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Medicine year 4 CDM > Block 9: gout, osteoarthritits, osteoporosis, PMR, Psoriasis > Flashcards

Block 9: gout, osteoarthritits, osteoporosis, PMR, Psoriasis Flashcards

1
Q

Crystals in gout and CPPD

A
  • Gout: negatively birefringent, needle shaped, monosodium urate
  • Pseudogout: Positively birefringent, Rhomboidal, Calcium pyrophosphate
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2
Q

Clinical diagnosis of gout

A
  • Mono-articular involvement of a foot/ankle joint
  • Previous episodes of a similar nature
  • Rapid onset
  • Erythema
  • Male
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3
Q

Treatment of gout

A
  • Acute flare: NSAID (first line), Colchicine (caution in renal impairement, causes diarrhoea)
  • Steroids (oral or injection): if NSAID’s and colchine are contraindicated can have intra-articular steroid injections, IL1 inhibitors
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4
Q

Treatment of gout: prevention

A
  • Prevention and management: lifestyle modification, change diet, reduce alcohol, weight loss, Allopurinal or febuxostat. Probenecid
  • Allopurinol is first like prophylaxis form of urate lowering therapy (ULT) and is started when inflammation has settled. If refractory use urate oxidase or pegloticase
  • Increase vitamin C
  • Use losartan if co-existent hypertension
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5
Q

Gout complications

A
  • Tophi
  • Bone complications: degenerative arthritis due to bone erosion and weakening of joints
  • Osteoporosis
  • Kidney disease
  • Mental health: depression
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6
Q

Crystal arthropathy management

A
  • Acute: NSAIDs + PPI, Colchine, Corticosteroids oral/IA, Interleukin 1B inhibitor if refractors
  • Chronic: attain normal BMI, stop alcohol, stay hydrated. After an acute attack Allopurinol. Febuostat, Probenecid, Rasburicase (severe/refractors)
  • Chronic CPPD: identify and treat and underlying metabolic abnormalities. NSAIDs and PPI, Colchine, Corticosteroids, Methotrexate, Hydroxylchloroquine
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7
Q

x ray of a joint affected by gout shows

A
  • Maintained joint space(no loss of joint space)
  • Lytic lesionsin the bone
  • Punched out erosions
  • Erosions can havesclerotic borderswithoverhanding edges
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8
Q

Fibromyalgia

A
  • Commonest cause of widespread MSK pain in women 20-55
  • No abnormalities in blood tests or imaging
  • Normal examination findings except tenderness
  • Possible disorder of pain regulation: overlap with MH issues
  • Difficult to treat
  • Chronic- major cause of disability
  • Poor prognosis: no cure and long course
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9
Q

Fibromyalgia symptoms

A
  • Widespread pain in muscles, tendons and ligaments (but not joints)
  • Fatigue
  • Morning stiffness <1 hour
  • Pins and needles in hands and feet
  • Unrefreshing sleep, insomnia
  • Low mood: could do PHQ9
  • Cognitive symptoms: brain fog
  • Can co-exist with other MSK conditions: may be primary or secondary to it
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10
Q

Diagnosis of fibromyalgia

A
  • Widespread pain for >3 months
  • Fatigue, sleep disturbance
  • Cognitive disturbance
  • Headaches, IBS symptoms
  • Tenderness but no swelling/inflammation on examination: diagnosis more likely id tender in at least 11 out of 18 points on the body
  • Non specific- can fulfil criteria even if you have different condition
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11
Q

Management of fibromyalgia

A
  • Difficult
  • Drugs: Analgesics mainly ineffective, Tricyclic anti-depressants may have some effect, Pregabalin, duloxetine, amitriptyline
  • CBT, “talking therapies”
  • Graded exercise
  • Explanation of disorder
  • Local heat application
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12
Q

Investigations fibromyalgia

A

Do bloods to exclude other disorders for example,hypothyroidism, inflammatory disorders, andhepatitis C. Example Blood tests iclude:U+Es, FBC, TFTs,LFTs, CRP / ESR, Rheumatoid factor,Ca2+, ANA, immunoglobulins.

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13
Q

Kellgren-Lawence grading scale for knee arthritis

A
  • Normal: no features of OA
  • Doubtful: minute osteophytes, doubtful significance
  • Mild: definite osteophytes, normal joint space
  • Moderate: moderate joint space reduction
  • Severe: joint space is greatly reduced, subchondral sclerosis
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14
Q

OA hands changes

A
  • Herberden’s nodes- distal interphalangeal joint
  • Bouchard nodes- proximal interphalangeal joint
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15
Q

Non inflammatory arthritis i.e. Osteoarthritis

A
  • 4 cardinal symptoms: pain, stiffness, swelling, loss of function/ difficulty in activities of daily living
  • Pain: worse during or after activity
  • Stiffness: can be in the mornings (tend to be less than 30 minutes) and on or after activity
  • Bony swelling
  • Difficulty in ADL
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16
Q

Joint involvement in osteoarthritis

A

spine (spondylosis), carpometocarpal joint, distal interphalangeal joint, knees, in the big toe the metatarsal pharyngeal joint

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17
Q

Joint involvement in RA

A

wrists, metacarpal pharyngeal joints, PIP, ankles and metatarsal pharyngeal joints

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18
Q

Inflammatory arthritis (RA)

A
  • 4 cardinal symptoms: Pain, stiffness, swelling, loss of function/difficulty in activities of daily living
  • Pain: often worse in the mornings and on activity
  • Stiffness: worse in the mornings (prolonged early morning stiffness >30 minutes) and on inactivity
  • Swelling in joints
  • Difficulty in ADL
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19
Q

Bone remodelling

A
  • Trabecular bone (spongy bone): replaced every 3-4 years
  • Cortical bone (compact bone): replaced every 10 years
  • Bone breakdown: osteoclasts
  • Bone formation: osteoblasts
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20
Q

Pathology of osteoporosis

A
  • Thinning of cortical bone
  • Fewer trabecular
  • Bone cells are normal with normal mineralisation
  • There is more bone breakdown with osteoclasts then bone formation with osteoblasts
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21
Q

Risk factors for osteoporosis

A
  • Age
  • Low oestrogen: post menopause or early menopause
  • Low serum calcium: after bones have been formed
  • Smoking
  • Alcohol
  • No weight baring exercise
  • Steroids
  • Co-morbidities: Crushings, diabetes, hyperthyroidism
22
Q

Secondary causes of osteoporosis

A
  • Endocrine: Hyperthyroidism, Hyperparathyroidism, Crushings disease, Diabetes mellitus, Hyperprolactinaemia, Early menopause
  • Gastrointestinal: Coeliac disease, IBD, chronic liver disease
  • Rheumatoid arthritis
  • Metabolic: CKD
  • Drug induced: steroids, antiepileptics

Complications of osteoporosis: Fractures

23
Q

DEXA scan

A
  • Dual energy x-ray absorptiometry
  • Analyses bone density to diagnose osteoporosis
  • Hip, radius, back
24
Q

FRAX score

A

Evaluates fracture risk, gives a 10 year probability of a fracture. It considers:

  • Age
  • Sex
  • Weight
  • Height
  • Previous fracture
  • If the parent had a fractured hip
  • Current smoking
  • Corticosteroids
  • Rheumatoid arthritis
  • Secondary osteoporosis
  • Alcohol 3 or more units/day
  • Femoral neck BMD (g/cm)
25
Q

Osteoporosis treatment

A
  • Conservative: quit smoking, reduced alcohol, regular exercise, Balanced diet
  • Medical: Bisphosphonates (oral alendronic acid, IV zoledronate), Teripartide, Denosumab. Calcium and vitamin D replacement
  • Surgical: bony fractures
26
Q

When to do a FRAX score

A
  • Do FRAX score in women >65 and men >75
  • OR
  • In women <65 and men <75 with risk factors
27
Q

When to offer a DEXA scan

A
  • Offer DEXA scan without initial FRAX score to anyone >50 with history of fragility fracture
  • Consider starting treatment without DEXA scan in people with a vertebral fracture
  • For patients with risk factors for osteoporosis do a FRAX score first. High risk patient should have DEXA
28
Q

Polymyalgia rheumatica (PMR)

A
  • An inflammatory condition causing pain and stiffness in the shoulder and pelvic girdle
  • More common in women >50 and caucasian
  • Respond well to steroids, treatment tends to be over 2-3 months
  • 15% develop GCA
29
Q

Clinical features of PMR

A
  • Shoulder and/or pelvic girdle pain and morning stiffness lasting at least 45 minutes (may be initially unilateral but then becomes bilateral). Worse in the morning and after rest, interferes with sleep
  • Improvement in symptoms one week after a trial of corticosteroids (usually prednisolone)
  • Systemic features: low grade fever, fatigue, anorexia, weight loss and depression
  • Peripheral oligoarticular arthritis (wrist, knee and metacarpophalangeal joint)
  • Associated features: muscle tenderness, carpel tunnel syndrome, peripheral oedema
30
Q

Patients requiring referral to rheumatologists due to atypical features of PMR

A
  • Have red flags of serious pathology (includingweight loss. night pain or neurological features) and don’t have a identifiable cause
  • Younger than 60
  • Do not have the core symptoms of PMR: Bilateral shoulder/pelvic girdle pain, >45 minutes of morning stiffness
  • Have unusual features of PMR: Normal, or very high inflammatory markers, Chronic onset of symptoms, Limited response to steroids
31
Q

PMR investigations

A
  • CRP/ESR: normally elevated. CRP is more sensitive but ESR is associated with higher risk of relapse
  • Bloods: FBC, U&E, LFT, TSH, Calcium, Creatine kinase, Serum protein electrophoresis, RF, anti-CCP
  • Urine dip
  • Chest x-ray: before commencing methotrexate
  • US: subacromial bursitis is associated with PMR
32
Q

Diagnosing PMR

A
  • Age >50
  • Acute or subacute bilateral pelvic and/or shoulder girdle aching, morning stiffness lasting >45 minutes
  • A good response to corticosteroids
  • Acute phase response: elevated CRP or ESR
  • Exclusion of other conditions that mimic PMR: infection, active cancer and GCA
33
Q

PMR management

A
  • Oral corticosteroids and gradually weaned off with dose adjustments being every 4-8 weeks and reviews one week after each dose adjustment
  • If symptoms begin again after dose reduction then dose may need to be increased. Don’t need routine bloods can rely on reported symptoms
34
Q

Complications of PMR

A
  • Chronic relapsing course- symptoms exacerbate frequently when reducing the corticosteroid dose
  • Risks of corticosteroids: osteoporosis, increased infection risk, T2D, hypertension, cataracts, glaucoma, skin changes (thinning or bruising)
  • GCA
35
Q

PMR reducing regime of prednisolone

A
  • 15mg until the symptoms are fully controlled, then
  • 12.5mg for 3 weeks, then
  • 10mg for 4-6 weeks, then
  • Reducing by 1mg every 4-8 weeks
36
Q

PMR: addition measures for long term steroids ‘Dont Stop’

A
  • Don’t–steroid dependenceoccurs after 3 weeks of treatment, and abruptly stopping risksadrenal crisis
  • S–Sick day rules (steroid doses may need to be increased if the patient becomes unwell)
  • T–Treatment card – patients should carry asteroid treatment cardto alert others that they are steroid-dependent
  • O–Osteoporosis prevention may be required (e.g.,bisphosphonatesandcalcium and vitamin D)
  • P–Proton pump inhibitors are considered forgastro-protection(e.g., omeprazole)
37
Q

Giant cell arteritis (temporal arteritis)

A

A type of systemic vasculitis affecting the medium and large arteries. Key complication is visual loss which can be irreversible

38
Q

GCA presentation

A
  • Unilateral headache: severe and around the temple and forehead
  • Temple artery is tender and thickened to palpation with reduced or absent pulsation
  • Scalp tenderness (e.g., noticed when brushing the hair)
  • Jaw claudication
  • Blurred or double vision
  • Loss of vision if untreated
39
Q

GCA diagnosis

A
  • Clinical presentation
  • Raised inflammatory markers, particularly ESR (usually more than50mm/hour)
  • Temporal artery biopsy(showingmultinucleated giant cells)
  • Duplex ultrasound(showing thehypoechoic“halo”signandstenosisof the temporal artery)
40
Q

GCA management

A
  • Steroids: started immediately before confirming diagnosis. 40-60mg prednisolonedaily with no visual symptoms or jaw claudication. 500mg-1000mg methylprednisolonedaily with visual symptoms or jaw claudication
  • Once condition is controlled steroid dose is weaned over 1-2 years
  • Aspirin75mg daily decreases vision loss and strokes
  • Proton pump inhibitor(e.g., omeprazole) for gastroprotection while on steroids
  • Bisphosphonatesandcalcium and vitamin Dfor bone protection while on steroids
41
Q

GCA complications

A
  • Steroid-related complications (e.g., weight gain, diabetes and osteoporosis)
  • Visual loss
  • Cerebrovascular accident (stroke)
42
Q

Chronic plaque psoriasis

A
  • 85-90%
  • Well defined patches of redness with a thick silver scale
  • Typically on extensor surfaces like elbows and knees
  • Increased itch
43
Q

Causes of psoriasis

A
  • Intense proliferation and abnormal keratinocytes proliferation, triggered by an active cellular immune system
  • Role for T cells, dendritic cells and cytokines
  • Genetic factors: HLA-B13, -B17 and Cw6
  • Type 1 psoriasis (young onset) most strongly associated with CW0602 (PSORS1)
  • Environmental triggers i.e. trauma, infection, drugs, EtOH. Improved by sunlight
44
Q

Psoriasis histology

A
  • Psoriatic epidermis contains scattered neutrophils
  • Neutrophil microabcesses can form
  • Psoriasis may be pustular
45
Q

Types of psoriasis

A
  • Guttate psoriasis
  • Erythrodermic psoriasis
  • Scalp psoriasis
  • Flexural psoriasis

Features of psoriasis: nail pitting, onycholysis

46
Q

Treatment for psoriasis

A
  • First line treatment of Psoriasis: Calcipotriol, Tar, Dithranol (anthralin) for chronic plaque psoriasis, topical steroids
  • Photo: PUVA, UVB
  • Systemic: biologics, ciclosporin, methotrexate, retinoids
  • The systemic treatment is more toxic then first line
47
Q

Features of chronic plaque psoriasis

A
  • Erythematous plaque covered in silvery white scale
  • Clear delineation between normal and affected skin
  • Typically effects extensor surfaces like elbows and knees
  • Plaques 1 to 10cm in size
  • If the scale is removed, a red membrane with pinpoint bleeding points may be seen (Auspitz’s sign)
48
Q

Stepwise treatment for chronic plaque psoriasis

A
  • Regular emollients to reduce scale loss and pruritis
  • First line: potent corticosteroids once daily plus vitamin D analogue applied once daily for up to 4 weeks
  • Second line: if no improvements after 8 weeks then a vitamin D analogue twice daily
  • Third line: if no improvements after 8-12 weeks then either a potent corticosteroid twice daily up to 4 weeks or a coal tar preparation OD or BD. Short acting dithranol can be used.
49
Q

Psoriasis complications

A
  • Psoriatic arthropathy
  • Increased incidence of metabolic syndrome
  • Increased incidence of cardiovascular disease
  • Increased incidence of venous thromboembolism
  • Psychological distress
50
Q

Guttate psoriasis

A
  • More common in children and adolescents.
  • May be precipitated by a streptococcal infection 2-4 weeks prior to the lesions appearing.
  • Tear drop papules on the trunk and limbs. Pink scaly patches or plaques of psoriasis
  • Tends to be acute over days
  • Tends to resolve spontaneously within 2-3 months. Use topical agents as per psoriasis, UVB phototherapy. Tonsillectomy might be necessary with recurrent episodes

Medicine year 4 CDM (44 decks)

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