Etiology and morphological substrate of endocrinopathies
The development of any endocrine disease is based on impaired adequate hormone production. This can manifest as excessive secretion (hyperfunction), insufficient production (hypofunction), or qualitative alteration of glandular function (dysfunction).
For a gland to malfunction, structural changes must occur within its tissues. The morphological substrates of such disorders are:
- Increase in cell number (hyperplasia) or their decrease (hypoplasia, atrophy).
- Replacement of active glandular tissue with connective tissue (sclerosis).
- Appearance of neoplasms (tumors).
- Other structural rearrangements.
The causes of endocrinopathy development are extremely diverse. The main etiological factors include:
- Enzymopathies—congenital (hereditary) or acquired defects of enzyme systems that often manifest against the background of previous infections or severe intoxications.
- Nutritional deficiency—lack of vital proteins and trace elements. Striking examples include iodine or zinc deficiency, without which the synthesis of a number of hormones is impossible.
- Direct glandular damage—can be caused by ionizing radiation, mechanical trauma, toxic effects, 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:
- Absolute deficiency—a condition in which the gland is physically incapable of synthesizing the required amount of hormone (e.g., due to the destruction of its cells).
- Relative deficiency—a situation in which the level of hormone synthesis and secretion is within the physiological norm, but the body's demand for these hormones increases sharply, and the current amount becomes insufficient to maintain homeostasis.
Diabetes mellitus: the primary endocrine disease
Among all diseases of the endocrine part of the pancreas and the endocrine system as a whole, diabetes mellitus is the absolute leader. This is a chronic pathology based 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 lesions of the endocrine glands. In the 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 common causes of profound disability and mortality in patients.
Pathogenesis and manifestations
Insulin deficiency triggers a cascade of destructive processes in the body:
- There is a total disruption of all types of metabolism. Carbohydrate metabolism suffers first, which is clinically and laboratory manifested by hyperglycemia.
- Systemic damage to the vascular bed develops—angiopathies.
- Structures of the nervous system are damaged—neuropathies.
- As a consequence, severe secondary pathological changes occur in various tissues and target organs.
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.
Its pathogenesis is based on the physical destruction of β-cells of 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:
- Autoimmune—cell destruction occurs due to a malfunction of the body's own immune system.
- Idiopathic—the exact cause of β-cell death cannot be established.
Briefly: answers to topical 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 changes in β-cells 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 unusual forms of immune-mediated diabetes.
- Gestational diabetes mellitus—diabetes of 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 acute decompensations of glucose levels (hypoglycemia, hyperglycemia, ketoacidosis, comas).
- Late complications—based on systemic damage to the vascular bed and nervous tissue, including microangiopathies (retinopathy, nephropathy, neuropathy) and macroangiopathies.
- Infectious complications—develop against the background of secondary immunodeficiency (pyodermas, furunculosis, sepsis, tuberculosis).
- Mauriac syndrome—a specific complication in children with a decompensated course of the disease.
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. The exhaustion of the functional capacity of β-cells is promoted by:
- Pancreatic lipomatosis—develops against the background of generalized 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 the development of insulin resistance.
The development of islet atrophy, primarily of β-cells, leads to absolute insulin deficiency, which is characteristic of severe diabetes mellitus.
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 in 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 atrophy of the islets, proliferation of connective tissue, and a significant decrease in the number of β-cells are observed.
- Compensatory hyperplasia — in the first years of the disease, isolated islets with β-cell hyperplasia may be observed.
After 1–2 years, the manifestations of insulitis subside until complete disappearance.
Which target organs are most commonly 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 the capillary basement membrane, glomerulosclerosis).
- Eyes — diabetic retinopathy occurs.
- Nervous system — diabetic neuropathy develops (due to damage to the vessels supplying the nerves — vasa nervorum).
- Heart and blood vessels — macroangiopathy leads to cardiovascular diseases, including myocardial infarction.
- Lower extremities — macro- and microangiopathy cause the ischemic variant of diabetic foot syndrome.
To remember the classic triad of diabetes mellitus manifestations, use the "GAN" rule: Hyperglycemia, Angiopathy, Neuropathy. These are the three pillars of pathogenesis leading to secondary organ damage.
Class and exam questions
Why is any endocrine disease considered pluriglandular?
Because all endocrine glands are tightly interconnected into a single network, primarily through the hypothalamic-pituitary system. Morphological or functional damage to one gland inevitably causes compensatory or pathological changes in others.
What is relative hormonal deficiency?
This is a condition where the gland produces a normal amount of hormones, but due to increased metabolic demands, this volume is insufficient for normal metabolism.
What is the basis of type 1 diabetes mellitus according to the WHO?
It is based on the destruction of pancreatic islet β-cells, leading to a state of absolute insulin deficiency. It is divided into autoimmune and idiopathic subtypes.
What else to study on this topic
- Type 2 diabetes mellitus and specific types of diabetes according to the WHO classification
- Morphological changes in target organs in diabetic micro- and macroangiopathy
- Pathogenesis of autoimmune destruction of pancreatic β-cells
- The role of the hypothalamo-hypophyseal system in the development of pluriglandular syndromes
- The effect of iodine and zinc deficiency on the histological structure of endocrine glands
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "General Pathology of the Endocrine System" and 4,414 more pages on the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in Chapter 19: Diseases of the Endocrine System
Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.