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WVSOM -- Physio
WVSOM -- GI Test Review
| Question | Answer |
|---|---|
| What two functions do epithelial cells have in the GI tract? | secretion or absorption |
| What are the layers of the GI tract? | Epithelial cells, Lamina Propria, Muscularis Mucosae, submucosal plexus, circular muscle, myenteric plexus, longtiduinal muscle, serosa |
| What does the circular muscle do? | Contraction causes a decrease in diamter of the lumen. |
| What does longitudinal muscle do? | Contraction causes a shortening of a segment of the GI tract |
| What are the two submucosal plexus of the GI system? | submucosal and myenteric |
| What makes up the enteric nervous system of the GI tract? | Submucosal plexus and myenteric plexus |
| What is another name for the submucosal plexus? | Meissner's plexus |
| What is the extrinsic innervation of the GI tract? | The ANS has efferents from the brainstem and spinal cord to the GI tract and Afferent fibers that carry information to the brain stem and spinal cord |
| What affect does the parasympathetic nervous system have on the GI tract? | usually excitatory |
| How is parasympathetic infomation carried to the GI tract? | Vagus nerve and pelvic nerves |
| What does the vagus nerve innervate? | esophagus, stomach, pancreas and upper large intestine |
| What do the pelvic nerves innervate? | lower large intestine, rectum and anus |
| What does the sympathetic nervous system usually do to the GI tract? | usually inhibitory |
| What is the enteric nervous system? | coordinates and relays information from teh PNS and SNS to the GI tract via local reflexes |
| What nervous system controls most of the GI tract functions? | enteric nervous system |
| What does teh myenteric plexus control? | motility of the GI smooth muscle |
| What does the submucosal plexus control? | secretion and blood flow |
| What is the action of gastrin? | Increases H+ secretion. Stimulates growth of gastric mucosa. |
| What cells release the H+? | Gastric parietal cells |
| What stimulates the secretion of Gastrin? | Amino Acids, distention of the stomach, and GRP mediated vagal response. |
| What is GRP? | Gastrin-releasing peptide. |
| What does GRP do? | Mediates vagal stimulation for secretion of gastrin |
| What inhibits gastrin release? | H+ in the lumen of the stomach and somatostatin. |
| What is Zollinger-Ellison Syndrome | Occurs when gastrin is secreted by non-beta-cell tumors of the pancreas. |
| What are the actions of CCK? (5) | Stimulates contraction of the gallbladder and relaxation of the sphincter of Oddi. Stimulates Pancreatic enzyme secretion. Potentiates secretin-induced stimulation of pancreateic HCO3 secretion. Stimulates growth of the exocrine pancreas. Inhibits gastric |
| Why does CCK inhibit gastric emptying? | To allow more time for intestinal digestion |
| What stimulates release of CCK? | amino acids and monoglycerides |
| Do triglycerides stimulate CCK release? WHY? | NO!!!!! Because they cannot cross intestinal cell membranes. |
| What is the action of secretin? | Stimulates pancreatic bicarb secretion and increases growth of the exocrine pancreas. Stimulates bicarb and water secretion by the liver and increases bile production. INHIBITS H+ secretion by parietal cells |
| What is GIP? | Glucose-dependent insulinotropic peptide |
| What are the actions of GIP? | Stimulates insulin release and inhibits H+ secretion |
| What stimulates GIP release? | fatty acids, amino acids and orally administered glucose |
| What are the 4 basic GI hormones? | Gastrin, cholecystokinin, secretin and Glucose-dependent insulinotropic peptide |
| What are the 2 paracrines of the GI system? | Somatostatin and Histamine |
| What does somatostatin do? | Inhibits the release of ALL GI hormones |
| What does histamine do? | Increases gastric H+ secretion directly and by potentiated the effects of gastrin and vagal stimulation |
| What stimulates somatostatin release? | H+ in the lumen. |
| What inhibits somatostatin release? | Vagal stimulation |
| What are the 3 Neurocrines of the GI system? | Vasoactive intestinal peptide, Gastrin Releasing Peptide and enkephalins. |
| What the action of VIP? | produces relaxation of GI smooth muscle and stimulates pancreatic bicarb secretion. It inhibits gastric H+ secretion |
| What does GRP do? | stimulates gastron release |
| What do enkephalins stimulate? | contraction of GI smooth muscle, particularly sphincters |
| What do enkephalins inhibit? | intestinal secrion |
| What is an example of an enkephalin and what would we use it in the treatment of? | Morphine in the treatment of diarrhea |
| What part of the GI system are striated muscle? | upper 1/3 of the esophagus and the external anal sphincter |
| Where do phasic contractions occur in the GI system? | esophagus, gastric antrum and small intestine |
| What do phasic contractions mean? | contract and relax periodically |
| What part of the GI system is tonic contractions? | lower esophageal sphincter, orad stomach, and ileocecal and insternal anal sphincters. |
| What do the cells of Cajal do? | pacemaker for the GI smoth muscles |
| What do slow waves do? | NOT action potentials but determine the pattern of action potentials and the pattern of contraction. |
| What are slow waves? | oscillating membrane potentials |
| Do slow waves happen spontaneously? | yes |
| What is the mechanism of slow wave production | is the cyclic opening of Ca channels followed by opening of K channels |
| What happens during the depolarization of the slow waves? | brings the membrane potential of smooth muscle cells closer to threshold and increases the probability that action potentials occur. |
| What do the frequency of slow waves do? | sets the maximum frequency of contractions for each part of the GI tract. |
| Where are slow wave frequencies the slowest? | stomach (3 slow waves/min) |
| Where are slow wave frequencies the fastest? | duodenum (12 slow waves/min) |
| What is the purpose of chewing? | lubricates food by mixing it with saliva and decreases the size of food particles to facilitate swallowing |
| What are the 3 events of swallowing? | 1. nasopharynx closes and breathing is inhibitied. 2. laryngeal muscles contract to close the glottis and elevate the larynx. 3. peristalsis begins in the pharynx to propel the food bulus toward the esophgus and the upper esophageal sphincter relaxes to |
| Where is the swallowing reflex? | medulla |
| What nerves carry the swallowing reflex? | vagus nerve and the glossopharyngeal nerves |
| What does the esophagus do? | propels swallowed food into the stomach |
| What is the purpose of the sphincters at eitehr end of the esophagus do? | Prevents air from entering the upper esophagus and gastric acid from entering the lower esophagus |
| What is the sequence of food movement in the esophagus? (6) | 1. upper esophageal sphincter relaxes 2. upper esophageal sphincter contracts to prevent regurgitation 3. Primary peristaltic contractions creates high pressure behind bolus 4. Secondary peristaltic contgraction clears esophagus of any remaingin food. |
| What relaxes the lower esophageal sphincter | vagal nerve and VIP |
| What is receptive relaxation? | Allows the food bolus to enter the stomach. |
| What causes gastroesophageal reflux? | If tone of the lower esophageal sphincter is decreased and gastric contents reflux into the esophagus. |
| What is achalasia? | The lower esophageal sphincter does not relax and food accumulates in the esophagus. |
| How many layers of smooth muscle does the stomach have and what are they? | 3!!! Longitudinal and circular as well as a third oblique layer |
| What are the 3 anatomic divisions of the stomach? | Fundus, body and antrum |
| What makes up the orad region? | Fundus and proximal body. |
| What does the orad region do? | contains oxynic glands and is responsible for receiving teh ingested meal. |
| What makes up the caudad region? | Antrum and distal body |
| What is the caudad region responsible for? | contractions that mix food and propel it into the duodenum |
| What is receptive relaxation? | orad region relaxes to acommodate the ingested meal |
| What initiates receptive relaxation? | vagovagal reflex initiated by distention of the stomach |
| How does CCK participate in receptive relaxation? | increases the distensibility of the orad stomach |
| Where in the stomach do mixing and digestion occur? | Caudad region of the stomach |
| What does contraction of the caudad stomach do to food? | mixes it with gastric secretions and begins digestion. Food particles are also reduced. |
| What does a wave of contraction in the stomach do? | closes the distal stomach and contracts the caudad stomach resulting in food being propelled back into the stomach to be mixed. |
| What is retropulsion? | a wave of contraction closes the distal stomach and contracts the caudad stomach resulting in food being propelled back into the stomach to be mixed. |
| How does CCK participate in receptive relaxation? | increases the distensibility of the orad stomach |
| Where in the stomach do mixing and digestion occur? | Caudad region of the stomach |
| What does contraction of the caudad stomach do to food? | mixes it with gastric secretions and begins digestion. Food particles are also reduce |
| How does CCK help in receptive relaxation? | increasing the distensiblity of the orad stomach |
| How does CCK participate in receptive relaxation? | increases the distensibility of the orad stomach |
| Where in the stomach do mixing and digestion occur? | Caudad region of the stomach |
| What does contraction of the caudad stomach do to food? | mixes the food with gastric secretions and reduces the size of food particles. |
| What does a wave of contraction in the stomach do? | closes the distal stomach and contracts the caudad stomach resulting in food being propelled back into the stomach to be mixed. |
| What is retropulsion? | A wave of contraction that closes the distal stomach and contracts the caudad stomach resulting in food being propelled back into the stomach to be mixed. |
| What increases gastric contraction? | vagal stimulation |
| What decreases gastric contraction? | sympathetic stimulation |
| What is migrating myelectric complex? | Contractions that occur at 90 minute intervals and clear the stomach of risdual food. |
| What mediates the migrating myoelectric complex? | motilin |
| How does food empty into the duodenum? | The caudad region of the stomach contracts. |
| When is the rate of gastric emptying the fastest? | When the stomach contents are isotonic. |
| What kind of food inhibits gastic emptying and why? | fat because it stimulates release of CCK. |
| What does H+ in the duodenum do? | Inhibits gastric emptying. |
| What is the function of the small intestine? | digestion and absorption of nutrients |
| What sets the basic electrical rhythm of the small intestine? | Slow waves at a rate of 12 waves/min |
| What are segmentation contraction? | Mix the intestinal contents by sending food in both the orad and caudad directions. |
| What does the back and forth movement of the segmentation contractions produce? | mixing without any net forward movement of the chime. |
| What are peristaltic contractions? | propel the chime thru the small intestine to the large intestine. |
| When do peristaltic contractions take place? | Ideally after digestion. |
| How does peristaltic contraction occur? | Contraction behind the bolus with simultaneous relaxation in front of the bolus. |
| What coordinates the peristaltic reflex? | enteric nervous system. |
| What is the gastroileal reflex? | Presence of food in the stomach triggers increased peristalsis in the ileum and relaxation of the ileocecal sphincter resulting in intestinal contents being delivered to the large intestine. |
| What mediates gastroileal reflex? | Extrinsic ANS and gastrin. |
| What are haustra? | Sac-like segments that appear after contractions of the large intestine. |
| What is the path of travel of fecal matter thru the large intestine? | cecum -> ascending colon -> transverse colon -> Descending colon -> sigmoid colon -> rectum -> anal canal |
| What is responsible for the appearance of the haustra? | segmentation contractions in the proximal colon. |
| What do segmentation contractions do? | mix the contents in the cecum and proximal colon |
| How often do mass movements occur? | 1-3 times a day |
| Where does most colonic water absorption occur? | proximal colon |
| What happens to fecal matter in the distal colon? | Becomes semisolid. |
| What are the 3 events of defication? | 1. Rectosphincteric reflex 2. Urge to deficate 3. External anal sphincter is relaxed and smooth muscle of the rectum contracts forcing the feces out of the body. |
| What is the rectosphincteric reflex? | As the rectum fills with fecal material, it contracts and the internal anal sphincter relaxes. |
| When does a person have an urge to defecate? | 25% capacity. |
| What is Valsalva maneuver? | intra-abdominal pressure is increased by expiring against a closed glottis. |
| What is the gastrocolic reflex? | Presence of food in the stomach increases the frequency of mass movements. |
| What is irritable bowel syndrome? | Results in constipation or diarrhea due to emotional stress relayed by the extrinsic ANS |
| What is megacolon? | Hirchsprung’s disease. Absence of the colonic enteric nervous system. Results in constriction of the involved segment, marked dilation and accumulation of intestinal contents proximal to the contriction and severe constipation. |
| What are the characteristics of saliva? | High bicarb, high K+, hypotonic, α-amylase, lingual lipase. |
| What inhibits saliva secretion? | sleep, dehydration and atropine. |
| What stimulates saliva secretion? | PNS and SNS |
| What makes up gastric secretion? | HCl Intrinsic factor and Pepsinogen |
| What stimulates HCl secretion? | Gastrin, PNS, and histamine |
| What inhibits HCl secretion? | Decreased stomach pH, chime in duodenum, somatostatin, atropine, omeprazole |
| What stimulates pepsinogen? | PNS |
| What is the functions of saliva? (3) | initial starch digestion, lubrication and protection. |
| How does the composition of saliva vary? | flow!!! At low flow rates it has lowest osmolatiry. At high flow rates it is close to plasma. |
| What forms saliva? | parotid, submandibular and sublingual glands |
| What are the two parts of a saliva gland? | acinus and ducts |
| What does the acinus secrete? | produces an intial saliva similar to plasma. Has Na, K, Cl, and HCO3 |
| What do the ducts secrete? | K and HCO3 |
| What do the ducts reabsorb? | Na and CL |
| What does aldosterone do to ducts of saliva glands? | increases the reabsorption of Na and secretion of K |
| What does saliva become in the ducts? | Hypotonic |
| What PNS nerves stimulate saliva production? | Cranial nerves VII and IX |
| What are the cholinergic receptors on acinar and ductal cells? | muscarinic |
| What is the secondary messenger for saliva production? | IP3 and intracellular Ca |
| What is a side effect of atropine? | Dry mouth |
| What are the SNS receptors in saliva glands? | β-adernergic |
| What is the SNS secondary messenger? | cAMP |
| What increases saliva production? | food in mouth, smells, conditioned reflexes and nausea |
| What decreases saliva production? | sleep, dehydration, fear and anticholinergic drugs |
| What are the three gastric cell types? | Parietal, chief and G cells |
| What do parietal cells secrete? | HCl and intrinsic factor |
| What do Chief Cells secrete? | pepsinogen |
| What do G cells secrete? | gastrin |
| Where are G cells? | antrum |
| What is the mechanism of gastric H+ secretion? | Parietal cells secrete HCl into the lumen of the stomach while absorbing HCO3 into the bloodstream |
| What is the carbonic equation? | CO2 + H20 = H2CO3 = H + HCO3 |
| What is the enzyme that converts CO2 and H2O to H and HCO3? | carbonic anhydrase |
| How is H secreted into the lumen of the stomach? | By H-K ATPase pump |
| What drug inhibits the H-K ATPase pump? | Omeprazole |
| What happens to the HCO3 that is produced? | absorbed into the blood stream in exchange for Cl |
| How is HCO3 and Cl exchanged? | Cl-HCO3 exchanger |
| What is the alkaline tide? | The HCO3 added to the venous blood increases blood pH and will be secreted in the pancreatic secretions to neutralize H+ in the small intestine. |
| How does metabolic alkalosis occur with vomiting? | H+ never arrives at the small intestine so there is no stimulus for pancreatic HCO3 secretion and the arterial blood becomes alkaline |
| What stimulates gastric H+ secretion? | vagal stimulation, Gastrin, histamine, and potentiating effects of ACh. |
| How does Vagal stimulation work on gastric H+ secretion? | Vagus nerve innervates parietal cells to stimulate H+ stimulation as well as innervating G cells to release gastrin. |
| How does gastrin stimulate H+ secretion? | Interacts with CCK-B receptor on parietal cells |
| How does histamine stimulate H+ secretion? | Released by enterochromaffin-like cells and binds to H2 receptors on parietal cell membranes. |
| How does the binding of Histamine get activated? | cAMP pathway |
| How is ACh, histamine and gastrin potiating factors on H+ secretion? | Each agent has a different mechanism of action on the parietal cell |
| How is gastric H+ secretion inhibited? | negative feedback mechanisms on the parietal cells |
| What are the negative feedback factors on parietal cells? | Low pH, Somatostatin, and prostaglandins |
| How does low pH inhibit parietal cells? | pH lower than 3.0 inhibits gastrin secretion. |
| How does somatostatin inhibit parietal cells? | Binds to receptors on the parietal cell that are coupled to G proteins and decrease cAMP levels. |
| How does prostaglandins inhibit gastric H+? | activated G1 protein inhibiting adenylyl cyclase decreasing cAMP levels |
| What is peptic ulcer disease? | an ulcerative lesion of the gastric or duodenal mucosa |
| How does peptic ulcer disease occur? | Loss of protective mucous barrio and/or excessive secretion of H+ and pepsin. |
| What are the protective factors of the GI tract? | Mucus, HCO3, prostaglandins, mucosal blood flow and growthfactors |
| What are damaging factors to the GI tract? | H+, pepsin, H. pylori, NSAIDs, stress, smoking and EtOH |
| What is a gastric ulcer? | gastric mucosa is damaged decreasing H+ and gastrin levels |
| What is the major cause of gastric ulcers? | H. pylori |
| What are duodenal ulcers? | Duodenal mucosa is damaged |
| What is Zollinger-Ellison syndrome? | occurs when a gastrin-secreting tumor of the pancreas causes increased H+ secretion. H+ secretion does not stop because because gastrin that is secreted by these tumor cells are not subject to negative feedback. |
| What 3 drugs block H+ secretion? | Atropine, Cimetidine and Omeprazole |
| What is the action of Cimetidine? | blocks H2 receptors and inhibits histamine stimulation of H+ secretion. |
| What is the composition of pancreatic secretion? | High concentration of HCO3, Na, K, Cl, pancreatic lipase, amylase and proteases. |
| What do acinar cells of the pancreas produce? | Small volume of initial pancreatic secretion which is mainly Na and Cl |
| What do ductal cells of the pancreas produce? | Secretes HCO3 and absorbe CL via a Cl-HCO3 exchange. |
| Does water move thru the ducts? | YES, the ducts are permeable to water and it is what makes pancreatic secretion isomotic. |
| What stimulates pancreatic secretion? | secretin, CCK and ACh |
| How does secretin stimulate pancreatic secretion? | Is secreted by S cells of the duodenum in response to H+, acts on pancreatic ductal cells to increase HCO3 secretion. |
| How does CCK stimulate pancreatic secretion? | Secreted by I cells of the duodenum in response to amino acids and fatty acids and stimulates acinar cells to increase enzyme secretion. |
| What Enzymes do acinar cells secrete? | Amylase, lipases and proteases |
| How does ACh stimulate pancreatic secretion? | Vagovagal reflex in response to H, amino ancids and fatty acids in the duodenal lumen. Stimulates secretion by the acinar cells. |
| How do ACh and CCK potentiate secretin? | extra Cl release by acinar cells provides for more HCO3/Cl exchange in the ducts. |
| What is cystic fibrosis? | disorder of pancreatic secretion. Results from a defect in Cl channels that is caused by a mutation in the CFTR gene. |
| What is cystic fibrosis associated with? | deficiency of pancreatic enzymes resulting in malabsorption and steatorrhea. |
| What is the composition of bile? | bile salts, phospholipids, cholesterol and bilirubin |
| What do bile salts do in aqueous solution? | orient themselves around droplets of lipid and keep them emulsified |
| What do bile salts do in digestion? | aid in the intestinal digestion and absorption of lipids by emulsifying and solubilizing them in micelles. |
| What are micelles? | Bile salts form on the outside with a center made up of free fatty acids and monoglycerides that are prepared for absorption. |
| What makes bile? | hepatocytes |
| What are cholertic agents? | increases the formation of bile |
| What makes secondary bile salts? | bacteria |
| What contracts the gall bladder? | CCK and ACh |
| What does CCK do to the gall bladder? | tells the gallbladder that bile is needed and contracts the gall bladder while relaxing the sphincter of Oddi |
| What happens during ileal resection? | Bile is not re-absorbed and steatorrhea results because fat absorption is impared. |
| What is digested and absorbed in the small intestine? | carbs, protein and lipids |
| What increases the surface area of the small intestine for absorption? | Brush border |
| Where are bile acids absorbed? | Ileum |
| What kind of carbohydrates are absorbed? | ONLY MONOSACCHARIDES!!!!! |
| What hydrolyzes the 1,4-glycosidic bonds in polysaccharides? | α-amylases |
| What are the two kinds of α-amylases? | salivary and pancreatic |
| What hydrolyzes the oligosaccharides to glucose? | maltase, α-dextrinase and sucrose |
| What degrades lactose? | Lactase |
| What degrades sucrose? | sucrase |
| What transports Glucose and galactose from the lumen into cells? | SGLT1 by a Na dependent cotransport. |
| What transports Glucose and galactose from cells to blood? | GLUT2 |
| How is fructose absorbed? | facilitated diffusion |
| What do endopeptidases? | degrade proteins by hydrolyzing interior peptide bonds |
| What are exopeptidases? | hydrolyze one amino acid at a time from the C terminus of proteins and peptides |
| What is pepsin? | helps digest proteins |
| How is pepsin secreted? | secreted as pepsinogen by chief cells in the stomach |
| How is pepsinogen activated to pepsin? | gastric H+ |
| What is the optimum pH for pepsin? | between 1 and 3 |
| What are the pancreatic proteases? | trypsin, chymotrypsin, elastase, carboxypeptidase A and carboxypeptidase B |
| How are pancreatic proteases secreted? | In inactive forms that are activated in the small intestine |
| How are proteins absorbed? | as amino acids, dipeptides and tripeptides |
| What is absorbed faster? Dipeptides/tripeptides or free amino acids? Why? | Dipeptides and tripeptides because of H dependant co transport while free amino acids share its transporter with glucose and galactose (Na dependant amino acid transport) |
| How are free amino acids absorbed? | Na dependent amino acid transport. |
| How are lipids digested in the stomach? | The stomach mixes the lipids and breaks them into droplets. Lingual lipases digest some of the ingested triglycerides to monoglicerides and fatty acids. |
| How are lipids digested in the small intestine? | Bile acids emulsify lipids in the small intestine and pancreatic lipases hydrolyze lipids to fatty acids, monglycerides, cholesterol and lysolecithin. |
| What enzymes are used to digest lipids in the small intestine? | pancreatic lipase, cholesterol ester hydrolase and phopholipase A2. |
| What happens to the hydrophobic products of lipid digestion? | Solubilized in miceles by bile acids |
| How are lipids absorbed? | micelles bring products of lipid digestion into contact with the absorptive suface. FA, monglycerides and cholesterol diffuse across the luminal membrane into cells. |
| What happens to lipids in intestinal cells? | re-esterified into triglycerides, cholesterol ester and phospholipids to form chylomicrons? |
| What happens to chylomicrons? | transported out of cells by exocytosis and transferred to lymph vessels and added to blood stream via the thoracic duct. |
| Why do chylomicrons go into lymph? | They are too big for capillaries |
| What 6 things can cause malabsorption of lipids? | Pancreatic disease, hypersecretion of gastric, ileal resection, bacterial overgrowth, decreased number of intestinal cells and failure to synthesize apo B |
| How can electrolytes and water cross intestinal epithelial cells? | by either cellular or paracellular routes |
| Which epithelium are impermeable to water and electrolytes? | colon |
| Which epithelia are “leaky”? | small intestine and gallbladder are permeable |
| How is NaCl absorbed? | Na moves into the intestinal cells across luminal membrane and down an electrochemical gradiant. |
| How is Na moved down its gradient? (4) | passive diffusion, Na-glucose or Na – aa co transport, Na-Cl co-transport, and Na-H exchange |
| How is Na transported in the colon? | passive diffusion va Na channels |
| What stimulates Na transport in the colon? | aldosterone |
| How is Cl absorption accompanied by NA absorption? (3) | passive diffusion, Na-Cl co-transport, and Cl-HCO3 exchange |
| How is K absorbed? | in the small intestine by passive diffusion |
| How is K secreted? | in the colon by stimulation of aldosterone |
| What happens to K secretion in diarrhea? | increased because of a flow rate-dependant mechanism similar to that in the renal distal tuble. |
| What does excessive loss of K lead to? | hypokalemia |
| How is water absorption compared to solute absorption? | it is secondary to solute absorption |
| Where are electrolytes secreted? | GI tract secretes electrolytes from blood to lumen |
| Where are secretory mechanisms located? | crypts |
| What is the primary ion secreted? | Cl |
| What does V. cholera cause? | diarrhea by stimulating Cl secretion. |
| How are fat-soluble vitamins absorbed? | They are incorporated into micells and absorbed along with other lipids. |
| How are water soluble vitamins absorbed? | Na dependant co-transport mechanisms |
| How is Vitamin B12 absorbed and what is required? | in the ileum and requires intrinsic factor |
| How does intrinsic factor work? | It binds to B12 and then that complex binds to receptros on the ileal celsl and is absorbed. |
| What is pernicious anemia? | Vitamin B12 deficiancy usually due to not enough intrinsic factor. |
| How is calcium absorbed? | Vitamin D is needed |
| What is the active form of Vitamin D? | 1,25-dihydroxycholecalciferol |
| Where is the active form of Vitamin D produced? | Kidney |
| What does vitamin D deficiency or chronic renal failure lead to? | inadequate intestinal Ca absorption |
| What does 1,25-dihydroxycholecalciferol induce? | synthesis of calbindin D-28k which is a calcium binding protein |
| How is iron absorbed? | As heme iron or as free iron. |
| How is free iron absorbed? | binds to apoferritin and transported into the blood |
| How is heme iron absorbed? | It is degraded to free iron and then bound to apoferritin and transported into the blood |
| What is the most common cause of anemia? | iron deficiency |
| How does Fe circulate in the blood? | Bound to transferrin |
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