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Phase 2a Medicine > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What are degenerative MSK disorders

A

disorders involving progressive impairment of both the structure and function of part of the body.

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2
Q

3 examples of Degenerative disorders

A

Degenerative arthritis (osteoarthritis), disc disease and degenerative scoliosis.

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3
Q

What are inflammatory MSK disorders

A

disorders involving a local response to cellular injury that is marked by redness, heat, pain, swelling and often loss of function.

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4
Q

4 examples of inflammatory MSK disorders

A

Rheumatoid arthritis, gout, vasculitis, spondyloarthropathies, infection.

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5
Q

pain profile of inflammatory joint disorders

A

pain eases with use

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6
Q

stiffness profile of inflammatory joint disorders

A

significant (longer than 60mins) in the morning/at rest

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7
Q

swelling profile of inflammatory joint disorder

A

synovial +/- bony

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8
Q

patient demographics of inflammatory joint disorders

A

young, psoriasis, family history

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9
Q

joint distribution for inflammatory joint disorders

A

hands and feet

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10
Q

response to NSAIDs of inflammatory joint disorders

A

Yes

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11
Q

pain profile of degenerative joint disorders

A

increases with use
clicks/clunks

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12
Q

stiffness profile of degenerative joint disorders

A

not prolonged (<30mins)
morning/evening

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13
Q

swelling profile for degenerative joint disorders

A

none or bony

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14
Q

patient demographics of degenerative joint disorders

A

older, prior occupation/sport

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15
Q

joint distribution of degenerative joint disorders

A

1st CMC, DIP, knees

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16
Q

response to NSAIDs for degenerative joint disorders

A

not convincing

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17
Q

4 pillars of inflammation

A

rubor- red
dolor- painful
calor- hot
tumour- swollen

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18
Q

ESR

A

erythrocyte sedimentation rate
Rises with inflammation/ infection
Increased fibrinogen makes RBCs stick together, so the number of RBCs falls faster
When ESR rises, rate of fall is quicker
ESR rises and falls slowly (days to weeks)

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19
Q

What causes ESR false postives

A

Age, female, obesity, racial difference, hypercholesterolaemia, high immunoglobulins, anaemia

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20
Q

CRP

A

C-reactive protein
Acute phase protein – pentameric peptide
Released in inflammation/ infection
Produced by liver in response to IL-6
Rises and falls rapidly (high at 6 hours and peaks at 48 hours)

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21
Q

Osteoarthritis

A

A group of diseases characterised by joint degeneration. It is an age-related, dynamic reaction pattern of a joint in response to insult or injury.

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22
Q

features of osteoarthitis

A

Affects synovial joints
All tissues of the joint are involved
Articular cartilage is the most affected
Changes in underlying bone at the joint margins

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23
Q

causes of osteoarthritis

A

Primary osteoarthritis: most common with no clear cause
Secondary osteoarthritis: brought about by conditions causing damage to joints e.g. rheumatoid arthritis (RA), gout, trauma

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24
Q

pathology of OA

A

Insult to joint tissue initiating a cycle of cellular events, including low-grade chronic inflammation of the synovium, release of metalloproteinases, and degradation of articular cartilage matrix.
Originally considered to be an inevitable consequence of ageing and trauma
Main pathological features:
Loss of cartilage
Disordered bone repair

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25
Q

Risk factors for OA

A

Age
Female
OA hip less common in Afro-Caribbean and Asian populations
Obesity
Occupation
Local trauma
Inflammatory arthritis e.g. RA
abnormal biomechanics

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26
Q

3 examples of occupations causing OA

A

Manual labour associated with OA of small joints of hands
Farming associated with OA of hips
Football associated with OA of knees

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27
Q

3 examples of abnormal biomechanics causing OA

A

Joint hypermobility
Congenital hip dysplasia
Neuropathic conditions

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28
Q

clinical presentations of OA

A

Joint pain
Tenderness
Swelling (small joints)
Synovitis
Stiffness
Symptoms typically worsen during the day with activity
Alteration in gait
Heberden’s nodes
Bouchard’s nodes

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29
Q

principal joints affected by OA

A

hip, knee, spine, and small joints of the hands

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30
Q

location of heberdens and bouchards nodes

A

Heberden’s nodes – DIP joint
Bouchard’s nodes – PIP joint

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31
Q

differential diagnosis for OA

A

Fibromyalgia
Rheumatoid arthritis
Gout and pseudogout

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32
Q

Xray findings for OA

A

LOSS;
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

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33
Q

non-medical management of OA

A

Activity and exercise – improve local muscle strength and general aerobic fitness.
Weight loss if overweight
Physiotherapy
Occupational therapy
Walking aids – sticks/frames

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34
Q

Pharmalogical management of OA

A

Analgesia;
Topical – NSAIDs/ capsaicin
Oral – paracetamol/ NSAIDs/ opioids
Transdermal patches

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35
Q

Surgical management of OA

A

Joint replacement (hips or knees)
Arthroplasty (surgical reconstruction or a replacement of a joint)– if uncontrolled pain and significant limitation of function
Arthroscopy (keyhole surgery on a joint)

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36
Q

rheumatoid arthritis

A

A multisystem autoimmune disease in which the brunt of disease activity falls upon the synovial joints.

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37
Q

causes of RA

A

The initial trigger remains unknown
Once inflammation begins, it appears to become self-perpetuating

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38
Q

Which auto-antibodies are found for RA

A

rheumatoid factor, anti-CCP

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39
Q

pathology of RA

A

Infiltration of synovium by CD4+ T-cells, B-cells (lymphocytes), plasma cells and macrophages
Chronic inflammation reaction

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40
Q

clinical presentations of RA

A

Symmetrical, swollen, painful, stiff, small joints of hands and feet
Symptoms are typically worse in the morning
Systemic illness e.g. fatigue, weight loss, pericarditis and pleurisy

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41
Q

Extra-articular manifestations of RA

A

Cardiac disease: ischaemic heart disease, pericarditis
Vascular disease: accelerated atherosclerosis, vasculitis
Haematological disease: anaemia, splenomegaly
Pulmonary disease: pulmonary fibrosis, pleuritis
Skin: rheumatoid nodules, erythema nodosum
Neurological: peripheral neuropathy, stroke

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42
Q

later signs of RA

A

Ulnar deviation and subluxation of the wrist and fingers
Boutonniere and swan-neck deformities of fingers
Z thumbs

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43
Q

differential diagnosis for RA

A

Osteoarthritis
Fibromyalgia
SLE

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44
Q

first line investigations for RA

A

Serology: anti CCP positive, rheumatoid factor positive
Bloods: anaemia, CRP/ESR raised
x-ray: less lost joint space, erosion, soft tissue swelling, soft bone

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45
Q

Gold standard investigations for RA

A

Clinical diagnosis, serology, inflammatory markers

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46
Q

Management for RA

A

1st line – DMARDs (disease modifying anti-rheumatic drugs) e.g., methotrexate, leflunomide, sulfasalazine
2nd – Add biological agent (infliximab, adalimumab, etanercept, rituximab)
3rd – corticosteroid (prednisolone), NSAIDs (ibuprofen)

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47
Q

management for pregnant RA patients

A

prednisolone, sulfasalazine, hydroxychloroquine

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48
Q

pathological bonefractures

A

A fracture is a soft tissue injury in which there is also a break in the continuity of a surface or substructure of bone.

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49
Q

7 fracture patterns

A

Transverse
Oblique
Spiral – generated from twisting injury
Butterfly
Comminution – generate from high energy impact
Segmental
Greenstick

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50
Q

features of greenstick fractures

A

Specific to children
Unicortical fracture in which the bone bends and breaks due to thick periosteum
Bones not completely broken, easy to treat

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51
Q

risk factors for pathological fractures

A

Osteoporosis
Metabolic bone disease – Osteomalacia and rickets
Paget’s disease
Bone infiltrated by malignant tumours

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52
Q

management of fractures

A

Analgesia
Examination – neurovascular
Reduce
Immobilise
Rehabilitate

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53
Q

Fracture healing steps when not touching

A

Immediately after the fracture there will be a haemorrhage within the bone from ruptured vessels in the marrow cavity and also around the bone.
A haematoma at the fracture site facilitates repair by providing a foundation for the growth of cells.
There will also be devitalised fragments of bone and soft tissue damage nearby. So the initial phases of repair involve removal of necrotic tissue and organisation of the haematoma.
The capillaries in the haematoma are accompanied by fibroblasts and osteoblasts, which deposit bone in an irregularly woven pattern; a callus.
Woven bone is subsequently replaced by more orderly, lamellar bone, which in turn is gradually remodelled according to the direction of mechanical stress.

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54
Q

what delays fracture healing

A

if bone ends are mobile, infected very badly, misaligned or avascular.

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55
Q

osteoporosis

A

A metabolic bone disease characterised by a generalised reduction in bone mass, increased bone fragility, and predisposition to fracture.

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56
Q

primary causes of osteoporosis

A

post-menopausal and age-related (>70y)

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57
Q

7 causes of osteoporosis

A

Therapeutic agents; glucocorticoid therapy, anti-androgens and anti-oestrogens
Cushing’s syndrome
Hyperparathyroidism, hyperthyroidism
Hypogonadism (low levels of testosterone)
Coeliac disease
IBD
Alcohol, poor nutrition, immobilisation

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58
Q

risk factors for osteoporosis

A

SHATTERED
Steroid use (>5mg/d prednisolone)
Hyperthyroidism, hyperparathyroidism, hypercalciuria
Alcohol and tobacco use
Thin (BMI <18.5)
Testosterone levels low
Early menopause
Renal or liver failure
Erosive/ Inflammatory bone disease e.g. RA
Dietary low calcium/ malabsorption

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59
Q

what is bone mass in later life determined by

A

the peak bone mass attained in early adulthood and the subsequent rate of bone loss

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60
Q

what is peak bone mass determined by

A

largely genetically determined but is modified by factors such as nutrition, physical activity and health early in life

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61
Q

What causes bone loss with age

A

decreasing bone turnover, decreasing physical activity, reduced sex hormones and reduced calcium absorption from the gut

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62
Q

what causes women to be more susceptible to osteoporosis

A

oestrogen deficiency after the menopause markedly accelerates bone loss

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63
Q

affect of glucocorticoids in osteoporosis

A

decrease osteoblastic activity and lifespan, reduce calcium absorption from the gut, and increase renal calcium loss.

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64
Q

characterisation of post-menopausal osteoporosis

A

High bone turnover
(resorption>formation)
Predominantly cancellous bone loss
Microarchitectural disruption

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65
Q

osteoporosis of ageing

A

there are changes to the trabecular architecture.
Decreases in trabecular thickness, more pronounced for non-load bearing horizontal trabeculae
Decrease in connections between horizontal trabeculae
Decrease in trabecular strength and increased susceptibility to fracture

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66
Q

clinical presentations of osteoporosis

A

Most cases are clinically silent until fragility fractures occur
Vertebral fractures lead to loss of height and kyphosis. May occur spontaneously and after lifting, coughing, and bending down.
If trabecular bone is affected, crush fractures of vertebrae are common
If cortical bone is affected, long bone fractures are more likely e.g. femoral neck (big cause of death and orthopaedic expense)

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67
Q

classic sites of involvement for osteoporotic fractures

A

vertebrae, distal radius, neck of femur following a fall

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68
Q

differential diagnosis for osteoporosis

A

Paget Disease
Hyperparathyroidism
Scurvy

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69
Q

first line investigations for osteoporosis

A

Bone mineral density with DEXA bone scan, FRAX score, Calcium, phosphate, ALP normal

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70
Q

FRAX score

A

10-year probability of major osteoporotic fracture or hip fracture

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71
Q

Ranges for DEXA scan

A

(normal = T > -1, osteopenia = -2.5 < T < -1, osteoporosis = T < -2.5)

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72
Q

Gold standard investigations for osteoporosis

A

DEXA bone scan – dual energy x-ray absorptiometry yields T score

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73
Q

lifestyle changes for osteoporosis

A

Quit smoking and reduce alcohol consumption
Weight-bearing exercise may increase bone mineral density
Balance exercises such as tai chi reduce risk of falls
Calcium and vitamin D rich diet

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74
Q

First line pharmalogical management for osteoporosis

A

Bisphosphonates: alendronic acid (alendronate)
Anti-resorptive: decreases osteoclast activity and bone turnover

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75
Q

benefits of HRT

A

reduce risk of fractures by 50%, stop bone loss, reduce risk of colon cancer

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76
Q

risks of HRT

A

breast cancer, stroke, CVD, venous thrombo-embolic disease

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77
Q

4 alternative pharmological managements for osteoporosis

A

Teriparatide: increases bone density, improves trabecular structure
Anabolic drugs: increases osteoblast activity and bone formation
Calcium and vitamin D: offer if evidence of deficiency
Calcitonin: pain management after a vertebral fracture
Testosterone: may help in hypogonadal men by promoting trabecular connectivity

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78
Q

pathological changes in systemic sclerosis

A

scleroderma (skin fibrosis), internal organ fibrosis and microvascular abnormalities.

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79
Q

investigations for Systemic sclerosis

A

90% are ANA positive
anti-SCL70 present

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80
Q

limited systemic scleroderma

A

involves face, hands and feet. Associated with anticentromere antibodies. Pulmonary hypertension is often present sub-clinically.

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81
Q

diffuse scleroderma

A

can involve the whole body, prognosis is poor. Control BP meticulously. Perform annual echocardiogram and spirometry.

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82
Q

potential complications for systemic sclerosis

A

organ fibrosis: lung, cardiac, GI and renal.

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83
Q

management of systemic sclerosis

A

No cure. Immunosuppressive regimens, including IV cyclophosphamide.
Monitor BP and renal function

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84
Q

polymyositis and dermatomyositis

A

Rare conditions characterised by insidious onset of progressive symmetrical proximal muscle weakness and autoimmune-mediated striated muscle inflammation.

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85
Q

complications of muscle weakness in polymyositis and dermatomyositis

A

may cause dysphagia, dysphonia, or respiratory weakness

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86
Q

skin signs of dermatomyositis

A

Macular rash
Lilac-purple rash on eyelids often with oedema
Nailfold erythema (dilated capillary loops)
Gottron’s papules: roughened red papules over the knuckles

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87
Q

extramuscular signs of polymyositis and dermatomyositis

A

Fever
Arthralgia
Raynaud’s
Interstitial lung fibrosis
Myocardial involvement (myocarditis, arrhythmias)

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88
Q

1st line investigations for polymyositis and dermatomyositis

A

Lactate dehydrogenase raised, AST and ALT raised, myoglobin raised, creatinine kinase raised (>1000 U/L. Normal = <300.)
Serology: anti-Jo-1 (polymyositis), anti Mi2 (dermatomyositis), anti-nuclear antibodies (dermatomyositis). Electromyograph

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89
Q

gold standard investigations for polymyositis and dermatomyositis

A

Muscle fibre biopsy – inflammation, necrosis

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90
Q
A
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91
Q

management of polymyositis and dermatositis

A

Start prednisolone
Immunosuppressives and cytotoxics are used in early resistant cases.

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92
Q

systemic lupus erythematosus

A

A multisystem autoimmune disease characterised by autoantibody production against a number of nuclear and cytoplasmic autoantigens.

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93
Q

pathophysiology of SLE

A

Anti-nuclear antibodies are antibodies which attack proteins in the person’s cell nucleus. This generates an inflammatory response and damage.

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94
Q

key presentations of SLE

A

Photosensitive red malar butterfly rash, glomerulonephritis (nephritic), arthralgia, fatigue, fever, hair loss, mouth ulcers, lymphadenopathy

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95
Q

signs of SLE

A

Butterfly rash, ulnar deviation, mouth ulcers, anaemia, Raynaud’s, lymphadenopathy and splenomegaly, pleuritic chest pain, hair loss, seizures and psychosis

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96
Q

symptoms of SLE

A

Weight loss, fever, fever, joint pain, myalgia, shortness of breath

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97
Q

1st line investigations for SLE

A

FBC (anaemia, leukopenia, thrombocytopenia), Normal CRP, raised ESR, raised urea and creatinine, urine protein:creatinine (proteinuria)
urine dipstick (haematuria, proteinuria)
anti-nuclear (ANA) and anti-double-stranded DNA (aDsDNA) antibodies present

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98
Q

gold standard investigations for SLE

A

Antinuclear antibodies (ANA)and clinical diagnosis

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99
Q

differential diagnosis for SLE

A

Rheumatoid arthritis, antiphospholipid syndrome, HIV, glomerulonephritis

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100
Q

management of SLE

A

1st line – Hydroxychloroquine
Consider: NSAIDs, corticosteroid, immunosuppressant (methotrexate), biologics (rituximab)

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101
Q

complications of SLE

A

Cardiovascular disease, infection, pericarditis, pleuritis, interstitial lung disease, anaemia

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102
Q

Sjorgens syndrome

A

A chronic inflammatory autoimmune disorder, which may be primary or secondary, associated with connective tissue disease.

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103
Q

what can sjorgens syndrome be secondary to

A

SLE, rheumatoid arthritis, scleroderma, primary biliary cirrhosis

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104
Q

key presentations of Sjorgens syndrome

A

Dry mucous membranes – dry mouth (xerostomia), dry eyes (keratoconjunctivitis sicca), dry vagina

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105
Q

1st line investigations for Sjorgens

A

Anti-Ro and anti-La antibodies. Schirmer test – tears travelling <10mm (>15mm is normal)

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106
Q

gold standard test for sjorgens

A

Anti-Ro and anti-La antibodies

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107
Q

Differential diagnosis for Sjorgens

A

Systemic lupus erythematosus, systemic sclerosis, rheumatoid arthritis

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108
Q

management of sjorgens

A

1st line – artificial tears, artificial saliva, vaginal lubricant.
Hydroxychloroquine used to halt progression

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109
Q

complications of sjorgens

A

Eye infections (conjunctivitis, corneal ulcers), oral problems (candida infection, dental cavities), vaginal problems (candidiasis, sexual dysfunction). Lymphomas

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110
Q

Raynauds phenomenon

A

Peripheral digital ischaemia due to paroxysmal vasospasm, precipitated by cold or emotion

111
Q

features of raynauds

A

Fingers or toes ache and change colour.
Pale -> ischaemia
Blue -> deoxygenation
Red -> reactive hyperaemia

112
Q

causative conditions for raynauds

A

Connective tissue disorders e.g. systemic sclerosis, SLE
Occupational e.g. using vibrating tools
Obstructive e.g. thoracic outlet obstruction, atheroma
Blood e.g. thrombocytosis, cold agglutinin disease, polycythaemia rubra vera
Drugs - β-blockers
Others – hypothyroidism

113
Q

treatment of raynauds

A

Keep warm e.g. hand warmers
Stop smoking
Chemical or surgical (lumbar or digital) sympathectomy may help in those with severe disease

114
Q

seronegative spondyloarthropathies

A

A group of inflammatory joint diseases characterised by arthritis affecting the spinal column and peripheral joints, and enthesitis (inflammation at the insertion site of tendons and ligament to bone).
Seronegative = rheumatoid factor is negative.

115
Q

genetic factor for spondyloarthopathies

A

Strong association with possession of HLA-B27 allele.

116
Q

pathology of seronegative spondyloarthropathies

A

Traditional theories proposed than an unidentified ‘arthritogenic peptide’ is present by HLA-B27 to CD8+ cytotoxic T cells, leading to joint inflammation.

117
Q

clinical features of spondyloarthropathies

A

Seronegativity (-ve rheumatoid factor)
HLA B27 association
Axial arthritis: pathology in spine and sacroiliac joints
Asymmetrical large-joint oligioarthritis or monoarthritis
Enthesitis: inflammation of the site of insertion of a tendon or ligament into bone
Dactylitis: inflammation of an entire digit due to soft tissue oedema and tenosynovial and joint inflammation
Extra-articular manifestations: iritis, psoriaform rashes, oral ulcers, IBD

118
Q

ankylosing spondylitis

A

A chronic inflammatory disease of the spine and sacroiliac joints, of unknown aetiology.

119
Q

clinical presentations of ankylosing spondylitis

A

Lower back pain due to sacroiliitis
Typical patient: man <30yrs with gradual onset of low back pain, worse during the night with morning stiffness relieved by exercise.
Pain radiates from sacroiliac joints to hips/buttocks, usually improves later in the day.
Progressive loss of spinal movement in all directions
Extra-articular manifestations include;
Iritis
Pulmonary fibrosis
Aortitis

120
Q

1st line investigations for ankylosing spondylitis

A

Pelvic x-ray, CRP and ESR raised, HLA B27 genetic test, MRI spine (bone marrow oedema in early disease before x-ray changes)

121
Q

gold standard investigation for ankylosing spondylitis

A

X-ray of spine and sacrum:
* Bamboo spine (fusion of vertebral bodies)
* Sacroiliitis
* Squaring of vertebral bodies
* Subchondral sclerosis and erosions
* Syndesmophytes (bony outgrowths in spinal ligament)
* Ossification of ligaments, discs and joints
* Fusion of facet, sacroiliac and costovertebral joints

122
Q

management of ankylosing spondylitis

A

Exercise for backache, including intense exercise regimens to maintain posture and mobility
NSAIDs relieve symptoms within 48h, may slow radiographic progression
Local steroid injections provide temporary pain relief
Surgery: hip replacement to improve pain and mobility. Rarely spinal surgery.

123
Q

presentation of psoriatic arthitis

A

Symmetrical polyarthritis (like RA)
DIP joints
Asymmetrical oligoarthritis
Spinal (similar to AS)
Psoriatic arthritis mutilans

Mostly affects the interphalangeal joints and may lead to severe deformation

124
Q

1st line investigations for psoriatic arthritis

A

CRP/ESR raised, joint x-ray, rheumatoid factor -ve, anti-CCP negative, joint aspiration negative for crystals or bacteria

125
Q

gold standard investigation for psoriatic arthritis

A

Joint X-ray:
* erosion in distal interphalangeal joint and periarticular new bone formation.
* Osteolysis.
* Pencil-in-cup deformity (central erosions of bone beside the joints causing one to look hollow like a cup, and one to sit in the cup)
* Periostitis (periosteum inflammation causing thickened, irregular outline of bone)
* Ankylosis (joints fuse causing stiffness)
* Dactylitis (finger inflammation appears as soft tissue swelling)

126
Q

management for psoriatic arthritis

A

1st line – NSAIDs for pain (naproxen, ibuprofen, indomethacin), intra-articular corticosteroid injection if severe
DMARDs (methotrexate, sulfasalazine, leflunomide), TNF inhibitor or monoclonal Ab (etanercept, adalimumab, infliximab), last resort – ustekinumab (Mab targeting IL 12 and 23)

127
Q

reactive arthritis

A

A condition in which arthritis and other clinical manifestations occur as an autoimmune response to infection elsewhere in the body – typically GI or GU, although preceding infection may have resolved or be asymptomatic by the time arthritis presents.

128
Q

pathophysiology of reactive arthritis

A

Occurs within 1 month of an infection elsewhere in the body. Usually related to a genitourinary infection with chlamydia or a GI infection with shigella, salmonella or campylobacter.

129
Q

clinical presentations of reactive arthritis

A

Pain and stiffness in lower back, knees, ankles and feet.
Enthesitis (inflammation at the insertion site of tendons and ligament to bone).
Keratoderma blenorrhagica (brown, raised plaques on soles and palms).
Patients may present with a triad of urethritis, arthritis and conjunctivitis.

130
Q

1st line investigation for reactive arthritis

A

ESR and CRP raised, antinuclear antibodies negative, rheumatoid factor negative, x-ray (sacroiliitis or enthesopathy), joint aspiration negative (exclude septic arthritis and gout), stool cultures, urine dipstick

131
Q

goldstandard investigation for reactive arthritis

A

No GS. Joint aspiration MC+S to rule out organism in synovial fluid. Polarised light microscopy rules out crystal arthropathy

132
Q

management of reactive arthritis

A

No cure.
Splint affected joints acutely; treat with NSAIDs or local steroid injections
Consider methotrexate if symptoms >6 months.
Treating the original infection may make little difference to the arthritis

133
Q

crystal arthropathies

A

A group of joint diseases caused by deposition of crystals in joints.

134
Q

pathology of crystal arthropathies

A

Crystals are deposited in joints
Neutrophils ingest the crystals and degranulate, releasing enzymes that damage the joint

135
Q

pathology of Gout

A

caused by deposition of monosodium urate crystals in joint
Most cases are related to hyperuricaemia due to impaired excretion of urate by the kidneys.

136
Q

clinical manifestations of gout

A

Acute, painful, swollen, red joint
Any joint may be involved, but the first metatarsophalangeal joint is typical
Individuals with high urate levels may develop chronic tophaceous gout, in which large deposits of urate (tophi – chalky white material) occur in the skin and around joints.

137
Q

differential diagnoses for gout

A

Reactive arthritis
Hemarthrosis
CPPD
Palindromic RA

138
Q

risk factors for gout related to reduced urate excretion

A

Elderly, men, post-menopausal women, impaired renal function, hypertension, metabolic syndrome, diuretics, antihypertensives, aspirin.

139
Q

Gout risk factors relating to excess urate production

A

Dietary (alcohol, sweeteners, red meat, seafood), genetic disorders, myelo- and lymphoproliferative disorders, psoriasis, tumour-lysis syndrome, drugs.

140
Q

1st line investigations for gout

A

Joint aspiration, Increased serum uric acid

141
Q

gold standard investigations for gout

A

joint aspiration and polarised light microscopy (needle-like crystals, negative birefringent of polarised light, monosodium urate crystals)

142
Q

differential diagnoses for gout

A

Septic arthritis, pseudogout, trauma, rheumatoid arthritis, psoriatic arthritis

143
Q

management of Gout

A

Lifestyle changes (decreased purines, more diary – antigout)
Acute flare: NSAIDs, Colchicine, corticosteroids
Prevention: allopurinol (xanthine oxidase inhibitor > reduces uric acid

144
Q

Pseudogout

A

(Calcium Pyrophosphate Deposition-CPPD)
caused by deposition of calcium pyrophosphate crystals in a joint
Shedding of crystals into a joint precipitates an acute arthritis which mimics gout

145
Q

Acute CPPD crystal arthritis

A

acute monoarthropathy usually of larger joints in elderly. Usually spontaneous but can be provoked by illness, surgery or trauma.

146
Q

Chronic CPPD

A

inflammatory RA-like (symmetrical) polyarthritis and synovitis

147
Q

key presentations of psuedogout

A

Often polyarticular with knee commonly involved. Hot swollen painful red joint. Other joints commonly affected: shoulder, wrist, hips

148
Q

1st line investigations for pseudogout

A

Joint aspiration, x-ray: chondrocalcinosis (thin white line in the middle of joint space caused by calcium deposition), serum calcium/PTH/iron elevated

149
Q

gold standard investigation for pseudogout

A

Joint aspiration and polarised light microscopy (rhomboid shaped crystals, positive birefringent of polarised light, calcium pyrophosphate crystals)

150
Q

differential diagnoses for psuedogout

A

Septic arthritis, osteoarthritis, gout, rheumatoid arthritis, psoriatic arthritis

151
Q

management for psuedogout

A

1st line – NSAIDs, colchicine, corticosteroids/intra-articular steroid injection

152
Q

risk factors for psuedogout

A

Old age
Hyperparathyroidism
Haemochromatosis
Hypophosphatemia

153
Q

Giant cell arteritis

A

A vasculitis of medium and large vessels which preferentially affects head and neck arteries

154
Q

presentation of Giant cell arteritis

A

Presents over weeks or months with;
Fever
Anorexia
Weight loss
Involvement of the temporal artery causes headache, scalp tenderness, and jaw claudication
Involvement of ocular vessels can cause blindness
Aortic involvement may lead to thoracic or abdominal aortic aneurysm formation

155
Q

1st line investigations for giant cell arteritis

A

Raised CRP, Raised ESR >50mm/hr. FBC (anaemia), LFT/RFT may be abnormal
Halo sign (wall thickening) on vascular ultrasonography of temporal and axillary artery

156
Q

Gold standard investigations for giant cell arteritis

A

Temporal artery biopsy (shows giant cells, granulomatous inflammation – patchy lesions therefore take big sample)

157
Q

differential diagnoses for giant cell arteritis

A

Polymyalgia rheumatica, rheumatic arthritis, Takayasu’s arteritis

158
Q

management for giant cell arteritis

A

1st line – high dose corticosteroid (e.g., prednisolone 40-60mg)
Consider: tocilizumab, methotrexate. Amaurosis fugax – high dose IV methylprednisolone.

159
Q

POLYARTERITIS NODOSA

A

Polyarteritis nodosa affects medium blood vessels

160
Q

key presentations of polyarteritis nodosa

A

Peripheral neuropathy (mononeuritis multiplex – ischaemia of vasa nervorum), cutaneous/SC nodules, abdominal pain, unilateral orchitis (testicle inflammation), livedo reticularis (mottled, purple lace rash), AKI/CKD, hypertension

161
Q

1st line investigations for polyarteritis nodosa

A

Raised ESR, raised CRP, HBsAg (Hep B antigen), CT angiogram (beaded appearance – aneurysms)

162
Q

gold standard investigation for polyarteritis nodosa

A

Biopsy e.g., kidney (transmural fibrinoid necrosis)

163
Q

management of polyarteritis nodosa

A

Hep B negative: corticosteroids and cyclophosphamide (DMARDs)
Hep B positive: antiviral agent, plasma exchange and corticosteroids

164
Q

Granulomatosis with polyangiitis (GPA)

A

A systemic ANCA-associated vasculitis characterised by dominant upper respiratory tract, lung, and renal involvement and cANCA positivity.

165
Q

presentation of GPA

A

Nasal symptoms
Acute renal failure
Pulmonary symptoms

166
Q

diagnosis of GPA

A

Renal biopsies show a focal segmental necrotizing glomerulonephritis with crescent formation (identical to microscopic polyangiitis).
Lung biopsies show large geographical areas of necrotising granulomatous inflammation and a necrotising vasculitis.

167
Q

management of GPA

A

Aggressive immunosuppression is needed to prevent mortality

168
Q

pathological staging of soft tissue tumours

A

Primary tumour (T)
pT1a: superficial tumour 5cm in size
pT1b: deep tumour 5cm in size
pT2a: superficial tumour >5cm in size
pT2b: deep tumour >5cm in size

Regional lymph nodes (N)
N0: no regional lymph node metastasis
N1: regional lymph node metastasis

169
Q

pathological staging of bone tumours

A

Primary tumour (T)
pT1: tumour 8cm or less in greatest dimension
pT2: tumour >8cm in greatest dimension
pT3: discontinuous tumour in the primary bone site

Regional lymph nodes (N)
N0: no regional lymph node metastasis
N1: regional lymph node metastasis

170
Q

naming tumours- prefixes

A

Prefix will be the tissue of origin, for example:
Osteo = bone
Chondro = cartilage
Rhabdomyo = skeletal muscle
Lipo = fat

171
Q

naming tumours- suffix

A

Suffix tells you whether it is benign or malignant
Oma = benign tumour
Sarcoma = malignant connective tissue tumour
Carcinoma = malignant epithelial/ endothelial tumour
Blastoma = malignant tumour of embryonic cells

172
Q

management of MSK tumours

A

MDT management
Histological tests help to show sensitivity of tumour to chemotherapy agents and radiotherapy
Chemo/radiotherapy can be given:
Neo-adjuvant i.e. before surgery
Adjuvant
Radiotherapy: Ewing’s, myeloma, lymphoma, STS, metastasis
Surgery can either be limb-sparing or limb-sacrificing
Local recurrence vastly increases risk of future amplification

173
Q

intralesional MSKoma surgery

A

the plane of surgery goes through the tumour

174
Q

marginal MSKoma surgery

A

the plane of surgery goes through the reactive zone of the lesion (the reactive zone contains oedema, tumour cells, fibrous tissue, and inflammatory cells)

175
Q

Wide MSKoma surgery

A

the plane of dissection goes through normal tissue

176
Q

radical MSKoma surgery

A

the entire anatomic compartment of the lesion is removed

177
Q

4 types of Bone cancer

A

benign-
osteoid osteoma
osteoblastoma
osteochondroma
malignant-
osteosarcoma

178
Q

3 types of cartilage tumour

A

benign-
enchrondroma
chondroblastoma
malignant-
chondrosarcoma

179
Q

3 types of fibrous tumours

A

benign-
fibrous dysplasia
non-ossifying fibroma
malignant-
fibrosarcoma

180
Q
A
181
Q

osteochondroma

A

A benign conventional cartilaginous-forming tumour of bone.

182
Q

features of osteochondroma

A

Typically grows as a solitary metaphyseal exophytic tumour
Multiple osteochondromas: inherited in an autosomal dominant manner, Langer-Giedion syndrome and DEFECT-11 syndrome.

183
Q

presentation of osteochondroma

A

Generally presents in young children with;
Reduction in skeletal growth
Bony deformity, restricted joint motion, and shortened stature
Painless lump – may have a narrow stalk or broad base

184
Q

management of osteochondroma

A

Surgical excision if symptomatic

185
Q

osteoid osteoma

A

A benign bone-forming tumour of bone

186
Q

presentation of osteoid osteoma

A

Commonly arises in the cortex of a long bone of a child or young adult
Characteristically painful, especially at night

187
Q

investigation of osteoid osteoma

A

Readily identified on plain radiographs as a small lucent nidus <1cm in size
Best appreciated on CT

188
Q

management of osteoid osteoma

A

Pain relieved by NSAIDs
Surgical: radiofrequency ablation

189
Q

osteoblastoma

A

A benign bone-forming tumour of bone

190
Q

presentation of osteoblastoma

A

Most commonly arises in the medullar in the axial skeleton of a child or young adult but can present later in life
Pain, not self-limiting
Spine lesions can present with neurology

191
Q

investigation for osteoblastoma

A

Radiographs: bone destruction surrounded by reactive new bone that can be misdiagnosed as a malignancy
Can be difficult to diagnose/ mistaken for osteosarcoma

192
Q

management for osteoblastoma

A

Excision with at least a marginal line of excision

193
Q

chondromas

A

A benign conventional cartilaginous-forming tumour of bone.

194
Q

enchondroma site

A

arise in the medulla of the bone, most commonly in the hands and feet

195
Q

periosteal chondroma site

A

arises on the bone surface, the proximal humerus being a characteristic site

196
Q

endochondromas features

A

Tend to occur in small bones (hands, foot)
Can occur anywhere in the skeleton
Do not destroy bone
Hot on bone scan

197
Q

chondroblastoma

A

A benign conventional cartilage-forming tumour of bone.

198
Q

presentation of chondroblastoma

A

Typically involves the epiphyses of the long bones in skeletally immature patients but may present later in life
Usually distal femur

199
Q

5 most common tumour to metastasise to bone

A

Lung
Breast
Kidney
Thyroid
Prostate

200
Q

metastatic bone deposits interaction with bone

A

Most metastatic deposits are osteolytic (they destroy bone), but some are osteoblastic (induce bone formation) e.g. prostate.

201
Q

myeloma

A

The most common tumour arising in bone. A disseminated bone marrow-based plasma cell neoplasm associated with a serum and/or urine paraprotein.

202
Q

pathology of myelomas

A

The neoplastic plasma cells secrete cytokines which activate osteoclasts, causing lytic bone lesions
Circulating paraprotein depresses normal immunoglobulin production, increasing the risk of infections.
Free light chains passing through the kidney contribute to renal failure.
The interaction between myeloma cells and bone marrow stromal cells increases myeloma cell growth and it is a target for new treatments.

203
Q

presentation of myeloma

A

Bone pain, pathological fractures, recurrent infections
Anaemia, increased ESR, hypercalcaemia and renal impairment are common

204
Q

management of myeloma

A

Myeloma is an incurable disease.

205
Q

conventional osteosarcoma

A

A malignant bone-forming tumour
The most common malignant primary bone tumour

206
Q
A
207
Q

presentation of osteosarcomas

A

Persistent deep pain within a long bone.
A palpable mass may be present

208
Q

management of osteosarcoma

A

If left untreated will be fatal
Multi-agent chemotherapy
Aims to kill tumour cells, reduce further spread, treat micro-metastases

209
Q

chondrosarcoma features

A

A malignant cartilage forming tumour.
The most common site is the pelvic bones
Atypical chondrocytes distributed in a cartilage matrix

210
Q

benign fibrous dysplasia

A

A benign intramedullary fibro-osseous lesion.

211
Q

features of benign fibrous dysplasia

A

Presents in a wide age range, with peak incidence <30y
Not inherited – a mosaic disorder
Can occur in any bone, proximal femur is the most common
Progressive in children, non-progressive in adults
Can worsen during pregnancy

212
Q

xray presentation of benign fibrous dysplasia

A

ground glass lesion with sclerotic margin

213
Q
A
214
Q

benign non-ossifying fibroma

A

Variants of normal growth
Become more diaphyseal as child grows

215
Q
A
216
Q

fibromyalgia

A

A long term condition that causes pain all over the body. Very similar to chronic fatigue syndrome.

217
Q
A
218
Q

risk factors for fibromyalgia

A

Female
Middle age
Low household income
Divorced
Low educational status
Psychosocial factors;
Sickness behaviours such as extended rest
Social withdrawal
Problems or dissatisfaction at work
Emotional problems such as low mood, anxiety or stress

219
Q

clinical features of fibromyalgia

A

Allodynia: pain in response to a non-painful stimulus
Hyperaesthesia: exaggerated perception of pain in response to a mildly painful stimulus
Diagnosis depends on a pain that is chronic (>3 months), and widespread (involves left and right sides, above and below the waist, and the axial skeleton)
Profound fatigue
Complaint of unrefreshing sleep
Significant fatigue and pain with small increases in physical exertion

220
Q

differential diagnoses for fibromyalgia

A

Rheumatoid arthritis
Vasculitis
Hypothyroidism
Myeloma

221
Q

investigations for fibromyalgia

A

All normal. Diagnosis is clinical
Over-investigation can consolidate illness behaviour, but exclude other causes of pain and/or fatigue

222
Q

management of fibromyalgia

A

Patient encouraged to remain as active as they feel able, and to continue to participate in the workforce.
New symptoms reviewed to exclude an alternative diagnosis
Graded exercise programmes – improve functional capacity
Relaxation, rehabilitation and physiotherapy may help
Cognitive-behavioural therapy aims to help patients develop coping strategies and set achievable goals.

223
Q

pharmacotherapy for fibromyalgia

A

Low-dose amitriptyline has been shown to relieve pain and improve sleep.
Steroids or NSAIDs are not recommended because there is no inflammation.

224
Q

mechanical lower back pain

A

Back pain is very common, and often self-limiting, but be alert to sinister causes i.e. malignancy, infection or inflammatory causes.

225
Q
A
226
Q
A
227
Q

causes of mechanical back pain for those 15-30

A

Prolapsed disc, trauma, fractures, ankylosing spondylitis, spondylolisthesis, pregnancy

228
Q

causes for mechanical back pain for those 30-50

A

Degenerative spinal disease, prolapsed disc, malignancy

229
Q

causes for mechanical back pain for those >50

A

Degenerative, osteoporotic vertebral collapse, Paget’s, malignancy, myeloma, spinal stenosis

230
Q

investigations for mechanical back pain

A

SOCRATES, clinical examination, x-ray if serious pathology suspected, e.g., myeloma, neuropathic pain. MRI

231
Q
A
232
Q
A
233
Q

septic arthritis

A

Infection within a joint.

234
Q

pathology of septic arthritis

A

Establishment of infection is favoured by the relative inability of phagocytes to enter the joint space
Acquisition of infection: infection is usually via haematogenous spread, occasionally may follow penetrating trauma
Infection spreads quickly, leading to rapid and irreversible joint destruction if antibiotic treatment is not started early.

235
Q

risk factors for septic arthritis

A

Pre-existing joint disease (especially rheumatoid arthritis)
Diabetes mellitus
Immunosuppression
Chronic renal failure
Recent joint surgery/ prosthetic joints

236
Q

clinical presentations for septic arthritis

A

An extremely painful, hot, red, swollen joint
Fever
Knee > hip > shoulder

237
Q

differential diagnosis for septic arthritis

A

Crystal arthropathies

238
Q

first line investigations for septic arthitis

A

Urgent aspirate joint for microscopy and culture (polarised light microscopy to identify organism), synovial fluid raised WCC, blood culture, raised CRP/ESR, FBC: raised WCC

239
Q

gold standard investigation for septic arthitis

A

Joint aspiration MC+S (ID organism)

240
Q

management of septic arthritis

A

Start empirical IV antibiotics (after aspiration) until sensitivities are known.
Common causative organisms are Staph. aureus, streptococci, Neisseria gonococcus, and gram -ve bacilli.
Consider flucloxacillin
For suspected gonococcus or meningococcus, consider ceftriaxone.
Antibiotics are required for a prolonged period, conventionally 2 weeks IV.
Analgesia

241
Q

osteomyelitis

A

Infection of a bone.

242
Q

acquisition of osteomyelitis

A

Haematogenous spread – this is typically the case in acute osteomyelitis in children
Penetrating trauma, e.g. open fracture
Iatrogenic e.g. following joint replacement or root canal treatment
Direct spread from an adjacent infection, e.g. as a complication of a foot ulcer in a diabetic

243
Q

pathology of osteomyelitis

A

Infection leads to an influx of acute inflammatory cells into the bone and suppurative inflammation
Destruction of bone leads to necrotic bone known as sequestrum
Failure to eradicate infection may lead to chronic osteomyelitis with areas of infected necrotic bone surrounded by areas of new bone formation (involucrum)

244
Q

clinical presentations of osteomyelitis

A

Fever and pain in the affected bone
Children may present with failure to weight-bear
May be aggravated by movement
Tenderness, warmth, erythema and swelling

245
Q

differential diagnosis of osteomyelitis

A

Avascular necrosis of bone
Fracture
Malignancy

246
Q

1st line investigation for osteomyelitis

A

FBC – raised WCC, raised CRP/ESR, blood culture MC+S, x-ray (osteopenia - thinning, periosteal reaction – changes to bone surface, destruction of bone), MRI (bone marrow oedema)

247
Q

gold standard investigation for osteomyelitis

A

Bone marrow biopsy and culture (identify organism)

248
Q

management for osteomyelitis

A

Aggressive treatment is needed with intravenous antibiotics and surgical debridement of any necrotic bone if cure is to be achieved.
Surgical – hardware replacement or removal
Antimicrobial therapy

249
Q

osteomalacia

A

a metabolic bone disease characterised by inadequate mineralisation of bone in the mature skeleton.

250
Q

rickets

A

a metabolic bone disease characterised by inadequate mineralisation of bone and epiphyseal cartilage in the growing skeleton of children.

251
Q

causes of calcium deficiency

A

Calcium deficiency which is usually due to vitamin D deficiency (source: sunlight)
Calcium deficiency is also caused by nutritional deficiency: diet, malabsorption of calcium due to chronic liver disease, CKD, GI bypass surgery, nutritional

252
Q

hypophosphataemic rickets

A

characterised by low serum phosphate levels and resistance to treatment with UV radiation and vitamin D, mainly caused by genetic defects involving renal absorption of phosphate

253
Q

pathology of osteomalacia/ rickets

A

Inadequate mineralisation of bone matrix (osteoid) due to lack of calcium and occasionally phosphate
Bones become abnormally soft and prone to deformity and fracture
In children, the soft bone formed at the epiphyseal plate results in skeletal deformity and short stature

254
Q

clinical presentation of rickets

A

Growth retardation, hypotonia, apathy in infants
Once walking – knock-kneed, bow-legged

255
Q

clinical presentation of osteomalacia

A

Bone pain and tenderness, fractures, proximal myopathy (waddling gait)

256
Q

1st line investigations for osteomalacia

A

X-ray (loss of cortical bone – defective mineralisation, looser zone), U&E (low calcium and phosphate), raised PTH, low serum 25-hydroxyvitamin D (<25 nmol/L = deficiency)

257
Q

gold standard investigation for osteomalacia

A

bone biopsy (incomplete mineralisation)

258
Q

management of osteomalacia/rickets

A

Vitamin D supplementation usually results in rapid mineralisation of bone and resolution of symptoms, though some deformity may remain.
If due to malabsorption give vitamin D2
If due to renal disease/ vit D resistance give alfacalcidol

259
Q

pagets disease

A

A metabolic bone disease characterised by excessive chaotic bone turnover in localised parts of the skeleton.

260
Q

pathology of pagets disease

A

The disease passes through a number of stages, all of which may be seen simultaneously within the same bone or in different bones
Initially, there is intense osteoclastic bone resorption
Osteoblastic activity then becomes exaggerated with laying down of grossly thickened, poorly organised weak bone which is prone to deformity and pathological fracture

261
Q

presentation of pagets disease

A

The vast majority of patients are asymptomatic, the diagnosis being made incidentally on radiology
Symptomatic disease usually presents with bony pain and deformity

262
Q

1st line investigation for pagets disease

A

x-ray (bone enlargement + deformity, osteoporosis circumscripta – well defined osteolytic lesions, cotton wool appearance of skull – poorly defined areas of sclerosis and lysis, V-shaped defects in long bones)
urinary hydroxyproline (protein constituent of collagen)
bloods: raised ALP, normal calcium and phosphate

263
Q

gold standard investigation of pagets

A

X-ray of bones

264
Q

management of pagets disease

A

Bisphosphinates to reduce bone turnover + NSAIDs

265
Q

capsaicin

A

Symptomatic relief in osteoarthritis

266
Q

side effects of capsaicin

A

Cough
Sneezing, watering eye
Asthma exacerbated

267
Q

paracetamol side effects

A

Thrombocytopenia
Bronchospasm
Rash
Hepatic function abnormal

268
Q

side effects of NSAIDs

A

Diarrhoea
Dizziness
GI discomfort / nausea

269
Q

bisphosphonates action

A

Bisphosphonates are adsorbed onto hydroxyapatite crystals in bone, slowing both their rate of growth and dissolution, and therefore reducing the rate of bone turnover
e.g. alendronic acid

270
Q

side effects of bisphosphonates

A

Alopecia
Anaemia
Constipation/ diarrhoea
Headache/ fever/ malaise

271
Q

methotrexate action and use

A

Methotrexate inhibits the enzyme dihydrofolate reductase, essential for the synthesis of purines and pyrimidines.
Used to treat moderate to severe active rheumatoid arthritis by mouth, and severe RA by IM/SC injection.
DMARD

272
Q

side effects of methotrexate

A

Fever/ headache/ nausea/ vomiting
Anaemia
Diarrhoea
Fatigue/ drowsiness

273
Q

use of hydroxychloroquine

A

Active rheumatoid arthritis
DMARD

274
Q

side effects of Hydroxychloroquine

A

Abdominal pain
Diarrhoea/ vomiting
Vision disorders
Headache

Phase 2a Medicine (10 decks)

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