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Human Diseases > W5 23 anti-bacterial drugs > Flashcards

W5 23 anti-bacterial drugs Flashcards

1
Q

What are antibacterial drugs?

A

Substances/chemicals killing or preventing the growth of bacteria

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2
Q

What is the difference between bacteriostatic and bactericidal?

A

Bacteriostatic = halts the growth of the bacteria without killing
Bactericidal = kills the bacteria, can’t come back after finishing antibiotic therapy

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3
Q

What is selective toxicity?

A

Kills bacteria without harming the host

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4
Q

Features of bacterial cells

A

Peptidoglycan cell wall (good target for selective toxicity)
Plasma membrane
Singular, circular chromosome
Protein synthesis
Energy metabolism - no mitochondria

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5
Q

Bacteria has 3 classes of mechanisms for their metabolism. What is class I and is it a good therapeutic agent?

A

Class I reactions are the reactions that utilise the nutrients and resources from the environment to make the precursor molecules that are needed for the macromolecules of the cells and needed for the production of ATP. (Not a good therapeutic target because these reactions are similar in human cells).

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6
Q

Bacteria has 3 classes of mechanisms for their metabolism. What is class II and is it a good therapeutic agent?

A

Class II reactions utilise the precursor molecules that are made by the cell to make the first building blocks of the macromolecules (hexosamines, amino acids, nucleotides)
Better targets than class I, some of these are specific for bacteria.

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7
Q

Bacteria has 3 classes of mechanisms for their metabolism. What is class III and is it a good therapeutic agent?

A

Class III reactions lead to the production of the large macromolecules like peptidoglycan, proteins, RNA and DNA
Best targets - specific macromolecules to the bacteria, good selective toxicity

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8
Q

What are some potential targets Class II reactions?

A

Folate metabolism
Folate utilisation
Sulphonamides

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9
Q

What is the difference between folate metabolism in humans and bacteria?

A

Human cells don’t make folate, we take it up from the environment. Used to make DNA.
Bacteria make their own folate from precursor PABA, and unable to take up folate from the environment.

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10
Q

How does inhibiting folate metabolism stop bacteria growth?

A

Interrupting the folate metabolic pathway in bacteria will inhibit DNA synthesis in these cells. Would be bacteriostatic, halting growth of the colony and division but not killing the bacteria.

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11
Q

What’s the difference between sulphonamides and trimethoprim?

A

Sulphonamides as antibiotics stop the production of folate from PABA in bacterial cells, interfering with DNA production. Bacteriostatic.
Trimethoprim interfere with the utilisation of folate by bacteria (only in bacterial cells). Bacteriostatic.

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12
Q

Why would we not use sulphonamides in dental practice?

A

Sulphonamides are competitive antagonists of PABA, so if there is excess PABA it won’t be effective. Procaine, an LA, produces PABA esters, so provide the competitive antagonist the the drug. So unuseful.
Pus has purines and pyramidine bases as breakdown products. Bacteria can use these when they cannot make folate to make their DNA.
Plasmid-mediated resistance

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13
Q

What antibiotics inhibit peptidoglycan synthesis? (Targeting class III reactions)

A

Penicillins
Cephalosporins
Cycloserin
Vancomycin
Bacitracin

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14
Q

What are penicillins the first drug choice for?

A

First choice drug for bone and joint infections
- can be given IM or IV
- absorption from GI tract variable

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15
Q

Why has resistance to penicillin spread among bacteria?

A

Bacteria produce b-lactamases - an enzyme that deactivates penicillin
Some gram-negative bacteria are resistance due to a reduction of membrane permeability so don’t uptake it
Modified penicillin binding sites by mRSA

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16
Q

Downsides of penicillin

A

GI disturbances like nausea and diarrhoea (treatable after antibiotics stop GI flora returns to normal)
Serious side effects - hypersensitivity reactions

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17
Q

Is there resistance by bacteria to cephalosporins?

A

Yes, same reasons as penicillin

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18
Q

What are the side effects of cephalosporins?

A

Unpleasant side effects - diarrhoea, nausea, intolerance to alcohol
Serious side effects - hypersensitivity reactions, neurotoxicity

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19
Q

Which types of antibiotics inhibit protein synthesis (class III)?

A

Tetracyclines
Aminoglycosides
Erythromycin

20
Q

What is the mechanism of protein synthesis in bacterial cells?

A

mRNA brings message along
tRNA brings amino acid into the A side
Process and new site moves over to the P side and cycle gets repeated
(Can interfere at some sites at the ribosome that will not affect human cells)

21
Q

What mechanism do tetracyclines inhibit protein synthesis of bacteria, and why do humans not respond?

A

They compete with tRNA for the A site, prohibiting the insertion of the tRNA bringing new amino acids.
Tetracyclines cannot go into human cells, they are selectively taken up by prokaryotes. Selective toxicity.

22
Q

What is the spectrum of bacteria that tetracyclines can affect?

A

Wide spectrum - gram + and gram - bacteria
Mycoplasma, Ricketsia, Neisseria meningitis

23
Q

Are tetracyclines absorbed from the GI?

A

Absorption from GI variable

24
Q

What are the unpleasant side effects of tetracyclines and how are they treatable?

A

GI disturbances, dizziness and nausea, diarrhoea, vitamin B complex deficiency (since they kill the gut bacteria that help us absorb this)
Deficiency treated with supplements. GI disturbances stop after finishing therapy.

25
Q

What are serious side effects of tetracyclines?

A

Hepatotoxicity
Renal damage (mainly affecting people with already damaged liver and kidney functions)
Teratogenic - can cause dental hypoplasia and bone deformities in unborn babies (don’t give to women of reproductive age unless certain they aren’t pregnant).

26
Q

By what mechanism do aminoglycosides work?

A

Aminoglycosides interfere with anticodon recognition, so bacteria ribosomes misinterpret the mRNA message, producing an unfunctional protein.

27
Q

What spectrum antibiotics are aminoglycosides?

A

Efficient against gram - enteric organisms eg Streptococcus, Listeria, Pseudomonas aeruginosa
Used mainly in sepsis

28
Q

How are aminoglycosides administered?

A

IM or IV, not intra-oral because they are not absorbed from the GI

29
Q

Side effects of aminoglycosides

A

Ototoxicity - toxic to the auditory nerve, can lead to nerve deafness
Nephrotoxicity

30
Q

By what mechanism does erythromycin act?

A

It inhibits translocation of tRNA from A site to P site of the ribosome, after new amino acid has been added to the chain. Thus polypeptide chain cannot be continued, producing a short dysfunctional peptide fragment rather than full protein.

31
Q

Why is erythromycin good to use?

A

Similar to penicillins, but people are not as allergic. Given to penicillin-sensitive patients. Resistance might still occur however.

32
Q

What are all the side effects of erythromycin?

A

Unpleasant - GI disturbances, similar to penicillin, can be tolerated
Treatable - opportunistic infections (mainly Candida albicans)
Serious - cholestatic jaundice (very rare), hypersensitivity (rare)

33
Q

Clindamycin inhibits protein synthesis of bacteria. Many dentists use it. Describe it.

A

Broad spectrum, easily tolerated, can be given by mouth

34
Q

What is the issue with clindamycin?

A

If you use it, it will kill a lot of the gut bacteria, potentially providing C. difficile with a growth advantage. Can cause severe problems. Particular associated with pseudomembranous colitis. Will kill the patient within a week.

35
Q

What advice should you give patients on clindamycin?

A

Warn them that any (even minor) GI disturbance, diarrhoea, bloating, immediately stop the drug and return, and need treatment if they get pseudomembranous colitis.

36
Q

What drugs interfere with energy metabolism?

A

Metronidazole

37
Q

How does metronidazole work?

A

Effective against anaerobic bacteria and protozoa (including C difficile)
In cells that don’t have mitochondria, the breakdown products of metronidazole will become cytotoxic and destroy the cell from within. Thus saves pt from pseudomembranous colitis.

38
Q

Side effects of metronidazole

A

Nausea, metallic taste
Disulfiram-like reaction with alcohol (don’t drink on this!)

39
Q

How do bacteria share their antibiotic resistance genes?

A

Bacteria can share their plasmids with one another via:
- conjugation - process of sharing a plasmid with a resistance gene from one live bacteria to another
- transduction - viruses can transport genes from one bacterium to another
- when a bacterium dies it releases contents to the environment and live bacteria can pick up these fragments of DNA and increase their arsenal of resistance for the future, sharing these further.

40
Q

How do genes in bacteria cause antibiotic resistance?

A

Genes in plasmid can:
- make an enzyme to drag de the antibiotic
- make efflux pumps that get rid of the antibiotic
- make enzymes that alter the antibiotic rendering it inefficient against the bacteria itself

41
Q

How do resistance bacteria have a selective advantage over antibiotic sensitive bacteria!

A

They multiply more easily producing larger numbers, facilitating spread

42
Q

Which drugs have which mechanisms of drug resistance?

A

Altered drug targets or metabolic pathways - eg acyclovir, rifampicin
Decreased access/increases export - eg chloroquine
Drug inactivation - penicillin, aminoglycosides

43
Q

Contraindications of antibiotics

A

Site of infection determining effective dose
Other drugs can interact
Pregnancy - watch women at reproductive age
Immune system - immunocompromised patients might need strong antibiotics
Drug resistance - previous use of antibiotics
Side effects - age, renal, hepatic function
Hypersensitivity reactions

44
Q

How can site of infection determine effective dose of antibiotics!

A

Small ineffective doses will promote resistance and development of sensitisation and won’t kill the bacterium.
Most infections are in bone, which need higher doses than soft tissues

45
Q

How might other drugs interact with antibiotics?

A

Might affect half life of the antibiotic
Antibiotic might affect other drugs and increase their toxicity
Combinations might be additive, synergistic, antagonistic. Can increase risk of adverse reactions.

46
Q

When can antibiotics be used in dental surgery?

A

Used to supplement:
- persistent/advanced infections
- complex gum or implant surgery
- patients with a weak immune system
- prevention of bacterial endocarditis in patients at HIGH risk

Human Diseases (75 decks)

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