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Pharmacology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What does selective toxicity mean

A

Drugs which target invaders not host cells

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2
Q

Explain the structure of penecillin

A

Beta lactam ring with 3C and 3N

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3
Q

What do b lactam penecillin target

A

Peptidoglycan wall

They inhibit transpeptidase enzyme from forming peptide cross links

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4
Q

Why are gram -ve harder to kill with penecillin (first class of penecillin)

A

Thin peptidoglycan and can’t penetrate through the outer membrane

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5
Q

What is the name of the original penecillin and what is its problems

A

Benzyl penecillin

It works only on gram +ve
It is acid labile (degraded in stomach)
Poor absorption orally

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6
Q

Why other than the large om are gram -ve harder to kill

A

Larger amounts of b lactamase

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7
Q

Which penecillins can now work also on gram -ve unlike benzyl penecillin

A

Broad spectrum

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8
Q

What makes broad spectrum penecillins able to penetrate gram -ve outer membrane

A

Addition of amino group

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9
Q

Why are broad spectrum penecillins easier absorbed/last longer than benzyl

A

Addition of hydroxyl OH

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10
Q

Name the other 3 penecillins other than the benzyl and broad spectrum

A

B lactamase resistant forms

Extended spectrum

Reverse spectrum

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11
Q

What do extended spectrum penecillins kill

A

Pseudomonads

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12
Q

What do reverse spectrum penecillins mean

A

Kill more gram -ve than +ve

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13
Q

Where is penecillin not distributed unless meningitis inflammation

A

Csf

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14
Q

Why are penecillin taken regularly

A

Short half life (30-80mins) - excreted 90% via tubular secretion

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15
Q

What are the 3 major adverse effects of penecillin

A

Hypersensitive (rash etc)

Blood clotting

GI changes in gut flora

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16
Q

What do sulphonamides and trimethoprim do

A

They are inhibitors of enzymes (because same shape as paba) which convert paba to tetrahydrofolate then to nucleotides

(Stop dna synthesis)

17
Q

Why don’t sulphonamides/ trimethoprim stop dna synthesis of host

A

We don’t produce folate ourselves we get it from diet

18
Q

What is good kinetically about sulphonamides

A

80-100% absorbed easily orally

19
Q

What is diff about distribution of sulphonamides to penecillin

A

Penecillin can’t cross csf

Sulphonamides do go to cns

20
Q

Where are sulphonamides metabolised

A

Liver

21
Q

Which antibiotics target type II isomerases and type IV to stop dna rep

A

Fluroquinolones

22
Q

Which topoisomerase is targeted in gram -ve by fluroquinolone and which gram +ve

A
  • = dna gyrase

+ = IV

23
Q

What is an issue with fluroquinolones in ADME

A

They are inhibitors of CYP 1a2 (stop metabolism of other drugs)

24
Q

Which drugs target ribosomes/protein synthesis

A

Macrolides and tetracycline

25
Q

What do macrolides do

A

Bind to the 50s subunit and prevent the translocation of the AA on the trna from the A site to the peptide site = no peptide bond

26
Q

Where on the 50s do macrolides bind

A

Exit site (PAE)

27
Q

Why do macrolides have to be coated for absorption

A

Destroyed in the stomach

28
Q

Where can’t macrolides distribute

A

Cns can’t cross BBB like penecillins

29
Q

How are macrolides metabolised

A

Cyp3a4

30
Q

How are macrolides excreted

A

Bile

31
Q

Name some adverse effects of macrolides

A

GI disturbance like penecillin

Hypersensitive reactions

Damage to ear drum

32
Q

How does tetracycline work

A

Binds to 30s and stops the binding of new trna

Stops ELONGATION

33
Q

When is absorbance of tetracycline highest

A

In fasting state

34
Q

Which drugs have large half life

A

Tetracycline (18hra)

35
Q

How is tetracycline excreted

A

Bile and kidney filtration

Pharmacology (24 decks)

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