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Med-Surg Final Exam Verified Updates 2025/26, Exams of Nursing

Musculoskeletal (New Material)  Bones  Bones support, protect internal organs, voluntary movement, blood cell production & mineral storage. They provide supporting framework that keeps the body from collapsing & also allows the body to bear weight.

Typology: Exams

2024/2025

Available from 06/16/2025

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Med-Surg Final Exam
Musculoskeletal (New Material)
Bones
Bones support, protect internal organs, voluntary movement, blood cell production & mineral storage. They
provide supporting framework that keeps the body from collapsing & also allows the body to bear weight.
Epiphyseal Plate
Also called growth zone, it is the cartilaginous area between the epiphysis & metaphysis, it actively produces
bone to allow longitudinal growth in children. Injury to the growth plate in children can lead to a shorter extremity
that can cause significant functional problems. In adults the epiphysis & metaphysis become joined as the plate
hardens to mature bone.
Joints
Articulation is a place where the ends of two bones are in proximity & move in relation to each other, joints are
classified by the degree of movement that they allow.
Cartilage
Hyaline Cartilage: the most common, contains a moderate amount of collagen fibers, found in the trachea,
bronchi, nose, epiphyseal plate. & articular surfaces.
Fibrous Cartilage: consists mostly of collagen fibers & is a tough tissue that often functions as a shock
absorber, it can be found between the vertebral discs & also forms a protective cushion between the bones of the
pelvic girdle. Knee, & shoulder.
Elastic Cartilage: contains both collagen & elastic fibers, is more flexible than hyaline cartilage, it is found in
ear, epiglottis, & larynx.
Muscle
Cardiac Muscles: found in the heart, its spontaneous contractions propel blood through the circulatory system.
Smooth Muscles: occurs in the walls of hollow structures such as airways, arteries, GI tract, urinary bladder, &
uterus. Smooth muscle contraction is modulated by neural & hormonal influences.
Skeletal Muscles: requires neuronal stimulation for contraction, accounts for half of a human begins weight.
Contractions
Isometric Contractions: increases tension within a muscle but does not produce movement, repeated
isometric contractions make the muscles grow larger & stronger.
Isotonic Contractions: shorten a muscle to produce movement, most contractions are a combination of
isometric & isotonic.
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Med-Surg Final Exam

Musculoskeletal (New Material)

 Bones

 Bones support, protect internal organs, voluntary movement, blood cell production & mineral storage. They provide supporting framework that keeps the body from collapsing & also allows the body to bear weight.

 Epiphyseal Plate

 Also called growth zone, it is the cartilaginous area between the epiphysis & metaphysis, it actively produces bone to allow longitudinal growth in children. Injury to the growth plate in children can lead to a shorter extremity that can cause significant functional problems. In adults the epiphysis & metaphysis become joined as the plate hardens to mature bone.

 Joints

 Articulation is a place where the ends of two bones are in proximity & move in relation to each other, joints are classified by the degree of movement that they allow.

 Cartilage

Hyaline Cartilage: the most common, contains a moderate amount of collagen fibers, found in the trachea, bronchi, nose, epiphyseal plate. & articular surfaces.  Fibrous Cartilage: consists mostly of collagen fibers & is a tough tissue that often functions as a shock absorber, it can be found between the vertebral discs & also forms a protective cushion between the bones of the pelvic girdle. Knee, & shoulder.  Elastic Cartilage: contains both collagen & elastic fibers, is more flexible than hyaline cartilage, it is found in ear, epiglottis, & larynx.

 Muscle

Cardiac Muscles: found in the heart, its spontaneous contractions propel blood through the circulatory system.  Smooth Muscles: occurs in the walls of hollow structures such as airways, arteries, GI tract, urinary bladder, & uterus. Smooth muscle contraction is modulated by neural & hormonal influences.  Skeletal Muscles: requires neuronal stimulation for contraction, accounts for half of a human begins weight.

 Contractions

Isometric Contractions: increases tension within a muscle but does not produce movement, repeated isometric contractions make the muscles grow larger & stronger.  Isotonic Contractions: shorten a muscle to produce movement, most contractions are a combination of isometric & isotonic.

 Ligaments

 Connect bones to bones, have a higher elastic content than tendons, they provide stability while permitting controlled movement at the joint.  Ligaments & tendons have a relatively poor blood supply, usually making tissue repair slow process after injury.

 Tendons

 Attach to muscles to bone as an extension of the muscles sheath that adheres to the periosteum. Both tendons & ligaments are composed of dense, fibrous, connective tissue that contains bundles of closely packed collagen fibers arranged in the same plane for additional strength.

 Fascia

 Refers to layers of connective tissue with intermeshed fibers that can withstand limited stretching. Can be either superficial or deep.

 Bursae

 Small sacs of connective tissue lined with synovial membranes & containing viscous synovial fluid. They are typically located in the bony prominences or joints to relieve pressure & decreases friction between moving parts.

 Older Adult Related Changes

Muscles: decreased number & diameter of muscle cell, loss of elasticity in ligaments, tendons, & cartilage, reduced ability to store glycogen, decreased ability to release glycogen as quick as energy is needed during stress, & decreased basal metabolic rate.  Joints: increased risk for cartilage erosion that contributes to direct contact between bone & ends & overgrowth of bone around joint margins, loss of water from discs between vertebrae, decreased height of intervertebral spaces.  Bone: decreased bone density & strength, brittleness, & slowed remolding process.

Fractures Lewis 1511

Etiology Diagnostic Indicators Factors Effecting Healing Manifestations Nursing Interventions Medical Treatment A disruption or break in the continuity of the structure of the bone. Although traumatic injuries account for the majority of fractures, some are secondary to a disease process. -history & physical -X-ray (most common) -CT scan -MRI Ongoing Assessment Ongoing monitoring -Vital signs, level of consciousness, -site of the fracture -blood supply to the area -displacement or fixation devices -infections -poor nutrition -age -hormones -smoking -edema & swelling -pain & tenderness -muscle spasm -deformity -loss of function (in the affected area) -crepitation -ecchymosis, contusion Table 63- -immediate localized pain with -neurovascular assessment think 6 P’s -immobilization -proper nutrition is essential -teach ROM exercise -assess for complications associated with immobility -manipulation, traction, closed or open reduction, fixation devices -surgical debridement & irrigation -prophylactic antibiotic therapy & DTaP shot -muscle relaxants including flexeril,

Callus Formation: as minerals & new bone matrix are deposited in the osteoid an unorganized network of bone is formed that is woven about the fractures parts. Callus is primarily composed of cartilage, osteoblasts, calcium, & phosphorous. It usually appears by the end of the second week after injury (evidence of callus formation can be verified by x-ray.  Ossification: ossification of the callus tissue occurs from 3 weeks to 6 months after the fracture & continues until the fracture has healed, this is sufficient to prevent movement at the fracture site when the bones are gently stressed, however the fracture is still evident on x-ray, during this stage clinical union, the patient may be allowed limited mobility or the cast may be removed.  Consolidation: as callus continues to develop, the distance between bone fragments diminished & eventually closes. During this stage ossification continues, it can be equated to radiologic union, which occurs when there is x-ray evidence of complete bony union, this phase can occur up to 1 year after injury.  Remolding: excess bone tissue is reabsorbed in the final stage of bone healing, & union is complete. Gradual strength & shape of the injured bone occurs, bone remodels in response to physical loading stress. New bone is deposited in sites subjected to stress & resorbed at areas where there is little stress.

 Complications of Healing

Delayed healing: heals slower than expected  Nonunion: fracture fails to heal  Malunion: heals but in unsatisfactory position, resulting in deformity  Angulation: heals in abnormal position  Pseudoarthrosis: false joint is formed with abnormal movement at the site  Refracture: new fracture at the original site  Myositis Ossifcans: deposition of Ca+ in muscle tissue at the injury site

 Types of Fractures

Colles’ Fracture - fracture of distal radius, one of most common fractures in adults. Usually occurs when client attempts to break a fall. Most often occurs in pts over 50 whose old bones are osteoporotic. symptoms include immediate pain, swelling, dorsal placement of distal fragment (obvious deformity of wrist). Major complication includes vascular insufficiency secondary to edema; carpal tunnel syndrome can occur later. Managed by closed manipulation of fracture & immobilization. Nursing measures: prevent/reduce edemas, frequent neuro checks, support/protection of extremity, encourage active movement of thumb/fingers to reduce edema/ increase venous return. Instruct patient to perform active movements of shoulder to prevent stiffness.  Humerus Fracture: common among young to middle-aged adults. Symptoms: obvious displacement of humerus shaft, shortened extremity, abnormal mobility, & pain. Major complications include radial nerve injury & vascular injury to brachial artery. Treatment depends on location/displacement: hanging arm cast, shoulder immobilizer, sling & swathe. When these devices used, elevate HOB, allow arm to hang freely when sitting/standing, measures to prevent skin breakdown. During rehab, exercise program to improve strength/motion (helps prevent stiffness).  Pelvic Fracture: may cause serious intraabdominal injury such as paralytic ileus, hemorrhage, & laceration of urethra, bladder, or colon. Can cause acute pelvic compartment syndrome. Physical exam of abdomen

demonstrates local swelling, tenderness, deformity, unusual pelvic movement, & ecchymosis. Assess neuro status of lower extremities & manifestations of associated injuries. Diagnosed by x-ray & CT scan. Treatment: bed rest for stable fractures maintained for few days to 6 weeks w/ early ambulation encouraged. Complex fractures require pelvic sling traction, skeletal traction, external fixation, open reduction, or combo of these. ORIF necessary if pelvis displaced. Turn pt only when ordered by HCP, assess bowel/urinary elimination and distal neuro status. Provide back care while pt is raised from bed  Hip Fracture: common in older adults (90% resulting from fall). Symptoms include external rotation, muscle spasm, shortening of affected extremity, & severe pain/tenderness around fracture site. Can cause disruption in blood supply= avascular necrosis of femoral head. Affected extremity may be temporarily immobilized by Buck’s traction (relieves painful muscle spasms & used for up to 24-48 hrs). Surgical options include repair w/ internal fixation, devices, replacement of part of femur w/ prosthesis (partial hip replacement), & total hip replacement. Pre-op: analgesics/muscle relaxants, comfy positions, & properly adjusted traction, encourage exercising other extremities and using trapeze bar to aid in hanging positions. Post-op: assess neuro, elevate leg whenever in a chair to alleviate edema, pillow between knees when turning to relieve pain, tub bath/driving not allowed for 4- weeks. Complications= nonunion, avascular necrosis, dislocation, and degenerative arthritis  Femoral Shaft Fracture: more common in young adults. Symptoms: deformity/angulation, shortening of extremity, inability to move hip or knee, & pain. Complications= fat embolism, nerve/vascular injury, problems associated w/ bone union, open fracture, soft tissue damage. Immobilize fracture. Traction may be used temporarily. Internal fixation is preferred. Ensure patient uses ROM & strengthening exercises for uninvolved extremities.  Tibia Fracture: more common site of stress fracture. Complications= compartment syndrome, fat embolism, problems associated w/ bony union, possible infection w/ open fractures. Assess neuro of affected extremity at least q2h during first 48 hrs. Must be non-weight bearing for 6-12 weeks  Stable Vertebral Fracture: fracture or fragment is not likely to move or cause spinal cord damage. Complications= displacement which can damage spinal cord. Pain/tenderness in affected region, sudden loss of function below level of fracture can indicate spinal cord paraplegia. Goal is to keep spine in good alignment until union has been accomplished. Treatment: pain meds, early mobilization and bracing.  Facial Fracture: maintain patent airway & provide adequate ventilation, suctioning may be necessary. All pts w/ facial injuries should be treated as if also have cervical fracture (until proven otherwise w/ x-ray & CT scan). Perform oral/facial exams after patient stabilized

 Open Reduction

 The correction of alignment through a surgical incision, it usually includes internal fixation of the fracture with wires, screws, pins, plates intramedullary rod, or nails. Early initiation of ROM of the joint, machines can provide continuous passive motion (CPM) to various joints. The main disadvantages of open reduction include infection, complications associated with anesthesia, & effect of preexisting medical conditions.

 Closed Reduction

 Stages of Bruising

 Red: At their onset, bruised look red or pink in color because of the presence of iron-rich hemoglobin in the

pooled blood. The area around the bruise may also get tender and swollen.  Dark blue or purple: Within one to two days from the time of injury or trauma, the bruise will then turn its color to dark blue or purple. This will continue through to the fifth day. It is attributed to low oxygen supply in the site of bruising as a result of swelling, which then causes the normally red hemoglobin to change its color

accordingly.

Greenish: After day 5, the bruise then turns greenish as hemoglobin undergoes biochemical breakdown. The green coloration is usually an indication of high levels of biliverdin in the pooled blood and will continue to day 7

 Yellow or Brown : After day 7, the bruise then turns pale yellow (usually as a result of presence of large

amounts of bilirubin) or brown. This is the final stage of bruise healing and the bruise will not undergo any further color changes but instead fade away gradually until it is no more.

Cast Care Table 63-

DO Do Not Apply ice directly over fracture site for first 24hrs (avoid getting cast wet by keeping ice in plastic bag & protecting cast with cloth) Get cast wet Check with HCP before getting fiberglass cast wet Remove any padding Dry cast thoroughly after exposure to water (blot dry with towel, use hair dryer on low setting) Insert any objects inside cast Elevate extremity above heart level Cover cast with plastic for prolonged periods Move joints above & below cast regularly Bear weight on new cast for 48hrs (not all cast are made for weight bearing so check with CHP) Use hair dryer on cool setting for itching Keep appointment to have fracture & cast checked Report s/s of possible problem to HCP (increasing pain despite elevation, ice, or analgesia, swelling associated with pain & discoloration of toes or fingers, pain during movement, burning or tingling under the cast, & sores or foul odor under the cast)

Compartment Syndrome Lewis 1522

Etiology Patho Risk Factors/Causes Manifestations Nursing interventions Medical Treatment A condition in which swelling & increased pressure within a limited space (a Two basic causes of CS are; (1) decreased compartment size resulting from -trauma -fractures -extensive soft tissue damage -crush injury Six P’s -Pain (distal to the injury that is not relieved by pain medication) -neurovascular assessment -assess urine output

  • do not elevate -fasciotomy (surgical decompression), the site may be left open for

compartment) press on & compromise the function of blood vessels, nerves, and/or tendons that run through the compartment. Most commonly associated with trauma, fracture (especially of the long bones), extensive soft tissue damage, & crush injury. restrictive dressings, splints, casts, excessive traction, or premature closure (2) increased compartment contents related to bleeding, inflammation, edema, or IV infiltration -after knee or leg surgery -fractures of the distal humerus & proximal tibia are the most common fractures associated with compartment syndrome -Pressure (increasing pressure in the compartment) -Paresthesia -Pallor -Paralysis

  • Pulselessness -ischemia can occur within 4-8hrs after onset the extremity (elevation may cause venous pressure & slow arterial perfusion) -do not use cold therapy several days to ensure adequate soft decompression -in severe cases amputation

Fat Embolism Lewis 1523

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Medical Treatment Systemic fat globules from fractures that are distributed into tissue & organs after a traumatic skeletal injury. FES is a contributory factor in mortality associated with fractures. Fractures most often causing FES are those of long bones, ribs, tibia, & pelvis. No specific lab examinations are available but certain diagnostic abnormalities may be present; -fat cells in blood, urine, or sputum -changes in EKG -prolonged pTT time -decrease in hematocrit & platelet count, & PaO 2 Two theories about FES exist; -mechanical theory is that fat emboli may originates from the fat that is released from the marrow of injured bone, the fat then enters the systemic circulation where it embolizes to other organs such as the brain. -biochemical theory is that hormonal changes caused by trauma or -early recognition is crucial to prevent a potentially lethal course, symptoms usually develop within 24-48hrs -in a short time skin color changes from pallor to cyanosis -coma -fat emboli in the lungs cause a hemorrhagic interstitial pneumonitis that produces s/s of acute respiratory distress syndrome such as; -chest pain -tachypnea -careful immobilization of long bone fractures are probably the most important factor in prevention of FES -encourage coughing & deep breathing -reposition the patient as little as possible -Treatment is directed at prevention & is mostly supportive & related to management of symptoms -corticosteroids (can be controversial) -oxygen therapy -fluid resuscitation (to correct acidosis & replacement of blood loss)

Causes of Osteoarthritis Table 65-1, 1562

Trauma Dislocation or fractures may lead to avascular necrosis or uneven stress on cartilage Mechanical Stress Repetitive physical activities cause cartilage deterioration Inflammation Release of enzymes in response to local inflammation can affect cartilage Joint Instability Damage to supporting structures causes instability, placing uneven stress on articular cartilage Neurological Disorders Pain & loss of reflexes from neurologic disorders such as diabetic neuropathy, Charcot’s joints (causes abnormal movements that contribute to cartilage deterioration) Skeletal Deformities Congenital or acquired conditions such as legg-calve-perthes disease or dislocated hip contribute to cartilage deterioration Drugs Such as Indocin, colchicine, & corticosteroids can stimulate collagen digesting enzymes in joint synovium Hematologic or Endocrine Disorders Chronic hemarthrosis contributes to cartilage deterioration

Osteoporosis Lewis 1553

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Medical Treatment Porous bone (fragile bone disease), is a chronic progressive metabolic bone disease characterized by low bone mass & structural deterioration of bone tissue, leading to increased fragility. -bone mineral density (BMD) which includes DEXA & quantitative ultrasound -initial bone scan is recommended before the age of 65 -DXA results are reported as T- scores (number of standard deviations below average for normal bone density) -T-score -1 or higher indicates normal bone density -T-scores -2.5 is defined as -Postmenopausal women -family history -diet low in calcium -alcohol abuse -vitamin D deficiency -low testosterone in men -age (>65) -female -low body weight -smoking -sedentary lifestyle -white or Asian -nontraumtic fractures -long term corticosteroid use -back pain -spontaneous fractures -gradual loss of height -dowagers hump (kyphosis) -calcium supplements (must be taken in divided doses with food to enhance absorption) -prevention of fractures -vitamin D -smoking cessation -weight bearing exercise -Bisphosphonates -Calcitonin -Selective estrogen receptor modulators -Teriparatide (Forteo) -Denosumab (Prolia), subQ injection q6months -Management of patients receiving corticosteroids -vertebroplasty or kyphoplasty (minimally invasive procedures used to treat osteoporosis vertebral fractures)

osteoporosis -T-score -1 to -2. is defined as osteopenia (bone loss that is more than normal but not yet a diagnosis of osteoporosis)

Osteomyelitis Lewis 1539

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Medical Treatment A severe life- threatening infection of the bone, bone marrow, & surround soft tissue. The infecting microorganism can enter directly or indirectly. After gaining entry into the blood, the microorganisms grow resulting in an increase in pressure because of the nonexpanding nature of most bones. This increasing pressure eventually leads to ischemia & vascular compromise of the periosteum. Once ischemia occurs, -bone or soft tissue biopsy -blood and/or wound cultures -elevated WBC count & erythrocyte sedimentation rate -x-ray (signs usually do not appear until the 10 th^ day) -MRI & CT scans -radionuclide bone scan

  • staph. Aureus -staph. Epidermidis -strep. Viridians -E. coli -mycobacterium tuberculosis -Neisseria gonorrhoeae -pseudomonas -salmonella -fungi, mycobacteria Acute Infection <1 month in duration, symptoms include local & systemic; Local Symptoms -Pain unrelieved by rest; worsens with activity -Swelling, tenderness, warmth -Restricted movement Systemic Symptoms -Fever -Night sweats -Chills -Restlessness -Nausea -Malaise -Drainage (late) Chronic Infection that persists longer than 1 month & failed to respond to antibiotic therapy, symptoms are -Immobilization and careful handling of affected limb -Assess and treat pain -Dressing care -Proper positioning to prevent complications of immobility -monitor trough levels -teach patient adverse signs & toxic reactions to antibiotic therapy (hives, diarrhea, bloody stool, throat & mouth sores, tendon rupture, ototoxicity, nephrotoxicity, & neurotoxicity) Acute -vigorous & prolonged IV therapy is the treatment of choice for acute osteomyelitis, as long as bone ischemia has not yet occurred -culture & bone biopsy before starting antibiotic therapy -IV antibiotic therapy for 4- weeks but up to 6 months Chronic -oral fluoroquinolone (Cipro) for 6 to 8 weeks -debridement of devitalized & infected tissue, the wound may be closed & a suction irrigation

Chronic Low Back Pain Lewis 1547

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Medical Treatment Low back pain that lasts longer than 3 months or is repeated incapacitating episodes. Is often progressive. Spinal stenosis which is narrowing of the spinal canal is a common cause of chronic low back pain, can be acquired including OA, RA, tumors, & Paget’s disease. Inherited conditions include scoliosis or congenital spinal stenosis. Same as acute -degenerative conditions such as arthritis or disc disease -osteoporosis or other metabolic bone disease -prior injury (scar tissue weakens the back) -chronic strain on the lower back from obesity, pregnancy, or job related stooping -congenital abnormalities in the spine -lower back pain that radiates to the buttocks & legs -pain that worsens when standing particularly when standing & not walking -heaviness in the legs or buttocks -lesser pain when bending forward or sits down -Weight reduction -Sufficient rest periods -Local heat and cold application -Physical therapy -Exercise and activity throughout day -Complementary and alternative therapies -Back School -Mild analgesics -Antidepressants -Gabapentin (Neurontin) -Duloxetine (Cymbalta) -Epidural corticosteroid injections -Implanted devices to deliver analgesia

Low Back Do’s & Don’ts Table 64-

DO DO NOT

Use lumbar roll or pillow for sitting Lean forward without bending knees Use local heat or cold application Lift anything above level of elbows Maintain appropriate body weight Stand in one position for prolonged time Carry light items close to the body Sleep on back or abdomen with legs straight Sleep side lying with knees & hips bent Exercise without consulting HCP if severe pain Sleep on back with lift under knees to flex hips & knees Exceed prescribed amount & type of exercise without consulting HCP Avoid straining the lower back by placing a foot on a step or stool during prolonged standing Exercise 15min in the morning & evening, begin exercise with 2-3min warm-up by moving arms & legs, alternating relaxing & tightening muscles & exercise slowly with smooth movements

Intervertebral Disc Disease Lewis 1547

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Medical Treatment Separates the vertebrae of the spinal column & provides a shock absorption of the spine. Is a condition that involves the deterioration, herniation, or other dysfunction of the intervertebral discs. Structural degeneration of discs is often caused by degenerative disc disease (DDD), this progressive degeneration is a normal process of aging & results in intervertebral discs losing their elasticity, flexibility, & shock- absorbing capabilities. -history & physical -x-ray -CT scan & MRI -myelogram -diskogram -electromyogram (EMG) -positive straight leg -natural degeneration -age -repeated stress of the spine -trauma -low back pain -decreased ROM -paresthesia -radicular pain that radiates down the buttocks & below the knee, along the sciatic nerve -back pain when flexing the foot 90 degrees -depressed reflexes -pain that radiates into the arms & the hands (called cervical disc disease) -multiple nerve root compression (cauda equina) from a herniated disc, a tumor, or an epidural abscess may be manifested as bowel or urinary incontinence, this is a medical emergency! -teach limitation of movement (avoid extreme flexion & torsion) -use of heat or ice -back strengthening exercises -teach good body mechanics -ultrasound & massage -skin traction -TENS unit -NSAIDs -short term opioids -muscle relaxants -antiseizure drugs -antidepressants -epidural corticosteroid injections -surgical therapy is indicated when conservative treatment fails, constant pain, loss of bowel or bladder control, persistent neurological deficits, & radiculopathy worsens

 Spinal Surgery Postoperative

Intradiscal electrothermoplasty (IDET): Minimally invasive outpatient procedure, needle inserted into affected disc & wire threaded into disc and heated → denervates nerve fibers  Radiofrequency Discal Nucleoplasty (Coblation Nucleoplasty): Needle inserted similar to IDET, radiofrequency probe generates energy → breaks up nucleus pulposus, up to 20% of nucleus is removed, & Decompresses disc  Interspinous Process Decompression System (X Stop): Titanium that fits into mount placed on vertebrae, is used to treat lumbar spinal stenosis & Lifts vertebrae off pinched nerve

 C-Reactive Protein (CRP)

 Used to diagnose inflammatory disease, infections, & active widespread malignancy. Is synthesized by the liver & is present in large amounts in serum 18-24hrs after onset of tissue damage. Is done through a simple venipuncture.

 Human Leukocyte Antigen (HLA)-B

 Antigen often present in autoimmune disorders such as ankylosing spondylitis & RA. Is done through a simple venipuncture.

 Creatine Kinase (CK)

 Highest concentration found is skeletal muscle, increased levels are found in progressive muscular dystrophy, polymyositis, & traumatic injuries. Is done through a simple venipuncture.

 Potassium

 Increased in muscle trauma as cell destruction releases this electrolyte into serum. Is done through a simple venipuncture.

 Arthrocentesis

 Incision or puncture of joint capsule to obtain samples of synovial fluid from within joint cavity or to remove excess fluid. Is useful in diagnosis of joint inflammation, infection, meniscal tears, & subtle fractures. Inform patient that procedure is usually done at the bedside or in an exam room, send samples of synovial fluid to lab for examination, & after procedure apply compression dressing & observe for leakage of blood or fluid on dressing.

Fluid & Electrolytes

Respiratory Acidosis (Hypoventilation) pH ↓^ PaCO2 ↑

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Carbonic excess is caused by hypoventilation which results in buildup of Co2, subsequently, carbonic acid accumulates in the blood. Carbonic acid dissociates, liberating H+ & a decrease in pH occurs. If CO2 it not eliminated from the blood, acidosis results from the accumulation of carbonic acid. (CO2 IS RETAINED, CAUSED BY SUDDEN FAILURE OF VENTILATION) CO2 retention from hypoventilation, compensatory response is HCO3 retention by kidneys -decreased pH (below 7.35) -increased PaCO 2 (above 45)

-COPD

-Infections -Cardiac disease Gillian-Barre syndrome -Obesity -Inadequate mechanical ventilation -Anesthetics & sedatives -Atelectasis -Chest wall abnormality Respiratory muscle weakness -Hypoventilation w/ hypoxia -Tremors -Seizures -Hypotension -Lethargy -Tachycardia -Treat the underlying cause -Mechanical ventilator -Respiratory support -Cautious with oxygen administration as it may create a CO retention -Administer an alkali (sodium bicarbonate) Respiratory Alkalosis (Hyperventilation) pH↑PaCO2 ↓

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Carbonic acid deficit caused by hyperventilation (anxiety, CNS disorders, & mechanical over ventilation also increases ventilation rate), hypoxemia from acute pulmonary disorders (CO2 IS BLOWN OFF, CAUSED BY MECHANICAL VENTILATION & ANXIETY W/ HYPERVENTILATION) Increased CO2 excretion from hyperventilation, compensatory response is HCO3 excretion by kidneys -increased pH (above 7.45) -decreased PaCO 2 (below 35) -Pulmonary disorders -Acute anxiety -Stimulant drug -Neural disorders -Hyperventilation -Hyperventilation -Paresthesia -Light-headedness, -Confusion -Tachycardia -Tetany -Numbness -Tingling of extremities

-Treat of underlying

disorder

-Respiratory support

-Re-breathing

If acute aggressive tx

of the cause of

hypoxemia is

essential & usually

does shifting of

bicarbonate into cells

in exchange for

chloride

Metabolic Alkalosis pH ↑^ HCO3 ↑

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Base bicarbonate excess caused by prolonged (LOSS) vomiting or gastric suction or (GAIN) of HCO (loss of acid or gain of base) (EXCESS OF BICARBONATE IN RELATION TO THE AMOUNT OF HYDROGEN ION) Loss of strong acid or gain of base, compensatory response is retention by the lungs -increased pH (above 7.45) -increased PaCO 2 (above 45) -increased HCO (over 26) -Vomiting -Long term gastric suctioning -Administration of NaHCO3 (sodium bicarbonate) -Overuse of diuretics -Potassium deficit -Adaptive hypoventilation -Lethargy -Confusion -Tachycardia -Seizures -Tetany -Tremors -Muscle cramps -Treat the underlying cause -Promote loss of bicarbonate acetazolamide sodium (Diamox) -Administer exogenous acid

Metabolic Acidosis pH ↓^ HCO3↓

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Occurs when an acid other than carbonic acid -decreased pH (below 7.35) -Ketoacidosis -Lactic acidosis -Bradycardia -Weak peripheral -Treatment of underlying cause

-Hydrostatic pressure increases, pushing fluids into the interstitial spaces -Peripheral vascular resistance (PVR) -Pulmonary edema & heart failure develop -Heart failure -Renal failure -Long term use of corticosteroids -Primary polydipsia -Excessive isotonic or hypotonic IV fluid -Osmolality less than 275 -Sodium less than 135 -Hematocrit less than 45% -BUN less than 8mg/dl -Specific gravity less than 1. -Peripheral edema -Jugular venous distention -Bounding pulse -Dyspnea -Crackles in the lungs -Pulmonary edema -Muscles spasms -Weight gain -Seizures -Headache & confusion -Lethargy

-RESTRIC FLUIDS

-Restrict sodium -Promote urine output Frequent Assessment: -Vital Signs -Lung sounds -Edema -Intake & output -Lab values -Reduce sodium & fluid intake -Mobilized fluids -Diuretics & Digitalis -Improve myocardial function -Angiotensin converting enzyme (ACE) inhibitors & beta blockers

Respiratory

Influenza

Etiology A Etiology B & C Diagnostic Indicators Manifestations Nursing interventions Medical Treatment Influenza Type A ; subtyped by based on the presence of two surfaces proteins hemagglutinin (H) & neuraminidase (N). The H antigens enable the virus to enter the cell, & N antigens facilitate cell-to-cell transmission. Influenza A can infect humans & a variety of animals, the virus mutates which allows it to infect different species. Type A can cause both epidemics or pandemics Influenza Type B & C; these are not divided into subgroups & only infects humans. B can cause regional epidemics but it is usually milder than type A. C cannot cause epidemics or pandemics & is mild. -Rapid flu test (nasal secretions), also called Antigen detection tests -Viral cultures (gold standard, can tell you which strain of virus it is), can take up to 3-10 days for results -Serology (antibodies in the serum) Immunofluoresce nce

Transmission

The virus has an incubation period of 1 to 4 days with a peak transmission risk starting at day 1 before onset of symptoms & continuing for 5 to 7 days. Symptoms should subside within 7 days; -Abrupt onset -Chills -Headache (severe) -Fever -Anorexia -Myalgia (muscle pain, severe) -Cough -Rhinorrhea (runny nose) -Sore throat COMPLICATIONS Dyspnea & diffuse crackles are signs of pulmonary complications, The most common complication is pneumonia (especially in older adults) -Put the pt on contact precautions -saline gargles -monitor respiratory status & fluid intake & outtake -teach the pt proper hand washing & coughing techniques -increase fluid intake & rest -avoid traveling & crowded places CONTRAINDICATI ONS Do not take the flu vaccine if you are allergic to eggs, or have a history of Guillain-Barre syndrome within 6 weeks following the previous flu vaccine. Antiviral medications (Relenza or Tamiflu), therapy should begin within 2 days of onset of symptoms, these drugs are neuraminidase inhibitors that prevent the virus from budding & spreading to other cells

Pneumonia

Etiology Diagnostic Indicators Risk Factors/Causes Manifestations Nursing interventions Medical Treatment Pneumonia is more likely to occur when the defense mechanisms become more -CBC (elevated WBC) -ABG’s (decreased PaO2, less than 80) -Blood culture -Serum electrolyte -Sputum culture & Bacteria, viruses, Mycoplasma organisms, fungi, parasites, & chemicals are all -Anxiety -fatigue & weakness -fever & chills (>100.4) -Position pt in high-fowlers position -encourage coughing or -Antibiotics IV or PO (get a culture BEFORE giving the antibiotics) -Bronchodilators to