Pain and Anesthesia

Pain and Anesthesia

Pain is the unpleasant sensory and emotional condition caused by the valid or possible damaging influence on a tissue.

Pain is spent to a CNS on two basic conduction paths: the Specific path - back horns of a spinal cord specific kernels of a thalamus a cortex of a back central gyrus. This path is little neuronic, fast, spends threshold, emotionally uncolored, precisely localised pain (epicritic a pain). Nonspecific (paleospinothalamic) a path - back horns of a spinal cord nonspecific kernels of a thalamus a cortex frontal and a parietal lobe diffusively. Spends the subthreshold, emotionally imbued, badly localised pain (a protopathic pain). Is slow, multineural since forms numerous collaterals to myelencephalon, a reticular formation, limbic system, a hippocampus. Subthreshold painful impulses are exposed to a summation in a thalamus. Impulses spent on a nonspecific painful path provoke the emotional centres of limbic system, the vegetative centres of a hypothalamus, myelencephalon. Therefore the pain is accompanied by pavor, burdensome experiences, increase of breath, sphygmus, BP lifting, a mydriasis, dyspeptic disorders. Action of painful nociceptive system is counteracted antinoceptive by the system which basic neurones are localised in aqueduct grey matter (a Sylvian aqueduct bridges III and IV ventricles). Their axons form descending pathes to prolate and to a spinal cord and ascending pathes to a reticular formation, a thalamus, a hypothalamus, limbic system, basal ganglions and a cortex. Mediators of these neurones are pentapeptideses: Met-enkephalin and Leu-enkephalin, having as trailer amino acids accordingly methionine and Leucinum.

Enkephalins provoke opiate receptors. In encephalinergetic synapses opiate receptors are on a postsynaptic membrane, but the same membrane is presynaptic for other synapses. Opiate receptors are associated with adenylatecyclase and cause its inhibition, breaking in neurones synthesis cyclic adenosine monophosphate. The orifice of calcium and remission of mediators, including pain mediators - peptides As a result decreases: substance P, cholecystokinin, a somatostatin, a glutamic acid.

Opiate receptors provoke not only MEDIATORS-enkefalinami, but also other components antinoceptive systems - brain hormones - endorphines (beta-endorphine, a dynorphin). Peptide agonists of opiate receptors are formed at a proteolysis of peptide materials of a brain: a proopiomelanocortin, proenkephalins And and V.Vse these peptides are formed in a hypothalamus. Opiate receptors are sectioned into some types:

  • mu-opiate receptors provoke beta-endorphine, cause a supraspinal analgesia, euphoria, medicinal dependence, respiratory centre oppression, a bradycardia
  • kappa-opiate receptors provoke a dynorphin, cause a spinal analgesia, a sedation and a miosis
  • delta-opiate receptors provoke enkephalins, cause an analgesia

Thus, peptide ligands of opiate receptors provoke these receptors in all structures of a brain participating in carrying out and perception of a pain, formation of emotionally imbued reactions to a pain. Abjection of mediators of a pain thus decreases and all reactions accompanying a pain are relaxed.

Analgesic medical products. The analgetic (Acidum acetylsalicylicum, paracetamol, Morphinum) is the medical product reducing a pain of a different genesis. The medical products reducing a pain, provoked by only certain causative factor, or eliminating a specific painful syndrome, for example antiacid agents, Ergotaminum (migraine), carbamazepine (neuralgia), Nitroglycerinum (stenocardia), do not concern classical analgetics. Corticosteroids depress inflammatory reaction and the pain caused by it, but, not looking on their wide use with these purposes, they also do not represent classical analgetics.

Analgetics are categorised as narcotic, reacting on structures a CNS and causing drowsiness, for example opioids, and not narcotic, reacting mainly on peripheric structures, for example paracetamol, Acidum acetylsalicylicum.

The additional agents intensifying action of analgetics. Preparations of this bunch in itself are not analgetics, but at a pain are used in a combination with analgesic agents since can variate the attitude to a pain, its perception and level disturbing, pavor, depression (tricyclic antidepressants can even cause reduction of requirement for Morphinum in the patient in a terminal state). Psychotropic preparations, and also influencing the mechanisms of painful sensations for example eliminating a spastic stricture of smooth and transversely striated muscles can be such agents.

Narcotic analgetics - the vegetative and synthetic agents selectively reducing perception of a pain, pains raising shipping as a result of reduction of an emotional coloration of a pain and its vegetative support, cause euphoria and medicinal dependence.

Narcotic analgetics reduce carrying out and perception of a pain only in limens a CNS, depress mainly nonspecific path. Preparations of this bunch provoke opiate receptors and imitate effects of peptides antinoceptive systems. Therefore the basic mechanisms of anaesthetising action is the following:

  • Disturbance of carrying out of painful impulse from an axon of I neurone which body is in a spinal ganglion, on II neurone localised in a gelatinous substance of back horns of a spinal cord.
  • Depressing of a summation of subthreshold impulses in a thalamus.
  • Reduction of participation in a pain reaction of myelencephalon, hypothalamus, limbic system (the indifferent attitude to a pain).
  • Appearance of euphoria and weakening of emotional and mental reaction to a pain, bound to cortex excitation.

Classification of narcotic analgetics and their antagonists

  • Full agonists mu - and kappa-opiate receptors:
    • Derivatives Piperidine - Phenanthrene:
      • Morphinum
      • Codeinum (Methylmorphinum, in 5-7 times is more weak than Morphinum as an analgetic)
      • Ethylmorphinum (Dioninum, it is peer on force to Morphinum)
    • Derivatives phenylephrine
      • Promedolum (in 3-4 times is more weak than Morphinum)
      • Fentanylum (in 100-400 times is stronger than Morphinum)
    • Diphenylmethane derivatives
      • Piritramidum (dipidolor) - is peer to Morphinum
      • Tramadol (tramal) - concedes to Morphinum a little
  • Agonists-antagonists
    • Agonists mu-opiate receptors and antagonists kappa-opiate receptors - a buprenorphine (Norfinum) - at 25-30 time are stronger than Morphinum.
    • Agonists kappa-opiate receptors and antagonists mu - opiate receptors - Pentazocinum (Lexirum) - in 2-3 times are more weak than Morphinum and the butorphanol (Moradol) - is peer to Morphinum.
    Agonists-antagonists are much rarer and more weak than full agonists cause euphoria and medicinal dependence.
  • Antogonisty-AGONISTS. The antagonist mu-opiate receptors, an agonist kappa-opiate receptors (the opposing effect prevails over effects of a narcotic analgetic). Nalorfinum - it is independent (for example at a poisoning with barbiturates) and at an easy venenating with Morphinum anaesthetising an effect has, causes a miosis, a bradycardia, aggravates respiratory centre oppression. At a serious venenating with Morphinum and other agonists supersedes them from opiate receptors of a respiratory centre and recovers breath. Causes a dysphoria - irritability, depression, disturbance of focusing of a look.
  • Full antagonists mu - and kappa-opiate receptors:
    • Naloxonum - independent action has no, is effective as an antidote at venenatings with narcotic analgetics.

To apply narcotic analgetics follows only at an acute pain quickly. To the patient doing not report what preparation it receives, since in development of euphoria psychologic preparation has great value. An acute pain - the best counterpoison for narcomania development. Most often use at traumas, combustions, a myocardial infarction, a peritonitis (after specification of the diagnosis and the decision of a question on operation). Narcotic analgetics are a part of lytic admixtures for narcosis potentiation. Preparations of this bunch apply at a postoperative pain in a combination from M - choline blocker and myotropic spasmolyticses. Them prescribe for cupping hepatic (Pentazocinum) and renal (Promedolum) of gripes.

The chronic pain is contraindication for appointment of narcotics, an exception - the started forms of a malignant tumour (a dipidolor, a tramadol, agonists-antagonists).

Narcotic analgetics combine with psychotropic drugs for carrying out of special kinds of anaesthesia:

  • Neuroleptanalgesia - anaesthesia by Fentanylum combination (strong, 30-40 minutes react) and Droperidolum (a soft neuroleptic). Droperidolum has soft sedative, antiemetic, antishock an effect, eliminates any emotional reaction, reduces a tonus of a sceletal musculation. Doses - 1:50. The combined preparation - Thalamonalum. A neuroleptanalgesia use at not traumatic operations, neurosurgery, a myocardial infarction, etc.
  • Analgesia or trankvilon analgesia - Fentanylum + a strong tranquilizer of a type of Sibazonum, Phenazepamum. The basic disadvantage - a strong respiratory depression Fentanylum, consciousness conservation.
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