DIABETES MELLITUSNelia S. Bañaga – Perez RN, MSN

Northeastern College

Nursing Department

Santiago City, Philippines

DIABETES MELLITUS• An endocrine disorder in which there is

insufficient amount or lack of insulin secretion to metabolize carbohydrates.

• It is characterized by hyperglycemia, glycosuria and ketonuria.

Diabetes MellitusPathophysiology

• The beta cells of the Islets of Langerhan of the Pancreas gland are responsible for secreting the hormone insulin for the carbohydrate metabolism.

• Remember the concept - sugar into the cells.

Diabetes MellitusTypes

• Type 1 - IDDM– little to no insulin

produced– 20-30% hereditary– Ketoacidosis

• Gestational– overweight; risk for Type

2

• Type 2 - NIDDM– some insulin produced– 90% hereditary

• Other types include Secondary Diabetes :– Genetic defect beta cell or

insulin– Disease of exocrine pancreas– Drug or chemical induced– Infections-pancreatitits– Others-steroids,

INSULIN

• Insulin is a protein made of 2 chains- alpha and beta• Preproinsulin is produced initially– Precursor molecule that is inactive– Must be made smaller before becoming active

• Proinsulin – Precursor that includes alpha and beta chains– Also has a C-peptide chain– C-peptide levels are used to measure rate that beta cells

secrete insulin

INSULIN• Insulin allows glucose to move into cells to make energy• Liver is first major organ to be reached– Promotes production and storage of glycogen (glycogenisis)– Inhibits glycogen breakdown into glucose (glycogenolysis)– Increases protein and lipid synthesis– Inhibits tissue breakdown by inhibiting liver glycogenolysis

(ketogenesis- converts fats to acids) & gluconeogenisis (conversion of proteins to glucose)

– In muscle, promotes protein and glycogen synthesis– In fat cells, promotes triglyceride storage

INSULIN

• Pancreas secretes 40-50 units of insulin daily in two steps:– Secreted at low levels during fasting ( basal insulin

secretion– Increased levels after eating (prandial)– An early burst of insulin occurs within 10 minutes

of eating– Then proceeds with increasing release as long as

hyperglycemia is present

GLUCOSE HOMEOSTASIS

• Glucose is main fuel for CNS• Brain cannot make or store, therefore needs

continuous supply• Fatty acids can be used when glucose is not

available ( triglycerides)• Need 68-105 mg/dL to support brain• Decreased levels of glucose, insulin release is

stopped with glucagon released

GLUCOSE

• Glucagon causes release of glucose from liver– Liver glucose is made thru glycogenolysis (glucogen to

glucose) &– Gluconeogenesis

• When liver glucose is not available, lypolysis occures ( breakdown of fat) OR

• Proteinlysis (breakdown of amino acids)

ABSENCE OF INSULIN

• Insulin needed to move glucose into cells• Without insulin, body enters a state of

breaking down fats and proteins• Glucose levels increase (hyperglycemia)

Absence of Insulin • Hyperglycemia• Polyuria• Polydipsia• Polyphagia• Hemoconcentration, hypervolemia,

hyperviscosity, hypoperfusion, and hypoxia• Acidosis, Kussmaul respiration• Hypokalemia, hyperkalemia, or normal

serum potassium levels

Assessment • History• Blood tests– Fasting blood glucose test: two tests > 126 mg/dL– Oral glucose tolerance test: blood glucose > 200 mg/dL

at 120 minutes– Glycosylated hemoglobin (Glycohemoglobin test) assays– Glucosylated serum proteins and albumin

• FSBS – (finger stick) monitoring blood sugar

Urine Tests

• Urine testing for ketones• Urine testing for renal function• Urine testing for glucose

Diabetes MellitusClinical Manifestation

• Hyperglycemia– Three P’s -

• Polyuria

• Polyphagia

• Polydispsia

• Gradual Onset

• Hypoglycemia– Weak, diaphoretic, sweat,

pallor, tremors, nervous, hungry, diplopia, confusion, aphasia, vertigo, convulsions

– Treatment - OJ with sugar, or IV glucose

• Sudden onset

Hyperglycemia - Clinical Manifestations

• Three P’s – polyuria, polydypsia,

polyphagia• Glycosuria• Dehydration• Hypotension• Mental Changes

• Fever• Hypokalemia• Hyponatremia• Seizure• Coma

Life Threatening!!!

Risk for Injury Related to Hyperglycemia

• Interventions include:– Dietary interventions, blood glucose

monitoring, medications– Oral Drugs Therapy

(Continued)

Risk for Injury Related to Hyperglycemia (Continued)

– Oral therapy• Sulfonylurea agents• Meglitinide analogues• Biguanides• Alpha-glucosidase inhibitors• Thiazolinedione antidiabetic agents

Oral HypoglcemiasKey Points

• Monitor serum glucose levels• Teach patient signs and symptoms of

hyper/hypoglycemia• Altered liver, renal function will affect medication

action• Avoid OTC meds without MD approval• Assess for GI distress and sensitivity• Know appropriate time to administer med

Diet Therapy • Goals of diet therapy• Principles of nutrition in diabetes– Protein, fats and carbohydrates, fiber,

sweeteners, fat replacers– Alcohol– Food labeling– Exchange system, carbohydrate counting– Special considerations for type 1 and type 2

diabetes

Diabetes MellitusDiet

• American Diabetic Association

• Food groups/ exchanges

• Carbohydrates - 60%• Fats - 30%• Protein - 12-20%

Diabetes - Monitoring Glucose Levels

• Urine - Ketones

• FSBS

• Wear ID Bracelet

Diabetes - TreatmentExercise

• Purpose - controls blood glucose and lowers blood glucose

• Purpose - reduce the amount of insulin needed

Exercise Therapy

• Benefits of exercise• Risks related to exercise• Screening before starting exercise program• Guidelines for exercise• Exercise promotion

Drug Therapy

• Drug administration• Drug selection• Insulin therapy:– Insulin analogue– Short-acting insulin– Concentrated insulin– Intermediate

(Continued)

Drug Therapy (Continued)

– Fixed-combination– Long-acting– Buffered insulins

Insulin Regimens

• Single daily injection protocol• Two-dose protocol• Three-dose protocol• Four-dose protocol• Combination therapy• Intensified therapy regimens

Pharmacokinetics of Insulin

• Injection site• Absorption rate• Injection depth• Time of injection• Mixing insulins

Complications of Insulin Therapy

• Hypoglycemia• Lipoatrophy• Dawn phenomenon• Somagyi's phenomenon

Alternative Methods of Insulin Administration

• Continuous subcutaneous infusion of insulin • Implanted insulin pumps• Injection devices• New technology includes:– Inhaled insulin– Transdermal patch (being tested)

Client Education

• Storage and dose preparation• Syringes• Blood glucose monitoring• Interpretation of results• Frequency of testing• Blood glucose therapy goals

Diabetic Education - Preventive Medicine

• Proper skin and foot care

• Proper Eye Exam

• Proper diet and fluids

• Diabetic Neuropathy

• Diabetic Retinopathy

• Diabetic Nephropathy

• Diabetic gastroparesis

Diabetes MellitusComplications

• Hyperglycemia

• Hypoglycemia

• Diabetic Ketoacidosis

• Hyperosmolar Hyperglycemic Nonketotic

Syndrome

Acute Complications of Diabetes

• Diabetic ketoacidosis • Hyperglycemic-hyperosmolar-nonketotic

syndrome• Hypoglycemia from too much insulin or too

little glucose

Diabetic Ketoacidosis

Potential for Diabetic Ketoacidosis

• Interventions include:– Monitoring for manifestations– Assessment of airway, level of consciousness,

hydration status, blood glucose level– Management of fluid and electrolytes

(Continued)

Potential for Diabetic Ketoacidosis (Continued)

– Drug therapy goal: to lower serum glucose by 75 to 150 mg/dL/hr

– Management of acidosis– Client education and prevention

Complication – KetoacidosisTreatment

• Patent airway• Suctioning• Cardiac monitoring• Vital Signs• Central venous pressure• Blood work – ABG, BS,

chemistry panel

• Administration of Na Bicarb

• Foley – monitor urinary output

• I & O• Frequent Repositioning

Complication – HHNCHyperosmolar Hyperglycemic

Non-Ketotic Coma

• Fluid moves from inside to outside cell vausing diuresis and loss of Na+ and K+

• Treatment - Give insulin and correct fluid and electrolytes imbalance

• Signs and Symptoms– Hypotension– Mental changes– Dehydration– Hypokalemia– Hyponatremia

– Life Threatening!!!

Chronic Complications of Diabetes

• Cardiovascular disease• Cerebrovascular disease• Retinopathy (vision) problems• Diabetic neuropathy• Diabetic nephropathy• Male erectile dysfunction

Diabetes MellitusNursing Process

• Assessment – Medicines, Allergies, Symptoms, Family Hx

• Nursing Diagnosis- Anxiety and Fear, Altered Nutrition, Pain, Fluid Volume Deficit

• Planning – Address the nursing diagnosis

• Implementation – Prevent complications, monitor blood sugars, administer meds and diet, teach diet and meds, Asess , Assess, Assess

• Evaluation- Goals, EOC’s

Whole-Pancreas Transplantation

• Operative procedure• Rejection management• Long-term effects• Complications• Islet cell transplantation hindered by

limited supply of beta cells and problems caused by antirejection drugs

Risk for Delayed Surgical Recovery

• Interventions include:–Preoperative care– Intraoperative care–Postoperative care and monitoring

includes care of:• Cardiovascular• Renal• Nutritional

Risk for Injury Related to Sensory Alterations

• Interventions and foot care practices:–Cleanse and inspect the feet daily.–Wear properly fitting shoes.–Avoid walking barefoot.–Trim toenails properly.–Report nonhealing breaks in the skin.

Wound Care

• Wound environment• Debridement• Elimination of pressure on infected area• Growth factors applied to wounds

Chronic Pain

• Interventions include:– Maintenance of normal blood glucose levels– Anticonvulsants– Antidepressants– Capsaicin cream

Risk for Injury Related to Disturbed Sensory Perception: Visual

• Interventions include:– Blood glucose control– Environmental management• Incandescent lamp• Coding objects• Syringes with magnifiers• Use of adaptive devices

Ineffective Tissue Perfusion: Renal

• Interventions include:– Control of blood glucose levels– Yearly evaluation of kidney function– Control of blood pressure levels– Prompt treatment of UTIs– Avoidance of nephrotoxic drugs– Diet therapy– Fluid and electrolyte management

Potential for Hypoglycemia• Blood glucose level < 70 mg/dL• Diet therapy: carbohydrate replacement• Drug therapy: glucagon, 50% dextrose,

diazoxide, octreotide• Prevention strategies for:– Insulin excess– Deficient food intake– Exercise– Alcohol

Potential for Hyperglycemic-Hyperosmolar Nonketotic Syndrome and Coma

Interventions include:MonitoringFluid therapy: to rehydrate the client and restore normal blood glucose levels within 36 to 72 hrContinuing therapy with IV regular insulin at 10 units/hr often needed to reduce blood glucose levels

Health Teaching

• Assessing learning needs• Assessing physical, cognitive, and emotional

limitations• Explaining survival skills• Counseling• Psychosocial preparation• Home care management• Health care resources

Diabetes MellitusSummary

• Treatable, but not curable.• Preventable in obesity, adult client.• Diagnostic Tests• Signs and symptoms of hypoglycemia and

hyperglycemia.• Treatment of hypoglycemia and hyperglycemia – diet

and oral hypoglycemics.• Nursing implications – monitoring, teaching and

assessing for complications.

DIABETES SELF CARE STAR• MEALS

MONITORING * PLASMA *FEET

MEDICATIONS *INSULIN *ORAL AGENTS

MANAGEMENT *SICK DAY *HYPOGLYCEMIA * HYPERGYCEMIA

MOTION

If there are none, If there are none, please prepare ½ please prepare ½ crosswise yellow crosswise yellow

paper….paper….