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

31: Antibiotics and Antifungals Flashcards

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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)

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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

Study These Flashcards
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

Study These Flashcards
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?

Study These Flashcards
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?)

Study These Flashcards
A

bind to the pentapeptide preventing PtG synthesis

24
Q

What is the MOA of ß-lactams?

Study These Flashcards
A

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

25
Which ABX classes are ß-lactams?
* Carbapenems * Cephalosporins * Penicillins Inhibit PtG incooperation into bacterial cell wall
26
What is the MOA of Carbapenems?
ß-lactam * lactams bind covalently to transpeptidase inhibiting PtG incorporation into cell wall
27
What is the MOA of Penicillins?
ß-lactam ## Footnote ß-lactams bind covalently to transpeptidase inhibiting PtG incorporation into cell wall
28
What is the MOA of Cephalosporins?
ß-lactam ß-lactams bind covalently to transpeptidase inhibiting PtG incorporation into cell wall
29
Which ABX classes interfere with cell membrane stability?
* **Lipopeptide** - (e.g. daptomycin) disrupt Gram +ve cell membrane * **Polymyxins** - binds to LPS (lipopolysaccharide) & disrupts Gram -ve cell membranes
30
What is the MOA of Lipopeptide ABX?
-(e.g. daptomycin) disrupt Gram +ve cell membrane
31
What is the MOA of Polymyxins?
Polymyxins - binds to lipopolysaccharide & disrupts Gram -ve cell membranes
32
What are the main causes of bacterial drug resistance?
* unncessary perscription * lifestock farming * lack of regulation (otc availibility) * lack of development
33
What are the Mechanisms by which bacteria can gain resistance?
HEADD * **H**yperproduction * **E**nzyme alteration * **A**dditional target * **D**estruction enzymes * **D**rug Permeation
34
Explain how production of Production of destruction enzymes can lead to ABX resistance
Enzyme is produced that destorys the ABX * b-lactamases hydrolyse C-N bond of the b-lactam ring
35
Explain how production of an additional target can lead to ABX resistance
Bacteria produce another target that is unaffected by the drug * e.g. producing a different DHF reductase enzyme that fulfils the function
36
Explain how Alterations in target enzymes can lead to ABX resistance
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
Explain how Alteraltions in drug Permeation can lead to ABX resistance
Expecially importnatn in Gram -ve Less drug can get into the cell due to * decreased entry (e.g. reduction in aquaporins) * increased efflux
38
Explain how Hyperproduction can lead to ABX resistance
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
Explain the way Fungal infections can be classified according to their affected tissue or organ
1. Superficial - Outermost layers of skin 2. Dermatophyte - Skin, hair or nails 3. Subcutaneous - Innermost skin layers 4. Systemic - Primarily respiratory tract
40
What are the two most common anti-fungal categories?
1. Azoles: **Fluconazole** 2. Polyenes: **Amphotericin**
41
What is the MOA of Fluconazole?
It is an Azole Antifungal * Inhibit cytochrome P450-dependent enzymes involved in membrane sterol synthesis
42
When are Azole ABX (e.g. Fluconazole) used? What is its ROA?
Used (orally) candidiasis & systemic infections
43
Waht is the MOA of Amphotericin?
It is a Polyenes Antifungal * Interact with cell membrane sterols forming membrane channels
44
What is the ROA and indication of the Use of Polyenes Antifungals Name an example
Amphotericin (I-V) for systemic infections
45
What is the general way in which Antifungal drugs work?
Interfere with Fungal cell membrane via interfering with ergosterol production/ integrety

Year 2 LCRS Pharmacology (38 decks)

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