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GI physiology and clinical > Physiology lectures > Flashcards

Physiology lectures Flashcards

1
Q

What are the 4 main functions of the digestive system?

A
  • digestion
  • secretion
  • motility
  • absorption
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2
Q

What are the 4 histological layers of the gut tube?

A

1) Mucosae: epithelium, lamina propria and muscularis mucosae
2) Submucosa: submucosal plexus
3) Muscularis externa: inner circular and outer longitudinal layer; myenteric plexus in between
4) Serosa/adventitia

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3
Q

What are the different types of epithelium found din the gut tube?

A
  • stratified squamous found in the mouth, oesophagus and anal canal
  • simple columnar found in the stomach and intestines
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4
Q

Which 2 reflexes provide autonomic control of the alimentary system?

A

Long (parasympathetic) and short (ENS) reflexes.

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5
Q

Name 3 monosaccharides.

A

Glucose, galactose and fructose.

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6
Q

Name 3 disaccharides.

A

Lactose, maltose and sucrose.

Broken down to monomers by brush border enzymes in the small intestine.

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7
Q

Name 3 polysaccharides.

A

Starch, cellulose and glycogen.

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8
Q

Which bonds link glucose monomers in glycogen and starch?

A

Alpha-1,4 glycosidic bonds.

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9
Q

How is cellulose digested in humans?

A

By bacteria in the large intestine - major source of dietary fibre.

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10
Q

Which enzyme digests starch and glycogen?

A

Alpha-amylase.

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11
Q

How is glucose transported across the cell membrane?

A

Via the SGLT1 symporter. This is the main mechanism of water reabsorption from the gut tube. Na is pumped out via Na/K pump and glucose leaves via GLUT-2 into the blood.

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12
Q

Which transporters do fructose and galactose use to enter epithelial cells?

A

Fructose - GLUT-5
Galactose - SGLT1

Both leave via GLUT-2.

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13
Q

What is the difference between endopeptidases and exopeptidases?

A
  • endopeptidases act in the middle of a protein and cut it in half
  • exopeptidases act at either end (C or N) and remove 1 AA at a time

Both act by hydrolysis.

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14
Q

How are proteins absorbed in the stomach?

A
  • Via SAAT transporters (NA-coupled AA transporters)
  • Via PepT1 for transport of tri and dipeptides
  • Via the NHE3 exchanger
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15
Q

Which enzyme is responsible for fat digestion and where does this act?

A

Pancreatic lipase - all fat digestion occurs in the small intestine.

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16
Q

What molecule are all fats ingested as?

A

Triacylglycerols.

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17
Q

Describe the process of emulsification.

A

The process of dividing large fat droplets into smaller ones to provide a larger surface area for the actions of pancreatic lipase.

Mechanical disruption of large droplets into smaller ones, then emulsifying agents make sure that these don’t congregate together again.

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18
Q

Name the main emulsifying agents.

A

Bile salts, phospholipids and amphipathic molecules.

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19
Q

What are the components of a micelle, and how large are they?

A

Micelle = bile salts + FA + monoglyceride + phospholipid

Micelle’s are 4-7 um.

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20
Q

What happens to FA’s and monoglygerides once they are inside enterocytes?

A

Taken into the SER where they are reformed into TAG’s. These are emulsified, passed through the golgi and endocytosed.

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21
Q

What are extracellular fat droplets called?

A

Chylomicrons - these contain phospholipids, cholesterol and fat-soluble vitamins.

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22
Q

Name the fat-soluble vitamins.

A

A, D, E and K.

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23
Q

Name the water-soluble vitamins.

A

B group, C and folic acid.

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24
Q

What is pernicious anaemia?

A

Vitamin B12 deficiency - this is usually absorbed in the distal ileum by forming a complex with intrinsic factor in the stomach. Pernicious anaemia causes a failure of RBC maturation.

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25
Q

Where is iron absorbed?

A

At the brush border membrane of the duodenum via DMT1 - only recognises Fe2+.

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26
Q

How does the body regulate intracellular iron?

A

If there is too much iron in the blood, this is taken up by ferritin which is the intracellular storage form of iron.

If there’s not enough iron in the blood, iron is released from ferritin, enters the blood and binds to transferrin. Ferritin expression is decreased so that more iron is absorbed from the gut.

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27
Q

What happens to iron when it is in the blood?

A

It is transported to the liver and incorporated into haemoglobin.

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28
Q

What is saliva made of?

A
  • 99% water (solute)
  • mucin (major protein component)
  • electrolytes (tonicity)
  • lysozyme (bacteriocidal)
  • alpha-amylase (starch and glycogen digestion)
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29
Q

How is secretion of saliva controlled?

A
  • parasympathetic via CNVII and CNIX (profuse watery secretion)
  • sympathetic (alpha-1 high mucous, beta-2 high amylase)
  • reflex (chemoreceptors/pressure receptors)
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30
Q

Which type of epithelium lines the oesophagus?

A

Stratified squamous non-keratinised (provides flexibility).

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31
Q

Which type of muscle lines the oesophagus?

A

Muscularis externa:

  • upper 1/3 is skeletal muscle
  • lower 2/3 is smooth muscle
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32
Q

What are the 3 phases of swallowing?

A

1) oral phase (voluntary)
2) pharyngeal phase (involuntary)
3) oesophageal phase (involuntary)

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33
Q

What is the maximum volume the stomach can hold?

A

1500ml

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34
Q

What are the main functions of the stomach?

A
  • dissolves food particles and initiates protein digestion
  • temporary storage
  • controls the rate of particle movement to the duodenum
  • sterilisation
  • produces intrinsic factor
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35
Q

What are the 3 main cell types of the stomach?

A
  • surface mucous cells
  • parietal cells (HCl and intrinsic factor)
  • chief cells (pepsinogen)
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36
Q

How many layers does the muscularis externa of the stomach have?

A

3 –> additional inner oblique layer.

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37
Q

What is the function of rugae in the stomach?

A

To increase surface area.

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38
Q

Which part of the stomach has the thickest wall and what is the function of this?

A

Antrum - for mixing/grinding of gastric contents.

39
Q

What are the 3 mechanisms by which gastric secretion is controlled?

A

1) Neurocrine - vagus and local reflexes
2) Endocrine - gastrin
3) Paracrine - histamine

40
Q

Which mechanisms stimulate gastric secretion?

A

Cephalic phase:

  • sight, smell and taste of food
  • increased vagal activity (G cell secretion of gastrin and ACh acts on parietal cells)
  • gastrin/ACh acts on ECL cells which produce histamine which stimulates parietal cells

Gastric phase:

  • distension of stomach due to arrival of food: vagal and enteric reflexes stimulate parietal cells
  • peptides in the lumen –> G cells –> gastrin –> parietal cells
  • gastrin/ACh –> ECL cells –> histamine –> parietal cells
41
Q

Which mechanisms inhibit gastric secretion?

A

Cephalic phase:

  • stopping eating decreases vagal activity

Gastric phase:

  • decreased pH due to increased [HCl] causes decreased gastrin

Intestinal phase:

  • presence of acid in duodenum –> secretin release –> decreased gastric secretion and decreased HCl secretion from parietal cells
  • fat in duodenum –> GIP release –> decreased gastric secretion and decreased HCl secretion from parietal cells
42
Q

What are enterogastrones?

A

Hormones released from duodenal gland cells in the duodenal mucosa which act to prevent further buildup of HCl - CCK, GIP and secretin.

  • released in response to acid, hypertonic solutions, FA’s or monoglycerides
  • either inhibit gastric secretion or reduce gastric emptying
43
Q

Which mechanisms keep the stomach lumen at pH 2?

A

H/K pump - it is essential that this is switched on at all times, this is done by 3 mechanisms:

1) G cells secrete gastrin –> binds to gastrin receptor –> GPCR mechanism that increases intracellular Ca –> ON
2) histamine type 2 receptors –> ATP to cAMP –> pKA –> ON
3) ACh from Vagus –> ON

44
Q

Which molecules are inhibitory for gastric secretion?

A

Prostaglandins

45
Q

How is stomach acid produced?

A

CO2 + H2O = H2CO3 which is unstable so breaks down to bicarbonate and H+. Bicarbonate goes into the blood which is why it is slightly alkaline. Protons are pumped out via the H/K pump and Cl comes from the blood (so does water) –> HCl in lumen of stomach.

46
Q

Which cells produce gastric mucous?

A
  • surface epithelial cells

- mucous neck cells

47
Q

What is the role of gastric mucous?

A
  • protects the mucosal surface from mechanical injury

- neutral pH (HCO3) –> protects from pepsin digestion and gastric corrosion

48
Q

What is the only essential function of the stomach?

A

To produce intrinsic factor - this is the only function of the stomach that isn’t compensated elsewhere.

49
Q

How are stomach contents mixed?

A

By contractions of the gastric antrum, and when chyme enters the duodenum and is forced back towards the body.

50
Q

What produces peristaltic waves?

A
  • peristaltic rhythm (3/min): produced by pacemaker cells in longitudinal muscle layer
  • slow wave rhythm (basic electrical rhythm): conducted through gap junctions in longitudinal muscle layer, depolarisation is subthreshold –> need further depolarisation to induce AP’s
51
Q

AP’s are…

A

All or nothing

52
Q

The force of contraction in the stomach is proportional to…

A

The number of AP’s

53
Q

What is the function of gastrin?

A

Increases contraction of stomach and stimulates HCl secretion from parietal cells

54
Q

How is gastric motility controlled?

A

Neural and hormonal controls:

  • gastrin
  • distension of stomach wall
  • fat/AA etc in duodenum –> closure of pyloric sphincter
55
Q

How is stomach acid neutralised in the duodenum?

A

HCO3 secretion is stimulated by secretin in response to acid in the duodenum - enzymes in duodenum are denatured below pH 5 and stomach acid is pH 2 so this needs to be neutralised. This also stimulates secretin release from liver and pancreas.

56
Q

What are the 3 sources of HCO3?

A

Brunner’s glands, liver and pancreas.

57
Q

What is the function of enterokinase?

A

Conversion of trypsinogen to trypsin –> this then converts all other digestive enzymes to their active forms.

58
Q

What happens if there is FA/AA in the duodenum?

A

CCK released in response to FA/AA in duodenum which stimulates zymogen release to digest fats and protein.

59
Q

Which structures form the porta hepatis?

A

Hepatic portal vein, hepatic artery and hepatic duct.

60
Q

What is carried in the hepatic duct?

A

Secretions of the liver, predominantly bile.

61
Q

What is the primary role of hepatocytes?

A

Make bile and secrete it into the canaliculi which then secrete bile into the hepatic duct.

62
Q

Name some other functions of hepatocytes.

A
  • nutrient storage
  • detoxification
  • nutrient interconversion
63
Q

What is the alimentary role of the liver?

A

Production and secretion of bile.

64
Q

What are the 6 components of bile?

A

1) bile acids
2) lecithin
3) cholesterol
4) bile pigment
5) toxic metals
6) bicarbonate

1-5 made in the liver; 6 made in pancreatic duct cells.

65
Q

What is the predominant bile pigment?

A

Bilirubin

66
Q

What are bile acids conjugated with?

A

Either taurine or glycine to increase their solubility.

67
Q

What are the 3 layers of the gall bladder wall?

A
  • mucosa (rugae)
  • muscularis (smooth muscle)
  • serosa
68
Q

How is bile secretion controlled?

A

By the sphincter of Oddi. When this is closed it forces bile back up to the gall bladder, where it is stored and concentrated.

69
Q

What happens if there is fat in the duodenum?

A

CCK release:

  • relaxation of sphincter of Oddi and contraction of GB
  • bile solubilises fat
  • decreased gastric emptying and increased pancreatic secretions
70
Q

What are the functions of the 3 parts of the small intestine?

A

Duodenum: acid neutralisation, digestion and Fe absorption

Jejunum: 95% nutrient reabsorption

Ileum: chyme dehydration by NaCl reabsorption

71
Q

What do crypt cells secrete?

A

Cl and water

72
Q

What is the average SA of the small intestine?

A

200 m^2. Enhanced by circular folds, villi and microvilli.

73
Q

How are nutrients absorbed in the small intestine?

A

Na-coupled secondary active transport.

74
Q

How much fluid is secreted into the intestinal lumen per day and how does this happen?

A

1.5L per day. Cl moves into the intestinal lumen via active transport through CFTR –> water moves by osmosis.

75
Q

Why does there need to be fluid in the intestinal lumen?

A
  • keeps luminal contents in liquid state
  • promotes mixing of luminal contents with digestive enzymes
  • dilutes and washes away potentially harmful substances
  • aids nutrient presentation to absorbing surface
76
Q

What are the 2 types of contractions that occur in the small intestine?

A

1) segmentation: during a meal

2) peristalsis: after nutrient absorption

77
Q

What is the function of segmentation vs perstalsis?

A

Segmentation mixes chyme thoroughly with digestive enzymes and brings it into contact with the absorptive surface.

Peristalsis moves undigested material into the large intestine and prevents bacterial colonisation of the small intestine.

78
Q

How are segmentation contractions generated?

A
  • depolarisation of pacemaker cells in longitudinal muscle layer
  • intestinal BER produces oscillations in membrane potential
  • reaches threshold
  • AP’s fire (frequency determines strength of contraction)

Vagus increases contraction, sympathetic decreases. No input by autonomic.

79
Q

How does peristalsis occur in the small intestine?

A

Migrating motility complex (MMC) moves from gastric antrum to distal ileum - moves undigested material into large intestine and limits bacterial colonisation.

MMC initiated by the hormone motilin.

80
Q

What happens if smooth muscle of the small intestine is distended,

A

Muscle on oral side contracts and muscle on anal side relaxes –> neurones of the myenteric plexus.

81
Q

Describe the gastroileal reflex.

A

Gastric emptying cause segmentation contraction in the ileum which opens the ileocaecal valve. This allows chyme into the large intestine and distends the colon which closes the ileocaecal valve to prevent backflux into the small intestine.

82
Q

Describe the muscle layers of the large intestine.

A
  • Inner circular is complete
  • Outer longitudinal layer is incomplete: 3 bands called tenaei coli which contract and form haustra (pouches)

There are also large, straight crypts lines with goblet cells for lubrication.

83
Q

What is the rectum?

A

Straight muscular tube between the end of the sigmoid colon and the anal canal. Lined by simple columnar epithelium.

84
Q

What is the anal canal?

A

2-3 cm between distal rectum and anus. Thick muscularis, internal anal sphincter (autonomic) and external anal sphincter (skeletal - voluntary).

Change in epithelium to stratified squamous.

85
Q

What happens in the colon?

A

Water reabsorption (non nutrient reabsorption). Dehydrates chyme for defaecation. Also, bacterial fermentation of undigested carbohydrate –> short chain FA’s, vitamin K etc.

86
Q

Describe the defaecation reflex.

A

Wave of intense contraction (mass movement contraction) following a meal from colon to rectum –> distension of rectal wall –> sensed by mechanoreceptors –> defaecation reflex.

Contraction of rectum –> relaxation of internal and contraction of external anal sphincter a –> increased peristalsis in colon which increases pressure on external anal sphincter –> relaxes under voluntary control and expulsion of faeces.

87
Q

How is the defaecation reflex controlled?

A

Completely by parasympathetic pelvic splanchnic nerves.

88
Q

Which pathways control voluntary delay of defaecation?

A

Descending pathways.

89
Q

What are the symptoms associated with constipation?

A

Nausea, headaches, appetite loss and abdominal distension.

90
Q

During constipation, are toxins absorbed from faecal material?

A

No, not even after long periods of retention.

91
Q

Name 2 enterotoxigenic bacteria.

A

V.cholerae and E.coli.

92
Q

How do enterotoxigenic bacteria work?

A

Produce protein enterotoxins which maximally turn on Cl secretion from intestinal crypt cells, which increases H2O secretion into the lumen. They do this by increasing intracellular second messengers (cAMP, cGMP and Ca).

93
Q

What is the consequence of enterotoxins?

A

H2O secretion swamps the absorptive capacity of intestinal villus cells which leads to profuse, watery diarrhoea (up to 25l per day for cholera).

94
Q

How is severe diarrhoea treated?

A

Give Na/glucose therapy to drive H2O absorption –> oral rehydration.

GI physiology and clinical (2 decks)

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