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Y1 FHD > Antibiotics > Flashcards

Antibiotics Flashcards

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1
Q

Explain “bacteriostatic”

A

prevents bacterial replication

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2
Q

what is bactericidal

A

toxic to bacteria - kills them

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3
Q

When would a bacteriostatic not be indicated for patient

A

When the patient is immunosuppressed they will not be able to clear bacteria even if replication is reduced by the antibiotic dose, because their immune system is not working properly. A bacteriocidal antibiotic will be better in this case.

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4
Q

what is selective toxicity in reference to antibiotics

A

they must be highly effective against the microbe but have minimal or no toxicity to humans

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5
Q

What are the ideal characteristics of an antibiotic? (4 concepts here)

A
  • Selective toxicity
  • Slow emergence of resistance
  • Non-toxic to host
  • No interference with other drugs
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6
Q

What are beta lactamases

A

An enzyme produced by bacteria that catalyses hydrolysis of the beta-lactam ring (inactivates beta-lactamase drugs eg penicillins and cephalosporins)
Means bacteria have a type of antibiotic resistance

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7
Q

how to overcome beta lactam resistance
give an example

A

add in Beta-Lactamase inhibitors
e.g. Clavulanic acid (there are others)
‘Kamikaze’ drugs

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8
Q

how do Beta-Lactamase inhibitors work

A

irreversibly bind the beta lactamase - mop up the enzyme so it is no longer available to inactivate the antibiotic

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9
Q

What Beta lactam antibiotics are there?

A

Penicillins e.g., benzylpenicillin, flucloxacilin, amoxicillin

Cephalosporins e.g., cephalexin, cefuroxime

less mainstream

Carbapenems e.g., imipenem, meropenem

Monobactams e.g., aztreonam

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10
Q

How do beta lactams work

A

Binding bacterial transpeptidases which are enzymes essential for peptidoglycan synthesis
Transpeptidases ≡ Penicillin Binding Proteins
Inhibits cell wall formation and leads to cell lysis
Bactericidal
Functional unit – Beta lactam ring

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11
Q

Amoxicillin
Mechanism of action ?
Activity?

A

Mechanism of action
Inhibition of bacterial cell wall synthesis

Activity - Broad spectrum
S. pyogenes (sore throat, skin infections)
Pneumococcal infections (resp. tract)
Coliform infections (urinary tract infections)

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12
Q

Amoxicillin

GI Absorption?

Protein binding?

Metabolism?

Half-life?

Excretion?

A

GI Absorption Good

Protein binding 20%

Metabolism Not significant

Half-life 1 hour

Excretion Urine

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13
Q

Amoxicillin

Adverse effects?

Interactions?

co prescription?

A

Adverse effects

Allergy (penicillin antibiotic)

Damage to commensal microflora (GI disturbance, opportunistic infections from Candida albicans,..)

Interactions

Can increase levels of other protein bound drugs

Co-amoxiclav

Amoxicillin + clavulanic acid

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14
Q

Cephalosporins – Broad Spectrum
what is their activity

A

Activity against transpeptidases of different bacterial species

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15
Q

Glycopeptides
e.g. Vancomycin, teicoplanin, telavancin? G+ve or -ve bacteria?

A

– only active in G+ve because too large to cross the wall of gram -ve

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16
Q

When are glycopeptide antibiotics used? How to administer?

A

Used (intravenous) for serious Gram positive organisms which produce beta-lactamases or are not responding to other treatments

Oral: not absorbed but used to treat Clostridium difficile (anaerobic) associated with diarrhoea (vancomycin)

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17
Q

what are Glycopeptide antibiotics?

A

Glycopeptide antibiotics are a type of antibiotic that inhibits bacterial cell wall formation by inhibiting peptidoglycan synthesis

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18
Q

What are the risks of glycopeptide antbs

A

Important: Nephrotoxicity (renal toxicity)

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19
Q

Core Drug: Vancomycin
Activity?
Mechanism of action?

A

Activity
Only Gram-positive
Many resistant strains including Methicillin Resistant S. aureus (MRSA)

Mechanism of action
Inhibits bacterial cell wall (peptidoglycans) formation by a different target to beta lactams

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20
Q

Core Drug: Vancomycin
What to be wary of?

A

Narrow therapeutic window
Dose by drug levels in blood
Adverse effects
Nephrotoxic
Ototoxic (ear toxicity)

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21
Q

Core Drug: Vancomycin
GI absorption
Protein binding
Metabolism
Half-life
Excretion

A

GI absorption Very low
Protein binding 50%
Metabolism None (we don’t metabolise, pass through and excrete)
Half-life 4-8 hours
Excretion Urine

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22
Q

Ribosomal subunits in humans v bacteria

A

Humans (60/40) (???
Bacteria 50/30s (80)

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23
Q

How do antibiotics inhibit protein synthesis

A

act on 70s ribosomes (50s+30s)

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24
Q

What are Macrolides

A

Bacteriostatic or bactericidal (conc dependant)
Erythromycin, clarithromycin, azithromycin
Activity: Gram positives, Gram negatives and cell wall deficient bacteria
Similar spectrum to (broad spectrum) penicillins so can be prescribed instead for cases of allergy or resistance to penicillins

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25
Core Drug: Clarithromycin activity? MoA? adverse effects?
Activity - Broad spectrum Similar to amoxicillin S. pyogenes (sore throat, skin infections) Pneumococcal infections (resp. tract) Coliform infections (urinary tract infections) (patients with penicillin allergy) Cell wall deficient bacteria (e.g., Chlamydia) Mechanism of action Inhibition of protein synthesis in the bacterial ribosome (50S subunit) Adverse effects Nausea and diarrhoea May alter cardiac conduction - arrhythmias
26
Core Drug: Clarithromycin Oral Bioavailability Protein binding Metabolism Half-life Excretion
Oral Bioavailability Good Protein binding High Metabolism Hepatic Half-life 1~6 hours Excretion Metabolites in bile
27
Which drugs inhibit proteins synthesis?
Aminoglycosides Bactericidal Gentamicin Nephrotoxicity, ototoxicity Tetracyclines Bacteriostatic – broad spectrum Doxycycline, minocycline Phototoxicity, chelation\* of metal ions \*Deposition in teeth Bone growth inhibition
28
Aminoglycosides how do they work
inhibit proteins synthesis Bactericidal Gentamicin Nephrotoxicity, ototoxicity
29
Tetracyclines how do they work
inhibit proteins synthesis Bacteriostatic – broad spectrum Doxycycline, minocycline Phototoxicity, chelation\* of metal ions \*Deposition in teeth Bone growth inhibition
30
What is the risk of Tetracycline, especially in children
Deposition in teeth Bone growth inhibition
31
drugs affecting bacterial genetic material and metabolism - mechanisms
Inhibitors of DNA replication Drugs that damage DNA Inhibitors of RNA polymerase Antimetabolites inhibiting precursor synthesis e.g., sulphonamides, trimethoprim (co-trimoxazole)
32
how do Quinolones work
Inhibition of enzymes (DNA gyrases) needed for supercoiling, replication and separation of circular bacterial DNA - Rapid bacterial cell death
33
4 examples of Quinolones
Ciprofloxacin, nalidixic acid, norfloxacin, ofloxacin
34
cautions against Quinolones
Important: several interactions; caution in children can lead to resistant bacteria?
35
how does Metronidazole work
Prodrug – only anaerobic organisms can metabolite to its active form Metabolites produced are toxic to DNA – bactericidal Considered potentially mutagenic, carcinogenic, and teratogenic\* maximum of 10 days prescription because of side effects/risks. not good with alcohol!!
36
how does Rifampicin work
Bactericidal – Mycobacteria (M. tuberculosis, M. leprae) Binds to RNA polymerase → inhibits mRNA synthesis
37
risks of rifampicin
Important Metabolic interactions: strong induction of CP450 Orange colour: saliva, tears and sweat!!
38
what is an Antimetabolite
\*Antimetabolites - drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways
39
what is cp450
cytochrome p450 more than 50 enzymes, six of them metabolize 90 percent of drugs, with the two most significant enzymes being CYP3A4 and CYP2D6. Cytochrome P450 enzymes can be inhibited or induced by drugs, resulting in clinically significant drug-drug interactions that can cause unanticipated adverse reactions or therapeutic failures. Interactions with warfarin, antidepressants, antiepileptic drugs, and statins often involve the cytochrome P450 enzymes.
40
what is Synergistic association
Synergistic association - interaction or cooperation of two or more organisations, substances, or other agents to produce a combined effect greater than the sum of their separate effects
41
what is co-trimoxazole
Co-trimoxazole is generally bactericidal; it acts by sequential blockade of folic acid enzymes in the synthesis pathway. The sulfamethoxazole component inhibits formation of dihydrofolic acid from para-aminobenzoic (PABA), whereas trimethoprim inhibits dihydrofolate reductase. Both drugs block folic acid synthesis, preventing bacterial cell synthesis of essential nucleic acids.
42
Sulfonamide + trimethoprim is what sort of combination?
synergistic association 1+1 = more than 2 in effect strength
43
What is antibiotic resistance?
drug resistance bacteria Can be a consequence of antibiotic use and misuse Too long Too broad Ineffective
44
what is impact of antibiotic resistance on patient?
Patients with infections caused by drug-resistant bacteria are generally at increased risk of worse clinical outcomes and death
45
What are hospital acquired infections and why are they a problem?
A hospital-acquired infection (HAI) is an infection whose development is favoured by a hospital environment, such as one acquired by a patient during a hospital visit. for example MRSA Hospital-acquired infections (methicillin-resistant Staphylococcus aureus (MRSA) or multidrug-resistant Gram-negative bacteria)
46
what are the Resistance Mechanisms for bacteria (3 main?)
--Inherent (natural) resistance Acquired arises from --Mutations in cell genes (chromosomal mutation) leading to cross-resistance --Gene transfer (vertical or horizontal) Antibiotics do not CAUSE resistance, they affect the rate of spread
47
Antibiotic resistance - can antibiotics cause antibiotic resistance?
not at a molecular level. they create a selection pressure toward resistant strains and this is exacerbated by inappropriate use
48
How can bacteria resist antibiotics? (6 methods)
- Inactivation or modification of the antibiotic - Alteration of microbial enzymes that transform pro-drugs to the effective moieties - Alteration of the target - Reduced uptake of the antibiotic - Enhanced export of the antibiotic (efflux pumps) - Development of alternative pathways
49
How to fight antibiotic resistance??
Preventing infections from occurring and preventing resistant bacteria from spreading Tracking resistant bacteria Improving the use of antibiotics – how? Promoting the development of new antibiotics and new diagnostic tests for resistant bacteria NICE guidance - good prescribing practice
50
5 examples of antibiotic resistance currently of concern
- Methicillin-resistant Staph Aureus (MRSA) - Vancomycin resistant enterococcus (VRE) - Extended Spectrum β-lactamase producing organisms (ESBL/AMPC) - resistant TB - Acinetobacter
51
t/f Broad spectrum penillins do not disturb normal gut flora.
false
52
t/f Penicillins are bactericidal by binding to bacterial ribosome sites.
false
53
t/f Individuals who are allergic to penicillins can not be given cephalosporins.
false (although there is some cross activity, so some could be allergic to cephalosporins if already allergic to penicillin)
54
t/f/ Macrolides can cause GI disturbances.
true - broad spectrum
55
t/f Tetracyclines should be avoided during pregnancy and for young children
true - chelates calcium and inhibits bone growth
56
t/f Gentamicin (aminoglycoside) is not active when given orally.
true - is not absorbed (but still
57
t/f/ Gentamicin (aminoglycoside) has low incidence of adverse effects.
false
58
t/f Rifampicin is an important drug for the treatment of tuberculosis.
true adverse effect is orange tears/saliva/sweat cytochrome p450 strong induction and cross inhibition of other drugs
59
t/f Trimethoprim administration can result in tetrhydrofolate deficiency.
true - inhibits pathway to produce nucleic acids
60
t/f Resistance to antibiotics may be due to mutations in bacterial ribosomes.
true
61
80yr patient who has chronic leg oedema (fluid swelling) because of heart failure After a trip to the chiropodist she develops cellulitis (infection of the skin) over her leg Her GP knows the most common pathogen causing cellulitis is…?
Her GP knows the most common pathogen causing cellulitis is Streptococcus pyogenes And knows these are always susceptible to penicillins
62
80yr patient who has chronic leg oedema (fluid swelling) because of heart failure After a trip to the chiropodist she develops cellulitis (infection of the skin) over her leg Her GP knows the most common pathogen causing cellulitis is Streptococcus pyogenes And knows these are always susceptible to penicillins However, the patient is allergic to penicillin What could be the alternative?
Another broad spectrum antibiotic such as erythromycin, clarithromycin or azithromycin
63
what are macrolide's MoA
The mechanism of action of macrolides is inhibition of bacterial protein biosynthesis, and they are thought to do this by preventing peptidyltransferase from adding the growing peptide attached to tRNA to the next amino acid (similarly to chloramphenicol) as well as inhibiting bacterial ribosomal translation.
64
(Patient with cellulitis) 3 days later she returns A culture result has confirmed her strep IS sensitive to clarythromycin and her leg is better She is complaining of a sore mouth Why is her mouth sore?
Antibiotics select out commensals like candida which may then cause symptoms The patient was presenting oral thrush Candida albicans was probably a commensal in this patient but antibiotic therapy has made it a pathogen
65

Y1 FHD (12 decks)

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