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Psychopharmacology > test 3 > Flashcards

test 3 Flashcards

1
Q

When is anxiety considered to be a normal emotion?

A

under circumstances of threat and is thought to be part of the evolutionary “fight or flight” reaction of survival.

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2
Q

What core symptoms characterize anxiety?

A

excessive fear and worry

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3
Q

Stahl states that all anxiety disorders have overlapping symptoms of anxiety/fear coupled with what?

A

Anxiety disorders all seem to maintain the core features of some form of anxiety or fear coupled with some form of worry.

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4
Q

What symptom is hypothetically linked to the functioning of cortico-striato-thalamo-cortical (CSTC) loops?

A

worry (anxious misery, apprehensive, expectation, obsessions)

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5
Q

What is an almond-shaped brain center located near the hippocampus that has important anatomical connections that allow it to integrate sensory and cognitive information and then determine whether there will be a fear response?

A

The amygdala

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6
Q

What key areas of the prefrontal cortex regulate feelings of fear via reciprocal connections with the amygdala?

A

orbitofrontal cortex and anterior cinglulate cortex

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7
Q

In regards to fear and motor responses, depending upon circumstances and one’s temperament, those responses could be fight, flight, or freezing in place. What connections and parts of the brain regulate motor responses of fear?

A

Motor responses of fear are regulated in part by connections between the amygdala and the periaqueductal gray area of the brainstem.

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8
Q

Endocrine reactions accompany fear and so what hormone is often involved?

A

cortisol

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9
Q

What medical comorbidities can occur with chronic and persistent activation of the HPA and cortisol release?

A

increased rates of coronary artery disease, type 2 diabetes, and stroke, and potentially to hippocampal atrophy as well.

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10
Q

What regulates breathing during a fear response?

A

connections between amygdala and the parabrachial nucleus in the brainstem.

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11
Q

Know about the fear responses, fight or flight response, and various symptoms that go along with this.

A

accelerate respiratory rate, can lead to exacerbation of asthma, or a false sense of being smothered. All symptoms common during anxiety, and especially during attacks of anxiety such as panic attacks.

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12
Q

Know the areas of the brain areas involved in the fear, fight or flight response.

A

The automomic and cardiovascular responses are mediated by connections between the amygdala and the locus coeruleurs (home of the noradrenergic cell bodies)

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13
Q

What specific anxiety condition can be triggered internally from traumatic memories stored in the hippocampus and activated by connections with the amygdala?

A

Post traumatic stress disorder

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14
Q

What are the neurobiological regulators and neurotransmitters that have an effect on the amygdala?

A

GABA, 5HT, and NE,

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15
Q

What does Stahl say the symptoms of worry include?

A

anxious misery, apprehensive expectations, catastrophic thinking, and obsessions

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16
Q

What part of the brain is linked to worry?

A

cortico-striato-thalamo-cortical feedback loops from the prefrontal cortex

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17
Q

Differences in dopamine availability may impact the risk for worry & anxiety disorder & help determine what?

A

whether you are “born worried” and vulnerable to developing an anxiety disorder, particularly under stress.

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18
Q

What is the difference between Met and Val variants of COMT?

A

Met-lower COMT activity and high dopamine levels
Val- higher COMT enzyme and lower dopamine levels.
Stress increases dopamine and to much dopamine decreases the efficiency of information processing under stress and creates the symptoms of anxiety and worry.

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19
Q

What is one of the key neurotransmitters involved in anxiety and in the anxiolytic action of many drugs used to treat the spectrum of anxiety disorders?

A

GABA (Y-aminobutyric acid) is one of the key neurotransmitters involved in anxiety andin the anxiolytic action of many drugs used to treat the spectrum of anxiety disorders.
GABA is the principal inhibitory neurotransmitter in the brain and normally plays an important reulatory role in reducing the activity of many neurons, including those in the amygdala and those in the CSTC loops.

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20
Q

What are the three major types of GABA receptors?

A

GABA-A, GABA-B GABA-C

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21
Q

What receptors are targets of benzodiazepines, sedative hypnotics, barbiturates, and/or alcohol?

A

Various subtypes of GABA-A receptors

22
Q

What receptors are G-protein-linked that may be coupled to calcium and/or potassium channels and may be involved in pain, memory, mood, and other CNS functions?

A

GABA-B

23
Q

Which two alpha 2 delta (α2δ) ligands have demonstrated anxiolytic actions in social anxiety disorder and panic disorder, and are also proven to be effective for the treatment of epilepsy and certain pain conditions, including neuropathic pain and fibromyalgia?

A

gabapentin and pregabalin

24
Q

What is a key neurotransmitter that innervates the amygdala as well as all the elements of the CSTC circuits, namely, the prefrontal cortex, striatum, and thalamus, and thus is poised to regulate both fear and worry?

A

serotonin

25
Q

What are the potential anxiolytic actions of buspirone?

A

Buspirone is a 5HT1A partial agonist and is recognized as a generalized anxiolytic. Works at both presynaptic and postsynaptic 5HT1A receptors with actions at both sites resulting in enhanced serotonergic activity in projections into the amygdala, prefrontal cortex, striatum, and thalamus. Effect is delayed not instant making researcherss think that the therapeutic effects are virtue of adaptive neuronal events and receptor events. pg 406

26
Q

When excessive noradrenergic output from the locus coeruleus triggers numerous central symptoms of anxiety and fear, what would you expect the symptoms to be?

A

nightmares, hyperarousal states, flashbacks, and panic attacks. Excessive noradrenergic activity can also reduce the efficiency of information processing in the prefrontal cortex and thus in the CSTC circuits and theoretically cause worry.

27
Q

What is an α1 - adrenergic blocker? And what is it used for?

A

Symptoms of hyperarousal such as nightmares can be reduced in some patients with an α1 - adrenergic blocker such as prazocin. Symptoms of fear and worry can be reduced by norepinephrine reuptake inhibitors.

28
Q

Is there a possibility of dependence, abuse, and withdrawal reactions with benzodiazepines?

A

benzodiazepines have a possibility of dependence, abuse, and withdrawal reactions.

29
Q

Remission from all symptoms of GAD in patients taking SSRIs or SNRIs may be slower in onset than for depression by how much longer?

A

Remission from all symptoms in patients with GAD who are taking an SSRI or SNRI may be slower in onset than it is in depression and may be delayed for 6 months of longer.

30
Q

Is PTSD treated with just one medicine?

A

most PTSD cases do not take monotherapy

31
Q

Chronic pain conditions of peripheral origin can be successfully targeted for relief by psychotropic drugs that work on what?

A

central pain mechanisms

32
Q

Painful conditions without identifiable peripheral lesions and that were once linked only to psychiatric disorders are now hypothesized to be forms of what?

A

hypothesized to be forms of chronic neuropathic pain syndromes that can be successfully treated witht the same agents that treat neuropathic pain syndromes not associated with psychiatric disorders.

33
Q

What can chronic neuropathic pain syndromes be successfully treated with?

A

SNRI serotonin-norepinephrine reuptake inhibitors and the alpha 2 delta (α2δ) ligands (anticonvulsants that block voltage gated calcium channels or VSCCs)

34
Q

What is the “on” switch which is localized within the tuberomammillary nucleus (TMN) of the hypothalamus?

A

The wake promoter

35
Q

What is the “off” switch which is localized within the ventrolateral preoptic (VLPO) nucleus of the hypothalamus?

A

The sleep promotoer

36
Q

Know about the two sets of neurons that regulate the sleep/wake switch and where they are located in the brain?

A

orexincontaining neurons of the lateral hypothalamus (LAT) and melatonin sensitive neurons of the suprachiasmatic nucleus SCN).

37
Q

What is the brain’s internal clock, or pacemaker, and regulates circadian input to the sleep/wake switch in response to how it is programmed by hormones, such as: melatonin and by the dark/light cycle?

A

The SCN; suprachiasmatic nucleus

38
Q

Know about orexin and narcolepsy.

A

The lateral hypothalamus serves to stabilize and promote wakefulness via a peptide neurotransmitter known by two different names : orexin and hypocretin. These lateral hypothalamic neurons and their orexin are lost in narcolepsy, especially narcolepsy with cataplexy. New hypnotics on the horizon (orexin antagonists) block the receptors for these neurotransmitters.

39
Q

Which novel neurotransmitter is linked to homeostatic drive, and appears to accumulate as this drive increases during the day, and to diminish at night?

A

adenosine

40
Q

What are the two key neurotransmitters that regulate the sleep/wake switch?

A

Histamine from the TMN and GABA from the VLPO

41
Q

What can help to reset the circadian clock?

A

Histimine=wake GABA=sleep, no light=melatonin

42
Q

What is the wake promoting drug that promotes the release of histamine from TMN neurons?

A

modafinil

43
Q

Know about Histamine, H1 receptors and neurons.

A

There are a number of histamine receptors. H1 receptors are well known because they are the target of antihistamines. (H1 antagonist). When histamine acts at H1 receptors it activate a G-protein linked second messenger system that activates phosphatidyl inositol and the transcription facto cFOS and results in wakefulness, normal alertness and pro-cognitive actions. When H1 receptors are blocked in the brain they cause sedation.

44
Q

Know why it is important to know the half-life of a hypnotic before prescribing it?

A

having half-lives that are too long can cause drug accumulation and hip fractures from falls. Long half life can cause next day carryover effects and sedation and memory problems from residual daytime drug levels. Other agents have half-lives that are too short and their effects can wear off before it is time to wake up, causing insufficient sleep maintenance and nocturnal awakenings, as well as restless and disturbed sleep in some patients.

45
Q

Know about Melatonin, Trazodone, Doxepin and over-the-counter sleep medicine.

A

Melatonin works on the phase shifts of the circadian rhythms. They are not known to help sleep maintenance but will induce natural sleep in those who suffer mostly from initial insomnia.
Trazodone- antidepressant, half life 6-8 hours, effect hypnotic at lower dose needed for antidepressant effects. Give just one dose a day at night.
DOXEPIN- tricyclic antidepressant workds at the H1 receptor. low doe. long term administration provides rapid sleep industion with all night sleep maintenance but without next day carryover effects, development of tolerance to its hypnotic efficancy, or weight gain.

46
Q

What are the first line treatments for restless leg syndrome?

A

dopamine antagonis such as ropinirole or pramipexole.

47
Q

What are the three treatments for excessive daytime sleepiness?

A

Modafinil, stimulant (methylphenidate and amphetamine, especially d-amphetamine), Caffeine

48
Q

What are the potential dangers of excessive daytime sleepiness?

A

loss of sleep causes performance decrements equivalent to intoxication with alcohol and traffic accidents and fatalities.

49
Q

Know the symptoms of ADHD, what specific areas of the brain are affected, and what areas of the brain are affected by specific symptoms?

A

trio of symptoms: inattention, hyperactivity, and impulsivity. It is hypothesized that the symptoms arise from abnormalities in various circuits involving the prefrontal cortex.

50
Q

What is the usual age of onset for ADHD?

A

by age 7

51
Q

What is the deal about nicotine and ADHD?

A

Adults with ADHD smoke as frequently as adults with schiaophrenia about twice the rate of the normal adult population in the US. This may be due to the fact that nicotine subjectively improves ADHD symptoms especially in patients who are not treated for their ADHD. Nicotine enhances DA release and enhances arousal so it is not surprising that it may be subjectively effective for ADHD symptoms.

52
Q

Know the various treatments for ADHD.

A

methlyphenidate, amphetamine, Atomoxetine, Alpha 2A-adrenergic agonist read 489-500

Psychopharmacology (4 decks)

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