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REGIS PSYCH 643 Study Guide Module 5 : Depression
Familiarize yourself with theories of bipolar spectrum disorder and their criticism (Article: Bipolar Spectrum: A Critical Perspective) with consideration of the following:
- Patient presentation rarely fits neatly into unipolar depression, bipolar I and bipolar II diagnostic criteria.
- Treatment decisions can be guided by the bipolar spectrum classification. What are the 3 neurotransmitters most implicated in mood disorders? Serotonin, Dopamine, Norepinephrine Describe the synthesis of norepinephrine. Tyrosine Hydroxylase convert amino acid Tyrosine into DOPA, DOPA decarboxylase convert DOPA to DA, Dopamine b hydroxylase converts DA into NE How is norepinephrine metabolized? Monoamine oxidase (MAO) A or B, Catechol-o-methyl-transferase (COMT) What is the significance of presynaptic alpha- 2 receptors? Presynaptic alpha 2 receptors are located in both the axon terminal and soma. Only a receptors can act as presynaptic autoreceptors, presynaptic alpha 2 receptors regulate norepinephrine release Describe how norepinephrine regulates serotonin. NE regulates 5HT neuros via alpha 1 and alpha 2 receptors, a1 accelerate and a2 brake Compare the monoamine hypothesis of depression to the monoamine receptor hypothesis and the proposed validity of each. (This information is also covered in Chapter 7.) Monoamine hypothesis conclude that depression is due to a deficiency of monoamine neurotransmitters and mania is due to an excess of monoamine neurotransmitters. Monoamine receptor hypothesis posits that abnormality in the receptors for monoamine neurotransmitters leads to depression. Describe the role of stress, BDNF and brain atrophy in depression. What is the relationship between monoamines and BDNF? Under stress brain-derived neurotrophic factor (BDNF) is repressed. Stress lower 5HT levels and can acutely increase, then chronically deplete both NE and DA. These
monoamine neurotransmitters changes together with deficient amounts of BDNF may lead to atrophy of neurons in the hippocampus and other brain areas like the prefrontal cortex. What is stress sensitization and its presumed role in depression? Certain types of stress such as child abuse can sensitize brain circuits and render them vulnerable to future stressors. Patients with vulnerable brain circuits who become exposed ti multiple life stressors can result in development of depression. What is the significance of neural circuits in depression? Inefficient information processing in neural circuits leads to depression Stahl Chapter 7 + Supplemental Materials Define treatment response, remission, relapse and recovery in depression. According to the Star D study, which symptoms are most likely to respond to antidepressant treatment? Depressed mood, suicidal ideation and psychomotor retardation Describe the mechanism of action of SSRIs. For the following SSRIS, how do their secondary mechanisms of action differ? What is the clinical significance of these differences? Are their particular patient profiles that are best matched to these medications? Describe the unique mechanism of action of vilazodone. Vilazodone SERT inhibition + 5HT1a partial agonisim Describe the mechanism of action of trazodone. How does treatment effect differ for dose strengths? What are the clinical findings for the 4 newest antidepressants, vilazodone, Describe the mechanism of action of MAO-inhibitors? Describe the mechanism of action of hypertensive crisis in MAOIs. Describe symptoms associated with hypertensive crisis and describe its treatment. Identify foods that are contraindicated while taking MAO-I. What are the roles of folate, SAMe and thyroid in depression? (Brain stimulation will be covered in the next module.) How does symptom presentation guide antidepressant selection? Know, understand and apply the implications of all warnings and safety risks associated with antidepressants including:
best tolerated SSRI with fewest CYP-mediated drug
interactions
5. Paroxetine (Paxil)- an SSRI with Muscarinic anticholinergic and
norepinephrine transporter (NET) inhibitory action- tends to be
more calming and sedating in early treatment. Paroxetine
inhibits the enzyme nitric oxide synthetase which contributes
to sexual dysfunction especially in men. Associated with
withdrawal upon sudden discontinuation
6. Citalopram (Celexa)- Two enantiomers R and S(aka racemic
citalopram)- R enantiomers is bad, QTc prolongation with dose
increase.
· Review dry mouth as a symptoms with antidepressant use
· Review food and monoamine oxidase inhibitors
Ingesting food containing tyramine like aged cheese, wine and
beers ( Hypertensive crisis/blood pressure elevation).
Selegiline transdermal patch does not have any dietary
restriction/it bypass the gut.
· Review the best treatment for sexual side effects caused by
antidepressants
Combining either a stimulant or sildenafil with an SNRI
· Review which drug class serotonin/norepinephrine/dopamine are
key targets for
· Review medication profile for tricyclic antidepressants
· Review medication profile for Trazodone
Block 5HT2a and 5HT2c as well as serotonin. Also know as
serotonin antagonist/reuptake inhibitor (SARI).
At lower dose Trazodone is effective a treating insomnia.
At higher dose it treat depression by recruiting SERT inhibition
and raise serotonin levels
· Review briefly the findings of the STAR D study
Only one third of patients remit on their first antidepressant
treatment, and even after a year of treatment with a sequence
of 4 different antidepressants given for 12 weeks, only about 2
thirds of depressed patients achieve remission of their
symptoms.
· Review what medication may cause increase bleeding with
antidepressant use.
· Review comparison of desvenlafaxine to venlafaxine
Venlafaxine(Effexor) is a substrate for CYP 2D6, which converts
it to an active metabolite Desvenlafaxine( Pristiq).
Desvenlafaxine has greater NET inhibition relative to SERT
inhibition compared to Venlafaxine
· Review definition of treatment resistant
· Review dietary tyramine and MAO inhibitors
Ingesting food containing tyramine like aged cheese, wine and
beers ( Hypertensive crisis/blood pressure elevation).
Selegiline transdermal patch does not have any dietary
restriction/it bypass the gut.
· Review factors important to consider when treating a depressed
treatment resistant patient
· Review what effect ECT has on depression
ECT is the only effective therapeutic agent for Depression that is resistant to
antidepressant.
· Review side effects of mirtazapine
Drowsiness and weight gain
· Review antidepressant use and suicide with patients > 65...
outcome
>65 may not respond as quickly to antidepressant. Do not
have increased suicide risk from taking antidepressant
· Review side effect profile for Duloxetine (Cymbalta)
Have a lower incidence of hypertension and milder withdrawal
reactions than venlafaxine.
· Review side effects of Venlafaxine at higher doses
Sweating and elevated blood pressure, Nausea
· Review the role of neural circuits in depression
· Review Unique roles of certain antidepressants (Matching)
SSRI
MAOI’s
TCA’s
· Review which side effect of antidepressant use may resolve with
time.
Agitation/activation, Sedation, Insomnia,Appetite changes, Headache, Stomach
upset
· Review rules associated with rTMS
In 2008, the FDA approved rTMS as a treatment for adults with MDD who “have
not responded to a single antidepressant medication in the current episode
rTMS was more likely to produce remission (moderate strength of evidence);
patients receiving rTMS were more than 5 times as likely to achieve remission as
those receiving sham (relative risk = 5.07; 95% CI, 2.50 to 10.30).”
- Which psychotherapies have the capacity to create epigenetic changes in the brain?
CBT and Interpersonal Therapy
Week 8 Quiz: Bipolar, Anxiety & Sleep
Bipolar Study Guide Stahl, Chapter 8 What is the hypothesized mechanism of action of lithium? P. 372. Lithium may work by affecting the signal transduction through its inhibition of secondary messenger enzymes such as inositol monophosphatase by modulation of G proteins or by interaction at various sites within downstream signal transduction. Which anticonvulsants have proven efficacy in bipolar disorder? P. 373 Carbamazepine (Tegretol) and Valproate (Depakene) What is the hypothesized mechanism of action of each? P. 373 Carbamazepine (Tegretol) – Blocking Voltage - sensitive sodium channels. 1st anticonvulsant shown to be effective in manic phase of bipolar. Enhance the inhibitory actions of GABA, binding to subunit of VSSC, Calcium and potassium channels as well. Treat neuropathic pain. Valproate (Depakene) - Inhibiting VSSC, Boosting neurotransmitter GABA, and regulating the downstream transduction cascade – p. 374. Treat migraine Which mood stabilizers have less evidence of efficacy in bipolar disorder? P. 379 Oxcarbazepine/eslicarbazepine, Topiramate(Topamax), Gabapentin/Pregabalin
What is the hypothesized mechanism of action of each? P. 377 - 379 Oxcarbazepine/ eslicarbazepine – Binding to the open channel confirmation of the VSSC at the site within the channel itself on the alpha subunit. Topiramate (Topamax)- enhance GABA function and reduce glutamate function by interfering with both sodium and calcium channels. Gabapentin and Pregabalin- a2 ligands, they bind selectively and with high affinity to the a2 site of voltage-sensitive calcium channels. Prevent seizures and anxiety but does not stabilize mood. How are atypical antipsychotics theorized to be effective in bipolar disorder? P. 380 By reduction of Glutamate hyperactivity from overly active pyramidal neurons by serotonin 2a antagonist actions (5HT2a). Traditional Antipsychotics Used BEFORE Lithium
- Atypical Antipsychotics include the following, which are ALL EFFECTIVE for Acute Mania and Maintenance:
- Olanzapine (Zyprexa)
- Risperidone (Risperdal)
- Quetiapine (Seroquel)
- Ziprasidone (Geodon)
- Aripiprazole (Abilify)
- Lurasidone (Latuda) Describe the use of benzodiazepines in the treatment of bipolar disorder? P. 381 Benzo’s works on GABAa receptors, and can have a calming effect immediately, providing valuable time for mood stabilizers with long action of onset to work. What are the recommendations for antidepressants in the treatment of bipolar depression? P. 382- 385 It Varies. Boston brew never uses antidepressants. California careful cocktail cautiously adds on an antidepressant when a patient’s depression is not in remission, and Tennessee mood shine adds an antidepressant for treatment resistance or the dx changes from unipolar to bipolar and the condition is evolving. What are the drawbacks to starting lamotrigine? P. 383 Long titration times (2 months) and Increased doses of lamotrigine increases the risk of a serious rash. In what circumstances are benzodiazepines appropriate in the treatment of bipolar disorder? P. 381.
For each of the following, what are safety issues, dosing considerations, and serious side effects? (Can also use concept map) Carbamazepine - Before : CBC, electrolytes (for sodium), LFTs, pregnancy test2, HLA-B* reaction in Asians! (Steven Johnson syndrome) After : CBC monthly x 2 months, then every 3– 6 months, then yearly; electrolytes, LFTs every 6–12 months; CBZ level 1 week after dose changes, every 6 – 12 months otherwise. Therapeutic level 4 - 12 mcg/ml toxic >12. Lamotrigine Before: Cr Opth exam. Monitor for worsening depression suicide, bipolar symptoms. Severe immune system reaction and rash! Lithium Before : TSH, BUN/creatinine5, pregnancy test, ECG if cardiac disease or older patient After : BUN/creatinine every 6–12 months; Li level one week after dose changes, every 6– 12 months; TSH 2 weeks, 6 months, then annually. Therapeutic level 0.6-1.2 meq/l toxic > 1. Oxcarbazepine No black box warning. Before : Sodium After: Sodium at 1–3 months, then if symptoms of hyponatremia appear Depakote Before: Major hepatotoxicity (liver failure). Monitor LFT’s, then frequently during the first 6 months, CBC, Coag tests, pregnancy, and drug levels. Therapeutic 50 - 125 mcg/ml. Toxic >
1. Review if new learning can modulate a conditioned fear response. P. 409
Yes fear that are learned and not forgotten may hypothetically progress to anxiety
disorders or major depressive disorder
2. Review if short & long acting benzodiazepine risk is associated with an increased
risk of dementia.
Short answer, yes. Long term use only.
3. Review if Z-drugs can be taken mid-sleep cycle for mid-sleep walking.?
No. zolpidem, are associated with complex behaviors such as sleepwalking
4. Review the use of clonidine and propranolol in the treatment of anxiety p. 415
Clonidine Propranolol Beta-blockers, also known as beta-adrenergic blocking agents, block norepinephrine and epinephrine (adrenaline) from binding to beta receptors on nerves. These hormones are what cause the physical symptoms of anxiety and blocking them reduces these effects, helping control some of the physical symptoms of anxiety.
5. Review the origin of anxiety in some individuals of the brain to include the locus
coeruleus. P. 392- 395
Locus Coeruleus-Area of the brain linked with increased noradrenergic activity
and anxiety
6. Matching column match mood stabilizer to recommended lab monitoring. EX:
Valproic Acid Depakote Before: Major hepatotoxicity (liver failure). Monitor LFT’s, then frequently during the first 6 months, CBC, Coag tests, pregnancy, and drug levels. Therapeutic 50 - 125 mcg/ml. Toxic >
Carbamazepine Before: CBC, electrolytes (for sodium), LFTs, pregnancy test2, HLA-B*
reaction in Asians! (Steven Johnson syndrome) After: CBC monthly x 2 months, then every 3 – 6 months, then yearly; electrolytes, LFTs every 6–12 months; CBZ level 1 week after dose changes, every 6 – 12 months otherwise. Therapeutic level 4 - 12 mcg/ml toxic >12.
Quetiapine Before: Lipids, BS, Slit lamp, CBC. After: monitor for leukopenia,
neutropenia.
Lithium Before: TSH, Na+ BUN/creatinine 5, pregnancy test, ECG if cardiac disease or older
patient After: BUN/creatinine every 6 – 12 months; Li level one week after dose changes, every 6 – 12 months; TSH 2 weeks, 6 months, then annually. Therapeutic level 0.6-1.2 meq/l toxic > 1. Lamotrigine Before: Cr Opth exam. Monitor for worsening depression suicide, bipolar symptoms. Severe immune system reaction and rash!
7. Review second line meds for Bipolar D/O p. 371 on
Risperidone (Risperdal); Olanzapine (Zyprexa); Quetiapine (Seroquel); Ziprasidone (Geodon); Aripiprazole (Abilify)
8. ID meds for Bipolar D/O favorable for the individual with liver disease
Lithium, Olanzapine, Ziprasidone, Gabapentin Valproate , Risperidone, Quetiapine, Lamotrigine, Topiramate, Carbamazepine (reduce dose)
9. Review risk associated with abrupt Benzo cessation
Most common SE: drowsiness, sedation, impaired motor coordination-ataxia,
weakness, dizziness, confusion, memory loss, seizures
10. Review if Benzos medications are appropriate for treatment of acute Bipolar
Mania. P. 381
Benzos provide valuable adjunctive treatment to proven mood stabilizers,
especially in emergent situations.
clonazepam [Klonopin])
11. Review medication for shift workers with excessive daytime sleepiness? P. 465 -
Caffeine, Modafinil, stimulants – methylphendate and Gamma-hydroxybutyrate
(GHB).
21. Review Buspirone indication for which type of anxiety D/O p. 414.
Buspirone is indicated for GAD.
22. Review which neurotransmitter responsible for action of ramelteon P. 457
Ramelteon is an Melatonin 1 and 2 (MT1/MT1) agonist used for the treatment of
insomnia
23. Review adjunctive use of benzodiazepines with mood stabilizers p. 381
benzodiazepines can have calming action immediately and can be used short term
to allow time for mood stabilizers with a longer onset of action to begin working
24. Review standard of care when prescribing hypnotics to treat insomnia
- Asking/educating pt. about sleep hygiene
- Cognitive Behavioral therapy
- Work-up for underlying cause insomnia; may still prescribe sleeping pill in the intermediate time
- Sedative-Hypnotic
25. Review first line monotherapy and antidepressant use in bipolar depression.
First Line Monotherapy in Bipolar Depression- Lamotrigine, QUETIAPINE
26. Review tapering guidelines regarding long term benzodiazepines use
if tx > 12 weeks, taper at rate of 10-25%/ week
-persistent abstinence syndrome can last up to 1 yr, worse in 1st month, may take > 6
months before noticeable benefits to patient and family members
-Gabapentin may be helpful
27. Review fear and the amygdala p. 392 - 394
The processing of fear response is regulated by the numerous neuronal
connections flowing in and out of the amygdala. The neurobiology regulators of
the amygdala including the neurotransmitters GABA, 5HT, NE, the voltage-gated
calcium channels.
28. Review medication treatment for overlapping symptoms of anxiety and
depression p. 414 - 416
First Line of treatment SSRI/SNRI augmenting with benzodiazepine
29. Review Side effects of Topamax regarding cognition
Poor concentration, confusion, speech difficulty, cognitive slowing.
30. Review the uses of Hydroxyzine in Alcohol dependence and anxiety disorder
Hydroxyzine (brand names Vistaril, Atarax) is a first-generation antihistamine hydroxyzine functions principally as an inverse agonist of the H1 histamine receptor. However, dissimilar to other first-generation antihistamine agents, it doesn’t significantly impact mACh (muscarinic acetylcholine receptors); this is favorable in reducing occurrence of anticholinergic side effects. Hydroxyzine also elicits antiserotonergic effects, meaning it inhibits action at serotonin (5-HT) receptors, which in turn, yields a therapeutic anxiolytic response.
31. Review the purpose/role of the amygdala in anxiety p. 392
The processing of fear response is regulated by the numerous neuronal
connections flowing in and out of the amygdala. The neurobiology regulators of
the amygdala including the neurotransmitters GABA, 5HT, NE, the voltage-gated
calcium channels.
32. Review important aspects of sleep hygiene practices especially if unable to fall
asleep
- Set a sleep/wake schedule
- Exercise daily, but not at night
- Avoid caffeine, cigarettes, alcohol, and drugs
- Invent a relaxing bedtime ritual
- Use the bed only for sleeping & sex
- Keep the room dark and wake up to the sun
- Adjust the room temperature as desired
33. Review the Carlatt Psychiatry report recommendations for patients experiencing
poor sleep quality.
Valerian has been compared head-to-head with Serax
(oxazepam) 10 mg QHS in 202 patients with insomnia, and
the herbal was every bit as effective as the benzo ( Eur J Med
Res 2002; 25:480-486).
34. Review how the class of anticonvulsants work in the treatment of bipolar disorder
p. 373
Carbamazepine (Tegretol) – Blocking Voltage - sensitive sodium channels. 1st anticonvulsant shown to be effective in manic phase of bipolar. Enhance the
the prefrontal cortex that regulate emotion, namely the orbitofrontal cortex and the anterior cingulate cortex. a. How does fear response differ from fear conditioning? What additional brain structures are involved? P.408- 409 Fear conditioning is a learned fear that is crucial for survival example: fearing dangerous situations. Other fears that are “learned” and not “forgotten” may hypothetically prograss to anciety disorders or MDD. The amygdala is involved in remembering the various stimuli associated with a given fearful situation.
- Describe the role of GABA in anxiety and fear. GABA is a key neurotransmitters involved in anxiety and anxiolytic action of many drugs. It reduce activity in the amygdala and CSTC loops. Benzo act by enhancing GABA actions at the level of the amygdala and at the prefrontal cortex within CSTC loops to reduce anxiety
- Which GABA receptor subunits modulate anxiety? Which are targets for hypnotic effects of benzodiazepines?
GABAa modulate anxiety
- What is the mechanism of action of benzodiazepines? What effect to benzodiazepines have on GABA receptors? P. Benzo act by enhancing GABA actions at the level of the amygdala and at the prefrontal cortex within CSTC loops to reduce anxiety. GABAa mediate inhibitory neurotransmission.
- How is serotonin believed to work as an anxiolytic?
Symptoms, circuits and neurotransmitters linked to anxiety disorders overlap
extensively with those for major depressive disorder. Serotonin is a key
neurotransmitters that innervates the amygdala as well as the element of the
CSTC circuits.
- Describe the differences between fear response, fear conditioning, fear extinction, memory reconsolidation? P. 408 - 411 - 414
Fear extincsion is the progressive reducation of the response of the response to a
feared stimulus.
Reconsolidation-
- Describe the role of beta blockers in fear condition and fear extinction.
b-blockers can mitigate the conditioning of the original traumatic memory
- What are the first line treatments for each of the following disorders? Support your responses with treatment guidelines, PowerPoint presentation.
- Generalized anxiety- Paroxetine, Escitalopram, Venlafaxine XR, Duloxetine
- Panic Disorder- Fluoxetine, Sertraline, Paroxitine, Venlafaxine
- Social Anxiety Disorder- Sertraline Poraxitine, Venlafaxine
- Posttraumatic Stress Disorder- Sertraline, Paroxetine
Study Guide: Anxiety Stahl Chapter 11
- Which neurotransmitters are implicated in the arousal spectrum? Histamine, Dopamine, Norepinephrine, Serotonin and acetylcholine
- Describe the brain region and neurotransmitters involved in sleep and wake cycles. The on switch localize in the tuberomammillary nucleus (TMN) of the hypothalamus. The off switch localized within the ventrolateral preoptic (VLPO) nucleus of the hypothalamus. Orexin and hypocretin. Two key neurotransmitters that regulate sleep/wake switch are: Histamine from TMN and GABA from VLPO
- How can light and melatonin to be used in phase delayed sleep disorders?
- What is the role of histamine at the H1 Receptor and the H3 Receptor? H1 receptors activates G-protein-linked second messenger that activate phosphatidyl inositol and the transcription factor cFOS and result in wakefulness, normal alertness and pro-cognitive actions. H3 receptors are presynaptic and function as autoreceptors. When histamine bind to it it turns off further release of histamine,
- How do zaleplon, zolpidem and zopiclone, differ from conventional benzodiazepines? Which receptors are targets of these medications? Zaleplon, zolpidem and zopiclone appear to bind to the GABAa receptor in a way that does not cause a high degree of tolerance to their therapeutic actions, dependence, or withdrawal upon discontinuation from long term treatment. Whereas benzodiazepine bind in a manner that changes the conformation of the GABAa receptor such that tolerance generally develops as well as withdrawal.
- Which sleep aids are best for which situations - insomnia, difficulty initiating sleep, mid sleep waking, early morning waking, nightmares?
- Which medications are approved for excessive daytime sleepiness and shift work disorders? Modafinil, Methylphenidate and amphetamine, GHB PowerPoint Presentation
Sleep apnea, Substance abuse, Sleep hygiene issues, Chronic insomnia, Acute stress induce insomnia, insomnia comorbid with a psychiatric disorder Sleeping Pills, Which ones for which patients? TCPR:
- What are the basic principles of sleep hygiene? No caffeine, no alcohol, avoid exercise at night, no smoking.
- Per Carlat, what recommendation is best for improving sleep quality?
Exercise is the single best way to increase the overall quality of your
sleep. So encouraging patients to get onto a regular exercise program is
crucial.
- What are sleep restriction techniques? Sleep restriction means reducing time in bed to sleep time only. I tell patients, “I want you to stay in bed only during times that you are asleep. So if you get in bed at 10 o’clock, but you don’t really fall asleep until 12, don’t go to bed until 12:30. If you wake up at 6 and you don’t usually get out of bed until 7, then start getting out of bed at 6. Try to restrict the time in bed to almost less time than you are actually sleeping. Practical Sleep Hygiene Tips
Week 9 ADHD Study Guide
Stahl
- Which neural circuits are implicated in symptoms of inattention, selective attention, hyperactivity and impulsivity in ADHD?
• Inattention- DLPFC,
• Selective attention- Dorsal anterior cingulate cortex ,
• Hyperactivity- Prefrontal motor cortex,
• Impulsivity- orbitofrontal cortex
- How are symptoms of impulsivity and compulsion modulated in the brain? P. 474 Impulsivity- is Modulated by the Orbitofrontal cortex.Impulsivity is associated with a cortico-striato-thalamocortical (CSTC) loop that involves the orbitofrontal cortex (OFC)
- Describe tonic versus phasic neuronal firing. p. 475
- Tonic – normal firing of DA and NE at baseline is slow and “Tonic”.
- Phasic- is a burst of firing of DA release Slow release of NE and DA = Tonic firing, and Bursts of DA release = Phasic firing
- What hypothetical actions to ADHD medications need to have to make them effective for ADHD? P. 487 Increase signal strength and output by dialing up the release of both DA and NE until they reach optimal levels.
- Describe signal to noise ratio as it pertains to ADHD. What is the role of norepinephrine? P. 477 NE increases the incoming signal by allowing for increase connectivity of the pre-frontal networks. What is the role of dopamine? DA decreases the noise by preventing inappropriate connections from taking place.
- How is ADHD treatment prioritized when it is comorbid with other psychiatric disorders? P. 487 Substance abuse problems must be managed top line. Treating ADHD may also have to await improvement from mood and anxiety disorder treatments.
- How does the mechanism of action of amphetamine differ from methylphenidate?
