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Pharmacology Mod 5 > Pharmacology of Neurodegenerative diseases, epilepsy and migraine > Flashcards

Pharmacology of Neurodegenerative diseases, epilepsy and migraine Flashcards

1
Q

what are the someone symptoms for parkinsons disease

A

progressive disease
tremor of rest
bradykinesia, rigidity
postural defect: tendency to stoop

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2
Q

what is the mortality of parkinsons disease

A

due to complications of severe rigidity

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3
Q

what is the pathophysiology of parkinsons

A

progressive degeneration of neurons in the substantia nigra: loss of DA transmission

leads to imbalance of input to the cortex - DA/ACh balance

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4
Q

what medication can quickly produce parkinsonian symtpoms

A

injection of MPTP
(a neurotoxin that kills dopamine-producing neurons)

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5
Q

what are the classes of dopamine receptors

A

D1 receptors (excitatory) and D2 receptors (inhibitory)

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6
Q

what is the effect of D1 receptor class

A

Excitatory
Increase cAMP
PIP hydrolysis
Ca2+ mobilization and PKC activation

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7
Q

what is the effect of D2 receptor class

A

Inhibitory
decrease cAMP
increase K+ currents
decrease Ca2+ currents

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8
Q

what does parkinsons inhibit

A

the thalamus and reduces thalamic stimulation of the cortex

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9
Q

What is the goal of Parkinson therapy

A

re-establish balance of striatal signaling
increase DA signaling and Decrease mACh signaling

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10
Q

what type of medication is levodopa

A

DA precursos

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11
Q

what is the MOA of levodopa

A

crosses the BBB
actively taken up into neurons (amino acid transporter)
converted to DA by DA decarboxylase

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12
Q

what are the adverse effects of Levadopa

A

dyskinesia
hallucinations/confusion (cautiously treat psychosis with antipsychotics)
peripheral effects: Nausea, hypotension, arrhythmia

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13
Q

why can Levadopa cause Nausea

A

DA receptors in the gut are affected

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14
Q

What is Carbidopa

A

adjunct therapy - peripheral inhibitor of levadopa (l-aa decarboxylase)

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15
Q

what is the purpose of Carbidopa

A

prevents conversion to DA in periphery
does NOT cross the BBB
reduces peripheral side effects (nausea) and allow more drug to reach the brain

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16
Q

what is the mainstay treatment for parkinsons disease

A

Levodopa-Carbidopa

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17
Q

what is Entacapone

A

a levodopa adjunct therapy - inhibits COMT enzyme mostly in the periphery
prevents degradation of Levodopa

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18
Q

what is COMT

A

catechol-o-methyl transferase
secondary pathway to metabolize levodopa as well as DA and NE

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19
Q

what are the adverse effects of Entacapone

A

dyskinesia, nausea and diarrhea

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20
Q

what is the efficacy of levodopa

A

extremly effective early in treatment

overtime one may develop motor flunctuation

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21
Q

how is motor fluctuation effect reduced

A

by increasing number of dosages

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22
Q

what is the benefit of increasing the number of levodopa dosages

A

to decrease motor fluctuation

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23
Q

what is the MOA Selegiline

A

Beta inhibitor that prevents metabolism of DA
selective for striatum, mild effect
reduced the dose of devodopa needed

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24
Q

what is another beta inhibitor that can be used for parkinsons treatment

A

Rasagiline

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25
Q

what are the adverse effects of selegiline

A

some amphetamine - like side effects (partly metabolized to amphetamine)
possibility of serotonin syndrome

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26
Q

what is the metabolism of selegiline

A

metabolized in the liver by CYP450 enzymes
possible serotonin syndrome induced by foods containing tyramine or combining with SSRIs or CYP450 substrates

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27
Q

what is a dopamine receptor agonist medication

A

Bromocriptine
Ropinerole
(pramipexole, perogolide, apomorphine)

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28
Q

what is Bromocriptine

A

DA receoptor agnoist: ergot alkaloid - D2 receptor agnoists
some avitivty at D1, D3 and 5-HT receptors
used to delay the need for using levodopa and also for advanced parkinsons

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29
Q

what are the side effects of Bromocriptine

A

more risk of psychotic effects and risk of cardiac valve fiborsis in long-term use

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30
Q

what is Ropinerole

A

dopamine receptor agonist
less selective than bromocriptine has D2, D3, D4 receptor agonist receoptos

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31
Q

what is ropinerole also beneifical in treating

A

restless leg syndrome

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32
Q

what are the adverse effects of ropinirole

A

metabolized by CYP450 thus could cause drug interaction
mostly has replaced bromocriptine therapeutically due to reduced side effects - less risk of cardiac valve fibrosis and D3 agonisms is linked to increased risky behavior

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33
Q

the agnoism of D3 is linked to what

A

increased risky behavior (gambling, hypersexuality)

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34
Q

what are non-DA parkinson treatments

A

MACh receptor agonists and antivirals

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35
Q

what is trihexyphenidyl

A

mACh receptor agonists
effective at reducing dyskinetic movements and spastic contractions - often given in combination with DA agonists

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36
Q

what is another option for mACh receptor agonists that is less commonly used

A

Benztropine

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37
Q

what are the adverse effects of trihexyphenidyl

A

anticholinergic side effects: sedation, confusion, constipation, urinary retention
pharmacokinets: excreted unchanged

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38
Q

what is amantadine

A

anti-viral drugmechanism by increaseing DA release and blocking NMDA gluamate receptors
less effective than levodopa

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39
Q

what may amatadine casue

A

confusion/psychosis

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40
Q

what is huntinggtons disease

A

dominant inherited disorder characterized by involunatary movements, personality changes and bradykinesia

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41
Q

what type of vulnerability does huntingtons disease have

A

selective,

mutant gene expressed throughout brain
neuronal loss is limited to caudate/putamen, striatum and loss of GABA function

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42
Q

what is the treatment for huntingtons

A

very difficult to treat becasuse of its effects on multiple neuronal systems

based on most pronounced symptoms: psychosis and chrea

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43
Q

what is the psychosis treatment for huntingtons

A

neuroleptic D2 blockers such as Haloperidol

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44
Q

what is the chorea treatment for huntingtons

A

inhibitor of neurotransmitter storage such as Deutetrabenazine

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45
Q

what is Deutetrabenazine

A

inhibitor of VMAT-2
prevents storage of neurotransmitter in vesicles
reduced uncontrolled hyperkinetic movements

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46
Q

where is Deutetrabenzine metabolized

A

P450 (CYP2D6)
some patient sare poor metabolizers
long half-life relative to tetrabenazine

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47
Q

what are the side effects of deutetrabenzine

A

similar to antipsychosis
Akathisia, drowsiness, tremor, depression

48
Q

when is deutetrabenazine contraindicated

A

with MAO inhibitors and uncontrolled depression (suicide risk)

49
Q

what are other conditions that deutetrabenzine is useful for

A

tourettes and tardive dyskinesia

50
Q

what are the drug types for alzheimers

A

cholinesterase inhibitor and NMDA antagonists

51
Q

what are cholinesterase inhibitor drugs used in the treatment of alzheimers

A

DONEPEZIL (aricept)
rivastigmine
galantamine

52
Q

what are the NMDA antagonist drugs used in treatment to Alzheimers

A

MEMANTINE (nemenda)
typcially used in combination with Donepezil

53
Q

what is the pathophysiology of Alzheimers dementia

A

neuritic plaques, containing beta-amyloid
neurofibrillary tangles
selective neuronal loss in Hippocampus and Cortex
CHOLINERGIC DAMAGE

54
Q

What is lost with Cholinergic Damage in connection to Alzheimers Dementia

A

loss of enzymes for ACh synthesis
loss of cholinergic neurons in basal forebrain

55
Q

what is the goal of Donepezil

A

raise ACh levels in damaged areas of the brain
readily enters CNS, relatively long lasting

56
Q

what are other affects of Donepezil

A

may increase ACh synthesis and release

57
Q

what are the adverse effects of Donepezil

A

GI distrubances from chilinergic effects, N/V/D (can be severe due to overactive gut motility)
Sleep distrbances- vivid dreams

58
Q

what is the metabolism of Donepezil

A

metabolism is through acetylcholinesterase activity, thus no major drug interactions

59
Q

what is the mechanism of Memantine

A

NMDA receptor antagonists
blocks pathological activation of NMDA receptors
thought to reduce excitotoxicity

60
Q

what are the common side effects of Memantine

A

Dizziness, headache, constipation, confusion

61
Q

when is Memantine used

A

it is not as effective as Donepezil, but useful for patients that do not response or cannot tolerate the side effects

can be used in addition to Donepezil

62
Q

what antioxidants are used in the treatment of Alzheimers

A

Vitamin E and Selegeline

63
Q

why is Vitamin E important

A

lipid soluble antioxidant
scavenges damaging free radicals
limited effectiveness, difficult to monitor

64
Q

what is selegeline

A

MAO inhibitor in Striatum
has neuroprotective effect (antioxidant?)

65
Q

what is the treatment for behavioral effects of alzheimers

A

antipsychotics
anxiolytics
antidepressants

66
Q

what is epilepsy

A

abnormal electrical activity can result in a variety of events including LOC, abnormal movements, atypical or odd behavior and distorted perceptions that are of limited duration but recur if untreated

67
Q

what are the common types of epilepsy

A

idiopathic and symptomatic

68
Q

what is idiopathic epilepsy

A

no specific anatomic cause for the seizure, such as truama or neoplasm, is evident, a patient may be diagnosed with idiopathic or cryptogenic (primary) epilepsy

69
Q

how is idiopathic epilepsy treated

A

with antiseizure drugs or vagal nerve stimulation

70
Q

what is symptomatic epilepsy

A

caused by illict drug use, tumor, head injury, hypoglycemia, meningeal infection or withdrawal from alcohol

71
Q

how is symptomatic epilepsy treated

A

antiseizure drugs and vagal nerve stimulators used to treat as well as treating the underlying cause

72
Q

what are the subtypes of seizures

A

partial and generalized

73
Q

what are partial seizures

A

conciousness preseved entirely or partially
simple vs complex

74
Q

what is simple partial seizures

A

consciousness normal - cauaed by a group of hyperactive neurons exhibiting abnormal electrical activity which are confined to a single locus in the brain

  • no LOC
75
Q

what is complex partial seizures

A

consciousness altered/no memory

exhibits complex sensory hallucinations and mental distortion

76
Q

what are the categories of generalized seizures

A

tonic-clonic
absence
myoclonic
status epilepticus
infantile spasm

77
Q

what is generalized seizures

A

consciousness lost / no memory

78
Q

what is generalized tonic - clonic seizures

A

loss of consciousness, followed by tonic and clonic

79
Q

what is tonic

A

continuous contraction

80
Q

what is clonic

A

rapid contraction and relaxation phases

81
Q

what is generalized absence seizures

A

brief abrupt self limiting loss of consciousness. may stare and exhibit rapid eye blinking lasting 3-5 seconds

82
Q

what is generalized myoclonic seizures

A

short episodes of muscle contractions that may recur within several minutes

83
Q

what is status epilepticus

A

two or more seizures occur without recovery of full consciousness between them. LIFE THREATENING

84
Q

What is the MOA of antiseizure drugs

A

blocking voltage-gated channels (Na+ or Ca2+)
enhancing inhibitory y-aminobutyric acid (GABA)-ergic impulses
interfering with excitatory glutamate transmission

85
Q

what is the MOA for Benzodiazepines

A

bind to GABA inhibitory receptors to reduce firing rate

86
Q

what are the most common Benzodiazepines

A

diazepam and lorazepam are most offen used as an adjuctive therapy for myoclonic as well as partial and generalized tonic-clonic seizures

87
Q

what is the benefit of Lorazepam

A

shorter half life - but stays in the brain longer than diazepam

88
Q

what is the benefit of Diazepam

A

available for rectal administration to avoid or interrupt prolonged generalized tonic-clonic seizures or clusters

89
Q

what population is diazepam typcially used in

A

childen and patients with AMS

90
Q

what is the MOA for Carbamazepine

A

reduces the propagation of abnormal impulses in the brain by blocking sodium channels, thereby inhibits the generation of repetitive action potentials in the epileptic focus and preventing their spread

91
Q

what are carbamazepine used for

A

effective for treating partial seizures and secondarily generalzied tonic-clonic seizures

92
Q

what patient should not be treated with Carbamazepine

A

patient with absence seizures becuase it may casue an increase in seizures - inducer of isozyme families CYP1A2, CYP2C, and CYP3A and UGT enzymes

Elderly

93
Q

how is carbamazepine metabolized

A

absorbed slowly and erratically following oral administration, resulting in large variations of serum concentration

94
Q

what is Ethosuximide

A

effective in treating primary generalized absence seizures

95
Q

what is the MOA for ethosuximide

A

reduces propagation of abnormal electrical activity in the brain, most likely inhibiting T-type calcium channels

96
Q

what is the MOA for Gabapentin

A

analog of GABA, but does not act on GABA receptors and it neither enhances GABA actions not is converted to GABA

MOA is not known

97
Q

what is Gabapentin approved for

A

approved as adjunct therapy in partial seizures and for treatment of postherpetic neuralgia

98
Q

when is gabapentin dose reduced

A

patients with renal disease - does not bind to plasma proteins and is excreted unchanged through the kidneys

99
Q

what is the MOA for Lamotrigine

A

blocks sodium channels as well as high voltage dependent calcium channels

100
Q

what is lamotrigine used for

A

effective in a wide variety of seizure types including partia, generlized and typical absnse seizures in the Lennox-Gastaut syndrome

101
Q

what other conditions are treated with Lamotrigine

A

bipolar disorder

102
Q

how is lamotrigine metabolized

A

through the N-2 glucuronide through the UGT pathway
half life is 24-35 hours and is decreased by enzyme inducing drugs like carbamazepine and phenytoin

103
Q

when lamotrigine is used in combination, what is important to remember

A

reduce doing if given in combination

104
Q

what are serious adverse reactions to lamotrigine

A

SJS
overall tolerated by elderly with partial seizures due to relatively minor effects

105
Q

what is Levetiracetam approved for

A

adjunct therapy of partial onset seizures, myoclonic seizures and primary generalized tonic-clonic seizures in adults and children

106
Q

how is Levetiracetam metabolized

A

does not interact with CYP or UGT metabolism systems

well absorbed orally and excreted in urine unchanged

107
Q

what are the side effects of levetiracetam

A

dizziness, sleep disturbances, headache and weakness

108
Q

what is the MOA for Oxcarbazepine

A

prodrug that is rapidly reduced to 10-monohydroxy (MHD) metabolite responsible for its anticonvulsant activity
MHD blocks sodium channels, preventing spread of abnormal discharge

109
Q

what is oxcarbazepine approved for

A

use in adult and children with partial onset seizures

110
Q

what are the adverse effects of oxcarbazepine

A

N/V, headaches, visual disturbances

111
Q

what is the MOA for phenobarbital

A

enhancing the inhibitory effects of GABA-mediated neurons

112
Q

what should phenobarbital be used for

A

primarily for the treatment of status epilepticus

113
Q

what is the MOA for phenytoin and fosphenytoin

A

blocks voltage-gated sodium channels by selectively binding to the channel in the inactive state and sling its rate of recovery

114
Q

what treatments are phenytoin and fosphenyotin used for

A

treatment of partial seizures and generalized tonic-clonic seizures and in the treatment of status epilepticus

115
Q

how are phenytoin and fosphenytoin metabolized

A

induces drugs metabolized by the CYP2C and CYP3A families and the UGT enzyme system

Pharmacology Mod 5 (3 decks)

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