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Pharmacology > Treatment of Pain > Flashcards

Treatment of Pain Flashcards

1
Q

Pain is difficult to catch up with; (…) are more effective when given (…) pain increases

A
  • analgesics
  • before
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2
Q

What is the chemical name for acetaminophen and the abbreviation?

A
  • N-acetyl-para-aminophenol
  • APAP
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3
Q

What is the mechanism of action of acetaminophen?

A
  • not full understood
  • possibly blocks central (not peripheral) prostaglandin production
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4
Q

What are the uses of acetaminophen?

A
  • antipyretic
  • analgesic
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5
Q

What are the different formulations of acetaminophen?

A
  • oral: capsule, tablet (chewable and ER), elixir, gel, liquid, solution, suspension, syrup, sachet (tear open and put into water)
  • rectal suppository
  • IV
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6
Q

What are the advantages to using acetaminophen vs other pain medications?

A
  • no GI irritation
  • almost no allergy
  • no bleeding issues
  • very safe at usual doses (TI approx. 10)
  • safe in pregnancy
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7
Q

What are the disadvantages of using acetaminophen vs other pain medications?

A
  • poor anti-inflammatory action (treats pain/reduces fever but no inflammation)
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8
Q

What are the side effects associated with acetaminophen use?

A
  • methemoglobinemia, leukopenia rare (hemoglobin abnormal; cyanosis in babies)
  • liver toxicity due to metabolite accumulation (more concerned about)
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9
Q

What is the 2nd most common cause of liver disease that requires transplant?

A

liver toxicity due to acetaminophen use

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10
Q

What are the different metabolite forms of acetaminophen?

A
  • sulfate form
  • glucuronide form
  • N-acetyl-p-benzoquinone imine (NAPQI)
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11
Q

What is acetaminophen normally metabolized by?

A

glucuronidation and sulfation with minor CYP2E1

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12
Q

In acetaminophen, (…) is overwhelmed and metabolism shifts to (…), producing the toxic metabolite (…)

A
  • phase II
  • phase I
  • NAPQI
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13
Q

Describe the steps of normal acetaminophen metabolism and what happens when an overdose of acetaminophen occurs.

A
  • acetaminophen is mainly metabolized through glucuronidation and sulfation (phase II) with a little being metabolized by CYP2E1 (oxidation/CYP450)
  • when overdose occurs, there isn’t enough molecules for glucuronidation and sulfation to occur so more acetaminophen goes through CYP2E1 (phaseI) to be converted to NAPQI, which is toxic
  • usually the small amt of NAPQI is detoxified/eliminated by glutathione conjugation, but there is only a certain amount of this to allow it to occur
  • so in overdose, glutathione conjugation is overwhelmed from the large amount of NAPQI and NAPQI remains in the system to interact with cellular macromolecules and cause toxicity
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14
Q

Toxic chronic doses of acetaminophen can occur when taken over time in a period longer than (…)

A

4 hours

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15
Q

A normal dose of acetaminophen is (…) in patients with liver impairment

A

toxic

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16
Q

What are risk factors for toxicity with acetaminophen? Explain each.

A
  • malnutrition (decreased glutathione)
  • chronic alcohol ingestion (induces 2E1)
  • concomitant use of drugs that are CYP2E1 inducers
  • young, febrile children (usually less serious, not intentional OD so severity will be less)
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17
Q
  • Describe adult acetaminophen OD?
  • Describe child acetaminophen OD?
A
  • more severe, more fatal
  • more frequent, less severe
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18
Q

Anything that induces (…) will facilitate acetaminophen to be converted to (…) causing toxicity

A
  • 2E1
  • NAPQI
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19
Q

What are the different phases of acetaminophen toxicity?

A
  • phase 1: up to 24 hours after intake
  • phase 2: 18-72 hours later
  • phase 3: 72-96 hours later
  • phase 4: 4 days to 3 weeks later
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20
Q

What are the symptoms associated with each phase of acetaminophen toxicity?

A
  • phase 1: GI upset or no symptoms at all
  • phase 2: RUQ pain +/- tenderness (liver); continued or new onset of GI issues
  • phase 3: all of the above continue; hepatic dysfunction begins
  • phase 4: resolution of symptoms and organ failure, if patient survives; complete resolution of hepatic damage may take months
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21
Q

What is associated with hepatic dysfunction (acetaminophen toxicity)?

A
  • coagulopathy
  • jaundice/encephalopathy
  • hypoglycemia (failing liver doesn’t product a lot of sugar)
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22
Q

What are ways you can treat acetaminophen toxicity?

A
  • activated charcoal (if ingestion occurred w/in an hour and patient is stable)
  • n-acetylcysteine/NAC (acetadote) - always use in overdose situations w/ acetaminophen
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23
Q
  • How does n-acetylcysteine work in acetaminophen toxicity?
  • What are the regimens for it?
  • Which may be more effective in what time frames?
A
  • provides cysteine group for glutathione synthesis (so NAPQI can be detoxified/eliminated)
    regimens:
  • 72-hour oral or 21-hour IV
  • oral mixed w/soda or juice and chilled
    effectiveness:
  • oral may be more effective for pts presenting > 18 hours after ingestion
  • IV is more effective for pts presenting within 12 hours
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24
Q

What is the revised Rumack-Matthew Nomogram for the Acute Ingestion of Acetaminophen? (what it is used for)

A
  • used to interpret serum concentrations of acetaminophen in relation to time since ingestion measured from ingestion of first dose, in order to assess potential hepatotoxicity
  • acute = under 24 hours
  • NAC administration to any patient with a blood level above the treatment line
  • above treatment line: treat them; below treatment line: don’t treat them
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25
Q

What are the different formulations of acetaminophen and associated doses?

A
  • regular strength: 325 mg
  • extra strength: 500 mg
  • arthritis formula: 650 mg
  • PM or nighttime formulations: tylenol PM contains (per tablet) 500 mg acetaminophen, 25 mg diphenhydramine (benedryl)
  • excedrin: APAP 250 mg, ASA 250 mg (aspirin), 65 mg caffeine
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26
Q

What is the max daily dose of acetaminophen in children/adults?

A
  • children: 75 mg/kg/day and no more than 4000 mg
  • adults: 4000 mg
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27
Q

What is the minimum hepatotoxic single dose of acetaminophen in children/adults?

A
  • children: 150 mg/kg
  • adults: 7.5-10 grams
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28
Q

Describe the arachidonic acid pathway.

A
  • phospholipids are found in cells
  • when cellular injury occurs, phospholipase A2 becomes active, releasing arachidonic acid into the system
  • COX-1 enzyme can convert arachidonic acid into prostaglandins (PG) for GI mucosal protection and thromboxane (TXA) for platelet aggregation and vasoconstriction
  • this pathway is constitutive so it is always on doing something, it just becomes enhanced in cellular injury situations
  • COX-2 enzyme can convert arachidonic acid into prostaglandins (PG) to aid in pain, inflammation, fever, uterine contraction, vasodilation, and inhibition of platelet aggregation (decreased clotting)
  • this pathway is inducible so it needs to be turned on
  • LOX enzyme converts arachidonic acid to leukotrienes
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29
Q

Corticosteroids can inhibit the enzymes associated with the (…) pathway, decreasing the amount of (…) produced

A
  • arachidonic acid pathway
  • prostaglandins, TXA, and leukotrienes
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30
Q
  • Cortisol is a (…). Describe this.
  • Cortisol enhances the (…) response
  • It stimulates the (…) leading to (…)
  • Cortisol decreases (…) which can (…) response
  • Cortisol can stabilize (…) which can (…)
A
  • endogenous glucocorticoid - “gluco:” increase blood sugar via catabolism of protein and subsequent conversion into sugars and fats; gluconeogenesis
  • enhances the sympathetic(stress) response
  • stimulates the CNS leading to irritability, insomnia
  • decreases WBCs which can lower the immune response
  • stabilize intracellular lysosomes which can decrease cell injury
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31
Q

What is the MOA of cortisol?

A
  • inhibits synthesis of histamine, kinins, and prostaglandins (inhibit phospholipase A2)
  • decrease inflammation and allergy (there are steroidal anti-inflammatory products)
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32
Q

In fight/flight situations, the body releases (…) for energy

A

cortisol (increases blood sugar)

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33
Q
  • The body doesn’t know the difference between (…) cortisol
  • You shouldn’t have cortisol released for (…)
A
  • endogenous and exogenous cortisol
  • extended periods of time
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34
Q
  • What is a prototypical agent glucocorticoids/cortisol?
  • This mimics the actions of (…)
  • What does this inhibit?
A
  • prednisolone (active form)/prednisone (inactive form) - and every agent after
  • mimics the actions of cortisol
  • inhibits phospholipase A2
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35
Q

What are the uses of prednisolone/prednisone?

A
  • anti-inflammatory
  • immunosuppressant
  • decrease cell injury
  • inhibit collagen synthesis - decrease scar tissue formation
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36
Q

Describe the MOA of prednisolone/prednisone?

A
  • inhibits phospholipase A2
  • won’t release arachidonic acid
  • COX-1 and COX-2 won’t be able to convert arachidonic acid to prostaglandins
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37
Q

Prednisolone/prednisone is very (…)

A

very potent

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38
Q
  • Should patients with severe liver disease receive prednisolone or prednisone?
  • Why?
A
  • prednisolone
  • liver will have a harder time breaking down prednisone (inactive) to make it active
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39
Q
  • Which corticosteroid is most similar to the bodies natural cortisol?
  • How is this given?
  • What are other corticosteroid drug names?
A
  • hydrocortisone
  • topical
    other corticosteroids:
  • hydrocortisone
  • cortisone (injection)
  • prednisolone/prednisone
  • methylprednisolone
  • triamcinolone
  • dexamethasone
  • betamethasone
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40
Q

What are the anti-inflammatory activity levels of all the corticosteroid drugs?

A
  • hydrocortisone - 1
  • cortisone - 0.8
  • prednisolone/prednisone - 4
  • methylprednisolone - 5
  • triamcinolone - 5
  • dexamethasone - 25-30
  • betamethasone - 25
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41
Q

What are the equivalent doses of corticosteroids?

A
  • hydrocortisone - 20 mg
  • cortisone - 25 mg
  • prednisolone/prednisone - 5 mg
  • methylprednisolone - 4 mg
  • triamcinolone - 4 mg
  • dexamethasone - 0.75 mg
  • betamethasone - 0.75 mg
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42
Q

Which corticosteroid may be the least potent? Most potent?

A
  • hydrocortisone
  • betamethasone
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43
Q
  • What corticosteroids have the longest duration of effect?
  • What are their associated plasma/biologic half-lives?
A

dexamethasone:
- plasma half-life: 100-300 minutes
- biologic half-life: 36 hours
betamethasone:
- plasma half-life: 100-300 minutes
- biologic half-life: 35 hours

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44
Q

What are some examples of corticosteroid uses?

A
  • pulmonology/allergy - asthma, COPD, anaphylaxis
  • dermatology - urticaria, contact dermatitis
  • endocrinology - adrenal disorders
  • GI - IBD
  • hematology - hemolytic anemia, leukemia, lymphoma
  • rheumatology - rheumatoid arthritis, dermatomyositis, lupus
  • others - ophthalmology, organ transplant, lung maturation in newborns, cerebral edema, MS, post-MI
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45
Q
  • How do corticosteroids assist in post-MI or cerebral edema patients?
  • What do corticosteroids do in patients with lymphoma, leukemia, multiple myeloma?
  • Corticosteroids can be used as replacement therapy for (…) insufficiency, which is also known as (…) disease
A
  • stabilize cells
  • work by decreasing lymphocytes
  • glucocorticoid insufficiency; Addison’s disease
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46
Q
  • What are the different routes of administration of corticosteroids?
  • What is the route of administration determined by?
  • You should always treat (…) when possible to avoid (…) exposure
  • Adverse effects are (…) and (…) dependent in most cases
A
  • oral, inhaled (ocular, intranasal), parenteral (IM, IV, intraarticular, intralesional)
  • determined by illness
  • locally; systemic exposure
  • dose and duration dependent
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47
Q

What are some short term adverse effects of corticosteroid use?

A
  • decreased immune response (candidiasis; new or worsening bacterial infection)
  • GI bleeding and ulcers
  • hyperglycemia (releasing glucose)
  • mood changes (irritability/instability; worsening psychiatric problems)
  • increased appetite
  • insomnia
  • mineralocorticoid effects (sodium retention-increased BP; hypokalemia)
  • pancreatitis
  • electrolyte abnormalities
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48
Q

Why are GI bleeds/ulcers a short term adverse effect of corticosteroids?

A

corticosteroids inhibit phospholipase A2, inhibiting arachidonic acid release and production of prostaglandins, so there is less protection of the stomach from mucosal lining and acid causes damage in the stomach

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49
Q

What are some long term effects of corticosteroid use?

A
  • growth suppression in children
  • Cushing’s syndrome (moon face, buffalo hump, redistribution of fat on the body)
  • adrenal suppression - atrophy of adrenal cortex (weakness, lethargy, anorexia, nausea, myalgia)
  • cataracts and glaucoma
  • cardiac effects (new onset afib, heart failure, ischemia)
  • androgenic effects (amenorrhea, hirsutism-excessive hair growth)
  • skin (thinning, bruising, stretch marks, acne)
  • obesity
  • hyperlipidemia
  • muscle atrophy
  • osteoporosis
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50
Q

Why can corticosteroid use cause osteoporosis?

A
  • inhibits osteoblasts and increases osteoclast activity
  • affects collagen in bone
  • decreases Ca+2 absorption in gut
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51
Q

Corticosteroid use is contraindicated in what conditions/situations?

A
  • systemic fungal infection
  • don’t give with live vaccines when using immunosuppressive doses - delay for 3 months after discontinuation of corticosteroid use
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52
Q

When should you use corticosteroids cautiously? (individuals with what conditions)

A
  • diabetes
  • PUD or active GI bleeding
  • osteoporosis
  • myasthenia gravis - may worsen symptoms (weakness in skeletal mm)
  • cataracts/glaucoma
  • pregnancy (cleft palate, hypoadrenalism-close to birth, baby will become dependent on corticosteroids)
  • CNS disorders
  • uncontrolled viral/bacterial infections
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53
Q

What should you give to patients taking corticosteroids who have PUD?

A

proton pump inhibitor

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54
Q

Why does adrenal suppression happen if taking corticosteroids long-term?

A
  • glucocorticoids suppress pituitary release of ACTH
  • zona fasciculata (cells that produce cortisol in adrenal gland) do not receive stimulation
  • adrenal atrophy occurs
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55
Q

How long does adrenal suppression take when using corticosteroids?

A
  • several weeks of treatment are required
  • long-acting and high dose products have highest risk
  • topical and inhaled products are not a concern
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56
Q

What can we do to decrease adrenal suppression in corticosteroid use?

A
  • do not abruptly discontinue
  • gradually taper doses over weeks to months (consider 6-15 months and monitor)
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57
Q

What is the preferred treatment for adrenal insufficiency (corticosteroids)? Why?

A

hydrocortisone is preferred treatment for adrenal insufficiency as it more closely acts like endogenous cortisol (will probably be on for life)

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58
Q
  • Patients taking corticosteroids for (…) can stop abruptly?
  • (…) often occurs even in short courses to avoid flare
A
  • one week or less
  • tapering
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59
Q
  • Abrupt discontinuation of corticosteroids when taking (…) can lead to adrenal suppression or flare of disease that was being treated
  • Treatment over (…) can be tapered quickly to physiologic dose then weaned slowly
  • (…) and (…) therapies require longer tapers over months in most cases
  • (…) of patients is important
A
  • for one week or less
  • over 3 weeks
  • long-term and high dose therapies
  • close monitoring
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60
Q

If a patient have a systemic fungal infection, what should they not receive/take?

A

corticosteroids

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61
Q

What is the MOA of NSAIDS?

A
  • block the production of prostaglandins via cyto-oxygenase inhibition (COX)
  • COX converts arachidonic acid to other things, so when it is inhibited, you just have arachidonic acid sitting in your system
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62
Q

What is the general function of NSAIDS?

A
  • antipyretic
  • anti-inflammatory
  • analgesic
  • inhibit platelet congregation
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63
Q

What is the original, prototypical NSAID?

A

Aspirin

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64
Q

What is another prototype for NSAID (other than aspirin)?

A

ibuprofen

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65
Q

Efforts to decrease side effects and increase efficacy have led to the development of several (…)

A

NSAIDs

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66
Q

What are the different types of NSAIDs?

A
  • aspirin
  • magnesium salicylate, diflunisal, salsalate, tolmetin
  • fenoprofen, flurbiprofen, ketoprofen
    ibuprofen
  • naproxen
  • oxaprozin, meclofenamate, mefanamic acid, diclofenac, etodolac, indomethacin, sulindac, ketoralac
  • nabumetone
  • meloxicam, piroxicam
  • celecoxib
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67
Q

What is more potent the acetaminophen?

A

corticosteroids

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68
Q
  • Celecoxib is an NSAID that is selective for only (…)
  • Low-dose Aspirin is an NSAID that is selective for (…)
A
  • COX-2
  • COX-1
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69
Q

What is the general pharmacokinetics of NSAIDs:
- absorption
- metabolism
- excretion

A
  • absorption: well absorbed; no interference from food
  • metabolism: undergoes phase I, II, or both
  • excretion: mostly renal; some undergo enterohepatic recycling; some may be excreted through bile
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70
Q
  • Repeated dosing of NSAIDs produces detectable levels in (…)
  • Shorter half-life drugs stay present in (…) longer than would be expected, which could be important in ortho surgeries
A
  • synovial fluid
  • synovial fluid
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71
Q

What are some general NSAID indications?

A
  • headache
  • fever
  • rheumatoid arthritis
  • osteoarthritis
  • gout
  • spondylitis
  • soft-tissue injuries
  • menstrual pain
  • tendonitis
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72
Q

Why would you not use corticosteroids instead of NSAIDs?

A

many of the indications for NSAIDs are long-term conditions and corticosteroids can cause severe effects if used for a long-amount of time

73
Q
  • Aspirin specifically irreversibly binds (…) inhibiting (…), having (…) benefits
  • All other NSAIDs are (…) bound
A
  • COX-1
  • inhibiting platelet aggregation
  • cardiac benefits
  • reversibly bound
74
Q

Indomethacin (NSAID) is used to close what?

A

PDA (patent ductus arteriosis)

75
Q

Describe the use of Ketorolac (NSAID)? (how long it is used, why it isn’t used longer)

A
  • short-term use (5 days total) for opioid-level pain
  • very high rate of GI events and renal toxicity
  • poor inflammatory effects
76
Q

What are general NSAID side effects?

A
  • GI
  • Renal
  • Cardiovascular
77
Q

What are the GI NSAID side effects? Why?

A
  • ulcers, bleeding
  • because COX-1 is inhibited, so there is less mucosal protection
78
Q

What are the renal NSAID side effects?

A
  • prevents afferent arteriolar vasodilation
  • hypertension
  • acute kidney injury
  • decreased sodium excretion
79
Q

What are the cardiovascular NSAID side effects?

A

increased risk of stroke or MI

80
Q

What is the mechanism of NSAIDs preventing afferent arteriolar vasodilation causing renal damage?

A
  • NSAIDs don’t allow afferent arteriolar vasodilation so when it clamps down, afferents can open it back up
  • efferent arterioles take fluid out, so when afferent arterioles are clamped down, there is less fluid in the glomerulus which you want it to be full
  • causes renal damage
81
Q

You should use NSAIDs with caution in patients with what conditions?

A
  • MI/CHF
  • HTN
  • renal disease
  • anticoagulant or antiplatelet meds
82
Q

If you use NSAIDs in patients on anticoagulants or antiplatelets, what do you run the risk of?

A

patient developing an uncontrollable bleed

83
Q

What are some more general side effects and cautions of NSAID use?

A
  • GI issues (nausea, vomiting, GI bleed, ulceration)
  • bleeding
  • fluid retention
  • allergy
  • anemia/dyscrasias
  • tinnitus (esp. w/ high doses)
84
Q

Why do NSAIDs cause nausea and vomiting?

A

drug itself is acidic

85
Q

What side effects of NSAID use are more common in chronic and/or high dose administration?

A
  • fluid retention
  • anemia/dyscrasias
  • tinnitus
86
Q

What are the NSAID black box warnings?

A
  • cardiovascular risk: can increase thrombotic events, can be fatal; ibuprofen contraindicated in setting of coronary artery bypass graft surgery
  • GI risk: bleeding, ulceration, perforation of stomach or intestine, can be fatal; elderly patients are at greater risk for serious GI events
87
Q
  • Ibuprofen is contraindicated in the setting of what?
  • (…) patients are at a greater risk for serious GI events with NSAID use
A
  • coronary artery bypass graft surgery
  • elderly patients
88
Q
  • Aspirin irreversibly inhibits (…) and (…)
  • At low doses, aspirin is selective for (…)
  • Platelets cannot make new enzymes; it takes (…) to reverse the effects of ASA on platelet inhibition
  • Platelets cannot be (…)
A
  • COX-1 and COX-2
  • COX-1
  • 7-10
  • activated
89
Q

What are the uses of aspirin?

A
  • inflammation
  • pain
  • fever
90
Q

What can you use aspirin for at low doses?

A
  • MI prophylaxis
  • transient ischemic attack
91
Q

When using aspirin for cardioprotection, what should you not do?

A

do not take other NSAIDs within 2 hours of ASA

92
Q

Why can you use ASA for MI prophylaxis and transient ischemic attacks in low doses?

A
  • prevents platelets from aggregating
93
Q

Why does it take 7-10 days to reverse the effects of ASA on platelet inhibition?

A

because binding of ASA is irreversible, so the body needs to make new platelets not bound to ASA

94
Q

If you take ASA with other NSAIDs, what do you increase the risk of?

A

increase the risk of bleeding

95
Q
  • What are the most common side effects of aspirin use?
  • Aspirin is contraindicated in patients with a history of what? Why?
A
  • GI upset and ulcers
  • patients with a history of GI bleed, hemophilia, and other bleeding disorders
  • Because ASA side effects include bleeding
96
Q

Which NSAID is the only one considered an antiplatelet?

A

aspirin

97
Q

How many patients will develop a bleed within 1 year of taking ASA regularly?

A

1 in 1000

98
Q
  • (…) can occur with long term use or high doses of ASA.
  • This can cause what to happen?
  • ASA use increases risk of (…) attack
  • You should use ASA with caution in patients who have (…)
A
  • salicylism (increased salicylate)
  • vomiting, tinnitus, hearing loss, vertigo
  • gout attack
  • asthma - can cause asthmatic attack
99
Q

If aspirin is being used with another NSAID and we want the effects of aspirin to occur, what do we need to do and why?

A
  • give ASA first: there is a binding site on COX-1 and we want aspirin to get there first and irreversibly bind
  • if another NSAID is given first, it will get there before ASA so ASA cannot bind
100
Q

Aspirin overdose is commonly seen at (…) tablets of (…) each

A
  • 20-35 tablets
  • 325 mg each
101
Q

What are aspirin overdose symptoms?

A
  • respiratory alkalosis and metabolic acidosis
  • hyperthermia
  • seizures, coma, death
102
Q

How is aspirin overdose treated?

A
  • treated with activated charcoal (if ingestion is recent)
  • hemodialysis if very severe or worsening
  • no antidote, only supportive care and hope they get better
103
Q

Why should you not have children and teens take aspirin?

A

reye’s syndrome (swelling in the brain and liver)

104
Q
  • Celecoxib blocks (…)
  • It is preferable to use after (…) because there is no risk of (…)
  • This is also good for (…) therapy
A
  • COX-2
  • surgery; no risk of bleeding
  • long term therapy
105
Q

Celecoxib is a safe alternative with patients on (…)

A

anticoagulants

106
Q

What is the process of choosing an NSAID?

A
  • illness (consider FDA approval)
  • response to different NSAID varies among patients; ask if anything has worked for them in the past
  • consider comorbidities
  • bleeding risk
  • pain level
  • side-effects
  • drug interactions
  • dosing frequency
  • cost
  • length of therapy
  • availability
107
Q
  • What is the dosing of ibuprofin,ASA, and naproxin for inflammation?
  • Why is this important?
A
  • Ibuprofen: 600 mg QID
  • ASA: 1200-1500 mg TID
  • Naproxen: 375 mg BID
  • importance: bottle instructions do not tell you this, so it may be better to write a prescription for this rather than having pt go by it OTC
108
Q

Crude resin from opium poppy seeds containing several alkaloids, one of which is morphine (10%)

A

opium

109
Q

Naturally occurring compounds: morphine, codeine, thebaine, and papaverine

A

opiate

110
Q

All agents with the same functional and pharmacological properties of opiates

A

opioid

111
Q

Per DEA: “refers to opium, opium derivatives, and their semi-synthetic substitutes”

A

narcotic

112
Q

What is 10% of what comes out of opium?

A

morphine

113
Q

(…) are endogenous morphine

A

endorphins

114
Q

What is the background of opioids?

A
  • used for 1000s of years to treat pain
  • 1803: morphine isolated from opium
  • 1973: radioactive morphine showed specific areas of uptake in mice - morphine receptors
115
Q
  • When researchers found that there was uptake of morphine in mice, they found (…)
  • They discovered that physiologic receptors bind to (…)
  • Looking for endogenous ligand led to the discovery of (…) in the 1980s
  • What were some of these endorphins?
A
  • morphine receptors
  • endogenous substances
  • endorphins
  • enkephalins, endorphins, dynorphins
116
Q
  • After the discovery of morphine receptors and endorphins, we now know that there are many (…) in the body
  • Opioids primarily act on which receptors (each have subtypes)?
  • (…) are the most important analgesic receptors
A
  • receptors
  • mu, kappa, delta
  • mu receptors
117
Q
  • What was the opioid prototype?
A

morphine

118
Q
  • Morphine is a very strong (…) agonist
  • What is the primary target for opioids?
  • Other opioids have been compared against (…) to determine potency
  • Why is the structure of morphine important?
A
  • mu receptor agonist
  • mu-receptor
  • morphine
  • changing the structure can change things like efficacy, potency, side-effects, etc.
119
Q

What are therapeutic uses of opioids?

A
  • pain
  • adjunct to anesthesia (improve sedation; provide pain control)
120
Q

(…) is inactive until it is broken down in the body to (…) which is its prodrug

A
  • codeine
  • morphine
121
Q
  • Long-term use of opioids can lead to (…)
  • Short-acting opioids are more likely to be (…)
A
  • dependence
  • addictive
122
Q

As analgesics, opiates can control (…) pain, but (…) doses will be needed over time depending on frequency of dosing. Sharp, intermittent pain may be best controlled with (…), but only treat when treatment is needed

A
  • severe, chronic pain
  • increased doses
  • short-acting opiates
123
Q
  • Fentanyl is a (…) agonist
  • Codeine is a (…) agonist
  • Buprenorphine is a (…) agonist
  • Butorphanol, Nalbuphine, and Pentazocine are (…)
  • Which opioids are used as reversal agents or deterrents and are antagonists?
A
  • strong
  • moderate/low
  • partial
  • mixed agonists/antagonists
  • Naloxone, Naltrexone
124
Q

What are the different classes of opioids?

A
  • phenanthrenes
  • benzomorphans
  • phenylpiperidines
  • dephenylheptanes
  • phenylpropylamines
125
Q

What drugs are phenanthrenes?

A
  • morphine
  • codeine
  • oxycodone
  • oxymorphone
  • hydromorphone
  • hydrocodone
  • levorphanol
  • buprenorphine
  • nalbuphine
  • butorphanol
  • naloxone
  • naltrexone
126
Q

What drugs are benzomorphans?

A

pentazocine

127
Q

What drugs are phenylpiperidines?

A
  • fentanyl
  • alfentanil
  • remifentanil
  • sufentanil
  • meperidine
128
Q

What drugs are diphenylheptanes?

A

methadone

129
Q

What drugs are phenylpropylamines?

A
  • tramadol
  • tapentadol
130
Q
  • Transmission of pain occurs via the (…) pathway
  • Once the pain message is received by the brain, the (…) pathway releases (…) to modulate pain
A
  • ascending pathway
  • descending pathway
  • endorphins
131
Q
  • Ascending pain transmission pathway: (…) painful stimuli
  • Descending pain transmission pathway: (…) pain
A
  • transmits painful stimuli
  • modulates pain
132
Q
  • What is the MOA in pain control?
  • In the spinal cord, pain information is (…) to the brain
  • In the brain, the (…) is activated (as if painful stimuli were received); inhibitory neurons are (…) and (…) are released
A
  • bind opioid receptors promoting K+ conductance and inhibiting Ca+2 conductance
  • not transmitted to the brain
  • descending pathway
  • inhibited
  • endorphins
133
Q
  • What do opioid agonists do?
A
  • stimulate the receptor (block pain receptors and release endorphins)
134
Q

What has high affinity but low efficacy at the mu receptor?

A

partial agonists

135
Q
  • Partial agonists may act as an (…) in the presence of an (…)
  • This precipitates withdrawal but to a lesser-extent than (…)
A
  • antagonist
  • agonist
  • agonist/antagonist
136
Q
  • Partial agonists have (…) bioavailability due to (…); formulations avoid the (…)
  • Partial agonists exhibit a (…) effect
  • Antagonists can be found at the (…) receptor
A
  • very poor bioavailability
  • high first-pass effect
  • gut
  • ceiling effect
  • kappa receptor
137
Q

If someone is overdosing on opioids, what can you give them?

A

partial agonists - can make some of the drug jump off

138
Q
  • Agonists-antagonists have (…) at the mu receptor, so essentially it blocks more (…) from binding, which may cause (…)
  • Agonists at (…) receptor; may cause (…) and (…)
  • These can exhibit a (…) effect
A
  • poor efficacy
  • efficacious opioids
  • withdrawal
  • kappa receptor
  • dysesthesias
  • dysphoria
  • ceiling effect
139
Q

Describe the ceiling effect

A

you can only attain a certain amount of pain relief with opioids, so once you give too much, it can lead to toxicity

140
Q

What has high affinity for the mu receptors but no efficacy so it will block anything that binds to the mu receptors?

A

antagonists

141
Q
  • Uptake of opioids is primarily determined by (…) and (…)
  • Most opioids are well absorbed via the (…)
  • What are exceptions to this?
  • Distribution of opioids will depend on what?
A
  • efflux transporters (like P-gp)
  • solute carrier influx transporters (SLCs)
  • GI tract
  • fentanyl (and its cousins), buprenorphine
  • will depend on whether the drug is a substrate for efflux transporters or SLCs
142
Q

What do SLCs do?

A

help bring drugs into the nervous system

143
Q

What do efflux transporters do?

A
  • spit drug out from where it is supposed to go
  • harder to cross a barrier and get into the nervous system
  • may only work peripherally, not centrally
144
Q
  • Phenylpiperidines are metabolized via (…)
  • Phenanthrenes are metabolized primarily via (…) as well as others
  • Those with free hydroxyl groups undergo (…)
  • Active and toxic metabolites are possible with some opioids in the (…) class
A
  • CYP3A4
  • CYP2D6
  • glucuronidation
  • phenanthrenes
145
Q
  • Ultimately, it is possible that not all opioids will (…) or be (…) for all patients
  • Because of extensive (…) metabolism, IV doses of opioids are often (…) than oral doses
  • How are opioids excreted?
A
  • relieve pain or be safe
  • hepatic
  • smaller
  • mostly renally
146
Q

What is an active metabolite?

A

metabolizes into another form that does the same thing

147
Q

Describe tolerance of opioids?

A
  • decrease in apparent effectiveness of a drug with repeated exposure
  • patient is given opioid, says pain is back, have to increase dose to get same effect
148
Q

Is tolerance reversible?

A

yes, it is reversible and surmountable

149
Q

Describe dependence of opioids?

A
  • neuronal adaptation to repeated exposure resulting in withdrawal syndrome upon cessation
  • body starts to depend on drug to do its function of daily life
150
Q

What is inevitable with continuous and extended use of opioids?

A

dependence

151
Q

What are effects of opioids that we have high tolerance to and can adjust to?

A
  • analgesia
  • euphoria/dysphoria
  • mental clouding
  • sedation
  • respiratory depression
  • antidiuresis
  • nausea/vomiting
  • cough suppression
152
Q

What are effects of opioids that we have moderate tolerance to and can adjust to?

A
  • bradycardia
153
Q

What are effects of opioids that we have minimal or no tolerance to and can never adjust to?

A
  • miosis
  • constipation
  • convulsions
154
Q

What is a behavioral pattern characterized by compulsive use of a drug and overwhelming involvement with its procurement and use?

A

addiction

155
Q
  • Addiction effects the (…) in the brain
  • It can be caused by (…) or (…) of withdrawal
A
  • reward center in the brain
  • avoidance or alleviation
156
Q
  • What is not an end result for all patients on opioids?
  • What should you not mistake this for?
  • Substances with (…) lives have greatest risk for this due to frequent ups and downs
A
  • addiction
  • dependence
  • short half-lives
157
Q

What are the effects of opioids?

A
  • analgesics
  • nausea/vomiting
  • euphoria/dysphoria
  • sedation w/o amnesia; disrupted sleep architecture
  • respiratory depression
  • constipation d/t decreased GI motility
  • hyperalgesia
  • miosis
  • cough suppression
  • urinary retention
  • truncal rigidity
  • minor bradycardia
158
Q

The more opioids you give a person (specifically a naive opioid user), the more likely it is they will have (…)

A

respiratory depression

159
Q
  • Why do opioids cause respiratory depression?
  • What is this dependent on?
  • How do you overcome this?
A
  • inhibit respiratory drive in the brainstem
  • dose-dependent
  • can be overcome by external stimuli
160
Q
  • Miosis caused by opioids is (…) dependent
  • No (…) develops
  • Miosis is useful in identifying (…)
A
  • dose dependent
  • tolerance
  • OD
161
Q
  • Truncal rigidity is seen with (…) doses of drugs like (…)
  • How is this prevented?
A
  • high doses
  • fentanyl
  • administering a neuromuscular blocker
162
Q

What should you give to patients who have constipation due to opioids?

A

a stimulant, not a stool softener

163
Q

What is the drug that is the exception of the opioid bradycardia effect in that it may cause tachycardia due to antimuscarinic effects?

A

meperidine

164
Q

Why should you not use opioids in patients who have COPD or cystic fibrosis?

A
  • allows cough suppression but does not allow mucus excretion
165
Q

In what patients should you use opioids cautiously?

A
  • pts w/ history of drug/alcohol abuse
  • pts w/ depression or other psychiatric illnesses (d/t dysphoria)
  • pts using other narcotics or CNS depressants (increased risk of respiratory depression)
  • pts with respiratory disease
  • pts with gallbladder disease
  • pts with epilepsy
  • pregnant pts
166
Q

In patients with gallbladder disease, opioids may cause (…) or (…)

A
  • biliary stasis
  • constriction of sphincter of oddi
167
Q

Why should you use caution giving opioids to pts with seizures?

A

opioids may lower seizure threshold in some pts

168
Q

Why should you use caution giving opioids to pregnant patients?

A
  • birth defects
  • restricted intrauterine growth
  • preterm birth
  • still birth
  • neonatal abstinence syndrome
169
Q
  • Since 1999, (…) people have died as a result of OD
  • When opioids bind to (…) receptors, it can cause OD pieces, especially respiratory distress
  • Not all synthetic opioids will cause (…)
A
  • 165,000
  • mu receptors
  • miosis
170
Q

How many MME should you avoid using?

A

> 50 MME

171
Q

When a pt is at an increased risk of opioid related harm, what should you consider offering?

A

naloxone

172
Q

What are the numbers associated with these:
- 50-99 MME/day: (…) increased risk of OD
- > 100 MME/day: (…) increased risk of OD

A
  • 3.7
  • 8.9
173
Q

What is the MOA of naloxone?

A
  • high affinity for mu receptor (higher than opioids)
  • displaces opioids to reverse respiratory depression; opioids still circulate body
  • no dependence/tolerance (can use again)
  • no clinical effects in absence of opioids (very safe)
174
Q

How can naloxone be given?
- What are the associated time to onset and half-lives?

A
  • IM: 2-3 mins; 30-90 mins
  • intranasal: 2-3 mins; 120 mins
175
Q
  • Naloxone is poorly absorbed via the (…) route
  • Why is the half-life of naloxone important to note?
A
  • oral route
  • shorter half-life than opioids so when they jump off mu receptors, opioids can hop back on and cause respiratory depression
176
Q

What are symptoms of opioid acute wthrawal?

A
  • HA
  • watery eyes
  • runny nose
  • sweating
  • craving opioids
  • MSK pain
  • abdominal pain
  • N/V/D
  • tremors
  • restlessness/irritability
177
Q

What are product specific reactions to naloxone?

A
  • nasal dryness
  • IM site discomfort
178
Q

You will only use naloxone when?

A

when patient is not breathing

179
Q
  • Naloxone can cross (…) in pregnancy and precipitate (…) withdrawal
  • Naloxone can cause (…) in neonates
  • During lactation, it is (…) if naloxone gets into lactate to be transported to the baby
  • What can naloxone cause in geriatrics and why?
A
  • placenta; fetal withdrawal
  • seizures
  • unclear
  • increased systemic exposure due to hepatic/renal/and cardiac function

Pharmacology (13 decks)

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