 Diminished or absent insulin  Insufficient insulin production

production.  Ketoacidosis not common

 Most often at age of 15 y.o. Classification  Adult and 40 y.o. mostly
 Autoimmune destruction of Type I/ IDDM Type II/NIDDM
 Familial
pancreatic islets
 Familial and lifelong  Obesity creates insulin
demand that cannot be met
by amount of circulating
 Hormone produce insulin present
Gestational
by the placenta has
 May need insulin
↑ insulin resistance
 4% of pregnant
women
 Goes away during Diabetes
delivery
 May develop Type Mellitus
3 P’s
Assessment Type I & II
II after 2 years Type I &II
Insulin Complica
 Polyphagia
tions Type I: Type II: (much eating)
 Hypoglycemia
 Lipodystrophy
↓weight ↑weight  Polydipsia
↑thirst Eye
 Hormone counter T Bed problem
(↑ thirst)
Action
Poorly Controlled Diabetes R wetting Slow  Polyuria
 Diabetic Ketoacidosis E Rapid onset (↑urine
 Hyperosmolar Hyperglycemia A onset volume)
(now Ketotic Coma) T
 Electrolyte Imbalance M
Long Term E
N Dx  Fasting (above
T 125mg/100cc)
Angiopathy  Glucose Tolerance Test
Peripheral Vascular Disease ( 2 hour value greater than
Retinopathy  Insulin 200 mg/dl)
Nephropathy  Glycosylated Hemoglobin
 Oral
Neuropathy is ↑
Infection Hypoglycemic
 Diet
↓insulin need, ↑Glucose
 Exercise Submitted by: Leslie Marie D. Rendon BSN II-Beneficence
storage, ↓Glucose Fluctuation