Medicines that act on the nervous system. Agents acting on the central nervous system. What is nefopam

1. List the signs of the state of anesthesia.

Ø unconscious state

Ø loss of sensation (primarily pain)

Ø loss of reflexes

Ø decreased skeletal muscle tone

2. Name the main means for inhalation anesthesia.

A) liquid drugs for inhalation anesthesia: Halothane (fluorothane), enflurane, isoflurane, diethyl ether(non-halogenated anesthetic)

B) gas anesthetics: Nitrous oxide.

3. Name the main means for non-inhalation anesthesia.

A) barbiturates: Sodium thiopental

B) non-barbituric anesthetics: Ketamine (calypsol), etomidate, propofol, propanidide (sombrevin), sodium oxybate

4. Requirements for drugs for anesthesia.

ü quick introduction to anesthesia without the stage of excitation

Ensuring sufficient depth of anesthesia for the necessary manipulations

good controllability of the depth of anesthesia

ü quick recovery from anesthesia without aftereffect

ü 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)

ü no or minimal side effects

ü simplicity in technical application

ü fire safety of preparations

ü acceptable cost

5. Name the stages of anesthesia.

For classical anesthesia, caused by one of the first anesthetics - ether, the following stages are characteristic:

1. Stage of analgesia- from the moment of administration of the anesthetic to the loss of consciousness.

2. Excitation stage- from the moment of loss of consciousness to the beginning of the movement of the eyeballs.

3. Stage of surgical anesthesia– 4 levels depending on the depth of anesthesia.

I. Superficial surgical anesthesia(level of eyeball movement).

II. Light surgical anesthesia(level of disappearance of the pharyngeal reflex).

III. Deep surgical anesthesia(level of disappearance of the corneal reflex).

IV. Super deep surgical anesthesia(the level of suppression of the pupillary reflex).

4. Awakening stage(when the anesthetic is discontinued) or agonal stage(with continued administration of the anesthetic).

With modern anesthetics The combination of these 4 stages of anesthesia is qualitatively and quantitatively different from classical ether anesthesia

6. Functional characteristics of the state of anesthesia.

7. What is the minimum alveolar concentration (MAC). What properties of inhalation drugs for anesthesia can be judged by the value of this indicator?

Minimum alveolar concentration (MAC)- the minimum concentration of anesthetic gas in the alveoli, which prevents a motor reaction (the equivalent of pain) in 50% of patients. MAC expresses the strength of inhalation anesthetics, that is, it is the main pharmacodynamic characteristic of NS. The stronger the anesthetic, the lower the MAC value it has. During surgical anesthesia, the concentration of the anesthetic should be 0.5-2.0 MAC.

8. Mechanism of analgesic action of anesthetics.

General mechanism: a change in the physicochemical properties of membrane lipids and the permeability of ion channels → a decrease in the influx of Na + ions into the cell while maintaining the exit of K + ions, an increase in the permeability for Cl - ions, a cessation of the flow of Ca2 + ions into the cell → hyperpolarization of cell membranes → a decrease in the excitability of postsynaptic structures and a violation release of neurotransmitters from presynaptic structures.

9. Advantages of halothane anesthesia.

V high narcotic activity (5 times stronger than ether and 140 times more active than nitrous oxide)

V rapid onset of anesthesia (3-5 minutes) with a very short stage of excitation, severe analgesia and muscle relaxation

V is easily absorbed in the respiratory tract without causing irritation of the mucous membranes.

V 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

V does not cause disturbances in gas exchange

V does not cause acidosis

V does not affect kidney function

V is rapidly excreted from the lungs (up to 85% unchanged)

V halothane anesthesia is easy to manage

V big narcotic latitude

V is safe in terms of fire

V slowly decomposes in air

10. Advantages of ether anesthesia.

V pronounced narcotic activity

V anesthesia when using ether is relatively safe and easy to manage

V pronounced myorelaxation of skeletal muscles

V does not increase myocardial sensitivity to adrenaline and norepinephrine

V sufficient narcotic latitude

V relatively low toxicity

11. Advantages of anesthesia caused by nitrous oxide.

V does not cause side effects during the operation

V does not have irritating properties

V does not adversely affect parenchymal organs

V causes anesthesia without prior excitation and side effects

V is safe in terms of fire (does not ignite)

V is excreted almost invariably through the respiratory tract

V quick exit from anesthesia without aftereffects

12. Advantages of thiopental anesthesia.

V rapid onset of anesthesia without the stage of excitation

V prolonged anesthesia (20-30 min)

V pronounced muscle relaxant effect

V is rapidly degraded in the liver and excreted from the body

13. Interaction of adrenaline and halothane.

Halothane activates the allosteric center of myocardial β-adrenergic receptors and increases their sensitivity to catecholamines. The administration of epinephrine 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.

14. Interaction of adrenaline and ethyl ether.

Does not increase the sensitivity of the myocardium to the arrhythmogenic effect of catecholamines.

15. Disadvantages of halothane anesthesia.

bradycardia (as a result of increased vagal tone)

ü hypotensive effect (as a result of inhibition of the vasomotor center and direct myotropic effect on the vessels)

ü arrhythmogenic effect (as a result of a direct effect on the myocardium and its sensitization to catecholamines)

ü hepatotoxic effect (as a result of the formation of a number of toxic metabolites, therefore, repeated use is not earlier than 6 months after the first inhalation)

ü increased bleeding (as a result of inhibition of sympathetic ganglia and expansion of peripheral vessels)

pain after anesthesia, chills (as a result of a quick exit from anesthesia)

ü enhances blood flow from the vessels of the brain and increases intracranial pressure (cannot be used in operations on people with head injury)

ü inhibits the contractile activity of the myocardium (as a result of a violation of the process of calcium ions entering the myocardium)

ü depresses the respiratory center and can cause respiratory arrest

16. Disadvantages of ether anesthesia.

ü ether vapors are highly flammable, form explosive mixtures with oxygen, nitrous oxide, etc.

ü causes irritation of the mucous membranes of the respiratory tract ® reflex changes in breathing and laryngospasm, a significant increase in salivation and secretion of bronchial glands, bronchopneumonia

ü a sharp increase in blood pressure, tachycardia, hyperglycemia (as a result of an increase in the content of adrenaline and norepinephrine, especially during arousal)

vomiting and respiratory depression in the postoperative period

a prolonged stage of arousal

slow onset and slow recovery from anesthesia

Seizures are observed (rarely and mainly in children)

ü Inhibition of liver and kidney function

development of acidosis

development of jaundice

17. Disadvantages of anesthesia with nitrous oxide.

ü low narcotic activity (can only be used for anesthesia in combination with other drugs and to provide surface anesthesia)

nausea and vomiting in the postoperative period

ü neutropenia, anemia (as a result of the oxidation of the cobalt atom in the composition of cyanocobalamin)

ü diffusion hypoxia after the cessation of inhalation of nitrous oxide (nitric 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

18. Disadvantages of thiopental anesthesia.

ü weak analgesia with preservation of vegetative reflexes to surgical manipulations

ü does not cause muscle relaxation, it is able to slightly increase muscle tone, cause their convulsions

convulsive muscle twitches

ü laryngospasm

ü abundant secretion of bronchial glands

ü inhibitory effect on the respiratory, vasomotor centers, myocardium (with a rapid increase in concentration) up to apnea and collapse

ü local irritant effect (aseptic phlebitis with rapid intravenous administration)

ü in high doses, thiopental causes hypotension, reduces myocardial contractility

ü prolonged post-anesthetic sleep (about 8-10 hours) as a result of the repeated release of thiopental into the bloodstream from the fat and muscle depot

the appearance of garlic taste in the mouth

19. What is neuroleptanalgesia?

Neuroleptanalgesia- a kind of general anesthesia - the combined use of antipsychotics (neuroleptics) with active analgesics, in which the patient is given analgesia and anterograde amnesia while maintaining consciousness.

Most often, the analgesic fentanyl is used together with the ultrashort-acting antipsychotic droperidol in a ratio of 1:50 (0.05 mg fentanyl together with 2.5 mg droperidol).

20. What is combined anesthesia? Example.

Combined anesthesia- combined administration of various in action and different in the way of administration (inhalation and non-inhalation) anesthetics, aimed either at enhancing the narcotic effect, or at eliminating side effects or shortcomings of the drugs used.

Benefits of combined anesthesia:

A) the stage of excitation is eliminated and a quick introduction to anesthesia is provided

B) the doses of the components of combined anesthesia are less than when using one agent for anesthesia ® reducing the toxicity of anesthetics

Examples: barbiturate or other fast-acting drug for non-inhalation anesthesia + halothane (enflurane, isoflurane) + nitrous oxide.

21. What is potentiated anesthesia? Example.

Potentiated anesthesia- a type of combined general anesthesia, in which the necessary anesthesia is achieved by using a complex of neuroplegic, antihistamine and other non-narcotic drugs with small doses of the main drug.

Example: neuroleptic (droperidol) + benzodiazepine anxiolytic (sibazon) + antihistamine (diprazine).

22. What is induction anesthesia? Example.

Introductory anesthesia- a kind of combined anesthesia, in which the patient falls asleep, bypassing the stage of excitement.

Example: general non-inhalation anesthetics: sodium thiopental, calypsol, propofol.

23. Name the aids used for anesthesia.

Ø sedatives (anxiolytics, antipsychotics): Droperidol

Ø morphine-like analgesics: Morphine, promedol, fentanyl

Ø M-anticholinergics: Atropine etc.

Ø Curare-like muscle relaxants: tubocurarine chloride, dithylin

Ø short-term ganglion blockers: Hygronium

24. Interaction of drugs for anesthesia and muscle relaxants.

All muscle relaxants are currently administered only against the background of the introduction of general anesthetics. The introduction of pure muscle relaxants is unacceptable.

general anesthetics, Usually enhance the effect non-depolarizing muscle relaxants (classic example: halothane).

Solutions of non-depolarizing relaxants are destroyed in an alkaline environment, so they cannot be used in the same syringe, for example, with Thiopental.

25. Local effect of ethyl alcohol.

A) antiseptic action

B) local effect on the gastrointestinal tract:

26. The central action of ethyl alcohol.

A) action on the psyche - 3 stages.

Stage 1 - excitation: inhibition of the inhibitory mechanisms of the brain, euphoria, increased mood, excessive sociability, talkativeness, inadequate assessment of the environment, reduced performance

Stage 2 - anesthesia: analgesia, drowsiness, impaired consciousness, inhibition of spinal reflexes

3rd stage - agonal

With prolonged use: addiction and drug dependence (mental and physical).

B) action on the vasomotor center:

C) influence on the posterior pituitary gland: decrease in the production of ADH ® increase in diuresis

D) psychogenic effect on the gastrointestinal tract

E) participation in energy exchange: 1 g of ethyl alcohol - 7.1 kcal.

27. Pharmacokinetics of ethyl alcohol.

1) when taken orally, 80% is absorbed - the small intestine, 20% - the stomach

2) quickly absorbed on an empty stomach; fats and carbohydrates delay absorption

3) 90% of ethanol is metabolized to carbon dioxide and water with the release of energy in the liver, the rest of unchanged ethanol is excreted: a) lungs b) kidneys c) sweat glands

28. Effect of ethanol on diuresis.

Decreased ADH production → increased diuresis.

29. Effect of ethanol on thermoregulation.

Inhibition of the vasomotor center ® vasodilation of the skin ® increased heat transfer

30. Effect of ethanol on the gastrointestinal tract.

The effect of ethanol on the gastrointestinal tract It has Central and local genesis:

10% concentration: increased secretion of the salivary and gastric glands (as a result of the release of gastrin, histamine), secretion of hydrochloric acid

20% concentration: reduced secretion of hydrochloric acid and gastric juice

40% concentration: increased mucus production, pyloric spasm, decreased gastric motility

Effect on the liver: inhibition of gluconeogenesis, hypoglycemia, ketoacidosis, accumulation of fats in the liver parenchyma.

31. Effect of ethanol on the cardiovascular system.

o alcoholic cardiomyopathy

- alcoholic arrhythmias

o arterial hypertension

ü reduced risk of atherosclerosis

32. The use of ethyl alcohol in medical practice.

Ø external antiseptic

Ø irritant rubdown and compresses

Ø for the manufacture of infusions, extracts, dosage forms for external use

Ø antishock agent

Ø hypnotic or sedative (rare)

Ø cachexia

33. Measures of assistance in acute ethanol poisoning.

1) Restore breathing:

A) holding the toilet of the oral cavity and upper respiratory tract

B) atropine to reduce the secretion of the salivary and bronchial glands

C) oxygen + mechanical ventilation

D) analeptics: Corazole, cordiamine, caffeine, etc.

2) Gastric lavage

3) Correction of BOS (intravenously sodium bicarbonate etc.)

4) Antiemetics in case of severe nausea ( metoclopramide and etc.)

5) In severe condition, hemodialysis is indicated

6) Symptomatic therapy, heat.

34. What is alcoholism?

Alcoholism is a chronic abuse of alcohol (ethyl alcohol - a substance with a sedative-hypnotic effect), which leads to damage to a number of organs (liver, gastrointestinal tract, central nervous system, cardiovascular system, immune system) and is accompanied by psycho-physical dependence.

35. What is disulfiram?

A drug taken orally for the treatment of chronic alcoholism, in cases where it is not possible to obtain a therapeutic effect by other methods of treatment (psychotherapy, vitamin therapy, taking apomorphine, etc.).

Mechanism of action: blockade of metal ions and sulfhydryl groups of alcohol biotransformation enzymes → an increase in the concentration of acetaldehyde in the blood after alcohol intake → reddening of the skin, a feeling of heat in the face and upper body, a feeling of tightness in the chest, difficulty breathing, noise in the head, palpitations, a feeling of fear, sometimes chills , hypotension → development of a negative conditioned reflex to the taste and smell of alcoholic beverages → alcohol intolerance.

36. Medicines for the treatment of alcoholism.

1) Teturam (antabuse, disulfiram)- see above

2) Esperal (radother)- long-acting teturam, subcutaneously implanted tablets

3) Apomorphine(taken in combination with alcohol) - an emetic of central origin

In addition to these drugs, psychotherapy and psychotropic drugs are used.

37. Means of stopping alcohol withdrawal.

alcohol withdrawal- a sharp interruption of alcohol consumption with the occurrence of motor excitations, anxiety, and a decrease in the convulsive threshold.

The main objective of treatment: prevention of convulsions, delirium, arrhythmias

1) thiamine therapy

2) detoxification - replacement of alcohol with a long-acting sedative-hypnotic agent with a gradual decrease in its dose (benzodiazepines)

3) antihistamines

4) phenytoin - sometimes as a means of preventing seizures

38. Principles of drug correction of extrapyramidal disorders.

The pathogenesis of parkinsonism:

A) primary: gradual loss of subcortical dopaminergic neurons in the area of ​​the basal ganglia of the brain in senile age → decrease in dopamine production → various disturbances in the regulation of tone and the nature of skeletal muscle movements.

B) secondary: taking antipsychotics, reserpine → blockade of dopamine synthesis in the basal ganglia.

Principles of drug correction:

1) elimination of dopamine deficiency

A) dopamine precursors ( Levodopa drug of choice for parkinsonism

B) dopamine D2 receptor agonists (ergot alkaloid Bromocriptine)

2) inhibition of the destruction of dopamine

A) DOPA decarboxylase inhibitors ( Carbidopa)

B) inhibitors of monoamine oxidase B ( Selegiline)

C) catechol-O-methyltransferase inhibitors ( Entacapon)

3) elimination of symptoms - M, N-anticholinergics in the central nervous system ( trihexyphenidyl, biperiden)

4) drugs that increase the release of dopamine ( Amantadine- an antiviral drug that has the ability to reduce the manifestations of parkinsonism with an unknown mechanism of action)

39. Name dopaminergic antiparkinsonian drugs.

Levodopa(precursor of dopamine) Amantadine(drug that increases the release of dopamine), Bromocriptine(agonist of dopamine D2 receptors), Selegiline(monoamine oxidase B inhibitor), Entacapon(catechol-O-methyltransferase inhibitor)

40. Name the inhibitors of DOPA-decarboxylase. Why are they used in combination with levodopa?

DOPA decarboxylase inhibitors: carbidopa, benzserazide.

There are two types of DOPA decarboxylase - in the periphery and in the CNS. These drugs do not cross the blood-brain barrier and do not affect DOPA decarboxylase in the CNS, which converts levodopa to dopamine. At the same time, these drugs competitively inhibit DOPA-decarboxylase of the intestine, liver, lungs (i.e., the peripheral form), preventing the destruction of levodopa on the periphery → most of the levodopa reaches the central nervous system, where it is converted into dopamine and exerts its therapeutic effect.

DOPA-decarboxylase inhibitors are used in combination with levodopa, because Potentiation effect(increased therapeutic effect of levodopa). As a result, smaller doses of levodopa can be administered, avoiding many undesirable effects.

41. Name the antiparkinsonian drugs from the group of anticholinergics.

Trihexyphenidyl (cyclodol), biperiden.

42. Mechanism of antiparkinsonian action of levodopa.

In the nuclei of the central nervous system, levodopa undergoes decarboxylation to dopamine → replenishment of its own deficiency in the neurons of the substantia nigra of the extrapyramidal system.

43. Mechanism of antiparkinsonian action of selegiline.

There are two isoforms of the MAO enzyme in the human body:

MAO-A - located mainly on the periphery (intestines, liver, lungs); conducts oxidative deamination of norepinephrine, serotonin, dopamine, tyramine.

MAO-B - located mainly in the central nervous system; conducts oxidative decarboxylation of dopamine and tyramine.

Selegelin - selective MAO inhibitor type B.

Selegiline selectively binds to MAO-B → impaired ability of the enzyme to destroy dopamine → enhancement and prolongation of the antiparkinsonian effect of dopamine formed from levodopa (selegelin itself has a minimal antiparkinsonian effect, since patients in this group already have an endogenous dopamine deficiency)

44. Mechanism of antiparkinsonian action of bromocriptine.

Agonist of postsynaptic D2-dopamine receptors:

1) activation of D2 receptors of neurons of the caudate nucleus → antiparkinsonian effect

2) activation of D2 receptors of the pituitary and hypothalamus → inhibition of prolactin secretion, normalization of growth hormone levels

45. Mechanism of antiparkinsonian action of amantadine.

Until the end, the mechanism of action of amantadine is unclear. It is believed that several processes play a role in the implementation of its anti-Parkinsonian activity:

blockade of glutamate receptors on the surface of cholinergic neurons of the caudate nucleus

ü increased release of dopamine into the synaptic cleft from the neurons of the substantia nigra and inhibition of its reverse neuronal uptake

ü weak M-anticholinergic activity

46. ​​Mechanism of antiparkinsonian action of trihexyphenidyl.

Blockade of M- and H-cholinergic receptors on inhibitory neurons of the caudate nucleus → antiparkinsonian effect

47. Mechanism of antiparkinsonian action of biperiden.

Blockade of M- and H-cholinergic receptors on inhibitory neurons of the caudate nucleus → antiparkinsonian effect.

Unlike Trihexyphenidyl (cyclodol) biperiden more active, better eliminates tremor, has more rare undesirable effects from the central nervous system.

48. What is nakom? Its mechanism of action and purpose.

On whom Levodop Y (precursor of dopamine) and carbidopa

Mechanism of action: the combination of levodopa with carbidopa leads to inhibition of the decomposition of levodopa in peripheral tissues and blood → an increase in the level of levodopa in brain tissues → the formation of more dopamine at lower doses of levodopa taken (potentiation of the effect).

49. What is Madopar? Its mechanism of action and purpose.

Madopar - a combined preparation containing Levodopa(precursor of dopamine) and benserazide(DOPA decarboxylase inhibitor).

Mechanism of action: the combination of levodopa with benserazide leads to inhibition of the decomposition of levodopa in peripheral tissues and blood → potentiation of the effect of levodopa in the central nervous system (see Nakom).

50. Side effects of levodopa.

Peripheral adverse effects (due to accumulation of levodopa in peripheral tissues):

ü tachycardia, arrhythmia, angina pectoris (as a result of dopamine activation of b-Ap myocardium)

ü polyuria (activation of D1 receptors of the vessels of the glomeruli of the kidneys → vasodilation)

ü anorexia, nausea and vomiting (as a result of stimulation of D1 and D5 receptors of the stomach, as well as D2 receptors of the trigger zone of the vomiting center of the medulla oblongata)

Central unwanted effects:

ü orthostatic hypotension (as a result of a decrease in the activity of the sympathetic centers of the central nervous system)

ü oral hyperkinesis - licking, baring, smacking.

ü choreic hyperkinesis - rapid violent, uncontrolled movements (as a result of a sharp increase in the concentration of dopamine after taking levodopa)

ü muscular dystonia - sudden freezing in an abnormal posture (as a result of a drop in the concentration of dopamine before the next medication)

ü the phenomenon of "on-off" or "on-off"-phenomenon - sudden transitions from movement to complete immobility.

ü anxiety, insomnia, nightmares (as a result of the influence of dopamine on the hypnogenic zone of the brain

ü visual hallucinations, delusions, psychosis (as a result of stimulation of the D2 receptors of the limbic system)

ü "withdrawal" syndrome: complete immobilization, gross tremor, malignant hyperthermia, respiratory and heart failure (as a result of sudden discontinuation of levodopa after prolonged use)

51. Side effects of trihexyphenidyl.

1) from the side of the central nervous system:

Ø drowsiness, slow thinking, impaired attention

Ø inexplicable mood swings, vivid colorful hallucinations, illusory perception of the world

2) peripheral effects associated with the blockade of M-cholinergic receptors

Ø dry mouth, throat

Ø pain in the eyes, disturbance of accommodation and photophobia, increased intraocular pressure

Ø tachycardia, constipation, urinary retention

52. Side effects of biperiden.

See side effects of trihexyphenidyl above.

Difference: undesirable effects from the central nervous system with biperidene are rarer compared with trihexyphenidyl.

53. What are antiepileptic drugs?

Antiepileptic drugs - drugs that reduce the frequency and severity of seizures in epilepsy.

NB! 1) antiepileptic drugs are not prescribed for the relief of already developed seizures (with the exception of status epilepticus), they are used solely for the purpose of preventing seizures in a sick person

2) antiepileptic drugs only make it possible to restrain the development of the disease or even stop it, but are not able to completely eliminate epilepsy.

54. Name the antiepileptic drugs that are effective in generalized tonic-clonic seizures of epilepsy.

Carbamazepine, phenytoin (difenin), sodium valproate, phenobarbital, primidone (hexamidine), lamotrigine.

55. Name the antiepileptic drugs effective in absence seizures.

Ethosuximide, sodium valproate

56. Name the antiepileptic drugs effective in myoclonic seizures.

Sodium valproate, clonazepam, ethosuximide, lamotrigine.

57. Name the antiepileptic drugs effective in partial epileptic seizures.

Carbamazepine, sodium valproate, phenytoin, gabapentin, lamotrigine.

58. The mechanism of action of antiepileptic drugs.

1) facilitation of inhibitory GABA-dependent transmission (phenobarbital, sodium and magnesium valproate, gabapentin)

2) suppression of usually excitatory glutamatergic transmission (lamotrigine)

3) modification of ionic currents

A) inhibition of the activity of Na + channels of neuronal membranes (phenytoin, carbamazepine)

B) inhibition of the activity of Ca2+ channels of T- and L-types (ethosuximide)

59. Side effects of antiepileptic drugs.

A) disorders of the gastrointestinal tract, a negative effect on the function of the liver and pancreas (nausea, vomiting, constipation and anorexia, ulcerative colitis and cholangitis, toxic hepatitis)

B) hematological adverse reactions (aplastic and megaloblastic anemia, agranulocytosis, leukopenia)

C) adverse reactions from the skin and mucous membranes (skin rashes, erythema, gingival hyperplasia)

D) damage to the respiratory system (acute interstitial pneumonia of allergic origin, respiratory rhythm disturbance, hyperbronchorea)

E) damage to the cardiovascular system (impaired cardiac conduction, arterial hypertension and congestive heart failure)

E) impaired renal function (urinary retention, nephrolithiasis)

G) endocrine disorders (fluctuations in body weight, etc.)

H) neuropsychiatric disorders (psychoses)

I) an increase in the frequency of epileptic seizures (as a result of a perverted pharmacodynamic response)

At Long-term long-term use: depression, drowsiness, lethargy, psychosis.

60. Indications for the use of phenytoin.

61. Indications for the use of carbamazepine.

Ø generalized tonic-clonic seizures of epilepsy

Ø partial epileptic seizures

Ø for the relief of pain syndrome of predominantly neurogenic origin, including essential trigeminal neuralgia, trigeminal neuralgia in multiple sclerosis, essential glossopharyngeal neuralgia

Ø diabetic neuropathy with pain syndrome

Ø prevention of seizures in alcohol withdrawal syndrome

Ø as a prophylaxis for affective and schizoaffective psychoses

Ø diabetes insipidus of central origin, polyuria and polydipsia of neurohormonal nature

62. Indications for the use of sodium valproate.

Ø partial epileptic seizures of epilepsy

Ø myoclonic convulsions

Ø absences

Ø specific syndromes (West, Lennox-Gastaut)

63. Indications for the use of ethosuximide.

A drug with a very narrow spectrum of activity: effective only when absences sometimes used as an analgesic For trigeminal neuralgia.

64. Indications for the use of sodium phenytoin.

The difference from phenytoin is that Phenytoin sodium Soluble and administered parenterally, which allows you to quickly achieve a therapeutic effect.

Ø status epilepticus with tonic-clonic seizures

Ø Treatment and prevention of epileptic seizures in neurosurgery

Ø ventricular arrhythmias with glycoside intoxication or associated with intoxication with tricyclic antidepressants

Also Phenytoin sodium can be used according to the indications of phenytoin:

Ø generalized tonic-clonic seizures of epilepsy

Ø partial epileptic seizures

Ø to eliminate pain in trigeminal neuralgia

65. Indications for the use of sodium phenobarbital.

Ø generalized tonic-clonic seizures of epilepsy

Ø for emergency treatment of acute seizures, including those associated with epileptic status, eclampsia, meningitis, toxic reactions to strychnine

Ø as a sedative to reduce anxiety, tension, fear

Ø for the prevention and treatment of hyperbilirubinemia (phenobarbital reduces the content of bilirubin in the blood due to the induction of glucuronyl transferase, the enzyme responsible for binding bilirubin)

66. Indications for the use of diazepam.

Ø status epilepticus

Ø neurosis, borderline states with symptoms of tension, anxiety, anxiety, fear

Ø sleep disorders, motor excitation of various etiologies in neurology and psychiatry

Ø Withdrawal syndrome in chronic alcoholism

Ø spastic conditions associated with damage to the brain or spinal cord

Ø myositis, bursitis, arthritis accompanied by skeletal muscle tension

Ø premedication before anesthesia

Ø as a component of combined anesthesia

Ø Facilitation of labor activity

Ø tetanus

67. Name the means for relief of convulsive syndrome.

Diazepam, clonazepam, magnesium sulfate, anesthetics, antipsychotics, muscle relaxants, paracetamol.

68. Name the means of relief of hyperthermic convulsions.

Paracetamol. diazepam.

69. Name the means used to reduce spasticity.

Mydocalm.

70. Name the means of relief of status epilepticus.

Diazepam, clonazepam, lorazepam, sodium phenobarbital, sodium phenytoin, clomethiazole , Means for anesthesia (thiopental, propofol).

71. What is an analgesic effect?

The analgesic effect is the selective suppression of pain sensitivity without suppressing other types of sensitivity and turning off consciousness.

72. What is an anesthetic effect?

Suppression of all types of sensitivity (pain, tactile, temperature, etc.) often with loss of consciousness.

73. What specific effect do opioids have?

Opioids selectively They suppress pain, increase its tolerance, reduce the emotional coloring and vegetative accompaniment of pain.

74. Mediators of the antinociceptive system.

Three families of peptides are mediators of the antinociceptive system:

V endorphins: b-endorphin;

V enkephalins: leu - and met-enkephalin;

V dynorphins: dynorphin A and B.

75. Do opioids have a general anesthetic effect?

No, opioids predominantly suppress pain sensitivity while preserving other types of pain sensitivity.

76. Name the main pharmacological effects of opioids.

ü analgesic effect (decrease in the perception of pain, change in emotional coloring for pain)

ü euphoria (feeling of emotional satisfaction, elimination of fear, anxiety)

ü sedative effect (drowsiness, decreased motor activity, weakening of concentration, indifference)

ü respiratory depression (due to a direct inhibitory effect on the respiratory center and a decrease in the sensitivity of its neurons to an increase in the concentration of carbon dioxide in the blood)

suppression of the cough center

ü activation of the vomiting center, nausea, vomiting (as a result of exposure to the chemoreceptor trigger zone of the bottom of the IV ventricle) or inhibition of vomiting (due to inhibition of the center of vomiting)

ü constriction of the pupil (as a result of influence on the nuclei of the third pair of cranial nerves)

ü bradycardia (due to the stimulating effect on the nuclei of the vagus nerve)

ü increased tone of skeletal muscles (as a result of increased reflex excitability of spinal cord neurons)

ü increased tone of the GMC of the gastrointestinal tract, spasm of sphincters, slowing down and weakening of peristalsis: constipation, decreased diuresis, impaired outflow of bile from the gallbladder

ü an increase in the duration of labor (as a result of a central action and a direct effect on the MMC of the uterus)

ü vasodilation of the skin, hyperemia, itching, sweating (due to the induction of histamine release)

ü increased secretion of prolactin, growth hormone and ADH, a decrease in the release of cortico - and gonadoliberins (which causes a decrease in blood levels of ACTH, FSH, LH, cortisol, estrogens and progesterone, testosterone)

77. What causes the action of opioids?

The action of opioids is due to their ability to interact with opiate receptors (μ, σ, κ, δ, υ), resulting in:

A) the body's own antinociceptive system is activated, its inhibitory effects on the nociceptive system are activated

B) the pathways for the transmission of pain signals to the central nervous system are inhibited (as a result of a decrease in the excitability of neurons and a decrease in the release of neurotransmitters from presynaptic endings)

C) the emotional perception of pain changes (as a result of the influence of opioids on opiate receptors in the limbic structures of the brain)

78. Mechanism of analgesic action of opioid analgesics.

Activation of μ-receptors (responsible for supraspinal analgesia, euphoria) and κ-receptors (responsible for spinal analgesia, sedation) →

A) activation of the antinociceptive system and an increase in its inhibitory effects on the nociceptive system

B) increased activity of adenylate cyclase → formation of cAMP → activation of cAMP-dependent protein kinases →

1. in presynaptic endings: inactivation of calcium channels → violation of calcium intake into presynaptic endings → violation of neurotransmitter release → difficulty in transmitting impulses in the nociceptive system

2. on the postsynaptic membrane: inactivation of calcium channels and opening of potassium channels with the release of potassium from neurons → hyperpolarization of the membrane, decreased excitability of the neuron → difficulty in perceiving the pain signal in the nociceptive system

C) activation of opiate receptors in the limbic structures of the brain → a change in the emotional perception of pain (pain is perceived as insignificant)

79. Central effects of narcotic analgesics.

ü analgesia

ü euphoria

the sedative effect

o respiratory depression

suppression of the cough reflex

ü rigidity of the muscles of the body

o nausea, vomiting

80. Effect of opioids on the vomiting center.

The action on the vomiting center is twofold:

A) opioids, binding to the opioid receptors of the vomiting center, cause its inhibition.

B) opioids activate the trigger zone of the vomiting center, which have a stimulating effect on this center.

Since the trigger zone lies outward from the BBB, it is activated before inhibition of the vomiting center begins, therefore, at the first administration of morphine (in 20-40% of patients), nausea and vomiting may occur, which is replaced by a rapid suppression of the gag reflex.

81. Effect of narcotic analgesics on the cardiovascular system.

1. Stimulation of the nuclei of the vagus nerve → bradycardia

2. Dilatation of intracranial vessels (especially with hypercapnia) → increased intracranial pressure.

3. Sometimes peripheral vasodilation (due to histamine release) → hypotension.

4. Morphine: dilatation of the vessels of the pulmonary circulation → reduction of preload on the myocardium, reduction of pressure in the vessels of the lungs.

82. Influence of narcotic analgesics on the gastrointestinal tract.

ü obstipation effect (constipation) as a result of increased tone of smooth muscles and sphincters of the gastrointestinal tract and segmentation of the intestine with the disappearance of propulsion

ü Decreased motility and basal secretion of the stomach.

Decreased secretion of intestinal juice and increased absorption of water from feces

ü reduction of SMC of the biliary tract, the occurrence of colic

Decreased secretion of the pancreas and bile

83. Influence of narcotic analgesics on diuresis.

ü decrease in renal blood flow and increase in the level of ADH → decrease in diuresis

ü increased tone of the sphincter of the bladder and ureters

84. Neuroendocrine effect of opioids.

ü enhances the secretion of: prolactin, STH and ADH

ü lowers the release of: cortico - and gonadoliberins (which causes a decrease in blood levels of ACTH, FSH, LH, cortisol, estrogens and progesterone, testosterone)

85. Dependence of t ½ of opioids on liver function.

Inactivation of opioids occurs in the liver by its binding to glucuronic acid. The half-life in young people is about 3 hours, it increases significantly:

A) in elderly and senile people

B) with liver diseases (cirrhosis, etc.)

86. Effect of opioids on the respiratory center.

It depresses the respiratory center, reducing its excitability to carbon dioxide and reflex effects.

87. Effect of opioids on the cough center.

Depress the cough center (especially Codeine)

88. Effect of opioids on the vasomotor center.

It practically does not affect the vascular-motor center in therapeutic doses. Toxic doses depress the vasomotor center.

89. Neuroendocrine effects of opioids.

See c. 84. I wonder why it is necessary to duplicate questions? To make them seem more?;)

90. Side effects of narcotic analgesics.

restlessness, trembling, hyperactivity (with dysphoria)

o respiratory depression

o Nausea, vomiting, constipation

ü increased intracranial pressure

Postural hypotension exacerbated by hypovolemia

o urinary retention

ü itching in the area of ​​​​the wings of the nose, urticaria (more often with parenteral administration)

91. Indications for the use of narcotic analgesics.

ü acute pain in injuries, burns, operations

ü chronic severe pain not associated with neoplastic diseases (i.e. with tumors)

pain associated with malignant neoplasms

acute period of myocardial infarction

shortness of breath (dyspnea) and acute pulmonary edema

ü labor pain relief

ü premedication in the pre-aesthetic period, pain relief in the postoperative period

ü renal and hepatic colic

92. Contraindications to the use of narcotic analgesics

conditions accompanied by depression of the respiratory center, bronchial asthma

ü trauma to the head and brain, accompanied by an increase in intracranial pressure

ü pregnancy, childbirth (since the tone of the uterus decreases and childbirth is lengthened, there may be respiratory depression in the newborn)

ü children under two years of age (due to the high sensitivity of the respiratory center to opioids)

ü with caution to people of senile age (due to slow metabolism of morphine)

93. Effects of opioid overdose (acute poisoning).

Acute opioid poisoning is the result of an absolute overdose of opioids (intentional or unintentional).

Dynamics of changes in acute poisoning:

1. The first signs of poisoning - 20-30 minutes after ingestion of toxic doses of opioids: dizziness, weakness, vomiting, drowsiness, euphoria, turning into stupor, a sharp symmetrical constriction of the pupils, oliguria, hypothermia

2. Complete analgesia quickly sets in, sleep, then complete loss of consciousness (coma)

3. Breathing is rare (sometimes 2-4 breaths per minute), arrhythmic, often Cheyne-Stokes breathing, accompanied by cyanosis, sometimes pulmonary edema due to hypoxia, collapse.

4. A sharp drop in blood pressure, convulsions are possible in children

Pathognomic signs of morphine poisoning: miosis, coma and respiratory depression with preserved and even enhanced tendon reflexes.

With an unfavorable outcome, death occurs within 6-18 hours as a result of paralysis of the respiratory center and respiratory failure.

With a favorable outcome: the transition of coma into sleep lasting 24-36 hours with withdrawal symptoms at the exit (manifested by a feeling of weakness, headache, vomiting).

94. Help with acute opioid poisoning (Sequence is important)

1. Measures to restore and maintain breathing:

transfer of the patient to artificial respiration (AVL) with positive pressure on inspiration. The most critical are the first 10-12 hours during which it is necessary to ensure continuous ventilation.

ü conducting antidote detoxification - Administration of intravenous naloxone with subsequent repeated injections if there are no clinically significant signs of improvement in breathing (naloxone competitively blocks the action of opioids on κ- and μ-receptors and simultaneously excites σ-receptors, which lead to excitation of the respiratory center)

ü repeated gastric lavages using a probe and a suspension of activated charcoal, a weak solution of KMnO4 (because opioids undergo gastroenterohepatic circulation)

2. Careful monitoring of the patient to prevent recurrent respiratory depression (for example, due to the fact that naloxone has a shorter duration of action than opioids) and withdrawal symptoms.

3. Administration of a long-acting opioid antagonist of the type Naltrexone.

4. Symptomatic treatment: restoration of cardiovascular activity, etc.

95. Effects of chronic opioid intoxication.

With prolonged use, morphine causes the rapid formation of:

A) mental dependence - an irresistible, uncontrollable (compulsive) desire for repeated administration of morphine, associated with its ability to cause euphoria

B) physical dependence - a deep restructuring of neuroendocrine functions, in which the synthesis of one's own endogenous opiopeptides is inhibited by the mechanism of a negative connection, while the cessation of regular administration of an opioid into the body causes a painful condition - deprivation syndrome or withdrawal syndrome.

The following changes are gradually increasing:

further decline in mental and physical performance

Decreased skin sensitivity, hair loss

ü an increase in changes in the gastrointestinal tract: emaciation, thirst, constipation

96. Manifestation of withdrawal syndrome in morphinism.

Not a “dreary state”, but slow death takes possession of a morphine addict, as soon as you deprive him of morphine for an hour or two. The air is not satisfying, it cannot be swallowed… there is no cell in the body that would not crave… What? It cannot be defined or explained. There is no human word. He's off. The corpse moves, yearns, suffers. He wants nothing, thinks of nothing but morphine. Morphine! Death from thirst is a heavenly, blissful death compared to the thirst for morphine. So buried alive, probably, catches the last insignificant air bubbles in the coffin and tears the skin on the chest with his nails. So the heretic groans and stirs at the stake when the first tongues of flame lick his feet...M. A. Bulgakov. Notes of a young doctor. Morphine"

Withdrawal syndrome (deprivation syndrome) occurs 6-10 hours after the last injection and reaches a maximum by day 2, after which it weakens by day 5-7, manifested by the development of effects opposite to those observed with the introduction of morphine:

rhinorrhea, lachrymation (lacrimation), sweating, sneezing

ü anxiety, insomnia, weakness, agitation, alternating with anxiety

ü severe muscle and joint pain, involuntary movements, tremors, convulsive muscle contractions, cold extremities, followed by a feeling of heat

ü back pain, abdominal pain

ü mydriasis

o nausea and vomiting

✓ Sharp fluctuations in blood pressure

ü hyperthermia with chills

arrhythmic tachypnea

Despite the apparent severity of the withdrawal syndrome, it Rarely ends in death(as opposed to barbituric withdrawal syndrome).

The constant triad of signs in withdrawal syndrome is pathognomic:

1) pupil dilation (mydriasis)

2) pilomotor reaction ("goosebumps"

3) dehydration of the body, accompanied by ketosis, violation of the acid-base balance, sometimes collapse.

97. Means of help with morphine withdrawal.

1. β-blockers (nadolol, sotalol)

2. neuroleptics (droperidol)

3. M-cholinolytics ( Atropine sulfate, dicycloverine, hyoscine butyl bromide)

4. drugs that promote detoxification of the body ( Hemodez, B vitamins, sodium sulfate)

98. Interaction of narcotic analgesics and anesthetics.

Means for anesthesia potentiate the action of narcotic analgesics.

99. Interaction of narcotic analgesics and anxiolytics.

benzodiazepine anxiolytics Enhance analgesic effect narcotic analgesics.

Ataralgesia is the combined administration of a tranquilizer (usually Diazepam) and analgesics (usually Fentanyl).

100. Interaction of narcotic analgesics with atropine, α-blockers.

Atropine and α-blockers potentiate the action of narcotic analgesics.

101. Interaction of narcotic analgesics with ethyl alcohol.

Ethyl alcohol potentiates the action of narcotic analgesics.

102. Name the analgesic preparations of opium alkaloids.

Morphine, codeine, dihydrocodeine.

103. Name the agonists of opioid receptors - derivatives of diphenylpropylamine.

Methadone.

104. Name opioid receptor agonists from the group of phenylpiperidine.

Trimeperidine (promedol), fentanyl.

105. Name agonists-antagonists of opioid receptors.

Pentazocine, butorphanol, nalbuphine.

106. Name partial agonists of opioid receptors and analgesics with a mixed (opioid and non-opioid) mechanism of action.

Partial opioid receptor agonists: Buprenorphine.

Analgesics with a mixed mechanism of action: Tramadol.

107. Name antagonists of opioid receptors.

Naloxone, naltrexone.

108. Comparative antitussive activity of morphine and codeine.

Codeine has a pronounced antitussive effect, like morphine, but differs from it in the following properties:

1) weaker analgesic ability

2) to a lesser extent depresses the respiratory center

3) to a lesser extent inhibits intestinal motility

4) constriction of the pupil is mild

5) causes less mental depression, its use is associated with less danger of addiction

109. What is codeine?

Moderate agonist of opioid receptors (mainly μ- and κ-receptors), a derivative of the natural opium alkaloid.

110. What is methadone?

A strong agonist of opioid receptors (mainly μ- and κ-receptors), a derivative of diphenylpropylamine.

111. What is trimeperidine?

Moderate agonist of opioid receptors (mainly μ- and κ-receptors), a derivative of phenylpiperidine.

112. What is pentazocine?

Opioid receptor agonist-antagonist (κ- and σ-agonist, μ-receptor antagonist).

113. What is buprenorphine?

Partial opioid receptor agonist (primarily μ receptors)

114. What is tramadol?

Analgesic with a mixed mechanism of action - narcotic (agonist-antagonist of μ- and κ-receptors) and non-narcotic.

115. What is naloxone?

Competitive opioid receptor antagonist.

116. What drugs are used for neuroleptanalgesia?

Neuroleptanalgesia = neuroleptic + analgesic. Antipsychotics: Droperidol. Analgesic: Fentanyl.

Combined drug "Talamonal" for neuroleptanalgesia contains fentanyl and droperidol in a ratio of 1:50.

117. The main effects of non-narcotic analgesics - antipyretics.

ü analgesic effect

ü antipyretic effect (reduce only elevated body temperature, without affecting normal)

ü antiaggregatory effect

118. Name the main non-narcotic analgesics - centrally acting cyclooxygenase inhibitors.

Paracetamol.

119. Name non-narcotic analgesics - inhibitors of cyclooxygenase in peripheral tissues.

Acetylsalicylic acid, ibuprofen, keterolac, metamizole sodium (analgin)

120. What is dantrolene?

Non-narcotic analgesic, drug for the treatment of malignant hyperthermia.

121. What is nefopam?

A non-narcotic analgesic of central action, an agonist of dopamine, adrenaline and serotonin receptors, has some m-anticholinergic and sympathomimetic activity.

According to the chemical structure and properties, it does not belong to either opioid analgesics or NSAIDs.

122. What is baralgin?

Spasmoanalgesic, a combination drug containing analgin, papaverine-like antispasmodic and ganglionic blocker.

123. What is sumatriptan?

Specific selective agonist of serotonin 5HT1 receptors (5-hydroxytryptamine-1-like), located mainly in the cranial blood vessels.

It is used to treat acute migraine attacks.

124. What is ergotamine?

Ergot alkaloid used to treat acute migraine attacks.

125. Mechanism of analgesic action of non-narcotic analgesics.

Inhibition of cyclooxygenase → inhibition of the synthesis of prostaglandins PG E2, PG F2α, PGI2 → prostaglandins that cause hyperalgesia (increased sensitivity of nociceptors to chemical and mechanical stimuli) are not synthesized → prevention of hyperalgesia, an increase in the sensitivity threshold of neurons to pain stimuli.

126. The mechanism of antipyretic action of non-narcotic analgesics.

Inhibition of cyclooxygenase COX-2 → inhibition of the synthesis of fever mediators (mainly PG E1) → a decrease in the pyrogenic effect of fever mediators on the thermoregulatory center of the hypothalamus → antipyretic effect

127. Indications for the use of non-narcotic analgesics.

Headache, toothache, postoperative pain

ü rheumatic diseases, arthralgia, myalgia

ü non-rheumatic diseases of the musculoskeletal system, injuries

Neurological diseases (neuralgia, sciatica)

dysmenorrhea (algomenorrhea)

NB! Non-narcotic analgesics are not effective for visceral pain (myocardial infarction, renal colic, acute abdomen, etc.) and do not eliminate the emotional component of pain (fear, anxiety, agitation), unlike narcotic analgesics.

128. Contraindications to the use of non-narcotic analgesics.

ü erosive and ulcerative lesions of the gastrointestinal tract, especially in the acute stage

Severe impairment of liver and kidney function

ü cytopenia

ü individual intolerance

ü pregnancy

129. Side effects of non-narcotic analgesics.

ü dyspeptic disorders (abdominal pain, nausea, vomiting)

ü erosion and ulcers of the stomach and duodenum, bleeding and perforation (as a result of systemic inhibition of COX-1)

ü negative effect on kidney function (direct effect, vasoconstriction and decrease in renal blood flow → renal ischemia, impaired renal function, hypernatremia, hyperkalemia, increased blood pressure, interstitial nephritis)

ü hematotoxicity (aplastic anemia, agranulocytosis)

ü hepatotoxicity (change in transaminase activity, jaundice, sometimes drug-induced hepatitis)

hypersensitivity reaction (Quincke's edema, anaphylactic shock, bronchospasm)

ü neurotoxicity (headache, dizziness, impaired reflex reactions)

ü Reye's syndrome: encephalopathy, cerebral edema, liver damage ( In children with viral infections when they are prescribed aspirin)

130. Comparative characteristics of narcotic and non-narcotic analgesics.

131. List spasmoanalgesics.

Baralgin, spazmolgon, novigan.

132. What is Pentalgin ICN and Pentalgin - N? indications for their use.

Pentalgin ICN: metamizole + paracetamol + caffeine + codeine + phenobarbital

Pentalgin-N: Metamizole + naproxen + caffeine + codeine + phenobarbital

Indications for use:

Ø fever of various origins (including with colds accompanied by pain and inflammation)

Ø moderate pain syndrome of various origins (headache, toothache, neuralgia, myalgia, arthralgia, primary dysmenorrhea, sciatica)

133. Name the drugs used in acute migraine attacks.

A) non-narcotic analgesics - Acetylsalicylic acid, paracetamol, etc.

B) serotonin agonists (5HT1 - receptors) - sumatriptan, naratriptan

C) ergot alkaloids - Ergotamine

D) antiemetics - metoclopramide, domperidone

134. Name the drugs used to prevent migraine attacks.

Pizotifen,B- blockers, tricyclic antidepressants, sodium valproate, C blockersA ++ channels, cyproheptadine.

135. Name the drugs used for various neuralgia (postherpetic,

trigeminal and glossopharyngeal nerves, etc.).

Carbamazepine, phenytoin, sodium valproate, tricyclic antidepressants.

136. Name the aids used in acute and chronic pain syndromes.

Ø Clonidine(myocardial infarction, tumors, postoperative pain, etc.)

Ø Amitriptyline(chronic pain, tumors, phantom pain, etc.)

Ø Ketamine(tumors)

Ø Calcitonin(tumor metastases to bone)

Ø Somatostatin(hormone-secreting tumors of the gastrointestinal region and pancreas)

Ø Corticosteroids(compression neuropathy)

Ø Benzofurocaine(pancreatitis, peritonitis, acute pleurisy, colic, etc.)

Ø other drugs with analgesic effect: Baclofen(GABAergic agent), Diphenhydramine(antihistamine)

137. Name the main groups of psychopharmacological agents.

1. CNS depressants:

a) antipsychotics (neuroleptics)

b) anxiolytics (tranquilizers) and sedative-hypnotics

c) normotimics (means for stopping manic states)

2. CNS stimulants

a) antidepressants (timoleptics)

b) psychostimulants (stimulants of physical and mental activity)

c) nootropic drugs (restore mental and mnestic functions)

d) psychodysleptics (psychotomimetics)

138. Name the groups of CNS depressants.

A) antipsychotics (neuroleptics)

B) anxiolytics (tranquilizers) and sedative-hypnotics

C) normotimics (a remedy for stopping manic states)

139. Name the molecular targets of action of psychotropic drugs.

Targets of molecular action of PPP: processes of chemical communication ( Synaptic signal transmission) at various levels of brain organization.

PFP application points:

1) action potential in the presynaptic fiber

2) mediator synthesis

3) mediator storage

4) mediator metabolism

5) mediator release

6) mediator recapture

7) mediator degradation

8) mediator receptor

9) receptor-dependent increase or decrease in ionic conductivity

140. Anxiolytic, sedative and hypnotic effects - essence, similarities and differences.

Anxiolytic effect- due to the influence on emotional excitability and affective tension of a neurotic nature:

A) decreased emotional excitability

B) elimination of fear, anxiety, worry

C) sedation, the onset of sleep in adequate conditions

D) increase in healthy threshold of emotional excitability

Sedation- calming, reducing emotional excitability.

Sedative effect in contrast to anxiolytic:

1) less specific

2) has a less pronounced calming and antiphobic component

3) does not cause muscle relaxation and ataxia

hypnotic effect- causes drowsiness, accelerating the onset of sleep and maintaining its duration.

141. List the main psychotropic effects of anxiolytics.

Anxiolytics suppress:

• Emotional reactivity to aversive stimuli
• Phobic reactions (fear, worry, anxiety)
• Painful experiences (frustration)

Anxiolytics reduce:

• Hypochondriacal reactions
• Incontinence
• Irritability

As a result of the action of anxiolytics:

Ø streamlined behavior

Ø CNS depletion decreases

Ø social adaptation improves

Ø vegetative disorders are reduced

142. Name the pharmacological effects of benzodiazepines.

1) sedation - suppression of the reaction to constant stimuli with a decrease in the level of spontaneous activity and thinking

2) sleeping pills

3) anesthesia

4) anticonvulsant (anticonvulsant) effect

5) muscle relaxation

6) anxiolytic effect:

a) antiphobic - inhibition of the inhibitory effect of aversive stimuli on behavior

b) anterograde amnesia - loss of memory for previous events

c) disinhibition - euphoric effect, decreased self-control

7) depression of the respiratory center of the medulla oblongata and vasomotor center in diseases of the respiratory and cardiovascular systems

143. List the most commonly used anxiolytics.

a) benzodiazepines:

Anxiolytics with pronounced activity

Alprazolam (Xanax), Lorazepam, Phenazepam Middle Duration of action (t 1/2 5 – 24 h);

Chlordiazepoxide (Elenium), Diazepam (Relanium)– long-acting (t 1/2 > 24 h);

Day anxiolytics :

Tofizepam, oxazepam

medazepam, dipotassium clorazepate Long acting

B) non-benzodiazepine (atypical anxiolytics): Buspirone hydrochloride, mexidol

144. Main pharmacokinetic properties of benzodiazepines.

1. Absorption.

Usually given orally. They are best absorbed in the duodenum (depending on lipophilicity and pH).

2. Distribution

A) the main role in the rate of entry of drugs into the CNS is played by their solubility in lipids.

B) benzodiazepines actively bind to plasma proteins (60-95%)

C) Benzodiazepines can reach the fetus through the placental barrier.

3. Biotransformation

A) almost all benzodiazepines are transformed into hydrophilic substances for subsequent excretion

B) determining in the metabolism of benzodiazepines is the microsomal system of the liver

C) drugs with a long half-life are characterized by cumulation

4. Excretion: the main part is excreted by the liver, trace amounts are excreted unchanged by the kidneys with urine

145. Molecular mechanism of action of benzodiazepines.

Benzodiazepine + benzodiazepine region of the chloride channel GABA receptor → increased GABA affinity for the receptor → increased chloride conductivity → hyperpolarization of neurons → inhibition of depolarization caused by an excitatory mediator.

146. Features of the action of "daytime" tranquilizers.

Possess Tranquilizing activity, but have a number of properties:

1) do not cause drowsiness during the day and do not impair the quality of life

2) do not have a muscle relaxant and anticonvulsant effect

147. Name "daytime" tranquilizers.

Tofizepam, oxazepam- average duration of action

Medazepam, dipotassium clorazepate Long acting

148. What is buspirone?

Atypical anxiolytic.

Peculiarities:

ü non-benzodiazepine anxiolytic, azaspirodecanedione by structure

ü does not act through GABAergic systems

ü does not have hypnotic, anticonvulsant and muscle relaxant properties

ü has a low addiction potential

the effect reaches a maximum within a week

149. What is medazepam?

Long acting daytime tranquilizer.

150. What is alprazolam?

Benzodiazepine anxiolytic with a pronounced activity of medium duration of action.

151. What is temazepam?

Benzodiazepine with a pronounced hypnotic effect of medium duration of action

152. What is oxazepam?

Daytime tranquilizer of average duration of action.

It has a pronounced anxiolytic effect and a minimal sedative-hypnotic effect.

153. What is chlordiazepoxide?

Benzodiazepine anxiolytic with pronounced long-acting activity.

154. What is flumazenil?

Antagonist of benzodiazepines.

Blocks benzodiazepine receptors, eliminating or reducing the severity of most of the central effects of benzodiazepines.

155. Distinctive properties of buspirone in comparison with benzodiazepines.

It does not have hypnotic, anticonvulsant and muscle relaxant properties.

156. Name the main side effects of benzodiazepine anxiolytics.

weakness, drowsiness, delayed motor reactions

memory loss, headache

ü nausea, in some cases jaundice, increased activity of hepatic transaminases

ü menstrual irregularities, decreased sexual potency

o skin rashes

addiction, the development of mental and physical drug dependence with long-term use

157. Indications for the use of diazepam (Relanium, Seduxen).

See question 66. Another original follow up question.

158. Name the areas of medical application of anxiolytics.

Ø as sedative-hypnotics in psychiatry

Ø during anesthesia to potentiate the action of other anesthetics

Ø as antiepileptic drugs

Ø for muscle relaxation

159. Name the benzodiazepines used as hypnotics.

A) short acting Triazolam

B) Average duration of action - temazepam

B) long acting Nitrazepam, flurazepam, flunitrazepam

B) cyclopyrrolones - Zopiclone (Imovan);

B) imidazopyridines - Zolpidem;

D) antihistamines

D) chloral hydrate;

E) barbiturates - Amobarbital;

160. Name benzodiazepines of short duration of action.

Triazolam, midazolam.

161. Name benzodiazepines of medium duration of action.

Temazepam, oxazepam.

162. Name long-acting benzodiazepines.

Nitrazepam, flurazepam, flunitrazepam.

163. Name hypnotic drugs of non-benzodiazepine nature.

A) cyclopyrrolones - Zopiclone (Imovan);

B) imidazopyridines - Zolpidem;

B) antihistamines diphenhydramine (diphenhydramine), promethazine;

G ) chloral hydrate;

D) barbiturates - Amobarbital;

164. Influence of hypnotic agents on the structure of sleep.

1) decrease in the duration of the period of falling asleep (latent period of the onset of sleep)

2) prolongation of stage 2 of MDH sleep (sleep with slow eye movements)

3) shortening the stage of slow-wave sleep

4) decrease in the duration of REM sleep (sleep with rapid eye movements)

The first two effects are clinically significant and useful.

165. Arrange the following drugs in order of decreasing effect on sleep structure: zolpidem, nitrazepam, triazolam, zopiclone, amobarbital, temazepam.

1) Amobarbital(barbiturates change the structure of sleep the most)

2) Nitrazepam, temazepam, triazolam long-acting, intermediate-acting and short-acting benzodiazepines, respectively

3) zolpidem and zopiclone(approximately the same effect on the structure of sleep).

Thus, the sequence, in decreasing order of influence on sleep structure, is as follows: Amobarbital, nitrazepam, temazepam, triazolam, zolpidem, and zopiclone.

166. The use of melatonin as a pharmacological agent.

ü disorder of the normal circadian rhythm as a result of rapid movement between the time zones of the Earth, manifested by increased fatigue

ü sleep disorders, including in elderly patients

depressions that are seasonal

167. The main side effects of hypnotic drugs.

ü abundance of dreams, nightmares, interrupted sleep

ü after sleep: prolonged drowsiness, fatigue, impaired coordination of movements, nystagmus

o respiratory depression

o vascular collapse

o increase in body temperature

- Decreased diuresis

o Increased sensitivity

Decreased tone and peristalsis of the gastrointestinal tract

168. Name some of the most commonly used sedatives.

Valerian, motherwort, proxybarbal, corvalol.

169. Indications for use and side effects of sedatives.

Indications for the use of sedatives:

ü neuroses of various etiologies with increased irritability

ü insomnia

ü for the prevention of withdrawal syndrome of certain sedatives and hypnotics

ü for muscle relaxation in specific neuromuscular diseases

ü sedation and amnesia before medical and surgical procedures

for diagnosis and treatment in psychiatry

Side effects:

o drowsiness and slight dizziness

ü violation of judgment

Difficulty in motor functions and decreased performance

dose-dependent depression of CNS functions

ü Allergic reactions in the form of a skin rash (rarely)

170. What are antipsychotics?

Antipsychotics (the old term is neuroleptics) are drugs intended for the treatment of severe diseases of the central nervous system with thought disorders (endogenous and exogenous psychoses, schizophrenia).

171. Name the main classes of APS (do not specify drugs).

A) phenothiazine derivatives: aliphatic, piperidine, piperazine

B) thioxanthene derivatives

C) derivatives of butyrophenone

D) derivatives of other groups (atypical APS)

172. The main clinical effect of neuroleptics.

Gradual weakening of psychotic symptoms, delusions, hallucinations, emotions, restoration of normal behavior in patients with psychosis.

The state of neuroplegia, drowsiness, lethargy, stupor in healthy people.

173. Name neuroleptics from the class of phenothiazines.

Ø aliphatic - Chlorpromazine (chlorpromazine)

Ø piperidine - Thioridazine

Ø piperazine - Fluphenazine, trifluoperazine (triftazine)

174. Name neuroleptics from the class of butyrophenone.

Haloperidol, droperidol

175. Name neuroleptics from the class of thioxanthene.

Chlorprothixene, flupentixol

176. The essence of the antipsychotic action of neuroleptics.

Elimination of productive symptoms of psychosis (delusions, hallucinations) and delaying the further development of the disease.

177. Parts of the brain responsible for the antipsychotic effect of neuroleptics.

Ø black substance

Ø limbic system

Ø neocortex

Ø hypothalamus

Ø pale nucleus

Ø caudate nucleus

Ø posterior pituitary gland

Ø periventricular neurons

Five main connections between neurons responsible for the antipsychotic effect:

1. Mesolimbic-mesocortical pathway: the connection between the substantia nigra and the limbic system with the neocortex.

2. Nigrostriatal pathway: connection between the substantia nigra and the caudate nucleus with the globus pallidus.

3. Tuberoinfundibular pathway: connection between the arcuate nuclei, periventricular neurons and the hypothalamus, the posterior pituitary gland.

4. Medullary-periventricular pathway: connection between neurons of the motor nucleus of the vagus nerve and periventricular neurons.

5. Incertohypothalamic pathway: connections between the nuclei of the hypothalamus and the lateral neurons of the septum.

178. Mechanism of antipsychotic action of APS.

Blockade of D2 receptors of the central nervous system, which normally carry out pre- and postsynaptic inhibition → removal of the activity of D2 receptors (in psychosis, the activity of these receptors is pathologically increased) → antipsychotic activity.

179. Pharmacokinetic features of APS.

1. Absorbed in the gastrointestinal tract quickly, but not completely

2. Partially undergo significant presystemic elimination

3. Highly lipophilic, accumulate in the brain

4. Transformed in the liver, excreted as polar metabolites

5. A small part is displayed unchanged.

180. What is chlorpromazine?

Aliphatic antipsychotic from the class of phenothiazines.

181. What is chlorprothixene?

Antipsychotic from the thioxanthene class.

182. What is haloperidol?

An antipsychotic from the butyrophenone class.

183. What is sulpiride?

Atypical antipsychotic (from the group of antipsychotics - derivatives of other groups)

184. What are clozapine and risperidone?

Atypical antipsychotics (from the group of antipsychotics - derivatives of other groups)

185. Name the pharmacological effects of APS used in medical practice.

ü antipsychotic effect - due to the blockade of D2 receptors of the central nervous system

ü sedative (calming) effect - due to the blockade of adrenoreceptors of the reticular formation of the brain stem

ü antiemetic effect - due to the blockade of D2 receptors of the vomiting center

186. Side effects of APS associated with the effect on the central nervous system.

Development of diverse Extrapyramidal disorders:

ü acute dystonia - spastic contractions of the skeletal muscles of the face, opisthotonus, dysphagia, laryngospasm, etc.

ü parkinsonian syndrome - bradykinesia, skeletal muscle rigidity, tremor, monotonous speech

akathisia - uncontrollable motor restlessness, restlessness

ü neuroleptic malignant syndrome - hyperemia, diffuse muscle rigidity, autonomic disorders (tachycardia, hypertension, tachypnea, etc.)

tardive dyskinesia - choreo-like stereotypical facial muscle contractions

ü perioral tremor - hyperkinesis of the circular muscle of the mouth

187. Influence of APS on vegetative functions.

A) cardiovascular system: hypotension, negative inotropic and bathmotropic effects, tachycardia, collapse

B) respiratory system: respiratory failure

C) digestive system: dry mouth, constipation, dynamic intestinal obstruction, cholestatic obstructive jaundice with bilirubinemia

D) organs of vision: conjunctival melanosis, possibly increased intraocular pressure, mydriasis

D) blood system: inhibition of leukopoiesis, agranulocytosis

E) genitourinary system: urination disorder, urinary retention, ejaculatory dysfunction

G) skin: photosensitivity, hyperpigmentation, urticaria, petechiae

188. Influence of APS on the endocrine system.

hyperglycemia (typical of chlorpromazine)

ü violation of ovulation, aminorrhea / galactorrhea, increased libido in women

ü Gynecomastia, weight gain, sexual dysfunction (decreased libido, erectile dysfunction and ejaculation, priapism) in men

189. Name the means used to stop acute psychosis.

Haloperidol, risperidone, loxapine.

190. Name the main groups of antidepressants (do not specify drugs).

1. Monoamine reuptake inhibitors

2. MAO inhibitors

3. Phytopreparations with antidepressant activity

191. Name the subgroups of inhibitors of re-uptake of monoamines (do not specify drugs).

A) inhibitors of predominantly re-uptake of noradrenaline (tricyclic antidepressants)

B) selective serotonin re-uptake inhibitors

B) atypical antidepressants

192. Name inhibitors of predominantly re-uptake of norepinephrine.

Imipramine, amitriptyline, doxepin, amoxapine.

193. Name selective serotonin re-uptake inhibitors.

fluoxetine,sertraline, Paroxetine, venlafaxine.

194. Name atypical antidepressants.

Trazadone, mianserin, Tianeptine

195. Name MAO inhibitors of irreversible and reversible action.

A) MAO inhibitors of irreversible action - Nialamide

B) reversible MAO inhibitors - Moclobemide

196. Name phytopreparations with antidepressant activity.

St. John's wort (Negrustin), Hypericin

197. Basic pharmacokinetic properties of antidepressants.

1. Tricyclic antidepressants:

ü incompletely absorbed in the gastrointestinal tract

undergo active first pass metabolism

ü large volume of distribution due to good protein-binding ability and high fat solubility

2. Selective serotonin reuptake blockers:

ü well absorbed in the gastrointestinal tract

are metabolized to active metabolites

Other properties are similar to those of tricyclic antidepressants

3. MAO inhibitors:

ü quickly and well absorbed in the gastrointestinal tract

ü metabolized in the liver, excreted by the kidneys in the form of metabolites

198. Influence of tricyclic antidepressants on catecholaminergic mechanisms of the brain.

1) inhibit the reuptake of noradrenaline (predominantly) and / or serotonin

2) block α-adrenergic receptors, causing tachycardia and orthostatic hypotension

199. Influence of sertraline on the mediator processes of the brain.

selective blocker of neuronal reuptake of serotonin in the brain

ü does not affect the uptake of norepinephrine and dopamine

ü does not have specific affinity for adreno - and m-cholinergic receptors, GABA receptors, dopamine, histamine, serotonin or benzodiazepine receptors

It is inhibited by MAO

200. Influence of MAO inhibitors on monoaminergic processes in the brain.

MAO inhibitors (especially selective MAO-A inhibitors, which primarily metabolize norepinephrine, serotonin, tyramine, prevent the destruction of monoamines and help prolong their action, providing an antidepressant effect).

201. What is imipramine?

202. What is amitriptyline?

Tricyclic antidepressant, predominantly norepinephrine re-uptake inhibitor.

203. What is sertraline?

204. What are fluoxetine and paroxetine?

Selective serotonin re-uptake inhibitor.

205. What is moclobemide?

Reversible MAO inhibitor.

206. What are trazadone and tianeptine?

Atypical antidepressants from the group of monoamine re-uptake inhibitors.

207. Side effects of tricyclic antidepressants.

A) sedative effects: drowsiness, potentiation of the action of other sedatives

B) sympathomimetic effects: tremor, insomnia

C) M-anticholinergic effects: blurred vision, constipation, urinary retention, thought disorders

D) cardiovascular: orthostatic hypotension, conduction blockade, arrhythmias

D) psychiatric: exacerbation of psychosis, withdrawal syndrome

E) neurological: convulsions

G) metabolic-endocrine: weight gain, sexual dysfunction

208. Side effects of MAO inhibitors.

o Headache, drowsiness

o dry mouth

o weight gain

o orthostatic hypotension

ü Sexual dysfunction

209. Diet restriction when using MAO inhibitors.

MAO inhibitors enhance the vasoconstrictive effect of tyramine contained in a number of foods (cheese, chocolate, etc.) and can lead to the development of a hypertensive crisis, therefore, products containing this substance should be excluded from the diet if possible or limited in their use.

210. Side effects of selective serotonin re-uptake inhibitors.

o anxiety, insomnia

asthenia, tremor

ü sweating

ü symptoms of gastrointestinal disorders

Allergic reactions (rash)

211. Indications for prescribing antidepressants.

1) depression:

a) major (endogenous) depression - primarily due to biochemical disorders of the brain

b) depressive states as part of psychosis

2) panic disorders, panic attacks (MAO-A inhibitors are especially effective)

3) obsessive-compulsive disorders (obsessive-compulsive disorders, serotonin reuptake inhibitors are especially effective)

4) enuresis (tricyclic antidepressants are especially effective)

5) chronic pain of unknown origin (tricyclic antidepressants are especially effective)

212. Benefits of atypical antidepressants:

1) block predominantly serotonin reuptake

2) have the properties of agonists and antagonists of serotonin and catecholamine receptors

3) do not have atropine-like and alpha-adrenergic blocking action

213. Benefits of serotonin re-uptake inhibitors versus tricyclic antidepressants.

Unlike tricyclic antidepressants, which inhibit both norepinephrine and serotonin uptake, serotonin re-uptake inhibitors selectively inhibit Serotonin reuptake only with low vegetative toxicity.

214. Spectrum of pharmacological activity of antidepressants.

Ø depression

Ø panic states

Ø obsessive-compulsive disorders

Ø chronic pain syndromes

Ø other indications (bulimia and anorexia nervosa, school phobia, attention deficit hyperkinetic syndrome)

215. Name antidepressants with a pronounced sedative effect.

Amitriptyline, doxapen, imipramine, amoxapine.

216. Name antidepressants with an activating component of psychotropic action.

Moclobemide, Nialamide.

217. Name the main groups and preparations of normothymic drugs.

A) lithium salts - Lithium carbonate, lithium oxybate

B) anticonvulsants - Carbamazepine, sodium valproate

C) antipsychotics and benzodiazepines

218. The mechanism of action of lithium ions.

1. Serotonin 5-HT1A receptor agonist ® increased activity of the hippocampus ( Currently, this mechanism is receiving the most attention.)

2. Influence on ion transport: replacement of sodium ions in biological membranes ® lithium is not able to support ion transport in sodium channels ® antagonistic action in relation to sodium ions, the impossibility of generating an action potential on the neuron membrane

3. Inhibition of synaptic release of norepinephrine and dopamine in the brain, increased inactivation of these catecholamines ® decreased activity of brain neurons

4. Blocking the formation of inositol and depletion of phosphatidylinositol-4,5-biphosphate, a precursor of DAG and IP3.

Thus, lithium blocks neuronal hyperactivity in mania by selectively blocking the resynthesis of DAG and IP3 precursors and suppressing excessive neuronal activity.

219. Basic pharmacokinetic properties of lithium preparations.

Ø suction almost 100%

Ø is distributed mainly in liquid media, slowly penetrates into cells, does not bind to proteins

Ø not metabolized

Ø is almost completely excreted in the urine, the plasma half-life is about a day

220. What are lithium salts used for?

bipolar affective disorders (manic-depressive psychosis)

Prevention of mania and depression

repeated exacerbations of acute endogenous depression

ü schizoaffective disorders (combination of symptoms of schizophrenia with depressive manifestations)

affective disorders in alcoholism

schizophrenia (when combined with neuroleptics)

ü correction of aggressive and conflict behavior in prison inmates

221. Side effects of lithium preparations.

1. Neurological and mental: tremor, motor hyperactivity, ataxia, dysarthria, aphasia

2. Effect on thyroid function: decreased function, hypothyroidism

3. Action on the kidneys: polydipsia, polyuria, nephrogenic diabetes mellitus, chronic interstitial nephritis and glomerulopathy with nephrotic syndrome

5. Action on the heart: bradycardia, tachycardia (they are a contraindication for the appointment of lithium)

5. During pregnancy and feeding in a newborn: lethargy, cyanosis, decreased sucking reflex, hepatomegaly.

6. Others: skin rashes, sexual dysfunction.

222. Name the main groups of nootropics.

A) improving predominantly metabolic processes - Piracetam (nootropil), pyritinol, meclofenoxate, cerebrolysin;

B) improving predominantly cerebral blood flow - Vinpocetine (Cavinton), Nimodipine.

C) activators of central cholinergic processes - Donepezil hydrochloride, rivastigmine.

223. Name a few nootropic drugs.

Piracetam (Nootropil), Vinpocetine (Cavinton), Donepezil Hydrochloride.

224. The main effects of nootropics.

stimulation of mental activity (thinking, learning, memory)

ü antihypoxic effect, increasing the resistance of brain tissue to hypoxia

ü Moderate anticonvulsant activity

ü positive effect on metabolic processes and blood circulation of the brain, increased glucose utilization

Improvement of microcirculation in ischemic areas

inhibition of activated platelet aggregation

ü protective effect in case of brain damage caused by hypoxia, intoxication, electric shock

225. Indications for the use of nootropics.

memory impairment, dizziness, decreased concentration

o emotional lability

ü dementia due to cerebrovascular accident (ischemic stroke), brain injury, Alzheimer's disease, in old age

ü coma of vascular, traumatic or toxic genesis

ü treatment of abstinence and psychoorganic syndrome in chronic alcoholism

ü learning disabilities in children that are not associated with inadequate education or the characteristics of the family environment (as part of combination therapy)

sickle cell anemia (as part of combination therapy)

226. Main effects of bemitil (actoprotector).

ü psychoactive effect

ü antihypoxic activity

increase the body's resistance to hypoxia

ü Increased physical activity

227. Name a few psychoactive drugs.

Caffeine, Methylphenidate (meridyl), mesocarb, amphetamine (phenamine), bemityl

228. Main pharmacological effects of methylxanthines.

1. Impact on the central nervous system:

A) low and medium doses - excitation of the cortex, increasing the level of wakefulness, reducing the feeling of fatigue

B) high doses - stimulation of the medulla oblongata, convulsions

2. Action on the cardiovascular system:

A) direct positive chronotropic and inotropic action

B) in high doses - relaxation of the SMC of all vessels, except for the brain, while the tone of the brain increases

C) decrease in blood viscosity, improve blood flow

3. Impact on the gastrointestinal tract: stimulation of the secretion of hydrochloric acid and enzymes in the stomach

4. Action on the kidneys: an increase in diuresis (due to a) an increase in glomerular filtration and b) a decrease in tubular reabsorption of sodium)

5. Impact on SMC: bronchodilation without the development of tolerance to the action of methylxanthines.

6. Impact on skeletal muscles: restoration of contractility and removal of fatigue of the diaphragm in patients with chronic obstructive pulmonary disease.

229. Effect of caffeine on the central nervous system.

In small doses - a stimulating effect:

ü enhances and regulates excitation processes in the cerebral cortex

ü enhances positive conditioned reflexes, increases motor activity, mental and physical performance

ü reduces fatigue and drowsiness

NB! Large doses of caffeine have Inhibitory effect on the CNS and may lead to Depletion of nerve cells.

230. Effect of caffeine on the respiratory center.

Stimulation of the respiratory center.

231. The effect of caffeine on the cardiovascular system.

A) central effects: stimulation of the vasomotor center and centers of the vagus nucleus.

B) peripheral effects:

ü an increase in vascular tone through excitation of the vasomotor center, a decrease in vascular tone with a direct effect on the SMC (in this case, the coronary vessels expand more often, and the brain vessels become toned)

ü direct stimulating effect on the myocardium

increase in blood pressure with hypotension

232. Action of caffeine on bronchi and kidneys.

ü Moderate antispasmodic effect on SMCs (bronchi, biliary tract, etc.).

ü a slight increase in diuresis (as a result of inhibition of the reabsorption of sodium and water ions, expansion of the renal vessels and increased filtration in the glomeruli)

233. Effect of caffeine on the gastrointestinal tract.

increased secretion of gastric glands

ü moderate myotropic antispasmodic effect on the biliary tract

234. Effect of caffeine on platelets.

Reduces platelet aggregation.

235. The use of caffeine in medical practice.

ü infectious and other diseases accompanied by depression of the functions of the central nervous system and the cardiovascular system

ü poisoning with drugs and other poisons that depress the central nervous system

spasms of cerebral vessels (with migraine, etc.)

to improve mental and physical performance

ü to eliminate drowsiness

with enuresis in children

236. Indications for the use of mesocarb (psychomotor stimulant)

ü asthenic conditions after intoxication, infections and injuries of the central nervous system, physical and mental overwork

ü neurotic disorders with lethargy, sluggish schizophrenia

withdrawal syndrome in chronic alcoholism

ü developmental delay in children as a result of organic lesions of the central nervous system with adynamia

ü asthenic phenomena associated with the use of neuroleptics and tranquilizers

ü lethargy, apathy, decreased performance in depression

237. Name the main analeptics.

Niketamide, bemegride, etimizole, caffeine sodium benzoate

238. How are analeptics subdivided into groups according to the direction of action on the respiratory center?

A) direct-acting respiratory stimulants: Bemegrid, etimizol.

B) respiratory stimulants of direct and reflex action: Niketamide (cordiamine), carbonic acid

239. Side effects of analeptics.

o nausea, vomiting

muscle twitching, spasms

o allergic reactions

restlessness, dizziness, sleep disturbances

Rp.: Alprazolami 0.0005

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

S. Inside, one tablet 3 times a day.

Rp.: Amitriptylini 0.025

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

S. Inside, one tablet 4 times a day.

Rp.: Sol. Amitriptylini 1% - 2 ml

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

S. Intramuscularly, 2 ml 3 times a day.

Rep.: Tab. Baralginum N. 20

Rp.: Baralgini 5 ml

D.t.d. N.5 in amp.

S. Intramuscularly, 5 ml.

Rp.: Natrii valproatis 0.15

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

S. Inside, 1 tablet 2 times a day.

Rp.: Natrii valproatis 0.15

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

S. Inside, 1 capsule 2 times a day.

Rp.: Zolpidemi tartrati 0.01

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

S. Inside, 1 tablet at bedtime.

Rp.: Carbamazepini 0.2

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

Rp.: Lorazepami 0.001

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

S. Inside 1 tablet 1 time per day

Rp.: Lithii carbonatis 0.3

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

S. Inside 1 tablet 1 time per day

Rp.: Medazepami 0.01

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

S. Inside, 1 tablet 3 times a day.

Rp.: Mesocarbi 0.005

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

S. 1 tablet 1 time per day.

Rep.: Tab. "Nakom" No. 20

D.S. Orally 1 tablet 3 times a day

Rp.: Dragee Tolperisoni 0.05

Rp.: Nefopami 0.03

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

S. Inside, 2 tablets 3 times a day

Rp.: Sol. Nefopami 2% - 1 ml

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

S. Intramuscularly, 1 ml every 6 hours.

Rp.: Nitrazepami 0.005

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

S. Inside, 1 tablet half an hour before bedtime.

Rp.: Piracetami 0.2

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

S. Inside 1 tablet 2 times a day

Rp.: Piracetami 0.4

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

Rp.: Sol. Piracetami 20% - 5 ml

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

S. Intramuscularly 5 ml 1 time per day

Rp.: Sertalini hydrochloridi 0.05

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

S. Inside 1 tablet 1 time per day

Rp.: Sumatriptani succinati 0.025

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

S. Inside 1 tablet 1 time per day

Rp.: Sol. Sumatriptani succinati 1.2% - 0.5 ml

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

S. Subcutaneously, 0.5 ml once a day

Rp.: Tramadoli 0.05

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

S. By mouth 1 capsule up to 3 times a day

Rp.: Sol. Tramadoli 5% - 1 ml

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

S. Intramuscularly 1 ml 1 time per day

Rp.: Sol. Tramadoli 10% - 1 ml

D.S. Inside, 20 drops in a small amount of water 6 times a day.

Rp.: Supp. cum Tramadolo 0.1

S. Rectally 1 suppository.

Rp.: Trimeperidini hydrochloridi 0.025

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

Rp.: Sol. Trimeperidini hydrochloridi 1% – 1 ml

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

S. Subcutaneously 1 ml 1 time per day

Rep.: Tab. "Phenytoinum" No. 20

D.S. Orally 1 tablet 3 times a day

Rp.: Fluoxetine 0.02

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

S. Inside 1 capsule 1 time per day

Rp.: Dragee Chlorpromazini hydrochloridi 0.025

S. Inside 1 tablet 3 times a day

Rp.: Sol. Chlorpromazini hydrochloridi 2.5% - 2 ml

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

S. Intramuscularly 2 ml 3 times a day

Rp.: Sol. Ergotamini hydrotartratis 0.05% – 1 ml

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

S. Intramuscularly 1 ml 1 time per day.

Rp.: Sol. Ergotamini hydrotartratis 0.1% – 10 ml

D.S. Inside 10 drops 3 times a day

Rp.: Ergotamini hydrotartratis 0.001

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

S. Inside 1 tablet 3 times a day

Rp.: Dragee Ergotamini hydrotartratis 0.001

S. Inside 1 capsule 3 times a day

Rp.: Ethosuximidi 0.25

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

S. Inside 1 tablet 1 time per day

Rp.: Sol. Ethosuximidi 5% - 50 ml

D.S. Inside, 15 drops.

Rp.: Trigexiphenidili 0.001

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

S. Inside 1 tablet 1 time per day

List the symptoms of anesthesia.

The state of anesthesia is characterized by:

Analgesia - suppression of pain sensitivity;

Amnesia;

Loss of consciousness;

Suppression of sensory and autonomic reflexes;

Relaxation of skeletal muscles.

Name the main means for inhalation anesthesia.

1) Liquid volatiles:

- halothane (halothane), enflurane, isoflurane, non-halogenated NS ( diethyl ether).

2) Gas drugs:

- nitrous oxide

Name the main means for non-inhalation anesthesia.

1) barbiturates: sodium thiopental.

2) non-barbituric NS: ketamine (calypsol), etomidate, propofol, propanidide, sodium oxybate.

Requirements for drugs for anesthesia.

· Smooth introduction to anesthesia without the stage of excitation.

Sufficient depth of anesthesia, providing optimal conditions for the operation.

Good controllability of the depth of anesthesia.

Quick recovery from anesthesia.

Large therapeutic latitude - the range between the concentration in which the drug causes anesthesia, and its minimum toxic concentration. The narcotic latitude is judged by their concentration in the exhaled air, and the means for non-inhalation - by the doses administered. The greater the narcotic latitude, the safer the drug.

· No side effects.

· Simplicity in technical application.

· Fire safety.

· Acceptable cost.

Name the stages of anesthesia.

1) The stage of analgesia.

2) Stage of excitation.

3) Stage of surgical anesthesia:

1st level – superficial anesthesia.

2nd level - light anesthesia.

Level 3 - deep anesthesia.

4th level superdeep anesthesia.

4) Stage of awakening (agonal - in case of overdose).

Functional characteristics of anesthesia.

1) stage of analgesia.

It is characterized by the suppression of pain sensitivity. Consciousness is preserved, but the orientation is broken. Typical amnesia.

2) Excitation stage.

Difficulty introducing anesthesia. Consciousness is lost, motor and speech excitement is observed, pupils are dilated, breathing quickens, tachycardia, blood pressure fluctuates, coughing, hypersecretion of bronchial and salivary glands, and vomiting may occur. Possible cardiac arrest.

3) Stage of surgical anesthesia:

Consciousness is turned off, pain sensitivity is absent, reflex activity is suppressed, pupils are constricted, blood pressure stabilizes, breathing becomes regular. With the deepening of anesthesia, the pulse rate changes, cardiac arrhythmias are possible, breathing is gradually depressed, relaxation of skeletal muscles, jaundice may occur, kidney function may be impaired

4) Awakening stage.

Analgesia persists for a long time, vomiting often occurs, but bronchopneumonia may develop.

What is the minimum alveolar concentration (MAC). What properties of inhalation drugs for anesthesia can be judged by the value of this indicator?

During general anesthesia, the partial pressure of the inhaled anesthetic in the brain is equal to that in the lungs when a steady state is reached. The minimum alveolar concentration (MAC) is the concentration at which 50% of patients do not respond to the impact of a damaging factor (surgical incision). MAC is used to determine the effectiveness of an anesthetic.

The mechanism of the analgesic action of drugs for anesthesia.

1) Interaction with the postsynaptic neuronal membrane, which causes a change in the permeability of ion channels, which disrupts the process of depolarization and, consequently, interneuronal transmission of impulses.

2) An increase in the intracellular concentration of calcium ions, a decrease in their uptake by mitochondria. This causes hyperpolarization of the membrane, an increase in the permeability for potassium ions and, in general, a decrease in the excitability of neurons.

3) Presynaptic action leading to a decrease in the release of excitatory mediators (ACh).

4) Interaction with GABA-benzodiazepine-barbiturate receptor complex and potentiation of GABA action.

5) Inhibition of metabolic processes of CNS neurons.

Benefits of halothane anesthesia.

High drug activity.

Anesthesia occurs quickly with a short stage of arousal.

Anesthesia with halothane is easily controlled.

When the inhalation is stopped, the patient wakes up within 5-10 minutes.

Anesthesia proceeds with quite satisfactory muscle relaxation. Fluorotan enhances the myoparalytic effect of antidepolarizing curariform drugs.

Does not cause irritation of mucous membranes, acidosis, nausea and vomiting in the post-anesthetic period.

Advantages of ether anesthesia.

Expressed narcotic activity.

Sufficient narcotic latitude.

Relatively low toxicity.

Ether anesthesia is fairly easy to manage.

Good muscle relaxation.

Benefits of anesthesia caused by nitrous oxide.

Does not cause side effects during surgery.

Does not have irritating properties.

It does not have a negative effect on parenchymal organs.

The rate of induction and recovery from anesthesia is very high.

Advantages of thiopental anesthesia.

Causes anesthesia after 1 minute without the stage of excitation.

The duration of anesthesia is 20-30 minutes.

Causes stronger muscle relaxation than hexenal.

Interaction of adrenaline and halothane.

When applied halothane (halothane) possible cardiac arrhythmias. They are due to the direct influence halothane on the myocardium, including its sensitization to adrenaline. In this regard, against the background of halothane anesthesia, the introduction adrenaline contraindicated.

Interaction of adrenaline and ethyl ether.

Interaction adrenaline and ethyl ether prevents possible reflex slowing of breathing and heart rate up to apnea and cardiac arrest.

Disadvantages of halothane anesthesia.

Bradycardia associated with an increase in the tone of the vagus nerve.

A decrease in blood pressure as a result of inhibition of the vasomotor center and sympathetic ganglia, as well as a direct myotropic effect on the vessels.

Cardiac arrhythmias are possible due to a direct effect on the myocardium, including its sensitization to adrenaline.

Fluorotan inhibits the secretory activity of the salivary, bronchial, and gastric glands.

In the body, a significant part of halothane (20%) undergoes biotransformation.

Disadvantages of ether anesthesia

A pronounced stage of excitation, which is accompanied by tachycardia, fluctuations in blood pressure, cough, hypersecretion of the bronchial and salivary glands, and vomiting.

Low rate of induction and recovery from anesthesia.

Sometimes there is jaundice.

Renal function is inhibited, albuminuria is possible.

acidosis develops.

Postoperative bronchopneumonia is possible.

Disadvantages of anesthesia with nitrous oxide.

Low narcotic activity (there is no stage of deep anesthesia).

Does not cause muscle relaxation.

Nausea and vomiting are possible.

With prolonged use, the development of leukopenia, megaloblastic anemia, neuropathy is possible, this is due to the oxidation of cobalt in the cobalamin molecule.

Disadvantages of thiopental anesthesia.

Convulsive twitching of the muscles.

Laryngospasm.

Depressing effect on the respiratory and vasomotor centers, also the heart.

With rapid administration, apnea and collapse are possible.

Local irritant.

What is neuroleptanalgesia?

Neuroleptanalgesia is a special kind of general anesthesia. It is achieved by the combined use of antipsychotics (neuroleptics), such as droperidol, with an active narcotic analgesic (especially fentanyl). In this case, the antipsychotic effect is combined with pronounced analgesia. Consciousness is preserved. Both drugs act quickly and for a short time. This facilitates the introduction and exit from neuroleptanalgesia.

What is combined anesthesia? Example.

Combined anesthesia is the combined administration of two or more drugs for anesthesia. Combine means for inhalation anesthesia with inhalation or non-inhalation administered drugs. Positive is the rapid introduction into anesthesia and the elimination of the stage of excitation. For example, anesthesia begins with the introduction thiopental-sodium, which ensures the rapid development of anesthesia without the stage of excitation. One of the most commonly used drug combinations for anesthesia is the following: a barbiturate or an arc potent drug for non-inhalation anesthesia + halothane + nitrous oxide. The advantage of combined anesthesia is also that the concentrations (doses) of the components in the mixture are less than when using a single drug for anesthesia, therefore, it is possible to reduce their toxicity and reduce the frequency of side effects.

What is potentiated anesthesia? Example.

Potentiated anesthesia is a combination of drugs for anesthesia with drugs of various effects, which is aimed at enhancing the narcotic effect. For example, midazolam. Its sedative and hypnotic effects are important.

What is induction anesthesia? Example.

Introductory anesthesia - in / in the introduction of general anesthetics, which ensures the rapid development of anesthesia without the stage of excitation. Sodium thiopental may be used.

Effect of ethanol on diuresis.

Diuretic action ethyl alcohol has a central genesis (the production of ADH in the posterior pituitary gland decreases).

The effect of ethanol on the gastrointestinal tract.

Enhances the secretory activity of the salivary and gastric glands. This is the result of a psychogenic, reflex, as well as a direct action on the glands. An increase in the secretion of the gastric glands with the direct effect of alcohol on the mucous membrane is associated with the release of humoral substances (gastrin, histamine). It should be borne in mind that alcohol enhances the secretion of hydrochloric acid. At low concentrations of alcohol, the activity of pepsin does not change, and at high concentrations it decreases. When taking strong drinks (40% and above), the activity of the stomach decreases. In response to an irritant action, the activity of goblet cells secreting mucus increases. The motility of the stomach also changes: pyloric spasm and decreased motility. Alcohol has little effect on bowel function.

Effect of ethanol on CCC.

Even when consumed in moderation ethanol marked inhibition of contractile function of the myocardium. As the cause of cardiac disorders, the accumulation of acetaldehyde is considered, leading to a change in the reserves of catecholamines in the myocardium. Arrhythmias occur with alcohol withdrawal. An increase in blood pressure is associated with the amount of alcohol taken, regardless of obesity, salt intake, coffee and smoking. there is also an expansion of skin vessels and, as a result, an increase in heat transfer.

What is alcoholism?

Alcoholism is a chronic poisoning with ethyl alcohol, which is characterized by various symptoms: a decrease in mental performance, attention, memory, mental disorders may occur, peripheral innervation is also affected, and dysfunction of internal organs.

What is disulfiram?

White with a slight yellowish-greenish tint crystalline powder. It is difficult to dissolve in alcohol, practically insoluble in water, acids and alkalis. It is taken orally for the treatment of chronic alcoholism, in cases where it is not possible to obtain a therapeutic effect by other methods of treatment (psychotherapy, vitamin therapy, taking apomorphine and etc.).

The action of the drug is based on its ability to specifically affect the metabolism of alcohol in the body. Alcohol undergoes oxidative transformations, passing through the phase of acetaldehyde and acetic acid. With the participation of acetaldehyde hydroxidase, acetaldehyde is usually rapidly oxidized.

Teturam, blocking the enzymatic biotransformation of alcohol, leads to an increase in the concentration of acetaldehyde in the blood after alcohol intake.

Side effects of levopoda.

When using the drug, various side effects are possible: dyspeptic symptoms (nausea, vomiting, loss of appetite), orthostatic hypotension, arrhythmias, chronic and choreoathetoid hyperkinesis, headache, hyperhidrosis, etc. These phenomena decrease with lower doses. To avoid dyspeptic symptoms and for more uniform absorption, the drug is taken after meals.

What is codeine?

Synonym methylmorphine. An alkaloid found in opium; produced semi-synthetically. It has a pronounced antitussive activity.

What is methadone?

Opioid receptor agonist, diphenylpropylamine group.

What is trimepiridin?

trimeperidine (promedol)) is a synthetic derivative of phenylpiperidine and, according to its chemical structure, can be considered as an analogue of the phenyl-N-methylpiperidine part of the molecule morphine.

What is pentazacin?

Pentazocine- a synthetic compound containing the benzomorphan core of the morphine molecule, but devoid of the oxygen bridge and the third six-membered core characteristic of compounds of the morphine group. It is a delta and kappa receptor agonist and a mu receptor antagonist.

What is buprenorphine?

Mu and kappa receptor partial agonist and delta receptor antagonist.

What is tramadol?

Analgesic with a mixed (opioid and non-opioid) type of action.

What is naloxone?

Pharmacologically, naloxone differs in that it is a "pure" opiate antagonist, devoid of morphine-like activity. It acts by the type of competitive antagonism, blocking the binding of agonists or displacing them from opiate receptors. Naloxone has the highest affinity for mu and kappa receptors. In large doses, the drug may have a slight agonistic effect, which, however, has no practical significance.

What is dantrolene?

Muscle relaxant of central action. Applied for the treatment of malignant hyperthermia, tk. inhibits the activation of catabolic processes.

What is nefopam?

Non-narcotic (non-opioid) analgesic.

What is baralgin?

Spasmoanalgesic.

What is sumatriptan?

Serotonin agonist (5HT 1 - receptor)

What is ergotamine?

Ergot alkaloid is used to treat acute migraine attacks.

What is buspirone?

Nonbenzodiazepine, atypical anxiolytic. Has a less pronounced sedative effect.

What is medazepam?

Benzodiazepine anxiolytic, long-acting daytime tranquilizer.

What is alprazolam?

Benzodiazepine anxiolytic, structurally similar to triazolam.

What is temazepam?

A hypnotic agent of the benzodiazepine series with a pronounced hypnotic effect of medium duration.

What is oxazepam?

Daytime tranquilizer of a benzodiazepine series of average duration of action.

What is chlordiazepoxide?

Long-acting benzodiazepine tranquilizer.

What is flumazenil?

Tranquilizer, benzodiazepine antagonist.

What is chlorpromazine?

APS, a phenothiazine derivative, an aliphatic agent.

What is chlorprothixene?

APS, a derivative of thioxanthene.

What is haloperidol?

APS, a derivative of butyrophenone.

What is sulpiride?

Sulpiride is a derivative of sulfonylbenzamide. In structure and some pharmacological properties, sulpiride is also close to metoclopramide.

What is imipramine?

Imipramine is the main representative of typical tricyclic antidepressants. This is one of the first antidepressants, but due to its high efficiency, it is still widely used.

What is amitriptyline?

Amitriptyline, like imipramine, is one of the main representatives of tricyclic antidepressants. It differs in structure from imipramine in that the nitrogen atom in the central part of the tricyclic system is replaced by a carbon atom. It is an inhibitor of neuronal reuptake of mediator monoamines, including norepinephrine, dopamine, serotonin, etc. Does not cause MAO inhibition.

What is sertraline?

Sertraline is an active selective serotonin reuptake inhibitor; has little effect on the reuptake of norepinephrine and dopamine.

What is moclobemide?

Moclobemide is an antidepressant - a reversible MAO inhibitor and also affects predominantly MAO type A.

The main effects of bemitil.

It has a psychostimulating effect, has antihypoxic activity, increases the body's resistance to hypoxia and increases efficiency during physical exertion. Considered as a representative of a new group - actoprotective drugs. Slowly absorbed when taken orally. It is prescribed for adults with asthenic conditions, neuroses, after injuries and in other conditions in which stimulation of mental and physical functions is indicated. There is evidence of the immunostimulating effect of bemitil and its effectiveness in connection with this in the complex therapy of certain infectious diseases.

The effect of caffeine on the central nervous system.

Physiological features of action caffeine on the central nervous system were studied by I.P. Pavlov and his colleagues, who showed that caffeine enhances and regulates excitation processes in the cerebral cortex; in appropriate doses, it enhances positive conditioned reflexes and increases motor activity. The stimulating effect leads to an increase in mental and physical performance, a decrease in fatigue and drowsiness. Large doses can, however, lead to the depletion of nerve cells. The action of caffeine (as well as other psychostimulants) largely depends on the type of higher nervous activity; dosage of caffeine should therefore be made taking into account the individual characteristics of nervous activity. Caffeine weakens the effect of sleeping pills and narcotic drugs, increases the reflex excitability of the spinal cord, excites the respiratory and vasomotor centers.

The effect of caffeine on the cardiovascular system.

Cardiac activity under the influence caffeine increases, myocardial contractions become more intense and become more frequent. In collaptoid and shock conditions, blood pressure is influenced by caffeine increases, with normal blood pressure no significant changes are observed, since simultaneously with the excitation of the vasomotor center and the heart, under the influence of caffeine, the blood vessels of the skeletal muscles and other areas of the body (heart, kidneys) expand, but the vessels of the abdominal organs (except kidneys) narrow. The vessels of the brain under the influence of caffeine narrow, especially when they are dilated.

The effect of caffeine on the gastrointestinal tract.

Under the influence caffeine stimulates the secretory activity of the stomach. This can be used to diagnose functional stomach diseases from organic ones.

Drugs affecting the central nervous system.

The nervous system regulates the interaction of organs and organ systems with each other, as well as the whole organism with the environment. The nervous system is divided into central and peripheral. The central nervous system (CNS) includes the brain and spinal cord, while the peripheral nervous system consists of 12 cranial and 31 spinal nerves.

According to the morphological structure of the CNS, it is a collection of individual neurons, the number of which in humans reaches 14 billion. Communication between neurons is carried out by contact between their processes with each other or with the bodies of nerve cells. These interneuronal contacts are called synapses. (viparviv- connection). The transmission of nerve impulses in the synapses of the nervous system is carried out with the help of chemical carriers of excitation - mediators, or transmitters (acetylcholine, norepinephrine, dopamine, etc.).

In medical practice, drugs are used to change, suppress or stimulate the transmission of nerve impulses in synapses. Influence on the synaptic transmission of nerve impulses leads to changes in the function of the central nervous system, resulting in various pharmacological effects. Medicines are classified according to their main effects: anesthetics, ethyl alcohol, hypnotics, antiepileptic, antiparkinsonian, analgesic, analeptics, psychotropic.

Means for anesthesia

Means for anesthesia - where drugs, as a result of the introduction of which a state of anesthesia occurs in the body (narcosis- numbness).

anesthesia- this is a reversible depression of the function of the central nervous system, which is accompanied by loss of consciousness, loss of pain and other types of sensitivity, inhibition of reflex activity and relaxation of skeletal muscles while maintaining cardiovascular activity and respiration.

anesthesia- one of the methods of general anesthesia.

The pharmacodynamics of anesthetic agents has not been fully studied. All drugs interfere with synaptic transmission to the CNS. According to the sequence of CNS depression, four stages of anesthesia are distinguished:

I. Stage of analgesia. First, pain sensitivity decreases, and then amnesia occurs. Other types of sensitivity, skeletal muscle tone and reflexes are preserved.

II. Excitation stage. This stage is characterized by language and motor activation, an increase in blood pressure, respiratory failure, and an increase in all reflexes (there may be cardiac arrest, vomiting, broncho and laryngospasm).

III. Stage of surgical anesthesia. The patient lacks all kinds of sensitivity, suppressed muscle reflexes; normal breathing is restored, blood pressure stabilizes. The pupils are dilated, the eyes are open. There are four levels at this stage.

After the cessation of the introduction of drugs for anesthesia, stage IV begins - awakening - restoration of the functions of the central nervous system, but in the reverse order: reflexes appear, muscle tone and sensitivity are restored, consciousness returns.

Classification of drugs for anesthesia

1. Means for inhalation anesthesia:

a) volatile liquids - ether, halothane (halothane), methoxyflurane, desflurane, enflurane, isoflurane, sevoflurane and the like;

b) gases - dianitrogen oxide, cyclopropane and the like.

2. Means for non-inhalation anesthesia:

a) powders in vials - sodium thiopental b) solutions in ampoules - sodium hydroxybutyrate, propanidide (Somba-Revin), tropofol (Diprivan), ketalar (ketamine, calypsol).

Means for inhalation anesthesia:.

They are introduced using special equipment;

The anesthesia is easily managed;

Most drugs cause irritation of the mucous membrane of the respiratory tract, a feeling of suffocation, injure the patient's psyche;

They enter the atmosphere and can adversely affect the health of medical personnel.

Ether for anesthesia- a volatile liquid with a pungent odor, quickly decomposes in the light, so it is necessary to check the quality of the drug before use. Boiling point - 35 ° C. Flammable. Ether is highly soluble in water, fats and lipids. Is a strong anesthetic. It has a wide range of narcotic effects and a high safety factor for use.

Side effects: pronounced stage of arousal; promotes the release of catecholamines, which can lead to arrhythmias, increased blood glucose levels; after anesthesia, nausea, vomiting and constipation may occur; due to the rapid evaporation of ether from the surface of the respiratory tract, pneumonia may develop in children, may cause convulsions. To eliminate them, thiopental is used.

Fluorotan(halothane) is a volatile liquid. Decomposes in the light, boiling point - 50 ° C. Fluorotan does not burn and, mixed with ether, prevents the latter from burning. Fluorotan is poorly soluble in water, but well - in fats and lipids. A strong anesthetic (exceeds the properties of ether as an anesthetic three times, and nitrous oxide - 50 times), but has a moderate analgesic effect.

Side effects: respiratory depression arrhythmia associated with the excitation of p-adrenergic receptors of the myocardium, therefore, catecholamines (adrenaline, noradrenaline) cannot be administered during anesthesia. In case of arrhythmia, β-blockers (propranolol) are administered; heart failure; arterial hypotension; mental changes; hepatotoxic, nephrotoxic, mutagenic, carcinogenic and teratogenic effect; people working with halothane may have allergic reactions.

Isoflurane, enflurane, desflurane- have less effect on the cardiovascular system.

dianitrogen oxide- gas, does not explode, but supports combustion. The drug does not irritate the mucous membranes of the respiratory tract. Enter in a mixture of 80% nitrogen oxide and 20% oxygen. Anesthesia occurs in 3-5 minutes. There is no arousal stage. Anesthesia is superficial, so nitrous oxide is used for basic anesthesia and neuroleptic analgesia. The drug is used for pain relief in severe injuries, acute pancreatitis, myocardial infarction, during childbirth, and the like.

Side effects: rarely, nausea, vomiting, arrhythmia, arterial hypertension; hypoxia occurs as a result of prolonged administration of nitrous nitrogen. It is important to maintain the oxygen content in the gas mixture at a level of at least 20%. After the end of the nitrogen supply, the nitrous oxides continue to give oxygen for 4-5 minutes.

Means for non-inhalation anesthesia:

They are administered intravenously, intramuscularly or rectally;

Anesthesia occurs immediately without the stage of excitation;

Does not pollute the atmosphere;

The drug is poorly managed.

Classification of drugs for inhalation anesthesia by duration of action.

1. Preparations of a short duration of action (duration of anesthesia - 5-10 minutes): propandide (sombrevin), ketamine (ketalar, calypsol).

2. Drugs of medium duration of action (duration of anesthesia - 20-40 minutes): thiopental-sodium, hexenal.

3. Drugs with a long duration of action (duration of anesthesia - 90-120 minutes): sodium oxybutyrate.

Thiopental sodium- powder of yellowish or yellowish-green color, easily soluble in water. The solution is prepared ex tempore in sterile water for injection. Administered intravenously (slowly) or rectally (in children). Anesthesia occurs immediately and lasts 20 minutes.

Side effects: respiratory depression, arterial hypotension, laryngospasm, bronchospasm, reflex cardiac arrest, increased secretion of bronchial glands.

Sodium hydroxybutyrate is a white powder, easily soluble in water. Produced in ampoules of 10 ml of a 20% solution. Enter intravenously slowly, occasionally - intramuscularly or administered orally. As a result of the introduction, the stage of anesthesia occurs after 30 minutes and lasts 2-4 hours.

Side effects: motor excitation, convulsive trembling of the limbs and tongue due to rapid administration; vomiting motor and speech excitation upon recovery from anesthesia.

Ketamine(ketalar, calypsol) - white powder, easily soluble in water and alcohol. Ketamine causes dissociated general anesthesia, which is characterized by catatonia, amnesia, and analgesia. The drug is administered intravenously or intramuscularly. The duration of anesthesia is 10-15 minutes, depending on the method of administration. It is used to introduce anesthesia, as well as to maintain it. Ketamine can also be used on an outpatient basis for minor surgical interventions.

Side effects: arterial hypertension, tachycardia increased intracranial pressure; hypertonicity, muscle pain; Hallucinatory syndrome (patients need to be monitored after surgery).

Means that depress the central nervous system

Ketamine anesthesia should not be performed in patients with mental disorders and epilepsy.

propanidide(sombrevin) - administered intravenously slowly. Anesthesia occurs in 20-40 seconds and lasts 3-5 minutes. The drug is used for anesthesia, as well as on an outpatient basis for short operations and for diagnostic studies (biopsy, removal of sutures, catheterization).

Side effects: bradycardia, arterial hypotension, heart failure bronchospasm, anaphylactic shock thrombophlebitis.

Pharmacosecurity:

- Sodium thiopental and other barbiturates cannot be mixed in the same syringe with ketamine, dithylin, pentamine, chlorpromazine and pipolfen, since a precipitate forms as a result of physicochemical interaction;

- It is forbidden to write out prescriptions for drugs for anesthesia.

Measures to prevent complications as a result of the use of drugs for anesthesia:

Explosive substances are combined with halothane;

Non-inhalation anesthetics are combined with inhalation anesthetics to reduce or eliminate the stage of arousal, feelings of suffocation, mental trauma;

Before anesthesia, to reduce reflex reactions and limit gland secretion, patients are given premedication (preparation for surgery) - atropine (or another M-anticholinergic) is administered to eliminate pain - analgesics (fentanyl, promedol, etc.); to enhance relaxation of skeletal muscles - muscle relaxants (tubocurarine) to reduce the manifestations of allergies - antihistamines (diphenhydramine, pipolfen) drugs. For premedication, tranquilizers, neuroleptics, ganglion blockers, clonidine and other drugs are also prescribed.

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On the topic: "Drugs affecting the central nervous system"

Introduction

Antidepressants

Antipsychotics

Used Books

Introduction

This group of drugs includes substances that change the functions of the central nervous system, having a direct effect on its various parts of the brain or spinal cord.

According to the morphological structure of the CNS, it can be considered as a set of many neurons. Communication between neurons is provided by contact of their processes with the bodies or processes of other neurons. Such interneuronal contacts are called synapses.

The transmission of nerve impulses in the synapses of the central nervous system, as well as in the synapses of the peripheral nervous system, is carried out with the help of chemical transmitters of excitation - mediators. The role of mediators in the CNS synapses is performed by acetylcholine, norepinephrine, dopamine, serotonin, gamma-aminobutyric acid (GABA), etc.

Medicinal substances that affect the central nervous system change (stimulate or inhibit) the transmission of nerve impulses in synapses. The mechanisms of action of substances on the CNS synapses are different. Substances can excite or block receptors on which mediators act, affect the release of mediators or their inactivation.

Medicinal substances acting on the central nervous system are represented by the following groups:

Means for anesthesia;

Ethanol;

sleeping pills;

Antiepileptic drugs;

Antiparkinsonian drugs;

Analgesics;

Psychotropic drugs (neuroleptics, antidepressants, lithium salts, anxiolytics, sedatives, psychostimulants, nootropics);

Analeptics.

Some of these drugs have a depressing effect on the central nervous system (anesthesia, hypnotics and antiepileptic drugs), others have a stimulating effect (analeptics, psychostimulants). Some groups of substances can cause both excitatory and depressant effects (for example, antidepressants).

Drugs that depress the CNS

The group of drugs that most strongly depress the central nervous system is general anesthetics (anesthetics). Next come sleeping pills. This group is inferior to general anesthetics in terms of potency. Further, as the strength of action decreases, there are alcohol, anticonvulsants, antiparkinsonian drugs. There is also a group of drugs that have a depressing effect on the psycho-emotional sphere - these are central psychotropic drugs: of these, the most powerful group is antipsychotic antipsychotics, the second group, which is inferior in strength to antipsychotics, is tranquilizers, and the third group is general sedative.

There is such a type of general anesthesia as neuroleptanalgesia. For this type of analgesia, mixtures of antipsychotics and analgesics are used. This is a state of anesthesia, but with the preservation of consciousness.

For general anesthesia, inhalation and non-inhalation methods are used. Inhalation methods include the use of liquids (chloroform, halothane) and gases (nitrous oxide, cyclopropane). Inhalation drugs now usually go in combination with non-inhalation drugs, which include barbiturates, steroids (preulol, veadrin), eugenal derivatives - sombrevin, hydroxybutyric acid derivatives, ketamine, ketalar. Advantages of non-inhalation drugs - complex equipment is not needed to obtain anesthesia, but only a syringe. The disadvantage of such anesthesia is that it is uncontrollable. It is used as an independent, introductory, basic anesthesia. All these remedies are short-acting (from several minutes to several hours).

There are 3 groups of non-inhalation drugs:

1. Ultra-short action (sombrevin, 3-5 minutes).

2. Medium duration up to half an hour (hexenal, termital).

3. Long-term action - sodium oxybutyrate 40 min - 1.5 hours.

Today, neuroleptanalgesics are widely used. This is a mixture, which includes antipsychotics and analgesics. From neuroleptics, droperidol can be used, and from analgesics, phentamine (several hundred times stronger than morphine). This mixture is called thalomonal. You can use chlorpromazine instead of droperidol, and instead of phentamine - promedol, the action of which will be potentiated by any tranquilizer (seduxen) or clonidine. Instead of promedol, you can even use analgin.

ANTIDEPRESSANTS

These drugs appeared in the late 50s, when it turned out that isonicotinic acid hydrazide (isoniazid) and its derivatives (ftivazid, soluzide, etc.), used in the treatment of tuberculosis, cause euphoria, increase emotional activity, improve mood (thymoleptic effect) . At the heart of their antidepressant action is the blockade of monoamine oxinase (MAO) with the accumulation of monoamines - dopamine, norepinephrine, serotonin in the central nervous system, which leads to the removal of depression. There is another mechanism for enhancing synaptic transmission - blockade of the reuptake of noradrenaline, serotonin by the presynaptic membrane of nerve endings. This mechanism is characteristic of the so-called tricyclic antidepressants.

Antidepressants are divided into the following groups:

1. Antidepressants - monoamine oxidase (MAO) inhibitors:

a) irreversible - nialamide;

b) reversible - pirlindol (pyrazidol).

2. Antidepressants - neuronal uptake inhibitors (tricyclic and tetracyclic):

a) non-selective inhibitors of neuronal capture - imipramine (imizin), amitriptyline, pipofezin (azafen);

b) selective neuronal uptake inhibitors - fluoxetine (Prozac).

The thymoleptic effect (from the Greek thymos - soul, leptos - gentle) is the main one for antidepressants of all groups.

In patients with severe depression, depression, feelings of uselessness, unmotivated deep melancholy, hopelessness, suicidal thoughts, etc. are removed. The mechanism of thymoleptic action is associated with central serotonergic activity. The effect develops gradually, after 7-10 days.

Antidepressants have a stimulating psycho-energizing effect (activation of noradrenergic transmission) on the central nervous system - initiative is increased, thinking is activated, normal daily activities are activated, physical fatigue disappears. This effect is most pronounced in MAO inhibitors. They do not give sedation (unlike tricyclic antidepressants - amitriptyline and azafen), but the reversible MAO inhibitor pyrazidol may have a calming effect in patients with anxiety and depression (the drug has a regulatory sedative-stimulating effect). MAO inhibitors inhibit REM sleep.

By inhibiting the activity of liver MAO and other enzymes, including histaminase, they slow down the biotransformation of xenobiotics and many drugs - non-inhalation anesthetics, narcotic analgesics, alcohol, antipsychotics, barbiturates, ephedrine. MAO inhibitors increase the effect of narcotic, local anesthetic and analgesic substances. The blockade of hepatic MAO explains the development of a hypertensive crisis (the so-called "cheese syndrome") when taking MAO inhibitors with foods containing tyramine (cheese, milk, smoked meats, chocolate). Tyramine is destroyed in the liver and in the intestinal wall by monoamine oxidase, but when its inhibitors are used, it accumulates, and deposited norepinephrine is released from the nerve endings.

MAO inhibitors are reserpine antagonists (even pervert its effect). Sympatholytic reserpine reduces the level of norepinephrine and serotonin, leading to a drop in blood pressure and depression of the central nervous system; MAO inhibitors, on the contrary, increase the content of biogenic amines (serotonin, norepinephrine).

Nialamide - irreversibly blocks MAO. It is used for depression with increased lethargy, lethargy, trigeminal neuralgia and other pain syndromes. Its side effects include: insomnia, headache, disruption of the gastrointestinal tract (diarrhea or constipation). When treating with nialamide, it is also necessary to exclude foods rich in tyramine from the diet (prevention of "cheese syndrome").

Pirlindol (pyrazidol) - a four-cyclic compound - a reversible MAO inhibitor, also inhibits the reuptake of norepinephrine, a four-cyclic compound, has a thymoleptic effect with a sedative-stimulating component, has nootropic activity (increases cognitive functions). Basically, the destruction (deamination) of serotonin and norepinephrine is blocked, but not tyramine (as a result, the "cheese syndrome" develops very rarely). Pyrazidol is well tolerated, does not have an M-anticholinergic effect (unlike tricyclic antidepressants), complications are rare - slight dryness of the mouth, tremor, tachycardia, dizziness. All MAO inhibitors are contraindicated in inflammatory liver diseases.

Another group of antidepressants are neuronal uptake inhibitors. Non-selective inhibitors include tricyclic antidepressants: imipramine (imizin), amitriptyline, azafen, fluacizine (fluorocyzine), etc. The mechanism of action is associated with inhibition of neuronal uptake of norepinephrine, serotonin by presynaptic nerve endings, as a result of which their content in the synaptic cleft increases and the activity of adrenergic and serotonergic transmission. A certain role in the psychotropic effect of these drugs (except for Azafen) is played by the central M-anticholinergic action.

Imipramine (imizin) - one of the first drugs in this group, has a pronounced thymoleptic and psychostimulant effect. It is mainly used for depression with general lethargy and lethargy. The drug has a central and peripheral M-anticholinergic, as well as an antihistamine effect. The main complications are associated with M-anticholinergic action (dry mouth, disturbance of accommodation, tachycardia, constipation, urinary retention). When taking the drug, there may be a headache, allergic reactions; overdose - insomnia, agitation. Imizin is close in chemical structure to chlorpromazine and, like it, can cause jaundice, leukopenia, and agranulocytosis (rarely).

Amitriptyline successfully combines thymoleptic activity with a pronounced sedative effect. The drug has no psychostimulating effect, M-anticholinergic and antihistamine properties are expressed. It is widely used for anxiety-depressive, neurotic conditions, depression in patients with somatic chronic diseases and pain syndromes (CHD, hypertension, migraine, oncology). Side effects are mainly associated with the M-anticholinergic effect of the drug: dry mouth, blurred vision, tachycardia, constipation, impaired urination, as well as drowsiness, dizziness, and allergies.

Fluacizine (fluorocyzine) is similar in action to amitriptyline, but has a more pronounced sedative effect.

Azafen, unlike other tricyclic antidepressants, does not have M-anticholinergic activity; a moderate thymoleptic effect in combination with a mild sedative effect ensures the use of the drug in mild and moderate depression, in neurotic conditions and long-term use of antipsychotics. Azafen is well tolerated, does not disturb sleep, does not give cardiac arrhythmias, can be used for glaucoma (unlike other tricyclic antidepressants that block M-cholinergic receptors).

Recently, drugs fluoxetine (Prozac) and trazodone have appeared, which are active selective serotonin reuptake inhibitors (the antidepressant effect is associated with an increase in its level). These drugs have almost no effect on the neuronal uptake of norepinephrine, dopamine, cholinergic and histamine receptors. Well tolerated by patients, rarely cause drowsiness, headache. nausea.

Antidepressants - inhibitors of neuronal uptake are more widely used in psychiatry, however, drugs of this group cannot be prescribed simultaneously with MAO inhibitors, since severe complications (convulsions, coma) can occur. Antidepressants have become widely used in the treatment of neuroses, sleep disorders (anxiety-depressive conditions), in the elderly with somatic diseases, with prolonged pain to prolong the action of analgesics, to reduce severe depression associated with pain. Antidepressants also have their own pain-relieving effect.

PSYCHOTROPIC DRUGS. NEUROLEPTICS

Psychotropic drugs include drugs that affect the mental activity of a person. In a healthy person, the processes of excitation and inhibition are in balance. A huge flow of information, various overloads, negative emotions and other factors affecting a person are the cause of stressful conditions that lead to the emergence of neuroses. These diseases are characterized by the partiality of mental disorders (anxiety, obsession, hysterical manifestations, etc.), a critical attitude towards them, somatic and autonomic disorders, etc. Even with a protracted course of neurosis, they do not lead to gross behavioral disorders. There are 3 types of neuroses: neurasthenia, hysteria and obsessive-compulsive disorder.

Mental diseases are characterized by more serious mental disorders with the inclusion of delusions (impaired thinking that causes incorrect judgments, conclusions), hallucinations (imaginary perception of non-existent things), which can be visual, auditory, etc.; memory disorders that occur, for example, when the blood supply to the brain cells changes with cerebral vascular sclerosis, during various infectious processes, injuries, when the activity of enzymes involved in the metabolism of biologically active substances changes, and in other pathological conditions. These deviations in the psyche are the result of a metabolic disorder in nerve cells and the ratio of the most important biologically active substances in them: catecholamines, acetylcholine, serotonin, etc. Mental illnesses can occur with a sharp predominance of excitation processes, for example, manic states in which motor excitation is observed and delirium, as well as with excessive inhibition of these processes, the appearance of a state of depression - a mental disorder accompanied by a depressed, dreary mood, impaired thinking, suicide attempts.

Psychotropic drugs used in medical practice can be divided into the following groups: neuroleptics, tranquilizers, sedatives, antidepressants, psychostimulants, among which a group of nootropic drugs is singled out.

Preparations of each of these groups are prescribed for the corresponding mental illnesses and neuroses.

Antipsychotics. The drugs have an antipsychotic (eliminate delusions, hallucinations) and sedative (reduce feelings of anxiety, restlessness) effect. In addition, antipsychotics reduce motor activity, reduce skeletal muscle tone, have hypothermic and antiemetic effects, potentiate the effects of drugs that depress the central nervous system (anesthesia, hypnotics, analgesics, etc.).

Antipsychotics act in the area of ​​the reticular formation, reducing its activating effect on the brain and spinal cord. They block adrenergic and dopaminergic receptors in different parts of the central nervous system (limbic system, neostriatum, etc.), and affect the exchange of mediators. The effect on dopaminergic mechanisms can also explain the side effect of neuroleptics - the ability to cause symptoms of parkinsonism.

According to the chemical structure, antipsychotics are divided into the following main groups:

¦ phenothiazine derivatives;

¦ derivatives of butyrophenone and diphenylbutylpiperidine;

¦ thioxanthene derivatives;

¦ indole derivatives;

¦ neuroleptics of different chemical groups.

CNS stimulant drugs

CNS stimulants include drugs that can increase mental and physical performance, endurance, reaction speed, eliminate the feeling of fatigue and drowsiness, increase the amount of attention, the ability to memorize and the speed of information processing. The most unpleasant characteristics of this group are the general fatigue of the body that occurs after the cessation of their effects, a decrease in motivation and performance, as well as a relatively quickly emerging strong psychological dependence.

Among the stimulants of the mobilizing type, the following groups of drugs can be distinguished:

1. Adrenomimetics of indirect or mixed action:

phenylalkylamines: amphetamine (phenamine), methamphetamine (pervitin), centedrine and pyriditol;

piperidine derivatives: meridyl;

sidnonimine derivatives: mesocarb (sidnocarb), sidnofen;

purine derivatives: caffeine (caffeine-sodium benzoate).

2. Analeptics:

acting mainly on the respiratory and vasomotor centers: bemegride, camphor, nikethamide (cordiamin), etimizol, lobelin;

acting mainly on the spinal cord: strychnine, securinine, echinopsin.

Phenylalkylamines are the closest synthetic analogues of the world-famous psychostimulant - cocaine, but differ from it in less euphoria and a stronger stimulating effect. They are able to cause an extraordinary spiritual uplift, a desire for activity, eliminate the feeling of fatigue, create a feeling of cheerfulness, clarity of mind and ease of movement, quick wit, confidence in one's strengths and abilities. The action of phenylalkylamines is accompanied by high spirits. Amphetamine use began during World War II as a means of relieving fatigue, combating sleep, increasing alertness; then phenylalkylamines entered psychotherapeutic practice and gained mass popularity.

The mechanism of action of phenylalkylamines is the activation of adrenergic transmission of nerve impulses at all levels of the central nervous system and in the executive organs due to:

displacement of norepinephrine and dopamine into the synaptic cleft from the easily mobilized pool of presynaptic endings;

Increase the release of adrenaline from the chromaffin cells of the adrenal medulla into the blood;

inhibition of neuronal reuptake of catecholamines from the synaptic cleft;

reversible competitive inhibition of MAO.

Phenylalkylamines easily penetrate the BBB and are not inactivated by COMT and MAO. They implement the sympathetic-adrenal mechanism of urgent adaptation of the body to emergency conditions. Under conditions of prolonged stress of the adrenergic system, under severe stress, exhausting loads, in a state of fatigue, the use of these drugs can lead to depletion of the catecholamine depot and a breakdown in adaptation.

Phenylalkylamines have psychostimulating, actoprotective, anorexigenic and hypertensive effects. The drugs of this group are characterized by an acceleration of metabolism, activation of lipolysis, an increase in body temperature and oxygen consumption, a decrease in resistance to hypoxia and hyperthermia. During physical exertion, lactate increases excessively, which indicates an inadequate expenditure of energy resources. Phenylalkylamines suppress appetite, cause constriction of blood vessels and increase pressure. Dry mouth, dilated pupils, rapid pulse are observed. Breathing deepens and ventilation of the lungs increases. Methamphetamine has a more pronounced effect on peripheral vessels.

In very low doses, phenylalkylamines are used in the United States to treat sexual disorders. Methamphetamine causes a sharp increase in sexual desire and sexual potency, although amphetamine has little activity.

Phenylalkylamines are shown:

For a temporary rapid increase in mental performance (operator's activity) in emergency conditions;

For a one-time increase in physical endurance in extreme conditions (rescue work);

To weaken the side psychosedative effect of drugs that depress the central nervous system;

· for the treatment of enuresis, weakness, depression, withdrawal syndrome in chronic alcoholism.

In psychoneurological practice, amphetamine is used to a limited extent in the treatment of narcolepsy, the consequences of encephalitis and other diseases accompanied by drowsiness, lethargy, apathy, and asthenia. With depression, the drug is ineffective and inferior to antidepressants.

For amphetamine, the following drug interactions are possible:

Strengthening the analgesic and reducing the sedative effect of narcotic analgesics;

weakening of the peripheral sympathomimetic effects of amphetamine under the influence of tricyclic depressants due to the blockade of amphetamine entry into adrenergic axons, as well as an increase in the central stimulating effect of amphetamine due to a decrease in its inactivation in the liver;

It is possible to potentiate the euphoric action when used in combination with barbiturates, which increases the likelihood of developing drug dependence;

lithium preparations can reduce the psychostimulant and anorexigenic effects of amphetamine;

Neuroleptic drugs also reduce the psychostimulant and anorexigenic effects of amphetamine due to the blockade of dopamine receptors and can be used for amphetamine poisoning;

amphetamine reduces the antipsychotic effect of phenothiazine derivatives;

amphetamine increases the body's endurance to the action of ethyl alcohol (although the inhibition of motor activity remains);

under the influence of amphetamine, the hypotensive effect of clonidine is reduced; amphetamine enhances the stimulating effect of midantan on the central nervous system.

Among the side effects are possible tachycardia, hypertension, arrhythmias, addiction, drug dependence, exacerbation of anxiety, tension, delirium, hallucinations, sleep disturbances. With repeated use, depletion of the nervous system, disruption of the regulation of CCC functions, and metabolic disorders are possible.

Contraindications to the use of phenylalkylamines are severe cardiovascular diseases, diabetes mellitus, obesity, productive psychopathological symptoms.

Due to a variety of side effects, most importantly, the possibility of developing drug dependence, phenylalkylamines are of limited use in medical practice. At the same time, the number of patients with drug addiction and substance abuse, who use various derivatives of phenylalkylamines, is constantly growing.

The use of mesocarb (sidnocarb) causes a psychostimulating effect more slowly than that of amphetamine, and it is not accompanied by euphoria, speech and motor disinhibition, does not cause such a deep depletion of the energy reserve of nerve cells. According to the mechanism of action, mesocarb is also somewhat different from amphetamine, since it mainly stimulates the noradrenergic systems of the brain, causing the release of norepinephrine from stable depots.

Unlike amphetamine, mesocarb has a less pronounced stimulation with a single dose, its gradual increase from dose to dose is observed. Sidnocarb is usually well tolerated, it does not cause dependence and addiction, when it is used, an increase in blood pressure, a decrease in appetite, as well as hyperstimulation phenomena are possible.

Mesocarb is used for various types of asthenic conditions, after overwork, CNS injuries, infections and intoxications. It is effective in sluggish schizophrenia with a predominance of asthenic disorders, withdrawal symptoms in chronic alcoholism, developmental delay in children as a result of organic lesions of the central nervous system with adynamia. Mesocarb is an effective remedy that stops asthenic phenomena associated with the use of neuroleptic drugs and tranquilizers.

Sidnofen is similar in structure to mesocarb, but less stimulates the central nervous system and has a pronounced antidepressant activity (due to a reversible inhibitory effect on MAO activity), therefore it is used to treat asthenodepressive conditions.

Meridil is similar to mesocarb, but less active. Increases activity, associative abilities, has an analeptic effect.

Caffeine is a mild psychostimulant, the effects of which are realized by inhibiting the activity of phosphodiesterase and, consequently, prolonging the life of secondary intracellular mediators, to a greater extent cAMP and somewhat less cGMP in the central nervous system, heart, smooth muscle organs, adipose tissue, skeletal muscles.

The action of caffeine has a number of features: it does not excite adrenergic transmission in all synapses, but enhances and lengthens the work of those neurons that are currently involved in current physiological reactions and in which cyclic nucleotides are synthesized in response to the action of their mediators. There is information about the antagonism of xanthines in relation to endogenous purines: adenosine, inosine, hypoxanthine, which are ligands of inhibitory benzodiazepine receptors. The composition of coffee includes substances - antagonists of endorphins and enkephalins.

Caffeine acts only on neurons that can respond to neurotransmitters by producing cyclic nucleotides. These neurons are sensitive to adrenaline, dopamine, acetylcholine, neuropeptides, and only a few neurons are sensitive to serotonin and norepinephrine.

Under the influence of caffeine are realized:

stabilization of dopaminergic transmission - psychostimulating effect;

Stabilization of b-adrenergic transmission in the hypothalamus and medulla oblongata - increased tone of the vasomotor center;

stabilization of cholinergic synapses of the cortex - activation of cortical functions;

· stabilization of cholinergic synapses of the medulla oblongata - stimulation of the respiratory center;

Stabilization of noradrenergic transmission - increased physical endurance.

Caffeine has a complex effect on the cardiovascular system. Due to the activation of the sympathetic effect on the heart, there is an increase in contractility and conductivity (in healthy people, when taken in small doses, it is possible to slow down the frequency of contractions due to excitation of the nuclei of the vagus nerve, in large doses - tachycardia due to peripheral influences). Caffeine has a direct antispasmodic effect on the vascular wall in the vessels of the brain, heart, kidneys, skeletal muscles, skin, but not the limbs! (stabilization of cAMP, activation of the sodium pump and hyperpolarization of membranes), increases the tone of the veins.

Caffeine increases the secretion of digestive glands, diuresis (reduces tubular reabsorption of metabolites), enhances basal metabolism, glycogenolysis, lipolysis. The drug increases the level of circulating fatty acids, which contributes to their oxidation and utilization. However, caffeine does not suppress appetite, but, on the contrary, excites it. In addition, it enhances the secretion of gastric juice so that the use of caffeine without food can lead to gastritis and even peptic ulcer.

Caffeine is shown:

To improve mental and physical performance;

for emergency care for hypotension of various origins (trauma, infection, intoxication, overdose of ganglionic blockers, sympatho- and adrenolytics, deficiency of circulating blood volume);

with spasms of cerebral vessels;

in mild forms of bronchial obstruction as a bronchodilator.

The following side effects are characteristic of caffeine: increased excitability, heart rhythm disturbances, retrosternal pain, insomnia, tachycardia, with prolonged use - myocarditis, trophic disorders in the limbs, hypertension, caffeinism. Acute caffeine poisoning produces early symptoms of anorexia, tremors and restlessness. Then nausea, tachycardia, hypertension and confusion appear. Severe intoxication can cause delirium, convulsions, supraventricular and ventricular tachyarrhythmias, hypokalemia and hyperglycemia. Chronic use of high doses of caffeine can lead to nervousness, irritability, anger, persistent tremors, muscle twitches, insomnia, and hyperreflexia.

Contraindications to the use of the drug are states of excitation, insomnia, hypertension, atherosclerosis, glaucoma.

Caffeine is also characterized by various types of drug interactions. The drug weakens the effect of drugs that depress the central nervous system, so it is possible to combine caffeine with histamine blockers, antiepileptic drugs, tranquilizers to prevent CNS depression. Caffeine reduces the depression of the central nervous system caused by ethyl alcohol, but does not eliminate the violation of psychomotor reactions (coordination of movements). Caffeine and codeine preparations are used in combination for headaches. Caffeine is able to enhance the analgesic effect of acetylsalicylic acid and ibuprofen, enhances the effect of ergotamine in the treatment of migraines. In combination with midantan, it is possible to increase the stimulating effect on the central nervous system. When taken simultaneously with cimetidine, it is likely that the side effects of caffeine will increase due to a decrease in its inactivation in the liver. Oral contraceptives also slow down the inactivation of caffeine in the liver, overdose symptoms may occur. When taken together with theophylline, the total clearance of theophylline decreases by almost 2 times. If necessary, the joint use of drugs should reduce the dose of theophylline.

Analeptics (from the Greek. analeptikos - restoring, strengthening) - a group of medicines that contribute to the return of consciousness in a patient who is in a state of fainting or coma.

Among analeptic drugs, a group of drugs is distinguished that primarily stimulates the centers of the medulla oblongata: vasomotor and respiratory. In high doses, they can stimulate the motor areas of the brain and cause seizures. In therapeutic doses, they are usually used for weakening vascular tone, collapse, respiratory depression, circulatory disorders in infectious diseases, in the postoperative period, poisoning with sleeping pills and narcotic drugs. Previously, a special subgroup of respiratory analeptics (lobelin) was distinguished from this group, which have a reflex stimulating effect on the respiratory center. Currently, these drugs have limited use.

One of the safest analeptics is cordiamine. In structure, it is close to nicotinamide and has a weak antipellagric effect. Cordiamin stimulates the central nervous system with a direct effect on the respiratory center and reflexively through the chemoreceptors of the carotid sinus. In small doses, the drug does not affect the CCC. Toxic doses can increase blood pressure, cause tachycardia, vomiting, cough, arrhythmias, muscle rigidity, and tonic and clonic convulsions.

Etimizole, in addition to stimulating the respiratory center, induces the secretion of corticoliberin in the hypothalamus, which leads to an increase in the level of glucocorticoids in the blood; inhibits phosphodiesterase, which contributes to the accumulation of intracellular cAMP, enhances glycogenolysis, activates metabolic processes in the central nervous system and muscle tissue. Depresses the cerebral cortex, eliminates the state of anxiety. In connection with the stimulation of the adrenocorticotropic function of the pituitary gland, etimizole can be used as an anti-inflammatory agent for arthritis.

Analeptics, primarily increasing reflex excitability, include: strychnine (an alkaloid from the seeds of the African liana chilibukha), securinine (an alkaloid from the herb of the Far Eastern securinegi shrub) and echinopsin (obtained from the seeds of the common muzzle). According to the mechanism of action, they are direct antagonists of the inhibitory mediator glycine, blocking the receptors of brain neurons that are sensitive to it. The blockade of inhibitory influences leads to an increase in the flow of impulses in the afferent pathways of activation of reflex reactions. The drugs stimulate the sense organs, excite the vasomotor and respiratory centers, tone up the skeletal muscles, are indicated for paresis, paralysis, fatigue, functional disorders of the visual apparatus.

The main effects of drugs in this group are:

increase in muscle tone, acceleration and intensification of motor reactions;

Improving the functions of the pelvic organs (with paralysis and paresis, after injuries, strokes, poliomyelitis);

Increased visual acuity and hearing after intoxication, trauma;

Increase in general tone, activation of metabolic processes, functions of the endocrine glands;

Some increase in blood pressure and heart function.

The main indications for the use of this group: paresis, paralysis, fatigue, asthenic conditions, functional disorders of the visual apparatus. Previously, strychnine was used to treat acute barbiturate poisoning, now the main drug used in this case is bemegride.

Securinin is less active compared to strychnine, but also much less toxic, it is also used for hypo- and asthenic forms of neurasthenia, with sexual impotence due to functional nervous disorders.

With an overdose of drugs, there is tension in the masticatory and occipital muscles, difficulty in breathing, swallowing, attacks of clonic-tonic convulsions. They are contraindicated in case of increased convulsive readiness, bronchial asthma, thyrotoxicosis, ischemic heart disease, arterial hypertension, atherosclerosis, hepatitis, glomerulonephritis.

Due to the high toxicity of reflex-type analeptics, they are used extremely rarely and only in a hospital setting.

medicinal nervous system antidepressant psychotropic

Used Books

Katzung B.G. «Basic and clinical pharmacology. In 2 volumes" 1998

V.G. Kukes "Clinical pharmacology" 1999

Belousov Yu.B., Moiseev V.S., Lepakhin V.K. "Clinical pharmacology and pharmacotherapy" 1997

Alyautdin R.N. "Pharmacology. Textbook for universities "2004

Kharkevich D.A. "Pharmacology" 2006

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1. oppressive

2. exciting

Drugs that depress the CNS

Means for anesthesia

Anesthesia is a reversible state of the body, in which pain sensitivity is turned off, consciousness is absent, reflexes are suppressed, at the same time, the normal function of respiration and the cardiovascular system is preserved, i.e. artificially induced deep sleep with loss of consciousness and pain sensitivity. During anesthesia, favorable conditions are created for surgical operations.

Means for anesthesia have a depressing effect on the transmission of nerve impulses in the synapses of the central nervous system. The sensitivity of the synapses of different parts of the central nervous system to narcotic substances is not the same. Therefore, the oppression of these departments under the action of drugs does not occur simultaneously: first, the more sensitive, then the less sensitive departments of the central nervous system are inhibited. Therefore, in the action of drugs for anesthesia, certain stages are distinguished, which replace each other as the concentration of the drug increases.

I stage– stunning (analgesia)(analgesia - loss of pain sensitivity (from Greek - an - denial, algos - pain).

When a narcotic substance enters the body, depression of the centers of the cerebral cortex develops first, which is accompanied by a decrease in pain sensitivity and a gradual depression of consciousness. By the end of the analgesia stage, pain sensitivity is completely lost, and at this stage some surgical manipulations (opening of abscesses, dressings, etc.) can be performed - round anesthesia.

II stage–arousal

It manifests itself in the form of motor and speech excitement, unconscious attempts to get up from the operating table, respiratory rhythm disturbances, etc. Consciousness is completely lost, muscle tone sharply increases. Respiration and pulse are quickened, blood pressure is increased. According to I.P. Pavlov, the cause of excitation at this stage is the switching off of the inhibitory influences of the cerebral cortex on the subcortical centers. There is a "rebellion of the subcortex."

III stage–surgical anesthesia

It is characterized by suppression of the function of the cerebral cortex, subcortical centers and spinal cord. Excitation phenomena disappear, muscle tone decreases, reflexes are inhibited. The vital centers of the medulla oblongata - the respiratory and vasomotor continue to function.

IV stage–awakening (restoration)

Occurs after the cessation of drug administration. CNS functions are restored.

V stage –paralysis (agonal)

In case of an overdose of an anesthetic agent, breathing becomes superficial, the activity of the intercostal muscles gradually fades away, and breathing is disturbed. Oxygen deficiency develops. Death can occur from paralysis of the respiratory and vasomotor centers.

Ethanol

It is a narcotic substance that has a depressant effect on the central nervous system. However, it cannot be used as an anesthetic agent, because. has little narcotic latitude(the maximum possible range between the concentrations of a substance in the blood, causing surgical anesthesia and paralysis of vital functions) and causes a long stage of excitement (intoxication). This stage is characterized by emotional arousal, an increase in mood, a decrease in a critical attitude towards one's own actions, a disorder in thinking and memory, working capacity decreases, etc.

With an increase in the dose of ethyl alcohol, the stage of excitation is replaced by depression of the central nervous system, coordination of movements and consciousness are disturbed. There are signs of oppression of the respiratory and vasomotor centers.

Ethyl alcohol is easily absorbed from the gastrointestinal tract, mainly in the small intestine and about 20% in the stomach. Especially quickly resorptive action is manifested when taken on an empty stomach. Delays the absorption of alcohol in the presence of foods such as potatoes, meat, fats in the gastrointestinal tract.

Alcohol affects the digestive system. Gastric secretion increases when exposed to alcohol at a concentration not exceeding 20%. A further increase in alcohol concentration leads to a temporary decrease in secretion.

Under the influence of small doses of alcohol, first the superficial vessels expand (the face turns red), a feeling of warmth appears. With an increase in the concentration of alcohol in the blood, blood vessels expand, especially in the abdominal cavity, and heat transfer increases. Therefore, people who are in a state of intoxication freeze faster than sober ones.

In medical practice, the resorptive effect of ethyl alcohol is rarely used. Sometimes it is used as an anti-shock agent (given its analgesic effect).

Ethyl alcohol finds practical application in connection with its antimicrobial, astringent, irritating properties. The antimicrobial effect of alcohol is due to its ability to cause denaturation (clotting) of proteins of microorganisms and increases with increasing concentration. 95% ethyl alcohol is used to treat surgical instruments, catheters, etc. For processing the hands of the surgeon and the operating field, 70% alcohol is more often used. This is due to the fact that alcohol of a higher concentration intensively coagulates the protein, but on the surface it does not penetrate well into the skin pores.

The astringent action of 95% alcohol is used to treat burns. Ethyl alcohol 40% concentration has pronounced irritating properties and is used to apply compresses for inflammatory diseases of internal organs, muscles, joints.

Drinking alcohol can lead to acute poisoning, the degree of which depends on the concentration of alcohol in the blood. Intoxication occurs at 1-2 g / l, pronounced signs of poisoning appear at 3-4 g / l. In acute alcohol poisoning, a state of deep anesthesia develops, characterized by loss of consciousness, reflexes, sensitivity, and a decrease in muscle tone. Blood pressure drops, body temperature drops, breathing is disturbed, the skin becomes pale. Death can occur from paralysis of the respiratory center.

First aid for acute poisoning with ethyl alcohol is to stop its further absorption into the blood. To do this, the stomach is washed, a saline laxative is given (20-30 g of magnesium sulfate per glass of water), if the patient is conscious, vomiting can be induced. For detoxification, a 40% glucose solution is administered intravenously, to eliminate acidosis - a 4% solution of sodium bicarbonate. If necessary, carry out artificial respiration or introduce oxygen and analeptics (bemegride, caffeine, etc.). It is necessary to warm the patient.

In chronic alcohol poisoning (alcoholism), working capacity is sharply reduced, higher nervous activity, intelligence, attention, memory suffer, mental illness often occurs. There are serious changes in the internal organs: chronic gastritis, cirrhosis of the liver, dystrophy of the heart, kidneys and other diseases.

Treatment of alcoholism is carried out in hospitals. The main task is to stop taking alcohol and develop disgust for it, negative reflexes to alcohol. One of the most effective drugs is Disulfiram(teturam). It delays the oxidation of ethyl alcohol at the level of acetaldehyde, the latter accumulates in the body and causes intoxication: headache, dizziness, palpitations, shortness of breath, sweating, nausea, vomiting, fear. Long-acting disulfiram is available for implantation under the skin - Esperal.

Sometimes emetics (apomorphine) are used to develop negative conditioned reflexes.

Treatment must be combined with psychotherapy.

Sleeping pills

Hypnotics (hypnotics - from the Greek hypnos - sleep) - substances of various chemical structures, which, under certain conditions, contribute to the onset and maintenance of sleep, normalize its indicators (depth, phase, duration).

Sleep is a vital need of the body. The mechanism of sleep is very complex. I.P. Pavlov made a great contribution to the study of it.

Sleep is not a homogeneous state and two phases are distinguished in it, several times (4-5) replacing each other. Sleep begins with a phase of "slow" sleep, which is characterized by a decrease in the bioelectric activity of the brain, pulse, respiration, body temperature, secretion of glands and metabolism. This phase accounts for 75-80% of the total duration of sleep. It is replaced by the second phase - "REM" sleep, during which the bioelectric activity of the brain increases, the pulse and respiration become more frequent, and metabolism increases. The phase of "REM" sleep is 20-25% of the total duration, it is accompanied by dreams.

Insomnia (sleep disorders) can be manifested by a slowing down of falling asleep or the nature of sleep (sleep is short or intermittent).

Sleep disorders are caused by various reasons:

Overwork;

Violation of the biological rhythm of life;

Pain, disease;

The stimulating effect of drinks, drugs, etc.

There are two types of insomnia:

- transitory which occurs when changing the usual way of life, emotional stress, stress, etc.

- chronic, which is an independent disease of the central nervous system.

In case of mild sleep disorders, hygiene measures are recommended: adherence to the regimen, walks before bedtime, going to bed at the same time, the use of medicinal plants, etc. The use of sleeping pills should be the last way to correct sleep. The duration of prescription of sleeping pills should not exceed three weeks.

There are three groups of sleeping pills:

1 - derivatives of barbituric acid;

2 - benzodiazepines;

3 - means of different chemical structure.

The mechanism of action of sleeping pills lies in their ability to inhibit the transmission of impulses in various parts of the central nervous system. They stimulate inhibitory GABA-ergic processes in the brain through barbituric (barbiturates) or through benzodiazepine (benzodiazepine) receptors (Fig. 13). The weakening of the exciting action of the reticular formation on the cerebral cortex is important.

Barbituric acid derivatives

Sleep induced by barbiturates (as well as by most other sleeping pills) differs in structure from natural sleep. Barbiturates make it easier to fall asleep, but shorten the duration of REM sleep.

Phenobarbital(luminal) - long-acting drugs: the hypnotic effect occurs after 1 hour and lasts 6-8 hours. It has a sedative, hypnotic, anticonvulsant effect depending on the dose. Has cumulation. It is slowly neutralized in the liver, while stimulating the activity of microsomal enzymes, it is excreted mainly by the kidneys in unchanged form.

Cyclobarbital is part of the combined drug " Reladorm».

BDR - benzodiazepine receptor BRR - barbituric receptor

Fig. 13 Scheme of the GABA-benzodiazepine-barbiturate complex

with chlorine ionophore

Barbiturates are usually administered orally, less often rectally. After awakening, drowsiness, weakness, and impaired coordination of movements can be observed.

Undesirable side effects are manifested in the occurrence of drug dependence with prolonged use, respiratory depression, impaired kidney and liver function, allergic reactions (rash), lowering pressure.

Currently, they are rarely used as sleeping pills.

Acute poisoning barbiturates result from an accidental or intentional drug overdose. There comes depression of the central nervous system, respiratory depression, weakening of reflexes, blood pressure falls; in severe poisoning - there is no consciousness (coma).

Treatment of acute poisoning is to accelerate the excretion of drugs from the body and to maintain vital functions. If the drug is not completely absorbed from the gastrointestinal tract, gastric lavage is done, adsorbents, saline laxatives are given. In connection with respiratory depression, oxygen therapy and artificial respiration are carried out.

To speed up the excretion of an already absorbed substance, diuretics are prescribed, the method of forced diuresis is used. At high concentrations of barbiturates in the blood, peritoneal dialysis or hemodialysis is performed. Analeptics are used in mild forms of poisoning and are contraindicated in deep respiratory depression.

benzodiazepine derivatives

They are safer drugs, have some advantages compared to barbiturates: they have less effect on the structure of sleep, however, with their long-term use, especially in large doses, daytime sleepiness, lethargy, weakness, dizziness are possible, drug dependence may develop.

These drugs have a tranquilizing effect (see "Psychotropic drugs"). The mechanism of the hypnotic action (and other effects) of benzodiazepines is associated with an increase in the inhibitory effect of GABA (gamma-aminobutyric acid) in the central nervous system. GABA is the main inhibitory mediator of the CNS, performing this function in all parts of the brain, including the thalamus, cortex, spinal cord, etc. From 30 to 50% of brain neurons are inhibitory GABAergic. Derivatives of benzodiazepine, interacting with specific benzodiazepine receptors that are part of one of the subunits of the GABA receptor, increases the sensitivity of the latter to its mediator. Upon activation of the GABA receptor, the chloride channel opens; increased entry of chloride ions into the cell causes an increase in the membrane potential, while the activity of neurons in many parts of the brain decreases. (Fig.10)

Benzodiazepines shorten the period of falling asleep, reduce the number of nocturnal awakenings, and increase the total duration of sleep. They can be recommended both for difficulty falling asleep (especially associated with increased anxiety), but mainly for sleep disorders in general and for short sleep in the elderly.

Nitrazepam(radedorm, nitrosan) exhibits a strong hypnotic effect, affecting the subcortical structures of the brain, reduces emotional arousal and stress. It is used for insomnia, as well as for neuroses of various origins. Sleep comes in 20-45 minutes. after taking the drug and lasts 6-8 hours.

Triazolam(halcion) has a pronounced hypnotic effect, accelerates falling asleep, increases the total duration of sleep. Drug dependence rarely occurs.

flunitrazepam(Rohypnol) has a sedative, hypnotic, anticonvulsant, muscle relaxant effect. It is used for sleep disorders, for premedication before anesthesia.

Contraindications to the use of benzodiazepines and other hypnotics are: pregnancy, lactation, impaired liver and kidney function, alcoholism, CNS depression. Should not be administered during work to drivers, pilots and other professions that require a quick response.

These benzodiazepine hypnotics differ in duration of action and have different half-lives. T 0.5 of nitrazepam (and its active metabolites) is 24 hours, flunitrazepam - 20 hours, triazolam - up to 6 hours.

A specific benzodiazepine antagonist is flumazenil. It blocks benzodiazepine receptors and completely eliminates or reduces the severity of most of the central effects of benzodiazepine anxiolytics. Typically, flumazenil is used to eliminate the residual effects of benzodiazepines (for example, when used in surgical practice or in diagnostic procedures), as well as in their overdose or acute poisoning.

The drug is usually administered intravenously. It acts for a short time - 30-60 minutes, so if necessary it is administered again.

Sleeping pills of different chemical structure

Zopiclone(imovan, somnol, sonnat), Zolpidem(ivadal, nitrest) are representatives of a new class of compounds, derivatives of cyclopyrrolone, structurally different from benzodiazepines and barbiturates. The sedative-hypnotic effect of these drugs is due to the activation of GABAergic processes in the central nervous system. They quickly induce sleep without changing its structure, do not cause weakness and drowsiness in the morning, do not have cumulation and do not cause drug dependence. Used to treat various types of insomnia. They have T 0.5 for about 3-5 hours.

Undesirable effects: metallic taste in the mouth, nausea, vomiting, allergic reactions.

Bromisoval exhibits a predominantly sedative-hypnotic effect. To obtain a hypnotic effect, it is taken orally in powders and tablets, washed down with sweet warm tea or milk. Cumulation and addiction are absent. Low toxicity. In case of overdose and hypersensitivity to the drug, the phenomena of "bromism" are possible: skin rash, conjunctivitis, dilated pupils, rhinitis.

doxylamine(donormil) is a blocker of H 1 -histamine receptors. Reduces sleep time. It has anticholinergic action. Causes dry mouth, constipation, urination disorders. Other antihistamines also have a hypnotic effect (see "Antiallergic drugs").

Analgesics

Analgesics (from the Greek - an - negation, algesis - sensation of pain) are medicinal substances that, with a resorptive action, selectively suppress the feeling of pain. Pain is a symptom of many diseases and various injuries.

Pain sensations are perceived by special receptors, which are called nociceptors(from lat. noceo - I damage). Irritants can be mechanical and chemical influences. Endogenous substances such as histamine, serotonin, bradykinin, etc., can cause pain by acting on nociceptors. Several types and subtypes of these receptors are currently known.

The body also has an antinociceptive (pain) system. Its main elements are opioid peptides(enkephalins, endorphins). They interact with specific opioid(opiate) receptors involved in the conduction and perception of pain. Opioid peptides released in both the brain and spinal cord cause analgesia (pain relief). An increased release of endogenous analgesic peptides is noted when severe pain occurs.

Analgesics, unlike drugs for anesthesia, selectively suppress only pain sensitivity and do not disturb consciousness.

Pyrazolone derivatives

Metamizole-sodium(analgin) has an anti-inflammatory, antipyretic effect, but an analgesic effect is more pronounced. It dissolves well in water, so it is often used for parenteral administration. Included in the combined drugs " Tempalgin», « Pentalgin», « Benalgin", as well as in combination with antispasmodics in the composition of drugs" Baralgin», « Spazgan», « Maxigan”, effective for spasmodic pain.

Undesirable side effects: oppression of hematopoiesis (agranulocytosis), allergic reactions, gastrotoxicity. In the process of treatment, it is necessary to control the blood test.

Aniline derivatives

Acetaminophen(paracetamol, panadol) has an analgesic and antipyretic effect and almost no anti-inflammatory effect. It is used mainly for headaches, neuralgia, injuries, fever. Widely used in pediatrics in the form of syrups and effervescent tablets - E fferalgan, tylenol, Kalpol, Solpadein, Paracet and other drugs practically do not cause irritation of the gastric mucosa. Possible impaired liver and kidney function. The antagonist of paracetamol is acetylcysteine.

Non-narcotic analgesics are contraindicated in gastric and duodenal ulcers, impaired liver and kidney function, bronchospasm, impaired hematopoiesis, pregnancy, lactation.

Chapter 3.3 Drugs affecting the central nervous system

The central nervous system is of paramount importance for the life of the body. Violation of its normal functioning can lead to serious illnesses.

All medicinal substances acting on the central nervous system can be conditionally divided into two groups:

1. oppressive CNS functions (anesthetics, hypnotics, anticonvulsants, narcotic analgesics, some psychotropic drugs (neuroleptics, tranquilizers, sedatives);

2. exciting CNS functions (analeptics, psychostimulants, general tonic, nootropic drugs).