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During an active tonic-clonic seizure, which nursing actions take priority?
positioning
airway protection
environmental safety
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
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
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
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
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
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
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
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
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.
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.
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
Findings requiring prompt provider notification when antiseizure medications are abruptly stopped?
signs of toxicity
inadequate seizure control
respiratory depression
withdrawal symptoms
parkinsons disease results from
an imbalance between dopamine (DA) and acetylcholine (ACh) caused by degeneration of neurons in the substantia nigra of the midbrain
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
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
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)
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
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
The carbidopa-levodopa combination directly addresses
the underlying dopamine depletion, helping restore the neurotransmitter balance needed for normal motor function.
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)
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
adverse movement disorder effects requiring monitoring for carbidopa-levodopa
Dyskinesia (impaired voluntary movement) may occur with high levodopa dosages
Dystonic movement (involuntary abnormal movement)
adverse cardiovascular effects requiring monitoring for carbidopa-levodopa
Orthostatic hypotension (especially during early use)
Increased heart rate during early use
Palpitations and angioedema
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
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.
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
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
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
How does benztropine reduce selected Parkinson symptoms?
by restoring the balance between dopamine and acetylcholine in the brain, thereby alleviating tremors and rigidity.
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
Central Nervous System Effects for Benztropine
Restlessness and confusion may occur in older adults 2
Mental disturbances
Medication Interactions and Precautions for Benztropine
Avoid Combining with:
Other anticholinergic medications (additive effects increase risk of toxicity)
CNS depressants (can enhance sedative effects)
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.
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.
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
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
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.
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.
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.
What is the end result of AChE inhibitor therapy in MG?
Improved neuromuscular transmission and increased skeletal muscle strength.
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
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
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
skeletal muscle relaxant work by
depressing neuron activity in the spinal cord or brain and enhancing neuronal inhibition of skeletal muscles
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.
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.
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
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
common side effects of Alemtuzumab
Fatigue (most common non-infusion-related effect)
Flu-like symptoms
Nausea, blood pressure changes, hyperglycemia, hypoxia
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
cardiac monitoring for Alemtuzumab
Report palpitations, chest pain, or shortness of breath
Risk of arrhythmias, heart failure, cardiomyopathy, and decreased ejection fraction