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

Medications for Inflammation Flashcards

(86 cards)

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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
Aspirin Class
NSAID (1st gen)
26
Aspirin MOA
Irreversibly inhibits COX (COX-1 > COX-2)
27
Aspirin ADE
Bleeding, GI bleeding, renal dysfunction, tinnitus, Reyes syndrome (rare brain swelling), hypersensitivity reactions (including anaphylaxis)
28
Aspirin Contraindications
< 18 y.o. 30+ weeks gestation
29
Aspirin Warnings/Considerations
Low-dose aspiring can be given to pregnant people to prevent preeclampsia and in certain clotting disorders Discontinue 7-10 days before surgery
30
Aspirin Drug interactions
Anticoagulants, glucocorticoids, EtOH, NSAIDS can cause more bleeding
31
Ibuprofen Class
NSAID (1st gen)
32
Ibuprofen MOA
Inhibits COX (COX-1 = COX-2 --- 50/50)
33
Ibuprofen ADE
Bleeding, GI bleeding, renal dysfunction, increased risk of MI/stroke
34
Ibuprofen Contraindication
30+ weeks gestation
35
Ibuprofen Warnings/Considerations
Can cause oligohydramnios past 20 weeks gestation Avoid 20-30 weeks gestation Discontinue 3 days before surgery
36
Ibuprofen Interactions
Low-dose aspirin (block COX binding site) Glucocorticoids
37
Celecoxib Class
NSAID (2nd gen)
38
Celecoxib MOA
Selectively inhibits COX-2
39
Celecoxib ADE
Renal impairment, risk of MI/stroke
40
Celecoxib Warnings/Considerations
Caution with sulfonamide allergy ("sulfa" allergy) Can cause oligohydramnios past 20 weeks gestation Risk-benefit calculation in lactation
41
Celecoxib Contraindications
Past 30 weeks gestation
42
Celecoxib Interactions
Warfarin (enhance anticoagulant effects) COX inhibitors (additive effect)
43
What do glucocorticoids mimic?
Cortisol
44
What effects do glucocorticoids cause?
Anti-inflammatory and immunosuppressant effects
45
Prednisone Class
Glucocorticoid/corticosteroid/steroid
46
Prednisone MOA
inhibits pro-inflammatory mediator synthesis via gene transcription mechanism
47
Prednisone Elimination
Is a PRODRUG Converted via CYP3A4 enzyme
48
Prednisone Interactions
NSAIDs (GI bleed risk), diabetes medications (bc incr BG)
49
Prednisone Pregnancy/Lactation Considerations
Conflicting evidence possible growth suppression, fetal adrenal hypoplasia Use lowest possible dose for shortest amount of time
50
Prednisone ADE
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
How is Adrenal Suppression caused?
Long-term glucocorticoid use with abrupt cessation
52
Prednisone teaching points
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
What are DMARDs? What do they do?
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
DMARDs vs. NSAIDs (action, toxicity)
DMARDs are slower acting. and more toxic than NSAIDs
55
Methotrexate Class
Non-biologic DMARD
56
Methotrexate MOA
Not entirely understood
57
Methotrexate Patient teaching point
Onset is 3-6 weeks, takes time to have an effect
58
Methotrexate Contraindications
Severe liver disease Pregnancy
59
Methotrexate ADE
Hepatic fibrosis, bone marrow suppression, GI ulceration
60
Methotrexate Warnings/Considerations
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
Methotrexate Warnings/Considerations
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
What are monoclonal antibodies?
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
Infliximab Class
Biologic DMARD
64
Infliximab MOA
TNF-alpha antagonist Binds both soluble and receptor-bound TNF-alpha --> bound TNF-alpha cannot function nor signal inflammation effects
65
Infliximab Warning/Considerations
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
Infliximab ADE
BBW: severe infection Infusion reaction
67
Infliximab Interactions
Immunosuppressants, immunomodulators (except methotrexate), corticosteroids, (live) vaccines
68
Thromboxane A2 is synthesized in:
Platelets
69
_____________ T cells recognize Class I MHC and ____________ T cells recognize Class II MHC
CYTOTOXIC T cells recognize Class I MHC and HELPER T cells recognize Class II MHC.
70
A blood transfusion reaction is which type of hypersensitivity reaction?
Type II
71
Your patient has just been prescribed diphenhydramine (Benadryl) for his allergies. Patient teaching should include avoidance of which beverage?
Alcohol
72
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?
"If I can't attend my 2-month follow-up appointment, I will just stop taking this medication".
73
The mechanism of action of Celecoxib (Celebrex) can be described as:
COX-2 inhibitor
74
In an allergic reaction, which type of antibody/immunoglobulin binds to mast cells?
IgE
75
This cell type can release reactive oxygen species (ROS) and proteases that have the potential to damage nearby healthy tissue
Neutrophils
76
Which med is a prodrug?
Prednisone
77
Which med requires testing for CBC and platelet count?
Methotrexate
78
Which med calls for folic acid supplementation?
Methotrexate
79
Which med causes anticholinergic effects?
Diphenhydramine
80
Which meds selectively inhibit COX-2?
Celecoxib
81
Which two meds given together increase one of their efficacy?
Infliximab and Methotrexate
82
Which med can activate late TB?
Infliximab
83
NSAIDs on this exam
Aspiring (1st gen) Celecoxib (2nd gen) Ibuprofen (1st gen)
84
DMARDs on this exam
Methotrexate (non-biologic) Infliximab (biologic)
85
Which med is contraindicated in people less than 18 y.o.?
Aspirin
86
Which med can result in Reye's Syndrome?
Aspirin

NURS 1650 - Here We Go Again (20 decks)

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