Physiology of Digestion Flashcards

1
Q

what organs is the ailmentary canal made of

A

mouth, oesophagus, stomach, duodenum, jejunum, ilium( small intestine) large intestine, rectum and anus

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2
Q

what are the accessory digestive components

A

teeth, salivary gland, liver, gall bladder annd pancrease

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3
Q

process of digestion

A

ingestion, secretion, peristalsis, digestion and absorption, excretion

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4
Q

parts of the stomach

A

cardia
fundus

corpus(body)- pits made of surface epithelial cells, mucus neck cells, cheif cells and parietal cells.
parietal cells secrete HCL and intrinsic factor which is used for vitamin B12 absorption
cheif cells secrete pepsinogen, which is used for protein digestion

antrum- pits dont contain parietal cells so dont take part in acid secretion. they do contain G and D cells.
G cells secrete gastrin which causes HCL release from parietal cells.
D cells release somatostatin which stops G cells from secreting gastrin

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5
Q

preparation of acid secretion

A

occurs in parietal cells
NKCC1 channel moves 1 Na+, 1K+ and 2 Cl- from interstitium to parietal cell
Cl moves to gastric lumen via diffusion through Cl- channels
H20 and CO2 enter parietal cell from interstitium via basolateral membrane
carbonic anhydrase turns these compounds into H+ and bicarbonate
bicarbonate is pumped back into interstitium via AE2 channel which pumps more Cl- into parietal cell
H+ pumped from parietal cell to gastric lumen and K+ pumper other way via K+-H+ ATPase (inhibited by proton pump inhibitor drugs such as omeprazol)
H+ reacts with Cl- in gastric lumen to form HCl

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6
Q

acid secretion

A

vagus nerve can stimulate parietal cells directly to acid secretion or it can stimulate ECL cells to secrete histamine which acts on parietal cells
histamine is also release from ECL cells when gastrin act on CCK-2 receptors on parietal and ECL cells
the overall effect of this is the H-K ATPase expression is increased which releases more H+ ions
histamine receptor antagonists can reduce these effects to treat reflux

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7
Q

consequences of excess stomach acid

A

can damage small intestine as its layer of protective mucus is thin
pancreatic enzymes are PH sensitive so can denature die to excess acid
gastric acid entering small intestines cant be completely neutralised as theres too much
can degrade gastric mucosa leading to reduced amount of mucus producing cells

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8
Q

macronutrients

A

cant be used as energy is this original form
carbohydrates- broken down to glucose by hydrolysis and an enzyme (amylase, sucrase, lactase)
triglyceride
proteins- broken down to smaller peptide chains or single amino acids via hydrolysis

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9
Q

carbohydrate digestion (mouth, pancreas)

A

in the mouth parotid gland releases enzyme ptyalin which breaks down 5% of the carbohydrate (starch to maltose)
most carbohydrate digestion is in duodenum
acinar cells in pancreas secrete amylase which converts starch to maltose

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10
Q

carbohydrate digestion (small intestine)

A

occurs in enterocytes on villi in small intestines
lactase breaks down lactose into glucose and galactose
sucrase breaks down sucrose into glucose and fructose
maltase breaks down maltose into 2 glucose
alpha-dextrinase breaks down dextrin to maltose
is also the site of sugar absorption

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11
Q

lactose intolerance

A

lactase gene is not expressed from birth so body can’t produce lactase and break down lactose
thought to be due to be through evolutionary selection pressure due to some people drinking cow milk

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12
Q

protein digestion (stomach)

A

gastric distention and vagal stimulation cause G-cells to release gastrin
gastrin and vagal stimulation cause parietal cells to release HCl and chief cells to release pepsinogen
HCl and pepsinogen combine to form pepsin which breaks down proteins into smaller polypeptides
this makes up about 20% of breakdown

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13
Q

protein digestion (duodenum)

A

majority of protein digestion
partially digested food from stomach enters duodenum and is met with trypsin, chymotrypsin, carboxypeptidase and elastase from the pancreas
enteropeptidase activates trypsin which activates other digestive enzymes

remaining proteases break down polypeptides into amino acids
most of these amino acids are absorbed into circulation

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14
Q

fat digestion

A

fat enters duodenum as large gobules made of triglyceride, cholesterol and phospholipids
enteroendocrine cells are stimulated to release CCK hormone which causes the gall bladder to contract and release bile into small intestines

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15
Q

fat digestion (bile)

A

bile enters duodenum and emulsifies fats which makes them into smaller fat droplets which greatly increases their surface area

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16
Q

fat digestion (lipase)

A

lipase enters duodenum and breaks down triglyceride into 2 fatty acids and monoglyceride via hydrolysis
phospholipids and cholesterol are broken down into fatty acids

17
Q

fat digestion (micelles)

A

bile forms micelles out of monoglycerides and fatty acids to avoid making triglycerides
they trap fatty acids and monoglycerides by having a water soluable outside
enetrocytes use a H+Na+ pump to acidify environment around it which breaks down the micelles so the fatty acids and monoglycerides enter the cell and get repackaged by RER and golgi apparatus for further use