NEET MDS Lessons
Pharmacology
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.
VITAMIN -K
- Group of lipophilic, hydrophobic vitamins.
- Needed for the post-translational modification of coagulation proteins.
- Phylloquinone (vitamin K1) is the major dietary form of vitamin K.
- Vitamin K2 (menaquinone, menatetrenone) is produced by bacteria in the intestines.
SULPHONAMIDES
Derivative of sulphonilamide (Para-amino Benzene (PABA ) sulphonamide).
Anti-bacterial spectrum
Bacteriostatic to gram + and gram - bacteria. but bactericidal concentrations arce attained in urine. S pyogencs. H influenzae.E coli, few- Staph aureus. gonococci. pneumococci, proteus, shigella and Lymphogranuloma venereum.
Mechanism of action
Inhibits bacterial folate synthetase as they compete with PABA
Less soluble in acid urine and may precipitate to cause crystalluria.
Accumulate in patients with renal failure and can cause toxicity
Classification
Shart Acting (4-8 Hrs) sulphadiazine, sulphamethizole.
Intermediate acting(8-16 Hrs): sulphamethoxazole , sulphaphenazole
Long Acting(l-7days): sulphamethoxypyridazine.
Ultralong Acting(3-8days): sulfaline
Adverse effects
I. nausea, vomiting and epigastric pain
2. crystalluria
3. hypersensitivity-like polyarthritis nodosa. Steven-Johnson Syndrome. photosenstivity
4.hemolysis in G-6PD deficiency
5. kernicterus
They inhibit metabolism of phenytoin. tolbutamide. methotrexate
Therapeutic Use
UTI Meningitis, Streptococcal pharyngitis, Bacillary Dysentery
ANTIASTHMATIC AGENTS
Classification for antiasthmatic drugs.
I. Bronchodilators
i. Sympathomimetics (adrenergic receptor agonists)
Adrenaline, ephedrine, isoprenaline, orciprenaline, salbutamol, terbutaline, salmeterol, bambuterol
ii. Methylxanthines (theophylline and its derivatives)
Theophylline
Hydroxyethyl theophylline
Theophylline ethanolate of piperazine
iii. Anticholinergics
Atropine methonitrate
Ipratropium bromide
II. Mast cell stabilizer
Sodium cromoglycate
Ketotifen
III. Corticosteroids
Beclomethasone dipropionate
Beclomethasone (200 µg) with salbutamol
IV. Leukotriene pathway inhibitors
Montelukast
Zafirlukast
Gabapentin (Neurontin): newer; for generalized tonic-clonic seizures and partial seizures (partial and complex)
Mechanism: unknown but know doesn’t mimic GABA inhibition or block Ca currents
Side effects: dizziness, ataxia, fatigue; drug well-tolerated and no significant drug interactions
CARDIAC GLYCOSIDES
Cardiac glycosides (Digitalis)
Digoxin
Digitoxin
Sympathomimetics
Dobutamine
Dopamine
Vasodilators
α-blockers (prazosin)
Nitroprusside
ACE-inhibitors (captopril)
Pharmacology of Cardiac Glycosides
1. Positive inotropic effect (as a result of increase C.O., the symptoms of CHF subside).
2. Effects on other cardiac parameters
1) Excitability
2) Conduction Velocity; slightly increased in atria & ventricle/significantly
reduced in conducting tissue esp. A-V node and His-Purkinje System
3) Refractory Period; slightly ^ in atria & nodal tissue/slightly v in ventricles
4) Automaticity; can be greatly augmented - of particular concern in ventricle
3. Heart Rate
-Decrease due to 1) vagal stimulation and 2) in the situation of CHF, due to improved hemodynamics
4 Blood Pressure
-In CHF, not of much consequence. Changes are generally secondary to improved cardiac performance.
-In the absence of CHF, some evidence for a direct increase in PVR due to vasoconstriction.
5. Diuresis
-Due primarily to increase in renal blood flow as a consequence of positive inotropic effect (increase CO etc.) Possibly some slight direct diuretic effect.
Mechanism of Action of Cardiac Glycosides
Associated with an interaction with membrane-bound Na+-K+ ATPase (Na-K pump).
Clinical ramifications of an interaction of cardiac glycosides with the Na+ K pump.
I. Increase levels of Ca++, Increase therapeutic and toxic effects of cardiac glycosides
II. Decrease levels of K+ , Increase toxic effects of cardiac glycosides
Therapeutic Uses of Cardiac Glycosides
- CHF
- CHF accompanied by atrial fibrillation
- Supraventricular arrhythmias
Oxycodone
About equal potency to morphine. Very effective orally.
It is combined with aspirin or acetaminophen for the treatment of moderate pain and is available orally
Oxycodone is a semisynthetic compound derived from thebaine, with agonist activity primarily at mu receptors.