Case 2 Flashcards
physiologically, what is the stomach divided into?
two parts:
- Orad portion – this is the first 2/3 of the ‘body’ of the stomach.
- Caudad portion – this is the last 1/3 of the ‘body’ of the stomach + antrum.
what are the three motor functions of the stomach?
- Storage of large quantities of food until the food can be processed in the stomach, duodenum, and lower intestinal tract.
- Mixing of this food with gastric secretions until it forms a semifluid mixture called chyme.
- Slow emptying of the chyme from the stomach into the small intestine at a rate suitable for proper digestion and absorption by the small intestine.
storage function of the stomach
- how does food sit in stomach
- what does distention cause
- maximal capacity
• Food entering forms concentric circles of food in the orad portion of the stomach.
• The newest food is closest to the oesophageal opening, whilst the old food lies nearest to the outer wall of the stomach.
• When this food stretches the stomach wall, a ‘vagovagal reflex’ occurs.
• Signals are sent from the stomach to the brainstem and back, thus reducing the muscle tone of the muscular wall of the body of the stomach so that the wall can expand outwards progressively.
• This accommodates for greater quantities of food entering the stomach.
The maximal stomach volume/ capacity is between 0.8-1.5 litres.
what are digestive juices of the stomach secreted by and where are they found?
- The digestive juices of the stomach are secreted by the gastric glands, which are present in almost the entire wall of the body of the stomach except along the lesser curvature of the stomach.
- These come into direct contact with the food lying against the mucosal surface of the stomach.
as long as food is in the stomach, what happens?
- The digestive juices of the stomach are secreted by the gastric glands, which are present in almost the entire wall of the body of the stomach except along the lesser curvature of the stomach.
- These come into direct contact with the food lying against the mucosal surface of the stomach.
what are these mixing waves initiated by?
the gut wall basic electrical rhythm, consisting of electrical “slow waves” that occur spontaneously in the stomach wall.
what happens as these constrictor waves progress from the body of the stomach into the antrum?
- As the constrictor waves progress from the body of the stomach into the antrum, they become more intense.
- Some of these waves become extremely intense, providing powerful peristaltic action potential–driven constrictor rings that force the antral contents under higher and higher pressure toward the pylorus.
how do these constrictor rings also play an important role in mixing the stomach contents?
Each time a peristaltic wave passes down the antral wall toward the pylorus, it digs deeply into the food contents in the antrum.
The opening of the pylorus is small - only a few millilitres or less of antral contents are expelled into the duodenum with each peristaltic wave.
Also, as each peristaltic wave approaches the pylorus, the pyloric muscle itself often contracts, which further impedes emptying through the pylorus.
Therefore, most of the antral contents are squeezed upstream through the peristaltic ring toward the body of the stomach, not through the pylorus.
Thus, the moving peristaltic constrictive ring, combined with this upstream squeezing action, called “retropulsion,” is an exceedingly important mixing mechanism in the stomach.
what does the degree of fluidity of chyme leaving the stomach depend on?
on the relative amounts of food, water, and stomach secretions and on the degree of digestion that has occurred.
• Chyme appears like a murky semifluid or paste.
hunger contractions
- when do they occur
- what are they
- who most intense in
- what also triggered by
- what also experienced with this
- Hunger contractions occur in the stomach when it is has been empty for several hours or more.
- They are rhythmical peristaltic contractions in the body of the stomach.
- Hunger contractions are most intense in young, healthy people who have high degrees of GI tonus (i.e. a constant low-level activity of a body tissue, especially muscle tone).
- They are also triggered by a hypoglycaemic state.
- When hunger contractions occur in the stomach, the person sometimes experiences mild pain in the pit of the stomach, called hunger pangs.
what is stomach emptying brought about by?
strong peristaltic contractions in the stomach antrum.
what are stomach contractions mainly involved in? how do they change and what do they become involved in? what happens as the stomach becomes more empty?
- The stomach contractions are mainly involved in mixing the food as they are weak with regards to causing emptying of the stomach.
- However, for about 20%of the time while food is in the stomach, the contractions become intense, beginning in mid-stomach and spreading through the caudad stomach no longer as weak mixing contractions but as strong peristaltic, very tight ring-like constrictions that can cause stomach emptying.
- As the stomach becomes progressively more and more empty, these constrictions begin farther and farther up the body of the stomach, gradually pinching off the food in the body of the stomach and adding this food to the chyme in the antrum.
when pyloric tone is normal, how much can each strong peristaltic wave force into the duodenum?
up to several milliliters of chyme
thus, what do the peristaltic waves do?
- Cause mixing in the stomach.
2. Provide a pumping action called the “pyloric pump.”
what is the thickness of the circular wall muscle of the pylorus like compared to earlier portions of the stomach antrum? what state is it normally in? what is the pyloric circular muscle called? what does this allow and not allow through?
- Here the thickness of the circular wall muscle becomes 50 -100% greater than in the earlier portions of the stomach antrum, and it remains slightly tonically contracted.
- Therefore, the pyloric circular muscle is called the pyloric sphincter.
- Despite normal tonic contraction of the pyloric sphincter, the pylorus usually is open enough for water and other fluids to empty from the stomach into the duodenum with ease.
- Conversely, the constriction usually prevents passage of food particles until they have become mixed in the chyme to almost fluid consistency.
what is the degree of constriction of the pylorus affected by?
• The degree of constriction of the pylorus is increased or decreased under the influence of nervous and humoral reflex signals from both the stomach and the duodenum.
what is regulation of stomach emptying controlled by?
- The rate at which the stomach empties is regulated by signals from both the stomach and the duodenum.
- However, the duodenum provides by far the more potent of the signals, controlling the emptying of chyme into the duodenum at a rate no greater than the rate at which the chyme can be digested and absorbed in the small intestine.
describe and explain the effect of gastric food volume on rate of emptying
- Increased food volume in the stomach promotes increased emptying from the stomach.
- This increased emptying is not due to increased storage pressure of the food in the stomach, because in the usual normal range of volume, the increase in volume does not increase the pressure much.
- However, stretching of the stomach wall elicits local myenteric reflexes in the wall that greatly accentuate activity of the pyloric pump and at the same time inhibit the pylorus.
what is gastrin released by?
G cells of the antral mucosa
what is gastrin released as a result of?
Stretching of the stomach wall.
Presence of protein food contents in the stomach.
what are the functions of gastrin?
- It has potent effects to cause secretion highly acidic gastric juice by stomach glands:
Gastrin activates ECL (enterochromaffin-like) cells, which release histamine, which is the primary initiator for parietal cell acid production. - It has some effects on the motor function of the stomach:
It enhances the activity of the pyloric pump, thus promoting stomach emptying.
what effect does the duodenum have on stomach emptying?
• Upon food entering the duodenum, multiple nervous reflexes are initiated from the duodenal wall that pass back to the stomach to slow or even stop stomach emptying if the volume of chyme in the duodenum becomes too much.
what are the three routes that these reflexes from the duodenum are mediated through?
- Directly from the duodenum to the stomach through the enteric nervous system in the gut wall.
- Through extrinsic nerves that go to the prevertebral sympathetic ganglia and then back through inhibitory sympathetic nerve fibres to the stomach.
- Through the vagus nerves to the brainstem, where they inhibit the normal excitatory signals transmitted to the stomach through the vagi. (this pathway only plays a minor role)
what effects do these enterogastric inhibitory reflexes have?
• These parallel pathways have two effects on the emptying of the stomach:
- Strongly inhibit the pyloric pump propulsive contractions.
- Increase the tone of the pyloric sphincter.
what are the types of factors that are continually monitored in the duodenum and that can initiate enterogastric inhibitory reflexes?
- Degree of distention of the duodenum
- Degree of irritation of the duodenal mucosa (if any) – especially sensitive to this
- Degree of acidity of the duodenal enzyme – especially sensitive to this
When the pH of the chyme in the duodenum falls below about 3.5-4, the reflexes frequently block further release of acidic stomach contents into the duodenum until the duodenal chyme has been neutralised by pancreatic and other secretions. - Degree of osmolality of the chyme
Hypertonic and hypotonic (especially hypertonic) fluids elicit the inhibitory reflex.
Too rapid flow of non-isotonic fluids into the small intestine is prevented, thereby also preventing rapid changes in electrolyte concentrations in the whole body extracellular fluid during absorption of the intestinal contents. - Presence of certain breakdown products in the chyme, especially breakdown products of proteins and perhaps to lesser extent of fats
By slowing the rate of stomach emptying, sufficient time is ensured for adequate protein digestion in the duodenum and small intestine.
what is the stimulus for hormone release from the upper intestine?
fats entering the duodenum, although other foods can increase this hormone release to a lesser extent:
o Fats bind to receptors on the duodenal and jejunal epithelium, thus extracting different hormones from the epithelium.
o These hormones are then carried by blood to the stomach, where they inhibit the pyloric pump and at the same time increase the strength of contraction pyloric sphincter.
what is the hormone that has the most potent effect in regards to hormonal feedback to inhibit gastric emtpying?
cholecystokinin (CCK)
where is CCK released from and what is the stimulus?
released from the duodenal and jejunal mucosa in response to fatty substances in the chyme.
what hormone does CCK act as an inhibitor against?
• CCK acts as an inhibitor to block increased stomach motility caused by gastrin.
what are other inhibitors of stomach emptying?
the hormones secretin (opposite - don’t secrete chyme) and gastric inhibitory peptide (GIP).
where is secretin released from?
duodenal mucosa (S cells in the crypts of Lieberkuhn).
what is secretin released in repsonse to?
gastric acid passed from the stomach through the pylorus.
GIP
- what effect does it have
- where released from
- what released in response to
- what’s its primary function
o This has a general but weak effect of decreasing GI motility.
o Released from the duodenal and jejunal mucosa.
o Released in response to fat in the chyme, but to lesser extent carbohydrates as well.
o Although GIP weakly decreases the GI motility, its primary function is to stimulate secretion of insulin by the pancreas.
summarise the regulation of stomach emptying
• Emptying of the stomach is controlled only to a moderate degree by stomach factors such as the degree of filling in the stomach and the excitatory effect of gastrin on stomach peristalsis.
• Probably the more important control of stomach emptying resides in inhibitory feedback signals from the duodenum, including both enterogastric inhibitory nervous feedback reflexes and hormonal feedback by CCK.
• These feedback inhibitory mechanisms work together to slow the rate of emptying when
1. Too much chyme is already in the small intestine.
2. The chyme is excessively acidic, contains too much unprocessed protein or fat, is hypotonic or hypertonic, or is irritating.
• In this way, the rate of stomach emptying is limited to that amount of chyme that the small intestine can process.
what are the gastric factors that increase stomach emptying?
Increased stretching of the stomach wall – increased pressure in the stomach
Gastrin – enhanced pyloric pump + increased HCl production in parietal cells
what are the duodenal factors that decrease stomach emptying?
Nervous reflexes (via enteric nervous system, extrinsic nerves and vagus nerve) – inhibit pyloric pump + increase pyloric sphincter tone
The following factors affect the duodenal mucosa and initiate the nervous reflexes: • Distention • Irritation of mucosa • Acidity of digestive enzymes • Osmolality of chyme (hyper-/hypotonic) • Protein breakdown products
Hormonal feedback - inhibit pyloric pump + increase pyloric sphincter tone
The hormones are secreted due to the presence of fat in the duodenum.
The hormones released are:
• Secretin (released from duodenal mucosa in response to gastric acid) – inhibit gastrin, thus lowering acid secretion
• Cholecystokinin/ CCK (released from jejunal mucosa in response to fat in chyme) – inhibit gastrin, thus lowering acid secretion
• Gastric inhibitory peptide/ GIP(released from jejunal mucosa in response to fat in chyme) – weakly decrease GI motility
what are the two types of tubular glands that the stomach mucosa also has? what are they composed of? where are they located? how much of the stomach do they constitute?
- Oxyntic glands/ Gastric glands
Acid forming glands composed of three types of cells:
1) Mucous neck cells – secrete mucus
2) Peptic (chief) cells – large quantities of pepsinogen
3) Parietal (oxyntic) cells – HCl and intrinsic factor
These are located on the inside surfaces of the body and fundus of the stomach, constituting the proximal 80% of the stomach. - Pyloric glands
Secrete mainly mucus for protection of the pyloric mucosa from the stomach acid and they also secrete the hormone gastrin.
These are located in the antral portion of the stomach, the distal 20% of the stomach.
where si HCl formed?
- The parietal (oxyntic) cell contains large branching intracellular canaliculi.
- The HCl is formed at the villus-like projections inside these canaliculi and is then conducted through the canaliculi to the secretory end of the cell (the apical end).
what is the mechanism of HCl secretion in the gastric glands?
The movement and exchange of ions in and out of parietal cells is primarily powered by ATP from the numerous mitochondria present in the parietal cells.
1) Cl- ions are actively transported from parietal cell cytoplasm into the lumen of the canaliculus via a chloride pump. Na+ ions are actively transported out of the canaliculus into the cytoplasm of the parietal cell via a sodium pump. This creates a negative potential (-40 to -70 mV) in the canaliculus. This causes K+ ions (and some Na+ ions) to enter the canaliculus from the cytoplasm. Thus, in effect, mainly KCl and smaller amounts of NaCl enter the canaliculus.
2) Water dissociates into hydrogen ions (H+) and hydroxyl ions (OH-) in the cytoplasm. H+ ions are actively secreted into the canaliculus in exchange for K+ ions. This is catalysed by the H+/K+ ATPase (proton pump).
Also, Na+ ions are ions are actively reabsorbed by a separate sodium pump. Therefore, the Na+ ions and K+ ions that were initially secreted into the canaliculus have ben reabsorbed, whilst H+ ions have been added to the canaliculus. This gives us the HCl in the canaliculus.
3) Water passes into the canaliculus by osmosis because of the increased ionic concentration in the canaliculus. The final secretion from the canaliculus contains water, HCl (conc = 150-160mEq/L), KCl (conc = 15mEq/L) and small amounts of NaCl.
4) OH- combines with CO2 under the influence of carbonic anhydrase to form bicarbonate ions (HCO3-). These diffuse into the extracellular fluid in exchange for Cl- ions.
where is pepsinogen secreted by? what type of pepsinogen? what is their function?
• Different types of pepsinogen are secreted by the peptic (chief) cells of the gastric/oxyntic gland.
• All pepsinogens have the same function:
It has no digestive activity.
As soon as it comes into contact with HCl, it is activated to form active pepsin.
Pepsin functions as an active proteolytic enzyme for protein digestion, in an acid medium.
what is the optimum pH for pepsinogen? at what pH does it lose activity?
Optimum pH is 1.8 - 3.5 but above a pH of 5 it has almost no proteolytic activity and becomes completely inactivated is a short time.
describe regulation of pepsinogen secretion
• Regulation of pepsinogen secretion by the peptic cells in the oxyntic glands occurs in response to two types of signals:
1. Stimulation of peptic cells by acetylcholine released from the vagus nerves or from the gastric enteric nervous plexus.
2. Stimulation of peptic cell secretion in response to acid in the stomach.
Acid doesn’t stimulate the peptic cells directly, instead it elicits additional enteric nervous reflexes that support the original nervous signals to the peptic cells.
The rate of pepsinogen secretion is influenced by the amount of acid in the stomach.
what is intrinsic factor essential for?
the absorption of vitamin B12 in the ileum. (protein that binds to B12 and is required for B12 uptake in the ileum)
what is intrinsic factor secreted by?
parietal (oxyntic) cells along with the secretion of HCl.
what happens when the acid-producing parietal cells of the stomach are destroyed?
• When the acid-producing parietal cells of the stomach are destroyed, which frequently occurs in chronic gastritis, the person develops not only achlorhydria (lack of stomach acid secretion) but often also pernicious anemia because of failure of maturation of the red blood cells in the absence of vitamin B12 stimulation of the bone marrow.
describe the regulation of gastric acid
increase by histamine, ACh, gastrin
decrease by somatostatin, GIP, prostaglandin, secretin
where are bicarbonate ions produced? what is their action? how are they regulated?
- mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner’s glands (duodenum)
- neutralises acid
- increase pancreatic and biliary secretion with secretin
- HCO3- is trapped in mucus that covers the gastric epithelium
how are pyloric glands different to parietal cells? what do cells of the gland secrete?
- The pyloric cells are structurally similar to oxyntic glands but contain few peptic cells and almost no parietal cells.
- Instead, they contain mainly mucous cells that are identical with the mucous neck cells of the oxyntic glands.
• These cells secrete:
Small amounts of pepsinogen.
Large amounts of thin mucus that helps lubricate food movement, as well as to protect the stomach wall from digestion by the gastric enzymes.
describe surface mucous cells
- where are they
- what do they secrete
- what is the mucus like and why
- what stimulates these cells
- The entire surface of the stomach mucosa between glands has a continuous layer of a special type of mucous cells called simply “surface mucous cells.”
- They secrete large quantities of viscid mucus that coats the stomach mucosa, thus providing protection for the stomach and lubrication.
- This mucus is alkaline (presence of bicarbonate ions), therefore, the normal underlying stomach wall is not directly exposed to highly acidic, proteolytic stomach secretion.
- Even the slightest contact with food or any irritation of the mucosa directly stimulates the surface mucous cells to secrete additional quantities of this thick, alkaline, viscid mucus.
what are the only cells that secrete HCl?
parietal cells
which cells do parietal cells operate in close association with? describe this association
enterochromaffin-like cell (ECL cell)
ECL cells secrete histamine which binds to H2 histamine receptors on parietal cells.
This activates the parietal cells to form and secrete HCl.
Rate of formation and secretion of HCl is dependent on the amount of histamine secreted by ECL cells.
how are ECL cells activated?
- Gastrin – when G-cells of the antral mucosa come into contact with amino acids, they pass gastrin to ECL cells through the digestive juices, which in turn secrete histamine.
- Acetylcholine – this is released from stomach vagal nerve endings.
- Hormonal substances secreted by the enteric nervous system of the stomach wall.
where is gastrin secreted from?
by gastrin cells (G-cells) located in the antral mucsoa (pyloric glands).
what are the two forms that gastrin is secreted in?
a. G-34 = this contains 34 amino acids
b. G-17 = this contains 17 amino acids (and is more abundant)
what stimulates gastrin release and what effect does this have?
- When amino acids reach the antral end of the stomach, they have a stimulatory effects on the G-cells in the pyloric gland.
- This causes release of gastrin into the digestive juices of the stomach.
- The vigorous mixing of the digestive juices transports the gastrin rapidly to the ECL cells in the body of the stomach, causing release of histamine directly into the deep oxyntic glands, which stimulates the parietal cells to form and secrete HCl.
what are the phases of gastric secretion?
- Cephalic phase
- Gastric phase
- Intestinal phase
cephalic phase
- what is it
- what stimulates it
- what signals does this produce - from where to where
- This occurs before food enters the stomach, especially whilst in the mouth.
- It results from the sight, smell, thought, or taste of food.
- The greater the appetite, the more intense the stimulation.
- Neuronal signals from appetite centres of the amygdala and hypothalamus are transmitted through the dorsal motor nuclei of the vagi through the vagus nerves to the stomach.
what are the stimulatory effects of the cephalic phase? how important for gastric secretion?
• This phase has stimulatory effects on HCl secretion:
It stimulates the vagus nerve to release more ACh, thus activating more ECL and parietal cells.
It stimulates the vagus nerve to activate gastrin-releasing-peptide (GRP), which increases the secretion of gastrin, thus activating parietal cells.
• This phase accounts for about 20% of gastric secretion associated with eating a meal.
gastric phase
- when does this phase occur/what stimulates it
- what are stimulatory and inhibitory effects
- how important for gastric secretion
• This occurs once food has entered the stomach.
• This phase has both stimulatory and inhibitory effects:
Stimulatory effects on HCl secretion:
It stimulates the vagus nerve to release more ACh, thus activating more ECL and parietal cells.
It stimulates the vagus nerve to activate gastrin-releasing-peptide (GRP), which increases the secretion of gastrin, thus activating parietal cells.
It increases the pH of the food, thus causing an increase in gastrin secretion.
It stimulates secretagogues, which increase H+ secretion.
Inhibitory effects on HCl secretion (I think this means if there is less acid):
It inhibits the G-cells (antrum), which decreases the secretion of gastrin and so increases the pH in the stomach.
• This phase accounts for about 70% of gastric secretion associated with eating a meal.
intestinal phase
- what does it occur as a result of
- what are the stimulatory and inhibitory effects
- This occurs as a result of the presence of food in the upper portion of the small intestine, particularly in the duodenum.
- This phase has both stimulatory and inhibitory effects:
Stimulatory effect:
It stimulates the G-cells (duodenum), which secrete more gastrin, resulting in an increase in the secretion of H+.
Inhibitory effect: (bigger part of intestinal phase)
It inhibits chemoreceptors, which cause a decrease in nerve reflexes, thus decreasing H+ secretion.
Secretin, CCK and GIP increase the secretion of somatostatin, thus decreasing H+ secretion.
• The presence of food will continue to cause stomach secretion of small amounts of gastric juice because small amounts of gastrin is released by the duodenal mucosa.
how does chyme influence gastric secretion? what causes these influences?
- Chyme initially increases gastric secretion.
- However, later chyme inhibits gastric secretion.
- Presence of food in the small intestine initiates a reverse enterogastric reflex, transmitted through the myenteric nervous system and vagus nerves, that inhibits stomach secretion.
This reflex can be initiated by distending the small bowel, by the presence of acid in the upper intestine, by the presence of protein breakdown products, or by irritation of the mucosa. - The hormone secretin is secreted as a result of the presence of… (listed above). It is important in the control of pancreatic secretion. Secretin opposes stomach secretion.
Other hormones have a slight effects on inhibiting gastric secretion – GIP, vasoactive intestinal polypeptide and somatostatin.
what is the purpose of intestinal factors inhibiting gastric secretion?
to slow passage of chyme from the stomach when the small intestine is already filled or already overactive.
what does somatostatin do?
inhibits G-cells, ECL cells and if there is an excess of acid in the duodenum, it inhibits the parietal cells.
is gastric juice secreted in the interdigestive period?
Yes
• This is non-oxyntic secretion, consisting mainly of mucus, but little pepsin and almost no acid.
• Emotional stimuli increase interdigestive gastric secretion.
what are the actions of gastrin?
- increase gastric H+ secretion
- increase growth of gastric mucosa
- increase gastric motility
where is cholecystokinin released by?
I cells (duodenum, jejunum)
what is the action of cholecystokinin?
- increase pancreatic secretion
- increase gall bladder contraction
- decrease gastric emptying
what is the action of secretin?
- increase pancreatic HCO3- secretion
- decrease gastric acid secretion
- increase bile secretion
where is somatostatin produced?
D cells (pancreatic islets, GI mucosa)
what is the action of somatostatin?
- decrease gastric acid and pepsinogen secretion
- decrease pancreatic and small intestine fluid secretion
- decrease gallbladder contraction
- decrease insulin and glucagon release
(sommm, hoommm = relax, calm, less acid, less everything)
what enzyme in saliva breaks down carbohydrates? what does this enzyme do?
ptyalin = a-amylase
• This enzyme hydrolyzes starch into the disaccharide maltose and other small polymers of glucose that contain three to nine glucose molecules.
what percentage of all starches are hydrolysedby the time the food has been chewed and is swallowed? what about by the time it has reached the stomach?
5%
• By the time the food reaches the stomach, 30-40% of all starches have been hydrolysed mainly to form maltose.
• Starch digestion sometimes continues in the body and fundus of the stomach for as long as 1hour before the food becomes mixed with the stomach secretions.
what happens to salivary amylase in the stomach?
• Then activity of the salivary amylase is blocked by acid of the gastric secretions because the amylase is essentially non-active as an enzyme once the pH of the medium falls below about 4.0.
at what pH is pepsin most active? when is it inactive?
- Pepsin is most active at a pH of 2.0 to 3.0 and is inactive at a pH>5.0.
- For pepsin to cause digestive action on protein, the stomach juices must be acidic.
how are gastric glands responsible for getting the optimum pH for pepsin?
• The gastric glands (parietal cells) secrete a large quantity of HCl at a pH = 0.8, but by the time it is mixed with the stomach contents and with secretions from the non-oxyntic glandular cells of the stomach, the pH then averages around 2.0 to 3.0, a highly favorable range of acidity for pepsin activity.
what is pepsin involved n the digestion of?
- One of the important features of pepsin digestion is its ability to digest the protein collagen, an albuminoid type of protein that is affected little by other digestive enzymes.
- Collagen is a major constituent of the intercellular connective tissue of meats.
- In persons who lack pepsin in the stomach juices, the ingested meats are less well penetrated by the other digestive enzymes and, therefore, may be poorly digested.
- Pepsin only initiates the process of protein digestion, usually providing only 10-20% of the total protein digestion to convert the protein to proteoses, peptones, and a few polypeptides.
- This splitting of proteins occurs as a result of hydrolysis at the peptide linkages between amino acids.
gastritis
- what is it
- is it serious
- what caused by
- treatment
- what are common irritants that are especially damaging to the protective gastric mucosal barrier
- Gastritis – inflammation of the gastric mucosa.
- The inflammation of gastritis may be only superficial and therefore not very harmful, or it can penetrate deeply into the gastric mucosa, in many long-standing cases causing almost complete atrophy of the gastric mucosa.
- In a few cases, gastritis can be acute and severe, with ulcerative excoriation of the stomach mucosa by the stomach’s own peptic secretions.
- Gastritis is caused by chronic bacterial infection of the gastric mucosa.
- This is treated by an intensive antibacterial therapy.
• In addition, certain ingested irritant substances can be especially damaging to the protective gastric mucosal barrier (mucous glands and the tight epithelial junctions between the gastric lining cells), often leading to severe acute or chronic gastritis.
Two of the most common of these substances are excesses of alcohol or aspirin.
what does the ‘gastric barrier’ consist of? what does form a barrier against?
- Highly resistant mucous cells that secrete a viscid and adherent mucus.
- Tight junctions between the adjacent epithelial cells.
- These two form a barrier against gastric absorption of food into the blood.
- The gastric barrier is resistant to diffusion of ions across it.
what happens in gastritis due to resistant barrier being removed?
- The permeability of the barrier is greatly increased.
Hydrogen ions can now diffuse into the stomach epithelium, leading to stomach mucosal damage and atrophy. - The mucosa becomes susceptible to digestion by the peptic digestive enzymes.
This causes gastric ulcers.
what is gastric atrophy? what does it lead to?
- Gastric atrophy is the damage to the mucosal glands of the stomach, such that little or no gastric gland digestive secretion remains.
- Gastric atrophy can also occur as a result of an autoimmune response against the gastric mucosa.
- Loss of stomach secretions in gastric atrophy leads to ‘achlorydria’ and, occasionally, ‘pernicious anaemia’.
what is achlorhydria?when is it diagnosed? what does this cause?
- Achlorhydria – this means that the stomach fails to secrete HCl.
- Hypochlorhydria – this literally means “decreased acid secretion”.
- It is diagnosed when the pH of the gastric secretions fails to decrease below 6.5 after maximal stimulation.
- When acid is not secreted, pepsin also usually is not secreted; even when it is, the lack of acid prevents it from functioning because pepsin requires an acid medium for activity.
describe how intrinsic factor is involved with B12 absorption
- Intrinsic factor must be present for absorption of vitamin B12 from the ileum.
- The intrinsic factor binds with vitamin B12 in the stomach and protects it from being digested and destroyed as it passes into the small intestine.
- Then, when the intrinsic factor–vitamin B12 complex reaches the terminal ileum, the intrinsic factor binds with receptors on the ileal epithelial surface.
- This in turn makes it possible for the vitamin B12 to be absorbed.
what is pernicious anaemia?
- In the absence of intrinsic factor, only about 1/50 of the vitamin B12 is absorbed.
- Vitamin B12 is not made available from the foods to cause young, newly forming red blood cells to mature in the bone marrow.
- This is called pernicious anaemia.
peptic ulcers
- what are they
- how common
- most common symptom
- most serious complicatino
- Peptic Ulcer – localised breach of the gastric or duodenal mucosa that extends through the mucosa into the submucosa or muscularis propria, caused by the digestive action of gastric juice or upper small intestinal secretions.
- Epidemiology – 10% of UK population during life
- Most common symptom is pain.
- Most serious complication is bleeding or perforation which are life threatening.
ulcer = acid/enzyme damage to stomach or intestinal wall
what are the causes (not specific) of peptic ulcers?
- Excess secretion of acid and pepsin by the gastric mucosa.
- Diminished ability of the gastrodudenal mucosal barrier to protect against the digestive properties of the stomach acid-pepsin secretion.
- Occur due to increase acid and/or decrease protection
what are the mechanisms for protection from gastric juices?
- Any area exposed to gastric juices is well supplied by mucous glands to provide a viscid coating of alkaline mucus.
- The duodenum is protected by intestinal secretions.
An important secretion is pancreatic secretion – this contains large amounts of sodium bicarbonate that neutralise the HCl of the gastric juice, thus also inactivating pepsin and preventing digestion of the mucosa. - Also, large amounts of bicarbonate ions are provided in:
The secretions of the large Brunner’s glands in the proximal duodenal wall. This gland also secretes mucus which helps provide an alkaline environment.
In bile coming from the liver.
what are the feedback mechanisms for neutralisation of gastric juices?
- When excess acid enters the duodenum, it reflexly inhibits gastric secretion and peristalsis in the stomach, both by nervous reflexes and by hormonal feedback from the duodenum, thereby decreasing the rate of gastric emptying.
- The presence of acid in the small intestine liberates secretin from the intestinal mucosa, which then passes by way of the blood to the pancreas to promote rapid secretion of pancreatic juice. This juice causes neutralization of the acid.
what are specific causes of peptic ulcers in humans?
1) Bacterial Infection by Helicobacter Pylori (H-pylori)
2) NSAIDS (e.g. Aspirin)
3) Zollinger-Ellison Syndrome
4) Other Causes
- Smoking
- Alcohol
- Caffeine
- Stress ulcers (most likely occur when you are already under medical care for a major illness, surgical procedure, trauma, or injury – the presence of a stress ulcer adds another complication to your other medical conditions that lead to the ulcer)
- Steroids, Crohn’s, drugs…
what is H. pylori? how common?
are flagellated gram negative bacteria found on the luminal surface of the gastric epithelium that induces chronic mucosal inflammation.
- 50% of people across world are colonised with H. Pylori, but only 0.5% in this country
what does H. pylori contain high levels of?
the enzyme urease - these bacteria metabolise urea