• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/191

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

191 Cards in this Set

  • Front
  • Back

Name 2 large vessels, 2 medium vessels, 2 small vessels (ANCA positive), and 2 small vessels (ANCA negative) vasculitides.

Large


Giant cell arteritis


Takayasu arteritis




Medium


Polyarteritis nodosa


Kawasaki disease




Small ANCA+


Granulomatous polyangiitis


Microscopic polyarteritis




Small ANCA-


Hypersensitivity


Henoch-Schonlein purpura


Churg-Strauss


Cryoglobulinaemia


Infections


Neoplasms


Autoimmune

What is Wegener's granulomatosis

The past name of granulomatous polyangiitis

What vessels are affected by GCA?

Largest in the body (eg aorta and carotids)

Name one condition with a significant overlap with GCA

Polymyalgia rheumatica (50% patients with GCA have PMR and 20% patients with PMR have GCA)

3 main symptoms of GCA

Headache


Scalp tenderness (pain when combing)


Jaw claudication (chewing fatigue)


Visual disturbance (central or amaurosis fugax)

Two investigations in GCA

CRP/ESR


Temporal artery biopsy

Treatment of GCA (including dose)

Steroids (high dose – 1mg/kg/day up to a max of 60mg/kg/day)


Bone protection (alendronate, Vit D, Ca)


Gastroprotection

Demographic most affected by Takayasu arteritis

Young Japanese women

How does Takayasu arteritis present?

Signs, symptoms and complications of vascular blockage




Absence of pulses


Bruits


Claudication


Loss of vision


Stroke




as well as dramatic weight loss and constitutional upset

Treatment of Takayasu arteritis

Steroids and cyclophosphamide (think of it as even more dramatic than GCA and therefore requiring even more potent treatment)




(like PAN, granulomatous polyangiitis and microscopic polyangiitis)

P/C


Malaise


Weight loss


Cough productive of blood-stained sputum


Acute renal failure




History


Never smoked


TB unlikely




CXR


Cavitating lesions in both upper lobes




Likely diagnosis and first test for investigation?

Granulomatous polyangiitis ⇒ Test for ANCA

Name of the sign and potential cause

Name of the sign and potential cause

Coin lesion


Granulomatous polyangiitis

Which vasculitis may present with positive Hep B antigen or antibody?

Polyarteritis nodosa

Patient presents with nephritic syndrome (oliguria, hypertension). Serum blood test is positive for ANCA. Likely cause?

Vasculitis


Granulomatous polyangiitis


Microscopic polyangiitis (mPA)

Patient presents with nephritic syndrome (oliguria, hypertension). Serum blood test is positive for ANA. Likely cause?

SLE

What tissues are mostly affected by polyarteritis nodosa (5)?

Nerves


Intestinal tract


Kidney


Skin


Joints

Name of the sign and disease where it occurs

Name of the sign and disease where it occurs

Rosary sign (chain of aneurysm – here in coronary vessels)


Polyarteritis nodosa

What nerve disease occurs in polyarteritis nodosa?

Mononeuritis mutliplex


Simultaneous or sequential involvement of noncontiguous nerve trunks, evolving over days to years and typically presenting with acute or subacute loss of sensory and motor function of individual nerves.

Investigations in polyarteritis nodosa (3)

ESR


Hep B positive


Angiography (microaneurysm and occlusions)


Biopsy




All serology is negative !

Treatment of polyarteritis nodosa

Steroids


Cyclophosphamide




(like Takayasu, granulomatous polyangiitis and microscopic polyangiitis)

T/F: PAN presents with positive ANCA

False (ANCA is a feature of some small vessel vasculitis, not medium vessels)

What demographic is affected by Kawasaki disease?

Children

Name of the sign and disease where it occurs

Name of the sign and disease where it occurs

Strawberry tongue


Kawasaki disease (think of children who like strawberries)




Note also the fissuring lips that is another sign of Kawasaki disease

Most feared complication of Kawasaki disease

Coronary arteritis

What organs are typically affected by Kawasaki disease?

All

Treatment of Kawasaki disease (2)?

Aspirin


IV Ig

5 clinical features of Kawasaki disease

Strawberry tongue


Fissuring/Crusting lips


Fever


Conjunctivitis


Lymphadenopathy


Palmar erythema and dry hands

Significance of raised ANCA?

Small vessel vasculitis, mostly


Granulomatous polyangiitis


Microscopic polyangiitis



What does ANCA stand for?

Anti-neutrophil cytoplasmic antibody

Name two types of ANCA and their significance in diagnosis of small vessel vasculitis

cANCA – Granulomatous Polyangiitis


pANCA – Microscopic Polyangiitis




(think of proximity of letters in the alphabet)

How does granulomatous polyangiitis present?

Classic triad


Upper airway – sinusitis/otitis media unresponsive to treatment


Lower airway – pulmonary haemorrhage


Renal disease – Glomerulonephritis

What investigations would you consider in a patient with granulomatous polyangiitis (4)?

ESR/CRP


cANCA


CXR


CT sinuses

What marker correlates with activity of disease in granulomatous polyangiitis?

cANCA

Treatment of granulomatous polyangiitis

Steroids


Cyclophosphamide




(like Takayasu, PAN and microscopic polyangiitis)

Treatment of microscopic polyangiitis

Steroids


Cyclophosphamide




(like Takayasu, PAN and granulomatous polyangiitis)

Treatment of the following vasculitides:


GCA


Takayasu


PAN


Kawasaki


Granulomatous polyangiitis (gPA)


Microscopic polyangiitis (mPA)


ANCA negative small vessel vasculitides

GCA


Steroids




Takayasu, PAN, gPA, mPA


Steroids


Cyclophosphamide




Kawasaki (think kids)


Aspirin


IV Ig




ANCA negative


Consider steroids

Besides the classic triad, what other organ may be affected by granulomatous polyangiitis?

Skin (gange


Joints


Neuro

How does microscopic polyangiitis present?

Renal disease


Pulmonary haemorrhage


Gangrene


Stroke and MI


Bowel infarcts

Compare gPA and mPA in terms of their impact on lungs, URT, kidneys, joints, skin, histology, CV, GI

Demographics most affected by Henoch-Schonlein purpura

Children

3 main symptoms of Henoch-Schonlein purpura and main complication

Symptoms


Purpura


Arthralgia


Abdominal pain




Main complication


Renal failure

What class of antibodies causes Henoch-Schonlein?

IgA

Pathogenesis of Henoch-Schonlein?

Immune complexes deposition containing IgA

Pathogenesis of cryoglobulinaemia

Cryoglobulins are proteins that precipitate at low temperatures blocking blood vessels

How does cryoglobulinaemia present? What other disease presents similarly? How do they differ?

Purpura, Arthralgia, Glomerulonephritis




Similar to Henoch-Schonlein purpura but


1) CG mostly affects adults while HSP mostly affects kids


2) CG does not present with abdo pain


3) CG is often caused by Hep C



What causes cryoglobulinaemia?

Usually Hep C

A patient presents with vasculitis and asthma and eosinophilia. Diagnosis?

Churg-Strauss sydnrome

Which vasculitis can be caused by Hep C?

Cryoglobulinaemia

Which vasculitis is associated with asthma?

Churg-Strauss syndrome

Which vasculitis occurs in children and associated with abdo pain?

Henoch-Schonlein purpura

RF for gout (7)

Unmodifiable


Male


Family history




Production ➚


Alcohol


Polycytaemia rubra vera


Haemolysis


Surgery


Rich diet (red meat)


Chemotherapy




Excretion ➘


Alcohol


Renal failure


Diuretics (thiazide)


Dehydration

3 clinical features of gout

Monoarthropathy (acute)


Renal impairment (uric acid stones and Calcium oxalate stones)


Skin tophi

Where do skin tophi occur in gout (2)?

Extensor tendons and tip of ear

Extensor tendons and tip of ear

Investigation in gout (1)

Joint aspirate


Needle shaped crystals with negative birefringement

Treatment of gout:


Acute – 1st, 2nd and 3rd line


Long-term

Acute


NSAIDs


Colchicine


Steroids (local or systemic)




Long-term


Allopurinol

What should we be careful about when giving allopurinol?

It may initially precipitate symptoms so give with colchicine or NSAIDs for first 6 weeks

Characterise and distinguish the presentations of polymyositis and dermatomyositis

Polymyositis


Proximal muscle weakness




Dermatomyositis


Polymyositis + Rash

Pathogenesis of polymyositis and dermatomyositis

Polymyositis


T–cell infiltration in muscles




Dermatomyositis


T–cell infiltration in muscles


Antibody and complement deposition in the skin

Investigation of polymyositis and dermatomyositis and how these relate to pathogenesis (3)

CRP/ESR ➚


Creatine kinase ➚ (due to muscle damage)


ANA +ve (in 50% of patients)


Anti–Jo1 +ve (if lung involvement)


Muscle biopsy

3 rashes in dermatomyositis

Shawl-like rash
Lilac-coloured rash (mostly around eyes)
Gottron's papules (raised erythema over MCP and PIP)

Shawl-like rash


Lilac-coloured rash (mostly around eyes)


Gottron's papules (raised erythema over MCP and PIP)


Linear erythema on fingers



Besides the rash, what do patients with dermatomyositis complain of?

Profound proximal weakness with little pain


Examples: difficulty putting up laundry, combing hair, getting out of chair, going up the stairs

Treatment of dermatomyositis

Steroids (IV if severe)

How does polymyalgia present?

A bit like fibromyalgia but more focal and with low-grade fever and anaemia

T/F: The diagnosis of osteoporosis is based on a z-score < -2.5

False: the diagnosis is based on difference with bone mass density at peak age (t-score) rather than at similar age (z-score)

BMD on DXA shows a t-score of -2.2. Diagnosis?

Osteopenia


Anything between -1.0 and -2.5

Disease

Disease

Scleroderma

What is definitely affected in scleroderma? What is variably affected?

Definitely – Skin (Thickening and fibrosis)


Variably – Internal organ




Exception: scleroderma sine scleroderma (only organs)

Incidence of scleroderma

Very rare (20/1,000,000/year)

Distinguish limited and diffuse scleroderma in terms of:


Skin involvement


Raynaud's phenomenon onset


Pulmonary fibrosis


Pulmonary hypertension


Renal crisis


Antibody present



Name the 3 organ most commonly affected by limited and diffuse scleroderma alike

Hands, Raynaud's phenomenon (95%)
Skin (90%)
Oesophagus (80%)

Hands, Raynaud's phenomenon (95%)


Skin (90%)


Oesophagus (80%)

First symptom of scleroderma

Raynaud's phenomenon

Sequence of colour change in Raynaud's

White, Blue, Red

4 triggers of Raynaud's phenomenon

Cold


Change in temperature


Stress


Vibration



Raynaud's phenomenon

Characterise the skin disease in scleroderma (distribution, initial presentation, later presentation)

Symmetrical


Initially: oedema


Later: fibrosis with subcutaneous atrophy

Name two skin complications of scleroderma

Ulcers at end of fingers (very painful)


Depigmentation

Facial scleroderma

Name 5 clinical features of scleroderma

CREST


Calcinosis (deposition of Ca in the skin)


Raynaud's
Esophegeal dysfunction
Sclerodactyly (skin thickening in fingers)
Telangiectasia

Why is calcinosis concerning in scleroderma?

Why is calcinosis concerning in scleroderma?

Because it may damage a nerve

What might you hear on auscultation of the lungs in scleroderma?

Bibasal inspiratory 'Velcro' crepitations


indicating pulmonary fibrosis (hence more likely in diffuse scleroderma)

What might you see on pulmonary function test in scleroderma?

FVC ➘➘


FEV1 ➘


FEV1/FVC > 0.8


Diffusion capacity ➘

What oesophageal symptoms occur in scleroderma?

Dysphagia and dyspepsia

Besides oesophagus, what GI disease occur in scleroderma (3)

Delayed motility


Fibrosis ⟹ Decreased colonic flexibility ⟹ diverticula


Anorectal dysfunction ⟹ Faecal incontinence

Why might a patient with scleroderma have malignant hypertension? What is the prevalence of this condition?

Renal crisis (20% of patients with scleroderma)

Strategy for the management of scleroderma

Symptomatic and aim to treat complications


(Immunosuppression has no effect)

T/F: Immunosuppression is effective in scleroderma

False

Treatment of Raynaud's phenomenon (4 steps)

1) Cold avoidance (gloves & hat)


2) Oral vasodilator


a) CCB (Amlodipine or nifedipine)


b) ACEI


3) IV vasodilator


4) Sympathectomy

Treatment of pulmonary fibrosis in scleroderma

IV cyclophosphamide

Treatment of renal crisis in scleroderma

ACEI


Renal replacement therapy if necessary

Patient has dry eyes and dry mouth. He has a PMH of SLE. What is the likely diagnosis?

Sjögren's syndrome

Pathogenesis of Sjögren's syndrome

Lymphocytic infiltration of glandular organs

Demographics most affected by Sjögren's

50 yo female

Serology of Sjögren's

ANA +ve ➙ Anti Ro/La

Particular severe complication of Sjögren's

Lymphoma (x 40)


Lifetime risk 8%

Treatment of Sjögren's

Lubricants (eg eye drops)


NSAIDs


HCQ

Serology in scleroderma

Anti-Scl70 (diffuse)


Anti-centromere (limited)

Clinical sign of pulmonary hypertension (as useful in limited scleroderma)

Raised JVP with cannon a-waves

Besides examination and LFT, what other investigation may you organise for a patient with scleroderma and respiratory symptoms?

Echocardiogram to check for right-sided heart failure

Significance of positive RNP in lupus

Worse prognosis

Significance of anti-histone antibodies in lupus

Likely drug-induced lupus

One possible sign of GCA on ophthalmoscopy

Pale retina due to ischaemia

What do you examine for in suspected GCA

Temporal artery tenderness


Facial artery tenderness (1/3 on mandibular edge from ear)

72 year old lady had headache and pain when combing. On further questioning she tells you that she also has muscle fatigue when chewing. Bloods reveal raised CRP. Temporal artery biopsy is negative. Likely diagnosis?

GCA – Negative biopsy may be due to skip lesions

Pattern recognition


Claudication in a young (20s-30s)

Takayasu

Pattern recognition


Pulseless

Takayasu

One sensitive sign of Takayasu

Subclavian bruit

Distinguish appearance of Takayasu and atheroma on angiogram

Much neater and symmetrical over a cross section of the artery than atheroma and with lots of collateral vessels because patients are otherwise young and healthy

T/F: PAN may present with synovitis

False, only arthritis

Patient is not cold. Name the sign and 2 differentials

Patient is not cold. Name the sign and 2 differentials

Livedo reticularis


SLE (antiphospholipid syndrome)


PAN

Impact of PAN on:


Muscle


Joints


Skin


Nerve


Lung


Kidney


GI


GU

Muscle – Myalgia (but not myositis)


Joints – Arthritis (but no synovitis)


Skin – Livedo reticularis


Nerve – Mononeuritis Multiplex


Lung – None


Kidney – Failure


GI – Mesenteric ischaemia


GU – Orchitis (sterile)

How does Mesenteric ischaemia present?

Pain after meal

What does cANCA and pANCA refer to?

Cytoplasmic ANCA
Perinuclear ANCA
The difference can be visualised on microscope.

Cytoplasmic ANCA


Perinuclear ANCA


The difference can be visualised on microscope.

What part of the body is best at distinguishing granulomatous polyangiitis from microscopic polyangiitis? How?

Nose – Affected only in GPA


Epistaxis, nasal crusting, discharge, collapsed nose septum

3 ΔΔ for collapsed nose septum

3 ΔΔ for collapsed nose septum

GPA


Cocaine use


Congenital syphilis

Why may patients with granulomatous polyangiitis have deafness?

Conductive – Upper airway disease


Sensory – Mononeuritis multiplex

Pattern recognition


Adult onset asthma

Churg-Strauss

Pattern recognition


Palpable purpura, sky high Rheumatoid factor

Cryoglobulinaemia (RF is even higher than in RA)

Name of the sign. In what disease does it occur?

Name of the sign. In what disease does it occur?

Hyperaemic nail bed


Dermatomyositis

Besides the rash and muscle weakness, what other two features may be present in dermatomyositis

GI


Dysphagia (indicates a bulbar involvement and may cause aspiration)




Lung


Diaphragmatic weakness causing orthopnoea


Interstitial lung disease (if ANA +ve – Anti-Jo1) ➙ Very poor prognosis

3 investigations and their results in dermatomyositis

ESR/CRP ➚


CK ➚


ANA +ve (Jo-1)

Most common rheumatological disease in kids

Juvenile idiopathic arthritis

At what ages does juvenile idiopathic arthritis (JIA) develop?

Before 16

Outline the ILAR classification of JIA (6). Which is most common?

◾ Systemic onset JIA (SOJIA)


◾ Oligoarticular (persistent or extended) – Most common


◾ Polyarticular (RF + or -)


◾ Psoriatic


◾ Enthesitis related


◾ Undifferentiated

Define diagnosis of systemic JIA

Arthritis with or preceded by a fever and accompanied one or more of:


◾ Evanescent rash (ie transient)


◾ Lymphadenopathy


◾ Hepatosplenomegaly


◾ Serositis

What defines oligoarticular JIA?

≤ 4 joints affected for the first 6/12 regardless of the number of joints eventually affected

3 year old girl has arthritis in the left ankle, right knee and left hip which has been symptomatic for 2/12. Likely diagnosis (as precise as possible)

Oligoarticular JIA

4 year old girl has had arthritis in the left ankle, right knee and left hip which has been symptomatic for 2/12 last year. She now presents with a 1/12 history of arthritis in most joints. Likely diagnosis (as precise as possible)

Extended oligoarticular JIA




(It is still oligoarticular JIA since what matters is the first 6/12 but is called extended because more joints are now affected)

Serology of JIA

Oligoarticular


ANA + or -




Polyarticular


RF + or -

3 RF for chronic anterior uveitis in oligoarticular JIA

ANA +ve


Girls


< 8 years

3 complications of anterior uveitis

Cataract


Glaucoma


Cystoid macular oedema

4 year old girl has had arthritis in most joints of the lower limbs for 2/12 . Likely diagnosis (as precise as possible)

Polyarticular JIA

Which joints are affected in polyarticular JIA and how does age influence this?

Younger ⟹ Large joints


Older ⟹ Small joints

3 year old girl has arthritis in the left ankle, right knee and left hip which has been symptomatic for 2/12. Her mother has psoriasis. Likely diagnosis (as precise as possible)

Oligoarticular JIA

3 year old girl has arthritis in the left ankle, right knee and left hip which has been symptomatic for 2/12. O/E, there is nail pitting. Her mother has psoriasis. Likely diagnosis (as precise as possible)

Psoriatic JIA

Define the diagnosis of psoriatic JIA

A) Arthritis with psoriasis


B) Arthritis and ≥ 2 of:


◾ Dactylitis


◾ Nail pitting/Onycholysis


◾ Psoriasis in first degree relative

T/F Psoriatic JIA involves that the patient has psoriasis

F: patient can also have ≥2 of dactylitis, nail pitting/onycholysis, psoriasis in first degree relative

Define the diagnosis of enthesitis related JIA

A) Arthritis with enthesitis


B) Arthritis with ≥ 2 of:


◾ HLA B27


◾ First degree relative HLA B27


◾ Sacro-iliac joint tenderness or inflammatory spinal pain


◾ Anterior uveitis


◾ Boy > 8

In what JIA can anterior uveitis occur?

Oligoarticular JIA


Enthesitis-related JIA

Main complication of JIA

Leg length discrepancy

3 causes of acute joint swelling in a child

Trauma


Sepsis


ReA

5 causes of chronic joint swelling in a child

JIA


Other inflammation (sarcoid, SLE...)


Malignancy


TB


Haemophilia

What is the key in the management of JIA to achieve good outcome?

Diagnose early

Medication ladder for JIA

NSAIDs


Corticosteroids (injection or oral)


MTX and other DMARDs


Biologics

Indications for MTX in JIA

Either of:


Recurrent joint injections


Polyarticular JIA


Uncontrolled eye disease

What biologics would you use in JIA

Anti-TNF (Etanercept or adalimumab)


Anti-IL6 (Tocilizumab) for SOJIA

How is uveitis diagnosed and managed in JIA?

Screen every 3/12 (as it may be asymptomatic)


Managed with topical steroids and MTX


Multi-disciplinary team

Name 6 polyarticular disease that may occasionally present as monoarthritis

PsA


IBD


ReA


RA


JIA


Viral arthritis

What organisms causing septic arthritis are most aggressive?

Gram positive bacteria (eg staph, strep)

Seven questions to ask in history of monoarticular disease and their significance

A) HPC


Onset of pain?


◾ Sec - Min: trauma


◾ Hrs-Days: infection, crystal, inflammatory conditions, palindromic RA


◾ Days-Wks: mycobacteria, fungi, OA, tumour




Joint damage/overuse?




Other symptoms: rash, low back pain, diarrhoea, urethral discharge, conjunctivitis, mouth sores? (ReA, PsA, IBD)




Risk of infections (eg IVDU)?




B) PMH


History of similar episode in other joints?(crystals, inflammatory joint syndromes)




History of bleeding? Use of anticoagulants? (Haemarthrosis)




C) DH


Prolonged steroid use? (infection or osteonecrosis)



T/F: fever with monoarthritis means septic arthritis

No, many inflammation of the joint can present with fever and septic arthritis may present without

Pattern recognition


Polyarticular migratory arthritis that then settles into one joint

Gonococcal septic arthritis

Pattern recognition
Monoarthritis with tender pustular lesions on an erythematus base and haemorrhagic papules

Pattern recognition


Monoarthritis with tender pustular lesions on an erythematus base and haemorrhagic papules

Gonococcal septic arthritis

Single most useful diagnostic study in the initial evaluation of monoarthritis

Synovial fluid analysis

4 reasons to do synovial fluid analysis in a patient with monoarthritis

1) Confirm diagnosis of septic arthritis and identify organism


2) Confirm and treat crystal arthritis


3) Confirm haemarthrosis


4) Distinguish inflammatory from non-inflammatory arthritis

What is arthrocentesis?

Joint aspiration

T/F: The following presentation rules out septic arthritis: patient presents with monoarthritis and joint aspirate reveals many negatively birefringent crystals.

False: gout may coexist with infection

Besides synovial fluid analysis, name 2 investigations that are almost always indicated in monoarthritis

1) Radiograph of the joint
2) FBC (mostly for WCC)

T/F: serum uric acid level is a relatively good marker of gout

False: it is notoriously useless

You suspect septic arthritis in a patient but you could not confirm it clinically. You have just sent blood and synovial fluid for cultutre. What do you do now?

Start treating as if it was septic arthritis until culture results come back

Name 5 chronic monoarticular arthritis (4 inflammatory and 1 non-inflammatory)

Inflammatory


TB


Fungal


Spondyloarthropathies


RA (monoarticular presentation)




Non-inflammatory


OA

Synovial fluid analysis in OA

Normal (non-inflammatory)

Besides adult onset asthma, name one symptom of Churg Strauss

Nasal polyp

Painful hands and knees with morning stiffness and history of miscarriages

SLE

What defines antiphospholipid syndrome?

Antiphospholipid antibody positive and symptoms (DVT, PE)

Impact of MTX on the lung. When can it occur?

Pneumonitis (inflammation of the walls of the alveoli)


Present with: very dry cough, terrible exercise tolerance (Sats fall to 50% when walking for 200m), very rapid onset




Can occur at any stage of the course of MTX

Two most specific features of RA on Xray

Erosion


Periarticular osteopenia

What part of LFT are you interested in when patients are on MTX?

ALT and AST (both can go up)

How are DMARDs most commonly administered

Subcut

T/F: When biologics are started, DMARDs can be stopped.

False: DMARDs protect the biologic agent and so should be taken alongside. If DMARD was not tolerated (a valid reason to start biologics), then keep them at a low dose (10mg) just to keep the biologic protected.

In which disease is HCQ not indicated?

PsA as it causes more skin problems

First question to ask in acute monoarthritis?

Are you otherwise well (to investigate septic arthritis)

When is "Rash? Bowel? Eyes?" most useful?

In seronegative arthritis

What is important to ask about the diet in gout?

Red meat
Shellfish

Three drugs to ask about in history of gout

Aspirin


Thiazide diuretics


Chemo

Management of septic arthritis

Theatre, wash out, broad-spectrum ABx

First question to ask in a patient in whom you suspect AS

Family history

Four extra-articular features of ankylosing spondylitis

Aortic Regurgitation


Apical Scarring (fibrosis)


Achilles Tendinitis


Anterior Uveitis

One investigation of choice in AS

T2w MRI

T/F: DMARD are useless for axial disease (eg AS)

True

What might you see in the hands of a patient with dermatomyositis (3)?

Gottron's papules (raised erythema over MCP and PIP)


Linear erythema on fingers


Mechanical hands

Sausage-like fingers

RA – Rheumatoi nodules



RA (Early stage) – Active synovitis



Psoriatic arthritis – Sausage-like fingers and destroyed nails



Scleroderma

Why might a patient with dermatomyositis be SOB?

Aspiration (oesophageal involvement)


Diaphragmatic paralysis


Interstitial lung disease (if anti-Jo-1 positive)

Besides blood tests, name 2 tests that you might consider in dermatomyositis

T2w MRI of the most affected part and biopsy



EMG (outdated but still in textbooks)

What separates diffuse from limited scleroderma in terms of skin involvement

Above the elbow ⟹ Diffuse

pGALS: 3 screening questions to ask

Do you have any pain or difficulty in moving your arms, legs, neck or back?




When you get dressed, are you able to do this yourself without any help?




Can you walk up and down the stairs without any problems?

pGALS: what is the 3 fingers in the mouth test used for?

Temporomandibular joint disease

5 broad causes of limping and how they can be differentiated clinically

LIMPS




Leg length discrepancy


Equal time spent on each limp




Incoordinated


Abnormal rhythm and controlled falls



Muscle weakness


Hip - Trenderlenberg's sign


Knee – Weak quads


Ankle – Lifts foot high in the air to avoid tripping




Pain


Shorter time spent on painful limb




Stiffness


Hip – Sway back and fort and hoist pelvis up


Knee – Swing leg out to the side


Ankle – Foot rocks forward from heel to toe