NEET MDS Lessons
Pharmacology
Mixed Narcotic Agonists/Antagonists
These drugs all produce analgesia, but have a lower potential for abuse and do not produce as much respiratory depression.
A. Pentazocine
- Has a combination of opiate analgesic and antagonist activity.
- Orally, it has about the same analgesic potency as codeine.
- In contrast to morphine, cardiac workload tends to increase due to an increase in pulmonary arterial and cerebrovascular pressure. Blood pressure and heart rate both also tend to increase.
- Adverse reactions to Pentazocine
• Nausea, vomiting, dizziness.
• Psychotomimetic effects, such as dysphoria, nightmares and visual hallucinations.
• Constipation is less marked than with morphine.
B. Nalbuphine
- Has both analgesic and antagonist properties.
- Resembles pentazocine pharmacologically.
- Analgesic potency approximately the same as morphine.
- Appears to be less hypotensive than morphine.
- Respiratory depression similar to morphine, but appears to peak-out at higher doses and to reach a ceiling.
- Like morphine, nalbuphine reduces myocardial oxygen demand. May be of value following acute myocardial infarction due to both its analgesic properties and reduced myocardial oxygen demand.
- Most frequent side effect is sedation.
C. Butorphanol
- Has both opiate agonist and antagonist properties.Resembles pentazocine , pharmacologically., 3.5 to 7 times more potent than morphine., Produces respiratory depression, but this effect peaks out with higher doses. The respiratory depression that does occur lasts longer than that seen following morphine administration.
- Butorphanol, like pentazocine, increases pulmonary arterial pressure and possibly the workload on the heart.
- Adverse reactions include sedation, nausea and sweating.
D. Buprenorphine
- A derivative of eto`rphine. Has both agonist and antagonist activity. 20 to 30 times more potent than morphine.Duration of action only slightly longer than morphine, but respiratory depression and miosis persist well after analgesia has disappeared.
- Respiratory depression reaches a ceiling at relatively low doses.
- Approximately 96% of the circulating drug is bound to plasma proteins.
- Side effects are similar to other opiates:
- sedation, nausea, vomiting,
- dizziness, sweating and headache.
ANTIDEPRESSANTS
Monoamine uptake inhibitors
1. Tricyclic antidepressants (TCAs)
2. Selective serotonin reuptake inhibitors (SSRIs)
3. Serotonin-norepinephrine reuptake inhibitors(SNRIs)
4. Norepinephrine reuptake inhibitor
Monoamine oxidase inhibitors (MAOIs)
Monoamine receptor antagonists
Ether (diethylether)
Ether (diethylether) MAC 2.0%, Blood/gas solubility ratio 15
- Ether is generally mixed with 3% ethanol to retard oxidation. Peroxides form on exposure to air and can enhance the danger of an explosion.
- Slow rate of induction and recovery due to its high blood/gas solubility ratio.
- Produces profound muscular relaxation.
- Both the rate and the minute volume of ventilation tend to be elevated during the inhalation of ether.
- Ether maintains good circulatory stability and does not sensitize the heart to the arrhythmogenic action of catecholamines.
- More than 90% of the absorbed ether can be recovered unchanged in the expired air. Metabolism is not extensive and the metabolites are not hepatotoxic.
- Ether is a versatile anesthetic of unexcelled safety, but it is flammable and irritating to breathe. Secretions can be blocked with anticholinergics.
Metabolism
Hepatic Drug-Metabolizing Enzymes: most drug metabolism in the liverperformed by the hepatic microsomal enzyme system.
Therapeutic Consequences of Drug Metabolism
- Accelerated Renal Drug Excretion: The most important consequence of drug metabolism is the promotion of renal drug excretion. Metabolism makes it possible for the kidney to excrete many drugs that it otherwise could not.
- Drug Inactivation
- Increased Therapeutic Action: Metabolism may increase the effectiveness of some drugs.
- Activation of Prodrugs: A prodrug is a compound that is inactive when administered and made active by conversion in the body.
- Increased or Decreased Toxicity
Factors that influence rate of metabolism:
- Age: Hepatic maturation doesn't occur until about a year old.
- Induction of Drug-Metabolizing Enzymes: Some drugs can cause the rate of metabolism to increase, leading to the need for an increased dosage. May also influence the rate of metabolism for other drugs taken at the same time, leading to a need for increased dosages of those drugs as well.
- First-Pass Effect: Hepatic inactivation of certain oral drugs. Avoided by parentaral administration of drugs that undergo rapid hepatic metabolism.
- Nutritional Status
- Competition between Drugs
Class III Potassium Channel Blockers
Prolong effective refractory period by prolonging Action Potential
Treatment: ventricular tachycardia and fibrillation, conversion of atrial fibrillation or flutter to sinus rhythm, maintenance of sinus rhythm
– Amiodarone (Cordarone) – maintenance of sinus rhythm
– Bretylium (Bretylol)
– Ibutilide (Corvert)
– Dofetilide (Tykosyn)
– Sotalol (Betapace)
Amiodarone
- Has characteristics of sodium channel blockers, beta blockers, and calcium channel blockers
- Has vasodilating effects and decreases systemic vascular resistance
- Prolongs conduction in all cardiac tissue
- Decreases heart rate
- Decreases contractility of the left ventricles
Class III - Adverse Effects
- GI- Nausea vomiting and GI distress
- CNS- Weakness and dizziness
- CV-Hypotension, CHF, and arrhythmias are common.
- Amiodarone associated with potentially fatal Hepatic toxicity, ocular abnormalities and serious cardiac arrhythmias.
Drug – Drug Interactions
These drugs can cause serious toxic effects if combined with digoxin or quinidine.
Ciclopirox:Ciclopirox is a synthetic antifungal agent for topical dermatologic use.
Paracetamol
Paracetamol or acetaminophen is analgesic and antipyretic drug that is used for the relief of fever, headaches, and other minor aches and pains.
paracetamol acts by reducing production of prostaglandins, which are involved in the pain and fever processes, by inhibiting the cyclooxygenase (COX) enzyme.
Metabolism Paracetamol is metabolized primarily in the liver. At usual doses, it is quickly detoxified by combining irreversibly with the sulfhydryl group of glutathione to produce a non-toxic conjugate that is eventually excreted by the kidneys.