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Y1 FHD > Antibiotics > Flashcards

Antibiotics Flashcards

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
Q

Core Drug: Clarithromycin
activity?
MoA?
adverse effects?

A

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

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26
Q

Core Drug: Clarithromycin

Oral Bioavailability
Protein binding
Metabolism
Half-life
Excretion

A

Oral Bioavailability Good
Protein binding High
Metabolism Hepatic
Half-life 1~6 hours
Excretion Metabolites in bile

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27
Q

Which drugs inhibit proteins synthesis?

A

Aminoglycosides
Bactericidal
Gentamicin
Nephrotoxicity, ototoxicity

Tetracyclines
Bacteriostatic – broad spectrum
Doxycycline, minocycline
Phototoxicity, chelation* of metal ions
*Deposition in teeth
Bone growth inhibition

28
Q

Aminoglycosides how do they work

A

inhibit proteins synthesis
Bactericidal
Gentamicin
Nephrotoxicity, ototoxicity

29
Q

Tetracyclines how do they work

A

inhibit proteins synthesis
Bacteriostatic – broad spectrum
Doxycycline, minocycline
Phototoxicity, chelation* of metal ions
*Deposition in teeth
Bone growth inhibition

30
Q

What is the risk of Tetracycline, especially in children

A

Deposition in teeth
Bone growth inhibition

31
Q

drugs affecting bacterial genetic material and metabolism - mechanisms

A

Inhibitors of DNA replication

Drugs that damage DNA

Inhibitors of RNA polymerase

Antimetabolites inhibiting precursor synthesis e.g., sulphonamides, trimethoprim (co-trimoxazole)

32
Q

how do Quinolones work

A

Inhibition of enzymes (DNA gyrases) needed for supercoiling, replication and separation of circular bacterial DNA - Rapid bacterial cell death

33
Q

4 examples of Quinolones

A

Ciprofloxacin, nalidixic acid, norfloxacin, ofloxacin

34
Q

cautions against Quinolones

A

Important: several interactions; caution in children can lead to resistant bacteria?

35
Q

how does Metronidazole work

A

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
Q

how does Rifampicin work

A

Bactericidal – Mycobacteria (M. tuberculosis, M. leprae)
Binds to RNA polymerase → inhibits mRNA synthesis

37
Q

risks of rifampicin

A

Important
Metabolic interactions: strong induction of CP450
Orange colour: saliva, tears and sweat!!

38
Q

what is an Antimetabolite

A

*Antimetabolites - drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways

39
Q

what is cp450

A

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
Q

what is Synergistic association

A

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
Q

what is co-trimoxazole

A

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
Q

Sulfonamide + trimethoprim is what sort of combination?

A

synergistic association 1+1 = more than 2 in effect strength

43
Q

What is antibiotic resistance?

A

drug resistance bacteria
Can be a consequence of antibiotic use and misuse
Too long
Too broad
Ineffective

44
Q

what is impact of antibiotic resistance on patient?

A

Patients with infections caused by drug-resistant bacteria are generally at increased risk of worse clinical outcomes and death

45
Q

What are hospital acquired infections and why are they a problem?

A

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
Q

what are the Resistance Mechanisms for bacteria (3 main?)

A

–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
Q

Antibiotic resistance - can antibiotics cause antibiotic resistance?

A

not at a molecular level. they create a selection pressure toward resistant strains and this is exacerbated by inappropriate use

48
Q

How can bacteria resist antibiotics? (6 methods)

A
  • 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
Q

How to fight antibiotic resistance??

A

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
Q

5 examples of antibiotic resistance currently of concern

A
  • Methicillin-resistant Staph Aureus (MRSA)
  • Vancomycin resistant enterococcus (VRE)
  • Extended Spectrum β-lactamase producing organisms (ESBL/AMPC)
  • resistant TB
  • Acinetobacter
51
Q

t/f Broad spectrum penillins do not disturb normal gut flora.

A

false

52
Q

t/f Penicillins are bactericidal by binding to bacterial ribosome sites.

A

false

53
Q

t/f Individuals who are allergic to penicillins can not be given cephalosporins.

A

false (although there is some cross activity, so some could be allergic to cephalosporins if already allergic to penicillin)

54
Q

t/f/ Macrolides can cause GI disturbances.

A

true - broad spectrum

55
Q

t/f Tetracyclines should be avoided during pregnancy and for young children

A

true - chelates calcium and inhibits bone growth

56
Q

t/f Gentamicin (aminoglycoside) is not active when given orally.

A

true - is not absorbed (but still

57
Q

t/f/ Gentamicin (aminoglycoside) has low incidence of adverse effects.

A

false

58
Q

t/f Rifampicin is an important drug for the treatment of tuberculosis.

A

true
adverse effect is orange tears/saliva/sweat
cytochrome p450 strong induction and cross inhibition of other drugs

59
Q

t/f Trimethoprim administration can result in tetrhydrofolate deficiency.

A

true - inhibits pathway to produce nucleic acids

60
Q

t/f Resistance to antibiotics may be due to mutations in bacterial ribosomes.

A

true

61
Q

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…?

A

Her GP knows the most common pathogen causing cellulitis is Streptococcus pyogenes
And knows these are always susceptible to penicillins

62
Q

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?

A

Another broad spectrum antibiotic such as erythromycin, clarithromycin or azithromycin

63
Q

what are macrolide’s MoA

A

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
Q

(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?

A

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
Q
A

Y1 FHD (12 decks)

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