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23 spring: pharm > Test 2: lecture 28 GI part 1 antacids > Flashcards

Test 2: lecture 28 GI part 1 antacids Flashcards

1
Q

Reflexive relaxation or accommodation — stomach muscle activity during filling phase

A

inhibits

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2
Q

what part of the stomach breaks food into 2 mm pieces

A

antrum (pyloric pump)

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3
Q

slow constrictor waves in the stomach is controlled by — nerve

A

vagal

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4
Q

superficial epithelial cells of the stomach make

A

mucin and bicarb

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5
Q

mucous neck cells of the stomach make

A

mucin

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6
Q

parietal cells of the stomach make

A

acid and intrinsic factor

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7
Q

chief cells make

A

pepsinogen

which is turned into pepsin

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8
Q

Enterochromaffin-like (ECL) cells make

A

histamine

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9
Q

what is intrinsic factor

A

A glycoprotein required for cobalamin (Vitamin B12) absorption in the ileum

made by parietal cells in the stomach

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10
Q

Pepsin is an enzyme that preferentially cleaves at — amino acids such as phenylalanine and tyrosine

A

carboxylic groups of aromatic

breaks up proteins

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11
Q

When pH — ,pepsinogen is activated to form the active enzyme pepsin

A

is less then 3

feed forward cycle, pepsin can make more pepsin

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12
Q

Pepsin preferentially cleaves at carboxylic groups of aromatic amino acids such as —

A

phenylalanine and tyrosine

cuts proteins into smaller pieces

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13
Q

Gastric acid lowers the pH in the proximal duodenum, enhancing the solubility and uptake of dietary —

A

iron

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14
Q

3 functions of gastric acid

A

protein digestion
iron absorption
inactivation of bacteria, viruses and parasites

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15
Q

CNS and stretch if stomach cells will cause release of — by — acting on M3 receptors to cause a — in acid secretion

A

ACh
vagus
increase

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16
Q

ACh and gastrin if stomach cells will cause release of — by — acting on H2 receptors to cause a — in acid secretion

A

histamine
ECL cells
increase

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17
Q

ACh, peptides and amino acids on stomach cells will cause release of — by — acting on CCKb receptors to cause a — in acid secretion

A

Gastrin
G cells
increase

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18
Q

release of — by many cell types acting on EP2 receptors to cause a — in acid secretion

A

prostaglandin (PGE2)
decrease

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19
Q

pH of the stomach will cause release of — by — acting on SST receptors to cause a — in acid secretion

A

somatostatin
D cells (antrum and corpus)
decrease

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20
Q

decrease pH in the duodenum will cause release of — by — acting on SCTR receptors to cause a — in acid secretion

A

secretin
S cells (small intestine)
decrease

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21
Q

Fatty acids and amino acids on stomach cells will cause release of — by — acting on CCKb receptors to cause a — in acid secretion

A

Choleystokinin (CCK)
I cells (small intestine)
decrease

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22
Q

direct stimulation of gastric acid secretion

A

acts directly on parietal cells of stomach to secrete acid

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23
Q

indirect stimulation of gastric acid secretion

A

Signals or transmitters stimulate other cells that release transmitters/hormones that then stimulate parietal cells to secrete acid

increased gastrin, and ACh from ENS will trigger ECL to release histamine which cause parietal cell to release acid

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24
Q

3 ways of direct stimulation of gastric acid secretion

A

enteric ACh on M3 receptors

histamine on H2 receptors

gastrin on CCKb receptors

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25
2 ways of indirect stimulation of gastric acid secretion
gastrin on CCKb receptors on ECL cause release of histamine ENS release ACh which binds to M3 receptors on ECL cell, ECL releases histamine histamine binds to H2 receptor on parietal call
26
cephalic phase of gastric activity is contolled by
the brain (CNS)
27
gastric phase of gastric activity is contolled by
stomach
28
intestinal phase of gastric activity is contolled by
intestine
29
3 phases of gastric activity
cephalic gastric intestinal
30
chief cells make
pepsinogen
31
Preganglionic parasympathetic nerve efferent impulses activated by cephalic phase are carried by the vagus nerves to the stomach where enteric plexus --- neurons are activated
postganglionic
32
how does gastrin stimulate release of histamine by the ECL cell?
G cells make gastrin gastrin **leaves stomach**, moves through **circulation** then comes back and causes ECL to release histamine
33
how does cephalic phase of gastric activity work
34
Distention of stomach stimulates mechanoreceptors (stretch receptors) and activates a --- reflex.
parasympathetic Activation of stretch receptors initiates **afferent** nerve impulse along vagal nerve back to **medulla oblongata in CNS**
35
Medulla oblongata processes the stretch information from the stomach and initiates efferent nerve impulses that travel back down vagus nerves to stimulate ---
**parietal cells** → acid **chief cells** → pepsinogen **ECL cells** → histamine
36
Stomach distention also activates local reflexes --- stomach secretions
increasing Enteric nervous system is **quasi-autonomous** can partially act without CNS
37
Enteric nervous system is --- can partially act without CNS
**quasi-autonomous**
38
During gastric phase, local distention will cause G cells to release Gastrin which travels via circulation back to stomach to cause ---
parietal cells →acid ## Footnote gastric phase of gastric activity
39
simply the gastric phase of gastric activity is controlled by distention of the stomach which causes ---
**PARA** to brain by **vagus nerve** → causes **increased secretions** of parietal (acid), chief (pepsingogen) and ECL (histamine) **local stretching** causes **gastrin** release by G cells, which travel through circulation to also cause **parietal cells** to secrete more acid
40
Chyme (partly digested food mash) in the duodenum with pH--- and/or containing digested fat products (lipids) --- gastric secretions
< 2 inhibits
41
three ways chyme with high fat and ph < 2 cause decrease in gastric secretions
(1) Chemoreceptors in duodenum are activated by H+ (Low pH) or by lipids initiates afferent nerve impulses along vagus nerve back to medulla oblongata * This impulse **blocks the generation of an efferent parasympathetic** impulses and thereby decreases gastric secretions (2) **Local reflexes** (involving ENS, not involving CNS) are activated by H+ (Low pH) and by lipids * These local reflexes act to inhibit further gastric secretions (3) The duodenum produces and releases the **peptides secretin and cholecystokinin (CCK)** * Secretin and CCK act to inhibit further gastric secretions
42
Chemoreceptors in duodenum are activated by H+ (Low pH) or by lipids initiates --- nerve impulses along vagus nerve back to medulla oblongat
afferent will block efferent PARA to stomach = decreases gastric secretions ## Footnote intestinal phase of gastric phase
43
Secretin and CCK will --- gastric secretions
inhibit
44
explain
intestinal phase of gastric activity
45
gastric phase
46
cephalic phase
47
NSAIDs are non-selective inhibitors of ---
COX 1 and COX2 prevents the formation of prostaglandins Cox1 inhibition leads to decrease in GI protection→ **gastric ulcers**
48
--- is a selective Cox2 inhibitor used in dogs
deracoxib (deramaxx) Large doses can cause COX-1 inhibition with concomitant gastric issues
49
--- is a first class cox 2 inhibitor that was withdrawn due to MI in humans
rofecoxib (vioxx) caused increased clotting and strokes
50
--- is a nonselective COX 1 and 2 inhibitor in humans, but a selective COX 2 inhibitor in dogs
carprofen (rimadyl) High doses can still cause COX-1 inhibition with concomitant gastric issues in dogs
51
--- secretions Helps buffer (neutralize) acid in layer adjacent to mucous cells
bicarb
52
Mucus acts as a barrier to --- and also for pepsins, and traps --- solution
H+ alkaline
53
how can you manage gastric ulcers through diet
(1) Provide adequate nutrition during ulcer (ulcer weight loss ) (2) Maintain continuous neutralization of gastric acid (3) Minimize acid secretions in stomach (4) Reduce mechanical, thermal and chemical irritation to the gastric mucosa
54
Sodium Bicarbonate (Alka-Seltzer) side effects
water soluble, it can be absorbed systemically can cause **alkalosis** (increase pH of blood) which can lead to **kidney stones** **belching** ## Footnote **antiacid:** sodium bicarbonate (alka seltzer) Calcium Carbonate (Tums) Magnesium Hydroxide (“Milk of Magnesia”) Aluminum Hydroxide (Maalox) magaldrate (Riopan)
55
Calcium Carbonate (Tums) side effects
**constipation** increased Calcium can cause **kidney stones** ## Footnote **antiacid:** sodium bicarbonate (alka seltzer) Calcium Carbonate (Tums) Magnesium Hydroxide (“Milk of Magnesia”) Aluminum Hydroxide (Maalox) magaldrate (Riopan)
56
Magnesium Hydroxide (“Milk of Magnesia”) side effects
cause diarrhea systemically absorbed pts with CKD: hypermagnesemia → cardiac complications and CNS depression ## Footnote **antiacid:** sodium bicarbonate (alka seltzer) Calcium Carbonate (Tums) Magnesium Hydroxide (“Milk of Magnesia”) Aluminum Hydroxide (Maalox) magaldrate (Riopan)
57
Aluminum Hydroxide (Maalox) side effects
**constipation** form insoluble Al-Phosphate complexes leading to **hypophosphatemia** decreases stomach acids and inhibits pepsin and increases mucus secretions ## Footnote **antiacid:** sodium bicarbonate (alka seltzer) Calcium Carbonate (Tums) Magnesium Hydroxide (“Milk of Magnesia”) Aluminum Hydroxide (Maalox) magaldrate (Riopan)
58
magaldrate (Riopan) side effects
none Contain mixture of Aluminum ( constipation) and Magnesium(diarrhea) -based antacids → offset each other ## Footnote **antiacid:** sodium bicarbonate (alka seltzer) Calcium Carbonate (Tums) Magnesium Hydroxide (“Milk of Magnesia”) Aluminum Hydroxide (Maalox) magaldrate (Riopan)
59
--- neutralize acids in the gastric lumen
antacids Rapid onset of action (within 30 min) but short duration of action (2 - 3 hours) ## Footnote **antiacid:** sodium bicarbonate (alka seltzer) Calcium Carbonate (Tums) Magnesium Hydroxide (“Milk of Magnesia”) Aluminum Hydroxide (Maalox) magaldrate (Riopan)
60
antacids have --- onset and --- duration
Rapid onset of action (within 30 min) but short duration of action (2 - 3 hours) ## Footnote **antiacid:** sodium bicarbonate (alka seltzer) Calcium Carbonate (Tums) Magnesium Hydroxide (“Milk of Magnesia”) Aluminum Hydroxide (Maalox) magaldrate (Riopan)
61
what is acid rebound phenomenon
If stomach pH goes above pH = 4 the stomach is stimulated to secrete acid to maintain pH lower then 4 magnesium antacids can increase pH=7 aluminum salts (maalox) do not increase pH if you stop taking magnesium, the stomach will be making to much acid→ need to stop med slowly to stop rebound
62
what type of antacid can cause acid rebound phenomenon
Mg2+ ions salts CAN raise gastric pH to pH = 7 and therefore can stimulate compensatory homeostatic HCl secretion to try to keep pH < 4 **need to stop Mg slowly to prevent rebound** Aluminum salts DO NOT raise gastric pH > 4
63
magaldrate (Riopan) cause
no symptoms contains both aluminum (constipation) and magnesium (diarrhea) symptoms balance each other out ## Footnote **antiacid:** sodium bicarbonate (alka seltzer) Calcium Carbonate (Tums) Magnesium Hydroxide (“Milk of Magnesia”) Aluminum Hydroxide (Maalox) magaldrate (Riopan)

23 spring: pharm (46 decks)

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