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Pharmacology > Chapter 4: Bone and Joint Disorders > Flashcards

Chapter 4: Bone and Joint Disorders Flashcards

1
Q

NSAID drugs

A

ASA

Tylenol

Ibuprofen

Mobic

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2
Q

GI upset with NSAID usage

A

prescribe an H2 blocker with it

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3
Q

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

A

follow up is needed if routine use exceeds 3 days

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4
Q

Perferred NSAID for mild-moderate pain with no inflammation

A

Acetominophen

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5
Q

Preferred NSAID for fever reduction

A

Ibuprofen

ASA

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6
Q

How long does it take to see improvement in arthritic conditions

A

Can take up to 2 weeks

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7
Q

Higher than recommended doses of NSAIDs

A

does not increase effect but does increase liklihood of side effects

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8
Q

NSAIDS pharmacokinetics

A

absorption: rapidly and completely from the GI tract
distribution: crosses placenta
metabolism: liver
excretion: urine

half-life: varies

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9
Q

Do NSAIDS enter breast milk

A

naproxen does

ibuprofen does not

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10
Q

NSAIDs and low dose aspirin

A

May lower cardioprotective effect

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11
Q

NSAIDs and diabetic medications

A

may increase hypoglycemic effect

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12
Q

Medications that cause increased bleeding risk when given with NSAIDs

A

Cefotan

valproic acid

thrombolytics

warfarin

drugs affecting platelets

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13
Q

What natural substances increase bleeding risk if given with NSAIDs

A

arnica

chamomile

garlic

ginger

ginseng

ginko

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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

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15
Q

Comorbidities that contraindicate NSAID usage

A

renal impairment

heart failure

hypertension

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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

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17
Q

Aspirin generic name

A

Acetylsalicylic acid

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18
Q

Aspirin actions

A

Analgesic

Antipyretic

anti-inflammatory

antiplatelet

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19
Q

salicylism

A

salicylate intoxication

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20
Q

symptoms of salicylism

A

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

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21
Q

how soon is treatment needed in severe salicylism

A

1-2 hours

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22
Q

Anagesic action of ASA

A

low-moderate pain (HA, myalgia, arthraligia)

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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

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24
Q

Duration of usage for acetominophen

A

5 days in children and no more than 10 in adults because of hepatic risks

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25
Q

Anti-inflammatory effect of ASA

A

inhibition of prostaglandin and thromboxane synthesis is the mechanism of anti-inflammatory action

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26
Q

Why are higher doses of ASA needed for anti-inflammatory effect than analgesic and antipyretic effects?

A

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

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27
Q

Anti-platelet effect of ASA

A

causes alteration of platelet aggregation

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28
Q

Acetylation effect of ASA

A

reduces the formation of thromboxane needed for platelet aggregation.

This inhibitory effect lasts up to 8 days until new plateets are formed

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29
Q

ASA absorption

A

absorption: some in stomach but mostly in upper small intestines

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30
Q

ASA plasma concentration levels

A

significant after 30 minutes with peak at 1-2 hours

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31
Q

ASA distribution

A

rapid and primarily by pH dependent passive diffusion

crosses placenta and enters breast milk

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32
Q

ASA metabolism

A

primarily in liver

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33
Q

metabolism of high-toxic doses of ASA

A

metabolism is limited and occurs according to zero-order kinetics

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34
Q

metabolism of low doses of ASA

A

proceed according to first-order kinetics

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35
Q

why is it important to understand the biphasic metabolism of ASA

A

the difference in rate of metabolism is important to drug accumulation with repeated high doses

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36
Q

ASA excretion

A

In urine (dependent on pH)

alkalization of urine (raise in pH) can markedly increase clearance

from 2-80%

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37
Q

ASA half-life

A

low dose: 3-6 hours

high dose: 15-30 hours

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38
Q

ASA dose: mild pain and fever

A

325-650mg

4-6 times a day

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39
Q

ASA dose: antiplatelet

A

40-80mg/day

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40
Q

ASA dose: moderate arthritic pain

A

1gm 4-6 times/day

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41
Q

ASA side effects: CV

A

hypotension, tachycardia, dysrythmias, edema

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42
Q

ASA side effect: DERM

A

rash, angioedema, urticaria

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43
Q

ASA side effects: EENT

A

hearing loss

tinnitus

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44
Q

ASA side effects: GI

A

N/V, dyspepsia, heartburn, ulcers, gastric erosions, duodenal ulcers, hepatotoxicity, increased transaminases, hepatits

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45
Q

ASA side effects: GU

A

Interstitial nephritis, proteinuria, increased BUN/creat, papillary necrosis

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46
Q

ASA side effects: HEME

A

prolonged PT, iron deficiency anemia, thrombocytopenia

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47
Q

ASA side effects: MISC

A

ANAPHYLAXIS

Reye’s syndrome, low birth weight, prolonged labor

STILLBIRTH

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48
Q

ASA side effects: MS

A

rhabdomyolysis, weakness

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49
Q

ASA side effects: NEURO

A

fatigue, insomnia, nervousness, agitation, confusion, dizziness, headache, lethary, hyperthermia, coma

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50
Q

ASA side effects: PULM

A

asthma, bronchospasm, dyspnea, hyperpnea, tachypnea, respiratory alkalosis

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51
Q

ASA drug interactions

A

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

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52
Q

Acetominophen and coumadin

A

Chronic high dosing can increase bleeding risk

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53
Q

Acetominophen and alcohol use

A

Chronic high dosing with alcohol abuse can increase risk of hepatotoxicity

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54
Q

Tylenol actions

A

Analgesic

antipyretic

significantly less gastric iiritation

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55
Q

What does Acetominophen poisoning cause

A

hepatic necrosis over 7-8 days

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56
Q

Acetominophen poisonind Day 1

A

N/V diaphoresis

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57
Q

Acetominophen poisoning day 1-2

A

liver enzymes, ALT, bilirubin, and PT rise

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58
Q

Acetominophen poisoning day 3-4

A

peak hepatotoxicity

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59
Q

Acetominophen poisoning day 7-8

A

recovery or death

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60
Q

Tylenol’s anti-inflammatory effects

A

Not effective as an anti-inflammatory

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61
Q

What makes Tylenol preferable to aspirin

A

Des not have the gastric irritation, erosion, and bleeding

does not show evidence of crossover sensitivity

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62
Q

Tylenol mechanism of action

A

Inhibits COX-3 substances in brain and spinal cord

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63
Q

Why does Tylenol not cause the same gastric side effects as aspirin

A

It has no effect on COX-1 or COX-2

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64
Q

Tylenol: pharmacokinetics

A

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)

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65
Q

Tylenol dose:

Adults and chilren over 14

A

325-650mg q4-6h

Not to exceed 4gm/day in people with renal impairment

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66
Q

Tylenol dose:

Children under 12

A

SHould not have more than 5 doses in a 24 hour period unless prescribed by health professional

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67
Q

Tylenol dose:

Osteoarthritis in adults

A

up to 1gm QID

not to exceed 4gm daily

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68
Q

Tylenol side effects: DERM

A

rash, urticaria

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69
Q

Tylenol side effect: GI

A

hepatic failure, hepatotoxicity

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70
Q

Tylenol side effects: GU

A

renal failure in high doses or chronic use

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71
Q

Tylenol Interactions

A

hepatotoxicity and liver damage additive with barbituates, alcohol

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72
Q

Misoprostol trade names

A

Arthrotec, Cytotec

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73
Q

What is the purpose of Cytotec

A

increase the production of mucus in the stomach and decreasing gastric acid secretion to decrease gastric mucosal injury of NSAIDs

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74
Q

cytotec: pharmacokinetics

A

absorption: rapid after oral administration
distribution: good bioavailability d/t methyl group
metabolism: parietal cells
excretion: urine

half-life: 20-40 minutes

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75
Q

Uses of cytotec

A

Patients with osteoarthritis at high risk for gastric ulcers

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76
Q

cytoec side effects: GI

A

abdominal pain, diarrhea, dyspepsia, N/V, flatulence

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77
Q

Cytotec side effects: NEURO

A

headache

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78
Q

cytotec side effects: OB/GYN

A

miscarriage, mentsrual disorders

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79
Q

medications which potentiate toxicity with cytotec

A

methotrexate

digoxin

cyclosporine

lithium

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80
Q

cytoec and K+ sparing diuretic

A

increased potassium

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81
Q

cytotec contraindications

A

pregnancy

patients senstive to prostaglandins

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82
Q

Patient education for cytotec

A

Avoid antacids (diarrhea)

diarrhea/black tarry stools may persist for one week

avoid alcohol

pregnancy implications

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83
Q

Ibuprofen uses

A

anti-inflammatory

relieves mild-moderate pain

antipyretic

rheumatoid arthritis

osteoarthritis

dysmenorrhea

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84
Q

Ibuprofen trade names

A

advil, motrin

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85
Q

ibuprofen mechanism of action

A

propionic acid derivative that inhibits cyclooxygenase

(inhibits prostaglandin synthesis)

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86
Q

ibuprofen: pharmacokinetics

A

absorption: rapidly (bound to protein)
distribution: hepatic
metabolism: hepatic via oxidation
excretion: renal

half-life: 2-4 hours

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87
Q

ibuprofen side effects: CV

A

arrythmias, edema

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88
Q

ibuprofen side effects: DERM

A

rash

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89
Q

ibuprofen side effects: EENT

A

amblyopia, blurry vision. tinnitus

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90
Q

ibuprofen interactions

A

may increase hypoglycemic effect of diabetic medications

increased bleeding risk

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91
Q

ibuprofen contraindications

A

sensitivity to ASA and other NSAIDs

chewable is contraindicated for patients with phenylketonuria

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92
Q

ibuprofen: caution in patients with

A

CV, renal, hepatic disease

especially elderly

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93
Q

meloxicam (mobic) mechanism of action

A

inhibits cyclooxygenase witch decreases biosynthesis of prostaglandins

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94
Q

Meloxicam pharmacokinetics

A

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

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95
Q

meloxicam clinical uses

A

rheumatoid arthritis

osteoarthritis

anti-inflammatory

analgesic

antopyretic

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96
Q

meloxicam side effects: DV

A

edema

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97
Q

meloxicam side effects: DERM

A

steven-johnson syndrome, toxic epidermal necrosis

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98
Q

meloxicam side effects: GI

A

bleeding, abnormal LFTs, diarrhea, dyspepsia, nausea

99
Q

meloxicam side effects: HEM

A

anemia, leukopenia, thrombocytopenia

100
Q

meloxicam drug interactions

A

may reduce effects of ACEIs

may reduce effects of furosemide and thiazide diuretics

101
Q

benefit of COX-2 inhibitors

A

relatively free of GI side effects

102
Q

how can COX-2 inhibitors produce NSAID-like nephrotoxicity

A

kidney expresses COX-2

(plays a role in maintaining normal physiologic function)

103
Q

COX-2 inhibitor drug names

A

celecoxib (Celebrex)

104
Q

Celebrex mechanism of action

A

inhibits prostaglandin synthesis by decresing activity of COX-2 enzyme

does not inhibit antiplatelet activity

105
Q

celebrex pharmacokinetics

A

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
Q

celebrex clinical uses

A

rheumatoid arthritis

osteoarthritis

dysmenorrhea

107
Q

celebrex side effects: CV

A

LE edema, HTN, increased risk of MI and CVA

108
Q

celebrex side effects: DERM

A

rash, swelling hands/feet/ankles/LE, itching

109
Q

celebrex side effects: GI

A

stomach pain, diarrhea, heartburn, black tarry stools, frank blood in stools, bloody vomit, weight gain, GI bleeding

110
Q

celebrex side effects: GU

A

renal toxicity worse than with other NSAIDs

111
Q

celebrex side effects: MISC

A

fatigue, flu-like symptoms

112
Q

celebrex side effects: NEURO

113
Q

celebrex drug interactions

A

warfarin, diazepam, glyburide, norethindrone, ethinyl estradiol, omeprazole, dextromethorphan, ASA

114
Q

Osteoarthritis

A

most common joint disease

increased ncidence of self-medicating

degree of pain/dysfunction guides intervention

115
Q

Purpose of DMARDs

(disease-modifying antirheumatic drugs)

A

influence disease process of rheumatoid arthritis by preventing bone loss and cartilage erosion

116
Q

DMARDs are often prescribed with

A

biologic modifiers

NSAIDs

other DMARDs

with/without corticosteroids

117
Q

why are DMARDs prescribed with other agents

A

ineffective as monotherapy

118
Q

what 3 situation warrant corticosteroids with DMARDs

A

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
Q

Drugs used to treat acute attacks of gout

A

colchicine, probenecid (Probalan), allopurinal (Zyloprim), sulfinpyrazone (Anturane), corticosteroids, NSAIDs

120
Q

low dose ASA in a person with gout

A

increased risk for flare-up as it interferes with uric acid excretion

121
Q

things patients with gout should avoid

A

alcohol, foods high in purines

122
Q

use of Allopurinol (Zyloprim)

A

prevent gout flare-ups

treat chronic gout

123
Q

allopurinol mechanism of action

A

inhibits xanthine oxidase blocking conversion into uric acid

reduces serum uric acid concentrations

124
Q

Allopurinol pharmacokinetics

A

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
Q

How is Methotrexate (Rheumatrex) used

A

antineoplastic

immunosuppressant

DMARD

(alone or in combination with other treatments)

126
Q

Methotrexate mechanism of action

A

folate antimetabolite that inhibits DNA synthesis

127
Q

Action when methotrexate is used for arthritis

A

Appears to act as a cell anti-proliferative with multiple effects

128
Q

Methotrexate pharmacokinetics

A

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
Q

Methotrexate uses

A

psoriasis

SLE (lupus)

sarcoidosis

chemotherapeutic

rheumatoid arthritis

130
Q

Methotrexate side effects: EENT

A

blurred vision, transient blindness

131
Q

methotrexate side effects: DERM

A

alopecia, photosensitivities, pruritis, urticaria,

132
Q

methotrexate side effects: GI

A

N/V, ulcers, hepatotoxicity, anorexia, stomatitis,

133
Q

methotrexate side effects: GU

A

infertility

134
Q

methotrexate side effects: HEM

A

anemia, leukopenia, thrombocytopenia

135
Q

methotrexate side effects: MISC

A

nephropathy, chills, fever, soft tissue necrosis

136
Q

methotrexate side effects: MS

A

hyperuricemia, osteonecrosis, stress fractures

137
Q

methotrexate side effects: NEURO

A

dizziness, headache, malaise, drowsiness

138
Q

methotrexate side effects: PULM

A

PULMONARY FIBROSIS

139
Q

methotrexate interactions: what increases hematological toxicity

A

high doses of salicylates, NSAIDs, oral hypoglycemics, tetracyclines, sulfonamides

140
Q

methotrexate interactions: herbal

A

echinacea and melatonin interefere with immunosuppression

141
Q

methotrexate: implications of teratogenics

A

women should wait one menses before attempting pregnancy

men should wait 3 months

142
Q

methotrexate conscientious considerations

A

use soft toothbrush/electric razor

ask before using OTC

use sunscreen

ask before getting vaccines

143
Q

DMARD drug names

A

methotrexate

leflunomide (Arava)

hydroxychloroquine (Plaquenil)

penicillamine (Cuprimine)

144
Q

What type of drug is Leflunomide (Arava) besides DMARD

A

immunomodulator

145
Q

leflunomide mechanism of action

A

inhibits de novo RNA synthesis (arrests cell in G1 phase)

146
Q

therapeutic goals of leflunomide

A

pain and inflammation relief

slows progression of disease

improves joint function

147
Q

Leflunomide pharmacokinetics

A

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
Q

leflunomide side effects: DERM

A

alopecia, pruritic rash, dry skin

149
Q

leflunomides side effects: EENT

A

rhinitus, sinusitis

150
Q

leflunomide side effects: GI

A

diarrhea, nausea, abdominal pain, abnormal LFTs, hepatotoxicity

151
Q

leflunomide side effects: META

A

hypokalemia, weight loss

152
Q

leflunomide side effects: MISC

A

paresthesia, flu-like symptoms, infections

153
Q

leflunomide side effects: MS

A

back pain, arthralgia, leg cramps, synovitis

154
Q

leflunomide side effects: NEUO

A

headache, dizziness, weakness

155
Q

leflunomide side effects: PULM

A

bronchitis, cough

156
Q

leflunomide contraindications

A

pregnancy, liver disease

157
Q

leflunomide patient education

A

tetratogenic, may cause dizziness (avoid driving), coping with hair loss, avoid vaccines

158
Q

hydroxychloroquine (plaquenil) clinical uses

A

suppress malaria

antirheumatic

lupus

159
Q

plaquenil mechanism of action

A

suspected to decrease T cell response

160
Q

plaquenil pharmacokinetics

A

absorption: rapidly in GI tract (safest if given orally)
distribution: slow
metabolism: liver
excretion: urine

half-life: 30-60 days

161
Q

plaquenil side effects: DERM

A

rashes, pruritus, exacerbation of psoriasis, hair bleaching, alopecia

162
Q

plaquenil side effects: EENT

A

ototoxicity, tinnitis, visual disturbances, retinopathy

163
Q

plaquenil side effects: GI

A

cramps, anorexia, diarrhea, vomiting, hepatic failure

164
Q

plaquenil side effects: HEM

A

aplastic anemia, agranulocytosis

165
Q

plaquenil side effects: MS

166
Q

plaquenil side effects: NEURO

A

dizziness, aggressiveness, anxiety, apathy, fatigue, headache, irritability, personality changes, psychosis

167
Q

plaquenil contraindications

A

liver/renal disease

alcohol use

168
Q

plaquenil conscientious considerations

A

frequent eye exams to check for retinopathy and resultant blindness

not first-line (last resort drug)

169
Q

what kind of DMARD is Penicillamine (Cuprimine)

A

Heavy metal DMARD

chelation action promotes copper excretion

170
Q

penicillamine mechanism of action

A

thought to decrease cell-mediated responses and inhibit new collagen formation which causes it to act as an antiinflammatory

171
Q

severe adverse reactions of penicillamine

A

aplastic anemia, agranulocytosis

172
Q

penicillamine pharmacokinetics

A

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
Q

penicillamine clinical uses

A

rheumatoid arhtritis

174
Q

penicillamine interactions

A

antacids can block absorption

175
Q

penicillamine side effects

176
Q

how long does it take to establish the effects of penicillamine

177
Q

penicillamine contraindications

A

pregnancy

aplastic anemia

renal failure

178
Q

Gold compound mechanism of action

179
Q

why are gold compounds used as a last resort for inflammation

A

slow acting, toxic

180
Q

examples of gold compounds

A

aurothioglucose suspension (Solganal)

gold sodium aurothiomalate (Myochrysine)

auranofin (Ridaura)

181
Q

Gold compounds pharmacokinetics

A

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
Q

Gold compound clinical

A

rheumatoid arthritis

juvenile arthritis

183
Q

gold compound: serious side effects

A

toxicity, decreased HGB, leukopenia, reduced granulocytes, proteinuria, throat ulcers

Other side effects: p. 58

184
Q

gold compound contraindications

A

blood dyscrasias, CHF, dermatitis, colitis, use of antimalarials

185
Q

conscientious considerations for gold compounds

A

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
Q

gold compoumd patient education

A

watch for mouth ulcers

187
Q

Tumor necrosis factor inhibitors

A

anticytokine therapy that targets the rheumatoid process

188
Q

examples of TNF inhibitors

A

etanercept (Enbrel)

infliximab (Remicade)

anakinra (Kineret

189
Q

Enbrel mechanism of action

A

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
Q

Remicade mechanism of action

A

mouse/human monoclonal antibody that targets TNF-alpha to neutralize and prevent its activity

191
Q

Kineret mechanism of action

A

blocks interleukin-1

192
Q

TNF inhibitors pharmacokinetics

A

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
Q

clinical uses of TNF inhibitors

A

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
Q

TNF inhibitor side effects

A

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
Q

TNF inhibitor contraindications

A

serious infections, children, allergic to proteins in formulations, pregnancy, TB

196
Q

Purpose of gout medications

A

end painful attacks

prevent formation of uric stones in kidney

prevent complications of uric stone formation in joints

197
Q

examples of drugs that treat gout

A

allopurinol

colchicine

probenecid

sulfinpyrazone

198
Q

Patient education regarding gout

A

Avoid alcohol and foods high in purines

199
Q

conscientious prescribing of gout medications

A

all patient on low dose ASA are at risk

determine cause of hyperuricemia to guide treatment

200
Q

Allopurinol (Zyloprim) mechanism of action

A

inhibits enzyme xanthine oxidase

blocks formation of uric acid

reduces serum uric acid

201
Q

Allopurinol pharmacokinetics

A

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
Q

clinical uses for allopurinol

A

chronic gouty arthritis

prevention of uric acid calculi

203
Q

allopurinol side effects: DERM

A

rash following injection, consider toxic if rash is severe

204
Q

allopurionol side effects: GI

A

diarrhea, hepatitis, N/V

205
Q

allopurinol side effects: GU

A

renal failure

206
Q

allopurinol side effects: HEM

A

bone marrow depression

207
Q

allopurinol side effects: MISC

A

sensitivity reactions after prolonged use possible

208
Q

allopurinol side effects: NEURO

A

drowsiness

209
Q

allopurinol and probenecid

A

probenecid increases clearance of oxypurinol so higher doses of allopurinol are needed

210
Q

allopurinol and azathioprine

A

allopurinol inhibits metabolism of the other one as it requires normal protein synthesis for action

211
Q

allopurinol and ACE inhibitors

A

produces stevens-johnson syndrome

(fever, arthraligias, skin eruptions)

212
Q

allopurinol and aluminum hydroxide

A

aluminum inhibits allopurinol response

213
Q

allopurinol contraindications

A

nursing mothers

history of hypersensitivity reactions

214
Q

conscientious cnsiderations for allopurinol

A

gouty attacks may increase initially

serum uric acids levels may take 1-3 weeks to achiev

215
Q

allopurinol patient education

A

take with food, avoid alcohol

216
Q

Colchicine mechanism of action

A

plant alkaloid that interferes with WBC ability to perpetuate inflammatory response which results in uric acid crystals

217
Q

Colchicine affect on uric acid levels

A

does not affect in circulatory system

218
Q

clochicine pharmacokinetics

A

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
Q

clinical use of colchicine

A

treatment of acute gout attacks

relief in 12 hours with symptoms gone in 48

220
Q

colchicine side effects

A

alopecia, N/V, diarrhea, abdominal pain, anuria, hematuria, renal damage, agranulocytosis, aplastic anemia, leukopenia, thrombocytopenia, phlebitis at injection site, peripheral neuritis

221
Q

colchicine interactions

A

additive GI effects with NSAIDs

222
Q

colchicine contraindications

A

cardiac, renal, hepatic, GI diseases

renal impairment (reduce dosage if needed)

safety not established in lactation

223
Q

conscientious considerations for colchicine

A

overdose can be fatal, once limit has been reached no more for 21 days

224
Q

colchicine patient education

A

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
Q

Pobenecid mechanism of action

A

lowers serum levels of urate by competitive inhibition in the renal tubules

226
Q

probenecid pharmacokinetics

A

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
Q

probenecid clinical uses

A

chronic gout

gonorrhea or neurosyphillis by delaying excretion of PCN

228
Q

probenecid side effects

A

flushing, rash, N/V, abdominal pain, diarrhea, sore gums, drug-induced hepatitis, uric acid stones, urinary frequency, aplastic anemia, headache, dizziness

229
Q

probencid interactions

A

increases levels of many drugs

increases clearance of oxypurinol

230
Q

probenecid contraindications

A

renal failure

231
Q

probenecid patient education

A

do not take ASA (decreases effects)

erratic compliance may cause attacks

report side effects

2,000-3,000 ml of fluid daily

232
Q

sulfinpyrazone (Anturane) mechanism of action

A

inhibits reabsorption of urates at the proximal tubule

increases uric acid excretion

233
Q

Sulfinpyrazone pharmacokinetics

A

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
Q

clinical use for sulfinpyrazone

A

chronic gout

235
Q

sulfinpyrazone side effects

A

rash, flushed face, N/V, stomach pain, frequent urination, agranulocytosis, aplastic anemia, headache, dizziness

236
Q

sulfinpyrazone interactions

A

increased toxicity with acetominophen

reduces effect of beta blockers

inhibits warfarin metabolism

237
Q

sulfinpyrazone contraindications

A

blood dyscrasias, renal failure

238
Q

sulfinpyrazone patient education

A

take with food, drink plenty of fluids, avoid ASA

239
Q

Pregnancy class B gout medications

A

etanercept, infliximab, anakinra, penicillamine, ibuprofen, diclofenac, other NSAIDs

240
Q

pregnancy category class C gout medications

A

allopurinol, aurothiomalate, aurothioglucose, hydroxychloroquine, celecoxib, etodolac

241
Q

pregnancy class D gout medications

A

colchicine, methotrexate

242
Q

pregnancy class X gout medications

A

leflunomide

243
Q

pregnancy unclassified gout medications

A

probenecid, sulfinpyrazone

Pharmacology (28 decks)

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