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Clinical Medicine 1 > degenerative and inflammatory disorders of musculoskeletal tissues > Flashcards

degenerative and inflammatory disorders of musculoskeletal tissues Flashcards

1
Q

inflammatory disorders of bone and joints

A
  • osteoarthritis
  • inflammation of soft tissues
  • osteomyelitis
  • septic arthritis
  • adult rheumatoid arthritis
  • juvenile rheumatoid arthritis
  • ankylosing spondylitis
  • gout and gouty arthritis
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2
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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3
Q

prevelence

A

the number of cases of a disease present in a specific population at a given time

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4
Q

itis vs osis

A

osis: more degenerative, no inflammation
- problem bc inflammation helps healing
- itis: tissue response to irritation, damage, injury

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5
Q

osteoarthritis

A
  • degenerative disorder of joint
  • slow, progressive degeneration of joint structures which can lead to loss of mobility, chronic pain, deformity, and loss of function
  • single most common joint disease
  • most commonly affected areas are the hip, knee, lumbar and cervical spine, carpometacapal and metatarsophalangeal joints
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6
Q

capsular patterns

A

typical patterns of movement inhibited by arthritis in each joint

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7
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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8
Q

secondary OA

A

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

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9
Q

osteoarthritis: incidence and risk factors

A

age: a high percentage of the pop aged 60 and over have some degree of articular cartilage damage, but only 15-20% have symptoms
- more frequent in males before the age of 45, females after 55

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10
Q

etiology of OA

A
  • primary etiology=unknown
  • wear and tear arthritis (mechanical stress and ability of body to resist
  • theorized that articular cartilage breaks down bc of an imbalance between mechanical stresses and the ability of the joint structures to handle the loads
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11
Q

pathogenesis of OA

A

once cartilage begins to break down, excessive mechanical stresses begin to fall on other joint structures

  • eventually fissuring and eburnation (whitening of bone/density increase) of cartilage can occur
  • joint space narrows as cartilage thins, and sclerosis (developing bone where it shouldnt be) of the subchondral bone occurs as new bone is formed in response to the now excessive mechanical load
  • new bone forms at joint margins
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12
Q

varous

A

medial osteoarthritis/deformation(bow legged)

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13
Q

vagus

A

lateral deformity from OA (knock kneed)

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14
Q

pathogenesis oa: immobilization

A

articular cartilage depends on repetitive mechanical loading and unloading for nutrition to reach the chondrocytes and for the cellular waste products to return to the synovial fluid and eventually the bloodstream
-nutritional mechanism of articular cartilage is interrupted by immobilization

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15
Q

clinical manifestations of oa

A

onset of symptoms may be sudden or insidious, usually slowly and gradually

  • pain often described as deep ache (sclerotome)
  • stiffness can occur after periods of inactivity
  • loss of flexibility is associated with significant disease and can occur secondary to soft tissue contractures, inta-articular loose bodies, large osteophytes, and loss of surface congruity
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16
Q

OA-treatment and prognosis

A

prognosis dependent on pts age, chronicity, and co-morbities

-treatment may involve physical agents, exercises according to direction of preference, core stabilization, unloading

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17
Q

tendinitis

A

inflammation of the fibrous connective tissue serving as connection of muscle to bone
-resisted isometrics

18
Q

tenosynovitis

A
  • inflammation of the lubricating fluid of the joint due to contractile tissue involvement
  • effusion
19
Q

synovitis

A
  • inflammation of a synovial membrane due to damaged cartilage or exposure to cold and dampness
  • damaged cartilage
20
Q

bursitis

A
  • inflammation of the padlike sac found in connective tissue (usually in the vicinity of joints)
  • empty end feel (pain before resistance)
21
Q

osteomyelitis

A

inflammation of bone, bone marrow

22
Q

osteomyelitis: pathophys

A

inflammation of bone (marrow) caused by an infectious organism (bacteria, fungi, parasites, viruses)

  • usually caused by direct inoculation into bone. infection is spread hematogenously in children and develops in the metaphysis of the distal femur, proximal humerus, and radius
  • vertebral osteomyelitis in adults is also spread hematogenously usually from pelvic or urinary tract infections
23
Q

osteomyelitis: incidence

A
  • occurs more often in children then adults and affects boys more often than girls
  • acute hematogenous osteomyelitis is most common and usually seen in children
  • chronic osteomyelitis is more common in adults, particularly immunocompromised people
  • incidence is decreasing with use of antibiotics
24
Q

osteomyelitis: etiology

A
  • staphlococcus aureus is the usual cause
  • organisms such as group B streptococcus, pneumococcus, pseudomonas, haemophilus influenza, and escherichia coli also produce bone infections
25
Q

osteomyelitis: clinical picture

A
  • unfortunately, pain may not be a factor in the initial phases because of lack of pain fibers in the cancellous bone
  • can spread rapidly to outer surface of bone which may then be painful
  • pain may be described as a deep, continuous pain which may increase with weightbearing
  • may produce intermittent or constant back pain aggravated by motion and described as throbbing at rest
26
Q

osteomyelitis: diagnosis

A

lab studies may show an increase in white blood cells (WBC) and erythrocyte sedimentation rate

  • radionucleotide bone scans may detect early stage disease
  • identification of the infectious pathogen is critical because the type of medication is dependent upon the specific microorganism
27
Q

medical/surgical management of osteomyelitis

A

-treatment is oral or intravenous antibiotics. surgery is indicated if the infection has spread to the joints

28
Q

septic arthritis (pyogenic=pus): pathophysiology

A
  • bacteria, viruses, and fungi are capable of infecting a joint
  • predisposing factors include systemic corticosteroids, preexisting arthritis, arthrocentesis, distant infection, diabetes mellitus, trauma
  • hisotry of alcohol abuse, iv drug abuse, hiv, joint prosthesis, rheumatoid arthritis, or other infectious disease increases the likelihood of having a septic joint
29
Q

incidence

A

incidence may be increasing as a result of greater number of people with immunosuppressed conditions. any person with an acute onset of joint pain and disability should be evaluated for possible sepsis

30
Q

septic arthritis: clinical picture

A
  • people with septic arthritis may be of any age and present with acute onset of joint pain, swelling, tenderness, and loss of motion
  • symptoms may be accompanied by fever, chills, and other systemic symptoms depending on the stage of the illness
  • a child with a septic joint will often refuse to bear weight and be extremely tender to palpation at the joint and along the metaphysis
31
Q

septic arthritis: medical management

A
  • diagnosis is made by analysis of the joint fluid obtained by aspiration
  • treatment with antibiotics such as penicillin, nacillen, or gentamicin is required
  • surgical drainage is often required to preserve function and prevent complications
32
Q

adult Rheumatoid Arthritis (RA)

A
  • chronic, SYSTEMIC, inflammatory disease. wide range of articular and extra-articular findings are associated with RA. Chronic polyarthritis can result in severe deformity and disability
  • the joints of the cervical spine are often involved and laxity of the transverse ligament can lead to antlanto axial subluxation and spinal cord compression
  • RA may involve the cardiovascular, pulmonary, and gastrointestinal systems. eye lesions, infection, and osteoporosis are other potential extra-articular manifestations
33
Q

adult RA: incidence

A
  • approximately 1-2% of the adult population has RA

- although less common, 60,000-200,000 children can develop the disorder

34
Q

adult RA-etiology

A

the cause of ra is unknown, but appears to arise from an autoimmune disease

35
Q

autoimmune

A

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

36
Q

autoantibodies

A

AAbs are produced by B lymphocytes and attack normal cells whose surface contains a self antigen or autoantigen (AAg) causing destruction of tissue

37
Q

RA-pathogenesis

A
  • approximately 80% of people with RA are rheumatoid factor positive
  • rheumatoid factors are antibodies that react with immunoglobin antibodies found in the blood
  • rheumatoid factor has also been found in synovial fluid and synovial membranes of those with the disease
  • it is hypothesizd that the interaction btwn RA factor and immunoglobin triggers the events that initiate an inflammatory reaction
  • as the attracted leukocytes, monocytes, and lymphocytes phagocytose the immune complexes, destructive lysosomal enzymes are released, leading to articular cartilage destruction and synovial hyperplasia (thickening of synnovial joint)
  • these changes can result in the development of a destructive vascular granulation tissue called pannus
38
Q

pannus

A

tissue unique to RA

  • pannus can proliferate and encroach joint space
  • inflammatory cells found with the pannus are destructive, affecting cartilage, bone, and other periarticular tissues
  • end result can be joint instabiliaty, joint deformity, or ankylosing
39
Q

adult RA-SYMPTOMS

A

patient reported, subjective

  • joint stiffness
  • joint pain
  • fatigue
  • weakness
  • psychological depression
40
Q

adult RA-SIGNS

A

objective measurements we take

  • swelling
  • palmar erythema
  • cool, moist skin
  • muscular atrophy
  • contracture of joints
  • nodules
  • synovial hernias
  • weight loss
41
Q

RA-clinical manifestations

A
  • symptoms usually begin insidiously and progress slowly
  • multiple joints are usually involved, with wrist, knee, and joints of fingers, hands, and feet most frequent
  • involved joints may be edematous, warm, painful, and stiff
  • after periods of rest, intense joint pain and stiffness (post-rest gel) may last from 30 min to several hours
  • deformities include ulnar deviation of the fingers, swan neck and boutonniere deformity

Clinical Medicine 1 (7 decks)

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