NEET MDS Lessons
Pharmacology
Ketorolac
Mechanism of action
primary action responsible for its anti-inflammatory/antipyretic/analgesic effects is inhibition of prostaglandin synthesis through inhibition of the enzyme cyclooxygenase (COX). Ketorolac is not a selective inhibitor of COX enzymes
Indications: short-term management of pain
Contraindications
hypersensitivity to ketorolac, and against patients with the complete or partial syndrome of nasal polyps, angioedema, bronchospastic reactivity or other allergic manifestations to aspirin or other non-steroidal anti-inflammatory drugs (due to possibility of severe anaphylaxis).
Fluconazole: an antifungal used orally, intravenously or vaginally to treat yeast and fungal infections. Side-effects of systemic administration include hepatotoxicity (liver damage).
- For vaginal candidiasis (vaginal thrush), a once-only oral dose is often sufficient.
Doxycycline
Commonly prescribed for infections and to treat acne. treat urinary tract infections, gum disease, and other bacterial infections such as gonorrhea and chlamydia., as a prophylactic treatment for infection by Bacillus anthracis (anthrax). It is also effective against Yersinia pestis and malaria.
Mucosal protective agents.
These are locally active agents that help heal gastric and duodenal ulcers by forming a protective barrier between the ulcers and gastric acid, pepsin, and bile salts. They do not alter the secretion of gastric acid. These drugs include sucralfate and colloid bismuth compounds. (e.g. tripotassium, dicitratobismuthate). Colloidal bismuth compounds additionally exert bactericidal action against H.pylori. Also, Prostaglandins have both antisecretory and mucosal protective effects.
Example: Misoprostol- used for prevention of NSAID – induced ulcer.
- Drugs that exert antimicrobial action against H.pylori such as amoxicillin, metronidazole, clarithromycin and tetracycline are included in the anti-ulcer treatment regimens.
Mechanism of Action
When a local anesthetic is injected, it is the ionized [cation] form of the local anesthetic that actually binds to anionic channel receptors in the sodium channel, thus blocking the influx of sodium ions which are responsible for lowering the -70mv resting potential towards the firing threshold of -55mv which then results in depolarization of the nerve membrane. However, only the lipid soluble nonionized [base] form of the local anesthetic can penetrate the various barriers [e.g., nerve membrane, fibrous tissue] between the site of injection and the targeted destination which is the sodium channel.
Indomethacin
commonly used to reduce fever, pain, stiffness, and swelling. It works by inhibiting the production of prostaglandins, molecules known to cause these symptoms.
Indications
ankylosing spondylitis, rheumatoid arthritis, osteoarthritis, juvenile arthritis, psoriatic arthritis, Reiter's disease, Paget's disease of bone, Bartter's disease, pseudogout, dysmenorrhea (menstrual cramps), pericarditis, bursitis, tendonitis, fever, headaches, nephrogenic , diabetes insipidus (prostaglandin inhibits vasopressin's action in the kidney)
Indomethacin has also been used clinically to delay premature labor, reduce amniotic fluid in polyhydramnios, and to treat patent ductus arteriosus.
Mechanism of action
Indomethacin is a nonselective inhibitor of cyclooxygenase (COX) 1 and 2, enzymes that participate in prostaglandin synthesis from arachidonic acid. Prostaglandins are hormone-like molecules normally found in the body, where they have a wide variety of effects, some of which lead to pain, fever, and inflammation.
Prostaglandins also cause uterine contractions in pregnant women. Indomethacin is an effective tocolytic agent, able to delay premature labor by reducing uterine contractions through inhibition of PG synthesis in the uterus and possibly through calcium channel blockade.
Indomethacin easily crosses the placenta, and can reduce fetal urine production to treat polyhydramnios. It does so by reducing renal blood flow and increasing renal vascular resistance, possibly by enhancing the effects of vasopressin on the fetal kidneys.
Adverse effects
Since indomethacin inhibits both COX-1 and COX-2, it inhibits the production of prostaglandins in the stomach and intestines which maintain the mucous lining of the
gastrointestinal tract. Indomethacin, therefore, like other nonselective COX inhibitors, can cause ulcers.
Many NSAIDs, but particularly indomethacin, cause lithium retention by reducing its excretion by the kidneys.
Indomethacin also reduces plasma renin activity and aldosterone levels, and increases
sodium and potassium retention. It also enhances the effects of vasopressin. Together these may lead to:
edema (swelling due to fluid retention)
hyperkalemia (high potassium levels)
hypernatremia (high sodium levels)
hypertension (high blood pressure)
Sulindac: Is a pro‐drug closely related to Indomethacin.
Converted to the active form of the drug.
Indications and toxicity similar to Indomethacin
Mefenamic acid
Analgesic, anti‐inflammatory properties less effective than aspirin
Short half‐lives, should not be used for longer than one week and never in pregnancy and in children.
Enhances oral anticoagulants
Used to treat pain, including menstrual pain. It decreases inflammation (swelling) and uterine contractions.