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Musculoskeletal Block Module > Pathology: Bone and Joint Disease > Flashcards

Pathology: Bone and Joint Disease Flashcards

1
Q

Function of cartilage

A

Weight distribution

Shock absorber during normal joint movement

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2
Q

What is the major proteoglycan in articular cartilage?

A

Aggrecan

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3
Q

What is the function of proteoglycans, especially aggregan and Type II collagen?

A

Prevent wear by protecting bone ends from grating together

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4
Q

What is the function of the synovium (synovial membrane)

A

Lines the non-articulating aspects of the joint

Secretes synovial fluid = lubricant in movement process

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5
Q

What is the function of the supporting ligaments and joint capsule?

A

Prevent instability

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6
Q

What causes OA?

A

Wear and tear disease (strongly associated with age)
Mechanical stresses - affects mostly weight bearing joints e.g. knee, hip, lumbar spine
Genetic factors
Chronic, low-level inflammation and inflammatory cytokines are implicated in disease progression

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7
Q

What is the pathogenesis behind OA?

A

Altered chondrocyte homeostasis with decrease in proteoglycans and cleavage of collagen type II fibres and disordered repair
= degradation of cartilage

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8
Q

Name the pathological changes that occur in OA.

A 
Fibrillation of cartilage 
Eburnation
Sclerosis 
Subchondral cysts 
Osteophytes 
Herbeden and Bouchard Nodules
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9
Q

Describe the fibrillation of cartilage in OA.

A

Early in disease - chondrocytes proliferate
Later chondrocytes die, cartilage is dehydrated & begins to break down
Exposed surface becomes frayed or fibrillated
Eventually cartilage is lost completely

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10
Q

What is the name given to pieces of cartilage tumbling into the joint space due to the fibrillation of cartilage in OA?

A

Joint mice

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11
Q

What happens as a result of loss of cartilage in OA?

A

Narrowing of the joint space - particularly seen in X-rays

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12
Q

What is eburnation?

A

Bone becoming ivory like

Bone that is devoid of cartilage is polished by the grinding action of bone on bone

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13
Q

What is sclerosis?

A

Bone below the area of cartilage loss becomes dense. q

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14
Q

What are subchondral cysts?

A

Small fractures occur through the eburnated bony surface due to loss of cartilage.
Joint fluid is forced under pressure into the subarticular area in one way direction.
Fluid incites a host response and becomes surrounded by a fibrous capsule.

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15
Q

What are osteophytes?

A

Mushroom shaped bony outgrowths that develop at the margins of the articulating bone.

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16
Q

What are Herbeden nodules?

A

Osteophytes of the distal interphalangeal joints.

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17
Q

What are Bouchard Nodules?

A

Osteophytes in the proximal interphalangeal joints in women

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18
Q

What are the current treatments/preventive strategies for OA?

A

No ways of preventing OA.
No effective treatment to date.
Therapy = physiotherapy, management of pain, modification of activity
Severe cases = arthroplasty (joint replacement)

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19
Q

What is RA?

A

Systemic autoimmune disease mainly affecting the joints leading to a chronic inflammatory polyarthritis.

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20
Q

Who is more affected by RA?

A

Women are 3x affected

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21
Q

What is the hallmark of RA?

A

Symmetric involvement of small joints of the hands and feet, wrists, elbows, ankles, knees

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22
Q

What auto-antibodies are found in RA?

A 
RF (Rheumatoid Factor) - antibody against patient's IgG (present in 80% of patients) 
Anti CCPs (antibodies against citrullinated peptides) - amino acid arginine ahs been converted to citrulline (therefore foreign to immune system)
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23
Q

What is the pathogenesis behind RA?

A

Multifactorial disease
Both genetic and environmental factors involved
Genetics - HLA alleles that presumably encode for MHC molecules with specific binding sites for presentation of the triggering antigen to the T cells.

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24
Q

What environmental factors are involved in RA?

A

Smoking: though to promote citrullination of self proteins
Infections: provide microbial agents and promote citrullination

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25
Q

Describe how the inflammatory synovitis of RA occurs.

A

Initiated by antigen presentation (bound to MHC) to T helper lymphocytes. These produce cytokines and activate macrophages and antibody producing plasma cells in the synovium.
Activated T lymphocytes and macrophages produce further cytokines that stimulate proliferation of fibroblasts, synovial cells and chondroblasts.
These proliferate and secrete proteolytic enzymes that destroy the cartilage.
Osteoclasts are activated by T cells and lead to bone resorption.

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26
Q

What is the end result of the inflammation of RA?

A

Chronically inflamed, thickened synovium = pannus

Destruction of underlying cartilage, bone and possibly capsule and ligaments in the affected joint

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27
Q

What is the pannus seen in RA?

A

Thickened opaque synovium instead of normal thin transparent membrane.

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28
Q

What is found in the pannus?

A

Inflammatory cells, granulation tissue and fibrosis

29
Q

What will you see in the histology of the pannus?

A

Synovial thickening formation - synovial cell hyperplasia with formation of villi.
Dark colour caused by inflammatory cells nuclei
Heavy infiltration by chronic inflammatory cells mainly plasma cells and lymphocytes
Granulation tissue and fibrosis also present

30
Q

Name the local complications of RA.

A

Joint instability and deformity (destruction of joint capsule, tendons and ligaments by proteases)
Cartilage and cortical bone eroded
Bony ends may be fused together to joint fixation (Ankylosis)

31
Q

What is ankylosis?

A

Fusion of bony ends leading to joint fixation in RA

32
Q

Name the systemic complications of RA.

A

Hallmarks of chronic disease - anaemia of chronic inflammation, fatigue, loss of appetite, high CRP and acute phase proteins, intermittent fever, weight loss
Subcutaneous rheumatoid nodules may develop as an extra-articular manifestation of the disease.

33
Q

Describe a knee removed from an RA patient and what you will expect to see.

A

Remnants of pannus (red inflammed material)
Eroded cartilage, exposing underlying bone
Underlying bone is pitted and eroded

34
Q

What causes the bone and cartilage erosion in RA?

A

Proteolytic enzymes and osteoclast activation

35
Q

What will an x-ray of a knee with RA show?

A

Erosion of the periphery of the joint by the pannus

Loss of joint space due to erosion of articular cartilage

36
Q

Describe the clinical picture of the hands of a person with RA.

A

Radial deviation of the wrist
Ulnar deviation of the fingers
Swelling of the wrist, MCP and PIP joints

37
Q

What is boutonniere deformity in RA?

A

Finger permanently points downwards

Flexion of PIP, extension of DIP

38
Q

What is swan neck deformity in RA?

A

PIP extension, DIP flexion

39
Q

List the treatment principles for RA.

A 
Control of pain 
Early treatment to avoid joint destruction and deformity/disability 
Active monitoring of disease progress
Prevention of disease complications 
Improving quality of px life
40
Q

List the treatment options for RA.

A

Pain relief - NSAIDs
Physiotherapy
Immunosuppression: steroids, DMARDs e.g. TNF antagonists, methotrexate

41
Q

What is osteomyelitis?

A

Inflammation of the bone marrow

42
Q

What causes osteomyelitis?

A

Usually caused by pyogenic (pus forming) bacterial infection
Therefore called pyogenic osteomyelitis

43
Q

What are the main bacteria causing pyogenic osteomyelitis?

A

Staph. aureus

44
Q

What other bacteria can cause osteomyelitis (rarely)

A

E coli, group B strep, salmonella, M. TB

45
Q

How do organisms gain entry into the bone in osteomyelitis?

A

Haematogenous (blood borne) dissemination from some other focus due to bacteraemia
Spread of infection from bone to adjacent site
Trauma
Surgical - Iatrogenic

46
Q

Describe what occurs in pyogenic osteomyelitis?

A

Pus forms within the bone shaft and the increasing pressure compresses the blood supply leading to necrosis of the medullary bone.
Pus is then forced through the bone cortex to locate under the periosteum.

47
Q

What is sequestrum and what disease does it fall under?

A

Lifting of the periosteum leads to further loss of blood supply to the cortical bone, which becomes necrotic and trapped.
Found in pyogenic osteomyelitis
Dead bone resulting from either pressure within the marrow cavity or loss of the blood supply because of the lifting periosteum.

48
Q

What is involucrum and what disease does it occur in?

A

Periosteum laying down new bone on the surface of the bone which entraps the dead sequestrum underneath
Pyogenic osteomyelitis

49
Q

What are sinuses and what disease are they found in?

A

Pus may break into soft tissue, forming abscesses which may open into the skin surface.
Sequestrum may also be extruded through a sinus

50
Q

What is pus in the bone marrow formed of?

A

Necrotic tissue debris, neutrophils and dead fragmented neutrophils

51
Q

What is the treatment for osteomyelitis?

A

Antibiotics according to culture and sensitivity

Surgical debridement to remove dead tissue and pus and therefore relieve pressure

52
Q

When is debridement undertaken in osteomyelitis?

A

Undertaken if there is no clinical improvement in 24-48 hours

53
Q

What is gout?

A

Arthritis initiated by deposition of urate crystals within and around joints
Px have excess uric acid in tissues and plasma = hyperuricemia

54
Q

What is uric acid?

A

End product of metabolism of purines

55
Q

What causes Primary gout?

A

Unknown cause

56
Q

What is the majority of gout caused by?

A

Primary cause - 90% of cases, no known cause

57
Q

What is secondary gout caused by?

A

Conditions that lead to the production of uric acid (increased cell turnover e.g. leukaemias) or decreased excretion of uric acid (renal failure)

58
Q

What is acute gout?

A

Attacks of acute gouty arthritis arise when monosodium urate (MSU) crystals precipitate within the joints - triggering an acute inflammatory reaction (infiltration by neutrophils)

59
Q

Where do urate crystals accumulate in acute attacks of gouty arthritis?

A

Peripheral joints where synovial fluid is a poor solvent and temp is low

60
Q

Which joint is usually affected in acute attacks of gout?

A

Big toe - shows all signs of acute inflammation: loss of function, heat, redness, swelling/oedema, pain

61
Q

What is chronic gout?

A

Repeated attacks of acute gouty arthritis, aggregates of urate crystals eventually deposit within the synovial membrane.

62
Q

What are the aggregates called in chronic gout and what is the condition called?

A

Aggregates are called tophi and condition is chronic tophaceous gout

63
Q

What happens in chronic gout?

A

Intense chronic inflammatory reaction in the synovium with pannus formation and cartilage/bone destruction
Tophi extend to the periarticular soft tissue

64
Q

Name some features seen on a chronic gout x-ray.

A

First MTP joint shows destruction of joint
Radiolucent (darker than bone) tophi (aggregates of crystals) are seen bilaterally extending to the soft tissue
Loss of joint space = damage to joint by inflamed synovium

65
Q

What is the treatment for gout?

A

NSAIDs - anti-inflammatory action and pain relief
Colchicine - inhibits neutrophil mobility and activity
Low dose steroids
Hydration
Medical assessment to reduce risk factors

66
Q

What is septic arthritis?

A

Infection of the joint leading to acute inflammation and pus formation within the joint cavity (replacing the clear synovial fluid)

67
Q

How do organisms gain entry for septic arthritis?

A

Bacteraemia (hematogenous spread)
Trauma
Surgery (iatrogenic)

68
Q

What is the most common causative organism in septic arthritis?

A

Staph Aureus

69
Q

What is the classic picture of septic arthritis?

A

Young child with fever and severe localized joint pain, swelling and marked limitation in range of movement

Musculoskeletal Block Module (10 decks)

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