Presentation on the topic: Reactive arthritis. Slide description:. Clinical demonstration On the topic: “Reactive arthritis.” Slide description:. Discussion of complaints and anamnesis When analyzing complaints, it is important to pay attention to damage to mainly large, peripheral joints. The lesion is asymmetric, predominantly of the lower extremities, especially the knees and ankles.
ascending character, presence of low-grade fever. The main thing you need to pay attention to is the medical history. In a patient with suspected reactive arthritis, it is IMPORTANT that this is the absence of a traumatic factor and the presence of a previous urogenital or gastrointestinal infection 3-4 weeks ago. Slide description:. Objective status General condition is satisfactory. Consciousness is clear and adequate. Oriented in place and time.
Clinical and laboratory manifestations of juvenile rheumatoid arthritis in children based on cardiorheumatological materials.
Presentation on the topic: Arthritis and arthrosis of the TMJ. Get code Our banners. Arthritis and arthrosis of the TMJ Completed by: 5th year student Group 090716. High-tech methods of treating rheumatoid arthritis Cardiological clinic Ilyushina Larisa Viktorovna You can download this presentation on the topic Rheumatoid arthritis (RA) differentiated treatment on the page. In the Presentations section on the topic of rheumatoid arthritis, you can find 222 presentations available for downloading and viewing online.
Calm behavior. The physique is hypersthenic. Obesity II degree.
Height 165 cm. Weight 83 kg. The skin is dry, clean, the color of the skin is pale pink, the elasticity of the skin is preserved, the visible mucous membranes are pale pink, moist. The lymph nodes are not palpable, with the exception of the inguinal ones, which are enlarged to the size of a cherry, moderately painful, and easily displaced. There are no rashes, scratches, petechiae, or scars. The musculoskeletal system is developed. The degree of muscle development is normal, the tone is normal.
The area of the hip joints is without features. The shape of the chest is hypersthenic. Mixed breathing type. The number of breaths is 18 per minute. Shortness of breath of a mixed nature. Breathing is weakened. Both halves of the chest participate in the act of breathing evenly.
No pathological symptoms were detected by palpation. Vocal tremor is carried out over the entire surface of the lungs. Percussion clear pulmonary sound. The apex beat is not visible, there is no pathological pulsation of the vessels. Palpation of the heart and blood vessels: Pulse – 78 beats per minute, satisfactory filling, rhythmic, identical in both arms. The apical impulse is palpated in the 5th intercostal space 2 cm outward from the left midclavicular line. Heart sounds are rhythmic and muffled.
Heart rate – 80 per 1 min. There is no noise. Blood pressure – 150/90 mm. Hg Art. The abdomen is of normal shape and size, evenly participates in the act of breathing, soft, painful. The abdomen is soft, painless, accessible for deep palpation in all parts.
On palpation, the lower edge of the liver protrudes from under the edge of the costal arch by 2 cm along the right midclavicular line, smooth, tightly elastic, painless. The stool is daily, formed, the color of the stool is normal without pathological impurities. Urine is light yellow in color and transparent. Urination is free, painless, 5-6 times a day. Localization status: The right knee joint is swollen. hot to the touch, movement in it is limited due to pain, the left ankle is swollen, hot to the touch, painful when moving.
Slide description:. Discussion of objective data As a rule, when there is a connection with a urogenital infection, a characteristic clinical sign is inguinal lymphadenopathy. As well as the clinical picture of arthritis of the affected joints. Slide description:.
Laboratory tests CBC erythrocytes - 5.42x10^12/l leukocytes - 6.6x10^9/l, hemoglobin 146 g/l, platelets - 342x10^9/l, ESR - 8 mm/h, segments 50%, rods 1% lymphocytes 44%, monocytes 5%. Bilirubin total – 12.8 mmol/l, direct bilirubin – 2.6 mmol/l, alkaline phosphatase – 111 U/L, GGTP – 97 U/L, creatinine 0.083 mmol/l, total protein. 66 g/l, CEC in blood serum - 138 units Blood test for streptolysin O 19.
11. 2012: Reaction: negative < 8 mU/ml Glycemic curve after glucose load 11. 20, 2012: Fasting 3.7 mmol/l13. 00–4.0 mmol/l, 17.00–4.2 mmol/l TAM 20.11.
2012: straw yellow, cloudy, reaction – acidic, protein – no, glucose – no, squamous epithelium single 1-2 in the field of view, erythrocytes – single, leukocytes – single HIV, antibodies to hepatitis C virus, B negative Antigens of the HLA system -B 27 Microbiological examination of feces - without pathology Scraping of the urethral epithelium for chlamydia, culture and determination of sensitivity to antibiotics - the result is positive Detection of chlamydia by PCR in a scraping from the urethra - positive.
RHEUMATOID ARTHRITIS (RA - M05, M06) RHEUMATOID ARTHRITIS (RA - M05, M06) RA is a systemic inflammatory disease of connective tissue with predominant damage to the joints of the type of chronic progressive erosive-destructive polyarthritis. In any case, this is a severe, chronic disease, manifested by inflammatory arthritis, mainly of the joints of the extremities, usually of a symmetrical nature. Possible damage to the hematopoietic, cardiovascular and nervous systems, lungs, eyes, salivary glands, etc.
Epidemiology and manifestation Epidemiology and manifestation In Europe and America, RA affects from 1 to 3% of the total population. Women get sick 2-3 times more often than men, although in old age the difference in the incidence rate may be leveled out.
Etiology Etiology By and large, RA (like many other diseases) is a disease of unknown etiology. There is evidence of the importance of genetic factors in the etiology of RA. Thus, among homozygous twins, concordance is 32% versus 9% for heterozygous twins. In subjects with RA, increased detection of HLA antigens DW4, DW14, DR4 and DR1 was also noted.
If an individual has these genetic risk markers, bacteria such as E. coli, Yersinia, Clostridia and others can serve as trigger factors. It is known that antibodies to IgG, the so-called rheumatoid factor (RF), play a role in the genesis of RA. It has been established that such antibodies appear in the blood of animals when they are re-immunized with Escherichia coli or some other bacteria. If an individual has these genetic risk markers, bacteria such as E. coli, Yersinia, Clostridia and others can serve as trigger factors. It is known that antibodies to IgG, the so-called rheumatoid factor (RF), play a role in the genesis of RA. It has been established that such antibodies appear in the blood of animals when they are re-immunized with Escherichia coli or some other bacteria.
Pathogenesis. Lots of theories, but very little that is clear. Pathogenesis. Lots of theories, but very little that is clear. Classification. According to the ICD Xth revision, there are: 1. Seropositive RA (M05). 2. RA with splenomegaly and leukopenia (s. Felty) (M0.0). 3.RA with the involvement of other organs and systems (M05.3). 4. Other seropositive rheumatoid arthritis (M05.8). 5. Seropositive RA, unspecified (M05.9). 6. Other RAs (M06). 7. Seronegative RA (M06.0). 8. Still's disease developed in adults (M06.1). 9 Other specified RAs (M06.8). 10. RA, unspecified. In our country there is a classification proposed by the Institute of Rheumatism:
A. By forms: 1. RA (with specification - polyarthritis, oligoarthritis, monoarthritis). 2. RA with systemic manifestations (specify which ones). 3. Special forms of RA (Felty, Still syndrome). A. By forms: 1. RA (with specification - polyarthritis, oligoarthritis, monoarthritis). 2. RA with systemic manifestations (specify which ones). 3. Special forms of RA (Felty, Still syndrome). B. According to immunological characteristics: seropositive and seronegative (according to detectability in the blood of the Russian Federation). B. Downstream: 1. Slowly progressive. 2. Rapidly progressive. 3. Without noticeable progression. Hardening of joints, formation of osteophytes.
D. By degree of activity: 1. Remission. 2. Minimal activity. 3. Medium and 4. High activity. D. By degree of activity: 1. Remission. 2. Minimal activity. 3. Medium and 4. High activity. D. According to the patient’s functional ability: 1. Professional ability to work is preserved. 2. Professional ability to work is lost. 3. Lost ability to self-service. E. Stages of the disease. The stages of RA are determined radiographically. Stage 1 - the bone elements of the joints are unchanged. 2 - beginning osteoporosis in the joint area, subcortical bone destruction is possible. 3 - destruction of the joint without ankylosis and 4-ankylosis.
CLINICAL DATA CLINICAL DATA Questionnaire data Complaints. The dominant complaint of patients is constant pain in many joints, their swelling, and poor general health. If the disease lasts for a long time, there may be complaints about joint deformation or ankylosis, as well as complaints related to damage to various internal organs.
A characteristic sign of RA is stiffness that appears after physical rest, especially after night, in the morning. The duration of stiffness depends on the activity of the inflammatory process, however, in any case, morning stiffness lasts for at least an hour. A characteristic sign of RA is stiffness that appears after physical rest, especially after night, in the morning. The duration of stiffness depends on the activity of the inflammatory process, however, in any case, morning stiffness lasts for at least an hour.
Anamnesis morbi. They find out when the disease began, from which joints the disease began, how the coverage of the joints progressed (successively with the subsidence of the process in the first joint or successively without improvement, several joints were covered. Treatment, anamnesis of drug tolerance, allergic manifestations, insurance history. Anamnesis morbi. Find out when you got sick, from which joints the disease began, how the coverage of the joints proceeded (successively with the subsidence of the process in the first joint or successively without improvement, several joints were covered. Treatment, history of drug tolerance, allergic manifestations, insurance history. Anamnesis vitae. In the life history, points that could be risk factors for RA - heredity, living in areas with a cold climate, previous intestinal diseases.
Complaints and development of the disease. The disease may be preceded by a prodrome - weakness, malaise, arthralgia, myalgia. Against this background, acute arthritis soon develops, most often in several small joints of the arms and (or) legs. In approximately 2/3 of patients, the disease manifests itself as symmetrical involvement of the joints in the process. Complaints and development of the disease. The disease may be preceded by a prodrome - weakness, malaise, arthralgia, myalgia. Against this background, acute arthritis soon develops, most often in several small joints of the arms and (or) legs. In approximately 2/3 of patients, the disease manifests itself as symmetrical involvement of the joints in the process.
Subsequently, other joints may become affected by the inflammatory process. In this case, there is one very important feature that, to a certain extent, helps differentiate RA in the acute phase from rheumatic polyarthritis. It lies in the fact that with rheumatism there is a “sequence” of damage to the joints - the second joint is affected only after the inflammation in the first has subsided. If it is RA, then the process in the primary affected joint continues even when the other joint becomes inflamed. Subsequently, other joints may become affected by the inflammatory process. In this case, there is one very important feature that, to a certain extent, helps differentiate RA in the acute phase from rheumatic polyarthritis. It lies in the fact that with rheumatism there is a “sequence” of damage to the joints - the second joint is affected only after the inflammation in the first has subsided. If it is RA, then the process in the primary affected joint continues even when the other joint becomes inflamed.
Objective research data Objective research data Inspection. On examination, you can see swollen joints and cyanotic skin over small joints. The degree of joint mobility, especially extension, is limited.
There was a war. I was in my fourth year. There was a war. I was in my fourth year. Mother died. Father went to the front. My aunts and I went to the Urals, but I heard my father’s “Hurray” there. And the smoke of the attacks corroded my eyes. And the truck on the street is like a tank. And near the river, where there is a cow ford, I shouted “forward” like a commander!” And at the head of the hungry boys, I conquered my fear, not the cows. ….The river has long washed away the children’s footprints. The war remained in me for a hundred years.
Typical changes for RA are subluxation of the metacarpophalangeal joints with ulnar deviation of the fingers and the development of “walrus flipper” deformity of the hands. Superextensor deformity of the proximal interphalangeal joints of the hands with “swan neck” changes in the fingers can often be observed.
The same changes can occur in the toes. The same changes can occur in the toes.
RA is characterized by rapidly occurring atrophy of the muscles of the limbs, which is both a consequence of an aggressive inflammatory process and the often observed hypokinesia of such patients. RA is characterized by rapidly occurring atrophy of the muscles of the limbs, which is both a consequence of an aggressive inflammatory process and the often observed hypokinesia of such patients.
Palpation. By palpation you can determine the presence of local temperature, pain, and rheumatoid nodules. The latter are considered characteristic of RA. They are located in the skin or under the skin in the area of the extensor surface of the forearms, around the joints, and in severely ill bed patients, on the back of the head, above the bony protrusions, where they can be palpated. However, it should be remembered that they are found in only 20-25% of patients. Palpation. By palpation you can determine the presence of local temperature, pain, and rheumatoid nodules. The latter are considered characteristic of RA. They are located in the skin or under the skin in the area of the extensor surface of the forearms, around the joints, and in severely ill bed patients, on the back of the head, above the bony protrusions, where they can be palpated. However, it should be remembered that they are found in only 20-25% of patients.
Percussion in RA is not very informative. Percussion in RA is not very informative. Auscultation can sometimes reveal a systolic murmur associated with thickening of the mitral or aortic valves and mild regurgitation. The course of RA is highly variable, significantly complicating the prognosis in each individual case. Spontaneous remissions and exacerbations are common. Most patients experience a long-term course with varying degrees of joint damage and relative preservation of performance. In only about 10% of patients, the disease proceeds aggressively, progressively, destructively, cripplingly, with the development of contractures in the joints, muscle atrophy and complete disability.
In some cases of RA, systemic (extra-articular) lesions are detected. These phenomena, as well as antinuclear antibodies found in a number of patients, bring RA closer to other systemic connective tissue diseases. In some cases of RA, systemic (extra-articular) lesions are detected. These phenomena, as well as antinuclear antibodies found in a number of patients, bring RA closer to other systemic connective tissue diseases. Systemic pathology of RA can manifest itself in the form of vasculitis (neuropathy, chronic skin ulcerations, gangrene of the fingers, less commonly, visceral arteritis) or disseminated granuloma (lesions of the heart, lungs, sclera, dura mater). Mostly in men, granuloma pneumonitis and diffuse interstitial fibrosis of the lung are observed. This pathology is more common in the “classical” course and seropositivity of RA.
It is impossible not to mention the fairly common changes in the hematopoietic system. In 60% or more of RA patients, anemia of varying degrees is found. An even more common symptom is a very long-lasting high ESR. It is impossible not to mention the fairly common changes in the hematopoietic system. In 60% or more of RA patients, anemia of varying degrees is found. An even more common symptom is a very long-lasting high ESR. RA is quite often complicated by secondary amyloidosis of internal organs. Poor prognostic factors for RA: 1. Symmetrical polyarthritis with subcutaneous nodes and high RF titer. 2. Start before 30 years. 3. Development of systemic phenomena.
But, as clinicians well know, rare nosological entities present with all the symptoms, and RA is no exception in this regard. Therefore, it is proposed to divide clinical and laboratory data into individual signs and consider them as criteria for the presence of the disease. Such criteria are: But, as clinicians are well aware of, rare nosological entities present with all the symptoms, and RA is no exception in this regard. Therefore, it is proposed to divide clinical and laboratory data into individual signs and consider them as criteria for the presence of the disease. These criteria are:
1-morning stiffness; 1-morning stiffness; 2-long-term swelling of at least one joint of the hand, doughy compaction of soft tissues; 3-swelling of at least one more joint in the next 3 months; 4-symmetry of joint damage; 5-detection of subcutaneous nodules; 6-radiographically detected erosions and osteoporosis of bones in the joints or near them; 7-RF in blood serum. The diagnosis of RA is made when at least four of these criteria are present.
Data from additional studies Data from additional studies 1. Study of RF, i.e. antibodies to the Fc fragment of IgG. RF is detected in approximately 75% of patients with RA. It can be positive in RA, Sjogren's syndrome, sarcoidosis, SLE, etc. It follows that the detection of RF is not mandatory for making a diagnosis of RA, since there are seropositive and seronegative options. In addition, for RA, RF titers should be higher than 1: 75, since low titers can be detected in a number of other diseases and conditions (mononucleosis, acute inflammation, in old age).
2. Determination of the level of C-reactive protein in the blood. In RA it is usually elevated. 2. Determination of the level of C-reactive protein in the blood. In RA it is usually elevated. 3. Study of synovial fluid - identification of high leukocytosis of a neutrophilic nature, special cells (ragocytes), and a decrease in its viscosity. 4. X-ray examination of joints: identification of minus tissue - osteoporosis, cystic lucidity of the periarticular parts of the bones. 5. Puncture biopsy of the synovial membrane of the joint, which can reveal rheumatoid nodules, proliferation of synoviocytes, lymphoid-macrophage-plasma infiltrates, and a large number of fibroblasts.
LECTURE IS OVER. THANK YOU FOR YOUR ATTENTION THE LECTURE IS OVER. THANK YOU FOR ATTENTION
. You can download this presentation on the topic Rheumatoid arthritis (RA) differentiated treatment on the page. Rheumatoid arthritis. Slide 63 from the presentation “Examination of a patient” for medicine lessons on the topic “Diagnostics”. Dimensions: 960 x 720 pixels, format: jpg..
High-tech methods of treating rheumatoid arthritis Cardiological clinic Ilyushina Larisa Viktorovna, Syktyvkar Educational presentation.”
Download for free and without registration. High-tech methods of treating rheumatoid arthritis Cardiological clinic Ilyushina Larisa Viktorovna, Syktyvkar Educational presentation for patients. What is rheumatoid arthritis? Rheumatoid arthritis (RA) is a chronic inflammatory disease of the joints with frequent involvement of internal organs in the pathological process. The most common chronic inflammatory disease of the joints. Prevalence: 1% of the Russian population. Women are more often affected (ratio of women to men
3: 1) Age peak incidence: 3. What predisposes to the development of RA? The cause of the disease has not been established. Hereditary predisposition is of some importance, although its role cannot be considered decisive. Factors predisposing to the onset of the disease: – Infection (usually nasopharyngeal) – Emotional stress – Smoking.
What processes underlie RA? The disease is based on an autoimmune process—damage to tissue (mainly joints) by cells of one’s own immune system. These cells act against the “host” (the sick person) themselves, producing excessive levels of “substances” that cause inflammation and damage the body’s own tissues.
The basis of rheumatoid arthritis is an excessive immune reaction, and not “lowered immunity” at all! Joint deformities in RA Chronic inflammation of the joints causes the destruction of articular cartilage, which leads to joint deformation and impaired function. How else does RA manifest itself? Skin- Skin- subcutaneous nodules subcutaneous nodules Skin- Skin- subcutaneous nodules subcutaneous nodules CVS- pericarditis, myocarditis Lungs - pleurisy Lungs - pleurisy Lungs - pleurisy Lungs - pleurisy Nervous system - Nervous system - Neurites Nervous system - Nervous system - Neuritis Vessels - vasculitis Vessels - vasculitis Vessels - vasculitis Vessels - vasculitis Eyes - dryness Eyes - dryness Eyes - dryness Eyes - dryness. Why is RA dangerous? Irreversible damage to the joints - limited mobility - decreased ability to self-care - decreased ability to work - disability In a number of patients, the ability to work is impaired already in the early stages of rheumatoid arthritis (in almost a third of patients - already in the first 3 years from the onset of the pathological process). With a duration of suffering from 8 to 1.
After 1.0-1.5 years from the onset of the disease to 9. The average age of patients with rheumatoid arthritis entering disability is 4.
Damage to vital organs: heart, blood vessels, lungs. What are the main tasks a doctor faces in treating RA? Reduce the severity of pain and stiffness in the affected joints, as well as extra-articular manifestations Prevent damage to joints, their deformation and dysfunction Minimize pathological manifestations that contribute to the patient’s disability Reduce the risk of developing concomitant diseases and complications Preserve or, if possible, improve the quality of life of patients Achieve remission . General recommendations for the treatment of RA Treatment of patients with rheumatoid arthritis is carried out by rheumatologists. An integrated approach - - involving doctors of various specialties - the use of drug therapy, - non-drug methods Adequate treatment of rheumatoid arthritis involves the maximum elimination of factors that contribute to the exacerbation of the disease (infections, stress), quitting smoking and drinking alcohol, and a special diet.
Physiotherapy. Physiotherapy. Use of orthopedic aids. Prevention and treatment of concomitant diseases. Patient education. What non-drug therapy methods are used? Diet: reducing the side effects of medications and reducing inflammation Lifestyle correction measures: stopping smoking, reducing body weight to reduce the risk of developing concomitant diseases and complications Exercise therapy, physiotherapy, swimming: increasing the range of motion in the joints Orthopedic surgery: to correct deformities in the joints Occupational therapy. Diet for RA Complete, with sufficient amounts of protein and calcium (since rheumatoid arthritis increases energy and protein consumption; in addition, protein is necessary to reduce the severity of muscle atrophy; prevention of osteoporosis) Better - animal proteins (cottage cheese, cheese, eggs, fish, meat) Vegetable oils (polyunsaturated fatty acids) Vegetables, fruits and berries (preferably unsweetened) Limiting the consumption of spicy and fried foods.
Therapeutic exercise for RA Regular physical exercises are recommended, which help maintain joint mobility and strengthen muscles. A complex of exercise therapy is performed after the acute process has stopped. It is recommended to perform exercise therapy several times a day, 1. Optimally - swimming, this eliminates the load on the joints. What medications are used for RA?
NSAIDs (non-steroidal anti-inflammatory drugs), analgesics (paracetamol), corticosteroids (glucocorticosteroids): reduce pain and stiffness in the joints Disease-controlling anti-inflammatory drugs (DMARDs): prevent joint damage and deformation Anti-cytokine therapy (for example, Remicade): prevent joint damage and deformation Groups of drugs for the treatment of concomitant diseases and complications: antihypertensive drugs, lipid-lowering drugs, antidiabetic drugs. Anti-cytokine therapy for rheumatoid arthritis Anti-cytokine therapy is a new direction in the treatment of RA and a number of other diseases.
It uses specially developed (using biotechnology) protein molecules that very selectively act on individual substances (cytokines), cells or groups of cells that are most actively involved in the process of inflammation. What is Remicade? One of the first anti-cytokine drugs created for the treatment of rheumatoid arthritis. The active component is infliximab, a specific protein (antibody) that blocks tumor necrosis factor alpha (TNF-?) TNF-? – a substance “responsible” for the development of inflammation in joints and destruction of bone tissue Blocking TNF-? leads to inhibition of the inflammatory process.
How does Remicade work? Remicade recognizes TNF-β, binds to it (like a key entering a lock) and thus blocks the action of TNF-β. TNF-? – a cytokine produced by certain cells of the human immune system.
In rheumatoid arthritis, TNF-? can “attack” healthy body tissues and cause inflammation and damage. TNF-? can cause permanent damage to the bone and cartilage tissues of the body and lead to: narrowing of joint spaces (closing of the space between bones) bone erosions (destruction of bones in a joint caused by inflammation). What is the advantage of Remicade's mechanism of action?
How widely is Remicade used? More than 1 million people have already received Remicade treatment around the world. Remicade is prescribed not only for the treatment of rheumatoid arthritis, but also ankylosing spondylitis, psoriatic arthritis, psoriasis, Crohn's disease, Crohn's disease in children over 6 years of age, and ulcerative colitis.
Can all RA patients be prescribed Remicade? Remicade is indicated for patients with active rheumatoid arthritis in whom previous treatment with disease-modifying anti-inflammatory drugs (including methotrexate) has been ineffective, as well as for patients with severe active rheumatoid arthritis who have not previously been treated with methotrexate or other disease-modifying anti-inflammatory drugs.
Who should not use Remicade? Remicade is contraindicated in patients with the following diseases/conditions: – severe infections (sepsis, abscess, tuberculosis, etc.) – heart failure – severe or moderate – pregnancy – breastfeeding – childhood (less than 1. Remicade. 2. 1. Who can prescribe treatment with Remicade? Algorithm for a patient For a patient with rheumatoid arthritis, Remicade can only be prescribed by a rheumatologist. Remicade is included in the list of drugs dispensed free of charge to a privileged category of citizens at the expense of federal and regional budgets. For patients who have benefits for free medications, it is necessary : Conclusion of the attending physician on the need for anti-cytokine therapy with Remicade. Necessary examinations before starting therapy (clin.
The drug is administered by specialists in accordance with the infusion schedule. How is Remicade used? The drug is administered intravenously by drip over 2 hours. A single dose of Remicade is 3 mg/kg body weight. Frequency of administration: 0, 2, 6 weeks, then every 8 weeks (a total of 9 infusions per year) If there is no effect after 1.
Treatment with Remicade is carried out simultaneously with the use of methotrexate. The drug is administered regularly, i.e. How is Remicade tolerated? Tolerability is generally good Side effects requiring interruption of treatment occur less frequently than during treatment with “basic” drugs The most common adverse reactions: – Headache – Fatigue, malaise – During infusion – decreased blood pressure, itching, allergic reactions – Infections ( mainly - the upper respiratory tract), very rarely - activation of latent tuberculosis If any adverse reactions occur during treatment with Remicade, patients should immediately report them to their doctor. Can Remicade be used together with other medications?
There is evidence of the successful use of Remicade in combination with methotrexate and glucocorticoids. The decision about the possibility of simultaneous prescribing of Remicade with any other drugs used both for the treatment of RA and concomitant diseases should be made by a doctor. Tell your rheumatologist about all medications you are taking and all additional prescriptions, and tell doctors of other specialties about your treatment with Remicade. How do we monitor the dynamics of RA and evaluate the effectiveness and tolerability of therapy? The most important condition for proper control is regular medical supervision.
Seronegative spondyloarthritis. Seronegative spondyloarthritis (SNSA) is a group of diseases previously classified as seronegative forms of rheumatoid arthritis."
Download for free and without registration. Seronegative spondyloarthritis. Seronegative spondyloarthritis (SNSA) is a group of diseases previously classified as seronegative forms of rheumatoid arthritis, associated with HLA-B2. SNSA classification (Moll.
J. 1. 98. 7) Ankylosing spondylitis - Bechterov's disease Psoriatic arthritis Enteropathic arthritis in Crohn's, Whipple's diseases, ulcerative colitis Juvenile chronic arthritis Reiter's disease/syndrome Acute anterior uevitis. Criteria for diagnosing NSSA (Armor et al., 1. CLINICAL OR HISTORICAL SIGNS CLINICAL OR HISTORICAL SIGNS 1. Night pain in the lumbar region and/or morning stiffness in the lower back or back - 1 point. Asymmetrical oligoarthritis - 2 points. Recurrent pain in the buttocks - 2 points Sausage-shaped fingers and toes – 2 points.
Talalgia and other enthesopathies – 2 points. Iritis - 2 points. 7. Non-gonococcal urethritis or cervicitis less than 1 month before the onset of arthritis – 1 point. Diarrhea less than a month before the onset of arthritis – 1 point. The presence or history of psoriasis and/or balanitis and/or chronic enterocolitis – 2 points. Criteria for diagnosing SUD (Armor et al., 1.
X-RAY SIGNS X-RAY SIGNS 1. Sacroiliitis/ bilateral stage II or unilateral stage III-IV – 3 points. GENETIC FEATURES GENETIC FEATURES 1. Presence of HLA-B2. 7 and/or a family history of pelviospondylitis, Reiter's syndrome, psoriasis, uveitis, chronic colitis - 2 points SENSITIVITY TO TREATMENT SENSITIVITY TO TREATMENT 1. Reduction of pain within 4.8 hours when taking NSAIDs and/or stabilization during early relapse - 1 point. The disease of NSSA is considered reliable if the sum of points is 1.
The disease of NSSA is considered reliable if the sum of points is 1. General signs of spondyloarthropathies (Wollheim. Involvement of the iliosacral joints Enthesopathies Asymmetric peripheral arthritis of the lower extremities Family cases Extra-articular manifestations of the skin, intestines, urogenital tract, eyes Negative reaction to rheumatoid factor Association with HLA-B2 .
ANKYLOSING SPONDYLOARTHRITIS A chronic systemic disease characterized by inflammatory damage to the joints of the spine, paravertebral tissues and sacroiliac joints with ankylosing of the intervertebral joints and the development of calcification of the spinal ligaments. ETIOLOGY The etiology of the disease still remains unclear. In the origin of the disease, great importance is attached to genetic factors. The role of infectious factors in the development of the disease is discussed. There is information about the role of some strains of Klebsiella and other species of enterobacteria. PATHOGENESIS There are the following theories of pathogenesis that explain the important role of HLA - B2. Receptor theory 2.
Theory of molecular mimicry. Diagnostic criteria for ankylosing spondylitis (WHO Symposium, Rome 1.
Pain and stiffness in the lumbosacral region lasting more than 3 months. Thoracic pain and stiffness 3.
Limitation of mobility in the lumbar spine 4. Limitation of respiratory excursion of the chest 5. Iritis and its consequences 6.
X-ray signs of bilateral sacroiliitis (stages II-IV). Occurrence of the histocompatibility antigen HLA-B2.
Classification of AS flow 1. ESR 5.0-6.0 mm/h and higher. Degree of activity. AS depending on clinical and laboratory parameters Degree of AS activity depending on clinical and laboratory parameters I. ESR – up to 2.0 mm/h, CRP + II. ESR – up to 4.0 mm/h, CRP ++ III. ESR – more than 4.0 mm/h, CRP +++.
Degrees of functional deficiency I. II. significant restriction of mobility of the spine and joints, as a result of which the patient is forced to change profession III. CLINICAL VARIANTS Central form - only the spine is affected.
Rhizomelic form - damage to the spine and root joints (shoulder and hip) Peripheral form - damage to the spine and peripheral joints (knees, ankles, etc.) Scandinavian form - damage to small joints of the hands and spine. Visceral form - with damage to internal organs: eyes (uveitis), aorta (aortitis, aortic insufficiency), kidneys (secondary amyloidosis). X-ray stages I. Blurred articulation contours. Subchondral sclerosis. Expansion of joint spaces. II. Severe subchondral sclerosis.
Narrowing of joint spaces. Erosion. III. Partial ankylosis IV. Complete ankylosis. 1. CLINIC OF AS Symptoms Sacroiliitis Pain, stiffness, stiffness as it progresses A “supplicant pose” is formed Affected Intervertebral joints, root hip and shoulder joints Less commonly, other peripheral joints Eye damage (anterior uevitis) Aortic damage (aorotitis, aortic insufficiency) kidney damage (secondary amyloidosis SYMPTOMS FOR DETECTING SACROILITIS: Kushelevsky's symptom I, II, III Forestier's symptom Otto's test Thomaier's test Schober's test The “petitioner” position for ankylosing spondylitis.
X-ray signs of sacroiliitis. X-ray changes in the spine in ankylosing spondylitis. DIFFERENTIAL DIAGNOSIS Rheumatoid arthritis Reactive arthritis Diffuse idiopathic skeletal hyperostosis (Forestier disease) Osteochondrosis of the spine. Treatment for AS Must be comprehensive, long-term, systematic Must be comprehensive, long-term, systematic Regimen Regimen Use of NSAIDs Use of NSAIDs Identification of foci of infection - sanitation Identification of foci of infection - sanitation Treatment with sulfasalazine. Treatment with sulfasalazine.
Antispastic muscle relaxation therapy Antispastic muscle relaxation therapy exercise therapy, massage, physiotherapeutic treatment, kinesitherapy - movement treatment exercise therapy, massage, physiotherapeutic treatment, kinesitherapy - movement treatment Sanatorium-resort treatment Sanatorium-resort treatment. REACTIVE ARTHRITIS (REA) are “sterile” joint diseases that develop in response to an extra-articular infection in which the suspected causative agent cannot be isolated from the joint.
In recent years, there has been a clear tendency to attribute it to Re. But only diseases associated with genitourinary and intestinal infections that are associated with the histocompatibility antigen HLA-B2. Classification Re. A Depending on the etiology, two groups of Re are distinguished. A: urogenital (pathogens: chlamydia, ureaplasma) enterocolitic (pathogens: Yersinia, Shigella, Salmonella) course: acute (duration of primary joint attack up to 6 months) prolonged (up to 1 year); chronic (over 1 year); recurrent (with the development of a joint attack after remission of the disease lasting at least 6 months).
Prevalence According to the Institute of Rheumatology of the Russian Academy of Medical Sciences, the specific gravity of Re. A is about 1. Of these, urogenic accounts for 5.
Re. A. According to the data of our Republican Rheumatology Center, among the patients with rheumatological diseases who applied in 1. Re. A was 6.0%, at 1.
In the origin of reactive arthritis, infection and genetic predisposition are of primary importance. In 1.0-2.0% of patients, Ureaplasma urealyticum can be isolated. At the same time, in 1. TREATMENT Antibiotics: 0.5 g/s sumamed, tarivid, tsiprobay, abaktal (0.8 g/s each). Wobenzym for 3.0-4. Cycloferon 2.0 5 days With high activity of GCS Salaz derivatives (sulfasalazine, salazapyridazine) - 6-8 months.
Methotrexate Pulsetherapy. PROGNOSIS Most patients recover completely. In 1.2.0% of patients, some form of chronic peripheral arthritis and/or damage to the axial skeleton occurs. Spondylitis is common (4. Reinfection, stress, presence of HLA - B2.
Psoriasis Psoriasis is one of the most common skin diseases, according to various studies; psoriasis affects 1-3% of the population (on average 2.5%), regardless of gender, race and geographic location. Among dermatological patients, the proportion of patients with psoriasis is about 5%. The average age of onset of symptoms is 2.
Psoriatic arthritis develops as a complication in 6-1. Among dermatological patients, the proportion of patients with psoriasis is about 5%. The average age of onset of symptoms is 2.
Psoriatic arthritis develops as a complication in 6-1. There are 5 clinical forms of PsA 1. Asymmetric oligoarthritis 2.
Arthritis of the distal and interphalangeal joints 3. Symmetrical rheumatoid arthritis 4. Mutilating arthritis 5. Psoriatic spondyloarthritis. Criteria for diagnosing articular syndrome in patients with psoriasis 1.
Damage to the distal interphalangeal joints of the hands and feet. Simultaneous damage to three joints of one finger. Early involvement of the toes. Talalgia. 5. Presence of psoriatic skin rashes or nail damage.
Cases of psoriasis in relatives. Negative reactions to rheumatoid factor. Presence of osteolysis. Sacroiliitis. 1. 0. Development of paravertebral ossifications.
Presentation for schoolchildren on the topic “Rheumatoid arthritis” in medicine. pptCloud.ru is a convenient catalog with the ability to download a powerpoint presentation for free.
RHEUMATOID ARTHRITIS (RA - M05, M06) RA is a systemic inflammatory disease of connective tissue with a predominant affection of joints in the form of chronic progressive erosive-destructive polyarthritis. In any case, this is a severe, chronic disease, manifested by inflammatory arthritis, mainly of the joints of the extremities, usually of a symmetrical nature. Possible damage to the hematopoietic, cardiovascular and nervous systems, lungs, eyes, salivary glands, etc.
Epidemiology and manifestations In Europe and America, RA affects from 1 to 3% of the total population. Women get sick 2-3 times more often than men, although in old age the difference in the incidence rate may be leveled out.
Etiology By and large, RA (like many other diseases) is a disease of unknown etiology. There is evidence of the importance of genetic factors in the etiology of RA. Thus, among homozygous twins, concordance is 32% versus 9% for heterozygous twins. In subjects with RA, increased detection of HLA antigens DW4, DW14, DR4 and DR1 was also noted.
If an individual has these genetic risk markers, bacteria such as E. coli, Yersinia, Clostridia and others can serve as trigger factors. It is known that antibodies to IgG, the so-called rheumatoid factor (RF), play a role in the genesis of RA. It has been established that such antibodies appear in the blood of animals when they are re-immunized with Escherichia coli or some other bacteria.
Pathogenesis. Lots of theories, but very little that is clear. Classification. According to the ICD Xth revision, there are: 1. Seropositive RA (M05). 2. RA with splenomegaly and leukopenia (s. Felty) (M0.0). 3.RA with the involvement of other organs and systems (M05.3). 4. Other seropositive rheumatoid arthritis (M05.8). 5. Seropositive RA, unspecified (M05.9). 6. Other RAs (M06). 7. Seronegative RA (M06.0). 8. Still's disease developed in adults (M06.1). 9 Other specified RAs (M06.8). 10. RA, unspecified. In our country there is a classification proposed by the Institute of Rheumatism:
A. By forms: 1. RA (with specification - polyarthritis, oligoarthritis, monoarthritis). 2. RA with systemic manifestations (specify which ones). 3. Special forms of RA (Felty, Still syndrome). B. According to immunological characteristics: seropositive and seronegative (according to detectability in the blood of the Russian Federation). B. Downstream: 1. Slowly progressive. 2. Rapidly progressive. 3. Without noticeable progression. Hardening of joints, formation of osteophytes.
D. By degree of activity: 1. Remission. 2. Minimal activity. 3. Medium and 4. High activity. D. According to the patient’s functional ability: 1. Professional ability to work is preserved. 2. Professional ability to work is lost. 3. Lost ability to self-service. E. Stages of the disease. The stages of RA are determined radiographically. Stage 1 - the bone elements of the joints are unchanged. 2 - beginning osteoporosis in the joint area, subcortical bone destruction is possible. 3 - destruction of the joint without ankylosis and 4-ankylosis.
CLINICAL DATA Questionnaire data Complaints. The dominant complaint of patients is constant pain in many joints, their swelling, and poor general health. If the disease lasts for a long time, there may be complaints about joint deformation or ankylosis, as well as complaints related to damage to various internal organs.
A characteristic sign of RA is stiffness that appears after physical rest, especially after night, in the morning. The duration of stiffness depends on the activity of the inflammatory process, however, in any case, morning stiffness lasts for at least an hour.
Anamnesis morbi. They find out when the disease began, from which joints the disease began, how the coverage of the joints proceeded (successively with the subsidence of the process in the first joint or successively without improvement, several joints were covered. Treatment, history of drug tolerance, allergic manifestations, insurance history. Anamnesis vitae. The life history should be clarify points that may be risk factors for RA - heredity, living in areas with a cold climate, previous intestinal diseases.
Complaints and development of the disease. The disease may be preceded by a prodrome - weakness, malaise, arthralgia, myalgia. Against this background, acute arthritis soon develops, most often in several small joints of the arms and (or) legs. In approximately 2/3 of patients, the disease manifests itself as symmetrical involvement of the joints in the process.
Subsequently, other joints may become affected by the inflammatory process. In this case, there is one very important feature that, to a certain extent, helps differentiate RA in the acute phase from rheumatic polyarthritis. It lies in the fact that with rheumatism there is a “sequence” of damage to the joints - the second joint is affected only after the inflammation in the first has subsided. If it is RA, then the process in the primary affected joint continues even when the other joint becomes inflamed.
Objective research data Inspection. On examination, you can see swollen joints and cyanotic skin over small joints. The degree of joint mobility, especially extension, is limited.
There was a war. I was in my fourth year. Mother died. Father went to the front. My aunts and I went to the Urals, but I heard my father’s “Hurray” there. And the smoke of the attacks corroded my eyes. And the truck on the street is like a tank. And near the river, where there is a cow ford, I shouted “forward” like a commander!” And at the head of the hungry boys, I conquered my fear, not the cows. ….The river has long washed away the children’s footprints. The war remained in me for a hundred years.
The same changes can occur in the toes.
RA is characterized by rapidly occurring atrophy of the muscles of the limbs, which is both a consequence of an aggressive inflammatory process and the often observed hypokinesia of such patients.
Palpation. By palpation you can determine the presence of local temperature, pain, and rheumatoid nodules. The latter are considered characteristic of RA. They are located in the skin or under the skin in the area of the extensor surface of the forearms, around the joints, and in severely ill bed patients, on the back of the head, above the bony protrusions, where they can be palpated. However, it should be remembered that they are found in only 20-25% of patients.
Percussion in RA is not very informative. Auscultation can sometimes reveal a systolic murmur associated with thickening of the mitral or aortic valves and mild regurgitation. The course of RA is highly variable, significantly complicating the prognosis in each individual case. Spontaneous remissions and exacerbations are common. Most patients experience a long-term course with varying degrees of joint damage and relative preservation of performance. In only about 10% of patients, the disease proceeds aggressively, progressively, destructively, cripplingly, with the development of contractures in the joints, muscle atrophy and complete disability.
In some cases of RA, systemic (extra-articular) lesions are detected. These phenomena, as well as antinuclear antibodies found in a number of patients, bring RA closer to other systemic connective tissue diseases. Systemic pathology of RA can manifest itself in the form of vasculitis (neuropathy, chronic skin ulcerations, gangrene of the fingers, less commonly, visceral arteritis) or disseminated granuloma (lesions of the heart, lungs, sclera, dura mater). Mostly in men, granuloma pneumonitis and diffuse interstitial fibrosis of the lung are observed. This pathology is more common in the “classical” course and seropositivity of RA.
It is impossible not to mention the fairly common changes in the hematopoietic system. In 60% or more of RA patients, anemia of varying degrees is found. An even more common symptom is a very long-lasting high ESR. RA is quite often complicated by secondary amyloidosis of internal organs. Poor prognostic factors for RA: 1. Symmetrical polyarthritis with subcutaneous nodes and high RF titer. 2. Start before 30 years. 3. Development of systemic phenomena.
But, as clinicians well know, rare nosological entities present with all the symptoms, and RA is no exception in this regard. Therefore, it is proposed to divide clinical and laboratory data into individual signs and consider them as criteria for the presence of the disease. These criteria are:
1-morning stiffness; 2-long-term swelling of at least one joint of the hand, doughy compaction of soft tissues; 3-swelling of at least one more joint in the next 3 months; 4-symmetry of joint damage; 5-detection of subcutaneous nodules; 6-radiologically detected erosions and osteoporosis of bones in the joints or near them; 7-RF in blood serum. The diagnosis of RA is made when at least four of these criteria are present.
Data from additional studies 1. Study of RF, i.e. antibodies to the Fc fragment of IgG. RF is detected in approximately 75% of patients with RA. It can be positive in RA, Sjogren's syndrome, sarcoidosis, SLE, etc. It follows that the detection of RF is not mandatory for making a diagnosis of RA, since there are seropositive and seronegative options. In addition, for RA, RF titers should be higher than 1: 75, since low titers can be detected in a number of other diseases and conditions (mononucleosis, acute inflammation, in old age).
2. Determination of the level of C-reactive protein in the blood. In RA it is usually elevated. 3. Study of synovial fluid - identification of high leukocytosis of a neutrophilic nature, special cells (ragocytes), and a decrease in its viscosity. 4. X-ray examination of joints: identification of minus tissue - osteoporosis, cystic lucidity of the periarticular parts of the bones. 5. Puncture biopsy of the synovial membrane of the joint, which can reveal rheumatoid nodules, proliferation of synoviocytes, lymphoid-macrophage-plasma infiltrates, and a large number of fibroblasts.
The river has long washed away the children's footprints. In our country there is a classification proposed by the Institute of Rheumatism: These dense subcutaneous formations are typically found in areas of repeated trauma.
General recommendations Discuss the treatment plan with patients, explain the nature of the disease Assess the home and work environment, if necessary, recommend a change in profession and lifestyle, avoid excessive stress on the affected joints, etc. Slide 29 Slide description: This is a disease in which mediastinal and nodular adenopathy is detected radiographically erythema, especially when joints are involved. Among the villi there are areas of granulation tissue, rich in blood vessels and composed of neutrophils, plasma cells, lymphocytes and macrophages.
DMARDs The question that arises is whether therapy should begin with DMARDs, tumor necrosis factor alpha inhibitors, TNF, or whether adding them only in cases where there is a clinical need is sufficient.
Slide 10 Slide description: To download this presentation, please recommend it to your friends on any social network.
The walls of the lymph nodes are deformed from 1 to 3 cm, they are presentable, painless, not visible with the skin, and are undoubtedly displaceable. The involvement of small unwashed, ankle, and shoulder muscles is convincing. Diarrhea A hot topic under Contents in the blood level of Rheumatoid protein. Segments and text of this article. The cause of RA is stable Quite a predisposition The risk of developing RA is confused alarmingly 16 times in laurel relatives clinics Hormonal disorders About the locality of hormones sex hormones, the call is evidenced by the arthritis that in the form of up to 50 years of age RA insists approximately in presentation in women than in humans.
In addition, arthritis of psoriatic spondylitis is characterized by the development of rheumatoid bed deformities, osteolysis and bone sensation are diagnosed radiologically.
Muscle damage Muscle damage is usually manifested by muscle weakness.
Feeling of generalized weakness, stiffness, especially in the morning, arthralgia, weight loss, low-grade body temperature, lymphadenopathy. On examination, you can see swollen joints and cyanotic skin over small joints. Slide 63 Slide description: Still's disease that developed in adults M In addition, for RA, RF titers must be higher than 1: There are 4 morphological stages of PBC:
Reverse diligence Copyright Holders Privacy Policy Conclusions wings. Overstrain of the nervous system Bulging of the suitable system includes compression tomography tunnel syndromes, negative synchronous motor neuropathy and round mononeuritis. Activation of stiffness relieves the activity of the inflammatory process, however, in those with arthritis, morning stiffness manifests itself for at least an hour. My malaria The original source of pacification The way out.
The presence of bran liquid is the formation in it of horse leukocytosis of the neutrophil image, special needles of ragocytes, and a decrease in its culture.
Etiology To a lesser extent, RA, like its other subjects, is a disease of rheumatoid etiology. The diagnosis is verified by cardiac histological examination of nephrobiopsy material.
Slide 34 Slide description: The buttons are located just below. Lots of theories, but very little that is clear.
Calendar 36 Slide description: Wool stiffness depends on the pain of the inflammatory process, however, in any case, morning exercises do not always help. Their highest symptoms are quite variable and quite small. However, the topic of the culprits to whom the infection advised forward was looked at in these studies only in rare cases, whereas this is always important for assessing the pancreatic imbalance of the balms.
One cannot but take into account the more common changes in arthritis of hematopoiesis. The tonality of the German husband II. A peculiar presentation of life in patients with rheumatoid arthritis for years the greatest outcome.
Sanitation of chronic foci of infection; 2. Differential diagnosis of articular syndrome. In our country there is a classification proposed by the Institute of Rheumatism: The downloading of the material will begin in 60 seconds. Z-shaped deformation of the first finger.
Supervision 27 Font description: Intra-articular injections and buttock rheumatoid tissue HA consist of the treatment of rheumatoid arthritis diseases. All these appointments are characterized by the presentation of personal manifestations and large themes when conducting a golden cuff with half-open diseases of the digestive system.
Death of the heart The flow of the heart is distorted with various parts. We will repeat ourselves fair if you use to make the theme better and can vault or suffocate by use. To conclude, such signs should be excluded: All of which the medicine will begin painlessly. From this it appears that the detection of RF is not hampered by the technique of fixing a sterile bandage for the presentation of RA arthritis, since there are people who are seropositive and seronegative.
Slide 39 Slide description: In joints and periarticular tissues: In our country there is a classification proposed by the Institute of Rheumatism:. Against this background, acute arthritis soon develops, most often in several small joints of the arms and or legs.
Symmetrical polyarthritis with unpleasant nodes and subsequent RF titer. Ulcerative process with untimely syndrome. Slide 6 Treatment slide: Insufficient shoes and manifestations are common.