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Clinical Pathology > Antibacterial Agents > Flashcards

Antibacterial Agents Flashcards

1
Q

Define antibiotic

A

Chemical products of microbes that inhibit/kill other organisms

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2
Q

Define Antimicrobial agents

A
  • Antibacterial, antiviral, antifungal
  • Antibiotics
  • Synthetic/semi-synthetic compounds with similar effects
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3
Q

What are the different types of bacterial killing?

A
  • Bacteristatic= inhibit bacterial growth (protein synthesis inhibitors)
  • Bactericidal= kill bacteria (cell-wall active agents)
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4
Q

What is the minimum inhibitory concentration?

A

Minimum conc of antibiotic at which visible growth is inhibited
-Some antibiotics are bacteriostatic at low conc and bactericidal at high conc

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5
Q

What types of antimicrobial interactions are there?

A
  • Synergism (activity of 2 antimicrobials given together is greater than the sum of their activity separately)- B-lactam/aminoglycoside combination for strep endocarditis
  • Antagonism (one agent diminishes activity of another)
  • Indifference (activity unaffected by addition of another agent)
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6
Q

Name some cell wall synthesis inhibitors

A
  • B-lactams
  • Glycopeptides
  • Cycloserine (antiTB agent)
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7
Q

Describe the structure of a bacterial cell wall

A
  • Peptidoglycan major component in gram +ve & -ve bacteria
  • Polymer of glucose-derivatives NAG & NAM
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8
Q

How do B-lactam antibiotics work?

A

Interfere with function of penicillin binding proteins- Transpeptidase enzymes involved in the peptidoglycan cross-linking

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9
Q

Describe the general structure of B-lactams

A
  • Four membered B-lactam ring structure (C-C-C-N)

- Structural analogue of D-alanyl-D-alanine

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10
Q

Name the groups of B-lactam antibiotics, members of each family and their spectrum

A
  • Penicillins (benzylpenicillin, amoxicillin, flucloxacillin- narrow spectrum)
  • Cephalosporins (Cefuroxime, ceftasidime- broad spectrum)
  • Carbapenems (meropenem, imipenem-extremely broad spectrum)
  • Monobactams (aztreonam- gram -ve activity only)
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11
Q

Name types of glycopeptides and how they work

A
  • Vancomycin, teicoplanin
  • Bind directly to terminal D-Alanyl-D-alanine on NAM pentapeptides
  • Inhibit binding of transpeptidases thus peptidoglycan cross-linking
  • Unable to penetrate gram -ve outer membrane porins
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12
Q

How are proteins synthesised in bacteria?

A
  • Translation of RNA to a protein
  • Takes place in ribosome
  • 50S + 30S= 70S
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13
Q

Give examples of Aminoglycosides, where they bind and what they are known for?

A
  • Gentamicin, amikacin
  • Protein synthesis inhibitors
  • Bind to 30S ribosomal subunit
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14
Q

Give examples of MLS, what it stands for, where they bind and what they are known for?

A
  • Macrolides, Lincosamides, Streptogramins
  • Protein synthesis inhibitors
  • M= erythromycin, clarithromycin
  • L= clindamycin
  • Bind to 50S ribosomal subunit= blockage of exit tunnel or inhibit protein elongation
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15
Q

Where do tetracyclines bind to, what are they known for?

A
  • Protein synthesis inhibitors
  • Bind to 30S ribosomal subunit
  • Inhibit RNA translocation= interfere with binding of tRNA to rRNA
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16
Q

Give an example of an Oxazolidinone, where it binds and what it is known for?

A

-Protein synthesis inhibitor
-Linezolid
-Binds to 50S ribosomal subunit- may also bind to 70S subunit
-Inhibits initiation of protein synthesis
-Inhibit assembly of initiation complex
-

17
Q

What are Trimethoprim & Sulphonamides inhibitors of and how? What is their combined name?

A
  • DNA synthesis
  • Inhibit folate synthesis (folic acid= purine synthesis precursor)
  • T=Dihydrofolate reductase
  • S=Dihydropteroate synthase
  • Combined= Co-Trimoxazole
18
Q

Give examples of Quinolones & fluoroquinolones, what they inhibit and how?

A
  • Ciprofloxacin, Nalidixic acid
  • Inhibit 1 or more of 2 related enzymes- DNA gyrase & topoisomerase IV
  • Involved in remodelling of DNA during DNA replication
19
Q

What is Rifampicin and how does it do this?

A
  • RNA synthesis inhibitor
  • RNA polymerase inhibitor
  • Prevents synthesis of mRNA
20
Q

Name some plasma membrane agents

A
  • Colistin (gram -ve)
  • Daptomycin (gram +ve)
  • Destruction of cell membrane
21
Q

What are adverse effects of antibiotics?

A
  • C.Diff
  • Antibiotic resistance
  • Fungal infection (candidiasis)
  • Nausea/vomiting, rashes
22
Q

What are the adverse reactions of aminoglycosides?

A
  • Reversible renal impairment on accumulation
  • Irreversible ototoxicity
  • Therapeutic drug monitoring indicated
23
Q

What are the adverse reactions of B-lactams?

A

Allergic reactions: Generalised rash or anaphylaxis

24
Q

What are the adverse reactions of Linezolid?

A

Bone marrow depression

25
Q

What are signs of intolerance or allergy to B-lactams?

A 
I= nausea, diarrhoea, headache
A= skin rash, anaphylaxis, urticaria, angio-oedema, severe skin rash, bronchospasm
26
Q

Describe C.Diff infection

A
  • Combination of enterotoxin & spore production
  • Hypervirulent strain 027 causes more severe disease
  • Produces toxins A & B
  • Assumed caused by abolition of colonisation resistance
27
Q

What are the most common precipitating antibiotics of C.Diff?

A
  • Co-amoxiclav
  • Cephalosporins
  • Ciprofloxacin
  • Clindamycin
28
Q

What are the best antibiotics to use against:

  • Staph Aureus
  • Strep Pyogenes
  • Gram -ve Bacilli
  • Anaerobes
  • MRSA/gram +ve
  • last option for gram -ves
A
  • SA=Flucloxacillin
  • SP=Benzylpenicillin
  • GB=Cephalosporins- avoid in elderly
  • A=Metronidazole
  • MRSA= Vancomycin
  • Last= Colistin
29
Q

Which antibiotics have a good and poor availability in the CSF?

A 
Good= B-lactams in presence of inflammation
Poor= Aminoglycosides & Vancomycin
30
Q

Which antibiotics have a good and poor availability in urine?

A 
Good= Trimethoprim & B-lactams
Poor= MLS antibiotics
31
Q

What are concentration dependent pharmacodynamics?

A

Main determinant of bacterial killing is the factor by which concentration exceeds MIC, administered intermittently

32
Q

What are time dependent pharmacodynamics?

A

Main determinant of killing is the amount of time for which antibiotic concentration exceeds MIC, administered frequently to maintain high levels

33
Q

Why is combination therapy used?

A
  • Reduce resistance
  • Provide adequately broad spectrum
  • Increase efficacy

Clinical Pathology (56 decks)

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