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Phase 2a > MSK/Rheumatology > Flashcards

MSK/Rheumatology Flashcards

1
Q

What is the most common arthritis?

A

Osteoarthritis.

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2
Q

What is osteoarthritis?

A

Non-inflammatory degenerative mechanical shearing - wear and tear.

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3
Q

What are the most commonly affected joints in osteoarthritis?

A

Hips, knees, sacro-iliac, wrists, cervical spine, thumbs.

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4
Q

What are seven risk factors for osteoarthritis?

A

Higher age, female, obesity, family history, occupation, sports, trauma.

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5
Q

Describe the pathophysiology of osteoarthritis.

A

Imbalanced cartilage breakdown and repair which leads to cartilage loss.
-Chondrocytes repair this which leads to structural issues.

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6
Q

How does osteoarthritis present?

A

Joint pain and stiffness with little morning pain but worsened as the day goes on and with exercise.

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7
Q

What are two signs of osteoarthritis? Where is affected?

A

Heberden’s and Bouchard’s nodes - asymmetrical, hard, non-inflamed joint.
-Affects big toe, hips and knees.

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8
Q

How is osteoarthritis diagnosed?

A

Over 45 with activity pain and no morning stiffness.
-Normal bloods.
-XRAY (LOSS).

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9
Q

What are the XRAY findings in osteoarthritis?

A

LOSS:

-Loss of joint space.
-Osteophytes.
-Subchondral sclerosis.
-Subchondral cysts.

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10
Q

What is the management of osteoarthritis?

A

-Lifestyle changes - weight loss and physio.
-NSAIDs for pain relief.
-Steroid injections.
-Last resort - Joint replacement.

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11
Q

What is rheumatoid arthritis?

A

Chronic inflammatory autoimmune polyarthritis which is symmetrical.

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12
Q

Where does RA usually affect?

A

Multiple joints - wrist, hand, feet.

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13
Q

What are the three risk factors for RA?

A

Women aged 30-50.
Smoking.
Family history - HLA-DR4, HLA-DR1.

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14
Q

Describe the pathophysiology of RA.

A

Autoantibodies:

-Rheumatoid factor (RF) autoantibody is present in 70%.
-Anti-CCP autoantibodies more sensitive and specific than RF.

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15
Q

How does someone with RA present?

A

Symmetrical distal polyarthritis (pain, swelling, hot, stiffness) that is worse on a morning and eases as the day goes on and with activity.

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16
Q

What are the signs of RA?

A

Hands - Boutonnieres deformity (flexed), swan neck deformity, Z thumb.
Extra-articular - Pulmonary fibrosis/bronchiolitis, CVD, CKD, elbow skin nodules.

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17
Q

How is RA investigated?

A

Bloods, serology, XRAY.

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18
Q

What are the blood and serology results of RA?

A

Raised ESR and CRP, normocytic normochromic anaemia.
-Positive anti-CCP and RF serology.

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19
Q

What are the XRAY findings on RA?

A

LESS:

-Loss of joint space.
-Eroded bone.
-Soft tissue swelling.
-Soft bones.

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20
Q

What are the first and second line medication treatments for RA?

A

DMARDs - methotrexate and leflunomide.

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21
Q

What are the 3rd and 4th line medication treatments for RA?

A

-Methotrexate and infliximab (anti-TNF).
-Methotrexate and rituximab (anti-CD20).

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22
Q

What is gout?

A

A crystal arthropathy associated with high blood uric acid levels.

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23
Q

What is the most common inflammatory arthritis in the UK?

A

Gout

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24
Q

What is the typical patient with gout?

A

Middle aged overweight men.

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25
Q

Describe the pathophysiology of gout.

A

Sodium urate crystal are deposited into the joint causing it to become hot, swollen and painful.

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26
Q

What is gouty tophi?

A

Subcutaneous deposits of uric acid typically affecting the small joints and connective tissues of the hands, elbows and ears.

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27
Q

What are the three joints most affected by gout?

A

-Metatarsophalangeal joints (base of big toes).
-Wrists.
-Carpometacarpal joints (base of thumbs).

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28
Q

What are seven risk factors of gout?

A

Male, obesity, family history, diuretics, alcohol, CVD/CKD, purine rich foods (meat, seafood).

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29
Q

What is a key differential diagnosis of gout?

A

Septic arthritis.

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30
Q

How does gout present?

A

Monoarticular sudden onset, severely swollen red toe that you can’t put weight on.

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31
Q

How is gout diagnosed?

A

Aspiration of fluid from the joint.

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32
Q

What are the results of joint aspiration in gout?

A

-Needle shaped crystals.
-Monosodium urate crystals.
-Negatively befringement of polarised light.
-No bacterial growth.

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33
Q

What is the acute treatment for gout?

A

1st line - NSAIDs.
2nd - Colchicine.
3rd - Steroids.

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34
Q

What is the prophylaxis for gout?

A

Allopurinol and lifestyle changes (less purines and more dairy).

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35
Q

What is pseudogout?

A

Crystal arthropathy caused by calcium pyrophosphate deposits.

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36
Q

What is another name for pseudogout?

A

Chondrocalcinosis.

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37
Q

Who does pseudogout usually affect?

A

Elderly females.

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38
Q

What are three risk factors for pseudogout?

A

Diabetes, metabolic disease, osteoarthritis.

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39
Q

What is the presentation of pseudogout?

A

Polyarticular with knee commonly affected (also hips, shoulders and wrists). Swollen, hot and red joint.

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40
Q

How is pseudogout diagnosed?

A

Joint aspiration.

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41
Q

What does aspiration fluid show in pseudogout?

A

-Calcium pyrophosphate crystals.
-Rhomboid shaped crystals.
-Positive befringement in polarised light.
-No bacterial growth.

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42
Q

What does an XRAY show in pseudogout?

A

Same as OA - LOSS.

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43
Q

What is the management for pseudogout?

A

-Chronic changes require no management.
-Acutely: NSAIDs, colchicine, steroids.
-Severe: Joint washout.

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44
Q

What is osteoporosis? What is a complications?

A

A condition characterised by a reduction in bone density. This makes bones more weak and prone to fractures.

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45
Q

What is osteopenia?

A

A less severe reduction in bone density than osteoporosis.

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46
Q

Who does osteoporosis usually affect?

A

Post-menopausal white woman above 50y.

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47
Q

What are the risk factors for osteoporosis?

A

SHATTERED:

-Steroids, hyperthyroid/para, alcohol/smoking, thin, testosterone low, early menopause, renal/liver failure, erosive + inflammatory disease, DMT1/malabsporption.

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48
Q

What are the four main causes of osteoporosis?

A

Endocrine (Cushing’s, parathyroid).
Haematology (myeloma).
GI (malabsorption).
Iatrogenic (steroids).

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49
Q

What is a T score?

A

Young adult bone density.

0 < T < 1 is normal.
1 < T < 2.5 - Osteopenia.
t > 2.5 - Osteoporosis.

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50
Q

How does osteoporosis present?

A

With fractures:

-Femur, Colle’s (wrist), compression vertebral crush.

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51
Q

What is the gold standard investigation for osteoporosis?

A

DEXA scan - yields a T score.

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52
Q

After a diagnosis of osteoporosis, which score is performed?

A

FRAX score - fracture risk assessment tool.

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53
Q

What is the 1st line treatment for osteoporosis?

A

Bisphosphonates (alendronate) which reduce osteoclast activity.

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54
Q

Which supplements are given to someone with osteoporosis?

A

Calcium and vitamin D.

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55
Q

What are other treatment options for osteoporosis?

A

Denosumab, HRT and raloxifene.

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56
Q

What is septic arthritis?

A

A bacterial infection within a joint (native or replacement).

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57
Q

What is the mortality of septic arthritis?

A

10%.

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58
Q

What are the organisms that can cause septic arthritis?

A

S. aureus (mc).
H. influenzae (children).
Gonorrhoea (sexually active).
E. coli and pseudomonas (IVDU).

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59
Q

What are six risk factors for septic arthritis?

A

IVDU, immunosuppression, surgery, trauma, prosthetic joints, RA.

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60
Q

How does septic arthritis present?

A

Acutely inflamed, hot, red joint with fever usually at the knee.
-Extremely painful with stiffness and reduced motion.

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61
Q

How is septic arthritis diagnosed?

A

Joint aspiration then mc + s - shows bacteria.
Bloods - Raised ESR and CRP.

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62
Q

What are four differential diagnoses of septic arthritis?

A

Gout, pseudogout, reactive arthritis and haemarthrosis.

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63
Q

What is the management of septic arthritis?

A

Joint aspiration and empirical antibiotics.
NSAIDs for pain.

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64
Q

Describe the antibiotic management of septic arthritis.

A

3-6 week antibiotics:
-1st line - Flucloxacillin and rifampicin.
-MRSA, prosthetic joint, penicillin allergy - Vancomycin and rifampicin.

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65
Q

What is osteomyelitis?

A

Infection of the bone or bone marrow.

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66
Q

How does osteomyelitis occur?

A

Local - Directly to the bone due to fracture.
Hematogenous - To bone through blood after entering body from another route.

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67
Q

What are the organisms responsible for osteomyelitis?

A

S. aureus (mc - 90%).

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68
Q

Who is osteomyelitis most common in?

A

Young boys under 10y.

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69
Q

What are seven risk factors for osteomyelitis?

A

Open bone fracture, bone surgery, immunocompromised, IVDU, sickle cell anaemia, HIV, TB.

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70
Q

How does osteomyelitis present?

A

Acutely and chronic:

Pain with swelling, tenderness and refusing to bear weight. May have fever.

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71
Q

What are the investigations for osteomyelitis and what their findings?

A

XRAY/MRI.
Bloods - Raised ESR and CRP.
BM biopsy - mc + s to ID causative organism.

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72
Q

What is the management of osteomyelitis?

A

Immbolisation and antibiotics (vancomycin).
May need surgery/drainage.

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73
Q

What are spondyloarthropathies?

A

Inflammatory seronegative (RF) arthritis associated with HLAB27.

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74
Q

What are the general features of spondyloarthropathies?

A

SPINEACHE:

-Sausage fingers, psoriasis, inflammatory back pain, NSAIDs good, enthesitis, arthritis, Crohn’s/colitis, HLAB27, eyes (uveitis).

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75
Q

What is ankylosing spondylitis?

A

Inflammatory spondyloarthropathy mainly affecting the spine with abnormal stiffening and pain.

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76
Q

Which joints does ankylosing spondylitis mostly affect?

A

Sacro-iliac joints and the vertebral column.

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77
Q

Describe the genetic link to ankylosing spondylitis.

A

Associated with HLAB27:

-90% with AS have HLAB27.
-2% with HLAB27 develop AS.

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78
Q

What is a complication of ankylosing spondylitis?

A

Vertebral fractures.

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79
Q

What is the typical presentation of AS?

A

Young male (teens/20s) with progressively worsening back stiffness. Develops over a few months and can have flare ups.
-Worse in the morning and night, improves with exercise.

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80
Q

What are four signs of ankylosing spondylitis?

A

Anterior uveitis, enthesitis, dactylitis, lumbar pathology (decreased lordosis and flexion).

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81
Q

What is Schober’s test?

A

A test to assess the mobility of the spine.
-Making marks above and below L5 vertebrae and seeing if the distance increases, if movement is restricted - AS.

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82
Q

What are the investigations of AS?

A

-Raised ESR and CRP.
-XRAY - Bamboo spine with squared vertebral bodies and syndesmophytes.
-HLAB27 positive.

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83
Q

What is the management of AS?

A

NSAIDs and exercise for pain.
Steroids during flare ups.
Anti-TNF medications - infliximab.

84
Q

What is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis.

85
Q

How strong is the link between psoriasis and psoriatic arthritis?

A

20% of those with psoriasis develop it arthritis within 10y.

86
Q

When does psoriatic arthritis usually occur?

A

Middle age but can occur at any age.

87
Q

How severe is psoriatic arthritis?

A

Can range from mild stiffening to arthritis mutilans.

88
Q

How common is arthritis mutilans in psoriatic arthritis?

A

5% develop arthritis mutilans.

89
Q

What is the screening tool for psoriatic arthritis?

A

PEST - asks about joint pain, swelling, arthritis history and nail pitting.

90
Q

What is arthritis mutilans?

A

Severe arthritis in the fingers and toes that presents in psoriatic arthritis.
-There is osteolysis which leads to progressive shortening of the finger and skin folding leading to ‘telescope finger’.

91
Q

What are the patterns of psoriatic arthritis?

A

-Symmetrical polyarthritis - Presents similar to RA, more common in women. Affects hands, wrists, ankles and DIP joints.
-Asymmetrical polyarthritis - Mainly affects digits and feet.
-Spondylitic - Back stiffness, sacroiliitis.

92
Q

What are five signs of psoriatic arthritis?

A

Psoriasis plaques, nail pitting, onycholysis, dactylitis, enthesitis.

93
Q

What are three associations of psoriatic arthritis?

A

Eye disease (conjunctivitis/uveitis).
Aortitis.
Amyloidosis.

94
Q

How is psoriatic arthritis diagnosed?

A

XRAY.

95
Q

What are the XRAY changes in someone with psoriatic arthritis?

A

Ankylosis, dactylitis, osteolysis, pencil-in-cup deformity.

96
Q

What is the management for psoriatic arthritis?

A

DMARD - Methotrexate.
Anti-TNF - Infliximab.
Last line - Ustekinumab.
NSAIDs for analgesia.

97
Q

What is reactive arthritis?

A

Inflammation of the synovial membranes due to recent infective trigger.

98
Q

What is the difference between septic and reactive arthritis?

A

In reactive arthritis there is no infection in the joint.

99
Q

What are the triggers of reactive arthritis?

A

Gastroenteritis or STI (chlamydia).

100
Q

What is the presentation of reactive arthritis?

A

Reiter’s triad - can’t pee, can’t see, can’t climb a tree.
-Uveitis, urethritis, arthritis.

101
Q

How is reactive arthritis diagnosed?

A

Joint aspiration and mc + s - No organism and negative for crystalarthropathy.
-Raised ESR and CRP, HLAB27.

102
Q

What is the management of reactive arthritis?

A

NSAIDs, steroid injections.
-If recurrent - DMARD (methotrexate) and infliximab.

103
Q

What is systemic lupus erythematous (SLE)?

A

An inflammatory autoimmune connective tissue disorder
-Systemic and involves multiple organs.

104
Q

What is the pattern of disease in SLE?

A

Usually relapse-remitting with flare ups.

105
Q

What type of reaction is SLE?

A

T3 hypersensitivity (Ab-Ag complex deposition).

106
Q

What is the typical patient affected by SLE?

A

Afro-Caribbean females aged 20-40.

107
Q

What are five risk factors for SLE?

A

Female, HLAB8, HLADR2, HLADR3 and drugs.

108
Q

What is the pathophysiology of SLE?

A

Anti-nuclear autoantibodies (ANA), these attack proteins in the cell nucleus. The immune system attacks these and an inflammatory response is generated.

109
Q

How does SLE present?

A

Photosensitive malar rash (butterfly shaped).
-Fatigue, fever, weight loss, myalgia, arthralgia.
-SOB, chest pain, hepatosplenomegaly.
-Hair loss, mouth ulcers, Raynaud’s.

110
Q

What are the investigations in SLE and what are their findings?

A

Bloods - Anaemia, raised ESR and CRP. Decreased C3 and C4.
Urinalysis and renal biopsy - Lupus nephritis.
Serology:
-ANA and anti-dsDNA are common.
-Types of ANA:
Anti-RO, anti-SM, anti-LA.

111
Q

What is the management of SLE? Severe?

A

Lifestyle - less sunlight and suncream.
Prednisolone, hydroxychloroquine and NSAIDs.
-Severe - Methotrexate and rituximab.

112
Q

What are five severe complications of SLE?

A

CVD, infection, anaemia, nephritis, antiphospholipid syndrome.

113
Q

What is vasculitis?

A

Inflammation of the blood vessels.

114
Q

What are the types of vasculitis?

A

Affecting:
-Large vessels, medium vessels and small vessels.

115
Q

What are the two types of vasculitis affecting large vessels?

A

Giant cell arteritis, Takayasu’s arteritis.

116
Q

What are the three types of vasculitis affecting medium vessels?

A

Polyarteritis nodosa, Kawasaki’s disease and Buerger’s disease.

117
Q

What are two types of vasculitis affecting small vessels?

A

Granulomatosis with polyangitis, Henoch-Schoenlein purpura.

118
Q

What is the general treatment for vasclitis?

A

Corticosteroids.
-If long term consider gastric and bone protection.

119
Q

What is giant cell arteritis?

A

Systemic vasculitis of the medium and large arteries, typically presents affecting the temporal artery.

120
Q

What is a severe complication of giant cell arteritis?

A

Sudden painless vision loss in one eye.

121
Q

What are the typical patients affected by giant cell arteritis?

A

White females 50 and above.

122
Q

How does giant cell arteritis present?

A

Severe unilateral headache around temple and forehead with scalp tenderness, jaw claudication and double/blurred vision.

123
Q

How is giant cell arteritis diagnosed?

A

-Temporal artery biopsy - granulomatous inflammation and multinucleated giant cells.
-Raised ESR and CRP.

124
Q

What is the management of giant cell arteritis?

A

Prednisolone, aspirin and PPI for gastric protection.

125
Q

What are three complications of giant cell arteritis?

A

Vision loss, stroke, aortitis (aneurysm/dissection).

126
Q

What is polyarteritis nodosa?

A

Medium vessel arteritis associated with hepatitis B and C and HIV.

127
Q

What does polyarteritis nodosa affect?

A

The skin, GI tract, kidneys and the heart - causes CKD/AKI, strokes, MI and skin nodules.

128
Q

What does polyarteritis nodosa cause?

A

Livedo reticularis - mottled purple rash.

129
Q

What is granulomatosis with polyangitis?

A

Small vessel arteritis that affects the respiratory tract and kidneys.

130
Q

What does granulomatosis with polyangitis cause?

A

Nose bleeds, crusty nasal secretions, hearing loss and sinusitis.

131
Q

What can granulomatosis with polyangitis progress to?

A

Glomerulonephritis.

132
Q

What is fibromyalgia?

A

Chronic widespread pain for 3+ months with all the other causes ruled out.

133
Q

What are the five risk factors for fibromyalgia?

A

60+, females, depression, stress, poor.

134
Q

How does fibromyalgia present?

A

Stressed, depressed 60y woman with fatigue and pain.
Sleep disturbance, morning stiffness.

135
Q

How is fibromyalgia diagnosed?

A

Diagnosis of exclusion and clinically made.
-No serological markers, normal ESR and CRP.
-Pain in 11 out of 18 regions.

136
Q

What is the treatment for fibromyalgia?

A

Educating patients, physiotherapy.
Antidepressants and CBT.

137
Q

What is the key differential diagnosis of fibromyalgia?

A

Polymyalgia rheumatica.

138
Q

What is Sjogren’s syndrome?

A

Chronic inflammatory autoimmune condition affecting exocrine glands.

139
Q

What are the types of Sjogren’s syndrome?

A

Primary - in isolation.
Secondary - in relation to SLE or RA.

140
Q

What are the four risk factors for Sjogren’s syndrome?

A

Females, middle aged, family history, HLAB8/DR3.

141
Q

How does Sjogren’s syndrome present?

A

Dry mucous membranes:
-Dry eyes, dry mouth and dry vagina.

142
Q

What are the investigations for Sjogren’s syndrome?

A

Serology - Anti-Ro, anti-La antibodies.
Schirmer tear test - Induce tears and place paper filter under eyes. Tears should travel 20mm, significant is <10mm.

143
Q

What is the management for Sjogren’s syndrome?

A

Artificial tears, saliva and lubricant for sex.
Hydroxychloroquine - slows progression.

144
Q

What are four complications of Sjogren’s syndrome?

A

Eye infections, dental/oral problems, vaginal problems, sexual dysfunction.

145
Q

How common are primary bone tumours?

A

Rare, seen mostly in children.
-Secondary bone tumours are more common.

146
Q

What are the four primary bone tumours?

A

Osteosarcoma, Ewing sarcoma, chondrosarcoma, fibrosarcoma.

147
Q

What are the cancers that metastasise to bone?

A

BLTKP:

-Breast, lung, thyroid, kidney, prostate.

148
Q

What is osteosarcoma?

A

Most common primary bone cancer, associated with Paget’s.

149
Q

What is Ewing sarcoma?

A

Very rare bone cancer from mesenchymal stem cell.

150
Q

What is chondrosarcoma?

A

Cancer of the cartilage.

151
Q

What is the general presentation of bone cancer?

A

Severe pain worse at night with weight loss, fatigue, fever and malaise.

152
Q

How is bone cancer diagnosed and treated?

A

XRAY.
Chemo, radio, bisphosphonates and surgery.

153
Q

What is systemic sclerosis?

A

An autoimmune inflammatory and fibrotic connective tissue disorder with unclear cause.

154
Q

What is the most common type of systemic sclerosis?

A

Limited cutaneous scleroderma.

155
Q

What does systemic sclerosis put you at risk for?

A

Pulmonary hypertension and fibrosis.

156
Q

What are the features of systemic sclerosis?

A

CREST:

-Calcinosis - calcium deposits under the skin at fingertips.
-Raynaud’s phenomenon - blue fingers when cold.
-oEsophageal dysmotility - swallowing difficulties.
-Sclerodactyly/scleroderma - skin hardening, thickening and tightening on hands which restricts mobility.
-Telangiectasia - spider veins on face.

157
Q

How is systemic sclerosis diagnosed?

A

ACA antibodies seen in 70%, ANA also positive.

158
Q

What is the management of systemic sclerosis?

A

No cure, treat symptoms and complications.
-Steroids and immunosuppressants.
-Treat complications: GI symptoms (PPI), Raynaud’s (hand warmers).

159
Q

What is polymyositis?

A

An autoimmune disorder where there is chronic inflammation of the muscles.

160
Q

What is dermatomyositis?

A

Autoimmune connective tissue disorder where there is chronic inflammation of the muscles and skin.

161
Q

What can cause dermatomyositis and polymyositis? What does this make them?

A

Underlying malignancy - paraneoplastic syndromes.

162
Q

Which cancers are most commonly associated with dermatomyositis and polymyositis?

A

Lung, breast, ovarian and gastric.

163
Q

How does polymyositis present?

A

Symmetrical wasting of muscles mostly the shoulder and pelvic girdle.
-With muscle pain, fatigue and weakness.

164
Q

What is the difference between polymyositis and dermatomyositis?

A

Dermatomyositis have skin changes involved.

165
Q

What are four features of dermatomyositis?

A

Gottron lesions - scaly knuckles.
Photosensitive erythematous rash.
Purple rash on face and eyelids.
Periorbital swelling.

166
Q

Which investigations are used for polymyositis and dermatomyositis?

A

Muscle biopsy for definitive diagnosis.
-Raised creatine kinase.
-Autoantibodies:
Anti-Jo1 for polymyositis.
Anti-Mi2 and ANA for dermatomyositis.

167
Q

What is the management of polymyositis and dermatomyositis?

A

1st line - Corticosteroids (prednisolone).
-Others: Immunosuppressants, IV Ig, biological therapy (infliximab).

168
Q

What is antiphospholipid syndrome?

A

Disorder associated with antiphospholipid antibodies where the blood is prone to clotting - hypercoagulable state.

169
Q

What is antiphospholipid syndrome associated with?

A

Thrombosis (stroke, MI, DVT, PE) and recurrent miscarriages.

170
Q

What are the types of antiphospholipid syndrome?

A

Primary (idiopathic) and secondary to other diseases (e.g. SLE).

171
Q

How does antiphospholipid syndrome present?

A

Clots and pregnancy complications:
-DVT, PE, MI, stroke.
-Recurrent miscarriage, preeclampsia, stillbirth.

Others:
-Livedo reticularis (purple rash).
-Thrombocytopenia.

172
Q

How is antiphospholipid diagnosed?

A

History of thrombus and pregnancy complications with autoantibodies:

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

173
Q

How is antiphospholipid syndrome managed?

A

Long term warfarin to prevent thrombi.
-If pregnant - LMWH and aspirin.

174
Q

What is mechanical lower back pain?

A

Lower back pain often due to trauma or work.
-Normal in 20-55, very common and self-limiting.

175
Q

What are the signs for serious pathology in back pain?

A

Elderly (myeloma), neuropathic pain (spinal cord compression).

176
Q

What is lumbar spondylosis?

A

Degeneration of intervertebral discs, loses its compliance and thins over time.

177
Q

What is osteomalacia?

A

Defective bone mineralisation causing soft bones.

178
Q

How does osteomalacia occur?

A

Due to vitamin D deficiency.

179
Q

What is the difference between Ricket’s and osteomalacia?

A

Ricket’s is in children before epiphyseal fusion whereas osteomalacia is in adults after epiphyseal fusion.

180
Q

Describe the pathophysiology of osteomalacia.

A

Vitamin D is essential for the absorption of calcium and phosphate from the intestine. If deficient, there is a lack of calcium and phosphate which leads to defective bone minerlisation.
-Low calcium causes secondary hyperparathyroidism as there is increased PTH to increase the calcium level, stimulating bone resorption which causes further problems with bone mineralisation.

181
Q

What are three causes of osteomalacia?

A

-Malabsorption/less intake/poor sunlight - No vitD.
-CKD/renal failure - Less active vitD formation.
-Liver failure.

182
Q

How does osteomalacia and Ricket’s present?

A

May be asymptomatic.
-Fatigue, bone pain, muscle weakness and aches.
-Fractures and difficulty weight bearing.

Rickets:
-Skeletal deformities (knocked knees, bowed legs).

183
Q

What are the investigations for osteomalacia?

A

Bloods - Low vitD (serum 25-hydroxyvitamin D), low calcium, low phosphate.
XRAY - Osteopenia.
BM biopsy - Incomplete minerlisation.
DEXA scan - Low bone mineral density.

184
Q

What is the treatment for osteomalacia?

A

Supplementary vitamin D and increased dietary intake.

185
Q

What is Paget’s disease?

A

Disorder of bone remodelling due to excessive activity of osteoclasts and osteoblasts.
-Leading to patchy areas of high and low density (sclerosis and lysis).
-Results in enlarged and misshaped bones with structural problems.

186
Q

What causes Paget’s disease?

A

Idiopathic.

187
Q

How does Paget’s disease present?

A

Older patients with: Bone pain, bone deformities, fractures and hearing loss (damaged inner ear bones).

188
Q

What are the investigations in Paget’s disease?

A

XRAY and bloods.

189
Q

What are the blood results in someone with Paget’s disease?

A

Raised ALP, normal calcium and normal phosphate.

190
Q

What are the XRAY findings in Paget’s disease?

A

Osteoporosis circumscripta - osteolytic lesions.
Cotton wool appearance - areas of sclerosis and lysis in skull.
V-shaped defects - in long bones, V shaped osteolytic lesions.

191
Q

What is the management of Paget’s disease?

A

Bisphosphonates and analgesia for pain.

192
Q

What are two major complications of Paget’s disease?

A

Osteosarcoma and spinal cord compression.

193
Q

What is polymyalgia rheumatica?

A

Inflammatory condition that causes pain and stiffness in the shoulders, neck and pelvic girdle.

194
Q

Which condition is PR strongly linked to?

A

Giant cell arteritis.

195
Q

What is the typical patient with polymyalgia rheumatica?

A

White women over 50y.

196
Q

How does polymyalgia rheumatica present?

A

Bilateral shoulder and pelvic girdle pain which is worse with movement and interferes with sleep.
-Stiffness for at least 45m in the morning.
-Systemic symptoms - weight loss, fatigue, low mood.

197
Q

How is PR diagnosed?

A

With clinical presentation and response to steroid treatment.

198
Q

What are the investigations for PR?

A

Bloods to exclude other things - Raised ESR and CRP., FBC, U+E, LFTs, TFTs, CK, RF, calcium, urine dipstick and Bence-Jones protein.

199
Q

What are seven differential diagnoses of PR?

A

OA, RA, SLE, myositis, osteomalacia, fibromyalgia, thyroid pathology.

200
Q

How is PR treated? How do you know that is it PR?

A

With prednisolone - poor response probably isn’t PR.
-If they work start a reducing regime.

201
Q

What are the long term steroids precautions?

A

DONT STOP:

DON’T - Steroid dependent, Adrenal crisis.
S - Sick day rules.
T - Treatment card.
O - Osteoporosis prevention.
P - PPI for gastric protection.

202
Q

What do connective tissue disorders lead to?

A

Weak valves and weak vessels - regurgitation murmurs and aortic aneurysm rupture.

203
Q

What are two connective tissue disorders?

A

Marfan’s and Ehlers-Danlos syndrome.

204
Q

What is Marfan’s syndrome?

A

Autosomal dominant FB1 mutation resulting in decreased connective tissue strength.

205
Q

How does Marfan’s syndrome present?

A

Tall and thin patients with long fingers and pectus excavatum.
-Aortic complications - Regurgitation murmur, AAA and aortic aneurysm.

206
Q

What is Ehlers-Danlos syndrome?

A

Autosomal dominant mutations affecting collagen proteins.

207
Q

How does ED syndrome present?

A

Joint hypermobility and CV complications (mitral regurgitation, AAA, AD).

Phase 2a (14 decks)

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