Diabetes Mellitus
Outline
Diabetes Mellitus 1. Types
2. Risk Factors
3. Metabolic Effects of Diabetes 4. Acute Complications
a. Hypoglycemia
b. Diabetic Ketoacidosis (DKA)
c. Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNK)
5. Chronic Complications
Objectives
•
At the end of the lecture, the student vocational nurse
will be able to:
•
Compare and contrast the two types of diabetes
mellitus
•
Summarize the risk factors associated with both
•
Describe the systemic metabolic effects of diabetes by
each body system
•
Formulate a nursing care plan which addresses the
physiological and psychosocial integrity, health
Diabetes Mellitus
• Metabolic Disorder of the Pancreas
– Affects CHO, fat, and protein metabolism; – Chronic disorder
– Affected people experience many debilitating and life-threatening
complications before death
• Metabolic Syndrome
– Abdominal obesity; HTN; Elevated LDP, triglycerides, blood glucose
levels; Low HDL
• 90-95% Acquire Disorder as Adults
• 7th Cause of Death in U.S.; 23.6 million in U.S. have DM (estimate)
• Incidence increased among African Americans, Latinos, Native
Americans, Asian Americans
Diabetes Mellitus
•
Two major forms:
•
Type I
– formerly called insulin-dependent diabetes mellitus (IDDM) – Characterized by no insulin production by the beta cells in the
islets of Langerhans of the pancreas
– Onset: childhood and adolescence
•
Type II
– formerly called non-insulin dependent diabetes mellitus
(NIDDM)
– Characterized by insulin resistance or insufficient insulin
production
Diabetes Mellitus
• Prediabetes Mellitus – Can lead to
• Type 2 diabetes • Heart disease • Stroke
– Impaired fasting glucose
(IFG): 100 to 125 mg/dL
– Impaired glucose tolerance
(IGT): 140 to 199 mg/dL
– A significant number of those
with pre-diabetes will develop the disease
– Weight loss and increase
physical activity can delay or avoid onset of Type II DM
Islet of Langerhans
Diabetes Mellitus
•
Hyperglycemia
– An elevated blood glucose level
– Associated: Other disorders; Management – Pancreatitis; Adrenocortical hormones
•
Insulin
– Functions:
• Carries glucose into body cells as their preferred
source of energy
Diabetes Mellitus
•
Pathophysiology and Etiology
– Type 1 diabetes mellitus (IDDM)
• No insulin production of the islet cells, or endocrine
portion of the pancreas
• Lipolysis (breakdown of fat) results in accumulation of
fatty acids and ketones (metabolic byproducts of fat metabolism)
• Ketoacidosis (a form of metabolic acidosis)
• Autoimmune disorder (genetic mutation causes killer
(CD8) T-cell lymphocytes to attack and destroy the insulin-producing islet cells
Diabetes Mellitus
•
Pathophysiology and Etiology
– Type 2 diabetes mellitus (NIDDM) • Inherited
• Obesity causes changes in liver function
accompanied by hyperglycemia and insulin
resistance (decreased sensitivity to insulin at the tissue level)
• Insufficient insulin
Diabetes Mellitus
•
Pathophysiology and Etiology
–
Type 2 diabetes mellitus (NIDDM)
• Insulin resistant; Insufficient insulin; Inherited
• Obesity—trigger;
• Glycosuria (Caused by an excessive glucose in the blood; appears when BS level >180mg/dL)
• Impaired renal threshold (kidney’s ability to
reabsorb glucose and return it to the bloodstream) • Ketonemia (increased ketones in the blood)
Diabetes Mellitus
•
Assessment Findings
– Signs and symptoms
• Polyuria (excessive urine production) • Polydipsia (excessive thirst)
• Polyphagia (feels hungry and eats more) • Weight loss
• Dehydration • Blurred vision • Thirst
Diabetes Mellitus
•
Diagnostic findings
– Urinary tests
• presence of glucose and ketones – Blood tests
• random blood sugar, fasting blood glucose, postprandial glucose, oral glucose tolerance test
– Glucometer
• measures capillary blood glucose from finger stick blood
sample
– Hemoglobin A1c test (glycosylated hemoglobin)
• Measures amount of glucose stored in the hgb molecule
Diabetes Mellitus
•
Medical Management
– Depends on type of diabetes
– Diet and weight loss: Major component of treatment • Dietary allowances (calories, percentages of CHO,
fats, and proteins)
• Carbohydrate counting
• Glycemic index (measures how fast CHO food raises
blood sugar)
– Exercise
Insulin: Four categories
• Rapid acting– Insulin lispro (Humalog)
• Onset: 5-15min; Peak: 1-2hr; Duration: 3-4hr – Aspart (Novolog)
• Onset: 5min; Peak: 1hr; Duration: 3-4hr
• Short acting
– Regular insulin (Humulin R, Novolin R, Iletin II Regular) • Onset: 30min-1hr; Peak: 1-3hr; Duration: 6-8hr
• Intermediate acting
– Isophane insulin suspension (NPH, Humulin N, Novolin N) • Onset: 1-1.5hr; Peak: 4-12hr; Duration: 24hr
– Insulin zinc suspension (Lente)
Insulin: Four categories (cont’n)
• Long acting– Extended insulin zinc suspension (Ultralente, Humulin U) • Onset: 4-8hr; Peak: 8-10hr; Duration: 18-30hr
– Glargine (Lantus)
• Onset: 2-4hr; Peak: none; Duration: >24hr
• Insulin mixtures
– Humulin 50/50
• Onset: 15min; Peak: 2-4hr; Duration: 20-22hr – Humulin 70/30
• Onset: 30min; Peak: 7-12hr; Duration: 16-24hr – Novolin 70/30
• Onset: 30min; Peak: 3-8hr; Duration: 10-16hr – Humalog 75/25
Diabetes Mellitus
•
Medical Management
–
Types of Insulin
•
Human, beef, pork
–
Administration of insulin
•
Dosage:
U-100; Type
•
IV
•
Subcutaneous;
•
Lipoatrophy
•
Lipohypertrophy
•
Insulin pen
Diabetes Mellitus
• Medical Management
– Oral antidiabetic agents-type 2 • Sulfonylureas and meglitinides
– “insulin releasers”
– Stimulates pancreas to secrete more insulin • Biguanides and thiazolidinediones
– “insulin sensitizers”
– Help tissues use available insulin more efficiently • Alpha-glucosidase inhibitors into glucose
– Breaks down complex CHO – Adjuvant drugs
• Glucose-regulating function – Pancreas transplantation
Acute Complications:
Diabetic Ketoacidosis (DKA)
•
Pathophysiology and Etiology
– Occurs when there is an acute insulin deficiency or an
inability to use whatever insulin the pancreas secretes
– Brittle (unstable) diabetes
– Noncompliance with treatment; Infection – Acidotic state; Coma
•
Assessment Findings
– Weakness; Thirst; Anorexia; Vomiting; Drowsiness;
Abdominal pain; Kussmaul respirations; Low BP
– Blood glucose 300-1000mg/dL; Urine test; Laboratory
Diabetic Ketoacidosis (cont’n)
•
Medical Management
–
Main goals
•
Reduce the elevated blood glucose
•
Correct fluid and electrolyte imbalances
•
Clear the urine and blood of ketones
–
IV Insulin; Glucose
–
Isotonic fluid
–
Potassium replacements
Hyperosmolar Hyperglycemic Nonketotic
Syndrome (HHNKS)
•
Pathophysiology and Etiology
– Hyperglycemia without ketosis
– Results from serious illness; Diuresis – Blood glucose >500
– pH normal range (7.35-7.45)
•
Assessment Findings
– Hypotension; Mental changes
– Extreme thirst; Dehydration; Tachycardia – Fever; Neurologic signs
Hyperosmolar Hyperglycemic Nonketotic
Syndrome (cont’n)
•
Diagnostic Findings:
–
Blood glucose
–
Serum potassium, sodium
–
Serum osmolarity
•
Medical Management
–
Insulin administration
–
Correction of fluid and electrolyte imbalances
–
CVP
Hypoglycemia
•
Pathophysiology and Etiology
– Hyperinsulinism
• blood glucose <60 mg/dL – Contributing factors:
• Diet; Exercise; Alcohol
•
Assessment Findings
– Signs and symptoms:
• Nausea; Drowsiness; Hunger; Malaise; Excessive
perspiration; Confusion; Coordination difficulty; Personality or behavior changes
•
Diagnostic Findings:
Hypoglycemia (cont’n)
•
Medical Management
–
Administration of 15 to 20 g of simple
carbohydrate as soon as possible
–
Glucagon
–
IV administration of 50% glucose
–
Complex carbohydrates
Chronic Complication:
Peripheral Neuropathy
•
Pathophysiology and Etiology
– Pathologic changes in nerves
– Develops 10 or more years after the onset of DM – Poor glucose control
– Decreased blood circulation to nerve tissue – Motor neuropathy
• When motor nerves are affected, the muscles weaken and
atrophy
– Sensory neuropathy
• Leads to paresthesias (abnormal sensations such as
prickling, tingling, burning, or needle-like pain) – Autonomic neuropathy
Peripheral Neuropathy (cont’n)
•
Assessment Findings
– Signs and symptoms:
– Pain; Swollen feet; Disturbing sensations; Digestive, urinary,
and sexual dysfunction; Dizziness; Smaller skeletal muscles
•
Diagnostic findings: Neurologic examination;
Screening test; Electromyography
•
Medical Management
– Diet; Exercise; Pain relief measures
– Drug therapy; Antibiotic therapy; Drugs to reverse diabetic
neuropathies
Diabetic Nephropathy
•
Pathophysiology and Etiology
– Progressive decrease in renal function – Glomerular deterioration
– Five stages:
• Stage I Hyperfiltration, Glomerular hypertrophy; 10 yrs after • Stage II Microalbuminuria; 15 yrs after dx of DM
• Stage III Gross albuminuria; 15 yrs
• Stage IV Advanced dysfunction; 15-20 yrs • Stage V End-stage renal failure; 20-25 yrs
•
Assessment Findings:
– Swollen feet and hands; Gradually increasing BP;
Diabetic Nephropathy (cont’n)
•
Diagnostic Findings:
–
Serum creatinine test; Renal creatinine clearance test
•
Medical Management:
–
Control blood glucose levels, hypertension
–
Drug therapy; Dietary protein reduction; Smoking
cessation
Diabetic Retinopathy (cont’n)
•
Pathophysiology and Etiology
–
Vascular changes in retina
–
Develops 10 or more years after
onset of diabetes
–
Types
•
Nonproliferative
•
Proliferative—blindness
•
Assessment Findings
Diabetic Retinopathy (cont’n)
•
Medical Management
– Laser photocoagulation – Vitrectomy
– ACE inhibitor
•
Nursing Management
– Encourage therapeutic regimen for tight glucose control – Client education
• Complications of diabetes
Vascular Disturbances
•
Pathophysiology and Etiology:
– Thickening of arterial walls– Coronary artery disease – Hyperlipidemia
•
Assessment Findings:
– Cool extremities; Leg cramps; Gangrene; Skin ulcers;
Myocardial infarctions
•
Diagnostic Findings:
– Laboratory tests– Angiography
Vascular Disturbances (cont’n)
•
Medical and Surgical Management:
–
Lipid-lowering measures
–
Vasodilators
–
Platelet aggregation reduction drugs
–
Amputation
–
Insulin
Reference
•
Timby, B. & Smith, N. (2010). Introductory