Podcast
Questions and Answers
What is the mechanism of action of clindamycin?
What is the mechanism of action of clindamycin?
- Disruption of bacterial DNA replication
- Inhibition of cell wall synthesis
- Activation of bacterial autolysins
- Inhibition of protein synthesis (correct)
Which type of bacteria is clindamycin effective against?
Which type of bacteria is clindamycin effective against?
- Both Gram-positive and Gram-negative
- Gram-positive, including MRSA and streptococcus (correct)
- Anaerobic bacteria only
- Gram-negative, including E. coli and Pseudomonas
How is clindamycin primarily eliminated from the body?
How is clindamycin primarily eliminated from the body?
- Renal excretion
- Excretion into bile and urine (correct)
- Exhalation through the lungs
- Metabolism by the liver
What is the main modification in fluoroquinolones compared to the 1st generation quinolones?
What is the main modification in fluoroquinolones compared to the 1st generation quinolones?
Why are fluoroquinolones considered 2nd line options for various indications?
Why are fluoroquinolones considered 2nd line options for various indications?
Which type of bacteria are fluoroquinolones effective against?
Which type of bacteria are fluoroquinolones effective against?
What is the mechanism of action of Amphotericin B?
What is the mechanism of action of Amphotericin B?
What is the drug of choice for several life-threatening mycoses?
What is the drug of choice for several life-threatening mycoses?
How is oral amphotericin B primarily used?
How is oral amphotericin B primarily used?
What is the primary route of excretion for amphotericin B?
What is the primary route of excretion for amphotericin B?
What is the resistance factor associated with amphotericin B?
What is the resistance factor associated with amphotericin B?
What is the primary method of administration for amphotericin B?
What is the primary method of administration for amphotericin B?
What is the treatment duration for multidrug-resistant TB (MDR-TB)?
What is the treatment duration for multidrug-resistant TB (MDR-TB)?
How is isoniazid activated in the body?
How is isoniazid activated in the body?
What is the mechanism of action of rifampin?
What is the mechanism of action of rifampin?
Which drug is specific for mycobacteria and inhibits arabinosyl transferases required for cell wall synthesis?
Which drug is specific for mycobacteria and inhibits arabinosyl transferases required for cell wall synthesis?
What is a potential adverse effect of isoniazid?
What is a potential adverse effect of isoniazid?
Why may rifabutin be used as an alternative to rifampin?
Why may rifabutin be used as an alternative to rifampin?
What is the primary route of excretion for trimethoprim?
What is the primary route of excretion for trimethoprim?
What is a potential adverse effect of methenamine?
What is a potential adverse effect of methenamine?
What is the mechanism of action of nitrofurantoin?
What is the mechanism of action of nitrofurantoin?
What is the mechanism of action of trimethoprim?
What is the mechanism of action of trimethoprim?
What can cause resistance to trimethoprim?
What can cause resistance to trimethoprim?
What is the first-line therapy for uncomplicated cystitis?
What is the first-line therapy for uncomplicated cystitis?
What is the mechanism of action of quinolones and fluoroquinolones?
What is the mechanism of action of quinolones and fluoroquinolones?
Which infections are quinolones and fluoroquinolones effective against?
Which infections are quinolones and fluoroquinolones effective against?
How can resistance to quinolones and fluoroquinolones occur?
How can resistance to quinolones and fluoroquinolones occur?
How are quinolones and fluoroquinolones absorbed in the body?
How are quinolones and fluoroquinolones absorbed in the body?
What are the adverse reactions to quinolones and fluoroquinolones?
What are the adverse reactions to quinolones and fluoroquinolones?
What is the mechanism of action of sulfonamides?
What is the mechanism of action of sulfonamides?
What is the primary mechanism of resistance associated with fluoroquinolones?
What is the primary mechanism of resistance associated with fluoroquinolones?
Which type of bacteria are fluoroquinolones primarily effective against?
Which type of bacteria are fluoroquinolones primarily effective against?
What is the primary route of excretion for clindamycin?
What is the primary route of excretion for clindamycin?
How are fluoroquinolones primarily eliminated from the body?
How are fluoroquinolones primarily eliminated from the body?
Which type of infections are clindamycin primarily used to treat?
Which type of infections are clindamycin primarily used to treat?
What is the primary method of administration for fluoroquinolones?
What is the primary method of administration for fluoroquinolones?
What is a potential adverse effect of quinolones and fluoroquinolones?
What is a potential adverse effect of quinolones and fluoroquinolones?
How are quinolones and fluoroquinolones primarily excreted from the body?
How are quinolones and fluoroquinolones primarily excreted from the body?
What is the mechanism of resistance to sulfonamides?
What is the mechanism of resistance to sulfonamides?
Which adverse effect is associated with sulfonamides?
Which adverse effect is associated with sulfonamides?
How are sulfonamides primarily metabolized in the body?
How are sulfonamides primarily metabolized in the body?
What is a potential adverse effect of folate antagonists like sulfonamides?
What is a potential adverse effect of folate antagonists like sulfonamides?
What is the primary method of administration for amphotericin B?
What is the primary method of administration for amphotericin B?
What is the mechanism of action of amphotericin B?
What is the mechanism of action of amphotericin B?
What is the resistance factor associated with amphotericin B?
What is the resistance factor associated with amphotericin B?
How is amphotericin B primarily excreted from the body?
How is amphotericin B primarily excreted from the body?
In addition to intravenous infusion, in what other form can amphotericin B be administered?
In addition to intravenous infusion, in what other form can amphotericin B be administered?
What is the drug of choice for several life-threatening mycoses?
What is the drug of choice for several life-threatening mycoses?
What is the treatment duration for latent tuberculosis infection (LTBI) with isoniazid monotherapy?
What is the treatment duration for latent tuberculosis infection (LTBI) with isoniazid monotherapy?
Which enzyme is required for the activation of isoniazid in the body?
Which enzyme is required for the activation of isoniazid in the body?
What is the primary mechanism of action of rifampin against mycobacteria?
What is the primary mechanism of action of rifampin against mycobacteria?
Which drug disrupts mycobacterial cell membrane metabolism and transport functions?
Which drug disrupts mycobacterial cell membrane metabolism and transport functions?
What is the primary target of ethambutol in mycobacteria?
What is the primary target of ethambutol in mycobacteria?
What is the reason for the increased incidence of mycoses?
What is the reason for the increased incidence of mycoses?
What is the mechanism of action of methenamine?
What is the mechanism of action of methenamine?
What is the first-line therapy for uncomplicated cystitis?
What is the first-line therapy for uncomplicated cystitis?
What is the resistance factor associated with trimethoprim?
What is the resistance factor associated with trimethoprim?
What is the primary route of excretion for methenamine?
What is the primary route of excretion for methenamine?
What are the adverse effects of nitrofurantoin?
What are the adverse effects of nitrofurantoin?
What is the spectrum of activity for methenamine?
What is the spectrum of activity for methenamine?
Which of the following is true about clindamycin?
Which of the following is true about clindamycin?
What is the primary mechanism of resistance associated with fluoroquinolones?
What is the primary mechanism of resistance associated with fluoroquinolones?
What is the primary route of excretion for fluoroquinolones?
What is the primary route of excretion for fluoroquinolones?
Which enzyme is required for the activation of isoniazid in the body?
Which enzyme is required for the activation of isoniazid in the body?
What type of bacteria are fluoroquinolones primarily effective against?
What type of bacteria are fluoroquinolones primarily effective against?
What is the reason for the increased frequency of C. difficile associated with fluoroquinolones?
What is the reason for the increased frequency of C. difficile associated with fluoroquinolones?
What is the primary route of excretion for amphotericin B?
What is the primary route of excretion for amphotericin B?
What is the mechanism of action of amphotericin B?
What is the mechanism of action of amphotericin B?
What is the drug of choice for several life-threatening mycoses?
What is the drug of choice for several life-threatening mycoses?
What is the resistance factor associated with amphotericin B?
What is the resistance factor associated with amphotericin B?
In addition to intravenous infusion, in what other form can amphotericin B be administered?
In addition to intravenous infusion, in what other form can amphotericin B be administered?
How is oral amphotericin B primarily used?
How is oral amphotericin B primarily used?
Which of the following is a potential adverse effect of quinolones and fluoroquinolones?
Which of the following is a potential adverse effect of quinolones and fluoroquinolones?
What is the primary mechanism of resistance associated with quinolones and fluoroquinolones?
What is the primary mechanism of resistance associated with quinolones and fluoroquinolones?
How are sulfonamides primarily metabolized in the body?
How are sulfonamides primarily metabolized in the body?
What is the spectrum of activity for sulfonamides?
What is the spectrum of activity for sulfonamides?
How are quinolones and fluoroquinolones excreted from the body?
How are quinolones and fluoroquinolones excreted from the body?
What is the primary route of excretion for sulfonamides?
What is the primary route of excretion for sulfonamides?
Which antimycobacterial drug disrupts mycobacterial cell membrane metabolism and transport functions, is active at low pH, and used for a short period in combination with other drugs?
Which antimycobacterial drug disrupts mycobacterial cell membrane metabolism and transport functions, is active at low pH, and used for a short period in combination with other drugs?
What is the primary target of ethambutol in mycobacteria?
What is the primary target of ethambutol in mycobacteria?
Which antimycobacterial drug is a prodrug activated by mycobacterial catalaseperoxidase (KatG) and targets enzymes required for mycolic acid synthesis?
Which antimycobacterial drug is a prodrug activated by mycobacterial catalaseperoxidase (KatG) and targets enzymes required for mycolic acid synthesis?
What is the treatment duration for latent tuberculosis infection (LTBI) with isoniazid monotherapy?
What is the treatment duration for latent tuberculosis infection (LTBI) with isoniazid monotherapy?
Which antimycobacterial drug blocks RNA transcription and is bactericidal against intracellular and extracellular mycobacteria?
Which antimycobacterial drug blocks RNA transcription and is bactericidal against intracellular and extracellular mycobacteria?
What is the adverse effect associated with rifampin?
What is the adverse effect associated with rifampin?
Which drug can be used alone for UTIs and bacterial prostatitis?
Which drug can be used alone for UTIs and bacterial prostatitis?
What is the primary route of excretion for trimethoprim?
What is the primary route of excretion for trimethoprim?
What is the mechanism of action of methenamine?
What is the mechanism of action of methenamine?
Which drug is contraindicated in renal insufficiency?
Which drug is contraindicated in renal insufficiency?
What is the first-line therapy for uncomplicated cystitis?
What is the first-line therapy for uncomplicated cystitis?
What is the mechanism of action of trimethoprim?
What is the mechanism of action of trimethoprim?
Clindamycin is a chlorine-substituted derivative of lincomycin.
Clindamycin is a chlorine-substituted derivative of lincomycin.
The mechanism of action of clindamycin is the same as macrolides.
The mechanism of action of clindamycin is the same as macrolides.
Clindamycin is primarily effective against Gram-positive bacteria such as MRSA, streptococcus, and anaerobic bacteria.
Clindamycin is primarily effective against Gram-positive bacteria such as MRSA, streptococcus, and anaerobic bacteria.
Clindamycin distributes well to all body fluids, including CSF.
Clindamycin distributes well to all body fluids, including CSF.
C. difficile is susceptible to clindamycin treatment.
C. difficile is susceptible to clindamycin treatment.
Fluoroquinolones are considered 2nd line options for various indications due to resistance to Gram-negative and Gram-positive organisms.
Fluoroquinolones are considered 2nd line options for various indications due to resistance to Gram-negative and Gram-positive organisms.
Amphotericin B is a water-soluble drug for the treatment of mycotic infections
Amphotericin B is a water-soluble drug for the treatment of mycotic infections
Amphotericin B binds to ergosterol, disrupting membrane function and leading to cell death
Amphotericin B binds to ergosterol, disrupting membrane function and leading to cell death
Amphotericin B is primarily excreted through the kidneys
Amphotericin B is primarily excreted through the kidneys
Amphotericin B is the drug of choice for several life-threatening mycoses
Amphotericin B is the drug of choice for several life-threatening mycoses
Amphotericin B is primarily administered orally for subcutaneous and systemic mycotic infections
Amphotericin B is primarily administered orally for subcutaneous and systemic mycotic infections
Amphotericin B has a wide antifungal spectrum, including Candida albicans and Aspergillus
Amphotericin B has a wide antifungal spectrum, including Candida albicans and Aspergillus
Quinolones and fluoroquinolones are primarily effective against Gram-negative organisms only.
Quinolones and fluoroquinolones are primarily effective against Gram-negative organisms only.
Sulfonamides are bacteriostatic and compete with PABA for binding sites.
Sulfonamides are bacteriostatic and compete with PABA for binding sites.
Resistance to quinolones and fluoroquinolones can occur through altered target binding, decreased accumulation, and enzymatic degradation.
Resistance to quinolones and fluoroquinolones can occur through altered target binding, decreased accumulation, and enzymatic degradation.
Sulfonamides are well absorbed orally, except for sulfasalazine.
Sulfonamides are well absorbed orally, except for sulfasalazine.
Adverse reactions to quinolones and fluoroquinolones include gastrointestinal and central nervous system effects, tendinitis, and tendon rupture.
Adverse reactions to quinolones and fluoroquinolones include gastrointestinal and central nervous system effects, tendinitis, and tendon rupture.
Folate antagonists like sulfonamides inhibit de novo synthesis of pyrimidines.
Folate antagonists like sulfonamides inhibit de novo synthesis of pyrimidines.
Trimethoprim is primarily hepatically metabolized
Trimethoprim is primarily hepatically metabolized
Methenamine is effective against E. coli, Enterococcus spp., Staphylococcus spp., and Pseudomonas aeruginosa
Methenamine is effective against E. coli, Enterococcus spp., Staphylococcus spp., and Pseudomonas aeruginosa
Nitrofurantoin inhibits protein synthesis in bacteria
Nitrofurantoin inhibits protein synthesis in bacteria
Cotrimoxazole is a combination of trimethoprim and sulfamethoxazole
Cotrimoxazole is a combination of trimethoprim and sulfamethoxazole
Resistance to trimethoprim can occur due to altered dihydrofolate reductase
Resistance to trimethoprim can occur due to altered dihydrofolate reductase
Nitrofurantoin is the first-line therapy for uncomplicated cystitis
Nitrofurantoin is the first-line therapy for uncomplicated cystitis
Rifampin is primarily used to treat multidrug-resistant TB (MDR-TB)
Rifampin is primarily used to treat multidrug-resistant TB (MDR-TB)
Isoniazid is a prodrug activated by mycobacterial catalaseperoxidase (KatG)
Isoniazid is a prodrug activated by mycobacterial catalaseperoxidase (KatG)
Pyrazinamide is active at high pH
Pyrazinamide is active at high pH
Ethambutol inhibits arabinosyl transferases required for cell wall synthesis
Ethambutol inhibits arabinosyl transferases required for cell wall synthesis
Antifungal drugs target bacteria's rigid cell wall (chitin) and cell membrane (ergosterol)
Antifungal drugs target bacteria's rigid cell wall (chitin) and cell membrane (ergosterol)
Isoniazid's adverse effects include convulsions and rashes
Isoniazid's adverse effects include convulsions and rashes
Clindamycin is a first-generation quinolone antibiotic
Clindamycin is a first-generation quinolone antibiotic
Clindamycin is effective against MRSA, streptococcus, and anaerobic bacteria
Clindamycin is effective against MRSA, streptococcus, and anaerobic bacteria
Fluoroquinolones have an expanded spectrum of activity compared to 1st generation quinolones
Fluoroquinolones have an expanded spectrum of activity compared to 1st generation quinolones
Fluoroquinolones are considered 1st line options for various indications due to resistance to G -ve and G +ve organisms
Fluoroquinolones are considered 1st line options for various indications due to resistance to G -ve and G +ve organisms
Clindamycin is excreted primarily through the kidneys
Clindamycin is excreted primarily through the kidneys
C. difficile is resistant to clindamycin treatment
C. difficile is resistant to clindamycin treatment
Amphotericin B is primarily administered orally for systemic mycotic infections
Amphotericin B is primarily administered orally for systemic mycotic infections
Amphotericin B binds to ergosterol, disrupting membrane function and causing cell death
Amphotericin B binds to ergosterol, disrupting membrane function and causing cell death
Amphotericin B is extensively distributed in the CSF, vitreous humor, peritoneal fluid, and synovial fluid
Amphotericin B is extensively distributed in the CSF, vitreous humor, peritoneal fluid, and synovial fluid
Amphotericin B is primarily excreted through the urine over a long period of time
Amphotericin B is primarily excreted through the urine over a long period of time
Resistance to Amphotericin B is primarily associated with altered ergosterol structure
Resistance to Amphotericin B is primarily associated with altered ergosterol structure
Amphotericin B is primarily used for local gastrointestinal tract treatment
Amphotericin B is primarily used for local gastrointestinal tract treatment
Quinolones and fluoroquinolones are primarily effective against Gram-negative organisms only.
Quinolones and fluoroquinolones are primarily effective against Gram-negative organisms only.
Sulfonamides are primarily metabolized in the liver through acetylation and conjugation.
Sulfonamides are primarily metabolized in the liver through acetylation and conjugation.
Resistance to quinolones and fluoroquinolones can occur through altered target binding, decreased accumulation, and enzymatic degradation.
Resistance to quinolones and fluoroquinolones can occur through altered target binding, decreased accumulation, and enzymatic degradation.
Sulfonamides are well absorbed orally, with high bioavailability for sulfasalazine.
Sulfonamides are well absorbed orally, with high bioavailability for sulfasalazine.
Adverse reactions to quinolones and fluoroquinolones include hematopoietic disturbances and kernicterus.
Adverse reactions to quinolones and fluoroquinolones include hematopoietic disturbances and kernicterus.
Folate antagonists like sulfonamides are bactericidal and primarily effective against Gram-negative organisms.
Folate antagonists like sulfonamides are bactericidal and primarily effective against Gram-negative organisms.
LTBI can be treated for 6 months with isoniazid monotherapy
LTBI can be treated for 6 months with isoniazid monotherapy
Rifampin is primarily used to treat multidrug-resistant TB (MDR-TB)
Rifampin is primarily used to treat multidrug-resistant TB (MDR-TB)
Pyrazinamide disrupts mycobacterial cell membrane metabolism and transport functions
Pyrazinamide disrupts mycobacterial cell membrane metabolism and transport functions
Ethambutol inhibits arabinosyl transferases required for RNA transcription in mycobacteria
Ethambutol inhibits arabinosyl transferases required for RNA transcription in mycobacteria
Antifungal drugs primarily target fungi's DNA synthesis
Antifungal drugs primarily target fungi's DNA synthesis
Increased incidence of mycoses is primarily due to antibiotic resistance
Increased incidence of mycoses is primarily due to antibiotic resistance
Trimethoprim is primarily hepatically metabolized
Trimethoprim is primarily hepatically metabolized
Methenamine is primarily effective against Escherichia coli and Pseudomonas aeruginosa
Methenamine is primarily effective against Escherichia coli and Pseudomonas aeruginosa
Nitrofurantoin inhibits protein synthesis in bacteria
Nitrofurantoin inhibits protein synthesis in bacteria
Mycobacterium tuberculosis is treated with first-line drugs like isoniazid, rifampin, pyrazinamide, and ethambutol
Mycobacterium tuberculosis is treated with first-line drugs like isoniazid, rifampin, pyrazinamide, and ethambutol
Cotrimoxazole has different pharmacokinetics and adverse effects compared to its individual components, trimethoprim and sulfamethoxazole
Cotrimoxazole has different pharmacokinetics and adverse effects compared to its individual components, trimethoprim and sulfamethoxazole
Nitrofurantoin is contraindicated in renal insufficiency
Nitrofurantoin is contraindicated in renal insufficiency
Study Notes
Antibiotics Pharmacology Lecture Summary
- Quinolones and fluoroquinolones inhibit bacterial DNA gyrase and topoisomerase IV, leading to rapid cell death.
- They are effective against Gram-positive and Gram-negative organisms, anaerobic infections, and are used for conditions like anthrax, UTIs, and respiratory infections.
- Resistance to quinolones and fluoroquinolones can occur through altered target binding, decreased accumulation, and enzymatic degradation.
- These antibiotics are well absorbed orally, with high bioavailability for levofloxacin and moxifloxacin, but their absorption is affected by certain antacids and supplements.
- Quinolones and fluoroquinolones are distributed widely in the body, penetrate well into tissues, and are excreted renally.
- Adverse reactions to quinolones and fluoroquinolones include gastrointestinal and central nervous system effects, tendinitis, tendon rupture, and drug interactions.
- Folate antagonists like sulfonamides inhibit de novo synthesis of folate, essential for cell growth and division, and are often used in combination with trimethoprim.
- Sulfonamides compete with PABA, are bacteriostatic, and effective against both Gram-positive and Gram-negative organisms.
- Resistance to sulfonamides can occur through natural mechanisms or acquired alterations in cellular permeability and PABA production.
- Sulfonamides are well absorbed orally, except for sulfasalazine, and are widely distributed in the body, including the central nervous system and placental barrier.
- Metabolism of sulfonamides involves acetylation and conjugation in the liver, with potential adverse effects like crystalluria and kidney damage.
- Adverse effects of sulfonamides include crystalluria, hypersensitivity, hematopoietic disturbances, kernicterus, and contraindications for specific patient populations.
Pharmacology Overview by Dr. Osama Abusara
- Trimethoprim is a potent inhibitor of bacterial dihydrofolate reductase, selectively toxic to bacteria, and prevents the formation of folic acid.
- Trimethoprim is 20-50 times more potent than sulfonamides and can be used alone for UTIs and bacterial prostatitis.
- Resistance to trimethoprim can occur due to altered dihydrofolate reductase.
- Trimethoprim is rapidly absorbed after oral administration, widely distributed, and primarily renally excreted.
- Adverse effects of trimethoprim include megaloblastic anemia, leukopenia, and hyperkalemia.
- Cotrimoxazole, a combination of trimethoprim and sulfamethoxazole, has a similar spectrum, resistance, pharmacokinetics, and adverse effects to the individual drugs.
- Methenamine and nitrofurantoin are urinary tract antiseptics used for treatment or suppression of UTIs.
- Methenamine is hydrolyzed to ammonia and formaldehyde in acidic urine, denaturing bacterial cell components.
- Methenamine is effective against E. coli, Enterococcus spp., Staphylococcus spp., and some activity against Proteus and Pseudomonas aeruginosa.
- Methenamine has adverse effects such as GI distress and is contraindicated in renal insufficiency.
- Nitrofurantoin is the first-line therapy for uncomplicated cystitis, inhibiting DNA and RNA synthesis.
- Mycobacterium tuberculosis causes tuberculosis (TB), and its treatment involves first-line drugs like isoniazid, rifampin, pyrazinamide, and ethambutol, with second-line drugs used for resistant TB or intolerance.
Pharmacology Overview by Dr. Osama Abusara
- Trimethoprim is a potent inhibitor of bacterial dihydrofolate reductase, selectively toxic to bacteria, and prevents the formation of folic acid.
- Trimethoprim is 20-50 times more potent than sulfonamides and can be used alone for UTIs and bacterial prostatitis.
- Resistance to trimethoprim can occur due to altered dihydrofolate reductase.
- Trimethoprim is rapidly absorbed after oral administration, widely distributed, and primarily renally excreted.
- Adverse effects of trimethoprim include megaloblastic anemia, leukopenia, and hyperkalemia.
- Cotrimoxazole, a combination of trimethoprim and sulfamethoxazole, has a similar spectrum, resistance, pharmacokinetics, and adverse effects to the individual drugs.
- Methenamine and nitrofurantoin are urinary tract antiseptics used for treatment or suppression of UTIs.
- Methenamine is hydrolyzed to ammonia and formaldehyde in acidic urine, denaturing bacterial cell components.
- Methenamine is effective against E. coli, Enterococcus spp., Staphylococcus spp., and some activity against Proteus and Pseudomonas aeruginosa.
- Methenamine has adverse effects such as GI distress and is contraindicated in renal insufficiency.
- Nitrofurantoin is the first-line therapy for uncomplicated cystitis, inhibiting DNA and RNA synthesis.
- Mycobacterium tuberculosis causes tuberculosis (TB), and its treatment involves first-line drugs like isoniazid, rifampin, pyrazinamide, and ethambutol, with second-line drugs used for resistant TB or intolerance.
Antimycobacterial Drugs Overview
- Tuberculosis (TB) treatment ranges from months to years, with at least 6 months for TB and 2 years for multidrug-resistant TB (MDR-TB)
- LTBI can be treated for 9 months with isoniazid monotherapy
- Standard TB regimen involves multiple drugs, while MDR-TB requires 2nd line drugs and any effective drug from 1st line
- Isoniazid is a prodrug activated by mycobacterial catalaseperoxidase (KatG) and targets enzymes required for mycolic acid synthesis
- Resistance to isoniazid can result from mutation or deletion of KatG, mutations of acyl carrier proteins, or overexpression of InhA
- Rifampin, a broader spectrum antimycobacterial drug, blocks RNA transcription and is bactericidal against intracellular and extracellular mycobacteria
- Pyrazinamide disrupts mycobacterial cell membrane metabolism and transport functions, is active at low pH, and used for a short period in combination with other drugs
- Ethambutol, specific for mycobacteria, inhibits arabinosyl transferases required for cell wall synthesis
- Antifungal drugs target fungi's rigid cell wall (chitin) and cell membrane (ergosterol)
- Increased incidence of mycoses is due to various reasons such as cancer chemotherapy, HIV, and organ transplantation causing immune suppression
- Isoniazid's adverse effects include hepatitis, peripheral neuropathy, convulsions, rashes, fever, and drug-drug interactions
- Rifampin's adverse effects include nausea, vomiting, rash, GI upset, flu-like syndrome, and rare hepatitis and death; rifabutin may be used as an alternative
Pharmacology Overview by Dr. Osama Abusara
- Trimethoprim is a potent inhibitor of bacterial dihydrofolate reductase, selectively toxic to bacteria, and prevents the formation of folic acid.
- Trimethoprim is 20-50 times more potent than sulfonamides and can be used alone for UTIs and bacterial prostatitis.
- Resistance to trimethoprim can occur due to altered dihydrofolate reductase.
- Trimethoprim is rapidly absorbed after oral administration, widely distributed, and primarily renally excreted.
- Adverse effects of trimethoprim include megaloblastic anemia, leukopenia, and hyperkalemia.
- Cotrimoxazole, a combination of trimethoprim and sulfamethoxazole, has a similar spectrum, resistance, pharmacokinetics, and adverse effects to the individual drugs.
- Methenamine and nitrofurantoin are urinary tract antiseptics used for treatment or suppression of UTIs.
- Methenamine is hydrolyzed to ammonia and formaldehyde in acidic urine, denaturing bacterial cell components.
- Methenamine is effective against E. coli, Enterococcus spp., Staphylococcus spp., and some activity against Proteus and Pseudomonas aeruginosa.
- Methenamine has adverse effects such as GI distress and is contraindicated in renal insufficiency.
- Nitrofurantoin is the first-line therapy for uncomplicated cystitis, inhibiting DNA and RNA synthesis.
- Mycobacterium tuberculosis causes tuberculosis (TB), and its treatment involves first-line drugs like isoniazid, rifampin, pyrazinamide, and ethambutol, with second-line drugs used for resistant TB or intolerance.
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Test your knowledge of antibiotics pharmacology with this quiz covering quinolones, fluoroquinolones, and sulfonamides. Learn about their mechanisms of action, indications, resistance mechanisms, pharmacokinetics, and adverse effects.
