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CP1 = Core Micobiology > Introduction to Antimicrobials > Flashcards

Introduction to Antimicrobials Flashcards

1
Q

Symptoms of severe allergic reaction =

A 
> Anaphylaxis
> Urticaria (Hives) 
> Angio-oedema 
> Bronchospams
> Severe skin rash
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2
Q

What is the major component of bacterial cell wall?

A

Peptidoglycan.

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3
Q

What do Quinolones and Fluroquinolones do?

A

Inhibit enzymes DNA Gyrase and Topoisomerase IV. (END IN FLOXACIN)

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4
Q

GENERAL Adverse Effects include:

A 
> Nausea, vom, headache
> Allergic and Infusion
> Anti'b resistance
> Fungal infection - C.diff
> Ototoxicity (ear)
> Renal impairment
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5
Q

What is Peptidoglycan made from?

Hint : Gly –> Think Glucose

A

Polymer of:
> NAM = N-acetyl Muramic Acid.
> NAG = N-acetyl glucosamine.

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6
Q

What anti’bs commonly cause C.Diff?

Hint: Think “C”

A

> Cephalosporins
Ciprofloxacin (Quinolones and Flouroquinolones)
Clindamycin

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7
Q

Define: Synergism (antimicrobials)

A

Activity of two antimicrobials together = greater than their individual activity.

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8
Q

How do aminoglycosides work?

A

Bind to 30S subunit.

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9
Q

What is Co-trimoxazole made up of?

A

> Trimethoprim

> Sulfamethoxazole

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10
Q

What is an example of a plasma membrane agent?

A

Daptomycin.

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11
Q

Antibacterial Mechanisms target what kind of cells?

A

Enzymes & other critical processing cells.

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12
Q

Aminoglycoside adverse effect =

A

Reversible renal impairment.

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13
Q

How do Tetracyclines work?

A

Bind to 30S subunit.
Think “T’s” !!
> –I RNA TRANSLATION
> Interfere with tRNA bind to rRNA.

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14
Q

What drug can you use in pt’s with severe penicillin allergy?

A

AZT (Monobactam)

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15
Q

What forms 70S initiation complex?

A

50S and 30S.

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16
Q

What component do animal cell walls lack?

A

Peptidoglycan –> good for selective toxicity.

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17
Q

When should single dose anaphylaxis be used?

A

Surgical Prophylaxis.

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18
Q

Determinants of Bacterial Killing are:

A

Concentration and Time Dependant where Anti’b > MIC.

Conc Dependant = Aminoglycosides

Time Dependant = B-lactams

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19
Q

Examples of cell wall synthesis inhibitors?

A

> Beta-lactams - MAIN ANTIBIOTIC.

> Glycopeptides

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20
Q

What type of spectrum do Carbapenems have?

A

Very Broad.

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21
Q

Stages of bacteria protein synthesis?

A

> Initiation
Elongation
Termination
Ribosome recycling

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22
Q

What type of bacteria do Monobactams only work on?

A

Gram-negative bacteria.

> AZT

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23
Q

Less commonly precipitating anti’bs to C.diff?

A

> Aminoglycosides

> Glycopeptides

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24
Q

What does Trimethoprim treat?

A

UTI’s.

25
Q

How do Macrolides, Lincosamides Streptogramins (MLS) work?

A

Bind to 50S subunit - inhibit protein elongation.

ALL END IN MYCIN

26
Q

What is a common feature of all B-Lactams?

A

B-lactam ring - Analogue of D-alanyl-D-alanine.

27
Q

Antibiotic is also known as?

A

Anti-bacterial agent.

28
Q

Define: Antibiotics

A

Chemical products of microbes –> kill/inhibit other organisms.

29
Q

What does Glycopeptide binding prevent?

A

Transpeptidase binding –I Peptidoglycan cross-linking.

30
Q

What does Rifampicin target?

A

RNA Polymerase –I Stop mRNA forming.

31
Q

Linezolid adverse effect =

A

Bone marrow depression

32
Q

What does Bacteriostatic mean?

A

Inhibit bacteria growth/division –I Protein synthesis.

33
Q

What are Aminoglycosides?

A

Protein synthesis inhibitors.

> Gentamicin, Amikacin

34
Q

How do Glycopeptides work?

A

Bind to D-Alanyl-D-Alanine (B Lactam Ring) on NAM - Peptidoglycans.

35
Q

What drugs can you use in pt’s with minor penicillin allergy?

A

Carbapenems and Cephalosporins.

36
Q

Define: Selective Toxicity

A

Toxic to bacteria, not to host.

  • Attack target present in bacteria, not in human.
  • Attack significantly different target in human host.
37
Q

Where does protein synthesis in bacteria occur?

A

Ribosome.

38
Q

B-lactams adverse effect =

A

ALLERGIC REACTION
General = ~10%
Anaphylaxis = 0.01%

39
Q

What does a Ribonucleoprotein complex consist of?

A

2/3 RNA, 1/3 Protein

40
Q

What strain of C.Diff causes severe disease?

A

Hypervirulent strain 027.

41
Q

What do enzymes DNA Gyrase and Topoisomerase IV do?

A

Supercoiling/strand seperation - DNA remodelling during replication.

42
Q

Define: Indifference (antimicrobials)

A

Anti’m activity unaffected if another added.

43
Q

Synergism - Streptococcal endocarditis therapy. Which drug combo?

A

Beta-lactam & Aminoglycoside.

44
Q

What does Trimethoprim target?

A

Dihydrofolate Reductase.

45
Q

Which types of bacteria have peptidoglycan?

A

Gram +ve and Gram -ve.

46
Q

What does Bactericidal mean?

A

KILL Bacteria –> Cell wall - active agents.

47
Q

What type of bacteria do Glycopeptides work on?

A

ONLY Gram +ve.

> Can’t penetrate Gram -ve outer membrane.

48
Q

What type of spectrum do Penicillins have?

A

Narrow.

49
Q

What do Sulphonamides target?

A

Dihydroperoate Synthetase

50
Q

What most commonly causes anti-b assc diarrhoea?

A

C.Difficile Infection –> make toxins A/B.

51
Q

Define : Minimum Inhibitory Concentration

A

MIC = Minimum anti’b concentration @ which visible growth inhibited.

52
Q

What is Benzylpenicillin?

A

A Beta Lactam.

53
Q

How do Oxazolidinones work?

A

Bind to 50S (maybe 70S) –I Protein synthesis.

–I Initiation complex forming.

54
Q

How do Plasma Membrane Agents work?

A

CYCLIC LIPOPEPTIDE- Have lipophilic tail and peptide ring.
> Insert tail into membrane –> depolarise –> ion loss
> Gram +ve only.

55
Q

What type of spectrum do Cephalosporins have?

A

Broad.

56
Q

Define: Antagonism (antimicrobials)

A

One agent diminishes another’s activity

57
Q

How do B-Lactams work?

A

They interfere with penicillin binding proteins.

> Transpeptidase enzymes involved in peptideoglycan cross linking.

58
Q

What do Trimethoprim and Sulphonamides inhibit?

A

Folate synthesis (Folid acid = Purine synthesis precursor)

59
Q

Combination Therapy reasons =

A

> Synergistic combination
Polymicrobial infection
Sepsis treatment
Reduce resistance, anti-TB chemo

CP1 = Core Micobiology (7 decks)

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