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Physio II > Exam 4- Gastric Secretion & Motility > Flashcards

Exam 4- Gastric Secretion & Motility Flashcards

1
Q

What are the 3 layers of the stomach?

A

Longitudinal layer, circular layer, inner oblique layer

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2
Q

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

A

Distal

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3
Q

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

A

Pressure

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4
Q

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

A

Receptive relaxation

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5
Q

Gastric stretch recetor activate what to cause GI relaxation?

A

Vagovagal reflex (afferents and efferents carried by vagus)

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6
Q

What 2 types of glands exist in the stomach wall?

A

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

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7
Q

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

A

Gastric pits = parietal and chief

Pyloric glands = G cells and mucous neck cells

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8
Q

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

A

VIP

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9
Q

What are the 4 major components of gastric juice?

A

HCL, pesinogen, mucus, intrinsic factor

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10
Q

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

A

Body of the stomach; HCl and intrinsic factor

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11
Q

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

A

Antrum; gastrin

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12
Q

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

A

Body of the stomach; pepsinogen

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13
Q

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

A

Antrum; mucus, pepsinogen

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14
Q

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

A

HCL

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15
Q

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

A

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

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16
Q

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

A

Mucus

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17
Q

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

A

Intrinsic factor

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18
Q

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

A

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

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19
Q

What cell secrete HCL?

A

Parietal cells

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20
Q

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

A

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

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21
Q

How is Cl secreted from the parietal cell?

A

Diffusion down it’s concentration gradient

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22
Q

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

A

Omeprazole (proton pump inhibitor)

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23
Q

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?

A

Alkaline tide

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24
Q

What hormones stimulates acid and pepsinogen secretion?

A

Gastrin

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25
Q

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

A

Gastrin

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26
Q

What hormone stimulates antral and intestinal motility?

A

Gastrin

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27
Q

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

A

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

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28
Q

Gastrin release is inhibited by what 3 things?

A

Low pH (< 3), somatostatin, PGE2

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29
Q

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

A

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

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30
Q

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

A

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

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31
Q

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

A

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

32
Q

What effect does somatostatin have on stomach acid production?

A

Inhibits acid formation

33
Q

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

A

Directly binding to parietal cells → Gi, inhbits ECL cells

34
Q

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

A

Atropine

35
Q

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

A

Cimetidine (H2 blocker)

36
Q

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

A

Taste, smell, chewing, swallowing, hypoglycemia

37
Q

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

A

Release gastric acid

38
Q

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

A

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

39
Q

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

A

Gastrin releasing peptide (GRP)

40
Q

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

A

Cephalic phase

41
Q

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

A

Gastric phase

42
Q

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

A

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

43
Q

Distension stimulates HCl secretion by which reflex arcs?

A

Local and vasovagal reflex arcs

44
Q

Alcohol and caffeine stimulate the release of what?

A

HCl

45
Q

What converts pepsin to pepsinogen?

A

Acids with optimum pH of 1.5-2.0 (autocatalytic)

46
Q

At what pH is pepsin denatured?

A

7

47
Q

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

A

Cephalic phase

48
Q

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

A

vagus nerve (ACh)

49
Q

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

A

Luminal HCl (locally), gastrin, secretin

50
Q

Where is mucus secreted from?

A

Mucous neck cells and surface epithelium

51
Q

What is the glycoprotein and carbohydrate component of mucus?

A

Mucins

52
Q

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

A

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

53
Q

What stimulates mucus and bicarbonate secretion? (3)

A

PNS (vagus), gastric distension, prostaglandins

54
Q

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

A

Gastric mucosal barrier

55
Q

What are the protective factors of the gastric mucosal barrier?

A

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

56
Q

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

A

Lead to damage of the gastric mucosal barrier

57
Q

What are the 3 components of gastric motility?

A

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

58
Q

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

A

Increases it

59
Q

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

A

Decreases it

60
Q

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

A

Antral peristaltic waves (generated by thick walls)

61
Q

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

A

Only allows very small particles to pass into duodenum

62
Q

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

A

Via duodenal distension (enterogastric reflex)

63
Q

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

A

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

64
Q

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

A

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

65
Q

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

A

Vomiting reflex

66
Q

What happens to the diaphragm during vomiting?

A

Diaphragm lowered to inspiratory position just above stomach

67
Q

What relaxes to allow for vomiting? (4)

A

Stomach, esophagus, LES, UES

68
Q

What contracts to increase intra-abd pressure during vomiting?

A

Abd wall muscles

69
Q

Closure of what prevents asipration of vomitus?

A

Glottis

70
Q

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

A

Stomach sqeezed between diaphragm and viscera

71
Q

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

A

Peptic ulcer disease

72
Q

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

A

Helicobacter pylori bacteria (damages mucosal layer)

73
Q

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

A

Histamine is released and it sitmulates acid secretion

74
Q

Overuse of what can result in peptic ulcer disease?

A

NSAIDS (inhibits cyclooxygenase → decreased prostaglandins)

75
Q

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

A

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

Physio II (14 decks)

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