On this page, is a study guide with practice questions for Mood Stablizers Exam . The guide has been made based on the 5th edition Test Bank for Stahl's Essential Psychopharmacology Neuroscientific Basis and Practical Applications by Stephen M. Stahl
1.Another way to refer to mood stabilizers are: treat from above, stabilize from above treat from below, stabilize from below p 370-371
2.treat from above, stabilize from above: a mania minded drug that reduces symptoms of mania and prevent relapse and recurrence of mania p. 370
3.treat from below, stabilize from below: drugs can be depression minded and reduce symptoms of bipolar depression or stabilize to prevent relapse and recurrence of depression p.370-371
4.do all mood stabilizers treat the four therapeutic actions: No p. 371
5.Lithium is an: ion, its mechanism of action is not positive p. 371
6.mechanism of action explanations for Lithium are unknown but postulated as: second messengers, such as the phosphatidyl inositol system where Lithium inhibits enzyme inositol monophosphatase; modulation of G proteins; and regulation of gene expression for growth factors and neuronal plasticity by interaction with DOWNSTREAM signal transduction cascades, including inhibition of GSK-3 and protein kinase C p 372-373
7.Lithium is well proven effective in: manic episodes and maintenance of recurrence (treat from above & stabilize from above) p. 372
8.Lithium is established to prevent: suicides in patients with mood disorders p. 372
9.lithium has equal or better efficacy in bipolar disorder compared to: valproate for manic depressive, or mixed episodes, though valproate is more frequently prescribed p. 372
10. theoretically, lithium can, through inhibition of GSK-3: inhibit the phosphoylation of tau proteins, thus slow formation of plaques and tangles in Alzheimer's disease, and possible prevent progression from mild cognitive impairment to Alzheimer's disease and reduce phosphorylated tau levels if give > than a year, even at low doses p. 373
11. side effects of lithium include: gastrointestinal symptoms, weight gain, hair loss, acne, tremor, sedation, decreased cognition, and incoordination, there are long-term adverse effects upon the thyroid and kidney p. 372-373
12. valproate and carbamazepine are two anticonvulsant mood stabilizers that: treat epilepsy (++++) treat from above (++++) stabilize from above (++++) treat from below (+)
stabilize from below (+/-) equally p. 373, table 8-1
13. lamotrigine is an anticonvulsant mood stabilizer that: treat epilepsy (++++) treat from above (+/-) stabilize from above (++++) treat from below (+++) stabilize from below (++++) equally p. 373, table 8-1
14. topiramate, zonisamide, gabapentin, pregabalin, levetiracetam are anticonvulsant mood stabilizers that ONLY treat: treat epilepsy (++++) treat from above (+/-) stabilize from above (+/-) p. 373, table 8-1
15. mechanism of action explanations for valproate acid is uncertain but postulated as:
1. inhibiting voltage-sensitive sodium channels
2.boosting the actions of GABA
3.regulating downstream signal transduction p. 373
16. valproate acid possibly acts on:
- DIMINISHING flow of ions through VSSC
- valproate may change the SENSITIVITY of sodium channels by altering their phosphorylation by binding directly to the VSSC, or regulatory units or by inhibiting phosphorylating enzymes
- If less sodium is able to pass into neurons, this may lead to DIMINISHED release of glutamate , and less excitatory neurotransmission (theory only)
- valproate enchances the actions of GABA by INCREASING its release, decreasing its reuptake or slowing its metabolic inactivation
- downstream actions on complex signal transduction cascades, inhibitGSK-3, Block of phosphokinase C (PKC), and MARCKS to PROMOTE neuroprotection and long-term plasticity p. 374
17.Valproic acid side effects: GI, distress, hepatotoxicity (rare, fatal, LFT & pancreatic measured), neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated for pregnancy, insulin resistance may be associated in women, polycystic ovaries, hyperandrogenism p. 374-375
18.Carbamazepine is hypothesized to act by: BLOCKING VSSCs at a site within the channel itself, known as alpha subunit p.375
19.valproate action on GABA sites may be due to: enhancement of GABA , perhaps by inhibiting GABA reuptake, or interfering with the metabolism of GABA by GABA transaminase (GABA-T) p. 376 figure 8-6
20.valproate is also effective in treating: migraine p. 376
21.carbamazepine is effective in treating: neuropathic pain p. 376
22.Side effects of carbamazepine: suppressant effect on bone marrow, requiring initial monitoring of blood counts, induction of 3A4, sedating and cause feta toxicity such as neural tube defects p. 376
23.Lamotrigine is approved as a mood stabilizer to prevent: recurrence of both mania and depression p. 376
24.Lamotrigine (Lamictal) appears to: reduce the release of glutamate p. 376
25.Lamotrigine is generally well: tolerated, except for Stevens-Johnson syndrome
26.Oxcarbazepine (Trileptal)/eslicarbazepine is structurally related to: carbamazepine the S enantiomer is eslicarbazepine, thus oxcarbazepine works via conversion to eslicarbazepine p. 377
27.Oxcarbazepine is an anticonvulsant that: BINDS to the open channel of the VSSC within the alpha subunit p. 377-378
28.Oxcarbazepine is: less sedating, less bone marrow toxicity, fewer 3A4 interactions than carbamazepine p. 379
29.Oxcarbazepine (Trileptal) has never been proven to work as a: mood stabilizer, but is used as "off-label_, especially for the manic phase of bipolar p. 379 30. Topiramate (Topamax) is approved for: anticonvulsant, migraine, and in combination with bupropion, weight loss in obesity p. 379
31. Topiramate (Topamax) exact binding is not known, but seems to: ENHANCE GABA function, and REDUCE glutamate by interfering with both sodium and calcium channels p. 379
32. Gabapentin and Pregabalin have little or no action as: mood stabilizers, yet treat pain condition from neuropathic pain to fibromyalgia and various anxiety disorders p. 379
33. Gabapentin and Pregabalin are classified as: ±2ligands since they bind se-´ lectively with high affinity to the ±2site of VSSC, thus blocking these VSCC (calcium ´ channels) when open causes improvement of seizures, pain, and anxiety but not stabilization of mood p. 379
34. N, P/Q, and L type channels are targeted by: ±2ligands, L channel on vascular ´ smooth muscle that are targeted by various antihypertensive and antiarrhythmic drugs are called calcium channel blockers, some evidence suggest dihydropyridie calcium channel blockers may be useful for some patient with bipolar disorder p. 379 35. Riluzole was developed to slow the progression of: amyotropic lateral sclerosis (ALS, Lou Gehrig's disease) p. 379-380
36. Riluzole works similarly to lamotrigine by: diminishing glutamate release, however it is expensive and has frequent liver function abnormalities associated with it p. 380
37. D2 antagonist actions have proven effective for: nonpsychotic symptoms of mania and maintenance to prevent recurrence of mania p. 380
38. all atypical antipsychotics are approved for schizophrenia, most are approved for mania, but only for for bipolar depression is: quetiapine, with another having multiple positive clinical trials in bipolar depression (lurasidone). p.381
39. Boston bipolar brew are proponents of: any combo, but NEVER utilize an antidepressant p. 384, 385
40. California careful cocktail proposes the possibility of patients: earning the right to add an antidepressant, carefully, and once exhausting other options for a bipolar depressed patient whose depression is not in remission p. 384, 385
41. Tennessee mood shine provides the option of: treating bipolar depression that arises when giving an antidepressant and discovering the patient either has activating side effects or treatment resistance, in this case, rather than stopping the antidepressant, an atypical antipsychotic is added p. 384, 385
0
1511