Antibiotics Flashcards
what is empiric therapy
may be one or multiple agents to give sufficient coverage
an “educated guess”
samples are good but takes several days for results
routes of administration for antibiotics?
topical, oral, intramuscular, IV, intravitreal (into the eye), or combination
what is drug resistance
bacteria evolve mechanisms to survive antibiotics
can occur if antibiotics are overprescribed, not thoroughly finished
What is the difference between Gram-positive and Gram-negative bacteria?
Gram-positive bacteria have a thick peptidoglycan layer and appears purple 2° retaining the stain
Gram-negative bacteria have a thin peptidoglycan layer and appears pink 2° being counterstained with safranin.
What role does peptidoglycan play in bacterial cells?
provides structural rigidity to the bacterial cell wall.
examples of diseases caused by gram-positive bacteria?
strep throat, staph infections
examples of diseases caused by gram-negative bacteria?
e. coli and salmonella
why are Gram-negative bacteria often more resistant to antibiotics?
Their outer membrane acts as a barrier that can make it difficult for antibiotics to penetrate.
What is the significance of lipopolysaccharides (LPS) in Gram-negative bacteria?
LPS can be toxic when released into the body, contributing to disease.
What is a bactericidal agent?
a type of antibiotic that kills bacteria directly.
What is a bacteriostatic agent?
an antibiotic that inhibits bacterial growth and reproduction but does not directly kill the bacteria.
How do bactericidal and bacteriostatic agents differ in their mechanism of action?
Bactericidal agents disrupt essential processes, leading to bacterial cell death, while bacteriostatic agents interfere with protein synthesis or other functions to prevent bacteria from multiplying.
When might a bacteriostatic agent be preferred over a bactericidal agent?
Bacteriostatic agents are often preferred in cases where the immune system can effectively clear the infection after bacterial growth is inhibited.
What are the classes of antibiotics affecting cell wall synthesis?
Examples: Penicillins (e.g., Amoxicillin), Cephalosporins (e.g., Cefazolin), Vancomycin
Action: Inhibit the formation of the bacterial cell wall, leading to cell lysis and death.
What are the classes of antibiotics affecting the cell membrane?
Examples: Polymyxins (e.g., Polymyxin B) ((antibiotics for gram-negative bacteria))
Action: Disrupt the integrity of the bacterial cell membrane, causing leakage of cellular contents and cell death.
What are the classes of antibiotics affecting protein synthesis?
Examples: Tetracyclines, Macrolides, Aminoglycosides
Action: Inhibit bacterial ribosomes, preventing protein synthesis, which is essential for bacterial growth and reproduction.
What are the classes of antibiotics affecting folate metabolism?
Examples: Sulfonamides (e.g., Bactrim)
Action: Inhibit the bacterial enzyme involved in folate synthesis, disrupting nucleic acid synthesis and bacterial growth.
What are the classes of antibiotics affecting bacterial DNA synthesis?
Examples: Fluoroquinolones (e.g., Ciprofloxacin)
Action: Inhibit DNA gyrase and topoisomerase IV, enzymes necessary for DNA replication, leading to bacterial cell death.
Type I Drug Allergy Reaction Symptoms (basic)
immediate
urticaria rash
angioedema
can be life threatening
discontinue immediately and seek emergency services - epi-pen
Type II Drug Allergy Reaction Symptoms (basic)
Cytotoxic - delayed by several days/weeks
hemolytic anemia=
Life threatening
discontinue drug - self resolves
Type III Drug Allergy Reaction Symptoms (basic)
autoimmune - 1-3 wks
serum sickness, vasculitis
arthritis/arthalgia
fever/malar rash
discontinue drug: prognosis is excellent and self-resolves
Type IV Drug Allergy Reaction Symptoms (basic)
cell mediated hypersensitivity
symptoms: contact dermatitis - rash
discontinue offending agent and can use steroids
what are key safety concerns for penicillins?
V site reactions (burning, phlebitis), CNS effects (headache, dizziness, confusion, seizures), blood dyscrasias, altered bacterial flora (risk of superinfections), severe allergic reactions (urticaria, anaphylaxis), and potential failure of oral contraceptives.
What are the characteristics of 1st Generation Cephalosporins?
Effective against gram (+) bacteria; relatively weak against gram (-) bacteria.
What are the characteristics of 2nd Generation Cephalosporins?
Increased activity against certain gram (-) pathogens; still effective against some gram (+) bacteria
What are the characteristics of 3rd Generation Cephalosporins?
Somewhat less active against gram (+) cocci; more active against enteric gram (-) bacteria.
What are the characteristics of 4th Generation Cephalosporins?
Extended spectrum against both gram (+) and gram (-) organisms; usually reserved for wide-spectrum activity and possible nosocomial infections.
What are key side effects of cephalosporins?
hypersensitivity (urticarial rash, bronchospasm, anaphylaxis), cross-sensitivity (especially with earlier generations), risk of superinfection, possible bleeding (due to vitamin K disruption), and potential for renal impairment.
what are the two contraindications for cephalosporins?
known allergies or hypersensitivity
those w/ history of hemophilia
what are the key concepts of antiviral pharmacology?
Antivirals interfere with viral replication to stop multiplication and demonstrate selective toxicity by inhibiting viral processes while sparing host cells.
Note: Antivirals are ineffective against bacteria or fungi.
what are some limitations for fungal anti-infectives?
significant side effects
narrow spectrum
poor tissue penetration
resistance
what are the 3 main classes for antifungal drugs
polyene
antifungal azoles
allyamines
MOA of Penicillins?
inhibiting synthesis of the bacterial cell wall
MOA of Cephalosporins?
Interferes with the terminal step in bacterial cell wall formation by preventing proper cross-linking of the peptidoglycan
MOA of Bacitracin?
Inhibits bacterial cell wall synthesis by inhibiting the movement of a precursor of peptidoglycan through the cell membrane from the cytoplasm to the cell wal
MOA of Aminoglycosides
Inhibit bacterial protein synthesis by binding to the 30s subunit of the bacterial ribosome which inhibits bacterial protein synthesis and causes incorrect reading of genetic code
MOA of Tetracyclines
Inhibit bacterial protein synthesis by binding 30s subunit of ribosome which block the aminoacyl-tRNA to receptor site on the messenger RNA-ribosome complex
MOA of Macrolides
Inhibit bacterial protein synthesis by binding to the 50s ribosomal subunit and preventing elongation of the peptide chain
MOA of Sulfonamides
Sulfonamides act by inhibiting bacterial synthesis of folic acid (needed for nucleic acid and protein)
MOA of Fluoroquinolones
Act by rapidly inhibiting bacterial DNA synthesis causing cell death
MOA of Neurominidase Inhibitors?
Stops release of new viral particles from infected cells
MOA of antiviral for HIV (truvada)?
Combination therapy for antiretroviral therapy (ART) and stops the formation of viral RNA to DNA
what antibiotics not to use with pregnant women
macrolides
tetracycline
fluoroquinolones
sulfonamides
