PATH EXAM 2016 Flashcards
1.
Briefly outline pathological events in ACUTE DISC (8 marks)
In an aging disc we see a range of biochemical changes:
- decreased proteoglycan size and synthesis
- decreased elastin content
- increased collagen content
- increased water content
These biochemical changes cause the disc to have:
- decreased disc height
- decreased hydrostatic pressure
- nucleus pulposis changes from a turgid, gelatinous structure to a soft, brownish dessicated structure
AS a result, the disc has altered biomechanical properties and therefore:
- the disc has a decreased ability to resist shear forces
- there is an increased force on the vertebral endplate
The decreased ability to resist shear forces results in a annulus fibrosis fissures which run parallel to the end plates. The annulus is weakened, and nucleus pulposis can hernitate out of the annulus. This could occur posteriolaterally and impinge on the spinal cord or exiting nerve roots. Alternatively/ simultaneously, as a result of increased force on the end plates, the nucleus pulposis can herniate through the vertebral end plate, causing the formation of schmorls nodes.
Herniations through the end plates can cause reactive bone growth around the vertebral margins and around the schmorls nodes in the form of lipping and osteophyte production.
As the degenerative continues, the IVD flattens, causing the facet joints to become malaligned. This causes reactive bone growth and osteophyte formation which collectively can be referred to as spondylosis or ‘spinal degeneration’. In time we see
- narrowing of the IVF.
- narrowing of the spinal canal
- fibrosis of the affected structures
- the nucleus pulposis becomes fibrocartilage
- increased osteophyte production.
Eventually the increase in osteophytic growth and fibrotic change causes narrowing of the spinal canal and IVF, results in spinal canal stenosis, which can cause a variety of nervous system manifestations depending on the spinal level.
2a.
Discuss stages of pathology in ANKYLOSING SPONDYLITIS (6 marks)
In AS the primary sites of inflammation are the entheses of the vertebral and pelvic region, and the synovium of vertebral facet joints, SIJ’s and costovertebral joints.
As as result we see 2 presentations:
- Synovitis of the facet joints, SIJ’s and costovertebral joints
- Enthesitis of the IVD’s, SIJ ligs, pubic symphysis and bony insertions of the ligs and tendons
AS pathology is a 4 stage process that involves both involvement of the entheses and the synovium as stated above.
STAGE 1: INFLAMMATION
Inflammation of the fibrocartilage in cartilagenous joints, followed by changes in the fibrous tissue of the joint capsule, cartilage that surrounds the IVD, entheses and periosteum.
We see:
- infiltration by inflammatory cells
- granulation tissue formation
- erosion of:
- adjacent bone and fibrocartilage in enthesitis
- subchondral bone and articular cartilage in synovitis
STAGE 2: FIBROSIS
Replacement of granulation tissue by fibrous scar tissue
STAGE 3: OSSIFICATION AND ANKYLOSIS Reactive new bone formation in: - articular bone (sclerosis) - adjacent ligs - other joint structures e.g. annulus fibrosis
Ossification of the fibrous tissue of the joint causes ankylosis of the joint.
STAGE 4: REMISSION
2b.
List radiological manifests in ANKYLOSING SPONDYLITIS (5 marks, 5 responses)
Cardinal signs of AS on xray include:
- erosion and fuzziness of SIJ and periarticular sclerosis eventually leading to ankylosis
We see changes in the SIJ:
- symmetrical, bilateral, subchondral sclerosis
- starts on the iliac side of the joint then later on both sides
- ghost sign: joint is mostly osteopoenic with sclerosis of sacroiliac ligaments and subchondral bone
- star sign: ossification of the iliolumbar ligaments
We also see changes in the vertebral joints:
- Involvement of the lumbar spine after the SIJ
- Barrel vertebrae - squaring off of the vertebrae
- Ossification of the longitudinal ligaments and annulus fibrosis, creating marginal syndesmophytes and eventually creating the image of a bamboo spine.
- Trolley tracks - due to ankylosis of the facet joints
- Dagger sign - ossification of the supraspinous ligaments
3.
Discuss PSORIATIC ARTHRITIS. Talk about the joints affected (5 marks)
Presentation of joints affected depends on the clinical subtype of psoriatic disease:
PERIPHERAL SYMMETRICAL SERONEGATIVE POLYARTHRITIS (25%-50%)
Most common form of PsA
Generally has warm, tender and red joints.
Usually mild but 50% can develop varying degrees of progressive, destructive disease which may be disabling.
- DIPS’s and PIP’s usually ankylose
- Hands, wrist, feet and ankles may also be involved
ASYMMETRICAL MONO- & OLIGOARTICULAR ARTHRITIS (35%)
Most common presentation of PsA, slow progressing and mild with asymmetric joint involvement
- PIP’s, DIP’s and MCP’s affected first
- Large joints can be affected in 80% of cases
- Often see Dactylitis: flexor tendonitis and synovitis
SPONDYLITIS AND SACROILIITIS (AXIAL ARTHRITIS): (25%)
Male predominant
Asymmetrical
Spondylitis is predominant
- Neck, Low back, SIJ’s and vertebrae
- Can have some peripheral joint involvement too (hands arms, hips and feet)
PERIPHERAL TYPE/ DIP DOMINANT POLYARTHRITIS: (5%-10%)
- DIP’s mostly affected
- Terminal tuft involvement is classic and unique to PsA
- Nail involvement with significant paronychial inflammation and swelling of finger ends
- Nail changes include: pitting, ridging and separation
ARTHRITIS MUTILANS: (<5%)
Severe, deforming and destructive
Resorption of bone with dissolution of joint
Affects:
- small joints of the hands and feet
- can have Cx and low back involvement
- ‘pencil in cup’
4a.
Describe typical pt for SYSTEMIC LUPUS ERYTHEMATOSUS (3 marks)
Female (90%)
20-40yoa
Caucasian
4b.
Pathological process in SYSTEMIC LUPUS ERYTHEMATOSUS (6 marks)
A genetically susceptible individual is exposed to a trigger. This causes T - helper cells to become reactive to self-peptides and activate ‘B’ cells to synthesise antibodies which target self antigens.
This results in IgG autoantibody production (especially ANA’s)
This production of ANA’s can be aimed towards a variety of nuclear antibodies, hence the wide variety of clinical signs and symptoms.
The ANA’s cause manifestations by:
- attacking and causing direct damage to target cells and tissues
- form immune complexes which deposit in tissues and cause complement activation and subsequent inflammation.
This usually leads to polyarthritis and small cell vasculitis among other manifestations.
4c.
Symptoms/signs common for SYSTEMIC LUPUS ERYTHEMATOSUS (4 marks) — past exam says list 4, but learn 8
SMALL VESSEL VASCULITIS
- skin, pleura, GIT, CNS, heart and kidneys affected
- seen as digital gangrene, diarrhoea and GIT bleeding secondary to perforation
LYMPHOID SYSTEM HYPERPLASIA
- lymphadenopathy
- splenomegaly
(due to lymphocyte hyperactivity)
SKIN INVOLVEMENT:
- Photosensitivity
- Rashes: malar
- Skin atrophy
- Raynauds phenomenon
- Skin ulceration
SEROSITIS:
- pericarditis
- pleuritis
GIT INVOLVEMENT:
- Diarrhoea
- Bleeding
- Perforation
CNS INVOLVEMENT:
- Encephalopathy
- CN palsies
- SC lesions
RENAL DAMAGE:
- Glomerulonephritis
ARTHRITIS/ARTHRALGIA:
- Commonly affects fingers, wrists, knees and toes
- Less commonly affects elbows, shoulders, ankles
(usually mild and non-erosive)
HAEMOTOLOGICAL INVOLVEMENT:
- Thrombocytopenia
- Haemolytic anaemia
- Neutropenia
5a.
Define REACTIVE/REITER’S (2 marks)
A seronegative spondylarthropathy associated with
- non-bacterial urethritis/cervicitis
- conjunctivitis
- mucocutaneous lesions
It is characterised by sterile inflammation of the joints from infections at a non-articular site.
5b.
Discuss the epidemiology/aetiology of REACTIVE/REITER’S (6 marks)
2 forms:
SEXUALLY TRANSMITTED:
- mainly males 20-40
- usually infected with chlamydia trachomatis
DYSENTERIC:
- usually females, children and elderly
- most often follows enteric bacterial infection by shigella, salmonella, yersinia, campylobacter
6a.
Describe the pathological processes in PMDM (6 marks)
Caitie - Pretty men VIBE on skin and muscle of FARNAPs
Cat - Pretty men have SKINy change when they VIBE and Pretty Men have muscular CHANting FANs when they PR
A trigger (possible environmental or genetically predisposed) causes T-cell activation, these T cells activate the B cells and also attack myocytes directly. T cell attack is directed as muscle tissue, where as B cell activation causes immune complex formation, whose effects are most seen in the skin:
The following are generally seen:
SKIN CHANGES: “VIBE”
These are secondary to immune complex deposition in the vessels occurring at the interface between the epidermis and the dermis, causing immune mediated vasculitis and inflammation.
- vascular dilation
- infiltration of lymphocytes in the dermis
- basal cell liquefaction/degeneration
- epidermal atrophy
MUSCLE CHANGES: MYOSITIS CAITIE - FARNAP Characterised by direct T-Cell mediated muscle injury, where the T cells cause direct myocytic damage and chronic inflammation: - necrosis - phagocytosis - atrophy and degeneration - fibrosis - regenerative activity (in damaged but living myocytes)
NECROTISING VASCULIITS:
Immune complexes also deposit in the arteries and in striated muscles causing:
- vasculitis
- thrombosis (may result in vascular obstruction)
- ischaemia
6b. *
Describe the signs in PMDM (6 marks)
MUSCLE WEAKNESS:
- symmetrical
- progressive
- proximal
- ssx depend on mm affected
CUTANEOUS ERUPTION: Due to vasculitis
Dusky erythematous rash: over chest and neck
- associated with
- muscle pain and tenderness
- induration
*Gottrons papules: rash is slightly elevated and smooth or scaly e.g. over knuckles
*Heliotrope rash: periorbital purple skin discolouration
*Periorbital oedema
* = Pathognomonic
- Might have an SLE malar rash
Subcutaneous calcification and dermal atrophy pccurs late stage
POLYARTHRALGIA: Mild - Swelling - Joint effusion - Raynauds
VISCERAL INVOLVEMENT:
- Interstitial pneumonitis
- Cardiac involvement
- Acute renal failure due to rhabdo
6b.**
Describe the signs in PMDM (6 marks)
Pretty men sign their Initials, DR SPAMS
INITIAL MANIFESTATIONS Dysphagia Raynauds Systemic ssx Proximal muscle weakness Arthralgia of multiple joints Muscle tenderness and pain Skin rash
Pretty men typically drive RV’s to the SPA
TYPICAL CLINICAL MANIFESTATIONS Skin rash Proximal muscle weakness Arthralgia of multiple joints Raynauds phenomenon Visceral involvement
6b.**
Describe the signs in PMDM (6 marks)
Pretty men sign poorly DR CRAPS
SIGNS OF POOR PROGNOSIS
Dysphagia/Malnutrition
Respiratory failure secondary to infection
Cardiac involvement
Respiratory failure secondary to infection
Aspiration pneumonia
Pulmonary involvement
Severe proximal weakness
7a.
Discuss the clinical manifestations of CHRONIC GOUT (6 marks)
College girls take pictures at College PARTI’S
TYPICAL PICTURE IN CHRONIC GOUT Chronic joint pain Polyarticular involvement (as a result of recurrent attacks) Acute attacks (recurrent) Renal manifestations Tophi - may ulcerate skin Involvement of tendons Stiffness and deformity of the joints
7b.
How is CHRONIC GOUT diagnosed (4 marks)
Clinical picture and examination
History of
- family incidence
- past attacks
Hyperuricaemia
- usually preceeds acute attack
- common in middle aged men
- NOT pathognomonic for gout, merely supportive evidence
Presence of negatively birefringent urate crystals in the synovial fluid or in phagocytes IS PATHOGNOMONIC
