MSK 2 Flashcards

(64 cards)

1
Q

what is gout?

A

Gout is a type of crystal arthropathy associated with chronically high blood uric acid levels. Urate crystals are deposited in the joint causing acute inflammatory arthritis, trophi around the joints and possible joint destruction, renal glomerular, tubular and interstitial disease and uric acid urolithiasis

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2
Q

where does gout commonly affect?

A

the first toe (podagra), foot, ankle, knee, fingers, wrist, and elbow; however, it can affect any joint.

*it usually affects cool parts of the body

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3
Q

what causes gout?

A

There is a causal relationship between hyperuricaemia (high urate level) and gout

Hyperuricaemia is due to renal under-excretion of urate in 90% of cases and to over-production in 10%

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4
Q

what are risk factors for gout?

A

risk factors for hyperuricaemia:

  • dietary - seafood, meat. alcohol, especially beer
  • obesity
  • insulin resistance
  • hypertension
  • diuretic can increase urate levels
  • high cell turnover - haematological cancer and chemotherapy - leads to urate production
  • ciclosporin or tacrolimus (lead to increased tubular re-absorption of urate and well as decrease GFR
  • Pyrazinamide - increase re-absorption of urate
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5
Q

how does gout present?

A
rapid onset of severe pain 
joint stiffness - usually in morning 
swelling and joint effusion 
tenderness 
tophi - subcutaneous deposits of uric acid (typically in hands, elbows, ears, achilles tendon)
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6
Q

how is gout diagnosed?

A

joint aspiration - synovial fluid analysis - this will provide a definate diagnosis and exclude septic arthritis and differentiate from pseudogout (calcium pyrophosphate deposition disease)

  • no bacterial growth
  • needle shaped crystals
  • strongly negative birefringent of polarised light
  • monosodium urate crystals

you could also perform a Joint x-ray which would show:

  • Typically the space between the joint is maintained
  • Lytic lesions in the bone
  • Punched out erosions
  • Erosions can have sclerotic borders with overhanging edges
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7
Q

how would you manage gout?

what are the indicaitons for urate lowering therapies?

A

ACUTE GOUT
1st line - NSAIDs or colchicine
2nd line - corticosteroid - prednisolone

*colchicine has slower onset and can cause diarrhoea

RECURRENT GOUT - 2-3 weeks post acute episode
1st line - allopurinol plus naproxen
2nd line - febuxostat

lifestyle changes

** exam tip - do not start allopurinol until acute attack is settled

the British Society of Rheumatology Guidelines now advocate offering urate-lowering therapy to all patients after their first attack of gout
ULT is particularly recommended if:
>= 2 attacks in 12 months
tophi
renal disease
uric acid renal stones
prophylaxis if on cytotoxics or diuretics

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8
Q

what are the complications of gout?

A

acute uric acid nephropathy

nephrolithiasis

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9
Q

what is pseudogout?

A

Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals. Calcium pyrophosphate crystals are deposited in the joint causing joint problems. It is also known as chondrocalcinosis.

can be both acute and chronic

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10
Q

how does pseudogout present?

A

tender painful joints
typically an older adult with a hot swollen, stiff, painful knee
other joint that may be affected: shoulders, wrists and hips

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11
Q

what are the risk factors of pseudogout?

A
advanced age (it is rare in people younger than 60) 
Injuries or previous joint surgeries 
hyperparathyroidism 
haemochromatosis 
family history 
hypomagnesaemia 
hypophosphatasia
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12
Q

what are the investigations for pseudogout?

A

joint aspiration with synovial fluid analysis - important for diagnosis, to exclude septic arthritis and differentiate from gout. It will show:

  • calcium pyrophosphate crystals
  • intracellular or extracelllular positively birefringent of polarised light
  • rhomboid-shaped crystals under polarised light.
  • no bacterial growth

X-ray - chondrocalcinosis is the classical xray change in pseudogout. It appears as a thin white line in the middle of the joint space by the calcium deposition - this is diagnostic of gout
other joint x-ray changes are similar to osteoarthritis - loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts

serum calcium - exclude hyperparathyroidism
serum parathyroid hormone - exclude hyperparathyroidism
serum magnesium
serum alkaline phosphatase

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13
Q

what is the treatment for pseudogout?

A
intra-articular corticosteroids 
NSAIDs if injection declined or joint not accessible 
second line - colchicine 
3rd line - joint aspiration 
add paracetamol for analgesia 

for severe cases joint wash out - arthrocentesis

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14
Q

what is Paget’s disease?

A

a chronic bone disorder that is characterised by focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone

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15
Q

what areas are most commonly affected in paget’s disease?

A

skull
spine/pelvis
long bones of the lower extremities

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16
Q

what are the risk factors for Paget’s disease?

A

increasing age
male sex
family history

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17
Q

how does Paget’s disease present?

A
    • only 5% of patients are symptomatic
  • *the stereotypical presentation is an older male with bone pain and an isolated raised ALP
  • bone pain - in the pelvis, lumbar spine, femur
  • if untreated - bowing of tibia, bossing of skull
  • raised ALP
  • other markers of increased bone turnover - PINP, CTx, NTx and urinary hydroxyproline
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18
Q

what investigations would you perform for Paget’s disease?

A

plain XR - mostly lytic changes, V shaped lytic lesions in the long bones, occasional fractures, skull XR - may show thickening of the calvarium
Isotope bone scan - areas of dense uptake - may identify all areas involved and often picks up non-symptomatic regions
ALP - may be normal or raised
bone specific ALP - sensitive blood test for diagnosis
calcium will usually be normal
P1NP and CTX - will initially be elevated - markers of bone turnover

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19
Q

what is the management for Paget’s disease?

A

if asymptomatic - observation, regular follow up, patient education and preventive measurs. If there is highly active disease and high risk of complications - bisphosphonate or calcitonin

If they are symptomatic
- bisphosphonate (IV zoledronic acid or oral riseronate) or calcitonin
plus supportive therapies e.g. physiotherapy

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20
Q

what are the complications of Paget’s disease?

A
deafness (cranial nerve entrapment)
bone sarcoma (1% if affected for > 10 years)
fractures
skull thickening
high-output cardiac failure
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21
Q

what is osteomalacia?

A

Osteomalacia is a metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix (osteoid) following growth plate closure in adults.

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22
Q

what causes osteomalacia?

A

vitamin D deficiency (can be from lack of sun exposure, malabsorption or chronic kidney disease)
VD is essential in calcium and phosphate absorption from the intestine and kidneys.
Vitamin D is also responsible for regulating bone turnover and promoting bone bone reabsorption to boost the serum calcium level.
Inadequate VD leads to a lack of calcium and phosphate in the blood.
Low calcium causes a secondary hyperparathyroidism as the parathyroid gland tries to raise the calcium level by secreting parathyroid hormone. Parathyroid hormone stimulates increased reabsorption from the bones. This causes further problems with bone mineralisation.

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23
Q

how does osteomalacia present?

A
may be asymptomatic 
Fatigue
Bone pain
Muscle weakness
Muscle aches
Pathological or abnormal fractures
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24
Q

how is osteomalacia investigated?

A

Serum 25-hydroxyvitamin D

Serum calcium is low
Serum phosphate is low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high (secondary hyperparathyroidism)
Xrays may show osteopenia (more radiolucent bones)
DEXA scan shows low bone mineral density

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25
how is osteomalacia managed?
calcium plus vitamin D - ergocalciferol or colecalciferol and calcium carbonate or calcium citrate
26
what is fibromyalgia?
it is a syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites.
27
what are the features of fibromyalgia?
``` chronic pain - at multiple sites, sometimes pain all over lethargy cognitive impairment - fibro fog sleep disturbances headaches dizziness ``` on examination there may be diffuse tenderness
28
what are risk factors for fibromyalgia?
``` family history rheumatological conditions age between 20 and 60 female sex associated conditions - IBS, tension headaches, chronic fatigue syndrome, temporomandibular joint disorder ```
29
what are some differentials for fibromyalgia?
``` RA osteoarthritis SLE chronic fatigue syndrome ankylosing spondylitis polymyalgia rheumatica ```
30
What investigations are performed for fibromyalgia?
diagnosis is usually clinical | - you would do investigations to rule out differential diagnosis
31
What criteria is used to diagnose fibromyalgia?
American College of Rheumatology (ACR) criteria for fibromyalgia syndrome The criteria include: > Generalised pain, defined as pain in at least 4 of 5 regions. > Symptoms have been present at a similar level for at least 3 months. > Widespread Pain Index (WPI) ≥7 and symptom severity scale (SSS) score ≥ 5 or WPI 4-6 and SSS score ≥ 9. > A diagnosis of fibromyalgia is valid irrespective of other diagnosis. A diagnosis of fibromyalgia does not exclude the presence of other clinically important illnesses.
32
how is fibromyalgia managed?
management is often difficult and needs to be tailored to individual patients explanation aerobic exercise - good evidence to help symptoms CBT Medication 1st line = amitriptyline or cyclobenzaprine 2nd line - pregabalin, duloxetine or gabapentin Analgesia such as naproxen or tramadol can be added
33
what is osteomyelitis?
infection in the bone
34
how can osteomyelitis be classified?
haematogenous osteomyelitis - results from bacteraemia - is usually monomicrobial - most common form in children - vertebral osteomyelitis is the most common form of haematogenous osteomyelitis in adults - risk factors include: sickle cell anaemia, intravenous drug user, immunosuppression due to either medication or HIV, infective endocarditis non-haematogenous osteomyelitis: - results from the contiguous spread of infection from adjacent soft tissues to the bone or from direct injury/trauma to bone - is often polymicrobial - most common form in adults - risk factors include: diabetic foot ulcers/pressure sores, diabetes mellitus, peripheral arterial disease
35
what bacteria causes osteomyelitis?
S-aureus = most common in children other causes - GBS, aerobic gram -ve bacilli, strep pyogenes, H influenzae drug users - pseudomonas aeruginosa sickle cell disease - salmonella species
36
how does osteomyelitis present?
- non-specific pain at the site of infection - malaise and fatigue - local inflammation, erythema or swelling - low grade fever
37
what investigations would you perform for osteomyelitis?
``` WBC count ESR CRP plain x-ray - in acute disease - osteopenia appears and evidence of bone destruction and cortical breaches and periosteal reaction follow qucikly MRI ```
38
how is osteomyelitis managed?
antibiotics usually flucloxacillin for 6 weeks clindamycin if penicillin allergy
39
what is septic arthritis?
it is where infection occurs in a joint | it can be in a native joint but is also a common and important complication of joint replacement
40
how does septic arthritis present?
usually just one single joint (most commonly in the knee) Hot, red, swollen and painful joint Stiffness and reduced range of motion Systemic symptoms such as fever, lethargy and sepsis
41
what are the common causes of septic arthritis?
Staphylococcus aureus is the most common causative organism. Other bacteria: Neisseria gonorrhoea (gonococcus) in sexually active individuals Group A Streptococcus (most commonly Streptococcus pyogenes) Haemophilus influenza Escherichia coli (E. coli)
42
what are differentials of septic arthritis?
Gout (fluid shows urate crystals that are negatively birefringent of polarised light) Pseudogout (fluid shows calcium pyrophosphate crystals that are rod-shaped intracellular crystals positively birefringent of polarised light) Reactive arthritis typically triggered by urethritis or gastroenteritis and associated with conjunctivitis Haemarthrosis (bleeding into the joint)
43
what investigations would you perform for septic arthritis?
``` synovial fluid microscopy, gram stain and polarising microscopy synovial fluid culture and sensitivities synovial fluid WCC blood cultures and sensitivities WCC ESR and CRP U&E LFTs plain X-ray USS ```
44
how is septic arthritis managed?
Empirical IV antibiotics should be given until the sensitivities are known. Antibiotics are usually continued for 3 – 6 weeks in total. Choice of antibiotic depends on the local guidelines. Example regimes are: Flucloxacillin plus rifampicin is often first line Vancomycin plus rifampicin for penicillin allergy, MRSA or prosthetic joint Clindamycin is an alternative
45
what are the complications of septic arthritis?
osteomyelitis | joint destruction
46
what is behcet's syndrome?
Behcet's syndrome is a complex multisystem disorder associated with presumed autoimmune-mediated inflammation of the arteries and veins.
47
what is the classic triad of symptoms in behcet's syndrome? | what are other features
triad - oral ulcers, genital ulcers, anterior uveitis other features - thrombophlebitis and DVT - arthritis - aseptic meningitis - abdo pain, diarrhoea, colitis - erythema nodosum - retinal haemorrhage - headaches and migraines - memory impairment
48
what investigations are done for Behcet's disease?
Behçet’s disease is a clinical diagnosis based on the features of the condition. The only particular investigation to be aware of is the pathergy test. The pathergy test involves using a sterile needle to create a subcutaneous abrasion on the forearm. This is then reviewed 24 – 48 hours later to look for a weal 5mm or more in size. It tests for non-specific hypersensitive in the skin. It is positive in Behçet’s disease, Sweet’s syndrome and pyoderma gangrenosum.
49
how is Behcet's disease managed?
Management involves a combination of: Topical steroids to mouth ulcers (e.g. soluble betamethasone tablets) Systemic steroids (i.e. oral prednisolone) Colchicine is usually effective as an anti-inflammatory to treat symptoms Topical anaesthetics for genital ulcers (e.g. lidocaine ointment) Immunosuppressants such as azathioprine Biologic therapy such as infliximab
50
what is discoid lupus erythematosus?
Discoid lupus erythematosus is a non-cancerous chronic skin condition. It is more common in women and usually presents in young adults between ages 20 to 40. It is more common in darker-skinned patients and smokers. It is associated with an increased risk of developing systemic lupus erythematosus, however this risk is still below 5%. Rarely the lesions can progress to squamous cell carcinoma (SCC) of the skin.
51
how does discoid lupus erythematous present?
The lesions typically occur on the face, ears and scalp. They are photosensitive, meaning that they are made worse by exposure to sunlight. They are associated with scarring alopecia (hair loss in affected areas that does not grow back) and hyper-pigmented or hypo-pigmented scars. ``` The appearance of the lesions are: Inflamed Dry Erythematous Patchy Crusty and scaling ```
52
how is discoid lupus erythematous managed?
Skin biopsy can be used to confirm the diagnosis. Treatment is with Sun protection Topical steroids Intralesional steroid injections Hydroxychloroquine
53
what is antisynthetase syndrome characterised by?
Antisynthetase syndrome is caused by autoantibodies against aminoacyl-tRNA synthetase e.g. anti-Jo1. ``` It is characterised by myositis interstitial lung disease thickened and cracked skin of the hands (mechanic's hands) Raynaud's phenomenon ```
54
what are bisphosphonates used for?
``` They inhibit osteoclasts by reducing recruitment and promoting apoptosis. Clinical uses prevention and treatment of osteoporosis hypercalcaemia Paget's disease pain from bone metatases ```
55
what are the adverse effects of bisphosphonates?
oesophageal reactions: oesophagitis, oesophageal ulcers (especially alendronate) osteonecrosis of the jaw increased risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate acute phase response: fever, myalgia and arthralgia may occur following administration hypocalcaemia: due to reduced calcium efflux from bone. Usually clinically unimportant
56
what is dermatomyositis?
an inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions may be idiopathic or associated with connective tissue disorders or underlying malignancy (typically ovarian, breast and lung cancer, found in 20-25% - more if patient older). Screening for an underlying malignancy is usually performed following a diagnosis of dermatomyositis polymyositis is a variant of the disease where skin manifestations are not prominent **usually ANA positive
57
what are the features of dermatomyositis?
Skin features photosensitive macular rash over back and shoulder heliotrope rash in the periorbital region Gottron's papules - roughened red papules over extensor surfaces of fingers 'mechanic's hands': extremely dry and scaly hands with linear 'cracks' on the palmar and lateral aspects of the fingers nail fold capillary dilatation ``` Other features proximal muscle weakness +/- tenderness Raynaud's respiratory muscle weakness interstitial lung disease: e.g. Fibrosing alveolitis or organising pneumonia dysphagia, dysphonia ```
58
what drugs can cause drug induced lupus erythematous?
Most common causes procainamide hydralazine Less common causes isoniazid minocycline phenytoin
59
what is Ehler-danlos syndrome?
an autosomal dominant connective tissue disorder that mostly affects type III collagen. This results in the tissue being more elastic than normal leading to joint hypermobility and increased elasticity of the skin. Features and complications elastic, fragile skin joint hypermobility: recurrent joint dislocation easy bruising aortic regurgitation, mitral valve prolapse and aortic dissection subarachnoid haemorrhage angioid retinal streaks
60
what is McArdle's disease?
autosomal recessive type V glycogen storage disease caused by myophosphorylase deficiency this causes decreased muscle glycogenolysis ``` Features muscle pain and stiffness following exercise muscle cramps myoglobinuria low lactate levels during exercise ```
61
what is lateral epicondylitis?
Lateral epicondylitis typically follows unaccustomed activity such as house painting or playing tennis ('tennis elbow'). It is most common in people aged 45-55 years and typically affects the dominant arm.
62
what are the features of lateral epicondylitis?
pain and tenderness localised to the lateral epicondyle pain worse on wrist extension against resistance with the elbow extended or supination of the forearm with the elbow extended episodes typically last between 6 months and 2 years. Patients tend to have acute pain for 6-12 weeks
63
how is lateral epicondylitis managed?
advice on avoiding muscle overload simple analgesia steroid injection physiotherapy
64
what are the rotator cuff muscles and what do they do?
Supraspinatus - abducts the arm before deltoid Infraspinatus - rotates arm laterally teres minor - adducts and rotates arm laterally Subscapularis - adducts and rotates arm medially