Appendages hurt: symptoms and treatment. The best antibiotic for pneumonia. Heart disease: myocardial infarction and dry pericarditis

The word pain combines two contradictory concepts. On the one hand, according to the popular expression of ancient Roman doctors: “pain is the watchdog of health,” and on the other hand, pain, along with a useful signaling function that warns the body of danger, causes a number of pathological effects, such as painful experience, limited mobility, impaired microcirculation, decreased immune defense, dysregulation of organ and system functions. Pain can lead to severe dysregulatory pathology and can cause shock and death [Kukushkin M. L., Reshetnyak V. K., 2002].

Pain is the most common symptom of many diseases. WHO experts believe that 90% of all diseases are associated with pain. Patients with chronic pain are five times more likely to seek medical help than other people in the population. It is no coincidence that the first section of the fundamental 10-volume manual on internal medicine, published under the editorship of T. R. Harrison (1993), is devoted to a description of the pathophysiological aspects of pain. Pain is always subjective, and its perception depends on the intensity, nature and localization of the damage, on the nature of the damaging factor, on the circumstances under which the damage occurred, on the psychological state of the person, his individual life experience and social status.

Pain is usually divided into five components:

1. A perceptual component that allows one to determine the location of damage.
2. An emotional-affective component that forms an unpleasant psycho-emotional experience.
3. Autonomic component, reflecting reflex changes in work internal organs and tone of the sympatho-adrenal system.
4. A motor component aimed at eliminating the effects of damaging stimuli.
5. Cognitive component that forms a subjective attitude towards the pain experienced at a given moment based on accumulated experience [Waldman A. V., Ignatov Yu. D., 1976].

Main factors influencing pain perception, are:

1. Age.
2. Constitution.
3. Upbringing.
4. Previous experience.
5. Mood.
6. Anticipation of pain.
7. Fear.
8. Russa.
9. Nationality [Melzack R., 1991].

First of all, the perception of pain depends on the gender of the individual. When presented with painful stimuli of equal intensity in women, the objective indicator of pain (pupil dilation) is more pronounced. Using positron emission tomography, it was found that women experience significantly more pronounced activation of brain structures during painful stimulation. A special study conducted on newborns showed that girls exhibit a more pronounced facial reaction in response to painful stimulation than boys. Age also has a significant impact on pain perception. Clinical observations in most cases indicate that the intensity of pain perception decreases with age. For example, the incidence of silent heart attacks increases in patients over 65 years of age, and the incidence of silent gastric ulcers also increases. However, these phenomena can be explained various features manifestations of pathological processes in old age, and not a decrease in pain perception as such.

When modeling pathological pain by applying capsaicin to the skin, young and elderly people experienced pain and hyperalgesia of the same intensity. However, in the elderly, there was a longer latency period before the onset of pain and before the development of maximum pain intensity. In older people, pain and hyperalgesia last longer than in younger people. It was concluded that in elderly patients, the plasticity of the central nervous system during prolonged painful stimulation is reduced.

Clinically, this results in slower recovery and prolonged increased pain sensitivity following tissue injury. [Reshetnyak V.K., Kukushkin M.L., 2003]. It is also known that ethnic groups living in the northern regions of the planet tolerate pain more easily compared to southerners [Melzack R., 1981]. As mentioned above, pain is a multicomponent phenomenon and its perception depends on many factors. Therefore, it is quite difficult to give a clear, comprehensive definition of pain. The most popular definition is considered to be the one proposed by a group of experts from the International Association for the Study of Pain: “Pain is an unpleasant sensation and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” This definition indicates that the sensation of pain can occur not only when tissue is damaged or in conditions of risk of tissue damage, but even in the absence of any damage.

In the latter case, the determining mechanism of pain is the psycho-emotional state of a person (presence of depression, hysteria or psychosis). In other words, a person’s interpretation of the pain sensation, his emotional reaction and behavior may not correlate with the severity of the injury . Pain can be divided into somatic superficial (in case of damage to the skin), somatic deep (in case of damage to the musculoskeletal system) and visceral. Pain can occur when the structures of the peripheral and/or central nervous systems involved in conducting and analyzing pain signals are damaged. Neuropathic pain is pain that occurs when peripheral nerves are damaged, and when the structures of the central nervous system are damaged, it is called central pain. [Reshetnyak V.K., 1985]. A special group consists of psychogenic pain, which occurs regardless of somatic, visceral or neuronal damage and is determined by psychological and social factors. According to time parameters, acute and chronic pain are distinguished.

Acute pain- this is a new, recent pain that is inextricably linked with the damage that caused it and, as a rule, is a symptom of some disease. This pain disappears when the damage is removed. [Kalyuzhny L.V., 1984].Chronic pain often acquires the status of an independent disease, lasts for a long period of time and the cause that caused this pain in some cases may not be determined. The International Association for the Study of Pain defines it as “pain that continues beyond the normal healing period.” The main difference chronic pain What is important is not the time factor, but qualitatively different neurophysiological, biochemical, psychological and clinical relationships. The formation of chronic pain significantly depends on a complex of psychological factors. Chronic pain is a favorite mask for hidden depression. The close connection between depression and chronic pain is explained by common biochemical mechanisms . The perception of pain is ensured by a complex nociceptive system, which includes a special group of peripheral receptors and central neurons located in many structures of the central nervous system and responding to damaging effects. The hierarchical, multi-level organization of the nociceptive system corresponds to neuropsychological ideas about the dynamic localization of brain functions and rejects the idea of ​​a “pain center” as a specific morphological structure, the removal of which would help eliminate the pain syndrome.

This statement is confirmed by numerous clinical observations indicating that neurosurgical destruction of any of the nociceptive structures in patients suffering from chronic pain syndromes brings only temporary relief. Pain syndromes that arise as a result of activation of nociceptive receptors during injury, inflammation, ischemia, and tissue stretching are classified as somatogenic pain syndromes. Clinically, somatogenic pain syndromes are manifested by the presence of constant pain and/or increased pain sensitivity in the area of ​​damage or inflammation. Patients, as a rule, easily localize such pain and clearly determine its intensity and nature. Over time, the area of ​​increased pain sensitivity can expand and go beyond the damaged tissue. Areas with increased pain sensitivity to damaging stimuli are called zones of hyperalgesia.

There are primary and secondary hyperalgesia. Primary hyperalgesia covers damaged tissues, secondary hyperalgesia is localized outside the damaged area. Psychophysically, areas of primary cutaneous hyperalgesia are characterized by a decrease in pain thresholds and pain tolerance to damaging mechanical and thermal stimuli.

Areas of secondary hyperalgesia have normal pain threshold and reduced pain tolerance to mechanical stimuli only. The pathophysiological basis of primary hyperalgesia is sensitization (increased sensitivity) of nociceptors - A- and C-fibers to the action of damaging stimuli. Sensitization of nociceptors is manifested by a decrease in their activation threshold, an expansion of their receptive fields, an increase in the frequency and duration of discharges in nerve fibers, which leads to an increase in the afferent nociceptive flow [Wall P.D., Melzack R., 1994]. Exogenous or endogenous damage triggers a cascade of pathophysiological processes affecting the entire nociceptive system (from tissue receptors to cortical neurons), as well as a number of other regulatory systems of the body. Exogenous or endogenous damage leads to the release of vasoneuroactive substances leading to the development of inflammation. These vasoneuroactive substances or so-called inflammatory mediators cause not only typical manifestations of inflammation, including a pronounced pain reaction, but also increase the sensitivity of nociceptors to subsequent irritations. There are several types of inflammatory mediators.

I. Plasma inflammatory mediators

1. Kallikriin-kinin system: bradykinin, kallidin
2. Complement components: C2-C4, C3a, C5 - anaphylotoxins, C3b - opsonin, C5-C9 - membrane attack complex
3. System of hemostasis and fibrinolysis: factor XII (Hageman factor), thrombin, fibrinogen, fibrinopeptides, plasmin, etc.

II. Cellular mediators of inflammation

1. Biogenic amines: histamine, serotonin, catecholamines
2. Arachidonic acid derivatives: - prostaglandins (PGE1, PGE2, PGF2?, thromboxane A2, prostacyclin I2), - leukotrienes (LTV4, MRS (A) - slow-reacting substance of anaphylaxis), - chemotactic lipids
3. Granulocyte factors: cationic proteins, neutral and acidic proteases, lysosomal enzymes
4. Chemotaxis factors: neutrophil chemotactic factor, eosinophil chemotactic factor, etc.
5. Oxygen radicals: O2-superoxide, H2O2, NO, OH-hydroxyl group
6. Adhesion molecules: selectins, integrins
7. Cytokines: IL-1, IL-6, tumor necrosis factor, chemokines, interferons, colony-stimulating factor, etc.
8. Nucleotides and nucleosides: ATP, ADP, adenosine
9. Neurotransmitters and neuropeptides: substance P, calcitonin gene-related peptide, neurokinin A, glutamate, aspartate, norepinephrine, acetylcholine.

Currently, more than 30 neurochemical compounds are identified that are involved in the mechanisms of excitation and inhibition of nociceptive neurons in the central nervous system. Among the large group of neurotransmitters, neurohormones and neuromodulators that mediate the conduction of nociceptive signals, they exist as simple molecules - stimulating amino acids - BAK(glutamate, aspartate) and complex high-molecular compounds (substance P, neurokinin A, calcitonin gene-related peptide, etc.).

VACs play an important role in the mechanisms of nociception. Glutamate is contained in more than half of the neurons of the dorsal ganglia and is released under the influence of nociceptive impulses. BACs interact with several subtypes of glutamate receptors. These are primarily ionotropic receptors: NMDA receptors (N-methyl-D-aspartate) and AMPA receptors (β-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid), as well as metalbolotropic glutamate receptors .

When these receptors are activated, Ca 2+ ions intensively enter the cell and its functional activity changes. Persistent hyperexcitability of neurons is formed and hyperalgesia occurs. It must be emphasized that the sensitization of nociceptive neurons resulting from tissue damage can persist for several hours or days even after the cessation of the receipt of nociceptive impulses from the periphery. In other words, if hyperactivation of nociceptive neurons has already occurred, then it does not require additional recharge by impulses from the site of damage. A long-term increase in the excitability of nociceptive neurons is associated with the activation of their genetic apparatus - the expression of early, immediately responding genes, such as c-fos, c-jun, junB and others. In particular, a positive correlation has been demonstrated between the number of fos-positive neurons and the degree of pain. In the mechanisms of activation of proto-oncogenes, an important role is played by Ca 2+ ions. With an increase in the concentration of Ca 2+ ions in the cytosol, due to their increased entry through Ca channels regulated by NMDA receptors, the expression of c-fos, c-jun occurs, the protein products of which are involved in the regulation of long-term excitability of the cell membrane . Recently, nitric oxide (NO), which in the brain plays the role of an atypical extrasynaptic transmitter, has been given importance in the mechanisms of sensitization of nociceptive neurons.

Its small size and lack of charge allow NO to penetrate the plasma membrane and participate in intercellular signal transmission, functionally connecting post- and presynaptic neurons. NO is produced from L-arginine in neurons containing the enzyme NO synthetase. NO is released from cells during NMDA-induced excitation and interacts with the presynaptic terminals of C-afferents, enhancing the release of the excitatory amino acid glutamate and neurokinins from them. [Kukushkin M.L. et al., 2002; Shumatov V.B. et al., 2002]. Nitric oxide plays a key role in inflammatory processes. Local injection of NO synthase inhibitors into the joint effectively blocks nociceptive transmission and inflammation.

All this indicates that nitric oxide is formed in inflamed joints . Kinins are among the most powerful algogenic modulators. They are rapidly formed upon tissue damage and cause most of the effects observed in inflammation: vasodilation, increased vascular permeability, plasma extravasation, cell migration, pain and hyperalgesia. They activate C-fibers, which leads to neurogenic inflammation due to the release of substance P, calcitonin gene-related peptide and other neurotransmitters from nerve terminals.

The direct excitatory effect of bradykinin on sensory nerve endings is mediated by B2 receptors and is associated with activation of membrane phospholipase C. The indirect excitatory effect of bradykinin on the endings of nerve afferents is due to its effect on various tissue elements (endothelial cells, fibroblasts, mast cells, macrophages and neutrophils) and stimulation the formation of inflammatory mediators in them, which, interacting with the corresponding receptors on nerve endings, activate membrane adenylate cyclase. In turn, adenylate cyclase and phospholipase C stimulate the formation of enzymes that phosphorylate ion channel proteins.

The result of phosphorylation of ion channel proteins is a change in the permeability of the membrane for ions, which affects excitability nerve endings and the ability to generate nerve impulses. Bradykinin, acting through B2 receptors, stimulates the formation of arachidonic acid with the subsequent formation of prostaglandins, prostacyclins, thromboxanes and leukotrienes. These substances, having a pronounced independent algogenic effect, in turn, potentiate the ability of histamine, serotonin and bradykinin to sensitize nerve endings. As a result, the release of tachykinins (substance P and neurokinin A) from unmyelinated C-afferents increases, which, increasing vascular permeability, further increases the local concentration of inflammatory mediators [Reshetnyak V.K., Kukushkin M.L., 2001].

The use of glucocorticoids prevents the formation of arachidonic acid by suppressing the activity of phospholipase A2. In its turn, non-steroidal anti-inflammatory drugs (NSAIDs) prevent the formation of cyclic endoperoxides, in particular prostaglandins. Under common name NSAIDs combine substances with different chemical structures that have an inhibitory effect on cyclooxygenase. All NSAIDs have anti-inflammatory, antipyretic and analgesic effects to varying degrees. Unfortunately, almost all NSAIDs have a pronounced side effect. They cause dyspepsia, peptic ulcers and gastrointestinal bleeding. An irreversible decrease in glomerular filtration rate may also occur, leading to interstitial nephritis and acute renal failure. NSAIDs have negative action on microcirculation, can cause bronchospasm [Filatova E. G., Vein A. M., 1999; Chichasova N.V., 2001; Nasonov E.L., 2001].

It is currently known that there are two types of cyclooxygenases. Cyclooxygenase-1 (COX-1) is formed under normal conditions, and cyclooxygenase-2 (COX-2) is formed during inflammation. Currently, the development of effective NSAIDs is aimed at creating selective COX-2 inhibitors, which, unlike non-selective inhibitors, have significantly less pronounced side effects. However, there is evidence that drugs with “balanced” inhibitory activity towards COX-1 and COX-2 may have more pronounced anti-inflammatory and analgesic activity compared to specific COX-2 inhibitors [Nasonov E. L., 2001].

Along with the development of drugs that inhibit COX-1 and COX-2, the search for fundamentally new analgesic drugs is underway. It is assumed that B1 receptors are responsible for chronic inflammation. Antagonists of these receptors significantly reduce the manifestations of inflammation. In addition, bradykinin is involved in the production of diacylglycerol and activates protein kinase C, which, in turn, enhances the sensitization of nerve cells.

Protein kinase C plays a very important role in nociception, and drugs that can inhibit its activity are being sought. . In addition to the synthesis and release of inflammatory mediators, hyperexcitability of spinal nociceptive neurons and increased afferent flow to the central structures of the brain, the activity of the sympathetic nervous system plays a certain role. It has been established that an increase in the sensitivity of the terminals of nociceptive afferents upon activation of postganglionic sympathetic fibers is mediated in two ways. Firstly, due to an increase in vascular permeability in the area of ​​damage and an increase in the concentration of inflammatory mediators (indirect pathway) and, secondly, due to the direct effect of neurotransmitters of the sympathetic nervous system - norepinephrine and adrenaline on a2-adrenergic receptors located on the nociceptor membrane. During inflammation, the so-called “silent” nociceptive neurons are activated, which in the absence of inflammation do not respond to various types of nociceptive stimuli.

Along with an increase in afferent nociceptive flow during inflammation, there is an increase in descending control . This occurs as a result of activation of the antinociceptive system. It is activated when the pain signal reaches the antinociceptive structures of the brain stem, thalamus and cerebral cortex. [Reshetnyak V.K., Kukushkin M.L., 2001]. Activation of the periaqueductal gray matter and the raphe major nucleus causes the release of endorphins and enkephalins, which bind to receptors, triggering a series of physicochemical changes that reduce pain. There are three main types of opiate receptors: ? -, ? - And? -receptors. The largest number of analgesics used exert their effect through interaction with? -receptors. Until recently, it was generally accepted that opioids act exclusively on the nervous system and produce an analgesic effect through interaction with opioid receptors located in the brain and spinal cord. However, opiate receptors and their ligands are found on immune cells , V peripheral nerves , in inflamed tissues . It is now known that 70% of the receptors for endorphin and enkephalins are located in the presynaptic membrane of nociceptors and most often the pain signal is suppressed (before reaching the dorsal horns of the spinal cord).

Does dynorphin activate? -receptors and inhibits interneurons, which leads to the release of GABA, which causes hyperpolarization of dorsal horn cells and inhibits further signal transmission . Opioid receptors are located in the spinal cord mainly around the terminals of C-fibers in the first plate of the dorsal horns . They are synthesized in the small cell bodies of the dorsal ganglia and transported proximally and distally along axons . Opioid receptors are inactive in non-inflamed tissues; after the onset of inflammation, these receptors are activated within a few hours . Synthesis of opiate receptors in neurons of the dorsal horn ganglia also increases during inflammation, but this process, including the time of transport along axons, takes several days . Clinical studies have found that injection of 1 mg of morphine into the knee joint after removal of the meniscus gives a pronounced long-term analgesic effect . Subsequently, the presence of opiate receptors in inflamed synovial tissue was shown .

It should be noted that the ability opiates causing a local analgesic effect when applied to tissue was described back in the 18th century. Thus, the English physician Heberden published a work in 1774 in which he described the positive effect of the application of opium extract in the treatment of hemorrhoidal pain. . Shows good analgesic effect diamorphine with its local application to bedsores and malignant areas of the skin , when removing teeth in conditions of severe inflammation of the surrounding tissue . Antinociceptive effects (occurring within a few minutes after the application of opioids) depend primarily on the blockade of the propagation of action potentials, as well as on a decrease in the release of excitatory mediators, in particular substance P, from nerve endings .Morphine is poorly absorbed through normal skin and is well absorbed through the inflamed area. Therefore, application of morphine to the skin provides only a local analgesic effect and does not act systemically.

IN last years An increasing number of authors are beginning to talk about the advisability of using balanced analgesia, i.e. combined use of NSAIDs and opiate analgesics, which makes it possible to reduce doses and, accordingly, side effects both the first and the second [Ignatov Yu. D., Zaitsev A. A., 2001; Osipova N. A., 1994; Filatova E. G., Vein A. M., 1999; Nasonov E.L., 2001]. Opioids are increasingly being used for arthritic pain [Ignatov Yu. D., Zaitsev A. A., 2001]. In particular, a bolus form of tramadol is currently used for this purpose. This drug is an agonist-antagonist [Mashkovsky M.D., 1993], and therefore the likelihood of physical dependence when adequate doses are used is low. It is known that opioids belonging to the group of agonist-antagonists cause significantly less physical dependence compared to true opiates [Filatova E. G., Vein A. M., 1999].

It is believed that opioids, used in the correct doses, are safer than traditional NSAIDs [Ignatov Yu. D., Zaitsev A. A., 2001]. One of the most important factors in chronic pain is the addition of depression. According to some authors, antidepressants should always be used in the treatment of chronic pain, regardless of its pathogenesis [Filatova E. G., Vein A. M., 1999].

Anti-pain effect antidepressants achieved through three mechanisms. The first is a reduction in depressive symptoms. Second, antidepressants activate serotonic and noradrenergic antinociceptive systems. The third mechanism is that amitriptyline and other tricyclic antidepressants act as NMDA receptor antagonists and interact with the endogenous adenosine system. Thus, a large number of different neurophysiological and neurochemical mechanisms are involved in the pathogenesis of pain syndromes arising from inflammation, which inevitably lead to changes in the psychophysiological status of the patient. Therefore, along with anti-inflammatory and analgesic drugs, for complex pathogenetically based therapy, as a rule, it is necessary to prescribe antidepressants.

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Answers:

Anastasia...

Pain in the lungs when taking a deep breath, sneezing or coughing can appear not only as a result of pathologies respiratory organs or disorders in the pericardial zone, but also as a result of diseases and injuries of the spine, rib cage, with neuralgia. Pain in this case is mainly localized on the right or left side of the chest, can occur with varying frequency, and can be dull or sharp. In this article we will look at the main causes of pain when inhaling, however, to accurately identify their origin and determine effective treatment methods, it is necessary to undergo a medical examination. What causes pain in the lungs when taking a deep breath?
Let's look at the varieties pain manifestations in the lung area with a deep breath.
Acute, piercing, almost “dagger-like” attacks of pain in the chest area, especially at the height of inspiration, accompanied by low-grade fever.
A possible cause of such pain may be pleurisy.
Pleurisy is a disease of the respiratory organs, or more precisely, inflammation of the pleura. In the pleura, due to fibrinous plaque on its surface, the composition of the lubricating secretion between its petals is disrupted, due to this friction of the petals occurs, which causes pain.
Pleurisy is a consequence of complications of various diseases of internal organs, the result surgical interventions and chest injuries. As a rule, pleurisy is secondary, but in the clinical picture, due to acute pain symptoms, often comes to the fore, hiding the primary disease.
Treatment for pleurisy should be prescribed by a specialist. The doctor determines medications only after diagnosing and identifying the exact cause of the disease and, depending on it, prescribes treatment. He may prescribe antibiotics, anti-inflammatory and painkillers, ensure fluid drainage from pleural cavity(drainage is resorted to in case of effusion).
Due to pain in the chest area, the patient has to breathe shallowly. He complains of a feeling of lack of air. It's painful to cough. Pain in the lungs when taking a deep breath is accompanied by chills and high temperature (above 38°C).
These symptoms may indicate pneumonia.
Pneumonia is an infectious inflammation of the lungs. Infection in the lungs, in this case, penetrates the respiratory tract from the environment or through the blood, due to infectious diseases such as influenza, tuberculosis, histoplasmosis.
Pneumonia is treated with antibacterial therapy. It is advisable to carry out treatment on an outpatient basis.
Pain in the lungs that manifests itself acute attack with a deep breath, but is constantly present. The pain is localized in the central part of the chest.
Expressed in the form of tingling. Sometimes accompanied by more rapid breathing, shortness of breath, swelling of the jugular vein, and hemoptysis.
Such pain may indicate pericarditis.
Pericarditis is an inflammation of the serous membrane that covers the heart.
This disease manifests itself by an increase in the volume of pericardial fluid in the pericardial cavity, thereby increasing the pressure in it and squeezing the heart from the outside and complicating its work. “Dry” pericarditis is characterized by a slight increase in fluid in the pericardial cavity and forms adhesions that interfere with the normal movement of the heart.
Secondary. It occurs as a complication of other (infectious, autoimmune, tumor) diseases.
Neutralized by curing the underlying disease. To drain excess fluid from the pericardial cavity, I prescribe diuretics.
Acute stabbing, burning, “shooting” pain in the lungs when taking a deep breath, manifesting itself along the ribs and accompanied by increased sensitivity of the skin.
The described symptoms usually characterize the process of intercostal neuralgia or myalgia.
Intercostal neuralgia is an inflammatory process, pinching or other irritation of nerve endings

Dimon Dimonov

pneumonia

Marina Nikolaeva

Too bad, call a doctor.

What temperature is observed during pneumonia?

Many people are interested in pneumonia, what temperature they may have and whether the course of the disease is possible without fever. To answer these questions, it is necessary to understand the mechanism of development of pneumonia and the forms of its course.

Modern medicine understands pneumonia as an acute infectious disease characterized by an inflammatory process in the lungs. Its cause is most often bacteria (pneumococcus, staphylococcus, Klebsiella), less often viruses (influenza, rhinovirus), fungal microorganisms (candida, aspergillus).

Based on the prevalence of inflammation, the following types of pneumonia can be distinguished:

1. Focal (or bronchopneumonia): inflammation is observed in the form of one or several foci, covering the smallest fragments of the lung (lobules, their groups).
2. Segmental: the disease affects a larger area of ​​lung tissue (segment).
3. Lobar (or lobar): infectious process spreads on lung lobe, consisting of several segments, or several shares.
4. Confluent: many separate foci of inflammation, merging, affect a large area of ​​lung tissue.
5. Total: the inflammatory process covers the entire lung.

In addition, the disease can be unilateral (inflammation affects one lung) or bilateral (both lungs are affected). All these features determine the temperature during pneumonia.

High temperature (39 – 40°C)

A temperature of 39–40°C is observed in severe forms of pneumonia, when the inflammatory process covers a significant area of ​​the lung. Fever is characteristic of lobar, confluent, total pneumonia, and is also characteristic of bilateral pneumonia.

Thus, the lobar form, the causative agent of which is pneumococcus, begins abruptly, with a sudden severe chill, lasting from several minutes to 2 - 3 hours. The temperature quickly rises to 39–40°C and is constant, remaining for 7–10 days.

Daily fluctuations in body temperature do not exceed 0.5 – 1°C. With timely and adequate antibacterial treatment, the period of fever can be reduced to 3–4 days.

Under the influence of temperature intoxication, the patient feels weak and weak. When pleural tissue is involved in the inflammatory process, disturbing pain appears from the affected lung, breathing becomes difficult and becomes more frequent. A person complains of a dry, raw cough, which after a few days becomes wet and is accompanied by sputum streaked with blood.

If during the day the temperature during pneumonia fluctuates by 1 - 2°C and is accompanied by chills with each increase, one can suspect septic and purulent-destructive complications of pneumonia: sepsis, lung abscess, pleural empyema, etc.

Febrile temperature (38 – 39°C)

This temperature most often accompanies focal and segmental pneumonia. The focal form sometimes occurs as an independent disease, but in most cases it is a complication of previous bronchitis, tracheitis, or acute respiratory viral infection. Reduced immunity leads to the fact that the inflammatory process of the bronchial tissue spreads to the pulmonary tissue, affecting one or more lobules.

At an early stage of the disease, ARVI symptoms are observed; the temperature can be either normal or low-grade. However, on the 5th – 7th day of illness, during treatment, the temperature begins to rise and remains at 38 – 39°C. The cough intensifies, breathing becomes rapid. The patient feels the consequences of temperature intoxication: fatigue, weakness, headache. These symptoms indicate the addition of pneumonia as a complication of the disease. Therefore, if the fever during ARVI persists and does not fall for more than 5-7 days, it is necessary to seek medical help.

Low-grade fever (37 – 38°C)

Low-grade fever with pneumonia is observed in a focal form, as well as with decreased immunity, in elderly, weakened people. There may be daily fluctuations in temperature: from normal to elevated. Patients complain of general weakness, sweating, chest pain, cough, and lack of appetite.

Normal temperature

There are frequent cases of latent pneumonia, when the inflammatory process occurs without fever. This form of the disease is extremely dangerous, since the lack of adequate treatment can lead to chronic pneumonia or even death.

Asymptomatic pneumonia occurs against a background of weakened immunity, when the body does not have the strength to fight the infection. Other typical manifestations of the disease may be absent: cough, pain. This course of the disease often occurs in very young children, whose immune system is still very weak, as well as in elderly and weakened people. In this case, you can suspect pneumonia based on the following symptoms:

• lethargy;
• drowsiness;
• general malaise;
• sweating;
• lack of appetite.

If these symptoms persist for a week or more, you should not postpone your visit to the doctor. Ignoring symptoms of illness or self-medicating can be very dangerous.

Diagnosis of disease by temperature

We found out what temperature is most often observed during pneumonia.

Often, pneumonia occurs with an increase in temperature, but there are cases of asymptomatic disease. Only a doctor can make a correct diagnosis in this case by examining blood tests and X-ray results.

With adequately prescribed therapy, the temperature drops on days 3–5 of illness. If the fever does not go away despite treatment, this may be a reason to change the drug or treatment regimen.

Drinking plenty of fluids: water, teas, fruit drinks, juices can alleviate temperature intoxication during illness. They promote increased sweating and a subsequent decrease in temperature.
Antipyretic drugs for pneumonia can only be used after consultation with your doctor.

respiratoria.ru

Do your lungs hurt? What to do?

Answers:

Arimanta

The lungs themselves rarely hurt. The most common complaint with lung disease is cough. If something hurts in the chest and it is associated with breathing, then it looks like pleurisy (inflammation of the lining of the lung). If it is not related to breathing, then it may be a disease of the stomach, heart, esophagus, trachea. In this case, it is best to do an X-ray of the lungs and an electrocardiogram to rule out heart disease. And then with the results he will contact a therapist for interpretation, diagnosis and treatment.

***SKARLETT***

Svetochka

Urgently see a pulmatologist, you most likely have pneumonia!

Sasha

It's time to see a doctor, and it's been a while. Take more care of yourself.

Nataly

the lungs cannot hurt, they have no nerves

Lydia S.

No pain is felt in the lungs. Maybe you have intercostal neuralgia, when everything pierces when you inhale or exhale? But see the doctor! urgently! Don't joke about it!

Marina Yakovleva

Pain in the lungs. As a rule, the lungs themselves do not hurt, even with pneumonia. If you feel pain in the chest area, there may be several reasons: intercostal neuralgia, osteochondrosis, problems with the thoracic spine. In some cases, the pain may be due to pleurisy (the pleura is the membrane that covers the lungs), but then there must be a high temperature.
In any case, you need to take a chest x-ray and consult a therapist.

Tanyushka Batyuk

I read everything written above. Good answers, I won’t hide it, but going to the doctors... My relative reached group 2 and asthma. And I was cured after 2 months of drinking Noni juice. Now my family drinks it and doesn’t get sick. If interested, write. I'll tell you in more detail. I invite everyone!! ! Health to everyone.

Vitaly Kulikov

I was told at the 70th Central Clinical Hospital that my lungs don’t hurt, there are no/few nerve endings, nothing to hurt.
this is said by those who have not had the disease, that is, theoretically there are few endings (although the central nervous system is somewhere around there, and its key areas are also there)
different gradations of pain - such a state when “not coughing” there is pain (of course it doesn’t hurt mortally, like when wounded - they think that pain is when there is a pain syndrome and they die from pain - no, it’s not mortal pain, it’s just not pleasant) but there is no full exhalation - sharply on flurry, pneumonia is nearby.
secondly, when you cough so much that you piss, it’s either COPD or asthma, the patient also doesn’t always consider it appropriate to give details, and the doctor will first work on the classic “go away” and then immediately put him on prendisalone
and yes, there is a stereotype that “the lungs don’t hurt”

A person who is at least a little familiar with physiology and anatomy knows that there are practically no nerve endings in the lungs - therefore, it is quite difficult to determine the presence of pain in them. But how then can you understand when you feel pain in the chest, is it your lungs that hurt or something else? There are certain additional symptoms that indicate lung problems.

Inflammatory diseases

Most often, pain in the lungs is concentrated in the bronchi, pleura or trachea, so to determine them you need to be able to find out the nature of the pain. If there is pain on one side and discomfort that increases with coughing, most likely the problem is ordinary pleurisy. You can confirm the diagnosis if you lie on the side that hurts - this will limit the mobility of the pleura, and the pain will gradually begin to subside. Dry pleurisy must be treated immediately, since it is prone to transition to exudative pleurisy, which is characterized by a dry, hysterical cough that stops only after the accumulation of exudate.

Exudative pleurisy is a sign of such a serious disease as tuberculosis, therefore, when its symptoms appear, measures must be taken immediately.

If the pain occurs due to severe infectious disease– for example, pneumonia, painful sensations in the chest accompanied by chills and fever. In addition, pneumonia is characterized by difficulty breathing, redness of the face, blue lips and other symptoms characteristic of an infectious infection. Pneumonia usually begins with a painful, dry cough, which later turns into a wet cough, with expectoration of blood and sputum. If the above symptoms appear, you should immediately go to the hospital and undergo inpatient treatment.

Other lung diseases

Pain caused by other lung diseases is less common than pneumonia and pleurisy. It can usually be caused by pneumothorax, a spontaneous disease that occurs as a result of lung tumors or various injuries. The main symptom of pneumothorax is acute pain in the chest, which increases with breathing or increased exercise. This pain continues for a long time, accompanied by a dry cough, pallor, severe weakness, low blood pressure, rapid heartbeat, sweating and difficulty breathing.

Basic distinctive feature pneumothorax is the patient's attempt to sit up to relieve painful sensations in the chest.

Pain of a different origin in the lungs can be caused by a wide variety of reasons, including diseases of other organs, pain from which radiates to the lungs and forces a person to suspect a non-existent problem. To accurately determine the cause of pain in the lungs, it is necessary to do fluorography or computed tomography.

A large number of different neurophysiological and neurochemical mechanisms are involved in the pathogenesis of pain syndromes arising from inflammation, which inevitably lead to changes in the psychophysiological status of the patient. Exogenous or endogenous damage triggers a cascade of pathophysiological processes affecting the entire nociceptive system (from tissue receptors to cortical neurons), as well as a number of other regulatory systems of the body. Exogenous or endogenous damage leads to the release of vasoneuroactive substances leading to the development of inflammation. These vasoneuroactive substances or so-called inflammatory mediators cause not only typical manifestations of inflammation, including a pronounced pain reaction, but also increase the sensitivity of nociceptors to subsequent irritations.

There are several types of inflammatory mediators that increase the sensitivity of nociceptors to irritation.

. Plasma mediators of inflammation 1. Kallikriin-kinin system: bradykinin, kallidin 2. Complement components: C2-C4, C3a, C5 - anaphylotoxins, C3b - opsonin, C5-C9 - membrane attack complex 3. Hemostasis and fibrinolysis system: coagulation factor XII (Hageman factor), thrombin, fibrinogen, fibrinopeptides, plasmin, etc.

Cellular mediators of inflammation 1. Biogenic amines: histamine, serotonin, catecholamines 2. Arachidonic acid derivatives:

– prostaglandins (PGE1, PGE2, PGF2α, thromboxane A2, prostacyclin I2), leukotrienes (LTV4, MRS (A) - slow-reacting substance of anaphylaxis), chemotactic lipids 3. Granulocyte factors: cationic proteins, neutral and acidic proteases, lysosomal enzymes 4. Chemotaxis factors: neutrophil chemotactic factor, eosinophil chemotactic factor, etc. 5. Oxygen radicals: O 2 -superoxide, H 2 O 2, NO, OH-hydroxyl group 6. Adhesive molecules: selectins, integrins 7. Cytokines: IL-1, IL-6, tumor necrosis factor, chemokines, interferons, colony-stimulating factor, etc. 8. Nucleotides and nucleosides: ATP, ADP, adenosine 9. Neurotransmitters and neuropeptides: substance P, calcitonin gene-related peptide, neurokinin A, glutamate, aspartate, norepinephrine, acetylcholine.

Currently, more than 30 neurochemical compounds are identified that are involved in the mechanisms of excitation and inhibition of nociceptive neurons in the central nervous system. Among the large group of neurotransmitters, neurohormones and neuromodulators that mediate the conduction of nociceptive signals, there are both simple molecules - excitatory amino acids - BAK (glutamate, aspartate), and complex high-molecular compounds (substance P, neurokinin A, calcitonin gene-related peptide, etc.) . VACs play an important role in the mechanisms of nociception. Upon activation of ionotropic receptors: NMDA receptors , AMPA receptors and metallobolotropic glutamate receptors cause an intensive entry of Ca 2+ ions into the cell and a change in its functional activity. Persistent hyperexcitability of neurons is formed and hyperalgesia occurs.

Recently, important importance has been attached to the mechanisms of sensitization of nociceptive neurons. nitric oxide(NO), which in the brain acts as an atypical extrasynaptic transmitter. Nitric oxide plays a key role in inflammatory processes. Local injection of NO synthase inhibitors into the joint effectively blocks nociceptive transmission and inflammation.

Kinins are one of the most powerful algogenic modulators. The direct excitatory effect of bradykinin on sensory nerve endings is mediated by B2 receptors and is associated with activation of membrane phospholipase C. The indirect excitatory effect of bradykinin on the endings of nerve afferents is due to its effect on various tissue elements (endothelial cells, fibroblasts, mast cells, macrophages and neutrophils) and stimulation the formation of inflammatory mediators in them, which, interacting with the corresponding receptors on nerve endings, activate membrane adenylate cyclase. In turn, adenylate cyclase and phospholipase C stimulate the formation of enzymes that phosphorylate ion channel proteins. The result of phosphorylation of ion channel proteins is a change in the permeability of the membrane to ions, which affects the excitability of nerve endings and the ability to generate nerve impulses.