PATHOPHYSIOLOGY Of Type I DM

Genetic predisposition Lifestyle (HPN, hyperlipidemia) (smoking, improper diet) Environmental Trigger (viral disease, spring or fall season)

Acute autoimmunity directed toward the pancreas Increase ICAs, Decrease insulin autoimmunity Beta cell destruction (resolution)
STRESS/ ACUTE ILLNESS

Hyperglycemia

No signs ands symptoms of DM HONEYMON PERIOD (312 MONTHS) (Pancreas produce adequate amount of insulin)
Ends when beta cells can no longer produce endogenous insulin to sustain life MGT: injected with exogenous insulin to sustain life

Decrease glucose increase protein utilization utilization hyperglycemia wasting

Increase fat metabolism ketones in the body protein

kidney eliminate excess emaciated sugar through urination water loss

ketones in the urine

Na excreation

Fluid volume deficit

Fluid volume deficit

PATHOPHYSIOLOGY Of Type II DM
Limited Beta cell response are chronically- 6 mos to hyperglycemia sugar in the blood Beta cells Expose to level of

Desensitization

Beta cells becomes less efficient in further In blood sugar due to insulin resistance sensitivity
STRESS/ ACUTE ILLNESS

Hyperglycemia

No signs ands symptoms of DM HONEYMON PERIOD (312 MONTHS) (Pancreas produce adequate amount of insulin)
Ends when beta cells can no longer produce endogenous insulin to sustain life MGT: injected with exogenous insulin to sustain life

Decrease glucose increase protein utilization utilization

Increase fat metabolism

hyperglycemia wasting

ketones in the body

protein

kidney eliminate excess emaciated sugar through urination water loss Fluid volume deficit

ketones in the urine

Na excretion Fluid volume deficit