ATM 200

Dosage

Children: Refer to specific product information for dosing, as anhydrous forms can vary widely in dosage recommendations.

Adults: Refer to specific product information for dosing, as anhydrous forms can vary widely in dosage recommendations.

Mechanism of action

Anhydrous compounds often function similarly to their hydrated counterparts but may have altered solubility and absorption characteristics. For example, anhydrous caffeine acts as a central nervous system stimulant primarily through antagonism of adenosine receptors, leading to increased neuronal firing and the release of neurotransmitters such as dopamine and norepinephrine. This results in improved alertness and reduced perception of fatigue.

Pharmacodynamics

The pharmacodynamics of anhydrous compounds can vary depending on the specific substance. In general, anhydrous forms may exhibit increased bioavailability due to their lower molecular weight and rapid absorption. This can lead to quicker onset of action and potentially enhanced effects compared to their hydrated forms. The exact pharmacodynamic profile will depend on the specific drug and its intended use.

Pharmacokinetics

Pharmacokinetics of anhydrous compounds typically involves absorption, distribution, metabolism, and excretion (ADME) processes similar to their hydrated forms. However, anhydrous forms may be absorbed more quickly due to their reduced size and increased solubility. Metabolism can occur in the liver, while excretion is generally through the kidneys. The half-life can vary widely based on the specific drug.

Pregnancy

Consult healthcare provider, as safety has not been established.

Breast-feeding

Consult healthcare provider, as safety has not been established.

Storage

Store in a cool, dry place away from moisture and light.

Indications

• Bacterial infections
• Mild to moderate typhoid due to multiple-antibacterial resistant organisms
• Respiratory-tract infections
• Otitis media
• Skin and soft tissue infections
• Chlamydia trachomatis genital infection
• Chronic Pseudomonas aeruginosa infection in cystic fibrosis
• Prevention of group A streptococcal infection in patients allergic to penicillin

Dosage

Children: Child 6 months–17 years: 10 mg/kg once daily (max. per dose 500 mg) for 3 days, repeated after 1 week if necessary. Refer to BNF for Children for specific dosing based on age and weight.

Adults: 500 mg once daily for 3 to 5 days depending on the infection being treated. For certain cases, doses may be adjusted based on clinical judgment.

Mechanism of action

Azithromycin binds to the 50S ribosomal subunit of bacteria, inhibiting protein synthesis and thus preventing bacterial growth.

Pharmacodynamics

Azithromycin exhibits bacteriostatic activity against susceptible bacteria. It has a long half-life, allowing for once-daily dosing and effective treatment of infections.

Pharmacokinetics

Azithromycin is well-absorbed after oral administration, with a bioavailability of approximately 37%. It penetrates well into tissues, with a half-life of about 68 hours, and is primarily excreted in bile, with minimal renal excretion.

Adverse effects

• Appetite decreased
• Diarrhoea
• Dizziness
• Gastrointestinal discomfort
• Headache
• Hearing impairment
• Insomnia
• Nausea
• Pancreatitis
• Paraesthesia
• Skin reactions
• Taste altered
• Vomiting
• Angioedema
• Anxiety
• Arrhythmias
• Chest pain
• Constipation
• Drowsiness
• Eosinophilia
• Hepatic disorders
• Leucopenia
• Neutropenia
• Palpitations
• QT interval prolongation
• Severe cutaneous adverse reactions (SCARs)
• Tinnitus
• Vertigo
• Antibiotic associated colitis
• Myasthenia gravis
• Nephritis tubulointerstitial
• Hallucination
• Hypotension
• Seizure
• Acute kidney injury
• Aggression
• Akathisia
• Hemolytic anemia
• Syncope

Interactions

• Azithromycin + ticagrelor: Moderate (increases exposure)
• Azithromycin + aliskiren: Unknown (increases exposure)
• Azithromycin + aminophylline: Unknown (increases exposure)
• Azithromycin + colchicine: Unknown (increases exposure)
• Azithromycin + erlotinib: Unknown (increases exposure)
• Azithromycin + lomitapide: Unknown (increases exposure)
• Azithromycin + rimegepant: Unknown (increases exposure)
• Azithromycin + taxanes: Unknown (increases exposure)
• Azithromycin + docetaxel: Unknown (increases exposure)
• Azithromycin + paclitaxel: Unknown (increases exposure)

Precautions

• Use with caution in patients with electrolyte disturbances
• Use with caution if estimated glomerular filtration rate is less than 10 mL/minute/1.73 m2
• Predisposition to QT interval prolongation may be aggravated

Mechanism of action

In order to replicate, bacteria require a specific process of protein synthesis, enabled by ribosomal proteins. Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit,. This results in the control of various bacterial infections,. The strong affinity of macrolides, including azithromycin, for bacterial ribosomes, is consistent with their broad‐spectrum antibacterial activities. Azithromycin is highly stable at a low pH, giving it a longer serum half-life and increasing its concentrations in tissues compared to erythromycin. Azithromycin usually is bacteriostatic, although the drug may be bactericidal in high concentrations against selected organisms. Bactericidal activity has been observed in vitro against Streptococcus pyogenes, S. pneumoniae, and Haemophilus influenzae. Azithromycin inhibits protein synthesis in susceptible organisms by penetrating the cell wall and binding to 50S ribosomal subunits, thereby inhibiting translocation of aminoacyl transfer-RNA and inhibiting polypeptide synthesis. The site of action of azithromycin appears to be the same as that of the macrolides (i.e., erythromycin, clarithromycin), clindamycin, lincomycin, and chloramphenicol. The antimicrobial activity of azithromycin is reduced at low pH. Azithromycin concentrates in phagocytes, including polymorphonuclear leukocytes, monocytes, macrophages, and fibroblasts. Penetration of the drug into phagocytic cells is necessary for activity against intracellular pathogens (e.g., Staphylococcus aureus, Legionella pneumophila, Chlamydia trachomatis, Salmonella typhi).

Pharmacodynamics

Macrolides stop bacterial growth by inhibiting protein synthesis and translation, treating bacterial infections. Azithromycin has additional immunomodulatory effects and has been used in chronic respiratory inflammatory diseases for this purpose.