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Final Exam Pharm > Moods > Flashcards

Moods Flashcards

1
Q

amitriptyline (Elavil)

A

TCA

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2
Q

imipramine (Tofranil)

A

TCA

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3
Q

Tricyclic Antidepressent

A

block reuptake of serotonin and norepenephrine

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4
Q

TCA Use

A

Depression
* Anxiety disorders (OCD)
* Insomnia
* Panic disorders
* Enuresis
* Neuropathic pain (chronic pain)

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5
Q

TCA Adverse Effect

A

Weight gain
* Sedation (blocks histamine receptors in CNS)
* *Anticholinergic effects (block acetylcholine – blurred vision, urinary retention, dry mouth,
constipation, confusion)
* *Tachycardia & may prolongation of QRS & PR/QT intervals (need initial ECG & repeat in 3 weeks)
* Lower seizure threshold
* Orthostatic hypotension

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6
Q

OD is fatal of TCA at what dose?

A

8 times

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7
Q

TCAs mnemonic

A

Tip the scales
Cardiac
Anticholinergic
sleepy

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8
Q

Monamine Oxidase Inhibitors

A

Inhibit monoamine oxidase enzyme, which metabolizes amines,
norepinephrine and serotonin

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9
Q

isocarboxazid (Marplan)

A
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10
Q

phenelzine/ Nardil

A

MAO
Nardil

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11
Q

tranylcypromine / Parnat

A

MAO
Parnat

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12
Q

seleglitine patch

A

EMSAM

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13
Q

MOAI Interactions

A

Tyramine is a monoamine precursor of norepinephrine
* It is normally deactivated/metabolized by MAO in GI tract & liver
* Therefore, dietary tyramine doesn’t reach general circulation
* However, MAO inhibitors prevent this deactivation of tyramine
* Avoid tyramine containing foods b/c they may cause a
hypertensive crisis (S/S = HA, tachycardia, palpitations, N/V):
* aged cheeses (cheddar, swiss, bleu)
* beer
* red wines
* smoked meats
* fermented sausages (pepperoni, salami, bologna)
* soy sauce
* sour cream * Dietary tyramine restriction continued for 14 days after stopping MAOIs
and initiating SSRI or SNRI (risk of fatal serotonin syndrome)
* fluoxetine (Prozac) is 3 week “wash out” period due to long half-life
* Onset is 1-2 weeks
* Many drug-drug interactions
* Should not be used with patients that are impulsive, cognitively impaired,
or cannot follow the dietary restrictions

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14
Q

Selective Serotonin Reuptake Inhibitors

A
  • MOA: inhibits serotonin reuptake
  • Increases availability of serotonin & prolongs stimulatory potential of
    receptors and elevates mood and decreases anxiety
  • Uses:
  • Depression
  • OCD
  • Panic disorder
  • Social phobia
  • PTSD
  • Anxiety
  • PMDD (Premenstrual dysphoric disorder)
  • Bulimia
  • Pregnancy category B, C & D (paroxetine – Paxil)
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15
Q

fluoxetine

A

Prozac
Longer half-life (good if forgetful to take meds); no need to taper off when
drug DC’d; greatest P450 interactions; more stimulating (“jittery”)

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16
Q

paroxetine

A

Paxil*
Shortest half-life; more sedating; more nausea; greatest P450 interactions;
must taper (don’t go cold turkey…flu-like symptoms – N/V/D, chills)

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17
Q

sertraline

A

Zoloft* SSRI
Short half-life; geriatric population (less drug-drug interactions & better
safety profile); good for anhedonia

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18
Q

citalopram

A

Celexa SSRI
>40 mg/day may cause prolonged QT interval; also good in elderly

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19
Q

escitalopram

A

SSRI
Lexapro
The lest P450 Interactions: good for anxiety; also good in elderly

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20
Q

vortioxetine / brintelix

A

Brintellix
Newest in class
Few side effects

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21
Q

SSRI Adverse Effects

A

Headache &/or nausea (initially)
* Sexual dysfunction (may decrease dose or change to other drug in same class)
* Early wt loss (then wt gain)…depends on the person…other factors?
* WD S/S if abruptly DC (high doses taper over 4 wks)
* Serotonin syndrome (“shivering,” chills, N/D, sweating, hyperthermia, hypertension, tremors, agitation,
disorientation, ataxia)

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22
Q

SSRI Primary Advantages

A

Primary advantages
* Many may be used in children
* Lack of cardiac effect
* No anticholinergic effect
* Not effective for pain management
* Do NOT prescribe with TCAs (causes increased risk of cardiac conduction problems)
* Take 3-4 weeks to observe full therapeutic effectiveness
* Observe for suicidal thinking/behavior during first 2-3 weeks

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23
Q

Serotonin Norepenephrine Reuptake Inhibitors

A

MOA: increases serotonin and norepenephrine at the synapse
Use
major depression
bipolar mood
anxiety disorders
PTSD
neuropathic pain

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24
Q

venlafine

A

EffexorLower doses = use for anxiety
synapse * higher doses may cause HTN
* Immed release (IM) more AEs than
ER

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25
Q

venlafine

A

EffexorLower doses = use for anxiety
synapse * higher doses may cause HTN
* Immed release (IM) more AEs than
ER

26
Q

duloxetine (Cymbalta)

A

SNRI
Good for nerve pain
Cymbalta
inhibits 5-HT and NE reuptake at all doses.
a. It is extensively metabolized and should be avoided in patients with severe liver
or kidney disease.
b. The major side effects are GI effects and sexual dysfunction.

27
Q

bupropian

A

Wellbutrin*
Exerts effect through dopamine (precursor to norepinephrine)
* No sexual adverse effects (b/c little serotonin involvement)
* “jittery” (may be transient)
* Wellbutrin XL for adult ADD

28
Q

trazodone

A

Oleptro
Used for sleep

29
Q

mirtazapine

A

Atypical antidepressent
RemeronBlocks presynaptic alpha2-adrenergic receptors, which increases release of
norepinephrine and serotonin
* Sedating (may be used sleep aid); lower doses more sedating (targets dopamine receptors)
* Monitor LFTs

30
Q

Neurotransmitters

A

Norepinephrine (primarily excitatory)
* Serotonin (excitatory in raphe nuclei; inhibitory in cerebral
cortex)
* Dopamine (inhibitory)
* Acetylcholine (excitatory)
* Gamma aminobutyric acid (GABA) (inhibitory)
* Glutamate (excitatory)

31
Q

Anxiety Therapy First Lines for chronic

A

SSRI
SNRI

32
Q

buspirone (BuSpar)

A

Anti anxiety
Not a controlled substance
* Doesn’t cause CNS depression or sedation
* Little risk of dependence
* Few drug interactions
* Begin to see effects 1-2 weeks (bridge with benzo only if SEVERE anxiety; no more than 7-10 days)
* Optimal effects may take 4-6 weeks
* Pregnancy category B
* CYP 450 3A4

33
Q

Anxiety Acute First line

A

Benzodiazepines

34
Q

Benzodiazepines MOA

A

potentiate inhibitory effect of GABA (gamma-aminobutyric acid)
* Work with GABA to stabilize cell membranes so they are less responsive to excitatory
neurotransmitters such as norepinephrine

35
Q

Benzo - four drugs - name them and recommendations

A

alprazolam (Xanax) – short-acting; highly abused
* diazepam (Valium) – long ½ life; highly abused; avoid in elderly
* lorazepam (Ativan) – short-acting; doesn’t accumulate with repeated dosing; good in
elderly
* clonazepam (Klonopin) – longer acting (preferred for long-term tx of anxiety)

36
Q

Sedative Hypnotics for Sleep

A
37
Q

zolpidem (Ambien, Intermezzo)

A
  • Rapid onset; short half-life; short duration
  • Take within 30 minutes of bedtime
  • No morning grogginess
  • Schedule IV
  • For short term use (ideally less than 3 months)
  • Withdrawal symptoms if chronic use & abruptly withdrawn
  • AE:
  • HA
  • Nausea
  • Somnolence
  • Transient amnesia
  • Reports of strange behavior (driving; eating; no memory of these events)* zolpidem (Ambien, Intermezzo)
  • Avoid ETOH and other CNS depressants
  • CYP 3A4
  • Pregnancy category C
  • Lower dose with elderly
  • Sublingual tablet available for middle-of-the night awakening (Intermezzo only)
38
Q

Levodopa / carbidopa

A

Sinemet*
Dopamine will not cross the BBB
* Levodopa is the precursor to dopamine (it will cross the BBB)
* Decarboxylase is the enzyme that converts levodopa to dopamine
* Decarboxylase is more abundant in the peripheral tissue than the brain
* Carbidopa is a dopamine decarboxylase inhibitor that reduces conversion in the
periphery so more will reach the brain* Adverse Effects:
* Orthostatic hypotension
* CNS stimulation
* Tachycardia
* On-off phenomenon (loses efficacy in 5 yrs)
* Levodopa effectiveness decreased with high protein diet & Vit B6

39
Q

Dopamine Receptor Agonist

A
  • MOA: stimulate dopamine receptors in the basal ganglia
  • First line therapy in younger patients; may delay need for dopamine replacement
  • May delay symptoms for 5 years
  • Ex: bromocriptine (Parlodel)
    ropinirole (Requip) (drowsiness & sleep attacks)
    pramipexole (Mirapex) (drowsiness & sleep attacks)
  • Adverse Effects:
  • N/V
  • Postural hypotension
  • Cardiac dysrhythmias
40
Q

repoinirole

A

Requip

41
Q

Catechol-O-Methyl Transferase (COMT)
Inhibitors

A
  • MOA: COMT is the enzyme that breaks down dopamine
  • Ex: entacapone (Comtan)
    tolcapone (Tasmar)
  • Hepatotoxic: LFTs q 2 wks for first year
  • DC if significant improvement not seen in 3 wks
  • Prescribed by neurologist
42
Q

selegilene

A

Antidepressent treats parkinsons
Eldyprel

43
Q

rasagiline

A

Azilect, selective irreversible MAO inhbitor

44
Q

amantadine

A

Symmetrel* MOA: antiviral agent; promotes release of dopamine from dopaminergic
terminals
* AE: CNS stimulation
* Relieves symptoms rapidly (2-3 days), but…
* Loses efficacy rapidly (3-6 months)
* May give for 2-3 wks with initiation of longer-acting agents or when
symptoms worsen (intermittent dosing)

45
Q

benztropine

A

Cogentin / anti tremor

46
Q

trihexyphenidyl

A

Artane

47
Q

Acetylcholinesterase Inhibitors

A

Alzheimers Treatment

  • Ex:
    1. donepezil (Aricept)
  • HS
  • Not hepatotoxic
  • Metabolized by cytochrome P450
    1. rivastigmine (Exelon)
  • BID or patch
  • NOT metabolized by cytochrome P450
  • Adverse Effects:
  • Bradycardia, nausea, vomiting, diarrhea
48
Q

NMDA Receptor Antagonist

A
  • MOA: glutamate antagonist that blocks
    excitation; this excitation is believed to lead
    to greater destruction of neurons
  • Ex. memantine HCl (Namenda) – indicated
    for mod/severe AD
  • Low incidence of side effects
  • Minimal drug interactions
  • Sexual disinhibition
49
Q

Lithium

A

Exact MOA unclear; however thought that lithium replaces sodium during depolarization in neuronal pathways,
effectively stopping the transmission of electrical impulses. It is also known to affect the synthesis, release & reuptake of
several neurotransmitters in the brain; it may increase the activity of GABA, an inhibitory neurotransmitter.

50
Q

Lithium Elimination *** Important

A

80% of lithium dose is reabsorbed in the proximal renal tubule.
* Amount of reabsorption depends on the concentration of Na in the proximal renal tubule
* Deficiency of Na causes increased lithium to be reabsorbed (increased toxicity)
* Dehydration may precipitate lithium toxicity
* Excess Na causes more lithium to be excreted
* Inverse relationship (lithium/sodium)
* Need good renal function (assess creatinine/BUN)

51
Q

Lithium AE

A
  • Long-term administration may cause hypothyroidism (monitor TSH)
  • Nephrotoxic
  • GI – N/V/D
  • Fine hand tremors
  • Drowsiness
  • Contraindicated in children < 12 yo
  • Pregnancy category C
  • Cautious use with diuretics
52
Q
  • Long ½ life = 1-2 weeks to reach maximum efficacy
  • Not used for acute mania
  • Narrow therapeutic index: 0.6-1.5 mEq/L
  • S/S of toxicity =
  • N/V/D
  • Coarse hand tremors
  • Polydipsia (increased thirst)
  • Polyuria
  • Confusion
  • Muscle weakness
  • Ataxia
  • Arrhythmias (baseline ECG at time of initiation of therapy)
  • Frequent monitoring initially; then maintenance q 3 months
  • Draw lab in am 12 hrs after last pm dose & before am dose
A

Lithium

53
Q

Lithium Labs

A

12 hours after the last dose. Its is a trough dose

54
Q

Typical Antipsychotics vs atypical

A

T

55
Q

Phenothiazines

A

chlorprmioazine
fluphenazine

56
Q

Atypical Antipsychotics

A

Examples:
* clozapine (Clozaril)
* olanzapine (Zyprexa)
* aripiprazole (Abilify) (can be activating)
* quetiapine (Seroquel)
* risperidone (Risperdal)
* ziprasidone (Geodon) (needs food in
stomach to increase efficacy)

57
Q

Clozaril

A

Tx for schizophrenia
Primary concern is decreased WBC agranulosytosis

58
Q

phenytoin

A

Dilantin

Anticonvulsant
* Most commonly used
* Least sedation
* AEs:
* Gingival hyperplasia
* N/V; anorexia
* Can interfere with vitamin K metabolism and disrupts clotting factors
* Hypotension (IV)
* Liver damage (uncommon)
* Therapeutic level = 10-20 mcg/ml
* S/S toxicity:
* Nystagmus, sedation, ataxia, diplopia, cognitive impairment
* Nonlinear relationship b/w Dilantin dosage & plasma levels
* zero order kinetics; the more on board, less quickly eliminated

59
Q

carbamazepine (Tegretol)

A

Tegretol
autoinduction of its own metabolism; may require increased dosages; Asian descent (risk of Toxic
Epidermal Necrolysis TEN; gene HLA-B*1502)
* May cause agranulocytosis (monitor CBC)
* May also be used as mood stabilizer

60
Q

Anticonvulsants

A
  • zonisamide (Zonegran) – risk of metabolic acidosis
  • phenobarbital – barbiturate (rapid development of tolerance, fatalities by OD, severe WD symptoms)
  • primidone – also used with essential tremors
  • gabapentin (Neurontin) – may also be used for pain management & mood stabilizer
    14
  • pregabalin (Lyrica) – also used in neuropathic pain & fibromyalgia
  • lamotrigine (Lamictal) - used as mood stabilizer and migraine headache
  • topiramate (Topamax) used as mood stabilizer and migraine headache* Also used for migraine headache prophylaxis, neuropathic pain syndromes & mood stabilizer
  • May cause weight LOSS
  • Risk of metabolic acidosis
  • levetiracetam (Keppra) - nuerologist
  • clonazepam (Klonopin) - benzodiazepine

Final Exam Pharm (12 decks)

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