March 19 - Gastrointestinal Physiology Flashcards
1
Q
What are the five functions of the GI system?
A
- Propulsion
- Secretion
- Digestion
- Absorption
- Barrier function
2
Q
Describe propulsion
A
Movement from mouth to anus
Deglutition
Peristalsis
Mass movements (elimination)
3
Q
Describe secretion
A
It is equally important (we would not be able to digest or absorb without secretion)
Mucous production for protection
Water
Enzymes
4
Q
Describe digestion
A
Mechanical
Chemical
5
Q
Describe absorption
A
Transcytosis
6
Q
Describe the barrier function
A
We need to keep the bacteria of our stomach from getting into our body
7
Q
What is MALT?
A
Mucosa associated lymphoid tissue
8
Q
What is GALT?
A
Gastrointestinal associated lymphoid tissue
9
Q
What is the importance of GALT?
A
There are more lymphocytes in the intestines than in the spleen; they determine that if anything should cross if it is either benign or if it requires the mounting of an immune response. Intestines are inflamed at all times; partly due to GALT
10
Q
What are the organs of the alimentary canal?
A
Mouth (addition of saliva, beginning of digestion)
Esophagus (upper two thirds is skeletal muscle, the lower two thirds is smooth muscle; swallowing begins as voluntary and transitions to involuntary)
Stomach
Small intestine (proximal section is the duodenum (first 10-15%), the middle bulk section is the jejunum and the distal section (last 10%) is the ileum)
Caecum (appendix: has a little digestion activity and is important for immunity)
Large intestine (formation of feces)
Rectum
Anus
11
Q
What are the accessory organs of the alimentary canal?
A
Liver (production of bile)
Gall bladder (storage of bile)
Pancreas (enzymatic role, buffering role)
12
Q
What are the seven sphincters of the GI tract?
A
Upper esophageal Lower esophageal Pyloric Ileocecal Colorectal Internal anal External anal
13
Q
What are the four tissue layers of the GI tract?
A
The mucosa
The submucosa
The muscularis
The serosa
14
Q
What makes up the mucosa?
A
A single columnar epithelium (with the exception of the esophagus - it has a stratified squamous epithelium) Lamina propria (connective tissue) Muscularis - thin layer of smooth muscle (anatomical landmark - it separates the mucosa from the submucosa)
15
Q
Describe the submucosa?
A
Complex tissue Lots of blood vessels Extensive lymphatic system Lots of fatty tissue Submucosal plexus
16
Q
Describe the submucosal plexus
A
Nervous tissue - a neuron network that is highly organized but not a in a tract (like in the spinal cord); it exists more as a network around the entire structure and it controls the functions of the submucosa and mucosa
17
Q
What makes up the muscularis?
A
Circular smooth muscle - when it constricts the diameter of the lumen decreases Myenteric plexus (similar to the submucosal plexus; it control the muscularis) Longitudinal smooth muscle - when it constricts, that segment of gut gets shorter
18
Q
How is the gut controlled?
A
The gut has more neurons than the spinal cord. There are many chemoreceptors, baroreceptors, interneurons to integrate signals, motor neurons. We have whole reflex arcs that occur entirely within the gut, so the gut can control itself using these neurons (however it is still influenced by the CNS)
19
Q
Describe the serosa
A
Basically just the visceral peritoneum
20
Q
Describe the small intestine ultrastructure
A
The epithelium of the small intestine is folded over on itself. It has a lot of finger-like projections call villi, which increase surface area by about 20x. The apical membrane of each epithelial cell has bristles created by the extending of the cytoskeleton called microvilli. This further increase the surface area by about 50x. This is where transport proteins are found and there are lots of enzymes here.
21
Q
Compare smooth muscle to skeletal muscle
A
There is no actin myosin striations There is more actin There is less mysoin It is organized very loosely There are no sarcomeres; dense bodies, attached together by intermediate filaments, organize the actin
22
Q
What causes contraction of smooth muscle?
A
When stimulated (neuronal signal, hormonal signal, gap junction communication, etc.) a smooth muscle cell membrane’s voltage-gated ion channels open, calcium enters the cell (in smooth muscle the SR is underdeveloped, so the bulk of the Ca comes from the ECF). The concentration of calcium increases. Calcium binds to calmodulin creating the calcium-calmodulin complex. This complex activates the enzyme myosin light chain kinase (MLCK). MLCK phosphorylates myosin. The phosphorylated form of myosin is active and can bind to actin, which causes contraction
23
Q
What causes relaxation of smooth muscle?
A
The smooth muscle actively pump out the calcium. The concentration of calcium decreases so the calcium-calmodulin complex dissociates. This causes the inactivation of MLCK. Also myosine phosphatase inhibits MLCK by dephosphorylation. All this ends cross bridging, which causes relaxation
24
Q
Name three different GI movements
A
Segmentation
Peristaltic waves
Migrating motor complexes
25
Describe segmentation
Parts of the tissue contracts and the other parts relax (chopping motion). When the muscle contracts, the contents are forced away in opposite directions (homogenization of contents)
26
Describe peristaltic waves
Allows movement from one organ to the next.
Very short, weak waves (one wave will travel about 1 cm. However, hundreds of thousands of them cause efficient movement of contents down the GI tract. We don't want to move things too fast; we want time for digestion and absorption
27
Describe migrating motor complexes
These are very strong, long waves that move like peristaltic waves. They go long distances (one wave can travel the stomach and intestines). They occur between meals. They keep things moving. They prevent infection. They rid the body of waste and accumulating toxins
28
What are gastric movements?
There are three layers smooth muscle specific to the stomach; when they contract, they twist. There are mixing or churning waves, which produce liquid chyme. Throughout the first wave, the pyloric sphincter is closed Peristaltic waves, a second, stronger wave, which increases pressure, which overcomes the tonicity of the pyloric sphincter and it will open up. The pyloric sphincter is under precise control. The amount of chyme that is released into the duodenum at one time is very small
29
Describe the control of the myenteric plexus
It is under local control via the enteric nervous system (a division of the ANS). In this plexus there are sensory, motor and interneurons. They have excitatory functions; they increase muscle tone (mainly in the sphincters). We automatically control the intensity and the frequency of these contraction, and thus we automatically control the speed of peristalsis. There are inhibitory functions as well, so when material needs to move past the sphincter, it needs to relax. In most cases we want to inhibit the back flow (exception: there's a little backflow in the stomach and occasionally we need to vomit)
30
Describe the intrinsic control of GI function
Smooth muscle membrane potential fluctuates. When they are at rest, the values are below threshold. The reason is due largely to Na/K pumps. If the waves become depolarized and the peaks reach threshold, we get these spike potentials. This is stimulated by a number of functions (e.g., stretch when food is present). The greater the depolarization, the higher the frequency of spike potential and the stronger the contraction. The are also inhibitory functions; any stimulus that causes hyperpolarization
31
Describe the extrinsic control of GI function
The initiation and the development of motility is controlled internally by the ENS but there are external influences (extrinsic coordination). Acetylcholine and the parasympathetics promote digestion. Norepinephrine and the sypmathetics control fight, flight and reproduction so they will redirect blood away from the GI tract. Other controls include hormones, as well as cognitive and emotional control
32
Describe the cognitive control
Modulation of gastric functions (anger and stress)
| Direct neurological pathways (acid production, motility, blood flow)
33
Describe GI reflexes
There is communication between the different parts of the GI tract (intragut). Various stimuli send signals (distention, chemicals, irritants). When your stomach is stretched, this will have an excitatory effect on the distal areas of the GI. Proximal to distal tend to be excitatory. In contrast, distal to proximal tend to be inhibitory (slow motility); if the colon is full, there is not room to accept new contents (distal to proximal will override proximal to distal signals; the material needs to be handled properly).
34
What happens if motility is increased too much?
This leads to diarrhea (increased migrating motor complexes). This can be a protective mechanism (if there is a parasite, etc.)
35
What happens if motility is decreased too much?
This leads to constipation. It allows more time to take the water out of feces, which makes it harder to move. Consequences include: distention, perforation, death. This can be caused by Chagas disease (caused by a parasite that destroys the myenteric plexus)
36
How does codeine lead to constipation?
Codeine binds to opioid receptors to alleviate pain and increase sympathetic activity (norepinephrine). In the myenteric plexus, codeine binds to u-Opioid receptors, which causes serotonin and norepinephrine release. Serotonin has antimotility effects, as does norepinephrine (via decreasing the release of ACh). In addition, norepinephrine is an antisecretagogue, so less water gets into the stools
37
What are prokinetic agents?
Used to treat constipation. They stimulate the secretion of ACh at the gut. Serotonin agonists turn off inhibitory signals and turn on excitatory signals. Dopamine-R antagonists turn off inhibitory signals
38
What is retropulsion?
Aka vomiting. It is a very special type of GI movement. The emetic centre controls vomiting. The process is incredibly complex. Peristalsis needs to change direction, the epiglottis needs to be closed, contraction of stomach muscles need to be controlled and everything needs to be done in the right order at the right time. There are many paths that lead to the emetic centre. Vomiting is a good thing in small doses (to get rid of toxins). Too much can cause the body to lose to many hydrogen ions (alkalosis)
39
How is excess vomiting treated?
With antiemetics. They are receptor antagonists (serotonin-R, histamine-R, muscarinic-R, dopamine-R)
40
How much is secreted throughout the GI tract daily?
8.5L
41
What are the various functions of fluid secretions of the GI tract?
Liquefaction (converting solid or semi solid food into liquid chyme)
Lubrication (mucous to help keep things moving smoothly so that we don't damage the epithelium)
Digestion (enzymes)
42
What controls secretion?
Local control by the submucosal plexus. Secretion is typically due to the presence of luminal contents (biggest stimulus)
43
Describe the secretion of saliva
Multiple glands secrete 1.5 L of saliva daily. Its functions include: moistening, lubrication (mucin), defence (lysozyme, which breaks down the cell walls of bacteria, IgA)
44
What controls salivation?
It is controlled locally or centrally. Stimulations include: tactile, parasympathetic, cognitive. The autonomic nervous system have a big effect over salivation
45
What cells are responsible for gastric secretions?
Gastric pits, which lead to gastric glands. Here the epithelial cells include surface mucous cells, mucous neck cells, parietal cells, chief cells and endocrine cells (Enterochromaffin-like cells, G cells and D cells)
46
Describe the gastric acid secretion
Approximately 2500 ml/day of gastric juice are secreted today by the H/K exchange pump. Functions include: bacteriocidal role, digestion of protein (acid hydrolysis, denaturation), digestion of bone
47
What happens if there is too much gastric acid secretion?
Peptic ulcer disease, gastroesophageal reflux disease (GERD)
48
Describe the process of acid secretion by the
Water and carbon dioxide become carbonic acid, which then dissociates into bicarbonate and a proton. The proton is pumped into the lumen of the stomach in exchange for a potassium ion. The bicarbonate is pumped into the blood stream in exchange for a chloride ion. The chloride ion then flows into the lumen of the stomach
49
How are gastrin secretions increased?
Via secretagogues, such as actetylcholine, gastrin and histamine. Acetylcholine increases the rate of proton pumping. Gastrin acts on the parietal cells to increase gastric secretion. Histamine has a similar effect
50
How are gastrin secretions decreased?
Via anti-secretagogues, such as prostaglandin E2 (PGE2) and norepinephrine
51
What is pepsinogen?
A proenzyme secreted by chief cells
52
What is intrinsic factor?
Factor secreted by parietal cells that is essential for vitamin B12 uptake
53
What is alkaline mucous?
A substance that is secreted and found on the surface of goblet cells and is responsible for the protection against acid and abrasion
54
What is thin mucous?
A substance secreted by mucous neck (goblet) cells that is responsible for lubrication
55
What are minor digestive enzymes?
Enzymes such as gastric lipase, gastric amylase and gelatinase
56
What is the alkaline tide?
There are a million times more protons in the stomach than in the blood. When protons are actively pumped into the stomach, the gradient gets bigger and some of these protons are going to wash into the basolateral side, which will decrease the pH of the blood. For every one proton that is pump out into the lumen, one bicarbonate is pumped into the blood stream. So if a proton leaks into the blood stream, it will be mopped up by the bicarbonate. The alkaline tide refers to the bicarbonate across the basolateral surface that keeps the blood pH constant at around 7.4
57
What are the three phases in the control of stomach secretions? Why are they named so?
Cephalic phase
Gastric phase
Intestinal phase
The phases are named after the site where the stimulus is coming from
58
Describe the cephalic phase?
From the brain, there is direct innervation down to the enteric nervous system via the vagus nerve. When you see food, it goes to your brain and your stomach starts secreting. The vagus nerves stimulates the ENS and there is direct innervation of the parietal cells (acid production). The ENS synapses with G cells (gastrin release, HCl and pepsinogen secretion) and ECL cells (histamine release, acid secretion)
59
What happens if there is stimulation via the cephalic phase but no food is consumed right away?
When the pH of the stomach becomes too low due to unnecessary acid secretion, there is a negative feedback mechanism which causes D cells to release somatostatin, which inhibits the G cells and directly inhibits the parietal cells
60
Describe the gastric phase
This is the second phase when food is present in the stomach. The gastrogastric reflex is stimulated when the gut organs are communicating with itself. The luminal contents stimualte baroreceptors, which measure pressure, and chemoreceptors, which respond to molecultes in the food, especially to lipids. Signals from the pressure and chemicals are sent via the vagus nerve to the medulla, which responds back.. This causes an excitatory response which stimulates the goblet cells (mucous production). This also stimulates parietal cells (acid secretion), as well as G cells and chief cells.
61
How does the luminal contents affect the pH
The food in the stomach will buffer the gastric contents. If the pH drops too much, the movement of food slows down (negative feedback when the pH is below 2)
62
Describe the intestinal phase
The enterogastric reflex is stimulated when chemoreceptors in the duodenum detect low pH or food contents. The low pH and high lipid content leads to secretin secretion. Secretin inhibits gastric function (gastric juice production/secretion). It acts directly on parietal cells and chief cells to inhibit their secretion. The enterogastric reflex also stimulates the release of gastric inhibitory peptide (GIP) hormone and cholecystokinin (CCK) hormone. GIP reduces all action of secretory cells within the stomach line. CCK inhibits stomach function (but to a lower extent than others)
63
Describe the result of parasympathetic stimulation of G cells, parietal cells, ECL cells and chief cells
Stimulation of G cells causes the secretion of gastrin, which stimulates ECL cells, parietal and chief cells. ECL cells release histamine, which has stimulates parietal and chief cells. Chief cells secrete pepsinogen. Parietal cells secrete intrinsic factor which help with vitamine B12 absorption. Parietal cells also secrete H ions, which activtes pepsinogen to the active form pepsin (cleaves peptides at a very high rate). If the concentration of H ions is too high causes a negative feedback, which is detected D cells, which release somatostatin, which inhibits ECL cells, G cells and parietal cells
64
What are the two major therapeutic targets for the prevention of acid secretion?
Histamine (H2) blockers (Tagamet, Zantac, Pepcid) - chemically inhibiting histamine blockers can reduce the total amount of acid released, especially in a patient that releases too much
Proton pump inhibitors (Prilosec, Prevacid) - the drug irreversibly binds to the proton pump and prevents it's action. Once the drug is bout, that effect is permanent until the cell makes a new pump
65
What is the problem with NSAIDs with regards to the GI tract
Non steroidal antiinflammatory drugs (ibuprofen, naproxen, aspirin) are painkillers block COX, the enzyme that produces prostaglandins. COX-1 is constitutive (continuously produced) and is responsible for keeping a low concentration of prostaglandins to regulate gastric secretions. COX-2 is inducible, and when it is activated, it produces a high concentration of prostaglandins that are pro-inflammatory. Chronic, non selective inhibition of COX enzymes can lead to development of peptic ulcer disease
66
What is the difference between first and second generation NSAIDs?
First generation NSAIDs were nonspecific (they block both COX-1 and COX-2 (e.g., Advil prevents the production of PGE2, which removes the protective effect, allowing histamine to have a fuller effect, increasing acid production)
Second generation NSAIDs selectively block COX-2 (Celecoxib, Refocoxib), however this can have some undesirable side effects (e.g., heart attacks)
67
What are NO-NSAIDs?
They are experimental, modified NSAIDs that have a side group added on that releases nitric oxide (NO) into the the tissue. These drugs are called CINOD (COX-inhibiting nitric oxide donators). CINODs are non selective COX inhibitors, but the NO causes vasodilation, which increases blood flow to the stomach (protective effect)
68
How is the pancreas divided?
```
Endocrine pancreas (pancreatic islets)
Exocrine pancreas (pancreatic duct)
```
69
Describe the exocrine pancreatic secretions
There are two components: the aqueous component and the enzyme component. The two components are under separate control. There are about 1500 ml of pancreatic juice secreted per day.
70
Describe the aqueous component of the exocrine pancreatic secretions
In the aqueous component contains sodium, bicarbonate (buffer the contents leaving the stomach). A chloride bicarbonate exchanger pumps bicarbonate into the lumen of the pancreas or intestine from the pancreatic duct cell or duodenal cell in exchange for a chloride ion. A Na/K exchanger pumps sodium into the interstitial fluid in exchange for a potassium. Water and sodium passively move down sodium's gradient from the interstitial fluid to the lumen of the pancreas or intestine
71
Describe the enzyme component of the exocrine pancreatic secretions
In the enzyme component, there are proteolytic enzymes (zymogens, to avoid self digestion), pancreatic amylase (break down of starch) and pancreatic lipases
72
What controls pancreatic secretion?
The vagus nerve
Cholecystokinin
Secretin
73
Describe the vagal control of pancreatic secretion
Parasympathetics (via acetylcholine) stimulates pancreatic secretions (rest and digest)
Sympathetics (via norepinephrine) inhibits pancreatic secretions (fight or flight)
74
Describe the control of pancreatic secretions via cholecystokinin
When the chemoreceptors detect lipids in the duodenum, this triggers the enzymatic secretion of CCK, which has a positive effect on pancreatic secretion but a negative effect on gastric secretion (gastric emptying)
75
Describe the control of pancreatic secretions via secretin
Secretin secretion is stimulated via acidic chyme in the duodenum (low pH). Secretin goes through the circulatory system to the pancreas to increase the secretion of the aqueous component. It also decreases gastric emptyhing
76
Describe bile production
The liver continuously produces fairly dilute bile, making about 500 ml/day. The gallbladder stores and concentrates the bile (5-15x). The gallbladder will store bile until stimulated to release it
77
What are the functions of bile?
Neutralization of the acidic chyme via bicarbonate
| Emulsification of oil (lipids) via bile salts
78
What controls the emptying of the gallbladder?
Cholecystokinin (chole means bile, cys means sac, kinin means move) is released when there are fats present in the duodenum. It causes contraction of the gallbladder and relaxation of the sphincter of Oddi
Parasympathetics (via acetylcholine) causes weak contraction of the gallbladder
Secretin stimulates bile production
79
Describe the architecture of the small intestine
There are villi (which increase the surface area for digestion and absorption). There are crypts (of Lieberkuhn), which look similar to the gastric glands of the stomach. The youngest cells are at the bottom of the crypts, and as we go up the villi, the cells get older and older until they reach the top of the villus. The young cells have secretory role and as they mature, they lose their secretory role and become important for absorption. So the crypts are the sites of secretion and the villi are the sites of absorption. The stem cells, which develop into the cells of the crypt, are found near the bottom of the crypt. Each cell has a lifespan of 5 days
80
Describe the secretions of the small intestine
This is a very important role of the small intestine. About 1500 ml is secreted each day. The small intestine secretions include a watery secretion (a salty watery secretion out of the crypts) and a mucoid secretion
81
Describe the secretion from the crypts of Lieberkuhn
The crypts secrete a watery fluid containing electrolytes. The secretion moves out of the opening to ensure the crypts are clean of bacteria. Cysticfibrosistransmembrane conductor (CFTR) is activated by cAMP and it moves chloride ions from one side of the epithelium to the other (the crypt lumen). Water and sodium move to into the crypt lumen to balance the charge
82
What are paneth cells?
They are cells found in the crypts of Lieberkuhn. Granules within the paneth cells release cryptidins and defensins that defend the crypts from bacteria
83
What are goblet cells
They are cells that secrete mucous
84
What controls small intestine secretion?
Local distention (has the largest impact on control)
Secretin and CCK play a minor role
Other secretagogues affect secretion. Products of inflammation are often potent secretagogues
85
How can infection affect small intestine secretion?
The cholera toxin is a powerful secretagogue. Other secretagogues can open calcium channels or increase the concentration of cAMP. Too much secretion leads to diarrhea
86
Describe the large intestine
The large intestine is not that exciting in terms of secretion. It's a flat surface with deep crypts of Lieberkuhn and no villi. There are lots of inflammatory cells here. There are lots of goblet cells secreting about 1000 ml per day. The mucous is important for lubrication and creating an adhesive medium (important for the conversion of chyme into feces)
87
What controls large intestinal secretion
Tactile stimulation and local distention. Parasympathetics increase secretion via acetylcholine. Some emotions (stress) affect secretion (can lead to mucoid diarrhea)
88
What is cholera?
Infection causes by Vibrio cholerae in contaminated water/food. It causes severe diarrhea, which can lead to dehydration and death
89
Describe the cholera toxin
The toxin is made up of 2 different subunits. The B subunit binds to glycoproteins and other molecules on the surface of the enterocyte membrane with high affinity. The A subunit is inserted/released in the plasma mambrane, where it splits into two smaller subunits (A1 and A2). One of the new subunits activates adenylate cyclase. The concentration of cAMP increases (cAMP is a potent chloride secretagogue)
90
Describe the effects of the cholera toxin
It increases chloride secretion, which increases the amount of sodium and water that is secreted (hypersecretion). This causes severe diarrhea. Patients can pass 23 L of diarrhea/day
91
How are cholera patient's treated?
Oral rehydration therapy (ORT): it is important to measure the amount of diarrhea that is passed to ensure that at least the same amount of a salty/sweet solution (basically gatorade) is replaced.
92
Describe digestion
Starts in the mouth and continues in the stomach, and is completely done by the time it reaches the large intestin. There is mechanical digestion (chewing, churning of the stomach, etc.)
There is chemical digestion (acid hydrolysis, enzymatic digestion)
93
Describe absorption
Bringing the building blocks (nucleic acids, amino acids, carbohydrates, lipids) into the epithelial cells
Largely done in the small intestine (some is done in the stomach, like alcohol, aspirin and some other drugs, etc.)
Vitamins and minerals are mostly absorbed by the small intestine but some are absorbed in the large intestine
94
Describe transport
Nutrients from the epithelial cells are put into circulation (across the basolateral border)
95
Where are digestive enzymes secreted from?
Salivary glands
Gastric pits
Exocrine pancreas
Liver
96
What are brush border enzymes?
Aka tethered enzymes. They are enzymes that are physically attached to the apical membrane of the small intestine. They usually do the final steps of steps of digestion before absorption
97
What are the dietary carbohydrates
There are complex carbohydrates (polysaccharides like starch, glycogen and cellulose)
There are simple carbohydrates (disaccharides likes sucrose, lactose and maltose, and monosaccharides like glucose and fructose
98
Describe carbohydrate digestion
Amylase breaks down amylose, mostly into maltose. This digestion is all luminal. Amylase can be salivary, gastric or pancreatic
Brush border enzymes like sucrase-isomaltase (the sucrase breaks down sucrose, the maltase breaks down maltose) and lactase (breaks down lactose into monomers) also participate
99
Describe the absorption of carbohydrates
Monosaccharides are absorbed through the apical membrane of the epithelial cells via SGLT1 and GLUT5. SGLT1 is a secondary active transporter that pumps glucose and galactose. GLUT5 facilitates diffusion to move fructose
Monosaccharides cross the basolateral membrane via GLUT2 tranporter (facilitated diffusion)
100
What happens to galactose and fructose after absorption?
They are converted into glucose in the liver. They can be stored as glycogen or converted into lipids
101
Why is glucose absorbed via a secondarily active transporter?
Normal blood glucose is between 4 and 7 mM
Cytoplasmic glucose is about 10 mM
Luminal glucose ranges from 1 to 40 mM
Facilitated diffusion is almost always bidirectional. If the absorption of glucose was passive, right after a meal, glucose would easily be absorbed. However, between meals, when luminal glucose is closer to 1 mM, glucose would go down it's gradient into the lumen from the blood (you would die). Active transporters are unidirectional, so glucose can't be lost
102
Why is fructose absorbed via facilitated diffusion?
Blood fructose is 0 mM so there's none to be lost between meals
103
Describe protein digestion
It's much more complicated (there's 20 different monomers)
There's mechanical digestion (mastication). There's denaturation via the low pH of the stomach (globular proteins start unfolding). Acid hydrolysis cleaves peptide bonds randomly. There's enzymatic digestion - proteases specifically break down peptide bonds to create shorter polypeptides
104
What are the general types of peptidases?
Endopeptidases break down peptide bonds in the centre of the protein (pepsin, trypsin, chymotrypsin)
Exopeptidases break down at the terminal ends. Aminopeptidases cleave the amino terminal residue. Carboxypeptidases cleave the carboxy terminal residue. The end result: single amino acids, dipeptides and tripeptides
105
Describe protein absorption
Apical cotransporters, secondarily active transporters, carry amino acids, di- and tripeptides across the apical membrane of the epithelial cells. Amino acids are transported with a sodium ion. Di- and tripeptides are transported with a hydrogen ion. Cytoplasmic peptidases break down di- and tripeptides into amino acids (basolateral transporters can only transport amino acids)
106
Describe lipid digestion via lipases
Lipids are different; they aren't water soluble. We ingest triglycerides (saturated fats, unsaturated fats). We have salivary lipase and gastric lipase. These enzymes combined do a very small amount of lipid digestion because they can only work on the surface of lipid droplets. Lipases cleave two of the fatty acids, leaving a monoglyceride. Churning of the stomach keeps the lipid droplets suspended and small (but they are still relatively large)
107
Describe lipid digestion via bile salts
Bile salts emulsify lipid droplets and make smaller micelles (increased surface area)
108
Describe lipid absorption
It is poorly understood. Monoglycerides and free fatty acids are lipid soluble, so they easily diffuse across the plasma membrane and then, through a poorly understood mechanism, end up in the endoplasmic reticulum (ER). Within the smooth ER, monoglycerides and free fatty acids are reassembled into triglycerides. Then they are transported to the Golgi apparatus. Triglycerides, cholesterol and proteins are assembled into chylomicrons aka apolipoproteins (for transportation of lipids throughout the circulation). The proportions of triglyercides/proteins/cholesterol are variable. Chylomicrons leave the cell through exocytosis into the interstitial fluid. They are too large to be picked up by the capillary so they enter the lacteal (lymphatic vessels).
109
What happens to empty chylomicrons?
They are recycled
110
Describe water absorption
We secrete approx. 8.5 L/dayThe small intestine is the primary site of water absorption. We reabsorb 9 L via osmosis (more than we secrete because there's water in our diets)
111
What happens if there is poor uptake of water?
If there is poor uptake (can't absorb properly) e.g., because there is poor digestion of carbohydrates, they won't be absorbed and water follows -> diarrhea
112
What happens if there is too much uptake of water
If we absorb too much from the lumen, this leads to constipation
113
What are tight junctions?
Highly regulated multi-protein complex. They have a barrier function. They keep the epithelial cells together. There are contractile cytoskeletal elements, cytoplasmic complex and integral membrane proteins. They can open up and they can tighten up (barrier function).
