Antiseizure Drugs, Medications for Parkinson and Alzheimer Disease

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Last updated 11:07 PM on 9/21/26
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52 Terms

1
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During an active tonic-clonic seizure, which nursing actions take priority?

  • positioning

  • airway protection

  • environmental safety


2
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positioning during seizure

  • Do NOT restrain the patient - allow seizure activity to occur naturally 

  • Position on the side (lateral/recovery position) if possible to facilitate drainage of oral secretions and prevent aspiration 

  • If patient falls, ease them gently to the floor 

  • Place padding under the head to prevent injury 


3
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airway protection during seizures

  • Maintain patent airway but do NOT force anything into the mouth 

  • Do NOT insert anything between the teeth during active seizure - this can cause injury, broken teeth, or airway obstruction 

  • Loosen tight clothing around the neck 

  • Position head to allow secretions to drain 

  • Suction oral secretions after seizure concludes if necessary 

  • Administer oxygen as needed after seizure 

 

4
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environmental safety during seizures

  • Remove harmful objects from the immediate area (furniture, sharp objects) 

  • Protect from injury by clearing space around the patient 

  • Lower bed to floor level if patient is in bed 

  • Pad side rails if already in place (but don't attempt to raise them during active seizure) 

  • Ensure privacy by moving onlookers away 


5
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critical actions to avoid during seizures

  • Do NOT restrain the patient's movements 

  • Do NOT force objects into the mouth (padded tongue blades, oral airways, fingers) 

  • Do NOT give anything by mouth during the seizure 

  • Do NOT attempt to move the patient unless in immediate danger 

  • Do NOT leave the patient alone 


6
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What teaching should a client receiving phenytoin receive regarding dose timing?

  • Take phenytoin at regular intervals to maintain steady therapeutic levels  

  • Consistency in timing is crucial due to phenytoin's narrow therapeutic range (10-20 mcg/mL) 

  • Phenytoin has a half-life of approximately 22 hours; steady state takes about 3½ days to achieve  


7
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What teaching should a client receiving phenytoin receive regarding missed or extra doses? 

  • If a dose is missed: Take it as soon as remembered, unless it's close to the next scheduled dose 

  • Never double up on doses to make up for a missed one 

  • Contact healthcare provider if multiple doses are missed 

  • Never take extra doses - phenytoin has a narrow therapeutic index requiring close monitoring  

  • Drug levels above the therapeutic range can result in toxicity  

  • Drug levels below the therapeutic range may fail to control seizure activity 

 

8
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What teaching should a client receiving phenytoin receive regarding driving? 

  • Do not drive or operate machinery until seizure control is established and drug levels are stable 

  • Phenytoin can cause drowsiness and dizziness initially 

  • Discuss return to driving with healthcare provider based on seizure control and state laws 

  • Avoid activities requiring alertness until response to medication is known 


9
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What teaching should a client receiving phenytoin receive regarding laboratory monitoring? 

  • Regular blood level monitoring is essential to ensure the drug level remains within therapeutic range  

  • Therapeutic plasma/serum level: 10-20 mcg/mL (equivalent to 1-2 mcg/mL unbound/free phenytoin)  

  • Monitoring ensures drug effectiveness and prevents toxicity  

  • Dosage adjustments are made based on therapeutic plasma levels  

  • Newborns, patients with liver disease, and older adults may require lower doses due to decreased metabolism  


10
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How should the nurse interpret a subtherapeutic phenytoin level in a client experiencing seizure activity?

A subtherapeutic phenytoin level (below 10 mcg/mL) in a client experiencing seizure activity indicates that the patient is not receiving the required drug dosage to control seizure activity.  

When the drug level falls below the therapeutic range of 10-20 mcg/mL, the medication cannot effectively prevent seizures 1. This explains why breakthrough seizure activity is occurring. 

11
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Which action should be anticipated for a patient with a subtherapeutic phenytoin level experiencing seizure activity?

Dosage Adjustment 

- The healthcare provider will likely increase the phenytoin dosage 

- Drug dosage is adjusted according to the therapeutic plasma or serum level  

- The goal is to bring levels within the therapeutic range (10-20 mcg/mL) where benefits become apparent. 

12
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Why should antiseizure medications generally not be stopped abruptly?

  • Breakthrough seizures or increased seizure frequency 

  • Status epilepticus (prolonged, life-threatening seizure activity) 

  • Withdrawal seizures (particularly with benzodiazepines and barbiturates) 

  • The drug dosage should be gradually decreased over a period of days, depending on the dose or length of time on the drug


13
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Findings requiring prompt provider notification when antiseizure medications are abruptly stopped?

  • signs of toxicity

  • inadequate seizure control

  • respiratory depression

  • withdrawal symptoms


14
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parkinsons disease results from

an imbalance between dopamine (DA) and acetylcholine (ACh) caused by degeneration of neurons in the substantia nigra of the midbrain

15
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dopamine movement connection in normal state

  • DA is an inhibitory neurotransmitter released from dopaminergic neurons  

  • ACh is an excitatory neurotransmitter released from cholinergic neurons  

  • DA normally maintains control over ACh and inhibits its excitatory response  


16
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dopamine movement connection in parkinson disease

  • Unexplained degeneration of dopaminergic neurons occurs 3 

  • With less DA production, the excitatory response of ACh exceeds the inhibitory response of DA3 

  • Excessive ACh stimulates neurons that release gamma-aminobutyric acid (GABA) 3 

  • With increased GABA stimulation, the symptomatic movement disorders of PD occur 


17
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The cardinal symptoms resulting from dopamine depletion include: 

  • Rigidity (abnormal increased muscle tone) 

  • Tremors (involuntary movements, often at rest) 

  • Gait disturbances (shuffling gait, absence of arm swing) 

  • Bradykinesia (slow movement) 


18
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The Problem with Levodopa Alone

  • The blood-brain barrier admits levodopa but not DA 2 

  • The enzyme dopa decarboxylase converts levodopa to DA, but this enzyme exists in both the brain AND peripheral nervous system 2 

  • 99% of levodopa is converted to DA before reaching the brain2 

  • Only about 1% reaches the brain, requiring large doses that cause significant side effects  


19
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how carbidopa helps levodopa

  • Carbidopa inhibits the enzyme dopa decarboxylase in the peripheral nervous system 

  • By blocking peripheral conversion, more levodopa reaches the brain 

  • Once in the brain, levodopa is converted to DA, which the striatal neurons can use  

  • The combination allows smaller doses of levodopa to achieve the desired effect  

  • More DA becomes available to restore the balance between DA and ACh, improving motor control 


20
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The carbidopa-levodopa combination directly addresses

the underlying dopamine depletion, helping restore the neurotransmitter balance needed for normal motor function. 

21
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Which findings indicate that carbidopa-levodopa is effective

  • Decreased rigidity (reduced muscle stiffness) 

  • Reduced tremors (less involuntary shaking) 

  • Improved mobility and gait (better walking pattern, return of arm swing) 

  • Decreased bradykinesia (faster, smoother movements) 

  • Improved facial expression (less masked facies) 

  • Enhanced ability to perform activities of daily living 

  • Fewer "off episodes" (periods when symptoms return between doses)  

 

22
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adverse gastrointestinal effects requiring monitoring for carbidopa-levodopa

  • Nausea and vomiting are common because DA stimulates the chemoreceptor trigger zone (CTZ) in the medulla  

  • Anorexia and GI disturbances  


23
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adverse movement disorder effects requiring monitoring for carbidopa-levodopa

  • Dyskinesia (impaired voluntary movement) may occur with high levodopa dosages  

  • Dystonic movement (involuntary abnormal movement)  


24
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adverse cardiovascular effects requiring monitoring for carbidopa-levodopa

  • Orthostatic hypotension (especially during early use)  

  • Increased heart rate during early use  

  • Palpitations and angioedema  

 

25
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adverse neuropsychiatric effects requiring monitoring for carbidopa-levodopa

  • Psychotic behavior 

  • Nightmares  

  • Sudden sleep onset (falling asleep without warning)  

  • Mental disturbances  

  • Impulse control symptoms 

  • Suicidal tendencies 


26
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What administration teaching should accompany carbidopa-levodopa? 

Patients should take with food to enhance absorption and reduce gastric irritation, and avoiding high protein meals may improve medication effectiveness. Never double doses or take extra medication.

 

27
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What safety teaching should accompany carbidopa-levodopa regarding cardiovascular precautions? 

  • Orthostatic hypotension can occur, especially during early use 

  • Change positions slowly (lying to sitting to standing) 

  • Report palpitations, dizziness, or fainting  


28
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What safety teaching should accompany carbidopa-levodopa regarding movement and activity safety? 

  • Dyskinesia (impaired voluntary movement) may develop with high doses  

  • Sudden sleep onset can occur without warning during activities of daily living  

  • Avoid driving or operating dangerous machinery until response to medication is established 

  • Report involuntary movements or sudden sleep episodes immediately 


29
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What safety teaching should accompany carbidopa-levodopa regarding neuropsychiatric monitoring? 

  • Watch for psychotic behavior, hallucinations, nightmares, or mental disturbances 

  • Report impulse control symptoms (compulsive behaviors like gambling, shopping, eating)  

  • Monitor for suicidal thoughts  

  • Confusion and restlessness may occur, especially in older adults 

 

30
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How does benztropine reduce selected Parkinson symptoms?

by restoring the balance between dopamine and acetylcholine in the brain, thereby alleviating tremors and rigidity.

31
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Common Anticholinergic Side Effects

  • Dry mouth and dry secretions 

  • Urinary retention (decreased bladder contraction)  

  • Constipation (decreased GI motility)  

  • Blurred vision (pupil dilation/mydriasis)  

  • Increased heart rate 


32
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Central Nervous System Effects for Benztropine

  • Restlessness and confusion may occur in older adults 2 

  • Mental disturbances 


33
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Medication Interactions and Precautions for Benztropine

Avoid Combining with: 

  • Other anticholinergic medications (additive effects increase risk of toxicity) 

  • CNS depressants (can enhance sedative effects) 

 

34
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Why are acetylcholinesterase inhibitors such as donepezil and rivastigmine are used in Alzheimer disease? The Problem in Alzheimer Disease: 

Acetylcholinesterase (AChE) is an enzyme responsible for breaking down acetylcholine (ACh). In Alzheimer disease, this breakdown reduces the available ACh needed for cognitive function. 

35
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How AChE inhibitors work in alzheimer patients

AChE inhibitors like donepezil and rivastigmine block the enzyme that breaks down ACh, permitting more ACh in the neuron receptors. By increasing ACh at the cholinergic synapses, cholinergic transmission is increased, which helps improve cognitive function. 

36
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What Families Should Understand About Expected Outcomes of AChE Inhibitors for Alzheimers

Realistic Expectations - Symptom Management, Not Cure: 

  • These medications increase cognitive function for patients with mild to moderate AD 

  • They may slow the disease process  

  • These drugs do not delay progression of AD 

  • There is no cure for AD 


37
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Which adverse effects should be monitored with AChE Inhibitors for Alzheimer Disease treatment

  • Monitor for GI distress (most common side effects) 

  • Assess liver function, especially with rivastigmine 

  • Watch for signs of bradycardia or cardiac irregularities 

  • Monitor older adults closely for cumulative effects 

  • Assess for respiratory changes 

  • Note any changes in urination patterns 

 

38
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How do AChE inhibitors improve muscle strength in myasthenia gravis?

They block acetylcholinesterase, so acetylcholine is not broken down as quickly. This leaves more ACh at the neuromuscular junction for longer, allowing it to bind to the remaining ACh receptors and improve muscle contraction.

39
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What happens to acetylcholine at the neuromuscular junction when an AChE inhibitor is given?

ACh builds up and stays available longer because its breakdown is inhibited.

40
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Why does having more ACh help in myasthenia gravis?

MG causes a reduced number of functional ACh receptors, so keeping more ACh around increases the chance that it will bind to the receptors that remain.

41
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What is the end result of AChE inhibitor therapy in MG?

Improved neuromuscular transmission and increased skeletal muscle strength.

42
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Which findings demonstrate a therapeutic response to AChE Inhibitors in MG

  • Increased muscle strength 

  • Reduced ptosis (drooping eyelids) 

  • Improved extraocular muscle function (less diplopia) 

  • Better ability to chew and swallow 

  • Improved respiratory muscle function 

  • Reduced generalized muscle weakness 


43
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which findings suggest excessive cholinergic stimulation? 

SLUDGE/DUMBELS Symptoms: 

  • Increased salivation (drooling) 

  • Excessive sweating 

  • Increased bronchial secretions 

  • Miosis (abnormal pupil constriction)  

  • Bradycardia 

  • Abdominal pain and cramping 

  • Nausea and vomiting  

  • Diarrhea  

  • Hypotension  

  • Fasciculations (involuntary muscle twitching)  

  • Pallor and vertigo  


44
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For acute painful skeletal muscle spasm, identify the expected role of a skeletal muscle relaxant

are used to: 

  • Decrease pain 

  • Increase range of motion 

  • Relieve muscular spasms associated with traumatic injuries  


45
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skeletal muscle relaxant work by

depressing neuron activity in the spinal cord or brain and enhancing neuronal inhibition of skeletal muscles

46
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safety teaching of skeletal muscle relaxants

includes advising patients about potential drowsiness, avoiding alcohol, dependency risk. and not operating heavy machinery while on these medications.

47
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Explain how alemtuzumab affects immune activity in multiple sclerosis

Alemtuzumab works by targeting and depleting CD52-expressing lymphocytes, reducing immune activity against myelin in multiple sclerosis. This results in decreased inflammation and potential slowing of disease progression.

48
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expected benefits of Alemtuzumab

  • Reduction in MS relapses 

  • Slowing of disease progression 

  • Used for relapsing forms of MS 

  • More effective in blood and bone marrow disease 


49
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infection risk due to Alemtuzumab

Severe Infection Risk Due to Lymphopenia: 

  • Severe lymphopenia increases infection risk significantly 

  • Prolonged immunosuppression and myelosuppression 

  • Patients are vulnerable to opportunistic infections 

  • Risk of fatal infections exists 

 

Additional Serious Risks: 

  • Fatal autoimmune pancytopenia 

  • Prolonged myelosuppression  

 

50
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common side effects of Alemtuzumab

  • Fatigue (most common non-infusion-related effect)  

  • Flu-like symptoms 

  • Nausea, blood pressure changes, hyperglycemia, hypoxia  


51
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safety instructions for Alemtuzumab

  • Report any signs of infection immediately (fever, chills, sore throat, unusual bruising/bleeding) 

  • Monitor for cardiac symptoms: arrhythmias, heart failure signs, decreased exercise tolerance  

  • Watch for bleeding or bruising (pancytopenia risk) 

  • Attend all scheduled lab appointments for blood count monitoring 

  • Avoid crowds and people with infections 

  • Practice good hand hygiene 

  • Do not receive live vaccines during treatment 


52
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cardiac monitoring for Alemtuzumab

  • Report palpitations, chest pain, or shortness of breath 

  • Risk of arrhythmias, heart failure, cardiomyopathy, and decreased ejection fraction