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WK 7- Antimicrobial drugs Flashcards

(78 cards)

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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
What are the adverse effects of cephalosporins
same as penicillins→ those that are sensitive to penicillin are also likely to be allergic to cephalosporins
26
What is the MOA of glycopeptides
inhibit release of the PG building block unit from carrier, preventing addition to the growing peptidoglycan chain→ bactericidal action
27
What are the indications for use of glycopeptides
narrow spectrum, reserved for treatment of resistant infections (eg MRSA)
28
What are the adverse effects of glycopeptides
nephrotoxicity, ototoxicity (damage to hair cells in the cochlear causes hearing loss)
29
What ribosomal subunits are present in a prokaryote | -why does this aid in selective toxicity
50S and 30S | -human (eukaryotes) have 40S and 60S
30
What is the MOA of tetracyclines
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
31
What are the indications for tetracyclines
broad spectrum against Gram+ve and Gram-ve bacteria, eg chlamydia, rickettsia, mycoplasma, spirochaetes, some mycobacteria protozoa→ can also be used as malaria prophylaxis
32
What are the adverse effects of tetracyclines
- tooth discolouration and enamel dysplasia in children→ not used for kids under 8 - GI damage
33
Why is tetracyline contrindicated in pregnancy
Due to cell hypoplasia
34
What do tetracylines interact with (another drug)
antacids
35
What is the MOA of aminoglycosides
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
What are the indications for aminoglycoside use
aerobic gram neg organisms
37
What are the adverse effects of aminoglycosides
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
What is the MOA of chloramphenicol
prevents protein chain elongation by inhibiting the peptidyl transferase activity of the bacterial ribosome (works on transpeptidation step)→ bacteriostatic action
39
What are the indications for chloramphenicol
bacterial eye or ear infections, broad spectrum→ active against may gram pos and gram neg bacteria
40
What are the adverse effects of chloramphenicol's
bone marrow suppression (systemic), aplastic anaemia
41
What are the interactions of chloramphenicol
inhibitor of CYP2C19 and CYP3A4→ these are vital in the breakdown of multiple drugs
42
What is the MOA of macrolides
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
What are the indications of macrolides
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
What are the interactions of macrolides
some are potent inhibitors of CYP3A4
45
What are the adverse effects associated with macrolides
mainly GI--> nausea, vomiting, diarrhoea
46
What is the MOA of a lincosamides
protein synthesis inhibitor through inhibiting ribosomal translocation (similar to macrolides)
47
What are the indications for lincosamides
broad spectrum→ used for serious infections and treatment of Propionibacterium acnes
48
What are the adverse effects of lincosamides
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
What are the 5 main ways to interfere with nucleic acid synthesis
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
What is the MOA of sulfonamides
- 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
What is tetrahydrofolate
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
What are the contraindications of sulfonamides
-should not be used in those with folate deficiency or in early preg (due to teratogenic effects)
53
What is the MOA of quinolones
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
What is the indiction of quinolones
broad spectrum, reserved for treatment of infections resistant to other drugs
55
What are the adverse effects of quinolones
rash, GIT disturbances
56
What is the MOA of nitroimidazoles
metabolised to active metabolites that covalently bind to DNA→ disrupt its helical structure, inhibiting nucleic acid synthesis→ bactericidal action
57
What are the indications for nitroimidazoles
antibacterial and antiprotozoal agent, radiation sensitizer (makes cell cycle halt in areas sensitive to radiation)
58
What is the MOA of rifamycins
inhibits bacterial RNA synthesis by binding to the beta subunit of DNA-dependent RNA polymerase→ blocks initiation of RNA transcription
59
What are the indications for rifamycins
G+ve, some G-ve bacteria, mycobacteria (TB)→ always be used in combination, due to resistance
60
What are the adverse effects of rifamycins
hepatotoxicity due to direct effects of toxic metabolites on hepatocytes
61
What are two types of resistance
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
What are the 3 basic mechanisms by which acquired resistance is spread
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
What are the 4 biochemical mechanisms of resistance
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
What are the 3 main antifungal drug classes
azoles, polyenes and terbinafine
65
What is the MOA of azoles
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
What is the indication for azoles
broad antifungal
67
What are the adverse effects of azoles
rash, headache, GIT effects
68
What is the MOA of polyenes
binds to ergosterol in fungal cell membranes altering their permeability and allowing leakage of intracellular components
69
What is the indication for polyenes
candidiasis
70
What is the MOA of terbinafine
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
What is the indication of terbinafine
ringworm, fungal infections of nails, given orally or topically
72
What are the 4 main types of anti-helminthic drugs
ivermectin, benzimidazoles, praziquantel and pyrantel
73
What is the MOA of pyrantel
stimulates nematode nAChR, causing muscle paralysis (Sustained depol and inhibition of nicotinic receptors causing muscle paralysis in the worm allowing it to pass)
74
What is the MOA of benzimidazoles
-inhibit β-tubulin polymerisation, interfering with microtubule-dependent functions such as glucose uptake
75
What is the MOA of ivermectin
-opens glutamate-gated Cl-channels; also binds to allosteric site on the nAChR, leading to paralysis (cause chloride movement= Ca+ influx= paralysis)
76
What is the MOA of praziquantel
-binding to PKC sites on VGCCs, leads to Ca2+ influx, prolonged contraction & paralysis
77
What is the most common reason for drug interactions
Competition/inhibition of cytochromes--> one will not be metabolised and have no activity
78
What therapy would be appropriate if the patient had otitis media but with no systemic signs of infection?
- 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

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