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Stahl Chapter 6 Mood Disorders

Stahl Chapter 6 Mood Disorders

Stahl Chapter 6 Mood Disorders

Last updated 28 December 2024

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On this page, is a study guide for Stahl Chapter 6 practice questions on Mood Disorders. The guide has been made from 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 recur- rence 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 recur- rence (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: val- proate 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 phospho- ylation 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 anticon- vulsant 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: 1. DIMINISHING flow of ions through VSSC

2. 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

3. If less sodium is able to pass into neurons, this may lead to DIMINISHED release of glutamate , and less excitatory neurotransmission (theory only)

4. valproate enchances the actions of GABA by INCREASING its release, decreas- ing its reuptake or slowing its metabolic inactivation

5downstream actions on complex signal transduction cascades, inhibit

GSK-3, Block of phosphokinase C (PKC), and MARCKS to PROMOTE neuropro- tection and long-term plasticity p. 374

17. Valproic acid side effects: GI, distress, hepatotoxicity (rare, fatal, LFT & pan- creatic 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 syn- drome

26. Oxcarbazepine (Trileptal)/eslicarbazepine is structurally related to: carba- mazepine

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 interac- tions than carbamazepine p. 379

29. Oxcarbazepine (Trileptal) has never been proven to work as a: mood stabi- lizer, 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 com- bination with bupropion, weight loss in obesity p. 379

31. Topiramate (Topamax) exact binding is not known, but seems to: EN- HANCE 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: ±2li´gands since they bind se- lectively with high affinity to the ±2s´ite 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: ±2li´gands, 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 scle- rosis (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 ap- proved 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

Also Study: Stahl Antipsychotics Chapter 5

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