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PMCOL 200 > OTC Analgesics > Flashcards

OTC Analgesics Flashcards

1
Q

what do OTC drugs not include?

A

supplements

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2
Q

what are the 2 kinds of pharmaceutical drugs?

A

prescription and over the counter (OTC)

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3
Q

what neurons detect sensory info in the periphery?

A

primary afferents

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4
Q

what do primary afferents synapse onto?

A

secondary afferents (in spinal cord)

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5
Q

where do secondary afferents send info to?

A

brain

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6
Q

what do motor efferents do?

A

send motor info from brain to periphery (muscles)

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7
Q

what are nocireceptors?

A

specific class of primary afferents that detect pain

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8
Q

what do polymodal nociceptors detect?

A

thermal, mechanical, chemical and electrical pain

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9
Q

where are nociceptors found?

A

on every surface of our body

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10
Q

how are different stimuli detected by polymodal nociceptors?

A

specific receptors are expressed on polymodal nociceptors

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11
Q

what are transient receptor potential (TRP) channels?

A

temperature sensitive ligand-gated channels

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12
Q

what do TRPM8 and TRPV1 detect?

A

M8: <10ºC
V1: >43ºC

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13
Q

what ligands activate TRPM8 and TRPV1 receptors?

A

TRPM8: menthol (cool)
TRMV1: capsaicin (chili peppers-hot)

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14
Q

what are inflammatory molecules? what can they bind to?

A

released from immune system after injury or infection; nociceptors

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15
Q

what is arachidonic acid?

A

fa in all phospholipids of pmemb and a key inflammatory mediator (2)

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16
Q

how is arachidonic acid freed from a phospholipid molecule?

A

by phospholipase A2 enzyme

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17
Q

what 2 enzymes metabolize arachidonic acid into prostaglandins, prostacyclins and thromboxanes?

A

cyclooxygenase 1 and 2 (COX1 and COX2)

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18
Q

what enzyme metabolizes arachidonic acid into leukotrienes?

A

5-lipoxygenase

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19
Q

what do prostaglandins and leukotrienes do? (3)

A

drive inflammation (vasodilators, pyrogenic, leukotactic-attract immune cells)

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20
Q

what cells is COX1 expressed in?

A

non-inflammatory cells (blood vessels, platelets, gastric mucosa)

21
Q

what cells is COX2 expressed in?

A

inflammatory cells

22
Q

what are NSAIDS?

A

aspirin or other non-selective anti-inflammatory drugs

23
Q

what do NSAIDS do generally?

A

treat inflammation

24
Q

how do NSAIDS work?

A

block COX1 and 2 (mainly) to inhibit production of pro-inflammatory prostaglandins and leukotrienes, reducing pain

25
Q

what is the antipyretic action of NSAIDS?

A

suppression of prostaglandin synthesis in brain (stimulated by pyrogens) to reduce fever (COX 2&3)

26
Q

what are non-selective NSAIDS associated with? why?

A

gastric toxicity; inhibit COX1 in gastric mucosa

27
Q

what can chronic use of non-selective NSAIDS cause? (3)

A

gastric ulceration, upper GI bleeding and renal failure

28
Q

how can gastric toxicity from NSAIDS be bypassed?

A

using specific COX2 inhibitors (reduce inflammation in chronic inflammatory disease)

29
Q

what is a con of specific COX2 inhibitors?

A

incr risk of cardiovascular toxicity

30
Q

what does specific COX2 inhibitors reducing inflammation but not pain suggest?

A

other mechanisms drive analgesic effects beyond blocking inflammation

31
Q

what is acetaminophen? (2)

A

an analgesic and antipyretic (no anti-inflammatory effects/not an NSAID)

32
Q

how does acetaminophen work?

A

a weak COX1 and 2 inhibitor (does not work like other NSAIDS), inhibits COX3 in cerebral cortex

33
Q

what are the side effects of acetaminophen?

A

overdose w/ liver impairments leads to liver damage or death

34
Q

what was the first anesthetic drug discovered?

A

cocaine

35
Q

how did Albert Niemann discover the anesthetic properties of cocaine in the late 19th century?

A

isolated cocaine from cocoa leaves and it numbed his tongue (used as a topical anesthetic for ophthalmoplegic surgery)

36
Q

what are the 3 most common topical anesthetics?

A

procain, lidocaine and bupivacaine

37
Q

what 3 functional groups do most local anesthetic contain?

A

hydrophobic aromatic moiety (ring), linker region and subs. amine (hydrophilic)

38
Q

what does the nature of the linker region of local anesthetics determine?

A

pharmacological properties (how long, well and fast it works)

39
Q

what does the ester linkage in local anesthetics (procaine) allow for? (2)

A

easy hydrolysis by plasma esterase and a short duration of action

40
Q

how do topical anesthetics work?

A

bind reversibly to site in pore of Na channels (block ion movement) - only accessible intracellularly

41
Q

what do topical anesthetics do?

A

block active neurons (ex: nociceptors when there is pain) thus blocking all sensation/causing motor paralysis

42
Q

how does the hydrophobicity of topical anesthetics affect its action? why?

A

incr potency and duration; Na channel binding pocket is hydrophobic and must cross pmemb

43
Q

how do local anesthetics preferentially block active neurons?

A

have a high affinity for open conf. of Na channels (can bind to pore easier)

44
Q

what is capsaicin?

A

agonist for TRPV1 receptor (active ingredient in chili peppers, causes burning pain)

45
Q

what does chronic activation of TRPV1 receptors (by capsaicin) cause?

A

desensitization and loss of TRPV1+ nociceptors leading to analgesia

46
Q

what does capsaicin do in a cell? (4)

A

prolonged opening of TRPV1 channels causes influx of cations, Ca overload, mitochondrial dysfunction and nerve ending dies off

47
Q

what is capsaicin most effective at treating?

A

burning or inflammatory pain from arthritis

48
Q

what do 3 OTC treatments for pain target?

A

inflammation/fever (NSAIDS), non-specific sensory pathways (topical anesthetics), and nociceptors (capsaicin cream)

PMCOL 200 (27 decks)

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