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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
Q

2 ways of indirect stimulation of gastric acid secretion

A

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

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26
Q

cephalic phase of gastric activity is contolled by

A

the brain (CNS)

27
Q

gastric phase of gastric activity is contolled by

A

stomach

28
Q

intestinal phase of gastric activity is contolled by

A

intestine

29
Q

3 phases of gastric activity

A

cephalic
gastric
intestinal

30
Q

chief cells make

A

pepsinogen

31
Q

Preganglionic parasympathetic nerve efferent impulses activated by cephalic phase are carried by the vagus nerves to the stomach where enteric plexus — neurons are activated

A

postganglionic

32
Q

how does gastrin stimulate release of histamine by the ECL cell?

A

G cells make gastrin
gastrin leaves stomach, moves through circulation
then comes back and causes ECL to release histamine

33
Q

how does cephalic phase of gastric activity work

A
34
Q

Distention of stomach stimulates mechanoreceptors (stretch receptors) and activates a
— reflex.

A

parasympathetic

Activation of stretch receptors initiates afferent nerve impulse along vagal nerve back to medulla oblongata in CNS

35
Q

Medulla oblongata processes the stretch information from the stomach and initiates efferent nerve impulses that travel back down vagus nerves to stimulate —

A

parietal cells → acid
chief cells → pepsinogen
ECL cells → histamine

36
Q

Stomach distention also activates local reflexes — stomach secretions

A

increasing

Enteric nervous system is quasi-autonomous can partially act without CNS

37
Q

Enteric nervous system is — can partially act without CNS

A

quasi-autonomous

38
Q

During gastric phase, local distention will cause G cells to release Gastrin which travels via circulation back to stomach to cause —

A

parietal cells →acid

gastric phase of gastric activity

39
Q

simply the gastric phase of gastric activity is controlled by distention of the stomach which causes —

A

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
Q

Chyme (partly digested food mash) in the duodenum with pH— and/or containing digested fat products (lipids) — gastric secretions

A

< 2

inhibits

41
Q

three ways chyme with high fat and ph < 2 cause decrease in gastric secretions

A

(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
Q

Chemoreceptors in duodenum are activated by H+ (Low pH) or by lipids initiates — nerve impulses along vagus nerve back to medulla oblongat

A

afferent

will block efferent PARA to stomach = decreases gastric secretions

intestinal phase of gastric phase

43
Q

Secretin and CCK will — gastric secretions

A

inhibit

44
Q

explain

A

intestinal phase of gastric activity

45
Q
A

gastric phase

46
Q
A

cephalic phase

47
Q

NSAIDs are non-selective inhibitors of —

A

COX 1 and COX2

prevents the formation of prostaglandins

Cox1 inhibition leads to decrease in GI protection→ gastric ulcers

48
Q

— is a selective Cox2 inhibitor used in dogs

A

deracoxib (deramaxx)

Large doses can cause COX-1 inhibition with concomitant gastric issues

49
Q

— is a first class cox 2 inhibitor that was withdrawn due to MI in humans

A

rofecoxib (vioxx)

caused increased clotting and strokes

50
Q

— is a nonselective COX 1 and 2 inhibitor in humans, but a selective COX 2 inhibitor in dogs

A

carprofen (rimadyl)

High doses can still cause COX-1 inhibition with concomitant gastric issues in dogs

51
Q

— secretions Helps buffer (neutralize) acid in layer adjacent to mucous cells

A

bicarb

52
Q

Mucus acts as a barrier to — and also for pepsins, and traps — solution

A

H+

alkaline

53
Q

how can you manage gastric ulcers through diet

A

(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
Q

Sodium Bicarbonate (Alka-Seltzer)
side effects

A

water soluble, it can be absorbed systemically

can cause alkalosis (increase pH of blood) which can lead to kidney stones
belching

antiacid:
sodium bicarbonate (alka seltzer)
Calcium Carbonate (Tums)
Magnesium Hydroxide (“Milk of Magnesia”)
Aluminum Hydroxide (Maalox)
magaldrate (Riopan)

55
Q

Calcium Carbonate (Tums) side effects

A

constipation
increased Calcium can cause kidney stones

antiacid:
sodium bicarbonate (alka seltzer)
Calcium Carbonate (Tums)
Magnesium Hydroxide (“Milk of Magnesia”)
Aluminum Hydroxide (Maalox)
magaldrate (Riopan)

56
Q

Magnesium Hydroxide (“Milk of Magnesia”) side effects

A

cause diarrhea

systemically absorbed

pts with CKD:
hypermagnesemia → cardiac complications and CNS depression

antiacid:
sodium bicarbonate (alka seltzer)
Calcium Carbonate (Tums)
Magnesium Hydroxide (“Milk of Magnesia”)
Aluminum Hydroxide (Maalox)
magaldrate (Riopan)

57
Q

Aluminum Hydroxide (Maalox) side effects

A

constipation

form insoluble Al-Phosphate complexes leading
to hypophosphatemia

decreases stomach acids and inhibits pepsin and increases mucus secretions

antiacid:
sodium bicarbonate (alka seltzer)
Calcium Carbonate (Tums)
Magnesium Hydroxide (“Milk of Magnesia”)
Aluminum Hydroxide (Maalox)
magaldrate (Riopan)

58
Q

magaldrate (Riopan) side effects

A

none

Contain mixture of Aluminum ( constipation) and Magnesium(diarrhea) -based antacids → offset each other

antiacid:
sodium bicarbonate (alka seltzer)
Calcium Carbonate (Tums)
Magnesium Hydroxide (“Milk of Magnesia”)
Aluminum Hydroxide (Maalox)
magaldrate (Riopan)

59
Q

— neutralize acids in the gastric lumen

A

antacids

Rapid onset of action (within 30 min) but short duration of action (2 - 3 hours)

antiacid:
sodium bicarbonate (alka seltzer)
Calcium Carbonate (Tums)
Magnesium Hydroxide (“Milk of Magnesia”)
Aluminum Hydroxide (Maalox)
magaldrate (Riopan)

60
Q

antacids have — onset and — duration

A

Rapid onset of action (within 30 min) but short duration of action (2 - 3 hours)

antiacid:
sodium bicarbonate (alka seltzer)
Calcium Carbonate (Tums)
Magnesium Hydroxide (“Milk of Magnesia”)
Aluminum Hydroxide (Maalox)
magaldrate (Riopan)

61
Q

what is acid rebound phenomenon

A

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
Q

what type of antacid can cause acid rebound phenomenon

A

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
Q

magaldrate (Riopan) cause

A

no symptoms

contains both aluminum (constipation) and magnesium (diarrhea)

symptoms balance each other out

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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