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Immunology Drugs > Antibacterials 3 > Flashcards

Antibacterials 3 Flashcards

1
Q

What are examples of folic acid synthesis?

A

Sulfonamides
Trimethoprim

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2
Q

What is an example of antifolates?

A

Sulfonamindes

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3
Q

Are sulphonamides bactericidal or bacteriostatic?

A

Bacteriostatic

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4
Q

What are examples of sulfonamides?

A

Sulfisoxazole
Sulfamethoxazole
Sulfadiazine
Sulfacetamide
Silver sulfadiazine

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5
Q

What is the mechanism of action of Sulphonamides?

A

They are competitive inhibitors of dihydropteroate synthase enzyme

Interfere with the pathway responsible for the synthesis of folic acid and thereby nucleic acid synthesis in bacteria.

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6
Q

What are the pharmacokinetics of sulfonamides?

A

Rapidly absorbed after oral administration

Bind to plasma proteins; distributed into most body tissues and fluids

Metabolised in the liver

Excreted in unchanged and metabolized form through kidneys.

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7
Q

What is the spectrum of sulfonamides?

A

Gram +
Gram -

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8
Q

Which bacteria do sulfonamides have potent activity against?

A

H. ducreyi
Nocardia
K. granulomatis

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9
Q

Which bacteria develop resistance against sulfonamides?

A

S. pyrogens
S. pneumoniae
S. aureus
H. influenza
N. meningitides
Shigella
E. coli

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10
Q

What happens if bacteria develop resistance to sulfonamides?

A

Limits their usefulness, particularly in empiric therapy

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11
Q

What are the therapeutic use of sulfonamides?

A

UTIs
Otitis media
Ocular infections
Burns

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12
Q

What are the adverse effects of sulfonamides?

A

Anorexia
GI disturbances
Jaundice
Hypersensitivity reactions
Haemolytic anémia (rare)
Crystalluria

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13
Q

Which sulfonamide is responsible for crystalluria?

A

Sulfamethoxazole

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14
Q

What causes resistance to sulfonamides?

A

Random mutation and selection or by transfer through plasmids, leading to reduced affinity of the drug or the enzyme, permeability barrier and efflux pump.

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15
Q

Is Trimethoprim a bacteriostatic or bactericidal?

A

Bacteriostatic

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16
Q

What is the mechanism of action of Trimethoprim?

A
  1. Interferes with the pathway responsible for the synthesis of DNA & RNA in bacteria
  2. NADPH cannot be converted into NADP
  3. Inhibition of dihydrofolate reductase
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17
Q

What is the spectrum of activity of Trimethoprim?

A

Similar spectrum as sulfamethoxazole

20 to 100 times more potent than sulfonamides

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18
Q

Which bacteria are resistant to Trimethoprim?

A

P. aeruginosa,
B. fragilis,
Enterococci

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19
Q

What is the therapeutic use of Trimethoprim?

A

UTI and bacterial prostatitis

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20
Q

What is the preferred medication for bacterial prostatitis?

A

Fluoroquinolones

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21
Q

What are the pharmacokinetics of Trimethoprim?

A

Rapidly absorbed following oral administration

Reaches higher concentrations in the relative acidic prostatic and vaginal fluids

Widely distributed into body tissues and fluids

60% to 80% is excreted unchanged via the kidneys

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22
Q

Which kind of bacteria usually tend to develop resistance against Trimethoprim?

A

Gram (-) bacteria due to an altered DHFR (lower affinity)

Decrease in permeability barrier and efflux pumps

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23
Q

What are the adverse effects of Trimethoprim?

A

Effects of folic acid deficiency (especially in patients with poor diets)

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24
Q

What can reverse the adverse effects of Trimethoprim?

A

Simultaneous administration of folinic acid

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25
Q

What is the combination of sulfamethoxazole + Trimethoprim?

A

Co-trimoxazole

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26
Q

What is the mechanism of action of Co-trimoxazole?

A

Blockade of two sequential steps of THF biosynthesis

Inhibition of DHPS & DHFR

Better antibacterial activity than either alone

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27
Q

What is the mechanism of synergism of Co-trimoxazole?

A

They show greater inhibition of bacterial growth.

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28
Q

Is Co-trimoxazole bactericidal or bacteriostatic?

A

Even though each drug exerts bacteriostatic activity, when the organism is sensitive to both then there is bactericidal activity.

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29
Q

What is the spectrum of Co-trimoxazole?

A

Broader spectrum than sulfa drugs alone

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30
Q

What is the therapeutic use of co-trimoxazole?

A

Effective in UTI

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31
Q

What are the pharmacokinetics of co-trimoxazole?

A

Orally
Distributed throughout the body; 65% of sulpha and 40% of trimethoprim bound to plasma proteins
Crosses BBB
Both drugs exerted in urine

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32
Q

In which case is co-trimoxazole given through IV?

A

Severe cases of pneumonia

33
Q

What is the therapeutic uses of co-trimoxazole?

A

Uncomplicated UTI, bacterial prostatitis
MRSA
Bacterial respiratory infections
Septicemia
Meningitis
GI disturbances

34
Q

What are the adverse effects of co-trimoxazole?

A

Skin rash
Nausea
Hematologic toxicities
Hyperkalemia
Prolonged prothrombin times

35
Q

What bacteria usually develop resistance co-trimoxazole?

A

E.coli
MRSA

36
Q

What are examples of Inhibitors of DNA synthesis and structure?

A

Rifamycins
Quinolones

37
Q

What are examples of quinolones?

A

Ciprofloxacin
Norfloxacin
Levofloxacin

38
Q

Are quinolones bactericidal or bacteriostatic?

A

Potent bactericidal

39
Q

What is the MOA of quinolones?

A

Enter the bacterium by passive diffusion through porins in the outer membrane

Inhibit DNA gyrase & Topoisomerase IV

Inhibit DNA replication

Bacterial cell death

40
Q

What inhibits DNA gyrase?

A

Topoisomerase II

41
Q

Which kinds of drugs exhibit PAE?

A

Aminoglycosides and Fluoroquinolones

42
Q

For Gram (+) bacteria what is the primary target?

A

Topoisomerase IV

43
Q

For Gram (-) bacteria what is the primary target?

A

DNA gyrase

44
Q

What is the function of DNA gyrase?

A

It catalyses and breaks down the super-coiling of the double stranded DNA

45
Q

What happens if DNA gyrase is inhibited?

A

Disruption of DNA synthesis –> cell death

46
Q

What is the function of Topoisomerase IV?

A

To unlink daughter chromosomes following DNA replication, and resolve DNA knots

47
Q

What happens if Topoisomerase IV is inhibited?

A

Slow decline in DNA synthesis –> cell death

48
Q

What is the selectivity of Fluoroquinolones?

A

Human, mammalian enzymes are NOT affected by bactericidal concentrations of quinolones because they are structurally different

49
Q

What is the general spectrum of Fluoroquinolones?

A

Broad gram (-)
Some gram + and mycobacteria

50
Q

What is an example of 1st generation Fluoroquinolones?

A

Nalidixic acid

51
Q

What is the spectrum of 1st generation Fluoroquinolones?

A

Gram (-) organisms

52
Q

Which gram (-) organism is not targeted by 1st generation Fluoroquinolones?

A

Pseudomonas sp.

53
Q

What is an example of 2nd generation of Fluoroquinolones?

A

Lomefloxacin

54
Q

What is the spectrum of 2nd generation Fluoroquinolones?

A

Improved against gram (-)
Some activity against gram (+) and atypic pathogens
Aerobic

55
Q

What are the atypical organisms targeted by 2nd generation Fluoroquinolones?

A

Legionellaceae
Chlamydiaceae

56
Q

What is an example of 3rd generation Fluoroquinolones?

A

Sparfloxacin
Gatifloxacin

57
Q

What is the spectrum of the 3rd generation of Fluoroquinolones?

A

Same as 2nd generation
Improved activity against Gram + and atypical organism

58
Q

What are examples of 4th generation Fluoroquinolones?

A

Gemifloxacin
Trovafloxacin

59
Q

What is the spectrum of activity of the 4th generation Fluoroquinolones?

A

Increased activity against gram +
Broad ANAEROBIC coverage

60
Q

How do bacteria build resistance against Fluoroquinolones?

A

Altered target
(mutations in bacterial genes –> reduced affinity for Fluoroquinolones)

OR
Decreased accumulation
(porin channels - reduced
efflux pumps - increased)

61
Q

What are the pharmacokinetics of Fluoroquinolones

A

Oral or Iv
Distributes well in all tissues and body fluids
High Vd
Do not cross BBB, unless inflamed
Cleared by kidney

62
Q

What substances reduce the absorption of Fluoroquinolones?

A

Antacids, iron and zinc

63
Q

Which Fluoroquinolones are detected in breast milk?

A

Ciprofloxacin
Ofloxacin
Levofloxacin

64
Q

What are the adverse effects of Fluoroquinolones?

A

GI disturbances
Headaches and dizziness
Phototoxicity
Articular cartilage erosion
Tendon rupture
Peripheral neuropathy (rare)

65
Q

What are the therapeutic uses of Fluoroquinolones?

A

RTI
Bone, joint, skin and soft tissue infections
GI and intra-abdominal infections
UTI
STI

66
Q

What are examples of Rifamycins?

A

Rifampin
Rifabutin
Rifapentine

67
Q

What is the first-line drug for TB?

A

Rifampicin

68
Q

Are Rifamycins bacteriostatic or bactericidal?

A

Bactericidal

69
Q

What is the MOA of Rifamycins?

A

Interfere with β-subunit of mycobacterial DNA-dependent RNA polymerase
Blocks RNA synthesis

70
Q

What is the spectrum of Rifamycins?

A

Intracellular and extracellular mycobacteria

Effective against both gram +/- bacteria

71
Q

What are examples of the mycobacteria that are targeted by Rifamycins?

A

M. tuberculosis
M. kansasii
MAC
M. leprae

72
Q

How do bacteria develop resistance to Rifamycins?

A

Mutations in bacterial DNA-dependent RNA polymerase –> reduced affinity for drug

73
Q

What are the PK of Rifamycins?

A

Orally taken
Distributes well
Induces hepatic CYP450 enzymes
Half-life reduced during first 2 weeks
Eliminated in the bile, feaces and urine

74
Q

Why does the half-life of Rifamycins decrease during the first 2 weeks?

A

Due to auto-induction

75
Q

What colour does Rifamycin stain urine, and feaces?

A

Orange-red

76
Q

What are the adverse effects of Rifamycin?

A

GI disturbances
Skin rash
Hepatitis
Flu-like symptoms

77
Q

What are the rare side effects of higher doses of Rifamycin?

A

Acute renal failure
Haemolytic anémia
Shock

78
Q
A

Immunology Drugs (7 decks)

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