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Defence > Antio > Flashcards

Antio Flashcards

1
Q

What are most antibiotics derived from?

A

→natural products by fermentation

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2
Q

Why are antibiotics chemically modified?

A

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

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3
Q

What is an example of totally synthetic antibiotics?

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?

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

→intracellular

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7
Q

What are the principles of selective toxicity?

A

→Due to the differences in structure and metabolic pathways between host and pathogen
→Harm microorganisms, not the host
→Target in microbe, not host (if possible)
→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) versus toxic effect

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9
Q

What types of drugs have narrow therapeutic margins?

A

→toxic drugs

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10
Q

Why is microbial antagonism important?

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

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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 colitis?

A

→Fluoroquinolones
→clindamycin,
→broad-spectrum lactams

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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

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16
Q

How are antibiotics classified?

A

→Type of activity

→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 eg tetracyclin

→Used when the host defense 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

A

→Cefotaxime

→

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21
Q

Example of narrow spectrum antibiotics

A

→Penicillin G

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22
Q

What are cephalosporins now most effective against?

A

→gram negatives

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23
Q

What are basic penicillin active against?

A

→streptococci,
→pneumococci,
→meningococci,
→treopnemes

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24
Q

Which bacteria are resistant against basic penicilin?

A

→Staphylococcus aureus

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25
Q

What type of natural substance does penicilin have?

A

→Beta-lactams

26
Q

What are anti-staphylococcal penicillin?

A

→narrow spectrum,
→G+ves,
→beta-lactamase resistant

27
Q

Compare Pen G and Pen V?

A

Pen G
→not acid stable
→i/v or i/m
→good for some G-ves as well as G+ves

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

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

29
Q

What are anti-pseudomonal penicillin?

A

→extended spectrum beta-lactam antibiotic

→also G+ve, G-ve, anaerobes

30
Q

Example of anti-pseudomonal penicillin

A

→piperacillin

31
Q

What are beta-lactam/lactamase inhibitors?

A

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

32
Q

What are pseudomonal?

A

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

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

35
Q

Why are beta-lactams important?

A

→Without B lactam there will be no antimicrobial property

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

36
Q

Which bacteria have beta lactams?

A

→penicillin

37
Q

What are carbepenams?

A

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

38
Q

What are the modes of actions of bacteria?

A 
→cell wall synthesis
→DNA
→folic acid →metabolism
→cell membrane
→protein sythesis- 50S and 30S
→DNA and RNA processing- Gyrase, DNA-directed RNA polymerase
39
Q

Is tetracycline -cidal or static?

A

→static

40
Q

How do antibiotics reach membrane of gram negatives?

A

→porins in outer membrane mediate the passive diffusion of antibiotics

41
Q

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

A

→cytoplasm- synthesis of cell wall precursors
→cytoplasmic membrane- synthesis of cell wall subunits
→cell wall- new wall unit attachment

42
Q

What are D-alanines?

A

→incorporated by PBPs 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 inhibit bacteria cell wall synthesis?

A

→inhibit enzymes which catalyse cross linking

47
Q

Which bacteria is resistant against penicillin?

A

→mycoplasma pneumoniae

→have sterol packed cell membrane

48
Q

What type of antibiotic 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?

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
→antiseptic creams
→burns

58
Q

What does minimum inhibition concentration depend on?

A 
→age
→weight
→renal and liver function
→severity of infection
→susceptibility of the organism
→properties of the antibiotic
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

Defence (31 decks)

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