Quinolone

Quinolones and fluoroquinolones form a group of  broad-spectrum antibiotics. They are derived from nalidixic acid.

Fluoroquinolone antibiotics are highly potent and considered relatively safe.

MOA : Quinolones act by inhibiting the bacterial  DNA gyrase enzyme. This way they inhibit nucleic acid synthesis and act bacteriocidically.

Drugs  :Nalidixic acid, Ciprofloxacin , Levofloxacin,  Norfloxacin ,Ofloxacin,  Moxifloxacin  , Trovafloxacin

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

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

Gastric acid secretion inhibitors (antisecretory drugs):

 HCl is secreted by parietal cells of the gastric mucosa which contain receptors for acetylcholine (muscarinic receptors: MR), histamine (H2R), prostaglandins (PGR) and gastrin (GR) that stimulate the production, except PGs which inhibit gastric acid production.
 
Therefore, antagonists of acetylcholine, histamine and gastrin inhibit gastric acid secretion (antisecretory). On the other hand, inhibitors of PGs biosynthesis such as NSAIDs with reduce cytoprotective mechanisms and thus promote gastric mucosal erosion. Also, the last step in gastric acid secretion from parietal cells involve a pump called H+ -K+-ATPase (proton pump). Drugs that block this pump will inhibit gastric acid secretion. Antisecretory drugs include:

1. Anticholinergic agents such as pirenzepine, dicyclomine, atropine.
2. H2-receptors blocking agents such as Cimetidine, Ranitidine, Famotidine, Nizatidine (the pharmacology of these agents has been discussed previously).
3. Gastrin-receptor blockers such as proglumide.
4. Proton pump inhibitors such as omeprazole, lansoprazole.

Major clinical indications of antisecretory drugs:

• Prevention & treatment of peptic ulcer disease.
• Zollinger Ellison syndrome.
• Reflux esophagitis. 

Itraconazole:

The drug may be given orally or intravenously.

Roxithromycin

It is used to treat respiratory tract, urinary and soft tissue infections. Roxithromycin is derived from erythromycin, containing the same 14-membered lactone ring. However, an N-oxime side chain is attached to the lactone ring.

Roxithromycin has similar antimicrobial spectrum as erythromycin, but is more effective against certain gram-negative bacteria, particularly Legionella pneumophilae.

When taken before a meal, roxithromycin is very rapidly absorbed, and diffused into most tissues and Phagocytes Only a small portion of roxithromycin is metabolised. Most of roxithromycin is secreted unchanged into the bile and some in expired air