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M2 Pathology > MSK Joint Pathology > Flashcards

MSK Joint Pathology Flashcards

1
Q

Osteoarthritis is the ______ progressive ________ of articular cartilage, resulting in _________.

A

Osteoarthritis is the CHRONIC progressive DESTRUCTION of articular cartilage, resulting in REDUCED JOINT SPACE.

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2
Q

State 4 common secondary causes of osteoarthritis

A
  1. Congenital abnormality
  2. Avascular necrosis
  3. Trauma
  4. Joint diseases
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3
Q

State the common pathological changes of osteoarthritis.

A
  1. Eburnation with smooth, polished surface due to constant friction of bone surfaces
  2. Formation of subchondral cyst
  3. Formation of osteophytes
  4. Thickening of subarticular bone
  5. Reactive thickening of synovium
  6. Destruction of articular cartilage
  7. Secondary changes to surrounding tissue
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4
Q

State the two types of osteophytes formed in OA, state their corresponding locations.

A

Hebedern’s nodes = DIPJ
Bouchard’s nodes = PIPJ

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5
Q

State the common clinical presentations of OA.

A
  1. pain
  2. swelling
  3. decreased ROM
  4. formation of osteophytes/bone spurs
  5. cervical spondylosis spinal nerve compression
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6
Q

State the 3 types of OA.

A
  1. primary generalised OA
  2. erosive inflammatory OA
  3. hypertrophic OA
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7
Q

State the difference between erosive inflammatory OA and hypertrophic OA.

A

erosive inflammatory OA - rapid progression

hypertrophic OA - slow progression

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8
Q

State the common group of individuals that present with primary generalised OA.

A

menopause women!

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9
Q

Hypertrophic OA is a _____, inflammatory, reparative activity involving _____ cartilage and _____ bone. It has secondary effects on ____, _____ and ____.

A

Hypertrophic OA is a DEGENERATIVE, inflammatory, reparative activity involving ARTICULAR cartilage and SUBARTICULAR bone. It has secondary effects on SYNOVIUM, MUSCLE and NERVES.

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10
Q

State the 2 common pathological changes associated with hypertrophic OA.

A
  1. florid osteophyte formation
  2. bone sclerosis
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11
Q

State the common causes of hypertrophic OA.

A
  1. increased unit load on joint
  2. degradation of articular cartilage
  3. biochemical abnormalities (reduction of prosteoglycans, protein synthesis, chondrocyte replication)
  4. genetic abnormalities (familial mutation of type 2 collagen COL2A1)
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12
Q

State the 2 most important parts of the intervertebral disc.

A
  1. nucleus pulposus (inner) = contains water and proteoglycans
  2. disc annulus (outer) = obliquely oriented collagen fibres and cartilaginous end plate
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13
Q

State some causes of degenerative intervertebral disc.

A
  1. age related wear and tear - nucleus pulposus dehydrated, fibrotic and atrophied
  2. mechanical factors
  3. genetic predisposition
  4. nutrition, metabolic, infection
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14
Q

State the stages of disc herniation.

A
  1. Degeneration
  2. Prolapse - weakened annulus, outer layers of annulus still intact
  3. Extrusion
  4. Sequestration - part of nucleus pulposus spurts out through a tear in annulus into the spinal foramen
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15
Q

State the common complications of intervertebral disc degeneration. Give 1 example for each complication.

A
  1. Posterior compression –> injury to spinal cord (eg: cervical myelopathy)
  2. Posterolateal compression –> injury to nerve roots (eg: radiculopathy)
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16
Q

Rheumatoid arthritis is a _____ chronic ______ ______ disease affecting many tissues but specifically the joints.

A

Rheumatoid arthritis is a SYSTEMIC chronic INFLAMMATORY AUTOIMMUNE disease affecting many tissues but specifically the joints.

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17
Q

Which parts of the body does RA usually affect?

A

Joints of hand (PIP, MCP), wrists, elbows, knees

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18
Q

RA is most common in _____.

A

RA is most common in MIDDLE-AGED WOMEN.

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19
Q

What are the elevated serum markers of RA?

A
  1. RF (rheumatoid factor)
  2. ACPA (anticitrullinated protein antibody)
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20
Q

State the pathogenesis of RA

(hint: very very long)

A

Step 1:

  • genetic predisposition = HLA-DR4
    -> unregulated lymphocyte activation
    -> loss of immune tolerance
  • environmental factors (infection, smoking) = formation of autoantibodies against CCP
    -> citrullination of self-proteins - recognised as foreign

Step 2: T and B lymphocyte response to self-Ag present in joint tissues

  • Th17 -> secrete IL-17 -> activates other immune cells to inflame joint
  • Th1 -> secrete cytokines (IL-1, TNF-a) -> promote inflammatory response
  • B lymphocyte -> secrete RF and ACPA -> form immune complexes

Step 3: Proliferation of chondryocytes, synovial cells, fibroblasts

Step 4: Release of elastase, stromelysin, collagenase, PGE2

Step 5: Pannus formation, ankylosis, fibrosis, desturction of bone and cartilage

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21
Q

State the common pathological features of RA

A
  1. Pannus formation - composed of granulation tissue that grows and destroys articular cartilage -> fibrosis across joint -> ankylosis
  2. Synovial inflammation - swelling and villous formation of synovium
  3. Destruction of adjacent bone - joint deformity
  4. Formation of rheumatoid nodules
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22
Q

Is RA or OA systemic?

A

RA is a systemic disease!!
- 25% of patients have subcutaneous rheumatoid nodules (has central zone of fibrinoid nodules)
- found in other organs
- presents with…
1. necrotising vasculitis of small vessels (affects GIT, lung, heart, kidneys)
2. amyloidosis

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23
Q

How do we differentiate OA and RA?

A

Morning stiffness:
RA >30 minutes, OA <30 minutes

Serum markers:
RA - RF and ACPA, OA none

Pannus:
RA - present, OA - absent

Nature:
RA - inflammatory and autoimmune, OA - non-inflammatory and degenerative

Cause:
RA - autoimune attack on synovium, OA - wear and tear of cartilage

Affected joints:
RA - small joints (PIP, MCP, wrists, elbow, knees) , OA - weight-bearing joints (knees, hips, spine)

Findings:
RA - synovial hyperplasia with dense inflammation, pannus, eroding cartilage, bony and fibrous ankylosis, subchondral cyst
OA - synovium with mild inflammation, osteophytes, thinned (destruction) of cartilage, subchondral cyst, subchondral sclerosis, no ankylosis

Systemic symptoms:
RA - yes, OA - no

Gender preference:
RA - older females, OA - none

24
Q

State two other types of inflammatory arthritis.

A
  1. Seronegative spondyloarthropathies
  2. Autoimmune arthritis - SLE, RF, systemic sclerosis
25
Q

State some unique features of seronegative spondyloarthropathies.

A
  • lacks RF (since seronegative)
  • high incidence of HLAB27
  • either axial location (vertebrae, sacr-iliac joint) or asymmetric involvement of the peripheral joints in digits
  • USE MRI OVER SACRO-ILIAC JOINT
  • hip pain -> sacroiliac -> lumbar -> thoracic (with some cervical pain)
  • pathology found in ligamentous attachments instead of synovium
26
Q

State the 3 commoner types of seronegative spondyloarthropathies.

A
  1. ankylosing spondylitis = destruction of vertebral column and sacroiliac joint
  2. psoriatic arthropathy (@DIPJ)
  3. reactive arthritis (post infection of conjunctivitis, polyarthritis, urethritis)
27
Q

State the common clinical presentation and determining factor for ankylosing spondylitis.

A
  • commonly presents with inflammatory back pain
  • patient is unable to bend on any axis due to stiff axial skeleton (uniquely cannot bend sideways)
28
Q

State 2 common inflammatory joint pathologies related to infection.

A
  1. Septic arthritis
  2. Osteomyelitis
29
Q

Septic arthritis is the _______ inflammation of the _____ and ________ _______ due to ______.

A

Septic arthritis is the SUPPURATIVE inflammation of the SYNOVIUM and JOINT STRUCTURES due to INFECTION.

30
Q

State the common clinical presentations of septic arthritis

A
  1. acute onset of severe joint pain
  2. warm and swollen joints (AT HIP AND KNEE)
  3. fever
  4. systemic symptoms
31
Q

State the common sources of infection for septic arthritis. State the common causative agents.

A
  1. Haematogenous dissemination (most common)
  2. Direct inoculation through skin
  3. Contiguous infective spread from adjacent soft tissue abscess or osteomyelitis

Common causative agents:
- Staph aureus
- Grp B strep
- Pseudomonas
- Gram negative bacilli

32
Q

State the laboratory tests used to investigate septic arthritis and the histological features seen under microscopy,

State the most appropriate treatment for patients with septic arthritis.

A

Laboratory tests:
- gram stain and culture
- high wcc count with predominance of neutrophils
- joint aspiration for histological and microbiological analysis

Histology
- acute inflammation, purulent exudate
- destruction of synovium and stroma

Treatment:
- joint washout and antibiotics for 2-6 weeks

33
Q

Osteomyelitis is a bone infection involving _____, ____ and ____.

A

Osteomyelitis is a bone infection involving MEDULLA, CORTEX and PERIOSTEUM.

34
Q

State the clinical presentations of osteomyelitis and their common sites of presentation.

A

Clinical presentation:
- fever
- swelling
- pain
- constitutional symptoms

Sites of presentation:
- Children - long bones and jaw
- Adults - small bones, femur, vertebral spine (lumbar > thoracic > cervical)

35
Q

State the main causative agent of osteomyelitis and modes of transport into bone.

A

Main causative agent = Staph aureus

Modes of transport:
1. Direct implantation - trauma with open wound/ wound and surgery
2. Bloodborne spread (more common in children)
3. Extension from contiguous site

36
Q

State the investigations used in osteomyelitis.

State the appropriate treatment needed for osteomyelitis.

A

Investigations:
- MRI > CT > X-ray
- Tissue culture or CT guided biopsy > wound swab
- If blood culture is positive and clinical signs fit -> immediately diagnose

Treatment:
- Avoid empirical antibiotic treatment to increase chances of growing causative pathogens from tissue sampling
- Treat for 6 weeks minimally
- Surgery to remove necrotic tissue or bone or manage neurological emergency

37
Q

State the progression of OM.

A
  1. Healed OM -> resolution or healing with scarring
  2. Complicated OM (acute OM -> chronic/subacute OM)
38
Q

State the complications of OM.

A
  1. Pathological fracture with deformities
  2. Spread of infections -> skin-cellulitis, endocarditis, blood-septicaemia
  3. Bone abscess (brodie’s abscess)
  4. Necrosis of bone (sequestrum)
  5. Proliferative periostitis and involucrum over sequestrum
  6. Sinus
  7. Secondary amyloidosis
  8. Malignant transformation to bone (osteosarcoma) and skin (SCC)
39
Q

State everything you know about suppurative OM

A
  • Active on chronic suppurative OM
  • Bacteria proliferates in bone -> induces acute inflammation and cell death (bone necrosis)
  • If infection extends to joints or synovium -> septic arthritis

Histology:
- neutrophils
- necrosis

Progression
- suppurative injury causes tissue destruction
- elevation of periosteum -> inflammation leads to sizable subperiosteal pus or abscess -> causes further bone necrosis
- rupture of periosteum -> leads to inflammation and abscess in surrounding skin and soft tissue (cellulitis) and eventual formation of draining sinus

40
Q

State everything you know about non-suppurative OM

A
  • chronic OM
  • lacking/minimal pus, mainly chronic inflammation and fibrotic/scar

Histology:
- diffuse or focal sclerosing
- proliferative periostitis

41
Q

State everything you know about chronic OM

A
  • 5-25% acute OM progresses to chronic OM
  • causes:
    1. delay in diagnosis and treatment
    2. extensive bone necrosis
    3. incomplete surgical debridement of necrotic bone
    4. weakened immunity
  • complications:
    1. pathological fractures and deformity
    2. secondary amyloidosis
    3. sepsis
    4. malignant transformation
42
Q

State everything you know about Garre’s Sclerosing OM.

A

CHRONIC OM WITH PROLIFERATIVE PERIOSTITIS
- presentation: mild irritation, dental infection, trauma
- involves jaw -> new bone formation obscuring underlying native bone structure
- mainly affects children and adolescents
- easily misdiagnosed as malignant (osteosarcoma, chondrosarcoma0

43
Q

State everything you know about Tuberculous OM

A

CHRONIC OM
- mainly affects very young or very old, immunosuppressed, lower SES with MTB infection
- blood borne or lymphatic drainage
- involves vertebral spine (thoracic and lumbar)
- highly destructive with extensive necrosis -> difficult to treat
- Histology:
1. epitheloid granulomas
2. caseating necrosis
- Complications:
1. compression fracture
2. severe deformities (scoliosis, kyphosis)
3. neurological deficits due to cord and nerve compression

44
Q

Crystal arthropathies is the ______ of ____ in joints and soft tissues.

A

Crystal arthropathies is the DEPOSITION of CRYSTALS in joints and soft tissues.

45
Q

State the presentation of crystal arthropathies.

State the investigations common to crystal arthropathies.

A
  1. Acute pain
  2. Swelling
  3. Erythema at joints (foot and big toe)

Investigation:
Joint fluid analysis (gram stain and culture)

46
Q

Gout is characterised by increased serum _____ ____ and _____ ____ deposition.

A

Gout is characterised by increased serum URIC ACID and URATE CRYSTALS deposition.

47
Q

State the primary and secondary causes of gout.

A

Primary causes:
- obesity
- alcohol
- HTN
- fatty diet

Secondary causes:
CONDITIONS THAT PROMOTE HYPERURICEMIA
- renal failure
- familial juvenile hyperuricaemic neuropathy
- congenital enzyme defects

48
Q

State the pathogenesis of gout.

State the lab observations of gout.

A

Problems of purine metabolism -> increased uric acid production and decreased uric acid elimination

  1. overproduction of purines (high purine diet)
  2. increased catabolism of nucleic acids due to high cell turnover (infection or cancer)
  3. decreased uric acid excretion by kidneys

Lab: strongly birefringent needle shaped crystals

Recap: purine is the precursor for uric acid

49
Q

State the presentation of gout and its associated complications.

A

Presentation: deposition of urate crystals -> erythematous inflammation

Complications
- gouty tophi
- deformities
- erosions of joints
- interstitial nephritis
- kidney disease and kidney stones

50
Q

State the pathogenesis of acute gouty arthritis.

A
  1. urate crystals are phagocytosed by macrophages
  2. activation of inflammaotey mediators that release IL-1
  3. IL-1 recruit neutrophils -> release of cytokines (TNF-A) -> free radicals and proteases
  4. neutrophils phagocytose crystals which together with macrophages damage the membranes of the lysosomes leading to release of enzyme
51
Q

Pseudogout is the deposition of _____ _____ ______ in joints.

A

Pseudogout is the deposition of CALCIUM PYROPHOSPHATE DIHYDRATE in joints.

52
Q

State the common causes of pseudogout.

State the presentation of pseudogout.

State the lab findings of pseudogout.

A

Common causes:
1. Idiopathic - trauma association
2. Hyperparathyroidism
3. Haemochromatosis

Presentation:
- mostly asymptomatic
- acute, subacute or chronic arthritis

Lab: crystals are rhomboid-shaped and positively birefringent under polarised light

53
Q

State the presentation of prosthetic joint infections

A

Acute infection = <6 months post surgery
Chronic infection = 6 months-2 years post surgery

Presents as…
1. fever
2. joint pain

54
Q

State the causative agents of prosthetic joint infections.

State the investigations of prosthetic joint infections.

A

Causative agents:
- >70% due to staph, can be due to any skin flora related bacteria
- CONS (coagulative negative staph) - insidious presentation
- Staph aureus - acute presentation

Investigations:
- DO NOT DO NOT DIAGNOSE WITH GRAM STAIN
- Multiple (>3,6) intraoperative tissue or pus culture
- DO NOT USE WOUND SWAB

55
Q

State the appropriate way to treat prosthetic joint infection.

A
  • antibiotic usage is guided by culture results
  • use antibiotics with ability to penetrate biofilm (rifampicin, ciprofloxacin)
  • combination antibiotic therapy preferred
  • start with IV antibiotics -> switch to PO provided antibiotics with excellent bioavailability

Acute infection
- local debridement with retention of prosthesis and prolonged antibiotics (>6 weeks)
- chances of cure without removal of prosthesis is pessimistic especially for bacterias (staph, enterococci, pseudomonas)

Infected prosthesis
1. one stage exchange arthroplasty = remove infected prosthesis, insert new prosthesis during the same operation with antibiotic loaded cement
2. two stage approach = remove infected prosthesis, install antibiotic loaded cement to stabilise bone -> treat with weeks or months of antibiotics -> insert new prosthesis after prolonged course of antibiotics

M2 Pathology (20 decks)

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