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0:00

Вступление

0:23

Достоинства и недостатки снотворных средств

4:11

Классификация снотворных средств

12:40

Классификация снотворных средств: общая схема

12:43

Механизм действия ГАМКергических средств

19:17

Фармакологические эффекты бензодиазепинов

27:38

Фармакологические эффекты Z-препаратов

29:11

Как снотворные влияют на структуру сна?

37:27

Блокаторы гистаминовых H1-рецепторов

40:32

Мелатонин

41:09

Сравнительная характеристика снотворных средств

Бессонница. 13 Серия. Боевик. Сериал

Бессонница. 13 Серия. Боевик. Сериал

Channel: Star Media

Базисная фармакология противоэпилептических средств

Базисная фармакология противоэпилептических средств

Channel: SciDrugs

Базисная фармакология антидепрессантов: основы патофизиологии депрессии

Базисная фармакология антидепрессантов: основы патофизиологии депрессии

Channel: SciDrugs

Базисная фармакология антипсихотических средств

Базисная фармакология антипсихотических средств

Channel: SciDrugs

Инсомния

Инсомния

Channel: ВИА Месхи – Thema

Бессонница (Версия)

Бессонница (Версия)

Channel: Светлана Разина – тема

Базисная фармакология противоаритмических средств

Базисная фармакология противоаритмических средств

Channel: SciDrugs

Бессонница. 14 Серия. Боевик. Сериал

Бессонница. 14 Серия. Боевик. Сериал

Channel: Star Media

Бессонница. 8 Серия. Боевик. Сериал

Бессонница. 8 Серия. Боевик. Сериал

Channel: Star Media

Базисная фармакология анксиолитиков и средств, применяемых в терапии тревожных расстройств

Базисная фармакология анксиолитиков и средств, применяемых в терапии тревожных расстройств

Channel: SciDrugs

Диазепам

Феназепам

Фенобарбитал

Нитразепам

Димедрол

Дифенгидрамин

Доксиламин

Золпидем

Зопиклон

Залеплон

Инсомния

Бессонница

Снотворные

Кудряшов

Фармакология

ЦНС

00:00:02

Viktorovich Kudryashov, and today we will talk about

00:00:04

sleeping pills, I hope that my

00:00:06

lecture will not cause you the mentioned

00:00:08

effect, what are sleeping pills,

00:00:11

this is a group of medications that

00:00:13

facilitate the process of falling asleep and induce

00:00:16

sleep, which in its electrophilic

00:00:18

graphic characteristics is close to

00:00:21

normal physiological to sleep, sleeping

00:00:23

pills, like almost any

00:00:26

group of medicines, have both

00:00:27

their bright and dark sides,

00:00:30

let's start by looking at the

00:00:32

obvious advantages of sleeping pills, their

00:00:34

advantages, what are the obvious

00:00:38

advantages of sleeping pills, firstly,

00:00:42

sleeping pills facilitate the process of

00:00:44

falling asleep, they facilitate rashes, why is

00:00:51

this a plus, well, I I think this is clear here and

00:00:54

obviously we have insomnia that is

00:00:57

caused precisely by the fact that a person’s

00:00:59

process of falling asleep is disrupted

00:01:00

just above vorne and they make it easier to

00:01:03

fall asleep, in general, it eliminates insomnia. The

00:01:05

second advantage of sleeping pills

00:01:07

is that they reduce the number of

00:01:11

night awakenings, they reduce the number of

00:01:16

night awakenings why this is

00:01:19

a plus; again, there is a form of

00:01:24

insomnia that is associated with the fact that a

00:01:26

person constantly wakes up in the middle of

00:01:27

the night, as a result of which the

00:01:29

integrity of sleep is lost, the person is not able to

00:01:31

properly rest during the day, and the remedies

00:01:33

solve this problem; they reduce

00:01:35

the number of night awakenings, as a result the

00:01:37

person regains complete sleep. the

00:01:41

third advantage is that sleeping pills

00:01:44

provide a sufficient

00:01:47

duration of sleep; they provide a

00:01:51

sufficient duration of

00:01:58

sleep; the advantage here is that there

00:02:04

is, again, a form of insomnia that is

00:02:07

associated with the fact that a person wakes up

00:02:08

ahead of time; he cannot fall asleep anymore; it’s

00:02:11

as if he did not receive his dose sleeping pills and

00:02:15

sleeping pills are able

00:02:18

to prolong sleep and ensure its

00:02:21

sufficient duration for a

00:02:22

person with insomnia can also be

00:02:25

attributed to the obvious disadvantage of sleeping pills as a

00:02:29

group of

00:02:32

drugs; firstly,

00:02:33

sleeping pills can be addictive and

00:02:37

addictive; they can be

00:02:39

addictive and

00:02:44

drug dependence; the

00:02:54

second disadvantage is that

00:02:58

sleeping pills disrupt the structure of

00:03:00

sleep, which is why in the definition we

00:03:03

say that they induce sleep

00:03:04

that is close to physiological but not

00:03:08

physiological, it is sleep that disrupts the

00:03:11

structure of sleep. Finally, the third disadvantage

00:03:22

is that they have after the

00:03:27

action and have after the action all

00:03:36

these three characteristics they are not uniform

00:03:38

for different groups of drugs

00:03:41

that are included in the category of sleeping pills,

00:03:43

respectively, with different strengths,

00:03:46

different sleeping pills can

00:03:48

be addictive and dependent, they do

00:03:50

not equally affect the structure of

00:03:53

sleep, some sleeping pills will

00:03:55

disrupt the structure of sleep to a greater extent, some will be

00:03:57

less and, of course, the severity after

00:04:00

action, it is different for all groups, it can

00:04:03

be either very low or quite

00:04:05

noticeable high and pronounced, but

00:04:08

we will talk about this a little later. You

00:04:13

can classify hypnotics according to several principles, but we will

00:04:17

consider the classification according to the

00:04:18

predominant mechanism of action of

00:04:20

hypnotics I

00:04:22

like it Most of all, the most

00:04:24

extensive group of

00:04:26

hypnotic drugs will be called gam

00:04:28

karmic drugs, what does this mean, this

00:04:33

means that drugs from this subgroup

00:04:38

will enhance inhibitory processes

00:04:41

that are mediated by the

00:04:43

main inhibitory mediator

00:04:45

gamma-aminobutyric acid and due to

00:04:47

this,

00:04:49

their own hypnotic effect will be realized, the other two groups are

00:04:52

smaller include

00:04:56

histamine h 1 receptor blockers

00:04:59

histamine h 1 receptor blockers and the

00:05:11

last group includes

00:05:14

melatonin receptor agonists

00:05:18

melatonin receptor agonists we

00:05:26

will begin to consider hypnotics

00:05:27

from the largest group with oncological

00:05:30

drugs to understand the classification then

00:05:33

what is the basis for the classification of

00:05:34

gankergic drugs we need to

00:05:37

look in detail at the structure of

00:05:40

gamma-aminobutyric acid receptors and

00:05:43

not just receptors of gamma-aminobutyric acid

00:05:45

receptors, type A, before us is the structure of the

00:05:49

gang and receptor, it consists of five

00:05:51

subunits 2 alpha 2 beta 2 hama

00:05:54

subini whose composition can change, in addition, the

00:05:56

subunits have different

00:05:58

isoforms that allows us to distinguish

00:06:01

different subtypes of GHB receptors, but more on

00:06:03

this again a little later, where we

00:06:07

have sites connected to this recipe,

00:06:10

while gamma-aminobutyric acid itself

00:06:12

has a binding site between alpha and

00:06:14

beta subunits, but

00:06:16

beta subunits still play a greater role, and

00:06:19

gamma acts -aminobutyric acid and

00:06:22

so homc

00:06:24

we bind here, this is the

00:06:26

binding site of the mediator itself, in addition to the

00:06:29

binding site with the gamma

00:06:31

acid machine itself, we have two more

00:06:34

important sites, in fact, a whole bunch of them

00:06:36

for homc recipes, but in the context of

00:06:38

sleeping pills, what is important to us is what

00:06:41

we have there is a site connected between the alpha

00:06:44

and gamma subunits and this site

00:06:49

is called

00:06:50

benza diaza pin site benza diaze

00:06:55

pin site or it can be called

00:07:00

benza diaza pin receptor means site

00:07:04

or receptor again there is a site

00:07:11

between two subunits but the alpha subunit plays a decisive

00:07:14

role for the binding of benzodiazepines On the

00:07:16

other

00:07:20

hand, between the beta and

00:07:25

alpha subunits, we also have

00:07:27

another receptor

00:07:29

or Ig site called barbiturate

00:07:33

barbiturate receptor or

00:07:35

barbiturate site barbiturate

00:07:40

site or receptor

00:07:46

drugs belonging to the

00:07:49

mentioned groups of drugs

00:07:51

or benzodiazepine derivatives or

00:07:54

barbituric acid derivatives pittura there they

00:07:57

are able to bind to these sites or

00:08:00

receptors

00:08:01

allosterically regulate the entire gamut to the

00:08:03

receptor, they do this in such a way

00:08:06

that by

00:08:07

binding in this center they change the

00:08:09

conformation of the entire gamut of the receptor and

00:08:12

improves the affinity of gamut butyric

00:08:14

acid to the ganga

00:08:15

receptor, but in more detail the mechanism

00:08:18

we will of course Let's look

00:08:20

at these sites

00:08:24

or receptors accordingly, we can classify

00:08:25

gun karmic means and 1 subgroup of

00:08:28

gam karmic means, as you

00:08:30

probably already guessed,

00:08:32

are agonists of the benzodiazepine

00:08:35

receptor or benzodiazepine site,

00:08:37

so the first subgroup is agonists of the

00:08:44

benzodiazepine receptor, I will reduce

00:08:47

benzodiazepines to two

00:08:50

letters, respectively. they can,

00:08:53

in turn, be divided into two

00:08:55

subgroups depending on their

00:08:57

chemical structure; they can be

00:08:58

benzodiazepine derivatives

00:08:59

or simply benzodiazepines, but they

00:09:07

can also be, no matter how stupid it sounds,

00:09:10

die special non-

00:09:12

benzodiazepine, you and benz and

00:09:14

diaza pin receptor agonists are not benza diaza

00:09:18

pins to penza diaza pins include such

00:09:25

well-known

00:09:27

drugs as midazolam

00:09:35

phenazepam diazepam

00:09:46

metro zapom

00:09:48

and so on, they are all

00:09:52

derivatives of benzodiazepines horse birds

00:09:57

for the first drug we have

00:10:00

drugs of various

00:10:02

chemical groups but I like that

00:10:06

this group there is a slang name

00:10:07

that allows you to better remember this

00:10:10

group of drugs, by the way, the

00:10:13

slang name is not just

00:10:14

colloquial, it is even found in the

00:10:16

scientific literature,

00:10:17

they are called z drugs z drugs,

00:10:23

respectively, they received this name due to the fact

00:10:26

that all the drugs in this group begin

00:10:28

in Latin, Latin spelling in the letter

00:10:32

z in the Russian version they will begin

00:10:35

with the letter z

00:10:37

hall tdm zopiclone

00:10:43

and

00:10:46

for lepland as you can see they all

00:10:55

start with the letter z

00:10:57

and in this case you can equate it with

00:11:04

z that’s why they are called for the drugs

00:11:07

I personally like to name this drug

00:11:10

I don’t see there is nothing reprehensible in it, I

00:11:11

quite believe that it can be

00:11:13

used in the classification

00:11:15

of the second group of Hamburg drugs

00:11:17

for compliance includes

00:11:19

barbiturate receptor agonists or barbiturate

00:11:21

new site

00:11:24

barbiturate receptor agonists here

00:11:29

we have only one drug since these

00:11:31

drugs are no longer particularly used as

00:11:33

stimulants this is

00:11:34

phenobarbital phenobarbital the

00:11:41

next group is blockers

00:11:44

of histamine h 1 receptors, we

00:11:48

can include this step about the well-known

00:11:51

drug as defiant hydra min yoongi

00:11:55

drummen is probably better known

00:11:58

under the trade brand dimidrol

00:12:01

and the second drug which I still

00:12:04

use more as a natural

00:12:06

remedy is this dag forces

00:12:09

so strength min we belong to the third group as

00:12:12

agonists of tanya new

00:12:13

receptors and here it is completely logical

00:12:15

that the drug will be the pineal gland hormone

00:12:19

melatonin itself. Normally melatonin regulates the

00:12:22

changes in sleep and alertness cycles and simply the

00:12:25

circadian rhythm and but in this case we are

00:12:28

not talking about

00:12:29

endogenous melatonin and which are

00:12:31

produced by snakes, the introduction of

00:12:33

exogenous melatonin is like this, this is how the

00:12:37

classification of hypnotic

00:12:40

drugs looks like, the mechanism of action, we will begin to

00:12:44

look at the GABA arctic drugs,

00:12:46

since this is really the main group of

00:12:47

hypnotic drugs, and before we

00:12:50

proceed to our own mechanism of action of

00:12:52

gram karmic drugs, let's

00:12:53

look at how they are structured how

00:12:56

the gang functions and the receptor frame the receptor is a

00:13:00

receptor for the main inhibitory

00:13:01

transmitter gamma-aminobutyric acid,

00:13:04

we have already said earlier that

00:13:07

it consists of five subunits alpha 2 pieces btd

00:13:11

pieces and gamma with an increased composition can

00:13:14

change subunits can have

00:13:15

different isoforms this itself the receptor

00:13:19

is nothing more than an

00:13:21

ion channel; roughly speaking, it forms a

00:13:23

funnel through which

00:13:26

chlorine ions can pass into the cell at the moment when the gang

00:13:29

contacts the receptors in its

00:13:31

area, the channel opens and

00:13:34

chlorine ions rush into the cell; they

00:13:37

accumulate on the inside

00:13:39

membranes and are called hyperpolarization of

00:13:41

nerve cells, as a result,

00:13:44

inhibition processes develop in the central

00:13:46

nervous system, this is how the

00:13:51

gang itself works,

00:13:52

but you and I remember that

00:13:54

there are other sites on the surface of the GOM receptors,

00:13:59

firstly, this benzodiazepine site

00:14:02

is located between the alpha and gamma

00:14:04

subunits on this site we have a

00:14:09

direct effect of benzodiazepines

00:14:14

benzodio, how do benzodiazepines act

00:14:23

benzodiazepines and bind to

00:14:26

benzodiazepine receptors

00:14:28

or benzodiazepine sites on the

00:14:31

surface of the ganga

00:14:32

receptor the conformation of the entire

00:14:37

benzodiazepine receptor changes as a

00:14:39

result the affinity of

00:14:42

benzodiazepines for the ganga receptor

00:14:48

increases the frequency of opening of chloride

00:14:51

channels, the process of

00:14:53

hyperpolarization develops and, accordingly, the

00:14:56

pharmacological effects of

00:14:59

benzodiazepines develop, and so the mechanism of action of the

00:15:01

laws will once again be duplicated in text

00:15:04

form. The basis for the mechanism of action of

00:15:06

benzodiazepines, as well as the

00:15:08

barbiturates themselves, which we will now

00:15:09

discuss, is based on the principle of all historical

00:15:12

regulation of homc and the receptor when

00:15:14

interaction with it by the active center

00:15:15

leads to a change in the conformation of

00:15:17

another active center, the mechanism

00:15:20

of action of barbiturates is in many ways similar to the

00:15:22

mechanism of action of benzodiazepines, but

00:15:25

unlike benzodiazepines, barbiturates

00:15:27

bind to the barbiturate site of the

00:15:29

hamka receptor, which also leads to a change in the

00:15:31

conformation of the entire homka receptor,

00:15:35

as a result of which the affinity of the gang gang increases

00:15:38

and the receptor, as a result, increases in

00:15:42

duration opening of chlorine

00:15:45

channels and increased inhibition

00:15:47

since more

00:15:48

chlorine is able to enter the cell,

00:15:50

accordingly this will intensify

00:15:51

the processes of hyperpolarization, again, what is

00:15:54

the difference? This is highlighted in red

00:15:56

on the slide. Benzodiazepines increase the

00:15:58

purity of the opening of chlorine channels.

00:16:00

Barbiturates increase the

00:16:02

duration of the

00:16:03

channel being in the open state,

00:16:06

both lead to to the fact that more

00:16:08

chlorine enters the cell, both of

00:16:11

which lead to increased inhibition, this is

00:16:14

the mechanism of action that

00:16:15

barbiturates and benzodiazepines have, but

00:16:18

what kind of drugs do you ask and what kind of

00:16:22

drugs have their own mechanism of

00:16:25

action, and the drugs

00:16:28

are also associated with the same benzodiazepine with

00:16:31

your recipes because how you hope

00:16:34

to remember from the classification they are

00:16:36

they are without back azapine new agonists without

00:16:39

delays of pin receptors but with one

00:16:43

caveat they bind to day video,

00:16:47

receptors only if the

00:16:50

gang

00:16:52

and receptor contains an alpha-1

00:16:55

subunit while

00:16:57

benzodiazepines bind with those gang

00:17:00

receptors that contain

00:17:03

alpha-1 alpha-2 alpha 3 or alpha 5

00:17:09

subunit because alpha 4 and alpha 6

00:17:18

subunits are insensitive to

00:17:20

benzodiazepines, insensitive to

00:17:23

benzodiazepines, let’s note this, they

00:17:28

are insensitive to benzodiazepines precisely because of this

00:17:31

selectivity z

00:17:35

drugs will be significantly different

00:17:38

from benzodiazepines,

00:17:40

and we’ll talk about this now,

00:17:42

let’s understand what the

00:17:45

difference is between z drugs and

00:17:47

benzodiazepines,

00:17:48

firstly, we talked about the fact that the

00:17:50

subunits can have different compositions due to the

00:17:53

shape of the race of the

00:17:55

alpha subunits, there are as many as 6

00:17:58

subtypes with 6 forms, while 4 and 6

00:18:01

are considered insensitive to

00:18:03

benzodiazepines,

00:18:05

and receptors that include

00:18:07

various isoforms of alpha subunits are

00:18:09

heterogeneously located in the brain,

00:18:12

predominantly in an instant to the megogo receptor of the

00:18:14

brain are lumpy receptors that

00:18:16

include alpha 1 subunit,

00:18:20

about 60 percent of them gomka

00:18:23

receptors of the brain they are located

00:18:26

mainly in the fields of the mantle of the brain in the

00:18:28

thalamus and in the brainstem

00:18:30

gomka receptors including the alpha 2 su

00:18:33

unit located in the hippocampus

00:18:35

information striatum and olfactory

00:18:37

bulbs a alpha 3

00:18:39

gomka receptors are located in the

00:18:41

lateral septum of the reticular nuclei

00:18:43

of the thalamus in some games of the brain stem

00:18:46

also in the motor neurons alpha 5 gomk and the

00:18:50

recipe are located in the olfactory

00:18:52

bulb and in the pyramidal cells of the

00:18:54

hippocampus and it is quite obvious that 1

00:18:58

gomk receptors contain different

00:19:01

alpha subunits and are heterogeneously

00:19:03

distributed throughout the brain then

00:19:05

benzodiazepines that bind to

00:19:08

alpha 1 alpha 2 alpha 3 alpha 5 gam to the

00:19:11

receptors will have several

00:19:14

pharmacological effects,

00:19:16

so benzodiazepines have six

00:19:19

important pharmacological effects, and

00:19:22

these effects are dose-dependent in

00:19:25

nature, let's try to

00:19:28

depict this, for this we will draw with you

00:19:31

such a line

00:19:33

that will go from low doses to

00:19:39

high doses high doses

00:19:47

according to the effects, as I said,

00:19:49

we have 6, so let’s conditionally divide this straight

00:19:54

line into 6 segments and begin

00:19:59

to consider the effects that appear

00:20:02

as the dose of benzodiazepines increases. The

00:20:06

first

00:20:07

effects are anxiolytic anxiolytic.

00:20:13

Politically, the

00:20:15

same effect can be called anti-

00:20:17

anxious, since the anxiolytic

00:20:19

effect is an effect associated with

00:20:22

suppression feeling of fear the second

00:20:26

effect in this ladder of

00:20:28

doses we will have the effect of sedation

00:20:32

sedative effect there is a difference

00:20:37

between anxiolytic and sedative

00:20:39

effect analytical effect is a

00:20:41

selective suppression of the feeling of fear

00:20:43

while sedation

00:20:46

is a decrease in the response of the central nervous

00:20:50

system to external stimuli which

00:20:52

is accompanied by a decrease in

00:20:54

concentration and general lethargy therefore

00:20:59

there is a clear difference in the effect of the anx

00:21:00

political effect a

00:21:01

sedative drug may have

00:21:03

a sedative but not have anx

00:21:05

political effect the drug may

00:21:06

have an

00:21:07

anx synthetic effect but does not

00:21:09

have a sedative or it can, like a

00:21:11

movie without delay, combine these

00:21:13

effects the third effect in our

00:21:15

ladder will be the

00:21:17

hypnotic effect sleeping pills, accordingly, it

00:21:23

occupies an honorable third step in our

00:21:28

ladder. Above we will have a

00:21:31

nice relaxing effect, which is

00:21:33

associated with the fact that benzodiazepines due to

00:21:35

central mechanisms, in particular the

00:21:37

presence of some GOMK receptors of the

00:21:41

motor neurons of the spinal cord, will be associated

00:21:44

with the relaxation of skeletal muscles, boldly

00:21:45

relaxing, relaxing, it occupies

00:21:52

the fourth step is relaxation of

00:21:54

skeletal muscles, higher we will

00:21:58

have an anticonvulsant effect.

00:22:00

Benzodiazepines are able to relieve seizures

00:22:05

in some forms of

00:22:08

epilepsy; moreover, knitting bumpers

00:22:11

is used, among other things, to relieve

00:22:13

such a serious condition as

00:22:14

status epilepticus;

00:22:16

anticonvulsant;

00:22:20

and at the very, very top of our ladder

00:22:25

there is such an interesting effect how

00:22:27

amnestic benzodiazepines

00:22:33

can cause antara grodno amnesia,

00:22:37

and this effect is reminiscent of the

00:22:40

amnestic effect of alcohol, let's say

00:22:42

4 people got drunk,

00:22:43

let him do some social

00:22:46

action, say it to someone, hit him in the

00:22:49

face there, beat someone, beat him somewhere,

00:22:51

broke furniture, a display window, not beyond the point it’s important

00:22:54

and the next morning when he sobered up, he’s like I didn’t

00:22:56

do anything, I don’t remember anything,

00:22:58

I don’t know anything, I didn’t do it, he

00:22:59

really doesn’t remember, but as soon as he

00:23:01

takes alcohol again, the memory voila

00:23:05

returns, that is, this effect is

00:23:08

associated with a specific state of the

00:23:10

central nervous system, that is

00:23:12

memorization occurred against the background of

00:23:14

alcohol intoxication to

00:23:15

reproduce these

00:23:18

memories before retrieving them again

00:23:21

requires the use of alcohol, the

00:23:23

same thing in general practically causes and

00:23:25

benzodiazepines are precisely because of this they

00:23:28

have a mystical effect there, again

00:23:30

this effect is not necessarily something that will develop

00:23:31

in a person taking benzodiazepines

00:23:33

then perhaps the effects again, as you see,

00:23:35

they strictly depend on the dose, but what about

00:23:39

these effects of benzodiazepines

00:23:42

associated with the presence of a specific

00:23:46

subunit in the race recipe to please with

00:23:48

its let's look at the alpha 1 subunit,

00:23:50

which is part of the loud

00:23:52

receptor is responsible for the hypnotic

00:24:00

oxidative

00:24:06

amnestic effect

00:24:13

and is partially partially responsible for

00:24:17

anticonvulsant activity since

00:24:19

this is an effect partially dependent on alpha-1,

00:24:21

I will designate it in a different color in the diagram

00:24:24

anticonvulsant anticonvulsant well

00:24:33

again, the mark is partial,

00:24:37

that is, not completely, this effect

00:24:39

is realized through alpha-1 alpha-2,

00:24:43

for which the alpha-2 subunit itself is responsible

00:24:50

is responsible for the development of the analytical

00:24:53

effect alpha 2 subunit is also

00:25:02

responsible for it the relaxing effect

00:25:11

alpha three subunits will be responsible for

00:25:13

chalk relaxing alpha 5 will also be

00:25:23

responsible for the world relaxing effect but

00:25:31

at the same time alpha 5 will also be responsible for the

00:25:33

amnesic effect amnestic this is what

00:25:44

we have you have a

00:25:45

distribution of effects that are

00:25:48

currently clearly

00:25:49

established in relation to the presence of a

00:25:52

specific alpha subini pike perch leti, not

00:25:54

all of our effects have a clear

00:25:59

link to the subunit. What I would like to

00:26:02

add about the

00:26:04

amnestic effect of benzodiazepines is the

00:26:06

magnitude of this effect not only depends

00:26:09

on the dose but also on properties as well as

00:26:11

lipophilic benzodiazepines, the more

00:26:13

benzodiazepines are soluble in lipids,

00:26:15

the more it is not according to the film, the higher the risk of an

00:26:18

amnestic effect, how can you

00:26:20

remember the dependence of the effects of Penza

00:26:24

Spin-off on the dose, but there is

00:26:27

no such graphic memory here, but you can’t

00:26:30

remember it loudly in such a very simple way

00:26:32

logical reasoning 5 there is no

00:26:35

scientific basis for it, but in

00:26:38

principle it is logical, at first the

00:26:41

feeling of fear decreases, remember this, the

00:26:43

feeling of fear is immediately eliminated, an

00:26:45

anxiolytic effect develops, respectively,

00:26:47

if the feeling of fear has disappeared, you can not

00:26:51

pay attention to the environment,

00:26:53

you can not monitor it, accordingly,

00:26:55

develop a sedative effect and only 1

00:26:57

is associated with a decrease in concentration of

00:26:59

attention and a decrease in the response of the central nervous system to an

00:27:01

external stimulus; at first, the feeling of

00:27:03

fear disappears, then you can stop

00:27:06

reacting to excess stimuli, and

00:27:08

then you can fall asleep in a dream;

00:27:12

sooner or later, muscle relaxation occurs; the

00:27:13

anticonvulsant effect just

00:27:17

needs to be remembered that it comes second to last

00:27:20

since the effect of the highest ones after there is

00:27:23

mystical, that is,

00:27:24

in high doses, benzodiazepines simply

00:27:27

deal a powerful blow to the brain, the

00:27:29

memory sings along,

00:27:31

well, somehow, in an unscientific way, you can

00:27:33

try to remember this dose depending on how to

00:27:35

simply not memorize these effects,

00:27:38

what is the beauty of these drugs?

00:27:42

act only in relation to

00:27:44

receptors that contain the alpha 1

00:27:46

subunit, which means in our table we

00:27:50

can highlight the

00:27:53

localization of the alpha 1 subunit and the

00:27:56

effects associated with it. The fact is that

00:27:59

due to the selectivity of the

00:28:01

drugs, firstly, they have a weakly

00:28:06

expressed anxiolytic effect,

00:28:08

respectively, anxiolytic

00:28:15

muscle relaxant

00:28:16

and anticonvulsant effects the effects are expressed to a

00:28:25

very very insignificant extent,

00:28:32

the effects are

00:28:36

weakly expressed, well, clinically, you can

00:28:42

say there are none and there are none; secondly,

00:28:47

zerg drugs

00:28:51

change the structure of sleep to a lesser extent and not to a lesser

00:29:00

extent change the structure of sleep, and now

00:29:02

we will just figure out what the

00:29:05

structure of sleep is and what we

00:29:07

mean by what we say that

00:29:08

drugs interfere with the structure of sleep

00:29:10

what is the effect of sleeping pills on the

00:29:13

structure of sleep but for simplicity we can

00:29:16

divide sleep into the rim phase this is the

00:29:18

paradoxical phase of sleep

00:29:19

rapid eye moment phase rapid eye movement

00:29:22

and nose rap sleep in the paradoxical phase of

00:29:25

sleep and so the growth phase of sleep, which

00:29:27

is responsible for dreaming and without which

00:29:29

complete mental and

00:29:31

physical rest of a person is impossible, the rome phase

00:29:34

is so called because in this phase

00:29:36

complete muscle paralysis occurs,

00:29:38

the person does not control the posture, but at the same time

00:29:41

the eyes move quickly during the phase of

00:29:44

men, you can also act

00:29:45

additionally, erection is a phase that

00:29:48

normally accounts for approximately 25 percent

00:29:50

of all sleep, it occurs

00:29:53

again approximately every 90 minutes, and here

00:29:56

is a line

00:29:57

that indicates the

00:29:59

percentage of rem sleep in a healthy person,

00:30:03

but what if we inject this person with

00:30:06

benzodiazepines or barbiturates

00:30:10

benzodiazepines or

00:30:16

these barbiturates drugs will reduce the stage of the rim

00:30:24

phase, the stage of paradoxical sleep,

00:30:27

ultimately what will this lead to if we

00:30:29

stop abruptly at this point, yes,

00:30:32

let’s say at this point we

00:30:35

cancel the drug,

00:30:39

cancel the drug,

00:30:42

this will lead to a compensator for us in the

00:30:45

growth of the fish phase and to the formation of a

00:30:51

syndrome or rebound phenomenon the rim phase of

00:30:55

sleep will increase, the increase in rm

00:31:01

phase, when

00:31:03

the drug is withdrawn, it will be

00:31:10

pleasant not the drug, this will

00:31:13

lead to the person’s

00:31:15

problems becoming worse for

00:31:18

which you actually used

00:31:19

benzodiazepines or barbiturates,

00:31:22

he will begin to see very vivid

00:31:24

dreams, usually of a nightmare

00:31:26

nature, because the withdrawal does not proceed

00:31:28

only due to the hypnotic effect but the

00:31:29

political membrane he will see

00:31:32

dreams that are vivid, usually

00:31:34

colored in a nightmare color he will often

00:31:36

wake up at night please it turns out

00:31:38

insomnia is associated with frequent awakenings at night

00:31:41

me of course this phenomenon

00:31:43

disappears when a

00:31:46

certain number of days have passed from the moment of

00:31:48

drug withdrawal, not immediately where then from

00:31:51

three days, maybe up to a week,

00:31:52

holding the price for and counting how much the person

00:31:55

took, in what dose he took the chainsaw,

00:31:57

what is recommended to do so that

00:31:59

this withdrawal syndrome does not develop, how to

00:32:03

prevent it, he warned, you just need to

00:32:05

gradually reduce the dose of the drug and

00:32:08

then there will be such a sharp return of such a

00:32:10

spring phenomenon will not happen

00:32:12

occurs from compensatory because the

00:32:14

body did not receive enough of

00:32:15

this phase, it is associated with rest with the

00:32:19

necessary mental and physical

00:32:20

rest during sleep, naturally, after

00:32:23

stopping the drug, the body tries

00:32:25

to compensate for the lack of this phase, a

00:32:27

spring phenomenon occurs, that is, if

00:32:29

the springs are compressed for a long time and then suddenly

00:32:31

released, this will actually happen the

00:32:33

same effect and the rebound effect of the

00:32:36

rebound phenomenon, therefore, prevention is a gradual

00:32:38

reduction in the dose of benzodiazepine,

00:32:42

which is interesting which drugs have a lesser

00:32:45

effect on the structure of sleep, the mechanism

00:32:49

due to which this happens

00:32:51

cannot be precisely named, but

00:32:52

even the neurotransmitter

00:32:54

mechanism of this paradoxical

00:32:56

sleep is not completely known but apparently

00:33:00

this is due to the fact that this drug

00:33:02

selectively acts on alpha 1 gom k

00:33:05

receptors. If we nevertheless turn to

00:33:09

attempts to analyze

00:33:12

what the rim phase of sleep consists of there and

00:33:15

low, we will clearly see that at the moment of the m phase

00:33:18

we have an increase in the concentration of acetylcholine

00:33:22

and glutamate Moreover, the main processes

00:33:25

will occur in the area of the

00:33:27

pons from which the projection of the preparation of the

00:33:29

rub will occur, cortical activation will occur

00:33:31

and will occur with inhibition of

00:33:33

motor neurons, which will cause

00:33:36

muscle paralysis during sleep, how will

00:33:40

benzodiazepines, unlike z drugs, affect

00:33:43

these neurotransmitters and the system well

00:33:45

in -the first GHB allergic drugs,

00:33:47

they generally are in reverse

00:33:51

interactions with the glutamate system,

00:33:53

since the gang system is the

00:33:54

inhibitory system of glutamate on the

00:33:57

excitatory system, this system

00:33:59

is usually in reverse interactions, the

00:34:01

more we strengthen the gang system, the

00:34:04

more glutamate is weakened, the logical

00:34:07

system is the first point, but here it is explained

00:34:09

how, just for the presence of this, here is the

00:34:11

effect on the phase of paradoxical sleep in

00:34:14

all gankergic drugs,

00:34:15

barbiturates enhance gang, can

00:34:17

weaken glutamate, benzodiazepines,

00:34:20

accordingly, also enhance gonorrhea

00:34:22

processes, which means they can weaken

00:34:24

processes associated with glutamate, but because of the

00:34:26

drugs, they still have an effect, but to a lesser extent

00:34:28

degrees in the structure of sleep by 5 why is this

00:34:30

taken to a lesser extent because they

00:34:32

again, as a means of ganker gical,

00:34:34

are in reverse interactions with the

00:34:38

tragic glutamate system,

00:34:41

everything is interesting in relation to acetylcholine, the fact is

00:34:45

that the neurons are just the neuron

00:34:47

located at the level of the neuronal bridges,

00:34:51

which contains acetylcholine and

00:34:53

release it,

00:34:54

they contain

00:34:59

gamma-aminobutyric acid receptors on their surface,

00:35:01

this is a cholinergic neuron that

00:35:04

releases

00:35:05

acetylcholine, which means a cholinergic

00:35:08

neuron, which is interesting, on the surface of an

00:35:16

allergic neuron there may be

00:35:20

a gang and a receptor race receptor and not

00:35:26

just a protein receptor agam k a receptor

00:35:28

containing

00:35:29

alpha three subunits, that is alpha 3

00:35:33

gang is a recipe and, accordingly, if

00:35:38

benzodiazepines are able to

00:35:41

bind to alpha 3 gang and the receptors

00:35:43

will initially bind from the GA

00:35:46

receptors that are located on the

00:35:48

surface of the cholinergic neuron, so far

00:35:50

what will this lead to if benzodiazepines

00:35:53

act on the alpha 3 gang receptor it

00:35:57

will enhance the effect of the gang itself on this

00:36:03

receptor and this will lead to inhibition of the

00:36:08

cholinergic neuron and accordingly

00:36:11

will decrease in the release of acetylcholine,

00:36:13

which is believed to play one of the

00:36:15

leading roles in the development of this

00:36:18

paradoxical sleep in the rim phase of sleep, and

00:36:21

perhaps this is why benzodiazepines

00:36:24

are able to act on alpha 3 HMC

00:36:26

receptors that are located on

00:36:28

cholinergic neurons This is partly why they

00:36:31

are able to change the structure of sleep more strongly

00:36:33

than drugs that do not act on

00:36:35

alpha three receptors, but again

00:36:38

the drugs are not absolutely

00:36:40

selective for alpha-1 GHB

00:36:44

receptors; it’s just that their affinity is

00:36:45

maximum and it decreases in relation to

00:36:49

others, respectively, GHB receptors, they

00:36:51

can, in principle, bind but to a

00:36:53

lesser extent with alpha 2 gom to

00:36:54

receptors, and to an even lesser extent with alpha

00:36:57

3 and alpha 5, this is possible; therefore, the

00:36:59

selectivity is not absolute and, again,

00:37:01

due to this, the

00:37:03

influence of the sleep structure is retained, but due to the lower

00:37:06

affinity and activity in relation to the structure

00:37:10

there will be less sleep for these drugs,

00:37:12

these are the features we have a

00:37:15

corner of logical means

00:37:18

and now we will move on to the two

00:37:20

remaining groups of sleeping pills:

00:37:22

histamine h 1 receptor blockers and

00:37:25

melatonin receptor agonists,

00:37:27

it’s time to consider the mechanism of

00:37:29

histamine h 1 receptor blockers,

00:37:30

their mechanism hypnotic effect for

00:37:34

this, I depicted

00:37:36

the brain very schematically, what do we need in this mask?

00:37:39

Actually, we are interested in the

00:37:42

projections of histamine in the hypothalamus, we

00:37:47

have ditches there and a nucleus that

00:37:49

contains a cluster of neurons,

00:37:52

neurons containing a large number of neurons containing

00:37:54

histamine and the bodies of these neurons are located

00:37:57

here oxana, respectively diffusely

00:38:01

projected to other areas of the brain, what is important to us is

00:38:04

that histamine has a projection to the

00:38:07

thalamus in the basal forebrain and to the

00:38:11

cortex, respectively, these projections are

00:38:15

important to us what is the function of histamine histamine

00:38:18

activating here here here here here here here here here

00:38:23

and here

00:38:27

h1 receptors maintain wakeful sleep and

00:38:32

because this system the histamine system

00:38:34

is one of those systems that

00:38:35

help maintain wakefulness,

00:38:38

these are all histamine receptors,

00:38:41

green dots, these are all

00:38:45

histamine receptors in the brain,

00:38:47

respectively, the action of histamine of these

00:38:49

receptors is the maintenance of wakefulness

00:38:52

if we introduce blockers of histamine h

00:38:56

1 receptors, for example dimidrol

00:38:59

or dak forces,

00:39:05

then they what they do is block

00:39:10

histamine h1 receptors in the

00:39:14

brain and disrupt the function of histamine,

00:39:18

which was to maintain

00:39:21

wakefulness, respectively, histamine

00:39:25

could directly activate the cortex, respectively,

00:39:27

blockade of histamine by the

00:39:29

relationship of punishment receptors, videos of the

00:39:31

impossibility of maintaining age, they are

00:39:33

not able to be activated by karatekas,

00:39:35

histamine activated the basal

00:39:38

forebrain, also maintaining alertness and that

00:39:41

the important histamine activated the

00:39:43

thalamus and the thalamus line also has an

00:39:46

ascending projection to the cortex and

00:39:48

maintains functions while awake in

00:39:50

conditions of blocked non-Stamenov h

00:39:52

1 receptors,

00:39:53

respectively, the energy

00:39:56

system of the brain cannot maintain

00:39:58

wakefulness and step on the product for a

00:40:01

sedative effect, what is the

00:40:03

difference between diphenhydramine by forces to us

00:40:05

so by forces of us kinship histamine is

00:40:07

lower to their receptors due to which after the

00:40:09

effect of using ducks the forces

00:40:12

will be lower than that of Dimitrov Dimitrov

00:40:14

as a creature is not used

00:40:15

ducks lamin as a sleeping pill

00:40:17

is used the

00:40:19

main disadvantage of this group of

00:40:21

sleeping pills is their

00:40:24

ability to block muscari

00:40:25

sensitive halim on the receptors,

00:40:28

accordingly, they can cause

00:40:29

atropine and similar effects, and it remains

00:40:33

for us to analyze the mechanism of action of

00:40:35

melatonin; melatonin is a complete

00:40:38

analogue of endogenous melatonin and

00:40:41

is capable of stimulating melatonin; you and the

00:40:43

receptors for them have at

00:40:47

least two types;

00:40:48

melatonin receptor of the first type; their

00:40:50

stimulation is associated with facilitating

00:40:51

sleep while the stimulation of

00:40:53

melatonin Bax receptors type 2

00:40:55

leads to the restoration of normalization of

00:40:57

circadian rhythms, when

00:41:00

we use melatonin, it is advisable

00:41:03

to take it first of all when there is a

00:41:05

failure in time zones when

00:41:08

jet lag has occurred at the end of the lecture we

00:41:10

will compare different groups of

00:41:12

sleeping pills with each other according to

00:41:15

parameters, severity after action,

00:41:17

influence on the structure of sleep, we are interested in the

00:41:20

effect on the rim phase of sleep, therapeutic

00:41:23

breadth, the ability to cause addiction and

00:41:26

dependence,

00:41:27

the ability to cumulate, the ability to

00:41:30

induce microsomal

00:41:31

liver enzymes, the ability to suppress the activity of the

00:41:33

cardiovascular and respiratory systems,

00:41:36

and that is, each of the extensive depression

00:41:38

and the presence of a specific antidote

00:41:41

let's start filling out our table

00:41:44

the severity after the action of

00:41:47

benzodiazepines it is moderate moderate

00:41:55

barbiturates it is quite significant

00:42:01

pronounced significant after the action of

00:42:07

uther drugs low for up to xiaomi

00:42:15

very low

00:42:21

in influence on the orem phase of sleep chainsaws

00:42:24

of course disrupt the structure of sleep, but to a

00:42:27

greater extent the ram phase is suppressed by

00:42:30

barbiturates

00:42:31

to a lesser extent z drugs and

00:42:35

practically does not influence so by forces

00:42:38

therapeutic latitude for benzodiazepines

00:42:43

significant barbiturates narrow already

00:42:53

drugs significant impact by forces on

00:43:00

significant what does this mean it

00:43:05

speaks of safe dosing of the

00:43:07

drug physiotherapeutic latitude

00:43:09

large is our range of doses from

00:43:11

minimal therapeutic to

00:43:12

maximum large with us there is a choice of a

00:43:15

large number of doses, if the

00:43:16

theoretical latitude is narrow, this means

00:43:19

that the drug has a therapeutic

00:43:21

effect in a fairly small range of

00:43:22

doses, everything above this range is already

00:43:25

forgive the dose, toxic ability

00:43:28

to cause addiction and dependence,

00:43:30

benzodiazepines are capable of long-term

00:43:32

use, as a rule, with long-term

00:43:35

use,

00:43:42

unlike barbiturates cause

00:43:45

rapid and persistent dependence fast and

00:43:49

persistent dependence addiction

00:43:53

ability quickly

00:43:54

and persistent z drugs but with long-term

00:43:59

use can cause but to a lesser

00:44:01

extent than benzodiazepines with

00:44:03

long-term use why dependence is typical for both them and

00:44:09

benzodiazepines

00:44:11

because the

00:44:13

drug dependence on benzodiazepines

00:44:15

develops due to alpha -1 race

00:44:19

of receptors, as you remember, drugs

00:44:21

also act on the alpha 1 loud

00:44:23

receptor, but accordingly, the

00:44:24

drug’s action is more selective

00:44:28

in relation to other receptors, but

00:44:31

this parameter makes it somewhat easier, and

00:44:33

therefore dependence is still less

00:44:36

typical for this drug in

00:44:37

than for benzodiazepines, but it is

00:44:39

characteristic of both the former and the

00:44:42

latter; for dak forces, the

00:44:44

ability to accumulate is low for

00:44:49

benzodiazepines, while for

00:44:51

barbiturates it is high;

00:45:04

liver in for benzodiazepines it is

00:45:07

expressed to a small extent characteristic to a

00:45:11

small extent for barbiturates it

00:45:16

is expressed expressed for z drugs not

00:45:23

established for running by forces

00:45:26

not established cardiorespiratory

00:45:29

depression in case of overdose it is

00:45:32

characteristic of benzodiazepines in case of

00:45:35

overdose, that is, in high doses

00:45:38

or in the presence of respiratory

00:45:41

and cardiovascular diseases -vascular systems, it is also

00:45:43

possible benzodiazepines, but

00:45:45

barbiturates in therapeutic doses, a

00:45:48

challenge from depression of the respiratory and

00:45:50

cardiovascular system,

00:45:55

therapeutic doses in drugs in case of

00:46:00

overdose, the

00:46:04

same can be said regarding the

00:46:06

same forces on in case of overdose, now

00:46:14

about a specific anti-dota, we

00:46:16

only have a specific antidote in relation to the

00:46:19

benzodiazepine site, we have an

00:46:21

antagonist albenza diaza pin site

00:46:23

or without gas pin receptors it

00:46:26

is called in the Duma vinyl

00:46:29

flom rated it is used either for the

00:46:33

correction of benzodiazepine poisoning

00:46:36

or for eliminating the residual effects

00:46:38

of benzodiazepines, respectively, the antidote

00:46:42

we will have is characteristic of benzodiazepines

00:46:44

from their drug, that is those

00:46:47

directly on the ground that

00:46:50

are able to bind to benzine for beer

00:46:52

or to benzodiazepines, we have

00:46:54

receptor clones behind it luma you

00:46:58

nil for barbiturates so

00:47:02

there is no specific antidote, this is how the

00:47:07

comparative characteristics of hypnotics look like,

00:47:12

I thank you for your attention, I hope you

00:47:15

liked it this lecture

00:47:17

until next time

Description:

В лекции рассмотрены основы фармакологии снотворных средств. ** ВНИМАНИЕ! Вся информация, представленная в данном видео, носит исключительно образовательный и ознакомительный характер. Автор не несет ответственности за возможные последствия самолечения упомянутыми в видео лекарственными средствами (препаратами). Помните, что назначать лекарственные средства, равно как и изменять схему лечения, может только лечащий врач при очной консультации. 0:00 Вступление 0:23 Достоинства и недостатки снотворных средств 4:11 Классификация снотворных средств 12:40 Классификация снотворных средств: общая схема 12:43 Механизм действия ГАМКергических средств 19:17 Фармакологические эффекты бензодиазепинов 27:38 Фармакологические эффекты Z-препаратов 29:11 Как снотворные влияют на структуру сна? 37:27 Блокаторы гистаминовых H1-рецепторов 40:32 Мелатонин 41:09 Сравнительная характеристика снотворных средств

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