CNS 1 Flashcards

1
Q

MOA of phenytoin (dilantin)

A

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

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2
Q

phenytoin uses

A

complete partial seizures, tonic-clonic seizures

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3
Q

difference between phenytoin and dilantin

A

dilantin can be taken once a day..phenytoin cannot

THEY ARE NOT INTERCHANGEABLE

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4
Q

drug-drug interactions of phenytoin

A
effects are reduced by:
phenobarbital
carbamazepine
rifampin
antacids
gingko
ETOH
azole drugs
may reduce effectiveness of oral contraception pills
corticosteroids
anticoagulants
levodopa
TH
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5
Q

phenytoin considerations

A

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

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6
Q

what is therapeutic range for phenytoin? at what ranges do you start seeing specific symptoms?

A

therapeutic: 10-20 mcg/ml
20-30 –> nystagmus
30-40 –> ataxia
>40 –> decreased LOC

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7
Q

phenytoin adverse effects

A
nystagmus - dyplopia
sedation
ataxia
hirsutism
gingival hyperplasia

skin reactions - Stevens Johnson, toxic epidermal necrolysis - higher in Asian population

hypotension
dysrhythmias

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8
Q

Carbamazapine (tegretol) MOA

A

same as phenytoin

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9
Q

carbamazepine uses

A

partial and generalized tonic-clonic seizure

mixed seizure types

complex partial seizures (DOC)

relieves pain R/T trigeminal neuralgia

bipolar disorder

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10
Q

therapeutic blood level of carbamazepine

A

8-12 mcg/ml

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11
Q

carbamazepine drug interactions

A
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

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12
Q

warnings with carbamazepine

A

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

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13
Q

valproic acid drugs

A

Depakote, Depakane

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14
Q

MOA of valproic acid

A

unknown, thought to increase GABA, an inhibitory neurotransmitter, as well as having direct membrane stabilizing effect

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15
Q

uses of valproic acid

A

absence, myoclonic, tonic-clonic, partial, neonatal seizures
prevent migraine
bipolar disorder

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16
Q

therapeutic range of valproic acid

A

50-100 mcg/ml

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17
Q

considerations with valproic acid

A

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

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18
Q

valproic acid - pregnancy category

A

X

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19
Q

patient teaching with anticonvulsants

A

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

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20
Q

what is levodopa used for?

A

Parkinson’s disease

we want to correct the neurotransmitter imbalance by increasing dopamine and decreasing Ach

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21
Q

levodopa MOA

A

relieves motor symptoms by conversion to dopamine by decarboxylase in surviving nerve terminals in the brain

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22
Q

levodopa disadvantages

A

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

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23
Q

what is the on-off syndrome with levodopa?

A

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

24
Q

what is a drug holiday and what drug does it help with?

A

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

25
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%
26
what drugs are levodopa/carbidopa
sinemet, parcopa
27
adverse effects of levodopa/carbidopa
N/V CV: postural hypotension, arrhythmias psychosis dyskinesias
28
drug interactions of levodopa/carbidopa
non-selective MAO inhibitors 1st gen antipsychotics anticholinergics pyridoxine (vitamin B6) - more with levodopa alone
29
contraindications of levodopa
angle-closure glaucoma - increased intra-ocular pressure undiagnosed skin conditions - can activate malignant melanoma
30
levodopa food interactions
high protein meals --> slows absorption --> reduce therapeutic effect vitamin B6 - fish, beef, liver
31
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
32
what drugs are COMT inhibitors
entacapone | tolcapone
33
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
34
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 ```
35
anticholinergic drugs MOA
goal is to inhibit cholinergic effects block PNS activity --> decrease acetylcholine
36
anticholinergic uses
tremors rigidity (cog wheeling) control sialorrhea
37
anticholinergic drugs
benzotropine (Cogentin) biperiden (Akineton) procyclidine trijexyphenidyl
38
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
39
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
40
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
41
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
42
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
43
lithium toxic effects
confusion, lethargy slurred speech hyperreflexia seizures pregnancy category D
44
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
45
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)
46
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 ```
47
centrally acting muscle relaxant drugs
``` Carisoprodol (Soma) Chlorzoxazone (Lorzone) Cyclobenzaprine (Flexeril) Metaxalone (Skelatxin) Methocarbamol (Robaxin) Orphendrine (Norflex) Tizanidine (Zanaflex) ```
48
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
49
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
50
Baclofen uses
spasticity associated with spinal cord injury multiple sclerosis trauma
51
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
52
Diazepam MOA
acts in CNS - mimics GABA
53
Diazepam adverse effects
sedation
54
Dantrolene MOA
act directly on skeletal muscle - suppresses release of Ca++ from sarcoplasmic reticulum
55
Dantrolene uses
spasticity associated with MS, cerebral palsy, spinal cord injury treatment for malignant hyperthermia
56
Dantrolene adverse effects
``` hepatotoxicity muscle weakness drowsiness diarrhea acne like rash ```
57
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