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MSK > Pathology > Flashcards

Pathology Flashcards

1
Q

Name the types of arthritis

A
  • osteoarthritis
  • rheumatoid arthritis
  • seronegative spondyloarthopathies
  • infectious arthritis
  • crystal induce arthritis
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2
Q

Describe connective tissue diseases

A
  • autoimmune conditions
  • inflammatory diseases characterised by the presence of autoantibodies
  • 1-2% of the population
  • often present with MSK and rheumatological symptoms and signs but have potential for systemic manifestations
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3
Q

Describe synovial joints

A
  • have a joint space that allows movement
  • strength from capsule, ligaments and muscle
  • joint space is bounded by synovial membrane; produce synovial fluid for lubrication and nutrition
  • articular surfaces formed of hyaline cartilage; elastic shock absorber and wear resistant surface
  • disseminate shear forces effectively
  • type 2 collagen gives strength
  • water and proteoglycans give elasticity and reduce friction
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4
Q

Describe osteoarthritis

A
  • the most common form of joint disease; an important cause for joint replacement surgery
  • a degenerative form of joint disease; degenerative changes in the articular cartilage, structural changes and functional impairment
  • pathogenesis; aging and biomechanical stress
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5
Q

What is primary osteoarthritis?

A
  • insidious
  • no overt cause
  • age related
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6
Q

What is secondary osteoarthritis?

A
  • predisposing condition

- excess / inappropriate weight bearing, deformity, injury, systemic conditions

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7
Q

Describe the clinical correlations of osteoarthritis

A
  • insidious onset
  • primary form present from age >50
  • secondary forms may arise earlier
  • aches and pain; worse with use
  • usually hips, knees, lower lumbar and cervical vertebrae, PIP and DIP joints of fingers
  • wrists, elbows and shoulders usually spared
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8
Q

Describe the early events of pathogenesis in osteoarthritis

A
  • degeneration of the cartilage and disordered repair
  • injury to chondrocytes and matrix
  • chondrocyte injury; genetic and biochemical factors
  • chondrocytes proliferate; release inflammatory mediator, proteases, collagen and proteoglycans, remodelling and degeneration of cartilage
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9
Q

Describe the late events of pathogenesis in osteoarthritis

A
  • stimulate inflammatory changes in synovium and subchondral bone
  • repetitive injury and chronic inflammation
  • loss of chondrocytes
  • disruption to and loss of cartilage matrix
  • further changes in subchondral bone and synovium
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10
Q

Describe the early pathological features of osteoarthritis

A
  • damage to cartilage
  • clusters of chondrocytes
  • small fissures in cartilage
  • fibrillation
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11
Q

Describe the later pathological features of osteoarthritis

A
  • cartilage is completely worn away; bone on bone
  • subchondral cysts
  • surface becomes polished - eburnation
  • remodelling to cope with stress
  • formation of osteophytes
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12
Q

Describe eburnation

A
  • loss of articular cartilage

- joint space being formed by the bone that normally lies underneath the cartilage becomes smooth through trauma

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13
Q

Osteophytes can do what?

A

They can innervate nerves

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14
Q

Describe rheumatoid arthritis

A
  • a chronic inflammatory disorder
  • autoimmune
  • 2nd to 4th decades
  • 3F:1M
  • often presents with features of arthritis
  • a systemic disorder
  • extra-articular lesions are common; may occur in the absence of joint symptoms
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15
Q

Describe the presentation of rheumatoid arthritis

A
  • vague systemic features; malaise, fever
  • generalised musculo-skeletal pain
  • joint involvement become more apparent
  • symmetrical; swollen, warm, painful, limited movement in morning and after inactivity
  • small joints before large joints; hands and feet (MCP, MTP, PIP), wrists, ankles, elbows, knees, cervical spine, usually spares hips and lumbosacral joints
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16
Q

Describe the progression of symptoms in rheumatoid arthritis

A
  • joint swelling, decreased range of movement, joint fusion (ankylosis)
  • associated involvement of tendons ligaments; joint deformity
  • unstable (very) limited ROM
  • synovial herniation; cysts eg bakers cyst
  • joint effusions, peri-articular bone loss, loss of articular cartilage
  • disease can show periods of remission
  • 10% patients have acute presentation; severe symptoms and polyarticular disease
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17
Q

Describe the genetic factors of rheumatoid arthritis

A
  • HLA DRB1 alleles linked to RA have common structure in the beta chain (shared eptiope), a site for binding arthritogens
  • initiate autoimmune inflammatory reaction
  • immune tolerance compromised
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18
Q

Describe environmental factors of rheumatoid arthritis

A
  • environmental factors
  • precise trigger uncertain
  • infection and smoking increase citrullinated peptide
  • citrullination of self proteins
  • modify epitopes and trigger autoimmune reactions
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19
Q

Describe the immunology of rheumatoid arthritis

A
  • auto-immune inflammation triggered
  • CD4+T cells may be critical
  • cytokine production results from initiation of inflammation
  • IFNg activates macrophages and synovial cells
  • IL-17 recruits neutrophils and monocytes
  • TNF and IL-1 stimulate production of proteases from synovium
  • RANKL expressed on activated T cells stimulates bone resorption
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20
Q

What is involved in the acute phases of rheumatoid arthritis?

A
  • pannus formation; inflammatory granulation tissue
  • hyperplastic / reactive synovium
  • cartilage is destroyed by inflammatory process; loss of joint space
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21
Q

Describe the extra-articular disease involved with rheumatoid arthritis

A
  • 40% of cases
  • before, with or after joint symptoms become apparent
  • high titres of RF most at risk
  • tendons, ligaments and fascia
  • many other sites of involvement
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22
Q

What are rheumatoid nodules?

A

Areas of necrotic cartilaginous tissue surrounded by a periphery of inflammatory cells

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23
Q

Describe the skin manifestations of rheumatoid arthritis

A
  • rheumatoid nodules; 25% of patients, often severe disease, pressure points, internal organs eg lung, spleen, heart
  • necrotising granuloma
  • small vessel vasculitis; splinter haemorrhages, peri-ungal infarcts, ulcers, gangrene
  • associated with episcleritis, pleural and pericardial effusions
  • pyoderma gangrenosum
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24
Q

What are necrotising granulomas?

A
  • central area collagen necrosis

- surround palisade of macrophages (lymphocytes and plasma cells)

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25
Q

What are the ocular manifestations of rheumatoid?

A
  • keratoconjunctivitis

- episcleritis and scleritis

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26
Q

What are the oral manifestations of rheumatoid?

A
  • salivary gland swelling

- sjogrens syndrome

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27
Q

What are the GI manifestations of rheumatoid?

A
  • mesenteric vasculitis (rare)

- related to medication

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28
Q

What are the pulmonary manifestations of rheumatoid?

A
  • pleuritis and effusion
  • rheumatoid nodules
  • interstitial lung disease; interstitial fibrosis
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29
Q

What are the cardiac manifestations of rheumatoid?

A
  • pericarditis and effusion
  • myocarditis; conduction anomalies
  • endocarditis; valve dysfunction
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30
Q

What are renal manifestations of rheumatoid?

A
  • forms of glomerulonephritis

- amyloid disease; nephrotic syndrome

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31
Q

What are neurological manifestations of rheumatoid?

A
  • peripheral neuropathy

- cervical myelopathy; atlanto-axial disease

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32
Q

What are haematological manifestations of rheumatoid?

A
  • anaemia; chronic disease, iron deficiency
  • other abnormal indices
  • lymphadenopathy; hyperplasia
  • splenomegaly (feltys syndrome)
  • increased risk of lymphoma
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33
Q

What are seronegative spondyloarthopathies ?

A
  • group of diseases with some common features
  • HLA B27 association
  • No rheumatoid factor
  • involve sacro-iliac joints +/- others
  • affect ligamentous attachments
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34
Q

Describe psoriatic arthritis

A
  • > 10% of patients with psoriasis
  • predominantly affects joints of hands and feet
  • 20% of cases involve sacro-iliac joints
  • joint involvement may be asymmetrical
  • DIP joints characteristically affected
  • similar histology to RA
35
Q

Describe infectious arthritis

A
  • potentially destructive process
  • suppurative
  • haematogenous spread of organisms; s aureus in adults, gonococcal infection in young adults, sickle cell predisposes to salmonella arthritis
  • typically involves single joint (knee most common)
  • systemic features of infection
  • acutely painful and swollen joint; aspirate purulent fluid
  • mycobacterial, lyme disease, viral
36
Q

Describe hyperurucaemia

A
  • can be a problem with excess synthesis or problem with excretion
37
Q

Describe synthesis of uric acid

A
  • from purine catabolism
  • reflects abnormal purine metabolism
  • synthesis from non-purine precursors
  • salvage from dietary intake and catabolism of purine nucleotides
38
Q

Describe excretion of uric acid

A
  • renal filtration
  • reabsorbed in proximal tubule
  • limited excretion from distal tubule
39
Q

Describe the increased production of uric acid

A
  • usually idiopathic; unknown enzyme defect
  • known enzyme defect; HGPRT deficiency; lesch nyhan syndrome (rare), impairs purine nucleotide salvage pathway, degraded to urate
  • increased cell turnover; psoriasis, cancer and tumour lysis following chemotherapy
40
Q

Describe the reduced excretion of uric acid

A
  • under excretion; a common cause of gout, chronic renal disease
  • drug side effect; thiazide diuretics reduce urate excretion
41
Q

Deposition of crystals into soft tissues causes what

?

A

Gouty tophus

42
Q

Describe the cytology findings in gout

A
  • joint fluid examined under cross polarised light to detect needle shaped crystals
43
Q

Describe the histology of gout (tophus)

A
  • amorphous eosinophilic debris and inflammation (giant cells)
  • crystals lost during tissue processing
  • NB; pyrophosphate arthropathy
44
Q

Describe calcium pyrophosphate

A
  • common crystal arthropathy; pseudogout or chondrocalcinosis
  • usually older invidiuals - large joints
  • may be known cause - hypercalcaemia, haemochromatosis, hypomagnesaemia, ochronsis, hypothyroidism
  • usually idiopathic
  • dense deposits on xray
45
Q

Describe pseudogout

A
  • usually asymptomatic
  • incidental finding on xray
  • also range of joint pain; acute chronic etc
  • crystals aren’t distinct histologically
  • under polarised light; rhomboid shaped crystals, weak positive birefringence, thicker and bigger than needle shaped urate crytsals
  • crystals form in cartilage, menisci and discs
46
Q

Name some examples of non-neoplastic bone disease

A
  • osteoperosis
  • osteomalacia
  • hyperparathyroidism
  • avascular necrosis
  • pagets
47
Q

Describe osteoperosis

A
  • decreased bone mass
  • osteoperosis >2.5 SD below mean peak bone mass
  • associated with significant risk of fracture; atraumatic or vertebral compression fracture
  • localised; disuse
  • generalised; primary and secondary
  • generalised most associated with osteoperosis
48
Q

Describe causes of secondary osteoperosis

A
  • endocrine disorders; cushing, hyperparathyroidism, hyperthyroidism
  • GI disorders; hepatic insufficiency, malabsorption, malnutrition, deficiency of vit C and D
  • drugs; alcohol, corticosteroids
  • immobilisation
49
Q

Describe age related changes and osteoperosis

A
  • reduced proliferative and biosynthetic capacity of osteoblasts
  • response to growth factors attenuated
50
Q

Describe reduced physical activity and osteoperosis

A
  • disuse, elderly and astronauts vs athletes

- load magnitude more effective than endurance

51
Q

Describe genetic factors and osteoperosis

A
  • polymorphisms in genes regulating osteoclastic activity and vitamin D receptors
52
Q

Describe calcium and osteoperosis

A

-Ca deficiency, elevated PTH and low vitamin D

53
Q

Describe hormonal effects and osteoperosis

A
  • post menopausal
  • low oestrogen causes high bone turnover but osteoclasis exceeds osteoblastic activity
  • monocytes release inflammatory mediators
54
Q

Deficiency of vitamin D leads to what?

A
  • hypocalcaemia and PTH elevated
  • increase calcium absorption
  • increased osteoclastic activity and release of Ca from bone
  • reduce renal calcium loss
  • increase renal excretion of phosphate; low phosphate impairs bone mineralisation
55
Q

Describe osteomalacia

A
  • impaired mineralisation of bone matrix
  • bone remodelling occurs normally
  • newly formed osteoid is not fully mineralised; thick osteoid seams
  • bone is weakened - prone to fracture; micro-fractures, gross fractures
56
Q

Describe avascular necrosis (AVN)

A
  • necrosis of bone and marrow; can be asymptomatic, resultant bone and joint damage can lead to THR
  • the result of loss of effective vascular supply; can result from fractures (scaphoid, femoral head)
57
Q

Name predisposing conditions of AVN

A
  • alcohol
  • corticosteroids, biphosphonates
  • connective tissue disorders
  • decompression (the bends)
  • sickle cell disease
  • infection, pregnancy, pancreatitis, radiation
58
Q

Describe PTH

A
  • activated osteoclasts; increased bone resorption, releases calcium
  • increased resorption of calcium by renal tubules
  • increased urinary phosphate excretion
  • increased synthesis of active forms of vitamin D
59
Q

Describe parathyroidism

A
  • elevates serum calcium, normally inhibits PTH release
  • continued osteoclasis; decreased bone mass, deformity and degenerative joint disease
  • osteoperosis, brown tumours and osteritis fibrosa cystica
60
Q

Describe osteoporosis

A
  • generalised
  • phalanges, vertebrae and femur
  • prominent changes in cortical bone; medullary cancellous bone also affected, dissecting osteitis
  • fibrovascular tissue in marrow spaces
61
Q

Describe brown tumours and hyperparathyroidism

A
  • osteoporotic bone prone to fracture
  • associated haemorrhage elicits macrophage reaction and processes of organisation and repair
  • includes giant cells
  • mass of reactive tissue known as a brown tumour
  • can become cystic
62
Q

Describe pagets disease

A
  • abnormality of bone turnover
  • osteitis deformans
  • late adulthood
  • geographic variation in incidence
  • often asymptomatic
  • cause uncertain
  • genetic elements
63
Q

Describe the three stages of pagets disease

A
  • osteolytic; resorption pits with large osteoclasts
  • mixed; osteoclasis and osteoblastic activity
  • osteosclerotic
64
Q

What is the net result of pagets disease?

A
  • thick excess bone with abnormal reversal lines; mosaic pattern
  • bone matures but is soft and porous
65
Q

Name some causes of pathological fracture

A
  • many causes
  • osteoporosis is very common
  • tumours
  • benign; usually children and primary
  • malignant; adults and metastatic
66
Q

What causes avascular necrosis?

A
  • usually asymptomatic
  • trauma (scaphoid), alcohol, dysbarism, steroid injection, sickle cell disease, infection etc
  • alcohol; unclear mechanism, atherosclerosis related?
67
Q

Describe the practical issue with biopsy procedure

A
  • the more tissue the better
  • may need extensive examination
  • suspected malignancy can require numerous stains
  • ancillary investigation eg genetic studies may be crucial
68
Q

Name examples of soft tissue tumours

A
  • ganglion cyst, rheumatoid nodules, gouty tophus, tenosynovitis
  • proliferative conditions; nodular fasciitis, fibromatoses
  • benign tumours; lipoma, haemangioma, neurofibroma, schwannomas, leiomyoma
  • malignant tumours
69
Q

What are the karyotypic abnormalities of synovial sarcoma?

A

t(X;18)

70
Q

What is the karyotypic abnormalities of alveolar rhabdomyosarcoma?

A

t(2;13)

71
Q

What is the karyotypic abnormality of ewings sarcoma?

A

t(11;22)

72
Q

Name some common and benign lesions

A
  • ganglion cyst
  • giant cell tumour
  • fibromatosis
  • rarer; fibrous cortical defect
  • fibrous dysplasia
73
Q

Describe ganglion cysts

A
  • lump near a joint capsule or tendon sheath
  • commonly arise around the wrist
  • degenerative change within connective tissue
  • not a true cyst; no epithelial lining
  • histologically; space with myxoid material
  • secondary inflammatory changes
  • synovial cysts can result from herniation of synovium or bursal enlargement eg bakers cysts
74
Q

Describe nodular fasciitis

A
  • superficial or deep
  • usually less than 5cm
  • circumscribed usually
  • very cellular, lots of mitoses
  • plump cells; stellate and spindle
  • tissue culture appearance
  • haemorrhage
  • mature towards periphery
  • correlates with site and history
  • spontaneous resolution; do not recur
75
Q

Describe myositis ossificans

A
  • similar to nodular fasciitis
  • history of preceding trauma
  • associated with insertions of large muscles of arms and legs
  • cellular proliferation but with evidence of bone formation and, critically, zonation
  • recognition of organisation is critical
  • may also be evident radiologically
  • but in early stages can e difficult and suggest malignancy
76
Q

Describe dupuytrens

A
  • common superficial fibromatoses
  • knuckle pads, plantar
  • penile - peyronies
  • M>F
  • average age 60
  • idiopathic
  • recognised associations; alcohol, DM and anticonvulsants
77
Q

Describe deep fibromatosis

A
  • desmoid tumour
  • large infiltrative masses
  • do not metastasise
  • often young adults (teenage to 30s)
  • sites; musculo-aponeurotic tissue of abdominal wall, mesenteric tissue, limb girdles
  • mutations of APC or b catenin genes; gardners syndrome predisposed to develop deep fibromatoses
78
Q

Describe tenosynovitis

A
  • giant cell tumour of tendon sheath
  • digits and wrist
  • reactive proliferation
  • excise and rarely recur
  • pigmented villonodular synovitis
  • similar histology
  • large joints
  • more likely to recur
79
Q

Describe angiolipomas

A
  • usually multiple and peripheral
  • vascular with fibrin thrombi
  • one of the painful subcutaneous lesions
80
Q

Describe liposarcoma

A
  • one of the most common sarcomas
  • adults, 50 to 60s
  • deep soft tissue of extremities or retroperitoneum
  • histological subtypes; well differentiated, myxoid, pleomorphic, amplification
81
Q

Grading of sarcomas relied on what three features?

A
  • degree of differentiation
  • degree of proliferation; mitotic count
  • presence of coagulative necrosis
82
Q

Describe leiomyosarcomas

A
  • 10-20% soft tissue sarcomas
  • F>M
  • deep soft tissues of the extremities and retroperitoneum
  • can arise from great vessels eg IVC
  • size, location and grade affect treatment options and prognosis
  • if excision not complete recur and can be lethal due to local invasion and metastasis - haematogenous to lungs
83
Q

Describe leiomyomas

A
  • leiomyomas are one of the most common tumours in the body; uterine
  • rarely encountered in orthopaedic practice
84
Q

Describe rhabdomyosarcoma

A
  • aggressive tumours
  • surgery plus adjuvant therapy
  • embryonal subtype arising in walls of hollow structures (botryoid variant) has best prognosis
  • pleomorphic forms may be hard to identify without ancillary investigations

MSK (10 decks)

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