Gout is a chronic disease that results from violations of metabolism which is accompanied by the deposition of urine acid sodium in various organs and tissues and which leads to disruption of their functions most often affects the joints and kidneys.

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.

Glomerulonephritis is a kind of allergic infectious disease of the kidneys, mainly affecting glomerular apparatus. We are to distinguish primary glomerulonephritis that develops after 1 – 3 weeks after exposure to communicable and so called “non-infectious factors” being secondary glomerulonephritis occurred due to various diseases like systemic lupus erythematosus, etc. Acute glomerulonephritis is characterized by hypertension, edema and urinary syndrome which is the most common symptom and appears suddenly within 1 – 3 weeks after exposure to various factors.

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 a contagious acute disease characterized by lesions of the small intestine, a violation of water-salt metabolism, varying degrees of dehydration because of fluid loss with watery feces and vomit. Refers to the number of quarantine infections. Pathogen is called Vibrio cholerae existing in the form of curved rods which dies after boiling for 1 minute. Some biotypes long persist and multiply in iodine, in the mud and among the inhabitants of water organisms. The source of infection is a person both the patient and the carrier. Vibrios are excreted either with feces or vomit. Epidemics of cholera are known being caused by water, food and mixed with susceptibility to cholera is being rather high.

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.

Though it is perceived the human beings have successfully combated plague in the 20th century we still have some cases “crop up” in some countries and everyone has to be aware what that decease is and how to face it.

Epidemiology

The Yersinia Pestis bacteria causes sporadic cases in humans and is transmitted by bites of fleas and rodents. Pulmonary form of plague can be transmitted from person to person.

Clinical manifestations

Bubonic plague which is characterized by painful lymphadenopathy or buboes, fever, headache, immobility, pain and defeat of the abdominal cavity after the 2-7-day incubation period. Insect bite usually goes unnoticed, but a small crust may indicate the place of the introduction of the parasite. Untreated bubonic plague is usually leading to sepsis and decrease blood pressure being followed by death in 2-10 days. Pneumonia develops in 10-20% of the cases and it is characterized multilobular defeat and release Y. pestis from sputum. The disease proceeds rapidly if left untreated and death occurs after 2-6 days.

Diagnosis

Diagnosis is based on the result of staining with Giemsa aspirate from the bubo in a smear detect bipolar shape, similar to safety pins. Results of studies are normally being seen in 48-72 h and are generally positive. Serological results may also confirm the diagnosis.

Plague treatment

• Assign streptomycin in a dose 7,5-15 mg / kg every 12 h for 10 days.
• Tetracycline in 5-20 mg / kg every 6 hours.
• Patients with pneumonic plague should be strictly isolated, and contact persons should undertake a course of tetracycline 250 mg by mouth 4 times a day.

The fall in blood pressure during bubonic form itself must be regarded as a sign of the generalization process, a sign of sepsis, while there is a need for resuscitation, administration of dopamine, the establishment of a permanent catheter. When the pulmonary and septicemic forms of plague dose of streptomycin is increased up to 4-5 g / day for forms that are resistant to streptomycin, chloramphenicol can enter suktsinatdo 6-8 g. In order to improve the state of doses of antibiotics reduce: streptomycin, 2 g / day to normalize the temperature, but at least 3 days, tetracycline, 2 g / daily by mouth, chloramphenicol with the doze of up to 3 g / day, total 20-25 g. Biseptol is also a very effective remedy in a battle with plague.