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First year semester 2 > Stomach > Flashcards

Stomach Flashcards

1
Q

What is swallowing

A
  1. Deglutition
  2. The propulsion of food from the oral cavity into oesophagus
  3. Food molded into bolus by tongue and moved upwards and backwards to pharynx: voluntary control, forces soft palette up to seal off nasal cavity
  4. Pressure sensitive sensory cells stimulated - swallowing centres in medulla initiate swallowing reflex: involuntary control.
  5. epiglottis closes off trachea
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2
Q

What is the anatomy of oesophagus

A
  1. most inside: Mucosal layer
  2. Submucosal layer
  3. Muscular layer
  4. Serosal layer - adventitia (loose connective tissue) only in neck.
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3
Q

What is the innermost layer of the oesophagus called and and what type of epithelium is present and why?

A
  1. Mucosal layer

2. Stratified squamous epi - protection

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4
Q

Why is the muscular layer in the oesophagus important?

A

Important for coordinating contractions of smoother or skeletal muscle when swallowing

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5
Q

What type of motility occurs in oesophagus

A

Peristalsis- movement of food in aboral direction

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6
Q

What is the arrangement of the muscular layer and why.

A
  1. inner arrangement is circular
  2. outer is longitudinal
  3. allows diff types of motility to occur
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7
Q

What type of muscle is in the oesophagus?

A
  1. varies according to species

2. Striated (can contract quickly) and smooth muscle

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8
Q

Comparative anatomy of oesophagus - dog, pig, cat, horse, bird

A
  1. DPC lot of striated muscle as bolt food down
  2. H, B rely lot more on smooth muscle
    * ** still involuntary!
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9
Q

How si the oesophagus innervated

A

Sympathetic:
1. via cervical sympathetic chain
Parasympathetic:
1. Special visceral efferent/ autonomic afferent via recurrent laryngeal (cranial division of XI) to cranial cervical oesophagus.
2. AE/AA via VAGUS (X) to caudal cervical/ thoracic oesophagus

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10
Q

Transport down the oesophagus after shut off soft palette and closed epiglottis

A
  1. physiological valve: upper oesophageal sphincter closes behind food bolus - stops food going back into mouth
  2. epiglottis opens to allow respiration
  3. complicated peristaltic contractions force food down oesophagus
  4. lower oesophageal sphincter opens to allow passage of food into stomach
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11
Q

What is the relationship of the oesophagus and diaphragm

A
  1. Oesophagus passed though D and joins stomach at an oblique angle
  2. so as stomach gets fuller it forces the two sides of D closer together which helps to shut off lower O sphincter so when contraction of stomach = more difficult for food to pass up. = prevents regurgitation of acidic stomach contents
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12
Q

What would a diagram of a food bolus travelling down oesophagus look like?

A
  1. contraction of smooth muscle behind bolus
  2. relaxation of circular smooth muscle infront of bolus
  3. coordinated contraction of longitudinal muslce to force food down.
    Like squeezing food down!
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13
Q

What is vomiting?

A

EMESIS

  1. The ACTIVE propulsion of stomach contents into oral cavity
  2. Deep inspiration to inc pressure of thorax via dia
  3. simultaneous closure of trachea/ nasal cavity
  4. Forceful contraction of lateral abdominal muscles
  5. cardiac sphincter opens, food propelled up oesophagus
  6. upper O sphincter opens
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14
Q

What controls vomiting and how is it stimualted?

A
  1. vomiting centre in medulla

2. stimualted by phyaryngeal/ gastric distension or irritation

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15
Q

What is a key difference between vomiting and regurgitation?

A
  1. Vomiting = contraction of abdominal wall muscle

2. Regurgitation = passive = contraction of smooth muscle

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16
Q

What are the functions of the stomach

A
  1. Digestion
  2. Protection - kill bacteria
  3. Storage
  4. Mechanical breakdown
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17
Q

What processes in stomach digestion

A
  1. Continuation of starch digestion
  2. Initiation of protein digestion
  3. from acid and pepsinogen
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18
Q

What is the “simple stomach” equivalent to in ruminants

A

Abomasum

Ruminants have 1 stomach, 4 compartments

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19
Q

What are the areas of the stomach

A
  1. top = fundus
  2. middle = corpus
  3. bottom = pylorus
  4. bottom bottom = pyloric sphincter
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20
Q

What cells line the stomach

A
  1. Cylindrical glands lined by
  2. Mucous (goblet) cells- prominent at exit to stomach lumen
  3. Parietal (oxyntic) cells - secrete HCl to digest protein
  4. Chief (peptic) cells = secrete pepsinogen (inactive pepsin) to digest protein
  5. Entero-endocrine cells - secrete hormones into blood stream
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21
Q

What do goblet cells secrete and why is this important in the stoamch

A
  1. mucous

2. protects the acid that goes into the middle of the stomach from digesting the stomach cells

22
Q

What activates pepsinogen

A

HCl

23
Q

What is the point of motility?

A
  1. Relaxation of stomach to receive meal
  2. contractions to mix and mechanically break down: acid and pepsinogen, empty into SI
  3. Prevent regurgitation of stoamch contents into O
24
Q

What is stomach relaxation when starts eating regulated by. What neurotransmitter

A
  1. regulated by swallowing centre via vagus nerve

2. Vasoactive inhibitory peptide transmitter

25
Q

Motility of stoamch: 6 marks

A
  1. mainly peristalsis
  2. Starts in fundus- weak contractions
  3. Propogate down corpus
  4. Pyloric sphincter opens to allow chyme into duodenum
  5. When contractions reach pylorus, pyloric sphincter closes
  6. food forced back into corpus helps mixing
  7. only small bolus of food out at a particular time - mainly because need to neutralise with bicarbonate
26
Q

How is stomach emptying stimulated

A
  1. Neural regulation - Expansion of stomach walls, nerves inc strength of contraction to reduce expansion as excessive = pain
  2. Hormonal regulation - gastrin released = dilation of pyloric sphincter and inc strength of contraction
27
Q

Why is stomach emptying inhibited?

A
  1. too much acidic food through SI too quick to be neutralised = stop stomach sending more
  2. Distend Duodenal wall
  3. too much nutrients
  4. high osmoregulatity
28
Q

How is stomach emptying inhibited

A
  1. Neural regulation via sympathetic/ dec para, via vagus
29
Q

Explain the digestion of carbohydrate in the stomach

A

species

30
Q

Explain the digestion of protein in the stomach

A

Explain the regulation of protein digestion in the stomach

31
Q

How is starch digested?

A
  1. Initiated by salivary amylase in mouth
  2. food not too much time in mouth
  3. newly swallowed food = forced into centre of stomach
  4. Acid secreted from stomach walls - delay for acid to reach centre = helps carbo digestion to carry on unhindered before acid comes along and deactivates salivary amylase
32
Q

Which species have and which don’t have salivary amylase?

A

humans, pigs, horses DO

Carnivores (not too much hydrolysabale carbo in diet), Dogs cats, ruminants DON’T

33
Q

How are Omnivores adapted to starch digestion

A
  1. High levels of starch in diet
  2. Pigs have adapted their stomachs to allow starch digestion to continue longer as hihgly reliable on hydrolysable carbo
  3. Sectioned off blind ending fundus = lined by epi that secreted mucous ONLY NOT acid
34
Q

How are Herbivores adapted to starch diets

A
  1. not tooooo much starch

2. stomach adapted to allow starch digestion to continue longer: blind ending fundus = stratified squamous epithelium

35
Q

How are carnivores adapted to starch diets

A
  1. no adaptation - no salivary amylase
36
Q

Comparison of salivary amylase levels in different species

A
  1. High in pigs
  2. Low in horses as their diet usually contains low levels of starch
  3. absent in carnivores and ruminants
  4. V high in humans (don’t have a stomach adapted for starch digestion such as horse and pigs)
37
Q

Explain digestion of protein in stomach

A

Explain regulation of protein digestion in stomach

38
Q

What is gastric juice

A
  1. Gastric juice = consists primarily HCL and Pepsinogen (which must be converted into pepsin to digest protein)
    2.
39
Q

Functions of HCL and what cell secreted from?

A
  1. convert inactive pepsinogen into active pepsin
  2. Provide required acidic environment for pepsin to digest protein
  3. Prevents fermentation by killing microorganisms
  4. from Parietal cell
40
Q

How is HCL secreted?

A
  1. CO2 out of blood stream into cell and combines with water in parietal cell forming bicarbonate H2CO3
  2. Carbonic splits into bicarbonate = out of cell into blood stream, and H+ which is secreted into lumen of gut (ATP requires)
  3. combines with Cl-
  4. bicarbonate into urine to ensure blood stream doesn’t inc pH
41
Q

Pepsinogen

A
  1. synthesised and stored in chief (peptic) cells
  2. Pepsinogen secreted, activated by HCl in stomach
  3. Pepsin breaks peptide links
  4. autocatalyst as pepsin can activate more pepsinogen
42
Q

How is secretion of gastric juice regulated?

A
  1. HORMONAL Acetylcholine, Histamine and Gastrin
  2. NERVOUS: long reflex arc via vagus, short locally within enteric
  3. Ach adn Histamine receptors stimulate acid
  4. gastrin receptors on ECL cell activated by gastrin, produce histamine which stimulates acid production - gastrin mediates its effect by stimulating ECL
43
Q

when is gastric juice secreted/ produced?

A
  1. Cephalic phase = Neural stimulation (before food entered stomach). Stimulates secretion Ach and gastrin
  2. Gastric phase - when food reaches stomach. Distension of stomach and presence of peptides in stomach lumen
  3. Intestinal phase = control outflow food from stomach to small I: inhibit or stimulate
44
Q

How is gastric juice inhibited

A
  1. Duodenal stretching inhibits stomach motility and gastric juice secretion
  2. Controlled neurally (vagus) and hormonally (secretin, CCK, gastric inhibitory peptide)
45
Q

When pH less than 2.0 what stops being released into stomach adn what mechanism

A
  1. GASTRIN
  2. to protect gastric mucosa from damage leading to ulceration
  3. Localised mechanism
  4. Protein can act as a buffer, binds to H+ = stimulates stomach to produce more acid for digestion
  5. Once protein digested = H+ accumulates = decrease urge for stomach to produce acid
46
Q

How is the stomach mucosa protected from HCL

A
  1. secretion of mucous layer
  2. Epithelial cell membrane and interconnecting tight junctions impenetrable by H+
  3. Epithelial cells are replaced every 2-3 days
47
Q

What is pathophysiology?

A

When physiology goes wrong

48
Q

How are duodenal and gastric stomach ulcers produced?

A
  1. D = increased acid production
  2. G = decreased protective function (layer of mucous)
    Same clinical effect
49
Q

If damaged epithelial cell why could this make the issue even worse?

A
  1. damaged cells produce histamine which stimulates acid secretion, intensifying the issue
50
Q

What is a clinical effect of gastric/ duodenal ulceration?

A
  1. lot of stuff secreted into lumen of gut
  2. Damaged absorptive capacity of gut = bleeding and less absorption
  3. fluid remains in lumen
  4. DIARRHOEA - dark red/ black blood
  5. vomit = bright red blood
51
Q

What things cause GI bleeding adn what colour blood and why?

A

Depends on where GI bleeding has occured

  1. Worms in LI = damage to mucosal surface. As distal = bright red
  2. Ulcer = proximal = partly digested = black
52
Q

Ulceration aetiology

A
  1. Non Steroidal anti inflammatory drugs (NSAIDs) = most common. Inhibit stomach’s ability to protect itself = less mucous and bicarbonate
  2. MAst cell tumours = produce EX histamins = inc gastric juice secretion = inc acid
  3. Gastrin producing tumours = inc HCl production

First year semester 2 (50 decks)

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