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1

 

 

NSAID drugs

 

ASA

Tylenol

Ibuprofen

Mobic

2

 

 

GI upset with NSAID usage

 

 

prescribe an H2 blocker with it

3

 

 

Duration of Ibuprofen/ASA usage before re-evaluation is necessary

 

 

follow up is needed if routine use exceeds 3 days

4

 

 

Perferred NSAID for mild-moderate pain with no inflammation

 

 

Acetominophen 

5

 

 

Preferred NSAID for fever reduction

 

 

Ibuprofen

ASA

6

 

 

How long does it take to see improvement in arthritic conditions

 

 

Can take up to 2 weeks

7

 

 

Higher than recommended doses of NSAIDs

 

 

does not increase effect but does increase liklihood of side effects

8

 

 

NSAIDS pharmacokinetics

 

absorption: rapidly and completely from the GI tract

distribution: crosses placenta

metabolism: liver

excretion: urine

half-life: varies

9

 

 

Do NSAIDS enter breast milk

 

 

naproxen does

ibuprofen does not

10

 

 

NSAIDs and low dose aspirin

 

 

May lower cardioprotective effect

11

 

 

NSAIDs and diabetic medications

 

 

may increase hypoglycemic effect

12

 

Medications that cause increased bleeding risk when given with NSAIDs

 

Cefotan

valproic acid

thrombolytics

warfarin

drugs affecting platelets

13

 

 

What natural substances increase bleeding risk if given with NSAIDs

 

arnica

chamomile

garlic 

ginger

ginseng

ginko

14

 

 

Comorbidities that can contraindicate NSAID usage d/t increased risk of GI bleeding

 

 

 history of ulcers

advanced age

poor health

smoking

alcohol use

15

 

 

Comorbidities that contraindicate NSAID usage

 

renal impairment

heart failure

hypertension

16

 

 

NSAIDs in pregnancy

 

may cause pulmonary HTN in fetus

contraindicated in 3rd trimester as it can cause premature closing of ductus arteriosus after birth

17

 

 

Aspirin generic name

 

 

Acetylsalicylic acid

18

 

 

Aspirin actions

 

Analgesic

Antipyretic

anti-inflammatory

antiplatelet

19

 

 

salicylism

 

 

salicylate intoxication

20

 

 

symptoms of salicylism

 

 

headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation, N/V, diarrhea

21

 

 

how soon is treatment needed in severe salicylism

 

 

1-2 hours

22

 

 

Anagesic action of ASA

 

 

 

low-moderate pain (HA, myalgia, arthraligia)

23

 

 

ANtipyretic effect of ASA

 

reset the thermostat of the hypothalmus to normal

heat is lost as a result of cutaneous vasodilation and sweating

24

 

 

Duration of usage for acetominophen

 

 

 

 

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

 

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