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Year 2 LCRS Pharmacology > 31: Antibiotics and Antifungals > Flashcards

31: Antibiotics and Antifungals Flashcards

1
Q

What is the most important characteristic of a Gram +ve bacterium? (e.g. Staphylococcus Aureus)

A

Has a cell membrane surrounded by a

  • prominent peptidoglycan cell wall
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2
Q

What is the most importnat structural characteristic of a Gram -ve bacterium (e.g. E.coli) ?

A

Has an inner cell membrane

a thin peptodoglican cell wall and an outer

membrane with lipopolysaccharide

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3
Q

What are the most important characteristics of Mycolic bacteria (e.g. M tuberculosis)?

A

Outer mycolic acid layer (on top of cell wall and membrane)

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4
Q

Summarise bacterial Nucleic Acid Synthesis

A
  • Dihydropteroate (DHOp)
    • Produced from paraaminobenzoate (PABA) by DHOp synthase
    • Converted into dihydrofolate (DHF)
  • Tetrahydrofolate (THF)
    • Produced from DHF by DHF reductase
    • THF is Important in DNA synthesis
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5
Q

Which enzyme is important in bacterial DNA replication and a common target for ABX?

A

DNA gyrase

  • –> Topoisomerase releases tension during replication
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6
Q

How is bacterial RNA synthesis exploited in ABX treatment?

A

Bacterial RNA polymerase is diffrent from eukariotic RNA polymerase

  • Produces RNA from DNA template
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7
Q

Explain how bacterial protein Synthesis can be exploited as an ABX treatment target

A

Bacterioal Ribosomes differ from eukaryotic ribosomes

  • Produce protein from RNA templates
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8
Q

What is the MOA of Sulphonamides?

A

Sulphonamides inhibit (Dihydropteroate) DHOp synthase

  • –> disrupt bacterial Nucleic acid production
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9
Q

What is the MOA of Trimethoprim?

A

Trimethoprim inhibits DHF reductase –> no production of THF (Tetrahydrofolate)

  • disrupt bacterial nucleic acid synthesis
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10
Q

Which Antibiotocs target bacterial nucleic acid synthesis?

A
  • Dihydropteroate (DHOp)
    • Sulphonamides inhibit DHOp synthase
  • Tetrahydrofolate (THF)
    • Trimethoprim inhibits DHF reductase
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11
Q

What are the two Ways Antibiotics can interfere with normal bacterial function?

A
  1. Disrupt intracellular mechanisms
  2. Membrane disruption (or disruption of membrane production)
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12
Q

Which ABX class targets bacterial DNA replication?

How?

A

Fluoroquinolones (e.g. Ciprofloxacin) inhibit DNA gyrase & topoisomerase IV

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13
Q

What is the MOA of Fluoroquinolones?

A

Inhibit bacterial DNA replication via

inhibition of DNA gyrase & topoisomerase IV

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14
Q

Which ABX class targets bacterial RNA synthesis?

How?

A

The rifamycins (e.g. Rifampicin) inhibits bacterial RNA polymerase

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15
Q

Explain how and which class of ABX interfere with bacterial protein Synthesis

A

Inhibit procaryotic Ribossomes (in different ways but same result)

  • Macrolides (e.g. Erythromycin)
  • Aminoglycosides (e.g. Gentamicin)
  • Chloramphenicol
  • Tetracyclines
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16
Q

What is the MOA of rifamycins

A

Rifamycins inhibit bacterial RNA polymerase

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17
Q

What is the MOA of Macrolides?

A

Inhibit Bacterial Ribosomes –> protein synthesis

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18
Q

What is the role of Peptidoglycan in bacteria?

A

It is the most important part of the bacterial cell wall

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19
Q

Explain the synthesis of Peptidoglycan (PtG)

A
  • A pentapeptide is created on N-acetyl muramic acid (NAM)
  • N-acetyl glucosamine (NAG) associates with NAM forming PtG
20
Q

Explain the transportation of PtG in bacterial cell wall formation

A
  1. PtG transportation
    * PtG is transported across the membrane by bactoprenol (into periplasm)
21
Q

Explain the PtG incoorperation into the existing cell wall in bacteria

A

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

22
Q

Which class of ABX interferes with PtG synthesis?

A

PtG needed for Cell wall

  • Glycopeptides (e.g. Vancomycin) bind to the pentapeptide preventing PtG synthesis
23
Q

What is the MOA of glycopeptides (e.g. Vancomycin?)

A

bind to the pentapeptide preventing PtG synthesis

24
Q

What is the MOA of ß-lactams?

A

b-lactams bind covalently to transpeptidase inhibiting PtG incorporation into cell wall

25
Q

Which ABX classes are ß-lactams?

A
  • Carbapenems
  • Cephalosporins
  • Penicillins

Inhibit PtG incooperation into bacterial cell wall

26
Q

What is the MOA of Carbapenems?

A

ß-lactam

  • lactams bind covalently to transpeptidase inhibiting PtG incorporation into cell wall
27
Q

What is the MOA of Penicillins?

A

ß-lactam

ß-lactams bind covalently to transpeptidase inhibiting PtG incorporation into cell wall

28
Q

What is the MOA of Cephalosporins?

A

ß-lactam

ß-lactams bind covalently to transpeptidase inhibiting PtG incorporation into cell wall

29
Q

Which ABX classes interfere with cell membrane stability?

A
  • Lipopeptide - (e.g. daptomycin) disrupt Gram +ve cell membrane
  • Polymyxins - binds to LPS (lipopolysaccharide) & disrupts Gram -ve cell membranes
30
Q

What is the MOA of Lipopeptide ABX?

A

-(e.g. daptomycin) disrupt Gram +ve cell membrane

31
Q

What is the MOA of Polymyxins?

A

Polymyxins - binds to lipopolysaccharide & disrupts Gram -ve cell membranes

32
Q

What are the main causes of bacterial drug resistance?

A
  • unncessary perscription
  • lifestock farming
  • lack of regulation (otc availibility)
  • lack of development
33
Q

What are the Mechanisms by which bacteria can gain resistance?

A

HEADD

  • Hyperproduction
  • Enzyme alteration
  • Additional target
  • Destruction enzymes
  • Drug Permeation
34
Q

Explain how production of Production of destruction enzymes can lead to ABX resistance

A

Enzyme is produced that destorys the ABX

  • b-lactamases hydrolyse C-N bond of the b-lactam ring
35
Q

Explain how production of an additional target can lead to ABX resistance

A

Bacteria produce another target that is unaffected by the drug

  • e.g. producing a different DHF reductase enzyme that fulfils the function
36
Q

Explain how Alterations in target enzymes can lead to ABX resistance

A

Alteration to the enzyme targeted by the drug

  • Enzyme is not anymore destoryed by drug and still works
  • E.g. Mutations in DNA gyrase enzyme
37
Q

Explain how Alteraltions in drug Permeation can lead to ABX resistance

A

Expecially importnatn in Gram -ve

Less drug can get into the cell due to

  • decreased entry (e.g. reduction in aquaporins)
  • increased efflux
38
Q

Explain how Hyperproduction can lead to ABX resistance

A

Bacterial increases production of drug target (enzyme) so that though some is destroyed there is still enough for its normal function

  • E.g. Over-production of DHF reductase
39
Q

Explain the way Fungal infections can be classified according to their affected tissue or organ

A
  1. Superficial - Outermost layers of skin
  2. Dermatophyte - Skin, hair or nails
  3. Subcutaneous - Innermost skin layers
  4. Systemic - Primarily respiratory tract
40
Q

What are the two most common anti-fungal categories?

A
  1. Azoles: Fluconazole
  2. Polyenes: Amphotericin
41
Q

What is the MOA of Fluconazole?

A

It is an Azole Antifungal

  • Inhibit cytochrome P450-dependent enzymes involved in membrane sterol synthesis
42
Q

When are Azole ABX (e.g. Fluconazole) used?

What is its ROA?

A

Used (orally) candidiasis & systemic infections

43
Q

Waht is the MOA of Amphotericin?

A

It is a Polyenes Antifungal

  • Interact with cell membrane sterols forming membrane channels
44
Q

What is the ROA and indication of the Use of Polyenes Antifungals

Name an example

A

Amphotericin (I-V) for systemic infections

45
Q

What is the general way in which Antifungal drugs work?

A

Interfere with Fungal cell membrane via interfering with ergosterol production/ integrety

Year 2 LCRS Pharmacology (38 decks)

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