DTC203 Final Exam Review Guide PDF

**DTC203 Final Exam Review Guide Dr. Carbone** The final exam will include 5 T/F (1pt each), 40 multiple choice (1.5pts each), 10 matching (1.5pts each) and choose 2 of 3 possible short answer questions (10pts each). As I believe I said in class, it is overwhelmingly based on the material covered...

**DTC203 Final Exam Review Guide Dr. Carbone** The final exam will include 5 T/F (1pt each), 40 multiple choice (1.5pts each), 10 matching (1.5pts each) and choose 2 of 3 possible short answer questions (10pts each). As I believe I said in class, it is overwhelmingly based on the material covered since exam \#3. The matching include some basic comprehensive nutrition-related concepts that have been covered repeatedly throughout the semester. As for this study guide, I\'m not sure if I got carried away or if we just covered a lot of really important stuff that I thought would be useful to have in writing.  Probably a combination of the two, but regardless, this is decently long... but full of good info.   [Upper GI Disorders] If something's not working correctly somewhere along the GI tract, chances are that it's going to affect nutrition. Usually, this means impairment in the nutritional status of our patients. In the upper GI, we're talking about anything going wrong from the mouth on down to the pyloric sphincter, at the base of the stomach. Let's start at the mouth; the relationship between oral health and nutritional status should (hopefully) be somewhat intuitive. If oral health is impaired, chances are you're not going to be eating very well, if at all. No one wants to crunch some healthy fruits & veggies when they're dealing with the pain and discomfort of gingivitis, glossitis (tongue inflammation) or open sores in the mouth. Similarly, malnutrition can impair oral health and create a vicious cycle. Remember 7^th^ grade Social Studies discussions of historical explorers dealing with scurvy and the eventual "Limey" nicknaming of British sailors. They ate limes and drank lime juice because they found out that doing so would prevent their teeth from falling out of their jaws as their gums receded. All because citrus fruits are a good source of Vitamin C which is very important in collagen formation and integrity (e.g., holding the teeth in the mouth). A lot of the drugs that we use to help our patients also cause some unfortunate side effects. A common one is dry mouth (aka- xerostomia). Xerostomia changes the taste and mouthfeel of foods and also makes it pretty uncomfortable to swallow. Imagine pouring a box of bread crumbs into your mouth, swishing them around, spitting them out and then sitting down to eat a peanut butter & jelly sandwich (without drinking anything in-between). We, thankfully, have saliva substitutes that we can use to counteract xerostomia. A couple of spritzes in the mouth before a meal help to moisten the mouth or stimulate salivary gland activity, depending on the type of spray. With patients like these, we encourage the use of gravies, oils, butter, etc. to lubricate foods and help them form a bolus that can be comfortably swallowed. Since the lack of saliva also tends to change the taste of the food, bland foods are better tolerated because a distinct taste isn't associated with them. If you sit down to a plate of pesto, you want to be able to taste the basil and it's disappointing when you can't. If, instead, you sit down to a bowl of mashed potatoes, it's not as huge of a letdown if it tastes like, well, potatoes. With severe mouth sores (think really, really bad canker sores), we tend to use oral anesthetics and soft, bland foods. Nothing with coarse edges and nothing that's acidic because we don't want to irritate these open wounds. Some institutions also utilize capsaicin candies. Capsaicin is the chemical in hot peppers that gives them their heat. The idea is that the capsaicin in these sucking candies numbs the nerves in the mouth so that sucking them before mealtime makes the actual meal more enjoyable. An enjoyable meal tends to mean increased consumption and a better overall nutritional status. As a side note, dry mouth and/or mouth sores don't tend to lead to a patient being admitted. You'll usually see these as comorbidities, so the diet plan will also be tailored around the major medical reason that's keeping your patient in the hospital. The esophagus is the tube that takes the food you swallow from the mouth and deposits it into the stomach. The major issue with the upper esophagus is dysphagia. When we swallow, usually the epiglottis covers over the trachea and our food gets passed down into the stomach. With dysphagia, there's usually a nervous or muscular issue that's preventing a functional swallow from taking place. Sometimes food gets stuck; sometimes it passes into the trachea and on to the lungs. Bad news for gas exchange (CO~2~ ↔ O~2~) and a great way to foster pneumonia. Dysphagia comes in various types; some patients can't swallow anything, others can handle pretty much any food, as long as it's of a consistent consistency (repetitive phrasing, but appropriate). Our friends from Speech & Language Pathology will usually assess these patients and determine what they can swallow. For a quick review, take a look at the 3 levels of the National Dysphagia Diet and what types of foods fit within each level. (Level 1- Dysphasia pureed: well mashed, homogenous (can't see separate parts), and cohesive) (Level 2-Dysphasia Mechanically altered: moist, cohesive, soft-textured) (Level 3- Dysphasia Advances: moist, bite-sized, mixed textures) Besides playing with the consistency of the foods, liquids can also be thickened when necessary. Remember nectar-thick, honey-thick, and spoon-thick? You will very likely see patients with dysphagia, especially if you work on a neuro floor (a lot post-stroke) or with older patients (diminished nervous response to food in the upper esophagus and limited muscle control). Separating the esophagus and stomach is the lower esophageal sphincter. It works to regulate passage of food into the stomach and, more importantly, keeps stomach contents from making a return trip back into the esophagus. A hiatal hernia is usually due to a tear in the diaphragm; the upper portion of the stomach can then move up into the thoracic cavity. This creates a small upper stomach pouch that can limit passage of food down into the rest of the stomach and can often precipitate GERD. GastroEsophageal Reflux Disease (GERD) is just what the name implies, stomach contents refluxing back into the esophagus. If this continues to happen, the esophagus can develop a condition called Barrett's Esophagus, which increases the risk of esophageal cancer. The best treatment for hiatal hernia & GERD is weight loss. Excess body fat can increase pressure on the abdominal cavity which pushes its contents (like the stomach and/or its contents) upward. Small feedings can also reduce symptoms of both. With GERD, keeping the stomach very relaxed is a good thing. That means limiting alcohol, tobacco, high fat foods, spicy foods, etc. Antacids (proton pump inhibitors, H2-blockers, buffers) can also help moderate GERD. Surgery can also help with severe GERD. The typical procedure is called a Lap Nissen, short for laparoscopic Nissen fundoplication. Basically, the upper portion of the stomach (fundus) is wrapped around the esophagus to aid the lower esophageal sphincter in keeping the stomach contents in the stomach (remember the lap Nissen video?). We've also recently seen the introduction of magnetic collars that can be placed around the LES to increase stricture; these look promising. The opposite of GERD is achalasia, a constant state of LES contraction. Balloon dilation can help, as can surgical removal of the LES, but an injection of Botox is a lot less invasive and oftentimes very effective. We've finally reached the stomach! The stomach can have some issues, the most common are nausea and vomiting. Nausea and vomiting can be induced by infection, meds, and certain foods and can cause serious problems if it's repeated and intense. Dehydration (removing fluid), hypokalemia (removes potassium), hyponatremia (removes sodium), and alkalosis (pulling out acidic contents) can occur; rationalize how excessive vomiting can lead to each of these issues. Gastroparesis can obviously complicate digestion. For MNT, we usually decrease the intake of foods that need a lot of mechanical digestion in the stomach, like high fat foods and high fiber foods. We can provide a full liquid diet for a little while to see if the situation resolves, but a gastric pacemaker can be implanted to signal the stomach to contract and churn up its contents. The final stomach issue we discussed was peptic ulcer disease (we can also see ulcerations in the proximal small intestine). The majority of peptic ulcers are precipitated by infection with *H. pylori*. These bacteria get under the stomach's mucosal layer and set up shop, neutralizing stomach acid and eventually degrading the stomach's epithelial cells. This leads to degradation of the lining and, in severe cases, perforation of the stomach. Bad news! The key to managing peptic ulcer disease is killing the bacteria; that means antibiotics. The antacids discussed above can alleviate some of the stress on the stomach lining, but you've got to kill the *H. pylori* to make things better for the long term. If things get really bad and it can't be rectified and we're dealing with perforated ulcers, gastric resectioning can be an option. [Lower GI Disorders] Now we're moving from the pyloric sphincter all the way down to the anus. The two most common lower GI issues, that I guarantee you will see, are constipation and diarrhea. Let's talk about constipation first. Key MNT here (after this bout has resolved) is increasing daily fiber intake, which has to be accompanied by increased water intake. If water intake doesn't increase, the problem doesn't get fixed, it probably gets worse. The idea is that the increased fiber and the water that it will absorb and retain will help move things along. Laxatives can be used to stimulate peristalsis and stool softeners do what their name implies by increasing gut secretions in order to make it easier to move the feces towards the anus. Diarrhea, pretty much the opposite of constipation, can be life-threatening if not corrected or properly managed. Correction requires you to know what's causing the diarrhea. We have 3 major forms of diarrhea: secretory, osmotic & motility. Secretory diarrhea is usually related to a bacterial infection which is causing the enterocytes to secrete excessive fluid into the lumen which moves things along quicker than we'd like. Osmotic diarrhea occurs when the contents of the intestinal lumen are hypertonic. This is often a result of malabsorption. If our gut doesn't absorb all the glucose and amino acids that have been broken down, then they're going to sit in the lumen and pull wer into the lumen (remember oncotic pull). This creates that great waterslide analogy, moving things along too quickly. Motility diarrhea is just an issue of fluids moving too quickly through the intestine; water can't be absorbed quickly enough and we get that same waterslide. Meds are often an underlying cause of motility diarrhea. Rehydration and the correction of electrolyte imbalance are crucial. Excessive diarrhea can lead to hypokalemia and acidosis if not managed well. We have a number of malabsorption issues to discuss. Lactose intolerance simply means that we have insufficient lactase activity, so lactose isn't broken down and absorbed which can lead to osmotic diarrhea. Pancreatitis is often caused by gallstones blocking the pancreatic duct, which leads to pancreatic enzymes backing up and becoming activated in the pancreas. Bad news, these enzymes break things down and can do just that to the pancreas. So let's give the pancreas a break, so that it slows down enzyme production. That means NPO, hydrolyzed enteral formulas, fat restrictions, and also oral pancreatic enzyme replacement therapy (PERT); treatment depends on the patient (individualization!). Cystic fibrosis is a disease usually associated with impaired lung function, marked by very thick mucosal secretions. These thickened secretions can also block the pancreatic duct and lead to the same issues and treatments we just discussed with pancreatitis. (has the same treatments as pancreatitis but backwards) Celiac disease and tropical sprue are marked by sloughing off of intestinal cells. This means we lose our absorptive surface area... malabsorption's going to be an issue. In celiac, this is because of a gluten intolerance. Remember gluten? It's the protein found in grains, which means no wheat, rye, oats or barley for Celiac patients (gluten content isn't the true issue with oats, but rather the fact most of them are processed in the same facilities that process wheat, rye & barley). Tropical sprue is mediated by a bacterial infection. That means maintenance of fluids & electrolytes & vitamins & minerals (maybe TPN) until the antibiotics kick in and kill the bacteria causing this problem (or the immune system takes care of it). Crohn's disease is marked by inflammation of the intestine (usually ileum & colon) and a cobblestone-like appearance. Key here is working with the patient to help them realize which foods are triggering flare-ups and then helping to avoid them. Ulcerative colitis is believed to be an autoimmune disorder leading to destruction of portions of the intestine. In both of these diseases, we're worried about malabsorption during flare-ups and in managing short bowel syndrome after repeated resections. The ileum does a pretty good job of adapting to absorb nutrients usually absorbed at other places, but if the ileum's gone and we're lacking a good amount of the rest of the intestines, we might be looking at long-term TPN. Depends on the patient, how much intestine has been removed, and what other symptoms are present. If parts of the colon or the whole colon are removed, we're dealing with an ostomy. When the ileum connects directly to the outside, it's an ileostomy. When it's the colon, we call it a colostomy. MNT depends again on what portions are removed and what's remaining. If we lose a lot of large intestine, we need to increase fluid intake. Remember that the colon is the major water absorber of the gut. [Diabetes] There are two types of diabetes mellitus, appropriately named Type I and Type II. Type I is an autoimmune disease which results in destruction of pancreatic beta cells. That means no more insulin production which means lack of regulation of glycemia and chronic hyperglycemia. Type II is related to insulin resistance. Individuals are hyper insulinemic but not responding to that insulin. Obesity is usually a contributing factor to type II. We talked about excessive intake, constant hyperglycemia, resultant hyperinsulinemia and, eventually, insulin resistance. Sound familiar? Take a look at the slide of "DM Symptoms" and think about how each of these happens. Why are people with uncontrolled diabetes so thirsty? Stuff like that. If hyperglycemia is persistent, we can get some nasty complications, all related to excess glucose floating around in the blood, altering the osmolarity of the vasculature. We're looking at neuropathy, retinopathy, and nephropathy as the big 3. We also have an increased risk of CVD here, because diabetics tend to have dyslipidemia associated with their hyperglycemia. (Symptoms: polyphagia (increased hunger), polydipsia (THIRSTY), Unintentional weight loss, hyperglycemia (high blood sugar), glucosuria polyuria (excessive urination). Treatment is all about glucose control. We primarily use blood glucose monitoring and hemoglobin A1C as indicators of glycemic control. What is HbA1C and how does it relate to blood glucose? (a blood test that measures blood glucose over a period of time) Good question. It's also prudent to examine the retina for capillary degradation, the urine for ketones (lipolysis product resulting from insulin resistance) and protein (nephropathy), and the feet (remember the pic of the infected cut?). MNT is focused on glycemic control and that means controlling carbohydrate intake, usually keeping it around 50% of total caloric intake. We like complex carbohydrates and low glycemic load foods. It's a good idea to know the difference between glycemic index and glycemic load. (Glycemic index -- food CHO vs food CHO and Glycemic load is food serving size vs food serving size) There's a lot of misconstrued info out there about glycemic index/load, so you're likely to get questions when you're a practicing health professional. As dietitians, we used to use exchange lists for diabetic meal planning but have now shifted to carb counting because it's, in theory, easier for our patients to understand. The basic premise is that 15g of carbohydrate equals one carbohydrate serving. Based on a patient's energy needs, we can then figure out how much carbohydrate they need (50%), convert that to grams (4kcal/g), and then break that down into carb servings (15g/serving) and allocate those throughout the day. There are plenty of lists/tables out there describing how much of a certain food makes up one carb serving. Check out Table 20-5 for a refresher. Type I diabetics need insulin to manage their hyperglycemia. They can't make it, so we give it via injection. Can't do it in a pill because insulin is a protein and would be degraded before it could be absorbed into the blood. There are a number of insulins on the market, with various times of onset and duration. We can use a combination of injections of long-acting and short-acting to keep glycemia in control and to manage the increases that are typical following a meal. In practical terms, most Type I diabetics use an insulin pump that allows for basal insulin infusion and bolus infusion based on carbohydrate intake. Type II diabetics, however, have a number of drugs available to manage their disease. The major classes are insulin secretories, insulin sensitizers, glucagon suppressors, hepatic glucose regulators, glucose absorption inhibitors, and peptide analogs. Take a look at these 6 slides and Table 20-7 to review these drugs. (Stimulate pancreas to secrete insulin -- Sulfonylureas (Glucotrol), Meglitinides (Starlix), Increase insulin sensitivities- Thiazolidinediones (Avandia, Actos), Supress pancreatic glucagon secretion- Amylin analogs (Pramlintide), Inhbit hepatic glucose production- Biguanides (Metformin), Delay intestional CHO absorption- Alpha-Glucosidase Inhibitors (Precose), Peptide Analogs- Glucagon-like peptide (Byetta) and Dipeptidyl peptidase-4 (Januvia) Physical activity is usually a good idea for Type II diabetics since obesity is often a precursor to the disease. It's important to remember that activity increases insulin sensitivity and decreases plasma glucose. This is especially important for those using insulin, since we don't want to induce hypoglycemia. [Cardiovascular Disease] CVD is a major killer of Americans and, for the most part, it's a preventable disease. When we have a lot of lipoproteins and fatty acids floating around in our blood (↑VLDL/LDL, ↑TG), some of it gets deposited along and inside the walls of our blood vessels. That means that the passageway for blood flow becomes smaller and can get blocked off. Well, that's bad news for any major organs downstream of the blockage because they're no longer going to receive fresh, oxygenated blood. If this happens in a coronary artery, it's a heart attack. If it happens in a cerebral artery, it's an ischemic stroke. The other bad thing about fatty deposits in the blood vessels (aka- atherosclerosis), is that they tend to weaken the BV wall. If it gets weak enough, it can pop (aka- aneurysm). These atherosclerotic lesions are also relatively sticky, when compared to the usually smooth interior of the BV. That means that we may get platelets hanging out here and forming a clot (aka- thrombus). If a piece of that clot breaks off and starts cruising around the cardiovascular system it can get stuck in smaller capillaries or at branch points and bends of the vasculature and block things up (aka- embolism, think of a pulmonary embolism). We talked about two types of stroke. The majority of strokes (\~80%) are ischemic strokes; one of those emboli mentioned before has made its way to the brain and gets stuck in a cerebral artery/vein/capillary. That means no more oxygen exchange in that region of the brain and some potentially severe consequences depending on the area of brain and duration of hypoxia. Clot busting drugs are the primary means of treatment here and need to be administered quickly -- call 911 anytime someone starts slurring their speech, gets tingly/numb on one side of the body, has a seizure, etc. Time is of the essence. The other type of stroke is a hemorrhagic stroke which occurs when a cerebral aneurysm pops. Clot busting drugs are absolutely the wrong move here, since they'll only contribute to increased bleeding. Surgery is often the best fix or the provision of pro-clotting drugs. The risk factors for stroke are the same as those for CVD described above. (Age, male gender, fam history of Hdx, high blood LDL cholesterol, low blood LDL cholesterol, hypertension, diabetes, obesity, no physical activity, smoking, "atherogenic diet: high saturated fats, low veggies, fruits, and whole grains.) We're still dealing with blood vessels, they just happen to be in the brain, a rather sensitive and important organ. We discussed a number of CVD risk factors, some modifiable, some not. It's a good idea to be able to think about each of those risk factors and rationalize how it relates to cardiovascular health and why it might be a contributor to CVD. (LOOK uo Like I said, CVD is overwhelmingly preventable and a big piece of that prevention is diet. Step 1 in prevention is eliminating *trans* fat intake and limiting saturated fat intake (\