Term
1) in the absence of a history of gout, asymptomatic hyperuricemeia does not require treatment
2) acute gouty arthritis may be treated effectively with short courses of high dose non-acetylated NSAIDs, corticosteroids, or colchicine
3) cholchicine is highly effective at relieving acute attacks of gout but has the lowest benefit/toxicity ratio of the available agents
4) uric acid nephroliathisis should be treated with immediate adequate hydration (2-3 L/day), a urine alkalinizing agent, and 60-80 mEq of KHCO3 or K citrate
5) treatment with urate lowering drugs to reduce risk of recurrent attacks is considered cost effective with 2 or more attacks/year
6) uricosuric agents should be avoided in renal impairment (CrCl < 50 mL/min), a history of nephrolithiasis, or uric acid overproduction
7) slowly titrate xanthine oxidase inhibitors to achieve suppression of uric acid < 6 mg/dL. Allopurinol first line, febuoxostat intolerant or with mild to moderate renal impairment. These drugs should not be started during an acute attack or unopposed without colchicine or NSAIDs |
|
Definition
|
|
Term
EtOH intake
renal impairment
FHx
medications: thiazide diuretics, loop diuretics
obesity
HTN
advanced age
metabolic syndrome
elevated uric acid |
|
Definition
|
|
Term
freely filtered across glomerulus
proximal tubule reabsorption of urate follows Na
high Na intake/dehydration promote reabsorption
normally production = elimination
24 hour urine collection:
< 800 mg = underexcretor
> 800 mg = overproducer |
|
Definition
|
|
Term
idiopathic:
underexcretor
overproducer
secondary:
myeloproliferative disorders
"tumor lysis syndrome" - may get gout from chemotherapy; chemotherapy kills cells in the tumor and those cell release a large amount of uric acid into the circulation
renal failure
drug related: diuretics, nicotinic acid, salicylates (<2 g/day), ethanol, pyrazinamide, levodopa, ethambutol, cytotoxic drugs, cyclosporine |
|
Definition
| classification of gouty arthritis: idiopathic and secondary |
|
|
Term
elevated serum uric acid:
men: > 7 mg/dL
women: > 6 mg/dL
urate crystal formation in joint space
excruciating pain, swelling, redness, fever
first MTP joint (big toe) 50% or initial attacks
most common in peripheral joints
ankles, knees, wrists, fingers |
|
Definition
| acute gouty arthritis signs and symptoms |
|
|
Term
urate stone formation in the kidney
associated with low urinary pH (<6)
urate less ionized (less soluble) in acidic urine
concentrated urine (dehydration)
urinary uric acid excretion > 1100 mg/day
increased risk for uric acid-Ca oxalate stones |
|
Definition
| definition of uric acid nephrolithiasis |
|
|
Term
acute and chronic uric acid nephropathy
precipitation of uric acid crystals in collecting ducts and ureters
most commonly associated with:
myeloproliferative disorders
tumor-lysis syndrome |
|
Definition
| definition of gouty nephropathy |
|
|
Term
urate deposits
late complications of chronic hyperuricemia
great toe, ears, olecranon bursae, achilles tendon, knees, wrists, hands
can lead to joint space erosions and deformities |
|
Definition
| definition of tophaceous gout |
|
|
Term
[image]
colchicine
NSAIDs
corticosteroids |
|
Definition
|
|
Term
reduces macrophage migration
most effective if started within 24 hours of attack
initiate 1.2 mg now, then in 1 hour take 0.6 mg
GI side effects (N/V/D)
toxicities:
neutropenia, myopathy (statin use), liver toxicity, avoid IV use |
|
Definition
| MOA and dose (acute) of colchicine |
|
|
Term
sulindac
indomethacin
naproxen |
|
Definition
| FDA approved NSAIDs for gout |
|
|
Term
GI (history of ulcer)
renal (CHF, HTN)
bleeding (concurrent anticoagulant use)
consider PPI if must be used in high risk patient |
|
Definition
|
|
Term
ADR of corticosteroids
increase in immature WBCs
patient will still be immunosuppressed b/c the WBCs are immature |
|
Definition
|
|
Term
patients with multiple attacks (2-3 attacks/year)
probenecid
sulfinpyrazone
allopurinol
febuxostat: if they cannot tolerate allopurinol or have renal insufficiencies
colchicine
DO NOT START PREVENTATIVE THERAPY DURING AN ACUTE ATTACK
start preventative therapy 2 weeks after the attack
DO NOT START PREVENTATIVE THERAPY WITHOUT AN NSAID OR COLCHICINE
if this is done, it may cause an acute flare |
|
Definition
prophylactic gout threrapy
NOT for acute treatment |
|
|
Term
uricosuric
increases clearance of uric acid
decreases proximal tubular reabsorption
NOT useful in patients with poor renal function (< 50 mL/min)
DO NOT use in overproducers
start with low dose to prevent stones |
|
Definition
|
|
Term
uricosuric
increased clearance of uric acid
decreased proximal tubular reabsorption
NOT useful in patients with poor renal function (< 50 mL/min)
DO NOT use in overproducers
start with low dose to prevent stones
side effects more prominent
antiplatelet effect: do not use with other antiplatelets/anticoagulants |
|
Definition
|
|
Term
xanthine oxidase inhibitor
has an active metabolite, oxypurinol
DO NOT USE IN ACUTE GOUT!
can be used in overproducers or underexcretors
ADJUST FOR RENAL FUNCTION
used to prevent gout attacks |
|
Definition
|
|
Term
xanthine oxidase inhibitor
NOT FOR USE IN ACUTE GOUT!
use in overproducers or underexcretors
no renal dosing, like there is with allopurinol
used to prevent gout attacks |
|
Definition
|
|
Term
fluid intake 2-3 L/day
alkalinization of urine
K bicarb or K citrate
acetazolamide
reduce dietary purine/protein intake
reduce urinary excretion (allopurinol) |
|
Definition
| treatment of nephrolithiasis |
|
|
Term
fenobibrate: increases clearance of hypoxanthing
losartan: inhibits renal tubular reabsorption of uric acid, increasing excretion; alkalinizes urine (may reduce risk of stones); unique to this ARB |
|
Definition
| miscellaneous gout treatments |
|
|
Term
generally does NOT require treatment
increase fluids, reduce dietary purines, reduce Na
elevated uric acid levels implicated in HTN and CAD
asymptomatic hyperuricemia is NOT a contraindication to use of HCTZ/diuretics |
|
Definition
| treatment of asymptomatic hyperuricemia |
|
|
Term
pain following prolonged use of joint
morning stiffness < 15-20 minutes or prolonged rest
joint bony enlargement
decreased range of motion
tenderness on palpitation usually absent
crepitus at late state disease |
|
Definition
| signs and symptoms of osteoarthritis |
|
|
Term
predominantly a diagnosis of exclusion
ESR normal, althought may not be sensitive to specific type of inflammatory process
joint radiography:
normal early
narrowed joint space
osteophyte formation
subchondral bony sclerosis
joint aspiration if clinical picture unclear:
< 500 cells = OA
> 2000 cells (neutrophils) = RA |
|
Definition
| diagnosis of osteoarthritis |
|
|
Term
rheumatoid arthritis:
primary joints affected - metacarpophalangeal, proximal interphalangeal
Heberden's nodes - absent
joint characteristics - soft, warm, and tender
stiffness - sorse after resting (morning stiffness)
lab findings - positive rheumatoid factor, positive anti-CCP antibody, elevated ESR and C reactive protein
osteoarthritis:
primary joints affected: distal interphalangeal, carpometacarpal
Heberden's nodes - frequently present
joint characteristics - hard and bondy
stiffness - if present, worse after effort, may be described as evening stiffness
lab findings - normal ESR and C reactive protein |
|
Definition
|
|
Term
weight loss!
joint protection
range of motion exercises
1st line pharmacotherapy = tylenol 1000 mg QID +/- glucosamine/chondroitin
2nd line pharmacotherapy = NSAIDs (nonacetylated salicylates, IBU, or naproxen) +/- glucosamine/chondroitin |
|
Definition
|
|
Term
[image]
NAPQI binds with proteins in the liver to cause a progressive hepatitis |
|
Definition
| metabolism of acetaminophen |
|
|
Term
|
Definition
|
|
Term
|
Definition
| nomogram used to predict if a patient should get N-acetyl-cysteine |
|
|
Term
decreased pain scores
increased mobility
decreased joint space narrowing
major limitation is reliability of ingredients
glucosamine and chondroitin help replace damaged cartilage in degenerative OA joints
enhances aggrecan which provides cartilage with its "shock absorbing" characteristics
more aggrecan is formed in vivo when chondrocytes are mixed with glucosamine |
|
Definition
| MOA of glucosamine/chondroitin |
|
|
