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PMCOL 200 > OTC Digestion > Flashcards

OTC Digestion Flashcards

1
Q

what are 4 common maladies of the GI tract that can be treated w OTC drugs?

A

peptic ulcers, gastroesophageal reflux disease (GERD, heartburn), nausea/vomiting, GI motility problems (constipation, diarrhea)

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2
Q

what are acid-peptic diseases?

A

excessive acid secretion or erosion of mucosal lining of GI tract (GERD, peptic ulcers, gastritis)

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3
Q

what do drugs that treat acid-peptic diseases do? (3)

A

decr GI acidity by decr acid secretion, incr mucosal defense, or eradicate H. pylori

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4
Q

what bacteria is associated with peptic ulcers?

A

Helicobacter pylori (breaks down mucosal barrier)

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5
Q

what drugs can cause peptic ulcers?

A

NSAIDs

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6
Q

what cells in the stomach secrete H+?

A

parietal cells (in the fundus)

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7
Q

what are the 2 regions of the stomach?

A

fundus (top) and antrum (bottom)

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8
Q

what pump do parietal cells use to make the stomach acidic?

A

H+/K+ ATPase pump (H+ against conc. grad.)

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9
Q

what 3 compounds control acid production from parietal cells?

A

gastrin, histamine, acetylcholine

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10
Q

how does gastrin stimulate acid production from parietal cells?

A

G cells in antrum detect protein/a.a. and release gastrin which binds to CCK receptors on P cells

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11
Q

how does histamine stimulate acid production from parietal cells?

A

gastrin stimulates enterochromaffin cells (H cells) in fundus to release histamine which binds to H2 receptors on P cells

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12
Q

how does ACh stimulate acid production from parietal cells?

A

vagus nerve (parasymp.) stimulates postgang. neurons of ENS to release ACh which binds to muscarinic (M3) receptors on P cells

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13
Q

what is the negative feedback loop to decr acid production from P cells?

A

D cells in antrum detect low pH (<3) and release somatostatin which inhibits gastrin release from G cells

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14
Q

what are the dangers of excess acid production in stomach?

A

erodes mucosal layer and LES

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15
Q

what can lead to acid in eso. (GERD)?

A

loss of LES integrity (from pregnancy, obesity, etc.)

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16
Q

what are antacids?

A

weak bases that neutralize stomach acid by reacting w H+

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17
Q

what are antacids used to treat?

A

peptic ulcers (decr recurrence rate if taken frequently and in high doses)

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18
Q

what are 2 popular antacids?

A

magnesium hydroxide (Mg[OH]2) and aluminum hydroxide (Al[OH]3)

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19
Q

what are the diff side effects of Mg(OH)2 and Al(OH)3?

A

(both not absorbed from bowel)
Mg(OH)2: laxative effect
Al(OH)3: constipation action

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20
Q

what are proton pump inhibitors?

A

lipophilic weak bases that diffuse into P cells and inactivate H+/K+ ATPase

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21
Q

what is an example of a proton pump inhibitor?

A

Omeprezole

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22
Q

what can prolonged use of proton pump inhibitors cause?

A

hypergastrinemia (acid secretion inhibits gastrin) which can incr cancer risk

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23
Q

what is a side effect of proton pump inhibitors?

A

decr bioavailability of vit B12 or other drugs that require acidity to be absorbed

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24
Q

what are OTC drugs called that treat nausea and vomiting caused by motion sickness or other conditions?

A

antiemetics

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25
Q

what is bismuth subsalicylate?

A

antiemetic, active ingredient in Pepto Bismol

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26
Q

what happens to bismuth subsalicylate in the stomach?

A

hydrolyzes to bismuth oxychloride (salt) and salicylic acid

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27
Q

what does salicylic acid do (from bismuth subsalicylate)?

A

is absorbed by gut and acts as a COX2 inhibitor (anti-inflammatory)

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28
Q

what do bismuth salts do (from bismuth subsalicylate)?

A

not absorbed by gut but has antibacterial effects (can bind to toxins from E. Coli and H. pylori)

29
Q

what are 3 other effects of bismuth subsalicylate?

A

weak antacid properties, slows gut motility, stimulates fluid absorption

30
Q

what is dimenhydramine?

A

competitive antagonist at H1 receptor (active ingr in Gravol)

31
Q

what does dimenhydramine do?

A

block histamine activity in vestibular system

32
Q

what is the ENS?

A

intrinsic neural plexuses that control GI motility (= second brain)

33
Q

what modulates ENS?

A

CNS and ANS (para: vagus nerve and symp)

34
Q

what results from removing extrinsic ANS control from ENS?

A

disorganized gastric activity but returns to normal over time (by ENS)

35
Q

what are the 2 plexuses of the ENS?

A

myenteric and submucosal

36
Q

what does the myenteric plexus do?

A

provide motor innervation to muscular layer of gut (peristalsis)

37
Q

what does the submucosal plexus do?

A

provide secretomotor innervation to submucosa (induce gland to produce mucus)

38
Q

what type of neurons are in the ENS plexuses primarily?

A

cholinergic (also has serotonin and dopamine)

39
Q

what do pregang ANS neurons release?

A

ACh (cholinergic)

40
Q

what do postgang ANS neurons release?

A

para: ACh (cholinergic)
symp: NA (adrenergic)

41
Q

what do pregang parasym neurons innervate?

A

postgang myenteric muscarinic (ACh) neurons in eso, stomach, and upper intest

42
Q

what does ACh binding to GI smooth muscle cause?

A

contraction (motility)

43
Q

what does vagus release of ACh also stimulate?

A

acid production from parietal cells

44
Q

what do postgang symp neurons innervate?

A

adrenergic myenteric and submucosal enteric neurons in intes and colon

45
Q

what receptors does NA from postgang symp neurons bind to?

A

alpha2 adrenergic receptors

46
Q

what is effect of sympathetic innervation of the GI tract?

A

inhibition of gut motility

47
Q

what is constipation?

A

less frequent bowel movements that are more difficult to pass

48
Q

what causes contipation?

A

low fiber diet and decr water intake

49
Q

what are laxatives?

A

substances that loosen stool or stimulate bowel movements

50
Q

what are 4 kinds of laxatives?

A

bulk-forming, osmotic, lubricant and stimulant

51
Q

what do bulk-forming laxatives do?

A

draw water into stool to make them larger and easier to pass by containing plant fibers such as psyllium and methyl cellulose (must take w/ water)

52
Q

what do osmotic laxatives do?

A

draw fluid into bowel from nearby tissues by containing polyethylene and Mg

53
Q

what do lubricant laxatives do?

A

coat surface of stool or anus to make it easier for stools to pass by containing glycerin suppositories (mineral oil)

54
Q

what do stimulant laxatives do?

A

cause bowels to squeeze stool out by containing senna and bisacodyl

55
Q

what is diarrhea?

A

loose, watery stool as colon doesn’t absorb fluid from food

56
Q

what causes dairrhea?

A

bacterial or viral infections

57
Q

what are 2 common OTC treatments for diarrhea?

A

loperamide and bismuth subsalicylate

58
Q

what is loperamide?

A

full mu opioid agonist

59
Q

where are mu opioid receptors in GI tract?

A

submucosal and myenteric (mainly) plexus

60
Q

what are mu opioid receptors?

A

Gi GPCRs

61
Q

what does loperamide do?

A

binds to mu opioid receptors to slow peristalsis and inhibit secretion of water and mucus

62
Q

what is different btwn loperamide and other opioid agonists?

A

has weak analgesic effects (not rewarding/addicting, no resp depression)

63
Q

why can’t loperamide cause any physiological effects in the brain?

A

is a substrate for P-gp (permeability-glycoprotein), which is a pump in the endothelial cells of the BBB that actively removes drugs from the brain

64
Q

what drugs interfere with P-gp?

A

tricyclic antidepressants (amitriptyline)

65
Q

what are some adverse effects of taking amitriptyline with loperamide?

A

respiratory depression and abuse as amitriptyline blocks P-gp allowing [loperamide] in brain to incr

66
Q

why are some OTC drugs for common digestive problems counterproductive?

A

bacterial or viral infections should be removed through vomiting/anal/urethral excretion

67
Q

Mucosal surface cells secrete mucous that provides a barrier btwn __________ and __________

A

Mucosa (top layer of stomach) and lumen

68
Q

what kind of receptors are alpha2 adrenergic receptors?

A

Gi GPCR

PMCOL 200 (27 decks)

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