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physiology Flashcards

1
Q

what is the alimentary canal

A

serious of hollow tubes running from mouth to anus (oral to aboral) separated by sphincters

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2
Q

what are the components of the GI tract

A

mouth and oropharynx, oesophagus, stomach, small intestine, large intestine, rectum and anus

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3
Q

where is the principle site of digestion and absorption

A

small intestine

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4
Q

what happens in the large instestine

A

holds the colon where fluids and electrolytes are reabsorbed and stored as faeces

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5
Q

what are the assessory features of the alimentary canal

A

salivary glands, pancreas, liver and gall bladder

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6
Q

how long is the GI tract

A

7-10m

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7
Q

what are the components of the digestive tract wall

A

mucosa, submucosa, muscularis externa, serosa

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8
Q

what is the function of the mucosa

A

fat absorption

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9
Q

what dies the muscularis externa do

A

changes shape to facillitate absorption

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10
Q

what are the 4 major functions of the alimentary canal

A

motility, secretion, digestion, absorption

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11
Q

what is the main type of muscle in the GI tract and what are the exceptions

A

mostly smooth, skeletal in mouth, pharynx, upper oesophagus and external anal sphincter

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12
Q

when does secretion occur and what does it do

A

in response to food, hormones or nerves, needed for digestion, protection and lubrication

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13
Q

what happens during digestion

A

chemical breakdown by hydrolysis of complex food to absorbable units

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14
Q

what happens during absorption

A

transfer from digestive tract to blood

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15
Q

when circular muscles contract what happens to the lumen

A

narrower and longer

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16
Q

when longitudinal muscles contract what happens to the lumen

A

shorter and fatter

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17
Q

adjacent cells are coupled by?

A

gap junctions

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18
Q

when the cells depolarise in a synchronous wave what is this called

A

single unit smooth muscle

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19
Q

what type of wave occurs in stomach, small and larger intestines

A

slow wave

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20
Q

what type of cells cause slow wave depolarisation

A

interstitial cells of Cajal (ICC’s), these are pacemakers

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21
Q

where are ICCs found

A

between circular and longitudinal muscle

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22
Q

when does depolarisation of slow waves result in contraction

A

when there are frequent enough AP’s to get to the threshold. (AP’s increase force not speed)

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23
Q

the upstroke is due to an influx of what

A

Ca++

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24
Q

what are short waves also known as

A

basic electrical rhythm

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25
Q

what type of outflow is involved in the PARASYMPATHETIC autonomic innervation and which nerves are involved

A

cranio-sacral, vagus and pelvic nerves

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26
Q

where to preganglionic fibres synapse with ganglion cells in parasympathetic.

A

enteric nervous system.

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27
Q

what are the excitatory influences of parasympathetic outflow

A

increased gastric, pancreatic and small intestinal secretion, increased blood flow and increased muscle contraction

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28
Q

what are the inhibitory influences of parasympathetic outflow

A

relaxation of sphincters, relaxation of stomach

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29
Q

what is more significant in the GI tract parasympathetic or sympathetic

A

parasympathetic

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30
Q

where to preganglionic fibres synapse in SYMPATHETIC outflow

A

prevertebral ganglia, (post release NA)

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31
Q

what are excitatory influences of sympathetic outflow

A

increased sphincter tone

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32
Q

what are inhibitory influences of sympathetic outflow

A

decreased motility, decreased secretion, decreased blood flow

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33
Q

what does the enteric nervous system act on

A

the gut

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34
Q

give an example of local, short and long nerve reflexes

A

local: peristalsis, short: intestino-intestinal inhibitory reflex, long: gastroileal

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35
Q

what is peristalsis

A

wave of relaxation followed by a contraction, usually over short distances and oral–>aboral

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36
Q

in the oral section, what muscle relaxes and what contracts

A

longitudinal relaxes and circular contracts

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37
Q

in the aboral section, what muscle relaxes and what contracts

A

longitudinal contracts and circular relaxes

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38
Q

what causes relaxation of longitudinal/ circular muscle

A

NO and VIP

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39
Q

what causes contraction of longitudinal/ circular muscle

A

ACh and substance P

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40
Q

what are the 5 major motility functions of the GI tract

A

peristalsis, segmentation, colonic mass movement, migrating motor complex (MMC), tonic contractions

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41
Q

what happens in segmentation, what is it called in large intestine

A

rhythmic contractions of circular muscle for mixing/ churning. Occurs in small and large intestine (haustration)

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42
Q

what are the 6 sphincters

A

upper oesophageal, lower oesophageal, pyloric, illeocacal, internal anus, external anus

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43
Q

which sphincters are controlled by skeletal

A

upper oesophageal and external anus

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44
Q

food entering the oesophagus does what to stomach

A

relaxes receptively to prepare, vagus activity

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45
Q

What are the 4 main anatomical areas of the stomach?

A

Fundus
Body
Antrum
Pylorus

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46
Q

what are the 2 mechinal sections of stomach

A

orad and caudad

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47
Q

what happens in orad section

A

relaxes in preparation for food, tonic contractions

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48
Q

what happens in caudad section

A

slow waves (3/min) when threshold met, peristalsis i antrum, propels chyme towards pylorus. also retropulsion of chyme

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49
Q

where does mixing occur

A

antrum

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50
Q

What is the substance produced when food mixes with gastric secretions

A

chyme

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51
Q

Name a substance which can be absorbed by the stomach

A

ethanol

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52
Q

What occurs in Retropulsion?

A

Peristaltic wave forces chyme against closed pyloric sphincter, so chyme bounces back and undergoes more mixing

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53
Q

what are some gastric factors promoting gastric emptying

A

volume of chyme, consistency of chyme, muscle strength, increases vagus nerve and gastrin release

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54
Q

Which 2 duodenal factors delay gastric emptying?

A 
Enterogastric reflex (decreases antral activity) 
Release of enterogastrones (inhibit stomach contractions eg CKK)
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55
Q

What is the enterogastric reflex?

A

Duodenum signals to stomach that it has enough chyme so slow down emptying/peristaltic contraction

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56
Q

which stimuli in duedendum can decrease stomach emptying

A

fat, acid, hypertoncity, osmotically active, distension

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57
Q

Where is the oxyntic mucosa area located?

A

fundus and body

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58
Q

Where is the pyloric gland area located?

A

antram

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59
Q

Which cells are contained in the oxyntic mucosa amd what do they secrete?

A

Parietal cells: HCL
Enterochromaffin-like cells (ELC): histamine
Chief cells: pepsinogen

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60
Q

Which cells are contained in the pyloric gland area and what do they secrete?

A

D cells: somatostatin

G cells: gastrin

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61
Q

What does autocatalytic mean with regards to pepsinogen and pepsin?

A

Pepsin formation triggers further pepsin formation from pepsinogen

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62
Q

what does HCL do (oxyntic mucosa)

A

converts pepsinogen to pepsin, denatures enzymes and kills bacteria (parietal cell)

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63
Q

what does histamine do (oxyntic mucosa)

A

stimulates HCL release (ECL cell)

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64
Q

what does pepsinogen do (oxyntic mucosa)

A

converted to pepsin which breaks down proteins (chief cells)

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65
Q

What is the role of intrinsic factor and in the oxyntic mucosa?

A

Binds vitamin B12

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66
Q

What is the role of gastrin in the pyloric gland area?

A

Stimulates HCl secretion (G cell)

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67
Q

What is the role of somatostatin in the pyloric gland area?

A

Inhibits HCl secretion (D cell)

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68
Q

in the parietal cell, which enzyme forms H2CO3 from which to substrates

A

carbonic anhydrase, Co2 and H2O

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69
Q

what does H2CO3 dissociate to

A

HCO3 (bicarbonate) and H+

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70
Q

what does H/KATPase do

A

actively pumps K in and H+ out at apical end to canaliculus

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71
Q

How does bicarbonate exit cell, what enters in the exchanger

A

antiporter into plasma, chlorine enters

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72
Q

what channel does Cl exit to canaliculus

A

CFTR

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73
Q

CL and H then form to make acid true/false

A

true :)

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74
Q

What are Secretagogues?

A

Substances promoting secretion of HCl (gastrin, ACh, histamine)

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75
Q

What are the 3 phases of gastric secretion?

A

Cephalic
Gastric
Intestinal

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76
Q

What is involved in the cephalic phase?

A

Stomach is prepared to receive food by conditioned reflex, chewing or swallowing, leading to gastric secretion through ACh and GRP

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77
Q

What is involved in the gastric phase?

A

Distension of stomach causes G cells to be activates and D cells to be inhibited

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78
Q

what inhibits gastric secretion in cephalic stage

A

vagal nerve activity once you’ve stopped eating

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79
Q

what inhibits gastric secretion in gastric stage

A

fall in antral pH after eating, prostaglandin E2 removing histamine

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80
Q

what inhibits gastric secretion in intestinal stage

A

Gastric secretion is halted through secretin, CCK and somatostatin as the stomach empties

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81
Q

What is the importance of the mucus gel layer on the surface of mucous secreting cells?

A

Prevents pepsin/HCl reaching the apical surface of the cells and damaging the cells

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82
Q

how does the mucus gel layer prevent damage

A

produces PGE2 and PGL2 to reduce acid, increases mucous and bicarbonate secretion, increased mucous blood flow

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83
Q

Place the parts of the small intestine in order from shortest to longest

A

Duodenum (0.25m)
Jejunum (2.5m)
Ileum (3m)

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84
Q

what does the small intestine recieve

A

chyme, pancreatic juices, bile from gallbladder

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85
Q

Which 3 components increase the SA of the small intestine?

A

Circular folds
Villi
Microvilli

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86
Q

Where is gastrin secreted from?

A

G cells of stomach + duodenum

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87
Q

Where is secretin secreted from?

A

S cells of duodenum

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88
Q

Where is CCK secreted from?

A

I cells of duodenum + jejunum

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89
Q

Where is motilin secreted from?

A

M cells of duodenum + jejunum

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90
Q

Where is ghrelin secreted from?

A

Gr cells of stomach, small intestine + pancreas

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91
Q

what factors increases small intestine secretion

A

gastrin, CCKm distension and parasympathetic stimulation

92
Q

does segmentation occur in small intestine

A

yes, to mix chyme,

93
Q

what is the migrating motor complex

A

strong peristaltic contraction between meals, clears stuff from stomach to ileum, activated by motilin

94
Q

what does the endocrine pancreas secrete

A

insulin and glucagon

95
Q

what does the exocrine pancreas secrete and from which cells

A

anicar cells: digestive enzymes

duct cells: aqueous salts (NaHCO3)

96
Q

where do exocrine secretions go

A

duodenum

97
Q

explain neutralisation in small intestine (involving pancreas)

A

duodenum has high acid which causes S cells to release secretin. Secretin travels in blood to pancreas, it then releases aqueous salts from duct cells (NaHCO3) to duodenum lumen

98
Q

explain digestion in small intestine (involving pancreas)

A

fat and protein in duodenum causes I cells to release CKK in blood to pancreas, it then releases digestive enzymes from anicar cells to duodenum lumen

99
Q

name some forms of carbs

A

starch, cellulose, disaccharides, glycogen

100
Q

name some types of lipids

A

triglycerides, free fatty acids, cholesterol, phospholipids

101
Q

what is luminal digestion

A

digestion by pancreatic enzymes secreted into duodenum

102
Q

what is membrane digestion

A

by enzymes at brush of epithelial cells

103
Q

what is the combined term for digestion and absorption

A

assimilation

104
Q

Name two polysaccharides

A

starch glycogen

105
Q

what are 2 forms of starch

A

amylose, amylopeptin

106
Q

what bonds does amylose have

A

alpha 1,4

107
Q

what bonds does amylopeptin have

A

alpha 1,4 and 1,6 in branches

108
Q

Name two disaccharides (oligosaccharides)

A

Sucrose

Lactose

109
Q

Name three monosaccharides

A

Glucose
Fructose
Galactose

110
Q

what do carbs have to be broken into for absorption

A

monosaccharides

111
Q

what happens in intraluminal hydrolysis

A

eg starch –> ogliosaccharides by alpha amylase

112
Q

what happens in membrane hydrolysis

A

ogliosaccharides –> monosaccharides by ogliosaccharidases

113
Q

what does lactase do

A

breaks down lactase to glucose and galactose

114
Q

what does maltase do

A

degrades alpha 1,4 bonds

115
Q

what does isomaltase do

A

only enzyme that breaks down alpha 1,6

116
Q

what does sucrose hydrolyse

A

sucrose + glucose –> fructose

117
Q

What is lactose intolerance?

A

Inability to digest lactose, caused by lactase insufficiency

118
Q

what side of enterocytes are monosaccharides absorbed

A

apical

119
Q

how doe glucose and galactose enter enterocytes

A

secondary transport, by SGLT1

120
Q

how does fructose enter enterocytes

A

facilitated diffusion by GLUT 5

121
Q

how do all monosaccherides exit monocytes

A

GLUT 2

122
Q

What denatures proteins in the stomach?

A

HCl

123
Q

Which enzyme cleaves protein into peptides in the stomach and is it essential for digestion

A

pepsin, no.

124
Q

What are the active enzymes that digest protein in the duodenum from the pancreas

A 
Trypsin
Chymotrypsin 
Elastase 
Procaroxypeptidase A 
Procaroxypeptidase B
125
Q

What are the ranges for normal BMI?

A

18.5-25

126
Q

What are the ranges for BMI classed as overweight?

A

25-29.9

127
Q

What are the ranges for BMI classed as obese?

A

30-39.9

128
Q

What are the ranges for BMI classed as morbidly obese?

A

> 40

129
Q

How is obesity “a disease of the brain”?

A

The brain sees new fat/weight as normal, and attempts to lose weight are seen as a threat to survival, so the new weight is defended

130
Q

what part of the brain regulates body weight

A

hypothalamus

131
Q

Which lesioning part of the hypothalamus causes leanness?

A

lateral

132
Q

Which lesioning part of the hypothalamus causes obesity

A

ventromedial

133
Q

define satiation

A

feeling full during/ end of a meal

134
Q

define satiety

A

fasting between means

135
Q

when do satiation signals increase and why

A

when you are eating, Increased signals limit meal size, i.e. you can’t eat anymore

136
Q

name some satiation singals

A

CKK, peptide YY, GLP1, OXM, obestatin

137
Q

What is ghrelin?

A

a hunger signal

138
Q

what are adiposity signals, give examples

A

signal fat stores to the brain, leptin and insulin, higher levels = more fat

139
Q

how can obesity affectin leptin and insulin

A

alter transduction, damage receptors

140
Q

what is the ‘food reward’

A

hedonistic affect, releases dopamine

141
Q

name some ways to tackle obesity

A

drugs: orlistat
gastric bypass
heat therapy

142
Q

name some types of lipids

A

Fats/ oils, phospholipids, fatt acids, cholesterol

143
Q

what is emulsion

A

creating droplets suspending lipids in water to increase surface area.

144
Q

what are the stages of lipid digestion

A

lingual phase –> gastric phase (gastric lipase in stomach) –> intestinal (small intestine, most important)

145
Q

what is released to the duodenum from the gall bladder in lipid digestion

A

bile salts

146
Q

what are bile salts released in response to and what do they do

A

CCK, emulsify lipids

147
Q

what cofactor is needed for pancreatic lipase so it can access triglycerides

A

colipase

148
Q

how is colipase activated

A

procolipase –> colipase by trypsin

149
Q

what is a mixed micelle

A

product of digestion, emulsified globule containing TAGs, esterified cholesterol, bile salts, phospholipids and fatty acids

150
Q

where do short/ medium exit enterocytes to capillaries and how do they do this

A

basolateral membrane by passive diffusion and membrane fatty-acid translocase

151
Q

how are long fatty acid chains and monoglycerides digested

A

resnythesized to triglcyerides in the ER and made to chylomicrons

152
Q

how are chylomicrons formed

A

triglycerides synthesised to cholesterol esters –> chylomicrons and coated with apolipoproteins

153
Q

where are chylomicrons released to

A

lymphatic system by exocytosis

154
Q

how is cholesterol absorbed

A

NPC1L1

155
Q

how does NPC1L1 move around the cell

A

by myosin

156
Q

how is Ca absorbed

A

passive diffusion in small intestine, is regulated by calcitrol

157
Q

what does Vit D do in relation to Ca absorption

A

increased expression for Ca channels when Ca conc is low

158
Q

what binds to Fe2+ in the stomach

A

gastroferrin

159
Q

how does Fe2+ enter cells

A

contransporter iron

160
Q

which acid is absorbable ferric or ferrous

A

ferrous (Fe2+) is bit ferric (Fe3+) is not, must be converted

161
Q

how does haem increase iron levels in the blood

A

degradation of haem oxidase

162
Q

what is the storage form of iron

A

ferratin

163
Q

what are the fat soluble vitamins

A

ADEK

164
Q

how is vit B12 absorbed

A

haptocorin binds to vitB12 in stomach, stomach parietal cells release intrinsic factor and in small intestine the intrinsic factor binds to it. It is then absorbed by endocytosis

165
Q

what diet can lead to vit B12 deficiency

A

vegans, only present in animal produce

166
Q

what is the large intestine made up of

A

caecum and appendix, ascending, transverse, descending and sigmoid colon, rectum, anal canal and anus

167
Q

what type of muscle is in the caecum and colon

A

longitudunal smooth muscle that divides into 3 strands called taeniae coli

168
Q

what surrounds the internal anal sphincter

A

the external skeletal sphincter

169
Q

what does the colon mainly absorb

A

Na, Cl and H2O, also short chain fatty acids

170
Q

what does the colon mainly secrete

A

K, HCO3 and mucus

171
Q

what are the 4 functions of the colon

A

absorption, secretion, storing faeces and eliminating faeces

172
Q

what does the colon have instead of villi

A

colonic folds, crypts and microvilli

173
Q

what do epithelial cells (colonocytes) mediate in the colon

A

electrolyte absorption

174
Q

what do crypt cells mediate

A

ion secretion

175
Q

what do goblet cells secrete

A

mucous

176
Q

what are haustra

A

saccule in colon from haustration

177
Q

what is the mass movement of the colon, what reflex causes it

A

contraction of large sections of the colon at the same time towards the rectum, gastrocolic response

178
Q

describe the defaecation reflex

A

reflex stretch receptors activate pelvic nerve, activates parasympathetic efferents causing internal sphincter to relax (rectum not normally filled with faeces)

179
Q

which nerves control the external anal sphincter

A

pudenal nerve (S2,3,4)

180
Q

why are colonic flora important

A

compete with pathogenic microbes, promote motility,, synthesise vit K2 and free fatty acids

181
Q

what is flatus

A

intestinal gas, from swallowed air, bacteria and gases

182
Q

what can cause constipation

A

enhances absorption of H20, suppressing the need, decreases motility obstruction, hirschprung disease

183
Q

what can hardened calcified matter cause

A

appendicitis

184
Q

how does chyme enter the caecum

A

through ileocal valve by gastroileal reflex in response to gastrin and CCK

185
Q

what does the caecum relax in response to

A

distension of the duodenum

186
Q

where is the appendix attached to the caecum

A

distal via appendiceal orifice

187
Q

what can happen if appendiceal orifice is obstructed by faecalith

A

appendicitis

188
Q

when should laxatives and purgatives not be used

A

bowel obstruction

189
Q

what can laxatives be used for

A

to increase peristalsis and soften faeces, clean bowel before surgery, when pooing is sore

190
Q

name 2 chronic bowel disease

A

irritable (IBS) and inflammatory (IBD)

191
Q

what causes vomiting and nausea

A

reverse peristlasis from upper

192
Q

where is the vomiting centre (VC)

A

medulla oblongata

193
Q

describe how the mediator is released in the vomiting pathway

A

toxic materials in gut lumen stimulate enterchromaffin cells in mucosa to release mediates (5-HT)

194
Q

describe how the nerves cause vomiting in pathway

A

sensory afferent terminals in mucosa depolarise, AP discharge in vagal nerve afferents to brainstem, VC causes you to throw up

195
Q

what are the events of vomiting

A

sphincters relax and retrograde contractions from ileum to stomach. proceeded by lack of saliva, sweating, high BP and nausea

196
Q

what are some consequences of severe vomiting

A

dehydration, loss of protons and chloride (met alkalosis), raised pH, hypokalaemia

197
Q

how much water is lost on faeces, what else does it contain

A

100ml, cellulose, bilirubin and bacteria

198
Q

what is the main solute that drives absorption of water

A

Na

199
Q

what are the major mechanisms in postorandiral period in jejunum

A

Na/glucose co-transport and Na/ amino acid co-transport

200
Q

do cAMP and cGMP increase or decrease NaCl absorption

A

decrease

201
Q

what is the definition of diarrhoea

A

loss of fluid and solutes in excess of 500ml a day

202
Q

what can cause diarrhoe

A

infectious agents, chronic disease, toxins, impaired absorption of NaCl, excession secretion of Cl and Na (cholera), poorly absorbable intestinal lumen

203
Q

what are some consequences of diarrhoea

A

dehydration (Na+H2O loss), metabolic acidosis (HC03 loss), hypokalaemia

204
Q

how does rehydration therapy work

A

Na and glucose translocate from extracellular to intracellular and water follows

205
Q

how do opiods act as anti-diarrhoeal

A

increase fluid absorption, contrict pyloric, iliocaecal and anal sphincters and decrease peristalsis

206
Q

name some opiods

A

codeine, diphenoxylate (least abuse potential), loperamide

207
Q

what 3 things does the liver metabolise

A

carbs, fat and protein

208
Q

describe carb metabolism in the liver

A

gluconeogenesis, glycogenesis, glycogenolysis

209
Q

describe fat metabolism in the liver

A

processes chylomicron remains and synthesises lipoproteins and cholesterol, ketogenesis

210
Q

what does the liver degrade

A

insulin, glucagon, ADH, steroid hormones

211
Q

what does the liver activate

A

thyroid –> throxine, vit D

212
Q

what does the liver store

A

fat soluble vitamens (ADEK), water soluble vit b12, iron copper, glycogen

213
Q

what does the liver synthesis

A

coagulation factors (II, VII, IX, X), albumin, apoliproteins

214
Q

what does the liver do for protection

A

kupffer cells digest and destroy old and bad stuff. produce immune cells

215
Q

what does the liver detoxify

A

bilirubin, drugs and ethanol

216
Q

where is bile stores and concentrated between meals

A

gall bladder

217
Q

how is bile released during a meal

A

chyme stimulates gall bladder to contract (via CCK and vagal impulses), sphincter of Oddi opens via CCK and bile exits

218
Q

where is primary bile secreted and what does it contain

A

hepatocytes: cholic + chenodeoxycholic acids

219
Q

what is the most common bilary system problems

A

cholelithiasis (gall stones), happens when bile crystallises

220
Q

what is best treatment for gall stones

A

laparoscopic cholectystectomy

221
Q

how are bile salts recycled

A

enterohepatic recycling

222
Q

how are some primary bile acids converted to secondary

A

dehydroxylated by bacteria and returned to liver

223
Q

what does the liver do to drugs

A

converts them to less pharmacologically active metabolites

224
Q

where does phase 1 happen and what does it do

A

right side, makes drugs more polar eg oxidation, reduction, hydrolysis

225
Q

where does phase 2 happen and what does it do

A

conjugation, adding something. glucuronidation is common

226
Q

what mediates oxidation reactions in phase I

A

CYP450

My1 GI (26 decks)

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