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Flashcards in CNS 1 Deck (57):
1

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

2

phenytoin uses

complete partial seizures, tonic-clonic seizures

3

difference between phenytoin and dilantin

dilantin can be taken once a day..phenytoin cannot
THEY ARE NOT INTERCHANGEABLE

4

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

5

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

6

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

7

phenytoin adverse effects

nystagmus - dyplopia
sedation
ataxia
hirsutism
gingival hyperplasia

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

hypotension
dysrhythmias

8

Carbamazapine (tegretol) MOA

same as phenytoin

9

carbamazepine uses

partial and generalized tonic-clonic seizure

mixed seizure types

complex partial seizures (DOC)

relieves pain R/T trigeminal neuralgia

bipolar disorder

10

therapeutic blood level of carbamazepine

8-12 mcg/ml

11

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

12

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

13

valproic acid drugs

Depakote, Depakane

14

MOA of valproic acid

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

15

uses of valproic acid

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

16

therapeutic range of valproic acid

50-100 mcg/ml

17

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

18

valproic acid - pregnancy category

X

19

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

20

what is levodopa used for?

Parkinson's disease
we want to correct the neurotransmitter imbalance by increasing dopamine and decreasing Ach

21

levodopa MOA

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

22

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

23

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

24

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

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