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
Q

Septic Arthritis Managment

A

Diagnosed by analysis of joint fluid
Treatment w/ antibiotics
Surgical drainage may be required

26
Q

Adult Rheumatoid Arthritis

A

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
Q

Adult RA Incidence

A

~1-2% of adult pop

Less common, but still present in children

28
Q

Adult RA Etiology

A

Unknown cause, but may arise from autoimmune disease

29
Q

Autoimmune Disease

A

A disease produced when the body’s normal tolerance of its own antigenic markers on cells disappears

30
Q

Autoantibodies

A

Produced by B lymphocytes and attack normal cells whose surface contains a “self” antigen or autoantigen, causing destruction of tissue

31
Q

RA Pathogenesis

A

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
Q

Pannus

A

A destructive vascular granulation tissue;

Can proliferate and encroach the joint space; results in joint instability, joint deformity, or ankylosis

33
Q

Ankylosis

A

Ligaments turn to bone

34
Q

Adult RA Symptoms

A

Joint stiffness; Joint Pain; Fatigue; Weakness; Psychological depression

35
Q

Adult RA Signs

A

Swelling;Palmar erythema; cool moist skin; muscular atrophy; joint contracture; nodules; synovial hernias; weight loss

36
Q

RA Clinical Manifestations

A

Insidious; multiple joint usually; Periods of rest increase symptoms; ulnar deviation; Swan Neck; Boutonniere deformity

37
Q

Juvenile RA

A

Chronic Inflammatory disease; mild to severe, destructive arthropathy with extra-articular manifestations; anti-inflamatory meds used

38
Q

Still’s Disease

A

Form of Juvenile RA marked by fever and a rash on trunk or extremities

39
Q

Ankylosing Spondylitis

A

Inflammartory arthropathy of the axial skeleton, including the sacroiliac joints, apophysial joints, costovertebraljoints, and the discs;
can lead to fibrosis, calcification, and ossification

40
Q

Ankylosing Spondylitis Pathophysiology

A

Nongranulomatous inflammation; disrupts ligamentous-osseus junction
Progressive ossification

41
Q

Ankylosing Spondylitis Etiology

A

Unknown, but there is a genetic or environmental link

More prevelent in males between 20-40

42
Q

Ankylosing Spondylitis Clinical Manifestions

A

Insidious onset back pain
“Ache”
Tolerating recumbant positions is difficult with progression of disease

43
Q

Ankylosing Spondylitis Medical Management

A

Loss of spinal mobility in multiple plains is typical

Diagnosis by history, physical exam, laboratory, and radiography

44
Q

Gout and Gouty Arthritis Pathophysiology

A

Elevated level of serum uric acid and deposition of crystals in the joints, soft tissues, and kidneys.

45
Q

Primary Gout

A

Hyperuricemia without any other disease

46
Q

Secondary Gout

A

Hyperuricemia in the presence of an antecedent disease

47
Q

Gout and Gouty Arthritis Pathogenesis

A

Sodium urate crystals precipitate from supersaturated body fluids. Aggregate and result in local necrosis

48
Q

Tendinitis impairments

A

Active motion loss, Tenderness, pain w/ isometric resistance

49
Q

Bursitis Key impairments

A

End Feel, Local Pain

Mimics L5-S1 and C4/C5 myotomal problems