Stomach & Stomach Acid Secretions Flashcards

1
Q

Name the 5 Functions of the Stomach

A
  1. Receiving & storing food & liquids
  2. Secretion of acid, pepsinogen, gastric lipase
  3. Mixing of food & liquid with gastric juice
  4. Grinding to reduce particle size (into chyme)
  5. Regulating the exit of chyme into the duodenum
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2
Q

Name the 5 Regions of the Stomach

A
  1. Cardia
  2. Fundus
  3. Body (corpus)
  4. Antrum
  5. Pylorus
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3
Q

What is the surface area of the stomach important for?

A
  • Secretion
  • Absorption
  • Access
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4
Q

What are the secreting cells of the stomach

A
  • Mucous cell
  • Parietal cells
  • Chief cells
  • Enteroendocrine cells
    • ECL - (Enterochromaffin - like cells)
    • G cells
    • D cells
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5
Q

Describe Mucous neck cells and their function

A
  • Secrete mucins - viscous glycoproteins
  • Secrete bicarbonate - HCO3-
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6
Q

What is the function of Parietal cells?

A
  • Produce HCl
  • Secrete intrinsic factor - req for B12 absorption
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7
Q

What is the function of Chief cells, and their secretions?

A
  • Secrete gastric lipase
  • Secrete pepsinogens
    • Pepsinogens → pepsins at pH < 3
    • Initiate protein digestion by hydrolysis
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8
Q

How do Parietal cells make HCl?

A
  • CO2 from bloodstream enters parietal cell
    • CO2 +H2O → H2CO3 (carbonic acid)
  • Carbonic acid deprotonates
    • H2CO3 → H+ + HCO3-
  • H+/K+ ATPase pump exchanges H+ into lumen in exchange for K+
  • HCO3- diffuses back into blood
  • Cl- diffuses from blood, across parietal cell into lumen following gradient
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9
Q

Key secretions from pyloric region of the stomach

A
  • Gastrin
  • Mucus
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10
Q

What are the 3 Enteroendocrine cells and their secretions?

A
  • ECL / Enterochromaffin like cells
    • Histamine - stimulates gastric acid secretion
    • Ghrellin - hunger, energy homeostasis
  • G cells
    • Gastrin - ↑ - acid secretion
  • D cells
    • Somatostatin - ↓ stomach acid secretion
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11
Q

Key secretions from the body of the stomach

A
  • HCl
  • Intrinsic Factor (IF)
  • Pepsinogens
  • Mucus
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12
Q

Name some causes of impairments to the gastric mucosal barrier

A
  • Alcohol
  • NSAIDs (Ibuprofen)
  • Salicylates (Aspirin)
  • Bile acids
  • Infection
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13
Q

3 main stimulating factors that act directly on parietal cells to increase acid production

A
  • Acetylcholine → vagus nerve → M3 muscarinic receptors
  • Gastrin → Antral G cells → CCK receptors
  • Histamine → Enterocromaffin like (ECF) cells → H2 histamine receptors
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14
Q

2 factors causing indirect stimulation of gastric acid

A

Stimulation of ECL cells to release histamine via:

  • ACH
  • Gastrin
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15
Q

3 phases of gastric acid secretion

A
  • Cephalic
  • Gastric
  • Intestinal
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16
Q

Explain the cephalic phase of gastric acid secretion

A
  • ~30% acid response to meal
  • Occurs before food reaches stomach - smell, taste, chewing, conditioning
  • Mediated by branches of Vagus nerve
    • Vagus → ACh → direct stimulation parietal cells
    • Vagus → GRP (gastrin releasing peptide) → gastrin
17
Q

Explain gastric phase of gastric acid secretion

A
  • ~60% acid prod
  • Food reaches stomach - distention, presence of amino acids & small peptides in stomach
  • Vagal stimulation
    • ACh → parietal cells
    • ACh → G cells → gastrin
  • Amino acids → G cells → gastrin
  • High pH → G cells → gastrin
18
Q

Explain intestinal phase of gastric acid secretion

A
  • ~10% acid response
  • Chyme in duodenum stimulates neural & hormonal mechanisms
  • First stimulate, then inhibit acid production
19
Q

Stimuli for gastric acid inhibition

A
  • pH <1.5
  • Acidic solutions in duodenum
  • Chyme in duodenum
  • Hyper-osmotic solutions in duodenum
20
Q

Stop signals to inhibit gastric acid secretion

A
  • Somatostatin from D cells
    • Inhibit parietal cells - stop HCl release
    • Inhibit G cell - stop gastrin release
    • Inhibit ECL cell - histamine release

Also:

  • Secretin → S cells
  • Gastric Inhibitory Polypeptide → K cells
21
Q

Damage to gastric mucosa can occur from:

A

↑ HCl production
↑ Pepsin production
↓ Thickness mucus layer
↓ Mucosal blood flow
↓ Bicarbonate secretion
Mucosal erosion (aspirin, NSAID’s)
Helicobacter pylori infection

22
Q

How does H-pylori survive the acidic environment

A
  • Produces large amounts of urease
  • Breaks down UREA → AMMONIA (NH3) + BICARBONATE (HCO3-)
  • Bicarbonate neutralises stomach acid → basic cloud
  • Ammonia is toxic to cells - increases damage to gastric epithelia

Urea + Water Urease Ammonia and Carbon dioxide

(NH2)2CO + H2O → 2NH3 + CO2

23
Q

3 drugs for “triple therapy” of H. Pylori

A
  • Amoxycillin - antibiotic → inhibits cell wall synthesis
  • Clarithromycin - antibiotic → inhibits protein synthesis
  • Omeprazole - proton pump inhibitor
24
Q

How does H-pylori contribute gastritis?

A
  • H-pylori excrete urease enzyme to break down urea to form basic cloud to help neutralise stomach acid to survive in the harsh stomach environment
  • Excretion of urease causes abundance of ammonia and bicarb
  • Ammonia is toxic to gastric epithelial cells
25
Q

Name the stimuli for Gastrointestinal Endocrine Hormones, and where they come from:

Gastrin

A

G cells, Stomach

⇑Proteins. amino acids

⇑ Neuronal stimulation → vagus

⇑ Stretch

⇓ Acid

26
Q

Name the stimuli for Gastrointestinal Endocrine Hormones, and where they come from:

CCK (CholyCystoKinin)

A

I cells, Duodenum

⇑ Proteins/amino acids

⇑ Fatty acids

27
Q

Secretin is a gastrointestinal Endocrine Hormone.
Where does it come from?
What promotes secretion?
What does it do?

A

S Cells,
Duodenum and small amounts of Jejunum

Released due to low duodenal pH ie, when chyme is released from pyloric sphincter

Targets pancreas to secrete bicarbonate rich fluid.
It also reduces acid secretion of gastric parietal cells

28
Q

Name the stimuli for Gastrointestinal Endocrine Hormones, and where they come from:

GIP (Glucose-dependent-Insulinotrophic-Peptide AKA Gastric-Inhibitory-Polypeptide)

A

K cells, Duodenum

⇑ Proteins/amino acids

⇑ Fatty acids

⇑ Glucose

29
Q

Describe the pathological features of erosion of the gastric mucosa

A

Erosion indicates an ulcer formed with death of gastric epithelial cells is shallow, and does. not penetrate beyond the mucosa

30
Q

One long term complication of untreated H-pylori infection

A

Gastric Adenocarcinoma

Gastric Lymphoma

31
Q

Carcinoma Vs Adenocarcinoma

A

Carcinoma is the most common form of cancer. It starts in the epithelial tissue of your skin or internal organs.

Adenocarcinoma is a subtype of carcinoma.

Starts in “glandular cells” that secrete mucus and other fluids

32
Q

What tumour suppressor gene is mutated in about 75% of colorectal cancers that is crucial or initiating apoptosis in cells with irreparable genetic damage in Go of the cell cycle?

A

p53

33
Q

A 28-year-old man complains of nausea, vomiting, diarrhoea and abdominal discomfort. His symptoms have developed over night following a social BBQ. He tells you that a number of his friends have developed similar symptoms.

What organism is the most-like responsible for his symptoms?

A

Campylobacter spp.

34
Q

How does secretin reduce gastric parietal cell acid secretion?

A

When released from duodenal S- cells, secretin:

  • Stimulates somatostatin release from D-cells (pyloric antrum, duodenum, pancreatic islets)
  • inhibit gastrin release from pyloric antrum G-cells
  • Directly down regulates parietal cells