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Physiology Flashcards

1
Q

functions of the digestive system

A

absorption
digestion
secretion
motility

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2
Q

where do nutrients primarily enter the circulatory system

A

small intestine

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3
Q

how many salivary glands are there

A

3 pairs (6)

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4
Q

what occurs in the mouth

A

foodstuffs broken down by chewing: saliva added as lubricant

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5
Q

what is oesophagus

A

muscular conduit between stomach and mouth

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6
Q

what happens in stomach

A
  • digestion of proteins:
  • foodstuffs reduced to liquid form
  • storage
  • sterilisation
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7
Q

what can be found in the pancreas

A

digestive enzymes for digestion of fats, carbohydrates and proteins

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8
Q

what can be found in liver

A

bile salts for digestion/ absorption of fats in the small intestine

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9
Q

what happens in large intestine

A
  • water absorption,
  • bacterial fermentation
  • formation of faeces
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10
Q

what are essential for fat digestion

A

bile salts in the liver

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11
Q

how long from oesophagus to rectum

A

8m ish

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12
Q

4 distinctive layers of alimentary canal

A
  • mucosa
  • submucosa
  • muscularis externa
  • serosa
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13
Q

2 layers of musculaisr externa

A

longitudinal

circular

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14
Q

function of muscularis externa

A

provide motility

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15
Q

type of epithelium in mouth, oesophagus and anal canal

A

stratified squamous

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16
Q

type of epithelium in stomach, small and large intestine

A

simple columnar

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17
Q

functions (3) of epithelium in GI tract

A
  • barrier separating lumen of alimentary canal from body
  • synthesis and secretion of digestive enzymes, hormones, mucus
  • absorbs products of digestion
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18
Q

components of mucosa

A
  • epithelium
  • lamina propria
  • muscularis mucosae
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19
Q

what is lamina propria

A

loose connective tissue (glands, blood/lymph vessels)

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20
Q

what is muscularis mucosae

A

thin, smooth muscle layer

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21
Q

what is submucosa

A

thick, irregular connective tissue

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22
Q

function of submucosa

A

support mucosa

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23
Q

what is contained in submucosa

A

neurons, blood and lymphatic vessels

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24
Q

where are submucosal glands found

A
  • oesophagus

- duodenum

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25
Q

what is the function of neurones in submucosa

A

form extensive network - the submucosal plexus (parasympathetic)

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26
Q

what is serosa/ adventitia

A

connective tissue outer layer of alimentary canal

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27
Q

function of serosa outside peritoneal cavity

A

adventitia attaches oesophagus and rectum to surrounding structures

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28
Q

function of serosa inside peritoneal cavity

A

serosa surrounds stomach, small intestine and large intestine

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29
Q

what is muscularis externa composed of

A
  • two thick layers of muscle
Inner = circular
Outer = longitudinal
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30
Q

where is myenteric plexus located

A

between circular and longitudinal layers of muscularis externa

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31
Q

What makes up the enteric nervous system?

A

submucosal and myenteric plexuses

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32
Q

function of enteric nervous system

A

indépendant control of gut function

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33
Q

what enables independent control of gut function

A

enteric nervous system

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34
Q

what is meant by a long reflex in alimentary system

A

gut - CNS

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35
Q

what is meant by a short reflex in alimentary system

A

just in gut (gut control)

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36
Q

Parasympathetic nerve innervation of alimentary system

A

vagus nerve

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37
Q

sympathetic nerve innervation of alimentary system

A

splanchnic nerve

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38
Q

effect of parasympathetic nervous system

A

stimulatory

increases secretion and motility

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39
Q

effect of sympathetic nervous system

A

inhibitory (reduces secretion and motility)

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40
Q

exception to stimulatory/ inhibitory rule for alimentary tract

A

salivation (no effect)

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41
Q

autonomic control

A

automatic control

you cannot influence it

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42
Q

long vs short reflexes in the gut

A

long: goes to CNS
short: remains in the gut

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43
Q

foregut contents

A
  • abdominal part of oesophagus
  • liver
  • pancreas
  • spleen
  • upper part of duodenum
  • stomach
  • gall bladder
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44
Q

midgut contents

A
  • ileum
  • jeudenum
  • lower part of duodenum
  • large intestine
  • proximal 2/3 transverse colon
  • appendix
  • ascending colon
  • caecum
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45
Q

hindgut structures

A
  • distal 1/3 transverse colon
  • descening colon
  • sigmoid colon
  • rectum
  • upper anal canal
  • urogenital sinus
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46
Q

blood supply to foregut

A

coeliac trunk

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47
Q

blood supply to midgut

A

superior mesenteric artery

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48
Q

blood supply to hindgut

A

inferior mesenteric artery

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49
Q

venous drainage of stomach

A

gastric veins

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50
Q

venous drainage of pancreas

A

splenic veins

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51
Q

venous drainage of midgut structures:

  • small intestine
  • caecum
  • ascending colon
  • transverse colon
A

superior mesenteric vein

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52
Q

venous drainage of hindgut structures:

  • descending colon
  • sigmoid colon
  • rectum
A

inferior mesenteric vein

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53
Q

name the components of the hepatic portal vein:

A
  • splenic vein
  • inferior mesenteric artery
  • superior mesenteric artery
  • gastric veins
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54
Q

where does blood go after leaving GI organs (pathway)

A
  1. portal vein tributaries
  2. hepatic portal vein (goes through liver)
  3. hepatic vein
  4. inferior vena cava
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55
Q

what organ does all blood go through before leaving the gut

A

liver

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56
Q

purpose of all blood going to the liver after leaving the gut

A

liver screens/ purifies blood to prevent any toxins absorbed from food from entering the circulatory system

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57
Q

principle dietary constituents

A
  • carbohydrates
  • protein
  • fat
  • vitamins
  • minerals
  • water
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58
Q

monosaccharide examples:

A

Hexose sugars (6c)

  1. glucose
  2. galactose
  3. fructose
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59
Q

description disaccharides

A

two monosaccharides linked together by glycosidic bonds

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60
Q

how are disaccharides broken down

A

brush border enzymes in small intestine break them down to monosaccharides

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61
Q

what is lactose broken down to

A

glucose and galactose

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62
Q

what breaks down lactose

A

lactase

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63
Q

what is sucrose broken down to

A

glucose and fructose

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64
Q

what breaks down sucrose

A

sucrase

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65
Q

what is maltose broken down to

A

glucose x2

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66
Q

what breaks maltose down

A

maltase

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67
Q

2 forms of starch

A
  • a-amylose

- amylopectin

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68
Q

what is a-amylose

A

glucose linked in straight chains

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69
Q

what is amylopectin

A

highly branched glucose chains

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70
Q

what type of bonds link glucose monomers in starch

A

a-1,4-glycosidic bonds

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71
Q

what type of reaction breaks down starch

A

hydrolyse

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72
Q

what enzyme is used to break down starch

A

amylase

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73
Q

why can vertebrates not break down cellulose by themselves

A

brecause they/ we don’t have the enzyme cellulase which is required to break down B-1,4-glycosidic bonds

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74
Q

what is celluloses function in humans

A

dietary fibre

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75
Q

glycogen function

A

animal storage form of glucose

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76
Q

glycogen structure

A

glucose monomers linked by a a-1,4-glycosidic bonds

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77
Q

what are people who are lactose intolerant not have

A

lactase enzyme

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78
Q

texture of villi in small intestine

A

velvety when it doesn’t have mucus

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79
Q

2 membrane types of epithelium

A
  • apical (facing outside e.g. vein)

- basolateral (facing inside e.g. other cells)

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80
Q

what does a brush border look like

A

bart simpsons hair

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81
Q

transcellular pathway

A

goes through the cell

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82
Q

paracellular pathway

A
  • goes between cells through tight junctions
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83
Q

how many transporter proteins are needed to pass a molecule through a cell

A

at least 2 - one at apical and one at basolateral membranes respectively

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84
Q

what transporter protein is used for getting glucose into a cell

A

SGLT1

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85
Q

what needs to be present for getting glucose into a cell

A

Na, Glucose, SGLT1

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86
Q

what transporter protein gets glucose out of a cell (down the concentration gradient)

A

GLUT-2

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87
Q

what is a normalise blood glucose

A

5 mmol/l

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88
Q

what transporter protein gets fructose into a cell

A

GLUT-5

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89
Q

what transporter protein gets fructose out of a cell

A

GLUT-2

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90
Q

why does fructose transport into a cell not require any energy?

A

because there is no blood fructose concentration

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91
Q

what other molecules are involved in fructose transportation

A

NONE ahahahah fooled ya ;)

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92
Q

who is awesome

A

you are

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93
Q

what is a protein

A

polymer of amino acids linked together by peptide bonds

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94
Q

what are described as natures lego and why

A

proteins

infinitely variable

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95
Q

what are enzymes that hydrolyse peptide bonds and reduce proteins/ peptides to amino acids called?

A
  • proteases

- peptidases

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96
Q

function of proteases and peptidases

A

break down proteins and peptides to form amino acids

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97
Q

endopeptidases

A

breaks down internal amino acids

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98
Q

exopeptidase

A

breaks down terminal end of amino acid (snipping at the end making it 1 shorter everytime)

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99
Q

aminopeptidases

A

work on amino end of protein

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100
Q

carboxypeptideases

A

work on carboxyl end of protein

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101
Q

how do most amino acids enter a cell

A

the same way as glucose; with a transporter and Na

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102
Q

how do amino acids leave a cell

A

using specific transporters to cross basolateral membrane

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103
Q

PepT1

A

protein transporter that can carry virtually any di/tripeptides into a cell using H

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104
Q

where does H come for transporting amino acids across apical membranes into a cell

A

acid microclimate around the surface

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105
Q

what form are almost all ingested fats found in

A

triglycerol

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106
Q

what enzyme digests fats in the small intestine

A

pancreatic lipase

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107
Q

definition of a ‘lipase’

A

water-soluble enzyme

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108
Q

emulsification

A

dividing large lipid droplets into smaller droplets

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109
Q

what is required for emulsification of fats to take place?

A
  • mechanical disruption

- emulsifying agent

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110
Q

ampiphatic

A

has polar and non polar components (like phospholipid membrane)

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111
Q

how does mechanical disruption of fats in the stomach take place

A

muscularis externa contraction grinds and mixes lumen contents.

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112
Q

function of micelles

A

‘vehicles’ for emulsion droplets to get to the cell surface for absorption

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113
Q

components of a micelle

A

bile salt + monoglycerides + fatty acids + phospholipids

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114
Q

fate of micelles when they have released the fatty acid inside onto the surface of the cell

A

they are reused, going back to pick up more fatty acids to transport

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115
Q

how does micelle release fatty acid at cell surface

A

micelle destabilises in the extreme acidic microclimate immediate to the cell, releasing the fatty acids onto cell surface

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116
Q

what happens to fatty acids when they enter the cell

A
  1. they enter the smooth endoplasmic reticulum,
  2. where they are resythesised by enzymes to for triacylglycerols,
  3. emulsified with amphipathic protein found in sER
  4. processed through Golgi apparatus
  5. exotysed into extracellular fluid at serial membrane
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117
Q

difference smooth and rough endoplasmic reticulum

A

smooth - no ribosomes

rough - ribosomes

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118
Q

chylomicron

A

extracellular fat droplet

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119
Q

extracellular fat droplet

A

chylomicron

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120
Q

where do chylomicrons go

A

pass into lacteals between epithelial cells (cannot pass through capillary basement membrane0

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121
Q

where does fat go after leaving a cell

A

into lymphatic system, then circulatory system via thoracic duct/ vena cava

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122
Q

what are the 2 classes of vitamins

A
  • fat soluble

- water soluble

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123
Q

which vitamins are fat soluble

A

A,D,E,K

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124
Q

which vitamins are water soluble

A

B, C, Folic Acid

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125
Q

how are fat soluble vitamins absorbed

A

same pathway as fat

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126
Q

how are water soluble vitamins absorbed

A
  • passive diffusion
    or
  • carrier mediated transport (like micelle for fat)
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3
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127
Q

how is vitamin B12 absorbed

A

it binds to an intrinsic factor in the stomach to form complex which is absorbed via a specific transport mechanism in the distal ileum

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128
Q

what can occur as a result of B12 deficiency

A

pernicious anaemia

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129
Q

what is pernicious anaemia?

A

failure of red blood cell maturation

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130
Q

what causes pernicious anaemia?

A

B12 deficiency

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131
Q

how much of daily iron intake is absorbed into the blood?

A

10%

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132
Q

how is iron stored

A

incorporated into ferritin

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133
Q

what does iron in blood bind to

A

transferrin

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134
Q

what is the only nutrient that has controlled absorption?

A

iron

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135
Q

hyperaemia

A

increase ferritin levels - more iron bound in enterocytes

136
Q

anaemia

A

decrease ferritin levels -more iron released into the blood

137
Q

how is chewing controlled

A

VOLUNTARY
-skeletal muscles of mouth/ jaw
REFLEX
-contraction of jaw muscles ->pressure of food against gums, hard palate and tongue -> mechanoreceptors -> inhibition of jaw muscles -> reduced pressure -> contraction … etc…

138
Q

components of saliva

A 
water
mucins
a-amylase
electrolytes
lysozyme
139
Q

purpose of water in saliva

A

softens
moistens
dilutes particles
solvent

140
Q

purpose of lysozyme in saliva

A

bactericidal (cleave polysaccharide component of bacterial cell wall)

141
Q

purpose of electrolytes in saliva

A

maintains tonicity/ pH

142
Q

exocrine duct

A

leads to the outside

143
Q

endocrine duct

A

leads onto a surface

144
Q

types of salivary gland

A
  • parotid gland
  • submandibular gland
  • sublingual gland
145
Q

effect of parasympathetic and sympathetic nervous system on salivary excretion

A

both stimulatory

146
Q

sympathetic stimulus reaction - type of saliva

A

viscous, less water, more protein

147
Q

parasympathetic stimulus reaction - type of saliva

A

very runny, lots of water, like a dog drooling

148
Q

reflex control of salivary excretion - description

A

presence of food in mouth -> chemoreceptors/ pressure receptors

149
Q

what type of epithelium lines oesophagus

A

stratified squamous epithelium

150
Q

describe the control of muscularis externa in the oesophagus

A

upper 1/3 = skeletal

lower 2/3 = smooth

151
Q

purpose oesophageal sphincters

A

regulate movement of material into and out of oesophagus

152
Q

function of soft palate in mouth upon swallowing

A

it is reflected backwards and upwards, closing off nasopharynx to stop food coming out of the nose

153
Q

what happens when food/ liquid approaches the oesophagus

A
  • upper oesophageal sphincter relaxes and epiglottis covers opening to larynx (preventing food from entering the trachea)
154
Q

what happens once food has entered the oesophagus?

A

upper oesophageal sphincter contracts preventing food reflux

155
Q

how long does it take to get food from mouth to stomach

A

about 10 seconds

156
Q

what happens as food nears the stomach

A

lower oesophageal sphincter relaxes - food enters the stomach

157
Q

describe the change in pressure of the stomach when food enters (up to 1.5l)

A

there is no change in pressure due to Rugae (folds in the stomach lining) moving out

158
Q

5 functions of the stomach

A
  • store food temporarily
  • sterilise ingested material
  • dissolve food particles and initiate digestive process
  • control delivery of contents to the small intestine
  • produce intrinsic factor needed for vitamin B absorption
159
Q

what is the only non-compensatable function of the stomach

A

producing the intrinsic factor that enables vitamin B12 absorption

160
Q

what is serosa

A

connective tissue outer layer

161
Q

what type of cells are found in gastric glands

A
  • surface mucous cell
  • mucous neck cell
  • parietal cell
  • chief cell
162
Q

where are gastric glands found

163
Q

what is produced in the body of the stomach

A

mucous
HCL
Pepsinogen
Intrinsic Factor

164
Q

what is a fundus

A

hollow part of an organ

165
Q

what is the purpose of the fundus in the stomach

A

food storage

166
Q

function of the antrum of the stomach

A
  • mixing/ grinding food

- producing gastrin

167
Q

explain pepsin storage in stomach

A

pepsin digests protein, so if left by itself in the stomach it would digest the stomach. it is therefore stores in an inactive precursor form; pepsinogen.

168
Q

what produced gastrin

169
Q

function mucous neck cells

A

produce mucous

170
Q

function chief cells

A

produce, store and secrete pepsinogens

171
Q

function parietal cells

A
  • secrete HCl

- secrete intrinsic factor

172
Q

what happens to the cells as you go further down a gastric gland?

A

they become more specialised

173
Q

describe the journey of gastrin

A

produced in the antrum of the stomach, travels all the way round the circulatory system only to end up 1cm above where it started in the stomach

174
Q

what 3 regulatory molecules stimulate acid secretion in the stomach?

A

gastrin
histamine
acetylcholine

175
Q

what do these 3 molecules have in common?

  • gastrin
  • acetylcholine
  • histamine
A

they all stimulate acid secretion in the stomach

176
Q

function of prostaglandins in the stomach?

A

inhibit acid secretion

177
Q

what molecule inhibits acid secretion in the stomach

A

prostaglandins

178
Q

what molecule is a lot of produces when stimulating acid production? (and not the acid itself)

179
Q

what 3 mechanisms is gastric acid secretion controlled by

A

neurocrine
endocrine
paracrine

180
Q

how does neurocrine control gastric acid secretion

A

vagus/ local reflexes

181
Q

how does endocrine control gastric acid secretion

A

gastrin (hormone)

182
Q

how does paracrine control gastric acid secretion

183
Q

explain paracrine

A

hormone which only has an effect on the vicinity of the gland secreting it - it doesn’t travel anywhere else

184
Q

what happens when we see/ smell/ taste food?

A

vagus nerve is stimulates, causing an increase in production of ACh and gastrin, which stimulates parietal cells resulting in an increased production of gastric acid

185
Q

what happens when there is a large amount of gastrin/ ACh

A
  • stimulates parietal cells

- activates ECL cells, which release histamine, again stimulates parietal cells

186
Q

Cephalic Stimuli for Parietal cells

A
  • smell/ sight/ taste of food
187
Q

Gastric stimuli of parietal cells

A
  • distension of stomach (arrival of food)
  • peptides in lumen
  • gastrin/ ACh
188
Q

what happens upon distension of stomach (arrival of food)

A

vagal/ enteric reflexes activated producing ACh, which activates parietal cells

189
Q

what happens when there are peptides in the lumen

A

G Cells activated, gastrin produced activating parietal cells

190
Q

cephalic mechanisms inhibiting gastric acid secretion

A

stopping eating = decrease in vagal activity

191
Q

gastric mechanisms inhibiting gastric acid secretion

A

decrease in pH = increase in HCl = decrease in gastrin

192
Q

intestinal mechanisms inhibiting gastric acid secretion

A

acid shouldn’t be in the duodenum cause that means theres an excess thats not being used; therefore if any appears here this inhibits it

193
Q

different areas for inhibition of gastric acid secretion

A
  • intesine (duodenum)
  • cephalic (head)
  • gastric (stomach)
194
Q

enterogastrones

A

hormones released from gland cells in duodenal mucosa

195
Q

why are enterogastrones released

A

in response to acid, hypertonic solutions, fatty acids or monoglycerides in duodenum.

196
Q

what do enterogastrones do

A

act collectively to prevent further acid build up in duodenum

197
Q

what 2 strategies do enterogastrones employ to prevent acid build up in duodenum?

A
  • inhibit gastric secretion

- reduce gastric emptying (inhibit motility/ contract pyloric sphincter)

198
Q

what is pepsinogen secreted by?

A

chief cells in gastric glands

199
Q

what happens to pepsin below pH 3

A

becomes pepsinogen

200
Q

what happens to pepsins at neutral pH?

A

inactivated

201
Q

what produces gastric mucus

A
  • surface epithelial cells

- mucous neck cells

202
Q

cytoprotective role of gastric mucous?

A
  • protects mucosal surface from mechanical injury

- neutral pH - protects against gastric acid corrosion and pepsin digestion

203
Q

what is produced by parietal cells other than gastric acid?

A

intrinsic factor required for vitamin B12 absorption

204
Q

2 major lobes of the liver

A

right> left

205
Q

2 minor lobes of the liver

A

caudate, quadrate

206
Q

where is the entry/ exit point of blood and lymphatic vessels, and nerves in the liver

207
Q

what is the porta

A

the entry/ exit point of blood and lymphatic vessels, and nerves in the liver

208
Q

Sphincter of Oddi

A

Mucular valve that controls the release of digestive juices (pancreatic enzymes and bile) from the first part of the duodenum into the second.

209
Q

falciform ligament

A

separates right and left lobes of the liver, but also keeps them attached

210
Q

which part of the liver attaches to the under side of the diaphragm?

211
Q

septa meaning

212
Q

what is the liver covered by?

A

connective tissue capsule and visceral peritoneum except for the bare area

213
Q

how is the liver divided and by what

A

into hexagonal lobules and by septa

214
Q

what is portal triad composed of?

A
  • hepatic portal vein
  • hepatic artery
  • hepatic duct
215
Q

where are portal triads located

A

at each corner of hexagonal lobule

216
Q

what are the functional units of the liver

217
Q

what are hepatic cords composed of?

A

hepatocytes

218
Q

function of hepaocytes

A

functional cells of the liver: remove rubbish and dump into canaliculus.

219
Q

where does clean blood from the liver go to

A

hepatic sinusoids

220
Q

what are the spaces between hepatic cords known as

A

hepatic sinusoids

221
Q

where do toxins go once they have been thrown out of your liver?

A

intestine then out of body

222
Q

six components of bile

A

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

223
Q

what is the only bile component not secreted by hepatocytes?

A

bicarbonate (HCO3)

224
Q

how is HCO3 produced?

A

secreted by duct cells

225
Q

how do bile pigments occur?

A

breakdown products of haemoglobin from old/damaged erythrocytes

226
Q

what is the predominant bile pigment

227
Q

what colour does bilirubin turn bile

228
Q

what causes bilirubin to turn brown

A

modification by bacterial enzymes

229
Q

what happens to reabsorbed bilirubin and what is it’s effect

A

excreted in urine - turns urine yellow

230
Q

how much bile acid has to be synthesised every day to replace lost volume

231
Q

what is bile acid synthesised from?

A

cholesterol

232
Q

what happens to bile acids before secretion?

A

they are conjugates with glycine or taurine to make bile salts

233
Q

purpose of turning bile acids to bile salts?

A

increase solubility

234
Q

how are secreted bile salts recycled

A

via enterohepatic circulation

235
Q

describe the shape/ location of the gallbladder

A

saclike structure on inferior surface of the liver

236
Q

3 layers in the gallbladder wall

A
  • mucosa
  • muscularis
  • serosa
237
Q

what happens when the sphincter of Oddi is closed?

A

bile is forced back into the gall bladder

238
Q

what effects does the gallbladder have on bile concentration?

A

increases it 5-20x (dependent on how long its in there)

239
Q

what happens when there is fat in the duodenum?

A

CCK is released, the sphincter of oddi relaxes and the gallbladder contracts, releasing bile

240
Q

over what area do peristaltic waves occur?

A

body –> antrum of stomach

241
Q

describe motility of the body of the stomach

A

thin muscle
weak contraction
no mixing

242
Q

describe motility of the antrum of the stomach

A

thick muscle
powerful contraction
mixing

243
Q

describe the effects of peristaltic waves on movement of stomach contents to duodenum

A

cause contraction of pyloric sphincter, squeezing a small quantity of gastric contents into the duodenum

244
Q

what produces and, conducts gastric peristaltic waves?

A

pacemaker cells in the longitudinal muscle layer. conducted through gap junctions along longitudinal muscle layer

245
Q

how many gastric peristaltic waves are there per minute

246
Q

what causes the slow wave rhythm of gastric peristaltic wave?

A

BER/ Basic Electrical Rhythm

247
Q

what determines the strength of contraction of a peristaltic wave?

A

number of action potentials per wave

248
Q

what can cause an increase in strength of contraction of peristaltic wave?

A
  • gastrin

- distension of stomach wall (when it fills with food)

249
Q

what can cause an decrease in strength of contraction of peristaltic wave?

A
  • fat/ acid/ amino acid/ hypertonicity in duodenum (means too much stuff is going through too quickly)
250
Q

where is bicarbonate (HCO3) produced?

A

Brunner’s gland duct cells (submucosal)

251
Q

what is triggered by acid in the duodenum that results in HCO3 secretion

A
  • long (vagal) and short (ENS) reflexes

- release of secretin from S Cells

252
Q

explain the pathway of secretin and HCO3

A

secretin released from S Cells -> HCO3 secreted from pancreas and liver -> acid neutralisation -> inhibits secretin release

negative feedback control pathway

253
Q

4 sections of pancreas

A

head (located within curvature of duodenum)
neck
body
tail

254
Q

explain endocrine portion of pancreas

A

there are pancreatic islets which produce hormones

255
Q

what hormones are produced by the endocrine portion of the pancreas

A
  • insulin
  • glucagon
  • somatostatin
256
Q

what does somatostatin do?

A

controls secretion of insulin and glucagon in the pancreas

257
Q

explain exocrine portion of the pancreas

A

acinar cells produces enzymes which are secreted into the duodenum via ducts
responsible for digestive function of the pancreas

258
Q

What proportion of the duodenum is taken up by exocrine-ness

259
Q

function of exocrine pancreas

A
  • secretion of bicarbonate by duct cells

- secretion of digestive enzymes by acinar cells

260
Q

where is sphincter of oddi located?

A

between pancreas and duodenum

261
Q

function of Islet of Langerhans

A

secrete insulin

262
Q

what do acinar cells contain

A

digestive enzymes stored as inactive zymogen granules

263
Q

what prevents auto digestion of the pancreas?

A

the ability of acinar cells to store digestive enzymes inactively as zymogen granules

264
Q

function enterokinase

A

converts trypsinogen to trypsin

265
Q

location enterokinase

A

bound to brush border of duodenal enterocytes

266
Q

function trypsin

A

converts all other zymogens to active forms

267
Q

different categories of pancreatic enzymes (6)

A 
proteases
nucleases
elastase
phospholipases
lipases
a-amylase
268
Q

proteases

A

cleave peptide bonds

269
Q

nucleases

A

hydrolyse DNA/RNA

270
Q

elastases

A

collagen digestion

271
Q

phospholipases

A

phospholipids -> fatty acids

272
Q

lipases

A

triglycerides -> fatty acids and glycerol

273
Q

a-amylases

A

starch -> maltose and glucose

274
Q

what stimulates zymogen secretion

A

cholecystokinin (CCK)

275
Q

what causes CCK (cholecystokinin) to be released?

A
  • Fat/ amino acids in duodenum

- organic nutrients in duodenum (local reflexes due to distension)

276
Q

approximate length small intestine

277
Q

approximate lengths of parts of small intestine

A
  1. duodenum = 25cm
  2. jejunum = 250cm
  3. ileum =. 350cm
278
Q

functions duodenum

A
  • gastric acid neutralisation
  • digestion
  • iron absorption
279
Q

functions jejunum

A
  • 95% nutrient absorption
280
Q

functions ileum

A
  • NaCl/ H2O absorption (chyme dehydration)
281
Q

chyme

A

gastric contents coming out of stomach

282
Q

how is the absorptive surface area of the small intestine increased

A

folds
villi
microvilli

283
Q

name of folds inside small intestine

284
Q

difference in appearance of villi in vegetarians

A

flatter than meat eaters

285
Q

how often are small intestinal cells replaced

A

every 5 days

286
Q

consequences of rapid dividing time of small intestinal cells

A

they can be affected by drugs targeting rapidly dividing cells e.g. cancer treatment

287
Q

explain cell movement on villi

A

cells start at the bottom and migrate upwards, specialising as they go

288
Q

what is secreted/ absorbed by crypts in small intestine

A

H2O + Cl secreted, nothing absorbed

289
Q

explain crypts in terms of someone with cystic fibrosis

A

they don’t secrete water, meaning that mucous layer on top of villi begins to build up and nutrients cannot be absorbed

290
Q

what is absorbed by a villus cell in small intestine

A 
NaCl
Monosaccharides
Amino Acids
Peptides
Fats
Vitamins
Minerals
Water
291
Q

how much fluid does the small intestine secrete per day

A

1500ml ish

292
Q

how does H2O secretion in small intestine occur

A

passively, along osmotic gradient cause theres a high amount of choride in intestinal lumen

293
Q

why is H20 secretion in the small intestine important for normal digestive process

A
  • maintains lumen contents in liquid state
  • promotes mixing of nutrients with digestive enzymes
  • aids nutrient presentation to absorbing surface
  • dilutes and washes away potentially injurous substances (protective function)
294
Q

what are the 2 distinct types of intestinal movement

A
  1. segmentation

2. peristalsis

295
Q

explain segementation in the small intestine

A
  • most common during a meal
  • contraction/ relaxation of small segments
  • chyme moves up and down from contracted areas to relaxed areas, then these switch
296
Q

benefits of the segmentation movement

A
  • provides a thorough mixing of contents

- brings chyme into contact with absorbing surface

297
Q

difference between gastric peristaltic wave creation and intestinal segmentation contractions

A

whereas the rate of contraction in the stomach remains the same throughout its length, the BER decreases slowly as it moves from intestine -> rectum

298
Q

reasoning for change of rate of contraction. throughout the intestine

A

more is being squeezed down from the top than up from the bottom

299
Q

can we conciously influence rate of contraction of intestine, stomach etc.

300
Q

what happens following the absorption of nutrients in the small intestine

A

peristalsis movement replaces segmentation

301
Q

what is the MMC (Migrating Motility Complex)

A

pattern of peristaltic activity travelling down small intestine (starts in gastric antrum)

302
Q

what causes the cessation of MMC and the initiation of segmentation

A

arrival of food in stomach

303
Q

functions MMC

A
  • move undigested material to large intestine

- limit bacterial colonisation of small intestine

304
Q

what hormone is involved in MMC?

305
Q

difference between peristalsis and segmentation

A

peristalsis only squishes food one way - no reverse peristalsis

306
Q

law of small intestine

A

if intestinal smooth muscle is distended (e.g. by bolus of chyme), muscle on oral side contracts, muscle on anal side relaxes.

307
Q

gastroilieal reflex - explain

A
  1. opening of ileocaecal valce
  2. entry of chyme into large intestine
  3. distension of colon
  4. reflex contraction of ileocecal sphincter (prevents reflux back into small intestine)
308
Q

how long is colon/ large intestine

309
Q

4 parts of large intestine

A

ascending
transverse
descending
sigmoid

310
Q

describe muscle layers colon

A

circular complete, longitudinal incomplete - hence puffs jacket look because circular pops through

311
Q

what happens upon contractions of tiniae coli in large intestine

A

pouches (puffa jacket appearance)

312
Q

what are pouches in large intestine called

313
Q

surface of mucosa in large intestine:

A

large, straight crypts lines with a large number of goblet cells (lubrication for movement of faeces)

314
Q

describe rectum

A

straight, muscular tube between sigmoid colon and anal canal

315
Q

describe epithelium mucosa of rectum and large intestine

A

similar columnar epithelium

316
Q

describe muscularis externa of rectum

A

thick compared to other regions of alimentary canal

317
Q

describe anal canal

A

2-3cm between distal rectum and anus

318
Q

describe muscularis externa of anal canal

A

thicker than rectum

319
Q

what is the external anal sphincter made of

A

skeletal muscle (we have voluntary control over it)

320
Q

epithelium anal canal

A

stratified squamous

321
Q

purpose of colon

A

actively transports Na from lumen to blood -> osmotic absorption of water -> dehydration of chyme -> solid faecal pellets

322
Q

describe presence of bacteria in colon

A

around 10^14 - about 1kg of colonic microflora

323
Q

purpose of bacteria in colon

A

fermentate undigested carbohydrate into short chain fatty acids, vitamin K and gas (flatus/pops)

324
Q

problems associated with not having bacteria in your colon when you’re born

A

you can’t fermentate the undigested bacteria, and therefore can’t make vitamin K, so are at risk of bleeding

325
Q

function of vitamin K

A

blood clotting

326
Q

what happens following a meal with regards to MMC and defaecation

A

wave of intense contraction resulting in distension of rectal wall as a mass movement of faecal material into the rectum occurs, initiating a defaecation reflex and an urge to defaecate.

327
Q

what nerve supply controls defaecation

A

pelvic splanchnic nerves (parasympathetic)

328
Q

3 stages of defaecation

A
  1. contraction of rectum
  2. relaxation of internal and contraction of external anal sphincters
  3. increased peristaltic activity in colon
  4. an increase in pressure on external sphincter, which relaxes under voluntary control
  5. expulsion of faeces
329
Q

why do children under 2ish have to wear nappies

A

because voluntary delay of defaeciation has to be learned

330
Q

symptoms of constipation

A

headaches
nausea
loss of appetite
abdominal distension

331
Q

what causes constipation

A

distension of rectum

332
Q

causes of diarrhoea

A 
pathogenic bacteria
protozoans
viruses
toxins
food
nervousness
333
Q

type of bacteria causing diarrhoea and examples

A

enterotoxigenic bacteria

e. g.
- vibrio cholerae
- e. coli

334
Q

effect bacteria have that causes diarrhoea

A

they turn on intestinal chloride solution, which in turn increases H2O secretion. large intestine doesn’t have a large surface area, so can’t absorb the water efficiently- hence the diarrhoea
dont damage villi

335
Q

treatment of secretory diarrhoea

A
  • give sodium/glucose solution cause this drives H2O absorption, rehydrating

GI (35 decks)

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