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Pharm III Final

Pharmacology: Bipolar, Anxiety, Psychosis

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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