Lecture 4: gastrointestinal Function Flashcards
What functions do GI peptides regulate in the GI tract
Contraction and relaxation of smooth muscle wall and sphincters
Secretion of enzymes for digestion
Secretion of fluid and electrolytes
Trophic (growth) effects
Some regulate secretion of other GI peptides
GI peptides: Hormones
- What are they secreted by
- Where are the target cells, local or elsewhere?
- Examples of the peptide
Peptides released from endocrine cells of GI tract
Secreted into portal circulation and enter systemic circulation
Target cells may be in GI tract or may be located elsewhere in body
Gastrin, Cholecystokinin, Secretin, and Gastric Inhibitory Peptide
GI peptides: Pancrines
- What are they secreted by
- Where are the target cells, local or elsewhere?
- Examples of the peptide
Secreted by endocrine cells of GI tract
Act locally within same tissue that secretes them
Somatostatin and Histamine
GI peptides: Neurocrines
- What are they secreted by
- Examples of the peptide
Released by neurons of GI tract following an Action Potential
ACh, norepinephrine, Vasoactive Intestinal Peptide (VIP), Gastrin-Releasing Peptide (GRP), Neuropeptide Y, and Substance P
GI peptides: Gastrin
- What are they secreted by
- Stimuili
Inhibit/stimulate what?
Secreted by G cells in stomach in response to eating
Stimuli include proteins, distention of stomach, and vagal stimulation
Gastrin-releasing peptide (GRP) is released from vagal nerve endings onto G cells
Secretion is inhibited by low pH in stomach
Promotes H+ secretion by gastric parietal cells
Stimulates growth of gastric mucosa
GI peptides: Cholecytsokinin:
Secreted by.. in response to…
5 Actions
Cholecystokinin
Secreted by I cells of small intestine in response to fatty acids and small peptides
5 Actions:
- Contraction of gallbladder
Eject bile from gallbladder into small intestine necessary for emulsification lipids
- Secretion of pancreatic enzymes
Digest lipids, carbohydrates, and proteins - Secretion of bicarbonate (HCO3-) from pancreas
- Growth of exocrine pancreas and gallbladder
-Inhibition of gastric emptying
Ensures adequate time for digestive and absorptive
GI peptides: Secretin:
Secreted by what cells… in response to…
Purpose
Secreted by S cells of duodenum in response to H+ and fatty acids
Promotes secretion of pancreatic HCO3-
Neutralizing H+ allows for pancreatic enzymes to digest fats
Inhibits effects of gastrin on parietal cells (H+ secretion and growth)
GI peptides: Gastric Inhibitory Peptide:
Secreted by… in response to…
stimulates and inhibits..
Secreted by small intestine in response to all 3 types of nutrients
Stimulates insulin secretion by pancreas
Inhibits gastric H+ secretion
GI Pancrines: Somastatin
Secreted by.. in response to…
Inhibits..
Secreted by endocrine cells in response to decreased luminal pH
Inhibits secretion of other GI hormones
Inhibits gastric H+ secretion
GI Pancrines: Histamine
Secreted by…
Secreted in H+-secreting region of stomach
Stimulates H+ secretion by gastric parietal cells (along with gastrin and ACh)
GI Neurocrines:
Where is Ach released from
Where is Norpinephrine released from
ACh (released from cholinergic neurons)
Norepinephrine (released from adrenergic neurons)
What does gastirc muscosal cells secrete and their assosicated purpose
HCl and pepsinogen initiate protein digestion
Intrinsic factor required for absorption of vitamin B12
Mucus protects gastric mucosa from HCl
Cell types of gastric mucosa
Body of stomach contains oxyntic glands
- Parietal cells → HCl and Intrinsic Factor
- Chief cells → Pepsinogen
Antrum of stomach contains pyloric glands
- G cells → Gastrin into the circulation
- Mucous neck cells → Mucus, HCO3-, and Pepsinogen
Cell type (below), location (body or antrum of stomach) and secretion
- Parietal Cells
- Cheif Cells
- G cells
- Mucous cells
- Body, HCl and intrinsitic factor
- Body, pepsinogen
- Antrum, Gastrin
- Antrum, Mucous, pepsingon and HCO3-
How does Ach regulate HCl secretion?
Released from..
Binds to..
Drug that prevents HCl release..
Released from vagus nerve
Binds to receptors on parietal cells
Produces H+ secretion by parietal cells
Atropine blocks muscarinic receptors on parietal cells
How does Histamine regulate HCl secretion?
Released from..
Binds to..
Drug that prevents HCl release..
Released from mastlike cells in gastric mucosa
Binds to H2 receptors on parietal cells
Produces H+ secretion by parietal cells
Cimetidine blocks H2 receptors
How does gastrin regulate HCl secretion?
Released from..
Binds to.. to simtulate…
Gastrin
Released into circulation by G cells of stomach antrum
Binds to receptors on parietal cells
Stimulates H+ secretion
Phases of acid secretion: Cephallic
Stimulus and diagram
sight, smell, taste or thought of food.
These stimuli, processed by the brain, activate enteric neurons via parasympathetic preganglionic neurons traveling in the vagus nerve.
Lecture slide
Phases of acid secretion: Gastric
Stimulus and diagram and role of food as a buffer
Lecture slide for diagram
Food in the stomach, which stimulates acid secretion.
Peptides and amino acids in food stimulate G cells to release gastrin (blue).
Food also acts as a buffer, raising the pH and thus removing the stimulus for somatostatin secretion (light blue-green).
Phases of acid secretion: Intestinal
Chyme effect
What is enterogastrones
Diagram
Lecture slides
Chyme enters the duodenum, intestinal phase stimuli activate negative feedback mechanisms to reduce acid secretion and prevent the chyme from becoming too acidic.
Enterogastrones are hormones that inhibit stomach processes (in this case, acid secretion).
CCK, secretin, GLP-1, and GIP
Maldigestion vs Malabsorption definition
Maldigestion:
impaired breakdown of nutrients (carbohydrates, protein, fat) to absorbable splitproducts (mono-, di-, or oligosaccharides; aminoacids; oligopeptides; fatty acids; monoglycerides)
Malabsorption:
defective mucosal uptake and transport of adequately digested nutrients including vitamins and trace elements.
Malabsorption symptoms diagnosis
Malabsorption causes diarrhea, weight loss, and bulky, extremely foul-smelling stools.
The diagnosis is based on typical symptoms along with testing of stool samples for fat and sometimes examination of a tissue specimen removed from the lining of the small intestine.
Mechanism of H.Pylori causing peptic uclers
- H. pylori secretes urease (generates ammonia), protease (breaks down glycoprotein in the gastric mucus) or phospholipases.
- Bacterial lipopolysaccharide attracts inflammmatory cells to the mucosa. Neutrophils release myeloperoxide.
- A bacterial platelet-activating factor promotes thrombotic occlusion of surface capillaries.
- Mucosal damage allows leakage of tissue nutrients in the surface microenvironment , sustaining the bacillus.
- Damage of the protective mucosal layer. The epithelial cells are exposed to the damaging effect of acid-peptic digestion.
- Inflammation of the gastric mucosa.
- Chronically inflamed mucosa more susceptible to acid- peptic injury and prone to peptic ulceration.
Ulcers occur at sites of chronic inflammation .
Other causes of Peptic ulcers?
Peptic ulcer caused due to high gastrin level (increased parietal mass) and excess acid production.
Peptic ulcers caused due to impaired mucosal defense.
The gastric acid and pepsin levels are normal and no H.pylori are present:
- Chronic use of aspirin causes suppression of mucosal prostaglandin and direct irritative topical effect.
- Repeated use of corticosteroid in high dose.
- Cigarette smoking impair healing and favour recurrences.
- Alcoholic cirrhosis.
What is pyloric obstruction and characteristics of it?
The outlet of the stomach is constricted by the contraction of an ulcer, malignancy or congenital abnormality.
Obstruction is characterized by vomiting, nausea, abdominal detention and loss of hydrochloric acid, leading to severe hypochloremic metabolic alkalosis.
Zollinger-Ellison syndrome
A rare condition characterized by severe and recurrent peptic ulcers in the stomach, duodenum, and upper small intestine, caused by a tumor, or tumors, usually found in the pancreas.
The tumor secretes the hormone gastrin, which stimulates the stomach and duodenum to produce large quantities of acid, leading to ulceration.
How does Laxatives cause constipation
Due to laxative clearing out the intestine, this causes longer time to refil it, thus misconception of constipation
- Enteral loss of water and salts causing release of aldosterone
- Stimulates reabsorption in intestine but increases renal excretion of K+
- Double loss of K+ (hypokalemia) which reduces peristalsis.
Relevant tests for chronic diarrhoea
Bile acid malabsorption testing
Assess malabsorption of vitamin B12
Dissacharides testing: maltase, lactase and sucrase on biopsy sample
Hormone measurement
Intestine Functions
Recovery of water and electrolytes from ingesta
Formation and storage of feces
Microbial fermentation
Common intestinal disorders:
Crohns: Inflammatory bowel disease (not restricted to either intestine but occurs from any point from mouth ot anus )
Colon polyps - in large intestine and not cancerous but can lead to colon cancer.
Diverticular Disease:
Can be found in both small and large intestine, but typically large intestine. Occurs when there is formation of pouches in the intestinal wall
Intestinal parasites:
Tapeworm or roundworm in intestines
Ulcerative colitis
An inflammatory bowel disease than is typically limited to large intestine
IBD (inflammatory bowel disease) factors
visceral hyperalgesia,
genetic and environmental factors
infection, inflammation, gut motility
psychological factor
Tests to detect Lactose intolerant
Hydrogen breath test:
if lactose is not digested in the small intestine, it passes into the large intestine and is fermented by microbes to a number of products, including hydrogen, which can be detected in breath; in normal circumstances, hydrogen is present in extremely low concentrations in exhaled breath.
Genetic testing: simple tests are now available to determine the lactase polymorphism associated with intolerance.
Lactose tolerance test: blood samples are collected at intervals following consumption of a lactose solution and assayed for glucose.
The measurement of intestinal disaccharidases (lactase, sucrase, isomaltase or palatinase, and maltase) through a small bowel biopsy is considered the gold standard for diagnosing Genetic Sucrase-Isomaltase Deficiency.
Faecal fat quantitative and Qualitative tests
quantitative:
“Gold standard” to diagnose maldigestion
72 hour collection optimal
Normal < 7 g/day
Qualitative
Random spot sample
Sudan stain
Semi-quantitative (#/size of droplets)
Less sensitive for mild-moderate steatorrhea
