Jesús Ramón Giraudo and Julio Libman 

Anorexia is understood as the abnormal lack of hunger, which means that despite having a clear need for nutrients, the individual does not experience the unpleasant sensations that lead him to eat food. Hunger is defined as a physiological phenomenon that comprises a group of unpleasant and imperious sensations that include the desire to eat without selectivity, and that arises from the need to maintain the supply of nutrients to the body. Appetite is a more conscious phenomenon, constituting the pleasant physiological sensation or normal psychic desire to selectively eat certain foods, even after hunger has disappeared. Satiety is the normal loss of the desire to eat following the ingestion of food.

Physiology and pathophysiology

Psychological and social factors play a fundamental role in the regulation of food intake. In the central nervous system the hypothalamus has a basic function in this regard. There are bilateral nuclei in the ventromedial portion of the nucleus whose ablation produces hyperphagia and morbid obesity, called nuclei of satiety. In the lateral hypothalamic areas there are other centers, whose injury causes the desire to ingest nutrients to be lost, constituting the feeding centers. The latter appear to be permanently active, unless inhibited by the satiety centers.

An important regulatory factor of the center of satiety is the levels of glucose and glucagon in the blood. When it reaches certain values, blood glucose stimulates the center of satiety, which in turn inhibits that of food; when blood glucose falls below a certain limit, it stops stimulating the satiety center, thereby releasing the appetite center. The presence of insulin would be necessary for glucose to penetrate the cells of the mentioned nucleus of satiety.

The uptake of fatty acids and the release of fats from the body's deposits would also play an important role in the regulation of appetite. On the other hand, the increase in blood glucagon decreases food intake, which indicates the suppression of the feeding center by the satiety center, probably through the hyperglycemia it produces. Sympathomimetic amines also inhibit nutrient intake. In addition to glucose, various neuro-transmitters and hormones act on the satiety center, such as serotonin, catecholamines, cholecystokinin, pancreatic polypeptide, thyrotrophin-releasing hormone (TRH) and insulin. Dopamine, endorphins, enkephains, and secretin influence the activity of the food center. An empty stomach contracts more vigorously, contributing to the feeling of hunger. These mechanisms and factors are illustrated in Figure 8-1.

The pathophysiological mechanism by which a wide variety of conditions produce anorexia is poorly understood. In the case of tumors, for example, the existence of a humoral factor that would somehow affect the hypothalamic center of satiety has been postulated, as well as distortions in the senses of taste and smell. Likewise, the mechanism through which, in anorexia nervosa, personality disorders with a high incidence of schizophrenic characteristics can affect the subcortical centers is unknown.

Causes of anorexia

They include the following:

  1. Neoplasms. Different malignancies can cause anorexia. Pancreatic cancer is a classic example. As in patients with gastric malignancy, anorexia can be selective for some foods, particularly meat.
  2. Liver disease Active, acute and chronic alcoholic hepatitis.
  3. Diseases of the digestive tract.
  4. Endocrinopathies. Acute and chronic adrenal insufficiency, hypothyroidism, hypopituitarism, hypercalcemia of any origin (when it reaches sufficient levels) and diabetic ketoacidosis have anorexia as one of its important manifestations.
  5. Kidney diseases with uremia.
  6. Systemic diseases. Lupus erythematosus and other collagenopathies, etc.
  7. Bronchopulmonary conditions with respiratory failure.
  8. Heart disease with severe heart failure, either due to a central mechanism or due to liver congestion and a feeling of abdominal fullness.
  9. Hematopoietic system disease: anemias, leukemias.
  10. Bacterial infections, mycoses, virosis.
  11. Fever of any etiology.
  12. Psychiatric conditions. Anxiety, depression, anorexia nervosa.
  13. Medications, cardiac glycoside poisoning, etc.
  14. Tobacco, alcohol.

Interrogation and study methodology

Since anorexia is such a non-specific manifestation, and may be the first symptom of a serious or non-acute or chronic condition, the questioning must be systematic and comprehensive. Its magnitude, form of onset, which may be abrupt or gradual, time of evolution and selectivity will be established. All concomitant clinical manifestations will be carefully evaluated. The study methodology depends on the clinical orientation that arises from the interrogation and the physical examination. Thus, for example, if the history reveals, together with anorexia, the presence of asthenia, weight loss, temperature, cough, haemoptoic sputum and perspiration, the methodology may be oriented towards pulmonary tuberculosis (chest x-ray, sputum examination, Mantoux reaction, etc.). In a patient with polyuria, polydipsia, weight loss, Kussmaul-type dehydration and dyspnea will be thought of as diabetic ketoacidosis (blood glucose, ketonernia, glycosuria, ketonuria, alkaline reserve, excess base, etc.). If jaundice, coluria and acolia exist, the study methodology will be oriented towards a hepato-biliary pathology (bilirubin, transaminase, 5-nucleotidase, alkaline phosphatase, prothrombin time, Australian antigen, proteinogram by electrophoresis, complete urine, ultrasound of the liver and airways). bile, etc.).