Treating otitus is usually a task of a doctor – otolaryngologist. Treatment starts from diagnostics. Seeing a doctor is necessary in order to indicate the type of otitus and to reduce the risk of choosing the wrong treatment tactics. However if you are not able to see doctor within several hours, you should start home treatment anyway.

Basic otitus treatment

Usually otitus flow together with a basic disease that led to ear inflammation. And otitus cure is possible only after the basic disease has been cured. The treatment of upper airways and nasal breathing recovery are always necessary. A patient should avoid exposure to cold. Immunogens and vitamin complexes are usually prescribed.

During otitus bed rest and light, calorie rich, vitaminized food are recommended.

Antibacterial otitus treatment

This treatment is aimed at microorganisms that caused the inflamation. Antibiotics are applied for such purpose, sometimes together with sulfanamides. All the remedies should be prescribed by the doctor, however some of the drops can be applied right away: Otipax, Otinum, Sofradex. It is forbidden to use the antibiotics that can injure hearing apparatus: Gentamicin, Streptomycin, Amikacin! To reduce the allergization of the body antihistaminic medicine is prescribed. In case of acute ear pain analgesic remedies are taken.

It is necessary to repeat that the exact complex, dosage, optimal way of taking of necessary drugs for otitus treatment should be chosen by a doctor if you want effective results.

Local otitus treatment

When curing otitus the external acoustic duct gets regularly desinfected by 40% ethyl alcohol or irrigated by 2% boric acid solution with further drying by probe covvered with a cotton, or treated 10% synthomycine emulsion.

In case of abundant secretion from an ear during otitus it is recommended to timely (with a help of gauze turundas or probe covered with cotton) remove the discharge, preliminary pouring 5-7 drops of 3% hydrogen peroxide solution pouring into acoustic duct. External acoustic duct is oiled by sterile vazeline or any other liquid oil in order to avoid skin injure.

To provide free breathing more you should drop vasoconstrictive drops in your nose – Naphthyzinum, Halazolin, Sanorin, Farmazolinum.

Hot compress is usually placed on parotid area, however consultation with a doctor on this procedure is strongly recommended. This can be semi-alcohol compress or dry heat (of heated enough, thoroghly wrapped coarse salt).

Physiotherapy otitus treatment

While curing otitus ultrahigh frequency waves are applied to the ear area, ultraviolet irradiation (quartz) of the external acoustic duct, auricle. Entotic laser therapy is also effective. Ear inflation is also an otitus treatment procedure. All the treatment activities of this type must be only iniciated by otolaryngologist in the outpatient setting. Hospitalization is indicated only in cases of atypical or severe course of atitus.

Usually the success of otitus treatment directly depends on which procedures are chosen. Proper treatment in 99% of cases leads to favorable outcome, while improper methods usually result in cronical otitus that develops from accute form.

The classification of stomatitis is based on various criteria:

1) the clinical course: acute and chronic stomatitis;

2) the nature of morphological changes – Primary (catarrhal, fibrinous, alterative and proliferative inflammation) and Secondary (erosion, aphthae, ulcers, spots, scars);

3) by reason of:

• damages arising from mechanical, physical and chemical injury (abrasion, AFTA Bednar, radiation, chemical and thermal burns);
• diseases are caused by viral infections (herpes, measles, vetryanochny canker), bacterial infections (streptococcal, scarlatinal, tubercular, gonorrheal sores), fungal infections (thrush, chronic oral candidiasis), spirochetes and fuzospirilleznoy Flora (syphilis, ulcer-necrotic Vincent’s stomatitis);
• diseases caused by allergic reactions in the contact, microbial and drug allergy;
• changes in the oral mucosa in some systemic diseases and illnesses exchange.

Consider the most famous among the public and common forms of stomatitis. Previously, stomatitis was considered purely child disease, and divided into fungal (or yeast), and aphthous (or herpes) stomatitis. At the present time, as seen from the above classification, the structure of diseases of the oral mucosa increased, but the proportion of infectious stomatitis is fairly high.

At the oral mucosa many infectious diseases are revealed. The main feature of most of them – the possibility of transmission from patient healthy organism under appropriate conditions. Infection occurs as a result of the interaction of three main factors: the microbe, microorganism and the environment. The main role may belong to one or another of these factors in different cases. The presence of the agent – compulsory, but not always a fundamental condition.

Mouth is normally abundantly populated by microorganisms, most of which are opportunistic. Under the influence of certain factors the virulence of certain species of flora increase, from opportunistic they become pathogenic. This contributes to reducing local and general immunity, the penetration of microbes into the tissues after trauma, disruption of their symbiotic equilibrium (with the use of certain drugs). Diseases caused by conditionally pathogenic flora, called endogenous, or self-infection. They include candidiasis, pustular infection and others.

Stomatitis treatment

World Health Organization in 1981 has given a definition of diabetes like a state of chronic hyperglycemia which may develop as a result of exogenous and causes genetic factors that complement each other.

Thus, the most important feature of diabetes is increasing blood sugar levels known also as hyperglycemia. The content of sugar in the blood of healthy human fasting 3.33 – 5.55 mg / dL.

Also, it is well known that a leading role in carbohydrate metabolism plays a pancreas performs two main functions:

• exocrine which is production of digestive enzymes and which fall on the pancreatic duct into the duodenum and are involved in digestion: break down proteins, fats and carbohydrates to less complex compounds, and then be absorbed into the bloodstream;
• internal secretion i.e. hormone in the so called “islets of Langerhans”;

These places in the body are unevenly distributed in the tissue of the pancreas and they distinguish four main types of cells known as Beta cells which produce insulin, Alpha calls which are in charge of glucagon, Delta cells for somatostatin and P cells for pancreatic.

Due to the total number of cells and their parameters for “health”, “full” and “quality” we can work out their insulin dependent cherished numbers of health from 3.33 to 5.55 mmol / l glucose in the blood.
Insulin is seen as the “key” for the penetration of glucose into the cells of the liver, brain, muscles i.e. the organs which are not able to function without glucose properly.
Blood glucose level is maintained in the main two hormones:

• insulin which is lowering it;
• glucagon which is increasing it.

If grossly interfere in nature – it severely punishes us diseases. The main factors contributing to, the development of diabetes are:

1) Refined foods of modern man, is deprived of crude fiber, forced to work the intestine, impeding absorbability of fats, cholesterol, lipids, and consequently prevents the development of atherosclerosis, unloads insulin y apparatus;
2) humanity has less to move and increase the mass of his body for tens of kilograms;
3) humanity lives in conditions of constant stress;
4) simply overeating;
5) breathing fire and eating masses of chemicals;
6) adverse effects of some drugs on carbohydrate metabolism;
7) cells of the pancreas are sensitive to different viruses.

The twentieth century gave people insulin and hypoglycemic agents which can not only extended but really has saved millions of lives and made it possible for people affected by diabetes but just to live, work actively, make love and have children.

Establish a genetic predisposition to diabetes

The frequency of diabetes mellitus type I in the 0,2 – 0, 3% of the population. In families where one child is suffering from diabetes type I, his brother or sister of risk to get diabetes about 5%. In families where the father has Type I diabetes risk of the disease, 5 – 10%. If the mother is ill, the risk of disease in children 2.5 – 5%. The risk of developing type I diabetes mellitus is higher in those families in which there is diabetes, a third child’s risk to get 10%. In the case of type I diabetes mellitus in relatives of 2 nd degree relatives (uncle, aunt, grandchild) the risk of developing diabetes mellitus 1 – 2%.

The frequency of diabetes mellitus type II is higher than type I diabetes. Among the relatives of the patient with diabetes mellitus type II diabetes risk 25 – 30%, and if both parents have type II diabetes, the risk of developing diabetes in their children after the age of 40 years – 65 – 75%.

Folk methods for treatment and relief

1. Salad of beets and carrots with oranges

Requires: 4 beets 1 carrot 4 cloves of garlic, 0.3 liters of water, 1 orange, 1 teaspoon lemon juice, 4 tablespoons sour cream, 2 tablespoons chopped dill.

Preparation. Take raw beets which are cleaned and rubbed on a coarse grater, add lemon juice. Carrot shred straw to be mixed with beets and pour hot water bringing to a boil at the end. Then the stuff has to be cool. Serve with oranges, sour cream, minced garlic, dill.

2. Cowberry juice

Washed berries are to be poured in boiled water (2 cups of water per 700 g of berries) forl 10 minutes to be rub the berries with the pestle and sieve. Juice has to be filled with Xylitol, Sorbitol or saharitom. Is chilled on 1/2–1 glasses a day.

3.Drink “Autumn”

In brine sauerkraut pour tomato juice, squeeze the juice of half a lemon there, add removed from 1 / 4 lemon zest crushed, cooled boiled water, salt to taste. Stir well. Serve chilled.

For 6 servings: 1 / 2 liters of brine, 1 / 2 liters of juice, 1 / 2 lemon, 1 / 2 cup water.

4.Tomato drink with cheese

You need for 1 serving the following: 2 tablespoons of tomato juice, 50 grams grated cheese, 1 / 2 cup of cold milk.

Preparation. In blender pour grated cheese, pour the tomato juice and cold milk and beat for 1 minute. Serve well chilled.

5. Carrot Cocktail

Required for 4 servings: 2 cups of carrot juice, 2 oranges, 1 lemon, 2 teaspoons honey, 1 cup yogurt or sour milk, 4 – 8 cubes of edible ice.

Preparation. In a mixer whip the good carrot, orange and lemon juices, yogurt or fermented baked milk, honey.

The cardinal sign of glaucoma is violation of the regulation of intraocular pressure. Increased intraocular pressure for the second time leads to the development of all the other symptoms characteristic of the glaucomatous process.

The boundaries of normal intraocular pressure normally ranges from 18 to 27 mm Hg. The so called “top ophthalmotonus” for the most of people is in the early morning and later during the day the intraocular pressure is reduced by 2 – 5 mm Hg.

Glaucoma treatment

The most common treatment of congenital glaucoma is the surgical one. In fact, before that you are supposed to take the drug treatment with 1 – 2% solution of pilocarpine and 2 – 3% solution of atseklidiya or 0.25% solution optimola.

The so called youth glaucoma means that developed glaucoma at a young age. There is a hereditary transmission and usually the sick persons are the ones who are under 30 years. The clinical picture is diverse i.e. in some patients with marked changes in the iris, the other symptoms progressed slowly, the cornea of normal size, anterior chamber depth.

Basic principles of medical treatment of primary glaucoma

• local application of pilocarpine, optimola, klodilina,
• in the absence of compensation glaucomatous process for the deterioration of visual function the surgery is needed.

Currently, pharmacological treatment of glaucoma conducted in three main areas:

• normalization of intraocular pressure (therapy of local and general);
• treatment, contributing to improve the blood supply of the inner shells eye and optic nerve;
• treatment aimed at normalizing the metabolism in tissues of the eye to influence the degenerative processes typical of glaucoma.

Secondary glaucoma

Glaucoma may develop at different times after the removal of cataracts. Sometimes glaucoma may be as a manifestation of primary open-angle glaucoma and not diagnosed before cataract extraction. Treatment is done with 1 – 2% solution of pilocarpine joined with 0,25 – 0, 5% solution of clonidine 2 – 3 times per day and a 50% solution of glycerol or glycerin with ascorbic acid and fruit syrup.

Secondary glaucoma, disturbed circulation in the vessels of the eye, orbit and intraocular hemorrhages occur more frequently in the central vein thrombosis of the retina, with fewer violations of the venous circulation in the orbit (inflammation, swelling, throbbing enzoftalmy, edematous exophthalmos), with obliteration of the veins after diathermy coagulation of the sclera and its resection, with intraocular hemorrhages.

Therapeutic agents can help relieve hemorrhage: local – instillation of 3% solution of potassium iodide; 0,1% aqueous solution of lidasa or ronidazy; intramuscular use of lidasa, vitreous body.

Acute and chronic conjunctivitis may have contagious nature caused by viruses and bacteria. Well, there may be also conjunctivitis caused by physical and chemical hazards as well as allergic conjunctivitis and conjunctivitis in common diseases.

Infectious conjunctivitis have expressed greater prevalence of contagious especially in kindergartens, nurseries, schools, educational institutions and industrial enterprises. Conjunctivitis are often caused by staphylococcus also.

Acute conjunctivitis starts first in one but soon comes to the other eye. Patients complain of a sense of debris or so called “sand” in the eye followed by pain and redness in the eyes as well as a watery or mucous-purulent discharge from the eye. Waking up in the morning, the patient normally had difficulty opening his / her eyes as the eyelids glued together with dried pus on the eyelashes. This may be preceded by entering the eye dust, cooling or overheating, swimming in non-flowing water and the general weakening of the organism, diseases of the nose, cold in the chest, etc.

For treatment of acute conjunctivitis in order to remove purulent discharge it is necessary to conduct by frequent washing of the eyeball. For the successful treatment they use 2% solution of boric acid and solution furacilinum of 1:5000 or 1:5000 of potassium permanganate solution (pale pink in terms of color). When doing washing the eyelids one should be well diluted and use a rubber spray.

Between washing the conjunctivitis cavity should be done in 2 – 3 hours antibacterial drops. As is often acute conjunctivitis caused coccal flora, the most appropriate to apply the sulfonamides and antibiotics: 30% solution of sodium sulfacyl and 1% solution of tetracycline and 1% solution of tetramitsina.

In acute conjunctivitis in any case it is not possible to apply the bandage on the eye patch since under the bandage blinking is not possible which contributing to the evacuation of the conjunctival cavity of purulent discharge.

Overall treatment normally should be done in a long time period and during the treatment some drugs which have the lack of effectiveness must be replaces in 1 – 2 weeks. You are to use 1% of erythromycin ointment and 1 % emulsion of chloromycetin.

Prevention of acute conjunctivitis is to comply with the rules of personal hygiene and do not touch eyes with dirty hands, do not apply common goods. All persons who were in contact with the patient, prophylaxis is recommended for 2 – 3 days instilled into the eyes of a 30% solution of sodium sulfacyl, in other words albutsid. Also, one should change daily towel and linen until the termination of purulent discharge and it is strictly prohibited to use common items of daily use. Infection can occur from an infected person via dirty hands, as well as by airborne droplets.

Most acute conjunctivitis are caused by adenovirus and may occur in the form of fever with the rise of temperature, inflammation of the upper respiratory tract and increasing the submandibular lymph nodes.

Catarrhal conjunctivitis is the most mild manifestation of the disease and lasts an average of 5 – 7 days. Full recovery might be achieved in 15 days.

Pseudomembranous form of decease is rather rarer. The thin transparent covers are usually soft, grayish-white and easy to remove moist cotton swab. However, in some cases form a fairly dense fibrinous covers with difficulty separating from the subject of inflamed mucosa. After removing the exposed surface of the transparent cover can bleed. Follicular form is characterized by rash follicles or vesicles on the conjunctiva of the cartilage and transitional folds. Follicles may be many in quantities and large and sprinkle the entire loosening mucous membrane century. The disease is very similar to the initial stage of trachoma.

Treatment of conjunctivitis

The following remedies are successfully applied:

• Florenalum (0,1% solution in drops),
• Oxolinum (0,1 – 0, 2% in the form of burial),
• Tebropheum (0,1% solution and 0.5% ointment Nye)
• Gludantanum (0,1% aqueous solution in drops 6 times a day).

Sulfanilamide (30% solution of sodium sulfacyl) and antibiotics do not have a specific effect on the adenovirus, but they are appropriate for the prevention of secondary infection. The best effect is observed with drugs tetracycline and chloromycetin because these antibiotics have strong virus-stopping effect.

The overall resistance to adenovirus infection increases dibasol, salicylates, vitamins and desensitization drugs.

Сonjunctivitis, caused by physical and chemical hazards, is in most cases professional chronic diseases of conjunctiva. The polluted air, dust, smoke and vapors of various chemicals can cause chronic conjunctivitis. The harmful effect of these agents to be observed in various industrial enterprises here are coal, cement, flour milling, sawmilling, many kinds of chemical industry, where workers have to deal with acids, alkalis, pairs of other compounds.

Complaints of patients include redness, feeling debris eye, tearing, burning, heaviness in the eyelids, growing in the evening. In the morning at the inner corner of eye slit is collected and separated in the form of lumps of mucus.

Treatment of chronic conjunctivitis is more often implies the use of drops and cold compresses of binding agents (infusion of tea, 0.25% solution of resorcinol), with exacerbations and the presence of discharge – 30% solution of sodium sulfacyl and antibiotics. Desinfecting ointments are usually applied nights. In case of professional conjunctivitis it is required to to comply with preventive measures to eliminate the impact of harmfull influence.

The disease was known in ancient Egypt, but until now the reasons for it remain unclear.

The spots usually appear on the intact skin with gradually increasing and merge forming large foci.

Most affected exposed skin places are: face, neck, hands and skin of large folds, genitals and anus.

The hair on the depigmented areas of skin are usually loosing their normal color too. The skin deprived of pigment is very sensitive to the sun light and under the influence of the sun they quickly turn red, but not tanned and discolored spots in particular stand out against tanned skin.

Folk medicine treatment

Folk medicine recommendationss are various but mainly herbal:

1. Hypericum perforatum herb – 30,0 gr.
calendula flowers drug – 30,0 gr.
Chamomile pharmacy – 20,0 gr.
Grass Sage – 40,0 gr.
herb Oregano – 20,0 gr.
grass succession – 20,0 gr.
nettle leaves – 40,0 gr.

From the mixture of herbs you have to prepare infusion as follows: 1 – 2 tbsp. collection pour with 1 cup of hot boiled water then cover and heat on a water bath (note! The water in the bank must be boiling) for 15 minutes then cool at room temperature for 45 minutes. The remaining raw overcome. Volume bring boiled water to 200 ml. Take 1 / 2 cup 2 times a day before meal for 1 – 2 months.

2. The infusion is prepared the same way as in the first recipe, but has a slightly different composition:
St. John’s herb – 20,0 gr.
Calendula officinalis (flowers) – 10,0 gr.
sage (herb) – 20,0 gr.
origanum (grass) – 10,0 gr.
Chamomile pharmacy (flowers) – 10,0 gr.
Plantago major (leaf) – 15,0 gr.
nettle (leaf) – 15,0 gr.

Take a glass of 1/3-1/2. It is highly recommended 3 times daily before meals.

Chinese folk medicine recommends for treatment of small Vitiligo which is floating on the surface of the water plant also known as “duckweed the little”.

You are to take 1 tbsp. of it cleanly washed and chopped and insist duckweed for 3 – 4 days in 1 cup of vodka, then strain. Allow to the patient consume 15 – 20 drops from 2 – 3 tbsp. l. water 2 – 3 times a day.

Also washed crushed duckweed mixed with honey in equal quantities are allowed to be teken1 g 2 – 3 times a day.

Inadequate intake of calcium from food or violation of its absorption in the intestine is accompanied by a decrease in calcium levels, and its ionized fraction in serum. Hypocalcemia stimulates production and secretion of parathyroid hormone which leads to reduction of calcium from bones and increase its level in serum as well as increasing its reflection in the kidneys and increase the synthesis of calcium in the kidneys which is known as Triolet. Homeostasis of phosphate is often regulated by the kidneys i.e. they are absorbed in the intestine almost completely, and their excretion in the urine determines their level in the blood. Excessive absorption of phosphate in the intestine leads to a reduction in serum ionized calcium and increased parathyroid hormone secretion, manifested phosphaturia accompanied by a decrease in phosphate content in the serum and the increase in the amount of calcium. Hypophosphataemia blocks the secretion of parathyroid hormone and activates the synthesis of the calcitriol in the kidneys. This connection enhances the absorption of phosphate in the intestine. Understanding the metabolism of vitamin D is necessary for the understanding of rickets.

The skin contains an enzyme that is under the influence of ultraviolet radiation is converted into vitamin D3. Unavailability of skin to ultraviolet radiation due to smog or clothing also leads to rickets.

There are seven natural substances containing vitamin D with activity but in medical practice they use only 2 of them known as vitamin D2 – called “calciferol” and D3 which is called “cholecalciferol”. In the organism the vitamin itself does not function but its active metabolites, in particular calcitriol.

Calcitriol and other vitamin D metabolites penetrate cell membranes and in cells of organs targeting and interact with specific receptors, forming a complex with them, penetrating into the nucleus of cells and initiates protein synthesis in them. Proteins may be specific (proteins, calcium binding – BSK) and nonspecific – collagen, alkaline fosfatoza. Formed in the brush rim mucosal cells of intestine alkaline fosfatoza participates in an active capturing of calcium ions from the intestinal lumen into the cell with which it interacts with the protein binds calcium, facilitating the passage of calcium through the gut wall into the blood.

Under the influence of metabolites of vitamin D in the intestinal-specific form factors which are also necessary stuff for the absorption of phosphate and magnesium ions. The protein binds calcium circulating in the blood, helps transport calcium in the tissue. In the bones under the influence of calcium Triola is synthesized protein binding calcium, alkaline fosfatoz and normal collagen structure. In the diaphysis kaltsiytriol intensifying resorption of bone tissue it is demonstrated in increasing intake of calcium acetate in blood plasma, which in the kidney is filtered into the primary urine, and from it and then reabsorbed (with normal vitamin D in the body), maintaining a healthy level and citrate, calcium and blood . Resorption of bone with normal vitamin A in the body occurs with a low rate in terms of the resumption of bone tissue. In the kidneys under the influence of calcitriol and is synthesized protein binding calcium, alkaline phosphatase, required for the reabsorption in the proximal tubules of kidneys of calcium, sodium, phosphate, amino acids.

Deficiency of mineral salts violates bone mineralization. Their failure in the areas of growth, shown slowdown and lag bone age is called rickets. The lack of mineralization of trabecular bone means leading to a high content nonmineralized osteoid which is called osteomalacia. Rickets is sick only a growing child and the process in this case is localized mainly in the epiphyses and osteomalacia can occur at any age. All patients revealed osteomalacia rickets, but not all patients with osteomalacia rickets develops.

The disease can occur as a background of deficiency of calcium or phosphorus. Since the ions of calcium and phosphorus are the mineral part of bone, the lack of any of them in the extracellular fluid bathing the mineralized surface, leads to rickets.

Periods of disease are: initial, peak, recovery, residual effects.

The initial stage of the disease accounts for up to the third month of life and shows changes in the nervous system: the child becomes irritable, often crying, sweating, there is a disorder of the fecalium and balding. This period lasts 2 – 3 weeks. In the blood decreases the amount of phosphorus with alkaline phosphatase is activated. In the midst of illness the changes in bone occur: strain softening of skull bones, soften the edges, sternum forward. As a result we see the chest being deformed, deformed limb bones, bone tissue becomes brittle and along with rickets osteoporosis. The X-ray shows not just proper bones but the contours of the bones lubricated. Tubular bone-shaped, fringed edge of the metaphysis. When rickets II – III degree enlarged liver and spleen, expressed anemia.

In acute course has been a rapid increase in symptoms of rickets. Acute course in children during the first months of life, especially in preterm good gain in weight.

Pathogenetic mechanism lies in the violation of phosphate reabsorption in the proximal tubules of the kidneys, the transformation of the inactive metabolite of vitamin D in the active form. Left untreated, the overall body length of an adult does not exceed 130 – 160 cm.

Radiographic signs are to enhance and destruction metaphysis, rough structure of trabecular bone. Goblet change occurs in the metaphysis of the proximal and distal tibia, radius and ulna bones.

Laboratory tests: serum calcium levels did not change or slightly decreased (90 – 94 mg per liter), moderately reduced levels of phosphate (15 – 30 mg / l) and increased activity of alkaline phosphatase. Phosphate excretion in the urine is significant.

The earlier a child develops kidney failure, the longer its course and so more likely to develop osteodystrophy. The early symptoms include slow growth as a result of metabolic acidosis, inadequate diet, a violation of mineral metabolism. Growth retardation sometimes occurs without radiological changes of the skeleton. With progression of the disease develop muscle weakness, bone pain, bone deformities, fractures and epiphyseal displacement in the metaphysis. Particularly noticeable in small children varus curvature of the knee joint, protruding frontal bone, pathological changes of teeth.

Unfortunately, currently the most common type of rickets we face is a classic D i.e. deficient rickets. This is due to a lack of vitamin D from food to both the mother and her child, in connection with the socio – political upheaval, amazing our country.

Important!
Ti is of great importance in the treatment of hypervitaminosis. Patients need to consume vitamin E, stabilizing cell membranes and vitamin A which is able to block the entry of calcium in the tissue. Should be the take of Furosemide, which accelerates the excretion of calcium in the urine. At the same time usually drugs are prescribed drugs that increase the alkaline reserves, liquidate acidosis (sodium bicarbonate, etc.) to be combined with Asparcam and a diet with restriction of calcium.

The term “gout” itself is derived from the Greek word podagra which literally means “foot trap” or “leg, a victim” (in direct translation podas means leg and agra is a trap or victim) reflecting the relatively frequent clinical observations defeat leg joints while disease.

This suffering from gout was known since antiquity. The great physician and founder of Medicine Hippocrates who was born 460 BC in six aphorisms provides information concerning the nature, origin, clinical course and treatment of gout, as well as an attempt to differentiate this disease from other arthritis. Famous Roman physician Galen (born 131 AD) described well the essential feature of this disease which is known uratoma or tofus.

An important landmark study of this disease was the discovery of uric acid Seheele and Bergmann in 1976 and in 1797 Mr.Wollaston discovers lithate contents gouty nodes. The final recognition of the primary role of uric acid in gout essentially proves in 1848 Dr. Garran by showing that the string, dropped in the blood of the patients covered by crystals of uric acid compounds. This fact was not observed in the study of blood of healthy people.

There are primary (essential) gout and secondary gout.

Primary gout occurs as a distinct disease, often caused by genetically determined defects in the enzymes which regulate the synthesis of nucleic acids, respectively, and uric acid, as well as in violation of the mechanisms of excretion by the kidneys. Thus, the known primary gout which occurs due to the presence in the body of congenital defective enzyme hypoxanthine-guanine-fosforiboziltransferaty appears already in childhood and leads to hyperuricemia (high levels of uric acid in the blood), as well as the accumulation and deposition of various tissues.

Secondary gout develops in the presence of certain pre-illness or pathogenic factor that is seen as a complication of a pathological process – it can be a variety of blood diseases (leukemia), chronic lead intoxication, the effects of some medicines such as riboksin, diuretics etc.

In the development of primary gout, as we already noted, somewhat importance belongs to the hereditary factor. According to various researchers, the existence of familial predisposition to the disease varies from 12 to 81% of cases. The presence of giperuremia (sometimes asymptomatic) was observed on average amongst 25% of relatives of the patients with gout examined. The role of heredity in the etiology of gout is confirmed by the prevalence of the disease within nations and whole races. Thus, in the literature mentioned that the number of cases detected gout in the Philippines is 20 times greater than rates of neighboring states. However, most often, the role of heredity are not so fatal, and, apparently, needed by many other factors influencing the occurrence of this disease.

Many researchers point out to the impact of “nutritional” factors explaining the increased incidence of gout in recent decades, people with increased material prosperity, abundant food, sedentary lifestyles, frequent alcohol use (it is believed that high-fat foods and alcohol to block the secretion of uric acid by the kidneys). It is known that after the Second World War in countries with high welfare population has increased dramatically the number of patients with gout. At the same time in those countries where the diet of lean meat and prevails, mostly carbohydrates (India and African countries), gout is quite rare. Despite these facts, the present role of nutritional factors not considered valid proof of the development of gout depending on the nature of power.

Folk methods of treatment

Of the non-traditional or so called “folk” methods of treatment for gout should be mentioned the action of radioactive substances on the patient’s body. Effective factor is the adoption of radon baths or inhalation of radium emanation. In the treatment procedure of radioactive substances in most cases there was an overall clinical improvement of the patient often seen in decrease or even disappearance of tofusov, positive dynamics of the functional abilities of the affected joints. Similarly we notice the same effect from the action of hydrogen sulfide baths.

A favorable factor for this disease is the heat. Local and overall thermal procedures promote resorption of tissue deposits of uric acid compounds. The mechanism of action due to increased blood flow in the zone, as well as the reaction of affected tissue with subsequent phenomena of phagocytosis and resorption of uric acid compounds exudates. The thermal procedure is shown to apply only in interracial periods.

Fasting is also one of the most ancient and proven methods of healing, cleansing and rejuvenation of the body, acquiring in recent years an increasing number of supporters. Here is what it says about domestic luminary of the method.

In the development of glomerulonephritis the leading role belongs to the streptococcus infection. Nephrotoxic properties has a beta-hemolytic streptococcus of group A with its types 12, 4, 25, 49. However, for the realization of the pathogenic effect of streptococcus in the body requires certain conditions, as indicated by statistics upon the development of glomerulonephritis in a few cases so called nephrotoxic types of streptococcus. When strep glomerulonephritis is not found in the kidney tissue its etiologic role is to antigenic stimulation with subsequent formation of antibodies and circulating immune complexes that damage the kidney tissue. The emergence of acute glomerulonephritis may be influenced by viral infection, as evidenced by the discovery of its symptoms in the glomeruli of the kidneys in so called nefrobiopsia. Acute glomerulonephritis may develop after vaccination, when vaccine and serum act as antigens or destructive factors of immune responses in previously sensitized organism. Obviously, prior sensitization is important in the development of glomerulonephritis after being bitten by bees, snakes, etc. In a certain percentage of cases there is a direct relationship between the development of glomerulonephritis with cooling of the body under the action of which, obviously, change the properties of the protein with the acquisition of its antigenic characteristics (e.g. cryoglobulins) or activated latently current streptococcal infection.

Based on clinical and experimental research we distinguish 2 major immune mechanisms responsible for the development of acute glomerulonephritis which are:

• primary autoimmune with antibodies to the basal membrane of glomerular capillaries
• immunocomplex i.e. in primary autoimmune genesis of glomerulonephritis develop antibodies to glomerular basement membrane as a result of the acquisition of its antigenic characteristics with the subsequent formation of immune complexes in glomeruli and their damage.

In such a mechanism of the disease among people 10 – 15% of cases, the reaction of antigen are antibody binding which occurs with complement and with the participation of the blood coagulation system, histamine, serotonin and other factors. When the mechanism of immune deposit glomerulonephritis observed in 85 – 90% of cases, kidney damage occurs under the action of circulating soluble antigen with antibody complexes that are deposited in the glomerular capillaries. This antigen may be autologous or more with respect to exogenous origin (streptococcal, etc.).

Immune origin of streptococcal have glomerulonephritis, nephritis associated with serum sickness, caused by malaria and viral infection. In the transition of acute glomerulonephritis in a chronic form of autoimmune mechanisms to align. Clinical manifestations of acute glomerulonephritis usually appear within 7 – 21 days after infection. In other words after a certain latent period characterized by the formation and deposition of immune complexes in glomeruli. Most patients comprising 85 – 95% of cases experience the dynamics of clinical signs of acute glomerulonephritis characterized by cyclical and fit into 3 main periods:

• detailed clinical manifestations – the initial period;
• regression of symptoms;
• complete clinical and laboratory remission, while maintaining a more than 5 years can speak about healing the patient.

With non-cyclical or unfavorable course of acute glomerulonephritis may become chronic and fatal diseases of various complications that often occur in the first period.

Glomerulonephritis treatment

Radical treatment is impossible, as the process is autoimmune out of intensification, in most cases a nephroprotection is prescribed. Other preventive measures include: long bed rest, avoiding physical load and exposures to cold, working seated in dry warm room, diet, limit in salt to 2-3 grams per day, in protein, healthy food.

In severe cases glucocorticosteroids (dexamethasone, hydrocortisone), cytostatic agents (mercaptopurine, azatioprine, cyclophosphan), curantyl are taken. Sanatorium-and-spa treatment in dry hot climate is recommended.

In case of intensification a hospitalization is needed. Any worsening of urine test should be considered as intensification. The treatment is the same as for accute glomerulonephritis. However the treatment becomes much more difficult for patients with gastric ulcer, pancreatic diabetes, renal insufficiency, high hypertension or within first 15 weeks of pregnancy due to contra-indications.

Cholera is periodically extended to many countries and whole continents, claimed millions of lives and the last pandemic disease began in 1961. So far the epidemiological situation of cholera in the world remain tense and annually infects up to several thousand people. In South and South-East Asia and some countries in Africa with the African continent recorded more than half of cases. There are endemic foci of cholera epidemics occur periodically.

Symptoms and flow

Symptoms are very diverse starting from an asymptomatic carrier state to severe dehydration states with sharp and lethal. When treating patients with cholera is very important to care for the sick. In the ward for patients must be maintained impeccable cleanliness, the strict disinfection regime. It should eliminate all impacts which can irritate patients and adversely affect their nervous system. Those need special care for the skin and mucous membranes of the mouth as well as eyes, urinary and sexual organs. The wards must be maintained sufficiently high temperature.

Treatment of patients with cholera should necessarily be in the specialized infectious hospitals. The sooner treatment is started, the better results and fewer opportunities for the development of complications. The first treatment is aimed at compensation for the loss of fluid and salts, the correction of metabolic disturbances and suppression of vital activity of the vibrios.

Effective treatment measures

First comes the rehidration treatment:

• Number of injected liquid should be about 10% of the patient’s body weight.
• The solutions injected heated to 38 – 40 C°. The introduction of the first 2 – 4 liters is a drip rate of 5 – 10 ml / min. Then produce a more accurate calculation of solution, which depends on fluid loss from the vomit and feces.
• In mild form of disease with dehydration I – II degree held oral rehydration, for this purpose using a glucose-salt mixture “Oral”.
• If necessary, oral rehydration can be carried out through the probe. Emerging sometimes vomiting is not a contraindication for rehydration.

In addition to rehydration therapy, antibiotics required. The most frequently used tetracycline in doses of 0,3 – 0, 5 grams 4 times a day for 5 days. You can apply chloramphenicol in a quantity of 0,5 g every 6 hours for 5 days.

Vibriocarrier takes 5-day course of antibiotics. During the period of cessation of vomiting, the patient is allowed to eat slimy soups, porridge, yogurt, the butter, vitamins, as a rule, special power of cholera patients is not required.