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Drug Mechanisms of action > Antibacterial > Flashcards

Antibacterial Flashcards

1
Q

Define Bacteriostatic

A

An antibacterial agent that inhibits the growth of bacteria

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2
Q

Define Bactericidal

A

An antibacterial agent that kills the bacteria

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3
Q

Define Antibiotic

A

A drug used to treat infections caused by microorganisms

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4
Q

Name 3 root causes of infection

A
  1. Viral
  2. Fungal
  3. Bacterial
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5
Q

Name the 4 stages of infection

A

Stage 1 - Exposure to pathogen
Stage 2 - Pathogen crosses protective barrier
Stage 3 - Pathogen multiplies
Stage 4 - Pathogens move around the body

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6
Q

What 3 things are looked at in bacteria classification

A
  1. Cell wall structure - Gram +ve / Gram -ve
  2. Shape - Cocci (Round) / Bacilli (Rod)
  3. Oxygen requirements - Aerobic / Anaerobic
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7
Q

Name 3 Gram positive organisms

A
  1. Staphylococcus aureus (Cocci)
  2. Streptococcus pneumonias (Diplococci)
  3. Clostridium Difficile (Rod)
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8
Q

Name 3 Gram negative organisms

A
  1. Eschrichia Coli (Rod)
  2. Klebsiella pneumoniae
  3. Pseudomonas aerguinosa
  4. Salmonella typi (rods)
  5. Neisseria Meningitidis (diplococci)
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9
Q

Name the 5 main targets for antibacterials

A
  1. Cell wall synthesis
  2. Protein synthesis
  3. Nucleic acid synthesis
  4. Metabolic pathways
  5. Cell membrane function
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10
Q

Name the three main classifications of antibacterial agents

A
  1. Bacteriostatic/Bactericidal
  2. By chemical structure
  3. Bacterial spectrum
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11
Q

Describe what is meant by high therapeutic index

A

A high therapeutic index is good ! The Therapeutic Index of a drug is the ratio of the toxic to the therapeutic dose. Drugs with a low therapeutic index may only require a small increase in dose to produce toxic effects

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12
Q

What 3 main factors would guide your antibiotic choice

A
  1. The presumed site of infection - suspected or know organisms, positive micro results
  2. Poperties of the antibiotic - Route/cost/spectrum/pharmacokinetics
  3. Patient status - Immunosuppression/allergies/renal or hepatic dysfunction/contraindications/response to treatment
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13
Q

Describe the mechanism of action of β-lactame antibiotics

A

Inhibit the synthesis of the bacterium cell wall by affecting synthesis of peptidoglycan
This results in the dividing cells not being able to maintain the osmotic gradient
net effect is cell swelling, rupture, and death of the bacterium

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14
Q

What is peptidoglycan

A

Peptidoglycan is the cell wall that surrounds most bacteria and is essential for their survival

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15
Q

Describe the pharmacokinetics of β-lactame antibiotics

A

Absorption - may vary depending on stability in acidic conditions - Penicillin tablets are acid stable (Labile) so ideally taken 1-2 hours before food. Absorption can be altered by absorption of food in the gut

Excretion - Rapidly excreted (90% renal route) and so relatively short half life.

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16
Q

Describe some side effects and cautions when using β-lactame antibiotics

A

Allergic reaction - Up to 10% of exposed individuals (anaphylaxis less common at 0.05%)
Minor hypersensitivity
GI disturbances such as diarrhoea and nausea

17
Q

Describe how resistance can occur with β-lactame antibiotics

A

Inactivation of the β-lactame ring by an enzyme called β-lactamase. β-lactamase is produced by the bacteria itself. This splits open the β-lactame ring causing structural changes so unable to bind

18
Q

Describe a Type A drug reaction

A

Type A Reactions Type A (augmented) reactions result from an exaggeration of a drug’s normal pharmacological actions when given at the usual therapeutic dose and are normally dose-dependent. Examples include respiratory depression with opioids or bleeding with warfarin. Type A reactions also include those that are not directly related to the desired pharmacological action of the drug, for example dry mouth that is associated with tricyclic antidepressants.

19
Q

Describe a Type B drug reaction

A

Type B Reactions (bizarre) reactions are novel responses that are not expected from the known pharmacological actions of the drug. These are less common, and so may only be discovered for the first time after a drug has already been made available for general use. Examples include anaphylaxis with penicillin or skin rashes with antibiotics.

20
Q

Describe the action of a β-lactamase inhibitor

A

β-lactamase inhibitors have no bacterial activity and are useful where resistance is due to β-lactamase enzyme.

Increases spectrum of activity to include bacteria that produces the β-lactamase enzyme.

Example - Clavulanic Acid is a β-lactamase-inhibitor

Augmenting = Amoxicillin + Clavulanic acid

21
Q

Name members of the β-lactame group

A 
Penicillins
Cephalosporins
Carbapenems
Flucloxacillin
Co amoxiclav
22
Q

Describe Macrolides mechanism of action

A

Macrolides are protein synthesis inhibitors

They inhibit bacterial protein synthesis by binding to bacterial 50S subunit of the ribosome. These proteins are essential for the bacteria for functions such as growth, repair and reproduction. This action is considered bacteriostatic.

Macrolides are actively concentrated with leukocytes and are, therefore transported to the site of infection.

23
Q

What is a macrolide

A

Erythromycin, clarithromycin, azithromycin

Similar antibacterial spectrum to penicillin agents

Bacteriostatic, useful in both Gram +ve and some -ve

Allows the body natural immune system to fight the infection

Can be effective agains unusual organisms (Mycoplasma pneumonia)

24
Q

Describe the pharmacokinetics of Macrolides

A

Metabolised by the liver - Erythromycin and azithromycin are prepared for elimination - Clarithromycin is converted to an active metabolite.

Macrolides can inhibit cytochrome P450 leading to risk of toxicity/side effects

Variation in plasma half life - Erythromycin - 90mins, up to 24hours for Azithromycin

25
Q

What is a Tetracycline

A

Tetracycline, Doxycycline, Minocycline

Broad spectrum antibiotics

Bacteriostatic

Issues with widespread resistance so limits use, good at treating intracellular infections.

26
Q

Describe Tetracyclines mechanism of action

A

Inhibits bacterial protein synthesis by binding to bacterial 30S subunit.

Accumulates in cells by active transport and passive diffusion. Resistance occurs if efflux pump exists

27
Q

Describe the side effects and cautions when using Tetracyclines

A

Oral absorption is effected by Calcium, magnesium, iron and food.

Should be avoided in pregnancy, breast feeding and children under 12 (Binds to calcium in growing bones and teeth causing discolouration)

May cause photosensitivity

GI upsets are common

28
Q

What are Amino glycosides

A

Gentamicin, Streptomycin, Amikacin, Neomycin

Narrow spectrum (Gram -ve mainly)
Reserved for serious Gram-ve infections e.g. pseudomonas

Bactericidal

Narrow therapeutic index (Requires close monitoring)

All given IV for systemic infections

29
Q

Describe the mechanisms of action of Amino glycosides

A

Inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit

This stops translation of mRNA into the proteins

They also cause transient holes in the cell membranes causing polysaccharide links to break (This is linked to bactericidal activity)

30
Q

Describe the pharmacokinetics of Amino glycosides

A

Not absorbed in the GI tract so given IM or IV.
Half life is 2-3 hours

Excreted via renal glomerular filtration - in renal impairment accumulation occurs rapidly resulting in toxicity.

Regular plasma monitoring essential
Dose adjustment is essential in renal impairment

31
Q

Describe cautions and side effects to consider when prescribing Amino glycosides

A

Ototoxicity - can lead to progressive damage to sensory cells, results can be irreversible including, vertigo, loss of balance, auditory disturbances, deafness.

Ototoxic effects are increased by the ototoxic drugs - i.e. loop diuretics

Nephrotoxic - Damage to kidney tubules

32
Q

What is a Quinolone

A

Ciprofloxacin, Levofloxacin, Norfloxacin

Broad spectrum of activity

Bactericidal

33
Q

Describe the mechanism of action of a Quinolone

A

Block the action of the enzyme DNA gyrate. DNA gyrate is responsible for forming DNA supercoils for replication and repair

Inhibition of the replication of bacterial DNA

Drug Mechanisms of action (2 decks)

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