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Diabetes

Type 1 Pathophysiology

Stage 1: genetic predisposition
Stage 2: environmental triggers
Spring and fall
Epidemics of various viral diseases
Stage 3: active autoimmunity
ICA's and insulin antibodies progressively decrease the effective circulating insulin level
Stage 4: progressive beta cell destruction
Stage 5: overt diabetes mellitus

Type 2 Pathophysiology

Insulin is a building (anabolic) hormone. w/o 3 metabolic problems occur
Decreased glucose utilization
Increased fat mobilization
Increased protein utilization

Decreased Glucose Utilization
Cells that require insulin as a carrier for glucose can take in only 25% of the glucose they require for fuel

Do Not Require Insulin for Glucose Transport Require Insulin
Nerve tissue Adipose tissue
Erythrocytes Skeletal muscle
Cells of intestines Cardiac muscle
Liver
Kidney tubules

Inadequate amounts of insulin = levels of glucose rise

Elevation continues to rise b/c liver cannot store glucose as glycogen w/o sufficient insulin levels

Return to homeostasis = kidney excretes excess glucose = urine acting as osmotic diuretic = increased water loss aka fluid volume deficit.

Increased Fat Mobilization
Body turns to fat stores for energy production when glucose unavailable
Type 1
Type 2 w/severe stress

Fat metabolism causes breakdown products called ketones

Ketones accumulate in the blood, are excreted through kidney & lungs, is measured in blood and urine.

High levels = uncontrolled diabetes

Ketones interfere w/body's acid-base balance by producing hydrogen ions

Decreased pH = metabolic acidosis

Sodium follows excreted ketones = sodium depletion and further acidosis

Excreted ketones also = increase in osmotic pressure = increased fluid loss

B/c fats are primary source of energy body lipids increase to 5x normal = atherosclerosis

Increased Protein Utilization
Protein wasting = lack of insulin

w/o insulin to...