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notes to flashcards year 2 - LCRS1 > Antibiotics and antifungals > Flashcards

Antibiotics and antifungals Flashcards

1
Q

state some general features of bacteria

A
  • single cell microorganisms: cell wall, cell membrane
  • entire phylogenetic domain
  • 1/3 are pathogenic
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2
Q

describe the properties of gram +ve bacteria

A
  • prominent peptidoglycan cell wall

e. g. S Aureus

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3
Q

describe gram -ve bacteria

A

outer membrane with LPS

e.g. E Coli

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4
Q

describe mycolic bacteria

A

e.g. M. tuberculosis

outer mycolic acid layer

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5
Q

what are 4 important steps in prokaryotic protein synthesis?

A
  • nucleic acid synthesis
  • DNA replication
  • RNA synthesis
  • protein synthesis
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6
Q

describe nucleic acid synthesis

A
  1. PABA –> DHOp (by DHOp synthase)
  2. DHOp –> DHF
  3. DHF –> THF (by DHF reductase)
    THF important in DNA synthesis
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7
Q

what enzymes are important in DNA replication?

A
  • DNA gyrase/ topoisomerase

- unwinds bacterial DNA, released tension

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8
Q

describe RNA synthesis

A
  • RNA polymerase

- produces RNA from DNA template

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9
Q

describe protein synthesis

A
  • produce protein from RNA templates

- differ from eukaryotic ribosomes

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10
Q

what drugs target nucleic acid synthesis?

A
  • sulphonamides inhibit DHOp synthase

- trimethoprim inhibits DHF reductase

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11
Q

what drugs target DNA replication?

A
  • flurorquinolones inhibit DNA gyrase and topoisomerase
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12
Q

what drugs target RNA synthesis?

A

Rifamycins inhibit bacterial RNA polymerase

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13
Q

wjat drugs inhibit ribosomes in protein synthesis?

A
  • aminoglycosides
  • chloramphenicol
  • macrolides
  • tetracyclines
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14
Q

what are the 3 steps to bacterial wall synthesis?

A
  1. peptidoglycan (PtG) synthesis
  2. PtG transportation
  3. PtG incorporation
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15
Q

describe PtG synthesis

A
  • pentapeptide created on N-acetyl muramic acid (NAM)

- N-acetyl glucosamine (NAG) associates with NAM forming PtG

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16
Q

describe PtG transportation

A

PtG transported across membrane by bactoprenol

17
Q

describe PtG incorporation

A

PtG incorporated into cell wall when transpeptidase enzyme cross-links PtG pentapeptides

18
Q

what drugs inhibit PtG synthesis

A

glycopeptides bind to pentapeptide preventing PtG synthesis

19
Q

what drugs inhibit PtG transportation?

A
  • bacitracin inhibits bactoprenol regeneration

- prevents PtG transportation

20
Q

what drugs inhibit PtG incorporation?

A
  • beta lactams bind covalently to transpeptidase
  • inhibits PtG incorporation into cell wall
    e. g. carbapenems, cephalosporins, penicillins
21
Q

what 2 drugs affect cell wall stability (but target cell membrane)?

A
  • lipoprotein - disrupt gram +ve cell membranes

- polymyxins - binds to LPS and disrupts gram -ve cell membranes

22
Q

what are the causes of antibiotic resistance?

A
  • unnecessary prescription
  • livestock farming
  • lack of regulation
  • lack of development
23
Q

state the 5 resistance mechanisms

A
  • production of destructive enzymes
  • additional target
  • alterations in target enzymes
  • hyperproduction
  • alterations in drug permeation
24
Q

describe the production of destruction enzymes

A
  • beta lactamases hydrolyse C-N bond of beta lactam ring
  • e.g. Pencillins G and V = gram +ve
  • flucloxacilin and temocilin are beta lactamase resistant
25
Q

describe additional target mechanism

A
  • bacteria produce another target that is unaffected by drug
26
Q

give an example of the additional target mechanism

A

E coli produce different DHF reductase enzyme making them resistant to trimethoprim

27
Q

describe alterations in target enzymes

A
  • alteration to enzyme targeted by drug
  • enzyme still effective but drug now ineffective
    e. g. S Aureus
28
Q

describe hyperproduction

A
  • bacteria significantly inc. levels of DHF reductase
29
Q

give an example of a bacteria that uses the hyperproduction method

A

E coli produce additional DHF reductase enzymes making trimethoprim less effective

30
Q

describe alterations in drug permeation

A
  • reductions in aquaporins and inc. efflux systems

- primarily of importance in gram -ve bacteria

31
Q

how can fungal infections be classified?

A
  • superficial: outermost layers of skin
  • dermatophyte: skin, hair, nails
  • subcutaneous: innermost skin layers
  • systemic: primarily resp tract
32
Q

what are the 2 most common categories of anti-fungals?

A
  • azoles: fluconazole

- polyenes: amphotericin

33
Q

what do azoles do?

A
  • inhibit cytochrome P450-dependent enzymes involved in membranes sterol synthesis
34
Q

what is the azole, flucanazole used to treat?

A

candidiasis and systemic infections

35
Q

what do polyenes do?

A
  • interact with cell membrane sterols forming membrane channels
36
Q

what is the polyene, amphotericin used to treat?

A

systemic infections

notes to flashcards year 2 - LCRS1 (58 decks)

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