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Physiology 1 > Regulation And Disorders Of Gastric Secretion > Flashcards

Regulation And Disorders Of Gastric Secretion Flashcards

1
Q

What are the contents of gastric juice in the fasting state?

A

Cations, anions, pepsinogen, lipase, mucus, intrinsic factors

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2
Q

What does the body of the stomach secrete?

A

Mucus, pepsinogen and HCL

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3
Q

What does the antrum of the stomach secrete?

A

Mucus, pepsinogen and gastrin

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4
Q

What is trefoil peptide important for?

A

Protection of stomach wall

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5
Q

How is gastric acid made in the stomach lumen?

A
  • HCO3 exchanged for Cl- in the blood
  • excess Cl- diffuses out into stomach
  • potassium hydrogen ATPase pumps hydrogen ions out into the stomach lumen
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6
Q

What are the 5 types of cells in gastric glands?

A 
Surface mucous cells
Mucus neck cells
Parietal cells
ECL cells
Chief cells
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7
Q

What do surface mucus cells do?

A

Secrete mucus, trefoil peptide and bicarbonate

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8
Q

What do mucus neck cells do?

A

Stem cell compartment

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9
Q

What do parietal cells secrete?

A

Acid and intrinsic factor secretion

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10
Q

What do ECL cells secrete?

A

Histamine

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11
Q

What do chief cells secrete?

A

Pepsinogen

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12
Q

What is resting juice?

A

Alkaline plasma (basically)

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13
Q

What is the mucus’ function?

A

Thick and sticky- forms water insoluble gel on epithelial surface

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14
Q

What does mucus do (in stomach)?

A

Increased HCO3 - protects against hydrogen ion secretion

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15
Q

What is renin replaced by?

A

Pepsinogen

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16
Q

What does intrinsic factor do?

A

Helps with absorption of vit B12

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17
Q

What is the function of gastric acid?

A

Kills bacteria, acidic denature of digested food, creates the optimum pH for activation of pepsinogen, promotes the activation of gastric lipase and secretion of pancreatic HCO3

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18
Q

What do G cells secrete?

A

Gastrin

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19
Q

What happens in the cephalic phase?

A

ACh stimulates histamine release from ECL cells and can also act on parietal cells -> HCL secretion

Gastrin stimulates histamine release and can act directly on parietal cells -> HCL secretions

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20
Q

What happens when too much acid is produced?

A

D cells are stimulated and release somatostatin

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21
Q

What is somatostatin?

A

Paracrine factor

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22
Q

What happens in the gastric phase?

A

Stomach distends, peptic concentration and acidity increases

Peptides in food buffer acid and increase pH so somatostatin inhibitition

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23
Q

What happens in the intestinal phase?

A

Balances the secretory activity of the stomach and the digestive and absorbitive capacities of small intestine
High duodenal acidity reflexively inhibits acid secretion

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24
Q

What inhibits acid secretion?

A

Duodenal distension, hypertonic solution, amino acids, fatty acids and monosaccharides

25
Q

What does inhibition of acid secretion in the small intestine depend on?

A

Composition of chyme, volume of chyme and distension of the duodenum

26
Q

What is HCL secretion regulated by?

A

Neuronal pathways and duodenal hormones

27
Q

What is the direct pathway of acid secretion?

A

Acts on parietal cells-> increased Acid secretion

28
Q

What is the indirect pathway of HCL secretion?

A

Influencing the secretion of gastrin and histamine,which increase acid secretion

29
Q

What stimulates HCL secretion?

A

Histamines, ACh, gastrin, caffeine, alcohol, NSAIDs, nicotine, helicobacter pylori,

30
Q

Why is pepsinogen secreted?

A

Inputs of chief cells from the nerve plexus when the [H+] is high

31
Q

What does PGE2 do?

A

Inhibits parietal cells and stimulate mucus secreting cells

32
Q

What do NSAIDs inhibit?

A

PGE2

33
Q

How does the mucus layer prevent the auto digestion of the stomach?

A

Protects from low pH

34
Q

How do the epithelial cells prevent autodigestion of the stomach?

A

Remove excess H+ via membrane transport systems

35
Q

How are H+ ions prevented from back diffusing?

A

Tight junctions of epithelial cells

36
Q

How do prostaglandins prevent the autodigestion of the stomach?

A

Inhibit acid secretion and enhance blood flow

37
Q

What does mucosal blood flow remove?

A

Excess acid that has diffused across the epithelial layer

38
Q

What do NSAIDs do?

A

Cause tropical irritation of the gut

39
Q

What does the presence of acid in stomach promote?

A

NSAID-mediated gastric disorders

40
Q

What are the functions of the GIT?

A

Storage, secretions, digestion, absorption of nutrients, salts, water, metabolism and elimination of undigested wastes

41
Q

Where can peptic ulcers form?

A

Oesophagus, stomach and duodenum

42
Q

When do peptic ulcers form?

A

Where there’s a breakage in the mucosal barrier

43
Q

Where are peptic ulcers particularly common?

A

Duodenal cap, stomach- junction of antrum and body, distal oesophagus, meckels diverticulum and weight loss surgery

44
Q

What are the causes of peptic ulcers?

A

Hyperacidity, presence of H pylori, NSAIDs, genetic factors

45
Q

What are the outcomes of acute peptic ulcers?

A

Severe bleeding, healing with no scarring and chronic peptic ulcers

46
Q

What do acute peptic ulcers develop from?

A

Areas of corrosive gastritis or acute hypoxia of surface epithelium

47
Q

How does H pylori cause peptic ulcers?

A

They can permeate the gastric mucosa and cause ulcers

48
Q

What are the virulence factors of H pylori?

A
  • flagella move it closer to the epithelium
  • produces urease
  • cytotoxin-associated antigen (CagA)
  • vacuolating toxin A (VacA)
49
Q

How does urease make H pylori more virulent?

A

Converts urea to ammonia- buffers gastric acid and produces CO2

50
Q

How does Cytotoxin-associated antigen make H pylori more virulent?

A

Inserts pathogenicity islands and confers ulcer-forming potential

51
Q

How does vacuolating toxin A make H pylori more virulent?

A

Alters the trafficking of intracellular proteins in gastric cells

52
Q

What is the most common cause of peptic ulcers?

A

H pylori

53
Q

What does H pylori do once its in the cells?

A

Disregulates gastrin secretion

54
Q

What happens when gastrin secretion is disregulated?

A

Gastrin secretion increases

55
Q

What are the three ways you can diagnose peptic ulcers?

A

Endoscopy
Histological examination and staining of an EGD biopsy
Test for H pylori presence

56
Q

What are the tests you can do for the presence of H pylori?

A
  • stool antigen test
  • evaluate urease activity
  • urea breath test
57
Q

How do you carry out the urea breath test?

A

Work out how much CO2 is in urine and how much is in breath by tagging some C-14. There shouldn’t be any C-14 in breath

58
Q

When do you measure CO2 levels when carrying out the urea breath test?

A

Before and 10-30 mins after

59
Q

What are the complications of a peptic ulcer?

A 
Haemorrhage 
Perforation and penetration 
Leakage of luminal contents
Narrowing of pyloric canal or oesophageal stricture
Malignant change

Physiology 1 (65 decks)

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