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ID > WK 7- Antimicrobial drugs > Flashcards

WK 7- Antimicrobial drugs Flashcards

1
Q

What is an antibiotic

A

natural substance from a micro-organism that is used to kill another organism→ used interchangeably with the word antimicrobials

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2
Q

What is an antimicrobial

A

term used for drugs used to treat microbes

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3
Q

What does broad spectrum mean

A

wide range of activity eg effective against a range of gram positive and gram negative bacteria

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4
Q

What does narrow spectrum mean

A

limited range of activity, target organism specific

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5
Q

What does bacteriocidal mean

A

kills bacteria

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6
Q

What does bacteriostatic mean

A

inhibits growth/replication of bacteria→ by stopping the bug replicating, the immune system can kill and eradicate the organism

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7
Q

What does empirical theory mean

A

therapy (antibiotics) are given without the exact pathogen of cause known→ leads to drugs being prescribed inappropriately→ used when treatment is required urgently→ guided by clinical presentation

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8
Q

What is directed therapy

A

used when the causative agent has been identified- based on causative organism and antimicrobial susceptibility

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9
Q

What is prophylactic therapy

A

used to prevent infection in clinical situations where there is significant risk of infection (ie. Malarial, surgical antibiotic prophylaxis)

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10
Q

What does selective toxicity mean

A
  • toxic to invading microorganisms while having minimal adverse effects on host (targets specific aspects of bacterial cells that aid in survival/replication/growth)
  • ie. target bacterial cell wall, as humans don’t have a cell wall they will not be affected
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11
Q

What are the 4 groups of antimicrobials that act to destroy microbes

A
  1. Agents that affect bacterial cell wall synthesis
  2. Agents that affect bacterial protein synthesis
  3. Agents that affect bacterial nucleic acid synthesis
  4. Agents that disrupt bacterial cell membrane function
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12
Q

What are some of the potential targets for selective toxicity of antimicrobial drugs

A

→pathways utilising energy to synthesise small molecules such as amino acids and nucleotides
→pathways that convert small molecules into macromolecules such as proteins, nucleic acids and peptidoglycan (cell wall)

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13
Q

What is the bacterial cell wall mainly composed of

A

peptidoglycan–> amino sugars with peptide side chain

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14
Q

What are the 2 main groups of antimicrobials that target the cell wall

A
  • Beta lactams–> both penicillins and cephalosporins

- Glycopeptides

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15
Q

What are the 5 main drug groups used to attack bacterial protein synthesis (MACLT)

A

Macrolides, Aminoglycosides, Lincosamides, Chloramphenicol and Tetracyclines

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16
Q

What are the main drug groups that affect nucleic acid synthesis (FNQR)

A

Folate inhibitors (sulfenamides/trimethoprim), Nitroimidazoles, Quinolones, Rifamycins

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17
Q

What is the MOA of B-lactams

-how do they preferentially target bacteria

A

inhibit the final transpeptidation step by forming covalent bonds with penicillin-binding proteins, preventing formation of crosslinks→ inhibiting formation of crosslinks leads to inhibition of cell wall synthesis and causes cell death
-humans don’t have a cell wall to target

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18
Q

How do penicillins display resistance (most likely cause)

A

through production of β-lactamases

-these act to break down the B-lactam ring and prevent the action of the antimicrobial

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19
Q

How is resistance to penicillin combatted

A

through use of clavulonic acid–> this is an B lactamase inhibitor

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20
Q

What are the two types of B-lactam drugs

A

Penicillins and Cephalosporins

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21
Q

What are the indications for penicillin

A

infections caused by many Gram+ve bacteria or Gram -ve cocci

-spectrum of activity ranges; some narrow, some broad

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22
Q

What are the adverse effects of penicillin

A

well tolerated though can produce a hypersensitivity (allergy) reaction (presents as a rash or in severe cases anaphylaxis), can also cause diarrhoea (due to disruption of commensal flora)

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23
Q

Which type of beta lactam is less sensitive to beta lactamase

A

-cephalosporins

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24
Q

What are the indications for cephalosporins

A

activity against both gram –ve and gram +ve bacteria→ ranges from moderate to broad spectrum

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25
Q

What are the adverse effects of cephalosporins

A

same as penicillins→ those that are sensitive to penicillin are also likely to be allergic to cephalosporins

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26
Q

What is the MOA of glycopeptides

A

inhibit release of the PG building block unit from carrier, preventing addition to the growing peptidoglycan chain→ bactericidal action

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27
Q

What are the indications for use of glycopeptides

A

narrow spectrum, reserved for treatment of resistant infections (eg MRSA)

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28
Q

What are the adverse effects of glycopeptides

A

nephrotoxicity, ototoxicity (damage to hair cells in the cochlear causes hearing loss)

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29
Q

What ribosomal subunits are present in a prokaryote

-why does this aid in selective toxicity

A

50S and 30S

-human (eukaryotes) have 40S and 60S

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30
Q

What is the MOA of tetracyclines

A

inhibit bacterial protein synthesis by reversibly binding to 30S subunit of the ribosome
→prevents the amino-acyl tRNA from binding to the A site→ bacteriostatic action

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31
Q

What are the indications for tetracyclines

A

broad spectrum against Gram+ve and Gram-ve bacteria, eg chlamydia, rickettsia, mycoplasma, spirochaetes, some mycobacteria protozoa→ can also be used as malaria prophylaxis

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32
Q

What are the adverse effects of tetracyclines

A
  • tooth discolouration and enamel dysplasia in children→ not used for kids under 8
  • GI damage
33
Q

Why is tetracyline contrindicated in pregnancy

A

Due to cell hypoplasia

34
Q

What do tetracylines interact with (another drug)

A

antacids

35
Q

What is the MOA of aminoglycosides

A

bind to aminoacyl site of 16S ribosomal RNA within 30S unit→ leads to misreading of the genetic code and inhibition of protein synthesis/wrong protein being produced→ bactericidal action due to producing non-functional proteins

36
Q

What are the indications for aminoglycoside use

A

aerobic gram neg organisms

37
Q

What are the adverse effects of aminoglycosides

A

nephrotoxicity and ototoxicity
→but a single one off empirical dose using genatmicin in pts with renal impairments is supported as it can be life saving

38
Q

What is the MOA of chloramphenicol

A

prevents protein chain elongation by inhibiting the peptidyl transferase activity of the bacterial ribosome (works on transpeptidation step)→ bacteriostatic action

39
Q

What are the indications for chloramphenicol

A

bacterial eye or ear infections, broad spectrum→ active against may gram pos and gram neg bacteria

40
Q

What are the adverse effects of chloramphenicol’s

A

bone marrow suppression (systemic), aplastic anaemia

41
Q

What are the interactions of chloramphenicol

A

inhibitor of CYP2C19 and CYP3A4→ these are vital in the breakdown of multiple drugs

42
Q

What is the MOA of macrolides

A

inhibit bacterial protein synthesis by binding to the 50S ribosomal subunit and inhibiting translocation (movement of the ribosome down the mRNA→ prevents further tRNA binding→ no continuation of polypeptide chain growth)→ bacteriostatic action

43
Q

What are the indications of macrolides

A

has immunomodulatory and anti-inflammatory effects → used for broad spectrum against gram pos and neg (resp, skin and urethral infections)→ used for pt with penicillin allergy

44
Q

What are the interactions of macrolides

A

some are potent inhibitors of CYP3A4

45
Q

What are the adverse effects associated with macrolides

A

mainly GI–> nausea, vomiting, diarrhoea

46
Q

What is the MOA of a lincosamides

A

protein synthesis inhibitor through inhibiting ribosomal translocation (similar to macrolides)

47
Q

What are the indications for lincosamides

A

broad spectrum→ used for serious infections and treatment of Propionibacterium acnes

48
Q

What are the adverse effects of lincosamides

A

diarrhea, pseudomembranous colitis→ caused by over growth of clostridium defacale (due to being a broad spectrum agent→ will disrupt micoflora of the GIT and allow for growth of opportunistic infections→ causes inflamm response in GIT)

49
Q

What are the 5 main ways to interfere with nucleic acid synthesis

A
  1. inhibit the synthesis of the nucleotides (sulfonamides)
  2. alter the base-pairing properties of the DNA template
  3. inhibit either DNA or RNA polymerase (rifamycins)
  4. inhibit DNA gyrase, which uncoils supercoiled DNA to allow transcription (quinolones)
  5. direct effect on DNA (nitroimidazoles)
50
Q

What is the MOA of sulfonamides

A
  • most bacteria can synthesise folate required for synthesis of DNA→ done through converting PABA→ folate→ Tetrahydrofolate→ thymidilate→ DNA
  • Sulfonamides are competitive analogues of PABA (Prevent conversion to folate)
  • Dihydrofolate reductase (converts folate to tetrahydrofolate) is inhibited by trimethoprim
51
Q

What is tetrahydrofolate

A

Tetrahydrofolate is required for DNA synthesis and is a co-factor in thymidilate synthesis→ it cannot be synthesised by humans and must be obtained from diet

52
Q

What are the contraindications of sulfonamides

A

-should not be used in those with folate deficiency or in early preg (due to teratogenic effects)

53
Q

What is the MOA of quinolones

A

inhibit bacterial DNA synthesis by blocking DNA gyrase and topoisomerase IV→ both unravel chromosomes to allow for replication of mRNA to occur→ bactericidal action

54
Q

What is the indiction of quinolones

A

broad spectrum, reserved for treatment of infections resistant to other drugs

55
Q

What are the adverse effects of quinolones

A

rash, GIT disturbances

56
Q

What is the MOA of nitroimidazoles

A

metabolised to active metabolites that covalently bind to DNA→ disrupt its helical structure, inhibiting nucleic acid synthesis→ bactericidal action

57
Q

What are the indications for nitroimidazoles

A

antibacterial and antiprotozoal agent, radiation sensitizer (makes cell cycle halt in areas sensitive to radiation)

58
Q

What is the MOA of rifamycins

A

inhibits bacterial RNA synthesis by binding to the beta subunit of DNA-dependent RNA polymerase→ blocks initiation of RNA transcription

59
Q

What are the indications for rifamycins

A

G+ve, some G-ve bacteria, mycobacteria (TB)→ always be used in combination, due to resistance

60
Q

What are the adverse effects of rifamycins

A

hepatotoxicity due to direct effects of toxic metabolites on hepatocytes

61
Q

What are two types of resistance

A

Intrinsic resistance (due to intrinsic properties of the bacterium eg. many antibiotics are active against G+ve but not G-ve bacteria), and acquired resistance (occurs when bacteria that were previously susceptible become resistant)

62
Q

What are the 3 basic mechanisms by which acquired resistance is spread

A
  1. transfer of resistant bacteria between people
  2. transfer of resistance genes between bacteria (usually on plasmids)
  3. transfer of resistance genes between genetic elements within bacteria, on transposons
63
Q

What are the 4 biochemical mechanisms of resistance

A
  1. production of enzymes that inactivate the drug
    eg -β-lactamases (β-lactams)
    -acetyltransferases (chloramphenicol)
    -kinases (aminoglycosides)
  2. alteration of drug-binding sites -eg aminoglycosides, erythromycin, penicillin
  3. reduction of drug uptake by the bacterium -eg tetracyclines (ie. Efflux pumps in the membrane that allow for removal of drug from cell)
  4. Alteration of enzyme pathways -eg trimethoprim
64
Q

What are the 3 main antifungal drug classes

A

azoles, polyenes and terbinafine

65
Q

What is the MOA of azoles

A

inhibit fungal enzyme, lanosine 14α-demethylase→responsible for converting lanosterol to ergosterol in fungal cell membrane
-cell leakage and death occur by lytic activity of host defence→ also inhibit transformation of candidal yeast cells into hyphae

66
Q

What is the indication for azoles

A

broad antifungal

67
Q

What are the adverse effects of azoles

A

rash, headache, GIT effects

68
Q

What is the MOA of polyenes

A

binds to ergosterol in fungal cell membranes altering their permeability and allowing leakage of intracellular components

69
Q

What is the indication for polyenes

A

candidiasis

70
Q

What is the MOA of terbinafine

A

selectively inhibits squalene epoxidase
→involved in the synthesis of ergosterol from squalene in the fungal cell wall→ accumulation of squalene is toxic to cell

71
Q

What is the indication of terbinafine

A

ringworm, fungal infections of nails, given orally or topically

72
Q

What are the 4 main types of anti-helminthic drugs

A

ivermectin, benzimidazoles, praziquantel and pyrantel

73
Q

What is the MOA of pyrantel

A

stimulates nematode nAChR,
causing muscle paralysis (Sustained depol and inhibition of nicotinic receptors causing muscle paralysis in the worm allowing it to pass)

74
Q

What is the MOA of benzimidazoles

A

-inhibit β-tubulin polymerisation, interfering with microtubule-dependent functions such as glucose uptake

75
Q

What is the MOA of ivermectin

A

-opens glutamate-gated Cl-channels; also binds to allosteric site on the nAChR, leading to paralysis (cause chloride movement= Ca+ influx= paralysis)

76
Q

What is the MOA of praziquantel

A

-binding to PKC sites on VGCCs, leads to Ca2+ influx, prolonged contraction & paralysis

77
Q

What is the most common reason for drug interactions

A

Competition/inhibition of cytochromes–> one will not be metabolised and have no activity

78
Q

What therapy would be appropriate if the patient had otitis media but with no systemic signs of infection?

A
  • symptomatic treatment→ provide a prescription for antibiotics at initial treatment, and if the infection progresses then the pt is able to dispense the script
  • -> don’t give antibiotics until systemic symptoms show

ID (13 decks)

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