Q: Describe The Diagnostic Criteria & Lab Investigation of SLE. Ans

DR.HASNAT JAKI CHOWDHURY, Question bank By DR.
ABIR BIN SAJJ
Q: Describe the Diagnostic criteria & Lab Investigation of SLE.
Ans :
Diagnostic Criteria of SLE:
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DR.HASNAT JAKI CHOWDHURY, Question bank By DR.ABIR BIN SAJJ
Investigations :
The diagnosis is based on a combination of clinical features and laboratory abnormalities.
Checking of ANAs,
antibodies to ENAs and complement,
routine haematology,
biochemistry and
urinalysis are mandatory.
Q: Note down The CNS Manifestation of SLE.
Ans:
CNS Manifestation of SLE:
 Ischemic Stroke  Fatigue,
 Headache and
 Hemorrhagic stroke
 Poor concentration are common
 Headache
and often occur in the absence of
 Seizure laboratory evidence of active
 Acute confusional state disease.
 Psychiatric symptoms More specific features of cerebral lupus
 TIA include
 Abnormal movement  Visual hallucinations,
 Transverse mylitis  Chorea,
 Aseptic meningitis  Organic psychosis,
 Cavernous sinus  Transverse myelitis and
 Thrombosis  Lymphocytic meningitis
 Recurrent stroke
 Memory disturbance
Q:Note down The Cutaneous & GI Manifestation of SLE:
Ans:
Cutaneous Manifestation :
The skin is commonly involved in SLE, and many SLE skin eruptions are precipitated by
exposure to ultraviolet light. The main types of skin involvement are:
• Malar rash : The classic facial rash (up to 20% of patients). This is erythematous,
raised and painful or itchy, and occurs over the cheeks with sparing of the nasolabial folds.
Rosacea is a mimic of this rash.
• A discoid rash characterised by hyperkeratosis and follicular plugging, with scarring
alopecia if it occurs on the scalp.
• Diffuse, usually non-scarring alopecia, which may also occur with active disease.
• Urticarial eruptions.
• Livedo reticularis , which is also a feature of antiphospholipid syndrome and can
become frankly vasculitic.
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GIT manifestation :
 Mouth ulcers may occur and may or may not be painful.
 Peritoneal serositis can cause acute pain.
 Mesenteric vasculitis is a serious complication, which can present with abdominal pain,
bowel infarction or perforation.
 Hepatitis is a recognised, though rare, feature
Q:Discuss the Adverse effect of Cyclophosphamide and

Hydroxychloroquine . How will you evaluate its retinal toxicity?
Ans: [Ref: From Katzung ]

Adverse effect of Cyclophosphamide :
 Leukopenia,
 thrombocytopenia,
 anemia
 High doses can be cardiotoxic and sterilty may occur after chronic dosing at
anti-rheumatic doses, especially in women.
 Bladder cancer is very rare but must be looked for, even 5 years after
cessation of use.
Advarse effect of Hydroxychloroquine :
 Dyspepsia,
 Nausea,
 Vomiting,
 Abdominal pain,
 Rashes,
 Nightmares.
 Ocular toxicity
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Q: What are the diagnostic criteria of Rheumatoid arthritis?

Mentation the ocular manifestation of Rheumatoid arthritis.
Ans:
Rheumatoid arthritis (RA) is a common form of inflammatory arthritis.
Ocular Manifestation :
 Keratoconjunctivitis sicca
 Episcleritis
 Scleritis
 Scleromalacia
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Q: What are the Extra articular manifestation of RA?
Ans :
C/F Of Rheumatoid arthritis :
1. Articular :
a. Pain
b. Morning Stiffness
c. Swelling
d. Involve small joints of both hand and feet
e. Symmetrical
f. Joint Deformity ( Hand- swan neck Deformity, ‘button hole’ deformity,
Trigger finger ; Foot - cock-up’ toe deformities, flat foot,
2. Extra articular :
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Q: Enumerate the causes of anaemia in RA

Ans : [Ref :- KELLEY & FIRESTEIN’S Textbook of Rheumatology Tenth Edition ,Page 1180 ]
Causes of anaemia in RA:
Hematologic abnormalities are common in patients with autoimmune disease, and RA
is no exception. Patients with RA frequently manifest a mild normocytic normochromic anemia
that tends to correlate with increased disease activity and elevated inflammatory markers.
Patients with chronic inflammation have an increased synthesis of ferritin and hemosiderin,
abnormal retention of iron from senescent red blood cells, and increased lactoferrin, ultimately
contributing to the binding and lowering of serum iron. Although mild anemia is common, the
presence of more severe anemia (i.e., hemoglobin <10 g/ dL) suggests an alternative etiology.
Mixed anemia poses a frequent diagnostic challenge in RA.
In addition to its utility in evaluating causes of anemia, ferritin is an acute phase reactant and is
therefore affected by inflammation. In general, however, a serum ferritin less than 50 ng/mL is
indicative of iron deficiency, whereas values exceeding 100 ng/mL are indicative of adequate
iron stores, regardless of RA disease activity.
Q: Enumerate the DMARDs for treating RA. Make a checklist of

information before starting DMARDs in RA.
Ans :
DMARDs Used in Rheumatoid arthritis :

DMARDs therapy should be introduced in all patients of RA as this improves outcome. The
DMARDs are as followes :
a. Non biological : [ Ref: Davidson’s Principles and Practice of 23rd Edition;Page 1026 ]
1. Sulfasalazine,
2. Hydroxychloroquine
3. Azathioprine
4. Methotrexate,
5. Leflunomide,
6. Cyclophosphamide,
7. Mycophenolate
b. Biological : [ Ref :-Katzung Basic & Clinical Pharmacology Twelfth Edition;Page 643 ]
There are also several biologic DMARDs marketed for rheumatoid arthritis:
 T-cell-modulating biologic (abatacept),
 B-cell cytotoxic agent (rituximab),
 anti-IL-6 receptor antibody (tocilizumab),
 TNF-α-blocking agents
Checklist of information before starting DMARDs :

Before starting DMARDs, all patients should have baseline blood tests including full blood
examination, serum creatinine and liver enzymes. Abnormalities may alter the choice of
therapy and dosing (e.g. methotrexate is renally excreted). All patients should be screened for
hepatitis B virus, hepatitis C virus and tuberculosis as there is a risk of reactivation of latent
infections or worsening of active infection.
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Other important considerations include congestive heart failure, malignancy,

lymphoproliferative disease, multiple sclerosis, chronic obstructive pulmonary disease,
bronchiectasis and interstitial lung disease. Further evaluation is required before treatment.
Q: How will you educate a newly diagnosed patient with RA?
Ans : Nonpharmacologic therapies include treatments other than medications and are the
foundation of treatment for all people with rheumatoid arthritis. There are a wide variety of
nonpharmacologic therapies available.
Education and counseling — Education and counseling can help to better understand the
nature of rheumatoid arthritis and cope with the challenges of this condition.
Nonpharmacologic measures such as biofeedback and cognitive behavioral therapy may help
in controlling rheumatoid arthritis symptoms. These measures can reduce pain and disability
and improve self-esteem.
Rest — Fatigue is a common symptom of rheumatoid arthritis. Inflamed joints should be
rested, but physical fitness should be maintained as much as possible. Several studies have
shown that physical fitness improves the quality of sleep, which in turn helps with fatigue. The
advice of physical and occupational therapists should be sought for help with fitness programs
if joint pain or limited joint motion interferes with exercise activities.
Exercise — Pain and stiffness often prompt people with rheumatoid arthritis to become
inactive. Unfortunately, inactivity can lead to a loss of joint motion, contractions, and a loss of
muscle strength. Weakness, in turn, decreases joint stability and further increases fatigue.
Regular exercise can help prevent and reverse these effects . Several different kinds of
exercise can be beneficial, including range-of-motion exercises to preserve and restore joint
motion, exercises to increase strength (isometric, isotonic, and isokinetic exercises), and
exercises to increase endurance (walking, swimming, and cycling).
Physical and occupational therapy — Physical and occupational therapy can relieve pain,
reduce inflammation, and help preserve joint structure and function for patients with rheumatoid
arthritis.
Specific types of therapy are used to address specific effects of rheumatoid arthritis:
●The application of heat or cold can relieve pain or stiffness.
●Ultrasound may reduce inflammation of the sheaths surrounding tendons (tenosynovitis).
●Passive and active exercises can improve and maintain range of motion of the joints.
●Rest and rest splinting can reduce joint pain and improve joint function.
●Finger splinting and other assistive devices can prevent deformities and improve hand
function.
●Relaxation techniques can relieve secondary muscle spasm.
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Nutrition and dietary therapy — People with active rheumatoid arthritis sometimes lose their
appetite or are unable to eat an adequate amount of food. Dietary therapy helps to ensure that
you eat an adequate amount of calories and nutrients. However, weight loss may be
recommended for overweight and obese people to reduce stress on inflamed joints
People with rheumatoid arthritis have a higher risk of developing coronary artery disease. High
blood cholesterol is one risk factor for coronary disease that can respond to changes in diet. A
nutritionist can recommend specific foods to eat or avoid to achieve a desirable cholesterol
level.
Smoking and alcohol — Several different studies have shown that smoking is a risk factor for
rheumatoid arthritis and that quitting smoking can improve disease. People who smoke need to
quit completely
Measures to reduce bone loss — Rheumatoid arthritis causes bone loss, which can lead to
osteoporosis. Bone loss is more likely in people who are inactive. The use of glucocorticoids,
such as prednisone, further increases the risk of bone loss, especially in postmenopausal
women
Several measures can minimize the bone loss associated with steroid therapy :
●Use the lowest possible dose of glucocorticoids for the shortest possible time, when
possible, to minimize bone loss.
●Consume an adequate amount of calcium and vitamin D, either in the diet or by taking
supplements.
●Use medications that can reduce bone loss, including that which is caused by
glucocorticoids.
Q: What are the indication of steroid in Ankylosing spondylitis?

Ans:
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Q: Mantion 3 Disease under the heading of spondarthritidis ?

What are the extra articular manifestation of Ankylosing
Spondylitis?
Ans: : [ Ref: Davidson’s Principles and Practice of 23rd Edition;Page ]

3 Spondarthritidis are :
 Axial spondyloarthritis  Psoriatic arthritis arthritis with
inflammatory bowel disease
 Ankylosing spondylitis (enteropathic spondyloarthritis)
 Reactive arthritis
Extra articular manifestation of Ankylosing Spondylitis are :

 Fatigue, anaemia  Osteoporosis
 Anterior uveitis (25%)  Cardiovascular disease (aortic
 Prostatitis (80% of men) and sterile valve disease 20%)
urethritis  Amyloidosis (rare)
 Inflammatory bowel disease (up to  Atypical upper lobe pulmonary
50% have IBD lesions) fibrosis (very rare)
Q: What are the common collagen disease?

What investigations needed for diagnosis of AS?
Ans:
Common collagen disease are
 Lupus,  Osteogenesis imperfecta or brittle
 Scleroderma, bone disease
 Rheumatoid arthritis  Stickler syndrome
 Alport syndrome  sjogren’s syndrome
 Ehlers-danlos syndrome  Psoriatic arthritis
 Marfan syndrome
Investigation for AS
A. X-rays of the sacroiliac joint : show
 Irregularity and loss of cortical margins,
 Widening of the joint space and subsequently sclerosis,
 Joint space narrowing and fusion.
B. Lateral thoracolumbar spine X-rays : Show
 Anterior ‘squaring’ of vertebrae
 Bridging syndesmophytes
C. X ray Lumbosacral spine show
 Bamboo’ spine
 Erosive changes may be seen in the symphysis pubis, ischial tuberosities and
peripheral joints
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D. MRI is more sensitive for detection of early sacroiliitis than X-rays

E. ESR and CRP are usually raised in active disease but may be normal;
F. Hb% - anaemia is often present.
G. Autoantibodies, such as RF, ACPA and ANA, are negative
Q: Enumerate the role of HLA B-27 in Rheumatoid arthritis.
Q: Mention 3 disease related to HLA B-27.
Ans : ref- wiki

Diseases associated with the HLA-B27 subtype can be remembered with the
mnemonic PAIR, and include
Psoriasis,
Ankylosing spondylitis,
Inflammatory bowel disease,
Reactive arthritis.
Q: Write the difference between granulomatous & non –

granulomatous uveitis? What are the signs of acute anterior
uveitis?
Ans :
Difference between granulomatous & non –granulomatous uveitis: ref- NET
Traits Granulomatous uveitis Non-granulomatous uveitis

Aetiology Organism invasion Ag Ab reaction
Course
Onset Insidious Acute
Duration Chronic Short
Inflammation Moderate Sever
Pain Minimal Marked
Photophobia Slight Marked
Ciliary congestion Minimal Marked
Pathology
Lesion Circumscribed Diffuse
Iris Focal reaction Diffuse reaction
KP Mutton fat Fine plenty
Iris adhesion Coarse, few, thick Fine ,plenty, thin
Investigations May be positive Negative
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Acute anterior uveitis : Ref- prof. Shamsul haque ; page- 241

Symptoms :
1. Pain in the eye
2. Photophobia
3. Redness
4. Lacrimation
5. There may be decreased vision
Symptoms :
1. Visual acuity is usually good except in sever cases.
2. Ciliary congestion – congestion is more marked around the cornea.
3. Miosis – due to spasm of the Sphincter pupillae.
4. Keratic precipitates – deposition of inflammatory cells over the endothelial surface of the
cornea is known as KP. In acute anterior uveitis , there is endothelial dustings consisting
of numerous neutrophils
5. Cells – inflammatory cells present in the aqueous humour.
6. Flares – excess amount of protein present in aqueous humour.
7. Hypopyon – present in anterior chamber
8. Hyphaema – may be present in anterior chamber.
Q: Write down the treatment of uveitis in different rheumatoid

disease.
Ans : ref- Prof. Shamsul haque; page 217

Uveitis is common feature in many rheumatoid disease. So treatment should be according to
causes.
Treatment of uveitis in different rheumatoid disease:

1. Topical mydriatics and cycloplegic :
Atropin (1%) eyedrop- 6/8/12 hrly depending on the severity of disease for 2-3
weeks
2. Steroid
a. Topical
i. Fluromethanol - 1 drop ½ /1/2 hrly depending on the severity of disease
for 2-3weeks .
b. Periocular injection :
i. Methylprednisolone / triamcinolone 30-40 mg
c. Intra- vitreal injections :
i. Triamcinolone 4 mg in 0.1 ml
3. Systemic immune suppressive :
a. Anti-metabolite ;
i. Azathioprine – 1mg/ kg body wt/ day
ii. Methotrexate – 10-15 mg/ wk
b. Immune modulators
i. Cyclosporine
4. Specific treatments for underlying disease:
As uveitis occur in various rheumatoid disease, so treatment of those disease is
necessary . diseases are
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 Juvenile idiopathic arthritis

 Ankylosing spondylosis
 Systemic lupus erythematosus
 Sarcoidosis
 Reiter’s syndrome
 Polychondritis
5. Hot compression
6. Use dark glass
Q: What is scleritis? Classify it.
Ans: ref- Prof Shamsul alam; page 170

Scleritis: Inflammation of the sclera due to any causes is known as scleritis. Scleritis is
characterized by oedema and cellular infiltration of the entire thickness of the sclera.
Classifications:
Scleritis
Anterior Scleritis posterior

(98%) scleritis (2%)
Non Necrotizing Necrotizing

(85%) (13%)
With without
Diffuse Nodular
inflammation inflammation
Q: What is Iritis? Name the rheumatic disease causing irits?
Ans : ref- Prof Shamsul alam; page 215

Iritis: Inflammation of the iris due to any causes is known as iritis.
Rheumatic disease causing Iritis:

 Juvenile idiopathic arthritis
 Ankylosing spondylosis
 Systemic lupus erythematosus
 Sarcoidosis
 Reiter’s syndrome
 Polychondritis
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Q: What are the adverse effect of steroid overdose?
Ans:
Adverse effect of steroid:
CORTICOSTEROID:
 Burning/itchy skin.  Extreme sleepiness.
 Agitation or psychosis.  Worsening health conditions.
 Convulsions.  Nervousness.
 High blood pressure.  Depression.
 Muscle and bone weakness.  Swelling in the legs.
 Nausea or vomiting.
ANABOLIC STEROID OVERDOSE :
 Kidney/liver damage.  Major mood swings.
 Increased blood pressure.  Aggression and irritability.
 Enlarged heart.  Delusions.
 Dangerous cholesterol changes,  Stunted growth in young users.
even in younger users.
Q: Mechanism of action of Methotrexate?
Ans : Ref- Ketzang ; 12th ed; page- 645

Methotrexate’s principal mechanism of action at the low doses used
in the rheumatic diseases probably relates to inhibition of aminoimidazolecarboxamide
ribonucleotide (AICAR) transformylase and thymidylate synthetase. AICAR, which accumulates
intracellularly, competitively inhibits AMP deaminase, leading to an accumulation of AMP. The
AMP is released and converted extracellularly to adenosine, which is a potent inhibitor of
inflammation. As a result, the inflammatory functions of neutrophils, macrophages, dendritic
cells, and lymphocytes are suppressed. Methotrexate has secondary effects on
polymorphonuclear chemotaxis. There is some effect on dihydrofolate reductase and this affects
lymphocyte and macrophage function, but this is not its principal mechanism of action.
Methotrexate has direct inhibitory effects on proliferation and stimulates apoptosis in immune-
inflammatory cells. Additionally, it has also been shown to have inhibition of proinflammatory
cytokines linked to rheumatoid synovitis.
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Q: Classify vasculitis. Write down the checklist of clinical

features and laboratory findings to diagnose a case of PAN.
Ans:
Vasculitis: Vasculitis is characterised by inflammation and necrosis of blood-vessel walls, with
associated damage to skin, kidney, lung, heart, brain and gastrointestinal tract.
Classification of vasculitis : (Ref- KELLEY & FIRESTEIN’S Textbook of Rheumatology page 1513)
A. Large-vessel vasculitis:
 Takayasu’s arteritis
 Giant cell arteritis
B. Medium-vessel vasculitis:
 Polyarteritis nodosa
 Kawasaki’s disease
C. Small-vessel vasculitis:
 Anti-neutrophil cytoplasmic antibody–associated vasculitis
 Microscopic polyangiitis granulomatosis with polyangiitis
 Eosinophilic granulomatosis with polyangiitis
 Immune complex small vessel vasculitis:
 Anti-glomerular basement membrane disease
 Cryoglobulinemic vasculitis
 Iga vasculitis (henoch-schönlein purpura)
 Hypocomplementemic urticarial vasculitis
D. Variable vessel vasculitis:
 Behçet’s disease
 Cogan’s syndrome
E. Single-organ vasculitis :
 Cutaneous leukocytoclastic angiitis
 Cutaneous arteritis
 Primary central nervous system vasculitis
 Isolated aortitis
F. Vasculitis associated with systemic disease :
 Lupus vasculitis
 Rheumatoid vasculitis
 Sarcoid vasculitis
 Others (e.g., igg4 -related aortitis)
 Vasculitis associated with probable etiology :
 Hepatitis c virus–associated cryoglobulinemic vasculitis
 Hepatitis b virus–associated vasculitis
 Syphilis-associated aortitis
 Drug-associated immune complex vasculitis
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 Drug-associated anca-associated vasculitis

 Cancer-associated vasculitis
 Others
Clinical features of PAN (POLYARTERITIS NODOSA) : (Ref – Davidsons 23rd; page – 1042)
 Fever,
 Myalgia,
 Arthralgia
 Weight loss
 Skin lesions are - palpable purpura , ulceration, infarction and livedo reticularis
 Neuropathy
 Severe hypertension and/or renal impairment
Investigations : (Ref- Davidson 23rd ; page – 1042 + CMDT; page – 864 )

 Angiography (conventional or magnetic resonance )-
o Multiple aneurysms and smooth narrowing of mesenteric, hepatic or renal
systems,
 Muscle or sural nerve biopsy –
o Necrotising inflammation and vessel occlusion
o Arteritis of the vasa nervorum
 CBC :
o Mild anaemia
o Leucocytosis
 Acute-phase reactants
o Strikingly elevated
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 ANCA
o Negative
 Rheumatoid factor
o Low titre
 Antinuclear antibodies
o Low titers
Q: What is giant cell arteritis? Describe the temporal arteritis.
Ans : (Ref- Davidsons 23rd; Page – 1042)

Giant cell arteritis : Giant cell arteritis (GCA) is a granulomatous arteritis that affects any large
(including aorta) and medium-sized arteries.
(Ref- Kaniski 8th; Page – 787)
GCA is a granulomatous necrotizing arteritis with a predilection for large and medium-size
arteries, particularly the major aortic branches and the superficial temporal (STA), ophthalmic,
posterior ciliary and proximal vertebral arteries. The severity and extent of involvement are
associated with the quantity of elastic tissue in the media and adventitia and intracranial
arteries are usually spared as they possess little elastic tissue.
Temporal arteritis:
Symptoms
○ Scalp tenderness, first noticed when combing the hair, is common.
○ Headache, which may be localized to the frontal, occipital or temporal areas
or be more generalized.
○ Jaw claudication (cramp-like pain on chewing), caused by ischaemia of the
masseter muscles, is virtually pathognomonic.
○ Non-specific symptoms such as weight loss, fever, night sweats, malaise and
depression are common.
○ Double vision may occur.
○ Arteritic anterior ischaemic optic neuropathy
Other features
○ Superficial temporal arteritis is characterized by thickened, tender, inflamed
and nodular arteries ,though the signs may be subtle.
○ Pulsation is initially present, but later ceases, a sign strongly suggestive of
GCA, since a non-pulsatile superficial temporal artery is highly unusual in a
normal individual.
○ Ocular motor palsies, including a pupil-involving third nerve palsy, can
manifest.
○ Scalp gangrene may occur in very severe cases.
○ Rare complications include dissecting aneurysms, aortic incompetence,
myocardial infarction, renal failure and brainstem stroke.
Investigation :
For conformation
o Temporal artery biopsy (TAB)
o Colour Doppler and duplex ultrasonography:
 hypoechoic halo around the superficial temporal artery
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Others :
o Erythrocyte sedimentation rate (ESR) is often very high, with a level of >60
mm/hr
o C-reactive protein (CRP) is invariably raised
o Full blood count: elevated platelets and normocytic normochromic anaemia are
commonly present.
o Autoantibodies are normal.
Treatment :
Oral prednisolone ; 1mg/kg/day. Need treatment for 1-2 years.
Q: What is vasculitis? Mention the causes of arteriolar occlusion

in eye.
Ans:
Vasculitis: Vasculitis is characterised by inflammation and necrosis of blood-vessel walls, with
associated damage to skin, kidney, lung, heart, brain and gastrointestinal tract.
Causes of arteriolar occlusion in eye: (Ref- Davidson 23rd ; Page- 1178)

o Atherosclerosis
o Valvular heart disease,
o Arrhythmias and infective endocarditis.
o Vasculitis - mainly giant cell arteritis
OR (Ref- Kanski 8th ; page – 550 )
A. Triad of retinal artery occlusion-

1. Sickling haemoglobinopathies
2. Susac syndrome (retinocochleocerebral vasculopathy),
3. Microangiopathy
B. Thrombophilic disorders-
o Hyperhomocysteinaemia,
o Antiphospholipid antibody syndrome and
o Inherited defects of various natural anticoagulants.
C. Emboli -
o Refractile yellow–white cholesterol (hollenhorst) plaques,
o Greyish elongated fibrin-platelet aggregates ,
o Non-scintillating white calcific particles
o Rarely vegetations from bacterial endocarditis, cardiac myxomatous
material, fat and others
D. Inflammation in or around the vessel wall
o Giant cell arteritis – GCA,
o Systemic lupus erythematosus,
o Wegener granulomatosis,
o Polyarteritis nodosa
D. Vasospasm
Migraine
E. Systemic hypotension contribute in a minority.
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Q: What investigation will you do for diagnosis of mesenteric

vasculitis ?
Ans:
Diagnosis of mesenteric vasculitis :
Q: What are the complication of Takayasu’s arteritis may

present to you? What relevant physical examination &
investigations will you ask for?
Ans:
Takayasu arteritis is characterised by granulomatous inflammation of the vessel wall, leading to
occlusion or weakening of the vessel wall.
Presentation –
 Claudication,
 Fever,
 Arthralgia
 Weight loss.
Physical examination:
 Loss of pulses,
 Bruits,
 Hypertension and
 Aortic incompetence.
Investigations :
 Angiography - reveals coarctation, occlusion and aneurysmal dilatation
 MRI - inflammatory thickening of the walls of affected vessels, or
 CT angiography - images of the stenoses, occlusions, and dilations
characteristic of arteritis.
 C- reactive protein – elevated
 ESR – Elevated
 Anaemia - normocytic, normochromic anaemia
Q: What do you mean by Mononuritis multiplex? Outline the

rheumatological causes of mononeuritis multiplex.
Ans :
Mononeuritis multiplex (Multifocal neuropathy) is characterised by lesions of multiple nerve
roots, peripheral nerves or cranial nerves.
Rheumatological causes :
Mononeuritis multiplex can be associated with the following rheumatologic disorders:
 Wegener granulomatosis
 Henoch-Schönlein syndrome
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 Sjögren syndrome
 Behçet’s disease
 Temporal (giant cell) arteritis
 Systemic lupus erythematosus
 Rheumatoid arthritis
 Polyarteritis nodosa - A retrospective study by Criado et al of 22 cases of cutaneous
polyarteritis nodosa found that a quarter of the patients had mononeuritis multiplex
 Scleroderma
Q: Enumerate the C/F of Myotonic muscular dystrophy.
Ans :
Myotonic dystrophy, a slowly progressive, dominantly inherited disorder, usually manifests itself
in the third or fourth decade but occasionally appears early in childhood.
Clinical features: (Ref - https://jnnp.bmj.com/content/jnnp/81/4/358.full.pdf)

1. Myotonia
2. Ocular :
a. Cataract – Most commonly PSC
b. Ptosis – Due to slow relaxation of Orbicularis oculi muscle
3. Cardiac :
a. Conduction disturbance
b. Tachyarrhythmias
4. Central nervous system –
a. Minor intellectual deﬁcits,
b. Delayed development
5. Gastrointestinal tract
a. Cholecystitis
b. Cholelithiasis
c. Slow gastric emptying (28%)
d. Diarrhoea (50%)
e. Faecal incontinence (30%)
6. Endocrinopathy
a. Disturbances of the thyroid, pancreas, hypothalamus and gonads
b. Testicular atrophy
c. Infertility in men
d. Women, habitual abortion and menstrual irregularities
e. Insulin insensitivity – DM
7. Skin
a. Early frontalbalding
b. Pilomatrixomata
c. Epitheliomas
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8. Respiratory
a. Aspiration pneumonia
b. Myotonia of the diaphragm
9. Psychiatry
a. Anxiety
b. Depression
10. Pregnancy
a. Spontaneous abortion
b. Prolonged labour
c. Retained placenta
d. Postpartum haemorrhage
Q: Describe the extraocular features of Marfan syndrome.
Ans :
Marfan’s syndrome is an inherited disorder of connective tissue that is associated with a high
risk of aortic aneurysm and dissection.
AD inheritance
Extraocular features are: (Ref- Kaniski 8th; Page – 300)

A. Musculoskeletal features
1. A tall, thin stature with disproportionately long limbs (arm span > height),
2. Long fingers and toes (arachnodactyly),
3. A narrow high-arched (‘gothic’) palate.
B. Kyphoscoliosis,
C. Sternal abnormalities,
D. Mild joint laxity,
E. Muscular underdevelopment
F. Predisposition to hernias.
G. Cardiovascular lesions
a. Dilatation of the aortic root,
b. Mitral valve prolapse
c. Aortic aneurysm formation.
[*** Ocular features :
○ Bilateral ectopia lentis (80%); subluxation is most frequently superotemporal. The zonule is
frequently intact so that accommodation is retained, although rarely the lens may dislocate into
the AC or vitreous.
○ Other ocular features: angle anomaly may lead to glaucoma, and lattice retinal degeneration
to retinal detachment; there may be hypoplasia of the dilator pupillae, microspherophakia, and
strabismus. ]
20
Q: Briefly discuss the red flag sign of Low back pain.
Ans:
Red flag signs of LBP :

Red flags for possible spinal pathology
History:
• Age: presentation < 20 years or > 55 years
• Character: constant, progressive pain unrelieved by rest
• Location: thoracic pain
• Past medical history: carcinoma, tuberculosis, HIV, systemic glucocorticoid
use, osteoporosis
• Constitutional: systemic upset, sweats, weight loss
• Major trauma
Examination:
• Painful spinal deformity
•Severe/symmetrical spinal deformity
• Saddle anaesthesia
• Progressive neurological signs/muscle-wasting
• Multiple levels of root signs
Q: A 65 old presented red painful eye with inflammatory poly

arthritis. What are the D/D would you consider and what relevant
investigations you will do to reach the diagnosis?
21
Q: How will you differentiate between neuropathy and

myopathy?
Ans :
Neuropathy: Neuropathy is a term that refers to general diseases or malfunctions of the
nerves
Myopathy : Myopathy is a disease of the muscle in which the muscle fibers do not function
properly
Difference between Neuropathy and Myopathy :
Q: How will you differentiate between inflammatory and

mechanical pain?
Ans :
Inflammatory pain Mechanical pain
Age of onset < 40 yr Any age ( usually later)
Type of onset Insidious Acute
Symptom duration >3 mnths <4 weeks
Morning stiffness >30 min < 30 min
Nocturnal pain Common Absent
Effect of exercise Improvement Exacerbation
22
Sacroiliac joint Frequent Absent
tenderness
Back mobility Loss in all patient Abnormal flexion
Chest expansion Often decreased Normal
Neurological deficits Unusual Possible
Q: How will you differentiate between articular and periarticular

joint pain?
Ans :
Differentiate between articular and periarticular joint pain
Clinical feature Articular joint pain Periarticular joint pain
Anatomical stracture Synovium , cartilage, Tendon, bursa,
capsule ligament, muscle, bone
Painful site Diffuse, deep Focal point
Pain on movement Active /passive all In active movement
movement
Planes Pain in all planes Pain in plane of tendon
Swelling Common Uncommon
Q: Briefly discuss Shirmer test.
Ans : (Ref – Kaniski, 8th ; Page – 124)
Schirmer test
The Schirmer test is a useful assessment of aqueous tear production. The
test involves measuring the amount of wetting of a special filter paper, 5 mm
wide and 35 mm long. The test can be performed with or without topical
anaesthesia.
In theory, when performed with an anaesthetic (Schirmer 2) basic secretion is
measured and without anaesthetic (Schirmer 1) it measures maximum basic
23
plus reflex secretion. In practice, however, topical anaesthesia cannot abolish

all sensory and psychological stimuli for reflex secretion. The test is
performed as follows:
• Excess tears are delicately dried. If topical anaesthesia is applied the excess
should be removed from the inferior fornix with filter paper.
• The filter paper is folded 5 mm from one end and inserted at the junction of
the middle and outer third of the lower lid, taking care not to touch the cornea
or lashes
• The patient is asked to keep the eyes gently closed.
• After 5 minutes the filter paper is removed and the amount of wetting from
the fold measured.
• Less than 10 mm of wetting after 5 minutes without anaesthesia or less than
6 mm with anaesthesia is considered abnormal.
Results can be variable and a single Schirmer test should not be used as the
sole criterion for diagnosing dry eye, but repeatedly abnormal tests are highly
supportive.
Q: How will you differentiate clinically episcleritis from scleritis ?
Ans :
24
Q: Name the rheumatic disease affecting eye ?
Ans :
Rheumatic disease affecting eye :
Rheumatological/ musculoskeletal disease
a. Rheumatoid arthritis
b. Seronegative spondyloarthropathy
c. Connective tissue disease
i. Dermatomyositis
ii. Sjogren’s syndrome
d. Systemic vasculitis
i. Giant cell arteritis
ii. Wegener’s granulomatosis
iii. Polyartaritis nodosa
e. Disease of bone
i. Paget’s disease
Q: Name the investigations of eye diseases with indications

and/ or comments .
Ans :
Q: What is macula? Name the drug causing maculopathy?
Ans :
Macula:
Drugs causing maculopathy: (ref- Kanski , 8th ; Page – 854)
A. Anti malarial drugs :

a. Chloroquine b. Hydroxychloroquine
B. Phanothiazine :
a. Thioridazine b. Chlorpromazine
C. Tamoifen G. Interferrin alpha
D. Canthaxanthin H. Desferrioxamine
E. Methoxyflurane I. Nicotinic acid
F. Nitrofurantoin
25
Q: Mantion the ocular symptoms of Sjogran disease & discuss

test to confirm the eye findings.
Ans :
Sjögren syndrome (SS) is an autoimmune disorder characterized by lymphocytic inflammation
and destruction of lacrimal and salivary glands.
Ocular symptoms :
 The most common ocular symptoms are feelings of dryness, grittiness and burning that
characteristically worsen over the course of the day.
 Stringy discharge,
 Transient blurring of vision,
 Redness
 Crusting of the lids
 Lack of emotional or reflex tearing is unusual.
 The symptoms of KCS are frequently exacerbated on exposure to conditions
associated with increased tear evaporation (e.g. Air-conditioning, wind and central
heating) or prolonged reading or video display unit use, when blink frequency is
reduced
Tests to confirm the eye findings:
The aim of investigation is to confirm and quantify a clinical diagnosis of dry eye.
The tests are –
• Stability of the tear film as related to its break-up time (BUT).
• Tear production (Schirmer, fluorescein clearance and tear osmolarity).
• Ocular surface disease (corneal stains and impression cytology).
Q: A 65 yr old patient present to you with dry eye and dry

mouth. How will you proceed to rule out Sjogren Syndrome?
Q: What is sicca syndrome? Briefly discuss the management of

dry eye.
Ans :
Sicca syndrome: also known as Sjogren syndrome (SS) is an autoimmune
disorder characterized by lymphocytic inflammation and destruction of
lacrimal and salivary glands.
Management of dry eye: ( ref- Kanski 8th, page – 127 )

The underlying causative processes of dry eye are generally not reversible
and management is therefore structured around the control of symptoms and
26
the prevention of surface damage. DEWS have produced guidelines, in which

suggested treatment options depend on the level of severity of disease
graded from 1 to 4. The DEWS guidelines can also be applied in a graded
approach, proceeding to the next level if the preceding measures are
inadequate.
Level 1
• Education and environmental/dietary modifications
○ Establishment of realistic expectations and emphasis on the
importance of compliance.
○ Lifestyle review including the importance of blinking whilst reading,
watching television or using a computer screen (which should be
orientated below eye level to minimize palpebral aperture size), and the
management of contact lens wear.
○ Environmental review, e.g. increasing humidity may be possible for
some environments.
○ Instillation aids for eye drops should be advocated for patients with
reduced dexterity (e.g. rheumatoid arthritis).
○ Caution the patient that laser refractive surgery can exacerbate dry
eye.
• Systemic medication review to exclude contributory effects and eliminate
offending agents.
Discontinuation of toxic/ preserved topical medication if possible.
• Artificial tear substitutes including gels and ointments –
a. Drops and gels
i. Cellulose derivatives (e.g. hypromellose, methylcellulose)
ii. Carbomer gels
iii. polyvinyl alcohol (PVA)
iv. Diquafosol
b. Ointments containing petrolatum (paraffin) mineral oil can be
used at bedtime to supplement daytime drops or gel instillation
c. Eyelid sprays are applied to the closed eye and typically contain
a liposome-based
d. Artificial tear inserts
e. Mucolytic agents. Acetylcysteine 5% drops
• Eyelid therapy.
Basic measures such as warm compresses and lid hygiene for
blepharitis; reparative lid surgery (e.g. entropion, ectropion, excessive lid
laxity or scleral show) may be considered as an early measure. Nocturnal
lagophthalmos can be addressed by taping the lids closed at bedtime,
wearing swimming goggles during sleep, or in extreme cases by lateral
tarsorrhaphy.
Level 2
• Non-preserved tear substitutes
• Anti-inflammatory agents such as topical steroids, oral omega fatty acids
and other agents such as topical ciclosporin.
• Tetracyclines (for meibomianitis, rosacea).
• Punctal plugs.
27
• Secretagogues, e.g. pilocarpine, cevilemine, rebamipide.

• Moisture chamber spectacles and spectacle side shields.
Level 3
• Serum eye drops. Autologous or umbilical cord serum.
• Contact lenses.
• Permanent punctal occlusion.
Level 4
• Systemic anti-inflammatory agents.
• Surgery
○ Eyelid surgery, such as tarsorrhaphy.
○ Salivary gland autotransplantation.
○ Mucous membrane or amniotic membrane transplantation for corneal
complications.
Q: Mention the eye findings of a patient with sarcoidosis.
Ans :
Sarcoidosis is a multisystem granulomatous disorder of unknown aetiology
that is characterised by the presence of non-caseating granulomas.
Ophthalmic feature of sarcoidosisi are as follows :

 Anterior uveitis (granulomatosis)
 Mutton fat keratitic precipitates
 Iris nodules
 Choroidal granuloma
 Panuveitis
 Multifocal choroiditis
 Retinal periphlebitis
 Sicca syndrome, caused by lacrimal gland infiltration
 Exposure keratopathy, caused by corneal exposure secondary to facial
nerve palsy
 Optic neuropathy, caused by optic disc oedema secondary to meningeal
infiltration
Q:
28

Q: Describe The Diagnostic Criteria & Lab Investigation of SLE. Ans

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DR.HASNAT JAKI CHOWDHURY, Question bank By DR.

ABIR BIN SAJJ

Q: Describe the Diagnostic criteria & Lab Investigation of SLE.

Q: Note down The CNS Manifestation of SLE.

Q:Note down The Cutaneous & GI Manifestation of SLE:

Q:Discuss the Adverse effect of Cyclophosphamide and

Ans: [Ref: From Katzung ]

Advarse effect of Hydroxychloroquine :

Q: What are the diagnostic criteria of Rheumatoid arthritis?

Q: What are the Extra articular manifestation of RA?

Q: Enumerate the causes of anaemia in RA

Q: Enumerate the DMARDs for treating RA. Make a checklist of

DMARDs Used in Rheumatoid arthritis :

Checklist of information before starting DMARDs :

Other important considerations include congestive heart failure, malignancy,

Q: How will you educate a newly diagnosed patient with RA?

●The application of heat or cold can relieve pain or stiffness.

●Ultrasound may reduce inflammation of the sheaths surrounding tendons (tenosynovitis).

●Relaxation techniques can relieve secondary muscle spasm.

Q: What are the indication of steroid in Ankylosing spondylitis?

Q: Mantion 3 Disease under the heading of spondarthritidis ?

Ans: : [ Ref: Davidson’s Principles and Practice of 23rd Edition;Page ]

Extra articular manifestation of Ankylosing Spondylitis are :

Q: What are the common collagen disease?

D. MRI is more sensitive for detection of early sacroiliitis than X-rays

Q: Enumerate the role of HLA B-27 in Rheumatoid arthritis.

Q: Mention 3 disease related to HLA B-27.

Ans : ref- wiki

Q: Write the difference between granulomatous & non –

Difference between granulomatous & non –granulomatous uveitis: ref- NET

Traits Granulomatous uveitis Non-granulomatous uveitis

Acute anterior uveitis : Ref- prof. Shamsul haque ; page- 241

Q: Write down the treatment of uveitis in different rheumatoid

Ans : ref- Prof. Shamsul haque; page 217

Treatment of uveitis in different rheumatoid disease:

 Juvenile idiopathic arthritis

Q: What is scleritis? Classify it.

Ans: ref- Prof Shamsul alam; page 170

Anterior Scleritis posterior

Non Necrotizing Necrotizing

Q: What is Iritis? Name the rheumatic disease causing irits?

Ans : ref- Prof Shamsul alam; page 215

Rheumatic disease causing Iritis:

Q: What are the adverse effect of steroid overdose?

Q: Mechanism of action of Methotrexate?

Ans : Ref- Ketzang ; 12th ed; page- 645

Q: Classify vasculitis. Write down the checklist of clinical

 Drug-associated anca-associated vasculitis

Investigations : (Ref- Davidson 23rd ; page – 1042 + CMDT; page – 864 )

Q: What is giant cell arteritis? Describe the temporal arteritis.

Ans : (Ref- Davidsons 23rd; Page – 1042)

(Ref- Kaniski 8th; Page – 787)

Q: What is vasculitis? Mention the causes of arteriolar occlusion

Causes of arteriolar occlusion in eye: (Ref- Davidson 23rd ; Page- 1178)

OR (Ref- Kanski 8th ; page – 550 )

A. Triad of retinal artery occlusion-

Q: What investigation will you do for diagnosis of mesenteric

Q: What are the complication of Takayasu’s arteritis may

Q: What do you mean by Mononuritis multiplex? Outline the

Q: Enumerate the C/F of Myotonic muscular dystrophy.

Clinical features: (Ref - https://jnnp.bmj.com/content/jnnp/81/4/358.full.pdf)

Q: Describe the extraocular features of Marfan syndrome.

Extraocular features are: (Ref- Kaniski 8th; Page – 300)