Physiology Flashcards
1
Q
What do the words oral and aboral mean?
A
oral means moving towards the mouth
aboral means moving away from the mouth
2
Q
What are the parts of the small intestine?
A
duodenum, jejunum and the ileum
3
Q
What are the parts of the large intestine?
A
caecum, appendix and colon (ascending, descending, transverse and sigmoidal)
4
Q
What are the accessory organs of the digestive tract?
A
- salivary glands
- pancreas (makes digestive enzymes)
- liver (makes bile)
- gallbladder
5
Q
What are the layers of the digestive tract wall?
A
- mucosa
- submucosa
- muscularis externa
- serosa
6
Q
What does the mucosa consist of?
A
- mucous membrane (epithelial, exocrine and endocrine gland cells)
- lamina propria (capillaries, enteric neurones and gut-associated lymphoid tissue)
- muscularis mucosae
7
Q
What does the submucosa consist of?
A
connective tissue, larger blood and lymph vessels, glands and submucous plexus
8
Q
What does the muscularis external consist of?
A
mostly smooth muscle consisting of circular muscle and longitudinal muscle and between is the myenteric plexus
9
Q
What does serosa consist of?
A
connective tissue
10
Q
What are the four main functions of the alimentary canal?
A
- Motility: mechanical
- Secretion: required for digestion, protection and lubrication
- Digestion: enzymatic hydrolysis of food
- Absorption: transfer of products into blood or lymph
11
Q
What places use skeletal or smooth muscle?
A
skeletal= mouth, pharynx, upper oesophagus and external anal sphincter smooth= everywhere else
12
Q
What type of change does the circular muscle cause?
A
lumen becomes narrower and longer
13
Q
What type of change does the longitudinal muscle cause?
A
intestine becomes shorter and fatter
14
Q
What type of change does muscularis mucosae cause?
A
change in area for absorption and secretion and it causes a mixing motion
15
Q
What is smooth muscle made up of (cells and their connections)?
A
small cells connected by gap junctions making a low-resistance pathway so there is a single-unit sheet of smooth muscle
16
Q
What is spontaneous contracting activity driven by in the GI tract and what is it modified by?
A
driven by pacemaker cells
modulated by intrinsic/extrinsic nerves and hormones
17
Q
What does slow wave electrical activity determine in the GI tract?
A
frequency, direction and velocity of rhythmic contractions
18
Q
What is slow wave activity driven by?
A
ICCs which are the pacemaker cells in the circular and longitudinal muscle layers which form gap junctions with themselves and smooth muscle cells
19
Q
What is required for the slow wave activity to cause a contraction?
A
the depolarising waves only cause a contraction in the wave amplitude reaches threshold
20
Q
What determines the force of the slow-wave-induced contraction?
A
the longer the wave is above threshold, the more action potentials will be fired off
the starting potential of the cell also has an effect on how long the wave is above threshold
21
Q
What is the starting electrical potential of a cell determined by?
A
neuronal, hormonal and mechanical stimuli causing depolarisation
22
Q
What is the parasympathetic innervation of the GI tract?
A
preganglionic fibres that synapse with ganglion cells in ENS
23
Q
What influences does the parasympathetic part of the GI tract have?
A
Excitatory influences: increased secretion, blood supply and mechanical activity
Inhibitory influences: relaxing of sphincters and stomach
24
Q
What is the sympathetic innervation of the GI tract?
A
preganglionic synapse in the prevertebral ganglia and postganglionic fibres which innervate enteric neurons and others
25
What influences does the sympathetic innervation of the GI tract have?
Excitatory influences are increased sphincter tone
| Inhibitor influences are decreased motility, secretion and blood flow
26
What does the Enteric nervous system consist of?
- Myenteric plexus- regulates motility and sphincters
| - Submucous plexus- modulates epithelia and blood vessels
27
What are the three types of neurones in the ENS?
- sensory (mechano-, chemo- or thermo-receptors)
- interneurons (majority, for motor activity coordination)
- effector neurons (execution)
28
What are the main features of peristalsis?
- propulsive segment and ahead is receiving segment
- stretch from sensory neurons so there is altered activity of interneurons then altered activity of motoneurons around the bolus
- behind bolus, the circular muscle contracts and longitudinal relaxes
- in front of the bolus, the circular muscle relaxes and longitudinal muscle contracts
29
What does segmentation consist of?
mixing, churning by contractions of the circular muscle layer
30
What does colonic mass movement consist of?
force of faeces into rectum
31
What does the migrating motor complex consist of?
powerful sweeping of the small intestine
32
What do tonic contractions consist of?
low pressure (organs with major storage function) or high pressure (sphincter)
33
What are the sphincters of the GI tract?
- Upper oesophageal (skeletal): relaxes for swallowing and closes during inspiration
- Lower oesophageal: entry of food into stomach and prevents reflux of gastric contents to oesophagus
- Pyloric: gastric emptying and prevents reflux
- Ileocaecal valve: flow from ileum to caecum
- Internal and external anal: regulated by defecation reflex
34
What is energy homeostasis?
physiological process whereby energy intake is matched to energy expenditure over time so there is body fuel stability
35
What is the table of classification for BMI?
BMI <25 = thin/normal/acceptable
BMI 25-30 = overweight
BMI 30-40 = obese
BMI > 40 = morbidly obese
36
What is fat used for?
energy storage, prevention of starvation and as an energy buffer during prolonged illness
37
How does the CNS influence body weight?
behaviour (food and exercise), ANS activity (energy expenditure) and neuroendocrine system (hormone secretion)
38
How does the hypothalamus control food and how it is digested?
satiety signalling, adiposity negative feedback signalling and food reward
39
What do satiation, satiety and adiposity mean?
Satiation is the sensation of fullness
Satiety is the period of time between one meal ending and the start of the next
Adiposity is the state of being obese
40
What are some of the chemical satiation signals in the body?
- Cholecystokinin
- Peptide YY
- Glucagon-like peptide 1
- Oxyntomodulin
- Obestatin
41
What does Ghrelin do?
hunger signal and stimulates food intake, levels are raised by fasting
42
What are the two hormones that are produced in peripheral tissue that act on hypothalamic neurones?
- Leptin is made and released from fat cells
| - Insulin is made and released from pancreatic cels
43
What do Leptin and Insulin do in terms of obesity?
both increase as more fat is stored and they inform the hypothalamus that the body should eat less and increase energy burn
44
What is the current treatment for obesity?
- Orlistat which inhibits pancreatic lipase and reduces the efficiency of fat absorption in the small intestine
- Bariatric surgery which is gastric by-pass surgery produces substantial weight loss and cures Type 2 Diabetes
45
How can the stomach be mechanically divided?
- orad (fundas and proximal body)
| - caudad (distal body and antrum)
46
What are the mechanical characteristics of the orad?
- contractions are weak, maintained and tonic
- storage area so there is no slow wave activity
- minimal churning so there can be partial carbohydrate digestion
- weak contractions propel the food occasionally to the caudad region
- gastrin decreases the rate of contractions so there is little stomach emptying
47
What are the mechanical characteristics of the caudad?
- contractions are strong, phasic and intermittent
- slow waves occur in the caudad region at a rate of 3 slow waves per minute
- contents are propelled from the midstomach to the gastroduodenal junction towards the pylorus
48
How does the chyme leave the stomach?
- waves reach threshold, they cause peristaltic contraction that moves towards pyloric sphincter so a small volume of chyme moves out of the stomach
- slow wave reaches the pylorus before the peristalsis with the food so that the chyme bangs against the constricted sphincter which is retropulsion (mixes chyme)
49
What are the gastric factors that control stomach emptying?
Gastric: distension (increased stretch of smooth muscle, intrinsic nerve plexus stimulation and vagus nerve activity and gastrin release) and consistency of chyme
50
What are the duodenal factors that control stomach emptying?
Duodenal:
- duodenum delays emptying by neuronal (enterogastric reflex) and hormonal responses (release of enterogastrones eg CCK to inhibit stomach contraction)
- fat presence (fatty acids and glycerol delay stomach emptying)
- acid (must be neutralised for pancreatic enzymes to work) - hypertonicity (solution must not be hypertonic as water would be drawn out of the blood)
- distension
51
How can the stomach be functionally divided in terms of secretions?
- oxyntic (funds and most of body)
| - pyloric gland area (distal dory and antrum)
52
What are the secretions in the pyloric gland area of the stomach?
G cells (secrete gastrin) and D cells (secrete somatostatin)
53
What are the secretions in the oxyntic area of the stomach?
parietal cells (HCl, intrinsic factor and gastroferin), chief cell (pepsinogen) and enterochromaffin-like cell (histamine)
54
What substances promote HCl secretion in the stomach?
histamine
| gastrin
55
What does somatostatin do in the stomach?
inhibits HCl secretion
56
What do intrinsic factor and gastroferrin do in the stomach?
bind vitamin B12 and Fe2+ respectively to give absorption
57
How is HCl produced?
H+ actively pumped out by ATPase
| Cl- leaves by CFTR
58
What three stimuli cause acid secretion from the parietal cell?
ACh
Gastrin
Histamine
59
At rest, where are the H+ pumps in the stomach?
H+ pumps are not inserted in the apical membrane of the parietal cell, they are in intracellular structures called tubular vesicles so are inactive
They secrete protons at the canalicular membrane
60
What are the three phases of gastric secretion?
- cephalic phase: before the food reaches the stomach, the stomach is preparing
- gastric phase: physical and chemical mechanisms when food is in the stomach
- intestinal phase: chyme enters the upper small intestine causing weak stimulation of gastric secretion after food has left stomach via neuronal and hormonal mechanisms
61
What happens in the cephalic phase of gastric secretion?
- stimulation from food leads to vagal activation
- enteric neurones are stimulated
- increased GRP so G cells make gastrin
- increased ACh to ECL cell makes histamine and D cell makes less somatostatin (leading to more gastrin)
- these all lead to more HCl secretion form parietal cells
62
What happens in the gastric phase of gastric secretion?
- distension is detected by sensory neurons (mechanoreceptors) so enteric neurons activates to increase ACh and activates G cells
- protein digestion products activate G cell
- so more acid from parietal cells
63
What is involved in the process of inhibition of gastric secretion?
- Cephalic phase: vagal nerve activity decreases stops acid secretion
- Gastric phase: antral pH falls when food leaves, release of somatostatin from D cells and there is decreased gastrin secretion, also prostaglandin E2 is always secreted and reduces histamine and gastrin-caused HCl secretion
- Intestinal phase: factors that reduce gastric motility also reduce gastric secretion
64
What are the ways and drugs that reduce acid secretion?
- Inhibiting the proton-pump
E.g omeprazole
- Histamine H2 receptor antagonists block competitively so less histamine
Eg ranitidine
- NSAIDs block irreversibly cyclo-oxygenase so there is less PGE2 synthesised
Eg aspirin
- Muscarinic receptor antagonists block competitively so less ACh
Eg pirenzepine
65
What helps protect the stomach mucosa?
- mucous cells form gel layer
- bicarbonate is secreted to make pH gradient
- PGE2 and PGI2 reduce acid secretion, increase mucus and bicarbonate and increase mucosal blood flow
66
What bacteria forms peptic ulcers and can this be treated?
H.pylori
| reducing acid secretion, increasing mucosal resistance and eradicating H.pylori
67
What drug can cause peptic ulcers and how does it doe this?
NSAIDs reduce prostaglandin formation and trigger gastric ulceration and bleeding
68
How can you prevent NSAIDs forming peptic ulcers?
- stable PGE1 analogue called misoprostol
| - inhibits basal and food-stimulated gastric acid formation and maintains secretion of mucus and bicarbonate
69
What are the mechanisms of drugs that reduce acid secretion?
- Irreversible inhibition of proton-pump
- Competitive antagonism of histamine receptors
- Competitive antagonism of M1 and M3 ACh receptors
- Antagonism of gastrin receptors
70
What are drugs that reduce acid secretion used to treat?
peptic ulcer, gastro-oesophageal reflux disease and acid hypersecretion diseases (Zollinger-Ellison syndrome or Cushing’s ulcer)
71
What do proton-pump inhibitors do?
- inhibit active proton pump
- form in an acidic environment
- goes back to stomach (after systemic circulation) and enters parietal cells to enter canaliculus and irreversibly inhibits the proton pumps in the canalicular membrane
- Eg omperazole
- must be administered when proton pumps are active, one hour before breakfast, full effect is achieved after repeat dosing
72
What do histamine receptor antagonists do?
- Eg ranitidine and cimetidine
- Act as competitive antagonists of H2 receptors and completely block the histamine-mediated component of acid secretion and reduce secretion by gastrin and ACh
- Used for peptic ulcer and reflux oesophagitis
73
What are examples of mucosal strengtheners and how do they work?
- Sucralfate- requires an acid environment, binds to ulcer base, increases mucosal blood flow, mucus, bicarbonate and prostaglandin production
- Bismuth chealate- mucosal strengthening action and is toxic to H. pylori so is used with antibiotics
74
What does the small intestine receive?
- chyme
- pancreatic juice form the pancreas
- bile from the gallbladder
75
What are the forces that move chyme in small intestine?
segmentation, peristalsis and a migrating-motor complex
76
What are the hormones secreted from the small intestine and what do they do?
- Gastrin: acid secretion and growth of gastric mucosa
- Secretin released in response to H+ and fatty acids in lumen: promotes secretion of pancreatic and biliary HCO3-
- Cholecystokinin (CCK) released in response to nutrients: inhibits gastric emptying, causes secretion of pancreatic enzymes, relaxation of sphincter of Oddi and contraction of gallbladder so bile enters duodenum
- Glucose-dependent insulinotropic peptide: stimulates release of insulin from pancreas and inhibits gastric emptying
- Glucagon-like peptide-1: stimulates insulin secretion, inhibits glucagon secretion and decreases gastric emptying
- Motilin: initiates the migrating motor complex
- Ghrelin: stimulates appetite
77
What do juices from the small intestine contain?
- mucus from goblet cells
| - aqueous salt from crypts of Lieberkuhn
78
What is segmentation of the small intestine triggered by?
distension in the fed state but by gastrin from the stomach in the fasting state which is the gastroileal reflex
79
What is the migrating motor complex?
a strong wave that passes slowly over entire small intestine, this is triggered by motilin and is suppressed by gastrin and CCK, inhibited by feeding
80
What is in the pancreatic secretions?
- Endocrine: insulin and glucagon into the blood
| - Exocrine: digestive enzymes, aqueous NaHCO3- solution secreted to the duodenum collectively as pancreatic juice
81
What does the pancreatic secretion act to do?
neutralises acidic chyme with bicarbonate to provide the best pH for pancreatic enzyme function and to protect mucosa from acid
82
What are the main pancreatic enzymes?
- proteases
- amylases
- lipases
83
How is pancreatic secretion controlled?
- Cephalic: mediated by vagal stimulation of acinar cells
- Gastric: gastric distention causes vagovagal reflex so parasympathetic stimulation of acinar and duct cells
- Intestinal: acid increases amount of secretin so increased aqueous NaHCO3, fat and protein increases CCK so increased secretion of digestive enzymes
84
What are luminal and membrane digestion?
- luminal is mediated by pancreatic enzymes secreted into the duodenum
- membrane is mediated by enzymes situated at brush border of the epithelial cells
85
What is absorption?
products of digestion crossing both the apical and basolateral membranes of the enterocytes in the intestinal epithelium
86
How are carbohydrates broken down into a size that can be absorbed?
- must be a monosaccharide to be absorbed
- alpha ampfhylase breaks down into oligosaccharides in intraluminal hydrolysis
- lactase, maltase and sucrase-isomaltase form the monosaccharides
87
What type of enzyme is alpha amylase?
- endoenzyme
| - breaks down lineal alpha-1,4 linkages so no end bonds or branch bonds
88
What does isomaltase break?
1,6 branching chain bonds
89
What is lactase persistence?
being able to digest lactase
90
What is lactose intolerance and what can it result from?
inability to digest lactose and can result from primary lactase deficiency, secondary lactase deficiency or congenital lactase deficiency
91
What happens if a lactose intolerant patient consumes lactose?
- short-chain fatty acids, hydrogen, carbon dioxide and methane are produced
- these cause bloating, abdominal pain and flatulence
- undigested lactose causes acidification of the colon and an increased osmotic load
92
How are monosaccharides absorbed?
- in duodenum and jejunum across two membranes
- glucose and galactose are absorbed by secondary active transport mediated by SGLT1
- fructose absorbed by facilitated diffusion by GLUT5
- exit out of cells for all monosaccharides is by GLUT2
93
How does SGLT1 work?
- alternating access model
| - glucose binds and unbinds depending on the binding of sodium ions
94
How is protein digested in the stomach?
by pepsin which is an andopeptidase
95
How is protein digested in the duodenum?
```
- by endo and exo peptidases from pancreas:
= trypsin (endo)
= chymotrypsin (endo)
= elastase (endo)
= carboxypeptidase A (exo)
= carboxypeptidase B (exo)
```
96
What are the other types of peptidases?
- brush border can be endo or exo (amino or carboxypeptidases) and have affinity for larger oligopeptidases
- cytoplasmic peptidases primarily hydrolyse di and tri peptides
97
How do amino acids get absorbed in the small intestine?
- transported with sodium into cell by secondary active transport
- across basolateral membrane with sodium-potassium pump making the gradient
98
How do larger peptides get absorbed in the small intestine?
- moved by PepT1 with H+ by secondary active transport
- hydrolysis in cell and amino acids are released as normal
- sodium-hydrogen pump makes the gradient
99
Where are bile salts released into?
into duodenum from gall bladder in response to CCK
100
What does failure to secrete bile salts result in?
lipid malformation and secondary vitamin deficiency due to failure to absorb fat soluble vitamins
101
What is the problem with bile salts emulsifying lipids and how is this overcome?
increase surface area but block enzyme access so colipase is needed to bind them together and allow lipase to access triglyceride
102
What is colipase secreted as?
secreted as inactive procolipase which is activated by trypsin
103
How are mixed micelles formed?
- droplets of fat are stabilised by adding a coat of amphiphilic molecules
- droplets become smaller to eventually form mixed micelle
104
How does the stomach contribute to lipid digestion?
secretes gastric lipase in response to gastrin from chief cells (only important in pancreatic insufficiency and infants)
105
What does pancreatic lipase do and require to work?
- released from acing cells and stimulated bile flow
| - full activity requires: colipase, alkaline pH, Ca2+, bile salts and fatty acids
106
What does pancreatic lipase break down lipids to form?
2-monoacylglycerol and free fatty acids
107
How is cholesterol absorbed?
mediated by NPC1L1 which binds it
108
What does the drug Ezemtimibe do and what is it used to treat?
binds to NPC1L1 so there is no internalisation and absorption of cholesterol so is used with statins to treat hypercholesterolaemia
109
How are chylomicrons formed?
long chain fatty acids and monoglycerides are resynthesises din the cells in the ER into triglycerides and are then made into chylomicrons
110
How does the mixed micelle enter the cell?
makes contact with the apical membrane and diffuses across the membrane
- short and medium fatty acids diffuse through enterocyte and then through basolateral and into capillaries
- long chain are resynthesises to triglycerides in ER and are then made into chylomicrons
111
What happens to the chylomicrons in the cells?
leave by exocytosis and enter the central lacteal
112
How are calcium ions moved into the cells?
- passive or active
- calcium channels move in across apical
- calciumbinds to ferine molecule and taken out by active transport of calcium or by calcium.sodium exchanger
113
In what form is iron absorbed?
as ferrous (Fe2+) not ferric
114
How are fat-soluble vitamins absorbed?
requires bile secretion as they are incorporated into micelles then into chylomicrons and into lymphatic system
115
Why does there need to be a complex way to absorb B12?
it is only minutely in the diet but is necessary for life
116
What is the structure of the longitudinal smooth muscle in the large intestine?
not continuous but is three stands called teniae coli but circles internal and external anal spincters at rectum
117
What muscle forms the internal and external anal sphincters?
internal is smooth muscle
| external is skeletal muscle
118
What are haustra?
sac-like bulges in the large intestine which change shape in a living person
119
What regulates the ileocaecal valve?
regulated by the gastroileal reflex and gastrin and CCK, permits movement into the caecum
120
What affects the contraction and relaxation of the ileocaecal valve?
- relaxes in response to distention of the duodenum
- contracts in response to distention of the ascending colon
- under control of vagus nerve, sympathetic nerves, enteric neurones and hormonal signals
121
What connects the caecum and the appendix?
appendiceal orifice
122
What does the colon absorb?
sodium
choloride
water
short chain fatty acids
123
What does the colon secrete?
K+
HCO3-
mucus
124
What is the function of the different parts of the colon?
- ascending and transverse do fluid reabsorption and bacterial fermentation
- descending and sigmoid colon do final drying and storage
125
What is the more microscopic structure of the colon?
colonic folds, crypts, microvilli to increase surface area
126
What do the cells of the colon do?
- colonocytes mediate electrolyte absorption so drives absorption of water
- crypt cells are involved in ion secretion
- goblet cells are involved in mucus (contains glycosaminoglycans) secretion and trefoil proteins
127
What enhances the absorption of sodium and secretion of potassium in the large intestine?
aldosterone
128
What are the main patterns of motility in the large intestine?
- haustration
- peristaltic propulsive movement
- defecation
129
What does haustration involve?
- non-propulsive movement
| - haustra are caused by alternating contraction of circular muscle and slows movement of contents of large intestine
130
What does peristaltic propulsive movement involve?
- 1-3 times a day
- triggered by a meal via gastrocolic response involving gastrin and extrinsic nerve plexuses
- mass movement to rectum triggers the defecation reflex
131
What does defecation involve?
- rectum fills:
- 1) rectum stretch receptors activated, activation of afferents to spinal cord and then parasympathetic efferents so contraction of smooth muscle of sigmoid and rectu, relaxing of internal anal sphincter then either relaxation or contraction of external anal sphnicter
- 2) rectum stretch causes activation of afferents to brain then efferents to spinal cord giving same outcomes
132
What is the function of the bacteria in the colon?
- increase intestinal immunity
- promote motility
- synthesise vitamin K2 and free fatty acids
- activate some drugs
133
Where does gas in the GI tract come from?
swallowed air
| bacteria in the colon which attack carbohydrates that are indigestible to humans
134
What are the causes of constipation?
- not defecating
- decreased colonic motility
- obstruction of faecal movement
- paralytic ileum after abdominal surgery
- impairments of motility/defaecation reflex sue to a lack of enteric nervous system (Hirschprung disease)
135
What are the symptoms of constipation and what are they caused by?
- malaise
- abdominal pain
- headache
- loss of appetite
all caused by prolonged colonic distention
136
What is the difference between laxatives and purgatives?
laxatives are used to treat constipation but purgatives are used to cause a purging of the entire tract to clean the vowels before surgery or endoscopic procedure
137
When are both laxative and purgatives completely contraindicated?
when there is a physical obstruction of the bowel
138
What do laxatives do and when should they be used?
- increase peristalsis
- soften faeces
- stimulate enteric nervous system
- overused can cause atonic colon
- should be used when straining is painful or damaging, to purge bowel or to treat drug-induced constipation
139
What are the four main types of laxatives and purgatives?
- bulk laxatives
- osmotic laxatives
- stimulant purgatives
- faecal softeners
140
What do bulk laxatives do ?
- indigestible carbohydrate
- given orally
- increase bulk
- retain H2O
- increase peristalsis
eg methylcellulose
141
What do osmotic laxatives do?
- poorly absorbed solutes
- slow acting if given orally compared to rapidly when given rectally
- increase bulk, water and peristalsis
eg magnesium sulphate/hydroxide orally or sodium citrate rectally
142
What do stimulant purgatives do?
- stimulates enteric nervous system to increase frequency and force of peristalsis
eg bisacodyl orally/ suppository or sodium picosulphate
143
What do faecal softeners do?
detergent-like action to lubricate stool
| eg decussate sodium orally or arches oil in an enema
144
What are IBS and IBD?
- IBS is bouts of diarrhoea, constipation or abdominal pain
| - IBD can affect entire gut (Chrohn's) or just colon (ulcerative colitis)
145
What is IBS treated with?
treatment is symptomatic with diet change, anti-diarrheals, antispasmodics or laxatives as required
146
What is IBD treated with?
- glucocorticoids for acute attack not long term eg prednisolone
- aminosalicylates for maintenance eg -salazine
147
How is water absorbed from the GI tract?
- passive
| - driven by the movement of solutes (especially Na+) from lumen to bloodstream
148
What are the main ways in which sodium ions move in the GI tract to cause water movement?
- sodium/glucose cotransport
- sodium/amino acid cotransport
- sodium/hydrogen exchange
- epithelial sodium channels
- parallel sodium/hydrogen and chloride/bicarbonate exchange
149
What are the two mechanical ways that water can move into blood from GI tract?
transcellular
| paracellular
150
What is the mechanism of sodium/glucose and sodium/amino acid cotransport?
- happens in the jejunum
| - both are secondary active transport
151
What is the mechanism of sodium/hdrogen ion exchange?
- jejunum at both apical and basolateral membranes
- NHE2 and NHE3 move Na+
- exchange at apical end is stimulated by alkaline lumen
152
What is the mechanism of parallel sodium/hydrogen and chloride/bicarbonate exchange?
- occurs in interdigestive period
- in ileum and proximal colon
- absorption is electoneutral
- regulated by cAMP, cGMP and Ca2+ which all reduce NaCl absorption
- reduction in NaCl is a cause of diarrhoea
153
What is the mechanism of epithelial Na+ channels?
- ENaC mediate electrogenic Na+ absorption is the distal colon
- important in Na+ conservation
- increased by aldosterone which opens channels, puts more in membrane and increases synthesis of ENaC and sodium-potassium pump
154
How does Cl- absorption occur?
passively
| via transcellular or paracellular routes
155
What is the driving force of Cl- movement in the small intestine?
lumen negative potential due to Na+ movement
156
What is the driving force of Cl- movement in the large intestine?
lumen negative potential due to electrogenic movement through ENaC
157
What are the other methods of chloride movement in the tract?
- chloride/hydrogen carbonate exchange
| - sodium/hydrogen and chloride/hydrogen carbonate parallel exchange
158
Where does chloride secretion occur cellularly?
from cell in crypts not villi
159
What are the three chloride movement processes in the basolateral membrane?
- sodium/potassium pump
- sodium/potassium/chloride co-transporter
- potassium channels
160
How does chloride move into the lumen?
CFTR channels on apical membrane
161
How is CFTR activated?
- bacterial enterotoxins
- hormones
- immune cells
- laxatives
162
What does activation of CFTR cause?
- generation of second messengers including cAMP, cGMP and Ca2+ (causes secretory diarrhoea)
163
What are the causes of diarrhoea?
- Impaired absorption of NaCl: congenital, inflammation, infection or excess bile acid in colcon
- Non-absorbable solutes in intestinal lumen (eg lactase deficiency)
- Excessive secretion eg cholera
- Hypermotility
- Other causes include: infectious agents, chronic disease, toxins, drugs and psychological factors
164
What can diarrhoea result in?
can involve small or large intestine, can result in dehydration, metabolic acidosis and hypokalaemia and may be fatal
165
What is the treatment of sever diarrhoea?
maintenance of fluid and electrolytes, use of anti-infective agents and use of non-anti-microbial antidiarrheal agents
166
What does rehydration therapy for diarrhoea exploit?
SGLT1q
167
What are the anti-motility agents used in diarrhoea and how do they act?
- codeine, diphenoxylate and loperamide
- inhibit enteric neurons, decrease peristalsis, increase fluid absorption, constrict sphincters and increase the tone of the large intestine
168
What are the main functions of the liver?
- metabolism of carbohydrate, fat and protein
- deactivation or inactivation of hormones
- storage
- synthesis of proteins
- protection
- detoxification
169
How does the liver help with metabolism?
- Carbohydrate- convert different glucose units
- Fat- processing chylomicron remnants, synthesize lipoproteins and ketogenesis
- Protein- plasma protein synthesis, transamination and deamination of amino acids and conversion of ammonia to urea
170
How does the liver contribute to the deactivation of hormones?
Deactivated: insulin, glucagon, ADH or steroid
Activated: thyroid and vit D
171
How does the liver contribute to storage?
fat and water soluble vitamins, iron, copper and glycogen
172
What proteins does the liver produce?
coagulation factors, albumin, complement, apolipoproteins and carrier proteins
173
How does the liver act to protect?
Kupffer cells and production of immune factors
174
What does the liver produce to help with detoxification?
Endogenous and exogenous substances
175
What is in primary juice?
primary bile acids, electrolytes, lipids, IgA and bilirubin
176
What is cholelithiasis and the treatment for it?
gallbladder stones forming which can be treated with laparoscopic cholecystectomy, ursodeoxycholic acid (dissolves small stones)
177
What is biliary colic treated with?
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pain meds
(not morphine as it constricts sphincter)
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178
What is bilary spasm treated with?
atropine or GTN
179
What happens with bile before during and after a meal?
- Between meals: bile is stored and concentrates in the gall bladder
- During a meal: chyme makes gall bladder smooth muscle contract and bile goes into duodenum
180
What does bile do?
assists in micelle formation, neutralisation of chyme, pH adjustment and protection of the mucosa
181
How is bile reabsorbed?
- reabsorbed by active transport in the terminal ileum and undergoes enterohepatic recycling
- primary bile acid form secondary bile acids which are returned to the liver
182
What are resins?
act by binding to bile acids do they aren’t reabsorbed, converts cholesterol to bile acids and increases LDL receptor expression
183
What are resins used to treat and what are the side effects?
- used in hyperlipidaemia, cholestatic jaundice and bile acid diarrhoea
- can cause diarrhoea
184
When does hepatic encephalopathy occur?
detoxification of ammonia to urea fails so it becomes toxic
185
What is the treatment for hepatic encephalopathy?
- lactulose which acidifies the stool so ammonium is made
| - antibiotics which suppress flora and inhibit ammonia generation
