GI 7

Question 1

Ptyalin

Answer 1

A salivary amylase, breaks down carbs in the mouth

Question 2

Vitamin B12 absorption

Answer 2

Requires intrinsic factor from the parietal cells of the stomach, basically keeps it alive until it reaches the distal ileum, then its officially taken up into blood
Failure in this process results in pernicious anemia, a macrocytic anemia from not having the material to properly shrink down and mature into an RBC

Question 3

Where is mucin secreted

Answer 3

Secreted by all surface epithelial cells as well as all mucous neck cells
This includes regions like the cardia and pyloric gland as well as the fundus and corpus (aka body)

Question 4

How does the mucin protect the surface epithelial layer in the stomach lining

Answer 4

Surface epithelial cells are the most apical, no cell layers on top, next protective layer is the bicarbonate rich mucous gel layer, forms a matrix like layer, protects the cells from the acidity my simulating an environments of pH 7

Question 5

Muci-bicarb layer

Answer 5

Includes the mucous layer over the epithelial cells and the bicarbonate layer is for further neutralization and protection, H ions wont reach the epithelia
Note that the bicarb is secreted from the epithelial cells themselves, its teh reason the pH near epithelia is 7 and not 2

Question 6

GMB

Answer 6

Gastric mucosal barrier
Specialization of the epithelial cells of the stomach, basically extra protection by having more tight junctions near the apical surface to prevent acid from seeping through

Question 7

What protects the gastric mucosa (names no details)

Answer 7

The gastric mucosal barrier
The muci-bicarb layer
In a way the rapid cell turnover too

Question 8

Re-epithelialization

Answer 8

The process of replacing old/damaged gastric epithelia, high turn over rate due to the whole acid thing
Applies to whole GIT really

Question 9

What factors can contribute to ulcers

Answer 9

Ulcers are damage to the stomach or duodenum lining leading to pain and stuff
Weak barrier normal HCl: can be caused by drugs like aspirin or NSAIDs, or a bacteria like helicobactor pylori
Normal barrier high HCl: excessive HCl output, can be caused by a gastrin-producing tumor (would increase HCl output)

Question 10

Phases of gastric secretion (brief)

Answer 10

Cephalic: you see or taste food and that leads to gastric secretion in anticipation of this incoming food
Gastric: food reaches the level of the stomach and gastric secretions are triggered
Intestinal: food reaches intestine and we get secretions in stomach
All intertwined

Question 11

Neural regulation of secretion at the level of the stomach

Answer 11

Stimulus hits, stretch usually, those afférents will trigger excitatory efférents that will release ACh on secretory cells, triggering teh release of whatever substance it has (pepsinogen, acid, mucous, wtv)
Parasympathetic activation also gives us vasodilation and sym gives vasoconstriction
Vagal vagal variations are also possible, where ANS is involved to strengthen response

Question 12

Secretagogues

Answer 12

Amino acids or partially digested proteins that act of G cells, gastrin releasing cells, which will in response increase HCl secretions
Note gastrin is a hormone, gut derived, so this is an example of hormonal control

Question 13

Gastrin

Answer 13

A peptide hormone secreted by the G-cells in the antrum of the stomach, increase HCl levels
Secreted in response secretogogues, local enteric reflexes and even vagal vagal reflexes

Question 14

Cephalic phase and gastrin

Answer 14

Cephalic phase can trigger the release of gastrin via ANS channels, comes down to ENS level, activates the secretory cells but also the G cells

Question 15

Self regulating gastrin release

Answer 15

Presence of secretogogues leads to G cell activation, increases the release of gastrin, incoming food signals ANS which activates G cells as well as the other secretory cells, giving more HCl, gastrin circulates and further activates the secretory cells including parietal cells, we make more HCl which activates pepsinogen for protein degradation which makes more secretogogues, and its seems to be positive feedback from there
But theres a regulator that stops the release of gastrin as soon as it senses a pH less than 2, a cell that releases somatostatin, released in response to low pH, inhibits G cell and parietal cells

Question 16

Trophic effect fo gastrin

Answer 16

Gastrin not only increases HCl production, but also mediates a trophic effect where it stimulates the production of more parietal cells
It’s its way of increasing HCl levels, not only by more HCl per capita but by more cells secreting it all togetehr

Question 17

Histamine and HCl secretion

Answer 17

There’s lots of histamine in gastric mucosa and it increase HCl production, so high levels of histamine like from an allergic reaction can stimulate HCl production

Question 18

Common mediator hypothesis

Answer 18

Hypothesis that histamine was the main stimulator of HCl production and that gastrin and ACh were just making more histamine, not accurate

Question 19

Permissive hypothesis about histamine and gastrin

Answer 19

For this theory gastrin, Ach and histamine all have different receptors on parietal cells and can act independently but they work synergistically, as in where one is bound the others are more likely to bind, same is true if its blocked

Question 20

Why are H2 blockers effective for ulcer treatment

Answer 20

H2 is the receptor for histamine, if you block it theres already less HCl being produced but because they work synergistically the parietal cells will also be less likely to bind gastrin and Ach, so overall greatly reduces HCl secretions, will lower acid production and help ulcer

Question 21

Duodenal excitatory component of the intestinal phase

Answer 21

Part where secretogogues reach the duodenum, theres a brief excitatory part where we get more gastrin secreted in response, burst of HCl, but then we calm down, effects will shift to be inhibitory
What will stimulate inhibitory effect: acidity of chyme, stretch, high osmolarity (if its hypertonic), chemical composition, etc, and this inhibitory effect will slow gastric emptying

Question 22

What are the pre-intestinal conditions of the chyme

Answer 22

Carbs may be somewhat broken down by ptyalin (amylase), lipids may be somewhere broken down by lipase (secreted in saliva), proteins may be somewhat broken down from pepsin and HCl
Acidic like pH2 and hypertonic (will draw fluid to it)
Overall still a lot of work to do

Question 23

Ampulla of vater

Answer 23

The result of the joining of pancreatic duct and the common bile duct (note that the common bile duct is the joining of the liver and gallbladder ducts)
Leads to the sphincter of Oddi, which when open will allow these secretions to flood over food and continue its breakdown