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Neuro Drugs > Neuro Drugs > Flashcards

Neuro Drugs Flashcards

1
Q

levodopa- MOA

A

serves as a substrate for sopamine synthesis in the striatum. Dopamine biosynthesis occurs via hydroxylation of tyrosine to dihydrophenylalanin and subsequent decarboxylation of L-DOPA to dopamine. L-aromatic amino acid transporters function in transporting DOPA crossing the BBB. Dopamine does not cross the BBB

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2
Q

levodopa-pharmacokinetics

A

it is rapidly absorbed from the small intestine with peak plasma levels within two horus. DOPA is taken up from the GI tract via aromatic amino acid transporters. Aromatic amino acids may compete wit hDOPA for transport and food can delay absorption especially high protein meals
• Majority of oral dose of L-DOPA is excreted in urine within 8 hours as DOPAC and homovanillic acid
• Whne administered alone less than 3% of levodopa gets to the brain as much of peripheral DOPA is decarbozylated to dopamine, which does not cross the BBB> Conversion of L dopa to dopamine in periphery competes with l dopa available for dopamine in the CNS. Conversion of L-dopa to dopamine in the periphery alos leads to increased catecholamine synthesis in the periphery and associated toxicities

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3
Q

levodopa- Toxicity

A
  • Peripheral toxicity of levodopa includes GI symptoms and cardiovascular symptoms
  • CNS toxicity of Levodopa- neurologal symptoms and behavioral issues
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4
Q

levodopa on-off

A

related to alterations in drug availability unrelated to timing

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5
Q

levodopa drug interaction

A
  • Sympathomimetic drugs like beta agonists
  • Pyridozine- decreases efficacy of levodopa by increasing extracerebral metabolism of dopa
  • Antipsychotic durgs also decrease efficacy of levodopa by decreasing dopa levels
  • Monoamine oxidase a inhibitors can cuase hypertensive crisis by elevating peripheral norepinephrine
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6
Q

carbidopa- MOA

A

carbidopa functins as an inhibitor of peripheral aromatic l amino acid decarboxylase- it is the structural analog of L-dopa and functions as competitive inhibitor of dopa decarbozylase
• does not cross the BBB so only inhibits the peripheral decarboxylase enzyme so increases L-dopa reaching the brain. It also helps reduce peripheral toxicitity.

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7
Q

carbidopa- administration

A

combined with levodopa as sinemet- 1:4 c:L. Most patients require it 3 times as day

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8
Q

carbidopa- effect on levodopa

A

carbidopa decreases conversion of levodopa to dopamine in gut and blood

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9
Q

what does carbidopa do to levodopa half life

A

Increases half life of levodopa and decreased peripheral side effects

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10
Q

carbidopa- disadvatages

A

increased risk for CNS side effects if the dose of levodopa is not decreasd when used in conjunction with carbidopa

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11
Q

amantidine

A

anti-viral agent that was found to have anti-parkinsons activity

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12
Q

amantidine- MOA

A

increase synaptic concentration of dopamine by stimulating dopamine release and or inhibiting its reuptake into neurons

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13
Q

amantidine- advantages and disadvantages

A

less toxic than levodopa. Adverse effects are restlessness, depresseion, irratilbility, insomnia, agitation, excitement, hallucination, and confusion. Overdosage can cause acute toxic psychosis. Livedo reticualris and other derm reactions can be described. It is dilation of capillary blood vessels and stagnation of blood within these vessels cuase net like cyanotic cutaneous discoloration suriounding pale central areas. It happens on legs, arms, trunk and pronounced in cold weather.

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14
Q

selegiline- MOA

A

inhibits MAO-B and does not act on A in the periphery. Inhibiton of MAO-B blocks metabolism of dopamine to dihydroxyphenylactetic acid and results in the build up of dopamine in CNS. It has H2O2 production along side it. Treatmetn with selegiline reduces reactive oxygen species and has been reported to block progressive neurodegeneration: human epidemiological studies do not however support positive results in animal studies

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15
Q

selegiline- administration

A

given with levodopa. Increase advesr effects wit hlevodopa. Levodopa should be decreases when used in combination. Prolonges usefulness of levodopa. Decreased incidence of dyskinesias on and off fluctuation that occur with prolonged use of levodopa

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16
Q

selegiline- drug interactions

A

not used with meperidine- risk of toxic acute interactions

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17
Q

rasagiline

A

same as selegiline

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18
Q

entacapone/tolcapone

A

the COMT pathway is activated by inhibiton of DOPA decarboxylase by carbidopa. COMT is secondary pathway for metabolism of LDOPA and these enzymes also metabolize other catecholamine including dopamine. COMT converts L dopa to 3 Omethydopa whcich competes with DOPA for transport across the gut and BBB

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19
Q

entacapone/tolcapone- MOA

A

inhibit peripheral metabolism of levodopa. This inhibition will increase DOPA available for transport into the CNS. This adunct treatment is good for smoothing response to L-DOPA. TOlocapone inhibits COMT and the covertion of dopamine to 3-methoxytryptamine

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20
Q

entacapone/tolcapone- administration

A

either drug is given with levodopa and isfrequently paired with inhibitor s of DOPA decarboxylase

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21
Q

entacapone/tolcapone- pharmacokinetics

A

both entacapone and tolcapone are rapidly absorbed, bound to palasma proteins, and metabolized prior to excretion. They have a 2 hour half life

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22
Q

which is preferred entacapone or tolcapone

A

tolcapone is more potent. Tolcapone is more hepatotoxic.

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23
Q

ergot alkaloids

A

bromocriptine, pergolide- natural products isolated from the grain fungus ergot

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24
Q

ergot alkaloids- MOA

A

stimulate dopaminergic stingalling by acitng as dopamine receptor agonist. Bromocryptine is a D@ agonist. Pergolid is a D1 and D2 agonist that increases on-time amoung response fluctuatiors and reduces levodopa dose. Pergolid is associated with valcular heart disease and is no longer avialble

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25
Q

ergot alkaloids administration

A

• Additive therapeutic effects with levodopa

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26
Q

ergot alkaloids- toxicity

A

• Hypotension, nausea, hallucinations,

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27
Q

pramipexole and ropinrole- MOA

A

pramipexole is a D3 agonist, ropinirole is a D2 agonist

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28
Q

pramipexole and ropinrole- administration

A

potent agonists can be used alone for mild parkinsons disease. In advanced disease they are used in assocaiation with levodopa ot smoothen response to levodopa. Effects are similar to older agonists. Pramipexole and ropinirole have vauge structural similarity to dopamine. Both drugs have been prescribed for restless leg syndrome

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29
Q

pramipexole and ropinrole- pharmacokinetics

A

• Pramipexole- excreted unchanged in the ureine. Ropinirole is metabolized by CYP1A2- may affected clearance of other drugs

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30
Q

pramipexole and ropinrole- toxicity

A

compulsive gambling

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31
Q

apopmorphine- MOA

A

a morphine decomposition product but does not bind to morphine receptors and instead functionsas a non-selective dopamine receptor agonist

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32
Q

apomorphine- administration

A

temporary relief or rescue from off periods of akinesisa. Injected subcutaneously with rapid uptake in 10 minuts and persists for two horus. Treat with antiemetic first

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33
Q

apomorphine- toxicity

A

restlessness, depression, irritability, insomnia, agitation, excitement, hallucination, confusions. Toxic psychosis and livedo reticularis have been described

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34
Q

Trihexyphenidyl, benztropine, biperiden, orphenadrine, procycidine- MOA

A

muscarinic blockade corrects imbalance of NT acitvitiy with dopamine and is used to respore normal striatal function

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35
Q

Trihexyphenidyl, benztropine, biperiden, orphenadrine, procycidine- administration

A

benztropine, trihexyphenidylare have used adjunctively with other antiparkinsons agesnt . anticholinergic agents can helpf control tremor but are less effective for treating bradykinesia or rigidity. They can also block dopamine reuptake, prolonging dopamines effects. Less efficacy than levodopa in treating parkinsons syndrome. Most physicians no longer use it

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36
Q

Trihexyphenidyl, benztropine, biperiden, orphenadrine, procycidine-toxicities

A

dry moth, blurry vision, urinary retention, nausea, vomiting, CNS toxicity delirium and confusion. Exacerbated by other antimuscarinic drugs. Tricyclic antidepressants and antihistamines.

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37
Q

non pharm management of Parkinsons

A
  • Deep brain stimulation
  • Ablation
  • Transplantation of dopaminergic tissue
  • Gene therapy
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38
Q

acute migraine treatment

A

• Acute- abortive-
o Triptans
o Antiemetics/antinuaseants
• Promethazine, metoclopramide, prochlorperazine
o NSAIDs- naproxen, ibuprofen, aspirin, diclofenac
o Ergot alkaloids- dihydroergotamine, methylergonovine
o Combination analgesic- aspirin, acetominipen

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39
Q

preventives for migraines

A
  • Anticonvolusants, antidepressants, antihypertensives
  • Non-specific
  • Off label prescription
  • Do not use EEG or opiod of butabital except the last resort
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40
Q

trigeminal autonomic cephalgia and tension headache treatment

A
  • O2 by face mask, subcut sumatriptan, intranasal zolmitriptan
  • Predinisone for remission
  • Lithum, valproic acid
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41
Q

acute MS treatment

A

prednisone, ACTH, IVIG, plasma exchange

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42
Q

fingolimod

A

keeps lymphocytes sequestered but bad infections

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43
Q

tereflutamide

A
  • inhibit pyrimidine synthesis so more like chemo
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44
Q

natalizumab

A
  • monoclonal antibody- risk of PML- block lymphocytes off BBB so no lymphocytes in brain- fatal
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45
Q

aletuzamab

A

chemo reset the immune system. More regulatory once it comes back. 1 per year but need to be tested every month

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46
Q

daclizumab

A

change the NK cells so tend to act like pregnancy. Skin infections are common

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47
Q

goal of antiepileptic therapy

A

eliminate seizures, avoid side effects, achieve best psychosocial function

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48
Q

drugs for partial set seizures

A

all AEDs, but ethosuximide.

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49
Q

for absence seizures

A

ethosuximide, valproic acid, zonisamide

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50
Q

for primary generalized seizures

A

valproic acid, lamotrigine, topiramate, zonisamide, levetiracetam, perampanel. Ethosuximide is only used for this

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51
Q

for myoclonus

A

valproic acid, levetiracetam, zonisamide

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52
Q

which drugs are first line for generalized tonic-clonic seizures or with both

A

phenytoin and carbamazepine

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53
Q

complex partial seizures

A

ethosuximide is not used. Carbamazepine, phenytoin,or valproate. Mono therapy are oxcarbazepine, lamotrigine, lacosamide

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54
Q

phenytoin side effects

A

gum hypertrophy, facial coarsening, hirsuitism, osteopenia, neuropathy, anemia, teratogenesis, cerebellar degeneration, ataxia with high levels

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55
Q

valproate side effects

A

weight gain, tremor, hair loss, polycystic ovary

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56
Q

topiramate side effects

A

weight loss, kidney stones, glaucoma exacerbation

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57
Q

levetiracetam side effects

A

irritability or mood disorder exacerbation

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58
Q

broad spectrum CYP inducers

A

Carbamazepine
Phenytoin
Phenobarbital
Primidone

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59
Q

CYP3A inducers

A

Oxcarbazepine
Topiramate
Felbamate

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60
Q

Cytochrome P450 inhibitor

A

valproate

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61
Q

UDP- glucoronyltransferase

A

valproic acid, lamotrigine

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62
Q

which drugs do not effect CYP

A 
Levetiracetam
Gabapentin
Lamotrigine
Tiagabine
Zonisamide
63
Q

Which drugs are associated with Stevens Johnson Syndrome

A 
Carbamazepine
Oxcarbazepine
Valproate
Phenytoin
Phenobarbital
Ethosuximide
Lamotrigine
Zonisamide
64
Q

which AE are hepatotoxic

A 
Carbamazepine
Oxcarbazepine
Valproate
Phenytoin
Phenobarbital
Felbamate
65
Q

which AE cause leukopenia/aplastic anemia

A 
Carbamazepine
Oxcarbazepine
Valproate
Phenobarbital
Ethosuximide
Zonisamide
Felbamate
66
Q

AE with voltage gated sodium channel modulation

A

Phenytoin, carbamazepine, lamotrigine, oxcarbazepine, eslicarbazepine, felbamate, topiramate

67
Q

AE with GABA receptor modulation

A

All benzodiazepines
Diazepam, clobazam, lorazepam, clonazepam, clorazepate, etc.
All barbiturates
Phenobarbital, primidone, mephobarbital, butalbital, pentobarbital etc.
Uptake and metabolism
Tiagabine, vigabatrin

68
Q

AE MOA: AMPA or NMDA receptor modulator

A

Perampanel (AMPA) and felbamate (NMDA)

69
Q

AE MOA: potassium channel opener

A

retigabine

70
Q

AE Ca Channel Blocker

A

gabapentin, ethosuximide

71
Q

AE Synpatic protein modulator

A

levetiracetam, brivaracetam

72
Q

multiple MOA AE

A

Valproate, topiramate, zonisamide, acetazolamide

73
Q

felbamate- side effects

A

fatal aplastic anemia and hepatitis

74
Q

vigabatrin side effects

A

permanent visual loss

75
Q

AE with cormorbid for tremor

A

primidone

76
Q

AE with migraine

A

topiramate and valproate

77
Q

AE with pain

A

gabapentin and pregabalin

78
Q

AE with neurologic pain

A

NA channel modulators

79
Q

AE with mood

A

lamotrigine and valproate

80
Q

bromides

A

triple bormide elixer, available from compounding pharmacies. A mixture of sodium, potassium, and ammonium salts of bromide in 5 mL of syrup and water. Half life is 12 days. Probably enhanced Cl currents through GABA receptors. Br is more permeable in these channels than Cl-. Ammonium anion may also enhance GABA effects

81
Q

phenytoin

A

sodium channel modulator, partial onset seizures, liver metabolism,interacts with multiple drugs. Twice dosing and 22hr half life. Liver enzyme induction, osteopenia, gum hypertrophy, neuropathy, cerebellar degeneration

82
Q

phenytoin metabolism

A

it is non-linear

83
Q

ethosuximide

A

MOA is unknown, but it blocks T type Ca currents. Used exclusively for absence seizures

84
Q

carbamazepine

A

sodium channel modulator is a tricyclic compound like amitriptyline. Liver metabolism is induced, but it induces its own metabolism. TID dosing, half life of 8-22 hours. Hyponatrremia, hepatitis, aplastic anemia, blurry vision, ataxia.

85
Q

carbamazepine special things

A

SJS and inhibition of metabolism by erythromycin

86
Q

gabapentin

A

partial onset seizures, favorable pharm, start at 300mg and then go to 1800 mh TID QID dosing and half life of 5-7 hours. Doses over 5000 are not absorbed, not good for renal failure, toxic can cause myoclonus

87
Q

lamotrigine

A

partial onset serizures, metabolized in the liver. Half life is 12-60 hours in naive patients. 50mg and then increase.

88
Q

topiramate

A

partial onset seizures, generalized seizures, metabolized by the liver and excreted in the kidneys. Liver path may predominant in the prescence of enzyme inducers. BID dosing start low and slow

89
Q

special topiramate

A

exacerbates acute angle glaucoma, kidney stones, weight loss, cognitive slowing, metabolic acidosis

90
Q

special lamotrigine

A 
Half life is prolonged by valproate
Metabolism markedly increased in pregnancy
Oral contraceptives increase metabolism
Rash! (10%, more if on valproate)
May make myoclonus wors
91
Q

special gabapentin

A

Doses over ~5000 mg/day not absorbed
In toxic does may cause myoclonus
Dosing in renal failure

92
Q

levetiracetam

A

partial onset seizures, MOA unknown, most is excreted unchanged. BI dosing and half life is 6-8 hours. More than 3000 does not work

93
Q

special levetiracetam

A

Irritability, aggressiveness, drowsiness

94
Q

lacosamide

A

sodium channel modulator, indicated for partial onset seizures and tends to be mono therapy. Half life of 13 hours

95
Q

special lacosamide

A

dizziness

96
Q

line drawing 24 months

A

straight line

97
Q

line drawing 36 months

A

circle

98
Q

line drawing 48 months

A

draws a cross

99
Q

handedness before second year

A

demonstrates early motor dysfunction

100
Q

four month motor development

A

roll from side to back, reach for objects, bring hands together, autonomic sucking disappears

101
Q

six months of motor development

A

sit with support, switch objects from one hand to another

102
Q

18 month motor development

A

should be able to walk

103
Q

language development- 9 months

A

mama dada

104
Q

language dev at two years

A

speaks in two word phrases can discern half of speech

105
Q

language dev at 3 y

A

speaks in sentences, recognize three colors, understans ¾ of speech

106
Q

language dev at 4 y

A

understand all of speech

107
Q

language dev at 7 y

A

name the seven days of the week

108
Q

4 yo drawing

A

cross or looks like a four or draw a thing wit four sides

109
Q

7 yo drawing

A

figure with 6 parts

110
Q

neonatal neuro exam

A

o alert to sounds like bell or voice

o demonstrates visual preference for human voice

111
Q

2 month neuro exam

A

o begins to smile at people
o coos, makes gurgling sounds, turns head toward sound
o begins to follow things with eyes, recognize people at a distance
o can hold head up and begins to push up when lying on tummy

112
Q

4 month neuro exam

A

o smiles spontaneously
o babbels with expression and copies sounds
o reaches for toy with one hand
o follows moving things with eyes from side to side
o recognizes people and things at a distance
o holds head steady, unsupported
o when lying on stomach, pushed up to elbows

113
Q

6 month neuro exam

A

o knows faces and begins to recognize strangers
o responds to sounds by making sounds
o brings things to mouth
o beings to pass things from one hand to the other
o rolls over in both directions
o when standing supports weight and might bounce

114
Q

9 month neuro exam

A 
o	may be afraid of strangers
o	copies sounds and gestures of others
o	looks for things he sees you hide
o	stands holding on
o	sits without support
o	pulls to stand
115
Q

12 month neuro exam

A

o shy or nervous with strangers
o hands you book when child wants to hear story
o mama and dada and exclamation like uh-oh
o tries to say words you day
o explores things in different ways like shaking, banging, throwing
o copies gestures
o follows simple directions like pick up toy
o pulls to stand, walks holding onto furniture
o may take a few steps without holding

116
Q

18 month neuro exam

A 
o	may be afraid of strangers
o	says several single words
o	says and shakes head no
o	points to one body part
o	can follow one step verbal commands without any gestures
o	walks alone
o	drinks from cup
117
Q

2 year neuro exam

A

o copies others especially adults and older children
o says sentences with 2-4 words
o beings to sort shapes and colors
o might use one hand more than the other
o begins to run
o walks up and down stairs holding on

118
Q

3 year neuro exam

A 
o	understands of mine, his, hers
o	dresses and undresses self
o	can name more familiar things
o	says first name, age, sex
o	carries on conversation using 2-3 sentences
o	can work toys with buttons, levers, and moving parts
o	parallel play
o	climbs well
o	runs easily
119
Q

4 year neuro exam

A 
o	plays mom and dad
o	would rather play with other children than by himself
o	sings a song or says a poem from memry
o	tells stories
o	names some colors and numbers
o	understands same and different
o	draws a person with 2-4 body parts
o	catches a bounced ball most of the time
120
Q

5 year neuron exam

A

o likes to sing, dance, and act
o is aware of gender
o tells a simple story with full sentences
o counts 10 or more things
o hops may be able to skip
o can use the toilet on her own (females usually potty trained before males)

121
Q

Denver II developmental screening

A

o Most widely used developmental assessment tool- reflects percentage of age range that can perform a certain tast
o Can your child regard a raisen- three months
o Rake a raisin- 6 months

122
Q

Autism Spectrum Disorder

A

o Persistent deficits in social communication and social interaction across multiple contacts
o Restricted repetitive patterns of behavior, interests or activities
o Symptoms must be present in early developmental period
o Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning
o These disturbances are not better explained by intellectual disability or global developmental delay

123
Q

cerebral palsy

A

o Disorder of aberrant control of movement and posture appearing early in life secondary to a CNS lesion or dysfunction that is not the result of a recognized progressive or degenerative brain disease
• Motor impairment and non-progressive static
• Diagnosed before the age of two

124
Q

why is CP a descriptive term

A

o CP is more descriptor term. It is important to evaluate for the etiology of CP (hypoxic or in utero stroke). Prematurity is single most important risk factor for CP.

125
Q

what is the most common form of CP

A

• spastic diplegic CP is bilateral in the lower etremtities and the most common

126
Q

classification of CP

A

based on predominant motor abnormality

127
Q

alzheimers

A

memory deficits, aphasia, apraxia, agnosia

128
Q

drug induced dementia from

A

anticholinergics, hypomanic delirium from psych drug border, transit CI (digoxin)

129
Q

cholinesterase inhibitors

A

increase chonilergic activity- tacrine theorginial but difficult dosing and side effets

130
Q

which cholinesterase inhibitor is no longer used

A

tacrine

131
Q

N-methyl asparate glutamate antagonists

A

inhibit glutamate excitotoxicity

132
Q

blockade of M receptors does what in normal people

A

memory distrubances

133
Q

deficiency in cholinergic functioning leads to

A

impaired short term memory

134
Q

which are indicated for cholinesterase inhibitors

A

alzhemers, Parkinsons, lewy body, TBI, vascular dementia

135
Q

which are cholinesterase inhibitors

A

donepezil, glantamine, rivastigmine

136
Q

cholinergic projection in brainstem do what

A

regulate arousal and cognition

137
Q

cholinergic projections in the basal forebrain do…

A

memory

138
Q

donepezil MOA

A

selective inhibitor of AChE without inhibition of BuChE. Inhibits Ache in pre and post synpatic cholinergic neurosn

139
Q

Donepezil side effects

A

GI, low HR, increased bladder activity

140
Q

Rivastigmine MOA

A

pseudoreversible intermediate agent to inhibit AChE and BuCHe. Selectively inhibits ACHE aover BUCHE in the cote. Inhibits BUCHE in the glia which may contribute to enhanced ACH levels in the CNS

141
Q

rivastigmine side effects

A

more GI side effects and can develop gloss when cortical neurons die. Transdermal patch is more often used to prevent side effects

142
Q

Why does inhibition of BuChE matter>

A

some cholinergic neurons have it instead of ACHE. It is supportive of ACHE when ACHE is inhibited by too much substrate. . It is more associated wit glial cells and endothelial cells and neurons

143
Q

galantamine MOA

A

Ache inhibition and positive allosteric modulation of nicotinic cholinergic receptors.

144
Q

galantamine side effects

A

GI and procholinergic effects

145
Q

memantine- MOA

A

NMDa receptor antagonist

146
Q

glutamate hypothesis of cognitive deficiency in AD

A

neuronal death due to amyloid precursors causing plaques. Triggers neurofibrillary angels and neurotoxic inflammatory reaction. Plaques provide release of glutamate leading to excitotoxicity. normally glutamate is quiet and NMDA receptor is blocked by Mg

147
Q

MOA of memantine

A

noncompetitive low affinitiy for NMDA receptor binds to Mg site when channel is open. Memantine blocks downstream effects of toxic glutamate release by plugging the receptor. When there is a phasic burst, this is removed to allow normal conduction of the impulse

148
Q

drug burden for dementia

A

additional until of drug burden has negative effect on physical function. Each additional rug burden unit has a negative effect on cognitive task performance

149
Q

what level of atropine shows levels of significant effects on self care of elders

A

.83ng/ml

150
Q

what antibody reduces AB plaques in alzheimer’s disease

A

aducanumab

151
Q

PRIME study

A

tested aucanumab helps to reduce plaques measured by PET

152
Q

reversal of cognitive decline study

A

multimodal approach include diet and behavior modification. It treats it as a chronic disease that dementia can be from lifestyle. Good outcomes

153
Q

neurologic changes with age

A

brain atrophy, significant cellular loss, plus disease loss. Proprioception decreases with age. Worsened by benzos, alcohol, and vitamin deficiency.

Neuro Drugs (1 decks)

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