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Sirpi's Phase 2A Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is Osteomyelitis?

A

Infection and inflammation of the bone.

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2
Q

Aetiology/Risk Factors for Osteomyelitis

A

Immunodeficiency (immunosuoppressants, HIV, etc)
DM - diabetic foot ulcers
Inflammatory arthritis e.g rheumatoid arthritis
Trauma
Sickle cell anaemia
Intravenous drug usage

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3
Q

Bacterial Aetiology of Osteomyelitsi

A

Staphylococcus aureus - most common
S.epidermidis - prosthetic joints
Salmonella - sickle cell disease
H.influenzae
P.aeruginosa - IVDU

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4
Q

What are the methods in which a bone can become infected?

A

Direct Inoculation - trauma, open wound

Contiguous Spread - infection of adjacent joint/tissue

Haematogenous Seeding - IVDU, catheter

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5
Q

Pathophysiology of Osteomyelitis

A

Inflammation due to infection causes inflammatory exudate in bone marow.
Results in increased intramedullary pressure - oedema.
Exudate can then go into the bone cortex and rupture periosteum.
Can interrupt perfusion and cause necrosis.
Leaves separated pieces of dead bone called sequestra.
New bone formation known as involucrum.

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6
Q

What is the most common site affected in children from haematogenous seeding osteomyelitis?

A

Metaphysis of long bones

Because blood flow is slower

Lack of endothelial basement membrane

Capillaries lack phagocytic lining cells.

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7
Q

What is the most common site affected in adutls from haematogenous seeding osteomyelitis?

A

Spinal vertebrae

Vertebrae get more vascular with age, allowing for increased likelihood of bacterial endplate seeding.

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8
Q

Acute pathophysiological changes seen in osteomyelitis

A

Oedema
Bone inflammation
Vascular congestion
Small vessel thrombi

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9
Q

Chronic pathophysiological changes seen in osteomyelitis

A

Necrotic bone ‘sequestra’
New bone formation - ‘involucrum
Lymphocytes and histiocytes
Exudate

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10
Q

Clinical Presentation of Acute Osteomyelitis

A

Onset over several days.

Dull pain at site which may be aggravated by movement.

Inflamed, swollen, tender at site of infection.

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11
Q

Clinical Presentation of Chronic Osteomyelitis

A

Deep / large ulcers that fail to heal despite several weeks treatment*
Non-healing fractures

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12
Q

Investigation of Osteomyelitis

A

FBC - leukocytosis
Raised CRP

First line: X-ray - can show osteopaenia - changes can be seen within 2 weeks of infection.

MRI scan - marrow oedema

GS: Blood cultures and bone biopsy

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13
Q

Differential Diagnoses of Osteomyelitis

A

Charcot joint - damage to sensory nerves due to diabetic neuropathy.
Cellulitis
Avascular necrosis of bone
Gout
Fracture

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14
Q

Medical Management of Osteomyelitis

A

Empirically vancomycin + ceftriaxone

Once organism is identified,

6 weeks IV antibiotics is considered minimum.

Stopping treatment is guided by CRP monitoring.

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15
Q

Surgical Management of Osteomyelitis

A

Debridement

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16
Q

Aetiolgy of Septic Arthritis in Adults

A

S.aureus
Streptococcus spp.
Neisseria gonorrhoeae
P.aeruginosa
Mycobacteria
Fungi

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17
Q

Aetiology of Septic Arthritis in children

A

S.aureus
H.influenzae
Kingella kingae

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18
Q

Risk Factors for Septic Arthritis

A

Immunosuppression (including steroids only)
Old age
Rheumatoid arthritis (or other immune-driven disease)
Diabetes mellitus
Prosthetic joint

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19
Q

Clinical Presentation of Septic Arthritis

A

Painful, red, swollen, hot joint

Mainly monoarthritis - single joint affected.

In children - may present as hesitation to use the joint.

Fever

Knee > hip > shoulder

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20
Q

Clincal Presentation of Gonococcal Septic Arthritis

A

Polyarthritis

Maculopapular – pustular rash

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21
Q

Investigation of Septic Arthritis

A

FBC: Leukocytosis
Raised CRP

Joint aspiration + culture - diagnostic
Infected joint fluid is turgid, viscous.

Blood cultures - mostly caused by bacteraemia seeding.

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22
Q

Management of Septic Arthritis

A

6 weeks minimum antibiotics

S.aureus - IV flucloxacillin

Gonococcal - IV ceftriaxone + azithromycin

Analgesia

Joint aspiration until no recurrent effusion.

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23
Q

What must be done for patients on corticosteroids with septic arthritis?

A

Temporary stoppage of short term immunosuppression.

If on long term steroids, prednisolone dose needs to be doubled in order to maintain glucocorticoid levels.

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24
Q

Investigation of Prosthetic Joint Infection

A

Serology: Alpha defensin positive - antimicrobial peptide found in synovial fluid.

Joint aspiration is diagnostic.

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25
Q

Mangement of Prosthetic Joint Infection

A

Antibiotic Suppression

Debridement and Implant Retention (DAIR) of Prosthesis - not for chronic infections.

Excision Arthroplasty

Exchange Arthroplasty

Amputation

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26
Q

Aetiology/RIsk Factors of Rheumatoid Arthritis

A

Female gender
HLA-DR4 presence
Smoking

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27
Q

Pathophysiology of Rheumatoid Arthritis

A

Overproduction of TNF-a leads to synovitis.

Further cytokine release causes synovium to grow past joint margins to form a pannus.

The pannus destroyed articular cartilage and subchondral bone resulting in erosions.

Mutation in process of arginine to citrulline conversion causes presence of anti-CCP (citric citrullinated peptide) antibodies.

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28
Q

Clinical Presentation of Rheumatoid Arthritis

A

Is a polyarthritis which affects joints symmetrically.

Swollen, painful and stiff joints.

Worse in the morning, improves throughout day.

Prolonged early morning stiffness (>60 mins)

Affects mainly small joints of hands such as MCP, PIP and feet like MTP.

DIP and spine sparing

Can affect elbows, shoulders, knees and ankles too.

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29
Q

Extra-Articular Manifestations of Rheumatoid Arthritis

A

Pericarditis (cardiovascular)
Episcleritis (ophthalmological)
Amyloidosis (renal)
Bronchiectasis (respiratory)
Peripheral neuropathy (neurological)
Subcutaneous nodules (dermatological)

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30
Q

Examination of Rheumatoid Arthritis

A

Decreased grip strength - cannot form fist.

Ulnar deviation of hand

Z-thumb

Boutonniere deformity - flexed PIP, extended DIP to form “^” shape at PIPJ.

Swan neck deformity - flexed DIP, extended PIP to form “^” shape at DIPJ.

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31
Q

Investigation of Rheumatoid Arthritis

A

FBC - may show normocytic normochromic anaemia
Raised CRP

Serology - Rheumatoid factor and Anti-CCP (cyclic citrullinated peptide) positive.

X-rays (may be normal at presentation but will get worse later)

Biopsy of nodules - cholesterol deposits.

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32
Q

What would be seen on an X-Ray for Rheumatoid Arthritis?

A

LESS

Loss of joint space
Erosion of bone
Soft tissue swelling
Soft bone (osteopaenia)

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33
Q

Management of Rheumatoid Arthritis

A

First line: DMARDs (Disease Modifying Anti-Rheumatic Drugs)

GS: Methotrexate 10-25mg per week

Sulphasalazine 2-3g daily
Leflunomide 10-30mg daily
Hydroxychloroquine 200mg

+ NSAIDs -Naproxen, Ibuprofen

Corticosteroids - Oral prednisolone or intra-articular injection

Biologics:

Anti TNF medications such as infliximab, adalimumab
Anti IL-6 such as tocilizumab.
Anti CD20 such as rituximab - last line.

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34
Q

Complication of Rheumatoid Arthritis

A

Felty Syndrome

Triad of RA + splenomegaly + granulocytopaenia.
More prone to infections since neutropaenia.

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35
Q

Pharmacodynamics of Methotrexate

A

Folate antagonists through inhibiting dihydrofolate reductase to reduce nucleic acid synthesis and cell replication.

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36
Q

Contraindications of Methotrexate

A

Contraindicated in pregnancy

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37
Q

Side effects of Methotrexate

A

Nausea, mouth ulcers, anaemia

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38
Q

Contraindications of adalimumab

A

Heart failure, ongoing infection.

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39
Q

Side effects of adalimumab

A

Agranulocytosis, anaemia, arrhythmias

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40
Q

What is the composition of gout crystals?

A

Monosodium urate

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41
Q

What is the composition of pseudogout crystals?

A

Calcium pyrophosphate

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42
Q

Epidemiology of crystal arthropathies

A

Gout - more common in males
Pseudogout - more common in females.

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43
Q

Physiology of purine metabolism

A

Xanthines are converted into uric acid by xanthine oxidase enzyme.

Humans lack uricase enzyme to further metabolise uric acid so it is excreted by kidneys.

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44
Q

Aetiology/Risk Factors of Gout

A

Hyperuricemia
Dietary - beer, red meats, high fructose diet.
CKD - limited excretion of purines
Drugs - Diuretics, aspirin

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45
Q

Pathophysiology of Gout

A

Caused by the deposition of sodium urate crystals within joint

The immunological reaction initiated to try and remove them, leads to acute pain and swelling

Soft drinks - fructose shares renal uric acid transporter which minimizes excretion of uric acid.

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46
Q

Clinical Presentation of Gout

A

Onset is usually at night.

Normally monoarticular, asymmetric arthritis.

Can be aggravated after high purine diet such as meats, seafood, alcohol.

Initial presentation of inflammation/pain of big toe - first MTP joint

Affect feet, ankles, knees, elbows, hands
Lower limbs are affected earlier on, upper limbs later.

If left to progress, can lead to tophi - erosion away from the articular margin.

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47
Q

Investigation of Gout

A

GS - Joint aspiration + microscopy
Negative birefringent needle-like crystals seen under polarized light.

FBC - leukocytosis due to inflammation
U + E - kidney status

Serum uric acid - often normal during attacks since the uric acid is not in the blood but in the form of joint crystals, but often raised in between attacks.

X-ray if recurrent episodes.

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48
Q

Lifestyle Management of Gout

A

Increased dairy intake
Reduced fructose intake
Reduced red meat and alcohol intake.

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49
Q

Management of Chronic Gout

A

Aim of management is to reduce uric acid below <300 micromols/L

Allopurinol – Xanthine Oxidase Inhibitor
Febuxostat – more potent Xanthine Oxidase Inhibitor

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50
Q

Complications of Gout

A

Renal calculi
Acute and chronic urate nephropathy

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51
Q

Clinical Presentation of Pseudogout

A

Polyarticular arthropathy.

Often affects the knee and wrist.

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52
Q

Investigation of Pseudogout

A

Joint aspiration + microscopy - rhomboid crystals, positive birefringence under polarized light.

X-ray: Chondrocalcinosis - cartilage calcification parallel to articular surface

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53
Q

Management of Acute Gout and Pseudogout

A

1st line: Oral NSAIDs (short course) unless renal failure, peptic ulcers

2nd line: Oral Colchicine 500ug 2-3 times daily

3rd line: Corticosteroids - Intra-articular injection or oral low dose (5-10mg short course) e.g prednisolone

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54
Q

Pharmacodynamics of Colchicine

A

Disrupts tubulin activity causing loss of microtubule based inflammatory chemotaxis.

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55
Q

Side effects of Colchicine

A

Abdo pain, nausea/vomiting, melena.

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56
Q

What is Osteoporosis?

A

A systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture

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57
Q

Epidemiology of Osteoporosis

A

50% of women and 33% of men will experience an osteoporotic fracture.

20% of people with hip fractures die within the first year.

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58
Q

Aetiology/Risk Factors of Osteoporosis

A

SHATTERED

Steroid use
Hypoparathyroidism & Hyperthyroidism
Alcohol and tobacco
Testosterone decrease - increased bone turnover
Early menopause - increased bone turnover
Renal failure
Erosive bone disease e.g RA
Dietary calcium decrease (malabosorption)

Previous and family history of fracture

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59
Q

Screening for Osteoporosis

A

FRAX Score

Gives risk of fractures over the next 10 years

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60
Q

Components of FRAX Score

A

Age
Smoking
Family history of hip fracture
Glucocorticoid use (eg, Prednisone)
Arthritis
Femoral neck bone mineral density

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61
Q

Pathophysiology of Osteoporosis

A

Osteoporosis results from increased bone breakdown by osteoclasts and decreased bone formation by osteoblasts, leading to loss of bone mass

Bone mass decreases with age, but will depend on the ‘peak’ mass attained in adult life and on the rate of loss in later life

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62
Q

What factors affect peak bone mass?

A

Genetic factors - most important

Dietary Vit.D intake

Levels of physical activity

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63
Q

Factors affecting bone strength

A

Bone density
Bone size
Bone quality (turnover, architecture, mineralization).
Age (increasing age increases fracture risk)

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64
Q

Changes in Trabecular Architecture with Ageing

A

Decrease in trabecular thickness

Decrease in horizontal inter-trabecular connections in order to preserve integrity of vertical trabecular connections.

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65
Q

Investigation of Osteoporosis

A

Bone Densitometry

DEXA scan (dual energy x-ray absorptiometry)
Measures the risk of having a fracture.

T-score

Standard deviation compared with gender matched young adult average.

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66
Q

What is the range and meaning of T-scores?

A

> -1 = normal
-1 to -2.5 = osteopaenia
< -2.5 = osteoporosis
< -2.5 + fracture = severe osteoporosis

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67
Q

Management of Osteoporosis

A

First line - bisphosphonates e.g IV zoledronate, oral alendronate

Denosumab - RANK ligand inhibitor

Teriparatide - PTH analogue

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68
Q

Pharmacokinetics of bisphosphonates

A

Inhibit farnesyl pyrophosphate synthase (FPP synthase) in the cholesterol synthesis pathway.

Reduces the ruffled border of osteoclasts, decreasing their activity and bone resorption.

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69
Q

Side effects of denosumab

A

Skin itching, back pain, cloudy urine.

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70
Q

Contraindications for bisphosphonates

A

Hypocalcaemia

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71
Q

Pharmacodynamics of denosumab

A

RANK receptor is expressed on osteoclast precursor.

RANK ligand expressed on osteoblasts.

Binding of ligand to receptor causes maturation into osteoblasts.

Is a monoclonal antibody to RANK ligand to does not allow osteoclast differentiation, reducing bone resorption.

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72
Q

Side effects of bisphosphonates

A

Increased risk of jaw osteonecrosis, oesophageal issues e.g oesophagitis, dysphagia.

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73
Q

Pharmacodynamics of teriparatide

A

PTH analogue that stimulates osteoblastic activity.

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74
Q

What are some inherited connective tissue disorders?

A

Marfan’s Syndrome
Ehler Dahnos Syndrome

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75
Q

What are some autoimmune connective tissue disorders?

A

Systemic Lupus Erythematosus
Sjorgen syndrome
Systemic Sclerosis
Dermatomyositis

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76
Q

Aetiology of Marfan’s Syndrome

A

Autosomal dominant FBN1 gene mutation on chromosome 15 affecting fibrillin-1 protein.

77
Q

Pathophysiology of Marfan’s Syndrome

A

FIbrillin-1 is a glycoprotein that forms a sheath around elastin and sequesters TGF-β, a growth factor for connective tissue.

Lack of connective tissue structure and growth.

78
Q

Clinical Presentation of Marfan’s Syndrome

A

Very tall, lanky people

Chest wall deformity - Pectus carinatum (pigeon chest), pectus excavatum (deep indentation at and around sternum)

79
Q

Investigation of Marfan’s Syndrome

A

Diagnose through genetic testing for FBN-1 mutation.

80
Q

Aetiology of Ehler-Danlos Syndrome

A

Mutation in Type V collagen gene causing defective collagen synthesis.

81
Q

Clinical Presentation of Ehler-Danlos Syndrome

A

Joint hypermobility
Flexible skin
Easy bruising/bleeding.

82
Q

Complications of Ehler-Danlos and Marfan’s Syndrome

A

Aortic aneurysms
Mitral regurgitation
Subarachnoid haemhorrage

83
Q

Epidemiology of SLE

A

More common in women of childbearing age, Afro-Caribbean

84
Q

Aetiology/Risk Factors for SLE

A

Drugs e.g isoniazid, sulfasalzine
UV light
EBV
Family history

85
Q

Pathophysiology of SLE

A

T3 hypersensitivity reaction.
Recognition of self-antigens causes production of anti-nuclear autoantibodies. Results in immune complex deposition in tissues which results in cytokine release and systemic inflammation.

86
Q

Clinical Presentation of SLE

A

FAME PEG

Fever
Arthritis (deforming, non-erosive arthritis)
Mouth ulcers
Episcleritis

Photosensitive malar rash
Erythema
Glomerulonephritis (haematuria)

Pericarditis, pleural effusion.
Reynaud’s = white fingers due to vasoconstriction and lack of blood flow.
Seizures (neuropsychiatric lupus)
P.E

87
Q

Investigation of SLE

A

Raised ESR but not CRP
FBC: Normocytic anaemia , leukopenia.
Serology: Anti nuclear antibody positive, anti double stranded DNA.
Biopsy will show IgG and complement deposition.

88
Q

Management of SLE

A

Reduce sunlight exposure
NSAIDs
Hydroxychloroquine - antimalarial.
Cyclophosphamide
Biologics - rituximab, belimumab.

89
Q

What are the different types of systemic sclerosis (scleroderma)?

A

Limited cutaneous scleroderma (most common)

Diffuse cutaneous scleroderma

90
Q

Pathophysiology of Systemic Sclerosis

A

Increased synthesis of T1 and T2 collagen causing connective tissue fibrosis and widespread vascular damage

91
Q

Clinical Presentation of Systemic Sclerosis

A

CRESS

Calcinosis (subcutaneous calcium deposition)

Raynaud’s phenomenon

Esophageal dysmotility

Sclerodactyly - thickening and tightening of fingers and skin around fingers.

Spider veins

92
Q

Investigation of Systemic Sclerosis

A

Serology: Anti-centromere antibodies in LCS, Anti-topoisomerase, anti-Scl-70 antibodies in DCS
Anti-nuclear antibodies in both.

93
Q

Pathophysiology of Sjorgen Syndrome

A

Autoimmune exocrine gland destruction through lymphocytic infiltration.

94
Q

Clinical Presentation of Sjogren Syndrome

A

Keratoconjunctivitis sicca (Dry eyes)
Joint pain
Xerostomia (decreased saliva production

95
Q

Investigation of Sjogren Syndrome

A

Serology: RF positive, ANA positive, anti-Ro and anti La antibody positive.

Schirmer test where tears are put onto filter paper and travel <10mm when normally should be >20mm.

96
Q

Management of Sjorgen Syndrome

A

Artificial tears and saliva administration

Hydroxychlroquine.

97
Q

What is Polymyositis/Dermatomyositis

A

Inflammation + necrosis of skeletal muscle

If skin involved then dermatomyositis.

98
Q

Clinical Presentation of Polymyositis

A

Symmetrical progressive muscle weakness.

Hard to stand from sitting

99
Q

Clinical Presentation of Dermatomyositis

A

Gottron’s papules (scales on knuckles).

Heliotrope - purple eyelid.

100
Q

Investigation of Polymyositis/Dermatomyositis

A

Muscle enzymes: Raised creatinine kinase, lactate dehydrogenase

GS: Muscle biopsy - shows necrosis and inflammationvo
Serology: ANA positive, anti-Jo-1 Ab positive

101
Q

Management of Polymyositis/Dermatomyositis

A

IV corticosteroids like prednisolone.

102
Q

What is Vasculitis

A

Inflammation and necrosis of blood vessel walls.
Can result in aneurysm and rupture.

103
Q

Examples of large vessel vasculitis

A

Giant cell arteritis
Takayasu’s arteritis

104
Q

Examples of medium vessel vasculitis

A

Classical polyarteritis nodosa
Kawasaki’s disease

105
Q

Examples of small vessel vasculitis

A

ANCA associated:

p-ANCA: Microscopic polyangitis and eosiniphilic granulomatosis with polyangitis (Churg-Strauss)

c-ANCA: granulomatosis with polyangitis

Not ANCA associated:
Essential cryoglobulinaemia

106
Q

General Investigations for Vasculitis

A

Raised ESR/CRP

FBC: Anaemia

Serology: Either negative or positive for p-ANCA or c-ANCA

107
Q

General Management of Vasculitis

A

Steroids e.g prednisolone
Immunosuppression e.g cyclophosphamide.

108
Q

Epidemiology of Giant Cell (Temporal) Arteritis & Polymyalgia Rheumatica

A

Normally affects women over 50

109
Q

Pathophysiology of Giant Cell Arteritis

A

Can affect branches of the external carotid artery
E.g facial, ophthalmic, temporal artery.

110
Q

Clinical Presentation of Giant Cell Arteritis

A

Unilateral headache on the temples.
Temporal artery tenderness
Jaw claudication

Can prevent with painless acute loss of sight.

111
Q

Clinical Presentation of Polymyalgia Rheumatica

A

Pain occurs above and below torso (shoulders, thighs, neck, knees)

Can have systemic symptoms of fever, weight loss, night sweats.

112
Q

Diagnostic Investigation of Giant Cell Arteritis & Polymyalgia Rheumatica

A

Temporal artery biopsy - can show inflammation and giant cells.

113
Q

Managment of Temporal Arteritis

A

Oral prednisolone
If visual symptoms - IV methylprednisolone.

Can give oral aspirin prophylaxis.

114
Q

Complications of Giant Cell Arteritis

A

Optic neuropathy causing sudden painless vision loss.

115
Q

Aetiology/Risk Factors of Polyarteritis Nodosa

A

Associated with hepatitis B

More common in males

116
Q

Clinical Presentation of Polyarteritis Nodosa

A

Weight loss
Melena
Numbness
Fever
Hypertension
Livedo reticularis - lace like purple rash.

117
Q

Clinical Presentation of Microscopic Polyangitis

A

Dyspnoea
Renal failure

118
Q

Investigation of Microscopic Polyangiitis

A

Serology: P-ANCA positive

119
Q

Henoch-Schonlein Purpura

A

IgA Associated small vessel vasculitis
Associated with IgA nephropathy.

120
Q

Investigation of Henoch-Schonlein Purpura

A

Immune complex deposition on tissue biopsy.

121
Q

Investigation of Eosinophilic Granulomatosis with Polyangitis (Churg-Strauss)

A

Eosinophilia
Raised serum IgE
Serology: p-ANCA

122
Q

Pathophysiology of Granulomatosis with Polyangitis

A

Necrotizing vasculitis
Necrotizing glomerulonephritis
Necrotizing granulomas in respiratory tract.

123
Q

Investigation of Granulomatosis with Polyangitis (Wegener’s)

A

Serology: c-ANCA positive
CXR: Large nodular densities.

124
Q

What is fibromyalgia?

A

A chronic pain syndrome

125
Q

Clinical Presentation of Fibromyalgia

A

Chronic widespread pain despite exclusion of other disease.
Areas of tenderness
Arthralgia - stiffness
Sleeplessness
Cognitive disturbances.

126
Q

Differential Diagnoses of Fibromyalgia

A

Polymyalgia rheumatica
Inflammatory arthritis

127
Q

Management of Fibromyalgia

A

Physiotherapy
Regular exercise
Low does antidepressants e.g TCAs like amitryptiline

128
Q

What are the serongative spondyloarthropathies?

A

Ankylosing spondylitis (axial spondyloarthritis)

Psoriatic arthritis

Acute anterior uveitis (acute iritis - synonymous with anterior uveitis)

Enteropathic arthritis (IBD)

Reactive arthritis

Undifferentiated spondyloarthritis

129
Q

What immune molecule are all the seronegative spondyloarthropathies asssociated with?

A

HLA B27

130
Q

Where is HLA B27 present?

A

On all cells except erythrocytes.

131
Q

What are two theories for the pathophysiology of HLA-associated seronegative spondyloarthropathies?

A

Molecular Mimicry

HLA B27 misfolding

132
Q

What is the HLA B27 molecular mimicry theory?

A

If antigen similar to HLA B27 is present on pathogens, there can be autoimmunity against existing HLA B27 containing cells.

133
Q

What is the HLA B27 misfolding theory?

A

Misfolding of HLA-B27 heavy chains causes stress on endoplasmic reticulum causing an inflammatory and immune response.

IL 12/23 involvement.

134
Q

Clinical Presentation of Sernoegative Spondyloarthritis

A

SPINEACHE

Sausage digit (dactylitis - swelling of whole finger or whole toe, synovitis + tenosynovitis)
Psoriasis - typically on extensor surfaces - back of elbows, front of knees
Inflammatory back pain
NSAID good response
Enthesitis (inflammation of tendon) - achilles tendon, heel.
Arthritis - normally asymmetric , large joint affecting.
Crohns/colitis/elevated CRP
HLA B27
Eye (uveitis)

135
Q

What is ankylosing spondylitis?

A

Chronic inflammatory disorder of the spine, ribs, sacroiliac joints.

More common im men below age of 45.

136
Q

Pathophysiology of Ankylosing Spondylitis

A

Repeated inflammation can result in fatty deposits and bone erosion.
Replacement by syndesmophyte formation occurs.
Causes bone fusion resulting in reduced mobility.
Affects areas like spine, ribs, sacroiliac joint, etc.

137
Q

Clinical Presentation of Ankylosing Spondylitis

A

Back pain - can occur at night and gets better with exercise.

Kyphosis

Sacroiliac (buttock) pain.

138
Q

Investigation of Ankylosing Spondylitis

A

Spinal X-ray: Bamboo spine appearance

MRI: periarticular bone marrow oedema

139
Q

Management of Ankylosing Spondylitis

A

First line - NSAIDS e.g naproxen.

Second line - biologics
Anti TNF e.g infliximab, adalimumab
IL-17 blockers e.g secukinumab.

DMARDS are not very effective.

140
Q

Clinical Presentation of Psoriatic Arthritis

A

Asymmetrical polyarthritis

DIP inflammation
Dactylitis – sausage digit / toe
Nail dystrophy
Enthesitis

Regions of psoriatic rash: Behind ears, scalp, under nails

141
Q

Clinical presentation of Arthritis Mutilans

A

Complication of psoriatic arthritis.

Is where there is very destructive bone changes.

Causes floppy fingers and shortened fingers due to joint degeneration.

142
Q

Investigation of Psoriatic Arthritis

A

X ray - pencil in cup sign in interphalangeal joints.

143
Q

Management of Psoriatic Arthritis

A

First line: DMARDs - e.g methotrexate

Second line: Anti-TNF e.g adalimumab, infliximab.

Third line: Anti IL 12/23 e.g Ustekinumab

144
Q

Reactive Arthritis

A

Sterile inflammation of synovial membrane, tendon and fascia triggered by an infection at a distal site.

Mostly post STI or enteric infection.

145
Q

Aetiology/Risk Factors of Reactive Arthritis

A

Sexual activity

Gastrointestinal infection - shigella, salmonella, c.jejuni

STI - chlamydia, gonorrhoea

146
Q

Clinical Presentation of Reactive Arthritis

A

Reiter’s Triad

Assymetrical, lower limb monoarthritis + enthesitis
Conjunctivitis
Urethritis

Keratoderma blennorrhagica - red-brown papules on plantar surface of feet
Genital inflammation

147
Q

Management of Reactive Arthritis

A

First line: NSAIDs e.g as naproxen

If persisting: DMARDs e.g methotrexate.

148
Q

Aetiology of Clinical Presentation of Enteropathic Arthritis

A

Associated with crohn’s disease and UC

Large joint, asymmetrical arthritis.

149
Q

Examples of Primary Bone Tumours

A

Osteosarcoma
Chondroma
Ewing’s sarcoma

150
Q

Clinical Presentation of Primary Bone Tumours

A

Localised pain, often worse at night (can wake up at night).
Can cause symptoms of hypercalcaemia.
Loss of mobility
Lumps

151
Q

Features of Osteosarcoma

A

Associated with Paget’s disease
Can metastasize to lung
Has pleiomorphic osteoblasts.
Occurs in the metaphysis of long bones.
Most commonly knee and proximal humerus

152
Q

Investigation of Osteosarcoma

A

X-Ray: Sunburst appearance

153
Q

What is a Chondrosarcoma?

A

Cartilage cancer

154
Q

Features of Ewing’s Sarcoma

A

Arises from mesenchymal stem cells
Most common in diaphysis of long bones.
Mostly affects children and young adults <15 years old.

155
Q

Investigation of Ewing’s Sarcoma

A

X-ray - onion skin appearance.

156
Q

Investigations of Bone Tumours

A

X-ray is first line.
Full length of bones imaging.
Can be evidence of bone destruction, periosteal/soft tissue swelling.

CT
Used to determine bone/tumour morphology
CT-CAP for primary tumour staging.

Biopsy
Diagnostic test
Fine needle aspiration cytology - carcinomas
Core biopsy for sarcomas

157
Q

Staging of Musculoskeletal Tumours

A

Grade - low (G1) or high (G2)
Extent of Tumour (T) - intra (T1)/extracompartmental (T2)
Intra if not crossing the intramuscular septum
Metastasis

AJCC TNM
Size of the primary tumor (T)
Spread to nearby lymph nodes (N)
Metastasis to distant sites (M)

158
Q

Surgical MSK Tumour Management

A

Bone:
Limb salvage - autograft, allograft, endoprosthetic replacement
Amputation

Soft Tissue:
Tumour excision
Angioembolization of feeding artery to tumour.

159
Q

Medical MSK Tumour Management

A

Adjuvant or neo-adjuvant chemotherapy.

Radiotherapy - Definitive management of radiosensitive primary tumour.

160
Q

What is Osteoarthritis?

A

Most common condition affecting synovial joints.

Age related, dynamic reaction pattern of a joint in
response to insult or injury.

Articular cartilage is most affected.

161
Q

Risk Factors for Osteoarthritis

A

Age - cumulative effect of trauma on joints
Female gender - esp. Postmenopausal
Obesity
Occupation - jobs involving manual labour

162
Q

Pathophysiology of Osteoarthritis

A

Mediated by cytokines (IL-1, TNF-a, NO)

Imbalance in degradation of cartilage and production by chondrocytes causing progressive destruction and loss of articular cartilage with an accompanying periarticular bone response

163
Q

General Clinical Presentation of Osteoarthritis

A

Pain - improves with rest but gets worse throughout the day with weight bearing

Functional impairment - walking, gripping

Joint swelling - bony swelling

Short-lived morning stiffness

164
Q

Clinical Presentation of Osteoarthritic Hand

A

Can involve DIP, PIP, CMC joints - especially 1st CMC (base of thumb)

Heberden’s nodes at DIP joints

Bouchard’s nodes at PIP

165
Q

Investigation of Osteoarthritis

A

X-Ray - LOSS

Loss of joint space
Osteophyte formation
Subchondral sclerosis
Subchondral cysts

Abnormalities of bone contour.

166
Q

Non-pharmacological management of Osteoarthritis

A

Physio/occupational therapy
Lifestyle changes - weight loss, increased exercise.
Walking aids e.g stick, walking frame

167
Q

Pharmacological Management of Osteoarthritis

A

First line: Topical/oral NSAIDs or capsaicin

Second line: Add paracetamol

Intra-articular steroid injections

168
Q

Surgical management of Osteoarthritis

A

Joint arthroscopy, arthrodesis, arthroplasty.

169
Q

What is Osteomalacia?

A

Defect in bone mineralisation.
Occurs after fusion of epiphysis.
Rickets is defective bone mineralisation in children which occurs during bone growth.

170
Q

Aetiology of Osteomalacia

A

Vitamin D deficiency
Hyperparathyroidism (causing hypophosphataemia)
CKD - no activation of vitamin D.
Drugs - anticonvulsants and rifampin.

171
Q

Clinical Presentation of Osteomalacia

A

Muscle weakness - waddling gait, difficulty getting out of chair.
Bone pain
Pathological fractures - especially femoral neck.

172
Q

Investigation of Osteomalacia

A

U + E
Low calcium, phosphate,
High ALP, High PTH

X-Ray - osteopaenia, looser’s zones

Diagnostic is bone biopsy - shows decreased mineralisation.

173
Q

Management of Osteomalacia

A

Calcitriol supplementation

174
Q

What is Paget’s Disease?

A

Focal disorder of bone remodelling.

175
Q

Pathophysiology of Paget’s Disease

A

Uncoordinated excessive activity of osteoclasts and osteoblasts causes patchy areas of sclerosed and lytic new bone.
Increases the risk of pathological fractures.

176
Q

Clinical Presentation of Paget’s Disease

A

Bone pain
Deformities such as bowed tibia
Deafness

177
Q

Investigation of Paget’s Disease

A

Raised ALP
Normal calcium, phosphate

X ray
Areas of sclerosis and lytic regions
Cotton wool appearance of skull

178
Q

Management of Paget’s Disease

A

Bisphosphonates e.g IV zoledronate, oral aledronate.
NSAIDs for pain

179
Q

Aetiology of Antiphospholipid Syndrome

A

Can be primary or secondary to another autoimmune disorder e.g SLE.
More common in females.

180
Q

Pathophysiology of Antiphospholipid Syndrome

A

Antiphospholipid antibodies (aPL) bind to
phospholipid on the surface of cells such as endothelial cells and platelets causing a state of hypercoagulability.

Cause CLOTS:
Coagulopathies
Livedo reticularis
Obstetric issues such as miscarriage
Thrombocytopaenia

181
Q

Clinical Presentation of Antiphospholipid Syndrome

A

Livedo reticularis
Thrombosis
Ischaemic stroke
DVT

182
Q

Investigation of Antiphospholipid Syndrome

A

Serology: Presence of antiphospholipid antibodies such as lupus anticoagulant, anticardiolipin antibodies, B2 glycoprotein antibodies.

183
Q

Management of Antiphospholipid Syndrome

A

First line: Long term Warfarin
If pregnant: Heparin + aspirin

184
Q

Aetiology of Mechanical Lower Back Pain

A

Scoliosis
Lumbar spondylosis - loss of intervertebral disc compliance
Facet joint syndrome
Sciatica
Vertebral disc degeneration - can cause prolapse
Osteoarthritis

185
Q

Risk Factors of Mechanical Back Pain

A

Manual labour
Increasing age
Female gender
Smoking

186
Q

Clinical Presentation of Mechanical Back Pain

A

Pain - often short lived & relieved by rest
Stiff back and scoliosis
Muscle spasms

187
Q

Pathophysiology of Lumbar Spondylosis

A

Loss of compliance of intervertebral discs.
Most commonly in L4-S1.

188
Q

Investigation of Mechanical Lower Back Pain

A

X-ray

189
Q

Management of Mechanical Lower Back Pain

A

Analgesia - e.g NSAIDs, paracetamol,
Physiotherapy

Sirpi's Phase 2A Medicine (13 decks)

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