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LCRS Pharmacology and Therapeutics > Antibiotics and antifungals > Flashcards

Antibiotics and antifungals Flashcards

1
Q

Give a basic overview of structure of gram positive bacteria and name a common example?

A

Prominent peptidoglycan cell wall

e.g. staph aureus

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2
Q

Give a basic overview of the structure of gram negative bacteria and name a common example?

A

Outer membrane that contains lipopolysaccharide

e.g. E. coli

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3
Q

What are mycolic bacteria like?

A

They have an outer mycolic acid layer e.g. mycobacterium tuberculosis

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4
Q

In nucleic acid synthesis, what is dihydropterate (DHOp) synthesised by?

A

Paraaminobenzoate (PABA) by the enzyme dihydrojpterate synthase

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5
Q

What happens to DHOp after formation?

A

It is then converted to dihydrofolate (DHF)

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6
Q

What is produced from DHF?

A

Tetrahydrofolate (THF) by DHF reductase

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7
Q

What is THF important in?

A

DNA synthesis

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8
Q

What is DNA gyrase the same as?

A

Topoisomerase

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9
Q

What is DNA gyrase important for?

A

Unwinding DNA to allow protein binding required for DNA replication- releases tension in the DNA

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10
Q

What does RNA polymerase do?

A

Produces RNA from a DNA template

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11
Q

What do ribosomes do?

A

Produce proteins from RNA templates

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12
Q

What is the difference between eukaryotic and prokaryotic ribosomes

A 
Eukaryotes= 60s +40s
Prokaryotes= 50s + 30s
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13
Q

Why are ribosomes good drug targets?

A

They are different in prokaryotes and eukaryotes

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14
Q

What do sulphonamides do?

A

They inhibit dihydropterate synthase thus inhibit prokaryotic nucleic acid synthesis

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15
Q

Why are sulphonamides not really used anymore?

A

Widespread antibiotic resistance

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16
Q

What does trimethoprim do?

A

Inhibits DHF reductase

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17
Q

What is co-trimoxazole?

A

Combined preparation of sulphonamides and trimethoprim

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18
Q

What do fluoroquinolones do?

A

They inhibits bacterial DNA gyrate and topoisomerase IV

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19
Q

What is the difference between fluoroquinolones and quinolones?

A

Same mechanism but less resistance

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20
Q

What do rifamycins do?

A

Inhibit bacterial RNA polymerase- prevent RNA synthesis

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21
Q

What inhibit ribosomes?

A

Aminoglycosides e.g. Gentamicin
Chloramphenicol
Macrolide’s e.g. erythromycin
Tetracyclines

22
Q

In bacterial cell wall synthesis, how is peptidoglycan formed?

A

A pentapeptide is created on N-acetyl muramic acid (NAM). N-acetyl glucosamine (NAG) associated with NAM forms peptidoglycan

23
Q

Where is the peptidoglycan formed?

A

Inside the bacterial cell

24
Q

What happens to peptidoglycan once formed?

A

It is transported across cell membrane and periplasm to cel wall using bactoprenol

25
Q

When peptidoglycan is at the cell wall, what happens?

A

The proteoglycan is incorporated into the cell wall when transpeptidase enzymes cross links the peptidoglycan pentapeptides

26
Q

What do glycopeptides e.g. vancomycin do?

A

They bind to the pentapeptide thus preventing PtG synthesis

27
Q

When are glycopeptides used?

A

As a last resort mainly for Gram positive bacteria that are resistant to other antibiotics

28
Q

What does bacitracin do?

A

Inhibits bactopreol regeneration thus prevents PtG transportation

29
Q

What do beta-lactams do?

A

They bind covalently to transpeptidase which inhibits PtG incorporation into the cell wall

30
Q

Give examples of beta lactams?

A

Carbapenems
Cephalosporins
Penicillins

31
Q

What do lipopeptides e.g. daptomycin do?

A

Disrupt Gram Positive cell walls

32
Q

What do polymyxins do?

A

They bind to lipopolysaccharide and disrupts gram negative cell membranes

33
Q

What are the causes of antibiotic resistance?

A

Unnecessary prescription
Livestock farming
Lack of regulation
Lack of development

34
Q

How does the additional target mechanism work?

A

Bacteria produce another target that is similar to actual target but this one fools the drug as it is unaffected by the drug so the actual target can function properly

35
Q

Give an example of the additional target mechanism?

A

E coli produce different DHF reductase enzymes making them resistant to trimethoporin

36
Q

How does the hyperproduction mechanism work?

A

Bacteria significantly increase production of DHF reductase so increases DNA synthesis

37
Q

Why is hyper production not a common mechanism of antibiotic resistance?

A

Hyper production requires a lot of energy

38
Q

How does alterations in target enzymes lead to antibiotic resistance?

A

There is an alteration to the enzyme that is targeted by drug so enzyme will still be effective but drug will be ineffective
Widely used method

39
Q

Give an example of the alteration in target enzyme mechanism?

A

S.aureus- Mutation in ParC region of topoisomerase IV confers resistance to quinolone

40
Q

What are aquaporins required for?

A

To allow drugs access to cells

41
Q

How does the alterations in drug permeation mechanism work?

A

The bacteria decreases number of aquaporins- reduces access to the cell
Another mechanism is increase efflux systems- drug gets kicked out quickly
Common method

42
Q

How does the production of destruction enzymes work?

A

Beta lactamases hydrolyse the C-N bond of beta lactic ring

43
Q

Give examples of production of destruction enzymes mechanism?

A

Pencillins G and V commonly used for gram positive bacteria
Flucloxacillin and temocillin are relatively beta lactamase resistant
Amoxicillin is broad spectrum antibiotic which isn’t resistant to beta lactamases

44
Q

Give all the mechanisms of antibiotic resistance?

A 
Additional target
Hyperproduction
Alteration in target enzymes
Alteration in drug permeation 
Production of destruction enzymes
45
Q

What are fungal infections classified based on?

A 
In terms of tissues/organs affected:
Superficial-outermost layers of skin
Dermatophyte- Skin, hair or nails
Subcutaneous- innermost skin layers
Systemic- Primarily respiratory tract
46
Q

What are the two most common categories of anti-fungals?

A

Azoles- Fluconazole

Polyenes- Amphotericin

47
Q

What do azoles do?

A

Inhibit cytochrome p450 dependent enzyme involved in ergosterol synthesis

48
Q

What is fluconazole used for?

A

Azole that is used in candiadis and systemic infections

49
Q

What do polyenes do?

A

Interacts with membrane sterols forming membrane channels- punch holes in cell membrane which destroys cell viability

50
Q

What is amphotericin used for?

A

Systemic infections

LCRS Pharmacology and Therapeutics (33 decks)

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