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General Pathology of the Endocrine System

*Systema endocrinum*

For medical students2 min readUpdated 2026-10-10

Endocrine pathology is based on impaired hormone secretion: hyperfunction, hypofunction, or dysfunction of glands. Due to the close interconnection via the hypothalamic-pituitary axis, any endocrine disorder is pluriglandular in nature—an alteration in the function of one organ inevitably affects the entire system.

Main PrincipleAny endocrinopathy is pluriglandular (systemic).
Scope of the ProblemDiabetes mellitus accounts for up to 50% of all endocrine pathologies.
Types of DeficiencyAbsolute and relative hormone deficiencies are distinguished.
MorphologyThe structural substrate includes hyperplasia, atrophy, sclerosis, or tumors.

Etiology and Morphological Substrate of Endocrinopathies

The development of any endocrine disorder is based on impaired adequate hormone production. This may manifest as excessive secretion (hyperfunction), insufficient production (hypofunction), or qualitative alteration in gland activity (dysfunction).

For a gland to malfunction, structural changes must occur within its tissues. The morphological substrates of such disorders include:

Causes of endocrinopathies are extremely diverse. The main etiological factors include:

  1. Enzymopathies — congenital (hereditary) or acquired defects in enzyme systems, which often manifest following infections or severe intoxications.
  2. Nutritional deficiency — lack of vital proteins and trace elements. Clear examples include iodine or zinc deficiency, without which the synthesis of a number of hormones is impossible.
  3. Direct gland injury — can be caused by ionizing radiation, mechanical trauma, toxic exposure, or autoimmune aggression.

Types of Hormonal Deficiency

Functional hormone deficiency is a key mechanism in the development of many pathological syndromes. In pathological anatomy and endocrinology, two fundamental types of hormonal deficiency are distinguished:

Diabetes Mellitus: The Major Endocrine Disease

Among all diseases of the endocrine pancreas and the endocrine system as a whole, diabetes mellitus is the undisputed leader. This is a chronic pathology founded on absolute or relative insulin deficiency.

Epidemiology and Medical-Social Significance

Diabetes is not just an endocrinopathy; it is a global medical and social problem. It accounts for up to 50% of all endocrine gland disorders. In the general population, this disease occurs in 2–4% of people, and in the age group over 70, this figure exceeds 10%.

Along with oncological pathology and cardiovascular diseases, diabetes mellitus firmly holds the lead among the most frequent causes of severe disability and patient mortality.

Pathogenesis and Manifestations

Insulin deficiency triggers a cascade of destructive processes in the body:

Type 1 Diabetes Mellitus

According to the etiological classification adopted by the World Health Organization (WHO) in 1999, diabetes mellitus is divided into several types. One of the key types is type 1 diabetes mellitus.

The pathogenesis is based on the physical destruction of β-cells in the pancreatic islets (islets of Langerhans). Due to the death of insulin-producing cells, the patient develops absolute insulin deficiency.

Within type 1, two main subtypes are distinguished:

  1. Autoimmune — cell destruction occurs due to a malfunction of the body's own immune system.
  2. Idiopathic — the exact cause of β-cell death cannot be established.

Mnemonic

To remember the classic triad of diabetes mellitus manifestations, use the rule "GAN": Glycemia (hyperglycemia), Angiopathy, Neuropathy. These are the three pillars of pathogenesis leading to secondary organ damage.

Frequently asked questions

What types of diabetes mellitus are distinguished according to the WHO etiological classification?

According to the WHO etiological classification, the following groups of diabetes mellitus are distinguished:

  • Type 1 diabetes mellitus — caused by the destruction of pancreatic islet β-cells, leading to absolute insulin deficiency; includes autoimmune and idiopathic subtypes.
  • Type 2 diabetes mellitus — characterized by β-cell alterations leading to relative insulin deficiency, along with insulin resistance.
  • Other specific types of diabetes — include genetic defects in β-cell function, genetic defects in insulin action, and uncommon forms of immune-mediated diabetes.
  • Gestational diabetes mellitus — diabetes diagnosed during pregnancy.
What systemic complications develop against the background of insulin deficiency in diabetes mellitus?

Against the background of insulin deficiency in diabetes mellitus, acute and delayed systemic complications develop:

  • Early complications — associated with sharp glucose decompensations (hypoglycemia, hyperglycemia, ketoacidosis, coma).
  • Late complications — based on systemic damage to the vascular bed and nervous tissue, including microangiopathies (retinopathy, nephropathy, neuropathy) and macroangiopathies.
  • Infectious complications — develop due to secondary immunodeficiency (pyoderma, furunculosis, sepsis, tuberculosis).
  • Mauriac syndrome — a specific complication in children with decompensated disease progression.
What is the pathogenesis of type 2 diabetes mellitus?

The pathogenesis of type 2 diabetes mellitus is based on insulin resistance and impaired insulin secretion, leading to relative insulin deficiency. Exhaustion of the functional capacity of β-cells is promoted by:

  • Pancreatic lipomatosis — develops against the background of general obesity.
  • Focal amyloidosis of the islets — local senile amyloid is formed from the polypeptide amylin; amylin causes hyperglycemia, insulin resistance, and is cytotoxic to β-cells.
  • Excess leptin — in obesity, it suppresses insulin secretion and promotes insulin resistance.

The development of islet atrophy, primarily of β-cells, leads to absolute insulin deficiency, which is characteristic of severe diabetes.

What morphological changes occur in the islets of Langerhans in type 1 diabetes mellitus?

In type 1 diabetes mellitus, sequential destruction of β-cells occurs within the islets of Langerhans:

  • Immune insulitis — occurs in the initial stages of the disease, characterized by an inflammatory infiltrate of T- and B-lymphocytes, macrophages, and NK cells.
  • Atrophy and fibrosis — subsequently, progressive islet atrophy, connective tissue proliferation, and a significant decrease in the number of β-cells are observed.
  • Compensatory hyperplasia — in the first years of the disease, individual islets with β-cell hyperplasia may be encountered.

After 1–2 years, insulitis phenomena subside up to complete disappearance.

Which target organs are most frequently affected in diabetic angiopathy?

In diabetic angiopathy, the following target organs are most frequently affected, leading to their dysfunction and failure:

  • Kidneys — diabetic nephropathy develops (thickening of capillary basement membranes, glomerulosclerosis).
  • Eyes — diabetic retinopathy occurs.
  • Nervous system — diabetic neuropathy forms (due to damage to vessels nourishing nerves — vasa nervorum).
  • Heart and vessels — macroangiopathy leads to cardiovascular diseases, including myocardial infarction.
  • Lower extremities — macro- and microangiopathy cause the ischemic variant of the diabetic foot syndrome.
Why is any endocrine disorder considered pluriglandular?

Because all endocrine glands are tightly interconnected into a single network, primarily via the hypothalamic-pituitary system. Morphological or functional damage to a single gland inevitably triggers compensatory or pathological changes in others.

What is relative hormonal deficiency?

It is a condition where the gland produces a normal amount of hormones, but due to increased bodily demand, this volume is insufficient for normal metabolism.

What is the basis of type 1 diabetes mellitus according to the WHO?

Its basis is the destruction of pancreatic islet β-cells, leading to absolute insulin deficiency. It is divided into autoimmune and idiopathic subtypes.

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