bactericidal effect. Other side effects include

Antibiotics are a huge group of bactericidal drugs, each of which is characterized by its spectrum of action, indications for use and the presence of certain consequences.

Antibiotics are substances that can inhibit the growth of microorganisms or destroy them. According to the definition of GOST, antibiotics include substances of plant, animal or microbial origin. At present, this definition is somewhat outdated, since a huge number of synthetic drugs have been created, but it was natural antibiotics that served as the prototype for their creation.

The history of antimicrobial drugs begins in 1928, when A. Fleming was first discovered penicillin. This substance was just discovered, and not created, since it has always existed in nature. In wildlife, it is produced by microscopic fungi of the genus Penicillium, protecting themselves from other microorganisms.

In less than 100 years, more than a hundred different antibacterial drugs have been created. Some of them are already outdated and are not used in treatment, and some are only being introduced into clinical practice.

How antibiotics work

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All antibacterial drugs according to the effect of exposure to microorganisms can be divided into two large groups:

• bactericidal- directly cause the death of microbes;
• bacteriostatic- prevent the growth of microorganisms. Unable to grow and multiply, the bacteria are destroyed by the sick person's immune system.

Antibiotics realize their effects in many ways: some of them interfere with the synthesis of microbial nucleic acids; others interfere with the synthesis of the bacterial cell wall, others disrupt the synthesis of proteins, and others block the functions of respiratory enzymes.

Groups of antibiotics

Despite the diversity of this group of drugs, all of them can be attributed to several main types. This classification is based on the chemical structure - drugs from the same group have a similar chemical formula, differing from each other in the presence or absence of certain molecular fragments.

The classification of antibiotics implies the presence of groups:

1. Derivatives of penicillin. This includes all drugs created on the basis of the very first antibiotic. In this group, the following subgroups or generations of penicillin preparations are distinguished:

• Natural benzylpenicillin, which is synthesized by fungi, and semi-synthetic drugs: methicillin, nafcillin.
• Synthetic drugs: carbpenicillin and ticarcillin, which have a wider range of effects.
• Mecillam and azlocillin, which have an even wider spectrum of action.

1. Cephalosporins are close relatives of penicillins. The very first antibiotic of this group, cefazolin C, is produced by fungi of the genus Cephalosporium. Most of the drugs in this group have bactericidal action i.e. kill microorganisms. There are several generations of cephalosporins:

• I generation: cefazolin, cephalexin, cefradin, etc.
• II generation: cefsulodin, cefamandol, cefuroxime.
• III generation: cefotaxime, ceftazidime, cefodizime.
• IV generation: cefpir.
• V generation: ceftolosan, ceftopibrol.

The differences between different groups are mainly in their effectiveness - later generations have a greater spectrum of action and are more effective. Cephalosporins of the 1st and 2nd generations are now used extremely rarely in clinical practice, most of them are not even produced.

1. - drugs with a complex chemical structure that have a bacteriostatic effect on a wide range of microbes. Representatives: azithromycin, rovamycin, josamycin, leukomycin and a number of others. Macrolides are considered one of the safest antibacterial drugs - they can be used even by pregnant women. Azalides and ketolides are varieties of macrolides that differ in the structure of active molecules.

Another advantage of this group of drugs is that they are able to penetrate the cells of the human body, which makes them effective in the treatment of intracellular infections:,.

1. Aminoglycosides. Representatives: gentamicin, amikacin, kanamycin. Effective against a large number of aerobic gram-negative microorganisms. These drugs are considered the most toxic, can lead to quite serious complications. Used to treat urinary tract infections,.
2. Tetracyclines. Basically, this semi-synthetic and synthetic drugs, which include: tetracycline, doxycycline, minocycline. Effective against many bacteria. The disadvantage of these drugs is cross-resistance, that is, microorganisms that have developed resistance to one drug will be insensitive to others from this group.
3. Fluoroquinolones. These are completely synthetic drugs that do not have their natural counterpart. All drugs in this group are divided into the first generation (pefloxacin, ciprofloxacin, norfloxacin) and the second (levofloxacin, moxifloxacin). They are most often used to treat infections of the upper respiratory tract (,) and respiratory tract (,).
4. Lincosamides. This group includes the natural antibiotic lincomycin and its derivative clindamycin. They have both bacteriostatic and bactericidal effects, the effect depends on the concentration.
5. Carbapenems. It is one of the most modern antibiotics acting on a large number of microorganisms. The drugs of this group belong to the reserve antibiotics, that is, they are used in the most difficult cases when other drugs are ineffective. Representatives: imipenem, meropenem, ertapenem.
6. Polymyxins. These are highly specialized drugs used to treat infections caused by. Polymyxins include polymyxin M and B. The disadvantage of these drugs is toxic effects on the nervous system and kidneys.
7. Anti-tuberculosis drugs. This is a separate group of drugs that have a pronounced effect on. These include rifampicin, isoniazid, and PAS. Other antibiotics are also used to treat tuberculosis, but only if resistance has developed to the mentioned drugs.
8. Antifungals. This group includes drugs used to treat mycoses - fungal infections: amphotyrecin B, nystatin, fluconazole.

Ways to use antibiotics

Antibacterial drugs are available in different forms: tablets, powder, from which a solution for injection is prepared, ointments, drops, spray, syrup, suppositories. The main ways to use antibiotics:

1. Oral- intake by mouth. You can take the medicine in the form of a tablet, capsule, syrup or powder. The frequency of administration depends on the type of antibiotics, for example, azithromycin is taken once a day, and tetracycline - 4 times a day. For each type of antibiotic, there are recommendations that indicate when it should be taken - before meals, during or after. The effectiveness of treatment and the severity of side effects depend on this. For young children, antibiotics are sometimes prescribed in the form of syrup - it is easier for children to drink a liquid than to swallow a tablet or capsule. In addition, the syrup can be sweetened to get rid of the unpleasant or bitter taste of the medicine itself.
2. Injectable- In the form of intramuscular or intravenous injections. With this method, the drug enters the focus of infection faster and acts more actively. The disadvantage of this method of administration is pain when injected. Injections are used for moderate and severe diseases.

Important:injections should only be given by a nurse in a clinic or hospital! Doing antibiotics at home is strongly discouraged.

1. Local- applying ointments or creams directly to the site of infection. This method of drug delivery is mainly used for skin infections - erysipelas, as well as in ophthalmology - for infectious eye damage, for example, tetracycline ointment for conjunctivitis.

The route of administration is determined only by the doctor. This takes into account many factors: the absorption of the drug in the gastrointestinal tract, the state of the digestive system as a whole (in some diseases, the absorption rate decreases, and the effectiveness of treatment decreases). Some drugs can only be administered one way.

When injecting, you need to know how you can dissolve the powder. For example, Abaktal can only be diluted with glucose, since when sodium chloride is used, it is destroyed, which means that the treatment will be ineffective.

Sensitivity to antibiotics

Any organism sooner or later gets used to the most severe conditions. This statement is also true in relation to microorganisms - in response to prolonged exposure to antibiotics, microbes develop resistance to them. The concept of sensitivity to antibiotics was introduced into medical practice - with what efficiency this or that drug affects the pathogen.

Any prescription of antibiotics should be based on knowledge of the susceptibility of the pathogen. Ideally, before prescribing the drug, the doctor should conduct a sensitivity test and prescribe the most effective drug. But the time for such an analysis at best is a few days, and during this time the infection can lead to the saddest result.

Therefore, in case of an infection with an unknown pathogen, doctors prescribe drugs empirically - taking into account the most likely pathogen, with knowledge of the epidemiological situation in a particular region and medical institution. For this, broad-spectrum antibiotics are used.

After performing a sensitivity test, the doctor has the opportunity to change the drug to a more effective one. Replacement of the drug can be made in the absence of the effect of treatment for 3-5 days.

Etiotropic (targeted) prescription of antibiotics is more effective. At the same time, it turns out what caused the disease - with the help of bacteriological research, the type of pathogen is established. Then the doctor selects a specific drug to which the microbe has no resistance (resistance).

Are antibiotics always effective?

Antibiotics only work on bacteria and fungi! Bacteria are unicellular microorganisms. There are several thousand species of bacteria, some of which coexist quite normally with humans - more than 20 species of bacteria live in the large intestine. Some bacteria are conditionally pathogenic - they become the cause of the disease only under certain conditions, for example, when they enter an atypical habitat for them. For example, very often prostatitis is caused by Escherichia coli, which enters from the rectum in an ascending way.

Note: antibiotics are completely ineffective in viral diseases. Viruses are many times smaller than bacteria, and antibiotics simply do not have a point of application of their ability. Therefore, antibiotics for colds do not have an effect, since colds in 99% of cases are caused by viruses.

Antibiotics for coughs and bronchitis may be effective if these symptoms are caused by bacteria. Only a doctor can figure out what caused the disease - for this he prescribes blood tests, if necessary - a sputum examination if it departs.

Important:Do not prescribe antibiotics to yourself! This will only lead to the fact that some of the pathogens will develop resistance, and the next time the disease will be much more difficult to cure.

Of course, antibiotics are effective for - this disease is exclusively bacterial in nature, it is caused by streptococci or staphylococci. For the treatment of angina, the simplest antibiotics are used - penicillin, erythromycin. The most important thing in the treatment of angina is compliance with the frequency of taking drugs and the duration of treatment - at least 7 days. You can not stop taking the medicine immediately after the onset of the condition, which is usually noted for 3-4 days. True tonsillitis should not be confused with tonsillitis, which may be of viral origin.

Note: untreated angina can cause acute rheumatic fever or!

Inflammation of the lungs () can be of both bacterial and viral origin. Bacteria cause pneumonia in 80% of cases, so even with empirical prescription, antibiotics for pneumonia have a good effect. In viral pneumonia, antibiotics do not have a therapeutic effect, although they prevent the bacterial flora from joining the inflammatory process.

Antibiotics and alcohol

The simultaneous use of alcohol and antibiotics in a short period of time does not lead to anything good. Some drugs are broken down in the liver, like alcohol. The presence of an antibiotic and alcohol in the blood gives a strong load on the liver - it simply does not have time to neutralize ethyl alcohol. As a result of this, the likelihood of developing unpleasant symptoms increases: nausea, vomiting, intestinal disorders.

Important: a number of drugs interact with alcohol at the chemical level, resulting in a direct decrease in therapeutic effect. These drugs include metronidazole, chloramphenicol, cefoperazone and a number of others. The simultaneous use of alcohol and these drugs can not only reduce the therapeutic effect, but also lead to shortness of breath, convulsions and death.

Of course, some antibiotics can be taken while drinking alcohol, but why risk your health? It is better to abstain from alcoholic beverages for a short time - course antibiotic therapy rarely exceeds 1.5-2 weeks.

Antibiotics during pregnancy

Pregnant women suffer from infectious diseases no less than everyone else. But the treatment of pregnant women with antibiotics is very difficult. In the body of a pregnant woman, a fetus grows and develops - an unborn child, very sensitive to many chemicals. The ingress of antibiotics into the developing organism can provoke the development of fetal malformations, toxic damage to the central nervous system of the fetus.

In the first trimester, it is advisable to avoid the use of antibiotics altogether. In the second and third trimesters, their appointment is safer, but also, if possible, should be limited.

It is impossible to refuse the prescription of antibiotics to a pregnant woman with the following diseases:

• Pneumonia;
• angina;
• infected wounds;
• specific infections: brucellosis, borreliosis;
• genital infections:,.

What antibiotics can be prescribed to a pregnant woman?

Penicillin, cephalosporin drugs, erythromycin, josamycin have almost no effect on the fetus. Penicillin, although it passes through the placenta, does not adversely affect the fetus. Cephalosporin and other named drugs cross the placenta in extremely low concentrations and are not capable of harming the unborn child.

Conditionally safe drugs include metronidazole, gentamicin and azithromycin. They are prescribed only for health reasons, when the benefit to the woman outweighs the risk to the child. Such situations include severe pneumonia, sepsis, and other severe infections in which a woman can simply die without antibiotics.

Which of the drugs should not be prescribed during pregnancy

The following drugs should not be used in pregnant women:

• aminoglycosides- can lead to congenital deafness (with the exception of gentamicin);
• clarithromycin, roxithromycin– in experiments they had a toxic effect on animal embryos;
• fluoroquinolones;
• tetracycline- violates the formation of the skeletal system and teeth;
• chloramphenicol- dangerous in late pregnancy due to inhibition of bone marrow function in a child.

For some antibacterial drugs, there is no evidence of a negative effect on the fetus. This is explained simply - on pregnant women, they do not conduct experiments to determine the toxicity of drugs. Experiments on animals do not allow with 100% certainty to exclude all negative effects, since the metabolism of drugs in humans and animals can differ significantly.

It should be noted that before you should also stop taking antibiotics or change plans for conception. Some drugs have a cumulative effect - they are able to accumulate in a woman's body, and for some time after the end of the course of treatment they are gradually metabolized and excreted. Pregnancy is recommended no earlier than 2-3 weeks after the end of antibiotics.

Consequences of taking antibiotics

The ingestion of antibiotics into the human body leads not only to the destruction pathogenic bacteria. Like all foreign chemicals, antibiotics have a systemic effect - in one way or another they affect all systems of the body.

There are several groups of side effects of antibiotics:

allergic reactions

Almost any antibiotic can cause allergies. The severity of the reaction is different: a rash on the body, Quincke's edema (angioneurotic edema), anaphylactic shock. If allergic rash practically not dangerous, then anaphylactic shock can lead to death. The risk of shock is much higher with antibiotic injections, which is why injections should only be given in medical facilities - emergency care can be provided there.

Antibiotics and other antimicrobial drugs that cause cross-allergic reactions:

Toxic reactions

Antibiotics can damage many organs, but the liver is most susceptible to their effects - against the background of antibiotic therapy, toxic hepatitis can occur. Some drugs have a selective toxic effect on other organs: aminoglycosides - on the hearing aid (cause deafness); tetracyclines inhibit bone growth in children.

note: the toxicity of the drug usually depends on its dose, but with individual intolerance, sometimes smaller doses are enough to show the effect.

Impact on the gastrointestinal tract

When taking certain antibiotics, patients often complain of stomach pain, nausea, vomiting, stool disorders (diarrhea). These reactions are most often due to the local irritating effect of drugs. The specific effect of antibiotics on the intestinal flora leads to functional disorders its activities, which is most often accompanied by diarrhea. This condition is called antibiotic-associated diarrhea, which is popularly known as dysbacteriosis after antibiotics.

Other side effects

Other side effects include:

• suppression of immunity;
• the emergence of antibiotic-resistant strains of microorganisms;
• superinfection - a condition in which microbes resistant to a given antibiotic are activated, leading to the emergence of a new disease;
• violation of vitamin metabolism - due to the inhibition of the natural flora of the colon, which synthesizes some B vitamins;
• Jarisch-Herxheimer bacteriolysis is a reaction that occurs when bactericidal drugs are used, when, as a result of the simultaneous death of a large number of bacteria, a large amount of toxins are released into the blood. The reaction is clinically similar to shock.

Can antibiotics be used prophylactically?

Self-education in the field of treatment has led to the fact that many patients, especially young mothers, try to prescribe themselves (or their child) an antibiotic for the slightest sign colds. Antibiotics do not have a preventive effect - they treat the cause of the disease, that is, they eliminate microorganisms, and in the absence of only side effects of drugs appear.

There are a limited number of situations where antibiotics are given before clinical manifestations infection, in order to prevent it:

• surgery- in this case, the antibiotic in the blood and tissues prevents the development of infection. As a rule, a single dose of the drug administered 30-40 minutes before the intervention is sufficient. Sometimes, even after an appendectomy, antibiotics are not injected in the postoperative period. After "clean" surgical operations, antibiotics are not prescribed at all.
• major injuries or wounds(open fractures, soil contamination of the wound). In this case, it is absolutely obvious that an infection has entered the wound and it should be “crushed” before it manifests itself;
• emergency prevention of syphilis carried out with unprotected sexual contact with a potentially sick person, as well as with health workers who have got the blood of an infected person or other biological fluid on the mucous membrane;
• penicillin can be given to children for the prevention of rheumatic fever, which is a complication of tonsillitis.

Antibiotics for children

The use of antibiotics in children in general does not differ from their use in other groups of people. Pediatricians most often prescribe antibiotics in syrup for young children. This dosage form is more convenient to take, unlike injections, it is completely painless. Older children may be prescribed antibiotics in tablets and capsules. In severe infections, they switch to the parenteral route of administration - injections.

Important: the main feature in the use of antibiotics in pediatrics is dosages - children are prescribed smaller doses, since the drug is calculated in terms of a kilogram of body weight.

Antibiotics are very effective drugs while having a large number of side effects. In order to be cured with their help and not harm your body, you should take them only as directed by your doctor.

What are antibiotics? When are antibiotics needed and when are they dangerous? The main rules of antibiotic treatment are told by the pediatrician, Dr. Komarovsky:

Gudkov Roman, resuscitator

The global action of antibiotics on bacteria or other microorganisms can be expressed in two forms: bactericidal and bacteriostatic effects. With the bactericidal action of the antibiotic, bacterial growth does not resume. Antibiotics destroy the cell wall. The invention relates to medical and veterinary bacteriology and can be used to differentiate antibiotics by bactericidal bacteriostatic action.

The bacteriostatic effect of drugs is a temporary suppression of the ability of microorganisms to reproduce in the body. Antibiotics such as various penicillins, streptomycin, neomycin, kanamycin, vancomycin, polymyxin have a bactericidal effect. When the antibiotic is removed from the environment, microorganisms can develop again. In most cases, in the treatment of infectious diseases, the bacteriostatic effect of antibiotics, together with the protective mechanisms of the body, ensures the recovery of the patient.

Use of antibiotics in veterinary medicine and animal husbandry - The use of antibiotics in veterinary medicine began immediately after their discovery. ANTIBIOTICS are chemicals produced by microorganisms that can inhibit the growth and cause death of bacteria and other microbes. In the first case, the microorganisms die, and then they talk about the bactericidal action of this preservative, in the second, the vital functions of the microorganism are deeply inhibited.

In order to manifest their action, antibacterial drugs in most cases must penetrate into the cell, and the main barrier in their path is the cell wall of the microorganism. When identifying a microorganism, it is necessary to use an antibacterial agent that has the narrowest spectrum of action. This means that it should have a damaging effect on the microorganism only, without affecting the macroorganism.

For many antimicrobial agents, the intimate mechanism of action has not been fully elucidated. Antimicrobial agents can have a bactericidal or bacteriostatic effect by the depth of impact on the microorganism. The bactericidal action leads to the death of the microorganism, for example, beta-lactam antibiotics, aminoglycosides act. The bacteriostatic effect consists in the temporary suppression of the growth and reproduction of microorganisms (tetracyclines, sulfonamides).

Bacteriostatic drugs should not be combined with bactericidal. However, the concepts of bactericidal and bacteriostatic are not absolute, since very often an increase in the concentration of a bacteriostatic drug can give a bactericidal effect.

There are two main mechanisms of action of antibiotics:

A certain influence on the type of action of antibiotics is exerted by the microorganism, the properties of the antibiotic, as well as their concentration. However, the most accessible and proven bactericidal type of action is the lack of cells' ability to grow and multiply after removal of the antibiotic. These enzymes are called extended-spectrum beta-lactamases.

With the bacteriostatic effect of the antibiotic on bacteria, after the addition of penicillinase, bacterial growth appears in those wells where it was not found after the second stage of the study. Example 1. Determination of the bactericidal and bacteriostatic effect of the sodium salt of benzylpenicillin on museum cultures of bacteria. However, for St. aureus, Y. pseudotuberculosis, and B. cereus were highly sensitive to the antibiotic; this difference did not exceed a twofold value.

Possibility of using antibiotics in pregnant and lactating women

In a parallel row with the added penicillinase, in all wells, including at the maximum concentration of the antibiotic, bacterial growth was observed (yellowing and turbidity of the medium). All wells added detachable 6th T-va. After 6 hours, growth inhibition of bacteria was found in the first three wells at the antibiotic concentration. 3. The method according to claim 1, characterized in that the concentration of the antibiotic is reduced by the method of serial dilutions.

How can antibiotics be introduced into the body?

1) Bactericidal mechanism - complete suppression of bacterial growth by acting on the vital cellular structures of microorganisms, therefore, causing their irreversible death. If you do not endure the full course of treatment and stop taking the bacteriostatic antibiotic early, the symptoms of the disease will return. After taking the antibiotic is in the blood, and then in a specific organ.

Currently, there is an acute problem of antibiotic resistance of microorganisms (resistance of microorganisms to the action of antibacterial drugs). In small doses, antibiotics are dangerous and affect the formation of bacterial resistance. Milk and dairy products should be taken no earlier than 4 hours after taking the antibiotic, or completely abandoned during the course of therapy. For example, action hormonal contraceptives decreases with antibiotics.

According to statistics, up to 70-85% of children with purely viral infections receive antibiotics in Russia, that is, these children have not been shown antibiotics. Also, one should not hesitate to prescribe antibiotics for mycobacterial infections (tuberculosis), where specific antibacterial drugs are key in the treatment regimen. This is primarily due to the inevitable side effects of drugs of any severity. Antibiotics are a group of organic substances of natural (natural) or semi-synthetic origin that have the ability to destroy or slow down the growth of bacteria, fungi and tumors.

What is an antibiotic?

This substance is a natural antibiotic - a chemical weapon of the microworld. Indeed, the development of antibiotics is one of the most advanced methods of competition between microorganisms in nature.

Features of taking antibiotics:

But that was only the beginning of the era of antibiotics. It turned out that some antibiotics can be used to treat fungal infections or to destroy malignant tumors. The most important point in understanding the phenomenon of antibiotics is to determine the horizon of their action. And vice versa: antibiotics are absolutely ineffective against viruses, which are known to be subcellular microorganisms.

With bacteriostatic action, the death of microorganisms does not occur, only the cessation of their growth and reproduction is observed. One of the most important features for antibiotics is the type of their action on microorganisms - bacteriostatic and bactericidal (Navashin S.M., Fomina I.P. Rational antibiotic therapy. The purpose of the invention is to increase the reliability of the method and speed up the determination with a distinction between the type of bacteriostatic and bactericidal action of antibiotics.

The body's balance between health and disease is called Homeostasis.

Homeostasis largely depends on the relationship of the body to the bacteria with which it lives. For example, bacteria are always present on human skin.

When the skin is injured, bacteria can enter the body and can cause an infection. Invading bacteria tend to destroy the phagocytes.

phagocytes- cells of the immune system that protect the body by engulfing (phagocytosis) harmful foreign particles, bacteria, and dead or dying cells. However, when there are too many bacteria in the body to process, disease occurs and antibiotics are needed to help restore homeostasis.

Antibiotics can be bacteriostatic (prevent bacteria from multiplying) or bactericidal (kill bacteria).

Bacteriostatic action characterized by the ability of antimicrobial agents to interfere with the metabolic-enzymatic processes of the pathogen (blocking oxidative processes, growth substances, etc.), disrupt its growth and reproduction. Some bacteriostatic agents with increasing concentration have a bactericidal effect. Bacteriostatic is characterized by selectivity of action against certain types of bacteria.

Bactericidal action drugs - the ability of some antibiotics, antiseptics and other drugs to cause the death of microorganisms in the body.

The mechanism of bactericidal action, as a rule, is associated with the damaging effect of these substances on the cell walls of microorganisms, leading to their death.

For most infections, these two types of antibiotics are equally effective, but if the immune system is impaired or the person has a severe infection, bactericidal antibiotics are usually more effective. Bactericidal preparations can have a bacteriostatic effect against some microorganisms, and vice versa.

In most infections, including some types of pneumonia (pneumococcal) and urinary tract infections, there is no advantage between bactericidal and bacteriostatic drugs. However, bactericidal activity is necessary in infections in which the host organism, from which the bacteria get their nutrition, defense mechanisms were partially absent locally or systemically (in the entire system), for example, endocarditis (inflammation of the inner lining of the heart membrane), meningitis (inflammation of the membranes spinal cord or brain), or serious staph infections.

Each of the different types of antibiotics kills microorganisms differently.

1. Violate the structure of the bacterial cell wall;
2. interfere with the production of essential proteins;
3. They interfere with the transformation (metabolism) of nucleic acids (substances contained in the cells of all living beings);

Testing the action of antibiotics in the laboratory shows how much exposure is needed to reduce the growth of bacteria, or to kill the bacteria. A large dose of an antibiotic taken at one time can kill the bacteria that causes the disease, but a large dose is likely to cause serious side effects. Thus, antibiotics are given in small doses. This method ensures that the bacteria are either killed or sufficiently reduced in number so that the body can fight on its own. On the other hand, when too little antibiotic is taken, the bacteria can develop methods to protect themselves from it. Thus, the next time the same antibiotic is needed against these bacteria, it will not be effective.

Conclusion: antibiotics should be taken according to the doctor's prescription, strictly according to the instructions.

Attention! Before using medications, you should consult your doctor. The information is provided for informational purposes only.

1. Definition of chemotherapeutic agents.

2. The difference between chemotherapeutic drugs and antiseptics and disinfectants.

3. Essence of concepts: empirical (probabilistic) and combined antimicrobial therapy, antimicrobial chemoprevention.

Empirical (probabilistic) therapy- the use of antimicrobial drugs until information about the pathogen and its sensitivity to certain drugs is obtained.

Combination antimicrobial therapy- the use of two or more chemotherapeutic agents in order to potentiate or expand antimicrobial effects.

Antimicrobial chemoprophylaxis- the use of chemotherapeutic agents in order to reduce the risk of infectious diseases and complications.

4. Essence of concepts: antibiotic, probiotic (eubiotic).

Antibiotics (microbiotics)- chemotherapeutic substances of microbial, semi-synthetic or synthetic origin, which in low concentrations cause inhibition of reproduction or death of microbes and tumor cells sensitive to them in the internal environment (endosomatically) of the animal organism.

Probiotics (eubiotics, antonyms of antibiotics, "life promoters")- These are bacterial preparations from live microbial cultures, designed to correct the host microflora, eliminate dysbacteriosis, treat (aftercare) a number of acute intestinal infections.

Probiotics are able to increase the body's anti-infective resistance, in some cases have an anti-allergic effect, regulate and stimulate digestion.

Probiotic Examples: Lactobacterin, bifidum-bacterin, colibacterin, bifikol, acylact.

5. Essence of concepts: bactericidal and bacteriostatic action.

Bacteriostatic action- the ability of drugs to temporarily inhibit the growth of microorganisms (this action is typical for tetracyclines, chloramphenicol, erythromycin, lincosamides, etc.)

Bactericidal action- the ability of drugs to cause the death of microorganisms (this type of action is typical for b-lactam antibiotics, aminoglycosides, polymyxins, II and III generation macrolides, fluoroquinolones, etc.).

It should be noted that the division of drugs into bactericidal and bacteriostatic is conditional, since almost any bactericidal agent in small doses is bacteriostatic, and a number of bacteriostatic agents in large doses have a bactericidal effect.

6. Essence of concepts: means of choice (first-line drugs, main means) and reserve means (second-line drugs, alternative means).

Means of choice (first-line drugs, fixed drugs)- it medicines, which are most indicated for the treatment of this pathology and allow a course of therapy with minimal costs and a minimum of undesirable consequences

Reserve funds (second-line drugs, alternative drugs)- these are drugs that can be used to treat this pathology, but they are usually not used due to undesirable effects and / or high cost; the use of this group of drugs should be carried out only as a last resort (ultima ratio) in case of ineffectiveness of first-line drugs.

7. The essence of the concepts of the minimum inhibitory (suppressive) concentration and the minimum bactericidal concentration.

Minimum inhibitory concentration (MIC)- the minimum concentration of a chemotherapeutic or antiseptic substance that causes Complete suppression visible to the naked eye Growth of this microorganism on media under standard experimental conditions.

It is measured in µg/ml or units. actions. It is established by sowing the test culture on solid or liquid media containing various concentrations of the drug.

Minimum bactericidal concentration (MBC)- the minimum concentration of a chemotherapeutic or antiseptic agent that causes Complete destruction bacteria under standard experimental conditions.

Measured in µg/ml or units. actions. It is established by sowing the test culture on solid or liquid nutrient media containing various concentrations of the drug. To distinguish from MICs from sterile zones or transparent tubes, inoculation is done on media without the drug (the appearance of growth indicates a static effect, the absence of it indicates a cidal effect).

MBC and MIC are used in chemotherapy and antiseptics to select effective drugs and doses for a given patient.

8. The essence of the concepts of sensitivity and resistance of the pathogen, post-antibiotic effect.

Exciter sensitivity- lack of mechanisms of resistance to cholesterol; while the reproduction of the pathogen is suppressed by an average therapeutic dose exceeding the minimum inhibitory concentration by 2-4 times.

Pathogen resistance- the presence of mechanisms of resistance to cholesterol; the growth of the pathogen is not suppressed by the concentration of the drug, which has a toxic effect in vivo.

Post-antibiotic effect- persistent inhibition of the vital activity of bacteria after their short-term contact with an antibacterial drug.

9. Determinants of selective toxicity of chemotherapeutic agents.

1) cholesterol accumulate in microbial cells at concentrations many times higher than in mammalian cells

2) CS act on structures that are present only in the microbial cell (cell wall, type II DNA gyrase) and are absent in the mammalian cell

3) CS act on biochemical processes that occur exclusively in microbial cells and are absent in mammalian cells.

10. The essence of the difference between pharmacodynamic and chemotherapeutic properties.

1. Pharmacodynamic therapy operates at the level of architecture of functional systems, its effects are usually reversible. For chemotherapy, agents with the most irreversible action are most valuable.

2. Pharmacodynamic agents cause a gradual response of the body system, for chemotherapeutic agents the most desirable effects are "all or nothing".

3. Chemotherapy has an etiotropic strategy aimed at the destruction of the pathogen or transformed cells of the body, and pharmacodynamic therapy can be both etiotropic and pathogenetic.

11. Basic principles of rational chemotherapy.

1. The pathogen must be sensitive to AB

The rule of "best offer" - reference tables, taking into account regional population characteristics of antibacterial sensitivity.

2. AB should create a therapeutic concentration in the focus.

3. Mostly adequate dosing regimen, depending on:

ü pathogen

the dynamics of the clinical course of infection

the localization of the infection

ü the duration and nature of the course of infection (acute, chronic or bacteriocarrier)

4. The optimal duration of antimicrobial chemotherapy (example: streptococcal pharyngitis is curable in 10 days, acute uncomplicated gonococcal urethritis in 1-3 days, acute uncomplicated cystitis in 3 days).

For a warning adverse reactions, the development of superinfection or resistance, the duration of treatment should correspond to the eradication period of the pathogen.

5. Accounting for patient factors:

Allergy history, immunocompetence

function of the liver and kidneys

ü tolerability of AB when taken orally; compliance

the severity of the condition

ü age, gender, pregnancy or breastfeeding, oral contraceptives

ü side effects

6. Combined antibiotic therapy.

12. Indications for combined antibiotic therapy.

treatment of critically ill patients with suspected infection of unknown origin

ü prevention of development of resistant strains in some clinical situations

ü expansion of the spectrum of antimicrobial activity (therapy of mixed infections)

ü increased antimicrobial effects in severe conditions

ü reducing the toxicity of individual ABs

13. Principles of combined antibiotic therapy.

1. It is impossible to combine bactericidal and bacteriostatic antibiotics.

2. Antibiotics with similar side effects should not be used together.

4. Combination antibiotic therapy should be convenient for the patient and, if possible, cost-effective.

14. Principles of classification of antibiotics.

A) by the nature of the antibacterial action:

1. bactericidal - cause the death of bacteria (penicillins, cephalosporins, etc.)

2. bacteriostatic - prevent the growth and reproduction of bacteria (tetracyclines, amphenicols, etc.)

B) according to the spectrum of antibacterial action:

1. agents acting primarily on Gr+ microorganisms (MB)

2. Funds acting primarily on Gr-MB

3. Broad-spectrum AB

C) according to the mechanisms of antibacterial action:

1. ABs disrupting the structure of the cell wall in MB

2. ABs that disrupt the permeability of the cytoplasmic membrane in MB

2. ABs that disrupt protein synthesis in MB

3. ABs that disrupt RNA synthesis

D) by chemical structure

D) by duration of action

15. The main mechanisms of action of antibiotics.

1. Inhibition of cell wall synthesis:

ü Violation of the synthesis of pentapeptide-monomer

ü Violation of the synthesis of peptidoglycan from monomers

ü Violation of the synthesis of peptidoglycan cross-links (inhibition of the transpeptidase reaction)

2. Dysfunction of the cell membrane:

ü Increased membrane permeability

ü Violation of the synthesis of sterols that make up the cell membrane

3. Violation of protein synthesis processes:

ü Violation of the function of the 30S subunit of the ribosome

ü Violation of the function of the 50S subunit of the ribosome

4. Violation of the processes of nucleic acid synthesis:

ü Violation of the DNA structure

ü Violation of RNA synthesis

16. Name the side effects of antibiotics due to their allergenic action.

A) allergic reactions:

ü fever

o angioedema

o Serum sickness

ü polyarthritis

ü systemic lupus erythematosus

o anaphylactic shock

B) skin reactions:

measles rash, hemorrhagic rash (purpura)

ü urticaria

Erythema nodosum and multiforme

exfoliative or contact dermatitis

B) oral cavity

ü dryness, burning, soreness

ü itching of the mouth and tongue

ü stomatitis, acute glossitis, cheilosis, black or brown coating on the tongue

D) gastrointestinal tract: nausea, vomiting, diarrhea

17. Name the side effects and complications of antibiotic therapy associated with pharmacodynamic action.

A) nervous system:

lesion of the 8th pair of cranial nerves

ü paresthesia

sleep disturbance or emotional status

o peripheral neuritis

psychosis or seizures

o respiratory depression

B) blood

ü eosinophilia (sensitization to any AB)

aplastic or hemolytic anemia

ü thrombocytopenia

ü leukopenia

hyperkalemia, hypernatremia, hypokalemic alkalosis

B) excretory system:

hematuria, crystalluria, impaired urine outflow

acute tubular necrosis, nephrotoxicity

D) Gastrointestinal: jaundice, hepatitis, steatorrhea

18. Name the side effects and complications of antibiotic therapy associated with chemotherapeutic action.

A) Dysbacteriosis- develops with the use of broad-spectrum AB, accompanied by suppression, changes in the spectrum of intestinal microflora, colonization of the intestine by pathogenic microflora.

Manifestations: pseudomembranous colitis, enterocolitis, candidiasis (oral, pharyngeal, rectal, perianal)

B) immunosuppression

V) Aggravation reactions (Jarish-Gersheimer reaction): bacteriolysis, endotoxin shock.

19. Mechanisms of development of resistance of microorganisms to antibiotics.

Acquired resistance is formed by modifying the determinants of natural sensitivity:

A) Reducing the permeability of the external structures of the microorganism to AB(either with the cessation of AB entry into the MB cell, or with an increase in the processes of removing AB from the cell; typical for tetracyclines, aminoglycosides)

B) Masking or modification of the target of the AB action:

ü chromosomal resistance to beta-lactams as a result of modification of the penicillin-binding protein

ü resistance to aminoglycosides as a result of loss or damage to L-proteins of the 30S subunit of the bacterial ribosome, etc.

V) Induction of expression or emergence of new forms of AB biotransformation enzymes(beta-lactamases for penicillins; aminoglycoside transferases, acetyltransferases, phosphorus transferases, nucleotidyl transferases for aminoglycosides)

G) Transition to collateral metabolic pathways(replacement of PABA with folic acid when using sulfonamides)

20. Ways to overcome the resistance of microorganisms to antibiotics.

1) the use of drugs that inhibit the enzymes of microorganisms that destroy AB (for example, b-lactamase inhibitors)

3) timely detection of the sensitivity of microorganisms to antibiotics in certain regions and the replacement of some ABs with others in order to prevent the development of MB addiction to ABs

4) selection of optimal doses and duration of AB use

21. Reasons for the ineffectiveness of antimicrobial therapy.

A) at the level of choosing a drug for antimicrobial therapy:

ü Wrong choice, inadequate doses or route of administration

ü poor absorption of drugs, increased rate of excretion or inactivation

ü poor penetration of drugs into the focus of infection (CNS, bone, heart valves, prostate, eyeball)

ü Insufficient duration of therapy

delay initiation of antimicrobial therapy

error in determining the sensitivity of the pathogen

B) at the level of the patient's body:

ü low resistance (granulocytopenia, leukopenia, AIDS)

the presence of an undrained purulent focus (abscess)

presence of an infected foreign body, sequester

ü inactivating effect of biological media (urine pH)

C) at the level of the pathogen:

development of drug resistance to antibiotics

ü superinfection

the presence of an initial mixed infection

22. Name the groups of antibiotics that inhibit cell wall synthesis.

1. b-lactam antibiotics (penicillins, cephalosporins and cephamycins, monobactams, carbapenems)

2. Glycopeptides

3. Cycloserine

23. Name the groups of antibiotics that disrupt the permeability of the cytoplasmic membrane.

1. Polypeptides.

2. Polienes .

24. Name the groups of antibiotics that inhibit RNA synthesis.

1. Ansamycins.

2. Griseofulvin

25. Name the groups of antibiotics that inhibit protein synthesis.

1. Aminoglycosides (aminocyclitols)

2. Tetracyclines

3. Macrolides and azalides

4. Amphenicols

5. Lincosamides

6. Antibiotics of steroid structure ( Fusidic acid)

26. Name the groups of antibiotics with bactericidal action on resting microbial cells.

Aminoglycosides, fluoroquinolones, polymyxins.

27. Name the groups of antibiotics with bactericidal action on dividing microbial cells.

B-lactam antibiotics (penicillins, cephalosporins and cephamycins, monobactams, carbapenems), ansamycins (rifampicin).

28. Name the groups of bacteriostatic antibiotics.

Aminoglycosides (aminocyclitols), tetracyclines, macrolides and azalides, amphenicols, lincosamides, steroid antibiotics ( Fusidic acid)

29. Name the groups of β-lactam antibiotics.

1) penicillins

2) cephalosporins and cefamycins

3) monobactams

4) carbapenems

30. Classification of penicillins (specify highly active drugs).

1) Biosynthetic penicillins:

A) for parenteral administration: Benzylpenicillin (Naand K salt), benzylpenicillin procaine, benzathine benzylpenicillin (bicillin -1.)

B) for oral administration: Phenoxymethylpenicillin (penicillinV).

2) Isoxazolpenicillins (anti-staphylococcal penicillins resistant to β-lactamases): oxacillin, flucloxacillin,cloxacillin.

3) Aminopenicillins (broad spectrum): Amoxicillin, ampicillin .

4) Carboxypenicillins (antipseudomonas): Carbenicillin, ticarcillin .

5) Ureidopenicillins (antipseudomonas): piperacillin, azlocillin.

6) Combined preparations of penicillins with β-lactamase inhibitors: Amoxiclav (aMoxicillin + potassium clavulanate), unazine (ampicillin + sulbactam), tazocine (piperacillin + tazobactam).

31. Classification of cephalosporins (specify highly active drugs).

Cephalosporins	For parenteral administration	For oral administration
I generation (narrow spectrum, highly active against Gr + bacteria and cocci (except for enterococci, methicillin-resistant staphylococci), much less active against Gr - flora (E. coli, Klebsiella pneumonic, indole-negative Proteus)	Cefazolin Cephradine	Cefalexin Cephradine
II generation (broad-spectrum, more active against Gr-microflora (Haemophilus influenzae, Neisseria, Enterobacteria, indole-positive Proteus, Klebsiella, Moraxella, Serration), resistant to b-lactamases)	Cefuroxime Cefoxitin Cefamandol	Cefuroxime axetil Cefaclor
III generation (broad-spectrum, highly active against Gr-bacteria, including those producing b-lactamase; active against Pseudomonas, Acinetobacter, Cytobacter ; Penetrate into the CNS	Cefotaxime Ceftazidime Ceftriaxone	Cefixime Cefpodoxime
IV generation (broad-spectrum, highly active against bacteroids and other anaerobic bacteria; highly resistant to extended-spectrum b-lactamases; in relation to Gr - floras are equal in activity to III generation cephalosporins, in relation to Gr + flora are less active than cephalosporins 1st generation)	cefepime Cefpir

32. Name the most active antibiotics of the group of monobactams and carbapenems.

Monobactams: Aztreonam.

Carbapenems: Imipenem (thienam), meropenem.

33. Name the most active antibiotics glycopeptides and polypeptides.

Glycopeptides: Vancomycin, teicoplanin

Polypeptides: Polymyxins B, M, E (colistin).

34. Name the most active antibiotics ansamycins and amphenicols.

Ansamycins: : Rifampicin, rifabutin.

Amphenicols: Chloramphenicol (levomycetin)

35. Name the most active antibiotics aminoglycosides (aminocyclotols).

1st generation: Streptomycin, kanamycin, neomycin.

II generation: Gentamicin.

III generations: Amikacin, netilmicin, tobramycin.

36. Name the most active antibiotics tetracyclines and lincosamides.

Tetracyclines:

a) synthetic: Tetracycline, oxytetracycline

b) semi-synthetic: Doxycycline, demeclocycline, minocycline, metacycline

Lincosamides: Clindamycin, lincomycin.

37. Name the most active antibiotics macrolides and azalides.

Macrolides and azalides:

a) with a 14-membered ring: Erythromycin, Clarithromycin

b) with a 15-membered ring (azalides): Azithromycin

c) with a 16-membered ring: Spiramycin

38. Name antifungal antibiotics.

griseofulvin, Polyena (nystatin, amphotericin B)

39. Indicate belonging to a group, spectrum antimicrobial activity, resistance to β-lactamase and the route of administration of the following antibiotics: Cefazolin, cephalexin, cephradine.

1. First generation cephalosporins.

2. Narrow spectrum, highly active against Gr+ bacteria and cocci (except for enterococci, methicillin-resistant staphylococci), much less active against Gr-flora (E. coli, Klebsiella pneumonic, indole-negative Proteus)

3. Not resistant to β-lactamases.

4. Are administered parenterally ( cefazolin, cephradine) and inside ( cephalexin, cephradin)

40. Indicate the belonging to the group, the spectrum of antimicrobial activity, resistance to β-lactamase and the route of administration of the following antibiotics: Cefuroxime, cefoxitin, cefamandol, cefaclor.

1. Second generation cephalosporins.

2. Broad spectrum of activity, more active against Gr - microflora (hemophilic bacterium, neisseria, enterobacteria, indole-positive proteus, klebsiella, moraxella, serrations)

3. Resistant to b-lactamase

4. Are administered parenterally ( Cefuroxime, cefoxitin, cefamandol) and inside ( Cefaclor)

41. Indicate belonging to the group, spectrum of antimicrobial activity, resistance to β-lactamase and route of administration of the following antibiotics: Cefotaxime, ceftazidime, cefixime, ceftriaxone.

1. Third generation cephalosporins.

2. Broad spectrum of action, highly active against Gr-bacteria, including those producing b-lactamase; active against Pseudomonas, Acinetobacter, Cytobacter ; Penetrate into the CNS

3. Highly resistant to b-lactamase

4. Are administered parenterally ( Cefotaxime, ceftazidime, ceftriaxone) and inside ( Cefixime)

42. Indicate belonging to the group, spectrum of antimicrobial activity, resistance to β-lactamase and the route of administration of the following antibiotics: cefipime, cefpirome.

1. Fourth generation cephalosporins.

2. Broad spectrum of action, highly active against bacteroids and other anaerobic bacteria; in relation to Gr - floras are equal in activity to third-generation cephalosporins, in relation to Gr + flora are less active than first-generation cephalosporins

3. Highly resistant to extended spectrum b-lactamases

4. Are administered only parenterally.

43. Indicate belonging to a group, distribution features, spectrum of antimicrobial activity and side effects Fusidic acid.

Fusidic acid- an antibiotic of a steroid nature (refers to bacteriostatic antibiotics that inhibit protein synthesis).

Spectrum of AB activity (SABA): Gr + cocci (all staphylococci) and anaerobe (Cl. difficile).

Distribution Features: accumulates in bones and joints, does not penetrate through the BBB.

Side effects : dyspeptic and dyspeptic disorders.

44. Indicate belonging to a group, spectrum of antimicrobial activity Cycloserine.

Cycloserine- anti-tuberculosis antibiotics (from the group of bactericidal antibiotics that inhibit cell wall synthesis)

SABA: broad spectrum: inhibits gram-positive and gram-negative bacteria, inhibits the growth of Mycobacterium tuberculosis.

45. Name the drugs of choice for the treatment of infections caused by methicillin-resistant staphylococci.

First choice drug Vancomycin(glycopeptide).

Alternative drug: Co-trimaxosole(combination preparation, 5 parts Sulfamethoxazole(mid-acting sulfonamide) + 1 part trimethoprim(antimetabolite folic acid).

46. ​​Name the groups of chemotherapeutic agents active against intracellular microorganisms.

1) antiprotozoal drugs

2) anti-tuberculosis drugs

3) antiviral drugs

4) antibiotic drugs

47. Name the main chemotherapeutic drugs active against anaerobes.

Group of microorganisms	First choice drug	Alternative drugs
Gram-positive anaerobes (Peptococcus, Peptostreptococcus, Clostridia)	Penicillin: PenicillinG PenicillinV(for oral)	1. Clindamycin(lincosamides) 2. Tetracycline 3. Cephalosporins of the 1st generation. 4. Cefoxitin(2nd generation cephalosporin for parenteral administration)
Gram-negative Bacteroides fragilis	1. Metronidazole(nitroimidazole derivative) 2. Clindamycin(lincosamides)	1. Chloramphenicol(amphenicols) 2. Imipenem(carbapenems) 3. Unazine(ampicillin + sulbactam)
Other gram-negative anaerobes, except Bacteroides fragilis	1. Penicillin: PenicillinG(for parenteral administration) or PenicillinV(for oral) 2. Metronidazole(nitroimidazole derivative)	1. Clindamycin(lincosamides) 2. Tetracycline(biosynthetic tetracyclines) 3. Cephalosporin 1st generation 4. Cefoxitin

48. Name chemotherapy drugs with high anti-pseudomonas activity.

First choice drugs: aminoglycosides of the second ( Gentamicin) or third ( Amikacin, netilmicin, tobramycin) generations + broad-spectrum penicillins: (carboxypenicillins ( Carbenicillin, ticarcillin) or ureidopenicillins ( piperacillin, azlocillin}.

Alternative drugs: Ceftazidime(3rd generation cephalosporin for parenteral administration), Aztreonam(monobactams), Imipenem(carbapenems)

49. Indications for the prescription of tetracyclines.

upper respiratory infections (acute sinusitis)

lower respiratory tract infections (exacerbation of chronic bronchitis, community-acquired pneumonia)

o biliary tract infections

ü Orodental infections (periodontitis, etc.).

ü yersiniosis

ü eradication H. pylori(tetracycline in combination with other antibiotics and antisecretory drugs)

ü acne, with the ineffectiveness of local therapy

syphilis (allergic to penicillin)

ü non-gonococcal urethritis caused by chlamydia, mycoplasmas

o pelvic infections

ü rickettsiosis

ü especially dangerous infections: plague, cholera.

ü zoonotic infections: leptospirosis, brucellosis, tularemia, anthrax

50. Indications for prescribing chloramphenicol.

o bacterial meningitis

a brain abscess

ü generalized forms of salmonellosis

o typhoid fever

ü rickettsiosis

o gas gangrene

51. Indications for the appointment of streptomycin.

ü tuberculosis

brucellosis, tularemia, plague (in combination with tetracycline)

o Urinary tract and respiratory infections

ü bacterial endocarditis caused by viridescent streptococci or enterococci

52. Characterization of imipenem and meropenem by spectrum of action, resistance to β-lactamases and dihydropeptidase I.

1. Action spectrum: broader spectrum than penicillins, including P. aeruginosa and non-spore-forming anaerobes.

2. Imipenem and meropenem are b-lactamase resistant

3. Imipenem is degraded by dihydropeptidase I, meropenem has significant resistance to dihydropeptidase I.

53. Indications for the appointment of carbapenems.

ü severe infections, including nosocomial, caused by multiresistant microorganisms, as well as mixed microflora:

Ø lower respiratory tract (nosocomial pneumonia, lung abscess)

Ø urinary tract

Ø Intra-abdominal and pelvic infections

Ø skin, soft tissues, bones and joints

neutropenic fever

o bacterial endocarditis

54. Side effects of penicillins.

1. Allergic reactions (rash, eosinophilia, angioedema, cross-allergy) - most often to natural penicillins.

2. Neurotoxic effects (in high doses, with endolumbar administration) - convulsions, meningism, hallucinations, delirium, coma (GABA antagonists)

3. Carboxypenicillins and ureidopenicillins - acute interstitial nephritis, dysbacteriosis, thrombocytopenia, neutropenia, leukopenia.

55. Side effects of cephalosporins.

1. Allergic reactions (in 5-10% of patients): anaphylaxis, fever, rashes, nephritis, granulocytopenia, hemolytic anemia, cross-allergy to penicillins.

3. Dyspeptic disorders

4. Nephrotoxicity

5. Neurotoxicity (nystagmus, behavioral disturbances, seizures, hallucinations)

6. Hepatotoxicity, hypoprothrombinemia, clotting disorders

7. Superinfection, dysbacteriosis

56. Side effects of carbapenems.

1. Allergic reactions

2. Local irritant action

3. Reversible disorders of leukopoiesis

4. Headache

5. Gastrointestinal tract: nausea, vomiting (often with rapid intravenous administration), in rare cases, diarrhea.

6. Dysbacteriosis

7. Neurotoxicity: convulsions (with rapid intravenous administration in patients with severe CNS diseases, renal failure), headache.

57. Side effects of aminoglycosides.

1. Nephrotoxicity - a picture of interstitial nephritis

2. Ototoxicity - vestibular and cochlear disorders of an irreversible nature

3. Sometimes neuromuscular blockade

58. Side effects of tetracyclines.

They are characterized by a high frequency of adverse reactions.

1. General catabolic effect, inhibition of protein metabolism, hyperazotemia.

2. Dyspeptic phenomena, esophagitis.

3. Inhibition of the normal microflora of the gastrointestinal tract and vagina, superinfection.

4. In children, a violation of the formation of bone and dental tissue: discoloration of the teeth, enamel defects, slowing down the longitudinal growth of bones.

5. Photosensitization (more often doxycycline).

6. Hepatotoxicity, up to liver tissue necrosis - especially in liver pathology and rapid intravenous administration.

7. Pseudotumor brain syndrome: increased intracranial pressure with long-term use.

8. Nephrotoxicity: the development of tubular necrosis when using expired drugs.

59. Side effects of chloramphenicol.

1. Myelotoxicity (anemia, leukopenia, neutropenia, thrombocytopenia)

2. Acute drug hemolysis, non-hemolytic anemia, Iron-deficiency anemia, malnutrition, myodystrophy.

3. "Gray collapse" of newborns, children 2-3 months old (in newborns, due to the immaturity of the liver enzyme systems that metabolize chloramphenicol, the drug accumulates and has a cardiotoxic effect, which leads to the development of collapse, heart failure; while skin take on a gray tint).

4. Neurotoxicity: defeat optic nerve, peripheral polyneuropathies

5. Dyspeptic and dyspeptic phenomena

60. Side effects of macrolides.

1. Dyspepsia

2. Hepatotoxicity

3. Local reactions: phlebitis, thrombophlebitis

61. Name the groups of synthetic antimicrobial agents.

1. Sulfa drugs (SA) and trimethoprim

2. Oxyquinolines.

3. Nitrofurans.

4. Quinolones.

5. Fluoroquinolones.

6. Nitroimidazoles.

7. methenamine (urotropine).

62. Classification of sulfa drugs for resorptive action according to its duration.

A) short-term action (T1 / 2< 10 ч): Sulfanilamide (Streptocide),

Sulfadimidine (sulfadimezin), sulfaetidol (etazol).

B) medium duration of action (T1 / 2 10-24 hours) : Sulfadiazine.

C) long-acting (T1 / 2 24-48 hours): Sulfamethoxypyridazine, sulfadimethoxine, Sulfadoxine d) super-long action (T1 / 2 > 60 hours): Sulfalen.

63. Name the sulfonamides acting in the intestinal lumen.

Phthalylsulfathiazole (phthalazole), phthalylsulfapyridazine (phthazine) , Salazosulfanamides ( Sulfasalazine and etc.)

64. Name sulfa drugs for topical use.

Sulfacetamide (sulfacyl sodium),silver sulfadiazine, mafenide.

65. Features of the therapeutic effect of sulfonamides combined with salicylic acid.

These drugs are more effective for inflammatory bowel disease: Sulfasalazine cleaved by intestinal microflora to release Sulfapyridine and 5-aminosalicylic acid; 5-aminosalicylic acid in the intestinal lumen creates a high concentration and has its main anti-inflammatory effect)

66. Indications for use Sulfasalazine.

ü non-specific ulcerative colitis

o Crohn's disease

67. Mechanism of antimicrobial action of sulfa drugs.

For the formation of vital folic acid (which is involved in the synthesis of nucleic acids), microorganisms need extracellular para-aminobenzoic acid (PABA). Sulfonamides compete with PABA for the enzyme dihydropteroate synthetase, which leads to the formation of non-functional analogues of folic acid.

68. Antibacterial spectrum of sulfonamides.

Initially, many gram-positive and gram-negative cocci, gram-negative rods were sensitive to sulfonamides, but now they have become resistant.

Sulfonamides remain active against Nocardia, toxoplasma, chlamydia, malarial plasmodia.

69. Mechanism of antimicrobial action of trimethoprim.

See diagram for question 67.

Trimethoprim inhibits bacterial dihydrofolate reductase, which converts dihydrofolic acid to tetrahydrofolic acid and prevents the synthesis of folic acid, which is necessary for the growth of microorganisms.

70. How will the chemotherapeutic properties of sulfonamides change when they are combined with trimethoprim? Why?

The combination of sulfonamides with Trimethoprim leads to a significant increase (synergism) in the chemotherapeutic activity of both drugs, since together they cause inhibition of two successive stages in the formation of tetrahydrofolic acid.

71. Why is it necessary to prescribe sulfa drugs in high doses?

Sulfanilamide drugs must be prescribed in large doses, because their competitive mechanism of action requires the creation of a high concentration of drugs in the patient's blood for successful treatment of infections.

To do this, you should prescribe the first shock dose, 2-3 times higher than the average therapeutic dose, and at certain intervals (depending on the half-life of the drug) prescribe maintenance doses.

72. Name the most dangerous sulfonamides in relation to crystalluria.

Sulfadiazine, sulfadimethoxine, sulfalene(poorly soluble sulfonamides)

73. Complications of sulfonamide therapy.

1. Two types of nephrotoxicity:

a) crystalluria with acidic urine

b) hypersensitive nephritis

2. Dyspeptic phenomena (nausea, vomiting, diarrhea)

3. Skin reactions (rash, exfoliative dermatitis)

4. Neurological reactions

5. Hypothyroidism

6. Violations of hematopoiesis (anemia, leukopenia)

7. Hepatotoxicity

74. Name the drugs that have cross-hypersensitivity with sulfonamides.

Carbonic anhydrase inhibitors ( Acetazolamide), thiazide diuretics ( Hydrochlorothiazide), loop diuretics ( Furosemide, bumetanide) and oral antidiabetic agents from the group of sulfonylurea derivatives ( Glibenclamide).

75. Why do local anesthetics weaken the bacteriostatic effect of sulfonamides.

Sulfonamides are ineffective in environments where there is a lot of PABA (for example, in the focus of tissue decay), because of their mutual competition for the same enzyme dihydropteroate synthetase.

Novocaine (procaine) and benzocaine (anestethine) are hydrolyzed to form PABA and therefore weaken the bacteriostatic effect of sulfonamides.

76. Precautions necessary during therapy with sulfonamides.

1. To prevent crystalluria, patients taking sulfanilamide preparations should receive a plentiful alkaline drink.

2. Correct choice of the drug (when using long-acting drugs, side effects are usually less pronounced, which is explained by taking these drugs in lower doses)

NB! However, it should be borne in mind that due to the slow release from the body and the possibility of cumulation, side effects in long-acting sulfonamides may be more persistent than when taking short-acting sulfonamides.

3. Careful adherence to the dosing regimen

77. Name the drugs derivatives of 8-hydroxyquinoline.

Nitroxoline, chlorquinaldol

78. Spectrum of chemotherapeutic action of chlorquinaldol and nitroxoline.

Gr+ and Gr-bacteria (the main clinical significance is activity against Gr-bacteria from the family Enterobacteriaceae); some fungi (genus Candida, etc.) and protozoa.

79. Features of the pharmacokinetics of 8-hydroxyquinoline derivatives having a nitro group in the structure and containing halogens.

Unlike other derivatives of 8-hydroxyquinoline, these drugs are rapidly absorbed from gastrointestinal tract and is excreted unchanged by the kidneys, and therefore there is a high concentration of drugs in the urine.

80. Indications for the use of nitroxoline.

ü infectious inflammatory diseases predominantly of the genitourinary tract (pyelonephritis, cystitis, urethritis, epididymitis, infected adenoma or prostate carcinoma), caused by microorganisms sensitive to nitroxoline

ü prevention infectious complications for diagnostic and therapeutic manipulations on the urinary tract (catheterization, cystoscopy)

81. Indications for the use of chlorquinaldol.

ü intestinal infectious diseases (dysentery, salmonellosis, food poisoning, intestinal infections caused by staphylococcus, proteus and other enterobacteria)

ü dysbacteriosis

82. Side effects of nitroxoline and chlorquinaldol.

1. Dyspeptic disorders (nausea, vomiting, abdominal pain, diarrhea)

2. Tachycardia (rare)

3. Allergic reactions: rash, skin rashes

4. CNS disorders: in isolated cases - ataxia, headache, paresthesia

83. Name the preparations of the nitrofuran group.

Nitrofurantoin (furadonin), furagin (solafur), furazolidone

84. The mechanism of action of nitrofurans.

Nitrofurans damage DNA and enzyme systems of microorganisms.

85. Indications for the use of furazolidone.

bacillary dysentery, paratyphoid, food poisoning

ü Trichomonas colpitis

ü giardiasis

86. Indications for the use of nitrofurantoin.

pyelitis, pyelonephritis, cystitis, urethritis

ü prophylaxis during urological operations, cystoscopy, catheterization

87. Why is it necessary to limit the use of products containing a lot of tyramine during treatment with furazolidone?

Furazolidone is a monoamine oxidase inhibitor, and the use of foods containing a lot of tyramine (cheese, chocolate, etc.) while taking furazolidone can lead to an increase in the vasoconstrictive effect of tyramine and to the development of a hypertensive crisis.

88. Effect of furazolidone on ethanol metabolism.

Furazolidone has the ability to sensitize the body to the effects of alcohol and is used to treat alcoholism when other drugs are not effective enough or there are contraindications to their use.

After taking furazolidone (within 10-12 days), a negative conditioned reflex reaction to alcoholic drink. Taking alcohol against the background of furazolidone causes a feeling of heat in the face and neck, burning sensation throughout the body, heaviness in the occipital region, increased heart rate, and a decrease in blood pressure.

89. Complications in nitrofurantoin therapy.

1. Dyspeptic phenomena: most often nausea and vomiting.

2.Hepatotoxicity.

3. Hematotoxicity.

4. Neurotoxicity: damage to the central nervous system and peripheral department, especially in renal failure and long-term courses (more than 1.5 months).

5. Pulmonary reactions:

A) acute (90%): pulmonary edema, bronchospasm;
b) chronic (10%): pneumonitis, accompanied by difficulty breathing, fever, eosinophilia

90. Side effects of furazolidone.

1. Dyspeptic symptoms: nausea, vomiting, decreased appetite.

2. Allergic reactions: exanthems and enanthems.

91. The difference in the antibacterial spectrum of acids: nalidixic, oxolinic and pipemidic.

AB spectrum Nalidixic acid: Gram(-) sticks ( E. coli, Shigella, Salmonella, Proteus, Klebsiella).

AB spectrum oxolinic acid: such as At nalidixic acid.

AB spectrum pipemidic acid: like u Nalidixic acid+ active against Pseudomonas

92. Difference in antimicrobial activity of oxolinic and nalidixic acids.

Antimicrobial activity oxolinic acid 2-4 times higher than activity Nalidixic acid(not differing from it in terms of AB spectrum of action), however Oxolinic acid is also more neurotoxic.

93. Difference and similarity of pharmacokinetic properties of acids: nalidixic, oxolinic and pipemidic.

Similar pharmacokinetic properties:

A) all are well absorbed in the gastrointestinal tract, food can slow down absorption, but does not affect the bioavailability of drugs

B) do not create therapeutic concentrations in the blood, many organs and tissues; therapeutically significant concentrations only found in urine

Differences in pharmacokinetic properties: most actively metabolized in the liver Nalidixic and oxolinic acids, least - pipemidic acid.

94. Side effects of nalidixic acid.

1. Dyspeptic disorders.

2. Cytopenias.

3. Hemolytic anemia(rarely).

4. Excitation of the central nervous system: lowering the convulsive threshold.

5. Cholestasis.

95. Which drug from quinolone derivatives causes fewer side effects from the side of the central nervous system and why?

Norfloxacin, since it does not penetrate the blood-brain barrier

96. Indications for the use of quinolones.

1. Urinary tract infections in children: cystitis, anti-relapse therapy chronic pyelonephritis(in adults in such cases it is better to use fluoroquinolones)

2. Shigellosis in children.

97. The fundamental difference between the structure of fluoroquinolones and quinolones, which radically changed them pharmacological properties and antimicrobial activity.

Fluoroquinolones, unlike quinolones, contain:

A) in position 7 of the quinolone core, an unsubstituted or substituted piperazine ring

B) in position 6 - a fluorine atom

Due to these features, fluoroquinolones have a wider spectrum of action; they are superior in activity against a number of bacteria. Nalidixic acid 10 - 20 times.

98. Name the most used fluoroquinolones in clinical practice.

A) II generation quinolones ("gram-negative"): Norfloxacin, ciprofloxacin, ofloxacin, lomefloxacin

B) III generation quinolones (“respiratory”): Levofloxacin, sparfloxacin.

C) IV generation quinolones (“respiratory” + “antianaerobic”): Moxifloxacin

99. Mechanism of action of fluoroquinolones.

Inhibition of the enzyme DNA gyrase of bacterial cells, which belongs to topoisomerases that control the structure and functions of DNA ® death of bacteria (bactericidal effect)

Quinolones also affect:

A) bacterial RNA and bacterial protein synthesis

B) membrane stability and other life processes of bacterial cells

100. Antimicrobial spectrum of fluoroquinolones.

Compared to quinolones, they have a wider spectrum of activity., including:

A) staphylococci (including penicillin-resistant S. aureus (PRSA) and some methicillin-resistant strains of S. aureus (MRSA)

B) gram-negative cocci (gonococcus, meningococcus, M. catarrhalis)

B) gram-positive rods (listeria, corynebacteria, anthrax pathogens)

D) Gram-negative rods of the Enterobacteriaceae family, including multidrug-resistant (E. coli, Salmonella, Shigella, Proteus, Enterobacter, Klebsiella), P. aeruginosa.

D) some intracellular microorganisms (legionella)

Individual drugs ( Ciprofloxacin, ofloxacin, lomefloxacin) Active against M. tuberculosis

101. Pharmacokinetic properties of fluoroquinolones.

1. All are well absorbed in the gastrointestinal tract, food can slow down absorption, but does not affect bioavailability.

2. The degree of metabolism in the liver depends on the type of drug

3. Fluoroquinolones have a large volume of distribution, create high concentrations in many organs and tissues, penetrate into cells

4. Excreted mainly by the kidneys, partly with bile.

102. Indications for the appointment of fluoroquinolones.

lower respiratory tract infections (exacerbation of chronic bronchitis, nosocomial pneumonia)

o biliary tract infections

o urinary tract infections

ü prostatitis

ü Intra-abdominal and pelvic infections

intestinal infections (shigellosis, salmonellosis)

ü severe infections of the skin, soft tissues, bones, joints

ü gonorrhea

tuberculosis (as second-line drugs)

103. Side effects of fluoroquinolones.

1. Inhibition of the development of cartilaginous tissue (therefore, it is contraindicated in pregnant and lactating mothers, in children under 18 years of age it can be used only for special indications)

2. Development of tendonitis (inflammation of the tendons, especially Achilles), tendon ruptures during physical exertion (in rare cases)

3. Prolongation of the QT interval on the electrocardiogram, which can provoke the development of ventricular arrhythmias

4. Photodermatitis

5. Influence on the central nervous system (rare): convulsions, psychosis, hallucinations, headache, dizziness, insomnia

6. Dyspeptic disorders: nausea, vomiting, diarrhea

7. Changes in the functional parameters of the liver

8. Skin rashes

9. Superinfection (streptococcal, candidal)

104. Contraindications to the appointment of fluoroquinolones.

Ø hypersensitivity to fluoroquinolones

Ø deficiency of glucose-6-dehydrogenase

o Pregnancy, breastfeeding

Ø childhood(up to 18 years old)

105. Name the drugs from the nitroimidazole group.

Metronidazole (trichopolum), tinidazole.

106. The mechanism of action of metronidazole.

Direct bactericidal and antiprotozoal action:

A) the electron-withdrawing nitro group of metronidazole is restored intracellularly only by anaerobes or microaerophiles with the formation of toxic metabolites ® reduction of redox potential, despiralization and destruction of DNA in susceptible microorganisms

B) increases the sensitivity of tumor cells to ionizing radiation (because it inhibits tissue respiration)

107. Spectrum of antibacterial and antiprotozoal action of metronidazole.

1. Most anaerobes: bacteroids (including B. fragilis), clostridia (including Cl. difficile), peptostreptococci, fusobacteria

2. Some protozoa: Trichomonas, Giardia, Leishmania, Amoeba, Balantidia

3. Helicobacter pylori

108. Pharmacokinetics of metronidazole.

1. Well absorbed when taken orally, bioavailability does not depend on food intake.

2. Metabolized in the liver with the formation of active and inactive metabolites.

3. It is well distributed, passes through the BBB, placenta, penetrates into breast milk, saliva, gastric juice.

4. Completely excreted from the body in the urine unchanged and in the form of metabolites, partially excreted in the feces.

5. With repeated injections, cumulation is possible.

109. Indications for the use of metronidazole.

ü postoperative anaerobic infection (colorectal surgery, appendicitis, hysterectomy)

Purulent anaerobic and mixed infection

acute ulcerative gingivitis

ü trophic ulcers, bedsores

anaerobic infection of the urinary tract, respiratory and gastrointestinal tract
pelvic inflammatory disease

o bacterial vaginosis

ü enterocolitis

o brain abscesses

ü trichomoniasis of the urinary tract, amoebiasis, giardiasis

110. Side effect of metronidazole.

1. Dyspeptic phenomena: nausea, vomiting, anorexia, metallic taste in the mouth

2. Hematotoxicity: leukopenia, neutropenia

3. Neurotoxicity: headache, incoordination, tremor, convulsions, impaired consciousness

4. Disulfiram-like effect

5. Allergic reactions: rash, itching

6. Local reactions: phlebitis and thrombophlebitis after intravenous administration

111. Name the drugs that cause bright yellow coloration of urine.

Nitroxoline.

112. Name the targets of action of antimalarial drugs.

A) erythrocyte schizonts

B) tissue schizonts:

1) preerythrocytic (primary tissue) forms

2) paraerythrocyte (secondary tissue) forms

C) sexual forms of plasmodia (gamonts)

113. Name the drugs that affect erythrocyte schizonts.

Mefloquine, chloroquine (chingamine), quinine, pyrimethamine (chloridine), fansidar (pyrimethamine + sulfadoxine), Maloprim(Pyrimethamine + yesPson)

114. Name the drugs that affect preerythrocyte forms malarial plasmodium.

pyrimethamine, proguanil (bigumal)

115. Name the drugs that affect the sexual forms of malarial plasmodium.

A) gamontocidal: Primakhin

B) gamonostatic: Pyrimethamine

116. The principle of using antimalarial drugs for personal chemoprophylaxis.

Means affecting pre-erythrocyte and erythrocyte forms of plasmodium.

117. Principle of using antimalarial drugs for the treatment of malaria

Drugs affecting the erythrocyte forms of plasmodium.

118. The principle of using antimalarial drugs to prevent recurrence of malaria (radical treatment).

Drugs affecting paraerythrocyte and erythrocyte forms of plasmodia.

119. The principle of the use of antimalarial drugs for public chemoprophylaxis.

Means that affect the sexual forms (gamonts) of Plasmodium.

120. Spectrum of antimalarial action of mefloquine, chloroquine, quinine.

Mefloquine: hemantoschizontocidal action (Pl. falciparum, Pl. vivax)

Chloroquine: hemantoschizontocidal, gamonotropic action (Pl. vivax, Pl. ovale, Pl. malariae, but not Pl. falciparum)

Quinine: hemantoschizontocidal action (Pl. vivax, Pl. ovale, Pl. malariae, but not Pl. falciparum), gamontocidal (Pl. vivax, Pl. ovale, less by Pl. falciparum)

121. Spectrum of antimalarial activity of pyrimethamine and proguanil.

pyrimethamine and proguanil: histoschizotropic action (Pl. falciparum)

122. Spectrum of antimalarial action of primaquine.

Primakhin: histotropic action (P. vivax and P. ovale ) , gamototropic action (all types of Plasmodium), hematotropic action (Pl. vivax).

123. Name drugs for personal chemoprophylaxis.

Chloroquine, mefloquine; chloroquine + proguanil; chloroquine + primaquine; pyrimethamine; doxycycline

124. Name the drugs for the treatment of malaria.

Chloroquine.

If: a) chloroquine resistant Pl. falciparum b) the causative agent is unknown or c) mixed malaria, apply: Mefloquine, quinine, quinil + doxycycline, pyrimethamine + sulfadoxine, pyrimethamine + dapsone.

125. Name drugs for prevention of malaria recurrence (radical treatment).

Primakhin.

126. Name drugs for public chemoprophylaxis.

Primakhin.

127. What kind of malarial plasmodium does not form paraerythrocyte forms?

128. What form of malaria does not relapse after treatment? Why?

Tropical form, called Pl. falciparum, since it lacks paraerythrocyte forms that contribute to the resumption of the erythrocyte cycle of Plasmodium development and the onset of distant relapses.

129. Name the remedies that are effective in any localization of amoebas.

Metronidazole, tinidazole (Fasigine)

130. Name the agents effective in intestinal localization of amoebas.

A) direct action, effective in the localization of amoebae in the intestinal lumen - Quiniofon, diloxanide, etofamide;

B) indirect action, effective in the localization of amoebae in the lumen and intestinal wall - Doxycycline

131. Name the agents acting on tissue forms of amoebas.

A) effective in the localization of amoebae in the intestinal wall and liver: Emetine hydrochloride

B) effective in the localization of amoebae in the liver: Chloroquine.

132. The mechanism of action of the quiniophone.

Antimicrobial and antiprotozoal action, has antiamebic activity.

A) disrupts the systems of oxidative phosphorylation of amoebas due to the halogenation of enzymes and the formation of chelate complexes with them

B) binds to Mg2+ and Fe, which are part of the structure of some amoeba enzymes and causes their inactivation

C) causes denaturation of pathogen proteins due to their halogenation

133. Pharmacokinetic properties of quiniofon providing amebocidal action.

It is absorbed from the gastrointestinal tract only by 10-15%, due to which high concentrations of the substance are created in the intestinal lumen, which provide the amoebicidal effect of quiniofon.

134. Pharmacokinetic properties of diloxanide furoate.

Diloxanide furoate breaks down in the intestine and is almost completely (90%) absorbed and excreted in the urine in the form of glucuronides. The part of diloxanide furoate that has not entered the bloodstream is an active anti-amoebic substance that is not affected by the intestinal flora.

135. Side effects of quiniophone.

A) allergic reactions

B) diarrhea

B) optic neuritis

136. Side effects of emetine hydrochloride.

A) dyspeptic and dyspeptic disorders

B) cardiotoxicity: ECG changes, heart pain, tachycardia, arrhythmias, decreased cardiac output, hypotension.

C) skeletal muscles: pain, stiffness, weakness, possible formation of abscesses and necrosis

D) skin: eczematous, erythematous or urticarial rashes

D) nephrotoxicity

E) hepatotoxicity

137. Side effects of diloxanide furoate.

A) dyspeptic disorders: nausea, flatulence

B) skin allergic reactions: urticaria, itching

138. Name antitrichomonas drugs for oral use.

Tinidazole

139. Name antitrichomonas drugs for oral and intravaginal use.

Metronidazole, trichomonacid, furazolidone

140. Name antitrichomonas drugs for intravaginal use.

Polyvidone-iodine, polycresulene

141. Principles of treatment of trichomoniasis.

1) treatment must be carried out simultaneously for both sexual partners, even in the absence of laboratory confirmation of Trichomonas invasion in one of them

2) both patients with inflammatory phenomena and trichomonas carriers are subject to treatment

3) in acute uncomplicated forms of trichomoniasis, one can limit oneself to prescribing specific antitrichomoniasis drugs orally, however, in prolonged, complicated and chronic cases, general etiotropic drug treatment must necessarily be supplemented by methods of stimulating the body's immune responses, local procedures and complex physiotherapy treatment

4) Sexual life and alcohol are prohibited during treatment

142. Name the drugs used in giardiasis (giardiasis).

Metronidazole, tinidazole, mepacrine (Acriquin), furazolidone

143. The mechanism of action of mepacrine.

It is not precisely established, it is believed that mepacrine wedged between two strands of DNA, interfering with the work of transcriptase and RNA synthesis.

144. Side effects of mepacrine.

A) neurotoxicity: dizziness, headache

B) dyspeptic disorders: nausea, vomiting, toxic psychosis, convulsions

C) reversible yellow discoloration of the skin or urine, blue-black discoloration of the palate and nails

D) hepatotoxic effect (rarely)

E) hematotoxicity: anemia (rare)

145. Name the drugs used in toxoplasmosis.

Pyrimethamine in combination with Sulfonamides ( Sulfadiazine or Sulfadimidine) and in combination with AB ( Clindamycin, azithromycin, spiromycin)

146. Features of therapy of toxoplasmosis against the background of AIDS.

The main place in the treatment of chronic forms of toxoplasmosis against the background of AIDS is Hyposensitizing and immunomodulatory therapy, showing:

1) carrying out specific hyposensitization with toxoplasma allergen ( Toxoplasmin)

2) application Levomisola(has immunomodulatory properties)

3) the use of chemotherapy drugs in the event of general toxic effects (pyrimethamine in combination with sulfazil),

4) inclusion in the course of treatment of vitamins, desensitizing agents, lidase, cerebrolysin

5) treatment of organ lesions

147. Features of the treatment of toxoplasmosis with the threat of infection of the fetus.

Drugs used in toxoplasmosis are used in combination with antibiotics.

148. Drugs used for the treatment of visceral leishmaniasis.

Sodium stibogluconate, solusurmin, pentamidine

149. Drugs used for the treatment of cutaneous leishmaniasis.

mepacrine, monomycin

150. Side effects of sodium stibogluconate.

A) dyspepsia

B) hypersensitivity reactions: rash, fever, arthralgia, myalgia, cough, pneumonitis

B) nephrotoxicity

D) neurotoxicity: headache, general weakness

E) cardiotoxicity: ECG changes, heart pain, rhythm disturbances

E) pain at the injection site

G) increased activity of serum transaminases and amylase, pancreatitis (often in subclinical form)

151. Side effects of pentamidine.

For inhalation use:

Allergic reactions: cough, shortness of breath, bronchospasm, rash, fever

o anorexia, metallic taste in the mouth

neurotoxicity: fatigue, dizziness

For parenteral use:

arterial hypotension, syncope

ü nausea

ü increased levels of urea and creatinine in the blood plasma, hyperkalemia

hematuria, proteinuria

Hypoglycemia followed by hyperglycemia

o acute pancreatitis

leukopenia, anemia, thrombocytopenia

152. Name the drugs used for pneumocystosis.

Co-trimoxazole, pentamidine

153. Specify the reasons why the treatment of viral infections is a difficult problem.

2) viruses use the protein biosynthesis apparatus of macroorganism cells, modifying it, so it is difficult to find selectively acting antiviral agents that would infect the virus without damaging the host cell

154. The main stages of virus reproduction, "vulnerable" to the effects of antiviral agents.

A) adsorption of the virus (blockade Gammaglobulins)

B) "undressing" viruses (blockade Amantadine)

C) synthesis of nucleic acids of viruses (blockade by antimetabolites, analogs of purine and pyrimidine bases, reverse transcription inhibitors)

D) synthesis of late viral proteins (blockade Metisazon, saquinar)

D) virus packaging (blockade Rifamipicin)

E) the release of the virus from the cell (blockade amantadines)

155. Name the inhibitors of adsorption, penetration and "undressing" of the virus.

Gammaglobulins Against measles, hepatitis B and C, rabies, cytomegalovirus infection , amantadine, rimantadine.

156. Name the inhibitors of the synthesis of nucleic acids of the virus.

A) Nucleoside analogues (reverse transcriptase inhibitors):

1) antiherpetic:

2) anticytomegalovirus: Ganciclovir

3) for the treatment of HIV infections:

B) non-nucleoside reverse transcriptase inhibitors:

for the treatment of HIV infection: nevirapine, ifavirenz

C) derivatives of phosphonomoric acid (organic phosphates)

antiherpetic and anticytomegalovirus: Foscarnet

157. Name the inhibitors of the synthesis of RNA and late viral proteins.

A) Interferons and interferonogens are broad-spectrum antiviral drugs:

ü monocytic interferons ( Interferon alfa, Interferon alfa-2a, Interferon alfa-2B), fibroblastic (interferon beta), leukocyte ( Interferon gamma-1B)

ü interferonogens: Tiloron,Arbidol

B) Inhibitors of the synthesis of late viral proteins - For the prevention and treatment of smallpox : Metisazon

V) Protease inhibitors (peptide derivatives)- for the treatment of HIV infection:

158. Name the inhibitors of virus self-assembly.

Rifampicin.

159. Name anti-influenza drugs.

Aminoadomantanes: Amantadine, rimantadine

160. Name antiherpetic drugs.

A) nucleoside analogues: Trifluridine, idoxuridine, acyclovir, famciclovir, valaciclovir, inosine pranobex, vidarabine

Foscarnet

161. Name anticytomegalovirus drugs.

A) nucleoside analogues: Ganciclovir

B) a derivative of phosphonoformic acid: Foscarnet

162. Name the drugs for the treatment of HIV infection.

A) reverse transcriptase inhibitors - nucleoside analogues: Zidovudine, didanosine, lamivudine, stavudine, zalcitabine, abacavir sulfate

B) non-nucleoside reverse transcriptase inhibitors: nevirapine, ifavirenz

C) protease inhibitors - derivatives of peptides: Saquinavir, indinavir, ritonavir

163. Name the drugs for the treatment of respiratory syncytial infection.

Ribavirin

164. Name broad-spectrum antiviral drugs.

A) monocytic interferons ( Interferon alfa, Interferon alfa-2a, Interferon alfa-2B), fibroblastic (interferon beta), leukocyte ( Interferon gamma-1B)

B) interferonogens: Tiloron,Arbidol

165. Name virucidal preparations of local action.

Oksolin, tebrofen, butaminophen, bonafton

166. Name the gamma globulins used for the treatment of viral infections.

Rabies gamma globulin, purified human measles gamma globulin, gamma globulins against hepatitis B and C, cytomegalovirus infection.

167. Mechanism of action of aminoadamantanes.

ü block the "undressing" of viruses

block the release of viruses

inhibit the release of the virus from the cell

168. The mechanism of action of ribovirin.

Inhibits the synthesis of viral RNA (reduces the formation of GMF) and proteins.

169. The mechanism of action of zidovudine.

Inhibition of reverse transcriptase of viruses ® violation of the synthesis of DNA of the virus, inhibition of its replication.

170. The mechanism of action of ganciclovir.

Inhibits DNA polymerase predominantly of cytomegalovirus ® disruption of viral DNA synthesis, inhibition of its replication

171. The mechanism of action of foscarnet.

Inhibits DNA polymerase ® disruption of virus DNA synthesis, inhibition of its replication

172. The mechanism of action of trifluridine.

Inhibits viral DNA synthesis by replacing thymidine.

173. The mechanism of action of acyclovir.

Acyclovir + virus thymidine kinase ® phosphorylation of acyclovir, formation of acycloguanosine triphosphate ® inhibition of viral DNA polymerase ® inhibition of viral DNA synthesis, inhibition of virus replication

174. The mechanism of action of nevirapine.

Connects with reverse transcriptase and blocks its activity, causing the destruction of the catalytic site of the enzyme ® inhibition of viral NK synthesis, inhibition of virus replication.

175. The mechanism of action of saquinavir.

Reduces the activity of proteases that cleave the virus polyprotein ® disruption of the formation of functionally active enzyme proteins and structural proteins of the virus.

176. The mechanism of action of interferons.

A) interfere with the penetration of the viral particle into the cell

B) inhibit the synthesis of mRNA and the translation of viral proteins by influencing a number of enzymes (protein kinase, phosphodiesterase, adenylate synthetase)

C) block the assembly process of the viral particle and its exit from the cell

D) are powerful endogenous immunomodulators and lymphokines, activate the immune defense mechanisms of host cells.

177. The mechanism of action of tilorone.

A) stimulates the formation of interferons alpha, beta, gamma in the body

B) has an immunomodulatory effect (stimulates bone marrow stem cells, increases antibody production depending on the dose, increases the ratio of high-avidity / low-avidity antibodies, reduces the degree of immunosuppression, restores the ratio of T-helpers / T-suppressors)

178. Indications for the use of acyclovir.

ü primary herpes of the genital organs - accelerates healing, but does not prevent relapses

recurrence of primary genital herpes

o herpetic encephalitis

mucocutaneous herpes

ü shingles - prevents new rashes, reduces pain, accelerates healing

o chicken pox

Prevention of cytomegalovirus infection after bone marrow transplantation

179. Indications for the use of trifluridine.

Only locally for keratoconjunctivitis caused by the herpes simplex virus

180. Indications for the use of idoxuridine.

o herpetic keratitis

ü deep stromal herpetic keratitis (together with glucocorticosteroids)

181. Indications for the use of foscarnet.

ü infectious and inflammatory diseases of the skin and mucous membranes caused by herpes viruses

o Cytomegalovirus retinitis

ü as a reserve drug for herpes against the background of AIDS with resistance to acyclovir

182. Indications for the use of ganciclovir.

cytomegalovirus pneumonia, retinitis

retinitis with HIV

ü colitis, liver damage in AIDS

183. Indications for the use of zidovudine.

ü AIDS in adults with CD4-T-lymphocytes below 500/µl of blood

AIDS in children older than 3 months

184. Indications for the use of amantadine and rimantadine.

Prevention of influenza A (but not B)

Indications for the prophylactic use of rimantadine (recommendations of the Centers for Disease Control, USA, 1997):

O Family members of a person with influenza.

O Persons who have close contact with a person who has the flu.

O Persons at high risk for severe influenza: the elderly over 65 years of age, patients with chronic bronchopulmonary, cardiovascular or renal pathology, with diabetes mellitus, with immunosuppression, with hemoglobinopathies

O Children 6 months to 18 years of age on long-term aspirin use (high risk of Reye's syndrome).

O Medical staff.

ü treatment of influenza A during an epidemic (should be started in the first 2 days after the onset of clinical symptoms)

ü with late vaccination against influenza (if less than 2 weeks have passed since the vaccination)

ü to protect people with IDS from influenza

185. Indications for the use of ribavirin.

ü treatment of diseases of the lower respiratory tract caused by the respiratory syncytial virus in newborns, children younger age(preparation of the 1st line)

ü influenza A and B in severe infection in adolescents (2nd line drug)

hemorrhagic fever with renal syndrome

ü hepatitis C (in combination with interferon)

186. Anti-rabies agent.

Rabies immunoglobulin, rifampicin.

187. Means of choice for anogenital warts.

Podophyllotoxin (cytostatic)

188. Means of choice for herpetic keratitis.

Idoxuridin.

189. Means of choice for herpetic conjunctivitis.

Trifluridine.

190. Belarusian virucidal agent of local action.

Butaminophen

191. Means of choice for the treatment of genital herpes.

Acyclovir

192. Side effects of acyclovir.

Usually well tolerated, adverse effects are rare.

o Nausea, vomiting, diarrhea

o headache

ü Allergic skin reactions

ü Increased fatigue

ü an increase in the content of urea, creatinine and bilirubin in the blood serum, an increase in the activity of liver enzymes (with parenteral administration)

193. Side effects of foscarnet.

It has a fairly high toxicity.

A) at the injection site: phlebitis, thrombophlebitis

B) nephrotoxicity - proteinuria, kidney failure, acute tubular necrosis, crystalluria, interstitial nephritis
c) electrolyte imbalance - hypocalcemia, hypomagnesemia, hypokalemia, hypophosphatemia; may be accompanied by arrhythmias, convulsions, mental disorders
d) dyspeptic and dyspeptic disorders

E) neurotoxicity - headache, hallucinations, depression, tremor, convulsions

E) hematotoxicity - anemia, granulocytopenia

G) fever

194. Side effects of ganciclovir.

A) hematotoxicity: neutropenia, thrombocytopenia, anemia

B) nephrotoxicity - renal failure, azotemia
c) neurotoxicity - headache, lethargy, psychosis, encephalopathy
d) dyspeptic and dyspeptic disorders.

D) phlebitis (locally)
f) rash, fever, eosinophilia, elevated liver enzymes

195. Side effects of zidovudine.

A) hematotoxicity: anemia, neutropenia, leukopenia, thrombocytopenia, pancytopenia with bone marrow hypoplasia

B) dyspeptic and dyspeptic disorders: nausea, vomiting, anorexia, taste perversion, abdominal pain, diarrhea, hepatomegaly, fatty degeneration of the liver, increased levels of bilirubin and liver transaminases

C) neurotoxicity: headache, dizziness, paresthesia, insomnia, drowsiness, weakness, lethargy, anxiety, depression, convulsions.
e) increased urination.
f) allergic reactions: skin rash, itching.
g) increased sweating

H) myalgia, myopathy, chest pain, shortness of breath

196. Side effects of aminoadamantanes.

As a rule, they are well tolerated, sometimes there may be neurotoxic reactions in the form of irritability, impaired concentration, and insomnia.

197. Side effects of interferons.

A) early (more often in the first week of treatment): flu-like syndrome, manifested by fever, myalgia, soreness of the eyeballs.

B) late (at 2-6 weeks of therapy):

hematotoxicity: anemia, thrombocytopenia, agranulocytosis

ü neurotoxicity: drowsiness, lethargy, depression, less often seizures

Cardiotoxicity: arrhythmias, transient cardiomyopathy, arterial hypotension

o autoimmune thyroiditis

ü hyperlipidemia

alopecia, skin rashes

198. Side effects of ribavirin.

A) local reactions: rash, irritation of the skin, mucous membranes of the eyes and respiratory tract, bronchospasm

B) hematotoxicity: anemia, lymphocytopenia (in AIDS patients), hemolytic anemia

C) neurotoxicity: headaches, fatigue, irritability, insomnia

D) metallic taste in the mouth, abdominal pain, flatulence, nausea

E) teratogenic effect

199. Antibiotic with antiviral activity.

Rifampicin.

200. The effectiveness of the use of drugs for the treatment of HIV infection.

HIV quickly develops resistance to the action of all currently existing antiviral drugs, so antiviral therapy is able to Only slow the progression of the disease.

201. An example of the combined use of antiviral drugs in the treatment of AIDS.

Combined drug Trizivir(GlaxoWellcom, UK), consisting of abacavir sulfate, lamivudine and zidovudine. Lamivudine, zidovudine and abacavir are nucleoside analogues and reverse transcriptase inhibitors - selective inhibitors of HIV-1 and HIV-2.

202. Name the main antispirochetal drugs.

BenzylpenicillinNaand K salt, benzathine benzylpenicillin (bicillin 1), erythromycin, azithromycin, tetracyclines, cephalosporins.

203. Means of choice for the treatment of syphilis.

Benzathine benzylpenicillin, penicillin(with neurosyphilis)

204. The mechanism of action of bismuth preparations.

A) stimulate the formation of prostaglandins and their secretion of the gastric mucosa gastroprotective effect

B) adsorption of the bismuth preparation on the outer membrane of the MB, followed by a critical for bacteria decrease in the content of intrabacterial ATP ® antimicrobial action against a significant number of pathogenic and opportunistic bacteria.

205. Side effects of bismuth preparations.

A) dyspeptic disorders: nausea, vomiting, frequent stools,

B) swelling of the eyelids and gums, vesicles and pigmentation on the tongue

C) rarely - allergic reactions in the form of skin rash and itching

D) hematotoxicity: methemoglobinemia.

206. Anti-tuberculosis drugs - definition.

Anti-tuberculosis drugs- chemotherapeutic agents that inhibit the growth of acid-resistant mycobacteria, reduce virulence, prevent and reduce the incidence of tuberculosis.

207. Name the main anti-tuberculosis drugs

Isoniazid, rifampicin (rifampin), ethambutol, pyrazinamide, streptomycin

208. Name the reserve anti-tuberculosis drugs.

Ethionamide, prothionamide, cycloserine, capreomycin, kanamycin, florimycin, rifabutin, amikacin, lomefloxacin, thioacetazone, PAS

209. Name other drugs (except for the main and reserve ones) that can be used in the treatment of tuberculosis.

Azithromycin, clarithromycin, dapsone, clofazimine, tetracyclines

210. Name the most active anti-tuberculosis drugs.

Isoniazid, rifampicin (rifampin), rifater (rifampicin + isoniazid + pyrazinamide), rifakom (isoniazid + pyridoxine)

211. Name anti-tuberculosis drugs of medium activity

Streptomycin, kanamycin, pyrazinamide, prothionamide, ethionamide, ethambutol, cycloserine, florimycin, semozid, methozid, ftivazid, capreomycin.

212. Name anti-tuberculosis drugs of moderate activity.

PASK, thioacetazone, solutizone, pasomycin

213. Name the most active synthetic anti-tuberculosis agent.

Isoniazid.

214. Name the most active anti-tuberculosis antibiotic.

Rifampicin

215. Name bacteriostatic anti-tuberculosis drugs.

A) bactericidal and bacteriostatic : isoniazid, rifampicin

B) only bacteriostatic: pyrazinamide, ethambutol, prothionamide, PAS, thioacetazone.

216. Name anti-tuberculosis drugs acting on mycobacteria localized intracellularly.

Isoniazid, rifampicin, streptomycin, cycloserine

217. Name bactericidal anti-tuberculosis drugs.

Isoniazid, rifampicin, streptomycin, lomefloxocin.

218. The spectrum of action of anti-tuberculosis drugs.

Synthetic anti-tuberculosis drugs - narrow spectrum of action (mycobacterium tuberculosis only, sometimes mycobacterium leprosy)

Antibiotics used to treat tuberculosis - broad spectrum (many MBs)

219. The difference between the spectrum of action of synthetic anti-tuberculosis drugs and antibiotics used to treat tuberculosis.

Synthetic anti-tuberculosis drugs affect only Mycobacterium tuberculosis and sometimes Mycobacterium leprosy, while antibiotics used to treat tuberculosis are characterized by a wide spectrum of antimicrobial activity.

220. Name the spectrum of action of synthetic anti-tuberculosis drugs.

Effective only against Mycobacterium tuberculosis, some compounds are effective against Mycobacterium leprosy. Other MBs are practically unaffected.

221. Name the spectrum of action of anti-tuberculosis antibiotics.

Broad spectrum of antimicrobial activity.

222. The mechanism of action of isoniazid.

Inhibition of enzymes necessary for the synthesis of mycolic acids in the cell wall of mycobacteria.

223. The mechanism of action of ethambutol.

1. Inhibits enzymes involved in the synthesis of the cell wall of mycobacteria, has a bacteriostatic effect.

2. Inhibits the synthesis of RNA of mycobacteria.

224. The mechanism of action of pyrazinamide.

The mechanism of action is not exactly known, but the most important condition for its antimicrobial activity is the conversion to pyrazinocarboxylic acid. It acts mainly bacteriostatically, has sterilizing properties.

225. Why can treatment with isoniazid be complicated by polyneuritis?

Pyridoxine is an inhibitor of the formation of pyridoxal phosphate, which is necessary for the conversion of AA, as a result of which polyneuritis may develop.

226. What drugs should be prescribed for the prevention of polyneuritis in the treatment with isoniazid.

For the prevention of polyneuritis, it is imperative to take pyridoxine in a daily dose of 60-100 mg. It is also recommended to take glutamic acid, thiamine.

227. What anti-tuberculosis drugs are used to treat leprosy.

Dapsone, clofazimine, rifampicin

228. Features of tuberculosis chemoprophylaxis in infected and uninfected individuals.

In uninfected persons, primary prophylaxis is carried out with BCG vaccine; in infected persons, secondary prophylaxis is carried out with one drug ( Isoniazid) in a short course, if there are no clinical and radiological manifestations of tuberculosis.

229. Primary chemoprevention of tuberculosis. Who to spend? How?

Primary chemoprophylaxis of tuberculosis is the use of anti-tuberculosis drugs in people with a negative reaction to tuberculin. It is carried out for newborns (the first 2 months of life without a preliminary reaction to tuberculin), children (with a negative or doubtful reaction to tuberculin) and persons from foci of tuberculosis infection. The BCG vaccine or its variety (BCG-M) is used

230. Secondary prevention of tuberculosis. Who to spend? How?

Secondary chemoprophylaxis of tuberculosis is the use of anti-tuberculosis drugs in infected individuals who do not have clinical and radiological manifestations of tuberculosis.

Isoniazid is used in a short course, which must be taken regularly.

231. What is the difference between primary and secondary tuberculosis chemotherapy.

Primary chemotherapy- chemotherapy for newly diagnosed patients with tuberculosis.

Secondary chemotherapy- chemotherapy of patients previously treated with anti-tuberculosis drugs.

232. What is the difference between chemoprevention and treatment of tuberculosis?

Chemoprophylaxis is aimed at preventing the appearance of clinical and radiological manifestations of tuberculosis, and treatment is aimed at slowing down their progression and eliminating them.

233. Principles of treatment of tuberculosis.

1) Treatment should start as soon as possible when there are still no morphological changes in the organs

2) Regularity of reception

3) long(course up to 18 months) continuous(strict adherence to the drug regimen) treatment

4) Stages of treatment(main course - 2 stages: 1) intensive treatment for translation open form closed, elimination of decay cavities; 2) consolidation of the achieved results, prevention of relapses)

5) Continuity of treatment at various stages: as a rule, the sequence of treatment is as follows: hospital (or day hospital) -” sanatorium -” ambulatory treatment -” dispensary observation with anti-relapse courses

6) Combination of drugs(up to 6 according to WHO, the use of isoniazid is mandatory; doses of drugs are usually not reduced; drugs with the same side effects cannot be combined)

7) Individual approach to the patient

234. Duration of a standard course of tuberculosis treatment.

6-18 months (average 1 year)

235. What determines and how does the duration of tuberculosis treatment change?

The optimal timing of chemotherapy is determined The form of tuberculosis, the effectiveness of treatment and range from 6 to 18 months (average 1 year).

Premature and early termination of treatment leads to exacerbations and relapses of the tuberculous process. In patients with untimely detected and neglected (hyperchronic) forms of tuberculosis, chemotherapy is Run for several years.

236. "Short" course of tuberculosis treatment recommended by WHO. Its rationale and duration.

DOTS (Directly Observed Tuberculosis Treatment Short Course) is a multi-targeted comprehensive TB control strategy proposed by WHO and the International Union Against Tuberculosis and Lung Disease.

DOTS provides:

ü political and financial support from the government for the TB program;

ü detection of tuberculosis by sputum examination in all patients who applied with symptoms suggestive of tuberculosis;

the standard course of treatment Within 6-8 months with direct control over medication;

ü regular and uninterrupted provision of all essential anti-tuberculosis drugs;

ü registration and reporting to evaluate the results of treatment for each patient and the TB program as a whole

DOTS allows:

ü reduce the "storage" of infection, the risk of contracting and getting sick with tuberculosis

ü stop the increase in the number of chronic patients with resistant forms of tuberculosis, reducing the increase in mortality and morbidity

237. What is the difference between standard and "short" (recommended by WHO) course of tuberculosis treatment?

1) in the terms of chemotherapy (standard course 6-18 months, "short" - 6-8 months)

2) in the specifics of the "short" course program (direct control of the doctor over medication)

238. Principles of combination of anti-tuberculosis drugs.

ü a combination of 2-3 drugs is desirable (up to 6 according to WHO)

Isoniazid must be used

Doses of drugs in combination are not reduced

Do not combine drugs with the same side effects

239. Name combined preparations for the treatment of tuberculosis.

Rifater (rifampicin + isoniazid + pyrazinamide), rifakom (isoniazid + pyridoxine)

240. Rifampicin, rifabutin. Comparative characteristics their antimycobacterial activity.

Rifampicin is a broad-spectrum antibiotic that is effective against:

A) Mycobacterium tuberculosis, atypical mycobacteria of various types

B) Gr+ cocci (methicillin-resistant staphylococci, multi-resistant pneumococci)

C) Gr - cocci (gonococci, meningococci)

D) Gr - sticks ( H. influenzae, legionella, rickettsia)

Rifabutin - a derivative of natural rifampicin - in contrast to it:

A) is active against some strains of Mycobacterium tuberculosis resistant to rifampicin

B) more active against atypical mycobacteria (complex M. avium-intracellulare, M. fortuitum)

In terms of other characteristics of antimicrobial action, it is close to rifampicin.

241. Side effects of isoniazid.

A) hepatotoxicity: temporary asymptomatic increase in transaminase activity, rarely hepatitis

B) neurotoxicity: irritability, insomnia, tremor, difficulty urinating, rarely - encephalopathy, memory impairment, psychosis, depression, anxiety, peripheral polyneuropathy, optic nerve damage
c) hypersensitivity reactions: fever, flu-like syndrome, rash, eosinophilia, arthropathy, pancreatitis

D) hematotoxicity: sideroblastic anemia, sometimes thrombocytopenia, agranulocytosis

D) endocrine disorders: gynecomastia, dysmenorrhea, cushingoid

242. Side effects of ethambutol.

A) optic neuritis, peripheral neuropathies

B) hypersensitivity reactions - dermatitis, arthralgia, fever

C) a metallic taste in the mouth

D) dyspeptic disorders

243. Side effects of pyrazinamide.

A) dyspepsia: nausea and vomiting

B) hepatotoxicity: increased activity of transaminases

C) nephrotoxicity: interstitial nephritis

D) hyperuricemia, accompanied by arthralgia and myalgia (the main metabolite - pyrazinoic acid - inhibits renal excretion of uric acid)

D) hematotoxicity - thrombocytopenia, sideroblastic anemia.

244. Side effects of rifampicin.

A) dyspeptic and dyspeptic phenomena

B) staining of urine, saliva and lacrimal fluid in an orange-red color

C) hepatotoxicity (up to the development of hepatitis)

D) hematotoxicity: thrombocytopenia, hemolytic anemia

D) flu-like syndrome (fever, arthralgia, myalgia

245. Prevention of side effects of anti-tuberculosis drugs

ü the introduction of vitamins B1, B6, B12, C

ü fractional prescription of the drug or its cancellation for a short time

ü the use of bismuth preparations to reduce irritation of the gastrointestinal mucosa

ü the introduction of glutamic acid, antihistamines, calcium preparations to prevent allergic reactions

avoid the use of drugs that are incompatible with anti-tuberculosis drugs

ü monitoring of the functional state of body systems, which are affected by the drugs used

246. Antifungals, definition.

Antifungal agents are drugs used to prevent and treat fungal infections.

247. Principles of therapy of mycoses.

1) the drug is selected taking into account the sensitivity of the fungus

2) the most effective dose of the antifungal agent is applied

3) continuous treatment until the effect is achieved

4) combination of local and resorptive (systemic) treatment

5) complexity of treatment

6) the result of treatment is determined using mycotic analysis

7) with a persistent course of the disease, change the drug once every 12 weeks

248. Name antifungal antibiotics.

Polyene antibiotics ( Amphotericin B, nystatin) Griseofulvin

249. Name antifungal polyene antibiotics.

Amphotericin B, nystatin

250. What is the significance of the polyene structure of antibiotics for the manifestation of antifungal activity.

Polyene AB molecules contain a) a lipophilic polyene part and b) a hydrophilic part.

The lipophilic part interacts with the fungal cell membrane ergosterol and forms a ring, inside which the hydrophilic part of the molecule forms a channel. Through this channel, ions and macromolecules are removed from the cell.

251. The mechanism of action of polyene antibiotics.

AB + ergosterol fungal cell membrane ® formation of pores in membranes ® loss of cellular macromolecules and ions, irreversible damage to membranes.

252. Mechanism of action of griseofulvin.

Not fully elucidated, two mechanisms are suggested:

1) griseofulvin binds to the tubulin protein of microtubules of fungi, preventing the growth and division of their cells

2) griseofulvin disrupts the synthesis and polymerization of fungal nucleic acids

253. Mechanism of antifungal action of azoles.

Violate the synthesis of ergosterol at one of the intermediate stages (inhibit lanosterol-14-demethylase)

254. Can fungi develop resistance to antifungal drugs?

Perhaps, for example, when using polyene ABs, the content of ergosterol in the cell membrane of fungi decreases or its structure is modified, as a result, these ABs bind to the membrane to a limited extent or practically do not bind.

255. Name antifungal agents - imidazole derivatives for local action.

Clotrimazole, Bifonazole (Mycospor), Econazole

256. Name antifungal agents - imidazole derivatives for systemic and local action.

Ketoconazole, miconazole

257. Name derivatives of triazole.

fluconazole, itraconazole

258. Terbinafine, features of action and application.

Terbinafen disrupts the initial stage of ergosterol synthesis in the cell membrane of fungi (inhibits squalene epoxidase).

When ingested, it is well absorbed, quickly accumulates in the stratum corneum of the skin and its appendages (hair, nails).

Apply once a day inside and topically (in the form of a solution, cream, spray) for dermatomycosis, superficial candidomycosis, onychomycosis (nail lesions).

259. Nystatin, features of action and application.

Nystatin - highly toxic, applied only topically in the form of ointments; when taken orally, it also acts locally, since it is not absorbed in the lumen of the gastrointestinal tract.

Applied topically in the form of an ointment for candidiasis of the skin, mucous membranes of the mouth ("thrush"), genitals and inside for the prevention and treatment of intestinal candidiasis.

260. What fungi can be affected by penicillins and tetracyclines?

Penicillins and tetracyclines are active against actinomycetes.

261. At what mycosis are sulfonamides and streptomycin effective?

Sulfonamides and streptomycin are active against actinomycetes.

But! Fungal diseases are a contraindication for the appointment of AB, the use of AB, on the contrary, often provokes the growth of fungi (of the genus Candida)

262. Why are systemic and especially deep mycoses difficult to treat?

Systemic and deep mycoses occur with widespread damage to internal organs, accompanied by a septic-like condition and immunosuppression, which makes their therapy difficult and sometimes impossible.

263. Why are keratolytic, depilatory agents used together with antifungal agents?

Keratolytic, depilatory agents are used to dissolve and remove old nail plates and crusts along with mycelium, which contributes to rapid healing affected surfaces and more effective treatment.

264. Mechanism of action and application of ciclopirox.

Cyclopirox inhibits the capture of precursors (precursors) of the synthesis of macromolecules by acting on the cell membrane of fungi.

Application: topically in the form of a cream and solution for dermatomycosis, superficial candidomycosis, in the form of nail polish for onychomycosis.

265. Which pathogens are most sensitive to polyene antibiotics: yeast-like fungi, pathogens of deep mycoses (coccidia, histoplasma, cryptococci, sporotrichia), mold fungi, dermatophytes?

Yeast-like fungi, pathogens of deep mycoses (coccidia, histoplasma, etc.)

266. Which pathogens are less sensitive to polyene antibiotics: yeast-like fungi, pathogens of deep mycoses (coccidia, histoplasma, cryptococci, sporotrichia), mold fungi, dermatophytes?

Molds (less sensitive), dermatophytes (not sensitive)

267. What protozoa are inhibited by polyene antibiotics?

Trichomonas, Leishmania, some amoeba

268. How does the toxicity of polyene antibiotics change depending on the route of administration?

The toxicity of polyenes is minimal when applied topically and orally (because they are not absorbed in the lumen of the gastrointestinal tract) and quite high when administered intravenously (although polyenes are most effective with this method of administration).

P. S. For help in preparing the work, we thank the team of authors: lecturers of the Department of Pharmacology of the Belarusian State Medical University, Kharkevich D. A., Katzung B. G., Kukes V. G., Starodubtsev A. K., Mashkovsky M. D., authors of the Vidal Handbook. Medications in Russia”, Yu. B. Belousov, V. V. Maisky, M. I. Perelman, et al. (“Tuberculosis”), L. S. Strachunsky and S. N. Kozlov (“Antibiotics: Clinical Pharmacology. A Guide for Physicians ”), etc. SPECIAL THANKS to the almighty Internet, which is always ready to help out in difficult situations, and the Department of Skin and Venereal Diseases, which gladly comes to the aid of students in mastering chemotherapy issues.

We have tried to make these works as easy to understand and study as possible, while maintaining Modern level of pharmacological knowledge. Good luck with your study!

Recipe for the colloquium "Chemotherapeutic drugs"

Rp.: Azithromycini 0.5

D.t.d. No. 10 in tab.

S. One tablet by mouth once a day.

Rp.: Azithromycini 0.25

D.t.d. N.10 in caps.

S. Take two capsules by mouth once a day.

Rp.: Amikacini sulfatis 0.5

S. Dissolve the contents of the vial in 2 ml of sterile water for injection. Intramuscularly 0.5 three times a day.

Rp.: Amoxicillini 0.5

D.t.d. No. 20 in tab.

Rp.: Amoxicillini 0.5

D.t.d. No. 20 in tab. obd.

S. Inside 1 tablet 3 times a day

Rp.: Amoxicillini 0.5

D.t.d. N. 20 in caps.

Rp.: Sol. Amoxicillini 10% - 1 ml

D.S. Inside 1 ml 3 times a day

Rp.: Suspensionis Amoxicillini 5% – 5 ml

D.S. Inside, 1 teaspoon 3 times a day

Rp.: Acicloviri 0.25

S. Dissolve the contents of the vial in 10 ml of isotonic NaCl solution. Intravenously, 5 mg/kg three times a day.

Rp.: Acicloviri 0.2

D.t.d. No. 20 in tab.

S. 1 tablet by mouth five times a day

Rp.: Ung. Acicloviri 3% - 5.0

D.S. Place in the conjunctival sac every 4 hours.

Rp.: Benzylpenicillinum sodium 500.000 ED

S. Dilute the contents of the vial in 2 ml of 0.25% novocaine solution. Inject intramuscularly at 500,000 IU 4 times a day.

Rp.: Benzylpenicillin-Benzatini 600.000 ED

S. Dilute the contents of the vial in 2 ml of 0.25% novocaine solution. Administer intramuscularly at 600,000 IU once every two weeks.

Rp.: Sol. Gentamycini sulfatis 4% - 2 ml

D.t.d. N. 10 in amp.

S. Intramuscularly 2 ml 3 times a day

Rp.: Ung. Gentamycini sulfatis 0.1% - 10.0

D.S. Apply to damaged skin 3 times a day

Rp.: Sol. Gentamycini sulfatis 0.3% - 10 ml

D.S. Instill in the eye one drop 3 times a day

D.t.d. N. 10 in caps.

Rp.: Doxycyclini hydrochloridi 0.1

D.t.d. No. 10 in tab. obd.

S. Inside, 1 capsule 1 time per day.

Rp.: Doxycyclini hydrochloride 0.1

D.t.d. N. 10 in amp.

S. Dissolve the contents of the ampoule in 100 ml of isotonic NaCl solution. Enter intravenously at 0.1 once a day.

Rp.: Zidovudini 0.1

D.t.d. N. 10 in caps.

S. Oral 2 capsules 6 times a day

Rp.: Isoniazidi 0.1

D.t.d. No. 20 in tab.

S. One tablet twice a day.

Rp.: Sol. Isoniazidi 10% - 5 ml

D.t.d. N. 20 in amp.

S. Intramuscularly, 5 ml once a day.

Rp.: Sol. Idoxuridini 0.1% - 10 ml

D.S. Instill two drops into the conjunctival sac every hour during the day and every two hours at night.

Rp.: Tienam 0.75

S. Pre-dilute the bottle with 10 ml of solvent, shake, add 100 ml of 0.9% NaCl solution. Administer intravenously in drops of 0.75 every 6 hours.

NB! Tienam - a combination drug containing Imipenem and Cilastatin

Rp.: Clindamycini 0.15

D.t.d. N. 20 in caps.

S. Inside 1 capsule 4 times a day

Rp.: Sol. Clindamycini 15% - 6 ml

D.t.d. N. 20 in amp.

S. Intramuscularly 6 ml once a day.

Rp.: Metronidazoli 0.5

D.t.d. No. 10 in tab.

Rp.: Supp. cum Metronidazolo 0.5

S. Intravaginally 2 times a day

Rp.: Sol. Metronidazoli 0.5% - 100 ml

D. S. Intravenous drip 100 ml once a day

Rep.: Tab. Nystatini obd. 250,000 units N. 40

D.S. 2 tablets 3 times a day

Rp.: Supp. cum Nystatino 500.000 ED

S. Intravaginally 1 suppository 2 times a day

Rp.: Ung. Nystatino 100.000 ED - 1.0

D.S. Apply to affected areas 2 times a day.

Rp.: Oxacillinum sodium 0.25

S. Pre-dilute the contents of the vial with the solvent supplied in the package. Enter intramuscularly at 0.25 four times a day.

Rp.: Ofloxacini 0.2

D.t.d. No. 20 in tab.

S. Inside 1 tablet 2 times a day

Rp.: Piperacillini 2.0

S. Dilute the contents of the vial in isotonic solution NaCl. Enter intramuscularly at 2.0 every 6 hours.

Rp.: Acidi pipemidici 0.1

D.t.d. N. 20 in caps.

S. Inside 2 capsules 2 times a day

Rp.: Acidi pipemidici 0.4

D.t.d. No. 10 in tab.

S. Inside 1 tablet 2 times a day

Rp.: Supp. cum Acido pipemidico 0.2

S. Intravaginally 1 suppository twice a day.

Rp.: Remantadini 0.05

D.t.d. No. 20 in tab.

S. Inside 2 tablets 2 times a day

Rp.: Rifampicini 0.15

D.t.d. N. 20 in caps.

S. Inside 2 capsules 1 time per day

Rp.: Rifampicini 0.15

D.t.d. N. 10 in amp.

S. Dilute the contents of the ampoule in 3 ml of sterile water for injection, shake, then in 125 ml of 5% glucose solution. Administer intravenously in drops of 0.15 once a day

Rp.: Streptomycini sulfatis 0.5

S. Dissolve the contents of the vial in 5 ml of isotonic NaCl solution. Enter intramuscularly at 0.5 twice a day.

Rp.: Sol. Sulfacetamidum-natrii 30% - 5 ml

D.t.d. N. 10 in amp.

Rp.: Sol. Sulfacetamidum-natrii 30% - 10 ml

S. Inject slowly 5 ml intravenously 2 times a day.

Rp.: Sol. Sulfacetamidum-natrii 20% - 1.5 ml

D. S. Instill into the conjunctival sac 2 drops 3 times a day

Rp.: Ung. Sulfacetamidum-natrii 30% - 10.0

D. S. Put in the conjunctival sac 2 times a day

Rp.: Terbinafini 0.25

D.t.d. No. 10 in tab.

S. 1 tablet 1 time per day

Rp.: Ung. Terbinafini 1% - 30.0

D.S. Apply to affected areas 2 times a day

Rp.: Tetracyclini 0.1 (100.000 ED)

D.t.d. No. 20 in tab.

S. Inside 1 tablet 3 times a day

Rp.: Ung. Tetracuslini 10, 0

D.S. Lay behind the lower eyelid 5 times a day

Rp.: Ung. Tetracuslini 3% - 10.0

D.S. Apply to affected areas 3 times a day.

Rp.: Chloramphenicoli 0.25

D.t.d. No. 10 in tab.

S. Inside 1 tablet 3 times a day

Rp.: Chloramphenicoli 0.25

D.t.d. No. 10 in tab. obd.

S. Inside 1 tablet 3 times a day

Rp.: Chloramphenicoli 0.25

D.t.d. N. 20 in caps.

S. Inside 1 capsule 3 times a day

Rp.: Sol. Chloramphenicoli 0.25% - 10.0 ml

D. S. In the conjunctival sac 1 drop 3 times a day

Rp.: Chlorochini 0.25

D.t.d. No. 20 in tab.

S. 2 tablets by mouth every 6 hours

Rp.: Sol. Chlorochini 5% – 5 ml

D.t.d. N. 20 in amp.

S. Intramuscularly 5 ml 4 times a day

Rp.: Cefaclori 0.5

D.t.d. N. 10 in caps.

S. Inside, 1 capsule 3 times a day.

Rp.: Suspensionis Cefaclori 5% – 5 ml

D.S. 5 ml orally 3 times a day

Rp.: Ceftazidimi 0.5

S. The contents of the vial must first be diluted in isotonic NaCl solution. Administer intramuscularly every 8 hours at 1.0

Rp.: Ciprofloxacini 0.25

D.t.d. No. 10 in tab. obd.

S. Inside 1 tablet 2 times a day

Rp.: Sol. Ciprofloxacini 0.2% - 50 ml

D. S. Intravenous drip 50 ml 2 times a day

Rp.: Sol. Ciprofloxacini 1% - 10 ml

D.t.d. N. 10 in amp.

S. Administer intravenously by bolus 10 ml 3 times a day

Rp.: Erythromycini 0.25

D.t.d. No. 20 in tab.

S. Inside, 1 tablet 4 times a day.

Rp.: Ung. Erythromycini 1% - 10.0

D.S. Apply to affected areas 2 times a day. If eye ointment - in the conjunctival sac 2 times a day.

Rep.: Tab. “Co-Trimoxazole” N. 20

D.S. Inside, 2 tablets 2 times a day.

Rp.: Suspensionis Co-Trimaxazoli 4% – 480 ml

D.S. Inside 5 ml 3 times a day

Rp.: Sol. Co-Trimoxazoli 8% - 3 ml

D.t.d. N. 20 in amp.

S. Intramuscularly, 3 ml 2 times a day.

Rp.: Nitrofurantoini 0.1

D.t.d. No. 20 in tab.

S. Inside 1 tablet 3 times a day

Rp.: Fluconazoli 0.02

D.t.d. N. 10 in caps.

S. Inside 1 capsule 3 times a day

The bactericidal action is characterized by the fact that under the influence of an antibiotic, the death of microorganisms occurs. With bacteriostatic action, the death of microorganisms does not occur, only the cessation of their growth and reproduction is observed.

11. What methods determine the sensitivity of microorganisms to antibiotics?

Determining the sensitivity of bacteria to antibiotics:

1. Diffusion methods

Using antibiotic discs

With the help of E-tests

2. Breeding methods

Breeding in a liquid nutrient medium (broth)

Breeding in agar

12. What is the diameter of the zone of growth inhibition of a microorganism, sensitively
go to the antibiotic?

Zones, the diameter of which does not exceed 15 mm, indicate a weak sensitivity to the antibiotic. Zones from 15 to 25 mm are found in sensitive microbes. Highly sensitive microbes are characterized by zones with a diameter of more than 25 mm.

13. What diameter of the zone of growth inhibition indicates the absence of sensitivity of the microorganism to it?

The absence of microbial growth inhibition indicates the resistance of the microbe under study to this antibiotic.

14. Classify antibiotics by chemical composition.

β-lactams (penicillins, cephalosporins, carbapenems, monobactams);

Glycopeptides;

Lipopeptides;

Aminoglycosides;

Tetracyclines (and glycylcyclines);

macrolides (and azalides);

Lincosamides;

Chloramphenicol / levomycetin;

Rifamycins;

Polypeptides;

Polyenes;

Various antibiotics (fusidic acid, fusafungine, streptogramins, etc.).

15. How do antibiotics differ in their spectrum of action?

Broad-spectrum antibiotics - act on many pathogens (for example, tetracycline antibiotics, a number of macrolide drugs, aminoglycosides).

Narrow-spectrum antibiotics - affect a limited number of pathogenic species (for example, penicillins act mainly on Gram + microorganisms).

16. List several broad-spectrum antibiotics.

Antibiotics of the penicillin group: Amoxicillin, Ampicillin, Ticarcycline;

Antibiotics of the tetracycline group: Tetracycline;

Fluoroquinolones: Levofloxacin, Gatifloxacin, Moxifloxacin, Ciprofloxacin;

Aminoglycosides: Streptomycin;

Amphenicols: Chloramphenicol (Levomycetin); Carbapenems: Imipenem, Meropenem, Ertapenem.

17. Describe the methods of obtaining antibiotics.

According to the method of obtaining antibiotics are divided:

on natural;

Synthetic;

semi-synthetic (at the initial stage, they are obtained naturally, then the synthesis is carried out artificially).

18. How antibiotics of the 1st, 2nd, 3rd and subsequent are obtained
generations?

The main ways to obtain antibiotics:

Biological synthesis (used to obtain natural antibiotics). In the conditions of specialized industries, microbes-producers are cultivated, which secrete antibiotics in the course of their life;

Biosynthesis with subsequent chemical modifications (used to create semi-synthetic antibiotics). First, a natural antibiotic is obtained by biosynthesis, and then its molecule is changed by chemical modifications, for example, certain radicals are attached, as a result of which the antimicrobial and pharmacological properties of the drug are improved;

Chemical synthesis (used to obtain synthetic analogues of natural antibiotics). These are substances that have the same structure as a natural antibiotic, but their molecules are synthesized chemically.

19. Name some antifungal antibiotics.

Nystatin, levorin, natamycin, amphotericin B, mycoheptin, miconazole, ketoconazole, isoconazole, clotrimazole, econazole, bifonazole, oxiconazole, butoconazole

20. The action of what antibiotics leads to the formation of L-forms of bacteria?

L-forms - bacteria, partially or completely devoid of a cell wall, but retaining the ability to develop. L-forms arise spontaneously or induced - under the influence of agents that block cell wall synthesis: antibiotics (penicillins, cycloserine, cephalosporins, vancomycin, streptomycin).

21. Specify the sequence of the main stages of obtaining antibiotics
from natural producers.

selection of high-performance producer strains (up to 45 thousand units/ml)

choice of nutrient medium;

The biosynthetic process

isolation of the antibiotic from the culture fluid;

antibiotic purification.

22. Name the complications that most often occur in the macroorganism during antibiotic treatment.

Toxic effect of drugs.

Dysbiosis (dysbacteriosis).

Negative effect on the immune system.

Endotoxic shock (therapeutic).

23. What changes occur in a microorganism when exposed to
antibiotics?

The nature of the action of antibiotic substances is diverse. Some of them retard the growth and development of microorganisms, others cause their death. According to the mechanism of action on the microbial cell, antibiotics are divided into two groups:

Antibiotics that disrupt the function of the microbial cell wall;

Antibiotics that affect the synthesis of RNA and DNA or proteins in a microbial cell.

Antibiotics of the first group mainly affect the biochemical reactions of the microbial cell wall. Antibiotics of the second group affect metabolic processes in the microbial cell itself.

24. With what forms of variability is the emergence of resistant forms associated
microorganisms?

Under the resistance (resistance) understand the ability of a microorganism to tolerate significantly higher concentrations of the drug than other microorganisms of a given strain (species).

Resistant strains of microorganisms arise when the genome of a bacterial cell changes as a result of spontaneous mutations.

During the selection process, as a result of exposure to chemotherapeutic compounds, sensitive microorganisms die, while resistant microorganisms persist, multiply and spread in environment. Acquired resistance is fixed and inherited by subsequent generations of bacteria.

25. In what ways does the microorganism protect itself from the effects of antibiotics?

Often, bacterial cells survive after the use of antibiotics. This is explained by the fact that bacterial cells can go into a dormant state or a state of rest, thereby avoiding the action of drugs. The dormant state occurs as a result of the action of a bacterial toxin, which is secreted by bacterial cells and deactivates cellular processes such as protein synthesis and energy production of the cell itself.

26. What role does penicillinase play?

Penicillinase is an enzyme that has the ability to break down (inactivate) β-lactam antibiotics (penicillins and cephalosporins).

Penicillinase is formed by certain types of bacteria that, in the process of evolution, have developed the ability to suppress penicillin and other antibiotics. In this regard, resistance of such bacteria to antibiotics is noted.

27. What is "efflux"?

Efflux is a mechanism of antimicrobial resistance, which consists in the active removal of antibiotics from the microbial cell due to the activation of stress defense mechanisms.

28. Name the plasmids involved in the formation of antibiotic resistance
stent microorganisms.

Plasmids perform regulatory or coding functions.

Regulatory plasmids are involved in compensating for certain defects in the metabolism of a bacterial cell by inserting into the damaged genome and restoring its functions.

Coding plasmids bring new genetic information into the bacterial cell, encoding new, unusual properties For example, resistance to

antibiotics.

29. List the ways to overcome the antibiotic resistance of microorganisms.

The main ways to overcome the resistance of microorganisms to antibiotics:

Research and introduction into practice of new antibiotics, as well as obtaining derivatives of known antibiotics;

The use for the treatment of not one, but simultaneously several antibiotics with a different mechanism of action;

The use of a combination of antibiotics with other chemotherapy drugs;

Suppression of the action of enzymes that destroy antibiotics (for example, the action of penicillinase can be suppressed with crystal violet);

Freeing resistant bacteria from multidrug resistance factors (R-factors), for which some dyes can be used.

30. How is the development of candidomycosis prevented in patients with
treatment with broad-spectrum antibiotics.

Along with antibiotics, antifungal drugs are prescribed, such as nystatin, miconazole, clotrimazole, polygynax, etc.