Mobility Fall 2024 Student Copy PDF

Mobility Exemplars: Osteoarthritis, Parkinson’s disease, Spina bifida Fall 2024 Rebecca Jones MN, RN, GNC(C), LC Learning Objectives Discuss osteoarthritis, its incidence, pathophysiology, risk factors, clinical manifestations, and management Demonstrate an understanding of the knowled...

Mobility Exemplars: Osteoarthritis, Parkinson’s disease, Spina bifida Fall 2024 Rebecca Jones MN, RN, GNC(C), LC Learning Objectives Discuss osteoarthritis, its incidence, pathophysiology, risk factors, clinical manifestations, and management Demonstrate an understanding of the knowledge of osteoarthritis and its relevance to nursing Discuss Parkinson’s disease, its incidence, pathophysiology, risk factors, clinical manifestations, and management Demonstrate an understanding of the knowledge of Parkinson’s disease and its relevance to nursing Discuss spina bifida, its three categories, its incidence, pathophysiology, risk factors, clinical manifestations, and management Demonstrate an understanding of the knowledge of Spina Bifida and its relevance to nursing Arthritis Osteoarthritis Inflammation of the joint or joints Systemic Gout Lupus Erythematosus Arthritis Rheumatoid Fibromyalgia Arthritis Osteoarthritis (OA) The most common chronic condition of the joints – “overuse arthritis” The most common type of arthritis and a significant cause of disability worldwide With a growing and aging Canadian population, its prevalence and burden of disability are predicted to increase – Approximately 5 million Canadians live with diagnosed osteoarthritis OA – Etiology Cause Effect on joint cartilage Medication Certain meds can stimulate collagen-digesting enzymes in the joint Hematological or endocrine Chronic hemarthrosis (e.g. hemophilia) can contribute to cartilage disorders deterioration Inflammation Release of enzymes in response to local inflammation affects cartilage integrity Joint instability Uneven stress placed on articular cartilage Mechanical stress Repetitive physical activities (e.g. sports) causes cartilage deterioration Neurological disorders Pain and loss of reflexes from neurological disorders cause abnormal movements that contribute to cartilage deterioration (e.g. diabetic neuropathy) Skeletal deformities Congenital or acquired conditions contribute to cartilage deterioration (e.g. dislocated hip) Trauma Dislocations or fractures may lead to avascular necrosis or uneven stress on cartilage OA – Etiology *Not a normal part of aging, but aging is a risk factor Decreased estrogen at menopause may contribute to the increased incidence of OA in aging women Obesity Regular moderate exercise ACL injury Occupation Family history Anatomy Review OSTEO-ARTHR-ITIS – Bone – joint – inflammation Important: 2 bones are needed to form a healthy joint - EACH with their own layer of cartilage – guide without friction Synovial membrane (synovium) is a specialized connective soft-tissue membrane that lines the inner surface of articular capsule – Composed of connective tissues and blood vessels. Communicate with rest of body, transports nutrients, remove waste Chondrocyte – cells that make up cartilage – Produce and maintain healthy cartilage – Make a gel like material containing: collagen and proteoglycans (hyaluronic acid, chondroitin sulfate, keratin) – Gives cartilage elasticity which facilitate weight distribution in joint Anatomy Review OA – Pathophysiology OA involves the gradual loss of articular cartilage with formation of bony outgrowths (spurs or osteophytes) at the joint margins The surface of the cartilage becomes rough and worn, interfering with easy joint movement Tissue damage appears to cause release of enzymes from the cells, which accelerates the disintegration of the cartilage (metabolic response at the level of the chondrocytes) Eventually the subchondral bone may be exposed and damaged, and bony outgrowths develop around the margin of the bone Pieces of the osteophytes and cartilage break off into the synovial cavity, causing further irritation The joint space becomes narrower (easily seen on x-rays) There may be secondary inflammation of the surrounding tissues in response to altered movement and stress on the joint OA – Pathophysiology The normally smooth, white, translucent articular cartilage becomes dull, yellow, and granular Affected cartilage steadily becomes softer, less elastic, and less able to resist wear with heavy use. Surfaces become cracked and worn Inflammation may occur – causes pain and stiffness – early symptoms of disease Articular cartilage is lost – bony surfaces rub together – later symptoms of disease The body’s attempts at cartilage repair cannot keep up with the destruction OA – Clinical Manifestations How is our patient going to present? OA – Systemic Clinical Manifestations What systemic clinical manifestations will we see with OA? OA – Diagnosis How is our patient diagnosed? OA – Radiographic Findings Diagnosis – Kellgren & Lawrence Scale The most common radiographic grading system for OA is the Kellgren and Lawrence grade, which scores the severity on a scale of 0 to 4 OA – Interprofessional Care No cure à treatment focused on managing pain and inflammation* How are we going to manage our patient? Quick Recap – OA Osteoarthritis - degenerative joint disease with slow destruction of the articular cartilage Women more affected than men Joints - weight bearing joints (knees, hips), fingers, hands, sometimes wrists Swelling and edema but not redness or “heat” complaints to joints Stiffness/pain - better in the morning, worse as day goes on. Can be aggravated by activity, improved with rest. Crepitus possible Genetic predisposition likely Obesity is exacerbating factor No labs X-ray findings- joint space narrowing, osteophytes, subchondral bone Pharmacological management - Acetaminophen, NSAIDS, Celebrex Supportive care – weight loss, use cane on opposite side, ice, moist heat, physiotherapy, referral for possible joint replacement Parkinson’s Disease A progressive, neurodegenerative disease of the CNS (basal ganglia) characterized by delayed initiation and execution of movement (bradykinesia), increased muscle tone (rigidity), tremor at rest, and impaired gait changes 2nd most common neurodegenerative disease (after Alzheimer’s) Cause remains unknown No cure 85% of cases diagnosed after the age of 65 – Diagnosed before 50 years old = early-onset PD PD Parkinson’s is a progressive adult onset disease resulting from the degeneration of ___________-producing neurons located in the Substantia Nigra In patients with PD, unusual aggregations of protein that develop inside nerve cells known as __________ are found within the brain. It is not known what causes them to form. – Their presence can lead to abnormal brain functioning that can affect cognition, movements, mood, and behaviors PD – Pathophysiology PD – Risk Factors Single most important factor – increasing age Male sex Some genetic factors Head trauma Occupation – farmers, healthcare providers PD – Clinical Manifestations PD – Clinical Manifestations Resting tremor – Cease with voluntary movement & during sleep – *Often the first sign Bradykinesia – slowness of movements Muscle rigidity Postural instability Repetitive “pill-rolling” motion of the hands Motor impairment Difficulty in initiating movement PD – Clinical Manifestations Lack of associated involuntary movement occurs; for example, loss of arm- swinging when walking The characteristic standing posture is stooped, leaning forward with the head and neck flexed Propulsive gait (short, shuffling steps with increasing acceleration), occurs as postural reflexes are impaired, leading to falls Complex activities, such as getting up out of a chair, become slow and difficult PD – Clinical Manifestations As disease advances: Voice becomes low and loses inflection (monotone) Chewing and swallowing become difficult Eating time becomes prolonged Constant drooling Face appears masklike Blinking of the eyelids is reduced, resulting in a blank, staring face Autonomic dysfunction – urinary retention, constipation, and orthostatic hypotension à increase in falls, and injury With advance disease, tremors affect hands, feet, face, tongue and lips PD – Complications As the disease progresses, complications increase Severe dementia, which is associated with an increase in mortality Akinesia (total immobility) Depression, hallucinations, psychosis Dysphagia (as swallowing becomes more difficult) à aspiration Pneumonia, UTI, skin breakdown (due to weakness) PD – Diagnosis Thorough clinical exam by a neurologist to diagnose PD – No specific diagnostic tests are available History will contain symptoms suggestive of bradykinesia, rigidity, resting tremor, and/or postural instability – Presence of “TRAP” A complete neuro exam should provide evidence of Parkinsonism Often, simple observation reveals generalized slowness and lack of spontaneous movement If unsure – can challenge with dopamine medication, if there is improvement – diagnosis confirmed (positive response to antiparkinsonian medications) PD – Management Dopamine replacement therapy has been used to reduce motor impairment Levodopa (l-dopa), a precursor of dopamine, is administered because dopamine itself does not cross the blood-brain barrier – Sign of toxicity: dyskinesia Selegiline (Eldepryl), – blocks the breakdown of l-dopa in the brain Pramipexole – Stimulates dopamine receptors in the brain Anticholinergic drugs Surgical procedures – Deep brain stimulation – Transplants of fetal dopamine-producing cells or adult stem cells Antidepressant drugs Treatment is symptomatic as no curative or disease modifying options exist* PD – Monitoring PT/OT are helpful with maintaining movement History and neuro exam every 4-6 months by specialist recommended If cognitive changes appear – brain MRI and full panel lab work recommended Spina Bifida Neural tube defect (CNS) “Split spine” à good descriptor Results from failure of the neural tube to close during embryonic development – Ectoderm develops a ridge that eventually becomes a neural tube – Neural tube goes on to become spinal cord, brain & tissue (including meninges) – Spina bifida occurs when portion of neural tube fails to close properly Preventable with maternal folate supplementation or fortification – Recommended to start prenatal vitamins 3 months prior to planning to conceive Types of Spina Bifida Spina Bifida Occulta – Most common and least severe type of spina bifida – Opening of the gap in the spinal arches is very small and covered in skin, stopping the spinal cord and membranes from pushing out – Skin is intact – Sometimes you will see a tuft of hair – Cases usually aren’t accompanied by a noticeable bulge in the back – These patients are usually asymptomatic – may never know they have spina bifida. May be picked up later in life during diagnostics for an unrelated reason Meningocele – Similar to the above, except only the protective membranes protrude out of the opening in the spine (not the spinal cord itself) – The spinal cord and nervous system are left intact, so this type of spina bifida can usually be corrected via surgery, with no further treatment required Types of Spina Bifida Myelomeningocele – Most serious form of spina bifida – Individuals with this type of spina bifida will have a sac in their back; this happens because the spinal cord and the protective membrane surrounding it protrude through the opening in the spinal arches – There is an opening in the skin – the nerves and meninges may be exposed - ++ infection risk – People with myelomeningocele spina bifida may be at risk of significant damage to the spinal cord and infections of the nervous system. – Although this isn’t the most common type of spina bifida, this is very often the form of the condition that people are referring to when they talk about spina bifida – Most severe symptoms Types of Spina Bifida Signs and Symptoms Occulta: Typically, there are no s/s related to this type, although, you can sometimes see signs on the newborns skin, above the spinal problem. This includes a tuft of hair, a small dimple, or birthmark v unexplained incontinence, chronic back pain, or changes in the muscles of their legs Meningocele: This type causes problems with bladder and bowel function Myelomeningocele: The spinal canal remains open along the lower or middle back. The spinal cord or nerves protrude at birth, forming a sac. Tissues and nerves are usually exposed (Mayoclinic, 2022) Causes Exact cause unknown Maternal folate deficiency Other Risk Factors Spina Bifida – Clinical Manifestations Orthopedic abnormalities (e.g. club foot or hip dislocation) Bladder and bowel control problems (incontinence, UTIs, poor renal function) Pressure sores and skin irritations Abnormal eye movement 68% of children with SB have an allergy to latex Paralysis Scoliosis Back pain Spina Bifida – Clinical Manifestations Partial or complete lack of sensation Weakness of hips, legs, or feet of a newborn Hair at the back part of the pelvis (called the sacral area) Dimpling of sacral area Difficulty swallowing (can lead to choking) Hoarseness Breath-holding and problems during sleep Spina Bifida – Diagnosis For myelomeningocele: – Often done prenatally – Looks for alpha fetoprotein in mother’s serum – Due to the leaking into bloodstream – Can be increased in other disorders (so not 100% - this is why we do other labs as well) – Other labs: – Human Chorionic Gonadotropin – Inhibin A – Estradiol – Amniocentesis – Sample obtained directly from amniotic sac – *Most conclusive but higher risk* Spina Bifida - Assessment Depends on the spinal cord involvement Visible spinal defect Flaccid paralysis of the legs (no muscle tone) Altered bladder and bowel function Hip and joint deformities Hydrocephalus Seizures Spina Bifida – Treatment Prenatal surgery – For closing myelomeningocele – Dangers to fetus and mother Postnatal surgery – Within several days of birth – Minimizes risk of meningitis Individuals often require additional support such as catheterization, crutches, walking aids à due to underdeveloped spinal nerves Spina Bifida – Nursing Interventions Prevent infection of, or injury to, the sac Correct positioning to prevent pressure on sac Prevent development of contractures Good skin care Adequate nutrition Accurate observations and charting Education of the parents Continued medical supervision Monitor for risk of hydrocephalus Monitor for risk of UTI, meningitis, or pneumonia (at high risk for) Urological monitoring Monitor for potential for latex allergy