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Year 2 - LCRS - Pharmacology > Antibiotics and Antifungals (13.03.2020) > Flashcards

Antibiotics and Antifungals (13.03.2020) Flashcards

1
Q

General Information about bacteria

A
  • Single-cell microorganisms - cell wall & cell membrane
  • An entire phylogenetic domain
  • ~ 1/3 are pathogenic
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2
Q

Membrane characteristics of different bacteria + name an example for each of the three categories

A

Gram Positive Bacteria

  • Prominent peptidoglycan cell wall, cell membrane below
  • E.g. Staphylococcus Aureus

Gram Negative Bacteria

  • Outer membrane with lipopolysaccharide (then a peptidoglycan layer and another inner membrane)
  • E.g. Escherichia Coli

Mycolic Bacteria

  • Outer mycolic acid layer (reasonable peptidoglycan layer below, they don’t fall under g+ or g-)
  • E.g. Mycobacterium Tuberculosis
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3
Q

Prokaryotic protein synthesis

A
  1. Nucleic Acid Synthesis
    a) Dihydropteroate (DHOp)
    - Produced from paraaminobenzoate (PABA)
    - Converted into dihydrofolate (DHF)
    b) Tetrahydrofolate (THF)
    - Produced from DHF by DHF reductase
    - THF -> Important in DNA synthesis
  2. DNA replication
    - DNA gyrase (same as topoisomerase, uses tension)
    - Topoisomerase - releases tension
  3. RNA synthesis
    - RNA polymerase
    - Produces RNA from DNA template
    - Differ from eukaryotic RNA polymerase
  4. Protein synthesis
    - Ribosomes
    - Produce protein from RNA templates
    - Differ from eukaryotic ribosomes
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4
Q

Ribosomes in eukaryotes and prokaryotes

A

P: 30-50s

E: 40-60s

-> protein synthesis

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5
Q

Nucleic acid synthesis in baacteria

A
  1. PABA

(via DHOp synthase) ->

  1. Dihydropteroate DHOp
    - >
  2. DHF

(via DHF reductaasae) ->

  1. THF (Tetrahydrofolate)
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6
Q

DNA replication in bacteria

A
  • uses DNA gyrase

- it is a topoisomerase -> releases tension

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7
Q

RNA synthesis in bacteria

A
  • RNA polymerase -> different in eukaryotes

- makes RNA from DNA template

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8
Q

Bacterial protein synthesis inhibitors - where do they interfere?

A
  • Sulphonamindes -> inhibit DHOp synthase
  • Trimethoprim -> inhibits DHF reductase
  • Fluoroquinolones inhibit DNA gyrase and topoisomerase IV
  • rifamycins -> inhibit bacterial RNA polymerase
  • Macrolides, Aminoglucosides, Chloramphenicol and Tetracyclines inhibit bacterial ribosomes.
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9
Q

Rifamycins

A
  • only used to treat TB

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

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10
Q

Sulphonamides

A
  • Sulphonamides inhibit DHOp synthase (nucleic acid synthesis)
  • not much used anymore
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11
Q

Trimethoprim

A
  • inhibits DHF reductase

- used sometimes but in combination moslty

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12
Q

Fluoroquinolones

A
  • inhibit DNA gyrase and topoisomerase IV

- e.g. Ciprofloxacin

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13
Q

Macrolides

A
  • e.g. erythromycin

- inhibit prokaryotic ribosomes

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14
Q

Which drugs inhibit prokaryotic ribosomes?

A

Aminoglycosides (e.g. Gentamicin)
Chloramphenicol
Macrolides (e.g. Erythromycin)
Tetracyclines

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15
Q

Which drugs inhibit bacterial intracellular processes?

A 
Sulphonamides
Tetracyclines
Trimethoprim
Fluoroquinonoles
Rifaamycins
Aminoglycosides (e.g. Gentamicin)
Chloramphenicol
Macrolides (e.g. Erythromycin)
Tetracyclines
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16
Q

Bacterial Wall synthesis

A

PtG synthesis -> transportation -> incorporation

  1. Peptidoglycan (PtG) synthesis
    - A pentapeptide is created on N-acetyl muramic acid (NAM)
    - N-acetyl glucosamine (NAG) associates with NAM forming PtG
  2. PtG transportation
    - PtG is transported across the membrane by bactoprenol
  3. PtG incorporation
    - PtG is incorporated into the cell wall when transpeptidase enzyme cross-links PtG pentapeptides

PtG is the most important component of the cell wall.

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17
Q

List the antibiotics that interfere with the bacterial cell wall and where they interfere

A
  1. PtG synthesis
    - Glycopeptides (e.g. Vancomycin) bind to the pentapeptide preventing PtG synthesis
  2. PtG transportation
    - Bacitracin inhibits bactoprenol regeneration preventing PtG transportation
  3. PtG incorporation
    - beta-lactams bind covalently to transpeptidase inhibiting PtG incorporation into cell wall
    - beta-lactams include:
    - Carbapenems
    - Cephalosporins
    - Penicillins
  4. Cell wall stability
    - Lipopeptide - (e.g. daptomycin) disrupt Gram +ve cell membranes
    - Polymyxins - binds to LPS & disrupts Gram -ve cell membranes
18
Q

Name different beta lactams

A
  • penicillins
  • carbapenems
  • cephalosporins
19
Q

Simply list the antibiotics that interfere with the bacterial cell wall

A
  • beta lactams (carbapenems, penicillins, cephalosporins)
  • glycopeptides
  • bacitracin
  • lipopeptide
  • polymyxins
20
Q

What do glycopeptides do?

A

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

21
Q

What does bacitracin do?

A

Bacitracin inhibits bactoprenol regeneration preventing PtG transportation (bactoprenol transports PtG across the membrane)

22
Q

What do beta-lactams do?

A
  • bind covalently to transpeptidase
  • inhibit PtG incorporation in the cell wall
  • transpeptidase enzyme cross-links PtG pentapeptides
23
Q

What do lipopeptides do?

A
  • disrupt gram+ve cell membranes
  • interfere with cell wall stability
  • e.g. daptomycin
24
Q

What do polymyxins do?

A
  • interfere with cell wall stability

- bind to LPS and disrupt gram-ve cell membranes

25
Q

Why is AB resistance a threat?

A
  • ‘CATASTROPHIC’, ‘APOCALYPTIC’, ‘AS BIG A RISK AS TERRORISM’ UK Chief Medical Officer
  • ~ 70% of bacteria developed resistance
  • 25000 yearly death rate - Europe & US
26
Q

What are the causes of AB resistance?

A

Unnecessary prescription
-> ~ 50% of antibiotic prescriptions not required

Livestock farming
-> ~ 30% of UK antibiotic use in livestock farming (and reducing)

Lack of regulation
-> OTC availability in Russia, China, India

Lack of development
-> Very few antibiotics in recent years (it is not very profitable for pharmaceutical companies to make drugs which are made to keep in case of emergency and try no t to use to prevent resistance) -> financially not favourable

27
Q

Name the types of AB resistance

A
  • destruction enzymes
  • additional targets
  • alteration of target
  • alteration in drug permeation
  • hyper production
28
Q

Production of destruction enzymes as a resistance mechanism

A
  • beta-lactamases hydrolyse C-N bond of the beta-lactam ring
  • Example:
  • Penicillins G & V -> Gram +ve
  • Flucloxacillin (naturally resistant due to stereo hindrance) & Temocillin -> beta-lactamase resistant
  • Amoxicillin -> Broad spectrum AB
    - Gram -ve activity
    - Co-administered with Clavulanic acid (then it is resistant to the beta-lactamases but not by itself)
29
Q

What does broad spectrum mean in terms of antibiotics?

A

an antibiotic that acts on the two major bacterial groups, gram-positive and gram-negative, or any antibiotic that acts against a wide range of disease-causing bacteria.

30
Q

Resistance mechanism: additional target

A
  • Bacteria produce another target that is unaffected by the drug
  • Example: E Coli produce different DHF reductase enzyme making them resistant to trimethoprim
31
Q

Resistance mechanism: alterations in target enzymes

A

Alterations in target enzymes

  • Alteration to the enzyme targeted by the drug.
  • Enzyme still effective but drug now ineffective
  • Example: S Aureus - Mutations in the ParC region of topoisomerase IV confers resistance to quinolones
32
Q

Resistance: alteration in drug permeation

A
  • Reductions in aquaporins
  • & increased efflux systems

Examples
- Primarily of importance in gram –ve bacteria

33
Q

Resistance: hyperproduction

A
  • Bacteria significantly increase levels of DHF reductase

- Example: E Coli produce additional DHF reductase enzymes making trimethoprim less effective

34
Q

What are the main categories of anti-fungal drugs?

A
  • Azoles: Fluconazole

- Polyenes: Amphotericin

35
Q

Fungal Infections

A
  • Can be classified in terms of tissue/organs:
  • Superficial - Outermost layers of skin
  • Dermatophyte - Skin, hair or nails
  • Subcutaneous - Innermost skin layers
  • Systemic - Primarily respiratory tract

-> down the list the infection becomes more serious

36
Q

Azoles

A
  • Inhibit cytochrome P450-dependent enzymes involved in membrane sterol synthesis
  • Fluconazole (oral) -> candidiasis & systemic infections
37
Q

Polyenes

A
  • Interact with cell membrane sterols forming membrane channels
  • Amphotericin (I-V) -> systemic infections
38
Q

Drug details (antifungals)

A

15 anti-fungal drugs licensed in the UK

Two most common categories:

  • Azoles: Fluconazole
  • Polyenes: Amphotericin
39
Q

LO1: Antibiotic classes: identify the main classes of antibiotic drugs and distinguish between them in terms of mechanism of action

A

Intracellular targets

  • Nucleic acids - Sulphonamides (DHOp), Trimethoprim (DHFR)
  • DNA gyrase - Fluoroquinolones e.g. Ciprofloxacin
  • RNA polymerase - Rifampicin
  • Bacterial ribosomes – Macrolides (Aminoglycosides, Tetracyclines)

Cell membrane targets

  • Peptidoglycan (PtG) synthesis - Vancomycin inhibits pentapeptide
  • PtG incorporation - Carbapenems, Cephalosporins & Penicillins inhibit transpeptidase
  • Membrane stability - Lipopeptides & Polymyxins
40
Q

LO2: Antibiotic resistance: recall the mechanisms commonly used by bacteria to become resistant to drugs

A
  • Destruction enzymes - beta-lactamases
  • Additional target - Different DHFR enzyme
  • Hyper-production - More DHFR enzyme
  • Changes to target - Changing DNA gyrase
  • Alterations in permeation - Increased efflux mechanisms
41
Q

LO3: Anti-fungals: differentiate between the drugs used to treat fungal infections

A
  • Azoles - Inhibit ergosterol production

- Polyenes - Bind to ergosterol and create pores

Year 2 - LCRS - Pharmacology (34 decks)

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