Physiology Flashcards
1
Q
What is the function of the mouth and oropharynx?
A
chops and lubricates food, starts carbohydrate digestion, propels food to oesophagus.
2
Q
What is the function of the oesophagus?
A
propels food to the stomach.
3
Q
What is the function of the stomach?
A
stores/churns foods continues carbohydrate digestion, starts protein digestion, regulates delivery of chyme to duodenum.
4
Q
What is the function of the small intestine?
A
principle site of digestion and absorption of nutrients.
5
Q
What is the small intestine made of?
A
duodenum, jejunum and ileum
6
Q
What is the function of the large intestine?
A
colon reabsorbs fluid and electrolytes, stores faecal matter before delivery to rectum
7
Q
what is the large intestine made of?
A
caecum, appendix and colon
8
Q
What is the function of the rectum and anus?
A
regulated expulsion of faeces
9
Q
What are the four major functions of the alimentary canal?
A
- Motility (movement)
- secretion
- digestion
- absorption
10
Q
What type of muscle is mostly involved in motility?
A
smooth muscle
11
Q
where would skeletal muscle be found which assists motility?
A
mouth, pharynx, upper oesophagus and external anal sphincter
12
Q
what is secretion of the alimentary canal required for?
A
digestion, protection and lubrication
13
Q
what chemical process are foods digested by?
A
enzymatic hydrolysis
14
Q
what happens during circular muscle contraction?
A
lumen becomes narrower and longer
15
Q
what happens during longitudinal muscle contraction?
A
intestine becomes shorter and fatter
16
Q
what happens during muscularis mucosae contraction?
A
change in absorption and secretory area of mucosa, mixing activity.
17
Q
what are adjacent smooth muscle cells coupled by?
A
gap junctions, electrical currents flow from cell to cell.
18
Q
what is a synchronous wave?
A
hundreds of cells are depolarised and contract at the same time as a single unit smooth muscle.
19
Q
what is spontaneous activity across the coupled cells driven by?
A
specialised pacemaker cells and modulated by intrinsic and extrinsic nerves and hormones.
20
Q
what does slow wave electrical activity determine?
A
frequency, direction and velocity of rhythmic contractions
21
Q
what is slow wave electrical activity driven by?
A
interstitial cells of cajal (ICCs) - pacemaker cells located between circular and longitudinal muscle layers.
22
Q
where do ICCs sometimes form bridges?
A
between nerve endings and smooth muscle cells
23
Q
when does contraction of the intestines occur?
A
when the slow wave amplitude is sufficient to reach a threshold to trigger smooth muscle cell calcium action potentials.
24
Q
what factors affect whether slow wave amplitude threshold is reached?
A
neuronal stimuli
hormonal stimuli
mechanical stimuli
25
what excitatory influences are due to parasympathetic stimulation?
- increased gastric, pancreatic and small intestinal secretion
- blood flow and smooth muscle contraction
26
what inhibitory influences are due to parasympathetic stimulation?
relaxation of some sphincters, receptive relaxation of stomach
27
what is the parasympathetic nerve supply?
preganglionic fibres (releasing Ach.) synapse with ganglion cells within the enteric nervous system (ENS)
28
where is the symapthetic innervation?
preganglionic fibres (reelasinf ACh) synapse in the prevenertebral ganglia.
29
what excitatory influences are due to sympathetic stimulation?
increased spincher tone
30
what inhibitory influences are due to sympathetic stimulation?
decreased motility secretion and blood flow
31
what is peristalsis?
a wave of relaxation, followed by contraction, that normally proceeds a short distance along the gut in an aboral direction triggered by distension of the gut wall.
32
what is segmentation?
rhythmic contractions of the circular muscle that mix and divide luminal contents.
33
where does segmentation occur?
in the small intestine (in the fed state)
34
what is segmentation called in the large intestine?
haustration
35
what is colonic mass movement?
powerful sweeping contraction that forces faeces into the rectum - occurs a few times a day
36
what is migrating motor complex (MMC)?
powerful sweeping contraction from stomach to terminal ileum
37
How many sphincters are there in the GI tract?
6 excluding the sphincter of Oddi
38
what are sphincters?
act as one way valves by maintaining a positive resting pressure relative to two adjacent structures
39
what does the upper oesophageal sphincter do?
relaxes to allow swallowing, closes during inspiration
40
what is the upper oesophageal sphincter made of?
skeletal muscle
41
what does the lower oesophageal sphincter do?
relaxes to permit entry of food to stomach, closes to prevent reflux of gastric contents to the oesophagus
42
what does the pyloric sphincter do?
regulates gastric emptying, usually prevents duodenal gastric reflux
43
what does the iloecaecal valve do?
regulates flow from ileum to caecum
44
what are the internal and external anal sphincters regulated by?
defaecation reflex
45
what does the myenteric plexus do?
mainly regulates motility and sphincters
46
what does the submucous plexus do?
mainly modulates epithelia and blood vessels
47
what is an example of the local reflex?
peristalsis
48
what is an example of short reflex?
intestino-intestinal inhibitory reflex
49
what is an example of long reflex?
gastroileal reflex
50
what is energy homeostasis?
physiological process whereby energy intake is matched to energy expenditure over time
51
what are some consequences of metabolic stress?
```
metabolic syndrome
central obesity
dyslipidemia
insulin resistance
type 2 diabetes
cardiovascular disease
```
52
how do you calculate body mass index?
weight (kg) / square of . height (m)
53
what does the brain do when you try to lose weight?
brain views extra weight sd normal and dieting may be a threat to body survival e.e defends new weight
54
how does the CNS influence energy balance and body weight?
behaviour - feeding and physical activity
ANS activity - regulates energy expenditure
neuroendocrine system - secretion of hormones
55
what is the site of integration?
brain
56
which part of the brain is responsible for energy homeostasis
hypothalamus
57
which part of the hypothalamus causes obesity?
lesioning ventromedial hypothalamus
58
which part of the hypothalamus causes leanness?
lesioning lateral hypothalamus
59
what basic concepts underlie control of energy intake and body weight?
1. satiety signalling
2. adiposity negative feedback signalling
3. food reward
60
which hormone is the hunger hormone?
Ghrelin
61
which two hormones report fat status to brain?
leptin and insulin
62
what molecules are responsible for digestion?
pepsin and HCL
63
what molecule is responsible for carbohydrate digestion in the stomach?
salivary amylase
64
what does food mixed with gastric secretions produce?
semi-liquid chyme
65
what are the two mechanical regions of the stomach?
orad and caudad stomach
66
what is the relaxation of the orad region of the stomach driven by?
vagas nerve
67
what does orad region not have that the caudad region does?
no slow wave activity
68
why are tonic contractions in the orad region weak?
due to thin musculature
69
how are contents propelled to the claudad region?
by low amplitude tonic contractions of about 1 minute duration - stomach size decreases after
70
what does gastrin do?
decrease contractions and hence the rate of stomach emptying
71
how many slow waves are produced by the caudad region of the stomach?
3 waves per minute
72
do contractions occur from every slow wave in the caudad region in the stomach?
no, only contract when threshold is reached
73
what are phasic peristalic contractions driven by?
suprathreshold slow waves
74
what do the phasic peristalic contractions do?
progress from midstomach to gastroduodenal junction propelling contents towards pylorus through which a very small volume of chyme flows into the duodenum
75
what is retropulsion?
velocity of contraction increases towards junction, overtaking the movement of chyme that rebounds against constricted distal antrum back into the relaxed body of the stomach
76
what does retropulsion do?
mixes gastric contents reducing chyme to small particles that pass through the pylorus
77
what determines the escape of chyme through the pyloric sphincter?
strength of antral wave
78
what factors effect how much chyme escapes the stomach?
gastric factors and duodenal factors
79
why does distension increase motility in the stomach?
stretch of smooth muscle, stimulation of intrinsic nerve plexuses, increased vagus nerve activity and gastrin release
80
what gastric factors are there that affect chyme rate?
rate of emptying proportional to volume of chyme in stomach and consistency of chyme
81
what neuronal response delays stomach emptying?
the enterogastric reflex - decreases antral activity by signals from intrinsic nerve plexuses and the ANS
82
what hormonal response delays stomach emptying?
release of enterogastrones e.g. cholecystokinin CCK from dueodenum inhibits stomach contraction
83
what stimuli within the duodenum drive the neuronal and hormone responses?
- fat
- acid
- hypertonicity
- distension
84
why does fat delay gastric emptying?
required for digestion and absorption in small intestine
85
why does acid delay gastric emptying?
time is required for neutralisation of gastric acid by bicarbonate secreted from the pancreas - important for optimal pancreatic digestive enzyme function
86
why does hypertonicity delay gastric emptying?
products of carbohydrate and protein digestion are osmotically active and draw water into the small intestine - danger of reduced plasma volume and circulatory disturbances (e.g. dumping syndrome)
87
what are the two secretion regions of the stomach?
oxyntic gland area and pylorlic gland area
88
what is the gastric mucosa composed of?
surface lining the stomach, pits, invaginations of the surface, glands, at the base of the pits responsible for several secretions
89
what is the function of HCL?
- activates pepsinogen to pepsin
- denatures protein
- kills most micro-organisms ingested with food
90
what is the function of pepsinogen?
- inactive precursor of the peptidase, pepsin.
91
what is the function of intrinsic factor and gastroferrin?
binds vitamin B12 and Fe2+ respectively, facilitating subsequent absorption
92
what is the function of histamine?
stimulates HCL secretion
93
what is the function of mucus in the stomach?
protective
94
what is the function of gastrin?
stimulates HCL secretion
95
what is the function of somatostatin?
inhibits HCL secretion
96
what is a secretagogue?
an agent that causes secretion
97
what are the three important secretagogue that induce acid secretion from the parietal cells?
acetylcholine (ACh)
gastrin
histamine
98
how do the secretagogue work in the direct pathway?
ACh, gastrin and histamine stimulate the parietal cell, triggering the secretion of H+ into the lumen
99
how do the secretagogue work in the indirect pathway?
ACh and gastrin also stimulate ECL cell, resulting in secretion of histamine. the histamine then acts on parietal cells
100
which molecules are responsible for sending satiation signals?
- cholecystkinin (CKK)
- Peptide YY
- glucagon-like peptide 1
- oxyntomodulin (OXM)
- obestatin
101
where is gherlin produced?
oxyntic cells in the stomach
102
what are the functions of leptin?
- food intake/energy expenditure/fat deposition
- peripheral glucose homeostasis
- maintenance of immune system
- maintenance of reproductive system
- angiogenesis
- tumourigenesis
- bone formation
103
During the resting state of the parietal cell where is H+/K+ATPase?
within the cytoplasmic tubulovesicles
104
where is H+/K+ATPase during the stimulated phase of the parietal cell?
traffics to the apical membrane taking residence in extended microvilli
105
what are the three phases of gastric acid secretion?
- cephalic phase
- gastric phase
- intestinal phase
106
when does the cephalic phase of gastric acid secretion happen?
when the stomach is preparing to receive food
107
what is the cephalic phase driven by?
CNS and vagus nerves
108
when does the gastric phase of gastric acid secretion happen?
when food is in the stomach - involves both physical and chemical mechanism
109
when does the intestinal phase of gastric acid secretion happen ?
after food has left stomach- chyme entering the upper small intestine causes weak stimulation of gastric section via neuronal and hormonal mechanisms
110
what are some other stimulants of G cells apart from amino acids?
Ca2+
caffeine
alcohol
111
how is gastric acid secretion inhibited during the cephalic phase?
vagal activity decreases upon cessation of eating and following stomach emptying.
pain, nausea and negative emotions also decrease vagal nerve activity which reduces gastric acid secretion
112
How is gastric acid secretion inhibited during the gastric phase?
pH falls when food exits stomach - release of somatostatin from D cells recommences, decreasing gastrin secretion
prostaglandin E2 works to reduce histamine and gastrin mediated HCL secretion
113
How is gastric acid secretion inhibited during the intestinal phase?
factors that reduce gastric motility also reduce gastric secretion e.g. neuronal reflexes, enterogastrones
114
what do prostaglandins (PGE2 and PGI2) do?
- reduce acid secretion
- increase mucus and bicarbonate secretion
- increase mucosal blood flow
115
What things does the small intestine receive from other organs?
- chyme from stomach
- pancreatic juice from pancreas
- bile from gall bladder
116
what liquid does the small intestines secrete?
intestinal juice (succus entericus)
117
what does the small intestine move residue to the large intestine via?
ileocaecal valve
118
Where is gastrin released from?
G cells of gastric antrum and duodenum
119
what peptide hormones does the small intestine secrete?
```
gastrin
cholecystokinin (CCK)
secretin
motilin
glucagon-like insulinotropic peptide (GIP)
glucagon-like peptide-1 (GLP-1)
Ghrelin
```
120
where is CCK released from?
from I cells of duodenum and jujunum
121
where is secretin released from?
from S cells of duodenum, released in response to H+ and fatty acids in lumen
122
where is motilin released from?
from M cells of duodenum and jejunum
123
where is GIP released from?
from K cells of duodenum and jejunum
124
where is GLP-1 released from?
from L cells of the gut
125
where is ghrelin released from?
from Gr cells of the gastric antrum, small intestine and elsewhere
126
what do all various peptide hormones secreted in the small intestines work on?
G-protein coupled receptors
127
what control mechanisms enhance secretions of the small intestine?
- distension/irritation
- gastrin
- CCK
- secretin
- parasympathetic nerve activity
128
what control mechanisms decrease secretions of the small intestine?
sympathetic nerve activity
129
why do secretions contain aqueous salt?
for enzymatic digestion
130
what is segmentation in the empty ileum triggered by?
gastrin from the stomach (gastroileal reflex)
131
what is strength of segmentation enhanced by?
parasympathetic activity
132
what is strength of segmentation decreased by?
sympathetic activity
133
what does the migrating motor complex (MMC) do?
clears small intestine of debris, mucus and sloughed epithelial cells between meals
134
what is the migrating motor complex inhibited by?
feeding and vagal activity
135
what is the MMC triggered by?
motilin
136
what is the MMC suppressed by?
gastrin and CCK
137
what are the endocrine pancreatic secretions?
insulin and glucagon
138
what are the exocrine pancreatic secretions?
digestive enzymes (acinar cells), aqueous NaHCO3- solution (duct cells) - secreted to the duodenum collectively as pancreatic juice
139
what does the pancreatic fluid do?
- neutralises acidic chyme entering duodenum
- provides optimum pH for pancreatic enzyme function
- protects the mucosa from erosion by acid
140
what can pancreatic enzymes do in the absence of all other enzymes?
completely digest food
141
how is the cephalic phase of control of pancreatic secretion mediated?
by the vagal stimulation of mainly the acinar cells
142
what does the gastric phase of control of pancreatic secretion evoke? what does this cause?
a vagovagal reflex resulting in parasympathetic stimulation of acinar and duct cells
143
define digestion
enzymatic conversion of complex dietary substances to a form that can be absorbed
144
what is luminal digestion mediated by?
pancreatic enzymes secreted into the duodenum
145
what is membrane digestion mediated by?
enzymes situated at the brush border of epithelial cells
146
what is absorption?
process by which the absorbable products of digestion are transferred across the atpical and basolateral membranes of enterocytes
147
what is assimilation?
overall process of digestion and absorption
148
what does secretin do?
promotes secretion of pancreatic and biliary HCO3-
149
what does CCK do?
- inhibits gastric emptying
- causes secretion of pancreatic enzymes required for digestion
- stimulates relaxation of sphincter of Oddi and contraction of gall bladder to eject bile into duodenum, - - - potentiates the action of secretin
150
what must dietary carbohydrates be converted to before absorption?
monosaccharides
151
what does GIP do?
- simulates release of insulin from pancreatic Beta cells
| - inhibits gastric emptying
152
what is the function of alpha- amylase?
breaks down linear internal alpha-1,4 linkages but not terminal alpha-1,4 linkages. hence, no production of glucose
153
what are the products of alpha-amylase?
linear glucose oligomers (maltotriose, maltose) and alpha-limit dextrins
154
what are oligiosaccharidases?
integral membrane proteins with a catalytic domain that faces the lumen of the GI tract
155
what does lactase do?
breaks down lactose to glucose and galactose
156
what do all oligosaccharidases apart from lactase do?
cleave the terminal alpha-1,4 likages of maltose, maltotriose and alpha-limit dextrins
157
what is sucrase specifically responsible for?
hydrolysing sucrose to glucose and fructose
158
why is isomaltase unique?
only enzyme that can split the branching alpha-1,6 linkages of alpha-limit dextrins
159
what can maltase do?
degrade the alpha-1,4 linkages in straight chain oligomers up to nine monomers in length
160
what is lactose intolerance a consequence of?
inability to adequately digest lactose caused by lactase insufficiency
161
what is primary lactase deficiency (primary hypolactasia)?
due to lack of the lactase persistence (LP) allele
162
what is secondary lactase deficiency?
caused by damage to/infection of/ the proximal small intestine
163
what is congenital lactase deficiency?
rare autosomal recessive disease - no ability to digest lactose from birth
164
what does the ileum colonic microflora from the colon produce when lactose is delivered in a lactose intolerant person?
short-chain fatty acids
hydrogen
carbon dioxide
methane
165
what do the by products of the ileum colonic microflora in lactose intolerant people cause?
bloating
abdominal pain
flatulence
166
what does undigested lactose cause?
- acidification of the colon
| - an increased osmotic load: loose stool and diarrhoea
167
where does the digestion of the final products of carbohydrate digestion occur?
duodenum and jejunum
168
what happens during the absorption of the final products of carbohydrate digestion?
- two step process involving entry and exit from the enterocytes via the apical and basolateral membranes
169
what is glucose and galactose absorbed by?
secondary active transport mediated by SGLT1
170
what is fructose absorbed by?
facilitated diffusion mediated by GLUT5
171
what is exit for all monosaccharides mediated by?
facilitated diffusion by GLUT5
172
how does SGLT1 work?
1. 2 Na+ binds
2. affinity for glucose increases, glucose binds
3. Na+ and glucose translocate from extracellular to intracellular
4. 2 Na+ dissociate, affinity for glucose falls
5. glucose dissociates
6. cycle is repeated
173
what must proteins be digested to for efficient absorption?
oligopeptides and amino acids
174
how many different pathways are there for protein digestion?
four
175
how much daily energy intake is from protein assimilation?
10-15%
176
which pancreatic proteases in the duodenum act as endopeptidases?
trypsin, chymotrypsin and elastase
177
which pancreatic proteases in the duodenum act as exopeptidases?
procarboxypeptidase A and procarboxypeptidase B
178
what is the product of endopeptidases?
oligopeptides
179
what is the product of exopeptidase?
single amino acids
180
what is pepsin?
an endopeptidase
181
what does pepsin prefer?
bonds between aromatic and larger neutral amino acids
182
where are the additional proteases present?
at the brush border and within the cytoplasm of the enterocyte
183
what do brush border peptidases have an affinity for?
larger oligopeptides (3-8 amino acids)
184
what are bursh border peptidases?
numerous, either endopeptidases or exopeptidase, the latter comprising both aminopeptidases and carboxypeptidases
185
what do cytoplasmic peptidases do?
primarily hydrolyse dipeptides and tripeptides
186
how are amino acids transported across the apical membrane?
via a variety of amino acid transporters some of which are Na+ dependant and others Na+ independant
187
how are oligopeptides transported across the apical membrane?
the H+/oligopeptide co-transporter, pepT1
188
how are oligopeptides within the cytoplasm hydrolysed to amino acids?
by peptidases within the enterocyte
189
how do amino acids exit the enterocyte across the basolateral membrane?
by several, Na+ independent transporters
190
How much of the daily energy requirement is provided by ingested lipids?
55-60%
191
why do ingested lipids cause problems for digestion and absorption?
they are either insoluble or poorly soluble
192
What must ingested lipids be converted to?
emulsion of small oil droplets suspended in water
193
what does emulsion of small oil droplets occur by?
- mouth: chewing
- stomach: gastric churning and squirting through the narrow pylorus. content mixed with digestive enzymes from mouth and stomach
- small intestine: segmentation and peristalsis mix the luminal content with pancreatic and biliary secretions
194
How are emulsion droplets stabilised?
by the addition of a 'coat' of amphiphilic molecules that form a surface layer that includes certain products of lipid digestion, biliary phospholipids, cholesterol and bile salts.
195
what is the name of the enzyme which digests food in the stomach during the gastric phase?
gastric lipase (lingual lipase in saliva)
196
when is gastric lipase secreted?
in response to gastrin from chief cells
197
what is the main lipid digestive enzyme in adults during the intestinal phase?
pancreatic (TAG) lipase
198
when is pancreatic lipase secreted?
from acinar cells of pancreas in response to CCK which also stimulates bile flow
199
what does the full activity of pancreatic (TAG) lipase require?
- colipase co-factor
- alkaline pH
- Ca2+
- bile salts
- fatty acids
200
what does digestion by lipase produce?
2-monoacylglycerol and free fatty acids
201
where does pancreatic lipase mainly hydrolyse TAGs?
at the 1 and 3 positions
202
when are bile salts released?
into the duodenum in bile from the gall bladder in response to CCK
203
what is the role of bile salts?
act as detergents to help emulsify large lipid droplets to small droplets (they are amphipathic)
204
what does failure to secrete bile salts result in?
- lipid malabsorption - steatorrhoea (fat in feaces)
| - secondary vitamin deficiency due to failure to absorb fat soluble vitamins (A,D,E,K)
205
what do bile salts do?
increase surface area for attack by pancreatic lipase, but block access of the enzyme to the TAGs
206
what is colipase secreted as?
inactive procolipase which is activated by trypsin
207
what does colipase do?
binds to bile salts and lipase allowing access by the latter to tri- and di-acylglycerols
208
what happens hen TAGs towards the surface of the emulsion droplets are hydrolysed?
they are replaced, by TAGs within the core, decreasing droplet size until a mixed micelle results
209
what do short chain (<6 carbon) and medium (8-12 carbon) fatty acids do during lipid absorption?
diffuse through the enterocyte, exit through the basolateral membrane and enter the villus capillaries
210
what do long chain (>12 carbon) fatty acids and monoglycerides do during lipid absorption?
they are resynthesized to triglycerides in the endoplasmic reticulum and are subsequently incorporated into chylomicrons
211
how is cholesterol absorbed?
- due to transport by endocytosis in clatherin coated pits by niemann-picj C1-like 1 (NPC1L1) Protein
212
How is cholesterol absorption prevented?
- ezetimibe binds to NPC1L1, Prevents internalisation and thus cholesterol absorption.
213
how is Ca2+ absorbed?
occurs by passive (i.e. paracellular; whole length of small intestine) and active (i.e. transcellular; mainly duodenum and upper jejunum) transport mechanisms
214
what is active Ca2+ regulated by?
1,25-dihydroxyvitamin D3 (calcitriol) and parathyroid hormone (increases 1,25-dihydroxyvitamin D3 synthesis)
215
what does a deficiency of iron result in?
aneamia
216
what does an excess of iron result in?
toxic
217
what is Fe3+ reduced to Fe2+ by?
- HCL
- Vitamin C
- brush border cytochrome B ferric reductase
218
what does Fe2+ bind to in the stomach?
gastroferrin
219
what is expression of divalent metal transporter 1 (DMT1 aka SLC11A2) increased/reduced by?
increased - blood loss
| reduced- human haemochromatosis protein (HFE)
220
what is the storage form of iron called?
ferratin
221
what is ferroportin 1 (aka SLC40A1) negatively regulated by?
the hormone hepcidin released from liver when body iron are high
222
how is vitamin B12 (cobalamin) absorbed?
1. vitamin B12 ingested in food bound to proteins
2. stomach acid releases vitamin B12 from protein
3. haptocorin, secreted in saliva binds vitamin b12, Released in stomach
4. stomach parietal cells release intrinsic factor
5. pancreatic proteases digest haptocorin in small intestine, vitamin B12 release
6. vitamin B12 binds to intrinsic factor in small intestine
7. Vitamin B12 intrinsic factor complex absorbed in terminal ileum by endocytosis
223
which group of people are susceptible to vitamin B12 deficiency?
vegans - no vitamin B12 in vegetables
224
what does absorption of fat soluble vitamins require?
adequate bile secretion and an intact intestinal mucosa
225
how are fat soluble vitamins usually transported?
passively into enterocytes
226
what are fat soluble vitamins incorporated into?
chylomicrons or VLDLs
227
what are fat soluble vitamins distributed by?
intestinal lympathics
228
how are water soluble vitamins transported?
may be either Na+ dependant or Na+ independant
229
what are the water soluble vitamins?
B complex vitamins (not B12), C and H
230
what is the longitudinal smooth muscle layer in caecum and colon divided into?
three strands - the taeniae coli
231
when is smooth muscle thickened in the large intestine?
at the internal anal sphincter, which is surrounded by the skeletal muscle of the external anal sphincter
232
what does activity of the taeniae coli and circular muscle layers in colon cause?
'sac-like' bulges - the haustra - that very slowly change in location
233
what does the caecum normally receive?
approx. 1-2l of material (undigested residues, unabsorbed biliary components, unabsorbed fluid) per day from the terminal ileum
234
how is entry into the caecum permitted?
by the gastroileal reflex in reponse to gastrin and CCK through the 'one way' ileocaecal valve
235
How does the ileocaecal valve act by?
- maintaining a positive resting pressure
- relaxing in response to distension of the duodenum
- contracting in response to distension of the ascending colon
- being under the control of the vagus nerve, sympathetic nerves, enteric neurones and hormonal signals
236
what is the appendix?
a blind-ended tube with extensive lymphoid tissue connected to the distal caecum via the appendiceal orifice
237
how is appendicitis caused?
appendiceal orifice obstructed by a faecalith
238
what are the primary functions of the colon?
- absorption of Na+, Cl- and H20 to condense ileocaecal material to solid or semi solid stool
- absorption of short fatty acids
- secretion of K+, HCO3- and mucus
- reservoir of storage of colonic contents
- periodic elimination of faeces
239
what does the mucosa of the colon have that increases its surface area?
colonic folds, crypts and microvilli
240
what do surface epithelial cells (colonocytes) of the colon do?
mediate electrolyte absorption which, by osmosis, drives absorption of H20
241
what do crypt cells in the colon do?
mediate ion secretion
242
what do goblet cells in the colon secrete?
- copious mucus containing glycosaminoglycans
| - trefoil proteins involved in host defence
243
what is Na+ absorption and K+ secretion enhanced by?
aldosterone
244
when might significant loss of K+ in the faeces occur?
secretory diarrhoea
245
what are the patterns of motility in the large intestine?
- haustration
- peristaltic propulsive movements
- defaecation
246
what is haustration?
- haustra are saccules caused by alternative contraction of the circular muscle
- disappear before and reappear a mass movement
- probably generated by slow wave activity
- mixes content - allows time for fluid and electrolyte reabsorption
247
what is mass movement of the colon?
simultaneous contraction of large sections of the circular muscle of the circular muscle of the ascending and transverse colon, powerfully drives faeces into distal regions
248
what does mass movement in the distal colon do?
propels faeces in the rectum triggering the defaecation reflex in response to rectal stretch
249
why are the bacteria in the colon beneficial?
- increase intestinal immunity by competition with pathogenic microbes
- promote motility and help maintain mucosal integrity
- synthesise vitamin K2 and free fatty acids that are absorbed
- activate some drugs
250
where does gas in the colon arise from?
- swallowed air that enters the small intestine is either absorbed or passed onto colon
- bacteria in the colon which attack forms of carbohydrate that are indigestible to humans
- gas that is not absorbed in the large intestine is expelled through the anus
251
what is constipation?
presence of hard faeces within the colon (results from delay in defaecation and enhanced absorption of H2O)
252
what are some causes of constipation?
- ignoring/suppressing, the urge to defaecate
- decreased colonic motility
- obstruction of faecal movement
- paralytic ileus following abdominal surgery
- impairment of motility/defaecation reflex
253
what symptoms may arise from constipation?
- abdominal discomfort
- headache
- loss of appetite
- general malaise (caused by prolonged distension of the large intestine - not toxins)
254
if hardened, calcified, faecal matter gets into the appendix what may happen?
causes appendicites
255
what is nausea?
subjective, highly unpleasant, sensation - normally felt in throat and stomach as 'sinking' sensations
256
what does nausea usually involve?
- pallor, sweating excessive salvation and relaxation of stomach and lower oesophagus
- upper intestinal contractions, forcing intestinal contents by reverse peristalsis into the stomach
257
what does retching involve?
- rhythmic reverse peristalsis of the stomach and oesophagus
- forceful, involuntary, contraction of abdominal muscles and the diaphragm
- upper intestinal contractions, forcing intestinal contents by reverse peristalsis into the stomach
- pallor, sweating excessive salvation
258
what is the medical term for vomiting?
emesis
259
how does vomiting commence?
with forceful inspiration, reflex closure of the glottis and elevation of the soft palate to close off the airways and nasal passages
260
what is vomiting co-ordinated by?
by the vomiting centre (VC) in the medulla oblongata of the brain stem
261
what is the steps of the vomiting cycle?
1. suspension of intestinal slow wave activity
2. retrograde contractions from ileum to stomach
3. suspension of breathing (closed glottis - prevents aspiration)
4. relaxation of LOS-contraction of diaphragm and abdominal muscles compresses stomach
5. ejection of gastric contents through open UOS
6. Repeat of cycle
262
what is vomiting often preceded by?
- profuse salvation
- sweating
- elevated heart rate
- sensation of nausea
263
What is the pathway of vomiting when induced by toxics?
1. toxin materials in gut lumen/ systemic toxins
2. stimulate enterochromaffin cells in mucosa (release of mediators)
3. depolarisation of sensory afferent terminals in mucosa
4. action potential discharge in vagal afferents to brainstem (CTZ and NTS)
5. co-ordination of vomiting by the 'vomiting centre'
264
What does mechanical stimuli (e.g. pharynx); pathology within the GI tract (e.g. gastritis) or other visceral organs (e.g. myocardial infarction) stimulate that causes vomiting?
vagal afferents to brainstem (CTZ and NTS)
265
what do absorbed toxic materials and drugs in blood stimulate that causes vomiting?
CTZ within the AP of brainstem (lacks an affective BBB)
266
what does the vestibular system (e.g. motion sickness) signal through to cause vomiting?
vestibular nuclei > CTZ
267
what does stimuli within the CNS (e.g. pain, repulsive sights and odours, fear, anticipation, psychological factors) signal through to cause vomiting?
cerebral cortex, limbic system > medulla
268
what is the 'vomiting centre'?
a group of interconnected neurones within the medulla that are driven by a central pattern generator (CPG) that receives input from the NTS
269
what are the consequences of severe vomiting?
- dehydration
- loss of gastric protons and chloride (causes hypocholoraemic metabolic alkalosis, raising blood pH)
- hypokalaemia
- rarely, loss of duodenal bicarbonate may cause metabolic acidosis
- rarely, oesophageal damage (mallory-weiss tear)
270
what is absorption of water?
a passive process driven by the transport of solutes (particularly Na+) from the lumen of the intestines to the blood stream
271
what is diarrhoea?
loss of fluid and solutes from the GI tract in excess of 500ml per day
272
How is the osmotic force for reabsorption of water provided?
by the reabsorption of Na+
273
where does the Na+/glucose co-transport and the Na+/amino acid co-transport occur?
throughout the small intestine and is the most important in the postprandial period (also occurs in the colon in the new born)
274
where does Na+/H+ exchange occur? what is it stimulated by?
in the duodenum and jejunum and is stimulated by the alkaline environment of the lumen due to the presence of luminal HCO3-
275
where does the parallel Na+/H+ and Cl-/HCO3- exchange occur?
ileum and colon most important in the interdigestive period
276
where does epithelial Na+ channels (ENaC) occur?
in the colon (distal particularly)
277
what are Na+/glucose co-transport and the Na+/amino acid co-transport examples of?
secondary active transport
278
what does electorgenic mean?
producing a change in the electrical potential of a cell
279
what does the overall transport of Na+ generate in the Na+/glucose co-transport and the Na+/amino acid co-transport?
a transepithelial potential (VTE) in which the lumen is negative - this drives the parallel absorption of Cl-
280
what is the parallel Na+/H+ and Cl-/HCO3- regulated by?
intracellular cAMP, cGMP and Ca2+, all reduce NaCl absorption
281
what does reduction in NaCl absorption cause?
diarrhoea
282
what is epithelial Na+ channels (ENaC) regulated by?
increased by aldosterone
283
what are the actions of aldosterone in epithelial Na+ channels (ENaC)?
1. opens ENaC (seconds)
2. inserts more ENaC into membrane from intracellular vesicle pool (minutes)
3. increases synthesis of ENaC and Na+/K+-ATPase (hours)
284
what is the driving force in the small intestine for Cl- absorption?
provided by lumen negative potential due to electrogenic transport of Na+ (Na+/glucose and Na+/amino acid)
285
what is the driving force in the large intestine for Cl- absorption?
provided by the lumen negative potential due to electrogenic movement of Na+ through ENaC
286
which cells secrete Cl-?
crypt cells
287
what does low intracellular Na+ drive forward?
inward movement of Na+, K+ and Cl- via NKCC1
288
why does little secretion of Cl- normally occur?
because apical CFTR is either closed or not present
289
what is CFTR indirectly activated by?
- bacterial enterotoxins (e.g. cholera toxin (V. cholerae), heat stable enterotoxin (E.coli), C. difficile toxin)
- hormones and neurotransmitters (e.g. vasoactive intestinal peptide (VIP), guanylin, acetylcholine, bradykinin, 5-HT (serotonin)
- immune cells products (e.g. prostaglandins, histamine)
- some laxatives (e.g. bile acids)
290
Activation of CFTR occurs indirectly as a result of the generation of second messengers, what do these include?
cAMP (e.g. cholera toxin, VIP, histamine)
cGMP (e.g. heat stable enterotoxin, guanylin)
Ca2+ (e.g. acetylcholine, bradykinin, 5-HT)
291
what does the Cl- conductance mediated by CFTR result from?
- opening of channels at the apical membrane
| - insertion of channels from intracellular vesicles into the membrane
292
what are the causes of diarrhoea?
- infectious agents -viruses, bacteria
- chronic disease
- toxins
- drugs
- psychological factors
- excess bile in colon
- inflammation
- congenital defects
- impaired absorptions of NaCl
- lactase deficiency
293
what are the consequences of diarrhoea?
can result in dehydration (Na+ and H2O loss), metabolic acidosis (HCO3- loss) and hypokalaemia (K+ loss)
may be fatal if severe (e.g. cholera)
294
what is the treatment of severe acute diarrhoea?
- maintenance of fluid and electrolyte balance
- use of anti-infective agents
- use of non- antimicrobial antidiarrhoael agents
295
what are the major metabolic functions of the liver?
regulation of carbohydrate, lipid and amino acid metabolism
296
what is glycogenolysis?
to release glucose, as required
297
what is included in fat metabolism?
- processing of chylomicron remnants
- synthesis of lipoproteins and cholesterol
- ketogenesis
298
what is included in protein metabolism?
- synthesis of plasma proteins
- transamination an deamination of amino acids
- conversion of ammonia to urea
299
which hormones are deactivated by the liver?
- insulin
- glucagon
- anti-diuretic hormone (ADH, vasopressin)
- steroid hormone
300
which hormones are activated by the liver?
- conversion of thyroid hormone
| - conversion of vitamin D to 25-hydroxyvitamin D
301
what does the liver store?
- fat soluble vitamins
- water soluble vitamin B12
- iron, copper
- glycogen
302
which proteins are synthesised in the liver?
- coagulation factors II,VII,IX and X
- protein C and S
- albumin
- complement proteins
- apolipoproteins
- carrier proteins
303
what do kupffer cells do?
digest/destroy particulate matter (e.g. bacteria) and senescent erythrocytes (metabolism of haemoglobin)
304
what does the liver detoxify?
```
many endogenous substances (e.g. bilirubin)
exogenous substances (xenobiotics) e.g. drugs and ethanol
```
305
what does bile do between meals?
stored and concentrated in the gall bladder
306
what does bile do during a meal?
1. chyme in duodenum stimulates gall bladder smooth muscle to contract
2. spinchter of oddi opens
3. bile spurts into duodenum via cystic and common bile ducts
307
what does neutral/ slightly alkaline bile assist?
- micelle formation
- neutralisation of chyme
- pH adjustment for digestive enzyme action
- protection of the mucosa
308
what do hepatocytes do?
secrete primary juice into canaliculi which drain into biliary ductules and ducts
309
what is the most common pathology of the biliary tract?
cholelithiasis
310
what may cholesterol do over time in the gall bladder?
crystallise and grow into a gall stone
311
what happens to bile salts that are not lost in feaces?
reabsorbed by active transport in the terminal ileum and undergoes enterohepatic recycling
312
what do bacteria do to some primary bile acids?
dehydroxylate them to form secondary bile acids which return to the liver. they are then conjugated with glycine or taurine and recycled as bile salts
