Summary

This presentation by Dr. Madelyn Carey in Spring 2024 details various disorders affecting mobility, including Parkinson's Disease, multiple sclerosis and others.

Full Transcript

Disorders of Mobility Dr. Madelyn Carey Spring 2024 Disorders Affecting Motor Function Overview Chronic degenerative neurologic disorders Unknown etiologies Most are labeled movement disorders but are typically multisystem disorders Genetic and environmental risk factors identified Musculoskeletal S...

Disorders of Mobility Dr. Madelyn Carey Spring 2024 Disorders Affecting Motor Function Overview Chronic degenerative neurologic disorders Unknown etiologies Most are labeled movement disorders but are typically multisystem disorders Genetic and environmental risk factors identified Musculoskeletal System Supports body weight, controls movements, provides stability Gross and fine movements Works with circulatory and nervous systems Nerves innervate muscles CNS coordination Conditions That Limit Mobility Pain Fatigue Nervous system disorders Respiratory disorders Musculoskelet al diseases or injuries Cardiovascula r disease Inability to cope Parkinson Disease Idiopathic, chronic, progressive degenerative disorder of CNS Has motor, nonmotor, neuropsychiatric manifestations Affects individuals over age 50 Second most common neurodegenerative disorder Conditions that cause secondary parkinsonism Head trauma Toxins Metabolic disorders Infections Multiple strokes in basal ganglia Atypical antipsychotics and antiemetics Parkinson Disease Causes Idiopathic (90%) Genetic (10%) Increased risk factors Increased age (most significant) Male gender Exposure to pesticides, metals, other compounds Family history of PD Genetic mutations Clinical Manifestations Motor Features Tremor “Pill-rolling” resting tremor of hand Tremor of lips, chin, jaw, tongue, legs Rigidity increased muscle stiffness and tone Cogwheeling Bradykinesia Postural instability Nonmotor Features Fatigue, sleep disturbances Olfactory dysfunction Pain Autonomic dysfunction Neuropsychiatric symptoms Cognitive dysfunction, dementia, psychosis, hallucinations Mood disorders, depression, anxiety Stage Stage 1 Stage 2 Stage 3 Stage 4 Stage 5 Parkinson Disease Symptoms Mild signs and symptoms; on one side only Tremor of one limb Changes in posture, locomotion, facial expression Bilateral symptoms Minimal disability; posture and gait affected Significant slowing of body movements Early impairment of equilibrium on walking or standing Generalized dysfunction that is moderately severe Severe symptoms Rigidity and bradykinesia but can still walk to a limited extent Unable to live alone Tremor may be less than in earlier stages Cachectic stage Invalidism; cannot stand or walk Treatment Pharmacologic replenishment with dopaminergic drugs Dopamine agonists Amantadine Catechol-O-methyltransferase inhibitors Ablation surgery Deep brain stimulation Complementary and supportive therapies Multiple Sclerosis Chronic, inflammatory, demyelinating and axonal degenerative disorder of CNS Inflammatory autoimmune disease Lesions throughout the CNS Progressive disease Risk factors Age: 20-50 Gender: more common women over men Ethnicity: more common in Caucasians of northern European descent Geography related to latitude Genetics Causes Exact cause unknown Autoimmune reaction (theorized) Multiple Sclerosis Relapsing-Remitting Multiple Sclerosis (RRMS) Stable for 10–20 years Secondary Progressive Multiple Sclerosis (SPMS) Gradual worsening with or without occasional relapses, minor remissions, plateaus Primary Progressive Multiple Sclerosis (PPMS) Progressive deficits with occasional plateaus, temporary improvements, or acute relapses Clinical Manifestations Sensory symptoms in the extremities or face Visual loss, double vision, nystagmus Weakness Vertigo Gait and balance disturbances Bladder problems Pain Dysarthria: difficulty or unclear speech Fatigue Cognitive dysfunction Multiple Sclerosis Diagnosis Treatment Demonstration of CNS lesion disseminated in time and space MRI Immunomodulatory therapy (IMT) McDonald criteria Blood tests to rule out other disorders Evoked potentials recording timing of CNS response to various stimuli Electroencephalography (EEG) Lumbar puncture slow the progress of disability, not a cure Education: avoid live attenuated vaccines Spasticity Physical therapy Routine stretching program Medications Nerve blocks Amyotrophic Lateral Sclerosis (ALS) Progressive neurodegenerative disease Causes weakness, disability, and death within 3–5 years Also known as Lou Gehrig’s disease Neurodegeneration Upper motor neurons in corticospinal tract Lower motor neurons in anterior horn cells of spinal cord Risk factors Age and family history Caucasian males and in individuals aged 60– 69 years About 5-10% of cases are inherited Clinical Manifestations Insidious onset Slowly progressive, painless weakness in one or more body parts Upper motor neuron (UMN) signs and symptoms Lower motor neuron (LMN) signs and symptoms Bulbar dysfunction Frontotemporal executive dysfunction Stage Description Stage 1 Symptom onset (involvement of first body region) Stage 2A Diagnosis (35% of way through disease course) Stage 2B Involvement of second body region (38% of way through disease course) Stage 3 Involvement of third body region (61% of way through disease course) Stage 4A Need for gastrostomy/feeding tube (77% of way through disease course) Stage 4B Need for noninvasive ventilation (80% of way through disease course) Amyotrophic Lateral Sclerosis Diagnosis Based primarily on clinical manifestations Tests Electromyography Nerve conduction studies MRI or CT scan of brain and spinal cord Muscle or nerve biopsy Genetic Blood tests Treatment Riluzole (glutamate pathway antagonist) Noninvasive ventilation Percutaneous endoscopic gastrostomy tube feeding Medications to relieve symptoms and maximize remaining function Multidisciplinary approach to care Huntington Disease Progressive, incurable, neurodegenerative disease of brain Autosomal dominant inherited Neuronal loss in cerebral cortex Varying degrees of atrophy in other areas in midbrain and cerebellum Causes uncontrolled involuntary movements; dementia; and behavior changes Onset of symptoms: ages 35–44 years Duration: mean of 19 years Primary causes of death Pneumonia Cardiovascular disease Grade Pathology Grade 0 No detectable histologic neuropathology and no gross striatal atrophy in presence of clinical manifestations and positive family history Grade 1 Neuropathologic changes detected microscopically but without gross atrophy Grade 2 Striatal atrophy present; caudate nucleus remains convex Grade 3 Striatal atrophy more severe; caudate nucleus flat Grade 4 Striatal atrophy most severe; medial surface of caudate nucleus concave Clinical Manifestations Involuntary movements Chorea Parkinsonian features Akinetic–rigid syndrome Dysarthria Dysphagia Abnormal eye movements Tics Myoclonus Cognitive impairment Short-term memory loss Impaired intellectual function Dementia Psychiatric manifestations Behavioral changes Irritability, moodiness, depression, OCD Untidiness Antisocial behavior Apathy Huntington Disease Diagnosis Treatment Genetically proven family history Reduce symptoms and improve quality of life Autosomal dominant Clinical presentation MRI or CT scan measure brain atrophy Referral to neurologist who specializes in HD Tetrabenazine for chorea Antidepressant or antipsychotic medications Levodopa or dopamine agonist medications Seizure Disorders Abnormal electrical discharges within brain Results in involuntary movement and/or behavior and sensory alterations Involuntary movements May encompass entire body or just certain muscle groups Changes in level of consciousness, behavior, or sensory perception Classifications Febrile Seizures Result from rapid temperature rise above 102.2°F Acute illness Generalized seizures lasting only few minutes Partial Seizures Focal seizures Contained within limited area of brain May be simple or complex Generalized Seizures Intractable Seizures Abnormal electrical discharges originate from both hemispheres of brain Types Tonic–clonic Absence Status epilepticus Associated with loss of awareness or consciousness; muscle stiffness and twitching Refractory Occur even with optimal medical management Require referral to epilepsy center Clinical Manifestations Loss of conscious awareness of environment Varying patterns of muscular rigidity and relaxation Aura Generalized Seizures Tonic Phase (15–60 seconds) Muscular rigidity Sudden loss of consciousness Pupils fixed and dilated Increased metabolic demands Hypoxia Skin pallor and cyanosis Urinary and bowel incontinence Clonic Phase (60–90 seconds) Alternating muscular contraction and relaxation in extremities Hyperventilation Eyes roll back, froth at mouth Postictal Period Decreased level of consciousness; sleepy Quiet and relaxed breathing Gradual regaining of consciousness Status Epilepticus Life-threatening condition Enhanced and sustained electrical activity over 30 minutes Increased neuronal excitation with reduced inhibition Intervention: Establish and maintain an open airway - PRIORITY Pad the bed frame to protect from injury. Document characteristics of the seizure. Administer 50% glucose. Seizure Disorder Diagnosis Laboratory tests Complete blood cell count Blood chemistry Urine culture Lumbar puncture EEG Lead level, toxicology screening CT scan or MRI and angiography Treatment Antiseizure medications Surgical intervention Acute Musculoskeletal Disorders Overview Musculoskeletal system is scaffolding of human body Motor function hindered by: Injuries Infections Disease processes Most frequently reported injuries in children vs. older adults Fractures Break in a bone Result of increase in energy beyond what bone can tolerate Direct force or indirect force Fractures can be classified as Open or Compound Fracture Closed or Simple Fracture Complicated Fracture Risk Factors Age Younger patients: sports-related injuries Older patients: falls and disease Presence of bone disease Poor nutrition Vitamin D Calcium Phosphorus Lifestyle habits: dangerous activities Clinical Manifestations Pain (most common) Deformity, edema, numbness Muscle spasms, skin bruising Hypovolemia, crepitus Healing of Fractures Indirect Healing Inflammatory stage Bleeding causes hematoma Inflammatory cells degrade debris and bacteria Reparative stage Fibrocartilage formed Soft callus joins fractured bone Hard callus develops Blood vessels form Remodeling stage Lamellar bone replaces woven bone Union vs Delayed Union vs Malunion Direct Healing Use of surgical procedure to realign bone Fractures that benefit from direct healing Long-term complications Severely comminuted; threatened vascularity Surgical procedures External fixation Internal fixation Closed reduction Infecti on Common agents Pseudomonas Staphylococcus Clostridium Those at increased risk Greater soft tissues damage Compromised immune system Treatment Antibiotics Proper hygiene of infection site Hip Fracture Displaced Hip Fracture With older patients with displaced fractures which have a higher likelihood of damaging the blood supply to the head of the femur usually receive replacement surgery Replacement Surgery Hemi-arthroplasty Replaces just the head of the femur Total hip replacement Replaces the ball and the socket Compartment Syndrome Medical Emergency Edema and swelling cause increased pressure in muscle compartment Decreased blood flow Possible muscle and nerve damage Ischemia may cause muscles and nerves to die Limb might need to be amputated Most common in lower leg and forearm Prevention: elevation and ice Symptoms: severe pain and tenderness, swelling, paresthesia, pallor, numbness or paralysis, and decreased or absent pulse Treatment: remove cast, surgical relief of pressure Additional Complications Fracture blisters Tense vesicles or bullae arising swollen skin directly overlying fracture Contain sterile fluid that can contribute to infection Fat embolism syndrome Closed long bone or pelvic fractures Fat emboli becomes trapped in pulmonary and dermal capillaries No symptoms in most patients Large amounts of fat released may cause fat embolism Treatment Oxygen administration Mechanical ventilation Prophylactic treatment with corticosteroids and early immobilization of injury Dislocations and Subluxation Dislocation Ends of bones moved out of normal position Attachment to joint lost Subluxation Bones of joint remain in partial contact Cause: trauma Clinical manifestations Pain Limb or joint deformity Altered mobility of affected joint Treatment: manual traction or reduction, immobilization Carpal Tunnel Syndrome Nerve entrapment Neuropathy causing nerve damage and muscle weakness or atrophy Body areas most prone Where nerves pass over rigid areas or through narrow canals Clinical manifestations Numbness and tingling of thumb, index finger, and lateral ventral surface of middle finger Hand weakness Diagnosis Tinsel test Phalen maneuver Nerve conduction studies with ultrasound Treatment Splinting and application of ice or heat Surgery to enlarge tunnel Bursitis Inflammation of bursa Results from: Overuse of joint Direct trauma to joint Clinical manifestations Tenderness of area around Pain with extension and flexion of joint Warm, red, swollen skin over bursa Treatment Rest, Ice (acute inflammation), compression, elevation NSAIDs Gentle stretching and strengthening exercises Corticosteroid injection Arthroscopic surgery Antibiotics (infectious cause) Strain Overstretching injury to muscle or muscle–tendon unit Forces muscle to extend beyond capacity, resulting in microscopic tears Most common sites: lower back and neck Sprain Ligaments around joint stretched or torn Oppositional forces cause ligament to overstretch and tear Most common site: ankle Treatment RICE, NSAIDs Casts, splints, immobilizers, or slings Surgery for severe injuries Physical therapy Clinical Manifestations Strains Sprains Immediate pain, reduced ranged of motion (ROM) Muscle spasms Edema Muscle weakness Bleeding, swelling, bruising Severely hindered ROM “Pop” or “rip” when injury occurs Bruising, pain, immediate swelling Anterior Cruciate Ligament (ACL) Injuries One of four major ligaments that connects femur to tibia Injuries occur when stressed, strained, or torn Pathogenesis Tear down middle of ligament Ligament torn completely from femur Anterior Cruciate Ligament (ACL) Injuries Clinical manifestations Intense pain Feeling that knee “popped” and “gave out” Swelling Diagnosis X-ray and MRI Treatment Ice, elevation, and pain medication (NSAIDs) Non-weight bearing until swelling subsides Physical therapy Surgery if symptoms persist Meniscus Injury Injury to cartilage located between femur and tibia Results from forced twist or rotation Clinical manifestations Popping sound at knee joint Pain when knee touched Edema Restricted joint mobility Knee “locks up” or does not move smoothly Knee feels weak or is “buckling” Meniscus Injury Diagnosis ROM assessment Testing (x-ray, MRI, ultrasound) Treatment Ice, elevation, NSAIDs Rest and no weight bearing; crutches Elastic bandage NSAIDs Physical therapy Arthroscopic surgery Osteochondral Lesions Occur at the end of the bone Causes Lack of blood supply Direct trauma to joint Repetitive use Clinical manifestations Pain with weight bearing Swelling Tenderness Limited mobility; occasional “locking” of knee Treatment NSAIDs and use of growth hormone Weight loss Rest/ Ice Use of assistive devices to walk Physical therapy Arthroscopic surgery Rotator Cuff Tear Tendon supporting muscle(s) rips or tears from the bone Causes Fall on shoulder Attempt to break fall with outstretched hand Repeated overhead motions Clinical manifestations Dull ache in joint from microscopic tears Weakness when raising arm Inability to reach behind back Rotator Cuff Tear Diagnosis Shoulder ROM assessment X-ray CT scan or MRI Ultrasound or arthrogram Treatment Rest, application of cold or heat to area, electrical stimulation of muscles Cortisone injections and NSAIDs Surgery: open vs arthroscopic Physical Therapy: ROM Immobilization for the first 4-6 weeks after surgery with passive exercising. Active exercising begins during the next 4-6 weeks and progresses until full or maximum shoulder ROM and arm function return. Adhesive Capsulitis (Frozen Shoulder) Acute inflammation of ligaments in shoulder joint capsule Shoulder bones unable to move freely in joint No known cause Associated with some conditions Clinical manifestations Self-imposed immobility of shoulder because of pain Stiffness, more pain, continued loss of motion Unable to move arm above head or behind back Adhesive Capsulitis (Frozen Shoulder) Diagnosis Shoulder ROM assessment X-ray to rule out other disease processes MRI Treatment NSAIDs and steroid injections Physical therapy Arthroscopic surgery Can resolve within 2 years with minimal loss of shoulder function without treatment Osteomyelitis Bone infection Occurs after penetrating wound, from blood infection, skin breakdown Joint replacement and internal fixation surgeries Causes Bacteria, fungi, parasites, viruses Infection from another body area carried to bone Clinical Manifestations Local Indications Systemic Indications Bone pain Drainage and ulceration Swelling, redness, warmth, tenderness Lymph node swelling Fever with chills, general malaise Tachycardia Nausea, vomiting Anorexia Osteomyelitis Diagnosis Imaging evidence of an abscess or bone changes X-ray, bone scan, MRI White blood cell count and sedimentation rate Blood cultures Bone biopsy/tissue samples Treatment Antibiotics: IV 2-6 weeks Surgery (for severe ischemia) Drainage tubes inserted in bone Procedure to fill dead tissue space with muscle Osteonecrosis Death of bone Risk factors Long-term use of steroids Heavy alcohol intake Direct injury to bone or joint Chemotherapy or radiation Organ transplantation Diseases Clinical manifestations Insidious; no symptoms Pain when pressure or weight applied to joint Inability to use limb Osteonecrosis Diagnosis X-rays, MRI or CT scan Bone scan Bone biopsy Measurement of bone pressure Treatment NSAIDs Non-weight bearing status ROM exercises Electrical stimulation Surgery Benign Bone Tumor Abnormal growth of normal tissue Do not metastasize/interfere with body organ function Occur in children and young adults up to age 30. Affected by growth hormones Clinical manifestations Lump associated with ache or pain Treatment Tumor heals when fracture heals Stops growing when growth hormone slows Surgery Malignant Bone Tumor Come from cartilage, bone cells, collagen, bone marrow Exact cause unknown Possibly related to: High bone growth or bone overstimulation by disease Radiation, bone marrow transplantation Osteolysis Clinical manifestations Deep bone pain Skin over mass warm, erythematous Malignant Bone Tumor Diagnosis X-rays CT scans MRI Bone biopsy Treatment Surgery Chemotherapy Radiation Metastatic Bone Disease Cancer from another body site that migrates to bone Most common in spine, pelvis, thigh Clinical manifestations Sometimes asymptomatic If symptomatic Bone pain Fractures Changes in urinary and bowel continence Limb weakness Chronic Musculoskeletal Disorders Overview Chronic musculoskeletal disorders Persist despite treatment for injury, or Develop as a part of pathologic condition Causes Lifestyle choices Employment Strenuous recreational activity Genetic predisposition Affected areas Bones Muscles Joints May begin with acute ailment Concepts Related to Chronic Disorders Mobility Inflammation Oxidative stress Immunity Comfort and pain Stress and coping Sensory perception Issues with mood and affect Depression and/or anxiety Gout Metabolic disorder that disrupts the body’s control of uric acid production or excretion Gout manifests high levels of uric acid in the blood and other body fluids Occurs when the uric acid concentration increases to high enough levels to crystallize Crystals deposit in connective tissues throughout the body Risk factors: Obesity Diabetes Family hx Use of certain meds: Thiazide diuretics, Niacin, Aspirin Dietary Modifications Avoid food with high purine content Scallops Mussels Organ and game meats Beans Spinach Asparagus Oatmeal Wine Low Back Pain Common occurrence for most people Decreases quality of life Decreased mobility Increased pain and frustration Loss of work hours Linked to: Certain lifestyle habits Occupational risk factors Diseases Intervertebral Disc Degeneration Intervertebral discs Pads of fibrocartilage between vertebrae Resist spinal compression while permitting limited movements Causes of degeneration Normal wear and tear Arthritic conditions Inherited genetic disorder Clinical manifestations Pain in back May spread to buttocks and upper thighs Numbness and tingling in leg or foot Intervertebral Disc Degeneration Diagnosis Treatment Physical examination to assess for the location on spine affected Spinal x-rays MRI Initial Aspirin and NSAIDs Periods of rest After initial period Physical therapy (palliative only) Back brace with heat or ice, massage, ultrasound, and electrical stimulation Options for persistent pain Narcotic analgesic Nerve block with steroid injections Herniated or Ruptured Disc Rupture of disc causing fluid to leak out and impinge on and irritate nearby nerves Decrease in cushioning of vertebral joints Back pain and limited mobility Can cause sciatica Risk factors Age 30 to 50 years Excess weight Regular heavy lifting, bending, and twisting Previous back problems Smoking and genetic factors Most common locations C5–C6 C6–C7 L4–L5 L5–S1 Clinical Manifestations With abrupt herniation Nerve root compression Severe pain Muscle spasms With gradual herniation Slow onset of pain Weakness or tingling Other symptoms Forward tilt to trunk when standing Changes in mobility, motor function, knee and ankle reflexes Cauda equina syndrome (CES) Factors affecting presenting symptoms Presence of nerve compression Location of the compression Herniated or Ruptured Disc Diagnosis Treatment Mobility tests CT, MRI, or myelography Nerve conduction studies Blood tests NSAIDs Opioids Antispasmodics Cortisone or corticosteroids; anesthetics Hot or cold packs Mild, low-impact exercise to help strengthen back Surgery Laminectomy Discectomy Spinal fusion Artificial disc surgery Laser surgery Spinal Stenosis Narrowing of spinal column Etiology and pathogenesis Vertebral bone degeneration with aging Clinical manifestations (if present) Slow progressive symptoms Numbness/ tingling in buttocks or legs Weakness in the legs / “foot drop” Cramping General/ “burning” pain (may radiate down arm or leg) Patient states that “flexing” lower back relieves the pain Spinal Stenosis Diagnosis Medical history and physical examination X-ray, MRI, and CT scan Myelography Treatment NSAIDs Steroid injections; nerve blocks Physical therapy; lumbar brace Chiropractic treatments and acupuncture Surgery Laminectomy Cauda Equina Rare condition that usually is a surgical emergency Compression of the spinal nerve roots Damage may lead to incontinence and possibly permanent paralysis of the legs Bladder dysfunction Perineal sensory loss Anal laxity Neurological deficit in lower extremities Including motor weakness Skeletal Irregularities Lordosis Spinal column more concave Pregnancy or obesity Kyphosis Spinal column convex Scoliosis Lateral curve of spine C shaped or S shaped Severe scoliosis Rotation of spine, leading to deformities and disability Scoliosis Risk factors Age 9 to 15 years Neuromuscular disorder Family history Sideways curvature Mild scoliosis: 10 to 20 degrees Moderate scoliosis: 20 to 40 degrees Severe scoliosis: over 40 degrees Scoliosis Clinical manifestations Spinal curvature to one side, uneven hips or shoulders Differences in leg length Tiredness of spine Prominent shoulder blade Rib bump Complications Heart and lung problems Paralysis Scoliosis Diagnosis Treatment Adam forward bend test X-ray MRIs, CT scans, or bone scans Pain management OTC analgesics, prescription NSAIDs, opioids Physical therapy (15–25 degrees) Brace (20–40 degrees) Spinal fusion surgery (over 40 degrees) Rheumatic and Arthritic Disorders More than 100 rheumatic diseases Rheumatic diseases caused by immune system dysfunction Degenerative conditions caused by wear and tear Osteoarthritis (OA) Most common form of arthritis Degenerative and localized Wear and tear on joints breaks down cartilage Causes bone to rub on bone Idiopathic OA vs Secondary OA Gender differences Men: OA in hips, knees, spine Women: OA in hips, knees, hands Risk factors Jobs requiring hard labor or repetitive motion Obesity Certain medical conditions Clinical Manifestations Mild symptoms that worsen over time Pain associated with joint degeneration Worsened by activity and relieved by rest Pain and stiffness with prolonged inactivity Tenderness, swelling, effusion, crepitus, bone spurs Enlargement of the joint Limited motion Deformity Osteoarthritis Diagnosis Treatment Most common: x-ray Others: MRI, ultrasound, blood tests, and joint fluid analysis OTC analgesics Prescription NSAIDs or opioids Topical analgesics Cortisone injections Hyaluronic acid injections Various nonpharmacologic therapies, such as: Heat and cold application Assistive technology Surgery Rheumatoid Arthritis Chronic systemic autoimmune disorder Most common form of autoimmune arthritis Cause unknown Various factors may be involved Pathogenesis Antibodies in RA bind with other proteins and tissues Create immune complexes that cause inflammation Enzymes cause further joint tissue degradation Pannus forms Clinical Manifestations Joint swelling, stiffness, warmth, tenderness, pain Joint deformation (if not treated) Systemic manifestations Fatigue, anorexia, weight loss, weakness, low-grade fever Rheumatoid nodules Pleural effusion Vasculitis Pericarditis Enlarged spleen Rheumatoid Arthritis Diagnosis Blood tests Anti-cyclic citrullinated peptide (CCP) test Examination of synovial fluid Treatment Pharmacologic treatment NSAIDs Low-dose oral corticosteroids Disease-modifying antirheumatic drugs (DMARDs) Intra-articular steroid injection Nonpharmacologic treatment Spondyloarthropathie s Group of diseases affecting joints Ankylosing spondylitis Reactive arthritis Psoriatic arthritis Enteropathic arthritis Clinical manifestations Low back pain Morning stiffness of back or neck Generalized fatigue Spondyloarthropathies Diagnosis Treatment Laboratory tests X-ray and MRI NSAIDs Stretching exercises Osteopenia Decrease in bone density which can lead to fractures Common causes Chronic eating disorders or issues with metabolism Chemotherapy or glucocorticoids Radiation exposure Family history of low bone density Being white or of Asian descent Thin body structure Limited physical activity, smoking, high alcohol intake Clinical manifestations Spontaneous fracture; limited pain Osteopenia Diagnosis Treatment DEXA scan Addresses risk factors Increased calcium and vitamin D intake Increased weight-bearing exercises Smoking cessation Reduction of alcoholic beverages Osteoporosis Most commonly diagnosed metabolic bone disorder Low bone density due to low intake of nutrients for bone growth or increase in bone resorption due to aging Classifications Primary osteoporosis Type 1: menopause Type 2: decreased bone formation from aging Secondary osteoporosis Disease process; renal hypercalciuria Effect of drug Osteoporosis Diagnosis Treatment DEXA scan May not be diagnosed until fracture occurs Serum bone G1a (osteocalcin) level Focuses on preventing fractures Nutritional support; calcium and vitamin D Exercise Measures to prevent falls Medications Paget Disease Metabolic disorder Causes select bones to overgrow and become weak Skull, spine, pelvis, femur Bone resorption faster than bone formation Body compensates by accelerating creation of new bone New tissue weak, brittle, easily fractured Genetic disorder initiated by environmental factor Clinical manifestations Pain Enlarged bones; deformed bones Fractures; damaged joint cartilage Paget Disease Diagnosis Presence of fracture X-ray Blood tests Treatment Bisphosphonates Calcitonin Calcium and vitamin D supplements Exercise Surgery Repair of fractures Correction of malformations Replacement of arthritic joints

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