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Gout and Pharm for Gout Flashcards

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1
Q

colchicine

A

depolimerization of microtubules, inhibits the function of polymorphonuclear lymphocytes
Tx: gout (ACUTE, PROPHYLAXIS of attack, FAMIAL MEDITERRANEAN FEVER)
SE: GI (acute), Blood dyscrasia (chronic), MYOPATHY (proximal weakness and elevated CPK), peripheral neuropathy, rhabdomyolysis
does NOT reduce uric acid
CI: renal disease
monitor: CBC, ALK PHOS
metab: hepatic de-acetylation
not removed by dialysis, no antidote

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2
Q

indomethacin

A

with ANTACID
COX inhibitor: analgesic, antipyretic
inhibits leukocyte motility
Tx: ACUTE gout
SE: GI, CNS (severe frontal headache), hematopoietic
CI: antagonize furosemide and HCTZ (antagonize diuretics)

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3
Q

allopurinol

A

xanthine oxidase inhibitor (competitive)
metabolite (oxypurinol) inhibits xanthine oxidase (non-competitive: irreversible: suicide inhibitor)
effect: reduces uric acid levels in plasma and urine: increases xanthine and hypoxanthine, dissolves crystals, prevent kidney stones
Tx: gout in primary and secondary hyperuricemia
AE: FLARE UPs (acute gout), hypersensitivity: DERMATITIS
monitor: LFTs
CI: 6-MP, ampicillin (and related antibiotics)
can use in RENAL IMPAIRMENT (adjust dose for insufficiency)

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4
Q

probenecid

A

interferes with uric acid reabsorption by BRUSH BORDER transporter (more UA in urine)
Tx: gout in patients that excrete less than 1 g of UA/day (dissolves uric acid in joints)
DRINK LOTS of WATER
CI: renal impairment, salicylates and other NSAIDs (inhibit uricosuric action of probenecid)
SWITCH to acetaminophen
HYDROCHLOROTHIAZIDE diminishes availability: effects transport across tubule

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5
Q

febuxostat

A

xanthine oxidase inhibitor
Tx: gout in people allergic to allopurinol
AE: FLARE UP (must give PROPHYLACTIC)
CAN USE in RENAL IMPAIRMENT

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6
Q

pegloticase

A

IV (expensive)
LONG acting: 2 weeks
urate oxidase: uric acid to allantoin (easily excreted in urine)
lowers uric acid in serum and urinary excretion
AE: acute gout (need PROPHYLAXIS)
Tx: SEVERE gout in those that conventional therapy is CI or has been ineffective
can develop Ab against PEG (most patients)

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7
Q

6-mercaptopurine

A

metabolized by xanthine oxidase
ALLOPURINOL inhibits metabolization and increases its blood levels
MUST REDUCE DOSE

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8
Q

uricosuric agents

A

increase renal excretion of uric acid
PROXIMAL CONVOLUTED TUBULE: filtered uric acid is completely reabsorbed early, next segment secretes, next segment partially reabsorbs (brush border transporter)

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9
Q

gout

A

monoarticular arthritis: DISTAL LOWER EXTREMITY (1st MTP)
late stage: asymmetric polyarticular
Dx: urate crystals neg. birefringence (yellow parallel)
Sx: PAIN, tophi, multiple attacks, mx inflammation in 1 day, REDNESS, hyperuricemia
MONOSODIUM URATE crystals
risks: alcohol (BEER), seafood, red meat, genetics
protective: milk, yogurt

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10
Q

hyperuricemia

A

plasma rate greater than 6.8-7 mg/dL

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11
Q

tophi

A

monosodium urate accumulation

locations; extensor surface of extremities

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12
Q

urolithiasis

A

5-10% of urinary stones in US
40% in hot, arid climates with low urine volumes and acidic pH
20% of un-Tx’ed gout patients have them
80% of stones in gout patients are completely uric acid, rest just have nidus of uric acid
urinary stone of uric acid
risk factors: increased uric acid excretion, reduced urine volume, low urine pH

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13
Q

Where in the kidney can monosodium rate deposit?

A

interstitium

leads to renal impairment

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14
Q

podagra

A

gout in big toes

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15
Q

Does rate precipitate at high or low pH?

A

low: acidotic conditions precipitate urate

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16
Q

xanthine oxidase

A

converts xanthine to uric acid

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17
Q

uricase

A

in animals not humans

converts uric acid to allantoic acid

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18
Q

hypoxanthine guanine phosphoribosyl transferase (HGPRT)

A

purine salvage pathway

hypoxanthine and guanine to IMP and GMP

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19
Q

How does the kidney deal with uric acid?

Study These Flashcards
A
  1. glomeruli: freely filtered
  2. PROXIMAL tubule: completely reabsorbed
  3. PROXIMAL tubule: half secreted, largely reabsorbed
    overall: 8-12% excreted
    lots of transporters: URAT, OAT, ABCG, MRP, NPT1
20
Q

In what ways does hyperuricemia develop? Which is more common?

Study These Flashcards
A

90%: decreased efficiency of uric acid excretion

10%: increased uric acid production (typically inherited defects)

21
Q

Do underexcretors of uric acid have a normal rate of urinary uric acid excretion?

Study These Flashcards
A

YES, production and clearance are relatively equal
REDUCED EFFICIENCY of urate excretion that obligates a higher serum rate concentration to achieve the necessary rate of uric acid excretion

22
Q

Who has more total body urate: men or women?

Study These Flashcards
A

men have twice as much (1200mg)

women may have increased excretion due to estrogen

23
Q

Do the intestines play a role in urate metabolism?

Study These Flashcards
A

bacteria degrade uric acid
1/3 of total urate metabolism
high uric acid may cause rate to deposit occutly

24
Q

When does primary hyperuricemia begin in men?

25
When do women get hyperuricemia?
post menopause
26
When is the highest incidence of gout in men? women?
men: 30 - 45 yrs women: 55 - 70 yrs two decades later than initial physiologic increase in serum urate
27
inflammatory cycle of gout attack
complement (C5a), macrophages, fibroblasts, mast cells, 1. IL-1B: activate neutrophils and endothelial cells in blood 2. NEUTROPHILS move into tissue and phagocytose urate crystals 3. crystals coated with Ig: IL-1B, IL-8, TNF, proteases, ROS; uncoated crystals: lyse phagolysosome 4. local tissue damage lease to additional neutrophil recruitment
28
Lesch-Nyhan syndrome
X-linked HPRT deficiency overproduction of uric acid, self-mutilation
29
systemic conditions promoting hyperuricemia: overproduction
hemolytic anemia, sickle cell disease, polycythemia vera, megaloblastic anemia, thalassemia, myelodysplastic syndrome, leukemia, lymphoma, multiple myeloma, Waldenstrom's macroglobulinemia, essential thrombocytosis, tumors, tumor less syndrome, psoriasis, sarcoidosis, metabolic myopathies, mitochondrial myopathies
30
systemic conditions promoting hyperuricemia: underproduction
renal insufficiency, dehydration, lactic acidosis, ketoacidosis
31
systemic conditions promoting hyperuricemia: over and underproduction
MI, CHF, sepsis
32
systemic conditions promoting hyperuricemia: metabolic states
hyper/hypothyroidism, hyper/hypoparathyroidism, obesity
33
drugs that cause hyperuricemia
CYCLOSPORINE, ALCOHOL, LEAD POISONING other: CSFs, ethambutol, thiazide and loop diuretics salicylates, nicotinic acid, pyrazinamide
34
drugs that increase uric acid excretion
clycopyrrolate, iopanoic acid, Ca ipodate, probenecid, salicylates, calcitonin, citrate, estrogens, fenofibrate, acetohexamide, amflutizole, ascorbic acid, azapropazone, azauridine, benzbromarone, dicumarol, difluisal, glycerol guaiacolate, glycine, iodopyracte, losartan, meclofenamic acid, orotic acid, outdated tetracyclines, phenolsulfonphthalein, sulfinpyrazone
35
Tx for acute gout
NSAIDs, colchicine, steroids, adrenocorticotropic hormone
36
Tx for chronic gout
give acute gout Tx first to prevent flare lowest dose to maintain serum rate below 6.8 mg/dL- preferably below 6 allopurinol, febuxostat, pegloticase DON'T use these for just hyperuricemia
37
What should hyperuricemic people be screened for?
HTN, CAD, DM, obesity, alcoholism
38
Diseases gout is associated with
obesity, hypertriglyceridemia, glucose intolerance, metabolic syndrome, HTN, atherosclerosis, hypothyroidism renal insufficiency
39
What situations may lead to uric acid nephropathy?
chronic hyperuricemia | acute hyperuricemia in tumor lysis syndrome
40
Do you treat asymptomatic hyperuricemia?
NO | try to identify cause
41
pseudogout
old people (70-75 yrs) CALCIUM PYROPHOSPHATE DIHYDRATE recurrent/chronic inflammatory monoarticular/oligoarticular arthritis: joints not affected by osteoarthritis: wrist, knee, ankle, MCP, elbow; hemarthrosis Sx: pseudo-polymyalgia rheumatica, FEVER, carpal tunnel, CNS disease complicating ligamentum flavum or transverse ligament of atlas incidental finding blue and rhomboid on parallel, BIREFRINGENCE familial: ANKH, chromosome 5p dysregulated chondrocyte differentiation NLRP3 Dx: ultrasound (can't always see chonedrocalcinosis on X-ray) Dx before 55: consider underlying disease, familial Dx older than 55: consider HYPERPARATHYROIDISM
42
pseudogout associations
osteoarthritis, trauma, familial metabolic: hyperparathyroidism, hemochromatosis, hypophosphatasia, hypomagnesemia, ochronosis NOT renal disease or diuretic use (unless dialysis dependent)
43
ANKH
AD chromosome 5p encodes transmembrane protein with functions including PPi transport FAMILIAL PSEUDOGOUT
44
calcium hydroxyapatite (HA) deposition disease
chronic renal failure, hyperphosphatemia enhances HA deposits both in and around joints elderly: HA released from bone causing acute synovitis in osteoarthritis knee, shoulder (Milwaukee shoulder) joint destruction: attenuation/ rupture of supporting structures subacromial bursitis, pseudopodagra (found female) Tx: NSAIDs, selective COX-2 inhibitors, local steroid injection, local irrigation, high freq. ultrasound association: severe OSTEOARTHRITIS no biofringence
45
calcium hydroxyapatite
primary mineral of bone and teeth | abnormal accumulations in areas of its damage
46
NLRP3 (cryopyrin)
CPPD | activates inflammasome leading to activation of capsize-1 and IL-1B

Musculoskeletal (13 decks)

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