Brainscape's Knowledge GenomeTM

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


See full index

Microbiology > Antimicrobials > Flashcards

Antimicrobials Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

-cidal Antimicrobials

A
  • Faster onset
  • Functional immune syst not required
  • Used in immunocompromised individuals
  • Used in life-threatening infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

-static Antimicrobials

A
  • Slower onset
  • Does require functional immune system in pt
  • Not advised in immunocompromised individuals
  • Not advised in life-threatening infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Selective Toxicity

A

Goal: minimal/no effect against host but maximum effect against infecting microorganism
*low selective toxicity = higher risk of side effects

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

Broad-spectrum Antimicrobials

A

Effective against a wide range of infectious micro organisms which includes both G+ve and G-ve bacteria

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

Narrow-spectrum Antimicrobials

A

Active against selected group of bacterial types

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

Broad-spectrum Used when:

A

Wide differential dx, delayed tx to identify microorganism would be detrimental to pt, tx of drug resistant pathogens where their resistance is to narrow spectrum compounds, or polymicrobial infections

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

Synergistic Interaction

A

Compounds are more effective in combination with one another

E.g. - penicillin is -static on its own but add genamicin the duo becomes -cidal

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

Target sites for Abx:

A
  1. Metabolism
  2. Protein synthesis
  3. CW
  4. Nucleic acid synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sulfonamides

A

Target: folic acid synthesis
Structure: analog of PABA (component of folic acid in bacteria)
Selective toxicity: no equivalent mammalian pathway (bacteria must synthesize their own folic acid)

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

Cyclines

A

Mechanism: bind aminoacyl site of 30s ribosome; aminoacyl tRNA is unable to bind bc of this

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

Aminoglycosides

A

Mechanism: interfere w/ formation of 30S initiation complex

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

Macrolides

A

Mechanism: bind to 23S component of 50S rRNA, blocks exit of peptide chain

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

Inhibitors of PG/CW synthesis

A

Groups: penicillins, cephalosporins, monobactgams, carbapenems
*bacteria must be actively replicating for these compounds to work (active ONLY on growing cells)

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

B-lactams

A

Target: mecA gene that encodes for penicillin binding protein (PBP) aka transpeptidases
Mechanism: interfere w/ transpeptidase enzymes that cross-link the PG/CW of the bacterium, the (must be replicating/growing) microorganism will lyse
Effect: bacterial cell lysis

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

Inhibitors of nucleic acid synthesis

A

Mechanism: inhibitors of DNA gyrase
Quinolone: synthetic abx
Fluoroquinolone: addition of side chain to quinolone to change the activity of the abx

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

Inherent Resistance

A
  • Lack of target for drug to act against (mycoplasma has no CW so resistant to penicillin)
  • Structural restriction (G-ve outer membrane blocks abx access)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Acquired Resistance

A

Via genetic diversity the bacterium transfer resistant genes to offspring, and random mutations occur causing resistance

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

Aminoglycosides

A

Ineffective against: anaerobes

Reason: ox-phos is absent in anaerobes

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

Glycopeptides

A

Ineffective against: G-ve

Reason: large abx and can’t penetrate the outer membrane

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

Nitroimidazoles

A

Ineffective against: aerobes

Reason: aerobes lack flavodoxin (which activates the nitroimidazoles)

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

Altered Uptake

A

Decrease/block uptake to prevent intracellular accumulation of abx to therapeutic level
Mechanism: often involves multi-drug resistance efflux pumps

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

Altered Target

A

Change in receptor site affinity, reduces binding of abx to cellular target
Mechanism: mecA gene encodes for a modified transpeptidase (so there is lower binding affinity for B-lactam abx)
*no inhibition of CW synthesis

23
Q

Drug Inactivation

A

B-lactamases, chloramphenicol acetyltransferases
Mechanism: hydrolytic enzymes that cleave the abx, constitutive or inducible
*partial solution: give Abx plus B-lactamase inhibitor

24
Q

Extended-Spectrum B-Lactamases

A

Allow bacteria to be resistant to almost all B-lactam abx, and frequently to aminoglycosides and fluoroquinolones
Exceptions: Cephamycins and Carbapenems
*main producers are E. coli and Klebsiella

25
Q

Transformation (recombination)

A

Uptake of DNA released by bacterial cell lysis, facilitated by DNA binding proteins, requires Ca2+, bacterial cell is called “competent cell” if it does transformation

26
Q

Conjugation (recombination)

A

Acquisition of free-floating DNA by plasmid called F factor which codes for a sex pilus, the cell w/ plasmid called F+ comes in contact with the F- cell an F- becomes F+
**only in G-ve bacteria

27
Q

Transduction (recombination)

A

Mediated by bacteriophages (bacterial viruses), in temperate virus the phage DNA integrates w/ host cell DNA
*e.g. - Diptheria toxin

28
Q

Transposition (recombination)

A

Transposon mediated non-homologous recombination, transposons are mobile genetic elements and can move around w/in the cell
*aka “jumping genes”

29
Q

Flucytosine (5-FC)

A

What? pyrimidine analogue
Mechanism: intracellular deamination of drug to 5-FC by fungal cytosine deaminase
Effect: inhibits synth of DNA, RNA and proteins
*fungicidal activity against Candida and Cryptococcus

30
Q

Polyenes

A

Mechanism: binds to Ergosterol in fungal cell membrane, causes pores in the membrane disrupting osmotic integrity then ion leakage and membrane destabilization
Effect: cell lysis due to disruption of membrane stability
*fungicidal activity against most yeasts and filamentous fungi

31
Q

Azoles

A

Target: Ergosterol (250-fold affinity for fungal sterols)
Mechanism: stops ergosterol synthesis by binding to 1,4a-demythylase
Effect: hinder growth can be fungistatic or fungicidal depending
*some have anti-parasitic effects

32
Q

Fluconazole

A

Azole drug that targets Lanosterol

33
Q

Echinocandins

A

Target: (1,3)-B-D-glucan synthase
Mechanism: disrupts CW (chitin) formation
Resistance: dec affinity for (1,3)-B-D-glucan synthase

34
Q

Neuraminidase Inhibitors

A

Target: neuraminidase (influenza virus) which normally cleaves sialic acid from glycoproteins to prevent virus being trapped in mucus
Mechanism: blocks neuraminidase causing formation of viral aggregates at cell surface (i.e. release is blocked)
E.g. - Oseltamivir

35
Q

IFNs (viral interference)

A

Mechanism: stimulate uninfected cells to produce antiviral proteins
Affect: blocks transcription and protein synthesis

36
Q

Acyclovir

A

Compound: nucleoside analog (guanine)
Mechanism: viral thymidine kinase is only present in virally infected cells and is required to activate Acyclovir, it is the first enzyme needed to convert ACV from monophosphate to diphosphate (most important step)
Effect: chain termination (HSV 1 and 2)

37
Q

Viral load

A

Amount of virus present in plasma, CSF, or other fluids

  • copies of nucleic acid per ML
  • monitors antiretroviral therapy in HIV
38
Q

Integrate Strand Transfer Inhibitors (INSTIs)

A

Target: integrase enzyme
Mechanism: blocks bonding of host and viral DNA so it can’t be incorporated into genome
E.g. - Raltegravir and Elvitegravir

39
Q

Reverse Transcriptase Inhibitors (RTIs)

A 
Target: Reverse Transcriptase
Mechanism: prevents viral RNA to DNA 
Types of RTIs:
1. NucleoSide analogues (NRTIs)
2. NucleoTide analogues (NtRIs)
3. Non-nucleoside (NNRTIs)
40
Q

Nitroimidazole

A

Characteristics: antiparasitic and antibacterial (against anaerobes)
Mechanism: ferredoxins donate electrons to nitro group of drug and activate to reduced form; acts as terminal electron acceptor and binds to DNA
Effect: loss of helical structure of DNA, impaired ability to act as template, breakage of strand

41
Q

Pentamidine

A

Antifungal, antiprotozoal (giardiasis and cryptosporidosis)
Mechanism: inhibition of DNA, RNA and protein synth
*toxic; largely replaced by other compounds now

42
Q

Antimalarials

A
  • single drug usually targets single stage of the Plasmodium lifecycle (blood or liver, etc)
  • stage specificity can vary w/ Plasmodium species
    E.g. - quinines, doxycycline (protein synth inhib), artemisinin
43
Q

Aminoquinoline Analogs

A

Likely mechanism: interferes w/ parasites he matin detoxification
*blood schizontocides

44
Q

Doxycycline

A

Mechanism: interferes w/ apicoplast (disrupts 70S ribosome)
Effect: inhibits protein synthesis
Target: both blood and liver stages of plasmodium

45
Q

Artemisinin

A

Mechanism: release free-radicals into parasite vacuoles, damaging membranes
Effect: inhibition of major metabolic processes like glycosiysis
*usually combined w/ aminoquinolone (ACT) to delay dev of resistance

46
Q

Ivermectin

A

Mechanism: interfere w/ Glu-gated Cl channels resulting in hyperpol of cells
Effect: paralysis and death of parasite
Target: nematodes, crestodes, and trematodes
*potent against: onchocerciasis and lymphatic filariasis

47
Q

Benzimidazoles

A

Mechanism: binds to beta-tubulin of cytoskeleton and inhibits something we dk what?
Target: intestinal nematodes, various cestodes
E.g. - Albendazole and Mebendazole

48
Q

Praziquantel

A

Mechanism: interferes w/ Ca2+ transport in tegument
Effect: worm paralysis (detachment, breakdown and expulsion)
Target: trematodes and crestodes (e.g. - liver flukes, cysticercosis, schistosomiasis)

49
Q

Biofilms (inherent resistance)

A

Multiple Abx cannot target the species that produce biofilms due to reduced microbial metabolic activity; lack of penetration

50
Q

NucleoSide and NucleoTide Analogues

A

Both lack 3’ hydroxyl group which causes chain termination because the polymerase cannot add on to the N3 group

51
Q

Amantadine/Rimantadine

A

Target: inhibit uncoating
Mechanism: viral M2 protein blocked so viral RNAs remain bound to M1, H+ ion channel formation is disrupted and viral RNA can’t enter nucleus
Affect: viral replication halted

52
Q

Antiparasitic Resistance (malaria)

A

Mutation, change in gene copy # causing change in drug target or increased efflux pumps

53
Q

Oseltamivir (Tamiflu)

A

Target: NA
Mechanism: virus binds to its own sialic acid and forms useless clumps blocking release/budding from host cell

Microbiology (14 decks)

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