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85 Cards in this Set
- Front
- Back
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What are the GI regulatory and secretory substances released in the stomach? |
Regulatory:
- Gastrin Secretory: - Intrinsic Factor - Gastric acid - Pepsin - HCO3- |
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What are the GI regulatory and secretory substances released in the duodenum?
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Regulatory:
- Cholecystokinin - Glucose-dependent insulinotropic peptide - Motilin - Secretin - VIP Secretory: - HCO3- |
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What are the GI regulatory and secretory substances released in the jejunum?
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Regulatory:
- Cholecystokinin - Glucose-dependent insulinotropic peptide - Motilin - VIP |
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What are the GI regulatory and secretory substances released in the ileum?
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Regulatory:
- Motilin - VIP |
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What is the source of Cholecystokinin?
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I cells (duodenum and jejunum)
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What is the source of Gastrin?
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G cells (antrum of stomach)
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What is the source of Glucose-dependent insulinotropic peptide?
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K cells (duodenum and jejunum)
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What is the source of Motilin?
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Small intestine
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What is the source of Secretin?
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S cells (duodenum)
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What is the source of Somatostatin?
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D cells (pancreatic islets and GI mucosa)
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What is the source of Vasoactive Intestinal Peptide (VIP)?
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- Parasympathetic ganglia in sphincters
- Gallbladder - Small intestine |
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What is the source of Intrinsic Factor?
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Parietal cells in stomach
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What is the source of gastric acid?
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Parietal cells in stomach
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What is the source of Pepsin?
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Chief cells in stomach
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What is the source of HCO3-?
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- Mucosal cells in stomach, duodenum, salivary glands, pancreas
- Brunner glands in duodenum |
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What is secreted from I cells? Location? Action?
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Cholecystokinin - duodenum and jejunum
- ↑ pancreatic secretion - ↑ gallbladder contraction - ↓ gastric emptying - ↑ sphincter of Oddi relaxation |
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What is secreted from G cells? Location? Action?
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Gastrin - antrum of stomach
- ↑ gastric H+ secretion - ↑ growth of gastric mucosa - ↑ gastric motility |
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What is secreted from K cells? Location? Action?
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Glucose-dependent insulinotropic peptide - duodenum and jejunum
- Exocrine: ↓ gastric H+ secretion - Endocrine: ↑ insulin release |
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What is the action of Motilin? Source?
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Motilin - small intestine
- Produces migrating motor complexes (MMCs) |
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What is secreted from S cells? Location? Action?
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Secretin - duodenum
- ↑ pancreatic HCO3- secretion - ↓ gastric acid secretion - ↑ bile secretion |
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What is secreted from D cells? Location? Action?
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Somatostatin - pancreatic islets and GI mucosa
- ↓ gastric acid and pepsinogen secretion - ↓ pancreatic and small intestine fluid secretion - ↓ gallbladder contraction - ↓ insulin and glucagon release |
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What is the action of Nitric Oxide in the GI tract?
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↑ smooth muscle relaxation, including LES
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What is the action of Vasoactive Intestinal Peptide (VIP)? Source?
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Parasympathetic ganglia in sphincters, gallbladder, and small intestine:
- ↑ intestinal water and electrolyte secretion - ↑ relaxation of intestinal smooth muscle and sphincters |
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What is secreted from Parietal cells? Location? Action?
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Intrinsic Factor - stomach
- Vitamin B12 binding protein (required for B12 uptake in terminal ileum) Gastric Acid - stomach - ↓ stomach pH |
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What is secreted from Chief cells? Location? Action?
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Pepsin - stomach
- Protein digestion |
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What is secreted from mucosal cells and Brunner glands? Location? Action?
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HCO3-
- Mucosal cells in stomach, duodenum, salivary glands, and pancreas - Brunner glands in duodenum - Acts to neutralize acid |
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Which regulatory substance ↑ pancreatic secretion, ↑ gallbladder contraction, ↓ gastric emptying, and ↑ sphincter of Oddi relaxation? Source? Regulation? Other?
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- Cholecystokinin (from I cells in duodenum and jejunum)
- Regulation: ↑ by fatty acids and amino acids - CCK acts on neural muscarinic pathways to cause pancreatic secretion |
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Which regulatory substance ↑ gastric H+ secretion, ↑ growth of gastric mucosa, and ↑ gastric motility? Source? Regulation? Other?
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- Gastrin (from G cells in antrum of stomach)
- Regulation: ↑ by stomach distention/alkalinization, amino acids, peptides, and vagal stimulation; ↓ if stomach pH <1.5 - Phenylalanine and troptophan are potent stimulators - Gastrin ↑↑ in Zollinger-Ellison Syndrome - Gastrin ↑ by chronic PPI use |
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Which regulatory substance ↓ gastric H+ secretion (exocrine) and ↑ insulin release (endocrine)? Source? Regulation? Other?
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Glucose-dependent insulinotropic peptide (aka Gastric Inhibitory Peptide = GIP)
- From K cells in duodenum and jejunum - Regulation: ↑ by fatty acids, amino acids, and oral glucose - Oral glucose load is used more rapidly than the equivalent given by IV due to GIP secretion |
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Which regulatory substance produces migrating motor complexes (MMCs)? Source? Regulation? Other?
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Motilin - from small intestine
- Regulation: ↑ in fasting state - Motilin receptor agonists (eg, erythromycin) are used to stimulate intestinal peristalsis |
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Which regulatory substance ↑ pancreatic HCO3-, ↓ gastric acid secretion, and ↑ bile secretion? Source? Regulation? Other?
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Secretin - from S cells in duodenum
- Regulation: ↑ by acid and fatty acids in lumen of duodenum - ↑ HCO3- neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function |
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Which regulatory substance ↓ gastric acid and pepsinogen secretion, ↓ pancreatic and SI fluid secretion, ↓ GB contraction, and ↓ insulin and glucagon release? Source? Regulation? Other?
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Somatostatin - from D cells in pancreatic islets and GI mucosa
- Regulation: ↑ by acid and ↓ by vagal stimulation - Inhibitory hormone - Antigrowth hormone effects (inhibits digestion and absorption of substances needed for growth) |
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Which regulatory substance ↑ smooth muscle relaxation including that of the LES? Other?
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Nitric Oxide
- Loss of NO secretion is implicated in ↑ LES tone of achalasia |
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Which regulatory substance ↑ intestinal water and electrolyte secretion and ↑ relaxation of intestinal smooth muscle and sphincters? Source? Regulation? Other?
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Vasoactive Intestinal Polypeptide (VIP)
- Source: parasympathetic ganglia in sphincters, GB, and SI - Regulation: ↑ by distention and vagal stimulation, ↓ by adrenergic input - VIPoma: non-α, non-β islet cell pancreatic tumor that secretes VIP → copious Watery Diarrhea, Hypokalemia, and Achlorhydria = WDHA syndrome |
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What is WDHA syndrome?
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Watery Diarrhea, Hypokalemia, and Achlorhydria:
- Caused by VIPoma, a non-α, non-β islet cell pancreatic tumor that secretes VIP - VIP ↑ intestinal water and electrolyte secretion, as well as ↑ relaxation of intestinal smooth muscle and sphincters |
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Which secretory substance is responsible for binding vitamin B12 (required for B12 uptake in terminal ileum)? Source? Other?
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Intrinsic factor
- Released from parietal cells in stomach - Auto-immune destruction of parietal cells → chronic gastritis and pernicious anemia |
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Which secretory substance ↓ stomach pH? Source? Regulation? Other?
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Gastric Acid
- Released from parietal cells in stomach - Regulation: ↑ by histamine, ACh, and gastrin; ↓ by somatostatin, GIP, prostaglandin, and secretin - Gastrinoma: gastrin-secreting tumor that causes high levels of acid secretion and ulcers refractory to medical therapy |
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Which secretory substance is responsible for protein digestion? Source? Regulation? Other?
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Pepsin
- Released from chief cells in stomach - Regulation: ↑ by vagal stimulation and local acid - Inactive pepsinogen → active pepsin via H+ |
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Which secretory substance neutralizes acid? Source? Regulation? Other?
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HCO3-
- Released from mucosal cells in stomach, duodenum, salivary glands, and pancreas - Released from Brunners glands in duodenum - Regulation: ↑ by pancreatic and biliary secretion with secretin - HCO3- is trapped in mucus that covers the gastric epithelium |
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Which substance is ↑↑ in Zollinger-Ellison syndrome? Action?
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Gastrin
- ↑ gastric H+ secretion - ↑ growth of gastric mucosa - ↑ gastric motility |
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Which substance is ↑ with chronic use of PPIs? Action?
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Gastrin
- ↑ gastric H+ secretion - ↑ growth of gastric mucosa - ↑ gastric motility |
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Which drug is a motilin receptor agonist? Action?
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Erythromycin
- Used to stimulate intestinal peristalsis - Motilin produces migrating motor complexes (MMCs) |
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Which substance is ↑ in VIPoma? Action?
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Vasoactive Intestinal Polypeptide (VIP)
- ↑ intestinal water and electrolyte secretion - ↑ relaxation of intestinal smooth muscle and sphincters - Leads to copious Watery Diarrhea, Hypokalemia, and Achlorhydria (WDHA syndrome) |
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Which substance is ↑ in Gastrinoma? Action?
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Gastrin
- Causes high levels of acid secretion and ulcers refractory to medical therapy |
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Which secretory cells are found in the body of the stomach? Action?
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- Parietal cells: release HCl and Intrinsic Factor
- Chief cells: release pepsinogen |
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Which secretory cells are found in the antrum (bottom) of the stomach? Action?
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- G cells: release Gastrin to circulation
- Mucous cells: release mucus - D cells: release Somatostatin |
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Which secretory cells are found in the duodenum?
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- I cells: release CCK
- S cells: release Secretin - K cells: release GIP |
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What is the action of ECL cells? Regulation?
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- Release Histamine → activates parietal cells in body of stomach to release HCl and Intrinsic Factor
- Stimulated by Gastrin (from G cells) |
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How does gastrin increase acid secretion?
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- Primarily through its effects on Enterochromaffin-Like (ECL) cells → release histamine which stimulates Parietal cells
- Also directly stimulates Parietal cells |
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Which receptors are found on gastric parietal cells? What do they bind?
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- M3 receptor - binds ACh
- CCK-B receptor - binds Gastrin - H2 receptor - binds Histamine - Other receptors that bind prostaglandins/misoprostol and somatostatin |
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What is the action/mechanism of the Vagus nerve on the gastric parietal cell?
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- Releases ACh which stimulates the M3 receptor
- Stimulates Gq → IP3 and Ca2+ → stimulates ATPase on gastric lumen to secrete H+ - Stimulates G cells via GRP to release Gastrin - Gastrin binds to CCK-B receptor - Stimulates Gq → IP3 and Ca2+ → stimulates ATPase on gastric lumen to secrete H+ |
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What is the action/mechanism of the ECL cells on the gastric parietal cell?
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- ECL cells are stimulated by gastrin to release Histamine
- Histamine binds H2 receptor on parietal cell - Stimulates Gs → cAMP → stimulates ATPase on gastric lumen to secrete H+ |
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What is the action/mechanism of the prostaglandins / misoprostol on the gastric parietal cell?
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- Binds to receptor on parietal cell
- Stimulates Gi → ↓ cAMP → no activation of ATPase on gastric lumen to secrete H+ |
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What is the action/mechanism of somatostatin on the gastric parietal cell?
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- Binds to receptor on parietal cell
- Stimulates Gi → ↓ cAMP → no activation of ATPase on gastric lumen to secrete H+ |
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How can you inhibit the gastric parietal cell from releasing acid, pharmacologically?
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- Atropine: inhibits ACh activation of M3 receptor
- H2 blockers: inhibits Histamine activation of H2 receptor - Proton Pump Inhibitors: inhibits H+/K+ ATPase on gastric lumen of parietal cell |
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What is the function and location of Brunner glands?
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- Secrete alkaline mucus (hypertrophy seen in peptic ulcer disease)
- Located in duodenal submucosa |
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Which histologic sign would you see in peptic ulcer disease?
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Hypertrophy of Brunner glands in duodenal submucosa (act to secrete alkaline mucus)
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What are the characteristics of pancreatic secretions?
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- Isotonic fluid
- Low flow → high Cl- - High flow → high HCO3- |
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What enzymes are released by the pancreas?
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- α-amylase
- Lipase, Phospholipase A, Colipase - Proteases - Trypsinogen |
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What is the action of α-amylase? Source? Other?
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- Starch digestion
- From pancreas - Secreted in active form |
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Which pancreatic secretions are involved in fat digestion?
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- Lipase
- Phospholipase A - Colipase |
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Which pancreatic secretions are involved in protein digestion?
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Proteases secreted as proenzymes (aka zymogens)
- Trypsin - Chymotrypsin - Elastase - Carboxypeptidase |
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What is the action of Trypsinogen? Source?
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- Converted to active enzyme Trypsin → activates other proenzymes and cleaves additional Trypsinogen molecules into active Trypsin (positive feedback loop)
- From pancreas |
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How does Trypsinogen get activated to Trypsin?
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- Enterokinase / Enteropeptidase - brush-border enzymes on duodenal and jejunal mucosa
- Activated Trypsin can also self-activate more Trypsinogen molecules (positive feedback loop) |
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How are carbohydrates absorbed?
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- Only monosaccharides (glucose, galactose, and fructose) are absorbed by enterocytes
- Glucose and Galactose are taken up by SGLT1 (Na+ dependent) - Fructose taken up by facilitated diffusion by GLUT-5 - All transported to blood by GLUT-2 |
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What is the action of SGLT1?
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Na+ dependent uptake up Glucose and Galactose on lumenal border of enterocytes
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What is the action of GLUT-5?
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Facilitated diffusion uptake of Fructose on lumenal border of enterocytes
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What is the action of GLUT-2?
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Transports Galactose, Glucose, and Fructose into blood from enterocytes
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What test distinguishes GI mucosal damage from other causes of malabsorption?
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D-xylose absorption test
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What is the function of the D-xylose absorption test?
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Distinguishes GI mucosal damage from other causes of malabsorption
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Which important vitamins/minerals are absorbed in the small intestine? Which part?
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- Iron (Fe2+) in duodenum
- Folate in jejunum and ileum - B12 in terminal ileum along with bile acids, requires intrinsic factor |
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What are Peyer Patches? Location?
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- Unencapsulated lymphoid tissue
- Found in lamina propria and submucosa of ileum |
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What takes place in Peyer Patches?
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- Specialized M cells sample and present antigens to immune cells
- B cells stimulated in germinal centers differentiate into IgA-secreting plasma cells - Plasma cells ultimately reside in lamina propria - IgA receives protective secretory component and is then transported across the epithelium to gut to deal with intraluminal antigen |
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Which antibody is important in the gut?
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IgA = the Intra-gut Antibody
Always say SECRETORY IgA - this is important so it can be transported into the gut out of the Peyer patch to deal with the intraluminal antigen |
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What are the contents of bile?
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- Bile salts (bile acids conjugated to glycine or taurine)
- Phospholipids - Cholesterol - Bilirubin - Water - Ions |
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How are bile salts made? Why?
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- Bile acids are conjugated to glycine or taurine to form bile salts
- This makes them water soluble |
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What enzyme catalyzes the rate-limiting step of bile synthesis?
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Cholesterol 7α-hydroxylase
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What are the functions of bile?
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- Digestion and absorption of lipids and fat-soluble vitamins
- Cholesterol excretion (body's only means of eliminating cholesterol) - Antimicrobial activity (via membrane disruption) |
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What is bilirubin made from?
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Product of heme metabolism - removed from blood by liver, conjugated with glucuronate, and excreted inb ile
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What are the two forms of bilirubin? Difference?
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- Direct bilirubin: conjugated with glucuronic acid, water soluble
- Indirect bilirubin: unconjugated, water insoluble |
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How is unconjugated bilirubin made?
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Takes place in macrophages:
RBCs → Heme → Unconjugated bilirubin |
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How is conjugated bilirubin made?
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- Unconjugated/indirect bilirubin (from macrophages) is bound to albumin to travel in bloodstream to liver
- Once in liver, it is conjugated via UDP-glucuronosyl-transferase to Direct Bilirubin |
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What happens to conjugated bilirubin made in the liver?
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- Released into gut
- Gut bacteria convert it to Urobilinogen - 80% of urobilinogen is excreted in feces as Stercobilin (giving it brown color) - 2% sent to kidney and excreted as Urobilin (giving it yellow color) - 18% sent through enterohepatic circulation back to liver |
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What form of bilirubin is excreted in feces?
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Stercobilin
- Conjugated bilirubin → Urobilinogen via gut bacteria - Urobilinogen → Stercobilin (excreted in feces giving stool its brown color) |
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What form of bilirubin is excreted in urine?
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Urobilin
- Conjugated bilirubin → Urobilinogen via gut bacteria - Urobilinogen → Urobilin (excreted in urine giving it its yellow color) |
