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1402- Digestion > Physio - Digestion In The Stomach And Peptic Ulcers > Flashcards

Physio - Digestion In The Stomach And Peptic Ulcers Flashcards

1
Q

Describe the control of the gastric motility in the stomach.

A
  1. Parasympathetic stimulations and Gastrin increase the force of gastric smooth muscles contractions.
  2. Sympathetic stimulations and secretin and cholecystokinin decrease the force of gastric smooth muscle contractions.
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2
Q

List the factors that support the reservoir function of the proximal part of the stomach

A

Tonic contractions
Rugae- allow stomach to expand
Receptive relaxation - induced via the vagovagal reflex and increase the stomach volume.

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3
Q

List the types of phasic contractions of the stomach.

A

Propulsion - when food moves down to the antrum
Retropulsion - when food is forced back into the body of the stomach
Gastric emptying - food is move down to the duodenum

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4
Q

Gastric emptying involves what two events?

A
  1. Phasic contractions of the stomach antrum
  2. Relaxation of the pyloric sphincter.
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5
Q

State the regulation of gastric emptying.

A
  1. Fatty acids stimulate the release of CCK and inhibits gastric contraction.
  2. Low pH stimulates the release of secretin and inhibits gastric contraction.

Facts that inhibits gastric emptying.

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6
Q

List the three types of exocrine cells in the gastric glands.

A
  1. Mucous cells - mucus
  2. Parietal cells - hydrochloric acid and intrinsic factor
  3. Chief cells - pepsinogen and gastric lipase.
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7
Q

What does gastrin stimulate? State what its secretion is increases and reduced by.

A

A. Parietal cells - secrete HCL acid
B. Gastrin secretion is increased by vagal stimulation and presence of amino acids
- Gastrin secretion is decreased by high amount of HCL acid in the stomach.

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8
Q

Describe the process of secretion of hydrochloric acid.

A
  1. Carbonic anhydrate catalyzed the formation of carbonic acid.
  2. Carbonic acid is dissociated into H+ and HCO3- ions
  3. The proton pump pumps the H+ into stomach lumen and brings K+ into the parietal cell.
  4. The increase K+ concentration causes K+ to diffuse back into the gastric lumen
  5. HCO3- exits the cell into the blood steam in exchange for the CL-
  6. The Cl- ion diffuse from the cell into the gastric lumen via the channel and form HCl acid.
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9
Q

Hydrochloric acid is stimulated and inhibited by what agents?

A

Stimulates-
AcH, Gastrin, Histamine, secretin and Cholecystokinin
Inhibited-
Somatostatin and prostaglandin E2.

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10
Q

State the roles of hydrochloric acids.

A
  1. Kills microbes
  2. Denatures proteins
  3. Converts pepsinogen
  4. Creates optimum pH
  5. Stimulates the release of enteric hormones.
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11
Q

Pepsin is derived from and what is its function?

A

Pepsinogen which was derived from the chief cells.
It acts as an endopeptidase which acts on peptide bonds.

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12
Q

What is pepsin stimulated by?

A

ACh
Gastrin
Histamine
CCK
Secretin

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13
Q

What stimulates Gastric acid?

A

Secretin and cholecystokinin.

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14
Q

What is the most frequent site for peptic ulcers?

A

Duodenum
Lesser curvature of antral part of the stomach
Lower end of the esophagus

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15
Q

State the significance of Gastric lipase.

A
  1. Produced by the chef cells
  2. Breaks down triglycerides into fatty acids and glycerol
  3. Significant in newborn infants
  4. Is deactivated by pancreatic proteases once contents of the stomach move into the duodenum.

Note: The continued action of gastric lipase is permitted when there is an issue with pancreatic proteases.

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16
Q

List the three phases of gastric secretion.

A
  1. Cephalic
  2. Gastric
  3. Intestinal
17
Q

Describe the cephalic phase of gastric secretion.

A
  1. Sight, smell and taste stimulates the brain.
  2. The vagus nerve stimulates the secretion of gastrin directly via the parietal cells or indirectly via the G cells to release gastrin.

Note: neural mechanisms play an important role in this.

18
Q

Describe the gastric phase of gastric secretion.

A
  1. When food is swallowed and enters the stomach, it initiates a mechanical and chemical stimulation of the mucosa
  2. This activates both the vague nerve and the release of gastrin and histamine from the mucosa

Note: neural and hormonal mechanisms play an important role.

19
Q

Describe the intestinal phase of gastric secretion.

A
  1. When chyme is evacuated from the stomach, induces mechanical and chemical stimulation of the gastic mucosa.
  2. It activates a neural reflex and release the hormones, secretin and CCK, which inhibits gastric motility and acid secretion

Note: neural and hormonal mechanism play an important role.

20
Q

What are three functions of the stomach?

A

Motor function-
— acts as a reservoir for food
— mixes food tin gastric secretions
— propels food into the duodenum

Secretory function -
— produces gastric/ HCL acid
— secretion of pepsinogen and gastric lipase, mucus and bicarbonates.

Source of humoral agents that regulate the digestion -
— Gastrin, histamine and somatostatin

21
Q

How are peptic ulcers developed?

A

develop due to an imbalance between that factors that protects the gastric mucosa and factors that cause an injury.

22
Q

List the components of the mucosal diffusion barrier.

A

Mucus
Bicarbonates
Mucosal lining

23
Q

Briefly describe each layer of the mucosal diffusion barrier.

A
  1. Mucus -
    formed by mucin, phospholipid and H2O.
    High viscosity, gel layer
    Physical barrier- slows diffusion of acid and pepsin
  2. Bicarbonate-
    - covers the surface of the mucosal cells
    - forms a chemical barrier that protects the mucosal lining
    - neutralizes, preventing the destructive effect of acids on the mucosal cells.

Note: bicarbonate layer inactivates pepsin

24
Q

What happens when the mucosal protective barrier is damaged?

A

When an acids penetrated the mucosal layer:
1. It stimulates the conversion of pepsinogen to pepsin, damages gastric mucosa
2. It stimulates release of histamine which stimulates acid production, pepsinogen production, increase vasodilation and capillary permeability.

Note: Histamine causes inflammation of gastric mucosa.

25
Q

How are peptic ulcers induced?

A
  1. Increased gastric/ HCL acid and pepsin
  2. Reduced mucus and bicarbonate (protective barriers)
  3. Damage (impaired integrity) of the mucosal lining
  4. Reduced mucosal cells regeneration.
26
Q

Causes of peptic ulcer disease?

A

Helicobacter pylori
Non steroids anti-inflammatory drugs (NSAIDs)
Stressful lifestyle
Irritating diet
Smoking
Genetics

27
Q

How is Helicobacter pylori (H. Pylori) able to survive in an acidic environment?

A
  1. Flagella
  2. Urease - which converts urea into ammonia. Ammonia neutralizes gastric acid in the location of the H. Pylori and facilitates migration
  3. Settles in antrum
  4. Produces catalase, protects the microbe
  5. Inhibits protoglandin E2 and somatastatin
28
Q

How does H. Pylori affect the gastric mucosa of the GI layer?

A
  1. Secretes toxins that caused persistent inflammation (chronic gastritis)
  2. Damages the mucosal cells making cells permeable to gastric acid
  3. Mucosal lining become extremely leaky and loses it protective properties.
29
Q

How does NSAIDs (aspirin) promote the development of peptic ulcers.

A

It suppresses prostaglandin E2 (inhibits cyclooxygenase and inhibits the secretion of HCL) and increases the secretion of HCL

30
Q

Briefly describe the Zollinger- Ellison syndrome.

A
  1. Associated with increases secretion of gastrin.
  2. The gastrin is secreted by gastrinoma
  3. The gastric acid secreted from gastrin inactivates protein lipase, resulting in steatorrhea.
31
Q

List the treatment options of peptic, gastic and Duodenal ulcers.

A
  1. Proton pump inhibitors
  2. Histamine H2 receptor blockers - block acid secretion
  3. Oral antacids - buffer gastric acid
  4. Antibiotics to remove H. Pylori
32
Q

What is the pathophysiology of GERD

A
  1. Develops due to weak lower esophageal sphincter
  2. Precipitated by increased abdominal pressure via vomiting, coughing, lifting weights, bending.
  3. Delayed gastric emptying due to narrow pylorus.
33
Q

State the clinical manifestations of GERD.

A
  1. Gastric acid regurgitation
  2. Chest pain
  3. Chronic cough
  4. Laryngitis.
34
Q

State the clinical manifestations of peptic ulcer disease.

A
  1. Nausea.
  2. Epigastric burning pain
  3. Admoninal upset (dyspepsia)
35
Q

State the pathogenesis difference between gastric and duodenal ulcers.

A

Gastic ulcers occur when the gastric acid is of normal levels and even lesser than normal.

Duodenal ulcers occur when they is an increase in gastric acid secretion and pepsin (like peptic ulcers)

36
Q

State the treatment of GERD.

A

Proton pump inhibitors
Histamine H2 receptor antagonist
Antacids
Metaclopramide
Alginate

1402- Digestion (21 decks)

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