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Alimentary > Oesophagus+ Stomach > Flashcards

Oesophagus+ Stomach Flashcards

1
Q

Digestion definition

A

Breaking down macromolecules to allow absorption

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2
Q

Absorption defintion

A

Process of moving nutrients and water across a membrane

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3
Q

Components of GI system

lecture 1, slide 5

A

-

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4
Q

Gut wall layers+ functions

A

Mucosa/ epithelium- single cell lining facing gut contents
Lamina propria- connective tissue, connects epithelium to muscle
Muscularis mucosae (allow shape of folds in the mucosa to change)
Submucosa- connective tissue containing nerve plexus
Oblique muscle layer- only in stomach, able to create more forceful contractions
Muscularis- muscle, propel food along GI (smooth muscle= circular, then myenteric plexus, then longitudinal)
Serosa- connective tissue holding gut to rest of body
Epithelium

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5
Q 
Anatomy of oesophagus
Start?
End?
Goes through?
Close to?
A

Starts at C5
Ends at T11
Goes through diaphragm at T10
Close to trachea, aorta, recurrent laryngeal nerves (voice control), pericardium
Anatomically only in abdomen for a short space before stomach connection

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6
Q

Oesophagus epithelium structure and function

A

Oesophagus: Stratified squamous epithelial cells
Epithelium= thicker than other parts of the gut because no absorption+ need to withstand abrasive damage without loss of function.
Mucus-producing glands (as well as saliva) to ensure easy passage of food towards stomach

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7
Q 
Oesophagus muscle structure and function
Muscles at rest (no food)?
Muscles when swallowing?
Process of swallowing?
If the bolus is too big?
A

Upper + lower oesophageal sphincter
Upper made of skeletal muscle only
Lower made of skeletal and smooth muscle
Closed at both ends rest
Swallowing opens both up but upper one up more
Swallowing= peristaltic effect, nerve stimulus of food bolus responds to contract muscle above bolus+ relax muscle immediately below it so food forced down
Swallowing= independent of gravity
If bolus= too big, signal sent to brain+ second peristaltic wave initiated

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8
Q

Oesophagus function

A

Conduit for food, drink and swallowed secretion from pharynx to stomach

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9
Q

Gasto-oesophageal structure+ function

A

Epithelial transition from stratified squamous to simple columnar which is better for absorption

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10
Q

Gasto-oesophageal sphincter
Why is it less defined?
How is food prevented from going back up from the stomach
How can the stomach change size?

A

Diaphragm+ folding of stomach (opening is much more narrow when there is no food)
Diaphragm prevents food from going back up (not in pregnancy which is why they get heartburn)
Lining of stomach= ridged= gastric folds= allows stomach to change size when it’s empty+ can expand to smooth lining when full

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11
Q

Stomach function

A

Break food down into smaller particles
Hold food and release at a controlled steady rate into duodenum
Kill parasites+ certain bacteria

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12
Q

Sections of the stomach

A

Order from top to bottom:
Fundus, Cardiac, Body, Pyloric Antrum, Pyloric, Pylorus
Cardiac+ Pyloric= immediately entering+ leaving stomach= more mucus produced
Body+ Fundus (top part above entrance)= acid+ pepsinogen produced as well mucus
Antrum= after the body, endocrine element, gastrin produced to help facilitate stomach function

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13
Q

Types of cells in Antrum, Body and Fundus, Cardia and Pyloric

A

Cardia+ Pyloric: mucus producing cells, closest to stomach contents, produce mucus+ bicarbonate trapped in mucus gel= allows pH of cells to be maintained at 6/7, also goblet cells producing mucus
Body+ Fundus: produce HCl= denatures proteins
Antrum: Chief cells that produce pepsinogen (precursor that produces pepsin to break down protein)+ G cells (enteroendocrine cells) that produce gastrin

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14
Q

How much stomach fluid is produced a day?

A

2L/day

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15
Q 
Peristalsis
% of stomach contraction?
Beginning+ end?
Change in peristalsis across stomach?
How are larger materials dealt with?
What is it also driven by?
Small intestine?
A

Propels chyme towards colon
Begin as gentle muscle contractions near lower oesophogeal sphincter+ end at pyloric sphincter
20% stomach contractions
Contractile waves near distal end become stronger+ forceful= mixed chyme before passing
Also driven by CNS (vagus nerve)
Sequential contraction of adjacent rings of smooth muscle

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16
Q 
Segmentation
Involves?
% of stomach contraction?
Fluid chyme vs solid chyme
Driven by?
Small intestine?
A

Mixes ingested food with stomach secretions to form chyme, less coordinated
Fluid chyme pushed towards pyloric sphincter, solid part pushed back towards stomach body
80% stomach contractions
Driven by enteric nervous system (local nervous stimulation)
Chyme moves in both directions but net effect= forward
Stationary contractions of circular muscles at intervals, more frequent at duodenum compared to ileum= pancreatic enzymes+ bile can mix with chyme

17
Q

Gastric Chief Cell features

What else is required for gastric cell secretion to function?

A 
Pepsinogen secreting epithelial cells
Abundant RER
Golgi packaging+ modifying
Masses of apical secretion granules
Acid required to facilitate pepsinogen breaking down= protein breakdown
18
Q

Parietal Cell features
Resting
Active
Function

A

Acid secreting cell
Resting:
1. Canaliculi= large internal resevoirs (look like large mitochondria)
2. Cytoplasmic tubulovesicles that contain H+/K+ ATPase
Active:
Tubulovesicles fuse with membrane+ microvilli project into canaliculi= larger SA for H+/K+ ATPase + resevoir to come into contact with lumen

Function= protein digestion

19
Q

Parietal cell activation

A
  1. CO2 from interstital fluid/ capillaries+ H20 from cell required to generate H2CO3 which dissociates to H+ and HCO3- with carbonic anhydrase enzyme in cell
  2. Na/ K ATPase on basal cell membrane pumps Na out of cell, K+ into cell
  3. HCO3- produced by carbonic anhydrase exchanged for Cl-
  4. K+ and Cl- diffuse out into gastric lumen and lots of mitochondria= ATP used to drive H+ ions against conc. gradient in exchange for K+ with H+/ K+ ATPase on apical cell membrane
20
Q 
Enteroendocrine cells
Example?
Found?
Releases?
Stimulates what from where?
A

Found in pyloric antrum
G cells release gastrin if there is food in stomach= indirect acid secretion
Stimulates histamine release from entero-chromaffin cells (also an enteroendocrine cell)= direct acid secretion
Gastrin+ Histamine stimulate acid release from parietal cells (as well as acetylcholine from vagus nerve)

21
Q

1st phase of gastric secretion

See slide 34 lecture 1 for summary

A

Cephalic phase- Before food in stomach

Stimulated by conditioned response to sensory stimuli which activates vagus nerve= acid production

22
Q

2nd phase of gastric secretion

See slide 34 lecture 1 for summary

A

Gastric phase- food in stomach
Nerves in stomach lining respond to chemical and physical change in stomach + activate muscles and glands.
Also central control (stomach distension detected by vagus= muscle contraction)

23
Q

3rd phase of gastric secretion
When is it not inhibitory?

See slide 34 lecture 1 for summary

A

Intestinal phase- food has left stomach into intestine
Signal goes to brain causing enterogastric reflex: cells in intestine produce gastric inhibitory peptide, cholecystokinin and secretin which switch off HCl+ pepsin production
Not inhibitory when protein conc in stomach is higher than expected= signals stomach hasn’t completely broken down protein= antrum produces more gastrin= exitatory response

24
Q

Two drugs used to decrease acid secretion

A

Omenprazole- inhibits H+/K+ ATPase

Ranitidine- targets histamine receptor

25
Q

Summary diagram of secretions

slide 38, lecture 1

A

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Alimentary (12 decks)

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