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Finals > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What type of joints are affected in osteoarthritis?

A

Synovial

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2
Q

What are 4 risk factors for osteoarthritis

A

obesity, age, occupation, trauma, being female and family history

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3
Q

What are the most commonly affected joints in osteoarthritis?

A

Hips
Knees
Distal interphalangeal (DIP) joints in the hands
Carpometacarpal (CMC) joint at the base of the thumb
Lumbar spine
Cervical spine (cervical spondylosis)

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4
Q

What x-ray changes may be present in osteoarthritis?

A

L – Loss of joint space
O – Osteophytes (bone spurs)
S – Subarticular sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone)

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5
Q

what are some general signs of osteoarthritis?

A

Bulky, bony enlargement of the joint
Restricted range of motion
Crepitus on movement
Effusions (fluid) around the joint

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6
Q

What are some hand signs seen in osteoarthritis

A

Heberden’s nodes (in the DIP joints)
Bouchard’s nodes (in the PIP joints)
Squaring at the base of the thumb (CMC joint)
Weak grip
Reduced range of motion

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7
Q

NICE guidelines state that a diagnosis of osteoarthritis can be made without any investigations if what?

A

the patient is over 45, has typical pain associated with activity and has no morning stiffness (or stiffness lasting under 30 minutes)

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8
Q

What are 3 non-pharmacological management options for osteoarthritis

A

exercise
weight loss
occupational therapy

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9
Q

What are the pharmacological management options for osteoarthritis?

A

Topical NSAIDs first-line for knee osteoarthritis
Oral NSAIDs where required and suitable (co-prescribed with a proton pump inhibitor for gastroprotection)

Weak opiates and paracetamol are only recommended for short-term, infrequent use.

Intra-articular steroid injections
Joint replacement

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10
Q

How would you describe the pattern of arthritis in rheumatoid arthritis?

A

symmetrical polyarthritis

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11
Q

What are 4 risk factors for rheumatoid arthritis

A

female
smoking
obesity
family history

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12
Q

What is the most common gene associated with rheumatoid arthritis?

A

HLA DR4

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13
Q

What antibodies can be present in rheumatoid arthritis?

A

Rheumatoid factor (present in 70%)
anti-CCP antibodies (more sensitive + specific, in 80%)

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14
Q

What 3 joint symptoms are present in rheumatoid arthritis?

A

Pain
Stiffness
Swelling

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15
Q

What are the most commonly affected joints in rheumatoid arthritis

A

Metacarpophalangeal (MCP) joints
Proximal interphalangeal (PIP) joints
Wrist
Metatarsophalangeal (MTP) joints (in the foot)

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16
Q

What are some associated systemic symptoms of rheumatoid arthritis?

A

Fatigue
Weight loss
Flu-like illness
Muscles aches and weakness

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17
Q

What is palindromic rheumatism

A

self-limiting episodes of inflammatory arthritis, with pain, stiffness and swelling typically affecting only a few joints. The symptoms last days, then completely resolve. Joints appear normal between episodes. Rheumatoid factor or anti-CCP antibodies may indicate that it will progress to rheumatoid arthritis.

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18
Q

What are some hand signs in advanced rheumatoid arthritis ?

A

Z-shaped deformity to the thumb
Swan neck deformity (hyperextended PIP and flexed DIP)
Boutonniere deformity (hyperextended DIP and flexed PIP)
Ulnar deviation of the fingers at the MCP joints

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19
Q

What is Atlantoaxial subluxation

A

Synovitis and damage to the ligaments around the odontoid peg of the axis (C2) allow it to shift within the atlas (C1). Subluxation can cause spinal cord compression and is an emergency.

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20
Q

What are some extra-articular manifestations of rheumatoid arthritis

A

Pulmonary fibrosis
Felty’s syndrome (a triad of rheumatoid arthritis, neutropenia and splenomegaly)
Sjögren’s syndrome (with dry eyes and dry mouth)
Anaemia of chronic disease
Cardiovascular disease
Eye manifestations
Rheumatoid nodules (firm, painless lumps under the skin, typically on the elbows and fingers)
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis
Bronchiolitis obliterans (small airway destruction and airflow obstruction in the lungs)
Caplan syndrome (pulmonary nodules in patients with rheumatoid arthritis exposed to coal, silica or asbestos dust)

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21
Q

What are some eye manifestations related to rheumatoid arthritis and it’s treatment?

A

Dry eye syndrome (keratoconjunctivitis sicca)
Episcleritis
Scleritis
Keratitis
Cataracts (secondary to steroids)
Retinopathy (secondary to hydroxychloroquine)

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22
Q

What initial investigations would you do in a patient with suspected rheumatoid arthritis?

A

Rheumatoid factor
Anti-CCP antibodies
Inflammatory markers
X-rays of the hands and feet
Ultrasound or MRI can be used to detect synovitis

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23
Q

What are the x-ray changes in rheumatoid arthritis

A

Periarticular osteopenia
Boney erosions
Soft tissue swelling
Joint destruction and deformity

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24
Q

State 2 scoring systems used in rheumatoid arthritis

A

Health Assessment Questionnaire (HAQ)
Disease Activity Score 28 Joints (DAS28)

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25
Q

Management options for rheumatoid arthritis

A

Short term steroids may be used at initial presentation
first: Monotherapy with methotrexate, leflunomide or sulfasalazine
second: Combination treatment with multiple cDMARDs
third: Biologic therapies (usually alongside methotrexate)

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26
Q

What DMARDs are considered safe in pregnancy

A

Hydroxychloroquine and sulfasalazine
(extra folic acid is required with sulfasalazine).

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27
Q

Name 3 types of biologics used in rheumatoid arthritis

A

Tumour necrosis factor (TNF) inhibitors (e.g., adalimumab)
Anti-CD20 on B cells (e.g., rituximab)
Anti-interleukin-6 inhibitors
JAK inhibitors
T-cell co-stimulation inhibitors

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28
Q

What are some side effects of Methotrexate

A

Mouth ulcers and mucositis
Liver toxicity
Bone marrow suppression and leukopenia (low white blood cells)
Teratogenic

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29
Q

What are some side effects of Leflunomide

A

Mouth ulcers and mucositis
Increased blood pressure
Liver toxicity
Bone marrow suppression and leukopenia
Teratogenic
Peripheral neuropathy

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30
Q

What are some side effects of Sulfasalazine?

A

Orange urine
Reversible male infertility (reduced sperm count and quality)
Bone marrow suppression

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31
Q

What are some side effects of Hydroxychloroquine?

A

Retinal toxicity (reduced visual acuity (macular toxicity)
Blue-grey skin pigmentation
Hair lightening

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32
Q

Psoriatic arthritis occurs in what percentage of patients with psoriasis?

A

10-20%

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33
Q

Name 2 extra-articular manifestations of psoriatic arthritis

A

Uveitis
Inflammatory bowel disease

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34
Q

What are the 5 patterns of psoriatic arthritis?

A

Asymmetrical oligoarthritis
Symmetrical polyarthritis
Distal interphalangeal predominant pattern
Spondylitis
Arthritis mutilans

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35
Q

What are some signs of psoriatic arthritis?

A

Plaques of psoriasis on the skin
Nail pitting
Onycholysis (separation of the nail from the nail bed)
Dactylitis (inflammation of the entire finger)
Enthesitis (inflammation of the entheses, which are the points of insertion of tendons into bone)

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36
Q

What tool can you use to screen patients for psoriatic arthritis

A

Psoriasis Epidemiological Screening Tool (PEST)

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37
Q

What are some x-ray changes seen in psoriatic arthritis?

A

Periostitis (inflammation of the periosteum, causing a thickened and irregular outline of the bone)
Ankylosis (fixation or fusion of the bones at the joint)
Osteolysis (destruction of bone)
Dactylitis (inflammation of the whole digit, seen as soft tissue swelling)

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38
Q

What disease is the x-ray finding ‘pencil-in-cup’ associated with?

A

psoriatic arthritis

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39
Q

What is the management of psoriatic arthritis?

A

NSAIDs
steroids
DMARDs
Biologics - anti-TNF, Ustekinumab

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40
Q

What is a significant differential in reactive arthritis ?

A

Septic arthritis

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41
Q

What are the most common triggers for reactive arthritis

A

Gastroenteritis
STI’s e.g. Chlamydia

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42
Q

What gene is associated with reactive arthritis

A

HLA B27

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43
Q

What are some associated symptoms of reactive arthritis?

A

Bilateral conjunctivitis (non-infective)
Anterior uveitis
Urethritis (non-gonococcal)
Circinate balanitis (dermatitis of the head of the penis)

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44
Q

How is reactive arthritis managed?

A

Joint aspiration to rule our septic arthritis
treat trigger
NSAIDs
Steroid injections
systemic steroids

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45
Q

What joints are mainly affected in Ankylosing spondylitis?

A

sacroiliac joints
Vertebral column joints

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46
Q

90% of patients with ankylosing spondylitis have what gene

A

HLA-B27

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47
Q

what are the main presenting features of ankylosing spondylitis?

A

Pain and stiffness in the lower back
Sacroiliac pain (in the buttock region)

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48
Q

What are some additional symptoms of osteoarthritis

A

Chest pain related to the costovertebral and sternocostal joints
Enthesitis
Dactylitis
Vertebral fractures
Shortness of breath relating to restricted chest wall movement)

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49
Q

What conditions are associated with ankylosing spondylitis?

A

A – Anterior uveitis
A – Aortic regurgitation
A – Atrioventricular block (heart block)
A – Apical lung fibrosis (fibrosis of the upper lobes of the lungs)
A – Anaemia of chronic disease

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50
Q

What test can be done to assess spinal mobility on ankylosing spondylitis

A

Schober’s test (length of <20cm indicates restriction)

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51
Q

What key investigations can be done for ankylosing spondylitis

A

Inflammatory markers (e.g., CRP and ESR) may rise with disease activity
HLA B27 genetic testing
X-ray of the spine and sacrum
MRI of the spine can show bone marrow oedema early in the disease

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52
Q

What x-ray changes can be seen in Ankylosing spondylitis?

A

Bamboo spine
Squaring of vertebral bodies
Subchondral sclerosis + erosions
Syndesmophytes
Ossification
Fusion

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53
Q

How is Ankylosing spondylitis managed?

A

NSAIDs
ANti-TNF
biologics
Inter-articular steroid injections
physio, exercise, avoid smoking

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54
Q

What is the epidemiology of systemic lupus erythematosus

A

Women
Asian, African, Caribbean and Hispanic
Young to middle-aged

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55
Q

SLE is characterised by which antibody?

A

anti-nuclear antibodies (ANA)

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56
Q

What are some non-specific symptoms SLE may present with?

A

Fatigue
Weight loss
Arthralgia (joint pain)
Non-erosive arthritis
Myalgia (muscle pain)
Fever
Photosensitive malar rash
Lymphadenopathy
Splenomegaly
Shortness of breath
Pleuritic chest pain
Mouth ulcers
Hair loss
Raynaud’s phenomenon
Oedema (due to nephritis)

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57
Q

What may an FBC show in a patient with SLE?

A

anaemia of chronic disease, low white cell count and low platelets

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58
Q

What will happen to C3 and C4 in SLE?

A

levels decreased in active disease

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59
Q

Name 4 autoantibodies that may be present in SLE

A

anti-nuclear antibodies
Anti-double stranded DNA antibodies (highly specific)
Anti -Sm
Anti-centromere antibodies
Anti-Ro, Anti-La
Antiphospholipid antibodies

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60
Q

What are some complications of SLE?

A

CVD
Infection
Anaemia
Pericarditis
Pleuritis
Lupus nephritis
Interstitial lung disease
Neuropsychiatric SLE
Recurrent miscarriage
VTE

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61
Q

How is SLE managed?

A

Hydroxychloroquine
NSAIDs
Steroids (prednisolone)
DMARDs
Biologics (Rituximab, Belimumab)

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62
Q

What is the appearance of the lesions in discoid lupus erythematosus

A

Inflamed
Dry
Erythematous (red)
Scaling

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63
Q

What is an association of discoid lupus erythematous

A

scarring alopecia
hyper/hypopigmentation

64
Q

How is discoid lupus erythematous diagnosed

A

skin biopsy

65
Q

How is discoid lupus erythematous managed?

A

Sun protection
Topical steroids
Intralesional steroid injections
Hydroxychloroquine

66
Q

What are the 2 main patterns of systemic sclerosis?

A

Limited cutaneous systemic sclerosis
Diffuse cutaneous systemic sclerosis

67
Q

What are the features of limited cutaneous systemic sclerosis?

A

C – Calcinosis
R – Raynaud’s phenomenon
E – oEsophageal dysmotility
S – Sclerodactyly
T – Telangiectasia

68
Q

What are some systemic symptoms of diffuse cutaneous systemic sclerosis?

A

Cardiovascular problems (e.g., hypertension and coronary artery disease)
Lung problems (e.g., pulmonary hypertension and pulmonary fibrosis)
Kidney problems (e.g., scleroderma renal crisis)

69
Q

What are the colour changes in Raynaud’s and why

A

First white, due to vasoconstriction
Then blue, due to cyanosis
Then red, due to reperfusion and hyperaemia

70
Q

What are the management options for Raynauds

A

keep hands warm
calcium channel blocker (nifedipine)
others: losartan, ACEi, sildenafil, fluoxetine

71
Q

Name 3 autoantibodies associated with systemic sclerosis

A

Antinuclear antibodies (ANA) are positive in most patients with systemic sclerosis. They are non-specific.

Anti-centromere antibodies are most associated with limited cutaneous systemic sclerosis.

Anti-Scl-70 antibodies are most associated with diffuse cutaneous systemic sclerosis and more severe disease.

72
Q

How is systemic sclerosis managed?

A

DMARDs
biologics
symptomatic treatment

73
Q

What condition is polymyalgia rheumatica strongly associated with?

A

Giant cell arteritis

74
Q

Where to patients typically get pain in polymyalgia rheumatica?

A

Shoulders
Pelvic girdle
Neck

75
Q

What are some associated features of polymyalgia rheumatica?

A

Systemic symptoms (e.g., weight loss, fatigue and low-grade fever)
Muscle tenderness
Carpel tunnel syndrome
Peripheral oedema

75
Q

What are the characteristic features of the pain and stiffness in polymyalgia rheumatica

A

worse in morning, after rest or with inactivity
Interfere with sleep
Take atleast 45 mins in morning
slightly improves with activity

75
Q

Name 3 differential diagnoses for polymyalgia rheumatica

A

osteoarthritis
cervical spondylitis
Rheumatoid arthritis
Myeloma

76
Q

What is the treatment for polymyalgia rheumatica?

A

steroids (15mg prednisolone) - reducing regime

77
Q

What additional management is required for patients on long term steroid therapy?

A

Don’t – steroid dependence occurs after 3 weeks of treatment, and abruptly stopping risks adrenal crisis
S – Sick day rules (steroid doses may need to be increased if the patient becomes unwell)
T – Treatment card – patients should carry a steroid treatment card to alert others that they are steroid-dependent
O – Osteoporosis prevention may be required (e.g., bisphosphonates and calcium and vitamin D)
P – Proton pump inhibitors are considered for gastro-protection (e.g., omeprazole)

78
Q

What size of arteries does GCA affect?

A

medium and large arteries

79
Q

What is the key complication of GCA?

A

vision loss

80
Q

How may GCA present?

A

Unilateral headache (Around temple and forehead)
scalp tenderness
jaw claudication
blurred/double vision
loss of vision if untreated

81
Q

What are some associated symptoms of GCA?

A

Symptoms of polymyalgia rheumatica
Systemic symptoms
Muscle tenderness
Carpel tunnel syndrome
Peripheral oedema

82
Q

What investigations may be carried out for GCA

A

Clinical presentation
Raised inflammatory markers, particularly ESR (usually more than 50 mm/hour)
Temporal artery biopsy (showing multinucleated giant cells)
Duplex ultrasound (showing the hypoechoic “halo” sign and stenosis of the temporal artery)

83
Q

how is GCA managed?

A

Steroids (40-60mg prednisolone daily if no visual/jaw claudication, if present then 500mg-1000mg methylprednisolone daily)
others: aspirin, PPI, bisphosphonates

84
Q

Name 3 complications of GCA

A

Steroid-related complications (e.g., weight gain, diabetes and osteoporosis)
Visual loss
Cerebrovascular accident (stroke)

85
Q

What are the 2 main skin changes seen in Dermatomyositis

A

Gottron papules on back of hands
Heliotrope rash affecting eyelids

86
Q

What may be some underlying triggers/causes for poly/dermatomyositis?

A

underlying cancer
viral infection (Coxsackie, HIV)

87
Q

How does polymyositis and dermatomyositis typically present?

A

gradual-onset, symmetrical, proximal muscle weakness, causing difficulties standing from a chair, climbing stairs or lifting overhead
Myalgia

88
Q

What blood test is critical for myositis

A

Creatine kinase

89
Q

What are some causes of a raised creatine kinase

A

polymyositis/dermatomyositis
Rhabdomyolysis
AKI
MI
Statins
Strenuous exercise

90
Q

What antibody is most associated with polymyositis?

A

anti-Jo-1

91
Q

How is polymyositis and dermatomyositis managed?

A

1st: Corticosteroids
2nd: immunosuppressants, Biologics, IVIg

92
Q

What are the specific antiphospholipid antibodies?

A

Lupus anticoagulant
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

93
Q

What are 3 key complications of antiphospholipid syndrome?

A

VTE
Arterial thrombosis
Pregnancy-related complications

94
Q

What are some associated signs in antiphospholipid syndrome?

A

Livedo reticularis (purple, lace like rash)
Libmann-Sacks endocarditis
Thrombocytopenia

95
Q

How is antiphospholipid syndrome managed?

A

Long term warfarin (INR target 2-3)
LMWH/ aspirin in pregnancy

96
Q

What are some key features of Sjogren’s syndrome

A

Dry eyes
Dry mouth
Dry vagina

97
Q

What 2 antibodies are associated with Sjogren’s?

A

Anti-Ro
Anti-La

98
Q

What test can be done for the symptoms of Sjogren’s syndrome?

A

Schirmer test

99
Q

How is Sjogren’s syndrome managed?

A

Artificial tears/saliva
vaginal lubricants
Pilocarpine (can stimulate production)
Hydroxychloroquine if associated joint pain

100
Q

What are some complications of Sjogren’s syndrome?

A

Eye problems, such as keratoconjunctivitis sicca and corneal ulcers
Oral problems, such as dental cavities and candida infections
Vaginal problems, such as candida infection and sexual dysfunction

101
Q

What type of glands does Sjogrens affect?

A

Exocrine (lacrimal and salivary)

102
Q

What are some rare organ complications of Sjogren’s?

A

Pneumonia
Bronchiectasis
Non-Hodgkins lymphoma
Peripheral neuropathy
Vasculitis
Renal impairment

103
Q

Name 3 types of small vessel vasculitis

A

Henoch-Scholein Purpura
Microscopic Polyangiitis
Granulomatosis with Polyangiitis
Eosinophilic Granulomatosis with Polyangiitis

104
Q

Name 2 medium vessel vasculitis

A

Polyarteritis Nodosa
Kawasaki Disease

105
Q

Name 2 large vessel vasculitis

A

Giant cell arteritis
Takayasu’s arteritis

106
Q

What are some key features of Henoch-Schonlein Purpura

A

Purpura
IgA nephritis

107
Q

What are some key lab findings and features of Microscopic Polyangiitis

A

p-ANCA
Glomerulonephritis
Diffuse alveolar haemorrhage

108
Q

What are some key lab findings and features of Granulomatosis with Polyangiitis

A

c-ANCA
Nasal symptoms
Respiratory symptoms
Glomerulonephritis

109
Q

What are some key lab findings and features of Eosinophilic granulomatosis with polyangiitis

A

p-ANCA, raised eosinophils
Late-onset asthma
Sinusitis and rhinitis

110
Q

What are some key features of Polyarteritis Nodosa

A

Renal impairment
HTN
CV events
Tender skin nodules

111
Q

What are some key features of Kawasaki’s disease

A

High fever (>5d)
widespread rash
strawberry tongue
Coronary artery aneurysms

112
Q

What are some key features and lab findings in Giant cell arteritis

A

raised ESR
Unilateral headache
scalp tenderness
vision loss

113
Q

What are some key features of Takayasu’s arteritis?

A

aortic arch affected
‘pulseless’ disease

114
Q

What are some general vasculitis features

A

Joint and muscle pain
Peripheral neuropathy
Renal impairment
Purpura (purple-coloured non-blanching spots caused by blood leaking from the vessels under the skin)
Necrotic skin ulcers
Gastrointestinal symptoms (e.g., diarrhoea, abdominal pain and bleeding)

115
Q

What associated systemic symptoms may be present in a patient with vasculitis?

A

Fatigue
Fever
Night sweats
Weight loss
Anorexia (loss of appetite)
Anaemia

116
Q

What investigations can be done in a patient with suspected vasculitis?

A

CRP + ESR
p-ANCA - microscopic polyangiitis + eosinophilic granulomatosis with polyangiitis
c-ANCA - granulomatosis with polyangiitis

117
Q

How is vasculitis managed?

A

1st: Steroids
2nd: cyclophosphamide, rituximab

118
Q

What are the 4 classic features of Henoch-Schonlein Purpura

A

Purpura
Joint pain
Abdominal pain
Renal involvement (IgA nephritis)

119
Q

How is Henoch-Schonlein Purpura managed?

A

Supportive - rest, hydration, analgesia
urine dip + blood pressure monitoring

120
Q

What are the key features of Behcet’s disease

A

Oral ulcers with red halo
Genital ulcers
erythema nodosum, eye problems, MSK, GI, CNS, aneurysms, DVT

121
Q

What test can be done for Behcet’s disease

A

Pathergy test

122
Q

How is Behcet’s disease managed?

A

Topical + systemic steroids
Colchicine
Topical anaesthetics
Immunosuppressants
Biologics

123
Q

What is the most common type of Ehlers-Danlos syndrome

A

Hypermobile Ehlers-Danlos syndrome

124
Q

What is the most severe type of Ehlers-Danlos syndrome and what are some features?

A

Vascular
thin, translucent skin, fragile blood vessels
autosomal dominant

125
Q

What are some key features of Ehlers-Danlos syndrome

A

Joint pain
Hypermobility
Soft and stretchy skin
Joint dislocations
Striae
easy bruising
poor wound healing
bleeding
chronic pain
autonomic dysfunction

126
Q

What score is used to test hypermobility on Ehlers-Danlos syndrome

A

Beighton score

127
Q

How is Ehlers-Danlos syndrome managed?

A

Supportive - physio, OT, moderating activity

128
Q

Name 4 risk factors for gout

A

Male
Family history
Obesity
High purine diet (e.g., meat and seafood)
Alcohol
Diuretics
Cardiovascular disease
Kidney disease

129
Q

What are the most commonly affected joints in gout

A

MTP of big toe
CMC - base of thumb
wrist

130
Q

How is gout diagnosed/investigated?

A

clinically
raised serum urate on bloods
Aspirated joint - monosodium urate crystals (needle shaped, negative birefringent)

131
Q

What may an x-ray of a joint affected by gout show?

A

No loss of joint space
lytic lesions in bone
punched out erosions which may have sclerotic boarders with overhanging edges

132
Q

How is gout managed?

A

Acute - NSAIDS (1st naproxen, 2nd Colchicine, 3rd oral steroids)
Prophylaxis - Allopurinol, Febuxostat

133
Q

What would joint aspiration show in a patient with pseudogout?

A

calcium pyrophosphate crystals, rhomboid-shaped, positive birefringent

134
Q

What is the classic x-ray change in pseudogout?

A

Chondrocalcinosis
Others: LOSS (loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts)

135
Q

How is pseudogout managed?

A

NSAIDS (Naproxen)
Colchicine
Intra-articular steroid injections
Oral steroids

136
Q

What T score is seen in Osteopenia

A

-1 to -2.5

137
Q

What T score is seen in Osteoporosis

A

<-2.5

138
Q

What T score is seen in severe Osteoporosis

A

Less than -2.5 plus a fracture

139
Q

How is bone mineral density measured?

A

DEXA scan

140
Q

What is the difference between a Z and T score?

A

Z-score is the number of standard deviations the patient is from the average for their age, sex and ethnicity.
T-score is the number of standard deviations the patient is from an average healthy young adult.

141
Q

What are some risk factors for osteoporosis?

A

Older age
Post-menopausal women
Reduced mobility and activity
Low BMI
Low calcium or vitamin D intake
Alcohol and smoking
Personal or family history of fractures
Chronic diseases
Long-term corticosteroids Certain medications (e.g., SSRIs, PPIs, anti-epileptics and anti-oestrogens)

142
Q

The 10-year risk of a major osteoporotic fracture and a hip fracture can be calculated using either:

A

QFracture tool (preferred by NICE)
FRAX tool (NICE say this may underestimate the risk in some patients)

143
Q

How is osteoporosis managed?

A

Lifestyle changes
Adequate vitamin D and calcium
Bisphosphonates e.g. Alendronate
other: Denosumab

144
Q

What are some important side effects of Bisphosphonates?

A

Reflux and oesophageal erosions
Atypical fractures (e.g., atypical femoral fractures)
Osteonecrosis of the jaw (regular dental checkups are recommended before and during treatment)
Osteonecrosis of the external auditory canal

145
Q

What causes osteomalacia?

A

defective bone mineralisation resulting from insufficient vitamin D

146
Q

How does osteomalacia present?

A

Fatigue
Bone pain
Muscle weakness
Muscle aches
Pathological or abnormal fractures

147
Q

How is osteomalacia treated

A

Colecalciferol (vitamin D3)

148
Q

What is the pathophysiology behind Pagets’s disease of the bone

A

excessive bone turnover (reabsorption and formation) due to increased osteoclast and osteoblast activity

149
Q

How would Paget’s disease of the bone present?

A

Bone pain
Bone deformity
Fractures
Hearing loss

150
Q

What x-ray findings can be seen in Paget’s disease of the bone?

A

Bone enlargement and deformity
Osteoporosis circumscripta (well-defined osteolytic lesions that appear less dense compared with normal bone)
Cotton wool appearance of the skull (poorly defined patchy areas of increased and decreased density)
V-shaped osteolytic defects in the long bones

151
Q

What would blood tests show in a patient with Paget’s disease of the bone

A

Raised alkaline phosphatase
Normal calcium
Normal phosphate

152
Q

How is Paget’s disease of the bone managed?

A

Bisphosphonates
others: Calcitonin, analgesia, calcium + vit D, surgery

153
Q

What are some key complications of Paget’s disease of the bone?

A

Hearing loss (if it affects the bones of the ear)
Heart failure (due to hypervascularity of the abnormal bone)
Osteosarcoma
Spinal stenosis and spinal cord compression

Finals (21 decks)

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