Antimicrobial chemotherapy Flashcards

1
Q

what do anti-fungal drugs target

A

class 2 reactions

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2
Q

what do fungal cell membranes contain

A

ergosterol
instead of cholesterol

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3
Q

what do drugs that inhibit ergosterol synthesis do

A

impair fungal membrane function without affecting the host cell membrane

e.g. fluconazole

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4
Q

drugs targeting endoplasmic reticulum

A

allylamines
benzylamines
imidazoles
triazoles

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5
Q

drugs targeting cell wall

A

echinocandins

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6
Q

drugs targeting plasma membrane

A

polyenes (amphotericin B)

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7
Q

drugs targeting DNA synthesis

A

flucytosine

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8
Q

drugs targeting the mitotic spindle

A

griseofulvin

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9
Q

what is fungal synthesis of nucleic acid dependent on

A

folate mechanism
some anti-fungals are converted to anti-metabolites (false substrates) in fungi but not in host cells

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10
Q

what is flucytosine metabolised to in fungi

A

5-FU

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11
Q

which stages of the cell cycle to anti-viral drugs target

A

entry to host cells
nucleic acid replication
viral protein synthesis
exit from host cells

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12
Q

how do anti-viral drugs target the entry to host cells

A

drugs may inhibit fusion of virus with host cell membrane following binding to surface receptor

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13
Q

how do anti-viral drugs target nucleic acid replication

A

drugs may inhibit DNA/RNA polymerases e.g. aciclovir or retroviral reverse transcriptase (zidovudine)

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14
Q

how do anti-viral drugs target viral protein synthesis

A

may inhibit girl proteases involved in processing large poly proteins

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15
Q

how do anti-viral drugs target exit from host cells

A

may inhibit neuraminidase-catalysed cleavage (oseltamivir)

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16
Q

attachment and entry inhibitor anti-virals

A

maraviroc
enfuvirtide

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17
Q

ion channel blockers anti-virals

A

amantadine
rimantadine

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18
Q

polymerase inhibitors anti-virals

A

acyclovir
zidovudine
efavirenz

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19
Q

integrase inhibitors anti-virals

A

raltegravir

20
Q

protease inhibitors anti-virals

A

saquinavir
ritonavir

21
Q

neuraminidase inhibitors anti-virals

A

zanamivir
oseltamivir

22
Q

remdesivir mechanism of action

A

RNA- dependent RNA polymerase inhibitor

23
Q

ribavirin mechanism of action

A

RNA dependent RNA polymerase inhibitor

24
Q

Lopinavir-ritonavir mechanism of action

A

3CL protease inhibitor

25
Q

favipiravir mechanism of action

A

RNA dependent RNa polymerase inhibitor

26
Q

chloroquine mechanism of action

A

viral entry inhibitor

27
Q

hydroxychloroquine mechanism of action

A

viral entry inhibitor

28
Q

oseltamivir mechanism of action

A

neuraminidase inhibitor

29
Q

umifenovir mechanism of action

A

spike protein/ ACe2 membrane fusion inhibitor

30
Q

examples of immunomodulatory agents

A

tocilizumab
interferons

31
Q

examples of adjunctive agents

A

arithromycin
corticosteroids

32
Q

tocilizumab mechanism of action

A

IL-6 inhibitor

33
Q

interferon mechanism of action

A

activate interferon-stimulated genes
-interfere with viral replication
-immunomodulatory effects

34
Q

azithromycin mechanism of action

A

antibacterial, used in combination with hydroxychloroquine for synergistic antiviral effect

35
Q

corticosteroid mechanism of action

A

cytokine gene expression inhibitor

36
Q

camostat mesylate mechanism of action

A

serine protease inhibitor

37
Q

ACE inhibitor mechanism of action

A

Ace inhibitor; inhibitor the formation of angiotensin 11
ARB; angiotensin 11 receptor antagonist

38
Q

how do bacteria transmit resistant

A

spontaneous mutation
gene transfer or transferred resistance

39
Q

spontaneous mutations

A

happens when cells replicate
within a population there will be some bacteria with acquired resistance
drug eliminates the sensitive organisms and the resistant ones proliferate

40
Q

gene transfer or transferred resistance

A

usually spread through conjugative transfer of R plasmid (may be virally mediated)

41
Q

4 mechanisms responsible for resistance to antimicrobial drugs

A
  1. inactivating enzymes that destroy the drug (beta lactamases)
  2. decreased drug accumulation (tetracyclins, beta lactams)
  3. altering the binding sites ( aminoglycosides and erythromycin)
  4. development of alternative metabolic pathways (sulphonamides e.g. dihydropteroate synthease and trimethoprim e.g. dihydrofolate reductase)
42
Q

increased elimination

A

drug enters cell but efflux pump ejects it

43
Q

drug-inactivating enzyme

A

enzyme modifies drug
inactivates it

44
Q

alteration in target

A

drug can’t bind to the target

45
Q

decreased uptake

A

prone proteins prevent entry into the cell

46
Q

4 ways to slow the emergence and spread of antimicrobial resistance

A
  1. understand the mechanisms
  2. use of combination therapies
  3. responsibilities of physicians: work to identify the microbe and prescribe suitable antimicrobials, educate patients
  4. responsibilities of patients: carefully follow instructions
47
Q

in the absence of drug will a sensitive or resistant cell grow faster

A

the sensitive cell
resistant cells use more energy