ESP Flashcards
What does an abnormally increased excretion of protein in stool suggest?
Normally, very little protein is lost in the stool. If protein is being lost, it is due to damage to the intestinal mucosal epithelium resulting in a protein losing gastroenteropathy. Clinically, will see hypoalbuminemia. Associated with alpha1-antitrypsin deficiency.
Does heart failure predispose to invasive infections of the intestine?
When you have heart failure, you have decreased cardiac output. Dec. cardiac output -> decreased BP -> decreased blood flow into the mesenteric arteries -> Intestinal mucosal hypoxia -> villus necrosis -> loss of villus allows for entry of pathogens and toxins into bloodstream ->septicemia
What is bacterial overgrowth in the small intestine?
Can be the result of a number of things inc. achlorhydria, lack of ileocecal valve, diverticular in jejunum, etc. May lead to malabsorption. To test for this, do a hydrogen breath test.
Basis for hydrogen breath test: ingest an amount of lactose; bacteria utilize lactose and convert it into hydrogen. If have lots of hydrogen, lots of bacteria.
Where is short bowel syndrome most likely to cause malabsorption?
If the jejunum is resected, you will have compromised nutrient absorption mores than a comparable length of ileum. If you resect ileum, will have impaired vitamin B12 absorption.
What are the effects of VIP?
Increases blood flow in the intestine; increases secretion of Na, Cl, and water; relaxes intestinal smooth muscle; peripheral vasodilation; and inhibition of gastric acid secretion (achlorhydria); Somatostatin reverses all these, so use a somatostatin analogue, octreotide, to take care of VIPoma’s.
Why do you get hypokalemia with chronic diarrhea?
Due to losses of K from the colon as a result of chronically increased K secretion and accelerated transit of chyme through the intestine.
Hypokalemia can lead to acute renal failure.
What is the anion gap in serum?
Anion gap is [Na] - {[Cl]+[HCO3]}
It is the measured difference between measured cations and measured anions and is normally between 8-14 mM
Elevated anion gap means there’s an increase in serum concentration of unmeasured anions such as lactate, phosphate, protein anions, sulfate, or other anions.
Why does diarrhea lead to metabolic acidosis?
In a disease process, much of the intestinal epithelium is damaged and the absorptive capacity of the small intestine is reduced. This leads to an increased load of Na, Cl, and water being presented to the colon. With the more Cl presented, the more bicarbonate secreted into the lumen in exchange for chlorine absorption. So, there is a net secretion of bicarbonate in the colon - this serves to minimize the amount of Cl lost in the stool and minimize the decrease in ECF volume that might occur although at the expense of bicarbonate.
What is congenital chloride diarrhea?
Can present with hypochloremic metabolic alkalosis. It is due to a deficiency in CLD, a Cl-HCO3 exchanger in apical membrane of colonic enterocytes. Deficiency in this means that bicarbonate cannot be secreted in exchange for chlorine and thus will have a loss of chlorine.
What controls the reflexive action of the EAS?
The EAS is made up of striated and smooth muscle. The smooth muscle is innervated by postganglionic cholinergic motor neurons in the ENS which are in turn innervated by parasympathetic preganglionic neurons from S2-S4.
The striated muscle is innervated at the S2-S4 level also, but its mediated by the pudendal nerve.
What is the normal composition of stool?
The stool is normally 75% water and about 30% bacteria. The remainder of fat and fat derivatives, desquamated mucosal cells, mucus, and small amounts of digestive enzymes.
What is the fate of unabsorbed carbohydrate entering the colon?
It is excreted as short-chain fatty acids. Bacteria in the colon metabolize it to SCFA’s with acetate, propionate, and butyrate being the major SCFA anions. This process is dependent on the rate of colonic peristalsis and the complement/function of colonic microbes.
What is the function of aldosterone in the gut?
It works to facilitate Na, Cl, and H20 reabsorption and secretion of K by duct epithelial cells in the salivary glands and it has a similar function in the distal colon. MOA is done through up regulation of epithelial Na channels and K channels as well as Na-K ATPase on the basolateral membrane.
What is the most important lipase?
Pancreatic lipase. The amount of salivary and gastric lipase cannot take over for the action of pancreatic lipase if it is lost. However, the pancreatic acini have to lose like 90% of their function before steatorrhea develops.
What is the mechanism of vitamin B12 absorption?
When vitamin B12 is ingested, it binds to R-binders/haptocorrins within the stomach. Within the duodenum, pancreatic proteases release the B12 from R-binder and it then binds to intrinsic factor. This complex is resistant to further proteolysis and binds to specific receptors in the terminal ileum.
What is the mechanism of iron deficiency?
HCl in the stomach keeps iron in the Fe2+ state which it is normally absorbed in. Almost all dietary iron is absorbed in the duodenum, so loss of this will lead to problems.
What is the secretin-CCK test?
Secretin and CCK are given intravenously and then the output of juices from the duodenum is measured. This evaluates the exocrine function of the pancreas.
What is the basis of the D-xylose test?
It is for evaluation of suspected malabsorption on the basis that D-xylose is not digested before its absorbed. If there’s a problem in the intestinal epithelium, then the D-xylose test will be abnormal. But the test is normal in the following situations: lactase deficiency, deficiency of bile, and deficiency of pancreatic enzymes. The reason its normal is because these digestive processes don’t damage the epithelium directly.
How is Cl, Na, and H2O secreted by the crypt cells of the small intestine?
Chloride enters enterocytes by the 1Na-1K-2Cl symporter on the basolateral membrane. It then passes through CFTR to be excreted into the lumen giving the lumen a negative voltage in relation to the plasma. Na+ leaks into the lumen and then water follows Na
How does the cGMP cascade work in crypt cells?
Guanylate cyclase is located in the apical membrane of intestinal epithelial cells. Binding of a ligand for the enzyme leads to increased intracellular levels of cGMP which in turn activate protein kinases that activate CFTR.
How does Oral Rehydration Solution ork?
Does not inhibit secretion of Na and Cl by the crypt cells. The coadministration of Na and glucose together allows for coabsorption via the SGLT1 in villus cells. The potential difference across the epithelial cell as a result draws in the chloride from the lumen to the interstitium.
Crypt cells vs. villus cells
Crypt cells are primarily involved in secretion of Na, Cl, and water whereas villus cells are involved in absorption of nutrients and electrolytes
How do you calculate osmotic gap and what is its role in diarrhea?
Calculated osmolality= 2 [Na+K]
Normal measured osmolality is assumed to be 290-300 mOsm which is close to the osmolality of human plasma.
Osmotic gap = Measured osmolal - calculated osmolal
If osmotic gap > 50 mOsm, then this suggests osmotic diarrhea. Osmotic gap is normal for secretory diarrhea
How are medium chain triacylglycerols absorbed?
Medium-chain TAGs do not require pancreatic lipolysis and can be absorbed by just the epithelial cell. This is limited to those that are only 8-10 C atoms long. They do not need to be re-esterified within the enterocytes and they are absorbed by the blood stream rather than the lymphatics
Could a deficiency in salivation predispose to symptomatic gastroesophageal reflux?
Yes. Saliva helps to raise the pH of refluxate in the lower end of the esophagus. Without this function, lower esophagus will be exposed to much lower pH which can damage the epithelium.
How do you maintain an adequate concentration of bile acids in the upper small intestine?
Common mechanism of fat malabsorption is through obstruction to bile flow in the intrahepatic bile canaliculi/extrahepatic biliary tree. When there is bacterial overgrowth in the bowel or infection of the biliary tree, premature deconjugation of bile acids by bacteria can occur before digestion of fat is complete. Deconjugated bile acids get absorbed by the jejunum by nonionic diffusion, but cannot arrange in micelles for fat absorption
How are bile acids and bile salts reabsorbed in the terminal ileum?
Unconjugated bile acids are absorbed by nonionic diffusion across mucosal cells in the small intestine, but 90-95% of bile salt recovery occurs in the terminal ileum via the Na-bile salt cotransporter in the luminal membrane of enterocytes.
This enterohepatic circulation occurs about 2-3 times each meal and 6-8 times per day.
Liver can only partially compensate for decreased enterohepatic circulation.
Bile acid diarrhea can occur following surgical resection of the terminal ileum - primarily a secretory diarrhea
How does decreased pH lead to steatorrhea?
Pancreatic lipase is active at a more alkaline pH. If a gastrinoma or process that decreases pH enough is found, then there will be inactivation of pancreatic lipase. Gastric lipase and lingual lipase cannot make up for a deficiency in pancreatic lipase - it is the main fat absorber.
