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Clinical Neuroscience 2 > Pharm- 32 > Flashcards

Pharm- 32 Flashcards

0
Q

What are the 3 ways to have selective toxicity?

A
  1. attack target unique to pathogen/cancer but not to host (best)
  2. attack similar target to host
  3. attack targets shared by host but try to be selective about it
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1
Q

What is selective toxicity?

A

Targeting things the in the pathogen/cancer but that dont exist in the host

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2
Q

Why is it harder to target cancer cells rather than microbes?

A

cancer cells are host cells. microbes are totally different.

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3
Q

What is the therapeutic index?

A

the ratio of the toxic dose tot he therapeutic dose. indicates how safe and selective the drug is.

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4
Q

Do drugs like cancer drugs have a higher or lower therapeutic index?

A

lower, cuz they are less selective –> larger EC50 –> decreased TI cuz TI = LD50/EC50

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5
Q

Why do B-lactams have a good selectivity against microrbes?

A

cuz it targets the cell wall, which is unique to bacteria

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6
Q

Generally, how to B-lactams work?

A

inhibit transpeptidation of the cell wall, .’. only work on replicating cells.

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7
Q

What are the ribosome subunits for bacteria?

A

50s + 30s = 70s

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8
Q

What are the ribosome subunits for humans?

A

40s + 60s = 80s

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9
Q

What are the 2 ways we can target cancer cells using selectivity?

A
  1. variations inc ell growth behavior

2. increases susceptibility to apoptosis

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10
Q

What is the mechanism of action for 5-FU?

A

inhibits DNA synthesis in dividing cells by inhibiting thymidylate synthase, which is required for pyrimidine synthesis

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11
Q

Which NORMAL cells can be damaged by apoptosis from5-FU?

A

Those which rapidly divide normally: bone marrow, GI mucosa, hair (think cancer pt)

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12
Q

What do bacteriostatic drugs do?

A

They inhibit further bacterial growth but do not kill the current bacterial residents.

leaves them “in static”

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13
Q

What did Rihanna say when she was asked why she was working with Chris Brown again?

A

“Beats me.”

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14
Q

1 more: what do you call a mexican who had his car stolen?

A

Carlos

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15
Q

In what types of pts can you use bacteriostatic drugs?

A

immune COMPETENT because they rely on host systems to kill the left-over population.

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16
Q

What do bactericidal cells do?

A

KILL KILL KILL

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17
Q

What types of pts do u use bactericidal drugs in?

A

immnocompromised pts cuz thy cant clear the current infection.

18
Q

Why cant u give tetracycline and PCN together?

A

PCN requires bacterial growth to work, but since tetracycline is a bacteriostatic drug, no bacteria will grow –> PCN is worthless

19
Q

Why are PCN and aminoglycosides synergists?

A

PCN destroys the cell wall and aminoglycosides can get into the cell to wreck proteins.

20
Q

What is the mech of action of aminoquinolones to treat malaria?

A

They inhbiit the alteration of heme by the parasite –> heme builds up –> kills parasite.

21
Q

Why does ACV not kill host cells?

A

ACV needs viral kinases to activate it (viral polymerase)

22
Q

What are the 3 Polymaerase inhibitors for viral infections?

A

Efavirenz, Acyclovir, Zidovudine

“PEAZ”

23
Q

What are the 2 neuraminidase inhbitors (inhibit viral relase form cell)?

A

Oseltamivir, Zanzmivir

“-ivir”

24
Q

Neuraminidase inhbiitors are good for treating what type of viral infection?

A

influenza

25
Q

Why do most anti-cancer drugs not affect cancer cells in the G0 stage?

A

antineoplastic drugs target dividing cells, and since theyre in G0 and not dividing,they dont work.

26
Q

How do taxanes and vinca alkaloids target microtubules?

A

they interfere with the spindle formation during M phase.

27
Q

What do alkylating agents do to kill cancer cells?

A

they damage DNA and other macromolecules and are toxic to allphases int he cell cycle, including the M phase

28
Q

What is the vertical transmission of bacterial resistance?

A

bacteria passe son resistance gene to daughter cell

29
Q

What happens in the horizaontal transmission of bacterial drug resistance?

A

bacteriaacquires resistance by gaining geneticmaterialfrom other bacteria

30
Q

What is conjugation?

A

bacteria sex. chromosomal/plasmid dDNA is transferred directly.

31
Q

What is transduction?

A

viral stork. a phage transfers resistnace DNA from 1 bacteria to another.

32
Q

What is transformation?

A

turkey baster. naked resistance DNA in environment is taken up by a bacteria.

33
Q

Why can p-glycoproteins cause multidrug resistance?

A

P-glycoproteins are on the membrane of cells and actively pumps out antineoplastic drugs, so they cant work.

34
Q

What i the most improtant cause of increased drug resistance in a population?

A

Over-prescribing antibiotics.

35
Q

What are the 4 advantages to using multiple drugs in antimicrobial/neoplastic treatments?

A
  1. multiple ways to kill
  2. decreases resistance.
  3. reduces adverse effects cuz u can use lower doses
  4. many have antineoplastic drugs.
36
Q

What does SMZ inhibit?

A

DHP synthase (which converts PABA to DHP)

37
Q

What does TMP inhibit?

A

DHFR (which does DHF –>THF)

38
Q

Why is TMP-SMZ given for UTI’s?

A

It’s excreted unchanged in the urine –> tx of UTI’s

39
Q

What is the condition in which primethamine is the only effective agent?

A

toxoplasmosis

40
Q

What drug is used when u give a lethaldose of methotrexate to kill cancer cells?

A

Leukovorin (folinic acid)

41
Q

What is the mechanism of action of methotrxate (MTX)?

A

folate analogue to inhibit DHFR –> shortage of THF –> cessation of de novo purine/thymidylate –> cessation of DNA and RNA synthesis

42
Q

What cells are suceptible to MTX attacks?

A

It attacks rapidlydividing cells, so bone marrow cells are susceptible.

Clinical Neuroscience 2 (16 decks)

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