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House Clinical Pathology > DISORDERS OF URIC ACID METABOLISM > Flashcards

DISORDERS OF URIC ACID METABOLISM Flashcards

1
Q

PURINE DEGRADATION REVIEW
The end product of purine metabolism in humans is _______

A

uric acid.

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2
Q

PURINE DEGRADATION REVIEW

The nucleotide monophosphates (_____,_____,_____ ) are converted to their respective ______ forms (_____,________,______ ) by the action of __________.

A

AMP, IMP & GMP

nucleoside

adenosine, inosine & guanosine

nucleotidase

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3
Q

PURINE DEGRADATION REVIEW

The _____ group, either from AMP or adenosine, can be removed to produce _______ or _________.

A

amino

IMP or ionosine

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4
Q

PURINE DEGRADATION REVIEW

Inosine & guanosine are converted to _______ and ———- (______ bases) by purine ___________ —————.

________ is not degraded by this enzyme, it has to be converted to ______.

A

hypoxanthine & guanine

purine

nucleoside phosphorylase

Adenosine; inosine

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5
Q

PURINE DEGRADATION REVIEW

Guanine undergoes deamination by ______ to form ________.

____________ converts hyr.

A

guanase

xanthine

Xanthine oxidase

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6
Q

Uric acid metabolism

Normal blood level of uric acid

Females: ___-___ mg/dl.
Males: ___-____ mg/dl.

The daily excretion varies from ____-____ mg.

A

2 -5

3 -7

500 – 700

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7
Q

Nucleic acid content is (more or less?) in
non – vegetarian diet.

A

More

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8
Q

Uric acid is very soluble in water.

T/F

A

F

Uric acid is sparingly soluble in water.

.

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9
Q

HYPERURICEMIA

Hyperuricemia refers to an elevation in the ________ concentration.

This is sometimes associated with increased ___________ (_____uria)

A

serum uric acid

uric acid excretion

uricos

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10
Q

Purine Catabolism

Purine bases are converted first into ______ and then into _____ for excretion.

______________ catalyzes two steps in this process.

A

xanthine

urate

Xanthine oxidase

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11
Q

GOUT & PATHOPHYSIOLOGY

It is a metabolic disease associated with _____________ of _______

A

overproduction of uric acid.

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12
Q

GOUT & PATHOPHYSIOLOGY

At the physiological pH, uric acid is found in a __________ form as ___________.

A

more soluble; sodium urate.

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13
Q

GOUT & PATHOPHYSIOLOGY

In severe hyperuricemia, ______ of _______ get deposited in the ________ ,particularly in the _______.

Such deposits are commonly known as ______.

A

crystals of sodium urate

soft tissues; joints

tophi

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14
Q

GOUT & PATHOPHYSIOLOGY

Deposit of Tophi
This causes ______ in the joints resulting in a (painful or painless?) __________.

A

inflammation

Painful; gouty arthritis

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15
Q

GOUT & PATHOPHYSIOLOGY

Sodium urate or uric acid may also precipitate in ________ and ________ that results in ________ and _______ formation.

A

kidneys & ureters

renal damage & stone

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16
Q

Gout is of two types.

List

A

Primary Secondary

17
Q

GOUT & ITS PATHOPHYSIOLOGY

Primary
Increased _____________

Mostly affecting the (males or females?)

A

production of uric acid

Males

18
Q

GOUT & ITS PATHOPHYSIOLOGY

Primary

CAUSES:

Increase in substrate levels of _______

Increased ___________,

A

PP-ribose-P

nucleic acid turnover

19
Q

GOUT & ITS PATHOPHYSIOLOGY
Primary

CAUSES:

Specific ——— ______ defects

_________

Deficiency of enzymes of ________

A

heritable enzyme

PRPP synthetase

salvage pathway.

20
Q

GOUT & ITS PATHOPHYSIOLOGY
Primary

CAUSES:
Increase in substrate levels of PP-ribose-P, e.g. _______,________

Increased nucleic acid turnover, e.g. ——— (especially during _____), infection, __________ anaemias, psoriasis.

A

obesity, idiopathic.

tumors; treatment

chronic haemolytic

21
Q

GOUT & ITS PATHOPHYSIOLOGY
Primary

CAUSES:

Specific heritable enzyme defects, e.g. ______ or ______ deficiency, _______________ overactivity.

Deficiency of _______ of _______

A

HGPRT or G6PD

PP- ribose P synthetase

enzymes of salvage pathway.

22
Q

GOUT & ITS PATHOPHYSIOLOGY

SECONDARY; Is due to various diseases causing ____________ or _________

A

increased synthesis or decreased excretion of uric acid.

23
Q

GOUT & ITS PATHOPHYSIOLOGY

SECONDARY : CAUSES

_____________ defect (the cause in the commonest form of primary gout)

Decrease in ___________

______ or _______ affecting _________

A

Specific renal tubular

renal functional mass

Drugs or metabolites

tubular secretion

24
Q

GOUT & ITS PATHOPHYSIOLOGY

SECONDARY: CAUSES.

Decrease in renal functional mass, e.g. ___________ or _____________

Drugs or metabolites affecting tubular secretion, e.g. ———,________,________ (in low dosage), _______ ,_________

A

acute or chronic renal failure

thiazides, ethanol, salicylates

lactate, β-hydroxy- butyrate

25
Q

RISK FACTORS

(Men or Women?) get gout more than (Men or Women?) by about _____ to ______.

A

Men; women

three to one.

26
Q

How is gout diagnosed?

Diagnosis of gout usually involves:
A ___________ of the ______

________ of _________

_______ of ________ of an affected joint to ___________ of uric acid.

A

physical exam of the joints

X-rays of affected joints

Extraction of synovial fluid

look for crystals

27
Q

Risk factors

Having one or more of the following conditions puts someone at a higher risk for gout.

_______ dysfunction
_______ disease
Obesity
High _______
High _________
____________

A

Kidney

Heart

cholesterol

triglycerides

Diabetes

28
Q

A definitive diagnosis of gout requires that ____ of the following 12 markers must be present:

A ______
An episode of _______ in a ______
A history of ________________________
________ of the skin around a joint
_________ or _________ ——joint
________ of the ________ joint on _____ only
_____ of ______ joints on _____ only

A

6

tophus

arthritis in a single joint

more than one such episode of arthritis

Redness

Swollen or painful big toe

Inflammation; big toe ; one foot

Inflammation; one or more midfoot; one foot

29
Q

A tophus (________ deposits in the joints or body)

Redness of the skin around a joint ( _____)

Swollen or painful big toe joint (the _______ or _______ joint)

A

urate crystal

erythema

metatarsophalangeal or MTP

30
Q

A definitive diagnosis of gout requires that ____ of the following 12 markers must be present:

(Slow or Rapid?) joint _____ that reaches a maximum level within a _____ period

_______ levels of uric acid in the blood

An X-ray showing __________ in a joint

An X-ray showing ________ or ________ without any indication of prior inflammation

Joint _______ where the joint fluid tests _______ for infection.

A

6

Rapid; swelling; 24-hour

Elevated

uneven (asymmetric) swelling

joint cysts or bone erosions

inflammation; negative

31
Q

TREATMENT OF GOUT

The drug ______ is used for primary gout

It is a _______ of _______ that _______vely inhibits enzyme _______

Changes in diet to avoid foods ___________ reduce the inflammation and pain in _____ cases.

Your doctor may also prescribe ______ (to alleviate pain and swelling).

A

Allopurinol

structural analog of hypoxanthine

competiti; xanthine oxidase

high in purines ; mild; NSAIDs

32
Q

TREATMENT OF GOUT

For more severe gout, other medications are needed to lower the uric acid. These may include one or more of the following:

_______ (Uloric)

_________ (Colcrys)

_________ (Zurampic)

__________ (Zyloprim)

______________(Krystexxa)

A

Mnemonic: Fucking CLAP!

Febuxostat

Colchicine

Lesinurad

Allopurinol

Pegloticase

33
Q

OTHER URIC ACID METABOLISM DISORDERS

Lesch-Nyhan syndrome

It is due to the deficiency of ___________________ an enzyme of ________

It is a/an (autosomal or sex linked?) metabolic disorder affects ______

A

hypoxanthine guanine phosphoribosyl transferase (HGPRT)

purine salvage pathway.

sex linked; only male

34
Q

OTHER URIC ACID METABOLISM DISORDERS
Lesch-Nyhan syndrome

_______, _______ behaviour, _____ disability etc
Irresistible urge to __________, often causing _______

A

Mental retardation

aggressive ; learning

bite their fingers and lips

self mutilation.

35
Q

OTHER URIC ACID METABOLISM DISORDERS

XANTHINURIA
____eased uric acid levels in the serum (___mg/dl) called as hyperuricemia

Mostly associated with a rare genetic defect in the enzyme ______
Leads to the _____eased excretion of ________ and _______

A

Decr

Less than 2

xanthine oxidase; incr

xanthine and hypoxanthine

36
Q

OTHER URIC ACID METABOLISM DISORDERS

XANTHINURIA

Xanthinuria frequently causes the formation of ________ in the ________

A

xanthine stones

urinary tract.

House Clinical Pathology (45 decks)

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