Pathogenesis of exogenous allergic bronchioalveolitis

Pathogenesis of exogenous allergic bronchioalveolitis

Allergic predisposition factors in patients with exogenous allergic bronchioalveolitis have not been established, although HLA-BW40 and HLA-B8 are more common. Immunological and non-immunological mechanisms are involved in the development of the disease. Allergic reactions of various types are expected to be involved: delayed-type hypersensitivity, immune complexes, immediate-type allergic reactions caused by antibodies related to immunoglobulin E, mediated by cytotoxicity antibodies. There is currently no evidence of a predominance of a particular type of immunological reaction.
Existing ideas about exogenous allergic bronchioloalveolitis as a disease caused by the immune complex are questioned for the following reasons: there is no parallelism between the level of precipitating antibodies related to immunoglobulin G and the severity of the disease; precipitins are found in a large number of healthy individuals in contact with the antigen; in the acute period of the disease, granulomas are formed that are uncharacteristic of the Arthus phenomenon; skin reactions according to the type of Arthus phenomenon to specific antigens are not constantly detected in patients;
deposits of immune complexes in biopsies of human lungs are noted only at an early stage of the process; histological signs with exogenous allergic bronchioalveolitis are more characteristic of cellular reactions, fibrinoid necrosis of the vascular walls and perivascular infiltration by segmented cells. Many authors assign the leading role of HRT. The role of GNT due to immunoglobulin E is not clear, antibodies related to immunoglobulin E have not been identified, although certain antigens (pigeon proteins, pituitary powder) can cause GNT. It is assumed that immunoglobulin E does not participate in the development of a typical granulomatous lesion, but can mediate GNT. The question of the role of immunoglobulin E needs to be studied in connection with recent data on late-type allergic reactions caused by immunoglobulin E and characterized by mononuclear cell infiltration without the presence of vasculitis. Perhaps the participation of a secondary autoimmune cytotoxic mechanism associated with chronic inflammation and tissue destruction. Non-immunological mechanisms are associated with the characteristics of disease-causing antigens that are resistant to lysosomal enzymes, are not destroyed by alveolar macrophages, are able to activate the complement system in an alternative way and have a nonspecific adjuvant effect on the induction of cell-mediated reactions and activation of alveolar macrophages. Immuno-non-immunological mechanisms activate alveolar macrophages, which, through soluble mediators, induce inflammation and stimulate the activity of fibroblasts, which leads to fibrosis. There is an opinion that it is activated alveolar macrophages that occupy a central place in the pathogenesis of exogenous allergic bronchioloalveolitis.

Pathomorphology of exogenous allergic bronchioalveolitis

With the fulminant form of exogenous allergic bronchioalveolitis, ending with the rapid death of the patient, intense inflammatory exudate in the alveolar septa, hemorrhagic edema inside the alveoli, necrosis of the bronchioles with obliteration are detected. In the acute period, infiltration of the alveoli and bronchioles with lymphocytes, plasma cells and a large number of alveolar macrophages is detected. Noncaseating sarcoid-like granulomas, consisting of lymphocytes, activated macrophages, epithelioid and giant cells, are characteristic. In a very early period of the disease, deposits of immune complexes on the alveolar membrane and necrotizing vasculitis are found. In the chronic form, infiltration by lymphocytes and plasma cells is less pronounced, granulomas are scattered in areas of interstitial fibrosis, destruction of the bronchioles mural structure with macrophage obliteration of the lumen, hypertrophy of the cuboid epithelium of the alveoli, and sometimes of the “emphysema” zone due to uneven destruction of the alveoli are observed. At the final stage, destruction of the alveoli, fibrosis, and the picture of the “cell lung” develop.

Clinic of exogenous allergic bronchioloalveolitis

Clinical signs of the disease depend on the nature of the organic particles, the intensity and frequency of inhalation, and the characteristics of the immunological response of the patient. The allergy period is different – from several months to several years. Usually, 4-6 hours after inhalation of organic dust, a cough appears, dry or with viscous yellow sputum, which may contain blood; there is an increase in temperature to 38-40 ° C, heavy sweat, chills, myalgia, weakness, retrosternal pain. Inspiratory dyspnea progresses rapidly. Over the lungs, dullness of the sound and crepitus are determined. In the acute period, tachycardia and bronchial obstruction resistant to the action of bronchodilators may occur, which indicates the prevalence of inflammation over increased bronchial tone. Fever lasts up to 24 hours, shortness of breath and weakness sometimes lasts up to several weeks. In other cases, the symptoms spontaneously disappear within a day. Upon contact with certain antigens (pigeon proteins, pituitary powder), HNT can occur, which occurs rarely if actinomycetes are the cause of exogenous allergic bronchioloalveolitis. With repeated exposures of the antigen, shortness of breath intensifies, anorexia, weight loss are noted – the disease acquires a chronic course, which can develop without an acute attack – in cases of prolonged contact with small stumps of antigen. This form is formed by bird lovers, especially budgerigar owners, workers in contact with heating and conditioning systems, and is characterized by progressive shortness of breath, coughing, weakness, malaise, and emaciation. Wet cracking rales (“cracking cellophane”) are heard over the lungs, but this is less typical of a disease than an idiopathic fibrosing alveolitis; in 10% of patients, after a gradual onset, subsequent antigen inhalations cause acute symptoms and GNT. Rare clinical signs of exogenous allergic allergic bronchioalveolitis are also described: chest tightness, impaired consciousness, changes in sensitivity and paralysis of the facial nerve.

The course of the disease is usually acute or subacute when inhaled enough antigen; with massive inhalation, the disease can last no more than a day. In cases of prolonged exposure to small doses of antigen, the disease progresses with the development of fibrosis.

The prognosis for acute and subacute currents is favorable, elimination of antigen and glucocorticosteroid therapy lead to the reverse development of the process. The prognosis is less favorable if the disease lasts several years, especially in the elderly.

Diagnosis of exogenous allergic bronchioalveolitis

There are no specific diagnostic methods for exogenous allergic bronchioloalveolitis. The diagnosis is based on the following criteria: typical allergic history (contact with organic dust); dynamics of clinical signs; positive allergic diagnostic tests intradermally for the corresponding antigens such as GNT and HRT; detection of precipitating antibodies related to immunoglobulins G; lack of eosinophilia of peripheral blood and sputum; radiological changes; restrictive ventilation disorders; positive RBTL and RTML; inhibition of macrophage migration under the influence of a specific antigen; HRT, GNT or a double bronchospastic reaction or crepitation over the lungs after allergological diagnostic tests of provocative inhalation with extracts of specific antigens.

X-ray data in the acute phase of the disease may be normal. As the disease develops, bilateral middle and lower lobe focal shadows appear with a tendency to merge and diffuse. Comparison of radiographs with lung biopsy data reveals that focal shadows correspond to granulomas and interstitial infiltrates. In acute cases, the radiograph of the lungs normalizes within 10-20 days after eliminating contact with the antigen. For the chronic form of exogenous allergic bronchioloalveolitis, fibrosis is characteristic; a cell lung pattern may develop.

Functional disorders of the respiratory system consist in restrictive ventilation failure, a decrease in the diffusion capacity of the lungs and static pulmonary volumes in the absence of airway obstruction. In severe cases, hypoxemia and hypercapnia may occur. In the later stages, a third of patients develop irreversible airway obstruction with a change in the relationship between ventilation and blood flow. In the acute phase of exogenous allergic bronchioalveolitis with fever, leukocytosis of up to (15-20) 109 leukocytes per 1 liter with a neutrophilic shift is observed, eosinophilia, hypergammaglobulinemia are sometimes noted; the level of immunoglobulins is increased, with the exception of immunoglobulin E.
Positive delayed and immediate skin tests for the introduction of antigen, antibodies related to immunoglobulin E, positive cell-type reactions (RBTL and RTML) with specific antigens are observed not only in patients with exogenous allergic bronchioalveolitis, but also in a certain contingent of people in contact with the same antigens, but not having symptoms of the disease. Cell-type reactions are of great diagnostic value compared to the detection of precipitating antibodies. RBTL remains positive for many months, while the precipitation reaction quickly becomes negative after cessation of contact with the antigen. Conducting provocative inhalation tests with specific antigens is unsafe, but in some cases it is possible. The diagnosis is helped by a study of bronchial lavage water, in which an increased number of lymphocytes is detected (the larger the more acute the form of the disease) – from 35 to 90% (average 50-60%). These results differ from those obtained for persons also exposed to organic dust, but without signs of disease. Despite the presence of specific precnpitins in the latter, the cellular composition of lavage fluid remains normal, which coincides with the absence of clinical signs of the disease. Lavage fluid lymphocytosis has not only diagnostic, but also prognostic value, as it quickly disappears with effective treatment or a spontaneous favorable course and is again detected during exacerbation.

Differential diagnosis of exogenous allergic bronchioloalveolitis

Differential diagnosis of the acute form is carried out with acute viral infectious diseases (influenza, etc.), acute pneumonia, allergic bronchopulmonary aspergillosis, chronic – with other diffuse lung lesions with progressive pulmonary and general symptoms.

Treatment of exogenous allergic bronchioloalveolitis

The main event is the elimination of the etiological factor. In particular, if the cause of the disease is pituitary powder (in patients with diabetes insipidus), then when switching to synthetic vasopressin, the symptoms of the disease disappear. If the disease progresses after removal of the antigen, then pharmacological therapy is necessary. The main treatment is glucocorticosteroid drugs, which are most effective in the acute form of exogenous allergic bronchioalveolitis, with a chronic effect is insufficient. The duration of glucocorticosteroid therapy is determined by clinical and laboratory data. GNT during provocative inhalation tests with specific antigens is prevented by the intal, but its effectiveness in conditions of professional contact with organic dust has not been proved. Antihistamines and bronchodilators are not effective. In cases of infection, antibiotics are prescribed, with appropriate indications, antimycotic drugs.
Prevention consists in storing organic materials under conditions that exclude their moisture, heating and decay.

Obliterate bronchiolitis

Obliterating bronchiolitis is rarely observed, mainly in children in the first months of life, and can occur as a complication of ARVI.

Clinic of obliterating bronchiolitis

At the onset of the disease, symptoms of acute bronchiolitis or bronchopneumonia appear. At a blood test neutrophilia, sometimes moderate leukocytosis is noted. After the acute period of the disease, relative remission sets in, lasting 3 to 4 weeks. However, in this period auscultatory changes are detected (rales of different sizes, wheezing exhalation), localized on the side of the lesion.
Then comes the third period in which, at an unstable febrile body temperature, bronchopulmonary changes intensify and respiratory failure increases. With bilateral damage during the next exacerbation, a fatal outcome is possible. With a unilateral lesion, a rapid decrease in the lung occurs due to atrophy of the alveolar tissue and a significant secondary violation of the functional pulmonary blood flow. Patients develop symptoms characteristic of McLeod’s syndrome (signs of chronic bronchitis in the affected lung and severe respiratory failure).
Radiologically, in the initial period of the disease, massive shadow formations due to the presence of atelectasis are detected mainly on one side . In the period of remission, these changes disappear, however, after such relative well-being, a rapidly progressive decrease in the lung occurs with the development of pneumosclerosis.
The deformity of the proximal parts of the bronchi, ending blindly (non-filling of peripheral branches with contrast medium), is bronchographically detected.
Diffuse endobronchitis of the affected lung is bronchoscopically detected.

Treatment of obliterating bronchiolitis

In the initial period of the disease, the use of antibiotics and glycocorticoids is indicated, symptomatic therapy (oxygen, with indications – antispasmodic and antihistamine drugs). Inhalations of semisynthetic penicillins in combination with other drugs, physical therapy, chest massage, etc. are effective. The
prognosis for diffuse obliterating bronchiolitis is serious and more favorable in children in whom obliteration is limited to a small number of bronchioles.

Atherosclerosis obliterans 

Obliterating atherosclerosis of the aorta and major vessels of the lower extremities in frequency is in first place among other diseases of the peripheral arteries. It occurs mainly in men over 40 years old. The disease often causes severe limb ischemia, condemning patients to excruciating suffering and depriving them of working capacity. The process is localized mainly in large vessels (aorta, iliac arteries) or medium-sized arteries (femoral, popliteal). 

Etiology, pathogenesis of obliterating atherosclerosis

Atherosclerotic lesions of the arteries are a manifestation of general atherosclerosis. In its occurrence, the same etiological factors and pathogenetic mechanisms play a role that are responsible for the formation of atherosclerosis of any other localization. The main changes in atherosclerosis develop in the intima of the arteries. A young connective tissue appears around the foci of lipoidosis , the maturation of which leads to the formation of fibrous plaque. Platelets and fibrin clots settle on plaques. With abundant accumulation of lipids, there is a violation of blood circulation in plaques, the necrosis of which causes the appearance of atheromas, i.e. cavities filled with atheromatous masses and tissue detritus. Atheromatousmasses are rejected into the lumen of the vessel. Getting with a blood stream into the distal bloodstream, they become the cause of embolism. At the same time, calcium salts are deposited in the altered tissue of plaques, in areas of degenerating elastic fibers, which is the final stage in the development of atherosclerosis and leads to impaired patency of the vessel.

Clinic for obliterating atherosclerosis

During obliterating atherosclerosis, the same 4 stages are distinguished as with obliterating endarteritis. For several years obliteri – ruyuschy atherosclerosis may be asymptomatic, but after the first clinical manifestations progress rapidly. In some cases, due to the joined thrombosis, the clinical manifestations of the disease appear suddenly. A characteristic symptom of obliterating atherosclerosis is intermittent claudication, manifested by pain in the calf muscles, which appears when walking and disappears after a short rest. With atherosclerotic lesions of the terminal abdominal aorta and iliac arteries ( Leriche syndrome ), the pain is localized not only in the legs, but also in the gluteus, lumbar and thigh muscles. Intermittent claudication intensifies when climbing stairs or uphill. Chilliness , increased sensitivity of the lower extremities to cold, and a feeling of numbness in the feet are noted. Due to ischemia, the color of the skin of the lower extremities changes, which in the initial stages of the disease become pale, and in patients with Lerish’s syndrome have the color of ivory. In the later stages of the disease the skin of feet and toes becomes purplish-bluish okrasku.Razvitie trophic disorders leading to hair loss, breach of nail growth. One of the manifestations of occlusion of the aorto-iliac segment is impotence due to circulatory disorders in the system of internal iliac arteries. This symptom occurs in 50% of patients.

Diagnosis of obliterating atherosclerosis

When examined in patients with obliterating atherosclerosis, hypotrophy or atrophy of the muscles of the lower extremities is often noted. In obliterating atherosclerosis, the femoral- iliac segment is most often affected , therefore, starting from the place of discharge of the deep femoral artery, the pulsation in the vast majority of patients is not determined either on the popliteal artery or on the arteries of the feet. With the occlusion of the abdominal aorta and iliac arteries, it is not determined on the femoral arteries. Systolic murmur is usually heard over stenotic arteries. With stenosis of the abdominal aorta and iliac arteries, it can be determined not only above the anterior abdominal wall, but also on the femoral arteries under the inguinal ligament. Rheovasography with obliterating atherosclerosis records a decrease in the main blood flow in the lower extremities. In severe cases of lower limb ischemia, rheovasographic curves take the form of straight lines, additional teeth disappear on the catacrotis , the rheographic index decreases, the infrared radiation intensity recorded by the thermal imager decreases until the thermal pattern is completely darkened, thermal asymmetry increases. Ultrasound examination makes it possible to determine the level of atherosclerotic and the degree of blood supply to the distal parts of the affected limb. The main method of topical diagnosis in obliterating atherosclerosis is angiography. It allows you to determine the localization and extent of the pathological process, the degree of damage to the arteries (occlusion, stenosis), the nature of collateral circulation, the state of the distal bloodstream. By angio graphic signs of atherosclerosis include edge defects filling ize – degeneracy circuit portions of the arteries to the stenosis, the presence or segmental common occlusions with filling through distal collaterals network.

Differential diagnosis of obliterating atherosclerosis

Differential diagnosis should be made with obliterative endarte – Riitta and trombangiitom.Endarteriitom ill young people. Overcooling, frostbite, emotional stress contribute to its development. The arteries of the distal segments of the limbs are mainly affected, a long, undulating course of the disease is characteristic. In patients with atherosclerosis may occur symptoms of other vascular beds (heart, brain, kidneys, etc..), Giperholesterine – mia , diabetes that occurs very endarteriite redko.Differentsialnaya diagnosis of arteriosclerosis obliterans and thromboangiitis usually straightforward. The main difference lies in the fact that Trom – Bang occurs predominantly in young men and is characterized by a combination of symptoms of arterial insufficiency and migratory thrombophlebitis of superficial veins.

Etiology, pathogenesis of obliterating endarteritis

The development of endarteritis is promoted by prolonged hypothermia, frostbite, injuries of the lower extremities, smoking, vitamin deficiencies, severe shock, mental disorders, infections, disorders of autoimmune processes and other factors that cause persistent spasm of the vessels. Long-term spasm of the arteries and their accompanying vasa vasorum leads to chronic and walls, resulting in intimal hyperplasia, adventitious fibrosis and degenerative changes in the nervous system of the vascular wall. Against the background of altered intimacy, a blood clot forms, narrowing and obliteration of the lumen of the vessel occur. If at the beginning of the disease mainly the distal vessels of the lower extremities (lower leg and foot) are affected, then subsequently larger arteries (popliteal, femoral, iliac) are involved in the pathological process. A sharp weakening of blood flow through the arteries leads to a deterioration in blood flow in the vessels of the microvasculature providing tissue metabolism, reduced oxygen delivery to tissues and tissue hypoxia develops, which is enhanced by the opening of arteriovenular anastomoses. Under these conditions, blood viscosity increases, erythrocyte aggregation increases, the adhesion-aggregation increases, and the disaggregation properties of platelets decrease . Formed platelet agreganty that block the microvasculature. Chronic hypoxia leads to the disintegration of the lysosomes with the release of hydrolases, Lizzie – ruyuschih cells and tissues. Tissue necrosis, the accumulation of proteolytic enzymes. The body is sensitized to protein breakdown products. Pathological autoimmune processes occur, exacerbating microcirculation disorders and enhancing local hypoxia and tissue necrosis.

Clinic of obliterating endarteritis

Depending on the degree of insufficiency of arterial blood supply to the affected limb, 4 stages of obliterating endarteritis are distinguished:
Stage I – functional compensation. Patients note chilliness, sometimes tingling and burning at the fingertips, increased fatigue. When cooled, the limbs become pale, cold to the touch. When passing at a speed of 4-5 km / h a distance of more than 1000 m in patients with intermittent claudication. It lies in the fact that the patient begins to experience pain in the calf muscles or foot, causing him to stop. In the pathogenesis of this symptom, a number of factors are important, in particular, insufficient blood supply to the muscles, impaired oxygen utilization, and the accumulation of under-oxidized metabolic products in the tissues. The pulse on the arteries of the feet in this stage is weakened or not determined; Stage II – subcompensation . Intermittent claudication increases and at the indicated pace of walking it occurs already after passing 200 m or a little earlier, the skin of the feet and lower legs loses its inherent elasticity, it becomes dry, flaky, hyperkeratosis develops on the plantar surface. Nail growth slows down, they thicken, become brittle, dull, acquire a matte or brown color. Disturbed and hair growth on the affected limb, which leads to the appearance of areas of baldness. Atrophy of the subcutaneous base and small muscles of the foot begins to develop. Ripple in the arteries of the feet is not determined; Stage III – decompensation. There is pain in the affected limb at rest. Walking becomes possible at a distance of 25-50 m. The color of the skin changes dramatically depending on the position of the affected limb. Her rise is accompanied by blanching, lowering – by redness of the skin. The skin becomes thinner and easily vulnerable. Minor injuries – scuffs, bruises, after cutting off nails – lead to the formation of cracks and superficial painful ulcers. To alleviate the suffering, patients give the limb a forced position, lowering it down, sitting asleep. Atrophy of the muscles of the leg and foot progresses. Disability of patients is significantly reduced; IV stage – destructive changes. Pain in the foot and fingers becomes constant and unbearable. The resulting ulcers are usually located in the distal extremities, often on the fingers. Their edges and bottom are covered with a dirty gray coating, there are no granulations, and there is inflammatory infiltration in the circle. Swelling of the foot and lower leg joins. Developing gangrene of the fingers and feet often proceeds as wet. Ripple may be absent due to ascending arterial thrombosis. Disability in patients at this stage is completely lost.

The course of obliterating endarteritis is usually long, over several years. It is characterized by periods of exacerbation and remission. Exacerbation is more often observed in autumn and spring. There are two main clinical forms of the course of the disease: 1) limited, in which, as a rule, arteries of one or both lower extremities are affected. This form is benign, changes progress slowly; 2) generalized , characterized by damage not only to the vessels of the limbs, but also to the visceral vessels of the abdominal part of the aorta, branches of the aortic arch, coronary and cerebral arteries.

Diagnosis of obliterating endarteritis

Diagnosis of obliterating endarteritis is based on the clinic of the disease, the results of functional tests and special research methods. Among the functional tests, indicating a lack of arterial blood supply is certainly the most revealing symptom of plantar ischemia Oppel , sample Goldflama , Samuels and Shamova , knee phenomenon Panchenko. Rheovasography , ultrasound flowmetry , thermography and angiography of the lower extremities help to establish the diagnosis . Obliterating endarteritis is characterized by a decrease in the amplitude of the main wave of the rheographic curve in the leads from the lower leg and especially the foot, smoothness of its contours, the disappearance of additional waves, a significant decrease in the value of the rheographic index. Rheograms recorded from the distal sections of the affected limb are straight lines. Ultrasound findings usually indicate a marked decrease in pressure in the arteries of the feet, a decrease in the linear velocity of blood flow, and help to clarify the level of vascular damage.
A thermographic study reveals a decrease in the intensity of infrared radiation in the distal extremities. On angiograms , normal patency of the aorta, iliac and femoral arteries is usually visible, the popliteal artery is narrowed, often occluded , the leg arteries are usually obliterated , and a network of small corkscrew collaterals is traced. If the contrast medium fills the affected vessels, then their contours are even, there is no scalloped edges, so characteristic for obliterating atherosclerosis.

Etiology, pathogenesis of Raynaud’s disease

The disease is characterized by spasm of the vessels of the fingers of the upper and lower extremities and very rarely – the tips of the ears and nose. The process is localized mainly on the upper limbs, the lesion is usually bilateral and symmetrical. The main reasons for the development of Raynaud’s disease are prolonged hypothermia, chronic trauma to the fingers, impaired functions of some endocrine organs (thyroid, genital glands), severe emotional stress. Triggers in the development of the disease are disorders of the vascular innervation.

Raynaud’s Clinic

There are three stages of the disease:
stage I – angiospastic . It is characterized by a pronounced increase in vascular tone. There is a short-term spasm of the vessels of the terminal phalanges. Fingers (often II and III hands and I-III feet) become pale, cold to the touch and insensitive. After a few minutes, the spasm is replaced by vasodilation. Due to active hyperemia, redness occurs and the fingers darken. Patients notice a strong burning sensation and sharp pain in them, swelling appears in the area of ​​interphalangeal joints. When the vascular tone normalizes, the color of the fingers becomes normal and the pain disappears. Stage II – angioparalytic . Attacks of pallor of the “dead finger” in this stage are rarely repeated, the brush and fingers become bluish. When lowering the arms down, it intensifies and acquires a purple hue. Swelling and pastiness of the fingers become permanent. The indicated stages last on average 3 years — 5 years. Stage III – trophoparalytic . At this stage, panaritiums and ulcers appear on the fingers. Foci of necrosis are formed, capturing the soft tissues of 1-2 terminal phalanges, less often of the entire finger. With the development of demarcation, necrotic areas are rejected, after which slowly healing ulcers remain, the scars from which are pale in color, painful, fused to the bone.

Differential diagnosis of Raynaud’s disease

Differential diagnosis includes obliterans endarte – Riitta and diseases in which circulatory disorder in the upper limb caused extravasal compression subclavian artery.
In contrast to obliterating endarteritis in Raynaud’s disease, pulsation in the arteries of the feet and radial arteries persists. The disease is more benign. Compression of the subclavian artery can be caused by an additional cervical rib or a highly located I rib (costoclavicular syndrome), a hypertrophied anterior scalene muscle, or its tendon (anterior scalene syndrome), or a pathologically altered pectoral muscle (pectoralis minor syndrome). With the above syndromes, both arteries and brachial plexus are compressed, so their clinic consists of vascular and neurological disorders. Constant trauma to the artery leads to cicatricial changes in its wall, periarteritis and may result in vascular thrombosis. The result of severe disturbances in the blood supply to the upper limb are trophic disorders. The correct assessment of the clinical picture, the results of samples with a change in the position of the limb allows you to differentiate these syndromes from Raynaud’s disease . In patients with an additional VI rib, as well as costal-clavicular syndrome, an x-ray study is important in the diagnosis.

Etiology and pathogenesis of nonspecific aortoarteritis

The etiology is unknown. The combination with diseases such as rheumatoid arthritis, ankylosing spondylitis, ulcerative colitis, suggests the possibility of an autoimmune nature. It is assumed that the disease is associated with tuberculosis, streptococcal infection.
A partial or generalized lesion of the ascending and (or) descending aorta and its branches, sometimes the pulmonary artery, is observed . The middle and outer shell of the vessel or all of the membranes ( panarteritis ) are affected . Infiltration by lymphocytes, plasma cells, histiocytes, sometimes neutrophils and multinuclear giant cells is characteristic. In the terminal stages, the infiltrates disappear, fibrosis develops. Thickening of the inner membrane and fibrosis of the middle and outer membranes lead to a narrowing or obliteration of the lumen of the vessel. There may be aneurysms, stratification of the vessel wall, sometimes with its rupture. Sometimes the aortic valve and coronary vessels are affected, the aortic opening becomes dilated, which leads to aortic insufficiency.

Clinic of nonspecific aortoarteritis

At an early stage, systemic signs are noted – fatigue, weight loss, low fever, arthralgia, or moderate synovitis . Later, ischemic symptoms appear – a decrease in heart rate and (or) noise. The upper limbs become cold, weakness in the arms develops, rapid fatigue, intermittent claudication, pain along the vessels. Dizziness and fainting are often observed, especially when moving from horizontal to vertical, as a result of occlusion of the carotid arteries. Nausea, headache, blurred vision, or ischemic ulcers; narrowing of the aorta or renal larter can lead to arterial hypertension. II far-reaching cases of arterial insufficiency can cause atrophy and ulceration of the skin on the face, scalp, hair and (or) forehead loss, dementia, abdominal pain, myocardial ischemia. Ruptured aneurysms or stratified arteries can lead to sudden death.
During the examination, the determination of the pulse on the radial, brachial, carotid arteries, aorta, auscultation of large vessels, blood pressure should be measured on both arms and legs is of primary importance. Characteristic asymmetric weakening or disappearance of the pulse on the hands, asymmetry of blood pressure. Over stenotic vessels, a rough systolic murmur can be heard. More than half of patients with increased blood pressure.
Collateral circulation can be detected on the shoulders or elsewhere. Aortic insufficiency may be observed. In the active phase of the disease, ESR is increased, moderate anemia may be noted. The white blood cell count is usually normal or slightly elevated. Serum gamma globulins are often elevated.

Diagnosis and differential diagnosis of nonspecific aortoarteritis

At an early stage of the disease, when there are only general nonspecific symptoms (weight loss, fever, arthralgia), it is difficult to make a diagnosis, but the possibility of aortoarteritis should always be considered when developing such symptoms in a young woman. Recognition of aortoarteritis in such cases is based on the detection of noise or decreased heart rate in large arteries. With an expanded picture of the disease, the diagnosis is based on the detection of cerebral ischemic syndrome, ischemic lesion of the extremities with a decrease in heart rate in large vessels, and vasorenal hypertension.
The diagnosis is confirmed by angiography or dopplerography, rheovasography . On arteriogram reveals narrowing – or patchy throughout the valley – vascular segments, expanding areas. These changes are more often observed in the proximal aorta and its branches. The affected arteries are usually too large to biopsy, but they must be examined with surgical intervention.
Differential diagnosis is carried out with arthritis observed with rheumatism, ankylosing spondylitis, Reiter’s disease, syphilis, vasorenal hypertension with atherosclerosis and fibromuscular dysplasia of the renal vessels.

Etiology of embolism

In 92–95% of patients, the causes of arterial embolism are heart diseases and, first of all, myocardial infarction (especially in the first 2-3 weeks of illness), complicated by severe cardiac arrhythmias, acute or chronic left ventricular aneurysm. Cause emboli may be combined rheumatic mitral heart disease with a prevalence of stenosis complicated intraatrial thrombosis due to atrial arrhythmia. Subacute bacterial endocarditis and congenital heart defects lead less often to arterial embolism. Sources of emboli can be aneurysms of the abdominal part of the aorta and large main arteries (in 3-4% of patients with embolism), ulcerative atheromatosis of the thoracic and abdominal parts of the aorta.

Embolism pathogenesis

As a rule, emboli are localized in the area of ​​branching or narrowing of the arteries. Embolism is accompanied by a pronounced reflex arterial spasm, responsible for the formation of an extended thrombus, which blocks the collateral network. With thrombosis and embolism of the main arteries of the limbs in the corresponding vascular pools, acute tissue hypoxia occurs, the main cause of which is a violation of blood flow in the vessels of the microvasculature. In the affected tissues, an excess of under-oxidized metabolic products is formed, which leads to the development of metabolic acidosis. The latter promotes platelet adhesion and the formation of platelet aggregates in the capillary lumen , exacerbating the severity of ischemia.
The increase in hypoxia adversely affects the course of redox processes in the tissues. They increase the content of membrane – toxins – histamine, serotonin, kinins , prostaglandins , which increase the permeability of cell membranes and intracellular membranes. As a result of impaired cellular permeability, subfascial edema of the muscles appears , in which the blood flow deteriorates even more due to compression by the bone-fascial cases. Changes in bone metabolism and cell death lead to the breakdown of lysosomes with the release of hydrolases that lyse tissues. The consequence of this is the development of soft tissue necrosis. From the ischemic tissues in the bloodstream fed suboxide – lennye metabolic products resulting in metabolic acidosis, toxic products, potassium, myoglobin. Severe disturbances in the activity of the cardiovascular system occur, manifested by a deterioration in cardiac activity, heart rhythm disturbances, and gross changes in central hemodynamics. Circulatory hypoxia increases, and renal filtration decreases.

Hypertonic conditions

An increase in blood pressure in older children and adolescents occurs, filed by various authors, in 5 – 10% of cases. It should be emphasized that the increase in blood pressure does not yet give rise to a diagnosis of hypertension, since in many cases these phenomena are transient in nature. However, the detection of arterial hypertension must necessarily lead to a comprehensive examination of the child to establish its cause.

Etiology and pathogenesis of hypertensive conditions

Arterial hypertension in childhood can be caused by various diseases: glomerulonephritis , pheochromocytoma , congenital malformations of the heart ( coarctation of the aorta), kidneys and their vessels; in young children – infectious diseases that occur with toxicoexicosis and sensitization of the body, the consequences of a birth injury to the skull. A hereditary predisposition and neurohumoral dysregulation of vascular tone play a role . There is an activation of the function of the sympathetic-adrenal system, an increase in the sensitivity of adrenoreceptors to catecholamines (which may be hereditary). This leads to an increase in systolic ejection and cardiac output with normal peripheral vascular resistance (i.e., with normal vascular tone). In some patients, vasoconstriction occurs with an increase in peripheral vascular resistance.
In children of high school age and adolescents, neuropsychic overstrain and mental fatigue with limited physical activity (irrational daily routine) may be important, especially with prolonged exposure to these factors. These points may be the cause of primary arterial hypertension.

Classification of hypertonic conditions

Three forms of arterial hypertension in children are distinguished (M. Ya. Studenikin ): vascular vegetative dystonia of the hypertensive type, hypertension, and symptomatic (secondary) hypertension.

Clinic of hypertonic conditions

In most cases, children do not complain, increased pressure is detected by chance during mass preventive examinations. However, in some cases, headache, increased irritability and fatigue, dizziness are noted. From the side of the heart, a resistant apical impulse is detected, functional noise is heard, sometimes an II tone accent above the aorta. Systolic blood pressure exceeds the age norm, and during exercise rises by 2.7 – 5.4 kPa.
In the development of hypertension, there are three stages: transient, labile and stable. Changes in blood pressure with an increase in systolic and then diastolic in parallel with changes in organs (heart, kidneys, on the fundus) are gradually increasing.

Diagnosis and differential diagnosis of hypertensive conditions

Primary arterial hypertension must be differentiated with diseases in which an increase in pressure is the leading symptom ( glomerulonephritis , pituitary and adrenal tumors, etc.). A typical clinic of these diseases helps to establish the correct diagnosis.

Hypertensive prognosis

Arterial hypertension is more often reversible. In some cases, increased blood pressure is persistent and is the initial phase of hypertension.

Hypertensive treatment

With secondary arterial hypertension, therapy of the underlying disease is necessary. Primary arterial hypertension in some cases with the vegetodystonic genesis of vascular disorders and a slight increase in blood pressure requires only the organization of a rational regime of the day, the expansion of motor activity with limited mental work. It is necessary to slightly reduce the training load, to ensure prolonged sleep and stay in the fresh air. Useful sports and exercise, but without participating in competitions. The purpose of sedatives (valerian, bromides, seduxen, elenium, trioxazine ), antihistamines and others, physiotherapy (electrophoresis according to the method of G. Kassil with solutions of calcium, magnesium salts) are shown .
In the absence of a therapeutic effect and high blood pressure, the patient is sent to a hospital and p- adrenoblockers ( anaprilin , inderal , obzidan , trazikor , wisken ) are included in the treatment regimen . Treatment begins with minimal doses, and then after 10 days the dose is increased ( anaprilin , trazikor 0.01 – 0.02 g 2 times a day, then – 0.03 g 2 times a day). Continue treatment for 2 to 3 months or more. Rauwolfia preparations in such patients are ineffective. B- Adrenergic blockers can not be used for bronchial asthma, signs of myocardial damage (according to ECG). In the absence of effect, especially in adolescents, as well as in stage II and III arterial hypertension, rauwolfia – raunatin preparations are used (0.002 – 0.003 g 1 – 2 times per day), reserpine (0.1 – 0.15 mg 3 times a day). Parallel used dihlotiazid – hydrochlorothiazide (1 every 2 – 3 days).
Treatment with rauwolfia preparations is carried out until a clear effect is obtained (lowering blood pressure), after which they are transferred to maintenance doses (2 to 3 months). If this therapy does not work, patients with high blood pressure are prescribed ganglion blockers – pentamine , isoprine and others with mandatory hemodynamic control and compliance with the appropriate regimen.

Prevention of hypertensive conditions

The correct regime of the day, physical education, sports, a fairly long sleep.

Etiology, pathogenesis of the open ductus arteriosus

The arterial ( botall ) duct (OAP) in the prenatal period connects the aorta to the pulmonary artery. This is the necessary anatomical structure of the embryonic circulation. After the birth of the baby, the duct function stops almost immediately. The process of anatomical closure of it lasts no more than 2-8 weeks . In some cases, the closure of the duct does not occur. Such a defect accounts for 10-25% of all congenital heart abnormalities. The arterial duct moves away from the aortic arch opposite the left subclavian artery, goes obliquely anteriorly and downward, falling into the bifurcation of the pulmonary trunk or into the left pulmonary artery. The duct has the shape of a cylinder or a truncated cone 10-25 mm long and up to 20 mm wide.

The primary violation of hemodynamics is associated with a difference in pressure in the aorta and the pulmonary artery, which leads to persistent systolic- diastolic aortopulmonary discharge of blood (from left to right). At the same time, there is a volume increase in pulmonary blood flow, which depends on the ratio of the diameters of the aorta and duct. With a significant diameter of the latter, most of the blood pumped into the left ventricle enters the pulmonary artery from the aorta. As a result, pulmonary blood flow may exceed that in a large circle of blood circulation. Due to chronic oxygen starvation of the body, the child lags behind in physical development. Significant volume overload of the vessels of the pulmonary circulation leads to frequent bronchitis and pneumonia. Hemodynamic compensation is initially supported by shock and minute volumes of the left ventricle due to its diastolic overload. In the future, there comes a spasm of pulmonary arterioles with their subsequent sclerosis , which leads to a significant decrease in the vascular capacity of the pulmonary circulation. This process at certain stages causes pressure balancing in the aorta and the pulmonary artery, and sometimes even leads to an inversion of blood discharge (from right to left). From this moment, blood begins to flow into the arterial bed, cyanosis appears ( cyanotization of the defect). At the same time, systolic overload of the right ventricle increases and OAA becomes its salvage drainage, the closure of which can cause acute right ventricular failure. However, in OAP, cyanotization is rare.

Clinic of the open arterial duct

The clinic depends on the magnitude of the OAA, the pressure level in the pulmonary artery and the ratio of the resistance of the vessels of the small and large circles of blood circulation. Allocate 4 stages of OAP: I – systolic pressure in the pulmonary artery is less than 40% blood pressure; II – moderate hypertension (systolic pressure in the pulmonary artery is 40-45% of blood pressure; III – severe hypertension (systolic pressure in the pulmonary artery is more than 75% of blood pressure, blood discharge is preserved from left to right); IY – state of extreme severity (systolic pressure in the pulmonary arteries is equal to or higher than blood pressure, cyanotization of the defect).

Complaints of patients with OAP are nonspecific. The most common complaints are fatigue, shortness of breath with physical exertion , sometimes sensations of interruptions in the work of the heart, palpitations, pneumonia. The lag in physical development, pallor of the skin is characteristic. When straining, cyanosis is more pronounced in the lower half of the trunk and on the lower extremities. On palpation of the chest determines the gain of the apical impulse, systolic or systolic -diastolicheskoe jitter in the projection base of the heart. The borders of the heart are expanded, but their quantitative characteristics are different. With a large arteriovenous discharge, the pulse is fast and high. Pulse pressure – with a tendency to increase. In young children, diastolic pressure can be reduced to 0. Auscultation reveals the main diagnostic sign of OAP – a rough, “machine” systolic- diastolic murmur in the second intercostal space to the left of the sternum. Noise is carried into the interscapular space and on the vessels of the neck. The diastolic component is better heard when straining ( Valsalva test ). As pulmonary hypertension there is a tendency to disappear first Diastolic – of the noise component, and subsequently – and systolic. Patients with stage IV it is virtually wrinkle ” Afonichev ” or accompanied by the appearance Protodeacon – stolicheskogo noise relative valvular insufficiency, pulmonary arterial (noise Graham Stille ). Against this background, II tone over the pulmonary artery progressively amplifies. Sometimes it can be split and the accent of the pulmonary component of II tone is heard

Diagnosis of open ductus arteriosus

In typical cases, a rhomboid-like systolo- diastolic murmur is recorded on the FCG over the pulmonary artery . As pulmonary hypertension increases, the tendency to the disappearance of the diastolic and decrease in the systolic component of the noise correlates with the amplification and splitting of II tone over the pulmonary artery. In the later stages of the defect, the protodiastolic murmur of Graham Still is recorded . There are no specific changes on the ECG. A normogram or levogram is marked . In the future, signs of hypertrophy of both ventricles with an outcome in the rightogram and isolated hypertrophy of the right ventricle are determined . When x-ray examination in the initial stages are noted: increased vascular pattern, left ventricular hypertrophy, increased aortic pulsation. In the future, a tendency to swelling and an increase in the pulse amplitude of the pulmonary artery, depletion of the pulmonary pattern, and hypertrophy of the right ventricle is determined . Dopplerographic examination in some cases captures the aorto-pulmonary shunt. When catheterization of the right heart revealed an increase in oxygen saturation of the blood in the pulmonary artery compared with the right ventricle by at least 2 vol. % Aortography makes it possible to obtain simultaneous contrasting of the pulmonary artery, into which the contrast medium enters through the OAA.

Etiology, pathogenesis of aortic coarctation

Coarctation of the aorta accounts for 4-15% of all congenital heart defects. The origin of this defect is associated with an abnormality in the transformation of the aortic isthmus during the formation of extrauterine circulation. The disease is 2–2.5 times more common in males. Bonnet proposed to distinguish between two types of coarctation of the aorta: 1) “infantile”, in which the aorta is narrowed over a large distance above the place of discharge of the OAP; 2) “adult”, in which the narrowing is observed only on a short segment of the aorta (segment), usually in the area of ​​transition of the arch to the descending part below the site of the OAA (isthmus of the aorta). For practical purposes, it is convenient to consider 4 options for coarctation of the aorta: I) isolated, 2) coarctation of the aorta in combination with OAP; 3) coarctation of the aorta in combination with DMS; 4) coarctation of the aorta in combination with other congenital heart defects.

Circulatory disorder is manifested by severe hypertension in the arterial vascular pool above coarctation and hypoperfusion below it. In this case, hemodynamic compensation is achieved due to the development of collateral arteries connecting the upper and lower parts of the body (intercostal, internal mammary arteries, internal mammary arteries). Decompensation is manifested by malignant hypertension, deep sclerotic changes in the walls of the arteries. HELL sometimes reaches 300 mm Hg . (40 kPa). The consequence of this are cerebrovascular disorders up to the development of hemorrhagic stroke, heart and kidney failure. The expansion of the intercostal arteries leads to a compressed – NIJ roots of the spinal cord, severe spinal disorders (paralysis, disruption of the pelvic organs). In the origin of arterial hypertension, in addition to the mechanical cause, a significant role is given to renal vasopressor , a weed factor that is a direct consequence of renal ischemia.

Depending on the type of defect, various hemodynamic disorders occur. With the “adult” type of coarctation with a closed arterial duct, systolic overload of the left ventricle comes to the fore. In the “infantile” type, when there is OAP, pulmonary hypertension develops rapidly with an outcome in cyanosis of the lower half of the body. The combination of defect with defects of the septa significantly accelerates the onset of pulmonary hypertension.

Clinic for aortic coarctation

In most cases, with this defect, imbalance is detected due to the pronounced development of the muscles of the shoulder girdle in comparison with the relative underdevelopment of the muscular system of the lower extremities. Moreover, blood pressure in the upper extremities is significantly increased. The pulse on the arteries of the thigh is sharply weakened or absent. The pulsation of the abdominal aorta is also not determined. In some cases, it is possible to detect the pulsation of the dilated intercostal arteries during tissue capture in the subscapular region. When ascultation is determined: a pronounced accent of II tone above the aorta, systolic murmur under the right clavicle, in the interscapular space on the left and on the vessels of the neck. The rest of the clinical picture in adult patients repeats all the signs of defects stenosing the outlet arterial tract of the left ventricle (aortic stenosis) with its pronounced systolic overload. In general, the physical picture is changeable and meager. That is why this anomaly requires special attention of doctors, since it is associated with frequent diagnostic errors.

Diagnosis of aortic coarctation

Under normal conditions, blood pressure in the lower extremities is 29-30 mm Hg higher . (2.7-4 kPa) than on the top. When comparing blood pressure levels under coarctation of the aorta, the pressure on the lower extremities (the auscultation point in the popliteal fossa with the location of the cuff on the thigh) is not determined or significantly reduced. Coarctation should be considered pronounced if the pressure gradient between the upper and lower extremities reaches 40 mm Hg . (5.3 kPa). Depending on the level of blood pressure, 3 stages of the defect are distinguished: I – moderate (blood pressure below 150 mmHg (20 kPa); II – moderate severity (blood pressure – 150-200 mmHg (20-28.7 kPa ); III – severe (blood pressure greater than 200 mmHg (26.6 kPa). X-ray and ECG data for this anomaly are characteristic of hypertension and are signs of left ventricular hypertrophy. Dopplerography and chest tomography are of great help in the diagnosis in the sagittal plane.With a typical isolated form, the anomalies of the listed means are sufficient to establish final diagnoza.V doubtful cases should resort to aortography . Thus aorta contrasted through the arterial branch of the shoulder belt with a mandatory recording layer the pressure gradient in the coarctation . When concomitant congenital heart diseases shows angiocardiography and sensing cardiac cavities.

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Etiology of peripheral arterial aneurysm

The most common causes of non-traumatic aneurysms are atherosclerosis and syphilis. Traumatic aneurysms, or false, are formed after gunshot and stab wounds, less often – due to a blunt injury. Their development is possible in the presence of a narrow wound channel, a small area of ​​damage to soft tissues, covering the wound opening with skin or tissues. Under these conditions, blood poured from the damaged vessel accumulates in the surrounding tissues, exfoliating them, and a periarterial pulsating hematoma occurs . The clots that form in it are pushed to the periphery by a stream of blood, condense, organize, as a result of which a connective tissue capsule is formed and a pulsating hematoma turns into a false aneurysm . Pathological anatomy. Three types of traumatic aneurysms are distinguished: arterial, arteriovenous and combined . An arterial aneurysm has an aneurysmal sac that communicates with the lumen of the artery. Arteriovenous aneurysm is the result of simultaneous damage artery and vein, which leads to the formation or arteriovenous – th fistula or aneurysms intermediate. With combined aneurysms, a combination of these types of aneurysms is observed. With the prolonged existence of an arteriovenous aneurysm, the wall of the leading artery changes significantly , which is manifested by its thinning, a change in the internal elastic membrane, resulting in an increase in the diameter of the artery. On the contrary, in the wall of the vein extending from the aneurysm, hypertrophy of the muscle membrane and the development of the internal elastic membrane are noted. The diameter of the vein also increases.

Pathogenesis of peripheral arterial aneurysm

Arteriovenous and combined aneurysms cause severe hemodynamic disorders. In this case, not only peripheral blood circulation is disturbed, but also central hemodynamics. A pathological discharge of arterial blood into the venous system leads to difficulty in the outflow of venous blood from the affected limb, as well as to an increase in the volume of blood flowing to the right atrium. Due to venous stasis, superficial veins expand, swelling and trophic changes in the distal extremities occur. Working myocardial hypertrophy develops, which is then replaced by myogenic dilatation with cardiac decompensation.

Clinic of peripheral arterial aneurysm

The main complaint of patients is the presence of a pulsating formation in one or another segment of the limb. When viewed at the site of an arterial aneurysm, a swelling is visible, often pulsating. On palpation, it has a densely elastic consistency, is clearly delimited, round or oval, pulsates synchronously with the contractions of the heart. With auscultation over the area of ​​the aneurysm, systolic murmur is determined, which disappears when the leading artery is compressed. Ripple to the periphery from the aneurysm is often weakened. Hand applied to the site of the aneurysm, the jitter can be felt or purling (symptom of feline purring) .Patognomonichnym symptomatic arteriovenous aneurysm is a slowing of heart rate for 15-30 min in 1, combined with an increase in blood pressure in the artery leading cross-clamping (Dobrovolskaya symptom). The slowdown of the pulse is due to an improvement in cardiac activity due to a decrease in blood flow to the right atrium.

Complications of peripheral arterial aneurysm

Complications of the aneurysm are rupture of the aneurysmal sac, accompanied by profuse, life-threatening bleeding, thromboembolism and thrombotic masses contained in the aneurysm. With a traumatic aneurysm, an outbreak of a dormant infection, the development of soft tissue phlegmon are possible. A number of patients develop severe trophic disorders and cardiac disturbances, depriving them of their ability to work.

Diagnosis of peripheral arterial aneurysm

Diagnosis is not difficult when there is a pulsating swelling and vascular noise. To clarify the true shape and size of the aneurysm, localization, the state of the distal and proximal arterial bed and the degree of development of collateral blood flow, arteriography is necessary .

Temporal Giant Cell Arteritis

Temporal giant cell arteritis , cranial arteritis, temporal arteritis , Horton’s disease is a systemic lesion of arteries, mainly of muscular-elastic and muscle types.
In temporal giant cell arteritis, the vessels of the head (primarily the temporal arteries) and the thoracic aorta are most often affected. As a rule, elderly people are older than 50 years old, most often women. Several family cases of the disease are described. Temporal giant cell arteritis belongs to the group of allergic vasculitis .
The etiology is not known, possibly viral. There is a connection with respiratory infections, the content of birds (parrots) in the house, and the detection of hepatitis B surface antigen in serum.

Pathomorphology of the temporal giant cell arteritis

In areas of vascular lesions, fixed immunoglobulin M and immunoglobulin G, components of the complement of the system, are detected. The acute phase is characterized by the phenomena of mucoid swelling, fibrinoid degeneration in the intima and middle lining of the arteries with thromboangiitis obliterans, necrotic changes and the transition to sclerosis. As part of the granulation tissue, giant multinuclear cells similar to Pirogov- Langgans cells are detected .

Clinic of the temporal giant cell arteritis

The onset of the disease is most often gradual – with the appearance of pain and stiffness in the neck, shoulder girdle, malaise, nausea, loss of appetite. An acute onset is also possible – high fever , sharp headaches in the area of ​​the affected vessels, sometimes with impaired and loss of vision. A painful and throbbing temporal artery is palpated. In temporal giant cell allergy, there may be a combined lesion of the coronary and abdominal vessels.
There is a frequent combination of this disease and rheumatic polymyalgia ( Forestier – Sertonsini syndrome ), which consists in the appearance of symmetric polymyalgia in the elderly , especially in the neck muscles. shoulder girdle, and accompanied by low-grade fever, asthenia , anorexia.
In both cases, there is a sharp increase in ESR – from 50 to 100 mm / h, hyper-A2-globulinemia, hypoalbuminemia , moderate hyperchromic anemia.

Treatment of temporal giant cell arteritis

There is a pronounced effect of glucocorticosteroid therapy (differential diagnostic sign of temporal giant cell arteritis). Symptom attenuation occurs within a few days after the administration of the glucocorticosteroid drug (initial dose of 40-50 mg, followed by a decrease to a maintenance dose of 5-10 mg). Long-term use of delagil , indomethacin is indicated , for relieving pain during an attack – novocaine chipping of near-arterial tissues.