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Pharmacology > Chapter 32 > Flashcards

Chapter 32 Flashcards

1
Q

What is the practice of “inhibiting pathways or targets that are critical for pathogen or cancer cell survival and replication at concentrations of drug lower than those required to affect host pathways.”?

A

Selective Toxicity

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2
Q

What are the three (3) components of selective toxicity?

A

Attacking:

  1. targets unique to pathogen or cancer
  2. targets in pathogen or cancer that are similar but not the same as host
  3. targets that are in both, but more important to pathogen or cancer
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3
Q

What is therapeutic index?

A

TI= TD50/ED50

-indication of how selecitve a drug is

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4
Q

Why is selective toxicity harder when targeting cancer cells than with microbes?

A
  • Because they are our cells!!!
  • share common biochemical, physiological, and reproductive pathways.
  • common molecular machinery
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5
Q

Why do beta-lactams have good selectivity?

A

-They target peptidoglycan cell wall synthesis, we dont have peptidoglycan cell walls.

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6
Q

What are two differences between bacterial and human protein synthesis?

A
  • Different size ribosomes
  • different ribosomal RNA and proteins
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7
Q

What is the basis of selectivity for most antinoplastic drugs?

A
  • Cancer cells divie more rapidly
  • drugs targeting processes involved in DNA systhesis are the target
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8
Q

What types of normal cells are adversely affected by 5-fluorouracil?

A
  • all cells undergoing DNA synthesis, esp. rapidly dividing tissues:
  • Bone marrow and GI mucosa
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9
Q

What is the difference between and bacteriostatic agent v. a bactericidal agent?

A
  • Bascteriostatics inhibit cell growth bu not not kill the bacteria (protein synth. inhib.)
  • bactericides kill bacteria (cell wall synth. inhib.)
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10
Q

What is the significance of bacteriostatics v. bactericides in immunocompromised patients?

A
  • Bacteriostatics rely on healthy host immune to eliminate the non-growing but viable bacteria
  • Bactericides do not= better for immunocompromised patients.
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11
Q

Why do Bacteriostatics like tetracycline have an an antagonistic interaction with bactericides like penicillin?

A
  • tetracycline inhibits protein synthesis and retards growth
  • penicillin requires cell growth to be effective
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12
Q

How do penicillins have a synergistic effect with amino glycosides?

A

-**penicillins inhibit cell wall synthesis which allows for increased entry and effectiveness of the aminoglycoside. **

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13
Q

What is the mechaism of aminoquinolines? What is an example of this type of drug?

A
  • Inhibit polymerization of heme within RBC
  • Thought to be toxic to malaria plasmodia

E.g. Chloroquine

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14
Q

Why would an antiviral that needs to be phosphorylated by a viral enzyme to be active have a higher selective toxicity than a drug that did no requrire this step?

A
  • the phosphorylation step ensures that the drug is only active at the site of viral infection.
  • no action against host.
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15
Q

What is the mecanism of action of acyclovir?

A

-nucloside analogue that competitively inhibits viral DNA and RNA synthesis once activated by phosphorylation.

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16
Q

What are three polymerase inhibitor drugs?

A

-Acyclovir

-Zidovudine

-Efavirenz

17
Q

What are two (2) neuramidase inhibitors?

A

-Zanamivir

-Oseltamivir

18
Q

Why do anticancer drug not affect cells in the Go phase?

A

-they aren’t activy dividing

19
Q

What kind of cells are killed by anti-cancer drugs and cause dose-limiting toxicity?

A

-Bone marrow and GI mucosa

20
Q

What are two kinds of drugs that interfere with dividsion at M phase?

A

-Taxanes

-Vinca alkaloids

21
Q

What is conjugation?

A

-Direct transfer of plasmid or DNA between microbes

22
Q

What is transduction?

A

-transfer of plasmid or DNA from bacteria to bacteria through a bacteriophage or virus.

23
Q

What is transformation?

A

-Acquisition of naked DNA of plasmid from the environment

24
Q

What is the signifance of p-glycoprotein in MDR?

A

-p-glycoprotein allows a cell to pump out different kinds of drugs therefore allowing resistace to several kinds.

25
Q

What is the most important cause of increased drug resistance in a population?

A

-overprescription of antibiotics

26
Q

Why is treatment of cancer or infection with multiple agents advantagous?

A

-it can significantly decrease the probability that resistance will develop

27
Q

What are four (4) major reasons to administer multiple drugs simutaneously?

A
  1. multiple MOA acheives maximum killing rate
  2. more difficult for resistance to develop
  3. lower doses of synergistically acting drugs means less side effect (important in anticancer).
  4. combination allows each drug to acheive maximally tolerated dose and increased killing.
28
Q

What is the action of sulfa drugs?

A

-prevent syntheiss of folic acid by acting as PABA analogues

29
Q

What is a sequential blockade?

A

-blockage of sequential steps in a syntetic pathway

30
Q

What is the action of trimethoprim?

A
  • Targets and inhibits dihydrofolate reductase (DHFR)
  • second step in sythesis
31
Q

What is the reason for the synergistic effect seen between trimethoprim and sulfamethoxazole?

A

-The sulfonamide decreases the intracellular concentration of DHF, this increases the effectiveness of the DHFR inhibitor (trimethoprim)

32
Q

Why is trimethoprim significant in the treatment of UTI?

A

-Trimethoprim is excreted unchanged in the urine.

33
Q

What is pyrimethamine the only effective treatment of?

A

-Toxoplasmosis

34
Q

What drug is used in folinic acid rescue in methotrexate overdose?

A

Leucovorin

35
Q

How is methotrexate effective in the treatment of cancer, tumors, and arthritis, but cause bone marrow problems?

A
  • Methotrexate (MTX) inhibits DHFR which causes a critacal shortage of THF in cells.
  • rapidly dividing cells (tumors, cancer, bone marrow, GI mucosa) can not continue DNA synthesis due to the halted purine sythesis.

Pharmacology (17 decks)

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