CNS 1 Flashcards
MOA of phenytoin (dilantin)
stabilize nerve cells to keep them from getting overexcited, works in the motor cortex of the brain where it stops the spread of seizure activity
phenytoin uses
complete partial seizures, tonic-clonic seizures
difference between phenytoin and dilantin
dilantin can be taken once a day..phenytoin cannot
THEY ARE NOT INTERCHANGEABLE
drug-drug interactions of phenytoin
effects are reduced by: phenobarbital carbamazepine rifampin antacids gingko ETOH azole drugs
may reduce effectiveness of oral contraception pills corticosteroids anticoagulants levodopa TH
phenytoin considerations
enteral feedings may interfere with absorption of oral phenytoin –>stop feedings 2 hrs before or after
not compatible with D5W –> precipitates
avoid giving IV push into back of hand –> discoloration “purple glove syndrome”
discard any unused drugs after 4 hrs
what is therapeutic range for phenytoin? at what ranges do you start seeing specific symptoms?
therapeutic: 10-20 mcg/ml
20-30 –> nystagmus
30-40 –> ataxia
>40 –> decreased LOC
phenytoin adverse effects
nystagmus - dyplopia sedation ataxia hirsutism gingival hyperplasia
skin reactions - Stevens Johnson, toxic epidermal necrolysis - higher in Asian population
hypotension
dysrhythmias
Carbamazapine (tegretol) MOA
same as phenytoin
carbamazepine uses
partial and generalized tonic-clonic seizure
mixed seizure types
complex partial seizures (DOC)
relieves pain R/T trigeminal neuralgia
bipolar disorder
therapeutic blood level of carbamazepine
8-12 mcg/ml
carbamazepine drug interactions
reduces effects of : oral anticoagulants haloperidol bupropion TCAs oral contraception other anticoagulants
increases levels of: diltiazem, INH, selective SSRIs, azole drugs valproic acid verapamil
Lithium and carbamazepine taken together leads to increase risk of toxic neurological effects
warnings with carbamazepine
contraindicated if glaucoma, cardiac, renal, or hepatic disease
can cause SIADH - monitor Na+
avoid ETOH
avoid grapefruit juice
can depress bone marrow - watch for s/s of infection or bleeding
photosensitivity
watch for low sodium - HA, confusion, slurred speech, weakness, feeling unsteady
valproic acid drugs
Depakote, Depakane
MOA of valproic acid
unknown, thought to increase GABA, an inhibitory neurotransmitter, as well as having direct membrane stabilizing effect
uses of valproic acid
absence, myoclonic, tonic-clonic, partial, neonatal seizures
prevent migraine
bipolar disorder
therapeutic range of valproic acid
50-100 mcg/ml
considerations with valproic acid
monitor CBC, AST
monitor for N/V, lethargy, impaired PT/PTT, hair loss, leukopenia, hepatotoxicity
increases serum phenobarbital level and alter serum phenytoin levels
monitor for drowsiness, blood dyscrasia, ataxia, nystagmus, GI distress
valproic acid - pregnancy category
X
patient teaching with anticonvulsants
take drug exactly as prescribed, don’t stop without HCP approval
take with food–> reduce GI upset and loss of appetite
don’t change brand/dosage forms
avoid hazardous activities that require mental alertness
space activities throughout day to allow time for rest
report persisten/bothersome effects
may cause pink, red, brown urine
ETOH may diminish drug’s benefit
perform oral hygiene
what is levodopa used for?
Parkinson’s disease
we want to correct the neurotransmitter imbalance by increasing dopamine and decreasing Ach
levodopa MOA
relieves motor symptoms by conversion to dopamine by decarboxylase in surviving nerve terminals in the brain
levodopa disadvantages
full therapeutic effect can take months
highly effective by benefits diminish over time
orally administered, rapid absorption in the small intestine
food delays absorption - take on empty stomach
proteins compete with levodopa for intestinal absorption and for transport across BBB so don’t take with high protein meal
what is the on-off syndrome with levodopa?
works for 2-5 years –> loss of response over time
gradual wearing off at the end of dose
abrupt loss of effect can happen anytime
need to let doctor know if this is happening so adjustments can be made
what is a drug holiday and what drug does it help with?
helps with the effectiveness of levodopa
with long term use of levodopa, adverse effects tend to increase and therapeutic effects tend to diminish. For some patients, taking time off (~10 days) may produce a beneficial effect with lower doses
drug holidays must take place in the hospital because drug withdrawal immobilizes the patient. The patient is at risk for all of the physical and psychological effects of this stress
why do we use carbidopa?
so levodopa is broken down in the gut by decarboxylase –> need large doses to get adequate levels in the CNS –> high peripheral levels of dopamine –> increased adverse effects
confusion, dyskinesia, GI distress, hypotension, dysrhythmias
so levodopa is given with carbidopa, a peripheral decarboxylase inhibitor
carbidopa inhibits decarboxylase –> less levodopa is broken down –> more levodopa can make it to the brain –> we can use lower doses of levodopa
allows dose of levodopa to be reduced by 75%
what drugs are levodopa/carbidopa
sinemet, parcopa
adverse effects of levodopa/carbidopa
N/V
CV: postural hypotension, arrhythmias
psychosis
dyskinesias
drug interactions of levodopa/carbidopa
non-selective MAO inhibitors
1st gen antipsychotics
anticholinergics
pyridoxine (vitamin B6) - more with levodopa alone
contraindications of levodopa
angle-closure glaucoma - increased intra-ocular pressure
undiagnosed skin conditions - can activate malignant melanoma
levodopa food interactions
high protein meals –> slows absorption –> reduce therapeutic effect
vitamin B6 - fish, beef, liver
levodopa nursing implications
may be taken with food to reduce N/V (avoid high protein meals - take med 30 min before/1 hr after)
inform patient that benefits maybe delayed for weeks to months
evaluate for improvements in ADLs and reductions in bradykinesia, postural instability, tremors, rigidity
to reduce off times, combine with dopamine agonist, COMT inhibitor, or MAO-B inhibitor
what drugs are COMT inhibitors
entacapone
tolcapone
COMT inhibitor MOA
inhibit metabolism of levodopa in the periphery
blocks enzyme COMT which breaks down levodopa –> reduces wearing off of levodopa –> prolongs time that levodopa is available to the brain
COMT inhibitor adverse effects
liver failure GI dyskinesia diarrhea brown-orange urine discoloration (entacapone) hyper/hypokinesia syncope hypotension abd pain constipation dry mouth back pain diaphoresis
anticholinergic drugs MOA
goal is to inhibit cholinergic effects
block PNS activity –> decrease acetylcholine
anticholinergic uses
tremors
rigidity (cog wheeling)
control sialorrhea
anticholinergic drugs
benzotropine (Cogentin)
biperiden (Akineton)
procyclidine
trijexyphenidyl
lithium MOA
unknown, may regulate catecholamine release by the CNS by
1) increasing norepinephrine and serotonin uptake
2) reducing the release of norepinephrine from the synaptic vesicles (where neurotransmitters are stored) in the presynaptic neuron
3) inhibiting norepinephrine’s action in the postsynaptic neuron
lithium therapeutic uses
bipolar disorder: DOC for manic episodes and long term prophylaxis and preventing suicide
other uses: alcoholism, migraines, bulimia, anorexia, schizophrenia, glucocorticoid-induced psychosis
lithium facts
excreted by the kidneys with same mechanism as sodium - lithium excretion is low when sodium level is low
effects begin in 5-7 days but full effect after 2-3 weeks
narrow therapeutic range - must monitor drug levels
for management of acute mania, a lithium serum level of 1-1.5 is usually required
desirable long term maintenance levels range between 0.6-1.2
lithium drug interactions
loss of Na+ –> kidney retain lithium to compensate –> lithium toxicity
loss of Na+ can occur with:
1) thiazide or loop diuretic
2) severe salt restricted diet
3) dehydration: N/V, hot weather
risk of toxicity increases when taking NSAIDS
administration of lithium with haloperidol, phenothiazines, carbamazepine may produce increased risk of neurotoxicity
lithium may increase hypothyroid effects of potassium iodine
sodium bicarbonate may increase lithium excretion –> reduce effects
lithium adverse effects
fatigue, HA, confusion, memory problems
poor concentration
N/V
weight gain
hair loss
acne
renal toxicity - check renal function before starting every year
fine tremors
polyuria/thirst (DI) - drink 8-12 glasses of fluid daily
goiter and hypothyroidism - Li inhibits TH secretion
lithium toxic effects
confusion, lethargy
slurred speech
hyperreflexia
seizures
pregnancy category D
lithium patient teaching
take with 2-3 liters of water/day and after meals to minimize GI upset
expect transient nausea, thirst, discomfort first few days of therapy
avoid activities that require alertness and psychomotor coordination
don’t switch brands or take OTC without HCP approval
wear/carry medical identification
lithium has narrow therapeutic window:
1) blood level that is even slightly high can be dangerous
2) watch for s/s of toxicity including diarrhea, vomiting, tremor, drowsiness, muscle weakness, ataxia
3) withhold one dose and call HCP if toxic symptoms appear - don’t stop drug abruptly
what are the two groups of drugs for muscle spasms and spasticity
localized muscle spasms
Diazepam (Valium)
Tizanidine (Zanaflex)
spasticity
Baclofen (Lioresal)
Diazepam (Valium)
Dontrolene (Dantrium)
therapeutic use of centrally acting muscle relaxants
relieve local muscle spasm decrease local muscle pain increase ROM neither drug is better than another - drug selection is based on prescriber preference and patient response NOT FOR SPASTICITY
centrally acting muscle relaxant drugs
Carisoprodol (Soma) Chlorzoxazone (Lorzone) Cyclobenzaprine (Flexeril) Metaxalone (Skelatxin) Methocarbamol (Robaxin) Orphendrine (Norflex) Tizanidine (Zanaflex)
adverse effects of muscle relaxants
generalized CNS depression - safety issues
drowsiness, dizziness
hypotension (Tizanidine)
severe reactions: allergic reactions, arrhythmias, bradycardia
hepatotoxicity - Tizanidine, Metaxalone
hepatitis and necrosis - chlorzoxazone
long term drug use can lead to physical dependence
less common: abd distress, N/V, constipation/diarrhea, heartburn, ataxia
NOT MEANT FOR CHRONIC USE - TAKEN FOR SHORT TIME ~2-3 WEEKS
Baclofen MOA
chemically similar to GABA, probably acts on spinal cord
reduces nerve impulses from the spinal cord to skeletal muscle, decreases number and severity of muscle spasms and associated pain
Baclofen uses
spasticity associated with spinal cord injury
multiple sclerosis
trauma
Baclofen withdrawal
avoid abrupt discontinuation –> baclofen withdrawal
classic symptoms are sudden increase or return of spasticity or tone, profuse sweating and itching without rash, fever, high HR or RR, high/low BP, confusion
severe symptoms include hallucinations, delirium, seizures, rhabdomyolysis, organ failure, death
use diazepam to offset withdrawal symptoms
Diazepam MOA
acts in CNS - mimics GABA
Diazepam adverse effects
sedation
Dantrolene MOA
act directly on skeletal muscle - suppresses release of Ca++ from sarcoplasmic reticulum
Dantrolene uses
spasticity associated with MS, cerebral palsy, spinal cord injury
treatment for malignant hyperthermia
Dantrolene adverse effects
hepatotoxicity muscle weakness drowsiness diarrhea acne like rash
S/S of malignant hyperthermia
dramatic rise in body temp –> as high as 113 F
rigid/painful muscles, esp in jaw
flushed skin
sweating
abnormally rapid/irregular heart beat
rapid/uncomfortable breathing
brown urine
very low BP
confusion
muscle weakness or swelling
