DIABETES

n A problem of transportation and/or storage

n Diabetes has far reaching and devastating physical, social, and economic consequences

n Diabetes Mellitus is a group of metabolic diseases characterized by elevated blood glucose.

n Glucose sources are absorption of ingested food and formation of glucose by the liver from food substances.

U.S. DIABETES STATISTICS

n 17 MILLION AMERICANS HAVE IT.

n UP TO 50% OF PEOPLE OVER 65 HAVE SOME DEGREE OF GLUCOSE INTOLERANCE

n 5.9 MILLION OF THOSE DON’T KNOW IT.

n THE LEADING CAUSE OF NEW CASES OF BLINDNESS.

n SINGLE MOST COMMON CAUSE OF ESRD REQUIRING DIALYSIS OR TRANSPLANT.

n LEADING CAUSE OF LOWER LIMB AMPUTATION

n Diabetes is the seventh leading cause of death in the United States

n Diabetes >>49% from 1990--2000

n ? How many diabetes death are unreported

n Major risk factor for morbidity and mortality due to coronary disease, cerebrovascular disease, and peripheral vascular disease

$98 billion spent annually for diabetes care

n Risk factor for diabetes mellitus

n family history--hx gestational diabetes

n obesity 20% over desired body weight or BMI>27

n race, ethnicity

n >45 years old

n HTN 140/90

n HDL <35 - triglycerides>250

n HX OF GESTATIONAL DIABETES..DELIVERY OF INFANTS>9 POUNDS

n In a diabetic state the cells may stop responding to insulin or the pancreas may stop producing insulin entirely

n GLUCAGON RELEASES GLUCOSE FROM CELL STORAGE SITES WHENEVER BLOOD GLUCOSE LEVELS ARE LOW

n INSULIN IS THE KEY TO OPEN THE GATES, TURN ON THE PUMPS, AND HELPS PUSH SUGAR OUT OF THE BLOODSTREAM INTO THE SURROUNDING TISSUE.

GLUCOSE HOMEOSTASIS

n GLUCOSE:

n PRIMARY FUEL FOR THE CENTRAL NERVOUS SYSTEM

n FAT HAS 9 CALORIES OF STORED ENERGY PER GRAM..PROTEINS AND CARBS HAVE 4CALORIES PER GRAM

n 65 TO 105 MG/DL TO SUPPLY GLUCOSE FOR CNS FUNCTIONS

n WHEN BLOOD GLUCOSE LEVELS DROP INSULIN SECRETION STOPS AND GLUCAGON IS RELEASED

ABSENCE OF INSULIN

n INSULIN:

n INSULIN IS NEEDED TO SUPPLY GLUCOSE TO TO MOST OF THE BODY’S TISSUES

n WITHOUT INSULIN FAT AND PROTEIN BREAK DOWN

n HYPERGLYCEMIA FROM ELEVATED BLOOD GLUCOSE

• ELECTROLYTE INBALANCES LEAD TO THE CLASSIC SYMPTOMS

• POLYURIA

• POLYDIPSIA

• POLYPHASIA

n INSULIN DEFICIENCY LEADS TO KETONES THAT LEAD TO METABOLIC ACIDOSIS

n ASSOCIATED DEHYDRATION CAUSES:

n HEMOCONCENTRATION

n HYPOVOLEMIA

n HYPERVISCOSITY

n HYPOPERFUSION

n HYPOXIA

n Insulin

n Transports and metabolizes glucose for energy

n Stimulates storage of glucose in the liver and muscle

n Signals the liver to stop the release of glucose

n Accelerates transport of amino acids.

n Classification of diabetes mellitus

n Type 1

n Type 2

n Other specific types (associated with other conditions or syndromes)

n Gestational diabetes

n Type 1

n 5%-10% of diabetes is Type 1

n Insulin producing beta cells are destroyed by an autoimmune or idiopathic process

n Genetic susceptibility

n Acute onset -usually before the age of thirty

n Abrupt onset, thirst, weight loss

n Usually non obese

n Insulin dependent

n Type 2

n 90%--95% of diabetics

n Decreased sensitivity to insulin or reduction in the amount of insulin produced

n Maturity onset, peaks in 50’s

n Frequently no symptoms

n Diet and exercise is 1st treatment

n 60% to 80% obese

n Genetic factors

n Ketones

n Byproducts of fat breakdown

n Acids that disturb acid base balance

n Problematic in Type 1 not Type 2

n Gestational Diabetes

• Any degree of glucose intolerance during pregnancy.

• Normal glucose post delivery

n PREVENTION

n HEALTHY PEOPLE 2010 GUIDELINES

n CLINICAL MANIFESTATIONS

n POLYURIA, POLYDIPSIA, POLYPHASIA CAUSED BY OSMOTIC DIURESIS AND CATABOLICBREAKDOWN OF PROTEINS AND FATS

n FATIGUE, WEAKNESS, VISION CHANGES, SLOW WOUND HEALING CHRONIC INFECTIONS.

n TYPE 1 ONSET MAY BE SUDDEN (DKA)

ASSESSMENT

n HISTORY

n RISK FACTORS

n WEIGHT AND WEIGHT CHANGE

n MAJOR OR MINOR INFECTIONS (YEAST)

n HEALING TIME

n FAMILY HISTORY

LAB ASSESSMENT

n BLOOD

n FASTING BLOOD GLUCOSE

• + DIABETES IS 126MG/DL

• RANDOM TEST 200MG/Dl ON MORE THAN ONE OCCASION

n ORAL GLUCOSE TOLERANCE

• MOST SENSITIVE

• NOT ROUTINELY USED (INCONVENIENT)

• + DIABETES IF BLOOD GLUCOSE 200 MG/DL AT 120 MINUTES

n HbA1c

• BEST INDICATOR OF AVERAGE BLOOD GLUCOSE LEVEL

• MEASURES 120 DAYS (LIFE OF RBC)

• NORMAL RANGE FROM 4% --6%

n Self monitoring of glucose

n Allows for detection and prevention of hypoglycemia and hyperglycemia

n Optimal blood glucose control possible with smbg.

n Advantages and disadvantages

n Consider patients

• Visual acuity cost

• Fine motor coordination cognitive ability

n URINE TESTING

n KETONES

• ACUTE ILLNESS OR STRESS

• BLOOD GLUCOSE 300

• PREGNANCY

• WEIGHT LOSS PROGRAM

PLANNING AND IMPLEMENTATION

n GOAL IS TO MAINTAIN GLUCOSE LEVEL WITHIN NORMAL RANGE

n HbA1c MAINTAINED AT 7% OR BELOW

n PREMEAL BLOOD GLUCOSE 80-120

n BEDTIME BLOOD GLUCOSE BETWEEN 100-140

n AVOID ACUTE AND CHRONIC COMPLICATIONS

MANAGEMENT

n NON-SURGICAL

n DRUG THERAPY

n DIETARY INTERVENTIONS

n MONITORING BLOOD GLUCOSE LEVELS

n PLANNED EXERCISE

n Nutritional management

n all essential food constituents

n achieve and maintain a reasonable weight

n meet energy needs

n prevent wide daily fluctuations in blood glucose levels

n decrease serum lipids (if >)

n PROTEIN,FAT AND CARBS, FIBER

n Exchange lists

n Nutritional counseling

n Exercise

n Exercise lowers blood glucose by increasing uptake of glucose by body muscles

n improves insulin utilization

n improves circulation and muscle tone

n alters lipids >HDL < total cholesterol and triglycerides

n EXERCISE BENEFITS

n REGULATES BLOOD GLUCOSE LEVELS

n IMPROVES DIABETIC CONTROL

n DECREASES FACTORS FOR CARDIOVASCULAR DISEASE

n INCREASES HDL

n EXERCISE RISKS

n INJURY

n PROLONGED HYPOGLYCEMIA

n HYPERGLYCEMIA

n EXERCISE SCREENING

n GUIDELINES

DRUG THERAPY

n ORAL THERAPY

n SULFONYLUREA AGENTS

• SOME REMAINING PANCREATIC FUNCTION

• DRUGS STIMULATE INSULIN SECRETION

• ENHANCE NUMBER OR SENSITIVITY OF RECEPTOR SITES

• GI SYMPTOMS AND DERMATOLOGIC REACTIONS

• HYPOGLYCEMIA IS MOST SERIOUS COMPLICATION

n MEGLITINIDES

n PRANDIN

n STARLIX

• BEFORE MEALS

• RAPID ONSET

• LIMITED DURATION OF ACTION

• HYPOGLYCEMIA ETC.

• GOOD CHOICE FOR CLIENTS THAT SKIP MEALS

n BIGUANIDES

n METFORMIN

• DECREASES LIVER GLUCOSE RELEASE

• DECREASES CELLULAR INSULIN RESISTANCE

• NO INSULIN STIMULATION-NO HYPOGLYGEMIA

• NOT INDICATED WITH RENAL DISEASE

• WITHOLD 48 HOURS FOR CONTRAST

• NO ALCOHOL INTAKE

n ALPHA-GLUCOSIDASE INHIBITORS

n PRECOSE AND GLYSET

• REDUCES POSTPRANDIAL HYPERGLYCEMIA BY SLOWING DIGESTION AND CARB ABSORPTION IN THE INTESTINE

• FLATULENCE, DIARRHEA AND ABDOMINAL DISCOMFORT

n THIAZOLIDINEDIONES

n AVANDIA AND ACTOS

• ENHANCE INSULIN ACTION

• CHECK LIVER FUNCTION

• REDUCES EFFECTIVENESS OF ORAL CONTRACEPTIVES

n COMBINATION THERAPY

n GLUCOVANCE

n 2002 RECOMMENDATIONS ENCOURAGE EARLY INTERVENTION WITH COMBINATION THERAPY

n Insulin therapy

n Insulin History--Discovered in 1922

n Experiments with dog pancreas--slaughterhouse cattle pancreas provided original pure insulin extract

n Banting and Best, MccLoud and Collip shared Nobel Prize in 1923

n 1978 insulin became the first human protein manufactured through biotechnology

INSULIN THERAPY

n USE IN TYPE 1 DIABETES AND SOME CASES OF TYPE 2 DIABETES

n INSULIN REGIMENS

n SITES AND ABSORPTION RATES

n ONSET- PEAK- DURATION

n MIXING INSULINS

n COMPLICATIONS OF INSULIN THERAPY

n HYPERTROPHIC LIPODYSTROPHY

n DAWN PHENOMENON

n SOMOGYI’S PHENOMENON

n INSULIN PUMPS

n BLOOD GLUCOSE MONITORING

n FREQUENCY

n THERAPY GOALS

n ACCURACY

n NEW TECHNOLOGY

n Acute complication of diabetes

n diabetic ketoacidosis

n hyperglycemic hyperosmolar nonketotic syndrome

n hypoglycemia

DIABETIC KETOACIDOSIS

n CAUSED BY TOTAL OR PARTIAL LACK OF INSULIN COMBINED WITH THE ACTION OF REGULATORY HORMONES

n USUALLY PRECIPITATED BY INFECTION

n ADDITION HEALTH PROBLEMS ADD TO INCIDENCE OF MORTALITY

n MAIN CLINICAL FEATURES

n HYPERGLYCEMIA

n DEHYDRATION AND ELECTROLYTE LOSS

n ACIDOSIS

n Polyuria, polydipsia, polyphagia precede CNS depression with various stages of lethargy

n Dehydration with extreme fluid loss

n Metabolic acidosis with associated symptoms

n Sodium low or normal-potassium can be ok—drop with treatment

n MAIN CAUSES OF DKA

n DECREASED OR MISSED DOSE OF INSULIN

n ILLNESS OR INFECTION

n UNDIAGNOSED DIABETES

n CLINICAL MANIFESTATIONS

n WBC’s--- 20,000 dehydration—30,000 indicate infection

n BLOOD GLUCOSE—300-800MG/DL

n HYPERGLYCEMIA MANAGEMENT

n FLUID AND ELECTROLYTE MANAGEMENT

n DRUG THERAPY

n ACIDOSIS MANAGEMENT

n CLIENT EDUCATION

n SICK DAY RULES

n MEDICAL MANAGEMENT

n REHYDRATION

n RESTORING ELECTROLYTES

n REVERSING ACIDOSIS

n NURSING MANAGEMENT

HYPERGLYCEMIC-HYPEROSMOLAR
NON-KETOTIC SYNDROME

n Absence of ketosis

n Blood glucose > 800

n Usually seen with elderly

n Type 2 diabetes

n Mortality 10% to 40%

n Does not occur without dehydration

n Profound osmotic diuresis

n CLINICAL MANIFESTATIONS

n HYPOTENSION

n PROFOUND DEHYDRATION

n TACHYCARDIA

n VARIABLE NEUROLOGIC SIGNS

n MEDICAL MANAGEMENT

n MONITORING

n FLUID THERAPY

n CONTINUING THERAPY

• INJURY PREVENTION FOR MENTAL STATUS CHANGES

HYPOGYLCEMIA

n CNS REQUIRES CONTINUOUS SUPPLY OF GLUCOSE

n BLOOD GLUCOSE 80 MG/DL INSULIN SECRETION DECREASES

n BLOOD GLUCOSE 68 MG/DL GLUCOSE COUNTERREGULATORY ACTIVATED

n GLUCAGON AND EPINEPHRINE

n TYPE 1 DIABETIC

n HAVE IMPAIRED RESPONSE TO HYPOGLYCEMIA

n HYPOGLYCEMIC UNAWARENESS

n CLINICAL MANIFESTATIONS

n ADRENERGIC

n CENTRAL NERVOUS STSTEM

n SWEATING

n TREMORS

n TACHYCARDIA

n PALPITATIONS

n NERVOUSNESS

n HUNGER

n DISORIENTED BEHAVIOR

MANAGEMENT

n HYPOGLYCEMIC MANAGEMENT

n DIET THERAPY

• LO FAT CARB REPLACEMENT

• 15 GM FAST ACTING CARB

n DRUG THERAPY

• 50% DEXTROSE

PREVENTION STRATEGIES

n INSULIN EXCESS

n DEFICIENT FOOD INTAKE

n EXERCISE

n ALCOHOL

CLIENT EDUCATION

n COMMUNITY BASED CARE

n HOME CARE MANAGEMENT

n Chronic Complications of Diabetes

n Macrovascular

• cardiovascular disease

• peripheral vascular disease

• cerebrovascular disease

n Microvascular complications

• ocular complications

• diabetic neuropathy

• diabetic nephropathy

• male erectile dysfunction

n SENSORY ALTERATIONS

n DIABETIC FOOT

n WOUND CARE

n CHRONIC PAIN

n VISUAL SENSORY-PERCEPTUAL ALTERATIONS

n ALTERED TISSUE PERFUSION

SPECIAL ISSUES IN DIABETES CARE

n MANAGEMENT OF HOSPITALIZED DIABETIC

n SELF CARE ISSUES

n DIETARY ALTERATIONS

• NPO

• CLEAR LIQUIDS

• TUBE FEEDING

n HYPO AND HYPER GLYCEMIC EPISODES