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MBChB Final Exam Essentials > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is articular cartilage composed of?

A

High water content

Type II collagen and proteoglycans

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2
Q

What condition is anti-citrullinated peptide antibodies (ACPA) highly specific for?

A

Rheumatoid arthritis

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3
Q

What does the presence of serum anti-dsDNA indicate?

A

Systemic Lupus Erythematosus (SLE)

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4
Q

What does the presence of serum anti-Ro indicate?

A

Primary scleroderma or systemic lupus erythematosus

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5
Q

What does the presence of serum anti-La indicate?

A

Primary scleroderma or systemic lupus erythematosus

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6
Q

What does the presence of serum anti-Smith indicate?

A

Systemic Lupus Erythematosus

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7
Q

What does the presence of serum anti-Jo-1 indicate?

A

Polymyositis and dermatomyositis

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8
Q

What does the presence of serum anti-phospholipid indicate?

A

Antiphospholipid syndrome

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9
Q

Name the muscles of the rotator cuff muscles

A

Supraspinatus
Infraspinatus
Subscaularis
Teres minor

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10
Q

What is meralgia paraesthetica?

A

Lateral cutaneous nerve of thigh compression

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11
Q

What are the symptoms of meralgia paraesthetica?

A

Numbness and increased sensitivity to light touch over the anterolateral thigh - usually self-limiting

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12
Q

What are the characteristics of mechanical back pain?

A

Sudden onset

Often unilateral and may be helped by rest

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13
Q

Outline some causes of mechanical back pain

A 
Lumbar disc prolapse
Osteoarthritis 
Fractures 
Spondylolithiesis
Spinal stenosis
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14
Q

There a certain ‘red flag’ symptoms in the presentation of lumbar back pain. List them.

A 
Aged <20 or >50 
Constant pain without relief 
History of TB, HIV, steroid use or carcinoma 
Systemically unwell 
Localised bone tenderness
Bilateral signs in legs
Neurological deficit 
Bladder, bowel or sexual dysfunction

Any thoracic back pain is considered a ‘red flag’

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15
Q

What course of action is indicated in the presence of ‘red flag’ symptoms for lower back pain?

A

Spinal X-ray

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16
Q

In the presence of neurological symptoms with concurrent back pain, what imaging modality is of most value?

A

Spinal MRI

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17
Q

How is mechanical back pain, in the absence of obvious pathology, managed?

A

Analgesia
Breif rest
Physiotherapy

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18
Q

What is the pathophysiology of acute disc disease?

A

Prolapse of the intervertebral disc resulting in acute back pain with/without sciatica

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19
Q

What demographic is acute intervertebral disease most common in?

A

Younger people

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20
Q

What is the more common cause of sciatica in older patients?

A

The result of compression of the nerve root by osteophytes in the lateral recess of the spinal cord

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21
Q

What is the typical presentation of acute vertebral prolapse?

A

Sudden onset of severe back pain (often following strenuous activity)

Pain is related to position and is aggrevated by movement

Muscle spasm leads to sideways tilt when standing

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22
Q

How is acute vertebral prolapse managed?

A

Symptom control - analgesia, bed rest (on firm mattress)

In severe disease consider epidural corticosteroid injection or surgery

Physiotherapy in the recovery period

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23
Q

What pathological process is chronic disc disease associated with?

A

Degenerative changes in the lower lumbar discs and facet joints. Pain is the mechanical type

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24
Q

What area of pain may arise from an S1 lesion?

A

From buttock down the back of thigh and leg to the foot

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25
Q

What area of pain may arise from an L5 lesion?

A

Buttock to the lateral aspect of the leg and dorsum of the foot

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26
Q

What area of pain may arise from an L4 lesion?

A

Lateral aspect of the shin to the medial side of the calf

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27
Q

What area of sensory loss may arise from an S1 lesion?

A

Sole of foot and posterior calf

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28
Q

What area of sensory loss may arise from an L5 lesion?

A

Dorsum of the foot and anterolateral aspect of leg

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29
Q

What area of sensory loss may arise from an L4 lesion?

A

Medial aspect of the calf and shin

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30
Q

What area of motor weakness may arise from an S1 lesion?

A

Plantar flexion of ankle and toes

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31
Q

What area of motor weakness may arise from an L5 lesion?

A

Dorsiflexion of foot at toes

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32
Q

What area of motor weakness may arise from an L4 lesion?

A

Dorsiflexion and inversion of the ankle; extension of the knee

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33
Q

What reflex is associated with the S1 spinal level?

A

Ankle jerk

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34
Q

What reflex is associated with the L4 spinal level?

A

Knee jerk

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35
Q

What is spondylolithesis?

A

Slipping forward of one vertebra on another, most commonly L4/L5.

Arising from a defect in the pars interarticularis

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36
Q

How is spondylolisthesis managed?

A

Minor pathology is treated conservatively

Major pathology is treated with spinal fusion

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37
Q

What is spinal stenosis?

A

Narrowing of the lower spinal canal compresses the cauda equina.

Typically coming on after a period of walking and resolving after rest

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38
Q

List some causes of spinal stenosis

A

Disc prolapse
Degenerative osteophytes formation
Tumour
Congenital narrowing

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39
Q

What position can a patient adopt that will open the spinal canal?

A

Bending forwards

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40
Q

What is the curative treatment for spinal stenosis?

A

Surgical decompression

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41
Q

What is the pathophysiology of osteoarthritis?

A

Arises from reparative processes characterised by progressive destruction and loss of articular cartilage

Attempts at repair produce cartilaginous growths at the margins of the joint which later calcify (osteophytes)

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42
Q

What is the typical presentation of osteoarthritis?

A

Joint pain made worse on movement and relieved by rest

Stiffness occurs after rest (called gelling)

Most common joints affected are distal interphalangeal joitns (DIPJs), first carpalmetacarpal, metatarsophalangeal and weight-bearing joints

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43
Q

What are some differential diagnoses of osteoarthritis?

A

Chondrocalcinosis
Chronic trophaeceous gout
Psoriatic arthritis

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44
Q

Outline the management of osteoarthritis

A

Focus on symptoms and disability:

Analgesia
Surgery
Physiotherapy

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45
Q

There are three main subgroups to inflammatory arthritis; what are they?

A

Rheumatoid arthritis
Seronegative Spondyloarthritis
Crystal arthritides

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46
Q

What is the pathophysiology of rheumatoid arthritis?

A

Chronic systemic autoimmune disorder characterised chiefly by synovitis (inflammation of the synovial lining of the joints, tendon sheathes and bursae)

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47
Q

What is the clinical presentation of rheumatoid arthritis?

A

Insidious onset of pain, early-morning stiffness (lasting 30mins or more) and symmetrical swelling in the proximal small joints of the hands and feet

Weakening of the joint capsule later occurs leading to instability, subluxation and deformity

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48
Q

Explosive and palindromic presentations of rheumatoid arthritis are much less common. Outline them.

A

Explosive - sudden onset of widespread arthritis

Palindromic - relapsing and remitting monoarthritis of different large joints

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49
Q

What pathology might you expect in a patient with disproportionate involvement of a single joint in the context of rheumatoid arthritis?

A

Must exclude septic arthritis

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50
Q

List some non-articular manifestations of rheumatoid arthritis (12)

A 
Fever
Fatigue
Weight-loss
Sjögren's syndrome
Carpal tunnel syndrome 
Cord compression
Anaemia 
Pleural effusion
Thrombocytosis 
Pericarditis
Nail fold infarcts
Amyloidosis

Not exhastive list

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51
Q

Outline the management of rheumatoid arthritis

A

NSAIDs and Coxibs
Corticosteroids
Disease-modifying antirheumatic drugs (DMARDs)
Biologics

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52
Q

What are the commonly used disease-modifying antirheumatic drugs (DMARDs) for rheumatoid arthritis?

(3)

A

Sulfasalazine
Methotrexate
Leflunomide

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53
Q

What characteristics are common across all the seronegative spondyloarthritides?

(5)

A

Predilection for axial (spinal and sacroiliac) inflammation
Asymmetrical peripheral arthritis
Absence of rheumatoid factor (seronegative)
Inflammation of the enthesis
Strong association with HLA-B27

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54
Q

List the common seronegative spondyloarthritides

A

Axial Spondyloarthritis
Psoriatic arthritis
Reactive arthritis
Enteropathic arthritis

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55
Q

What is axial spondyloarthritis?

A

Inflammatory disorder of the spine, affecting mainly young adults

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56
Q

What is the term used to describe axial spondyloarthritis with radiographic changes at the sacroiliac joints?

A

Ankylosing spondyloarthritis

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57
Q

What are the clinical features of axial spondyloarthritis?

A

Typically young male presenting with increasing pain and prolonged morning stiffness in the lower back which improves with exercise but not rest

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58
Q

What examination findings would be expected in the case of axial spondyloarthritis?

A

Loss of lumbar lordosis
Reduced spinal flexion (Schober test)
Reduction in chest expansion
Non-articular features (aortic incompetence, lung fibrosis)

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59
Q

Describe the radiographic changes associated with ankylosing spondyloarthritis

A

Sclerosis/ankylosis of sacroiliac joints

Progressive calcification of interspinous ligaments producing ‘bamboo spine’

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60
Q

What is the management strategy for axial spondyloarthritis?

A

Morning exercises to maintain posture and spinal mobility

Slow release NSAIDs (usually taken at night)

Methotrexate (to help with peripheral disease)

TNF-alpha highly effective in both axial and peripheral disease

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61
Q

Psoriatic arthritis has several different subtypes. List them.

A 
Distal interphalangeal arthritis 
Mono- or oligoarthritis 
Symmetrical seronegative polyarthritis 
Arthritis mutilans 
Sacroiliitis
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62
Q

What is the most common subtype of psoriatic arthritis?

A

Distal interphalangeal arthritis

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63
Q

Outline the treatment of psoriatic arthritis

A

Analgesia and NSAIDs

Local synovitis responds to intra-articular corticosteroid injections

In severe cases, methotrexate and TNF-alpha is effective

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64
Q

What is reactive arthritis?

A

Sterile synovitis following a gastrointestinal or sexually acquired infection.

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65
Q

The presence of what immunological marker increases the susceptibility to reactive arthritis?

A

HLA-B27 positivity

66
Q

What bacteria are associated with reactive arthritis?

6

A 
Shigella
Salmonella
Yersinia
Campylobacter
Chlamydia trachomatis 
Ureaplasma urealyticum
67
Q

What is the classical triad of Reiter’s syndrome?

A

Urethritis
Reactive arthritis
Conjunctivitis

68
Q

How is reactive arthritis managed?

A

NSAIDs and local corticosteroid injections

Persisting infection is treated with antibiotics

Relapsing cases can be treated with sulfasalazine, methotrexate and TNF-alpha inhibitors

69
Q

What is enteropathic arthritis?

A

Large joint mono- or asymmetrical oligoarthritis occuring in 10-15% of patients with ulcerative colitis/Crohn’s disease

70
Q

What is the pathophysiology of gout?

A

Caused by hyperuracaemia and intra-articular sodium urate crystals

71
Q

Hyperuracaemia and deposition of sodium urate crystals result in four clinical syndromes. What are they?

A

Acute sodium urate synovitis (acute gout)
Chronic interval gout
Chronic polyarticular gout
Chronic tophaceous gout

72
Q

What are the two biological mechanisms leading to hyperuracaemia?

A

Imapired excretion of uric acid e.g. chronic kidney disease or hyerprtension

Production of uric acid e.g. HGPRT (Lesh-Nyan syndrome) or myeloproliferative disorder

73
Q

How does acute gout present?

A

Sudden onset of severe pain, swelling, redness and warmth over the affected joint

Most typically the first metatarsophalangeal joint

74
Q

What may precipitate an attack of acute gout?

A

Dietary or alcohol excess

Dehydration (dietary or starting a diurectic)

75
Q

How does chronic trophaecous gout present?

A

Large, white smooth white deposits (tophi) in the skin and around the joints (particularly the ears, fingers and on the Achilles tendon)

76
Q

What investigations are indicated in a case of suspected gout?

A

Joint fluid microscopy - negatively bifringent under polarised light
Serum uric acid is raised
Serum urea and creatinine for signs of renal impairment

77
Q

How is acute gout treated?

A

NSAIDs
Cochicine
Corticosteroids (intramuscular or intra-articular)

78
Q

How is hyperuracaemia treated?

A

Allopurinol

79
Q

When are uricosuric agents e.g. allopurinol contra-indicated?

A

In the immediate period (1 month) after an attack of acute gout as it has a risk to induce a further attack of acute gout

80
Q

What is pseudogout?

A

Deposition of calcium pyrophosphate dihydrate in articular cartilage and peri-articular tissues producing the radiological appearence of chondrocalcinosis

81
Q

How do pseudogout crystals appear under polarised light?

A

Positively bifringent

82
Q

Delay in treatment of septic arthritis can lead to what complications?

A

Sepsis, irreversible joint destruction, long-term disability or death

83
Q

What is the most common bacteria responsible for causing septic arthritis?

A

Staphylococcus aureus

84
Q

In the elderly and immunosuppressed patients, what type of bacteria is the most common cause of septic arthritis?

A

Gram-negatives

85
Q

What is the classic presentation of septic arthritis?

A

Hot, painful, swollen and red joint

86
Q

Joint aspiration is necessary in the investigation of acute monoarthritis. How does it normally appear and what is the normal white cell count?

A

Straw coloured with <3000 WCC/mm^3

87
Q

Joint aspiration is necessary in the investigation of acute monoarthritis. How does it appear and what is the normal white cell count during an inflammatory but not septic disease?

A

Cloudy and contains 3000 WCC/mm^3

88
Q

Joint aspiration is necessary in the investigation of acute monoarthritis. How does it appear and what is the normal white cell count in septic disease?

A

Opaque and containing up to 75,000 WCC/mm^3 (mostly neutrophils)

89
Q

What is the empirical treatment of acute non-gonococcal bacterial arthritis?

A

Flucloxacillin 1-2g hourly IV
Oral fusidic acid 500mg 8-hourly
Add gentamicin in immunosuppressed patients

90
Q

What is the most common cause of septic arthritis in previously young and fit adults?

A

Gonnococcal arthritis

91
Q

How is gonococcal septic arthritis treated?

A

Penecillin, ciprofloxacin or doxycyclin for two weeks and joint rest

92
Q

What is meningococcal arthritis?

A

Complicates the clinical picture of meningococcal septicaemia and presents as a migratory polyarthritis

93
Q

How is meningococcal arthritis treated?

A

Penecillin

94
Q

What is tuberculosis arthritis?

A

Approx. 1% of tuberculosis patients have joint/bone involvement

Hip, knee and spine (intervertebral disc) are most commonly affected

95
Q

What is the presentation of tuberculosis arthritis?

A

Insidous onset of pain, swelling and dysfunction.

Systemically the patient is febrile, has night sweats and loses weight.

96
Q

How is tuberculosis arthritis treated?

A

Common tuberculosis treatment (rifampicin, isoniazid, ethambutol, pyrazinimide) but extended for nine months with intital joint rest and immobilisation

97
Q

How can osteomyeltis develop?

A

Occurs due to haematogenous spread (e.g. from a boil) or due to local infection

98
Q

What is the most common causative agents in osteomyelitis?

A

Staphylococcus aureus
Haemophilus influenzae
Salmonella

99
Q

What are the symptoms of osteomyelitis?

A

Fever, pain and local eythema

Sinus formation in chronic osteomyelitis

100
Q

How is osteomyelitis diagnosed?

A

CT/MRI
Blood cultures
Bone biopsy and cultures

101
Q

How is osteomyelitis treated?

A

Flucloxacillin and fusidic acid for at least of 4-6 weeks (IV initially with switch to oral therapy when tolerated)

102
Q

What are autoimmune rheumatic diseases?

A

Autoimmune rheumatic diseases are a collection of diseases in which non-organ specific autoantibodies target joints among other sites

103
Q

List the autoimmune rheumatic diseases

A

Systemic autoimmune erythematosus (SLE)

Antiphospholipid syndrome

Systemic sclerosis (scleroderma)

Polymyositis and dermatomyositis

Sjögren’s syndrome

‘Overlap’ syndromes and undifferentiated autoimmune rheumatic disease

104
Q

What is systemic lupus erythematosus (SLE)?

A

Inflammatory multisystem disease characterised by the presence of serum antibodies against nuclear components

105
Q

Describe the epidemiology of systemic lupus erythematosus (SLE)

A

A disease mostly of young women with a peak age of onset between 20 and 40

106
Q

What is the clinical presentation of systemic lupus erythematosus? List five features.

A

Any of the following:

Symmetrical small joint arthralgia

Skin manifestations (malar flush)

Non-specific features - fever, malaise and depression

Blood - anaemia, leucopenia, thrombocytopenia

Serositis (pleuritis and pericarditis)

Alopecia

Glomerulonephritis

107
Q

Outline the managment of systemic lupus erythematosus (SLE)

A

NSAIDs useful for mild disease/arthralgia

Chloroquine and hydroxychloroquine when

NSAIDs are insufficient

Corticosteriods (mainstay of treatment)

Immunosuppressives

108
Q

What is discoid lupus?

A

Benign variant of SLE which just manifests as skin disease - characterised by facial rash with erythematous plaque and scarring

109
Q

What is antiphospholipid syndrome?

A

Syndrome characterised by thrombosis/recurrent miscarriages and persistently positive blood tests for antiphosophlipid antibodies (including anticardiolipin and lupus anticoagulant)

110
Q

What are the clinincal features of antiphosphlipid syndrome?

A

Arterial: stroke, TIA, myocardial infarction

Venous: DVT

Placental: recurrent miscarriages

Other features: migrain, epilepsy, renal impairment, accelerated atheroma

111
Q

What is the management of antiphosphlipid syndrome?

A

Long-term warfarin

Pregnant patients recieve aspirin and heparin

112
Q

What is systemic sclerosis (scleroderma)?

A

A multi-system disease with involvement of the skin and Raynaud’s phenomenon occuring early

113
Q

What is the pathophysiology of scleroderma?

A

Uncontrolled and irreversible proliferation of connective tissue and thickening of vascular walls with narrowing of the lumen

114
Q

What are the two clinical manifestations of scleroderma?

A

Limited cutaneous scleroderma (LcSSc, 70% of cases)

Diffuse cutaneous scleroderma (DcSSc, 30% of cases)

115
Q

What is the disease course of limited cutaneous scleroderma?

A

Starting with Raynaud’s phenomenon before skin disease

Skin of the lower legs, proximal arms and face is thickened and tethered

Sclerodactyly, microstomia, painful digital ulcers, calcinosis in the fingers

116
Q

What was the term previosuly used to describe limited cutaneous scleroderma?

A

CREST syndrome

117
Q

What does CREST syndrome stand for?

A 
Calcinosis
Raynaud's phenomenon
Eosophageal involvement
Sclerodactyly 
Telangiectasia
118
Q

What is the difference between limited and diffuse cutaneous scleroderma?

A

Skin changes are more rapid and widespread with early involvement of other organs.

119
Q

Outline the non-skin organ involvement of diffuse cutaneous scleroderma

A

Gastrointestinal - atony of oesophagus (headburn and dysphagia), small intestine (bacterial overgrowth, malabsorption), colon (pseudo-obstruction)

Renal - acute/chronic kidney disease, acute hypertensive crisis

Lung - fibrosis, pulmonary hypertension

Heart - myocardial fibrosis (causing arrythmias), hypertension

120
Q

What investigations are indicated in scleroderma?

A

Blood count - anaemia, raised ESR

Urea/creatinine - increased in renal disease

Serum autoantibodies - anti-Ro/La, ANA, anticentromere

Radiology - showing calcinosis of hands

Barium swallow - oesophageal dysfunction

121
Q

How is scleroderma treated?

A

Hypertension - ACEIs

Pulmonary hypertension - oral vasodilators, oxygen, warfarin

Pulomary fibrosis - cyclophosphamide/azothioprine with prednisolone

122
Q

What is polymyositis/dermatomyositis?

A

Polymyositis is a rare muscle disorder of unknown aetiology in which there is inflammation and necrosis of skeletal muscle fibres

When skin is involved it becomes dermatomyositis

123
Q

What are the clinical features of polymyositis?

A

Symmetrical progressive muscle weakness and wasting of proximal muscles of the shoulder and pelvic girdle

Involvement of respiratory muscles can lead to dystonia, dysphagia and respiratory failure

124
Q

What are the characteristic skin changes of dermatomyositis?

A

Heliotrope rash (purple discolouration of the eyes)

Gottron’s papules (scaly, erythematous plaques on the knuckles)

125
Q

What investigations are relevant for the diagnosis of polymyositits/dermatomyositis?

A

Muscle biopsy is the definitive test

Serum muscle enzymes (creatine kinase, aminotransferases) are elevated

Anti-JO antibodies are positive

Electromyography show characteristic changes

126
Q

What is the treatment of choice for polymyositis/dermatomyositis?

A

Oral prednisolone

Immunosuppressive therapy (azathioprine, methotrexate, ciclosporin) if the disease relapses

127
Q

What is Sjögren’s syndrome?

A

A disorder characterised by immunologically mediated destruction of epithelial exocrine glands, especially lacrimal and salivary glands

128
Q

What are the symptoms of Sjögren’s syndrome?

A 
Keratoconjunctivitis sicca (dry eyes)
Xerostomia (dry mouth)

Other features: arthritis, Raynaud’s phenomenon, renal tubular defects, pulmonary fibrosis

129
Q

What investigations are indicated in Sjögren’s syndrome?

A

Serum autoantibodies: anti-nuclear, anti-Ro and rheumatoid factors

Labial gland biopsy (shows lymphocytic infiltration and acinar destruction)

Positive Schirmer test

130
Q

What is the Scirmer test?

A

A standrd strip of paper is placed on the inside of the lower eyelid; wetting of less than 10mm in 5 mins is positive

Confirms defective tear production

131
Q

How is Sjögren’s syndrome treated?

A

Symptomatic treatment with artificial tears and saliva replacement solutions

132
Q

What is an ‘overlap’ autoimmune rheumatic syndrome?

A

A collection of symptoms the combines features of more than one autoimmune rheumatic disease

133
Q

What is undifferentiated autoimmune rheumatic disease?

A

The term used to describe when patients have evidence of autoimmunity and some clinical features of autoimmune rheumatic diseases but not enough to make a diagnosis of any one specific condition

134
Q

What are systemic vasculitides?

A

A term used to describe a group of multisystem diseases in which vasculitis is the main feature

135
Q

What is polymyalgia rheumatica?

A

A condition characterised by abrupt onset of stiffness and intense pain in the hips and shoulder girdle pain.

136
Q

What is giant cell arteritis?

A

Inflammation of the superficial temporal artery causing headache, tenderness of the scalp and claudication of the jaw when eating

137
Q

What is the most devestating complication of giant cell arteritis?

A

Sudden loss of vision due to involvement of the ophthalmic artery.

138
Q

What is the management strategy of both giant cell arteritis and polymyalgia rheumatica?

A

Corticosteroids to create a dramatic reduction in symptoms

139
Q

What is polyangitis?

A

A condition involving the lungs and kidney.

Causing haemoptysis, haemturia, proteinuria and progressive renal failure

140
Q

How is polyangitis diagnosed?

A

Renal biopsy

141
Q

What is eosinophilic granulomatosis with polyangitis?

A

A rare disease characterised by the classic triad of asthma, eosinophilia and a systemic vasculitis affecting peripheral nerves and skin

142
Q

What is the treatment for eosinophilic granulomatosis with polyangitis?

A

Corticosteroids and immunosuppressive

143
Q

What is Henoch-Schönlein purpura?

A

A condition usually seen in children presenting as a purpuric rash of the lower legs and buttocks

Abdominal pain, arthritis and haematuria may also occur

144
Q

What is the pathophysiology of Henoch-Schönlein purpura?

A

Vascular deposition of IgA-dominant immune complexes.

145
Q

What cells secrete parathyroid hormone?

A

Secreted from chief cells in the parathyroid gland

146
Q

What are the effects of parathyroid hormone?

A

Increase plasma calcium and decrease plasma phosphate

147
Q

What is osteoporosis?

A

A reduction in bone mass density and micro-architectural deterioration of bone tissue; ultimately leading to fragility and increased fracture risk

148
Q

What is the diagnostic criteria of osteoporosis?

A

Bone mineral density (BMD) more than 2.5 standard deviations below the young adult mean value (T score < -2.5)

149
Q

What is the diagnostic criteria of osteopenia?

A

Bone mineral density (BMD) between than 1 and 2.5 standard deviations below the young adult mean value (T score < -2.5)

150
Q

What are the most common sites of osteoporotic fractures?

A

Thoracic and lumbar vertebrae, proximal femur and distal radius

151
Q

Recurrent vertebral fractures may lead to what deformity?

A

Kyphosis and loss of height (‘Widow’s stood’)

152
Q

What is the most important investigation for both the diagnosis and monitoring of osteoporosis?

A

Dual Energy X-ray Absorptiometry (DEXA) scan

153
Q

Outline some of the pharmacological treatments of osteoporosis

(7)

A 
Bisphosphonates - inhibit osteoclasts
Denosumab - anti-resorptive 
Selective oestrogen-receptor modulators
Recombinant human parathyroid peptide 
Oestrogen therapy 
Testosterone 
Strontium ranelate
154
Q

What is Paget’s disease?

A

Focal disorder of bone remodelling in which there is increased osteoclastic bone resorption followed by formation of weaker bone with increased vascularisation and fibrotic tissue

155
Q

What are the clinical features of Paget’s disease?

A

Pain in the bone/joints
Deformities: enlargement of the skull, bowing of tibia

Complications: nerve compression (deafness, paraperesis), pathological fractures, osteogenic sarcoma

156
Q

What are the indicated investigations for Paget’s disease?

A
  • Serum alkaline phosphatase (raised)
  • Urinary hydroxyproline
  • X-rays (shows bony enlargement, deformity, osteolytic regions)
  • Radionuclide bone scans
157
Q

What is the mainstay of treatment for Paget’s disease?

A

Bisphosphonates (mainly IV zoledronate)

158
Q

What is osteomalacia?

A

Inadequate mineralisation of osteoid framework leading to soft bones

Causes Rickets disease in children and osteomalacia (after closure of epiphysium) in adults

The cause is profound vitamin D deficiency

159
Q

What are the clinical features of osteomalacia?

A

Proximal muscle weakness and pain are the common symptoms (bone deformity in children with Rickets)

Severe vitamin D deficiency may present with hypocalcaemia, tetany and seizures

160
Q

What investigations are relevant to osteomalacia?

A

Serum vitamin D levels

Serum alkaline phosphatase

Serum PTH levels

Radiology: Looser’s pseudofractures (low density bands running perpendicular to the cortex)

161
Q

What are the common side effects of bisphosphonates?

A

Gastrointestinal: dyspepsia, nausea, diarrhoea

Osteonecrosis of the jaw

Atypical femoral fractures

MBChB Final Exam Essentials (18 decks)

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