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A2 ME3031 MSK > W10 - Metabolic Bone Disease, Crystal Arthopathy, Sero-neg Arthritis > Flashcards

W10 - Metabolic Bone Disease, Crystal Arthopathy, Sero-neg Arthritis Flashcards

1
Q

Discuss the definition of osteoporosis

A
  • low bone mass
  • microarchitectural deterioration bone tissue
    = bone fragility = fracture risk

*DXA bone scan =

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2
Q

Describe the investigations to confirm the diagnosis of osteoporosis as well as significant scoring methods used

A

DEXA scan = lifestyle interventions

  • FRAX = risk assessment tool
  • QFracture = prediction algorithm estimates the 10 year absolute risk of osteoporotic fractures and hip fractures in men and women
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3
Q

Discuss the types of drugs used to prevent and treat osteoporosis

A

(1)
* >BISPHOSPHONATES *
advise good dental health
*drug holiday for 1-2yrs after 10yr use
!oesophagitis; uveitis; CI in CKD, femoral #

> DENOSUMAB
MAb against RANKL = ⇩osteoclastic resorption
*6mos subcut injection
* preferred for renal impairment Pts
!hypocalcaemia risk, allergic rash
>Teriparatide (PTH)
!rare hypercalcaemia; allergy; COST
-----
>Hormone replacement Rx
!blood clots
! breast ca risk
! cvd risk

> RALOXIFENE (oestrogen R modulator)

  • nil effect on nonvertebral #
  • hot flushes, clotting risk, lack of protection at hip site
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4
Q

Associations with Osteoporosis

A

Endocrine Causes:
Thyroid+++;
Parathyroid(-) and (+)
Cushings

Rheumatic:
RA
Ankylosing Spondylitis
Polymyalgia Rheumatica

GI:
UC & CD
Liver disease
Malabs

Medications:
Steroids, PPI, antiepileptics, warfarin

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5
Q

VitaminD & Calcium Metabolism

A

The liver converts vitamin D to 25OHD.

The kidney converts 25OHD to 1,25(OH)2D and 24,25(OH)2D.

The liver is the main source for 25-hydroxylation, and the kidney is the main source for 1α-hydroxylation.

*Vit D stimulates calcium and phosphate abs from gut thus allowing their availability for bone mineralisation

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6
Q

Discuss the pathogenesis of osteomalacia

A

Vit D, Calcium Deficiency = Rickets (Child) / Osteomalacia (Adult)

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7
Q

Discuss the investigations to confirm the diagnosis of osteomalacia

A

Bloods for vitamin D metabolites, and calcium metabolism

Bone scan

Bone biopsy

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8
Q

Describe the clinical features of osteomalacia and rickets

A
  • wide bones, odd legs, curved out legs
  • odd curve to back

bone pain and muscle weakness. The dull, aching pain commonly affects the lower back, pelvis, hips, legs and ribs.
-worse at night or when you put pressure on the bones. –rarely relieved completely by rest.

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9
Q

Describe the biochemical and radiological abnormalities found in osteomalacia

A

*BMD: bone scan

  • high alkaline phosphatase; parathyroid hormone
  • low 25-hydroxyvitamin D and calcium and/or low phosphate
  • Looser’s Zone Fractures
  • Bone biopsy
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10
Q

Discuss the differential diagnoses of osteomalacia with other metabolic disease, including Paget’s disease

A

Osteomalacia must be differentiated from other diseases that cause lowering bone mineral density (BMD), such as osteoporosis, scurvy, osteogenesis imperfecta, multiple myeloma, and homocysteinuria.

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11
Q

Discuss the principles of prevention and treatment of osteomalacia

A

> Lifestyle: dietary suppl.

>

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12
Q

Describe the epidemiology and etiology of Paget’s Disease

A
  • Genetic familial component; anglo-saxon origin
  • environmental trigger = infective trigger within osteoclast
  • > 40yo
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13
Q

Discuss the clinical features of Paget’s disease

A

Abn bone turnover and remodelling = disorganised bone = risk of deform and #

Presents with bone pain, deform., excessive heat or neurological complications (hearing loss); rarely osteosarcoma

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14
Q

Discuss the investigations to confirm the diagnosis of Paget’s disease and how the results may differ from other metabolic bone disease

A

Isolated elevation of serum alkaline phosphatase

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15
Q

Discuss the principles of management of Paget’s disease

A

Skull = Sx intervention

> Intravenous Bisphosphonate therapy
One off zoledronic acid infusion

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16
Q

Crystal Arthropathy Presentation and associated deposits

A

GOUT = Monosodium urate = Tophi (swolleen bulbous growths)

PSEUDOGOUT = CPPD
= chrondrocalcinosis
= pyrophosphate crystals
CALCIFIC PERIARTHRITIS = BCP

*deposition within joints and peri-articular tissue

17
Q

Polymyalgia Rheumatica Presentation

A

Inflamm. condition of the elderly

Polymyalgia Rheumatica > GCA > High ESR, Anaemia
* cycle

  • SUDDEN shoulder/pelvic girdle stiffness
  • > 70y, F>M, ESR ~100
  • Anemia
  • Malaise, Wt. loss, fever, depression
18
Q

Why hyper/hypo uricaemia may occur

A 
(+)
malignancy: lymphoproliferative, tumour lysis syndrome
severe exfoliative psoriasis
drugs: ethanol, cytotox.
HGPRT deficiency
(-)
Renal impairment
HT
Thyroid(-)
Drugs: alcohol, low dose aspirin, diuretics, cyclosporin
Exercise, starvation, dehydration

*endogenous uric acid via purine degradation contributes to 2/3 of body urate pool with rest dietary. Normally then excreted via kidney.

19
Q

Management of Gout

A

Dx:
Joint fluid microscopy and culture
Serum uric acid (SUA) (4-6w after acute attack)
Joint X-ray

Acute Mgmt:
> NSAIDs
+PPI?

> COLCHICINE

> STEROIDS

20
Q

Management of Hyperuricaemia

A

prophylaxis - lowering uric acid: ensure acute attack settled before reduction attempts

> ALLOPURINOL = consider eGFR
CANAKINUMAB = sfx
+ COLCHICINE

In particular it is important to advise the use of urate-lowering therapy to people with:
Two or more attacks of acute gout in 12 months.
Tophi.
Chronic gouty arthritis.
Joint damage.
Renal impairment (eGFR less than 60 ml/min).
A history of urinary stones.
Diuretic use.
Young age of onset of primary gout.

21
Q

Polymyalgia Rheumatica Associations

A

Giant Cell Arteritis; immune complex deposits

22
Q

Management of Pollymyalgia Rheumatica

A

Dx:
Hx as well as STEROID RESPONSE

> Pred./day; 18-24mos course
Bone prophylaxis

23
Q

Lesch Nyan Syndrome

A

HGPRT deficiency, X-linked recessive

*HGPRT plays aa role in recycling of purine bases into purine
= purine synthesis accelerated

24
Q

Mgmt of Pseudogout

A

> NSAIDs
Steroids

nil prophylaxis d/t idiopathic nature

25
Q

Definition and classification of sero-negative (rheumatoid factor negative) inflammatory arthritis

A
  • negative rheumatoid factor
  • HLA-B27 association
  • asymmetric arthritis + AXIAL INVOLVEMENT
  • ENTHESITIS
  • extra-articular: uveitis, IBD
  1. ANKYLOSING SPONDYLITIS
  2. JUVENILE ANKYLOSING SPONDYLITIS
  3. PSORIATIC ARTHROPATHY
  4. INTESTINAL: UC; CD
  5. REACTIVE ARTHROPATHY (REITER SYNDROME)
26
Q

Understand the genetic basis for the grouping of sero-negative inflammatory arthritis and features spondylarthritides have in common

A

HLA-B27 association

27
Q

Describe the characteristic pattern of joint involvement in spondylo-arthropathies compared with other arthropathies

A

Symmetric (RA) vs Asymmetric (Sero-Neg)

28
Q

Describe the characteristic features and mgmt of ankylosing spondylitis

A

axial progression and entheses

  • M>f, younger decades
  • inflamm back pain (lower)
  • sacroiliitis on XR

MRI > CR > Syndesmophytes

extra-articular: uveitis, cardiac, pulmonary, IBD, neuro: CES, renal 2 amyloidosis

>Physio
> NSAID: large benefit, with decreased mSASSS change
> DMARD: Sulfasalazine
> ANTI-TNF; ANTI-IL-17
> Joint replacements and spinal sx
29
Q

Describe the characteristic features and mgmt of eneteropathic spondylo-arthropathies,

A

Associated with IBD: CD or UC
* Peripheral and/or axial disease
+ ENTHESOPATHY

(NSAID difficult)
> SULFASALAZINE
> STEROIDS
> Mtrx
> Anti-TNF
> Bowel-resection
30
Q

Describe the characteristic features and mgmt of psoriatic arthritis

A

Common joints: flexures, shoulder, base of spine
+nail pitting
+ DACTYLTIS
+ ENTHESITIS

  • Distal Interpharyngeal joint involvement subtype
  • Symmetrical subtype
  • Asymmetric subtype

> Sulfaalazine
Mtrx
Anti-TNF

31
Q

Describe the characteristic features of reactive arthritis, as well as management

A

Post-infection => sterile synovitis
+ SYSTEMIC?
+ dactylitis or enthesitis
+ eye, urinary symptoms (nil bg of infection)

  • mono or olioarthritis
  • skin and mucous membrane involvement

Prognostic
•Hip/heel pain
• ESR
• FHx, HLAB27+

--- Acute
>NSAID
> Joint injection
> Abx in Chlamydia
--- Chronic
>NSAID
>DMARD
32
Q

Describe the characteristic features of Reiter’s syndrome

A

reiter’s syndrome = (moono)ARTHRITIS, URETHRITIS, CONJUNCTIVITS

33
Q

Define the inclusive term of sero-negative spondarthritis and its subdivisions

A
  1. ANKYLOSING SPONDYLITIS
  2. JUVENILE ANKYLOSING SPONDYLITIS
  3. PSORIATIC ARTHROPATHY
  4. INTESTINAL: UC; CD
  5. REACTIVE ARTHROPATHY (REITER SYNDROME)
34
Q

Describe the extra-articular features of spondylarthritides

A

Uveitis

Skin/Mucosal Involvement

etc.

35
Q

Assessing Spinal Mobility

A

Modified Schober

Lateral Spine Flexion

Occiput to Wall

Cervical Rotation

36
Q

Grading of Sacroiliitis

A

for Ankylosing Spondy

0 - normal
1 - sus changes
2 - small local erosion/sclerosis; NIL JOINT WIDTH ALTERATION

3 - unequivocal abn = mod/adv sacroiliitis with erosions, sclerosis, widening etc.

4 - total ankylosis = fusion of bone

A2 ME3031 MSK (20 decks)

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