Narrative of Pathophysiology

Diabetes mellitus is a group of metabolic disease that characterized by elevated

levels of glucose in the blood (hyperglycemia) resulting from defect in insulin secretion,
insulin action or both. For the predisposing factors the possible are: family history of
DM, race, age and sex. It could really run in the family having the same gene from
generation to generation. For the precipitating factors, the possible are: diet, lifestyle
obesity and stress. Diet involves the individual who is habitually eating foods high in
sugar, fats or cholesterol, low fiber and salty diet. Sedentary lifestyle is believed to
precipitate the condition also.

This factors could lead to insulin deficiency resulting to catabolic state that affects
both fat and protein metabolism. Insulin deficiency coupled with glucagons excess
decreases peripheral utilization of glucose while causing hyperglycemia. Hyperglycemia
causes osmotic diuresis which is a sign of polyuria. It could cause to hyperosmolality
dehydration and volume depletion. It could further lead to water loss and electrolyte
imbalance. On the other hand, dehydration together with water loss and electrolyte
imbalance, it could trigger the thirst center of the brain. In this manner, polydipsia
appears. On the other hand, hyperglycemia could lead to viscosity of the blood increasing
the risk of clot formation. Therefore, it could lead to altered circulation decreasing the
blood supply to the vital organs of the body.

Insulin deficiency stimulates the adipose stores to break down increasing lipolysis
process of fat metabolism. This process could increase the levels of free fatty acids.
When free fatty acids reach the liver called as oxidation of fatty COA molecule produces
ketone bodies. Increase would further lead to ketonuria. If ketone excretion is
compromised by dehydration, it could increase the plasma hydrogen ion concentration.
This could further lead to metabolic acidosis. Signs and symptoms that can be manifested
are Kussmaul breath as a compensatory mechanism to acidosis. Acidosis can make the

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potassium shift from intracellular to extracellular space leading to hypokalemia, which in
turn can lead to arrhythmia and trigger myocardial infarction leading to death.

On the other hand, insulin deficiency can cause protein metabolism causing use of
gluconeogenesis by the liver. This can cause increase appetite since the body does not use
up glucose. Protein metabolism also causes derangement in capillary wall causing
increase permeability to plasma protein and other particles causing proteinuria. It can
cause deceased amount of albumin in the blood causing generalized edema,
immunoglobulin loss cause the patient to be more succeptible to infection and lipiduria.

If treated, it could lead to a good prognosis. If not, it could lead to chronic

complications to vital organs of the body. In lower extremities, it could cause tissue
hypoxia, causing foot ulceration and infection and turn into gangrenous area causing
amputation. In the brain, it could cause cerebral ischemia of infarction causing diabetic
neuropathy. In the heart , it could cause myocardial infarction. In the eyes, it increases
vascular permeability leading to glaucoma or cataract leading to retinopathy and
eventually visual loss. Tissue damage in the kidney decreases the delivery of oxygen to
the nerves causing atrophy of the nerves with loss of myelin and further damage to the
kidneys. All of these can cause, shock, leading to comatose, and eventually death.

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