Exam 4 Flashcards

(40 cards)

1
Q

What NTs mediate anxiety

A

Increased NE

Decreased Gaba or seratonin

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2
Q

Define GAD clinically

A

Excessive anxiety and worry for at least 6 months

Need anxiety plus:
Restlessness, fatigue, difficulty concentrating, irritabillity, muscle tension, sleep disturbance

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3
Q

What is the treatment goal for GAD

A

To restore or agonize GABA and 5HT

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4
Q

Define a panic attack

A

Discrete period of intense fear or discomfort with four or more symptoms setting in within 10 minutes:

Palpitatins, sweating, trembling, SOB, choking feeling, chest pain, NV, dizzy, derealization, fear of losing control, fear of dying, paresthesia, chills, hot flashes

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5
Q

What drugs can induce panic symptoms

A

Lactate infusion, yohimbine (alpha 2 antagonist)

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6
Q

What NTs may play a role in phobias or social phobia

A

Decreased seratonin in social phobia

Increased NE and DA in phobia

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7
Q

What is the order of drugs used to treat anxiety disorders

A

SSRI- SNRI- TCA- MOAi

Gaba-ergic: benzos

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8
Q

Name the 6 SSRIs

A

Escitalopram, citalopram, paroxetine, sertraline, fluoxentine,fluvcoamine

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9
Q

Name 3 SNRIs

A
  • increase NE and 5HT

Venlafaxine, dysyenlefaxine, duloxetine

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10
Q

Name two TCAs

A

Clomiparinamine, imipramine

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11
Q

Name an MAOi

A

Phenelzine

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12
Q

What is the suffix for benzos

A

Pam

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13
Q

What are non typical ways to treat anxiety

A

Beta blockers for performance anxiety- propanolol

Busprione - non benzo anxiolytic

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14
Q

What is first line treatment of GAD

A

CBT, behavioral techniques, relaxation training, systematic desensatizaiton, exposure response prevention

SSRIs

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15
Q

What brain centers drive the fear response and worry response. What NTs are used there

A

Fear- amygdala (panic and phobia), 5HT from raphe nuclues, NE from locus coerulues, GABA = inhibitory
Worry- cortical- strial- thalamic (anxious, OCD), 5HT, GABA= inhibitory

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16
Q

How does GABA work

A

GABA is inhibit NT, binds to GABA-A receptor and increases the frequency of opening of choloride channel = inhibition

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17
Q

What is MOA of SSRIs

A

SSRIs increase seratonin output by blocking SERT, increase 5HT = down regualtion of auto-receptors= more release 5HT at axon, increase at axon causes post-synaptic receptors to desensatize/downregulate and reduce side effects

18
Q

What is the MOA of SNRIs

A

Inhibit SERT and NET (directly increase 5HT NE, indirect increase in DA)

19
Q

What are the differences in SSRIs and SNRIs

A

Excessive NE from SNRIs can increase anxiety

They can be used people with panic disorder though

20
Q

Side effects of SNRI and SSRI include:

A

Sex dysfunction, GI upset, CNS- insominia or sedation, sweating, bruising easy, hyponatremia
RARE DANGEROUS- seizures, mania, increased Suicide in those less than 24

From NE only: urinary retention, increased BP, SIADH, nervousness, asthenia

21
Q

what is the side effects of too much 5HT. What is 5HT syndrome

A

-less DA release, emotional flattening, cognitive slowing, apathy

SS- confusion, flushing, diaphoresis, tremor, myoclonic jerks, hyperthermia, hypertonicity, rhabdomyolysis, renal failure, death

22
Q

What is MOA and SE of benzos

A

When GABA is present benzos increase the frequency of chloride channel opening- positive allosteric modulator

Work by reducing excessive amygadala action by increasing action of GABA

SE: sedation, fatigue, depression, dizziness, ataxia, slurred speech, weakness, forgetfulness, confusion, hyper-excitability, nervousness
Rare- hallucinations, manina, hypotension, hyper-salivation, dry mouth, hepatic or renal dysfunction, blood dysacrias
Withdrawl- grand mal seizures
Dangerous- respiratory depression

23
Q

What benzos are liver safe

A

LOT

Lorazopam, oxazepam, tomazapam

24
Q

What is MOA and SE of buspirone

A

seratonin 1 partial agonist at presynatpic autoreceptors and post-synaptic receptors, on set of action is delayed (downstream effects)

Tx GAD and anxiety

SE: Dizziness, headache, nervousness, sedation, excitement, nausea, restlessness, cardiac symptoms

25
What is the MOA and SE of TCAs, name them
Block NE and 5HT reuptake, antagonist at 5HT - disinhibit DA and NE release Doxepin, chlordiazepoxide, amytrypline, clomipramine SE limit use: anti-histamine action- sedation and weight garin Anti-cholinergic- dry mouth, blurred vision, urinary retention, constipation Alpha1 antagonist- orthostatic hypotension and dizziness Interfere with insulin release DANGEROUS: block Na channels in heart and brain- overdose= seizures coma, cardiac arrythmias, cardiac arrest and death
26
What is hydroxyzine MOA, use, and SE
Hydroxyzine- antagonist at H1 receptor, treat anxiety, shows skeletal muscle relaxation, bronchodilator activity, analgesic, and anti-emetic effects SE- anti-muscarinic (blurred vision, constipation, memory problems, dry mouth)
27
What is MOA of MAOi and SE
MOA= inhibit the breakdown of 5HT DA and NE Treat- 2nd line, panic disorder, social anxiety, PTSD, OCD SE= dizziness, sedation, headache, sleep problems, fatigue, weakness, tremor, movement problems, blurred vision, increased sweating -constipation, dr moutch, nausea, change in appetite, weight gain, sex dysfunction, ortho hypothensiion, and syncope DANGEROUS: HTN crisis, mania, suicidiality, seizures, hepatotoxicity So avoid high tyramine foods
28
Treatment for social anxiety
BB are second line
29
Tx for OCD
SSRI first line Clomiparamine- TCA second line Lithium buspirone, antipyschotics as add on Deep brain stimulation
30
Tx for PTSD
SSRI and SNRI - first line Benzos are not used or used with caution Pre-emptive treatment with BBs
31
What TCA at low doses can be used for sedation
Doxepin- at low doses it is selective for histamine receptors and is used as hypnotic
32
What is the dx criteria for PTSD
Exposure to actual or threatened death, serious injury, or sex violence in one or more way: directly experiencing event, witnessing event, learning of event to close friend or family, repeated exposure to events Presence of one or more INTRUSIVE SYMPTOMS associated with the traumatic event beginning after the event occurred: recurrent distressing memories of the event, dreams of event, dissociative reactions (flashbacks) which they believe the event is recurring, pyschological distress and reactions at cues of the event or trauma Persistant AVOIDANCE of stimuli associated with event: memores or reminders of the event Negative alterations in cognitions and mood associated with the trauma as two or more: inability to remember all of event, persistent negaitive beliefs about self or others, persistent cognitions about the cause or consequences of the trauma that lead the individual to blame self or others, persistent negative emotional states (fear, horror, anger, guilt, shame), markedly diminished interest or participation in activities, feelings of detachment of estrangement from others, persistent inability to experience positive emotions Marked alterations in arousal and reactivity associated with the trauma, as evidence by 2 or more: irritable outburts, reckless behavior, hypervigilance, exaggerated startle response, problems with concentration, sleep disturbances MUST BE GREATER THAN 1 months and clinically significant impairment Can be with or without dissociative symptoms Delayed onset after 6 months
33
What are co-morbid conditions of PTSD
SUD, interpersonal problems, sleep disturbance, somatization and chronic pain, suicidality, self destructive or impulsive behavior, anger and hostility, ID problems, TBI, anxiety disorders and phobias 20-40% have SUD, 40-60% of SUD have PTSD or three times more prevalent, makes treatment and sx worse
34
What are risk factors for PTSD
PRE TRAUMA Ongoing life stress, lack of social support, young age at time of trauma, SUB or pysch disorder, Hx of traumatic events Female, Low SES, low education and IQ, FHx of pysch disorders POST TRAUMA Life stress, lack of support, bereavement of traumatic grief, major loss of resources, negative social support, poor coping skills
35
What are the tx for PTSD
1) pyschotherapy- CBT or trauma focused therapy (prolonged exposure, congitive processing therapy, eye movement desensitization and reprocessing) 1) SSRIs - sertraline, fluoxetine, paroxetine SNRI- venlafaxine 2)antidepressants- mirtazepine, tricyclics- imipramine, amitripyline, MAOis - phenelzine Alppha 1 anatonists- prazosin for sleep or arousal symptoms 3) Risperidone- global symptoms, mood stabalizers Benzos are not recommended but sometimes used
36
What is acute distress disorder
Very similar to PTSD but lasts 3 days to 1 month
37
What is adjustment disorder
Development of emtional or behavioral symptoms in response to stressors within 3 months, less severe stressor than PTSD Symptoms: marked distress out of proportion to stressor, significant impairment in social or occupational functioning Symptoms not longer than 6 months Need to describe mood: depressed, anxious, mixed, disturbed conduct, mixed emotions and disturbed conduct
38
What are the MAOis and the MOA
Phenelzine, tranycypormine, isocarboxazid, selegilline (NON SELECTIVE MAO-A and B)
39
What are uses and contraindications to MAOi
Mood disorders- unipolar or bipolar depression, ATYPICAL DEPRESSION, OCD PTSD Neuro disorders- PD, fibromyalgia, chronic fatigue syndrome Contraindication: epilepsy, cardiac disease, DM, pheochromocytoma
40
What are the names of the two Seratonin modulators and stimulators
Voritoxetine- SSRI + agonist at 5HT1A and 1B | Vilazodone- SSRI + partial agonist 5HT1A