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MSK Flashcards

1
Q

Define osteoarthritis

A

Degenerative joint disorder, not inflammatory. Osteoarthritis is ‘wear and tear’ of synovial joints, resulting from mechanical and biological events that destabilise the normal degradation and synthesis of cartilage.

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2
Q

Describe the aetiology of osteoarthritis

A

Arthritis

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3
Q

Describe the risk factors for osteoarthritis

A

High intensity labour, old age, obesity, occupation/sports, genetic

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4
Q

Describe the pathophysiology of osteoarthritis

A

Non-inflammatory degenerative destruction of cartilage from repeated mechanical forces. Disruption of chondrocytes prevents rebuilding. Imbalanced cartilage breakdown > repair causing increased chondrocyte metalloproteinase secretion which degrades T2 collagen and causes cysts. Bone attempts to overcome this with T1 collagen which leads to abnormal bony growths (osteophytes) and cysts
Commonly affected joints: hips, knees, fingers, thumb, cervical spine

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5
Q

Describe the key presentations of osteoarthritis

A

Transient painful joints stiff for <30 mins in morning, worse throughout day. Proximal Bouchard nodes and distal Heberden nodes on fingers.

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6
Q

Describe the clinical manifestations of osteoarthritis

A

Signs: Hard asymmetrical bulky non-inflamed joint, squaring at the base of thumb (carpometacarpal saddle joint)
Symptoms: Restricted motion, crepitus on moving (popping/clicking), no extra-articular sx

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7
Q

What is the gold standard investigation for osteoarthritis

A

x-ray: loss of joint space, osteophyte formation (bony lumps), subchondral sclerosis, subchondral cysts.

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8
Q

Describe the first line investigations for osteoarthritis

A

x-ray. FBC (normal)

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9
Q

What are the differential diagnosis for osteoarthritis

A

Bursitis, gout, pseudo-gout, rheumatoid arthritis, psoriatic arthritis

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10
Q

Describe the management for osteoarthritis

A

1st line - lifestyle (less weight-bearing, physio), topical analgesics (capsaicin, NSAIDs – diclofenac, methyl salicylate), + paracetamol, + opioid (PPI for gastric protection)
joint replacement surgery (arthroplasty)

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11
Q

Describe the complications of osteoarthritis

A

Destruction of joint, loss of joint function, NSAID related GI bleeding/renal dysfunction

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12
Q

Define rheumatoid arthritis

A

Autoimmune condition causing inflammation of the synovial lining of joints, tendon sheaths and bursa. Inflammatory symmetrical polyarthritis

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13
Q

Describe the epidemiology of rheumatoid arthritis

A

Women 30-50 (3x more likely than men premenopausal)

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14
Q

Describe the aetiology of rheumatoid arthritis

A

Autoimmune, genetic (HLA DR4/DR1)

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15
Q

Describe the risk factors for rheumatoid arthritis

A

Young, female, FHx, other autoimmune conditions

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16
Q

Describe the pathophysiology of rheumatoid arthritis

A

Autoimmune destruction of the synovium. Inflammation causes damage to tendons, bone cartilage and ligaments.
Rheumatoid factor is an autoantibody which targets IgG antibodies causing activation of the immune system against IgG causing systemic inflammation.
Cyclic citrullinated peptide antibodies (anti-CCP) are autoantibodies which target healthy joint tissues.

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17
Q

Describe the key presentations of rheumatoid arthritis

A

Joint pain worse in morning (>30mins) gets better as day goes on. Symmetrical distal Polyarthropathy, hot inflamed joints, most common in wrist/hand + feet, knee, hip.

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18
Q

Describe the clinical manifestations of rheumatoid arthritis

A

Signs: Swan neck thumb, ulnar deviation, boutonniere deformity, Z shaped thumb deformity. DIP joint often spared. Extra-articular complications
Symptoms: Painful, swollen, stiff joints for more than 1hour in the morning, get better as the day goes on and with movement. Fatigue, weight loss, malaise, aches and cramps

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19
Q

What is the gold standard investigation for rheumatoid arthritis

A

Clinical diagnosis, serology, inflammatory markers

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20
Q

Describe the first line investigations for rheumatoid arthritis

A

Serology: anti CCP positive, rheumatoid factor positive
Bloods: anaemia, CRP/ESR raised
x-ray: less lost joint space, erosion, soft tissue swelling, soft bones

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21
Q

What are the differential diagnosis for rheumatoid arthritis

A

Osteoarthritis, psoriatic arthritis, gout, pseudo-gout

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22
Q

Describe the management for rheumatoid arthritis

A

1st line – DMARDs (disease modifying anti-rheumatic drugs) e.g., methotrexate, leflunomide, sulfasalazine
2nd – Add biological agent (infliximab, adalimumab, etanercept, rituximab)
3rd – corticosteroid (prednisolone), NSAIDs (ibuprofen)
Pregnant: prednisolone, sulfasalazine, hydroxychloroquine

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23
Q

Describe the complications for rheumatoid arthritis

A

Cervical spine cord compression (weakness and loss of sensation), lung involvement (interstitial lung disease, fibrosis), ischemic heart disease, vision problems, CKD. Work disability

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24
Q

Define Gout

A

Type of crystal arthropathy associated with high blood uric acid levels. Sodium urate crystals are deposited in joint causing it to become hot, swollen, and painful. Acute bouts of inflammatory arthritis

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25
Q

Describe the epidemiology of gout

A

Middle aged overweight males

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26
Q

Describe the aetiology of gout

A

Uric acid overproduction or excretion

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27
Q

Describe the risk factors for gout

A

High purine diet (meat, seafood, beer) increased cell turnover, CKD, diuretics

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28
Q

Describe the pathophysiology of gout

A

Purines oxidised to uric acid by xanthine oxidase. Uric acid is excreted by kidneys or converted to monosodium urate. Increased uric acid or CKD causing impaired excretion leads to more monosodium urate which forms crystals in joints.

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29
Q

Describe the key presentations of gout

A

Monoarticular (often big toe/DIPs/wrist/thumb) acute hot swollen painful joint

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30
Q

Describe the clinical manifestations of gout

A

Signs: Tophi – subcutaneous deposits of uric acid affecting small joints and connective tissue in DIPs, elbow, ears
Symptoms: Acute hot swollen painful inflamed joints.

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31
Q

What is the gold standard investigation for gout

A

Joint aspiration and polarised light microscopy (needle-like crystals, negative birefringent of polarised light, monosodium urate crystals)

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32
Q

Describe the first line investigations for gout

A

Joint aspiration, Increased serum uric acid

Other: Joint x-ray: maintained joint space, lytic lesions, punched out erosions with sclerotic borders or overhanging edges

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33
Q

What are the differential diagnosis for gout

A

Septic arthritis, pseudogout, trauma, rheumatoid arthritis, psoriatic arthritis

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34
Q

Describe the management for gout

A

Lifestyle changes (decreased purines, more diary – antigout)
Acute flare: NSAIDs, Colchicine, corticosteroids
Prevention: allopurinol (xanthine oxidase inhibitor > reduces uric acid)

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35
Q

Describe the complications for gout

A

Infection in tophi, joint destruction, nephrolithiasis, CKD

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36
Q

Define pseudogout

A

Type of crystal arthropathy caused by calcium pyrophosphate crystals deposited in joints.

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37
Q

Describe the epidemiology of pseudogout

A

Females over 70

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38
Q

Describe the aetiology of pseudogout

A

Calcium pyrophosphate crystals

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39
Q

Describe the risk factors for pseudogout

A

Females over 70, hyperthyroidism, hyperparathyroidism, excess iron or calcium, diabetes, metabolic diseases

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40
Q

Describe the pathophysiology of pseudogout

A

Damage to joint causes pathological formation of calcium pyrophosphate crystals.

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41
Q

Describe the key presentations for pseudogout

A

Often polyarticular with knee commonly involved. Hot swollen painful red joint. Other joints commonly affected: shoulder, wrist, hips

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42
Q

Describe the clinical manifestations for pseudogout

A

Signs: Recent injury to the joint in the history
Symptoms: Hot swollen tender joint, usually knees. Fever and malaise

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43
Q

What is the gold standard investigation for pseudogout

A

Joint aspiration and polarised light microscopy (rhomboid shaped crystals, positive birefringent of polarised light, calcium pyrophosphate crystals)

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44
Q

What are the differential diagnosis for pseudogout

A

Septic arthritis, osteoarthritis, gout, rheumatoid arthritis, psoriatic arthritis

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45
Q

Describe the management for pseudogout

A

1st line – NSAIDs, colchicine, corticosteroids/intra-articular steroid injection

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46
Q

What are the complications with pseudogout

A

Loss of joint function

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47
Q

Define osteoporosis

A

Reduction in the density of bones (by 2.5 standard deviations). Osteopenia is a less severe reduction in bone density.

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48
Q

Describe the epidemiology of osteoporosis

A

50+ postmenopausal Caucasian women

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49
Q

Describe the aetiology of osteoporosis

A

SHATTERED: steroids, hyper(para)thyroidism, alcohol, thin (low BMI), testosterone (low), early menopause, renal/liver failure, erosive/inflammatory bone disease, dietary low calcium

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50
Q

Describe the key presentations for osteoporosis

A

Fractures (proximal femur, colles wrist fracture, compression vertebral crush - kyphosis)

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51
Q

What is the gold standard investigation for osteoporosis

A

DEXA bone scan – dual energy x-ray absorptiometry yields T score (normal = T > -1, osteopenia = -2.5 < T < -1, osteoporosis = T < -2.5)

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52
Q

What are the differential diagnosis for osteoporosis

A

Osteomalacia, multiple myeloma, CKD bone-mineral disorder

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52
Q

Describe the first line investigations for osteoporosis

A

1st line: Bone mineral density with DEXA bone scan (normal = T > -1, osteopenia = -2.5 < T < -1, osteoporosis = T < -2.5) FRAX score (10-year probability of major osteoporotic fracture or hip fracture), Calcium, phosphate, ALP normal

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53
Q

Describe the management for osteoporosis

A

Lifestyle – exercise, weight, low alcohol and smoking. Vitamin D and calcium supplementation.
1st line –Bisphosphonates (reduce osteoclast activity), e.g., alendronate, risendronate, zoledronic acid.
2nd line – denosumab (monoclonal antibody which binds to RANK-ligand and blocks osteoclast)
Hormone replacement therapy, raloxifene (stimulates oestrogen bone receptor)

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54
Q

Describe the complications for osteoporosis

A

Fractures (hip, ribs, wrist), chronic pain

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55
Q

Define ankylosing spondylitis

A

Inflammatory condition mainly affecting sacroiliac joints and vertebral column and causing progressive stiffness and pain.
Spondyloarthropathies: chronic inflammatory disease that affect sacroiliac joints and axial skeleton. Seronegative (Rheumatoid Factor -ve) and associated with HLA B27.
SPINEACHE: sausage digits (dactylitis), psoriasis, inflammatory back pain, NSAIDs > good response, enthesitis (tendon/ligament insertion), arthritis, Crohn’s/colitis/CRP raised, HLA B27, eye (uveitis)

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56
Q

Describe the epidemiology of ankylosing spondylitis

A

Males 3x more common, young male/late teens, HLA B27 gene

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57
Q

Describe the aetiology of ankylosing spondylitis

A

HLA B27 gene

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58
Q

Describe the pathophysiology of ankylosing spondylitis

A

Inflammatory arthritis of spine and rib cage leads to formation of new bone and fusion of joints. Syndesmophytes replace spinal bone damaged by inflammation and make the spine less mobile

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59
Q

Describe the key presentations of ankylosing spondylitis

A

Progressively worse lower back pain and stiffness, worse with rest and improves with movement. Worse at morning and night. Sacroiliac pain. Flares of worsening symptoms.

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60
Q

Describe the clinical manifestations of ankylosing spondylitis

A

Signs: Anterior uveitis, dactylitis, enthesitis, lumbar pathology: decreased lumbar lordosis > more kyphosis, Schober test shows decreased lumbar flexion <20cm
Symptoms: Chronic pain, weight loss, fatigue, dyspnoea, sleep disturbance

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61
Q

What is the gold standard investigation for ankylosing spondylitis

A

X-ray of spine and sacrum:
* Bamboo spine (fusion of vertebral bodies)
* Sacroiliitis
* Squaring of vertebral bodies
* Subchondral sclerosis and erosions
* Syndesmophytes (bony outgrowths in spinal ligament)
* Ossification of ligaments, discs and joints
* Fusion of facet, sacroiliac and costovertebral joints

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62
Q

Describe the first line investigations for ankylosing spondylitis

A

Pelvic x-ray, CRP and ESR raised, HLA B27 genetic test, MRI spine (bone marrow oedema in early disease before x-ray changes)

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63
Q

What are the differential diagnosis for ankylosing spondylitis

A

Reactive arthritis, psoriatic arthritis, enteric/IBD arthritis

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64
Q

Describe the management for ankylosing spondylitis

A

1st line – NSAIDs (naproxen, indomethacin, ibuprofen)
Steroids during flares, anti-TNF drugs e.g., etanercept. Monoclonal antibodies against TNF (infliximab), physiotherapy and lifestyle advice, surgery for deformities

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65
Q

Describe the complications for ankylosing spondylitis

A

Vertebral fractures, osteoporosis, cardiac involvement, iritis

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66
Q

Define psoriatic arthritis

A

Inflammatory arthritis associated with psoriasis.
Spondyloarthropathies: chronic inflammatory disease that affect sacroiliac joints and axial skeleton. Seronegative (Rheumatoid Factor -ve) and associated with HLA B27.
SPINEACHE: sausage digits (dactylitis), psoriasis, inflammatory back pain, NSAIDs > good response, enthesitis (tendon/ligament insertion), arthritis, Crohn’s/colitis/CRP raised, HLA B27, eye (uveitis)

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67
Q

Describe the epidemiology of psoriatic arthritis

A

1 in 5 patients with psoriasis have psoriatic arthritis

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68
Q

Describe the aetiology of psoriatic arthritis

A

HLA B27, psoriasis

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69
Q

Describe the key presentations for psoriatic arthritis

A

Inflammatory joint pain, plaques of psoriasis (hidden – behind ears, under nails, scalp), onycholysis (separation of nail from nail bed), dactylitis (inflammation of finger), enthesitis (tendon/ligament insertion inflammation), nail pitting

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70
Q

Describe the clinical manifestations for psoriatic arthritis

A

Signs: Anterior uveitis, conjunctivitis, aortitis, amyloidosis
Symptoms: Joint pain and stiffness, reduced mobility

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71
Q

What is the gold standard investigation for psoriatic arthritis

A

Joint X-ray:
* erosion in distal interphalangeal joint and periarticular new bone formation.
* Osteolysis.
* Pencil-in-cup deformity (central erosions of bone beside the joints causing one to look hollow like a cup, and one to sit in the cup)
* Periostitis (periosteum inflammation causing thickened, irregular outline of bone)
* Ankylosis (joints fuse causing stiffness)
* Dactylitis (finger inflammation appears as soft tissue swelling)

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72
Q

Describe the first line investigations for psoriatic arthritis

A

CRP/ESR raised, joint x-ray, rheumatoid factor -ve, anti-CCG negative, joint aspiration negative for crystals or bacteria

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73
Q

What are the differential diagnosis for psoriatic arthritis

A

Reactive arthritis, rheumatoid arthritis, gout

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74
Q

Describe the management for psoriatic arthritis

A

1st line – NSAIDs for pain (naproxen, ibuprofen, indomethacin), intra-articular corticosteroid injection if severe
DMARDs (methotrexate, sulfasalazine, leflunomide), TNF inhibitor or monoclonal Ab (etanercept, adalimumab, infliximab), last resort – ustekinumab (Mab targeting IL 12 and 23)

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75
Q

Describe the complications for psoriatic arthritis

A

Arthritis mutilans (most severe psoriatic arthritis): occurs in phalanxes, osteolysis of bones around joints in digits > leads to progressive shortening > skin then folds as digit shortens > telescopic finger

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76
Q

Define reactive arthritis

A

Sterile inflammation of synovial membranes and tendons that occurs after exposure to certain GI or GU infections. Often monoarticular synovitis affecting single joint in lower limb (mc knee). Used to be called Reiter’s syndrome.
Spondyloarthropathies: chronic inflammatory disease that affect sacroiliac joints and axial skeleton. Seronegative (Rheumatoid Factor -ve) and associated with HLA B27.
SPINEACHE: sausage digits (dactylitis), psoriasis, inflammatory back pain, NSAIDs > good response, enthesitis (tendon/ligament insertion), arthritis, Crohn’s/colitis/CRP raised, HLA B27, eye (uveitis)

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77
Q

Describe the aetiology of reactive arthritis

A

Chlamydia trachomatis (most common), N. gonorrhoea
Gastroenteritis: campylobacter jejuni, salmonella enteritidis, shigella

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78
Q

Describe the risk factors of reactive arthritis

A

HLA B27 gene, male, preceding STI

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79
Q

Describe the pathophysiology of reactive arthritis

A

Immune-mediated syndrome triggered by recent infection

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80
Q

Describe the key presentations for reactive arthritis

A

1-4 weeks after infection. Asymmetrical oligoarthritis (joint swelling and stiffness in large joint e.g., knee). Painful swollen red and stiff joints. Dactylitis.
Classic triad: conjunctivitis, urethritis/balanitis (dermatitis of head of penis), arthritis (can’t see, can’t pee, can’t climb a tree)

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81
Q

Describe the clinical manifestations for reactive arthritis

A

Circinate balanitis (head of penis dermatitis), keratoderma blennorrhagicum (brown rash on foot)

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82
Q

What is the gold standard investigation for reactive arthritis

A

No GS. Joint aspiration MC+S to rule out organism in synovial fluid. Polarised light microscopy rules out crystal arthropathy

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83
Q

Describe the first line investigations for reactive arthritis

A

ESR and CRP raised, antinuclear antibodies negative, rheumatoid factor negative, x-ray (sacroiliitis or enthesopathy), joint aspiration negative (exclude septic arthritis and gout), stool cultures, urine dipstick

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84
Q

What are the differential diagnosis for reactive arthritis

A

Septic arthritis (painful red hot swollen joint + signs/Hx of infection), gout, ankylosing spondylitis, psoriatic arthritis

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85
Q

Describe the management for reactive arthritis

A

1st line – antibiotics and joint aspiration until septic arthritis is ruled out.
NSAIDs (naproxen, ibuprofen, indometacin), intra-articular corticosteroid injection, DMARDs (sulfasalazine) or TNF inhibitors in chronic arthritis

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86
Q

What are the complications for reactive arthritis

A

Secondary osteoarthritis, iritis/uveitis, keratoderma blennorrhagicum

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87
Q

Define septic arthritis

A

Infection of 1 or more joints caused by pathogenic inoculation of microbes – via direct inoculation or haematogenous spread. Medical emergency

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88
Q

Describe the aetiology of septic arthritis

A

Staphylococci (most common), streptococci, N. Gonorrhoea, E. coli/pseudomonas (IVDU)

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89
Q

Describe the risk factors for septic arthritis

A

Pre-existing joint disease (OA/RA), IVDU, joint prosthesis, immunosuppression, alcohol misuse, diabetes, intra-articular corticosteroid injection, recent joint surgery

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90
Q

Describe the pathophysiology of septic arthritis

A

Organism spreads to the joint via blood or through direct entry to the joint. Synovium has little defence against infection. Inflammation of the joint increases pressure and reduces blood flow within the joint, damaging the joint.

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91
Q

Describe the key presentations for septic arthritis

A

Acutely hot, swollen, painful, restricted joint. Onset < 2 weeks. Fever. Knee most common joint. Stiffness and reduced range of motion

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92
Q

Describe the clinical manifestations for septic arthritis

A

Fever, lethargy, sepsis (tachycardia, hypotension, cold, clammy, shaking)

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93
Q

What is the gold standard investigation for septic arthritis

A

Joint aspiration MC+S (ID organism)

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94
Q

What are the differential diagnosis for septic arthritis

A

Reactive arthritis (sterile, crystal free joint), gout (sterile, -ve birefringent needle crystals), pseudogout (+ve birefringent rhomboid crystals)

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95
Q

Describe the management for septic arthritis

A

Aspirate joint (drainage) then empirical antibiotic.
Pathogen-directed Abx e.g., flucloxacillin (gram -ve; E.coli/pseudomonas), vancomycin (MRSA, s. aureus), IM ceftriaxone + azithromycin (N. gonorrhoea).
NSAIDs for analgesia. If on steroids, double dose while infected

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96
Q

Describe the complications for septic arthritis

A

Osteomyelitis, joint destruction

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97
Q

Define systemic lupus erythmatosus

A

SLE is an inflammatory autoimmune connective tissue disorder, affecting multiple organs

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98
Q

Describe the epidemiology of SLE

A

Young Afro-Caribbean women

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99
Q

Describe the risk factors for SLE

A

Female, drugs (isoniazid), HLA link

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100
Q

Describe the pathophysiology for SLE

A

Anti-nuclear antibodies are antibodies which attack proteins in the person’s cell nucleus. This generates an inflammatory response and damage.

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101
Q

Describe the key presentations for SLE

A

Photosensitive red malar butterfly rash, glomerulonephritis (nephritic), arthralgia, fatigue, fever, hair loss, mouth ulcers, lymphadenopathy

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102
Q

Describe the clinical manifestations for SLE

A

Signs: Butterfly rash, ulnar deviation, mouth ulcers, anaemia, Raynaud’s, lymphadenopathy and splenomegaly, pleuritic chest pain, hair loss, seizures and psychosis
Symptoms: Weight loss, fever, fever, joint pain, myalgia, shortness of breath

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103
Q

What is the gold standard investigation for SLE

A

Antinuclear antibodies (ANA)and clinical diagnosis

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104
Q

Describe the first line investigations for SLE

A

FBC (anaemia, leukopenia, thrombocytopenia), Normal CRP, raised ESR, raised urea and creatinine, urine protein:creatinine (proteinuria)
urine dipstick (haematuria, proteinuria)
anti-nuclear (ANA) and anti-double-stranded DNA (aDsDNA) antibodies present

Other: Renal USS (for nephritis)

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105
Q

What are the differential diagnosis for SLE

A

Rheumatoid arthritis, antiphospholipid syndrome, HIV, glomerulonephritis

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106
Q

Describe the management for SLE

A

1st line – Hydroxychloroquine (anti-malarials)
Consider: NSAIDs, corticosteroid, immunosuppressant (methotrexate), biologics (rituximab)

107
Q

What are the complications for SLE

A

Cardiovascular disease, infection, pericarditis, pleuritis, interstitial lung disease, anaemia

108
Q

Define primary bone tumours

A

Sarcomas are cancers originating in muscle, bone, and other connective tissues. The main bone cancers are: osteosarcoma, chondrosarcoma, Ewing sarcoma

109
Q

Describe the epidemiology of primary bone tumours

A

Osteosarcoma most common primary tumour (10-20yo), commonly long bones

110
Q

Describe the aetiology of primary bone tumours

A

Mutation. Primary – osteosarcoma, chondrosarcoma (cartilage), Ewing sarcoma (bone and soft tissue), fibrosarcoma
Secondary (most common) – prostate, thyroid, lung, breast, kidney

111
Q

Describe the risk factors for primary bone tumours

A

Previous radiotherapy, previous cancer, Paget’s disease, benign bone lesions

112
Q

Describe the pathophysiology of primary bone tumours

A

Tumours which metastasise to bone: PROSTATE, THYROID, LUNG, BREAST, KIDNEY

KPBLT

113
Q

Describe the key presentations for primary bone tumours

A

Bone pain: worse at night, constant or intermittent, resistant to analgesia, may increase in intensity.
Atypical bony or soft tissue swelling/masses, pathological fractures, mobility issues (unexplained limp, joint stiffness, reduced motion), inflammation and tenderness over bone

114
Q

Describe the clinical manifestations for primary bone tumours

A

Cancer symptoms: weight loss, fever, fatigue, easy bruising, malaise

115
Q

What is the gold standard investigation for primary bone tumours

A

Bone biopsy

116
Q

Describe the first line investigations for primary bone tumours

A

1st line X-ray (osteosarcoma – sunburst appearance), bloods – FBC, raised ESR, ALP, lactate dehydrogenase, Ca, U&E.

Other: CT chest/abdomen/pelvis

117
Q

What are the differential diagnosis for primary bone tumours

A

Secondary bone tumours

118
Q

Describe the management for primary bone tumours

A

1st line – chemo, radiotherapy, surgery (limb sparing or amputation). Bisphosphonates

119
Q

Define fibromyalgia

A

Chronic pain syndrome characterised by widespread pain in body for 3+ months in addition to tenderness in 11 of 18 designated sites.

120
Q

Describe the risk factors for fibromyalgia

A

Women, low socioeconomic status, 20-50 yo, stress, depressed

121
Q

Describe the pathophysiology of fibromyalgia

A

Abnormal pain processing and signalling

122
Q

Describe the key presentations for fibromyalgia

A

Widespread chronic body pain and tenderness, insomnia, morning stiffness (back and neck)

123
Q

Describe the clinical manifestations for fibromyalgia

A

Fatigue, confusion, pain, morning stiffness

124
Q

Describe the first line investigations for fibromyalgia

A

1st line Clinical diagnosis: 11 tender points in 18 sites (9 pairs R+L).
No serology or inflammatory markers

125
Q

Describe the differential diagnosis for fibromyalgia

A

Polymyalgia rheumatica (chronic pain syndrome, Dx = raised CRP/ESR), osteoarthritis, rheumatoid arthritis

126
Q

Describe the management for fibromyalgia

A

1st line – tricyclic antidepressants, e.g., amitriptyline. Serotonin-noradrenaline reuptake inhibitors SNRIs, e.g., duloxetine. Gabapentinoids, e.g., pregabalin
Non-pharmacological: exercise, relaxation, CBT
Analgesia (naproxen, tramadol)

127
Q

Describe the complications for fibromyalgia

A

Poor quality of life, anxiety, depression, insomnia, opiate addiction

128
Q

Describe mechanical lower back pain and vertebral disc degeneration

A

Discogenic low back pain is a multi-factorial condition characterised by lower back pain and degenerative intervertebral disc disease. Mechanical back pain means it isn’t caused by a specific disease. Lumbar spondylosis is degeneration of intervertebral disc

129
Q

Describe the aetiology of mechanical lower back pain and vertebral disc degeneration

A

Trauma/work, muscle/ligament sprain, myeloma (elderly), spinal cord decompression (neuropathic pain), intervertebral disc degeneration (lumbar spondylosis), arthritis

130
Q

Describe the pathophysiology of mechanical lower back pain and vertebral disc degeneration

A

Vertebral disc degeneration: loses its compliance and thins over time. Usually L5/S1 or L4/L5

131
Q

Describe the key presentations for mechanical lower back pain and vertebral disc degeneration

A

Chronic lower back pain, movement restriction, neurological deficit (leg weakness, sensory loss, bladder and bowel symptoms)

132
Q

Describe the first line investigations for mechanical lower back pain and vertebral disc degeneration

A

SOCRATES, clinical examination, x-ray if serious pathology suspected, e.g., myeloma, neuropathic pain. MRI

133
Q

Describe the management for mechanical lower back pain and vertebral disc degeneration

A

Analgesia (1st line NSAIDs), education, exercise, physiotherapy

134
Q

Define osteomalacia

A

Poor bone mineralisation leading to soft bone due to lack of Ca2+. In adults
Rickets: inadequate mineralisation of the bone and epiphyseal cartilage in the growing skeleton of children

135
Q

Describe the aetiology of osteomalacia

A

Hyperparathyroidism – increased Ca2+ release from bone so less for mineralisation due to low Vit D
Vitamin D deficiency – malabsorption/reduced intake/poor sunlight.
CKD/renal failure – decreased active vitamin D production (25-hydroxyvit D > 1,25-dihydroxyvit D)
Liver failure – decreased reaction in vitamin D pathway (cholecalciferol > 25-hydroxyvitamin D)
Anticonvulsant drugs – increased CYP450 metabolism of vitamin D

136
Q

Describe the pathophysiology of osteomalacia

A

Calcium deficiency due to lack of vitamin D. vitamin D increased Ca2+ absorption from gut and reabsorption from kidney PCT
7-dehydrocholesterol converted by UVB to cholecalciferol (vitamin D3). > 25-hydroxyvitamin D in the liver. > 1,25-dihydroxyvitamin D in kidneys (active vitamin D) > bone, GIT, PCT kidney

137
Q

Describe the key presentations for osteomalacia

A

Osteomalacia: bone pain and tenderness. Dull ache, worse on weight-bearing exercises. Fractures (esp neck of femur), muscle weakness (waddling gait, difficulty with stairs)
Rickets: growth retardation, hypotonia, knock-kneed, bow-legged

138
Q

Describe the clinical manifestations for osteomalacia

A

Fatigue, bone pain, muscle weakness and aches

139
Q

What is the gold standard investigation for osteomalacia

A

bone biopsy (incomplete mineralisation)

140
Q

Describe the first line investigations for osteomalacia

A

X-ray (loss of cortical bone – defective mineralisation, looser zone), U&E (low calcium and phosphate), raised PTH, low serum 25-hydroxyvitamin D (<25 nmol/L = deficiency)

141
Q

Describe the management for osteomalacia

A

1st line - Vitamin D supplements (cholecalciferol)
Calcium supplements

142
Q

Define Paget’s disease of bone

A

Disorder of bone turnover. Areas of patchy bone due to excessive osteoclast and osteoblast activity. Leads to areas of sclerosis and lysis.

143
Q

Describe the aetiology of Paget’s disease

A

Idiopathic

144
Q

Describe the risk factors for Paget’s disease

A

Females 40+

145
Q

Describe the pathophysiology of Paget’s disease

A

Excessive bone turnover (formation and reabsorption) due to excessive activity of osteoclasts and osteoblasts. The excessive turnover is not coordinated, leading to patchy areas of high density (sclerosis) and low density (lysis). This results in enlarged and misshapen bones with structural problems that increase the change of pathological fractures.

146
Q

Describe the key presentations of Paget’s disease

A

Bone pain, bone deformity (bowed tibia and skull), fractures, hearing loss (if bones of ear are affected)

147
Q

What is the gold standard investigation for Paget’s disease

A

X-ray of bones

148
Q

Describe the first line investigations for Paget’s disease

A

x-ray (bone enlargement + deformity, osteoporosis circumscripta – well defined osteolytic lesions, cotton wool appearance of skull – poorly defined areas of sclerosis and lysis, V-shaped defects in long bones)
urinary hydroxyproline (protein constituent of collagen)
bloods: raised ALP, normal calcium and phosphate

149
Q

Describe the management for Paget’s disease

A

1st line – Bisphosphonates
NSAIDs for pain, calcium + vit D supplements

150
Q

Describe the complications for Paget’s disease

A

Osteosarcoma, spinal stenosis and cord compression, deafness (CN8 nerve compression), hydrocephalus (sylvian aqueduct blockage)

151
Q

Define Marfan’s syndrome

A

Connective tissue disorder. Autosomal dominant condition affecting the gene responsible for fibrillin production, an important component of connective tissue.

152
Q

Describe the aetiology of Marfan syndrome

A

Autosomal dominant condition

153
Q

Describe the risk factors for Marfan syndrome

A

Family history

154
Q

Describe the key presentations for Marfan syndrome

A

Tall stature, long limbs, long fingers (arachnodactyly), hypermobility, pectus carinatum (breastbone juts out of chest)/pectus excavatum (breastbone sunken in chest), high arch palate, heart murmur/aortic complications

155
Q

What is the gold standard investigation for Marfan syndrome

A

Genetic testing

156
Q

Describe the first line investigations for Marfan syndrome

A

Physical exam, Echocardiogram, MRI, eye exam. Ghent criteria:
MAJOR: enlarged aorta, lens dislocation, FHx, at least 4 skeletal problems
MINOR: myopia (near-sighted), loose joints, high arched palate

157
Q

Describe the differential diagnosis for Marfan syndrome

A

Aortic dissection, bicuspid aortic valve, Ehlers-Danlos syndrome

158
Q

Describe the management for Marfan syndrome

A

Lifestyle - avoid intense exercise, avoid caffeine
Medication – beta blockers, angiotensin receptor blockers
Surgery: aortic dissection, lens correction, bone problems.
Yearly echocardiogram, ophthalmologist

159
Q

Describe the complications for Marfan syndrome

A

Mitral/aortic valve prolapse with regurgitation, aortic aneurysms, aortic dissection, lens dislocation, GORD, pneumothorax, scoliosis

160
Q

Define Ehlers-Danlos syndrome

A

Group of inherited connective tissue disorders causing defects in collagen, resulting in hypermobility of joints and abnormalities in connective tissue

161
Q

Describe the aetiology of Ehlers-Danlos syndrome

A

Autosomal dominant mutation

162
Q

Describe the risk factors for Ehler-Danlos syndrome

A

Family history

163
Q

Describe the pathophysiology of Ehlers-Danlos syndrome

A

Hypermobile EDS (most common) > joint hypermobility, soft, stretchy skin
Classical EDS > stretchy skin (smooth, velvety to touch), joint hypermobility, joint pain, abnormal wound healing
Vascular EDS > vascular abnormalities, prone to rupture

164
Q

Describe the key presentations for Ehlers-Danlos syndrome

A

Joint hypermobility, easily stretched skin (hyperextensibility), easy bruising, chronic joint pain, re-occurring dislocations, cardiovascular complications (mitral regurg, AAA, dissection)

165
Q

What is the gold standard investigation for Ehlers-Danlos syndrome

A

Physical exam, Beighton score to assess hypermobility (touch ground with straight legs, elbows/knees/little finger hyperextend, thumb bend to touch forearm), collagen mutations

166
Q

Describe the differential diagnosis for Ehlers-Danlos syndrome

A

Marfan syndrome

167
Q

Describe the management for Ehlers-Danlos syndrome

A

No cure, focus on maintaining healthy joints: physiotherapy, occupational therapy, psychological support (chronic pain)

168
Q

Describe the complications for Ehlers-Danlos syndrome

A

Classical EDS: hernias, prolapse, valve/aortic problems (regurgitation, AAA, dissection), joint pain, abnormal wound healing
Vascular EDS: skin, internal organs, blood vessels prone to rupture

169
Q

Define antiphospholipid syndrome

A

Disorder associated with antiphospholipid antibodies where blood becomes prone to clotting = hypercoagulable state. Main associations are thrombosis and miscarriage

170
Q

Describe the aetiology of antiphospholipid syndrome

A

Primary – idiopathic. Secondary – autoimmune condition e.g., SLE

171
Q

Describe the risk factors for antiphospholipid syndrome

A

Young female, diabetes, hypertension, obesity, autoimmune condition, smoking, oestrogen therapy

172
Q

Describe the pathophysiology of antiphospholipid syndrome

A

Autoimmune condition where abnormal proteins, antiphospholipid antibodies are made in the blood, making it prone to clotting. This causes abnormal flow and clotting in veins and arteries which leads to thrombosis and pregnancy complications – miscarriage.

173
Q

Describe the key presentations for antiphospholipid syndrome

A

Thrombosis, recurrent miscarriages, livedo reticularis (purple discolouration of skin), thrombocytopenia

174
Q

What is the gold standard investigation for antiphospholipid syndrome

A

Hx of thrombosis/pregnancy complications + serology:
Anticardiolipin antibodies
Lupus anticoagulant
Anti-beta-2 glycoprotein 1 antibodies

175
Q

Describe the management for antiphospholipid syndrome

A

Long term warfarin (INR range 2-3)
Pregnant: LMWH (enoxaparin) + aspirin

176
Q

Describe the complications for antiphospholipid syndrome

A

Venous thromboembolisms (DVT, PE), arterial thromboembolism (stroke, MI, renal thrombosis), pregnancy complications (miscarriage, pre-eclampsia)

177
Q

Define dermatomyositis/polymyositis

A

Autoimmune disorders causing inflammation of muscles. Polymyositis = chronic inflammation of muscles. Dermatomyositis = connective tissue disorder with inflammation of muscles and skin

178
Q

Describe the aetiology of dermatomyositis/polymyositis

A

Autoimmune. Also caused by malignancy – lung, breast, ovarian, gastric (paraneoplastic syndromes)

179
Q

Describe the risk factors for dermatomyositis/polymyositis

A

Females, genetic link

180
Q

Describe the key presentations for dermatomyositis/polymyositis

A

Symmetrical wasting of muscles of shoulder and pelvic girdle.
Dermatomyositis = gottron lesions (scaly erythematous patches) on knuckles, elbows, and knees. Purple rash on face and eyelids. Photosensitive erythematous rash on back, shoulders and neck. Periorbital oedema. Subcutaneous calcinosis

181
Q

Describe the clinical manifestations for dermatomyositis/polymyositis

A

Muscle pain, fatigue, weakness. Hard to stand from sitting, to squat, to put hand on top of head

182
Q

What is the gold standard investigation for dermatomyositis/polymyositis

A

Muscle fibre biopsy – inflammation, necrosis

183
Q

Describe the first line investigations for dermatomyositis/polymyositis

A

Lactate dehydrogenase raised, AST and ALT raised, myoglobin raised, creatinine kinase raised (>1000 U/L. Normal = <300.)
Serology: anti-Jo-1 (polymyositis), anti Mi2 (dermatomyositis), anti-nuclear antibodies (dermatomyositis). Electromyograph

184
Q

Describe the differential diagnosis for dermatomyositis/polymyositis

A

Rhabdomyolysis, myasthenia gravis, muscular dystrophy

185
Q

Describe the management for dermatomyositis/polymyositis

A

1st line – prednisolone. Also, IV immunoglobulin
2nd line – immunosuppressant (methotrexate, azathioprine)
3rd line – rituximab or cyclophosphamide

186
Q

Describe the complications for dermatomyositis/polymyositis

A

Corticosteroid complications

187
Q

Define enteropathic arthritis/ IBD associated arthritis

A

Spondylarthritis and peripheral arthritis due to inflammatory bowel disease – ulcerative colitis, Crohn’s

188
Q

Describe the aetiology of enteropathic arthritis

A

HLA B27, ulcerative colitis, Crohn’s disease

189
Q

Describe the pathophysiology of enteropathic arthritis

A

Mainly affects peripheral joints, especially lower limbs

190
Q

Describe the key presentations of enteropathic arthritis

A

Abdominal pain, diarrhoea, blood in stool, weight loss.
Bony deformity, painful red hot swollen joints. Stiffness and reduced motion. SPINEACHE

191
Q

What is the gold standard investigation for enteropathic arthritis

A

Clinical diagnosis + symptoms + medical history

192
Q

Describe the first line investigations for enteropathic arthritis

A

Joint aspiration, stool culture, colonoscopy and biopsy, faecal-calprotectin raised, FBC (anaemia – malabsorption, raised WCC), CRP/ESR raised, joint x-ray

193
Q

Describe the differential diagnosis for enteropathic arthritis

A

Ulcerative colitis, Crohn’s, ankylosing spondylitis, reactive arthritis, psoriatic arthritis

194
Q

Describe the management for enteropathic arthritis

A

DMARDs (methotrexate, leflunomide, sulfasalazine), NSAIDs (naproxen, ibuprofen, indomethacin), TNF inhibitors (etanercept, infliximab)
Treat ulcerative colitis/Crohn’s disease

195
Q

Define giant cell arteritis

A

Vasculitis is a group of diseases causing inflammation of blood vessels. Giant cell arteritis affects large blood vessels

196
Q

Describe the aetiology of giant cell arteritis

A

Autoimmune attacking of blood vessels

197
Q

Describe the risk factors for giant cell arteritis

A

Over 50 y.o, northern European, females, Hx of polymyalgia rheumatica

198
Q

Describe the pathophysiology of giant cell arteritis

A

Affects aorta and/or its major branches (carotid and vertebral arteries). Temporal artery often involved > temporal arteritis

199
Q

Describe the key presentations of giant cell arteritis

A

Headache (new onset, unilateral over temporal area), scalp tenderness (hurts to brush hair), jaw claudication, visual disturbances (blurred, diplopia, amaurosis fugax – transient vision loss, blindness), thickened temporal arteries and weak pulses

200
Q

Describe the clinical manifestations for giant cell arteritis

A

Malaise, fatigue, weight loss, fever, aching and stiffness

201
Q

What is the gold standard investigation for giant cell arteritis

A

Temporal artery biopsy (shows giant cells, granulomatous inflammation – patchy lesions therefore take big sample)

202
Q

Describe the first line investigations for giant cell arteritis

A

Raised CRP, Raised ESR >50mm/hr. FBC (anaemia), LFT/RFT may be abnormal
Halo sign (wall thickening) on vascular ultrasonography of temporal and axillary artery

203
Q

Describe the differential diagnosis for giant cell arteritis

A

Large vessel vasculitis: Takayasu’s arteritis (Asian women, mainly affects aortic arch, Px: pulseless disease, arm claudication, syncope. GS = CT angiography)
Polymyalgia rheumatica, rheumatic arthritis

204
Q

Describe the management for giant cell arteritis

A

1st line – high dose corticosteroid (e.g., prednisolone 40-60mg)
Consider: tocilizumab, methotrexate. Amaurosis fugax – high dose IV methylprednisolone.

205
Q

Describe the complications for giant cell arteritis

A

Blindness (permanent if not given high dose IV methylprednisolone), irreversible neuropathy, large vessel stenosis

206
Q

Define osteomyelitis

A

Inflammatory condition of bone and bone marrow caused by an infectious organism, most commonly staph aureus. Spread via haematogenous spread or direct contamination of joint.

207
Q

Describe the epidemiology of osteomyelitis

A

Mainly children. Children = haematogenous spread most common. Adults = direct infection

208
Q

Describe the aetiology of osteomyelitis

A

Staphylococci aureus, salmonella in sickle cell patients

209
Q

Describe the risk factors for osteomyelitis

A

Previous osteomyelitis, penetrating injury, IVDU, diabetes (diabetic foot ulcers), HIV, recent surgery, infection, sickle cell, rheumatoid arthritis, chronic kidney disease, children (upper respiratory tract or varicella infection)

210
Q

Describe the pathophysiology for osteomyelitis

A

Direct inoculation/local spread/haematogenous > acute bone diagnosis = inflammation and bone oedema. Chronic bone diagnosis (complication) = sequestra (necrotic bone embedded in pus), involucrum (thick sclerotic bone placed around sequestra to compensate for support)

211
Q

Describe the key presentations for osteomyelitis

A

Acute = Limp or reluctance to weight-bear (children), hot, erythema and swollen joint, dull non-specific pain at site of infection, bone oedema
Chronic = sequestra (deep ulcers - necrotic bone embedded in pus)

212
Q

Describe the clinical manifestations for osteomyelitis

A

low grade fever, malaise, fatigue, muscle aches

213
Q

What is the gold standard investigation for osteomyelitis

A

Bone marrow biopsy and culture (identify organism)

214
Q

Describe the first line investigations for osteomyelitis

A

FBC – raised WCC, raised CRP/ESR, blood culture MC+S, x-ray (osteopenia - thinning, periosteal reaction – changes to bone surface, destruction of bone), MRI (bone marrow oedema)

215
Q

Describe the differential diagnosis for osteomyelitis

A

Charcot joint (damage to sensory nerves due to diabetic neuropathy, causes progressive degeneration of weight-bearing joint)
Tuberculosis osteomyelitis (bone marrow biopsy – caseating granuloma +ve), septic arthritis, reactive arthritis

216
Q

Describe the management for osteomyelitis

A

1st line – immobilise and antibiotics: vancomycin (MRSA, S. aureus), fusidic acid (S. aureus), flucloxacillin (salmonella)
Supportive therapy and surgical removal of necrotic bone

217
Q

Describe the complications for osteomyelitis

A

Chronic osteomyelitis, fracture, amputation

218
Q

Define polyarteritis nodosa

A

Vasculitis is inflammation of blood vessels. Polyarteritis nodosa affects medium blood vessels.

219
Q

Describe the epidemiology of polyarteritis nodosa

A

Associated with Hep B, developing countries

220
Q

Describe the aetiology of polyarteritis nodosa

A

Autoimmune

221
Q

Describe the pathophysiology of polyarteritis nodosa

A

Affects skins, kidney, GI tract and heart

222
Q

Describe the key presentations for polyarteritis nodosa

A

Peripheral neuropathy (mononeuritis multiplex – ischaemia of vasa nervorum), cutaneous/SC nodules, abdominal pain, unilateral orchitis (testicle inflammation), livedo reticularis (mottled, purple lace rash), AKI/CKD, hypertension

223
Q

Describe the clinical manifestations for polyarteritis nodosa

A

Malaise, fatigue, weight loss and fever

224
Q

What is the gold standard investigation for polyarteritis nodosa

A

Biopsy e.g. kidney (transmural fibrinoid necrosis)

225
Q

Describe the first line investigations for polyarteritis nodosa

A

Raised ESR, raised CRP, HBsAg (Hep B antigen), CT angiogram (beaded appearance – aneurysms)

226
Q

Describe the differential diagnosis for polyarteritis nodosa

A

Medium vessel vasculitis: Kawasaki disease (children, strawberry tongue, causes coronary artery aneurysm), eosinophilic granulomatosis with polyangiitis (Churg-Strauss – pANCA positive)

227
Q

Describe the management for polyarteritis nodosa

A

Hep B negative: corticosteroids and cyclophosphamide (DMARDs)
Hep B positive: antiviral agent, plasma exchange and corticosteroids

228
Q

Describe the complications for polyarteritis nodosa

A

GI perforation and haemorrhages, arthritis, renal infarcts, stroke, MI

229
Q

Define polymyalgia rheumatica

A

Inflammatory condition causing pain and stiffness in shoulders, pelvic girdle, and neck. Large cell vasculitis presenting as chronic pain syndrome. Affects joints and muscles

230
Q

Describe the epidemiology for polymyalgia rheumatica

A

Females, always 50+, associated with giant cell arteritis

231
Q

Describe the key presentations for polymyalgia rheumatica

A

Shoulder pain radiating to elbow, pelvic girdle pain, worse with movement, insomnia, morning stiffness >45 mins, rapid response to corticosteroids

232
Q

What is the gold standard investigation for polymyalgia rheumatica

A

Clinical presentation, Raised ESR and CRP, and response to steroids

233
Q

What are the further investigations for polymyalgia rheumatica

A

Temporal artery biopsy may show giant cell arteritis, FBC (anaemia of chronic disease)

234
Q

Describe the differential diagnosis for polymyalgia rheumatica

A

Fibromyalgia, giant cell arteritis, osteoarthritis, rheumatoid arthritis

235
Q

Describe the management for polymyalgia rheumatica

A

1st line – oral prednisolone

236
Q

Define scleroderma

A

Systemic sclerosis in which normal tissue is replaced with thick dense connective tissue. It affects skin, blood vessels and internal organs. 2 types: limited cutaneous systemic sclerosis (CREST syndrome) and diffuse cutaneous systemic sclerosis.

237
Q

Describe the aetiology of scleroderma

A

Autoimmune antibodies attacking connective tissue

238
Q

Describe the risk factors for scleroderma

A

Women 30-50yo, family history, exposure to environmental substances and toxins (silica dust, solvents)

239
Q

Describe the pathophysiology of scleroderma

A

Autoimmune response involving endothelial damage, inflammation and fibrosis

240
Q

Describe the key presentations for scleroma

A

CREST:
Calcinosis (calcified nodules under skin),
Raynaud’s phenomenon,
Esophageal dysmotility (strictures, food gets stuck on swallowing),
Sclerodactyly (tightening and thickening of skin over fingers distal to MCP joint),
Telangiectasia (prominent dilated capillaries, especially on cheeks)

241
Q

Describe the clinical manifestations for scleroderma

A

Signs: Coronary artery disease, pulmonary hypertension, pulmonary fibrosis, GORD, kidney failure
Symptoms: Swelling of hands and feet, finger pits/ulcers, fatigue, skin thickening and stiffening, myalgia, fatigue

242
Q

What is the gold standard investigation for scleroderma

A

Anti centromere antibodies (limited/CREST), Anti-SCL70 (diffuse)

243
Q

What are the first line investigations for scleroderma

A

Antinuclear antibodies maybe present - Anti-centromere antibodies present, anti-SCL70.

Other FBC, U&E, CRP normal. pulmonary function tests

244
Q

Describe the management for scleroderma

A

No treatment. Immunosuppressants to slow progression.
Treat symptoms: analgesia, CCB for Raynaud’s, PPI for oesophageal reflux, topical emollient, ACEi for kidneys

245
Q

Describe the complications for scleroderma

A

Malabsorption, pulmonary artery hypertension, hypothyroidism, kidney failure

246
Q

Define Sjogren’s syndrome

A

Autoimmune condition affecting exocrine glands causing dry mucous membranes

247
Q

Describe the aetiology for Sjogren’s syndrome

A

Autoimmune.
Primary – exists by itself. Secondary – complication of SLE with rheumatoid arthritis

248
Q

Describe the risk factors for Sjogren’s syndrome

A

Family history, female, 40+ yo

249
Q

Describe the key presentations for Sjogren’s syndrome

A

Dry mucous membranes – dry mouth (xerostomia), dry eyes (keratoconjunctivitis sicca), dry vagina

250
Q

What is the gold standard investigation for Sjogren’s syndrome

A

Anti-Ro and anti-La antibodies

251
Q

Describe the first line investigations for Sjogren’s syndrome

A

Anti-Ro and anti-La antibodies. Schirmer test – tears travelling <10mm (>15mm is normal)

252
Q

Describe the differential diagnosis for Sjogren’s syndrome

A

Systemic lupus erythematosus, systemic sclerosis, rheumatoid arthritis

253
Q

Describe the management for Sjogren’s syndrome

A

1st line – artificial tears, artificial saliva, vaginal lubricant.
Hydroxychloroquine used to halt progression

254
Q

Describe the complications for Sjogren’s syndrome

A

Eye infections (conjunctivitis, corneal ulcers), oral problems (candida infection, dental cavities), vaginal problems (candidiasis, sexual dysfunction). Lymphomas

255
Q

Define Wegener’s granulomatosis (granulomatosis with polyangitis)

A

Vasculitis is inflammation of blood vessels. Wegener’s granulomatosis affects small blood vessels.

256
Q

Describe the aetiology for Wegener’s granulomatosis

A

Autoimmune

257
Q

Describe the risk factors for Wegener’s granulomatosis

A

Young adult

258
Q

Describe the pathophysiology for Wegener’s granulomatosis

A

Small vessel vasculitis affecting ENT, lungs and kidneys

259
Q

Describe the key presentations for Wegener’s granulomatosis

A

ENT: Saddle shaped nose due to perforated nasal septum, epistaxis, crusty nasal/ear secretions > hearing loss, sinusitis,
Lungs: Cough, wheeze, haemoptysis, dyspnoea
Kidneys: glomerulonephritis > haematuria

260
Q

Describe the clinical manifestations for Wegener’s granulomatosis

A

Malaise, fatigue, weight loss, fever, night sweats

261
Q

What is the gold standard investigation for Wegener’s granulomatosis

A

cANCA positive and symptoms

262
Q

Describe the first line investigations for Wegener’s granulomatosis

A

FBC: raised eosinophils, raised CRP/ESR, tissue biopsy shows granulomas, CT chest shows lung nodules, urinalysis (haematuria), ANCA positive

263
Q

Describe the differential diagnosis for Wegener’s granulomatosis

A

Small vessel vasculitis: Henoch-Schoenlein purpura (IgA deposits, purpura, joint pain, abdo pain, renal involvement), microscopic polyangiitis (pANCA +ve), eosinophilic granulomatosis with polyangiitis (Churg-Strauss – asthma, pANCA positive, raised eosinophils)

264
Q

Describe the management for Wegener’s granulomatosis

A

Corticosteroids (methylprednisolone and prednisolone) and immunosuppression (rituximab, cyclophosphamide). Plasmapheresis, IV immunoglobulin.

265
Q

Describe the complications for Wegener’s granulomatosis

A

Glomerulonephritis, deafness, chronic renal failure

Conditions (9 decks)

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