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arthritis notes - exam study, Study notes of Nursing

Trocaire CollegeNursing

notes on arthritis - musculoskeletal

Typology: Study notes

2022/2023

Uploaded on 10/31/2023

J0e-mama
J0e-mama 🇺🇸

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Arthritis
Characterized by inflammation & loss of function of the affected joint
Often Dx in older individuals, also affects children
Osteoarthritis (OA) & rheumatoid arthritis (RA) = most prevalent types
Osteoarthritis: Etiology & Complications
Most common form of arthritis
Typically results from a known event or condition that directly
damages cartilage/causes joint instability
Not normal of the normal aging process, although it is as risk factor
for development
Most adults – affected by age 40; few pts experience s/s until after
age 50
More women affected after age of 55, w/ a ratio of 2:1 over men
Causes (complications that led to OA)
oTrauma – dislocations, fractures, avascular necrosis
oMechanical stress – repetitive physical activities (sports,
manual labor) causing cartilage deterioration
oInflammation – enzyme release damages joints
oObesity – joint instability = damage to supporting structures
oNeurologic disorders – diabetic neuropathy, Charcot’s foot
(causes: abnormal movements & cartilage deterioration)
oSkeletal deformities – congenital conditions, acquired
conditions, dislocated hip
oHematologic/endocrine disorders
Chronic hemarthrosis from hemophilia
Sickle cell disease
Diabetes mellitus
Paget’s disease
oMedications
Drugs that stimulate collagen-digesting enzymes in the
synovial joint include:
Indomethacin
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Arthritis  Characterized by inflammation & loss of function of the affected joint  Often Dx in older individuals, also affects children  Osteoarthritis (OA) & rheumatoid arthritis (RA) = most prevalent types Osteoarthritis: Etiology & Complications  Most common form of arthritis  Typically results from a known event or condition that directly damages cartilage/causes joint instability  Not normal of the normal aging process, although it is as risk factor for development  Most adults – affected by age 40; few pts experience s/s until after age 50  More women affected after age of 55, w/ a ratio of 2:1 over men  Causes (complications that led to OA) o Trauma – dislocations, fractures, avascular necrosis o Mechanical stress – repetitive physical activities (sports, manual labor) causing cartilage deterioration o Inflammation – enzyme release damages joints o Obesity – joint instability = damage to supporting structures o Neurologic disorders – diabetic neuropathy, Charcot’s foot (causes: abnormal movements & cartilage deterioration) o Skeletal deformities – congenital conditions, acquired conditions, dislocated hip o Hematologic/endocrine disorders  Chronic hemarthrosis from hemophilia  Sickle cell disease  Diabetes mellitus  Paget’s disease o Medications  Drugs that stimulate collagen-digesting enzymes in the synovial joint include:  Indomethacin

 Colchicine  Corticosteroids o Aging – years of use cause joint to wear down o Genetic factors – OA runs in families Osteoarthritis Patho  Results in o Progressive deterioration & loss of cartilage o Increased thickness of the subchondral plate o Osteophytes (new bone @ joint margins) o Subchondral bone cysts o Mostly caused by overuse/wear & tear on the joints  The remodeling process of the cartilage o Altered by a combo of mechanical, cellular, & biochemical processes – resulting in abnormal reparation of cartilage & an increase in cartilage degradation  Normal smooth, white cartilage is eroded & becomes yellow, dull, granular, & less elastic – the body is unable to make repairs as fast as the cartilage is being worn down  Disease progression – vascular invasion & further calcification of nearby articular cartilage may occur o This leads to decreased thickness of articular cartilage & over time causes bone remodeling & enhanced cartilage deterioration Osteoarthritis: clinical manifestations  Disease = pain, crepitation, & deformity of the affected joints  Affects weight-bearing joints & is not symmetric in occurance  Pain o Most prominent symptom; reported as:  Worsening w/ use  Relieved by rest in the early stages of the disease  Stiffness occurs

o Large # of WBCs are found in the synovial fluid (between 5, & 60,000 cells/uL) o X-rays show soft tissue swelling w/ possible osteoporosis; no signs of joint destruction yet  Stage 2 o Inflammation of the joints is increased o Gradual destruction of the cartilage w/ narrowing joint space will also occur  Stage 3 o Synovial pannus will be formed o Cartilage in joints erodes, showing bone o X-rays show extensive joint erosion & deformities  Stage 4 o End stage – inflammatory process stops o Includes loss of joint function & subcutaneous nodule formation RA Patho  No known cause, but a combo of environmental triggers & genetics is believed to be responsible o Theory = an autoimmune response in which response to the antigen initiates an abnormal immunoglobulin G (IgG) formation  Dx is established by the presence of abnormal autoantibodies called Rheumatoid factor (RF) o RF combines w/ IgG to = immune complexes that attach to the synovial membranes &/or the superficial articular cartilage in joints, leading to inflammation. RA clinical manifestations  Initially affects small joints, effects are symmetric (both hands, feet, etc have the same symptoms)

 Early Joint manifestations o Inflammation  Early systemic manifestations o Low-grade fever o Fatigue o Weakness o Anorexia o Paresthesias  Late joint manifestations o Deformities o Moderate-severe pain o Joint effusions o Morning joint stiffness (gel phenomenon)  Late systemic manifestations o Osteoporosis o Severe fatigue o Anemia o Subcutaneous rheumatoid nodules o Peripheral neuropathy o Vasculitis o Pericarditis o Fibrotic Lung tissue o Sjogren’s syndrome o Kidney disease o Felty’s syndrome Fibromyalgia  A chronic central pain syndrome that causes diffuse pain that affects muscle & connective tissue in multiple tender points

o Presence of Herberden’s & bouchard’s nodes  Dx tests to reveal bone/joint changes: o Xray – results reveal joint space narrowing, osteophytes, subchondral cysts, sclerosis  Used to confirm the condition & monitor progression of joint damage o Synovial fluid analysis – reveals WBC count <2000/uL (mild leukocytosis) o Erythrocyte sedimentation rate (ESR) – shows transient elevation in ESR related to synovitis o Bone scan – detects reactive bone turnover assoc w/ OA & provides images of the entire skeleton in one exam o MRI – demonstrates reactive bone edema or soft tissue swelling, as well as small cartilage or bone frags in the joint o CT – demonstrates the degree of osteophyte (bone spur) formation & its relationship to the adjacent soft tissues Diagnostic Studies for Rheumatoid Arthritis  Current dx criteria are @ least 6 points on a classification scale & one positive (confirmed) blood test result (refer to chart @ end)  Other dx tests: o CBC: includes hemoglobin & hematocrit- may reveal anemia also assoc w/ RA o Antinuclear antibody (ANA): may be increased in some pts w/ RA o Synovial fluid analysis: often reveals a straw-colored fluid w/ many fibrin flecks in early stages of RA; also shows elevated WBC count in synovial fluid (up to 25,000u/L) o ESR: elevated rate indicates inflammation during exacerbations, but is not diagnostic of disease Drug therapy for OA

 Mild pain meds o Acetaminophen o Topical analgesics  Capsaicin cream  Camphor  Eucalyptus oil  Menthol o Moderate  Ibuprofen  Naproxen (dose can be increased over time as pain worsens) o Severe  Piroxicam  Indomethacin  Sulindac  Tolmetin  Diclofenac  Meclofenamate  Nabumetone  Oxaprozin  Meloxicam  Celecoxib  Corticosteroid injections into affected joint  Prednisone  Methylprednisolone  Dexamethasone Drug Therapy for RA  Initial therapy may be short-term use of NSAIDS (aspirin, ibuprofen, & naproxen)  These drugs are RX’d to prevent disease progression after a dx of RA has been established o Disease-modifying antirheumatic drugs (DMARDs)