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Pharm III Final
Pharmacology: Bipolar, Anxiety, Psychosis
| Term | Definition |
|---|---|
| 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) |
| Only know anti-suicidal Tx for bipolar? What reduction has been seen? | Lithium; Greater than 50% reduction |
| True MOA for lithium? | Unknown |
| 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 |
| 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. |
| What baseline labs should you get before Rx lithium? (2) | Thyroid and Renal function |
| 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 |
| 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 |
| Level of moderate lithium toxicity and a few Sx | 2.0-2.5 mEq/L: anorexia, blurred vision, motor impairment, delirium |
| 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 |
| Level of severe lithium toxicity and a few Sx | Over 2.5 mEq/L: coma, decreased urine production, renal failiure |
| 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 |
| 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 |
| Specific levels of efficacy for valproate? | Not established |
| 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) |
| Helpful in Tx of of Bipolar 1 depression. Adverse? | Lamotrigine; Adverse: dizziness, HA, blurred vision, Nausea, RASH is the big one. |
| 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 |
| Typical adverse of anti-psychotics? (4) | 1) Wt gain 2) hyperglycemia/DM 3) Dyslipidemia 4) QT prolongation |
| When can anti-depressants be used in bipolar disorder? Why? | Only when a mood stabilizer or atypical anti-psychotic is in place |
| What is TSH not a reliable indicator of in mood disorder patients? Tx? | Subclinical hypothyroidism; Supplemental T4 |
| 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 |
| What is an Anxiolytic? | drug used to Tx anxiety |
| 6 depressant drugs | 1) alcohol 2) inhalants 3) barbiturates 4) benzodiazepines 5) anti-epileptic drugs 6) general anesthetics |
| 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; |
| Major excitatory NT: How does it work? | Glutamate; Opens Na and Ca channels making neuronal cell more responsive to stimulation |
| Chronic exposure to what causes these adverse: disinhibition, self-neglect, fatigue, sluggishness, impaired memory and concentration | Bromides |
| 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. |
| T/F: Barbituates cannot exert their actions in absence of GABA | False; Barbiturates can exert their actions in the absence of GABA |
| 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 |
| What adverse effect profile is similar to barbituates? | Alcohol. That pretty much tells the whole story |
| 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 |
| Non-barbituate sedative-hypnotic. Mixed w/ alcohol called "Mickey Finn" | Chloral hydrate |
| 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 |
| 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) |
| 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 |
| 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. |
| Who aren't Benzos not recommended for? (3) | 1) Those who rely on fine motor/cognitive/alertness skills 2) Receiving CNS depressants 3) Elderly |
| 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 |
| 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) |
| What are 3 indications for Duloxetine? | 1) Chronic neurologic pain 2) Depression 3) Anxiety |
| 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 |
| Cortical activation, dreams are vivid, emotional, bizarre, paralysis, rapid eye movements, autonomic fluctuations | REM Sleep |
| Cortical synchrony, difficult to wake up when deep, dreams brief and less vivid, increased parasympathetic activity | Non-REM Sleep (NREM) |
| 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 |
| 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 |
| Attenuation of circadian alerting signal | MT1 receptor |
| Circadian phase reinforcement or shifting | MT2 receptor |
| How to use Ramelteon and Tasimelteon? | Take single dose at the same time daily 30 minutes prior to bed time |
| 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 |
| sleep worsened relative to baseline for 1-2 days | rebound insomnia |
| slow return of original insomnia symptoms | Recrudescence |
| can result in new cluster of adverse symptoms not present prior to treatment | Withdrawal |
| 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 |
| 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 |
| 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) |
| 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 |
| 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) |
| Antihistamine and sedative properties; one of the first compounds used for psychosis...wasn't very effective. Now used for nausea | Promethazine (phenergan) |
| MOA of Chlorpromazine (one of the first effective Txs of psychosis) | Significantly lowers brain dopamine levels |
| 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 |
| Dopamine stimulant that, when abused, mimics positive psychotic Sx | Amphetamines |
| Glutamate NMDA type receptor antagonist | PCP, Ketamine |
| Dopamine D2 receptor antagonists | Phenothiazines |
| Antipsychotics that work well for positive Sx but may make negative Sx worse. Differ in potency, not effectivness | First generation or Atypical antipsychotics |
| Minimal anticholinergic effects but higher EPS (extra pyramidal symptoms) | Butyrophenones: Haloperidol and Thioxanthines: Thiothixene |
| Benefits of later generation antipsychotics | Better tolerated, lower occurrence of adverse effects, better compliance, less cognitive impairment |
| No EPS, block D2 receptors and 5-HT receptors (generally) | Atypical antipsychotics |
| 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 |
| 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 |
| 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 |
| If Clozapine is so effective, why isn't it used first line!? | Most dangerous of all atypicals...agranulocytosis. Works great but very dangerous |
| Adverse of Clozapine (4) | Highly anticholinergic (low EPS is a good thing), strong alpha blocker so sedating, HypoTN, agranulocytosis, myocarditis |
| 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 |
| May cause transaminitis (elevated liver enzymes), wt gain, hypercholesterolemia, hyperglycemia, orthostatic HypoTN | Quetiapine |
| MAJOR wt gain, hypertriglyceridemia, hyperglycemia, hyperprolactinemia (not much) | Olanzapine |
| QT prolongation,NO associated wt gain, absorption 100% w/ food | Ziprasidone |
| D2 partial agonist, low EPS, no QT prolongation, low sedation, no wt gain | Aripiprazole |
| motor restlessness, "feeling like jumping out of skin" | akathasia |
| jerky motion | dyskinesia |
| muscle rigidity. Tx? | dystonia; diphenhydramine IV and other anticholinergics work well |
| facial grimacing, tics, tongue protruding, lip smacking | tardive dyskinesia (irreversible) |
| tremors, pill rolling movement of fingers, cogwheeling rigidity | Drug-induced Parkinsonism |
| T/F: all typical anti-psychotics have some anticholinergic adverse | True, varies greatly |
| T/F: all typical anti-psychotics have some alpha1 receptor antagonism | True, varies greatly |
| 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 |
| 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 |
Created by:
crward88
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