Module 7 Study Guide/Practice Questions Flashcards

1
Q

What drugs in Module 7 prolong QT?

A
Chlorpromazine
Citalopram
Escitalopram
Haloperidol
Thioridazine
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2
Q

What are the six classifications of anxiolytics?

A
SSRIs
SNRIs
Azapirones
Benzodiazepines
Beta blockers
Sedative Antihistamines
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3
Q

Should benzodiazepines be prescribed for daily use for anxiety? Why or why not?

A

No, high risk for Abuse potential and Addictive

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4
Q

What could happen if benzodiazepines are abruptly stopped after chronic use?

A

Risk for seizures; should be tapered over many weeks

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5
Q

What other drug class must be avoided in the use of benzodiazepines?

A
CYP450 drugs (wondering if that’s what they mean?)
They are a CNS depressant. Don’t use with opioids.
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6
Q

Can you rate the onset of action of benzos with the likelihood of abuse or dependence?

A

They work quickly, with high abuse potential.
Xanax has the highest abuse potential due to its fast onset.
Take home: Prescribe cautiously and for as short as possible.

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7
Q

Are SSRIs a good choice for the relief of acute anxiety?

A

No because they may not be effective for several weeks

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8
Q

Can you list two drug-to-drug interactions with Buspirone (BuSpar)?

A

CYP450 3A4 inhibitors (fluoxetine, fluvoxamine, nefazodone) may reduce the clearance of buspirone and raise its plasma levels, so the dose of buspirone may need to be lowered when given concomitantly

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9
Q

What is the abuse potential when using hydroxyzine (Vistaril) in the treatment of anxiety?

A

From lecture: No risk.
From google: Due to its fast acting, sedative and relaxing nature, there is potential for abuse. However, there is no chance of addiction in that there are no physical side effects when discontinued.

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10
Q

Which patients should avoid the use of hydroxyzine (Vistaril)?

A

Risk of anticholinergic toxicity or delirium in the elderly or patients with neurocognitive disorders.

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11
Q

How do Beta-Blockers work to reduce anxiety related to public speaking?

A

Decreases symptoms caused by autonomic hyperactivity (tremors, sweating, tachycardia, palpitations)

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12
Q

Who should avoid Beta-Blockers?

A

Those taking it for BP management

Cardiac issues like heart failure

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13
Q

Can you list drug-to-drug interactions associated with St. John’s Wort?

A

triptans, benzos, contraceptives, digoxin, SSRIs, and antibiotics.

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14
Q

What are the two agents recommended in the treatment of chronic insomnia (greater than 6 months)?

A

Lunesta (eszopiclone) - schedule IV

Rozerem (ramelteon)

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15
Q

Discuss the required patient education that must be provided regarding sleep medications.

A

Do not take unless you have 7-8 hours to sleep
Take on an empty stomach at least 30 minutes before bedtime
Drugs with long half-lives (eszopiclone) are associated with a higher risk of next-day impairment
Sleepwalking, sleep driving, sleep eating, sleep sex have been reported with zolpidem and other “Z-drugs”
Do not use with other CNS depressants or alcohol

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16
Q

Which anxiolytics are considered safe in pregnancy?

A
(Confirming this info in the forum) 
short-term use of clonazepam (Klonopin) if nothing else works. 
Buspar (B) 
Clozaril (B) 
Zoloft (C) 
Prozac (C) 
Lexapro (C)
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17
Q

Which sleep medications are considered safe in pregnancy?

A

Visitril for short amount of time.

Ambien. Short, last resort.

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18
Q

How long does it take to see an initial response with antidepressants? How long for the full effect of antidepressants?

A

Some individuals see an initial effect after one week and up to four weeks to achieve a full effect.

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19
Q

What are the two main determinants for which antidepressant to use? Are there any others?

A

Tolerability and safety. Also to consider: D2D interactions, cost, and patient preference. (Ie low libido, do buspar. Fatigue, do a CNS stimulant, etc.)

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20
Q

What is serotonin syndrome? What causes it?

A

This can occur from overdose or drug-to-drug interaction, multiple serotonin drug uses. It is essential to review the current medication list prior to prescribing serotonergic drugs

Confusion, agitation, clonus, fever, tremor, or hyperreflexia and can result in respiratory failure and death.

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21
Q

How often should a patient be seen after initial treatment with antidepressants? Why?

A

Once a week for first month, biweekly for next four. because of high risk of suicide.

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22
Q

What is the BBW for antidepressants? Who is at greatest risk?

A

Suicide risk, especially early on, may increase.

Antidepressant-induced suicide applies mainly to children, adolescents, and adults younger than 25.

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23
Q

What is withdrawal syndrome? Are drugs with a short half-life or long half more likely to result in withdrawal syndrome? Why?

A

Starts within days and lasts up to 3 weeks. Dizziness, chills, lightheadedness. Brain “zaps.”

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24
Q

How do you discontinue an antidepressant?

A

Cross taper. Slowly decrease current while simultaneously titrating up the new drug to therapuetic drugs. Can take 1-2 weeks. Don’t cross-taper with MAOIs (need 14 day detox).

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25
Q

Which antidepressants are safe in pregnancy? Lactation?

A

Zoloft and Prozac in pregnancy (??)
Zoloft, Paxil, and Fluvox are safe and first-line in breastfeeding.
Avoid Paxil in pregnancy.
Avoid Prozac in BF.

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26
Q

What should people who are taking MAOIs avoid (think drug to drug and drug to food interactions)? What can happen if they do not avoid these foods/drugs?

A

Wine, meats, unfiltered beers, and cheeses that are high tyramine. Can spike blood pressure.

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27
Q

What happens if you treat a patient with bipolar by using an SSRI?

A

Can put them in a manic state. Want to rule out bipolar before starting.

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28
Q

What are some adverse effects of SSRIs and SNRIs?

A

Serotonin syndrome is a rare but serious complication.
Increased suicidal ideation the first 2-3 weeks.
May cause n/v, insomnia, weight gain, and sexual dysfunction.
Use caution with elderly. Start low and go slow
Venlafaxine (SNRI) may cause HTN and must be avoided with MAOI.

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29
Q

When is the risk for suicide greatest for children/adolescents on antidepressants?

A

First week.

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30
Q

Are there risks for the elderly taking antidepressants?

A

TCAs: Anticholinergic side effects. Use with caution in elderly.
MAOI’s contraindicated for elderly.
Due to decreased renal clearance, reduced hepatic function, and frequently reduced albumin levels, typically the dose is started at one-third to one-half of the usual starting adult dosage

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31
Q

Who is a good candidate for Wellbutrin, and why?

A

It is stimulating, so can be very beneficial for those individuals with depression that have symptoms of lethargy, apathy, and low motivation. Beyond its antidepressant effect, patients taking bupropion often report improved focus/concentration, reduction in appetite, increased libido, and greater motivation/energy.

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32
Q

When would a tricyclic antidepressant be appropriate?

A
  1. TCAs may still benefit some patients who do not respond to first-line agents
  2. TCAs may be beneficial to patients who have trouble sleeping.
  3. They have also been found to decrease pain in many patients with chronic pain including neuropathic pain.
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33
Q

How is bupropion (Wellbutrin) different from the other antidepressants?

A

bupropion boosts norepinephrine ( aka. noradrenaline ) and dopamine

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34
Q

What is the main concern with bupropion (Wellbutrin)?

A

it may increase the frequency and severity of seizures in those with a seizure disorder

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35
Q

What classes of drugs are used to treat ADHD?

A
Stimulants - first choice 
Non stimulants - Second Choice
Noradrenergic Agents: (Atomoxetine)
Alpha 2A Adrenergic Agonists:
Antidepressants
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36
Q

What is or is not the link between ADHD and long-term drug use?

A

Untreated attention deficit disorder increases the significant risk for addictions due to self-medication of symptoms.

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37
Q

What is the expected therapeutic effect of stimulants?

A
38
Q

What are the adverse side effects of stimulants?

A

decreased appetite, insomnia, and jitteriness

39
Q

Are stimulants or non-stimulants first-line treatment in ADHD?

A

Stimulants

40
Q

Are the non-stimulants controlled substances? What about stimulants?

A

No.

yes. Adderall is schedule 2.

41
Q

What is the expected symptom response time with both the stimulants and the non-stimulants?

A

Non-stimulants- develop slowly, initial response time = few days to develop, max response 1-4 weeks
Stimulants- Effects near max with first dose

42
Q

What are the adverse effects of the non-stimulants?

A
GI (N/V, dyspepsia)
Reduced appetite
Weight loss / growth delay in children
Dizziness
Somnolence
Mood swings
Trouble sleeping
In adults: sexual dysfunction, urinary retention
Liver injury
Can raise or lower BP
Suicidal thinking in children & adolescents
43
Q

What are the drug interactions with the non-stimulants?

A

Inhibitors of CYP2D6 (can raise levels) → e.g. Paxil, prozac and quinidine

44
Q

Why would you choose a non-stimulant over a stimulant?

A

Can be used as an add -on or may be preferred if there is abuse potential or strong aversion to stimulant tx

45
Q

What is the gold standard for treating Bipolar Disorder?

A

Lithium

46
Q

What are the black box warnings for mood stabilizers?

A

Toxicity levels can occur at doses close to therapeutic levels.

47
Q

What are the adverse effects of mood stabilizers?

A

Lithium:
Common: Nausea, fine-hand tremors, increased urination, and thirst.
Toxicity: Slurred speech, confusion, severe GI effect
Can cause hypothyroidism.

Carbamazepine:
Common: Nausea, dizziness, headache, dry mouth, constipation, skin rash
Rare: Agranulocytosis/aplastic anemia, Sevens-Johnson syndrome
BBW:Serious dermatologic reactions and HLA-B*1502 Allele and Aplastic anemia/agranulocytosis

Depakote:
Common: Nausea, diarrhea, abdominal cramps, sedation, tremor
Rare: Increased liver enzymes, Stevens-Johnson syndrome
BBW: Increased hepatotoxicity risk in mitochondrial disease, Fetal Risk, Pancreatitis

Lamictal:
Common: Dizziness, ataxia, somnolence, diplopia, nausea, headache, hepatotoxicity
Rare: Life-threatening rashes, including Stevens-Johnson syndrome, leukopenia
BBW: Serious rash

48
Q

What are the two major groups of antipsychotic drugs?

A

First (Haldol) and second generation (clozapime, etc.)

49
Q

What is the MOA of first and second-generation antipsychotics? What are the main concerns of FGAs and SGAs?

A

1st Gen:block dopamine, acetylcholine, histamine, and norepinephrine=decreased psychosis BBW:elderly mortality

2nd Gen:D2 and serotonin 2A antagonist BBW:clozaril=agranulocytosis

50
Q

What is the black box warning for antipsychotic drugs as a class?

A

Suicide.

Mortality in elderly.

51
Q

What are the adverse effects of antipsychotic drugs listed in your text?

A

First generation: Haloperidol (Haldol) and Chlorpromazine
Common: extrapyramidal side effects, acute dystonia, parkinsonism, akathisia, tardive dyskinesia, sedation, hypotension

Second generation: Clozapine, Olanzapine, Ziprasidone, Aripirazole
Common: QTc prolongation, sedation, weight gain, prolactin elevation
FDA warning issued on SGA (Not sure what SGA Is???)
Increased risk of hyperglycemia and diabetes
Noted some cases of extremely high blood sugar that led to ketoacidosis, hyperosmolar coma, or death

52
Q

What are three drug interactions with antipsychotic drugs?

A

First generation: anticholinergics, CNS depressants, Levodopa.

53
Q

What are the five basic mechanisms of action of antiseizure drugs?

A

Suppression of sodium influx (Tegretol, dilantin)
Suppression of calcium influx
Promiton of potassium influx
Blockade of receptors for glutamate
Increase of GABA (Ethosuximide (Zarontin) and Valproic acid (Depakote))

54
Q

What is the goal of treatment with AEDs?

A

To reduce seizures to the degree that the person can live a normal life. Ultimate goal is complete seizure inactivity.

55
Q

What are the reasons for monitoring blood plasma levels with AEDs?

A

Knowledge of levels can help us establish dosage and evaluating effectiveness of the drug. Also helps us determine patient adherence, determine cause of loss of seizure control, identifying causes of toxicity.

56
Q

What are the two classifications of antiseizure drugs?

A

Traditional: More side effects, more D2D, but more studies on efficacy and cheaper. (Depakote, Dilantin, Tegretol)

Newer: Safer, more effective, less D2D, less well established efficacy. (Lomictal, gabapentin)

57
Q

What are the concerns with contraception and pregnancy when it comes to antiseizure medications? What does this mean in terms of recommended patient education?

A

Decreased contraceptive effects (recommend barrier). Progesterone only pills also work better. IUDs/implanon.

58
Q

What is the black box warning for phenytoin (Dilantin)?

A

Rapid IV administration can cause severe hypotension and cardiac dysrhythmias.

59
Q

What is the black box warning for carbamazepine (Carbatrol, Tegretol)?

A

It may cause SJS and TEN. Aplastic anemia and agranulocytosis.

60
Q

What is the black box warning for valproate and valproic acid (Depacon, Depakote)?

A

Fatal hepatic failure risk. Fatal and rapidly progressing pancreatitis. Fetal teteragenic

61
Q

What are some of the important patient education points for patients using traditional antiseizure drugs? (adverse effects, drug interactions, food interactions).

A

Decreases effectiveness of BC, warfarin, gluccocorticoids
Increase levesl: Diazapam, alcohol (acute) cimitedine, grapefruit juice
Decrease levels: Alcohol (chronic), carbamezapine, phenobarbitol. (Breakthrough seizures!)
Other CNS depressants can increase depressive effects.
Can cause hirituism, gingival hyperplasia, rash.
Do not abrupty withdrawal.
Take folic acid.

62
Q

What is the MOA of lamotrigine (Lamictal)?

A

Acts as a use-dependent blocker of voltage-sensitive sodium channels
Interacts with the open channel conformation of voltage-sensitive sodium channels
Interacts at a specific site of the alpha pore-forming subunit of voltage-sensitive sodium channels
Inhibits the release of glutamate and aspartate

63
Q

What are the approved uses for lamotrigine (Lamictal)?

A

Bipolar I disorder, maintenance
Partial seizures
Seizures, primary generalized tonic-clonic
Migraine headache with aura prophylaxis

64
Q

What is the black box warning of lamotrigine (Lamictal)?

A

SJS-severe rash

65
Q

What is additional monitoring that is necessary for many of the AEDs?

A

Seizure activity, degree of CNS change, depression, suicide, behavior change.

66
Q

What are withdrawal seizures, and how are they prevented?

A

When AEDs are taken off too quickly, can result in seizures.
Withdraw slowly, over 6+ weeks.

67
Q

What are the neurotransmitters involved with Alzheimer’s disease?

A

Acetylcholine (responsible for memory function)

Glutamate (an excitatory neurotransmitter causing cell death)

68
Q

What are the two classes of drugs used in the treatment of AD?

A
Cholinesterase inhibitors (Aricept)  - mild to moderate AD
NMDA receptor antagonists. (Namenda)  - moderate to severe AD
69
Q

What is the MOA of cholinesterase inhibitors?

A

Prevents breakdown of acetylcholine

70
Q

What is the indication (disease severity) for using cholinesterase inhibitors?

A

Mild to moderate AD

71
Q

What are the adverse side effects of the cholinesterase inhibitors?

A

GI related

Weight loss
Nausea
Vomiting
diarrhea

Muscle cramps

72
Q

Which drugs have drug interactions with cholinesterase inhibitors

A

Anticholinergics (first-generation antihistamines, TCAs) reduce effectiveness
NSAIDs, increase risk of GI bleed
antifungals, inhibit metabolism increasing levels

73
Q

What is the therapeutic goal of cholinesterase inhibitors?

A

Improved cognition and function for patients with AD by increasing availability of acetylcholine at cholinergic synapses

74
Q

Regarding N-Methyl-D-Aspartate Receptor Antagonist (NMDA receptor antagonists), when is it used, and what are the therapeutic goals?

A

Used in moderate to severe AD
Therapeutic goals:
Slow cognitive and functional decline of patients with moderate to severe AD

75
Q

What is the MOA of memantine (Namenda)?

A

Blocks excessive excitation of NMDA receptors by glutamate as overexcitation by glutamate is cytotoxic

76
Q

What are some adverse effects of memantine (Namenda)?

A

Dizziness- FALL RISK
HA
Constipation
Use caution in pt’s with renal impairment

77
Q

What is the therapeutic goal of PD treatment?

A

Drugs can only provide symptomatic relief and cannot reverse damage
Improve pt’s ability to carry out activities of daily living
Improve bradykinesia, gait disturbance, postural instability

78
Q

What two types of drugs are used to treat PD?

A

Dopaminergic agents → drugs that directly or indirectly activate dopamine receptors
Anticholinergic agents → block receptors for acetylcholine

79
Q

Is Levodopa effective in PD, and how long does it take to see a full therapeutic response?

A

Highly effective;

Full therapeutic response takes several months to develop

80
Q

What happens with long-term therapy of Levodopa?

A

Symptoms typically well- controlled during first two years of tx but by year five ability to function may deteriorate to pretreatment levels

81
Q

What is the loss of effect? Describe both gradual and abrupt loss.

A

Gradual: “wearing off” develops near end of dosing interval → drug levels have declined to a subtherapeutic value. Can be minimized in 3 ways:
Shortening dosing interval
Giving a drug that prolongs levodopa plasma half life (e.g. entacapone)
Giving a direct acting dopamine agonist

Abrupt: “on-off” phenomenon
Can occur at any time during dosing interval (even if drug levels are high)
“Off” times can last from minutes to hours
Increase with development of disease

82
Q

What is the MOA of Levodopa? Why not use dopamine instead of Levodopa?

A

Levodopa crosses the BBB, undergoes uptake into remaining dopaminergic nerve terminals, and is converted into dopamine (active form)
Dopamine isn’t used because it doesn’t cross the BBB and has such a short half-life that it wouldn’t be “practical” even if it did cross the BBB

83
Q

What is the role of Carbidopa in Levodopa/Carbidopa?

A

Carbidopa inhibits decarboxylation of levodopa making it more available to the CNS
Carbidopa does not prevent conversion of levodopa to dopamine in brain b/c carbidopa is unable to cross BBB

84
Q

What are the adverse effects of Levodopa/Carbidopa?

A
Nausea and vomiting
Dyskinesias
CV effects
Psychosis
CNS effects (from anxiety & agitation to memory & cognitive impairment)
Darkened sweat/urine
85
Q

What is important patient education regarding Levodopa/Carbidopa when it pertains to diet?

A

High protein meals can reduce therapeutic responses to levodopa
High fat foods can decrease absorption
Drugs should be taken on an empty stomach

86
Q

What are the drug-to-drug interactions with Levodopa/Carbidopa?

A

First generation antipsychotic drugs - can decrease therapeutic levels of levodopa
MAOIs - levodopa can cause hypertensive crisis if given w/nonselective inhibitor or MAO
Anticholinergic drugs
Pyridoxine

87
Q

What is the therapeutic goal of dopamine agonists?

A

To maintain or improve the patient’s ability to carry out ADLs

88
Q

What are drug interactions with dopamine agonists?

A

Cimetidine (tagament) can inhibit renal excretion of pramipexole, increasing it’s blood level

89
Q

List the important patient education concerns for patients taking dopamine agonists.

A

N/V can be reduced by taking oral dopamine agonists w/food → tell provider if n/v persist or become severe (can be pre-treated w/antiemetic)
Orthostatic hypotension
Potential for movement disorders
DAs can cause hallucinations (especially in older adults)
Pramipexole, ropinirole, rotigotine and apomorphine can cause sleep attacks (avoid hazardous activities if they occur)
Use effective BC if taking ropinirole d/t harmful effects on developing fetus

90
Q

What does the patient on MAO-B inhibitor used with Levodopa need to avoid in their diet?

A

Tyramines

91
Q

How is Amantadine (antiviral) used in the treatment of PD?

A

Reduces tremor. Can be used alone, with Levadopa, and to reduce “off” times.

92
Q

Who should avoid tricyclic antidepressants? What can happen?

A

Contraindicated in patients with cardiac issues. Risk of cardiac toxicity. Lead to arrhythmias. Can cause death.