Chapter 4: Bone and Joint Disorders Flashcards
1
Q
NSAID drugs
A
ASA
Tylenol
Ibuprofen
Mobic
2
Q
GI upset with NSAID usage
A
prescribe an H2 blocker with it
3
Q
Duration of Ibuprofen/ASA usage before re-evaluation is necessary
A
follow up is needed if routine use exceeds 3 days
4
Q
Perferred NSAID for mild-moderate pain with no inflammation
A
Acetominophen
5
Q
Preferred NSAID for fever reduction
A
Ibuprofen
ASA
6
Q
How long does it take to see improvement in arthritic conditions
A
Can take up to 2 weeks
7
Q
Higher than recommended doses of NSAIDs
A
does not increase effect but does increase liklihood of side effects
8
Q
NSAIDS pharmacokinetics
A
absorption: rapidly and completely from the GI tract
distribution: crosses placenta
metabolism: liver
excretion: urine
half-life: varies
9
Q
Do NSAIDS enter breast milk
A
naproxen does
ibuprofen does not
10
Q
NSAIDs and low dose aspirin
A
May lower cardioprotective effect
11
Q
NSAIDs and diabetic medications
A
may increase hypoglycemic effect
12
Q
Medications that cause increased bleeding risk when given with NSAIDs
A
Cefotan
valproic acid
thrombolytics
warfarin
drugs affecting platelets
13
Q
What natural substances increase bleeding risk if given with NSAIDs
A
arnica
chamomile
garlic
ginger
ginseng
ginko
14
Q
Comorbidities that can contraindicate NSAID usage d/t increased risk of GI bleeding
A
history of ulcers
advanced age
poor health
smoking
alcohol use
15
Q
Comorbidities that contraindicate NSAID usage
A
renal impairment
heart failure
hypertension
16
Q
NSAIDs in pregnancy
A
may cause pulmonary HTN in fetus
contraindicated in 3rd trimester as it can cause premature closing of ductus arteriosus after birth
17
Q
Aspirin generic name
A
Acetylsalicylic acid
18
Q
Aspirin actions
A
Analgesic
Antipyretic
anti-inflammatory
antiplatelet
19
Q
salicylism
A
salicylate intoxication
20
Q
symptoms of salicylism
A
headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation, N/V, diarrhea
21
Q
how soon is treatment needed in severe salicylism
A
1-2 hours
22
Q
Anagesic action of ASA
A
low-moderate pain (HA, myalgia, arthraligia)
23
Q
ANtipyretic effect of ASA
A
reset the thermostat of the hypothalmus to normal
heat is lost as a result of cutaneous vasodilation and sweating
24
Q
Duration of usage for acetominophen
A
5 days in children and no more than 10 in adults because of hepatic risks
25
Anti-inflammatory effect of ASA
inhibition of prostaglandin and thromboxane synthesis is the mechanism of anti-inflammatory action
26
Why are higher doses of ASA needed for anti-inflammatory effect than analgesic and antipyretic effects?
ASA has a stronger effect on COX-1 than COX-2
inflammation mainly affects COX-2
therefore higher doses of aspirin are needed to properly inhibit COX-2
27
Anti-platelet effect of ASA
causes alteration of platelet aggregation
28
Acetylation effect of ASA
reduces the formation of thromboxane needed for platelet aggregation.
This inhibitory effect lasts up to 8 days until new plateets are formed
29
ASA absorption
absorption: some in stomach but mostly in upper small intestines
30
ASA plasma concentration levels
significant after 30 minutes with peak at 1-2 hours
31
ASA distribution
rapid and primarily by pH dependent passive diffusion
crosses placenta and enters breast milk
32
ASA metabolism
primarily in liver
33
metabolism of high-toxic doses of ASA
metabolism is limited and occurs according to zero-order kinetics
34
metabolism of low doses of ASA
proceed according to first-order kinetics
35
why is it important to understand the biphasic metabolism of ASA
the difference in rate of metabolism is important to drug accumulation with repeated high doses
36
ASA excretion
In urine (dependent on pH)
alkalization of urine (raise in pH) can markedly increase clearance
from 2-80%
37
ASA half-life
low dose: 3-6 hours
high dose: 15-30 hours
38
ASA dose: mild pain and fever
325-650mg
4-6 times a day
39
ASA dose: antiplatelet
40-80mg/day
40
ASA dose: moderate arthritic pain
1gm 4-6 times/day
41
ASA side effects: CV
hypotension, tachycardia, dysrythmias, edema
42
ASA side effect: DERM
rash, angioedema, urticaria
43
ASA side effects: EENT
hearing loss
tinnitus
44
ASA side effects: GI
N/V, dyspepsia, heartburn, ulcers, gastric erosions, duodenal ulcers, hepatotoxicity, increased transaminases, hepatits
45
ASA side effects: GU
Interstitial nephritis, proteinuria, increased BUN/creat, papillary necrosis
46
ASA side effects: HEME
prolonged PT, iron deficiency anemia, thrombocytopenia
47
ASA side effects: MISC
ANAPHYLAXIS
Reye's syndrome, low birth weight, prolonged labor
STILLBIRTH
48
ASA side effects: MS
rhabdomyolysis, weakness
49
ASA side effects: NEURO
fatigue, insomnia, nervousness, agitation, confusion, dizziness, headache, lethary, hyperthermia, coma
50
ASA side effects: PULM
asthma, bronchospasm, dyspnea, hyperpnea, tachypnea, respiratory alkalosis
51
ASA drug interactions
blocks transport of PCN from CSF to blood
can block the effects of gout medications
anticoagulants, beta blockers, hydantoins, lithium, loop diuretics, probenecid, and salicylates
52
Acetominophen and coumadin
Chronic high dosing can increase bleeding risk
53
Acetominophen and alcohol use
Chronic high dosing with alcohol abuse can increase risk of hepatotoxicity
54
Tylenol actions
Analgesic
antipyretic
significantly less gastric iiritation
55
What does Acetominophen poisoning cause
hepatic necrosis over 7-8 days
56
Acetominophen poisonind Day 1
N/V diaphoresis
57
Acetominophen poisoning day 1-2
liver enzymes, ALT, bilirubin, and PT rise
58
Acetominophen poisoning day 3-4
peak hepatotoxicity
59
Acetominophen poisoning day 7-8
recovery or death
60
Tylenol's anti-inflammatory effects
Not effective as an anti-inflammatory
61
What makes Tylenol preferable to aspirin
Des not have the gastric irritation, erosion, and bleeding
does not show evidence of crossover sensitivity
62
Tylenol mechanism of action
Inhibits COX-3 substances in brain and spinal cord
63
Why does Tylenol not cause the same gastric side effects as aspirin
It has no effect on COX-1 or COX-2
64
Tylenol: pharmacokinetics
absorption: incomplete and varies by dosage form
distribution: 80-40% protein bound
metabolism: liver
excretion: urine
half-life: 1-4 hours (may be prolonged in elderly)
65
Tylenol dose:
Adults and chilren over 14
325-650mg q4-6h
Not to exceed 4gm/day in people with renal impairment
66
Tylenol dose:
Children under 12
SHould not have more than 5 doses in a 24 hour period unless prescribed by health professional
67
Tylenol dose:
Osteoarthritis in adults
up to 1gm QID
not to exceed 4gm daily
68
Tylenol side effects: DERM
rash, urticaria
69
Tylenol side effect: GI
hepatic failure, hepatotoxicity
70
Tylenol side effects: GU
renal failure in high doses or chronic use
71
Tylenol Interactions
hepatotoxicity and liver damage additive with barbituates, alcohol
72
Misoprostol trade names
Arthrotec, Cytotec
73
What is the purpose of Cytotec
increase the production of mucus in the stomach and decreasing gastric acid secretion to decrease gastric mucosal injury of NSAIDs
74
cytotec: pharmacokinetics
absorption: rapid after oral administration
distribution: good bioavailability d/t methyl group
metabolism: parietal cells
excretion: urine
half-life: 20-40 minutes
75
Uses of cytotec
Patients with osteoarthritis at high risk for gastric ulcers
76
cytoec side effects: GI
abdominal pain, diarrhea, dyspepsia, N/V, flatulence
77
Cytotec side effects: NEURO
headache
78
cytotec side effects: OB/GYN
miscarriage, mentsrual disorders
79
medications which potentiate toxicity with cytotec
methotrexate
digoxin
cyclosporine
lithium
80
cytoec and K+ sparing diuretic
increased potassium
81
cytotec contraindications
pregnancy
patients senstive to prostaglandins
82
Patient education for cytotec
Avoid antacids (diarrhea)
diarrhea/black tarry stools may persist for one week
avoid alcohol
pregnancy implications
83
Ibuprofen uses
anti-inflammatory
relieves mild-moderate pain
antipyretic
rheumatoid arthritis
osteoarthritis
dysmenorrhea
84
Ibuprofen trade names
advil, motrin
85
ibuprofen mechanism of action
propionic acid derivative that inhibits cyclooxygenase
(inhibits prostaglandin synthesis)
86
ibuprofen: pharmacokinetics
absorption: rapidly (bound to protein)
distribution: hepatic
metabolism: hepatic via oxidation
excretion: renal
half-life: 2-4 hours
87
ibuprofen side effects: CV
arrythmias, edema
88
ibuprofen side effects: DERM
rash
89
ibuprofen side effects: EENT
amblyopia, blurry vision. tinnitus
90
ibuprofen interactions
may increase hypoglycemic effect of diabetic medications
increased bleeding risk
91
ibuprofen contraindications
sensitivity to ASA and other NSAIDs
chewable is contraindicated for patients with phenylketonuria
92
ibuprofen: caution in patients with
CV, renal, hepatic disease
especially elderly
93
meloxicam (mobic) mechanism of action
inhibits cyclooxygenase witch decreases biosynthesis of prostaglandins
94
Meloxicam pharmacokinetics
Absorption: plasma levels peak at 4-5 hours
distribution: unknown
metabolism: cytochrome P450 enzymes in liver to inactive metabolites
excretion: urine and feces
half-life: 15-20 hours
95
meloxicam clinical uses
rheumatoid arthritis
osteoarthritis
anti-inflammatory
analgesic
antopyretic
96
meloxicam side effects: DV
edema
97
meloxicam side effects: DERM
steven-johnson syndrome, toxic epidermal necrosis
98
meloxicam side effects: GI
bleeding, abnormal LFTs, diarrhea, dyspepsia, nausea
99
meloxicam side effects: HEM
anemia, leukopenia, thrombocytopenia
100
meloxicam drug interactions
may reduce effects of ACEIs
may reduce effects of furosemide and thiazide diuretics
101
benefit of COX-2 inhibitors
relatively free of GI side effects
102
how can COX-2 inhibitors produce NSAID-like nephrotoxicity
kidney expresses COX-2
(plays a role in maintaining normal physiologic function)
103
COX-2 inhibitor drug names
celecoxib (Celebrex)
104
Celebrex mechanism of action
inhibits prostaglandin synthesis by decresing activity of COX-2 enzyme
does not inhibit antiplatelet activity
105
celebrex pharmacokinetics
absorption: good orally, peak plasma levels at 2-4 hours
distribution: bound extensively to plasma proteins
metabolism: liver (CYP2C9 enzyme)
excretion: urine and feces
half-life: 11 hours
106
celebrex clinical uses
rheumatoid arthritis
osteoarthritis
dysmenorrhea
107
celebrex side effects: CV
LE edema, HTN, increased risk of MI and CVA
108
celebrex side effects: DERM
rash, swelling hands/feet/ankles/LE, itching
109
celebrex side effects: GI
stomach pain, diarrhea, heartburn, black tarry stools, frank blood in stools, bloody vomit, weight gain, GI bleeding
110
celebrex side effects: GU
renal toxicity worse than with other NSAIDs
111
celebrex side effects: MISC
fatigue, flu-like symptoms
112
celebrex side effects: NEURO
headache
113
celebrex drug interactions
warfarin, diazepam, glyburide, norethindrone, ethinyl estradiol, omeprazole, dextromethorphan, ASA
114
Osteoarthritis
most common joint disease
increased ncidence of self-medicating
degree of pain/dysfunction guides intervention
115
Purpose of DMARDs
(disease-modifying antirheumatic drugs)
influence disease process of rheumatoid arthritis by preventing bone loss and cartilage erosion
116
DMARDs are often prescribed with
biologic modifiers
NSAIDs
other DMARDs
with/without corticosteroids
117
why are DMARDs prescribed with other agents
ineffective as monotherapy
118
what 3 situation warrant corticosteroids with DMARDs
early in treatment while waiting for DMARD to work
chronic low doses for patients who fail to respond to DMARDs
treatment of acute flare-ups
119
Drugs used to treat acute attacks of gout
colchicine, probenecid (Probalan), allopurinal (Zyloprim), sulfinpyrazone (Anturane), corticosteroids, NSAIDs
120
low dose ASA in a person with gout
increased risk for flare-up as it interferes with uric acid excretion
121
things patients with gout should avoid
alcohol, foods high in purines
122
use of Allopurinol (Zyloprim)
prevent gout flare-ups
treat chronic gout
123
allopurinol mechanism of action
inhibits xanthine oxidase blocking conversion into uric acid
reduces serum uric acid concentrations
124
Allopurinol pharmacokinetics
absorption: rapidly from GI tract
distribution: peak plasma concentration in 60-90 minutes (negligible protein binding) enters breast milk
metabolism: in liver to oxypurinol (long half-life)
excretion: unabsorbed in feces or unchanged in urine (oxypurinol in urine)
half-life: 1-2 hours for allopurinol; 18-30 hours for oxypurinol
125
How is Methotrexate (Rheumatrex) used
antineoplastic
immunosuppressant
DMARD
(alone or in combination with other treatments)
126
Methotrexate mechanism of action
folate antimetabolite that inhibits DNA synthesis
127
Action when methotrexate is used for arthritis
Appears to act as a cell anti-proliferative with multiple effects
128
Methotrexate pharmacokinetics
## Footnote
absorption: small doses rapidly in GI tract (large doses relatively unabsorbed)
distribution: slow delivery
metabolism: minimally because hepatic enzymes convert it to inactive metabolite
excretion: urine
half-life: 3-10 hours (low dose), 8-15 hours (high dose)
129
Methotrexate uses
psoriasis
SLE (lupus)
sarcoidosis
chemotherapeutic
rheumatoid arthritis
130
Methotrexate side effects: EENT
blurred vision, transient blindness
131
methotrexate side effects: DERM
alopecia, photosensitivities, pruritis, urticaria,
132
methotrexate side effects: GI
N/V, ulcers, hepatotoxicity, anorexia, stomatitis,
133
methotrexate side effects: GU
infertility
134
methotrexate side effects: HEM
anemia, leukopenia, thrombocytopenia
135
methotrexate side effects: MISC
nephropathy, chills, fever, soft tissue necrosis
136
methotrexate side effects: MS
hyperuricemia, osteonecrosis, stress fractures
137
methotrexate side effects: NEURO
dizziness, headache, malaise, drowsiness
138
methotrexate side effects: PULM
PULMONARY FIBROSIS
139
methotrexate interactions: what increases hematological toxicity
high doses of salicylates, NSAIDs, oral hypoglycemics, tetracyclines, sulfonamides
140
methotrexate interactions: herbal
echinacea and melatonin interefere with immunosuppression
141
methotrexate: implications of teratogenics
women should wait one menses before attempting pregnancy
men should wait 3 months
142
methotrexate conscientious considerations
use soft toothbrush/electric razor
ask before using OTC
use sunscreen
ask before getting vaccines
143
DMARD drug names
methotrexate
leflunomide (Arava)
hydroxychloroquine (Plaquenil)
penicillamine (Cuprimine)
144
What type of drug is Leflunomide (Arava) besides DMARD
immunomodulator
145
leflunomide mechanism of action
inhibits de novo RNA synthesis (arrests cell in G1 phase)
146
therapeutic goals of leflunomide
pain and inflammation relief
slows progression of disease
improves joint function
147
Leflunomide pharmacokinetics
absorption: 80% rapidly absorbed
distribution: 99% protein bound
metabolism: rapidly converted to active metabolite
excretion: 1/2 feces, 1/2 urine
half-life: 14-18 days
148
leflunomide side effects: DERM
alopecia, pruritic rash, dry skin
149
leflunomides side effects: EENT
rhinitus, sinusitis
150
leflunomide side effects: GI
diarrhea, nausea, abdominal pain, abnormal LFTs, hepatotoxicity
151
leflunomide side effects: META
hypokalemia, weight loss
152
leflunomide side effects: MISC
paresthesia, flu-like symptoms, infections
153
leflunomide side effects: MS
back pain, arthralgia, leg cramps, synovitis
154
leflunomide side effects: NEUO
headache, dizziness, weakness
155
leflunomide side effects: PULM
bronchitis, cough
156
leflunomide contraindications
pregnancy, liver disease
157
leflunomide patient education
tetratogenic, may cause dizziness (avoid driving), coping with hair loss, avoid vaccines
158
hydroxychloroquine (plaquenil) clinical uses
suppress malaria
antirheumatic
lupus
159
plaquenil mechanism of action
suspected to decrease T cell response
160
plaquenil pharmacokinetics
absorption: rapidly in GI tract (safest if given orally)
distribution: slow
metabolism: liver
excretion: urine
half-life: 30-60 days
161
plaquenil side effects: DERM
rashes, pruritus, exacerbation of psoriasis, hair bleaching, alopecia
162
plaquenil side effects: EENT
ototoxicity, tinnitis, visual disturbances, retinopathy
163
plaquenil side effects: GI
cramps, anorexia, diarrhea, vomiting, hepatic failure
164
plaquenil side effects: HEM
aplastic anemia, agranulocytosis
165
plaquenil side effects: MS
myopathy
166
plaquenil side effects: NEURO
dizziness, aggressiveness, anxiety, apathy, fatigue, headache, irritability, personality changes, psychosis
167
plaquenil contraindications
liver/renal disease
alcohol use
168
plaquenil conscientious considerations
frequent eye exams to check for retinopathy and resultant blindness
not first-line (last resort drug)
169
what kind of DMARD is Penicillamine (Cuprimine)
Heavy metal DMARD
chelation action promotes copper excretion
170
penicillamine mechanism of action
thought to decrease cell-mediated responses and inhibit new collagen formation which causes it to act as an antiinflammatory
171
severe adverse reactions of penicillamine
aplastic anemia, agranulocytosis
172
penicillamine pharmacokinetics
absorption: 1/2 dose is absorbed (orally)
distribution: protein binds to albumin
metabolism: hepatic biotransformation in small amounts
excretion: feces and urine
half-life: 1.7-3.2 hours
173
penicillamine clinical uses
rheumatoid arhtritis
174
penicillamine interactions
antacids can block absorption
175
penicillamine side effects
Page 57
176
how long does it take to establish the effects of penicillamine
months
177
penicillamine contraindications
pregnancy
aplastic anemia
renal failure
178
Gold compound mechanism of action
unclear
179
why are gold compounds used as a last resort for inflammation
slow acting, toxic
180
examples of gold compounds
aurothioglucose suspension (Solganal)
gold sodium aurothiomalate (Myochrysine)
auranofin (Ridaura)
181
Gold compounds pharmacokinetics
absorption: Auranofin 29% gold (absorbed moderately in GI tract)
Aurothioglucose is 50% gold (aborbed slow and erraticly IM)
distribution: binds to albumin and accumulate in liver, kidney, bone marrow, spleen, lymph nodes
metabolism: livers (gold sodium thiomalate)
excretion: mostly kidney, sometimes liver
half-life: p. 58
182
Gold compound clinical
rheumatoid arthritis
juvenile arthritis
183
gold compound: serious side effects
toxicity, decreased HGB, leukopenia, reduced granulocytes, proteinuria, throat ulcers
Other side effects: p. 58
184
gold compound contraindications
blood dyscrasias, CHF, dermatitis, colitis, use of antimalarials
185
conscientious considerations for gold compounds
dc if ANY side effects are noted
monitor protein and blood counts
metallic taste is warning of stomatitis
pruritus is warning of cutaneous reaction
186
gold compoumd patient education
watch for mouth ulcers
187
Tumor necrosis factor inhibitors
anticytokine therapy that targets the rheumatoid process
188
examples of TNF inhibitors
etanercept (Enbrel)
infliximab (Remicade)
anakinra (Kineret
189
Enbrel mechanism of action
TNF receptor joined to a human IgG molecule that interferes with the inflammatory process initiated by TNF alpha. This lowers circulating cytokines making them inactive
190
Remicade mechanism of action
mouse/human monoclonal antibody that targets TNF-alpha to neutralize and prevent its activity
191
Kineret mechanism of action
blocks interleukin-1
192
TNF inhibitors pharmacokinetics
absorption: Anakinra no accumulation in tissues
Enbrel well absorbed (subQ)
Remicade IV gives complete bioavailability
distribution: unknown
metabolism/excretion: unknown except ANakinra in urine
half-life: anakinra 4-6h, enbrel 115h, remicade 7.7-9.5 days
193
clinical uses of TNF inhibitors
Enbrel and remicade for moderate to severe RA that dont respond to other DMARDs
moderate to severe active Chrohns
can be used with methotrexate
194
TNF inhibitor side effects
erythema, abdominal pain, N/V, constipaton, gas, oral and tooth pain, life-threatening infections, pain/pruritus at injection site, infusion reactions, low back pain, involuntary muscle spasm, myalgia, headache, fatigue, anxiety, paresthesias, bronchitis, cough, dyspnea, URIs, rhinitis
195
TNF inhibitor contraindications
serious infections, children, allergic to proteins in formulations, pregnancy, TB
196
Purpose of gout medications
end painful attacks
prevent formation of uric stones in kidney
prevent complications of uric stone formation in joints
197
examples of drugs that treat gout
allopurinol
colchicine
probenecid
sulfinpyrazone
198
Patient education regarding gout
Avoid alcohol and foods high in purines
199
conscientious prescribing of gout medications
all patient on low dose ASA are at risk
determine cause of hyperuricemia to guide treatment
200
Allopurinol (Zyloprim) mechanism of action
inhibits enzyme xanthine oxidase
blocks formation of uric acid
reduces serum uric acid
201
Allopurinol pharmacokinetics
absorption: rapidly from GI tract oral admin
distribution: peak concentration 60-90 minutes, enters breast milk
metabolism: liver to oxypurinol (long half-life)
excretion: unabsorbed in feces or unchanged in urine, oxypurinol in urine
half-life: allopurinol 1-2 hours, oxypurinol 18-30 hours
202
clinical uses for allopurinol
chronic gouty arthritis
prevention of uric acid calculi
203
allopurinol side effects: DERM
rash following injection, consider toxic if rash is severe
204
allopurionol side effects: GI
diarrhea, hepatitis, N/V
205
allopurinol side effects: GU
renal failure
206
allopurinol side effects: HEM
bone marrow depression
207
allopurinol side effects: MISC
sensitivity reactions after prolonged use possible
208
allopurinol side effects: NEURO
drowsiness
209
allopurinol and probenecid
probenecid increases clearance of oxypurinol so higher doses of allopurinol are needed
210
allopurinol and azathioprine
allopurinol inhibits metabolism of the other one as it requires normal protein synthesis for action
211
allopurinol and ACE inhibitors
produces stevens-johnson syndrome
(fever, arthraligias, skin eruptions)
212
allopurinol and aluminum hydroxide
aluminum inhibits allopurinol response
213
allopurinol contraindications
nursing mothers
history of hypersensitivity reactions
214
conscientious cnsiderations for allopurinol
gouty attacks may increase initially
serum uric acids levels may take 1-3 weeks to achiev
215
allopurinol patient education
take with food, avoid alcohol
216
Colchicine mechanism of action
plant alkaloid that interferes with WBC ability to perpetuate inflammatory response which results in uric acid crystals
217
Colchicine affect on uric acid levels
does not affect in circulatory system
218
clochicine pharmacokinetics
absorption: rapidly
distribution: high concentrations in liver, spleen, and kidney
metabolism: reneters biliary tract by biliary secretion and reabsorbed by intestines
excretion: feces primarily
half-life: 20 minutes in plasma, 60 hours in WBCs
219
clinical use of colchicine
treatment of acute gout attacks
relief in 12 hours with symptoms gone in 48
220
colchicine side effects
alopecia, N/V, diarrhea, abdominal pain, anuria, hematuria, renal damage, agranulocytosis, aplastic anemia, leukopenia, thrombocytopenia, phlebitis at injection site, peripheral neuritis
221
colchicine interactions
additive GI effects with NSAIDs
222
colchicine contraindications
cardiac, renal, hepatic, GI diseases
renal impairment (reduce dosage if needed)
safety not established in lactation
223
conscientious considerations for colchicine
overdose can be fatal, once limit has been reached no more for 21 days
224
colchicine patient education
take missed dose ASAP but do not double
if taking prophylactically do not increase dose if gouty attakc occurs
diet, weight loos, alcohol
stop for ANY GI symptoms
225
Pobenecid mechanism of action
lowers serum levels of urate by competitive inhibition in the renal tubules
226
probenecid pharmacokinetics
absorption: completely after oral w/ peak concentration 2-4 hours
distribution: crosses placenta
metabolism: hydroxylated to metabolites that retain carboxyl function and uricosuric activity
excretion: small amount in urine
half-life: ranges 5-more than 17 hours
227
probenecid clinical uses
chronic gout
gonorrhea or neurosyphillis by delaying excretion of PCN
228
probenecid side effects
flushing, rash, N/V, abdominal pain, diarrhea, sore gums, drug-induced hepatitis, uric acid stones, urinary frequency, aplastic anemia, headache, dizziness
229
probencid interactions
increases levels of many drugs
increases clearance of oxypurinol
230
probenecid contraindications
renal failure
231
probenecid patient education
do not take ASA (decreases effects)
erratic compliance may cause attacks
report side effects
2,000-3,000 ml of fluid daily
232
sulfinpyrazone (Anturane) mechanism of action
inhibits reabsorption of urates at the proximal tubule
increases uric acid excretion
233
Sulfinpyrazone pharmacokinetics
absorption: compleely with oral, peak concentration at 2-4 hours
distribution: widely in serum
metabolism: liver to 4 active metabolites
excretion: 50% unchanged in urine
half-life: 2.7-6 hours
234
clinical use for sulfinpyrazone
chronic gout
235
sulfinpyrazone side effects
rash, flushed face, N/V, stomach pain, frequent urination, agranulocytosis, aplastic anemia, headache, dizziness
236
sulfinpyrazone interactions
increased toxicity with acetominophen
reduces effect of beta blockers
inhibits warfarin metabolism
237
sulfinpyrazone contraindications
blood dyscrasias, renal failure
238
sulfinpyrazone patient education
take with food, drink plenty of fluids, avoid ASA
239
Pregnancy class B gout medications
etanercept, infliximab, anakinra, penicillamine, ibuprofen, diclofenac, other NSAIDs
240
pregnancy category class C gout medications
allopurinol, aurothiomalate, aurothioglucose, hydroxychloroquine, celecoxib, etodolac
241
pregnancy class D gout medications
colchicine, methotrexate
242
pregnancy class X gout medications
leflunomide
243
pregnancy unclassified gout medications
probenecid, sulfinpyrazone
