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Phase 2a > Rheumatology > Flashcards

Rheumatology Flashcards

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1
Q

What’s the function of oestoblasts?

A
  • Synthesis type I collagen rich matrix (osteoid).

- Secrete RANK-ligand.

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2
Q

What’s the function of osteoclasts?

A
  • Responsible for bone resorption.
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3
Q

What’s the function of RANK-ligand? What inhibitors RANK-ligand?

A
  • Binds to osteoclasts + essential for their formation, function + survival.
  • OPG.
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4
Q

What are ESR/CRP?

A

Inflammatory markers.

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5
Q

Briefly describe vitamin D synthesis

A
  • In liver, 25-hydroxylase converts cholecalciferol into calcifediol.
  • In kidneys, 1-alpha-hydroxylase converts calcifediol into calcitriol.
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6
Q

Describe the function of PTH.

A
  • Increases bone resporption + so calcium + phosphate.
  • Increases calcium reabsorption in DCT + decreases phosphate reabsorption in PCT.
  • Stimulates 1-hydroxylase release, increasing calcitriol + so calcium/phosphate absorption in intestine.
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7
Q

Describe uric acid metabolism.

A
  • Purines (A+G) > hypoxanthine > xanthine > uric acid > monosodium urate.
  • Xanthine oxidase converts hypoxanthine > xanthine.
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8
Q

OSTEOARTHRITIS

What is the pathophysiology of OA?

A
  • Non-inflammatory degernative disorder of synovial joints characterised by deterioration of articular cartilage + formation of new bone.
  • Progressive destruction of articular cartilage makes exposed subchondral bone become sclerotic, increases vascularity + subchondral cysts form where repair produces cartilaginous growths from chondrocytes which become calcified (osteophytes)
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9
Q

OSTEOARTHRITIS

What is the aetiology of OA?

A
  • Usually primary with no predisposing factors.

- Secondary OA sometimes occurs to damaged/congenitally abnormal joints.

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10
Q

OSTEOARTHRITIS

What are the risk factors of OA?

A
  • Female.
  • Family Hx.
  • Obesity.
  • Occupation (manual labour).
  • Increasing age (cumulative effect of trauma + decrease in neuromuscular function).
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11
Q

OSTEOARTHRITIS

What are the symptoms of OA?

A
  • Morning stiffness <30m.
  • Joint pain exacerbated by exercise.
  • Joint stiffness after rest (gelling).
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12
Q

OSTEOARTHRITIS

What are the signs of osteoarthritis?

A 
Bony swelling's...
- DIPJs = Herberden's nodes.
- PIPJs = Bouchard's nodes.
- Carpal metacarpal joints affected.
- Medial surface of knee affected.
Joint deformities/tenderness.
Reduced range of movement.
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13
Q

OSTEOARTHRITIS

What are the investigations for OA?

A

Plain X-ray = LOSS…

  • Loss of joint space.
  • Osteophytes.
  • Subarticular sclerosis.
  • Subchondral cysts.
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14
Q

OSTEOARTHRITIS

What is the non-medical treatment of OA?

A
  • Education.
  • Exercise to improve local muscle strength.
  • Weight loss.
  • PT/OT.
  • Walking aids.
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15
Q

OSTEOARTHRITIS

What is the medical treatment for OA?

A
  • Regular paracetamol ± topical NSAIDs.
  • Codeine.
  • Intra-articular steroid injections.
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16
Q

OSTEOARTHRITIS

What is the surgical treatment for OA?

A
  • Arthroscopy for loose bodies (can cause locking, e.g. knee).
  • Osteotomy (change bone length).
  • Arthroplasty (joint replacement).
  • Fusion (ankle + foot often).
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17
Q

OSTEOARTHRITIS

What is a negative to arthroplasty?

A
  • Prosthetic joint infection can be a serious complication, requires exchange arthroplasty.
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18
Q

RHEUMATOID ARTHRITIS

What is the pathophysiology of RA?

A
  • Autoimmune inflammatory synovial joint disease.
  • Chronic inflammation leads to B/T cells + neutrophils to infiltrate the synovium, formation of new synovial blood vessels occur causing synovium to proliferate leading to pannus formation, grows over articular cartilage + destroys it + subchondral bone leading to bony erosions.
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19
Q

RHEUMATOID ARTHRITIS

What is the epidemiology of RA?

A
  • 1% prevalence (increased in smokers).
  • F:M = 2:1.
  • Peak incidence in 40s.
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20
Q

RHEUMATOID ARTHRITIS

What is the aetiology of RA?

A
  • Autoantibodies such as rheumatoid factor (Anti-IgG) + anti-cyclic citrullinated peptide (CCP) lead to defective cell mediated immune response.
  • HLA DR4/DRB1 linked.
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21
Q

RHEUMATOID ARTHRITIS

What are the symptoms are RA?

A
  • Morning stiffness (>30m).
  • Pain eases with use.
  • Swelling.
  • Systemic illness like general fatigue, malaise.
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22
Q

RHEUMATOID ARTHRITIS

What are the extra-articular symptoms of RA?

A
  • Eyes = dry, scleritis.
  • Neuro = neuropathies like carpal tunnel.
  • Haem = lymphadenopathy, anaemia.
  • Resp = pleural effusion, nodules.
  • Cardio = pericardial effusion, IHD.
  • Kidneys = amyloidosis.
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23
Q

RHEUMATOID ARTHRITIS

What are the signs of RA?

A

Symmetrical swollen painful + stiff joints…
- Typically metacarpophalangeal + PIPJ + wrist affected.
Deformities…
- Ulnar deviation (Swelling of metacarpophalangeal + PIPJ joints).
- Boutonierre thumb (Z-thumb).
- Swan-neck deformity.
Polyarthropathy.

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24
Q

RHEUMATOID ARTHRITIS

What are the investigations for RA?

A 
Bloods...
- ESR/CRP raised.
- Anaemia (normochromic/cytic).
Test for serum antibodies...
- Rheumatoid factor (>70% present).
- Anti-CCP (specific, predicts disease progression).
X-ray shows LESS...
- Loss of joint space.
- Erosions.
- Soft tissue swelling.
- Soft bones (osteopenia).
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25
RHEUMATOID ARTHRITIS | What is the treatment for RA?
- Early use of 2x DMARDs = methotrexate + sulfasalazine + biological agents (rituximab) to slow progression + target parts of immune system involved in inflammation. - Steroids help rapidly reduce symptoms. - NSAIDs/analgesia. - PT/OT. - Encourage exercise.
26
GOUT | What is the pathophysiology of gout?
- Inflammatory arthritis caused by hyperuricaemia + intra-articular monosodium urate crystals. - Hyperuricaemia results from overproduction of uric acid/renal underexcretion. - Urate is derived form breakdown of purines.
27
GOUT | What is the aetiology + risk factors for gout?
- Hyperuricaemia – idiopathic with impaired renal excretions from CKD, diuretics, HTN. - Men >75y/o. - RFs = alcohol, red meat + seafood, chemotherapy.
28
GOUT | What are the mean differentials for gout?
- Septic arthritis. | - Reactive arthritis.
29
GOUT | What are the symptoms of gout?
- Hot + swollen joints. | - Toes commonly affected (metatarsophalangeal joint of big toe).
30
GOUT | What are the signs of gout?
- Tophi = aggregates of urate crystals w/ inflammatory cells, proteolytic enzymes are released leading to erosion. - Poly-articular inflammatory arthritis. - Erythema.
31
GOUT | What are the complications of gout?
Increased risk of developing... - HTN. - CVD like stroke. - Renal disease. - T2DM.
32
GOUT | What are precipitating factors for an acute attack of gout?
- Cold/trauma. - Drugs. - Dehydration. - Sepsis. - Sudden overload.
33
GOUT | What are the investigations for gout?
Joint fluid aspiration + microscopy... - Needle-shaped crystals, negatively birefringent under polarised light. Serum uric acid raised. Tophi.
34
GOUT | What is the treatment for gout?
Lifestyle = diet, weight loss, reduce alcohol. Rest + elevate joint, ice packs. - NSAIDs like diclofenac, colchicine if NSAIDs C/I. - Allopurinol. - Corticosteroids. - Switching bendroflumethiazide to cosartan.
35
GOUT | What is the mechanism of action of allopurinol?
- Blocks xanthine oxidase.
36
PSEUDOGOUT | What is the pathophysiology of pseudogout?
- Deposition of calcium pyrophosphate crystals on joint surfaces + the crystals ellicit an inflammatory response.
37
PSEUDOGOUT | What diseases is pseudogout associated with?
- Hyperparathyroidism. - Haemochromatosis. - Hypophosphataemia.
38
PSEUDOGOUT | What is the clinical presentation of gout?
- Acute, hot + swollen joints. | - Usually knee/wrist.
39
PSEUDOGOUT | What are the investigations of pseudogout?
Joint fluid microscopy... - Rhomboid-shaped crystals showing positive birefringence in polarised light. X-ray... Can show chondrocalcinosis (linear calcification parallel to articular surfaces).
40
PSEUDOGOUT | What is the treatment for pseudogout?
- Rest + elevate joint, ice packs. - Joint aspiration w/ NSAIDs/colchicine. - Intra-articular steroids. - Methotrexate.
41
ANKYLOSING SPONDYLITIS | What is the pathophysiology of ankylosing spondylitis?
- Inflammation of spine leads to erosive damage causing repair/new bone formation, resulting in bony spurs (syndesmophytes) that leads to irreversible fusion of the spine (ankylosis). - Typically asymmetrical large joints are affected in seronegative spondyloarthropathies.
42
ANKYLOSING SPONDYLITIS | What is the aetiology of ankylosing spondylitis?
- Unknown, M>F. | - Strong association with HLA-B27 antigen presenting cell.
43
ANKYLOSING SPONDYLITIS | What are the symptoms of ankylosing spondylitis?
- Typically young man. - Increasing pain + prolonged morning stiffness in lower back + buttocks, improves with exercise, not rest. - Progressive loss of spinal movement.
44
ANKYLOSING SPONDYLITIS | What are the signs of ankylosing spondylitis?
- Loss of lumbar lordosis (curve). - Increased kyphosis. - Limitation of lumbar spine mobility. - Enthesitis.
45
ANKYLOSING SPONDYLITIS | What are the investigations for ankylosing spondylitis?
Bloods... - ESR/CRP often raised. X-ray... - Erosion + sclerosis of margins of sarcoiliac joints > sacroilitis. - Bamboo spine = progressive calficiation of interspinous ligaments + syndesmophytes. HLA-B27 test, MRI.
46
ANKYLOSING SPONDYLITIS | What is the treatment for ankylosing spondylitis?
- Morning exercises to maintain posture + spinal mobility. - Slow release NSAIDs taken at night to relieve night pain + morning stiffness. - Methotrexate for peripheral arthritis. - TNF-alpha inhibitors like rituximab.
47
PSORIATIC ARTHRITIS | What is the pathophysiology + aetiology of psoriatic arthritis?
- Psoriasis occurs commonly at elbow, knees + fingers. | - Occurs in 10–40% of those with psoriasis.
48
PSORIATIC ARTHRITIS | What is the clinical presentation of psoriatic arthritis?
``` Skin rash, check behind/in ears + umbilicus... - Symmetrical distribution. - Itchy. - Well-circumscribed margins. - Deep red colour on extensor srufaces. DIPJ involvement. ```
49
PSORIATIC ARTHRITIS | What are specific psoriatic arthritis features?
- Symmetrical polyarthritis. - Dactylitis (inflammation of whole digit). - Spinal involvement.
50
PSORIATIC ARTHRITIS | What are the investigations for psoriatic arthritis?
X-rays... - Pencil in cup deformity in interphalangela joints where bone erosion create pointed appearance + articulating bone is concave.
51
PSORIATIC ARTHRITIS | What is the treatment for psoriatic arthritis?
- Analgesia + NSAIDs. | - Methotrexate, TNF-alpha inhibitor.
52
REACTIVE ARTHRITIS | What is the pathophysiology of reactive arthritis?
- Sterile inflammation of the synovial membrane in which arthritis occur as an autoimmune response to infection elsewhere in body, typically GI/GU.
53
REACTIVE ARTHRITIS | What is the aetiology of reactive arthritis?
- GI infection like Shigella, Salmonella. | - STI like chlamydia trachomatis.
54
REACTIVE ARTHRITIS | What is the clinical presentation of reactive arthritis?
Reiter's syndrome "can't see, pee or climb a tree" - Conjunctivitis. - Urethritis. - Arthritis. Acute onset malaise, fatigue, fever. Low back pain, asymmetrical, oligoarthritis.
55
REACTIVE ARTHRITIS | What are the investigations + treatments for reactive arthritis?
- Bloods = CRP/ESR raised. - Aspirated synovial fluid sterile with high neutrophil count. - NSAIDs + local corticosteroid injections, methotrexate in relapsing cases.
56
ENTEROPATHIC ARTHRITIS | What is it associated with? How does it improve? Treatment for resistant cases?
- IBD. - Improves w/ bowel symptoms. - DMARDs like methotrexate.
57
JIA | What is the diagnostic criteria + aetiology of juvenile idiopathic arthritis (JIA)?
- Joint swelling/stiffness >6w in children <16y/o + no other cause identified. - Idiopathic but autoimmune so genetic factors.
58
JIA | Where should you check especially in JIA + why? Other features of JIA.
- Eyes, lining of eyes + joints very similar so high risk of uveitis. - Oligoarthritis affecting ≤4 joints, often antinuclear antibody (ANA) positive. - Enthesitis related JIA is similar to adult ankylosing spondylitis + is HLA-B27 positive.
59
JIA | What is the treatment of JIA?
``` Non-medical = education, support, physiotherapy. Medical = steroid joint injections, NSAIDs + methotrexate. ```
60
JIA | What are the complications with JIA?
- Damage, deformity, disability.
61
SEPTIC ARTHRITIS | What is the pathophysiology + aetiology of septic arthritis?
- Acute infection of joint which can cause damaging inflammation + loss of function, can destroy joint in <24h. - Mostly S. aureus, Streptococci, Neisseria.
62
SEPTIC ARTHRITIS | What are the risk factors with septic arthritis?
- Pre-existing joint disease (Esp. RA). - Prosthetic joints. - IVDU. - Age >80y/o. - DM.
63
SEPTIC ARTHRITIS | What is the clinical presentation of septic arthritis?
- Fever. - Red/swollen/hot. - Single swollen joint w/ pain on movement (often knee).
64
SEPTIC ARTHRITIS | What are the investigations + treatment for sepetic arthritis?
- Bloods = ESR/CRP raised. - Joint aspiration for synovial fluid microscopy + culture prior to antibiotics. - Immediate empirical antibiotics (flocloaxicillin), aspiration to drain, rest/splinting.
65
OSTEOMYELITIS | What is osteomyelitis?
- Bone inflammation leading to destruction, secondary to infection of the bone marrow.
66
OSTEOMYELITIS | What are the two easiest routes for pathogens to get into the bone?
- Inoculation of infection into bone (trauma, open wound). | - Continguous spread of infection to bone from adjacent tissues.
67
OSTEOMYELITIS | What is the hardest way for pathogens to get into the bone?
- Haematogenous seeding, often seen in vertebrae in adults + as with age vertebrae become more vascular. - Bacterial seeding means bacterial can move from blood to bone e.c. due to cannula infection, IVDU.
68
OSTEOMYELITIS | What are host factors affecting pathogenesis of osteomyelitis?
- Behavioural (risk of trauma). - Vascular supply (arterial disease). - Pre-existing bone/joint problems (RA). - Immune deficiency.
69
OSTEOMYELITIS | What is the aetiology of osteomyelitis?
Local infection... - S. aureus, H. influenzae, Salmonella. - Metastatic haematogenous spread. - TB (caseating granuloma).
70
OSTEOMYELITIS | What are the risk factors for osteomyelitis?
- Pre-existing joint disease (Esp. RA). - Prosthetic joints. - Age >80y/o. - DM. - Immunosuppression.
71
OSTEOMYELITIS | What is the clinical presentation of osteomyelitis?
- Fever, dull, localised bone pain worse on movement. - Tenderness. - Erythema.
72
OSTEOMYELITIS | What are the investigations with osteomyelitis?
``` Bloods... - Raised ESR/CRP, WCC. - Cultures. X-rays first line. Bone biopsy + cultures = diagnostic. ```
73
OSTEOMYELITIS | What is the treatment for osteomyelitis?
- Surgical debridement (removal of damage tissue), drainage of abscess. - IV Abx (often flucloxacillin).
74
OSTEOPOROSIS | What is the pathophysiology of osteoporosis?
- Systemic skeletal disease characterised by low bone mass + micro-architectural deterioration where the patient is at increased risk of fracture.
75
What are 2 factors important in determining likelihood of osteoporotic fall? What makes bone strength?
- Propensity to fall leading to trauma + bone strength. | - Bone mineral density, size, micro-architecture + mineralisation.
76
OSTEOPOROSIS | Why does the bone become so much weaker in osteoporosis?
- Trabecular thickness decreases meaning there's fewer connections between trabecular + so overall decrease in strength. - Excessive bone resorption + inadequate formation of new bone during remodelling occurs.
77
OSTEOPOROSIS | What are the secondary causes of osteoporosis?
- Steroid use. - Hyper/hypothyroid. - Alcohol/smoking. - Thin (low BMI). - Testosterone low. - Early menopause. - Renal/liver failure. - Relatives (FHx). - Erosive bone disease (RA). - Dietary calcium low.
78
OSTEOPOROSIS | What is the clinical presentation of osteoporosis?
- Develops asymptoamtically. - Fracture often first sign... Distal radius = Colles' fracture. Thoracic vertebrae > kyphosis (widow's stoop). Proximal femur. Lumbar vertebrae.
79
OSTEOPOROSIS | What are the investigations for osteoporosis?
- Bloods normal (no issue with mineralisation). - Dual-energy X-ray absorptiometry (DEXA) scan is gold standard. - X-ray show fractures. - FRAX to assess someone's risk of osteoporotic fracture.
80
OSTEOPOROSIS | What is the DEXA T score and what does it tell you?
- T score is a standard deviation compared to a gender-matched young adult mean. - DEXA-T ≤ –2.5 = osteoporosis. - –2.5 < DEXA-T ≤ –1 = osteopenia (low bone mass).
81
OSTEOPOROSIS | What is the lifestyle advice for osteoporosis?
- Quit smoking, reduce alcohol. - Calcium + vitamin D supplement (AdCal D3). - HRT. - Balance exercise to reduce risk of falls.
82
OSTEOPOROSIS | What are the medical therapies for osteoporosis?
Anti-resorptive (decrease osteoclast activity + bone turnover)... - Bisphosphonates (alendronate). - Denosumab (human monoclonal antibody to RANK-L). - HRT in early post-menopausal women. Anabolic (increase osteoblast activity) - Teriparatide.
83
SLE | What is the pathophysiology of systemic lupus erythematosus?
- Inefficient phagocytosis > cell fragments transferred to lymphoid tissue where they're taken up by antigen presenting cells where self-antigens are present to T cells. - T cells stimulate B cells to produce autoantibodies against self-antigens. - Results in complement activation, influx of neutrophils + abnormal cytokine production leads to inflammation + tissue damage.
84
SLE | What are the risk factors + triggers of SLE?
``` Risk factors... - 90% young women. - Commoner in Afro-Caribbeans. - Genetic association. Triggers... - UV light. - EBV. ```
85
SLE | What are the symptoms of SLE?
- Weight loss. - Migraines. - Photosensitivity. - Myalgia + arthralgia.
86
SLE | What are the signs of SLE?
- Butterfly rash. - Pericarditis. - Raynaud's phenomenon. - Anaemia.
87
SLE | What is a major complication of SLE?
Antiphospholipid syndrome. - There are antiphospholipid antibodies which causes CLOTs... - Coagulation defect. - Livedo reticularis (mottled rash). - Obstetric (recurrent miscarriage). - Thrombocytopenia.
88
SLE | What are the investigations for SLE?
``` Bloods... - Raised ESR, normal CRP. - Normochromic/cytic anaemia. Serum autoantibodies... - ANA (specific, not sensitive). - Anti-dsDNA (sensitive, not specific). ```
89
SLE | What is the treatment for SLE?
Education + support, UV protection + smoking cessation, screening for organ involvement. - Corticosteroids, NSAIDs, DMARDs, monoclonal antibody. (rituximab).
90
PRIMARY BONE TUMOURS | What is a primary bone tumour? Give an example
- Bone tumours that originate in bone or from bone-derived cells + tissues. - Sarcoma is rare tumour of mesenchymal origin – malignant connective tissue neoplasm.
91
PRIMARY BONE TUMOURS | Give examples of benign + malignant tumours.
- Osteoid osteoma, osteoblastoma, osteochondroma. | - Osteosarcoma, chondrosarcoma, Ewing'd sarcoma.
92
PRIMARY BONE TUMOURS | What are bony sarcomas?
Make up 20% sarcomas. - Osteosarcoma (fast growing, aggressive, 15–17y/o). - Ewing's sarcoma (neural crest cells), onion-skin appearance on x-ray, responds well to chemotherapy.
93
PRIMARY BONE TUMOURS | What are red flag symptoms for primary bone tumours?
- Loss of function, non-mechanical bone pain present when still. - Weight loss, night pain, swelling. - Tiredness, pyrexia.
94
PRIMARY BONE TUMOURS | What are signs of primary bone tumours?
- Lump >5cm. - Lump increasing in size + deep to fascia. - Rest pain/pain at night. - Codman's triangle + sunburst appearance (osteosarcoma + Ewing's).
95
PRIMARY BONE TUMOURS | What are the investigations of primary bone tumours?
- Bloods, FBC, U+E, ALP. - Plain X-rays. - Bone scan. - Core needle biopsy. - CT/MRI scan.
96
PRIMARY BONE TUMOURS | What is the treatment of primary bone tumours?
- Chemo ± radiotherapy. - Surgery. - Bisphosphonates.
97
SECONDARY BONE TUMOURS | What are the most common secondary bone tumours?
- Breast. - Lung. - Prostate. - Kidney. - Thyroid.
98
SECONDARY BONE TUMOURS | What is the clinical presentation of secondary bone tumours?
- Bone pain. - Generally unwell. - Pathological fracture.
99
SECONDARY BONE TUMOURS | What are the investigations + treatment for secondary bone tumours?
- Bloods, FBC, U+E, ALP. - Plain X-rays, bone scan, core needle biopsy, CT/MRI scan. - Treat cause, surgery, correct metabolic abnormalities.
100
FIBROMYALGIA | What is the pathophysiology of fibromyalgia?
- Chronic widespread pain + sensitivity to pressure.
101
FIBROMYALGIA | What can increase/decrease the volume of pain?
- Increase = substance P, glutamate, serotonin. | - Decrease = opioids, GABA + cannabinoids.
102
FIBROMYALGIA | What are the associations + triggers of fibromyalgia?
Associations... - Depression, chronic fatigue, IBS. Triggers... - Physical trauma, infections, hormonal alterations.
103
FIBROMYALGIA | What is the clinical presentation of fibromyalgia?
- Morning stiffness. - Poor concentration, sleep disturbances. - Headaches. - Pain worse w/ stress, cold.
104
FIBROMYALGIA | What are the investigations for fibromyalgia?
- Chronic widespread pain lasting >3 months w/ other causes excluded. - Pain is at 11/18 tender sites.
105
FIBROMYALGIA | What is the treatment for fibromyalgia?
- Exercise + fitness important. - Acupuncture. - Low dose amitriptyline (sleep). - CBT, acupuncture.
106
MECHANICAL BACK PAIN | What is the pathophysiology of mechanical back pain?
- Back pain as a result of physical wear + tear.
107
MECHANICAL BACK PAIN | What is nerve root pain?
- Nerve root impingement due to herniated discs causes a sharp, well localised pain + can be associated with paraesthesia.
108
MECHANICAL BACK PAIN | What are risk factors with mechanical back pain?
- Manual labour work. - Smoking. - Low socioeconomic status. - Females.
109
MECHANICAL BACK PAIN | What's the clinical presentation of mechanical back pain?
- Back pain in lumbosacral area. - Worse on movement. - Systemically well.
110
MECHANICAL BACK PAIN | What are the investigations for mechanical back pain?
- FBC, ESR/CRP. | - Only x-ray if red-flags (IVDU, night sweats, incontinence, fever).
111
MECHANICAL BACK PAIN | What is the treatment for mechanical back pain?
- Resolves after 6w. - Education + self-management. - Analgesic ladder. - Acupuncture, physio.
112
OSTEMOMALACIA | What is the pathophysiology of osteomalacia + rickets?
- Manifestation of profound vitamin D deficiency where inadequate mineralisation of osteoid framework leads to soft bones + produces rickets during bone growth + osteolamalcia following epiphyseal closure. - Normal amount of bone but mineral content low.
113
OSTEMOMALACIA | What's the aetiology of vitamin D deiciency?
- Lack of exposure to sun. - Malabsorption/poor diet. - Renal disease.
114
OSTEMOMALACIA | What's the clinical presentation of osteomalacia + rickets?
- Osteomalacia = proximal muscle weakness + pain, fractures (esp. femoral neck). - Rickets = bowed legs + knock knees, growth retardation.
115
OSTEMOMALACIA | What are the investigations + treatment for osteomalacia?
``` Plasma... - Hypocalcaemia, high PTH, high ALP. - Low calcitriol + phosphate. Bone biopsy = incomplete mineralisation. X-ray = loss of cortical bone. - Oral calciferol. ```
116
SJÖGRENS SYNDROME | What is the pathophysiology of Sjögrens syndrome?
- Immunologically mediated destruction of epithelial exocrine glands, especially lacrimal + salivary. - Lymphocytic infiltration of exocrine glands.
117
SJÖGRENS SYNDROME | What's the aetiology of Sjögrens syndrome?
- Primary = idiopathic. | - Secondary = autoimmune related (RA).
118
SJÖGRENS SYNDROME | What is the clinical presentation of Sjögrens syndrome?
- Dry eyes + mouth = sicca complex. | - Arthritis.
119
SJÖGRENS SYNDROME | What are the investigations + treatment for Sjögrens syndrome?
- Schirmer's test = measure conjunctival dryness. - Serum autoantibodies like anti-Ro, rheumatoid factor, ANA. - Artifical tear + saliva replacement.
120
POLYMYOSITIS | What is the pathophysiology of polymyositis?
- Rare muscle disorder where there's autoimmune-mediataed striated muscle inflammation (myositis), mediated by cytotoxic T cells.
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POLYMYOSITIS | What is the clinical presentation of polymyositis.
- Symmetrical progressive muscle weakness. | - Skin invovlement with scaly erythematous plaques over knucles (dermamyositis).
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POLYMYOSITIS | What are the investigations + treatment for polymyositis?
- Serum muscle enzymes raised, muscle biopsy diagnostic. | - Oral prednisolone + immunosuppressive therapy.
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SCLERODERMA | What is the pathophysiology of scleroderma?
Multisystem autoimmune connective tissue disorder with involvement of skin, excessive collagen production + deposition, inflammation + autoantibody production.
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SCLERODERMA | What is the clinical presentation of limited cutaneous?
``` Face, forearms, lower legs up to knee... Calcinosis. Raynaud's phenomenon. oEsophageal involvement (dysmotility). Sclerodactyly. Telangiectasia. ```
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SCLERODERMA | What is the clinical presentation of diffuse cutaneous?
- Affects whole body. - Pulmonary fibrosis + HTN. - Poor prognosis.
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SCLERODERMA | What are the investigations + treatments for scleroderma?
``` Serum autoantibodies (antinuclear, anti-Ro). - Treat symptoms, PPIs for GORD, CCB for Raynaud's, annual echo. ```
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VERTEBRAL DISC DEGENERATION | What is the pathophysiology of vertebral disc degeneration?
- Pathological process of degeneration of intervertebral discs where there's protrusion, spondylosis +/or spinal stenosis.
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VERTEBRAL DISC DEGENERATION | What is the aetiology of vertebral disc degeneration?
- Disease of ageing, increased fragility of cartilage of disc can lead to pathology.
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VERTEBRAL DISC DEGENERATION | What is the clinical presentation of vertebral disc degeneration?
- Chronic lower back pain, sometimes radiating to hips _ buttocks.
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VERTEBRAL DISC DEGENERATION | What are the investigations + treatment for vertebral disc degeneration?
- Physical therapy, NSAIDs, surgery.
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POLYMYALGIA RHEUMATICA | What is the pathophysiology of polymyalgia rheumatica?
- Pain + stiffness results from inflammatory cells concentrating in tissues surrounding affecting joints, attacking the lining of joints. - Especially shoulders, neck + hip.
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POLYMYALGIA RHEUMATICA | What is the clinical presentation of polymyalgia rheumatica?
- Bilateral aching/tenderness. - Morning stiffness in shoulders, hips + proximal limbs. - Associated with giant cell arteritis.
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POLYMYALGIA RHEUMATICA | What are the investigations + treatment for polymyalgia rheumatica?
- Bloods, ESR/CRP raised. | - Corticosteroids.
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POLYARTERITIS NODOSA | What is the pathophysiology of polyarteritis nodosa?
- Necrotising arteritis that causes aneurysms + thrombosis in medium-sized arteries, leading to infarction in affected organs with severe systemic symptoms.
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POLYARTERITIS NODOSA | What is the clinical presentation of polyarteritis nodosa?
- Systemic = fever, malaise, weight loss, myalgia. | - Skin can show rash, punched out ulcers, nodules.
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POLYARTERITIS NODOSA | What are the investigations + treatment for polyarteritis nodosa?
Bloods = ESR, CRP, WCC raised. - Renal/mesenteric angiography or renal biopsy = diagnostic. - Control BP, corticosteroids.
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WEGENER'S GRANULOMATOSIS | What is the pathophysiology of Wegener's granulomatosis?
- Necrotising granulomatous inflammation + vasculitis of small + medium vessels, normally affects arterioles + capillaries.
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WEGENER'S GRANULOMATOSIS | What is the clinical presentation of Wegener's granulomatosis?
- Upper RT = sinusitis, otitis. - Lungs = pulmonary nodules. - Kidney = glomerulonephritis. - Skin = ulcers. - Eyes = uveitis.
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WEGENER'S GRANULOMATOSIS | What are the investigations + treatment for Wegener's granulomatosis?
- c-ANCA +ve. - Urinalysis for proteinuria/haematuria. - CXR nodules. - High dose steroids.
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PAGET'S DISEASE | What is the pathophysiology of Paget's disease?
- Increased bone turnover associated with increased numbers of osteoblasts + osteoclasts w/ resultant remodelling, bone enlargement, deformity + weakness as new bone is mechanically weaker, more vascularised + poorly organised (pathological fractures).
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PAGET'S DISEASE | What is the clinical presentation of Paget's disease?
- Mostly asymptomatic. - Deep, boring pain in bone/nearby joint. - Deformities like skull enlargement, bowing of tibia (bowed sabre tibia).
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PAGET'S DISEASE | What are the complications with Paget's disease?
- Pathological fractures. - Nerve compression. - OA.
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PAGET'S DISEASE | What are the investigations + treatment for Paget's disease?
- Bloods = high serum ALP. - X-ray = localised bony enlargement, distortion, sclerotic changes + osteolytic areas. - Bisphosphonates + analgesia.
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NSAIDs | What is the mechanism of action? Give some examples. List some side effects.
- Non-selective inhibitors of cyclo-oxygenase + so inhibit prostaglandins. - Naproxen, diclofenac, ibuprofen. - Peptic ulcers (co-prescribe PPIs), renal failure (AA vasoconstriction so reduced GFR), increased risk of MI/CVD.
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STEROIDS | Give an example. What are the side effects of steroids?
- Prednisolone. | - Acne, HTN, osteoporosis, skin atrophy.
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DMARDS | What is the mechanism? Give examples. Advice for when taking methotrexate?
- Non-specific inhibition of inflammatory cytokine cascade = reduced joint pain, stiffness + swelling. - Methotrexate, sulfasalazine. - Take once weekly, folic acid co-prescribed, can cause liver problems so regular bloods.
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TNF-ALPHA BLOCKER | Give an example.
Rituximab, adalimumab.
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BISPHOSPHONATES | Example + mechanism.
- Alendronate. | - Reduces bone tunrover by inhibiting osteoclast mediated bone resorption by targeting HMG-CoA reductase pathway.
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ANALGESIC LADDER | What are the three steps?What is the additional step?
``` Non-opioids, mild pain.. - NSAIDs, paracetamol. Weak-opioids, moderate pain... - Codeine + derivatives. Strong opioids, high pain... - Morphine, oxycodone. ?Nerve blocks. ```
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ANALGESIC LADDER | What does NICE recommend at each level of the ladder?
- Adjuvant pharmacological agents like muscle-relaxants, anti-depressants + corticosteroids.
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OSTEOMYELITIS | What is the difference between acute + chronic osteomyelitis?
Acute - dendritic cells, macrophages, oedema = resolution often. Chronic - necrotic bone (sequestra), new bone formation.

Phase 2a (12 decks)

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