Gout- Pathophysiology, Risk Factors, Symptoms

Question 1

Gout patho: where do purines come from?

Answer 1

Diet and tissue breakdown

Question 2

Breakdown of purines leads to what?

Answer 2

UA formation

Question 3

Is UA soluble?

Answer 3

Soluble at concentrations <6.7mg/dl, but otherwise insoluble

Question 4

In most mammals, what happens to UA?

Answer 4

It gets broken down by uricase into allantoin and excreted in the urine

Question 5

What happens in humans?

Answer 5

We don’t have uricase, so we’re forced to excrete UA

Question 6

What happens when UA solubility is saturated?

Answer 6

UA precipitates into monosodium urate crystals, which deposit in the joints, become phagocytosed, and triggers an immune response

Question 7

What is excess serum UA caused by?

Answer 7

Overproduction of urate
Underexcretion of urate

Question 8

Gout presentation in a flare

Answer 8

Rapid onset of severe pain, erythema, and swelling in single or multiple joints

Question 9

Podagra clinical presentation

Answer 9

Monoarticular arthritis, usually affects the big toe but can affect other joints of the lower extremity. Affected joint is swollen, erythematous, and tender

Question 10

Interval gout presentation

Answer 10

Asymptomatic period between attacks

Question 11

Tophaceous gout presentation

Answer 11

Deposits of monosodium urate crystals in soft tissues

Question 12

Complications of tophaceous gout

Answer 12

Soft tissue damage, deformity, joint destruction, nerve compression syndromes

Question 13

Atypical gout presentation

Answer 13

Polyarthritis affecting any joint, upper or lower extremity

Question 14

Atypical gout can be mistaken for what?

Answer 14

RA, OA

Question 15

Gouty nephropathy presentation

Answer 15

Nephrolithiasis
AKI, CKD

Question 16

Gout diagnosis

Answer 16

Diagnosed by synovial fluid aspiration and identification of monosodium urate crystals

Question 17

Gout is associated with what SUA level?

Answer 17

> 6.8mg/dl

Question 18

What generally confirms a gout diagnosis?

Answer 18

A flare/attack presentation

Question 19

Will SUA be elevated in an attack?

Answer 19

Not always

Question 20

Will all patients with hyperuricemia develop gout?

Answer 20

No

Question 21

If a patient has no synovial fluid aspiration and monosodium urate crystals but they have an elevated SUA and clinical presentation consistent with gout, can they be treated?

Answer 21

Yes

Question 22

Do patients who have no symptoms of a flare but have elevated UA levels need to be treated?

Answer 22

No

Question 23

Risk factors for gout: age

Answer 23

Increased age, increased risk

Question 24

Gout risk factors: sex

Answer 24

Men > women, ratio is 3-4:1 and decreases with age due to estrogen loss

Question 25

Disease states associated with gout

Answer 25

T2DM
HLD
Obesity
Renal insufficiency/CKD
HTN
Organ transplantation
CHF

Question 26

Gout risk factors: diet that precipitates gout

Answer 26

Hyperuricemic foods like meat, seafood, beer and liquor (not wine), soft drinks, fructose

Question 27

Gout risk factors: diet that will help gout

Answer 27

Uricosuric: coffee, dairy, vitamin C

Question 28

Gout risk factors: medications that precipitate gout

Answer 28

Thiazide diuretics, loops, nicotinic acid, <1g/d ASA

Question 29

Gout risk factors: medications that would work in gout

Answer 29

Losartan, fenofibrate

Question 30

Precipitating factors of gout

Answer 30

Alcohol and high purine ingestion, stress, medications (including UA lowering agents)

Question 31

Goal of therapy in acute gout

Answer 31

Reduce pain and duration of attacks

Question 32

Goal of therapy in chronic gout

Answer 32

Prevent future attacks and maintain SUA <6.0mg/dl