Antibiotics & Anti-fungals Flashcards Preview

Pharmacology Year 2 > Antibiotics & Anti-fungals > Flashcards

Flashcards in Antibiotics & Anti-fungals Deck (32)
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1
Q

Describe the distinctive features of:

a. Gram positive bacteria
b. Gram negative bacteria
c. Mycolic bacteria

Give an example of each.

A

a. Gram positive bacteria
Thick peptidoglycan cell wall (e.g. Staphylococcus Aureus)

b. Gram negative bacteria
Outer membrane that contains lipopolysaccharide
(e.g. E. coli)

c. Mycolic bacteria
Outer mycolic acid layer
(e.g. Mycobacterium Tuberculosis)

2
Q

Describe important reactions involved in the nucleic acid synthesis process in bacteria

A
  1. Paraaminobenzoate (PABA) is converted into Dihydropteroate (DHOp) - catalysed by DHOp synthase.
  2. DHOp is converted into dihydrofolate (DHF).
  3. DHF is converted into Tetrahydrofolate (THF) - catalysed by DHF reductase.

THF is important in DNA synthesis.

3
Q

What is DNA gyrase? What is it important in?

A

A type of topoisomerase that releases tension in DNA and is important in unwinding DNA to allow protein binding required for DNA replication

4
Q

Does bacterial RNA polymerase differ from eukaryotic RNA polymerase?

A

YES

5
Q

What is the key difference between ribosomes in eukaryotes and prokaryotes?

A

Eukaryote = 40S + 60S Prokaryote = 30S + 50S

6
Q

State two classes of drugs that interfere with nucleic acid synthesis and name the enzymes that they inhibit.

A

Sulphonamides – inhibits dihydropterate synthase

Trimethoprim – inhibits DHF reductase

7
Q

These two drugs are sometimes used together. What is this preparation called?

A

Co-trimoxazole

8
Q

Name a group of drugs that interfere with DNA replication and state its targets.

A

Fluoroquinolones (e.g. ciprofloxacin) inhibits bacterial DNA gyrase and topoisomerase IV

9
Q

Name a group of drugs that interfere with RNA synthesis and state its main target.

A

Rifamycins (e.g. rifampicin) – inhibits RNA polymerase

10
Q

List 4 groups of drugs that interfere with ribosomes.

A

Macrolides
Chloramphenicol
Aminoglycosides
Tetracyclines

11
Q

Describe how peptidoglycan is synthesised

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

* N-acetyl glucosamine (NAG) associates with NAM forming peptidoglycan

12
Q

How is the peptidoglycan is transported into the cell wall?

A

Transported across the cell membrane and into the cell wall by bactoprenol

13
Q

Describe how the peptidoglycan is incorporated into the cell wall.

A

The peptidoglycan is then incorporated into the cell wall when a transpeptidase enzyme cross-links the peptidoglycan pentapeptides

14
Q

Which groups of drugs interfere with peptidoglycan synthesis and how do they do this?

A

Glycopeptides (e.g. vancomycin) – they bind to the pentapeptides and inhibit peptidoglycan synthesis
This is used as a last resort for Gram-positive bacteria that are resistant to other antibiotics

15
Q

Name a drug that interferes with peptidoglycan transportation and state its target.

A

Bacitracin – this inhibits bactoprenol

16
Q

Name a class of drugs that inhibit peptidoglycan incorporation and explain how they do this.

A

Beta lactams – they bind covalently to transpeptidase.

17
Q

What are the three subsets of beta lactams?

A

Carbapenems
Cephalosporins
Penicillins

18
Q

Name two drugs that interfere with cell wall stability and explain how they do this.

A

Lipopeptides – disrupt Gram-positive cell membranes

Polymyxins – bind to lipopolysaccharide and disrupt Gram-negative cell membranes

19
Q

State the four main causes of antibiotic resistance

A
  1. Unnecessary prescription
  2. Antibiotic use in livestock farming
  3. Lack of regulation (OTC availability)
  4. Lack of development of new antibiotics
20
Q

List 5 antibiotic resistance mechanisms

A
  1. Production of destruction enzymes
  2. Bacteria produce another target that is unaffected by the drug
  3. Alteration to the enzyme targeted by the drug (enzyme still effective but drug now ineffective)
  4. Alterations in drug permeation
  5. Hyperproduction of drug target
21
Q

Describe an example of (1)

A

𝛽-lactamases hydrolyse C-N bond of the 𝛽-lactam ring

22
Q

What are penicillins G and V normally used to treat?

A

Gram-positive bacteria

23
Q

Name two drugs that are relatively beta lactamase resistant.

A

Flucloxacillin and temocillin

24
Q

Name a broad-spectrum antibiotic that must be administered with another drug to become resistant to beta lactamases. What is this other drug?

A

Amoxicillin (no antibiotic resistance on its own)

Administered with Clavulanic acid

25
Q

Describe an example of (2)

A

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

26
Q

Describe an example of (3)

A

S Aureus - Mutations in the ParC region of topoisomerase IV confers resistance to quinolones

27
Q

Describe an example of (4)

A

Reductions in aquaporins & increased efflux systems; primarily of importance in gram –ve bacteria

28
Q

Describe an example of (5)

A

E Coli produce additional DHF reductase enzymes making trimethoprim less effective

29
Q

What are the four types of fungal infection, characterised based on the tissues/organs affected?

A

Superficial – outermost layers of skin
Dermatophyte – skin, hair or nails
Subcutaneous – innermost skin layers
Systemic – primarily respiratory tract

30
Q

What are the two main groups of anti-fungals? Give an example of each.

A

Azoles (fluconazole)

Polyenes (amphotericin)

31
Q

Describe the mechanism of action of azoles. What is the example drug used to treat?

A

They inhibit CYP51p (enzyme of the CYP450 system), which is involved in membrane ergosterol synthesis.
e.g. Fluconazole (oral) treats candidiasis & systemic infections

32
Q

Describe the mechanism of action of polyenes. What is the example drug used to treat?

A

These interact with membrane ergosterols forming membrane channels (punching holes in the membrane)
e.g. Amphotericin treats systemic infections