150 Questions
What is the mechanism of action of clindamycin?
Inhibition of protein synthesis
Which type of bacteria is clindamycin effective against?
Gram-positive, including MRSA and streptococcus
How is clindamycin primarily eliminated from the body?
Excretion into bile and urine
What is the main modification in fluoroquinolones compared to the 1st generation quinolones?
Fluorination of the quinolone nucleus
Why are fluoroquinolones considered 2nd line options for various indications?
Due to resistance to Gram-negative and Gram-positive organisms
Which type of bacteria are fluoroquinolones effective against?
Both Gram-negative and Gram-positive
What is the mechanism of action of Amphotericin B?
It binds to ergosterol, forming pores, disrupting membrane function, leading to cell death
What is the drug of choice for several life-threatening mycoses?
Amphotericin B
How is oral amphotericin B primarily used?
For local GI tract treatment
What is the primary route of excretion for amphotericin B?
Urine
What is the resistance factor associated with amphotericin B?
Ergosterol content and structure
What is the primary method of administration for amphotericin B?
Parenterally (slow IV infusion)
What is the treatment duration for multidrug-resistant TB (MDR-TB)?
At least 2 years
How is isoniazid activated in the body?
By mycobacterial catalaseperoxidase (KatG)
What is the mechanism of action of rifampin?
Blocks RNA transcription
Which drug is specific for mycobacteria and inhibits arabinosyl transferases required for cell wall synthesis?
Ethambutol
What is a potential adverse effect of isoniazid?
Peripheral neuropathy
Why may rifabutin be used as an alternative to rifampin?
To reduce the risk of rare hepatitis and death
What is the primary route of excretion for trimethoprim?
Renal excretion
What is a potential adverse effect of methenamine?
GI distress
What is the mechanism of action of nitrofurantoin?
Inhibiting DNA and RNA synthesis
What is the mechanism of action of trimethoprim?
Inhibitor of bacterial dihydrofolate reductase
What can cause resistance to trimethoprim?
Altered dihydrofolate reductase
What is the first-line therapy for uncomplicated cystitis?
Nitrofurantoin
What is the mechanism of action of quinolones and fluoroquinolones?
Inhibit bacterial DNA gyrase and topoisomerase IV
Which infections are quinolones and fluoroquinolones effective against?
Gram-positive and Gram-negative organisms, anaerobic infections
How can resistance to quinolones and fluoroquinolones occur?
Altered target binding, decreased accumulation, enzymatic degradation
How are quinolones and fluoroquinolones absorbed in the body?
Well absorbed orally, with high bioavailability
What are the adverse reactions to quinolones and fluoroquinolones?
Gastrointestinal and central nervous system effects, tendinitis, tendon rupture, drug interactions
What is the mechanism of action of sulfonamides?
Inhibit de novo synthesis of folate
What is the primary mechanism of resistance associated with fluoroquinolones?
Altered DNA gyrase or topoisomerase IV enzymes
Which type of bacteria are fluoroquinolones primarily effective against?
Gram-positive and gram-negative
What is the primary route of excretion for clindamycin?
Bile and urine
How are fluoroquinolones primarily eliminated from the body?
Renal excretion
Which type of infections are clindamycin primarily used to treat?
Gram-positive, such as MRSA, streptococcus, and anaerobic bacteria
What is the primary method of administration for fluoroquinolones?
Oral and IV
What is a potential adverse effect of quinolones and fluoroquinolones?
Photosensitivity
How are quinolones and fluoroquinolones primarily excreted from the body?
Renally
What is the mechanism of resistance to sulfonamides?
Altered cellular permeability
Which adverse effect is associated with sulfonamides?
Thrombocytopenia
How are sulfonamides primarily metabolized in the body?
Conjugation
What is a potential adverse effect of folate antagonists like sulfonamides?
Megaloblastic anemia
What is the primary method of administration for amphotericin B?
Intravenous infusion
What is the mechanism of action of amphotericin B?
Disruption of membrane function
What is the resistance factor associated with amphotericin B?
Ergosterol content and structure
How is amphotericin B primarily excreted from the body?
Through urine
In addition to intravenous infusion, in what other form can amphotericin B be administered?
Intrathecal administration
What is the drug of choice for several life-threatening mycoses?
Amphotericin B
What is the treatment duration for latent tuberculosis infection (LTBI) with isoniazid monotherapy?
9 months
Which enzyme is required for the activation of isoniazid in the body?
KatG
What is the primary mechanism of action of rifampin against mycobacteria?
Inhibition of RNA transcription
Which drug disrupts mycobacterial cell membrane metabolism and transport functions?
Pyrazinamide
What is the primary target of ethambutol in mycobacteria?
Cell wall synthesis
What is the reason for the increased incidence of mycoses?
Immune suppression
What is the mechanism of action of methenamine?
It is hydrolyzed to ammonia and formaldehyde in acidic urine, denaturing bacterial cell components
What is the first-line therapy for uncomplicated cystitis?
Nitrofurantoin
What is the resistance factor associated with trimethoprim?
Altered dihydrofolate reductase
What is the primary route of excretion for methenamine?
Renal excretion
What are the adverse effects of nitrofurantoin?
GI distress and contraindicated in renal insufficiency
What is the spectrum of activity for methenamine?
Effective against E. coli, Enterococcus spp., Staphylococcus spp., and some activity against Proteus and Pseudomonas aeruginosa
Which of the following is true about clindamycin?
It is primarily excreted through the bile
What is the primary mechanism of resistance associated with fluoroquinolones?
Mutations in DNA gyrase and topoisomerase IV
What is the primary route of excretion for fluoroquinolones?
Urine
Which enzyme is required for the activation of isoniazid in the body?
KatG
What type of bacteria are fluoroquinolones primarily effective against?
Gram-negative
What is the reason for the increased frequency of C. difficile associated with fluoroquinolones?
Disruption of normal gut flora
What is the primary route of excretion for amphotericin B?
Renal excretion
What is the mechanism of action of amphotericin B?
Fungicidal - binds to ergosterol, forming pores and disrupting membrane function
What is the drug of choice for several life-threatening mycoses?
Amphotericin B
What is the resistance factor associated with amphotericin B?
Ergosterol content and structure
In addition to intravenous infusion, in what other form can amphotericin B be administered?
Intrathecal administration
How is oral amphotericin B primarily used?
For local GI tract treatment
Which of the following is a potential adverse effect of quinolones and fluoroquinolones?
Gastrointestinal and central nervous system effects
What is the primary mechanism of resistance associated with quinolones and fluoroquinolones?
Altered target binding
How are sulfonamides primarily metabolized in the body?
Acetylation and conjugation in the liver
What is the spectrum of activity for sulfonamides?
Bacteriostatic against Gram-positive and Gram-negative organisms
How are quinolones and fluoroquinolones excreted from the body?
Renally
What is the primary route of excretion for sulfonamides?
Renally
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?
Pyrazinamide
What is the primary target of ethambutol in mycobacteria?
Cell wall synthesis
Which antimycobacterial drug is a prodrug activated by mycobacterial catalaseperoxidase (KatG) and targets enzymes required for mycolic acid synthesis?
Isoniazid
What is the treatment duration for latent tuberculosis infection (LTBI) with isoniazid monotherapy?
9 months
Which antimycobacterial drug blocks RNA transcription and is bactericidal against intracellular and extracellular mycobacteria?
Rifampin
What is the adverse effect associated with rifampin?
Hepatitis
Which drug can be used alone for UTIs and bacterial prostatitis?
Nitrofurantoin
What is the primary route of excretion for trimethoprim?
Renal excretion
What is the mechanism of action of methenamine?
Denaturing bacterial cell components
Which drug is contraindicated in renal insufficiency?
Methenamine
What is the first-line therapy for uncomplicated cystitis?
Nitrofurantoin
What is the mechanism of action of trimethoprim?
Inhibition of folic acid formation
Clindamycin is a chlorine-substituted derivative of lincomycin.
True
The mechanism of action of clindamycin is the same as macrolides.
True
Clindamycin is primarily effective against Gram-positive bacteria such as MRSA, streptococcus, and anaerobic bacteria.
True
Clindamycin distributes well to all body fluids, including CSF.
False
C. difficile is susceptible to clindamycin treatment.
False
Fluoroquinolones are considered 2nd line options for various indications due to resistance to Gram-negative and Gram-positive organisms.
True
Amphotericin B is a water-soluble drug for the treatment of mycotic infections
False
Amphotericin B binds to ergosterol, disrupting membrane function and leading to cell death
True
Amphotericin B is primarily excreted through the kidneys
True
Amphotericin B is the drug of choice for several life-threatening mycoses
True
Amphotericin B is primarily administered orally for subcutaneous and systemic mycotic infections
False
Amphotericin B has a wide antifungal spectrum, including Candida albicans and Aspergillus
True
Quinolones and fluoroquinolones are primarily effective against Gram-negative organisms only.
False
Sulfonamides are bacteriostatic and compete with PABA for binding sites.
True
Resistance to quinolones and fluoroquinolones can occur through altered target binding, decreased accumulation, and enzymatic degradation.
True
Sulfonamides are well absorbed orally, except for sulfasalazine.
True
Adverse reactions to quinolones and fluoroquinolones include gastrointestinal and central nervous system effects, tendinitis, and tendon rupture.
True
Folate antagonists like sulfonamides inhibit de novo synthesis of pyrimidines.
False
Trimethoprim is primarily hepatically metabolized
False
Methenamine is effective against E. coli, Enterococcus spp., Staphylococcus spp., and Pseudomonas aeruginosa
False
Nitrofurantoin inhibits protein synthesis in bacteria
False
Cotrimoxazole is a combination of trimethoprim and sulfamethoxazole
True
Resistance to trimethoprim can occur due to altered dihydrofolate reductase
True
Nitrofurantoin is the first-line therapy for uncomplicated cystitis
True
Rifampin is primarily used to treat multidrug-resistant TB (MDR-TB)
False
Isoniazid is a prodrug activated by mycobacterial catalaseperoxidase (KatG)
True
Pyrazinamide is active at high pH
False
Ethambutol inhibits arabinosyl transferases required for cell wall synthesis
True
Antifungal drugs target bacteria's rigid cell wall (chitin) and cell membrane (ergosterol)
False
Isoniazid's adverse effects include convulsions and rashes
True
Clindamycin is a first-generation quinolone antibiotic
False
Clindamycin is effective against MRSA, streptococcus, and anaerobic bacteria
True
Fluoroquinolones have an expanded spectrum of activity compared to 1st generation quinolones
True
Fluoroquinolones are considered 1st line options for various indications due to resistance to G -ve and G +ve organisms
False
Clindamycin is excreted primarily through the kidneys
False
C. difficile is resistant to clindamycin treatment
False
Amphotericin B is primarily administered orally for systemic mycotic infections
False
Amphotericin B binds to ergosterol, disrupting membrane function and causing cell death
True
Amphotericin B is extensively distributed in the CSF, vitreous humor, peritoneal fluid, and synovial fluid
False
Amphotericin B is primarily excreted through the urine over a long period of time
True
Resistance to Amphotericin B is primarily associated with altered ergosterol structure
True
Amphotericin B is primarily used for local gastrointestinal tract treatment
False
Quinolones and fluoroquinolones are primarily effective against Gram-negative organisms only.
False
Sulfonamides are primarily metabolized in the liver through acetylation and conjugation.
True
Resistance to quinolones and fluoroquinolones can occur through altered target binding, decreased accumulation, and enzymatic degradation.
True
Sulfonamides are well absorbed orally, with high bioavailability for sulfasalazine.
False
Adverse reactions to quinolones and fluoroquinolones include hematopoietic disturbances and kernicterus.
False
Folate antagonists like sulfonamides are bactericidal and primarily effective against Gram-negative organisms.
False
LTBI can be treated for 6 months with isoniazid monotherapy
False
Rifampin is primarily used to treat multidrug-resistant TB (MDR-TB)
False
Pyrazinamide disrupts mycobacterial cell membrane metabolism and transport functions
True
Ethambutol inhibits arabinosyl transferases required for RNA transcription in mycobacteria
False
Antifungal drugs primarily target fungi's DNA synthesis
False
Increased incidence of mycoses is primarily due to antibiotic resistance
False
Trimethoprim is primarily hepatically metabolized
False
Methenamine is primarily effective against Escherichia coli and Pseudomonas aeruginosa
False
Nitrofurantoin inhibits protein synthesis in bacteria
False
Mycobacterium tuberculosis is treated with first-line drugs like isoniazid, rifampin, pyrazinamide, and ethambutol
True
Cotrimoxazole has different pharmacokinetics and adverse effects compared to its individual components, trimethoprim and sulfamethoxazole
False
Nitrofurantoin is contraindicated in renal insufficiency
True
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.
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.
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