Path Exam Qs Flashcards
(15 cards)
- Briefly outline the pathological events occurring during acute disc herniation. (8 marks)
- Trauma to IVDs, commonly due to:
- Jarring (especially Cs spine)
- Combined F/E with spine under load (especially LS spione)
- Sudden straining whilst in unstable position (especially LS spine) - Depending on mechanism, two different pathways (major force or repeated microtrauma):
Major force (eg car accident, fall from a height etc)
• Complete disc rupture – Outer layers of annulus fibrosis breached and rupture of PLL, immediate herniation of nuclear material
• Immediate onset of symptoms (dependent on extent and direction of herniation)
Repeated microtrauma (eg occupational or recreational overuse)
• Partial disc herniation – Outer layers of annulus fibrosis intact, but increased nuclear pressure causes protrusion of nuclear material into tears
• Gradual/progressive onset of symptoms (causes back pain as annulus fibrosis has nerve supply)
• May progress to complete rupture
- Directions of disc herniation:
- Central disc herniation – Spinal canal stenosis (spinal cord compression), causing UMN Ssx
- Postero-lateral disc herniation – IVF stenosis (compression of exiting spinal nerve or rootlet), causing LMN Ssx - May also get joint displacement/spondylolisthesis
Pathological events occurring during chronic disc degeneration
- Normal ageing
- Causes biochemical changes to the nucleus pulposis
↓ proteoglycan size + synthesis
↓ H2O and elastin content
á collagen content
- Nucleus pulposis becomes soft, brown, dessicated structure - Annulus fibrosis
Develops fissures parallel to endplates
Small herniations of nuclear material squeeze through annulus fibrosis
- Vert. endplates are perforated by nuclear material Schmorl’s nodes - Reactive bone formation
- Formation around Schmorl’s nodes and other sites of herniations
- Spondylosis flattening of IVD + osteophyte formation - Disc space collapse
- Displacement of facet joint resulting in OA (after months/years) - Severe OA
- á osteophyte formation
- Narrowing of spinal canal and IVF stenosis & neural compression Ssx (UMN/LMN) - End of degenerative process
- Fibrocartilage replaces gelatinous nucleus polposus
- Segmental fibrosis stabilisation of disc lesion + ↓ of ass. Back pain
Discuss stages of pathology in Ankylosing Spondylitis (AS) (6 marks)
- Inflammation – Inflammation and development of granulation tissue in:
- Entheses:
o Common sites: Vertebrae and pelvis,
o Destruction of: Bone and fibrocartilage
- Synovium:
o Common sites: Facets, CV joints, SIJs
o Destruiction of: Subchondral bone, articular cartilage - Fibrosis – Granulation tissue replaced by fibrous scar tissue
- Ossification and ankylosis – Reactive new bone formation in:
- Articular bone (results in sclerosis)
- Adjacent ligaments & other joint structures
- Ossification of fibrous tissue of joints ankylosis - Remission – Pathological processes recede.
List 5 radiological manifestation in ankylosing spondylitis (5 marks) – Could ask for SIJ findings or spinal findings
SIJ
Early:
- “Rosary beads” (articular erosions)
- “Pseudowidening” (Loss of articular cortex definition)
- Subchondral osteoporosis with patchy reactive sclerosis
- Diminished joint space
Late:
- “Ghost” joint margin – Visualisation of articular cortex through ankylosed joint
- “Star sign” – Ossification of superior sacroiliac ligaments (triangular opacity at superior SIJ)
Spine
- “Romanus lesion” – Lucent VB corner erosion due to inflammatory destruction
- “Squared” or “barrel-shaped” vertebrae
- Marginal syndesmophytes (ossification of annulus fibrosis) “bamboo spine” (multiple ankylosed IVDs/vertebrae
- “Trolley track” appearance – Due to fusion of facet joints
- “Dagger sign” – Due to calcification of supraspinous ligaments causing SP ankylosis
- “Ballooning” of IVDs - Due to osteopenic vertebral endplates that become concave due to excessive pressure
- Schmorl’s nodes
- Name the 5 clinical variants of psoriatic arthritis (PsA); and describe the number and type of joint typically affected in each variant
Peripheral (DIP dominant)
- 5-10%
- Men
- DIPs affected
- Oligo/polyarthtiris
- Asymmetric
- Nail changes
Peripheral symmetric seronegative polyarthritis
- 25-50%
- Females
- Similar to RA
- Polyarthritis (>5 joints)
- Small hand/feet joints: PIPs & MCPs
- Large joints: Knee, hip, ankle, wrist
- Psoriasis often severe
Asymmetric oligo/pauciartucular arthritis
- 35%
- Similar to OA (mild)
- Mono/oligoarthritis (1-3 small and large joints)
- Small joints: DIPs, PIPs & MCPs
- Large joints: Hip, knee
- Dactylitis
*To remember large joints for symmetric/asymmetric = ALSU (Asymmetric lower; symmetric upper [extremity joints]), both have wrist & ankle
Axial arthritis (spondylitis & sacroiliitis)
- 5-20%
- Male
- Oligo/polyarthritis
- Asymmetric
- Commonly: Cx, Lx, SIJs
- Also: Peripheral joints (hands, arms, legs, feet)
Arthritis Mutilans - <5% - Severe, destructive, erosive - Polyarthritis - Commonly: DIPs, small joints of hands & feet Also: Neck, lower back
Describe the typical SLE patient (3 marks)
- Female (90%), 20-40 years old (but may occur at any age)
- Australia: Increased frequency in Aboriginals and people of South-East Asian origin
- Potential history of CNS manifestations (cognitive dysfunction, HA, seizures, psychosis); GIT involvement (bleeding and diarrhea); and/or fever, fatigue, weight loss
- May have some type of skin rash: Malar rash (40% presenting Sx) or photosensitivity rash (29% presenting Sx)
Discuss mechanism of tissue damage in SLE (6 marks)
- Genetically predisposed individual (MHC class 2)
- Environmental trigger (eg drugs, viruses)
- Helper T-cells become reactive to self-peptides and:
Autoantibody mediated direct damage
- Differentiate into cytotoxic T-cells
- Cause direct tissue damage (Ssx dependent on specific mix of AutoAb’s present and tissues affected)
Immune complex deposition
- Activate B-cells (differentiate into plasma cells)
- Plasma cells produce IgG autoAb’s (especially ANAs)
- Immune complex formation and deposition into various body tissues
- Complement is released, causing:
- Small vessel vasculitis thrombosis, ischaemia and tissue necrosis (skin, pleura, GIT, CNS, kidney, heart)
- Polyarthritis/arthralgia – Distal joints affected more (fingers, wrists, knees and toes)
TISSUES AFFECTED:
- Lymphoid system (lymphadenopathy, splenomegaly)
- Skin inflammation
- Heart involvement (endocarditis, myocarditis, pericarditis)
- CNS
- Renal/kidneys
- Vasculitis
- Arthritis
List commonest early presenting symptoms in SLE (4 marks)
- Arthritis (69%)
- Malar rash (40%)
- Low-grade fever (36%)
- Photosensitivity rash (29%)
List the commonest overall symptoms which are seen in SLE in the course of time
- Haematologic (100%)
- Arthritis (90%)
- Skin (85%)
- Fever (83%
Define the term reactive arthritis (2 marks)
Syndromes characterized by sterile inflammation of joints from infections at non-articular sites (eg dysenteric or sexually transmitted infections) that are classified as a seronegative spondyloarthropathy.
Briefly compare the epidemiology and aetiology of the two forms of Reiter’s syndrome (6 marks)
Sexually Transmitted
epidemiology:
- Post-venereal infection ratio is 5-10M:1F
- Mainly males 20-40yo
- ~1-3% of all people with nonspecific urethritis develop an episode of arthritis
aetiology
- Usually chlamydia trachomatis
Dysenteric
epidemiology:
- Post-enteric infection ratio is 1M:1F
- Usually seen in women, children and elderly
- ~1-4% of all people will develop an episode of arthritis after an enteric infection
- 20-25% of HLA-B27 positive individuals will develop arthtirits after bacterial enteritis
aetiology
- Shigella
- Salmonella
- Yersinia
- Campylobacter
Describe the pathological process occurring in the skin in dermatomyositis (6 marks)
- Trigger (viral infection)
- Autoimmune reaction (T-lymphocytes activated B-cells differentiate into plasma cells Release autoAb’s)
- Deposition of immune complex into basal membrane of skin, and small blood vessels supplying skin
- Release of complement, causing vasculitis
- Vascular dilation and lymphocytic infiltration of dermis
- Basal cell liquefaction, leading to epidermal atrophy
Describe skin signs in dermatomyositis
- Dusky, erythematous rash – Often the first manifestation. A slightly raised, patchy bluish-purple rash that may be smooth or scaly and can be present on: forehead, chest and back, elbows and knees, forearms and lower legs, medial malleoli and radiodorsal surface of PIPs and MCPs
- Gottron’s papules – Pathognomonic for DM. Slighlt elevated, violaceous papules/plaques that occur over bony prominences (eg elbows, knees and finger joints)
- Heliotrope rash – A purple rash that occurs periorbitally (on and around eyes/eyelids).
- Telangiectasia – Small, red dots due to vasodilation that can be located anywhere on the body, but are typically noticed near nail beds where the skin is thin
- Dermal atrophy – Thin, shiny and dry skin caused by decreased dermal/epidermal thickness and regression of sebaceous glands.
Compare gout and pseudogout 10 marks)
Can compare based on:
- Aetiology (hyperuricaemia vs chondrocalcinosis)
- Type & appearance of crystal (sodium urate; negatively birefriengent needle-shaped VS calcium pyrophosphate; positively birefringent & polygonal)
- Pathophys stages (1. Asymptomatic hyperuricaemia 2. Acute gouty 3. Intercritical 4. Chronic tophaceous VS 1. Asymptomatic chondrocalcinosis 2. Acute pyrophosphate synovitis 3. Chronic pyrophosphate arthritis)
- Typical pt: (Men >30; diet high in purine & excess alcohol; HTN & obese VS elderly people)
- Joints (small VS large)
- Pain (severe VS mod)
- Swelling (severe VS mod)
- Crystal Ssx (tophi VS no lumps/crystals)
- Complications (renal calculi and insufficiency VS None)
- Lab tests (High uric acid VS serum calcium)
- Radiology (Tophi & joint erosion VS cartilage calcification & changes similar to OA)
Discuss the events occurring in joints and tendons as RA progresses through from early to advanced stages (10 marks)
Stage 1: Synovitis
- Early changes:
o Vascular congestion → vasodilation
o Proliferation of synoviocytes → synovial thickening
o Infiltration of articular cartilage and subchondral bone by polymorphs, lymphocytes and plasma cells
- Gradual thickening and villous formation of the synovium
- Effusion into joint and tendon sheaths
Stage 2: Destruction
- Persistent inflammation → Joint and tendon destruction
- Articular cartilage erosion, due to:
o Pannus (granulation tissue) formation and spread
o Action of proteolytic enzymes
o Vascular tissue in folds of synovial reflections (neoangiogenesis)
- Bone erosion, due to:
o Invasion of granulation tissue
o Osteoclastic resorption
- Tendon sheath destruction, due to:
o Tenosynovitis
o Invasion of collagen bundles by granulation tissue and inflammatory elements → eventual tendon rupture
Stage 3: Deformity
- Inflammation often subsides by end of this stage
- All of the following cause progressive joint instability and deformity; and structural/mechanical issues cause patient’s pain:
o Articular destruction
o Capsular stretching
o Tendon rupture
- Typical deformities:
o Fingers: Swan neck & Boutonniere’s (destruction of flexor/extensor tendons and sheaths), Bouchard’s (PIPs) & Hagarth’s (MCPs) nodes, ulnar deviation
o Wrist: Radial and palmar deviation
o Knees and ankles: Valgus deformities
o Toes: Claw & hammer toe
