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DM Basics
  • Energy in the form of glucose is essential for optimal human functioning
  • Glucose in excess is stored in the liver
  • Glucose in the blood triggers the release of insulin
  • An anabolic hormone
  • Required for uptake of glucose by liver cells (receptor sites to store glucose), muscle cells, adipose cells
  • Not required for uptake of glucose by neurons, RBCs, kidney, eye lens
  • Precursor proinsulin: A & B chain linked by c-peptide chain which cleaves off into serum & urine, leaving insulin
Insulin Functions
  • Promote glucose usage
  • Promote protein synthesis
  • Promote formation and storage of lipids
  • Facillitate transport of K+, PO4--, and MG++ into cells
  • Insulin production and availability closely related
  • has endocrine and exocrine functions
  • Endocrine function secretes hormones: inisulin, glucagon, amylin
  • Exocrine secretes: digestive acids, alkaline fluids
Islets of Langerhans
  • Alpha cells: secrete glucagon which mobilizes glycogen from liver, supresses insulin secretion, maintains BG between meals
  • Beta cells: secrete insulin which promotes glucose utilization
  • Delta cells: secrete gastrin & somatostatin which regulate A/B cell function
Increased Insulin secretion
  • increased blood glucose
  • increased amino acids
  • Increased K+, PO4-, MG+
  • when glucagon and gastrin have been active
Decreased Insulin Secretion
  • decreased blood glucose
  • high levels of insulin (negative feedback loop)
  • stimulation of alpha cells (more insulin would make hypoglycemia worse)
  • normal insulin metabolism facillitates a normal glucose range
  • 70-120 mg/dL
Counterregulatory Hormones
  • glucagon
  • epinephrine
  • growth hormone
  • cortisol
  • Oppose effects of insulin
  • move glucose out of storage and into blood
  • decrease cellular uptake
Diabets Mellitus
  • A group of disorders leading to multisystem disease
  • Characterized by: the inability to regulate the amount of glucose in the body, leading to inadequate metabolism of protein, fats, and carbs
  • Related to: abnomral insulin production, impaired insulin utilization, or both
  • Significant elevation of blood glucose coupled with the inability to move glucose and amino acids into the cells that require insulin for movement
  • Causes cell starvation and forces cells to turn to less efficient sources like body fat and proteins for enrgy
DM facts
  • leading cause of heart disease, stroke, adult blindness, and nontraumatic lower limb amputations
  • 7th leading cause of death in the U.S.
  • world health problem
  • 7.8% of US population, expected to increase by 175% over the next 50 years
  • Twofold risk for CAD and CVA, 73% for HTN
  • Estimated 116 billion/year medical costs
DM Type 1 Incidence
  • Fromerly known as juvenile onset or insulin dependent diabetes
  • Most often occurs in people under 40 (40% under 20)
  • peak onset between 11 and 13
  • 10% of all diabetics
  • 1.5-2 times prevalent in caucasians
DM type 1 Etiology and Pathphys
  • Causes: genetic predisposition r/t human leukocyte antigens (HLAs)
  • exposure to a virus
  • leads to autoimmune response and destruction of beta cells
DM type 1 etiology cont.
  • Progressive destruction of pancreatic beta cells may occur several years before signs
  • Autoantibodies have caused a reduction of 80%-90% of normal beta cell function
Type 1 onset
  • Manifestions develop when the pancreas can no longer produce insulin
  • rapid onset of symptoms
  • PResents at ER with ketoacidosis, fat oxidation produces hyerketonemia
  • acetoacetic acid, acetone, B-hydroxybutyric acid) ACID
Type 1 clinical manifestations
  • polyuria
  • polydipsia
  • polyphagia
  • weight loss
  • weakness and fatigue
  • ketoacidosis
Type 1 onset cont.
  • Diabetic ketoacidosis (DKA): occurs in the absence of endogenous insulin, life threatening condition, results in metabolic acidosis
  • Honeymoon perioid: lasts about 3-12 months from diagnosis, decreased need for insulin d/t some functioning beta cells
Type 2 incidence
  • Accounts for 90% of pts with DM
  • usually occurs in people over 35, but is increasing in children
  • 80-90% of pts overweight
  • family history
  • prevalent in african, hispanic, asian, & native american
Type 2 etiology and pathophys
  • Pancreas contines to produce some endogenous insulin
  • insulin produced is either insufficient or poorly utilized by the tissues
  • 4 main metabolic abnormalities play a role: insuli resistance, fatigued beta cells (decreased insulin production), inappropriate glucose productin by the liver, alteration inthe production of adipokines
Type 2 etiology and pathophys cont.
  • insulin resistance:
  • body tissues do not respond to insulin
  • may have decrease in receptor sites
  • results in hyperglycemia
Type 2 etiology and pathophys cont.
  • beta cells fatigued from overproduction
  • Impaired glucose tolerance (IGT) prediabetes:
  • ocurs when the alteration in beta cell function is mild
  • blood glucose levels are higher than normal, but not high enough for a diagnosis of diabetes
  • Fasting BG level between 100-125
Type 2 etiology and pathophys cont.
  • Inappropriate glucose production by liver not considered a primary factor in the development of type 2 DM
Metabolic Syndrome
  • Insulin resistance /syndrome X
  • Cluster of abnormalities that act synergistically to ↑ the risk of CV disease
  • ↑ triglycerides
  • ↑ LDL, low HDL
  • central obesity
  • sedentary lifestyle
  • age
  • HTN
  • ↑ insulin levels
  • westernization
  • NA, AA, hispanic
  • family history
Type 2 onset
  • gradual onset
  • person may go years with indeected hyperglycemia
  • may initially present with long term complication
  • Hyperosmolor hyperglycemic (non-ketotic) syndrome (marked hyperglycemia (>400-100 m/dL, marked ↑ serum osmolality
Type 2 Clinical Manifestations
  • Non-specific symptoms
  • Fatigue
  • Recurrent infections
  • Prolonged wound healing
  • vision changes
Gestational Diabetes
  • Develops during pregnancy
  • Increased Incidence: multiparous, family hc
  • Detected at 24-28 weeks of gestation
  • ↑ risk for c-section, perinatal death, and neonatal complications
  • diabetes resolves 6 wks after delivery
  • increases risk of mother developing type 2 later in life (within5-10 years)
Gestational diabetes: fetal complications
  • Fetal complications
  • Fetal macrosomia
  • Newborn hypoglycemia
  • 5-10% incidence of developmental anomolies: heart defects, spina bifida
Gestational diabetes: maternal complications
  • Risk of chronic HTN
  • C-section
  • DM 2 risk greater after delivery
Secondary diabetes
  • DM caused by treatments or other disorders
  • Excessive hormone production: cushing's, acromegaly
  • Drugs: glucocorticoids, thiazides
  • Pancreatic disease: neoplasm, pancreatitis
  • Infections: CMV, rubella
Diagnostic studies
  • fasting glucose >126
  • Random plasma glucose measurement >200 mg/dl plus symptoms
  • Two hours OGTT ≥200 mg/dl using a glucose load of 75g
  • A1C ≥ 6.5%
  • Impaired glucose tolerance (IGT): fasting blood lgucose ≥ 100 mg/dl but < 126 mg/dl
  • Hemoglobin A1C test (glycosated Hgb): normally < 6.5%
  • C peptide levels: normally 80-400 ng/dl
Collaborative care: goals of diabetes management
  • reduce symptoms
  • promote well-being
  • prevent acute complications
Collaborative Care
  • Pt teaching
  • nutritional therapy
  • drug therapy
  • exercise
  • self monitoring of blood glucose
DM drug therapy: Insulin
  • Exogenous insulin: required for type 1, prescribed for pts with type 2 who cannot control blood glucose by other means
Types of insulin
  • Human Insulin: most widely used types of insulin, cost-effective, ↓ likelihood of allergic reaction
  • Insulins differ in regard to onset, peak action, and duration
  • Different types of insulin may be used for combination therapy
Types of Insulin cont.
  • Rapid acting: lispro, novolog, glulisine (Apidra)
  • Short acting: regular, Novolin R, Humulin R
  • Intermediate acting: NPH, lente, Novolin N, Humulin N
  • Long acting: ultralente, lantus
  • Combination: 70/30, 75/25, (NPH/Regular)
Administration of Insulin
  • Cannot be taken orally, yet
  • SQ injection for self-administration
  • Draw up regular before NPH
  • IV administration for critical care only
  • Insulin pump; tight glycemic control
Problems with Insuling therapy
  • Hypoglycemia: administer juice if concious (15-30 grams cho), glucagon SQ/IM or D50 IVP if unconcious
  • Allergic reactions: administer benadryl or steroids
  • Lipodystrophy: rotate injection sitesif humulin is not being used, hypertrophy or atrophy causes sporadic absorption
  • Somogyi effect: need to decrease evening or night insulin dose, hypoglycemia with rebound hyperglycemia
  • Dawn phenomenon: moring hyperglycemia, limit or regulate snacks or meds
Type 2 treatment: oral glycemic agents
  • Not insulin
  • Work to improve the mechanisms in which insulin and glucose are produced and used by the body
Oral glycemic agents: Sulfonylureas
  • glipizide/Glucotrol, glyburide/Micronase & Diabeta, glimepiride/Amaryl)
  • stimulates secretion of insulin from pancreas
  • May cause antabuse reaction with alcohol
Oral glycemic agents: Meglitinides
  • repaglinide/Prandin
  • stimulates secretion of insuling from pancreas
  • short acting
Oral glycemic agents: Biguanides
  • metformin/Glucophage
  • prevents excess glucose release from the liver
  • increaes peripheral sensitivity to insulin
  • hold prior to procedures where dye in injected (can cause lactic acidosis)
  • dont use for ETOH, CHF, liver disease, renal disease
Oral glycemic agents: α-Glucosidase inhibitors
  • acarbose/Precose, miglitol/Glyset
  • acts on intestines to slow carbohydrate digestion
Oral glycemic agents: Thiazolidnediones
  • rosiglitazone/Avandia, pioglitazone/Actos
  • acts on muscle cells to increase sensitivity to insulin
  • Don't use with CHF
  • Increased risk for MI and CVA
Oral Glycemic Agents: dipeptidyl peptidase-f (DDP-4) inhibitors
  • decreased weight gain
Drug therapy: other agents
  • Amylin analog: pramlintide (symlin) for type 1/2
  • can cause profound hypoglycemia
  • Incretin mimetics (byetta): type 2, delays gastric emptying,
  • can cause acute pancreatitis and kidney problems
Drug interactions: drugs that affect blood glucose levels
  • B-adrenergic blockers
  • thiazide and loop diuretics
  • glucocorticoids
New developments in diabetic therapy
  • New delivery systems (not all yet approved by FDA)
  • skin patch
  • oral spray
  • insulin pills
  • jet injector
  • Taken off the market: inhaled insulin
Nutritional Therapy
  • American diabetes association (ADA)
  • guidelines indicante that within the context of an overall healthy eating plan, a person with diabetes can eat the same foods as a person who does not have diabetes
  • OVerall goal: assist people in making changes in nutrition and exercise habits that will lead to improved metabolic control
Nutritional therapy
  • Type 1: meal plan based on the individual's food intake and is balanced with insulin and exercise patterns
  • Type 2: emphasis placed on acheiving glucose, lipid, and BP goals, calorie reduction
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