Nrsg 3304 Lecture Notes on Nutritional Physiology PDF

Addison’s Disease Non-diabetic and Diabetic Hypoglycaemia Special diets (renal, heart health diet, malabsorption syndrome, iron deficiency anemia) 1  Lecture Outline Normal distribution of nutrients in the body Overview of normal glucose regulation...

Addison’s Disease Non-diabetic and Diabetic Hypoglycaemia Special diets (renal, heart health diet, malabsorption syndrome, iron deficiency anemia) 1  Lecture Outline Normal distribution of nutrients in the body Overview of normal glucose regulation Addison’s Disease- Aetiology, Pathophysiology, Nutrition Non-diabetic and Diabetic Hypoglycaemia- Aetiology, Pathophysiology, Nutrition Special diets (renal, heart health diet, 2  OVERARCHING THEMES OF LECTURE To support one’s biochemistry in a manner that supports health, one needs to get nutrients to where (W) they are needed, when (W) they are needed, in form(s) (F) needed and in the quantity (Q) of 3 Ingestion (I) is the just the start We must also have Digestion (D) Absorption (A) Transport (T) Metabolism (M) Excretion (E) 4  Ingestion (I) is getting nutrients into the body (oral, feeding tube, iv, central line) This lecture deals solely with oral ingestion 5  Ingestion (I) leads to Digestion (D) Digestion is the breaking up of the food and molecules in the mouth and gastrointestinal (GI) tract so that individual molecules and atoms can be 6  Digestion(D) leads to Absorption (A) Absorption is the movement of molecules and atoms (i.e. the nutrients) from the digested food and digested molecules into the blood or lymph 7  Digestion (D) leads to Absorption (A) http://wowzahttp.cengage.co m/digital-production/nutrition/ 0308.mp4 8  Absorption (A) leads to Transport (T) Transport is the movement of molecules and atoms that have been absorbed This movement gets molecules and atoms to where and when they need to be 9  Absorption (A) leads to Transport (T) Transport video http://wowzahttp.cengage.com/dig ital-production/nutrition/circulatio n_final.mp4 10  Transport (T) leads to getting molecules and atoms to where (W) and when (W) they are needed to be for metabolism (M) Various aspects of metabolism occur in different parts of the body so transport is important for molecules and atoms to get to where and when 11  Metabolism (M) gets molecules and atoms into the correct form (F) and quantity (Q) for usage in the body’s biochemistry 12  When the body is done with molecules and atoms they are excreted (E) and so one goes back to ingestion (I) Humans are one big never-ending metabolism reno job (constant tear down and build up) 13  Without this regulation of IDATME nutrients can not get to where (W) they are needed, when (W) they are needed, in form needed (F) and in quantity (Q) needed 14 Normal physiological mechanisms of plasma glucose concentration regulation (hormones involved) Insulin- glucose rises, insulin rises, glucose leaves blood and goes into cells Glucagon-glucose falls, glucagon rises, glycogen broken down into glucose and glucose enters blood Other hormones affect blood sugar levels Focus on insulin and glucagon 15 Regulation of Plasma Glucose Level 16 Normal physiological mechanisms of plasma glucose concentration regulation (hormones involved) https://www.youtube.com/watch?v=eDm9hE On8zc 17 Normal physiological mechanisms of plasma glucose concentration regulation (hormone receptor function) Insulin binds to an insulin receptor on liver, muscle, adipose tissue (major targets) Insulin receptor is a protein with a specific configuration that allows for the binding of insulin 18 19  Endocrine Pancreas  Pancreas is both an endocrine and an exocrine gland  Houses the islets of Langerhans  Secretion of glucagon and insulin  Cells: Alpha—glucagon Beta—insulin and amylin Delta—somatostatin and gastrin F cells—pancreatic polypeptide Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 20  Endocrine Pancreas (Cont.) From Patton, K.T., & Thibodeau, G.A. (2016). Structure & function of the body (15th ed.). St Louis, MO: Mosby. Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 21  Endocrine Pancreas (Cont.)  Insulin  Synthesized from proinsulin  Secretion is promoted by increased blood levels of glucose, amino acids, GI hormones  Facilitates the rate of glucose uptake into the cells of the body  Anabolic hormone Synthesis of proteins, lipids, and nucleic acids  Amylin  Peptide hormone cosecreted with insulin  Delays nutrient uptake  Suppresses glucagon secretion Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 22  Endocrine Pancreas (Cont.)  Insulin action on cells Redrawn from Levy, M.N., et al. (Eds.). (2006). Berne & Levy principles of physiology (4th ed.). St Louis, MO: Mosby. Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 23  Endocrine Pancreas (Cont.)  Glucagon  Secretion is promoted by decreased blood glucose levels  Stimulates glycogenolysis, gluconeogenesis, and lipolysis  Pancreatic somatostatin  Possible involvement in regulating alpha-cell and beta-cell secretions  Gastrin, ghrelin, and pancreatic polypeptides Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 24  Endocrine Pancreas (Cont.)  Secretion of insulin is: - inhibited by somatostatin - promoted by gastrin - inhibited by ghrelin - no indicated impact of pancreatic polypeptide  Pancreatic polypeptide may increase insulin sensitivity  Secretion of glucagon is: - inhibited by somatostatin - unaffected?/promoted? by gastrin - promoted by ghrelin - perhaps inhibited by pancreatic polypeptide Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 25 2. Insulin is secreted by the pancreas from which type of cell? A. F B. Beta C. Delta D. Alpha Copyright © 2019, Elsevier Canada, a division of Reed Elsevier Canada, Ltd. All rights reserved. 26 Insulin binds to an insulin receptor on liver, muscle, adipose tissue (major targets) Insulin receptor is a protein with a specific configuration that allows for the binding of insulin 27 Post-insulin binding causes a signalling cascade that ultimately allows glucose to come in side the cell) 28 Post-insulin binding signalling cascade causes a glucose transport protein to rise to the surface of the cell to bring glucose into the cell 29  Glucagon binds to an glucagon receptor on liver (major target for glucose release) Glucagon receptor is a protein with a specific configuration that allows for the binding of glucagon 30  Glucagon binding causes a signalling cascade that ultimately allows for the breakdown of glycogen to glucose and the release of glucose from the liver 31 Normal physiological mechanisms of plasma glucose concentration regulation (glut transporter for getting glucose into (in response to insulin) and out of liver –out of liver in response to signalling cascade arising from glucagon binding) 32 How Insulin Decrease Plasma Glucose Level? 33  Carbohydrate Metabolism  Carbohydrates are metabolized in the body to glucose.  CNS uses glucose as its primary energy source. This is independent of insulin.  Glucose is taken by the muscle to produce energy (insulin required).  Glucose is stored in the liver as glycogen and in adipose tissues as fat.  Insulin is produced and stored by the β- cells of the pancreas 34  Carbohydrate Metabolism (Cont’d) – Postprandial glucose metabolism in normal individuals:  After food is ingested, blood glucose concs rise and stimulate insulin release. – Insulin action: – glucose uptake by the tissues – liver glycogen formation and glycogen breakdown – lipid synthesis and inhibits fatty acid breakdown to ketone bodies – Promotes protein synthesis 35 Physiological significance of normal plasma glucose concentration regulation –must meet key roles of glucose by avoiding disruption of glucose homeostasis Healthy roles for glucose Upon glucose homeostasis dysregulation one sees unhealthy aspects of glucose elevations 36  OVERARCHING THEMES OF LECTURE Compromised WWFQ can result from aetiology and pathophysiology Compromised WWFQ means that specific dietary approaches are 37  OVERARCHING THEMES OF LECTURE As we go through each of the pathologies, please look for where WWFQ is disrupted and how nutrition is used to improve the WWFQ via IDATME 38  Addisons-Overview Dr Thomas Addison in 1855 Addison’s: –Affects 1 in 10000 – rare –Common presentation between ages of 30 and 50 –Affects women more  Aetiology continued Autoimmune attack on adrenal gland Tuberculosis- (most common worldwide but tuberculosis is most common in developing countries) Infections – AIDS, fungal Adrenal haemorrhage (caused by sepsis, meningitis) Metastatic spread to adrenals Amyloidosis Adrenalectomy Genetic/congenital defects Addison’ disease-pathophysiology Addison's disease, also called adrenal insufficiency uncommon disorder that occurs when your body doesn't produce enough of certain hormones. produce too little cortisol and, often, too little aldosterone. Addison's disease occurs in all age groups and both sexes, and can be life-threatening. 41 HPA axis PATHOPHYSIOLOGY OF ADDISON’S DISEASE  Hyponatremia due to low cortisol causing increase in vasopressin secretion/action and inability to excrete free water.  Low aldosterone causing hyperkalaemia  High adrenocorticotrophic hormone (ACTH) due to low cortisol  Low glucose (cortisol stimulates glycogenolysis (via increased glucagon release) and gluconeogenesis (via protein catabolism to generate gluconeogenic amino acids); low cortisol increases insulin sensitivity S&S  Complications – Addisonian Crisis severe dehydration pale, cold, clammy skin sweating rapid, shallow breathing dizziness severe vomiting and diarrhoea severe muscle weakness headache severe drowsiness or loss of consciousness coma and death  Addison’s disease-nutrition Higher sodium intake If on high dose corticosteroids- increased vitamin D and calcium as high dose corticosteroids are linked to higher risk of osteoporosis Lower potassium intake if warranted Comfort food (high simple) sugar reported 46 Hypoglycaemia Diabetic and non-diabetic 47 Hypoglycaemia: Aetiology and Pathophysiology -Failure of hypoglycaemia counter-regulatory mechanisms: decreases in insulin production first line of defense against hypoglycemia. hepatic glycogenolysis, low insulin levels are necessary as plasma glucose levels decline, beta cell secretion of insulin also decreases, thus leading to increased hepatic/renal gluconeogenesis and hepatic glycogenolysis. glycogenolysis maintains serum glucose levels over 8 to 12 hours until glycogen stores are depleted. Over time, hepatic gluconeogenesis contributes more to maintaining euglycemia when required. the decrease in insulin production occurs while the glucose level is in the low-normal range. This serves as a distinctive feature compared to other counter-regulatory measures. pancreatic alpha cell secretion of glucagon is the next line of defense against hypoglycemia. Should increased glucagon fail to achieve euglycemia, adrenomedullary 48 Hypoglycaemia: Aetiology and Pathophysiology -Failure of hypoglycaemia counter-regulatory mechanisms: Growth hormone stimulates gluconeogenesis and insulin resistance 49  Hypoglycaemia-aetiology Type of Non-diabetic Possible Causes Hypoglycemia Having pre-diabetes or being at risk for diabetes, which can lead to trouble making the right amount of insulin Stomach surgery, which can make food pass too quickly into Reactive hypoglycemia your small intestine Rare enzyme deficiencies that make it hard for your body to break down food Medicines, such as - salicylates (a type of pain reliever) - sulfa drugs (an antibiotic) - pentamidine (to treat a serious kind of pneumonia) - quinine (to treat malaria) Alcohol, especially with binge drinking Fasting hypoglycemia Serious illnesses, such as those affecting the liver, heart, or kidneys Low levels of certain hormones, such as cortisol, growth hormone, glucagon, or epinephrine Tumors, such as a tumor in the pancreas that makes insulin or a tumor that makes a similar hormone called IGF-II Not getting enough to eat 50 Non-diabetic Hypoglycaemia-Pathophysiology An irregular or fast heartbeat Fatigue Pale skin Shakiness Anxiety Sweating Hunger Irritability Tingling or numbness of the lips, tongue or cheek As hypoglycemia worsens, signs and symptoms can include: Confusion, abnormal behavior or both, such as the inability to complete routine tasks Visual disturbances, such as blurred vision Seizures 51 Non-Diabetic Hypoglycaemia- Nutrition immediate treatment of low blood glucose, eat or drink 15 grams carbohydrate (in form of juice, glucose tablets, or hard candy). eating small meals and snacks throughout the day, eating about every three hours having a variety of foods, including protein (meat and nonmeat), dairy foods, and high-fiber foods such as whole-grain bread, fruit, and vegetables limiting high-sugar foods 52  Diabetic Hypoglycaemia-aetiology Taking too much insulin or diabetes medication Not eating enough Postponing or skipping a meal or snack Increasing exercise or physical activity without eating more or adjusting one’s medications Drinking alcohol 53 Diabetic Hypoglycaemia-pathophysiology An irregular or fast heartbeat Fatigue Pale skin Shakiness Anxiety Sweating Hunger Irritability Tingling or numbness of the lips, tongue or cheek As hypoglycemia worsens, signs and symptoms can include: Confusion, abnormal behavior or both, such as the inability to complete routine tasks Visual disturbances, such as blurred vision Seizures 54  Diabetic Hypoglycaemia-Nutrition Don't skip or delay meals or snacks. If you take insulin or oral diabetes medication, be consistent about the amount you eat and the timing of your meals and snacks. Adjust your medication or eat additional snacks if you increase your physical activity. The adjustment depends on the blood sugar test results, the type and length of the activity, and what medications you take. Eat a meal or snack with alcohol, if you choose to drink. Drinking alcohol on an empty stomach can cause hypoglycemia. Alcohol may also cause delayed hypoglycemia hours later, making blood sugar monitoring even more important. 55  Special diets get each of the nutrients to where (W) they are needed, when (W) they are need, in the form (F) they are needed, and in the quantity (Q) they are needed so as to meet the metabolic needs of the body that would not otherwise be met due to the pathology 56  Special Diets Used to treat or prevent certain conditions. Specific modified diets include changes for:  Texture  Nutrient level  Frequency  Timing of meals  Exclusions  Examples of Special diets Renal 58  Examples of Special diets Excretion-diet for chronic kidney disease Necessary as kidney progressively loses its ability to play its role in water and electrolyte balance in the body and in ridding the body of urea and creatinine 59  Examples of Special diets Excretion-renal diet Chronic kidney disease  Examples of Special diets Excretion-chronic kidney disease diet – Used for patients with chronic kidney disease. – Protein restriction with restrictions of fluid, sodium, potassium, phosphorus – Diet becomes progressively more restricted as renal disease progresses stage 1- 4; dialysis required at stage 5  Examples of Special Diets Excretion-chronic kidney disease Foods Lower in Foods Higher in Phosphorus Phosphorus Fresh fruits and Meat, poultry, fish vegetables Bran cereals and Breads, pasta, rice oatmeal Rice milk (not enriched) Dairy foods Corn and rice cereals Beans, lentils, nuts Light-colored Dark-colored sodas/pop, such as sodas/pop, fruit punch, lemon-lime or some bottled or canned homemade iced tea iced teas that have  Examples of Special Diets Excretion-chronic kidney disease Foods Lower in Potassium Foods Higher in Potassium Apples, peaches Oranges, bananas, and Carrots, green beans orange juice White bread and pasta Potatoes, tomatoes White rice Brown and wild rice Rice milk (not enriched) Bran cereals Cooked rice and wheat Dairy foods cereals, grits Whole-wheat bread and Apple, grape, or cranberry pasta juice Beans and nuts Spironolactone (Aldolactone) can be used in CKD patients to lower blood pressure but is a potassium- sparing drug  Examples of Special Diets Excretion-chronic kidney disease Foods Lower in Sodium l Fresh or frozen fruits and vegetables l Rice, noodles l Cooked cereal without added salt l Fresh meat, poultry, seafood l Low-fat, low-sodium cheese l Unsalted nuts l Low- and reduced-sodium frozen dinners, peanut butter, salad dressings l Air-popped popcorn Foods Higher in Sodium l Bacon, corned beef, ham, hot dogs, luncheon meat, sausage l Bouillon, canned, and instant soups l Boxed mixes, like hamburger meals and pancake mix l Canned beans, chicken, fish and meat l Canned tomato products, including juice l Canned and pickled vegetables, vegetable juice l Cottage cheese l Frozen meals l Frozen vegetables with sauce l Olives, pickles, relish l Pretzels, chips, crackers, salted nuts l Salt and salt seasonings, like garlic  Examples of Special Diets Excretion-chronic kidney disease diet Aproteids High Protein Meat, such as pork, beef, chicken, turkey, duck, Eggs Dairy products, such as milk, yogurt, cheese, Fish Beans, peas, lentils,Soy foods, such as soy milk, tofu, Nuts and nut spreads, such as almond butter, peanut butter, soy nut butter, Sunflower seeds Low Protein  Examples of Special Diets Excretion-chronic kidney disease Protein Eat smaller portions of meat and dairy. This helps lower the amount of phosphorus in diet, because phosphorus is found in meat and dairy foods. – Meat, poultry, and fish: A cooked portion should be about 2 to 3 ounces or about the size of a deck of cards. – Dairy foods: A portion is ½ cup of milk or yogurt, or one slice of cheese. Plant proteins should make up the rest of the protein that you eat. A serving is: – ½ cup of cooked beans – ¼ cup of nuts – a slice of bread  Examples of Special diets Heart health diet LDL carries most of the cholesterol in the blood and elevated LDL-c contributes to the atherosclerotic process (arteries clogged with fat) 68  TLC diet-mainly post-onset management of metabolic syndrome Component TLC Diet Total fat 25-35% of total calories* Saturated fat