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General anaesthetics презентация, доклад

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General anaesthetics (GAs) are drugs which produce reversible loss of all sensation and consciousness. The cardinal features of general anaesthesia are:• Loss of all sensation, especially pain• Sleep (unconsciousness) and amnesia•

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Слайд 1General anaesthetics

General anaesthetics

Слайд 2 General anaesthetics (GAs) are drugs which produce reversible loss of

all sensation and consciousness.
The cardinal features of general anaesthesia

are:
• Loss of all sensation, especially pain
• Sleep (unconsciousness) and amnesia
• Immobility and muscle relaxation
• Abolition of somatic and autonomic reflexes.
The balanced anaesthesia is achieved by using combination of inhaled and i.v. drugs.
The first GAs were nitrous oxide (laughing gas in 1844. The first IV anaesthetic thiopentone was introduced in 1935.
General anaesthetics (GAs) are drugs which produce reversible loss of all sensation and consciousness. 	The cardinal features

Слайд 3Mechanism of action of anaesthetics
Anaesthetic potency correlates well with lipid

solubility. Anaesthetics might dissolve in the lipid bilayer of the

cell membranes and somehow produce anaesthesia by expanding the membrane or increasing its fluidity.
It is now believed that anaesthetics bind to a hydrophobic area of a protein (e.g. ion channel, receptor) and inhibit its normal function.
Anaesthetics can inhibit the function of glutamate receptors and can enhance γ‐aminobutyric acid (GABA)ergic transmission.
Mechanism of action of anaestheticsAnaesthetic potency correlates well with lipid solubility. Anaesthetics might dissolve in the lipid

Слайд 4Properties of an ideal anaesthetic
A. For the patient:
It should

be pleasant, nonirritating, should not cause nausea or vomiting.
Induction and

recovery should be fast with no after effects.
B. For the surgeon:
It should provide adequate analgesia, immobility and muscle relaxation.
It should be noninflammable and nonexplosive.

Properties of an ideal anaestheticA. For the patient: It should be pleasant, nonirritating, should not cause nausea

Слайд 5C. For the anaesthetist:
Its administration should be easy, controllable.

Heart, liver and other organs should not be affected.
It

should be potent so that low concentrations are needed and oxygenation of the patient does not suffer.
Rapid adjustments in depth of anaesthesia should be possible.
It should be cheap, stable and easily stored.

C. For the anaesthetist: Its administration should be easy, controllable. Heart, liver and other organs should not

Слайд 6Stages of general anaesthesia
I. Stage of analgesia starts from beginning

of anaesthetic inhalation and lasts up to the loss of

consciousness. Pain is progressively abolished. Patient remains conscious.
II. Stage of delirium. Apparent excitement is seen—patient may shout, struggle and hold his breath; muscle tone increases, jaws are tightly closed, breathing is jerky; vomiting, involuntary micturition or defecation may occur. Heart rate and BP may rise and pupils dilate due to sympathetic stimulation.
III. Surgical anaesthesia extends from onset of regular respiration to cessation of spontaneous breathing. This has been divided into 4 planes. These stages are not obvious with currently used anaesthetics.
Stages of general anaesthesiaI. Stage of analgesia starts from beginning of anaesthetic inhalation and lasts up to

Слайд 8General anaesthesia usually involves the administration of different drugs
For premedication,
For

induction of anaesthesia, and
For maintenance of anaesthesia.
Premedication has 4

main aims:
The prevention of the parasympathomimetic effects of anaesthesia (bradycardia, bronchial secretion): Muscarinic blockers – Atropine
The reduction of pain: Opioid analgesics, e.g. morphine
The relief from anxiety: Benzodiazepines produce anxiolysis and amnesia and are used in particularly anxious patients.
Postoperative antiemesis: The dopamine antagonist droperidol and metoclopramide are widely used for this purpose and is effective against opioid‐induced emesis.
General anaesthesia usually involves the administration of different drugsFor premedication,For induction of anaesthesia, and For maintenance of

Слайд 9CLASSIFICATION
Inhalational
Gas: Nitrous oxide
Volatile liquids: Ether, Halothane, Enflurane, Isoflurane, Desflurane,

Sevoflurane
Intravenous
Fast acting drugs: Thiopental sod., Propofol
Slower acting drugs: Sodium oxybutyrate
Benzodiazepines: Diazepam,

Lorazepam, Midazolam
Dissociative anaesthesia: Ketamine
Opioid analgesia: Fentanyl
CLASSIFICATIONInhalationalGas: Nitrous oxide Volatile liquids: Ether, Halothane, Enflurane, Isoflurane, Desflurane, SevofluraneIntravenousFast acting drugs: Thiopental sod., PropofolSlower acting

Слайд 10Nitrous oxide is not potent enough to use as a

sole anaesthetic agent, but it is commonly used as a

non‐flammable carrier gas for volatile agents, allowing their concentration to be significantly reduced. It is a good analgesic and a 50% mixture in oxygen is used when analgesia is required (e.g. in childbirth, road traffic accidents). Nitrous oxide has little effect on the cardiovascular or respiratory systems.
Halothane was the first fluorinated volatile anaesthetic. It is a potent and non‐irritant agent, induction is smooth and pleasant. More than 20% of the administered halothane is biotransformed by the liver to metabolites (e.g. trifluoroacetic acid) that may cause severe hepatotoxicity with a high mortality. It has been largely replaced by less toxic drugs. It sensitizes heart to catecholamines, causes hypotension, cardiac arrhythmias, hyperthermia.
Nitrous oxide is not potent enough to use as a sole anaesthetic agent, but it is commonly

Слайд 11Isoflurane is more soluble in blood than sevoflurane or enflurane

and so onset and recovery are slower. It causes dose-related

hypotension by decreasing systemic vascular resistance. Only 0.2% of the absorbed dose is metabolized and none of the metabolites has been associated with hepatotoxicity.
Sevoflurane. Emergence and recovery from anaesthesia are rapid. This may necessitate early postoperative pain relief. It is very pleasant to breath and is a good choice if an inhalation agent is required for induction, for example, in children.
Isoflurane is more soluble in blood than sevoflurane or enflurane and so onset and recovery are slower.

Слайд 12Propofol is the most widely used intravenous anaesthetic. It induces

anaesthesia within 30 s and is smooth and pleasant. Recovery

from propofol is rapid without nausea or hangover. Propofol is inactivated by redistribution and glucuronide conjugation in the liver. The rapid elimination of propofol prevents significant cumulation and recovery from continuous infusion is relatively fast.
Thiopental injected intravenously induces anaesthesia in less than 30 s because the very lipid‐soluble drug quickly dissolves in the rapidly perfused brain. Recovery from a single dose of thiopental is rapid because of redistribution into less perfused tissues. The liver subsequently metabolizes thiopental. Doses of thiopental only slightly above the ‘sleep dose’ depress the myocardium and the respiratory centre.
Propofol is the most widely used intravenous anaesthetic. It induces anaesthesia within 30 s and is smooth

Слайд 13Ketamine may be given by intramuscular or intravenous injection. It

is analgesic in subanaesthetic doses, but often causes hallucinations. It

induces a so called ‘dissociative anaesthesia’ characterized by profound analgesia, immobility, amnesia with light sleep. It increases cardiac work and blood pressure.
Sodium oxybutirate may be given intravenously or orally. It is used for induction and base anaesthesia. The effect persists up to 2-3 hours. It increases the brain resistance to hypoxia.
Ketamine may be given by intramuscular or intravenous injection. It is analgesic in subanaesthetic doses, but often

Слайд 14COMPLICATIONS OF GENERAL ANAESTHESIA
A. During anaesthesia
Respiratory depression. Cardiac

arrhythmias, asystole. Fall in BP.
Salivation, respiratory secretions. Aspiration of

gastric contents: acid pneumonitis. Laryngospasm and asphyxia.
Delirium, convulsions and other excitatory effects.
B. After anaesthesia
Nausea and vomiting. Pneumonia, atelectasis. Organ toxicities: liver, kidney damage.
Persisting sedation: impaired psychomotor function.
Cognitive defects.
COMPLICATIONS OF GENERAL ANAESTHESIAA. During anaesthesia Respiratory depression. Cardiac arrhythmias, asystole. Fall in BP. Salivation, respiratory secretions.

Слайд 15ANTIEPILEPTIC DRUGS
Epilepsy is a chronic disease in which seizures result

from the abnormal discharge of cerebral neurones. The seizures are

classified:
Generalised tonic-clonic seizures: commonest, lasts 1–2 min. The usual sequence is aura—cry—unconsciousness—tonic spasm of all body muscles—clonic jerking followed by prolonged sleep and depression of all CNS functions.
Partial seizures: lasts 1/2–1 min. Often secondary. Convulsions are confined to a group of muscles or localized sensory disturbance depending on the area of cortex involved in the seizure, without loss of consciousness.
ANTIEPILEPTIC DRUGSEpilepsy is a chronic disease in which seizures result from the abnormal discharge of cerebral neurones.

Слайд 17Absence seizures last about 1/2 min. Momentary loss of consciousness,

patient apparently freezes and stares in one direction, no muscular

component or little bilateral jerking.
Myoclonic seizures: Shock-like momentary contraction of muscles of a limb or the whole body.
Status epilepticus is defined as continuous seizures lasting at least 30 min or a state in which fits follow each other without consciousness being fully regained
Absence seizures last about 1/2 min. Momentary loss of consciousness, patient apparently freezes and stares in one

Слайд 18CLASSIFICATION
Generalised tonic-clonic seizures: Carbamazepine, Valproate, Phenytoin, Phenobarbital.
Partial seizures: Carbamazepine, Valproate,

Phenytoin, Gabapentin.
Absence seizures: Valproate, Lamotrigine, Ethosuximide, Clonazepam.
Myoclonic seizures: Valproate,

Clonazepam, Lamotrigine.
Status epilepticus: Diazepam (i.v.), Phenobarbital (i.v., i.m.), Gen. anaesthetics
CLASSIFICATIONGeneralised tonic-clonic seizures: Carbamazepine, Valproate, Phenytoin, Phenobarbital.Partial seizures: Carbamazepine, Valproate, Phenytoin, Gabapentin. Absence seizures: Valproate, Lamotrigine, Ethosuximide,

Слайд 19Carbamazepine, lamotrigine, valproate, phenytoin block neuronal Na+ channels, ↓ axonal

conduction.
Barbiturates and benzodiazepins ↑inhibitory tone by facilitation of GABA-mediated

hyperpolarisation.
Valproate also seems to increase GABAergic central inhibition by stimulation of glutamic acid decarboxylase activity and/or inhibition of GABA‐Transaminase.
Lamotrigine ↓excitatory effects of glutamic acid (block of NMDA receptors)
Ethosuximide and valproate ↓presynaptic Ca₂+ influx through type-T channels in thalamic neurons.

Carbamazepine, lamotrigine, valproate, phenytoin block neuronal Na+ channels, ↓ axonal conduction. Barbiturates and benzodiazepins ↑inhibitory tone by

Слайд 21Phenytoin. Pharmacokinetics – variable absorption, induction of P450s;
Side effects:

CNS depression, gingival hyperplasia, osteomalacia (↓ vit.D), megaloblastic anemia (↓

folate), hirsutism, teratogenicity (cleft lip and palate).
Carbamazepine is also used for trigeminal neuralgia. Induces P450s.
Side effects: CNS depression, osteomalacia (↓ vit.D), megaloblastic anemia (↓ folate, aplastic anemia), exfoliative dermatitis, ↑ ADH secretion (dilutional hyponatremia), teratogenicity (cleft lip and palate, spinal bifida).

Phenytoin. Pharmacokinetics – variable absorption, induction of P450s; Side effects: CNS depression, gingival hyperplasia, osteomalacia (↓ vit.D),

Слайд 22Valproate can be used for migraines. Inhibits P450s. Side effects:

hepatotoxicity, thrombocytopenia, pancretitis, alopecia, teratogenicity (spinal bifida).
Ethosuximide. Side effects:

nausea, vomiting, leukopenia.
Lamotrigine. Side effects: sleepiness, dizziness, diplopia, ataxia, vomiting and Steven-Johnson syndrome.
Gabapentin can be used for neuropathic pain. Side effects are mild sedation, tiredness, dizziness and unsteadiness.

Anticonvulsants are additive with other CNS depressants.
Avoid abrupt withdrawal, which may precipitate seizures.
Valproate can be used for migraines. Inhibits P450s. Side effects: hepatotoxicity, thrombocytopenia,  pancretitis, alopecia, teratogenicity (spinal

Слайд 23Antiparkinsonian Drugs.
These are drugs that have a therapeutic effect

in parkinsonism.
Parkinsonism. It is an extrapyramidal motor disorder characterized

by rigidity, tremor and hypokinesia.
Pathology: degeneration of nigrostriatal dopamine tracts with imbalance between dopamine (↓) and Ach (↑).

Antiparkinsonian Drugs. These are drugs that have a therapeutic effect in parkinsonism. Parkinsonism. It is an extrapyramidal

Слайд 26CLASSIFICATION
I. Drugs affecting brain dopaminergic system
Dopamine precursor : Levodopa

(l-dopa)
Peripheral decarboxylase inhibitors : Carbidopa, Benserazide.
Dopaminergic agonists: Bromocriptine, Ropinirole


MAO-B inhibitor: Selegiline,
Glutamate (NMDA receptor) antagonist (Dopamine facilitator): Amantadine.
II. Drugs affecting brain cholinergic system
Central anticholinergics: Trihexyphenidyl
Antihistaminics: Promethazine
CLASSIFICATIONI. Drugs affecting brain dopaminergic system Dopamine precursor : Levodopa (l-dopa)Peripheral decarboxylase inhibitors : Carbidopa, Benserazide. Dopaminergic

Слайд 28Levodopa. Mechanism of action: Levodopa is the immediate precursor of

dopamine and is able to penetrate the brain, where it

is converted to dopamine.
Carbidopa is a selective extracerebral decarboxylase inhibitor and it is used with levodopa.This combination is the most effective treatment for most patients with Parkinson’s disease.
Adverse effects are frequent: nausea and vomiting, vivid dreams, hallucinations, psychotic states and confusion, postural hypotension, dyskinesias
Levodopa. Mechanism of action: Levodopa is the immediate precursor of dopamine and is able to penetrate the

Слайд 30The DA agonists can act on striatal DA receptors

Bromocriptine is a potent agonist on D2receptors.
Side effects:

vomiting, hallucinations, hypotension, nasal stuffiness, conjunctival injection. Marked fall in BP with the ‘first dose’ has occurred in some patients, especially those on antihypertensive medication.
Ropinirole is а selective D2/D3 receptor agonist. Side effects: nausea, dizziness, hallucinations and postural hypotension
The DA agonists can act on striatal DA receptors Bromocriptine is a potent agonist on D2receptors.

Слайд 31Amantadine has muscarinic blocking actions and probably increases dopamine release.

It has modest antiparkinsonian effects in a few patients, but

tolerance soon occurs.
Side effects: atropine-like.
Selegiline selectively inhibits MAO-B present in the brain and reduces the metabolism of dopamine in the brain and potentiates the actions of levodopa.
Side effects: postural hypotension, nausea,confusion, insomnia and agitation.
Amantadine has muscarinic blocking actions and probably increases dopamine release. It has modest antiparkinsonian effects in a

Слайд 32Muscarinic antagonists produce a modest improvement in the early stages

of Parkinson’s disease.
Adverse effects: dry mouth, urinary retention and

constipation. Impairment of memory, organic confusional states and blurred vision are more common in the elderly.
The antihistaminics are less efficacious than anticholinergics, but are better tolerated by older patients. Their sedative action also helps.
Muscarinic antagonists produce a modest improvement in the early stages of Parkinson’s disease. Adverse effects: dry mouth,

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