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Pathology > Infectious and noninfectious arthritis > Flashcards

Infectious and noninfectious arthritis Flashcards

1
Q

Acute Suppurative Arthritis

How can it infect ?

A

• Bacterial etiology • Hematogenous spread

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2
Q

Acute Suppurative Arthritis
H. Influenza
Common in ?

A

Less than 2 years

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3
Q

Acute Suppurative Arthritis
Common in ?
Staph aureus

A

Older children and adults

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4
Q

Acute Suppurative Arthritis
Common in ?

gonorrhea?

A

Adolescent and young adults

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5
Q

Acute Suppurative Arthritis

Common in ? Salmonella?

A

patient with sickle cell disease

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6
Q

Acute Suppurative Arthritis
Predisposing factors
?

A
  • Immune deficiency
  • Debilitating illness
  • Joint trauma
  • IV drug abuse
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7
Q

Acute Suppurative Arthritis
Clinical presentation
?

A

• Sudden onset of acute joint

swelling and pain • Fever • Leukocytosis • Elevation of ESR

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8
Q

Non -infectious arthritis examples ?

A
  1. Osteoarthritis
  2. Rheumatoid arthritis
  3. GOUT
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9
Q

the most common degenerative joint

disease ?

A

Osteoarthritis

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10
Q

characterized by progressive degeneration of articular
cartilage in weight-bearing joints.
?

A

Osteoarthritis

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11
Q

Primary Osteoarthritis commonly affects ?

A
  • Elderly (90%), common above 50 years

* Oligoarthritis, few joints

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12
Q

Secondary Osteoarthritis coolly affects ?

A

Younger
• There is typically some predisposing condition, such as
previous traumatic injury, developmental deformity, or underlying systemic disease such as diabetes or marked obesity

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13
Q

Osteoarthritis

Normal articular cartilage performs two functions ?

A

1) Provides virtually friction-free movement within the joint along with the synovial fluid. (2) In weight-bearing joints, it spreads the load across the joint surface

These functions require the cartilage to be elastic (i.e., to regain normal
architecture after compression) and to have high stretchy strength. These
attributes are provided by proteoglycans and type II collagen, both
produced by chondrocytes

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14
Q

Pathogenesis of Osteoarthritis?

A
  1. Chondrocyte function is affected by a variety of influences (mechanical stresses , aging and Genetic factors. )
  2. an imbalance in the expression, activity, and signaling of cytokines and growth factors
  3. degradation and loss of matrix.
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15
Q

Early osteoarthritis is marked by ?

A
  • degenerating cartilage containing :
    mor water
    less proteoglycan

• The type II collagen network also is diminished, apparently as a result of
decreased local synthesis and increased breakdown

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16
Q

Morphology of Osteoarthritis?

A
  1. superficial layers of the cartilage are degraded.
  2. Fibrillation and cracking of the matrix
  3. Full-thickness portions of the cartilage are sloughed
  4. subchondral bone plate is exposed and is smoothened by friction.
  5. Small fractures can dislodge pieces of cartilage and subchondral bone into the joint, forming loose bodies.
  6. fracture gaps allow synovial fluid to be forced into the
    subchondral regions to form fibrous walled cysts.
  7. Mushroom-shaped osteophytes (bony outgrowths) develop at the
    margins of the articular surface
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17
Q

osteophytes

Common characteristic of ?

A

Osteoarthritis

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18
Q

Heberdens nodes Is ? In which condition ?

A

Osteophytes on the interphalangeal joints of the fingers

- osteoarthritis

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19
Q

Osteoarthritis

Commonly effects which area in women and in men?

A

Knees and hands are commonly affected in females and hips in

males

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20
Q

Osteoarthritis pain rate ?

A
  • Insidious onset of pain
  • Worsens with use
  • Limitation of range of movement

• Morning stiffness, crepitus (rough or cracking sensation in the joint)
Osteophyte formation in spinal joint leads to radicular pain

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21
Q

Osteoarthritis which joint are commonly involved. ?

A

First carpometacarpal joints, and first tarsometatarsal joints of the
feet

22
Q

Heberden nodes in ? Characteristics in women or men?

A

Heberden nodes in the fingers, representing prominent osteophytes
at the distal interphalangeal joints, are characteristic in women.

23
Q

Management treatment ? Osteoarthritis?

A

• No prevention and no specific therapy • +/- arthroplasty

24
Q

systemic, chronic inflammatory

autoimmune multisystem disease, principally attacking the joints. ?

A

Rheumatoid arthritis

25
Q

causes a nonsuppurative proliferative synovitis that
frequently progresses to destroy articular cartilage and
underlying bone with resulting disabilities.
?

A

Rheumatoid arthritis

26
Q

Rheumatoid arthritis

More common in which gender? Age ?

A

common in middle aged women.

27
Q

The joint inflammation in RA is mediated by ?

A

is immunologically mediated

28
Q

RA is initiated by ?

A
  1. some arthritogenic agent, possibly microbial, or to some self-antigen enter thec body
  2. activation of CD4+ helper T cells
29
Q

Pathogenesis of RA

A
  1. some arthritogenic agent, possibly microbial, or to some self-antigen enter thec body
  2. activation of CD4+ helper T cells
  3. activated T cells produce cytokines that:
  4. (1) Activate macrophages and other cells in the joint space, releasing degradative enzymes and other factors that produce inflammation.
  5. (2) Activate B cells, resulting in the production of antibodies, some of which are directed against self-antigens in the joint.
  6. autoantibodies; antibodies against cyclic
    citrullinated peptides (CCPs), which may contribute to the joint
    lesions in RA
  7. form immune complexes that deposit in the joints
30
Q

may contribute to the joint

lesions in RA ?

A 
antibodies against cyclic
citrullinated peptides (CCPs)
31
Q

DIAGNOSTIC
MARKERS FOR RA
?

A

immune complexes that deposit in the joints

32
Q

autoantibodies in RA what do they do ?

A

rheumatoid factor

1. serum IgM or IgA autoantibodies that
bind to the Fc portions of their own IgG
2. deposit in joints 
3. leading to inflammation and tissue damage
=

They are not specific.

33
Q

These
autoantibodies are called

RA. ?

A

rheumatoid factor

34
Q

Pathologic Features of RA?

A
  1. Synovial cell hyperplasia and proliferation
  2. Chronic synovitis; dense perivascular lymphoplasmacytic inflammatory infiltrates, frequently forming lymphoid follicles in the synovium.
  3. Pannus: formed by proliferating synovial cells, inflammatory cells, granulation tissue, and fibrous connective tissue

• Pannus fills up the joint space,

• Fibrosis and calcification may follow causing permanent
ankylosis
4. Increased osteoclast activity in the underlying bone  bone erosion.

35
Q

RA commonly effects which area ?

A
  • Symmetric arthritis, principally affecting
    the small joints of the hands and feet,
    ankles, knees, wrists, elbows, and shoulders.
  • proximal interphalangeal and
    metacarpophalangeal joints are commonly
    affected, but distal interphalangeal joints are
    spared.
  • Axial involvement, when it occurs, is limited
    to the upper cervical spine; similarly, hip
    joint involvement is extremely uncommon.
36
Q

RA Destruction of tendons, ligaments, and joint capsules

produces the characteristic deformities, including?

A

• 1.Radial deviation of the wrist
• 2.Ulnar deviation of the fingers.
• 3.Flexion-hyperextension abnormalities of the fingers:
• Swan neck deformity (hyperextension of PIP Joint with flexion
of DIP joint)
• Boutonnière deformity (hyperextension of the DIP with flexion
of the PIP joint)

37
Q

hyperextension of PIP Joint with flexion

of DIP joint?

A

Swan neck deformity

38
Q

hyperextension of the DIP with flexion

of the PIP joint?

A

Boutonnière deformity

39
Q

RA x-ray? Laboratory?

A

X ray: joint space narrowing, loss of articular cartilage, erosion. Laboratory:
Anti-CCP (cyclic citrullinated peptides) protein antibodies Rheumatoid factor ESR and C-reactive

40
Q

Leads to loss of cartilage matrix ?

A

Osteoarthritis

41
Q

disorder caused by the tissue
accumulation of excessive amounts of uric
acid, an end product of purine metabolism ?

A

Gout

42
Q

Gout

What is precedent in the joint? And what does it cause ?

A

Monosodium urate crystals precipitate in
joints and induce an acute inflammatory
reaction.

43
Q

Gout

Recurrent episodes of acute arthritis,
sometimes accompanied by the formation of
large crystalline aggregates called ?

A

tophi, and

eventual permanent joint deformity.

44
Q

Classification of Gout

?

A

PRIMARY GOUT (90% OF CASES) :
 Overproduction of uric acid
 Diet
 Unknown enzyme defects (80% to 90%)
 Known enzyme defects (e.g., partial HGPRT deficiency, rare)
 Reduced excretion of uric acid with normal production

SECONDARY GOUT (10% OF CASES) :
 Overproduction of uric acid with increased urinary excretion
 Increased nucleic acid turnover (e.g., leukemias and other aggressive neoplasms)
 Inborn errors of metabolism (e.g., complete HGPRT deficiency)
 Reduced excretion of uric acid with normal production
 Chronic renal disease

45
Q

Acute arthritis is characterized by ?

A

dense neutrophilic infiltrate
permeating the synovium and synovial fluid. Long, slender, needle-
shaped monosodium urate crystals frequently are seen

46
Q

repetitive precipitation
of urate crystals during acute attacks
What develops ? Gout?

A

Chronic tophaceous arthritis

47
Q

Gout

The synovium becomes?

A

hyperplastic, fibrotic, and thickened by inflammatory cells

48
Q

pathognomonic for gout. ?

A

Tophi

49
Q

are formed by large
aggregations of urate crystals surrounded by an intense
inflammatory reaction of lymphocytes, macrophages, and
foreign-body giant cells ?

A

Tophi

50
Q

appear in the articular cartilage of joints and in the
soft tissues, including the ear lobes & nasal cartilages
?

A

Tophi

51
Q

Gout most commonly affwected suite ?

A

first metatarsophalangeal

joint, swollen, red, and very painful.

52
Q

Renal manifestations of gout can appear as?

A

renal colic associated

with the passage of stones

Pathology (4 decks)

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