CLINICAL LECTURE MBBS 2017 Batch

CLINICAL LECTURE

(MBBS 2017 BATCH)

Dr. Lubna Zafar

Assistant Professor

Department of Medicine, JNMCH

24/6/2020 9 (Wednesday)

CASE SCENARIO

A 52-years-old male with 8-years history of recurrent arthritis was admitted for generalized articular pain. He had only taken traditional medicines for joint pains .

He complained of multiple hard swelling over his joints which had developed over 4 years, progressively increasing in size.

Ten hours before seeking medical assistance, a nodule located on the first metatarsophalangeal joint of his left foot had bursted releasing a viscous, chalk-like material.

Past History : Hypertensive for 4 years. On

Amlodipine 10 mg.

Personal History : Non-vegetarian

Alcohol Intake

o Family History : Nothing significant

Examination:

Pallor present (mild)

Icterus absent

Clubbing absent

No LAP

PR : 98/min, regular, no special character

BP: 158/94 mmHg Supine

RR: 18 /min

Temp: 100.2 F

BMI 30.4 kg/m2

Physical examination revealed that there were

multiple large firm tophi over bilateral hands,

feet, elbows, and knees .

A large tophus over MCP right second finger.

Some of them are ulcerated and discharged

white chalky material.

INVESTIGATIONS :

Hb 10 gm%

TLC 13600 cells/mm3

DLC P70L27M3

B.S. 142

Serum creatinine 2.8 mg/dl

Serum electrolytes normal

Serum uric acid 9.8 mg/dl

Thyroid profile normal

RA negative

Radiological examination of the feet showed

soft tissue swelling and total destruction of the

first left metatarsophalangeal joint

Abdominal ultrasonography revealed

bilateral caliceal calculi.

DIAGNOSIS

Systemic Hypertension. Chronic tophaceous gout.

Nephrolitiasis. Sepsis. Renal Insufficiency

GOUT

GOUT

Inflammatory response to MSU crystals formed

secondary to hyperuricaemia

Hyperuricaemia defined as plasma urate

concentration greater than 7 mg/dl in males and

6mg/dl in females.

In females, uric acid rises after menopause.

HISTORY

Was known as Disease of the ‘KINGS’ (Rich

foods have a higher concentration of protein. This

was believed to be causative of gout)

Famous personalities affected with the disease:

Benjamin Franklin

Thomas Jefferson

Sir Isaac Newton

Charles Darwin

King Henry VIII

PREDISPOSING FACTORS

Purine rich foods – meat, kidney, liver, seafood,

oatmeal, peas, beans,lentils, mushrooms

Drugs – Loop diuretics, NSAIDs, corticosteroids,

Niacin, Cyclosporine, Salicylates, Pyrazinamide

Trauma

Infection

Other disease – DM, HTN, vascular dx, renal dx,

thyroid dx, sarcoidosis, etc.

HYPERURICEMIA LEADS TO DEPOSIT OF

URATES IN THE JOINT FLUID, TRIGGERING AN

INFLAMMATORY CASCADE

STAGES OF GOUT

Asymptomatic hyperuricemia

Acute gout

Intercritical gout

Chronic tophaceous gout

ACUTE GOUT

Acute gout is a painful

condition that typically

affects only one or a few

joints.

o First metatarsopharangeal

joint classic site

o Throbbing, crushing, or

excruciating pain,typically at

night

o Joint appears warm and

red.

o Fever may be there.

The attack may resolve in a few days, but

relapses

Additional attacks often last longer.

CHRONIC GOUT

Joint damage

Loss of motion in the joints

Joint pain and other symptoms most of the time,

throughout the day

Is characterised by massive deposits of monosodium

urate crystals in articular cartilage, subchrondral

bone, synovial membrane, capsule, tendon sheaths

and peri articular tissues.

ADVANCED CHRONIC TOPHACEOUS

GOUT

Tophi can be seen

clinically, with

obvious deformity

demonstrated in

hands and foot

Tophi may be

associated with bony

destruction as seen on

the x-ray.

TOPHI

The tophaceous nodules consists of multicentric

deposition of urate crystals and intra cellular

matrix and foreign body granulomatous reaction.

As they enlarge in size, calcify, they can cause

pressure symptoms.

The tophi are firm yellow in colour and

occasionally discharge a chalky material.

RENAL INVOLVEMENT IN GOUT

Most common complication of hyperuricaemia

after gouty arthritis

Urate nephropathy: Deposition of MSU in renal

interstitial tissue

Uric acid calculi

Renal failure accounts for 10-25% deaths in gout

patients

INVESTIGATIONS

Plain radiographs

Serum Uric acid: ≥ 2 raised fasting levels ( may

be normal during acute attack)

Synovial fluid analysis

BUN ,Serum Creatinine

Synovial biopsy

24 hour Urinary urate

SYNOVIAL FLUID ANALYSIS

Turbid, with elevated

neutrophils ( Septic

arthritis is D/D)

Polarized Light Microscopy:

The Gold standard.

Crystals intracellular

during attacks

Needle & rod shapes

Strong negative

birefringence

DIFFERENTIAL DIAGNOSIS

Pseudogout: Chondrocalcinosis, CPPD

Psoriatic Arthritis

Osteoarthritis

Rheumatoid arthritis

Septic arthritis

Cellulitis

MANAGEMENT

ASYMPTOMATIC HYPERURICAEMIA

No drug therapy

Treatment indicated in tumor lysis syndrome,

uric acid levels more than 10mg/dl, presence of

risk factors or comorbidities

ACUTE GOUT

Treatment as soon as possible

NSAID , Colchicine, Steroids

Xanthine oxidase inhibitor 10-15 days after

resolution of inflammation

NSAID:

Inhibits pain & inflammation.

Inhibits urate crystal phagocytosis by decreasing

the migration of granulocytes into the inflammatory

area.

Indomethacin, Naproxen, Ketorolac.

COLCHICINE:

Produces its anti-inflammatory effects by binding

to the intracellular protein tubulin, preventing

its polymerization leading to the inhibition of

leukocyte migration into affected area.

Inhibits the synthesis & release of leukotrienes.

URICOSURIC AGENTS:

Probenecid & Sulfinpyrazone

They are weak organic acids .

Sulfinpyrazone is a metabolite of phenylbutazone.

Increase the excretion of Uric acid.

XANTHINE OXIDASE INHIBITOR

Allopurinol/ Febuxstat:

Inhibits synthesis of uric

acid by inhibiting xanthine

oxidase enzyme

URICASE ENZYMES

Catabolize urate to allantoin

More soluble, excretable form

Currently approved for hyperuricemia in tumor

lysis syndrome