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Pharmacology Exam 3 > CNS 1 > Flashcards

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
Q

why do we use carbidopa?

A

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
Q

what drugs are levodopa/carbidopa

A

sinemet, parcopa

27
Q

adverse effects of levodopa/carbidopa

A

N/V
CV: postural hypotension, arrhythmias
psychosis
dyskinesias

28
Q

drug interactions of levodopa/carbidopa

A

non-selective MAO inhibitors
1st gen antipsychotics
anticholinergics
pyridoxine (vitamin B6) - more with levodopa alone

29
Q

contraindications of levodopa

A

angle-closure glaucoma - increased intra-ocular pressure

undiagnosed skin conditions - can activate malignant melanoma

30
Q

levodopa food interactions

A

high protein meals –> slows absorption –> reduce therapeutic effect

vitamin B6 - fish, beef, liver

31
Q

levodopa nursing implications

A

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
Q

what drugs are COMT inhibitors

A

entacapone

tolcapone

33
Q

COMT inhibitor MOA

A

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
Q

COMT inhibitor adverse effects

A 
liver failure
GI
dyskinesia
diarrhea
brown-orange urine discoloration (entacapone)
hyper/hypokinesia
syncope
hypotension
abd pain
constipation
dry mouth
back pain
 diaphoresis
35
Q

anticholinergic drugs MOA

A

goal is to inhibit cholinergic effects

block PNS activity –> decrease acetylcholine

36
Q

anticholinergic uses

A

tremors
rigidity (cog wheeling)
control sialorrhea

37
Q

anticholinergic drugs

A

benzotropine (Cogentin)
biperiden (Akineton)
procyclidine
trijexyphenidyl

38
Q

lithium MOA

A

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
Q

lithium therapeutic uses

A

bipolar disorder: DOC for manic episodes and long term prophylaxis and preventing suicide

other uses: alcoholism, migraines, bulimia, anorexia, schizophrenia, glucocorticoid-induced psychosis

40
Q

lithium facts

A

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
Q

lithium drug interactions

A

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
Q

lithium adverse effects

A

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
Q

lithium toxic effects

A

confusion, lethargy
slurred speech
hyperreflexia
seizures

pregnancy category D

44
Q

lithium patient teaching

A

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
Q

what are the two groups of drugs for muscle spasms and spasticity

A

localized muscle spasms
Diazepam (Valium)
Tizanidine (Zanaflex)

spasticity
Baclofen (Lioresal)
Diazepam (Valium)
Dontrolene (Dantrium)

46
Q

therapeutic use of centrally acting muscle relaxants

A 
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
Q

centrally acting muscle relaxant drugs

A 
Carisoprodol (Soma)
Chlorzoxazone (Lorzone)
Cyclobenzaprine (Flexeril)
Metaxalone (Skelatxin)
Methocarbamol (Robaxin)
Orphendrine (Norflex)
Tizanidine (Zanaflex)
48
Q

adverse effects of muscle relaxants

A

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
Q

Baclofen MOA

A

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
Q

Baclofen uses

A

spasticity associated with spinal cord injury

multiple sclerosis

trauma

51
Q

Baclofen withdrawal

A

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
Q

Diazepam MOA

A

acts in CNS - mimics GABA

53
Q

Diazepam adverse effects

A

sedation

54
Q

Dantrolene MOA

A

act directly on skeletal muscle - suppresses release of Ca++ from sarcoplasmic reticulum

55
Q

Dantrolene uses

A

spasticity associated with MS, cerebral palsy, spinal cord injury

treatment for malignant hyperthermia

56
Q

Dantrolene adverse effects

A 
hepatotoxicity
muscle weakness
drowsiness
diarrhea
acne like rash
57
Q

S/S of malignant hyperthermia

A

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

Pharmacology Exam 3 (4 decks)

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