Rheumatism etiology pathogenesis clinic treatment dispensarization. Rheumatism: etiology, pathogenesis, clinic
The supercooling, genetic predisposition, nutrition disorders, physical and mental overwork plays a certain value in the development of rheumatic processes. The infectious and allergic origin of rheumatism is scientifically proven.
The primary causative agent of the disease - Streptococcus. The root cause of rheumatism may be angina (the probability of risk is 1-3%) or scarletine (very rarely). The protein shell of the beta-hemolytic streptococcus group A provokes the formation of M-antibodies and lysis (destruction) leukocytes. At the same time, the streptococcus is distinguished toxic substances, among which it includes streptolysin with a cardiotoxic effect. In 2/3 cases, Streptococcus is found when sowing from the oz.
In addition to hemolytic streptococcus, a certain response of the body is necessary for the development of inflammation (allergic theory). Rheumatic inflammation develops only after angina, scarletins in 2-3 weeks. Therefore, the pathogenesis of rheumatism is divided into 3 stages:
- It lasts about 2 weeks from acute angina until symptoms appear.
- Acute rheumatism is manifested by pronounced hypergic reactions, expressed symptoms.
- AutoSensitization is the formation of secondary antibodies that support recurrent inflammation due to non-specific infections or with re-penetration into streptococcus organism.
Rheumatism can for a long time Leak secretly. Symptomatics is determined by the localization of the inflammatory process and is very diverse.
The pathogenesis of the rheumatic process is very complex, and many of his parties are not yet clarified. However, the main stones of the pathogenesis of the disease are refined. The leading role is to be removed by the direct damaging effect of streptococcal toxins on the tissue structures of the heart and other organs, as well as impaired immunogenesis and neuroendocrine regulation mechanisms, etc.
Currently, great importance in the development of rheumatism is distinguished by perversion of immunological reactivity reactions as a result of hereditary or acquired features of the body. The effects of streptococcal toxins leads to the development of antiordinate antibodies. In the influence of streptococcal toxins (first of all, the products of their decay are distinguished on the tissue of the heart, which together with toxins form autoantigren.
The main value in the damage to the heart during rheumatism is given by the effect of streptococcal toxins on the tissue of the heart and impaired immunogenesis with the development of allergic and autoimmune reactions on the background genetic predisposition In conditions of violation of neuroendocrine regulation.
Intracellular soluble streptococcus antigens have tropiness to connective tissue Hearts and vessels, due to their antigenic relationship. This contributes to the constant and advantageous impact of the heart, as well as a long-term persistence of streptococcus in the body and tissues of the patient. Streptococcal toxins damage the membranes by lysosomes of cells in the focus of inflammation, which leads to the exit of them of enzymes (proteases, nucleus, phosphatases), causing the depolymerization of the connecting tissue elements with the destruction of its protein-polysaccharide complexes (glucosamineoglycans with proteins).
Morphofunctional changes in the cell elements of the connective tissue are developing, in particular fat cells - their quantity changes, degranulation increases, the severity of which reflects the activity of the rheumatic process. As a result, biologically active substances are published in the fabric and microcirculatory channel - inflammation mediators (histamine, serotonin, bradykin, etc.
Play the role of genetically determined (hereditary) features of fabrics, organs, as well as protective mechanisms for the fight against streptococcal infection (increased tendency to sensitization, reinforced response to irritant antigens, unusual stormy proliferation of lymphoid and plasma cells, tendency to hyperproduction of antibodies and perversion of immunological reactions ).
The various elements of the connective tissue of the vessels and myocardium walls (myocyto-sarchatum, sarcoplasma, discs and insert plates, glycoprotein valves, etc.) are affected. Myofibrils are cleavage, the smoothing of their transverse structure, the breaking and melting of the cells, which is clearly expressed in the acute phase of the disease.
Arising under the influence of long-term intoxication and other adverse factors of violation by the Central and Vegetative nervous systemas well as functions endocrine glasses (pituitary glands) lead to a change in the neuroendocrine regulation of immunological reactivity and other processes in the body and as a result - to the violation of adaptation mechanisms.
AT complex mechanism The development of the rheumatic process is a significant role in immunological reactions, which in this disease are more often proceeded by type immediately in acute and slow - with a protracted, sluggish flow. Immunological response by immediate type is due humoral factors - antibodies and intracellular soluble streptococcus antigens.
It leads to the development of the exudative component of the rheumatic process determining the severity clinical manifestations, sharpness of the flow and activity of the disease. The immunological reaction along the slowdown type is due to cellular factors and antibodies to intracellular soluble streptococcal antigens. At the same time, the specific component of the rheumatic process is developing - granuloma, which depends on the outcome of the disease.
Etiology: microflora gastroy.
Pathogenesis: meat food - meat chimus
Activates the MF, making it pathogenic.
Modern theory nervously vascular
(angioedema, ricker theory):
The process of vascular spasms begins
from musculature spasms is disturbed
Circulatory, hypoxia, led.
permeability of vessels, mo
in the wall, inflammation.
1. Easy simple - initial form (anemia,
swelling, hemosidery deposition - res-
impaired blood circulation, pain
syndrome).
2.Survenault appendicitis - in depth
Crypt arises a small focus of inflammation
(primary affect).
3.Flegemonous appendicitis - inflammatory
Process from primary affect on the OKR
Fabric, pus affects most
Ground walls.
4.Anatomatous (bunting) - in the wall
The process is formed by guncrow;
Group accumulates
leukocytes, focus of necrosis, leukocyte
Enzymes dilute necrosis, pus cavity,
Apostle (bunting).
5. Former-gangrenous - as a result
Long spasm of vessels, embolism.
6.Verial-gangrenous - inflammation
captures the wall of vessels before sex,
The vessel is thrombied, necrosis.
More severe changes arise in
The distal part of the process.
1.Clerosis (with uneven sclerosis in the wall
Flow M.B. Diverticulus - protrusion).
2. Valiteration (Loading) - Distal
part almost completely separated from
Proximal, bag with pus.
3. Empire process
4. Watering process - filling with liquid.
5. Inherit of the plots of mucous
Shell - mucus compliant
Part, bag of mucus, mucocelium.
6.pilifelbit, Tiflit.
Hypertonic disease - Chronic
disease, main clinical
the symptom of which is long
and persistent increase in blood pressure (hypertension).
Another essential hypertension is called.
Less frequent arterial hypertension is an
symptom of some other disease,
It is called secondary (symptomatic)
Hypertension.
1. Renal hypertension - kidney damage
- Xpielonephritis, oh. and xp. Glomerulonephritis,
Diabetic nephropathy, tumor
kidneys, renal artery stenosis.
2. Endocrine - disease or symptom
Itsenko Cushing, Feochromocytoma (tumor
adrenal gland - excess catecholamines)
3. Neurogenic - Increased intracranial
Pressure (injury, tumor, abscess,
Hemorrhage), defeat of the hypothalamus.
4. Others - coarctation of aortic and other vessels.
Etiology GB. Risk factors -
Multifactor disease - a combination
Genetic predisposition I.
Environmental factors. Most
Meaning psycho-emotional overvoltage
(stress, conflicts), excessive
Used NaCl, smoking, sedentary
Lifestyle.
Influences gender, age, cholesterol
in blood, smoking, hypercholesterolemia,
Diabetes, Obesity Strengthens Development
GB
Pathogenesis
1. T. Myasnikova - Reduced brake
The effects of big brain cortex on subcortical
Vegetative centers, first of all
pressor - over-use of these
Centers Sudsky
Spazmpus
Adveclusion
Renal endogenous mechanism
Hell regulation. Reduced brakes
The effects of the crust is due to long-term
stressful situations.
2. Membrane t. Poststly - initial
The factor in the development of GB is generalized
Local defect membrane ionic
Cell pumps. Decreases activity
Sa pump. Excess Ca 2I Na in the cytoplasm of smooth muscle cells
Causes them spasm and raising
Sensitivity to pressor factors.
Point of application with GB - artery and
Arterioles.
Stress News in the central regulation Adusing the activity of sympathetic-adrenal
Systemsgiperection
Catecholamines - due to persistent
Vascular spasm turns on
Renin-angiotensin S-A (ischemia) heart Emission - Raising
systolic pressure - benign
Current removal of reninangiotenzine II, development stimulation
Aldosterone Suitable Na and H2OP
HELL.
Etiology and pathogenesis of rheumatism
It is generally recognized by the role of in-hemolytic streptococcus Group A in the development of rheumatism. It has long been a link of rheumatism with acute and chronic streptococcal diseases (tonsillitis, pharyngitis, angina, scarletina, etc.), detected by about 80% of rheumatism patients. Repeated aggravation of chronic focal infections Or the layering of sharp streptococcal diseases is a resolution resulting in 2 weeks directly to the development of the rheumatic process.
The streptococcal ethnology of rheumatism is evidenced by the frequent sowing of streptococcus from the contents of the almond crypt and blood, the detection of streptococcal antigens in the blood and the urine of patients with rheumatism and the growth of the titer of anti-esthemonidase (anti-libtolized anti-esthetocinase antifibrinolysin), positive skin samples with streptococcal toxin, as well as significant Reducing the frequency of the primary incidence of rheumatism, its exacerbations and relapses in children who received the prevention of rational defendant therapy.
A certain meaning in the development of rheumatism, especially with protracted and sluggishly current forms of the disease, is currently given by L-forms of streptococcus filtering through bacterial filters and formed under the influence of damaging factors (V. D. Timakov and G. Ya. Kagan, 1962). The etiological role of viruses, including the cokes of AI3, as an independent factor, and in combination with Streptococcus (G. D. Zalessky) has not yet received convincing confirmation and requires further study.
3. Empire process
The course of the disease can be benign
(benign hypertension) and
malignant (malignant
Hypertension).
Malignant hypertension. More often
occurs after a period of benign
currents on average continues
10 years. Less often malignant flow
Observed from the very beginning.
Primary clinical manifestations -
Summary disorders, sharp head
Pain, hematuria. Diastolic pressure
Above 130 mm Hg. Diagnostic criterion
allowing differentiating evils.
from benign - disk swelling
Spectator nerve, with protein effusion,
Hemorrhage to the retina.
With malignant form dominate
manifestations characteristic for hypertensive
Crisse, i.e. A sharp increase in blood pressure.
Morphological changes - corrugation
and degradation of basal membranes of endothelium,
Endothelium cell location
Palkes, plasma impregnation
Arteriole walls, fibrinoid necrosis
Walls joining thrombosis. Behind
The account of this is developing heart attacks,
Hemorrhage.
1. Preclinical - Transit Hypertension
- Periods 1 hell, well amenable to correction.
Moderate compensatory hypertrophy
Left ventricle heart.
2. Stage of Changes
Arteries. Characterized persistent
Increased blood pressure. Arterioles -
The most typical sign - hyaline
(arteriosclerosis). Most often - kidneys,
brain, pancreas,
intestines, adrenal glands.
Changes in the arteries of muscle,
muscular and elastic and muscular types
- Elastofibrosis and atherosclerosis, elastofibrosis
- splitting internal elastic
Membranes and its sclerosis. Atherosclerosis
GB background has features more
widespread, involved
arteries of muscle type (which is not characteristic
for atherosclerosis in pure form),
fibrous plaques have circular, and
not segmental character that leads to
Development of stenosing atherosclerosis.
Most often in the arteries of the heart, the brain,
kidneys, vertebral arteries.
Myocardial hypertrophy increases thickness
left ventricle - 2-3 cm. arises
relative failure
blood supply to myocardium, which contributes
The emergence of diffuse small-scale
Cardiosclerosis
and the appearance of signs of cardiac
Insufficiency.
3. Stage of changes in internal organs.
Secondary amendments can
develop slowly what leads to
Development of Parenhim and Sclerosis atrophy
Stroms.
May occur sharp or complicated
changes due to the attachment of thrombosis,
long resistant spasm, fibrinoid
necrosis (during a chisosis) - heart attacks,
Hemorrhage. In vessels, especially
Brain develops microneviations,
What leads to intracerebral
hemorrhages.
ABOUT
Paying pericardis talk then
When the heart bag accumulates
Exudate. By the nature of Exudat
Paying pericarditis
distinguish: serous-fibrinous; serous; purulent; hemorrhagic.
Cluster
fluids in the pericardial cavity creates
Pressure on the outer surface of the heart
and that part of the vessels that lies in
The cavity of the window bag. it
pressure is the stronger than more
the amount of fluid in the pericardia and
It accumulates faster. Usually
Indoor Pressure Pressure
Negative and corresponds
Approximately 80-100 mm of water column.
In the upper and lower hollow veins as well
In the right atrium during diastole
Pressure is also negative - 30-40
mm water column. Thereby
lumen of hollow veins and right atrium
keeps open. Compared quite
Small and rapid pressure increase
in the window bag to make it difficult
The influx of blood to the right heart.
AT
The result of an exudative pericarditis
Development is developing
Pathogenesis based blood circulation
which lies the compression of the mouths of the hollow
and hepatic veins, right atrium
And difficulty diastole golders.
Complaints
patient. High temperature (more
38 ° -40 °), sweating, weakness, head
pain - symptoms of intoxication; dyspnea,
sickness of swallowing
esophagus), nausea, vomiting (irritation
Diaphragms), gulp pain in the region
Hearts, heartbeat (stagnation in veins -
The symptom of Bay - Bridge).
For
inspection is observed the pallor of the skin
Pokrovov, Lip Cyanosis, Outlook
Persons, swelling of the jugular veins. Dyspnea B.
Rest. Breith position
(knee-knelling
patient).
AT
Hearts area - intercostal
The gaps, or heart hump.
The top impulse is weak and is
In the middle of heart stupidity (since
hespped exudate up to
vertical position of the patient). AT
severe conditions may increase
Belly due to ascite.
Palpation.
Pulse of weak tension, frequent, soft.
Blood pressure is reduced -
Less than 100/60 mm Hg. Art. Venous pressure
increased to 300-400 mm of water column.
The top push is weak, determined
In the center of heart dullness.
Percussion.
Heart boundaries expand in all
Parties acquire a triangle shape
or trapezium. Disappears relative
Dullness of the heart smoothes
Cardiovascular corner. Revealed
Absolute characteristic of the presence of fluid
in the pericardia cavity when the left border
cardiac stupidity does not coincide with
Cardiac shock.
Auscultation.
Heart tones are weakened due to
The presence of fluid in the window
bag; Frillrad friction noise with a small
The number of exudate is more often listened
in zone III-IV
Intercostal on the left.
ECG
- low-voltage curve (occurs
Capacity of the potentials due to fluid).
Notes Svet St
from the isoelectric line in many
leads (concordant bias type).
For
X-ray study shadow
Hearts evenly expanded in
diameter and acquires the form
equilateral trapezium.
3. Vascular
failure. Classification,
etiology, clinic.
Inconsistency
between the capacity of the vascular bed
and circulating blood due to
Insufficiency of vascular tone
or (s) volume of circulating blood
(hypovolemia). The deficit of venous return
(blood flowing) can break
Pump function of the heart. In such cases
There are changes primarily
on the type of left vehicles
emissions with brain ischemia phenomena,
hearts, kidneys and other organs, with
hypovolemia - with centralization
blood circulation. Perhaps development
Disseminated syndrome
intravascular coagulation.
Vascular
deficiency call the state
arising from reduced tone, t.
e. constant voltage smooth muscles
Vascular walls. Reduced tone
Vessels leads to the fact that stretching
Their walls increase: respectively
The capacity of the vascular bed increases,
what lead to the first place to fall
blood pressure (hypotension).
Distinguish
acute and chronic vascular
failure.
Acute
Vascular failure manifests itself
In the form of fainting and collapse.
Syncoon occurs
Due to acute short-term
Half blood supply disorders
brain. Fainting are observed with some
Heart rhythm disorders, patients
With the lesions of the neck vessels
brain (so-called
Vertebrobasilar failure),
with certain turns of the head, in
in some cases (in weak patients
In some diseases of the nervous system,
in patients receiving certain
medicines) with a sharp transition from
horizontal position in vertical.
Collapse -
it is usually heavier than
faint, sharp vascular form
Insufficiency. The causes of Collapse
There may be acute infectious diseases,
under which the "Center" is affected
regulating tone of vessels and
In one of the brain departments
(oblong brain), as well as walls
vessels; very strong pain (traumatic
shock);
extensive burns (while developing
Collapse takes part not only
pain as such, but some
Toxic substances formed in
dead tissues): massive blood loss
(tone of vessels with blood loss reflex
rises to prevent fall
blood pressure then
catastrophically drops); acute
allergic reaction to hit B.
Blood of alien protein substance
(anaphylactic shock); Heart sharp
Insufficiency with myocardial infarction
(cardiogenic shock) and extremely heavy
arrhythmias (arrhythmogenic shock); overheating
(Sun and thermal blow).
Causes of rheumatism and mechanism for its development
CLASSIFICATION
For rheumatism, the variety of clinical manifestations is characterized, as well as the alternation of periods of exacerbation and attenuation of the process. Almost all organs may be affected, but the cardiovascular system, joints, serous shells, central nervous system are most often involved in the process.
In 1964, a working classification of rheumatism (A. I. Nesterov) was proposed, which was based on the determination of the phase of the rheumatic process and the degree of activity, the peculiarities of changes in the heart and other organs, the nature of the disease and the functional characteristic of blood circulation.
1 If possible, clarify the main localization of the heart lesion (myocarditis, endocarditis, pericarditis, pankarditis, coronaryig), indicate the number of attacks, and noted whether there is a valve vanity (which).
3. Empire process
The domestic rheumatological school strictly distinguishes the true R. (Sokolsky - buuche disease), putting not only sharp episodes into this concept ("acute rheumatic fever"), but also all stages of the development of the disease with its propensity to relapses and the formation of valve defects Hearts. Last variant of classification and nomenclature R.
adopted at the symposium of the All-Union Scientific Society of Rheumatologists In December 1964, they distinguish the active and inactive phase of the disease. At the same time, the possibility of transition of the active rheumatic process into the inactive phase of the disease and the division of the active phase by three degrees of activity is recognized. As the main component of the concept of "activity" implies primarily an inflammatory rheumatic process in organs and tissues in its clinical and laboratory mapping.
In addition, it is taken into account that the concept of "activity", as well as the concept of "disease", is not exhausted only by inflammation, but certainly includes elements of damage, dystrophy, multi-faceted protective, including immune, body response. By the nature of the flow, the acute, under-acute, protracted, continuous-re-cedizable and latent flow of the rheumatic process is isolated.
It should be noted that with the modern flow of rheumatism, the return myocarditis sometimes, especially in childhoodmay be without heart defect, as well as the inactive phase is characterized by the lack of changes from the heart (myocardioosclerosis or heart rate). In the active phase of the disease among lesions of other organs and systems, polyarthritis, serososites are isolated (pleurisy, peritonitis, abdominal syndrome), chorea, encephalitis, menin-goienphalitis, neuropsychiatric disorders, jade, hepatitis, leather damage, etc.
For the characteristics of the features of the flow of R. used clinical and temporal principle, in accordance with the to-ry, the active phase of the disease (rheumatic attack) may have acute, subacute and three versions of chronic flow: a protracted, continuous recurrent and latent (Table 2).
Thus, the working classification allows us to assess R. as a pathogenetically multifaceted disease in a particular patient with differentiation according to the degree of activity, the nature of the flow, indicating the primary or return nature of the rheumatic process, which largely helps the doctor in determining the tactics of the patient and the organization of an individualized dispensary Observations.
Symptoms and reasons
After streptococcal angina, the disease can only appear in a few weeks. Basic symptoms:
- increasing body temperature;
- appearance under the skin of small nodules;
- pain in the chest;
- arbitrary muscle twitching;
- rash on the skin;
- cardiopalmus.
In arthritis, the joints are affected by rheumatism. They scatter, hurt, their redness is observed, the local temperature increases, it is possible to form inside the liquid. The course of treatment can last from 2 weeks.
A carditis - heart rheumatism, initially manifested by the symptoms described above. Then the rapid heartbeat appears, the pain in the chest. It is possible to develop heart failure characterized shortness of breath, barking cough, abdominal pain, nausea and vomiting. Course treatment up to 5 months.
Abdominal syndrome has such symptoms: nausea, vomiting, sharp migrating abdominal pain, stool disorders. More often occurs in children.
The defeat of the lungs is accompanied by the development of rheumatic pneumonia or pulmonary vasculitis. In the second case, in addition to coughing and shortness of breath, hemochkali can be observed.
Kidney defeat is manifested by the development of glomerulonephritis, post-infectious jade, stagnant kidney (in rare cases).
Rheumatic chorea - meningoencephalitis. Inflammatory changes in the brain segments more often develop in pregnant women and girls. The main feature is muscular hypotension. It is difficult to swallow, the patient can not sit and walk. In this case, rheumatism is also manifested by aggressiveness, fatigue and scattered, emotional instability.
At the same time, drugs are prescribed to relieve inflammation, reduce destructive processes. The treatment regimen is selected only by the doctor according to the results of the diagnostic survey.
Pathogenesis
Criteria for diagnosis of rheumatism
Ticket
№ 29.
1. Inspection,
Percussion and auscultation of belly. I saw
spend in a standing and lying position.
Inspection standing gives an idea of
The condition of the abdominal wall. Wherein
Changes can be detected
abdomen, ware, bloating and asymmetrical
Plots. In case of inspection, lying in asthenics
in the region Stomach is sometimes revealed
Normal peristaltic movements
stomach.
Pathological is rude
Peristaltic movements in the form
shafts (deep waves coming from the left
hypochondrium to the right) periodically
raising stomach oblast and observed
In cases where there is a difficulty
In promotion of gastric content
due to the narrowing of the entry from the stomach (
Slip, tumor, scar). Great importance
have visible peristaltic
movements of the intestine that cause
Fancy changes in the belly relief.
Always associated with the feeling of pain,
stop with gases,
ration. Falpalpation
The most important diagnostic feature.
First conduct surfaces
Palpation, i.e. Approximate, for
this soft circular movement
Consistently palpit abdominal
the wall of the right and left iliac
paramatographic, hypochrites,
then epigastrine, backed,
suplocked areas.
It is possible
define local pain and
Abdominal muscle tension, hernia
and tumors.pr.
Deep methodically sliding
Palpation for sample hands
put the plafhmy and slightly bent
fingers at the time of the breath tend
penetrate the back of the abdominal wall.
Reaching her or the body under study
slide the tops of the fingers in the direction,
transverse to the axis of the body under study
or to its edge.
We start with sigmoid
guts. Blind, iliac. Cross-grained
intestine. Sigmoid is palpable in the left
iliac region, mobile, painless,
Thickness S. thumb Hands smooth.
Blooming in the form of a smooth one in two fingers
the thickness of the rumbling, painless,
moderately moving cylinder. Print
deep palpation in persons with a stomach ulcer
and 12 intestines are revealed pain points:
dot
Boas in the region of body 10 and 12 breast vertebrae.
At the same time the pain on the left of the vertebrae
testifies to localization of ulcers
On a small curvature, to the right of the vertebra
An ulcer of gatekeeper or 12 guts.
dot
Herbsta - in oblast transverse processes
3 lumbar vertebra.
points
Openhovsky in the region of octic processes
7 and 10 vertebrae.
Percussion. By
Mendel definition of sensitivity
Abdominal wall. Surability when hitting
According to the direct muscles of the abdomen talks about ulcers
12 guts.
Auscultation.
Lisviar
peristaltic bowel noise.
Despite the polymorphism of clinical manifestations R., in its development, clear patterns are noted, allowing to distinguish the disease as a strictly outlined nosological form. These, in particular, include the connection of R. with streptococcal infection (the presence of a hidden period between the end of infection and initial symptoms Diseases). For R. are also characterized by a tendency to polysindrome-sieves of clinical manifestations, the existence of typical options for the beginning and course of the disease, the presence in the clinical picture for the first time dedicated A. A.
Kisel "Absolute signs of rheumatism" and, finally, the tendency of R. to exacerbations and relapses. In a large part of cases, classic sharp forms R. end in full recovery. At the same time, mainly under the protracted flow and relapses of R., conditions may arise that contribute to the next transition of the disease into a chronic, trapidic, often exacerbating process.
A. I. Nesterov (1973) allocates three periods in the development of the rheumatic process. The first (hidden) period continues normally 2-4 weeks after the end of streptococcal infection to the initial manifestations of the rheumatic attack. It is characterized by the processes of toxic-infectious damage to the connective tissue structures and the immunological restructuring of the body in response to streptococcal antigenic effects.
Clinically, this period proceeds or asymptomatic, or with manifestations peculiar to the period of prolonged reconvalues. The second period is a period of hypero-tissue reactions with distinct and characteristic clinical manifestations of the disease (rheumatic attack). It is important to note that on the background of adequate anti-rheumatic therapy, the reverse development of clinical symptoms of attack does not occur simultaneously.
After the disappearance of bright inflammatory manifestations of the disease, it is natural to transition it to the hidden phase with a gradual normalization of immunological and biochemical indicators. The third period is manifested by diverse forms of return R. It is characterized by a certain tendency to a further impaired and qualitative occasion of protective and compensatory reactions with increasing immunological disorders, progression of dystrophic processes.
The primary and return R. Primary R. is also isolated, as a rule, it occurs in a children's and youthful age, is characterized mainly by acute and fiction variants of the course of the disease (in 88% of patients, according to 3. P. Annenkova, 1981). A clear age pattern is noted in the development of primary p.: Breast children, as a rule, do not ill, two-, three-year sick are extremely rare, and in subsequent years the incidence increases, reaching a maximum of 7-14 years old and adolescents. In childhood, the genital differences in the incidence of the primary R. is not observed, among adolescents, more often R. Female female face.
The initial clinical manifestations of acute primary R. refers fever, migrating polyarthritis (in 50-60% of the ill, based on the materials of the Institute of Rheumatology of the AMN of the USSR) or pronounced arthles-Gia are relatively rare - servers and signs of the defeat of other organs and systems. There is a relationship between high fever, polyarthritis and serosozit. A carditis, even pronounced, can only take place with a moderate temperature increase or at normal body temperature.
Primary-chronic variants of the flow R. relatively rare. The question of the specific gravity of the primary latent flow in the structure of the incidence of R. remains uncomputed
The primary R. is characterized by generalized exudative inflammatory reactions, but over the past 20-25 years (since the late 50s), the evolution of the primary R. is noted towards mitigating the bright exudative-hypergic forms of the disease. Relatively rare is now acute inflammatory lesions at the same time all the shells of the heart (Pankarditis), primary exudative pleurisites, pericardits, sharp meningoencephalitis. Much less often revealed primary rheumatic pneumonia, ring-shaped erythema, rheumatic nodules, rheumatic ferret flows softer.
The age features of the flow of primary river are noted, preschoolers prevail the protracted current, and in the younger school age - subacute. The greatest danger represents the 12-14-year-old age, with K-ROM, more often than in other age groups, is detected acute and subacute, and sometimes continuously recurring current. At the same time, in this, as in an older age (15-18 years), it is often observed primary latent flow with the involvement of heart valves.
Returning R. As a manifestation of the third period of development of the disease is characterized by a special inclination for exacerbations and relapses, progressive trophic disorders and regulatory processes with a predominance of protracted, continuous-but-recurrent flow options. According to the materials of the Institute of Rheumatology of the AMN of the USSR (V. A. Nononova, I. A. Bronzov, 1978), among 200 patients with primary R.
Like the primary, return R. can manifest itself with a polyarthritis, involvement in the inflammatory process of serous shells, light, nervous system and other organs. However, the most permanent carditis is, the clinical course of K-very often determines the nature of the flow of return R. in general. At the same time, as the occurrence of new exacerbations, along with the tightness of the frequency and the weakening of the severity of the lesion of the joints, there is a progressive weighting of cardiac pathology by increasing the damage to the valves and myocardium of the heart. Significantly occurring continuously recurring current.
Rheumatic Cardness (Rev Noise)
The rheumatic carditis is the leading manifestation of the active R., determining the severity of the flow and the forecast of the disease. The peculiarities of rheumatic carditis include a tendency to a consistent or simultaneous inflammatory damage to myocardium, endocardium and pericardium (see Pankardit). Due to the difficulties of distinguishing the defeat of individual heart shells in clinical practice, the generalized term "rheumokart" was widespread.
Primary rheumokard, according to different researchers, is recognized in 80-90% of children and in 95- 100% of adults, sick R. Despite the existence of some age-related features, fundamental differences in clinical manifestations of primary rheumlocks in children, adolescents and adults are not marked . The symptoms of the rheumlockardite is largely determined by the preferential defeat of a shell of the heart - myocardium, endocardium and pericardium.
Despite the achievements in the development of modern diagnostic methods, it is often established to establish a reliable diagnosis of R., especially its initial manifestations, is far from a slight task for a doctor. The absence of specific clinical and laboratory diagnostic tests determines the need for a syndromic approach to establishing the diagnosis of R. The essence of the latter is a reasonable idea that the nosological specificity of the disease can be established when the combination of nonspecific syndromes is detected.
It was this principle that the basis of the diagnostic criteria of acute R. proposed by A. A. A. Polya, polyarthritis, chores, rheumatic nodules, ring-shaped erythema, characteristic of this disease, induced to the diagnostic significance of this disease, he drew attention to the importance of their combinations for reliable recognition R. later The same five syndromes are attributed by the American cardiologist Jones (T. D.
TREATMENT
Treatment in rheumatism depends on the phase and the degree of activity of the process, the depth of the bodies, the nature of the course of the disease, as well as on the degree of circulatory disorders. Treatment should be aimed at an active struggle with streptococcal infection, suppressing the inflammatory process, a decrease in sensitization (outosenticization).
In our country, the method of stage treatment of patients with rheumatism was developed and was developed and widely implemented: in the hospital (first stage), in the sanatorium (second stage) and in the cardiorevmatology office, the polyclinic (third stage).
Patients in the active phase of rheumatism are subject to hospitalization. A bed is appointed, combined with individualized complexes of therapeutic physical education, a rational diet.
In the acute flow of rheumatism with the pronounced activity of the process, the patient should be in bed 2 - 6 weeks. With a quick improvement in the overall state, the normalization of laboratory research indicators and significant improvement from the heart side of the patient can be translated into a semi-respective mode before the specified period. And, on the contrary, in protracted cases or when developing blood circulation deficiency II - III degree, this period must be extended.
Care for a sick child is of great importance, especially with long bed mode. It is necessary to ventilate the room well. With increased sweating, the underwear should often be changed and wipe the skin with a solution of vinegar or cologne. The daily morning toilet is required, care for the oral cavity. It is necessary to monitor the chair (when the chair is delayed, it is possible to put a cleansing enema or prescribe a laxative).
With pronounced phenomena, blood circulation is necessary elevated position in bed. In order for the long-term bed mode to the child, it is necessary to think about board games, books, drawing pencils, threads for embroidery, etc. Classes of medical physical education are shown to children even with bed mode in the lying position, later the exercises are sitting, and then Standing.
The nutrition of the patients should be full, but not too abundant, since in bed mode, energy produces are minimal. Preferably four-member feeding. It is necessary that food is rich in vitamins. In hormone therapy, an increase in potassium food should be increased. The products containing a large number of potassium include baked potatoes, cabbage, raisins, uryuk, prunes, oatmeal and buckwheat, cottage cheese, milk.
From antibacterial agents aimed at combating streptococcal infection, the preparations of Penicillin are successfully used. In the acute period of rheumatism, the potassium or sodium salt of benzylpenicillin intramuscularly is prescribed in the usual age doses for 10 days, then they are moving to the injection of Bicillin-1 1 time in 10 days.
Anti-inflammatory therapy with rheumatism patients is currently being carried out by non-corporal and hormonal drugs. Among the first most widely used drugs salicylic acid, first of all - acetylsalicylic acid at a dose of 0.2 - 0.3 g per year of life (no more than 2 g per day); Pyrazolone derivatives - amidopin, analgin at a dose of 0.15 - 0.2 g per year of life (no more than 2 g per day).
An anti-inflammatory drug indomethacin (methindol) is also used for the treatment of patients with rheumatism (methindol) in a dose of 10-20 mg 2 - 3 times a day, followed by an increase in dose to 50-10 mg / day. Application with brupen rheumatism is justified - 20 mg 4 times in time for 1.5 - 2 months. Unfortunately, these drugs have a side effect. With long-term admission of acetylsalicylic acid, intestinal bleeding may occur as a result of tissue necrosis (ulcers).
The long-term reception of amidopyrin can lead to the development of agranulocytosis; Butadion and its derivatives - to the defeat of the urinary tract (hematuria). Therefore, in the process of treatment, careful observation of patients and repeated laboratory tests of blood and urine is needed. Good effectiveness, especially with the serious flow and high activity of the rheumatic process, possess glycocorticosteroids - prednisone, dexamethasone, triamcinolone.
The prednisone is prescribed at the rate of 0.5 - 1 (less often 2) mg / day, dexamethasone and triamcinolone - in a smaller dose, respectively, their comparative efficiency (dexamethasone - 7 times, triamcinolone is 2 times more active than prednisone). After 10 days of treatment, the daily dose of prednisolone is gradually reduced (every 5 to 7 days - 5 mg).
When determining the dose and duration of the use of hormonal drugs, it is necessary to focus on the degree of activity of the process and the nature of the flow. In acute flow with the pronounced activity of the dose of drugs, the highest, the duration of treatment should be on average 6 weeks, with a protracted flow - more than a long time. On the contrary, with a subacute or sluggish flow, a short (2 - 3-week) course of hormone therapy can be prescribed. In such patients with EF The effectiveness of steroid therapy is low.
In patients with phenomena, blood circulation deficiency PB - III degree hormone therapy should be carried out with caution. It is advisable to begin treatment with small doses of steroid preparations (for example, prednisone at 5 - 10 mg / day), and then for 7 to 10 days to increase to age doses, followed by a gradual decline.
In the acute course and high activity of the rheumatic process, the purpose of steroid hormones in combination with nonteroid drugs, most often - prednisone and acetylsalicylic acid. With a small activity of the process, the treatment is carried out only by non-steroidal preparations in maximum doses. In the continuous-recurrent and protracted flow of rheumatism, drugs of a quinoline series are used (made, resokokhin, plaque) of 5-10 mg / kg / day for 3 to 6 months. Treatment is carried out for a long time, can be combined with the reception of salicylates or steroid hormones.
Steroid drugs reduce the immunological reactivity of the body, so when they are taken, there may be exacerbated by chronic foci of infection. To prevent this, hormonal drugs under the cover of antibiotics are prescribed: Penicillin is first used, and then bicillin.
In patients with rheumatism, especially when conducting hormone therapyThe content in the body of ascorbic acid and vitamins of the group B is reduced, so it is necessary to assign them additionally. Cardiac means apply only with blood circulation deficiency phenomena.
Treatment in the hospital is carried out within 40 - 60 days with a gradual change of beddown to a semi-by-step.
After calming the rheumatic process and extracting from the hospital, the patient's treatment continues in the conditions of a rheumocardiological sanatorium or at home. If the disease proceeded sharply, the child needs a sanatorium mode for a month. With a sluggish current, this period may be somewhat reduced, and with a protracted - elongated to 8 - 12 weeks.
The patient's day after rheumatic attack should be strictly individualized depending on the nature of the process flow, the time passed after the discharge from the hospital, the functional state of the cardiovascular system.
The question of visiting the school should be decided taking into account the distance from the house to school. If the school is located close, visit it can be allowed a month after the end of the sharp period, if far - you can organize school at home. In some cases, the child is provided with an additional day off. Patients in the active phase of rheumatism are exempted from exams.
In the absence of signs of activity of rheumatism and a satisfactory reaction to physical activity after 4-6 months, exercises on the complex of the preparatory group can be resolved. A year later, the child may be allowed to exercise physical education in the scope of the main group, excluding various competitions and running to the distance. If for three years there was no exacerbation of rheumatism or phenomena of blood circulation deficiency, one can be allowed to engage in some sports.
When solving the issue of admissible exercise It is necessary to take into account the presence and nature of heart disease.
The child who had rheumatized, should be on a dispensary accounting in the rheumocardiological office of children's clinics, and in the countryside - in the district hospital or medical center. During the year after the attack, it will be examined monthly, and then 1 time in 3 months. The survey should include studies of the functional state of the cardiovascular system and laboratory indicators of the activity of the rheumatic process.
With a stubborn arthralgy, treatment with mud and hydrogen sulfide baths at Odessa resorts, Evpatoria, Matsesta and others 10 - 12 months after attack are shown. In other cases, patients should be heated in a planned manner in local sanatoriums and pioneering camps of a sanatorium type.
The idea of \u200b\u200bR. as a systemic disease with preferably damage to the cardiovascular system, clinical and morphological data on the stage of its development, taking into account the etiological role r-hemolytic streptococcus Groups and substantiated the creation of a domestic system of three-stage treatment R. nominated in the 60-70s A. I. Nesterov's clinical immunological direction in the study of R.
made a significant contribution to her further development. In modern form, this system includes: Treatment of the active phase of the disease in the hospital, continued treatment after extracting from the hospital in the rheumatology office Polyclinics for adults, or a cardio-rheumatological office of children's clinics, or in a suburban sanatorium with a connection of rehabilitation measures, subsequent long-term dispensary observation and preventive ambulatory treatment.
More than twenty years of experience in the fight against rheumatism in the USSR confirmed the high efficiency of three-stage treatment and systematic long-term observation of patients under polyclinic conditions. The success of treatment depends on how individualized its program is depending on the degree of activity, the variant of the flow of the rheumatic process, the severity of the carditis, the severity of the valve and muscle lesion of the heart, the presence of streptococcal infectedness.
4B. Atherosclerosis of brain vessels, kidneys, intestines, lower extremities: Patanatomy, complications.
3. Empire process
Atherosclerosis of the brain arteries
also manifests itself slowly progressive
with the development of crust atrophy
brain manifest
memory, intelligence up to development
senile marasma.
Complicated manifestations - ischemic
cerebral heart attack develops
The corresponding neurological
symptomatics.
4. Atherosclerosis of the renal arteries -
Formation of wedge-shaped ischemic
heart attacks, followed by scarring
- large-born atherosclerotically
Primary wrinkled kidney.
With steniting atherosclerosis for
An account of hrying tissue ischemia occurs
Symptomatic hypertension.
5. Atherosclerosis of the intestinal arteries -
complicated manifestations to gangrene
intestine due to thromboembolism or
Thrombosis of mesenteric arteries.
6. Atherosclerosis of the limbs -
more often amazed femoral artery —
Stenzing atherosclerosis
Insufficient collateral blood flow
leads to the development of the syndrome intermittent
Chromoty (pain in the muscles when walking, atrophy
muscles of the limbs). With thrombosis -
Gangrene develops lower limbs.
Prevention of rheumatism
The prevention of rheumatism is carried out in the direction of prevention of the disease (primary prevention) and preventing recurrences in over-time (secondary, anticorcidal prevention).
Primary prevention includes community events: hardening the body, physical education, sports. It is important to actively fight with streptococcal infection, i.e., the sanations of the chronic inflammatory process (tonsillitis, otitis, caries of teeth, sinusitis, cholecystocholangitis). It is necessary to eliminate the action of sensitizing factors (irrational nutrition, improper vaccination).
With an angina and exacerbation of chronic tonsillitis, pharyngitis prescribe a bed and treatment course with antibacterial and anti-inflammatory agents (Penicillin for seven days, followed by the introduction of bicillin-1) with simultaneous purpose of acetylsalicylic acid, polyvitamins, desensitizing drugs. Repeated blood test. Extract B. children's institution It is permitted only with normal blood indicators and a well-known state of the cardiovascular system.
In chronic tonsillit, it is necessary to conduct conservative treatmentAnd with ineffectiveness it, especially in children with a toxicallergic background, resort to tonsillectomy. In tonsilogenic intoxication for the prevention of rheumatism in spring and autumn, it is recommended to prescribe acetylsalicylic acid or amidopin for three weeks.
Secondary prophylaxis is based on an increase in the reactivity of the body by appointing chapel procedures gently-training regime, therapeutic physical education. Active identification and systematic planned rehabilitation of chronic infection foci, including the use of antibiotics and testimony - tonsillectomy should be widely carried out.
Patients with signs of heart lesions and the consequences of transferred primary rheumlockarditis, who suffered a chore with a protracted flow, returned rheumokard, prescribe a monthly continuous introduction of Bicillina-1 for five years. Children who suffered a primary rheumorite without forming a vice or chore without explicit heart changes, the term of the monthly year-round introduction of Bicillina-1 is limited to three years, seasonal prevention is carried out in the next two years.
In children with frequent respiratory infections Justified since the beginning of the disease, the use of repeated 2 - 3-week mefenamic acid courses (0.2 - 0.3 g 3 - 4 times a day), which has anti-inflammatory, desensitizing and interferonogenic effects. As a result of anti-inflicted treatment, the number of re-exacerbations is currently decreased by 3-4 times, the number of patients with the formation of heart defects has sharply decreased.
The identification of the role of streptococcal infection in the occurrence of R. and its recurrence allows for the primary prevention of the disease. It consists of measures aimed at the systematic and reasonable hardening of the body, the development of physical education and sports, carrying out wide sanitary and hygiene measures that reduce the possibility of streptococcal infection of the population, primarily children's teams.
The secondary prevention is aimed at preventing the recurrences and progression of the disease in individuals who have already undergone R. In addition to measures related to primary prevention, it includes the methods of year-round and seasonal biotillinomedic acid prophylaxis of recurrences carried out by the rheumatologists of the ambulatory-profile institutions or district doctors.
In the spring and autumn periods for 4 weeks. Adult acetylsalicylic acid is prescribed in a dose of 2.0 g, children 1.0-1.5 g per day or another non-steroidal anti-inflammatory drug. After a 3-year rate of year-round bicillino-prevention, in the absence of relapses, seasonal prevention is prescribed the following 2 years. It is carried out in spring and autumn for 6-8 weeks of Bicyllin-5 in a dose of 1,500,000 united monthly in combination with acetylsalicylic acid at a dose of 2.0 g per day.
Among the rehabilitation activities, an important place belongs to the operational treatment of heart defects, the results of a large degree depend on the preoperative preparation and postoperative observation of patients with the rheumatologists.
See also collagen diseases.
Forecast of rheumatism
Currently, there are almost no cases of a disease with a catastrophic flow and a fatal outcome. At the end of the disease, the age of the patient affects the nature of the first attack of rheumatism and the quality of the dispensary service.
Heavy cases of the disease are more often among young children. The severity of the first attack usually predetermines the further course of the disease. Of great importance for the forecast has timely rational treatment In the active phase and regularly conducted anti-relapse therapy in the inactive phase of the disease. As a rule, the forecast of repeated recurrences of the disease are aggravated.
Early diagnosis, timely appointed adequate therapy, proper use All stroke treatment links contribute to suppressing the activity of the rheumatic process, preventing the formation of a heart-to-significant reduction in the recurrence of the disease. Forecast R. Defined ch. arr. The outcome of the lesion of the heart, most often the valve endocarditis (Walvulite).
Therefore, prediction of the outcome of the primary rheumatic holvulite is of paramount importance for the forecast of R. in general. H. N. Kuzminina, A. V. Trufanova, T. G. Fishile (1978), developed with the help of computer prognostic tables for the children's contingent of patients with R., allowing to predict the outcome of the disease according to the results of a clinical processing examination;
Rheumatism
Rheumatism is an acute rheumatic fever - systemic inflammatory disease of the connective tissue, developing after transferred streptococcal infection in genetically predistened persons with predominant lesions of the heart and blood vessels.
Etiology, pathogenesis
The primary role in the development of rheumatism belongs to streptococcal infection (β-hemolytic streptococcus Group A), the immune violations are essential. The pathogenesis of the development of the pathological process in rheumatism is determined by two main factors: toxic effects of a number of enzymes produced by streptococcus having cardiotoxic properties, and the presence of common antigenic determinants with heart fabric in some strains.
Clinical picture
For this pathology, a protracted and continuous-recurrent flow with the gradual progression of organ changes and the emergence of severe complications that determine the unfavorable distant outcome of rheumatism are characterized.
Arthritis (or arthralgia) of several large joints is a symptom-leading disease in patients with the first attack of rheumatic fever. Sustainacles are often so pronounced that they lead to a significant limitation of their mobility. Simultaneously with pains appear swelling of the joints due to synovitis and damage to periarticular tissues, sometimes redness skin Pokrov over the joints. The most commonly damage to the knee, ankle, rays and elbow joints occurs. A characteristic feature of rheumatic arthritis is a migrating character when signs of lesion of one joints almost completely disappear within 1-5 days and are replaced by such a pronounced lesion of other joints.
The clinical symptoms of carditis is determined by the preferably lesion of one or another heart structure - myocardium, endocardium or pericardium. In the structure of rheumatic defects of the heart, mitral insufficiency prevails, less often the formation of the lack of aortic valve, mitral stenosis and combined heart defects.
Round-shaped (anular) erythema is a characteristic, but rare sign (it is noted about 10% of patients). Round-shaped pink unsmitted rashes are localized on the inner surface of the limbs, a torso, neck, usually combined with migratory arthritis. Subcutaneous rheumatic nodules - small (magnitude with a pea) of formation, localized in periarticular tissues at the places of attachment of tendons, over bone protrusions in the field of knee, elbow joints, occipital bone. Rheumatic nodules are found only in children, usually appear during the first attack and disappear without a trace after 2-4 weeks from the beginning of the disease.
Chorea, which is commonly referred to as small, is associated with the involvement in the pathological process of various brain structures (striped body, subtalameanic kernels and cerebellum). It is developing mainly in children 1-2 months after transferred acute streptococcal infection. The overwhelming majority of patients are the only sign, but sometimes it is combined with carditis and arthritis. Horie's symptoms - chaotic involuntary twitching of extremities and mimic muscles (hypercinesis), accompanied by a violation of the handwriting, violation of speech and awkward movements. The child cannot perform coordination samples.
Ophthalmological symptoms
The eye disease in rheumatism is observed, according to various authors, in 4-8% of cases. From the severity of the rheumatic process, the eye defeat does not depend in some cases, it may be its first manifestation. The most common episklerites, sclerites, rheumatic uveitis, vasculitis and retiniovasculitis.
Rheumatic iridocyclite in adults has a sharp start (on the background of a rheumatic attack) and a stormy course, in children the current is more sluggish, ashautive. Both eyes can be affected simultaneously or alternately. The process is a diffuse non-peculousatous nature. In the clinical picture, attention is drawn to the presence of a bright periodal injection, a large number of small bright precipitates on the rear surface of the cornea and abundant serous exudate; The iris is sluggish, swelling, the pupil is narrowed. The duration of the process is 3-6 weeks. The outcome is usually favorable, but as a result of frequent recurrences, the iris atrophy may develop, the reaction of the pupil becomes sluggish, the edge and planar fusion of iris with a lens are formed, the destruction of the vitreous body is developing, visual sharpness is developing.
With retiniova, destructive proliferative processes are developing in the vascular wall of the arterioles and arteries. On the eye day, the presence of grayish muft-cuffs around vessels of 2-3rd order, couplings can cover several vessels or located on one side of the "platives" vessel, resembling snow on the branch, is a pathogononic symptom of rheumatism. With a common vascular lesion, the phenomena of reactive papillitis are observed in the process of vessels of the optic nerve in the eye, the phenomena of the reactive papillitis are observed, the disk appears on the disk, covering the vascular funnel and most of the disk surface. In the presence of a macular edema, visual acuity is reduced.
In rheumatism, an acute circulatory disorder may develop in the retina vessels.
Diagnostics
In the acute initiation of the disease, the development of neutrophilic leukocytosis is already observed in the first days, an increase in ESR and the concentration of SRVs. The increase in ESP and the concentration of SRV is often preserved for a long time after the disappearance of clinical signs. Increasing the credits of anti-superstopococcal AT in the titer more than 1: 250 is observed in patients. In a bacteriological study, the β-hemolytic streptococcus of group A. The β-hemolytic streptococcus group is found in a single sowing streptococcus detecting in 20-45% of cases, more informatively detecting streptococci in serial sowing. Conducting echocardiography is suitable for identifying heart defects and pericarditis. ECG is important to clarify the nature of heart rhythm violations.
Treatment
Etiotropic therapy is carried out - Penicillin, Bicyllin-5 at 1500,000 units of potassium or sodium salt every 2 weeks or benzatin-benzylpenicillin, 2.4 million, every 3 weeks for 1.5-2 months, and then after 21 days for 5 Amoxicillin, erythromycin 250 mg 4 times a day, cephalosporins or azithromycin, roxitromycin can be used. NSAIDs are used, the voltar (orthophene) are preferred, Molovas. Acetylsalicylic acid can be used 4 times a day and ibuprofen (bruphen) 0.4 g 4 times a day. NSAIDs are prescribed with rheumatic polyarthritis, roetener, rheumatur with light and moderate severity. Upon the protracted and recurrent flow of the rheumlock, the NSAIDs are prescribed together with weak immunosperessants - aminohinoline preparations (made, resokokhin, chlorookhin) of 0.2-0.25 g per day. During the latent flow of the rheumlock, NSAIDs and aminohinoline preparations are prescribed in the same dose. The main indication for the purpose of aminohinoline compounds (made, composy, placled, etc.) is a rheumorite with a protracted, latent or continuous-absorbing flow. Most often used by 0.25 g or plated 0.2 g 1-2 times a day for 6-12 months. The effect is observed no earlier than 6 months after the start of treatment. Anti-inflammatory therapy continues outpatient times for 2-4 months (up to 12-24 months) in combination with aminohinoline compounds of 0.2-0.25 g per day.
With high activity of the disease, glucocorticosteroids are prescribed. According to the testimony symptomatic treatment It is carried out depending on the types of complications of rheumatism.
Rheumatic diseases
Rheumatic diseases are characterized by severe clinical polymorphism.
The most frequent and characteristic ophthalmologic manifestation of rheumatic diseases is defeat vascular shell Eyes will take away. Depending on the localization and length, it can be anterior (irrit, iridocyclite), medium (rear cyclitis, peripheral will take off), rear (horoite, chorioretinite) or total (PASNUIT). In some cases, preferably defeat the eyes with rheumatic diseases is retiniovasculit (damage to the vessels of the mesh eye envelope) and retinopapillitis, in which a visual nerve is involved in the process.
Rheumatoid arthritis
Rheumatoid arthritis - Inflammatory rheumatic disease of unknown etiology, characterized by symmetric chronic erosive arthritis (synovitis) of peripheral joints and systemic inflammatory damage in the internal organs.
Etiology
The etiology of rheumatoid arthritis is unknown. Various exogenous, toxic, endogenous (collagen type II collagen, stress proteins) and nonspecific factors can act as "arthritogenic". There are data on the relationship between rheumatoid arthritis and carriers of certain HLA class II alleles.
Pathogenesis
The essence of the pathological process with rheumatoid arthritis is generalized, immunologically determined (autoimmune) inflammation.
Clinic
In 50% of cases, the disease begins with a gradual increase in pain and stiffness in small peripheral joints. Approximately 10% of patients the disease begins and continuously proceeds in the form of mono- or oligoarthritis predominantly large joints. In the debut of the disease, clinical signs of joint inflammation are usually expressed very moderately - soreness appears in passive and active movements, during palpation; In the developed stage, swelling is formed, the skin temperature in the joint area increases, etc.
The defeat of tendons and muscle changes play a leading role in the formation of persistent deformations - "rheumatoid brush" and "rheumatoid stop". In the area of \u200b\u200belbow joints, rheumatoid painless, moderately dense, small sizes of the nodule can be detected. With the defeat of the knee joints, atrophy of the four-headed muscles of the thigh develops. Fibrous changes in the articular capsule and muscle tendons attached in the area knee Sustavacan lead to the development of bending contractures.
Polynereropathy (manifestation of vasculitis of vessels that feed peripheral nerves) - characterized by the defeat of the distal departments of nerve trunks, most often a small-terrestrial nerve, with the development of sensitivity disorders. Patients are disturbed by numbness, burning, chicness in the distal limbs. There are soreness during palpation of not only affected joints, but also tissues located in the distance from them, a decrease or increase in sensitivity in the zone of nerve damage.
Heart damage (pericarditis, myocarditis, extremely rarely - deficiency of the mitral valve or aortic valve) is most often occurring in the serious course of the disease.
Rheumatoid lung damage includes: diffuse fibrusing alveolo, nodule defeat pulmonary fabric (rheumatoid nodules), obloring bronchiolite, vasculitis.
Rheumatoid kidney damage - glomerulonephritis and amyloidosis (develops in 10-15% of patients, as a rule, after many years from the beginning of the disease).
In 10-15% of cases, the lesions of the exocrine glands are developing in rheumatoid arthritis, mainly salivary and tear - SHEGREEN syndrome.
Ophthalmological symptoms
Iridocyclite with rheumatoid arthritis in most cases the process of bilateral, the current - recurrent (recurrences are accompanied by articular attacks). The eyeball at palpation is usually painless, the perikornal injection is poorly pronounced, characterized by the presence of a large number of small bright precipitates on the back surface of the cornea and an abundant serous or fibrinous exudate in the front chamber. The outcome of iridocyclite is usually favorable. However, after frequent recurrences, the severity of signs of iris atrophy is gradually increasing, becomes a sluggish reaction of the pupil, the edges are formed first, and then the planar fusion of iris with a lens increases, the severity of clouds in the vitreous body increases, visual acuity increases.
In case of sernegative arthritis in 24.1% of cases, the retina vasculitis develops.
Diagnostics
For the diagnosis of rheumatoid arthritis, laboratory research methods are carried out - a general blood test (hypochromic anemia, an increase in ESP and CRB) and immunological studies (the rheumatoid class Ig M is detected in 70-90% of cases, antibodies to a cyclic citrulated peptide). The determining value for the diagnosis and assessment of the progression of rheumatoid arthritis has a rhenological or MRI study.
Treatment
Treatment begins with the selection of nonsteroidal anti-inflammatory funds. Among them are the most commonly used voltar (diclofenac), orthophene (0.15 g), Moviece, Ibuprofen (1.2 g). The intra-articular introduction of corticosteroids (Diprospan, Kenalog, Deposedrol), especially with a small number of affected joints, is widely used.
Mandatory with rheumatoid arthritis is the appointment of slowly valid ("basic") drugs (Hinghamine, hydroxychloroquine, etc.) or immunosuppressants. Hinghamine is used in 0.25 g per day, hydroxychloroquine (placled) - 0.2 g per day. At the same time, 1 time in 3-4 months. An inspection of a patient with an ophthalmologist to prevent complications from the bodies of vision is necessary. Traditional "basic" drugs are advisable to combine with biological agents - infliximab, rituximab, etc.
From immunosuppressants with rheumatoid arthritis, methotrexate in medium doses (5-7.5-10 mg per week) or leflomide are commonly used.
With progressive signs of systemics, for example, polyneuropathy, Digital Arteri, Felty syndrome is possible to use pulserapics.
Surgery Applied with rheumatoid arthritis in order to preserve, restore or improve the function of joints (synovectomy, tetosenovectomy, synovkapsulectomy, capsulotomy; arthrodesis, arthroplasty and endoprosthetics)
General principles of ophthalmological treatment
When you learn in the active period, GCS, NSAIDs and mydriatics (instillation, subconjunctive and parabulbar injections) are locally used. Instillations to the conjunctival cavity of 0.1% of the dexamethasone solution of 1-2 drops 3-6 times a day, 15-30 days; 0.1% diclofenac solution 1-2 drops 3 times a day, 15-30 days; With pronounced inflammation, an additional 0.2 ml of 1% phenylephine solution is subconjunctivally, 1 time per day, 5-10 days; With a serious flow, the appearance of macular edema - dexamethasone parabulbarno 2-3 mg (0.5-0.75 ml) 1 time per day, 5-10 days.
Juvenile rheumatoid arthritis (Synonym juvenile chronic arthritis) is an independent nosological form. Children are ill predominantly over 5 years; Girls sick almost 2 times more often than boys.
Clinic
Two options for the start of juvenile rheumatoid arthritis are distinguished: predominantly articular (monoarthritis, oligoarthritis, polyarthritis) and systemic (style syndromes and Wisters-Fanconi). For juvenile rheumatoid arthritis, regardless of the options for the beginning of the disease, the defeat is characterized by predominantly large and medium-sized joints (knee, ankle, ray-beam), the frequent involvement of the joints of the cervical spine, the development of uveitis and the extreme rare detection in the blood of rheumatoid factors.
The main signs of lesion of joints with juvenile rheumatoid arthritis are pain, swelling, morning stiffness. The severity of pain in the joints in children is usually less than in adults; Sometimes there are no complaints about pain, as well as morning stiffness.
From the very beginning of the disease, the polyarthritis is observed in 35-50% of patients. The number of affected joints is usually less than with rheumatoid arthritis in adults. The beginning of the disease can be acute, but more often happens gradual, accompanied by a subfebrile temperature, total weakness, decreased appetite, irritability and increased fatigue. The current is usually wave, exacerbations alternate with incomplete or even complete remissions of various durations. Mono- or oligoarthicultural arthritis is observed about patients, mostly large joints are affected.
The characteristic features of juvenile rheumatoid arthritis include the slowdown in physical development, the growth in growth, violation of the growth of individual skeletal segments (in the "zone" of the affected joints).
Syndromes Stilla and Wisters-Fanconi In addition to the lesion of the joints, the high body temperature (38-39 °) and chills are characterized by high body temperature. In the stylist syndrome, a rheumatoid rash appears during the lifting of the body temperature on the body and the proximal sections of the limbs. Typical embracing manifestations of Stilla syndrome are an exudative pericarditis, generalized lymphadenopathy, an increase in liver and spleen.
Changes in laboratory indicators are nonspecific. It is characterized by neutrophilic leukocytosis, especially expressed in the system variant of the disease. Many patients have no normal hypochromic anemia, an increase in ESP, an increase in the level of fibrinogen, α 2 -Гlobulins, the appearance of C-reactive protein. These changes usually correspond to the activity of the disease. The rheumatoid factor in blood serum is detected by no more than 20% of patients and, as a rule, after a long period of time from the beginning of the disease.
Ophthalmological symptoms
In the mono- and oligoarticular form of juvenile rheumatoid arthritis, the eye damage (front will uveitis) is found in 29-30% of cases (the rheumatologists are called "juvenile rheumatoid arthritis with eye damage" or "Little Girls Disease" - with the development of juvenile rheumatoid arthritis in girls in Aged up to 2 years and the presence of an antinuclear factor The risk of uveitis is almost 100%), with a polyarticular - at 8-9% and with systemic - extremely rare - no more than 2% of patients.
The oligoarticular form in children is found in 73% of cases, in 70-85% of cases the disease develops in girls, in this case, in this case, is a bilateral, more often (51-97% of cases) asymptomatic (sometimes revealed by changing the shape of the pupil when forming the rear synechs, Lack of pain, low-rise perikornal injection, a very small amount of cell suspension in moisture of the anterior chamber). At the boys, with this form of the disease, the eye defeat is more often preceded by arthritis than in girls, the process is more likely to be one-sided, the course of uveitis is acute with pronounced clinical symptoms and relapses, but more favorable. With a polyarticular form, the eye damage is favorable, without complications; As a rule, these are female patients.
Eye damage is developing in most cases (60-87%) for 5 years of rheumatoid arthritis, in some cases, it may precede (sometimes for 10 years there may be no signs of lesion of the joints) and develop much later - after 10-28 years.
The course of anterior uveitis with juvenile rheumatoid arthritis in most cases (80-93%), especially in children of preschool age and with the "uveitis of small girls", - chronic, for adolescent age is more characteristic of the acute course of the disease.
For juvenile rheumatoid, uveitis is characterized by the presence of small, dry precipitates; Fast formation of rear synechs of considerable length, infection of the pupil and subatrophy of the iris; The formation of a precrustic film due to the organization of fibrinous deposits, especially in young children, crust clouds in 42-68% of cases and cloues of the vitreous body, developing in children of preschool and adolescent age in 92% and 49% of cases, respectively. With the system version of juvenile rheumatoid arthritis (Still's disease) A classic triad of symptoms is developing: chronic plastic will inhabit, the ribbon dystrophy of the cornea and complicated cataract.
The rear segment of the eye is involved in the pathological process extremely rarely: papillilation, macular (cystic character) of the retina dystrophy may develop. In severe cases, the retractation retractor and subatrophia of the eyeball can develop.
For uveitis, during juvenile rheumatoid arthritis, the presence of normo or hypotension is characterized, in 15-20% of cases develops glaucoma.
Diagnostics
The following criteria for early diagnostics are proposed - arthritis lasting than 3 weeks (lesions of 3 joints during the first 3 weeks); Defeat of the cervical spine: accumulation of joints; Morning stiffness; Thawinit or bursitis; will take away; an increase in ESP is more than 35 mm per hour; detection of rheumatoid factor in blood serum; Synovial shell biopsy characteristic.
Treatment
In most cases, treatment is usually beginning with the purpose of acetylsalicylic acid (75-100 mg / kg per day) - well tolerated by children and has a pronounced analgesic and anti-inflammatory effect. After 1-2 weeks of treatment, the question of the continuation of the reception of this drug or the appointment of another non-steroidal anti-inflammatory agent is solved: indomethacin (daily dose - 1-3 mg / kg), orthophene (2-3 mg / kg), ibuprofen (20-30 m / kg).
In the absence of sufficient effect on the above treatment after 4-6 months, especially in the case of a polyarthritis, the use of slowly active drugs is shown. (quinoline derivatives, gold drugs - criesanol, penicilline, etc.). Hinghamine and hydroxychloroquine are prescribed in the first 6-8 weeks per day at the rate of 5-7 mg / kg per day (no more than 0.2-0.25 g per day), then highly recommended a smaller dose (under the control of an ophthalmologist). The presence of a pronounced positive effect in the treatment of these drugs is an indication to continue their reception.
Glucocorticosteroids for intakes are prescribed with rheumatoid arthritis rarely - only by special indications And usually for a short time. Immunosuppressants - in extreme cases with the system variant.
If you learn in the active period, GCS, NSAIDs and mydriatics (instillation, subconjunctive and parabulbar clients) are locally used. Surgical treatment is carried out with violations of transparency of optical media (cornea, lens, glassy body), infesses and dislocations of pupil, retinal traction destructive detachment and in the presence of testimony for anti-cloudsomatous surgical interventions.
Jet arthritis
Jet arthritis - inflammatory diseases of the joints, developing after certain infections (most often of the urinary or intestinal tract). A characteristic feature of reactive arthritis is an asymmetric inflammatory oligaritrite with a predominant defeat of the joints of the lower extremities, spondylitis, antisopathy, tendosiveit, osteite. The combination of arthritis with urethritis and conjunctivitis is called Reiter syndrome.
Etiology
Etheological agents include urogenative (ChLamiydia Tgashotis, Neisseria Gonorrhoeae, Ureaplasms igaa1outicum), intestinal (Shigella, Satr1Obacter, Salmonella, etc.), pulmonary (Chlamydia Pneumoniae) and other infections.
Pathogenesis
In the pathogenesis of jet arthritis, it is conventionally distinguished by several sequentially developing stages. At first, as a result of infection, the local infectious inflammation of the urinary tract or intestines is developing, which in most cases ends with spontaneous recovery. In some patients, the process passes into the second (acute) phase characterized by the development of peripheral arthritis, which also ends with recovery. The process chronization can be observed in NLA-B27 media.
Clinic
Reactive arthritis develops at the age of 20-40 during an infection or within 2-6 weeks after the sacrificing of acute manifestations. Arthritis begins, as a rule, soreness, edema and skin hyperthermia appear over joints. The damage to the joints is usually assymmetric, most patients are affected mainly joints of the lower extremities; The course of the disease is a recurrent, with an urgent form of reactive arthritis, there is a higher frequency of relapses. Often there are painless erosion of the oral mucosa and genital organs (ring-shaped balanitis), keratodermia - a typical skin lesion, resembling psoriatic plaques with abundant peeling, nail defeat (ongoing). In 50% of cases, the kidney damage is observed - proteinuria, hematuria, aseptic pyuria; Glomerulonephritis and Ig A-nephropathy are very rarely developed. Changes from the nervous system are manifested by radiculitis, peripheral neuritis, encephalopathy. With the syndrome of the Reather, the triad symptoms is developing - urethritis, polyarthritis and conjunctivitis.
Ophthalmological symptoms
In 60% of cases, patients develop double-sided mucous follicular conjunctivitis, in 20% of cases there is a non-growing uridocyclitis - the process is usually one-sided, the course of recurrent, but more favorable, sometimes keratitis (one-and two-way), episclerite, the rear will fly and panet.
Diagnostics
In general blood test, leukocytosis is determined to the acute phase (10-15. 10 9 / l), thrombocytosis (400-600-10 9 / l), an increase in ESR and the level of the CRP. In the chronic phase there is a moderate normal normal normocitar anemia, reflecting the development of chronic inflammation. NLA-B27 carriage more often occurs in patients with chronic recurrent flow and is associated with the development of iridocyclitis, sacroileitis, spondylitis.
Treatment
Non-steroidal anti-inflammatory agents are used (indomethacin, diclofenac, voltar, orthophene, Moviece, Kebrex, Nimesil), glucocorticoids (prednisone), immunocorrorizing drugs (sulfasalazine), non-coronal immunosuppressants-cytostatics (methotrexate, azathioprine, cyclosporin A, biological agents - EFCLCSIMAB, etc. ), Miorlaxants for removing muscle spasm (Middokalm), preparations for improving microcirculation in a ligament apparatus (trental, pentoxifyllin, nicotinic acid). Antibacterial therapy is carried out.
In the presence of ophthalmic symptoms, local treatment is carried out using NSAIDs, GKS, mydriatics.
To increase the sensitivity to basic therapy with high immunological activity, plasmapheres and plasmaSorption are produced, the lubl. In the inactive phase of the disease, physiotherapy and physical leaf are carried out.
Systemic Red Volchanka
System Red Volchanka (SC) - chronic polysindromic disease, developing against the background of genetically determined imperfection of immunoregulatory processes, leading to uncontrolled antibody products to its own tissues and their components with the development of autoimmune and immunocomplex chronic inflammation.
Etiology and pathogenesis Finally not installed. Among the factors of the external environment provoking the detection of SLE, generally recognized is excess insolation - ultraviolet irradiation stimulates apoptosis of skin cells, which leads to the appearance of autoantigen on the "apoptotic" cells and induction of an autoimmune process. There is a hereditary predisposition - the SLE is most often found in the presence of certain types of HLA - DR2, DR3, B9, B18. Equally important is the hormonal factor: a high level of estrogen in young women. There are indirect data on the role of chronic viral infection. A crucial role in pathogenesis play immune disorders in the form of a shortage of T-suppressors, the predominance of T-helpers and an increase in the activity of in lymphocytes. For SLE, the development of an immune response is characterized in relation to the components of the nuclei and cytoplasm of cells - antinuclear antibodies (ana), which are found in 50-60% of patients. The pathogenetic value of the ana consists in their ability to form a CEC, which, laying off in the structures of various organs, can cause their damage.
Clinic
The classic triad is dermatitis, arthritis, polysorozit. Skin lesions are one of the most frequent clinical manifestations of SLE - often develops in the debut of the disease, has several clinical options. Erythematous dermatitis (discoid foci with hyperemic edges, infiltration, scar atrophy and depigmentation in the center with teleangioectasis) is localized on the face, neck, chest, in the field of large joints; Characteristic location in the region of zilly arc and nose backs ("Butterfly"). Alopecia - hair loss can be generalized or focal. Other forms of skin lesions are possible: Pannacult, various manifestations of skin vasculitis (purple, urticaria), LiveDo Reticularis - branching nets, branch-purple spots on the skin associated with microtrombosis.
The defeat of the joints is distinctive features. Arthralgia develop in 100% of patients, intensity pain often do not correspond to external manifestations; Milk arthritis - symmetrical non-erosive, more often localized in small joints of brushes, rays and knee joints.
The lesion of the lungs at the SLE is represented by the following clinical forms: pleurisy dry or discharge develops in 50-80% of cases, a lupus pneumonite. Heart defeat is accompanied by the involvement of all its shells, most often pericardia; In the acute current of the SLE, the vasculitis of coronary arteries (coronet) and myocardial infarction can be developed. Kidney lesion (Lolve jade, Lupus nephritis) - Classic immunocomplex extras intra-block glomerulonephritis, is also observed in 50% of cases.
The damage to the CNS and the peripheral nervous system develops from the overwhelming majority of patients. Since almost all departments of the nervous system are involved in the pathological process, most of the patients may develop neurological violations: headache, more often than a migrane nature, convulsive seizures, defeat card nerves, acute violation of cerebral circulation, polyneuropathy, etc.
The pathological process is often involved in the liver - the filtration of stroma is developing with lymphoid, plasma cells, macrophages; Often revealed fatty dystrophy Liver, as well as coagulative necrosis of hepatocytes.
Ophthalmological symptoms
With a systemic red lupus, erythematous rash can appear on the skin of the eyelids, a specific blepharitis is developed in the form of a limited edema of the clarity edge of the century of the dark color, conjunctivitis, episclerite, keratitis, iridocyclite, will take away and retini. Retinionskilitis develops in 3-35% of cases, is usually diffusable. The process is accompanied by occlusion of retinal vessels (preacpillary arterioles, the central artery of the retina and its branches; venous capillaries, central veins of the retina and its branches) in 19% of cases, edema, exudative (soft exudates in 10% of cases - unfavorable prognostic criterion) and hemorrhagic manifestations ( seldom); As a result of retinal ischemia, neovascularization of the retina and / or disk of the optic nerve can develop. As a rule, changes in the retinal vessels appear in the process of developing the disease, sometimes with the angiitis of retinal vessels begins the manifestation of the disease. In the development of changes in the retinal vessels, especially occlusal, with a special role, a significant role belongs to AFS; Occlusions are developing in patients with APS and without it - at 14% and 0.9% of cases, respectively. The highest percentage (24%) of occlusal lesions of the retinal vessels is observed in the SLE with APS and thrombocytopenia (without thrombocytopenia - 6%), and mainly arterial recurrent occlusion develops.
In patients with SD with occlusions of the retinal vessels 2 times more often than patients with the damage of the retinal vessels without occlusion, and 3 times more often than in patients without damage to the vascular bottoms, thrombosis of other localization develops. In this regard, the results of ophthalmological examination of patients with SLE are a kind of criterion that allows indirectly to determine the likelihood of developing blood circulation disorders under a given disease.
The clinical ophthalmological picture, which is observed in violations of the cerebral circulation and in the blood circulation system, - see the chapter of "circulatory disorders".
Diagnostics
The most common criteria for diagnosing SLE - the criteria of the American rheumatological association - "Butterfly", discoid rash, arthritis, kidney damage, damage to the central nervous system, hematological disorders, immunological disorders, antibodies to DNK, SM antigens, histones, etc.
Treatment
Glucocorticoid therapy - small doses of glucocorticoids are prescribed patients with low activity (<10 мг/кг), с умеренной — средние (<40 мг/кг) в течение 2-4 недель с постепенным снижением дозы до минимальной поддерживающей и с высокой — большие дозы (1мг/кг/сут. и более). При СКВ эффективно применение пульстерапии (1000 мг метилпреднизолона в/в капельно 3 дня подряд).
The use of cytotoxic drugs depends on the peculiarities of the flow, the severity of the disease and the effectiveness of previous therapy. With the development of proliferative and membraneous lupus nephritis and severe damage to the CNS, a cyclophosphamide is considered to be a drug (0.5-1 g / m2 V / in monthly for at least 6 months, then every 3 months for 2 years). For the treatment of less severe, but aosatioprin (1-4 mg / kg / day), methotrexate (approximately 15 mg / week) and cyclosporine (less than 5 mg / kg / day) are used to treat the glucocorticoids of manifestations.
To relieve the muscular-skeletal manifestations of SLE and pronounced serosositis use NSAIDs. With damage to the skin, joints and in order to reduce the risk of thrombotic complications, aminohinoline preparations are used (hydroxychlorookhin); In the first 3-4 months, the dose of hydroxychlorochin is 400 mg / day., then 200 mg / day. When cytopenia, cryoglobulinemia, vasculite and thrombocytopenic purpura, the use of plasmapheresis is effective.
In the presence of retiniovasculitis, Parabulbarno administer DEXAX (2 mg per day, 10-15 days), direct anticoagulants - heparin (750 cells 1 time per day, 10-12 days), Trental (0.5 ml per day, 10-15 days) , Kenalog (20 mg 1 time in 7 days - 3 times; 1 time in 10 days - 3 times; 1 time in 14 days - 3-12 months) (see also the chapter "Blood Disturbance"). When identifying the presence of ischemic zones and non-disconnecting of the retina in an inactive period and under the cover of drug therapy, which includes the use of steroids, the lakescoagulation of the retina is carried out.
Systemic sclerodermia
Systemic Sclerodermia (SSD) - This is a systemic disease of the connective tissue and small vessels, characterized by common fibrous-sclerotic changes in the skin, stroma of internal organs and symptoms of obliterators endarterity in the form of a common Rhino syndrome.
Etiology and pathogenesis
The etiology of the SSD is unknown. In the development of SDS, the role of work associated with long-term cooling, vibration, vinyl chloride polymerization plays. There are immunogenetic markers, such as A9, B8 and B27, B40, DR5 and DR3. The basis of pathogenesis is the unrestrained collagen formation and vascular processes in combination with peculiar, almost impossible, inflammation.
Clinic
Rhino phenomenon - symmetric paroxysmal vasospasm; Detected in 95% of cases. It is manifested by sequential changes in the color of the skin of the fingers (whitewashing, cyanosis, redness) is accompanied by a feeling of tension and pain. Skin lesions develops from the overwhelming majority of Patients with CDS. Characterized by the stage of skin lesion. The initial stage continues for several months, is characterized by dense skin of the skin of the distal departments of the upper and lower extremities, often accompanied by the skin itch. The progressive damage to the skin of the face leads to well-known mascasoicity, the skin of the limbs - to bendable contractures, trophic disorders, hyperpigmentation and depreciation of the skin with the characteristic flappingness of the skin and the tissues subject to tissue.
The defeat of the joints is among the most frequent and early manifestations of the SSD. Patients impose complaints of swelling, stiffness and pain in the joints of the fingers, rays and knee joints. It is often developing osteolysis of the nail phalanx, manifested by shortening and deformation of the fingers and legs. In some patients, the manifestations of polyimosit (proximal muscular weakness) are found. Sometimes muscle atrophy is developed associated with mobility impaired and contractures.
The gastrointestinal lesion is detected in 80-90% of cases. During the defeat of the esophagus, dysphagia develops, the weakening of the peristalsis, signs of reflux-esophagitis; When damaged to the stomach and intestines, abdominal pain arise, bloating, suction impairment syndrome (diarrhea, weight loss). The lesion of the lungs is often combined with the damage to the cardiovascular system and refers to the number of unfavorable manifestations of the disease. The kidney damage is detected in most patients, is characterized by preferably damage to the kidney vessels. The most severe manifestation is sclerodermic kidney crisis, usually developing in the first 5 years of the disease (the main manifestations - arterial hypertension, fast-triping renal failure, hyperreninemia, microangiopathic hemolytic anemia, thrombocytopenia, stagnant heart failure, pericarditis and nonspecific symptoms - headaches, cramps).
Ophthalmological symptoms
The lesion of the organ of vision in scleroderma is found quite often and is diverse, which depends on the stage and the degree of activity of this disease. The pathological process is often involved in the eyelids and pairbital fabrics. First, edema phenomena are developing, then induced, later atrophic. The edema of the century with CDS is usually dense with fabric infiltration; Later, hyperemia appears (or the color of the eyelid becomes marble), whitish spots surrounded by a purple rim, develop scarmers, fall out eyelashes, narrowed and crushed the eye slit, blefrophomy develops (a peculiar view of the patient). Induration with an edema or atrophy of the eyelid, bilateral enofalm, the presence of ability to trigger the eyelids are specific to sclerodermia ophthalmic symptoms. In some cases, there are papillomas, atheromes, serous cysts, xantellasm, blefarochalasis and teleangectasis of the century. The vessels of the conjunctiva of the eyelid under the SSD ampuloid are expanded, in the late stages of the disease develops conjunctiva atrophy, subconjunctive hemorrhages and lymphangectas are observed. Dry keratoconjunctivitis with a pitchal secret develops when the lacrimal gland is developed, cases of the presence of corneal abscesses in patients with svd, thinning sclera, atrophy of the mesodermal leaf of iris, injection with heterochromy, complicated cataracts and secondary glaucoma (fux syndrome), degradation (without cellular elements), Perpends and rear tweeons of the vitreous body. With CDS, there may be violations of the function of the eye muscles (swelling, sclerosis). Signs of angiopathy, maculyodistrophy are detected on the eye day, circulatory disorders can develop in the retina vessels.
Diagnostics
The criteria of the American Rheumatological Association are used to diagnose the SSD. The proximal scleroderma includes a proximal scleroderma (symmetric thickening, sealing and induration of the skin of the fingers is proximal from the bulk-phalange and plus-phalange joints); Small criteria include: sclerodctification, scars on the tips of the fingers or the loss of the substance of the pillow of the fingers, double-sided pulmonary fibrosis. Common blood test - hypochromic anemia, an increase in ESP, leukocytosis or leukopenia - changes are not specific. General urine analysis - microhematuria, proteinuria, leukocyturia. Immunological studies - definition of "sclerodermic autoantibodes".
Treatment
The main directions of pharmacotherapy of SSDs - prevention and treatment of vascular complications, primarily the phenomenon of Rhine, suppressing the progression of fibrosis, the impact on the immunocipal mechanisms of SSD, prevention and treatment of the damage to the internal organs. The selection preparations in the phenomenon of the Rhine are - dihydropyridine blockers of slow calcium channels. The most efficient retarded forms of nifedipine (10-90 mg / day). The selective blockers of 5-HT2-serotonin receptors (ketaneserine 60-120 mg / day) and A-adrenoblays are fairly effective (Prazozin 1-2 mg 1-4 times a day). In severe cases (pulmonary hypertension, renal crisis) uses intravenous administration of synthetic PGA alprostadila or prostacyclin and plasminogen tissue activator. Antiagrams are included in the complex therapy: dipyridamol (300-400 mg / day), tickopidine (250 mg 2 times a day), low molecular weight dextre (REOPOLIGLUKIN). Penicilline is the main drug, overwhelming the development of fibrosis, the starting dose in the debut of the SSD is 125-250 mg every other day, with the ineffectiveness of the dose gradually increases to 300-600 mg per day. Glucocorticoids (no more than 15-20 mg / day) are shown in explicit clinical and laboratory signs of inflammatory and immunological activity (myiositis, alveolit, serozite) at an early scholar stage.
SHEGREEN DISTRICT
SHEGREEN DISTRICT (N. Sjogren, Swedish ophthalmologist, 1899-1986) - BSh - system autoimmune disease relating to diffuse diseases of the connective tissue; It is characterized by the damage to many secreting epithelial (exocrine) glands, mainly salivary and tear.
Etiology is unknown, most researchers consider BSh as a result of immunopathological reactions to viral infection, presumably retroviral.
Pathogenesis
The hypothesis of autoimmune genesis BSh is the most recognized, in whose benefits of the frequent detection in patients as organospecific (to the epithelium of ducts of salivary glands, etc.) and organonese-visual autoantipers (for example, rheumatoid and antinuclear factors, antibodies to some nuclear antigens - SS-A / RO and SS-B / LA).
Clinic
The clinical manifestations of the BSH can be divided into ferrous and extra-zeroisses. Irony symptoms are due to the lesion of secreting epithelial glands and are characterized mainly by their hypofunction.
Ophthalmological symptoms
In the development of pathological changes in the disease, the Shegon is distinguished by three stages: the hypoid design of the conjunctiva, dry conjunctivitis and dry keratoconjunctivitis. Complaints appear on bad portability of wind and air-conditioned air; The burning, light-friendly, the feeling of "sand" and the foreign body in the age of the century, the presence of a viscous separated (due to high viscosity, the conjunctive discharge is formed into thin mucosal threads), is characterized by the presence of a negative reaction to instillations of indifferent drops. Objectively reveals a decrease or lack of tear meniscoves from the edges; Local edema of bulbar conjunctiva with the transition to the free edge of the century; The presence of degenerative changes in the epithelium of conjunctiva within the open eye slit; formed (dust and knutri from the cornea) on the conjunctiva of whitish, a small size of plaques with a dry and rough surface (Iskober Bito plaques); With a deep parenchymal xerosis, the conjunction acquires a gray shade and becomes rough. With a sharp decline or complete absence of tear liquid products, xerosis and clouding of the cornea are developing. The clinical forms of corneal lesions correspond to the severity of the disease - epithelialism (point defects of the corneal epithelium - microerosia), cornea erosion, nitrate keratitis (epithelial threads on the cornea), corneal ulcer.
The second mandatory and constant feature of the BSH is the defeat of salivary glands by the development of chronic parenchymal vapor. It is characterized by xerostomy and an increase in the salivary glands. Often before the appearance of these signs there are dryness of the red border of the lips, snaps, stomatitis, an increase in regional lymph nodes, multiple caries of teeth. In a third of the patients, an increase in the parole glands is observed, leading to the characteristic change of the head of the face described in the literature as the "Khomyaka Mord". Easy glands at palpation are minorly cones.
Dry nasopharyasus to the formation of dry crusts in the nose, in the lumen of hearing pipes can lead to temporary deafness and the development of otitis. The dryness of the pharynx, as well as voice ligaments determine the witness of the voice. Supportic rinofaringolangitis develops.
Frequent complications are secondary infections: sinusites, recurrent tracheobronchitis and pneumonia. The defeat of the apocrytic glands of external genital organs is approximately in patients with BSh. The mucous membrane of the vagina is hyperemic, dry, atrophic, often patients are bothering burning pains and itching. Frequent sign BSH is dry skin. Changes in the digestion system of BSH are often observed and diverse in nature. Dysphagia is due to the presence of xerostomy, as well as, in some cases, the hypocine of the esophagus. Many patients have chronic atrophic gastritis with pronounced secretory insufficiency, clinically manifested gastric dyspepsia syndrome (heaviness and discomfort in epigastrics after eating, air exhaust, nausea, decline in appetite). Less often observe pain in the epigastric area. The pathology of the biliary tract (chronic cholecystitis) and the liver (persistent hepatitis) is observed in the majority of patients. There are complaints of gravity and pain in the right hypochondrium, bitterness in the mouth, nausea, bad tolerance of oily food. Involvement in the pancreas process (pancreatitis) is manifested by pain and dyspeptic syndromes.
Elderish manifestations are diverse, is systemic. Arthralgia, a small stiffness in the morning, recurring non-erosive arthritis of small, less often of large joints and pain flexible contractures are encountered about patients. Signs of polyimositis (Malgia, moderate muscle weakness, a slight increase in the level of creatine phosphocainase in the blood) are observed in 5-10% of patients. Most patients with BSh have regional lymphadenopathy.
Various respiratory lesions are powered by 50% of patients. Dry throat, allocating and scratching, dry cough and shortness of breath are the most frequent complaints. Dyspnea more often indicates the defeat of pulmonary parenchyma (interstitial pneumonia and interstitial fibrosis). Comparatively rarely, with BSh, recurrent dry and discharge pleurisites are observed. In 20-30% of patients, various lesions of kidney-chronic renal failure are noted, the diffuse glomerulonephritis is less likely. In patients, BSh is observed Reyno syndrome, more often - erased its forms. Clinical signs of peripheral polyneeropathy with a disruption of the sensitivity of "socks" and "gloves", paresthesia, less often - polyneurite and mononeurite, neurites of the facial and trigeminal nerves are observed in a third of the patients.
Diagnostics
The most informative laboratory indicators with BSH are high ESP, leukopenia, hypergammaglobulinemia (80-90%), the presence of antinuclear and rheumatoid factors (90-100%), as well as antibodies to soluble nuclear antigens SS-A / RO and SS-B / LA (60-100%). In a third of patients, poly- or monoclonal cryoglobulins are found.
Treatment
The main place in the treatment of BSh belongs to corticosteroids and cytostatic immunosperessants (chlorubutin, cyclophosphamide). In the initial stage of the disease in the absence of signs of systemic manifestations and moderate disorders of laboratory indicators, a long-term treatment of prednisone in small doses (5-10 mg / day) is advisable. In the pronounced and late stages of the disease, in the absence of signs of systemic manifestations, it is necessary to assign prednisolone (5-10 mg / day) and chlorobutin (2-4 mg / day) followed by long-term, for several years, receiving supportive doses of prednisolone (5 mg / day ) and chlorobutin (6-14 mg / week). Pulse therapy with high doses of prednisolone and cyclophosphane (1000 mg of 6-methylprednisolone intravenously daily for three days in a row and single intravenous administration of 1000 mg of cyclophosphane) followed by transfer to moderate doses of prednisolone (30-40 mg / day) and cytostatics (chlorubutin 4- 6 mg / day or cyclophosphamide 200 mg is intramuscularly 1-2 times a week) is the most effective method of treating patients with severe system manifestations of BSH. Extracorporeal methods of treatment (hemosorption, cryoadsorption, plasmapheresis, double plasma filtration) in combination with pulserates are most effective in the treatment of BSH patients with ulcerative-necrotic vasculitis, glomerulonephritis, polyneurite, myelopolyadiculine-neuritis, cerebrovasculitis caused by cryoglobulinemia.
Local therapy with dry keratoconjunctivitis is aimed at overcoming hypolacrymy, preventing a secondary infection, accelerating the processes of regeneration of the epithelium conjunctiva and cornea. Tears of tear-leather therapy replenish the deficit of the aqueous layer of precalar tear film and hold it in a stable position - a peer natural, polycin, lacryciphy, lacrimal, Lacripos, a Vicersik, an offagel, etc. (In addition to bioadhesia, increases the viscosity of tears, thickens mucin and aqueous layers of the lacrimal film). The frequency of use of various drugs depends on the severity and shape of the disease - from 4-6 to 10 times a day or more.
With a light severity of xerosis, it is recommended to use substitutes for low viscosity tear fluid substitutes containing polyvinyl alcohol (PVS) or polyvinylpyrrolidone (PVP) (OFTTAGEL, Lacrimal, Lakofal, Liquofilm). Polyvinyl alcohol has a surface pressure similar to the pressure of the water-muddy layer of a lacrimal film and has the ability to bind water. At the average degree of severity of the xerose, it is recommended to use substitutes for tear fluids containing cellulose (natural tear, lacryciphic, lacrimal) and polymers consisting of a carbomer (offagel, vocinery). The chemical basis of the carbomer is acrylic acid; A carbomer-based gel has a thixotropic property, i.e. It turns into a liquid under the influence of the shear forces, as a result, the drug is quickly distributed over the surface of the eyeball and holds longer on it.
In case of degenerative changes in the epithelium, conjunctiva and cornea are used drugs that provide reparative effects - decantennol (Cornelgel), 5% ointment, Actovegingel 20%, Salcossierl-gel 20%, Balarpan, Vitasik). In the signs of a local allergic reaction, the criterity acid (ledrooline), 2% rr or Loksamide, 0.1% rr and azelastine, 0.05% rr-p, are additionally prescribed. With a pronounced inflammatory process, a NSAIDs - diclofenac are used, 0.1% r-p; Indomethacin, 0.1% rr. With a pronounced reduction of tearoproduks (sample result for Schirmer O. less than 5 mm, and on Jones LT - 2 mm and lower), the inefficiency of drug therapy for 1 month, the presence of severe changes in the cornea (its thinning or ulceration, nitrate keratitis) is shown Points or tubules. This task is now being solved with the help of various means. The largest distribution was obtained by the polymer obturation of the tear paths (corks-obturators of tear dots and lamination of tear tubules). In order to assess the expected effect from the planned long-term obturation of the tear paths of Herrick R.S. (1994) recommends initially entering collagen obstructors in both tear tubers, which are independently absorbed in 4-7 days; If there is a noticeable clinical effect during this period, they introduce the same products, but already from the non-disseminating silicone.
In order to normalize the trophic and secretion of the salivary glands, novocaine blockades use. In cases of exacerbation of chronic vapotitis (and for the prevention of its recurrence), appliques of 10-30% solution of Dimekside are used. In cases of the development of purulent parotitis, antibiotics are administered to the ducts of the salivary glands and antifungal drugs are administered. To reduce the permeability of ducts intravenously or intramuscularly injected with calcium preparations. When drying the trachea and bronchi, a long-term reception of bromgexine is recommended (8-16 mg 3 times a day for 2-3 months). In the presence of symptoms of chronic gastritis with secretory failure for a long time, substitution therapy is carried out. Insufficiency of pancreatic secretion requires reception of enzymes: Panzinorma, Creon, Festal, 2-3 months courses. or constantly.
Gout
Gout - heterogeneous disease, characterized by deposits in various tissues of urates crystals in the form of sodium monorate or uric acid.
Etiology
The determination factor in the development of gouts are various violations of urinary acid metabolism (synthesis and / or derivation), leading to a resistant increase in its level in blood - hyperuricemia.
Pathogenesis
In the case of the content of uric acid in the blood or tissue fluid, more than 0.42 mmol / l occurs the risk of urates crystallization. When the temperature decreases, the crystallization of uric acid is facilitated, in connection with this, the deposition of ultrasound crystals occurs mainly in avascular tissues (articular cartilage and cartilaginous shells), in relatively poorly blooddered structures (tendons, ligaments) or in relatively poorly blood-made anatomical areas (in particular In the footsteps).
Clinical picture
Acute arthritis. For the first attack, the gout is typical monoarthritis and preferential defeat of the foot joints. Most of the gouty attacks are manifested at night and flows with a rapid increase in erythema and temperatures around the joint, swelling and soreness. During the attack of gouts, moderate fever, leukocytosis and an increase in ESP are often noted. The usual duration of the attack is a few days, less often a few weeks. A characteristic feature of gouty arthritis is spontaneous complete reverse development of symptoms.
Chronic gout. It is characterized by the development of certain permanent manifestations of the disease: tofuses (significant accumulations of urates crystals) of various localization, chronic arthritis, kidney damage or urolithiasis. From the first "attack" of the disease to the development of chronic gout passes an average of 11 years (from 3 to 42 years).
The most common localization of subcutaneously visible with the direct inspection is subcutaneously or intracutaneously arranged tofuses - in the area of \u200b\u200bfingers and stops, knee joints, protrusions on the elbow surface of the forearm, as well as synovial bags, tendons and ear-sinks. Sometimes skin can be used over the tofus, while its contents, having a pasty consistency and white color, spontaneously stands out.
Chronic arthritis for gout may involve a different number of joints. Often amazing small joints of the brushes and stop. The articular syndrome may include destructive signs, deformation and stability of the joints. The infiltration of articular tissues by urates is accompanied by an inflammatory reaction of tissues surrounding the joint.
Kidney damage can occur at any stage of the disease. The most frequent clinical signs are moderate proteinuria, a decrease in the relative urine density, the development of arterial hypertension. In renal dysfunction, the tubular disorders prevail. In 10% of cases, the terminal stage of CPN is developing.
Ophthalmological symptoms
The formation of gouty tofuses - whitish painless formations - possibly (rarely found) in the skin of the eyelids; Tufus is formed due to subcutaneous deposits of uric acid crystals, with spontaneous autopsy, the content of tofus content in the form of white or yellowish paste-like mass is detected; Secondary infection rarely occurs (urates have a bactericidal effect). Sometimes the gout develop conjunctivitis, sclerites, keratitis, iris and iridocyclites. Under the gaunt keratitis, the deposition of uric acid crystals is observed in the cornea appear infiltrates that have the form of the nodules of yellowish color; The nodules can merge and ulcerate. Gouty irrit and iridocyclite develop usually suddenly as an attack of gout; severe pain appear, a pronounced mixed injection of the eyeball, a rich fibrinous exudate and hemosis of conjunctiva; there is a damage to the deep layers of the iris, and the ciliary body; The process may be complicated by the clouding of the vitreous body; The course of iridocyclite for gout resistant with recurrences.
Diagnostics
In the acute fit of the gout in the general blood test, leukocytosis with a neutrophilic shift to the left and an increase in ESP, in biochemical blood test, typically elevated uric acid content in serum are found. The largest value in the diagnosis of gout has polarization microscopy of synovial fluid and other tissues (tofuses), at which it is possible to detect the characteristic urates crystals having a rich shape. The determination of daiety of uric acid with urine is important.
Treatment
To relieve acute gubric arthritis - colchicine inside, in the initial dose of 0.5 mg, then each hour additionally 0.5 mg of the drug until the arthritis is completely relocating, the drug takes no more than a day. Among the NSAIDs, preference is given to drugs with a rapid start of action and the most active in anti-inflammatory relation - indomethacin, diclofenacatriy (orally 50-100 mg or intramuscularly 75 mg), nimesulide, naproxen, etc. If necessary, after needed every 2-3 hours, the NSAVP is repeated (diclofenac -Trium 25-50 mg to 200 and even 400 mg per day). With their ineffectiveness, glucocorticoid therapy is carried out, more often. At nephropathy, plasmapheresis is widely used.
In the interconception period, urricauric agents are prescribed. In this group of drugs, Benzbromaron (Hipurik, Desuraric, Normurat) is beneficial (Hipuric, Desuuric, Normurat) - the preparation of prolonged action (0.08-0.6 g per day). Uricostatic means - allopurinol, starting dose 100 mg / day. With the subsequent increase in the dose of up to 300 mg / day. - 3-4 weeks.
Treatment of acute renal failure due to the blockade of intravenous urine outflows, urine crystals refers to the category of critical and requires immediate intensive therapy. Measures aimed at stimulating forced diuresis - intravenous administration of a large amount of liquid and the simultaneous use of saluretics in large doses (furosemid to 2 g per day). Allopurinol is prescribed inside in a daily dose at the rate of 8 mg / kg and the means leaning the urine (sodium bicarbonate intravenously, acetasolamide orally). Conducted therapy is considered effective if it is possible to achieve a diurere that constitutes at least 100 ml per hour for 1-2 days. In the absence of due effect, hemodialysis is used.
42. Rheumatism. Classification. Clinic rheumatic polyarthritis
Rheumatism- This is a systemic inflammatory disease of the connective tissue with a characteristic lesion of the heart.
Etiology, pathogenesis.The main etiological factor in acute forms of the disease is? -Gemolytic streptococcus group A. In patients with protracted and continuously recurrent forms of rheumloard, establish the connection of the disease with streptococcus often fails. In the development of rheumatism, immune violations are of particular importance.
It is assumed that sensitizing agents in the body (streptococcus, viruses, nonspecific antigens, etc.) can lead in the first stages to the development of immune inflammation in the heart, and then to a violation of the antigenic properties of its components with the conversion of them to autoantigentes and the development of the autoimmune process. A special role in the development of rheumatism plays a genetic predisposition.
Classification.It is necessary to identify before the inactive or active phase of the disease.
Activity may be minimal (I degree), the mean (II degree) and the maximum (III degree).
To determine the degree of activity, the severity of clinical manifestations, as well as changes in laboratory indicators, are used.
The classification of the localization of the activity of the rheumatic process (carditis, arthritis, chorea, etc.), the condition of blood circulation and the flow of the disease.
The acute flow of rheumatism is isolated, subacute, a protracted flow, continuously recurring the course and latent course of the disease. The release of latent flow is justified only for retrospective characteristics of rheumatism: latent formation of heart defect, etc.
Clinic.The most often the disease is developing in 1-3 weeks after the suffered angina, sometimes another infection.
When relapses, this period may be smaller. Disease recurrences are often developing after any inter-karrent diseases, surgical interventions, physical overloads. The manifestation of rheumatism is the combination of acute migratory and reversible fully polyarthritis of large joints with moderately pronounced carditis. The beginning of the disease is sharp, stormy, rarely subacute. The polyarthritis develops quickly, accompanied by a remitating fever up to 38-40 ° C with daily fluctuations in 1-2 ° C, a strong sweating, but more often without chill.
The first symptom of rheumatic polyarthritis is the sharp pain in the joints, growing and reinforcing with the slightest passive and active movements. The pain is joined by the swelling of soft tissues in the joints of the joints and simultaneously appears in the articular cavity. Skin covers over the affected joint are hot, when palpation is a sharp pain, the volume of movements is limited due to pain.
A characteristic feature is a symmetric lesion of large joints - more often knee, ray-crew, ankle, elbow. Typichna "volatility" of inflammatory changes, manifested in the rapid and reverse development of arthritic manifestations in some joints and the same rapid increase in other joints. All articular changes disappear without a trace even without treatment, they hold no more than 2-4 weeks.
From the Book Hospital Pediatrics: Lecture Abstract by N. V. Pavlova From the book Urology author O. V. Osipova From the book Urology author O. V. Osipova From the book Faculty Pediatrics by N. V. Pavlova From the book Faculty therapy author Yu. V. Kuznetsova Author From the book internal diseases Author Alla Konstantinovna Myshkin From the book internal diseases Author Alla Konstantinovna Myshkin From the book internal diseases Author Alla Konstantinovna Myshkin From the book General Surgery: Lecture Abstract Author Pavel Nikolaevich Mishinkin Children's diseases: Lecture Abstract by N. V. Gavrilova From the book Handbook of Feldscher Author Galina Yurevna Lazarev From the book Small Psychiatry of the Big City Author Samuel Yakovlevich Bronpers From the book Military Field Surgery Author Sergey Anatolyevich Lodkov From the book Improvement of the spine and joints: Methods of S. M. Bubnovsky, the experience of readers "Herald" Zozh " Author Sergey Mikhailovich Bubnovsky From the book How to Return Health to the Spine Author Gennady Petrovich Malakhov1. Rheumatism. Etiology and pathogenesis
Rheumatism (Sokolsky-Buuo disease) is a systemic inflammatory disease of the connective tissue with the preferential localization of the process in a cardiovascular system, which develops in the persons predisposed to it (as a rule, these are young people) due to acute infection B-hemolytic streptococcus group BUT.
This definition of the disease was given in 1989 V. A. Nononic.
The defeat of other organs and systems during rheumatism has a secondary value and does not define its gravity and subsequent forecast.
Etiology. Beta-hemolytic streptococci groups A are the cause of the defeat of the upper respiratory tract. That is why the emergence of rheumatism, as a rule, is preceded by the angina, the aggravation of chronic tonsillitis, and in the blood of the disease, the increased amount of streptococcal antigen and anti-government antibodies (ASL, ASG, ASC, anti-DNase C)) is detected in the blood.
In the development of rheumatism, the role of age, social factors (adverse living conditions, insufficient food) play, and genetic predisposition (rheumatism - polygnically inherited disease is well known, the existence of "rheumatic" families), which is a hyperimmune response to streptococcal antigens, the inclinations of the disease to autoimmune and immunocomplex processes.
Pathogenesis. With rheumatism there is a complex and diverse immune response (reaction of the hypersensitivity of immediate and slow-type) on numerous streptococcal antigens. In case of contact with infection, antiordinate antibodies are produced and immune complexes are formed (streptococcal + anti-antibodies to them + complement), which are circulated in the blood and settled in the microcirculatory line. Toxins and streptococcus enzymes also provide damaging effect on myocardium and connective tissue.
Due to the genetically determined defect of the immune system from the body of patients, streptococcal antigens and immune complexes are not fully eliminated and quickly eliminate. As a result, autoimmune processes are developed by the type of slow-type hypersensitivity, and lymphocytes reacting with heart tissue are found in the blood of patients. These cells are given great importance in the origin of organ lesions (mainly hearts).
In the connective tissue in rheumatism, phase changes occur: a mucoid swelling - fibrinoid changes - fibrino-shaped necrosis. The morphological expression of immune disorders are cellular reactions - infiltration of lymphocytes and plasmocytes, the formation of rheumatic, or Ashofftalalaevskaya, granuloma. The pathological process is completed by sclerosing.
With the defeat of the heart, the inflammatory process can spread to all the shells of the heart (Pankardit) or is isolated on each of the shells.
Rheumatism (rheumatic fever) is a systemic, inflammatory disease, with an autoimmune mechanism of occurrence, having a chronic course, mainly affects the shell of heart and joints, and is found mainly in children, adolescents from 7 to 15 years, and people who are predisposed to him .
Etiology beta-hemolytic streptococcus group A, in 90% of cases of rheumatism preceded diseases of sore throat, scarletina
Pathogenesis.It lies in the fact that some people have a hereditary predisposition, this explains that there are so-called, "rheumatic families", in which the incidence is 2-3 times, apparently, have such people with genetic changes in immune System. In this case, the body cannot give a proper immune response to an infection, then autoimmune and allergic mechanisms are included. The body, as if fights with himself, antibodies begin to fight the connective tissue, on which immune complexes settle, and it is damaged: joints, heart, kidney, etc., the whole thing is that the immune system perceives its own fabric like an antigen (Alien protein), which should be destroyed with Streptococcus. This situation is a direct consequence of breakage in the work of immunity.
With the first attack-damage to the joints in the lastness of the heart of a shortness of breath, heart pain, dizziness, swelling
Inspection: Ring Erythema, Rheumatic. Takes Palpation Increases CHSS-Golos Fucking Percussion: Displacement of the left heart of the heart, stupid percussion sound Auscultation: Rhythm Galopa, Systolic Noise, Fricond friction noise, Pericard friction noise, Oslable. 1Tadiagnostics: leukocytosis, hurt the SE with react.
ECG Extrasystolia, Avbonda Ist X-ray, Echo.FKG
Current: 1st-small vyat wedge of signs and weathered witnesses
2T-moderately pronounced clinical symptoms and sharp-phase indicators of mete \u003d 40
3st-vivid manifestations of the disease, a rivalent protein
Diagnostic criteria of Kisel_Juses_Nesterov
Main: carditis, polyarthritis, chorea, rheumat.uzelki, ring. Earthhem.
Additional: art pulmonary, fever, rheumatic anamnesis
2OSN + 2Dop \u003d Rheumatism 1OSN + 2Dop \u003d rheumatism
Ticket15.
1. High breathing formations
Hard breathing-character with gross hard breath and elongated exhale of hard Har-Ra
Fur Education:
1. Inseparable as a modified bronchial breathing. In cases of bronchitis and at focal pneumonia, when the acinuses are affected, the conditions for carrying the armor of breathing are being created, but the fabric is modified by changing it and occurs hard breathing \u003d wired
2. The narrowing of small bronchi (bronchiolitis) as a result of swelling of the mucous bronchi, it is narrowed by its lumen, and air friction occurs about the rough surfaces of the bronchus, the sound of the jignea) occurs \u003d local rigid breathing
.2. Radiological, radioisotope and ultrasound methods of renal research
For the study of the urethra, the bladder, ureters and kidney pellets resort to tool methods. The urethra is examined by jamming of a different caliber with a cystoscope "inspect the mucous membrane of the bladder, the outlet holes (mouths) of ureters are observed, as the urine from each ureter is distinguished. X-ray shots of the kidneys (without the introduction of a contrast substance) give only a general idea of \u200b\u200bthe position, kidney sizes , The presence of stones, tumors.
By producing kidney x-ray with the introduction of special means introduced into the blood, snapshots are obtained on which you can see the outlines of the kidney contours, an increase in the organ (for example, hydronephrosis, kidney tumor), as well as stones in the kidneys, ureters and bladder.
Pyelography is of great importance, i.e., X-ray shots of kidney pelvis. To do this, with the help of a cystoscope through the ureteral catheters in renal pelvis, any contrast agent is introduced, which delays X-ray-new rays (retrograde pyelography). Currently conduct pyelography with the help of contrasting substances (ser-gozin et al.), Which are poured into a vein (intravenous pyelography). Normally, after 15-20 minutes, this substance is derived by the kidneys and on the radiograph of the renal's outlines, renal pelvis, ureters and bladder.