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Neuro Drugs Flashcards

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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
ergot alkaloids administration
• Additive therapeutic effects with levodopa
26
ergot alkaloids- toxicity
• Hypotension, nausea, hallucinations,
27
pramipexole and ropinrole- MOA
pramipexole is a D3 agonist, ropinirole is a D2 agonist
28
pramipexole and ropinrole- administration
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
29
pramipexole and ropinrole- pharmacokinetics
• Pramipexole- excreted unchanged in the ureine. Ropinirole is metabolized by CYP1A2- may affected clearance of other drugs
30
pramipexole and ropinrole- toxicity
compulsive gambling
31
apopmorphine- MOA
a morphine decomposition product but does not bind to morphine receptors and instead functionsas a non-selective dopamine receptor agonist
32
apomorphine- administration
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
33
apomorphine- toxicity
restlessness, depression, irritability, insomnia, agitation, excitement, hallucination, confusions. Toxic psychosis and livedo reticularis have been described
34
Trihexyphenidyl, benztropine, biperiden, orphenadrine, procycidine- MOA
muscarinic blockade corrects imbalance of NT acitvitiy with dopamine and is used to respore normal striatal function
35
Trihexyphenidyl, benztropine, biperiden, orphenadrine, procycidine- administration
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
36
Trihexyphenidyl, benztropine, biperiden, orphenadrine, procycidine-toxicities
dry moth, blurry vision, urinary retention, nausea, vomiting, CNS toxicity delirium and confusion. Exacerbated by other antimuscarinic drugs. Tricyclic antidepressants and antihistamines.
37
non pharm management of Parkinsons
* Deep brain stimulation * Ablation * Transplantation of dopaminergic tissue * Gene therapy
38
acute migraine treatment
• 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
39
preventives for migraines
* Anticonvolusants, antidepressants, antihypertensives * Non-specific * Off label prescription * Do not use EEG or opiod of butabital except the last resort
40
trigeminal autonomic cephalgia and tension headache treatment
* O2 by face mask, subcut sumatriptan, intranasal zolmitriptan * Predinisone for remission * Lithum, valproic acid
41
acute MS treatment
prednisone, ACTH, IVIG, plasma exchange
42
fingolimod
keeps lymphocytes sequestered but bad infections
43
tereflutamide
- inhibit pyrimidine synthesis so more like chemo
44
natalizumab
- monoclonal antibody- risk of PML- block lymphocytes off BBB so no lymphocytes in brain- fatal
45
aletuzamab
chemo reset the immune system. More regulatory once it comes back. 1 per year but need to be tested every month
46
daclizumab
change the NK cells so tend to act like pregnancy. Skin infections are common
47
goal of antiepileptic therapy
eliminate seizures, avoid side effects, achieve best psychosocial function
48
drugs for partial set seizures
all AEDs, but ethosuximide.
49
for absence seizures
ethosuximide, valproic acid, zonisamide
50
for primary generalized seizures
valproic acid, lamotrigine, topiramate, zonisamide, levetiracetam, perampanel. Ethosuximide is only used for this
51
for myoclonus
valproic acid, levetiracetam, zonisamide
52
which drugs are first line for generalized tonic-clonic seizures or with both
phenytoin and carbamazepine
53
complex partial seizures
ethosuximide is not used. Carbamazepine, phenytoin,or valproate. Mono therapy are oxcarbazepine, lamotrigine, lacosamide
54
phenytoin side effects
gum hypertrophy, facial coarsening, hirsuitism, osteopenia, neuropathy, anemia, teratogenesis, cerebellar degeneration, ataxia with high levels
55
valproate side effects
weight gain, tremor, hair loss, polycystic ovary
56
topiramate side effects
weight loss, kidney stones, glaucoma exacerbation
57
levetiracetam side effects
irritability or mood disorder exacerbation
58
broad spectrum CYP inducers
Carbamazepine Phenytoin Phenobarbital Primidone
59
CYP3A inducers
Oxcarbazepine Topiramate Felbamate
60
Cytochrome P450 inhibitor
valproate
61
UDP- glucoronyltransferase
valproic acid, lamotrigine
62
which drugs do not effect CYP
``` Levetiracetam Gabapentin Lamotrigine Tiagabine Zonisamide ```
63
Which drugs are associated with Stevens Johnson Syndrome
``` Carbamazepine Oxcarbazepine Valproate Phenytoin Phenobarbital Ethosuximide Lamotrigine Zonisamide ```
64
which AE are hepatotoxic
``` Carbamazepine Oxcarbazepine Valproate Phenytoin Phenobarbital Felbamate ```
65
which AE cause leukopenia/aplastic anemia
``` Carbamazepine Oxcarbazepine Valproate Phenobarbital Ethosuximide Zonisamide Felbamate ```
66
AE with voltage gated sodium channel modulation
Phenytoin, carbamazepine, lamotrigine, oxcarbazepine, eslicarbazepine, felbamate, topiramate
67
AE with GABA receptor modulation
All benzodiazepines Diazepam, clobazam, lorazepam, clonazepam, clorazepate, etc. All barbiturates Phenobarbital, primidone, mephobarbital, butalbital, pentobarbital etc. Uptake and metabolism Tiagabine, vigabatrin
68
AE MOA: AMPA or NMDA receptor modulator
Perampanel (AMPA) and felbamate (NMDA)
69
AE MOA: potassium channel opener
retigabine
70
AE Ca Channel Blocker
gabapentin, ethosuximide
71
AE Synpatic protein modulator
levetiracetam, brivaracetam
72
multiple MOA AE
Valproate, topiramate, zonisamide, acetazolamide
73
felbamate- side effects
fatal aplastic anemia and hepatitis
74
vigabatrin side effects
permanent visual loss
75
AE with cormorbid for tremor
primidone
76
AE with migraine
topiramate and valproate
77
AE with pain
gabapentin and pregabalin
78
AE with neurologic pain
NA channel modulators
79
AE with mood
lamotrigine and valproate
80
bromides
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
phenytoin
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
phenytoin metabolism
it is non-linear
83
ethosuximide
MOA is unknown, but it blocks T type Ca currents. Used exclusively for absence seizures
84
carbamazepine
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
carbamazepine special things
SJS and inhibition of metabolism by erythromycin
86
gabapentin
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
lamotrigine
partial onset serizures, metabolized in the liver. Half life is 12-60 hours in naive patients. 50mg and then increase.
88
topiramate
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
special topiramate
exacerbates acute angle glaucoma, kidney stones, weight loss, cognitive slowing, metabolic acidosis
90
special lamotrigine
``` 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
special gabapentin
Doses over ~5000 mg/day not absorbed In toxic does may cause myoclonus Dosing in renal failure
92
levetiracetam
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
special levetiracetam
Irritability, aggressiveness, drowsiness
94
lacosamide
sodium channel modulator, indicated for partial onset seizures and tends to be mono therapy. Half life of 13 hours
95
special lacosamide
dizziness
96
line drawing 24 months
straight line
97
line drawing 36 months
circle
98
line drawing 48 months
draws a cross
99
handedness before second year
demonstrates early motor dysfunction
100
four month motor development
roll from side to back, reach for objects, bring hands together, autonomic sucking disappears
101
six months of motor development
sit with support, switch objects from one hand to another
102
18 month motor development
should be able to walk
103
language development- 9 months
mama dada
104
language dev at two years
speaks in two word phrases can discern half of speech
105
language dev at 3 y
speaks in sentences, recognize three colors, understans ¾ of speech
106
language dev at 4 y
understand all of speech
107
language dev at 7 y
name the seven days of the week
108
4 yo drawing
cross or looks like a four or draw a thing wit four sides
109
7 yo drawing
figure with 6 parts
110
neonatal neuro exam
o alert to sounds like bell or voice | o demonstrates visual preference for human voice
111
2 month neuro exam
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
4 month neuro exam
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
6 month neuro exam
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
9 month neuro exam
``` 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
12 month neuro exam
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
18 month neuro exam
``` 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
2 year neuro exam
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
3 year neuro exam
``` 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
4 year neuro exam
``` 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
5 year neuron exam
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
Denver II developmental screening
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
Autism Spectrum Disorder
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
cerebral palsy
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
why is CP a descriptive term
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
what is the most common form of CP
• spastic diplegic CP is bilateral in the lower etremtities and the most common
126
classification of CP
based on predominant motor abnormality
127
alzheimers
memory deficits, aphasia, apraxia, agnosia
128
drug induced dementia from
anticholinergics, hypomanic delirium from psych drug border, transit CI (digoxin)
129
cholinesterase inhibitors
increase chonilergic activity- tacrine theorginial but difficult dosing and side effets
130
which cholinesterase inhibitor is no longer used
tacrine
131
N-methyl asparate glutamate antagonists
inhibit glutamate excitotoxicity
132
blockade of M receptors does what in normal people
memory distrubances
133
deficiency in cholinergic functioning leads to
impaired short term memory
134
which are indicated for cholinesterase inhibitors
alzhemers, Parkinsons, lewy body, TBI, vascular dementia
135
which are cholinesterase inhibitors
donepezil, glantamine, rivastigmine
136
cholinergic projection in brainstem do what
regulate arousal and cognition
137
cholinergic projections in the basal forebrain do...
memory
138
donepezil MOA
selective inhibitor of AChE without inhibition of BuChE. Inhibits Ache in pre and post synpatic cholinergic neurosn
139
Donepezil side effects
GI, low HR, increased bladder activity
140
Rivastigmine MOA
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
rivastigmine side effects
more GI side effects and can develop gloss when cortical neurons die. Transdermal patch is more often used to prevent side effects
142
Why does inhibition of BuChE matter>
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
galantamine MOA
Ache inhibition and positive allosteric modulation of nicotinic cholinergic receptors.
144
galantamine side effects
GI and procholinergic effects
145
memantine- MOA
NMDa receptor antagonist
146
glutamate hypothesis of cognitive deficiency in AD
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
MOA of memantine
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
drug burden for dementia
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
what level of atropine shows levels of significant effects on self care of elders
.83ng/ml
150
what antibody reduces AB plaques in alzheimer's disease
aducanumab
151
PRIME study
tested aucanumab helps to reduce plaques measured by PET
152
reversal of cognitive decline study
multimodal approach include diet and behavior modification. It treats it as a chronic disease that dementia can be from lifestyle. Good outcomes
153
neurologic changes with age
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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