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MB1: Gastrointestinal > Physiology > Flashcards

Physiology Flashcards

1
Q

components of alimentary canal

A 
mouth/oropharynx 
oesophagus 
stomach 
small intestine 
large intestine 
rectum and anus
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2
Q

4 functions of alimentary canal

A

motility
secretion
digestion
absorption

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3
Q

describe lumen during circular muscle contraction

A

narrowed lumen and longer

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4
Q

describe lumen during longitudinal muscle contraction

A

shorter, fatter intestine

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5
Q

how is a synchronous wave of contraction achieved in the smooth muscle of the GI tract

A

gap junctions between cells

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6
Q

how is GI smooth muscle contraction driven

A

pacemaker cells

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7
Q

what do interstitial cells of cajal do?

A

drive slow waves coupled to smooth muscle to control rate of contraction

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8
Q

when does intestinal muscle contraction occur

A

when slow waves exceed threshold to contract

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9
Q

what increases force of contraction in intestinal muscle

A

number of APs discharged

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10
Q

true/false - frequency of slow waves vary along GI tract

A

true

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11
Q

where do parasympathetic nerves for the GI tract originate from

A 
vagus nerve
sacral outflow (S2-S4)
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12
Q

true/false - preganglionic parasympathetic fibres of the GI tract synapse with gaglia and connect to postganglionic neurons of parasympathetic system

A

false - synapses with ganglia then connects to postganglionic neurons of ENS

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13
Q

true/false - preganglionic neurons of the sympathetic system synapse at the sympathetic chain

A

false - they synapse at prevertebral ganglia

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14
Q

inflences of parasympathetic nervous system

A

increased gastric, pancreatic and small intestine secretion
increased blood flow and smooth muscle contraction
relaxation of sphincters

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15
Q

influences of sympathetic nervous system

A

increased sphincter tone

decreased motility, secretion and blood flow

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16
Q

true/false - ANS/hormones can modulate myenteric and submucosal plexus

A

true

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17
Q

what is peristalsis

A

wave of relaxation followed by contraction in aboral direction

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18
Q

in peristalsis, what happens behind the bolus

A

NO/VIP cause longitudinal muscle to relax

ACh causes circular muscle to contract to push bolus

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19
Q

in peristalsis, what happens in front of the bolus

A

longitudinal muscle contracts due to ACh

circular muscle relaxes due to VIP/NO

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20
Q

what is colonic mass movement

A

sweeping contraction that forces faeces into rectum

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21
Q

function of upper oesophageal sphincter

A

relaxes to allow swallowing and closes in inspiration

skeletal muscle

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22
Q

function of lower oesophageal sphincter

A

relaxes to allow food entry to stomach

prevents acid reflex into oesophagus

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23
Q

function of pyloric sphincter

A

regulates gastric emptying and prevents duodenal gastric reflux

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24
Q

function of ileocaecal valve

A

controls flow from ileum to caecum

ileal distention opens it and proximal colon distention closes it

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25
Q

internal and external anal sphincters

A

defaecation reflex

skeletal muscle - voluntary control

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26
Q

function of orad stomach

A

accomodate food in feeding

digestion by amylase

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27
Q

what effect does vagal tone have on the orad stomach

A

relaxation to allow for storage of ingested food

tonic contraction to propel food into caudad stomach

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28
Q

what is the orad stomach made up of

A

fundus and proximal body

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29
Q

what is the caudal stomach made up of

A

distal body and antrum

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30
Q

function of caudad stomach

A

digestion by pepsin and HCl, intrinsic factor and gastrograffin
phasic peristaltic contractions to allow chyme into duodenum

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31
Q

what is retropulsion

A

rebound of chyme back into caudad stomach due to faster contraction than chyme movement - churns chyme

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32
Q

gastric factors controlling stomach emptying

A 
stretch of smooth muscle 
intrinsic nerve plexus stimulation 
increased vagal activity 
increased gastrin 
thicker chyme
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33
Q

duodenal factors controlling stomach emptying

A

enterogastric reflex - decrease in antral activity due to decrease in ANS and intrinsic nerve plexus
release of enterogastrones from duodenum to inhibit contraction

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34
Q

stimuli for slower secretion of chyme into stomach

A

high fat
high acid concentration
hypertonicity - carbohydrates and protein
duodenal distention

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35
Q

what is the oxyntic gland area

A

fundus and body

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36
Q

what is the pyloric gland area

A

antrum

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37
Q

secreting cells and their secretions in the pyloric gland

A

G cells - gastrin
D cells - somatostatin
Mucus secretion

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38
Q

secreting cells and their secretions in the oxyntic gland

A

enterochromaffin - histamine
parietal cells - HCl, intrinsic factor, gastroferrin
Chief cells - pepsinogen
Mucus secretion

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39
Q

Function gastrin

A

stimulates gastric secretion and acid production
growth of gastric mucosa
G cells

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40
Q

function somatostatin

A

reduces astric secretion and acid production

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41
Q

function HCl

A

denatures proteins, kills microorganisms, pepsinogen to pepsin

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42
Q

function intrinsic factor

A

binds to vitamin B12 to facilitate absorption, sometimes iron

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43
Q

function gastroferrin

A

binds to iron to facilitate absorption

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44
Q

function pepsinogen

A

inactive precursor of pepsin, once activated it can further activate pepsin

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45
Q

function histamine

A

stimulates HCl secretion

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46
Q

describe HCl secretion by parietal cells

A

CO2 and H2O combine by carbonic anhydrase to form carbonic acid. dissociates to H, pumped into canaliculus by proton pump. bicarbonate removed by antiport with chloride, which leaves cell by CFTR at canaliculus

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47
Q

true/false - acid secretion is a passive process

A

false - it is active

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48
Q

name 3 secretagogues

A

ACh
Gastrin
Histamine

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49
Q

where does the proton pump translocate from on stimulation by secretagogues

A

cytoplasmic tubulovesicles

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50
Q

what is the cephalic phase of acid secretion and what drives it

A

anticipatory signal telling stomach to secrete acid

driven by vagus nerve

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51
Q

Vagus nerve stimulates enteric nervous system to release ACh in the cephalic and gastric phase. what does it do?

A

parietal cells- increase secretion
D cells - reduce somatostatin
ECL - increase histamine
(GRP not ACh) G cells- increase gastrin

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52
Q

what is the gastric phase, and besides vagal innervation what else drives it

A

when food enters stomach
distention of stomach
amino acids on g cell to increase gastrin
high pH decreases somatostatin

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53
Q

what drives acid secretion in the intestinal phase

A

chyme enters duodenum to cause weak gastric secretion stimulation

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54
Q

what causes decreased acid secretion in cephalic phase

A

decreased vagal activity

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55
Q

what causes decreased acid secretion in gastric phase

A

decreased vagal activity
low pH - somatostatin from D cells
PGE - reduce histamine and gastrin mediated HCl

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56
Q

3 ways small intestine increases surface area and better absorption

A

circular folds of kerckring
villi
microvilli

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57
Q

what is segmentation and when does it occur

A

digestive state

vigorous alternating contraction and relaxation of segments of circular muscle

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58
Q

cause of segmentation and how to increase strength

A

interstitial pacemaker cells emitting slow waves, reach threshold upon distention
Parasympathetic innervation

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59
Q

what is the gastroileal reflex

A

segmentation in empty ileum due to gastrin from stomach

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60
Q

what is the migrating motor complex

A

strong peristaltic contraction that passes slowly across small intestine to clear debris, mucus and cells every 90-120 mins

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61
Q

___ and ___ induce the MMC and ___, ___ and ___ inhibit it

A

increase- motilin, macrolides

decrease - vagus, gastrin, CCK

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62
Q

location of secretin secretion and function

A

S cell duodenum

promotes secretion of bicarbonate from pancreas and gallbladder due to protons/fatty acid

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63
Q

location of CCK secretion and function

A

I cells duodenum
inhibits gastric emptying and pancreatic enzyme secretion, contraction of gallbladder and relaxation of sphincter oddi due to monoglycerides, fatty acid, amino acids

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64
Q

location of GIP secretion and function

A

K cell duodenum, jejunum

insulin release and impaired gastric emptying due to glucose, amino acids, fatty acids

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65
Q

location of GLP-1 secretion and function

A

L cell small intestine
insulin secretion
inhibits glucagon secretion
decrease gastric emptying and appetite

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66
Q

location of motilin secretion and function

A

M cells duodenum and jejunum

stimulates MMC on fasting

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67
Q

location of ghrelin secretion and function

A

Gr of gastric antrum, small intestine

stimulates appetite

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68
Q

innervation for succus entericus

A 
distention 
gastrin 
CCK
secretin 
parasympathetic activity
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69
Q

contents of succus entericus

A

mucus - goblet cell

aqueous salt - crypt lieberkuhn - secreted by chloride ion secretion into lumen by CFTR, drawing Na and H2O

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70
Q

2 endocrine pancreatic secretions

A

insulin

glucagon

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71
Q

describe how digestive enzymes converge in pancreatic duct

A

acinar cells secrete digestive enzymes that travel from acinus to duct and then converge

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72
Q

describe the formation of bicarbonate by pancreatic duct cells

A

Na/Cl transporter provides some bicarbonate
CO2 into cell with H20 and carbonic anhydrase produces carbonic acid
H dissociates and is pumped out by proton pump and Na/H transporter
bicarbonate secreted in bicarbonate/Cl exchanger with CFTR pumping chloride back out

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73
Q

what enzyme catalyses trypsinogen to trypsin

A

enterokinase

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74
Q

trypsin in active form activates what other proteases

A

chymotrypsin and carboxypeptidase A&B

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75
Q

what increases pancreatic secretion in cephalic phase

A

vagal stimulation

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76
Q

what increases pancreatic secretion in gastric phase

A

gastric distention leading to vagal stimulation

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77
Q

what increases pancreatic secretion in intestinal phase

A

acid in duodenum - increased secretin

fat and protein - increased CCK

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78
Q

what is luminal digestion

A

enzymes secreted into lumen

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79
Q

what is membrane digestion

A

enzymes present at brush border of epithelial cells

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80
Q

what is assimilation

A

the collective term for digestion and absorption

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81
Q

what linkage does amylose have

A

straight chain with alpha-1,4 linkage

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82
Q

what linkage does amylopectin have

A

branched chain with alpha-1,4 and alpha-1,6 linkage

83
Q

what linkage does glucose have

A

alpha-1,4

alpha-1,6

84
Q

name 2 oligosaccharides

A

sucrose - glucose and fructose

lactose - glucose and galactose

85
Q

name 2 monosaccharides

A

glucose

fructose

86
Q

true/false - dietary carbohydrates must be converted to monosaccharides for absorption

A

true

87
Q

where are polysaccharides broken down

A

intraluminal digestion - pancreatic enzymes and alpha amylase

88
Q

what does alpha amylase break down

A

internal alpha-1,4 links but not terminal links so can only yield oligosaccharides

89
Q

where are oligosaccharides broken down into monosaccharides for absorption

A

brush border

90
Q

what does maltase do

A

degrades alpha 1,4 linkage in straight chain oligomers

91
Q

what does sucrase do

A

hydrolyses sucrose to glucose and fructose

92
Q

what does isomaltase do

A

splits branches of alpha 1,6 links of alpha limit dextrins

93
Q

where does carbohydrate absorption occur

A

duodenum and jejunum

94
Q

how do glucose and galactose move into enterocyte from lumen

A

SGLT1 - secondary transport

2 Na pumped in per one glucose/galactose

95
Q

how does fructose enter enterocyte

A

GLUT5 - facilitated diffusion

96
Q

how do monosaccharides leave enterocyte at basolateral membrane

A

GLUT2

97
Q

in what state must digested proteins be to be absorbed by small intestine

A

oligopeptides and amino acids

98
Q

what digests proteins in the stomach

A

pepsin and HCl

99
Q

what digests proteins in the duodenum

A

trypsin, chymotrypsin, elastase, procarboxypeptidase A&B

100
Q

true/false - there are a limited selection of brush border peptidases

A

false- there are many

101
Q

what do cytoplasmic peptidases do?

A

hydrolyse dipeptides and tripeptides

102
Q

describe protein absorption at the brush border

A

7 mechanisms of uptake - 5 require sodium and 2 dont

103
Q

what is system B0AT1

A

Na dependent uptake of neutral amino acids

104
Q

what is system b0+AT

A

Na independent uptake of cationic amino acids

105
Q

mechanisms of uptake at basolateral membrane

A

3 efflux and 2 influx

106
Q

what facilitates uptake of di,tri,tetra peptides at brush border

A

pepT1

107
Q

what happens to oligopeptides following brush border absorption

A

further hydrolysed to amino acids and then transported out of enterocyte

108
Q

lipids are poorly soluble on their own and so must form an emulsion to be properly digested and absorbed. what makes it up

A

chewing
gastric churning/segmentation/peristalsis
pancreatic/biliary secretion

109
Q

what enzyme digests TAGs in the stomach and what are the products

A

gastric lipase

diacylglycerol and free fatty acid

110
Q

what enzyme breaks down TAGS in the duodenum and what are the products

A

pancreatic lipase

monoacylglycerol and 2 free fatty acids

111
Q

what stimulates the release of pancreatic lipase and bile

A

CCK

112
Q

functions of bile salts

A

stabilise fat vesicle by acting as detergent

increase SA of lipid to pancreatic lipase

113
Q

what allows pancreatic lipase access to hard to reach TAGs in the lipid micelle and how is it secreted

A

colipase, secreted as procolipase and activated by trypsin

114
Q

waht does failure to secrete bile salts result in?

A

steatorrhoea

secondary vitamin deficiency

115
Q

what state must lipids be in, in order to be absorbed

A

fatty acids

monoacylglycerol

116
Q

describe absorption of short chain fatty acids

A

diffuse/transported into enterocyte and exit through basolateral membrane to enter villus capillary

117
Q

describe absorption of long chain fatty acids

A

diffuse/transported into enterocyte and resynthesised to TAG and synthesised to chylomicron
exocytosed

118
Q

describe cholesterol uptake

A

NPC1L1 endocytoses cholesterol and is recycled to be put back onto cell membrane, dependent on amount of cholesterol in cell

119
Q

calcium absorption is passive in _____ and active in ____ and _____

A

small intestine

duodenum and jejunum

120
Q

what increases calcium absorption

A

dihydroxyvitamin D3 and parathyroid hormone

121
Q

Absorption of iron is regulated/unregulated and loss of iron is regulated/unregulated

A

regulated

unregulated

122
Q

in what form is most digested iron found

A

ferric (3+)

123
Q

where would ferric iron be found and in what form

A

meat and veg
inorganic iron
haem
ferratin

124
Q

before ferric iron can be absorbed by an enterocyte what must happen

A

it must accept an electron to pass into the cytoplasm to become Fe2+

125
Q

what promotes electron acceptance in Fe?

A

HCl, vitamin C, gastroferrin, duodenal cytochrome B

126
Q

Fe influx is via _____

A

DMT1

127
Q

function of apoferratin

A

chaperone molecule to store iron at ferratin

128
Q

function of mobilferrin

A

chaperone molecule transferring iron to basolateral membrane for efflux

129
Q

how does iron exit cell via basolateral membrane

A

ferroportin 1

130
Q

when iron 2+ exits cell what must it be converted to

A

ferric iron

131
Q

how is haem converted to Fe 2+ for use in the enterocyte

A

haem oxidase converts it for binding with mobilferrin apoferrin

132
Q

where is vitamin B12 found

A

food, and bound to protein

133
Q

describe absorption of B12

A

HCl liberates from protein and binds it to haptocorin

intrinsic factor binds to B12 after haptocorin digested by pancreatic proteases

134
Q

where is B12 absorbed

A

terminal ileum

135
Q

describe absorption of fat soluble vitamins

A

incorporated into micelles and transported into enterocytes

incorporated into chylomicrons and distributed by lymphatics

136
Q

how are water soluble vitamins absorbed

A

Na dependent/independent manner

137
Q

vitamin C&H are Na dependent/independent

A

dependent

138
Q

folic acid is Na dependent/independent

A

independent

139
Q

true/false - the internal and external anal sphincters are fully separate

A

false - the external surrounds the internal

140
Q

what are the haustra

A

sac like bulges due to circular muscle and tenia coli

141
Q

what allows for chyme to pass from ileum to caecum

A

duodenal distention causes ileocaecal valve to relax

gastrin and CCK

142
Q

what does the colon have to make up for its lost surface area due to lost villi

A

colonic folds
crypts
microvilli

143
Q

function of colonocytes

A

mediate ion absorption to allow for water absorption

144
Q

function of crypt cells

A

mediate ion secretion

145
Q

what ion changes does aldosterone cause

A

increased Na absorption and K secretion

146
Q

what is contained in faeces

A 
cellulose 
bacteria 
bilirubin
salt 
water
147
Q

what is haustration and when is it present

A

alternating contraction of smooth muscle, segmentation with less frequency
disappear before and reappear after mass movement

148
Q

what is mass movement

A

driving of faeces distally by contraction of large sections of circular muscle

149
Q

what triggers mass movement

A

gastrocolic response

150
Q

describe rectal stretch leading to defaecation

A

rectal stretch sends afferent via spinal cord, efferent causes smooth muscle contraction in sigmoid colon and rectum to allow defaecation

151
Q

describe rectal stretch in delaying defaecation

A

efferent signal sent to brain to notify need to defaecate, efferent causes relaxation of external anal sphincter to cause defaecation or allows for delay as voluntary muscle

152
Q

3 functions of intestinal flora

A

intestinal immunity by competition
activation of certain drugs
promotes motility and mucosal integrity

153
Q

where does flatus come from?

A

swallowed air

bacteria attacking indigestible carbohydrates

154
Q

what is linaclotide and how does it work

A

peptide drug for moderate/severe IBS

increased chloride and bicarbonate secretion to ease constipation

155
Q

what is used for the acute and mild treatment of IBD

A

glucocorticoids - acute

aminosalicylates - mild

156
Q

how is water and Na absorbed in jejunum in the postprandial period

A

Na/glucose and Na/amino acid

ion flow into cell drags water with it and creates -ve transepithelial potential

157
Q

how is water and Na absorbed by jejunum in the interdigestive period

A

Na/H exchange

occurs at alkaline environment due to pancreas releasing bicarbonate

158
Q

how is water absorbed in ileum and proximal colon and what is it regulated by

A

Na/H and Cl/HCO3

cAMP, cGMP, Ca - cause less NaCl absorption

159
Q

what mediates water uptake in distal colon and describe its regulation

A

ENaC

increased by aldosterone, opening ENaC, inserting more in membrane and increasing synthesis

160
Q

how is Cl absorbed by small and large intestine

A

small - -ve driving force due to Na/Amino acid/glucose channel draws up
Large - -ve driving force from ENaC

161
Q

where is Cl secreted from and what increases secretion

A 
CFTR
bacterial enterotoxins 
hormones and neurotransmitters 
immune cell products 
laxatives
162
Q

causes of diarrhoea

A 
infection 
chronic disease
toxins 
drugs 
psychosocial factors
163
Q

physiological cause of diarrhoea

A

hypermotility
impaired NaCl absorption
poorly absorbable substances
excessive secretion

164
Q

describe how cholera causes secretory diarrhoea

A

toxin enters enterocyte to inhibit GTPase
increased cAMP and CFTR stimulation, release of Cl
further release of cAMP and Na uptake impaired so less water absorbed

165
Q

function of the liver in carbohydrate metabolism

A

gluconeogenesis
glycolysis
glycogenesis
glycogenolysis

166
Q

function of the liver in fat metabolism

A

synthesis of cholesterol and lipoproteins
ketogenesis
process chylomicrons

167
Q

function of the liver in protein metabolism

A

synthesise plasma proteins
transamination/deamination of AA
convert ammonia to urea

168
Q

what hormones does the liver activate

A

conversion of thyroid hormone

conversion of vitamin D

169
Q

what hormones does the liver deactivate

A

insulin
glucagon
ADH
steroid hormones

170
Q

what does the liver store

A

glycogen
copper
iron
fat soluble vitamins

171
Q

what proteins does the liver synthesise

A 
coag factors II, VII, IX, X
proteins C and S
albumin 
complement factors 
carrier proteins 
apolipoproteins
172
Q

what expogenous substances does the liver detox

A

ethanol

drugs

173
Q

what endogenous substances does the liver detox

A

bilirubin

174
Q

what protection does the liver offer

A

immune factor production

kupffer cells destroy old RBC and bacteria

175
Q

what cells produce bile

A

hepatocytes

cholangiocytes

176
Q

describe how bile exits the biliary tree to enter the duodenum during a meal

A

chyme stimulate vagus and CCK to release bile

gallbladder contracts and sphincter of oddi opens

177
Q

what is the function of bile

A

forms micelle with fat
acid neutralisation
pH optimisation
mucosal protection

178
Q

primary and secondary bile acids?

A

primary - cholic acid and chenodeoxycholic acid

secondary - deoxycholic and lithnocholic acid

179
Q

true/false - gallstones are painful so give morphine

A

false - morphine can make the pain worse

give Buprenorphine

180
Q

describe reuptake of bile salts

A

active in ileum and passive in rest of small intestine

returned to liver in portal circulation and undergo enterohepatic recycling

181
Q

name 3 bile acid sequestrants, indication and imitation

A

colveselam, colestipol, colestyramine
hyperlipidaemia, cholestatic jaundice
bile acid diarrhoea
large dose, cause diarrhoea, reduce vitamin absorption

182
Q

phase II drug metabolism is ___ and often occurs by ____

A

conjugation

glucuronidation

183
Q

what is cytochrome P450 monooxygenases

A

haem proteins in ER of hepatocytes mediating oxidation

184
Q

how does hepatic encephalopathy occur

A

hepatic failure causes failure of ammonia detox

toxic effect on CNS

185
Q

therapy for encephalopathy

A

lactulose - converts NH3 to NH4 to prevent reabsorption

rifamixin - suppress colonic flora to prevent ammonia generation

186
Q

characteristics of nausea

A 
feeling sick
pallor
sweating 
salivation
reverse peristalsis and upper stomach and lower oesophagus relaxation
187
Q

what is retching

A

rhythmic reverse peristalsis of stomach and oesophagus

188
Q

what is vomiting

A

forceful expulsion of gastric/intestinal contents out of mouth

189
Q

true/false - in vomiting the stomach is contracted

A

false - it is relaxed

190
Q

events of vomiting

A

suspended slow waves
retrograde contraction from ileum to stomach
closure of glottis
relaxed LOS, contracted diaphragm and abdomen
ejection of gastric contents

191
Q

how do toxic materials stimulate vomiting

A

stimulate enterochromaffin cells to release 5-HT - depolarises vagal afferents to reach NTS and CTZ

192
Q

what does the vestibular system pathway stimulate to invoke vomiting

A

CTZ

193
Q

what do stimuli within brain act on to stimulate vomiting

A

vomiting centre directly

194
Q

vagal efferents from VC

A

shortened oesophagus
proximal gastric relaxation
retrograde contraction

195
Q

somatic motor from VC

A

contracted diaphragm and anterior abdomen muscles

196
Q

autonomic efferent from VC

A

cold sweat, pallor, increased saliva
tachycardia
anal/bladder sphincter contraction

197
Q

consequences of severe vomitjng

A

dehydration
metabolic alkalosis due to loss of H and Cl
Metabolic acidosis due to bicarb loss - rare
hypokalaemia
mallory weiss tear

198
Q

causes of drug induced emesis

A 
cancer chemotherapy/radiotherapy 
operation with general anaesthetic 
agents with dopamine agonist properties 
morphine and opiates
cardiac glycosides 
drugs enhancing 5-HT - SSRI
199
Q

indication for ondansetron, palonosetron

A

chemotherapy/radiotherapy emesis
less effective over time
not indicated for motion sickness

200
Q

name an NK1 antagonist and what it is given with

A

aprepitant

5-HT3 antagonist and dexamethasone to treat highly emetogenic chemo

201
Q

when is domperidone/metoclopramide given, class, indication, contraindication

A

dopamine receptor antagonist in CTZ
drug induced vomiting esp parkinsons
domperidone less unwanted effects
contraindicated motion sickness and children

202
Q

name 2 H1 antagonists, action and side effect

A 
cyclizine/cinnarizine 
block H1 receptors in vestibular nuclei and NTS
drowsiness 
slight muscarinic action 
effective motion sickness
203
Q

name 2 muscarinic ACh receptor antagonists, indication, side effects

A

hyosine/scopolamine
motion sickness
blocks muscarinic receptors in vestibular nuclei, NTS, VC
inhibits GI movements
blurred vision, dry mouth, urine retention

MB1: Gastrointestinal (19 decks)

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