Lecture 15 - OTC Digestion Flashcards

1
Q

there are a number of common maladies that can afflict the GI tract, including:

A
  • peptic ulcers
  • gastroesophageal reflux disease (GERD)
  • nausea and vomiting
  • GI motility prblems (constipation and diarrhea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

a group of disorders involving either excessive acid secretion or erosion of the mucosal lining of the GI tract (particularly the stomach)

A

acid-peptic diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

the stomach is divided into the:

A

antrum (bottom) and fundus (top)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cells in the fundus of the stomach responsible for acid secretion (H+ ions)

A

parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

moves acid from the parietal cell into the gastric lumen

A

the H+/K+ ATPase proton pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cells in the antrum that respond to intraluminal dietary peptides to release gastrin

A

G-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

gastrin binds to:

A

cholecystokinin (CCK) receptors on parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

gastrin stimulates ______ to release ______ which binds to ______ on parietal cells

A

enterochromaffin cells (H cells), histamine, histamine (H2) receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

the vagus nerve stimulates postganglionic neurons of the enteric nervous system to release ______, which binds to ______ on parietal cells

A

acetylcholine, muscarinic receptors (M3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cells which release somatostatin and inhibit gastrin release from G cells

A

D cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what causes D cells to release somatostatin?

A

an increase in intraluminal acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what effect does excess acid production have on the stomach?

A

it erodes the mucosal barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

loss of sphincter integrity can lead to:

A

acid in the esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

most OTC treatment for peptic ulcer disease are focused on:

A

controlling acid production in the stomach (antacids and proton pump inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

weak bases that neutralize stomach acid by reacting with protons in the lumen of the gut

A

antacids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

popular antacids include:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when used regularly, in the large doses required to raise stomach pH, antacids reduce the:

A

recurrence rate of peptic ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

magnesium hydroxide has a strong:

A

laxative effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

aluminium hydroxide has a:

A

constipating action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

lipophilic weak bases that diffuse into the parietal cell and inactivate the H+/K+ ATPase transporter

A

proton pump inhibitors (ex: Omeprazole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

prolonged use of proton pump inhibitors can lead to:

A

hypergastrinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

proton pump inhibitors will decrease the bioavailability of:

A

vitamin B12 and certain drugs that require acidity for their absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

nausea and vomiting is an important defence against:

A

food poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

can help when dealing with nausea and vomiting caused by motion sickness caused by other conditions

A

OTC anti-emetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
the active ingredient in PeptoBismol
bismuth subsalicylate
26
bismuth subsalicylate hydrolyzes in the gut to:
bismuth oxychloride and salicylic acid
27
salicylic acid is absorbed in the gut and:
inhibits prostaglandin synthesis (anti-inflammatory properties)
28
bismuth salts are not absorbed from the gut, but have:
bactericidal effects
29
dimenhydrinate (gravol) is a theoclate salt composed of:
diphenhydramine and 8-chlorotheophylline
30
dimenhydrinate acts as a ______ at the ______ receptor
competitive antagonist/inverse agonist, H1
31
what is the effect of 8-chlorotheophylline?
reduces potency of dimenhydramine
32
what is the effect of dimenhydrinate?
blocks histamine activity in the vestibular system, but less sedation than diphenhydramine (less potent)
33
GI motility is controlled by:
intrinsic neural plexuses (enteric nervous system)
34
removing extrinsic autonomic control of the GI tract results in:
disorganized gastric activity (nausea and vomiting)
35
the enteric nervous system is also known as the:
"second brain"
36
enteric neurons are organized into a:
nerve plexus
37
provides motor innervation to the muscular layer of the gut (mediates peristalsis)
myenteric plexus
38
provides secretomotor (inducing a gland to secrete a substance) innervation to the gut mucosa
submucosal plexus
39
the neurons of the myenteric plexus and submucosal plexus are predominantly:
cholinergic
40
all preganglionic neurons in the autonomic nervous system are:
cholinergic
41
postganglionic parasympathetic neurons are:
cholinergic
42
postganglionic sympathetic neurons are:
adrenergic
43
preganglionic parasympathetic neurons release acetylcholine onto postganglionic neurons within:
myenteric neurons within the stomach and upper intestine
44
binds to muscarinic receptors (M2) on GI smooth muscle leading to contraction
acetylcholine
45
acetylcholine stimulates the production of:
acid from parietal cells
46
adrenergic postganglionic sympathetic fibers innervate:
enteric neurons (both myenetric and submucosal plexus)
47
what effect do adrenergic postganglionic sympathetic fibers have on gut motility?
inhibits gut motility
48
occurs when bowel movements become less frequent and stools are difficult to pass
constipation
49
substances that loosen stool or stimulate bowel movement
laxatives
50
what are the four major kinds of laxatives?
- bulk forming laxatives - osmotic laxatives - lubricant laxative - stimulate laxatives
51
contain naturally occuring plant fiber like psyllium and methyl cellulose that draw water into the stool to make them larger and easier to pass (must drink lots of water while taking)
bulk forming laxatives
52
contain ingredients like polyethylene glycol or magnesium that draw fluid into the bowel from nearby tissue
osmotic laxatives
53
glycerin suppositories (mineral oil) that coat the surface of stools or anus to make it easier for stools to pass
lubricant laxatives
54
contain ingredients like senna and bisacodyl that cause the bowels to squeeze out the stools
stimulant laxatives
55
loose, watery stool that occurs when the colon is unable to adequately absorb the liquid from ingested food/fluid
diarrhea
56
diarrhea is usually caused by:
a bacterial or viral infection
57
what is the most common OTC treatment for diarrhea?
loperamide and bismuth subsalicylate
58
loperamide is a:
mu opioid agonist
59
where in the GI tract are mu opioid receptors located?
on the myenteric plexus (controls peristalsis)
60
true or false: loperamide has weak analgesic activity despite being a full agonist at the mu opioid receptor
true
61
where is loperamide distributed to?
loperamide is widely distributed across the body, including the brain
62
what makes lopermaide different from codeine?
less analgesia, less respiratory depression, no effect on cough
63
loperamide is a substrate for:
P-glycoprotein (P-gp)
64
where is P-glycoprotein (P-gp) located?
endothelial cells at the blood brain barrier (actively pumps drugs out of the brain)
65
why isn't loperamide rewarding/addictive like morphine?
loperamide brain levels are kept low by P-gp activity
66
P-glycoprotein (P-gp) is inhibited by:
tricyclic antidepressants (amitriptyline)
67
blockin P-glycoprotein (P-gp) will increase brain concentration of:
loperamide