NCMB 316 LEC Week 7: Diabetes Mellitus

• NCMB 316 LEC Week 7 covers Diabetes Mellitus

Learning Objectives

• Differentiate between Type 1 and Type 2 diabetes
• Describe etiologic factors associated with diabetes
• Relate the clinical manifestations of diabetes to the associated pathophysiologic alterations
• Identify the diagnostic and clinical significance of blood glucose test results
• Explain the management of DM
• Use the nursing process as a framework for care of clients with diabetes

Pancreas

• The pancreas includes the bile duct, head, body, and tail as well as the inferior vena cava and the abdominal aorta

Pancreas: Endocrine part

• The Islets of Langerhans are located in the Pancreas
• The Islets of Langerhans are made up of alpha, beta and delta cells

Alpha Cells

• Glucagon increases glucose levels through gluconeogenesis

Beta Cells

• Insulin decreases glucose levels by:
• Transcellular membrane transport of glucose
• Inhibiting the breakdown of fats & CHON
• Requires Na+ for transport of CHON
• Requires K+ for production

Delta Cells

• Somatostatin inhibits the action of growth hormone

Diabetes Mellitus

• A chronic metabolic disease characterized by hyperglycemia due to a disorder of carbohydrate, fat, and protein metabolism

Predisposing Factors

• Heredity is strongly associated with Type II DM
• Obesity leads to adipose tissues being resistant to insulin, therefore glucose uptake by the cells is poor
• Stress stimulates secretion of epinephrine, norepinephrine, glucocorticoids increasing serum carbohydrates

Other Predisposing Factors

• Viral infection increases the risk to autoimmune disorders
• Autoimmune Disorders are more associated with Type I DM
• Multigravida

Types of Diabetes Mellitus

• Type I
• Type II
• Gestational Diabetes
• Diabetes associated with other conditions or syndromes
• Pancreatic disease, Cushing's syndrome
• Use of certain drugs like Steroids, Thiazide diuretics and Oral contraceptives

Type I (IDDM)

• Commonly Juvenile onset, Brittle DM, Unstable DM
• The Onset is less than 30 years
• Occurs in children or in non-obese adults (usually thin)
• There is no insulin production
• Prone for DKA
• Management includes diet, exercise and Insulin

Type II (NIDDM)

• Commonly Maturity – onset, Stable DM, Ketosis – resistant DM
• The Onset is 40 years
• Occurs in obese adults
• Inadequate insulin production or cells do not respond to insulin
• Prone for HHNKS
• Management includes diet, exercise and OHA, Insulin is given in STRESSFUL situations

Stress Response in Type II Diabetes

• STRESS: surgery, infections pregnancy, etc. causes a stress response which releases E, NE and Glucocorticoids
• This leads to hyperglycemia and the need to give insulin to get back to normal

Diabetes Mellitus: Pathophysiology - Normal Process

• The stomach converts food to glucose.
• Glucose enters the bloodstream.
• The pancreas produces insulin.
• Insulin allows glucose to enter the body effectively.
• Glucose levels are maintained in balance.

Diabetes Mellitus: Pathophysiology

• Insulin acts as the "key" to allow glucose to enter the cell

Insulin Deficiency

• Leads to hyperglycemia

Hyperglycemia leads to

• Polyuria, Polydipsia and Polyphagia

Polyuria

• Large amounts of glucose pass through the kidney.
• This causes it to exert high osmotic pressure within the renal tubules.
• This results in osmotic diuresis.

Polydipsia, Hypovolemia and Glycosuria

• Polydipsia is due to blood osmolarity, which means water moves from inside to outside the cell causing Intracellular Fluid (ICF) dehydration
• Hypovolemia can be expected which is Extracellular Fluid (ECF) dehydration)
• Glycosuria will occur if glucose in the blood is >180 mg/dl (renal threshold)

Hyperglycemia & Polyuria

• Can lead to a Loss of Fluids & electrolytes
• This can cause Hypovolemia, Hypotension, Renal failure, Coma & Death

Hyperglycemia & Cellular Starvation

• Glucose and Insulin are needed for the Cell, however the cellular starvation is due to lack of insulin
• A person will experience Hunger and increased appetite which is know as Polyphagia

Cellular Starvation and Alternative Energy

• Alternative energy source are Proteins and Fats
• However Fats breakdown ultimately lead to Ketone production

More consequences of Ketoacidosis

• Ketones increase Ketonuria
• Lipolysis leads to hyperlipidemia and ultimately atherosclerosis
• Hyperlipidemia increases Ketones and therefore leads to Ketonemia and Acetone breath
• Ketonemia increases Metabolic acidosis

Ketones

• Act as CNS depressants and may decrease brain pH leading to coma

Proteins

• Protein breakdown ultimately leads to a Negative nitrogen balance
• This leads to an increase in BUN and serum creatinine
• Which also manifests as Tissue wasting, Weight loss, and Debilitation

Increased Blood Viscosity

• Sluggish circulation
• Proliferation of microorganisms
• Infections, Periodontal, UTI, Vasculitis, Cellulitis, Vaginitis, and Furuncles, Carbuncles
• Retarded Wound Healing

Diabetic Foot Care

• Thoroughly inspect feet daily, and keep them clean and dry

Diabetes Mellitus: Pathophysiology - Complications

• Macroangiopathy
• Microangiopathy
• Neuropathy

Macroangiopathy

• Impacts
• Cerebrovascular accident of the Brain
• Myocardial infarction of the Heart
• Peripheral vascular disease of the Peripheral arteries

Microangiopathy

• Impacts
• Renal failure due to nephropathy of the Kidneys
• Cataract due to retinopathy of the Eyes

Microangiopathy of the Eyes

• Normal retina vs Retinopathy

Neuropathy

• Spinal Cord/ ANS
• Peripheral neuropathy
• Involves damage to the Peripheral Nervous System (PNS)
• Affects movement, sensation and bodily functions (numbness/ tingling)

Neuropathy continued

• Paralysis
• Gastroparesis (delayed gastric emptying)
• Neurogenic bladder (bladder does not empty properly)
• Decreased Libido, impotence

Diagnostic Tests for Diabetes Mellitus

• Random Blood Sugar (RBS)
• Blood specimen is drawn without preplanning
• ≥200mg/dl + symptoms indicates of DM
• Fasting Blood Sugar (FBS)
• Blood specimen after 8 hours of fasting -Normal (70-100 mg/dl), pre diabetes(101 but <126mg/dl) -DM- > 126 mg/dl
• Postprandial Blood Sugar
• Blood sample is taken 2 hrs after a high CHO meal -No DM (70-140mg/dl), prediabetes (≥140 but <200 mg/dl)
• Oral Glucose Tolerance Test (OGTT)
• Diet high in CHO is eaten for 3 days -Client then fast for 8 hours and a baseline blood sample drawn and a urine specimen collected -An oral glucose solution is given and ingestion time recorded -Blood is drawn at 30 minutes & 1, 2, and 3 hours after glucose ingestion plus urine collected -No DM is diagnosed if glucose returns to normal in 2-3 hours & urine is negative for glucose -DM is diagnosed if blood glucose returns to normal slowly and urine is positive for glucose
• Glycosylated hemoglobin (HbA1c)
• Requires a single sample of venous blood is withdrawn -The amount of glucose stored by the hemoglobin is elevated above 7% in the newly diagnosed client with DM, in one who is noncompliant, or in one who is inadequately treated

Diabetes Mellitus: Management

• A low caloric diet is recommended if obese
• Diet should be in proportion
• 20% CHON
• 30% Fats
• 50% CHO
• Consume complex CHO and HIGH fiber diet as it inhibits glucose absorption in the intestines

Exercise

• Increases CHO uptake by the cells
• Decreases insulin requirements
• Maintains ideal body weight, serum carbohydrates & serum lipids
• Guidelines require to allow additional sources of CHO like snacks during exercises
• Exercise is done 1-2hours after eating to prevent hypoglycemia
• Exercise must be regular pattern rather than sporadic to maintain stable serum carbohydrate levels

Medications

• Insulin is appropriate for Type I & II
• Oral Hypoglycemic Agents are good for Type II

Insulin preparations can consist of a mixture of

• Beef and pork insulin
• Pure beef
• Pure pork
• Human insulin - purest insulin and has the lowest

Types of Insulin Administration

• Human insulin is recommended for
• ALL newly diagnosed Type I diabetics
• Type II diabetics who need short-term insulin therapy
• Pregnant client
• Diabetic clients with insulin allergy or severe insulin resistance

Types of Insulin

• Rapid acting
• Lispro (Humalog)
• Onset is 5 minutes, Peak is at 30 mins - 1hr and Duration is 2 to 4 hrs
• Aspart (Novalog)
• Short acting
• Regular (Humulin R, Novolin R, Iletin II regular)
• Onset is 30 min to 1 hr, Peak is at 2 to 4 hrs and Duration is 6 to 8 hrs
• Intermediate
• NPH, Humulin N -Onset is 1 to 2 hrs, Peak is at 6-8 to 12 hrs and Duration is 18 to 24-28hrs -Lente, Humulin L
• Long acting -Ultralente -Onset is 5 to 8 hrs, Peak is at 14 to 20 hrs and Duration is 30 to 36 hrs -Lantus -Onset is 5 to 8 hrs, Peak is unknown and Duration is 24 hrs

Insulin Action

• Insulin level when taking various types of insulin - Aspart, lispro, glulisine, Regular, NPH, Detemir and Glargine

Insulin Types

• Humalog, Insulin R, Humulin N, Lantus

Nursing Responsibilities in Insulin Therapy

• Route: Subcutaneous
• slow absorption, less painful, use a 90° (thin) 45° on obese clients
• no need to aspirate, do not massage site of injection
• IV insulin: is given in emergency cases like DKA
• Administer insulin at room temperature
• Cold insulin can cause lipodystrophy, Lipoatrophy- loss of subcutaneous fat usually caused by animal insulin, Lipohypertrophy is development of bumps
• Nursing pt teaching:
• Store vial of insulin in current use at RT, can be stored for a month, place other vials in fridge
• Rotate the site of injection to prevent lipodystrophy
• Gently roll vial in between the palms to redistribute insulin particles
• DO NOT Shake (bubbles make it difficult to aspirate the amount needed)
• Observe for side effects of insulin therapy
• Localized: Induration or Redness, Swelling, Lesion at the site, Lipodystrophy
• Generalized: Edema (due to sudden resolution of hyperglycemia) and Hypoglycemia

Nursing pt teaching: Dawn vs Somogyi effect

• Lack of available insulin vs rebound effect
• The dawn phenomenon vs Dawn phenomenon

Insulin Pumps

• A computerized device delivers insulin to patients automatically throughout the day
• Dosage instructions are entered into the pump's small computer, then the appropriate amount of insulin is injected into the body in a calculated, controlled manner

Insulin Pumps

• Closely mimic normal pancreatic functioning
• It contains a 3 mL syringe attached to a narrow-lumen tube with a needle or Teflon catheter at the end
• The needle or Teflon catheter is inserted into the subcutaneous tissue (usually on the abdomen) and secured with tape

Insulin Pumps Continued

• The needle or catheter is changed at least every 3 days
• The pump is worn either on a belt or in a pocket
• The pump uses only regular insulin
• Insulin can be administered via the basal rate (usually 0.5-2.0 units/hr) and by a bolus dose

Types of Oral Hypoglycemics

• Sulfonylureas “insulin releasers”
• Stimulate the beta cells to secrete more insulin -Increases the ability of insulin cell receptors to bind insulin -SE: weight gain, hypoglycemia, secondary failure of pancreas due to overstimulation with Tolbutamide (Orinase), Acetohexamide (Dymelor), Tolazamide (Tolinase), Chlorpropamide (Diabenese), Glipizide (Glucotrol), Glyburide (micronase, Glynase), and Glimepiride (Amaryl)

Image relating to Sulfonylureas

• Sulfonylureas help the pancreas make extra insulin

Other Oral Hypoglycemic types

• Nonsulfonylureas - Biguanides
• Metformin (Glucophage
• Help tissues use available insulin more efficiently. They are “insulin sensitizers” -SE: Stomach upset, flatulence, diarrhea -No weight gain, no hypoglycemia unlike sulfonylureas

More Oral Hypoglycemic types

• Nonsulfonylureas Alpha-glucosidase inhibitors
• Miglitol (Glyset), Acarbose (Precose) Alpha-glucosidase stops an intestinal enzyme that breaks down carbohydrates into glucose. By inhibiting this enzyme, the process that forms glucose is slowed, and glucose is absorbed more slowly from the small intestine
• should be Taken 15 minutes before meal

Alpha-glucosidase inhibitors

• Alpha-glucosidase inhibitors slow the digestion of starches by the intestines

Other Oral Hypoglycemic types

• Nonsulfonylureas
• Thiazolidinediones (TZDs) - Rosiglitazone (Avandia), Pioglitazone (Actos) -Helps tissues use available insulin more efficiently and are “ insulin sensitizers” -SE: weight gain, edema & liver damage
• Meglitinides
• Repaglinide (Prandin) -“Insulin releaser" -SE: same as with sulfonylureas

ОНА

• Stress the importance of taking the drug regularly
• Avoid alcohol intake while on medication
• Sulfonylureas can precipitate extreme vomiting if given with EtOH

General Nursing Interventions:

• Monitor urine sugar and acetone (freshly voided specimen)
• Perform finger sticks to monitor blood glucose levels as ordered (more accurate than urine tests)
• Observe for signs of hypo and hyperglycemia
• Provide meticulous skin care and prevent injury
• Maintain intake and output; weigh daily

General Nursing Interventions Continued

• Provide emotional support; assist client in adapting to change in life-style and body image
• Observe for chronic complications and plan care accordingly
• Provide client teaching and discharge planning concerning:
• Disease process
• Diet
• Insulin - teach to gently roll vial between palms of hands and to draw up insulin using sterile technique
• If mixing insulin, teach to remember to draw up clear insulin before cloudy (refer to image on slide 66 & 67)

General Nursing Interventions Continued

• Provide many opportunities for return demonstration for proper and correct insulin administration
• Perform good oral hygiene and have regular dental exams
• Have regular eye exams
• Care for the diabetics under stress -Do not omit insulin or oral hypoglycemic agents if taking antibiotics since infection causes increased blood sugar

Hypoglycemia

• Look for typical symptoms such as Shaking, Sweating, Anxious, Dizziness, Hunger, Fast Heartbeat, Impaired Vision, Weakness and Fatigue, Headache and Irritability

Hypoglycemia: Causes

• Overdose
• Omission of insulin,
• Omission of meals,
• Strenuous exercise,
• G.I. upset (N&V)
• Assessment:
• <60mg/dl
• Other symptoms: Headache, Shaking, Sweating,Feeling tired and Weakness

Hypoglycemia: Management

• Simple Sugars p.o.
• 3-4 oz regular soft-drink, 8 oz fruit juice, 5-7 pcs lifesaver's candies, 3-4 pcs hard candies, 1 tbsp sugar, 5 ml pure honey/ karo syrup
• 10-15 gm CHO
• D50 W 20-50 ml IV push (if unconscious) or 1 mg glucagon Monitor BS (blood sugar)

Hyperglycemia Symptoms

• Extreme Thirst
• Frequent Urination
• Dry Skin
• Fruity breath
• Nausea

Hyperglycemia: Causes

• Stress (infection, surgery), Overeating, under dose of insulin
• Assessment:
• 3P'S (polyphagia if insulin is absent)
• Warm flushed dry skin, Soft eyeballs
• Tachycardia, N&V, Abdominal pain
• Kussmaul's breathing
• Urine (+) glucose & Ketones
• Altered LOC

Hyperglycemia: Management

• Patent AW
• O₂ therapy
• NSS + regular insulin IV
• D10W once glucose reaches 250 mg/dl level
• KCI / Slow IV drip, once urine output is adequate
• Monitor blood sugar

Diabetic Ketoacidosis (DKA)

• An acute complication of DM characterized by
• Hyperglycemia
• Accumulation of ketones in the body; causes metabolic acidosis
• Frequently occurs in DM Type I (IDDM)
• Precipitating factors:
• Undiagnosed diabetes
• Neglect of treatment
• infection, cardiovascular disorder
• Other physical or emotional stress

DKA Assessment Findings

• 3 P's
• N&V, abdominal pain
• Warm, dry, flushed skin
• Dry mucous membranes; soft eyeballs
• Kussmaul's respirations or tachypnea; acetone or fruity breath
• Altered LOC
• Hypotension
• Tachycardia

DKA Diagnostic Test

• Serum glucose (up to 600 mg/dL) and ketones elevated (positive urine ketones)
• BUN, Creatinine, Hematocrit are elevated (due to dehydration)
• Serum sodium decreased, potassium (elevated due to the acidosis)
• ABGs: metabolic acidosis with compensatory respiratory alkalosis

DKA: Nursing Management

• Maintain a patent airway
• Maintain F&E balance:
• Administer IV therapy as ordered:
• Normal saline (0.9% NaCl), then hypotonic (0.45% NaCl) sodium chloride When blood sugar drops to 250 mg/dl, may add 5% dextrose to IV Potassium will be added when the urine output is adequate
• Observe for fluid and electrolyte imbalances, especially fluid overload, hypokalemia
• Administer insulin as ordered: -ONLY Regular insulin is given IV (drip or push) and/or subcutaneously (SC) If given IV drip, give with small amounts of albumin since insulin adheres to IV tubing
• Monitor blood glucose levels frequently
• Check urine output every hour
• Monitor vital signs
• Assist client with self-care
• Provide care for the unconscious client if in a coma
• Discuss with client the reasons ketosis developed and provide additional diabetic teaching if indicated

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNKS)

• A complication of DM characterized by
• Hyperglycemia
• Hyperosmolar state without ketosis
• Occurs in Type II DM
• Precipitating factors are:
• Undiagnosed diabetes
• Infections, major burns, other stress
• Certain medications (Dilantin, Thiazide diuretics)
• Dialysis, Hyper-alimentation

HHNKS Assessment Findings

• Similar to ketoacidosis but without Kussmaul respirations and acetone breath

Laboratory Tests

• Blood glucose level extremely elevated
• BUN, creatinine, Hct elevated (due to dehydration)
• Urine positive for glucose

Nursing Interventions

• Treatment and nursing care is similar to DKA, excluding measures to treat ketosis and metabolic acidosis