Psychopharm Test 3 Flashcards

1
Q

What does the Supra Charismatic Nucleus do?

A

PPM of the brain - located in hypothalamus it is responsible for influencing the sleep/wake cycle.

It increases the release of GABA and other neurotransmitters so you can fall asleep

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2
Q

How does Adenosine effect sleep

A

Adenosine increases in your body the longer you are awake and as it increases it mildly depresses the body and promotes sleep.

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3
Q

What is coffee considered?

A

Adenosine antagonist; it prevents the effects of adenosine and helps you stay awake.

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4
Q

What is the pineal gland responsible for releasing?

A

Melatonin - melatonin levels increase in evening and help you fall asleep.

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5
Q

How does the Ascending Reticular Activating System work?

A

network of nerves in the brain that regulates consciousness and when we sleep. During deep sleep the activity in RAS is reduced. During REM sleep the activity is almost as active as when we are awake

Damage or blockage of the ARAS can lead to sleep disturbances and difficulty staying awake. Like comas,

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6
Q

How does histamine effect sleep

A

Histamine is a neurotransmitter found in Tuberomammillary nucleus and it keeps you awake. Less histamine = you are tired; antihistamines = decrease histamine and make you drowsy.

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7
Q

How does Orexin/Hypocretin effect sleep

A

Located in perifornical area, it mediates arousal and alertness in the body (helps keep you awake). In the case of sleep, blocking orexins can help to combat insomnia (help you sleep), while too little orexin can cause narcolepsy.

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8
Q

What is initial insomnia?
How do you treat it?

A

Inability/difficulty falling alseep (d/t neuropathic/musculoskeletal pain & certain meds)

Tx = Melatonin or Histamine Antagonist (aka antihistamine) - ex. would be diphenhydramine or Vistaril (hydroxyzine pamoate)

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9
Q

What is middle insomnia?
How do you treat it?

A

waking durig the night and not being able to fall back asleep.
*Can be d/t daytime fatigue, muscle spasm, nocturia etc.

Tx - Eszopixlone (Lunesta) and Zolpidem (Ambien) They both have longer half lives which is good for patients who need 6-8 more hours of sleep.

Hypnotics with half-lives that are short, but not ultra-short (approximately 6 hours: zolpidem CR, eszopiclone, and perhaps low doses of trazodone or doxepin), may provide rapid onset of action and plasma levels above the minimally effective concentration only for the duration of a normal night’s sleep.

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10
Q

What is terminal insomnia?
How do you treat it?

A

May be d/t mental illness or lack of exposure to daylight;

Tx - treat the underlying cause such as depression or anxiety

** Mirtazapine (atypical antidepressant/seritonergic hypnotic)

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11
Q

Where is the “off” setting or sleep promoter of the sleep/wake cycle located?

A

ventrolateral preoptic nucleus (VLPO) of the hypothalamus
When the VLPO is active and GABA is released to the TMN, the sleep promoter is on, and the wake promoter is inhibited.
Inhibiting GABA activity can promote wakefulness.

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12
Q

Where is the wake promotor located?

A

is localized within the tuberomammillary nucleus (TMN) of the hypothalamus. Two key neurotransmitters regulate the sleep/wake switch: histamine from the TMN and GABA from the VLPO.

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13
Q

A 75-year-old man in good physical shape is having sleep problems. He wakes up at 4am and, although he tries to stay awake in the evening to prevent this early rising, he usually falls asleep right after dinner, often before 7pm. Which of the following treatment options may be most beneficial for this patient?

A

Early morning melatonin
Late afternoon/Evening light

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14
Q

Why are benzos used for sleep?

A

act on the CNS to enhance the effects of GABA (helps increase it) which induces sleep

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15
Q

Name examples of benzos for sleep that are GABA-A positive allosteric modulators (PAMs)

A

Flurazepam
Quazepam
Estazolam
Trazolam

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16
Q

Are benzos considered a 1st or 2nd line treatment for sleep disorders?

A

2nd line therapy - this is because they cause long-term problems such as loss of efficacy over time (tolerance) and withdrawal sx including rebound insomnia

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17
Q

How dow Benzo GABA-PAMs work/mechanism of action?

A

Activates GABA in the VLPO which increases the persons need/drive to sleep
*it does this by opening Cl- channels more frequently

18
Q

What are Z drugs and what are they used for? Provide examples

A

All start with Z - and are GABA-PAMs, but they are NON-BENZOS and hypnotics

Ex. Zaleplon (Sonata)
Zolpidem (Ambien)
Eszopiclone (Lunesta)

19
Q

Melatonin Agonists - give ex and what do they do/why are they used?

A

Ex. Ramelteon
Tasimelteon
Agomelatine

Used for insomnia associated with jet lag or circadian rhythm disturbances.

MT-1 and MT-2 receptors agonist
promotes sleep and maintenance of circadian rhythm

20
Q

Mech of action of Modafinil and what is is used to treat?

** WAKE PROMOTING AGENT

A

Modafinil
act predominantly as inhibitors of DAT, enhancing dopamine tonic activity to promote wakefulness

  • Once dopamine is activate => downstream release of
    histamine from the TMN, and further activation of orexin (which helps keep you awake)

Not as powerful as stimulants, but is used to treat narcolepsy and OSA ans shift work

21
Q

SOLFIAMFETOL = wake promoting agent
What class/what is it used to treat?

A

NDRI - (norepi/dopamine reuptake inhibitor)
used for daytime sleepiness
more potent than wellbutrin, less abusable than stimulants

short-half life consistent w/ morning wearing off

22
Q

Pitolisant - WAKE PROMOTING AGENT

What class/what is it used to treat?

A

H3 antagonist = blocks H3 which enhances histamine release = keeps you awake

23
Q

Hydroxybutyrate aka
sodium oxybate/ GHB (gabba
hydroxybutyrate

WAKE PROMOTING AGENT

A

Day-time sleepiness AID
GHB receptor agonist
GABA-B partial agonist
increases slow-wave sleep and improves cataplexy, reduces hypnagogic hallucinations and sleep paralysis

potential abuse
* controlled substance
* labeled “date rape drug”
* Use w/ ETOH causes amnesia and involuntary intoxication

24
Q

What types of medications are beneficials for insomnia if the patient has a hx of addiction and wants to avoid benzos

A

Orexin antagonists/DORA (Duel Orexin Receptor Antagonists)

Suvorexant
Lemborexant
Daridorexant

25
Q

How do Orexin antagonists/DORAs work?

A

blockage of orexin receptors at both orexin-1 and orexin-2
has hypnotic actions by blocking wake-stabilizing effects
* Inhibit release of H, ACh, NE, DA, 5HT
improve initiation and maintenance of sleep
* lack-side effects of Z-drugs, such as dependence, withdrawal, rebound, unsteady gait, falls, confusion, amnesia, or respiratory depression
* at night, high ratio of drug/orexin; in morning, inhibitory actions of DORA reverse

26
Q

Impulsivity

A

inability to stop initiating actions
risk seeking

*Starts in the ventral striatum, but as you keep doing this impulse it no longer travels on its regular path (ACC/VMPFC to ventral striatum and back), but rather travels to dorsal striatum and becomes compulsive rather than impulsive.

27
Q

Compulsivity

A

OFC to Dorsal Striatum and back to OFC (orbitofrontal cortex)

performance of repetitive behaviors and often done to avoid consequences.
You are unable to terminate the actions and these behaviors are often done as a form of “harm reduction”

28
Q

Impulsivity is hypothesized to be related to the _____, while compulsivity is hypothesized to be related to the _____.

A

Ventral Striatum

Dorsal Striatum

29
Q

Mark, a 35-year-old cigarette smoker, would like to quit but is nervous because he typically craves a cigarette approximately every 2 hours. The craving and withdrawal are due to:

A

Resensitization of nicotine receptors

During cigarette smoking cessation, resensitized nicotinic receptors no longer receiving nicotine are craving due to an absence of dopamine release in the nucleus accumbens. Craving seems to be initiated at the first sign of nicotinic receptor resensitization. When the receptors resensitize to their resting state, this initiates craving and withdrawal due to the lack of release of further dopamine.

30
Q

Jenny is a 48-year-old nurse who suffers from shift work disorder. She has a history of depression and substance use disorder but is otherwise healthy. Which of the following wake promoting agents would be most appropriate to prescribe this patient?

.1 - methylphenidate
2. - caffeine
3. Solfiamfetol
4. Armodafinil

A

Armodafinil (also Modafinil) - wake promoting agent that is good for the tx of narcolepsy, shift work, and OSA

*not as potent as stimulants

31
Q

What is “harm reduction” related to opioid use/withdrawal

A

Putting the pt on the lowest dose of suboxone or naltrexone (long acting opioid antagonist) indefinitely to reduce cravings and prevent them from using dangerous levels of drug.

32
Q

Opioid Intoxication s/sx

A

Activation/rush
Euphoria/dysphoria
facial flushing/itching/feeling warm
impaired judgment
analgesia
Constipation
Constricted Pupils
Drowsiness
Resp Depression
Tachycardia
Apneia

33
Q

How does Naltrexone work in patients who struggle with ETOH abuse

A

If taking Naltrexone the patient will not have the “euphoric” effect from drinking because Naltrexone binds to the mu receptors preventing ETOH from binding, so ETOH cannont cause release of dopamine/euphoria.

34
Q

What is Wernike Encephalopathy of deficiency of?

A

ACUTE B1 (thiamine) deficiency

35
Q

What triad of sx is present in Wernicke Encephalopathy? How many do you ned for a clinical dx?

A
  1. Change in mental status/impairment
  2. Oculomotor dysfunction (nystagmus/opthalmoplegia (paralysis of motor eye - one slower than other or not at all)
  3. Cerebellar dysfunction ( eg. gait ataxia but not in upper limbs)
  4. Nutritional deficiency

need 2/4

36
Q

Other causes for Wernickies?

A

chronic etoh
cancer/malignancy
hyperemesis of pregnancy
bariatric surgery
anorexia nervosa

37
Q

What happens in WErnicke if you do not give Thiamine before glucose?

A

It can worsen the encephalopathy and cause the pt to develop Korsakoff syndrome (Chronic B1 deficiency - irreversible).

38
Q

How to treat ETOH when CIWA scoring

A

Benzos and taper

39
Q

What receptors does marijuana inhibit

A

34A (benzos and antipsychotics)
2C9 (depakote)
2C19 (lexapro/sertraline)

** this will increase the level of those meds in the body

40
Q

AcamPROSTATE/ Campral

A

Artificial ETOH
Assist with withdrawal of ETOH to dampen cravings
check KIDNEY function, GFr, BUN/Creatinine

direct blocking actions on certain glutamate receptors to inhibit, and enhances GABA