General fluid/electrolyte loss
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| What other treatment can help against bipolar instead of lithium? Advantages (1) and disadvantages (3)? | Valproate (valproic acid); A: rapid onset/baseline, not as effective. D: wt gain, pancreatitis, hepatotoxicity
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| Specific levels of efficacy for valproate? | Not established
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| Generally used only if other agents do not work, effective both for mania and refractory depression in bipolar, onset of action in mania 2 weeks and antidepressant effects 6 weeks. Adverse? | Carbamazepine; Adverse: aplastic anemia, Steven-Johnson Syndrome/TEN ESPECIALLY in East Asians (x10 more often)
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| Helpful in Tx of of Bipolar 1 depression. Adverse? | Lamotrigine; Adverse: dizziness, HA, blurred vision, Nausea, RASH is the big one.
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| Equivalent to lithium, superior to valproate and considered a first-line Tx for mania. General class and examples? (2) | Anti-psychotics: Olanzapine, Risperidone, Quetiapine, Ziprasidone, Aripiprazole
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| Typical adverse of anti-psychotics? (4) | 1) Wt gain 2) hyperglycemia/DM 3) Dyslipidemia 4) QT prolongation
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| When can anti-depressants be used in bipolar disorder? Why? | Only when a mood stabilizer or atypical anti-psychotic is in place
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| What is TSH not a reliable indicator of in mood disorder patients? Tx? | Subclinical hypothyroidism; Supplemental T4
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| What is last line for Bipolar depression? How does it work? | ECT or Electroconvulsive Shock Therapy; We don't know how it works...perhaps dumping of NTs and replenishment back to a stable number
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| What is an Anxiolytic? | drug used to Tx anxiety
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| 6 depressant drugs | 1) alcohol 2) inhalants 3) barbiturates 4) benzodiazepines 5) anti-epileptic drugs 6) general anesthetics
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| Major inhibitory NT: How does it work? What drugs effect it? | GABA; Opens Cl and K channels making neuronal membrane less responsive to stimulation. GABA magnified by barbituates, benzos, alcohol;
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| Major excitatory NT: How does it work? | Glutamate; Opens Na and Ca channels making neuronal cell more responsive to stimulation
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| Chronic exposure to what causes these adverse: disinhibition, self-neglect, fatigue, sluggishness, impaired memory and concentration | Bromides
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| Lethal in OD, low safety of margin, high potential for tolerance and abuse, interact dangerously w/ other drugs. Useful w/ head injuries. MOA? | Barbituates; MOA: Increase inhibition by increasing Cl influx.
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| T/F: Barbituates cannot exert their actions in absence of GABA | False; Barbiturates can exert their actions in the absence of GABA
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| T/F: Ultrashort duration of action of barbituates has a low lipid solubility | False, Ultrashort DoA has a high solubility while Long DoA has a low lipid solubility
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| What adverse effect profile is similar to barbituates? | Alcohol. That pretty much tells the whole story
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| T/F: Through tolerance, desired effect may take a higher dose, but death by respiratory depression has the same lethal dose | True. Same dosage would kill you whether you tried it for the first time or were tolerant of drug
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| Non-barbituate sedative-hypnotic. Mixed w/ alcohol called "Mickey Finn" | Chloral hydrate
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| Compound that lowers anxiety w/o producing excessive sedation and has less depression of respiratory centers. Replaced barbituates | Benzodiazepines. Note: Respiratory depression still does occur, and can have synergistic effects w/ other drugs
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| Do Benzos require GABA? (MOA of Benzos) | Yes, they are GABAa agonists. They increase number of times Cl channels open in response to GABA (so they require GABA to be effective)
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| Benzo effects in : 1) amygdala, frontal cortex, insula (4) 2) cerebral cortex and hippocampus (2) 3) spinal cord, cerebellum, brain stem (2) | 1) Reduce response to fearful stimuli, anxiety, panic, agitation 2) Can produce confusion and amnesia 3) Can produce muscle relaxation and mild sedation
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| Metabolism and Excretion of Benzos? Can Benzos be reversed? Why or why not? | Metabolism in liver, excretion though kidneys/urine. Reversed by Flumazenil by binding GABA receptor.
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| Who aren't Benzos not recommended for? (3) | 1) Those who rely on fine motor/cognitive/alertness skills 2) Receiving CNS depressants 3) Elderly
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| Reduces aggression, anxiety, irritability w/o sedation or respiratory depression, and little potential for abuse. Type of drug? Adverse? (2) | Buspirone; Type: Serotonin Receptor Partial Agonist. A: profound HypoTN w/ MAO-Is and non specific CP w/ those w/ prior cardiac disease
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| What is Kava and how does it work? Adverse? | beverage that may reduce anxiety but has significant hepatotoxicity. Blocks Na channels, acts on GABAa receptors and is a reversible inhibitor of MAO (is essentially a MAO-I)
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| What are 3 indications for Duloxetine? | 1) Chronic neurologic pain 2) Depression 3) Anxiety
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| Subjective patient complaint of difficulty falling asleep, difficulty staying asleep, poor quality sleep, or inadequate sleep despite adequate opportunity. What disorders are related to this disease? (2) | Insomnia; Anxiety disorders (OCD, PTSD, Panic, GAD, Hypochondirasis) and Substance abuse
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| Cortical activation, dreams are vivid, emotional, bizarre, paralysis, rapid eye movements, autonomic fluctuations | REM Sleep
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| Cortical synchrony, difficult to wake up when deep, dreams brief and less vivid, increased parasympathetic activity | Non-REM Sleep (NREM)
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| Endogenous neuropeptides that are critical to sleep and WAKEFULNESS through activation of cholinergic and monoaminergeric neurons in the hypothalamus and brain stem | Orexins or hypocretins
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| Act on suprachiasmatic nucleus (SCN) which sends signals to pineal gland to influence release of melatonin. 2 examples? Adverse? (2) | Selective Melatonin Receptor Agonists: Ramelteon and Tasimelteon; A: make you tired, hyperprolactinemia
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| Attenuation of circadian alerting signal | MT1 receptor
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| Circadian phase reinforcement or shifting | MT2 receptor
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| How to use Ramelteon and Tasimelteon? | Take single dose at the same time daily 30 minutes prior to bed time
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| Sedative adverse: All day? (3); Morning? (3) Unpredictable? (2) | All day: depressed cognition, somnolence, fatigue; Arising: dizziness, blurred vision, ataxia; Unpredictable: anterograde amnesia, complex sleep behavior
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| sleep worsened relative to baseline for 1-2 days | rebound insomnia
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| slow return of original insomnia symptoms | Recrudescence
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| can result in new cluster of adverse symptoms not present prior to treatment | Withdrawal
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| Suppresses wakefulness, significant reduction in time to continuous sleep. Effects doubled in obese. Adverse?(2) Major problem? | Suvorexant; A: daytime somnolence, unconscious nighttime activity. MP: Suicidal ideation w/ repeated dosages
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| Postsynaptic histaminic and muscarinic blockade. Most common OTC sleep aid ingredients. Adverse? (4) | Antihistamines, especially first generation (Diphenhydramine, Doxylamine). Adverse: Residual effects: dizziness/somnolence. Antimuscarinic effects (dry mouth, constipation, urinary retention), blurred vision, narrow angle glaucoma exacerbation
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| What are some other non-pharmological methods to insomnia? (2) | 1) Behavioral Tx like stimulus control therapy (assumes learned association btwn wakefulness and bedroom). 2) Relaxation Training (progressive muscle relaxation, guided imagery, biofeedback, self-hypnosis)
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| What does positive Sx mean and what are the positive schizophrenia Sx? (3) | Manifestations of psychosis; 1) Delusions 2) Auditory hallucinations 3) Thought disorder (false beliefs about self or others, paranoia
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| What are negative schizophrenia Sx and what does negative Sx mean? (5) | Absence of normal traits or abilities; 1) Flat affect 2) Alogia (poverty of speech) 3) Anhedonia 4) Asociality 5) Avolition (lack of motivation)
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| Antihistamine and sedative properties; one of the first compounds used for psychosis...wasn't very effective. Now used for nausea | Promethazine (phenergan)
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| MOA of Chlorpromazine (one of the first effective Txs of psychosis) | Significantly lowers brain dopamine levels
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| Dopamine Hypothesis of 1950s. Problems with it? | Excess dopamine leads to psychosis. Therefore blockade of D2 receptors should provide reversal of psychotic features immediately. BUT these patients usually take 2-4 weeks for a response to antipsychotics, and some never improve
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| Dopamine stimulant that, when abused, mimics positive psychotic Sx | Amphetamines
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| Glutamate NMDA type receptor antagonist | PCP, Ketamine
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| Dopamine D2 receptor antagonists | Phenothiazines
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| Antipsychotics that work well for positive Sx but may make negative Sx worse. Differ in potency, not effectivness | First generation or Atypical antipsychotics
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| Minimal anticholinergic effects but higher EPS (extra pyramidal symptoms) | Butyrophenones: Haloperidol and Thioxanthines: Thiothixene
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| Benefits of later generation antipsychotics | Better tolerated, lower occurrence of adverse effects, better compliance, less cognitive impairment
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| No EPS, block D2 receptors and 5-HT receptors (generally) | Atypical antipsychotics
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| We know that serotonin inhibits dopamine release. What are positive Sx associated w/ when blocking serotonin receptors? | HYPERdopaminergic condition because less serotonin means more dopamine
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| We know that serotonin inhibits dopamine release. What are negative Sx associated w/ when blocking serotonin receptors? | HYPOdopaminergic condition because more serotonin means less dopamine release
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| Effect on Positive Sx of Schizophrenia: 1st gen vs clozapine (2nd gen) | 1st: 70% helped, relapse from 75->20%. 2nd: 85% helped, relapse 10%. Helps 1/3 to 1/2 of those not helped by 1st gen
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| If Clozapine is so effective, why isn't it used first line!? | Most dangerous of all atypicals...agranulocytosis. Works great but very dangerous
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| Adverse of Clozapine (4) | Highly anticholinergic (low EPS is a good thing), strong alpha blocker so sedating, HypoTN, agranulocytosis, myocarditis
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| Predominantly blocks D2, then 5-HT. Lacks antichoinergic activity so better for youth or elderly. Increased EPS. Problem? | Risperidone; Elevated prolactin levels so contra in Breast Ca
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| May cause transaminitis (elevated liver enzymes), wt gain, hypercholesterolemia, hyperglycemia, orthostatic HypoTN | Quetiapine
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| MAJOR wt gain, hypertriglyceridemia, hyperglycemia, hyperprolactinemia (not much) | Olanzapine
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| QT prolongation,NO associated wt gain, absorption 100% w/ food | Ziprasidone
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| D2 partial agonist, low EPS, no QT prolongation, low sedation, no wt gain | Aripiprazole
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| motor restlessness, "feeling like jumping out of skin" | akathasia
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| jerky motion | dyskinesia
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| muscle rigidity. Tx? | dystonia; diphenhydramine IV and other anticholinergics work well
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| facial grimacing, tics, tongue protruding, lip smacking | tardive dyskinesia (irreversible)
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| tremors, pill rolling movement of fingers, cogwheeling rigidity | Drug-induced Parkinsonism
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| T/F: all typical anti-psychotics have some anticholinergic adverse | True, varies greatly
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| T/F: all typical anti-psychotics have some alpha1 receptor antagonism | True, varies greatly
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| Catatonic mental status, tachycardia, unstable BP, hyperthermia, muscle rigidity, tremors, increased WBC and CPK. Tx? (3) | Neuroleptic Malignant Syndrome (NMS). Didn't get this answer? Remember FEVER from serotonin syndrome. Tx: 1) D/C med 2) Bromocriptine to reverse dopamine blockade 3) Dantrolene to relax muscles
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| T/F: There is one oral medication available for Tx of acute agitation in psychosis. What is it? | LOL False. AND, unfortunately, parenteral meds are associated w/ significant adverse
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