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Pharmacology > Anti-epileptic Drugs > Flashcards

Anti-epileptic Drugs Flashcards

1
Q

What is epilepsy

A
  • Chronic disorder characterized by recurrent seizures
  • Sudden, transient disturbances in cerebral excitation
  • May remain localized in a specific area or may spread & become generalized
  • Physical convulsion due to neuronal activation of motor cortex leading to muscle contractions
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2
Q

Describe hyper excitable cerebral neurons

A
  • Inciting causes stroke, tumors, toxins, head trauma, CNS infection, & hypoxia
  • Congenital abnormalities & genetic factors
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3
Q

Describe innovative approaches to treatment of epilepsy

A
  • Surgery
  • Neuronal stimulation
  • Dietary control
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4
Q

Classifications of seizures

A
  • Focal (partial) seizures
  • Generalized seizures
  • Outward manifestations depend on the area of brain impacted
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5
Q

Describe focal/partial seizures

A
  • Older terminology includes terms such as partial
  • Only affect one part of the brain/typically one cerebellar hemisphere
  • May progress to affect the whole brain
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6
Q

Describe generalized seizures

A
  • Subclassification include tonic-clonic (grand mal) & absence
  • Affects the whole brain
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7
Q

Role of AEDs in epilepsy

A
  • Individual seizures are usually self-limiting
  • Recurrence of seizures may cause further damage to neurons; harmful to healthy cells
  • Biochemical changes, harmful proteins, oxidative stress
  • Increased susceptibility to additional seizures
  • Physical harm from LOC/falls
  • Goal is to suppress the excitability of neurons that initiate seizures
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8
Q

Lists the first generation AEDs

A
  • Barbiturates
  • Benzodiazepines
  • Hydantoins
  • Iminostilbenes
  • Succinimides
  • Valproates
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9
Q

Describe barbiturates

A
  • Phenobarbital & pentobarbital
  • Potentiate inhibitory effects of GABA, decreased the release of excitatory glutamate
  • Narrow therapeutic index
  • Very effective but mostly last-line
  • SE: sedation & ataxia
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10
Q

Describe benzodiazepines

A
  • Clonazepam & lorazepam
  • Potentiate inhibitory effects of GABA
  • Great for acute termination of seizures/status epilapticus
  • Longterm use limited to specific subtypes
  • SE: sedation, ataxia, behavioral changes
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11
Q

Describe hydantoins

A
  • Phenytoin & fosphenytoin
  • Stabilize neurons by blocking sodium channels, may increase concentrations of inhibitory NTs (GABA)
  • Narrow therapeutic index
  • SE: sedation, dizziness, HA, gastric irritation, hirsutism, skin reactions
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12
Q

Describe iminostilbenes

A
  • Carbamazepine & oxcarbamazepine
  • Stabilize neurons by blocking sodiumchannels; may inhibit presynaptic uptake and release of NE
  • SE: dizziness, drowsiness, ataxia, blurred vision, water retention (abnormal ADH release)
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13
Q

Describe succinimides

A
  • Ethosuximide
  • Inhibit spontaneous firing in thalamic neurons by limiting calcium entry
  • SE: GI distress, HA, dizziness,lethargy,dyskinesia, bradykinesia, skin rashes
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14
Q

Describe valproates

A
  • Vampiric acid & divalproex
  • May inhibit sodium channels; may hyperpolarize neurons through potassium channels; may increase GABA concentration
    -SE: GI distress, hair loss, weight gain/loss, impaired platelet function
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15
Q

Lists the 2nd generation AEDs

A
  • Gabapentin: sedation, dizziness
  • Lacosamide: dizziness, HA, double vision
  • Lamotrigine: ataxia, skin reactions
  • Levetiracetam: sedation, dizziness
  • Pregabalin:peripheral edema, temporary
  • Rufinamide: drowsiness, HA, nausea
  • Tiagabine: rare depression,anxiety
  • Topiramate: sedation, dizziness, ataxia
  • Vigabatrin: rare suicidal thoughts, confusion, weight gain
  • Zonisamide: sedation, loss of appetite
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16
Q

Describe 2nd generation AEDs compared to 1st generation AEDs

A
  • Not more effective
  • More favorable kinetics
  • Yes milder side effects
  • Similar ADEs to 1st generation. just less severe& less frequently seen
17
Q

Describe AEDs in pregnancy

A
  • Birth defects incidence is generally higher in women who take AEDs compared those w/o exposure
  • Risks of stopping AEDs exist
  • Individual decision to be discussed with physician & families
  • Consideration for narrowing therapy to a single agent at lowest effective dose
18
Q

What is status epilepticus

A
  • Series of seizures without appreciable recovery in between
  • Untreated SE will result in permanent damage
  • IV benzodiazepines followed by additional agents (levetiracetam, phenytoin, valproic acid, lacosamide); General anesthesia (propofol, pentobarbital)
19
Q

Other indications for AEDs

A
  • Commonly used for non-epilepsy indications
  • Neuropathic pain
  • Migraine prophylaxis
  • Bipolar disorder
  • Restless leg syndrome
  • Trigeminal neuralgia
  • Seizure prophylaxis following head trauma
  • Highlights importance of linking a medication to an indication
20
Q

Special concerns for rehab patients taking AEDs

A
  • Epileptic patients, even while on AEDs, are at risk for seizure activity
  • Close observation of patients may provide indications of non-compliance and undesirable side effects
  • Alert patients and providers of potential toxic effects of medications
  • Consider timing of therapy sessions when side effects are least bothersome
  • Identify when therapy modalities may be exacerbating conditions: Skin reactions with therapy tools, etc.; HA or nausea inducing activities
    -Recognize environmental triggers for seizures: Lighting, sounds, smells
21
Q

What is Parkinson disease

A
  • Slow, progressivedegeneration ofdopamine-secretingneurons
  • Clinical syndrome may also be precipitated byfactors such as trauma, variousantipsychotic drugs, CV disease, etc.
  • Movement disorder characterized byresting tremor, bradykinesia, rigidity,posturalinstability.
  • Advanced disease results inpersistently flexed posture; low, soft speaking voice
  • Untreated canlead to total incapacitation.
  • Nonmotor symptoms: depression,cognitive impairment, fatigue, chronic pain
22
Q

PD pharmacology

A
  • Symptom management is priority goal: Motor function > improved physiological and psychological well-being
  • Current pharmacology does not cure disease;motor deterioration tends to slowly progress
23
Q

PD pathophysiology

A
  • Degeneration of dopamine-producing cells in substantia nigra > loss of dopaminergic input in the corpus striatum
  • “Direct” (D1 receptors) and “indirect” (D2 receptors)pathways
  • Results in a cascading effect on the cortex
24
Q

Genetic etiology of PD

A
  • Mutations resulting in overproduction of certain proteins
  • Associated free-radical/reactive oxygen species cellular damage
  • “Vicious” cycle of the above results in degeneration & death of neurons
25
Q

Environmental etiology of PD

A
  • Designer drug use (MPTP)
  • Environmental toxins (herbicides, insecticides, fungicides, industrial agents); possible trigger for genetic pathways
  • Role of ‘antioxidants’ in prevention has no definitive evidence to date
26
Q

Describe Levodopa

A
  • Primary agent; cornerstone
  • Dramatic improvement in all symptoms; bradykinesia and rigidity: Small portion of patients don’t respond or cannot tolerate
  • Prolonged use > tolerance vs disease progression > loss of efficacy
  • Start with low doses, increase to symptom reduction or until ADEs become problematic
  • Levodopa conversion to dopamine in the periphery is a problem > less than 1% reaching the brain
27
Q

Describe Levodopa-carbidopa

A
  • Carbidopa is a peripheral decarboxylase inhibitor
  • Enables higher amounts of levodopa to reach the brain
  • Fixed C:L ratio at 1:4 or 1:10
  • Available in a controlled-release formulation to slow absorption, prolong benefits, and allow fewer doses per day
28
Q

Adverse drug reactions to Levodopa

A
  • Gastrointestinal is common: N/v can be severe at initiation of therapy, sx greatly reduce when given in combo with carbidopa
  • Cardiovascular: arrhythmias are minor unless prior Hx, orthostatic hypotension
  • Dyskinesias: develop after prolonged use, varies/pt specific, may be a factor of too much drug/dopamine, intricate relationship b/w BG neurons & endo/exo genous dopamine
  • Behavioral: psychotic sx are more prevalent, atypical antipsychotics may help reduce sx w/o worsening parkinsonism
29
Q

Describe the diminished and fluctuations of Levodopa

A
  • Tolerance to therapy can make it ineffective over time unless doses are increased
  • End of dose akinesia: drug effect wears off; resolved with adjustment in dose/timing
  • On-off phenomenon: unpredictable change in response to therapy, freezing can lead to falls/injury
30
Q

What are Levodopa drug holidays

A
  • Refractory response may be overcome w/ a holiday lasting 3 days to 3 wks
  • Goal is to be able to restart levodopa therapy at lower doses with better results
  • Risks of not taking therapy: severe immobility, VTE, pneumonia
  • Employed on limited basis
31
Q

Parkinson therapies other than Levodopa

A
  • Dopamine agonists
  • Anticholinergics
  • Amantadine
  • Monoamine Oxidate B inhibitors (MAO-B inhibitors)
  • Catechol-O-methyltransferase inhibitors (COM inhibitors)
32
Q

Describe dopamine agonists for PD therapy

A
  • Bromocriptine, cabergoline, pramipexole, rotigotine, ropinirole
  • Employed in those experiencingdecrease responsiveness
  • May be helpful for end-of-dose akinesia and on-off phenomenon
  • May normalize endogenous dopamine activity; neuroprotective
  • SE: N/V, orthostatic hypotension
33
Q

Describe anticholinergics for PD therapy

A
  • Limiting acetylcholine transmission may alleviate PD symptoms
  • SE limit use: sedation, mood change, confusion,blurred vision
34
Q

Describe amantadine for PD therapy

A
  • Helpful for reducing dyskinesias
  • SE: Orthostatic hypotension, confusion
35
Q

Describe MAO-B inhibitors for PD therapy

A
  • MAO-B enzyme breaks down dopamine
  • Inhibition leads to prolonged effects at CNS synapses
  • Selegiline/rasagiline are often used in early treatment to delay levodopa therapy then used in combination
  • SE: sleep and mood disturbances (S>R); dizziness, sedation, GI distress
36
Q

Describe COM inhibitors for PD therapy

A
  • Enzyme that converts levodopa to an inactive metabolite
  • Preventing metabolism of levodopa increases drug available in CNS
  • Used in combo with levodopa and carbidopa
  • SE: increase in dyskinesia with therapy initiation; N/V, muscle pains
37
Q

Describe the clinical course of PD

A
  • Early arguments to wait until advances staged to prescribe Levodopa
  • Use of dopamine agonists or MAO-B inhibitors might be suitable initial agents: Levodopa with significant motor sx
  • No consensus; patient & provides decisions
38
Q

Special considerations for. rehab for PD patients

A
  • Coordinate therapies with peak drug effects (Levodopa ~1hr post-dose)
  • Morning hrs may be ideal given late day fatigue
  • May encounter ‘drug holiday’ patients in inpatient: need to maintain as much mobility as possible
  • Monitor BP: orthostatic hypotension, dizziness, or syncope
  • Careful guarding given fall risk
  • Gait training, balance activities are essential to QOL

Pharmacology (12 decks)

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