Carbohydrate and Potein Metabolism

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Carbohydrate Metabolism

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.

Glucose Metabolism

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.

Diabetes Mellitus

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.

Fasting Blood Sugar or   Plasma Glucose

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

Sampling

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

Changes in Carbohydrate

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.

Oral Glucose Tolerance Test (GTT)

 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)

Glycohemoglobin and Hemoglobin A1C

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

            Hyperglycemia

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

Diabetic Ketoacidosis

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

Hyperglycemic Nonketotic Syndromes (HHNK)

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

Serum Acetone or Ketones

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.

Hypoglycemia

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

  1. Fasting = suggest serious organic disease (pancreatic tumor, Addison’s disease, liver disease, pituitary problem and alcohol induced)
  2. Postprandial “reactive” – hypoglycemia after a meal

Hypoglycemia

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.

Lactose Tolerance Test

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

Galactosemia

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

Slide 20

Protein Metabolism

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

Function of Albumin

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

Functions of Globulins

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

Total Protein

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

Serum Albumin

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

Globulin

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.

Hypoproteinemia

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.

Serum Ammonia (NH3)

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)

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