Outline the pathophysiology and clinical features of diabetes mellitus


(1) In diabetes mellitus, hyperglycemia occurs due to reduced entry of glucose into the cells (decreased peripheral utilization) and more importantly, due to the deranged glucostatic functions of the liver.

(2) The hyperglycemia causes glycosuria and osmotic diuresis leading to polyuria and polydipsia.

(3) Intracellular glucose deficiency, which occurs in all cells of the body, also occurs in the cells of hypothalamic satiety center, resulting in polyphagia.


(4) The rate at which aminoacids are catabolized to C02 and H20 is increased and protein synthesis is reduced, leading to a negative nitrogen balance, protein depletion and wasting. Protein depletion is also associated with poor resistance to infection.

(5) The plasma cholesterol level is elevated which plays a role in the accelerated development of atherosclerosis and vascular diseases.

(6) Due to accelerated lipid breakdown, there is excess formation of acetyl CoA that is converted in the liver to acetoacetate, resulting in ketosis and acetone breath.

(7) The large amounts of acetoacetic acid and β-hydroxy butyric acid (ketone bodies) result in acidosis. The acidosis stimulates hyperventilation, known clinically as Kussmaul breathing.


(8) Coma results from acidosis, dehydration and hyperosmolarity of plasma.

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