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POM > Antimicrobial Therapies > Flashcards

Antimicrobial Therapies Flashcards

1
Q

What is an antibiotic?

A

An antimicrobial agent produced by a microorganism that kills or inhibits other microorganisms

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2
Q

What is bactericidal?

A

Kills bacteria

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3
Q

What is bacteriostatic?

A

Stops bacteria growing but doesn’t kill them

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4
Q

What is prontosil?

A

First sulphonamide antibiotic
Eg. sulfamethoxazole. Sometimes used with trimethoprim
Used to treat UTIs, RTIs, bacteraemia and prophylaxis for a HIV+ patient
Only acts on gram positive bacteria

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5
Q

What is antiseptic?

A

Chemical that kills or inhibits microbes

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6
Q

What is antimicrobial?

A

Chemicals that selectively kill or inhibit microbes

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7
Q

What are aminoglycosides?

A

E.g. Gentamicin, Streptomycin
Bactericidal
Target protein synthesis (30S ribosomal subunit) and affect RNA proofreading and cause damage to cell membrane

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8
Q

What is rifampicin?

A

Bactericidal
Targets RpoB subunit of RNA polymerase
Makes secretions go orange/red- affects compliance

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9
Q

What is vancomycin?

A

Bactericidal

Targets lipid II component of cell wall synthesis as well as crosslinking via D- ala residues

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10
Q

What is linezolid?

A

Bacteriastatic
Inhibits initiation of protein synthesis by binding to 50S RNA subunit
Affects gram positive bacteria

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11
Q

What is daptomycin?

A

Bactericidal
Targets bacteria cell membrane
Targets gram positive bacteria

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12
Q

What are beta lactams?

A 
E.g. penicillin, methicillin
Inhibits bacterial cell wall peptidoglycan formation
Binds transpeptidases (penicillin binding proteins -PBPs)
PBPs catalyse a number of steps in the synthesis of peptidoglycans
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13
Q

What are macrolides?

A

E.g. erythromycin, azithromycin
Affect gram positive and some gram negative infections
Target 50S ribosomal subunit preventing amino-acyl transfer and translocation of polypeptides

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14
Q

What are quinolones?

A

Synthetic and bactericidal

Target DNA gyrase in gram negative bacteria and topoisomerase IV in gram positive bacteria

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15
Q

What is the minimal inhibitory concentration?

A

The lowest concentration of antibiotic required to inhibit growth

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16
Q

How does antimicrobial resistance develop?

A

Selection pressures: resistant mutants outcompete other strains

17
Q

Through what mechanisms does antibiotic resistance occur by?

A
  1. Altered target site: methicillin- resistant staphylococcus aureus encodes an alternate penicillin binding protein with low affinity for beta lactams
  2. Inactivation of antibiotic- Beta lactamase destroys beta lactam ring
  3. Altered drug metabolism- increased production of PABA- resistant to sulfonamides
  4. Decreased drug accumulation- antibiotic efflux pump
18
Q

How do bacteria alter their metabolism to resist effects of antibiotics?

A

Increased production of enzyme substrate can out-compete antibiotic inhibitor
Alternatively bacteria switch to other metabolic pathways reducing requirement for PABA

19
Q

How do resistant bacteria decrease drug accumulation?

A

Reduced penetration of antibacterials into bacteria cell and/or increased efflux of antibiotic out of cell

20
Q

What are the major gram negative antibiotic resistant bacterial pathogens?

A 
Pseudomonas aeruginosa
E.coli (ESBL)
E.coli Klebsiella spp. (NDM-1) 
Salmonella Spp (MDR)
Acinetobacter Bacmannia 
Neisseria gonorrhoeae
21
Q

What are major gram positive antibiotic resistant bacterial pathogens?

A 
Staphylococcus aureus (MRSA, VISA)
Streptococcus pneumoniae
Clostridium difficile
Enterococcus Spp
Mycobacterium Tuberculosis
22
Q

What are sources of antibiotic resistant genes?

A

Plasmids: extrachromosomal circular DNA, often multiple copies. Often carry multiple antibiotic resistant genes-selection for one maintains resistance to all

Transposons: integrate into chromosomal DNA and allow transfer of genes from plasmid to chromosome and vice versa

Naked DNA: DNA from dead bacteria released into environment

23
Q

What are 3 mechanisms for spread of antibiotic resistance genes?

A

Transformation- uptake of intracellular DNA
Conjugation- pilus mediated DNA transfer
Transduction- phage mediated DNA transfer

24
Q

What are non-genetic mechanisms of resistance?

A

Biofilm- communities of bacteria that are highly drug tolerant
Intracellular location- doesn’t change location so makes it hard for antibodies to access them
Slow growth- if bacteria doesn’t use many processes to replicate then it’s hard for antibiotics to inhibit them
Spores- extremely resistant to heat, antiseptics and antibiotics
Persisters: organisms not using any processes that are inhibited by antibiotics

25
Q

What are other reasons of treatment faliure?

A

Inappropriate choice for organism
Poor penetration of antibiotic into target site
Inappropriate dose
Inappropriate administration
Presence of antibiotic resistance with commensal flora

26
Q

Why is antibiotic resistance common in hospitals?

A

Large number of infected people receiving high doses of antibiotics- strong selection pressure

27
Q

What are risks for hospital acquired infections?

A 
High number of ill people
Crowded wards
Presence of pathogen
Broken skin
Indwelling devices
AB therapy may suppress normal flora
Transmission by staff
28
Q

What harm can come about when antibiotic therapy impares commensal flora?

A

Commensal organisms can outcompete pathogen for adhesion, metabolism and growth
Pathogen cannot colonise at levels sufficient for infection
After AB therapy pathogen has no competition which can lead to overgrowth
The pathogen produces toxins which damage the host and becomes a symptomatic infection

29
Q

How can we prevent the emergence of drug resistant bacteria?

A

Prescribing strategies- tighter controls
Reduce use of broad spectrum antibiotics
Quicker identification of infection caused by resistant strain
Knowledge of local strains/ resistance patterns
Modification of existing medications
Combination of antibiotic and inhibitor

30
Q

What are 3 broad classes of conditions that fungi cause in humans?

A

Allergy- allergic reaction to fungal products
Mycotoxicosis- ingestion of fungi and their toxic products
Mycoses- superficial, subcutaneous or systemic colonisation and invasion and destruction of human tissue

31
Q

What are the targets for antifungal therapy?

A

Cell membrane- fungi use ergosterol instead of cholesterol
DNA synthesis- some compounds may be selectively activated by fungi, arresting DNA synthesis
Cell Wall- unlike mammalian cells, fungi have a cell wall

POM (48 decks)

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