exam 2 Flashcards

Immune and connective tissue disorders, brain and spinal cord disorders, and PNS disorders

1
Q

immune disorders include:

A

1- medication induced immunosuppression
2- neutropenia
3-HIV/AIDS

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2
Q

medication induced immunosuppression and goal of therapy

A

-secondary immune dysfunction
-chemotherapy
-corticosteroids
Goal= 1-prevent infection, 2- treat infections promptly

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3
Q

chemotherapy induced immunosuppression

A

-cytotoxic= targets rapidly dividing cancer cells
-cells of the immune system are inadvertent targets of chemotherapy, which results in a decrease in lymphocytes and phagocytes
-causes general immunosuppression- remaining lymphocytes unable to release antibodies and lymphokines to facilitate immune response

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4
Q

corticosteroid induced immunosuppresion

A

-used to treat autoimmune disorders and prevent transplant rejection, interfering with cell-mediated immunity or production of antibodies
-also has anti-inflammatory effect
-suppression of cell-mediated immunity and lymphopenia as well as a decrease in the inflammatory response
(methylprednisolone, prednisone, dexamethasone, betamethasone, hydrocortisone)

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5
Q

neutropenia

A

a reduction in the number of neutrophils (WBC that fight bacteria) that are essential for fighting infection
-absolute neutrophil count= ANC
= mild: ANC 1000-1500
= moderate: ANC 500-1000
= severe: ANC <500
-if severe, the normal bacteria from mouth and digestive tract can cause serious illness

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6
Q

causes and risks for neutropenia

A

-causes: chemotherapy, radiation, bone marrow disorders, medications (medication induced), surgery, burns, malnutrition and infections like HIV
-risks: patients with severe neutropenia are at a higher risk for life-threatening infections, requiring close monitoring and preventative care

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7
Q

medication induced neutropenia

A

-most common mediation that can result in drug-induced neutropenia is chemotherapy!!!! this kills neutrophils

also includes medications for:
-overactive thyroid
-antibiotics
-antivirals
-anti-inflammatory meds for UC or RA
-antipsychotics
-antiarrhythmics

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8
Q

nursing assessment for neutropenia

A

-VS: monitor for signs of infection like fever, tachycardia, or hypotension
-skin and mucous membranes: assess for redness, swelling, or lesions, especially in the oral cavity and IV sites
-lab monitoring: regularly review CBC to track ANC levels
-symptoms: ask about any chills, sore throat, cough, nasal congestion, rhinorrhea, or urinary symptoms (cloudy or odor) that may indicate infection

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9
Q

nursing management/action for neutropenia

A

-hand hygiene before and after contact
-protective isolation= neutropenic precautions/reverse isolation: private room with isolation precautions to minimize potential pathogen exposure
-visitor restrictions: limit number of visitors, no sick visitors or care providers, ensure adherence to hygiene protocols
-use PPE like gloves, masks, and gowns
-low bacteria diet: diet restrictions to prevent ingestion of harmful bacteria
-oral care: meticulous oral hygiene to prevent infections in the mouth, soft toothbrushes, avoid flossing if platelets are low
-skin and IV care: maintain skin integrity, avoid invasive procedures, ensure sterile technique for dressing changes and catheter care
-psychosocial support: help patients cope with isolation and the emotional impact of prolonged treatment and infection risk
-fever management: patient with fever (>101F) is considered medial emergency- immediate assessment and prompt initiation of broad-spectrum abx may be required

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10
Q

patient teaching for neutropenia

A

-regular check ups
-report infections promptly
-universal precautions
-HANDWASHING
-avoid contact with people who have infections or are sick
-avoid large crowds or gatherings
-do not change cat litter boxes
-avoid turtles or reptiles as pets
-eat a low bacteria diet: avoid raw or undercooked meat, poultry, seafood, and eggs. avoid unpasteurized dairy products and juices. wash fruits and veges thoroughly, or opt for cooked versions. no raw nuts and seeds. ensure proper food handling, storage, and preparation to minimize contamination.

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11
Q

HIV/AIDS

A

HIV= human immunodeficiency virus: attacks the immune system, specifically targeting CD4 cells (T cells), which help the body fight off infections.

-over time if untreated, HIV can destroy so many of these cells that the body becomes unable to defend itself against infections and diseases.

AIDS= acquired immunodeficiency syndrome: the most advanced stage of HIV infection, characterized by a severely weakened immune system. this makes individuals vulnerable to opportunistic infections and certain cancers.

not everyone with HIV develops AIDS!! especially with proper treatment, as antiretroviral therapy (ART) can control the virus and prevent progression to AIDS.

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12
Q

HIV replication

A

-HIV belongs to a group of viruses known as retroviruses
-targets CD4 receptors, which are expressed on the surface of T lymphocytes, monocytes, dendritic cells, and brain microglia

complex life cycle of HIV: binding, fusion, reverse transcription, integration, transcription/replication, translation/assembly, budding, maturation.

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13
Q

risk factors for HIV/AIDS

A

-non-discriminatory: sexual orientation, race, ethnicity, gender, age
-transmission: unprotected sex, body fluid, IV drug abuse, occupational exposure, blood transfusions and organ transplant- less likely now due to testing.

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14
Q

diagnostic testing of HIV

A

-HIV antibody tests- rapid/POC
-EIA= enzyme immunoassay/ELISA=enzyme-linked immunosorbent assay

used to identify antibodies directed specifically against HIV

-western blot: used to confirm sero-positivity when the EIA result is positive

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15
Q

disease monitoring for HIV

A

the viral load and CD4 count are obtained at the time of diagnosis, and then routinely every 3-4 months for the first 2 years of therapy.
-interval may be extended to 6 months for adherent patients who viral load has been suppressed for more than 2 years
-viral load is used as a marker of response to ART (antiretroviral therapy)

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16
Q

classification of HIV stages

A

-HIV infection stage 1: at least 500 cells
-HIV infection stage 2: 200-499 cells
-HIV infection stage 3=AIDS: less than 200 cells

Four Fs:
-Flu-like= acute infection
-Feeling fine= asymptomatic, latent infection
-Falling count= symptomatic, opportunistic infections
-Final crisis= AIDS

HIV consists of several stages, ranging from acute infection to death:
-viral transmission, viral infection, and seroconversion
-asymptomatic chronic infection
-symptomatic chronic infection
-acquired immune deficiency syndrome=AIDS

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17
Q

HIV manifestations

A

-fever
-cough
-weakness
-NVD
-dysphagia
-forgetfulness
-skin lesions
-SOB, DOE
-HA
-vision changes
-pain
-night sweats
-lymphadenopathy

clinical manifestations indicating a deterioration in status requiring immediate attention by a healthcare provider: new cough, increased fatigue, temperature greater than 102, night sweats, new onset of HA, new onset of visual. blurring, recent change in mental status, new skin lesions, new onset of diarrhea, weight loss greater than 10% of previously recorded weight.

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18
Q

Antiretroviral therapy=ART

A

major goals for initiative ART
-reduce HIV associated morbidity and prolong the duration and quality of survival
-restore and preserve immunologic function
-maximally and durably suppress plasma HIV viral load
-prevent HIV transmission

evaluate hepatic and renal function prior to administration

ART targets different stages of the HIV life cycle:
-to achieve sustained viral suppression, patients are prescribed 2-3 medications from two different classes
-simplifying treatment regiments and decreasing the number of medications that must be taken each day increase patients’ adherence to therapy.

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19
Q

medical management for HIV

A

prophylaxis medications:
-administered in patients with CD4 count of 200 cells or less to reduce the risk of OI initiated prior to ART therapy.
-awareness of allergies to medications such as bactrim. the decreased CD4 cells may mask reactions. once the CD4 cell begin to increase, allergic reactions may manifest and can be life threatening.

immunizations:
-maintain up to date immunizations including pneumovax and influenza
-live virus for people with HIV and household members are contraindicated.

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20
Q

HIV/AIDS if untreated

A

-if an HIV infected individual who does not receive treatment, the length of time from infection to death is approximately 12 years.
-in resource limited countries, the time from infection to death is approximately 5 years
-malnutrition, TB, and malaria are co-morbidities that shorten the time the untreated patient survives.

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21
Q

HIV education

A

-prevention
-awareness
-testing
-follow up appointments
-pre-exposure prophylaxis: truvada-combo of two drugs (tenofovir and emtricitabine) used to reduce the risk of contracting HIV

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22
Q

HIV nursing management

A

-VS: temp, pulse, respirations, oxygen saturation
-weight trend
-CD4 count
-viral load
-adherence to ART: adherence rate of 95% or greater is essential to achieve viral suppression and prevent the development of resistance to one or more ART medications
-TB status
-Immunization status
-depression

-use universal precautions consistently
-administer ART as prescribed and on time
-provide nutritionally dense foods and small, frequent meals
-provide emotional support
-refer for social services evaluation
-education: avoid high risk behaviors, adhere to treatment regimen, implement infection control precautions at home, s/sx to report to HCP urgently, health maintenance needs.

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23
Q

connective tissue disorders

A

-systemic lupus erythematous=SLE
-GOUT

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24
Q

systemic lupus erythematous=SLE

A

autoimmune chronic inflammatory disorder of the connective tissue
-produces antinuclear antibodies=ANA
-causes widespread inflammation and tissue damage of most major body systems
-period of exacerbations and remissions

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25
Q

risk factors for SLE

A

-gender-female
-age: 20-40 year olds
-race: African American, asian, Native American
-environmental stimulus: infection, medications, sun exposure
-genetic predisposition

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26
Q

SLE diagnosis

A

-based on combination of clinical symptoms and lab findings
-criteria consists of 11 key signs and lab tests, and a diagnosis is made if a patient meets at least 4 of them

medical history and physical exam
laboratory tests:
-ANA test: most have positive, which indicates presence of autoantibodies
-Anti-dsDNA and anti-smith antibodies: more specific for SLE. presence of anti-double-stranded DNA and anti-smith antibodies can help confirm the diagnosis
-CBC: may cause anemia, low white blood cells (leukopenia), and low platelets (thrombocytopenia)
-urinalysis: checks for protein and blood in urine, which may indicate kidney involvement (lupus nephritis)
-complement levels (C3, C4): proteins are often low in active SLE because the immune system uses them up during inflammation.

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27
Q

signs and symptoms for SLE

A

-skin rashes: malar or butterfly rash on face
-photosensitivity
-lupus nephritis
-fatigue
-weakness
-malaise
-joint pain and swelling (arthritis)
-fever
-hair loss
-mouth sores
-anorexia, weight loss
-palm erythema

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28
Q

medications for SLE

A

-NSAIDs: for pain and inflammation in joints and muscles
-antimalarials: to control skin symptoms and joint pain, and to prevent flares
-corticosteroids: used to reduce inflammation during flare-ups but should be tapered and monitored for side effects
-immunosuppressants: help control the immune response, but increase risk of infections

adherence: stress importance of taking meds as prescribed, even when feeling well

side effects: discuss potential side effects of medications like weight gain, increased risk of infections, bone thinning, and the importance of regular monitoring (blood tests for liver and kidney function)

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29
Q

nursing care for SLE

A

-monitor for complications like renal failure
-identify factors contributing to fatigue
-diet: high vitamin and high iron, high protein if no evidence of kidney disease
-administer medications as prescribed
-monitor VS, Is and Os, daily weights for signs of fluid overload if corticosteroids are used
-monitor for bruising, bleeding, and injury
-monitor for signs of organ involvement such as pleuritis, nephritis, pericarditis, CAD, HTN, neuritis, anemia, and peritonitis
-provide support therapy as major organs become affected
-provide emotional support
-provide information regarding support groups, and encourage the use of community resources

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30
Q

education for SLE

A

-recognizing and managing flares: early signs of flare, rest and energy conservation, when to seek help (CP, SOB, urinary symptoms)
-preventing flares: sun protection, stress management, balanced diet, regular exercise, medication adherence
-infection prevention: handwashing, masks, avoid crowds and sick people, stay up to date on vaccines
-skin: clean skin with mild soap, avoiding harsh and perfumed substances
-coping: mental health care, support groups
-follow up care: emphasize the importance of regular medical checkups to monitor disease progression, medication effects, and organ function (kidneys, heart), may need to see multiple specialists

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31
Q

gout

A

-metabolic disease
-hyperuricemia (increased uric acid) and uric acid crystals in joints= tophi, and major organs (kidneys) causing organ dysfunction
-caused by overproduction of uric acid, medications (thiazide diuretics, BBs), another disease (CKD)

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32
Q

signs and symptoms of gout

A

-excruciating joint pain
-erythema
-swelling
-tophi in great toe
-low-grade fever
-malaise
-HA
-pruritus: urate crystals in the skin
-renal stones from elevated uric acid levels

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33
Q

risk factors for gout

A

-obesity
-HTN
-diet rich meat and seafood
-use of thiazide diuretics
-consuming large quantities of ETOH (beer)

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34
Q

phases of gout

A

-acute: acute onset of pain, redness, and swelling
-intercortical: asymptomatic period between attacks
-chronic: repeat attacks over many years causing the formation of tophi in the joints causing destruction

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35
Q

diagnosis of gout

A

-uric acid level
-synovial fluid exam and urate crystals
-x-ray
-CT scan

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36
Q

medical management for gout

A

-medications: allopurinol for chronic, colchicine for acute
-diet: avoid purine
-weight management
-limit ETOH
-splint affected joint
-monitor for kidney stones

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37
Q

nursing management for gout

A

-assess decreased ROM
-assess intense joint pain, and tenderness, swelling, and warmth to affected joint
-assess for presence of tophi

-use ice packs
-administer medications: NSAIDs, uric acid lowering agents, glucocorticoid therapy

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38
Q

nursing care and patient teaching for gout

A

-avoid purine rich foods: organ and red meat, shellfish, wine, aged cheese, lentils, asparagus, spinach, fructose drinks
-increase urinary pH to above 6 by eating alkaline ash foods such as green beans or broccoli
-avoid alcohol and starvation diets as these can cause attack
-high fluid intake of 2000 mL/day to prevent stone formation
-reduce stress
-bed rest with affected extremity elevated
-monitor joint ROM ability and appearance of joints
-protect the affected joint from excessive movement (immobilize), direct contact with sheets or blankets, no weight bearing
-provide cold to affected joint as prescribed
-administer medications as prescribed

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39
Q

brain disorders

A

affect cognition, personality, mobility, and ADLs

-chronic: primary headaches, seizure disorders, Parkinson’s disease, Alzheimer’s disease- require lifelong management and coping with exacerbations

-emergency: primary or metastatic brain tumors, meningitis, and encephalitis- may be life-threatening emergencies

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40
Q

brain tumors

A

-occupies space within the skull
-primary tumors: grow within the brain, benign or malignant, slow growing or aggressive
-secondary tumors: metastasis spread from cancer in another area of the body

effects of brain tumors are caused by inflammation, compression, and infiltration of tissue- cerebral edema, increased ICP, neurologic deficits, seizures, altered pituitary function

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41
Q

diagnosis of brain tumors

A

-CT
-MRI
-PET
-biopsy
-EEG
-CSF analysis
-toxicology to rule out substance use as cause

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42
Q

signs and symptoms of brain tumors

A

obtain patient and family history
thorough neuro assessment
symptoms vary with location of tumor, but some include:
-HA
-NV
-new onset seizures
-impaired sensory perceptions: facial numbness or tingling, visual changes (papilledema, loss of vision), hearing changes
-cranial nerve palsy
-loss of balance
-ataxia
-weakness or paralysis: one part or side of body (hemiparesis, hemiplagia)
-abnormal redlexes
-difficulty thinking, speaking, or articulating words-aphasia
-changes in cognition, mentation, or personality

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43
Q

gliomas

A

infiltrate any portion of the brain
-most common type of brain tumor!

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44
Q

medical management of brain tumors

A

nonsurgical management
-drug therapy: chemo, hormone suppressing meds, corticosteroids, osmotic diuretics, anticonvulsants, non-opioid analgesics
-radiation therapy

surgical management
-biopsies
-craniotomy
-complication: increased ICP, bleeding, cerebral edema, seizures, VTE

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45
Q

interventions for brain tumors

A

goal= compensate for self-care deficits, improve nutrition, reduce anxiety, enhance coping skills, free of complications
-frequent neuro and symptom assessments
-VS: watch for cushing’s triad- widened pulse pressure (HTN), bradycardia, irregular respirations: late increased ICP
-treat headaches: analgesics, upright position
-treat NV
-treat fatigue: conserve energy, promote rest
-treat pain
-medication management: dexamethasone, antiepiletics
-monitor elevtrolyes
-Is and Os
-urine specific gravity and osmolality
-cognition: reorientation, orienting devices, assistance with self care, monitoring and intervention for prevention of injury
-seizure precautions: educate on risk for seizures and prophylactic antiepileptics
-emotional support

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46
Q

taking action for brain tumors

A

-encourage independence for as long as possible
-measures to improve cognitive function
-allow patient to participate in decision making and to express fears and concerns
-presence of family, friends, spiritual advisor and health care personnel may be supportive
-referral to counselor, social worker, home health care, support groups, PT/OT/ST
-referral for hospice care
-improve nutrition: oral hygiene before meals, plan meals for times when patient is comfortable and well rested, measures to make mealtimes as pleasant as possible, offer preferred foods, dietary supplements, daily weight, record daily intake.

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47
Q

craniotomy for brain tumors

A

pre-operatoin
-treat anxiety: opening skull, head shaved, possible neuro deficits
-provide reassurance
-educate on post-op expectations

post-operation: monitor for changes in status, prevent complications
-VS and neuro checks q15-30 min for 4-6 hours, then q1 hour for first 24 hours
-report immediately: decreased LOC, weakness or paralysis, aphasia, decreased sensory perception, sluggish pupil reaction to light, personality changes
-periorbital edema and bruising around eyes- need cold compresses!
-cardiac monitoring for potential dysrhythmias
-monitor dressing for drainage- report immediately if dressing is saturated or drainage is >50mL in 8 hours
-record Is and Os, with a fluid restriction if SIADH develops
-treat electrolyte imbalance- Na!
-manage airway, ventilator
-medications as prescribed
-standard post-op care: cough and deep breathing, incentive spirometers, SCDs

48
Q

meningitis

A

an acute inflammation of the protective membranes covering the brain and spinal cord, known as the meninges
-an infectious organism crosses the BBB and enters the CSF, causing inflammation of the meninges
-caused by bacterial, viral, fungal, or parasitic infections- bacterial being the most severe and life-threatening
-early recognition and treatment are essential for reducing morbidity and mortality

49
Q

signs and symptoms of meningitis

A

-fever: high in bacterial meningitis
-neck stiffness= nuchal rigidity
-altered mental status
-severe headache
-photophobia
-NV
-seizures
-rash: in meningococcal meningitis, petechial or purpuric
-Kernig’s sign: inability to straighten the leg when the hip is flexed at 90 degrees due to pain and stiffness
-Brudzinski’s sign: involuntary flexion of the knees when the neck is flexed toward the chest
-signs in infants and older adults: infants-bulging fontanelle, irritability, poor feeding, lethargy, and a weak cry; older adults- atypical presentation like confusion, lethargy, and mild fever, dx more challenging

50
Q

diagnosis of meningitis

A

-lumbar puncture: GOLD STANDARD- increased WBC, elevated protein, decreased glucose in bacterial meningitis, presence of bacteria on gram stain and culture
-blood cultures
-CT or MRI scan

prevention through vaccine!

51
Q

pharmacological treatment for meningitis

A

-antibiotics: immediate empiric broad-spectrum antibiotics- 14 to 21 days of antibiotics, central line (PICC)
-antiviral drugs for viral meningitis
-anti-fungal therapy: fungal meningitis such as amphotericin B
-corticosteroids: dexamethasone to reduce inflammation and risk of complications like hearing loss
-supportive care: antipyretics for fever, anticonvulsants for seizures IVF for hydration

complications= increased ICP, seizures, SIADH, DI

52
Q

assessment of meningitis

A

-neuro status
-signs of meningeal irritation, such as nuchal rigidity, Brudzinski’s sign, Kernig’s sign
-VS
-fluid balance
-HA
-CSF results
-daily weight
-renal function
-vascular assessments

53
Q

actions for meningitis

A

-IVF
-antibiotics
-decrease stimuli
-HOB 30 degrees
-pain management
-seizure precautions
-bacterial meningitis-droplet precautions
-maintain temperature: antipyretics, cooling bath, cooling blankets
-educate on keeping follow up appointments and taking full course of abx

54
Q

neurodegenerative disorders

A

-disorders of the central and peripheral nervous system
-deterioration of cells or function of the nervous system
-slow onset of s/sx

-Parkinson’s disease
-Huntington’s disease
-Amyotrophic lateral sclerosis= ALS

55
Q

Parkinson’s disease

A

progressive neurodegenerative disease affecting movement, muscle control, and balance
-causes muscle rigidity, akinesia, involuntary tremor, postural instability, disability
-affects the dopaminergic neurons in the brain leading to a depletion of dopamine, which plays a key role in coordinating smooth, controlled movements
-loss of dopamine and increase in acetylcholine leads to abnormal nerve function causing motor symptoms of Parkinson’s
-abnormal masses of protein develop inside neurons leads to characteristic PD, contributing to neuron dysfunction and death

56
Q

diagnosis of parkinson’s disease

A

-symptoms
-rule out other neurological disease
-levodopa trial
-no specific diagnostic studies to confirm, so the presence of progressive decline in motor function accompanied by the tremors and rigidity is typically how the diagnosis is made

57
Q

assessment of parkinson’s

A

-history: when did symptoms start?
-physical assessment: motor symptoms include bradykinesia leading to akinesia, tremors and pill rolling, muscle rigidity, postural instability, slow/shuffling gait
-facial mask-like expression
-drooling
-dysphagia
-psychosis, hallucinations, dementia
-constipation, urinary incontinence
-excessive perspiration
-speech changes-slow and monotone
-orthostatic hypotension

58
Q

medications for parkinson’s

A

-levodopa: most effective drug, converted to dopamine in the brain, and often combined with carbidopa
-dopamine agonists: mimic dopamine and stimulate dopamine receptors in the brain
-MAO-B inhibitors: inhibit breakdown of dopamine in the brain
-COMT inhibitors: prolongs the effect of levodopa by. blocking its breakdown
-anticholinergics: reduce tremors by inhibiting the action of acetylcholine
-amantadine: used in combination with levodopa to manage dyskinesia

58
Q

stages of parkinson’s disease

A

-stage 1: mild symptoms- symptoms on one side of the body only; tremors, change in posture, facial expression, slowness of walking
-stage 2: mild symptoms- symptoms on both sides of the body; tremors, rigidity, bradykinesia, walking difficulties, postural instability, loss of facial expressions
-stage 3: moderate symptoms- loss of balance, slowness of movements, falls are more common
-stage 4: severe symptoms- unable to stand without assistance, posture instability, bradykinesia, rigidity
-stage 5: severe symptoms- stiffness in the legs may make it impossible to stand or walk, hallucinations and delusions occur

58
Q

interventions for parkinson’s

A

goal= promote mobility, manage cognitive dysfunction, maintain safety and quality of life

safety:
-gag reflex and swallowing: aspiration precautions, swallow evaluation and speech therapy, thickened liquids, modified texture diet, sit patient upright, have suction available
-fall precautions
-prevent constipation, pressure injuries, contractures

mobility
-progressive daily program of exercise
-PT
-walking techniques for safety and balance-stopping occasionally
-frequent rest periods
-proper shoes
-use of assistive devices

enhancing self-care activities
-encourage, educate, and support independence
-environmental modifications
-use of assistive and adaptive devices
-occupational therapy
-allow patient extra time to perform ADLs and answer questions

supporting coping abilities
-set achievable, realistic goals
-encourage social socialization, recreation, and independence
-planned programs of activity
-support groups and referral to supportive services: counselors, social workers, and home care

medications
-administer promptly on patient schedule for continuous therapeutic levels
-prevent “off” periods (times when the medication isn’t working effectively)

home care preparation:case manager may be helpful
self-management education: follow instructions for drug therapy, maintain or improve quality of life
health care resources: national parkinson foundation

58
Q

medial management for Parkinson’s

A

goal= control symptoms and maintain functional independence
-no medical approach prevents disease progression
-medications
-deep brain stimulation
-medical marijuana
-non-traditional exercise like yoga or tai chi
-SLP- sleep and dysphagia

59
Q

huntington’s disease

A

progressive, genetic neurodegenerative disorder characterized by motor dysfunction, cognitive decline, and psychiatric disturbances
-genetic disorder that results in degeneration of GABA neurons and increase dopamine in the cerebral cortex and basal ganglia
-premature death of cells in the striatum of the basal ganglia (control of movement), and the cortex (thinking, memory, perception, judgment)

59
Q

diagnosis of huntington’s disease

A

-genetic testing
-family history
-CT/MRI of brain

60
Q

assessment for huntington’s disease

A

motor dysfunction:
-chorea= rapid, jerky, involuntary, purposeless movements, during sleep and progresses to athetosis and uncontrollable movements of the entire body
-athetosis= twisting and writhing movements
-impaired gait- eventually bed bound

cognitive impairment:
-problems with attention and emotion recognition, psychosis, impaired judgment and memory, dementia

behavioral features: apathy, blunted affect, fits of anger, suicidal depression

-facial movements
-emaciated
-incontinence
-speech: slurred, eventually unintelligible
-chewing and swallowing difficulty

61
Q

medical management of huntington’s disease

A

-no treatment stops disease progression
-focus on quality of life
-medication to treat chorea: tetrabenazine, benzodiazepines, neuroleptics
-behavior management: SSRIs, tricyclic antidepressants, antipsychotics
-psychotherapy
-speech therapy: nutritional support when unable to eat (tube feed)
-PT/OT
-assistive services-home care, day care, respite, long term care
-palliative care
-end of life planning

62
Q

assessment and actions for huntington’s disease

A

assess:
-movements, ambulation, balance
-swallow, gag reflex, speech
-mental status
-oral intake

actions:
-aspiration precautions, position while eating
-suction at bedside
-pressure injury risk
-administer medications
-safety precautions-fall risk
-consult PT/OT/SLP
-involve family in care
-end of life

education:
-fall prevention
-aspiration precautions
-suicide prevention
-family: supportive care, facilitating favorite activities

63
Q

amyotrophic lateral sclerosis= ALS
“Lou Gehrig’s Disease”

A

neurodegenerative disease causing progressive muscle weakness and atrophy
-no cognitive dysfunction!
-graduation deterioration of the upper an lower motor neurons leads to loss of voluntary movement and muscle control

64
Q

risk factors and diagnosis of ALS

A

risk factors:
-age
-autoimmune disease
-environmental exposure to toxins
-family history
-smoking
-viral infections

diagnosis:
-symptoms
-rule out other neurologic disorders
-EMG
-muscle biopsy
-MRI

65
Q

signs and symptoms of ALS

A

-fatigue
-muscle atrophy, including tongue
-progressive muscle weakness
-twitching of face and tongue
-muscle cramps
-dysarthria
-dysphagia
-stiff, clumsy gait
-spasticity-upper motor neuron damage
-flaccidity- lower motor neuron damage
-abnormal reflexes
-emotional lability
-respiratory paralysis within 3-5 years
-death: infection, aspiration, respiratory insufficiency

66
Q

medical management for ALS

A

goal= maintain or improve function, well-being, and quality of life. there is no cure
-PT/OT
-treat depression
-palliative care, hospice
-noninvasive positive-pressure ventilation
-tracheostomy with mechanical ventilation
-PEG tube with tube feed
-medications:
riluzole- first developed to slow disease progression
edaravone- shown to reduce decline in daily functioning
spasticity: baclofen, diazepam, dantrolene sodium
fatigue: modafinil

67
Q

interventions for ALS

A

-maintain patent airway, O2 saturation
-monitor strength, ROM
-ability to swallow
-monitor for pneumonia and respiratory failure
-manage non-invasive positive pressure ventilation
-tracheostomy care
-manage mechanical ventilator
-medication management
-emotional support
-end of life care

68
Q

multiple sclerosis= MS

A

chronic, progressive, immune-mediated disorder that affects the CNS
-demyelination of nerve fibers, which disrupts the communication between the brain and other parts of the body
-demyelination leads to the immune system mistakenly attacking the myeline sheath, and the protective covering of the nerve fibers
-loss of myelin leads to the formation of hardened, scar-like areas (sclerotic plaques or lesions) in the brain and spinal cord

types:
-RRMS: relapsing-remitting MS
-SPMS: secondary progressive MS
-PPMS: primary progressive MS
-PRMS: progressive-relapsing MS

69
Q

signs and symptoms of MS

A

-motor dysfunction: weakness in one or more limbs, spasticity (muscle stiffness or spasms), unsteady gait or coordination problems (ataxia)
-sensory disturbances: numbness or tingling (paresthesia), pain, often described as burning or electric shock-like sensations (Lhermitte’s sign)
-vision problems: blurred or double vision (diplopia), optic neuritis (inflammation of the optic nerve, causing pain and vision loss)
-fatigue: often the most disabling symptom, overwhelming physical or mental exhaustion
-cognitive impairment: difficulty concentrating, with memory, or problem-solving
-emotional changes: depression, anxiety, or mood swings
-bladder and bowel dysfunction: urinary urgency, frequency, or incontinence, constipation or bowel incontinence
-speech and swallowing difficulties: dysarthria (slurred speech), and dysphagia (difficulty swallowing)
-heat sensitivity: worsening of symptoms in response to heat

70
Q

medical management for MS

A

diagnosis: difficult to diagnose because there is no one specific test, ruling out conditions with similar clinical presentations, h and p, rule out inflammatory or infectious diseases
-MRI: identify brain lesions (plaques)
-electrophysiological tests and evoked potentials to examine how quickly impulses are traveling through the nerves
THE PATIENT MUST HAVE AT LEAST TWO SEPARATE SYMPTOMATIC EVENTS OF MRI CHANGES IN AT LEAST TWO SEPARATE LOCATIONS. there is no cure for MS.

71
Q

treatment for MS

A

managing symptoms, reducing the frequency of relapses, and slowing disease progression
-adequate rest, healthy eating, exercise, staying cool, relieving stress, support groups
-DMTs= disease modifying therapies
-corticosteroids
-symptomatic treatments
-plasmapheresis= plasma exchange

72
Q

nursing management for MS

A

assess:
-neuromuscular function
-vision/eye movement
-skin integrity
-ability to perform ADLs
-bowel and bladder function

actions:
-encourage ROM exercises
-administer medications
-implement safety measures
-PT and exercise to maintain strength and coordination
-assistive devices to improve moility and reduce fall risk
-scheduled voiding, high fluid intake, and a high-fiber diet to manage urinary and bowel dysfunction
-teach intermittent catheterization if necessary
-monitor for infections like UTIs

teaching
-disease process and prognosis
-take meds as prescribed
-importance of rest periods, preventing fatigue, and overheating
-manifestations of exacerbation
-maintain ideal body weight
-safety: visual scanning, check water temp before entering shower/tub

73
Q

spinal cord injuries

A

-any damage to the spinal cord: direct damage or degenerative diseases
-clinical manifestations depend on level of injury
-diagnosis: history and physical, imaging tests
-treatment: depends on level of injury, rehabilitation
-nursing care: avoiding further injury, preventing complications

74
Q

low back pain

A

low-back pain often results from muscle strain, ligament injury, degenerative disc disease or herniation, spinal stenosis. these factors cause mechanical pressure on spinal nerves.

75
Q

manifestations of low back pain

A

-localized or radiating pain
-stiffness
-limited mobility
-muscle spasms
-difficulty with ambulation
-sciatica may occur with nerve root compression
-acute pain: exacerbated by movement
-muscle spams: limit mobility
-nerve involvement: numbness/tingling

76
Q

diagnosis of low back pain

A

-history and examination
-x ray
-CT scan
-MRI
-electromyography (EMG)
-myelogram

77
Q

conservative management for low back pain

A

-non-pharmacological: PT, patient education on posture and lifting techniques, limit movement (brace, corset, belt), back strengthening exercise, heat, transcutaneous electrical nerve stimulation (TENS), interventional therapy like nerve blocks with local anesthetics, steroids, and narcotics injected into affected areas, massage, traction, acupuncture, meditation/yoga, weight reduction

-pharmacological: acetaminophen, NSAIDs, muscle relaxations, opioids, corticosteroids, anti-seizure drug, antidepressants

78
Q

surgical intervention for low back pain

A

for cases unresponsive to conservative treatment
-spinal fusion
-disectomy
-laminectomy

79
Q

degenerative disc- spinal cord

A

normal part of aging, unless accompanied by pain!
-osteoarthritis=OA
-loss of fluid in the discs-lose elasticity, flexibility, shock absorbing abilities
-discs become thin, shrink, and dry out- this limits ability to distribute pressure between vertebrae causing progressive destruction to disc
-can cause disc herniation as disc weakens

80
Q

herniated disc- spinal cord

A

“slipped disc”
-most common sites: L4-5 and L5-S1, C5-6 and C6-7
-disc bulges outward between the vertebrae
-degeneration, repeated stress, trauma, spinal stenosis
-can press against these nerves “pinched nerve”- causes radiculopathy= radiating pain, numbness, tingling, decreased strength and ROM

81
Q

cauda equina (herniated disc and spinal cord)

A

Bundle of nerves at the end of the spinal cord that provides movement and sensation to the lower body

82
Q

cauda equina syndrome= CES

A

The nerves in the cauda equina are compressed, rare but serious condition that requires immediate surgery to prevent to prevent permanent nerve and muscle damage
-weakness or numbness in the legs
-numbness around the genitals, anus, or buttocks- saddle anesthesia
-difficulty urinating or controlling urination
-difficulty having a bowel movement or controlling bowel movements
-loss of sexual sensation

know the signs:
S=saddle anesthesia
P=pain
I=incontinence
N=numbness
E=emergency!

83
Q

nursing management and recognizing cues for cervical and lumbar spine

A

cervical spine:
-pain radiates to arms and hands
-shoulder pain (rule out other causes)
-weak or absent reflexes
-weak hand grip

lumbar:
-low back pain: shooting or stabbing
-radiculopathy: pain radiation, sciatica
-straight leg test
-depressed or absent reflexes
-paresthesia: numbness, tingling
-muscle weakness: limited ROM, inability to stand upright

84
Q

interventions for herniated discs

A

assess:
-VS
-pain
-mobility
-numbness and tingling
-bowel function
-depression/SI

actions:
-administer meds as ordered: pain, anti-inflammatory, stool softener
-range of motion exercises
-increase fluid intake
-William’s position
-avoiding painful positioning
-emotional support
-education
-post-surgical care

85
Q

post-op anterior cervical disectomy and fusion= ACDF

A

-assess airway, breathing, circulation
-frequent neuro assessments
-check for bleeding and drainage at incision site
-monitor VS
-assess swallowing ability
-monitor Is and Os
-assess ability to void
-manage pain
-assist with ambulation
-neck collar as ordered
-education/discharge teaching: someone to stay with patient for few days, medications, incision care, walk everyday, wear color, call if pain numbness tingling worsening or swallowing becomes difficult, activity restriction- no lifting , driving, or strenuous activity

86
Q

spinal cord injury= SCI

A

SCI results from trauma that damages the spinal cord, leading to partial or complete loss motor, sensory, and autonomic function below the injury site.

87
Q

risk factors and diagnosis of spinal cord injuries

A

risk factors:
-ages 16-18
-male gender
-high-risk physical activity
-driving under the influence of alcohol

diagnosis:
-neuro exam
-xray
-CT
-MRI

88
Q

medical treatment for spinal cord injury

A

acute management:
-immobilization
-maintain patent airway
-corticosteroids to reduce inflammation
-surgery to stabilize the spine-laminectomy, fusion

rehabilitation:
-physical therapy
-OT
-psychological support

88
Q

clinical manifestations for spinal cord injury

A

-complete SCI: total loss of motor and sensory function below the injury level
-incomplete SCI: varying degrees of motor and sensory loss

depends on level of injury: autonomic dysreflexia!!! hypotension, bradycardia, bowel/bladder dysfunction, inability to breathe, paraplegia, loss of sexual function, chronic pain, impaired temperature control
-higher the injury, greater loss of function

89
Q

complications of spinal cord injury

A

-autonomic dysreflexia: potentially life threatening condition that occurs in people with spinal cord injuries, typically at or above the level of T6. it is caused by an overreaction of the autonomic nervous system to a stimulus below the level of injury. the overreaction can lead to a dangerous increase in blood pressure. it is a medical emergency that requires immediate attention to prevent complications like stroke.

-triggers= full bladder (maybe due to blocked catheter), full. bladder (constipation, impaction), skin irritation (like tight clothing or pressure sores)

-s/sx: sudden, severe headache, flushed face, high blood pressure, bradycardia, sweating, cold, pale skin

90
Q

spinal cord injury interventions/nursing management

A

assessments:
-VS
-respiratory function
-motor function
-sensory function
-pain
-bowel function
-Is and Os
-post op care/pin care if applicable

actions:
-maintain suction
-facilitate cough
-maintain spinal immobilization
-passive ROM
-reposition and maintain body alignment
-perform routine pin care if halo in place post-op
-teaching: s/sx of respiratory distress, autonomic dysreflexia, skin care/management

90
Q

myasthenia gravis

A

-PNS disease
-chronic autoimmune disorder that affects nerve cell communication with muscles. the body produces antibodies that attack acetylcholine (ACh) receptors on the muscle surface necessary for muscle contraction.
this leads to:
-impaired transmission of nerve impulses to muscles
-fluctuation muscle weakness, particularly with repetitive use
-fatiguability that worsens with activity and improved rest

91
Q

clinical manifestations of myasthenia gravis

A

-muscle weakness: progressive weakness that worsens with activity and improves with rest
-ocular muscles: ptosis=drooping eyelids, diplopia=double vision
-facial and throat muscles: difficulty speaking=dysarthria, swallowing=dysphagia, and chewing
-limb muscles: difficulty with lifting, climbing stairs, and performing repetitive movements
-respiratory muscles: severe cases may cause respiratory weakness, leading to a myasthenic crisis (life threatening emergency!)
-fatiguability: muscle weakness worsens with repetitive use, typically improving after periods of rest. symptoms can fluctuate throughout the day, often worsening in the evening.

92
Q

myasthetic crisis

A

a severe life-threatening exacerbation of muscle weakness that can involve respiratory failure due to diaphragm weakness.
-triggers: infections, stress, surgery, or inadequate medications.

93
Q

diagnosis of myasthenia gravis

A

-acetylcholine receptor antibody test: measures the presence of anti-acetylcholine receptor antibodies, elevated in most MG patients
-electromyography (EMG): evaluates electrical activity of muscles, reveals muscle weakness and abnormal fatigability
-tensilon test= edrophonium test: short-acting acetylcholinesterase inhibitor (edrophonium) is administered to temporarily improve muscle strength, confirms MG
-chest CT or MRI: detect a thymoma, tumor of thymus gland

94
Q

treatment for myasthenia gravis

A

-medications: anticholinesterase drugs, immunosuppressants, corticosteroids, azathioprine, or mycophenolate, intravenous immunoglobulin=IVIG
-plasmapheresis
-surgery: thymectomy= surgical removal of thymus gland, which can result in long-term improvement or remission in some patients
-management of myasthenic crisis: mechanical ventilation, high-dose steroids, plasmapheresis, or IVIG

95
Q

myasthenia gravis assessments

A

-muscle weakness, difficulty with chewing, swallowing, or vision problems
-muscle strength, particularly in the ocular, facial, and respiratory muscles
-signs of fatigue and weakness, particularly after repetitive activity
-monitor respiratory function (rate, depth, and effort), pulse oximetry, especially during exacerbations

96
Q

guillain-barre syndrome= GBS

A

an acute, autoimmune disorder, in which the body’s immune system attacks the peripheral nervous system, leading to inflammation and demyelination of the nerves.
-results in impaired nerve signal transmission, primarily affecting motor function but can also involve sensory and autonomic nerves
-the exact cause is unknown, but often triggered by a preceding infection, such as a respiratory or GI illness or viral infection.

96
Q

interventions/actions for myasthenia gravis

A

-have emergency equipment available, like suction and ventilator
-timely administration of anticholesterase drugs to optimize muscle strength throughout the day
-support respiratory function with non-invasive or invasive ventilation
-coughing, deep breathing exercises, use of an incentive spirometer
-collaborate with speech therapy and dietitians to assess swallowing ability
-provide small, frequent meals, with soft or pureed foods if needed to prevent choking
-education: taking medications consistently, especially before meals to reduce aspiration risk, how to conserve energy and plan rest periods to avoid fatigue, recognizing signs of myasthenic crisis, infection prevention and management of stress, which can exacerbate symptoms

97
Q

diagnosis of guillain-barre syndrome

A

-lumbar puncture: increased protein levels in the CSF with a normal white blood cell count (albuminocytologic dissociation) is a key indicator
-electromyography (EMG) and nerve conduction studies: confirms nerve dysfunction by showing delated or absent conduction
-other: MRI to rule out other causes of weakness (spinal cord disorders), pulmonary function tests (PFTs) to assess respiratory involvement

98
Q

clinical manifestations of guillain-barre syndrome

A

-motor symptoms: ascending weakness starting in the legs and progressing to the upper limbs and face
-reduced or absent deep tendon reflexes= areflexia
-difficulty with ambulation, respiratory muscles involvement in severe cases
-sensory symptoms: tingling or numbness in extremities= paresthesia
-pain, which can be neuropathic in nature
-autonomic dysfunction: blood pressure fluctuations, cardiac arrhythmias
-bowel and bladder dysfunction

99
Q

assessment for guillain-barre syndrome

A

-motor function: progressive weakness, ascending paralysis
-respiratory function: RR, depth, effort, signs of respiratory distress
-cardiovascular status: autonomic instability, such as fluctuations in BP and HR
-pain: evaluate for neuropathic pain
-psychosocial status: signs of anxiety and depression

100
Q

interventions/actions for guillain-barre syndrome

A

-non-invasive ventilation (like BiPAP) or mechanical ventilation
-treat potential respiratory infection (such as pneumonia)
-cardiac monitoring
-gradual position changes to prevent orthostatic hypotension
-mobility: ROM, PT, OT- prevent contractures and other complications
-manage pain
-plasmapheresis
-administer IVIG
-provide emotional support, encourage family involvement, and consider involving mental health services

101
Q

trigeminal neuralgia

A

sudden, usually unilateral, severe, brief, stabbing, recurrent pain the distribution of one or m ore branches of the trigeminal nerve (CN 5)
-etiology is unknown! may be due to vascular compression, tumor, structural abnormality or the skull base, or MS
-diagnosis: Hx, physical, MRI

102
Q

clinical manifestations of trigeminal neuralgia

A

-intense, sudden, sharp, stabbing, or electric shock-like facial pain
-typically occurs unilaterally
-triggered by stimuli like chewing, talking, smiling, brushing teeth, or light breeze
-fear of triggering pain can cause the patient to avoid eating, speaking, or other daily activities

103
Q

treatment of trigeminal neuralgia

A

-medications: anticonvulsants, muscle relaxants, antidepressants, opioids, NSAIDs
-nerve block injections, acupuncture, relaxation techniques
-surgical options: microvascular decompression or nerve ablation for refractory cases

104
Q

assessments for trigeminal neuralgia

A

-obtain detailed history of the patient’s pain: location, intensity, triggers, duration, and any associated symptoms
-impact on daily activities and psychosocial status
-evaluate medication history, effectiveness, and any side effects from current treatments

105
Q

interventions/actions for trigeminal neuralgia

A

-administer meds: carbamazepine or baclofen as prescribed
-educate the patient about recognizing and avoiding triggers
-assist in planning meals and activities around times when pain is less likely to occur
-provide psychological support to help manage anxiety and depression associated with chronic pain
-consider referral to a mental health professional if needed
-teach patient and family about condition, treatment options, and importance of medication adherence
-inform them about potential side effects and when to seek medication attention (example- signs of drug toxicity)

106
Q

bells palsy

A

an acute, unilateral paralysis or weakness of the facial muscles due to inflammation or compression of cranial nerve 7 (facial nerve), inflammation of the facial nerve leads to interruption of nerve signals, exact cause is unknown, but often associated with viral infections such as herpes simplex virus=HSV, varicella-zoster virus, epstein-barr virus, or lyme disease

107
Q

clinical manifestations of bells’ palsy

A

-sudden onset over 48 hours
-facial dropping
-inability to close eye
-inability to smile or raise eyebrow
-difficulty speaking and eating
-excessive tearing or dry eye

108
Q

diagnosis of bell’s palsy

A

exam to rule out other causes of facial paralysis, like stroke, tumors, or lyme disease

109
Q

treatment of bell’s palsy

A

-medications: corticosteroids, antivirals, analgesics
-eye care: eye drops, protective patch, taping
-physical therapy
-speech therapy
-emotional support

110
Q

patient education for bell’s palsy

A

-understanding bell’s palsy: educate patient a bout the condition, its likely causes, and the typical course of recovery
-eye care at home: demonstrate how to apply artificial tears and protect the eye with patches or taping
-medication adherence: stress the importance of completing the corticosteroid course and taking antivirals if prescribed
-facial exercises: teach simple exercises, like smiling or frowning, to help improve muscle tone and recovery
-recovery expectations: most patients see improvement within weeks to months, but some may experience residual weakness. reassure them that recovery is favorable, though full recovery may take time.