Diabetes Mellitus: A syndrome with disordered metabolism and inappropriate hyperglycemia due to either a deficiency of insulin secretion or to a combination of insulin resistance and inadequate insulin secretion to compensate.  Type 2 results from insulin resistance with a defect in compensatory insulin secretion.

Etiology: Disease results from genetic susceptibility combined with environmental determinants and other risk factors.  Associated with long-duration obesity.

Pathophysiology:  The cause of the common form of type 2 is unknown although it clearly runs in families and results from a combination of genetic susceptibility and environmental factors. 

Treatment: The goal of treatment is restoration of eugylcemia (normal blood glucose level) and correction of related metaboolic disorders.  Dietary measures, including the restriction of the total caloric intake, are of primary importance in the overweight individual.  Oral hyperglycemic agents often are needed for optimal management and exercise is an essential component of treatnment.

Insulin therapy is used when oral medications fail to maintain eugylcemia.

Dementia: A progressive failure of many cerebral functions not caused by impaired level of consciousness.  The result may be a decrease in orienting, omemory, language and executive attentional networks.  Because of declining intellectual ability, the individual exhibits alteration in behavior.

Etiology: Degeneration, compression, atherosclerosis and trauma. 

Pathophysiology: mechanisms leading to dementia include degeneration, compression, atheroscelrosis, and trauma.  Genetic predispostion is associated with degenerative diseases.  CNS infections, including the human immunodeficiency virus (HIV) and slow-growing viruses associated with Creutzfeldt-Jokobn diseases are associated with dementai in addition to motor function.  Progressive dementias produce nerve cell degeneration and brain atrophy.

Treatments: Individuals with clinical manifestations of dementia should be evaluated with laboratory and neurophsychologic testing to identify underlying conditions that may be treatable.  Therapy is directed at maintaining and maximizing use of the remaining capacities, restoring functions if piossible and accomodating lost abilities.

Chronic Renal Failure:

Definition: the progressive loss of renal function over a period of months or years. 

Etiology: develops as a complication of systemic diseases, such as hypertension or diabetes mellitus, or as a complication of many renal diseases.  CRF decreases GFR and tubular functions with changes manifest throughout all organ systems.

Pathophysiology: The continued loss of functioning nephrons and the adaptive hyperfiltration probably results in further nephron injury and ultimately resuls in uremia and end-stage renal failure.

Treatments: Management involves dietary control, including moderate protein restriction, sodium, and fluid evaluation, potassium restriction, adequate caloric intake, management of dylipidemias, and erythropoietin as needed.  ACE inhibitors or receptor blockers are often used to provide renoprotection and control systemic hypertension.  End-stage renal failure related to diabetic nephropathy can be significantly reduced with control of hyperglycemia by intense insulin therapy.  End-stage renal failure is treated with dialysis, supportive therapy and renal transplantation 

Hypokalemia

Definition: potassium deficiency

Etiology: develops when the serum potassium concentration falls below 3.5 meq/L. 

Pathophysiology: can develop without losses of total body potassium. For example, potassium shifts into the cell during respiratory or metabolic alkalosis or after administration of insulin.  In alkalosis, potassium shifts into the cell in exchange for hydrogen to maintain plasma acid base balance. 

Treatments: Potassium supplements (?)