Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PoM > Immuno - Antimicrobial Therapies > Flashcards

Immuno - Antimicrobial Therapies Flashcards

1
Q

What is prontosil?

A

antibacterial drug used for blood infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of antibiotic is prontosil?

A

Sulphonamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some sulphonamide antibiotics?

A

Sulphamethoxazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are sulphonamides sometimes used together with

A

Trimethoprim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is prontosil used to treat?

A

UTIs. RTIs, bacteraemia, HIV prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is prontosil only effective against in terms of bacterial structure?

A

Only effective against gram negative bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is an antibiotic?

A

Antimicrobial agent produced by microorganism that kills or inhibits another microorganism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is an antimicrobial?

A

Chemical that selectively kills or inhibits microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a bactericidal?

A

Kills bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a bacteriostatic?

A

Stops the growth of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an antiseptic?

A

Kills or inhibits microbes - usually applied topically to prevent infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can we attribute to antimicrobial resistance?

A

Lack of new antibiotics and countries prescribing high levels of antibiotics to their patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does AMR lead to?

A

Increased mortality, morbidity and cost/burden on society.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does AMR lead to increased time to effective therapy?

A

We must spend more time trying to figure out what the patient responds well to

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does AMR lead to requirement for additional approaches?

A

For example, we may need surgery as the patient will not respond well to antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does AMR lead to use of expensive therapy?

A

We must try out many new methods of treatment rather than simply administering antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does AMR lead to use of more toxic drugs?

A

E.g. vancomycin is needed which is toxic, to generate the same response as the normal antibiotic that a microbe has become resistant to.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does AMR lead to use of less effective antibiotics?

A

We must resort to second choice antibiotics, as bacteria have developed resistance to our antibiotic of choice.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are aminogylcosides?

A

Potent bactericidal activity - target protein synthesis, membrane integrity and RNA proof reading.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does a lack of RNA proof reading lead to?

A

Abhorrent proteins which damage the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the downside of aminoglycosides?

A

They are toxic and can sometimes cause hearing loss - they are only used as other antibiotics are ineffective.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Rifampicin?

A

Bactericidal - targets the RpoB subunit of RNA polymerase and is very effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the downside of Rifampicin?

A

Spontaneous resistance can occur and can sometimes cause orange/red secretions from the patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is vancomycin?

A

Bactericidal that targets the lipid component of the cell wall biosynthesis and the wall cross linking via D-ala-residues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the downside of vancomycin?

A

Very toxic and needs to be given intravenously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

When do we use vancomycin?

A

Due to resistance e.g. MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is linezolid?

A

Bacteriostatic that inhibits the initiation of protein synthesis by binding to the 50s rRNA subunit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a limitation of linezolid?

A

Only affects gram positive but not negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is daptomycin?

A

Bactericidal that targets the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are some of the limitations of daptomycin?

A

Only positive against gram positive bacteria and is relatively toxic therefore needs to be given intravenously in inpatient settings

31
Q

What are beta-lactams?

A

Interfere with the synthesis of the peptidoglycan component of the bacterial cell wall

32
Q

What are examples of beta-lactams?

A

Penicillin

Methicillin

33
Q

How are antibiotics selectively toxic?

A

Machinery that the antibiotics target are specific to the targeted bacteria.

34
Q

What are macrolides?

A

Affect both gram positive and negative bacteria, and target the 50s subunit of ribosomes to prevent amino-acyl transfer, thus truncating polypeptides to stop growth.

35
Q

What are some examples of macrolides?

A

Erythromycin

Azithromycin

36
Q

What are Quinolones?

A

Synthetic broad spectrum antibiotics
Target the DNA gyrase in gram negative bacteria, and topoisomerase 4 in positive bacteria - causes DNA damage and subsequent death of an organism.

37
Q

What are the main misconceptions at the dawn of the antibiotic era?

A

Resistance against more than 1 class of antibiotic would not occur in the same bacterium.
Resistant bacteria would be significantly less potent/fit
Resistance arising from horizontal gene transfer would not occur

38
Q

When does resistance occur?

A

When a bacteria can grow at antibiotics at or above the breakpoint

39
Q

What is the breakpoint?

A

The clinically achievable concentration at which a microbe is susceptible

40
Q

What is the minimal inhibitory concentration?

A

Minimum concentration of an antibiotic required to inhibit growth - related to the breakpoint

41
Q

What arises from the routine use of antibiotics?

A

Selection pressure for the acquisition and maintenance of resistant genes.

42
Q

In the absence of selection pressure, what happens with the antibiotics?

A

Resistant strains do not gain an advantage therefore do not proliferate, as they do not have anything to gain an advantage over.

43
Q

What happens when you add a selection pressure to bacteria?

A

There is now an advantage for resistant bacteria, therefore they proliferate over other antibiotics and we gain a high population of resistant bacteria as long as there is pressure

44
Q

What are the mechanisms of resistance?

A

Altered target site
Inactivation of antibiotics
Altered metabolism by bacteria to bypass antibiotic
Decreased drug accumulation

45
Q

What is an altered target site?

A

Change to peptide sequence of bacteria so that the antibiotic can no longer bind to the bacteria

46
Q

What is an example of an altered target site?

A

MRSA encodes alternative PBP to PBP2a with a lower affinity to beta lactase therefore giving it resistance

47
Q

What is inactivation of the antibiotic?

A

Occurs via enzymes that degrade or alter antibiotics to render them ineffective

48
Q

What is an example of antibiotic inactivation?

A

Beta lactamase hydrolyses the beta-lactam ring and chloramphenicol acetyl transferase (CAT)

49
Q

What is altered metabolism?

A

Bacteria overproduce metabolic intermediates which can outcompete antibiotic for target site. or they can switch to other metabolic pathways from pathways which antibiotics would have otherwise targeted.

50
Q

What is decreased drug accumulation?

A

Efflux pumps in the bacteria eject antibiotics to stop then from reaching their MIC.

51
Q

When can multiple resistance mechanisms co-exist?

A

E.g. N.gonorrhoea - some strains encoded penicillinases, some encoded efflux pumps and also underwent target site modification to quinolones

52
Q

What are the exogenous sources of resistance

A

Bacteria can acquire plasmids
Bacteria can acquire transposons
Bacteria can acquire naked DNA from environment

53
Q

What are the main mechanism bacteria can share DNA?

A

Transformation
Transduction
Conjugation

54
Q

What is transformation?

A

Allows bacteria to take up DNA from their environment

55
Q

What is transduction?

A

Phage mediated transfer between a virus that infects bacteria and goes on to take up some of their DNA and spread it between different bacteria

56
Q

What is conjugation?

A

Plus mediated DNA transfer in which plasmids are shared.

57
Q

What are some of the non genetic mechanisms of resistance?

A
  • Biofilm - matrix encased communities of bacteria
  • Intracellular location in human cells
  • Slow growth of bacteria therefore too hard to target.
  • Spores can be resistant to heat, antiseptics and ABs
  • Persister bacteria - bacteria are dormant
58
Q

What are some miscellaneous reasons for treatment failure?

A

Wrong choice of treatment
Poor AB penetration
Inappropriate dose level/ technique
AB resistance within commensal flora which may secrete beta lactamases for example.

59
Q

Where do we typically find the highest rates of resistance?

A

Critical care units

Renal in patient units

60
Q

Where do we typically find the lowest rates of resistance?

A

Community settings

61
Q

What are some of the risk factors for acquiring resistant bacteria?

A 
Immunosuppression 
Crowded wards 
Broken skin
Indwelling devices e.g. catheter
AB therapy may suppress microbiota 
Transmission by staff.
62
Q

what are some of the ways in which we can address resistance?

A

New strategies for prescribing
Reserving/withdrawing certain classes of antibiotic
Reducing broad spectrum ABs which damage microbiota
Development of more rapid diagnosis
Combination therapy research/ more research in general

63
Q

What are broad spectrum antibiotics?

A

Effective against a wider number of bacteria types.

64
Q

How can we overcome resistance?

A

Modification of antibiotics e.g. amoxicillin
Infection control measures
Antibiotic combination

65
Q

What is an example of overcoming resistance?

A

Methicillin is modified so that its B-lactam ring is resistant to lactamases

66
Q

Along with bacteria, what organisms are also becoming affected by antimicrobial resistance?

A

Fungi

67
Q

How do fungi digest food?

A

Outside the cell by secreting hydrolytic enzymes which can break down biopolymers to be absorbed for nutrition

68
Q

What are the 3 broad classes of fungal conditions in humans?

A

Allergy
Mycotoxicoses
Mycoses

69
Q

what is allergic fungal condition?

A

Allergic reactions to fungal products e.g. Allergic Broncho-pulmonary aspergillosis (ABPA)

70
Q

What is mycotoxicoses?

A

Ingestion of fungi and their toxic products e.g. aflatoxin

71
Q

What are mycoses?

A

Superficial, subcutaneous or systemic colonisation, invasion and destruction of human tissue

72
Q

What are the 3 classes of mycoses?

A

Superficial
Subcutaneous
Systemic
(Mucosal too)

73
Q

What are the targets for anti fungal therapies?

A

Cell membrane - uses ergosterol instead of cholesterol
DNA synthesis
Cell wall - fungi have one unlike mammalian cells.

PoM (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions