Stomach Flashcards

1
Q

Describe the process of swallowing that occurs in the oesophagus.

A
  1. Food molded into bolus by tongue and moved upwards and backwards to pharynx.
  2. Forces soft palette up to seal off nasal cavity.
  3. Pressure-sensitive sensory cells stimulated; swallowing centre in medulla initiates swallowing reflex (under involuntary control).
  4. Epiglottis closes of trachea.
  5. Complicated contraction/relaxation of muscles forces food into oesophagus.
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2
Q

What are the layers of the oesophagus?

A
  1. Mucosa: Protects the oesophageal lining (stratified squamous epithelium)
  2. Submucosa: Contains glands that secrete mucus for lubrication.
  3. Muscularis: Two layers of muscle:
    Inner circular layer: Contracts to push food downward.
    Outer longitudinal layer: Shortens the oesophagus during swallowing.
  4. Adventitia/Serosa: Outer connective tissue layer for structural support.
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3
Q

How is food transported down the oesophagus?

A
  1. Upper oesophageal sphincter closes behind food bolus (epiglottis opens to allow respiration).
  2. Complicated peristaltic contractions force food down oesophagus.
  3. Lower oesophageal sphincter opens to allow passage of food into stomach.
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4
Q

Why is the lower oesophageal sphincter always closed except during swallowing?

A

Prevents regurgitation of acidic stomach contents.

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5
Q

Describe the process of vomiting.

A

Active propulsion stomach contents into oral cavity.
1. Deep inspiration with simultaneous closure of trachea / nasal cavity –> increases intra-abdominal pressure via diaphragm
2. Forceful contraction of abdominal muscles
3. Cardiac sphincter opens
4. Food propelled up oesophagus
5. Upper oesophageal sphincter opens

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6
Q

How is vomiting controlled?

A

By vomiting centre in medulla; stimulated by pharyngeal/gastric distension or irritation.

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7
Q

What is gastric torsion and in what animals does it occur?

A
  • Horses and dogs with wide chests
  • Life-threatening condition where the stomach fills with gas (dilatation) and twists on its axis (volvulus). This twisting obstructs the exit of gas and fluid (seals off cardiac sphincter), impairs blood flow (shuts off caudal vena cava), and causes severe systemic effects.
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8
Q

Describe the four functions of the simple stomach?

A
  1. Digestion - continuation of starch digestion, initiation of protein digestion.
  2. Protection - stomach acid kills bacteria.
  3. Storage - ensures food delivered to small intestine at controlled rate.
  4. Mechanical breakdown / mixing - breaks down food and mixes with gastric juice forming a semi-liquid chyme.
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9
Q

Draw the anatomy of the simple stomach.

A

Esophageal sphincter –> Cardia –> fundus –> corpus –> pylorus –> pyloric sphincter
(look at diagram)

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10
Q

What cell types are in the stomach?

A

Consists of cylindrical glands:
1. Mucous (goblet) cells - secrete mucus to protect against HCl.
2. Parietal cells - secrete HCl to digest protein.
3. Chief cells - secrete pepsinogen ( inactive pepsin) to digest protein.
4. Entero-endocrine cells - secrete hormones.

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11
Q

What motility occurs when animal starts eating and how?

A

An initial relaxation of stomach smooth muscle to accommodate the meal (= receptive relaxation).
Regulated by swallowing centre via vagus.

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12
Q

Describe the main type of motility in the stomach.

A

Peristalsis:
1. Start in fundus with weak contractions
2. Propogate down corpus
3. Pyloric sphincter opens to allow chyme into duodenum
4. When contractions reach pylorus the pyloric sphincter closes
5. Food forced back into corpus helps mixing

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13
Q

How is stomach emptying regulated?

A
  • Mainly regulated by strength of contraction
    Also opening / closing of pyloric sphincter
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14
Q

What’s stimulates emptying of stomach?

A

Neural regulation - Expansion of stomach walls increases strength of contraction
Hormonal regulation – Release of gastrin increases strength of contraction and dilates pyloric sphincter

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15
Q

What inhibits stomach emptying?

A

Factors in duodenum act to inhibit gastric contractions
Neural regulation via increased sympathetic activity / decreased parasympathetic activity (via vagus)
Hormonal regulation via secretin, cholecystokinin & gastric inhibitory peptide (GIP)

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16
Q

Explain the digestion of carbohydrate in the stomach

A

Salivary amylase, which begins carbohydrate breakdown in the mouth, is inactivated by the acidic environment of the stomach.

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17
Q

Explain the digestion of protein in the stomach.

A

Protein digestion begins in the stomach where pepsinogen, secreted by chief cells, is activated into pepsin by stomach acid. Pepsin breaks down proteins into smaller peptides, preparing them for further digestion in the small intestine.

18
Q

What is the point of salivary amylase of food doesn’t spend much time in mouth?

A
  1. Newly swallowed food forced into centre of stomach.
  2. Acid secreted from stomach walls.
  3. Hence there is a gradual decline in pH from centre of stomach to edge that allows starch digestion to continue for a while.
19
Q

Which species don’t have salivary amylase?

A

Carnivores and ruminants

20
Q

How is pepsin secreted and why?

A

Inactive form (pepsinogen) so that digestion of self doesn’t occur.

21
Q

What is stomach ulceration?

A

Breach of mucosal barrier.

22
Q

What are the functions of HCl?

A
  1. Converts inactive pepsinogen into active pepsin.
  2. Provides acidic environment for pepsin.
  3. Prevents fermentation by killing micro-organisms.
  4. Degrades large chunks of connective and muscle tissue.
23
Q

What secrets HCl?

A

Parietal cells

24
Q

What synthesises and stores pepsinogen?

A

Chief (peptic) cells

25
Q

What stimulates secretion of gastric juice?

A
  1. Reflex arcs: long via vagus and short locally.
  2. 3 substances: amplify each other, acetylcholine/histmamine (direct stimulation of chief, parietal and mucin cells)
    Gastrin (almost entirely via stimulation of ECL cells to produce histamine)
26
Q

What causes release of gastrin and where does it go?

A
  • Peptides in stomach and distension
  • Reaches target cells via blood
  • Mediates its effect almost entirely via stimulation of ECL-cells to release histamine
27
Q

What does maximal HCl secretion require?

A

Simultaneous stimulation by acetylcholine, histamine & gastrin.

28
Q

What inhibits secretion of gastric juice?

A
  1. Secretin - secreted by the duodenum in response to acidic chyme entering the small intestine.
  2. Enterogastric reflex - triggered when the small intestine becomes distended or acidic chyme enters and decreases vagal stimulation.
  3. Low pH in stomach - when the stomach contents become highly acidic (pH < 2), negative feedback mechanisms reduce gastrin secretion.
29
Q

What causes duodenal ulcers?

A

Increases acid production

30
Q

What causes gastric ulcers?

A

Decreased protective functions

31
Q

What are the main specific causes of gastric and duodenal ulcers and why?

A
  1. Nonsteroidal anti-inflammatory drugs (NSAIDs): These inhibit prostaglandin production, reducing mucosal protection.
  2. Excessive acid production: Overproduction of gastric acid.
32
Q

Explain how gastric/duodenal ulceration is treated.

A
  1. Aimed at reducing HCl secretion - anti-histamines and proton pump inhibitors.
  2. Protecting ulcerated mucosa - antacids and mucosal binding agents.
33
Q

What is the role of bile salts in fat digestion?

A

They emulsify large fat globules into smaller droplets, increasing surface area for lipase action and prevent them coalescing.

34
Q

What enzyme breaks down triglycerides into monoglycerides and free fatty acids?

A

Pancreatic lipase.

35
Q

What are micelles, and why are they important?

A

Micelles are structures formed by bile salts and lipids; come into contact with phospholipid cell membrane & diffusion of mono-glyerides & FFAs into enterocyte occurs.

36
Q

How are absorbed lipids transported in the body?

A

As chylomicrons, through lacteals into the lymphatic system.

37
Q

What happens to the FFAs and mono-glycerides once in the cell?

A
  1. Re-esterified to form triglycerides in endoplasmic reticulum.
  2. Tri-glycerides coalesce along with cholesterol & phospholipids to form chylomicrons in the golgi apparatus.
38
Q

What are the main routes of water transport?

A
  1. Para-cellular - across tight junctions between epithelial cells.
  2. Trans-cellular - across cell membrane via transporter proteins (aquaporins/osmosis through sodium co-tranpsorters)
39
Q

Describe the absorption of iron and what enhances its uptake.

A
  1. Regulated according to requirements.
  2. Secondary active transport coupled with H+ via divalent metal transporter 1 (DMT-1).
  3. Vitamin C enhances absorption by reducing Fe³⁺ to Fe²⁺.
40
Q

Describe the absorption of calcium.

A
  1. Absorbed according to body requirements.
  2. Occurs both by active & passive transport.
  3. High dietary Ca2+ increases rate of passive transport
  4. When body calcium low or requirement high (e.g. growth / lactation) active transport stimulated by calcitrol
41
Q

Draw a table of the embryological organs of the stomach (in a dog).

A

Look at notes