Diabetes Mellitus

Pancreas
is elongated gland located in the upper portion of the posterior abdominal wall, behind the stomach. it has important types of exocrine and endocrine tissues. the islets of Langerhans secrete insulin and glucagon directly into the bloodstream

The islets of Langerhans contain three major types of cells

a. Alpha cells secrete glucagon b. Beta cells secrete insulin

c. Delta cells secrete somatostatin.

Insulin
Glucose Metabolism
The average adult secretes approximately 35 50 units of insulin per day. Insulin facilitates the diffusion of glucose from the bloodstream into the cells, particularly liver, muscles, and fat cells. Therefore, a major function of insulin is to enhance the transport and utilization of glucose by most cells of the body.

 insulin causes glucose to be stored in the liver in the form of Glycogen. as blood glucose levels decline, the amount of insulin in the bloodsteam decreases and glycogen is broken down into glucose. insulin also causes the glucose in the liver to be converted into fatty acids, which are transported to adipose tissues of the body and deposited as fat.

 Generally, muscles utilize fatty acids for energy, except during exercise and a few hours after meal.

During exercise, the muscles become permeable to glucose, even in the absence of insulin. After meals, insulin secretion is increased, causing the transport of glucose into muscle cells, where it is used fro energy. If there is limited exercise after a meal, glucose is transported to the muscles and is stored in the form of glycogen.

 insulin promotes the entry of potassium and magnesium into the cells, lowering extracellular levels of electrolytes. the control of insulin release is related to the concentration of glucose in blood flowing through the pancreas. an increase in blood glucose levels stimulates the release of insulin. the insulin causes the rapid entry of glucose into cells, thereby reducing the level of blood glucose.

Synthesis of Fatty Acids

insulin promotes fatty acid synthesis by the liver and fat cells. most of the fatty acids synthesized by the liver are transported to adipose cells, where they are stored as fat.

Synthesis of Protein
Insulin promotes the synthesis of protein by causing active transport of many of the amino acids into the cells. Insulin inhibits the catabolism of proteins. This subsequently reduces the rate of protein catabolism and the release of amino acids from cells.

 an elevated amino acid concentration causes the release of insulin. the increase release of insulin subsequently increases the transport of amino acids into cells. reduced concentrations of amino acids inhibit the release of insulin. after a meal, several gastrointestinal hormones, including gastrin, secretin, and cholecystokinin, are released. These, in turn, cause an increase in insulin secretion.

Glucagon
the major effects of glucagon are opposite those of insulin. Glucagon increases the blood glucose concentration. this is accomplished through increased liver glycogenolysis, the breakdown of glycogen into glucose, and increased gluconeogenesis. Glucagon also stimulates lipolysis (breakdown of fat) and the release of fatty acids into the circulation.

 The secretion of glucagon is controlled by plasma concentrations of glucose and amino acids. a decrease in blood glucose and amino acids increases the secretion of glucagon. when blood glucose levels decrease, the pancreas secretes large amounts of glucagon, which rapidly mobilizes glucose from the liver.

 Exercise tends to increase the release of glucagon.

Blood glucose concentrations decrease with exercise, in turn, causing glucagon to mobilize glucose for use by the muscles.

Conversely, an increase in blood glucose and amino acids inhibit the secretion of glucagon.

Somatostatin
Functions:
slow gastric emptying decrease gastric acid secretion diminish contraction of gallbladder. the hormone prevents excessive levels of nutrients from entering the systemic circulation by inhibiting the rates at which food is digested and absorbed.

stimuli that cause the release of somatostatin from the pancreas include the presence of food in the gastointestinal tract and, ultimately, the increase in circulating levels of glucose and amino acids.

Diabetes Mellitus
is a group of metabolic deiseases characterized by elevated levels of glucose in the blood (hyperglycemia) resulting from: a. defects in insulin secretion b. insulin action or both normally a certain amount of glucose circulates in the blood.

Insulin
a hormone produced by the pancreas, controls the level of glucose in the blood by regulating the production and storage of glucose.

In the diabetic state:

the cells may stop responding to insulin

or
the pancreas may stop producing insulin entirely.

This leads to hyperglycemia, wich may result in acute metabolic complications such as:

1. Diabetic ketoacidosis (DKA) 2. Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) Long-term effects of hyperglycemia
a. Macrovascular complications (coronary artery disease, cerebrovascular disease, and peripheral vascular disease) b. Chronic microvascular complications (kidney and eye disease c. Neuropathic complications (disease of the nerve)

Classification of Diabetes
Type 1 diabetes (previously referred to as IDDM) Type II diabetes (previously NIDDM) Gestational Diabetes Mellitus Diabetes Mellitus associated with other conditions or syndromes

Overview
The terms insulin-dependent diabetes and noninsulin dependent and their acronyms (IDDM and NIDDM) are no longer used because they have

resulted in classification of patients on the basis of the treatment of their diabetes rather than the underlying etiolgy. Use of Roman numerals (type I and Type II) to distinguish the two types has been changed to type 1 and type 2 to reduce confusion.

Physiology and Pathophysiology

insulin is an anabolic, or storage hormone. When a person eats a meal, insulin secretion increases and moves glucose from the blood into muscle, liver, and fat cells.

In these cells, insulin:

Transports and metabolizes glucose for energy
Stimulates storage of glucose in the liver and muscle (in the form of glygogen)

Signals the liver to stop the release of glucose

Enhances storage of dietary fat in adipose tissue Accelerates transport of amino acids (derived from dietary protein) into cells.

Insulin also inhibits the breakdown of stored glucose, protein, and fat during fasting periods (between meals and overnight), the pancreas continuously releases a small amount of insulin (basal insulin)

another pancreatic hormone called glucagon is released when blood glucose levels decrease and stimulate the liver to release stored glucose. the insulin and the glucagon together maintain a constant level of glucose in the blood by stimulating the release of glucose from the liver.

Type 1 Diabetes
is characterized by destruction of the pancreatic beta cells. it is thought that combined genetic, immunologic, and possibly environmental (e.g. viral) contributes to beta cell destruction. although the events that lead to beta cell destruction are not fully understood, it is generaly accepted that a genetic susceptibility is a common underlying factor in its development.

 People do not inherit type 1 diabetes itself; rather, they inherit a genetic predisposition, or tendency, toward developing type 1 diabetes. The genetic tendency has been found in person with certain HLA (human leukocyte antigen) types. HLA refers to a cluster of genes responsible for transplantation antigens and other immune processes.

Autoimmune response in Type 1

is an abnormal response in which antibodies are directed against normal tissue of the body, responding to these tissues as if they are foreign. autoantibodies against islet cells and against endogenous (internal) insulin have been detected in people at the time of diagnosis and even several years before clinical sign developed.

Environmental factors
viruses or toxins may initiate destruction of the beta cells are being investigated.

Regardless of the specific etiology, the destruction of the beta cells results in decreased insulin production unchecked glucose production by the liver fasting hyperglycemia in addition, glucose derived from food cannot be stored in the liver but instead remains in the bloodstream and contributes to postprandial (after meals) hyperglycemia.

If the concentration of glucose in the blood exceeds the renal threshold for glucose, usually 180 to 200 mg/dL (9.9 to 11.1 mmol/L), the kidney may not reabsorb all of the filtered glucose; the glucose then appears in the urine (glucosuria).

When excess glucose is excreted in the urine, it is accompanied by excessive loss of fluids and electrolytes. This is called osmotic diuresis.

Insulin normally inhibits glycogenolysis (break down of stored glucose) and gluconeogenesis (production of new glucose from amino acids and other substrates) In people with insulin deficiency, these processes occur in an unrestrained fashion and contribute further to hyperglycemia. In addition , fat breakdown occurs, resulting in an increased production of ketone bodies, which are the byproducts of fat breakdown.

Type 2 Diabetes
The two main problems related to insulin in type 2 diabetes are
a. insulin resistance b. impaired insulin secretion

Insulin resistance refers to a decreased tissue

sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism.

the exact mechanisms that lead to insulin resistance and impaired insulin secretion are unknown, although genetic factors are thought to play a role. to overcome insulin resistance and to prevent the buildup of glucose in the blood, increased amount of insulin must be secreted to maintain the glucose level at a normal or slightly elevated. However, if the beta cells cannot keep up with the increased demand for insulin, the glucose level rises, and type 2 diabetes develops.

Despite the impaired insulin secretion that is characteristic of type 2 diabetes, there is enough insulin present to prevent the breakdown of fat and the accompanying production of ketone bodies. Therefore, DKA does not typically occur in type 2 diabetes.

 Because insulin resistance is associated with obesity, the primary treatment is weight loss Exercise is also important in enhancing the effectiveness of insulin. Oral antidiabetic agents may be added if diet and exercise are not successful in controlling blood glucose levels.

Gestational Diabetes
is any degree of glucose intolerance with its onset during pregnancy. Hyperglycemia develops during pregnancy because of the secretion of placental hormones, which causes insulin resistance.

Initial management
Dietary managemant Blood glucose monitoring Insulin medication if hyperglycemia persists After delivery of the infant, blood glucose levels return to normal However, many women will develop type 2 diabetes later in life Therefore, all women who have had gestational diabetes should maintain their ideal body weight and exercise regularly to reduce the risk for type 2 diabetes.

Clinical Manifestations
Clinical manifestations of all types of diabetes include the three Ps Polyuria (increased urination) Polydipsia (increased thirst)
they occur as a result of the excess loss of fluid associated with osmotic diuresis

Polyphagia (increased appetite)

results from the catabolic state induced by insulin deficiency and the breakdown of proteins and fats.

Diagnostic Findings
an abnormally high blood glucose level is the basic criterion for the diabetes diagnosis. Fasting Plasma Glucose (FPG) levels of 126 mg/dL (7.0 mmol/L) or more

Or
Random plasma glucose levels exceeding 200mg/dL (11.1mmol/L)

on more than one occassion are diagnostic of diabetes.

Diabetes Management
The main goal of diabetes treatment Normalize insulin activity and blood glucose levels to reduce the development of vascular and neuropathic complications.

Five Components of Diabetes Management 1. Nutritional Management 2. Excercise 3. Monitoring 4. Pharmacologic Therapy 5. Education

1. Nutritional Management
Nutrition, diet, and weight control are the foundation of diabetes management.
The most important objective in the dietary and nutritional management of diabetes

Control of total caloric intake to attain or maintain a reasonable body weight and control of blood glucose levels.

For obese diabetic patients

Weight loss is the key to treatment Overweight is considered to be a body mass index (BMI) of 25 to 29. BMI is weight-to-height ratio calculated by dividing body weight (in kilograms) by the square of the height (in meters)

Obesity is defined as:

20% above ideal body weight or a BMI equal to or greater than 30.

Caloric Distribution
A diabetic meal plan focuses on the percentage of calories to come from carbohydrates, proteins, and fats. In general, carbohydrate foods have the greatest effect on blood glucose levels because they are more quickly digested than other foods and are converted into glucose rapidly.

 Several decades ago it was recommended that diabetic diets contain more calories from protein and fat foods than from carbohydrates to reduce postprandial increases in blood glucose levels.

Carbohydrates
The American Dietetic Association (ADA) recommend that for all levels of caloric aintake, 50% to 60% of calories should be derived from carbohydrates, 20% to 30% from fat, and the remaining 10% to 20% from protein.

 Carbohydrates consist of sugars and starches. Little scientific evidence supports the belief that sugars, such as sucrose, promote a greater blood glucose level compared to starches (e.g. rice, pasta or bread) All carbohydrates be eaten in moderation to avoid high postprandial blood glucose levels.

 Foods high in carbohydrates,such as sucrose, are not eliminated from the diet but should be eaten in moderation because these foods are typically high in fat and lack vitamins, minerals, and fiber. One carbohydrate serving is equivalent to 15g of carbohydrate Example of one serving Apple 2 inches in diameter 1 slice of bread.

All carbohydrates, to some extent, affect the blood glucose to different degrees, regardless of equivalent serving size

Fats
Recommended diebetic diet
Reduce calories and saturated fat sources Limit cholesterol intake This approach may help to reduce risk factors such as elevated serum cholesterol levels, which are associated with the development of coronary artery disease, the leading cause of death and disability among people with diabetes.

Fiber
High-carbohydrate, high-fiber diet
this type of diet plays a role in lowering total cholesterol and low-density lipoprotein cholesterol in the blood. Increasing fiber in the diet may also improve blood glucose levels and decreased the need for exogenous insulin.

Two Types of Dietary Fiber

Soluble fiber
plays more of a role in lowering blood glucose and lipid level, although the clinical significance of this effect is probably small (legumes, oats, and some fruits). it is thought to be related to the formation of a gel in the GI tract. this gel slows stomach emptying and the movement of food through the upper digestive tract.

The potential glucose-lowering effect of fiber may be caused by the slower rate of glucose absorption from foods that contain soluble fiber.

Insoluble Fiber
is found in whole grain breads and cereals and in some vegetables. This type of fiber plays more of a role in increasing stool bulk and preventing constipation.

Both soluble and insoluble fibers increase satiety, which is helpful for weight loss.

Other Dietary Concerns

Alcohol Consumption
Patients with diabetes do not need to give up alcoholic beverages but mederation is recommended. The main danger of alcohol consumption by a diabetic patient is hypoglycemia,especially for patients who take insulin. Alcohol may decrease the normal physiologic reactions in the body that produce glucose (gluconeogenesis)

if a diabetic patient takes alcohol on an empty stomach, there is an increased likelihood that hypoglycemia will develop. in addition, excessive alcohol intake may impair the patients ability to recognize and treat hypoglycemia and to follow a prescribed meal plan to prevent hypoglycemia

Person with type 2 diabetes

Diabinese medication , a potential side effect of

alcohol consumption is a disulfiram (Antabuse) type of reaction which involves Facial flushing Warmth Headache Nausea Vomiting Thirst Sweating within minutes of consuming alcohol

Alcohol consumption may lead to excessive weight gain from the high caloric content of alcohol, hyperlipidemia, and elevated glucose levels.

2. Exercise
is extremely important in managing diabetes because of its effects on lowering blood glucose and reducing cardiovascular risk factors. Excercise lowers the blood glucose level by increasing the uptake of glucose by body muscles and by improving insulin utilization.

 It also improves circulation and muscle tone. it also alters blood lipid levels, increasing levels of high-density lipoproteins and decreasing total cholesterol and triglyceride levels.

this is especially important to the person with diabetes because of the increased risk of cardiovascular disease.

Exercise Precautions
Patients who have blood glucose levels exceeding 250 mg/dL (14mmol/L) and who have ketones in their urine should not begin exercising until the urine tests negative for ketones and the blood glucose level is close to normal.

 Exercising with elevated blood glucose levels increases the secretion of glucagon, growth hormone and catecholamines. The liver then releases more glucose, and the result is an increase in the blood glucose level.

 Blood glucose monitoring is the cornerstone of diabetes management, and self monitoring blood glucose (SMBG). Frequent SMBG enables patient with diabetes to adjust the treatment regimen to obtain optimal blood glucose control.

3. Monitoring Glucose Levels and Ketones

This allows for detection and prevention of hypoglycemia and hyperglycemia and plays a crucial role in normalizing blood glucose levels, which in turn may reduce the risk of long-term diabetic complications.

Glycosylated Hemoglobin
referred to as HgbA1C or A1C, is a blood test that reflects blood glucose levels over a period of approximately 2 to 3 months. when blood glucose levels are elevated, glucose molecules attach to hemoglobin in the red blood cell. The longer the amount of glucose in the blood remains above normal, the more glucose binds to the red blood cell and the higher the glycosylated hemoglobin level.

Urine Testing for Glucose

The advantages for urine glucose testing are that it is less expensive and is not invasive. The general procedure involves applying urine to a reagent strip or tablet and matching colors on the strip with a color chart at the end of a specified period.

Testing for Ketones

Ketones (or ketone bodies) in the urine signal that control of type 1 diabetes is deteriorating, and the risk of DKA is high. when there is almost no effective insulin available, the body starts to break down stored fat for energy.

Ketone bodies are byproducts of this fat breakdown, and they accumulate in the blood and urine. one of the ketone bodies is called acetone, and this term is used interchangeably with the term ketones

4. Pharmacologic Management
as stated earlier, insulin is secreted by the beta cells of the islets of Langerhans and works to lower the blood glucose level after meals by facilitating the uptake and utilization of glucose by muscle, fat, and liver cells. In the absence of adequate insulin, pharmacologic thearapy is essential.

Insulin Therapy and Insulin Preparations Because the body loses the ability to produce insulin in type 1 diabetes, exogenous insulin must be administered for life. In type 2 diabetes, insulin may be necessary on a long term basis to control glucose levels if diet and oral agents fail.

 in some patients in whom type 2 diabetes is usually controlled by diet alone or by diet an oral agent may require insulin temporarily during illness, infection, pregnancy, surgery, or some other stressful events.

Time Course of Action

Insulin may be grouped into several categories based on the onset, peak, and duration of action.

Human insulin preparations

have a shorter duration of action from animal sources because the presence of animal proteins triggers an immune response that results in the binding of animal insulin, which slows its availability.

Rapid-acting insulins (Humalog,

Novolog) are blood glucose lowering agents that produce a more rapid effect. onset :5 to 15 minutes peak : 1 hour after injection Duration: 2 to 4 hours. Because of their rapid onset, patients should be instructed to eat no more than 15 minutes after injection.

Short acting insulins, called Regular insulin (mark R on the bottle)

Onset: 30 minutes to 1 hour Peak: 2 to 3 hours Duration: 4 to 6 hours Regular insulin is a clear solution and is usually administered 20 to 30 minutes before a meal, either alone or in combination with a longer acting insulin.

Example: Humulin R and Novolin R

Intermediate acting insulins, called NPH insulin (neutral protamine Hagedorn) or

Lente insulin.

Onset: 3 to 4 hours Peak: 4 to 12 hours Duration: 16 to 20 hours it appear white and cloudy it is important for the patient to eat some foods around the time of the onset and peak of these insulins.

Long-acting insulin, called Ultralente insulin

are sometimes referred to as peakless insulins because they tend to have a long, slow, sustained action rather than sharp, definite peaks in action Onset: 6 to 8 hours Peak: 12 to 16 hours Duration: 20 to 30 hours Because the insulin is in suspension with a pH of 4, it cannot be mixed with other insulins because this would cause precipitation.

Species (Source)
in the past, all insulins were obtained from beef and pork pancreases. Human insulins are now widely available They are produced by recombinant DNA technology and have largely replaced insulin from animal sources.

Complications of Insulin Therapy

1. Local Allergic Reactions
local allergic reactions (redness, swelling, tenderness, and induration or a 2-to 4-cm wheal) may appear at the injection site 1 to 2 hour after the insulin administration.

these reactions, which usually occur during the beginning stages of therapy and disappear with continued use of insulin, are becoming rare because of the increased use of human insulins.

2. Insulin Lipodystropy
Lipodystrophy refers to a localized reaction, in the form of either lipoatrophy or lipohypertrophy, occuring at the site of insulin injections.

Lipoatrophy is loss of subcutaneous fat and appears as slight dimpling or more serious pitting of subcutaneous fat.

Lipohypertrophy
the development of fibrofatty masses at the injection site, is caused by the repeated use of an injection site. if insulin is injected into scarred area, absorption may be delayed. this is one reason that rotation of injection site is so important. the patient should avoid injecting insulin into these areas until the hypertrophy disappears.

3. Insulin Resistance
Most patients at one time or another have some degree of insulin resistance. This may occur for various reasons, the most common being obesity, which can be overcome by weight loss.

 clinical insulin resistance has been defined as a daily insulin requirement of 200 units or more. In most diabetic patients taking insulin, immune antibodies develop and bind the insulin, thereby decreasing the insulin available for use.

4. Morning Hyperglycemia
an elevated blood glucose level upon arising in the morning may be caused by an insufficient level of insulin due to several causes: The dawn phenomenon The Somogyi effect Insulin waning

 the dawn phenomenon is characterized by a relatively normal blood glucose level until approximately 3 a.m. when blood glucose levels begin to rise. the phenomenon is thought to result from nocturnal surges in growth hormone secretion that create a greater need for insulin in the early morning hours in patient with type 1 diabetes.

Insulin waning
the progressive increase in blood glucose from the bedtime to morning. is frequently seen if the evening NPH dose is administered before dinner and is prevented by moving the evening dose of NPH insulin to bedtime.

Somogyi effect
is a nocturnal hypoglycemia followed by rebound hyperglycemia

Oral Antidiabetic Agents

Sulfonylureas (Diabinese, Orinase)
exert their primary action by directly stimulating the pancreas to secrete insulin. these agents improve insulin action at the cellular level and may also directly decrease glucose production by the liver.

Side Effects
GI symptoms and dermatologic reactions Hypoglycemia may occur when an excessive dose is used or the patient omits or delays meals, reduces food intake, or increases activity. Disulfiram (Antabuse) type of reaction when alcohol is ingested.

Biguanides (Metformin)
produces its antidiabetic effects by facilitating insulins action on peripheral receptor sites. therefore, it can be used only in the presence of insulin. It has no effect on pancreatic beta cells. If used with sulfonylurea may enhance the glucose-lowering effect more than either medication used alone.

Medications thay may interact with Biguanides

Anticoagulants Corticosteroids Diuretics Oral contraceptives Is contraindicated for patients with renal impairement or those at risk for renal dysfunction.

5. Education
Because diet, physical activity, and physical and emotional stress affect diabetic control, patients must learn to balance a multitude of factors. They must learn daily self-care skills to prevent accute fluctuation in blood glucose.

They must become knowledgeable about nutrition, medication effects and side effects, exercise, disease progression, prevention strategies and blood glucose monitoring techniques.

Teaching Patients to Sellf-Administer Insulin 1. Storing insulin

Cloudy insulins should be thoroughly mixed by gently inverting the vial or rolling it between the hands before drawing the solution into a syringe. The insulin vial in use should be kept at room temperature to reduce local irritation at the injection site, which may occur when cold insulin is injected.

2. Withdrawing Insulin
Most of the printed materials available on insulin dose preparation instruct patients to inject air into the bottle of insulin equivalent to the number of units of insulin to be withdrawn. The rationale for this is to prevent the formation of a vaccum inside the bottle, which would make it difficult to withdraw the proper amount of insulin.

 Insulin bottles should also be inspected for flocculation, which is a frosted, whitish coating inside the bottle of intermediate-or long-acting insulins. This occurs most commonly with human insulins that are not refrigerated.

If a frosted, adherent coating is present, some of the insulin is bound and should not be used.

3. Selecting and Rotating the injection site

The four main areas for injection Abdomen Arms (posterior surface) Thighs (anterior surface) Hips The speed of absorption is greatest in the abdomen and decreases progressively in the arm, thigh, and hip.

Systematic rotation of injection sites with an anatomic area is recommended to prevent localized changes in fatty tissue (lipodystrophy).

To promote consistency of insulin absorption, patients should be encouraged to use all available injection sites within one area rather than randomly rotating sites from area to area.

4. Preparing the skin

Use of alcohol to cleanse the skin is not recommended, but patients who have learned this technique often continue to use it. They should be cautioned to allow the skin to dry after cleansing with alcohol. If the skin is not allowed to dry before the injection, the alcohol may be carried into the tissue, resulting in a localized reddened area.

5. Inserting the Needle

Injection that is too deep (e.g. IM) or too shallow may affect the rate of absorption of insulin. Aspiration is generally not recommended with self injection of insulin.

Acute Complications of Diabetes

There are three major complications of diabetes related to short-term imbalances in blood glucose levels: Hypoglycemia DKA HHNS

Hypoglycemia (InsulinReactions)
Hypoglycemia (abnormally low blood glucose
level) occurs when the blood glucose falls to less than 50 to 60mg/dL (2.7 to 3.3 mmol/L).

It ca be caused by:
too much insulin or oral hypoglycemic agents Too little food Excessive physical activity

it may occur at any time of the day or night. it often occurs before meals, especially if meals are delayed or snacks are omitted.

Clinical Manifestations
Grouped into two categories:
Adrenergic symptoms Central Nervous System symptoms

In mild hypoglycemia, as the blood glucose level

falls, the sympathetic nervous system is stimulated, resulting in a surge of epinephrine and norepinephrine. This causes symptoms such as sweating, tremor, tachycardia, palpitation, nervousness, and hunger.

In moderate hypoglycemia
the fall in blood glucose level deprives the brain cells of needed fuel for functioning.

Signs of impaired function of CNS

Inability to concentrate slurred speech Impaired coordination double vision Confusion drowsiness Memory lapses Irrational or combative behavior Any combination of these symptoms (in addition to adrenergic symptoms) may occur with moderate hypoglycemia

In severe hypoglycemia
CNS function is so impaired that the patient needs assistance of another person for treatment of hypoglycemia.

Symptoms may include:

disoriented behavior seizures difficulty arousing from sleep loss of consciousness.

Management
Immediate treatment must be given when hypoglcemia occurs. Three or four commercially prepared glucose tablets 4 to 6 oz of fruit juice or regular soda 6 to 10 Life Savers or other candies 2 to 3 teaspoons of sugar or honey.

 it is not necessary to add sugar to juice, even if it is labeled as unsweetened juice: the fruit sugar in juice contains enough carbohydrate to raise the blood glucose level. Adding sugar to juice may cause a sharp increase in the blood glucose level, and patient mat experience hyperglycemia for hours after treatment.

Teaching Patients
Patients are advised to refrain from eating high-calorie, high fat dessert foods (e.g. cookies, cakes, doughnuts, ice cream) to treat hypoglycemia. The high fat content of these foods may slow the absorption of the glucose, and the hypoglycemic symptoms may not resolve as quickly as they would with the intake of carbohydrates.

Initiating emergency measures

For patients who are unconscious and cannot swallow Glucagon injection is given (1 mg IM or subcutaneous)

Glucagon is a hormone produced by the

alpha cells of the pancreas that stimulates the liver to release glucose (through the breakdown of glycogen, the stored glucose)

In hospital
Patients who are unconscious and cannot swallow is treated with 25 to 50 ml 50% dextrose in water (D50 W) administered intravenously Assuring patency of the IV line used for injection of 50% dextrose is essential because hypertonic solutions are very irritating to the vein.

Diabetic Ketoacidosis
DKA is caused by the absence or markedly
inadequate amount of insulin. this deficit in available insulin results in disorders in the metabolism of carbohydrates, proteins, and fat.

The three clinical features of DKA are:

Hyperglycemia Dehydration and Electrolyte loss Acidosis

Pathophysiology
without insulin, the amount of glucose entering the cells is reduced and the liver increases glucose production. In an attempt to get rid the body of the excess glucose, the kidneys excrete the glucose along with water and electrolytes (sodium & potassium)

this osmotic diuresis, which is characterized by excessive urination, leads to dehydration and marked electrolyte loss.

Patients with severe DKA

may lose up to 6.5 liters of water up to 400 to 500 mEq each of sodium, potassium and chloride over a 24 hour period.

Another effect of insulin deficiency or deficit

is the breakdown of fat (lipolysis) into free fatty acids and glycerol the free fatty acids are converted into ketone bodies by the liver. In DKA there is excessive production of ketone bodies because of the lack of insulin that would normally prevent this from occuring.

Ketone bodies are acids; their

accumulation in the circulation leads to metabolic acidosis.

illness and infections are associated with insulin resistance.

in response to physical and emotional stressors, there is an increase in the level of stress hormones: Glucagon Epinephrine Norepinephrine Cortisol Growth hormone

these hormones promote glucose production by the liver and interfere with glucose utilization by muscle and fat tissue, counteracting the effect of insulin.

If insulin levels are not increased during times of illness and infection, hyperglycemia may progress to DKA.

Clinical Manifestations
The hyperglycemia of DKA leads to
polyuria and polydipsia Blurred vision, weakness and headache Orthostatic hypotension due to intravascular volume depletion. GI symptoms (anorexia, nausea, vomiting, abdominal pain)

 Patients may have acetone breath (a fruity odor), which occurs with elevated ketone levels

Hyperventilation (with very deep, but not labored, respiration) may occur.
these Kussmaul respirations presented the bodys attempt to decrease the acidosis, counteracting the effect of the ketone buildup.

Diagnostic Findings
Blood glucose levels may vary from 300 to 800 mg/dL (16.6 to 44.4 mmol/L). Evidence of ketoacidosis is reflected in low serum bicarbonate and low pH values. A low PCO2 level reflects respiratory compensation (Kussmaul respirations) for the metabolic acidosis.

Medical Management
In addition to treating hyperglycemia, management of DKA is aimed at correcting dehaydration, electrolyte loss, and acidosis.

Rehydration
is important for maintaining tissue perfusion. Fluid replacement enhances the excretion of excessive glucose by the kidneys. Patients may need up to 6 to 10 liters of IV fluid to replace fluid losses caused by polyuria, hyperventilation, diarrhea, and vomiting.

Restoring Electrolytes Potassium the major electrolyte of

concern during treatment of DKA. Although the initial plasma concentration of potassium may be low, normal or even high, there is a major loss of potassium from body stores and intracellular to extracellular fluid shift of potassium.

Some of the factors related to treating DKA that reduce the serum potassium concentration include:

a. Rehydration which leads to increased

plasma volume and subsequent decreases in the concentration of serum potassium. Rehydration also leads to increased urinary excretion of potassium. b. Insulin administration which enhances the movement of potassium from the extracellular fluid into the cells.

because extrcellular potassium levels drop during DKA treatment, potassium must be infused even if the plasma potassium level is normal.

Potassium replacement is withheld only if hyperkalemia is present or if the patient is not urinating.

Reversing Acidosis
Ketone bodies (acids) accumulate as a result of fat breakdown. The acidosis that occurs in DKA is reversed with insulin, which inhibits fat breakdown, thereby stopping acid buildup. Insulin is usually infused intravenously at a slow, continuous rate.

Nursing Management
Nursing care focuses on
Monitoring fluid and electrolye status Blood glucose level monitoring Preventing fluid overload Administer fluids, insulin and other medications. Urine output is monitored to ensure adequate renal function before potassium is administered to prevent hyperkalemia.

Hyperglycemic Hyperosmolar Nonketotic Syndrome

HHNS is a serious condition in which hyperosmolarity and hyperglycemia predominate, with alterations of the sensorium. The basic biochemical effect is lack of effective insulin (insulin resistance) The persistent hyperglycemia causes osmotic diuresis, resulting in losses of water and electrolytes.

What distinguishes HHNS from DKA?

in HHNS ketosis and acidosis do not occur partly because of differences in insulin levels. Insulin is too low to prevent hyperglycemia, but it is high enough to prevent fat breakdown.

In DKA no insulin is present, and this

promotes the breakdown of stored glucose, proteins, and fats which leads to the

production of ketone bodies and ketoacidosis.

Clinical Manifestation
The clinical picture of HHNS
Hypotension Dehydration (dry mucous membranes, poor skin turgor) Tachycardia variable neurologic signs (alteration of sensorium, seizures)

Medical Management
The overall approach to the treatment of HHNS is similar to that of DKA:

Fluid replacement Correction of electrolyte imbalances Insulin administration

Insulin plays a less important role in the treatment of HHNS because it in not needed for reversal of acidosis, as in DKA.

Insulin is usually administered to treat hyperglycemia

Nursing Management
Close monitoring of VS, fluid status and laboratory values. They should be monitered because of the risk for renal failure secondary to severe dehydration.

Long-Term Complications
1. Macrovascular Complications
Result from changes in the medium to large blood vessels. Blood vessel walls thicken, sclerose and become occluded by plaque that adheres to the vessel walls. Eventually, blood flow is blocked.

Three main types of macrovascular complications

Coronary artery disease Cerebrovascular disease Peripheral vascular disease Other factors that may play a role in diabetis related atherosclerosis include platelet and clotting factor abnormalities Decreased flexibility of red blood cells Decreased oxygen release changes in the arterial wall due to hyperglycemia

Management
Prevention of risk factors for atherosclerosis

Diet and exercise to manage obesity, hypertension and hyperlipidemia Compliance to medications Control of blood glucose level Smoking cessation

Microvascular complications
Diabetic microvascular disease
is characterized by capillary basement membrane thickening. The basement membrane surrounds the endothelial cells of the capillary

 Researchers believe that increased blood glucose levels react through a series of biochemical responses to thicken the basement membrane to several times its normal thickness. Two areas affecte by these changes are the retina and kidney.

Proliferative retinopathy
is characterized by the proliferation of new blood vessels growing from the retina into the vitreous. these new vessels are prone to bleeding. The visual loss associated with proliferative retinopathy is caused by this vitreous hemorrhage and/or retinal detachment.

 the vitreous is normally clear, allowing light to be transmitted to the retina. When there is hemorrhage, the vitreous becomes clouded and cannot transmit light, resulting in loss of vision.

Nephropathy
is the most common complication of diabetes soon after the development of diabetes, and especially if the blood glucose levels are elevated, the kidneys filtration mechanism is stressed, allowing blood proteins to leak into the urine.

 as a result, the pressure in the blood vessels of the kidney increases. It is thought that the elevated pressure serves as the stimulus for the development of nephropathy.

 As renal function decreases, the patient commonly has multiplesystem failure. One of the most important blood proteins that leaks into the urine is albumin.

Diabetic Neuropathies
refers to a group of diseases that affect all types of nerves, including peripheral (sensorimotor), autonomic, and spinal nerves.

Elevated blood glucose levels over a period of years have been implicated in the etiology of neuropathy.

 Capillary basement membrane thickening and capillary closure may be present. There may be demyelination of the nerves, which is thought to be related to hyperglycemia. Nerve conduction is disrupted when there are aberrations of the myelin sheaths.

Peripheral Neuropathy
Initial symptoms include Paresthesias (prickling, tingling, or heightened sensation) Burning sensations The feet become numb
Decreased sensations of pain and temperature place patients at increased risk for injury and undetected foot infections.

Decrease in deep tendon reflexes is found.

Autonomic Neuropathies
results in a broad range of dysfunctions affecting almost every organ system of the body Urinary retention A decreased sensation of bladder fullness Other urinary symptoms of neurogenic bladder

results from autonomic neuropathy.

Patients with neurogenic bladder are predispose to developing urinary tract infections due to inability to completely empty the bladder

Sudomotor Neuropathy
This neuropathic condition refers to a decrease or absence of sweating (anhidrosis) of the extremities, with a compensatory increase in body wasting. Dryness of the feet increase the risk for the development of foot ulcers.

Sexual Dysfunction
Reduced vaginal lubrication has been mentioned as a possible neuropathic effect. Vaginal infection, increased in incidence in women with diabetes, may be associated with decreased lubrication and vaginal itching and tenderness.

Some men with autonomic neuropathy have normal erectile function and can experience orgasm but do not ejaculate. Retrograde ejaculation occurs: seminal fluid is propelled backward through the posterior urethra and into the urinary bladder.

Foot and Leg Problems

Complications of diabetes that contribute to increased risk of foot infections include:
1. Neuropathy a. Sensory neuropathy leads to loss of pain and pressure sensation b. autonomic neuropathy leads to increased dryness and fissuring of the skin (secondary to decreased sweating). c. motor neuropathy results in muscular atrophy, which may lead to changes in the shape of the foot.

2. Peripheral vascular disease:

Poor circulation of the lower extremities contributes to poor wound healing and the development of gangrene.

3. immunocompromise:
Hyperglycemia impairs the ability of specialized leukocytes to destroy bacteria. Thus in poorly controlled diabetes, there is lowered resistance to certain infections.

The typical sequence of events in the development of a diabetic foot ulcer Begins with a soft tissue injury of the foot Formation of a fissure between the toes or in area of dry skin, or formation of a callus.

Injuries are not felt by the patient with an insentitive foot and may be

Thermal from using heating pads walking barefooted from hot concrete testing bath water

Chemical Burning the foot while using caustic agents on calluses, corns, or bunions Traumatic
Injuring the nails while cutting nails Walking with an undetected foreign object in the shoe Wearing ill-fitting shoes and socks.