PHARM 1 EXAM #3 Flashcards by LYNSE AMBERS

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)

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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.

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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

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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

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Which are the most common degenerative diseases of nerves?

1st = Alzheimer’s Disease
2nd = Parkinson’s Disease (PD)

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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

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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

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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

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What are the treatments (Tx) regimens for Parkinsonism?

– Anticholinergics
– Dopaminergics
– Dopamine agonists
– MAO-B inhibitors
– COMT inhibitors

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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

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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

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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.

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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.

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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

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Actions of Dopaminergics in treatment of Parkinson’s Disease

— Converts to dopamine
— A mimetic that mimics dopamine and becomes dopamine in the body

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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)

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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)

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Advantages of combining Carbidopa/Levodopa

More dopamine reaches the basal ganglia and that smaller doses of levodopa are required to achieve the desired effect

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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

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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

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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

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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!”*

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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

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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

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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