Rheumatism licks the joints and bites the heart!
Streptococcal infection is usually in the form of prolonged and / or recurrent purulent tonsillitis. The long presence of this organism in the pus on the tonsils entails as the second disease rheumatism. Of all the microorganisms only beta hemolytic streptococcus group A can lead to development of rheumatism. Why him?
After the usual inflammatory reaction can not cope with a cause of disease, the stage goes immune system . Antibacterial immunity is humoral. This means that in the fight against strep organism relies on the production of antibodies by plasma cells (activated B lymphocytes).
These cells for about ten days produce large amounts of antibodies (immunoglobulins) against the surface proteins of streptococci. Immunoglobulins are spread through the bloodstream to all tissues in order to seek and destroy the cause of inflammation (streptococci).
This germ, however, have surface antigens (membrane proteins) that are fully comparable with some antigens of human tissues. For example:
M-protein of streptococci is almost identical to the protein Myosin from human muscle cells; hialuronatnata capsule of the bacterium was identical in structure and composition with human hyaluronic acid which is present in the body povsevmestno as the main ingredient of connective tissue.
This similarity “wrong” antibodies and they are sasoyanie streptococci to differentiate the cells of normal tissue. Consequently, the antibodies circulate throughout the body and also to streptotokokite throat, they begin to attach to the membranes of normal cells.
These are called. cross-reactive antibodies that can be detected in the serum – elevated titers antistreptolizin O antistreptokinaza and antistreptohialuronidaza. These immunoglobulins deplete the body’s own cells, “thinking” that they are bacteria. Inflammatory processes in the bodies running from these “autoantibodies” defines the clinical presentation, severity of course of rheumatism and prognosis of the patient’s life.
Normal ESR exclude the presence of rheumatism!
Tissues for rheumatism are sterile. They did not detect microbiological testing streptococci (except in the pus of angina).
Organ damage in rheumatic
Damage to the heart and engage the three layers of the wall – pericardium (heart sac and the outer surface of the heart), myocardium (heart muscle) and endocardium (inner lining).
Outer covering (pericardium) prejudice in the form of acute fibrinous inflammation. The surface of the heart is covered with whitish exudate, which can be drained of fiber and heart to get ciliates species. This version of fibrinous pericarditis is called Cor villosum. Inflammatory exudate in most cases be absorbed, but remains rare focal adhesions not zatrunyavat cardiac function.
Involvement of the myocardium (heart muscle) of the inflammatory process leads to the development of revmatizmalen myocarditis. The typical morphological picture is presented by granulomatous inflammatory reaction in cardiac muscle. These focal chronic inflammatory infiltrates are called granulomas of Ashov and contain macrophages, histiocytes, Anichkov cells and giant cells of multi Ashov.
Effect on the inner lining of the heart in rheumatism goes through several phases:
Valves lanes are juicy, swollen. Microscopic changes are owned by their razrehavyavane stroma and change the basic substance of connective tissue, which is proved by the reaction metahromaziya stained with toluidine Blau. Altered tissue change background color of blue dye and dyed purple.
The jet of blood flow through the cardiac chambers is strongest in the center of the stream. There are edges of the canvas flaps that are already damaged by previous stages of rheumatic inflammation.
Endothelial cells on the edges of the boards are scaling the strength of blood flow, because they are no longer firmly attached to the stromal (base) of valves lanes. Coagulation system is activated at the drop endothelial cells form thrombotic sediments that look like beads of rosary.
These bradavitsovidni thrombi consisting mainly of platelets and fibrin are located on the surface of the sails flap, which is on the side of incoming blood. Thus, the knots in mitral valve is located on the side of the left ventricle and those of aortic valve – side left ventricle.
The growth of connective tissue valves lane as an exit from the inflammatory process distortions of the valves and the development of heart defects. Valve defects in rheumatism commit most often mitral valve and second valve of the aorta. Depending on how the strain of the sails flap, subject to the grown connective tissue, formed two major types of defects – stenosis and / or insufficiency.
Stenosis is a narrowing of the valves opening due to scarring of valves lanes. This narrowing prevents the entry of sufficient amounts of blood in the heart cavity. In mitral valve stenosis appears to be injured left ventricle. Due to the small amount of blood coming in, she made a long time less work (less redundancy) and over time undergoes atrophy (reduced size).
At the same time, retained blood in the left atrium leads to its enlargement (hypertrophy and dilatation). Vihrovidnite movements of blood created by compromised hemodynamics favor the development of thrombosis . Formed thrombus in the left ventricle can grow on the ground, spinning with blood flow in the heart cavity.
This thrombus has a round shape and can reach rozmeri to egg yolk. If at one point he went to pass through the funnel narrowed mitral orifice, most likely stuck in the narrowed valve and cause sudden death by stopping the flow.
You do not have patients with mitral stenosis wait for this moment!
Cardiac operations has long become routine and is successful in most major hospitals in the country!
Insufficiency of a valve is insufficient to tightly close the valves canvas, allowing the return of blood into the adjacent cardiac cavity
If you followed a new bout of rheumatism and the process is repeated again on the already strained valve canvas, it deepens and aggravates valve defects.
Myocarditis severity determines the course of acute rheumatism in, and valve defects remaining after endocarditis are responsible for disability and prognosis in these patients.
Joints – migratory polyarthritis
Are affected large joints – knee, ankle, elbow, wrist. Damaged joint is swollen, red and very painful. After two to three weeks resolved symptoms and inflammation is transferred to another joint. So called migratory arthritis.
For other types of joint damage read Arthritis and arthrosis
Cutaneous manifestations of rheumatic fever
Annular erythema marginatum
Rose-red, partly scattered spots on the body, especially around the navel (periumbilikalno) spots.
Red and blue spots, painful pressure and located usually legs.
Nervous system – Chorea Minor (Sydenham of)
Develops as a late-onset (within months!) of rheumatism and is expressed in uncontrolled movements of arms and signs of clumsiness in children. They spill the soup, broken vessels start to write ugly …
Initial symptoms of rheumatic fever:
- Increasing the temperature
- Headache, sweating
- Tachycardia (heart palpitations)
- Swelling and pain in large joints, which migrate from going into a joint
All these traits are developed 2-4 weeks after purulent tonsillitis!
Rheumatism can develop and unnoticed underground. His only event may be feeling unwell and subfebrilna temperature (37.2 to 37.4 0 C). Other hidden events could be revmatizmalni subcutaneous nodules and red spots on the skin (erythema, purpura). Effect on the nervous system (Sydenham Chorea minor on) can also make symptoms with valuable diagnostic value. The change in the student’s handwriting can be a sign of infantile rheumatism.
- Festering angina treated with an antibiotic prescribed by a doctor. Self-medication is as dangerous as lack of treatment!
- After completing the course with antibiotic therapy should be made examination to establish the effect of it!
- Treatment of streptococcal antgini is done with penicillin. In all streptococcal infections penicillin is the tool of choice, since without exception all streptococci are sensitive to it!
- Other prevention is also made with penicillin preparations and should continue over 10 years, up to age 25.
- Removing the tonsils (tonsillectomy) should be done under penicillin protection!
- Extraction of teeth too!
“Concepts such as” stubborn, “” stubborn, “” nepovratliv “are linguistic similarities with the word” stiff “and correspond to the nature of arthritis patients, whose personal profile is well known, thanks to psihosomatikata already half a century exploring this group patients.
These traits issue proper rigidity and hard-headed of those people and show how flexible and mobile enough is their consciousness. “
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Filed under: List of Diseases
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