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Bacteria Flashcards

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Biology 101 flashcards
1
Q

What is Beta lac-tam drugs

A

Drug inhibits the final step of Bacteria cell wall synthesis.
These drugs bind to beta receptors and inhibits formation of cell wall

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2
Q

What are beta-lactom drugs

A

penicillins and cephalosporins -

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3
Q

What is penicillin

A
  • Gram+ bacteria.
  • So, take phenoxymethylpenicillin.
  • Large Vd , but penetration into brain: poor, except when the meninges are inflammed.
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4
Q

What is board spectrum of penicillin?

A

Penne twin act aging Gram +
Bacteria

amoxicillin and ampicillin are more hydrophillic and therefore, are active against grambacteria.

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5
Q

Which drug is penicillinase resistant penicillin?

A

Flucloxacillin

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6
Q

What is penicillineage resistant pen?

A

By hindering access of the enzyme to beta lactam

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7
Q

Which bacteria increases the problem by- resisting fluclocicillin

A

Staph aureus

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8
Q

Ampicillin and amoxicillin are active against which bacteria’s?

A
  • against non beta lactamase producing Gram + Bacteria
  • also against Gram - Bacteria like e-colli, H influenza and salmonella typhimurium
    Ineffective
    . Against Steph aureoles, 50% E. coli, 15 %H influenza
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9
Q

Drug is effective against pancillinase producing organisms also inhibits beta- lactamases?

A

Co- anoxiclav

Indicated in respiratory and urinary tracks infection which resist to amoxicillin

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10
Q

Drug used for meningitis pneumonia and septicemia has same mechanism of penicillin?

A

Cephalosporins

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11
Q

What is bound spectrum of cephalosprine?.

A

_ Cedadroxil:-in case of antibatoral Resist

  • cefuroxime:- used in sever infection against beta lactamase
  • ceftazidine:- active against Gram - bacteria and less active than cefurozime agust Gram + Bacteria, used mostly aging meningitis caused by gram -ve
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12
Q

What is vancomycin?
How it affects Bacteria?
When it used as iv?
For which disease mostly use?

A
  • Inhibits peptidoglycan formation.
  • Active against most gram+ve organisms.
  • I.v. treatment for septicemia or endocarditis caused by MRSA.
  • Used for pseudomembranous colitis (super-infection of the bowel by Clostridium difficile – produces a toxin that damages the colon mucosa)
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13
Q

Which organ is target of antibiotics in inhibition of protein synthesis?

A

Ribosome is the target of antibiotics
•Aminoglycosides, binds to 30s subunit, block the translation.
. Tetracycline:. Bind to 30s subunit block attachment of tRNA
.macrolides: band to 50s subunit and prevents protein synthesis

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14
Q

What is amino-glycosides?
Effects which bacteria?
Side effects
Resistance

A
  • Against many gram-ve and some gram+ve..
  • Most important adverse side-effect: VIIIth cranial nerve. (ototoxicity) and kidney damage.

• Resistance – several mechanisms:
inactivation of the drug by acetylation, phosphoralation, or adenylation,

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15
Q

What are aminoglycosides group of drugs

A 
Gentamicin
Amikacin
Neomycin
 netilmicin
Streptomycin
Rifampiein
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16
Q

Explain gentamicin?
Which drug is used when there is resistance agent gentamicin?
Which drug is less toxic than gentamicin?

A
  • Gentamicin – used for acute, life-threatening gram- veinfections. Has synergism with penicillin and vancomycin and combination
  • Amikacin – used for bacteria that are gentamycin -resistant.
  • Netilmicin – less toxic than gentamicin
17
Q

What is neomycin

A

Neomycin iS on aminoglycosidees drug, which inhibits synthesis of bacterial proteins.. It is too toxic, it is used tropically for skin infection and orally in order to sterilize bowel befor surgery.

18
Q

Which drug is used for tb but it is too toxic?

And replaced by which drug?

A
  • Streptomycin – active against Mycobacterium tuberculosis. But because of its ototoxicity, rifampicin replaces.
  • Rifampicin – resistance develops quickly alone; so, with TB, combine with isoniazid, ethambutol, and pyrazinamide for the 1st 2 months of treatment,
19
Q

Define macrolide’s?

It is subgroup drugs?

A
  • Very safe drugs..
  • Effective against gram- ve and can be used as an alternative to penicillin-sensitive patients
  • Don’t cross the brain barriers – ineffective against meningitis.
  • Erythromycin and clarithomycin and Azithromycin
  • Erythromycin – in high doses, may cause nausea and vomiting
  • Azithromycin – very long t 1/2(~40-60 hr)
20
Q

Explain tetracyclines?
How they get into microorganisms?
How resistance is former?
Why they cause discolor to teeth?

A
  • Broad-spectrum.
  • Sensitive organisms accumulate it through partly passive diffusion and partly through active transport.
  • Resistant organisms develop an efflux pump and do not accumulate the drug.
  • Genes for tetracycliness-resistance transmitted by plasmids.

• Tetracyclines bind to Calcium in growing bones and teeth → can discolor teeth. So, should be avoided in children < 8 years old.

21
Q

Explain chloramphenicol?
It is side effect?
How effects other drugs?

A
  • large Broad-spectrum.
  • Large Vd , including CNS.
  • Serious side-effects: bone marrow aplasia, suppression of RBCs, WBCs, encephalopathy, optic neuritis.
  • So, periodic blood counts required, specially in high doses.
  • Inhibits the actions of other drugs and may increase the actions of phenytoin, sulphonlureas, and warfarin..
22
Q

What’s function of flubroquinolones.?

What is function of rifamycins?

A
  • Fluoroquinolones: inhibit enzymes that maintain the supercoiling of closed circular DNA
  • Rifamycins: block prokaryotic DNAdependent RNA polymerase from initiating transcription
23
Q

What is uses of trimethoprin?

What is Co- trimotarole?

A

. • Trimethoprin – used for UTIs and respiratory infections

. (trimethoprin + sulfamethoxazole) – used mostly for pneumonia, neo-carditis, and toxoplasmosis.

24
Q

What is quinolone?
It’s function?
And it’s group off drugs?

A

GABA antagonists

  • Inhibit DNA gyrase.
  • Nalidixic acid – used only for UTIs.
  • Ciprofloxin enhances its effectiveness against both gramand gram+ bacteria

Side-effects (headache, vomiting, nausea) are rare; but convulsions may occur.

25
Q

Define nitroimidazoles? And it’s group

A

It is nuctic acidsyuthess inhibiting drug

• Metronidazole – against anaerobic bacteria and protozoan infections.

• Tinidazole – longer duration of action.
. chemically reactive intermediates are formed that inhibit DNA synthesis and/or damage DNA.

26
Q

Which drug effect the plasma membrane?

A

• Polymyxin B: binds to membrane of G-ve bacteria and alters permeability

27
Q

What are drugs inhibits the entering or leaving of virus to host cell?

A

Amantadine, zanamivir, Ig

28
Q

Which drugs inhibits virus infection by inhibiting nuclei acid syuthes’s?

A

Acyclovir, cidofovir, lamivudine

29
Q

What is mechanism of action of acyclovir?

A

HSV and VZV contain thymidine kinase (tk) which convert acyclovir to acyclovir phosphate then by humane enzyme into acyclovir triphosphate.

  • Effective against HSV, but does not eradicate them.
  • Need high doses to treat shingles.
30
Q

When does ganciclovir is used?

And why acyclovir is not used?

A
  • Quite toxic (neutropenia) –so, given only for severe CMV infections in immunosuppressed patients.
  • CMV is resistant to acyclovir because it does not code for TK.
31
Q

What are antiretrovirals drugs?

A

Tenofovir, zidovudine, stavudine, didanosine, zalcitabine, nevirapine, efavirenz.

32
Q

What are enzyme inhibitors of viruses?

A

Zanamivir, oseltamivir phosphate, indinavir.

33
Q

What is mechanism action of indinavir?

A

• Indinavir- protease inhibitors. Inhibit the synthesis of essential viral proteins (e.g., RT) by viral-specific proteases.

34
Q

Define interferons?

A

Infected cells by virus produces

Interferons which inhibits further spread of the infection,

35
Q

How to determine drug susceptibility?

A

Drug susceptibilityis done by kirby- Bauer method:
1 prepare an agar plate contain Bacteria
2 place different anitmicrobicels on the disk
3 drug diffuse outward and kill susceptible Bacteria
4 calculate zone of inhibition
5 compare the size of zone to chart.

36
Q

What are mechanisms causes resistance to drugs?

A
  1. Inactivating enzymes
  2. Decreased drug accumulation
  3. Altering the binding sites
  4. Development of alternative metabolic pathways
37
Q

How bacteria became resistant?

A

1 spontaneous mutation.

2 Gene transfer

Microbiology (7 decks)

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