The inner mucosa of the respiratory tract is lined with epithelium. Respiratory system. Metabolic lung function


benign tumors. The most common benign tumors of the nasopharynx are papilloma and juvenile (juvenile) angiofibroma.

Papilloma more often localized on the posterior surface of the soft palate, less often on the lateral and posterior walls of the nasopharynx. Its appearance resembles small-tuberous growths on a wide base, the tumor has a soft texture. In childhood, nasopharyngeal papillomas are more often combined with pathology of the larynx; in adults, single forms can occur.

Surgical treatment. Papillomas can be removed using an ultrasonic disintegrator or a laser beam.

Juvenile angiofibroma- one of the most common tumors of the nasopharynx, histologically benign, has a locally destructive, progressive growth and is prone to recurrence without the formation of metastases.

This tumor develops in boys and young men from 14 to 25 years old, is located on the roof of the nasopharynx. It has a spherical surface, bluish-pink color, a wide base and a very dense texture.

The clinical picture is quite characteristic. The tumor grows relatively quickly. Nasal breathing progressively worsens, along with which hearing gradually decreases in one, less often in both ears. Angiofibromas are characterized by epistaxis. As the tumor grows, the intensity and frequency of bleeding increase. From the nasopharynx, angiofibroma penetrates into the nasal cavity and paranasal sinuses, primarily into the sinus of the sphenoid bone. The tumor can cause destruction of the base of the skull and penetrate into its cavity. At the same time, a headache joins the listed symptoms.

Differential diagnosis should be carried out with adenoid growths, papilloma, cancer, fibrosarcoma.

Treatment surgical. The main difficulty that arises when performing operations for angiofibroma is profuse, life-threatening bleeding of the patient. To prevent this complication, the external carotid artery is preliminarily ligated on the side of the tumor (sometimes both external carotid arteries). The tumor is removed from a wide external approach: a Moore incision is made with a dissection of the upper lip along the midline (Fig. 1d).

Malignant tumors. This pathology of the nasopharynx is characterized by a wide age range, although the disease predominates in the elderly. At a young age, sarcomas and lyphoepitheliomas are more common. In elderly and elderly patients, cancer predominates. Men get sick 3-4 times more often than women.

According to the histological structure, malignant tumors of the nasal part of the pharynx are divided into epithelial and non-epithelial neoplasms. Ratio cancer and sarcomas, according to most modern authors, is 2:1. The most common epithelial tumors of the nasopharynx are squamous and transitional cell carcinomas.

Nasopharyngeal cancer most often has the form of an asymmetric infiltrate, localized on the back or side walls, characterized by an endophytic-ulcerative form of the nose.

clinical picture. Symptoms of malignant tumors of the nasopharynx can be divided into early (nasal) and late (Fig. 2).

Early symptoms include - a gradually increasing violation of nasal breathing, a violation of the auditory function (according to the conductive type) on the side of the lesion, nosebleeds, concomitant sinusitis, headache.

Late symptoms indicate damage to the nervous structures.

When the tumor penetrates into the middle cranial fossa, III, IV, VI pairs of cranial nerves are affected and manifested by the following symptoms: ptosis, descending strabismus, impaired abduction of the eyeball outward, exophthalmos, diplopia. In severe cases - complete immobility - ophthalmoplegia.

When penetrating into the anterior cranial fossa, the second pair of cranial nerves (n. opticus) is affected - decreased vision, loss of visual fields.

The penetration of the pathological process into the pterygopalatine fossa is characterized by Troter's syndrome - neuralgia in the temporo-facial region, paresis of the soft palate, hypoesthesia or anesthesia of the cheek on the side of the lesion.

With damage to the parapharyngeal space, signs of damage to the IX, X, XI, XII pairs of cranial nerves appear - tongue deviation first to the healthy side, then to the diseased side (XII), impaired laryngeal mobility (X), prolapse of the soft palate (IX), prolapse of the shoulder on the affected side (XI).

Fig.2. Scheme of the spread of malignant tumors of the nasopharynx (Abyzov R.A., 2004)

Metastases in regional cervical nodes, according to most authors, are often the only sign of a malignant tumor of the nasopharynx at the first visit of the patient. It should be noted that regional metastasis is observed equally often in the case of cancer and sarcoma. Most often, regional metastases appear in the upper jugular lymph node under the digastric muscle and in the lymphadenoid tissue of the retropharyngeal space. In addition, the submandibular, mental, supraclavicular lymph nodes are affected, which is due to massive invasion of the jugular lymph nodes. Often, metastases occur in the lymph nodes of the opposite side, which is associated with the presence of numerous anastomoses between the lymphatic vessels of the neck.

Treatment. Among all ENT oncology, the nasopharynx remains a “non grata” (inviolable) organ for surgical intervention. This is due to the anatomical structure of this organ, the growth of neoplasms towards the cranial cavity or into the parapharyngeal space with the destruction of surrounding tissues, as well as early and regional metastasis. Radiation and drug (chemotherapeutic) treatment remain the main methods.

Experts cannot exactly name the cause of the development of such a disease as angiofibroma. There are several theories that are used to explain the causes of pathology:

  • hormonal theory.

Frequent diagnosis of the disease in children in adolescence suggested that a disturbed hormonal background could become a certain risk factor. However, information regarding this assumption is contradictory: some scientists do not admit the possibility of a negative impact of hormonal imbalance, while others confirm the involvement of the function of the gonads. Experts have not yet made a final conclusion.

  • genetic theory.

This assumption is considered one of the most common. Information about the complete or incomplete absence or violation of Y and X chromosomes in the cells of the neoplasm serves as confirmation. These conclusions are not final and require further research.

  • Theory of the influence of age.

Some experts tend to consider the disease as a result of age-related changes in the body.

In addition, there are suggestions about the influence of certain factors on the development of the disease.

Risk factors for developing angiofibroma may include:

  • injuries of the face, head, nose, etc.;
  • inflammatory diseases, especially inflammation with a chronic course (for example, chronic sinusitis, etc.);
  • the presence of hazards, poor ecology, unacceptable lifestyle, etc.

Pathogenesis

Angiofibroma can occur at almost any age, in people of any gender and race.

The most common neoplasm of the nasopharynx: angiofibroma develops on the basis of the pharyngeal main fascia and is a basal or basosphenoidal type of tumor. The proliferation covers the surface of the sphenoid bone and/or the area of ​​the posterior ethmoid cells (sphenoethmoidal appearance).

In some cases, the disease begins from the area of ​​the pterygopalatine fossa, spreading into the nasal cavity and into the space behind the jaw. This type of angiofibroma growth is diagnosed in the pterygo-maxillary variant of tumor development.

This neoplasm is considered to be benign, although it often has rapid growth, affecting adjacent tissues, cavities, and sinuses. Angiofibroma, which has grown into the cavity of the cranium, is especially dangerous.

Symptoms of angiofibroma

Angiofibroma outwardly resembles a small (3-15 mm) single nodule, which has clearly defined contours and an elastic structure. The color of the formation can vary from pinkish-yellow to brown.

The nodule, as a rule, rises slightly above the surrounding tissues.

In some cases, the nodule has a rich capillary network and has a translucent structure: this can be seen with a microscope.

The tumor is found in more cases on the mucous tissues of the upper respiratory tract, or on the upper or lower extremities, less often on organs (for example, the kidneys).

The first signs of a neoplasm depend on its location. For example, if the nasopharynx is affected, the patient complains of difficulty in nasal breathing, up to its complete absence. Congestion can occur only on one side, aggravated gradually. At the same time, no drops for the nose do not remove this problem.

Over time, snoring appears (even when awake), a feeling of dryness in the throat, one or two-sided hearing loss. There may be frequent pain in the head, bleeding from the nose of a spontaneous nature.

Angiofibroma at the initial stage is not always manifested by changes in the blood picture. In most patients, signs of anemia - a decrease in the number of red blood cells and hemoglobin - are already detected at later pathological stages.

Angiofibroma in a child may resemble signs of adenoids, so in childhood it is customary to differentiate these pathologies.

In children, non-ossifying fibromas and metaphyseal defects are most often diagnosed; these are relatively common skeletal pathologies in pediatric patients.

As the tumor grows, the patient's well-being worsens. Sleep becomes restless, appetite is disturbed, facial features change (deformation and asymmetry are possible).

stages

Juvenile angiofibroma is conditionally divided into several stages:

  1. The neoplasm has a limited growth that does not extend beyond the nasal cavity.
  2. The neoplasm grows into the pterygopalatine fossa or nasal sinuses.
  3. The tumor spreads in the orbit or infratemporal fossa without intracranial growth (stage) or with extradural growth (stage).
  4. The tumor is characterized by intradural growth without involvement of the cavernous sinus, pituitary gland, or optic chiasm (stage), or with the involvement of these areas (stage).

Forms

The species classification of the disease is associated with the localization of the tumor, as well as with some of its structural and pathogenetic features.

  • Angiofibroma of the nasopharynx is a benign formation that consists of vascular and connective tissue and develops in the nasopharyngeal cavity. Most often, a disease such as angiofibroma of the nose is found in adolescent boys, so it is also called the term "juvenile, juvenile angiofibroma", this is the most common neoplasm in pediatric patients.
  • Angiofibroma of the skin is often mistaken for a hemangioma: it is a connective tissue formation that looks like a wart. Such a tumor in most cases is round, has a base and penetrates deep into the skin. It is most often found on the upper and lower extremities, as well as in the neck and face. Mostly women 30-40 years old are ill.
  • Angiofibroma of the larynx is a benign formation that occupies the region of the vocal cords. A similar term for the disease is vocal cord angiofibroma. The tumor has a reddish or bluish tint, has an uneven structure and is located on the leg. The first signs of the disease are the appearance of characteristic hoarseness up to the complete loss of voice.
  • Angiofibromas of the face are located in different parts of it. You can find them at any age. The main clinical symptom of the disease is the sudden appearance of a small dense or elastic growth. There are usually no other symptoms. If the tumor is constantly touched and damaged, then it can bleed and grow rapidly. Often, education is found in the nasal or ear cavities, on the eyelids.
  • Angiofibromas of the face in tuberous sclerosis are typical manifestations of this pathology. Tuberous sclerosis is a hereditary neuroectodermal disease, the main features of which are convulsive seizures, mental retardation, and the appearance of neoplasms like angiofibromas. Neoplasms are found in more than half of patients suffering from tuberous sclerosis. You can find them already after 4 years of age.
  • Angiofibroma of the skull base is the rarest and, at the same time, the most severe form of the disease, in which a benign formation is formed in the bone structure of the skull base. The disease is difficult to diagnose at an early stage, due to its similarity with hypertrophic and inflammatory pathologies of the nasal and pharyngeal region. Angiofibroma of this type is prone to rapid growth with the destruction of cranial bones and spread to adjacent anatomical brain structures. The overwhelming majority of boys and young people aged 7-25 are ill.
  • Angiofibroma of soft tissues often develops in patients on the skin, on the mammary glands, and tendons. Affects predominantly soft tissues on the limbs, in the trunk, face or neck. In some cases, tumor processes also develop in the area of ​​internal organs - in the uterus, ovaries, lungs, and mammary glands.
  • Angiofibroma of the kidney is a benign formation that can proceed for a long time without showing any symptoms. Rarely, the disease is detected due to the appearance of pain in the kidney. The disease is cured surgically: with a small size of the neoplasm, dynamic monitoring of the tumor is possible.

Complications and consequences

In itself, such a neoplasm as angiofibroma belongs to a number of benign ones, and only in extremely rare cases can the disease become malignant.

However, tumor development often proceeds rapidly. A rapid increase in education can provoke the destruction of nearby structures: even dense tissues, such as bones, are damaged. Therefore, rapid tumor growth can cause prolonged and massive bleeding (often recurring), deformation of the facial part, disorders and respiratory visual function. In order to prevent complications of angiofibroma, it is very important to determine the presence of a neoplasm in a timely manner and begin treatment.

Diagnosis of angiofibroma

Diagnosis of the disease has its own characteristics. First of all, the doctor during the examination will pay attention to the number of pathological formations, their nature. The patient will be asked questions about the presence of such pathologies in family members and relatives, about the detection of malignant diseases in loved ones, about possible disorders of the central nervous system.

If multiple tumor foci are detected, then the patient is recommended to be screened for tuberculous sclerosis or MEN I.

Blood tests will indicate the presence of anemia and inflammation in the body. Thus, a decrease in the level of hemoglobin to 80 g / liter and erythrocytes to 2.4 per 10¹² / l can be observed. Blood biochemistry often demonstrates a decrease in total protein, albumin, and an increase in ALT, AST, and alkaline phosphatase.

Tissue biopsy - the study of part of the tissue with a microscope, will allow you to accurately determine the good quality of the neoplasm.

In addition, the doctor often prescribes a blood test for specific markers of tumors to rule out malignancy.

Additional instrumental diagnostics often includes fibroscopy or endoscopy. Such procedures are done using a special device - an endoscope, which will allow you to detect and examine the tumor in cavities, for example, in the nasopharynx. This method will help to assess the surface state of the tumor, visualize the vascular network, and determine the presence of an inflammatory reaction.

Angiofibroma treatment

In the vast majority of cases, patients with angiofibromas are prescribed surgical treatment. The volume and type of surgical intervention is selected taking into account the stage and localization of the pathological focus.

If the tumor process has a significant spread and is penetrated by a large number of vessels, then it may be necessary to prepare the patient in advance. This is done to reduce the risk of bleeding during and after surgery.

Treatment may include the following methods:

  • X-ray endovascular occlusion - is used when it is impossible to carry out a full-fledged surgical intervention, as the initial stage of radiation therapy. The application of the method allows to reduce the volume of intraoperative blood loss.
  • Radiation treatment - helps in about 50% of cases of angiofibroma, but can be accompanied by a large number of complications. For this reason, it is used only when it is impossible to carry out a full-fledged surgical intervention.

Medications

Drug treatment is aimed at eliminating the main painful signs of angiofibroma, as well as at alleviating and prolonging the life of patients.

  • When pain occurs, it is recommended to take Baralgin or No-shpu 1-2 tab. up to three times a day. Duration of admission - from one to four weeks.
  • To improve the functioning of organs and strengthen blood vessels, Stimol is prescribed in the amount of 1 package twice a day, as well as multivitamin complexes - for example, Duovit 2 tab. daily for 4 weeks, or Vitrum 1 tab. daily for 4-12 weeks.

Combination chemotherapy is used as needed on an individual basis. Can be offered:

  • a combination of Adriamycin, Sarcolysin and Vincristine;
  • a combination of Vincristine, Decarbazine, Adriamycin, Cyclophosphamide.

For example, such treatment may be applied before and/or after surgery.

vitamins

High-quality treatment of angiofibroma cannot be imagined without vitamin therapy. Eating certain vitamins does not affect tumor growth in any way, but it helps strengthen blood vessels, prevent anemia and normalize the function of the immune system.

  • Vitamin A will serve as a prevention of secondary infection, improve tissue turgor and speed up recovery. This vitamin can be obtained by eating plant foods, or purchased in pharmacies in capsules with an oily vitamin solution.
  • Tocopherol prevents the formation of blood clots in the vessels, rejuvenates and renews tissues. The drug is available at any pharmacy without a prescription, and is also present in products such as butter and sunflower oil, nuts, seeds and milk.
  • Ascorbic acid is involved in the regulation of regenerative reactions in the body, normalizes the production of hormones. Ascorbic acid can be obtained from vitamin preparations or from food products, which include berries, apples, kiwi, citrus fruits, greens, cabbage.
  • B vitamins regulate neuroendocrine function. They can be obtained in sufficient quantities by eating meat products, nuts, milk.
  • Vitamin K improves blood clotting, eliminates minor bleeding. Vitamin is part of many multivitamin products and monopreparations.

Physiotherapy treatment

With angiofibroma, physiotherapy can be prescribed, which enhances the effect of drugs on the tumor. Often, oncode-destructive effects are prescribed: photodynamics, high-intensity laser therapy, decimeter therapy, ultrasound. At the same time, it is possible to use cytolytic techniques, which include, in particular, cytostatic electrophoresis.

Comprehensive treatment of patients who underwent surgery to remove such a neoplasm as angiofibroma includes the following physiotherapeutic methods:

  • immunosuppressive procedures (electrophoresis with immunosuppressants);
  • chemo-modifying procedures (low-frequency magnetic therapy).

To normalize autonomic disorders, electrosleep therapy, transcranial electroanalgesia, low-frequency magnetic therapy, and galvanization are used.

After complete removal of angiofibroma, contraindications to physiotherapy are of a general nature.

Alternative treatment

To get rid of the tumor - angiofibroma, it is recommended to pay attention to the diet: certain products can help stop the spread of the disease.

  • Tomatoes are frequent guests on our table. Experts advise eating five large tomatoes daily, as well as adding tomato paste or juice to meals.
  • It is recommended to mix beetroot juice with honey in equal parts, and drink it three times a day before meals, 100 ml each.
  • Walnuts should be crushed together with the shell, pour boiling water over, insist for fifteen minutes. Proportion - 300 g of nuts per 1 liter of water. The infusion should be taken three times a day for 1 tbsp. l.

Angiofibroma grows quite quickly, but the clinical manifestations do not immediately begin to disturb patients.

Increasing difficulty in nasal breathing. Hyposmia and anosmia (decrease and disappearance of the sense of smell). Nasal. Hearing loss in one or both ears. nosebleeds; as the disease progresses, their intensity and frequency increase. Headache. Deformation of the facial skeleton (in the later stages leads to displacement of surrounding tissues).

When the tumor spreads to the eye area, visual impairment is possible (decreased visual acuity, exophthalmos (displacement of the eyeball forward (bulging eyes), sometimes with a shift to the side), limitation of eyeball mobility, double vision (diplopia), etc.).

Forms

There are three forms of angiofibroma depending on the direction of its growth:

the tumor can begin its growth on the vault of the nasopharynx and grow from there to the base of the skull; a tumor from the body of the sphenoid bone grows into the ethmoid labyrinth, sinuses, nasal cavity and orbit; angiofibroma can also begin its growth in the region of the pterygopalatine fossa and grow into the nasal cavity.

The type of deformation of the surrounding tissues depends on the direction of growth of angiofibroma, for example, angiofibroma growing in the direction of the orbit will cause a displacement of the eyeball, its growth can also disrupt the blood supply to various parts of the brain, compress nerve formations.

There is a clinical and anatomical classification of juvenile angiofibroma, in which two forms are distinguished:

basal-common: it is characterized by such clinical symptoms as difficulty in nasal breathing, anosmia (lack of odor recognition), nasality, hearing impairment (hearing loss in one, less often both ears), inflammation in the paranasal sinuses, signs of compression of II and III branches trigeminal nerve, exophthalmos (bulging eyes) and diplopia (double vision); intracranial-common: with it, the picture is supplemented by signs of damage to the I branch of the trigeminal nerve, swelling of the optic nerve head, swelling of the cheek from the side of the spread of the tumor, damage to the II, III and VI pairs of cranial nerves - ptosis (omission of the eyelid), swelling of the eyelid, decreased vision.

Classification by stages:

Stage I - the tumor is limited to the nasal cavity; Stage II - the spread of the tumor into the pterygopalatine fossa or maxillary, ethmoid or sphenoid sinuses; Stage IIIa - tumor spread into the orbit or infratemporal fossa without intracranial growth; IIIb stage - stage IIIa with spread outside the dura mater; IVa stage - the spread of the tumor under the dura mater without involving the cavernous sinus (a large vein at the base of the brain), the pituitary gland (the coordinator of the activity of all endocrine glands of the body) and the optic chiasm (the area where the optic nerves cross); IVb stage - involvement in the tumor process of the cavernous sinus, pituitary gland or optic chiasm.

The reasons

It is believed that this tumor is a consequence of an abnormal development in the embryonic period.

LookMedBook reminds you that the sooner you seek help from a specialist, the more chances you have to maintain your health and reduce the risk of complications:

Diagnostics

Analysis of complaints and anamnesis of the disease: progressive difficulty in nasal breathing; hyposmia and anosmia (reduction or complete absence of smell); nasality; hearing loss in one or both ears; nosebleeds; headache; visual disturbances (decreased visual acuity, bulging eyes, double vision, etc.). Anterior and posterior rhinoscopy allows you to see a rounded, smooth or bumpy surface of the tumor of a bright red or cyanotic color; during palpation with a probe, the tumor begins to bleed. Radiography (sometimes does not allow you to accurately determine the size of the tumor and the space it occupies). Computed tomography is a more accurate method for determining the boundaries of the tumor and its size. Nasal endoscopy or fibroscopy. Endoscopy is performed after local anesthesia, which saves the patient from discomfort during the procedure. The doctor inserts the endoscope into the nasal cavity through the nostril and examines the nasal cavity. Taking a biopsy (a tumor site for further histological examination) is accompanied by a high risk of bleeding, therefore it is not always used. Angiography allows you to visualize the relationship of the tumor with the carotid artery system (important when planning surgical treatment). A complete blood count will show anemia due to frequent nosebleeds. It is also possible to consult an oncologist.

Treatment of angiofibroma of the nasopharynx of youth

Treatment is surgical only. It is carried out under endoscopic control (an endoscope is an “optical device”, which is used for a more detailed examination of distant parts of the nasal cavity, provides visual control of the operation).

Operation types:

operations using access to the tumor through natural routes (through the nose or mouth); surgery using sparing access through the maxillary sinus and nasal cavity (with an incision under the lip); surgery using extended access through the maxillary sinus and nasal cavity (with a facial incision); operation using access through the sky.

Before surgery, to reduce the risk of bleeding, it is desirable to carry out embolization (artificial blockage) of the tumor vessels.

Complications and consequences

The development of profuse intractable bleeding and irreversible neurological complications (for example, loss of visual fields) when the tumor grows into the cranial cavity. Spread of the tumor into the nasal cavity. Anemia as a result of frequent heavy nosebleeds (a condition in which there is a reduced content of red blood cells in the bloodstream or an insufficient amount of hemoglobin in them).

Prevention of angiofibroma of the nasopharynx of youth

Prevention of this disease does not exist. When the first signs appear (increasing difficulty in nasal breathing, decreased sense of smell up to its complete disappearance, frequent nosebleeds), indicating the presence of this disease, you should immediately consult a doctor.

Additionally

Benign tumors are pathological formations resulting from a violation of the mechanisms that control cell division and growth. They have a structure similar to the tissues from which they originate (muscle tissue, bone, cartilage tissue, etc.). Benign tumors tend to grow slowly. As they grow, squeezing of neighboring organs and tissues occurs. Tumors characterized by benign growth, for the most part, are not prone to recurrence (that is, to the recurrence of the disease after successfully completed therapy), do not metastasize (that is, secondary tumor foci in other organs) and respond well to treatment.

In children during the period of hormonal adjustment (in the second decade of life), benign and malignant neoplasms sometimes occur, which are formed from a wide variety of tissues. Angiofibroma refers to those benign tumors, which are based on connective tissue (fibroma) and vascular tissue of varying maturity (angioma). If such a tumor is located in the region of the arch of the nasopharynx, then it is called angiofibroma of the nasopharynx.

Causes of angiofibroma of the nasopharynx

By the nature of the process, such a tumor is considered benign, but the peculiarity of its growth and development resembles a malignant process. This disease is different in that it occurs more in boys aged 9-10 to 16-18 years, which is why it has a different name - juvenile angiofibroma(juvenile). At the age of 20, it usually undergoes reverse changes and regresses. Much less often, the disease occurs in young men under the age of 28-30 years.

Currently, there is no specific opinion on why nasopharyngeal angiofibroma occurs, but many scientists agree that the main cause of tumor development is the remnants of undeveloped embryonic tissue that are located in the nasopharynx. The basis of the tumor is vessels of different sizes and thicknesses, which are located in a chaotic manner, as well as connective tissue. The vascular tumor feeds from the external carotid artery. Juvenile angiofibroma is located in the following places of the nasopharynx:

Basis of the sphenoid bone (body). Posterior wall of the ethmoid bone. Pharyngeal fascia.

From these anatomical formations of the nasopharynx, the tumor can grow into organs located in the neighborhood, namely, the nasal passages, eye sockets, the ethmoid labyrinth, the sphenoid and ethmoid sinuses, causing many problems and discomfort. This disease is prone to recurrence or recurrence of the development of pathological tumor growth into surrounding tissues even after therapy.

Clinical picture and diagnosis of angiofibroma of the nasopharynx

What does angiofibroma of the nasopharynx visually look like?

The clinic of the disease is quite characteristic and is distinguished by a number of pronounced symptoms. This is due to the rapid growth of the tumor in neighboring tissues. The clinical picture largely depends on the place where the vascular and connective tissues grow. Symptoms of angiofibroma of the nasopharynx include:

Sudden hearing loss (in one or both ears). Difficulty breathing through the nose. Nosebleeds that get worse as the tumor grows. Nasal congestion. Severe migraine-like headaches. Deformation of soft and hard tissues of the face and skull. Bulging (exophthalmos) or displacement of the eyeball. Facial asymmetry and drooping of the upper eyelids.

Diagnosis of the disease is based on the following tests and data:

Examination of the patient and collection of complaints. Arteriography (angiography) of the carotid arteries. Computed (magnetic resonance) tomography of the nose or skull. Tissue biopsy (with endoscopic examination of the nasal cavity).

Be sure to conduct a differential diagnosis with diseases such as adenoids in children, brain tumor, choanal polyps, sarcoma, papilloma. They try to conduct an analysis for tissue biopsy only in a hospital (in the operating unit), because after taking a biopsy, bleeding from the vessels of the nose may occur.

Treatment of angiofibroma of the nasopharynx

Given the fact that the disease often leads to relapses, treatment is always surgical and, if possible, radical. The disease can progress over several years, but in some cases it manifests itself as a malignant neoplasm, that is, it grows rapidly. Therefore, if angiofibroma of the nasopharynx is suspected and the diagnosis is established, a surgical operation is performed as early as possible.

Nosebleeds can occur during surgery, so the carotid artery (external) is often ligated before surgery. Usually, general anesthesia is used and, depending on the location of the tumor, one of the following approaches is chosen:

Endoral, when access to the nasal cavity is through the mouth. Endonasal - access is through the nasal passages. Transaxillary access, which requires endoscopic control.

During the operation, in some cases, when there is massive blood loss, donated blood is transfused. In the period after the operation, the following medications are prescribed:

Transfusion of solutions that improve blood rheology and replenish blood loss. Antibiotic therapy (reduces the risk of infection). Therapy aimed at increasing blood clotting.

To reduce the number of relapses, many ENT oncologists advise taking a course of radiation therapy after surgery. In rare cases, the disease can develop into a malignant neoplasm, but in general the prognosis is favorable.

In adolescent children, hormonal changes are sometimes accompanied by the appearance of neoplasms, benign and malignant. They can be formed from different tissues.

The great Hippocrates back in the 5th century BC. described the disease, which in modern medicine is called angiofibroma. This is a benign tumor that appears in the nasopharynx. It is based on tissue - fibroma (connective) and angioma (vascular). It affects the nasopharynx of boys from 10 years old and young men up to 21 years old (after 20 years, as a rule, regression begins), therefore it is also called "juvenile". Very rarely, the disease overtakes men 28-30 years old.

This neoplasm can grow with deep tissue damage extending to the vessels. And this is a big problem if you need to remove it.


Forms of juvenile angiofibroma

Focusing on the direction of growth of juvenile angiofibroma of the nasopharynx, experts call its forms:

the vault of the nasopharynx (beginning), develops into the base of the skull; the body of the sphenoid bone (origin), growing, affects the nasal cavity, orbit, sinuses, ethmoid labyrinth; from the beginning - the pterygopalatine fossa - into the nasal cavity.

The growth trend of the neoplasm affects the distortion of tissues adjacent to the nasopharynx. A tumor that grows towards the orbit is fraught with displacement of the eyeball, causes a disruption in the blood supply to the brain, and puts pressure on the nerve endings.

With clinical and anatomical classification, two forms of this disease are called: basal- and intracranial-common.

The development of neoplasms - angiofibromas of the nasopharynx - is benign, however, due to the characteristics of growth, predisposition to repetitions, the neoplasm is considered to be malignant.

Symptoms


A sharp deterioration in hearing accompanies the disease.

Since with angiofibromas nearby tissues are very quickly affected, the disease reveals itself as vivid signs:

a sharp deterioration in hearing (one or two ears); nasal bleeding (more frequent and become stronger with the growth of the tumor); nasality; difficulty breathing through the nose; debilitating headaches; a decrease (often disappearance) of smell.

Depending on the direction in which angiofibroma of the nasopharynx spreads, the clinical picture is supplemented by:

distortion of the facial skeleton, soft and hard tissues; weakening of the ability to distinguish the smallest details; limitation of mobility and damage to the eyeball (displacement or protrusion); diplopia; asymmetry of the face, lowered upper eyelids; swelling of the cheek (on the side affected by the tumor).

Disease recognition

Diagnosis may require endoscopy.

Diagnosis of pathology - angiofibroma of the nasopharynx - the result of examining the patient, analyzing his complaints and conducting:

MRI - the skull or nasopharynx is subject (to determine the size and border of the tumor); x-ray examination of the arteries; endoscopy (examination of the cavity with an endoscope); biopsy (of affected tissues for examination) is fraught with bleeding, is carried out in cases of emergency; a thorough examination of the nasal cavity with the help of tools (rhinoscopy) shows the surface (nature and color of the tissue) of the neoplasm; X-ray examination of the blood vessels shows whether the carotid artery is affected by the tumor (important to know in case of an inevitable operation).

A general blood test is required to determine the level of hemoglobin. Sometimes a consultation with an oncologist is prescribed.

When establishing a diagnosis, it is important to distinguish angiofibroma from the clinic with adenoids, brain tumors, polyps, papillomas, and sarcomas.

Treatment


Treatment is carried out surgically.

Angiofibroma of the nasopharynx involves decisive action in the treatment - surgery. Before surgical removal of the neoplasm, radiation therapy is usually performed. Since there is a high risk of bleeding during operations, the external carotid artery is often ligated.

Operations to remove angiofibromas are carried out using an endoscope for a detailed examination of remote areas of the nasal cavity.

Surgical intervention under general anesthesia is chosen depending on the location of the malignant formation by:

approach to the tumor through the nose or oral cavity; facilitated - with a dissection under the lip (through the nasal cavity and sinus of the upper jaw); deployed passage - facial incision; access through the sky.

If during the operation the patient suffers a large loss of blood, a donor transfusion is required. In the postoperative stage, the doctor prescribes:

antibiotics (protection against possible infection); transfusion of solutions that replenish blood loss; drugs that promote blood clotting.

Nasopharyngeal tumor: the likelihood of complications and consequences

Of the possible complications with nasopharyngeal angiofibroma, the following are likely:

severe bleeding with a difficult stop; lack of peripheral vision (neurological complication), when the tumor affects the cranial cavity; anemia due to severe and frequent nosebleeds; penetration of the neoplasm into the nasal cavity.

Juvenile angiofibroma of the nasopharynx does not imply preventive measures - it is impossible to prevent the formation of a tumor. However, in order not to start the course of the onset of the disease, you should immediately consult a doctor at the first characteristic manifestations: recurring nosebleeds, inability to distinguish odors, and others.

Topic 22. RESPIRATORY SYSTEM

The respiratory system includes various organs that perform air conduction and respiratory (gas exchange) functions: the nasal cavity, nasopharynx, larynx, trachea, extrapulmonary bronchi and lungs.

The main function of the respiratory system is external respiration, i.e., the absorption of oxygen from the inhaled air and the supply of blood to it, as well as the removal of carbon dioxide from the body (gas exchange is carried out by the lungs, their acini). Internal, tissue respiration occurs in the form of oxidative processes in the cells of organs with the participation of blood. Along with this, the respiratory organs perform a number of other important non-gas exchange functions: thermoregulation and humidification of the inhaled air, cleansing it of dust and microorganisms, deposition of blood in a richly developed vascular system, participation in maintaining blood clotting due to the production of thromboplastin and its antagonist (heparin), participation in the synthesis of certain hormones and in water-salt, lipid metabolism, as well as in voice formation, smell and immunological protection.

Development

On the 22-26th day of intrauterine development, a respiratory diverticulum, the rudiment of the respiratory organs, appears on the ventral wall of the foregut. It is separated from the foregut by two longitudinal esophagotracheal (tracheoesophageal) grooves protruding into the lumen of the foregut in the form of ridges. These ridges, approaching, merge, and the esophagotracheal septum is formed. As a result, the anterior intestine is divided into a dorsal part (esophagus) and a ventral part (trachea and pulmonary buds). As it separates from the foregut, the respiratory diverticulum, lengthening in the caudal direction, forms a structure lying along the midline, the future trachea; it ends with two saccular protrusions. These are the pulmonary buds, the most distal parts of which make up the respiratory bud. Thus, the epithelium lining the tracheal rudiment and pulmonary buds is of endodermal origin. The mucous glands of the airways, which are derivatives of the epithelium, also develop from the endoderm. Cartilage cells, fibroblasts, and SMCs originate from the splanchic mesoderm surrounding the anterior gut. The right pulmonary kidney is divided into three, and the left - into two main bronchi, predetermining the presence of three lobes of the lung on the right and two on the left. Under the inductive influence of the surrounding mesoderm, branching continues, and as a result, the bronchial tree of the lungs is formed. By the end of the 6th month, there are 17 branches. Later, 6 additional branches occur, the branching process ends after birth. By birth, the lungs contain about 60 million primary alveoli, their number increases rapidly in the first 2 years of life. Then the growth rate slows down, and by the age of 8-12, the number of alveoli reaches approximately 375 million, which is equal to the number of alveoli in adults.

Stages of development. Differentiation of the lungs goes through the following stages - glandular, tubular and alveolar.

glandular stage(5 - 15 weeks) is characterized by further branching of the airways (the lungs take on the appearance of a gland), the development of cartilage of the trachea and bronchi, the appearance of bronchial arteries. The epithelium lining the respiratory bud consists of cylindrical cells. On the 10th week, goblet cells appear from the cells of the cylindrical epithelium of the airways. By the 15th week, the first capillaries of the future respiratory department are formed.

tubular stage(16 - 25 weeks) is characterized by the appearance of respiratory and terminal bronchioles lined with cubic epithelium, as well as tubules (prototypes of alveolar sacs) and the growth of capillaries to them.

Alveolar(or the terminal sac stage (26-40 weeks)) is characterized by massive transformation of tubules into sacs (primary alveoli), an increase in the number of alveolar sacs, differentiation of type I and II alveolocytes, and the appearance of surfactant. By the end of the 7th month, a significant part of the cells of the cubic epithelium of the respiratory bronchioles differentiates into flat cells (type I alveolocytes), closely connected by blood and lymphatic capillaries, and gas exchange becomes possible. The rest of the cells remain cuboidal (type II alveolocytes) and begin to produce surfactant. During the last 2 months of prenatal and several years of postnatal life, the number of terminal sacs is constantly increasing. Mature alveoli before birth are absent.

lung fluid

At birth, the lungs are filled with fluid containing large amounts of chlorides, protein, some mucus from the bronchial glands, and surfactant.

After birth, lung fluid is rapidly resorbed by the blood and lymph capillaries, and a small amount is removed through the bronchi and trachea. The surfactant remains as a thin film on the surface of the alveolar epithelium.

Malformations

Tracheoesophageal fistula occurs as a result of incomplete splitting of the primary intestine into the esophagus and trachea.

Principles of organization of the respiratory system

The lumen of the airways and alveoli of the lung - the external environment. In the airways and on the surface of the alveoli - there is a layer of epithelium. The epithelium of the airways performs a protective function, which is performed, on the one hand, by the very fact of the presence of the layer, and on the other hand, due to the secretion of a protective material - mucus. It is produced by the goblet cells present in the epithelium. In addition, under the epithelium there are glands that also secrete mucus, the excretory ducts of these glands open to the surface of the epithelium.

The airways function as an air junction unit. The characteristics of the external air (temperature, humidity, contamination with different types of particles, the presence of microorganisms) vary quite significantly. But the air that meets certain requirements must enter the respiratory department. The function of bringing air to the required conditions is played by the airways.

Foreign particles are deposited in the mucosal film located on the surface of the epithelium. Further, contaminated mucus is removed from the airways with its constant movement towards the exit from the respiratory system, followed by coughing. Such a constant movement of the mucous film is ensured by synchronous and undulating oscillations of the cilia located on the surface of the epithelial cells directed towards the exit from the airways. In addition, by moving the mucus to the exit, it is prevented from reaching the surface of the alveolar cells, through which diffusion of gases occurs.

Conditioning of the temperature and humidity of the inhaled air is carried out with the help of blood located in the vascular bed of the airway wall. This process occurs mainly in the initial sections, namely in the nasal passages.

The mucous membrane of the airways is involved in defense reactions. The epithelium of the mucous membrane contains Langerhans cells, while its own layer contains a significant number of various immunocompetent cells (T- and B-lymphocytes, plasma cells that synthesize and secrete IgG, IgA, IgE, macrophages, dendritic cells).

Mast cells are very numerous in their own mucosal layer. Mast cell histamine causes bronchospasm, vasodilation, hypersecretion of mucus from the glands, and mucosal edema (as a result of vasodilation and increased permeability of the wall of postcapillary venules). In addition to histamine, mast cells, along with eosinophils and other cells, secrete a number of mediators, the action of which leads to inflammation of the mucous membrane, damage to the epithelium, reduction of SMC and narrowing of the airway lumen. All of the above effects are characteristic of bronchial asthma.

Airways do not collapse. The clearance is constantly changing and adjusting in connection with the situation. The collapse of the lumen of the airways prevents the presence in their wall of dense structures formed in the initial sections by bone, and then by cartilage tissue. The change in the size of the lumen of the airways is provided by the folds of the mucous membrane, the activity of smooth muscle cells and the structure of the wall.

Regulation of MMC tone. The tone of the SMC of the airways is regulated by neurotransmitters, hormones, metabolites of arachidonic acid. The effect depends on the presence of the corresponding receptors in the SMC. SMC walls of the airways have M-cholinergic receptors, histamine receptors. Neurotransmitters are secreted from the terminals of the nerve endings of the autonomic nervous system (for the vagus nerve - acetylcholine, for neurons of the sympathetic trunk - norepinephrine). Bronchoconstriction is caused by choline, substance P, neurokinin A, histamine, thromboxane TXA2, leukotrienes LTC4, LTD4, LTE4. Bronchodilation is caused by VIP, epinephrine, bradykinin, prostaglandin PGE2. The reduction of MMC (vasoconstriction) is caused by adrenaline, leukotrienes, angiotensin-II. Histamine, bradykinin, VIP, prostaglandin PG have a relaxing effect on the SMC of blood vessels.

The air entering the respiratory tract is subjected to chemical examination. It is carried out by the olfactory epithelium and chemoreceptors in the wall of the airways. Such chemoreceptors include sensitive endings and specialized chemosensitive cells of the mucous membrane.

airways

The airways of the respiratory system include the nasal cavity, nasopharynx, larynx, trachea, and bronchi. When the air moves, it is purified, moistened, the temperature of the inhaled air approaches the body temperature, the reception of gas, temperature and mechanical stimuli, as well as the regulation of the volume of inhaled air.

In addition, the larynx is involved in sound production.

nasal cavity

It is divided into the vestibule and the nasal cavity itself, consisting of the respiratory and olfactory regions.

The vestibule is formed by a cavity, located under the cartilaginous part of the nose, covered with stratified squamous epithelium.

Under the epithelium in the connective tissue layer there are sebaceous glands and bristle hair roots. Bristle hairs perform a very important function: they retain dust particles from the inhaled air in the nasal cavity.

The inner surface of the nasal cavity proper in the respiratory part is lined with a mucous membrane consisting of a multi-row prismatic ciliated epithelium and a connective tissue proper plate.

The epithelium consists of several types of cells: ciliated, microvillous, basal and goblet. Intercalated cells are located between the ciliated cells. Goblet cells are unicellular mucous glands that secrete their secret on the surface of the ciliated epithelium.

The lamina propria is formed by a loose, fibrous, unformed connective tissue containing a large number of elastic fibers. It contains the terminal sections of the mucous glands, the excretory ducts of which open on the surface of the epithelium. The secret of these glands, like the secret of goblet cells, moisturizes the mucous membrane.

The mucous membrane of the nasal cavity is very well supplied with blood, which contributes to the warming of the inhaled air in the cold season.

Lymphatic vessels form a dense network. They are associated with the subarachnoid space and perivascular sheaths of various parts of the brain, as well as with the lymphatic vessels of the major salivary glands.

The mucous membrane of the nasal cavity has abundant innervation, numerous free and encapsulated nerve endings (mechano-, thermo- and angioreceptors). Sensitive nerve fibers originate from the semilunar ganglion of the trigeminal nerve.

In the region of the superior nasal concha, the mucous membrane is covered with a special olfactory epithelium containing receptor (olfactory) cells. The mucous membrane of the paranasal sinuses, including the frontal and maxillary sinuses, has the same structure as the mucous membrane of the respiratory part of the nasal cavity, with the only difference that their own connective tissue plate is much thinner.

Larynx

The organ of the air-bearing section of the respiratory system, complex in structure, is involved not only in air conduction, but also in sound production. The larynx in its structure has three membranes - mucous, fibrocartilaginous and adventitial.

The mucous membrane of the human larynx, in addition to the vocal cords, is lined with multi-row ciliated epithelium. The mucosal lamina propria, formed by loose fibrous unformed connective tissue, contains numerous elastic fibers that do not have a specific orientation.

In the deep layers of the mucous membrane, elastic fibers gradually pass into the perichondrium, and in the middle part of the larynx they penetrate between the striated muscles of the vocal cords.

In the middle part of the larynx there are folds of the mucous membrane, forming the so-called true and false vocal cords. The folds are covered by stratified squamous epithelium. Mixed glands lie in the mucous membrane. Due to the contraction of the striated muscles embedded in the thickness of the vocal folds, the size of the gap between them changes, which affects the pitch of the sound produced by the air passing through the larynx.

The fibrocartilaginous membrane consists of hyaline and elastic cartilages surrounded by dense fibrous connective tissue. This shell is a kind of skeleton of the larynx.

The adventitia is composed of fibrous connective tissue.

The larynx is separated from the pharynx by the epiglottis, which is based on elastic cartilage. In the region of the epiglottis, there is a transition of the mucous membrane of the pharynx into the mucous membrane of the larynx. On both surfaces of the epiglottis, the mucous membrane is covered with stratified squamous epithelium.

Trachea

This is an air-conducting organ of the respiratory system, which is a hollow tube consisting of a mucous membrane, submucosa, fibrocartilaginous and adventitious membranes.

The mucous membrane, with the help of a thin submucosa, is connected with the underlying dense parts of the trachea and, due to this, does not form folds. It is lined with multi-row prismatic ciliated epithelium, in which ciliated, goblet, endocrine and basal cells are distinguished.

Ciliated prismatic cells flicker in the direction opposite to the inhaled air, most intensively at the optimum temperature (18 - 33 ° C) and in a slightly alkaline environment.

Goblet cells - unicellular endoepithelial glands, secrete a mucous secretion that moisturizes the epithelium and creates conditions for adherence of dust particles that enter with air and are removed when coughing.

The mucus contains immunoglobulins secreted by immunocompetent cells of the mucous membrane, which neutralize many microorganisms that enter with the air.

Endocrine cells have a pyramidal shape, a rounded nucleus and secretory granules. They are found both in the trachea and in the bronchi. These cells secrete peptide hormones and biogenic amines (norepinephrine, serotonin, dopamine) and regulate the contraction of airway muscle cells.

Basal cells are cambial cells that are oval or triangular in shape.

The submucosa of the trachea consists of loose fibrous unformed connective tissue, without a sharp border passing into dense fibrous connective tissue of the perichondrium of open cartilaginous semirings. In the submucosa are mixed protein-mucous glands, the excretory ducts of which, forming flask-shaped extensions on their way, open on the surface of the mucous membrane.

The fibrocartilaginous membrane of the trachea consists of 16–20 hyaline cartilage rings, not closed on the posterior wall of the trachea. The free ends of these cartilages are connected by bundles of smooth muscle cells attached to the outer surface of the cartilage. Due to this structure, the posterior surface of the trachea is soft, pliable. This property of the posterior wall of the trachea is of great importance: when swallowing, food boluses passing through the esophagus, located directly behind the trachea, do not encounter obstacles from its cartilaginous skeleton.

The adventitial membrane of the trachea consists of loose, fibrous, irregular connective tissue that connects this organ to the adjacent parts of the mediastinum.

The blood vessels of the trachea, as well as in the larynx, form several parallel plexuses in its mucous membrane, and under the epithelium - a dense capillary network. Lymphatic vessels also form plexuses, of which the superficial is directly below the network of blood capillaries.

The nerves approaching the trachea contain spinal (cerebrospinal) and autonomic fibers and form two plexuses, the branches of which end in its mucous membrane with nerve endings. The muscles of the posterior wall of the trachea are innervated from the ganglia of the autonomic nervous system.

Lungs

The lungs are paired organs that occupy most of the chest and constantly change their shape depending on the phase of breathing. The surface of the lung is covered with a serous membrane (visceral pleura).

Structure. The lung consists of branches of the bronchi, which are part of the airways (bronchial tree), and a system of pulmonary vesicles (alveoli), which act as the respiratory sections of the respiratory system.

The composition of the bronchial tree of the lung includes the main bronchi (right and left), which are divided into extrapulmonary lobar bronchi (large bronchi of the first order), and then into large zonal extrapulmonary (4 in each lung) bronchi (bronchi of the second order). Intrapulmonary segmental bronchi (10 in each lung) are subdivided into bronchi of III-V orders (subsegmental), which are medium in diameter (2-5 mm). The middle bronchi are subdivided into small (1–2 mm in diameter) bronchi and terminal bronchioles. Behind them, the respiratory sections of the lung begin, performing a gas exchange function.

The structure of the bronchi (although not the same throughout the bronchial tree) has common features. The inner shell of the bronchi - the mucous membrane - is lined like the trachea with ciliated epithelium, the thickness of which gradually decreases due to a change in the shape of the cells from high prismatic to low cubic. Among epithelial cells, in addition to ciliated, goblet, endocrine and basal, in the distal sections of the bronchial tree, secretory cells (Clara cells), bordered (brush), and non-ciliated cells are found in humans and animals.

Secretory cells are characterized by a dome-shaped top, devoid of cilia and microvilli and filled with secretory granules. They contain a rounded nucleus, a well-developed endoplasmic reticulum of an agranular type, and a lamellar complex. These cells produce enzymes that break down the surfactant that coats the respiratory compartments.

Ciliated cells are found in bronchioles. They are prismatic in shape. Their apical end rises somewhat above the level of adjacent ciliated cells.

The apical part contains accumulations of glycogen granules, mitochondria, and secretion-like granules. Their function is not clear.

Border cells are distinguished by their ovoid shape and the presence of short and blunt microvilli on the apical surface. These cells are rare. They are believed to function as chemoreceptors.

The lamina propria of the bronchial mucosa is rich in longitudinally directed elastic fibers, which provide stretching of the bronchi during inhalation and their return to their original position during exhalation. The mucous membrane of the bronchi has longitudinal folds due to the contraction of oblique bundles of smooth muscle cells that separate the mucous membrane from the submucosal connective tissue base. The smaller the diameter of the bronchus, the relatively thicker is the muscular plate of the mucosa. In the mucous membrane of the bronchi, especially large ones, there are lymphatic follicles.

AT submucosal connective tissue the terminal sections of mixed mucous-protein glands lie. They are located in groups, especially in places that are devoid of cartilage, and the excretory ducts penetrate the mucous membrane and open on the surface of the epithelium. Their secret moisturizes the mucous membrane and promotes adhesion, enveloping of dust and other particles, which are subsequently released to the outside. Mucus has bacteriostatic and bactericidal properties. There are no glands in the bronchi of small caliber (diameter 1–2 mm).

The fibrocartilaginous membrane, as the caliber of the bronchus decreases, is characterized by a gradual change of open cartilage rings in the main bronchi by cartilaginous plates (lobar, zonal, segmental, subsegmental bronchi) and islets of cartilaginous tissue (in medium-sized bronchi). In medium-sized bronchi, hyaline cartilage tissue is replaced by elastic cartilage tissue. In the bronchi of small caliber, the fibrocartilaginous membrane is absent.

outdoor adventitia built from fibrous connective tissue, passing into the interlobar and interlobular connective tissue of the lung parenchyma. Among the connective tissue cells, tissue basophils are found, which are involved in the regulation of the composition of the intercellular substance and blood coagulation.

The terminal (terminal) bronchioles are about 0.5 mm in diameter. Their mucous membrane is lined with a single layer of cubic ciliated epithelium, in which brush cells and secretory Clara cells occur. In the lamina propria of the mucous membrane of these bronchioles, longitudinally extending elastic fibers are located, between which individual bundles of smooth muscle cells lie. As a result, the bronchioles are easily distensible during inhalation and return to their original position during exhalation.

Respiratory department. The structural and functional unit of the respiratory section of the lung is the acinus. It is a system of alveoli located in the wall of the respiratory bronchiole, alveolar ducts and sacs that carry out gas exchange between the blood and air of the alveoli. The acinus begins with a respiratory bronchiole of the 1st order, which is dichotomously divided into respiratory bronchioles of the 2nd, and then of the 3rd order. In the lumen of the bronchioles, the alveoli open, which in this regard are called alveolar. Each third-order respiratory bronchiole, in turn, is subdivided into alveolar ducts, and each alveolar duct ends with two alveolar sacs. At the mouth of the alveoli of the alveolar ducts there are small bundles of smooth muscle cells, which are visible in transverse sections in the form of button-like thickenings. The acini are separated from each other by thin connective tissue layers, 12-18 acini form the lung lobule. Respiratory bronchioles are lined with a single layer of cuboidal epithelium. The muscular plate becomes thinner and breaks up into separate, circularly directed bundles of smooth muscle cells.

On the walls of the alveolar passages and alveolar sacs there are several dozen alveoli. Their total number in adults reaches an average of 300 - 400 million. The surface of all alveoli with a maximum inhalation in an adult can reach 100 m 2, and during exhalation it decreases by 2 - 2.5 times. Between the alveoli are thin connective tissue septa, through which the blood capillaries pass.

Between the alveoli there are messages in the form of holes with a diameter of about 10 - 15 microns (alveolar pores).

The alveoli look like an open vesicle. The inner surface is lined by two main types of cells: respiratory alveolar cells (type I alveolocytes) and large alveolar cells (type II alveolocytes). In addition, in animals, there are type III cells in the alveoli - bordered.

Type I alveolocytes have an irregular, flattened, elongated shape. On the free surface of the cytoplasm of these cells, there are very short cytoplasmic outgrowths facing the cavity of the alveoli, which significantly increases the total area of ​​air contact with the surface of the epithelium. Their cytoplasm contains small mitochondria and pinocytic vesicles.

An important component of the air-blood barrier is the surfactant alveolar complex. It plays an important role in preventing the collapse of the alveoli on exhalation, as well as in preventing them from penetrating through the wall of the alveoli of microorganisms from the inhaled air and transuding fluid from the capillaries of the interalveolar septa into the alveoli. Surfactant consists of two phases: membrane and liquid (hypophase). Biochemical analysis of the surfactant showed that it contains phospholipids, proteins and glycoproteins.

Type II alveolocytes are somewhat larger in height than type I cells, but their cytoplasmic processes, on the contrary, are short. In the cytoplasm, larger mitochondria, a lamellar complex, osmiophilic bodies, and an endoplasmic reticulum are revealed. These cells are also called secretory because of their ability to secrete lipoprotein substances.

In the wall of the alveoli, brush cells and macrophages containing trapped foreign particles and an excess of surfactant are also found. The cytoplasm of macrophages always contains a significant amount of lipid droplets and lysosomes. The oxidation of lipids in macrophages is accompanied by the release of heat, which warms the inhaled air.

Surfactant

The total amount of surfactant in the lungs is extremely small. There are about 50 mm 3 of surfactant per 1 m 2 of the alveolar surface. The thickness of its film is 3% of the total thickness of the air-blood barrier. The components of the surfactant enter the type II alveolocytes from the blood.

Their synthesis and storage in lamellar bodies of these cells is also possible. 85% of the surfactant components are recycled and only a small amount is resynthesized. Removal of surfactant from the alveoli occurs in several ways: through the bronchial system, through the lymphatic system and with the help of alveolar macrophages. The main amount of surfactant is produced after the 32nd week of pregnancy, reaching a maximum amount by the 35th week. Before birth, an excess of surfactant is formed. After birth, this excess is removed by alveolar macrophages.

Respiratory distress syndrome of the newborn develops in premature babies due to the immaturity of type II alveolocytes. Due to the insufficient amount of surfactant secreted by these cells to the surface of the alveoli, the latter are unexpanded (atelectasis). As a result, respiratory failure develops. Due to alveolar atelectasis, gas exchange occurs through the epithelium of the alveolar ducts and respiratory bronchioles, which leads to their damage.

Compound. Pulmonary surfactant is an emulsion of phospholipids, proteins and carbohydrates, 80% glycerophospholipids, 10% cholesterol and 10% proteins. The emulsion forms a monomolecular layer on the surface of the alveoli. The main surfactant component is dipalmitoylphosphatidylcholine, an unsaturated phospholipid that makes up more than 50% of the surfactant's phospholipids. The surfactant contains a number of unique proteins that promote the adsorption of dipalmitoylphosphatidylcholine at the interface between two phases. Among the surfactant proteins, SP-A, SP-D are isolated. Proteins SP-B, SP-C and surfactant glycerophospholipids are responsible for reducing surface tension at the air-liquid interface, while SP-A and SP-D proteins are involved in local immune responses by mediating phagocytosis.

SP-A receptors are present in type II alveolocytes and in macrophages.

Production regulation. The formation of surfactant components in the fetus is facilitated by glucocorticosteroids, prolactin, thyroid hormones, estrogens, androgens, growth factors, insulin, cAMP. Glucocorticoids enhance the synthesis of SP-A, SP-B and SP-C in the lungs of the fetus. In adults, surfactant production is regulated by acetylcholine and prostaglandins.

Surfactant is a component of the lung defense system. Surfactant prevents direct contact of alveolocytes with harmful particles and infectious agents that enter the alveoli with inhaled air. The cyclic changes in surface tension that occur during inhalation and exhalation provide a breath-dependent cleaning mechanism. Enveloped by the surfactant, dust particles are transported from the alveoli to the bronchial system, from which they are removed with mucus.

Surfactant regulates the number of macrophages migrating into the alveoli from the interalveolar septa, stimulating the activity of these cells. Bacteria entering the alveoli with air are opsonized by surfactant, which facilitates their phagocytosis by alveolar macrophages.

The surfactant is present in bronchial secretions, coating the ciliated cells, and has the same chemical composition as lung surfactant. Obviously, surfactant is needed to stabilize the distal airways.

immune protection

Macrophages

Macrophages make up 10-15% of all cells in the alveolar septa. Many microfolds are present on the surface of macrophages. The cells form rather long cytoplasmic processes that allow macrophages to migrate through the interalveolar pores. Being inside the alveolus, the macrophage can attach itself to the surface of the alveolus with the help of processes and capture particles. Alveolar macrophages secrete? 1-antitrypsin - a glycoprotein from the family of serine proteases that protects alveolar elastin from: splitting of leukocytes by elastase. Mutation of the gene? 1-antitrypsin leads to congenital emphysema (damage to the elastic framework of the alveoli).

Migration paths. Cells loaded with phagocytosed material can migrate in various directions: up the acinus and into the bronchioles, where macrophages enter the mucous membrane, which is constantly moving along the surface of the epithelium towards the exit from the airways; inside - into the internal environment of the body, i.e., into the interalveolar septa.

Function. Macrophages phagocytize microorganisms and dust particles that enter with the inhaled air, have antimicrobial and anti-inflammatory activity mediated by oxygen radicals, proteases and cytokines. In lung macrophages, the antigen presenting function is poorly expressed. Moreover, these cells produce factors that inhibit the function of T-lymphocytes, which reduces the immune response.

Antigen presenting cells

Dendritic cells and Langerhans cells belong to the system of mononuclear phagocytes, they are the main antigen-presenting cells of the lung. Dendritic cells and Langerhans cells are numerous in the upper respiratory tract and trachea. With a decrease in the caliber of the bronchi, the number of these cells decreases. As antigen-presenting pulmonary Langerhans cells and dendritic cells express MHC class 1 molecules. These cells have receptors for the Fc fragment of IgG, the fragment of the C3b complement component, IL-2, they synthesize a number of cytokines, including IL-1, IL-6, tumor necrosis factor, stimulate T-lymphocytes, showing increased activity against the antigen that first appeared in the body.

Dendritic cells

Dendritic cells are found in the pleura, interalveolar septa, peribronchial connective tissue, and in the lymphoid tissue of the bronchi. Dendritic cells, differentiating from monocytes, are quite mobile and can migrate in the intercellular substance of the connective tissue. They appear in the lungs before birth. An important property of dendritic cells is their ability to stimulate the proliferation of lymphocytes. Dendritic cells have an elongated shape and numerous long processes, an irregularly shaped nucleus, and typical cell organelles in abundance. There are no phagosomes, since the cells practically do not have phagocytic activity.

Langerhans cells

Langerhans cells are present only in the epithelium of the airways and absent in the alveolar epithelium. Langerhans cells differentiate from dendritic cells, and such differentiation is possible only in the presence of epithelial cells. Connecting with cytoplasmic processes penetrating between epitheliocytes, Langerhans cells form a developed intraepithelial network. Langerhans cells are morphologically similar to dendritic cells. A characteristic feature of Langerhans cells is the presence in the cytoplasm of specific electron-dense granules with a lamellar structure.

Metabolic lung function

In the lungs, it metabolizes a number of biologically active substances.

Angiotensins. Activation is only known for angiotensin I, which is converted to angiotensin II. The conversion is catalyzed by an angiotensin-converting enzyme localized in the endothelial cells of the alveolar capillaries.

inactivation. Many biologically active substances are partially or completely inactivated in the lungs. So, bradykinin is inactivated by 80% (with the help of angiotensin-converting enzyme). In the lungs, serotonin is inactivated, but not with the participation of enzymes, but by excretion from the blood, part of serotonin enters the platelets. Prostaglandins PGE, PGE2, PGE2a and norepinephrine are inactivated in the lungs with the help of appropriate enzymes.

Pleura

The lungs are covered on the outside with a pleura called the pulmonary (or visceral). The visceral pleura fuses tightly with the lungs, its elastic and collagen fibers pass into the interstitial tissue, so it is difficult to isolate the pleura without injuring the lungs. The visceral pleura contains smooth muscle cells. In the parietal pleura, which lines the outer wall of the pleural cavity, there are fewer elastic elements, and smooth muscle cells are rare.

Blood supply in the lung is carried out through two vascular systems. On the one hand, the lungs receive arterial blood from the systemic circulation through the bronchial arteries, and on the other hand, they receive venous blood for gas exchange from the pulmonary arteries, that is, from the pulmonary circulation. The branches of the pulmonary artery, accompanying the bronchial tree, reach the base of the alveoli, where they form a capillary network of the alveoli. Through the alveolar capillaries, the diameter of which varies within 5 - 7 microns, erythrocytes pass in 1 row, which creates an optimal condition for the implementation of gas exchange between erythrocyte hemoglobin and alveolar air. The alveolar capillaries gather into postcapillary venules, which merge to form the pulmonary veins.

Bronchial arteries depart directly from the aorta, nourish the bronchi and lung parenchyma with arterial blood. Penetrating into the wall of the bronchi, they branch out and form arterial plexuses in their submucosa and mucous membrane. In the mucous membrane of the bronchi, the vessels of the large and small circles communicate by anastomosis of the branches of the bronchial and pulmonary arteries.

The lymphatic system of the lung consists of superficial and deep networks of lymphatic capillaries and vessels. The superficial network is located in the visceral pleura. The deep network is located inside the pulmonary lobules, in the interlobular septa, lying around the blood vessels and bronchi of the lung.

innervation carried out by sympathetic and parasympathetic nerves and a small number of fibers coming from the spinal nerves. Sympathetic nerves conduct impulses that cause bronchial dilatation and constriction of blood vessels, parasympathetic - impulses that, on the contrary, cause bronchial constriction and dilation of blood vessels. The ramifications of these nerves form a nerve plexus in the connective tissue layers of the lung, located along the bronchial tree and blood vessels. In the nerve plexuses of the lung, large and small ganglia are found, from which nerve branches depart, innervating, in all likelihood, the smooth muscle tissue of the bronchi. Nerve endings were identified along the alveolar ducts and alveoli.

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On the walls of the alveolar passages and alveolar sacs there are several dozen alveoli. Their total number in adults reaches an average of 300 - 400 million. The surface of all alveoli with a maximum inspiration in an adult can reach 100 m2, and during exhalation it decreases by 2 - 2.5 times. Between the alveoli are thin connective tissue septa, through which the blood capillaries pass.

Between the alveoli there are messages in the form of holes with a diameter of about 10 - 15 microns (alveolar pores).

The alveoli look like an open vesicle. The inner surface is lined by two main types of cells: respiratory alveolar cells (type I alveolocytes) and large alveolar cells (type II alveolocytes). In addition, in animals, there are type III cells in the alveoli - bordered.

Type I alveolocytes have an irregular, flattened, elongated shape. On the free surface of the cytoplasm of these cells, there are very short cytoplasmic outgrowths facing the cavity of the alveoli, which significantly increases the total area of ​​air contact with the surface of the epithelium. Their cytoplasm contains small mitochondria and pinocytic vesicles.

An important component of the air-blood barrier is the surfactant alveolar complex. It plays an important role in preventing the collapse of the alveoli on exhalation, as well as in preventing them from penetrating through the wall of the alveoli of microorganisms from the inhaled air and transuding fluid from the capillaries of the interalveolar septa into the alveoli. Surfactant consists of two phases: membrane and liquid (hypophase). Biochemical analysis of the surfactant showed that it contains phospholipids, proteins and glycoproteins.

Type II alveolocytes are somewhat larger in height than type I cells, but their cytoplasmic processes, on the contrary, are short. In the cytoplasm, larger mitochondria, a lamellar complex, osmiophilic bodies, and an endoplasmic reticulum are revealed. These cells are also called secretory because of their ability to secrete lipoprotein substances.

In the wall of the alveoli, brush cells and macrophages containing trapped foreign particles and an excess of surfactant are also found. The cytoplasm of macrophages always contains a significant amount of lipid droplets and lysosomes. The oxidation of lipids in macrophages is accompanied by the release of heat, which warms the inhaled air.

Surfactant

The total amount of surfactant in the lungs is extremely small. There are about 50 mm3 of surfactant per 1 m2 of the alveolar surface. The thickness of its film is 3% of the total thickness of the air-blood barrier. The components of the surfactant enter the type II alveolocytes from the blood.

Their synthesis and storage in lamellar bodies of these cells is also possible. 85% of the surfactant components are recycled and only a small amount is resynthesized. Removal of surfactant from the alveoli occurs in several ways: through the bronchial system, through the lymphatic system and with the help of alveolar macrophages. The main amount of surfactant is produced after the 32nd week of pregnancy, reaching a maximum amount by the 35th week. Before birth, an excess of surfactant is formed. After birth, this excess is removed by alveolar macrophages.

Respiratory distress syndrome of the newborn develops in preterm infants due to the immaturity of type II alveolocytes. Due to the insufficient amount of surfactant secreted by these cells to the surface of the alveoli, the latter are unexpanded (atelectasis). As a result, respiratory failure develops. Due to alveolar atelectasis, gas exchange occurs through the epithelium of the alveolar ducts and respiratory bronchioles, which leads to their damage.

Compound. Pulmonary surfactant is an emulsion of phospholipids, proteins and carbohydrates, 80% glycerophospholipids, 10% cholesterol and 10% proteins. The emulsion forms a monomolecular layer on the surface of the alveoli. The main surfactant component is dipalmitoylphosphatidylcholine, an unsaturated phospholipid that makes up more than 50% of the surfactant's phospholipids. The surfactant contains a number of unique proteins that promote the adsorption of dipalmitoylphosphatidylcholine at the interface between two phases. Among the surfactant proteins, SP-A, SP-D are isolated. Proteins SP-B, SP-C and surfactant glycerophospholipids are responsible for reducing surface tension at the air-liquid interface, while SP-A and SP-D proteins are involved in local immune responses by mediating phagocytosis.