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Gastrointestinal
FA complete review part 2 Physiology
Question | Answer |
---|---|
What cells produce Gastrin? | G cells |
Where are G cells located? | Antrum of Stomach and Duodenum |
What actions are performed by Gastrin? | Increase in: - Gastric H+ secretion - Growth of gastric mucosa - Gastric motility |
Chronic use of PPI can cause an increase in secretion of which GI regulatory substance? | Gastrin |
What regulatory substance is seen in increased levels by chronic atrophic gastritis (H. pylori)? | Gastrin |
Gastrinomas produce elevated levels of ______________. | Gastrin |
What change in pH would cause an decrease in Gastrin production? | pH < 1.5 |
What conditions lead to the increase release of Gastric? | Increase by stomach distension/ alkalinization, amino acids, peptides, vagal stimulation via gastrin-releasing peptide (GRP) |
What substance is secreted by D cells? | Somatostatin |
Where are found D cells? | Pancreatic islets, and GI mucosa |
Which cells secrete somatostatin? | D cells |
What is the main role of Somatostatin? | Inhibits secretion of various hormones |
Analog of Somatostatin? | Octreotide |
What is the main use for Octreotide? | Acromegaly |
What drug is often used for treatment of Acromegaly? | Octreotide |
What are conditions often treated with Octreotide? | Acromegaly, Carcinoid syndrome, and variceal bleeding |
List of actions of Somatostatin: | Decrease release of: 1. Gastric acid and pepsinogen secretion 2. Pancreatic and small intestine fluid secretion 3. Gallbladder contraction 4. Insulin and glucagon release |
What substance decreases the release of insulin and glucagon? | Somatostatin |
What does the increase the release of Somatostatin? | Acid |
Vagal stimulation has what effect on Somatostatin? | Decrease release of Somatostatin |
What cells secrete Cholecystokinin? | I cells |
Which GI structures have I cells? | Duodenum and Jejunum |
I cells secrete | Cholecystokinin (CCK) |
What compounds increase the release of CCK? | Fatty acids and amino acids |
What actions are increased/ speed up by the release of CCK? | Pancreatic secretion and Gallbladder contraction, and Sphincter of Oddi relaxation. |
On which pathways does CCK act on to cause pancreatic secretions? | Neural muscarinic pathways |
What is the effect of CCK on gastric emptying? | Decreases |
S cell secrete ______________. | Secretin |
Which part of small intestine have S cells? | Duodenum |
What Pancreatic substance secretion is increased by Secretin? | HCO3- |
What is the role of the increasing amount to HCO3- in the duodenum? | Neutralize gastric acid, allowing pancreatic enzymes to function |
Which regulatory GI substance is secreted by K cells in the duodenum and Jejunum? | Glucose-dependent insulinotropic peptide |
What is another name for Glucose-dependent insulinotropic peptide? | GIP |
What conditions lead to an increase release of GIP? | - Fatty acids - Amino acids - Oral glucose |
What is the exocrine function of GIP? | Decreased gastric H+ secretion |
What is the Endocrine function of GIP? | Increase insulin release |
Motilin is secreted by the _______ _____________. | Small intestine |
What is the role or function of Motilin? | Produces migrating motor complexes (MMCs) |
What condition increases the production/release/secretion of Motilin? | Fasting state |
What is a common Motilin receptor agonist? | Erythromycin |
What is the MC use for Motilin receptor agonists? | Stimulate intestinal peristalsis |
What substance produces MMCs? | Motilin |
What GI structures produce VIP? | 1. Parasympathetic ganglia in sphincters 2. Gallbladder 3. Small intestine |
Known VIP tumor? | VIPoma |
non-a, non-B islet cell pancreatic tumor that secretes VIP? | VIPoma |
What are the known features caused by a VIPoma? | Watery diarrhea, Hypokalemia, and Achlorhydria |
WDHA | Mnemonic for VIPoma signs and symptoms |
What are the two actions or roles of VIP? | 1. Increase intestinal water and electrolyte secretion 2. Increase relaxation of intestinal smooth muscle and sphincters |
Which conditions lead to the increase secretion of VIP? | Distention and vagal stimulation |
What are the GI functions of Nitric oxide? | Increase smooth muscle relaxation, including the lower esophageal sphincter (LES) |
Which GI substance deficiency or loss is associated with the development of Achalasia? | Nitric oxide |
Achalasia can be partially due to the loss of _______________. | Nitric oxide |
Why is the deficiency of NO associated with Achalasia? | NO serves to relax the SM of LES |
Which GI structure/organ secretes Ghrelin? | Stomach |
GI relulator substnce responsable for incrased appetite? | Ghrelin |
What decreases the secretion of Ghrelin by the stomach? | Food |
In a fasting state, the release of Ghrelin is increased or decreased? | Increased |
Which congenital condition is characterized by elevated levels of Ghrelin? | Prader-Willi syndrome |
A decrease in Ghrelin secretion is seen with: | Gastric bypass surgery |
Which cells are known to secrete Intrinsic factor? | Parietal cells of the stomach |
What is the role or function of the Intrinsic factor (IF)? | Required for B12 uptake in the terminal ileum |
Vitamin B12-binding protein. | Intrinsic factor (IF) |
What is the result of the autoimmune destruction of parietal cells of the stomach? | Chronic gastritis and pernicious anemia (lack of IF) |
Which two GI secretory products are known to be secreted by Parietal cells of the stomach? | Intrinsic factor and Gastric acid |
Which substance decrease the stomach pH? | Gastric acid |
What actions/ substances produce an increase release of Gastric acid? | 1. Histamine 2. Vagal stimulation (ACh) 3. Gastrin |
Gastric acid is inhibited by: | 1. Somatostatin 2. GIP 3. Prostaglandin 4. Secretin |
Chief cell of the stomach secrete? | Pepsin |
Where are the Chief cells that secrete pepsin? | Stomach |
What is the main responsibility of Pepsin? | Protein digestion |
Protein digestion is done by: | Pepsin secreted by stomach Chief cells |
What is the inactive form of pepsin? | Pepsinogen |
What is pepsinogen? | Inactive form of pepsin |
How is Pepsinogen converted into pepsin? | Presence of H+ |
What would be the effect on Pepsin/Pepsinogen in a environment lacking of H+? | No conversion of pepsinogen into pepsin (active) |
What are 2 know actions that increase release of Pepsin? | 1. Vagal stimulation (ACh) 2. Local acid |
Vagal stimulation causes ____________________. | Increased concentration of ACh |
Which are the sources of Bicarbonate? | 1. Mucosal cells 2. Brunner glands |
Mucosal cells of which organs secrete bicarbonate, or a source of bicarbonate? | Stomach, doudenum, salivary glands, and pancreas |
Brunner glands are in the _________________. | Duodenum |
Which GI regulatory substance neutralizes acid? | Bicarbonate |
What causes an increase release of Bicarbonate? | Pancreatic and biliary secretion with secretin |
What is trapped in mucus that covers the gastric epithelium? | Bicarbonate |
What are three important cells located in the Duodenum? | I cells, S cells, and K cells. |
Which part of the stomach holds most of the mucous cells and D cells? | Antrum |
What cells are often found in the Body of the stomach? | Chief cells and Parietal cells |
What is the main effect of the Enterochromaffin-like cells? | Increased gastrin levels |
What substance is release by ECL cells? | Histamine |
What is the effect of Histamine on Parietal cells? | Increase secretion of IF and HCl |
What is the main role of a-amylase? | Starch digestion |
What is the role of Lipases? | Fat digestion |
What is the main role of Proteases? | Protein digestion |
Pancreatic proteases main role is to digest ______________. | Protein |
What are common Pancreatic secretions? | a-amylase, lipases, proteases, and trypsinogen |
What enzyme converts Trypsinogen into is active form (trypsin)? | Enterokinase/enteropeptidase |
Brush-border enzyme on duodenal and jejunal mucosa that converts trypsinogen into trypsin? | Enterokinase/enteropeptidase |
What are some common Proteases? | Trypsin, Chymotrypsin, elastase, carboxypeptidases |
What is another name for proenzymes? | Zymogens |
Which kind of sugars are the only ones absorbed by enterocytes? | Monosaccharides |
What are some common monosaccharides? | Glucose, galactose, and fructose |
Which monosaccharides are taken up by the cell through SGLT1? | Glucose and Galactose |
Which protein channel is used by Galactose and glucose for their uptake into the enterocyte? | SGLT1 |
SGLT is _______ dependent. | Na+ |
How is Fructose taken up by the enterocyte? | Via facilitated diffusion by GLUT5 |
Which GLUT is used by Fructose? | GLUT5 |
Which GLUT is used by all monosaccharides to be transported to the blood? | GLUT2 |
What is the D-xylose absorption test? | Simple sugar that requires intact mucosa for absorption, but does not require digetive enzymes |
What is one important use for the D-xylose test? | Distinguish GI mucosal damage from other causes of malabsorption |
Where is Iron absorbed? | Duodenum |
What important water soluble vitamin is absorbed in the small bowel? | Folate |
Where is Vitamin B12 absorbed? | Terminal ileum |
What is required for Vitamin B12 to be absorbed by the terminal ileum? | Intrinsic factor |
What else is absorbed along terminal ileum with cobalamin? | Bile salts |
Iron Fist, Bro? | Mnemonic to recall absorption of Fe (iron- duodenum), Fist (folate- small bowel), Bro (Vit B12 -- terminal ileum |
Unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum. | Peyer patches |
What structure contain specialized M cells that sample and present antigens to immune cells? | Peyer patches |
What are the antigen presenting specialized cells found in Peyer patches? | M cells |
What does the differentiation of germinal center B cells of Peyer patches convert into? | IgA-secreting plasma cells |
What is the purpose for IgA-secreting plasma cells in Peyer patches to travel to the lamina propria? | To receive protective secretory component |
How is Bile composed? | Bile salts + phospholipids + cholesterol + bilirubin + water + ions |
What properties of bile make it water soluble? | Bile salts (bile acids conjugated to glycine or taurine. |
What is the end result of bile acids conjugation with glycine or taurine? | Makes bile water soluble |
What enzyme catalyzes rate-limiting step of bile acid synthesis? | Cholesterol 7a-hydroxylase |
What are the 3 main functions of bile? | 1. Digestion and absorption of lipids and fat-soluble vitamins 2. Cholesterol excretion 3. Antimicrobial activity |
What conditions are associated with a decreased absorption of bile acids in the ileum? | Short bowel syndrome and Crohn disease |
Why is a patient with Crohn disease seen with abnormal fat absorption? | Due to decrease absorption of enteric bile salts in the distal ileum |
What kind of kidney stones are seen with abnormal bile absorption? | Calcium Oxalate kidney stones |
Increased levels of fat, due to decreased bile absorption in the distal ileum can produce ---> | Calcium Oxalate kidney stones |
What enzyme converts Heme ito biliverdin? | Heme oxygenase |
What is the reduced form of Biliverdin? | Bilirubin |
Direct bilirubin: | - Conjugated with Glucuronic acid -Water soluble |
Indirect bilirubin: | Unconjugated and water insoluble |
Direct bilirubin is conjugated with _________________________. | Glucuronate |
Which bilirubin state is water soluble? | Direct bilirubin |
Which organs removes unconjugated bilirubin? | Liver |
Conjugated bilirubin is removed/excreted from the body by ___________ or __________. | Urine or feces |
What is the enzyme involved in the conversion of Unconjugated bilirubin to Conjugated bilirubin? | UDP-glucuronosyltransferase |
Where is unconjugated bilirubin formed? | Macrophages |
At which point is albumin added to unconjugated bilirubin? | In the bloodstream |
At what organ is Direct (conjugated) bilirubin formed? | Liver |
What compound gives urine its yellow color and feces its brownish color? | Bile |
Most (80%) of bilirubin is excreted in the form of? | Stercobilin |