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Pathological Anatomy · Morphology of Metabolic Disorders — Dystrophies

Disorders of lipoprotein metabolism and other lipidemias

Lipomatosis cordis

Disorders of neutral fat metabolism manifest either as a pathological increase or a sharp decrease in body fat stores within specialized depots. The greatest clinical and morphological significance is attributed to excessive lipid accumulation—obesity. This process leads to serious structural changes in internal organs, among which cardiac involvement is particularly prominent, leading to severe functional disorders.

Cardiac obesityAdipose tissue proliferates beneath the epicardium and deeply invades the myocardial stroma.
Severity gradesFrom grade I (20–29% excess weight) to grade IV (more than 100% above normal).
MorphologyHypertrophic (increase in cell volume) and hyperplastic (increase in cell number) types are distinguished.
ComplicationsCardiomyocyte atrophy, heart failure, and rarely—right ventricular rupture.
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Etiology and external manifestations of obesity

According to the etiological factor, primary (idiopathic) and secondary obesity are distinguished. Secondary obesity has clearly defined causes and is divided into several types:

  • Alimentary — develops against the background of imbalanced nutrition and lack of physical activity (hypodynamia).
  • Cerebral — associated with brain lesions, especially hypothalamic tumors or as a consequence of neurotropic infections.
  • Endocrine — occurs in pathologies of the endocrine glands (for example, in Cushing's syndrome, hypothyroidism, hypogonadism, or adiposogenital dystrophy).
  • Hereditary — genetically determined forms, a striking example of which is von Gierke disease.

According to external manifestations and the distribution of adipose tissue, symmetric, upper, middle, and lower types of obesity are distinguished.

Morphological variants and severity grades

The severity of the pathology is assessed by the percentage by which the patient's actual body weight exceeds the normal weight. Four grades are distinguished:

GradeBody weight excess
Grade Iby 20–29%
Grade IIby 30–49%
Grade IIIby 50–59%
Grade IVby more than 100%

At the microscopic level, depending on the state of fat cells (adipocytes), two morphological variants are distinguished:

  1. Hypertrophic variant — characteristic of generalized obesity. The total number of fat cells is unchanged, but their size is significantly increased due to the excessive accumulation of triglycerides.
  2. Hyperplastic variant — characterized by a true increase in the number of adipocytes. From a clinical standpoint, the course of the disease with this variant is considered more favorable.
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Cardiac obesity (Lipomatosis cordis)

In generalized obesity, the most formidable complication is cardiac involvement. The macroscopic picture is quite specific: the dimensions of the organ are significantly increased, and a thick layer of fat is visualized beneath the epicardium, enveloping the heart like a "case".

The pathological process is not limited to the surface. Adipose tissue begins to actively grow into the myocardial stroma. This leads to mechanical compression of muscle fibers, resulting in cardiomyocyte atrophy.

Morphological changes are distributed unevenly: they are always more pronounced in the right side of the heart. Clinically, this condition manifests with the development of progressive heart failure. In extremely rare and severe cases, thinning of the wall can lead to a fatal complication—rupture of the right ventricle.

The antipode of obesity and cholesterol metabolism

The exact opposite of the excessive accumulation of neutral fats is cachexia (wasting). This condition represents generalized atrophy of all organs and tissues of the body, accompanied by a critical decrease in fat stores in depots.

In addition to neutral fats, a crucial role in pathological anatomy is played by disorders of cholesterol and cholesterol ester metabolism. This very imbalance is the fundamental basis for the development of atherosclerosis—a systemic vascular disease.

Briefly: answers to topical questions

What are the body weight excess criteria for each of the four grades of obesity?

The criteria for the four grades of obesity are determined depending on the percentage by which the patient's body weight is exceeded. The following grades are distinguished:

  • Grade I — excess body weight is 20–29%.
  • Grade II — excess body weight is 30–49%.
  • Grade III — excess body weight is 50–59%.
  • Grade IV — excess body weight is more than 100%.

What causes and diseases lead to the development of cachexia?

The development of cachexia (general pathological atrophy) is caused by various exogenous and endogenous factors, as well as a number of severe diseases. The following main causes and types of wasting are distinguished:

  • Alimentary wasting — occurs in starvation, food deficiency, and impaired food assimilation in gastrointestinal diseases.
  • Cancer cachexia — develops in malignant oncological neoplasms.
  • Cerebral and pituitary cachexia — occurs in lesions and diseases of the brain (for example, Simmonds' disease).
  • Traumatic wasting — forms after severe trauma, including against the background of suppurative-resorptive fever during prolonged suppuration.

Cachexia also acts as a symptom of many severe somatic and infectious diseases.

What stages of morphogenesis are distinguished in the development of atherosclerosis?

In the morphogenesis of atherosclerosis, four sequential stages are distinguished that reflect the dynamics of pathological processes in the vascular plaque:

  • Pre-lipid stage — characterized by intimal injury due to altered blood composition, which is visualized only under an electron microscope.
  • Stage of lipoidosis — manifests as focal lipid infiltration of the intima with the formation of fatty streaks and spots.
  • Stage of liposclerosis — accompanied by connective tissue proliferation and the formation of a fibrous plaque narrowing the vessel lumen.
  • Stage of complicated lesions — includes the sequential development of atheromatosis (breakdown of lipid masses), ulceration (destruction of the plaque fibrous cap), and atherocalcinosis (deposition of calcium salts).
How to memorize

To memorize the causes of secondary obesity, use the mnemonic: Hereditary (von Gierke disease), Alimentary (hypodynamia), Cerebral (hypothalamic tumors), Endocrine (Cushing's syndrome).

Class and exam questions

Which morphological variant of obesity has a more favorable clinical course?

Hyperplastic variant. In this variant, the number of adipocytes increases rather than their size, which has a better clinical prognosis.

What does the ingrowth of adipose tissue into the myocardial stroma lead to?

This causes compression and subsequent atrophy of muscle fibers (cardiomyocytes), ultimately leading to the development of heart failure.

Which half of the heart suffers more severely in lipomatosis?

Pathological changes are always more pronounced in the right side of the heart. In rare cases, this can lead to rupture of the right ventricle.

What is the morphological antipode of obesity?

Cachexia (wasting). It is characterized by generalized atrophy of all organs and tissues, including a sharp decrease in fat stores in depots.

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What else to study on this topic

  • Mechanisms of development of alimentary and endocrine obesity
  • Pathogenesis of cardiomyocyte atrophy in cardiac lipomatosis
  • Cholesterol metabolism disorders and the morphology of atherosclerosis
  • Von Gierke disease as an example of an inherited lipid metabolism disorder
  • Differences between hypertrophic and hyperplastic variants at the cellular level

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