Drug Resistance, Sulfonamides, Trimethoprin Flashcards

1
Q

Needs to be used with Dihydropteroate Synthase (DHPS) in folate biosynthesis to make 7,8-Dihydropteroate.

A

pABA

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2
Q

Folate (FH4) is made from this crucial molecule.

A

7,8-Dihydropteroate

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3
Q

These drugs competitively inhibit PABA.

A

Sulfonamides

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4
Q

Sulfonamides are a type of _______.

A

Anti-folate.

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5
Q

MOA of Sulfonamides.

A

Competitively inhibit pABA, which is needed for folate synthesis.

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6
Q

These drugs decrease the Dihydropteroate precursor.

A

Sulfonamides

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7
Q

Mammals and folates.

A

Mammals cannot make folic acid, so they have to get it in the diet.

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8
Q

These anti-folate drugs have a free para-amino acid.

A

Sulfonamides

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9
Q

Sulfonamides bacteriocidal or static?

A

Static.

Delayed bacteriostatic effect.

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10
Q

Concentrated in the urine, and effective in aerobic Gram + and -.

A

Sulfonamides

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11
Q

Folate is used for what kind of metabolism?

A

One-carbon unit transfer reactions

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12
Q

Converts dUMP to dTMP

A

Thymidylate cycle

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13
Q

Part of the Folate pathway and makes dTMP

A

Thymidylate cycle

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14
Q

These are needed in order for the Thymidylate cycle to work

A

Folate derivatives

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15
Q

Folate synthesis inhibitor.

A

Trimethoprim

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16
Q

A folic acid analog that inhibits folate synthesis by blocking DHFR (Dihydrofolic Reductase).

A

Trimethoprim

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17
Q

How do microbes prevent microbial disease?

A

Create an inhospitable environment by lowering the pH.

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18
Q

Host microbes make these, which insert into the cell walls of bad bacteria to create pores and cause cell death.

A

Colicins

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19
Q

What is a microbial disease?

A

An overpopulation of microbes that colonize sterile zones, and a small number of them are pathogenic.

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20
Q

How does microbial disease occur?

A

Exposure through ingestion, inhalation, or a wound, or thru a superinfection.

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21
Q

How do microbes cause disease?

A

1) Through tissue invasion and immune over-response.

2) Make exo and endotoxins (LPS).

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22
Q

Anti-microbial proteins found in body fluids that defend against bad bacteria.

A

Defensins.

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23
Q

Using a single drug to treat a disease.

A

Monotherapy.

24
Q

This therapy uses microbes to kill bad bacteria without harming the host.

A

Antimicrobial therapy.

25
Q

Bacterial shape and how they stain is known as bacterial ________.

A

Taxonomy

26
Q

These antimicrobial drugs are most used by general dentists.

A

Attack cell wall and protein synthesis.

27
Q

What does the gram stain tell you?

A

Thickness and composition of the cell wall.

28
Q

Bacteriostatic or cidal drugs recommended if you are immunocompromised?

A

CIDAL!

29
Q

A lack of antimicrobial effect at the highest drug concentration that’s tolerable to the host.

A

Drug resistance.

30
Q

When a protective substance, like pus, prevents the antibiotic from getting to the site of infection.

A

Escape

31
Q

Escape in the oral cavity.

A

Biofilm

32
Q

There’s a pre-existing mechanism in the bacteria that makes it naturally resistant to the drug.

A

Intrinsic/Natural resistance.

33
Q

When species that used to be sensitive to a drug are no longer sensitive to it.

A

Acquired resistance.

34
Q

Acquired drug resistance can be _______ or ________.

A

Chromosomal; Extrachromosomal

35
Q

Ways that bacteria can spread acquired drug resistance extrachromosomally.

A

Transformation
Transduction
Conjugation

36
Q

Chromosomal spread of resistance is through ______.

A

Replication

37
Q

Interfere with the normal metabolism within cells.

A

Antimetabolites

38
Q

What do bacteria use to make DNA?

A

Folate derivatives.

39
Q

These inhibit folate metabolism in bacteria to stop DNA synthesis.

A

Anti-folates.

40
Q

Can either inhibit a reaction or incorporate into the DNA as an analog and disrupt the metabolism.

A

Anti-metabolites.

41
Q

Synthetic antibiotics bc they’re man-made structural analogs.

A

Anti-folates

42
Q

These two things are needed to make 7,8-Dihydropteroate synthase.

A

pABA and Dihydropteroate Synthase

43
Q

Create a delayed bacteriostatic effect.

A

Sulfonamides

44
Q

Has a free para-amino group.

A

Sulfonamides

45
Q

This is needed to convert dUMP to dTMP in the Thymidylate cycle so that bacteria can make nucleotides.

A

Folate

46
Q

Inihibits DHFR

A

Trimethoprim (TMP)

47
Q

Folate analogue that inhibits DHFR

A

Trimethoprim

48
Q

Analogue of dTMP

A

TMP (Trimethoprim)

49
Q

Converts 7,8-Dihydrofolate to Folate.

A

DHFR

50
Q

Bacteriostatic and NOT delayed.

A

Trimethoprim

51
Q

Rationale for blocking the folate synthesis pathway at two steps rather than just one.

A

1) Decreased chance of drug resistance.

2) Has a greater effect at stopping bacterial replication if two steps are blocked rather than one.

52
Q

These drugs concentrate in the urine, so they’re used to treat UTI’s and p. cervicii pneumonia.

A

Sulfonamides + Trimethoprim

53
Q

Adverse event of Sulfonamides + Trimethoprim when used to treat p. cervicii pneumonia (PCP).

A

Increased CNS effects

54
Q

Oral manifestation of folate deficiency.

A

Chronic ulcers.

55
Q

Folate deficiency is commonly seen in:

A
  • Chronic alcoholics
  • Elderly
  • People with Folate malabsorption