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2-Anesthesia Pharm Exam 2 > Peripherally-Acting Analgesics and Corticosteroids > Flashcards

Peripherally-Acting Analgesics and Corticosteroids Flashcards

1
Q

What are the effects of NSIADs?

A

Have central & peripheral effects

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2
Q

What are the principle action of NSAIDs?

A

blockade of prostaglandin production

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3
Q

What does the NSAIDs inhibit?

A

the activity of cyclooxygenase enzymes (COX-1 and COX-2) that are required for the production of prostaglandins

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4
Q

What is the primary MOAC of NSAIDs?

A

inhibiting the biosynthesis of prostaglandins by preventing the substrate arachidonic acid from binding to the COX enzyme active site

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5
Q

What is arachidonic acid?

A

present in cellular tissues and is released when the cellular membranes are disrupted by injury or disease

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6
Q

What is prostaglandins?

A

localized hormones that are responsible for inflammatory activity (vasodilation, erythema, edema, fever) and nociceptor sensitization

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7
Q

NSAIDS can be classified by ______ selectivity

A

COX

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8
Q

What are the two COX forms?

A

cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2)

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9
Q

What is COX1?

A

catalyzes production of prostaglandins that maintain physiologic functions: – maintain normal renal function, mucosal protection in GI tract, proaggregatory thromboxane A2 in platelets

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10
Q

What is COX2?

A

expression induced by inflammatory mediators in tissues, role in mediation of pain, inflammation, & fever; some anticoagulation activity, modulation of cell proliferation and pain sensitization

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11
Q

What is COX-1 activity?

A
  • Hemostasis

- gastric mucosa protection

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12
Q

What is COX-1 inhibition benefits?

A
  • possible reduced neuro inflammation targets at microglia

- cardio-protective anti coagulation

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13
Q

What is COX1- inhibition risks?

A
  • can cause bleeding

- increased risk of gastric irritation & ulcers

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14
Q

What can COX-2 activity?

A
  • inflammatory response
  • fever
  • pain sensation
  • anticoagulation
  • modulation of cell proliferation
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15
Q

What can COX-2 inhibition benefits?

A
  • reduced inflammation
  • reduced fever
  • reduced pain sensation
  • possible reduction in cancer progression
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16
Q

What CO2 inhibition risks??

A

Increase risk of thrombotic activity

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17
Q

What properties of NSAIDS?

A

Antipyretic, anti-inflammatory and analgesic properties

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18
Q

What are the characteristics of NSAIDs?

A

Weakly acidic, highly protein bound, lipophilic, low volume of distribution, and only the unbound portion is effective

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19
Q

What is the pKa of NSAIDs? What formed does it exist?

A
  • NSAIDs are weak acids with pKa values typically lower than 5
  • Exists mostly in the ionized form at physiologic pH
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20
Q

What is the protein bind of NSAIDs?

A

> 90% bound to albumin

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21
Q

What can occur from hypoalbuminemia with NSAIDs?

A

hypoalbuminemia & displacement by other drugs that are albumin bound can result in greater unbound NSAID & increased risk for toxicity

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22
Q

What is the elimination of NSAIDs?

A

Elimination via hepatic oxidation and conjugation (less than 10% eliminated via renal activity)

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23
Q

What some principles of NSAIDs?

A
  • Decreased activation and sensitization of peripheral nociceptors
  • Attenuation of the inflammatory response
  • Absence of dependence or addiction potential
  • Synergistic effects with opioids
  • Preemptive analgesic effects
  • Absence of respiratory depression
  • Minimal N&V compared to opioids
  • Long duration of action
  • No effects on cognition
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24
Q

What is true about NSAIDs and hypersensitivity?

A
  • Hypersensitivity reactions more common in individuals w/nasal polyps or asthma
  • allergic reactions – bronchoconstriction, rhinitis, urticaria
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25
Q

What is the platelet effects of NSAIDs?

A

Platelet inhibition/dysfunction, increased intraoperative bleeding

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26
Q

What is the gi effects of NSAIDs?

A

ulcers, perforation, GI bleeds

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27
Q

What is the CV effects of NSAIDS?

A

increased risk of MI, heart failure, and HTN

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28
Q

What is the NSAIDs drug of choice for pt with cardiovascular complications?

A

Naproxen

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29
Q

What is the renal effects of NSAIDS?

A

changes in the excretion of sodium, changes in tubular function, potential for interstitial nephritis, and reversible renal failure – should be avoided in patients with renal failure

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30
Q

What is the liver effects of NSAIDS?

A

liver failure and increased hepatic transaminase level reported with some NSAIDs

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31
Q

What is the pulmonary effects of NSAIDS?

A

due to inhibition of prostaglandin synthesis in local tissues

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32
Q

Who is at increased risk for anaphylaxis for NSAIDs?

A

Patients with allergic rhinitis, nasal polyposis, asthma

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33
Q

What are some drug interactions of NSAIDs?

A
  • Increased bleeding risk for patients taking other antiplatelet agents
  • NSAIDs decrease lithium clearance and increase serum lithium concentrations
  • Conflicting data regarding interactions between NSAIDs and ACE inhibitors
  • Concurrent administration of digoxin can decrease renal clearance of of digoxin, increase plasma dig levels, and potentiates dig toxicity
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34
Q

What is the route for acetaminophen?

A

po, rectal, IV

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35
Q

What does acetaminophen lack?

A
  • Lacks significant anti-inflammatory properties

- Inhibits COX activity in the CNS rather than in the periphery

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36
Q

IV Acetaminophen: Analgesic and antipyretic for adults and children __________

A

> 2 years of age

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37
Q

IV Acetaminophen: Significant __________ sparing effect

A

opioid

38
Q

What is true regarding the effects of IV Acetaminophen?

A

Does not exhibit significant GI and CV effects associated with NSAIDs

39
Q

What is the onset, duration and peak effect of IV Acetaminophen?

A

10 minutes; peak effect 1 hour; duration of action 4-6 hours

40
Q

What is the dosing of acetaminophen > 13 years old?

A

1000 mg infused over 15 minutes

41
Q

What is the dosing of acetaminophen 2-13 years old

?

A

15 mg/kg

42
Q

When is hepatotoxicity a concern with IV acetaminophen?

A

Side effects rare but hepatotoxicity a concern with > 4000 mg/day

43
Q

What drug class is Acetylsalicylic Acid (Aspirin)?

A

Nonselective COX inhibitor

44
Q

What is the MOA of Acetylsalicylic Acid (Aspirin)?

A
  • Causes irreversible inhibition of COX enzymes (inhibition lasts approx. 7 days until new protein is produced)
  • Prevents production of prostaglandins
45
Q

What are the properties of Acetylsalicylic Acid (Aspirin)?

A

Excellent long-term antipyretic and anti-inflammatory properties

46
Q

What can be prolonged with Acetylsalicylic Acid (Aspirin)?

A

Significant impact on platelet aggregation that may be prolonged

47
Q

What is ketorolac?

A

Nonselective NSAID

48
Q

What is the characteristics of ketorolac?

A

Low incidence of nausea/vomiting and lack of respiratory depression

49
Q

What is the dosing of ketorolac?

A

30-60 mg IM/max IV dose = 30mg

50
Q

What is the onset and duration of action of ketorolac?

A

Onset 30 minutes; duration of action 4-6 hours

51
Q

When should ketorolac be used?

A

atopic or asthmatic patients, the elderly, patients with renal or GI dysfunction or bleeding disorders

52
Q

What negative effects of ketorolac can be seen (2)?

A

-Bone healing is delayed
(Blocks the mesenchymal stem cells chondrogenic differentiation)
-Bleeding may also be an issue in intracranial surgery

53
Q

What are the properties of Ibuprofen (Caldolor)?

A

Analgesic and antipyretic, Clinical effects similar to ketorolac

54
Q

What is the dose of Ibuprofen (Caldolor)?

A

400-800 mg IV over 30 minutes

55
Q

What is the onset and duration of Ibuprofen (Caldolor)?

A

Onset 30 minutes; duration 4-6 hours

56
Q

What are the contraindications of

Ibuprofen (Caldolor)?

A

Contraindications and precautions similar to ketorolac

57
Q

What is the derivative of Ibuprofen (Caldolor)?

A

Proprionic acid derivative

58
Q

What is the only COX2 selective inhibitor on the market?

A

Celecoxib (Celebrex)

59
Q

What is the dose of Celecoxib (Celebrex)?

A

loading dose = 400 mg followed by 200 mg q 12 hours

60
Q

What are the positive effects of Celecoxib (Celebrex)?

A

COX2 inhibitors have reduced incidence of GI ulceration and do not inhibit platelet function

61
Q

What can Celecoxib (Celebrex) cause?

A

fluid retention and hypertension

62
Q

When should Celecoxib (Celebrex) not be prescribed?

A

Should not be prescribed to patients with known history of CAD or cerebrovascular disease

63
Q

What can cause increase incidence of side effects with Celecoxib (Celebrex)?

A

Be wary of ketorolac at end of case of patient received full celebrex dose preoperatively (increased incidence of side effects)

64
Q

How do Celecoxib (Celebrex) (COX2 inhibitors) differ from nonspecific NSAIDs?

A

Highly lipophilic, neutral, non-acidic molecules with limited solubility in aqueous media

65
Q

What are the effects of Corticosteroids (Glucocorticoids)?

A

have analgesic, anti-inflammatory, and antiemetic effect

66
Q

When is Corticosteroids (Glucocorticoids) used?

A

Used in multimodal analgesia protocols to minimize opioid doses: dexamethasone at doses > 0.1 g/kg decreases acute postop pain & reduces opioid use esp. when administered preoperatively

67
Q

What causes the anti-inflammatory and analgesic effects of Corticosteroids (Glucocorticoids)?

A

inhibition of phospholipase A2 enzyme necessary for inflammatory chain reaction along both the lipoxygenase and COX enzyme pathways

68
Q

What does Corticosteroids (Glucocorticoids) inhibit?

A
  • Inhibits prostaglandin synthesis

- Also results in decrease in inflammatory cytokines

69
Q

What are side effects of Corticosteroids (Glucocorticoids)?

A

adrenal suppression, osteonecrosis, increased blood glucose, and impaired wound healing

70
Q

What is the primary corticosteroid?

A

hydrocortisone – standard against which synthetic corticosteroids are judged

71
Q

What is the MOA of Corticosteroids (Glucocorticoids)?

A
  • Attach to cytoplasmic receptors to enhance or suppress changes in the transcription of DNA & synthesis of proteins
  • Inhibit secretion of cytokines
72
Q

What is Glucocorticoids?

A

widely distributed; evoke anti-inflammatory response (glucocorticoid effect)

73
Q

What is a Mineralocorticoid?

A

present in distal renal tubules, colon, salivary glands, hippocampus; evokes distal renal tubular reabsorption of sodium in exchange for potassium ions (mineralocorticoid effect)

74
Q

Why are Glucocorticoids important during surgery?

A

critical for the maintenance of homeostasis during severe stress & mounting an appropriate stress response

75
Q

______physiologic steroid concentrations prepare the individual for responding to stress

A

Low

76
Q

_______ concentrations exert anti-inflammatory & immunosuppressive effects

A

Higher

77
Q

What is cortisol?

A

is released from the adrenal glands in an episodic manner, is linked to sleep-wake cycle

78
Q

What is max and min concentrations of cortisol?

A

maximal plasma concentrations of cortisol occur just before awakening & lowest levels 8-10 hours late

79
Q

What changes does stress-induce have on cortisol?

A

Stress-induced changes in plasma concentrations of cortisol occur (in addition to baseline release of cortisol)

80
Q

What controls cortisol synthesis?

A

governed by adrenocorticotropic hormone (ACTH) which is controlled by: hypothalamic hormones, corticotropin-releasing hormone, & arginine vasopressin

81
Q

What are endogenous corticosteroids?

A

cortisol, cortisone, coricosterone, desoxycortisosterone, aldosterone

82
Q

What are synthetic corticosteroids?

A

prednisolone, prednisone, methylprednisolone, betamethasone, dexamethasone, triamcinolone

83
Q

Review Clinical uses.

A

Slide 86-87

84
Q

What are the side effects of corticosteroids?

A
  • Suppression of the HPA (hypothalamic-pituitary-adrenal) axis
  • Electrolyte and metabolic changes
  • Osteoporosis
  • Peptic ulcer disease
  • Skeletal muscle myopathy
  • Inhibition of normal growth
  • Increased susceptibility to bacterial or fungal infection
85
Q

Who should receive corticosteroid supplementation?

A

Patients taking > 20mg/day of prednisone or its equivalent for > 3 weeks have a suppressed HPA axis

86
Q

Patients taking < 5mg/day of prednisone or its equivalent can be considered ___________ HPA axis

A

considered not to have suppression of the HPA axis

87
Q

Patients taking 5-20mg/day of prednisone or its equivalent for > 3 weeks __________ have suppression of the HPA axis

A

may or may not

88
Q

For patients with ________ (pts taking > 20mg/day of prednisone for > 3 weeks), glucocorticoid supplementation should consider the stress of surgery

A

Suppressed HPA axis

89
Q

What is the recommended minor surgical stress for corticosteroid supplementation?

A

(i.e., inguinal hernia repair) – hydrocortisone 25mg IV or methylprednisolone 5mg IV is sufficient

90
Q

What is the recommended moderate surgical stress for corticosteroid supplementation?

A

(i.e., non-laparoscopic cholecystectomy, colon resection, total hip replacement) – hydrocortisone 50-75mg/day IV for 1-2 days

91
Q

What is the recommended majoe surgical stress for corticosteroid supplementation?

A

(i.e., pancreatoduodenectomy, esophagectomy, cardiopulmonary bypass) – hydrocortisone 100-150mg/day IV for 2-3 days

2-Anesthesia Pharm Exam 2 (6 decks)

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