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Destructive Power of Cocaine

02 Oct 2018

Cocaine destroys the nose

The incredible increase in cocaine consumption in all walks of life began in the 1960s. He attracted attention when the drug played a major role in the Hollywood blockbuster Easy Rider. He became a super-popular drug, and there was an explosion of demand for it, which caused an increase in supplies from South America. Formed international supply chains and the names of drug cartels have become well known. The largest drug lord of them all, Pablo Escobar, was one of the richest people in the world, earning millions of dollars every day.

Since Escobar, the cocaine business has expanded its product range. Now there is cocaine for every budget. This stuff costs $40 per gram. Can you easily see the difference, because it's powdery, while the coke that costs $80 grams, it is crystalline, you can even see a bit of shine. Just grind it. It's good stuff, you can taste the difference. This is a cheap material, it slightly hurts his nose. From this coke does not hurt at all, it runs beautifully and smoothly.

Destructive Power of Cocaine

What is harmful about cocaine?
If you inhale too much of any type of coke, you can damage your nose. The mucous membrane inside the nostrils is affected, this causes the blood vessels to shrink and clot, depriving the surrounding tissues of supply with blood and oxygen. In the end, the tissues weaken and die. This can lead to a perforation in the nose. To treat these injuries, surgery is often required. Consultant Surgeon Sandeep Paun is a leading specialist in the field of nose reconstruction. As a result of regular use of cocaine, a hole formed in his nose in the nose. He wished to remain anonymous. Today we are going to carry out an operation to eliminate the perforation of your nasal septum. When did you do it last? I do it regularly, most recently six months ago. OK. there are no guarantees that we will be able to completely close the perforation. After consuming cocaine, the operation to close the perforation of the septum is quite difficult.

Destructive Power of Cocaine
I learned about the hole only when I went to the doctor, and he pulled blood clots from his nose that covered the hole that looked really scary. And all the fault was cocaine, a drug. When you look at Danielle Westbrook, as soon as you see her, you will understand what happened to her, her nose actually collapsed and the worst thing is that it can happen to you. During operation, the patient's nose will be cut and divided into two parts. The picture is very illustrative. We'll just look in the nose of this gentleman now. We move in through the nostrils, that's the inner view. On the front wall we can see this hole. In fact, this is a relatively small hole for a patient who abuses cocaine. It should be much more. Often these holes progress far beyond the size that we see here. Knife, please. Sometimes, when you make a strip, you experience a very strong, unbearable burning sensation from the very beginning of your nose to the back of your throat, very painful. The next day, you wake up with blood clots, and you, in fact, snot the pieces of your nose.

With chronic cocaine abuse, perforation becomes more and more, and the cartilage becomes weaker and weaker, because it lacks support. The upper part of the nose begins to collapse, and you can, ultimately, get a boxing appearance. Scissors please. I had patients who had destroyed the entire nasal septum. They had one nasal cavity, and everything just fell through. I sniffed coke every day. You do not worry when you do this. But then, the nose hurts scared, when the nose is bleeding you regret that they were doing it .. So, we see inside the nose, the mucous membrane, on the one hand, you can see the hole in the shell, first the cocaine forms a hole in the shell, and not in the cartilage, but then it corrodes the cartilage and eventually forms a through hole.

About coke
Cocaine is often mixed with all kinds of contaminants, including soda, glucose and, in the worst case, even with talc, which can lead to an intense inflammatory reaction. This inflammation can cause tissues in the nose to die even faster. Ironically, Mr. Pawn uses cocaine to stop the bleeding of the patient. Patients do not inhale it in advance, we give them a small amount in a liquid form. I just cut out a small piece of cartilage from the back of the nasal septum, which we then intend to insert into the front part, A little cartilage will close the hole. So, you can see here that the shell was completely closed, in the place where the hole was. If we look at the other side, There's no opening right now. I do quite a lot of nose surgery in London. There is a lot of money. About once every few weeks, I have a patient who has problems with cocaine use.


Second stage of alcoholism

01 Oct 2018

Duration 5-15 years.

Second stage of alcoholism

At this second stage all the symptoms of alcoholism become heavier. The pathological attraction to alcohol becomes more intense and arises not only in connection with "alcoholic situations", but also spontaneously. Patients are more likely to find motivation for alcoholization themselves than to use the appropriate situations.

Tolerance in the formation of the second stage continues to increase, reaches a maximum, and then, for a number of years, remains constant. Alcoholic amnesia becomes systematic, individual episodes of a significant part of the intoxication period are forgotten.

During this period of the disease, the form of alcohol abuse changes. This can be expressed in the tendency to periodic or constant abuse of alcohol throughout the disease. In the first case, frequent single drinks are replaced by drinking-bouts. Drinks are characterized by periods of daily drunkenness, the duration of which can range from a few days to several weeks.

There is a physical dependence on alcohol. A sharp break in drunkenness is accompanied by an abstinence syndrome: limb tremor, nausea, vomiting, lack of appetite, insomnia, dizziness and headache, pain in the heart and liver.

Alcoholics have changes in the mental sphere. The level of personality decreases, creative possibilities are lost, intellect is weakened. There is psychopathy and delusions of jealousy. In the future, it can go into a persistent delirium, extremely dangerous for the patient and his loved ones.


How to treat fungal diseases

21 Sep 2018

Currently, fungal - mycotic - infections affect about 20% of the world's population. More than 100 thousand mushrooms are known, of which about 50 thousand are pathogenic for humans. In this case mycosis is very contagious.

The most common mycoses with a lesion of smooth skin and nail plates - onychomycosis. The causative agent of onychomycosis can be dermatophytes (Trichophyton rubrum) that affect the nail plates on the toes of the feet, brushes, smooth skin, as well as long and hairy hair, and Trichophyton interdigitale - the nails that damage the toes and the interdigital folds, the upper third of the sole and the arch of the foot. Often, onychomycosis causes yeast-like fungi of the species Candida and mold fungi - Scopulariopsis brevicaulis, Aspergillus, Fusarium and others.

How to treat fungal diseases

The defeat of the nail plates can proceed according to the normotrophic type - only the color of the nails changes: in their lateral areas, spots and bands appear, the color of which varies from white to yellow, gradually the whole nail changes its color while retaining its thickness.

In hypertrophic type, subungual hyperkeratosis is attached to the changed color; the nail loses color, becomes dim, thickens and deforms.

For the onycholitic type, a dull brownish-gray color of the affected part of the nail, its atrophy and rejection from the bed is characteristic, the exposed area is covered with loose hyperkeratotic scales. In 15-25% of patients with mycosis, the stop fungal process spreads primarily to large skin folds, then to other parts of the skin. The effects of mycosis feet are quite serious. Under the influence of fungi and the products of their vital activity, polyvalent sensitization is formed, which leads to an increase in the frequency of allergic skin diseases, mucous membranes, attachment of eczematous complications, drug intolerance, especially antibiotics of the penicillin series. In addition, through erosion and cracks in the macerated, loosened horny layer of the skin, bacteria easily penetrate. Bacterial complications are characterized by resistance to therapy, bacteria under the influence of antibiotic substances produced by fungi, acquire increased resistance to antibiotics.

Combating the fungus from the outside and inside

Etiotropic treatment of onychomycosis happens:

- local (external) - the antifungal drug is applied to the smooth skin or the affected nail;
- systemic - the drug is prescribed inside, and it enters the nail plate through the blood.

To the requirements for antifungal drugs, in addition to their effectiveness, include a wide range of antifungal activity, rapid absorption, safety (the absence of common and local side effects), as well as ease of use.

Means of local therapy. If the patient has various diseases (chronic hepatitis, nephritis, pathology of the cardiovascular system), as well as with superficial mycosis and mycosis of smooth skin, the main principle of treatment is the appointment of local antifungal therapy (ointments, creams, gels, sprays, solutions and varnishes ). Antifungal components of these forms do not penetrate through the nail plate, so the drugs are applied to the smooth skin or to the naked nail bed - they are rubbed 2-3 times a day until a healthy nail plate grows.

Drugs containing only antimycotic are isolated, for example: bifonazole (1% cream, 1% solution, spray, powder), isoconazole (1% cream), ketoconazole (2% cream), clotrimazole (1% ointment, 1% solution, 1% cream, 2% cream, suppositories), miconazole (2% cream), econazole (1% cream, 10% solution), naphthiphine (1% cream, 1% solution), terbinafine (1% cream), natamycin (2% cream), chloronitrophenol (1% solution).

Drugs of double action, which, in addition to antimycotics, include anti-inflammatory substances: clotrimazole and betamethasone (cream), miconazole and mazipredon (ointment), isoconazole and diflucortolone (cream).

Preparations of triple action - with antifungal, antibacterial and anti-inflammatory action: clotrimazole, gentamicin and betamethasone (cream, ointment), natamycin, neomycin and hydrocortisone (cream, ointment, lotion).

Very convenient for use in local therapy of onychomycosis varnishes (with active substance 8% cyclopyrox and 5% amorolfin). They differ not only in high fungicidal activity against dermatophytes, molds and yeast-like fungi, but also antibacterial against gram-positive and gram-negative flora. To cure onychomycosis, 6 months of therapy is sufficient on the hands, 9-12 months on the feet.

A solution containing the active ingredient terbinafine hydrochloride (1%) is applied once a day. When applied, a thin film forms on the surface of the epidermis, from which the active component is released into the deeper layers in the therapeutic concentration for 13 days. Sprays, which include terbinafine and bifonazole, have a primary fungicidal effect.

At local use of preparations there are no systemic side effects, but when applied to the surface of the nail they do not always reach the pathogen capable of damaging not only the nail plate, but also penetrating into the nail bed, deep layers of the skin and even into the medullary canal of the fingers, especially with total defeat a nail plate. As practice shows, local treatment alone, in most cases, does not lead to complete recovery of patients.

Preparations of systemic action. Systemic therapy provides penetration of drugs into the nails through the blood. Although it does not allow you to immediately create in the nail such high concentrations as with topical application, but the supply of the drug in the nail bed and matrix with systemic therapy is guaranteed. Many systemic drugs accumulate in the nail matrix in quantities far exceeding the minimum inhibitory concentrations, and are able to remain there after the treatment is over.

There are 3 groups of compounds created for the systemic treatment of fungal infections in humans:

- inhibitors of ergosterol biosynthesis; it is the main sterol of the fungal cell and is necessary for the propagation of fungi;
- allylamines, squalene epoxidase inhibitors, blocking the conversion of squalene to squalene epoxide);
- azoles, inhibiting the activity of fungal cytochromes P-450;
- morpholines inhibiting delta14-reductase and delta8-delta7-isomerase.

Synthetic antimycotics of the azole series include itraconazole and fluconazole. Itraconazole has the widest spectrum of action on dermatophytes, different species of Candida and many mold fungi found in onychomycosis. At the distal ends of the nail plate, itraconazole can be detected after 1 week of treatment. In the matrix, the drug accumulates and is excreted only when the new nail plate grows, therefore, the effective concentration of the drug after its abolition is maintained in the nails on the hands for another 3 months, and on the legs - for 6-9 months with a 3-month course of treatment.

Fluconazole in the treatment of onychomycosis is used according to the pulse therapy scheme, the duration of which depends on the form and localization of onychomycosis: about 6 months with nail damage on the hands, up to 12 months on the legs.

Terbinafine (an allylamine derivative) is highly effective and safe in the treatment of onychomycosis, the drug can be used in children. But many yeast fungi, in particular Candida albicans, are resistant to terbinafine. At infections of fingernails or nails on arms or hand the term terbinafine treatment makes 6 weeks, at infections of fingernails or nails on legs or foots - 12 weeks (3 months).

The above drugs are metabolized in the liver with cytochrome P-450, but itraconazole, in addition, interacts with this enzyme, disrupting the metabolism of many medications, which it somehow influences. Hepatic complications from increasing the level of hepatic enzymes to the possibility of hepatitis are higher in itraconazole than in terbinafine (0.3-5% vs. 0.1%, respectively).

Ketoconazole, a synthetic preparation from the class of azoles, has a wide spectrum of action, but many mold fungi - causative agents of non-dermatophytic onychomycosis - are resistant to ketoconazole. With onychomycosis, the treatment takes 4-6 months and 8-12 months - with onychomycosis stops. The main toxic effect of ketoconazole is its effect on the liver. An increase in the concentration of hepatic transaminases during treatment is observed in 5-10% of patients taking ketoconazole.

The greatest efficacy of mycosis therapy is still achieved with combined etiotropic treatment, which combines the administration of a systemic antimycotic and a local drug.

It is also necessary to remember the prevention of the disease, which includes personal hygiene, nail and foot skin care, the prophylactic use of antifungals after exercise, visits to public institutions (saunas, swimming pools), disinfection of shoes and bath, sex and pedicure accessories, once a week For prevention, you can cover your toenails with antifungal lacquer.

Many people with foot mycosis try to start treatment on their own, which in most cases does not bring the desired effect, but only aggravates the course of the disease (spreading skin rashes, involving more nail plates and complications in the form of eczematiza- tion), so treatment should be done after consultation of a specialist - a doctor-mycologist who correctly diagnoses and selects treatment for each individual patient individually.


How to quickly remove hangover syndrome

14 Sep 2018

Dilute 5-6 drops of ammonia in a glass of cold water and drink. Dead drunk unclot your mouth and pour in. 20 drops of mint alcohol help in the same way.

Lay the one you want to bring back to life. With the palms of your hands, rub both his ears quickly and strongly. A rush of blood to the head should lead the drunk into consciousness.

How to quickly remove hangover syndrome

Strong sweet tea eliminates dizziness.

If things have gone too far, you should wash your stomach. A malicious but effective procedure: two fingers in the mouth - and vomiting. If it does not become easier, drink a weak solution of baking soda or potassium permanganate. Then take a laxative. Thus from you all the remnants of the holiday will come out.

A small, but a wide glass, moisten a few drops of vegetable oil (to cover the walls). Mix egg yolk with 10-20 drops of vodka and add a pinch of ground red and black pepper. Drink with a volley, pre-mixing properly.
The easiest method to combat a light hangover is a cup of coffee or tea on an empty stomach. These drinks relieve the feeling of weakness and fatigue. However, already a double dose can increase nervousness and irritability. In tea it is good to add lemon, honey or currant jam. All these additives can be consumed by mixing lemon or currant juices with mineral water. Folk remedies like brine or sour cabbage soup also fit into the pharmacological canons, although none of the medicines are listed. Paradoxically, these acutely acidic drugs are struggling with the acidification of blood, which is inevitable in a hangover. The weak acids contained in them, the blood only alkali.

When all standard brine-type methods have already been tried, and the soul craves something extravagant, try some foreign method. For example, out of solidarity with the Puerto Rican workers, get drunk according to their methods: take half a lemon and rub it under your armpits.

If the heart allows, go to the bath in the morning. Abundant sweating opens the pores and removes harmful metabolic waste from the body. After that, join the happy in marriage to men, from the earliest times, a borsch, a soup or broth brewed by good wives on the eve.

Maybe it's time for us, Slavs, to move on to cultural wine drinking? Then there would be no reason to write about alcohol poisoning.

Well, those who still decided to "tie" with alcoholic dope, but can not do it even with the help of official medicine, we will give some advice. The people have accumulated a lot of recipes to help people who pass before the green serpent. Here are some of them:

- Take 1 tbsp. a spoonful of centaury, one part of herb wormwood and one part of thyme - all dried. Pour 15 g of the mixture (5 g each) 200 ml of boiling water. Insist, wrapped, 2 hours, strain. Take 1 tbsp. spoon 4 times a day before meals;
- in 250 grams of vodka put a clean dried celery root and two dry leaves of the laurel of the noble. Insist for two weeks. To give a glass of such a tincture - most drinkers have a strong aversion to alcohol;
- 1 tbsp. Spoon the crushed dry roots of the claw into a glass of water. Boil for 10-15 minutes on low heat. Insist, wrapped, 30 minutes, strain, 1 tbsp. Spoon the decoction of the root of the claw into a glass with vodka, give a drink. Such a mixture will cause vomiting and a persistent dislike for alcohol. Precisely observe the dosage, since the plant is poisonous. The drunkard should not know that something has been mixed with vodka.

The use of glycine

In those ancient times, when every amateur photographer himself exhibited films and himself printed photographs, in the photoshop it was possible to buy glycine, a substance that was part of many developers. So called in everyday life the simplest of amino acids - aminoacetic acid.

Later, in the 80's, glycine began to produce the pharmaceutical industry. It was used as a metabolic corrector, that is, a substance capable of influencing delicate metabolic processes.

Not so long ago, a little over a decade ago, physicians paid attention to another property of glycine. It turned out that glycine is capable of neutralizing the toxic products of decomposition of ethyl alcohol and reduces the pathological attraction to alcohol. He was prescribed to people who abuse alcohol, or a patient with chronic alcoholism for interrupting drinking bouts and in an acute hangover period. Glycine prevents the development of alcohol "white fever" and alcoholic psychosis.

Glycine practically does not cause unpleasant side effects, except that the blood pressure decreases slightly and only in rare cases there is an individual intolerance of the drug. Habituation to it is not noted. The only thing that is not recommended is to use the drug along with sleeping pills, tranquilizers and neuroleptics - there can be unpredictable inhibition of the central nervous system.

Natural products containing glycine

Where to get the glycine? It is produced in a very primitive way from the cartilaginous tissue of cattle, if desired, you can get as many as you want. He is in the pharmacies of major cities, but should he chase after him?

The fact is that at the disposal of any hostess there are natural products containing glycine. This is a rich soup, an ear, a jellied fish, a cold. Even jelly marmalade contains glycine. In each 100 gram bag of gelatin contains not less than 20 g of glycine. Apparently not for nothing that our ancestors liked to have a snack of vodka with cold and jellied sturgeon!

In Armenia, for example, it is known as "hash". It is brewed from beef or mutton bones for a long time, and is eaten hot. They say that in Armenia you can not take a step so that you do not stumble upon "armenian cafe".

Now glycine is a part of many anti hangover means, it even went so far that some distilleries began to produce special alcohol-free vodka, which includes glycine.

Back in 1994, a group of astronomers from the University of Illinois announced the receipt of evidence of the existence in space of glycine. This is the simplest form of an amino acid - one of the building blocks of DNA, and, consequently, of life on Earth. Even earlier, newspapers wrote about clouds of alcohol found in space. Apparently, someone there, upstairs, decided to prepare a lot of alcohol-free vodka.


Phenotropil is not high and no euphoria? There is a solution!

11 Sep 2018

If you clicked here, then at least heard about Phenotropil, but rather even tried it! By the way, other names of Phenotropil are Carphedon and Phenylpyracetam. I will say at once, for a long time this carphedon was for me in the top of my favorite nootropics and I did not understand why so many people write that they do not feel it at all. Until he did not come to this .. After a few years of admission, it can take place once every 2 weeks. And then he began to gather the pieces in small pieces. It looked like this, that almost every day a few months passed through the western and our forums, by research and wrote out some notes, then tested himself and close friends of the scheme for several days.

Phenotropil high, Phenylpiracetam euphoria, tolerance

How to reduce tolerance to phenylpyricetam
- Break
Option, which he spoke about in several issues. The meaning is in the recoil of the nervous system to about the starting parameters. For a month, refuse any chemistry, booze, cigarettes, porn (Who loves that). A month later, a little add your favorite thing and you're a lot more from them, including from nootropics.

- Add Potassium, Choline, L-Carnitine
These substances will slightly increase the sensitivity to Carphedon. Especially if there was any deficit. If you want to look for additives, then eat extra 2-3 eggs a day, 2-3 bananas and beef or seafood.

- Mexidol and Vitamins
Mexidol has a bunch of analogues, so it's not important to take it exactly. This is a very good scheme in principle for the recovery of the central nervous system, if you or your friends addicted / thumped and otherwise killed your brain, then at least 2-3 weeks of taking these substances have a positive effect on the brain.

- Memantine
The substance reduces the activity of NMDA receptors of glutamate. On the feedback mechanism, after a mini-course in a few days, the sensitivity of glutamate and dopamine increases, which means stimulants work better.

On whom does Phenylpiracetam work best?

An interesting study that partly answers this question.

Scientists divided mice into 2 groups: with congenital low and high research activity. That is very and not very curious mouse. The first immediately exploring the new terrain, the latter are cautious. All 5 days were administered either phenotropil or placebo.

It turned out that initially the active and passive brain differed in the number of receptors. Active had more NMDA and less Acetylcholine. And almost in 1,5 times.

After the course, in groups with phenylpyricetam the passive norm was pulled to active. The active special changes were not. Changes have occurred in research behavior. Passive began to show average results for active.

If it works on animals that way, it can and for people will be similar. Therefore, a logical summary: Phenylpyracetam works best for people with low motivation or activity. DMAA by the way, on the contrary, it is better for who works better.

How to Take Carphedon

So, after numerous tests on yourself and friends, in search of an ideal scheme, here's the best option for you: To an empty stomach, 2-3-200 hours before a meal, 100-200 mg of the substance! In these 2-3 hours a maximum - tea with cookies, but certainly no complete meals. After 3-5 hours after taking phenylpyricetam, add 100-200 mg of caffeine. This is the most powerful scheme of all.

There was another option to "snort Phenylpiracetam", it works, but who knows what people would think)

Bottom line:

- Phenylpyricetam works in many ways and in different ways for each person

- In general, the effect of stimulation is more pronounced in low-motivated people, if you are so extrovert, you are always prey and a bunch of ideas - there will be no special improvements

- If phenylpyrazetam used to work, but now do not, then take a break from everything, drink vitamins and adjust nutrition. Of the substances can help: Mexidol, Potassium, L-Carnitine, Memantine.

- Carphedon is best taken on an empty stomach a few hours before meals, and then add caffeine.

- Fenotropil now removed from production

Well, the work was done great and at last some exemplary answers were found on the scheme for reducing addiction and correct reception of phenylpyracetam. If you had your observations on this matter - write in the comments.


Smoking is a narcotic addiction

08 Sep 2018

At present, there is no longer any doubt that tar of tobacco smoke provokes cancer, especially lung cancer. It is also known that tobacco tar is not the only life-threatening substance inhaled in the process of smoking.

Until recently, in tobacco smoke, there were 500, then 1000 components. According to modern data, the number of these components is 4720, including the most poisonous - about 200.

Stop smoking. Tabex buy

These thousands of chemicals are presented in tobacco smoke in the form of particles (tar, nicotine, benzpyrene, etc.) and gases (carbon monoxide, ammonium, dimethylnitrosoamine, formaldehyde, hydrogen cyanide, acrolein, etc.). Most of these substances have pronounced irritant properties, and about 60 are known or suspected carcinogens.

If the habit of tobacco, and especially the chemical dependence on it, arises from the influence of nicotine on the brain, the cause of most serious illnesses (often fatal) are tobacco tar, paralyzing purification processes in the lungs, reducing immunity, causing cancer and other diseases lungs.

Nicotine is one of the strongest poisons of plant origin. Birds perish if they bring a glass rod moistened with nicotine to their beaks; the rabbit dies from 1/4 drop, the dog - from 4. For the person a fatal dose - 2 - 3 drops; it's about 20 to 25 cigarettes. The smoker does not die because this dose of nicotine is introduced gradually (within 24 hours), but not in one step, and also as a result of partial neutralization of the poison with formaldehyde of tobacco tar.

It should be noted that smoking exists in two completely different clinical varieties: in the form of a habit of smoking and in the form of tobacco dependence. In the second variant (let's call it "thirst"), the smoker has a pathological, painful attraction to tobacco, and in the first one it does not form. Due to the fact that the outward signs of addiction to tobacco among all smokers are the same (regularity of smoking, a gradual increase in the number of cigarettes smoked per day, attracted to the smell of tobacco smoke), the difference between the two types of smokers can be established only when they try to quit smoking. Those who smoke only by force of habit, can become non-smoking completely painless, without any medical assistance and eventually forget that they were fooling. And those who have developed a tobacco dependence, at all desire can not quit smoking forever, even if the first days without tobacco they pass relatively safely. Sometimes, after a long break (several months and even years), they relapse. This means that smoking left a deep imprint in the mechanisms of memory, thinking, mood and metabolic processes of the body.

According to available data, 100 regularly smoking only seven smoke resulting habits remaining 93 patients - they become carriers of tobacco dependence, for which (as for any other type of addiction) characterized by craving to smoke, and on the thinking level, mental level processes.

It should be noted that severe somatic, bodily disorders affect equally both those who smoke by habit, and nicotine-dependent. These diseases do not appear immediately, they are as if deployed in time, and this often prevents the relationship between disease and smoking.

What is nicotine - the culprit of the formation of tobacco dependence?
Alkaloid nicotine (C10H14O2) in chemically pure form is a clear colorless oily liquid with a pungent taste and boiling point 246 C (730.5 mm Hg. V.), Well soluble in water, alcohol and other solvents. In the air it easily resists. Contained in tobacco (up to 2%) and some other plants.
Nicotine - an extremely strong poison, not inferior to the toxicity of hydrocyanic acid. In small doses, it acts excitantly on the nervous system, in large doses it causes paralysis: stopping breathing, stopping the work of the heart. Multiple absorption of nicotine with frequent smoking forms nicotinism - chronic poisoning, as a result of which memory and working capacity decrease, there is a constant cough with phlegm. One of the devastating effects of nicotine poisoning is also such signs: trembling of the hands, uncertain walk, the person throws something in the heat, then in the cold, the heart while it will happen as a hammer, then freezes.

Nicotine is the main component of tobacco smoke causing destructive changes in the spinal cord, inflammation of the lumbosacral plexus. Due to its effect on the adrenal glands, after each cigarette smoked, the number of circulating corticosteroids, as well as epinephrine and norepinephrine, involved in the regulation of the most important physiological functions of the body, significantly increases in comparison with the norm. Adrenaline, in particular, narrows the blood vessels, resulting in increased blood pressure. Nicotine increases the minute stroke volume of the heart and the rate of contraction of the myocardium. Attacks like coronary vessels of an inveterate smoker, as a rule, are narrowed and do not deliver myocardium with the necessary portions of oxygen, oxygen starvation of the heart muscle (coronary heart disease) occurs. The situation is further aggravated by the fact that less oxygen is supplied to other organs and tissues. After all, a part of hemoglobin, instead of transferring oxygen to them, attaches the carbon monoxide contained in the smoke of the cigarette.

The main metabolite of nicotine is cotinine, which, by its toxic properties, is close to its predecessor. In the blood serum of a person who smokes 10 cigarettes a day, 137.7 μg / l of cotinine is found; when smoking 20 cigarettes, its amount increases to 302 μg / l.

To learn about other, no less insidious components of tobacco smoke, consider them in order.

So, the cigarette was lit and the smoker began to breathe the smoke of burning tobacco. And its pollution and 384 thousand times exceeds the maximum permissible concentration (MPC) of the substances contained in it. Inhalation of tobacco smoke is more than 4 times more harmful than breathing the exhaust gases of a car directly from the exhaust pipe. In a perfectly clean atmosphere, the human body at the moment of smoking is exposed to the same toxic effects as if it were in case of air pollution at 1100 MAC (hygienic norms should not exceed 1 MAC). Such air pollution in industrial centers does not occur. In other words, for smokers, environmental problems practically do not exist. For them, the costs of cleaning up industrial gases are a waste of money, because they "have enough" of those poisons that they inhale with smoke; exhale, they are not more than 10% of the components of smoke absorbed during the inhaling, the rest remain in the body!

But let's go along the path of destructive following of tobacco smoke in the body. The mouth and nasopharynx are the first to contact him. Tobacco smoldering in a cigarette has a temperature of about 300 C. At the smoke which has passed through a layer of tobacco packing and got to the mouth, the temperature drops to 50 - 60 . To smoke through the nasopharynx into the lungs, the smoker, opening his mouth, inhales fresh air, the temperature of which is 35-40 C below the temperature of the smoke there. Only due to a multiple temperature drop on the tooth enamel cracks are formed - the "entrance gate" for infection. Hot smoke, in addition, contributes to the expansion of capillary vessels of the mucous cheeks, palate, gums and causes its chronic irritation, which can lead to an inflammatory process, and then to the development of leukoplakia, a precursor of cancer. The salivary glands of the oral cavity react to tobacco smoke. This leads to increased salivation, which the smoker has to either spit or swallow along with the poisonous components dissolved in it - aniline, hydrogen sulphide, ammonia, carcinogens. Getting on the mucous membrane of the stomach, these toxic compounds cause pain in the stomach, loss of appetite, alternating constipation and diarrhea, the development of gastritis. They can cause ulcers of the stomach and duodenum, stomach cancer.

No less harmful is the effect of tobacco smoke from the oral cavity through the vocal cords to the mucous membranes of the larynx, trachea, bronchi and alveoli. Dissolving in the moisture of mucous membranes, ammonia of tobacco smoke turns into ammonia, which causes increased secretion of mucus, which is why smokers suffer from chronic bronchitis.

The tar of tobacco smoke settles on the walls of the airways, accumulates in the pulmonary alveoli and also stands out when coughing in the form of gray sputum. The lungs are dirty brown. Their resistance to various infectious diseases, in particular tuberculosis, is declining. According to J. Petit and other French scientists, out of 100 cases of pulmonary tuberculosis, which began in adulthood, 25 account for smokers. The vital capacity of their lungs is 300-400 ml less than that of non-smokers. The presence of carcinogenic substances and radioactive compounds in tobacco smoke (as will be discussed in detail below) causes the highest level of lung cancer in smokers.

A number of studies have shown that the increase in lung cancer diseases increases in direct proportion to the number of cigarettes smoked. Those. who smoke a lot, this risk increases by 15-30 times compared with non-smokers. It has also been proven that the risk of the disease is exacerbated by factors such as smoke inhalation when smoking cigarettes, smoking from an early age, holding the cigarette in your mouth between puffs, igniting a cigarette that is not smoked. And, as already noted, the use of alcohol increases the harmful effect of smoking on the respiratory system. Active smokers develop extensive metaplastic changes in the bronchi, considered oncologists as precancerous. Those who quit smoking experienced the reverse development of metaplastic cells, which indicates the reversibility of precancerous changes.

It is estimated that smoking cessation and industrial countries lead to a reduction in the incidence of cancer by almost 40%. One of the main components of tobacco smoke - carbon monoxide - flows through the airways to the alveoli, where carbon dioxide is exchanged, not so much oxygen is enriched as carbon monoxide. Having combined with hemoglobin, it forms carboxyhemoglobin - a dummy molecule, unable to carry the cells of the body the oxygen they need. The average content of carboxyhemoglobin in the blood of smokers is 4.3%, in non-smokers - 0.93%. That's why a person who smoked a few cigarettes in a row or was in a smoke-filled room, kneading oxygen starvation, manifested in headaches, dizziness, nausea, pale skin.

Cyanic acid is another component of tobacco smoke that reduces the ability of body cells to utilize oxygen. Together with nicotine, ammonia, essential oils and methyl alcohol, prussic acid helps to reduce visual acuity, deterioration of color perception, smell, dullness of taste. (Tabex can help to stop smoking).

On this list of disasters, in which tobacco smoke is guilty, does not end. It also includes atherosclerosis, coronary thrombosis, chronic bronchitis, pulmonary emphysema, infertility, allergic diseases. Nicotine and tar entering the blood during smoking are one of the causes of the disease with obliterating endarteritis followed by spontaneous gangrene of the extremities, which arises from the severe narrowing of the peripheral vessels until the closure of their lumens with the necrosis of tissues devoid of blood supply. Manifestations of endarteritis: rapid fatigue of the legs, cramps, intermittent claudication, when a person can only go a few steps, and then one or both legs show numbness and unbearable pain. When you stop after a few minutes, the pain passes, but when you try to go on, it resumes. The vessels of the legs (and sometimes of the hands) are in a state of spasm with such a disease and are able to provide limbs with blood only in a state of complete rest, i. without any physical exertion. Movement increases metabolism in working muscles, and because of lack of oxygen and the accumulation of metabolic products, severe pain occurs. At the second stage of the disease, spasm increases, it also manifests itself in a state of rest. Fingers, starting with a large one, are always cold and blue. There are sores. Since the vessels do not provide for metabolism in the muscles even at rest, the foot, and then the entire limb, can become dead. At the same time the patient experiences unbearable unbearable pains. In severe cases, inevitable surgical intervention (plastic vessels, limb amputation).

Sometimes people think: where in the streets are there so many young people - legless and armless in camouflage uniforms? Not all of them are from the trenches of Afghanistan or Chechnya, not there they lost hands-feet, although this loss occurred just because of the "trench disease" - gangrene. During hard military times, she really got sick in the trenches from hypothermia in conditions of high humidity. And now it often suffers intensively smoking people, especially bums and vagabonds, whose lodging is served by ditches, gateways, cellars.


Allergic conjunctivitis

04 Sep 2018

Allergic conjunctivitis is an inflammatory reaction of the conjunctiva to the effect of allergens, characterized by hyperemia and edema of the lining of the eyelids, edema and itching of the eyelids, the formation of follicles or papillae on the conjunctiva, sometimes accompanying corneal damage with visual impairment. Allergic conjunctivitis occupies a significant place in the group of diseases united by the common name "red eye syndrome", they affect about 15% of the population on average, but conjunctivitis occurs more often among children.

Actovegin. Allergic conjunctivitis

The most common forms of allergic conjunctivitis are:
- pollinous conjunctivitis, which is usually a seasonal disease and is caused by pollen during the flowering of grasses, cereals, trees;
- spring conjunctivitis (spring catarrh), observed with increased sensitivity to the action of the ultraviolet part of the solar spectrum;
- drug allergy usually develops with prolonged use of eye drops to treat any eye disease (cataracts, glaucoma, iridocyclitis, etc.), but sometimes after a single application of eye medicinal forms;
- large-capillary conjunctivitis occurs as a result of prolonged contact of the upper eyelid with a foreign body - contact lenses (hard and soft), ocular prostheses, surgical sutures after cataract extraction, etc.

In the therapy of allergic conjunctivitis, several groups of drugs are used. Antiallergic - antihistamines LS azelastine, Allergodil, Allertec, Levokabastin (does not have sedative effect), etc., stabilizers of fat cells membranes Alomid, Allergokrom, Lecrolin, KromoGEXAL, Hi-Krom, etc .; glucocorticosteroids Dexapos, Oftan Dexamethasone, Garazon, Sofrax, and others.

In addition to the basis of therapy, with allergic conjunctivitis apply:

Anti-convoestants: Alergoftal, Afrin, nafazolin, Vizin, Sanorin, Nafkon-A and others.
Antiseptics and disinfectants: Ophthalmol, etc.

Vitamins: Riboflavin, Retinol palmitate, etc.

NSAIDs: indole derivatives - indomethacin, sulindac; derivatives of pyrazolone - phenylbutazone, oxyphenbutazone, azaprase, ketorolac; derivatives of propionic acid - ibuprofen, flurbiprofen, ketoprofen, naproxen; derivatives of anthranilic acid - mefenamic acid, meclofenamic acid.

Wound healing preparations: Actovegin (eye gel 20%), Taufon, etc.

Homeopathic medicines: Allergies, Mucosa compositum (appointed by a doctor).

Dietary supplements: Artromax, Neovitel - bioactive complex with Echinacea, etc.


Two sides of Meldonium

03 Sep 2018

After the scandal with Russian athletes, sales of Mildronate grew at times.

The doping scandal is becoming a decisive event for athletes, not all of whom are able to return to their careers after the shame, and for the country whose sports cordons were weakened on the eve of international competitions, and even for banned drugs. After reports that in early March in the samples of Russian athletes found illegal Meldonium, sales of the drug for a short time increased by different data in more than two or even ten times. Not so long ago, the product was associated with the consumer with another scandal, negatively affecting its sales. Now we can not doubt that the schedule of sales of the drug will again go up.

Meldonium buy. Mildronate buy

Sharp takeoff
Sales of Mildronate (INN meldonium) in tablets in a dosage of 250 mg from February 15 to March 15 this year. increased by 80% compared to December 2015, at a dosage of 500 mg - by 120-130%, said commercial director of the pharmaceutical company "Mizar-N" Arthur Belenko. "December was chosen as a comparison point as the month that demonstrates the maximum orders. Ampulated Mildronate showed no growth, "he said.

Spent Scheme
The expectation of sales growth is based on the similar experience of the pharma market. In 2006, Russian biathlete Olga Pyleva, who won a silver medal in the individual race at the Olympics in Turin, Italy, was deprived of the award and disqualified for two years for using Phentropil, the original Russian design. The drug was listed as banned after the representative of the Olympic Committee told WADA (World Anti-Doping Agency) that Russian athletes take it as doping. The career of the sportswoman crashed, the product produced by JSC "Valenta Pharmaceutics", on the contrary, has survived the heyday, demonstrating a significant increase in sales. The reason for this is associated with the popularization of its doping properties.

Mildronate and Phenotropil

The scandal with Mildronate began in a similar way. The US Anti-Doping Agency (USADA) received information that athletes from Eastern Europe use it as doping - it is only spread in this region. Since October 2014 Meldonium has been included in the list of drugs for which WADA monitors. At the end of the same year, according to the results of tests of urine samples in 2.2% of samples, a drug was found, all of them belonged to athletes from Eastern Europe.

In early March, meldonium was found in dope-samples of figure skaters Ekaterina Bobrova, skater Pavel Kulizhnikov, short track-players Semyon Elistratov and Ekaterina Konstantinova, rider Eduard Vorganov, volleyball player Alexander Markin, biathlete Eduard Latypov, rugby players Alena and Alexei Mikhaltsov. Tennis player Maria Sharapova voluntarily confessed to using Mildronate. Given the political situation of the past few years, the scale of the scandal has turned out to be much more serious than with Phentropil. However, experts are not ready to predict Mildronate the same success of sales, primarily because the properties of the drugs are completely different.

Not Phentropropyl

Phenotropil, as experts say, is a "serious drug", which is indicated in diseases of the central nervous system, intoxication, neurotic states, depression, psycho-organic syndromes, and due to the psychostimulating effect and increased endurance, it is able to influence physical achievements. "Mildronate is used as a second-line drug in cardiology and neurology, it improves the quality of life by reducing symptoms," explained Mehman Mammadov, head of the Laboratory of Assessment and Correction of Cardiovascular Risk. The drug increases the endurance of the body, but does not stimulate, he stressed. The manufacturer of Mildronate - the concern Grindeks (Latvia) - also insists that meldoniy can not improve sports results. Minister of Sports Vitaly Mutko and did call Mildronate "worthless". Nevertheless, from January 1, 2016, the substance is listed as prohibited WADA in both competitive and out-of-competition periods.

Phenotropil and Mildronate

The fact that the purpose of testing doping samples were representatives of Russia, is no longer surprising. The ability to deprive the country's strongest athletes of the right to participate in international competitions is probably one of the types of sanctions that allow the US to strike at the image of the country. But how did the drug whose doping properties unanimously reject the experts got into the "black" list? "It was noticed that the athletes used the substance to improve performance," WADA spokesman Ben Nichols replied to the "FV" request. However, evidence has not been submitted so far, although the Anti-Doping Code states that a substance or method is considered for inclusion on the list in the presence of medical or other scientific evidence, a pharmacological effect or experience indicating that they, or in combination with other substances or methods can improve athletic performance. According to the representatives of Grindeks, the replies to the inquiries about the justifications of the committee's decision have not yet been received.

Who is guilty
How did it happen that the athletes continued to take the drug that was suspected by WADA from the autumn of 2014? "On September 16, 2015, the executive committee of the World Anti-Doping Agency approved a prohibited list of substances and methods in 2016. In the fall of 2015, the Federal Medical and Biological Agency brought this information to the doctors of the national teams, the leaders of the subordinate organizations of FMBA of Russia were informed," in the department. On December 17, 2015, the head of the Ministry of Sports of the Russian Federation signed an order No. 1194 "On approving lists of substances and (or) methods prohibited for use in sports". Now, FMBA conducts an internal audit, the reasons for the emergence of positive doping tests. Athletes, in turn, took a position from frank confession and statements that the medication was completed long before January 1 of this year, to suspicion that the Meldonium was planted by him.

Lines of fate
Until now, the name "Mildronate" was clearly associated with a loud trial, stretching for several years. In 2009, after applying a solution of ampoules with the inscription "Mildronate" in 23 patients, adverse reactions were identified, two women were killed. As it turned out later, Listeron appeared in ampoules, which possesses other pharmacological properties. Five employees of Sotex were prosecuted (in 2008, JSC Grindeks concluded an agreement with the company on the production of 20% of Mildronate in the Russian market with injections). After all the vicissitudes, when the materials of the case were transferred from one court to another, and the judges could not determine the severity of the punishment, the defendants were released from responsibility in connection with the expiry of the limitation period.

Thanks to the doping scandal, Mildronate, previously associated with the consumer with a danger, has now acquired in his eyes the properties of a product that helps to discover new resources of the body. "It turned out very powerful advertising Mildronate. Now much depends on how the situation will develop. After all, the information is spread that the drug is addictive. Then the demand will fall, "said commercial director of the pharmacy chain" Kalina Farm "Artem Vardanyan.

Anyway, now the hype around Mildronate, Grindex's statements about its intention to fight for the exclusion of its product from the "black" list play into the hands of the drug and its manufacturer. As they say, in PR there is no superfluous.


Medicines for the protection of the liver

31 Aug 2018

Every day, every hour, every minute, the human body is exposed to the action of many factors that damage it, external and internal. But a complex and multilevel protection system is capable for the time being to make these impacts practically invisible and almost not dangerous for humans. Almost - because nothing in the body does not pass without a trace. Viral or bacterial attacks, inhaled air toxins, dyes and preservatives in food, overeating and alcoholic libations all affect the health, even if it does not affect well-being. Because all this increases the load on the liver, which cleanses blood from all sorts of decomposition products. And it is quite possible - will affect in the future. Because if the liver suffers, the whole body suffers.

Heptral. hepatoprotectors. B12

The liver is the largest internal organ. Its weight is about 2% of the body weight in adults (an average of 1.2-1.5 kg) and about 5% in children. In the body, this most massive organ performs several important functions: purification of blood from toxic substances, secretion and secretion of bile, synthesis of various biologically active substances and maintenance of the energy balance of the body. Its damage entails a variety of various disorders and, as a result, diseases of other organs and systems. Metabolic disorders, various allergic reactions, dysfunctions of the digestive system, a decrease in antimicrobial protection, weakness, lethargy, chronic fatigue - all this may be a consequence of damage to the liver and its cells.

Mechanisms of liver damage
Various natural substances, synthetic chemical compounds used in the food industry, as well as most medicines, can cause chemical damage to the liver - it is the liver cells that neutralize both natural toxins and synthetic xenobiotics.

At present, specialists identify 5 main mechanisms of chemical damage to the liver:
- damage to the plasma membrane of liver cells - hepatocytes;
- disturbances in the function of mitochondria, which lead to a decrease in ATP in the cell and its subsequent death;
- violation of intracellular ion homeostasis - an increase in the concentration of sodium and calcium ions and a decrease in potassium ions; this further leads to damage to the cytoplasmic membrane and / or disruption of mitochondrial functions and, as a consequence, to the death of hepatocytes;
- activation of substances degradation enzymes (proteinase, nuclease, phospholipase, etc.), which leads - to damage to cellular and mitochondrial membranes, followed by cell death;
- the action of free radicals.

In addition to chemical damage to the liver, there are other mechanisms that cause the death of liver cells. Not the least role in these processes is the activity of the immune system, designed to normally protect the body from the penetration of foreign agents and destroy them. Sometimes, immune reactions directly or indirectly lead to liver damage. The functioning of killer lymphocytes, hyperproduction of cytokines, autoantibodies that occur with allergies, and some other immune responses in a number of cases can cause hepatocyte death, dysfunction and liver diseases. And, of course, among the causes that cause liver disruption, we can not fail to mention hepatitis viruses that directly affect liver cells.

Treatment of liver diseases
When it comes to the pathology of the liver, there are two main areas of treatment. This is primarily etiotropic therapy - the fight against the cause of the disease. In clinical practice, this suppression of a pathogenic agent in viral hepatitis (with the parenteral mechanism of infection). The second area of complex treatment is the impact on various links of pathogenesis with the help of pharmacological agents. Pathogenetic therapy may include the following groups of drugs:

- vitamins, amino acids, peptides and other agents that positively influence the processes of tissue metabolism;
- adsorbents, antidotes, which reduce the load on the liver due to its detoxification activity;
- drugs that help metabolize xenobiotic substances (inhibitors and inducers of microsomal systems);
- immunomodulators;
- antiviral and antimicrobial agents;
- anti-inflammatory drugs;
- cholagogue;
- antioxidants;
- hepatoprotectors.

Hepatoprotectors - a special group of drugs
Despite such an abundance of liver damaging factors, there is one surprising property in the liver that inspires optimism: the ability to regenerate with the restoration of lost functions. It is on the maintenance and stimulation of this ability that the action of a special group of drugs - hepatoprotectors is mainly directed. In addition, their task is to increase the resistance of the liver to the action of damaging factors, to stop and prevent further destruction of the liver by suppressing fibrogenesis (replacing the hepatic tissue with fibrous tissue).

The arsenal of modern hepatoprotectors is quite wide. They differ in origin (natural and synthetic), chemical structure, mechanism of action, etc. There is no unified classification system for such funds, however, it is a common practice to divide hepatoprotective agents into the following groups:

- preparations of vegetable origin;
- preparations of animal origin;
- preparations containing essential phospholipids (EFL);
- amino acids or their derivatives;
- vitamins-antioxidants and vitamin-like compounds;
- preparations of different groups.

Plant hepatoprotectors. The most in demand at the moment are herbal preparations. More than half of all hepatoprotectors sold today are herbal remedies.

Milk thistle, as well as preparations based on its bioflavonoids, have proven themselves in the protection of the liver. The main substance thistle spotty - silibinin (in complex with other isomers makes silymarin) - has a membrane-protective, antioxidant and metabolic effects. Thanks to its action, the resistance of the cell membrane increases, the concentration of intracellular calcium decreases and the calcium-dependent activation of phospholipases decreases. In addition, there is evidence that silybinin is able to block the transport systems of certain toxins (in particular the toxins of pale toadstool) and to bind the radicals. In addition, silibinin stimulates the synthesis of proteins and accelerates the regeneration of damaged hepatocytes, slows liver fibrosis in cirrhosis. However, patients with cholestasis should be careful - in some cases, silibinin increases cholestasis. It is not recommended to use milk thistle preparations with long courses.

Also popular are the preparations based on the extract of another hepatoprotective plant - artichoke. Artichoke increases the antitoxic function of the liver, lowers cholesterol in the blood with cholesterolemia, and has choleretic action.

Licorice root, as well as preparations based on glycyrrhizin (an aqueous extract of licorice root), has antioxidant properties, reduces the activity of liver enzymes and reduces the severity of liver fibrosis. However, because of the possibility of developing hypokalemia as a side effect of glycyrrhizin treatment, the administration of licorice root preparations as hepatoprotectors requires careful additional examination and constant monitoring of the doctor.

The hepatoprotective effect is also exerted by biologically active substances contained in the pumpkin seed oil. Preparations based on them have membrane stabilizing, anti-inflammatory, choleretic properties. In addition, pumpkin seeds slow down the development of connective tissue and accelerate the regeneration of liver cells.

Hepatoprotectors of animal origin. These preparations are hydrolysates of liver extract of cattle or isolated hepatocytes obtained as a result of freeze drying of animal liver cells. Such drugs have a reparative effect, but their appointment requires mandatory testing for individual sensitivity.

Preparations containing essential phospholipids. The second most prevalent group of drugs for the protection of the liver. It accounts for about 16% of all hepatoprotectors. Essential phospholipids restore cell membranes of liver cells and promote their regeneration. The molecules of the esterial phospholipids are embedded in the phospholipid structure of the damaged hepatocytes, thereby restoring the barrier function of the lipid layer. In addition, essential phospholipids inhibit lipid peroxidation. Although in some cases they may themselves be involved in this process.

Amino acids and their derivatives. Ademethionine (adenosylmethionine) plays an important role in the synthesis of phospholipids and other substances necessary for the normal functioning of liver cells and regeneration processes. Its use promotes the removal of free radicals and other harmful metabolites from hepatocytes. Effective as a means of accompanying potentially hepatotoxic drugs. In addition, ademetionine has an antifibrotic effect. And, finally, this is the only drug that can not only protect the liver, but also have an antidepressant effect (on the 5th-7th day of admission). This property of ademetionine is successfully used in the treatment of patients with alcoholic liver damage, and the drug simultaneously acts as an antidepressant and hepatoprotector. Ademetionine is also recommended for use in pregnant patients with cholestasis as a means of resolving steroid cholestasis. The undoubted advantage of this drug is the possibility of its use in almost all hepatic pathologies without the risk of side effects.

Preparations based on amino acids ornithine and aspartate are involved in regulating the metabolism in hepatic cells and are used as a hepatoprotector for hepatitis, cirrhosis and hepatic encephalopathy.

Vitamins and vitamin-like compounds. To preserve the health of the liver, vitamins E and C are required, which have antioxidant activity, lipoic (alpha-lipoic) acid has proved to be particularly useful as a hepatoprotector. It acts as an antioxidant, has immunomodulating activity, helps slow down the development of liver fibrosis and even its regression.

Preparations of different groups. Ursodeoxycholic acid contributes to the removal of toxic substances from the liver, prevents the toxic effect of hydrophobic bile acids on the membranes of liver cells, inhibits the production of immunoglobulins that contribute to the destruction of the liver, has an antioxidant effect.

Today, in the pharmaceutical market of the country, more than 1,000 names of hepatoprotective drugs are presented, and their number continues to grow. And this is not surprising, because according to WHO data, for the last several decades in Russia, as well as in the whole world, there is a clear tendency to an increase in the number of liver diseases. And this means that drugs that support the liver, helping it cope with its functions, will be increasingly in demand. After all, the fairness of the expression: "The disease is easier to prevent than treat" is particularly evident when one of the main defenders of our body itself needs protection.


Syndrome of impaired digestion. How to treat?

30 Aug 2018

Syndrome of impaired digestion (maldigestia) is a complex of intestinal symptoms caused by insufficient digestion of nutrients. Maldigestia can be gastrogenic, pancreatic and enterogenic.


Classification, etiology and pathogenesis
Disturbances in digestion are more or less characteristic of all gastroenterological diseases, in which the production of digestive enzymes and bile acids decreases.
Syndrome of impaired digestion

1. Insufficiency of the cavitary digestion:
- pancreatogenic insufficiency of digestion;
- deficiency of bile acids;
- gastrogenic insufficiency of digestion.

2. Lack of membrane digestion:
- disruption of adsorption of pancreatic enzymes;
- deficiency of intestinal enzymes.

Disturbances in digestion can be associated with insufficiency of cavitary and membrane hydrolysis of food proteins, fats and carbohydrates. The most severe violations of cavitary digestion are observed in diseases of the pancreas with exocrine insufficiency. Pancreatic insufficiency develops as a result of a decrease in functioning pancreatic tissue in patients with chronic pancreatitis and pancreatic cancer.

The external secretory function of the pancreas is disrupted with a decrease in the secretion of pancreosimin, secretin and enterokinase in the mucosa of the duodenum when it is atrophy. In addition, the activity of enterokinase and pancreatic enzymes in the cavity of the small intestine decreases with the pH shifting in the lumen of the small intestine to the acid side. Intestinal digestion is also disturbed in the absence of sufficient bile acids necessary for digestion of fat (cirrhosis of the liver, mechanical jaundice, ileal resection, excessive growth of microbes in the small intestine).
The inadequacy of membrane digestion occurs when the intestinal enzymes themselves are deficient and the adsorption of pancreatic enzymes decreases on the membrane of the brush border of the enterocytes.

Patients complain of bloating, excessive gas formation, sensation of transfusion and rumbling in the abdomen. In more severe cases, there is polyphecal, steatorrhea, diarrhea and weight loss. Nevertheless, trophic disorders (dry skin, dullness and brittle nails and hair, cracks in the corners of the lips and in the tongue, etc.) with the syndrome of impaired digestion practically do not develop. This is the fundamental difference between the syndrome of maldigestia and the syndrome of impaired absorption.

In patients with chronic pancreatitis with severe impairment of the exocrine function of the pancreas, the volume of the stool increases, and the content of fat, muscle fibers and starch is increased. In diseases of the liver and bile ducts, accompanied by a deficiency of bile acids, digestion of fats is also disrupted and more or less pronounced steatorrhea appears. The cause of maldigestia in patients with secretory gastric insufficiency or after operations on it is excessive bacterial growth in the upper parts of the small intestine and a violation of contact between the chyme and digestive juices.

The inadequacy of membrane digestion is clinically manifested by poor tolerance of nutrients containing those oligomers whose digestion is impaired. Food intolerance, caused by a lack of membrane digestion, develops only when there is a deficit of intestinal (membrane) enzymes. Most often it is a deficiency of intestinal carbohydrases and poor tolerance of lactose (milk sugar), trehalose (disaccharide contained in mushrooms), sucrose and other disaccharides.

In patients with atrophy of the small intestine mucosa, violations of the membrane digestion are combined with impaired absorption.

Diagnosis, differential diagnosis
A simplest method of laboratory evaluation of the effectiveness of digestive processes is a coprological study. Disorders of digestion are accompanied by an increase in the daily volume of feces, the appearance in it of a large number of muscle fibers, corks of starch, drops of fat. One of the early symptoms of a violation of digestion of nutrients is steatorrhea. The feces become greasy, shiny, and sticky. At a microscopic examination, droplets of fat are visible. A more accurate representation of the degree of steatorrhea can be obtained by examining the fat content in the daily amount of stool according to the Van de Camera method. With pancreatic insufficiency, the amount of undigested fat, mostly neutral, exceeds 5-7 g.

In patients with insufficient digestion and absorption, favorable conditions are created for the reproduction of microbial flora in the upper parts of the small intestine. This is facilitated by the slow utilization of chyme, motor disorders and decreased production of lysozyme by enterocytes. Therefore, an important method of diagnosing maldigestia is to determine the amount and composition of microbes in intestinal juice.

A characteristic symptom of the failure of membrane digestion is the intolerance of food products, for example milk, sugar, fungi and other carbohydrates containing disaccharides. Unlike maldigestii of any origin for malabsorption syndrome, the main clinical symptoms are trophic disorders, not so much quantitative (weight loss) as qualitative ones. These include changes in the skin and its appendages, signs of a deficiency in the body of microelements, vitamins and other biologically active substances. Differential diagnostics is assisted by histological and histochemical studies of the small intestine mucosa.

In the complex therapy of intestinal digestion disorders, dietary nutrition plays a leading role, the characteristics of which depend on the underlying disease and the severity of intestinal disorders. Food should be mechanically sparing, contain an increased amount of protein (100-150 g) and carbohydrates (400-500 g), a reduced amount of fat (30-40 g). Excluded from the diet are hard-to-digest fats, raw vegetables and fruits. If milk, sugar, mushrooms or starch is poorly tolerated, an appropriate individual - elimination diet - is prescribed.

Medicamental therapy should be aimed at improving intestinal digestion, suppressing pathogenic microflora and regulating motor function.

With pancreatogenic steatorrhea, a good therapeutic effect is provided by the enzymes of the pancreas Creon, Mezim Forte and others.

In hepatogenic steatorrhea, preparations containing components of bile besides enzymes (Penzinorm forte, Digestal, Festal, Enzistal, etc.) are recommended. The effectiveness of substitution treatment with enzyme preparations is determined primarily by the choice of the optimal dose.

Of the regulators of motor activity are most effective in digestion disorders of Dicetel and Duspatalin.

In patients with impaired digestion, dysbiosis almost always develops.

Treatment of dysbacteriosis should be carried out taking into account the characteristics of the underlying disease. It includes:

- application of intestinal antiseptics in order to eliminate excess bacterial colonization of the intestine -with a conditionally pathogenic microflora;
- restoration of normal microbial flora of the intestines with the help of probiotics;
- enterosorbents;
- stimulation of the organism's reactivity.

Intestinal antiseptics
These drugs have a less harmful effect on symbiotic microbial flora than antibiotics. These include Intetriks, Ersefuril, Nitroxoline, Furazolidon, etc. Antibacterials are prescribed for 10-14 days. The use of an antibiotic is justified as a backup.

Probiotics were most widely used: Linex, Bifidumbacterin, Probiophore. The course of treatment should last 1-2 months.

This group of drugs does not inhibit the normal intestinal microflora. Their disadvantage is the indiscriminate sorption of opportunistic pathogenic microflora and its toxins. Preparations are prescribed by short courses from 5 to 10 days. Enterosorbents are used only as a monotherapy; can inactivate the action of other drugs. These include: Filtrum, Lactofiltrum (1 tablet 3-4 times a day), Enterosgel (1 tbsp., Dissolving in 1/4 cup water, 3 times a day).

Stimulants of body reactivity
To improve the reactivity of the weakened patients, it is advisable to apply Gepon, Timalin, Timogen, Immunal, Immunophane and other immunostimulating agents. The course of treatment should last for an average of 4 weeks. At the same time prescribe vitamins.

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