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IPT: Neuro > Block 3 > Flashcards

Block 3 Flashcards

1
Q

DSM-5 Criteria Bipolar I vs II

Which one has manic episodes?

A

I

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2
Q

DSM-5 Criteria Bipolar I vs II

Which one sometimes requires hospitilizations?

A

II

I always requires hospitalization

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3
Q

DSM-5 Criteria Bipolar I vs II

Which one must last for 4 consecutive days to be diagnosed?

A

II

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4
Q

DSM-5 Criteria Bipolar I vs II

Which one has hypomanic episodes?

A

II

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5
Q

DSM-5 Criteria Bipolar I vs II

Which one requires the episode to last for 1 week and being present most of those days?

A

I

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6
Q

What must occur for a cyclothymic disorder diagnosis?

A

Fluctuation between subsyndromal depression and hypomanic episodes

2 yrs for adults

1 yr for younger peeps

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7
Q

What is a mixed condition for bipolar?

A

Major depressive episode + manic episode almost daily for a week

Requires hospitalization

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8
Q

What is a rapid cycling condition for bipolar?

A

> 4 major depressive OR manic episodes in 12 months

Requires hospitalization

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9
Q

(T/F)

AD may trigger manic/hypomanic episodes

A

True

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10
Q

FDA approved agents for acute mania?

A

LARVA COZ Q

Lithium
Aripiprazole
Risperidone
Valproate
Asenapine

Carbamazepine
Olanzapine
Ziprasidone

Quetiapine

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11
Q

FDA approved agents for maintenance of bipolar?

A

ALDOL

Aripiprazole
Lithium
Divalproex
Olanzapine
Lamotrigine
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12
Q

FDA approved agents for bipolar depression?

A

Quetiapine + Lurasidone

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13
Q

Labs + Lithium?

A

PT BEER

Pregnancy (teratogenic
Thyroid

Blood (increase WBC)
EKG
Electrolytes (decreases sodium)
Renal (excreted)

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14
Q

Serum levels of lithium of acute mania and for maintenance?

A

Acute = 0.8 to 1.2

Maintenance = 0.6-1.0

Draw lvls 12hrs after last dose

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15
Q

Lithium + toxicity levels?

A
  1. 5 to 2.0 = N/V/D, ataxia, , lethargy, drowsiness
  2. 0 to 2.5 = anorexia, delirium, stubor, ECG changes

> 2.5 = seizures, renal damage, oliguria

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16
Q

Which Rx will increase concentration of lithium?

A

Thiazides, NSAIDs and ACE/ARBs

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17
Q

How do thiazides increase lithium concentration?

A

Sodium depletion results in increases proximal reabsorption of sodium and lithium

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18
Q

How do NSAIDs increase lithium concentration?

A

Enhanced reabsorption of sodium and lithium by inhibition of prostaglandin synthesis

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19
Q

How do ACE/ARBs increase lithium concentration?

A

Reduced GFR results in reduced lithium elimination

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20
Q

Which genes are associated w/ increased % of ADHD?

A

Dopamine transporters and receptors, SNAP25 and COMT genes

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21
Q

Environmental factors of ADHA?

A

FAS, lead poison, meningitis

Obstetric adversity, maternal smoking, adverse parent-child relationships

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22
Q

What are the neurotransmitters involved for ADHD?

A

DA and NE

Defect in receptor D4 (DRD4) receptor gene

Overexpression of DAT-1

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23
Q

DSM-5 Criteria for ADHD?

A

Must be present for ≥6 months

17+ yo = ≥5 symptoms

16 and below = ≥6 symptoms

Symptoms had to be present prior to age 12

Present in ≥2 settings

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24
Q

Most cases of ADHD are found in what age group?

A

School age; 6-11, realized from 6-9

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25
Q

Oppositional defiant disorder DSM 5 critera?

A

4 sx over 6 months (angry, argues, refuses to comply)

<5 yo = most days
>5 yo = once weekly

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26
Q

Conduct disorder DSM 5 criteria?

A

3 sx in the past 12 month but 1 in the past 6 months (bullies, fights, cruel to animals/humans, theft, property destruction)

Childhood onset <10
Adolescent >10yo

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27
Q

What are the brain regions involved in ADHD?

A

Prefrontal cortex + connection to basal ganglia and cerebellum

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28
Q

Specific NE receptors involved in ADHD

A

alpha 2A improves ADHD

alpha 1 impairs

Beta adrenoreceptors impair

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29
Q

What are the SNRIs used for ADHD?

A

Atomoxetine

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30
Q

What are the alpha 2 adrenergic agonists used for ADHD?

A

Clonidine + Guanfacine

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31
Q

What are the NDRIs used for ADHD?

A

Methylphenidate
Dexmethylphenidate

Amphetamines
Dextroamphetamines
Lisdexamfetamine

Bupropion

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32
Q

Methylphenidate formulations

A

Tablets, chewables, liquid = short acting (more flexibility, but can have peak/trough effects that might be uncomfortable)

Wax matrix tablets = intermediate (causes inconsistent release of Rx)

Osmotic release oral system = long-acting

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33
Q

Methylphenidate w/ food increases (Cmax/Tmax)

A

Cmax

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34
Q

(d/l) methylphenidate is more bioavailable

A

D

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35
Q

(T/F)

Methylphenidate has extensive first-pass metabolism

A

True

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36
Q

General structure of amphetamine

A

Ring with a basic carbon skeleton with a methyl group and amine

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37
Q

SAR of amphetamines?

A

Amine = primary is more potent than tertiary except in methamphetamines

Demethylation lowers lipophilicity and increased metabolism (S isomer more potent like in dextroamphetamines)

Adding groups to ring reduces CNS stimulation

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38
Q

Metabolism of amphetamines and urine?

A

Most are excreted unchanged

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39
Q

Lisdexamfetamine info?

A

Prodrug, needs to be hydrolyzed to form d-amphetamine

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40
Q

Stimulant AE?

A

Reduced appetite and weight loss

Insomnia, irritability, psychosis, rebound sx, and even sudden cardiac death

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41
Q

Bupropion vs other stimulants

Efficacy

A

Equal compared to methylphenidate

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42
Q

Bupropion vs other stimulants

AE?

A

Lower prevalence of appetite suppression and weight loss, but risk of seizure exists

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43
Q

Atomoxetine vs other stimulants

Efficacy

A

Less efficacious than methylphenidate OROS and has slower onset (2-4wks) vs stimulants 1-2hrs

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44
Q

Atomoxetine AE?

A

Liver injury and new-onset suicidality

Sexual AE too

More sedation vs stimulants

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45
Q

Clonidine vs Guanfacine, which one is more selective for alpha 2?

A

Guanfacine

Clonidine activates both alpha 1 and 2

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46
Q

When starting rx for ADHD, what should adults vs children start off?

A

Adults = amphetamines

Children = methylphenidates

Swap if they done work

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47
Q

Just know that in vyvanse, it doesnt have a dose-dependent effect but rather a dose dependent AE profile

A

k

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48
Q

Stimulant safety issues?

A

Psychiatric (just decrease dose)

CV risk

Growth

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49
Q

DI with atomoxetine?

A

CYP2D6 inhibitors and increased AUC with PM of CYP2D6

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50
Q

Which alpha 2 agonist for ADHD is affected by high fat meals?

A

Guanfacine (increases concentration)

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51
Q

What is pica?

A

Eat nonfood >1 month

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52
Q

What is rumination?

A

Regurgitation of food >1 month

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53
Q

DSM-5 Anorexia nervosa

A

Cant maintain >85% normal body weight or BMI >17.5

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54
Q

Anorexia nervosa types?

A

Restricting: lasts 3 months, has not engaged in binge eating or purging

Binge-eating/purging type: last 3 months

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55
Q

DSM-5 bulimia nervosa

A

Binges weekly for 3 months

vs binge-eating disorder which just requires once weekly for 3 months

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56
Q

What is the most common AE of AN and BN?

A

Cardiac complications

CV collapse due to refeeding syndrome

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57
Q

Prognosis of AN?

A

Most will reach remission, but 20% will remain chronically ill even if they reach a normal weight

2-4% of those will even die due to cardiac arrest or suicide

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58
Q

Considerations for hospitalizations for ppl with eating disorders?

A

BMI<12

Nonresponsive to outpatient tx after 3-4 months

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59
Q

Nonpharm Tx for AN?

A

Cognitive behavioral therapy for 6 months minimum

SLOW refeeding usually with liquids

Controlled wt gain (2-3lbs/wk)

Add 3500-7000 calories/week

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60
Q

Pharm Tx for AN?

A

No role for antidepressants in acute Tx

If used, SSRIs are preferred due to AE profile; Fluoxetine is the most widely studied one

Smaller study showed Olanzapine with positive results (but not FDA approved)

Works with BN too

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61
Q

What rx is used for binge eating disorder?

A

Lisdexamfetamine 50 and 70mg, NOT 30!!! (only one that is FDA approved)

SSRIs, Atomoxetine, venlafaxine

Topiramate, zonisamide, and orlistat

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62
Q

What are the environmental etiologies of alzheimer’s disease?

A

Increased age (#1 factor)

Decreased reserve capacity of brain

Head injury

Increased risk for vascular diseases

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63
Q

Which genes can cause early onset familial alzheimer’s disease?

A

Mutations in dominant alleles

Chromo 1 (PSEN 2)

Chromo 14 (PSEN 1)

Chromo 21 (APP)

64
Q

Which genes can cause late onset familial alzheimer’s disease?

A

ApoE

Chromo 19 (specifically epsilon 4 that increases risk)

ApoE4 (both epsilon 4 = most risk, no copies = least risk)

65
Q

What is the amyloid cascade hypothesis?

A

AD pt have amyloid plaques, which are beta-amyloid proteins

APP is typically cleaved by alpha then gamma secretase, but in AD alpha is replaced by beta

Causes 42 length beta-amyloid fragments which forms plaque

66
Q

What are neurofibrillary tangles?

A

Found inside AD pt, specially hippocampus and cerebral cortex

NFTs have hyperphosphorylated Tau proteins which fills cytoplasm

67
Q

What role does ApoE have in AD?

A

May clear beta-amyloids (binds strongest to E2, then E3 and lastly E4)

68
Q

Inflammation and AD?

A

Believed to be pro-inflammatory mediators such as cytokines

Studies show NSAIDs may reduce AD risk

69
Q

What is the cholinergic hypothesis?

A

Loss of cholinergic neurons cause decline in memory and cognition

Cell loss is a consequence of AD and doesnt cause AD

70
Q

How is excitotoxicity caused by glutamate?

A

NMDA and AMPA receptors exist in postsynaptic membranes

AMPA allows sodium influx which allows magnesium to block NMDA receptors

Glutamate binds to NMDA and causes calcium influx to that alone leads to neurotoxicity

71
Q

When can definitive diagnosis be made for dementia?

72
Q

What is unique with Creutzfeldt Jacob Disease in dementia?

A

No inflammatory response + amyloid plaques are not always observed

73
Q

Which phobias are the most common?

A

Animals and heights

74
Q

What does the amygdala control?

75
Q

What does the locus ceruleus control?

A

NE projections to areas responsible for fear response

76
Q

What does the hippocampus control?

A

Consolidates traumatic memory and fear conditioning

77
Q

What does the hypothalamus control?

A

Neuroendocrine + autonomic response to threats

78
Q

Drugs that decrease anxiety and produce sedation target GABA (A/B)

A

A

Decreases neuronal excitability via chloride channel

79
Q

Drugs that inhibit locus ceruleus such as ______, inhibit LC firing and do what?

A

EX: BZD, SNRIs, SSRIs

Decrease NE and block anxiogenic drugs

80
Q

How does stress affect the hypothalamus and brainstem?

A

Hypothalamus affects the pituitary and eventually the adrenal glands which produces cortisol and Epi

Brainstem (which contains locus ceruleus) increases sympathetic outflow which also affects the adrenal glands and autonomic effects

81
Q

How does serotonin activity affect locus ceruleus?

A

Increases serotonin = decreases locus ceruleus

82
Q

Unlike the other anxiety disorders, OCD involves what?

A

Serotonin AND dopamine

83
Q

To be diagnosed with generalized anxiety disorder, how long must you have it?

84
Q

To be diagnosed with panic disorder, how long must you have it?

85
Q

Which anxiety condition is linked with agoraphobia?

A

Panic disorders, must have escape routes

86
Q

Social anxiety disorder physical indicator?

87
Q

Acute stress disorder occurs when after a trauma?

A

Within 1 month and lasts 2 days and resolves around 4 wks

88
Q

What are the cholinesterase inhibitors used in dementia? MOA?

A

Tacrine
Donepezil
Galantamine
Rivastigmine

Binds REVERSIBLY to AchE which accumulates ACh

89
Q

What are the NMDA antagonists used for dementia? MOA?

A

Memantine

Blocks action of glutamate attaching to NMDA receptors

90
Q

Aducanumab MOA?

A

Reduces/dissolves beta-amyloid plaques

91
Q

Which drugs for alzheimer’s are primarily renally eliminated?

A

Rivastigmine and memantine

92
Q

Which AD drug has multiple MOA?

A

Galantamine

Competitively inhibits AChE + modulates pre/postsynaptic nicotinic receptors (can help release ACh? might be neuroprotective?)

93
Q

GABA A receptor info?

A

Ligand-gated channel

Channel is closed until GABA binds to it which allows chloride to enter

94
Q

BZD bind to which sites?

A

Allosteric site at alpha and gamma subunits

95
Q

Alpha 1 and alpha 2 sites of GABA, what effects do they lead to?

A

Alpha 1 = sedation

Alpha 2 = anxiolytic

96
Q

What do BZD require to exert their effects?

A

GABA because they are positive allosteric modulators

97
Q

What combo with BZD are fatal?

A

Ethanol and opioids due to them being CNS depressants

98
Q

BZD main structures?

A

3 rings, but the important ones are the two that are directly touching each other

Side ring = at C7, it enhances anxiolytic activity

Main ring = C3 have comparable potency and are excreted more rapidly

99
Q

Half life and BZD?

A

BZD are given based off of their half life

Short half life? For hypnotics

Long half life? Anxiolytics

100
Q

Which BZD are inactivated rapidly by non-P450 dependent ways? What the importance?

A

Lorazepam, Oxazepam, and Temazepam

DDI are less of a concern

101
Q

Buspirone class? Anxiolytic activity is due to what?

A

Aryl piperazine

5-HT1a partial agonist

102
Q

Buspirone metabolism?

A

Extensive first pass metabolism (2.5hr half life), gotta be dose 2-3 times/day

103
Q

What are the “Z” drugs?

A

Non BZD hypnotics

Zaleplon
Zolpidem
Eszopliclone

104
Q

Z drug MOA and use?

A

Target alpha 1 subunit of GABA

Treats insomnia

105
Q

Zolpidem metabolism? Adjustments?

A

Absorbed via GI with a 2.5hr half life which should cover a 8hr sleep period

Dose adjustments made for elderly and hepatic impairment

106
Q

Zaleplon metabolism?

A

Absorbed via GI with a 1hr half life

Metabolized by AO + CYP3A4 with inactive metabolites

107
Q

Eszopiclone metabolism?

A

Absorbed via GI with a 6hr half life

Only one of the Z drugs that is approved for long-term use

108
Q

AE of Z drugs?

A

Generally safe vs BZD but amnesic sleep-related behaviors can come up (sleep walking, sleep eating, etc)

109
Q

Ramelteon MOA?

A

Synthetic analog of melatonin and agonist at GPCR MT1 and 2 with much higher affinity than melatonin

110
Q

Ramelteon AE and metabolism?

A

Less AE than BZD, no abuse, and can be used chronically

If used with CYP1A2 inhibitors, ramelteon levels will increase

111
Q

Suvorexant MOA?

A

Orexin receptor antagonist that binds to orexin A and B to OX1 and 2

112
Q

Suvorexant AE and metabolism?

A

Low potential for abuse and can be used chronically, but next day drowsiness can occur

Metabolised by CYP3A4

113
Q

Lemborexant MOA?

A

Antagonist of OX1 and 2

114
Q

Lemborexant metabolism?

A

Via CYP3A4

Caution over 10mg due to impairment

115
Q

Esketamine class and indication?

A

S-isomer of ketamine (NMDA antagonist)

Used for TRD in certified clinics only

116
Q

Esketamine AE?

A

Sedation, cognitive impairment, must monitor pt for at least 2 hrs after admin

Similar to phencyclidine aka angel dust which is known to cause episodic hallucinations

117
Q

Brexanolone class and indication?

A

GABA receptor modulator

Used for postpartum depression over 60hrs of continuous infusion

118
Q

Which antipyschs are generally safe to give to nursing mothers?

A

Sertraline

Paroxetine

Fluvoxamine

119
Q

Psychotherapy should be used when in depression?

A

May be used alone in mild to moderate acute MDD

NOT RECOMMENDED ALONE in severe or psychotic MDD

120
Q

When is light therapy used?

A

For seasonal affective disorders

121
Q

When is ECT useful?

A

Rapid response is needed

Patient will be under anesthesia

Can be used in severe cases and MDD

122
Q

What is a transcranial magnetic stimulation?

A

Coil placed on patients head while they are awake (no anesthesia needed)

No cognitive AE

123
Q

What is vagus nerve stimulation?

A

Approved for epilepsy and TRD

Implanted in left chest wall area attached to left vagus nerve and applies to CN X

Required to be programed

124
Q

Most common AE of vagus nerve stimulation?

A

Voice modulation during the stimulation

125
Q

Disadvantages to vagus nerve stimulation?

A

Surgery, cost

126
Q

What is deep brain stimulation?

A

FDA approved for parkinson’s and tremors

127
Q

Statistic to know about homicide and suicide…?

A

Since 2010, suicide death outnumbered homicide deaths

128
Q

What is the number one drug that is used for suicide?

129
Q

What are the top mental health conditions of peeps that commit suicide?

A

Depression (#1), then anxiety and then bipolar

130
Q

Church and suicide?

A

Church attendance is NOT a factor

Church involvement IS a factor

131
Q

What is a overlooked contributor to “imminent” suicidal risk?

132
Q

DSM-5 Criteria Bipolar I vs II

Which one contains Mixed or Rapid cycling?

A

Bipolar I and II

133
Q

DSM-5 Criteria Bipolar I vs II

Which one can occur throughout the life cycle with a mean age of onset at 18 yo?

A

I

II mean age of onset is mid-20s

134
Q

DSM-5 Criteria Bipolar I vs II

Which one has several MDD prior to manic-like states?

A

II; Several episodes of MDD prior to hypomanic episode

I has mania then depression

135
Q

Bipolar and biological factors

Serotonin
NE
Glutamate
GABA
VMAT2

Which one affects mania/depression?

A

Decreased serotonin = depression

NE = linked w/ mania

Glutamate/GABA = affects mania and depression

VMAT2 = higher in bipolar pt

136
Q

How long does Lithium take to work?

A

7-10 days, but can take up to 6-8wks for full effect

137
Q

Li AE of tremor, how do you treat it?

A

Propranolol

138
Q

Li AE of polyuria, polydipsia?

139
Q

Valproic acid can treat for (mania/depression)

140
Q

Lamotrigine can treat for (mania/depression)

A

Just depression

141
Q

Atypical antipsychs are used to prevent relapse of (mania/depression)

142
Q

AAPPG + Tx for ADHD

Preschool
School age
Adolescents + Adults

A

Preschool = behavioral therapy + methylphenidate

School age = behavioral therapy AND stimulant, atomoxetine, guanfacine, or clonidine

Adolescents + adults = behavioral therapy AND FDA approved medications

143
Q

Pharmacologic Tx algorithm for ADHD?

A

> 18yo = uses Amphetamines
Dextroamphetamines
Lisdexamfetamine first

then Methylphenidate
Dexmethylphenidate

For Pediatric pt, its swapped

144
Q

Stimulant MOA?

A

Blocks DA and NE reuptake

Increases catecholamine release

Inhibits monoamine oxidase release

145
Q

Use of lisdexamfetamine and its efficacy?

A

Not dose dependent for efficacy, but has dose dependent AE profile

146
Q

Methylphenidate AE?

A

May increase concentration of TCAs

In combo with clonidine, will enhance CV effects

147
Q

DDI of stimulants and MAOIs?

A

14 day washout period with MAOIs

148
Q

Methylphenidate and psychosis risk?

A

If they have it, watch them for the first 9 months (especially 3 months)

149
Q

If patient is on stimulant + has reduced appetite or weight loss, what do you do?

A

Give high calorie meal

150
Q

Alpha 2 agonists for ADHD, MOA?

A

Inhibits NE and increases blood flow to prefrontal cortex

151
Q

Alpha 2 agonist for ADHD, efficacy?

A

Not really used as monotherapy, usually in addition to stimulants

152
Q

Weight in anorexia vs bulimia

A

Weight can be normal in bulimia

153
Q

Prevalence of anorexia, buliimia, and binge-eating

A

Binge-eating is the most prevalent

154
Q

What is the only FDA approved drug for bulimia?

A

Fluoxetine

155
Q

In bulimia, is bupropion okay to use?

A

No, increased seizure risk

156
Q

Fluoxetine is used for (anorexia/bulimia)

A

Bulimia, no FDA approved meds for anorexia

157
Q

What are some reversible causes of dementia?

A

B12 and hypothyroidism

IPT: Neuro (4 decks)

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