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Digestive System > Digestive System Physiology + GI investigations > Flashcards

Digestive System Physiology + GI investigations Flashcards

1
Q

What are the four main functions of the GI tract?

A

digestion
secretion
absorption
motility

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2
Q

what are the four main histological layers of the gut tube? what are their sublayers?

A

mucosa - epithelium, lamina propria, muscularis mucosae
submucosa
muscularis externa - concentric + longitudinal
serosa/adventitia

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3
Q

what is the Enteric Nervous System and where in the gut lining is it found?

A

nervous system without any brain input, controls GI tract.

made up of submucosal plexus (under submucosa) + myenteric plexus (between muscle layers of muscularis externa)

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4
Q

where in the GI tract is stratified squamous epithelium found?

A

mouth
oesophagus
anal canal

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5
Q

where in the GI tract is simple columnar epithelium found?

A

stomach
small intestine
large intestine

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6
Q

what is the arterial blood supply to the GI tract in the abdomen?

A

celiac trunk
superior mesenteric artery
inferior mesenteric artery

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7
Q

what are the main branches of the celiac trunk?

A

left gastric artery
splenic artery
hepatic artery

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8
Q

what is the venous drainage from the GI tract, and where does it lead to?

A

gastric veins
splenic veins
superior and inferior mesenteric veins
drain into the hepatic portal vein and into the liver

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9
Q

what is the parasympathetic action on the GI tract, and from which nerves?

A

increased salivation - CNVII (facial) and CNIX (glossopharyngeal)
increased motility - CNX (vagus)
increased secretion - CNX (vagus)

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10
Q

what is the sympathetic action on the GI tract, and from which nerves?

A

decreased motility - splanchnic nerves
decreased secretion - splanchnic nerves
some salivation

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11
Q

what are the main functions of the submucosa in the gut tube?

A

support of the mucosa

contain glands in oesophagus and duodenum

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12
Q

what is the reason behind the change in term between serosa and adventitia?

A

serosa - lined by peritoneum

adventitia - not lined by peritoneum (not in abdomen)

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13
Q

what is the function of the muscularis mucosae?

A

slight contraction to help glands secrete their contents

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14
Q

what is the function of the muscularis externa layers?

A

concentric layer - segmentation

longitudinal layer - peristalsis

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15
Q

what is dumping syndrome and how is it avoided in nature?

A
  • food entering the small intestine too fast and water entering the gut lumen through osmosis creating a huge load on the gut
  • avoided through the gradual breakdown of polimerised nutrients rather than intake of simple monomers of carbs/fats/proteins
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16
Q

what are three kinds of carbohydrate monosaccharides?

A

glucose
galactose
fructose

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17
Q

what are the three kinds of carbohydrate disaccharides, and what are they made up of?

A 
lactose = glucose + galactose
maltose = glucose + glucose
sucrose = glucose + fructose
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18
Q 
what are the three kinds of carbohydrate polysaccharides? 
which one(s) can the GI tract not digest and why?
A

starch
glycogen
cellulose (not digested by GI tract because made up of beta1-4 glycosidic bonds)

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19
Q

how is cellulose broken down by the GI tract?

A

digested by the bacteria colonising the colon

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20
Q

what are the two main types of starch and their differences?

A

alpha-amylose - unbranched alpha1-4 glycosidic bonds

amylopectin - branched alpha1-6 glycosidic bonds

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21
Q

which transport proteins carry which monosaccharides into enterocytes, and what other molecules do they co-transport?

A

glucose and galactose = SGLT1 transporter. co-transport of Na
fructose = GLUT5 transporter. no co-transport

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22
Q

what transport protein transports monosaccharides out of the enterocytes and into the bloodstream?

A

GLUT2 transporter

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23
Q

is there a movement of water from the gut lumen into the gut wall in monosaccharide absorption? be specific

A

glucose - yes, water enters the gut wall
galactose - yes, water enters the gut wall
fructose - no water movement

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24
Q

why is there no movement of water in fructose absorption?

A

because there is no co-transport of charged molecules into the enterocytes with fructose absorption

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25
Q

how does Na leave the enterocyte after being pumped into the cell through SGLT1 and GLUT5?

A

through the Na-K-ATPase pump (sodium potassium pump)

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26
Q

where in the epithelial cells of the GI tract are the sodium potassium pumps located?

A

all along the basolateral membrane

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27
Q

what are the membranes in enterocytes relevant for absorption barriers?

A

apical membrane

basolateral membrane

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28
Q

which enzymes breaks down which carbohydrates and where?

A

alpha-amylase - breakdown of polysaccharides in mouth and small intestine
sucrase/lactase/maltase - breakdown of disaccharides (sucrose/lactose/maltose) in small intestine

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29
Q

which types of alpha-amylase are there?

A

salivary amylase

pancreatic amylase

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30
Q

how are monosaccharides distributed around the body?

A

through the bloodstream

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31
Q

what enzymes break down proteins? what are the two classifications and their properties?

A

enzymes: peptidases or proteases
endopeptidases/endoproteases - cleave protein/peptide anywhere along peptide chain and split it in two or more peptides
exopeptidases/exoproteases - cleave one amino acid at a time from each end of the peptide chain

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32
Q

with what chemical process do proteases/peptisases break down peptide chains?

A

hydrolysis of peptide bonds

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33
Q

what is PepT1 and why is it important?

A

proton (H) coupled transporter which transports peptides into the epithelial cells
it’s important because it proves proteins aren’t only absorbed as amino acids, but as di/tripeptides

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34
Q

what percentage of proteins are absorbed as polypeptides through the PepT1 transporter?

A

~70%

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35
Q

what are the membrane transporters which allow proteins into epithelial cells, and what are they coupled to?

A

SAAT1 (coupled with Na transport) - carry amino acids

PepT1 (coupled with H transport) - carry di/tripeptides

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36
Q

how is H recycled after the use in the proton pump PepT1?

A 
through NHE3 (sodium hydrogen exchanger 3)
allows Na into the cell and pumps H back out into lumen
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37
Q

where along the GI tract are proteins digested?

A

stomach and small intestine

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38
Q

does amino acid transport across the gut epithelium trigger water absorption?

A

yes

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39
Q

what lumen environment does PepT1 require to function and what explains it?

A

acidic environment, because it needs H ions to be able to transport peptides

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40
Q

what are the membrane transporters involved in protein absorption from the gut?

A

SAAT1
PepT1
NHE3 (indirectly involved with PepT1)

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41
Q

what are the membrane transporters involved in carbohydrate absorption from the gut?

A

GLUT2
GLUT5
SGLT1

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42
Q

what is the main structure of lipids which enter our digestive tract?

A

triacylglycerides

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43
Q

how are fats globules reduced in size for absorption? what structure is responsible?

A

separated in smaller fat globules by oesophageal smooth muscle

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44
Q

how are small fat globules prepared for digestion, after separation by the oesophageal motility?

A

separated fat globules surrounded by emulsifiers (bile salts)

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45
Q

what enzyme breaks down fats once emulsified?

A

pancreatic lipase

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46
Q

which organs are responsible for the digestion of fats from the gut, and by what action?

A

pancreas - secretes pancreatic lipase

liver - secretes bile

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47
Q

what is the role of bile salts in the digestion of fats?

A

it emulsifies fat globules to keep them separate

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48
Q

how is absorption of fats maximised once fat globules are emulsified?

A
  • lipase breaks down fat globules into monoglycerides and free fatty acids
  • micelles formed which carry fats across the mucous layer to the epithelial brush border
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49
Q

what is the function or micelles?

A

they carry monoglycerides and free fatty acids through the mucous layer of the small intestine for absorption into the gut cells

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50
Q

what happens to the fatty acids once absorbed by gut cells? (4 stages)

A
  • reassembled into TAG in smooth endoplastic reticulum
  • processed in the Golgi body
  • exocitosed from cell to extracellular space
  • TAG picked up by lacteals in form of chylomicrons
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51
Q

how are fats distributed around the body from the gut, and in what form?

A

fats take form of chylomicrons which enter lymphatic system through lacteals

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52
Q

what makes micelles break down at the gut brush border?

A

the acidic microenvironment on the surface of the brush border

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53
Q

what are the possible ways vitamins can be absorbed from the gut? what is the exception?

A 
fat soluble (A,D,E,K) - same as lipids
water soluble (B, C) - diffusion or carrier mediated
exception: Vitamin B12 - needs intrinsic factor
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54
Q

what are the molecules responsible for fat emulsification?

A

bile salts

phospholipids

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55
Q

where are lipids digested in the gut?

A

small intestine

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56
Q

where is vitamin B12 absorbed?

A

distal ileum

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57
Q

what are molecules responsible for iron absorption and storage, and where are they found?

A

ferritin - in gut cells

transferrin - in blood

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58
Q

why is ferritin important? explain how it works

A

it regulates the amount of iron absorbed by the body:
low iron in body - less ferritin so more free iron
high iron in body - more ferritin so more iron trapped in gut cell

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59
Q

what does ferritin do?

A

it captures absorbed iron from the gut when there is no need for it

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60
Q

how much ingested iron is actually absorbed by the body?

A

~10%

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61
Q

what are micelles made up of?

A

bile salts
phospholipids
fatty acids
monoglycerides

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62
Q

why is emulsification of fats necessary?

A

because it would take lipase too long to break down fat globule otherwise

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63
Q

what are the main components of saliva and their respective functions? (5)

A

water - soften food
mucins - create mucous with addition of water
alpha-amylase - to break down complex carbs
electrolytes - maintain pH
lysozyme - break down bacteria

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64
Q

name the salivary glands

A

parotid gland
submandibular gland
sublingual gland

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65
Q

what are the types of glands in the salivary glands, and what are their functions? (2)

A

mucous glands - produce mucins

serous glands - produce amylase

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66
Q

how is salivation controlled?

A

parasympathetic system - facial and glossopharyngeal nerves (CN 7 and 9)
sympathetic system - adrenergic fibres (apha1 for mucins and alpha2 for serous)
reflex from chemoreceptors in wall of mouth and tongue - salivary secretion when food enters mouth

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67
Q

what type of muscle innervates the oesophagus?

A

upper third - skeletal
middle third - skeletal and smooth
lower third - smooth

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68
Q

what are the stages of swallowing and what happens during each? (4)

A
  1. oral phase - food moved back to soft palate by tongue
  2. pharyngeal phase - reflex contraction of pharyngeal muscles (controlled by medulla): nasopharynx and epiglottis close, upper oesophageal sphincter relaxes
  3. oesophageal phase - bolus moves down through peristalsis
  4. gastric phase - lower oesophageal sphincter relaxes, bolus enters stomach, stomach relaxes
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69
Q

what is the type of epithelium that lines the oesophagus and why?

A

non-keratinised stratified squamous epithelium

  • non-keratinised because if keratinised it would be too rigid
  • stratified squamous to provide enough thickness to withstand sharp bits of food
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70
Q

what is the histological structure of the gut tube wall?

A
  • mucosa (epithelium, lamina propria, muscularis mucosae)
  • submucosa
  • muscularis mucosae (circular, longitudinal, oblique in stomach)
  • adventitia (oesophagus)/serosa (in peritoneum)
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71
Q

what is the function of rugae in the stomach?

A

prevent the stomach lining to become too thin when it stretches in response to food entering the stomach

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72
Q

what are the main functions of the stomach? (5)

A
  • storage of food
  • control of gastric emptying
  • break down food and begin digestion (pepsin)
  • produce gastric acid to destroy pathogens - sterilisation
  • produce intrinsic factor
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73
Q

what are the three layers of the stomach muscle and what are their individual actions on the stomach?

A

inner oblique layer - wringing motion
circular layer - contraction
longitudinal layer - shortening

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74
Q

how is chewing controlled? (2)

A

voluntary control - skeletal muscle

reflexes

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75
Q

what are the three mechanisms that control gastric secretion?

A

neuroendocrine (ACh through vagus nerve)
endocrine (gastrin)
paracrine (histamine/prostaglandins)

76
Q

which mechanism has an inhibitory effect on gastric secretion?

A

paracrine through prostaglandins

77
Q

which mechanism causes a rise in intracellular calcium to trigger gastric secretion and how?

A

gastrin and ACh

they cause an increase in calcium, which activates Protein Kinase C and activates the H-K ATPase (proton pump)

78
Q

which intracellular mechanism steps are essential for maintaining a low pH in the stomach lumen? (4)

A
  • CO2 and H2O combining to form carbonic acid
  • carbonic acid dissociation into bicarbonate + H
  • H pumped out to lumen through proton pump
  • chloride pumped out to lumen as a result of H-K pump action
79
Q

which cells produce gastric acid, and what else do they produce?

A

parietal cells. also produce intrinsic factor

80
Q

what is the purpose of intrinsic factor?

A

it is essential for the absorption of vitamin B12 in the distal ileum

81
Q

what is gastrin, where is it secreted and how does it work?

A
  • gastrin is a hormone which promotes gastric acid secretion
  • gastrin is secreted by G-cells in the stomach antrum
  • gastrin is secreted into the circulation and goes to act on parietal cells which will produce HCl as a result
82
Q

what is produced in parallel with gastric acid, from which cells?

A

pepsinogen. produced from chief cells

83
Q

what is pepsinogen and how does it work?

A

it’s a zymogen secreted and stored by chief cells

when hydrolised by gastric acid at low pH it turns into active pepsin, which digests peptides

84
Q

how does the stomach protect itself from gastric acid and pepsin, and how is this different from the small intestine?

A

through secreting a layer of mucous on its epithelial surface
the mucous in the stomach has neutral pH, whereas the small intestine has an acidic mucous with low pH

85
Q

how are parietal cells stimulated?

A

through vagal input directly to parietal cells
through vagal input into G-cells –> gastrin acting on parietal cells
through ACh and gastrin input into ECL cells –> histamine production –> act on parietal cells

86
Q

what is histamine secreted by in the stomach, what triggers its secretion and what does it do?

A

secreted by enterochromaffin-like (ECL) cells
secretion triggered by ACh and gastric action
causes activation of parietal cells

87
Q

what is the function of parietal cells, chief cells and mucous cells in the stomach?

A

parietal cells - secrete HCl and intrinsic factor
chief cells - secrete pepsinogen
mucous cells - secrete neutral pH mucous for protection

88
Q

what inhibits gastric acid secretion?

A

inhibition of vagal input (stop eating)
lower pH, higher HCl levels in stomach
release of enterogastrones from the small intestine (CCK, secretin)

89
Q

what are enterogastrones?

A

they are hormones which inhibit gastric acid secretion and reduce gastric emptying

90
Q

what triggers release of enterogastrones?

A

the presence of acid/fat/carbs in the duodenum

91
Q

what is the purpose of enterogastrones?

A

reducing the amount of acid in the duodenum

92
Q

what are the two phases during which parietal cells are activated for gastric acid secretion?

A

cephalic phase

gastric phase

93
Q

where are G-cells found?

A

in antrum of stomach

94
Q

where are parietal cells and chief cells found?

A

in gastric glands of stomach epithelium

95
Q

how do histamines trigger production of gastric acid from parietal cells?

A

through G-protein coupled receptor (adenylyl cyclase) which turns ATP into cAMP –> activates Protein Kinase C –>activates proton pump

96
Q

how do ACh and gastrin trigger production of gastric acid from parietal cells?

A

through an increase in intracellular calcium, which activates Protein Kinase C and stimulates proton pump

97
Q

what triggers parietal cells during the gastric phase of gastric acid secretion?

A

distension of stomach (food arriving) - causes vagal reflex –> stimulates parietal cells
presence of peptides in stomach - stimulates G-cells –> act on parietal cells

98
Q

explain why pepsin creates a positive feedback loop

A

because once activated by low pH it can trigger more pepsinogen secretion from chief cells, which due to the low pH are in turn activated to pepsin

99
Q

what is a zymogen?

A

it’s an inactive form of an enzyme

100
Q

why is pepsin secreted by chief cells as a zymogen?

A

because the activated form of pepsinogen would digest the stomach itself, as it’s made of proteins

101
Q

what is a disease related to a lack of intrinsic factor, and why?

A

pernicious anaemia
because it impairs RBC maturation, but it takes long to show symptoms as even though a lack of intrinsic factor stops vitamin B12 absorption, the liver still has a 3 year supply of vitamin B12 before it runs out

102
Q

what is the electrical underlying current which controls peristaltic movement in the stomach?

A

base eletrical rhythm (BER)

103
Q

why does the BER not always cause contractions?

A

because it is normally sub-threshold, and needs neuronal or hormonal input to reach threshold and create an action potential

104
Q

what does the strength of gastric peristaltic contractions depend on?

A

the number of action potentials fired through neuronal and hormonal input

105
Q

what neuronal and hormonal input promotes peristaltic contractions of the stomach?

A

hormonal - gastrin

neuronal - vagal input/reflexes from stomach stretching

106
Q

where in the stomach is the muscle layer thickest and why?

A

antrum. because bolus gets churned and mixed here before gastric emptying

107
Q

what happens in the duodenum as soon as bolus has passed the pyloric sphincter into the duodenum itself? (3)

A

release of secretin from S-cells
release of bicarbonate from Brunner’s glands
release of cholecystokinin (CCK)

108
Q

what is the purpose of secretin being secreted on arrival of bolus into the duodenum? (3)

A

it promotes the secretion of bicarbonate from pancreatic duct cells
it decreases gastrin secretion
it reduces peristaltic movement in the stomach

109
Q

what is the point of pancreatic duct cells secreting bicarbonate?

A

it helps to neutralise the gastric acid which has entered the duodenum from the stomach

110
Q

what is the purpose of CCK being secreted on arrival of bolus into the duodenum? (3)

A

it promotes zymogen secretion from the pancreatic acinar cells
it promotes relaxation of Sphincter of Oddi
it promotes contraction of gallbladder –> bile release

111
Q

what happens to pancreatic enzymes (zymogens) when they reach the duodenum through the pancreatic duct?

A

they are activated by trypsin into active enzymes

112
Q

what allows active trypsin to activate pancreatic enzymes?

A

the membrane-bound enterokinase, which turns trypsinogen into trypsin

113
Q

what reduces the peristaltic movement of the stomach?

A

secretin secretion, in response to acid entering the duodenum

114
Q

what are Brunner’s glands, where are they located and what is their purpose?

A

they are glands in the duodenal submucosa which produce bicarbonate

115
Q

what are the names of the channels in the liver which hold 1. bile, 2. blood?

A
  1. bile canaliculi

2. hepatic sinusoids

116
Q

what is the characteristic of the blood in the liver sinusoids?

A

carry both arterial and venous blood

117
Q

what are the main alimentary functions of the liver? (2)

A
  • production of bile

- storage of nutrients from hepatic circulation

118
Q

what are the contents of bile? (6)

A
  • cholesterol
  • lecithin
  • bile acids
  • toxic metals
  • bile pigments (bilirubin)
  • bicarbonate
119
Q

which of the bile contents is produced by the hepatic duct cells?

A

bicarbonate

120
Q

what is bilirubin?

A

breakdown product of heme group from recycled RBC’s.

121
Q

what is the porta hepatis?

A

it’s the area of liver which allows access to the hepatic ducts, the hepatic artery and the hepatic portal vein

122
Q

list the 4 main functions of hepatocytes in the liver

A
  • store nutrients
  • nutrient interconversion (glucose to glycogen)
  • production of bile
  • detoxification
123
Q

what are the individual actions of CCK in response to fats/proteins in the duodenum? (3)

A
  • relaxation of Sphincter of Oddi
  • contraction of gallbladder
  • release of zymogens from pancreatic acinar cells
124
Q

what is the generic function of secretin and CCK?

A

secretin - neutralisation of acid through promotion of bicarbonate
CCK - digestion through bile and pancreatic acid secretion

125
Q

how are bile acids rendered more soluble?

A

through addition of glycine or taurine

126
Q

what are the three layers of the gallbladder wall?

A

mucosa
muscularis
serosa

127
Q

what are the fat emulsifying elements of bile? (3)

A

cholesterol
lecithin
bile acids

128
Q

what is the function of villi and crypts in the small intestine?

A

villi - absorption

crypts - secretion

129
Q

what do crypts of Lieberkuhn secrete in the small intestine?

A

chloride and water

130
Q

how is cystic fibrosis related to the secretion of chloride in the small intestine?

A

water follows osmotic gradient of chloride into the gut lumen. if the chloride channel isn’t working (CFRT) no chloride exits cell, so no water is secreted

131
Q

why is sodium absorption important in the small intestine?

A

because sodium transport is coupled to transport of other nutritional molecules (glucose, peptides etc)

132
Q

what is the purpose of microvilli?

A

increase surface area for absorption

133
Q

what is the difference between peristalsis and segmentation, and what are their functions?

A

segmentation - moves chyme back and forth - promotes mixing
peristalsis - sweeps chyme down small bowel towards large bowel - ensures nothing is left in small intestine and reduces risk of bacterial colonisation of small bowel

134
Q

when does segmentation start?

A

when chyme enters the small intestine

135
Q

when does peristalsis start?

A

when absorption is complete

136
Q

what is the gastro-ileal reflex?

A

closure of the ileocaecal sphincter in response to distension of colon, when chyme has entered large bowel

137
Q

in what parts of small intestine epithelium is water secreted and absorbed?

A

secreted - crypts of Lieberkuhn

absorbed - villi

138
Q

how is concentration of bile controlled?

A

absorption of water by gallbladder epithelium
lots of fatty food - lots of dilute bile
small amount of food - a little, concentrated bile

139
Q

what electrical mechanism controls small intestine peristalsis and segmentation?

A

peristalsis - BER and stimulation through action potentials

segmentation - Migrating Motility Complex (MMC)

140
Q

how does the small gut ensure that chyme only travels towards large bowel and not in the other direction?

A

because the BER contractions are stronger at the top of the small intestine, and tail down towards the rectum

141
Q

what is the pH of the mucous layer lining the small intestine?

A

acidic microclimate

142
Q

what is the pH of the mucous layer lining the stomach?

A

neutral pH - mucous containing bicarbonate

143
Q

what hormone initiates the action of the Migration Motility Complex (MMC) in the small intestine?

A

motilin

144
Q

where is the majority of nutrients absorbed in the small intestine?

A

in the jejunum

145
Q

during which phase of eating does segmentation occur?

A

when there is food in the stomach

146
Q

what’s the histological appearance of the colonic epithelium?

A

flat, deep crypts containing goblet cells

147
Q

what characteristics of the muscularis externa differentiate the colon from the small intestine?

A

incomplete longitudinal layer - teniae coli

circular layer bunched up - haustra

148
Q

what are the main functions of the colon? (2)

A
  • absorb water

- allow undigestible molecules to be broken down by gut flora

149
Q

how is water absorbed from the colon?

A

through the sodium-potassium ATPase which pulls in Na, driving passive water movement into epithelial cells

150
Q

what are the three breakdown products of cellulose by gut flora in the colon?

A
  • gas
  • vitamin K
  • short chain fatty acids
151
Q

what drives the movement of chyme through the colon?

A

MMC - Mass Movement Contraction

152
Q

what causes the urge to defecate?

A

the relaxation of the rectum wall

153
Q

what are the two checkpoints faeces have to go through prior to defecation, and what controls them?

A

internal anal sphincter - involuntary (pelvic splanchnic nerves)
external anal sphincter - voluntary (descending pathways)

154
Q

what are four common symptoms of constipation?

A

nausea
headaches
abdominal distension
loss of appetite

155
Q

what is the main reason for constipation?

A

distension of the rectum

156
Q

what causes diarrhoea?

A

increased secretion of chloride from crypts, causes passive movement of water into the colon lumen

157
Q

what is the main treatment for diarrhoea?

A

sodium and glucose infusion to promote water absorption

158
Q

what is the purpose of the bacterial colonisation in the colon?

A

to break down undigestable material (cellulose)

159
Q

how much of our body weight is derived from colonic bacteria?

A

about 1kg

160
Q

how much does a normal liver weigh?

A

~1.4kg

161
Q

how much does a normal spleen weigh?

A

~150g

162
Q

what are the sections of the large bowel? (5)

A 
ascending colon
transverse colon
descending colon
sigmoid colon
rectum
163
Q

what are the sections of the small bowel? (3)

A

duodenum
jejunum
ileum

164
Q

what kind of epithelium is found in the anal canal?

A

junctional epithelium - simple columnar to stratified squamous

165
Q

where is the thickest layer of muscularis externa found?

A

rectum and anal canal

166
Q

what neuronal mechanism controls the defecation reflex?

A

parasympathetic - pelvic splanchnic nerves

167
Q

what is the role of enterotoxins in diarrhoea, and which organisms are responsible for them?

A

organisms: vibrio cholerae; Escherichia coli

turn up the chloride secretion from crypts in colon through upregulation of cAMP, cGMP and calcium

168
Q

what is a significant complication of diarrhoea, and in which age groups?

A

dehydration in the elderly and very young

169
Q

where in the gut lining are immune cells found?

A

in the lamina propria, under the epithelium

170
Q

what are the lymphoid aggregations in the gut lining called?

A

Peyer’s Patches

171
Q

what is the importance of macrophages in the digestive tract?

A

effective at picking up and phagocytosing pathogenic organisms

172
Q

what is the position of dendritic cells, and what is their importance in the digestive tract?

A

sit in the lamina propria and in Peyer’s patches,with parts sticking through epithelium and into the lumen
they sample organisms in the lumen and present them to T cells for an appropriate response

173
Q

what are mature dendritic cells also known as?

A

antigen presenting cell (APC)

174
Q

what are M cells and what is their role?

A

specialised cells in the gut epithelium

responsible for sampling the gut lumen contents and present particles for analysis in Peyer’s Patches

175
Q

what are two examples of an imbalance of the immune system in the gut?

A

inflammatory bowel disease

coeliac disease

176
Q

what is the general pathology behind IBD?

A

leaky epithelial layer allowing pathogenic organisms to get through to lamina propria, causing an inflammatory response

177
Q

which immune cells are responsible for maintaining homeostasis in gut?

A

T reg cells

178
Q

what is the function of cytokines in the gut immune response?

A

they regulate the differentiation of T cells to act as pro-inflammatory or anti-inflammatory

179
Q

what is the general pathology behind coeliac disease?

A

exaggerated immune response to an indigestible particle derived from gluten

180
Q

what is the role ot Th1 cells in the gut?

A

trigger an appropriate response to pathogens

181
Q

what is the role of TReg cells in the gut?

A

maintain homeostasis and promote tolerance to self/benign antigens

182
Q

list some of the features to be picked up at the bedside for GI investigations

A
  • BMI changes
  • pulse
  • BP
  • ECG
  • temperature
  • urinalysis
  • capillary glucose
183
Q

list some tests done with stool samples for GI investigations, and what they look for

A
  • FOB (fecal occult blood)/FIT (fecal immunochemical test) - look for microscopic traces of blood in faeces
  • faecal calprotectin - detects/rules out inflammation
  • faecal elastase - measures pancreatic function
  • faecal culture - looks for bacteria
184
Q

name some examples of blood tests specifically carried out for GI investigations

A 
FBC, U&E, creatinine, CRP, ESR
LFT's, TFT's
haematinics: vit B12, folate, ferritin
calcium/magnesium/phosphate
serology (autoantibodies)
alpha-1 antitrypsin
alpha fetoprotein
glucose/HbA1c
lipid profile
185
Q

list some of the endoscopic imaging tests carried out for GI investigations

A
  • endoscopy
  • colonoscopy/sigmoidoscopy
  • ERCP
  • EUS
  • enteroscopy (+/- capsule)
186
Q

what are haematinics, and what are the most important ones?

A

haematinics are compounds found in diet that are important for RBC formation
the main ones are vitamin B12, folate and iron

Digestive System (6 decks)

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