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Pharm Exam 2 > Anti-inflammatory and Gout > Flashcards

Anti-inflammatory and Gout Flashcards

1
Q

Cyclosporine MOA

A

Calcineurin inhibitor, suppressing production of interleukin-2

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2
Q

Cyclosporine DOC

A

Preventing organ rejection in allogeneic transplants

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3
Q

Cyclosporine Other uses

A

Autoimmune
RA
Psoriasis

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4
Q

Cyclosporine A/E

A

Risk for infection and neoplasms
HTN
Tremor
Male pattern hair growth

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5
Q

Cyclosporine Drug interactions

A

NSAIDS ( Aspirin) – other nephrotoxic drugs
CYP450 (Azoles, Erythromycin, Grapefruit juice) – increase level of Cyclosporine
Rifampin – decreases level of Cyclosporine

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6
Q

Cyclosporine Toxicity

A

Nephrotoxic due to renal blood flow/ filtration

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7
Q

Cyclosporine Monitoring

A

BUN
Cr
Could be toxicity or organ rejection

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8
Q

Tacrolimus MOA

A

Calcineurin inhibitor, prevents helper T cells from producing interleukin-2, interferon gamma and other cytokines

Same MOA as Cyclosporine, different chemical structure and binding place

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9
Q

Tacrolimus Use

A

Prevent organ rejection

Autoimmune

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10
Q

Tacrolimus A/E

A 
GI (N/V/D)
HTN
Hyperkalemia
Hyperglycemic
Gum hyperplasia
Anaphylaxis 
Overgrowth of hair 
Risk for infection and neoplasms
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11
Q

Tacrolimus Toxicity

A

Nephrotoxic

Neurotoxic (HA, Tremors)

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12
Q

Cyclosporine given with

A

glucocorticoids

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13
Q

Tacrolimus given with

A

Glucocorticoids

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14
Q

Tacrolimus Drug interactions

A

CYP3A4: Erythromycin, Azoles, grapefruit juice – increase levels of Tacrolimus
Rifampin – decreases level of Tacrolimus

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15
Q

Aspirin MOA

A 
1st gen NSAID 
non selective (irreversible) inhibitor of cyclooxygenase
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16
Q

Aspirin Use

A 
analgesic 
anti-inflammation 
antipyretic (DOC for adults with fever) 
suppression of platelet aggregation 
dysmenorrhea
cancer prevention ( possibly colorectal)
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17
Q

Aspirin Dosing

A

low: (81mg) platelet aggregation inhibitor
high: (325+mg) pain

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18
Q

Aspirin A/E

A

GI: distress, heartburn, bleeding
increased risk for bleeding
hypersensitivity
Reye’s syndrome ( swelling of the liver and brain)
Salicylate poisoning ( fever, tinnitus, due to not fully developed kidneys)
Acute poisoning: hyperkalemia, respiratory depression, dehydration, acidosis – life threatening OD

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19
Q

Aspirin Toxicity

A

Nephrotoxicity

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20
Q

Aspirin Drug interactions

A

Anticoagulants: increase risk for bleeding
Glucocorticoids: increase r/f gastric ulceration
ETOH: increase r/f gastric bleeding
Ibuprofen: decrease antiplatelet aggregation effects
ACE/ARBs increase renal impairment

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21
Q

Aspirin Contraindications

A

Pregnancy –anemia/ postpartum hemorrhage

Infants

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22
Q

Salicylate poisoning

A

babies, tinnitus, fever, N/V, lethargy/excitability, hyperventilation

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23
Q

Ibuprofen MOA

A

1st gen NSAID
inhibits cyclooxygenase and has inflammatory, analgesic and antipyretic actions
COX 1 and 2 inhibitor

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24
Q

Ibuprofen Use

A 
Fever-- given to children >6mo
Mild- Mod pain
anti-inflammatory
arthritis
better for dysmenorrhea
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25
Q

Ibuprofen A/E

A 
GI bleed
SJS 
PUD
fluid retention 
renal impairment (decreased blood flow)
resistant HTN
platelet inhibitor
increase r/f CV disease
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26
Q

Ibuprofen Drug interaction

A

decreases effectiveness of BP meds

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27
Q

Celecoxib MOA

A

selective Cox 2 inhibitor

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28
Q

Celecoxib Use

A

osteoarthritis
RA
Acute pain
saved for last form of long term treatment (cardic effects)

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29
Q

Celecoxib Contraindications

A

Sulfa allergy

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30
Q

Celecoxib A/E

A 
Cardiovascular (heart attack, stroke, CV death)
dyspepsia
diarrhea
abdominal pain
URI
peripheral edema
GI discomfort/irritation
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31
Q

Celecoxib Toxicity

A

nephrotoxic (increase risk for HTN, HF, kidney disease)

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32
Q

Celecoxib Drug interactions

A

increase effects of warfarin
decrease effects of diuretics (furosemide), ACE inhibitors
increase level of Lithium
fluconazole increases level of celecoxib

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33
Q

Celecoxib Dose

A

give the smallest dose for the shortest time possible

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34
Q

Acetaminophen MOA

A

inhibits prostaglandin synthesis in the CNS

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35
Q

Acetaminophen Use

A

Analgesic

Antipyretic: DOC for children <6mo

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36
Q

Acetaminophen does not

A

have anti-inflammatory effects

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37
Q

Acetaminophen Max dose

A

healthy person: 4000mg/day
malnutrition: 3000mg/day
liver diseases: talk to MD <3000mg/day

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38
Q

Acetaminophen A/E

A

SJS
Acute generalized exanthematous pustulosis (AGEP)
Toxic epidermal necrolysis (TEN)

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39
Q

Acute generalized exanthematous pustulosis

A

rare skin reaction

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40
Q

Acetaminophen S/S of Toxicity/ OD

A 
Eary: 
-N/V/D
-Sweating
-abdominal pain 
Hepatic necrosis 
Hepatic failure
Coma- death
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41
Q

Acetaminophen Toxicity

A

Hepatotoxic

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42
Q

Acetaminophen Drug interactions

A

ETOH increases risk for liver injury
Warfarin increases risk for bleeding
Blunts vaccine response

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43
Q

Acetaminophen Antidote

A

Acetylcysteine (mucomyst)

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44
Q

Ketorolac MOA

A

Inhibition of prostaglandin synthesis by competitive blocking of the enzyme cyclooxygenase (COX)
Non selective COX inhibitor
1st generation NSAID

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45
Q

Ketorolac Use

A

short term pain relief– equivalent to morphine
C-section
mild anti-inflammatory effects

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46
Q

Ketorolac Dose

A

5 days max!– due to bleeding risk

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47
Q

Ketorolac A/E

A 
GI bleed 
Peptic ulcer
Prolonged bleeding time
renal impairment 
hypersensitivity reaction 
increase Cardiovascular disease
48
Q

Ketorolac Route

A

IV
IM
PO

49
Q

Indomethacin Use

A

1st choice for Acute gout attack – pain relief
Arthritis
Tendonitis
Bursitis

50
Q

Naproxen pt reports

A

works the best

51
Q

Indomethacin Contraindications

A

inflants, children <14y/o
PUD
Psych patients
Patients with seizures

52
Q

Indomethacin A/E

A 
Thrombosis**
smoking increases risk for CV events 
Frontal HA-- common
CNS: Confusion, dizziness, vertigo, depression, psychosis, seizures 
GI: N/V/D, bleeding
Hematologic anemias 
Platelet aggregation inhibitor (slight)
53
Q

Indomethacin Toxicity

A

Nephrotoxic

54
Q

Indomethacin metabolized

A

liver

55
Q

Indomethacin excreted

A

urine/ feces

56
Q

Glucocorticoids Drugs

A 
Hydrocortisone
Prednisone
Prednisolone 
Methylprednisolone
Dexamethasone
57
Q

Glucocorticoids MOA

A

Nearly identical to steroids produced by the adrenal cortex

Immune suppression

58
Q

Glucocorticoids Use

A 
Those who cannot take NSAIDs
Gout that is unresponsive to NSAIDS
Acute gout attack 
Concurrent use with Cyclosporine, Tacrolimus to prevent infection
Premedicate to chemo
RA
SLE
IBD
Other inflammatory disorders
Allergic conditions
Asthma
Dermatologic disorders
Neoplasms
Suppression of allograft rejection 
Prevents respiratory distress syndrome in preterm infants
59
Q

Prednisone Use

A

Pain relief– for those who cannot take NSAIDs

60
Q

Glucocorticoid Doses

A

low doses: physiologic effects (usually for adrenal insufficiency)
high doses: pharmacologic effects (immune suppression)

61
Q

Glucocorticoid Drug interactions

A 
Aspirin* cannot be combined due to GI bleed
Diabetes oral meds
K dumping drugs (hypokalemia) 
NSAIDs
Vaccines
62
Q

Glucocorticoid Contraindications

A

Systemic fungal infections
Receiving live Vaccine
Prone to hyperglycemia

63
Q

Glucocorticoid A/E in general

A

increase everything

64
Q

Glucocorticoid A/E

A 
Increase: 
-Bp
-BG
-infection
-wight
Adrenal insufficiency 
Osteoporosis 
Myopathy (rhabdomyolysis) 
Fluid retention 
Hypernatremia
Hypokalemia 
Growth suppression
Psychological disturbances
Glaucoma/ cataracts 
PUD
Iatrogenic Cushing syndrome (pot belly, moon face, buffalo hump)
Abnormal hair growth 
Thinning skin
Insomnia
Agitation
65
Q

Glucocorticoid withdrawal

A

Taper for 5-7 days

If stopped immediately can cause Addison’s disease

66
Q

Treatment for Addison’s disease

A

low dose of glucocorticoid, then taper off slowly

67
Q

Glucocorticoid Nursing implementation

A

Give in the morning because the body is producing the most cortisol at that time and it causes insomnia
Can be taken with food
Increase dose when under stress
Can be giving on alternating days
Avoid long term use
Use smallest dose for shortest time
Topical can cause systemic reactions if gets into wound

68
Q

Glucocorticoid Monitoring

A

BP

BG

69
Q

Colchicine MOA

A

Unknown

Does not decrease production or removal of uric acid

70
Q

Colchicine Use

A

Gouty arthritis
Acute gouty attack : 2nd line drug
Anti-inflammatory (when unresponsive to NSAIDs)

71
Q

Colchicine Doses

A 
Small dose (long term): prevents gout attacks 
High dose (short term): relieve attacks
72
Q

Colchicine A/E

A

GI: N/V/D – take with food
Abdominal pain
Myelosuppression
Myopathy (rhabdomyolysis)

73
Q

Colchicine Drug interactions

A

Statins: increase muscle injury
PGP inhibitors
CYP3A4 drugs

74
Q

Colchicine Contraindication

A

Renal/ Hepatic impairment

pregnancy

75
Q

Goal for hyperuricemia (gout)

A 
Promote dissolution of urate crystals 
Prevent new crystal formation 
Prevent disease progression 
Reduce frequency of acute attacks 
Improve quality of life
76
Q

Drugs for Hyperuricemia

A

Allopurinol
Febuxostat
Probenecid
Pegloticase

77
Q

DOC for acute gout attack

A

NSAIDs

78
Q

Allopurinol and Febuxostat

A

inhibits uric acid formation

79
Q

Probenecid

A

Increases uric acid excretion

80
Q

Pegloticase

A

Converts uric acid to allantoin, a compound readily excreted by the kidneys

81
Q

Allopurinol MOA

A

Inhibits xanthine oxidase (XO), an enzyme required for uric acid formation
-reduces blood levels of uric acid

82
Q

Allopurinol DOC

A

Chronic tophaceous gout

83
Q

Allopurinol Other uses

A

Hyperuricemia due to chemotherapy

84
Q

Allopurinol A/E

A

N/V/D - give with food
abdominal discomfort
HA
Drowsiness
Metallic taste
Hypersensitivity syndrome (rash, fever, kidney and liver dysfunction)
Initially may cause an acute gout attack
Renal impairment ** (nephropathy from deposition of urate crystals in the kidneys)

85
Q

Allopurinol Drug interactions

A

Warfarin

86
Q

Allopurinol Nursing implementations

A

Promote hydration- 2-3 L/ day at least

87
Q

Allopurinol Prevents

A

New tophus from forming and causing regression of tophi that have already formed

88
Q

Allopurinol Improves

A

Joint function

89
Q

Probenecid MOA

A

Acts on renal tubules to inhibit reabsorption of uric acid

Prevents formation of new topji and helps diminish existing tophi

90
Q

Probenecid A/E

A

Same as Allopurinol
N/V/D – take with food
Hypersensitivity reactions
May exacerbate acute gout attacks (add Indomethacin)

91
Q

Probenecid Toxicity

A

Nephrotoxic

92
Q

Probenecid Nursing implementation

A

Promote hydration 2.5-3L/ day
Need to alkalize urine to protect the kidneys
Increasing uric acid excretion

93
Q

Probenecid Drug interactions

A

Aspirin
Indomethacin
Sulfonamides (kidneys)

94
Q

Pegloticase MOA

A

Recombinant of uricase, an enzyme that catalyzes the conversion of uric acid to allantoin, an inert water-soluble compound

95
Q

Pegloticase Use

A

Last resort for Chronic gout (IV)

96
Q

Pegloticase A/E

A

Anaphylaxis

Infusion reactions

97
Q

Pegloticase Nursing implementation

A

Premedicate for reactions with antihistamine, acetaminophen, glucocorticoids

98
Q

Pegloticase Contraindication

A

G6PD deficiency

99
Q

DMARDS Drugs

A

Methotrexate
Cyclosporine
Etanercept

100
Q

Methotrexate MOA

A

Traditional DMARD

Immunosuppression effects

101
Q

Methotrexate DOC

A

Gold standard for RA (analgesic/ anti-inflammatory, start with in a year of Dx)
Prevents joint destruction
Prevents long term disability

102
Q

Methotrexate Other use

A

Psoriasis
Medical abortion
Cancer/ chemo

103
Q

Methotrexate Contraindication

A

Pregnancy

104
Q

Methotrexate A/E

A 
Bone marrow suppression 
Mucositis (ulcers) 
N/V
Fatigue 
Pneumonitis: acute inflammation of the lung (SOB) 
Pulmonary fibrosis 
Methotrexate lung
105
Q

Methotrexate lung

A

SOB
Dry cough
Fever
-Most often seen in the first 6 mo

106
Q

Methotrexate Toxicity

A

Hepatotoxic

Teratogenic

107
Q

Methotrexate Baseline information

A

Chest Xray
PFT
HIV, HBV, HCV test
Pregnancy test

108
Q

Methotrexate Monitoring

A

CBC
LFTs
Pregnancy tests
-every 4-8wk or every month or every other month

109
Q

Methotrexate Nursing implementation

A

Takes 6wk to start working

Always give 1mg folic acid every day

110
Q

Methotrexate Doses

A

low dose: RA

high dose: Cancer

111
Q

Methotrexate Antidote

A

Leucovorin

112
Q

Etanercept MOA

A

Produced by cells of immune system or inflammatory cells
Acts to decrease inflammatory and immunologic responses
Tumor Necrosis factor antagonists blockers (pro-inflammatory cytokine) – inactivates TNF

113
Q

Etanercept Use

A

Moderate to severe RA
Given in combo with Methotrexate
Psoriasis

114
Q

Etanercept Starts working

A

sooner than Methotrexate: 2wk, at 3 mo you see extreme benefits, at 5 yr most patients have no further progression

115
Q

Etanercept A/E

A 
Increased risk for infection and neoplasms, and reactivation of TB
Serious allergic reaction 
New or worsening Heart failure
Hematological disorders (fatal)
CNS demyelinating disorders
116
Q

Etanercept Toxicity

A

Hepatotoxicity

117
Q

Etanercept not often used because

A

VVVVVV expensive!!!

Pharm Exam 2 (4 decks)

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