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Pharmacology > viruses and bacteria > Flashcards

viruses and bacteria Flashcards

1
Q

what is the best protection against viruses?

A

vaccines, because developing viral selective drugs is very hard

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2
Q

what is the usual combination for HAART?

A
    • Two nucleoside reverse transcriptase inhibitors
    • one NNRT or a protease inhibitor
    • HAART does not eradicate HIV but it keeps it viral load down
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3
Q

how do interferons work?

A

those work by modulating the immune response
they bind to specific gangloside receptors which causes the production of enzymes that inhibit the translation of viral mRNA into viral proteins

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4
Q

what is Palivizumab?

A

this is given as prophyalxis to children who are at high risk of contracting RSV. This is an Ig which prevents the entry of the virus into the cell

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5
Q

what is enfuvritide?

A

this prevents entry of HIV-1 into cells, it is an analogue of gp41 which is essential to viral entry into the cell

given to patients who do not respond to normal HAART

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6
Q

What is the mechanism of action of amanatidine? and what is it used for?

A

used for:

  • prophylaxis and treatment of influenza A
  • it blocks the M2 channel which will allows proton influx, which is necessary for the viral uncoating
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7
Q

what is the mechanism of action for Zanamivir or Oseltmavir?

A

those are used as prophylaxis and treatment for influenza A and B

  • both those are sialic acid analogues
  • so they inhibit neuromindase action
  • prevent budding of the virus from host cells
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8
Q

what is the mechanism of action of acycloivr?

A

acyclovir is given as a pro-drug, it becomes mono-phosphorylated by viral thymidine kinase. then double phosphorylated by cellular kinases. this inhibits DNA polymerase of the virus and inhibits its viral replication

acyclovir as an acyloguanosine trisphosphate

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9
Q

give two reasons why acyclovir has selective toxicity

A

because only infected cells have thymidine kinase with a high affinity to mono-phospharylate the drug

also the triple phosphorylated drug has a higher affinity for viral DNA polymerase than cellular DNA polymerase

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10
Q

when is acyclovir used?

A

to treat HSV and VZV

high dosages can be used for shingles

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11
Q

when is ganciclovir used? and why?

A

in extreme causes of CMV (e.g. CMV retinitis) given I.V

given because CMV does not have thymidine kinase. the drug itself can cause neutropenia

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12
Q

how does Zidovudine work?

A

AZT; a thymidine analogue (N3 instead of OH)

  • triple phosphorylated by cellular kinases
  • but the phosphorylate drug has a much higher affinity for the reverse transcriptase than cellular DNA polymerase
  • this drug is a nucleoside analogue
  • the drug does not have OH at its 3’end so cannot form the phosphodiesterase bonds required for chain elongation
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13
Q

what is so special about the resistance of the NRTI

A

they do not have cross resistance. and using more than one type suppresses resistance

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14
Q

give the four stages of the viral response to AZT

A

1: this is a rapid decrease in viral plasma load (days)
2. (weeks) a rapid increase of viral plasma load, independent of resistance
3. months - slow increase in viral load probably due to resistance
4. this is rebound of virus load to baseline line because of withdrawal of treatment

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15
Q

what is nevarapine?

A

this is a NNRTI - which acts by denaturing RT

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16
Q

What is saquinavir and Indinavir?

A

those are protease inhibitors and they prevent the formation of mature viral particles

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17
Q

what is ribavarin?

A

this is a guanosine analogue
used in treatment of RSV
inhibits viral RNA polymerase
also inhibits GTP dependant enzymes which affects viral mRNA capping

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18
Q

What is saquinavir and Indinavir, ritonavir, idinavir

A

those are protease inhibitors and they prevent the formation of mature viral particles

this is because proteases are required for splicing viral proteins which are polycistronic

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19
Q

what is ribavarin?

A

this is a guanosine analogue
used in treatment of RSV
inhibits viral RNA polymerase
also inhibits GTP dependant enzymes which affects viral mRNA capping

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20
Q

what is the treatment for Hep B virus?

A

Treatment of Hepatitis B:
• The virus requires reverse transcriptase
• Usually use Lamivudine (a nucleoside reverse transcriptase inhibitor)
o But resistance quickly arises
o To phosphonate analogues are used: dAMP (Adefovir)
o dGMP: entecavir
o those are nucleotide analogues that inhibit viral DNA polymerase

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21
Q

what’s the difference between bacteriostatic and bactericidal agents?

A

bacteriostatic prevent bacterial proliferation, whereas the bactericidal agents actually kill the bacteria

22
Q

how is resistance in bacteria developed?

A

there is two ways:
selection:
- where the antibiotic will eliminate the sensitive bacteria and the resistant bacteria remain

transferred resistance:

  • a gene coding for resistance is passed from one bacteria to another
  • the gene for resistance can be within the plasmid which is easily passed between organisms via conjugation
23
Q

what enzyme do sulphonamides work?

A

they inhibit dihydropetroate synthetase, which is required for folate synthesis

24
Q

what enzyme does trimethoprim inhibit?

A

this inhibit dihydrofolate reductase, which is required for folate synthesis

25
Q

what are the sulphonamides and trimethoprim used for?

A

they’re used for UTIs

26
Q

what enzyme does the quinolone inhibit?

A

inhibits DNA gyrase (topoisomerase II) which is required to seal the nicks of DNA strands in the process of DNA supercoiling

27
Q

why are the quinolones specific?

A

because humans have no DNA gyrase

28
Q

giva an example of a quiolone

A

ciproflaxcin - which is a broad spectrum antibiotic

29
Q

what is the mechanism of action of Metronidazole, and why is it selectively toxic?

A

metronidazole penetrates into organism and becomes reduced by ferridoxin (which is only found in the bacterial electron chain, and not found in the human electron transport chain)

this reduced metabolites are toxic and bind to DNA inducing mutations and reduce replication

30
Q

what is the active product of penicillin

A

the beta lactam group, without this beta lactam the drug will not work, the beta lactam work because they mimic the D-alanyl D-alanine of the peptide chains of the bacterial walls

31
Q

what is flucloxacillin used for?

A

used in infections with staphylococci which produce Beta lactmase -

this is still effective because it has a steric group which prevents the access of the lactmase enzyme to the beta-lactam group

32
Q

give an example of a narrow spectrum penicillin

A

benzylpenicillin

33
Q

give example of broad spectrum penicillin?

A

amoxicilin and ampicillin

  • those are actually active against gram negative bacteria
34
Q

give example of broad spectrum penicillin?

A

amoxicilin and ampicillin

  • those are actually active against gram negative bacteria, therefore can be used in the treatment of E.coli, H.influenzae and salmonella
35
Q

what is co-amoxicillin?

A

this is clavulanic acid (which inactivates the beta lactamase) and amoxicillin. this is used when the infection is penicillin resistant

36
Q

what is the major side -effects with amino glycosides?

A

oto-toxicity (by damaging the 7th cranial nerve)
damage to the kidney
can impair neuromuscular transmission - so not recommended for patients with MG

37
Q

what is the mechanism of action for the amino glycosides?

A

they bind to the 30s sub-unit and inhibit binding of aminoacyl -RNA

they also cause misreading of MRNA forming non-functional proteins

38
Q

what are the side effects of the macrolides?

A

they’re generally quite safe drugs, but they inhibit p450 enzymes, so they can cause warfarin accumulation

39
Q

give examples of a macrolide

A

erythromycin and clarithromycin

40
Q

when are cephalosporins used>

A

they’re usually used for meningitis, pneumonia and septicaemia

41
Q

what are the main side-effects of tetracyclines

A

binds to calcium in growing teeth and bone (therefore, cause teeth discolouration in the young)
diarrhoea and nausea
nephrotoxicity

42
Q

what is the mechanism of action of the tetracyclines?

A

they bind to the 30-s subunit preventing the binding of aminoacyl tRNA

43
Q

what is the mechanism of action of chloramphenicol?

A

inhibits peptidyl transferase activity of 50s ribosomal subunit (and this inhibits peptide chain elongation)

44
Q

what is the side effect of chloramphenicol?

A

bone marrow depression, Grey baby syndrome and diarrhoea

45
Q

when is chloramphenicol used?

A

usually used to treat bacterial conjunctivitis

46
Q

what is zidovudine used for?

A

HIV

47
Q

What is nevarapine used for?

A

HIV - this is a non-nucleoside inhibitor

48
Q

what is indinavir and squanivir used for?

A

HIV

protease inhibitors

49
Q

what is acyclovir used for?

A

HSV, VZV, immunocomprosided patient (encephalitis, mucocutaneous infections and genital herpes and varicella

50
Q

what is ganciclovir used for?

A

this is used for cytomegalovrius retinitis - because acylcovir is inactive against it

51
Q

what can vidarabine be used for?

A

HSV, VZV, (same as acyclovir but stronger side-effects)

52
Q

idoxurdine

A

HSV, corneal infections

Pharmacology (17 decks)

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