Gout- Purine metabolism disorder

Gout- Purine metabolism disorder

Q. 1 Acute Gouty arthritis is seen early in treatment following
 A Probenecid
 B

Allopurinol

 C Colchicine
 D

Rasburicase

Q. 1 Acute Gouty arthritis is seen early in treatment following
 A Probenecid
 B

Allopurinol

 C Colchicine
 D

Rasburicase

Ans. B

Explanation:

Allopurinol REF: Goodman Gillman manual of pharmacology and therapeutics 2008 edition page 458

“The incidence of acute attacks of gouty arthritis mayincrease duringthe early months of allopurinol therapy as a consequence of mobilization of tissue stores of uric acid. Co-administration of colchicine helps suppress such acute attacks. After reduction of excess tissue stores of uric acid, the incidence of acute attacks decreases and colchicine can be discontinued”


Q. 2 A 40-yrs-old male has a uric acid level of 9 mg/dL. The patient has never had gout arthritis, renal disease, or kidney stones. Which of the following is correct?
 A Risk   of   urolithiasis requires institution of prophylactic therapy
 B Asymptomatic hyperuricemia is associated with an increased risk of gouty arthritis, but benefits of prophylaxis do not outweigh risks in this patient.
 C The presence or  absence of lymphoproliferative disease does not affect  the  decision  to use prophylaxis in hyperuricemia
 D Lowering serum uric acid will provide a direct cardiovascular benefit to the patient lowering CAD risk.
Q. 2 A 40-yrs-old male has a uric acid level of 9 mg/dL. The patient has never had gout arthritis, renal disease, or kidney stones. Which of the following is correct?
 A Risk   of   urolithiasis requires institution of prophylactic therapy
 B Asymptomatic hyperuricemia is associated with an increased risk of gouty arthritis, but benefits of prophylaxis do not outweigh risks in this patient.
 C The presence or  absence of lymphoproliferative disease does not affect  the  decision  to use prophylaxis in hyperuricemia
 D Lowering serum uric acid will provide a direct cardiovascular benefit to the patient lowering CAD risk.
Ans. B

Explanation:

Asymptomatic hyperuricemia is associated with an increased risk of gouty arthritis…………………. Asymptomatic hyperuricemia does increase the risk of acute gouty arthritis. However, the cost of lifelong prophylaxis in this patient would be high, and the prevalence of adverse drug reaction would be between 10 and25%. This expense is generally considered high compared to a more conservative approach of treating an attack when it does occur. Prophylactic therapy would be reserved for patients who already had one or more acute attacks. Although hyperuricemia is associated with arteriosclerotic disease, the association is not felt to be causal, and there is no proven cardiovascular benefit to reducing the uric acid level. In patients with lymphoproliferative disease, prophylaxis for the prevention of renal impairment is recommended. The risk of urolithiasis is sufficiently low that prophylaxis is not necessary until the development of a stone.


Q. 3 In gout tophi are not seen in? 
 A

Skin

 B Muscles 
 C Nasal cartilage
 D

Synovium

Q. 3 In gout tophi are not seen in? 
 A

Skin

 B Muscles 
 C Nasal cartilage
 D

Synovium

Ans. B

Explanation:

Muscles

REF: Apley 8th edition page 77

Tophi are nodular deposition of crystals of mono sodium urate which get deposited in connective tissues like:

  • Articular cartilage
  • Tendon
  • Synovium
  • Articular ends of bone
  • Periarticular tissue
  • Pinna
  • Cartilage
  • Ligaments
  • Kidney
  • Subcutaneous tissue

On X-ray: Tophi appears as punched out cysts with over hanging bony edges or G sign or martel’s sign.

Metatarsophalangeal joint is the most common and earliest joint affected by gout


Q. 4

True statements regarding acute attack of gouty arthritis is all EXCEPT:

 A

Joint aspirate reveals positive birefringent crystals

 B

Allopurinol should be started immediately

 C

Colchicine is known to provide relief

 D

Serum Uric acid levels may be absolutely normal

Q. 4

True statements regarding acute attack of gouty arthritis is all EXCEPT:

 A

Joint aspirate reveals positive birefringent crystals

 B

Allopurinol should be started immediately

 C

Colchicine is known to provide relief

 D

Serum Uric acid levels may be absolutely normal

Ans. B

Explanation:

Allopurinol should be started immediately REF: Goodman Gillman manual of pharmacology and therapeutics 2008 edition page 458, Katzung 9th edition page 599, Harrison 17th ed chapter 327

“The incidence of acute attacks of gouty arthritis may increase during the early months of allopurinol therapy as a consequence of mobilization of tissue stores of uric acid. Co-administration of colchicine helps suppress such acute attacks. After reduction of excess tissue stores of uric acid, the incidence of acute attacks decreases and colchicine can be discontinued”

During acute gouty attacks, strongly birefringent needle-shaped MSU crystals with negative elongation are typically seen both intracellularly and extracellularly

Serum uric acid levels can be normal or low at the time of the acute attack, as inflammatory cytokines can be uricosuric and effective initiation of hypouricemic therapy can precipitate attacks. This limits the value of serum uric acid determinations for the diagnosis of gout

MP mainstay of treatment during an acute attack is the administration of anti-inflammatory drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or glucocorticoids.


Q. 5 Acute Gouty arthritis is seen early following treatment with:
 A Rasburicase
 B Probenecid
 C Allopurinol
 D Sulfinpyrazone
Q. 5 Acute Gouty arthritis is seen early following treatment with:
 A Rasburicase
 B Probenecid
 C Allopurinol
 D Sulfinpyrazone
Ans. C

Explanation:

Allopurinol


Q. 6

In a patient with gouty arthritis, synovial fluid aspiration will show:

 A

Monosodium Urate crystals

 B

Calcium Pyrophosphate crystals

 C

Mononuclear Leucocytosis

 D

Polymorphonuclear Leukocytosis

Q. 6

In a patient with gouty arthritis, synovial fluid aspiration will show:

 A

Monosodium Urate crystals

 B

Calcium Pyrophosphate crystals

 C

Mononuclear Leucocytosis

 D

Polymorphonuclear Leukocytosis

Ans. A

Explanation:

Demonstration of intracellular Monosodium Urate Crystals (MSU) in synovial fluid from affected joint is diagnostic of gout.

Ref: Harrison’s Principles of Internal Medicine, 16th Edition, Page 2046; Current Rheumatology Diagnosis and Treatment, 2nd Edition, Page 467


Q. 7

Which of the following types of crystals would support the likely diagnosis of pseudogout?

 A

Negatively-birefringent needle-shaped crystals

 B

Negatively-birefringent oval crystals

 C

Negatively-birefringent rhomboidal crystals

 D

Positively-birefringent rhomboidal crystals

Q. 7

Which of the following types of crystals would support the likely diagnosis of pseudogout?

 A

Negatively-birefringent needle-shaped crystals

 B

Negatively-birefringent oval crystals

 C

Negatively-birefringent rhomboidal crystals

 D

Positively-birefringent rhomboidal crystals

Ans. D

Explanation:

Positively-birefringent rhomboidal crystals are classically found in cases of pseudogout.

Pseudogout, or calcium pyrophosphate dihydrate (CPPD) disease, tends to affect older individuals, tends to affect the knee, wrist, shoulder, ankle, elbow, and hands, and may develop more insidiously.

Nevertheless, the similarities between gout and pseudogout require aspiration of the joint for diagnosis.

Negatively-birefringent needle-shaped crystals are diagnostic for gout.

 

The other choices are not diagnostic or commonly occurring combinations.

 

Also Know:

 

Pseudogout (also called calcium pyrophosphate dihydrate (CPPD) deposition disease) is most often seen in persons age 60 or older, is characterized by acute, recurrent and rarely chronic arthritis involving large joints (most commonly the knees and the wrists and is almost always accompanied by chondrocalcinosis of the affected joints.

 

 

 

Identification of calcium pyrophosphate crystals in joint aspirates is diagnostic of pseudogout.
With light microscopy, the rhomboid-shaped crystals differ from the needle-shaped gout crystals.

 

Ref: Hellmann D.B., Imboden Jr. J.B. (2013). Chapter 20. Musculoskeletal & Immunologic Disorders. In M.A. Papadakis, S.J. McPhee, M.W. Rabow (Eds),CURRENT Medical Diagnosis & Treatment 2013.

 


Q. 8

 A person has severe pain and swelling in great toe, True statement is/are:

  1. Allopurinol used in acute control of gout
  2. Colchicine acts slowly
  3. Colchicine causes gastrointestinal disturbances
  4. High serum uric acid level may not be present
  5. Joint fluid aspiration is done for investigation
 A

1,2,3

 B

3,4,5

 C

2,4,5

 D

All are correct

Q. 8

 A person has severe pain and swelling in great toe, True statement is/are:

  1. Allopurinol used in acute control of gout
  2. Colchicine acts slowly
  3. Colchicine causes gastrointestinal disturbances
  4. High serum uric acid level may not be present
  5. Joint fluid aspiration is done for investigation
 A

1,2,3

 B

3,4,5

 C

2,4,5

 D

All are correct

Ans. B

Explanation:

“serum uric acid levels can be normal or low at the time of acute attack”. This limits the value of serum uric acid determination for the diagnosis of gout.

Nevertheless, serum urate levels are almost always elevated at some time and are important to use to follow the course of hyperuricemic therapy”

Acute gout
Acute gout manifests as sudden onset of severe inflammation in a small joint ( commonest is metatarso- phalangeal joint of great toe) due to precipitation of urate crystals ( sodium biurate) in the joint space.
The joint become red, swollen and extremely painful, require immediate treatment.
 
Drugs used
For acute gout: NSAIDS, colchicine and corticosteroids
For chronic gout/hyperuricemia
Uricosuric: Probenecid, Sulfinpyrazone
Urea synthesis inhibitor: allopurinol
 
Allopurinol
Allopurinol as well as uricosurics should not be started during acute attack of gout.
It is first choice drug in chronic gout and can be used in both overproducers and under excretors of uric acid.
During the initial 1-2 months of treatment, attacks of acute gout are common probably due to fluctuating plasma urate levels.
With long term allopurinol therapy, tophi gradually disappear and nephropathy is halted, even reversed
 
Colchicine
Colchicine is the fastest acting drug to control an acute attack of gout; 1 mg orally followed by 0.25 m 1-3 hrly till controll of attack is achieved ( occurs in 4-12 hrs)
Nausea, vomiting, watery or bloody diarrhea and abdominal cramps occur as dose limiting adverse effect. Chronic therapy with colchicine is not recommended because it causes aplastic anaemia, agranulocytosis, myopathy and loss of hair.
 
Confirmation of diagnosis: Urate crystals in the aspirate from a joint or bursa, high serum uric acid crystals.
 
Ref: Maheshwari 3/e, Page 251; KDT 6/e, Page 205-10; Harrison’s 17/e, Page 2166.

Q. 9

The cause of hyperuricemia and gout in glucose-6-phosphatase deficiency is:

 A

More formation of ribose 5-phosphate

 B

Decreased availability of glucose to tissues

 C

Increased accumulation of sorbitol

 D

Impaired degradation of free radicals

Q. 9

The cause of hyperuricemia and gout in glucose-6-phosphatase deficiency is:

 A

More formation of ribose 5-phosphate

 B

Decreased availability of glucose to tissues

 C

Increased accumulation of sorbitol

 D

Impaired degradation of free radicals

Ans. A

Explanation:

Type I glycogen storage disease (Von Gierke’s Disease) is an autosomal recessive disorder caused by glucose-6-phosphatase deficiency in liver, kidney, and intestinal mucosa. Purine overproduction and hyperuricemia in von Gierke disease (glucose-6-phosphatase deficiency) occurs secondary to enhanced generation of the PRPP precursor ribose 5-phosphate. An associated lactic acidosis elevates the renal threshold for urate, elevating total body urates.
 
Ref: Rodwell V.W. (2011). Chapter 33. Metabolism of Purine & Pyrimidine Nucleotides. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e.

 


Q. 10

False regarding gout is:

 A

Due to increased metabolism of pyrimidines

 B

Due to increased metabolism of purines

 C

Uric acid levels may not be elevated

 D

Has a predilection for the great toe

Q. 10

False regarding gout is:

 A

Due to increased metabolism of pyrimidines

 B

Due to increased metabolism of purines

 C

Uric acid levels may not be elevated

 D

Has a predilection for the great toe

Ans. A

Explanation:

Gout is due to disorder of purine metabolism which result in excess formation of uric acid which in turn accumulate in synovial fluid resulting in gouty arthritis.
 
Ref: Textbook of Biochemistry By DM Vasudevan, 3rd Edition, Pages 339 ; Lippincott Biochemistry, 2nd edition, Pages 350, 353 ; Harrison’s Principles of Internal Medicine, 14th Edition, Pages 2161, 15th Edition, Pages 1994-95 ; Davidson’s Medicine, 17th Edition, Page 882

Q. 11

Which of the following pathological agents are implicated in pseudogout?

 A

Sodium monourate

 B

Calcium oxalate

 C

Calcium pyrophosphate

 D

Sodium pyrophosphate

Q. 11

Which of the following pathological agents are implicated in pseudogout?

 A

Sodium monourate

 B

Calcium oxalate

 C

Calcium pyrophosphate

 D

Sodium pyrophosphate

Ans. C

Explanation:

Pseudogout is a result of synovitis caused by calcium pyrophosphate crystals.


Q. 12

Gout is a disorder of:

 A

Purine Metabolism

 B

Pyrimidine Metabolism

 C

Ketone Metabolism

 D

Protein metabolism

Q. 12

Gout is a disorder of:

 A

Purine Metabolism

 B

Pyrimidine Metabolism

 C

Ketone Metabolism

 D

Protein metabolism

Ans. A

Explanation:

Primary gout is a disorder of purine metabolism. Purine degradation result in the production of uric acid. Gout occur mainly from hyperuricemia secondary to reduced uric acid excretion from the kidney, and in a minority of cases it occur secondary to overproduction of uric acid.

Ref: Current medical diagnosis and treatment 2012, Chapter 20; Essentials of Medical Biochemistry: With Clinical Cases By N. V. Bhagavan, Page 345-6.


Q. 13

The triad of “saturnine” gout, hypertension and renal insufficiency seen in poisoning with which of the following metals?

 A

Arsenic

 B

Lead

 C

Copper

 D

Iron

Q. 13

The triad of “saturnine” gout, hypertension and renal insufficiency seen in poisoning with which of the following metals?

 A

Arsenic

 B

Lead

 C

Copper

 D

Iron

Ans. B

Explanation:

Heavy metals like cadmium and lead can lead to chronic tubulointerstitial disease. It is usually not commonly diagnosed. This leads to proximal tubular damage and hyperuricemia due to diminished urate excretion. The above mentioned triad should prompt a clinician to ask specifically about lead exposure. Lead chelation therapy can slow the disease progression.


Q. 14

The cause of hyperuricemia and gout in glucose-6­phosphatase deficiency is :

 A

More formation of pentose

 B

Decreased availability of glucose to tissues

 C

Increased accumulation of sorbitol

 D

Impaired degradation of free radicals

Q. 14

The cause of hyperuricemia and gout in glucose-6­phosphatase deficiency is :

 A

More formation of pentose

 B

Decreased availability of glucose to tissues

 C

Increased accumulation of sorbitol

 D

Impaired degradation of free radicals

Ans. A

Explanation:

A i.e More formation of pentose

Von Gierke’s (type Ia glycogen storage) disease d/t deficiency of glucose 6 phosphatase enzymeQ is autosomal recessive in inheritance. It is characterized by – Cells (of liver, renal tubular epithelium & intestinal mucosa) containing normal structured metabolically unavailable glycogen, hepato-renomegalyQ, doll like face, hypoglycemia, hyper-lipoemia, hyper cholesterolemia, fatty infiltration of liver, ketosisQ, acidemia, T lactic acid, t uric acid and stunted growth.


Q. 15

False regarding gout is :

 A

Due to increased metabolism of pyrimidines

 B

Due to increased metabolism of purines

 C

Uric acid levels may not be elevated

 D

Has a predilection for the great toe

Q. 15

False regarding gout is :

 A

Due to increased metabolism of pyrimidines

 B

Due to increased metabolism of purines

 C

Uric acid levels may not be elevated

 D

Has a predilection for the great toe

Ans. A

Explanation:

A i.e. Due to increased metabolism of pyrimidines


Q. 16

Gout is a disorder of :

 A

Purine metabolism

 B

Pyrimidine metabolism

 C

Oxalate metabolism

 D

Protein metabolism

Q. 16

Gout is a disorder of :

 A

Purine metabolism

 B

Pyrimidine metabolism

 C

Oxalate metabolism

 D

Protein metabolism

Ans. A

Explanation:

A i.e. Purine metabolism


Q. 17

What is not true about gout:

 A

Abrupt increase in serum urate levels is more common a cause for acute gout than an abrupt fall in urate levels.

 B

Patient may be asymptomatic with high serum uric acid for years

 C

Development of arthritis correlates with level of serum uric acid

 D

Uric acid crystals are best seen by polarising light microscope

Q. 17

What is not true about gout:

 A

Abrupt increase in serum urate levels is more common a cause for acute gout than an abrupt fall in urate levels.

 B

Patient may be asymptomatic with high serum uric acid for years

 C

Development of arthritis correlates with level of serum uric acid

 D

Uric acid crystals are best seen by polarising light microscope

Ans. A

Explanation:

A i.e. Abrupt increase in serum urate levels is more common a cause for acute gout than an abrupt fall in urate levels


Q. 18

Specific test for gout is:

 A

Raised serum uric acid level

 B

Raised uric acid in synovial fluid of joint

 C

Raised urea level

 D

Raised urease enzyme level

Q. 18

Specific test for gout is:

 A

Raised serum uric acid level

 B

Raised uric acid in synovial fluid of joint

 C

Raised urea level

 D

Raised urease enzyme level

Ans. B

Explanation:

B i.e. Raised uric acid in synovial fluid of joint

– Gout is a metabolic disorder of purine catabolismQ, and characterized by high level of uric acid in the blood . Uric acid is end product of purine catabolismQ

Pyrimidine nucleotide unlike purine rings can be opened & degraded to highly water soluble structure like, p- alanine, /3‑ amino isobutyrate, NH3 & CO2. Excess meabolism of pyrimidine therefore does not give rise to clinical manifestationQ Human catabolizes purine (Adenine & Guamine) to uric acid, which is relatively insoluble acid.


Q. 19

A sample to look for uric crystal (Gouty tophus) would be submitted to the pathology laboratory in:

 A

Formalin

 B

Distilled water

 C

Alcohol

 D

Normal saline

Q. 19

A sample to look for uric crystal (Gouty tophus) would be submitted to the pathology laboratory in:

 A

Formalin

 B

Distilled water

 C

Alcohol

 D

Normal saline

Ans. C

Explanation:

C i.e. Alcohol


Q. 20

Prolonged allopurinol therapy in a patient with gout is not indicated for –

 A

Acute gouty arthritis

 B

Tophi

 C

Urate nephropathy

 D

Evidence of bone/joint damage

Q. 20

Prolonged allopurinol therapy in a patient with gout is not indicated for –

 A

Acute gouty arthritis

 B

Tophi

 C

Urate nephropathy

 D

Evidence of bone/joint damage

Ans. A

Explanation:

Ans. is ‘a’ i.e., Acute gouty arthritis

o “Allopurinol as well as uricosuries should not be started during acute attack of gout”.             –

o Tophi, urate nephropathy and bone & joint damage are seen in chronic gout.

o Allopurinol is the drug of choice for chronic gout.


Q. 21

Best drug for chronic gout in patient with renal impairment is –

 A

Naproxen

 B

Probenecid

 C

Allopurinol

 D

Sulfinpyrazone

Q. 21

Best drug for chronic gout in patient with renal impairment is –

 A

Naproxen

 B

Probenecid

 C

Allopurinol

 D

Sulfinpyrazone

Ans. C

Explanation:

Ans. is ‘c’ i.e., Allopurinol

o NSAIDs like naproxen have no role in chronic gout.

o Uricosuric drugs like probenecid and sulfinpyrazone are ineffective in the presence of renal insufficiency.

o Allopurinol is drug of choice for most cases of chronic gout.


Q. 22

Gout is a disorder of:

 A

Purine Metabolism

 B

Pyrimidine Metabolism

 C

Ketone Metabolism

 D

Protein metabolism

Q. 22

Gout is a disorder of:

 A

Purine Metabolism

 B

Pyrimidine Metabolism

 C

Ketone Metabolism

 D

Protein metabolism

Ans. A

Explanation:

Answer is A (Purine Metabolism):

Gout is primarily a disorder of purine metabolism.

Uric acid is the final breakdown product of purine degradation in humans. Primary Gout results from either increased production or impaired excretion of metabolic end products of purine metabolism (Uric Acid)- Harrison


Q. 23

Clinical features of Gout include:

 A

Severe joint pain

 B

Involvement of small joints

 C

Deposition of monosodium urate crystals in syynovium

 D

All of the above

Q. 23

Clinical features of Gout include:

 A

Severe joint pain

 B

Involvement of small joints

 C

Deposition of monosodium urate crystals in syynovium

 D

All of the above

Ans. D

Explanation:

Answer is D (All of the above):

1present with all of the features mentioned as options in the above question.

Gout

A disorder of purine metabolism characterized by hyperuricaemia, deposition of mono – sodium urate- monohydrate crystals in joints and per-articular tissuese and recurrent attacks of acute synovitis. Late changes include cartilage degeneration, renal dysfunction & uric acid ttrolithiasis

Epidemiology

Pathology

Clinical Feature

Treatment

• Commoner in Caucasians

•  More wide spread in men than

in women° (may be 20 :1)

Usually men over the age of 30

yearse; women are seldom

affected until after menopause.

Often there is a family history.

Tophi

Acute attack is sudden onset of

severe joint pain that lasts for a

week or two. Usually comes out of

blue but may be precipitated by

-minor trauma

–    illness

– unaccustomed exercise

Antiinflammatory

 

•  Tophi are

nodular deposits

of monosodium

urate

monohydrate

crystals, with an

•  Mainstay of

treatment during

acute attack is

administration of

antinflammatory

drug such as

cokhicine, NSA

•   Sterotype patient is obese,

rubicund, hypertensive and fond

associated

foreign body

alcohol

(except aspirin) or

of alcohol and may be nudged

reaction. It is

– ACTCH

glucocorticoidsQ

into an attack by uncontrolled

deposited in

– steroid withdrawl

•  Glucocorticoids may

administration of diuretics or

aspirin°

minute clumps

in connective

– hypouricemic therapy, drugs

be used.

• Common in Hypercurecemic

patients

• The rate of urate deposition in

joint and articular destruction

correlate with the duration and

severity of hyperuricemia. The

complications of gout correlate

tissue eg.

– articular cartilage’

– tendon (not muscle)”

-(pyri mol), MI, stroke

– The commonest sites are

metatarsophalangeal joint of big

toe” > ankle & finger joints and

olecranon bursae.

– The skin is red, shiny, swollen,

hot and extremely tender

1Hypourecemics

•  Probenecid or sulfin

pyrazone can be

used if renal

function is normal.

Xanthine oxidase

inhibitors

with both duration & severity of

–    periarticular

suggesting a cellulitis or septic

 

hyperuriacemia

tissue

arthritis

•  Allopurinol, a

xanthine oxidase

– Although the risk of developing clinical features of gout increases with increasing levels of serum uric acid, only a fraction of those with hyper

– synovium & joints

_ pinnae (cartilage) of ear

Investigations

inhibitor is usually

preferred.

These drugs should

never be started in

••Characteristic negatively

birefringent monosodium urate

crystals in the synovial fluid

uricaemia develop symptoms

– ligaments

examined by polarizing

acute attack, and

– Any factor that causes either an abrupt increase or decrease in the serum urate levels may

– articular ends of bone

– subcutaneous

e.

microscopy is diagnostic

•  X- rays show only soft tissue

swelling. Chronic gout may result

they should always be covered by an anti inflammatory

provoke an acute attack, the

hest correlations being factors

tissue’

_ kidney

in joint space narrowing & ry seconda   OA

preperations or colchic colchicine; otherwise they may

that cause an abrupt fall’.

 

•  Tophi appear as characteristic

actually precipitate

Serum uric acid levels can be

normal or low at the time of

acute attacke

– Despite these limitations, serum

uric acid is almost always

elevated at some timee and can

be used to follow the cource of

hypouricemic therapy.

•  Tophi may

ulcerate through

h thro

skin or destroy

cartilage &

periarticular

bone

punched out cysts or deep

erosions with over hanging bony

edgesQ(Marters         G’ or G sign).

These well defined erosions are

larger & slightly further from joint

margin than typical RA erosions.

an acute attack’. In

chronic tophaceous

gout and in all

patients with renal

complications,

allopurinol is drug

of choice’.

 


Q. 24

All of the following conditions are observed in Gout except:-

 A

Uric acid nephrolithiasis

 B

Deficiency of enzyme Xanthine oxidase

 C

Increase in serum urate concentration

 D

Renal disease involving interstitial tissues

Q. 24

All of the following conditions are observed in Gout except:-

 A

Uric acid nephrolithiasis

 B

Deficiency of enzyme Xanthine oxidase

 C

Increase in serum urate concentration

 D

Renal disease involving interstitial tissues

Ans. B

Explanation:

Answer is B (Deficiency of enzyme Xanthine oxidase):

Deficiency of enzyme xanthine oxidase does not lead to gout.

Xanthine oxidase is the enzyme that is needed for synthesis of uric acid from purine.

Deficiency of xanthine oxidase will result in decreased formation of uric acid and hence will not lead to gout, rather this shall prove protective in gout.

Allopurinol is a xanthine oxidase inhibitor that mimic’s the deficiency of xanthine oxidase and is actually used in treatment of gout.


Q. 25

Crystals deposited in Pseudogout:       

March 2013 (d)

 A

Sodium biurate

 B

Calcium oxalate

 C

Sodium pyrophosphate

 D

Amyloid

Q. 25

Crystals deposited in Pseudogout:       

March 2013 (d)

 A

Sodium biurate

 B

Calcium oxalate

 C

Sodium pyrophosphate

 D

Amyloid

Ans. C

Explanation:

Ans. C i.e. Sodium pyrophosphate


Q. 26

In a patient with gouty arthritis, strongly birefringent needle-shaped crystals with negative elongation in synvial fuid aspiration are composed of:

September 2007

 A

Monosodium urate

 B

Calcium pyrophosphate

 C

Homogentisic acid

 D

Sodium pyrophosphate

Q. 26

In a patient with gouty arthritis, strongly birefringent needle-shaped crystals with negative elongation in synvial fuid aspiration are composed of:

September 2007

 A

Monosodium urate

 B

Calcium pyrophosphate

 C

Homogentisic acid

 D

Sodium pyrophosphate

Ans. A

Explanation:

Ans. A: Monosodium Urate

Gout is a metabolic disease most often affecting middle-aged to elderly men and postmenopausal women. It is the result of an increased body pool of urate with hyperuricemia.

It is typically characterized by episodic acute and chronic arthritis, due to deposition of Monosodium urate (MSU) crystals in joints and connective tissue tophi, and the risk for deposition in kidney interstitium or uric acid nephrolithiasis.

If the clinical appearance strongly suggests gout, the diagnosis should be confirmed by needle aspiration of acutely or chronically involved joints or tophaceous deposits.

Acute septic arthritis, several of the other crystalline-associated arthropathies, palindromic rheumatism, and psoriatic arthritis may present with similar clinical features.

During acute gouty attacks, strongly birefringent needle-shaped MSU crystals with negative elongation are typically seen both intracellularly and extracellularly.

Synovial fluid cell counts are elevated from 2000 to 60,000/


Q. 27

Most common joint involved in gout is ‑

 A

Knee

 B

Hip

 C

MP joint of great toe

 D

MP joint of thumb

Q. 27

Most common joint involved in gout is ‑

 A

Knee

 B

Hip

 C

MP joint of great toe

 D

MP joint of thumb

Ans. C

Explanation:

Ans. is ‘c’ i.e., MP joint of great toe

Gout is the common end point of a group of disorders that produce hyperuricemia.

It is marked by transient attacks of acute arthritis intitiated by crystallization of monosodium urate into the joints, leading eventually to chronic gouty arthritis and deposition of masses of urates in joints and other sites, creating tophi.

Most common joint involved in gout is big toe, i.e. metatarsophalangeal joint of great toe.

Tophi are pathognomic of gout. They are formed by large aggregations of urate crystals. The urate crystals are surrounded by –


Q. 28

Which joint is most commonly affected in pseudogout –

 A

Knee

 B

Hip

 C

MP joint great toe

 D

MP joint thumb

Q. 28

Which joint is most commonly affected in pseudogout –

 A

Knee

 B

Hip

 C

MP joint great toe

 D

MP joint thumb

Ans. A

Explanation:

Ans. is ‘a’ i.e., Knee

Pseudogout

It is one of the forms of “Calcium pyrophosphate dihydrate” (CPPD) arthropathy.

Pseudogout commonly involves the larger joints. Knee joint is most commonly involved; other sites are wrist, elbow, shoulder, ankle. Involvement of small joints is uncommon.

Age group is > 60 yrs.

In CPPD arthropathy, CPPD deposition occurs in articular tissues. It can present in any of the following three forms :‑

1) Asympatomatic chondrocalcinosis

2) Acute synovitis – Pseudogout

3) Chronic pyrophosphate arthropathy

The radiologic hallmark of CPPD is “chondrocalcinosis. Chondrocalcinosis is seen as punctate and/or linear radiodense deposits in fibrocartilaginous joint menisci or articular hyaline cartilage.

Definitive diagnosis is made by synovial fluid polarised light microscopy which shows weakly positive, birefringent, rhomboid crystals of CPPD. [In gout polarized light shows – strongly negative birefringent, needle shaped crystals of monosodium urate]


Q. 29

Drug of choice for the treatment of acute gout in patients in whom NSAIDs are contraindicated is‑

 A

Colchicine

 B

Allopurinol

 C

Xyloric acid

 D

Paracetamol

Q. 29

Drug of choice for the treatment of acute gout in patients in whom NSAIDs are contraindicated is‑

 A

Colchicine

 B

Allopurinol

 C

Xyloric acid

 D

Paracetamol

Ans. A

Explanation:

Ans. is ‘a’ i.e., Colchicine

Treatment of Gout

1) Acute gout

  • NSAIDs are the drugs of choice
  • Colchicine is the fastest acting drug. However it is reserved for the patients in which NSAIDs are contraindicated, because colchicine can cause gastrointestinal disturbances.
  • If neither NSAIDs nor colchicin are tolerated, oral prednisolone is used.
  • Allopurinol and uricosuric drugs (sulfinpyrazone, probenacid) are not effective in acute gout because they will not relieve symptoms as they don’t have anti-inflammatory property.

2) Chronic gout

  • Allopurinal is the drug of choice.
  • Other drugs are sulfinpyrazone and probenacid.

Q. 30

Crystal of pseudogout is made up of ‑

 A

CPPD

 B

Urate

 C

Calcium carbonate

 D

Xanthine

Q. 30

Crystal of pseudogout is made up of ‑

 A

CPPD

 B

Urate

 C

Calcium carbonate

 D

Xanthine

Ans. A

Explanation:

Ans. is ‘a’ i.e., CPPD


Q. 31

Drugs used in treatment of acute gout

 A

Allopurinol

 B

Colchicine

 C

Pamidronate

 D

Methotrexate

Q. 31

Drugs used in treatment of acute gout

 A

Allopurinol

 B

Colchicine

 C

Pamidronate

 D

Methotrexate

Ans. B

Explanation:

Ans. is ‘b’ i.e., Colchicine

Management of gout

Treatment of acute gout

  • To provide rapid and safe pain relief
  • Drugs used are :

i) NSAIDse:

  • These are the most frequently used drugs to treat gout because they are so well tolerated.
  • Indomethacin is the agent of choice but other NSAIDs may be just as effective. Aspirin is usually avoided because low doses of aspirin aggravate hyperuricemia.

ii) Cokhicinee:

  • Colchicine is effective but less well tolerated than NSAIDs

iii) Glucocorticoidse:

  • Usually reserved for patients in whom colchicines or NSAIDs are contraindicated or ineffective.

Treatment of chronic gout  (maintain serum urate levels at 5.0 mg/dl or less) Allopurino12:

  • Xanthine oxidase inhibitor
  • Agent of choice for most patients with gout
  • Uricosuric agents
  • Probenecid0
  • SulfinpyrazoneQ

Q. 32

Tophi in gout found in all regions except

 A

Prepatellar bursae

 B

Muscle

 C

Helix of ear

 D

Synovial membrane

Q. 32

Tophi in gout found in all regions except

 A

Prepatellar bursae

 B

Muscle

 C

Helix of ear

 D

Synovial membrane

Ans. B

Explanation:

Ans. is ‘b’ i.e., Muscle

Location of Tophi

  • They are classically located along the helix of the ear.
  • Can also be seen in :-
  • Fingers
  • Toes
  • Prepattelar bursa
  • Olecranon
  • Although gout typically cuases joint inflammation, it can also cause inflammation in other synovial-based structures, such as bursae and tendons.
  • Tophi are collections of urate crystals in the soft tissues. They tend to develop after about a decade in untreated patients who develop chronic gouty arthritis.
  • Tophi may develop earlier in older women, particularly those receiving diuretics.

Q. 33

The pathogonomic finding in pseudogout is ‑

 A

CPPD crystals under microscope

 B

Polyarthritis with urinary sediment

 C

Juxta – articular osteopenia

 D

Bone spurs

Q. 33

The pathogonomic finding in pseudogout is ‑

 A

CPPD crystals under microscope

 B

Polyarthritis with urinary sediment

 C

Juxta – articular osteopenia

 D

Bone spurs

Ans. A

Explanation:

Ans. is ‘a’ i.e., CPPD crystals under microscope

Pseudogout

  • It is one of the forms of “Calcium pyrophosphate dihydrate” (CPPD) arthropathy
  • Pseudogout commonly involves the larger joints. Knee joint is most commonly involved; other sites are wrist, elbow, shoulder, ankle. Involvement of small joints is uncommon.
  • Age group is > 60 yrs.
  • In CPPD arthropathy, CPPD deposition occurs in articular tissues. It can present in any of the following three forms‑
  1. Asympatomatic chondrocalcinosis
  2. Acute synovitis – Pseudogout
  3. Chronic pyrophosphate arthropathy
  • The radiologic hallmark of CPPD is “chondrocalcinosis”. Chondrocalcinosis is seen as punctate and/or linear radiodense deposits in fibrocartilaginous joint menisci or articular hyaline cartilage.
  • Definitive diagnosis is made by synovial fluid polarised light microscopy which shows weakly positive, birefkingent, rhomboid crystals of CPPD. [In gout polarized light shows – strongly negative birefringent, needle shaped crystals of monosodium urate]
  • In acute synovitis form, leucocytosis (thousands to 1 lac cells/ 1) is seen in synovial fluid examination.
  • It may be associated with certain underlying disease such as –
  1. Primary hyperparathyroidism
  2. Hemochromatosis
  3. Hypomagnesemia
  4. Hypophosphatasia
  5. Hypothyroidism

Q. 34

Gout is a metabolic disorder of –

 A

Purine

 B

Pyramidine

 C

Glycogen

 D

Fatty acid oxidation

Q. 34

Gout is a metabolic disorder of –

 A

Purine

 B

Pyramidine

 C

Glycogen

 D

Fatty acid oxidation

Ans. A

Explanation:

Ans. is `a’ i.e., Purine

Disorder of purine metabolism

  • Gout
  • Lesch-Nyhan syndrome
  • Adenosine deaminase deficeincy
  • Purine nucleoside phosphorylase deficiency 

Disorder of pyramidine metabolism

  • Orotic aciduria
  • (3 – hydroxybutyric aciduria
  • Uraciluria-thyminuria

Q. 35

Which of the following is not used in acute attack of severe pain due to gout ‑

 A

Indomethacine

 B

Colchicine

 C

Febuxostat

 D

Corticosteroids

Q. 35

Which of the following is not used in acute attack of severe pain due to gout ‑

 A

Indomethacine

 B

Colchicine

 C

Febuxostat

 D

Corticosteroids

Ans. C

Explanation:

Ans. is ‘c’ i.e., Febuxostat



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