2017 Exam

Question 1

Briefly outline pathological events occurring during chronic disc herniation.

Answer 1

With normal ageing the I/V disc gradually changes →

• annulus fibrosus develops fissures parallel to the vertebral endplates
• small herniations of nuclear material squeeze through the annulus in all directions

In time these herniations result in reactive bone formation around Schmorl’s nodes and other sites of herniations (vertebral margins).

These changes result in: flattening of the I/V disc ie “spondylosis” osteophyte formation

Collapse of the disc space results in displacement of the facet joints which results in osteoarthritis after many months and years.

Severe OA may result in →

• narrowing of spinal canal and I/V foramen
• increased osteophyte formation
• spinal stenosis

By the end of the degenerative process we observe the following:

• total replacement of the gelatinous mucoid material of the nucleus pulposus with fibrocartilage
• segmental fibrosis

Segmental fibrosis often results in stabilisation of the disc lesion and a decrease in associated backpain.

Question 2

List the stages of pathology in ankylosing spondylitis.

Answer 2

• Stage 1 (inflammation)
• Stage 2 (Repair):
• Stage 3 (Ossification)

Question 3

List radiological manifestations in ankylosing spondylitis

Answer 3

1. Cardinal sign: erosion and fuzziness of SI joints and periarticular sclerosis (eventually bony ankylosis occurs).
2. Vertebral changes: flattening of vertebral body concavity (squaring).
3. Ossification across the I/V discs creates “syndesmophytes” which span the gaps btw vertebrae.
4. Bridging at several levels results in a “bamboo spine” appearance.
5. Spotty ligamentous ossification.

Question 4

Name the five clinical variants of PsA. In each case, describe the number and type of joint typically affected in each variant.

Answer 4

Asymmteric OligoA.

Symmetric PolyA.

Peripheral DIP Dominant A.

Axial ‘Sacro/Spondy’ A.

Arthritis Mutilans

Question 5

Describe the typical SLE patient.

Answer 5

• F>M, 20-64yo
• Caucasian, Polynesian, African, Asian background
• Typically onset 20-40yo but can onset anywhere from childhood onwards

Question 6

Discuss the mechanism of tissue damage in SLE.

Answer 6

• Cellular damage in SLE is mediated by:
o immune complex mediated inflammation (via complement activation)
o direct action of autoantibodies on cells eg anti-RBC antibodies → anemia, anti-clotting factors → thrombocytopenia, etc)
• ANAs are not believed to be able to enter intact cells.

→ use examples of clinical pathology to explain Tx mechanism

e. g 1 immune complex deposition in small vessels, leads to inflammation, leads to vasculitis, leads to ischaemia (i.e. ischaemic tissue damage) of any tissue downstream.
e. g 2 immune complex deposition in glomerulus, leads to glomerulonephritis → tissue damage
e. g 3 immune complex deposition in basement membrane (point of attachment for epithelial cells) via small capillaries, activation of complement → inflammation of skin → external rash.

Question 7

List commonest early presenting symptoms in SLE

Answer 7

Arthritis
Malar rash
Fever
Photosensitivity
Raynaud's phenomenon
Serositis

Question 8

Define the term ReA.

Answer 8

A collection of syndromes characterised by sterile inflammation (DEF: lack of presence of infective agent DNA in urine test) of joints from infections at non-articular sites

Question 9

Briefly compare the epidemiology and aetiology of the two forms of ReA.

Answer 9

• Sexually transmitted
o mainly males 20-40 year olds
o usually infection with Chlamydia trachomatis

• Dysenteric:
o usually seen in women, children and the elderly.
o imost often follows enteric bacterial infection usually:
• Shigella
• Salmonella
• Yersinia
• Campylobacter

Question 10

Discuss the clinical manifestations of chronic gout.

Answer 10

• Recurrent acute attacks may eventually merge into polyarticular gout.

• Joint erosion results in:
o chronic pain
o stiffness
o deformity

• Tophi may be discovered; large tophi may ulcerate through the skin and discharge chalky material.

• In chronic gout we may observe the following renal manifestations:
o calculi: occur in 10-20% of cases
o parenchymal disease (due to deposition of MSU from blood) may result in renal failure
o renal tophi

Question 11

How is gout diagnosed?

Answer 11

• usually based on the clinical picture and physical examination.
• Presence of negatively birefringent urate crystals in the synovial fluid or in phagocytes → DIAGNOSTIC of gout.

Question 12

List the three main stages of RA progression from early to advanced. .

Answer 12

Stage 1: SYNOVITIS / EARLY

Stage 2: DESTRUCTION / ESTABLISHED

Stage 3: DEFORMITY/ADVANCED (Years+++)

Question 13

Describe the pathological process occurring in the skin in dermatomyositis

Answer 13

• Skin changes → secondary to immune mediated vasculitis and inflammation occurring at the interface between the epidermis and dermis.

•	Leads to:
o	epidermal atrophy 
o	vascular dilation
o	basal cell liquefaction/degeneration 
o	lymphocytic infiltration of dermis

Question 14

Describe the skin signs in dermatomyositis

Answer 14

• periorbital oedema
• heliotrope hue (purplish eyelids)
• Gottran’s Papules

Question 15

Describe the initial Inflammatory Stage of AS

Answer 15

Stage 1 (inflammation)
• Inflammation of fibrocartilage in cartilaginous joints, followed by changes in the fibrous tissue of the joint capsule, cartilage that surrounds the IV/discs, entheses (enthesitis) and periosteum.
o infiltration by inflammatory cells
o granulation tissue formation
o erosion of adjacent bone and fibrocartilage

Question 16

Describe the second Repair Stage of AS

Answer 16

Stage 2 (Repair):

• Replacement of granulation tissue by fibrous scar tissue (ie inflammation subsides; healing by fibrosis occurs).

Question 17

Discuss the third Ossification Stage of AS

Answer 17

Stage 3 (Ossification)
• Reactive new bone formation in:
o articular bone (results in sclerosis)
o adjacent ligaments
o other joint structures
• Ossification of the fibrous tissue of the joint cause ankylosis of the joint.

Question 18

Discuss PsA Clinical Form- Asymmetric Oligoarthritis

Answer 18

• Most common presentation of PsA (30-50%)
• Generally mildest form
• Asymmetric involvement of 1-3 large & small joints;
• digits of the hands & feet are usually affected first;
• Small joints: DIPs , PIPs and MCPs
• Large joints: knee, hip, ankle or wrist
• Dactylitis (arthritis & tendinitis in ray distribution) may occur in hand involvement

Question 19

Discuss PsA Clinical Form - Symmetric Polyarthritis

Answer 19

• most common form (25-50% Pts)
• c.f. RA -> usually milder with less deformity; may evolve from asymmetric form
• F>M
• Symmetric joint involvement commonly affecting >4 joints
• Commonly affects: fingers and toes
• Also : wrists, elbows, & ankles
• Can be severe & disabling -> joint deformity
• May have prominent nail involvement
• Swelling of digital tuft
• Severe Psoriasis associated

Question 20

Discuss PsA Clinical Form - DIP Dominant Peripheral Arthritis

Answer 20

• less common
• M>F
• DIPs in fingers, toes
• Nail and skin changes are common / prominent
• Nail Pitting: ice pick-like depressions
• Nail ridging
• Nail splitting
• Nail discoloration (yellow / orange)
• Onycholysis: separation of nail from the nail bed

Question 21

Discuss PsA Clinical Form - Axial Arthritis

Answer 21

• less common
• M>F
• asymmetric spondylitis & sacroiliitis
• Stiffness, pain & ↓ed ROM
• Structures affected
• Cx spine, Lx spine, SIJ:
• peripheral joints in the hands, arms, hips, legs and feet.
• Enthesitis is common

Question 22

Discuss PsA Clinical Form - Arthritis Mutilans

Answer 22

• rare
• severe, erosive, destructive, deforming arthritis
• asymmetric
• Structures affected:
• small joints (esp. DIPs) of the hands and feet;
• shortening of digits because of severe joint or bone lysis
• neck or lower back
• Enthesitis is common
• Observe exacerbations & remissions coincidental with skin flare ups.

Question 23

Describe the events in the early stage of RA.

Answer 23

Stage 1: SYNOVITIS / EARLY

1. early changes - vascular congestion
   - proliferation of synoviocytes
   - infiltration of the subsynovial layers by polymorphs, lymphocytes & plasma cells
   → ACUTE INFLAMMATORY RESPONSE!
2. Gradual thickening of the capsular structures.
3. Villous formation of the synovium
4. Effusion into the joints and tendon sheaths
5. SSX: pain, swelling, tenderness

NB: In spite of the above all the joint structures are mobile and intact, thus the condition is potentially reversible.

Question 24

Describe the events in the established / destructive stage of RA.

Answer 24

Stage 2: DESTRUCTION / ESTABLISHED

1. Persistent inflammation results in joint and tendon destruction
2. Articular cartilage erosion is due to:
   • proteolytic enzymes
   • vascular tissues in the folds of the synovial reflections
   • invasion of cartilage by a pannus of granulation tissue which spreads over the articular cartilage.
   • Definition: the pannus is a swollen, congested and thickened synovial membrane and a proliferation of granulation tissues which contains many lymphocytes and plasma cells.
3. Bone erosion due to:
   granulation tissues invasion
   osteoclastic resorption
4. Tendon sheaths:
   observe similar changes as in cartilage and bone.
   tenosynovitis
   invasion of collagen bundles by inflammatory elements causing the eventual rupture of the tendon.
5. Synovial effusion:
   may contain: increased amounts of fibrinoid material causing swelling of joints/tendon/bursae.

Question 25

Describe the events in the advanced / deforming stage of RA.

Answer 25

Stage 3: DEFORMITY/ADVANCED (Years+++)

progressive instability and deformity of joints d/t:

• articular destruction
• capsular stretching
• tendon rupture

→ Inflammation has often subsided at this stage and the patient’s problems are primarily due to the mechanical/functional affects of joint destruction.