Test 2: lecture 28 GI part 1 antacids Flashcards
Reflexive relaxation or accommodation — stomach muscle activity during filling phase
inhibits
what part of the stomach breaks food into 2 mm pieces
antrum (pyloric pump)
slow constrictor waves in the stomach is controlled by — nerve
vagal
superficial epithelial cells of the stomach make
mucin and bicarb
mucous neck cells of the stomach make
mucin
parietal cells of the stomach make
acid and intrinsic factor
chief cells make
pepsinogen
which is turned into pepsin
Enterochromaffin-like (ECL) cells make
histamine
what is intrinsic factor
A glycoprotein required for cobalamin (Vitamin B12) absorption in the ileum
made by parietal cells in the stomach
Pepsin is an enzyme that preferentially cleaves at — amino acids such as phenylalanine and tyrosine
carboxylic groups of aromatic
breaks up proteins
When pH — ,pepsinogen is activated to form the active enzyme pepsin
is less then 3
feed forward cycle, pepsin can make more pepsin
Pepsin preferentially cleaves at carboxylic groups of aromatic amino acids such as —
phenylalanine and tyrosine
cuts proteins into smaller pieces
Gastric acid lowers the pH in the proximal duodenum, enhancing the solubility and uptake of dietary —
iron
3 functions of gastric acid
protein digestion
iron absorption
inactivation of bacteria, viruses and parasites
CNS and stretch if stomach cells will cause release of — by — acting on M3 receptors to cause a — in acid secretion
ACh
vagus
increase
ACh and gastrin if stomach cells will cause release of — by — acting on H2 receptors to cause a — in acid secretion
histamine
ECL cells
increase
ACh, peptides and amino acids on stomach cells will cause release of — by — acting on CCKb receptors to cause a — in acid secretion
Gastrin
G cells
increase
release of — by many cell types acting on EP2 receptors to cause a — in acid secretion
prostaglandin (PGE2)
decrease
pH of the stomach will cause release of — by — acting on SST receptors to cause a — in acid secretion
somatostatin
D cells (antrum and corpus)
decrease
decrease pH in the duodenum will cause release of — by — acting on SCTR receptors to cause a — in acid secretion
secretin
S cells (small intestine)
decrease
Fatty acids and amino acids on stomach cells will cause release of — by — acting on CCKb receptors to cause a — in acid secretion
Choleystokinin (CCK)
I cells (small intestine)
decrease
direct stimulation of gastric acid secretion
acts directly on parietal cells of stomach to secrete acid
indirect stimulation of gastric acid secretion
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
3 ways of direct stimulation of gastric acid secretion
enteric ACh on M3 receptors
histamine on H2 receptors
gastrin on CCKb receptors
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
cephalic phase of gastric activity is contolled by
the brain (CNS)
gastric phase of gastric activity is contolled by
stomach
intestinal phase of gastric activity is contolled by
intestine
3 phases of gastric activity
cephalic
gastric
intestinal
chief cells make
pepsinogen
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
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
how does cephalic phase of gastric activity work
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
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
Stomach distention also activates local reflexes — stomach secretions
increasing
Enteric nervous system is quasi-autonomous can partially act without CNS
Enteric nervous system is — can partially act without CNS
quasi-autonomous
During gastric phase, local distention will cause G cells to release Gastrin which travels via circulation back to stomach to cause —
parietal cells →acid
gastric phase of gastric activity
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
Chyme (partly digested food mash) in the duodenum with pH— and/or containing digested fat products (lipids) — gastric secretions
< 2
inhibits
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
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
intestinal phase of gastric phase
Secretin and CCK will — gastric secretions
inhibit
explain
intestinal phase of gastric activity
gastric phase
cephalic phase
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
— is a selective Cox2 inhibitor used in dogs
deracoxib (deramaxx)
Large doses can cause COX-1 inhibition with concomitant gastric issues
— is a first class cox 2 inhibitor that was withdrawn due to MI in humans
rofecoxib (vioxx)
caused increased clotting and strokes
— 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
— secretions Helps buffer (neutralize) acid in layer adjacent to mucous cells
bicarb
Mucus acts as a barrier to — and also for pepsins, and traps — solution
H+
alkaline
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
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
antiacid:
sodium bicarbonate (alka seltzer)
Calcium Carbonate (Tums)
Magnesium Hydroxide (“Milk of Magnesia”)
Aluminum Hydroxide (Maalox)
magaldrate (Riopan)
Calcium Carbonate (Tums) side effects
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)
Magnesium Hydroxide (“Milk of Magnesia”) side effects
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)
Aluminum Hydroxide (Maalox) side effects
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)
magaldrate (Riopan) side effects
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)
— neutralize acids in the gastric lumen
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)
antacids have — onset and — duration
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)
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
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
magaldrate (Riopan) cause
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)
