Exam 4- Gastric Secretion & Motility

Question 1

What are the 3 layers of the stomach?

Answer 1

Longitudinal layer, circular layer, inner oblique layer

Question 2

Is the muscle wall of the stomach thickest in the proximal or distal end?

Answer 2

Distal

Question 3

The orad stomach enlarges with increased content volume but there is little change in what?

Answer 3

Pressure

Question 4

Distension of the lower esophagus relaxes the LES and orad stomach, a process known as what?

Answer 4

Receptive relaxation

Question 5

Gastric stretch recetor activate what to cause GI relaxation?

Answer 5

Vagovagal reflex (afferents and efferents carried by vagus)

Question 6

What 2 types of glands exist in the stomach wall?

Answer 6

Oxyntic glands (gastric pits) in body of stomach and pyloric glands in antrum of stomach

Question 7

What type of cells do the gastric pits and pyloric glands contain respectively? (2 each)

Answer 7

Gastric pits = parietal and chief

Pyloric glands = G cells and mucous neck cells

Question 8

What brain center is responsible for relaxation caused by the vagovagal reflex?

Answer 8

VIP

Question 9

What are the 4 major components of gastric juice?

Answer 9

HCL, pesinogen, mucus, intrinsic factor

Question 10

Where are parietal cells located and what do they secrete (2)?

Answer 10

Body of the stomach; HCl and intrinsic factor

Question 11

Where are G cells located and what do they secrete (1)?

Answer 11

Antrum; gastrin

Question 12

Where are chief cells located and what do they secrete (1)?

Answer 12

Body of the stomach; pepsinogen

Question 13

Where are musucs cells located in the stomach and what do they secrete (2)?

Answer 13

Antrum; mucus, pepsinogen

Question 14

What component of gastric juice reduces pH of the stomach, activates pepsin, aids in proteins digestion and kills bacteria?

Answer 14

HCL

Question 15

What component of gastric juice can be inactive or active? And when active, digests proteins by cleavage to peptides at aromatic links?

Answer 15

Intactive: pepsinogen (aka proenzyme). Active: pepsin (digests 10-20% proteins in a typical meal)

Question 16

What component of gastric juice protects the gastric mucosa from the corrosive actions of HCl, enzymes and physical damage?

Answer 16

Mucus

Question 17

What component of gastric juice is necessary for absorption of vitamin B12 in the ileum?

Answer 17

Intrinsic factor

Question 18

What pump is present on the basolateral surface of the cell that contributes to HCl production/ secretion?

Answer 18

Cl-/HCO3- exchanger (Cl- into cell from blood, HCO3- out of cell into blood)

Question 19

What cell secrete HCL?

Answer 19

Parietal cells

Question 20

What pump is present on the apical surface of the cell that contributes to HCl production/ secretion?

Answer 20

H/K-ATPase exchanger (H+ out, K+ in)

Question 21

How is Cl secreted from the parietal cell?

Answer 21

Diffusion down it’s concentration gradient

Question 22

What drug blocks the H/K exchanger on the apical surface of the cell, affecting production/ secretion of HCl?

Answer 22

Omeprazole (proton pump inhibitor)

Question 23

What condition is a result of a tempory increase in blood pH due HCO3 secreted into the blood from the gastric parietal cells after a meal?

Answer 23

Alkaline tide

Question 24

What hormones stimulates acid and pepsinogen secretion?

Answer 24

Gastrin

Question 25

What hormone stimulates growth of gastric and intestinal mucosa (trophic effects)

Answer 25

Gastrin

Question 26

What hormone stimulates antral and intestinal motility?

Answer 26

Gastrin

Question 27

What 3 things stimulate the release of gastrin from G cells of the antrum?

Answer 27

Small peptides/ AAs in stomach, distension of stomach, vagal stimulation

Question 28

Gastrin release is inhibited by what 3 things?

Answer 28

Low pH (< 3), somatostatin, PGE2

Question 29

How does gastrin directly affect the H/K exchanger on parietal cells thus impacting HCl production/ secretion? (4 steps)

Answer 29

Directly binding to CCKB receptor → Gq → IP3/Ca → H/K-ATPase

Question 30

How does gastrin indirectly affect the H/K exchanger on parietal cells thus impacting HCl production/ secretion? (6 steps)

Answer 30

Stimulation of enterochromaffin-like (ECL) cells → releases histamine → binds to H2 receptor→ Gs → cAMP→ H/K-ATPase

Question 31

How does the vagus nerve stimulate HCl secretion? (5 steps)

Answer 31

Releases Ach → M3 receptor → Gq → IP3/Ca → H/K-ATPase

Question 32

What effect does somatostatin have on stomach acid production?

Answer 32

Inhibits acid formation

Question 33

How does PGE2 inhibit the H/K-ATPase pump of parietal cells? (2)

Answer 33

Directly binding to parietal cells → Gi, inhbits ECL cells

Question 34

What drug blocks ACh from binding to M3 receptors on parietal cells?

Answer 34

Atropine

Question 35

What drug blocks histamine form binding to H2 receptor on parietal cells?

Answer 35

Cimetidine (H2 blocker)

Question 36

What things trigger cephalic inputs? (part of cephalic phase of HCl secretion) (5)

Answer 36

Taste, smell, chewing, swallowing, hypoglycemia

Question 37

What general effect do the cephalic inputs have on the stomach? (cephalic phase)

Answer 37

Release gastric acid

Question 38

What does the PNS stimulate during the cephalic phase? (2)

Answer 38

Vagus nerve (stimulate parietal cells), and G cells (release gastrin)

Question 39

What does the PNS release to stimualte the release of gastrin from G cells?

Answer 39

Gastrin releasing peptide (GRP)

Question 40

What phase of digestion is responsible for 30% of total HCl release?

Answer 40

Cephalic phase

Question 41

What phase of digestion is responsible for 60% of total HCl release?

Answer 41

Gastric phase

Question 42

During the gastric phase, what stimulates HCL release from the parietal cells?

Answer 42

Amino acids, small pepetides (from g cells), distention of stomach

Question 43

Distension stimulates HCl secretion by which reflex arcs?

Answer 43

Local and vasovagal reflex arcs

Question 44

Alcohol and caffeine stimulate the release of what?

Answer 44

HCl

Question 45

What converts pepsin to pepsinogen?

Answer 45

Acids with optimum pH of 1.5-2.0 (autocatalytic)

Question 46

At what pH is pepsin denatured?

Answer 46

7

Question 47

What phase is the most improtant phase for the regulation of pepsinogen secretion?

Answer 47

Cephalic phase

Question 48

Release of pepsinogen from chief cells is directly stimulated by what?

Answer 48

vagus nerve (ACh)

Question 49

During the gastric phase, what 3 things stimulate the release of pepsinogen?

Answer 49

Luminal HCl (locally), gastrin, secretin

Question 50

Where is mucus secreted from?

Answer 50

Mucous neck cells and surface epithelium

Question 51

What is the glycoprotein and carbohydrate component of mucus?

Answer 51

Mucins

Question 52

Mucus layer contains high levels of what? What impact does this have on it's pH?

Answer 52

High levels of bicarb. Mucus w/ alkaline pH, resulting in pH gradient (pH 7 at cell surface, pH ~ 2 at top of mucus layer)

Question 53

What stimulates mucus and bicarbonate secretion? (3)

Answer 53

PNS (vagus), gastric distension, prostaglandins

Question 54

What does the gel on the epithelial surface of the stomach create?

Answer 54

Gastric mucosal barrier

Question 55

What are the protective factors of the gastric mucosal barrier?

Answer 55

HCO3- and mucus > prostaglandins, mucosal BF, growth factors

Question 56

H+ and pepsin, H. pylori, NSAIDs, stress, smoking and alcohol have what effect on the gastric mucosal barrier?

Answer 56

Lead to damage of the gastric mucosal barrier

Question 57

What are the 3 components of gastric motility?

Answer 57

Receptive relaxation (vagal reflex/ VIP), mixing motions (reduce bolus size), propulsion of chyme (past pyloric valve into duodenum)

Question 58

How does PNS stimulation, gastric distension, gastrin and motilin affect gastric mixing and emptying?

Answer 58

Increases it

Question 59

What impact does SNS stimulation, secretin, CCK, and GIP have on gastric emptying and mixing?

Answer 59

Decreases it

Question 60

What drives the bolus towards the pyloric valve and is increased by distension, PNS, and gastrin?

Answer 60

Antral peristaltic waves (generated by thick walls)

Question 61

What is the result of the pyloric valve being largely closed?

Answer 61

Only allows very small particles to pass into duodenum

Question 62

How does H+, and digestion production of fats and proteins decrease gastric emptying and mixing?

Answer 62

Via duodenal distension (enterogastric reflex)

Question 63

What happens to the larger particles that are not able to make it through the pyloric valve?

Answer 63

Reflected back into antrum (retropulsion) → (process repeated until particles are small enough)

Question 64

What area of the brain detects chemicals/ toxins in blood to trigger the vomiting reflex?

Answer 64

Vomiting center in brain (chemoreceptive area of meduallary brain center), no BBB

Question 65

Intracrainal pressure, irradiation, visual stimulus, and toxins/meds can stimulate what reflex?

Answer 65

Vomiting reflex

Question 66

What happens to the diaphragm during vomiting?

Answer 66

Diaphragm lowered to inspiratory position just above stomach

Question 67

What relaxes to allow for vomiting? (4)

Answer 67

Stomach, esophagus, LES, UES

Question 68

What contracts to increase intra-abd pressure during vomiting?

Answer 68

Abd wall muscles

Question 69

Closure of what prevents asipration of vomitus?

Answer 69

Glottis

Question 70

Simultaneous contraction/ relaxation of structures allows for what to happen, resulting in vomiting?

Answer 70

Stomach sqeezed between diaphragm and viscera

Question 71

Excess acid secretion and/or damage to mucosal barrier results in what disease?

Answer 71

Peptic ulcer disease

Question 72

Infection via what pathogen is implicated in many cases of peptic ulcers?

Answer 72

Helicobacter pylori bacteria (damages mucosal layer)

Question 73

What is released during the destruction of mucosal cells by gastric acid? What does this result in?

Answer 73

Histamine is released and it sitmulates acid secretion

Question 74

Overuse of what can result in peptic ulcer disease?

Answer 74

NSAIDS (inhibits cyclooxygenase → decreased prostaglandins)

Question 75

What is the treatment for peptic ulcer disease? (4)

Answer 75

Antibiotics (for H. pylori), H2-blockers (Cimetidine), proton pump inhibitors (Omeprazole), colloidal bismuth (coats and protects ulcer)