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Pharmacology. > 11. Antimicrobials > Flashcards

11. Antimicrobials Flashcards

1
Q

What kind of drug is linezolid?

A

Reversible MAO inhibitor

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2
Q

What type of organism are bacteria and what does this mean?

A

Prokaryotes,

Single called without nuclei

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3
Q

What is the overall aim of antibiotic therapy and what are the targets?

A

Selective toxicity of prokaryotes very eukaryote cells

  1. Attack bacterial targets but not human e.g. bacterial cell wall or folate metabolism
  2. Attack bacterial physiological/metabolic mechanisms that are different from humans e.g. ribosome or nucleic acid synthesis.
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4
Q

How are bacterial cell walls made?

A

Contain call wall and cell membrane.

Cell wall Made of two linear peptidoglycan polymers of alternating NAG and NAM amino sugars he,d together by glycosidic bonds. NAM amino acids have side chains that can link to chains on the other strand via transpesidases.

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5
Q

What is the difference in cell walls of gram negative vs. Gram positive cell walls?

A

Gram positive = cell membrane with thick outer well wall

Gram positive = membrane, then wall (thinner) then membrane.

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6
Q

What are the different categories of antibiotics?

What do they target

A

Cell wall:
Beta lactams = penicillins, carbapenems, monbactams and cephalosporins
Glycopeptides

Bacterial protein synthesis:
Aminoglycosides
Tetracyclines
Macrolides
Lincosamides
Fusidanes

Folate synthesis and metabolism:
Sulphonamides

DNA inhibitors:
Quinolones
Nitromidazoles
Rifamycins

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7
Q

Are beta lactams bacteriocidal or static?

How do they work?

A

Cidal

Beta lactam ring resembles D-alanyl D-alanine which is an amino acid attached to NAM in bacterial cell wall. Suicide substrate for transpepsidase enzymes, weakening cell wall and causing osmotic lysis.

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8
Q

What are transpepsidase enzymes in bacterial cell walls otherwise known as?

A

Penicillin binding proteins.

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9
Q

What causes penicillin resistance?

How can this be avoided?

A

Bacteria produce beta lactamase which degrades the beta lactam ring.

Clavulanic acid and tazobactam inhibit beta lactamase

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10
Q

What do penicillins cover and what are the names?

A

Gram positive and negative

-illins

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11
Q

What are the gram positive and negative bacteria?

A

Positive = staph and streps

Negative = everything else

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12
Q

What are the carbapenems?

How do they work?

What do they cover?

A

Meropenems and other -enems.

Broad spectrum with high affinity for PBP’s so can get in gram -be cell wall.

Used for resistant gram negatives.

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13
Q

What are the monobactams?

How do they work?

A

Aztreonam

Can traverse cell wall due to high affinity for PBP’s. Only cover gram negative.

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14
Q

What are the cephalosporins and how do they work?

A

Call the cefs-

Beta lactam ring fused to dihydrothiazine ring.

Bind to PBP’s

Cover both gram positive and negative, but more so negative.

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15
Q

Are the glycopeptides static or cidal?

What are the drugs?

What do they cover?

A

Static. Bind to peptidoglycan monomers to block PBP’s.

Too bulky to penetrate gram negative so only positive.

Vanc and teicoplanin.

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16
Q

How do vanc and Tesco compare to each other?

What are the side effects?

A

Vanc = no oral BA, so oral only for c-diff.
Toxicity = ototoxicity, histamine release = red man, tachy and hypotension, and phlebitis (dilute).

Teicoplanin = 4 x as strong as vanc. More active against steep and enterococci.

Both cover MRSA.

17
Q

How do bacterial ribosomes compare to human?

A

Bacterial = 30s and 50s. Human = 40s and 60s.

18
Q

What are the aminoglycosides?

How do they work?

What are they inhibited/amplified by?

A

Amikacin and the -micins like gent.

Bind to ribosomal 30s, but are large and polar so are moved by active transport.

Inhibited by: mg, ca, acidosis and low O2.
Amplified by beta lactams which have a synergistic effect (disrupt cell wall, so help entry)

19
Q

What are the side effects of the aminoglycosides?

A

Ototoxicty, nephrotoxicity and muscle weakness.

20
Q

What are the tetracyclines?

How do they work?

What inhibits them?

When should they be avoided?

A

-cycline

Bind to 30s

Chelated by calcium, milk, mg and antacids.

Avoid in renal and hepatic failure, pregnant and kids. Deposited in growing bones and teeth causing hypoplasia and staining.

21
Q

Are the macrolides static or cidal?

What are the drugs?

How do they work?

What do they cover?

Side effects?

A

Both

Mycins e.g. erythromycin, clari and azithro

Bind to 50s (inhibit translocation)

Most gram positive and negative anaerobes.

Inhibit CYP3A4 and PGP. Cause prolonged QT and pro kinetic e.g. the runs.

22
Q

Are the linacosamides static or cidal?

Drugs?

How do they work?

What do they cover?

A

Both

Clindamycin

Bind to 50s

Cover gram positive and anaerobes. Good for bone penetration.

23
Q

What are the fusidanes?

How do they work?

What are they good for?

A

Fusidic acid

Cidal, preventing protein synthesis, by preventing elongation.

Cover gram positive and are good for bone and cerebral abscesses.

24
Q

What human/bacterial difference is exploited in folate synthesis?

What antibiotics target this?

A

PABA is an essential metabolite for folate synthesis. Humans have to get folate from diet.

Sulphonamides e.g. sulfamerhoxazole are PABA analogues and also interfere with dihydropholate synthetase.

Trimethoprim and Co-trimox (= trimethoprim plus above). Inhibits dihydrofolate reductase but is 50000x more attracted to bacterial.

25
Q

Are the quinolones cidal or static?

What are the drugs?

How do they work?

Side effects?

A

Cidal

-floxacins

Target topoisomerase (DNA production) in mostly gram negative. Good for atypical.

Can cause: seizures, Achilles tendon rupture, prolonged QT and haemolytic reactions in G6PD.

26
Q

What are the nitromidazoles?

How do they work?

What are they good for?

S/E?

A

Metronidazole

Diffuses into cell and disrupts DNA via free radical damage. 100% oral BA

Anaerobes and protozoa

S/E: nausea, metallic taste, alcohol gives disulfiram reaction, ill and flushed and hypotension.

27
Q

How does rifampicin work?

S/E:

A

Binds to RNA polymerase stopping transcription

CYP450 inhibitor causing red secretions

28
Q

How does aciclovir work?

What does it cover?

What are the side effects?

A

Infected cells have enzyme thymidine kinase, aciclovir is a substrate for this. It is converted to aciclovir mono phosphate then active triphosphate which inhibits DNA polymerase

Herpes simplex and varicella zoster

Renal impairment, thrombophlebitis and CNS issues e.g. tremor and confusion.

29
Q

What is zidovudine for and what does it target?

A

HIV and targets nucleoside reverse transcriptase

30
Q

What are the two different classes of anti fungal?

A

Polyenes and azoles

31
Q

How do polyenes work?

Drugs?

S/E?

A

Targets fungal cell wall and creates a pore.

Amphotericin B (IV)

S/E: nephrotoxicity

32
Q

What are the azoles?

How do they work?

S/E?

A

Triazoles: fluconazole and itraconazole
Imidazole: ketoconazole and miconazole

Prevent amino acid conversion of essential component of fungal cell wall.

Inhibit CYP450.

Pharmacology. (22 decks)

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