NEET MDS Lessons
Pharmacology
ANTIBIOTICS
Chemotherapy: Drugs which inhibit or kill the infecting organism and have no/minimum effect on the recipient.
Antibiotic these are substances produced by microorganisms which suppress the growth of or kill other micro-organisms at very low concentrations.
Anti-microbial Agents: synthetic as well as naturally obtained drugs that attenuate micro-organism.
SYNTHETIC ORGANIC ANTIMICROBIAL DRUGS
Sulfonamides
Trimethoprim-sulfamethoxazole
Quinolones – Ciprofloxacin
ANTIBIOTICS THAT ACT ON THE BACTERIAL CELL WALL
Penicillins
Cephalosporins
Vancomycin
INHIBITORS OF BACTERIAL PROTEIN SYNTHESIS
Aminoglycosides - Gentamicin
Antitubercular Drugs: Isoniazid & Rifampin
Tetracyclines
Chloramphenicol
Macrolides – Erythromycin, Azithromycin
Clindamycin
Mupirocin
Linezolid
ANTIFUNGAL DRUGS
Polyene Antibiotics (Amphotericin B, Nystatin and Candicidin)
Imidazole and Triazole Antifungal Drugs
Flucytosine
Griseofulvin
ANTIPROTOZOAL DRUGS
Antimalarial Drugs – Quinine, Chloroquine, Primaquine
Other Antiprotozoal Drugs – Metronidazole, Diloxanide, Iodoquinol
ANTIHELMINTHIC DRUGS
Praziquantel
Mebendazole
Ivermectin
ANTIVIRAL DRUGS
Acyclovir
Ribavirin
Dideoxynucleosides
Protease inhibitors
Erythromycin
used for people who have an allergy to penicillins. For respiratory tract infections, it has better coverage of atypical organisms, including mycoplasma. It is also used to treat outbreaks of chlamydia, syphilis, and gonorrhea.
Erythromycin is produced from a strain of the actinomyces Saccaropolyspora erythraea, formerly known as Streptomyces erythraeus.
Carbonic anhydrase inhibitors
Acetazolamide, Dichlorphenamide, Methazolamide, Ethoxzolamide
Mechanism of Action
1. Carbonic anhydrase (CA) facilitates excretion of H+ and recovery of bicarbonate by the proximal renal tubule and ciliary epithelium of the eye. Sodium is recovered in exchange for H+.
2. Inhibitors block CA block sodium recovery. A very mild diuresis is produced (this is really a side effect of their use in glaucoma) because relatively unimportant mechanism for Na recovery and because proximal tubule site means that other sodium recovery mechansims continue to process their normal fraction of the sodium load.
Treatment modifications to consider if there are concerns regarding vasoconstrictors
- Monitor blood pressure and heart rate preoperatively
- Minimize administration of epinephrine or levonordefrin
- Monitor blood pressure and heart rate 5 min after injection
- May re-administer epinephrine or levonordefrin if blood pressure and heart rate are stable
- Continue to monitor as required
- Consider limiting epinephrine to 0.04 mg, levonordefrin to 0.2 mg
- Avoid epinephrine 1:50,000
- Never use epinephrine-impregnated retraction cord
Flucloxacillin, important even now for its resistance to beta-lactamases produced by bacteria such as Staphylococcus species. It is still no match for MRSA (Methicillin Resistant Staphylococcus aureus).
The last in the line of true penicillins were the antipseudomonal penicillins, such as ticarcillin, useful for their activity against Gram-negative bacteria
A. Sympathetic Nervous System Depressants
1. Antagonists
Both α-adrenoceptor antagonists and β-adrenoceptor antagonists are useful antihypertensives.
- α-blocker Prazosin, phentolamine, phenoxybenzamine
- β-blocker Propranolol ,Metoprolol, atenolol
- α/β-blocker labetalol
2. Sympathetic depressants
a. Examples of peripherally acting agents include
- reserpine This agent interferes with the storage of norepinephrine
- quanethidine This agent interferes with the release of norepinephrine
- trimethaphan This agent blocks transmission through autonomic ganglia.
b. Examples of Centrally acting agents include
- alphamethyldopa
- clonidine. These agents act by decreasing the number of impresses along sympathetic nerves.
Adverse Effect
include nasal congestion, postural hypotension, diarrhea, sexual dysfunction, dry mouth. sedation and drowsiness.
B. Directly Acting Vasodilators
Act on vascular smooth muscle cells independently of adrenergic nerves and adrenergic receptors.
Relaxation of vascular smooth muscle which leads to a decrease in peripheral vascular resistance.
Sites of action of vasodilators are many. For example
Calcium Channel Blocker’s MOA
. Decrease automaticity & conduction thru SA & AV nodes
. Decreased myocardial contractility
. Decreased peripheral & coronary
smooth muscle tone = decrease SVR
Potassium channels activators
minoxidil, cause vasodilation by activating potassium channels in vascular smooth muscle.
An increase in potassium conductance results in hyperpolarization of the cell membrane which is associated with relaxation of smooth muscle.
Nitrovasodilators, such as sodium nitroprusside,
Increase in intracellular cGMP. cGMP in turn activates a protein kinase. Directly-Acting Vasodilators are on occasion used alone but more frequently are used in combination with antihypertensive agents from other classes (esp. a β-blocker and a diuretic.)
Chloral hydrate
1. Short-acting sleep inducer—less risk of “hangover” effect the next day.
2. Little change on REM sleep.
3. Metabolized to trichloroethanol, an active metabolite; further metabolism inactivates the drug.
4. Used for conscious sedation in dentistry.
5. Can result in serious toxicity if the dose is not controlled.