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Pharmacology > 32- Antimicrobials and Antineoplastics > Flashcards

32- Antimicrobials and Antineoplastics Flashcards

1
Q

What is the goal “selective toxicity” of antimicrobials and antineoplastics?

A

provide antimicrobial and antineoplastic (anti-cancer) drug therapy without affecting the host

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2
Q

What are the 3 ways of selectivity to kill harmful cells?

A

1) Targets unique to only pathogen or cancer cells (genetic or biochemical pathway) but not host
2) Targets in pathogen or cancer cell that are similar but not identical to those in the hosts
3) Targets in pathogen or cancer cells that are shared by the host. These targets are important for pathogens but not so much for the host.

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3
Q

Why is selective toxicity harder for cancer cells?

A

in order to target cancers, the drug targets pathways common to both cancer and host

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4
Q

What is the therapeutic index equation?

A

TI = TD50/ED50

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5
Q

What is better, a small or large therapeutic index?

A

large

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6
Q

What is the MOA of β-lactams?

A

inhibit the transpeptidase enzymes that catalyze the final cross-linking step in peptidoglycan synthesis

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7
Q

Why are β-lactams essentially nontoxic to humans?

A

target the peptidoglycan cell wall which is both biochemically unique and essential for the survival of growing bacteria

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8
Q

What is the difference between bacterial and eukaryotic ribosomes?

A

bacteria use 70S ribosomes made up of 30S and 50S. We use 80S ribosomes made up of 40S and 60S

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9
Q

Since cancer cells contain our own enzymes and structures, how do we target them?

A

target through variations in cancer cell growth behavior and from increased susceptibility of cancer cells to induction of apoptosis or senescence

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10
Q

Where is the basis for selectivity for antineoplastic drugs?

A

lies in the drug’s ability to induce apoptosis in cancer cells but not in most normal cells

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11
Q

What is 5-flurouracil (5-FU)?

A

inhibits DNA synthesis in dividing cells by inhibiting thymidylate synthase

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12
Q

What cells can be damaged by 5-FU therapy?

A

5-FU is toxic to all dividing human cells causing both therapeutic and adverse effects

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13
Q

What are the therapeutic effects of 5-FU therapy?

A

toxic for rapidly cycling tumor cells

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14
Q

What are bactericidal drugs?

A

drugs that kill bacteria

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15
Q

What are bacteriostatic drugs?

A

drugs that inhibit growth of pathogen without causing death by targeting metabolic pathways necessary for growth but not survival

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16
Q

What determines the effectiveness of bacteriostatic drugs?

A

depends on an intact host immune system to clear the nongrowing bacteria

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17
Q

Why are tetracyclines and beta lactams antagonists?

A

tetracycline is a bacteriostatic drug by inhibiting protein synthesis and penicillin is a bactericidal drug that requires cell growth and division to kill cells. no cell growth –> PCN can’t fxn

18
Q

How can a penicillin-aminoglycoside combination produces a synergistic effect?

A

inhibition of bacterial cell wall synthesis by penicillin allows increased entry of aminoglycoside

19
Q

What is the MOA of aminoquinolones?

A

Aminoquinolones work by inhibiting the polymerization of heme within the erythrocyte

20
Q

What does aminoquinolones treat?

A

Malaria

21
Q

What is the target of ACV?

A

viral DNA polymerase

22
Q

What are the 3 polymerase inhibitors?

A
  • Acyclovir (treats HSV and VZV)
  • Zidovudine (“AZT”, treats HIV)
  • Efavirenz (treats HIV)
23
Q

What are the 2 neuraminidase inhibitors?

A
  • Zanamivir (treats Influenza A and B)

* Oseltamivir (treats Influenza A and B)

24
Q

Why do most anticancer drugs not target cancer cells in the G0 phase?

A

Most antineoplastic drugs target dividing cells

25
Q

What types of human cells can be harmed with anticancer drugs?

A

bone marrow, GI mucosa, and hair follicles because these cells, like cancer cells, have a high turnover rate

26
Q

What is the MOA of Vinca alkaloids?

A

inhibit microtubule polymerization, preventing microtubule extension

27
Q

What is the MOA of Taxanes?

A

inhibit microtubule depolymerization, arresting the cell in mitosis (eventually leading to apoptosis)

28
Q

What are the 3 ways bacteria can trans mit genetic material for drug resistance?

A

conjugation (bacteria sex), transduction (bacteria UPS delivery), and transformation (naked baby bacteria adoption services)

29
Q

What protein are multidrug cancers (MDR’s) often associated with?

A

P-glycoprotein

30
Q

What does an overexpression of P-glycoproteins do?

A

actively pumps many types of antineoplastic drugs out of the cell, allowing pathogens or tumors to become resistant to multiple drugs of different classes

31
Q

What is the most important cause of increased antibiotic resistance?

A

overprescription of antibiotics that are not indicated for the clinical situation

32
Q

What is trimethoprim (TMP)?

A

folate analogue that competitively inhibits dihydrofolate reductase (DHFR)

33
Q

What is the MOA of TMP?

A

prevents the regeneration of THF, therefore there is no synthesis of purine nucleotides or methylation of dUMP to dTMP

34
Q

Why are folate analogues like TMP given with sulfonamides?

A

They’re synergistic by blocking 2 essential steps in folates.

35
Q

Why is TMP-SMZ given for UTI’s?

A

TMP is excreted unchanged in the urine, so it can be used even as a single agent to treat uncomplicated UTIs

36
Q

What is the MOA of Pyrimethamine?

A

a folate analogue that selectively inhibits parasitic DHFR

37
Q

What type of infection does Pyrimethamine given for?

A

toxoplasmosis

38
Q

What is methotrexate (MTX)?

A

a folate analogue that reversibly inhibits DHFR

39
Q

What must you give a few hours later if you give a very high dose of MtX to a pt? Why?

A

Folinic acid (leukovorin). The idea is that normal cells are “rescued” by the folinic acid while malignant cells are killed by the MTX

40
Q

What is MTX harmful to tissues like bone marrow?

A

MTX toxicity is primarily manifested in rapidly dividing host cells

Pharmacology (9 decks)

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