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Pharmacology 201 > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What is the difference between antibiotics and antibacterials?

A

Antibiotics were originally derived from a living source.

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2
Q

When was Penicillin discovered?

A

1928

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3
Q

What was the first antibiotic clinically used?

A

Prontosil

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4
Q

What are bacterial diseases?

A

Infections caused by bacteria that have deviations from normal flora, which is healthy bacteria necessary for normal function.

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5
Q

How do antibiotics work?

A

By directly attacking the source within damaging our own cells

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6
Q

What is the cell envelope and how does it relate to bacteria?

A

The cell envelope encompasses the cytoplasmic membrane. It is the basic that segregates gram (+) bacteria from gram (-) bacteria. The cell envelope impacts how easy antibiotics can access it and its selectivity.

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7
Q

What are gram (+) cells?

A

Gram (+) cells have many peptidoglycan linked together to provide rigidity and strength for the cell.

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8
Q

What are gram (-) cells?

A

These cells only have a small peptidoglycan layer, but they have a secondary membrane.

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9
Q

What mechanisms do antibiotics use to destroy bacteria?

A
  • Breakdown of the Cell Wall
  • Inhibition of Protein Production
  • Inhibit of DNA replication and hence cell division
  • Inhibition of Nucleotide Production
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10
Q

How do antibiotics break down the cell wall?

A

Primarily in gram (+) bacteria, binding proteins inhibit the growth and development of the cell wall by preventing peptidoglycan links from forming its structure. This renders the bacteria cell vulnerable to osmotic pressures and disrupts cell activity.

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11
Q

What kind of antibiotics use this MOA?

A

Antibiotics with a B-Lactam ring. These are Penicillins and Cephalosporins.

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12
Q

Where are Penicillins derived from?

A

Fungus

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13
Q

Do they treat gram (+) or gram (-)?

A

Primarily gram (+) but sometimes gram (-) are supsceptible.

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14
Q

Are all gram (+) strains treatable by Penicillin?

A

No, some gram (+) may have natural resistance due to the degradation by B-lactamase enzymes. If the B-lactam ring is broken down, the antibiotic is practically ineffective.

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15
Q

What family members are in the Penicillin family?

A

Penicillin V, Penicillin G, and Ampicillin

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16
Q

Explain the Pharmacokinetics for Penicillin

A

A - oral, but absorption can depend on the pH of the stomach
D - travels to all the tissues in equal concentrations, but has poor permeability in the CNS
M/E - Majority is excreted unmetabolized through the urine
Half Life: 30 mins - 1 hr

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17
Q

What are the side effects of Penicillin?

A

Although it is among one of the safest drugs in used today, about 5% of the population is sensitive to Penicillin.
- Rash, Edema, and Anaphylaxis

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18
Q

Why does cation toxicity occur with Penicillin?

A

This drug is given as a sodium/potassium salt. A large does can fluctuate concentrations of crucial ions/electrolytes in the body. This can cause Hyperkalemia, and Hypernatremia.

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19
Q

How are Cephalosporins classified?

A

Classified by generation such as:

  • effectiveness of penetrating gram (+) vs gram (-) strains
  • ability to cross BBB
  • cross sensitivity
  • resistance to B-lactamase
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20
Q

What can Cephalosporins do that Penicillin cannot?

A

A broad spectrum antibiotic that has the ability to cross the BBB. Some are also resistant to B-lactamase.

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21
Q

What are the side effects of Cephalosporins?

A
  • there is potential for cross sensitivity for those who are allergic to Penicillin.
  • people should avoid drinking alcohol when on Cephalosporins because it can induce Disulfiram like reactions in certain individuals
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22
Q

How do antibiotics inhibit protein production?

A

Antibiotics can bind to their (30s or 50s) ribosome subunits to block tRNA access. As a result, this inhibits translation/peptide elongation. If proteins cannot be synthesized, bacteria cannot grow.

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23
Q

Which antibiotics use this MOA? (MATC)

A

Tetracyclines, Aminoglycosides, Macrolides and Chloramphenicol.

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24
Q

How does Tetracycline use this MOA?

A

It binds to 30s ribosomal subunits, block tRNA access and peptide elongation.

25
Q

What kind of antibiotic is Tetracycline?

A

It is a broad spectrum antibiotic that can treat many gram (+) and (-) strains.

26
Q

How does Tetracycline travel?

A

Using passive diffusion and active transport.

27
Q

What is the pharmacokinetic process for Tetracycline?

A

A - oral
D - can distribute a bit to the CNS in BBB. It also binds to tissues undergoing calcification
M - short, medium, and long acting derivatives
E - urine

28
Q

Why should people avoid eating or drinking dairy products, taking Anti-acids or juice when on this medication?

A

Tetracycline binds to cations, which prevents the antibiotic from absorbing into the system.

29
Q

What are the side effects of Tetracycline?

A
  • gastric discomfort (which may cause non-compliance)
  • can cause calcium deposits in teeth which cause discolouration
  • temporary growth stunting (binds to calcium in the bone framework and prevents growth) (kids under 8 should avoid)
30
Q

Why should pregnant women avoid this drug?

A

Tetracycline passes through placenta

31
Q

How do aminoglycosides inhibit protein production?

A

Binds to the 30s ribosomal subunit

32
Q

Which strain is aminoglycosides most effective in treating?

A

Gram (-)

33
Q

How does Aminoglycosides travel throughout the body?

A

Active Transport. They require this because the drug is thick and bulky.

34
Q

Why are Aminoglycosides less susceptible to treating gram (+) bacteria?

A

Since they are very bulky, they get stuck in the peptidoglycan layer.

35
Q

How can this be used in combination to treat gram (+) strains?

A

If combined with a B-lactam, it can break down down the cell wall, and then a Amino-glycoside can be added.

36
Q

What are the Aminoglycosides?

A

Ototoxicity (hearing loss) and nephrotoxicity (can be reversible if drug is only used in short duration).

37
Q

What are names of some Aminoglycosides?

A

Streptomycin, Neomycin, and Gentamicin.

38
Q

How do Macrolides and Chloramphenicol inhibit protein production?

A

They bind to the 50s ribosomal subunits, thus inhibiting peptide formation.

39
Q

Which strains can Macrolides and Chloramphenicol treat?

A

many gram (+) and gram (-) strains. They are broad spectrum.

40
Q

What are examples of Macrolides?

A

Erythromycin, and Clarithromycin

41
Q

Can Chloramphenicol enter BBB?

A

Yes readily, which is good for CNS infections.

42
Q

How do antibiotics inhibit DNA replication?

A

They prevent bacteria cells from dividing and readily proliferating by blocking DNA replication by two very crucial enzymes known as DNA Gyrase, and Topoisomerase IV.

43
Q

Which type of antibiotics can use this MOA?

A

Fluroquinolones such as Norvoflacin, Ciproflaxcin, and Levofloxacin.

44
Q

How do Fluroquinelones enter body?

A

Passive diffusion

45
Q

How many generations of this drug are there?

A

4, and they generally progress towards those that have distribute more systemically, and increased effective against anaerobic gram (+) bacteria.

46
Q

What are the side effects of Fluroquinelones?

A
  • generally well tolerated
  • nausea, diarrhea
  • can break down cartilage and cause joint pain
  • avoid for pregnant women and in children under 18
  • may cause irregular heart beat
47
Q

How do antibiotics alter nucleotide synthesis?

A

They inhibit tetrahydrofolic, a folate derivative that is needed for nucleotide production. By inhibiting this, the building blocks form DNA cannot form, and bacteria cannot be synthesized.

48
Q

What type of antibiotics inhibit nucleotide synthesis?

A

Sulphonamides, and Trimethoprim.

49
Q

What strains of bacteria can they inhibit?

A

Both gram (+) and gram (-).

50
Q

Can they penetrate BBB?

A

Yes.

51
Q

What is Cotrimoxazole?

A

A combination antibiotic of both Sulphonamide and Trimethoprim. It completely inhibits the bacteria.

52
Q

Side effects of Sulphonamide?

A
  • acetylated metabolite that causes crystals in acidic or neutral pH.
  • Crystaluria (in urine)
  • hematouria (crystals that can cause bleeding)
  • obstruction of urine by large crystals
53
Q

Side effects of Trimethoprim?

A
  • can exacerbate folic acid deficiency
54
Q

How does on select an antibiotic?

A
  • decide what kind of strain by identifying bacteria through culture
  • check if it is resistant
55
Q

How about in critical situations?

A
  • pick a broad spectrum antibiotic to buy time
  • does it need to cross BBB
  • understand patient history
56
Q

what are some patient factors?

A

cost, safety of agent (sensitivities), renal/hepatic systems, pregnancy and age.

57
Q

What types of dosing are there?

A

Concentration dependent or time dependent.

58
Q

What is concentration dependent dosing?

A

Efficacy is related to Cmax. How large peak concentration is, rather than how long it is there is more important. Once a day therapy is usually enough. Ex: Aminoglycosides or Rifampin

59
Q

What is time depending dosing?

A

Time dependent dosing does depend on the peak concentration, but rather how long you are above the minimum inhibitory concentration. Usually dosing is multiple times a day. EXAMPLE: B-lactam

Pharmacology 201 (20 decks)

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