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Pharmacology Exam 3 > Pharm Kelsey and Amy > Flashcards

Pharm Kelsey and Amy Flashcards

1
Q

Can Conventional Synthetic drugs treat other conditions?

A

Yes - Cancer, Chron’s, RA, Ulcerative Colitis

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2
Q

Conventional Synthetic Drugs

A

Hydrocholorquine, Sulfasalazine, Leflunomide, Methotrexate

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3
Q

How do you decide what drug to use?

A

Drug safety, efficacy, disease severity, cost, patient experience

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4
Q

What is the initial treatment choice for RA?

A

Methotrexate

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5
Q

MOA for Methotrexate

A

Anti-inflammatory inhibits dihydrofolate reductase (inflammatory factors) which prevents folic acid (FH2) from converting to active form (FH4)

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6
Q

What must be given in combo with Methotrexate?

A

Folic Acid

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7
Q

What does Folic Acid supplementation prevent?

A

Reduces risk of folate depleting reactions Methotrexate Toxicity

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8
Q

Folic Acid prophylactic dose

A

1 gram

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9
Q

Methotrexate route of admin

A

PO, IM, SubQ

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10
Q

Methotrexate AE

A

Nausea, diarrhea, hepatotoxicity, alopecia, new cough, SOB, myelosuppression

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11
Q

Methotrexate contraindication

A

Hepatic Impairment

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12
Q

What to monitor with methotrexate use

A

CBC, creatinine, LFT (every 4-8 wks), signs of infection

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13
Q

What to avoid when taking methotrexate

A

Pregnancy, alcohol

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14
Q

What DMARDs medication is category X for pregnancy?

A

Methotrexate

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15
Q

What does methotrexate cause if taken when pregnant?

A

Spontaneous abortion, myelosuppression in fetus, limb defects, CNS abnormalities

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16
Q

Cautious measures with methotrexate

A

Birth control and dose adjustment for renal impairment

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17
Q

Signs of methotrexate toxicity

A

Stomatitis, diarrhea, nausea, alopecia, myelosuppression (fever, infection, easy bruising, bleeding), elevation in liver fxn tests

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18
Q

What do you give to prevent Methotrexate Toxicity? What do you give if Methotrexate Toxicity occurred?

A

Folic Acid or Leucovorin (cancer drug)

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19
Q

What does Leucovorin provide in the active form?

A

Folic Acid (X-FH4)

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20
Q

MOA for Hydroxychloroquin

A

Unknown

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21
Q

Use for Hydroxychloroquin

A

Low RA disease activity

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22
Q

Can Hydroxychloroquin be combined?

A

Yes - with methotrexate or sulfasalazine

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23
Q

Hydroxychloroquin route

A

Oral

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24
Q

Hydroxychloroquin AE

A

Nausea, diarrhea, headache, vision changes, skin pigmentation

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25
Q

Hydroxychloroquin onset time

A

Slow must use for 6 mo to determine if effective

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26
Q

When would Hydroxychloroquin be a good choice?

A

Renal, hepatic, or bone marrow suppression

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27
Q

What to monitor with Hydroxychloroquin use?

A

Annual eye exam

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28
Q

Sulfasalazine MOA

A

Unknown

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29
Q

When is Sulfasalazine used?

A

For low RA disease activity

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30
Q

Sulfasalazine onset time?

A

Slow onset - must use for 6 mo to determine if effective

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31
Q

When would Sulfasalazine be a preferred option?

A

Pregnancy!

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32
Q

Can you combine Sulfasalazine?

A

Yes - with methotrexate or hydroxychloroquin

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33
Q

What is Sulfasalazine’s route of administration?

A

Oral

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34
Q

How do you dose Sulfasalazine?

A

Start with low dose and titrate up slowly

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35
Q

Sulfasalazine AE

A

Nausea, abdominal discomfort, diarrhea, leukopenia, myelosuppression, rash, yellow-orange discoloration, photosensitivity (easily sunburn!)

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36
Q

What is a contraindication to taking Sulfasalazine?

A

Sulfa allergy

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37
Q

Who should avoid taking Sulfasalazine?

A

Those with hepatic impairment

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38
Q

Why should you adjust the dose of Sulfasalazine

A

Renal impairment status

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39
Q

What to monitor when taking Sulfasalazine

A

CBC every 2-4 weeks for 3 mo, then every 3 mo

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40
Q

MOA of Leflunomide

A

Inhibits t-lymphocyte response which halts the inflammatory cascade

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41
Q

What type of half life does Leflunomide have?

A

Long

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42
Q

How should you start a patient on Leflunomide?

A

Loading dose followed by a maintenance dose

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43
Q

Can you combine Leflunomide?

A

Yes - with Methotrexate, but it INCREASES RISK OF HEPATOTOXICITY!

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44
Q

How can you discontinue Leflunomide abruptly?

A

Give cholestyramine (removes from body quickly)

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45
Q

Why would you want to discontinue Leflunomide abruptly?

A

Pregnancy or toxicity

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46
Q

When should you use Biological DMARDs

A

If a patient fails trail of conventional DMARDs or used in combo with a conventional DMARD in early aggressive disease.

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47
Q

Do conventional or biological DMARDs work faster?

A

Biological

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48
Q

Can Biological DMARDs be used with methotrexate?

A

Yes

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49
Q

What do you base your choice of Biological DMARDs of off?

A

Comfort level, severity of disease, prognosis, frequency/route of administration, patient’s comfort level, cost, insurance

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50
Q

Who should avoid using Biological DMARDs?

A

Patients with serious infections, demyelinating disorders, hepatitis

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51
Q

Who should avoid using TNF antagonists?

A

Patients with heart failure

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52
Q

What other conditions use Biological DMARDs?

A

Patients with cancer and chrons

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53
Q

What are the classes of Biological DMARDs?

A

TNF antagonists, Interleukin-1 receptor antagonist, Costimulation modulators, Anti-CD20 monoclonal antibody, Anti-interleukin-6 receptor antibody

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54
Q

What are the drug names of the TNF Antagonists?

A

Etanercept (Enbrel)
Adalimumab (Humira)
Infliximab (Remicade)
Golimumab (Simponi)
Certolizumab (Cimzia)

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55
Q

What are the adverse reactions of TNF Antagonists?

A

Injection site reactions and Infusion reactions (can be helped by using topical corticosteroids, antipruritics, analgesics, rotate site).

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56
Q

What should you monitor in TNF Antagonists?

A

Serious infection

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57
Q

What should you screen for before giving a TNF Antagonist?

A

TB (could reactivate if TNF is inhibitied. TNF involved in forming granulomas that wall off TB) and Hepatitis

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58
Q

What is the MOA of TNF Antagonists?

A

Prevent action of TNF, causing a reduction in inflammation

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59
Q

What are the signs of an infusion reaction? What should you do if someone has a reaction?

A

Rash, urticaria, flushing, headache, fever, chills, nausea. Treatment is to temporarily d/c, slow infusion rate, corticosteroids/antihistamines.

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60
Q

What is the route of administration of Infliximab?

A

Given IV

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61
Q

What is the route of administration of Adalimumab (Humira)

A

SubQ

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62
Q

What is the route of administration of Golimumab (Simponi)

A

SubQ or IV

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63
Q

What are the drug names of Costimulation Modulators?

A

Abatacept (Orencia)

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64
Q

What is the MOA of Costimulation Modulators?

A

Blocks T cell signaling and activation (prevents response)

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65
Q

What are the adverse effects of Costimulation Modulators?

A

Headache, infection, infusion reaction, injection site reaction

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66
Q

What should you monitor Costimulation Modulators?

A

Infection

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67
Q

What is the use of Costimulation Modulators?

A

Monotherapy or combo therapy after inadequate response of methotrexate and/or anti-TNF

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68
Q

What are the Anti-CD20 Monoclonal Antibody drug names?

A

Rituximab (Rituxan)

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69
Q

What is the MOA of Anti-CD20 Monoclonal Antibody?

A

Causes B lymphocyte depletion in bone marrow and synovial tissue. Fewer B lymphocytes to cause inflammation response.

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70
Q

Do patients with rheumoatoid factor postive RA have a better or lesser response to Anti-CD20 Monoclonal Antibody?

A

Better

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71
Q

What is the Black box warning of Anti-CD20 Monoclonal Antibody?

A

Fatal infusion reactions, severe mucocutaneous reactions

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72
Q

When should you use Anti-CD20 Monoclonal Antibodies?

A

As LAST resort - HIGH RISK

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73
Q

What is the AE of Anti-CD20 Monoclonal Antibody?

A

Infusion reaction

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74
Q

What should you monitor for when taking Anti-CD20 Monoclonal Antibody

A

Infection

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75
Q

What are the Anti-interleukin-6 Receptor Antibody drug names?

A

Tocilizumab (Actemra)

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76
Q

What is the MOA of Anti-interleukin-6 Receptor Antibody?

A

Blocks interleukin-6 (causes joint damage, disease activity, and anemia)

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77
Q

What is the route of administration for Anti-interleukin-6 Receptor Antibody?

A

IV or SubQ

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78
Q

When would you use Anti-interleukin-6 Receptor Antibody?

A

After Biological DMARDs have failed

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79
Q

What is the AE of Anti-interleukin-6 Receptor Antibody

A

Elevated LFT/Total Chol/Trigs/HDL, nasopharyngitis, infection

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80
Q

What to monitor when using Anti-interleukin-6 Receptor Antibody

A

Infection, LFTs

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81
Q

Targeted Synthetic drug names

A

Tofacitinib

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82
Q

What is the MOA of Targeted Synthetic?

A

Inhibits specific kinases

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83
Q

What is the route of administration for Targeted Synthetic?

A

Oral

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84
Q

When would you use Targeted Synthetic drugs?

A

To treate moderate or severe RA

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85
Q

Can you combine Targeted Synthetic drugs?

A

Yes - with conventional DMARDs (but you can use it as monotherapy)

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86
Q

What is the AE of Targeted Synthetic drugs?

A

Infection, headache, HTN, elevated LFTs, diarrhea, worsening lipids

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87
Q

When should you adjust the dose of Targeted Synthetics?

A

When there is renal or hepatic impairment

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88
Q

What should you monitor when taking Targeted Synthetics?

A

CBC, hemoglobin, lipids, LFTs, infection

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89
Q

How should you think about Biosimilar drugs?

A

As “generic” Bio Originators

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90
Q

What DMARD medication is the drug of choice during pregnancy?

A

Sulfasalazine

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91
Q

What other RA medications are ok for pregnancy?

A

Low dose corticosteroids, hydroxychloroquine, azathioprine

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92
Q

What is the MOA of acetaminophen?

A

Centrally acting analgesic and antipyretic with minimal anti-inflammatory properties

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93
Q

What is the onset of acetaminophen?

A

One hour

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94
Q

What is the use of acetominophen?

A

Mild to moderate pain in general

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95
Q

What is the drug name for acetominophen?

A

Tylenol (APAP)

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96
Q

Can APAP be combined?

A

Yes - with NSAIDs (APAP has equal efficacy as NSAID)

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97
Q

What is the max daily dose for APAP?

A

4000 mg per day

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98
Q

What is the max dose of APAP given at a time

A

1000 mg at a time

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99
Q

What is the AE for APAP?

A

Renal toxicity, hepatic toxicity, GI upset

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100
Q

What is the leading cause of acute liver injury?

A

Acetaminophen Toxicity

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101
Q

What can cause Acetaminophen toxicity?

A

Overdose - many meds contain APAP

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102
Q

What can cause CHRONIC Acetaminophen Toxicity?

A

> 4g daily dose, use of alcohol (2.5 g daily in those drinking 2-3 beverages)

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103
Q

What can cause ACUTE Acetaminophen Toxicity?

A

200 mg/kg or 10g or 10x overdose

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104
Q

What are the common signs/sx’s of acute APAP toxicity?

A

Nausea, vomiting, abdominal pain

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105
Q

What is elevated after 24 hours of APAP ingestion?

A

ALT and AST

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106
Q

When do ALT and AST peak after ingestion or APAP?

A

2-3 days

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107
Q

What are the more serious effects of acute APAP toxicity?

A

Liver and renal dysfunction, hyperglycemia, lactic acidosis, coma, death (if serum concentration of APAP is > 500 mcg/mL)

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108
Q

True or false: hepatic and renal function return to normal if a Pt survives APAP overdose?

A

True!

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109
Q

What are the mild signs/sx’s of chronic supratherapeutic APAP overuse?

A

ALT elevation, malaise, nausea, vomiting, abdominal pain, hepatotoxicity

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110
Q

What are the severe signs/sx’s of chronic supratherapeutic APAP overuse?

A

Jaundice, hypoglycemia, coagulopathy, renal failure, fulminant hepatic failure encephalopathy, death

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111
Q

How do you treat mild/moderate supratherapeutic overuse of APAP?

A

1: Obtain APAP concentration in blood. 2: Start acetylcysteine (if risk of hepatic injury)

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112
Q

What is considered mild/moderate supratherapeutic APAP overuse?

A

If >200 mg/kg ingested or if >10 g ingested, or if APAP concentration can’t be measured, or if concentration is >150 mcg/mL at 4 hours post ingestion

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113
Q

How do you treat severe supratherapeutic APAP overuse

A

ER care: intubation, fresh frozen plasma, vasopressors, dialysis, airway management, fluid resuscitation
Start acetylcysteine if hepatic injury risk

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114
Q

What is acetylcysteine used for?

A

Hepatic injury due to severe APAP toxicity

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115
Q

What is one of the safest analgesics?

A

APAP

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116
Q

What analgesic is preferred for Pts with mild-moderate pain with hypertension or kidney issues?

A

APAP

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117
Q

What is the MOA of NSAIDs?

A

All NSAIDs block COX1 and COX2. Has analgesic and antipyretic activities by blocking COX1 and COX2, which causes inhibition of prostaglandins

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118
Q

What does COX1 affect?

A

Gastric mucosa (increase muscus, bicarb), kidney (dilate afferent arteriole), platelets (promote normal function)

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119
Q

What does COX2 affect?

A

Normally undetectable, but increases at sites of inflammation and local tissue injury

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120
Q

What COX does selective NSAIDs preferentially block?

A

COX2

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121
Q

What COX does nonselective NSAIDs preferentially block?

A

Not selective for either

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122
Q

What are the nonselective NSAIDs drug names?

A

Aspirin, salsalate, etodolac, diclofenac, indomethacin, nabumetone, ibuprofen, naproxen, meloxicam, prioxicam, prioxicam, sulindac, ketorolac

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123
Q

What nonselective NSAIDs are over-the-counter?

A

Aspirin, ibuprofen, naproxen

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124
Q

What are the selective COX2 inhibitors?

A

Celecoxib

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125
Q

What is the use of NSAIDs?

A

Used in mild-moderate pain in general. Can be combined with APAP.

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126
Q

What is the route of administration with NSAIDs?

A

Oral, topical

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127
Q

What is the efficacy of APAP compared to NSAIDs?

A

They are equal

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128
Q

What is the onset of pain relief with NSAIDs?

A

1 hour

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129
Q

What is the onset of anti-inflammatory effects?

A

2-3 weeks of continuous therapy

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130
Q

What do you choose NSAIDs based on?

A

Patient preference, previous response, tolerability, dosing frequency, cost, GI and CV risk. if one doesn’t work, try another NSAIDs

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131
Q

What is the route of administration of Diclofenac?

A

Gel, solution, patch

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132
Q

What are the adverse effects of Diclofenac?

A

NSAID specific are minimal. Appilcation site dermatitis, pruritus, and phototoxicity.

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133
Q

What joints should be used with Diclofenac?

A

Superficial joints. Hands, wrists, elbows, knees, ankles, feet.

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134
Q

What is the dose of Diclofenac?

A

Depends on the joint.

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135
Q

What are the pros of using Diclofenac?

A

Minimized systemic exposure. Has comparable pain relief to oral NSAIDs.

136
Q

What are the contraindicatations of Ketorolac?

A

CV disease, GI/peptic ulcer risk, advanced renal impairment, high bleeding risk (on anticoagulants), concomitant NSAIDs.

137
Q

What is the use of Ketorolac?

A

Commonly used for acute moderately severe pain that requires analgesia at opioid level. Initiate in office/ED with IM or IV then followu p to 5 days oral.

138
Q

How long can you use Ketorolac?

A

5 days maximum, only for adults

139
Q

What should you take Ketorolac with?

A

Food

140
Q

What is Salicylism?

A

Toxic syndrome that occurs due to excessive doses of aspirin, salicylic acid, consuming oil of wintergreen (5mL). Cuased mixed repiratory alkalosis and metabolic acidosis (anion gap). Can occur due to acute overdose (150mg/kg or 6.5g aspirin) or chronic overdose.

141
Q

What are the signs and symptoms of Salicylism?

A

Severe headache, nausea, vomiting, tinnitus, confusion, increased pulse, increased repiratory rate, can progress to seizures, coma, cerebral/pulmonary edema, death

142
Q

What is the treatment of Salicylism?

A

Urine alkalinization (sodium bicarb), hemodialysis, emergency care PRN

143
Q

What are the adverse reactions of all NSAIDs, especially in eldery?

A

GI (COX1 related), renal insufficiency, hepatic dysfunction, increased cardiovascular risk (COX2 related), CNS effects, increased BP/fluid retention, rarely causes tubulointerstitial nephropathy renal papillary necrosis.

144
Q

What are the adverse reactions of COX1 inhibitors?

A

Adverse effects on gastric mucosa (asymptomatic gastric/duodenal mucosal ulceration), direct irritant effect on GI (nausea, dyspepsia, anorexia, abdominal pain, flatulence, diarrhea), perforation, gastric outlet obstruction, GI bleeding

145
Q

What are the adverse reactions of COX2 inhibitors?

A

Increased risk of CV events. Degree of COX2 selectivity (dose, potency) dictates how much CV event risk.

146
Q

What selective COX2 inhbitor has the strongest association with CV events?

A

Celecoxib

147
Q

What nonselective NSAIDs have the strongest association with CV events?

A

Diclofenac, ibuprofen

148
Q

What increases the CV risk the most?

A

Selective COX2 inhbitor

149
Q

What NSAID should you use with patients at high risk fo GI complications and low risk for CV events?

A

Celecoxib (selective COX2 inhibitor)

150
Q

What NSAID should you use in high CV risk patients?

A

Use nonselctive NSAID, Naproxen. Has the lowest CV event risk. Should also be on aspirin.

151
Q

If high GI risk, use

A

Gastroprotection to nonselective NSAID or lower Gi risk NSAID (selective COX2 NSAID, celecoxib)

152
Q

If high CV risk +Gi risk

A

Add gastroprotection and use nonselective NSAID (naproxen)

153
Q

If low CV and GI risk

A

Use nonselective NSAID

154
Q

NSAID contraindications/cautions

A

At risk for peptic ulcers or GI risk, bleeding risk, renal insufficiency, uncontrolled HTN, HF. Caution if NSAID/asprin sensitive asthma.

155
Q

NSAIDs and pregnancy

A

Risk of feal bleeding. Possibly contraindicatied, associated with miscarriage in 1st trimester. Contraindicated after 30 weeks/3rd trimester, promotes closure of ductus arteriosus.

156
Q

NSAID interactions

A

Aspirin, warfarin, oral hypoglycemics, antihypertensives, lithium. Due to high protein binding, detrimental renal effects, antiplatlet activity.

157
Q

What medication is used to stop gout attacks?

A

Colchicine

158
Q

Can you use colchisine for an acute gout attack if already taking it for prophylaxis or recently taken (in last 14 days)

A

No!

159
Q

Could you give colchisine 48 hours after the acute attack begins?

A

No - it only works if given right away (<36 hrs)

160
Q

What fraction of people respond to colchisine w/in the first 24 hours of attack?

A

2 out of 3

161
Q

What is the MOA of Colchisine?

A

It interferes with the migration of neutrophils to sites of inflammation induced by deposits of monosodium urate crystals in synovial fluid anti-inflammatory

162
Q

Is Colchisine an analgesic or uricosuric (clears uric acid)?

A

No

163
Q

Is there a generic Colchisine drug?

A

No - it is brand name only (more expensive)

164
Q

Is Colchisine FDA approved?

A

Yes - recently! And now properly labeled and the dose changed (lower)

165
Q

What are the AE of Colchisine?

A

Toxicity

166
Q

What are the signs that Colchisine toxicity could happen?

A

Nausea, vomiting, diarrhea, abdominal pain

167
Q

What are the signs that Colchisine toxicity HAS happened?

A

Myopathy, bone marrow suppression (neutropenia)

168
Q

What should you be cautious of when taking Colchisine?

A

Renal insufficiency (toxicity is more likely adjust the dose!)

169
Q

What kind of therapeutic window does Colchisine have?

A

Low

170
Q

What class of drugs does Colchisine interact with?

A

P-glycoprotein or strong CYP3A4 inhibitions

171
Q

What specific drugs does Colchisine interact with?

A

Clarithromycin, Verapamil, Ritonavir, Cyclosporine, Ranolazine

172
Q

What should you do if Pt is experiencing numerous AE on Colchisine?

A

Adjust dose or try NSAIDs

173
Q

What is urate lowering therapy used for?

A

To prevent future gout attacks

174
Q

What is the criteria for using urate lowering therapy?

A

Recurrent attacks (>2xyear), Tophi, CKD Stage 2 or worse, past urolithiasis

175
Q

In what ways can urate lowering therapy prevent future gout attacks?

A

Either decrease uric acid production or increase uric acid secretion

176
Q

What is the goal of urate lowering therapy?

A

Decrease uric acid levels and prevent crystal formation

177
Q

What are the FIRST LINE Urate Lowering Therapy drugs?

A

Allopurinol and Feboxostat

178
Q

What are the ALTERNATE Urate Lowering Therapy drugs?

A

Probenecid

179
Q

What are the REFRACTORY Urate Lowering Therapy drugs?

A

Pegloticase

180
Q

Should you continue using Urate Lowering Therapy drugs during an acute flare?

A

YES! That is the key of urate lowering therapy

181
Q

What is the most common Urate lowering therapy drug?

A

Allopurinol and Feboxostat

182
Q

MOA of Allopurinol?

A

Both drug and metabolite reduce uric acid concentrations by inhibiting xanthine oxidase

183
Q

What does xanthine oxidase do?

A

Produces uric acid

184
Q

What is the primary metabolite of Allopurinol?

A

Oxypurinol

185
Q

What is the route of Allopurinol administration?

A

Oral

186
Q

What clears Allopurinol from the body?

A

Kidneys

187
Q

What is the half life of Allopurinol?

A

2-3 hours

188
Q

What is the half life of Oxypurinol?

A

24 hours

189
Q

What is the dosing of Allopurinol?

A

Once daily

190
Q

Why would you adjust the dose of allopurinol?

A

Based on renal function (decrease if renally impaired)

191
Q

Should you start Allopurinol with a high dose?

A

No - start with low, then increase q2-5 weeks prn and as tolerated

192
Q

What uric acid level should you titrate the dose of Allopurinol to?

A

<6 mg/dL or <5 mg/dL

193
Q

What is the max dose of Allopurinol?

A

800 mg daily

194
Q

What should you also give when initiating allopurinol during an acute gout attack?

A

Low dose colchisine or NSAID

195
Q

What does allopurinol do?

A

Prevents inflammation and crystal formation

196
Q

What causes crystals?

A

Rapid uric acid concentration shifts

197
Q

What should you monitor when taking Allopurinol?

A

Serum uric acid levels Q 2-5 weeks during titration, every 6 mo after target level is reached

198
Q

What interacts with Allopurinol?

A

Theophylline, Warfarin, Azathioprine, 6-mercaptopurine (can simply lower the doses of these), and Ampicillin (rash)

199
Q

What are the AE of Allopurinol?

A

Nausea, diarrhea, maculopapular rash

200
Q

What can Allopurinol AE progress to?

A

Stevens-Johnson Syndrome or Allopurinol Hypersensitivity syndrome

201
Q

What are the sx’s of Stevens-Johnson Syndrome?

A

Severe expression of erythema multiforme, top layer of affected skin dies and sheds, skin and mucous membranes affected - can lead to death!

202
Q

When does Stevens-Johnson Syndrome usually occur?

A

1-2 weeks after initiation

203
Q

Where are Stevens-Johnson Syndrome patients treated?

A

Burn unit

204
Q

What are the sx’s of Allopurinol Hypersensitivity Syndrome?

A

Severe desquamating skin lesions, high fever (>39 C), hepatic dysfunction, leukocytosis with predominant eosinophilia, renal failure

205
Q

When does Allopurinol Hypersensitivity usually occur?

A

Highest risk in in first months

206
Q

Is a mild skin rash a sign of Allopurinol Hypersensitivity?

A

No - you can actually desensitive patients with this reaction to be able to take Allopurinol

207
Q

What can you screen for to determine if Pt is at risk for Allopurinol Hypersensitivity?

A

HLA B*5801

208
Q

What groups are more at risk for Allopurinol Hypersensitivity?

A

Koreans with stage 3+CKD, Han Chinese or Thai descent

209
Q

When is it ok to give Allopurinol to HLAB*5801 positive pts or Pts with history of A Hypersenstivity?

A

NEVER

210
Q

What is the MOA of Febuxostat?

A

Xanthine oxidase inhibtor that acts to decrease uric acid

211
Q

What should you give during initiation and titration of Febuxostat?

A

Low dose colchicine or NSAID to prevent gout attack

212
Q

What are the cons of Febuxostat?

A

Expensive

213
Q

What are the pros of Febuxostat?

A

Structurally different than allopurinol, so if someone has an allergic reaction they can take Febuxostat

214
Q

What is use of Febuxostat?

A

If allopurinol is not tolerated or need additional therapy to reach uric acid level.

215
Q

What are the contraindications of Febuxostat?

A

CrCl <30

216
Q

What are the adverse effects of Febuxostat?

A

Nausea, arthralgias, rash, transient elevation of hepatic transaminases

217
Q

What should you monitor when on Febuxostat?

A

Liver function tests at baseline, 2 months, 4 months, periodically.

218
Q

What is the MOA of Probenecid?

A

Uricosuric. Blocks reabsorption of uric acid, increasing its excretion.

219
Q

What are the contraindications of Probenecid?

A

History of urolithiasis, urate nephropathy. Avoid if CrCl <50.

220
Q

What are the adverse reactions of Probenecid?

A

Generally well tolerated, nausea, fever, rash, hepatic toxicity, uric acid kidney stone formation

221
Q

Who is Probenecid not advised for?

A

Urate overproducers. It also less effective as renal function declines.

222
Q

What is the MOA of Pegloticase?

A

Recombinant form of uricase, an enzyme that exists in nonprimates to convert uric acid into soluble product that is easily excreted.

223
Q

When should you use Pegloticase?

A

When other therapies don’t work

224
Q

What are the severe AE of Pegloticase?

A

Gout flares, infusion reactions, anaphylaxis

225
Q

What is the route of Pegloticase administration?

A

IV (which is inconvenient)

226
Q

What are the contraindications of Pegloticase?

A

G6PD deficiency (risk of hemolysis and methemoglobinemia)

227
Q

What must you screen for before you give Pegloticase?

A

Methemoglobinemia

228
Q

Pros and Cons of Single Inhaler Products

A

Pro- Easier to adjust specific dose

229
Q

Pros and Cons of Combination Inhaler Products

A

Pro- May increase adherence
Con- Lose dosing flexibility

230
Q

Pros and Cons of Nebulizers

A

Pros- Helpful if patient can’t use inhaler (very young, difficulty breathing, etc.)
Cons- Not as portable, can be loud

231
Q

General Monitoring Considerations

A

-Efficacy/symptoms/control
-Adverse effects
-Inhaler technique
-Adherence

232
Q

Respiratory- Bronchodilator Sub Categories

A

Beta agonists
Anticholinergics
Methylzanthines (theophylline)

233
Q

Respiratory- Anti-inflammatory Sub Categories

A

Corticosteroids
Immunomodulators
PDE-4 Inhibitors

234
Q

Beta2 Adrenergic Agonists MOA

A

-Relax airway smooth muscle by direct stimulation of B2 receptors in airway (bronchodilation)
-Also increase clearance and transport of mucus in airways
-Also stabilize mast cell membranes

235
Q

Beta2 Adrenergic Agonists Adverse Effects

A

Tachycardia
Tremor
Hypokalema
Palpitations
Sleep disturbance (higher doses of LABAs)
-Inhaled preferred (Adverse effects not as severe)

236
Q

SABA Use in Treatment

A

Most effective agents for reversing acute airway obstruction caused by bronchoconstriction
SABAs are best at bronchodilating
-1st line for acute asthma
-1st line for chronic asthma symptoms
-1st line for preventing exercise induced bronchospasm
-Used for rescue prn use in COPD

237
Q

SABA Onset and Duration

A

Onset- 5 min
Duration- 4-6 hours

238
Q

SABA Delivery

A

Inhaler
Nebulizer

239
Q

SABA Drug Names

A

Albuterol
Levalbuterol
Terbutaline

240
Q

Dosing of SABA

A

Typically dosed 1-2 puffs every 4-6 hours

241
Q

Considerations of Levalbuterol

A

R-enantiomer of albuterol—equally effective, no fewer side effects (despite marketing)

242
Q

LABA Drug Names

A

Salmeterol
Formoterol
Arformoterol (R enant of formoterol)
Indacaterol*
Olodaterol*
Vilanterol *
*longer acting

243
Q

LABA Onset and Duration

A

Onset:
-Salmeterol: 30 min
-Formoterol: 5 min
Duration: 12-24 hours initially, decreases to 5 hours with chronic use

244
Q

LABA Delivery

A

Inhaler (alone, combo with ICS)
Nebulizer

245
Q

LABA Black Box Warning

A

Not for monotherapy in chronic asthma: increase risk of severe asthma exacerbations and asthma related deaths—must use with ICS
Monotherapy in COPD is common
(but add a SABA for rescue med)

246
Q

Inhaled Anticholinergics MOA

A

MOA: anti-inflammatory; inhibit the effects of acetylcholine on muscarinic receptors in airways causes bronchodilation
-Protect against cholinergic-mediated bronchoconstriction
-May decrease mucus secretion

247
Q

Adverse Effects of Inhaled Anticholinergics

A

Blurred vision Dry mouth
Urinary retention
Metalic taste (ipratropium)
Constipation
Tachycardia
Precipitation of narrow-angle glaucoma
Urinary retention
Increased CV events (with ipratropium, esp in CV disease or CKD)

248
Q

AVOID Ipratropium in COPD + CV disease

A

Aclidinium: CV risk also

249
Q

Inhaled Anticholinergic Drug Names

A

Ipratropium bromide Tiotropium bromide*
Aclidinium bromide
Umeclidinium bromide*
Glycopyrrolate

250
Q

Delivery of Inhaled Anticholinergics

A

Inhaler
Nebulizer (ipratropium)

251
Q

Onset of Inhaled Anticholinergics

A

Ipratropium 15 min
(not a rescue med, too slow)
Tiotropium 30 min
Aclidinium < 30 min

252
Q

Duration of Inhaled Anticholinergics

A

Ipratropium 4-8 hours
Tiotropium >24 hours
Aclidinium < 24 hours

253
Q

Methylxanthines MOA

A

MOA: anti-inflammatory + causes bronchodilation by inhibiting phosphodiesterase and antagonizing adenosine
-Act as a bronchodilator at high concentrations
-Anti-inflammatory effect at low concentrations

254
Q

Methylxanthines Drug Name

A

Theophylline

255
Q

Methylxanthines Considerations

A

-Narrow therapeutic index
-Life-threatening toxicity
-Many important drug interactions
-Only for patients who cannot use Inhaled meds or if symptomatic despite appropriate use of Inhaled meds

256
Q

How is Theophylline metabolized?

A

By CYP1A2, CYP2E1, CYP3A4

257
Q

Theophylline Drug Interactions

A

alcohol
ciprofloxacin diltiazem
erythromycin
oral contraceptives phenytoin propranolol
verapamil

258
Q

Theophylline Target Serum Concentration

A

Target serum concentration: 5-15mg/L

< 10: little bronchodilation (more anti-inflammatory: 5-10)
10-20: bronchodilation
> 15: increased adverse effects
(headache, nausea, vomiting, insomnia)
> 20: more serious adverse effects
(cardiac arrhythmias, seizures)

259
Q

Theophylline Pharmacokinetics

A

Dose changes, drug interactions, hepatic function, cigarette/marijuana have VARIABLE EFFECT on serum concentration

Tobacco increases clearance, current smokers may need higher dose

260
Q

Theophylline Adverse Effects

A

Heartburn
Restlessness
Insomnia
Irritability
Tachycardia
Tremor

With increased dose-
Nausea
Vomiting
Seizures
Arrhythmias

261
Q

Corticosteroids MOA

A

MOA: decrease airway inflammation, attenuate airway hyperresponsiveness, minimize mucus production/secretion, improve response to beta 2 agonists

262
Q

Delivery of Corticosteroids

A

Inhalers
Oral
Injectable

263
Q

Inhaled Corticosteroid Drug Names

A

Beclomethasone
Budesonide
Ciclesonide
Flunisolide
Fluticasone
Mometasone

*many in combo with LABAs

264
Q

Onset of Inhaled Corticosteroids

A

12 hours; 2+ weeks for max effect

265
Q

Inhaled Corticosteroid Considerations

A

-Equally effective at equipotent doses
-Cigarette smoking decreases response need higher dose

266
Q

Local Adverse Effects of Inhaled Corticosteroids

A

Oralpharyngeal candidiasis (thrush)
Cough
Dysphonia (hoarse voice)

-drug deposited in mouth/throat/swallowed—rinse mouth after use; use spacer
-decrease dose decrease hoarseness

267
Q

Inhaled Corticosteroids Interactions

A

Potent inhibitors of CYP3A4 (ritonavir, itraconazole, ketoconazole, etc) + high doses of ICS : cause Cushing syndrome and adrenal insufficiency

268
Q

What factors vary the response of Inhaled Corticosteroids

A

Age
Genetics
Smoking status
Race

269
Q

Consideration of Inhaled Corticosteroids

A

Abrupt discontinuation exacerbations

Changed dose does not increase exacerbation risk

270
Q

Systemic (oral) Corticosteroids Drug Names

A

Prednisone
Prednisolone
Methyprednisolone

271
Q

Use of Systemic (oral) Corticosteroids

A

Acute exacerbations of asthma or COPD

(rarely, some patients may be on longer term—serious cases)

272
Q

Onset of Systemic (oral) Corticosteroids

A

4-12 hours
-Therefore start early in exacerbation
-Continue 3-10 days until symptoms resolve
-Taper off is not necessary (short course)

273
Q

Adverse effects of Systemic (oral) Corticosteroids (also Inhaled Corticosteroids)

A

**More likely if long term, high dose, systemic route
**Adrenal suppression
**Decreased bone mineral density
**Skin thinning
**Cataracts
Easy bruising
**Steroid myopathy
Insomnia
Increased appetite
Agitation/irritation
Weight gain (longer term)

274
Q

Systemic (oral) Corticosteroids Interactions

A

Potent inhibitors of CYP3A4 (ritonavir, itraconazole, ketoconazole, etc) + high doses of ICS : cause Cushing syndrome and adrenal insufficiency

275
Q

Systemic (oral) Corticosteroid Considerations

A

-Minimize as much as possible if chronic therapy necessary
(once daily, every other day, taper off)
-AVOID LONG TERM use if possible
(unfavorable risk vs benefit, steroid myopathy can occur)

276
Q

Leukotriene Receptor Antagonists MOA

A

MOA: anti-inflammatory; act to antagonize the leukotriene receptor

-Improve FEV1
-decrease asthma symptoms
-decrease SABA use
-decrease asthma exacerbations
-Steroid sparing

277
Q

Leukotriene Receptor Antagonists

A

Montelukast
Zileuton
Zafirlukast

278
Q

Adverse Effects of Leukotriene Receptor Antagonists

A

Generally few
-Hepatotoxicity (zileuton and zafirlukast)
-Sleep disorders
-Aggressive behavior
-Suicidal thoughts
-Eosinophilic granulomatosis with polyangiitis (rare)
-Angioedema
-Urticartia

279
Q

Leukotriene Receptor Antagonists monitoring

A

Liver function monitoring at onset and frequently thereafter (Zileuton)

280
Q

Leukotriene Receptor Antagonists drug interactions

A

CYP2C9 drugs (significant: zileuton, zafirlukast)

281
Q

Monteleukast Considerations

A

Generally well tolerated, few interactions, minimal monitoring

282
Q

Immunomodulator (Omalizumab) MOA

A

Anti-inflammatory; inhibits binding of IgE to receptors on mast cells and basophils; results in inhibition of inflammatory mediator release/attenuation of early and late phase allergic response

283
Q

Immunomodulator Drug Name

A

Omalizumab
(recombinant humanized monoclonal anti-IgE antibiody)

284
Q

Delivery of Immunomodulator

A

Subcutaneous q2-4 weeks in office/clinic ($$$)

285
Q

Immunomodulator AE

A

Injection site reactions
-Bruising
-Redness
-Pain
-Stinging
-Itching
-Burning

Anaphylactic Reactions (rare, but can happen anytime)
-Monitor after injection
-Give epinephrine prescription

Increased risk of CV and cerebrovascular events

Increased risk of cancer

286
Q

Phosphodiesterase-4 Inhibitor MOA

A

Reduce inflammation by inhibiting breakdown of cAMP; do not cause direct bronchodilation

Used for preventing COPD exacerbations or for select chronic bronchitis patients

287
Q

AE of Phosphodiesterase-4 Inhibitor

A

Much more likely than other meds
-Diarrhea
-Weight loss
-Nausea
-Headache
-Insomnia
-Decreased appetite
-Abdominal Pain
-Anxiety
-Depression
-Increased suicidality

288
Q

Interactions of Phosphodiesterase-4 Inhibitor

A

-Theophylline (both inhibit PDE-4)

289
Q

Cromolyn MOA

A

MOA: decreases bronchospasm through anti-inflammatory effect

(may not have more benefit than a placebo)

290
Q

Cromolyn Considerations

A

Less effective & less cost effective than ICS
-Reserve for patients who can’t tolerate ICS

2nd line therapy for exercise induced asthma

291
Q

Smoking Cessation Meds

A

Nicotine replacement
(nicotine gum, lozenges, patches, inhaler, nasal spray)
Bupropion SR
Varenicline

292
Q

Smoking Cessation Considerations

A

Lowered risk of
COPD, Lung cancer, Cancer, CV disease, Infertility

Slows rate of decline in pulmonary function
(important in asthma and COPD)

Difficult! (often takes multiple quit attempts)
Patients need support, drugs can help!

293
Q

The 5 A’s for Brief Intervention

A

Ask: Identify and document tobacco-use status for every patient at every visit

Advise: Urge every tobacco user to quit

Assess: Is the tobacco user willing to make a quit attempt at this time?

Assist: Use counseling and pharmacotherapy to help patients willing to make a quit attempt

Arrange: Schedule follow-up contact, preferably within the first week after the quit date

294
Q

The 5 R’s to Motivate Smokers Unwilling to Quit at Present

A

Relevance: Tailor advice and discussion to each smoker

Risks: Help the patient identify potential negative consequences of tobacco use

Rewards: Help the patient identify the potential benefits of quitting

Roadblocks: Help the patient identify barriers to quitting

Repetition: Repeat the motivational message at every visit

295
Q

Nicotine gum/inhaler/lozenge/spray considerations

A

-Provides nicotine at a fixed dose
-Used prn for cravings

296
Q

Nicotine patch considerations

A

-Can be worn 24 hours/day
-Provides a consistent delivery of nicotine
-Reduces cravings; doesn’t take them away
-can be Used in combo with prn nicotine replacement
-8 week treatment longer treatment
-Change patch Q24 hours
Remove overnight if insomnia/weird dreams

297
Q

Nicotine replacement therapy dosing

A

Increase chances of quitting by 50-70%
Dosing/strength based on # cigs/day, if smoke immediately upon waking

298
Q

Nicotine Gum considerations

A

-Chew gum until it tingles
park it in cheek until it no longer tingles
-Repeat until gum no longer tingles
-Do not eat/drink 30 min after use
-AVOID if dentures/braces

299
Q

Nicotine Lozenge considerations

A

-Dissolve in mouth
-Do not eat/drink 30 min after use
-Contains 25% more nicotine than gum

300
Q

Bupropion SR MOA

A

Antidepressant (Blocks reuptake of dopamine and NE)

Doubles the odds of smoking cessation compared to placebo

301
Q

Bupropion SR considerations

A

-can combine with NRT -May benefit patients with Depression/history of Depression
-Not 1st line for adolescents

302
Q

Bupropion SR AE

A

Dry mouth
Insomnia (take early in day)
Lowers seizure threshold

303
Q

Bupropion SR contraindicated

A

-history of seizures
-history of eating disorder
-Use of MAOI in past 14 days (risk of hypertensive reactions)

304
Q

Black Box Warning of Bupropion SR

A

-May increase suicidality in patients with Depression
-Adolescents/young adults have Increased suicide risk while on antidepressants

305
Q

Bupropion SR Interactions

A

-MAO-is
-Drugs that lower seizure threshold (antipsychotics, antidepressants, Theophylline, systemic corticosteroids)

306
Q

Varenicline MOA

A

Nicotinic receptor partial agonist. Reduces cravings/withdrawal. Blocks effects of smoked nicotine

(works better than bupropion)

307
Q

Varenicline considerations

A

Use as monotherapy

Do not combine with NRT or bupropion

Begin 1 week before quit date; continue 12-24 weeks

308
Q

Varenicline AE

A

Insomnia
Black Box Warning of Varenicline

309
Q

Black Box Warning of Varenicline

A

Neuropsychiatric symptoms

-Changes in behavior
-Hostility
-Agitation
-Depressed mood
-Suicidal thoughts and behavior
-Attempted suicide

310
Q

Varenicline Cautions

A

Increased risk of CV events

311
Q

Smoking Cessation, Special Populations: Pregnant Women

A

-NRTs increase risk of birth defects
-Other meds not tested for safety/Efficacy
-Quitting smoking important encourage (without drugs)!

312
Q

Smoking Cessation, Special Populations: Coronary Heart Disease

A

Caution with bupropion
-Cardiotoxic at high doses
-Widens QRS complex

Caution with varenicline
-Increased CV events

NRT: generally benefits>risks
Caution at immediate post MI
Caution with serious arrhythmias
Caution with worsening angina

313
Q

Asthma is characterized by…

A

Airway narrowing
-Hyper-responsiveness—triggers cause exaggerated narrowing
-Results from smooth muscle contraction, Increased mucus secretion, airway edema, remodeling

Inflammation
-Initiated by trigger that induces immune response (immediate and later)

314
Q

Chronic asthma severity is based on…

A

Current Disease Impairment
-Frequency and severity of symptoms
-use of short acting B2 agonists (SABAs)
-Pulmonary function
-Impact on normal activity
-Quality of Life

Future Risk
-Potential for future severe exacerbations
-Potential for asthma-related death
-Potential for progressive loss of lung function (esp. adults)
-Potential for reduced lung growth (children)
-Occurrence of drug-related Adverse effects

315
Q

Chronic Asthma Tx Goals

A

-Prevent chronic/troublesome symptoms
-SABA use infrequent (< 2 days/week)
-Maintain normal/near normal Pulmonary function
-Maintain normal activity levels
-Prevent exacerbations/ED visits/hospitalizations
-Prevent progressive loss of lung function
-Minimize Adverse effects

316
Q

Acute Asthma classification

A

Not based on chronic classification (because anyone with asthma can have life threatening attacks!)

-Mild: dyspnea with activity; PEF (peak expiratory flow) >70%
-Moderate: dyspnea limits activity; PEF is 40-69%
-Severe: dyspnea interferes with conversation or occurs at rest; PEF < 40%
-Life threatening: not able to speak; PEF <25%

317
Q

Acute Asthma Tx goals

A

-Correct significant hypoxemia
-Reverse airflow obstruction rapidly
-Reduce likelihood of exacerbation relapse/recurrence of severe airflow obstruction in future
-Prevent death!

Mortality: usually due to
inappropriate assessment of severity/insufficient treatment or referral for medical care (TAKE IT SERIOUSLY!)

318
Q

Treating Asthma Considerations

A

-AVOID triggers (Prevent attacks)
-Quick relief meds (STOP attacks/RELIEVE symptoms)
-Long-term control meds (PREVENT attacks, DECREASE/SLOW damage)

319
Q

Non pharmacologic treatment

A

Avoid triggers

Allergens/irritants/foods/comorbid conditions
Influenza/pneumococcal vaccines recommended!

Drugs
Nonselective beta blockers (including eye drops)
Avoid unless benefits > risks
Selective BB (low dose) are better option!

Aspirin-sensitive asthma (Samter’s Triad)
Often co-occurs with rhinitis, nasal polyps and asthma
Acute asthma can occur in minutes of aspirin or other NSAIDs
AVOID!

320
Q

Quick Relief Meds for Asthma

A

ALL ASTHMA PATIENTS NEED SABA

Pretreatment with SABAs block early phase response to antigen/trigger
SABAs are best at bronchodilating
-1st line for acute asthma
-1st line for chronic asthma symptoms
-1st line for preventing exercise induced bronchospasm

Chronic Use: PRN (shorter duration of action if used chronically/all the time)

Exacerbation: Double the dose of SABA during exacerbation + schedule the dose

321
Q

Intermittent Astma Tx

A

SABA for dealing with symptoms
-infrequent trigger exposure
-Exercise-induced bronchospasm
-Seasonal asthma
-can pretreat with SABA before Exercise

322
Q

Persistant Chronic Asthma Tx

A

SABA for PRN use
Daily long term control therapy

323
Q

Control Therapy: First Line

A

ICS
-Most effective monotherapy (1st line)
-Additional agents can be added if needed
-LABAs Most effective add on (not for monotherapy)
-LTRAs 2nd best add on

ICS + LABA preferred therapy
For age 5+ with moderate persistent asthma

324
Q

Control Therapy: Alternatives

A

LTRAs as monotherapy for mild persi
Monoclonal antibodies
-Reserved for patients with uncontrolled severe symptoms
(expensive, risk of anaphylaxis)

Immunotherapy
-for patients with asthma triggered by allergies + Adverse effects with meds or comorbid allergic conditionsstent asthma (if patient prefers to avoid ICS, less effective than ICS)

325
Q

Step Up Therapy

A

-Initiate with low-dose treatment
-increase intensity at later visits if control is not achieved

326
Q

Step Down Therapy

A

-start with high dose regimen
-Reduce intensity as control is achieved

327
Q

Monitoring Asthma

A

After initiating med
2-6 weeks

If controlled asthma
q1-6 months

Consider step down if well controlled for > 3 months

328
Q

COPD cause

A

Caused by repeated inhalation of noxious particles/gasses
SMOKING: 85-90% of cases
Leads to chronic inflammation & pathologic changes that cause obstruction

329
Q

Goals of COPD Tx

A

-smoking cessation
-Symptom reduction (Reduce inflammation, bronchodilation)
-Improve Exercise tolerance
-Maintain/Improve Quality of Life
-Prevent/treat exacerbations (hospitalizations)
-SLOW disease progression
-Reduce mortality

330
Q

COPD Tx

A

Smoking cessation
Drug therapy
-short acting bronchodilators
-LONG acting bronchodilators
-Inhaled corticosteroids

Supplemental therapy
-Oxygen (Goal: O2 sat >90%)

Pulmonary Rehab
-Exercise training
-smoking cessation
-Nutrition counseling
-Education
Vaccinations
-Pneumococcal

331
Q

COPD Tx Based on Gold Guidelines

A

PATIENT GROUP
RISK/SYMPTOMS
INITIAL TREATMENT

A
low risk, fewer symptoms
Short acting anticholinergic
Or
SABA

B
low risk, more symptoms
LABA
Or
Long acting anticholinergic

C
high risk, fewer symptoms)
ICS + LABA or
Long acting anticholinergic
high risk, more symptoms
ICS + LABA or
Long acting anticholinergic

332
Q

COPD Tx: Bronchodilators

A

ALL patients: short acting bronchodilator (SABA OR short acting anticholinergic)
Step 1: Initiate with monotherapy bronchodilator (LABA or long acting anticholinergic)
Step 2: if needed, LABA + long acting anticholinergic OR LABA + ICS
Step 3: if needed, could consider LABA + long acting anticholinergic + ICS

333
Q

COPD Tx: Corticosteroids

A

Inhaled corticosteroids:
-For severe, v. severe COPD or frequent exacerbations not controlled by 1st line long acting bronchodilator
-monotherapy less effective than in combo with LABA
-Reduces inflammation
Oral corticosteroids
-For exacerbations (3-10 days)
-not recommended for LONG TERM treatment

334
Q

COPD Tx Contraindication

A

Antitussives
-Cough is important—clears secretions
-not for LONG TERM treatment

335
Q

Other meds possible used in COPD

A

Beta Blockers
-May be beneficial due to CV effects & B2 receptor up regulation (means inhales B2 agonists might work better)
-Selective B1 blockers preferred
Azithromycin prophylaxis
-Reduces incidence of acute exacerbation in some patients
-risk of LONG TERM use
-risk of QT prolongation
-More study needed
Leukotriene modifers
-May improve lung function(?), dyspnea, QoL, but studies are inadequate

Pharmacology Exam 3 (1 decks)

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