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KLowe Pharm 2 > Lecture 9-Neuropsychiatric Medications > Flashcards

Lecture 9-Neuropsychiatric Medications Flashcards

1
Q

Status epilepticus first phase = ___-___ minutes; ___ is treatment of choice

A

status epilepticus first phase = 5-20 minutes; benzo is treatment of choice (i.e.: versed, Ativan, valium)

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2
Q

Status epilepticus second phase = ___-___ minutes; there ___ (is/is no) evidence based first choice; may use ___, ___, or ___

A

status epilepticus second phase = 20-40 minutes; there is no evidence based first choice; may use fosphenytoin, valproic acid, or keppra

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3
Q

Status epilepticus third phase = ___-___ minutes; can repeat any ___ (first/second) line therapy; ___ doses of thiopental, midazolam, pentobarbital, or propofol

A

status epilepticus third phase = 40-60 minutes; can repeat any second line therapy; anesthetic doses of thiopental, midazolam, pentobarbital, or propofol

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4
Q

Anticonvulsant medications are only approved to treat seizures–T/F?

A

False–there are several approved/unapproved indications

i.e.: neuropathic pain, mood stabilization, migraines, alcohol dependence

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5
Q

Anticonvulsants MOA–___ channel blockade, ___ channel blockade

A

sodium channel blockade, calcium channel blockade

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6
Q

Anticonvulsants calcium channel blockade–particularly the ___-type channels located in the ___ which act as ‘pacemakers’ of normal rhythmic brain function

A

Anticonvulsants calcium channel blockade–particularly the T-type channels located in the thalamus which act as ‘pacemakers’ of normal rhythmic brain function

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7
Q

Anticonvulsants other MOAs–GABA ___ (enhancers/inhibitors); glutamate ___ (enhancers/blockers); carbonic anhydrase ___ (enhancers/inhibitors); ___ hormones; synaptic vesicle protein ___

A

GABA enhancers [remember GABA is inhibitory]; glutamate blockers [remember glutamate is excitatory]; carbonic anhydrase inhibitors; sex hormones; synaptic vesicle protein 2A (SV2A)

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8
Q

Anticonvulsant medications–carbamazepine, oxcarbazepine, eslicarbazepine, phenytoin/fosphenytoin, lamotrigine, zonisamide, lacosamide, and cenobamate are all ___ channel blockers

A

all sodium channel blockers

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9
Q

Carbamazepine multiple uses–___ and ___ seizures; mood ___; ___ pain; ___ neuralgia

A

partial and generalized seizures; mood stabilizer; neuropathic pain; trigeminal neuralgia

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10
Q

Carbamazepine ___ (induces/inhibits) its own metabolism

A

Carbamazepine induces its own metabolism

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11
Q

Carbamazepine is a CYP3A4 ___ (inducer/inhibitor)

A

Carbamazepine is a CYP3A4 inducer

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12
Q

What is the most important thing to consider about carbamazepine?

A

Drug interactions–because it is a CYP inducer/substrate, it ramps up the metabolism of other drugs and itself, clears medications from the bloodstream faster, and shortens the duration of action of other drugs

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13
Q

Carbamazepine side effects–___ea, ___ syndrome, ___ (increased/decreased) LFTs, ___natremia

A

nausea, Stevens-Johnson syndrome, increased LFTs, hyponatremia

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14
Q

If patient is on carbamazepine, check ___ levels

A

sodium levels

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15
Q

Why was oxcarbazepine created?–to eliminate the auto-___ of carbamazepine

A

to eliminate the auto-induction of carbamazepine

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16
Q

As a person takes carbamazepine for a longer period of time, it loses its effectiveness because it’s an inducer and substrate–T/F?

A

True

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17
Q

Eslicarbazepine is a ___drug

A

prodrug –> S-licarbazepine

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18
Q

If patient has renal impairment, you need to adjust the dose of eslicarbazepine–T/F?

A

True

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19
Q

Main concerns for the -carbazepine anticonvulsants–check ___ levels, check for drug ___, check ___/___s

A

check sodium levels, check for drug interactions, check CBC/LFTs

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20
Q

Most common side effects with eslicarbazepine (> 10%)–___ness, ___lence, ___ea, ___ache, ___opia

A

dizziness, somnolence, nausea, headache, diplopia

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21
Q

Phenytoin is a ___ channel blocker; has ___ (linear/non-linear) pharmacokinetics; CYP enzyme ___ and ___

A

Phenytoin is a sodium channel blocker; has non-linear pharmacokinetics; CYP inducer and substrate

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22
Q

What is the therapeutic range for phenytoin?

A

10-20

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23
Q

Dose adjustments for phenytoin are ___ (small/large)

A

Small because it has non-linear pharmacokinetics

Example: Patient is on 300 mg phenytoin. You check a level and it comes back at 5. You increase the dose to 300 mg bid. You re-check the level and it is 28, and patient is dizzy, nauseous, and having vision changes. You may just add 30-50 mg at a time to get to desired therapeutic levels for phenytoin.

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24
Q

Fosphenytoin = ___drug for ___ (oral/parenteral) administration

A

prodrug for parenteral administration

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25
Q

Fosphenytoin is safer, better tolerated, and can run at faster infusion rates than phenytoin–T/F?

A

True

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26
Q

Side effects of phenytoin/fosphenytoin–gingival ___plasia; ___mias, CV ___, ___tension mostly at toxic levels; ___mus; vitamin ___ and ___ deficiencies; if given during pregnancy–cleft ___/___, congenital ___ disease, slowed ___ rate, mental ___

A

Side effects of phenytoin/fosphenytoin–gingival hyperplasia; arrhythmias, CV depression, hypotension mostly at toxic levels; nystagmus; vitamin K and folate deficiencies; if given during pregnancy–cleft lip/palate, congenital heart disease, slowed growth rate, mental deficiency

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27
Q

Lamotrigine is a ___ channel blocker

A

sodium channel blocker

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28
Q

If patient is on depakote/lamictal and stops taking both prior to surgery, if they are both not restarted in 3-4 days and you have to reinitiate, there is a long cross-taper period of 4-8 weeks where you can only make minor incremental increases in the dosages–T/F?

A

True

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29
Q

What happens if you reinitiate a person’s regular doses of depakote/lamictal after having stopped both drugs for 3-4 days or more?

A

Steven Johnsons syndrome–very high rates, can cause devastating skin reactions

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30
Q

Lamotrigine drug interaction with depakote = high risk of ___

A

high risk of SJS

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31
Q

Zonisamide side effects–can cause renal ___ in 1.5% of patients

A

can cause renal stones in 1.5% of patients

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32
Q

Lacosamide (Vimpat) has a ___ (low/high) side effect profile; pregnancy category ___

A

Lacosamide has a low side effect profile; pregnancy category C–still unsure of what the true risk is in pregnancy

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33
Q

Benzodiazepines should be restarted as soon as possible if held before/after a surgical procedure to avoid withdrawal–T/F?

A

True–continue Benzos as long as possible, restart ASAP

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34
Q

Higher lipophilicity for benzos = ___ (slower/faster) onset of action, ___ (shorter/longer) duration of action

A

higher lipophilicity for benzos = faster onset of action, longer duration of action

i.e.: diazepam (Valium), clonazepam (Klonopin)

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35
Q

Lower lipophilicity for benzos = ___ (slower/faster) onset of action, ___ (shorter/longer) duration of action

A

lower lipophilicity for benzos = slower onset of action, shorter duration of action

i.e.: alprazolam (xanax), temazepam (restoril)

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36
Q

Which benzodiazepine is only used for seizures and is not appropriate to use for anxiety/sleep? If this medication is discontinued, it needs to be restarted ASAP otherwise patient will experience wild withdrawal symptoms and will start seizing really quick. This medication has a long taper if you want to get a person off of it.

A

Clobazam (Onfi)

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37
Q

Primidone is a prodrug that is metabolized to ___

A

Primidone is a prodrug metabolized to phenobarbital

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38
Q

Vigabatrin has a risk of permanent ___, and for this reason is only available through a very specific program with REMS monitoring

A

Vigabatrin has a risk of permanent vision loss, and for this reason is only available through a very specific program with REMS monitoring

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39
Q

Gabapentin is more often used for ___ than ___ control

A

Gabapentin is more often used for neuropathic pain than seizure control

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40
Q

Gabapentin ___ (is/is not) protein bound, ___ (is/is not) metabolized, is excreted completely ___ (changed/unchanged) by the ___, ___ (has/has no) PK drug interactions

A

Gabapentin is not protein bound, is not metabolized, is excreted completely unchanged by the kidneys, has no PK drug interactions

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41
Q

A meta analysis of RCTs suggests that gabapentin given 1x 30 minutes pre-operatively in regional anesthesia for multiple procedures ___ (improves/worsens) post-op pain and ___ (increases/reduces) opiate requirements with increased post op ___ being the highest safety risk

A

A meta analysis of RCTs suggests that gabapentin given 1x 30 minutes pre-operatively in regional anesthesia for multiple procedures improves post-op pain and reduces opiate requirements with increased post op sedation being the highest safety risk

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42
Q

You may see increased side effects of gabapentin in patients with poor kidney function–T/F?

A

True–because it is completely eliminated by the kidneys

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43
Q

Gabapentin is very well tolerated–T/F?

A

True

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44
Q

December 2019 FDA safety communication–gabapentinoids in combo with opiates may lead to severe ___ distress

A

gabapentinoids in combo with opiates may lead to severe respiratory distress

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45
Q

Pregabalin main use is in ___, but also may be used to treat ___ and ___

A

Pregabalin main use is in neuropathy, but also may be used to treat seizures and anxiety

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46
Q

Lots of people taking pregabalin complain of difficulty ___

A

Lots of people taking pregabalin complain of difficulty walking

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47
Q

Valproic acid drug interactions occur through ___ (stimulation/inhibition) of oxidation and glucuronidation pathways

A

Valproic acid drug interactions occur through inhibition of oxidation and glucuronidation pathways

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48
Q

In utero exposure to valproic acid leads to lower ___ in children compared to other anti-epileptics

A

In utero exposure to valproic acid leads to lower IQ in children compared to other anti-epileptics

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49
Q

Valproic acid is pregnancy category ___-___

A

Valproic acid is pregnancy category D-X

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50
Q

Valproic acid may cause ___penia

A

thrombocytopenia–just like carbamazepine family, heparin, H2 receptor antagonists, SSRIs

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51
Q

Valproic acid may cause ___ammonemia

A

Valproic acid may cause hyperammonemia

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52
Q

If someone is on depakote and becomes confused, what should you do?

A

Check ammonia level because depakote increases ammonia levels

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53
Q

What labs should be routinely checked if patient is on valproic acid?

A

Ammonia, LFTs, CBC

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54
Q

If patient is pregnant and in status epilepticus, you can give valproic acid–T/F?

A

False–never use depakote in pregnancy, even if patient is in status epilepticus

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55
Q

What are (3) glutamate blockers?–___bamate, ___ramate, ___ampanel

A

Felbamate (felbatol), topiramate (topamax), perampanel (fycompa)

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56
Q

Felbamate (felbatol) is very rarely used in the US because it has high risk of ___ anemia and fatal ___ failure

A

Felbamate (felbatol) is very rarely used in the US because it has high risk of aplastic anemia and fatal hepatic failure

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57
Q

What is one common side effect of topiramate (topamax)? ___ slowing

A

Psychomotor slowing–want to do something, but can’t make it happen

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58
Q

Perampanel black box warning–serious or life threatening ___ and ___ adverse effects

A

Perampanel black box warning–serious or life threatening psychiatric and behavioral adverse effects–aggression, hostility, irritability, anger, homicidal ideation, threats

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59
Q

Common side effect of perampanel (in 43% of patients) = ___

A

dizziness

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60
Q

Levetiracetam MOA is possibly related to synaptic vesicle protein ___, which appears to be important for the availability of __-dependent neurotransmitter vesicles ready to release their content

A

Levetiracetam MOA is possibly related to synaptic vesicle protein 2A, which appears to be important for the availability of calcium-dependent neurotransmitter vesicles ready to release their content

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61
Q

Keppra–without SV2A, reduced action potential-___ (independent/dependent) neurotransmission, while action potential-___ (independent/dependent) neurotransmission remains normal

A

Keppra–without SV2A, reduced action-potential dependent neurotransmission, while action potential-independent neurotransmission remains normal

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62
Q

Keppra also inhibits ___ release from IP3-sensitive stores

A

Keppra also inhibits calcium release from IP3-sensitive stores

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63
Q

A significant side effect of keppra is ___ impairment

A

A significant side effect of keppra is cognitive impairment–have a convo and don’t even remember having it

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64
Q

Baclofen is a ___ analog

A

Baclofen is a GABA analog

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65
Q

Substance ___ is released in response to pain impulses

A

Substance P is released in response to pain impulses

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66
Q

How does baclofen work?–it inhibits substance ___ release into the spinal cord to reduce pain

A

Baclofen inhibits substance P release into the spinal cord to reduce pain

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67
Q

Baclofen is primarily used to treat muscle ___

A

Baclofen is primarily used to treat muscle spasm

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68
Q

If baclofen is abruptly discontinued, patients will experience ___ symptoms–i.e.: ___nations, ___er, ___tation, ___or, ___cardia, ___ure

A

If baclofen is abruptly discontinued, patients will experience withdrawal symptoms–i.e.: hallucinations, fever, agitation, tremor, tachycardia, seizure

69
Q

Tizanidine is a centrally acting alpha ___–slows down ___ release using negative feedback

A

Tizanidine is a centrally acting alpha 2 agonist–slows down NE release using negative feedback

70
Q

Withdrawal is possible with abrupt discontinuation of tizanidine–T/F?

A

True

71
Q

Side effects of tizanidine–___ mouth, ___ation, anti___ effects

A

Side effects of tizanidine–dry mouth, sedation, anticholinergic effects

72
Q

Dantrolene blocks ___ channel, reduces ___ release from the ___

A

Dantrolene blocks ryanodine channel, reduces calcium release from the sarcoplasmic reticulum

73
Q

___ mutations are associated with malignant hyperthermia

A

RyR1 mutations are associated with malignant hyperthermia

74
Q

Dantrolene has dose dependent ___rrhea and ___toxicity (BB warning > ___mg/day with long term use)

A

Dantrolene has dose dependent diarrhea and hepatotoxicity (BB warning > 800 mg/day with long term use)

75
Q

Other side effects of dantrolene–___nea, ___phagia, ___lence

A

Other side effects of dantrolene–dyspnea, dysphagia, somnolence

76
Q

Skeletal muscle relaxants ___ (should/should not) be used long term

A

Skeletal muscle relaxants should NOT be used long term due to significant ADRs and increased duration

77
Q

Skeletal muscle relaxants have risks of ___ sedation and ___

A

Skeletal muscle relaxants have risks of over sedation and withdrawal

78
Q

Zolpidem (Ambien), Zaleplon (Sonata), and Eszopiclone (Lunesta) are all ___, AKA ___-drugs

A

Zolpidem (Ambien), Zaleplon (Sonata), and Eszopiclone (Lunesta) are all sedative hypnotics, AKA Z-drugs

79
Q

Ramelteon (Rozerem) is a ___ receptor agonist

A

Ramelteon (Rozarem) is a melatonin receptor agonist

80
Q

Suvorexant (Belsomra) is a ___ antagonist; is associated with significant sleep ___

A

Suvorexant (Belsomra) is a norexin 2 antagonist; is associated with significant sleep activities

81
Q

Our bodies release melatonin naturally every ___-___ hours ___ (before/after) we fall asleep

A

Our bodies release melatonin naturally every 2-3 hours before we fall asleep

82
Q

Sedative hypnotics ___ (should/should not) be used regularly in the hospital to help patients sleep

A

Sedative hypnotics should NOT be used regularly in the hospital to help patients sleep

83
Q

Sedative hypnotics like Zolpidem (Ambien) are benzodiazepine like drugs–T/F?

A

True

84
Q

Patients can go through withdrawal when they stop taking sedative hypnotics like ambien, sonata, and Lunesta–T/F?

A

True–withdrawal symptoms include insomnia and anxiety

85
Q

Sedative hypnotics help people fall asleep and provide restorative REM sleep–T/F?

A

FALSE–sedative hypnotics DO help people fall asleep, but they DO NOT provide restorative REM sleep

86
Q

“Sleep behaviors” are very common with Z drugs, i.e.: sleep eating, sleep fighting, sleep walking; patients can hurt themselves when they take these medications–T/F?

A

True

87
Q

Ramelteon and melatonin help you fall asleep–T/F?

A

True

88
Q

Ramelteon and melatonin will help if you have difficulty staying asleep–T/F?

A

False–do not help you stay asleep, just help you fall asleep

89
Q

(6) classes of antidepressant medications

A
  • TCAs
  • SSRIs
  • SNRIs
  • DNRIs
  • 5HT2A antagonists
  • Nuedexta
90
Q

TCAs MOA–___ and ___ reuptake inhibition, anti___, ___ antiarrhythmic

A

TCAs MOA–serotonin and norepinephrine reuptake inhibition, anticholinergic, 1A antiarrhythmic

91
Q

TCAs are not typically used to treat depression anymore, but may still be used to treat neuropathic pain/migraines–T/F?

A

True–have fallen out of favor to treat depression since prozac came out

92
Q

Side effects of TCAs–anticholinergic side effects–___pation, ___fusion, ___tation in elderly/children, urinary ___, ___ vision, ___ mouth; CV effects–QT ___, ___mias

A

Side effects of TCAs–anticholinergic side effects–constipation, confusion, agitation in elderly/children, urinary retention, blurred vision, dry mouth; CV–QT prolongation, arrhythmias

93
Q

TCA overdose–administer ___ d/t metabolic ___osis, supportive therapy

A

TCA overdose–administer NaHCO3 d/t metabolic acidosis, supportive therapy

94
Q

Serotonin excitatory receptors

A

2, 3, 4, 6, 7

Increase cAMP

95
Q

Serotonin inhibitory receptors

A

1, 5

Decrease cAMP

96
Q

Side effects of SSRIs–___natremia, ___cytopenia, ___ality, ___mias, ___ syndrome, ___/___/___, weight ___

A

Side effects of SSRIs–hyponatremia, thrombocytopenia, suicidality, arrhythmias, serotonin syndrome, nausea/vomiting/diarrhea, weight fluctuations

97
Q

All antidepressants, most anticonvulsant mood stabilizers, and most psychiatric medications have a black box warning for ___

A

suicidality

98
Q

Neuroleptic malignant syndrome is precipitated by ___ antagonists; onset is ___-___ days

A

Neuroleptic malignant syndrome is precipitated by dopamine antagonists; onset is 1-3 days

99
Q

Serotonin syndrome is precipitated by ___ agents; onset is < ___ hours

A

Serotonin syndrome is precipitated by serotonergic agents; onset is < 12 hours

100
Q

NMS and SS identical features–___tension, ___cardia, ___pnea, ___thermia, ___salivation, ___phoresis

A

NMS and SS identical features–hypertension, tachycardia, tachypnea, hyperthermia (> 40 C), hypersalivation, diaphoresis

101
Q

NMS demonstrates ‘___’ rigidity in all muscle groups

A

NMS demonstrates ‘lead-pipe’ rigidity in all muscle groups

102
Q

SS has ___ (increased/decreased) muscle tone, especially in ___ (upper/lower) extremities

A

SS has increased muscle tone, especially in lower extremities

103
Q

NMS distinct features–___reflexia, pupils ___ (normal/dilated), bowel sounds ___ (normal/increased/decreased)

A

NMS distinct features–hyporeflexia, pupils normal, normal bowel sounds

104
Q

SS distinct features–___reflexia, ___ unless masked by increased muscle tone, pupils ___ (normal/dilated), bowel sounds ___active

A

SS distinct features–hyperreflexia, clonus unless masked by increased muscle tone, pupils dilated, bowel sounds hyperractive

105
Q

What antibiotic can cause serotonin syndrome?

A

Linezolid (because it is an MAOI)

106
Q

Opioids can cause serotonin syndrome–T/F?

A

True

107
Q

Serotonin syndrome has a slower onset than neuroleptic malignant syndrome–T/F?

A

False–serotonin syndrome has a faster onset (<12 hours) than neuroleptic malignant syndrome (1-3 days)

108
Q

Neuroleptic malignant syndrome has ___reflexia, whereas serotonin syndrome has ___reflexia

A

Neuroleptic malignant syndrome has hyporeflexia, whereas serotonin syndrome has hyperreflexia

109
Q

Neuroleptic malignant syndrome pupils are ___, serotonin syndrome pupils are ___

A

Neuroleptic malignant syndrome pupils are normal, serotonin syndrome pupils are dilated

110
Q

How do SNRIs like duloxetine, venlafaxine, desvenlafaxine, and levomilnacipran work?–___ and ___ reuptake inhibition

A

serotonin and norepinephrine reuptake inhibition

111
Q

SRNIs side effects–___ syndrome, ___toxicity, ___tension, ___nia, abnormal ___, ___somnolence throughout the day d/t sleep interruptions throughout the night, ___/___/___, weight ___ (loss/gain), ___or, ___tation

A

SNRIs side effects–serotonin syndrome, hepatotoxicity, hypertension, insomnia, abnormal dreams, hypersomnolence throughout the day d/t sleep interruptions throughout the night, nausea/vomiting/diarrhea, weight loss, tremor, agitation

112
Q

SNRIs can also cause ___natremia and ___cytopenia just like SSRIs

A

SNRIs can also cause hyponatremia and thrombocytopenia just like SSRIs

113
Q

Bupropion (Wellbutrin) is a ___ and ___ reuptake inhibitor, has no ___ effects

A

Bupropion (Wellbutrin) is a dopamine and norepinephrine reuptake inhibitor, has no serotonergic effects

114
Q

Side effects of bupropion (wellbutrin)–___nia, ___tation, ___iety, ___cardia, ___tension, weight ___ (loss/gain)

A

Side effects of bupropion (Wellbutrin)–insomnia, agitation, anxiety, tachycardia, hypertension, weight loss

115
Q

Mirtazepine (Remeron) and Trazodone (Desryl) are ___ antagonists

A

Mirtazepine (Remeron) and Trazodone (Desryl) are 5HT2A antagonists

116
Q

Side effects of 5HT2A antagonists–highly ___, ___ (increased/decreased) appetite, ___toxicity

A

Side effects of 5HT2A antagonists–highly sedating, increased appetite, hepatotoxicity

117
Q

Think ___ with mirtazepine (remeron) and trazodone (desryl)

A

sedation

118
Q

Nuedexta is a combination of ___ and ___

A

Nuedexta is a combination of dextromethorphan and quinidine

119
Q

Nuedexta is the only medication approved by the FDA to treat ___

A

Nuedexta is the only medication approved by the FDA to treat pseudobulbar affect

120
Q

Pseudobulbar affect is inappropriate ___ or ___, seen in patients with ___

A

Pseudobulbar affect is inappropriate crying or laughing, seen in patients with TBI

121
Q

Nuedexta MOA–quinidine ___ (increases/decreases) dextromethorphan levels through enzyme inhibition; dextromethorphan may ___ (induce/inhibit) NMDA receptors, sigma 1 agonist

A

Nuedexta MOA–quinidine increases dextromethorphan levels through enzyme inhibition; dextromethorphan may inhibit NMDA receptors, sigma 1 agonist

122
Q

Side effects of nuedexta–QT ___, ___us, GI effects, ___ma, ___mia, ___cytopenia

A

Side effects of nuedexta–QT prolongation, lupus, GI effects, edema, anemia, thrombocytopenia

123
Q

Nuedexta drug interactions–quinidine is a strong 2D6 ___ (inducer/inhibitor)

A

quinidine is a strong 2D6 inhibitor

124
Q

Check ___ if someone is on a neuropsychiatric medication

A

platelets…many of these meds cause thrombocytopenia

125
Q

Lithium is a mood ___

A

Lithium is a mood stabilizer

126
Q

Side effects of lithium–diabetes ___, ___uria, ___dipsia

A

diabetes insipidus, polyuria, polydipsia

127
Q

It is important to check ___ levels and ___ levels in patients on lithium

A

It is important to check sodium levels and lithium levels in patients on lithium

128
Q

What is the difference between first and second generation antipsychotics?

A

First generation = mostly dopamine (D2) blockers; second generation = S2, D2 blockers

129
Q

Chlorpromazine (thorazine); prochlorperazine (compazine); and haloperidol (haldol) are all ___ (first/second) generation antipsychotics

A

first generation antipsychotics

130
Q

Aripiprazole (Abilify); clozapine (clozaril); olanzapine (zyprexa); quetiapine (Seroquel); risperidone (risperdal) are all ___ (first/second) generation antipsychotics

A

second generation antipsychotics

131
Q

Dopamine pathways in the CNS–meso___ = positive symptoms of schizophrenia and psychosis

A

Dopamine pathways in the CNS–mesolimbic = positive symptoms of schizophrenia and psychosis

132
Q

Dopamine pathways in the CNS–meso___ = negative symptoms, cognitive and affective symptoms

A

Dopamine pathways in the CNS–mesocortical = negative symptoms, cognitive and affective symptoms

133
Q

Dopamine pathways in the CNS–___ = Parkinsonian effects, i.e.: extrapyramidal symptoms, tardive dyskinesias

A

Dopamine pathways in the CNS–nigrostriatal = Parkinsonian effects, i.e.: extrapyramidal symptoms, tardive dyskinesias

134
Q

Dopamine pathways in the CNS–___ = hyperprolactinemia

A

Dopamine pathways in the CNS–tuberohypophyseal = hyperprolactinemia

135
Q

Side effects of antipsychotics–___ symptoms, ___ dyskinesias; metabolic side effects–weight ___ (gain/loss), ___glycemia; CNS side effects–___gy, ___ation, ___fusion; CV–QT ___, especially with ___

A

Side effects of antipsychotics–extrapyramidal symptoms, tardive dyskinesias; metabolic side effects–weight gain, hyperglycemia; CNS side effects–lethargy, sedation, confusion; CV–QT prolongation, especially with haldol

136
Q

Black box warning for clozaril 2008–___ related death, ___cytosis

A

Black box warning for clozaril 2008–dementia (CV/stroke) related death, agranulocytosis

137
Q

Antipsychotics should be used as a last resort when a patient is a risk to others and/or themselves–T/F?

A

True

138
Q

Carbidopa/Levodopa (Sinemet) and Carbidopa/Levodopa/Entacapone (Stalevo) are ___ analogs

A

dopamine analogs

139
Q

___ = dopamine precursor, looks and acts like dopamine

A

Levodopa = dopamine precursor, looks and acts like dopamine

140
Q

___ = false dopamine; confuses the enzymes MAO and COMT to prevent breakdown of levodopa

A

Carbidopa = false dopamine; confuses the enzymes MAO and COMT to prevent breakdown of levodopa

141
Q

___ = COMT inhibitor, has no effect on dopamine

A

Entacapone (Comtan) = COMT inhibitor, has no effect on dopamine

142
Q

Benztropine (Cogentin) and trihexyphenidyl (Artane) are anti___ used to treat ___ associated with antipsychotic administration

A

Benztropine (Cogentin) and trihexyphenidyl (Artane) are anticholinergics used to treat EPS associated with antipsychotic administration

143
Q

MAOB inhibitors rasaligine (azilect) and selegiline (eldepryl) ___ (increase/decrease) dopamine availability via enzyme inhibition

A

MAOB inhibitors rasaligine (azilect) and selegiline (eldepryl) increase dopamine availability via enzyme inhibition

144
Q

Side effects of MAOB inhibitors are similar to dopamine agents because they increase the amount of dopamine available–T/F?

A

True

145
Q

If you have a patient on MAOB inhibitors, you may see exaggerated effects of epi, NE, or ephedrine–T/F?

A

True

146
Q

Nuplazid (Pimavanserin) acts only at ___ receptors

A

Nuplazid (Pimavanserin) acts only at serotonergic receptors

147
Q

Two classes of Alzheimer’s medications–___ inhibitors, ___ receptor antagonist

A

acetylcholinesterase inhibitors, NMDA receptor antagonist

148
Q

Side effects of acetylcholinesterase inhibitors–‘___’ side effects–___cardia, ___ stools, ___ bladder

A

‘rest and digest’ side effects–bradycardia, loose stools, overactive bladder

149
Q

Acetylcholinesterase inhibitors drug interactions–anti___, ___choline, ___ neuromuscular blockers

A

anticholinergics, succinylcholine, non depolarizing neuromuscular blockers

150
Q

Acetylcholinesterase inhibitors ___ (potentiate/reduce) the effects of succinylcholine

A

Acetylcholinesterase inhibitors potentiate the effects of succinylcholine (because you’re flooding the receptors with acetylcholine)

151
Q

Acetylcholinesterase inhibitors ___ (potentiate/reduce) the effects of nondepolarizing neuromuscular blockers

A

Acetylcholinesterase inhibitors reduce the effects of nondepolarizing neuromuscular blockers

152
Q

Never discontinue a psych medication without reviewing the risk of withdrawal–T/F?

A

True

153
Q

What benzodiazepine has risk of wild withdrawal when stopped abruptly?

A

ONFI

154
Q

Psych medications may require a taper if absolutely required to be discontinued for several days–T/F?

A

True

155
Q

Withdrawal can be deadly–T/F?

A

True

156
Q

Delirium and dementia are two different things–T/F?

A

True

157
Q

Post op delirium may be fatal and is preventable in up to 40% of cases–T/F?

A

True

158
Q

Post op delirium may be hypo, hyperactive, or a mixed presentation–T/F?

A

True

159
Q

Almost 50% of cases of delirium are not reported–T/F?

A

True

160
Q

Post op delirium may occur in up to 75% of cases–T/F?

A

True

161
Q

JAMA Surgery 2018 STRIDE Trial–hip fracture repair, reducing sedation levels to reduce post op delirium–in the primary analysis, limiting the level of sedation provided no significant benefit in reducing incident delirium–T/F?

A

True

162
Q

JAMA Surgery 2018 STRIDE Trial–hip fracture repair, reducing sedation levels to reduce post op delirium–in a prespecified subgroup analysis, lighter sedation levels reduced postoperative delirium for persons with a Charlson Comorbidity Index of 0 (less sick patients)–T/F?

A

True

163
Q

Antipsychotics should not be used unless patient is at risk of harm to self or others–T/F?

A

True

164
Q

If using antipsychotics, use the ___ (lowest/highest) dose for the ___ (shortest/longest) duration

A

If using antipsychotics, use the lowest dose for the shortest duration

165
Q

Prophylactic low dose PO haloperidol did reduce delirium incidence in acutely hospitalized older patients–T/F?

A

FALSE–DID NOT reduce delirium incidence in acutely hospitalized older patients

166
Q

Prophylactic haldol reduces mortality in critically ill adults at high risk of delirium–T/F?

A

FALSE–prophylactic haldol DOES NOT reduce mortality in critically ill adults at high risk of delirium

167
Q

Do not initiate medications for dementia if not using prior to surgery–T/F?

A

True

168
Q

Benzos should never be used unless in the case of ETOH withdrawal–T/F?

A

True

169
Q

Benzos exacerbate delirium–T/F?

A

True

KLowe Pharm 2 (10 decks)

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