Degenerative and Inflammatory Disorders of Musculoskeletal Tissue Flashcards

1
Q

Incidence

A

The frequency with which a condition occurs over a period of time and in relation to the population in which it occurs

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2
Q

Prevelence

A

The number of cases a disease present in a specified population at a given time

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3
Q

Osteoarthritis

A

Slow, progressive degeneration of joint structures
Can lead to loss of mobility, chronic pain, deformity, and loss of function
Most common joint disease

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4
Q

Primary OA

A

Disorder of unknown cause and degenerative effects are thought to be related to defects in the articular cartilage

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5
Q

Secondary OA

A

Has known cause which may be trauma, infection, hemarthrosis, osteonecrosis

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6
Q

OA Incidence and Risk

A

High % of population over 60 have damage; only 20% have symptoms
More frequent in males before 45, females after 55

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7
Q

Etiology of OA

A

Primary etiology is unknown
“Wear and tear”
Imbalance between mechanical stresses and the ability of the joint structures to handle the loads

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8
Q

Pathogenesis of OA

A

Once cartilage breaks down, mechanical stresses fall on other joints.
Fissuring and eburnation of cartilage occurs
Joint space narrows
New bone forms at joint margins

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9
Q

Eburnation

A

Changes in bone causing it to become dense and hard like ivory

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10
Q

Immobilization effect on OA

A

Articular cartilage needs repetitive loading and unloading; nutritional mechanism is interrupted with immobilization

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11
Q

Clinical Manifestations of OA

A

Sudden or Insidious
Deep Ache
Stiffness after inactivity
Loss of flexibility

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12
Q

OA Treatment and Prognosis

A

Depends on patient’s age, chronicity, and co-morbidities

Treatment involves physical agents, exercises, core stabilization, and unloading

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13
Q

Tendinitis

A

Inflammation of the tendons

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14
Q

Tenosynovitis

A

Inflammation of the lubricating fluid of the joint due to contractile tissue involvement

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15
Q

Synovitis

A

Inflammation of the synovial membrane due to damaged cartilage or exposure to cold and dampness

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16
Q

Bursitis

A

Inflammation of the padlike sac found in connective tissue

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17
Q

Osteomyelitis Pathophysiology

A

Inflammation of bone caused by an infectious organism

Usually caused by direct innoculation into bone

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18
Q

Osteomyelitis Incidence

A

Occurs more often in kids than adults
Acute hematogenous osteomyelitis is most common
Chronic osteomyelitis is more common in adults
Decreasing with use of antibiotics

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19
Q

Osteomyelitis Etiology

A

Staphlococcus aureus is usual cause

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20
Q

Osteomyelitis clinical picture

A

Pain may not be an initial factor
Can spread rapidly to outer surface of bone
Pain may be described as deep, continous worse with weight
Intermittent, throbbing back pain at rest

21
Q

Osteomyelitis Diagnosis

A

Increase in WBC and Erythrocyte sedimentation rate
Radionucleotide bone scans detect early stage
Identification of pathogen is critical
Treatment is oral or IV; surgery indicated if in joints

22
Q

Septic Arthritis Pathophysiology

A

Bacteria, viruses, and fungi infect a joint

History of alcohol, drug, prosthesis, diabetes, and trauma increases risk

23
Q

Septic Arthritis Incidence

A

Increasing as a result of a greater number of people with immunosupressed conditions

24
Q

Septic Arthritis Clinical Picture

A

May be of any age
Acute onset of joint pain, swelling, tenderness, and loss of motion
Accompanied by fever, chills, and systemic symptoms

25
Septic Arthritis Managment
Diagnosed by analysis of joint fluid Treatment w/ antibiotics Surgical drainage may be required
26
Adult Rheumatoid Arthritis
Chronic, systemic, inflammatory disease. Chronic polyarthritis can result in severe deformity and disability Joints of the cervical spine often involved Can include cardiovascular, pulmonary, and gastrointestinal systems
27
Adult RA Incidence
~1-2% of adult pop | Less common, but still present in children
28
Adult RA Etiology
Unknown cause, but may arise from autoimmune disease
29
Autoimmune Disease
A disease produced when the body's normal tolerance of its own antigenic markers on cells disappears
30
Autoantibodies
Produced by B lymphocytes and attack normal cells whose surface contains a "self" antigen or autoantigen, causing destruction of tissue
31
RA Pathogenesis
Interaction between rheumatoid factor and immunoglobin triggers inflammatory reaction Attracted immune cells phagocytose immune complexes and lysosomal enzymes are released; leads to articular cartilage destruction and synovial hyperplasia
32
Pannus
A destructive vascular granulation tissue; | Can proliferate and encroach the joint space; results in joint instability, joint deformity, or ankylosis
33
Ankylosis
Ligaments turn to bone
34
Adult RA Symptoms
Joint stiffness; Joint Pain; Fatigue; Weakness; Psychological depression
35
Adult RA Signs
Swelling;Palmar erythema; cool moist skin; muscular atrophy; joint contracture; nodules; synovial hernias; weight loss
36
RA Clinical Manifestations
Insidious; multiple joint usually; Periods of rest increase symptoms; ulnar deviation; Swan Neck; Boutonniere deformity
37
Juvenile RA
Chronic Inflammatory disease; mild to severe, destructive arthropathy with extra-articular manifestations; anti-inflamatory meds used
38
Still's Disease
Form of Juvenile RA marked by fever and a rash on trunk or extremities
39
Ankylosing Spondylitis
Inflammartory arthropathy of the axial skeleton, including the sacroiliac joints, apophysial joints, costovertebraljoints, and the discs; can lead to fibrosis, calcification, and ossification
40
Ankylosing Spondylitis Pathophysiology
Nongranulomatous inflammation; disrupts ligamentous-osseus junction Progressive ossification
41
Ankylosing Spondylitis Etiology
Unknown, but there is a genetic or environmental link | More prevelent in males between 20-40
42
Ankylosing Spondylitis Clinical Manifestions
Insidious onset back pain "Ache" Tolerating recumbant positions is difficult with progression of disease
43
Ankylosing Spondylitis Medical Management
Loss of spinal mobility in multiple plains is typical | Diagnosis by history, physical exam, laboratory, and radiography
44
Gout and Gouty Arthritis Pathophysiology
Elevated level of serum uric acid and deposition of crystals in the joints, soft tissues, and kidneys.
45
Primary Gout
Hyperuricemia without any other disease
46
Secondary Gout
Hyperuricemia in the presence of an antecedent disease
47
Gout and Gouty Arthritis Pathogenesis
Sodium urate crystals precipitate from supersaturated body fluids. Aggregate and result in local necrosis
48
Tendinitis impairments
Active motion loss, Tenderness, pain w/ isometric resistance
49
Bursitis Key impairments
End Feel, Local Pain Mimics L5-S1 and C4/C5 myotomal problems