Musculoskeletal Flashcards
bones composed of?
- Composed of collagen fibers (Ca++,
* Osteoblasts and Osteoclasts
functions of bones
- Provide support for body
- Protect internal organs
- Store calcium, phosphorus, other minerals
- provide movement in conjunction with muscles
- produce red/white blood cells in bone marrow of long bones
problem with bone leads to?
anemia, leukopenia
MS assessment
Inspect for deformities (Ie in hip fx is one leg longer than other) Inspect and palpate any swelling Feel for increased temperature • Observe for redness Palpate for tenderness around joint Assess ROM
Pg 1493 has list of lab tests specifically r/t bone disorders that we should be familiar with
look
osteoporosis
• Skeletal disease: low bone mass, deterioration of bone tissue
• Most common metabolic bone disease
structure and mass change
osteoporosis etiology
Etiology/pathophysiology:
•Incompetent bone remodeling (more broken down than rebuilt)
• Primary or secondary (Primary: unsure why, relationship to hormone, just happens with age. Secondary: something is causing it ie steroids. With secondary can identify cause and treat cause. Primary much more common)
• Changes in both cortical and cancellous bone (Affects whole bone, every bone in body. But those that cause more problems are th weight bearing ones)
-changes in bone turnover process result in bone structure changes
Ververy common post menopausal becase lose protective function of estrogen
osteoporosis s/s
- Fractures after minor falls (Sometimes hip fx after a heavy step, putting too much weight on leg, THEN they fall.)
- Pathologic fractures (spine, femur) (Compression fx of spine, vertebrae themselves squish down with aging.)
- Spontaneous wedge fractures r/t dec density of spine, inability to manage weight on the spine
- Kyphosis r/t decreased density of spine and inability to manage the weight
- Height loss
- pain
- vertebral collapse
osteoporosis management/prevention
- Bone resorption inhibitor
- Hormone replacement therapy (HRT)
- Calcium supplements (Usually has vitamin D in it: teach pt to read label, buy the one with vit d in it.)
- Vitamin D
- Diet: protein, vitamins, minerals
- Exercise: high-impact (High impact as in weight bearing, not like crazy exercises)
- complementary/alternative therapy: biofeedback, yoga, massage, reflexology
osteoporosis severity determination
Osteoporosis is in degrees: bone density test may show how many standard deviations away from normal. Little loss = osteopenia (very early stages of osteoporosis). More than something like 1 SD = osteoporosis.
noninflammatory arthritis
OA
Inf/noninflamm as in the CAUSE, not as in the effect. Both have inflammation, but both don’t have it as the CAUSE.
• Related to overuse/ wear and tear: not equal on both sides. Esp if injury, wear/tear worse on side of injury. So worse in one knee or ONLY in one knee for example. Vs RA: is systemic! So everywhere. Equal.
• Unilateral and not systemic.
inflammatory arthritis
Rheumatoid arthritis
Systemic lupus erythematosus
Connective tissue disease that is inflammatory.
autoimmune diseases / tx
Some arthritis are autoimmune as in rheumatoid arthritis recognizing something in joint as foreign, causing inflammation from autoimmune response.
- Defect in immunologic mechanism
- Possible genetic component (Onset at much younger age for autoimmunes than for like OA.)
- Characterized by hypersensitivity
- Tend to be systemic and chronic (bilateral, often times disease itself goes beyond MS system and connective tissue of MS system, since it’s a connective tissue disorder, it’ll cause non MS symptoms as well. But early signs are usually in MS system.)
- Medications control or reduce immune system response: systemic meds, particularly immunosuppressants
OA, characterizations
Ask WHERE the OA is.
-Most common type of arthritis
-Joint pain and loss of function characterized by progressive deterioration and loss of cartilage in the joints
• Decrease in collagen synthesis so wearing down joint and weraing down ability to repair
• Increase in collagen breakdown
-Osteophytes (bone spurs)
-Synovitis (inflammation of the synovium which is lining of the joint itself)
-subluxation (weak joint, partial dislocation)
Get erosion of the bone itself after losing the protective coating.
Tends to be in larger joints: hips, knees, hands, spine. RA starts in very small joints.
OA etiology
Multiple factors
• Can be primary idiopathic (Don’t rly know whats causing it.)
Can be secondary to: Congenital joint defects, Trauma, Inflammatory, metabolic disorders
OA Pg 1566 has list of diagnostic tests for OA. Best most simple and low cost test is X RAY. Not a lot of detail, but first stop because it gives enough information.
look
nrsg assessment for OA
-History
-Physical assessment and clinical manifestations:
• Joint deformity
• Heberden’s nodes, In joint closer to tip
• Bouchard’s nodes, In 2nd joint
• Joint effusions
• Atrophy of skeletal
• Morning stiffness: Happens with OA and RA, but key is with oA, it gets better thru day with movement. RA gets WORSE with movement.
• Pain with overuse of joint: What was their job? OA in hand more commonly with someone who has done fine work with their hands ie sewing
OA nursing management
- Highest priority: pain relief (NSAIDS WOULD be great, but most ppl with OA are older and much higher risk for GIB. Nsaids should be short term only. Tylenol not that good for this because it doesn’t do inflammation, but its safer and appropriate doses.)
- Heat and cold applications
- Complementary and alternative therapies: Accupuncture, herbs
- Exercise, firm mattress, splints: If it’s in the back use mattress, splints for extremities. Don’t completely immobilize joints: need to move the joints. Splints would be temporary.
- Fall protocol in hospital and at home: Especially if its in a joint like hip or knee.
- Promotion of independence
- Weight loss
- support
- OA prevention
RA
- Chronic, progressive, systemic inflammatory autoimmune disease affecting primarily the synovial joints
- Autoantibodies (rheumatoid factors) formed that attack healthy tissue, especially synovium, causing inflammation; development of a pannus
- cartilage becomes fibrous and calcified (No erosion of cartilage, instead becomes very stiff.)
- affects synovial tissue of any organ/body system
RA pathology
Tissue hypersensitivity leads to inflammation in WHOLE CAPSULE unlike in OA.
Will start to see it in small joints like in the hands.
Get all WBCs and stuff so joint gets very full, inflammation.
RA clinical manifestations
- Remissions and exacerbations
- Early disease manifestations—joint stiffness, swelling, pain, fatigue, and generalized weakness (Pt will be very tired and weak on top of the other symptoms; key to look for that early because they’ll be weak from the inflammatory response)
- Systemic Manifestations: Swollen glands (Body responding), dry mouth, pleuritis, anemia, decreased WBCs, vasculitis
- Late disease manifestations—as the disease worsens, the joints become progressively inflamed and quite painful (joints become practically unusable)
RA pain relief
splints for immobilization
RA joint involvement
Ulnar deviation: damage to knuckle joints, deviating to one side instead of fingers going straight out.
Also swan neck deformity (subluxation at middle joint, bending wrong way). Classic in RA patients. Rly impt to recognize
RA lab/diagnostics
- Radiologic imaging (Cat, bone scan, x ray, but key is things significant to autoimmune disorders ie the things below)
- Blood tests include:
* Rheumatoid factor (This is what goes around causing inflammation. Means it’s a rheumatic disease, and its probably RA.)
* Antinuclear antibodies (Elevation of ANA is sign of autoimmune)
* Erythrocyte sedimentation rate (ESR) (Elevated, sign of inflammation. )
RA nrsg management
- Joint mobility, preventing contractures (Joint mobility when nOT having a flare up. Cause if not, they’ll get contractures. But during flare up they should rest, use splints, heat etc)
- Rest during flare-ups
- heat applications (paraffin bath)
- pain medications
- support, referral (Chronic, irreversible, progressive disease, lifelong. So make sure they have a good support.)
RA medical management
• Chronic condition; no cure
• Early intervention
• Can control disease and treat symptoms (They’ll use NSAIDs since they’re younger)
Treatment includes:
• Pharmacologic interventions
• Rest (Flare up), exercises (When not flare up), safeguarding joints
• surgical intervention includes: synovectomy, arthrodesis, and/or reconstructive surgery (Surgery to loosen contracture. Surgeries kinda rare.)
RA systemic complications
- Weight loss, fever, and extreme fatigue (LOW grade fever (not like 101 and up) from inflammation, and slight increase in WBC. Slight increase = inflammatory. Large inc = infection.)
- Exacerbations
- Subcutaneous nodules (Subcutaneous nodule. Seen in both diseases, but in RA theyre seen more in other areas while OA is mostly seen in joints. RA kinda more where lymph system is at.)
- Pulmonary complications
- Vasculitis (If vasculitis, stiffness and swelling in vessel itself: whatever organ is supplied by vessel is where u will see the problem.)
- Periungual lesions
- paresthesias
- cardiac complications (myo/pericarditis)
- resp fibrosis
Because there’s connective tissue in all these areas
gouty arthritis etiology/patho
Etiology:
• Imbalance in purine metabolism (Causes excessive uric acid, gets stuck in joints)
• Risk factors: heredity, enzyme defect, lead exposure.
• Strong genetic predisposition
Pathophysiology:
Uric acid crystals accumulate in joints
75% of patients affected in great toe (Can go other places in body, but this is most common.)
other joints: elbow, ankle, wrist, finger, knees
gouty arthritis pain:
Instead of the uric acid crystals being excreted through the kidneys, they accumulate in the joints. The crystals are needlelike, causing excruciating pain, usually in the joints of the elbows, wrists, fingers, knees, ankles, and toes, with 75% of patients affected in the great toe.
Buildup in distal AND proximal joints at same time, unlike other kinds of arthritis.
