Rheum2 Flashcards

(50 cards)

1
Q

What is osteoporosis

A

Condition characterised by low BMD and microarchitectural deterioration of bone ==> Leads to bone fragility and increased fracture risk

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2
Q

What investigations should be ordered in Ank Spond?

A

AP Pelvis and lumbar spine Xray

FBE, UEC, LFT

CRP, ESR

HLAB27

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3
Q

What are the two diagnostic categories for AS?

A

Radiographic Axial Spa (sacro-illitis on xray or mri plus one other feature of SPa)

Non-Radiographic Axial Spa (2 clinical features plus HLA B27 positive - no radiographic evidence yet)

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4
Q

What is the treatment of Ank SPond?

A
  1. Smoking cessation
  2. Spinal stretching and ankylosing spondylitis specific exercise program
  3. Patient Education and awareness of disease progression and red flags (Eg uveitis symptoms)
  4. Oral NSAIDs (proven benefit)
  5. IF not improving - DMARDS -sulfasalazine and/or methotrexate
  6. TNF alfa inhibitors are second line (rheum prescription)
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5
Q

How does enteropathic arthritis present?

A

Its the most common extra-articular manifestation of IBD (20%)

Can get spinal enthesitis (sacroillitis) and peripheral - achilles/plantar fasc

just like ank spond clinically

But in extra-articular - can also get conjunctivitis/episcleritis AND the skin manifestations of IBD

Erythema nodosum - CHRONS
Pyoderma Gangrenosum - Ulcerative colitis

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6
Q

Management of enteropathic arthritis

A

NSAID - if tolerated because of gut issues

Steroid injections

Exercise

DMARD’s in refractory

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7
Q

Clinical features of psoriatic arthritis?

A

Usually a peripheral arthritis - can get dactylitis

  • 50% peripheral arthritis affecting Up to 5 joints - starts oligoarticular but can become poly
  • polyarticular peripheral - can resemble rheumatoid (30%)
  • Predominant sacroillitis and spondylitis (10%)
  • Predom DIP involvement ( 5%)
  • arthritis mutilans (5%)- osetolysis! shortening of fingers and flail joints
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8
Q

Management of psoriatic arthritis?

A

1, NSAIDS - ibuprofen 400mg tds prn

  1. Corticosteroid injections
  2. DMARDS - methotrexate, sulfasalazine, leflunomide
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9
Q

What are the features of reactive arthritis?

A

Triad of peripheral arthritis, urethritis, conjunctivitis

  • 1-2 weeks after infection with either CHLAMYDIA TRACHOMATIS

or shigella, camylobacter, salmonella, yersinia

  • YOu need one or more of the triad and the typical history
  • usualy 20’s -40’s
  • Extra-articular - conjunctivitis, urethritis/prostatis/balanitis and Keratoderma Blenorrhagica (pustular hyperkeratosis to hands and feet).

ACUTE MX- oral NSAIDS

Corticosteroid injection

Prednisolone (10-50mg daily until symptoms improve - then taper dose and stop)

CHRONIC (20%)

exercise programs

NSAIDS

Corticosteroid injections

May need DMARDS

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10
Q

What’s the differential diagnosis for a monoarthritis?

A
  1. Crystal arthritis eg gout
  2. Septic arthritis
  3. Traumatic/Haemarthrosis
  4. Malignancy within joint
  5. Psoriatic/enteropathic/reactive arthritis can present as mono arthritis
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11
Q

Patient with widespread joint pain (everywhere)

A

fibromyalgia

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12
Q

What are the serum uric acid targets for patients with a) gout b)tophaceous gout?

A
  1. 36 mmol/L for gout
  2. 3 mmol/L for tophaceous gout
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13
Q

What is Gout?

A

Deposition of monosodium urate crystals in joints, tissues and kidneys

can present with acute or chronic joint disease

Nephrolithiasis

Chronic urate nephropathy (tubular interstitial nephritis)

Its managed with life long urate lowering therapy

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14
Q

Which foods are high in purines?

A

Red meat,

Offal

Shellfish

Alcoholic beverages

Sweetened soft drinks

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15
Q

How is uric acid made?

A

Made in liver from endogenous and dietary purines

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16
Q

Where is uric acid eliminated?

A

2/3 kidney

1/3 GIT

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17
Q

Which drugs inhibit uric acid excretion?

A
  1. Thiazide diuretics
  2. Loop diuretics
  3. Cyclosporin
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18
Q

What causes an acute attack of gout

A

Sudden change in uric acid levels - up or down

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19
Q

What are the risk factors for GOUT?

A

Hypertension

Dyslipidaemia

Diabetes

Obesity (increased endogenous insulin reduces uric acid b/down)

Ischaemic heart disease

Chronic kidney disease

(Basically all CV RF’s and kidney due to metabolic effect)

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20
Q

Differences in presentation between acute and chronic gout

A

acute - usually monoarticular - 1st MTP or other part of foot

Chronic - can be tophaceous - tophi usually occur at elbows, knees (causing bursitis) and in peripheral joints (fingers and toes)

Chronic tophaceous gout is DESTRUCTIVE and can cause significant disability

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21
Q

Investigations for gout?

A

definitive dx requires ID of monosodium urate crystals under polarised microscopy in synovial ( or bursal) fluid or tophi

Ix: Aspiration of joint with suspected acute gout - and microscopy for urate crystals

Serum uric acid

FBE, CRP, ESR

UEC - impaired RF is both risk factor and and consequence of gout

22
Q

Management of acute gout?

A

Indomethacin 50mg TDS for 3-5 days

OR

Local Corticosteroid injection - up to two sites

OR

Prednisolone 15mg orally 3-5 days

OR

Colchicine 1mg stat followed by 500mcg at one hour

can then give 500mcg TDS for next few days to a maximum of 6mg in 4 days

23
Q

Long term management of GOUT?

A
  1. Education regarding purine rich foods - give patient list of foods to avoid.
  2. Screen for metabolic syndrome - advise cardiovascular risk management and 150min/week of exercise
  3. Life long urate therapy - commence allopurinol at low dose 50mg/daily - increasing slowly every 4 weeks - titrate dose according to serum urate level (treat to target)
  4. 36 for gout
  5. 3 if tophi are present

If not starting allopurinol during acute flare - can start with flare prophylaxis.

24
Q

Whats the dose of colchicine for flare prophylaxis?

A

500mcg orally daily for 6 months

25
What is a side effect of allopurinol which patients should be informed of?
Allopurinol Hypersensitivity syndrome Maculopapular rash can be Desquamating fever hepatitis Eosinophilia Usually occurs in first 3 months of treatment CAN BE FATAL! **Tell patients to seek urgent medical attention if a skin rash develops**
26
Which group of people is allopurinol hypersensitivity more likely ? What drug can be given if allopurinol is inappropriate or does not work?
Asian descent (esp Han Chinese) HLA B\*5801 allele also ppl who commence on high dose renal impairment elderly **PROBENECID** is an alternative
27
What are common sites of minimal trauma fracture?
vertebral bodies distal radius proximal humerus pelvis proximal femur **CONSIDER OP in any person over 50 with a min trauma fracture** (NB fractures of fingers/toes/face/skull are usually not osteoporotic)
28
Whats the T score in OP
-1 to -2.5 = osteopenia Below minus 2.5 is osteoporosis Above minus 1 is normal bone This is number of SD's away from 'young normal mean' at any major skeletal site This is mainly done in older people
29
What is the Z score?
In premenopausal women, men younger than 50 and kids Z is the number of SD"s away from AGE and SEX matched mean **A Z score below -2 is below the expected range and warrants investigation for a secondary cause of low bone density**
30
Aside from BMD what other investigations are considered in Osteoporosis?
**Plain xrays** can identify fractures Vert fractures are painless in 70% of cases but can be used in patients with significant loss of height - **3cm or more or Kyphosis.** specialists use bone turnover markers like serum fasting P1NP and CTX (gps dont use these regularly)
31
When would you commence osteoporosis treatment?
1. Age over 50 with a minimal trauma fracture of **hip or vertebrae** 2. Age over 50 with minimal trauma fracture at proximal femur/humerus or distal radius AND BMD of less than **1.5(if bmd is higher - then refer to specialist)** 3. In a patient over 70 who is being screened for OP with a BMD of less than -2.5 (if BMD higher then do Garvan fracture risk calculation) 4. In a patient under 70 with risk factors for OP with a BMD of less than -2.5 (If BMD higher then do Garvan fracture risk calculation)
32
In whom should BMD be measured
Anyone over 70 Anyone under 70 with risk factors for OP
33
What are non modifiable risk factors for osteoporosis?
Ageing Female White/Asian race Previous low impact fracture Late Menarche Post Menopausal Family history of OP short stature
34
What are lifestyle associated risk factors for Osteoporosis?
Smoking Nutritional deficiencies - vitamin D deficency and low calcium intake Alcohol intake Sedentary lifestyle Immobilisation
35
Which diseases and drugs are risk factors for Osteoporosis
**CDC FEM W** **Chronic** - heart/liver/kidney **Drugs** - antiepileptics, thiozolidenediones, aromatase inhibitors, glucocrticoids **Connective tissue disease** - eg Rheumatoid **Falls** - visual impairment, balance disorders, muscle weakness, sedating drugs **Endocrine** - cushings, sex hormone deficiencies in women and men, hyperthyroid, hyperparathyroid **Malabsorption** - Coeliac disease, gastric/bowel resection, bariatric surgery **Weight** - low body weight, increased weight loss eg anorexia nervosa
36
37
Whats your approach for osteoporotic risk in a patient on long term glucocorticoids (eg 5mg over 3 months)?
Do a BMD If Less than - 1 - commence treatment as primary prevention
38
When would you consider a secondary cause in osteoporosis?
Pre-menopausal women young men (less than 50 years) SEEK SPECIALIST ADVICE TO GUIDE MX In men think about - hypogonadism, smoking, steroids, anti epileptics, etoh excess, vitamin D deficiency
39
40
What investigations to detect secondary causes of OP might be appropriate
ALP CMP TSH VITAMIN D LFT and UEC Then for different causes - eg PTH, Urine and serum protein electrophoresis, coeliac serology, sex hormones, 1mg overnight dexamethasone suppression test
41
Indications for specialist referral in OP
1. Secondary cause suspected 2. women of child bearing age and preg women 3. post transplant 4. patients with osteoporosis and CKD (esp if gfr is less than 35)
42
43
Non pharm management of osteoporosis?
1. Falls Prevention * Podiatric check for neuropathy * Podiatrist - cut toe nails * Podiatrist - optimise foot wear * OT home assessment - carpets, walking aids, lighting * Exercise FOR mobility, balance and strength * Review meds that can cause OP and Postural hypotension * Opthalmology review - assess and optimise vision * Referral to a FALLS prevention clinic 2. Advise and assist all patients at risk of minimal trauma fracture - PHYSIO review for improving balance and exercise program - 30mins/most days and 2-3 resistance sessions - Avoid Excess alcohol or coffee - Stop smoking - Maintain ideal body weight - Ensure adequate vitamin D and calcium intake CONSIDER an oral calcium supplement (600mg) if calcium intake is insufficient
44
What is the pharmacological management of osteoporosis?
1. BISPHOSPHONATE - Alendronate 70mg once weekly on an empty stomach Bisphosphonates inhibit osteoclasts to minimise upper GI adverse affects - 1. Take FIRST THING in the morning on an empty stomach 2. Remain upright at least 30 minutes after taking them 3. Avoid food and drink immediately after (affects absorption) no supplements eg calcium for 2 hours after. CONTRAINDICATIONS to BISPHOSPHONATES Dysphagia Achalasia unable to remain upright for 30 minutes
45
What are adverse effects of bisphosphonates?
Upper GI - gastritis, oesophagitis, nausea, constipation, Rarely osteonecrosis of the jaw Maintain good oral hygiene and see dentist before commencement
46
Dose of ZOledronic? ADR of Zoledronic acid?
5mg IV yearly Can cause flu like symptoms (usually at first dose) Can cause **hypocalcaemia - esp if low vit D or renal issues** Safe for use as long as: **Vitamin D over 50** **normal serum calcium** **EGFR is over 35** **Patient is well hydrated**
47
How long should bisphosponates be continued in patients with osteoporosis?
in High risk continue bisphosponates for 10 years and zoledronic for 6 years - 75 and older - previous hip or verteberal frac - Hip Tscore less than -2.5 - had a min trauma frac after commencement of treatment IF LOW RISK - then 5 years after bisphos or 3 years after zoledronic - consider stopping
48
How would you monitor osteoporosis treatment
Direct measurements of BMD at hip and spine 2 years after starting treatment 1-2 years after significant change in treatment If High risk patient or on glucocorticoid therapy consider more frequent monitoring
49
What is denosumab?
Its a MONOCLONAL ANTIBODY **60mg subcutaneous ever 6 months** which is also anti resorptive Decreases osteoclast formation and increases Apoptosis ITS a SUBCUTANEOUS DOSE every six months (useful if patient has adverse GI side effects) - WITHDRAWL OF Denosumab has been associated with MULTIPLE FRACTURES **CAN BE GIVEN TO RENAL PATIENTS**
50
When is raloxifene used for OP treatment?
IN women at risk of BREAST CANCER - can reduce risk most appropriate for younger Post menopausal women (under age of 60) Does increase VTE Risk and increases hot flushes