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Pharm 2 > Test 4: Multimodal Specific Drugs to Know > Flashcards

Test 4: Multimodal Specific Drugs to Know Flashcards

1
Q

What are NSAIDs used for?

A

-Treatment of mild-moderate post-op pain
-Pain r/t inflammation
-Most common analgesia adjuncts
-NSAIDs + Opioids = synergistic effect (!)
-Antipyretic, analgesic, and anti-inflammatory
-Inhibits cyclooxygenase (COX)
-Most are weak acids with pKa between 4-5

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2
Q

What is COX 1?

A

COX = enzyme that makes thromboxane, prostaglandins, and prostacyclins.
-Widespread throughout the body and necessary for homeostasis
-Responsible for platelet aggregation, gastric mucosal integrity, and renal function
-Inhibition causes gastric irritation, renal microvascular constriction, and platelet inhibition

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3
Q

What is COX 2?

A

COX = enzyme that makes thromboxane, prostaglandins, and prostacyclins.
-Inducible enzyme that releases prostaglandins in the presence of inflammation
-Mediates pain, fever, and carcinogenesis
-Inhibition causes analgesic effects
-Modulation of cell proliferation
-No issues with hemostasis and less GI issues.

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4
Q

What are the pharmacokinetics of Celecoxib (Celebrex)?

A

-Absorption: Bioavailability unknown
-Distribution: 97% protein bound
-Metabolism: Extensively hepatically metabolized via CYP450 to inactive metabolites
-Half-life = 11 hours
-Dose: 200 mg QD or 100 mg BID
-Caution use in patients with Hx of GI bleed

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5
Q

What is the MOA of Celecoxib (Celebrex)?

A

-COX-2 selective NSAID (reversible)
-Decreases formation of prostaglandin precursors
-Reduces inflammatory symptoms
-Relieves pain

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6
Q

What are the CNS effects of Celecoxib (Celebrex)?

A

Headache

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7
Q

What are the Respiratory effects of Celecoxib (Celebrex)?

A

-Potential for bronchoconstriction due to conversion of arachidonic acid to the precursor of leukotrienes.
-Technically contraindicated in asthmatics, even though they usually tolerate it well.

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8
Q

What are the cardiovascular effects of Celecoxib (Celebrex)?

A

-Can start or worsen hypertension
-DIC in children with systemic onset juvenile RA
-Can lead to MI formation

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9
Q

What are the uses of Celecoxib (Celebrex)?

A

Useful in arthritis, gout, dysmenorrhea, and orthopedic surgeries.
-Treatment of acute surgical pain, chronic pain syndromes, and cancer pain
-Often used in combination with other analgesics

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10
Q

What are the risks associated with long-term use of Celecoxib (Celebrex)?

A

Concern for duodenal ulcers, hemorrhage, or MI (if taking every day for long periods of time)

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11
Q

What are the contraindications / cautions to the use of Celecoxib?

A

-C/I if hypersensitivity to sulfonamides (contains sulfa), asthma, or hypersensitivity to NSAIDs/ASA.
-Caution in pts taking warfarin or phenytoin – cotherapy increases warfarin or phenytoin levels.

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12
Q

What are the Onset and Peak times of Ketorolac (Toradol)?

A

-IM Onset: 30min with Peak 2-3 hrs
-IV Onset: 15 min with Peak 2 hrs
-Well absorbed via PO

Would be administered at the end of the case - peaks in PACU. Ask if surgeon is concerned with use and with oozing.
Often in PACU standing orders - notify PACU RN of when you dosed.

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13
Q

What is the Distribution & Metabolism of Ketorolac (Toradol)?

A

Distribution:
-DOA 6-8 hrs
-Crosses placenta
-Enters breast milk
-99% protein bound

Metabolism: Hepatic
Excretion: Renal

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14
Q

What is the dose of Ketorolac (Toradol)?

A

Adults > 50 kg
-30mg IM = 12 mg Morphine = 100 mg Demerol.
-Should not be administered beyond 5 days (used for short-term, acute post-op pain)
-Very potent.

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15
Q

What is the MOA of Ketorolac (Toradol)?

A

-Non-selective COX inhibitor (COX 1 & 2)
-Inhibits prostaglandin synthesis by decreasing COX = decreased prostaglandin precursors

Causes platelet inhibition. Potent analgesic with moderate anti-inflammatory properties.

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16
Q

What are the CNS effects of Ketorolac (Toradol)?

A

-HA
-Hallucinations with concomitant use of psychoactive drugs

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17
Q

What are the Respiratory and CV effects of Ketorolac (Toradol)?

A

Respiratory:
-Bronchospasm
-Anaphylaxis

Cardiovascular:
-Edema (rare)
-HTN

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18
Q

What is important to know regarding Ketorolac and renal function?

A

-C/I with renal failure (renal excretion) and high grade renal insufficiency.
-Prolonged clearance with opioids on board
-½ life prolonged 30-50% in elderly. Look at Creatinine clearance. Dec dose in elderly due to decline in renal function.

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19
Q

What are contraindications for the use of Ketorolac (Toradol)?

A

-renal failure
-coagulopathies
-PUD
-GIB
-asthma
-hypersensitivity to NSAIDS
-surgery with high risk of bleeding
-Controversy with orthopedic procedures

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20
Q

Why is Ketorolac controversial with orthopedic procedures?

A

Interrupts normal prostaglandin effects on osteoblast and osteoclast activity that promote bone healing.

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21
Q

What are the pharmacokinetics of acetaminophen?

A

Absorption:
-IV onset 10 minutes
-Almost entirely neutral and absorbs rapidly from duodenum.
Distribution:
-DOA 4-6 hours
-8-43% protein bound
Metabolism:
-Hepatic
-Active metabolite: acetylimidoquinone
-1/2 life = 1-3 hours

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22
Q

What is the dose of acetaminophen?

A

Adults > 50 kg
-1000mg Q 6 hrs titrated over 15 min
-650mg Q 4 hrs titrated over 15 min
-Max 4000 mg/day

23
Q

What is the MOA of acetaminophen?

A

-Reduces prostaglandin synthesis via COX inhibition
-Minimal anti-inflammatory effects
-Mainly analgesic and antipyretic

Less stomach/intestinal irritation compared to NSAIDs.

24
Q

What are the contraindications / cautions for the use of acetaminophen?

A

Contraindicated in:
-Liver failure
-Severe hepatic impairment
-Hypersensitivity to NSAIDs

Caution in:
-Alcoholism
-Chronic malnutrition
-Severe hypovolemia
-Severe renal impairment

Do not administer IV with any other meds

25
Q

What are the effects of NSAIDs that are NOT present with acetaminophen?

A

Lacks negative effects of other NSAIDS:
-Platelet inhibition
-GI irritation
-Renal toxicity

26
Q

What is the difference between PO and IV acetaminophen?

A

-Bypasses first pass liver metabolism.
-More bioactive agent available of what you’re giving.
-Greater peak levels with IV acetaminophen.

27
Q

What are the pharmacokinetics of Ibuprofen?

A

Absorption:
-IV Onset 10 minutes (nagelhout says 30)
Distribution:
-DOA 4-6 hours
->90% protein bound
Metabolism:
-Hepatic via CYP
Elimination:
-Renal
1/2 Life = 2 hours

28
Q

What is the usual dose of Ibuprofen?

A

Adults > 50 kg
-400mg to 800mg IV over 30 min q6hr PRN
-Peds (6mon-12y): 10 mg/kg IV over 10 min up to max single dose of 400mg q4-6h
-3200 mg/day

29
Q

What is the MOA of Ibuprofen?

A

-Inhibits prostaglandin synthesis via COX 1 and 2 inhibition
-Minimal anti-inflammatory effects
-Mainly analgesic and antipyretic

30
Q

What are the CNS, Cardiovascular, and GI effects of Ibuprofen?

A

CNS: Mild - headache

CV: Risk of thrombotic events

GI: Increased risk of GI ulcer, bleeding, and perforation (if reaching max dose)

31
Q

What is the box warning associated with Ibuprofen?

A

RISK OF SERIOUS CARDIOVASCULAR AND GASTROINTESTINAL EVENTS
-Non-steroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use.

32
Q

What are the contraindications / cautions for the use of Ibuprofen?

A

C/I in CABG (risk of thrombosis)

Caution in:
-Alcoholism
-Chronic malnutrition
-Severe hypovolemia
-Severe renal impairment

Must be diluted, usually in 100-200 mL

33
Q

What is the MOA of Corticosteroids?

A

Achieves anti-inflammatory effects by:
-Inhibit phospholipase A2
-Prevents release of arachidonic acid
-⬇cytokines & prostaglandins

34
Q

What are corticosteroids used to treat?

A

-Work well with chronic pain syndromes.
-RA, OA, herpetic neuralgia, chronic LPB, chronic neck pain

35
Q

HPA suppression from 1 dose of steroids can last how long?

A

4 days to 5 weeks

36
Q

Full recovery of the HPA takes how long after suppression?

A

3-6 months
-Requires stress-dose steroids
-Suppression: >10 days of treatment
-Have to factor in stress level of procedure (Minor vs major procedure).

37
Q

What are symptoms associated with long-term corticosteroid therapy?

A

-Weight gain
-Steroid skin: tears easily
-GI upset (ulceration/gastritis)
-Insomnia, mood swings, depression

38
Q

What are the stress-dose steroid requirements for a Major surgery?

A

Continue preop + 25 mg of hydrocortisone on induction + 100 mg per day for 2-3 days.

39
Q

What are the pharmacokinetics of Methadone?

A

Absorption:
-PO peaks at 30-60 min
-IV peaks at 15-20 min
Distribution:
-Highly lipid soluble
Metabolism:
-Hepatic via CYP to inactive metabolites
1/2 Life = 15-60 hours. Ideal for maintenance programs. Use in acute pain is limited, but effective
Dose: Difficult to initiate & titrate

40
Q

What are the uses of Methadone?

A

-Historically used in treatment of opioid addiction
-Increasing use in the treatment of severe acute pain, chronic pain (malignant & non-malignant)
-Longer ½ life than most opioids.
-Use with acute pain is limited, but can be given pre-incision for big spine cases to dec opioid requirements.

41
Q

What is the MOA of Methadone?

A

-Synthetic opioid agonist
-Racemic
-D-isomer antagonizes NMDAR & inhibits serotonin & NE uptake (Treats neuropathic pain and prevents tolerance & hyperalgesia)
-L-isomer binds to the opioid receptor (analgesic effects)

42
Q

What are the CNS and Respiratory effects of Methadone?

A

CNS: Excessive sedation

Respiratory: Depression (later than analgesic effects)

Risk of dependence, tolerance, and addiction.

43
Q

What are the cardiovascular effects of Methadone?

A

-QT interval prolongation
-Lethal VT or Torsades
-EKG pretreatment, after 30 days and then annually (!!!)
-D/C if QT interval exceeds 500ms

44
Q

What are the contraindications for use of Methadone?

A

-CV pts on antiarrhythmics
-TCAs
-Ca++ Channel Blockers
-⬇K+
-hx of prolonged QT

45
Q

What is Physiologic dependence?

A

Manifestations of withdrawal symptoms after abrupt D/C.

46
Q

What are examples of withdrawal symptoms?

A

Irritability
Restlessness
Tremors
Chills
Muscle cramps
Sweating
Mydriasis
Abd pain
Diarrhea
Tachycardia

47
Q

What is Psychologic dependence?

A

-Craving for an opioid to achieve a psychological effect
-Continued use of a drug despite harm to self or others

48
Q

What is Opioid Induced Hyperalgesia (OIH)?

A

-Worsening pain with escalating doses of opioids
-Pain in different locations
-Whole-body hyperesthesia
-Allydonia, agitation
-Multifocal myoclonus
-Seizures
-Improves with reducing or d/c ing opioids. Switch them to non-opioid analgesics.

49
Q

What are the theories behind OIH?

A

1) Central activation NMDA receptors via glutamate
2) Shifting of a modulation system from a descending inhibitory pathway to a facilitating pronociceptive pathway
3) Prostaglandins stimulate glutamate release (refer to #1)

50
Q

What is tolerance?

A

-Change in the dose-response relationship
-Induced by repeated exposure
-Need for a higher dose to maintain analgesic effect

51
Q

What is Pseudoaddiction?

A

-Often confused with psychological addiction
-Pt behavior can be the same
-Drug seeking behavior due to inadequate analgesia

52
Q

What does Lidocaine do for pain control?

A

-Decreases opioid use in the post-op period

Dose:
-2mg/kg/hr intra-op
-Continued for up to 8 hours post op

53
Q

What does Esmolol do for pain control?

A

-Decreases anesthesia requirements
-Decreases opioid use
-Decreases PONV

Dose:
-Bolus 1mg/kg
-5-15mcg/kg/min
-Bolus 0.5mg/kg
-0.5mg/kg/hr

Pharm 2 (40 decks)

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