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Digestive MBChB 2 > Lecture 3; Gastric digestion and diseases of the stomach. > Flashcards

Lecture 3; Gastric digestion and diseases of the stomach. Flashcards

1
Q

What does gastric digestion begin with?

A

Saliva production

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2
Q

What generates saliva production?

A
  • Sight, smell of food (autonomic control)
  • Inhibited during sleep
  • Stimulated by acid in the oesophagus
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3
Q

What are the contents of saliva?

A
  • Electrolytes, hypotonic, HCO3- (basic)
  • Mucins; lubricates bolus and enhances chewing action
  • Silivary amylase initiates digestion
  • Lactoferrin; lysozyme with antibacterial action
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4
Q

What happens with the loss of saliva?

A
  • Increased risk of infection
  • drying of mouth
  • dental decay
  • loss of taste (saliva irrigates taste buds)
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5
Q

What can cause the loss of saliva?

A

1) Sjogrens disease causes loss of salivary secretion because of chronic inflammation of salivary glands
2) Anti-cholinergic drugs

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6
Q

What are the major functions of the stomach?

A

1) Reservoir for food during initial digestion, controlled flow of chyme into SI
2) Adjusts osmolarity of chyme to enter SI
3) Antrum acts as grinding mill
4) Pylorus regulates size of particles that can pass through to duodenum.
5) 1.5L acid release per day
6) Other secretions; Intrinsic factors, pepsinogen, mucous, prostaglandins.

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7
Q

What controls the rate of gastric emptying?

A

1) Feedback mechanisms from duodenum; Acid, Fat, amino acids, osmolarity
2) Requires antrum, pylrous and duodenum for normal function
3) Normal hormonal and vagal function

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8
Q

Describe the function of each part of the stomach?

A

1) Fundus acts as a food store (vasovagal reflex)
2) Body and antrum mix food
3) Pylorus contracts to limit exit of chyme

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9
Q

Describe the process of diarrhoea;

A

Food moves too fast through stomach, Enhanced gastric emptying

Undigested food enters the SI, hyperosmolar chyme causes water to enter the bowel. Intestinal distention = pain. Diarrhoea due to osmotic effect.

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10
Q

What are the class of drugs that speed up gastric emptying? and an example;

A

Prokinetics

i.e Metoclopramide; releases ACh at myenteric plexus.

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11
Q

What can cause delayed gastric emptying?

A

Diabetic gastroparesis

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12
Q

Describe diabetic gastroparesis;

A
  • Autonomic neuropathy
  • Variable rate of glucose absorption
  • Upper abdominal discomfort.
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13
Q

What are drugs that cause delayed gastric emptying?

A

Anti-cholinergic drugs

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14
Q

What is the role of gastric acid;

A
  • Sterilise stomach (apart H. pylori)
  • Limited digestion, denatures proteins
  • Helps B12 and iron absorption
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15
Q

What is the name for absent or low gastric acid?

A

Achlorhydria i.e

  • pernicious anemia
  • low iron absoprtion
  • Gastric cancer?
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16
Q

What are the cells of the stomach?

A

Parietal cells
ECL cells
G cells
D Cells

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17
Q

What do parietal cells do?

A

Secrete acid (H+)

H/K ATPase pump (proton pump)

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18
Q

Describe how parietal cells function;

A
  • H+ out, K+ in, ATP to function
  • HCO3 is formed as bi-product and released into the blood stream. Cl- is exchanged for this.

HCL secretion

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19
Q

Describe the pH of the stomach during the day;

A

Stomach pH is dynamic.
- Dilution by secretion and HCO buffering gives the stomach a pH of 1.5-2.0

Buffering with meals increases this to 5-6 and decreases overnight to 1.5 roughly.

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20
Q

How is the stomach protected from HCL secretions?

A

Mucous is secreted onto the luminal surface.

HCO3 is also secreted to act as a buffer.

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21
Q

What stimulates the stomach and what are the neurotransmitters?

A

Vagus nerve and enteric neurons.

Release ACh

22
Q

What is the function of ACh on the stomach;

A

Causes;

  • Parietal cells release HCl
  • ECL cells to release histamine (paracrine, stimulates parietal)
  • G cells to release gastrin -> Stimulates parietal and ECL cells.
23
Q

What are ECL cells?

A

Enterochromaffin-like cells

24
Q

What is the function of ECL cells?

A
  • Located in body of stomach

- Secrete histamine which acts in paracrine manner to stimulate adjacent parietal cells.

25
Q

What is the function G cells?

A
  • Located in antrum of the stomach
  • Secretes gastrin (endocrine)
  • Stimulates ECL->histamine->Parietal->HCL

Indirect acid secretion

26
Q

What is the function of D cells?

A
  • Antrum
  • Secretes somatostatin (endocrine and paracrine)
  • Inhibits acid secretion by acting on adjacent G cells and inhabiting gastrin release.
27
Q

What are the phases of digestion;

A
  • Cephalic phase
  • Gastric phase
  • Intestinal phase
28
Q

What is the cephalic phase of digestion;

A
  • Initiated by thought, sight, smell of food.

- Mediated by vagus nerve (Ach). (stimualtes parietal cells)

29
Q

What is the gastric phase;

A
  • Distension of both body and antrum causes acid secretion mediated by the vagus nerve
  • Peptides and AA in atrum stimulate G cells. - Gastrin release
30
Q

What is the intestinal phase;

A
  • Inhibits acid secretion
31
Q

Describe the intestinal phase;

A
  • HCl in the antrum causes somatostatin release from D cells. Inhibits gastrin release.
  • HCl in duodenum stimulates SECRETIN which inhibits gastric acid release and gastric emptying. Simulates pancreatic HCO3 secretion
  • Short Chain FA and peptides in duodenum stimulate CCK, inhibits GA and gastric emptying. Increases pancreatic enzyme release and gallbladder contraction to release bile.
32
Q

Summerise what stimulates gastric acid release and what inhibits it?

A

Stimulates;

  • ECL -> Histamine
  • G cells -> Gastrin
  • Vagus and enteric nerves (ACh)

Inhibits;
- D cells -> Somatostatin

33
Q

What can cause an abnormal increase in gastric secretion;

A
  • H. pylori gastritis

- Tumors that produce gastrin i.e gastrinoma

34
Q

What things can cause low gastric secretion?

A
  • Loss of parietal cells i.e pernicious anemia
  • Vagotomy (loss of vagal nerve)
  • Drugs i.e proton pump inhibitor, histamine 2 receptor antagonists
  • Gastric surgery: Removal of parts of the stomach that contain cells involved in HCL secretion
35
Q

What is pepsinogen secreted in the stomach?

A
  • Activated by low pH and converted into active pepsin
  • Secreted by chief cells
  • Degrades/hydrolyses aspartic amino acids
  • Increasing stomach pH is treatment option for ulcers as inactivates pepsinogen so it cant break down blood clots
36
Q

What else is secreted by the stomach?

A

Intrinsic factor;
- Protein secreted by parietal cells

Prostaglandins

  • Lipid molecules
  • Protection and repair of gastric mucosa
37
Q

What is peptic ulcer disease?

A
  • Break in the mucosa, leading to formation of ulcers
  • Pain; Epigastric, burning
  • Bleeding
  • Perforation
  • Obstruction in pylorus or duodenum from swelling or scarring.
38
Q

In peptic ulcers what causes the pain to worsen?

A

Gastric ulcers; Pain is worse with food i.e during and after meal

Duodenal ulcers; Pain is worse on empty stomach

39
Q

What is the medical treatment of peptic ulcers?

A
  • H+ pump inhibitors

- Histamine 2 antagonists

40
Q

What are the surgical treatments of peptic ulcers?

A
  • Gastrectomy (removes antrum thus gastrin)
  • vagotomy (reduces ACh)
  • Pyloroplasty; Relax pyloric sphincter, food in stomach for less time, less gastrin.
41
Q

What causes gastric ulcers;

A

H pylori

NSAIDS
Aspirin

42
Q

What makes H pylori able to survive?

A

Produces enzymes urease and degrades mucous

Elicits cellular immune response.

43
Q

What else can H pylori cause?

A
  • Gastritis
  • Peptic ulcer
  • Gastric cancer
  • Gastric MALToma
44
Q

What can long term H pylori cause?

A

Long term H. pylori gastratis can result in atrophic gastritis (loss of gastric cells i.e parietal -> Achlorydia -> bacterial colonisation -> increased chance of gastric cancer)

45
Q

How does H pylori lead to a duodenal ulcer?

A

H pylori can lead to increased gastrin -> HCL inc.

Can lead to gastric acid metaplasia in the duodenum, H pylori migrates to duodenum causing brakdown of mucosa.

46
Q

What are the two major types of gastric adenocarcinoma?

A

Intestinal and diffuse.

Association between gastric cancer and H pylori. (more intestinal type).

47
Q

Describe intestinal adenocarcinoma;

A
  • Well differentiated
  • cells arranged in tubular/glandular pattern
  • more likely to be in antrum
48
Q

Describe diffuse adenocarcinoma;

A
  • Poorly differentiated
  • Lack glandular differentiation
  • Can infiltrate gastric wall
  • Potential genetic factors (E-cadherin mutation)
49
Q

How does gastric cancer present;

A
  • Upper abdominal discomfort
  • Early satiety
  • Pain after meals
  • Anorexia
  • Weight loss

Palliative car treatment often.

50
Q

What can happen with H. pylori gastritis?

A

Atrophic gastritis

51
Q

What can H. Pylori stimulate the secretion of?

A

Gastrin -> excess HCL -> duodenal metaplasia -> duodenal ulcer

52
Q

What can H. Pylori stimulate the secretion of?

A

Gastrin -> excess HCL -> duodenal metaplasia -> duodenal ulcer

Digestive MBChB 2 (31 decks)

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