Lecture No. 11. Pain and analgesics

1. Pain

Pain is an unpleasant sensory and emotional state caused by real or potential pathological effects on tissues.

In the CNS, pain is conducted along two main pathways.

Specific path - the posterior horns of the spinal cord, specific nuclei of the thalamus, the cortex of the posterior central gyrus. This pathway is low-neuronal, fast, conducts threshold, emotionally uncolored, precisely localized pain (epicritic pain).

Non-specific way - the posterior horns of the spinal cord, non-specific nuclei of the thalamus, the cortex of the frontal and parietal lobes diffusely. Conducts subthreshold, emotionally colored, poorly localized pain. It is slow, multineuronal, as it forms numerous collaterals to the medulla oblongata, the reticular formation, the limbic system, and the hippocampus. Subthreshold pain impulses undergo summation in the thalamus. Impulses conducted along the nonspecific pain pathway excite the emotional centers of the limbic system, the autonomic centers of the hypothalamus, and the medulla oblongata. Therefore, pain is accompanied by fear, painful experiences, increased respiration, pulse, rise in blood pressure, pupil dilation, dyspeptic disorders. The action of the nociceptive pain system is counteracted by the antinoceceptive system, the main neurons of which are localized in the periaqueductal gray matter (the aqueduct of Sylvius connects the III and IV ventricles). Their axons form descending pathways to the medulla oblongata and spinal cord and ascending pathways to the reticular formation, thalamus, hypothalamus, limbic system, basal ganglia, and cortex. The mediators of these neurons are pentapeptides: methenkephalin and leuenkephalin, which have methionine and leucine as terminal amino acids, respectively. Enkephalins excite opiate receptors.

In enkephalinergic synapses, opiate receptors are located on the postsynaptic membrane, but the same membrane is presynaptic for other synapses. Opiate receptors are associated with adenylate cyclase and cause its inhibition by disrupting cAMP synthesis in neurons. As a result, calcium entry and release of mediators, including pain mediators - peptides decreases: substance P, cholecystokinin, somatostatin, glutamic acid. Opiate receptors are excited not only by mediators - enkephalins, but also by other components of the antinoceceptive system - brain hormones (endorphins). Peptide agonists of opiate receptors are formed during proteolysis of the peptide substances of the brain: proopiocortin, proenkephalins A and B. All these peptides are formed in the hypothalamus. Opiate receptors excite receptors in all brain structures involved in the conduction and perception of pain, the formation of emotionally colored reactions to pain. At the same time, the release of pain mediators decreases and all reactions accompanying pain are weakened.

2. Analgesic drugs

An analgesic (acetylsalicylic acid, paracetamol, morphine) is a drug that reduces pain of various origins. Drugs that reduce pain provoked only by a certain causative factor, or eliminate a specific pain syndrome, for example, antacids, ergotamine (migraine), carbamazepine (neuralgia), nitroglycerin (angina pectoris), do not belong to classical analgesics. Corticosteroids suppress the inflammatory response and the resulting pain, but despite their widespread use for these purposes, they also do not represent classical analgesics.

Analgesics are classified into narcotic, acting on CNS structures and causing drowsiness, such as opioids, and non-narcotic, acting mainly on peripheral structures, such as paracetamol, acetylsalicylic acid.

Additional drugs that enhance the effect of analgesics

The drugs of this group are not analgesics themselves, but are used in combination with analgesics for pain, as they can change the attitude towards pain, its perception and level anxiety, fear, depression (tricyclic antidepressants can even cause a decrease in the need for morphine in a patient in terminal state). Such drugs can be psychotropic drugs, as well as those that affect the mechanisms of pain, for example, eliminating spasm of smooth and striated muscles.

Narcotic analgesics are herbal and synthetic drugs that selectively reduce the perception of pain, increase pain tolerance by reducing the emotional coloring of pain and its vegetative accompaniment, cause euphoria and drug dependence. Narcotic analgesics reduce the conduction and perception of pain only within the boundaries of the central nervous system, suppressing mainly the nonspecific pathway. Means of this group excite opiate receptors, create an action similar to the effects of peptides of the anti-noreceptive system. Therefore, the main mechanisms of anesthesia are the following: a disorder in the conduction of a pain impulse from the axon of neuron I, whose body is located in the spinal ganglion, to neuron II, located in the gelatinous substance of the posterior horns of the spinal cord. Suppression of summation of subthreshold impulses in the thalamus. Decreased participation in the pain reaction of the medulla oblongata, hypothalamus, limbic system (non-accentuated attitude to pain).

Classification of narcotic analgesics and their antagonists

The classification is as follows.

1. Piperidine-phenanthrene derivatives:

1) morphine;

2) codeine (methylmorphine, 5-7 times weaker than morphine as an analgesic);

3) ethylmorphine (dionine, equal in strength to morphine).

2. Phenylpiperidine derivatives:

1) promedol (3-4 times weaker than morphine);

2) fentanyl (100-400 times stronger than morphine).

3. Derivatives of diphenylmethane:

1) pyritramide (dipidolor) - equal to morphine;

2) tramadol (tramal) - somewhat inferior to morphine.

4. Agonists-antagonists:

1) opiate receptor agonists and opiate receptor antagonists - buprenorphine (norphine) (25-30 times stronger than morphine);

2) opiate receptor agonists and opiate receptor antagonists - pentazocine (lexir) (2-3 times weaker than morphine) and butorphanol (moradol) (equal to morphine).

Agonists-antagonists are much less likely and weaker than full agonists to cause euphoria and drug dependence.

Narorphine - on its own (for example, with barbiturate poisoning) and with mild morphine poisoning, it has an analgesic effect, causes miosis, bradycardia, and exacerbates respiratory center depression. In severe poisoning with morphine and other agonists, it displaces them from the opiate receptors of the respiratory center and restores breathing. Causes dysphoria, irritability, depression, impaired focusing of the gaze.

Complete opioid receptor antagonists

Naloxone has no independent action, it is effective as an antidote for poisoning with narcotic analgesics.

Narcotic analgesics should be used only for acute pain for a short time.

Most often used for injuries, burns, myocardial infarction, peritonitis (after clarifying the diagnosis and deciding on the operation). Narcotic analgesics are part of lytic mixtures for potentiation of anesthesia. The drugs of this group are used for postoperative pain in combination with M-anticholinergics and myotropic antispasmodics. They are prescribed to stop hepatic (pentazocine) and renal (promedol) colic. Chronic pain is a contraindication for prescribing drugs, with the exception of advanced forms of a malignant tumor (dipidolor, tramadol, agonists-antagonists).

Narcotic analgesics are combined with psychotropic drugs for special types of anesthesia.

Neuroleptanalgesia is pain relief with a combination of fentanyl (strong, lasts 30-40 minutes) and droperidol (a mild antipsychotic). Droperidol has a mild sedative effect, stops emotional reactions and reduces the tone of skeletal muscles. Also important effects of droperidol are antiemetic and antishock. Doses of droperidol - 1: 50. Combined drug - thalamonal. Neuroleptanalgesia is used in low-traumatic operations, in the field of neurosurgery and in cardiology for myocardial infarction, etc. Atalgesia or tranquilizer analgesia - fentanyl in combination with a strong tranquilizer such as sibazon, phenazepam. The main disadvantage is the strong respiratory depression of fentanyl and the preservation of consciousness.

Author: Kolesnikova M.A.

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