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Drugs And Infectious Diseases > Antibacterial Pharmacology > Flashcards

Antibacterial Pharmacology Flashcards

1
Q

Discovery of abx

A

Alexander Fleming 1928 Penicillium mold on Petri dish Later used as a “cure all” drug, resulting in resistance

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2
Q

Cycle of ID

A

susceptible host -> causative agent -> reservoir -> Portal of Exit blood -> Mode of transmission -> portal of entry blood

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3
Q

Properties of bacteria

A
  • Prokaryotic cells - no membrane enclosed organelles - single cellular - reproduce through binary fission - plasmids and nucleoid DNA are easy to transport and communicate because they are free -> cause for resistance
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4
Q

Gram Positive Bacteria

A
  • thick peptidoglycan - relatively featureless - no outer membrane - susceptible to cell wall disruption
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5
Q

Gram Negative Bacteria

A
  • cytoplasmic and outer membranes - thin peptidoglycan - lots of lipids because of outer membrane - resistant to cell wall disruption
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6
Q

Cell wall structure

A

Peptidoglycan Layer: rigid glycerin cross-linked by flexible peptide bridges Periplasmic spaces: Very small on gram (+), multiple on gram (-): generate B-lactamases which inhibit abx Wall tetracholic acid: accessory protein on g(+) Lipoprotein, Porin protein, LPS: on gram (-) Lipoprotein: protection layer Porin: if needed bacteria can down regulate LPS: for inflammatory response

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7
Q

PBP

A
  • Important for MoA for abx - enzymes that catalyze: transglycosylation, transpeptidation, carboxypeptidation, endopetidation - for: cell wall synthesis (peptidoglycan), cell wall remodeling, cell division, cell shape
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8
Q

Bactericidal

A

direct action of bacteria - kill/lysis biochemical pathways in wall assembly compromised cell wall progressively weaker cells - daughter cells don’t have what is needed to keep cell wall up. eventually integrity of cell wall fails

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9
Q

Bacteriostatic

A

does not directly kill may be reversible - or relapse target nucleic acid synthesis and protein synthesis slow bacteria growth allows immune system to act and destroy the cells

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10
Q

Broad spectrum

A

Treat many kinds of infections - wide range of bacteria - targets common structures so can also go against commensal bacteria -> LEADS TO SUPERINFECTION - Once the agent is identified it should be discontinued

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11
Q

Superinfection

A

Bacteria that aren’t supposed to grow well in a particular area but do because the niche (normally keeps it away) is dead.

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12
Q

Narrow spectrum

A

Against a single or few bacteria (specific) - when agent is known - reduces chance of superinfection and abx resistance

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13
Q

Classification of bacteria

A

With 16s ribosome which share amplified DNA from a single cell. Polymer chain reaction is used to compare (DNA template to RNA to ribosomal subunits)

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14
Q

Where do abx come from?

A

Soil (but hard to isolate) Bottom feeders like roaches, catfish, alligators, bacteriophages (viruses that infect bacteria), cannabinoids. They are exposed to more bacteria than anyone else so they evolved to develop mechanisms to protect themselves.

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15
Q

MoA of abx

A
  • inhibition of bacterial cell wall synthesis - direct action on cell membrane - inhibition of protein synthesis - modification of protein synthesis (change how it works) - inhibition of nucleic acid synthesis - inhibition of biosynthetic pathways
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16
Q

Inhibition of Cell wall synthesis

A

Attack cell wall synthesis - Beta Lactams (PBP in periplasmic space)

Penicillins, cephalosporins - inhibit transpeptidase from creating long chains of glycopeptide polymer chains (D-ala addition) carbapenems, monobactams

Inhibit pathways of peptidoglycan and sugars: Vancomycin (periplasmic space) & Bacitracin (cytoplasm)

Attack cell membrane Polymyxins

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17
Q

3 places to attack

A
  1. cell wall synthesis
  2. Protein synthesis
  3. Nucleic acid synthesis
18
Q

Nucleic acid synthesis

A

Attack DNA and/or biosynthetic pathways

Folate synthesis Sulfonmides, Trimethoprim

DNA Gyrase/ topoisomerase (mRNA translation- unwinding and unkinking DNA) Quinolones

RNA polymerase (reads sequencing) Rifampin

19
Q

Protein synthesis

A

Intracellular - interfere with translation Together 50s and 30s make 70s subunit. 50s subunit: Macrolides, clindamycin, linezolid, chloramphenicol, streptogramins 30s subunit: Tetracyclines, aminoglycosides

20
Q

Detergents

A

Cell wall is degraded because it suck out lipids.

21
Q

Daptomycin

A

Inhibits cell wall by squishing lipid tail into cell wall lipids -> forms complexes -> forms into channels (from the subunits coming together) -> disrupts the normal order of cell/ influx and eflux of materials

22
Q

Penicillins and other B-lactam MoA

A

5 AA peptide ends in D-ala D-ala. The PBP removes the end alanine to form a cross-link with a nearby peptide (gives cell wall rigidity). B-lactam abx are analogues of D-ala D-ala which covalently bonds to PBP - inhibiting transpeptidation reaction and stops peptidoglycan synthesis - cell dies.

23
Q

Half life of penicillins & clinical

A

penicillins = 30 mins / 10 hours for renal failure. 1-2 hours before or after meals. without regard with amoxicillin amplicillins = 1 hour these are cleared with kidney so adjust when needed nafcillin - biliary excretion oxacilin, dicloxacillin - biliary and kidney -> no dose adjustment

24
Q

Tetracyclines MoA

A

Binds to 30s active site. can’t make proteins to let the chain grow

25
Q

Macrolides MoA

A

binds to 50s - interferes with peptide conjugation

26
Q

Aminoglycoside MoA

A

blocks initiation complex of 50s binding to 30s -> causes miscoding of proteins which won’t fold and bind to active site -> can’t move out of ribosome (translocation step)

27
Q

Folate synthesis Inhibition

A

PABA->Dihydrofolic acid->tetrahydrofolic acid ->purines ->DNA Sulfonamides competes with PABA at dihydropteroate synthase Trimethoprim inhibits dihydrofolate reductase

28
Q

Bacterial Resistance

A
  1. lots of bacteria - few are resistant
  2. use of abx - kills bad bacteria and good bacteria
  3. still some resistant that are left and grow (no good bacteria to protect)
  4. sharing of information to other bacteria -> more reisistance
29
Q

Topoisomerase 4

A

Divides/ seperates part of DNA so daughter cells can get equal amounts

Used in inhibition of nucleic acid synthesis

think DNA gyrase - unwinding DNA inhibited by fluroquinolones

30
Q

Origin of drug resistance

A
  • bacteria in inactive site (non dividing)
  • Genetics (horizontal gene transfer - ex) PBP dont bind to B-lactams on MRSA)
  • Spontaneious mutation: misreading, mutation
  • plasmid-encoded resistant gene products
  • cross resistance of one type: same MoA

drug doesnt reach the target

drug activity is decreased/ destroyed

drug target is altered

31
Q

How do bacteria exchange genetic information?

A

Transduction - bacterial virus - transfer its genes into bacteria ->resistance from virus

Transformation - naked DNA transfer
Ex) shock E. Coli then transfer DNA -> gets sucked up by another

Conjugation - transfer by direct cell-cell contact - through pilli of fusion of membrane

Transposition - transposon medicated exchange
: small segments jump out of DNA and go elsewhere to disrupt chromosomes

32
Q

Production of enzymes that destroy or inactivate the drug

A

B-lactamases inactivate B-lactam Abx

B-lactamases are normally in bacteria and activate Antibodies -> too much B-lactamases = resistance

Aminoglycosides altered by acetylation, phosphorylation. or adenylation

just enough change to not work with antibodies
Ex) kinases (protein that phosphorylates) can mutate so that it disrupts normal order

Chloramphenicol acetyltransferases in inactive chloramphenicol

33
Q

Decrease entry or increased efflus

A

Decreased active transport across membrane in anaerobic conditions - effect on channels -> can’t get in, can’t get out

Down regulation of porin expression -> throws everything out of the cell

Mutation in efflux transporter

34
Q

Altered structural target for the drug

A

Altered:

binding sites on ribosonal subunits (decreased affinity for macrolides - protein syn inhibitors)

binding proteins (B-lactams no longer able to bind to PBP)

mutation in DNA genes (decreased affinity for abx-fluroquinolones)

35
Q

Alterante metabolic pathway

A

Resistant strains produce D-ala D-lactate instead of D-ala D-ala (affinity for Vancomycin reduced)

Resistant strains overproduce PABA which antagonizes sulfonamide abx.

36
Q

MIC

A
  • Minimum inhibitory concentration
  • lowest concentration of abx required to inhibit bacterial growth
  • defines susceptibility of drug
  • DOES NOT indicate bactericidal activity
37
Q

MBC

A
  • Minimum Bacerial Concentration
  • concentration of abx required to inhibit bacterial growth by 99.9%
  • more quantitative than MIC
38
Q

PAE

A
  • Post abx effect
  • period of bacterial growth supression after brief exposure to drug
  • abx with PAE requires LESS frequent administration
    [abx] < MIC
    time afterward is still slowing growth
39
Q

PALE

A
  • Post-antibiotic Leukocyte effect
  • period during which bacteria are more susceptible to leukocyte action
  • After drug has cleared, stimulation of phagocytosis mechanism still at work
  • also explains drug efficacy below MIC
40
Q

Broth/Agar dilution Test

A

Same number of bacteria in each tube but at different concentrations of the drug.

The minimum inhibitory concentration of drug = not cloudy

41
Q

Disk diffusion test

A

Filter paper disks concentrated with abx.

Check for zone of inhibition.

No zone = resistant

Little zone = intermediate

Large zone = sensitive

42
Q

Gradient Diffusion Test

A
  • gradient of abx
  • higher concentration of abx as go up on strip
  • Find MIC/ decreasing growth as you go down (lower concentration of abx)

Drugs And Infectious Diseases (4 decks)

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