Please enable JavaScript.

Coggle requires JavaScript to display documents.

Antimicrobials - Coggle Diagram

- - - - MOA
        
        inhibits the gene transcription of mycobacteria by blocking the DNA dependent RNA polymerase, which prevents the bacillus from synthesizing messenger RNA and protein, causing cell death.
        
        Resistance:
        
        Resistance to rifampicin occurs due to mutations in the gene, which encodes the
        RNA polymerase beta chain
      - Pharmacokinetics
        
        orally administered
        
        hepatic metabolism
        
        if used to treat TB meningitis, then the concentration in the CNS will be higher
      - Note
        
        during pregnancy: give with vitamin K to avoid postpartum hemorrhage as an adverse effect is thrombocytopenia
        
        rifampicin is a cat C frug
        
        breastfeeding: small concentrations can pass into breast milk but is not sufficient to treat TB in infant
        
        infant should be monitored for jaundice
        
        kidney failure: no dose adjustment is needed
        
        contraindications: patients with history of hypersensitivity to this drug
      - DDI
        
        induces certain CYP450 enzymes
        
        increase metabolism of many drugs that are partially/completely metabolised by CYP450 enzyles
        
        eg wafarin, corticosteroids, hormonal contraceptives and HIV protease inhibitors
        
        use of isoniazid with rifampicin may increase potential for hepatotoxicity
    - - MOA
        
        activated by the catalase-peroxidase enzyme of M. tuberculosis. The activation of isoniazid produces oxygen-derived free radicals that can inhibit the formation of mycolic acids of the bacterial cell wall, cause DNA damage and, subsequently, the death of the bacillus.
        
        Resistance
        
        mutations to the catalase-peroxidase enzyme, and mutations of the regulatory genes involved in mycolic acid synthesis
      - PK
        
        orally administered
        metabolised in liver
        
        acetylation rate is related to genetic polymorphisms
        
        FYI: isonazid itself is not hepatoxic, it is only toxis when it is metabolised along the amidase pathway which forms hydrazine which is toxic
      - Note
- - - - natural penicillins
        
        Penicillin G and Penicillin V
        - route of administration
        - main organisms/indications
        - penetration into CSF
        - excretion (both by renal)
      - penicillase resistane penicillins
        
        cloxacillin
      - aminopenecillins (broad spectrum) + BL inhibitiors
        
        ampicillin, amoxicillin
      - anti pseudomonal penicillins (extended spectrum) + BL inhibitors
        - know the mechanism
        the idea is that one of it will bind to the beta lactamase to prevent it from working and the other will attack the virus
        
        Amoxicillin Clavulanic
        
        Ampicillin Sulbactam
        
        Piperacillin Tazobactam
    - - 1st to 5th generation
        
        increased activity against gram negative bacteria
        
        increased resistance against beta lactamase producing microbes
        
        the 5th generation one (ceftaroline) can target MRSA
      - adverse effects:
        
        hypersensitivity
        
        GI symptoms
    - - generally have poor bioavailability
        
        Imipenem and Cilastatin
        
        meropenem
        
        ertapenem
        
        need to add in the orgnaisms that are able to target p aeruginosa
      - adverse effects
        
        hypersensitivity
        
        GI symptoms
        
        neurotoxicity
    - - aztreonam
- - - - drugs
        
        Erythromycin
        
        Active against Gram-positive bacteria and Gram-negative bacteria.
        
        Treatment of community acquired pneumonia; S.pneumoniae and atypical bacteria
        
        • Clarithromyciin
        
        Most active of the three against both Gram-positive and Gram-negative pathogens, and it is also active against mycobacteria.
        
        Higher activity against atypical bacteria, such as Legionella, and Helicobacter pylori, than erythromycin.
        
        • Azithromycin
        
        More active than erythromycin against respiratory infections (CAP) due to H. influenzae and Moraxella catarrhalis.
        
        Active against atypical bacteria
        
        Preferred therapy for STD caused by Chlamydia trachomatis and Neisseria gonorrhoea (with ceftriaxone IM).
        
        Against some common bacterial enteric pathogens. (Campylobacter species, Salmonella species, Shigella species, and Vibrio cholerae)
      - MOA
        
        inhibit protein synthesis by reversibly binding to the 50S ribosomal subunits of sensitive organism
        
        inhibit the translocation step such that the nascent peptide chain residing at the A site of the transferase reaction fails to move to the peptidyl donor (P) site
      - adverse effects
        
        Gastric distress
        
        Hepatotoxicity
        
        Ototoxicity
        
        may prolong the QT interval and should be used with caution in those patients with pro-arrhythmic conditions.
    - - MOA:
        Binds exclusively to 50S subunit of
        bacterial ribosome and inhibit peptide synthesis.
      - adverse effects:
        
        Take with a full glass of water to reduce esophageal irritation.
        
        Gastrointestinal effects – Diarrhoea, vomiting
        
        Skin rashes
        
        Clostridioides difficile associated diarrhoea (CDAD); diarrhoea, caused by overgrowth of C. difficile. C. difficile is always resistant to clindamycin. Contraindicated in patients with pseudomembranous colitis or ulcerative colitis.
      - Clinical indications
        
        Treatment of infections caused by Gram-positive organisms, including MRSA and streptococcus, and penicillin resistant anaerobic bacteria.
        
        As alternatives for patients with penicillin allergies
        
        Toxic shock syndrome (anti-toxigenic effect)
        
        Often used in serious/severe anaerobic infections
        
        Anaerobic infections of skin and soft tissues (eg. necrotising fasciitis, diabetic foot) including Bacteroides, Clostridioides perfringen.
        
        Good spectrum of activity against oral pathogens.
        
        Almost all aerobic Gram-negative bacteria are RESISTANT.
    - - MOA:
        Binds the bacterial 23S ribosomal RNA of the 50S subunit and prevents the formation of a functional 70S initiation complex, which is an essential component of the bacterial translation process.
        
        used against gram positive
        
        not for gram neg
      - adverse effects:
        
        GI effects: nausea, diarrhea, headache, and rash.
        
        Bone Marrow Suppression: Thrombocytopenia has been reported in patients taking the drug for longer than 10 days. Need to monitor blood counts.
        
        Linezolid possesses nonselective monoamine oxidase inhibitory activity and may lead to serotonin syndrome if given concomitantly with selective serotonin reuptake inhibitors, or monoamine oxidase inhibitors. The condition is reversible when the drug is discontinued. Tyramine and histamine rich food needs to be avoided.
        
        Irreversible peripheral neuropathies and optic neuritis (causing blindness) have been associated with greater than 28 days of use, limiting utility for extended-duration treatments.
  - - - tetracycline
        
        route of adminstration: orally
        main orgnaisms/indications:
        Treatment of infections caused by susceptible
        
        Rickettsia (Rocky Mountain spotted fever)
        
        Chlamydia, and Mycoplasma pneumoniae.
        
        Vibrio cholerae, plague due to Yersinia pestis
      - doxycycline
        
        orally
        organisms
        Those covered above by tetracycline and
        
        Rickettsia
        
        Acne vulgaris
        
        Anthrax (Bacillus anthracis),
        
        community-acquired pneumonia, S.pneumoniae, Haemophilus influenzae, and
        
        skin and soft tissue infections caused by MRSA
      - minocycline
        
        orally
        organisms
        Active against some tetracycline resistant isolates and those covered by tetracycline.
        
        Used in treatment of severe acne,
        
        Respiratory tract infections caused by Haemophilus influenzae, Klebsiella spp, or Mycoplasma pneumonia,
        
        plague due to Yersinia pestis;
    - - tigecycline
        
        Tigecycline exhibits broad-spectrum activity that includes
        
        Methicillin resistant staphylococci (MRSA),
        
        Multidrug-resistant streptococci,
        
        Vancomycin-resistant enterococci (VRE),
        
        Extended-spectrum β-lactamase–producing (ESBL) Gram-negative bacteria, useful against carbapenem resistant strains
        
        adverse effects
        
        Gastric discomfort
        
        Effects on calcified tissues
        
        Hepatotoxicity
        
        Phototoxicity
        
        Vestibular dysfunction
        
        Renal
        
        Superinfection:
        
        contraindications
    - - drugs
        
        Gentamicin
        
        • Streptomycin
        
        • Tobramycin
        
        • Amikacin
        
        • Neomycin
      - adverse effects:
        
        Ototoxicity
        -Nephrotoxicity
        
        Neuromuscular paralysis
        
        Hypersensitivity reactions
        
        Contraindicated in Pregnancy
      - resistance to aminoglycosides