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HUBS192 GI > processes in GI tract > Flashcards

processes in GI tract Flashcards

1
Q

functions of motility in GI tract

A

Propulsion - at a controlled rate

Mechanical digestion - increase SA

Mixing - food, secretions and enzymes

Exposure to absorptive surfaces -> intimate contact

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2
Q

Basic electrical rhythm (slow wave)

A
  • These are spontaneous variations in membrane potential (pacemakers)
  • If they surpass threshold, we get action potentials and therefore contraction of smooth muscle
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3
Q

regulation of motility

A
  • BER determines the frequency of contractions
  • Strength of contraction regulated by nervous and hormonal reflexes
  • depolarise or hyperpolarise RMP to make it easier or harder to get to threshold
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4
Q

role of enteric nervous system

A
  • determines type of motility that occurs: peristalsis or segmentation
  • modified by stretch, nerves, hormones, loacl feedback loops
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5
Q

fasting motility pattern

A
  • migrating motor complex
  • coordinated movement from stomach to SI to LI for 4-5 hours after a meal
  • repeated every 2 hours
  • 3 period: inactivity, intermittent activity, intense activity
  • function = housekeeping
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6
Q

feeding motility patterns in GI tract

A
  • storage
  • peristalsis
  • segmentation
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7
Q

features of storage

A

Mainly stomach

Relaxation of smooth muscle (-> distension)

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8
Q

features of peristalsis

A

Esophagus, stomach, small & large intestine

Propulsive

Proximal squeeze, distal relax

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9
Q

features of segmentation

A

Small and large intestine

Mixing & exposure to absorptive surfaces - churning and squishing

Alternate contraction and relaxation of circular muscle

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10
Q

function of swallowing (deglutition)

A

rapid transfer of material from mouth to stomach via oesophagus

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11
Q

function of chewing (mastication)

A

Reduce size of food

Mix food with saliva

Taste

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12
Q

motility in esophagus

A
  • Oesophageal peristalsis transfers food from the mouth (following mastication and deglutition) to the stomach
  • May or may not be aided by gravity (i.e. still happens when we’re upside down)
  • Oesophageal sphincters prevent backflow of food
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13
Q

control of chewing

A
  • Under both voluntary and reflex control
  • We have to voluntarily masticate (skeletal muscle)
  • Reflexes control the strength, frequency, occlusion (how the teeth match up during biting), and side of chewing
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14
Q

control of swallowing

A
  • Initiated voluntarily but proceeds via reflexes (involuntary)
  • Involves the coordination of multiple muscles in order to pass the food to the stomach, whilst still protecting the airway
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15
Q

fasting stage of gastric motility

A

shrinks to small volume, MMC

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16
Q

fed stage of gastric motility

A
  • storage in proximal stomach
  • peristalsis
  • controlled delivery of chyme to the duodenum
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17
Q

storage in stomach

A
  • nervous reflex initiated by swallowing
  • relaxation of proximal gastric smooth muscle leads to increase in volume - distension of rugae
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18
Q

peristalsis in stomach

A
  • initiated on greater curvature that spread to antrum
  • propulsion moves food down to antrum
  • retropulsion moves food back from pyloric sphincter - helps mix food with secretions, and also mechanical digestion
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19
Q

controlled delivery of chyme to duodenum

A
  • rate depends on composition of food (solids slower than liquids, fats move slowly)
  • gastric inhibitory polypeptide (hormone) and enterogastric reflex (neural) are feedback from duodenum that influence gastric emptying
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20
Q

functions of small intestine motility

A
  • Facilitate the chemical digestion of food
  • Facilitate the absorption of nutrients, salts, and water
  • Mix chyme with intestinal secretions
  • Exposure chyme to absorptive surfaces
  • Propel chyme along the GI tract
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21
Q

fed small intestine motility

A

Mainly segmentation to aid in contact digestion and mixing of chyme with digestive enzymes and other chemicals

Also peristalsis to propel chyme through the small intestine

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22
Q

functions of large intestine motility

A

Temporary storage of faeces

Regulation of the salt and water content of faeces

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23
Q

motility patterns in large intestine

A

Inactivity

Segmentation to aid in mixing and slow propulsion

Peristalsis to move masses of faeces into the rectum for defecation. Occurs 3-4 times per day

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24
Q

what is chemical digestion

A

chemical hydrolysis of food by digestive enzymes into molecules that can cross epithelial lining of GI tract

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25
Q

functions of secretions in GI tract

A

digest food

dilute food

maintain optimal pH

protect and lubricate GI tract

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26
Q

features of digestive enzymes

A

extracellular

organic catalysts

display specificity (i.e. they will only act on a specific substrate).

Function optimally at a specific pH (different for different enzymes)

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27
Q

two stages of chemical digestion

A
  1. luminal digestion - initial digestion of food in the lumen of the GI tract
  2. contact digestion - completion of chemical digestion by brush border enzymes in the small intestine
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28
Q

luminal enzymes secreted by salivary glands, chief cells of stomach and acinar cells of pancreas

A

salivary glands: amylase

chief cells of stomach: pepsinogen

acinar cells of pancreas: trypsinogen, chymotrypsinogen, lipase and amylse

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29
Q

composition of carbohydrates

A

composed of chains of monosaccharides

main polysaccharides in our diet are starch and glycogen - joined by alpha-1,4-glycosidic bonds

a lof of cellulose in in our diet which we cant digest because our digestive enzymes cannot cleave beta-1,4-glycosidic bonds

some disaccharides such as sucrose, lactose and maltose

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30
Q

luminal digestion of carbohydrates

A

Polysaccharides are converted to disaccharides by salivary and pancreatic amylase (in lumen)

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31
Q

contact digestion of disaccharides

A

Disaccharides are converted to monosaccharides by substrate-specific enzymes (on brushborder)

Sucrose is broken down by sucrase

Lactose is broken down by lactase

Maltose is broken down by maltase

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32
Q

composition of proteins

A

exogenous (ones we ingest) and endogenous (ones we produce) proteins that the intestine digests

long chains of amino acids joined by peptide bonds

approximately 10 essentials amino acids

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33
Q

luminal digestion of proteins

A

Proteins are converted to polypeptides by a number of luminal enzymes

Pepsin in the stomach

Trypsin and chymotrypsin in the small intestine (but secreted by the pancreas as inactive precursors - trypsinogen and chymotrypsinogen)

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34
Q

contact digestion of polypeptides

A

Converts polypeptides into individual amino acids by numerous peptidases attached to the brush-border of the small intestine

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35
Q

composition of lipids

A

composed mainly of triglycerides which are composed of a glycerol backbone with 3 fatty acids attached by ester bond

contain fat soluble vitamins

fatty acids have variable chain length

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36
Q

type of digestion of lipids and why is this the case

A

only digested by luminal digestion because of their insolubility in water so must be dissolved in luminal fluid

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37
Q

4 stages of lipid chemical digestion

A
  1. Emulsification - motility
  2. Stabilisation - bile
  3. Hydrolysis - lipase
  4. Formation of micelles
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38
Q

emulsification of lipids

A

must be broken down into small uniform particles

motility separates large fat droplets into smaller droplets to increase SA for further digestion

retropulsion in stomach and segmentation in SI

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39
Q

stabilisation of lipids

A

lecithin and bile salts secreted in bile stabilise the emulsion droplets because they are amphipathic (have hydrophobic and hydrophilic part)

increases SA even more as allows formation of even smaller droplets

occurs in SI

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40
Q

production and secretion of bile salts and lecithin

A

produced in the liver, stored and secreted by the gallbladder

41
Q

hydrolysis of lipids

A

occurs in SI lumen at emulsion droplet surface

involves lipase and colipase (cofactor) which are both secreted by pancreas

colipase anchors to the surface of emulsion droplet

Lipase converts triglycerides into monoglyceride and two free fatty acids

42
Q

micelle formation of lipids

A

Because products of fat digestion (fatty acids and monoglycerides) are insoluble in water, they are kept in solution by the formation of micelles (i.e. they don’t reform large insoluble fatty clumps)

43
Q

micelle

A

small droplets (4-6nm) that are composed of amphipathic compounds (bile salts and lecithin), fatty acids, and monoglycerides

44
Q

2 stage process of saliva production

A
  1. Primary secretion: isotonic, serous solution produced by acinar cells
  2. Hypotonic saliva: reabsorption of various molecules (including Na+ and Cl-) in the salivary ducts to produce the final hypotonic saliva
45
Q

volume and rate of saliva secretion

A

volume = 1.5L/day

basal rate = 0.3 mL/min

stimulated rate = 1.5 mL/min

46
Q

composition of saliva

A

mucus for lubrication

dilute solution of NaHCO3 and NaCl to aid in dilution and maintain optimum pH

enzymes including alpha-amylase and lipase

47
Q

regulation of saliva secretion

A

autonomic nervous control in response to thought, smell and sight of food, as well as chewing

Parasympathetic NS: acetylcholine produces large amounts of saliva

Sympathetic NS: adrenaline produces small volumes of viscous saliva

48
Q

functions of saliva

A

lubrication to aid in mastication and deglutition

hygiene - irrigates mucosa

digestion - dissolves food to allow taste

49
Q

volume and rate of gastric secretions

A

volume = 2-3L/day

basal rate = slow - 15-30mL/hr

stimulated rate = 150mL/hour

50
Q

composition of gastric secretions

A

basal: mainly mucous
stimulated: gastric acid (150mM HCl), mucous, pepsinogen, intrinsic factor

51
Q

3 phases of gastric secretions

A

3 phases:

  1. cephalic phase - preparation
  2. gastric phase
  3. intestinal phase
52
Q

cephalic phase secretions

A
  • 30-40% of secretion associated with a meal
  • Parietal cells stimulated to produce secretions
  • Gastrin produced - upregulates parietal cell function
53
Q

stimuli for cephalic phase

A

This is the preparation phase - controlled by higher centres (brain) in response to the thought, smell, and sight of food. Also stimulated by mastication and taste

Parasympathetic NS controls gastric secretions via the ENS

54
Q

gastric phase secretions

A

60% of secretion associated with a meal

Ensures sufficient secretions are present to handle the ingested food

Parietal cells stimulated to produce secretions. Gastrin production is also stimulated, which upregulates parietal cell function

55
Q

control of gastric phase

A

Acts in response to stretch/distension of the stomach and also the presence of products of digestion

Local reflex: controlled by the ENS

External reflex: controlled by the parasympathetic NS

56
Q

intestinal phase secretions

A

5-10% of secretion associated with a meal

Controls the amount of acid delivered to the small intestine

gastric secretions inhibited by negative feedback processes

57
Q

control of intestinal phase

A

Acts in response to distension of the duodenum and arrival of acid and products of digestion into the duodenum

Gastric secretions are inhibited by negative feedback processes caused by hormones gastric inhibitory polypeptide (GIP), cholecystokinin (CCK), secretin, and nervous enterogastric reflex (via vagus nerve)

58
Q

function of intrinsic factor

A

facilitates absorption of vitamin B12 in the SI

59
Q

function of pepsinogen

A

converted to pepsin by acidic environments and starts digestion of proteins

60
Q

function of gastric acid

A

denatures protein, activated pepsinogen, optimum pH for pepsin, protection, dilute food

61
Q

volume, rate and composition of pancreatic solutions

A

volume = 1.5L/day

basal rate = slow during fasting

stimulated = higher when stimulated by hormones

composition = enzymes produced by acinar cells and HCO3 produced by duct cells

62
Q

cholecystokinin

A

Produced by duodenal ENDOcrine cells in response to digestive products (amino acids, fats, carbohydrates etc.) in the lumen

Stimulates enzyme secretion by pancreatic acinar cells

63
Q

secretin

A

Produced by duodenal ENDOcrine cells in response to an increased [H+] in the duodenal lumen

Stimulates HCO3 secretion by pancreatic duct cells

64
Q

enzymes in pancreatic secretions

A

lipolytic - lipase, phospholipase

amylytic - amylase

proteolytic - trypsin, chymotrypsin, carboxypeptidase

nucleolytic - ribonuclease, deoxyribonuclease

65
Q

activation of proteolytic enzymes

A

Proteolytic enzymes are secreted as inactive precursors (e.g. trypsinogen and chymotrypsinogen

In the small intestine, trypsinogen is converted to trypsin by the enzyme enterokinase. Trypsin then activates other enzymes

66
Q

function of pancreatic enzymes

A

multiple different types of enzymes that chemically digest all classes of food. Produced by acinar cells

67
Q

functions of pancreatic bicarbonate

A

basic, so neutralises the acidic chyme from the stomach. This creates an optimum pH (basic) for pancreatic and intestinal enzymes.

Bicarbonate is produced by duct cells

68
Q

volume and rate of biliary secretions

A

volume = 0.5L/day

rate = bile is secreted constantly and stored in gallbladder, which is delivered to SI when food is present

69
Q

composition of biliary secretions

A

excretory products (bile pigments and cholesterol) and digestion-aiding products (bile salts and lecithin)

70
Q

regulation of biliary secretions

A

delivery of bile from the gall bladder to the SI is controlled by cholecystokinin (CCK) in response to the products of digestion in the duodenum

CCK stimulates contraction of the gallbladder and relaxation of the sphincter of Oddi (opens up into the duodenum)

71
Q

functions of bile salts and lecithin

A

help to emulsify fats so that can be absorbed and digested

72
Q

small intestine secretion volume and composition/function

A

volume = 1.5L/day

composition/function = mucus for lubrication and NaHCO3 solution to neutralise chyme

73
Q

what is absorption

A

net passage of substances from the lumen, across the lining of the GI tract, into the into interstitial fluid and then into the blood or lymph

74
Q

absorption in mouth, oesophagus and stomach

A

minimal absorption - lipid soluble substances

75
Q

absorption in small intestine

A

main site of absorption - absorbs 90% of water and Na, and all nutrients

76
Q

absorption in large intestine

A

9% of water and Na absorption

77
Q

how does motility affect absorption

A

Absorption requires the correct rate of propulsion for digestion and sufficient exposure to absorptive surfaces

(too fast = not enough time to absorb, too slow = too much absorption)

78
Q

how does surface area affect absorption

A

The rate of absorption is proportional to the surface area available for absorption to occur

Anatomical adaptations maximise surface area (e.g. plicae circulares, villi, microvilli)

79
Q

how does transport affect absorption

A

molecules need to travel across interstitial epithelium in order to be absorbed.

Two pathways for absorption are paracellular and transcellular

80
Q

paracellular pathway of absorption

A

solutes travel through tight junctions between cells rather than crossing cell membrane

relatively non-selective - only selective based on size

passive so requires gradient

81
Q

transcellular pathway of absorption

A

solutes travel through cells, crossing two membranes (apical and basal)

substances which are not lipid soluble require transport proteins

can be passive or active, and is more specific (can be through specific transport proteins)

82
Q

how does removal of substances affect absorption

A

need to remove substances from interstitial space in order to maintain concentration gradients

requires large blood flow

lacteals in intestinal villi faciliate efficient removal of various substances

83
Q

absorption of water

A

via osmosis - passive movement down conc gradient

osmotic gradients set up by absorption of salts

secrete around 7-8L/day so important that it is absorbed again

84
Q

absorption of sodium

A

absorbed both passively (paracellular pathway) and actively (transcellular pathway)

3 mechanisms:

  1. Na+ transport alone
  2. glucose cotransport through SGLT-1
  3. amino acid cotransport
85
Q

absorption of carbohydrates

A

absorbed both actively and passively

  1. passive absorption through paracellular pathway - diffusion of monosaccharides through tight junctions down conc grad
  2. active absorption via transcellular pathway - cotransport with Na+
86
Q

absorption of proteins

A

both actively and passively

  1. passive absorption through paracellular pathway - diffusion of amino acids through tight junctions down conc grad
  2. active absorption via transcellular pathway - cotransport with Na+
87
Q

absorption of lipids

A

Monoglycerides and fatty acids are delivered to the brush border via micelles and diffuse into the cell without need for transporter- whole micelle not absorbed

In the cell, monoglycerides and fatty acids are synthesised into triglycerides and packaged into chylomicrons. Chylomicrons exit the cell via exocytosis, and enter the lacteals

88
Q

active absorption of glucose

A

Na+/K+ pump actively pumps Na+ out of epithelial cells into interstitial fluid so conc inside epithelial cell is low and Na+ diffuses in with glucose through SGLT-1

Then glucose can diffuse out through GLUT2 protein

89
Q

absorption of bile salts

A

majority of secreted bile salts are reabsorbed in the distal portions of the small intestine (e.g. ileum) to promote fat absorption, as bile salts stabilise micelles

  1. Bile salts are reabsorbed via active transport through apical Na-dependent bile acid transporter in terminal ileum
  2. Passive absorption in the jejunum
90
Q

absorption of vitamins

A

fat soluble vitamins (A, E, D and K) absorbed with fats

water soluble vitamins mostly have Na-dependent absorption

Vitamin B12 requires intrinsic factor in order to be reabsorbed

Receptors in the ileum bind the intrinsic factor/vitamin B12 complex - allowing vitamin B12 to be actively absorbed

91
Q

components of ENS

A

submucosal plexus - on inside, regulate secretions

myenteric plexus - on outside, regulate motility

92
Q

what initiates GI ENS reflexes

A

works independently of CNS and operate via a number of short, local GI reflexes:

distension

acidity of chyme

osmolarity of chyme

presence of products of digestion etc

93
Q

how are GI reflexes mediated

A

GI reflexes are mediated by receptors in the GI mucosa that sense (afferent signals) distension of the GI tract (mechanoreceptors)

chemical composition of the lumen (chemoreceptors)

osmolarity of the lumen (osmoreceptors)

94
Q

role of CNS in GI regulation

A

CNS modulates activity of CNS via long autonomic neural reflexes

Parasympathetic NS: in general stimulates motility and secretion

Sympathetic NS: in general inhibits motility and secretion

CNS regulation is bidirectional - has both afferent and efferent signals

e.g. vagovagal nerve

95
Q

gastrointestinal peptide hormones

A

gastrin

gastric inhibitory peptide (GIP)

secretin

cholecystokinin

96
Q

gastrin - produced and target

A

Produced by gastric G cells

Targets parietal cells and gastric muscle to stimulate gastric secretion and motility

97
Q

gastric inhibitory peptide - produced and target

A

Produced by small intestinal K cells

Targets gastric G cells and gastric muscle to inhibit gastric secretion and motility

98
Q

secretin - produced and target

A

Produced by duodenal S cells

Targets pancreatic duct cells to stimulate HCO3 secretion

Also targets gastric parietal cells to inhibit H+ secretion

99
Q

cholecystokinin - produced and target

A

Produced by small intestinal I cells

Targets pancreatic acinar cells to stimulate enzyme secretion

HUBS192 GI (2 decks)

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