Case: Atty.

Tom Ador San Miguel is 52 year old obese male who comes to his family doctor complaining of
severe pain in his first metatarsophalangeal joint (podagra) that began at night after an episode of binge
eating and drinking. He admits to be an avid meat eater and drinks red wine every night. His history is
significant for removal of kidney stones, which on the previous laboratory report was analyzed to be uric acid
stones. He is known hypertensive with diabetes mellitus type 2. He takes antidiabetic and antihypertensive
medicines very irregularly.

Pertinent PE findings: temperature of 38.2C, BP 140/100. His right MTP joint is red, hot and swollen, painful
to active and passive motion, with tophaceous deposits in the left ear and olecranon bursitis.

Laboratory findings CBC count revealed leukocytosis with neutrophilia, elevated serum uric acid, and
elevated ESR. Urinalysis showed urate crystals. Xray of the foot showed punched out erosions, in the right
big toe at MTP joint producing overhanging spicules.

A diagnosis of acute gouty arthritis was given by his doctor. He was immediately given colchicine and
prescribed allopurinol. His condition gradually improved. He was referred to the hospital dietary services for
a diet low in purines and advised to increase his fluid intake and follow up for his DM and hypertension.

1. What is acute gouty arthritis? (Hedder, Jaedt, Paulo, Czai)

Pau
- Acute gouty arthritis or commonly referred to as gout is a form of inflammatory arthritis
characterized by recurrent attacks of redness, tenderness, heat, and swelling typically on a joint
(most common is the metatarsal-phalangeal joint of the big toe). It is due to an elevated level of uric
acid in the blood. It can lead to kidney stones and urate nephropathy among other renal diseases.
- Bibo kid tayo so sagutin na din natin ung genetics part HAHA (pau)
- Gout is also 60% attributed to abnormalities in SLC2A9, SLC22A12, and ABCG2 genes which are
commonly associated with hyperuricemia, where a loss-of-function mutation especially on the
ABCG2 gene causes a defective or malformed protein component for the pump that actively
sequesters uric acid from the bloodstream into the urine.
Acute gouty arthritis- Gout is a form of inflammatory arthritis characterized by recurrent attacks of a
red, tender, hot, and swollen joint. Acute gout is a condition that often affects only one joint. The joint at the
base of the big toe is affected in about half of all cases. (Jaedt) omg meron pala dito haha (pau)

What are the precipitating factors that can lead to this condition? (Hedder)
Genetics. Many people with gout have a family history of the disease.
Gender and age. Gout is more common in men than in women and more common in adults
than in children.
Weight. Being overweight increases the risk of developing gout because there is more tissue
available for turnover or breakdown, which leads to excess uric acid production.
Alcohol consumption. D rinking too much alcohol can lead to a buildup of uric acid because
alcohol interferes with the removal of uric acid from the body.
Diet. Eating too many foods that are rich in purines such as liver, dried beans and peas,
anchovies and gravies, can cause or aggravate gout in some people.
Lead exposure. In some cases, exposure to lead in the environment can cause gout.
Other health problems. R enal insufficiency, or the inability of the kidneys to eliminate waste
products, is a common cause of gout in older people. Other medical problems that contribute to
high blood levels of uric acid include
high blood pressure
 hypothyroidism (underactive thyroid gland)
conditions that cause an excessively rapid turnover of cells, such as psoriasis,
hemolytic anemia, or some cancers
Kelley-Seegmiller syndrome or Lesch-Nyhan syndrome, two rare conditions in which
the enzyme that helps control uric acid levels either is not present or is found in
insufficient quantities.
Medications
diuretics, which are taken to eliminate excess fluid from the body in conditions like
hypertension, edema, and heart disease, and which decrease the amount of uric acid passed in
the urine
salicylate-containing drugs, such as aspirin
niacin, a vitamin also known as nicotinic acid
cyclosporine, a medication that suppresses the bodys immune system (the system that
protects the body from infection and disease). This medication is used in the treatment of some
autoimmune diseases and to prevent the bodys rejection of transplanted organs.
levodopa, a medicine used in the treatment of Parkinsons disease.

What is the relationship of alcohol and hyperuricemia? (Czai)

Increases production of uric acid by increasing production of lactic acid, hence lactic
acidosis
Increases the plasma concentrations of hypoxanthine and xanthine via the acceleration of
adenine nucleotide degradation, and is a possible weak inhibitor of xanthine
dehydrogenase
As a byproduct of its fermentation process, beer additionally contributes in increased purine
(predominantly guanosine) and UA production by accelerating the degradation of
adenosine triphosphate to adenosine monophosphate, a UA precursor
Ethanol decreases excretion of uric acid by competitively inhibiting UA secretion by the
proximal tubules

2. What are tophi? What is the appearance of tophi and uric acid crystals on synovial fluid
examination? (Ryan, Shannen, Dan, Jem)
Tophi(Tophus) are deposits of uric acid crystals, usually seen in people in long with long
standing hyperuricemia.
Tophi are characteristic for gout and they are usually found in joints such as elbows or
knees.
Common diagnosis for gout is synovial fluid examination. The presence of Monosodium
urate(Uric acid) crystals under the microscope. They are often described as needle like
crystals. Under polarized light, they tend to flare.
MSU crystals are routinely seen as needle-shaped crystals. They may be extracellular or
located within the cytoplasm of neutrophils. They are frequently seen sticking through the
cytoplasm of the cell.
The molecules in MSU crystals run parallel to the long axis of the crystal and, when aligned
with the slow vibration, the velocity of the slow light passing through the crystal is not
impeded as much as the fast light, which runs against the grain and produces a yellow
color. This is considered negative birefringence (subtraction of velocity from the fast ray).

3. What is the role of colchicine and allopurinol? (Shenna, Vini, Mako, Ches)
 Colchicine decreases swelling and reduces accumulation of uric acid crystals in the
affected joints. It works by reducing the number of white blood cells which travel into the
inflamed areas. This helps break the cycle of inflammation and reduces the swelling and
pain of the gout attack
Mechanism Of Action: Colchicines effectiveness as a treatment for gout has been
postulated to be due to its ability to block neutrophil-mediated inflammatory responses
induced by monosodium urate crystals in synovial fluid. Colchicine disrupts the
polymerization of -tubulin into microtubules, thereby preventing the activation,
degranulation, and migration of neutrophils to sites of inflammation. Colchicine also
interferes with the inflammasome complex found in neutrophils and monocytes that
mediates interleukin-1 (IL-1) activation.
Allopurinol is used to treat gout and certain types of kidney stones. It is also used to prevent
increased uric acid levels in patients receiving cancer chemotherapy. These patients can
have increased uric acid levels due to release of uric acid from the dying cancer cells.
Allopurinol works by reducing the amount of uric acid made by the body. Increased uric acid
levels can cause gout and kidney problems.
Mechanism of Action: Allopurinol and its active metabolite, oxypurinol, inhibits the enzyme
xanthine oxidase, blocking the conversion of the oxypurines hypoxanthine and xanthine to
uric acid. Elevated concentrations of oxypurine and oxypurine inhibition of xanthine oxidase
through negative feedback results in a decrease in the concentrations of uric acid in the
serum and urine. Allopurinol also facilitates the incorporation of hypoxanthine and xanthine
into DNA and RNA, leading to a feedback inhibition of de novo purin synthesis and a
decrease in serum uric acid concentrations as a result of an increase in nucleotide
concentration.

4. If left untreated, what are the possible complications of gout? (Reg, Mar, Des, Cel)
Hi. Since 4 tayo here, maybe we can give 1 each? - C
Tophi (sing. tophus):
deposit of uric acid crystals, in the form of monosodium urate crystals, in people
with longstanding hyperuricemia
Pathognomonic for the gout.
Chronic tophaceous gout is known as Harrison Syndrome
Form in the joints, cartilage, bones, and other places throughout the body.
Sometimes, tophi break through the skin and appear as white or yellowish-white,
chalky nodules
Limit joint function and cause bone destruction, leading to noticeable disabilities,
especially when gout cannot successfully be treated
Kidney stones
The same crystals can deposit in the kidneys. These stones are very painful and
can cause permanent kidney damage by 1) forming an obstruction that prevents
your kidneys from removing wastes and causing infection, and 2) scarring the
kidneys with rough or sharp edges.
Joint deformity
 If the cause of gout is not treated, acute attacks happen more and more often. The
inflammation caused by these attacks, as well as the growth of tophi, causes
damage to joint tissues. Joints can eventually come out of alignment and become
immobile.
Heart disease
Gout is caused by increased levels of uric acid in the blood, and this deposits as
crystals in the joints and sets off the inflammatory response of the body.
Inflammation is a part of the process that results in blood clots that can cause heart
attacks and stroke. source
Inflammation causes damage to the blood vessel, disrupting blood flow
causing blood clots to form source