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244 Cards in this Set

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Most common polyarthritis

Rheumatoid arthritis

What does Anti-CCP stand for?

Anti-cyclic citrullinated peptide

What is ACPA antibody?

Anti–citrullinated protein antibody – Antibodies present in RA which are detected by CCP and therefore referred to as Anti-CCP.

In practice: ACPA = Anti-CCP

What are entheses?

Connective tissue between tendon or ligament and bone

Supposed pathogenesis of RA

Presumed autoimmune-driven inflammation of synovial joints leads to destruction ofjoints and peri-articular tissues ± extra-articular features

Most common polyarthritis

RA

Where do Rheumatoid nodules locate?

Back of elbow or back of hands

Significance of rheumatoid nodules

Necessarily seropositive (RF present) and therefore worse prognosis

3 RF for RA

Women (3x)


Smoking


FHx

4 presentations of RA and their relative incidence

Insidious (70%) – progressively feeling poorer ➙ Worse prognosis


Acute (15%) – wakes up with stiff joints whilst being fine the day before ➙ Better prognosis


Systemic (10%) – low grade fever, weight loss, lethargic


Palindromic (5%) – Symptoms come and go

What defines polyarthriris

≥ 5 joints affected


2-4 is oligoarthritis

Name one classification system for RA. Why is it useful?

EULAR classification


Early diagnosis

Boutonière's deformity

Swan's neck deformity

Z-thumb

Name 4 deformities in the hand and wrist of RA

Wrist


Ulnar deviation




Hands


◾︎ Swan neck


◾︎ Boutonniere


◾︎ Z-Thumb

4 X-ray features of OA

◾︎ Joint space narrowing
◾︎ Osteophytes
◾︎ Osteosclerosis
◾︎ Cysts

◾ Joint space narrowing


◾ Osteophytes


◾ Subarticular sclerosis


◾ Subarticular cysts

4 X-ray features of RA

◾︎ Joint space narrowing
◾︎ Osteopenia 
◾︎ Erosion
◾︎ Soft tissue swelling

◾ Joint space narrowing


◾ Periarticular osteopenia


◾ Erosion


◾ Soft tissue swelling

What are the 4 criteria used in the EULAR diagnostic criteria for rheumatoid arthritis?

◾ Joint involvement (# and size): many small joints get more points


◾ Serology: RF and ACPA


◾ Acute phase: CPR and ESR


◾ Duration of symptoms: > 6weeks get one point

6 clinical features of the joint in rheumatoid arthritis

Pain


Stiffness


Swelling


Subluxation


Joint instability


Deformity

3 signs of RA in the skin

Palmar erythema


Nodules


Vasculitic rash and ulcers

Besides the skin and the joints, name 8 other systems affected by RA

Neurological


Cardiovascular


Haematological


Lymphatics


Musculoskeletal


Ocular


Pulmonary


Amyloid



4 CV features of RA

Think of diseases just surrounding but not into the heart




Cardio


Pericarditis


Conduction abnormalities




Vascular


Coronary vasculitis


Aortitis

3 neuro features of RA

Cervical cord compression


Mononeuritis multiplex (loss of all modalities of a peripheral nerve due to vascular occlusion)


Compression neuropathy (eg carpal tunnel syndrome)

1 MSK feature of RA

Muscle wasting

3 ocular features of RA

Episcleritis


Scleritis


Keratoconjunctivitis sicca (dry eyes)

What mostly distinguishes episcleritis from scleritis

Scleritis is more painful

3 pulmonary features of RA

Nodules


Effusion (exudates due to inflammation)


Fibrosis


Caplan's syndrome (rare)

2 haematological features of RA

Anaemia


Thrombocytosis

(Note: this is different from SLE in which there is usually thrombocytopenia)

Three complications of RA

Septic arthritis


AA amyloidosis


Side effects of drugs

Why may patients with RA have pitting oedema?

RA ⟹ AA amyloidosis ⟹ nephrotic syndrome

What tool enables to assess the progression of RA? Describe it.

Disease activity score (DAS28)


28 joints: shoulders, elbows, wrists, MCP, PIP, knees




◾︎ Swollen join count


◾︎ Tender joint count


◾︎ ESR/CRP


◾︎ Patient global health (visual analog scale)

DAS28 thresholds for remission and severe disease

DAS28 > 5.1 is severe


DAS28 < 2.6 is remission

6 broad biochemical tests to do in RA (to assess severity and help diagnose)

◾ ESR/CRP


◾ FBC


◾ Renal function


◾ Liver function


◾ Urinalysis


◾ Serology: RF and Anti-CCP

Which of the 4 presentations of RA has the worst prognosis?

Insidious

Which symptoms of RA lead to the worst prognosis if present?

Systemic symptoms

What is the basic principle for the management of RA

Treat to target


Define a target DAS28 with patient and treat until you reach it

4 broad strategies of management of RA

Education


PT/OT


Medication


Surgery

What medication would you use to kick-start the treatment of RA

Depo-medrone injection (steroid)

Name 4 drugs that can effectively modify the progression of RA and outline their MOA

Disease-modifying anti-rheumatoid drugs (DMARD)



Methotrexate (MTX)


Folic acid antagonist




Hydroxychloroquine (HCQ)


Inhibition of cellular enzyme release




Sulphasalazine (SSZ)


(Unknown)




Leflunomide (LEF)


Arrests activated lymphocytes

About the side effects of DMARD,


1) Which one(s) cause diarrhoea?


2) Which one(s) require FBC? Why?


3) Which one(s) require LFT? Why?


4) Which one(s) require optician review? Why?


5) Which one(s) are teratogenic?

1) LEF (but also MTX and SSZ)


2) LEF, MTX and SSZ because they may cause myelosuppression


3) LEF, MTX and SSZ because they may cause hepatitis
4) HCQ because it may cause macular damage


5) MTX and LEF

What monitoring is required for patients under MTX, SSZ, LEF and HCQ (separately)?

FBC


LEF, MTX and SSZ (may cause myelosuppression)




LFT


LEF, MTX and SSZ (may cause hepatitis)




Pregnancy test


LEF and MTX


Optician review


HCQ

What is the role of steroid treatment in RA?

No overall impact on progression of disease




Systemic steroids useful in active disease and flare




Local injections useful in early disease and flare

Criteria for use of biologics in RA

Two DMARD have been attempted, including MTX




and




DAS28 > 5.1

Patient with RA remains very symptomatic after MTX course (DAS28 = 4.9). What may you consider?

Another DMARD (eg HCQ)

Patient with RA remains very symptomatic after MTX course (DAS28 = 5.2). What may you consider?

Another DMARD since she hasn't tried two (even if DAS28 > 5.1)

Patient with RA remains very symptomatic after MTX and HCQ course (DAS28 = 4.9). What may you consider?

Try another combination since DAS28 < 5.1

First biologic that should be attempted in patient with RA

Anti-TNF

Name 3 anti-TNF and their MOA

Infliximab and adalimumab (destroy TNF)


Etanercept (receptor of TNF to neutralise them)

Three serious complications of anti-TNF

New infections


Reactivation of TB


Increased risk of cancer

1st, 2nd and 3rd line of biologics if Anti-TNF have failed (and their MOA)

Rituximab (anti CD20,i.e. anti middle age B-cells)


Abatacept (anti T-cells)


Tocilizumab (anti IL-6)

How often should rituximab (anti B-cells) be given in RA?

Twice 2 weeks apart, every 6 months

A patient with RA has DAS28 of 5.3, RF -ve and has tried MTX and adalimumab which were unsuccessful. What drug would you try now?

Abatecept (anti T-cells) or Tocilizumab (anti IL-6)


but not rituximab since she is RF -ve.

MOA of abatacept (with a bit of details)

Exogenous CTLA-4 which is an endogenous molecule that blocks T-cell/APC communication

Role of NSAIDs in RA

Can be used in acute flares

T/F: Anaemia is a good indicator of RA disease activity

False, thrombocytosis is. Anaemia can be due to multiple factors




(Note: in SLE, thrombocytopenia indicates worse prognosis)

4 contraindications to the use of anti-TNF

Pregnancy


Breast feeding


Septic arthritis within 12 months


Heart failure

At what age do we reach our peak bone mass

20-30

Name 4 factors that negatively affect peak bone mass

Smoking


Teenage pregnancy


Anorexia


Exercise amenorrhoea

Adequate calcium intake per day in mg, milk, cheese matchbox and pot of yoghurt units

700mg


1 pint of milk


3.5 matchboxes of cheese


3.5 pots of yoghurt

Besides age, name 6 factors that accelerate bone loss

Low oestrogen/Low testosterone


Vit D deficiency


Corticosteroids (oral)


Low weight/Low muscle mass


Smoking


ETOH XS

Examination of suspected osteoporosis



Diagnosis of osteoporosis

Dual energy X-ray absorptiometry (DXA)

What do T-score and Z-score refer to in DXA context

T-score – Compared to young adult female reference mean

Z-score – Compared to same gender and age

WHO diagnostic criteria for osteoporosis

DXA T-score ≤ -2.5 in the presence of one or more fragility fractures

What tool can be used to assess the fracture risk based on bone mineral density? How is the outcome of this tool used?

FRAX
Provides guidance on whether to treat or give lifestyle advice and reassurance

FRAX


Provides guidance on whether to treat or give lifestyle advice and reassurance

12 primary causes of secondary osteoporosis

Omit to take Vit D
Smoking
Thyroid hyperactive
Ethanol
Omit to eat (anorexia)
Parathyroid hyperactive
Osteodystrophy (renal)
Rheumatoid
Osteogenesis imperfecta
Steroid
IBD and Coeliac
Shitty bone cancers (mets or myeloma)

7 drugs that can be considered in osteoporosis

◾ Vit D/Calcium


◾ Raloxifene (oestrogen-like on bone and anti-oestrogen like on uterus and breast)


◾ Bisphosphonate (push osteoclasts to apoptosis)


◾ Strontium (Ca-like element)


◾ Teriparatide (PTH-like)


◾ Denosumab (RANKL inhibitor)


◾ Cathepsin K inhibitors (cathepsin K is secreted by osteoclasts to break down collagen)

MOA of raloxifene

Selective estrogen receptor modulator (SERM)


Oestrogen-like on bone and anti-oestrogen-like on uterus and breast

MOA of bisphosphonate

Push osteoclasts to apoptosis

MOA of strontium

Calcium-like element 

Calcium-like element

MOA of teriparatide

PTH (recombinant form)


Intermittent exposure to PTH increases osteoblasts activity (as achieved here) while chronic exposure to PTH increases bone resorption (as in hyperparathyroidism)

MOA of denosumab

RANKL inhibitor
(Of note: OPG is also produced by osteoblasts and inactivate RANKL)

RANKL inhibitor


(Of note: OPG is also produced by osteoblasts and inactivate RANKL)

MOA of cathepsin K inhibitors

Cathepsin K is secreted by osteoclasts to break down collagen

7 RF for bone fracture (3 related to clinical risk of fracture, 4 related to decreased bone mass density)

Clinical


Parental hip fracture


Alcohol ≥ 3U/day


RA




BMD


BMI < 22


IBD/AS


Immobility


Untreated premature menopause

Activation of Vitamin D



5 contraindications to HRT

Breast cancer (past, current or suspected)


Known or suspected oestrogen-sensitive cancer


IHD (recent or current)


Past or current thromboembolism


Untreated HTN


Active liver disease with deranged LFT

What are SERM?

Selective estrogen receptor modulator (SERM)


The class of drug of raloxifene

Two contraindications to SERM (such as raloxifene)?

DVT/PE


Pre-menopause

In one line, who is raloxifene recommended to?

Post-menopausal women with spinal osteoporosis and no DVT/PE hx

Major downside of bisphophonate in the treatment of OP

Very poor bioavailability so lots of precaution in taking and therefore poor compliance

What would you instruct to a patient to take bisphosphonate?

1. After overnight fast


2. With only tap water


3. Do not chew it


4. NBM for 30min afterwards


5. Remain upright for 30min (seated or standing)


6. No Ca supplement for 4h

4 contraindications to bisphosphonate (alendronate and risedronate)

Pregnancy


Recent upper GI event


Hypocalcaemia


Abnormal swallowing

Can bisphosphonate (alendronate and risedronate) be given to patient of childbearing age?

It should be avoided as much as possible and if given, foul-proof contraception should be added.

Can bisphosphonate (alendronate and risedronate) be given to men of any age?

Yes, the risk to pregnancy is only related to blood transmission to placenta

Alternative to alendronate and risedronate in patients with OP with recent GI event?

Zoledronate IV

Compare alendronate and zoledronate in terms of:


1) Frequency


2) Route


3) Contra-indications


4) Side effects

Frequency


Weekly (A) vs Annually (Z)




Route


PO (A) vs IV (Z)




Contraindications


Pregnancy (A and Z)


Hypocalcaemia (A and Z)


Upper GI events (A)


Abnormal swallowing (A)


Kidney disease (Z)




Side effects


Osteonecrosis of the Jaw (A and Z)


Renal impairment (Z>A)


Oesophagitis (A)


Acute inflammations, eg flu, colitis (Z)


Requires normal serum Ca and Vit D (Z)

Two contraindications to strontium for OP

Kidney disease (low eGFR)


Thromboembolism


Cardiovascular disease

One contraindication to denosumab for OP

Hypocalcaemia

4 contraindications for teriparatide in OP

Hypercalcaemia (opposite to denosumab and bisphosphonate)


Previous radiotherapy


Previous malignancy (except BCC)


Paget's disease

Treatment of vertebral collapse

Vertebroplasty (percutaneous cement injection)

A patient on bisphosphonate for OP starts experiencing bad taste and swelling of the jaw. Likely cause? What might you elicit on examination?

Osteonecrosis of the jaw
Examination: Exposure of mandibular or maxillary bone through lesions in the gingiva that do not heal

Osteonecrosis of the jaw


Examination: Exposure of mandibular or maxillary bone through lesions in the gingiva that do not heal

Which bones are most affected by osteonecrosis of the jaw?

Mandible and maxillary

Name 3 treatments of OP that may cause osteonecrosis of the jaw

Alendronate PO


Zoledronate IV


Denosumab (RANKL inhibitor)

T/F: bisphosphonate and denosumab reduce the probability of all fractures.

False: they increase the risk of atypical subtrochanteric fracture

Likely story 

Likely story

Atypical subtrochanteric fracture


Patient with OP treated with bisphosphonate or denosumab

Pathogenesis of Paget's disease of the bone

Multinucleate osteoclasts causing increased bone turnover with disorganised woven formation

Two genes whose mutations may lead to Paget's disease of the bone

Sequestome 1 (SQSTM1)


RANK-NF-kB

What inheritance pattern of Paget's disease is known?

Autosomal dominant with incomplete penetrance (SQSTM1)

Which genetic mutation leads to the worst prognosis of Paget's? Which leads to the earliest onset?

SQSTM1 for both

Most common presentation of Paget's disease of the bone?

Asymptomatic

When symptomatic, most common symptom of Paget's disease of the bone? Name one other symptom

Pain


Deformities

Characterise the pain in Paget's disease

Deep


Constant


Worse when lying flat


Worse with heat

6 complications of Paget's disease

◾ OA – 70%


◾ Nerve compression (deaf 60%, vertigo, spinal stenosis)


◾ Fracture – 10%


◾ Osteosarcoma – 0.4%


◾ High output heart failure (AV connections forming in the bones)


◾ Gout

Most, second and third likely site of Paget's disease

Polyostotic (72%)


Pelvis (70%)


Vertebra (40%)


Femur (30%)

T/F Osteoarthritis is a rare complication of Paget's disease

F: it occurs in 70% of patients

Levels of the following in Paget's:


ALP


Ca


Vit D


PO4


PTH

ALP ➚ (or bone-specific ALP)


Ca ➙


Vit D ➙


PO4 ➙


PTH ➙

Besides X-ray, what imaging can be used to help diagnose Paget's

Bone scan (scintigraphy)


= SPECT with Tc99 radioactive substance

Bone mets (focal areas and not whole bone affected)

Normal skeleton (activated areas are symmetrical and correspond to highly active bones)

Paget's disease: whole bone affected (asymmetrical)

Management of Paget's (3)

Reassure


Bisphosphonate


Monitor (including for malignancy)

T/F: In polyarticular diseases, imaging usually provide the bulk of the information for diagnosis

False: history and examination does

T/F: In polyarticular diseases, lab tests usually provide the bulk of the information for diagnosis

False: history and examination does

Definite diagnostic feature of SLE

Anti-dsDNA

Symmetrical synovitis and morning stiffness in small joints of the hands

Rheumatoid arthritis

For the following 3 broad aetiologies of polyarticular diseases, state whether it is acute or chronic:


1) Infective (eg Lyme)


2) Non-infective inflammatory (eg RA)


3) Non-inflammatory (eg OA)

1) Acute


2) Acute or Chronic


3) Chronic

Name 3 polyarthrites that present with a migratory pattern of joint involvement (comes and goes in some joints to reappear in others).

Rheumatic fever


Gonococcal arthritis


Lyme (early phase)

Name 5 polyarthrites present with intermittent pattern (come in several joints then complete remission then reappearance)

Reactive arthritis


Rheumatoid arthritis


Psoriatic arthritis


Polyarticular gout (rare)


Sarcoid arthritis

T/F: rheumatoid arthritis spare the spine

False: cervical spine can be affected but not thoracolumbar

Name 6 joints (or group of joints) commonly spared by OA

Upper limb


MCP


Wrist


Elbow


Glenohumeral




Lower limb


Ankle


Tarsal

RA (symmetrical and spine and DIP spared)



Psoriatic arthritis (any joints in an asymmetrical fashion)

AS (axial skeleton and large peripheral joints in an asymmetrical fashion)

OA (DIP, base of thumb, knees, hips, lumbar and cervical spine)

Which of the following polyarthritis may affect the spine:


Psoriatic arthritis


Ankylosing spondylitis


Osteoarthritis


Rheumatoid arthritis


Reactive arthritis


Lyme


Gonococcal arthritis


Enteric arthritis

All can except


Rheumatoid arthritis – only cervical


Lyme – Not at all


Gonococcal arthritis – Not at all

3 most common diagnosis in a patient with polyarticular symptoms who is:


1) Female between 25-50


2) Male between 25-50


3) Over 50

1) OA, RA, SLE, Fibromyalgia


2) Gonococcal arthritis, reactive arthritis, AS, OA


3) OA, RA, polymyalgia rheumatica

How is morning stiffness useful in the differential of polyarticular diseases?

Inflammatory polyarticular diseases (eg RA)


Morning stiffness for > 1hour




Non-inflammatory polyarticular diseases (eg OA)


Morning stiffness for 15min-1hour







Define tenosynovitis. Significance of its presence in polyarticular disease (5 differential)

Inflammation of the synovial-lined sheaths surrounding tendons elicited on exam as swelling and tenderness along tendons between joints.




RA, Gout, Reactive arthritis, gonococcal arthritis, TB and fungal arthritis

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Psoriatic plaque


Psoriatic arthritis

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Butterfly malar rash


SLE

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Erythema nodosum


Enteric arthritis, Sarcoid arthritis

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Rheumatoid nodules


RA

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Keratoderma blennorrhagica


Reactive arthritis



kerato–: keratinised


–derma: skin
blenn– : mucus


–rrhagia: discharge

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Palmar erythema


RA

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Circinate balanitis


Reactive arthritis

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Tophus


Gout

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Keratoderma blennorrhagica


Reactive arthritis

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Discoid rash


SLE

Name the skin condition and the polyarticular disease(s) associated with it

Name the skin condition and the polyarticular disease(s) associated with it

Pyoderma gangrenosum


Enteric arthritis

T/F the presence of circinate balanitis indicates that the primary infection was an STI.

False: it is reactive arthritis and therefore signs relate to immune reactions, not the infection itself which could be GI

6 polyarticular diseases that may have a positive ANA

SLE – dsDNA, Histone, RNP, Ro/La


RA – Histone (and RF is a false positive in tests)


Sjögren's – Ro/La


Polymyositis – Jo1


Scleroderma – Scl70/Topoisomerase


Mixed connective tissue disease – RNP

A patient with flu-like symptoms has a positive RF. What should you do and suspect?

Flu which usually causes RF to raise temporarily

Significance of low serum complement in polyarticular diseases

SLE or vasculitis


They consume complement by forming immune complexes

Suspected mechanism of RA

1) CD4 T cells trigger production of proinflammatory cytokines by Mϕ (e.g. IL-1 and TNFα)


2) Production of IgM and IgG by plasma cells

What two (groups of) joints are typically affected by RA?

PIP and MCP

PIP and MCP

What is a subluxation?

A partial dislocation

Name 5 seronegative spondyloarthropathies

Ankylosing spondylitis (AS)


Psoriatic arthritis (PsA)


Reactive arthritis (ReA)


Enteric arthritis (IBD)


Undifferentiated spondylitis

3 intra or periarticular characteristics of seronegative spondylitis

Sacroiliac (buttock) pain


Peripheral inflammatory arthropathy


Enthesopathy (insertional tendonitis)

Which is correct:


1) HLA-B27 has high sensitivity and high specificity for ankylosing spondylitis


2) HLA-B27 has high sensitivity but low specificity for ankylosing spondylitis


3) HLA-B27 has low sensitivity but high specificity for ankylosing spondylitis


3) HLA-B27 has low sensitvity and low specificity for ankylosing spondylitis

2 – 99% of AS patients have it but so does 10% of the population

What is HLA-B27 a sensitive marker of? a RF for? a non-sensitive marker of (2)?

Sensitive for Ankylosing spondylitis (99% have it)


Risk factor for reactive arthritis (20% of HLA-B27 positive develop ReA)


Non-sensitive for psoriatic arthritis and enteric arthritis




Remember PAIR (PsA, AS, IBD, ReA)

Demographic mostly affected by AS

Young (20-40) male

Pathological process of ankylosing spondylitis

1. Inflammation with fibrosis and ossification of ligaments, tendons and insertions2. Formation of syndesmophytes (bony growth originating in ligaments) and microfractures causing "Bamboo spine"
3. Fusion of the spine

1. Inflammation with fibrosis and ossification of ligaments, tendons and insertions
2. Formation of syndesmophytes (bony growth originating in ligaments) and microfractures causing "Bamboo spine"


3. Fusion of the spine



Bamboo spine caused by formation of syndesmophytes in ankylosing spondylitis

27 year old man with low back pain and pain in the back of his right ankle. Name one possible diagnosis and outline the pathological process explaining his back pain and ankle pain

Ankylosing spondylitis


Back pain – Spinal fusion and microfractures


Ankle pain – Enthesopathy (insertional tendonitis)

5 extra-articular features of ankylosing spondylitis

Constitutional + 4A


Aortic regurgitation


Apical fibrosis


Achilles tendinitis


Anterior uveitis

What fraction of patients with AS have anterior uveitis

40%

4 signs of anterior uveitis

Dilated ciliary vessels
Posterior synechiae: (hence irregular pupil)
Keratic precipitate (deposition of inflammatory cells on cornea)
Hypopyon (inflammatory cells in the anterior chamber of the eye)

Dilated ciliary vessels


Posterior synechiae (Iris adheres to the lens hence irregular pupil)


Keratic precipitate (deposition of inflammatory cells on cornea)


Hypopyon (inflammatory cells in the anterior chamber of the eye)

Name 4 conditions that may present with anterior uveitis and polyarticular disease

Spondyloarthropathies (AS, IBD, PsA, ReA)


Juvenile rheumatoid arthritis


Sarcoidosis


SLE

T/F: inflammatory markers is a good way of assessing severity of ankylosing spondylitis

False: there is little correlation

Imaging of choice in early diagnosis of ankylosing spondylitis and what you would see

T2w MRI


Romanus lesions (erosion involving the anterior and posterior edges of the vertebral endplates) followed by shiny corners (reactive sclerosis to erosions)



Role of XR in ankylosing spondylitis

Positive only after 8 years of disease


Demonstrates symmetrical sacroiliac changes, syndesmophytes, and ossification

Patient has ankylosing spondylitis and on examination, there are crepitations in apices. Name 2 potential reasons

Fibrosis (as an extra-articular feature)


TB (caused by anti-TNF alpha)

Name and quickly describe one tool used to assess AS disease activity

BASDAI


Self-reporting questionnaire

Name and describe one special test to do in OSCE in a patient with AS

Modified Schöber's test


A and B = Dimple of Venus (Posterior-superior iliac spine)


C = (A+B)/2


D = C + 10cm above


E = C - 5cm below


|DE| = 15cm


Ask patient to bend forward.


Positive if |DE| remains < 20cm

6 bad prognostic indicators of AS (3 that happen early, 1 extra sign, 1 blood, 1 aetiological)

Early: onset, loss of lumbar spine mobility, hip involvement


Dactylitis


ESR > 30


Sporadic (vs familial)

3 lines of management of AS

1) PT (including hydrotherapy)


2) NSAIDs


3) TNF blockade

Besides BASDAI which is useful for formalising history of AS, what formal scoring system exists for examination of AS? Describe it

BASMI
1) Lateral lumbar flexion
2) Tragus-to-wall distance (displayed)
3) Modified Schöber's test4) Maximal intermalleolar distance (separate your legs as much as you can)
5) Cervical rotation

BASMI


1) Lateral lumbar flexion


2) Tragus-to-wall distance (displayed)


3) Modified Schöber's test
4) Maximal intermalleolar distance (separate your legs as much as you can)


5) Cervical rotation

Demographics at risk of psoriatic arthritis

20-40 M and F

5 common presentations of psoriatic arthritis

◾︎ DIP (OA-like)


◾︎ Symmetrical polyarthritis (RA-like)


◾︎ Spondyloarthropathy (AS-like)


◾︎ Asymmetrical oligo


◾︎ Arthritis mutilans (severe, deforming and destructive)

What clinical feature of psoriasis is predictive of the development of PsA?

Nail lesions – Occur in 90% of patients with PsA

Radiological hallmark of PsA

Erosive change with bone proliferation, in a predominantly distal distribution

Name the sign and a condition in which it may occur

Name the sign and a condition in which it may occur

Pencil-in-a-cup finger


Occurs in PsA

What does juxtaarticular osteopenia suggest in polyarticular arthritis?

RA (not PsA)

Besides erosion and bone prolifeartion, name 3 other signs that you would see in a patient with PsA

Ankylosis
Pencil-in-cup deformities
Whittling of terminal phalanges (picture)

Ankylosis


Pencil-in-cup deformities


Whittling of terminal phalanges (picture)

Dactylitis

In which 2 conditions does dactylitis occur?

AS


PsA

Patient presents with pain in the distal phalange of the big toe, as well as in several joints in both hands. There is also an itchy rash on the skull. X-ray shows bone fusion and some erosion. Blood test reveals high level of uric acid. Diagnosis?

PsA which can present with hyperuricaemia


The rash and X-ray appearance is inconsistent with gout

Management of PsA

PT/OT




Mild to moderate


NSAID


MTX/LEF


If spinal or peripheral: SSE


Avoid HCQ


Severe


TNF blockage (etanercept or adalimumab)


Cyclcosporin A


Retinoids




Flares


Steroids injection



What is the best arthritis to have? Why?

Reactive arthritis usually remits after 2 year

Presentation of reactive arthritis

Classic triad


1) Monoarthritis


2) Rash


- Keratoderma blennorhagica (painless palms and soles pustules)


- Circinate balanitis on penis


3) Eye irritation (conjunctivitis then uveitis)

+ possibly systemic illness

In one line, what determines suspicion for reactive arthritis?

Spondyloarthropathies with associated urethritis, cervicitis or diarrhoea

About reactive arthritis following diarrhoea, when does the diarrhoea occur? What organisms (3) mostly cause it?

Within a month


Shigella, salmonella, clostridium (C. diff)

About reactive arthritis following urethritis, how does it present? What organism mostly causes it?

May be asymptomatic


Chlamydia

4 differentials to reactive arthritis

HIV


Lyme


Behcet’s
Parvovirus (mother of infected child)

How is reactive arthritis diagnosed?

History + Examination


Raised inflammatory markers


Serology


Cultures and swabs


Joint aspirate to rule out septic or crystal arthropathy

Role of joint aspirate in reactive arthropathy

Rule out septic arthritis and crystal arthropathy

Treatment of reactive arthritis

Usually


NSAIDs + Steroid injections will suffice for many patients (Remission occurs in 2 years)




Persistent disease


DMARDs (eg SSZ)

T/F: Treating the primary infection with ABx is very important in controlling reactive arthritis

False: ABx may have no effect on arthritis

Significance of HLA-B27 in reactive arthritis

HLA-B27 positive is a RF for persistent disease


(otherwise useless marker for diagnosis)

Distinguish the two types of enteric arthropathy in terms of joints affected, association with IBD symptoms, and incidence

Peripheral – 2/3


Coincide with symptoms of IBD


Mostly knees and ankles




Sacroiliitis – 1/3


Independent from symptoms of IBD


AS-like

Besides the joint and IBD, what clinical features would you look out for in enteric artrhopathy

Eye


Conjunctivitis then uveitis




Skin


Erythema nodosum


Pyoderma gangrenosum

Treatment of enteric arthropathy (symptom management, disease-modifying and refractory disease)

Symptoms


NSAIDs + Intra-articular or oral steroids




Disease-modifying


SSZ




Refractory disease


Anti-TNF

What sign of SLE might you see on ECG?

Saddle-shaped ST elevation in most leads due to pericarditis (serositis can be caused by SLE)

Pathogenesis of SLE (2)

1. Autoantibodies against nuclear antigens and other antigens ⇒ Direct effect on tissues and immune complex formations




2. Antibody against C1q and C4 complement ⇒ Complement defect ⇒ Cells debris are not collected ⇒ Nuclear antigens are presented to Th cells ⇒ Autoantibodies to nuclear antigens can act

What haematological changes are observed in SLE?

Anaemia of chronic disease + Possibly haemolytic anaemia (due to Ig against RBC)




Pancytopenia

Name one antibody class that can be tested for in SLE. How sensitive and specific is it?

Anti-nuclear antibodies (high sensitivity, low specificity)

What anti–nuclear antibody is most sensitive to SLE?

Anti-dsDNA

What biopsy investigation can be made in the diagnosis of SLE?

Biopsy of skin ⇒ Band of immune complex deposition between dermis and epidermis

Prognosis of SLE with treatment

Excellent (> 90% survival at 10 years)

Prevalence of SLE


F:M ratio


Peak age


and one demographic particularly at risk

0.1%


F:M = 9:1


Peak age: 45


Afro-Caribbeans (RR=5) and South-East Asian (RR=2)

At what stage of SLE is ANA positive

Very early on (even before symptoms)

How does the skin rash correspond to the chronicity of SLE

Malar (butterfly) rash – Acute


Discoid rash – Chronic

Discoid lupus

How does discoid lupus influences prognosis of SLE

Indicates milder disease

What fraction of patients with SLE develop renal disease? Cardiac disease? Stroke and seizures? Pleurisy?

60% – Glomerulonephritis


50% – Cardiac


20% – Stroke and seizures


50% – Pleurisy

How is skin disease in SLE managed (4)?

UV avoidance


Topical steroids


Topical calcineurin inhibitors (eg tacrolimus)


Systemic immunosuppressants if resistant

How is renal disease in SLE assessed?

Routinely: Dipstick, U&E, BP


Biopsy if suspicious

Initial and maintenance management of renal disease in SLE

Initial


Mycophenolate mofetil (MMF)


IV methylprednisolone




Maintenance


MMF


Prednisolone


Hyroxychloroquine


ACE inhibitor, statin, vaccinations

Patient with SLE has significant proteinuria but normal U&E. What should you do?

Treat as renal disease of SLE (this is likely membranous disease)

Patient with SLE has normal urine but abnormal U&E. What should you do?

Biopsy and treat if renal disease

What may cause neuro symptoms in SLE?

◾ Disease itself (vasculopathy or diffuse inflammation)
◾ Infection (immunosuppressed by medication)


◾ S/E of medications

Two most common neuro presentation of SLE

Cumulative incidence: 20%


Stroke


Seizure

Name one serological marker that is a RF for neuropsych disease in SLE

Anti-phospholipid antibodies

Patient with SLE has headaches, what may cause it?

Infection or venous sinus thrombosis


(Probably not SLE itself)

T/F: if a patient with SLE has delirium, then immunosuppression should be stopped.

False, infection should urgently be excluded following what intense immunosuppression may be beneficial.

Most common cardiac disease in SLE?

Pericarditis

What cardiac diseases are patients with SLE at risk of (3)? Give an approximate prevalence

Pericarditis – 50%


Endocarditis – 30%


Myocarditis – 10%

T/F: patients with SLE are at increased risk of IHD

True (> 2x)

Most common respiratory disease in SLE

Pleurisy (serositis)

Which of the following is least likely to be heard in a patient with SLE:


1) Pericardial rub


2) An ejection systolic murmur over the RUSE


3) A pansystolic murmur over the apex


4) Third heart sound

2 – Aortic stenosis is less common


1 – Common due to endocarditis


3 – Common due to mitral regurgitation in endocarditis (mitral valve is the most affected)


4 – Common due to pulmonary hypertension

What is a severe albeit rarer pulmonary complication of SLE

Acute pneumonitis

SLE can present with low blood cells of any sort. Which one is associated with more severe disease and poorer prognosis?

Thrombocytopenia




(Note: in RA, thrombocytosis correlates with disease activity)

Name 5 biochemical features of haemolytic anaemia

Normocytic anaemia


Positive Coomb's test


Raised LDH


Low haptoglobin (binding to free Hg for clearance)


Raised reticulocytes

Main 3 (groups of) joints affected in SLE

PIP


Wrists


Knees

Compare arthralgia in SLE and RA

SLE – Pain excessive compared to amount of swelling
RA – Opposite

Characterise the arthritis in SLE in terms of joints affected, synovitis, erosion, and deformities

Joints – PIP, Wrist, Knees


Synovitis – Little


Erosion – None


Deformities – Passively correctable (eg Jaccoud's)

4 GI manifestations of SLE

Oral ulcers


Mesenteric vasculitis


Pancreatitis


Peptic ulcer

Which antibody correlates with disease activity in SLE

dsDNA

Besides dsDNA, name 5 other antibodies that may be present in SLE

Sm


Ro/La (crossover with Sjögren's)


RNP (mixed connectivity tissue disease)


Phospholipids

Which two complements are typically measured and low in SLE?

C3 and C4

Which antibody in SLE is worrisome in neonates?

Anti-Ro – Indicating neonatal lupus causing complete heart block

Two drugs to give to all patients with SLE

Hydroxychloroquine


NSAIDs (eg ibuprofen)




(HIPIC)

Patient with SLE is started on NSAIDs and HCQ. Next stage in management if disease persists

Add Prednisolone




or azathioprine or methotreaxate to reduce steroid exposure




(HIPIC)

Patient with SLE is on NSAIDs, HCQ and prednisolone but start experiencing Cushing's. What should you do?

Replace prednisolone by MTX or azathioprine

Patient with SLE is on NSAIDs, HCQ and prednisolone but disease persists. What should you do?

Either of the following:


Increased steroid dose


Cyclophosphamide




MMF


Tacrolimus
Rituximab




(HIPIC)

Among the following drugs for SLE, which are not safe to use in pregnancy:


HCQ


NSAIDS


Prednisolone


Azathioprine


MTX


MMF


Cyclophosphamide

MTX


MMF


Cyclophosphamide

Name two anti-phospholipids that may be present in SLE

Anti-cardiolipin


Lupus anticoagulant

What are patients with anti-phospholipid syndrome at risk of (2)

Thrombosis


Fetal loss in pregnancy

How is anti-phospholipid syndrome treated in SLE?

Long-terms warfarin


or heparin if pregnant

Sign and condition

Sign and condition

Keratic precipitates (deposition of inflammatory cells on cornea)


Anterior uveitis

What is Z-thumb deformity? When does it occur?

RA

RA

In which polyarthritis should HCQ be avoided?

PsA

Passively correctable swan neck deformity. What disease?

SLE