The term " pathogenesis" comes from two words: Greek pathos - suffering (according to Aristotle, pathos - damage) and genesis - origin, development. Pathogenesis - this is the doctrine of the mechanisms of development, course and outcome of diseases, pathological processes and pathological conditions.

Pathogenesis – this is a set of mechanisms that are activated in the body when it is exposed to harmful (pathogenic) factors and manifested in the dynamic stereotypical deployment of a number of functional, biochemical and morphological reactions of the body that determine the occurrence, development and outcome of the disease.

classification of pathogenesis:

a) private pathogenesis, which studies the mechanisms of individual pathological reactions, processes, conditions and diseases (nosological units). Private pathogenesis is studied by clinicians, revealing the mechanism of specific diseases in specific patients (for example, the pathogenesis of diabetes mellitus, pneumonia, gastric ulcer, etc.). Private pathogenesis refers to specific nosological forms.

b) general pathogenesis involves the study of the mechanisms, the most general patterns underlying typical pathological processes or certain categories of diseases (hereditary, oncological, infectious, endocrine, etc.). General pathogenesis deals with the study of the mechanisms leading to the functional insufficiency of any organ or system. For example, general pathogenesis studies the mechanisms of development of heart failure in patients with pathology of the cardiovascular system: with heart defects, myocardial infarction, coronary heart disease, lung diseases with pulmonary hypertension.

The study of pathogenesis is reduced to the study of the so-called pathogenetic factors, those. those changes in the body that occur in response to the influence of an etiological factor and subsequently play the role of a cause in the development of the disease. The pathogenetic factor causes the emergence of new disorders of life in the development of the pathological process, disease.

The trigger mechanism (link) of any pathological process, disease is damage, arising under the influence of a harmful factor.

Damage can be:primary; they are caused by the direct action of the pathogenic factor on the body - these are damages at the molecular level, secondary; they are a consequence of the influence of primary damage on tissues and organs, accompanied by the release of biologically active substances (BAS), proteolysis, acidosis, hypoxia, impaired microcirculation, microthrombosis, etc.

The nature of the damage depends on the nature of the irritant (pathogenic factor), species and individual properties of the living organism. Damage levels can be different: molecular, cellular, tissue, organ and organism. The same stimulus can cause damage at a variety of levels.

Simultaneously with damage, protective-compensatory processes are activated at the same levels - molecular, cellular, tissue, organ and organism.

The primary link in this long chain is damage that occurs under the influence of a pathogenic factor, and which becomes the cause of secondary damage, causing tertiary, etc. (Influence of a mechanical factor - trauma - blood loss - centralization of blood circulation - hypoxia - acidosis - toxemia, septicemia - etc.).

In this complex chain of cause-and-effect relationships, there are always basic(synonyms: main, leading) link. Under the main (main) link of pathogenesis understand such a phenomenon that determines the development of a process with specific features characteristic of it. For example, arterial hyperemia is based on the expansion of arterioles (this is the main link), which causes an acceleration of blood flow, redness, an increase in the temperature of the hyperemic area, an increase in its volume and an increase in metabolism. The main link in the pathogenesis of acute blood loss is the deficiency of circulating blood volume (BCV), which causes a decrease in blood pressure, centralization of blood circulation, shunting of blood flow, acidosis, hypoxia, etc. When the main link is eliminated, recovery occurs.

Untimely elimination of the main link leads to a violation of homeostasis and the formation vicious circles pathogenesis. They arise when a deviation in the level of functioning of an organ or system begins to support and strengthen itself as a result of the formation positive feedback.

Regarding such a section of pathogenesis as flow diseases, the question of acute and chronic processes. Traditionally, one of the criteria for an acute or chronic course is temporary. If a pathogenic agent (or information about it recorded by the immune or nervous system) persists in the body, the disease acquires a protracted course, which is clinically referred to as subacute, and after a certain period - chronic.

Remission- this is a temporary improvement in the patient's condition, manifested in slowing down or stopping the progression of the disease, partial regression or disappearance of the clinical manifestations of the pathological process.

relapse- this is a new manifestation of the disease after its apparent or incomplete cessation.

Complication- this is a pathological process secondary to the existing disease, arising in connection with the peculiarities of the pathogenesis of the primary (main) disease or as an unforeseen consequence of the diagnostic and therapeutic measures carried out.

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Hypoxia - lack of oxygen a condition that occurs when there is insufficient supply of oxygen to the tissues of the body or a violation of its use in the process of biological oxidation. The compensatory reaction of the body is an increase in the level of hemoglobin in the blood. The trigger mechanism for the development of hypoxia is associated with hypoxemia - a decrease in the oxygen content in arterial blood.
A healthy body may be in a state of hypoxia if the need for oxygen (oxygen demand) is higher than the ability to satisfy it. The most common causes of this condition are:

2. temporary cessation or weakening of pulmonary ventilation when diving to different depths;

3. an increase in the need for oxygen during the performance of muscular work.

Short term adaptation mechanisms can only be effective at relatively low altitudes and for a short time. An increased load on the heart and respiratory muscles requires additional energy consumption, that is, it increases the oxygen demand. Due to intensive breathing (hyperventilation of the lungs), CO2 is intensively removed from the body. A drop in its concentration in the arterial blood leads to a weakening of breathing, since it is CO2 that is the main stimulator of the respiratory reflex. Acid products of anaerobic glycolysis accumulate in tissues.
D permanent adaptation - the shift of the main field of activity from the mechanisms of transport to the mechanisms of oxygen utilization, to increase the efficiency of the use of resources available to the body. This is achieved primarily by stimulating biosynthetic processes in the systems of transport, regulation and energy supply, which increases their structural potential and reserve capacity. In transport systems, this is the growth of the vascular network (angiogenesis) in the lungs, heart, brain, the growth of lung tissue, and an increase in the number of red blood cells. In regulatory systems, this is, on the one hand, an increase in the activity of enzymes responsible for the synthesis of mediators and hormones, and on the other hand, an increase in the number of receptors for them in tissues. Finally, in energy supply systems - an increase in the number of mitochondria and enzymes of oxidation and phosphorylation, the synthesis of glycolytic enzymes.

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Arterial hypertension is a persistent increase in blood pressure in the arteries of the systemic circulation, when the upper pressure is equal to or greater than 140 mm Hg. Art., lower pressure equal to or greater than 90 mm Hg. Art.

Arterial hypertension can be divided into two stages:

systolic pressure - 140-159 mm Hg. Art., or diastolic pressure - 90-99 mm Hg. Art.
systolic pressure - from 160 mm Hg. Art., or diastolic pressure - from 100 mm Hg. Art.

In almost 95% of patients, the causes of increased blood pressure remain unexplained, and such a disorder is classified as primary or essential arterial hypertension (EAH).

In hypertension, the causes of which are clearly established, they speak of secondary(or symptomatic) arterial hypertension (VAH). VAH is much less common than EAH, but the establishment of the causes of VAH often allows you to completely cure patients from high blood pressure.

Criteria for the diagnosis of hypertension set at DBP and/or SBP equal to or greater than 90 and 140 mm Hg. Art., respectively.

Common mechanisms of disease pathogenesis are nervous, hormonal, humoral, immune, genetic.

The significance of nervous mechanisms in the pathogenesis of diseases is determined by the fact that the nervous system ensures the integrity of the body, interaction with the environment (fast, reflex), and rapid mobilization of the body's protective and adaptive forces. Structural and functional changes in the nervous system lead to a violation of the triple nervous control over the state of organs and tissues, that is, there are violations of the function of organs and systems, blood supply to organs and tissues and the regulation of trophic processes.

Violation of the state of the nervous system can be the initial link of cortico-visceral (psychosomatic) diseases: hypertensive, ulcerative and resulting from psychogenic effects. The cortico-visceral theory of the pathogenesis of diseases is based on the reflex theory of I.M. Sechenov and I.P. Pavlov and is confirmed by the possibility of reproducing pathological reactions according to the mechanism of a conditioned reflex and the occurrence of functional disorders of internal organs in neurotic disorders.

The main pathogenetic factors that determine the development of cortico-visceral diseases are the following:

violation of the dynamics of nervous processes in the higher parts of the brain (in particular, in the cerebral cortex);

change in cortical-subcortical relationships;

formation in the subcortical centers of dominant foci of excitation;

blocking of impulses in the reticular formation and increased disturbance of cortical-subcortical relationships;

functional denervation of organs and tissues;

trophic disorders in the nervous tissue and on the periphery;

violation of afferent impulses from organs that have undergone structural and functional changes;

disorder of neuro-humoral and neuro-endocrine relations.

The shortcomings of the cortico-visceral theory can be attributed to the fact that specific causes and conditions that cause the development of various forms of cortico-visceral pathology have not been identified, and the provisions on the violation of cortico-subcortical relations are too general and do not allow explaining the different nature of pathological changes in internal organs in neurotic disorders.

The significance of hormonal mechanisms in the pathogenesis of diseases is determined by the fact that the endocrine system is a powerful factor in the overall regulation of the body's vital activity and its adaptation to changing environmental conditions. In pathological processes, the endocrine system provides long-term maintenance of functional activity and metabolic processes at a new level. The restructuring of hormonal regulation ensures the development of protective and adaptive reactions of the body.

The humoral mechanisms of the development of diseases include the formation in the focus of primary damage of various humoral biologically active substances (histamine, bradykinin, serotonin, etc.), which cause changes in blood circulation, the state of the blood, vascular permeability and the functions of many organs and systems in the hematogenous and lymphogenous pathways. the process of development and course of pathological processes.

Immune mechanisms are associated with the function of the immune system, which ensures the constancy of the protein composition of the body. Therefore, in all pathological conditions accompanied by a change in the structure of one's own proteins or the penetration of foreign proteins into the body, the immune system is activated, the altered and foreign proteins are neutralized and excreted from the body. This is its protective role. But in some cases, a violation of the function of the immune system can lead to the development of allergic and autoimmune diseases.

Formed connective tissue performs a supporting function and protects the body from mechanical damage, while unformed connective tissue performs the function of metabolism, synthesis of plastic substances and biological protection of the body. Connective tissue also performs the function of regulating the homeostasis of liquid media, protein composition, acid-base balance, barrier and phagocytic function, participates in the production, storage and release of biologically active substances. Violation or perversion of these functions leads to the development of pathological processes.

DAMAGE OF THE NERVOUS SYSTEM IN DISEASES OF THE INTERNAL ORGANS

LECTURE 14

The pathogenesis of damage to the nervous system in somatic diseases is mainly due to metabolic, toxic, vascular and reflex disorders. Shifts in homeostasis resulting from a violation of protein, carbohydrate, fat, water-electrolyte, vitamin metabolism, hypoxemia and tissue hypoxia, the accumulation of various toxins to be removed from the body, have a toxic effect on the nervous tissue (neurons and gliosis cells, synapses, axons). A certain role belongs to reflex disorders. There may be an excessive release of neurotransmitters, and then the depletion of their tissue reserves, for example, norepinephrine activates the enzyme adenylate cyclase, which catalyzes the formation of cyclic adenosine monophosphate (cAMP) from ATP. The latter is necessary for the normal course of complex intracellular metabolic reactions, since with a decrease in cAMP, the activity of the genetic apparatus and enzyme systems decreases. Therefore, in most cases, a number of interrelated factors influence, one or two of which are the most significant. With pulmonary embolism, this is acute hypoxia and reflex disorders (anoxic shock syndrome), with long-term nonspecific lung diseases - chronic hypoxia with severe changes in nerve cells and glia, kidney pathology - metabolic disorders and toxicosis (hypo-, and later hyperkalemia, creatininemia, azotemia, the effect of the whole complex of metabolites accumulating in the blood with the development of cerebral edema), obstructive jaundice - bilirubinemia. Clinical manifestations depend, in addition, on heredity, the constitution of the patient, age, living conditions and nutrition, bad habits, previous pathology, features of the work performed. Somatogenically caused disorders of the regulatory influence of the nervous system on the activity of internal organs and endocrine glands create a vicious circle, contributing to the deepening of insufficiency of both internal organs and the nervous system. The well-known commonality of the clinic of neuropsychiatric disorders in response to the pathology of internal organs, endocrine glands confirms that they are based on similar pathogenetic mechanisms - a combination of irritation and prolapse phenomena at various levels of the nervous system (cortex, subcortex, trunk, spinal cord, etc. ) with some emphasis on one or the other of them.

It has been established that even a relatively compensated insufficiency of the functions of an internal organ or an endocrine gland with an increased predisposition can lead to clinically pronounced changes in the nervous system (fatigue, headache, dizziness, memory loss, etc.). Against the background of somatic disorders and the accompanying shifts in hormonal-mediator-electrolyte balance and hypoxia, neuropsychiatric disorders develop earlier and more often with infections, intoxications, injuries, chronic and acute cerebrovascular accidents, hereditary and chronically progressive diseases are more severe.

The first signs indicating the involvement of the nervous system in somatic diseases are increased fatigue, irritability, headache, sleep disturbance, paresthesia and dysesthesia in the Zakharyin-Ged zones.

So, with heart damage, pain often spreads to the upper chest and to the inner surface of the shoulder and forearm on the left (Cvp-Thi-Thiv segment), with lung damage - to the neck and shoulder girdle (Csh-Civ), liver - to the right hypochondrium (Thvsh-Thix), stomach and pancreas - on the epigastric region (Thvn-Thix), kidneys and ureter - on the lower back and anterior upper surface of the thigh (Thxn-Li), small intestines - on the umbilical region (Thx-Thxi). When the vagus nerve is involved, pain is often felt in the face (trigeminal nerve) and the back of the head (Sp segment); phrenic nerve - in the area of the shoulder girdle and neck (Csh-Civ).

All these symptoms are initially expressed weakly and inconsistently. In the future, if the dysfunction of one or another organ or endocrine gland increases, then organic disorders may gradually develop - nystagmus, symptoms of oral automatism, changes in reflexes, motor and sensory disorders. Sometimes an acute disease of an internal organ (pulmonary embolism, pancreatitis, obstructive jaundice, hepatitis) debuts with neuropsychiatric disorders: agitation, motor anxiety, hallucinations, meningeal phenomena, etc. Increased neuromuscular excitability, spasms and paresthesias in the extremities are the first signs of hypocalcemia due to insufficiency of the function of the parathyroid glands and kidneys. Even in the presence of a clear picture of diseases of the liver, kidneys, lungs, pancreas, and pelvic organs, the establishment of a pathogenetic relationship between this disease and damage to the nervous system should be based on anamnesis, clinical data, and additional research methods. Neuropsychiatric disorders develop, as a rule, against the background of an already identified somatic or endocrine disease. The latter may precede the development of neuropsychiatric pathology by several years. Less often, there are inverse relationships: neuropsychic disorders are ahead of the clinical manifestations of somatic ones. In this case, the interval between them is usually shorter - it rarely exceeds a period of 2-3 months, sometimes six months - a year. During this period of time, the symptoms of a somatic disease, as a rule, become quite obvious. It is necessary to pay attention to the relationship between the severity and course of the underlying disease and the existing disorders of the nervous system.

Diseases of the heart and main vessels. Diseases of the heart and large vessels - congenital and acquired malformations, myocardial infarction, cardiac arrhythmias, septic endocarditis, aortic aneurysm and coarctation, nonspecific aortoarteritis (Takayasu's disease), thromboangiitis obliterans and some others may be accompanied by a variety of neuropsychiatric disorders. The pathogenesis of these disorders is due to changes in blood circulation and cerebrospinal fluid circulation, vascular occlusion, embolism, reflex disorders, and sometimes the spread of the inflammatory process to the vessels of the brain (for example, with vasculitis, septic endocarditis).

The initial period of heart and vascular disease is most often characterized by asthenic vegetative-vascular disorders - general weakness, fatigue, sleep disturbance, sweating, instability of the pulse and blood pressure (the so-called neurocirculatory asthenia). Cephalgic syndrome is manifested by paroxysmal or almost constant diffuse or more limited (temporal, nape) pain. With a significant duration and severity of the disease, in addition to headache and other cerebral symptoms (nausea, dizziness), there are small focal symptoms - nystagmus, reflexes of oral automatism, hand tremor, pathological reflexes, etc.

The symptomatology of congenital heart defects manifests itself in childhood, with a lag in physical and mental development, syncope or epileptiform seizures, paresis and other focal symptoms. Neurosis-like disorders are often noted - fear, anxiety, constant internal anxiety, sleep disorders, general weakness. The severity of symptoms depends on the severity of the underlying disease, premorbid personality traits, age and gender.

Extensive myocardial infarction can be complicated by various disorders of cerebral circulation (lethargy, lethargy, drowsiness or agitation, headache, meningeal symptoms, inhibition of reflexes, etc.), sometimes turning into cardiogenic shock, cardiocerebral syndrome (dizziness, impaired consciousness, motor and sensory disorders, pathological reflexes) or cardiospinal syndrome (weakness in the limbs, changes in tendon and periosteal reflexes, conductive or segmental sensory disturbances and pelvic disorders). One of the consequences of myocardial infarction can be a shoulder-hand reflex syndrome, which is characterized by severe pain in the shoulder joint, arm, especially in the hand, soft tissue swelling, and vasomotor disorders. In the future, trophic disorders are detected - atrophy of the muscles and skin of the hands, osteoporosis, etc.

Cerebral circulation disorders occur especially often against the background of hemodynamic disorders in children with congenital heart defects or in older patients suffering from acquired heart defects, hypertension or cerebral atherosclerosis.

In patients with congenital heart defects, paradoxical embolisms to the brain often occur, the source of which is thrombosis of the veins of the lower extremities or hemorrhoidal veins. The development of acute disorders of cerebral circulation in these cases is facilitated by both exogenous factors (physical stress, bending or turning the body, etc.), as well as compensatory polycythemia and increased blood viscosity observed in congenital heart defects. These patients often have early and late post-stroke pneumonia, which develop, respectively, in the first 3 days or 2-6 weeks after a stroke, as well as a violation of carbohydrate metabolism (post-stroke diabetic syndrome).

The rapid development of early pneumonia, its occurrence mainly in extensive foci with an impact on the hypothalamus and brain stem, more frequent development on the side contralateral to the focus in the brain, the presence in the lungs of signs of circulatory disorders in the form of plethora, hemorrhage and edema indicate the important role of central neurotrophic disorders in the pathogenesis of complications.

The hypostasis factor plays a lesser role in the development of early pneumonia, but a very important, and in some cases decisive role in the development of late forms of complications. In patients with stroke, whose activation is delayed for one reason or another (cardiac pathology, thrombophlebitis), prolonged stay in bed almost always leads to a violation of the ventilation capacity of the lungs.

In addition, for the development of both early and late forms of pneumonia, the initial background of the patient's health is important. They often occur in individuals with repeated cerebrovascular accidents and pseudobulbar and bulbar syndromes. Swallowing disorders in these patients contribute to the aspiration of saliva, pieces of food, mucus, and vomit into the respiratory tract.

An important provoking factor is coronary heart disease with small and large focal angiogenic cardiosclerosis, chronic lung diseases (bronchitis, bronchial asthma) with an outcome in pneumosclerosis (diffuse or limited) and emphysema, which leads to the development of pulmonary heart failure. The occurrence of a stroke in these patients further worsens the already disturbed aeration of the lungs.

Disorders of carbohydrate metabolism in the acute period of stroke develop very often. They are characterized by lability and the absence of ketoacidosis phenomena. The severity of disorders depends on the severity of the stroke, the size of the focus and the nature of the process, as well as on the outcome of the pancreas. In the recovery period after a stroke, carbohydrate metabolism gradually normalizes, however, if there is a compensated insufficiency of organs (primarily the pancreas) involved in the regulation of glycemia, then the risk of developing diabetes mellitus increases with the survival of the patient. A previous stroke is thus one of the risk factors contributing to the onset of the disease, especially in the elderly.

Changes in the heart rhythm (paroxysmal tachycardia, atrial fibrillation, bradycardia) are a common cause of syncope.

Fainting (syncope) conditions occur most often with atrioventricular blockade (Morgagni-Adams-Stokes syndrome) against the background of a slowing of the pulse to 30-10 beats / min. There is a feeling of lightheadedness, dizziness, general weakness, then loss of consciousness. Objectively - the face is pale, the pulse is very rare, weak filling. In severe cases develop tonic and clonic convulsions, loss of urine. Frequent paroxysms gradually lead to the formation of an encephalopathic syndrome.

The cerebral form of thromboangiitis obliterans is characterized by simultaneous involvement of the vessels of the brain, limbs and internal organs, for Takayasu's disease - obliteration of the vessels extending from the aortic arch. Both forms are manifested by symptoms of dyscirculatory encephalopathy and repeated transient ischemic attacks, accompanied by dizziness, impaired consciousness, speech, visual and motor disorders.

With septic endocarditis, damage to the nervous system due to cerebral embolism is possible. The entry of infected emboli into the vessels of the meninges can lead to the development of purulent meningitis, and into the deep vessels of the brain - single or multiple abscesses of the brain.

Coarctation of the aorta due to increased blood supply to the upper half of the body and insufficient lower half leads to hypertrophy of the chest, shoulder girdle, hands and atrophy of the pelvic girdle and legs. Against this background, symptoms of dyscirculatory encephalopathy and acute disorders of cerebral circulation usually develop - plethoric crises, parenchymal and subarachnoid hemorrhages. Symptoms of an aortic aneurysm - girdle pain at the level of its location, the intensity of which may vary depending on the position of the patient; in the future, signs of ischemic myelopathy appear.

If the aneurysm is localized in the region of the aortic arch, adjacent formations can be compressed - the left recurrent nerve (hoarseness, coughing, choking), the phrenic nerve (shortness of breath, hiccups), the borderline sympathetic trunk (Horner's symptom, burning pain in half of the face, lacrimation and redness of the eye, rhinorrhea).

The clinical picture of a dissecting aortic aneurysm is the sharpest radicular pain in the chest or back with irradiation to the lower abdomen and legs, sometimes the development of collapse or shock.

Acute occlusion of the abdominal aorta and the main arteries of the lower extremities is characterized by pronounced blanching of the legs and pain in them, the disappearance of the pulsation of large vessels, the development of lower flaccid paralysis or paraplegia with dysfunction of the pelvic organs, as well as sensory disorders of the conduction type.

Chronic obliteration of the abdominal aorta, bifurcation of the aorta and great vessels of the lower extremities is manifested by the gradual development of symptoms of discirculatory myelopathy. At the same time, vegetative-trophic, sensory and motor disorders are especially pronounced in the distal extremities (up to gangrene of the feet).

Treatment and prognosis. The most rational complex treatment regimen, taking into account the characteristics of both the underlying disease and the existing complication. If neurological disorders develop against the background of myocardial infarction or congenital and acquired heart defects, then therapeutic measures should be aimed primarily at compensating for cardiovascular insufficiency. In case of cardiac arrhythmias, antiarrhythmic drugs are indicated. Patients with a sharp decrease in heart rate (atrioventricular blockade) are prescribed anticholinergics, and in cases of their insufficient effectiveness with appropriate indications, electrical stimulation. Septic endocarditis is treated with large doses of antibiotics.

Therapy of systemic diseases with impaired vascular patency (Takayasu's disease, atherosclerotic obliteration of the vessels of the extremities) at the initial stage is usually conservative with the use of antispasmodics, vasodilators, ganglioblockers, sympathetic blockades, and oxygen therapy. With epileptic seizures - anticonvulsants, cerebrovascular accident - treatment corresponding to the clinical picture of a stroke.

The prognosis is determined by the course of the underlying disease, the nature of the neuropsychiatric complication, the timeliness and volume of therapeutic measures. It is relatively less favorable in severe chronic diseases of the heart and great vessels, complicated by cardiogenic shock, cerebrovascular accident, and stage II-III dyscirculatory encephalopathy.

Lung diseases. Neurological disorders can develop against the background of both acute lung diseases (thromboembolism of the main trunk, large, medium and small branches of the pulmonary artery, infarct pneumonia, severe bilateral pneumonia) and chronic nonspecific lung diseases (COPD) (pulmonary emphysema, chronic bronchitis, bronchial asthma , pneumosclerosis).

Pathomorphologically, in the brain of patients who died from acute lung diseases, edema, diapedetic hemorrhages and plasmorrhagia, foci of thrombotic and non-thrombotic softening, a combination of focal ischemia in the cortical regions with areas of plethora in deeper ones, as well as venous stasis with arterial ischemia are determined. There are hyaline and ring-shaped thrombi in the capillaries, dystrophic changes in nerve cells and glia, areas of massive primary karyocytolysis.

Chronic hypoxia is manifested primarily by neurocellular pathology - a severe form of damage to nerve cells with a slowly growing dystrophic process in the nucleus and cytoplasm of neurons and glial cells.

In the pathogenesis of damage to the nervous system in lung diseases, the leading role is played by the influence of hypercapnia and hypoxemia factors, which arise as a result of disorders of ventilation and gas exchange in the lungs. When examining the function of external respiration, depending on the nature and severity of the pathology, there is a decrease in vital capacity (VC) to 2400-1900 ml; maximum lung ventilation (MVL) up to 50-30 l and oxygen utilization factor (KI02) up to 30-28 ml; an increase in the minute volume of breathing (MOD) up to 8-10 l and the amount of oxygen uptake per minute (POg) up to 240-270 ml/min. The duration of breath holding (Stange-Gench test) is shortened to 10-15 s. The partial pressure of carbon dioxide (pCO2) rises to 50-60 mm Hg, the pH value shifts towards acidosis (up to 7.3). Arterial oxygen saturation (HbO2) gradually decreases (up to 80%), changing the level of standard bicarbonates (SB) and buffer bases (BB).

Deep metabolic disorders develop (the amount of fibrinogen increases, a - and g-globulins and amino acids, lactic acid, ammonia, inorganic phosphorus, decreases the amount of ATP, phosphocreatine, etc.). With thrombosis and embolism of the pulmonary artery, an important role belongs to severe hemodynamic disorders resulting from blockage of the pulmonary vessel and widespread vascular spasm. Following this, arterial ischemia and venous plethora of the brain and spinal cord develop, the permeability of the vascular walls increases with the release of erythrocytes per diapedesem into the subarachnoid space and brain substance, which causes massive primary karyocytolysis with the formation of extensive foci of neuron prolapse in the cortex.

The complexity of the pathogenesis of brain disorders (hypoxemia, a drop in blood pressure in the systemic circulation, vascular spasm, homeostasis disturbances) leads to a greater frequency than in other types of hypoxia, the frequency of focal brain lesions, the diversity of their nature (meningeal syndrome, encephalopathy with convulsive seizures, non-thrombotic softening , hemorrhages, etc.).

The appearance of local neurological symptoms (often in the absence of a macroscopic focus in the brain) is explained by the phenomenon of capillary ischemia, which is uneven in nature, with massive primary karyocytolysis and areas of cell loss in the cortex. Glia is more resistant to the action of hypoxia, although it exhibits a rough proliferative-dystrophic reaction, but basically retains its structure.

Clinic. Neurological disorders in the form of mild headache, photophobia, general hyperesthesia, small vegetative-dystonic manifestations are usually included in the clinical picture of uncomplicated pneumonia and are present to some extent in almost all patients. More pronounced neurological symptoms, which should be regarded as neuropsychiatric complications, are observed in approximately 6-8% of hospitalized patients with pneumonia. These complications are manifested by cerebral, meningeal, focal and autonomic symptoms, including severe headache, dizziness, psychomotor agitation, pain when moving the eyeballs, severe general hyperesthesia, epileptiform seizures, nystagmus, anisoreflexia, pathological symptoms, sensitivity disorders, changes in blood pressure, pulse, sweating, etc.

Encephalopathic and meningeal syndromes develop more often in severe forms of lobar pneumonia. Encephalopathic syndrome is manifested by polymorphic neuropsychiatric disorders: intense headache, a feeling of heaviness in the head and stuffiness in the ears, nausea, psychomotor agitation, mild focal symptoms - nystagmus, revival of tendon reflexes, anisoreflexia, increased muscle tone, as well as manifestations of vegetative-vascular dystonia in the form of instability of blood pressure, lability of the pulse, acrocyanosis, etc. Often, on the side of somatic pathology in the Zakharyin-Ged zones, hyperesthesia, hyperpathia or hypoesthesia are determined.

Meningeal syndrome is manifested by moderately severe headache, nausea, urge to vomit or vomit, pain when moving the eyeballs, photophobia, general hyperesthesia, sometimes psychomotor agitation, tonic symptoms (rigidity of the neck muscles, Bekhterev's zygomatic symptom, etc.). In the cerebrospinal fluid, only an increase in pressure is usually noted with an unchanged content of cells and protein. The course is short-lived (3-5 days). The indicated symptom complex (shell syndrome with normal CSF) is called meningism. However, severe forms of pneumonia can be complicated by purulent meningitis due to dissemination of the introduction of pathogens (most often pneumococci) into the subarachnoid space. In these cases, there is a sharp deterioration in the condition of patients - a new rise in temperature to high numbers and pronounced cerebral, meningeal, and sometimes focal symptoms. Neutrophilic pleocytosis and hyperalbuminosis are observed in the cerebrospinal fluid. The course is longer (2-4 weeks), the prognosis, especially in the elderly, is not always favorable.

The clinical picture of pulmonary embolism is extremely polymorphic. It can be manifested by the following neurological syndromes - psychomotor agitation, meningeal, focal brain damage, epileptiform. It should be remembered that thromboembolism can be the cause of acute coma development.

Syndrome of psychomotor agitation is particularly common. For thromboembolism of the main trunk or large branches of the pulmonary artery, an acute development of pronounced psychomotor agitation is characteristic: patients jump up, try to run, do not recognize relatives, hallucinate, and do not orient themselves in the environment. With prolonged forms of thrombosis and infarct pneumonia, such attacks occur periodically, more often at night. Usually, paroxysms of arousal are replaced by adynamia, a decrease in emotional reactions, lethargy, drowsiness, lethargy. In some cases, periods of motor excitation are accompanied by the appearance of focal symptoms.

Meningeal syndrome is observed in subacute and acute forms of the disease. The more severe the pulmonary heart failure, the more shell symptoms are usually found. Meningeal syndrome in patients with pulmonary thrombosis and infarction pneumonia appears with an increase in cerebral edema and serves as a poor prognostic sign.

Focal brain damage is observed in patients with predominantly prolonged forms of the disease. Of the transient symptoms of damage to the nervous system, the most common are nystagmus or nystagmoid twitching of the eyeballs, anisocoria, anisoreflexia, pathological reflexes, intentional trembling when performing coordinating tests. Often, against the background of a deterioration in the patient's condition, speech disorders occur such as sensory and motor aphasia, paresis, paralysis, etc. Cerebral local symptoms in some cases appear several hours earlier than severe respiratory and cardiac disorders. It should be noted that the favorable dynamics of pulmonary pathology is accompanied by a rapid complete or partial regression of neurological symptoms. If an increase in thrombosis in the pulmonary vessels is accompanied by a deepening of cerebral disorders, then in the case of a fatal outcome it is difficult to identify the immediate cause of death (impaired cerebral circulation or a process in the pulmonary artery). Spinal cord injury develops less frequently and predominantly in patients with subacute and protracted forms of the disease. Inhibition or complete extinction of tendon reflexes on the lower extremities (especially often the knee ones) and sensitivity disorders of the segmental type are noted. Positive dynamics of symptoms is characteristic with the normalization of the functions of the respiratory and cardiovascular systems. Torpidity of knee reflexes is an important symptom indicating the severity of the pulmonary process, even with a relatively satisfactory general condition of the patient. The progression of spinal disorders is a poor prognostic sign, as it usually indicates an increase in the thrombotic process in the pulmonary arteries.

The epileptic syndrome is characterized by the development of a generalized convulsive seizure. It can also complicate the course of pulmonary embolism (acute and subacute forms). Sometimes, after an attack in patients, the appearance or increase in focal neurological symptoms is noted, which simulates an acute violation of cerebral circulation. It is important to remember that post-seizure symptoms usually subside over the next 24 hours.

Polyneuropathic syndrome is occasionally observed in patients with prolonged form of pulmonary embolism. These disorders are transient and regress relatively well under the influence of treatment aimed at normalizing blood gases and hemodynamics.

The syndrome of “decompensation of the old focus” develops in patients with subacute and protracted forms of pulmonary embolism who have previously had a stroke or a transient cerebrovascular accident. Damage to the nervous system is fully compensated and does not manifest itself before the onset of a pulmonary disease. The sudden development of focal neurological symptoms (paresis, disorders of sensitivity, speech, etc.) simulates a repeated violation of cerebral circulation. The differential diagnosis is based on the history and clinical data (thrombophlebitis, shortness of breath, cyanosis, tachycardia, etc.) and the presence of symptoms indicating the localization of the lesion in the pool of the same vessel. Confirms the diagnosis of decompensation of the blood supply to the brain against the background of the presence of a cyst in the brain from a previous stroke, the rapid favorable dynamics of neurological symptoms with the relief of airway insufficiency. In patients suffering from atherosclerosis or hypertension, increasing pulmonary insufficiency may result in cerebrovascular accident - ischemic softening or hemorrhage.

Syndrome of chronic encephalopathy develops in COPD patients with long-term pulmonary insufficiency and is characterized by diffuse dull headache, especially intense in the morning, with physical exertion, coughing, fatigue, irritability, irascibility and small scattered focal symptoms (hyperreflexia, anisoreflexia, ataxia, trembling of outstretched fingers). hands). Sometimes there are syncope and paroxysms of the type of cough syncope (betolepsy).

Inflammatory lung diseases with the presence of a purulent focus (empyema, bronchiectasis, etc.) can lead to the formation of a metastatic abscess in the brain (single or multiple), which is expressed by an increase in cerebral and focal symptoms, epileptic seizures, etc.

Pulmonary tuberculosis is usually manifested by symptoms of general intoxication and autonomic dysfunction: headache, weakness, sweating, tachycardia, and instability of blood pressure. Tuberculous intoxication can lead to meningism (more severe headache, photophobia, nausea). In the case of generalization of tuberculosis infection, the development of tuberculous meningitis, tuberculoma of the brain or spinal cord, tuberculous spondylitis is possible.

Diagnosis of the diseases under consideration presents certain difficulties, especially in the initial stages of the disease or its atypical course. The reaction of the nervous system to some extent can be advanced, for example, with prolonged pulmonary thrombosis, in some cases, neuropsychic disorders (headache, nausea, vomiting, psychomotor agitation, meningeal symptoms, paresis) may come to the fore, and pulmonary-cardiac disorders (shortness of breath, cyanosis, tachycardia, decreased blood pressure) become pronounced in a more advanced stage of the disease.

The appearance of cerebral and focal disorders against the background of pulmonary insufficiency following the syndrome of psychomotor agitation (a typical sign of pulmonary embolism or infarct pneumonia), the instability of symptoms and their dependence on the dynamics of pulmonary heart failure are the main diagnostic signs of hypoxic encephalopathy. In the study of cerebrospinal fluid, only an increase in cerebrospinal fluid pressure (up to 200-300 mm of water column or more) is noted without cytosis and hyperalbuminosis.

Treatment of neuropsychiatric disorders in patients with pulmonary embolism is inextricably linked with the treatment of the underlying disease. Extremely severe thromboembolism of the trunk and main branches of the pulmonary artery is treated promptly (emergency embolectomy). The presence of neuropsychiatric disorders is not a contraindication to surgery, since it usually contributes to their regression. Severe pulmonary embolism, as well as embolism of its intermediate and lobar branches are indications for thrombolytic therapy with simultaneous correction of the hemostasis system (fibrinolysin or endogenous fibrinolysis activators, antiplatelet agents, thrombolytics, anticoagulants).

Conservative treatment can be combined with surgical prevention of recurrent pulmonary embolism (installation of a filter in the inferior vena cava). Along with drugs aimed at treating a pulmonary disease, drugs that normalize the functions of the nervous system (metabolics, vitamins, vasotropic drugs) should also be recommended.

Antipsychotics are most often used to relieve psychomotor agitation. Symptomatic treatment of other cerebral disorders is carried out - vomiting (droperidol, triftazin), hiccups (metoclopramide, torecan, etaperazine), pain syndromes (analgesics or lytic mixtures consisting of chlorpromazine or tisercin, diphenhydramine or pipolfen and promedol).

The prognosis of neuropsychiatric disorders in pulmonary embolism and infarct pneumonia is always serious.

Only the favorable dynamics of the underlying disease prevents the transition of transient disorders into persistent organic brain lesions. Neuropsychiatric disorders in chronic pneumonia, pulmonary emphysema, bronchitis, pulmonary tuberculosis are usually expressed moderately, and with systematic treatment and adherence to regimen recommendations, most patients remain able to work.

Liver diseases. Diseases of the liver and biliary tract are often complicated by neuropsychiatric disorders. The clinical manifestations of the latter are determined by the form, severity and duration of the underlying disease - cholecystitis, gallstone disease, cholangitis, cholepancreatitis, obstructive jaundice, liver cirrhosis, etc.

The most frequently observed asthenic manifestations are diffuse lesions of the brain and spinal cord, and sometimes of individual peripheral nerves, i.e., syndromes of encephalopathy, encephalomyelopathy and polyradiculoneuropathy.

Liver disease can be one of the causes of optic neuritis.

Pathogenesis lesions of the nervous system due to violations of the detoxification function of the liver and various types of metabolism - protein, lipid, carbohydrate, water-electrolyte, vitamin. Hyperglobulinemia develops, the formation of fibrinogen, prothrombin, vitamin metabolism (in particular, vitamins C and K) are disturbed, which causes a change in the coagulating properties of the blood and the development of hemorrhagic syndrome. The acid-base state of the blood shifts towards acidosis, the alkaline reserve of the blood decreases. The water-salt metabolism and the course of all redox processes in the nervous system are upset. With jaundice, the accumulation of bilirubin and bile acids in the blood has a toxic effect, hepatoportal disorders - ammonia. One of the links in the pathogenesis may be a violation of the function of other organs, which is confirmed by the frequent development of hepatocardial, hepatolienal, or hepatorenal syndromes.

Neurasthenic syndrome occurs in two variants - hypersthenic (irritability, irritability, emotional lability, incontinence, anger, excessive mobility) and asthenic (physical and mental fatigue, resentment, suspiciousness). The mood is unstable. Sleep superficial, disturbing. Usually complaints of headache, feeling of heaviness in the head, dizziness, as well as discomfort in the heart, palpitations, sexual disorders (impotence, menstrual irregularities, etc.). Some patients with sensitive character traits with obstructive or parenchymal jaundice experience severe itching and a burning sensation in any part of the body, causing a desire to “take everything off oneself”, sensations of electric current and hot waves passing through the body, “twitching and gurgling in the area abdomen”, “vibration in the spine”, etc.

Hepatogenic encephalopathy is manifested by headache, dizziness, sometimes nausea and mild scattered symptoms (nystagmus, cranial nerve paresis, coordination disorders, hyperkinesis, anisoreflexia, pathological reflexes). In the advanced stage of liver cirrhosis (ascites, splenomegaly), more severe forms of portal encephalopathy with impaired consciousness are observed. Due to the formation of anastomoses between the system of the vena cava and the portal vein, ammonia and other toxic products from the gastrointestinal tract enter the bloodstream (normally they pass through the liver filter and undergo detoxification). Against the background of polymorphic neurological symptoms, psychomotor agitation is often noted, as well as hyperkinesis (often of the type of choreoathetosis or fluttering tremor). Psychomotor agitation can turn into stunning, stupor and then coma. With an acute increase in the difficulty of blood flow from the portal vein to the liver, the likelihood of neurological disorders increases. The formation of ammonia is proportional to the content of proteins in the intestine, therefore, with bleeding from varicose veins of the esophagus, portal encephalopathy develops especially often.

The cause of the development of acute toxic-dyscirculatory encephalopathy (OTDE) is often obstructive jaundice. In milder cases, OTDE is manifested by severe apathy, adynamia, headache, and a diffuse decrease in muscle tone. With moderate OTDE, focal neurological symptoms (anisoreflexia, pathological reflexes, impaired cranial innervation, reflexes of oral automatism, meningeal signs) join, and with severe OTDE, in addition to an increase in organic cerebral symptoms, signs of damage to the spinal cord appear (paresis of the legs, decreased muscle tone, plantar and Achilles reflexes). There is a certain correspondence between the severity and duration of bilirubin autointoxication, on the one hand, and the depth of neurological disorders, on the other.

The symptomatology of polyradiculoneuropathy associated with liver pathology has the following features: at the beginning of the disease, a limited lesion of one or two roots or one nerve is typical, and only after a few weeks or months the process spreads to other nerves and gradually captures all limbs - a polyneuropathic syndrome occurs. Depending on the clinical manifestations, sensitive, motor and mixed forms are distinguished.

The most common is the sensitive (sensory) form, which is characterized by pain, paresthesia, a disorder of superficial sensitivity in the distal extremities, and vegetative-vascular disorders (coldness of the hands and feet, hyperkeratosis, hyperhidrosis, discoloration of the skin). The degree of motor disorders is different - from mild weakness to relatively deep paresis. On the hands there is a predominant lesion of the radial, on the legs - peroneal nerves.

Sometimes, with diseases of the liver and biliary tract, various visceral disorders develop - hepatocholecystocardial and hepatorenal syndromes. Most often, cholecystocoronary Botkin's syndrome is observed, which is manifested by recurrent cardialgia against the background of a diet disorder, dyspeptic symptoms, jaundice, etc. In elderly patients suffering from atherosclerosis involving the vessels of the brain and heart, pathology of the liver and biliary tract may be a risk factor for stroke or myocardial infarction.

Diagnosis is based on clinical data and additional research methods, among which the most important are EEG indicators (the appearance of three-phase waves is one of the early signs of the transition of hepatogenic encephalopathy to a coma) and EMG (decrease in the amplitude of myopotentials, rare fibrillations, changes in nerve conduction velocity are detected during subclinical forms of hepatogenic polyneuropathies). An increase in pressure is found in the cerebrospinal fluid. CT and MRI are important for assessing the state of the brain and liver.

Treatment. Assign detoxification, dehydration, lipotropic and restorative agents - rheopolyglucin, diacarb, cerebrolysin, retabolil, glutamic acid, methionine, pancreatin, intravenous infusions of glucose with insulin, isotonic sodium chloride solution, blood, plasma or blood substitutes (polyglucin, etc.), as well as diet with restriction of salt and proteins. To reduce the activity of the bacterial flora of the intestine, under the action of which ammonia is produced, short-term courses of antibiotics or sulfa drugs are sometimes prescribed. Excitation and restlessness can be stopped by the introduction of neuroleptics. When bleeding occurs, ascorutin, vikasol, calcium gluconate, dicinone, etc. are prescribed. A number of diseases of the liver and biliary tract are treated promptly (cholecystitis, cholelithiasis, liver cirrhosis, etc.). The appearance of neuropsychiatric disorders, as a rule, should not serve as a contraindication to surgical intervention.

The prognosis is more favorable with the development of neuropsychiatric disorders against the background of cholecystitis, cholangitis and cholelithiasis, less - against the background of liver cirrhosis, with porto-caval anastomosis, splenomegaly, ascites, bleeding from the veins of the esophagus.

Diseases of the pancreas. In hyperglycemic conditions due to diabetes mellitus, various symptoms are observed: headache, dizziness, general weakness, memory loss, skin itching, sensory disturbances, motor disorders. The following syndromes are distinguished: neurasthenic, encephalopathic, polyneuropathic, autonomic polyneuropathy, neuralgia and neuropathy of individual nerves, most often the facial one, as well as hyperglycemic (diabetic) coma.

Diabetic encephalopathy is characterized by headache, decreased memory and attention, nystagmus, impaired pupillary reactions to light and convergence, paresis of the facial and oculomotor nerves, etc. Severe forms of diabetes mellitus, especially in the elderly, may be complicated by a stroke. Pathological studies suggest that in the pathogenesis of encephalopathy and strokes in diabetes, an important role belongs to the macroangiopathy inherent in diabetes mellitus, i.e. damage to arterioles, precapillaries that vascularize the cortex, subcortical formations and the brain stem.

The frequency of non-thrombotic softening should be emphasized, which is explained by the excessive accumulation of carbon dioxide. The latter, by expanding the cerebral vessels, causes a regional drop in blood pressure, which, in the presence of an increased need for oxygen in the brain tissue of diabetic patients, leads to softening without the formation of a blood clot in the brain vessel.

Diagnosis of strokes occurring against the background of diabetes mellitus has certain difficulties. The neurological picture is masked by adynamia associated with diabetes, peripheral sensitivity disorders, anisoreflexia, areflexia, etc. In many patients in the acute period of a stroke, the course of diabetes also worsens: the blood sugar level rises to values unusual for this patient, acetonuria appears, etc. Coma states in these patients are characterized by a long duration (from 1 to 3-5-8 and more than 20 days).

A disorder of cerebral circulation can be complicated by the development of hyperglycemic coma. All this in cases of stroke with loss of consciousness, stupor, stupor complicates differential diagnosis with diabetic (hyperglycemic) coma.

Hemorrhagic stroke in patients with diabetes mellitus develops more often when combined with hypertension or as a complication of diabetic coma, apparently as a result of a toxic effect on the cerebral vessels of metabolic products, in particular ketone bodies.

Diabetic patients often have polyneuropathic disorders that occur with a predominance of sensory, vegetative and motor symptoms. The sensitive form is manifested by paresthesia, pain and a slight decrease in surface sensitivity, impaired coordination of movements, the motor form is manifested by mild flaccid paresis of the limbs and muscle atrophy, more pronounced in the proximal sections. For diabetic polyneuropathies, peripheral autonomic failure is highly characteristic. The most common manifestations of PVN are orthostatic hypotension, fixed tachycardia, nocturnal diarrhea, and pelvic disorders. There are also neuropathies and neuralgia of individual nerves, especially often the facial one.

Hyperglycemic diabetic coma often develops gradually - over several hours or days. Headache, dizziness, thirst, polyuria appear. Patients become lethargic, drowsy, apathetic, indifferent. Dry skin with traces of scratching is noted. If left untreated, the precomatous state turns into a coma: consciousness is completely lost, blood pressure drops, the pulse becomes weak, frequent, there is a smell of acetone from the mouth. The pupils are narrow, corneal, abdominal and tendon reflexes gradually decrease. With a coma of 1-11 degrees, pathological reflexes are usually determined.

Treatment. In the acute period of a stroke against the background of diabetes mellitus, insulin should be prescribed: by normalizing carbohydrate metabolism and reducing the effects of hypoxia, it improves the nutrition of the brain tissue. To avoid hypoglycemia, it is better to administer insulin in fractional doses. Dysfunction of the blood coagulation and anticoagulation system, the frequency of non-thrombotic softening and the presence of foci combined in the nature of the pathological process require caution when prescribing anticoagulants to patients with diabetes mellitus. In cases of diabetic coma, immediate intravenous administration of insulin is indicated, and hypoglycemic coma - glucose. Surgical interventions are used for purulent pancreatitis, pancreatic necrosis, pancreatic tumors (insulinoma).

The course of syndromes of diabetic polyneuropathy, diabetic and hypoglycemic encephalopathy is often recurrent with improvement under the influence of complex treatment.

Kidney diseases. Acute renal failure (acute glomerulonephritis, post-abortion sepsis, poisoning, trauma, etc.) and long-term kidney diseases (chronic glomerulonephritis, pyelonephritis, urolithiasis) in the stage of subcompensation and especially decompensation can cause a variety of neuropsychiatric disorders - polyneuropathy, encephalopathy, discalemia paralysis, uremic coma, etc.

Pathologically, a typical picture of toxic encephalopathy with a combination of vascular and parenchymal-cellular changes (edema, angionecrosis, diapedetic hemorrhages, degenerative changes in cells, etc.) is found in the brain.

The pathogenesis of neurological disorders in kidney diseases in the stage of decompensation is mainly due to intoxication caused by azotemia.

However, such syndromes as astheno-like, renovisceral, moderate encephalopathy can complicate subcompensated kidney failure when there are no symptoms of azotemia yet. Loss of sodium and chlorides, slight hypo- and hyperkalemia and hypoalbuminemia lead to a decrease in colloid osmotic blood pressure, an increase in vascular permeability with the development of edema in the brain, spinal cord and peripheral nerves, diapedetic hemorrhages and plasmorrhagia, and subsequently to a change in nerve cells, conductors , nerve plexuses and peripheral nerves, as well as impaired contractile function of muscles.

Toxic damage or mechanical compression of the branches of the autonomic plexus of the kidneys by stones can lead to pathological irritation of the pain impulse to the spinal nodes and segmental apparatus of the spinal cord and the appearance of pain and hyperesthesia in the renal zones of Zakharyin-Ged, pain in the region of the heart (renocardial syndrome), abdomen (renovisceral syndrome). ) or exacerbation of sciatica. In the advanced stage of renal failure, the combined toxic effects of azotemia and the entire complex of medium molecular weight metabolites, metabolic acidosis, protein and water-electrolyte imbalances, especially hyperkalemia and hypercreatininemia, and arterial hypertension are of primary importance.

Neurasthenic syndrome in the initial period of kidney disease is manifested by symptoms of hypersthenia (irritability, irascibility, mood instability, sleep disorders), later (stage of subcompensation and decompensation) hyposthenia symptoms begin to predominate (fatigue, absent-mindedness, touchiness, tearfulness). All disorders usually develop against the background of lower back pain, edema, dysuric disorders, etc.

The algic syndrome is characterized by pains that are localized in the lower back at the level of the Tmx-Li segments on one (renal colic) or on both (nephritis) sides, are permanent or paroxysmal in nature, do not always subside in the supine position and can spread to the inner surface of the thigh and inguinal crease.

In the study of sensitivity, in the area of the affected segments, hyperesthesia or hyperpathy is most often determined. The severity of symptoms of tension of the nerve trunks is negligible. Symptoms of loss in the motor and reflex areas, as a rule, are absent.

It should be borne in mind that kidney pathology can cause an exacerbation of lumbar ischial syndrome in patients suffering from deforming spondylosis and spinal osteochondrosis, which accordingly changes the clinical picture of the disease.

With polyneuropathic syndrome, moderate sensory, autonomic and reflex disorders are noted: pain, burning, numbness, acrocyanosis, hypesthesia or hyperesthesia in the distal parts of the arms and legs (mainly in the feet), sometimes a decrease in Achilles reflexes. Severe forms with paralysis and paresis of the extremities are now rarely observed due to improved treatment of renal failure.

Renocardial syndrome is characterized by prolonged aching pains in the left half of the chest, which are combined with lower back pain and are poorly relieved by nitroglycerin. An electrocardiographic study does not reveal significant deviations from the norm. Pain regresses as renal failure resolves. However, in patients with coronary heart disease, paroxysmal renal pain can provoke angina attacks.

Reno-abdominal syndrome develops at the height of an attack of urolithiasis and is manifested by epigastric pain, nausea, belching, heartburn (not associated with eating), hiccups, loss of appetite and other dyspeptic disorders. Can mimic diseases such as cholecystitis, appendicitis, pancreatitis, gastritis, peptic ulcer.

Acute encephalopathic disorders usually occur against the background of a sharp increase in renal failure. Patients develop cerebral (headache, dizziness, apathy or, conversely, agitation), as well as meningeal and small focal symptoms (anisocoria, horizontal nystagmus, muscle hypotension, increased reflexes, etc.). The most severe disorders are observed in the oligoanuric stage of the disease, when a sharp psychomotor agitation can be replaced by somnolence, and later - by a soporous or coma. In the fundus, there are varicose veins or even congestive nipples. There is an increase in pressure in the cerebrospinal fluid (up to 250-300 mm of water column) with a normal composition or slight pleocytosis and hyperalbuminosis.

With a significant increase in hypo- or hyperkalemia, dyskalemic paralysis often develops - weakness of the muscles of the arms, legs and torso, which can reach a degree of complete immobility, as well as respiratory and cardiac disorders (shortness of breath, bradycardia, arterial hypotension, etc.). Tendon reflexes and muscle tone are reduced. Hypokalemic paralysis is more pronounced in the proximal parts of the arms and legs, rarely captures the muscles of the face, hyperkalemic - usually spread to the muscles of the face, pharynx and larynx.

Clinical manifestations of acute encephalopathy and dyskalemic paralysis usually gradually disappear as renal failure compensates. But in cases of a long and severe course of a renal disease, neuropsychiatric disorders (headache, general weakness, decreased memory and attention, increased reflexes of oral automatism, revitalization of tendon reflexes, pathological reflexes, etc.) become persistent, i.e. develop chronic dysmetabolic encephalopathy. Sometimes it can proceed according to the type of pseudotumorous syndrome (headache, nausea, epileptic seizures, spontaneity, workload).

Violations of cerebral circulation (crises, transient disorders, strokes) are most often observed in chronic nephritis complicated by arterial hypertension.

Uremic coma is characterized by the presence of itching, scratching on the skin, ammonia breath, hiccups, vomiting, myoclonus, and often convulsive paroxysms. In the shallow stage of the coma, all tendon reflexes are brisk, and the corneal and pharyngeal reflexes are usually already reduced. Bilateral pathological pyramidal reflexes are caused.

It should be borne in mind that the course of chronic renal failure (CRF) has changed somewhat over the past two decades due to the development of effective methods of treatment. This largely applies to the terminal stage of CRF - uremia. Hemodialysis and kidney transplantation can prolong the life of patients for many years.

Neurological disorders in CRF should be considered as part of the body's overall response to impaired renal function. The influence of a complex of intoxication factors, including anemia, can manifest itself at different times depending on the sensitivity of certain parts of the nervous system. This underlies a certain staging in the development of neurological disorders in the terminal stage of CRF. The clinical dynamics is Initially, stem symptoms appear, then tendon reflexes and leg muscle strength gradually decrease; tendon reflexes on the hands remain elevated for some time, sometimes with the presence of pathological signs; then weakness and inhibition of tendon reflexes on the hands join against the background of even greater damage to the lower extremities - the appearance of deep lower atrophic paresis and paralysis with the absence of tendon reflexes and sensory disorders of the distal type. This process occurs against the background of progressive encephalopathy, as evidenced by increasing changes in the emotional and mental sphere, asterixis, multiple myoclonus.

It is known that phylogenetically younger parts of the nervous system are more sensitive to both hypoxia and intoxication. Therefore, with a mild degree of intoxication, the cortical level primarily suffers, and the functional state of the limbic-reticular complex also changes. In this case, symptoms of encephalopathy are revealed. With increased intoxication, the initial excitation is replaced by a sharp weakness, increased fatigue, lethargy, apathy, forgetfulness, and drowsiness. With a further increase in intoxication, spinal symptoms are increasingly revealed - a decrease in muscle strength, muscle tone and tendon reflexes, and sensory disorders in the legs. These symptoms may depend both on the violation of the descending influences of the reticular formation, and on the direct effect of intoxication on the spinal cord and peripheral nerves, which leads to a decrease in pyramidal symptoms and an increase in atrophic paresis.

The widespread introduction of chronic dialysis has led to the identification of a new form of neurological pathology - dialysis encephalopathy, the leading manifestation of which is dementia. So far, the pathogenesis of brain damage in such cases remains unclear; an excess of aluminum in the water used for dialysis has been cited as a possible cause. The presence of a permanent shunt sometimes leads to the development of a tunnel neuropathy of the median nerve in the carpal tunnel.

The pattern of regression of symptoms of focal lesions of the nervous system after successful kidney transplantation is inverse to the dynamics of their increase: initially, the symptoms of damage to the peripheral nerves and spinal cord disappear, then the symptoms of renal encephalopathy regress. The duration of the recovery process is up to 2-3 years. The symptoms remaining after this period are poorly reversible and must be attributed to persistent residual disorders. It should be remembered that cytomegalovirus infection sometimes occurs in patients with a transplanted kidney.

Treatment. Therapy should be carried out taking into account the form and stage of renal disease, clinical manifestations and pathogenesis. Usually it is aimed primarily at compensating for renal failure. Uremia with hypercreatininemia and hyperkalemia and an increase in cerebral, meningeal and general focal symptoms requires the mandatory use of hemodialysis (peritoneal dialysis) or hemosorption (which is often a preparation for a kidney transplant). With urolithiasis, pyelonephritis, hydronephrosis, kidney injuries, according to indications (ineffectiveness of conservative therapy, etc.), surgical intervention is used, after which there is a complete or partial regression of neuropsychiatric disorders. Treatment of emotional and mental disorders in the structure of the encephalopathic syndrome is carried out using tranquilizers, antidepressants, nootropics, restorative drugs, etc. Prescription of any drugs should be carried out only after consultation with a nephrologist, given the presence of severe renal failure in some patients.

The prognosis is determined by the form and severity of the underlying disease and partly by the features of the complication. Stable compensation of neurological symptoms can only be achieved with the elimination of renal failure. Neurostenoid-like, polyneuropathic, renocardial, renovisceral, encephalopathic disorders can completely regress if they are caused by acute and relatively mild kidney diseases or long-term diseases in the stage of subcompensation or compensation. An increasing or recurrent course of these syndromes is observed in patients with chronic glomerulonephritis or pyelonephritis in the decompensation stage.

Connective tissue lesions. Lupus erythematosus, polymyositis, dermatomyositis, periarteritis nodosa, scleroderma, temporal arteritis, thromboangiitis obliterans are often accompanied by neuropsychiatric disorders - encephalopathic, polyneuropathic, myasthenic, myopathic and some other syndromes.

The pathogenesis of these disorders is due to autoimmune degenerative-inflammatory changes in the membranes of the brain and spinal cord and blood vessels.

Rheumatism can be complicated by cerebral disorders with a predominant lesion of the subcortical nodes - minor chorea. Essentially, rheumatic brain damage is limited to chorea minor. The earlier concept of “cerebral rheumatic vasculitis” as an everyday cause of damage to the nervous system turned out to be untenable. The defeat of the cerebral vessels in rheumatism is a rarity.

Among the causes of cerebral strokes, a prominent place is occupied by both primary vasculitis and vasculitis in connective tissue diseases. Particular attention is drawn to Snedonn's syndrome associated with antiphospholipid factor - perhaps the most common cause of ischemic stroke in young patients.

Temporal arteritis (Horton's disease) is characterized by sharp local pain in the temporal region, which may be accompanied by lockjaw. The pathological basis of the disease is giant cell arteritis of the temporal artery. Palpation reveals a thickened and painful temporal artery. Sometimes it is visible on examination. Often, the optic nerve is involved in the process on the side of the lesion (decrease in visual acuity; in the fundus - a picture of ischemic neuritis). A sharp increase in ESR is characteristic.

Neurolupus- neurological manifestations of systemic lupus erythematosus. Most often, against the background of general malaise, fever, headache, dizziness, damage to the peripheral nervous system (neuropathy, polyneuropathy, etc.) is observed, but sometimes other levels of the nervous system are involved with the development of the syndrome of encephalopathy, myelopathy, encephalomyelopathy.

Nodular periarteritis is pathomorphologically characterized by lesions of small arteries with the development of dense nodules along the way. Since the vessels of almost all organs and tissues, including the nervous system, can be involved in the process, the clinical manifestations of the disease are extremely diverse. It occurs at any age, but is somewhat more common in men 30-50 years old. At the onset of the disease, fever, diffuse pain and polymorphic skin rashes are usually observed. In the course of the vessels, dense, painful nodules are felt on palpation. Already at an early stage of the disease, internal organs are involved - the spleen, liver, kidneys, gastrointestinal tract, which is manifested by abdominal pain, hematuria, intestinal bleeding and other symptoms. Over time, patients acquire a characteristic appearance - an earthy-pale color of the skin against the background of general exhaustion. In almost all cases, various neurological disorders are observed - neuropathies, polyneuropathy, encephalopathy, myelopathy, acute vascular disorders (subarachnoid, subdural, parenchymal hemorrhages). Most often, the peripheral nervous system suffers in the form of multiple mononeuropathies.

Diagnosis is based on the clinical picture (a combination of fever, skin disorders, kidney and peripheral nerve damage) and additional data (hypergammaglobulinemia, left shift leukocytosis, high ESR).

With polymyositis, edema, lymphoid cell accumulations, fiber destruction, etc. are detected in the muscle tissue.

The clinical picture is characterized by the appearance of diffuse or limited pain in the muscles, mainly in the proximal limbs, low-grade fever, and general fatigue. The muscles are slightly swollen, painful on palpation. Gradually, changes develop in the internal organs (heart, lungs, gastrointestinal tract), skin (depigmentation, swelling), nervous system (peripheral nerves, membranes, spinal cord, brain stem, etc. are involved) and muscles. Therefore, the disease can occur with syndromes of polyneuropathy, radiculoneuropathy, myelopathy, encephalopathy, myopathy, myasthenia gravis. In the blood - leukocytosis, hyperglobulinemia, increased ESR, as well as the activity of aminotransferases and aldolase.

Differential diagnosis is most often carried out with other forms of polyneuropathy and myopathy. In unclear cases, muscle biopsy data are helpful in establishing the diagnosis.

Treatment. All forms of collagenosis are treated with long-term repeated courses of anti-inflammatory (indomethacin, voltaren, brufen, reopyrin, delagil), antihistamines (suprastin, pipolfen, diazolin) and hormonal (prednisolone, urbazone, dexamethasone) drugs in various combinations. The inclusion of corticosteroids is mandatory in severe disease.

EPILEPSY.

According to the definition of WHO experts, epilepsy is a chronic brain disease of various etiologies, which is characterized by recurrent epileptic seizures resulting from excessive neural discharges, and is accompanied by a variety of clinical and paraclinical symptoms.

It is necessary to strictly distinguish between an epileptic seizure and epilepsy as a disease. Single, or, according to the terminological dictionary for epilepsy, random epileptic seizures or epileptic reaction, according to the terminology of domestic researchers, having arisen in a certain situation, do not recur in the future. Some cases of febrile convulsions in children can be cited as an example. Epilepsy should not include recurrent epileptic seizures in acute cerebral diseases, such as cerebrovascular accidents, meningitis, encephalitis. At the suggestion of S. N. Davidenkov, in such cases it is advisable to use the term “epileptic syndrome”.

Etiology. For the development of epilepsy, it is necessary to have a persistent focus of epileptic activity due to organic damage to the brain. At the same time, epileptization of neurons, i.e., a special state of neurons that determines the “convulsive readiness” of the brain in the foci of its organic lesion and the degree of epileptic influence of these foci on brain structures, depends on the premorbid characteristics of the organism and, in particular, on the epileptic predisposition of the genetic or an acquired character, which determines the greater likelihood of an epileptic seizure in a patient with brain damage.

The significance of the genetic factor is most clearly seen in typical absences (short-term loss of consciousness followed by amnesia), inherited in an autosomal dominant manner with incomplete gene penetrance, with primary generalized epilepsy beginning in childhood; the role of the genetic factor in partial seizures is less pronounced, however, as noted, in this case, seizures are more common among the closest relatives of patients than on average in the population.

Among the exogenous factors influencing the development of the disease are perinatal and postnatal neuroinfections, neurotoxicosis and traumatic brain injury, which are of the greatest importance. This does not exclude the role of other factors - intrauterine, vascular, toxic. As for perinatal pathology (from the 27th week of fetal life to the 7th day of a newborn’s life), traumatic factors play the greatest role here (discrepancy in the size of the fetal head and pelvis, the use of obstetric aids, etc.) and anoxic (fetal asphyxia during protracted labor, entanglement of the neck of the fetus with the umbilical cord, etc.).

Pathogenesis. In the pathogenesis of epilepsy, both changes in the functional state of a part of neurons in the area of epileptogenic lesions (epileptogenic focus), the totality of which constitutes an epileptic focus, and features of the interaction of a population of epileptic neurons are important. The electrical activity of epileptic neurons is characterized by the occurrence of paroxysmal

DAMAGE OF THE NERVOUS SYSTEM IN DISEASES OF THE INTERNAL ORGANS

LECTURE 14

Changes in the heart rhythm (paroxysmal tachycardia, atrial fibrillation, bradycardia) are a common cause of syncope.

1.2.6. nosological unit. Phenocopies and genocopies. Principles of disease classification

1.2.7. Methodological principles underlying the scientific understanding of the essence of the disease

2. Etiology

2.1. Control questions

2.2. Recommendations for answers

2.2.1. The concepts of "etiology", "etiological factor", "conditions", "reason", "cause of the disease". Principles of etiotropic prophylaxis and therapy of diseases.

2.2.2. Forms of interaction of exogenous etiological factors with the body. Features of the occurrence of pathology in the prenatal period of development

2.2.3. Division of diseases depending on the role of genetic and exogenous factors in etiology

2.2.4. Fundamentals of misconceptions in etiology

3. General pathogenesis of non-hereditary diseases

3.1. Control questions

3.2. Recommendations for answers

3.2.3. The main mechanisms of damage to the body and violation of its functions during the onset and development of the disease.

3.2.4. Adaptive phenomena in pathogenesis, their types

3.2.5. Stress as a general adaptation syndrome and its role in pathology.

3.2.6. Dialectical assessment of adaptive phenomena in the pathogenesis of the disease

4. Pathophysiology of cell damage

4.1. Control questions

4.2. Recommendations for answers

4.2.1. Definition of the concept of damage. Causes of cell damage. Selectivity and specificity of injury

4.2.2. Consequences of damage to the main cellular organelles.

4.2.3. Mechanisms that determine cellular reactivity and its changes.

4.2.4. The pathogenesis of cell damage

4.2.5. Sanogenetic mechanisms in the process of cell damage. Damage outcomes

5. The constitution of man. Mechanisms of formation of hereditary pathology

5.1. Control questions

5.2. Recommendations for answers

5.2.1. The human constitution, the role of heredity and the external environment in its formation

5.2.2. The value of the constitution for the body and

5.2.3. Some formation mechanisms

5.2.3.1. Formation of pathology on the basis of violations of enzymatic processes

5.2.4. Manifestations of constitutional pathology

5.2.5. Features of people of normal constitutional types and morbidity

5.2.6. Principles of prevention and therapy of constitutional pathology

6. Reactivity of the organism and its role in pathology

6.2. Recommendations for answers

6.2.1. Reactivity, its significance for the organism and forms of manifestation. Reactivity and resistance

6.2.2. Factors that determine the individual reactivity of the body

6.2.4. Pathogenesis of paraallergic processes such as the Schwartzman and Sanarelli phenomena

6.2.5. Tachyphylaxis, its mechanisms

7. Immunopathology

7.1. Control questions

7.2. Recommendations for answers

7.2.1. Allergy. 7.2.1.1. Definition, meaning, classification

7.2.1.2, Allergens, sensitization

7.2.1.3. Antibodies involved in allergic processes

7.2.1.4. Antibodies that prevent allergic phenomena

7.2.1.5. Regulation of allergogenesis

7.2.1.6. The pathogenesis of allergic processes

7.2.1.7. Allergy and heredity

7.2.1.11. Principles of prevention and therapy of allergic processes

8. Disseminated

8.2.3. ICE pathogenesis

8.2.3.1. Mechanisms of microcirculation disorder in DIC

8.2.3.2. Vicious circles in the development of internal combustion engines

8.2.4. Development stages of internal combustion engines

8.2.5. The course and clinical manifestations of DIC - thrombogemorragic syndrome (TGS)

9. Fever. hyperthermia

9.1. Control questions

9.2.2. Causes of fever

9.2.3. fever pathogenesis. Stages of its development

9.2.4. Features of the development of fever in children

9.2.5. Changes in metabolism and body functions during fever

9.2.6. Hyperthermia. Stages of development. The difference between fever and hyperthermia

9.2.7. The biological significance of fever

Content

3. General pathogenesis of non-hereditary diseases

3.1. Control questions

1. The concept of "pathogenesis". The main structure of the pathogenesis of the disease. Principles of pathogenetic therapy of diseases. 2. The main ways of distribution of damaging factors (and damage) in the body. 3. The main mechanisms of damage to the body and violation of its functions in the occurrence and development of diseases. 4. Adaptive phenomena in pathogenesis, their types. 5. Stress as a general adaptation syndrome and its role in pathology. 6. Dialectical assessment of adaptive phenomena in the pathogenesis of the disease.

3.2.1. The concept of pathogenesis. The main structure of the pathogenesis of the disease

Pathogenesis- the mechanism of development of pathological processes and diseases.

This is not a chaotic process, as it is closely related to the cause that caused the pathology, and with the anatomical, biochemical, and physiological characteristics of the body.

The pathogenesis of a disease is a complex branched structure of cause-and-effect relationships, where the consequences themselves become the causes of other consequences (Fig. 2).

When considering the pathogenesis of the disease, it is necessary to highlight a number of phenomena.

1. Distribution routes damaging factors in the body. 2. Mechanisms of damage and dysfunction organism. 3. Main links(A), usually one of the first, the impact on which can stop the development of the disease (pathogenetic therapy). 4. Vicious circles(B), that is, such phenomena when subsequent links reinforce the previous ones, creating an unfavorable trend in the development of the disease. They should be destroyed. 5. Adaptive(sanogenetic) processes(B) which, if they are insufficient, should be strengthened; if they are excessive, they should be limited.

3.2.2. The main ways of distribution of damagingfactors(and damage) in the body

1. By continuation of the tissue (for example, from the upper respiratory tract down the mucosa of the tracheobronchial system). 2. By contact (for example, from the visceral to the parietal sheet of the pleura or peritoneum). 3. Intracanalicular (for example, Koch's bacilli in the bronchi, intestines, urinary tract). 4. With blood or lymph flow (microbes, toxins, emboli, tumor cells). 5. Nerve trunks (rabies virus, poliomyelitis, tetanus toxin, many non-microbial poisons that can damage nerve fibers).

3.2.3. The main mechanisms of damage to the body and violation of its functions during the onset and development of the disease.

Immediate Damage cells, tissues at the site of action of the pathogenic factor by themselves, for example, with mechanical, thermal, chemical trauma. In this case, membranes, enzymes, organelles, the genetic apparatus or whole cells, tissue structures can be damaged in isolation (see the Cell Damage section).

mediated damage.

A. Neurogenic mechanisms.

Unconditioned pathological reflexes, causing a violation of regulated functions (for example, a blow to the epigastric region - cardiac arrest).

Unconditioned pathological reflexes that cause trophic disorders (neurogenic or nervous dystrophies) with excessive irritation of receptors or nerve centers, especially the hypothalamic region.

3. Disorders on the periphery (motor, secretory) with damage (switching off) of the corresponding nerve centers of regulation.

4. Tissue denervation (transection, destruction of afferent, efferent or mixed nerves), causing neurogenic dystrophies.

In the mechanisms of development of reflex neurodystrophic processes (neurogenic tissue non-circulatory disorders), an important role is played by an increased release of norepinephrine into the synaptic cleft of sympathetic terminals, followed by depletion of its reserves.

When cutting afferent nerves, when the pathological process is most difficult, there are: firstly, inadequate efferent influences as a result of pathological afferent impulses from the central stump of the cut nerve; secondly, the defenselessness of an organ devoid of sensitivity against injuries, infections, etc.; thirdly, the lack of complete information about metabolic changes, which limits the possibility of its correction; fourthly, pathological antidromic influences transmitted to the innervated tissues, as can be seen, through the synthesis of group E prostaglandins.

When deafferentation, the impulse activity of the nerve, transmitted through mediators, stops, which adversely affects the metabolism and causes atrophy from inactivity. Non-impulse activity also stops, which consists in the fact that fluid (axoplasmic current) with the substances necessary for normal metabolism constantly enters the innervated tissue. Among them, the main role is played by neurotrophic factors, which are different for different types of neurons. These are peptides or proteins with a molecular weight of 5 to 300 kD. They affect metabolism, division, cell differentiation and tissue regeneration. In addition, the denervated organ responds inadequately (usually intensely) to humoral stimuli.

In the cells of the denervated tissue, the function of the genetic apparatus changes, which leads to dysfermentosis and even to the appearance of autoantigens, followed by rejection.

Conditioned pathological reflexes, for example, vomiting, attacks of angina pectoris, bronchial asthma can occur as a conditioned reflex.

Mediation through the psycho-emotional sphere (psychotrauma, iatrogenic, etc.).

B. Humoral mechanisms: by increasing or decreasing the production of biologically active substances. This refers to hypo- or hyperneurosecretion, hypo- or hypersecretion of the endocrine glands, hypo- or hyperproduction of tissue biologically active substances.

V. Allergic mechanisms.

G. Combination of mechanisms, for example, direct damage, reflex and humoral disorders.

vbordo.ru

Pathogenetic mechanisms of various diseases. Pathogenesis: term, definition and classification. Damage. The main link of pathogenesis. The course of diseases. Disease outcomes. General pathogenesis of non-hereditary diseases

3. General pathogenesis of non-hereditary diseases

3.1. Control questions

3.2.1. The concept of pathogenesis. The main structure of the pathogenesis of the disease

3.2.3. The main mechanisms of damage to the body and violation of its functions during the onset and development of the disease.

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3. General pathogenesis of non-hereditary diseases

3.1. Control questions

3.2.1. The concept of pathogenesis. The main structure of the pathogenesis of the disease

3.2.3. The main mechanisms of damage to the body and violation of its functions during the onset and development of the disease.

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