Streptomycin

Streptomycin was the first of a class of drugs called aminoglycosides to be discovered, and was the first antibiotic remedy for tuberculosis. It is derived from the actinobacterium Streptomyces griseus.

Streptomycin cannot be given orally, but must be administered by regular intramuscular injection.

Chloramphenicol

derived from the bacterium Streptomyces venezuelae

Chloramphenicol is effective against a wide variety of microorganisms, but due to serious side-effects (e.g., damage to the bone marrow, including aplastic anemia) in humans, it is usually reserved for the treatment of serious and life-threatening infections (e.g., typhoid fever). It is used in treatment of cholera, as it destroys the

vibrios and decreases the diarrhoea. It is effective against tetracycline-resistant vibrios.It is also used in eye drops or ointment to treat bacterial conjunctivitis.

Mechanism and Resistance Chloramphenicol stops bacterial growth by binding to the bacterial ribosome (blocking peptidyl transferase) and inhibiting protein synthesis.

Chloramphenicol irreversibly binds to a receptor site on the 50S subunit of the bacterial ribosome, inhibiting peptidyl transferase. This inhibition consequently results in the prevention of amino acid transfer to growing peptide chains, ultimately leading to inhibition of protein formation.

Spectrum of activity: Broad-spectrum

Effect on bacteria: Bacteriostatic

EPHEDRINE

It act indirectly and directly on α and β receptors. It increases blood pressure both by peripheral vasoconstriction and by increasing the cardiac output. Ephedrine also relaxes the bronchial smooth muscles.

Ephedrine stimulates CNS and produces restlessness, insomnia, anxiety and tremors.
Ephedrine produces mydriasis on local as well as systemic administration.
Ephedrine is useful for the treatment of chronic and moderate type of bronchial asthma, used as nasal decongestant and as a mydriatic without cycloplegia. It is also useful in preventing ventricular asystole in Stokes Adams syndrome.

Acid-Peptic disorders

This group of diseases include peptic ulcer, gastroesophageal reflux and Zollinger-Ellison syndrome.

Pathophysiology of acid-peptic disorders

Peptic ulcer disease is thought to result from an imbalance between cell– destructive effects of hydrochloric acid and pepsin on the one side, and cell-protective effects of mucus and bicarbonate on the other side. Pepsin is a proteolytic enzyme activated in gastric acid (above pH of 4, pepsin is inactive); also it can digest the stomach wall. A bacterium, Helicobacter pylori, is now accepted to be involved in the pathogenesis of peptic ulcer.

In gastroesophageal reflux the acidic contents of the stomach enter into the oesophagus causing a burning sensation in the region of the heart; hence the common name heartburn or other names such as indigestion and dyspepsia.

However, Zollinger-Ellison syndrome is caused by a tumor of gastrin secreting cells of the pancreas characterized by excessive secretion of gastrin that stimulates gastric acid secretion.

These disorders can be treated by the following classes of drugs:

A. Gastric acid neutralizers (antacids)
B. Gastric acid secretion inhibitors (antisecretory drugs)
C. Mucosal protective agents
D. Drugs that exert antimicrobial action against H.pylori

Helicobacter Pylori Agents

  Antimicrobial

• Amoxicillin,

• Clarithromycin,

• Metronidozole

• Tetracycline

 Antisecreteory agents accelerates symptom relief and yield healing (omeprozole)

  Bismuth subsalicylate

Therapy For H. Pylori

  Original

• Tetracycline

• Metronidazole (Flagyl)

• Bismuth subsalicylate

• Given for 14 days

• >90% effective in eradicating microorganisms

 New triple therapy

• Amoxicillin

• Clarithromycin

• Omeprazole (Prilosec)

• Given for 7 days

• >90% effective in eradicating microorganisms

Dual Therapy

  Amoxicillin or clarithromycin

  Omeprazole

  Given for 14 days

  60-80% effective in eradication of H. Pylori

Needle selection

Nerve blocks:

Inferior alveolar- 25 G short (LLU technique)

PSA- 25 G short

Mental/Incisive- 25 G short

Palatal- 27/30 G short/ultrashort

Gow-Gates/Akinosi- 25 G long

Infraorbital- 25 G long

Field Block:

ASA 25/27 short

Infiltration:

Infiltration/SP 25/27 short

PDL/Intraosseous

PDL 27/30 short

Intraosseous 30 short/ultrashort