PHARM 1 EXAM #3 Flashcards
Neurotransmitters (NTs) + Receptors + Enzymes in Sympathetic vs Parasympathetic Nervous Systems
Sympathetic Nervous System (SNS)
NTs: Norepinephrine, Epinephrine, Dopamine
Receptors: a1, a2, b1, b2
Enzymes: Monoamine Oxidase (MAO), Catechol-O-Methyltransferase (COMT)
Parasympathetic Nervous System (PNS)
NTs: Acetylcholine (ACh)
Receptors: muscarnic, nicotinic
Enzymes: Acetylcholinesterase (ACh-ase)
What is Alzheimer’s Disease (AD)?
Alzheimer’s disease (AD) is characterized by progressive memory loss, impaired thinking, personality changes (neuropsychiatric symptoms), and inability to perform routine tasks of daily living.
Symptoms of Alzheimer’s Disease
— Memory loss
— Confusion
— Inability to communicate
— Aggressive behavior
— Depression
— Psychoses
— Progression to loss of memory, logical thinking, and judgment; time disorientation; personality changes; hyperactivity; tendency to wander; inability to express oneself; and later hostility, paranoia
Pathophysiology of Alzheimer’s disease
— Incurable dementia illness
— Chronic, progressive neurodegenerative conditions
— Marked cognitive dysfunction
— Onset usually occurs between ages 45 and 65 years, risk increases after 65.
— Neuritic plaques form (outside of neurons)
— Neurofibrillary tangles are in neurons.
— Cholinergic neurotransmitter abnormality
Which are the most common degenerative diseases of nerves?
1st = Alzheimer’s Disease
2nd = Parkinson’s Disease (PD)
Summarize the pathophysiology of Parkinsonism
Parkinson’s:
– Chronic neurologic disorder
– Imbalance of the neurotransmitters dopamine (DA) and acetylcholine (ACh)
– Marked by degeneration of neurons of the
extrapyramidal motor tract
– Reason for the degeneration of neurons is
unknown
Characteristics of Parkinsonism
– Tremors of head, neck, and limbs
– Rigidity (increased muscle tone)
– Bradykinesia (slow movement)
– Postural changes: head and chest thrown forward
– Shuffling walk
– Lack of facial expression
– Pill-rolling motion of hands
– Common non-motor symptoms: depression,
psychosis, dementia, sleep disturbances
Differences between depression vs. psychosis
Depression — lack of motivation, disinterest; “blah” feeling..don’t care
Psychosis — lack of being in touch with reality; hallucinations, paranoia present
What are the treatments (Tx) regimens for Parkinsonism?
– Anticholinergics
– Dopaminergics
– Dopamine agonists
– MAO-B inhibitors
– COMT inhibitors
Action of Anticholinergics in treatment of Parkinson’s Disease
oldest drugs used as treatment
— Inhibits release of acetylcholine (ACh); parasympatholytic
— Blocks cholinergic receptors in order to push the ACh influence down in CNS, which helps to restore the balance of ACh + Dopamine in the body
— Reduce the rigidity and some of the tremors characteristic of parkinsonism
— Minimal effect on bradykinesia
— Used to treat drug-induced parkinsonism, or pseudoparkinsonism
NON-DRUG Tx for Mirgraines
Adequate sleep
Exercise
Avoiding triggers
Once headache begins
Quiet, dark room with ice pack to neck
Supplements
Riboflavin (Vitamin B2)
Coenzyme Q-10
Feverfew
Butterbur
Interventions for taking Anticholinergic Drugs
— Counsel patients who take an anticholinergic to have routine eye exams because anticholinergics are contraindicated in patients with glaucoma.
— Encourage patients to relieve a dry mouth with hard candy, ice chips, or sugarless gum.
— Monitor urine output (I&Os) for early detection of urinary retention.
— Increase fluid intake, fiber, and exercise to avoid constipation.
Antiparkinsonism Drugs RN Interventions
— Monitor for orthostatic hypotension.
— Administer drug with low-protein foods.
— Avoid vitamin B6, alcohol, other depressants.
— Do not abruptly discontinue
— Warn of harmless brown discoloration of urine and sweat.
— Assess for suicidal tendencies.
— Assess symptom status and “on-off” phenomenon.
— Monitor blood cell counts, liver and kidney function.
Correlation with protein-rich foods + Medication + Parkinson’s Disease
— Food does slow drug absorption.
— High-protein foods interfere with drug transport to CNS.
— Foods high in vitamin B6 include lima, navy, kidney beans; cereals.
— Vitamin B6 inhibits conversion of levodopa to dopamine.
— A conservative amount of vitamin B6 is needed to prevent vitamin B6 deficiency (peripheral neuritis, muscle weakness).
— want low protein foods with PD medications
Actions of Dopaminergics in treatment of Parkinson’s Disease
— Converts to dopamine
— A mimetic that mimics dopamine and becomes dopamine in the body
Centrally Acting Anticholinergics: Benztropine (Cogentin) + Trihexyphenidyl (Artane)
— Reduce tremor and possibly rigidity
— No reduction of bradykinesia
— Less effective than levodopa or the dopamine agonists but better tolerated
— Used as second-line therapy for tremor
— Most appropriate for younger patients with mild symptoms
— Avoided in the elderly, who are intolerant of CNS side effects (for example, sedation, confusion, delusions, hallucinations)
Action of Dopamine Agonists in treatment of Parkinson’s Disease + Drugs
— Converted to dopamine and stimulates receptors to increase mobility
E.g. Carbidopa-levodopa (Sinemet)
Advantages of combining Carbidopa/Levodopa
More dopamine reaches the basal ganglia and that smaller doses of levodopa are required to achieve the desired effect
Contraindications to Dopaminergic therapy (carbidopa/levodopa (Sinemet))
— Narrow-angle glaucoma; severe cardiac, renal, hepatic disease; and suspicious skin lesions (activates malignant melanoma).
— Has a short half-life and must be taken 3-4 times per day
Side effects of Dopaminergics In Antiparkinsonism drugs
— Fatigue, insomnia
— Dry mouth
— Blurred vision
— Orthostatic hypotension, palpitations, dysrhythmias
— Urinary retention
— GI disturbance: nausea, vomiting
— Dyskinesia, psychosis, severe depression
Drug interaction with Carbidopa-levodopa (Sinemet) in Dopaminergics
Decrease levodopa effect with:
— Anticholinergics
— Phenytoin
— Tricyclic antidepressants
— MAO inhibitors
— Benzodiazepines (works in CNS)
— Phenothiazines (works CNS)
— Vitamin B6
Because PD patients have too much ACh, there will be an imbalance of ACh + dopamine levels r/t dopamine becoming less effective if taken concurrently
Side effects for Anticholinergics
Dizziness, drowsiness, anxiety, headache
Insomnia, paresthesia, restlessness
Blurred vision, ocular hypertension
Weakness, dry mouth, GI distress
Anhidrosis, urinary retention
”Can’t see, can’t spit, can’t pee, can’t sht!”*
Action of MAO-B Inhibitors in treatment of Parkinson’s Disease
MAO-I = Monoamine Oxidase B Inhibitors
— Inhibit MAO-B enzyme that interferes with dopamine
— MAO = enzyme that breaks down NTs in the peripheral nervous system (PNS)
— MAO-B = enzyme that breaks down dopamine, therefore if we inhibit the enzyme —> an increase availability of dopamine in the CNS
COMT inhibitors in the treatment of Parkinson
— Inhibit COMT enzyme that inactivates dopamine
— By stopping the breakdown of dopamine in the CNS + peripheral[P]NS in order to improve the effects of dopamine bioavailability
Side Effects for MAO-Is Selegiline + Parkinson’s Disease
— Dizziness, headache, nausea, dry mouth
— Orthostatic hypotension, hypertension
— Impulse control disorder, suicidal ideation
— Not as popular, but an option
_Interaction: foods high in tyramine can cause hypertensive crisis; hard to manage
Side Effects for COMT-Inhibitor + Parkinson’s Disease
COMT-I = Catechol-O-Methyltransferase Inhibitors
Drug: Tolcapone
— Dizziness, drowsiness, headache
— GI distress, excess dreams
— Insomnia, sudden sleep onset
— Orthostatic hypotension
— Impulse control disorder
— Hepatic dysfunction
Other than dyskinesia, name the non-motor symptoms that arise in patients with Parkinson’s Disease
— Depression
— Psychosis and dementia
— Sleep disturbances
90% of patients develop these nonmotor symptoms
What are some non-pharmacological treatments for Parkinson’s Disease?
— Exercise
— Balanced diet
— Support group
Compare the side effects of various anti-Parkinsonism drugs
Combination Preparation differences between Sinemet + Stalevo
levodopa/carbidopa (Sinemet)
— Carbidopa has no therapeutic effects of its own, but makes levodopa more available to the CNS, allowing the dosage of levodopa to be reduced by about 75%
** By combining carbidopa with levodopa, carbidopa can inhibit the enzyme decarboxylase in the periphery, thereby allowing more levodopa to reach the brain.**
levodopa/carbidopa/entacapone (Stalevo)
— Entacapone (Comtan) prolongs plasma level of levidopa/carbidopa, so if the effect of Simemet is wearing off entacapone can be added
Contraindications of MAO-Is + Parkinson’s
Can cause a hypertensive crisis when given within 2 weeks of levodopa
Apply the nursing process to anticholinergics, dopaminergics, and acetylcholinesterase
inhibitors
What is the contraindications when having a high-protein diet while taking Antiparkinson’s drugs?
— A high protein diet impairs levodopa absorption and transport across BBB
— High protein meal can trigger an “off” episode, where it appears a patient is “off” their meds, but they aren’t
Differentiate the phases of Alzheimer’s disease with corresponding symptoms
Side Effects + Adverse Rxns of Rivastigmine (Exelon)
Drug = Acetylcholinesterase Inhibitors/Cholinesterase Inhibitor
Side effects:
— Anorexia, nausea, vomiting, diarrhea, constipation, abdominal pain, GI bleeding, dizziness, depression, peripheral edema, dry mouth, dehydration, restless legs syndrome, nystagmus
Adverse reactions
— Seizures, bradycardia, orthostatic hypotension, cataracts, myocardial infarction, heart failure
Compare the side effects/adverse effects of acetylcholinesterase inhibitors that are used to
treat Alzheimer’s disease
Contrast the pathophysiology of myasthenia gravis and multiple sclerosis
Discuss the drug group used to treat myasthenia gravis
Discuss the drug group used to treat multiple sclerosis
— Immunomodulators: 1st-line Tx; slows disease progression and prevents relapses
— Immunosuppressants
— Sphingosine 1-phosphate receptor modulator (for worsening)
— Monoclonal antibody (made in lab + specific to d/o)
— Corticosteroids: reduces edema and acute inflammation
Immunomodulators
Administered by self-injection (IM, SubQ)
— Interferon beta (Avonex, Rebif); has flulike S/Sx
— Glatiramer acetate (Copaxone): gets severe chest pain, but WILL go away
IV infusion
— Natalizumab (Tysabri)
Differentiate between the muscle relaxants used for spasticity and those used for muscle
spasms
Spasticity
— tightening of muscle b/c of MS, stroke, TBI, SCI , trauma in nervous system causing this (neurologic impairment/disorder)
Meds: Baclofen (Lioresal); Tizanidine (Zanaflex)
Muscle spasms
— pull your back and muscle tightens up d/t trauma, injury, overuse
Meds: Dantrolene Sodium (Dantrium)
Skeletal Muscle Relaxants: Cyclobenzaprine (Flexaril)
Action
— Relax skeletal muscles
Use
— Relieves muscle spasms
Side Effects
—Anticholinergic effects (blurred vision, dry mouth, tachycardia, urine retention, constipation)
— Drowsiness, dizziness, headache, nervousness
— GI distress, unpleasant taste
— Dysrhythmias
contraindicated if patient has cardiovascular disorders, hyperthyroidism, hepatic impairment, or taking concurrent MAOIs. The nurse should note if there is a history of narrow-angle glaucoma or MG. Cyclobenzaprine is contraindicated with these health problems.
RN Interventions for Cyclobenzaprine (Flexaril)
— Observe for CNS side effects = drowsiness
— Teach patient not to stop abruptly but taper off over 1 week.
— Teach patient to avoid alcohol and CNS depressants.
— Take with food.
—Monitor liver function
— Check vital signs.
— Advise patient not to drive
— No EtOH + smoking
— Inform patient that most centrally acting muscle relaxants are prescribed for no longer than 3 weeks (NOT LONG TERM)
Determine the 2 ways of treating and affecting change in neuromuscular disorders
If your muscle is tight:
1) change in brain (centrally acting spasticity)
—Baclofen (Lioresal)
— Tizanidine (Zanaflex)
2) change at neuromuscular junction (direct acting spasticity)
— Dantrolene sodium (Dantrium)
Apply the nursing process to drugs used to treat myasthenia gravis and muscle spasms
Explain the pathophysiologic basis of five cardinal signs of inflammation
Compare the action of various nonsteroidal antiinflammatory drugs (NSAIDs)
Explain the use of disease-modifying antirheumatic drugs (DMARDs)
Differentiate between the side effects and adverse reactions of NSAIDs and DMARDs
Correlate the nursing processes associated with NSAIDs and corticosteroids, including
patient teaching
Apply the nursing process to the patient taking DMARDs
Compare the action of various antigout medications
Differentiate between acute and chronic pain
Compare indications for nonopioid and opioid analgesics
Describe the serum therapeutic ranges of aspirin and acetaminophen. Identify the recommended
maximum daily dosage of acetaminophen
Contrast the side effects of aspirin and opioids
Explain the methadone treatment program
Discuss nursing interventions and patient teaching related to nonopioid and opioid analgesics
Apply the nursing process to the patient with patient-controlled analgesia (PCA)
Discuss nursing implications and pharmacotherapy related to tension, cluster, and migraine headaches
Drugs that treat cluster + migraine headaches
Analgesics
Aspirin (caffeine), acetaminophen
NSAIDs: ibuprofen, naproxen (Aleve)
Opioid analgesics
Meperidine (Demerol)
Butorphanol nasal spray (Stadol NS)
Ergot alkaloids
Dihydroergotamine mesylate (Migranal) – IV, IM, subQ, nasal
Selective serotonin1 receptor agonists [triptans]
Sumatriptan (Imitrex)
Zolmitriptan (Zomig)
Discuss the differences between tension, cluster, migraine headaches
Tension —
Cluster — Severe unilateral nonthrobbing pain; usually located around the eye
Migraine — a neurovascular disorder involving dilation and inflammation of intracranial arteries.
Side Effects for COMT-Inhibitor + Parkinson’s Disease
