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ACEM viva > antibiotics pharmacology > Flashcards

antibiotics pharmacology Flashcards

1
Q

Describe the mechanism of action of penicillins

A

● Bacteriocidal
● Inhibition of bacterial cell wall synthesis
● Covalent binding to penicillin binding proteins
● Interfere with cross linking and formation of peptidoglycan

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2
Q

How does resistance to penicillins occur?

A

● Inactivation by beta-lactamase
● Modification of target penicillin binding proteins
● Impaired penetration of drug
● Efflux pumps

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3
Q

What is the microbial spectrum of penicillin G?

A

● Streptococci, meningococci, enterococci, some pneumococci
● Treponema pallidum
● Clostridia
● Non beta lactamase producing staph

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4
Q

What are the manifestations of penicillin allergy?

A

● Anaphylaxis
● Fever
● Skin pathology – rash, Steven Johnson Syndrome

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5
Q

What are some other side effects of penicillin?

A

● Renal failure
● Seizure at high doses
● GI disturbance
● Hepatitis

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6
Q

How are penicillins eliminated in the body?

A

● Renal excretion and active secretion
● Biliary secretion

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7
Q

How does probenecid alter the elimination of some penicillins?

A

● Inhibits secretion of weak acid from the proximal tubule.

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8
Q

What circumstances encourage the development of bacterial resistance to
antimicrobial agents?

A

ntimicrobial agents?
● Resistance is an example of natural selection and arises through spontaneous
mutations or DNA exchange between bacteria.
● It is promoted by :
● Dirty hospital environments with multiple species of bacteria cp-existing and
exchanging between hospital patients, the environment and staff.
● A course of antibiotics that only partially treats an infection - can result from both
overuse and underuse of antibiotics.
● Total consumption of antibiotics in a human population os the critical factor in
development of resistant strains.

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9
Q

What is the MOA of flucloxacillin?

A

● Bacteriocidal, beta lactam antibiotic
● Inhibits bacterial cell growth by binding to the active site of penicillin binding
proteins
● Interferes with cell wall synthesis which leads to cell death

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10
Q

What microorganisms are susceptible to flucloxacillin?

A

● Staphylococci (including beta lactamase producing) and streptococci.
● No activity against enterococci, anaerobes, gram negatives or MRSA.

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11
Q

What are the side effects of flucloxacillin?

A

● Allergy/anaphylaxis, GIT upset, cholestasis, interstitial nephritis, neutropaenia,
serum sickness

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12
Q

What is the frequency of cross allergenicity between flucloxacillin and
cephalosporins?

A

● 5-10%

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13
Q

Why is oral fluclox given before meals?

A

● It is inactivated by gastric acid and binds to food proteins which can decrease
absorption

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14
Q

What is the MOA of cephalosporins?

A

● Bacteriocidal, beta lactam antibiotic
● Inhibit bacterial cell wall synthesis by halting peptidoglycan synthesis

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15
Q

How are they classified and give an example of each class

A

● 1st generation – cephalexin and cefazolin. Active against gram positive cocci.
Not active against pseudomonas.
● 2nd generation – Added gram negative coverage. Cefuroxime, Cefaclor
● 3rd generation – Crosses BBB, more gram neg coverage. Ceftriaxone and
Ceftazidime which works against Pseudomonas.
● 4th generation – Extended gram negative cover, more resistant to beta
lactamase, pseudomonas cover, crosses BBB. Cefepime

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16
Q

Are there any CNS infections that cephalosporins do not cover?

A

Listeria, resistant strains of pneumococci and e.coli

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17
Q

What are the adverse effects of cephalosporins?

A

Hypersensitivity reaction similar to penicillin, 5-10% cross reactivity. Fever, skin
rashes, neutropaenia, haemolytic anaemia. Can cause interstitial nephritis and
ATN.

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18
Q

Can you Explain the microbial spectrum of activity of ceftriaxone?

A

● Not usual degraded by beta lactamases, so a broader spectrum of activity
● Expanded gram negative cover and crosses the blood brain barrier
● Active against neisseria and haemophilus
● Not active against pseudomonas

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19
Q

What is the clinical relevance of ceftriaxones half life?

A

Half life is 7-8 hours so it may be administered once daily

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20
Q

What is the mechanism of action of vancomycin?

A

● Bacteriocidal antibiotic.
● Inhibits cell wall synthesis by binding to peptidoglycan pentopeptide.
● Prevents cross linking of the wall, which leads to weakening of the wall and cell
membrane

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21
Q

What are the target organisms of vancomycin

A

● Gram positive staph including MRSA and enterococci
● Gram positive anaerobes like clostridium difficile

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22
Q

Which clinical conditions require dose adjustment?

A

Renal impairment and obesity

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23
Q

What class of antibiotic is gentamicin?

A

● Aminoglycoside

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24
Q

What is its mechanism of action?

A

● Bacteriostatic.
● Acts by binding irreversibly to the 30s subunit of the bacterial ribosome, inhibiting
protein synthesis in 3 ways;
● By interfering with the initiation complex of peptide formation
● Inducing misreading of mRNA to produce non functional proteins
● Causing the breakup of polysomes to non-functioning monosomes
● Exhibits concentration dependent killing and post antibiotic effect

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25
Q

Please describe the pharmacokinetics of gentamicin

A

● A: IV, IM, inhalational or topical (poor PO absorption)
● D: Small volume of distribution, <10% protein bound, achieves high
concentrations in renal cortex
● M: Not metabolised
● E: Renal dependent elimination, glomerular filtration. Half life 2-3 hours, given
daily. Dose adjustment required for renal failure.

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26
Q

What microorganisms is gentamicin active against?

A

● Gram negative bacteria – e.coli, pseudomonas, proteus, klebsiella, serratia
● Gram positive – staph, strep (in combination with beta lactams)
● No anaerobic activity

27
Q

What are the advantages of a single daily dosing regimen for gentamicin?

A

● Decreased toxicity time – less time above critical level for toxicity than multiple
dose schedule
● Concentration dependent killing (at increased concentration can kill more
bacteria at a faster rate)
● Post antibiotic effect (effects last longer than detectable serum levels)
● Easier to do outpatient therapy
● Cost effective
● Less nursing time
● What are the adverse effects of gentamicin?
● Nephrotoxic, ototoxic, prolongs neuromuscular blockade

28
Q

How do penicillins enhance the efficacy of gentamicin?

A

Transport of gentamicin into the cell is enhanced by penicillins because they act
on the cell wall.

29
Q

How does resistance to gentamicin develop?

A

● Transferase enzyme that inactivates drug
● Impaired cell entry via cell wall changes
● Alteration of ribosomal receptor proteins

30
Q

Doxycycline
What is the MOA of doxycycline?

A

● Bacteriostatic
● Protein synthesis inhibitor - binds to the 30s subunit of a ribosome
● Blocks the binding of tRNA to mRNA ribosome complex and stops the addition of
amino- acids to the peptide.
● Inhibits protein synthesis in malaria, where it is active against erythrocytic
shizonts of all malaria parasites. Used for prophylaxis.

31
Q

What are the pharmacokinetics of tetracyclines?

A

● A: generally well absorbed (>60% bioavailability) but absorption inhibited by
food, calcium, dairy products and alkaline pH.
● D: Distributed widely to tissues except the CSF, crosses the placenta and can
chelate to Ca in teeth and bones. 40-80% protein bound.
● M: Concentrated in bile, undergo enterohepatic circulation.
● E: Excreted in the bile and urine. Except for doxycycline which has no renal
elimination.

32
Q

What are the side effects of doxycycline?

A

● GI - nausea and vomiting
● Skin photosensitivity
● Hepatotoxicity
● Discolouration of teeth and bones (binds calcium in forming teeth ad bones so
cannot be used in pregnancy or children <8yrs)
● Intracranial hypertension

33
Q

Other than malaria, what are the other indications for doxycycline?

A

● Respiratory infections
● STIs (chlamydia, syphilis)
● Skin infections (acne)
● Rickettsia (Q Fever)
● Vibrio species (Cholera)
● Antihelminthis
● Anthrax
● Some gram negatives but not routinely used

34
Q

What is the mechanism of action of chloramphenicol?

A

● Chloramphenicol is bacteriostatic
● It directly interferes with substrate binding in the 50S subunit of the ribosome to
block protein synthesis

35
Q

What are the side effects of chloramphenicol?

A

● GIT: Nausea, vomiting, diarrhoea
● Bone marrow suppression
● Gray baby syndrome in newborns
● Drug interactions with phenytoin, warfarin

36
Q

Chloramphenicol
Which bacteria is it active against?

A

Aerobic and anaerobic gram positive and negative. Rickettsia but not chlamydia

37
Q

Can you list some examples of macrolide antibiotics?

A

Erythromycin, roxithromycin, azithromycin, clarithromycin

38
Q

Describe the MOA of macrolides

A

Bacteriostatic - at high concentrations can be bacteriocidal to some orgaisms
● Inhibit bacterial protein synthesis by binding to the 50s subunit of the ribosome,
blocking transpeptidation

39
Q

What organisms are macrolides effective against?

A

● Gram positive organisms like staph, strep, pneumococcus
● Atypicals: mycoplasma, legionella, chlamydia, listeria and some mycobacteria
● Gram negative organisms: Neisseria, pertussis, treponema pallidum,
campylobacter

40
Q

What are the adverse effects of erythromycin?

A

● GI upset – anorexia, nausea, vomiting
● Liver toxicity – acute hepatitis
● Allergic reaction – fever, rash
● Drug interaction via P450 enzymes

41
Q

What is the mechanism of the drug interactions with erythromycin and give some
examples?

A

● Erythromycin inhibits hepatic enzymes, inhibiting the metabolism of other drugs
and causing increased activity.
● Examples include benzodiazepines, digoxin, warfarin, theophylline

42
Q

How does azithromycin differ from other macrolides?

A

● Higher tissue penetration
● Long elimination half life (2-4 days rather than 2-4 hours)
● Single daily dosing
● More effective against chlamydia, haemophilus
● Less effective against staph and strep
● Excreted unchanged in the urine
● No inhibition of of hepatic P450 so drug interactions are uncommon
● Prolongs the QT interval

43
Q

Ciprofloxacin

A

● Describe the pharmacokinetics of ciprofloxacin
● A: PO or IV administration, bioavailability >80%
● D: 20 - 40% protein bound
● E: Elimination half life 3-5 hours, renal elimination, requires dose adjustment in
renal failure.

44
Q

Describe the mechanism of action of fluoroquinolones

A

● Blocks DNA synthesis by inhibiting bacterial topoisomerase II (also known as
DNA gyrase) and IV.
● Inhibition of Topoisomerase II - interferes with relaxation of supercoiled DNA,
required for normal transcription and replication
● Inhibition of Topoisomerase IV - interferes with separation of replicated
chromosomal DNA

45
Q

What are the clinical uses of ciprofloxacin?

A

Used to treat UTIs, bacterial diarrhoea, soft tissue/bone/joint infections and
atypical pneumonias or respiratory infections

46
Q

What is the microbial spectrum?

A

● Excellent gram negative activity, moderate gram positive activity
● Active against staph aureus, pseudomonas
● Agents of atypical pneumonia such as mycoplasma & chlamydia.
● Intracellular pathogens such as legionella & mycobacterium
● The drug of choice for treatment of anthrax

47
Q

How does the antibacterial activity of ciprofloxacin differ from norfloxacin?

A

● Ciprofloxacin has a greater activity (4-8 times lower minimum inhibitory
concentration) against gram negatives and has a much greater activity against
gram positives

48
Q

What are the potential adverse effects of fluoroquinolones

A

● Prolonged QT (with some)
● Nausea, vomiting, diarrhoea (including c.diff)
● Rash
● Abnormal LFTs
● Photosensitivity
● Hyperglycaemia in diabetes
● Damage to growing cartilage(not recommended for those <18 or in
pregnancy/lactation)
● Tendonitis and risk of tendon rupture
● Allergy

49
Q

What is the mechanism of resistance to fluoroquinolones?

A

enzyme or a change to the permeability of the organism

50
Q

What are the indications for acyclovir in the ED?

A

● HSV encephalitis
● Varicella Zoster
● Patients with HIV
● Neonatal HSV

51
Q

Describe the mechanism of action of acyclovir

A

● Inhibition of viral DNA synthesis via irreversible binding to DNA polymerase.
● Incorporation into viral DNA with termination.
● Specificity for virus-infected cell (virus specific thymidine kinase)

52
Q

Describe the pharmacokinetics of acyclovir

A

● Short half life of 2.5hrs ( 5 times daily dosing PO)
● Low PO bioavailability
● Excreted unchanged in the urine
● CSF concentration reaches 50% of plasma concentration
● Large volume of distribution

53
Q

Name some side effects of acyclovir

A

● Nausea, vomiting, diarrhoea
● Reversible renal toxicity
● Neurological effects - tremor, delirium, seizures

54
Q

List some anti-influenza agents

A

Oseltamivir, zanamivir, amantadine, rimantadine

55
Q

What is the MOA of Osteltamivir/tamiflu?

A

● Neuraminidase inhibitor - disrupts viral replication and release.
● Active against influenza A and B

56
Q

What is the relevance of these agents to emergency medicine?

A

● May be of use in higher risk groups i.e. pregnant women, immunocompromised
● Can limit the severity of disease in those infected
● Can be used in the early phases of a pandemic to limit spread and numbers
infected

57
Q

Describe the mechanism of action of trimethoprim

A

● Selectively inhibits bacterial enzyme dihydrofolate
reductase, which is required for the conversion of
dihydrofolic acid to tetrafolic acid.
● By this mechanism it inhibits purine and DNA synthesis
in the bacterium.
● Less efficient at inhibiting the human version of this
enzyme.

58
Q

What is the rationale for combining trimethoprim with
sulphonamides?

A

● Sulphonamides inhibit sequential steps in the DNA
synthesis pathway, leading to an enhanced effect.
● They inhibit the step before trimethoprim, which inhibits
the conversion of PABA to dihydrofolic acid.
● This means the combination is bacteriocidal, compared to the bacteriostatic
action of using just one.

59
Q

Describe the pharmacokinetics of metronidazole

A

● A: Well absorbed orally with 99% PO bioavailability, can also be given IV
● D: Low protein binding 10 - 20%
● M: Metabolised in the liver, can accumulate in liver disease
● E: half life 7.5 hours, excreted by the kidney

60
Q

What are the adverse effects of metronidazole

A

● GIT: nausea, diarrhoea, dry mouth, metallic taste
● Neuro: Headache, paraesthesia, dizziness
● Thrombophlebitis
● Disulfiram like effect so alcohol should be avoided

61
Q

What is an antiseptic

A

A chemical disinfectant applied to living tissue which decreases the number of
organisms by killing, removing or diluting and has generally low toxicity to tissues.

62
Q

Describe the actions and uses of chlorhexidine

A

● Low skin irritating capacity
● Low oral toxicity
● Active against bacteria (most effective against gram positive cocci)
● Not inhibited by blood or organic products

63
Q

When is chlorhexidine contraindicated

A

● Middle ear surgery (can cause sensorineural deafness)
● Neurosurgery as can cause neural toxicity
● Allergy

ACEM viva (25 decks)

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