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Type 1 diabetes
Insulin-producing beta cells in the pancreas are destroyed by an autoimmune process
Requires insulin
Onset is acute before 40 years
Manifestations occur when pancreas can no longer produce insulin
Type 2 diabetes
Insulin resistance and impaired beta cell function result in decreased insulin production
slow, progressive glucose intolerance
Treated initially with diet and exercise
Type 1 diabetes clinical manifestations
Polyuria
Polydipsia
Polyphagia
Weight loss
Weakness
Fatigue
Ketoacidosis
Type 2 diabetes clinical manifestations
nonspecific—classic symptoms of type 1 may manifest
Fatigue
Recurrent infection
Recurrent vaginal yeast or candida infection
Prolonged wound healing
visual problems
Diabetes diagnostic findings
A1C 6.5% or higher
FPG >126 MG/DL
Hyperglycemia symtoms—random plasma glucose >200
Type 2 Diabetes nutrition therapy
Moderate weight loss
Appropriate serving sizes
Reduced saturated and trans fats
Spacing meals
Regular exercise
Hypoglycemia
Cold, clammy skin
Numbness in fingers, toes, and mouth
Tachycardia
Emotional changes
Diabetic Ketoacidosis
Caused by profound deficiency of insulin
Characterized by hyperglycemia, ketosis, acidosis, dehydration
More likely in type 1
Sugar 250-500+
DKA clinical manifestations
Polydipsia
Headache
Nausea/vomiting/abd pain
polyuria
Leg cramps
Confusion, ketotic breath
Kussmaul breathing
Tachycardia, hypotension, dehydration
DKA emergency management
Ensure patent airway, administer o2
Establish IV access; begin fluid resuscitation to correct electrolyte imbalance
NACL 0.45% or 0.9%; add 5%-10% dextrose when glucose approaches 250
Monitor and replace potassium before insulin therapy
Hyperosmolar Hyperglycemia syndrome
Type 2 diabetes; over age of 60
Able to make enough insulin to prevent DKA but still have severe hyperglycemia, osmotic diuresis, and ECF depletion
sugar 600+
Slower onset, stable potassium