wk 5- antimicrobial stewardship Flashcards

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1
Q

antimicrobial resistance what is it?

A

Antimicrobial resistance arises via random mutations BUT is also a consequence of, and accelerated by antimicrobial overuse, underuse and misuse.

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2
Q

how do agents become resistant to antimicrobials? 3

A

Genetic material (DNA), which codes for resistance traits can be exchanged between microbial cells via:

Transformation: uptake of free DNA from lysed microbial cells in the environment into the genome of living cells.
Conjugation: horizontal gene transfer involving direct cell to cell contact to facilitate transfer of plasmids from donor to recipient cells.
Transduction: injection of viral genetic material into bacterial cells via bacteriophage

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2
Q

how do agents become resistant to antimicrobials?

A

Genetic material (DNA), which codes for resistance traits can be exchanged between microbial cells via:

Transformation: uptake of free DNA from lysed microbial cells in the environment into the genome of living cells.
Conjugation: horizontal gene transfer involving direct cell to cell contact to facilitate transfer of plasmids from donor to recipient cells.
Transduction: injection of viral genetic material into bacterial cells via bacteriophage

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3
Q

what is antimicrobial stewardship

A

safe and effective prescription and use of antimicrobial agents to improve patient outcomes, reduce adverse sequelae of antimicrobial use including antimicrobial resistance, and ensure cost-effective therapy

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4
Q

MINDME antimicrobial creed

A

M- microbiology samples collected for identification and antimicrobial susceptibility testing
I- indications should be evidence based with improved patient prognosis
N- narrow spectrum required. reduces collateral damage and suboptimal exposure to antimicrobials.
D- dosage appropriate to type and site of infection
M- minimise duration of therapy 5-7 days and not exceeding unless theres proof short duration isn’t adequate.
E- ensure monotheraphy in most cases. synergy of drugs is useful in treatment of multiple drug resistant infectious agents and extending spectrum of treatment of poly microbial infections.

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5
Q

risks of drug delivery 2

A
  1. route of administration affects the risk associated with portals of entry in the chain of infection
  2. also risks associated with distribution of the drug (restrict so endogenous microbiota isn’t destroyed and opportunistic resistant populations aren’t created
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6
Q

drug selection is importance because

A
  1. narrow spectrum agents restrict the effect of exposure to the targeted infectious agent. it reduces the development of antimicrobial resistance and collateral damage of endogenous microbiota.
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7
Q

importance of drug metabolism

A

drug must be able to reach the affected area at a therapeutic level. examples are neurological infections with the blood brain barrier restricting access and metabolism of liver before arrival at site.

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8
Q

types of antimicrobial agents 3

A
  • Drugs that inhibit the growth/replication of infectious agents (for example, bacteriostatic)
    -Drugs that kill the infectious agent (for example, bacteriocidal)
    -Drugs that lyse the infectious agent cells (for example, bacteriolytic)
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9
Q

what do antimicrobials target?

A

cellular structures and or functions in infectious agents

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10
Q

how can u reduce antimicrobial resistance? 2

A

-limiting exposure to antimicrobials
which reduces the selective pressure applied to infectious agents and the horizontal transfer of genetic information between cells of infectious agents.
-knowing the resistance profiles of circulating pathogens in population groups
the correct and effective antimicrobial agent can be chosen for first-line treatment. This reduces exposure of the pathogen and opportunists to sub-optimal doses of antimicrobial agents known to accelerate the development of resistance.

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11
Q

how to reduce antimicrobial resistance occurring? 4

A

-infection prevention and control (precautions in place)
-antimicrobial stewardship (prescription, restriction and administration reduces selective pressure)
-surveillance of resistance profiles
-drug development

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12
Q

therapeutic use of antimicrobials, when and who shouldn’t use them 4

A

Antimicrobial selection is complicated by factors associated with susceptible hosts. The optimal treatment options should be determined by evaluation of the patient’s clinical history, the identity of the infectious agent, and the results of antimicrobial susceptibility testing.

age- young and elderly susceptible to increased drug toxicity mostly elderly bc of poor renal function.

comorbidities- altered host physiology and medication interaction

pregnancy/breastfeeding- mode of action interferes with essential developmental processes

poly pharmacy- drug-drug interactions and adverse outcomes

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13
Q

empirical therapy is?

A

educated guess

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14
Q

drug targets for bacterial infections 4

A
  1. inhibition of cell wall synthesis- bactericidal and inhibit the formation of a rigid cell wall (include b-lactams and glycopeptides such as pennicillins)
  2. disruption of the cell membrane - bactericidal agents that increase the permeability of the cell membrane( membrane lysis)
  3. inhibition of protein synthesis- bacteriostatic that target ribosomal subunits
  4. inhibition of nucleic acid synthesis - inhibition of DNA gyrase that unwinds and supercoils DNA, also RNA polymerase and transcription and replication of binding of drug metabolites to DNA, these all inhibitions considered bactericidal and the interference with the metabolic pathway of folic acid being bacteriostatic
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15
Q

fungal antimicrobial drug class/target 3

A

inhibit ergosterol synthesis- azoles
bind to ergosterol - polyenes
inhibit B (1, 3)- D-glucan synthesis- echinoocandins

these are all broad spectrum atifungals, poorly soluble and highly toxic.

16
Q

types of worms

A

cestode- tape worm
nematode round worm
trematode - fluke

16
Q

types of worms

A

cestode- tape worm
nematode round worm
trematode - fluke

17
Q

how do amtihelmintic antimicrobials act as a drug target and class / spectrum

A
  1. increased membrane permeability- against cestodes and trematodes
  2. inhibit tubullin polymerization- against nematodes

broad spectrum

18
Q

protozoa drug target and class

A
  1. inhibit DNA replication, penetrate cell wall, activate upon entry by nitroreductase -
  2. inhibit nucleic acid synthesis and inhibit protein synthesis
19
Q

viral replication cannot occur unless

A

the virus infects a host cell and as a result antiviral medications are limited

20
Q

prions have no drug treatment for infection because?

A

they are not metabolically active

21
Q

bacteriostatic does what

A

stops replication/ growth of cells

22
Q

bacteriocidal

A

kills the cells

23
Q

bacteriolytic

A

lyse the cell and target functions of the cell

24
Q

what do the eurakytoic cells have in common with human host cells?

A

membrane bound organelles, ribosomes, cell membrane, nucleic acid

25
Q

what do prokayrotic cells have in common with human host cells

A

cell membrane

26
Q

what do viruses have in common with human host cells

A

nucleic acid

27
Q

what do prokayrotic have different to human cells

A

cell wall (not all)

28
Q

what do fungi/yeast have different to human cells

A

ergosterol

29
Q

what do protoza have different to human cells

A

metabolic pathways

30
Q

what do helminths have diff to human cells

A

mirotubules, microfilaments

31
Q

what do viruses have diff to human cells

A

enzymes

32
Q

drugs used to target these infectious agents would be relevant to what part of its structure?

A

target structures that they have that human cells don’t so theres no collateral damage