Normal Physiology Pancreas (Located in the upper abdomen)

Endocrine function (Islets of Langerhans)

Exocrine function

Alpha cells Glucagon

Beta cells Insulin

Delta cells Somastatin

Secretion of digestive pancreatic enzymes to GI tract

Pancreas continuously releases small amounts of insulin (basal insulin)

*during fasting periods (between meals and overnight)* Glucagon stimulates the liver to release stored glucose

*when meal is taken*

Exerts a hypoglycemic effect by interfering with the release of growth hormone from pituitary and glucagon from pancreas Insulin binds to special receptors on cell surfaces and initiates series of actions involved in glucose metabolism

Insulin secretion increases and moves glucose from blood into the muscle, liver and fat cells

- transport and metabolize glucose for energy -Stimulate storage of glucose in the liver and muscle (glucogen) -Signals the liver to stop the release of glucose -Enhances the storage of dietary fat in adipose tissues -Accelerates transport of amino acids into cells -Inhibits the breakdown of stored glucose, protein and fat

Maintain the constant level of glucose in the blood

Pathophysiology: Predisposing factors: - Hereditary factor (familial history of DM, fathers side) Precipitating factors: -diet (high sugar)

Diabetes mellitus is a group of metabolic diseases characterized by increase level of glucose in the blood Oral antihyperglycemics Insulin resistance (decrease tissue sensitivity to insulin) Impaired insulin secretion

Insulin

Intracellular reactions are diminished Cell starvation Insulin is less effective at stimulating glucose uptake by the tissues and at regulating glucose release by the liver Compensatory mechanism: increased amounts of insulin must be secreted to maintain the glucose level at normal or slightly elevated level Overtime, beta cells cannot keep up with the increased demand for insulin Management: Nutritional support Exercise Blood glucose monitoring Social and psychological support

Increased secretion of glucagon to stimulate liver to release stored glucose through breakdown of glycogen (glycogenolysis)

Metabolic syndrome: hypertension, hypercholesterolemia, and abdominal obesity Risk for unstable blood glucose level

Stored glucose runs out, liver forms glucose from breakdown of non carbohydrate substances including amino acids and fats

Glucose produced may not be enough for normal metabolic needs Brain interprets as need for food Polyphagia Decreased ATP production Decreased energy, weakness Risk for Activity Intolerance

Glucose level rises and builds up in the blood

Increase blood concentration

Increase in the viscosity of the blood (hyperviscosity)

Increased extracellular osmolarity Osmotic diuresis Polyuria

Decrease ability to perfuse effectively

Sluggish blood flow Polydipsia

Risk for ineffective tissue perfusion

Damage to macro and microvascular circulation

Risk for fluid and electrolyte imbalance

Injury to blood vessel wall

Attempt to repair

Activation of inflammatory process

Release of chemical mediators

Vascular changes

Increased blood flow

Increased capillary permeability

Leakage of plasma and protein components to injured tissue

Migration of leukocytes

Release of biochemical substances

Further damage to vascular tissue

Necrosis of injured tissue

Retinopathy

Nephropathy

Neuropathy

Decrease in sensory

Damage on the capillaries causing opacity

Increased stressed in glumerular filtration

Management: Nutrition: regulate CHON, Fluid, Na, K, increase caloric intake, and vitamins Avoid or delay complications

Numbness tingling sensation

Cataract

Prolonged inflammatory response (attempt to repair)

Scarring and loss of glumerular filtration membrane

Damage in capillary membrane

Ketoanalogues

Decrease glumerular filtration rate

Plasma protein leaked into the urine

Loss of protein

Decrease ability of kidney to remove bodys metabolic wastes

Decrease ability to perform regulatory functions Decrease ability to release erythropoietin Decrease stimulation of bone marrow to produce RBCs

Stimulates synthesis of lipoproteins

hypoalbuminemia

Build up of metabolic wastes in the body

hyperlipidemia

Decrease oncotic pressure

Further damage in the kidney and other parts of the body

Erythropoietin

Fluid shifting from intravascular to interstitial

Subjected to peritoneal dialysis

Unable to keep up with erythrocyte demand Risk for ineffective tissue perfusion

Risk for fluid and electrolyte imbalance

Creation of access

Anemia

Impaired tissue and skin integrity

Fe Sulfate

Acute pain/ impaired comfort

Risk for infection

Disturbed sleep pattern

Poor appetite

Imbalanced nutrition: less than body requirements