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Y2 - PHARM > Antibiotics and Anti-fungals > Flashcards

Antibiotics and Anti-fungals Flashcards

1
Q

Describe the distinctive features of:

1) Gram positive bacteria
2) Gram negative bacteria
3) Mycolic bacteria

A

1)

  • Thick peptidoglycan cell wall

2)

  • Outer membrane that contains lipopolysaccharide (LPS)

3)

  • Outer mycolic acid layer
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2
Q

State the steps involved in the production of THF from PABA

A
  1. PABA (paraaminobenzoate) –> DHOp (dihydropteroate) (enzyme = dihydropterase synthase)
  2. DHOp (dihydropteroate) –> DHF (dihydrofolate)
  3. DHF (dihydrofolate) –> THF (tetrahydrofolate) (enzyme = DHF reductase)
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3
Q

What is DNA gyrase and what is its function?

A
  • A type of topoisomerase
  • It releases tension in DNA and is important in unwinding DNA to allow protein binding required for DNA replication
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4
Q

What does RNA polymerase do?

A
  • Produces RNA from a DNA template
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5
Q

On a very basic level, what is one of the functions of ribosomes in regards genetics?

A
  • RNA molecules go through the prokaryotic ribosomes, which produce protein from RNA templates
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6
Q

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

A
  • Eukaryote = 40S + 60S
  • Prokaryote = 30S + 50S
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7
Q

1) State two classes of drugs that interfere with nucleic acid synthesis and name the enzymes that they inhibit
2) These two drugs are sometimes used together. What is this preparation called?

A

1)

  1. Sulphonamides – inhibits dihydropteroate synthase
  2. Trimethoprim – inhibits DHF reductase

2)

  • Co-trimoxazole
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8
Q

Name a group of drugs (with a named example) that interfere with DNA replication and state its targets

A
  • Fluoroquinolones (e.g. ciprofloxacin) - inhibits bacterial DNA gyrase and topoisomerase IV - thereby inhibiting DNA replication
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9
Q

Name a group of drugs (with a named example) that interfere with RNA synthesis and state its main target

A
  • Rifamycins (e.g. rifampicin) – inhibits RNA polymerase
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10
Q

List 4 groups of drugs that interfere with ribosomes

A
  1. Macrolides
  2. Chloramphenicol
  3. Aminoglycosides
  4. Tetracyclines
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11
Q

Describe the differences in the specificities that antibiotics that target intercellular mechanisms have for gram-positive and gram-negative bacteria

A
  • Gram-positive bacteria have a thickened outer wall
  • Gram-negative bacteria have a outer membrane containing LPS
  • It is therefore a lot harder for antibiotics targeting intercellular mechanisms to access gram positive bacteria than gram-negative bacteria
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12
Q

Describe how peptidoglycan is synthesized (basic outline), transported to, and incorporated into the bacterial cell wall in bacterial cell wall synthesis

A
  • A pentapeptide is created on N-acetyl muramic acid (NAM)
  • N-acetyl glucosamine (NAG) associates with NAM, forming peptidoglycan
  • The peptidoglycan is transported via the periplasm
  • The peptidoglycan is transported across the cell membrane and ultimately transported into the cell wall by bactoprenol
  • The peptidoglycan is then incorporated into the cell wall by transpeptidase enzyme, which cross-links the peptidoglycan pentapeptides
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13
Q

Which groups of drugs (and give a named example) 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
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14
Q

Name a drug that interferes with peptidoglycan transport and state its target

A
  • Bacitracin – this inhibits bactoprenol regeneration, hence preventing peptidoglycan transport
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15
Q

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

A
  • Beta lactams – they bind covalently to transpeptidase, which inhibits peptidoglycan incorporation into the cell wall
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16
Q

What are the three subsets of beta lactams?

A
  1. Carbapenems
  2. Cephalosporins
  3. Penicillins
17
Q

Name two drugs that interfere with cell wall stability and explain how they do this - also give a named example for one of these

A
  • Lipopeptides (e.g. daptomycin) – disrupt Gram-positive cell walls
  • Polymyxins – bind to lipopolysaccharide and disrupt Gram-negative cell membranes
18
Q

List five mechanisms of antibiotic resistance and give a brief description of each

A
  1. Production of destruction enzymes – beta-lactamases hydrolyse the C-N bond in the beta-lactam ring rendering the beta-lactams inactive
  2. Production of additional targets – the bacteria produce another target that is unaffected by the drug
  3. Altered target site – there is an alteration in the drug target so that the drug is no longer effective
  4. Hyperproduction – the bacteria increase the production of the target so the antibiotics are less effective (this is energy inefficient)
  5. Alteration in drug permeation – down regulation of aquaporins (responsible for allowing drugs into cells) or the upregulation of efflux systems
19
Q

What are penicillins G and V normally used to treat?

A
  • Gram-positive bacteria
20
Q

Name two drugs that are relatively beta lactamase resistant

A
  1. Flucloxacillin
  2. Temocillin
  • These are both beta-lactamase resistant penicillins
21
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)
  • Clavulanic acid
22
Q

Give an example of how a named example of a bacterium can be resistant to trimetophorins

A
  • E. Coli - produces another DHF reductase resistant enzyme so even if the DHF reductase inhibits the conversion of DHF to THF, the E. Coli can still survive
23
Q

Give an example of how a named example of a bacterium can be resistant to quinolones

A
  • S. Aureus - mutations in the ParC region of topoisomerase IV, confers resistance to quinolones which otherwise inhibit this topoisomerase IV enzyme to inhibit DNA replication
24
Q

Describe how bacteria can be resistant to antibiotics by alterations in drug permeation

A
  • Reductions in aquaporin - less internalisation of antibiotics
  • Increased efflux - more removal of antibiotics
25
Q

What are the two courses of treatment for mycobacterial infections?

A
  • Isoniazid + Rifampicin (6 months) Ethambutol +
  • Pyrazinamide (2 months)
26
Q

What are the mechanisms of action of isoniazid and rifampicin?

A
  • Isoniazid – inhibits mycolic acid synthesis
  • Rifampicin – inhibits RNA polymerase
27
Q

What else is rifampicin indicated for?

A
  • Leprosy
28
Q

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

A
  1. Superficial – outermost layers of skin
  2. Dermatophyte – skin, hair or nails
  3. Subcutaneous – innermost skin layers
  4. Systemic – primarily respiratory tract
29
Q

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

A
  1. Azoles (fluconazole)
  2. Polyenes (amphotericin)
30
Q

Describe the mechanism of action of azoles - also give a named example of an azole drug

A
  • They inhibit CYP51p (enzyme of the CYP450 system), which is involved in ergosterol production (a component of bacterial cell membranes). CYP450 converts lanosterol into ergosterol
  • E.g. Fluconazole
31
Q

Describe the mechanism of action of polyenes - also give a named example of a polyene drug

A
  • These interact with membrane sterols (e.g. ergosterol on fungal cell and form channels (punching holes in the membrane) resulting in lysis
  • E.g. Amphotericin
32
Q

Which of the 2 main types of anti-fungals have a greater side effect profile and why?

A
  • Polyene because they can interfere with the sterols on even host cell membranes and cause pore formation and lysis whereas azoles specifically interfere with the synthetic pathway for ergosterols which are unique to fungi

Y2 - PHARM (27 decks)

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