Unit 16 - Joint and Connective Tissue Diseases Flashcards

(40 cards)

1
Q

Heberden Nodes

A

Heberden’s nodes are hard or bony swellings that can develop in the distal interphalangeal joints (DIP) (the joints closest to the end of the fingers and toes). They are a sign of osteoarthritis and are caused by formation of osteophytes (calcific spurs) of the articular (joint) cartilage in response to repeated trauma at the joint.

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2
Q

Bouchard Nodes

A

hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (PIP) (the middle joints of fingers or toes.) They are seen in osteoarthritis, where they are caused by formation of calcific spurs of the articular (joint) cartilage. Much less commonly, they may be seen rheumatoid arthritis, where nodes are caused by antibody deposition to the synovium.

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3
Q

Vasculitis

A

a group of disorders that destroy blood vessels by inflammation.[2] Both arteries and veins are affected.
Found in RA and SLE.

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4
Q

Synovitis

A

inflammation of the synovial membrane in joints

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5
Q

Butterfly rash

A

present along nose and cheeks of patient with SLE

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6
Q

Swan neck deformity

A

hyperextension of PIP joints in RA.

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7
Q

ulnar deviation

A

fingers point towards ulna in RA.

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8
Q

pannus

A

proliferation of newly formed synovial tissue infiltrated with inflammatory cells

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9
Q

crepitus

A

continuous grating sensation felt or heard as OA patient goes through ROM.

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10
Q

discoid lesions

A

coinlike lesions found in SLE, scarring and ring shaped, above neck. DLE

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11
Q

tophi

A

Deposits of uric acid, found in gout

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12
Q

lupus nephritis

A

also known as SLE nephritis)[1] is an inflammation of the kidneys caused by SLE. It is a type of glomerulonephritis in which the glomeruli become inflamed. As the result of SLE, the cause of glomerulonephritis is said to be secondary and has a different pattern and outcome from conditions with a primary cause originating in the kidney

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13
Q

scleroderma

A

hard skin, smooth shiny appearance as a result of edema from inflammatory response. The skin then undergoes fibrotic changes, leading to loss of elasticity and movement. Eventually, the tissue degenerates and becomes nonfunctional. This chain of events, from inflammation to degeneration, also occurs in blood vessels, synovium, skeletal muscles, and internal organ(s) of the heart, lungs, GI tract, and kidneys

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14
Q

CREST

A

Calcinosis (calcium deposits in the tissues)
Raynaud’s phenomenon (spasm of blood vessels in response to cold or stress)
Esophageal dysfunction (acid reflux and decrease in mobility of esophagus)
Sclerodactyly (thickening and tightening of skin on fingers and hands)
Telangiectasia (capillary dilation that forms vascular red marks on surface of skin)

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15
Q

bursitis

A

inflammation of bursa sac joint structures

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16
Q

Osteoarthritis

A
  • A chronic, progressive disorder that causes cartilage deterioration in synovial joints and vertebrae
  • Major risk factors include age, obesity & overuse
  • Involves a complex combination of cartilage degradation, bone stiffening, and reactive inflammation of the synovium
  • Manifestations are pain, stiffness, and loss of movement and function
  • Main problem: Progression leads to disability
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17
Q

OA Defining Characteristics

A
  • Joint stiffness occurs after long periods of rest, static position and repetitive activity
  • Early morning stiffness usually resolves in < 10 minutes -30 minutes
  • Over activity can cause mild joint effusion, temporarily ↑ stiffness
  • Crepitus
  • Joint involvement in 1 or more joints
  • Heberden’s (DIP) and Bouchard’s nodes (PIP) r/t osteophyte formation
  • Loss of joint function and movement – limited ROM
  • Pain
18
Q

OA Dx

A

H&P - Limited passive ROM, crepitus, joint effusion, bony swelling (patellar tap or fluid thrill wave tesT) Herb or Bouch nodes.
Xrays- osteophytes, joiint space narrowing, sclerosis.

Arthroscopy - visualize cartilage integrity. Synovial fluid to differentiate OA from RA.

19
Q

OA Goals of Tx and interventions

A

Goals - : Pain management, improve joint function, prevent disability
• Non-pharmacologic treatment
• Alternative treatments
• Nutritional supplementation (glucosamine and chondroitin)
• Exercise: T’ai Chi, Yoga
• Positioning, ROM
• Joint support
• Balance rest with activity
• Heat & cold
• Pharmacologic management – adjunctive (aceto q6 <2600mg day, NSAID, if issues with NSAID misoprostol or celecoxib -SE’s : CV disease and GI distress)
Capsaicin, sodium hyaluronate (viscosuplementation)
• Arthroplasty – severe cases
R

20
Q

OA Teaching

A
Balance rest with activity
• Improve activity tolerance
• Self-care
• Home safety
• How to use medications
• Therapeutic exercise program
• Community wellness programs
21
Q

Rheumatoid Arthritis

A

• Autoimmune Systemic Disease (inflammation from immune complexes IgG)
Pannus - abnormal layer of fibrovascular/granulation tissue over joint, destructive to cartilage and bone.
• Remissions and exacerbations
• Extra-articular manifestations ie fever, weight loss, fatigue, anemia, lymph node enlargement, and Raynaud’s phenomenon, arteritis, neuropathy, scleritis, pericarditis, splenomegaly
• Felty - SANTA (splenomegly, anemia, neutropenia, thrombocytopenia, Arthritis)
Sjogrens (dry eyes and dry mucous membranes)
• Progressive disability
• Affects all ethnic groups

22
Q

RA Defining Char

A
  • Early morning joint stiffness lasting 30 – 45 minutes
  • Swelling, warmth, erythema & pain in affected joints
  • Loss of function
  • Joints feel spongey/boggy on palpation
  • Bilateral and symmetric symptoms
  • Systemic symptoms include: fever, weight loss, fatigue
  • Deformities of PIP and metatarsals
23
Q

RA Dx Criteria

A

4 of 7 of the following criteria for at least 6 weeks:
• Morning stiffness that lasts at least 30-45 min
• Swelling in three or more joints*
• Swelling in hand joints*
• Symmetric joint swelling*
• Erosions or decalcification seen on hand x-rays
• Rheumatoid nodules
• Presence of serum RF

24
Q

RA Dx

A

ESR - significantly elevated
• Serum Rheumatoid factor (RF) - present
• Antinuclear antibody (ANA) - elevated
• Anticyclic citrullinated (Anti CCP) marker/assay - present
• C-reactive protein (CRP) – elevated
• RBC and complements C3 and C4 (decreased)
• X-Ray: bony erosions and narrowed joint spaces
• Arthrocentesis – complement and inflammatory cells

Patients commonly have the inability to “wring out a wash cloth,” need to hold a cup with both hands, and may complain of the sensation of having a “stone in my shoe.”

25
RA Goals of Tx and Interventions
``` • Goals: Pain relief, decrease inflammation, slow progression of disability, address psychosocial needs • Non-pharmacologic pain relief • Nutrition: anti-inflammatory diet • Whole grain • Fresh fruits and Veggies • Legumes • Seeds and nuts • Avoid excessive high glycemic-load calories including simple sugars • Animal products in moderation • Dietary supplementation: omega 3 fatty acids • Psychosocial & self-care • Pharmacologic management R ```
26
RA Pharma
Disease-modifying antirheumatic drugs (DMARDs) • methotrexate : Drug of choice, Rapid anti-inflammatory, SE’s: myelosuppression, aplastic anemia and GI toxicity, teratogenic • sulfasalazine • leflunomide * Biologic Therapy: Serious infection risk, No live vaccines * etanercept, adalimumab & Infliximab: Injectable * SE’s: bacterial sepsis, invasive fungal infections and TB * manteaux testing before starting treatment is recommended * Antimalarial Therapy - Hydroxychloroquine * Anti-inflammatory works with methotrexate * Improves long-term outcomes * SE’s: BM suppression, GI ulcers, infection risk, rashes, alopecia and bladder toxicity
27
Other RA pharma
NSAIDS • Glucocorticoids - use with flareups. Prednisone, prednisolone (can cause oestoporosis, GI ulcer, adrenal suppression, DM) • Antibiotics - minocycline or doxycyline • Gold salts • Antidepressants amitryptiline, sertraline, paroxetine. • Sleep aids
28
RA Self Care
``` Pain Mgmt Med regimen Alternate rest w activity Maintain body alignment Positive self image Joint protection Self Help groups ```
29
Systemic Lupus Erythematous SLE
• Chronic inflammatory autoimmune disease • Characterized by exacerbations and remission • exaggerated production of autoantibodies and antigens • Multiple manifestations, including fatigue, myalgia's/arthralgia's and Reynaud's Phenomena • Young women
30
SLE Defining Chars
* Musculoskeletal * Cutaneous: Scleroderma * CREST syndrome * Butterfly rash * Discoid lesions * Photosensitivity • Renal - glomerulonephritis ``` • Central Nervous system Mood, depression, psychosis • Cardio-pulmonary system Pericarditis and pleuritis • Gastrointestinal system • Oral ulcers, esophageal dysfunction ``` • Hematologic system
31
SLE Dx
* *Antinuclear antibody (ANA) - increased * ESR - increased * Lupus cell prep. (LE cell prep) * Anti-DNA antibody – presence * Anti-Sm antibody - presence * Anti-Ro (SSA) * Skin biopsy – cellular changes * American College of Rheumatology (ACR) criteria
32
Goals of Tx and interventions for SLE
``` • Goals: Improve QOL, pain management, rest and activity, adequate nutrition, self-care • Maintain skin integrity • Management of fatigue and stress • Promotion of adequate nutrition • Sunscreen and protective clothing • Monitoring of strict I&O • Assessment of infection • Pharmacologic management R ```
33
SLE Pharma
Immunosuppressnt/cytotoxic. azathioprine, cyclophosphamide steroids, systemic and topical NSAIDS DMARDS -methotrexate Antimalarial - fatigue and moderate skin/joint problems Anticonvulsants
34
SLE Teaching
``` Alt rest and ativity Know when to call HCP Improve QOL Home safety Joint protection Adequate nutrition SUpport groups Pharma mgmt. ```
35
General Overview of Arthritis
Consists of more than 100 different types of disorders that affect joints, bones, skeletal muscles, and connective tissues • Major symptom is pain but may include joint swelling, limited movement, stiffness, weakness, fatigue and disability • Assessment includes a complete health history followed by a complete physical examination combined with a functional assessment • Treatment can be simple, aimed at localized relief, or complex, directed toward relief of systemic effects
36
Gout
• A metabolic disorder • Genetic • hyperuricemia (elevated level of uric acid in the blood) : **Serum uric acid >/= 6.8 mg/dl** • Primary & secondary • Risk factors: Common in males, increased age, increased BMI, and increasing uric acid levels • Risk for development of tophi and kidney stones
37
Gout defining characteristics
* Acute pain * Swelling * Erythema * Renal damage * Tophi * Great toe (podagra); other joints and cartilage
38
Gout pharma
Anti-inflammatories: Decreases inflammation only • colchicine it Interferes with the functions of the WBCs in initiating and perpetuating inflammatory response • Acute stage • SE’s: GI upset, diarrhea,N/V, abd. Pain, aplastic anemia • Take with meals, avoid grapefruit juice * NSAIDS * indomethacin * Ibuprofen * Uricosuric * Probenecid * inhibits renal reabsorption of urates & increases renal excretion – decreases serum uric acid * SE: Kidney stones, GI upset, aplastic anemia, flushing. Action is decreased by salicylats * Combination: Colbenemid
39
Gout pharma cont
• Xanthine Oxidase Inhibitors (XOI) • febustat • Interrupts the breakdown of purines • Allopurinol Prevents uric acid in the blood by blocking uric acid formation • SE: Increses action of antidiabetic agents, hypotension, hepatitis, bone marrow depression, N/V, flushing, rash, increases theophylline toxicity * Angiotension II Inhibitor (ARB) * losartan Good for the use in elderly patients with HTN & gout. * Promotes urinary excretion • Aspirin & Thiazide diuretics blocks renal excretion of uric acid
40
Goals of Tx and Interventions GOUT
• Goals: Pain Management, dietary modifications, prevention of deformity, decrease exacerbations • Prevention of exacerbations • Medications • Weight Loss strategies if indicated • Control hypertension • Hydration • Avoid alcohol use • Avoid excessive intake purines (organ meat and shellfish) • Maintain uric acid level less than 6.8 • Prevent deformity and maintain musculoskeletal function