Carbohydrate and Protein Metabolism
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| Carbohydrate (starch, sugar, milk, maltose etc) accounts for at least 50% of the American diet | ||
| Only monosaccharides (galactose,glucose, fructose) are absorbed by the intestinal mucosa | ||
| Complex carbo. (polysaccharides & oligosacharides) must be hydrolyzed to their simplest form | ||
| Salivary and pancreatic amylases break down starches to oligosaccharides | |
| Half of the starch hydrolysis occurs in the stomach and about half in duodenum. | |
| Most glucose comes from dietary intake of carbohydrates. Most complex carbo. are eventually broken down to glucose. | |
| The liver stores extra glucose in the form of GLYCOGEN. With excess glucose intake, glucose is not stored as glycogen but is converted to adipose tissue. | ||
| 4 major hormones influence serum glucose levels | ||
| 1. Insulin - secreted by beta cells of pancreas. Transport glucose into the cells. Lack of insulin increase blood glucose levels | ||
| 2. Glucagon - secreted by alpha cells of the pancreas, elevates blood glucose levels by promoting the conversion of glycogen to glucose | |
| 3. Other hormones can also increase blood glucose levels | |
| 4. Human placental lactogen (HPL) in pregnancy can increase blood glucose levels. |
| Type I - primarily due to pancreatic beta cell destruction. Can lead to ketoacidosis | |
| Type II - more prevalent and is related to some type of insulin problem | |
| Both Type I and II can cause multiple problems if not controlled. |
| A fasting blood sugar greater than 126 mg/dL two times indicates diabetes. | |
| Borderline results may be followed by a carbo. loading test for a definitive diagnosis. | |
| Fast the client for at least 8 hours before the test, but H2O intake is still allowed. If the patient is already on insulin both food and insulin are withheld |
| Plasma glucose levels are higher than whole blood because the RBCs are not as rich in glucose as in the plasma. | |
| The blood is collected in a tube with an fluoride mixture as a glycolytic inhibitor (Gray -topped vacuum tube) | |
| Postprandial or post cibum (p.c) means after a meal and the PC blood sugar test is used to determine how the body responds to the ingestion of carbo. after a meal |
| FBG across the lifespan | ||
| Newborn less than 40 mg | ||
| Adults 70 - 110 dL | ||
| Pregnancy slightly lower than adults | ||
| Older adults may be slightly higher | ||
| Blood glucose finger sticks common method to monitor blood sugar trends. A non invasive method using a laser device maybe a possibility in the future. | ||
| Excellent way to diagnose diabetes mellitus | |
| The patient must eat a “normal” diet for several days before testing. Have the pt. fast during the night except for H2O. At the start of the test a FBG may be drawn then have the pt. drink 75 -100 g of glucose dissolved in H2O. Fingerstick Glucose are taken at 1,2,& 3 hrs and plotted on a graph. Too long to return to baseline or never returning to fasting levels (reference values p. 195) |
| With prolonged hyperglycemia, the Hbg remains saturated with glucose by glycohemoglobin (GHB). The test is weighted average of glucose level over the last few months. | ||
| After age of 6 months at least 90% of Hbg is Hbg A. The glycolated part of Hbg is designated A1 with 3 subunits (A1a,A1b,A1c). A1c is the most abundant of the 3 so many labs only report A1c but many due a total A1. | ||
| The relationship between glucose and glycosylated hemoglobin cna be detailed. It must be obtained from individual labs. For KUMC it is: | ||
| GlycoHgb% | Estimated Avg. Glu mg/dl | |
| 5-8 | 110 | |
| 9 | 140 | |
| 10 | 170 | |
| 11 | 200 | |
| 13 | 260 | |
| 14 | 290 | |
| 15 | 320 | |
| 16 | 350 | |
| 17 | 380 | |
| Most common reason for persistently elevated blood glucose is diabetes mellitus and lead to acidosis and coma | ||
| Glucose levels | ||
| Mild = 300 - 450 mg/dL | ||
| Moderate = 450 - 600 mg/dL | ||
| Severe = 600 mg/dL | ||
| Many causes: diabetes, stress, pregnancy, drugs. | ||
| 3 Levels of glucose intolerance - hyperglycemia, ketosis, ketoacidosis | ||
| Signs and Symptoms | ||
| polyuria, freq. UTI, polydipsia | ||
| Wt. Loss if child onset, Wt. Gain if adult | ||
| poor turgor | ||
| blurred vision | ||
| nausea and vomiting | ||
| Ketosis | ||
| ketones in urine, weak, | ||
| metallic taste, acetone breath | ||
| Develops when there is a problem with usage or amount of insulin (Glucose 300-750 mg/dL) | |
| Increased risk with Type I diabetes and nondiagnosed diabetes | |
| Predisposing factors: stress = infection, accident, trauma, emotional stress, omission of insulin, medication | |
| Symptoms = dry mouth, headache, weight loss, N & V, pruritus, abd. Pain, lethargy, SOB, acetone odor, malaise, polyuria, polydipsia | |
| Free fatty acids in HHNKS are lower than those in DKA. Lack of ketosis. Glucose levels are considerably higher in HHNKS than DKA. Maybe due to lack of ketonemia in HHNKS permits greater synthesis of glucose and thus more severe hyperglycemia (600-2000 mg/dL) | |
| Therapy is focused to reduce blood sugar levels by replacing fluids & sometimes giving insulin. | |
| Increase chance of increased viscosity of blood so risk of venous thrombi | |
| If there is not enough glucose to the cells the body will mobilize fat and proteins for energy, KETONE bodies (acetoacetic acid, acetone and hydroxybutyric acid) are the by-products | |
| Need 2 ml of blood, hemolysis of specimen can interfere with measurement. | |
| Negative < 2 mg/dL is normal | |
| Purpose of test to distinguish between diabetic ketoacidosis and HHNK | |
| Red topped tube used for serum and if for plasma levels use gray-topped. | |
| Caused by in diabetic clients | ||
| Too much insulin and less freq. too high dose of oral hypoglycemic drugs | ||
| Too little food | ||
| Increased exercise without additional food | ||
| Is always a potential problem for pregnant women and infants | ||
| Nondiabetic clients – there are 2 groups | ||
| Fasting = suggest serious organic disease (pancreatic tumor, Addison’s disease, liver disease, pituitary problem and alcohol induced) | ||
| Postprandial “reactive” – hypoglycemia after a meal | ||
| Sign and Symptoms (pg 200, Table 8-3) | ||
| Diaphoresis, tachycardia, dizziness, tremors due to increase surge of epinephrine to try to increase blood sugar levels. Pts. on beta blockers will not have tachycardia or shakiness | ||
| Nursing should assess early if possible and provide treatment (4 oz O.J. = 10 g simple carbo., other sugar containing beverage or treat) | ||
| Can’t swallow, honey or cake gel can be put under the tongue. | ||
| After 30 mins be sure to give protein and complex carbo. | ||
| Lactase is an enzyme that is in the small intestine use to digest lactose the sugar that is in milk products. | |
| Some genetic and other factors cause pts. to be deficient in lactase so digestive problems | |
| Test lactose by giving a known amount of lactose and then test the blood glucose levels at various intervals. An increase of less than 20 mg of glucose – get GI problems (bloating, diarrhea) | |
| Treatment is to remove all lactose from the diet, reintroduce gradually or capsules with lactase before or with meals with dairy products |
| Inherited disorder in which galactose cannot be converted to glucose because of a missing enzyme. Galactose is wasted in the urine. It can be detected in urine. | |
| Diet without galactose should be instituted within a newborn period or the infant can have mental retardation, cataracts and other neurologic problems. So no mil products for newborn | |
| Early signs are vomiting, liver enlargement and jaundice |
| Protein intake varies but a person needs 44 - 56 g of protein per day. | |
| Approx. 20 - 30 g of protein is derived endogenously from the epithelial cells and plasma proteins | |
| Most protein is absorbed; only 5 -10% is eliminated in the stool | |
| Major protein hydrolysis in small intestine; broken down into amino acids | |
| Albumin is produced by the liver and is needed to maintain oncotic pressure in the vascular system | |
| Too low then fluid leaks out into the interstitial spaces and cavities | |
| Also important in transporting substances in the blood such as calcium and is a buffer to maintain acid-base balance in bloodstream | |
| Many drugs, lipids, hormones can bind to albumin | |
| Also a reserve nitrogen source for tissue growth and healing | |
| Globulins in general are either immunologic agents or enzymes | ||
| Very complex and diversified group of serum proteins | ||
| a-1 globulins contain lipoproteins, antitrypsin, glycoproteins | ||
| a-2 contain hormones such as erythropoietin | ||
| b-1 contain vitamins, transferrin, plasminogen, hormones | ||
| b-2 contain various parts of complement system and fibrinogen | ||
| Broad indicator of the quantity and concentration of all plasma proteins except fibrinogen. | ||
| Measures the amount of albumin and globulins combined | ||
| It is nonspecific test | ||
| Range: adult = 6-8 g/dL, newborn = 4.6-7.4 g/dL | ||
| Low value less than 4.0 g/dL together with a low serum albumin level cause EDEMA | ||
| Decreased – prolonged malnutrition, starvation, GI cancer, ulcerative colitis, Hodgkin’s disease, seer liver disease, chronic renal failure, water intoxication, malabsorption syndrome | ||
| Smallest molecule yet is the largest component of plasma proteins responsible for 80% of colloidal osmotic pressure | |
| Normal value – Adult > 60 = 3.4 – 4.8 g/dL, Adult 18-60 years 3.5-5 g/dL, newborn 2.8-4.4 g/dL | |
| Decreased – many reasons, acute & chronic inflammation disease, liver disease, inflam. bowel syndrome, malnutrition, peritonitis, ascites | |
| Increased – Loss of vascular fluid because a reduction in volume of fluids the albumin levels will rise because they are more concentrated in the blood |
| 2.5 times bigger than albumin, | |
| Many drugs affect this value – aspirin, bicarbonates, corticosteriods, salicylates, estrogen, testosterone etc. | |
| Also includes the gamma immune proteins (antibodies) such as IgG, IgA, IgM, IgE | |
| Normal globulin is 2.8-4.4 g/dL | |
| Decreased: Hypogammaglobulemia, multiple myeloma | |
| Increased: Inflammatory disease, cirrhosis, chronic active hepatitis, sarcoidosis | |
| Albumin/globulin ratio (A/G ratio) – normal > 1.0, used to identify the proportional amts. of these 2 proteins in the blood. Low in if pt. has cirrhosis, severe infections, ulcerative colitis, chronic nephritis etc. | |
| Caused by increase loss of protein in urine, burns, inadequate intake, decreased production (liver failure), malabsorption, true protein def (Kwashiorkor) | |
| Pt will be edematous when albumin fall be 2.0-2.5 g/dL, not just dependent edema | |
| Be sure to weight patient, measure abd. girth, prevent dependent edema, provide skin care, give diet high in protein and carbohydrates. |
| Ammonia is a byproduct of protein catabolism and is made during the process of deamination of amino acids. It is made by metabolizing tissues in the body and by bacterial activity on protein in the intestine. When ammonia enters the bloodstream the liver removes it from the portal vein circulation. Pts. with hepatic problems, ammonia is converted to urea then the kidneys remove the urea from the circulation and it is excreted in the urine. | |
| Elevated ammonia level is an indication of the failure of hepatic cells to function in the conversion of ammonia to urea & portal vein circulation problems which prevents ammonia from reaching the liver |
| Purpose of the test is to evaluate or monitor liver failure or impair portal vein circulation | ||
| Also used in children to diagnose Reye’s syndrome | ||
| Use green topped tube & collect 7-10 ml venous blood | ||
| Normal – adults=15-45 ug/dL, neonate 90-150 ug/dL | ||
| In severe liver disease blood urea nitrogen (BUN) drops as ammonia level rises | ||
| Preparation of pt. = Fasting, water allowed, 1 ml of venous or arterial blood. Blood must be heparinized and packed in ice & rotated immediately to chill the specimen | ||
| Interfering factors = tobacco smoke, high protein intake, GI hemorrhage, hyperalimentation (TPN) | ||