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Pharmacology Exam 2 > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

what is empiric therapy

A

may be one or multiple agents to give sufficient coverage
an “educated guess”
samples are good but takes several days for results

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2
Q

routes of administration for antibiotics?

A

topical, oral, intramuscular, IV, intravitreal (into the eye), or combination

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3
Q

what is drug resistance

A

bacteria evolve mechanisms to survive antibiotics
can occur if antibiotics are overprescribed, not thoroughly finished

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4
Q

What is the difference between Gram-positive and Gram-negative bacteria?

A

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.

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5
Q

What role does peptidoglycan play in bacterial cells?

A

provides structural rigidity to the bacterial cell wall.

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6
Q

examples of diseases caused by gram-positive bacteria?

A

strep throat, staph infections

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7
Q

examples of diseases caused by gram-negative bacteria?

A

e. coli and salmonella

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8
Q

why are Gram-negative bacteria often more resistant to antibiotics?

A

Their outer membrane acts as a barrier that can make it difficult for antibiotics to penetrate.

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9
Q

What is the significance of lipopolysaccharides (LPS) in Gram-negative bacteria?

A

LPS can be toxic when released into the body, contributing to disease.

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10
Q

What is a bactericidal agent?

A

a type of antibiotic that kills bacteria directly.

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11
Q

What is a bacteriostatic agent?

A

an antibiotic that inhibits bacterial growth and reproduction but does not directly kill the bacteria.

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12
Q

How do bactericidal and bacteriostatic agents differ in their mechanism of action?

A

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.

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13
Q

When might a bacteriostatic agent be preferred over a bactericidal agent?

A

Bacteriostatic agents are often preferred in cases where the immune system can effectively clear the infection after bacterial growth is inhibited.

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14
Q

What are the classes of antibiotics affecting cell wall synthesis?

A

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.

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15
Q

What are the classes of antibiotics affecting the cell membrane?

A

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.

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16
Q

What are the classes of antibiotics affecting protein synthesis?

A

Examples: Tetracyclines, Macrolides, Aminoglycosides
Action: Inhibit bacterial ribosomes, preventing protein synthesis, which is essential for bacterial growth and reproduction.

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17
Q

What are the classes of antibiotics affecting folate metabolism?

A

Examples: Sulfonamides (e.g., Bactrim)
Action: Inhibit the bacterial enzyme involved in folate synthesis, disrupting nucleic acid synthesis and bacterial growth.

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18
Q

What are the classes of antibiotics affecting bacterial DNA synthesis?

A

Examples: Fluoroquinolones (e.g., Ciprofloxacin)
Action: Inhibit DNA gyrase and topoisomerase IV, enzymes necessary for DNA replication, leading to bacterial cell death.

19
Q

Type I Drug Allergy Reaction Symptoms (basic)

A

immediate
urticaria rash
angioedema
can be life threatening
discontinue immediately and seek emergency services - epi-pen

20
Q

Type II Drug Allergy Reaction Symptoms (basic)

A

Cytotoxic - delayed by several days/weeks
hemolytic anemia=
Life threatening
discontinue drug - self resolves

21
Q

Type III Drug Allergy Reaction Symptoms (basic)

A

autoimmune - 1-3 wks
serum sickness, vasculitis
arthritis/arthalgia
fever/malar rash

discontinue drug: prognosis is excellent and self-resolves

22
Q

Type IV Drug Allergy Reaction Symptoms (basic)

A

cell mediated hypersensitivity
symptoms: contact dermatitis - rash
discontinue offending agent and can use steroids

23
Q

what are key safety concerns for penicillins?

A

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.

24
Q

What are the characteristics of 1st Generation Cephalosporins?

A

Effective against gram (+) bacteria; relatively weak against gram (-) bacteria.

25
Q

What are the characteristics of 2nd Generation Cephalosporins?

A

Increased activity against certain gram (-) pathogens; still effective against some gram (+) bacteria

26
Q

What are the characteristics of 3rd Generation Cephalosporins?

A

Somewhat less active against gram (+) cocci; more active against enteric gram (-) bacteria.

27
Q

What are the characteristics of 4th Generation Cephalosporins?

A

Extended spectrum against both gram (+) and gram (-) organisms; usually reserved for wide-spectrum activity and possible nosocomial infections.

28
Q

What are key side effects of cephalosporins?

A

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.

29
Q

what are the two contraindications for cephalosporins?

A

known allergies or hypersensitivity
those w/ history of hemophilia

30
Q

what are the key concepts of antiviral pharmacology?

A

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.

31
Q

what are some limitations for fungal anti-infectives?

A

significant side effects
narrow spectrum
poor tissue penetration
resistance

32
Q

what are the 3 main classes for antifungal drugs

A

polyene
antifungal azoles
allyamines

33
Q

MOA of Penicillins?

A

inhibiting synthesis of the bacterial cell wall

34
Q

MOA of Cephalosporins?

A

Interferes with the terminal step in bacterial cell wall formation by preventing proper cross-linking of the peptidoglycan

35
Q

MOA of Bacitracin?

A

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

36
Q

MOA of Aminoglycosides

A

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

37
Q

MOA of Tetracyclines

A

Inhibit bacterial protein synthesis by binding 30s subunit of ribosome which block the aminoacyl-tRNA to receptor site on the messenger RNA-ribosome complex

38
Q

MOA of Macrolides

A

Inhibit bacterial protein synthesis by binding to the 50s ribosomal subunit and preventing elongation of the peptide chain

39
Q

MOA of Sulfonamides

A

Sulfonamides act by inhibiting bacterial synthesis of folic acid (needed for nucleic acid and protein)

40
Q

MOA of Fluoroquinolones

A

Act by rapidly inhibiting bacterial DNA synthesis causing cell death

41
Q

MOA of Neurominidase Inhibitors?

A

Stops release of new viral particles from infected cells

42
Q

MOA of antiviral for HIV (truvada)?

A

Combination therapy for antiretroviral therapy (ART) and stops the formation of viral RNA to DNA

43
Q

what antibiotics not to use with pregnant women

A

macrolides
tetracycline
fluoroquinolones
sulfonamides

Pharmacology Exam 2 (6 decks)

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