Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

4.2 Medical Microbiology > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

Talk a little on the history of antibiotics

A

Greatest medical breakthrough of the 20th century

First antibiotic salvarson deployed in 1910

Penicillin in 1928 - golde age of natural produce antibiotic discovery

Over 100 years theyve drastically changed medicine

Extended human life span by 23 years

Invasive procedures now possible e.g. open heart surgery and infections now survivable

However no new antibiotics in recent years - were now in the postantibiotic era

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

Why are no new antibiotics being made?

A

theres no money in antibiotics

Any new drugs will eventually incur resistance - companies wont make money from them

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

Talk about the UK O’Neill report, what are some of the findings

A

A report on resistance comissioned by the UK government

Determined that 700,000 deaths occur due to resistant bacteria at the moment

Predict that 10 million deaths will occur due to resistant bacteria by 2050

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

How was Penicillin discovered

A

S. aureus plates were left in an incubater over the weekend

Fungus grew on plates

Observed antimicrobial affect of fungus on the S. aureus

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

What has been our most recent large discovery in antibiotics

A

Macrolides

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

Define antimicrobials, what are the three types?

A

Agents used to kill or inhibit the growth of microorganisms such as bacteria, fungi, viruses or pasites

Antibiotics are used to control bacterial growth
Annifungals are used to control fungal growth
Anivirals used to control viral growth

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

What three things must be balanced when selecting an antibiotic to use

A

Effective treatment
Minimisation of toxicity
Prevention of resistance

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

What are the different properties of an antibiotic, what properties of a drug should be considered

A

Spectrum of activity: broad or narrow
Mechanism of action: bacteriostatic vs bactericidal
Pharmacokinetic properties: absorption, distribution, metabolism, excretion
Pharmacodynamic properties: time-dependent killing, concentration-dependent killing
Toxicity and safety profile: organ toxicity, allergic reactions, side effects
Interactions with other drugs
Stability and formulation
Impact on normal flora
Cost and availability

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

Talk about broad spectrum antibiotics

A

Effective against both gram positive and negative organisms
Most commonly used is Norfloxacin
They are used in empirical treatment where we dont have time to ID the causative organism
They attack every bacteria and thus disrupt microbiome
Cause side effects such as GI distress and yeast infections in women

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

Talk about narrow spectrum antibiotics

A

Act against a limited number of bacteria
e.g. penicillin targetting peptidoglycan and thus only being affective against gram +/ves
We often switch to narrow spectrum to target therapy when we have ID’d the organism
More targetted therapy means more effective treatment - means patient needs to be treated for less time
Often has fewer side effects and little impact on normal flora

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

Compare baceriostatic vs bactericidal antibiotics

A

Bacteriostatic only inhibit bacteria from reproducing but doesnt actively kill them

Bactericidal actively kills bacteria - kills at least 99% in the first 4-8 hours

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

What is the most commonly used antibiotic in empirical treatment?

A

Norfloxacin

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

Some antibiotics can have both bacteriocidal and bacteriostatic affects, comment on this and give an example

A

Different affects on different organisms e.g.
Linezolid is bacteriostatic against staph and enterococcus but bactericidal against strep

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

What is pharmacokinetics

A

The study of how the body interacts wih administered substanced for the entire duration of exposure

Defined as the kinetics of drug absorption, distribution, metabolism and excretion (KADME)

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

Talk about the absorption PK property of antibiotics

A

How well the antibiotic is absorbed into the bloodstream when taken orally or through other routes

IV or oral etc

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

Talk about the distribution PK property of antibiotics

A

How the drug spreads throughout the body’s tissues and fluids

Some antimicorobials will penetrate well into specifric tissues e.g. CNS while others will not

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

Talk about the metabolism PK property of antibiotics

A

The process by which the drug is broken down
Some antimicrobials are metabolised in the liver, and understandin this helps avoid drug-drug interactions

Chronic illness e.g. those affecting liver and kidney can affect the metabolism of antimicrobials
The same can happen with other medications- they can interfere with metabolisation of antibiotics

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

Talk about the excretion PK property of antibiotics

A

How the drug is removed from the body, primarily through the kidneys or liver

Patients with renal or hepatic impairment may need dosage adjustments to compensate for this - might need lower dosage etc

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

What are pharmacodynamic properties

A

The effects of drugs in the body and the mechanism of their action

Time-dependent killing and conentration-dependent killing

Monitoring concentration of antibiotics done in bio lab to balance conc above MIC

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

Talk about time-dependent killing PD property of antimicrobials

A

The effectiveness of some antimicorbials such as B-lactams is dependent on how long the drug concentration remains above the minimum inhibitory concentration of the pathogen

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

Talk about concentration -dependent killing PD property of antimicrobials

A

Some antimicrobials such as aminoglycosides and fluoroquinolone effectiveness increases with higher concentration

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

What are the differences between pharmacokinetics and pharmacodynamics

A

PK is the study of what the body does to the drug
- absorption, metabolism etc etc

PD is the study of what the drug does to the body
- in tems of antimicrobials this is the effect of concentrations and time of drug on body

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

Talk about the organ toxicity property of antimicrobials, give examples

A

Some can be toxic to specific organs e.g. aminoglycosides are nephrotoxic and isoniazid is hepatotoxic

Monitoring is necessary for high-risk patients

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

Talk about allergic reactions in antimicrobials

A

Some such as penicillins can cause severe allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Talk about the side effects of antimicrobials
Can range from mild e.g. GI upset to severe eg. anaphylaxis or C. diff associated diarrhea
26
What are the properties of a good antibiotics
Selective toxicity ie. the ability to kill or inhibit growth of an organism without harming the cells of the host
27
Talk about the ability of antimicrobials to inteact with other drugs
Can inteact with others to either affect their own activity of the acivity of the othe drug Can reduce efficacy or increase toxicity
28
Talk about stability and formulation of antimicrobials
Stability: what tempeature does it have to be stored at, does it work best at certain pHs etc Formulation: does it have to be made up, oral, intravenous, topical etc
29
Talk about the impact of antimicrobials on normal flora
Broad spectrum disrupt normal flora Can potentially cause secondary infections usch as yeast Can cause superinfections such as C. diff
30
Talk about superinfections
Infections which follow treatment Either opportunistic e.g. C, diff or resistant following antimicobirl resistance
31
Talk about the cost and availability of antimicrobials
The expense and availability can impact their use especially in low-resource settings Generic formulations are often preferred to reduce costs
32
What are the four ideal properties of an antimicrobial
Selective toxicity Bactericidal activity Narrow spectrum of activity (if appropriate) Slow emergency of resistance
33
What does the duration of treatment depend on? Give examples of reflections of this
Nature of infection Site of infection Growth rate of pathogen 3-5days reatment for UTIs (updated guidelines, used to be 5-7) 2-3 weeks for BSIs 6 wekks for IEs 9 weeks for TB
34
What are the three main mechanisms of antibiotics
Disrupt cell structures or processes - by interfering with cell wall synthesis or maintenance Interfere with the function of enzymes required to synthesise or assemble macromolecules - by targetting nucleic acid replication or - by targetig protein synthesis Destroy structures already formed in the cell
35
Talk about cell wall inhibitors, give examples
These are bacteriocidal and are selectively toxic for bacterial cell walls Include B-lactams, bacitracin, vancomycin and isoniazid
36
Talk about protein synthesis antimicrobials, give examples
Bacteriostatic but selective Attack 30S and 50S ribosomoal subunits of bacteria that humans dont have e.g. azithromycin, clindamycin, aminoglycosides such as gentamycin, tetracyclines and linezolid
37
Talk about antimicrobials against cytoplasmic membrane, give examples
Bacteriocidal but not selective Targets both human and bacterial cells hence used with caution e.g. polymixin or daptomycin
38
How do cell wall antibiotics work, give examples
Target peptidoglycan - blcoking synthesis - cells lyse and die Beta-lactams: - Penicilins, cephalosporens, carbapenems, monobactams Glycopeptides: - Vancomycin and teicoplanin Polypeptides: - Bacitracin (strep)
39
What is peptidoglycan, describe its structure
A strong, mesh-like polymer that forms a protective layer around bacterial cells giving structural integrity and shape It is made up of glycan chains (sugars) that are cross-linked by peptide chains (amino acids) Its glycan backone consisits of alternating units of NAG and NAM Short peptide chain attached to NAM unit - D-alanine-D-alanine Traspeptidase facilitates cross linkage between peptides by acting on D-ala D-ala
40
What does NAM and NAG stand for?
NAM = N-acetylglucosamine NAG = N-acetylmuramic acid
41
How do Beta lactams work?
They mimic D-ala D-ala and thus confuse transpeptidase - thus blocking cross linkage of PG
42
What are the four major classes of beta lactams, ive examples
Penicillins: narro spectrum - augmentin - methicillin Cephalosporins: extended spectrum - cefotaxime Carbapenems: reserve - meropenem Monobactams: newest
43
Comment on the use and side effects of beta lactams
Most commonly used antimicrobials Rearded as safe but can be associated with diarrhoea and allergy Usage can range from superficial infections to bloodstream infections
44
What is the main strucutral component of beta lactam antibiotics how does this differ between classes?
The beta-lactam ring - a four-membered ring structure essential for action Classes are defined by the structure of the ring or attachments e.g. - five-membered ring in penicillins - six-membered ring in cephalosporins - side chains attached
45
Why do we make new classes of B-lactams and new generations
We develop new classes to increase the spectrum of activity and to address specific resistance mechanisms Within each class there are generational hierarchy e.g. 1st, second, thrid and fourth generation cephalosporins to target specific resistance
46
List the penicillins
Penicillin Methicillin Amoxicillin Ampicillin Ticarcillin Piperacillin
47
List the cephalosporins
Cefuroxime Cefotoxime Ceftazidime Cefepime Cefaroline
48
List the carbapenems
Imipenem Meropenem Ertapenem
49
Give an example of a monobactam
Aztreonam
50
Talk about the formation of peptidoglycan
Precursor of NAG and NAM are synthesised in cytoplasm NAM is attached to a short peptide chain (D-ala D-ala) used later in cross-linking NAG an NAM units are transported across the cell membrane by bactoprenol Bactoprenol delivers these units to the growing PG layer outside the cell membrane Once outside the NAG and NAM units link together to form a glycan chain which provid the backbone of PG layer which supports bacteial cell wall Penicillin-binding proteins such as transpptidases link the peptide side chains of NAM to form cross-links and thus a strong, mesh-like structure
51
What is bactoprenol and what does it do?
Bactoprenol is a lipid carrier molecule It helps deliver NaG and NAM units across the cell membrane to outside the cell membrane
52
What is transpeptidase, what does it do?
An example of a penicillin-binding protein Which cross links the D-ala D-ala s of NAM molecules to form cross linked PG
53
How exactly do B-lactams work?
They resemble D-ala-D-ala Thus they act as a flas substrate in PG synthesis They bind to transpeptidase enzymes (hence penicllin binding protein) responsible for final stages of cell wall cross-linkage Thus inhibit transpeptidation in PG synthesis This results in accumulation of precursors of cell wall units and activation of cells autolytic system and thus cell lysis
54
How do B-lactams affect gram positives?
Gram positive cell walls are rich in Peptidoglycan and thus the Penicillin binding proteins/transpeptidase are easily accessible Following exposure to B-lactams GPs release lipoteichoic acid fom the cell wall This lipoteichoic acid triggers a generalised autolytic dismantling of the PG i.e. suicidal activation of wall autolysins
55
What are released from GPs following exposure to Beta lactams?
Lipoteichoic acid
56
What does Leipoteichoic acid trigger
Activation of wall autolysins thus incurring cell suicide
57
How do B-lactams affect gram negatives?
In gram negatives the PBP/transpeptidase are not as easily accessed - they are inside the periplasmic space B-lactams need to cross the oute membrane through passive diffusion or pass through porin chanels to access the target PBPs
58
Talk about the Penicillin class, how do they work
Contain a B-lactam ring - this is the target for resistance (penicillinase) Work by inhibiting PG cross-linking They naturally target Gram positives and thus have a narow spectrum of activity Synthetic penicllins can have broader spectrum
59
Talk about synthetic penicillins, how do they work
New generations to extend the spectrum of activity and reduce vulnerability to evolving resistance mechanisms We now have beta lactamase producers so to combat this we made B-lactamase inhibitors such as clavulanate and tazobactam which have weak antibacterial activity but act false/suicide substrate for analogue for penicillin i.e. distract the Beta lactamase enzymes so that penicillins can work
60
Give three examples of synthetic penicillins
Augmentin: amoxicillin + clavulanate Timentin:: Ticarcillin + clavulanate Tazocin: Piperacillin + tazobactam
61
Talk about cephalosporins
They have an extended spectrum of activity compared to penicillins They have activity against gram -/ves 3rd and 4th generation have an extended spectrum of activity and are less susceptible to inactivation by beta-lactamases Theres a need for further generations to reduce vulnerability to ESBL and CPOs
62
Give some examples of cephalosporins and their usage
Ceftazidime/avibactam -> beta-lactamase gram -ves Ceftolozane/tazobactam -> beta-lactamase gram-ves Cefidirocol -> new drug throught to be useful against resistance without moving up a class to carbapenems
63
How do cephalosporins affect gram negative bacteria
They can penetrate the outer membrane through the porin channels
64
Talk about Carbapenems
Of all B-lactams, carbapenems posses the broadest spectrum of activity and greatest potency against gram-positive and gram negative bacteria They were meant to be our reserve but usage is now widespread Less susceptible than pen and ceph to B-lactamase activity but we now have CPEs
65
Talk about some of the different carbapenems and their uses
Imipenem was the first clinically used Meropenem provides the highest bacterial response Ertapenem can be given as a once a day therapy but lacks activity against P. aeruginosa and Acientobacter
66
Talk about the redesign of ertapenem
Redesigned in 2017 so that it could be used as a once a day treatment
67
Talk about monobactams
Mode of action similar to penicillins Newest form of B-lactam drugs Some capability in inhibiting B-lactamase but not ESBLs or carbapenemases Limited for gram-negative bacteria
68
Give some examples of monobactams
Aztreonam - primary monobactam used in gram-negative infections particularly in patients with penicillin allergies Aztreonam and avibactam combination is under development for resistant strains - avibactam is a beta lactamase inhibitor -> this combo is currently in phase 3 trials
69
What are the three main glycopeptides
Vancomycin Teicoplanin Dalbavancin and Oritavancin
70
Talk about Vancomycin Glycopeptide and its use
The most well known glycopeptide We tend to limit its use due to high nephrotoxic effect We tend to limit it to MRSA, endocarditis (and other severe GP infections) and C. diff infections
71
Talk about Teicoplanin Glycopeptide and its use
Tend to prescribe teicoplanin over vancomycin in Europe It has a longer half life then vancomycin -> hence have to dose less frequently than vancomycin Used for gram positive infections
72
Talk about Dalbavancin and Oritavancin
Newer glycopeptide with a longer half life Used for skin and soft tissue infections caused by resistant gram positive organisms These drugs allow for one-weekly dosing
73
List the modes of action of glycopeptides
Binding to Peptidoglycan Precursors: - bind directly to D-ala-D-ala portion of the peptidoglycan precursor Prevents Cross-linking: - binding to the D-ala-D-ala part of the precursor, glycopeptides block the cross-linking of peptidoglycan strands - cross-linking is essential for cell wall strength and integrity Prevents Incorporation of Subunits: -prevents transport of the subunit through the cytoplasmic membrane, stopping the insertion of new peptidoglycan units into the cell wall - inhibiting the transglycosylation and transpeptidation reactions, critical for peptidoglycan chain assembly and maturation NB: prevents cross linking and prevenys transport of precurosors across cytoplasm to PG chain *different glycopeptides have slight differences in binding profiles but we dont need to know these

4.2 Medical Microbiology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions