During this 20-25 minute pre-recorded lecture, Dr. Priya Simoes discusses the topic of TPN and nutrition. This in-depth review will provide an update on this topic for your clinical practice as well as supplement your learning for the ABIM Gastroenterology and Hepatology boards. CME pre-requiste of live Q & A webinar, 8th Annual Mount Sinai Intensive Board Review in Gastroenterology & Hepatology on Oct 6.
Hi I'm Preston, moist and welcome to today's talk on nutrition and TPN for the G. I. Boards. Um We're going to be going over a number of board review questions. Uh And then the rationale for the correct answers which I think is the best approach to um preparing for the boards. So the goals of today's talk to focus on specific vitamins and minerals that are essential to G. I. Health to recognize clinical manifestations of their toxicity and efficiencies to understand intestinal failure and short bowel syndrome and specific clinical situations. Um And the needs that arise from these situations. Um and briefly to discuss TPN and its complications. So question one a 45 year old man presents with fatigue and abdominal pain. He has a history of perforated appendicitis 15 years ago and then underwent an operation at that time. He had additional operations for bowel obstruction that resulted in having some part of his colon and small intestine removed. He reports that he rarely sees a doctor. He reports difficulty with amputation. His fecal fat is normal. His hemoglobin is 11.4 g for desolated with an M. C. V. Of 106. What is the next step in the treatment of this patient? A checkmate on moronic acid and start I am complement. Be check copper levels. See start folic acid supplementation. D. Check method, moronic acid and start oil, compliment or e start a multivitamin and the correct answer is a check metal moronic acid and start um compliment. So the closer the question stem. Um So this patient is reporting difficulty with amputation in the setting of a microscopic anemia. So neurological symptoms with microscopic anemia. He has a history of multiple bowel receptions. We're probably his terminal ilium, which is the site of B-12 absorption was respected. So he's not going to be able to absorb B 12 and he is ultimately going to develop a B 12 deficiency clinical manifestations and neurological symptoms with a microscopic anemia. Um The other answers are wrong because um fully deficiency does not tip and copper deficiency can cause a peripheral neuropathy, but it causes a microscopic anemia and not a microscopic. Um So briefly, vitamin B 12 is found in animal products like feet, fish, meat, dairy and shellfish. There is a large reserve pool stored in the liver and the major causes of deficiency are equally jadriyah, pernicious anemia, and those who have had a history of alien resection or a diseased terminal ilium, like in the case of Crohn's disease, or radiation enteritis. Um And those who have undergone gastric bypass surgery, Vitamin B 12 deficiency manifests as a microscopic metal plastic anemia, peripheral smear, Michelle hyper segmented neutrophils. Um and the presence of neurological symptoms like dementia, ataxia paris. These is, it primarily affects the posterior columns of the spinal cord. So patients will have a loss of the vibration and appropriate section sensations. Um important point to remember is the serum ethel moronic acid levels increased before B. 12 levels decrease and that's why checking serum it'll moronic acid um can give you a clue earlier in the course of the development of B. 12 deficiency. Folic acid. Also found an organ meats and green leafy vegetables also causes the mega plastic anemia, but not typically neurological symptoms before starting folic acid supplementation. You want to check B 12 levels and rule out B. 12 deficiency and then supplement folio required. All right question to a 35 year old man presents to the clinic with complaints of postprandial abdominal bloating and nausea. He reports that he has always been a picky eater, but his symptoms have further restricted his diet on physical exam. You know, several cuts on his arms and a few scattered, particularly when you questioned him about the cuts. He states that they happened several months ago but have not healed, which is the of the following is the most likely vitamin deficiency in this patient, a zinc B, vitamin B one C, niacin D, vitamin E. Or E. Vitamin C. And the correct answer is vitamin C. So the patient is suffering from scurvy or vitamin C deficiency. The symptoms that particular red swollen red bleeding gums and poor wound healing along with the presence of anemia. Um This happens uh in patients who do not have access to fruits and vegetables in those who are chronic alcoholics or who are suffering from a malabsorption state. Question three, A 55 year old man presents to the emergency room. He started on I. V Fluids as he appears dehydrated and reports drinking 10 to 15 beers a day. Which vitamin B. Deficiency should you first be concerned about in this type of patient A vitamin B. Six B. Vitamin C. Niacin or D. None of the above. And the correct answer is B fighting so close in the question stem uh someone who has a history of chronic alcoholism uh or history of a gastric bypass. And the clinical um situation of the clinical symptoms will be um one of two. So it presents is very very one is a higher output cardiomyopathy. Um And the other uh the so called dry very very uh is predominantly neurological symptoms which included peripheral neuropathy against paralysis or cerebellum dysfunction. Uh Remember that one cost cough syndrome can be exacerbated by giving ivy dextrose prior to administering timing. So if the question is asked um you want to always replace time in before starting the patient on I. B. Dextrose containing fluids. Um The other B. Vitamins will go through quickly. So vitamin B. Two or riboflavin again deficiency seen in chronic alcoholics or those with malabsorption um sort of classic clinical symptoms are um angular colossus which is uh inflammation and sort of cuts at the corners of the mouth. Um close iris um as well as other nonspecific symptoms. Nice Nrb three. Uh The classic clinical presentation ESP Allegra which is three things. Diarrhea dermatitis and dementia um vitamin B. Six deficiency um Usually seen in the setting of certain using certain drugs um Like I. N. H. D. penicillin. Mean so those are things to look out for the question stem. Um And also presents with close itis. And colossus biotin deficiency is rare. Um This will almost never be asked. All right question for a 57 year old man is admitted to the hospital after a gunshot wound to the abdomen he's taken to the O. R. And more than half of his small intestine is removed due to damage to the S. M. A. He is left with the Juno illegal anastomosis in continuity with the colon. You are asked to see him post operatively. Which of the following is the next best step in management a high fiber diet. Be convert medications to delayed release formulations, see electrodes restricted diet. D. Start acid suppression or e hypersonic oral beverages. And the correct answer is D. Start as suppression. So this patient has had a massive small bowel resection and is at risk for short bowel syndrome. Specific steps that need to be done in the postoperative period. So you want to start with acid suppression um then replace I. V. Fluids um and start parental nutrition is required um and transition to enter nutrition if possible, acid acid suppression is important because after a massive small bowel resection. There's rebound gastric acid hyper secretion. Um And this can cause and as demonic ulceration at the surgical site. It can also cause um fluid losses from the increased gastric acid that's been secreted and the gastric acid can inactivate pancreatic light based um and lead to fat malabsorption which will further deplete the patient's nutritional status. The other answers are wrong because you typically would not need to initiate a high fiber diet in the acute setting immediately. Post op. Yeah. Um There's no point in converting to delayed release formulations because most medications absorbed in the stomach and approximates mobile. So this patient who's had a resection of the distal small about doesn't really need his medications converted. Uh lactose restriction is not indicated unless the patient has a preexisting lactase deficiency and hyper tonic beverages will actually increase the secretion into the intestine. Aluminum cause further fluid losses. So you want to stay away from that question. Five, a 48 year old woman with a significant past medical history of eventual abdominal hernia status, post measure of death. That was complicated by small bowel bodiless and resulted in intestinal ischemia. The patient underwent an ex lap with small bowel resection and was left with 100 and 80 centimeters of small intestine and Juno and the original two transfers colonic anastomosis. She has continued to lose weight post operatively over the past few years and requires two leaders of I. V. Fluids daily. She is non compliant with her short bowel diet. The patient reports multiple symptoms including difficulty seen at night, muscle aches and dry skin when questioned further. She reports very foul smelling stools that often leads an oily residue in the toilet. She does take a daily chewable multivitamin which vitamins B. This patient required extra supplementation off A. Iron B. Vitamins A C, vitamin D. D. Vitamin B. One E, vitamin E. F. Um A. B. And C. That I. And vitamin A. And vitamin D. G. Is B. C. And E. So vitamin A. Vitamin D. Vitamin E. Or H. All of the above and the answer is G. That is vitamin B. Vitamin D. And vitamin E. So the patient in the questions stem likely has short bowel syndrome. She's had uh vulva list um and then had extensive smallville restrictions because of that. Uh And from the history with oily stools that are seen, she probably has fat malabsorption. So you want to monitor all the vitamins but specifically the fat soluble vitamins which are vitamins A. D. E. And K. Um And she's showing signs of vitamin A deficiency with night blindness. Um So as well as some neurological symptoms indicating vitamin E. Deficiency. Uh So remember the symptoms of vitamin D. Deficiency um are typically high podcast senior uh and muscle cramping symptoms of vitamin A deficiency are usually vision. So night blindness um as well as dryness of the eyes or zero Tommy uh vitamin E. Deficiency presents as neurological symptoms and a hemolytic anemia vitamin E deficiency like B. 12 effects the posterior columns of the spinal cord vitamin K deficiency. Um We all know presents as an increased tendency to bleeding. Um But this is rare if the patient has an intact colon as the bacteria in the colon will synthesise vitamin K. Uh an occasional iron on monitoring is usually sufficient alright um briefly to go over. So intestinal failure as a state where the nutritional demands of the patient cannot be met by the G. I. Absorptive surface and it can be um uh from either malabsorption or dis mortality. Um So diseased small bowel in the case of clones or radiation enteritis. Um Obviously large intestinal resection from vascular complications or intestinal obstruction and simple obstruction. Short bowel syndrome is sort of similar um which is loss of the functional bowel mass and is characterized by malabsorption, diarrhea, diarrhea fluid and electrolyte disturbances generally happens if there's less than 200 centimeters of small intestine and um factors that will affect whether the patient develops short bowel syndrome ana are the amount of small bowel that is respected. Um The uh time for the bout to adapt um And the presence of the musical segment. Um And that is because there is something called the iliad brake mechanism which is um when the when there is a lot of un absorbed fact that is reaching um the terminal ilium uh the ilium actually secretes peptide YY which causes uh a slowdown in the gastric emptying so that there is more time for absorption. So if you lose your musical segment, this little break mechanism is lost. Um And that you know sort of further um affects the amount of malabsorption that there is. Um And so can be a predictor of needing to stay on TPN or not. Um So the treatment is generally a specific diet. Some patients may require TPN if they've lost a large amount of small ball um replacement of fluid losses. Uh You can try anti motility agents if they're having um you know huge storm losses um Like Jeremiah LaMotta um tincture of opium opportunity. It is not recommended because a lot of patients will develop goldstone's uh as a result of being on our prototype. Uh And one of the few drugs that can sort of help to increase the intestinal absorptive surface is to do blood type which is a GLP two analog. Um But it does carry an increased risk of developing colon polyps. Uh And even colon cancer. All right, the next question. Um So a 35 year old woman with a history of chronic diarrhea presents with a very oral rash that also involves her gluteal region. She notes that food tastes bland. Um and has a £5 weight loss. What supplement might help this patient? A nice person be iron C, zinc D. Vitamin D. O. E. Filing. Um And the correct answer to this is C zinc. Um So the patient is describing a very oral rash and a rash on her perineum. Um This is the classic perry or official rash um Called acro dermatitis and terra Patika that is seen um in zinc deficiency uh And zinc needs to be supplemented either or early or potentially. Uh So a picture of the rash it's typically seen around the mouth or around the anus. Um And that's kind of what it looks like. This dry scaly red rash, Other non specific symptoms. Patients might have a disclosure and night blindness and remember that excessive zinc um into can result in uh copper deficiency and that's why it's used as one of the treatments for uh Wilson's disease. All right. I am. So I inefficiency we all know causes microscopic hyper chronic anemia. Um And it can be seen either when there's I am lost through bleeding or for absorption uh in the setting of celiac disease or a patient who's had uh the duodenum bypass like in a ruin. Why I guess bypass. So the next question. Uh 45 year old man presenting with fatigue and peripheral anesthesia. His labs are significant for hemoglobin of 10 and M. C. B. Of 78 a white blood cell count of 2.5. On further questioning you find out that he underwent a ruin y gastric bypass 10 years ago. Which of the following are you likely to find on further investigation a an elevated homocysteine. Be a loaf Sheraton. See alot method moronic acid D. And elevated methane moronic acid or e low copper. Um So the correct answer is e low copper. Close in the question stem. They're telling you that he had a gastric bypass surgery. Um So that means his duodenum was bypassed and he has a microscopic anemia with a hemoglobin of 10 and an M. C. B. Of 78. Um So important things to remember. So copper deficiency will present as a microscopic hyper chronic anemia and they will usually tell you that iron studies are normal indicating that this is not iron deficiency anemia. Um And the patient will have neurologic disturbances which are not typically seen in iron deficiency anemia. Clinical situations will be um uh either a patient who's had a gastric bypass. So um the duodenum is bypassed or a TPM dependent patient who is not getting a multivitamin. Alright the next question A 32 year old from Qatar presents with nausea and poor oral intake. She has a history of gastric bypass surgery. Two years ago um surgery and all her post op care was done abroad. She required TPN for two years to maintain her nutritional state. Her nutritional needs. After a surgically placed j two failed she has an £85 weight loss. Since surgery. Medical history is diabetes which improved with the weight loss and an idiopathic cardiomyopathy diagnosed within the past year exam is significant for bradycardia. A non tender abdomen with the intact colostomy side labs show normal electrolytes but E. K. G. Shows sinus bradycardia. She's scheduled to undergo an upper endoscopy and ethnography which of the following should be checked next couple levels, chromium levels, selenium levels, Sheraton or manganese levels. And the correct answer is c selenium levels. So this is just one of those things you have to remember. Um uh The patient is on TPN. She's developed selenium deficiency um as a result of inadequate replacement in her TPN. And the keywords to look out for uh cardiomyopathy or myocarditis. Um As well as Disney to um and cardiac rhythm disturbances. Um or like bradycardia um that you will see in the question stem. So the question stand for this patient uh sort of talked about bradycardia an exam E. K. G. Showing sinus bradycardia and the patient presented with Disney to all indicating that she has a cardiomyopathy which is specific for selenium deficiency. The other um the other options it's not manganese deficiency that causes non specific symptoms. Uh And they usually ask about manganese toxicity not deficiency. Uh iron deficiency presents differently with microscopic anemia patients can cause can have higher output uh heart failure. Um But this patient has no specific reasons to have a microscopic anemia or to have iron deficiency. And copper deficiency. Like we talked about can cause microscopic anemia and but also causes neurological symptoms which this patient is not really reporting. Alright um Question nine. A 48 year old woman presents the clinic with tremor and shuffling gait which have progressively worsened over the past two months. She has a history of short bowel syndrome and has been on TPN after a massive small bowel resection new to me, esoteric vascular thrombosis from an unknown hyper calculable state. She also sustained thrombosis, two branches of her hepatic artery which resulted in chronic biliary strictures. While she is able to tolerate some oil intake, she is really completely tP independent. She's on warfarin and vitamin supplements examination reveals a fine bilateral tremor of both hands and mental status exam reveals poor recall. Her cbc is normal. The most likely explanation for her symptoms is vitamin B 12 deficiency timing deficiency manganese excess, iron overload or nice and efficiency. And the correct answer is manganese excess. So close in the question stem that they're giving you uh is this patient is on TPN and she has called a static liver disease. So remember that patients who have called a static liver disease at increased risk for developing manganese toxicity. Um This question stem tells you that the patient had a vascular vascular damage to her hypnotic country which caused biliary strictures or secondary um sort of a secondary sclerosing cholangitis kind of picture. Um And that's why she is at risk the clinical manifestations, Pakistani like symptoms. So patients will present with a tremor shuffling memory loss. Um So these are specific to manganese access. It is not the other options because B 12 deficiency causes neurological symptoms. But the patient is unlikely to have a normal cbc. They probably have a microscopic anemia. Um This patient had a normal cbc. Nice and efficiency will cause Villagra. Like we talked about diarrhea, dermatitis. And um in addition to the dementia I an overload can cause a cardiomyopathy but uh should not be causing the other symptoms that are listed. And um timing deficiency has specific neurological symptoms that are different from these parking Tony in like symptoms. Um So those are mostly cerebral symptoms like ataxia, nystagmus. Um And less likely to develop on some in someone who is on uh sort of chronic stable tv. So a few key words to remember about trace element deficiencies and toxicities that will be asked. So selenium, you want to remember cardiomyopathy or myocarditis and symptoms of this. So Disney, a bradycardia um uh E. K. G abnormalities uh manganese. They will usually ask toxicity because deficiency is just non specific symptoms, toxicity is specific Pakistani in like symptoms. Um So that is a tremor shuffling gait memory loss. Um Copper so deficiency is a microscopic anemia with neurological symptoms and they will usually tell you the patient has normal iron studies. So you can rule out iron deficiency anemia. Alright. Um question 10. So a 52 year old man with solid food. Decision for several months now has now progressed to inability to swallow even liquids he presents to the to the hospital where on exam he's dry with Ortho static vital science. His ct chest and abdomen reveals thickening of the distal esophagus, which is suspicious for esophageal cancer. And GT. With tissue sampling his plan and TPN is started in the interim the next day. The patient is found to have severe new onset dystonia and inspires which of the following lab abnormalities is most likely to have led to this condition. Hypercholesterolemia, hyperglycemia, hypoglycemia, hyperglycemia or hypoglycemia. And the correct answer is hipAA hospital MIA. Um So it's likely that this patient developed re feeding syndrome. Um They tell you that he has had a long period of dysplasia with decreased oral intake to where he is now not even able to swallow liquids. And then he's admitted to hospital and started on TPN which is full nutritional support. So he's developed re feeding syndrome which is basically um when the patient is re fed or given a large glucose load unexpectedly that causes a sudden surge in insulin levels. And this surgeon insulin levels causes an intracellular shift of potassium magnesium and phosphorus. Um Also there's suddenly increased energy production um and that utilizes phosphorus or phosphate for 80 P production. Uh And so hyper hospital MIa develops. Um and the sudden hypercholesterolemia can cause um congestive heart failure with pulmonary oedema it can also cause diaphragmatic paralysis that can lead to sudden cardiac death. Um So important to remember that so the complications of TPN. Um that important important to remember. So infection uh patients may have uh persistent battery. Male of funky mia that generally requires removal of the capita uh an antibiotic or alcohol locks can decrease the rates of infection. Um In the short term TPN can cause elevated S. T. And LT levels as well as alkaline phosphate is in the long term. Uh it can cause liver damage that can be seen on liver biopsy uh including Seattle hepatitis. Um also because these patients are generally not eating. Um They developed stasis in the gold ladder and as a result um call it a diocese and gallbladder sludge. Uh You can decrease the liver related complications by cycling the TPM. That means um running it for only 12 out of the 24 hours um at a higher rate. Um minimizing the use of soy based lipid emulsions and restricting the calories and not overfeeding patients. Um Some of the last few questions. So 50 year old woman presenting with dry skin and hair loss. She reports the history of recurrent cellulitis uh and she underwent resection of 300 centimeters of small bowel um During resection of a dismal tumor she eats a very low fat diet with medium chain triglycerides supplementation on example has course and falls out with gentle tugging and her skin appears very dry. Which of the following is most likely needed for this patient paramedic acid linoleic acid, you trick acid, citric acid or Oleic acid and the correct answer is linoleic acid. So this is kind of that one. But um it did come on the boards a few years ago. Um the patient is exhibiting signs of essential fatty acid deficiency. So close in the question stem uh that she's eating a very fat restricted diet with only medium chain triglycerides and two of the essential fatty acids are long chain fatty acids, which are linolenic acid and linoleic acid. Um it's best to just remember this. Um so the symptoms are um that the patient will present with actually sound a little bit like zinc deficiency. So they come in with a scaly dermatitis, alopecia, um and they can also have poor wound healing and from beside opinion. Um so remember that um you know, if this kind of question is asked and linoleic acid or linolenic acid is um one of the options, then that will be the correct answer. And the last question, A 45 year old man with a history of Crohn's disease diagnosed at the age of 14 and currently maintained on Humira presents to your office um for consultation for diarrhea. He reports that he's been seeing the nephrologist for kidney issues on further questioning, he has undergone several operations resulting in at least 120 centimeters of his William respected. He continues to have diarrhea. The patient reports 3-4 loose foul smelling stools daily and stool cultures and see the toxins are negative figure fat is measured as 20 g a day and the CT scan demonstrates. And Ilya colonic anastomosis with no inflammation. So what is the patient at risk for developing calcium? Prospect? Natural synthesis? Copper deficiency, uric acid, natural archdiocese, calcium oxalate, natural with ISIS or struck by natural allies. And the correct answer is calcium oxalate natural with ISIS or calcium oxalate stones. So what happens in these patients is um that they've lost so much of the ilium that they have bile salt malabsorption because the terminal ilium is where bile salts are reabsorbed into the anterior lymphatic circulation, They've lost that. So they have bile salt malabsorption and this results in fat malabsorption. So usually oxalate, which is in which is bound to calcium in the small bowel and absorbed that way. Now what happens in these patients who have fat malabsorption is that there are a large number of free fatty acids in the small bowel. So calcium instead of binding to oxalate binds preferentially to these free fatty acids. Um So there's free oxalate or un absorbed oxalate that then reaches the colon and gets reabsorbed in the colon um and then that gets absorbed you know into the bloodstream and leads to calcium oxalate stone formation. Um And so that is the kind of kidney stone that will form uh So remember um that for this to happen, the patient has to have a large small powered reception. So more than 100 centimeters of ilium including the T. I. Um And the the small bowel has to be connected to the colon in continuity. So if they have an end Elias to be they're not going to develop cash amongst let stones because the um the free oxalate is re absorbed in the colon. So the small bowel has to be in continuity with the colon. Um And the treatment for this is to give them calcium supplementation. So if you give mega doses of calcium there's enough calcium um to buy into the free fatty acids as well as access to buy into the oxalate and prevent free oxalate reabsorption and you want to put them on a low oxalate diet. Um So that brings us to the end of this presentation. Um I'm happy to take
