Prescription writing rules
For the relief of severe pain, the drug is most commonly prescribed as a solution for intramuscular injection. Below is a classic example of a prescription written in Latin:
Rp.: Sol. Ketorolaci 3% – 1 ml D.t.d. N. 10 in ampull. S. 1 ml intramuscularly for severe pain.
Prescription breakdown:
- Rp. (Recipe) — traditional appeal to the pharmacist meaning "Take".
- Sol. (Solutionis) — indicates the dosage form (solution).
- Ketorolaci — the international nonproprietary name of the active substance in the genitive case.
- 3% – 1 ml — concentration of the active substance and volume of a single ampoule.
- D.t.d. N. 10 in ampull. (Da tales doses numero 10 in ampullis) — instruction to dispense ten such doses in ampoules.
- S. (Signa) — signature, where detailed instructions for use by the patient are written out.
Classification of NSAIDs and the place of ketorolac
To understand the characteristics of the drug, it is necessary to review the general classification of non-narcotic analgesics based on their effect on cyclooxygenase (COX) isoenzymes.
| NSAID group | Type of action | Representatives |
|---|---|---|
| Nonselective (COX-1 + COX-2) | Irreversible<br>Reversible | Acetylsalicylic acid<br>Diclofenac, ibuprofen, ketorolac, indometacin |
| Preferential COX-2 | Reversible | Nimesulide, meloxicam |
| Selective COX-2 | Reversible | Celecoxib |
As can be seen from the table, ketorolac shares its subgroup with ibuprofen and diclofenac. An important distinction within the nonselective group belongs to acetylsalicylic acid — it inhibits COX-1 irreversibly (via acetylation), whereas the action of other drugs is reversible.
Mechanism of action and pharmacodynamics
The pharmacodynamics of ketorolac is based on the inhibition of the cyclooxygenase enzyme. This blocks the biochemical cascade converting arachidonic acid into endoperoxides. As a result, the synthesis of prostaglandins (primarily PGE_2 and PGI_2) and thromboxane A_2 in tissues drops sharply.
The golden rule of NSAID pharmacology states: the therapeutic effect is always associated with the suppression of COX-2, while toxicity and adverse reactions are linked to the inhibition of COX-1.
The reduction in inflammatory mediator levels provides three main effects:
- Analgesic: sensitization (sensitivity) of pain receptors to histamine and bradykinin decreases.
- Anti-inflammatory: caused by a deficiency of prostaglandins PGE_2 and PGI_2 directly at the site of inflammation.
- Antipyretic: the drug acts on the thermoregulatory center located in the hypothalamus, leading to increased heat dissipation. Important nuance: the antipyretic effect manifests exclusively during febrile temperature (fever) and does not lower normal body temperature.
Indications and adverse reactions
Ketorolac is indicated for pain of inflammatory or traumatic origin, severe postoperative pain, and dysmenorrhea. Drugs of this group are also actively used for rheumatic diseases such as osteoarthritis and rheumatoid arthritis. When body temperature rises above 38.5 °C, these agents are used to combat fever.
Since ketorolac is a nonselective agent, its administration is accompanied by risks associated with the blockade of physiological COX-1:
- NSAID-induced gastropathy: due to a deficiency of gastroprotective prostaglandins, the defense of the gastric mucosa is impaired, leading to ulcer formation and gastrointestinal bleeding.
- Nephrotoxicity: renal blood flow is impaired.
- Bronchospasm: so-called "aspirin-induced asthma", resulting from the redistribution of arachidonic acid metabolic pathways.
- Thromboembolic complications: this side effect is more characteristic of selective COX-2 inhibitors, but safety profiles must always be kept in mind when choosing therapy.
To permanently remember the connection between isoenzymes and NSAID effects, use a simple rule: "COX-TWO IS FOR YOU (GOOD), COX-ONE IS DONE (BAD)." Therapeutic benefit comes from blocking the second cyclooxygenase, and side effects stem from the first.
Class and exam questions
Which selectivity group does ketorolac belong to?
It is a nonselective drug, meaning it reversibly inhibits both enzyme isoforms: both COX-1 and COX-2.
Do NSAIDs lower normal body temperature?
No, the antipyretic effect is realized exclusively at febrile temperatures (fever). These drugs do not affect normal body temperature.
Why does gastropathy occur when taking nonselective NSAIDs?
COX-1 blockade reduces the synthesis of gastroprotective prostaglandins, which normally protect the gastric mucosa. Their deficiency leads to ulcer formation and bleeding.
What is the specific feature of the mechanism of action of acetylsalicylic acid?
Unlike ketorolac and ibuprofen, acetylsalicylic acid inhibits COX-1 irreversibly by acetylating the enzyme.
What else to study on this topic
- Prescription writing for acetylsalicylic acid tablets
- Prescription writing for ibuprofen in arthralgia
- Biochemical mechanism of action of non-narcotic analgesics
- Characteristics of preferential and selective COX-2 inhibitors (meloxicam, celecoxib)
- Pathogenesis of "aspirin-induced asthma" development during NSAID intake
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