Requirements for the main narcotic substances used for general anesthesia.
They must have a greater breadth of therapeutic action, that is, doses that induce narcotic sleep must be far removed from doses that paralyze vital centers.
Must have a sufficient narcotic effect, allowing anesthesia with low concentrations of vapors or gas with a high oxygen content in the inhaled mixture when administered via inhalation.
Do not provide harmful influence on breathing and blood circulation, metabolism and parenchymal organs (liver, kidneys).
They should have a short period of induction of anesthesia, without a stage of excitement and without unpleasant subjective sensations for the patient.
Do not provide irritating effect on the mucous membranes of the airways.
Must have an elimination rate that ensures easy management of anesthesia and rapid awakening from narcotic sleep.
They must be cheap, stable during storage, explosion- and fireproof, and convenient for transportation.
Classification.
Anesthetics are divided into inhalation and non-inhalation.
Inhalation are divided into:
volatile liquids (ether, fluorotane, etc.).
gaseous (nitrous oxide, cyclopropane, etc.).
Non-inhalational anesthetics are divided into:
barbiturates (hexenal, sodium thiopental, sodium methohexital).
Non-barbituric drugs (Viadril, ketamine, sodium hydroxybutyrate, propofol, etomidate, altesin).
Characteristics of the drugs will be given when considering the types of anesthesia.
Inhalation anesthesia
Inhalation anesthesia is the administration of anesthetics through Airways in the form of vapors or gases. This type of anesthesia has several advantages. The main one is good control over the level of anesthesia. Inhalation anesthesia can be performed using mask, endotracheal and endobronchial methods.
Preparations for inhalation anesthesia. Liquid inhalational anesthetics
Ether – ethyl or diethyl ether. Colorless volatile liquid with a peculiar odor. The specific gravity of the ether is 0.714--.715 g/ml. Boiling point 34-35С. Highly soluble in fats and alcohol. 1 ml of liquid ether gives 230 ml of steam upon evaporation. Explosive, vapors burn well. It is stored in tightly sealed dark bottles, as it decomposes in light to form harmful products that irritate the respiratory tract. For anesthesia, specially purified ether (Aether pro narcosi) is used. It has a sufficient breadth of therapeutic action and a strong narcotic effect. Excreted from the body through the lungs.
Negative properties. Poorly tolerated by patients; prolonged sleep and awakening; the stage of excitement is expressed; stimulates the sympathetic-adrenal system; irritates the mucous membranes of the respiratory tract, causing an increase in the secretion of the bronchial glands; toxic to parenchymal organs; is eliminated from the body rather slowly; Nausea and vomiting are often observed.
Ftorotan (halothane, fluotane, narcotan)- transparent colorless liquid with a mild sweetish odor. Boiling point 50.2 °C. Highly soluble in fats. Explosion-proof. Stored in dark bottles. It has a powerful narcotic effect: approximately 4-5 times more powerful than ether, causes a rapid onset of anesthesia (3-4 minutes), with a pleasant sleep, practically without an excitation phase and quick awakening. Ftorotan does not irritate the mucous membranes of the respiratory tract, so it can be used in patients with respiratory diseases, and is quickly eliminated from the body. Fluorothane anesthesia is well controlled. A negative property is the small breadth of pharmacological action. In case of overdose, cardiovascular activity is inhibited, decreased arterial pressure. Toxic to the liver. Ftorotan increases the sensitivity of the heart muscle to adrenaline and norepinephrine, and therefore these drugs should not be used during anesthesia with Ftorotan.
Methoxyflurane (pentran, inhalan)– colorless clear liquid with a characteristic fruity smell. Boiling point 104°C, non-explosive. It has a powerful narcotic effect, stronger than ether. Narcotic sleep occurs slowly, after 8-10 minutes. A pronounced stage of excitation is characteristic; awakening occurs slowly. It has minimal toxic effects on the body. However, prolonged anesthesia and large doses have a negative effect on the heart, respiratory system and kidneys. Increases the sensitivity of the myocardium to adrenaline and norepinephrine.
Trilene- transparent liquid with pungent odor. Boiling point 87.5˚C. Not explosive. It decomposes in light, so it is stored in dark bottles. Has a pronounced analgesic effect. A negative property is the narrow range between the narcotic and therapeutic dose. Therefore it should not be used when long operations. In high concentrations, it reduces breathing and causes disturbances heart rate. Increases the sensitivity of the myocardium to adrenaline and norepinephrine.
Enflurane (ethrane) - clear, colorless liquid with a pleasant odor. Does not ignite. Has a powerful narcotic effect. Calls rapid attack narcotic sleep and rapid awakening. It has a good muscle relaxant effect, does not depress cardiac activity and respiration, and does not cause arrhythmia even at high concentrations of adrenaline and norepinephrine. The hepatotoxic effect is less than that of fluorotane. Is a good alternative to it.
Inhalation anesthetics such as chloroform and chloroethyl are not currently used. At the same time, in recent decades, modern anesthetics such as isoflurane, sevoflurane, desflurane, which have a powerful narcotic effect and less negative impacts on the body.
21. Neurotropic drugs of central action, classification. Anesthesia (general anesthesia) definition, classification of anesthesia; Comparative characteristics drugs for inhalation anesthesia. Means for non-inhalation anesthesia, their comparative characteristics. The concept of combined anesthesia and neuroleptanalgesia.
Neurotropic drugs of central action, classification(?)
Sleeping pills
Antiepileptic drugs
Antiparkinsonian drugs
Painkillers (analgesics)
Analeptics
Neuroleptics
Antidepressants
Anxiolytics
Sedatives
Psychostimulants
Nootropics
Anesthetics
Anesthesia is an insensible, unconscious state caused by anesthetic drugs, which is accompanied by loss of reflexes, decreased tone of skeletal muscles, but at the same time the functions of the respiratory, vasomotor centers and heart function remain at a level sufficient to prolong life. Anesthetic drugs are administered by inhalation and non-inhalation routes (into a vein, muscle, rectally). Inhalation anesthetic agents must satisfy a number of requirements: rapid onset of anesthesia and rapid recovery from it without discomfort; ability to control the depth of anesthesia; adequate relaxation of skeletal muscles; wide range of anesthetic action, minimal toxic effects.
Anesthesia is caused by substances of various chemical structures - monatomic inert gases (xenon), simple inorganic (nitrous oxide) and organic (chloroform) compounds, complex organic molecules(haloalkanes, ethers).
Mechanism of action of inhalation anestheticsGeneral anesthetics change the physicochemical properties of neuronal membrane lipids and disrupt the interaction of lipids with ion channel proteins. At the same time, the transport of sodium ions into neurons is reduced, the output of less hydrated potassium ions is maintained, and the permeability of chlorine channels controlled by GABA A receptors increases by 1.5 times. The result of these effects is hyperpolarization with increased inhibition processes. General anesthetics suppress the entry of calcium ions into neurons by blocking H-cholinergic receptors and NMDA-glutamic acid receptors; reduce the mobility of Ca 2+ in the membrane, therefore preventing the calcium-dependent release of excitatory neurotransmitters. The classic four stages of anesthesia are caused by ether:
Analgesia(3 - 8 min) Characterized by confusion (poor orientation, incoherent speech), loss of pain, then tactile and temperature sensitivity, at the end of the stage amnesia and loss of consciousness occur (suppression of the cerebral cortex, thalamus, reticular formation). 2. Excitation(delirium; 1 - 3 minutes depending on the individual characteristics of the patient and the qualifications of the anesthesiologist) Incoherent speech, motor restlessness with the patient’s attempts to leave the operating table are observed. Typical symptoms of excitement are hyperventilation, reflex secretion of adrenaline with tachycardia and arterial hypertension (operation is unacceptable.3 . Surgical anesthesia , consisting of 4 levels (occurs 10 - 15 minutes after the start of inhalation. Motion level eyeballs(light anesthesia).Level of corneal reflex (severe anesthesia) The eyeballs are fixed, the pupils are moderately constricted, the corneal, pharyngeal and laryngeal reflexes are lost, skeletal muscle tone is reduced as a result of inhibition spreading to the basal ganglia, brain stem and spinal cord. Level of pupil dilation (deep anesthesia) The pupils dilate, react sluggishly to light, reflexes are lost, skeletal muscle tone is reduced, breathing is shallow, frequent, and becomes diaphragmatic in nature.4. Awakening Functions are restored in the reverse order of their disappearance. IN agonal stage breathing becomes shallow, coordination in the respiratory movements of the intercostal muscles and diaphragm is disrupted, hypoxia progresses, blood becomes dark color, the pupils dilate as much as possible and do not react to light. Blood pressure quickly drops, venous pressure increases, tachycardia develops, and heart contractions weaken. If the anesthesia is not stopped immediately and emergency assistance is not provided, death occurs from paralysis of the respiratory center. Inhalational anesthetics are volatile liquids and gases.
Modern anesthetics - volatile liquids (fluorotane, enflurane, isoflurane, desflurane) are halogen-substituted derivatives of the aliphatic series. Halogens enhance the anesthetic effect. The drugs do not burn, do not explode, and have a high evaporation temperature. Surgical anesthesia begins 3 to 7 minutes after the start of inhalation. Muscle relaxation is significant due to the blockade of H-cholinergic receptors in skeletal muscles. Awakening after anesthesia is rapid (in 10 - 15% of patients, mental disturbances, tremors, nausea, and vomiting are possible). FTOROTANE in the stage of surgical anesthesia, it depresses the respiratory center, reducing its sensitivity to carbon dioxide, hydrogen ions and hypoxic stimuli from the carotid glomeruli (blockade of H-cholinergic receptors). Breathing disorders are caused by strong relaxation of the respiratory muscles. Ftorotan dilates the bronchi as a blocker of H-cholinergic receptors of the parasympathetic ganglia, which is used to relieve severe attacks of bronchial asthma. Ftorotan, by weakening heart contractions, reduces cardiac output by 20 - 50%. The mechanism of the cardiodepressive effect is due to a block in the entry of calcium ions into the myocardium. Ftorotan causes severe bradycardia, as it increases the tone of the center vagus nerve and directly inhibits the automatism of the sinus node (this action is prevented by the introduction of M-anticholinergics). Ftorotan causes severe hypertension due to several mechanisms: it inhibits the vasomotor center; blocks H-cholinergic receptors of the sympathetic ganglia and the adrenal medulla; has an α-adrenergic blocking effect; stimulates the production of the endothelial vasodilator factor - nitric oxide (NO); reduces minute volume of blood. A decrease in blood pressure during fluorotane anesthesia can be used as controlled hypotension, however, in patients with blood loss there is a risk of collapse; during operations on organs with a rich blood supply, bleeding increases. To stop the collapse, the selective α-adrenergic agonist mesaton is injected into the vein. Norepinephrine and adrenaline, which have β-adrenomimetic properties, provoke arrhythmia. Other effects of ftorotane include an increase in coronary and cerebral blood flow, an increase in intracranial pressure, a decrease in oxygen consumption in the brain, despite adequate delivery of oxygen and oxidation substrates in the blood; Fluorotane has hepatotoxicity, as it is converted in the liver into free radicals - initiators of lipid peroxidation, and also forms metabolites (fluoroethanol) that covalently bind to biomacromolecules. The incidence of hepatitis is 1 case per 10,000 anesthesia in adult patients. ENFLURANE And ISOFLURANE Both drugs severely depress breathing (artificial ventilation is required during anesthesia), disrupt gas exchange in the lungs, and dilate the bronchi; cause arterial hypotension; relax the uterus; do not damage the liver and kidneys. DESFLURANE evaporates at room temperature, has pungent odor, severely irritates the respiratory tract (danger of coughing, laryngospasm, reflex respiratory arrest). Depresses breathing, causes arterial hypotension, tachycardia, does not change blood flow in the brain, heart, kidneys, increases intracranial pressure.
GAS NARCASIS Nitrous oxide is a colorless gas, stored in metal cylinders under a pressure of 50 atm in a liquid state, does not burn, but supports combustion, is poorly soluble in the blood, but dissolves well in the lipids of the central nervous system, so anesthesia occurs very quickly. To obtain deep anesthesia, nitrous oxide is combined with inhalational and non-inhalational anesthetics and muscle relaxants. Application: for induction of anesthesia(80% nitrous oxide and 20% oxygen), combined and potentiated anesthesia (60 - 65% nitrous oxide and 35 - 40% oxygen), anesthesia for childbirth, trauma, myocardial infarction, acute pancreatitis (20% nitrous oxide). Contraindicated for hypoxia and severe lung diseases accompanied by impaired gas exchange in the alveoli, with severe pathology nervous system, chronic alcoholism, alcohol intoxication (danger of hallucinations, agitation). Not used for pneumoencephalography and operations in otorhinolaryngology.
Xenoncolorless, does not burn and has no odor, upon contact with the mucous membrane of the mouth creates a bitter sensation on the tongue metallic taste. It is characterized by low viscosity and high solubility in lipids, and is excreted unchanged by the lungs. The mechanism of the anesthetic effect is blockade of cytoreceptors of excitatory neurotransmitters - N-cholinergic receptors, NMDA-glutamic acid receptors, as well as activation of receptors for the inhibitory neurotransmitter glycine. Xenon exhibits antioxidant and immunostimulant properties, reduces the release of hydrocortisone and adrenaline from the adrenal glands. Xenon anesthesia (80%) mixed with oxygen (20%)
Awakening after stopping xenon inhalation is quick and pleasant, regardless of the duration of anesthesia. Xenon does not cause significant changes in pulse or heart contraction force, and at the beginning of inhalation it increases cerebral blood flow. Xenon can be recommended for anesthesia in patients with compromised cardiovascular systems oh, in pediatric surgery, during painful manipulations, dressings, for pain relief during childbirth, relief of painful attacks (angina pectoris, myocardial infarction, renal and hepatic colic). Xenon anesthesia is contraindicated during neurosurgical operations.
Non-inhalation anesthetics are administered into a vein, into muscles and intraosseously .
Non-inhalational anesthetics divided into three groups: Drugs short acting(3 - 5min)
· PROPANIDID(SOMBREVIN)
· PROPOFOL (DIPRIVAN, RECOFOL)
Drugs with medium duration of action (20 - 30 min)
· KETAMINE(CALIPSOL, KETALAR, KETANEST)
· MIDAZOLAM(DORMICUM, FLORMIDAL)
· HEXENAL(HEXOBARBITAL SODIUM)
· THIOPENTAL SODIUM (PENTOTHAL) Long-acting drugs (0.5 - 2 hours)
· SODIUM OXYBUTYRATE
PROPANIDID- ester, by chemical structure close to novocaine. When administered into a vein, it has an anesthetic effect within 3-5 minutes, as it undergoes rapid hydrolysis by blood pseudocholinesterase and is redistributed into adipose tissue. Blocks sodium channels in neuron membranes and disrupts depolarization. It turns off consciousness and in subnarcotic doses has only a weak analgesic effect.
Propanidide selectively stimulates the motor areas of the cortex, therefore causing muscle tension, tremors, and increases spinal reflexes. Activates the vomiting and respiratory centers. During anesthesia with propanidide, hyperventilation is observed in the first 20–30 s, followed by hypocapnia and respiratory arrest for 10–15 s. Weakens heart contractions (to the point of cardiac arrest) and causes arterial hypotension by blocking β - adrenergic receptors of the heart. When prescribing propanidide, there is a risk of allergic reactions due to the release of histamine ( anaphylactic shock, bronchospasm). Possible cross allergy with novocaine.
Propanidide is contraindicated in shock, liver disease, kidney failure, and is used with caution in cases of coronary circulation disorders, heart failure, and arterial hypertension.
PROPOFOL.He is the antagonistNMDA-glutamic acid receptors, enhances GABAergic inhibition, blocks voltage-dependent calcium channels neurons. It has a neuroprotective effect and accelerates the recovery of brain function after hypoxic damage. Inhibits lipid peroxidation, proliferation T-lymphocytes, their release of cytokines, normalizes the production of prostaglandins. The extrahepatic component plays a significant role in the metabolism of propofol; inactive metabolites are excreted by the kidneys.
Propofol induces anesthesia within 30 s. Possible at the injection site strong pain, but phlebitis and thrombosis occur rarely. Propofol is used for induction of anesthesia, maintenance of anesthesia, providing sedation without turning off consciousness in patients undergoing diagnostic procedures and intensive care.
During induction of anesthesia, twitching of skeletal muscles and convulsions sometimes appear, respiratory arrest develops within 30 s, due to a decrease in the sensitivity of the respiratory center to carbon dioxide and acidosis. Oppression of the respiratory center is potentiated by narcotic analgesics. Propofol, by dilating peripheral vessels, short-term reduces blood pressure in 30% of patients. Causes bradycardia, reduces cerebral blood flow and oxygen consumption by brain tissue. Awakening after propofol anesthesia is rapid, convulsions, tremors, hallucinations, asthenia, nausea and vomiting occasionally occur, and intracranial pressure increases.
Propofol is contraindicated in case of allergies, hyperlipidemia, cerebrovascular disorders, pregnancy (it crosses the placenta and causes neonatal depression), and children under one month of age. Anesthesia with propofol is carried out with caution in patients with epilepsy, pathology of the respiratory, cardiovascular systems, liver and kidneys, and hypovolemia.
KETAMINEcauses anesthesia when injected into a vein for 5 - 10 minutes, when injected into muscles - for 30 minutes. There is experience with the epidural use of ketamine, which prolongs the effect up to 10–12 hours. The metabolite of ketamine, norketamine, has an analgesic effect for another 3–4 hours after the end of anesthesia.
Ketamine anesthesia is called dissociative anesthesia: the drugged person has no pain (felt somewhere to the side), consciousness is partially lost, but reflexes are preserved, and the tone of the skeletal muscles increases. The drug disrupts the conduction of impulses along specific and nonspecific pathways to the associative zones of the cortex, in particular, it interrupts thalamo-cortical connections.
The synaptic mechanisms of action of ketamine are diverse. It is a non-competitive antagonist of the excitatory neurotransmitters glutamine and aspartic acid in a relationship NMDA-receptors ( NMDA-N-methyl- D-aspartate). These receptors activate sodium, potassium and calcium channels in neuronal membranes. When receptors are blocked, depolarization is disrupted. In addition, ketamine stimulates the release of enkephalins and β-endorphin; inhibits the neuronal uptake of serotonin and norepinephrine. Last effect manifested by tachycardia, increased blood pressure and intracranial pressure. Ketamine dilates the bronchi.
When recovering from ketamine anesthesia, delirium, hallucinations, and motor agitation are possible (these undesirable phenomena are prevented by the administration of droperidol or tranquilizers).
An important therapeutic effect of ketamine is neuroprotective. As is known, in the first minutes of brain hypoxia, excitatory mediators - glutamic and aspartic acids - are released. Subsequent activation NMDA-receptors, increasing
in the intracellular environment, the concentration of sodium and calcium ions and osmotic pressure cause swelling and death of neurons. Ketamine as an antagonist NMDA-receptors eliminates the overload of neurons with ions and the associated neurological deficit.
Contraindications to the use of ketamine - violations cerebral circulation, arterial hypertension, eclampsia, heart failure, epilepsy and other convulsive diseases.
MIDAZOLAM- a non-inhalation anesthetic with a benzodiazepine structure. When injected into a vein, it causes anesthesia within 15 minutes; when injected into the muscles, the duration of action is 20 minutes. Affects benzodiazepine receptors and allosterically enhances the cooperation of GABA with GABA type receptors A. Like tranquilizers, it has muscle relaxant and anticonvulsant effects.
Midazolam anesthesia is performed only with artificial ventilation lungs, since it significantly depresses respiratory center. This drug is contraindicated in myasthenia gravis, circulatory failure, in the first 3 months. pregnancy.
Barbiturates HEXENAL And THIOPENTAL SODIUM after injection into a vein, anesthesia is induced very quickly - “at the end of the needle”, the anesthetic effect lasts 20 - 25 minutes.
During anesthesia, reflexes are not completely suppressed, the tone of skeletal muscles increases (H-cholinomimetic effect). Laryngeal intubation without the use of muscle relaxants is unacceptable due to the risk of laryngospasm. Barbiturates do not have an independent analgesic effect.
Barbiturates depress the respiratory center, reducing its sensitivity to carbon dioxide and acidosis, but not to reflex hypoxic stimuli from the carotid glomeruli. They increase the secretion of bronchial mucus, independent of cholinergic receptors and not eliminated by atropine. The center of the vagus nerve is stimulated with the development of bradycardia and bronchospasm. They cause arterial hypotension because they inhibit the vasomotor center and block the sympathetic ganglia.
Hexenal and thiopental sodium are contraindicated in diseases of the liver, kidneys, sepsis, fever, hypoxia, heart failure, inflammatory processes in the nasopharynx. Hexenal is not administered to patients with paralytic intestinal obstruction (severely inhibits motility), thiopental sodium is not used for porphyria, shock, collapse, diabetes mellitus, bronchial asthma.
Non-inhalation anesthetics are used for induction, combined anesthesia and independently during short-term operations. In outpatient practice, propanidide, which has no aftereffects, is especially convenient. Midazolam is used for premedication and is also prescribed orally as a hypnotic and tranquilizer.
SODIUM OXYBUTYRATE (GHB) when administered into a vein causes anesthesia after 30 - 40 minutes, lasting 1.5 - 3 hours.
This drug is converted into the GABA mediator, which regulates inhibition in many parts of the central nervous system (cerebral cortex, cerebellum, caudate nucleus, pallidum, spinal cord). GHB and GABA reduce the release of excitatory transmitters and enhance postsynaptic inhibition by affecting GABA A receptors. During anesthesia with sodium hydroxybutyrate, reflexes are partially preserved, although strong muscle relaxation occurs. Relaxation of skeletal muscles is due to the specific inhibitory effect of GABA on the spinal cord.
Sodium hydroxybutyrate does not inhibit the respiratory, vasomotor centers, or the heart; it moderately increases blood pressure, sensitizing vascular α-adrenergic receptors to the action of catecholamines. It is a strong antihypoxic agent in the brain, heart, and retina.
Sodium hydroxybutyrate is used for introductory and basic anesthesia, pain relief during labor, as an antishock agent, in complex therapy hypoxia, including cerebral hypoxia. It is contraindicated for myasthenia gravis, hypokalemia, and is prescribed with caution for toxicosis of pregnancy accompanied by arterial hypertension, as well as for people whose work requires rapid mental and motor reactions.
COMBINED NARCASIS (multicomponent)
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A combination of two or more anesthetics (for example, hexenal and ether; hexenal, nitrous oxide and ether). Currently, in most cases, combined general anesthesia is performed, which is safer for the patient and more convenient for the surgeon in terms of performing the operation. The combination of several anesthetics improves the course of anesthesia (impairments in breathing, gas exchange, blood circulation, liver function, kidneys and other organs are less pronounced), makes anesthesia more manageable, eliminates or significantly reduces the toxic effect on the body of each of the drugs used. |
Neuroleptanalgesia (Greek neuron nerve + lepsis grasping, attack + Greek negative prefix ana- + algos pain) - combined method intravenous general anesthesia, in which the patient is conscious, but does not experience emotions (neurolepsy) and pain (analgesia). Thanks to this, the protective reflexes of the sympathetic system are turned off and the tissue need for oxygen is reduced. The advantages of neuroleptanalgesia also include: greater latitude therapeutic action, low toxicity and suppression of the gag reflex. Narcosis is an insensible, unconscious state caused by anesthetic drugs, which is accompanied by loss of reflexes, decreased tone of skeletal muscles, but at the same time the functions of the respiratory, vasomotor centers and heart function remain at a level sufficient to prolong life.
15. Means for inhalation anesthesia.
basic means for inhalation anesthesia.
a) liquid drugs for inhalation anesthesia: halothane (fluorothane), enflurane, isoflurane, diethyl ether(non-halogenated anesthetic)
b) gas anesthetics: nitrous oxide.
Requirements for anesthesia.
rapid induction of anesthesia without arousal stage
ensuring sufficient depth of anesthesia for the necessary manipulations
good control over the depth of anesthesia
quick recovery from anesthesia without aftereffects
sufficient narcotic breadth (the range between the concentration of the anesthetic that causes anesthesia and its minimum toxic concentration, which depresses the vital centers of the medulla oblongata)
no or minimal side effects
ease of technical use
fire safety of drugs
reasonable cost
The mechanism of the analgesic effect of anesthesia.
General mechanism: change in the physicochemical properties of membrane lipids and the permeability of ion channels → decreased influx of Na + ions into the cell while maintaining the output of K + ions, increased permeability for Cl - ions, cessation of the flow of Ca 2+ ions into the cell → hyperpolarization of cell membranes → decreased excitability of postsynaptic structures and impaired release of neurotransmitters from presynaptic structures.
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Anesthetic agent |
Mechanism of action |
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Nitrous oxide, ketamine |
Blockade of NMDA receptors (glutamine) coupled to Ca 2+ channels on the neuron membrane → a) cessation of Ca 2+ current through the presynaptic membrane → disruption of transmitter exocytosis, b) cessation of Ca 2+ current through the postsynaptic membrane - disruption of the generation of long-term excitatory potentials |
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1) Blockade of H n -cholinergic receptors associated with Na + channels → disruption of Na + current into the cell → cessation of generation of spike APs 2) Activation of GABA A receptors associated with Cl - - channels → entry of Cl - into the cell → hyperpolarization of the postsynaptic membrane → decrease in neuron excitability 3) Activation of glycine receptors associated with Cl - channels → entry of Cl - into the cell → hyperpolarization of the presynaptic membrane (transmitter release decreases) and postsynaptic membrane (neuron excitability decreases). 4) Disrupts the processes of interaction between proteins responsible for the release of transmitters from the vesicles of the presynaptic terminal. |
Advantages of halothane anesthesia.
high narcotic activity (5 times stronger than ether and 140 times more active than nitrous oxide)
rapid onset of anesthesia (3-5 min) with very short stage excitement, pronounced analgesia and muscle relaxation
easily absorbed in the respiratory tract without causing irritation of mucous membranes
inhibits the secretion of the glands of the respiratory tract, relaxes the respiratory muscles of the bronchi (the drug of choice for patients with bronchial asthma), facilitating mechanical ventilation
does not cause gas exchange disturbances
does not cause acidosis
does not affect kidney function
quickly excreted from the lungs (up to 85% unchanged)
Halothane anesthesia is easily manageable
large narcotic latitude
fire safe
decomposes slowly in air
Advantages of ether anesthesia.
pronounced narcotic activity
anesthesia when using ether is relatively safe and easy to manage
pronounced muscle relaxation of skeletal muscles
does not increase myocardial sensitivity to adrenaline and norepinephrine
sufficient narcotic breadth
relatively low toxicity
Advantages of anesthesia induced by nitrous oxide.
does not cause side effects during the operation
does not have irritating properties
does not provide negative influence to parenchymal organs
causes anesthesia without prior stimulation and side effects
fire safe (non-flammable)
excreted almost invariably through the respiratory tract
quick recovery from anesthesia without aftereffects
Interaction between adrenaline and halothane.
Halothane activates the allosteric center of myocardial β-adrenergic receptors and increases their sensitivity to catecholamines. Administration of adrenaline or norepinephrine against the background of halothane to increase blood pressure can lead to the development of ventricular fibrillation, therefore, if it is necessary to maintain blood pressure during halothane anesthesia, phenylephrine or methoxamine should be used.
Interaction between adrenaline and ethyl ether.
Does not increase the sensitivity of the myocardium to the arrhythmogenic effect of catecholamines.
Disadvantages of halothane anesthesia.
bradycardia (as a result of increased vagal tone)
hypotensive effect (as a result of inhibition of the vasomotor center and direct myotropic effect on blood vessels)
arrhythmogenic effect (as a result of a direct effect on the myocardium and its sensitization to catecholamines)
hepatotoxic effect (as a result of the formation of a number of toxic metabolites, therefore re-use no earlier than 6 months after the first inhalation)
increased bleeding (as a result of suppression of the sympathetic ganglia and dilatation of peripheral vessels)
pain after anesthesia, chills (as a result of quick exit from anesthesia)
increases blood flow to the vessels of the brain and increases intracranial pressure (cannot be used during operations in persons with TBI)
inhibits the contractile activity of the myocardium (as a result of disruption of the process of calcium ions entering the myocardium)
depresses the respiratory center and can cause respiratory arrest
Disadvantages of ether anesthesia.
ether vapors are highly flammable and form explosive mixtures with oxygen, nitrous oxide, etc.
causes irritation of the mucous membranes of the respiratory tract reflex change in breathing and laryngospasm, significant increase in salivation and secretion of the bronchial glands, bronchopneumonia
a sharp increase in blood pressure, tachycardia, hyperglycemia (as a result of an increase in the content of adrenaline and norepinephrine, especially during periods of excitement)
vomiting and respiratory depression in the postoperative period
prolonged stage of excitement
slow onset of anesthesia and slow recovery from it
convulsions are observed (rarely and mainly in children)
depression of liver and kidney function
development of acidosis
development of jaundice
Disadvantages of nitrous oxide anesthesia.
low narcotic activity (can only be used for induction of anesthesia in combination with other NS and to provide superficial anesthesia)
nausea and vomiting in the postoperative period
neutropenia, anemia (as a result of oxidation of the cobalt atom in the composition of cyanocobalamin)
diffusion hypoxia after cessation of nitrous oxide inhalation (nitrous oxide, poorly soluble in the blood, begins to be intensively released from the blood into the alveoli and displaces oxygen from them)
flatulence, headache, pain and congestion in the ears
Halothane (fluorothane), isoflurane, sevoflurane, dinitrogen, nitric oxide (nitrous oxide).
PHTOROTHANUM (Phthorothanum). 1, 1, 1-Trifluoro-2-chloro-2-bromoethane.
Synonyms: Anestan, Fluctan, Fluothne, Ftorotan, Halan, Halothane, Halothanum, Narcotan, Rhodialotan, Somnothane.
Ftorotan does not burn or ignite. Its vapors, when mixed with oxygen and nitrous oxide in the ratios used for anesthesia, are explosion-proof, which is a valuable property when used in a modern operating room.
Fluorotane slowly decomposes under the influence of light, so it is stored in orange glass bottles; thymol (O, O1%) is added for stabilization.
Ftorotan is a powerful narcotic, which allows it to be used independently (with oxygen or air) to achieve the surgical stage of anesthesia or as a component of combined anesthesia in combination with other narcotics, mainly with nitrous oxide.
Pharmacokinetically, fluorotane is easily absorbed from the respiratory tract and rapidly excreted unchanged by the lungs; Only a small part of fluorotane is metabolized in the body. The drug has a rapid narcotic effect, stopping soon after the end of inhalation.
When using fluorotane, consciousness usually turns off 1-2 minutes after the start of inhaling its vapors. After 3-5 minutes, the surgical stage of anesthesia begins. 3 - 5 minutes after stopping the supply of fluorotane, patients begin to awaken. Anesthesia depression completely disappears 5 - 10 minutes after short-term and 30 - 40 minutes after long-term anesthesia. Excitement is rare and weakly expressed.
Ftorotan vapors do not cause irritation of mucous membranes. There are no significant changes in gas exchange during anesthesia with fluorotane; blood pressure usually decreases, which is partly due to the inhibitory effect of the drug on the sympathetic ganglia and the expansion of peripheral vessels. The tone of the vagus nerve remains high, which creates conditions for bradycardia. To some extent, fluorotane has a depressing effect on the myocardium. In addition, fluorotane increases the sensitivity of the myocardium to catecholamines: the administration of adrenaline and norepinephrine during anesthesia can cause ventricular fibrillation.
Ftorotan does not affect kidney function; in some cases, liver function disorders with the appearance of jaundice are possible.
Under fluorotane anesthesia, various surgical interventions can be performed, including on the abdominal and thoracic cavities, in children and the elderly. Non-flammability makes it possible to use it when using electrical and X-ray equipment during surgery.
Ftorotan is convenient for use during operations on the chest organs, as it does not cause irritation of the mucous membranes of the respiratory tract, inhibits secretion, relaxes the respiratory muscles, which facilitates artificial ventilation. Fluorothane anesthesia can be used in patients with bronchial asthma. The use of fluorotan is especially indicated in cases where it is necessary to avoid agitation and tension of the patient (neurosurgery, ophthalmic surgery, etc.).
Fluorothane is part of the so-called azeotron mixture, consisting of two volume parts of fluorothane and one volume part of ether. This mixture has a stronger narcotic effect than ether, and less strong than fluorotane. Anesthesia occurs more slowly than with fluorotane, but faster than with ether.
During anesthesia with fluorotane, the supply of its vapor should be accurately and smoothly adjusted. It is necessary to take into account the rapid change of stages of anesthesia. Therefore, fluorotane anesthesia is carried out using special evaporators located outside the circulation system. The oxygen concentration in the inhaled mixture must be at least 50%. For short-term operations, fluorotan is sometimes also used with a regular anesthesia mask.
To avoid side effects associated with stimulation of the vagus nerve (bradycardia, arrhythmia), the patient is administered atropine or metacin before anesthesia. For premedication, it is preferable to use promedol rather than morphine, which stimulates the centers of the vagus nerve less.
If it is necessary to enhance muscle relaxation, it is preferable to prescribe relaxants of a depolarizing type of action (ditilin); when using drugs of a non-depolarizing (competitive) type, the dose of the latter is reduced compared to the usual one.
During anesthesia with fluorotane, due to inhibition of the sympathetic ganglia and dilation of peripheral vessels, increased bleeding is possible, which requires careful hemostasis and, if necessary, compensation for blood loss.
Due to the rapid awakening after cessation of anesthesia, patients may feel pain, so early use of analgesics is necessary. Sometimes chills are observed in the postoperative period (due to vasodilation and heat loss during surgery). In these cases, patients need to be warmed with heating pads. Nausea and vomiting usually do not occur, but the possibility of their occurrence should be considered in connection with the administration of analgesics (morphine).
Anesthesia with fluorotane should not be used in case of pheochromocytoma and in other cases when the level of adrenaline in the blood is increased, with severe hyperthyroidism. It should be used with caution in patients with cardiac arrhythmias, hypotension, and organic liver damage. During gynecological operations, it should be taken into account that fluorotane can cause a decrease in the tone of the uterine muscles and increased bleeding. The use of fluorotan in obstetrics and gynecology practice should be limited only to those cases where relaxation of the uterus is indicated. Under the influence of fluorotane, the sensitivity of the uterus to drugs that cause its contraction (ergot alkaloids, oxytocin) decreases.
During anesthesia with fluorotane, adrenaline and norepinephrine should not be used to avoid arrhythmias.
It should be taken into account that persons working with fluorotane may develop allergic reactions.
NITROGEN OXIDE (Nitrogenium oxidulatum).
Synonyms: Dinitrogen oxide, Nitrous oxide, Oxydum nitrosum, Protoxide d'Azote, Stickoxydal.
Small concentrations of nitrous oxide cause a feeling of intoxication (hence the name<веселящий газ>) and slight drowsiness. When pure gas is inhaled, a narcotic state and asphyxia quickly develop. When mixed with oxygen, when dosed correctly, it causes anesthesia without preliminary stimulation or side effects. Nitrous oxide has weak narcotic activity, and therefore it must be used in high concentrations. In most cases, combined anesthesia is used, in which nitrous oxide is combined with other, more powerful anesthetics and muscle relaxants.
Nitrous oxide does not cause respiratory irritation. In the body it remains almost unchanged and does not bind to hemoglobin; is in a dissolved state in plasma. After cessation of inhalation, it is excreted (completely after 10 - 15 minutes) through the respiratory tract unchanged.
Anesthesia using nitrous oxide is used in surgical practice, operative gynecology, surgical dentistry, and also for pain relief during childbirth.<Лечебный аналгетический наркоз>(B.V. Petrovsky, S.N. Efuni) using a mixture of nitrous oxide and oxygen is sometimes used in the postoperative period to prevent traumatic shock, as well as to relieve pain attacks in acute coronary insufficiency, myocardial infarction, acute pancreatitis and other pathological conditions accompanied by pain that cannot be relieved by conventional means.
To more completely relax the muscles, muscle relaxants are used, which not only enhances muscle relaxation, but also improves the course of anesthesia.
After stopping the supply of nitrous oxide, oxygen should be continued for 4 to 5 minutes to avoid hypoxia.
Nitrous oxide should be used with caution in cases of severe hypoxia and impaired diffusion of gases in the lungs.
To relieve labor pain, they use the method of intermittent autoanalgesia using a mixture of nitrous oxide (40 - 75%) and oxygen using special anesthesia machines. The woman in labor begins to inhale the mixture when signs of contraction appear and ends inhalation at the height of the contraction or towards its end.
To reduce emotional arousal, prevent nausea and vomiting and potentiate the effect of nitrous oxide, premedication with intramuscular injection of a 0.5% solution of diazepam (seduxen, sibazon) is possible.
Therapeutic anesthesia with nitrous oxide (for angina pectoris and myocardial infarction) is contraindicated in severe diseases of the nervous system, chronic alcoholism, and alcohol intoxication (excitement and hallucinations are possible).
| " |
Questions of computer tests in Pharmacology
In lesson No. 15 for Colloquium No. 2 on the topic
“Drugs affecting the central nervous system” - 2005
Means for inhalation anesthesia:
Thiopental sodium.
$Ftorotan.
$Nitrous oxide.
Ketamine.
$Isoflurane.
Gaseous substance for inhalation anesthesia
Ftorotan.
$Nitrous oxide.
Propofol
Isoflurane.
Volatile liquids for inhalation anesthesia
$Ftorotan.
Nitrous oxide.
Ketamine.
$Isoflurane.
Means for non-inhalation anesthesia:
$Ketamine.
Ftorotan.
$Thiopental sodium.
$Propofol.
Ftorotan:
$Has high narcotic activity.
$Increases the sensitivity of the myocardium to adrenaline.
$Enhances the effect of anti-depolarizing curare-like drugs.
Flammable.
Isoflurane:
$Unlike fluorotane, it causes tachycardia.
$Does not irritate the mucous membranes of the respiratory tract.
$Safe in terms of fire.
It has virtually no muscle relaxant effect.
Nitrous oxide:
$Has low narcotic activity.
Causes significant relaxation of skeletal muscles.
Irritates the mucous membranes of the respiratory tract.
$Has pronounced analgesic activity.
Thiopental sodium:
$Induces anesthesia 1-2 minutes after injection into a vein.
$Avails for 20-30 minutes.
Effective for 1.5-3 hours.
$Deposited in adipose tissue.
Has pronounced analgesic properties.
The short duration of the effect of sodium thiopental is due to
High metabolic rate in the liver.
Rapid excretion unchanged through the kidneys.
$Redistribution in the body (accumulation in adipose tissue).
Ketamine:
Causes deep surgical anesthesia.
$Causes loss of consciousness and general anesthesia.
Does not have analgesic properties.
$NMDA receptor antagonist.
$May cause dysphoria and hallucinations upon awakening.
What is characteristic of propofol?
$Induces anesthesia 30-40 seconds after injection into a vein.
Has a pronounced analgesic effect.
$Acts for a short time (3-10 minutes).
$Recovery from anesthesia is quick.
Side effects of Ftorotan
Tachycardia.
$Bradycardia.
Increased blood pressure.
$Hypotension.
$Cardiac arrhythmias.
Side effects of ketamine
Hypotension.
$Increased blood pressure.
$Tachycardia.
$Hallucinations after waking up.
Bradycardia, hypotension and cardiac arrhythmias are caused by:
Thiopental sodium.
Nitrous oxide.
$Ftorotan.
Propofol
The development of arrhythmias during fluorotane anesthesia is facilitated by:
Anaprilin.
$Adrenaline.
$Ephedrine.
The sensitivity of the myocardium to adrenaline increases:
Thiopental sodium.
$Ftorotan.
Propofol
Nitrous oxide.
The effect of anesthesia under the influence of antipsychotics (neuroleptics):
$Increases.
Weakening.
Doesn't change.
Identify the drug. Administered by inhalation, has high narcotic activity, causes bradycardia, lowers blood pressure, sensitizes the myocardium to adrenaline
Nitrous oxide.
Propofol
$Ftorotan.
Ketamine.
Identify the drug. Administered by inhalation, has low narcotic activity, usually used in combination with active means for anesthesia, causes virtually no aftereffects, has a pronounced analgesic effect, can be used to relieve pain during myocardial infarction
Ftorotan.
Ketamine.
Thiopental sodium.
$Nitrous oxide.
Identify the drug. After injection into a vein, it causes anesthesia in 1-2 minutes, the duration of anesthesia is about 30 minutes, it is deposited in adipose tissue, it is contraindicated in cases of liver dysfunction
Ketamine.
$Thiopental sodium.
Ftorotan.
Identify the drug. It is administered intravenously, acts for 5-10 minutes, causes<диссоциативную анестезию>, has a pronounced analgesic effect, can cause hallucinations
Ftorotan.
Propofol
Thiopental sodium.
$Ketamine.
The duration of action of sodium thiopental is 3-5 minutes.
Nitrous oxide is used for pain relief in the postoperative period.
Ketamine is a non-competitive NMDA receptor antagonist.
Check the correct statements:
Nitrous oxide is the most active agent for inhalation anesthesia.
$Sodium thiopental has weak analgesic properties.
Fluorotane is flammable.
Check the correct statements:
$Ketamine is a drug for non-inhalational anesthesia.
The duration of action of sodium thiopental is 1.5-2 hours.
$Ftorotan sensitizes the myocardium to adrenaline.
Check the correct statements:
Nitrous oxide has a pronounced analgesic effect.
Fluorotane is less active than nitrous oxide.
Fluorotane is flammable.
Check the correct statements:
Ftorotan is a drug for non-inhalation anesthesia.
$Thiopental sodium is deposited in adipose tissue.
Propofol is a drug for inhalation anesthesia.
Check the correct statements:
The duration of action of ketamine is 3-5 minutes.
Nitrous oxide is characterized by a long aftereffect.
Nitrous oxide is inferior in activity to fluorotane.
Check the correct statements:
Nitrous oxide sensitizes the myocardium to adrenaline.
Sodium thiopental is characterized by a pronounced stage of excitation.
$Ftorotan lowers blood pressure.
TETURAM PROMOTES THE ACCUMULATION OF ACETALDEHYDE IF TAKEN
ETHYL ALCOHOL BECAUSE:
INHIBES LIVER MICROSOMAL ENZYMES
$INDEPRESENTS ALDEHYDE HYDROGENASE
INHIBITS MONOAMINE OXIDASE
THE RESORPTIVE EFFECT OF ETHYL ALCOHOL IS CHARACTERISTIC:
$PSYCHOMOTOR EXCITATION
REDUCED HEAT TRANSFER
$ANTI-SHOCK EFFECT
ETHANOL:
$CAUSES EUPHORIA
$INCREASES HEAT TRANSFER
REDUCES DIURESIS
$CAUSES MENTAL AND PHYSICAL DEPENDENCE
WITH PROLONGED USE OF ETHYL ALCOHOL, DEVELOPMENT IS POSSIBLE:
$FUNCTIONAL CUMULATION
$MENTAL AND PHYSICAL DEPENDENCE
NONE OF THE ABOVE
ETHYL ALCOHOL PROMOTES HYPERCOOLING BECAUSE:
REDUCES HEAT PRODUCTION
$INCREASES HEAT TRANSFER TO A GREATER EXTENT THAN HEAT PRODUCTION
NONE OF THE ABOVE
TETURAM:
ACCELERATES THE OXIDATION OF ETHYL ALCOHOL
$BLOCKS THE OXIDATION OF ETHYL ALCOHOL AT THE ACETALDEHYDE STAGE
STIMULATES CHEMORECEPTORS OF THE TRIGGER ZONE OF THE VOMITIC CENTER
USE OF ETHYL ALCOHOL AGAINST THE EFFECT OF TETURAM CAUSES:
$FEELING OF FEAR
$HYPOTENSION
$NAUSEA AND VOMITING
CORRECT STATEMENTS:
$ETHYL ALCOHOL CAN CAUSE EUPHORIA
$TETURAM IS USED IN THE TREATMENT OF ALCOHOLISM
CORRECT STATEMENTS:
$ETHYL ALCOHOL IN LARGE DOSES DEPRESSES C.N.S.
$ETHYL ALCOHOL HAS A SMALL BREAD OF NARCOTIC EFFECT
TETURAM IS USED IN ACUTE ETHYL ALCOHOL POISONING
THERE ARE NO CORRECT STATEMENTS
CORRECT STATEMENTS:
$ETHYL ALCOHOL CAN CAUSE NARCASIS
$ETHYL ALCOHOL INCREASES HEAT TRANSFER
ETHYL ALCOHOL REDUCES DIURESIS
CORRECT STATEMENTS:
ETHYL ALCOHOL DOES NOT CAUSE EXCITATION
$WHEN USING ETHYL ALCOHOL, FUNCTIONAL CUMULATION IS POSSIBLE
$ETHYL ALCOHOL CAUSES PHYSICAL AND MENTAL DEPENDENCE
WHAT IS TRUE?
$ETHYL ALCOHOL CAUSES A STRONG STAGE OF EXCITATION
WHEN USING ETHYL ALCOHOL, MATERIAL CUMULATION IS OBSERVED
$ MENTAL AND PHYSICAL DEPENDENCE CAN DEVELOP TO ETHYL ALCOHOL
$TETURAM DISTURBS THE METABOLISM OF ETHYL ALCOHOL AT THE ACETALDEHYDE STAGE
THERE ARE NO CORRECT STATEMENTS
CORRECT STATEMENTS:
$ETHYL ALCOHOL IN LARGE DOSES DEPRESSIVES THE CENTRAL NERVOUS SYSTEM
$ETHYL ALCOHOL INCREASES DIURESIS
$ETHYL ALCOHOL IS USED AS AN ANTISEPTIC
THERE ARE NO CORRECT STATEMENTS
RIGHT:
ETHYL ALCOHOL REDUCES HEAT TRANSFER
ETHYL ALCOHOL IS USED AS AN ANESTHIC DRUG
ETHYL ALCOHOL IS NOT DEPENDENT
$ETHYL ALCOHOL HAS ANTI-SHOCK PROPERTIES
Sleeping pills from the group of benzodiazepines:
Zolpidem.
$Phenazepam.
$Diazepam.
Etaminal sodium.
$Nitrazepam.
Hypnotics - benzodiazepine receptor agonists:
Flumazenil.
$Diazepam.
$zolpidem.
$Nitrazepam.
<Небензодиазепиновый>benzodiazepine receptor agonist:
Diazepam.
Flumazenil.
$zolpidem.
Nitrazepam.
Etaminal sodium.
Narcotic sleeping pills
$Chloral hydrate.
$Etaminal-sodium.
Nitrazepam.
Zolpidem.
Sleeping pill from the group of barbiturates
Nitrazepam.
$Etaminal-sodium.
Zolpidem.
Chloral hydrate.
Hypnotic - a derivative of the aliphatic series
Nitrazepam.
Zolpidem.
Etaminal sodium.
$Chloral hydrate.
What effects can diazepam cause?
$Sedative.
$Sleeping pills.
$Anticonvulsant (antiepileptic).
$Anxiolytic.
Increased skeletal muscle tone.
Duration of REM sleep barbiturates:
Lengthen.
$Shortened.
They don't change.
The structure of sleep is least affected by:
Etaminal sodium.
Nitrazepam.
$zolpidem.
Compared to barbiturates, benzodiazepines reduce the duration of REM sleep:
To a greater extent.
$To a lesser extent.
To the same extent.
With a decrease in the activity of microsomal liver enzymes, the duration of action of etaminal sodium:
Decreases.
$Increases.
Doesn't change.
Barbiturates:
$Cause induction of microsomal liver enzymes.
Inhibits the activity of microsomal liver enzymes.
Do not affect microsomal liver enzymes.
Zolpidem:
Benzodiazepine receptor antagonist.
$Stimulates GABAergic processes in the central nervous system.
$Used as a sleeping pill.
Etaminal sodium:
Benzodiazepine derivative.
$Disturbs sleep structure.
$Causes a phenomenon<отдачи>upon sudden cancellation.
$Causes the induction of microsomal liver enzymes.
$May cause drug dependence.
Etaminal sodium:
Interacts with benzodiazepine receptors.
$Interacts with barbiturate receptors.
$Enhances GABAergic processes in the central nervous system.
Weakens GABAergic processes in the central nervous system.
Nitrazepam:
$Has an anxiolytic effect.
$Causes a hypnotic effect.
Relaxes skeletal muscles by blocking neuromuscular transmission.
$Muscle relaxant of central action.
$Has anticonvulsant properties.
$May cause drug dependence.
$Interacts with benzodiazepine receptors.
Nitrazepam enhances GABAergic processes in the brain due to:
Inhibition of GABA transaminase.
Interactions with GABA receptors.
$Interactions with benzodiazepine receptors.
Nitrazepam in contrast to etaminal sodium:
Does not have a sedative effect.
$Less influence on sleep structure.
Does not cause drug dependence.
Side effects of barbiturates:
Cramps.
$Sleep structure disturbance.
$Aftereffect.
$Drug dependence.
Phenomenon<отдачи>after stopping taking sleeping pills due to:
$Influence on sleep structure.
Material accumulation of drugs.
The most pronounced effect on sleep structure is exerted by:
Nitrazepam.
$Etaminal-sodium.
Phenazepam.
Zolpidem.
Ability to shorten phase<быстрого>sleep decreases in the series:
Zolpidem - nitrazepam - etaminal sodium.
Etaminal sodium - zolpidem - nitrazepam.
$Etaminal sodium - nitrazepam - zolpidem.
Which by-effect Is it related to the ability of hypnotics to disrupt sleep patterns?
Aftereffect.
$phenomenon<отдачи>.
Addiction.
Drug addiction.
Side effects when taking barbiturates are associated with:
Disturbance of sleep structure.
Induction of microsomal liver enzymes.
$Relatively slow removal from the body.
At acute poisoning sleeping pills are used to reduce their absorption in the digestive tract:
$ Gastric lavage.
$Adsorbents.
$Saline laxatives.
Drugs that reduce intestinal motility.
In case of acute poisoning by narcotic-type hypnotics, analeptics are used:
$Only for relatively mild forms of poisoning.
Only in case of severe poisoning.
For any form of poisoning.
In case of severe poisoning with sleeping pills, to ensure adequate breathing:
Analeptics are administered.
Reflex-type breathing stimulants are administered.
$Carry out artificial ventilation.
In case of acute poisoning with nitrazepam, the following is used:
Zolpidem.
$Flumazenil.
Cholinesterase reagents.
Flumazenil:
Sleeping pill.
$Benzodiazepine derivative.
Benzodiazepine receptor agonist.
$Benzodiazepine receptor antagonist.
Check the correct statements:
Zolpidem is a barbiturate.
Etaminal sodium is an aliphatic compound.
$Phenazepam is a benzodiazepine receptor agonist.
$zolpidem -<небензодиазепиновый>benzodiazepine receptor agonist.
Check the correct statements:
Etaminal sodium does not have narcotic potential.
Barbiturates do not disrupt sleep patterns.
Phenobarbital is used to treat epilepsy.
Check the correct statements:
$Barbiturates cause a phenomenon<отдачи>.
Diazepam inhibits GABAergic processes in the brain.
Zolpidem weakens GABAergic processes in the central nervous system.
Check the correct statements:
Nitrazepam is a barbiturate.
$Zolpidem has little effect on sleep patterns.
$Etaminal sodium enhances GABAergic processes in the central nervous system.
Check the correct statements:
Flumazenil is an antagonist of zolpidem.
Benzodiazepines are less likely to shorten REM sleep than barbiturates.
Phenazepam weakens GABAergic processes in the central nervous system.
Check the correct statements:
Etaminal sodium is excreted by the kidneys mainly unchanged.
$Zolpidem interacts with benzodiazepine receptors.
$Diazepam causes relaxation of skeletal muscles.
Check the correct statements:
$Etaminal sodium - barbiturate.
$Nitrazepam is less likely to disrupt sleep structure than barbiturates.
$Diazepam has an anxiolytic effect.
$Zolpidem has little effect on sleep structure.
Barbiturates reduce the activity of microsomal liver enzymes.
Check the correct statements:
$Nitrazepam is a benzodiazepine derivative.
$Etaminal sodium is largely metabolized in the liver.
Phenazepam is a barbiturate.
Flumazenil is a barbiturate antagonist.
Check the correct statements:
Zolpidem weakens GABAergic processes in the central nervous system.
$Phenazepam is an anxiolytic with a pronounced hypnotic effect.
$Nitrazepam increases the sensitivity of GABA receptors to the mediator.
$Phenazepam has narcotic potential.
Antiepileptic drugs:
$Sodium valproate.
Cyclodol.
$Lamotrigine.
$This is suximide.
$Difenin.
$Phenobarbital.
To prevent grand mal seizures, use:
$Carbamazepine.
Ethosuximide.
$Difenin.
$Lamotrigine.
$Sodium valproate.
To prevent minor seizures of epilepsy, use:
Difenin.
$This is suximide.
Phenobarbital.
Effective for focal (partial) epilepsy
$Sodium valproate.
$Carbamazepine.
$Phenobarbital.
Ethosuximide.
$Difenin.
$Lamotrigine.
Effective for myoclonus epilepsy
$Sodium valproate.
Ethosuximide.
$Clonazepam.
For status epilepticus the following is used:
Ethosuximide.
$Diazepam.
$Anesthetics.
Which two antiepileptic drugs have sedative-hypnotic properties?
Ethosuximide.
Difenin.
$Diazepam.
$Phenobarbital.
Antiepileptic, central muscle relaxant, hypnotic and anxiolytic effects are characteristic of:
Diphenina.
$Diazepam.
Ethosuximide.
The mechanism of antiepileptic action of diazepam and phenobarbital:
Strengthening the synthesis of GABA.
Direct stimulation of GABA receptors.
$Increasing the sensitivity of GABA receptors to the mediator.
Inhibition of the enzyme that inactivates GABA.
Sodium valproate
Inhibits glutamatergic processes in the brain.
$Enhances GABAergic processes in the brain.
$Promotes the formation of GABA and prevents its inactivation.
Carbamazepine is used to prevent:
$Focal epilepsy.
Difenin is used to prevent:
Minor seizures.
$Major convulsive seizures.
$Focal epilepsy.
Phenobarbital is effective in preventing:
$Major convulsive seizures.
Minor seizures.
Manifestations of myoclonus epilepsy.
Lamotrigine
Activates the GABAergic system of the brain.
$Reduces the activity of the glutamatergic system of the brain.
$Reduces the release of glutamate from presynaptic terminals.
$Effective for all forms of epilepsy.
Determine the drug: has antiepileptic, hypnotic and sedative properties; stimulates GABAergic processes in the brain; causes a pronounced induction of microsomal liver enzymes
Lamotrigine.
Difenin.
Carbamazepine.
$Phenobarbital.
Determine the drug: has antiepileptic, hypnotic, central muscle relaxant and anxiolytic properties; stimulates GABAergic processes
in the brain, used to relieve status epilepticus
Difenin.
Ethosuximide.
$Diazepam.
Lamotrigine.
Groups of antiparkinsonian drugs:
$Central anticholinergic blockers.
Drugs that block dopamine receptors.
$Medicines that enhance dopaminergic processes in the central nervous system.
$NMDA receptor blockers.
Stimulators of glutamatergic processes in the central nervous system.
Groups of antiparkinsonian drugs that stimulate dopaminergic processes in the brain:
$Precursor to dopamine.
Cholinergic receptor blockers.
$MAO-B inhibitors.
$Dopamine receptor agonists.
Antiparkinsonian drugs:
$Cyclodol.
$Levodopa.
Difenin.
$Midantan.
$Bromocriptine.
$Selegiline.
Antiparkinsonian drugs that stimulate dopaminergic processes in the brain:
$Bromocriptine.
$Levodopa.
Cyclodol.
$Selegiline
Drugs that increase the content of dopamine in the basal ganglia of the brain:
Cyclodol.
$Levodopa.
$Selegiline.
Inhibits cholinergic mechanisms in the brain:
$Cyclodol.
Selegiline.
Bromocriptine.
Midantan.
Levodopa.
Inhibits glutamatergic processes in the brain:
Cyclodol.
Selegiline.
Bromocriptine.
$Midantan.
Levodopa.
Levodopa:
$Precursor to dopamine.
$Increases the synthesis of dopamine in the brain and peripheral tissues.
Slows down the biotransformation of dopamine.
Inhibits MAO-B.
Stimulates dopamine receptors directly.
$In parkinsonism, it primarily reduces hypokinesia and muscle rigidity.
Levodopa is converted into dopamine under the influence of:
Monoamine oxidase B.
Catechol-o-methyltransferases.
$Dopa decarboxylase.
Which drug is combined with levodopa to reduce peripheral side effects and enhance antiparkinsonian effect?
Cyclodol.
Midantan.
Bromocriptine.
$Carbidopa.
Peripheral dopa decarboxylase inhibitor:
Midantan.
Cyclodol.
Selegiline.
$Carbidopa.
Carbidopa:
$Does not penetrate the blood-brain barrier.
Easily penetrates the blood-brain barrier.
Inhibits brain dopa decarboxylase.
$Inhibits dopa decarboxylase in peripheral tissues.
Carbidopa does not interfere with the formation of dopamine from levodopa in the central nervous system, since:
Brain dopa decarboxylase is not sensitive to carbidopa.
Carbidopa does not cross the blood-brain barrier.
Levodopa is combined with carbidopa because:
The inactivation of dopamine in the central nervous system slows down.
$The formation of dopamine in peripheral tissues is suppressed.
The conversion of levodopa to dopamine in the central nervous system is activated.
With simultaneous use of levodopa and carbidopa:
$Decreases side effect levodopa from peripheral tissues.
$The antiparkinsonian effect of levodopa is enhanced.
The antiparkinsonian effect of levodopa decreases.
To reduce the side effects of levodopa, use:
Non-selective monoamine oxidase inhibitors.
$Peripheral dopa decarboxylase inhibitors.
$Peripheral dopamine receptor blockers.
$Catechol-o-methyltransferase inhibitors.
Selegiline:
$MAO-B inhibitor.
Central cholinergic receptor blocker.
More effective than levodopa.
$Often used in combination with levodopa.
Cyclodol:
$Central anticholinergic blocker.
It is more effective against parkinsonism than levodopa.
$It is less effective in treating parkinsonism than levodopa.
$Contraindicated in glaucoma.
$Used for parkinsonism caused by antipsychotic drugs.
Midantan:
Stimulates cholinergic receptors.
$Non-competitive NMDA receptor antagonist.
Inhibits dopa decarboxylase.
$In parkinsonism, it reduces hypokinesia and rigidity.
$It is less effective than levodopa.
Opioid analgesics:
$Procedol.
Paracetamol.
$Butorphanol.
Amitriptyline.
$Buprenorphine.
$Fentanyl.
Full mu opioid receptor agonists:
Butorphanol.
$Fentanyl.
Buprenorphine.
Analgesics from the group of agonists-antagonists and partial agonists of opioid receptors:
Fentanyl.
Naloxone.
$Butorphanol.
$Buprenorphine.
Non-opioid (non-narcotic) centrally acting analgesic:
Butorphanol.
Buprenorphine.
$Paracetamol.
Non-opioid drugs from different pharmacological groups with analgesic activity
Butorphanol.
$Amitriptyline.
$Carbamazepine.
$Ketamine.
$Nitrous oxide.
Morphine:
$Opioid analgesic.
$Opium alkaloid.
Opioid receptor antagonist.
Inhibitor of cyclooxygenase in the central nervous system.
Analgesics from the group of full mu opioid receptor agonists cause:
$Euphoria.
$Respiratory depression.
Antipyretic effect.
$Drug dependence.
$Analgesia.
Morphine causes:
$Analgesia.
$Respiratory depression.
Anti-inflammatory effect.
Antipyretic effect.
$Antitussive effect.
$Euphoria.
$Slowing down the movement of contents through the intestines.
Sensitivity of the respiratory center to carbon dioxide under the influence of morphine:
$Decreases.
Increasing.
Doesn't change.
Excitability of the center of the cough reflex morphine:
Stimulates.
$Depressing.
Doesn't change.
Pupils under the influence of morphine:
Expanding.
$Narrow.
They don't change.
Gastrointestinal sphincter tone morphine:
Decreases.
$Raises.
Doesn't change.
When acting on the gastrointestinal tract, morphine:
$Increases sphincter tone.
$Reduces the secretion of the digestive glands.
Accelerates the movement of contents through the intestines.
$Slows down the movement of contents through the intestines.
Means for inhalation anesthesia.
This group includes liquid volatile and gaseous substances. The general anesthetic is inhaled, passes from the lungs into the blood and affects tissues, primarily the central nervous system. In the body, drugs are distributed evenly and excreted through the lungs, usually unchanged.
3.3.3.1.1. Liquid volatile substances.
These are drugs that easily pass from a liquid to a vapor state.
Ether for anesthesia gives characteristic stages general anesthesia (the stage of excitation can last up to 10-20 minutes, awakening - 30 minutes). Ether anesthesia is deep and quite easy to control. The muscles relax well.
The anesthetic may cause irritation of the respiratory tract and increased salivation. This can cause a reflex breathing spasm at the beginning of anesthesia. Heart rate may decrease and blood pressure may increase, especially during the period of awakening. After anesthesia, vomiting and respiratory depression are common.
Contraindications to the use of this product: acute diseases respiratory tract, increased intracranial pressure, some cardiovascular diseases, liver disease, kidney disease, exhaustion, diabetes and situations where excitement is very dangerous.
Ether vapors are highly flammable with oxygen, air, nitrous oxide and form explosive mixtures in certain concentrations.
Chloroform for anesthesia is a clear, colorless, heavy liquid with a characteristic odor and a sweet, pungent taste. Active general anesthetic, the surgical stage occurs in 5-7 minutes. after administration, and depression after this anesthesia occurs within 30 minutes.
Toxic: may cause various disorders in the heart, liver, metabolic disorders. Because of this, it is now used less often.
Ftorotan (Anestan, Fluctan, Halothane, Narcotan, Somnothane, etc.) is a colorless, odorous liquid. It is one of the most common and powerful means general anesthesia. Easily absorbed from the respiratory tract and quickly excreted unchanged (up to 80%). Anesthesia occurs quickly (within 1-2 minutes after the start of inhalation, consciousness is lost, after 3-5 minutes the surgical stage begins), and they quickly emerge from it (they begin to awaken after 3-5 minutes and depression disappears completely after 5-10 minutes after stopping breathing with fluorotane). Excitement (weak) is rare. Myorelaxation is less than from ether.
Anesthesia is well regulated and can be used for wide range surgical interventions. This anesthetic is especially indicated for surgical interventions, requiring avoidance of excitement and tension, for example, in neurosurgery, etc.
Ftorotan vapors do not irritate the mucous membranes, but reduce blood pressure and cause bradycardia. The drug does not affect kidney function, sometimes it interferes with liver function.
3.3.3.1.2. Gaseous substances.
These anesthetics are initially gaseous substances. The most common is nitrous oxide (N 2 O), cyclopropane and ethylene are also used.
Nitrous oxide is a colorless gas heavier than air. It was discovered in 1772 by D. Priestley, when he was making “nitrous air”, and was initially used only for entertainment, since in small concentrations it causes a feeling of intoxication with slight joyful excitement (hence its second, unofficial name “laughing gas”) and subsequent drowsiness. For inhalation general anesthesia it began to be used from the second half of the 19th century V. Causes mild anesthesia with analgesia, but the surgical stage is reached only at a concentration of 95% in inspired air. Under such conditions, hypoxia develops, so the anesthetic is used only in lower concentrations in a mixture with oxygen and in combination with other more powerful anesthetics.
Nitrous oxide is released unchanged through the respiratory tract within 10-15 minutes. after inhalation has stopped.
They are used in surgery, gynecology, for pain relief during childbirth and in dentistry, as well as for diseases such as heart attack, pancreatitis, i.e. accompanied by pain that cannot be relieved by other means. Contraindicated in serious illnesses nervous system, with chronic alcoholism and able alcohol intoxication(use of anesthetic may lead to hallucinations).
Cyclopropane is more active than nitrous oxide. Surgical anesthesia without the excitation phase occurs in 3-5 minutes. after the start of inhalation, and the depth of anesthesia is easily adjusted.
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