Antibiotics Flashcards

1
Q

Explain the different names for antibiotic effects on bacteria.

A

Bactericidal- kill bacteria

Bacteriostatic- inhibit growth of bacteria.

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2
Q

Explain the different antibiotic spectrum.

A

Broad spectrum- larger number of bacteria species
Narrow spectrum- limited number of bacteria
Limited spectrum- one species.

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3
Q

Explain the characteristics of bacteria.

A

Toxic only to bacteria.

Innocuous to humans- little to no side effects.

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4
Q

Explain the cell wall of bacteria.

A

Humans do not have a cell wall, it is a bacteria specific organelle
Responsible for integrity and protection.
Main target for antibiotics
No CW= death by autolysis.

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5
Q

What is unique about bacteria that stain purple?

A

They are gram positive bacteria with a thick layer of peptidoglycan.
Easier to target than gram- due to the thick chains between the peptidoglycan.

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6
Q

List a number of antibiotics that act on peptidoglycan biosynthesis.

A

Penicillin
Chephlaosporin
Carbapenems.
Vanomycin.

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7
Q

Explain B-lactam antibiotics.

A

Effective against growing and dividing cells.
Bactericidal
Inhibit transpeptidase cross-linking reaction.

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8
Q

What is a limitation of B-lactam antibiotics.

A

Resistant bacterial species produce B-lactamse- an enzyme that inactivates antibiotics by breaking down their B-lactam ring.

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9
Q

What are examples of B-lactam antibiotics?

A

Penicillins- drugs that end in cilin.
Cephlaosporins- drugs that start with cef.
Carbapenems- drugs that end in penem.

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10
Q

What are the key characteristics of penicillins?

A

Bactericidal

Very effective against G.negative.

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11
Q

What are the key characteristics of cephlaosporins?

A

Bactericidal
Effective against gram positive and negative bacteria.
Can be anaerobes.

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12
Q

What are the key characteristics of carbapenems?

A

Bactericidal
Broad spectrum drug
Administered IV.
Affective against all but MRSA and VRE.

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13
Q

Explain vancomycin.

A

Inhibitor of CW biosynthesis.
Glycopeptide antibiotic.
Administered IV.
Effective against MRSA however there are emerging cases of VRSE and VRE resistance.

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14
Q

Explain antibiotics that inhibit protein synthesis.

A

Broad spectrum- effective against positive and negative.
Most are bacteriostatic.
Associated with toxicity because mitochondrial ribosomes are inhibited too.

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15
Q

What are examples of antibiotics that inhibit protein components of 30S subunit?

A

Tetracycline

Aminoglucosid (gentamycin and streptomycin)

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16
Q

What are examples of antibiotics that inhibit protein components 50S.

A

Macrolides (erythromycin)

Chloramphenicol.

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17
Q

Explain fluoroquinolones.

A

Antibioitics that inhibit DNA biosynthesis.
Borad spectrum drugs that inhibit DNA gyrase.
Effective against gram negative bacteria and intracellular pathogens.
High toxicity

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18
Q

What are examples of fluoroquinolones?

A

Ciprifloxacin
Norfloxacin
Drugs that end in floxacin.

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19
Q

Explain rifampicin.

A

Antibiotics that inhibit RNA biosynthesis in bacterial RNA.

Used predominantly in the treatment of TB.

20
Q

Explain the target of nucleic acid in biosynthesis.

A

The biosynthesis of nucleotides requires folic acid.

Anti-metabolites target and inhibit folic acid synthesis.

21
Q

Explain sulfonamides.

A

Anti-metabolites.

Analogue of PABA- inhibits dihydropteroate syntheses.

22
Q

Explain trimethoprim.

A

Antimetabolites.

Inhibits dihydrofolate reductase.

23
Q

Explain co-trimoxazole.

A

Combination of sulphonamides and trimethoprim.

24
Q

What antibiotics are produced by fungi?

A

Penicillin and cephlaosporin.

25
Q

What antibiotics are produced by bacteria?

A

Erythromycin, rifampicin, streptomycin and tetracyline.

26
Q

What antibiotics are semi-synthetic?

A

Ampicillin.

27
Q

What bacteria are synthetic?

A

Sulfonamides and trimethoprim.

28
Q

What does the choice of antibiotic treatment depend upon?

A
Bacterial species
Susceptibility to drug
Site of infection
Safety of drug
Cost of therapy
Patient factors.
29
Q

Resistance to antibiotics arises due to?

A

Mutation of gene encoding targets of common antibiotics (VGT).
Transfer between organisms of resistant genes carried by plasmids (HGT)
Biofilm formation.

30
Q

Biochemical resistance is manifested by..?

A

Decreased accumulation of the drug.

Enzymatic inactivation.

31
Q

Where do superficial mycoses affect?

A

Scalp, nails, mucous membranes (mouth and vagina).

Are non-lifethreatening.

32
Q

Where do systemic mycoses effect?

A

Internal organs- lung, kidney, brain.

Can be fatal in immunocompromised patients.

33
Q

What puts a patient at a higher risk of fungal infections?

A

HIV, organ transplant, long term antibioitics, premature birth, cancer, mestrual cycle.

34
Q

What are echinocandins?

A

Anti fungal drug that inhibits gluten synthetase.

Fungicidal

35
Q

What are examples of echioncandins?

A

Caspofungin

Micafungin.

36
Q

What are the target for most antifungals?

A

The plasma membrane.

37
Q

What are the actions of antifungals that target the plasma membrane?

A

Target ergosterol.

38
Q

Explain polyene antifungals.

A

Bind to resident ergosterol and form pores in the plasma membrane. The poor disrupt the membrane integrity killing the cell.
Fungicidal.

39
Q

What is a disadvantage of polyene antifungals?

A

Prolonged use can lead to kidney failure.

40
Q

List examples of polyene antifungals.

A

Amphotericin B.
Nystatin
Both are of natural origin.

41
Q

Explain azoles.

A

Ergosterol biosynthesis inhibitors.
Inhibit Lanosterol C14.
Fungatisitc.

42
Q

What are two types of azalea antifungals?

A

Imidazole and triazole.

Triazole has a higher affinity for enzymes so is therefore more potent.

43
Q

What are examples pf allylamnes?

A

Drugs that end in fine.

44
Q

Explain flucytosine.

A

Taken up my fungal cells and are metabalised into 5-FU.
5FU inhibit fungal DNA and RNA.
Commonly used in combination with azoles.

45
Q

Resistance to antifungal durgs is caused by?

A

Decreased accumulation of the drug
Inactivation of the drug
Mutation in drug encoding genes
Biofilm formation.