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NURS 1650 - Here We Go Again > Medications for Inflammation > Flashcards

Medications for Inflammation Flashcards

1
Q

Which type of cells releases histamine?

A

Mast cells and basophils

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2
Q

What are two major effects of histamine when it is released?

A

Vasodilation

Increased vascular permeability

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3
Q

What happens when H1 (histamine) receptors are activated?

A

Causes alertness (bc are in the CNS)

Causes itching and pain

Promotes secretion of mucus in the upper respiratory system

Generally: promotes inflammation –> chemotaxis of eosinophils, neutrophils, increased activity of dendrites

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4
Q

Antihistamines MOA

A

Selectively antagonize H1 receptors (H1 blockers)

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5
Q

Diphenhydramine MOA

A

H1 receptor antagonist

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6
Q

Diphenhydramine Class

A

H1 blocker

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7
Q

Diphenhydramine ADE

A

Sedation, anticholinergic effects

Paradoxical CNS excitation in children

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8
Q

Diphenhydramine Contraindications

A

In breast-feeding

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9
Q

Diphenhydramine Warnings/Considerations

A

Risk-benefit for pregnant people bc it can cross the placenta

Avoid/minimize in older adults

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10
Q

Examples of anticholinergic effects

A

Dizziness
Drowsiness/sedation
Dry mouth & mucus membranes, eyes
Hypotension
Constipation
Blurry vision
Confusion

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11
Q

What is the first choice drug for the treatment of anaphylaxis?

A

Epinephrine IM

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12
Q

Epinephrine MOA

A

vasoconstrictor and bronchodilator

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13
Q

What can antihistamines treat and NOT treat?

A

Can be given for hives and itching

NOT for bronchospasm, hypotension, or shock

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14
Q

NSAIDs MOA

A

Inhibit COX, the enzyme that converts arachidonic acid to prostaglandins and related compounds

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15
Q

Immunosuppressants and immunomodulators MOA

A

Inhibit or limit the immune response more generally

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16
Q

Immunosuppressants vs immunomodulators

A

Immunosuppressants
- Tamp down the immune system
- Higher risk of infection and cancer

Immunomodulators
- Target a specific cytokine or signaling pathway
- Do not have a risk of infection and cancer

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17
Q

COX-1 vs COX-2

A

COX-1
- found in almost all tissues
- protects the gastric mucosa, supports renal function, promotes platelet aggregation
- “good COX”

COX-2
- found mainly at sites of tissue injury
- produced in response to cytokines
- mediates inflammation
- present in fever & pain (brain), kidneys, vasodilation
- “bad COX”

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18
Q

Harmful effects in the inhibition of COX-1

A

Gastric ulceration

Bleeding

Renal impairment

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19
Q

Beneficial effects in the inhibition of COX-1

A

Protection against myocardial infarction and stroke, 2/2 reduced platelet aggregation

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20
Q

Beneficial effect in the inhibition of COX-2

A

Suppression of inflammation

Alleviation of pain

Reduction of fever

Protection against colorectal cancer

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21
Q

Harmful effects in the inhibition of COX-2

A

Renal Impairment

Promotion of MI and stroke (2/2 suppressing vasodilation and production of prostacyclin and not suppressing platelet aggregation)

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22
Q

All NSAIDs can cause:

A

Renal impairment
Increase risk of bleeding (if COX-1 is inhibited)
Increase GI bleeding tendencies
Increase risk of MI and stroke (except aspirin)
Fetal abnormalities (except low-dose aspirin)

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23
Q

NSAIDs Contraindications

A

Past 30 weeks of gestation due to the risk of premature closure of the ductus arteriosus

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24
Q

NSAIDs should be avoided in patients with:

A

Severe renal impairment

Uncontrolled hypertension

Active peptic ulcer disease

Other bleeding tendencies

Sever liver disease (esp if cirrhosis is present)

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25
Q

Aspirin Class

A

NSAID (1st gen)

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26
Q

Aspirin MOA

A

Irreversibly inhibits COX (COX-1 > COX-2)

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27
Q

Aspirin ADE

A

Bleeding, GI bleeding, renal dysfunction, tinnitus, Reyes syndrome (rare brain swelling), hypersensitivity reactions (including anaphylaxis)

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28
Q

Aspirin Contraindications

A

< 18 y.o.

30+ weeks gestation

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29
Q

Aspirin Warnings/Considerations

A

Low-dose aspiring can be given to pregnant people to prevent preeclampsia and in certain clotting disorders

Discontinue 7-10 days before surgery

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30
Q

Aspirin Drug interactions

A

Anticoagulants, glucocorticoids, EtOH, NSAIDS

can cause more bleeding

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31
Q

Ibuprofen Class

A

NSAID (1st gen)

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32
Q

Ibuprofen MOA

A

Inhibits COX (COX-1 = COX-2 — 50/50)

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33
Q

Ibuprofen ADE

A

Bleeding, GI bleeding, renal dysfunction, increased risk of MI/stroke

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34
Q

Ibuprofen Contraindication

A

30+ weeks gestation

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35
Q

Ibuprofen Warnings/Considerations

A

Can cause oligohydramnios past 20 weeks gestation
Avoid 20-30 weeks gestation

Discontinue 3 days before surgery

36
Q

Ibuprofen Interactions

A

Low-dose aspirin (block COX binding site)
Glucocorticoids

37
Q

Celecoxib Class

A

NSAID (2nd gen)

38
Q

Celecoxib MOA

A

Selectively inhibits COX-2

39
Q

Celecoxib ADE

A

Renal impairment, risk of MI/stroke

40
Q

Celecoxib Warnings/Considerations

A

Caution with sulfonamide allergy (“sulfa” allergy)

Can cause oligohydramnios past 20 weeks gestation

Risk-benefit calculation in lactation

41
Q

Celecoxib Contraindications

A

Past 30 weeks gestation

42
Q

Celecoxib Interactions

A

Warfarin (enhance anticoagulant effects)
COX inhibitors (additive effect)

43
Q

What do glucocorticoids mimic?

A

Cortisol

44
Q

What effects do glucocorticoids cause?

A

Anti-inflammatory and immunosuppressant effects

45
Q

Prednisone Class

A

Glucocorticoid/corticosteroid/steroid

46
Q

Prednisone MOA

A

inhibits pro-inflammatory mediator synthesis via gene transcription mechanism

47
Q

Prednisone Elimination

A

Is a PRODRUG

Converted via CYP3A4 enzyme

48
Q

Prednisone Interactions

A

NSAIDs (GI bleed risk), diabetes medications (bc incr BG)

49
Q

Prednisone Pregnancy/Lactation Considerations

A

Conflicting evidence

possible growth suppression, fetal adrenal hypoplasia

Use lowest possible dose for shortest amount of time

50
Q

Prednisone ADE

A

Short-term: increased appetite, hyperglycemia, insomnia, delayed wound healing, GI ulcers/bleeding, blood clots

Medium-long-term: osteoporosis, infection, iatrogenic Cushing’s syndrome, adrenal suppression

51
Q

How is Adrenal Suppression caused?

A

Long-term glucocorticoid use with abrupt cessation

52
Q

Prednisone teaching points

A

Take once-daily doses

Do NOT abruptly discontinue taking

Monitor BG if diabetic

Avoid NSAIDs

Report early signs of infections

Report abdominal pain/bloody or black stools, swelling/edema, muscle weakness, irregular heart rhythms

Wear medical alert bracelet, have emergency supply if being used in long-term therapy

53
Q

What are DMARDs? What do they do?

A

Disease-Modifying Antirheumatic Drugs

They modify the underlying disease process, rather than simply treating the resulting inflammation

May suppress immune function

Types: biologic and non-biologic

54
Q

DMARDs vs. NSAIDs (action, toxicity)

A

DMARDs are slower acting. and more toxic than NSAIDs

55
Q

Methotrexate Class

A

Non-biologic DMARD

56
Q

Methotrexate MOA

A

Not entirely understood

57
Q

Methotrexate Patient teaching point

A

Onset is 3-6 weeks, takes time to have an effect

58
Q

Methotrexate Contraindications

A

Severe liver disease
Pregnancy

59
Q

Methotrexate ADE

A

Hepatic fibrosis, bone marrow suppression, GI ulceration

60
Q

Methotrexate Warnings/Considerations

A

Decrease dose in renal impairment

Folic acid supplement recommended to minimize hepatic, GI, and hematologic adverse effects

CBC, platelet count, LFTs required q 8-12 weeks

Excreted in breast milk, avoid use

61
Q

Methotrexate Warnings/Considerations

A

Decrease dose in renal impairment

Folic acid supplement recommended to minimize hepatic, GI, and hematologic adverse effects

CBC, platelet count, LFTs required q 8-12 weeks

Excreted in breast milk, avoid use

62
Q

What are monoclonal antibodies?

A

Biologic DMARDs

antibodies that are identical because they were produced by clones of a single-parent cells

used to treat autoimmune/chronic inflammatory disorders, considerable use in oncology as well

EXPENSIVE

63
Q

Infliximab Class

A

Biologic DMARD

64
Q

Infliximab MOA

A

TNF-alpha antagonist

Binds both soluble and receptor-bound TNF-alpha –> bound TNF-alpha cannot function nor signal inflammation effects

65
Q

Infliximab Warning/Considerations

A

Use concomitant methotrexate, improves efficacy of infliximab

Test for latent TB bc it can activate it! –> continue monitoring for it

Avoid 30+ weeks of gestation

Lactation

66
Q

Infliximab ADE

A

BBW: severe infection

Infusion reaction

67
Q

Infliximab Interactions

A

Immunosuppressants, immunomodulators (except methotrexate), corticosteroids, (live) vaccines

68
Q

Thromboxane A2 is synthesized in:

A

Platelets

69
Q

_____________ T cells recognize Class I MHC and ____________ T cells recognize Class II MHC

A

CYTOTOXIC T cells recognize Class I MHC and HELPER T cells recognize Class II MHC.

70
Q

A blood transfusion reaction is which type of hypersensitivity reaction?

A

Type II

71
Q

Your patient has just been prescribed diphenhydramine (Benadryl) for his allergies. Patient teaching should include avoidance of which beverage?

A

Alcohol

72
Q

Which statement by the patient with diabetes who has been prescribed prednisone (Deltasone), 10 mg daily x 60 days, requires further teaching by the nurse?

A

“If I can’t attend my 2-month follow-up appointment, I will just stop taking this medication”.

73
Q

The mechanism of action of Celecoxib (Celebrex) can be described as:

A

COX-2 inhibitor

74
Q

In an allergic reaction, which type of antibody/immunoglobulin binds to mast cells?

A

IgE

75
Q

This cell type can release reactive oxygen species (ROS) and proteases that have the potential to damage nearby healthy tissue

A

Neutrophils

76
Q

Which med is a prodrug?

A

Prednisone

77
Q

Which med requires testing for CBC and platelet count?

A

Methotrexate

78
Q

Which med calls for folic acid supplementation?

A

Methotrexate

79
Q

Which med causes anticholinergic effects?

A

Diphenhydramine

80
Q

Which meds selectively inhibit COX-2?

A

Celecoxib

81
Q

Which two meds given together increase one of their efficacy?

A

Infliximab and Methotrexate

82
Q

Which med can activate late TB?

A

Infliximab

83
Q

NSAIDs on this exam

A

Aspiring (1st gen)
Celecoxib (2nd gen)
Ibuprofen (1st gen)

84
Q

DMARDs on this exam

A

Methotrexate (non-biologic)
Infliximab (biologic)

85
Q

Which med is contraindicated in people less than 18 y.o.?

A

Aspirin

86
Q

Which med can result in Reye’s Syndrome?

A

Aspirin

NURS 1650 - Here We Go Again (20 decks)

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