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Foundations- Block 1 > Pharmacology: Antibiotics > Flashcards

Pharmacology: Antibiotics Flashcards

1
Q

Why are synthetic antibiotics not “true” antibiotics?

A

By definition, ABX are naturally occurring substances produced by a microorganism to target another microorganism

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2
Q

What is the ideal trait of antibiotics to effectively treat a patient? What microbes present an issue for this?

A

Selective toxicity

Viruses, cause they use our cell’s machinery
Fungi and Parasites: they’re euks and have similar functions

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3
Q

What is the minimum inhibitory concentration?

A

The concentration of an antibiotic where the colony cannot grow its numbers

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4
Q

What is the minimum bacteriocidal concentration?

A

The concentration that kills 99.9% of microorganisms in a colony

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5
Q

Why is MIC or MBC unreliable for clinical dosing?

A

Pharmacokinetic functions, such as first pass metabolism, protein binding, and metabolism, may decrease the effective dose of ABX in a patient

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6
Q

What areas are difficult to reach and may require a larger dose of antibiotics?

A

CNS, bone, adipose tissue

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7
Q

What is the reason some people have allergic responses to ABX?

A

ABX are antigenic, so they can react with the host immune system

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8
Q

What are bacteriostatic and bactericidal ABX?

A

Static: halt growth of bacterium

Cidal: kill and decrease concentration of ABX

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9
Q

Knowing the action of bacteriostatic ABX, how does a infection clear? What is a contraindication for this type?

A

Via host immune system

Compromised immunity

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10
Q

What are the chemotherapeutic spectrum types?

A

Broad, narrow, and extended

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11
Q

What are the three general areas that ABX target in a bacterial cell?

A

Nucleic acid synthesis, ribosomal protein synth, and the cell wall

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12
Q

Describe a few ways bacterium can defend and adapt against ABX?

A

Reduced entry or drug, efflux pumps (MDR protein), alteration of target proteins, alteration of metabolism

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13
Q

What kind of antibiotic destabilizes the cell wall of a bacterium?

A

Bactericidal

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14
Q

What enzyme links the layers of sugars in the peptidoglycan walls? What residues are used in this linkage?

A

Transpepditases

D-alanine

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15
Q

What do beta-lactam drugs target in a cell?

A

Transpeptidase in the cell wall

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16
Q

What is another name for transpeptidase?

A

Penicillin binding protein

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17
Q

What does penicillin target? What types of bacterium does this work against? What are its extended-spectrum agents? What do they work against?

A

1&2)Transpeptidases; & Gram positive bacterii and syphilis

3&4) amoxicillin, ampicillin, amniopenicillin; gram + and -

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18
Q

How effective is Penicillin against today’s bacterium?

A

Not good due to resistance; only acts well with syphilis

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19
Q

What class are cephalosporins? How can they be recognized via nomenclature?

A

Beta-lactams; largest B-lac class; have ceph- or cef- in name

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20
Q

What class is carbapenem ABX? What is its spectrum? Potency? What are common clinical uses?

A

B-lactam; broad spectrum and potent; usually used as a combination therapy drug; NEEDS INHIBITORS WITH ITS MOST UNSTABLE FORM

21
Q

Are monobactams considered true B-lactams? What does it target? What is its spectrum?

A

No; Gram -; narrow-spectrum

22
Q

What are common allergic responses to B-lactams?

A

Anaphylaxis/cytolytic anemia

23
Q

How are B-lactams allergenic? What if a patient is allergic to penicillin, what B-lactams can be prescribed?

A

Bind to human proteins;

NO B-lactams can be prescribed, it is a classwide (monobactams are safe since it does not have extra ring structure)

24
Q

What enzyme gives bacteria resistance to B-lactams?

A

B-lactamase

25
Q

What are some ways around B-lactamases? How does this work?

A

Combination therapy: strong B-lact with weak B-lact- weak B-Lac binds to enzyme, strong kills the bacteria

Chemical modifications to drugs (ie Methicillin from penicillin)

26
Q

How do glycopeptides work to be an ABX?

A

Bind to D-alanine and prevent crosslinking from transpeptidase

27
Q

What antibiotic is historically effective against MRSA? What class is this ABX? What is this drug not effective against? How has MRSA adapted to this drug?

A
  • Vancomycin
  • Glycopeptide
  • gram - bacteria
  • changed transpeptidases to not use D-alanine links in cell wall
28
Q

What type of antibacterial inserts into the plasmalemma and disrupts the cell wall? What are these effective against?

A

Lipopeptides (like Daptomycin)

-vancomycin resistant strains

29
Q

How do lipopeptides kill bacteria?

A

Create pores in the cell mem to disrupt osmolarity

30
Q

What does bacitracin do?

A

Prevents peptidoglycan subunits from reaching cell surface

31
Q

Are bacitracin and lipopeptides bacteriostatic or bactericidal? What are their draw backs? How are they typically administered?

A
  • cidal
  • very toxic to humans (nephrotoxic due to lipid mems in the kidney)
  • topical administration
32
Q

What are polymixins? What are they effective against? What are its drawbacks?

A

Positively charged peptides that disrupt cell membrane structure

  • gram -
  • cannot be taken orally due to charge
33
Q

Are direct nucleotide synthesis inhibitors cidal or static? Broad or narrow spectrum?

A

Cidal and broad

34
Q

How can bacteria become resistant to nucleotide synthesis disrupting ABX?

A

Changing the antibiotic, altered protein targets, expression of protective proteins

35
Q

What do quinolones do?

A

Inhibit topoisomerases on bacterial DNA during replication

36
Q

What does rifampin target?

A

RNA polymerase to prevent mRNA synth

37
Q

What does metronidazole do?

A

Cleaves daughter strand of DNA to prevent replication

38
Q

Are indirect DNA/RNA synth inhibs bacteriostatc or cidal? Broad or narrow?

A

Static; broad spectrum (even protozoa)

39
Q

How do sulfonamides function on bacteria?

A

Targets dihydropteroate synthase (in folic acid synthesis)

40
Q

How does trimethoprim target bacteria?

A

Inhibits dihydofolate reductase (in folic acid synthesis)

41
Q

How are indirect RNA/DNA synth inhibs resisted?

A

Increased substrates for their target proteins to overpower them

42
Q

Are protein synth inhibs bacteriocidal or static? Where do they function? Broad or narrow? Gram + or -?

A

Mostly static, but can be cidal

Mostly on the ribosome

Can be broad or narrow

Can be Gram - or +

43
Q

Why shouldnt protein synth inhibs be used as first line against infections?

A

Toxicity is abundant in this class

44
Q

Where does tetracycline bind? What does it do?

A

Binds to 30s subunit/ disrupts tRNA interaction

45
Q

Where does erythromycin bind? What does it do?

A

Binds to ribosome/ prevents translocation of peptide chain

46
Q

Where does chloramphenicol bind? What does it do?

A

Mimics/binds to amino group attached to tRNA; prevents formation of peptide chain

47
Q

What are some reasons to do combination therapy?

A

Multiple microbes, very ill patients, prevent spread of drug resistant pathogens, reduce chances of toxicity

Cons: drug-drug interactions

48
Q

What are addative and synergistic combinations?

A

Addative is the addition of each drug’s potency

Synergy is 1+1=4 (more than sum of parts)

49
Q

What is a good example of antagonistic combinations?

A

Tetracyclines and penicillins- tet reduce efficacy of penicillin

(Penicillin better on growing bacterial colonies)

Foundations- Block 1 (17 decks)

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