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DIABETES MELLITUS

DIABETES MELLITUS. Majuvy L. Sulse MSN, RN, CCRN Lola Oyedele MSN, RN, CTN. DIABETES MELLITUS. DEFINE CHRONIC SYSTEMIC DISEASE CHARACTERIZED BY EITHER A DEFICIENCY OF INSULIN OR A DECREASED ABILITY OF THE BODY TO USE INSULIN (insulin resistant). PANCREAS. CELL TYPES AND FUNCTION

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DIABETES MELLITUS

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  1. DIABETES MELLITUS Majuvy L. Sulse MSN, RN, CCRN Lola Oyedele MSN, RN, CTN

  2. DIABETES MELLITUS • DEFINE • CHRONIC SYSTEMIC DISEASE CHARACTERIZED BY EITHER • A DEFICIENCY OF INSULIN • OR A DECREASED ABILITY OF THE BODY TO USE INSULIN (insulin resistant)

  3. PANCREAS • CELL TYPES AND FUNCTION • BETA - INSULIN • HYPOGLYCEMIC FACTOR • ALPHA - GLUCAGON • HYPERGLYCEMIC FACTOR • DELTA - SOMASTATIN • INHIBITS SECRETION OF BOTH INSULIN AND GLUCAGON

  4. ROLE OF INSULIN • SKELETAL MUSCLE • INCREASE UPTAKE OF GLUCOSE, CONVERT TO GLYCOGEN • Liver • Increase uptake of glucose from blood and convert to glycogen • Inhibits production of glycogenolysis • Inhibits gluconeogenesis

  5. CARBOHYDRATES • BREAKS DOWN TO GLUCOSE, INSULIN TRANSPORTS ACROSS CELL MEMBRANE • ENZYMES BREAKS DOWN FOR ENERGY OR STORED AS GLYCOGEN • PROTEIN • INSULIN ENHANCES AMINO ACIDS TO PROTEIN • FATS • FREE FATTY ACIDS TO ADIPOSE

  6. Critical thinking • The process of breaking down material without insulin during metabolism is know as: • A. Ketogenesis • B. Lipolysis • C. Glycogenesis • D. Catabolism

  7. REGULATION • INSULIN •  BLOOD SUGAR = INSULIN SECRETED FOR TRANSPORT INTO CELLS • GLUCAGON •  BLOOD SUGAR = GLUCAGON SECRETED • STIMULATES LIVER TO BREAKDOWN GLYCOGEN TO GLUCOSE & RELEASE ( GLYCOGENESIS) • METABOLISE AMINO ACIDS TO GLUCOSE • LIPOLYSIS TO GLYCEROL ( GLUCONEOGENESIS)

  8. PITUITARY • GROWTH HORMONE • ACTH • CORTISOL •  GLUCONEOGENESIS •  LIPOLYSIS •  USE OF GLUCOSE BY CELLS • =  BLOOD SUGAR

  9. RISK FACTORS • FAMILY HISTORY • HISTORY OF GLUCOSE INTOLERANCE • OBESITY • HIGH FAT DIET • SEDENTARY LIFE STYLE • ELDERLY • ETHNECITY

  10. TYPES • TYPE 1 • IDDM ( 5-10%) • TYPE 2 • NIDDM ( 90%) • GLUCOSE INTOLERANCE • FBS  110 BUT  126 • SECONDARY DIABETES • 2ND TO DISEASE OR DISORDER • GESTATIONAL DIABETES • DURING PREGNANCY

  11. TYPE 1 (IDDM) • DEFINE • BETA CELL DESTRUCTION • ( AUTOIMMUNE, VIRAL, GENETIC) • INSULIN INSUFFICIENT TO SUSTAIN LIFE • REQUIRES EXOGENOUS INSULIN • REVERTS TO LIPOLYSIS & GLUCONEOGENESIS • ETIOLOGY •  30 YEARS, THIN, ABRUPT ONSET • S&S • POLYURIA, POLYDIPSIA, POLY PHASIA

  12. TYPE 2 (NIDDM) • DEFINE • DEFECIENT INSULIN TO MEET BODY DEMANDS • INSULIN RESISTENCE • DOES NOT REVERT TO LIPOLYSIS OR GLUCONEOGENESIS • ETIOLOGY •  30 YEARS, OBESE, GRADUAL ONSET • S&S • VAGUE, FATIGUE, IRRITABILITY, GRADUAL POLYURIA, POLYDIPSIA, POLYPHASIA

  13. Critical Thinking • Which of the following is true regarding Diabetes? • Diabetes is an acute disorder that responds only to insulin • Diabetes is curable • Diabetes is characterized by an abnormality of carbohydrate metabolism • Diabetes is not a significant cause of death.

  14. CONSEQUENCE OF INSULIN DEFECIENCY • LIVER • CANNOT STORE GLUCOSE AS GLYCOGEN • FREE FATTY ACIDS BREAK DOWN = KETONE BODIES • HYPERTRIGLYCERIDEMIA • SKELETAL MUSCLE • NO GLUCOSE FOR ENERGY, METABOLISE PROTEINS • ADIPOSE TISSUE • LIPOLYSIS = FREE FATTY ACIDS

  15. KIDNEY • KIDNEY CAN EXCRET 180 MG/DL • (GLUSOSURIA) • = OSMOTIC DIURESIS= (POLYURIA) • = FLUID VOLUME & ELECTROLYTE DEPLEATION • = HYPOVOLEMIA = THIRST (POLYDISPIA) •  GLUCOSE TO CELLS = STARVATION (POLYPHAGIA)

  16. Critical thinking • A diagnosis of diabetes suggests that a client’s symptom of polyuria is most likely caused by : • A. Increased insulin levels promote a diuretic effect • B. Glucose acting as a hypertonic agent, draws water from the intracellular fluid into the renal tubules • C. Electrolyte changes lead to the retention of sodium and potassium • D. Microvascular changes alter the effectiveness of the kidney

  17. DIAGNOSTIC STUDIES • FASTING BLOOD SUGAR  126 • RANDOM BLOOD SUGAR  200 • POST PRANDIAL BLOOD SUGAR  200 • GLYCOSYLATED HgB. (HgA1c)  7% • (life of RBC – 120 days) • GLYCOSYLATED ALBUMIN 1.5–2.7nmol/L

  18. MANAGEMENT OUTCOMES • PROMOTE PROPER NUTRITION • PROMOTE EXERCISE • ADMINISTER MEDICATION

  19. ORAL ANTIDIABETIC MEDICATIONS SULFONYLURES INCREASE RELEASE OF INSULIN ORINASE, TOLINASE GLUTROL, DIABETA WEIGHT GAIN, HYPOGLYCEMIA • MEGLITINIDES • INCREASE RELEASE OF INSULIN • PRANDIN, STARLIX • WEIGHT GAIN, HYPOGLYCEMIA

  20. ORAL ANTIDIABETIC MEDICATIONS • BIGUANIDES • REDUCE GLUCOSE BY LIVER, INCREASED INSULIN SENSATIVITY. • GLUCOPHAGE • DIRRHEA, LACTIC ACIDOSIS • A-GLUCOSIDASE INHIBITORS • DECREASE ABSORPTION OF CARBOHYDRATES • ACARBOSE, • DIRRHEA, ABD PAIN • THIAZOLIDINEDIONES • INCREASE GLUCOSE UPTAKE • ACTOSE, AVANDIA • WEIGHT GAIN, EDEMA

  21. ALTERED HEALTH MAINTENANCE • R/T LACK OF KNOWLEDGE OF DIETARY MANAGEMENT DIABETES • OUTCOME • CLIENT WILL STATE RELATIONSHIP OF DIETARY MANAGEMENT TO BLOOD GLUCOSE CONTROL • CLIENT WILL CHOOSE FOODS THAT MEET CALORC NEEDS AND OFFER A WELL BALANCED DIET

  22. Dietary Proportions • Carbohydrates 50-60% • Fats  30% • 10% saturated ( animal fats) • 10% polysaturated ( fish) • 10% monounsaturated ( olive oil) • Protein 10-20% • Fiber 40 gms daily

  23. Acute Complications of Diabetes Mellitus • Hypoglycemia = BS below 60 • Causes • Insufficient food • Missed meal, nausea/vomiting, interrupted enteral feeding • Increased insulin •  dose, NPO exam, peak action of insulin • Categories • Adrenergic • Neuroglycopenic

  24. Hyperglycemia • Causes • Undiagnosed type 1 • Know type 1 • Omission of insulin • Illness/infection/ trauma/ surgery • None DM • Cushing's syndrome/ hyperthyroid/ pregnancy • Medications ( Dilantin)

  25. Diabetic Ketoacidosis • Criteria = Blood sugar greater than 250 • Arterial Ph less than 7.30 • HCO3 less than 18 • Pathology •  cellular glucose = gluconeogenesis & glycogenolysis • Free fatty acids metabolized = ketone bodies • Ketones release hydrogen ions • Hydrogen ions exchanged for K at cell wall =  K

  26. Diabetic Ketoacidosis • Kidney regulates =  K •  blood glucose =  osmotic pressure • Kidney regulates = diuresis =  Na • Glucosuria, dehydration & electrolyte imbalance

  27. S&S • Polyuria, polydipsia, polyphagia • Headache with blurred vision • Nausea/vomiting r/t  peristalsis •  respirations/ fruity breath • Kussmaul's pattern

  28. Labs • Blood sugar = 300-800 • Na  ( reflect level of dehydration) • K first  (hydrogen ions exchanged for K at cell wall • then  (kidney regulates) •  Bun & Creatinine • ABG’s = metabolic acidosis

  29. Critical Thinking • Which terms would best describe the condition of a ketoacidotic client on admission? • A. warm, flushed, dry • B. Cool and clammy • C. cool and dry • D. Warm, pale and clammy

  30. Management • Rehydration • Replace electrolytes • Insulin • Vital signs hourly • Blood sugar hourly • Urine output hourly • Cardiac monitor

  31. Complications • Hypovolemic shock • Dysrhythmias • Myocardial infarction • Seizures • Coma • Acute renal failure

  32. Hyperglycemic Hyperosmolar Nonketotic Syndrome • Hyperglycemia, & Dehydration • W/O acidosis ( enough insulin) • Insidious onset • ( tolerate polyuria, polydipsia, polyphagia headache & weakness)

  33. HHNS • Dehydration R/T osmotic diuresis • Hypovolemia =  glomerular filtration rate =  glucose retained  Na retained  osmolarity.

  34. At risk • Elderly, type 2 or mild type 1 • Burns, infection, renal & heart disease • Acute illness • Dialysis, hyperalimentation • S&S • Profound dehydration • Blood sugar = 600-2000 •  BUN Creatinine • glycosuria

  35. Management • Rehydrate • Normal saline X 2 hours ( Isotonic) • .45 normal saline (hypotonic) • Electrolyte replacement • Insulin • Hourly vital signs, output, • Cardiac monitor

  36. Chronic Complications • Infections • monilia • Skin r/t glucose & moisture • Vaginal R/T glucose & altered Ph

  37. Vascular Complications • Macrovascular • Atherosclerotic changes earlier & greater frequency • Coronary artery disease • Cerebral vascular disease • peripheral vascular disease

  38. Microvascular • Unique to diabetics • Thickening of basement membrane of capillaries • Retinopathy - • Cataracts • Neuropathy • Nephropathy

  39. Retinopathy • R/t vascular fragility • Stages • Early -  capillary permeability = intra-retinal hemorrhage • Moderate- macular edema, micro hemorrhage • Progressive retinal ishemia, exudate, cotton-wool patches • Advanced - neo-vascularization, retinal detachment, blind

  40. Cataracts • Accumulation of sorbitol in the lens • Opacity gradual onset • Similar to senile cataracts

  41. Neuropathy • Most commonly affects peripheral nervous system • Most common complication •  sensation  motor function • Parasthesia ( tingle- burn, numbness) • Mononephropathy • Sporadic, single focal area • Symmetrical polyneuropathy • Distal symmetrical pattern ( stocking, glove) • Autonomic nephropathy • Cardiac, GI ( gastroparesis) , GU ( neurogenic bladder)

  42. NEPHROPATHY • Most common cause of end-stage renal disease • Type 1 = 45%, Type 2 = 20% • Damage to capillaries of glomeruli • Concomitant hypertension • Dx glycosylated albumin • Rx hypertension, maintain even blood sugar

  43. SICK DAY MANAGEMENT • TEST BLOOD SUGAR Q 2-4 HRS • TEST URINE FOR KETONES Q 2-4 HRS • TAKE INSULIN EVEN IF N/V • 10-15 GMS CARBOHYDRATES Q 1-2 HRS. • EX. 1 POPSICLE, 1/2 CUP JELLO • FLUIDS Q 30 MINS • EX. ICE CHIPS, GATORADE

  44. FOOT PROBLEMS • 75% OF ALL LOWER EXTREMITY AMPUTATIONS • 3 FOLD PROBLEM • NEUROPATHY •  SENSATION (INJURY) • PERIPHERAL VASCULAR DISEASE •  CIRCULATION ( POOR WOUND HEALING) • IMMUNOCOMPROMISED •  ABILITY OF LEUKOCYTES • RESISTANCE TO INFECTION

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