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Phase 2a > Musculoskeletal/Rheumatology > Flashcards

Musculoskeletal/Rheumatology Flashcards

1
Q

Give 3 causes of inflammatory joint pain.

A
  1. Autoimmune disease, e.g. RA, vasculitis, connective tissue disease
  2. Crystal arthritis
  3. Infection
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2
Q

Give 2 causes of non-inflammatory joint pain.

A
  1. Degenerative, e.g. osteoarthritis.
  2. Non-degenerative, e.g. fibromyalgia
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3
Q

What are the 5 cardinal signs of inflammation?

A
  1. Rubor (redness)
  2. Calor (heat)
  3. Dolor (pain)
  4. Tumor (swelling)
  5. Loss of function
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4
Q

How does inflammatory pain differ from degenerative non-inflammatory pain? Are you more likely to see swelling in inflammatory or degenerative pain?

A
  • Inflammatory pain tends to ease with use whereas degenerative pain increased with use
  • In inflammatory pain you are likely to see synovial swelling. There is often no swelling in degenerative pain
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5
Q

Name 2 inflammatory markers that can be detected in blood tests.

A
  1. ESR (erythrocyte sedimentation rate)
  2. CRP
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6
Q

Explain why ESR levels are raised in someone with inflammatory joint pain.

A

Inflammation leads to increased fibrinogen which means the RBC’s clump together. The RBC’s therefore fall faster and so you have an increased ESR

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7
Q

Explain why CRP levels are raised in someone with inflammatory joint pain.

A

Inflammation leads to increased levels of IL-6. CRP is produced by the liver in response to IL-6 and therefore is raised

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8
Q

What is vasculitis? How is vasculitides categorised? Name some diseases in each category.

A
  • Vasculitis = group of autoimmune diseases that cause inflammation of blood vessels
  • Vasculitides can be categorised blood vessel size: small, medium, large
  • Large vessel vasculitis: Giant cell arteritis, Takayasu’s arteritis
  • Medium vessel vasculitis: Polyarteritis nodosa, Kawasaki disease
  • Small vessel vasculitis: Henoch-Schonlein purpura, Granulomatosis with polyangiitis (Wegener’s granulomatosis)
  • EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS CAN BE SMALL OR MEDIUM VESSEL VASCULITIS
  • Variable vessel vasculitis = Behcet’s disease
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9
Q

What is the pathophysiology of Giant cell arteritis?

A
  • Affects aorta and/or its major branches (carotid and vertebral branches)
  • Temporal artery often involved (temporal arteritis)
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10
Q

What are the risk factors for Giant cell arteritis?

A
  • Almost exclusively in >50 year olds
  • Northern European
  • Female
  • Hx of polymyalgia rheumatica
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11
Q

What is the clinical presentation of Giant cell arteritis?

A
  • HEADACHE - new onset, typically unilateral over temporal area
  • Scalp tenderness
  • Jaw claudication
  • Visual disturbances: blurred vision, diplopia
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12
Q

What are the investigations for Giant cell arteritis?

A
  • Increased ESR and/or CRP (=highly sensitive) ESR >50mm/hr
  • Halo sign on ultrasound of temporal and axillary artery
  • TEMPORAL ARTERY BIOPSY = GOLD STANDARD (show multinucleate giant cells, granulomatous inflammation)
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13
Q

Describe the management for Giant cell arteritis.

A

High dose glucocorticoid ASAP - usually prednisolone 40-60mg

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14
Q

What are the complications of Giant cell arteritis?

A
  • Blindness
  • Irreversible neuropathy
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15
Q

What is the pathophysiology and epidemiology of Takayasu’s arteritis?

A
  • Pathophysiology: mainly affects aorta and its branches, also affects pulmonary branches
  • Epidemiology: <40 years, Asian, female
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16
Q

What is the clinical presentation of Takayasu’s arteritis?

A
  • PULSELESS DISEASE (difficulty in detecting peripheral pulse due to narrowing)
  • Arm claudication
  • Syncope
  • Non-specific symptoms: fever, malaise, muscle aches
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17
Q

What are the investigations for Takayasu’s disease?

A
  • CT angiography = GOLD STANDARD
  • Granulomatous inflammation on histology
  • Elevated ESR and CRP
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18
Q

Describe the management for Takayasu’s arteritis. What are the complications?

A
  • Management: prednisolone
  • Complications: aortic aneurysms
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19
Q

What is the epidemiology of Polyarteritis nodosa?

A
  • Associated with hepatitis B
  • More common in developing countries
  • Affects all ages, all racial groups, no sex predominance
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20
Q

What is the presentation of Polyarteritis nodosa?

A
  • CUTANEOUS/SUBCUTANEOUS NODULES (hallmark feature)
  • UNILATERAL ORCHITIS (characteristic feature)
  • Peripheral neuropathy - mononeuritis multiplex
  • Livedo reticularis
  • HTN
  • Abdominal pain
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21
Q

What are the investigations for Polyarteritis nodosa?

A
  • Increased ESR and/or CRP
  • HBsAg
  • Biopsy: shows transmural fibroid necrosis
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22
Q

Describe the management for Polyarteritis nodosa.

A
  • If Hep B negative - corticosteroids + cyclophosphamide
  • If Hep B positive - antiviral agent, plasma exchange and corticosteroids
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23
Q

What are the complications of Polyarteritis nodosa?

A
  • GI perforation and haemorrhages
  • Arthritis
  • Renal infarcts
  • Strokes
  • MI
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24
Q

What is the pathophysiology of Kawasaki disease?

A
  • Arteritis associated with mucocutaneous lymph nodes
  • Acute and self-limited
  • Usually affects coronary arteries
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25
Q

What are the risk factors for Kawasaki disease?

A
  • <5 years old
  • Males 1.5x more affected
  • More common in children of Japanese descent
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26
Q

What is the clinical presentation of Kawasaki disease?

A
  • Fever for >5 days
  • Non-purulent bilateral conjunctivitis
  • Strawberry tongue
  • Erythema + desquamation of palms and soles
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27
Q

What are the investigations for Kawasaki disease? Describe the management. What are the complications?

A
  • Investigations: increased ESR and/or CRP, echocardiogram
  • Management: aspirin and IV immunoglobulins
  • Complications: coronary artery aneurysm
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28
Q

What is the pathophysiology of Eosinophilic granulomatosis with polyangiitis (EGSA, or Churg-Strauss syndrome)? What is its epidemiology?

A
  • Pathophysiology: small and medium vasculitis, most associated with lung and skin problems (but can also affect kidneys)
  • Epidemiology: late teenage years, early adulthood
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29
Q

What is the clinical presentation of EGSA? What are the investigations? Describe the management.

A
  • Presentation: severe asthma, peripheral neuropathy, palpable purpura
  • Investigations: high eosinophils on FBC, diagnose with p-ANCA (MPO antibodies)
  • Management: inhaled corticosteroids - prednisone
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30
Q

What is the pathophysiology of Henoch-Schonlein purpura? What is its epidemiology?

A
  • IgA vasculitis
  • Due to IgA deposits in the blood vessels of affected organs such as skin, kidneys, GI tract
  • Often triggered by upper airway infection, e.g. tonsillitis or gastroenteritis
  • Epidemiology: < 10 years old
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31
Q

What is the clinical presentation of Henoch-Schonlein purpura?

A
  • Symmetrical purpuric rash affecting lower limbs or buttocks in children
  • Joint pain
  • Abdominal pain
  • Renal involvement (HTN)
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32
Q

What are the investigations for Henoch-Schonlein purpura?

A
  • Take BP (check for HTN)
  • Urinalysis (can see microscopic haematuria/proteinuria)
  • Perform abdominal exam (check for bowel obstruction)
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33
Q

Describe the management for Henoch-Schonlein purpura. What are its complications?

A
  • Supportive: simple analgesia, rest and plenty of fluids
  • Complications: IgA nephritis, INTUSSUSCEPTION, orchitis, arthralgia
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34
Q

What is the pathophysiology of Granulomatosis with polyangiitis? What are the risk factors?

A
  • Pathophysiology: small vessels vasculitis, affects respiratory tracts and kidney
  • Risk factors: late teenage years, early adulthood
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35
Q

What is the clinical presentation of Granulomatosis with polyangiitis?

A
  • CLASSIC SIGN ON EXAMS: SADDLE SHAPED NOSE
  • Epistaxis
  • Crusty nasal/ear secretions = hearing loss
  • Sinusitis
  • Cough, wheeze, haemoptysis
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36
Q

What are the investigations for Granulomatosis with polyangiitis?

A
  • High eosinophils on FBC
  • Histology shows granulomas
  • Presence of c-ANCA
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37
Q

Describe the management for Granulomatosis with polyangiitis. What are the complications?

A
  • (Nasal) corticosteroid
  • Cyclophosphamide
  • Complication: glomerulonephritis
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38
Q

Compare Giant cell arteritis, Takayasu arteritis, Polyarteritis nodosa and Kawasaki disease.

A
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39
Q

Compare GPA, EGPA, and MPA.

A
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40
Q

What is osteoporosis? What is it characterised by?

A
  • Osteoporosis = low bone mineral density
  • Characterised by an imbalance between bone formation and bone resorption
  • ↓ bone mass/density and micro-architectural deterioration
  • ↑ in bone fragility and susceptibility in fracture
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41
Q

What are the risk factors for osteoporosis? How can this be remembered?

A
  • Risk factors = ‘SHATTERED’:
  • Steroid use
  • Hyperthyroidism, hyperparathyroidism, hypercalciuria
  • Alcohol + tobacco use
  • Thin (BMI < 18.5)
  • Testosterone (low)
  • Early menopause
  • Renal or liver failure
  • Erosive/inflammatory bone disease, e.g. myeloma or RA)
  • Dietary low calcium/malabsorption or Diabetes type 1
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42
Q

What is the clinical presentation of osteoporosis?

A

FRACTURE - asymptomatic until this occurs

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43
Q

What are the investigations for osteoporosis? How about the risk assessment?

A
  • DEXA scan - decreased bone mineral density
  • Ca, phopshate, ALP (normal)
  • Risk assessment:
  • FRAX score - 10-year probability of a hip fracture >3% or osteoporosis-related fracture >20%
  • QFRACTURE
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44
Q

Describe the T-score categories for a DEXA scan.

A
  • Normal: T > -1.0
  • Osteopenia: -2.5 < T < -1.0
  • Osteoporosis: T < -2.5
  • Established osteoporosis: T < -2.5 with > 1 fragility fractures
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45
Q

Describe the management for osteoporosis.

A
  • Vitamin D + calcium supplementation - 1ST LINE
  • Bisphosphonates (reduce osteoclastic activity as osteoclasts absorb them), e.g. alendronate, risendronate, zolendronic acid - 1ST LINE
  • Denosumab (monoclonal Ab that blocks the activity of osteoclasts - bind to RANK-ligand) - 2ND LINE
  • Lifestyle advice - exercise, maintaining a healthy weight, stop smoking, reduce alcohol
  • HRT
  • Prompt surgery in the case of hip fracture
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46
Q

What is arthritis caused by?

A

Inflammation of the joints

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47
Q

What is the pathology of osteoarthritis? What are the risk factors?

A
  • NON-INFLAMMATORY degenerative progressive destruction of articular cartilage (underlying bone of synovial joints) from repeated mechanical forces
  • The damage to the articular cartilage causes the disruption of chondrocytes (cells responsible for cartilage formation) prevents rebuilding
  • Risk factors: high intensity labour, old age
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48
Q

What is the clinical presentation of osteoarthritis?

A
  • Painful joints that are stiff for 30 minutes or less in the morning. Worse throughout the day
  • Proximal Bouchard’s nodes, distal Herberden’s nodes - interphalangeal joints
  • Sharp pain worsened by activity
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49
Q

What are the investigations for osteoarthritis?

A
  • X-ray - LOSS (loss of joint space, osteophytes, subchondral sclerosis, subchondral cysts)
  • Serum ESR and CRP
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50
Q

Describe the management of osteoarthritis. What are the complications?

A
  • Analgesia, e.g. acetaminophen, tramadol, NSAIDs
  • Cortisol injections
  • Osteotomy
  • Complications: destruction of the joint and loss of function
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51
Q

What is the pathology of rheumatoid arthritis?

A

Autoimmune destruction of the synovium. The inflammation causes damage to bone, cartilage (connective tissue), tendons (muscle to bone), and ligaments (bone to bone)

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52
Q

What are the risk factors for rheumatoid arthritis?

A
  • Young
  • Female - 3x more than men
  • Family history
  • Other autoimmune diseases
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53
Q

Describe the clinical presentation of rheumatoid arthritis. What are the systemic symptoms?

A
  • Symptoms: painful, swollen, stiff joints for >1 hour in the morning, better with movement
  • Signs: SWAN NECK THUMB, ULNAR DEVIATION, Boutonnière deformity
  • Systemic symptoms: scleritis, pleural effusions, pericarditis
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54
Q

What are the investigations for rheumatoid arthritis?

A
  • Bloods: anti CCP (most sensitive), rheumatoid factor, raised ESR/CRP
  • X-ray = LESS: loss of joint space, erosion, soft tissue swelling, soft bones
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55
Q

What is the diagnostic criteria for rheumatoid arthritis?

A

RF RISES:

  • Rheumatoid factor positive
  • Finger/hand/wrist involvement
  • Rheumatoid nodules present
  • Involvement of ≥ 3 joints
  • Stiffness in the morning for > 1 hour
  • Erosions seen on X-Ray
  • Symmetrical involvement

More than 6 weeks, more than 4 of the above

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56
Q

Describe the management for rheumatoid arthritis.

A
  • DISEASE-MODIFYING ANTIRHEUMATIC DRUGS (DMARDs), e.g. methotrexate = hallmark of RA treatment. 2nd line = methotrexate + hydroxychloroquine. 3rd line = biologic DMARDs, e.g. rituximab (suppress B-cells) + methotrexate
  • Ibuprofen/NSAIDS
  • Short-term, low-dose glucocorticoid (class of corticosteroids = a class of steroids)
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57
Q

What are the complications of rheumatoid arthritis?

A
  • Cervical spinal cord compression - weakness and loss of sensation
  • Lung involvement - interstitial lung disease, fibrosis
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58
Q

What is Felty syndrome?

A

Rare disorder characterised by the presence of three conditions: RA, splenomegaly, granulocytopenia

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59
Q

What are the two types of crystal arthritis?

A
  • Gout
  • Pseudogout
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60
Q

What is the pathology of gout?

A

Over-production/under-excretion of uric acid

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61
Q

What are the risk factors for gout?

A
  • Middle-aged, overweight males
  • High purine diet (uric acid produced when these are broken down) - found in meat
  • Increased cell turnover
  • Heavy alcohol consumption
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62
Q

What is the clinical presentation of gout?

A
  • Symptoms: inflamed joints - 1st metatarsal and distal interphalangeal joints often affected
  • Signs: tophi-lumps of urate salts
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63
Q

What are the investigations for gout?

A
  • GOLD STANDARD = ARTHROCENTESIS (joint aspiration) with synovial fluid extraction and polarised light microscopy (NEEDLE-LIKE NEGATIVE BIREFRINGENT CRYSTALS)
  • 1st line = bloods - increased monosodium urate
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64
Q

Describe the management of acute and chronic gout.

A

ACUTE:

  • 1st line: NSAIDs (not good for kidneys which is a risk factor for gout, so careful when prescribing) or COLCHICINE (causes diarrhoea)
  • 2nd line: intra-articular steroid injection

CHRONIC:

  • 1st line: ALLOPURINOL (xanthase oxidase inhibitor, reduces uric acid production)
  • 2nd line: febuxostat
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65
Q

What are the complications of gout?

A
  • Infection of the tophi
  • Destruction of the joint
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66
Q

What are the side effects of allopurinol?

A
  • Triggers or worsens acute episodes of gout
  • Skin rash
  • Stevens-Johnson Syndrome
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67
Q

What is the pathology of pseudogout?

A

Damage to a joint causes pathological formation of calcium pyrophosphate crystals

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68
Q

What are the risk factors for pseudogout?

A
  • Females over 70
  • Hyperthyroidism
  • Hyperparathyroidism
  • Excess iron or calcium
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69
Q

What is the clinical presentation of pseudogout?

A
  • Symptoms: hot, swollen, tender joint, usually knees
  • Signs: recent injury to the joint in the history
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70
Q

What are the investigations for pseudogout?

A
  • Arthrocentesis with synovial fluid analysis and polarised light (RHOMBOID POSITIVE BIREFRINGENT CRYSTALS)
  • X-ray of affected joints
  • Serum calcium and PTH
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71
Q

Describe the management and complications of pseudogout.

A
  • NSAIDs with colchicine
  • Complications: damage to the joint - loss of function over time
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72
Q

What is septic arthritis? What is its pathophysiology? What is its aetiology?

A
  • Septic arthritis = infection in the synovial fluid and joint tissues
  • Pathophysiology: infection of joint = endotoxin production = cytokine release = neutrophil attraction = inflammation, damage of joint structures
  • Aetiology: predominant organisms responsible are S.aureus, Neisseria gonorrhoea, E.coli
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73
Q

What are the risk factors for septic arthritis?

A
  • Pre-existing joint disease (OA or RA)
  • IVDU, alcohol misuse
  • Immunosuppression
  • Intra-articular corticosteroid injection
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74
Q

What is the clinical presentation of septic arthritis?

A
  • Hot, swollen, painful, restricted joint
  • Onset < 2 weeks
  • Fever
  • Commonest → knee
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75
Q

What are the investigations for septic arthritis?

A
  • ASPIRATE JOINT and THEN GIVE ANTIBIOTICS (empirical until organism identified)
  • Blood culture
  • WCC → may be raised
  • ESR + CRP → raised
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76
Q

Describe the management for septic arthritis.

A
  • Joint aspiration
  • Empirical Abx, e.g. flucloxacillin (penicillin allergic = clindamycin), MRSA = vancomycin
  • Surgical wash out
  • Pathogen-directed Abx once identified
  • Pain medications, e.g. NSAIDs
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77
Q

What is osteomyelitis? What is it most commonly caused by?

A

Osteomyelitis is an inflammatory condition of bone caused by an infecting organism - most commonly STAPHYLOCOCCUS AUREUS

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78
Q

What are the risk factors for osteomyelitis?

A
  • Diabetes
  • Fractures
  • Recent surgery
  • IVDU
  • Distant or local infection
  • Children - upper respiratory tract or varicella infection
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79
Q

What is the clinical presentation of osteomyelitis?

A
  • Limp or reluctance to weight-bear (children)
  • Non-specific pain at site of infection
  • Low grade fever
  • Malaise + fatigue
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80
Q

What are the investigations for osteomyelitis?

A
  • FBC - elevated WCC, ESR and CRP raised
  • GOLD STANDARD = bone biopsy
  • Blood culture
  • X-ray
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81
Q

Describe the management for osteomyelitis.

A
  • Long-term IV antibiotics
  • Surgical removal of dead bone
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82
Q

What are spondyloarthropathies? What are they all associated with? Name the different conditions.

A
  • Spondyloarthropathies: family of chronic diseases of the joints
  • All associated with HLA-B27 (encoded by MHC on chromosome 6)
  • Seronegative (RF -ve)
  • Conditions:
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • Juvenile idiopathic arthritis
  • Enteropathic arthritis
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83
Q

What are the features of spondyloarthropathies?

A
  • SPINEACHE:
  • Sausage digit (dacytylitis)
  • Psoriasis
  • Inflammatory back pain
  • NSAID - good response
  • Enthesitis (heel)
  • Arthritis
  • Crohn’s/colitis/elevated CRP (can be normal)
  • HLA B27
  • Eye (uveitis)
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84
Q

What is ankylosing spondylitis? What is its pathophysiology? What are the risk factors?

A
  • Ankylosing spondylitis = chronic, multisystem inflammatory disorder involving primarily inflammation of the sacroiliac joints + axial skeleton
  • Pathophysiology: inflammatory arthritis of spine + rib cage → leads to new bone formation + fusion of joints = loss of spinal movements
  • Risk factors: HLA-B27 gene, male (3x more common)
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85
Q

Describe the clinical presentation of ankylosing spondylitis.

A
  • Typical presentation male in late teens or 20s
  • Lower back pain + stiffness → worse with rest + improves with movement
  • Sacroiliac pain
  • Flares of worsening symptoms
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86
Q

What are the complications of ankylosing spondylitis?

A
  • Aortic regurgitation
  • Uveitis
  • Enthesitis
  • Dactylitis
  • Decreased pulmonary function
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87
Q

What are the investigations for ankylosing spondylitis? Which criteria is used?

A
  • X-ray of spine + sacrum:
  • BAMBOO SPINE
  • Squaring of vertebral bodies
  • Subchondral sclerosis + erosions
  • Syndesmophytes
  • Ossification of ligaments, discs + joints
  • Fusion of facet, SI + costovertebral joints
  • MRI spine - bone marrow oedema in early disease before x-ray changes
  • CRP and ESR - raised
  • HLA-B27 genetic test
  • NEW YORK CRITERIA
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88
Q

Describe the management for ankylosing spondlyitis.

A
  • FIRST LINE = NSAIDs, e.g. ibuprofen
  • Steroids during flares. DMARDs during severe flare ups
  • MAbx against TNF-alpha: infliximab, adalimumab, certulizomab
  • Anti-TNF drugs: etanercept
  • Physiotherapy, lifestyle advice
  • Surgery for deformaties
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89
Q

What is psoriatic arthritis? What is its epidemiology?

A
  • Psoriatic arthritis = chronic inflammatory joint disease associated with psoriasis
  • 1 in 5 patients with psoraisis have psoraitic arthritis
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90
Q

What is the clinical presentation of psoraitic arthritis?

A
  • Inflammatory joint pain
  • Plaques of psoriasis
  • Onycholysis (separation of nail from nail bed)
  • Dactylitis (inflammation of full finger)
  • Enthesitis (inflammation of entheses - point of insertion of tendons into bone)
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91
Q

What are the investigations for psoriatic arthritis?

A
  • Plain film x-rays of hands and feet:
  • Erosion in DIPJ + periarticular new-bone formation
  • Osteolysis
  • PENCIL-IN-CUP/POT deformity
  • ESR + CRP - normal or raised
  • Rheumatoid factor -ve
  • Anti-CCP - negative
  • Joint aspiration - no bacteria or crystals
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92
Q

Describe the management for psoriatic arthritis.

A
  • NSAIDs (mild disease)
  • Physiotherapy
  • Steroid injection, e.g. cortisol
  • DMARDs - methotrexate, sulfasalazine
  • TNF inhibitor or MAbx, e.g. infliximab, etanercept, adalimumab
  • Ustekinumab - last line (MAb that targets IL 12 + 23)
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93
Q

What is arthritis mutilans?

A
  • Most severe form of psoriatic arthritis
  • Occurs in phalanges
  • Osteolysis of bones around joints in digits → leads to progressive shortening
  • Skin then folds as digit shortens → telescopic finger
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94
Q

What is reactive arthritis? What is its aetiology?

A
  • Reactive arthritis = inflammatory arthritis that occurs after exposure to certain GI or GU infections

  • Aetiology:
  • Chlamydia - C trachomatis v. common
  • Campylobacter jejuni
  • Salmonella enteritidis
  • Shigella
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95
Q

What is the clinical presentation of reactive arthritis?

A
  • Begin 1-4 weeks after onset of infection
  • Asymmetrical oligoarthritis
  • Painful, swollen, warm, red + stiff joints
  • Dactylitis
  • CLASSICAL TRIAD → conjunctivitis, urethritis + arthritis (CAN’T SEE, CAN’T PEE, CAN’T CLIMB A TREE) (good for exams)
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96
Q

What are the investigations for reactive arthritis?

A
  • ESR + CRP - raised
  • ANA - negative
  • RF - negative
  • X-ray - sacroiliitis or enthesopathy
  • Joint aspirate - negative (exclude septic arthritis + gout)
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97
Q

Describe the management for reactive arthritis.

A
  • NSAIDs
  • Corticosteroids
  • DMARDs - chronic arthritis
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98
Q

What is juvenile idiopathic arthritis?

A

Juvenile idiopathic arthritis (JIA) describes a group of chronic paediatric inflammatory arthritides. Characterised by onset before 16 years of age and the presence of objective arthritis (in one or more joints) for at least 6 weeks

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99
Q

What is the complication of juvenile idiopathic arthritis?

A

10% develop disability in adulthood

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100
Q

What is the clinical presentation of juvenile idiopathic arthritis?

A
  • Arthritis, e.g. joint pain, joint swelling
  • Rheumatoid nodules, RF usually absent
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101
Q

What are the investigations for juvenile idiopathic arthritis?

A
  • FBC
  • ESR and CRP
  • Antinuclear antibodies (ANA)
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102
Q

Describe the treatment for juvenile idiopathic arthritis.

A

Similar to RA treatment

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103
Q

What is systemic lupus erythmatosus? What is its pathology? What are the risk factors? What type of hypersensitivity reaction is this?

A
  • It is an autoimmune disease in which the immune system attacks its own organs, causing widespread inflammation and organ damage. It is the most common type of lupus
  • Pathology: characterised by the presence of ANTI-NUCLEAR ANTIBODIES (aNA). aNA and aDsDNA (anti-double stranded DNA) attack soft tissue causing inflammation and damage
  • Risk factors: biologically female and of reproductive age, black people
  • Type III hypersensitivity
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104
Q

What is the clinical presentation of SLE?

A
  • Symptoms: butterfly rash (over cheeks), weight loss, fever, fatigue, joint pain, mouth ulcers
  • Signs: correctable ulnar deviation, glomerulonephritis, depression
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105
Q

What are the investigations for SLE?

A
  • Bloods: ESR raised, CRP normal, aNA and aDsDNA present
  • Activated partial thromboplastin time
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106
Q

Describe the management of SLE.

A
  • FIRST LINE FOR MILD SLE = hydroxychloroquine (anti-malaria)
  • Ibuprofen (NSAID)
  • Prednisolone (steroid)
  • Methotrexate (more severe)
  • Cyclophosphamide (immunosuppressant)
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107
Q

What are the complications of SLE?

A

Cardiovascular disease, renal failure, lung involvement

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108
Q

What is Sjogren’s syndrome? What are the two types? What are its risk factors?

A
  • Sjogren’s syndrome = autoimmune condition that affects exocrine glands, especially the lacrimal or salivary glands
  • Two types:
  • Primary: the condition occurs in isolation
  • Secondary: it occurs related to RA or SLE
  • Risk factors: FHx (first degree relative = 7x increased risk), female, >40 years old
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109
Q

What is the clinical presentation of Sjogren’s syndrome?

A
  • Dry mucous membranes, i.e. dry mouth, dry eyes, dry vagina
  • Joint pain
110
Q

What are the investigations for Sjogren’s syndrome?

A
  • Presence of anti-Ro and anti-La antibodies
  • SCHIRMER TEAR TEST: tears travelling <10mm is significant (15mm in healthy adults)!
  • ROSE BENGAL STAINING AND SLIT LAMP EXAM
  • Salivary gland biopsy
111
Q

Describe the management for Sjorgen’s syndrome.

A
  • Artificial tears, artificial saliva, vaginal lubricants
  • Hydroxychloroquine used to halt progression
  • M3 agonist - pilocarpine
112
Q

What are the complications of Sjogren’s syndrome?

A
  • Eye infections (conjunctivitis, corneal ulcers)
  • Oral problems (dental cavities, candida infections)
  • Vaginal problems (candidiasis, sexual dysfunction)
113
Q

What is dermatomyotosis? What is it characterised by?

A

Dermatomyositis is an idiopathic autoimmune inflammatory myopathy characterised by distinctive skin manifestations

114
Q

What is the clinical presentation of dermatomyotosis?

A
  • Gottron’s papules
  • Heliotrope rash
  • Photosensitivity
115
Q

What are the investigations for dermatomyotosis?

A
  • Serum creatine kinase (muscle cells death so increased) and serum aldolase
  • Muscle biopsy - perivascular inflammation = diagnostic
116
Q

Describe the management for dermatomyotosis.

A
  • Prednisolone
  • Immunosuppressive agents, e.g. methotrexate
117
Q

What is the difference between polymyotosis and dermatomyotosis?

A

Polymyotosis causes muscle weakness, dermatomyotosis causes muscle weakness plus a skin rash

118
Q

What is scleroderma? What is it characterised by?

A
  • Scleroderma, also known as systemic sclerosis, is a multi-system, autoimmune disease in which there is INCREASED FIBROBLAST ACTIVITY (INCREASED COLLAGEN DEPOSITION)
  • Characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, and production of auto-antibodies
119
Q

What is the clinical presentation of scleroderma?

A
  • Skin involvement limited to HANDS, FACE, FEET AND FOREARMS
  • CHARACTERISTIC ‘BEAK’-LIKE NOSE AND SMALL MOUTH
  • Raynaud’s phenomenon
  • Microstomia
120
Q

What are the investigations for scleroderma?

A
  • Increased aNA
  • Anti-topisomerase, anti scl-70
  • Urea and serum creatinine
  • Upper GI endoscopy
121
Q

Describe the management for scleroderma.

A
  • Depends on disease subset:
  • PPIs for gastroesophageal reflux
  • CCBs for Raynaud’s phenomenon
  • ACEi for renal hypertensive crisis
  • Pulmonary fibrosis - cyclophosphamide
122
Q

What is Marfan syndrome? What is its pathophysiology? What are its risk factors?

A
  • Autosomal dominant disorder of connective tissue
  • Pathophysiology: affects gene involved in creating fibrillin-1, which is an important component of connective tissue
  • Risk factors = family history
123
Q

What is the clinical presentation of Marfan syndrome?

A
  • Tall stature
  • Long limbs (wide arm span)
  • Long fingers
  • Hypermobility
  • Pectus carinatum/pectus excavatum
  • High arch palate
  • Aortic root dilation
124
Q

What are the investigations for Marfan syndrome?

A
  • Physical examination (S+S, heart murmur etc.)
  • Echocardiography
  • Ghent criteria:
  • Major: enlarged aorta, lens dislocation, Fx, at least 4 skeletal problems
  • Minor: myopia, loose joints, high arched palate
  • MRI
  • Eye exam
125
Q

Describe the management for Marfan’s syndrome.

A
  • Lifestyle changes: avoid intense exercise, avoid caffeine
  • Beta-blockers/ARBs (both slow aortic dilation)
  • Yearly echocardiogram/review by opthamologist
126
Q

What are the complications of Marfan’s syndrome?

A
  • MITRAL/AORTIC VALVE PROLAPSE (WITH REGURGITATION)
  • AORTIC ANEURYSMS
  • LENS DISLOCATION
  • Pneumothorax
  • GORD
  • Scoliosis
127
Q

What are Ehlers-Danlos syndromes? What is their pathophysiology? What are their risk factors?

A
  • Group of inherited connective tissue disorders
  • Caused by FAULTY COLLAGEN
  • Risk factors: FHx
128
Q

What is the clinical presentation of Ehler’s-Danlos syndrome?

A

Varies between types but generally:

  • Joint hypermobility
  • Easily stretched skin (hyperextensibility)
  • Easy bruising
  • Chronic joint pain
  • Re-occuring dislocations
129
Q

What are the investigations for Ehler’s-Danlos syndrome?

A
  • Use Beighton score to assess hypermobility
  • Genetic testing
130
Q

Describe the management for Ehler’s-Danlos syndrome.

A
  • Physiotherapy
  • Occupational therapy
  • Psychological support (chronic condition + pain)
  • Pain medication, e.g. NSAIDs
131
Q

What are the complications of Ehler’s-Danlos syndrome?

A
  • Classical type: prone to hernias, prolapse, aortic root dilation, joint pain, abnormal wound healing
  • Vascular EDS: skin, internal organs, vessels are prone to rupture
132
Q

What is antiphospholipid syndrome? What is its pathophysiology? How does it occur?

A
  • Antiphospholipid syndrome = associated with antiphospholipid antibodies where blood becomes prone to clotting = hyper-coagulable state
  • Pathophysiology: those with APS make abnormal proteins called antiphospholipid autoantibodies in the blood. This causes blood to flow improperly and can lead to dangerous clotting in arteries and veins, problems for a developing fetus and pregnancy miscarriage
  • Can occur on its own or secondary to AI disorder, e.g. SLE
133
Q

What are the risk factors for antiphospholipid syndrome?

A
  • Diabetes
  • HTN
  • Obesity
  • Female gender
  • Underlying systemic AI disease
  • Smoking
  • Oestrogen therapy for menopause
134
Q

What is the clinical presentation of antiphospholipid syndrome?

A
  • Recurrent venous thromboses
  • Recurrent miscarriages
  • Livedo reticularis - purple lace-like rash
  • THROMBOCYTOPENIA
135
Q

Describe the investigations for antiphospholipid syndrome.

A
  • Hx of thrombosis/pregnancy complications + antibody screen with raised:
  • lupus anticoagulant
  • ANTICARDIOLIPIN antibodies
  • anti-beta-2 glycoprotein I antibodies
136
Q

Describe the management for antiphospholipid syndrome.

A
  • Long-term warfarin (INR range 2-3)
  • Pregnant women on low molecular weight heparin (e.g. enoxaparin) + aspirin
137
Q

What are the complications of antiphospholipid syndrome?

A
  • Venous thromboembolisms (e.g. DVT, pulmonary embolism)
  • Arterial thrombosis (stroke, MI, renal thrombosis)
  • Pregnancy complications (recurrent complications, pre-eclampsia)
138
Q

What is fibromyalgia? What is its pathology? What are its risk factors?

A
  • Fibromyalgia = chronic pain syndrome diagnosed by the presence of widespread body pain
  • Pathophysiology: unknown, possibly pain perception/hyper-excitability of pain fibres
  • Risk factors: women, poor socioeconomic status, 20-50 year olds
139
Q

What is the clinical presentation of fibromyalgia?

A
  • Widespread muscle pain
  • Fatigue
  • Cognitive dysfunction - brain fog
  • Morning stiffness
  • Extreme tenderness
140
Q

What are the investigations for fibromyalgia?

A

11 tender points in nine pairs (18) of sites for six months

141
Q

Describe the management for fibromyalgia.

A
  • Physical therapy
  • Relaxation
  • CBT
  • Analgesia (paracetamol, tramadol/codeine)
142
Q

What are the complications of fibromyalgia?

A
  • Can really affect Q.o.L
  • Anxiety, depression, insomnia
  • Opiate addiction
143
Q

What is Paget’s disease? What is it characterised by?

A
  • Paget’s disease = localised disorder of bone remodelling. Characterised by ↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
144
Q

What is the clinical presentation of Paget’s disease?

A
  • 60-80% asymptomatic, some will have these symptoms:
  • BONE PAIN
  • Bone deformity, in particular BOWED TIBIA and SKULL CHANGES
  • Fractures
  • Hearing loss (if bones of ear affected)
145
Q

What are the 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 + lysis)
  • V-shaped defects in long bones
  • Bloods: raised ALP, normal calcium + phosphate
  • Total serum alkaline phosphatase
146
Q

Describe the management of Paget’s disease.

A
  • Bisphosphonates (zoledronate, risedronate) - slow down bone thinning
  • NSAIDs for bone pain
  • Calcium and Vitamin D supplements
  • Surgery if need to correct fractures or malformations
147
Q

What are the complications of Paget’s disease?

A
  • Osteoarthritis
  • Osteosarcoma
  • Spinal stenosis + cord compression
148
Q

What is osteomalacia? What is the difference between osteomalacia and rickets?

A
  • Osteomalacia = POOR BONE MINERALISATION leading to soft bone due to a lack of Ca2+, phosphate or increased bone resorption. IN ADULTS. Normal bone but low mineral content (excess uncalcified osteoid/cartilage). Happens after fusion of epiphytes
  • Rickets = inadequate mineralisation of the bone and epiphyseal cartilage in the growing skeleton of CHILDREN. Same disease process but it happens during bone growth period so presentation differs slightly
149
Q

What is the clinical presentation of osteomalacia and rickets?

A
  • Osteomalacia:
  • WIDESPREAD BONE PAIN and TENDERNESS. Dull ache that is worse on weight-bearing exercises
  • Fractures
  • Muscle weakness - waddling gait, difficulty with stairs
  • Rickets:
  • LEG-BOWING and KNOCKED KNEES
  • Growth retardation
  • Hypotonia
150
Q

What are the investigations for osteomalacia?

A
  • X-ray - loss of cortical bone - defective mineralisation
  • Bloods - low calcium and phosphate, low 25-hydroxyvitamin D levels
  • Bone biopsies - incomplete mineralisation
151
Q

Describe the management for osteomalacia.

A
  • Vitamin D supplements – rapid mineralization of bone and resolution of symptoms
  • If dietary insufficiency – calcium D3 forte
  • If due to malabsorption, give IM calcitriol
  • If due to renal disease give alfacalcidol
152
Q

What is polymyalgia rheumatica? What does it manifest itself as? How does it occur? Is it acute or chronic?

A
  • Polymyalgia rheumatica (PMR) is an inflammatory rheumatological syndrome that manifests as pain and morning stiffness involving the neck, shoulder girdle, and/or pelvic girdle in individuals older than age 50 years
  • Either occurs as an isolated condition or associated with giant cell arteritis
  • Can regress after 1-2 years or remain chronic
153
Q

What is the clinical presentation of polymyalgia rheumatica?

A
  • Shoulder/hip girdle STIFFNESS and PAIN - typically lasts > 1 hour
  • Low-grade fever, fatigue, loss of appetite
154
Q

What are the investigations for polymyalgia rheumatica?

A
  • ESR and CRP - raised
  • FBC
  • Physical examination
155
Q

Describe the treatment for polymyalgia rheumatica.

A

Low-dose corticosteroids - suppress immune response

156
Q

What is polymyositis? What is dermatomyositis?

A
  • Polymyositis is a RARE MUSCLE DISORDER of unknown aetiology in which there is INFLAMMATION and NECROSIS of SKELETAL MUSCLE FIBRES
  • Dermatomyositis is poly + skin involvement
157
Q

What is the clinical presentation of polymyositis?

A

SYMMETRICAL PROGRESSIVE MUSCLE WEAKNESS and wasting affecting the PROXIMAL MUSCLES OF THE SHOULDER AND PELVIC GIRDLE

158
Q

What is the clinical presentation of dermatomyositis?

A
  • HELIOTROPE (PURPLE) DISCOLOURATION of EYELIDS
  • GOTTRON’S PAPULES - SCALY ERYTHEMATOUS PLAQUES OVER THE KNUCKLES
159
Q

What are the investigations for polymyositis?

A
  • Muscle biopsy
  • Bloods: serum creatine kinase, aminotransferases, lactate dehydrogenase and aldolase all ↑

Immunology: ANA, Anti jo1, anti mi2

160
Q

Describe the treatment for polymyositis.

A
  • Oral prednisolone
  • Stronger immunosuppresssants
  • Symptomatic treatment of skin disease
161
Q

What is a fracture? What are the long bones?

A
  • A fracture (or broken bone) is an abnormal disruption in the continuity of a bone
  • Long bone = bone that has a shaft and 2 ends and is longer than it is wide:
  • Humerus, radius, ulna, femur, tibia, fibula, metatarsals, phalanges
162
Q

What is the clinical presentation of a long bone fracture?

A
  • Pain
  • Soft tissue swelling
  • Ecchymosis
  • Altered nerve sensation
163
Q

What are the investigations for a long bone fracture?

A
  • X-ray limb
  • FBC, blood-typing
  • Whole body CT
  • MRI limb
164
Q

Describe the treatment for a long bone fracture.

A
  • ABCDE for all fracture types
  • Analgesia and assess pain
  • If stable, apply a splint
165
Q

What is the aetiology of mechanical lower back pain?

A
  • 70% are due to lumbar strain or sprain
  • 10% are due to age-related degenerative changes in disks and facets
  • 4% are due to herniated disks
  • 4% are due to osteoporotic compression fractures
  • 3% are due to spinal stenosis
166
Q

What is the primary purpose of the initial evaluation of lower back pain?

A

To evaluate whether the symptoms suggest a more serious underlying condition. Mechanical back pain = SPASMS IN CYCLIC NATURE

167
Q

What are the differential diagnoses for back pain?

A
  • Congenital - scoliosis
  • Infection - osteomyelitis
  • Inflammation - HLA B27/osteoporosis/osteoarthritis/pyelonephritis
  • Trauma - lumbar muscular strain/sprain, herniated nucleus pulposus (slipped disc), compression fracture
  • Iatrogenic
  • Malignant - MM/Metastases
  • Lifestyle - posture/overuse
168
Q

What are the red flag causes of mechanical back pain?

A

TUNA FISH:

  • Trauma, thoracic pain
  • Unexplained weight loss
  • Neurological findings (e.g. incontinence, weakness etc.). nocturnal pain
  • Age >55 or <25
  • Fever
  • Immunocompromised
  • Steroid
  • History of cancer, TB
169
Q

Which mnemonic should be used when assessing any type of pain?

A

When assessing any pain, you can use the SOCRATES mnemonic:

S – Site

O – Onset

C – Character

R – Radiation

A – Associations

T – Timing

E – Exacerbating and relieving factors

S – Severity

170
Q

What are the investigations for mechanical lower back pain?

A
  • Generally, patients with mechanical/non-specific lower back pain can be diagnosed clinically and do not require further investigations:
  • X-rays or CT scans for spinal fractures
  • Emergency MRI scan required in patients with suspected cauda equina
  • Investigations for suspected ankylosing spondylitis are:
  • CRP and ESR
  • X-ray of the spinal and sacrum - “bamboo spine”
  • MRI of the spine (may show bone marrow oedema early in the disease)
171
Q

Describe the management for mechanical back pain.

A
  • Encourage exercise and physiotherapy first
  • NSAIDS 1st line analgesia for lower back pain, codeine 2nd line
172
Q

What is vertebral disc degeneration? What is the most common cause of?

A
  • Vertebral disc degeneration/intervertebral disc disease/degenerative disc disease is a common condition characterised by the degeneration of one or more of the discs that separate the bones of the spine (vertebrae), causing pain in the back or neck and frequently in the legs and arms
  • Most common cause of back pain
173
Q

What are the signs and symptoms of degenerative disc disease?

A
  • Back pain that may radiate, decreased range of motion
  • Tingling, parasthesia, numbness
  • Atrophy
174
Q

What are the investigations for degenerative disc disease?

A
  • Erect lumbar spine x-ray - detects fracture
  • MRI spine
175
Q

Describe the management for degenerative disc disease.

A
  • Analgesics - NSAIDs, corticosteroids
  • Surgery: corpectomy (vertebral portion removal - enlarge intervertebral space), discectomy (herniated disc portion removal), nerve root injection
176
Q

What are the two types of bone tumours?

A
  • Primary: originate from the bone
  • Secondary: orginate from other organs
177
Q

What are the most common types of primary bone tumour?

A
  • Chondrosarcoma - v. common in M < 25, overproduction of bone which deposits on metaphysis
  • Osteosarcoma - KIDS, metastasis of long bones
  • Ewing sarcoma - super rare, from mesenchymal cells
178
Q

What are the risk factors for primary bone tumours?

A
  • Previous radiotherapy
  • Previous cancer
  • Paget’s disease
  • Benign bone lesions
179
Q

What is the clinical presentation of primary bone tumours?

A
  • More common in males and long bones
  • Bone pain - WORSE AT NIGHT, constant or intermittent, resistant to analgesia, may increase in intensity
  • ATYPICAL BONY OR SOFT TISSUE SWELLING/MASSES
  • PATHOLOGICAL FEATURES
  • Mobility issues - unexplained limp, joint stiffness, reduced ROM
  • Inflammation and tenderness of bone
  • Systemic symptoms
180
Q

Describe the investigations for primary bone tumours.

A
  • X-ray = first line. There will be a PERIOSTEAL reaction (irritation of the lining of the bone) that is classically described as a ‘SUN BURST’ appearance
  • Biopsy = gold standard
  • Bloods - FBC, ESR, ALP, lactate dehydrogenase, Ca, U+E
  • CT chest/abdomen/pelvis
181
Q

Describe the management for primary bone tumours.

A
  • Adjuvant chemotherapy
  • Radiotherapy
  • Surgery - limb sparing or amputation
182
Q

Where are the common sites that secondary bone tumours come from?

A
  • PBKTL (lead kettle):
  • Prostate
  • Breast
  • Kidneys
  • Thyroid
  • Lungs
183
Q

What is multiple myeloma? What is its pathophysiology?

A
  • Multiple myeloma = neoplastic proliferation of bone marrow plasma cells that affects multiple areas of the body
  • Pathophysiology: malignant plasma cells produce excess Immunoglobulin leading to multiple organ dysfunction (esp. kidneys). ⅔ = IgG, ⅓ = IgA
184
Q

What is the clinical presentation of multiple myeloma?

A
  • OLD CRAB (they love this in exams):

  • OLD age
  • Calcium elevated (think “bones, stones, groans, moans”)
  • Renal impairment - pts get nephrotic syndrome due to light chain deposition in distal loop of henle and Igs disrupt glomeruli. Also get Bence-Jones protein in urine
  • Anaemia
  • Bone lytic lesions (have a high index of suspicion if bone or back pain)
185
Q

What are the investigations for multiple myeloma?

A
  • FBC - normocytic normochromic anaemia
  • Films - Rouleaux formation (RBC aggregations)
  • U&Es - raised calcium, raised urea + creatinine
  • Haematinics - persistently raised ESR
  • X-Ray - lytic “punched out” lesions (pepper-pot skull, vertebral collapse, fractures). Salt and pepper skull actually refers to multiple tiny well-defined lucencies caused by resorption of trabecular bone in hyperparathyroidism. It’s actually called a raindrop skull for multiple myeloma lytic lesion
  • Serum / urine electrophoresis - BENCE JONES protein band
  • Bone marrow biopsy - raised plasma cells
186
Q

What is the diagnostic criteria for multiple myeloma?

A
  1. Monoclonal protein band (BENCE JONES) in serum or urine
  2. Raised plasma cells on BM biopsy
  3. End organ damage (hypercalcaemia, renal failure, anaemia)
  4. Bone lesions on skeletal survey (X-ray of chest, spine, skull, pelvis)
187
Q

Describe the management for multiple myeloma.

A
  • First line = combination of chemotherapy and bortezomib, thalidomide, dexamethasone
  • Analgesia → bone pain
  • Bisphosphonates → reduce fractures and bone pain
  • Local radiotherapy → reduce focal disease
  • Transfusion → correct anaemia
  • Fluids/dialysis → manage renal failure
  • Abx for infections
188
Q

A 53 year old man comes into A&E with his husband. His knee is painful, hot and swollen. His observations are: oxygen saturations of 96% on air, BP 99/68mmHg, temperature 38.1 degrees and HR of 101bpm. On examination, the knee is red and swollen with reduced movement. What is the first line management?

A) Aspirate joint

B) Give empirical antibiotics

C) X-Ray

D) Send him home

E) Give Ibuprofen

A

Answer: A - Aspirate Joint

Explanation: A, B/E then C in this order. Don’t give abx before aspiration as it will affect the culture grown

189
Q

A 55 year old female comes to A&E after tripping over and getting an intense pain in her arm. On examination, the arm is swollen and heavily bruised. X-Ray confirms there is a fracture, which makes this her second fracture this year. You decide to refer her for a DEXA scan which comes back as T = -2.6

Based on this score, what is the diagnosis?

A) Normal

B) Osteopenia

C) Osteoporosis

D) Established Osteoporosis

E) Hyper Osteobosteoporosis

A

D. Estabslished osteoporosis

190
Q

The lady is diagnosed with osteoporosis. What would be the 2nd line treatment for this condition?

A). ADcal

B). Alendronic acid

C). Allopurinol

D). Corticosteroids

E). Denosumab

A

Answer: E - Denosumab

Explanation: Adcal is a vit D and calcium supplement. Alendronic acid is a bisphosphonate, they are both 1st line treatments. Allopurinol is used for gout. Corticosteroids cause osteoporosis so don’t give this! Denosumab is a monoclonal antibody for RANK-ligand

191
Q

A 20 year old man comes to his GP with pain whilst urinating. The GP notes that he’s limping. The patient mentions he’s recently changed sexual partners. His new partner refuses to post selfies with him on her instagram due to his “gross” eyes. He is a member of the local Tree Climbing Society but has been kicked out due to poor performance. Based on this tragic tale, what is your suspected diagnosis?

A). Septic arthritis

B). Syphilis

C). Reactive arthritis

D). Optic Neuritis

E). Urinary Tract Infection

A

Answer: C

Explanation: for reactive arthritis the classic triad can be remembered by: “can’t see, can’t pee, can’t climb a tree”

192
Q

A 70 year old female develops osteomyelitis after a total hip replacement. A culture is sent to the lab, where a gram positive organism is grown which is also catalase positive. What is the causative organism?

A). Escherichia Coli

B). Haemophilus Influenzae

C). Salmonella

D). Staphylococcus aureus

E). Streptococcus Pneumonia

A

Answer: D - staphylococcus aureus

Explanation: options A, B and C are Gram negative. Option E is gram positive BUT catalase negative

193
Q

A 23 year old man visits his GP surgery complaining of lower back pain. The pain is worse in the morning and improves with movement. He is referred for an X-ray (image below). Based on the X-Ray, what is the diagnosis?

A). Psoriatic arthritis

B). Ankylosing spondylitis

C). Rheumatoid arthritis

D). Osteoarthritis

E). Septic arthritis

A

B - ankylosing spondylitis

History is consistent with this and image shows ‘bamboo spine’

194
Q

He is subsequently diagnosed with ankylosing spondylitis, what is the 1st line treatment?

A) Chemotherapy

B) Ibuprofen

C) Infliximab

D) Paracetamol

E) Spinal surgery

A

Answer: B - ibuprofen

Explanation: NSAIDs are 1st line treatment for ankylosing spondylitis. Paracetamol can be used if NSAIDs are contraindicated. Infliximab can be used in severe AK. There is a lack of red flags to warrant chemotherapy. Watch and wait will not address his symptoms

195
Q

Katy is coming to see you in the rheumatology clinic for a routine review. She was diagnosed with Paget’s disease 5 years ago. She says she is in good health but mentions she has bone pain in her right leg which is worse at night. What are you going to do?

a) Reassure her this is normal
b) Order an x-ray
c) Order a biopsy
d) Recommend ibuprofen for the pain
e) Prescribe methotrexate

A

Answer = B - order an x-ray

Paget’s disease is a risk factor for osteosarcoma. Katy has bone pain which is worse at night which is a red flag for this. X-ray is the 1st line investigation and a biopsy is the gold standard

196
Q

A 40 year old woman named Kim presents to A&E with a swollen hand and a painful elbow. Her hand is extremely red and swollen. You notice scaly erythematous plaques and some nail pitting. You send her for an X-Ray, what x-ray finding is most associated with this condition?

A) Pencil in cup deformity

B) Bamboo spine

C) Cotton wool appearance

D) Dactylitis

E) Pepper pot skull

A

Answer: A - pencil-in-cup deformity

Explanation: History is suggestive of psoriatic arthritis. Bamboo spine is seen in ankylosing spondylitis. Cotton wool appearance is seen in Paget’s disease. Dactylitis is a sign in psoriatic arthritis NOT an X-ray finding. Pepper pot skull is seen in myeloma

197
Q

A 70 year old man comes to see his GP for lower back and abdominal pain. The GP also notices that he seems low in mood. They order some bloods which show a raised calcium, normocytic anaemia and a raised creatinine. Based on the most likely diagnosis, what will you see on a blood film?

A) Reed Sternberg cells

B) Bence Jones proteins

C) Rouleaux formation

D) Sickle cells

E) Normal blood film

A

Answer: C - Rouleaux formation

Explanation: history is suggestive of multiple myeloma (OLD CRAB) so the film would be abnormal. Bence Jones proteins are present in the urine for myeloma (not blood films). Reed Sternberg cells are present in Hodgkin’s lymphoma, sickle cells are found in sickle cell anaemia

198
Q

Which of the following is false about SLE?

A: Patients may present with ulnar deviation

B: Cancer should be a differential diagnosis

C: The inflammatory markers ESR and CRP are raised

D: Hydroxychloroquine can be used to treat lupus

A

C - ESR raised but CRP tends to be normal

199
Q

What is the most sensitive test for rheumatoid arthritis?

A: Rheumatoid factor

B: X ray

C: Anti cyclic citrullinated peptide

D: ESR/CRP

A

C - anti-CCP

200
Q

Henry de Ate, a 50 year old male who is partial to a feast of red meat and wine, presents to you with an acutely inflamed big toe. You do a joint aspirate and look at the sample under the microscope. What would you expect to see?

A: -ve birefringent rhomboid crystals

B: +ve birefringent rhomboid crystals

C: +ve birefringent needle crystals

D: -ve birefringent needle crystals

A

D

201
Q

A 40 year old female presents to the GP saying she feels she constantly in pain. She is asking for higher and higher doses of opioids to combat this. What is not a valid concern about prescribing opioids for this patient?

A: The patient could develop respiratory depression

B: The patient could develop hyperanalgesia

C: The patient could develop chronic prefuse diarrhoea

D: The patient is a forklift operator

A

C - constipation is the chief complaint

202
Q

64 year old builder comes in with pain in his knees and hips. He says the pain is worse in the evenings on examination the joints are not swollen. There is some crepitus (clicking) when the joints are moved. What finding would you expect on X ray?

A: Increase in joint space

B: Osteophytes

C: Soft bones

D: Soft tissue swelling

A

B - osteoarthritis

203
Q

A 70 year old woman presents to the GP with a red swollen knee. She explains she fell a couple of weeks ago. What is not in your differential diagnosis?

A: Septic arthritis

B: Osteoarthritis

C: Pseudogout

D: Fractured patella

A

B - red swollen knee = septic arthritis until proven otherwise!

204
Q

A 68-year-old woman presents to accident and emergency with severe left-sided headache. She also mentions that the vision in her left eye is blurred. She has previously been fit and well but has been feeling increasing worn down in the last few months with aching, weak shoulders and legs. On examination, the left side of her scalp is painful to touch. Blood tests reveal a raised ESR. What is the most appropriate immediate management?

A: Discharge with advice to use paracetamol and safety net

B: IV hydrocortisone

C: Arrange urgent CT head

D: Oral prednisolone

A

D - giant cell arteritis, so give oral prednislone 40-60mg

205
Q

A 45-year-old woman presents to the rheumatology clinic with a three-month history of itchy, dry eyes and a persistently dry mouth. She also mentions that her fingers have been extremely cold, occasionally turning blue after going outside in the morning. Schirmer’s test is positive. What is the most likely diagnosis?

A: Systemic sclerosis

B: Raynaud’s disease

C: SLE

D: Primary Sjogren’s syndrome

A

D

A) Reduced tear production and salivation are not features of systemic sclerosis

B) Raynaud’s disease just affects hands (sometimes feet) – but Raynaud’s phenomenon is a systemic manifestation of Sjogren’s

C) Absence of features suggestive of other connective tissue disorders means SLE and secondary Sjogren’s syndrome are incorrect

D) Primary Sjogren’s is the correct answer

206
Q

Which of these is not associated with Ehlers-Danlos syndrome?

A: Easy bruising

B: Livedo reticularis

C: Joint hypermobility

D: Dislocations

A

B - livedo reticularis is seen in APS

207
Q

A 28-year-old man presents with a 2-day history of abdominal pain which he describes as constant, dull and around his umbilicus and occasionally migrating to his groin. You note that he has very long fingers and toes and a high-arched palate. Abdominal examination reveals a pulsatile and expansile mass just below the umbilicus. The most appropriate screening investigation is:

A: Ultrasound scan

B: Angiography

C: Abdo MRI

D: Abdo CT scan

A

A.

Suspect Marfan Syndrome: major complication is AAA

Most appropriate, least invasive first line Ix is

Angiography – Invasive, can’t always determine true size of aneurysm

Abdo CT scan (With contrast) = most accurate visualisation of an AAA but due to availability of resources / invasiveness it’s not first line

Abdo MRI – pt in pain not likely to stay motionless long enough

208
Q

A 30-year-old woman presents to your ED complaining of sudden onset SOB, right-sided pleuritic chest pain and haemoptysis. She has a PMHx of 3 miscarriages and a deep venous thrombosis in the right leg. CTPA confirms a pulmonary embolism.
A diagnosis of anti-phospholipid syndrome is suspected. Which of the following auto-antibodies would confirm the diagnosis if detected?

A: anti-centromere antibody

B: anti-nuclear antibody

C: anti-mitochondrial antibody

D: anti-cardiolipin antibody

A

D. Raised anti-cardiolipin antibodies would confirm Dx (also would see lupus anticoagulant antibodies and anti-beta-2 glycoprotein I antibodies)

209
Q

An adult male presents with a 6 week history of right sided headache, general malaise, early morning stiffness, and pain in his jaw when eating. His CRP is 63 (0-5), ESR 78 (0-15). Which of the following is true about his underlying disease?

A. It is associated with ANCA positivity

B. It typically affects those between 50 and 60 years old

C. It can present with acute sight loss

D. It rarely responds to corticosteroids

E. It is a vasculitis affecting small blood vessels

A

C. It is GCA or temporal arteritis

210
Q

Which of the following is now a rare cause for joint infection in infants, due to the standard childhood immunisation schedule in the UK?

A. Staphylococcus Aureus

B. Gp A (β haemolytic) Streptococcus

C. Varicella Zoster

D. Rubella

E. Haemophilus Influenzae

A

E

211
Q

A 64 year old woman with type 2 diabetes mellitus has been struggling with cellulitis of her right forefoot for 4 weeks. After making no progress with oral antibiotics, she has now had 14 days of intravenous flucloxacillin and co-amoxiclavulanic acid but the pain and erythema persist and her CRP has only fallen to 47 from its peak of 91. What is the next most appropriate investigation?

A. Blood cultures

B. MRI right forefoot

C. Plain X-ray right forefoot

D. Skin biopsy of right forefoot

E. Ultrasound scan of right forefoot

A

C.

The risk is that contiguous spread from the soft tissues has developed osteomyelitis in one of the bones of her feet. As this has now been going on a number of weeks, a plain film is likely to show something and this can be organised much more quickly than an MRI.

A The blood cultures will be unhelpful as likely to be negative if on antimicrobials

B MRI foot would be a good test but is less easily available and may not be necessary if plain film shows OM

D Skin biopsy will not show bacteria and not exclude OM

E Ultrasound right foot could be useful to exclude a soft tissue abscess but these are rare in the feet if not clinically apparent

212
Q

Which of the following is the most frequent infecting organism after hip replacement?

A. Methicillin resistant Staphylococcus aureus

B. Coagulase negative staphylococcus

C. Salmonella

D. Enterococcus faecalis

E. Propionibacterium acne

A

B

213
Q

A 37 year old man with a 10 year history of back pain presents with a “flare” of symptoms – pain in his lower back radiating out over his buttocks and down the back of his thighs, and pain between the shoulder blades. Ibuprofen has been helping significantly. He finds it very difficult to get moving in the mornings.
Which of the following features would support a diagnosis of inflammatory back pain?

A. Worsening pain on bending forwards

B. Worsening pain on bending backwards

C. Pain shooting down his leg to the ankle

D. Pain across the costochondral joints

E. Improved pain whilst sitting at work

A

D. B is facet joint pain, C is sciatica

214
Q

Which of the following is an extra-articular manifestation of rheumatoid arthritis?

A. Subcutaneous nodules

B. Episcleritis

C. Peripheral sensory neuropathy

D. Pericardial effusion

E. All of the above

A

E

215
Q

Which of the following is a classical feature of Rheumatoid Arthritis on X-ray?

A. Peri-articular sclerosis

B. Sub-chondral cysts

C. Osteophytes

D. Peri-articular erosions

E. New bone formation

A

D, all the others are osteoarthritis

216
Q

A 53 year old man presents to you with a 3 day history of pain in his lower back. The pain has started spontaneously and he first noticed it at work. He works as a builder, and has been unable to go to work for the last three days and is keen to have a ‘sick note’. Physical examination reveals him to be slightly overweight with a BMI of 29, but there are no neurological deficits or spinal deformity and the pain is not easily localised on examination.

Which of the following describes the best management for this gentleman?

A. Given his age, he should be referred to a specialist

B. He should be sent for an X-ray to look for any pathological changes to his spine

C. He should not be given a sick note, and advised to return to work straight away

D. He should be reassured and advised to take simple analgesics and return to normal activity as soon as he can manage

E. He should be advised to seek other employment

A

D

217
Q

For a lytic tumour to be visible on X-ray, it must have lost:

A. Greater than 6% bone density

B. Greater than 16% bone density

C. Greater than 60% bone density

D. Greater than 90% bone density

E. 100% bone density

A

C

218
Q

A 57 year old man presents with a 3 day history of a painful 1st MTP joint. On examination the area is red and very warm. He has a BMI of 32 and hypertension, and has had identical episodes before. Which of the following dietary changes would reduce his risk of future similar episodes?

A. A diet with a high red meat content

B. A diet rich in dairy products

C. Drinking >5 cans of non-diet fizzy drinks per day

D. A diet rich in sugary foodstuffs

E. Switching from drinking beer to drinking lager

A

B

219
Q

Which of the following is not an autoimmune connective tissue disease?

A. Systemic Lupus Erythematosus

B. Ehlers Danlos syndrome

C. Primary Sjorgen’s syndrome

D. Systemic sclerosis

E. Dermatomyositis

A

B

220
Q

A 23 year old woman presents with mouth ulcers, fever, painful white fingers and pleuritic chest pain. She is antinuclear antibody (ANA) (+), her ESR is 52 (0-15), and her white cell count is low (leucopenic). Which of the following features would you not expect to be associated with her illness?

A. Deforming arthritis

B. Photosensitive rash

C. Seizures

D. Pulmonary embolism

E. Thrombocytosis

A

E, this woman has SLE

221
Q

Which of the following is used in the treatment of SLE?

A. Anti-TNF

B. Anti-malarials

C. Ustekinuab (IL12/IL23 blocker)

D. Sulfasalzine

E. Allopurinol

A

B

222
Q

An adult male presents with a 6 week history of right sided headache, general malaise, early morning stiffness, and pain in his jaw when eating. His CRP is 63 (0-5), ESR 78 (0-15). Which of the following is true about his underlying disease?

A. It is associated with ANCA positivity

B. It typically affects those between 50 and 60 years old

C. It can present with acute sight loss

D. It rarely responds to corticosteroids

E. It is a vasculitis affecting small blood vessels

A

C

223
Q
A

E. Brachioradialis

224
Q
A

E. Serratus anterior

225
Q
A

B. Capitulum of the humerus

226
Q
A

A. Femoral nerve

227
Q
A

E. Median and radial nerve

228
Q
A

D. Flexor carpi radialis

229
Q
A

B. Axillary nerve

230
Q
A

A. Adductor longus

231
Q
A

D. Peroneus longus

232
Q
A

E. Median nerve

233
Q
A

C. Wrist drop

234
Q
A

A

235
Q
A

D. Claw hand

236
Q
A

D. Lateral epicondylitis

237
Q
A

C. Profunda femoris

238
Q
A

C. Scaphoid

239
Q
A

D. Periarticular erosions

240
Q

Which drug would be a suitable first-line treatment for a patient with rheumatoid arthritis?

a) Topical diclofenac
b) Leflunomide
c) Etanercept
d) IM methylprednisolone

A

B) Leflunomide

241
Q

A 65-year-old male patient sees his GP after developing a widespread skin rash. Which of his prescribed medication is most likely to have caused this and should be discontinued?

a) Atorvastatin
b) Ibuprofen gel
c) Allopurinol
d) Naproxen

A

C) Allopurinol

242
Q

A 26 year old male presents with haemoptysis, a strong cough, wheeze, chronic nosebleeds and a saddle-nose deformity. A urine dipstick reveals haematuria and proteinuria. Blood test reveals cANCA positive.

What is your differential diagnosis?

A. Polyarteritis Nodosa

B. Kawasaki Disease

C. Takayasu’s Arteritis

D. Granulomatosis with polyangiitis

E. Henoch-Schonlein Purpura

A

D. Granulomatosis with polyangiitis

243
Q

Mary is a 62y/o lady presenting with dry eyes. She has a PMH of SLE, for which she takes hydroxychloroquine. Mary tells you she has also been more tired than normal lately, and when you ask about her diet she tells you she drinks a lot of water as her mouth gets very dry.

A. What is the likely differential diagnosis for Mary?

B. Is this a primary or secondary diagnosis? Why?

C. How might you investigate this?

D. How might you explain the type of arthritis caused by this condition?

E. What is the most appropriate management?

A

A. Sjogren’s syndrome

B. Secondary - previously diagnosed SLE

C. Bloods - ANA, anti-Ro, anti-La, Rheumatoid Factor. Schirmer test (filter paper under lower eyelid). Salivary gland biopsy (not 1st line) - inflammation

244
Q

Michelle is a 42 year old who presents to her GP with joint and muscle pain. She also reports being short of breath recently. On examination you notice a malar rash. You complete an ANA blood test, which comes back positive for ANA and and anti-dsDNA.

Which of the following is the least likely to be a complication of this disease?

A. Interstitial Lung Disease

B. Pleuritis

C. Recurrent Miscarriage

D. Polycythaemia

E. Nephritis

A

D. Polycythaemia

245
Q

An 18 year old male presents to his GP with progressive back pain and stiffness. You decide to send him for a spinal x-ray to investigate which reveals a bamboo spine on the x-ray.

A. What gene would you associate with this disease?

B. Name 3 other findings you would expect to see on the x-ray.

C. Give an example of an Anti-TNF drug that you would prescribe this patient.

A

A. HLA-B27 (ankylosing spondilytis)

B. Squaring of vertebral bodies, syndesmophytes, subchondral sclerosis and erosions

C. Etanercept

246
Q

Margaret is a 61-year-old dear who has limped into your GP surgery looking in discomfort. She says she has pain in her left knee, which is worse when she has to walk down to the shops or walk her dog. When you ask about joint stiffness, she says they are stiff for about 25 minutes when she wakes up, and then after that it becomes the pain that limits her. It has gone on for some years but she has had enough.

A. What is your differential diagnosis?

B. What might you see on an X-Ray of her knee?

C. What is the cause of these changes? (think about cartilage physiology)

D. Other than analgesia, what management options does Margaret have?

A

A. Osteoarthritis

B. Loss of joint space, osteophytes, subarticular sclerosis (increased density along joint line) and subchondral cysts

247
Q

A 66 year old patient presents to the GP with bone pain. They have recently had a few fractures which resulted in them going to A+E. You also notice that when they walk in there is some bone deformity in their left leg. You send them for some testing.

A. How would the skull in this patient appear on x-ray?

B. Which LFT would you expect to be raised?

C. What type of drug would you use to treat this patient?

A

This is Paget’s disease.

248
Q

Sally is a 37-year-old lady who presents to the GP with tender, swollen joints. They are stiff for around an hour in the morning, though this improves throughout the day with activity. On examination, Sally has ulnar deviation and Boutonniere’s deformity.

Which of the following blood markers would be most specific to her likely diagnosis?

A. Rheumatoid Factor

B. Erythrocyte Sedimentation Rate

C. C-Reactive Protein

D. Anti-Cyclic Citrullinated Peptide Antibody

E. Anti-Ro and Anti-La antibodies

A

D. Anti-Cyclic Citrullinated Peptide Antibody

249
Q

Taylor presents to their GP complaining of muscle pain, fatigue and weakness in both hands and forearms, and their shoulders over the last few weeks. On examination you find Gottron lesions on their knuckles and elbows, a photosensitive rash on their face and some subcutaneous calcinosis. You conduct a blood test and their results show positive for ANA, a creatinine kinase of 1200 U/L, and Anti-Jo-1 antibodies.

What is the differential for this patient?

A. Polymyositis

B. Dermatomyositis

C. Vasculitis

D. Antiphospholipid syndrome

E. Fibromyalgia

A

B. Dermatomyositis

250
Q

Vitamin D metabolism is important for the absorption of calcium and phosphate from the intestine, therefore important for bone mineralisation.

Which of the following substances is not involved in bone metabolism?

A. Parathyroid Hormone

B. 1-alpha-hydroxylase

C. Antiphospholipid antibody

D. Oestrogen

E. Calcitonin

A

C. Antiphospholipid antibody

251
Q

Vitamin D metabolism is important for the absorption of calcium and phosphate from the intestine, therefore important for bone mineralisation.

i. What condition might cause an adult to have brittle bones due to insufficient vitamin D?
ii. What condition occurs in a child?
iii. Why do you not get this condition in adulthood?
iv. What does a T-Score of -2 mean?
v. What is the first-line treatment for osteoporosis?

A

i. Osteomalacia
ii. Ricket’s
iii. Occurs due to impaired bone mineralisation prior to epiphyseal closure
iv. Osteopenia
v. Bisphosphonates

252
Q

Susan is a 55 year old female who has presented to you with a severe unilateral headache in her forehead. She has also had some blurred vision and tenderness of the scalp. Her blood test results in an ESR of 73.

A. What test would you like to do to confirm the diagnosis?

B. What would you expect to find on this test to confirm your diagnosis?

A

a. Temporal artery biopsy
b. Multinucleate giant cell

253
Q

Which of the following is not a true regarding gout?

A. Negatively birefringent on polarised light microscopy

B. Monosodium urate crystals

C. Allopurinol is first-line treatment during acute flare

D. Tophi may deposit within the ear

E. Needle-shaped crystals

A

C. Allopurinol is first-line treatment during acute flare

254
Q

Sharon is a 54 year old female who presents to your GP practice with a main complaint of chronic widespread pain and tenderness. She complains that her muscles feel stiff in the morning. She also has had difficulty sleeping, and therefore is tired and has low mood and concentration. You determine that the pain is musculoskeletal, not arthritic.

What is your diagnosis?

A

Fibromyalgia

255
Q

Which of the following is not a risk factor for developing fibromyalgia?

A. Low income

B. Being divorced

C. Low educational status

D. Depression

E. Poor diet

A

E. Poor diet

256
Q

Colin is a 78-year-old man who has a long history of osteoarthritis. He underwent a knee replacement 3 days ago, and now has an acutely swollen knee that is hot to the touch, stiff, and he can’t move it due to severe pain. He has a fever of 38.1 and is lethargic.

A. What is the likely diagnosis?

B. What is the most appropriate investigation?

C. What is the most likely causative organism?

D. Which empirical antibiotic(s) are first line?

A

A. Septic arthritis

B. Joint aspiration and microscopy, culture and sensitivities

C. Staphylococcus aureus

D. Flucloxacillin (and rifampicin for the first 2 weeks)

257
Q

Jules is a 14 year old who has presented to you with a complaint of bone pain with swelling around their knee. The swelling hasn’t gone down despite ibuprofen use over the last week. Jules has a PMHx of hereditary retinoblastoma.

Based on their symptoms and PMHx:

A. What is the most likely diagnosis?

B. What tests would you like to do to confirm this?

C. How would you treat this?

A

A. Osteosarcoma

B. Needle/surgical biopsy, X-ray, CT, MRI, bone scan

C. Surgery to remove the cancer/affected limb/lower portion of the limb

258
Q

Mary is a 37 y.o lady presenting to her GP with a 2-week history of difficulties swallowing. She has no problem drinking but solid food tends to get stucked somewhere around her sternum. There is no pain on swallowing and she has not regurgitated food back out.

She denies any weight loss, fever or recent trauma.

Past medical history of GORD. Her mum had a disease which she could not recall but affected her skin badly.

O/E: Patches of shiny skin bilaterally on her arms up to her shoulder. Limited ROM of fingers. White discoloration over her knuckles

Based on the most likely diagnosis, which would be most useful for diagnosis of the pathology? (+++)

A. Nerve conduction study

B. Electromyography

C. Endoscopy

D. Serum nuclear antigens

E. Urine culture & sensitivity (MSU)

A

D.Serum nuclear antigens (Limited→ Anticentromere, Diffuse→ Antitopoisomerase, Anti-scl 70, Anti RNA polymerase III

259
Q

Chimdi is a 1 year-old boy who had recently moved from Nigeria to the United Kingdom. During his 1st week here, he started having fever and felt generally unwell. When you examined him, he was tender to touch over his left hip. His vitals are temp: 38, RR: 40, 120bpm, 95 O2%. Later, you had found out from his parents that he had sickle cell disease.

Further investigations were ordered and it was confirmed that Chimdi had osteomyelitis of his left hip and was given antibiotics for it.

Based on the history above, what is the most likely causative organism? (++)

A. Salmonella species

B. Staphylococcus aureus

C. Neisseria gonorrhoea

D. Pseudomonas aeruginosa

E. Pasturella

A

A. Salmonella species

260
Q

Malcolm is a 25 y.o gentleman presenting to his GP with pain in his lower back for 3 months. He also gets stiffness in the back in the morning, however that improves with exercise. He has a family history of arthritis. He has Crohn’s for which is well controlled with medications.

His obs are normal. On examination, he has redness in both eyes. Based on the above, what is the most likely diagnosis? (+)

A. Rheumatoid arthritis

B. Ankylosing spondylitis

C. Psoriatic arthritis

D. Reactive arthritis

E. Osteoarthritis

A

B. Ankylosing spondylitis

261
Q

A 82 y.o gentleman presents to the GP with a 2 month history of back pain. The pain is localised and does not radiate at all. He has also been feeling very tired recently and you notice that he seem to look really pale. Over the past 2 months, Jim been constantly getting pneumonia. Jim used to work in the petrol industry.

His obs are normal.

His relevant blood results are:

Hb: 97 (110-130)

Creatinine: 260 (<176)

Urea: 49 (<30)

CRP 63 (<40)

Based on the history, which is the best investigation to confirm the diagnosis. (++)

A. Serum LDH levels

B. Serum electrophoresis

C. X-ray of bone

D. MRI of bone

E. Serum calcium levels

A

B. Serum electrophoresis (IgG, IgA, light chain proteins)

262
Q

Malcolm has a red hot swollen joint. He also has a fever and is systemically unwell. His blood pressure is low.

A. How would you manage this patient? (2)

B. Name 3 risk factors for septic arthritis? (1)

C. Malcolm is sexually active, what is the most likely causative organism for his septic joint? (1)

A

A. Sepsis 6 and joint fluid aspiration

B. Immunosuppressants, diabetes, HIV, old age, IV drug use

C. Neisseria gonorrhoea

263
Q

63 y.o. Patient comes in with left sided knee pain. She says she’s had it for a few months now and hurts whenever she tries to move it. She also thinks she’s been having hearing difficulties on her right ear as of late. She is given a bone isotope test thats shows areas of abnormal bone turnover with decreased osteoclast action. The main areas found affected were the right side of skull and left knee.

What is the most likely diagnosis?

What is the first line treatment for her?

A. Calcitonin

B. Prednisolone

C. Zoledronate

D. Ibuprofen

E. No treatment needed

A

Most likely diagnosis: Paget’s disease of bone - abnormal bone turnover. C - zolendronate is the first line treatment for symptomatic patients as it is absorbed by overactive osteoclasts or osteoblasts and suppresses bone resorption

264
Q

John 42 y.o. Man comes to clinic with freaking out as he is afraid that he has lung cancer. He screams that he has recently had a cough and has been coughing out blood. He says he has hd weight loss recently too. His father had lung cancer while his mother had an autoimmune disease that he can’t remember the name of. He says recently he has been peeing less and the color is usually very dark reddish brown but he just thought it was because he had been drinking too much alcohol.

When investigated, his blood showed that he was positive for Anti glomerular basement membrane antibodies.

Urine dipstick showed:

Blood +++

Protein +

Nitrites

What is the most likely cause of his symptoms:

A. SLE

B. Antiphospholipid syndrome

C. Wegener’s Granulamotosis

D. Metastasized Small cell lung cancer

E. Goodpasture’s syndrome

A

E. Goodpasture’s syndrome

265
Q

Mary 33 y.o. Woman comes into clinic complaining of pain and swelling of joints all over. Her fingers, wrist and knees hurt the most on both sides. She says that the pain and stiffness is worse in the morning but thankfully gets better as the day goes by.

A. What is the best biochemical blood marker to test for to diagnose her?

B. Name two clinical features/ deformities commonly found on the arms/hands of patients.

C. Name one sign of this illness seen on X-rays.

D. What is the one joint never affected by this illness?

E. What marker is used to monitor progression of this illness?

A

A. Anti-CCP

B. Ulnar deviation, swan neck deformity

C. Soft tissue swelling (also loss of joint space and bony erosions)

D. DIPJ

E. CRP

266
Q

Mary is 34 y.o. Woman who has been trying to conceive for the last 10 years. However she is always unsuccessful as the last four times she was pregnant, she ended up having a miscarriage. She and her partner have had fertility consultation. Her ovaries, fallopian tube and uterus were all normal and she has no history of STD. His sperm count was also normal. When further questioned, Mary rememebered that her mom did also tend to have miscarriages a lot and so the doctor believes this could be autoimmune caused.

What is the most likely diagnosis?

A. Wegener’s granulomatosis

B. Goodpasture’s

C. SLE

D. Systemic sclerosis

E. Antiphospholipid syndrome

A

E. Antiphospholipid syndrome - antiphospholipid antibodies stop the egg from implanting and also inhibit growth of foetal cells commonly causing miscarriage

267
Q

Patient has been diagnosed with systemic lupus erythematosus (SLE).

A. List one risk factor for this illness?

B. List two clinical manifestations of this illness?

C. What are two gold standard biochemical marker used to diagnose this illness?

D. Describe the ESR and CRP changes caused by this illness?

E. What is the first line management for this illness?

A

A. Family history (others = idiopathic, EBV, medications: hydralazine, isoniazid

B. Malar flush (butterfly rash), glomerulonephritis

C. ANA (high sensitive low specific) and anti-dsDNA (high specific)

D. ESR raised, CRP normal

E. Oral corticosteroids (prednisolone) for mild; high dose corticosteroids (IV methylprednisolone) for severe

268
Q
A

E. Negatively birefringent needle shaped crystals

269
Q
A
270
Q
A
271
Q
A
272
Q
A

C. Excessive non-mineralised osteoid

Phase 2a (13 decks)

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