Endocrine System: Diabetes Mellitus Pathophysiology

Subject: Healthcare Research
Pages: 4
Words: 881
Reading time:
4 min
Study level: College


This article focuses on the endocrine system and its correlation with diabetes mellitus. Diabetes mellitus is an endocrine disorder characterized by either lack of insulin or lack of response to insulin in body tissues.

Structure of the endocrine system

The endocrine system and the nervous system have evolved principally to maintain homeostasis; the two are interlinked by the hypothalamus. The endocrine system has various components including endocrine glands proper, those with both endocrine and exocrine cells, and scattered endocrine cells. Endocrine glands proper include the pituitary gland. The endocrine gland proper is a pea-sized organ endocrine gland that is located in the Sella turcica, whose main function is to control functions of other endocrine glands. The anterior pituitary (adenohypophysis) gland has different types of cells: somatotrophs secrete growth hormone, lactotrophs secrete prolactin, gonadotrophs secrete luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Thyrotropin secrete thyroid-stimulating hormone (TSH), adrenocorticotrophic cells secrete adrenocorticotropin hormone (ACTH). The posterior pituitary gland (neurohypophysis) releases antidiuretic hormone (ADH, vasopressin) and oxytocin. The two hormones are secreted in the brain, are transported to the neurohypophysis through the pituitary stalk where they are released (Jain and Sharma, 2004).

The thyroid gland is a bilobed gland situated at the anterior portion of the neck, with the lobes connected by an isthmus. It has follicular cells which synthesize thyroid hormone that is stored in the colloid of the gland. The parathyroid glands are close to the thyroid and they secrete parathyroid hormone (PTH). The pineal body is attached to the brain. Its pinealocytes secrete melatonin. The adrenal cortex releases mineralocorticoids (aldosterone), and glucorcorticoids. The adrenal medulla secretes epinephrine and norepinephrine (Heuther and McCance, 2008).

The pancreas has both exocrine and endocrine cells. It is located posterior to the stomach, between the spleen and the duodenum. The endocrine portion mainly regulates carbohydrate metabolism. Its beta cells elaborate insulin; alpha cells secrete glucagon; delta cells secrete somatostatin, and PP cells secrete pancreatic polypeptide. The testes secrete testosterone and the ovary secretes progesterone and estrogens.

Alterations of the endocrine system

Manifestation of endocrine disorders occurs usually due to overproduction or underproduction of their respective hormones. For the pituitary, underproduction of hormones is termed hypopituitarism and it can be caused by tumors, mass lesion, Rathke cleft cyst, necrosis, Sheehan syndrome, genetic defects, iatrogenic factors, empty Sella syndrome, and pituitary apoplexy. Hyperpituitarism is usually caused by adenomas of one type or more of functioning secretory cells e.g. prolactinomas, growth hormone adenoma, corticotroph cell adenomas, gonadotroph adenomas, thyrotrophin adenoma.

Disorders of the thyroid include hyperthyroidism and hypothyroidism. Thyrotoxicosis is a feature of hyperthyroidism and can be caused by diffuse hyperplasia of the thyroid, hyper-functional multinodular goiter, or thyroid adenoma secondary hyperthyroidism is caused by excessive secretion of TSH by the pituitary gland. Classical clinical features include those of a hypermetabolic state.

Hypothyroidism is caused by iodine deficiency, autoimmune thyroiditis, inborn errors of metabolism, and iatrogenic factors. Secondary hypothyroidism is caused by insufficient production of TSH by the pituitary gland. Clinical features include cretinism in children and myxedema in adults. Primary hyperparathyroidism can occur due to an adenoma, hyperplasia, or carcinoma of the parathyroid gland. Features include hypercalcemia. Secondary hyperparathyroidism is caused by decreases in serum calcium commonly secondary to renal failure. Hypoparathyroidism is caused by surgery, congenital absence, or can be familial or idiopathic. Features include those of hypocalcemia (Magaji and Johnstone, 2011).

The pancreatic beta cells can fail to produce insulin completely to cause type 1 diabetes mellitus. Type 2 diabetes mellitus is caused by resistance to insulin. This is usually superimposed by a failure of the beta cells to compensate by increasing insulin production. Clinical features include polyuria, weight loss, polyphagia, excessive thirst, later blurring of vision, ketoacidosis coma, and nephropathy. Hyperadrenalism is characterized by excess cortisol (Cushing syndrome), hyperaldosteronism, and adrenogenital syndromes. Adrenocortical insufficiency is usually caused by lesions in the adrenal cortex. Secondary adrenocortical insufficiency is caused by disorders of the hypothalamus or pituitary causing low levels of corticotropin. Alterations in the adrenal cortex include pheochromocytoma which is a neoplasm that secretes excessive catecholamines. This usually causes hypertension. Zollinger-Ellison syndrome is a condition where excessive gastrin is produced. It is usually associated with peptic ulcer disease. Multiple endocrine neoplasias (MEN) is a hereditary disorder characterized by tumors of more than one endocrine gland. Clinical features vary depending on which gland is affected.

Diagnostic tests (case study)

The history and signs of the patient in the case study indicate that he has type 2 diabetes mellitus. This is diagnosed by measuring the amount of glucose in blood under different circumstances. The following includes a positive diagnosis for diabetes mellitus: random blood glucose of more than or equal to 11.1 mmol/L, fasting blood glucose of more than or equal to 7.0 mmol/L, and oral glucose tolerance test (OGTT) of equal to or more than 11.1 mmol/l. if fasting blood glucose is more than 125 mmol/l on two different occasions, the diagnosis is positive for diabetes.


Subcutaneous insulin injections are given if the patient cannot be managed solely on diet and oral ant-diabetic agents. Change of diet to low carbohydrate foods is mandatory, so the food labels should be examined carefully. Exercise reduces blood glucose. Oral medications like biguanides (e.g. metformin), sulfonylureas (tolbutamide), meglitinides (e.g. repaglide), Naneglinide, thiazolidinediones (e.g. pioglitazone) are also useful (Robbins, 2007).


Heuther, S.E. and McCance, K.L. (2008). Understanding pathophysiology (4th ed.). St. Louis: Mosby.

Jain, V. K., Sharma J. P. (2004). Comprehensive Objective Biology. New York, NY: Golden Bells.

Magaji, V., Johnstone J.M. (2011). Inpatient Management of Hyperglycemia and Diabetes. American Diabetes Association(R) Inc. Web.

Robbins., C. (2007). Pathologic Basis of disease 7thed. New York, NY: Prentice Hall.