Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Immunology Drugs > Antibacterials 3 > Flashcards

Antibacterials 3 Flashcards

1
Q

What are examples of folic acid synthesis?

A

Sulfonamides
Trimethoprim

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

What is an example of antifolates?

A

Sulfonamindes

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

Are sulphonamides bactericidal or bacteriostatic?

A

Bacteriostatic

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

What are examples of sulfonamides?

A

Sulfisoxazole
Sulfamethoxazole
Sulfadiazine
Sulfacetamide
Silver sulfadiazine

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

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

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

What is the spectrum of sulfonamides?

A

Gram +
Gram -

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

Which bacteria do sulfonamides have potent activity against?

A

H. ducreyi
Nocardia
K. granulomatis

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

Which bacteria develop resistance against sulfonamides?

A

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

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

What happens if bacteria develop resistance to sulfonamides?

A

Limits their usefulness, particularly in empiric therapy

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

What are the therapeutic use of sulfonamides?

A

UTIs
Otitis media
Ocular infections
Burns

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

What are the adverse effects of sulfonamides?

A

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

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

Which sulfonamide is responsible for crystalluria?

A

Sulfamethoxazole

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

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

Is Trimethoprim a bacteriostatic or bactericidal?

A

Bacteriostatic

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

What is the spectrum of activity of Trimethoprim?

A

Similar spectrum as sulfamethoxazole

20 to 100 times more potent than sulfonamides

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

Which bacteria are resistant to Trimethoprim?

A

P. aeruginosa,
B. fragilis,
Enterococci

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

What is the therapeutic use of Trimethoprim?

A

UTI and bacterial prostatitis

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

What is the preferred medication for bacterial prostatitis?

A

Fluoroquinolones

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

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

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

What are the adverse effects of Trimethoprim?

A

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

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

What can reverse the adverse effects of Trimethoprim?

A

Simultaneous administration of folinic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the combination of sulfamethoxazole + Trimethoprim?

A

Co-trimoxazole

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the mechanism of synergism of Co-trimoxazole?

A

They show greater inhibition of bacterial growth.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the spectrum of Co-trimoxazole?

A

Broader spectrum than sulfa drugs alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the therapeutic use of co-trimoxazole?

A

Effective in UTI

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

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

Immunology Drugs (7 decks)

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