ch1 module 1 review

parkinson’s cause

primary - not known, combo of genetic & environmental factors

secondary - antipsychotic drugs or another condition such as brain tumor or trauma

parkinson’s patho

chronic, terminal disease

degeneration of substantia nigra cells in the basal ganglia

decrease dopamine (helps promote voluntary muscle & sympathetic nervous system control)

works opposite acetylcholine

parkinson’s disease course

steady & gradual decline (10-20 years)

cognitive, mobility & ADL function from mild-severe

patients die from complications of immobility

4 cardinal symptoms: tremor, muscle rigidity, bradykinesia, postural instability, difficulty chewing, swallowing, drooling

• mask-like blank expression, pill-rolling tremors

• resting tremor in upper extremities

• emotional/speech changes

• bowel/bladder changes

parkinson’s risk factors

primary - male, >40 y/o, family hx, exposure to chemicals & metals

secondary - tbi, brain tumor or other lesion

parkinson’s incidence & prevalence

more men than women, less in black population

parkinson’s labs/diagnostics

no specific diagnostic tests

may do CSF, MRI or SPECT

what is levodopa/carbadopa

levodopa is converted to dopamine in brain, carbidopa is combined to decrease its breakdown (used for parkinson’s)

what are anticholinergics

treat tremors; watch out for dry mouth, constipation, urinary retention, acute confusion (used for parkinson’s)

ex. trihexyphenidyl & benztropine (used for parkinson’s)

what are antivirals

amantadine; stimulate the release of dopamine & prevent it's reuptake (used for parkinson’s)

what are monoamine oxidase type b (MAO-B) inhibitors

Selegiline taken with levodopa, increases dopamine levels; avoid foods with tyramine (used for parkinson’s)

what should patients know about taking MAOIs (selegiline)

avoid foods, beverages, drugs that contain tyramine (cheese & aged, smoked or cured foods and sausage, red wine and beer) to prevent severe headache and life-threatening hypertension

• patients should continue restrictions for 14 days after drug is discontinued

what are catechol-o methyltransferanse (COMT) inhibitors

Entacapone taken with levodopa to decrease its breakdown; dark urine is normal (used for parkinson’s)

what is dopamine agonists

pramipexole/ropinirole activate release of dopamine; can cause orthostatic hypotension, drowsiness, dyskinesias & hallucinations (used for parkinson’s)

parkinson’s procedures

ablative procedures - destroys a small portion of the globus pallidus; thalamotomy, pallidotomy

deep brain stimulation (DBS) - surgical choice, electrode implanted in the thalamus; current delivered through generator. decreases tremors & involuntary movements

cell transplantation - fetal tissue transplants are experimental

parkinson’s complications

aspiration pneumonia (swallowing precautions, pt/ot, dietary/speech consult)

altered cognition

parkinson’s nursing care

(afe environment, freeze gait issue, adls/independence maintenance, extra time for activities, fostering communication for depression, self-esteem

huntington’s cause

hereditary, autosomal-dominant trait at conception

huntington’s patho

chronic, terminal disease

alterations in dopamine, GABA and glutamate from the basal ganglia

huntington’s disease course

gradual decline (typically about 15 years)

cognitive & neuromuscular symptoms

characterized by progressive dementia & choreiform movements (uncontrollable rapid, jerky movements) in the limbs, trunk & facial muscles; patients usually die from complications of impaired mobility

huntington’s risk factors

dominant inheritance

30-50 years of age equally in men and women (when symptoms typically begin)

huntington’s labs/diagnostics

hd genetic test - gene present?

CT scans - frontal horn enlargement

MRI & PET

huntington’s medications

tetrabenazine - suppress involuntary chorea movements; SE - new/worse depression, drowsiness, nausea & restlessness

other antipsychotics may be used for psych symptoms

huntington’s procedures

no neuroprotective/neurorestortative treatment available

main medical management : supportive & symptomatic treatment

huntington’s complication

altered cognition (dementia, memory), mobility, aspiration pneumonia

huntington’s nursing care

emphasis on maintaining independence, exercise, yoga, assistive devices, ROM exercises, pace activities, foster communication, allow extra time to answer questions, pt/ot, drug therapy

huntington’s care coordination

decisional conflict r/t to have children

aspiration pneumonia

suicide prevention with depression

encourage 3 meals/day (dietary supplements may be necessary)

eventually help with ADLs, confined to bed & unable to speak

encourage planning for residential and EOL care

ALS (lou gehrig’s disease) patho

chronic, progressive, neurogenerative but NOT autoimmune

NO CURE and FATAL

targets the CNS & brain

loss of voluntary movement control, weakness (spasticity & flaccidity)

patients suffer from lack of physical ability

ALS risk

unknown could be genetic or environmental

ALS disease course

most die within 3-5 years when symptoms first start, only about 10% survive for 10 or more years

causes progressive muscle weakness & wasting. clients lose ability to speak, eat, move & eventually breathe (paralysis of respiratory muscles)

ALS expected findings

fatigue, muscle atrophy (wasting away, including tongue) & muscle weakness followed by spasticity & hyperactive reflexes

twitching (fasciculations) of face and tongue

dysarthria (uncoordinated or slurred speech)

dysphagia, stiff & clumsy gait

ALS prevalence

rare (40-60 y/o) more common in men

ALS labs & diagnostics

no definitive test to confirm the presence

diagnosis based on medical history, neurological examination, symptoms

lab tests to rule out other metabolic conditions

ALS medications

non-curable, drugs may improve quality of life but have limited ability to extend life

ex. muscle relaxants

what is edaravone

ALS; reduces oxidative stress. SE; blisters, itching, skin irriation, cough, confusion, tachycardia, weakness, easy bruising, GI disturbances, DIB. AE; glycosuria, respiratory failure

what are riluzole

reduces molecular stimulation preventing overstimulation & brain damage. SE; tachycardia, edema, dizziness, drowsiness, GI disturbances. AE; liver toxicity, DIB, rash, muscle/joint pain (used for ALS)

ALS complications

death anxiety - impending progressive loss of function leading to death

ineffective breathing pattern r/t compromised respiratory function

ALS nursing care

palliative care for symptom management, home health care, EOL planning, hospice

psychosocial support

multiple sclerosis patho

chronic, progressive, neurogenerative IS an autoimmune disease

NO CURE and NOT fatal

targets the brain & spinal cord (myelin sheath)

demyelination of white matter leads to decreased flow of nerve impulses

patient suffer from more cognitive dysfunction than those w ALS

sx worse in extreme heat & cold, stress, infection, fatigue, pregnancy

remissions & exacerbations

multiple sclerosis etiology

multiple factors, changes in immunity most likely, cold climates

multiple sclerosis disease course

no cure, progressive in severity, may progress to tetraplegia; normal life expectancy.

multiple sclerosis expected findings

fatigue, muscle spasticity

blurred or double vision (diplopia)

scrotomas (patches of blindness in peripheral vision)

uhthoff’s sign (temp bad vision usually after exertion or when exposed to heat)

nystagmus, tinnitus

pain or parethesia

hypoalgesia (sensitivity to pain)

areflexic (flaccid) or spastic bladder

sexual dysfunction

intention tremors (when performing activity), changes in gait

multiple sclerosis prevalence

ages 20-50, more common in whites and women (2x as likely)

multiple sclerosis labs & diagnostics

CSF reveals elevated protein level, slight increase in WBCs, IgG

MRI plaques of the brain and spine

evoke potential testing (give stimulation & see if sense is decreased)

multiple sclerosis medications

immunosuppressants/anti-inflammatories (secondary infections)

• interferon beta 1a/1b - immunomodulator with antiviral effects; watch out for flu-like symptoms

what are baclofen, dantrolene, diazepam

muscle relaxants - avoid stopping abruptly (MS)

what is dexamethasone (decadron)

steroid anti-inflammatory for managing relapses (infection, hyperglycemia, don’t stop abruptly) (MS)

what does medical marijuana do for MS

decreases spasticity, muscle stiffness & pain (can cause mental decline & dizziness)

glatiramer acetate side effects

injection site rxn, GI disturbances, weight gain, confusion/nervousness, depression, edema, difficulty swallowing, excessive sweating, rash, flu-like symptoms (MS)

multiple sclerosis complications

neurosensory/motor function baseline (w exacerbations may not recover 100% of the function)

multiple sclerosis nursing care

psychosocial support - depression, emotional lability

uti prevention (hydration, bathroom schedule); bowel & bladder training

eye patches for diplopia

activity planing for energy conservation

exercise planning to avoid fatigue & overheating

swallowing precautions

decrease risk of injuries (safe environment, no high impact activities), PT/OT

remain free of infection, maintains adequate visual acuity & cognition

sinus headache

pain is behind browbone and/or cheekbones

cluster headache

pain is in and around one eye

accompanied by ipsilateral sx: conjunctival hyperemia (bloodshot eyes), rhinorrhea & nasal congestion, swelling around eye, ptosis

pacing or agitation

cluster headaches patho

trigeminovascular system activation, trigeminal-autonomic reflex, posterior hypothalamus activation

tension headache

pain is like a band squeezing the head

treated with rest, hydration, & OTC pain meds

migraine headache

pain, nausea, fatigue & visual changes are typical classic forms

treated w/ rest, isolation in dark quiet space & OTC or RX (opioids & triptans)

migraine patho

recurrent episodic head pain (lasts 4-72hrs)

throbbing, intense, unilateral pain

can be accompanied by nausea, light/sound sensitivity

genetics & triggers

cerebral artery vasodilation → prostaglandins released → brain tissue inflammation

migraine expected findings

photophobia & phonophobia

nausea & vomiting

stress & anxiety

unilateral pain (often behind one eye or ear)

hx of headaches (family)

alterations in ADLS (4-72hr)

migraine with aura (classic)

prodromal stage → aware it’s coming before onset: irritated, depressed, food cravings, bowel issues & freq urination

aura stage → min-hr numbness & tingling of mouth, lips, face or hands; acute confusion, vision prob (light flashes, bright spots)

second stage → severe, incapacitating, throbbing HA → gets worse over time w/ n/v/drowsiness, vertigo

third stage → 4-72hr, dull

recovery → pain and aura subsides. muscle aches & contraction of head and neck muscles are common. physical activity worsens pain and client might sleep

older adult → can experience an aura without pain (visual migraine)

migraine without aura (common)

pain is aggravated by physical activity

unilateral, pulsating pain

one or more manifestations present; photophobia, phonophobia, n/v

persists for 4-72hr; often occurs in early AM during stress or with premenstrual tension or fluid retention

atypical migraine

• status migrainous >72hr

• migrainous infarction: neuro symp for 7 days; imaging may indicate ischemic infarct

• unclassified: does not fit other criteria

migraine risk factors

all ages (women>men)

overweight/obesity

fasting/low blood glucose

high bp, cholesterol

hx of stroke or CAD

psych disorders (depression, anxiety)

birth control, some drugs (opiates, barbiturates, triptans can develop into migraines)

migraine labs & diagnostics

neuroimaging if neuro symptoms are present or >50 y/o new onset

CT/MRI/EEG (r/p other diagnoses like tumor, MS, aneurism)

migraine prevention (oral)

beta blockers: propranolol, metoprolol, timolol, atenolol

- reduces adrenergic tone, norepinephrine release & synthesis & inhibits b-adrenergic receptors

AE: bradycardia, bronchospasm, depression, dizziness, fatigue, impotence

migraine prevention (injection)

onabotulinumtoxin A - inhibits neurotransmitter release from presynaptic nerve endings

AE: muscle paralysis

migraine avoidance and management

tyramine-containing foods (pickled products, aged cheeses, wine), preservatives & artifical sweeteners, diary with exposures & migraine history

mild migraine abortive therapy

initiate during the aura phase or as soon headache starts:

• NSAIDS (ibuprofen, naproxen) aceptaminophen

• antiemetics (metoclopramide) for n/v

severe migraine abortive therapy

• triptan preparations (sumatriptan, zolmitriptan, eletriptan) to produce vasoconstrictive effect

• ergotamine preparations with caffeine (dihydroergotamine) to narrow blood vessels & reduce inflammation

• isometheptene (vasoconstriction) in combination with caffeine when others meds don’t work

nonpharmacologic migraine interventions

avoid: medication overuse, try to limit analgesic medications to 2-3x/week

supplements: magnesium, riboflavin, melatonin, coq10

provide dark, quiet environment, avoid environmental odors, perfumes & tobacco smoke

lupus patho

chronic & progressive autoimmune disorder

inflammatory & immune attacks occur against multiple self-tissues and organs

progressive loss of tissue integrity through excessive inflammation and overactive immunity leads to organ failure & death

lupus etiology

triggering events include infections, hormones, environmental exposures to toxins/pollutants/uv radiation

common cause of death is CKD and CV collapse

lupus risk factors

present in women 30-44 y/o (10x more than men)

incidence declines after menopause

black americans compared to white americans 8:1

lupus disease course

slow onset (6 years from first symptoms to diagnosis)

lupus expected findings

chronic fatigue

recurrent fevers with unknown origin

persistent joint/muscle swelling/pain, tenderness, weakness

alopecia

blurred vision

pleuritic pain (pericarditis, pleural effusion)

anorexia, weight loss, anemia

depression

butterfly rash

raynaud’s phenomenon

lupus key features

red, macular, facial rash over the cheeks and nose in shape of a butterfly

coin-shaped lesions (discoid rash) on face, scalp, and sun-exposed areas

sensitivity to light (photosensitivity) with rash development after exposure

chronic lesions on the mucous membranes of mouth & throat

nonerosive arthritis of two or more peripheral joints

inflammation of serosal membranes (pericarditis and pleurisy)

kidney changes with persistent casts and protein in urine

presence of ANA, decreased WBC/lymphocytes/platelets

false positive results for syphilis

lupus labs & diagnostics

skin biopsy (lupus cells & cellular inflammation)

antinuclear antibodies (ANAs) positive

ESR elevated

BUN/Creatinine elevated with renal involvement

UA positive for protein, casts, RBCs

CBC

lupus medications

NSAIDs- anti-inflammatory, pain (no if renal dz)

what does antimalarial do for lupus ex. hydroxychlororquine

suppresses synovitis, fever, fatigue, and risk of UV-related lesions (frequent eye exams)

what are immunosuppressants for lupus

methotrexate, azathioprine, belimumab (reverse isolation, toxicity, bone marrow suppression, liver toxicity, hold vaccines 30 days before)

what are corticosteroids (-sone, -lone) ex. prednisone

anti-inflammatory and immunosuppressant (fluid retention, HTN, impaired kidney function, hyperglycemia, skin atrophy, pathological fractures)

• don’t stop abruptly (death) caution with elderly

(lupus)

lupus complications

pain/mobility/fatigue

HTN, edema, renal dysfunction (urine output)

diminished breath sounds (pleural effusion)

tachycardia & chest pain (pericarditis)

rubor, pallor, cyanosis in hands/feet (vasculitis/vasospasm/Raynaud’s)

arthralgias/myalgias/polyarthritis (joints/connective tissue)

changes in mental status (psychosis/paresis/seizures)

nutritional status

lupus patient education

avoid uv exposure, mild soaps/shampoos, pat skin dry/no rubbing, avoid drying agents, steroid cream for rashes, reverse isolation

epilepsy patho

chronic disorder in which repeated unprovoked seizure activity occurs

may be imbalance of electrical neuronal activity or neurotransmitters (GABA)

epilepsy etiology

primary - idiopathic, often associated with genetics

secondary - tumor or trauma, metabolic disorders, acute alcohol withdrawal, electrolyte disturbances, high fever, stroke, head injury, substance abuse, heart disease (esp arrhythmias)

status epilepticus

continuous or rapidly recurring seizures

medical emergency causes hypoxemia = brain damage, arrhythmias, acidosis

to do: IV push lorazepam or diazepam

might need endotracheal intubation

epilepsy acute care and management

protect patient from injury, maintain airway, time seizure

administer lorazepam or diazepam (1st); phenytoin or fosphenytoin

after seizure: apply oxygen & clear airway, check blood glucose, attempt to reorient patient

• EEG, CT, MRI, SPECT/PET

anticonvulsants (epilepsy)

all cause drowsiness, ataxia & CNS depression (monitor blood levels)

levetiracetam - no need to monitor blood levels

phenytoin - causes gingival hyperplasia, bone marrow suppression, rash, multiple drug interactions, IV vesicant

carbamazepine - causes bone marrow suppression

divalproex - causes hepatotoxicity, bone marrow suppression

epilepsy surgical treatment

hospitalized for continuous EEG monitoring

vagal nerve stimulation (pacemaker for brain) - prevent seizures by sending regular, mild electrical impulses to the brain. stimulator placed under skin in upper chest and electrode surgically placed in left neck around vagus nerve

epilepsy patient education

do not stop anticonvulsants abruptly, need for blood monitoring, avoid hazardous activities, avoid alcohol, fatigue, loss of sleep, medic-alert bracelet

seizure considerations

protect patient from injury

do not force anything into patient mouth

turn patient to the side to prevent aspiration and keep airway clear

suction oral secretions if possible

loosen restrictive clothing

do NOT restrain or try to stop patient’s movement

record time seizure began and ended

transient ischemic attack (TIA)

temporary neurologic dysfunction

brief interruption in cerebral blood flow, deficits resolve within 24 hours

common cause: carotid artery stenosis

RF: smoking, DM, advancing age, inadequate nutrition, hypercholesterolemia, BC, excessive alc, illicit drug use

stroke incidence

5th leading cause of death

women have higher incidence (women live longer)

“stroke belt” - 8 SE states with higher mortality rates

cardiovascular accident (stroke) patho

interruption in blood flow to brain

medical emergency - certain areas of brain can become damaged or infarcted

CVA symptoms

similar to TIA but do not resolve but can improve over time

facial drooping, arm & leg weakness, speech difficulties, vision loss, dizziness, confusion, incontinence, tingling or numbness, severe headaches

ischemic stroke

common form of stroke; occurs as a result of an obstruction within a blood vessel that supplies blood to the brain

hemorrhagic strokes

interruption in blood vessel integrity, bleeding into brain tissue or subarchnoid space

arterivenous malformation (avm)

tangled mass of abnormal blood vessels in which arterial blood flows directly into the venous system

cervical spine cord injury

above c4 requires mechanical ventilation

all injuries cause respiratory insufficiencies - decreased cough, vital capacity, high risk of atelectasis and pneumonia

spinal shock

decreased reflexes and flaccid paralysis below level of injury

complete but temporary loss of motor, sensory, reflex, & autonomic function (48hrs - several weeks)

neurogenic shock

high risk with injury above t6

disruption of sympathetic nervous system

hypotension, bradycardia, poikilothermia

sleep apnea patho

breathing stops during sleep > 10 sec, >5x/hour

muscles relax, tongue & other structures obstruct the airway (hypoxemia, hypercapnia, reduced pH, sleep depravation from repeating cycle)