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Therapeutics III > Barker Pharmacology of Non-opiate Drugs > Flashcards

Barker Pharmacology of Non-opiate Drugs Flashcards

1
Q

What are the different chemical structures classified as NSAIDs?

A

-Salicylates
-Arylpropionic acid
-Arylacetic acids
-Enolic acids

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2
Q

What are the salicylate NSAIDs?

A

Aspirin

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3
Q

What are the arylpropionic acid NSAIDs?

A

-Ibuprofen
-Naproxen

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4
Q

What are the arylacetic acid NSAIDs?

A

-Indomethacin
-Diclofenac
-Ketorolac
-Etodolac

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5
Q

What are the enolic acid NSAIDs?

A

-Piroxicam
-Meloxicam

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6
Q

Therapeutic applications of NSAIDs

A

-Analgesic
-Anti-inflammatory
-Antipyretic
-Prophylactic to reduce risk of myocardial infarction - aspirin

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7
Q

Examples of when NSAIDs will be used for analgesic purposes

A

-Chronic postsurgical pain
-Myalgias and arthralgias/sprains and strains
-Inflammatory pain
-Dysmenorrhea (specific PGE effect)

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8
Q

Examples of when NSAIDs will be used for anti-inflammatory purposes

A

-Bursitis and tendonitis
-Osteoarthritis
-Rheumatoid arthritis
-Gout and hyperuricemia
-Rib fracture

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9
Q

What is the inflammatory response to injury?

A

Rubor (redness), tumor (swelling), calor (heat), dolor (pain)

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10
Q

Three phases of the inflammatory response

A

-Acute - vasodilation leading to increase permeability
-Subacute - infiltration of neutrophils causing more inflammation
-Chronic - proliferation

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11
Q

What inflammatory mediators are recruited in an inflammatory response

A

Eicosanoids

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12
Q

What are the eicosanoids in an inflammatory response?

A

-Arachidonic acid metabolites
-Prostaglandins (redness, heat, pain)
-Thromboxanes
-Leukotrienes (swelling)
-Cytokines (pain)

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13
Q

Aspirin mechanism of action

A

-Irreversibly inhibits cyclooxygenase1/2 by acetylation of COX
-Modifies cyclooxygenase 2 activity -> produce lipoxins
-Duration of effect corresponds to time required for new protein synthesis

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14
Q

Mechanism of action of NSAIDs besides aspirin

A

-Competitive (reversible) inhibitors of cyclooxygenase 1/2
-Some arylacetic acids also inhibit leukotriene synthesis, contributing to anti-inflammatory effect (indomethacin and diclofenac)

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15
Q

Aspirin contraindication

A

Risk in treating children with fever or viral origin due to the development Reye’s syndrome

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16
Q

Aspirin clinical pearls

A

-Historically one of the most common and effective agents for analgesia, antipyresis, and anti-inflammatory use
-Frequently used as prophylactic for anti-coagulation
-No tolerance development to analgesic effects

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17
Q

How is aspirin absorbed?

A

-Rapidly absorbed
-Passive diffusion of unionized acid at gastric pH
-Delayed by presence of food

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18
Q

How is aspirin distributed in the body?

A

-Distributed throughout most tissues and fluids
-Competes with many drugs for protein binding sites

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19
Q

How is aspirin metabolized and excreted?

A

-Aspirin half-life 15 min - hydrolysis at multiple sites
-Salicylate half-life 6-20hrs - dose dependent conjugation (saturated)
-Active secretion and passive reabsorption in renal tubule
-Increased excretion with increased urinary pH

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20
Q

Mild effects of salicylism/aspirin poisoning

A

-Vertigo
-Tinnitus
-Hearing impairment

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21
Q

CNS effects (moderate -> severe) of salicylism/aspirin poisoning

A

-Nausea, vomiting, sweating, fever
-Stimulation followed by depression
-Delirium, psychosis -> stupor -> coma
-Respiratory alkalosis caused by hyperventilation (moderate for adults)
-Metabolic acidosis caused by lowering of blood pH (high dose or kids)

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22
Q

Treatment of salicylism/aspirin poisoning

A

-Increase urinary excretion using dextrose or sodium bicarbonate
-Trap in urine pKa of salicylate 3.0 -> ionized in urine -> can not go back
-Treat by correcting metabolic imbalance (usually potassium level)

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23
Q

Ibuprofen and naproxen clinical pearls

A

-All are potent reversible cyclooxygenase inhibitors
-Half-lives: ibuprofen 2 hr, naproxen 14 hr (otherwise drugs quite similar)
-Better tolerated than aspirin
-Inter-patient variation in response and adverse effects

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24
Q

Therapeutic use of diclofenac

A

-Excellent alternative to ibuprofen and naproxen
-Increased risk of peptic ulcer and renal dysfunction with prolonged use
-Arthrotec (diclofenac/misoprostol) for chronic use. Misoprostol=PGE1 analog

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25
Q

Therapeutic use of indomethacin

A

-One of the most potent reversible inhibitors of PG biosynthesis
-High incidence and severity of side effects long-term
-Acute gouty arthritis, ankylosing spondylitis

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26
Q

Therapeutic use of sulindac

A

-Less toxic derivative of indomethacin
-Still significant side effects
-Rheumatoid arthritis and ankylosing spondylitis

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27
Q

Pharmacology of enolic acids

A

-Used to treat arthritis
-Great joint penetration
-One of the least GI side effects
-At low doses meloxicam is cox-2 selective
-Long T1/2
-Meloxicam = 20 hours
-Piroxicam = 57 hours

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28
Q

Adverse renal effects of NSAIDs

A

-Inhibition of renal PGE2 synthesis can lead to increased sodium reabsorption, causing peripheral edema
-Higher risk with longer half-life NSAIDs
-Higher risk with long-term use

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29
Q

Adverse effects of NSAIDs

A

-Decreased renal function
-Transient inhibition of platelet aggregation (increased risk of GI bleeding)
-Inhibition of uterine motility
-GI distress/ilceration

30
Q

What is another therapeutic use of NSAIDs related to one of the adverse effects?

A

Delaying preterm labor

31
Q

Clinical pearls associate with NSAID GI distress side effect

A

-Risk increases with age
-Though less than salicylate NSAIDs
-Risk increases with long-term use
-20-50% depending on dose and duration
-Treat with misoprostol -> PGE1 analog (induces labor)

32
Q

Therapeutic use of acetaminophen

A

-Highly effective as an analgesic and antipyretic
-Limited anti-inflammatory activity

33
Q

Advantages of acetaminophen compared with NSAIDs

A

-No GI toxicity
-No effect on platelet aggregation
-No correlation with Reyes syndrome
-Liver disease patients <2 gr/day is ok

34
Q

Disadvantages of acetaminophen compared with NSAIDs

A

-Little clinically useful anti-inflammatory activity
-Acute overdose may lead to fatal hepatic necrosis
-Mechanism of action is still unclear

35
Q

Adverse effects of acetaminophen

A

-Renal toxicity, papillary necrosis (vasoconstriction by inhibition of PGE2) (more toxicity aspirin, NSAIDs)
-Dose-dependent potentially fatal hepatic necrosis
-Patients unaware that it is in multiple products

36
Q

What is the dose limit of acetaminophen before hepatic necrosis?

A

4 g/day

37
Q

What increases risk of hepatic necrosis in people who take acetaminophen?

A

High alcohol consumption (also nephrotoxic)

38
Q

Mechanism of action in alcohol induced acetaminophen toxicity

A

-Alcohol increases CYP450
-Increase in CYP450 activity leads to an increase in toxic acetaminophen metabolites

39
Q

How do you treat acetaminophen hepatotoxicity?

A

N-acetylcysteine

40
Q

Why were most selective COX-2 inhibitors withdrawn?

A

hgih chance of blood clots, strokes and heart-attacks

41
Q

Which selective COX-2 inhibitor is still available?

A

Celecoxib

42
Q

What side effects do selective COX-2 inhibitors not have?

A

Ulcers and GI bleeds

43
Q

Black box label for celecoxib

A

Serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal

44
Q

NSAID contraindications

A

-Chronic kidney disease
-Peptic ulcer disease
-History of GI bleed
-Cardiovascular risk in patients with coronary heart disease
-All NSAIDs, when used in high doses, can interfere with bone healing
-Can cause asthma exacerbations (less likely in COX-2 specific NSAIDs)

45
Q

Which NSAID has the highest cardiovascular risk?

A

Diclofenac

46
Q

Which NSAID has the lowest cardiovascular risk?

A

Naproxen

47
Q

What are the sodium channel blockers

A

-Lidocaine
-Bupivacaine
-Benzocaine

48
Q

When is lidocaine used?

A

Local analgesia, itch, burn

49
Q

Lidocaine onset

A

15 minute onset and lasts 30-120 min

50
Q

Bupivacaine duration of action

A

Longer lasting (3.5hr), epidural anesthesia

51
Q

Bupivacaine use

A

Epidural anesthesia

52
Q

Benzocaine use

A

-OTC use
-Oral ulcers
-Ear pain

53
Q

What differentiates benzocaine from the other sodium channel blockers?

A

It has an ester group which means it has a higher risk for allergies

54
Q

What is the most important sodium channel for pain?

A

NaV1.7

55
Q

Which anticonvulsants can also be used for treatment of pain?

A

-Lamotrigine
-Carbamazepine
-Oxcarbazepine

56
Q

Which tricyclic antidepressants can be used for the treatment of pain?

A

-Amitriptyline
-Nortiptyline

57
Q

SNRI mechanism of action

A

-Increase norepinephrine levels
-Can act on alpha2A-adrenergic receptors in spinal cord
-Provides analgesia

58
Q

Which SNRIs have sodium channel functionality?

A

-Duloxetine
-Venlafaxine

59
Q

What is duloxetine used for?

A

-Diabetic pain
-Fibromyalgia
-Peripheral neuropathy

60
Q

What is venlafaxine used for?

A

-Off label diabetic neuropathic pain
-Non-selective opioid effects

61
Q

Side effect of venlafaxine

A

Cardiac toxicity -> cardiac Nav channels

62
Q

What are the SNRIs lacking sodium channel functionality

A

-Milnacipran
-Tapentadol

63
Q

What is milnacipran used to treat?

A

Fibromyalgia

64
Q

What is tapentadol used to treat?

A

Diabetic neuropathic pain

65
Q

Tapentadol mechanism of action

A

NRI and MOR agonist

66
Q

What alpha2a adrenergic agonists are used to treat pain?

A

Clonidine

67
Q

Major function of calcium channel blockers as possible analgesics

A

Heart rate and blood pressure

68
Q

Which calcium channel blockers are used as analgesics?

A

-Gabapentin
-Pregabalin
-Ziconotide
-Levetiracetam

69
Q

What receptors do gabapentin and pregabalin target?

A

-Alpha2
-Delta
-Cav1, 2 selective

70
Q

Gabapentin and pregabalin clinical pearls

A

-Not metabolized, not protein bound
-No drug-drug interactions
T1/2=4-8hrs

71
Q

Ziconotide clinical pearls

A

-Snail toxin
-I.t. pump (expensive)
-Use in opioid tolerant patients

72
Q

Levtiracetam clinical pearls

A

-Well tolerated
-May cause mood symptoms

Therapeutics III (42 decks)

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