Origin and metabolism
The drug is obtained by extraction from the dried latex of the opium poppy (Papaver somniferum). Although total synthesis was accomplished back in 1952, isolation from plant material remains the most economically feasible.
The drug is rarely prescribed orally: due to intensive first-pass metabolism in the liver, bioavailability is low. With parenteral administration, the effect develops significantly faster. Morphine itself crosses the blood-brain barrier poorly (unlike its chemically modified derivative, heroin). In the liver, the substance actively binds to glucuronic acid. The resulting metabolite (morphine-6-glucuronide) exceeds the parent compound in both potency and duration of analgesic action. Excretion occurs predominantly via the kidneys.
Central pharmacological effects
The action is due to binding to opioid receptors in the central nervous system. Key manifestations:
- Analgesia and sedation: pain syndrome is eliminated, superficial sleep occurs without memory loss.
- Psychoemotional sphere: patients often experience euphoria (a sense of absolute comfort, suppression of hunger), which is a triggering factor for addiction. In healthy individuals without pain, dysphoria — a feeling of malaise and anxiety — may occur.
- Stem reflexes: the drug excites the oculomotor nerve centers, causing persistent miosis. It also stimulates the trigger zone of the vomiting center (provoking nausea, especially with motion), but paradoxically depresses the vomiting center itself. The cough reflex is suppressed very rapidly.
- Respiration: a vital effect. Morphine reduces the sensitivity of neurons to carbon dioxide. In case of overdose, breathing becomes shallow and extremely slow, up to complete cessation.
- Neuroendocrine regulation: the hypothalamus reacts by increasing the production of prolactin, somatotropin, and antidiuretic hormone, but decreases the secretion of adrenocorticotropic and gonadotropic hormones.
Peripheral action on organs and tissues
In addition to the nervous system, the drug actively affects smooth muscle and mediator release:
- Gastrointestinal tract: the motility of the stomach and intestines decreases, but the tone of sphincters sharply increases. Spasm of the sphincter of Oddi disrupts bile outflow. Together, this leads to pronounced constipation (obstipation).
- Urinary system: the ureters and urethral sphincter go into spasm, creating a direct threat of acute urinary retention.
- Histamine release: provokes cutaneous vasodilation, urticaria, and increases the risk of bronchospasm, which is especially dangerous for patients with bronchial asthma.
Tolerance, dependence, and indications
With regular intake, receptor sensitivity drops unevenly. The body quickly adapts to analgesia, euphoria, and respiratory depression — this allows dependent individuals to tolerate doses that are fatal to an ordinary person. However, tolerance to miosis and constipation practically does not develop.
Physical dependence manifests as a severe withdrawal syndrome. First, lacrimation, rhinorrhea, and "goosebumps" appear, followed by tachycardia, tremor, vomiting, and severe back and abdominal pain.
In clinical practice, morphine is the drug of choice for severe pain (oncology, extensive burns, myocardial infarction), for the prevention of traumatic shock, and for relieving acute pulmonary edema. Administration is strictly contraindicated in respiratory failure, high intracranial pressure, as well as in children under 2 years of age and pregnant women.
Briefly: answers to topical questions
What is the mechanism of the analgesic action of morphine at the spinal cord level?
The mechanism of the analgesic action of morphine at the spinal cord level consists in the direct inhibition of pain impulse transmission in the dorsal horns and enhancement of descending control.
The action is realized through the following processes:
- Presynaptic level — blockade of N-type calcium channels and a decrease in the release of pain mediators (substance P and glutamate), which disrupts signal transmission to interneurons.
- Postsynaptic level — stimulation of opioid receptors on the membrane of interneurons, leading to disruption of their depolarization and inhibition of activation.
Morphine also activates descending pathways that massively stimulate the release of enkephalins for additional inhibition of impulses.
What is the classic triad of symptoms in acute morphine poisoning?
The source does not single out a specific "classic triad", but describes the clinical picture of acute morphine poisoning:
- comatose state;
- slow shallow breathing;
- bradycardia.
A diagnostic sign is sharp miosis; as asphyxia develops, the pupils dilate.
To remember the effects to which tolerance never develops with prolonged morphine use, use the "MC" rule: Miosis and Constipation stay with the patient always.
Class and exam questions
Why is it effective to perform gastric lavage during a morphine overdose, even if the drug was administered intravenously?
Part of the drug in the form of glucuronides is excreted by the liver with bile into the intestinal lumen, from where it can be reabsorbed into the blood. Gastric lavage with a weak potassium permanganate solution interrupts this cycle of reabsorption.
Can morphine be used in pure form to relieve pain in hepatic or renal colic?
Categorically no. The drug significantly increases the tone of smooth muscle (sphincter of Oddi, ureters), which will only worsen the spasm. In colic, it is permitted to be administered only together with antispasmodics, for example, atropine.
What is the main danger of relapse after treatment for morphinism?
Upon drug refusal, resistance to its toxic effect rapidly disappears. If after a long pause a person injects their previous, "accustomed" high dose, paralysis of the respiratory center and death will occur.
What else to study on this topic
- Features of blood-brain barrier permeability for opiates in newborns
- Synthetic full opioid receptor agonists (fentanyl, methadone, trimeperidine)
- Pharmacodynamics of partial agonists and agonist-antagonists (buprenorphine, pentazocine)
- Mechanism of hypothermia development and changes in skeletal muscle tone upon morphine administration
- Comparative characteristics of opium alkaloids: phenanthrene derivatives vs. isoquinolines
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