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Flash Cards for Nursing

Musculoskeletal Assessment: Basic Assessment: •Past health history;Medications ;Surgeries ;ROM;Reflexes;Inspection, palpation;Muscle-strength testing;Measurement;Assessment for scoliosis •Pain, weakness, deformity, limitation of movement, stiffness, & joint crepitation
Bone support, protection of internal organs, voluntary movement, blood cell production, & mineral storage *SUPPORTING FRAMEWORK OF THE BODY, KEEPS BODY FROM COLLAPSING*
• Osteoblasts: bone forming
• Osteoclasts: bone remodeling & breaking down bone tissue
Joints: a place where the ends of two bones are in proximity & move in relation to each other *AN ARTICULATION*
Synovial joint: freely moveable each joint is enclosed in a capsule of fibrous connective tissue, which joins the two bones together to form a cavity. More other stuff.
Muscle: Cardiac • Cardiac (striated, involuntary): occurs only in the heart, spontaneous contractions propel blood through the circulatory system
Muscle: Smooth • Smooth (non-striated, involuntary): found in the walls of the hollow structures such as airways, arteries, GI tract, urinary bladder, & uterus. Smooth muscle contraction is modulated by neuronal and hormonal influences.
Muscle: Skeletal • Skeletal (striated, voluntary): Requires neuronal stimulation for contraction. Accounts for half a human’s body weight.
Bone Scan: Involves injection of radioisotope that is taken up by bone. Uniform uptake of the isotope is normal. Increased uptake is seen in osteomyelitis, primary & metastatic cancer of bone, and certain fractures. more
Bone Scan: Nursing responsibilities before o BEFORE: explain that radioisotope is given 2 hours before procedure. Ensure that bladder is emptied before scan. Inform patient that the procedure requires 1 hour while the patient lies supine. No harm or pain will result from the isotope.
Bone Scan: Nursing responsibilities After o AFTER: Increase fluids after scan.
Soft Tissue Injuries: sprains, strains, dislocations, & subluxations usually RESULT FROM TRAUMA
Sprain: ligament damage
Strain: excessive stretching of muscle
Manifestations: of Strains and Sprains • Pain • Edema • Decrease in function • Contusion • Pain aggravated by continued use
Acute Care Strains and Sprains Part 1 (of 3) Acute Care: • Stopping the activity and limiting movement • Applying ice packs to the injured area • Compressing the involved area • Elevating the extremity above heart level • Providing analgesia as necessary • RICE
Acute Care Strains and Sprains Part 2 (of 3) • Prolonged rest is not indicated unless the injury is severe • Cold: induces hypothermia in the injured body part & induces physiologic changes in soft tissue, including vasoconstriction & a reduction in the transmission & perception of nerve pain
Acute Care Strains and Sprains Part 3 (of 3) • APPLY ICE NO MORE THAN 20-30 MINUTES AT A TIME & AVOID APPLYING DIRECTLY TO SKIN • Elastic bandage wrap: prevents edema & encourages fluid return • Exercises to increase muscle flexibility&strength • Prevention: warm up muscles before exercising
Dislocations complete displacement of the joint surfaces, severe injury of the ligamentous structure that surround a joint • Patella is commonly dislocated
Subluxation partial/incomplete displacement of the joint surface • X-rays determine extent of dislocations
Clinical Manifestations: Dislocations and Subluxation • Deformity • Limb can be shorter/internally rotated on the affected side • Pain • Tenderness • Loss of function • Swelling
Acute Care: Dislocations and Subluxation 1 • ORTHOPEDIC EMERGENCY (prompt attention required) • MAY BE ASSOCIATED WITH SIGNFICANT VASCULAR INJURY • Realign the dislocation of the joint
Acute Care: Dislocations and Subluxation 2 • Treat quickly to avoid avascular necrosis (the longer the joint remains unreduced, the greater the possibility of avascular necrosis) • Compartment syndrome may also occur due to vascular injury & resulting ischemia
Acute Care: Dislocations and Subluxation 3 • NEUROVASCULAR ASSESSMENT IS CRITICAL • Pain relief • Support/protection of injured joint • Immobilization of affected joint (motion is usually restricted)
Acute Care: Dislocations and Subluxation 4 • Gentle ROM exercises • Clients with dislocations are at greater risk for repeat dislocations
Fracture a disruption or break in the continuity of a bone • Traumatic injuries account for the majority of fractures, but some fractures are secondary to disease processes (cancer or osteoporosis) • Unnecessary movement increases soft tissue damage
• Open fracture: skin is broken & bone is exposed, causing soft tissue injury
• Closed fracture: skin remains intact
Manifestations: Fractures • Immediate, localized pain • Decreased function • Inability to bear weight or use the affected part • Client guards or protects extremity against movement • Obvious bone deformity may or may not be present
Diagnostics: Fractures • Visual assessment: alignment • X-ray or MRI
Assessment: Fractures 1 • ASSESS FOR COMPARTMENT SYNDROME: PAINFUL CONDITION THAT OCCURS WHEN PRESSURE WITHIN THE MUSCLES BUILDS TO DANGEROUS LEVELS • Neurovascular assessment: color, temperature, capillary refill, peripheral pulses, & edema
Assessment: Fractures 2 • Compare both extremities to obtain an accurate assessment • Assess extremity color (pink, pale, cyanotic) • Asses extremity temperature (hot, cool, cold)
Assessment: Fractures 3 • Assess capillary refill (should be less than 3 seconds) • Accurate documentation & ongoing neurovascular assessment • When was patient’s last tetanus shot?
Emergency care: Fractures 1 • Immobilize site: above & below injury • Splint to maintain alignment & prevent dislocation • Tissue perfusion: apply pressure dressing • Assess pulses, movement, & sensation
Emergency care: Fractures 2 • Check circulation, motion, sensation, & CRT every 30 minutes & report any changes • Prevent infection by covering with sterile dressing • Prophylactic antibiotics if skin is broken • Tetanus booster if skin is broken
Emergency care: Fractures 3 • Antibiotics if open fracture • Analgesics & stool softener if constipated • Reduction of the fracture to realign • Preserve the proper alignment
Emergency care: Fractures 4 • Recheck regularly • Elevate as much as possible • Apply cold packs initially until swelling stops
Prevention of factures calcium, weight-bearing exercise
Reduction method of returning a joint to its normal alignment
Traction the application of a pulling force to an injured or diseased body part or extremity. Traction is used to: prevent or reduce pain & muscle spasm, immobilize a joint or part of the body, reduce a fracture or dislocation, & treat a pathologic joint
bennefits of casts • Common treatment following closed reduction. • Allows patient to perform many normal activities of daily living • Applied 1-2 days after injury once swelling has decreased • Synthetic often used because they dry more quickly and are lighter
Cast Care: • Keep clean & dry • ASSESS FOR SKIN BREAKDOWN • Elevate extremity above heart level to promote venous return • Do not put things in cast space
Cast care 2 • Teach to report signs of problems to the HCP: o Increased pain despite elevation, ice, & analgesia o Swelling associated with pain and discoloration of toes or fingers o Pain during movement o Burning or tingling under cast o Sores or foul odor und
Cast care 3 • Do not get cast wet • Do not remove any padding • Do not insert any objects inside the cast • Do not cover cast with plastic for prolonged periods
The 6 P’s: • PAIN & POINT OF TENDERNESS • PULSE: distal to the fracture site • PALLOR • PARASTHESIA: sensation distal to the fracture site • PARALYSIS: movement distal to the fracture site • POIKILOTHERMIA: temperature
Complications of fracture: • Infection: osteomyelitis • Venous thromboembolism (use Heparin or Lovenox to prevent) • Fat embolism (with long bone fractures) • Skin breakdown
• Acute Compartment Syndrome: swelling and pressure in compartments of tight casts. CIRCULATION IS DECREASED. *IRREVERSIBLE DAMAGE RESULTS IF PRESSURE NOT RELIEVED*
Signs of • Acute Compartment Syndrome: 1 of 3 o Pain out of proportion to the injury that is not relieved by opioid analgesics & pain on passive stretch of muscle o Increased pressure in the compartment o Paresthesia o Pallor, coolness, & loss of normal color of extremity
Signs of • Acute Compartment Syndrome: 2 of 3 o Paralysis or loss of function o Pulselessness or diminished/absent peripheral pulses o CRT greater than 3 seconds o Tissue is pale/cool
Signs of • Acute Compartment Syndrome: 3 of 3 o Numbness/tingling o May feel like a vice is on the extremity o CAST MUST BE CUT o FASCIOTOMY PERFORMED: fascia is cut to relieve tension or pressure
• Fat Embolism Syndrome: characterized by systemic fat globules from fractures that are distributed into tissues, lungs, and other organs after a traumatic skeletal injury.
o Manifestations: Fat Embolism Syndrome: Acute respiratory distress syndrome (chest pain, cyanosis, dyspnea, apprehension, tachycardia, & decreased PaO2), changes in mental status o Petechiae located places (eye, neck, chestwall,axilla,buccal)
Treatment: Fat Embolism Syndrome o Treatment aimed at prevention: reposition the patient as little as possible before fracture immobilization to prevent dislodging fat droplets into the general circulation
o Management of symptoms: Fat Embolism Syndrome fluid resuscitation to prevent hypovolemic shock, correction of acidosis, & blood transfusions o Encourage coughing & deep breathing o Administer O2 to treat hypoxia
Hip fractures common in older adults, with 95% of these fractures resulting from a fall • Occur more frequently in women than men (due to osteoporosis) • 1 in 5 people experiencing a hip fracture will die within 1 year of injury
• Extracapsular: fracture of trochanter, less complications related to blood supply to proximal fragment being maintained & the fracture unites easier
• Intrascapsular: fracture of the head or neck of the femur, greater complications related to less blood supply to proximal fragment & bone union may be difficult
Manifestations: Hip Fracture • External rotation • Muscle spasm • Shortening of the affected extremity • Severe pain & tenderness around the fracture site
Interprofessional care: Hip Fracture • Initially the affected extremity may be temporarily immobilized by Buck’s Traction until the patient’s physical condition is stabilized & surgery can be performed (Buck’s Traction relieves painful muscle spasms & can be used for 24-48 hours
Nursing Management: Hip Fracture • Medicate regularly for 48-72 hours • Notify provider if medication doesn’t relieve pain • Medicate before planned activity • Neurovascular assessment: circulation, movement, sensitivity • Potential for permanent impairment is present • 6 P’s
• Post-operative care: Hip Fracture 1 or 2 o Prevent internal rotation, adduction, & 90 degree flexion o Adduction pillow o Anticoagulant therapy o PT on day one with weight bearing or walker o MAINTAIN POST-OPERATIVE ABDUCTION
• Post-operative care: Hip Fracture 2 of 2 o Taking a tub bath & driving a car are not allowed for 4-6 weeks o Positioning: KNEES MUST BE KEPT APART, NEVER CROSS LEGS, NEVER TWIST TO REACH BEHIND o Assess for infection o PAIN MANAGEMENT
Osteomyelitis a severe infection of the bone, bone marrow, & surrounding soft tissue.
• Indirect entry: Osteomyelitis trauma (boys younger than 12), adults with GU & respiratory tract infections, or people with disorders marked by vascular insufficiency (diabetes mellitus) because they are at high risk for spread of a primary infection via the blood to the bone
• Direct entry when an open wound allows entry of microorganisms into the body
Manifestations: Osteomyelitis • Constant bone pain unrelieved by rest;Swelling;Tenderness;Warmth;Fever;Night sweats;Chills;Restlessness;Nausea;Malaise;Drainage
Management: Osteomyelitis • Vigorous & prolonged IV antibiotics • May need to remove dead tissue & bone • Hyperbaric oxygen therapy
Osteoporosis chronic, progressive metabolic bone disease marked by low bone mass & deterioration of bone tissue, leading to increased bone fragility • HOLES IN THE BONES • LOSS IN BONE • FIRST SIGN IS BACK PAIN OR SPONTANEOUS FRACTURES
• Risk factors: Osteoporosis greater than 65 years, female gender, low body weight, white or Asian ethnicity, cigarette smoking, sedentary lifestyle, corticosteroid use, low vitamin D levels, low calcium levels, being post-menopausal • NEED VITAMIN D & CALCIUM
silent thief Osteoporosis: occurs slowly, insidiously over many years & robs the skeleton of its banked nutrients/minerals • Current guidelines recommend an initial bone density test for all women over 65
Manifestations: Osteoporosis • Back pain or spontaneous fractures • Bone is thinner • Height shortens • Spine is curved • Over time: wedging & fracture of vertebra produce gradual loss of height & humped back (Dowager’s Hump/Kyphosis)
Diagnostics: Osteoporosis Serum tests (calcium, phosphorus), Bone Mineral Density (BMD), dual energy x-ray absorptiometry (DXA)
Management: Osteoporosis • Proper nutrition • Calcium supplements • Exercise • Vitamin D supplements • Prevent falls/fractures • Medications (estrogen, bisphosphonates, calcitonin)
Arthritis a type of rheumatic disease which involves inflammation of a joint or joints
Osteoarthritis: 1 of 3 a slowly progressive non-inflammatory disorder of the synovial joints • GRADUAL LOSS OF ARTICULAR CARTILAGE WITH FORMATION OF BONY OUTGROWTHS AT THE JOINT MARGINS
Osteoarthritis: 2 of 3 • Degeneration & loss of strength of the weight bearing joints with loss of cartilage and bone hypertrophy result and result in not being able to absorb energy/the force of a joint
Osteoarthritis: 3 of 3 • Bone outgrowth changes shape of joint causing spurs which can break, causing synovitis (inflammation of synovial fluid) • FORMATION OF NEW JOINT TISSUE IN RESPONSE TO CARTILAGE DESTRUCTION
• Risk factors: Osteoarthritis increased age, obesity, immobility, strenuous/repetitive exercise, low estrogen
• Causes: Osteoarthritis trauma, mechanical stress, inflammation, joint instability, neurologic disorders, skeletal deformities, hematologic/endocrine disorders, drugs
Manifestations: Osteoarthritis • Joint pain (primary symptom) • Usually affects joint on 1 side of body • Mild discomfort to significant disability • Pain worsens with use • Early: pain relieved with rest • Advanced: pain at rest and sleep disturbances • Deformities
Distinction between Osteoarthritis and inflammatory join disorders such as rheumatoid arthritis FATIGUE, FEVER, & ORGAN INVOLVEMENT ARE NOT PRESENT IN OA
Herberden’s nodes: OA occur on the distal interphalangeal (DIP) joints due to osteophyte formation & loss of joint space often red, swollen, & tender (same as Bouchard's nodes)
Bouchard’s nodes: OA occur on the proximal interphalangeal (PIP) joints due to osteocyte formation & loss of joint space often red, swollen, & tender (same as herberden's nodes)
Diagnostics: Osteoarthritis bone scan, MRI, CT scan, ESR
Management: Osteoarthritis 1 of 2 • Rest & joint protection • Heat/cold applications • Nutritional therapy • Weight reduction if needed • Exercise
Management: Osteoarthritis 2 of 2 • Use of assistive devices • ROM & strengthening exercises • Drug therapy: Salicylate, NSAIDS, corticosteroid injections • Physical therapy • Arthroscopy to debride joint • Osteotomy to change joint alignment • NO CURE
Rheumatoid Arthritis (RA): define chronic, systemic autoimmune disease characterized by inflammation of connective tissue in the synovial joints *INFLAMMATORY CONDITION*
Rheumatoid Arthritis (RA): points Typically marked by periods of remission & exacerbation;Typically has an insidious onset with non-specific manifestations;AUTOIMMUNE;JOINT SYMPTOMS OCCUR SYMMETRICALLY;CAN AFFECT NEARLY EVERY BODY SYSTEM;Incidence increases with age
Manifestations: Rheumatoid Arthritis 1 of 3 • Fatigue • Joint pain • Anorexia • Weight loss • Generalized stiffness • Joint stiffness • Morning stiffness
Diagnostics: Rheumatoid Arthritis Rheumatoid factor, ESR, c-reactive protein, antinuclear antibody (ANA), synovial fluid analysis
Complications: Rheumatoid Arthritis pleural effusion, pericarditis, splenomegaly, anemia, muscle atrophy
Medications: Rheumatoid Arthritis DMARDS (methotrexate), biologic targeted therapy, antibiotics, immunosuppressant drugs, NSAIDS/salicylates
Management: Rheumatoid Arthritis • Balance rest & activity • Prevent deformity with weight management, correct posture, & correct positioning • PT & OT: low impact exercise to maintain ROM • Use of assistive devices & splints • Heat & cold therapy
Manifestations: Rheumatoid Arthritis 1 of 2 (maybe 3) • Inflammation & fibrosis of joint capsule • Supporting structures may lead to deformity and disability • Rheumatoid nodules (fingers/elbows)
Manifestations: Rheumatoid Arthritis 2 of 2 (maybe 3) • Felty Syndrome: enlarged spleen & low WBC count, at risk for infection & lymphoma • Flexion contractions • Hand deformities
• Sjogren’s Syndrome: Rheumatoid Arthritis diminished lacrimal & salivary gland secretion, leading to a dry mouth & burning/itchy eyes with decreased tearing This is a manifestation of RA
Gout Define a type of acute arthritis characterized by elevation of uric acid and the deposit of uric acid crystals in 1 or more joints
Gout points Add
Manifestations: Gout • Acute phase: inflammation of joint, dusky or cyanotic joint, extremely tender, inflammation of big toe, low-grade fever • Chronic phase: visible deposits of sodium urate crystals
Diagnostics: Gout serum uric acid, WBC, ESR, 24-hour urine for uric acid, aspiration of synovial fluid for uric acid
Management: Gout • Limit purine intake;Increase fluids (200 mL);No alcohol;Bed rest;Elevate affected joint;Hot or cold therapies;Sodium bicarbonate to neutralize urine;Colchicine (anti-inflammatory medication for gout attacks);NSAIDS
Systemic Lupus Erythematosus (SLE) multisystem inflammatory autoimmune disease. • Complex disorder of multifactorial origin resulting from interactions among genetic, hormonal, environmental, & immunologic factors.
TISSUE DESTRUCTION: Systemic Lupus Erythematosus (SLE) Circulating immune complexes with antibodies against DNA are deposited in the basement membranes of capillaries in the kidneys, heart, skin, brain, & joints -> these complexes trigger inflammation and thus cause tissue destruction
Systemic Lupus Erythematosus (SLE) Risk Factors: • More common in African Americans, Asian-Americans, Hispanics, & Native Americans • Prevalence in families suggests a genetic influence
Manifestations: Systemic Lupus Erythematosus 1 of 3 • Dermatologic: butterfly rash, cutaneous vascular lesions, alopecia • Musculoskeletal: arthritis, polyarthralgia (pain in multiple joints) • Cardiopulmonary: tachypnea, cough, pleurisy, dysrhythmias
Manifestations: Systemic Lupus Erythematosus 2 of 3 • Renal: kidney damage (can lead to end-stage renal disease) • Nervous system: generalized or focal seizures, cognitive dysfunction as a result of immune complexes deposited on brain, depression, stroke
Manifestations: Systemic Lupus Erythematosus 3 of 3 • Hematologic system: anemia, leukopenia, thrombocytopenia, excessive bleeding, or excessive clotting • Infection: increased susceptibility
Diagnostic studies: Systemic Lupus Erythematosus NO SPECIFIC TEST, ANA present in most cases
Management: Systemic Lupus Erythematosus 1 of 4 • Drug therapy: NSAIDS, antimalarial drugs, steroid-sparing drugs, corticosteroids, immunosuppressive drugs • Assess pain and fatigue daily • Promote early diagnosis and treatment
Management: Systemic Lupus Erythematosus 2 of 4 • Observe: fever pattern, joint inflammation, limitation of movement, location & degree of discomfort, fatigueability • Monitor weight • Monitor I & O • Collect 24-hour urine
Management: Systemic Lupus Erythematosus 3 of 4 • Assess neurologic status • Explain nature of disease (no cure) • Provide support • Adherence to treatment does not half disease progression
Management: Systemic Lupus Erythematosus 4 of 4 • Minimize exposure to precipitating factors • Lupus & pregnancy: infertility can result from treatment regimen, women with serious SLE should not be pregnant, neonatal lupus may occur in infants born to a mother with SLE
Gullian Bone Syndrome: Definition Auto immune process that occurs a few days or weeks following a ural or bacterial infection. acute inflammatory demylinating polyneuropathy
Gullian Bone Syndrome: Symptoms Ascending, rapidly progressive, symmetric weakness of the limbs. maximal weakness is reached in 4 weeks. "Bar" Start low works up -> affects respiratory
Gullian Bone Syndrome: Clinical Manifestations Pain, Paresthesia, hypotonia, Areflexia, weakness/paralysis of the limbs, usually peak within 4 weeks. pain worse at night, facial flashing, diaphoresis. Decrease appetite, may interfere with sleep.respiratory failure. Autonomic nervous system dysfunction
Gullian Bone Syndrome: Autonomic nervous system dysfunction (manifestation) Orthostatic hypotension, HTN, abnomal vagal responses (brady cardia, heart block, asystole)
Gullian Bone Syndrome: Complications Respiratory infection/UTI, immobility from paralysis can cause paralytic ileus, muscle atrophy VTE, pressure ulcers, orthostatic hypotension, and nutritional deficiences
Gullian Bone Syndrome: Nursing Interventions Ventilatory Support; Plasma phresis - removes fantibodies/ immune factors; Assess motor/sensory function/ascending
Gullian Bone Syndrome: How will you evaluate respiratory/cardiac function; comparing to baseline; ABG's-hemodynamic status;Autonomic dysfunction;tachycardia;bradycardia;HTN;Hypotension;Abnormal Sweating,Paralytic ileus; Most w/ GBS will recover spontaneously 28~ days; 80% almost completely recover
Gullian Bone Syndrome: Diagnostic Study Patient History & Clinical Signs; Progressive weakness of more than one limb and dimminished or absent reflexes. CSF(increased protein) is helpful in excluding other causes. Nerve conduction studies/EMG (electromyography)
Gullian Bone Syndrome: EMG (electromyography) Evaluates and accesses electrical activity produced by skeletal muscles.
Bell's Palsy: Acute Peripheral facial paresis of unknown cause, it caused by facial nerve (CN VII) 7; Patients recover within (3 weeks - 9 months)
Bell's Palsy: Risk Factors Susceptible groups include women in third trimester of pregnancy/early postpartum, older adults, and people with diabetes or hypothyroidism
Bell's Palsy: Etiology/Pathophysiology: Acute Demylination: Most likely caused by reactivation of herpes simples virus (causes inflammation, leading to nerve compression and clinical features such as facial paralysis;
Bell's Palsy: Manifestations: Unilateral facial weakness (fast); pain around the ear;numbness of face,tongue,ear,tinnitus,headache,hearing deficit.Dropping on one side of the face,flaccidity.Paralysis inability to move. Bell's Phenomenon, Palpebral fissure, Overflow of tear production
Bell's Palsy: Diagnostic Studies No definitive existing tests. CT/MRI: can eliminate other causes for facial paralysis.
Bell's Palsy: Nursing Interventions Mild analgesics,moist heat,gentle massage-keeps muscle from becoming flaccid. Good Nutrition, chew on unaffected side. Prevent caries, dark glasses/artificial tears. eye shield/facial sling,exercises with OT/PT
Bell's Palsy: Medications Corticosteroids started before paralysis (the loss of the ability to move). Taper patient off of corticosteroids over 2 week period
Spinal Cord Injury: Caused by trauma or damage to the spinal cord. Results in temporary or permanent alteration in the function of spinal cord.
Spinal Cord Injury: Risk Factors Young men 16 - 30; High Risk activity
Spinal Cord Injury: Etiology/Pathophysiology Primary Primary:Can result from cord compression, bone displacement, interuption of blood supply to the cord, or tractrion from pulling on cord. (gun shot;stab wound)
Spinal Cord Injury: Etiology/Pathophysiology Secondary part 1 Ongoing Progressive damage hemmorage, vasospasm, thrombosis,loss of autoregulation,breakdown of BB barrier;infiltration of inflammatory cells that cause ischemia, edema,cellular necrosis;Aptosis(programmed cell depth); free radical information
Spinal Cord Injury: Etiology/Pathophysiology Secondary part 2 lipid peroxidrdrudction release of glutamate, and disruption of ionic balance of potassium sodium and calcium leads to neuronal cell depth and reduced spinal cord flow.
Spinal Cord Injury: Mechanism of injury Flexion, hypertension, flexion-rotation,extension-rotation,compression; flexion-rotation injury is the most unstable because ligaments that stabilize the spine are torn.
Spinal Cord Injury: Level of Injury Cervical,Thoracic,Lumbar, Sacral;Skeletal level of injury is the vertebral level with the most damage to the vertebral bones/ligaments.Neurologic level is the lowest segment of spinal cord with normal sensory and motor function on both sides of the body
Spinal Cord Injury: Cervical and Lumbar Most common becaue they are assosiated with the greatest flexibility/movement
Spinal Cord Injury: Cervical Cord is involved. Paralysis of all four extremities occurs, resulting in tetraplegia (quadriplegia)
Spinal Cord Injury (types that causes Paraplegia) Toracic, Lumbar, Sacral spinal cord is damaged.
Spinal Cord Injury: Complete Cord Involvement Results in loss of Sensory and Motor function
Spinal Cord Injury: Incomplete cord involvement Results in mixed loss of voluntary motor activity and sensation and leaves some tracts intact.
Spinal Cord Injury: 5 major syndromes Central Cord Syndrome; Anterior Cord Syndrome; Brown-Sequard syndrome; cauda-equina syndrome;conus medullaris syndrome
Spinal Cord Injury: Clinical Manifestations Motor/Sensory:Sensory regions called dermatonmes;each segment of the spinal cord innevating a particular area of skin;
Spinal Cord Injury: C4 Injury Tetraplegia results in complete paralysis below the neck (above c4 deflcullty breathing)
Spinal Cord Injury: C6 Injury Paraplegia results in paralysis below chest
Spinal Cord Injury: T6 Injury Paraplegia results in paralysis below chest
Spinal Cord Injury: L1 Injury Paraplegia results in paralysis below the waist.
Spinal Cord Injury: respiratory systems Above C4 total loss of respiratory muscle function; below c4 results in diaphagmatic breathing; too much edema; hemorrhaging could causes diaphragm to not function;hypoventilation and impairment of vital capacity and tidal volume; how much you can breath
Spinal Cord Injury: cardiovascular injury above t6 leads to dysfunction of the sympathetic nervous system; result may be brady cardia, peripheral vasodilation, and hypotension. (decreased circulation)/(decreased ability to compensate)
Spinal Cord Injury: Urinary System Won't work as well; acute SCI/spinal shock: bladder atonic, becomes overdisturbed, and fails to empty
Spinal Cord Injury: GI Systems Decrease function; Neurogenic boveliloss of voluntary cortisol;sphincter is tight;at risk for inpaction/constipation,paralytic ileus;incontinence/retention
Spinal Cord Injury: Integumentary system risk for skin breakdown/lack of sensation
Spinal Cord Injury: Thermoregulation Poikilothermism: adjustment of body temp to room temp. High cervical injury are associated with greater loss of ability to regulate temp.
Spinal Cord Injury: Metabolic Needs High Calories, protein, monitor potassium and sodium when patient has NG tube.
Spinal Cord Injury: Peipheral Vascular problems Leg girth: monitor VTE/DVT (won't be pain tenderness) Nociceptive
Spinal Cord Injury: Nociceptive PAIN: Visceral and or other types of injury. Patients describe musculoskelatal pain as dull or achy;VISCERAL PAIN: located in thoras abdomen, and/or pelvis, dull, tender, or cramping.
Spinal Cord Injury: Neuropathic pain Damage is spinal cord/nerve roots. Pain as hot, burning,tingling,pins,needles,cold shooting
Spinal Cord Injury: Diagnostics CT Scan Location and injury MR to assess soft injury
Spinal Cord Injury: Complications Spinal Shock may occur after accute SCI;temporary shock is decreased reflexes, loss of sensation, absent themoregulation and flaccid paralysis;Can last 7-20 days and patient wont know how severe injury is until it's up. Neurogenic shock
Spinal Cord Injury: Neurogenic Shock Loss of vasomotor tone caused by injury and characterized by hypotension/bradycardia
Spinal Cord Injury: Interventions Maintain ABC;Stabbalize/Immobilize;Assess Respiratory Failure in high cervical injuries;Spinal Shock assessment complete loss of reflex motor, sensory, and autonomic function below the Injury.
Spinal Cord Injury: Autonomic Dysreflexia part 1 Increased BP,pounding Headache,Sweating,Nasocongestion, bradycardia,goosebumps,bowel/bladder distension.watch for acute paralytic ileus.lack of gastric activity.asses bowel sounds frequently.initiate gastric suction to reduce distension. rectal tube
Spinal Cord Injury: Autonomic Dysreflexia part 2 suction with cautives to prevent vagus nerve stimulation which can cause cardiac arrest;high dose corticosteroids IV to decrease edema and reduce cord damage. Prevent UTI:Cranberry, prune, Tomato, water, cathertization;deep breathing exercises;Exercise
ALS rare progressive neuromuscular disorder characterized by loss of motor neurons."Lou Gehrigs" disease-stephen hawking/baseball player 1st in 1939
ALS Manifestations Progressive muscle weakness; Early Signs:tripping,dropping things,abnormal fatigue,slurred speach,muscle cramps/twitches. muscle wasting;pain esophangealreplek, constipation:doesn't affect a patient intelligence, but may have depression. No cure
ALS Nursing Interventions Riluzole; Facilitating communication;reducing aspiration;facilitate early identification of respiratory insufficiency. decrease pain secondary to muscle weakness.decrease risk of injury R/T falls. provide diversional activities/reading/companionship
ALS complications Respiratory Insufficency; Cognitevely intact and wastes away. Spporting patients cognitive/emotional function. help the patient/family manage disease process, grieving r/t end of life. Artificial directives and artificial methodes of ventilation.
What is Multiple Sclerosis Chronic progressive, degenerative disorder of the (CNS) characterized by demylination of the nerve fibers of the brain/spinal cord
Risk factors of MS Age between 20-50 years old, women are more affected than men, cold climates
Clinical manifestations of MS Aggrevated by heat, severe fatigue/muscle weakness, blurred double vision, red-green color distortion, blindness in one eye (optic neuroitis), gait disturbances, numbness, tingling, paresthesia, spastic bladder/hypotonic flaccid
Diagnostic studies for MS Rule out diagnosis two inflammatory demylination lesions in at least two different locations with CNS. Damage or attack occurring at different times. History and Physical. CSF analysis. Increase in immunoglobulin G
Meds for MS Corticosteroids "Sones" are most helpful to treat acute exacerbation of MS. Chemotherapy drugs shorten length of attack (Methotrexate).
Nursing interventions for MS Preventing triggers/exacerbation- which can be from infection, assist the patient in dealing with stress, bowel/bladder problems, vigorous early treatment, diet high in fiber, minimize caffinee
Complications of MS Use of immuno-modulator drugs. Decreases immune response
Parkinson's Disease Chronic progressive nuero-degenerative disorder characterized by slowness in the initiation and execution of movement (TRAP)
Risk factors of PD More common in men over 50, lack of dopamine, Lewy bodies: unusual clumps of protein are found in brains of patients with PD.
Clinical manifestations of PD TRAP: Tremor, rigidity, akinesia, postural instability. Tremor: often first sign and may be minimally initially. Akinesia: loss of control of voluntary muscle movement. Shuffling gait (festination) Postural instability Stop themselves from going forward
What is the two words that describe the "pull test" pertaining to Postural instability Stop themselves from going forward (populsion) or backward (retropulsion) assessment of postural instability includes "pull test"
Interventions of PD Schedule activities in the morning, do activities at peak of medication, eliminate noise, soft easy to swallow diet
Meds for PD Carbidopa/levadopa (sinemet). Monitor for signs of dyskinesia (abnormal increase movements of mouth), instruct patient or caregive to report any uncontrolled movement s of face, eyelid, mouth, tongue, arms, hands, legs
Complications of PD Hypomobility (inability to rise from chair), Dyskinesia, weakness, depression, dysphagia
Nutritional therapy of PD Easy to chew/swallow foods, adequate fiber fruits, cut food into bite sized pieces, eat six small meals a day
Interventions of PD Increase exercise to strengthen muscle and flexion of joints, step over real lines on the flood, drop rice kernels and step over them, rock from side to side to get up,
Myasthenia Gravis Autoimmune disease of the nueromuscular junction characterized by fluctuating weakness of certain skeletal muscle groups
Etiology of MG Reduction in receptor sites, antibodies attack receptors. Thymic hyperplasia and tumors are common in patients with MG suggesting autoantibody production occurs in thymus
Manifestations of MG Muscles used to move eye, eyelids, chew, swallow, speak, breathe are affected, occular muscles affected. Patients may difficulty chewing and swallowing. Exacerbation respiratory infections, stressful situations
Myasthenic crisis Muscle weakness triggered by stress can cause aspiration, respiratory insufficiency and respiratory tract infection
Diagnostic studies of MG History and physical exam. TENSLION TEST; improved muscle contractility after IV injection of edrophonium chloride (Tenslion). More definitive test tenslion.
Meds of MG anticholinterase drugs to enhance Ach breakdown, Corticosteroids
Interventions of MG Tracheostomy kit available if they have respiratory failure. Myasthenic crisis: muscle weakness in areas that affect swallowing/breathing. Bed rest often realizes symptoms bladder/respiratory infections recurring encourage cough/deep breath.
Cholinergic crisis Anticholintrase drug clinical features include muscle fasciulation (twitching), sweating, excessive, salivation, constricted pupils
Trigeminal Neurlagia TN Tic doulorex is characterized by sudden, usually unilateral, severe, brief, stabbing recurrent episodes of pain in trigeminal nerve (CN #5).
Risk factors TN Women are affected more than men. Middle aged people, HTN/MS. Side note: At risk for suicide
Etiology of TN artery compresses the nerve as it exits the braintem. Can be secondary to MS, shingles, masses in cerebellum, brainstem
Manifestations of TN abrupt onset of paroxysms of excruciating pain, described as burning, knifelike, or lightening like shock in upper lips. Frequent blinking 2-3 minutes (episodes, unilateral). Painful episodes initiated by triggering mechanisms of light touch.
Diagnostic of TN History and physical, MRI
Meds of TN T1 (Dilantin), T2 Analgesics/opioids
Interventions of TN Room should be kept at a moderate temp (free of drafts). Patient may prefer to complete all self care fearing someone else will cause pain. Serve lukewarm food, soft toothbrush or warm mouthwash, chew unaffected side, avoid hot food, 6 mon dental visits
Seizures Is a transient uncontrolled electrical discharge of neurons in the brain that interrupts normal function
Clinical manifestations of seizures Prodromal phase, Aural phase, ictal phase, postical phase
Prodromal phase with sensations or behavior changes that preced a seizure
Aural phase With a sensory warning that is similar each time a seizure occurs
ictal phase from first symptoms to the end of the seizure activity
Postical phase The recovery period after the seizure
Tonic-clonic (grand mal) lose of consciousness, falling to the ground, followed by stiffening of the body. Cyanosis, excessive salvation, tongue or cheek biting, incontinence may accompany the seizure
Postical phase The patient has muscle soreness, feels tired, and may sleep for several hours, some patients may not feel normal for several hours. Patient has no memory of seizure
Absence seizure Petitmal day dreaming less than 10 seconds, accompanied by blinking, chewing, hand gestures
Complication Statuse epilepticus (SE)
Status epilepticus State of continuous seizure or a condition in which seizures recur in rapid succesion without return to consciousness. Lasting longer than 5 min. Convulsive status is most dangerous: hypoxemia, cardiac dysrthmias, fatal ventilatory
Diagnostic studies of seizures Health history, CBC, urinalysis, electrolytes, creatnine, fasting blood glucose, EEG
Drugs for seizures Dilantin phenytonin, carbamezpine (tegretol), phenobrabital, divasproex, and primidone (mysoline). All used to treat tonic-clonic.
Status eplictus Requires immediate rapid acting IV antizeizure drugs. lorazepan (ativan/diazepam (valium)
Dilantin causes what Gum breakdown
S/E antiseizure drugs Diplopia, drowsiness, ataxia
Created by: craig.mcintire