Pathology Previous Exam Q Flashcards
Briefly outline the pathological events occurring during acute disc herniation. Where possible, present the events in the order in which they normally occur (10 marks)
- Physical stress is a major factor occurring via:
- major force (MVA/Fall) - annulus fibrosis ruptures immediately, disc herniates immediately
- repetitive microtrauma - lifting or jarring causing minor annular tears which result in eventual migration of the nucleus pulposus into torn region. this may eventually lead to protrusion and disc herniation - The above events cause:
- Partial herniation: outer annulus still intact
- Complete herniation: complete disc rupture with outer annulus breach - symptom onset depends on type of herniation
- Partial herniation - gradual progression of herniated material into annular tear and may result in neurological ssx
- Complete herniation: immediate neurological ssx - Tears may result in central, postero-lateral or lateral herniation. The type will determine the specific neurological compromise (i.e. L5/S1 causes S1 nerve root compression)
- Events in herniation
Partial:
- nucleus pulposus extrudes posteriorly
- Annular tissue bulges to one side of the PLL
- Degree of herniation gradually increased with successive injury
Complete:
- part if nucleus may break loose and lie free in the spinal cord of IVF - Healing of acute disc injuries
- Occurs naturally over time
- Shrinkage of extruded material
fibrosis of extruded material occurs
- Extruded material doesn’t reposition within the disc
a) Discuss the stages of pathology in Ankylosing Spondylitis (6 marks)
b) List the radiological manifestations of AS (5 marks)
a)
Pathological stages procede in three stages:
Stage one: Inflammation
- Inflammation of fibrocartilagenous joints, followed by changes in the fibrous tissue of the joint capsule, cartilage that surrounds IVDs, entheses and periosteum
> infiltration by inflammatory cells
> granulation tissue formation
> erosion of adjacent bone and fibrocartilage
Stage two: repair
- Replacement of granulation tissue by fibrous scar tissue (i.e. inflammation subsides; healing by fibrosis occurs)
Stage thee: ossification
- Reactive new bone formation in:
> articular bone (resulting in sclerosis)
> adjacent ligaments
> other joint structures
- Ossification of the fibrous tissue of the joint cause ankylosis
ENTHESES (vertebral and pelvis entheses)
Stage one: erosion of bone and fibrocartilage
stage two: granulation tissue replaced by fibrous scar tissue, in an excessive attempt to heal
*Fibrosis of joint capsule
Stage three: ankylosis of adjacent ligaments and other joint structures
SYNOVIUM (facets, SIJs, Costovertebral joints)
Stage one: causes destruction of articular cartilage and subchondral bone
Stage two: as entheses
Stage three: ankylosis of articular bone (sclerosis) and ossification of fibrous tissue of joints
b)
- Cardinal sign:
- Erosion and fuzziness over the SIJs (‘Rosary bead’) and periarticular sclerosis
- Vertebral changes:
- flattening of the vertebral body concavity (vertebral squaring)
- Ossification across the IVDs creates marginal syndesmophytes which spam the gaps between adjacent vertebrae
- bridging at several levels results in bamboo spine appearance
- Spotty ligamentous ossification of vertebral ligaments (dagger sign - supraspinous ligament)
Others:
- trolley track sign (fusion of facet joints)
- star sign (ossification of superior SI ligament)
- ghost joint (visualisation of posterior aspect of joint due to osteopenia and ankylosis)
Discuss the five subtypes of Psoriatic Arthritis (5 marks)
- Asymmetrical monoarthritis/oligoarthritis
- feet and hands, DIPs/PIPs primarily (2-4 joints)
- larger joints incl. wrist/elbows/ankles (1-3 joints)
- asymmetrical and oligo/pauciarticular as name suggests - Symmetrical polyarticular
- involves >5 joints symmetrically
- presents a bit like RS but milder and less deformity - Distal Interphalangeal dominant arthritis
- mainly DIPs of fingers and toes
- can be confused with OA
- peripheral distribution
- Asymmetrical - spondylitis or sacroiliitis (axial arthritis)
- Spondylitis is predominant
- Unilateral SIJ (differentiate form AS)
- asymmetrical distribution
- can have peripheral presentation in hands, arms, hips, legs and feet
- Inflammation with resultant pain and stiffness of Cx, Tx, Lx, and SIJ
- Polyarticular (extending up the spine)
Arthritis multilans
- Severe, deforming and destructive arthritis
- Small joints of hands and feet but can also affect Cx and Lx pain
- Polyarticular
- Asymmetrical
a) Define Rieter’s disease
b) compare the aetiology and epidemiology of the two types of Rieter’s disease
a)
An arthritis associated with non-bacterial urethritis/cervisitis, conjunctivitis and mucosutaneous lesions classified as a seronegative spondyloarthropathy along with ankylosing spondylitis, enteropathic arthritis and psoriatic arthritis
b)
STI
AGE/GENDER: Male 20-40 years
PATHOGEN: Chlamydia trachomatis
Dysenteric
AGE/GENDER: Women, Children, Elderly
PATHOGEN: Shigella, Salmonella, campylobacter
a) Describe the pathological processes occurring in the skin of DM
b) Describe characteristic skin rash/manifestations encountered in dermatomyositis
a)
Skin changes are secondary to immune mediated vasculitis and inflammation occurring at the interface between the dermis and epidermis.
Immune complexes are the result of an abhorrent immune response in which T cells are activated and cause B cells to differentiate into plasma cells and produce antibodies.
The antibodies attach to antigens to form Ag-Ab complexes which are deposited in vessels supplying the skin leading to complement mediated vasculitis.
1. epidermal atrophy
2. basal cell liquefaction
3. vascular dilation
4. lymphocytic infiltration of dermis
b)
- Dusky erythematous rash
> Generally over the chest and neck
- Gottron’s papules
> Slightly elevated, smooth or scaly rash, generally present over bony eminence (eg. knuckles)
- Heliotrope rash
> Periorbital purple skin discoloration on eyelids
- Telangiectasia
> Small dilations of blood vessels generally notices near the nail beds, but can be located anywhere on the body
- Dermal atrophy
> A reduction of epidermal and dermal thickness, regression of the sebaceous glands, loss of subcutaneous fat tissue and muscle layers
- Subcutaneous calcification
> Late stage
a) describe the typical SLE patient
b) discuss the mechanism of tissue damage in SLE
c) list the commonest early presenting symptoms in SLE
a)
- Female
- Child bearing age (20-40)
- Higher correlation in AUS with individuals of indigenous, south east asian or polynesian descent
- Potential Hx of CNS involvement (HA/seizures/ psychosis)
- May have a malaria rash (40% presenting sx)
b)
Pathological process
1. Genetically predisposed individual (gene associated - MHC class II)
2. Encounters an environmental trigger (drugs, emotion, virus) which causes an aberrant immune response in which:
3. CD4 T Helper cells become reactive to self peptides and activate B cells to differentiate into plasma cells (targeting nuclear antigens)
4. IgG autoantibodies are produced
- Autoantibody production causes direct damage to target tissues
5. Immune complex formation
results in:
> Immune complex deposition in various body tissues tissues and complement activation = inflammatory reaction
6. Complement is released causing - small vessel vasculitis, thrombosis, and ischemic tissue necrosis in various body systems (Skin, GIT, CNS, pleura, kidney and heart)
> Immune complex deposit into synovium results in polyarthritis/polyarthralgia (distal joints are more affected eg. fingers, wrists, knees and toes)
c)
- arthritis
- malar rash
- fever
- photosensitvity
- raynaud’s
OR more information
- Arthritis/arthralgia (69%)
> Non-erosive, may affect any joint
> Commonly affects: Small joints of hands and feet; wrists and knees
- Malar rash (40%) – Fixed erythema that may be flat or raised, commonly presents in “butterfly distribution” across maxillary and nasal areas.
- Fever – Low-grade (36%) due to chronic inflammation
- Photosensitivity rash (29%) – A raised, red, pruritic rash that can occur anywhere on the body and is caused by exposure to sunlight
- Raynaud’s phenomenon (18%) – Skin may appear pale (due to vasoconstriction) → Dusky/cyanotic (due to more severe ischaemia) → Red, erythematous, warm and swollen (due to NO and other vasodilators, influx of blood)
- Serositis (17%) – May present as pericarditis or pleuritis and require cardiac or respiratory examination.
- Nephropathy (16%) – May have urinary symptoms or and/or increased BP.
- Neurologic involvement (12%)
Compare two types of arthritides (10 points of comparison)
GOUT
Aetiology: Hyperuricaemia
Crystal type: sodium urate/uric acid crystals
Microscopic appearance: needle-shaped, negatively birefringent
Pathophysiological stages
- Asymptomatic hyperuricaemia
- acute gouty arthritis
- inter critical period
- chronic tophaceous gout
Typcial patient:
- Diet high in purines
- heavy drinker esp. beer
- hypertensive/overweight
Joints affected:
- smaller joints: 1st MTP, small joints of hands and feet, wrists
- also: ankles, knees and elbows
Pain levels:
- severe/intense ‘excruciating’
Complications:
- renal calculi and insufficiency
Labs:
- normal to high uric acid levels
Imaging:
- Tophi and joint erosion may be visible on x-ray in chronic disease
PSEUDO GOUT
Aetiology: Chondrocalcinosis
Type of crystal: calcium pyrophosphate
Microscopic appearance: Polygonal, positively birefringent
Path stages:
- chondrocalcinosis (asympt build up)
- acute pyrophosphate synovitis
- chronic pyrophosphate arthropathy
Typical Patient:
- Older individual (M:F)
Joints affected:
- Larger joints incl. knees, shoulders and hips
Pain:
- moderate
Complications:
- nil
Labs:
- normal/high calcium
Imaging:
- calcification of cartilage may be seen on x-ray (later stage)
Discuss the events occurring in Rheumatoid Arthritis
Stage one: synovitis
1. Early changes:
> vascular congestion
> Proliferation of synoviocytes
> Infiltration of the subsynovial layers by polymorphs, lymphocytes and plasma cells
2. gradual thickening of capsular structures
3. villious formation of the synovium
4. effusion into the joints and tendon sheaths (tenosynovitis)
5. ssx: pain, swelling and tenderness
*in spite of these changes condition is potentially reversible
Stage two: Destruction
1. persistent inflammation
2. articular cartilage erosion due to:
> proteolytic enzymes
> vascular tissues in the folds of the synovial reflections
> invasion of cartilage by a panes of granulation tissue which spreads over the articular cartilage
3. bone erosion due to:
> granulation tissue invasion
> osteoclastic resorption
4. Tendon sheaths
> observe similar changes as in articular cartilage and bone
> tenosynovitis
> invasion of collagen bundles by inflammatory elements causing the eventual rupture of tendons
5. synovial effusion:
> May contain: increased amounts of fibrinoid material causing swelling of joints/tendons and bursae
Stage three: Deformity
> articular destruction
> capsular stretching
> tendon rupture
ALL lead to progressive joint instability and deformity of joints
inflammation has often subsided at this stage and the patients problems are primarily due to the mechanical/functional affects of destruction
