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lolmyi > L13: Antibiotics > Flashcards

L13: Antibiotics Flashcards

1
Q

What are most antibiotics derived from?

A

→ natural products of fungi and bacteria - soil dwellers
→natural products by fermentation

then are chemically modified

→synthetic antibiotics are produced too

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2
Q

Why are antibiotics chemically modified?

A

→ increase pharmacological properties ie can they survive in the stomach
→increase antimicrobial effect

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3
Q

What is an example of a totally synthetic antibiotic?

A

→sulphonamides

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4
Q

What are natural products of fungi and bacteria derived from?

A

→- soil dwellers natural antagonism and selective advantage

→kill or inhibit the growth of other microorganisms

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5
Q

Why is there selective toxicity in antibiotics?

antibiotic has selective toxic effect against organism that is being treated and minimum effect on host

A

→Due to the differences in structure and metabolic pathways between host and pathogen

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6
Q

Why is selective toxicity difficult in viruses?

A

→viruses are intracellular

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7
Q

What are the principles of selective toxicity?

A

→differences in structure and metabolic pathways between host and pathogen
→Harm microorganisms, not the host
→Target in microbe, not host (if possible)
→selective toxicity Difficult for viruses (intracellular), fungi and parasites
→Variation between microbes
→effect on commensals

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8
Q

What is therapeutic margin?

A

→active dose (MIC) vs toxic effect

THERE IS NO SAFE DRUG - in balance

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9
Q

What types of drugs have narrow therapeutic margins?

A

→toxic drugs e.g. aminoglycosides, vancomycin, ototoxic, nephrotoxic

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10
Q

Why is microbial antagonism important?

inhibition of one bacterial organism by another

A

→Maintains flora

→Limits growth of competitors and pathogens

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11
Q

What happens with loss of flora?

A

→bacterial or pathogen overgrowth

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12
Q

Example of a disease cause by loss of flora

A

→Antibiotic Associated Colitis i.e. pseudomembranous colitis

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13
Q

Which bacteria can cause pseudomembranous colitis?

A

Clostridioides difficile

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14
Q

Which antibiotics most commonly cause (antibiotic associated) colitis?

A

→Fluoroquinolones
→clindamycin,
→broad-spectrum lactams

these antibiotics affect gut flora thus causes over growth of the bacteria Clostridioides difficile

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15
Q

What conditions cause immunosuppression?

A

→cancer chemotherapy,
→transplantations,
→myeloma,
→leukaemias,

→HIV with low CD4

→Neutropenics, 
→asplenics, 
→renal disease, 
→diabetes,
→ alcoholics
→babies and elderly
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16
Q

How are antibiotics classified?

A

→Type of activity e.g. bactericidal and bacteriostatic

→Structure

→ Target site for activity

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17
Q

What are bactericidal antibiotics?

A

→Kill bacteria

→Used when the host defense mechanisms are impaired

→Required in endocarditis, kidney infection

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18
Q

Describe bacteriostatic antibiotics

A

→Inhibit bacteria (at a certain concentration) eg tetracyclin

→Used when the host defence mechanisms are intact

→Used in many infectious diseases

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19
Q

What might a bacteriostatic antibiotic become if dose is increased?

A

→bactericidal if dose is increased

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20
Q

Examples of broad spectrum antibiotics:

antibiotics that are effective against many types

A

→Cefotaxime

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21
Q

Example of narrow spectrum antibiotics:

effective against very few types

A

→Penicillin G

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22
Q

What are cephalosporins now (third-generation) most effective against?

A

→gram negatives

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23
Q

What are basic penicillins active against?

A

→streptococci,
→pneumococci,
→meningococci,
→treopnemes

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24
Q

Which bacteria are resistant against basic penicilin?

A

→Staphylococcus aureus thus need a different type of penicillin to kill it

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25
Q

What type of natural substance does penicilin have?

A

→Beta-lactams

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26
Q

What are anti-staphylococcal penicillin?

A

→narrow spectrum,
→G+ves,
→beta-lactamase resistant (enzyme that breaks down penicillin produced by S. aureus)
→ less potent than PenG
→ not MRSA (type of bacteria resistant to several antibiotics)

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27
Q

Compare Pen G and Pen V

A

Pen G - benzylpenicillin
→not acid stable (cannot give orally)
→thus administered i/v or i/m
→good for some G-ves as well as G+ves

Pen V - phenoxymethylpenicillin
→oral (more acid-stable than penG)
→less active G-ves,
→ same activity with G+ves as in PenG

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28
Q

What are broader spectrum penicillins?

A

→Spectrum of activity is similar to basic penicillins but also includes some Gram-negative organsims and also enterococci

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29
Q

What are anti-pseudomonal penicillin?

A

→extended spectrum beta-lactam antibiotic

→also G+ve, G-ve, anaerobes

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30
Q

Example of anti-pseudomonal penicillin

A

→piperacillin

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31
Q

What are beta-lactam/lactamase inhibitors?

A

→Spectrum like amoxicillin plus activity against some Gram-negatives and Staph aureus

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32
Q

What are pseudomonal?

A

→a major cause of lung infections in people with cystic fibrosis.
→thrive in moist environments and equipment

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33
Q

What are the molecular structure classifications of antibiotics?

A 
→nalidixic acid
→ciprofloxacin
→erythromycin
→tetracycline
→vancomycin
→streptomycin(aminoglycosides)
34
Q

What are beta lactams?

A

→Structural mimics of natural substrates for enzymes

beta lactams antibiotics are antibiotics that have a beta lactic ring including:
→penicillins, 
→cephalosporins
→sulbactam 
→carbapenem 
→monobactam
35
Q

Why is the beta-lactam ring structure important?

A

→Without B lactam there will be no antimicrobial property
→ b lactam ring is the active structure in penicillin

→stop bacterial growth by inhibiting PBPs (penicillin-binding proteins) that are indispensable for the cross-linking process during cell wall biosynthesis

36
Q

Which antibiotics have beta lactams?

A 
→penicillins, 
→cephalosporins 
→sulbactam 
→carbapenem 
→monobactam
37
Q

What are carbepenams?

A

→effective antibiotic agents commonly used for the treatment of severe or resistant bacteria

38
Q

What are the bacterial targets for common antibiotics?

modes of actions of bacteria?

A 
→cell wall synthesis
→DNA
→folic acid metabolism
→cell membrane
→protein synthesis- 50S and 30S
→DNA and RNA processing- DNA Gyrase, DNA-directed RNA polymerase
→ generation of Free radicals

Thus many targets for selective toxicity

39
Q

Is tetracycline bactericidal or bacteriostatic?

A

→bacteriostatic

has anti-inflammatory effects; broad-spectrum thus used widely in community

40
Q

How do antibiotics reach membrane of gram negatives?

A

→porins in outer membrane mediate the passive diffusion of antibiotics

these bacteria have an impermeable barrier thus certain pores allow for entrance to periplasmic space and thus inhibit PEPTIDOGLYCAN SYNTHESIS ENZYMES

41
Q

What are the sites of action of inhibitors of bacterial cell wall synthesis?

A

→cytoplasm- synthesis of cell wall precursors (MONOMERS) e.g. cycloserine
→cytoplasmic membrane- synthesis of cell wall subunits attached to lipid carriers (DIMERS TO CHAIN FORMATION) e.g. vancomycin and bacitracin
→cell wall- new wall unit attachment to growing peptidoglycan (CROSS LINKING) e.g. beta lactams (penicillin)

42
Q

What are D-alanines?

A

→incorporated by PBPs (Penicillin-binding proteins) into peptidoglycan

43
Q

How does cycloserine inhibit bacteria cell wall synthesis?

A

→inhibits incorporation of alanine into cell wall precursor

44
Q

How does vancomycin inhibit bacteria cell wall syntesis?

A

→bind to terminal D-ala D-ala residues to prevent incorporation of subunit into peptidoglycan

45
Q

How does bacitracin inhibit bacteria cell wall synthesis?

A

→prevents dephosphorylation of phospholipid carrier which prevents regeneration of carrier to continue synthesis

46
Q

How do penicillin and cephalosporins (beta lactams) inhibit bacteria cell wall synthesis?

A

→inhibit enzymes which catalyse cross linking (PBPs)

induction of autolytic enzymes causing bacteria to die as cannot make peptidoglycan structure.

47
Q

Which bacteria is resistant against penicillin?

A

→mycoplasma pneumoniae

→have sterol packed cell membrane (not peptidoglycan thus use other antibiotics that target elsewhere in the bacteria)

48
Q

What type of antibiotics are folic acid synthesis inhibitors?

A

→bactericidal

→broad spectrum

49
Q

What are the targets of folic acid synthesis inhibitors?

A

→PABA

→dihydrofolate reductase- human DHFR is less inhibited hence selective toxicity

50
Q

How do aminoglycosides inhibit protein sythesis?

A

→Binding fmet t-RNA Initiation complex formation

→streptomycin

51
Q

How does gentamycin inhibit protein synthesis?

A

→Translocation of fmet t-RNA

to P site

52
Q

How does tetracycline inhibit protein synthesis?

A

→Competition with new Aminoacyl t-RNA at the A site

53
Q

How does chloramphenicol inhibit protein synthesis?

A

→Blocks formation of peptide bond peptidyl transferase

→Bind to 50S ribosome

54
Q

How do erythromycin and fusidic acid inhibit protein sythesis?

A

→Block translocation of peptidyl t-RNA

55
Q

What 2 infections can antibiotics be used prophylaxis (to prevent bacterial infection)?

A

→meningitis

→tuberculosis

56
Q

How is antibiotic given in a meningitis case?

A

→i/m injection

57
Q

Which conditions are antibiotics given topically?

A 
→conjunctivitis
→superficial skin infections
→antiseptic creams
→burns
heavy metal ointments
58
Q

What does minimum inhibition concentration depend on?

A

→age
→weight
→renal and liver function
→severity of infection
→susceptibility of the organism to the antibiotic
→properties of the antibiotic i.e. is it enough to give a concentration higher than MIC (minimum inhibitory concentration) at the site of infection -NOT JUST BLOOD

MIC levels vary between different antibiotics

59
Q

What are the two pharmacodynamic properties of antibiotics killing activity?

A

→time-dependence

→concentration-dependence = max or area above MIC

60
Q

Why are antibiotic combinations used?

A

→life-threatening infections e.g. endocarditis, septicaemia

→Polymicrobial infections

→Less toxic doses
→synergy eg. penicillin and gentamicin
→reduce antibiotic resistance e.g. Tuberculosis

61
Q

What is microbial antagonism?

A

Inhibition of one bacterial organism by another

62
Q

what is dysbiosis?

A

outgrowth of certain organisms due to antibiotics disrupting the flora

Normal microbiota prevent outgrowth of pathogens

63
Q

Clinical features of antibiotic associated colitis (pseudomembranous colitis by bacteria C. difficile)?

A

→Ulcerations - inflammations
→Severe diarrhoea
→ serious hospital cross-infection risks

64
Q

How is Clostridium difficile (bacteria) spread?

A

→ via endospores (spores)

65
Q

what 2 factors allow fro bacterial clearance?

A

antibiotics and immunity

66
Q

Example of basic penicillin

A

benzylpenicillin (PenG), penicillin V

67
Q

Examples of and MOA of antibiotics targeting cell wall synthesis

A

→penicillins
→ cephalosporins
→ cycloserine
→vanomycin

68
Q

Examples and MOA of antibiotics targeting folic acid metabolism:

Folate is made in bacteria; humans consume folate

A

Synergetic effect (given together):
→trimethoprim
→sulphonamides

69
Q

Examples and MOA of antibiotics targeting cell membrane:

A

→colistin (hugely toxic in human c=membranes thus only given if bacteria is multi drug resistant e.g. e.coli
→daptomycin

70
Q

Examples and MOA of antibiotics targeting protein synthesis - 50s inhibitors:

A

→erythromycin
→chloramphenicol (toxic drop so used topically as eye drops)
→clindamycin
→linezolid

71
Q

Examples and MOA of antibiotics targeting protein synthesis - 30s inhibitors:

A 
→tetracycline - bacteriostatic effect 
→spectinomycin 
→streptomycin
→gentamicin (toxic thus measure concentration to prevent overdosing)
→tigecycline
→doxycycline (modern tetracycline)
72
Q

Examples and MOA of antibiotics targeting DNA and RNA processing:

A

→Quinolones- inhibits DNA Gyrase by targeting DNA replication and mRNA synthesis
→ Rifampin- blocks ability of bacteria to produce mRNA binds to and inhibits bacterial DNA-directed RNA polymerase

73
Q

What is the enzyme that acts like DNA gyrase in humans?

A

topoisomerase IV

74
Q

Examples of antibiotics that generate free radicals:

A

→METRONIDAZOLE - used to treat anaerobic infections (deep ulcers, abscesses etc.)
→NITROFURANTOIN -treating simple infections thus decreases toxicity; good anti-microbial effects

These AB generate free radicals once inside the bacteria

75
Q

Why is the germination of free radicals helpful in killing bacteria?

A

Free radicals kill many of the bacterial structures thus killing the bacteria

76
Q

Are the enzymes making peptidoglycan the same in both gram positive and gram negative bacteria?

A

NO!

Different antibiotics required to treat the 2 types of bacteria even though in both cases u are targeting the peptidoglycan (cell wall synthesis antibiotics)

77
Q

What are PBPs?

A

Penicillin-binding proteins or transpeptidase

involved in the synthesis of peptidoglycan - enzyme cross-line sub-units of peptidoglycan to form peptidoglycan dimers which then exist as peptidoglycan.

78
Q

How are community infections administered antibiotics?

A

→Orally by GP

79
Q

How are serious infections, which have lead to hospitalisation, administered antibiotics?

A

→systemic treatment via I/v

I/v is rapid delivery and high [blood]
I/v when unable to take orally e.g. vomiting, consciousness, poor gut absorption due to trauma

80
Q

Does MIC levels vary between different antibiotics?

A

YES

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