RHEUM: Osteroporosis, osteomalacia, gout,fibromyalgia and hypermobility Flashcards Preview

Year 3 Medicine Block > RHEUM: Osteroporosis, osteomalacia, gout,fibromyalgia and hypermobility > Flashcards

Flashcards in RHEUM: Osteroporosis, osteomalacia, gout,fibromyalgia and hypermobility Deck (57)
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1
Q
A
2
Q

What is hypermobility?

A

Where joints move beyond normal limits due to laxity of ligaments, capsules and tendons. Can affect many joints.

3
Q

Who does hyper mobility affect?

A

People with familial history (but there isn’t any genetic testing)
Women, Asian people

4
Q

What is the clinical presentation of hypermobility?

A

PC: Presents in childhood, or young adulthood. Pain around the joints, worse after activity. Pain is generalised. Fatigued
PMH: Recurrent subluxations and recurrent dislocations
On examination:
- Soft tissue rheumatism, abnormal skin - thin, hyper extensible, striae, marfanoid habits, arachnodactyly, drooping eyelids, myopia, hernias, prolapses or uterine or rectal contents

5
Q

What scoring system is used for Hypermobility?

A

Beighton score - a point is given for each manoeuvre a pt can do. Score is out of 9.

6
Q

What is the aim of Hypermobility syndrome treatment?

A

Treated based on improving pain and reducing disability

7
Q

What non-drug treatment is available for hyper mobility?

A

Strengthening exercises to reduce joint subluxation.
Posture and balance exercises
Splinting
Specialist pain management

8
Q

What pharmacological treatment is available for hyper mobility?

A

Paracetamol

9
Q

What is a DEXA scan?

A

Measures the amount of radiation absorbed by the bones - indicating bone mineral density - BMD

10
Q

Where should a DEXA scan reading be done to classify and manage OA?

A

At the hip - neck of femur to confirm OA and monitor treatment .

11
Q

What scores can bone density be represented as?

Which score is key for the WHO classification of OA?

A

Z score ( how much bone mineral density falls below mean of pts age)

T score (how much bone mineral density falls below mean of healthy young person)

T SCORE - CLINICALLY IMPORTANT

12
Q

How is OA defined?

A

Degenerative joint disorder where there is progressive loss of articular cartilage accompanied by new bone formation and capsular fibrosis

13
Q

What are the aetiology possibilities for OA?

A

Failure of normal cartilage subject to abnormal or incongruous loading for long periods

Damaged or defective cartilage failing under normal conditions of loading

Break up of cartilage due to defective stiffened subchondral hone passing more load to it

14
Q

What are the key features of cartilage in OA

A

Loss of elasticity with reduced tensile strength

Cellularity and proteoglycan content are reduced

15
Q

What are the RF for OA?

A
Age- over 65 
Women are more symptomatic than men 
Obesity- hand and knee 
Trauma and joint malalignment  
Fhx
16
Q

What are the most common joints to be affected by OA?

A

Hip, knee and spine

17
Q

What are the symptoms of OA?

A

Pain provoked by movement and weight bearing
Pain starts off intermittent but as it progresses becomes constant
Knee-inactivity gelling and feeling that joint will give way is common

18
Q

What are the xray features of OA?

A

LOSS

loss of joint space
osteophytes
subchondral scerlosis
subchondral cysts

19
Q

What is the aim of treatment?
(regarding osteoarthritis)

A

Pain improvement and reduce disability

20
Q

What non-drug therapy is recommended in patients with OA?

A

Hip and Knee- strengthening and range of movement exercises
Weight loss to reduce joint loading
Laterally wedged insoles or walking stick

21
Q

What pharmacological therapy is given for OA?

A

Paracetamol is first line
NSAIDs- short term
Topical NSAIDS, topical rubefacients and capsaicin can be used.
Intra- articular corticosteroids can be offered.

22
Q

What surgical therapy is offered in OA?

A

If physio and pharmatherapy is not helpful- joint replacement surgery can be offered

23
Q

What is fibromyalgia

A

A common disorder of central pain processing characterized by chronic widespread pain in all 4 quadrants of the body (both sides and above and below the waist)

Allodynia, a heightened and painful response to innocuous stimuli, is often present.

24
Q

What is the pathogenesis of fibromyalgia?

A

It can be induced by deliberate sleep deprivation.
Reduced REM and delta wave sleep –>causes hyper-activation in response to noxious stimulation, and neural activation in brain regions associated with pain perception in response to non-painful stimuli.

25
Q

How would you assess a patient with osteoporosis?

A
  • Patients are categorised as low, intermediate or high risk based on the risk calculator. For QFracture, this is based on the percentage, and patients above 10% are considered for a DEXA scan.
  • For FRAX, this is based on the NOGG guideline chart (linked to on the online FRAX tool), which advises whether to arrange a DEXA scan or start treatment.

These suggestions do not apply to specific groups. For example, NICE CKS (April 2023) suggest:

  • A DEXA may be arranged without calculating the risk in patients over 50 with a fragility fracture
  • Treatment may be started without a DEXA in patients with a vertebral fracture

In FRAX: Using the T score (Bone mineral density score) use the FRAX assessment tool (plug in RF -AR, sex, age, steroid use) p242 Z2F

26
Q

What Management for osteoporosis ? Non-pharmacological?

A

Lifestyle:

Stop smoking 
Avoid falls
Activity and exercise 
Good Ca + Vit D intake 
Reduce alcohol 
Healthy weight
27
Q

What management for osteoporosis? Pharmacological?

A

Vit D + Ca supplements - Calcichew-D3

1st line for osteoperosis
Bisphosphonates e.g. Alendronate 70mg weekly

If above not tolerated :
Denosumab - monoclonal AB that blocks ostoeclasts
HRT for early menopause women

28
Q

How do Bisphosphonates work? What are some side effects ?

A

MOA: reduce activity of osteoclasts stopping resorption of bone

  1. Reflux and oesophageal erosions (empty stomach and sit upright for 30 mins)
  2. Atypical fractures e.g. femoral
  3. Osteonecrosis of the jaw
  4. Osteonecrosis of the external auditory canal
29
Q

Treatment of fibromyalgia ?

A

Tailor to pain, function and associated symptoms : depression / fatigue / sleep disturbance

Drug:
Low dose Amitryptytline
Pregabalin
CBT

30
Q

What blood tests to rule out other causes of fibromyalgia ?

A

BLOODS:

ESR, CRP, FBC, U+E, LFT, Ca, CK, TFT

31
Q

What is Gout ?

A

Crystal arthropathy related to hyperuricemia .

Depositition of monosodium urate crystals in joints and soft tissues.

32
Q

How does Gout present?

A

The monosodium urate crystals that deposit in soft tissues and joints cause acute and chronic arthritis.

Hot swollen joint
Can affect >1 joint but most commonly 1st metatarsal (podagra)
Soft tissue deposits of uric acid - tophi
urate nephropathy + uric acid stones.

33
Q

Typical joints affected by Gout?

A

Base of big toe - (metatarso-pharyhgeal joint)

Wrists

Base of thumb (carpo-metacarpal joint)

34
Q

Which type of Gout are older women with OA likely to get?

A

Pseudogout important DD in diagnosis of gout called by pyrophosphate crystals in older woman with OA

35
Q

What investigation and its result is patho-mnemonic for Gout?

A

Aspiration of joint will reveal:

Monosodium Urate Crystals are PM
also will find:
No bacterial growth 
MSU crystals = needle shaped
-ve befringement of polarised light
36
Q

What would you seen on XRay of a joint with Gout?

A

Joint space is maintained

Lytic lesions in bone

Punched out erosions of bone

Erosions can have sclerotic borders with overhanging edges

Joint effusion

37
Q

What is management of acute flare of Gout?

A

NSAIDs e.g. ibuprofen- 1st line

Colchicine - 2nd line

Steroids - 3rd line

38
Q

What should be used for Gout if NSAIDS are not suitable?

Give an example of pt where NSAIDS not suitable?

A

Pts not suitable for NSAIDS :
Renal impairment
Significant heart disease

2nd line choice:
Colchicine

Side effects of Colchicine are GI upset and diarrohea

39
Q

What is the prophylactic treatment of Gout? When specifically can you start this treatment?

A

Allopurinol - urate lowering

Only start once flare up has stopped. Once started can continue through subsequent flares

Lifestyle changes: 
lose weight
hydration 
reduce alcohol
reduce purine based food e.g. meat / seafood
40
Q

How would you differenciate between Pseudo-Gout and Gout ?

A

Aspiration fluid

Pseudo gout: pyrophosphate rhomboid crystals

Gout
Needle shaped monosodium urate crystals

41
Q

What are some non-modifiable and modifiable risk factors for Gout?

A

Nonmodifiable
* Male sex
* Age over 50 years
* Family history of gout
* Inherited syndrome with uric acid overproduction (eg. Lesch–Nyhan syndrome)

Modifiable
* Obesity
* Hypertension
* Chronic kidney disease
* Diabetes
* Metabolic syndrome
* Medications (eg. thiazide diuretics, ACE inhibitors and aspirin)

42
Q

What is pathognomonic Xray finding in pseudo gout ?

A

Chondrocalcinosis - thin white line in middle of joint space

Severe cases - joint washout (arthrocentesis)

Joint changes similar to )A
LOSS

L- loss of joint space
O- osteophytes
S- sub articular sclerosis
S- subchondral cysts

43
Q

What is osteoporosis?

A

low bone mass, deterioration of bone tissue, and disruption of bone architecture that leads to compromised bone strength and an increased risk of fracture

44
Q

Risk factors for osteoporosis?

A
Advanced age (>65 years)
Female gender
 Caucasian or south Asians
Fhx
Low body weight (58 kg or body mass index
[BMI] <21)
 early menopause (age<45)
- Calcium/vitamin D deficiency
- Inadequate physical activity
- Cigarette smoking
- Excessive alcohol intake (>3 drinks/day)
- Iatrogenic: e.g. corticosteroids, aromatase
inhibitors
45
Q

Characteristic gait of a patient with osteomalacia?

A

waddling gait

46
Q

Which medical conditions put patients at risk of developing Vit D deficiency and therefore osteomalacia?

A
Malabsorption disorders e.g. IBD Chrons 
Lack of sunlight 
diet
CKD - kidneys needed to metabolise to active form
Drug - anticonvulsants 
Inherited - hypophosphatemic rickets
liver disease - cirrhosis
47
Q

What risk factors for Vit D deficiency in population (therefore getting osteomalacia?)

A
Darker skin
Stay in doors a lot
colder / northern climates
Wear covered clothing 
low exposure to sunlight
48
Q
  1. Briefly explain relationship between Vit D, Ca, phosphate

2. How they become deranged in osteomalacia?

A
  1. Vit D essential for Ca and Phos absorption from intestines and kidney.
  2. Low vit D leads to lack of Ca and Phos in blood causing defective bone mineralisation.
    Low Ca causes increased PTH (2nd hyperparathyroidism) which makes mineralisation problem worse as it stimulates Ca resorption from bones.
49
Q

Symptoms of osteomalacia?

A
fatigue
Proximal myopathy - waddling gait 
Muscle /bone tenderness
Bone pain 
Pathological / abnormal fractures
50
Q

Treatment of osteomalacia?

A
Vitamin D (colecalciferol) e.g. 50,000 IU weekly for 6w
Vit D serum below 25 nmol/L is deficient
51
Q

Define osteomalacia

A

Defective bone mineralisation causing soft bones in adults due to low vitamin D. When this happens in children before growth plates have closed it is called Rickets.

52
Q

Which drugs can increase risk of gout?

A

Diuretics- particularly thiazide like and loop
pyrazinamide
ciclosporin
tarcolimus

53
Q

Signs and symptoms of fibromyalgia?

A
Unrefreshed sleep 
Joint and muscle stiffness 
Profound fatigue 
Numbness 
Headaches 
IBS/ Bladder syndrome 
Depression and anxiety 
Poor concentration and memory fibrofog.
54
Q

Risk factors of fibromyalgia?

A

Female
Age - 40-50 usually
May have obvious trigger = emotional trauma, physical e.g. painful arthritis.

55
Q

Allopurinol - mechanism of action?

A

Xanthine oxidase inhibitor so reduces rate formation.

56
Q

Compare gout and pseudo gout?

A

Gout = male, needle shaped negatively birefringent monosodium rate crystals (under polarised light)

Pseudogout = women, usually with PMH of OA. Weakly positive birefringent rhomboid crystals made of calcium pyrophosphate

57
Q

Late XR findings of gout?

A

Joint effusion
Punched out erosions
Reduced joint space

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