Antimicrobial chemotherapy Flashcards

(47 cards)

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

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
favipiravir mechanism of action
RNA dependent RNa polymerase inhibitor
26
chloroquine mechanism of action
viral entry inhibitor
27
hydroxychloroquine mechanism of action
viral entry inhibitor
28
oseltamivir mechanism of action
neuraminidase inhibitor
29
umifenovir mechanism of action
spike protein/ ACe2 membrane fusion inhibitor
30
examples of immunomodulatory agents
tocilizumab interferons
31
examples of adjunctive agents
arithromycin corticosteroids
32
tocilizumab mechanism of action
IL-6 inhibitor
33
interferon mechanism of action
activate interferon-stimulated genes -interfere with viral replication -immunomodulatory effects
34
azithromycin mechanism of action
antibacterial, used in combination with hydroxychloroquine for synergistic antiviral effect
35
corticosteroid mechanism of action
cytokine gene expression inhibitor
36
camostat mesylate mechanism of action
serine protease inhibitor
37
ACE inhibitor mechanism of action
Ace inhibitor; inhibitor the formation of angiotensin 11 ARB; angiotensin 11 receptor antagonist
38
how do bacteria transmit resistant
spontaneous mutation gene transfer or transferred resistance
39
spontaneous mutations
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
gene transfer or transferred resistance
usually spread through conjugative transfer of R plasmid (may be virally mediated)
41
4 mechanisms responsible for resistance to antimicrobial drugs
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
increased elimination
drug enters cell but efflux pump ejects it
43
drug-inactivating enzyme
enzyme modifies drug inactivates it
44
alteration in target
drug can't bind to the target
45
decreased uptake
prone proteins prevent entry into the cell
46
4 ways to slow the emergence and spread of antimicrobial resistance
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
in the absence of drug will a sensitive or resistant cell grow faster
the sensitive cell resistant cells use more energy