- prescription weight-loss drugs are used for pt. BMI >30 or BMI>27 with DM, HTN, dyslipidemia - serious side effects-cardiac, pulmonary ADRs-possibly fatal - avoid in patients with cardiac hx, drug/ETOH abuse - difficult to monitor pts with diabetes-increased glucose uptake from skeletal muscles

- overstimulation of CNS-agitation, insomnia, dizziness, HTN, etc - may cause withdrawal symptoms if suddenly stop - increased glucose uptake from skeletal muscles

- persistent hyperactivity and impulsivity - tx: behavior therapy and medication therapy (stimulant and non-stimulant options; used to help with alertness, focus, attention - most common drug: MPH (methylphenidate) - all stimulants are controlled substance

- amphitamines for ADHD - ? vyvanse less abuse potential - ADRs: decreased appetite, insomnia, abd pn - risk of sudden cardiac death

- loss of neurons in substantia nigra - presence of Lewy bodies - loss of dopamine 1 and 2-leading to increased cholinergic activity - symptoms: bradykinesia, resting tremor, postural instability - progression: depression and psychosis

chapter 15 CNS Flashcards by Maariannette Calon-Munoz

use of anorexiants

prescription weight-loss drugs are used for pt. BMI >30 or BMI>27 with DM, HTN, dyslipidemia
serious side effects-cardiac, pulmonary ADRs-possibly fatal
avoid in patients with cardiac hx, drug/ETOH abuse
difficult to monitor pts with diabetes-increased glucose uptake from skeletal muscles

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Anorexiants

-for short term use only
-related to amphetamines-suppresses appetite
-Diethylpropion (Tenuate, Tenuate Dospan Cat-IV)
-Orlistat (Xenical, Alli OTC)-only non-stimulant-lipase inhibitor; preg. cat. X
-phentermine (Adepex-P)
-Sibutramine (meridia)
-

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pharmacodynamics of anorexiants

release of norepi/dopamine from storage sites in lateral hypothalmic feeding center
decreases appetite

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pharmacokinetics of anorexiants

lipid soluble with wide distribution
crosses BBB
metabolized by liver and excreted by kidneys
duration of action 4-6 yrs

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pharmacotherapeutics of anorexiants

high risk of dependence (avoid pts with ETOH/drug dependence)
avoid pt who abuse cocaine/methamphetamines-d/t additional adrenergic stimulation

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ADRs for anorexiants

overstimulation of CNS-agitation, insomnia, dizziness, HTN, etc
may cause withdrawal symptoms if suddenly stop
increased glucose uptake from skeletal muscles

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drug interactions for anorexiants

off label in combo with SSRI: “Phen-Pro” (prozac and phentermine)
with serotonergic meds-blks seratonin production and causes seratonin syndrome (severe muscle rigidity can lead to death)
- cyproheptadine anecdote
MAO inhibitors could lead to HTN crisis
lithium toxicity
cautious with: adrenergic blks, insulin sulfonylureas, phenothiazines
Orlistat decreases level of levothyroxine and increases warfarin

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ADHD

persistent hyperactivity and impulsivity
tx: behavior therapy and medication therapy (stimulant and non-stimulant options; used to help with alertness, focus, attention
most common drug: MPH (methylphenidate)
all stimulants are controlled substance

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MPH

MAO: blks dopamine reuptake
M: de-esterification to inactive metabolite
AE: insomnia, decreased appetite, weight loss
Rare AE: tics, visual hallucinations
Caution: hx psychosis, mania, drug addiction
DI: carbamazepine, clonidine, warfarin, phenobarb, phenytoin, TCAs
-short and long acting available
* concerta with pt with esophageal motility issues-may increase risk of obstruction

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Adderall and Vyvanse

amphitamines for ADHD
? vyvanse less abuse potential
ADRs: decreased appetite, insomnia, abd pn
risk of sudden cardiac death

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non-stimulant meds for ADHD

atomoxetine (Strattera)
MAO: inhibitor of norepi reuptake
metabolized in CYP2D6
ADRs: dyspepsia, decreased appetite, wt. loss, no tics
can cause severe liver injuries, suicidal ideation

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adjunct meds for ADHD

buproprion
clonidine: cautious for sedation
TCA: monitor EKG first
guafacine: less sedation longer action
modanifil-not recommended-hallucinations, Stevens Johnson syndrome

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parkinsons disease

loss of neurons in substantia nigra
presence of Lewy bodies
loss of dopamine 1 and 2-leading to increased cholinergic activity
symptoms: bradykinesia, resting tremor, postural instability
progression: depression and psychosis

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dopaminergics/dopamine agonist

choice of tx for parkinson’s
attempt to restore functional balance of dopamine and acetylcholine-both responsible for smooth movements and balance
- either by increasing synthesis, increasing receptors, release from storage, or inactivating MAO leading to more amounts available
  i. e.: amantadine, bromocriptine, levodopa (carbidopa-levodopa), pramipexole, ropinirole
many drug intereactions
can not stop abruptly
cautious with patients with impulse-control disorders (pathologic gambling, binge eating, hypersexuality, excessive shopping etc)
“sleep attacks”-suddenly fall asleep
confusion and toxic psychosis

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cabidopa/levodopa

-combination enhances transmission of levodopa across BBB
-levodopa precursor to dopamine
-carbidopa: increases CNS penetration, prevents peripheral dopamine metabolism
ADRs: n/v, arrhythmias, postural hypotension, nightmares
-always given in combination
-absorption: levodopa protein bound, food delays gastric emptying
-controversial when to start tx, enhances neuron degradation, builds dose tolerance

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catechol-O-methyltranserase inhibitor (COMT)

blocks degradation of levodopa
entacopone-may have sleep attacks
tolcapone-hepatotoxicity-monitor LFTs
decreases levodopa requirements
adrs: dyskinesias, n/d, discolored urine

ergot derivatives for parkinsons

bromocriptine: limited efficacy, risk of pulmonary fibrosis
pergolide: removed from market d/t cardiac valve regurg

MAO-B inhibitors for parkinsons

selegiline, rasagiline
inhibits catabolism and reuptake of dopamine
can be mono or adjunctive therapy
caution with SSRIs, meperidine, tramadol
lower dose than for depression
adrs: nausea, orthostatic hypotension, may enhance adrs of levodopa

anticholinergics for parkinsons

trihexyphenidyl, benztropine, ethopropazine
limited role d/t ADRs
used for tremors and drooling

drugs associated with seizure activity

antidepressants: SSRIs, TCA, buproprion
quinolones
high dose pcn
cabepenems
theophylline
tramadol
cyclosporins
ETOH, drug, benzo withdrawal

anticonvulsants

seizures are result of abnormal discharge off neurons-anything that disrupts stability of neurons may cause
can be used for tx of mood disorders
precipitating factors: stress, high intake of caffeine, sleep deprivation, infection, sensory stimuli, hormonal change, metabolic disorders
classes: hydantoins, iminostilbenes, succinimides
main actions: stimulating influx of chloride ions-assoc. with GABA neurotransmitter
- delaying influx of Na+
- delaying influx of Ca+
may cause suicide ideation and depression
consider levels-toxicity and compliance
there are many drug interactions

hydantoins

phenytoin-most commonly used, ethotoin, fosphenytoin
inhibit and stabilize electrical discharge in motor cortex of brain
first line tx for tonic-clonic and partial complex seizures

phenytoin (Dilantin)

stabilize Na+ channels
dose: loading: 15-20mg/kg, maintenance: 4-7mg/kg/day
metabolized: non-linear kinetics enzyme inducer
many drug interactions
caution: hypothyroidism, carbohydrate intolerance, peripheral neuropathy
toxicity: n/v, tachycardia,
adrs: nystagmus, ataxia, drowsiness, cognitive impairment (dose related)
- gingival hyperplasia, hirsutism, acne, rash, coarse facial features, osteomalacia, vit D and folic acid deficiency

levetiracetam (Keppra)

for epilepsy and partial seizures/mono or adjunct therapy
prevents epileptiform burst firing
propagation of seizure activity
dose 500mg BID (max of 3g/day)-adjust for renal impairment
not largely metabolized-non-hepatic hydrolysis
adrs: sedation, fatigue, agitation, lethargy
levels: 12-46 mcg/ml
pregnancy C

iminostilbenes

- used to treat epilepsy, bipolar affective disorder, aggressive behavior, neuralgias - carbamazepine (tegretol)

carbemazepine (Tegretol)

- structurally related to TCAs - inhibits Na+ channels-to prevent seizure activity - metabolized by autoinduction-to induce its own metabolism; CYP3A4, 1A2 inducer - half life 25-65 hrs decreases to 12-16 hours adrs: black box warning blood dyscrasias, rash, ostomalacia, hepatotoxicity, lupus, diplopia, nystagmus levels: 4-12 mcg/ml

oxcarbazepine

- mono or adjunct therapy for partial seizures - Na+ channel blker - metabolized in liver: 3A4 inducers, 2C19 inhibitors - half life 9 hrs - adrs: hyponatremiz, rash, less blood dyscrasias than cabazepine levels: 3-35 mcg/ml - pregnancy cat C

phenobarbital

- for epilepsy low doses to not have dependence or tolerance - can be used for tonic-clonic seizures - increases aminobutyric acid and chloride influx-causing decrease activity and induce sleep - CYP enzyme inducer; half life 80-100 hrs - level 15-40 mcg/ml - drug interactions: other benzos - adrs: faitugue, depression, cognitive impairment, hyperactivity (pediatrics) - preg. class D - enhanced excretion: urinary alkaline, diuretics

valproic acid

- used for primary generalized, absent seizures in adults, myclonic, atonic - potentiates GABA, membrane stabilization, K+ channels - 10-15 mg/kg/day TID (ER 15% higher) - metabolized in liver-1 is hepatotoxic, 10 metabolites, CYP 2C9, 2C19 - many drug interactions including antacids - enzyme inducer adrs: GI, derm, wt gain, ataxia, hepatotoxicity, thombocytopenia - preg. class D levels: 40-100 mcg/ml

gabapentin

- inhibits Ca+ channels, enhances GABA - 2nd line for partial seizures - dose 300-400 mg; titrate, renal dosing - can be used for neuropathic pn adrs: somnolence, sedation - preg. class C

pregabalin

- GABA analog; potency>gabapentin - used for fibromylagia, postherpetic neuralgia - dose: 50 mg TID (max 600 mg/day), renal dose adrs: wt. gain, dizziness, somnolent - CNS depressant - avoid in CHF patients - controlled substance

succinimides

- treatment of absence seizures in children/adults - decreases nerve impulses/transmission in motor cortex leading to higher seizure threshold - ethosuximide, mehsuximide

ethosuximide

- inhibits Ca+ channels - dose: 250 mg BID (max 1.5 g/day) - used for absence seizures - level: 40-100 mcg/ml - metabolized in liver, hepatic hydroxylization, 3A4 involvement - excretion through renal and feces - half life 60 hrs - drug interactions with 3A4 meds adrs: GI upset, wt loss, CNS depression, derm, abnormal LFTs, blood dyscrasias - preg. class c

adjunctive therapies for seizures

- topiramate and zonisamide - topiramate-blocks Na+channels, potentiates GABA, blks glutamate, carbonic anhydrase inhibitor; can be used for migraines - zonisamide: suppresses focus of seizures via Na+ and Ca+ channels; avoid sulfa allergy, adrs: nephrolithiasis

migraines

3 categories: migraine with aura (classic), without aura (common), complicated migraine-treated by drugs the same - patho: vascular theory: aura created by vasoconstriction of intracranial vessels and vasodilation of affected vessels-disproven - sertonin: changes cause release of vasoactive neurotransmitter, causes inflammatory response, excitory serotonin receptors activated - acute abortive therapy v. prophylactic therapy