Pharm- 32 Flashcards
What are the 3 ways to have selective toxicity?
- attack target unique to pathogen/cancer but not to host (best)
- attack similar target to host
- attack targets shared by host but try to be selective about it
What is selective toxicity?
Targeting things the in the pathogen/cancer but that dont exist in the host
Why is it harder to target cancer cells rather than microbes?
cancer cells are host cells. microbes are totally different.
What is the therapeutic index?
the ratio of the toxic dose tot he therapeutic dose. indicates how safe and selective the drug is.
Do drugs like cancer drugs have a higher or lower therapeutic index?
lower, cuz they are less selective –> larger EC50 –> decreased TI cuz TI = LD50/EC50
Why do B-lactams have a good selectivity against microrbes?
cuz it targets the cell wall, which is unique to bacteria
Generally, how to B-lactams work?
inhibit transpeptidation of the cell wall, .’. only work on replicating cells.
What are the ribosome subunits for bacteria?
50s + 30s = 70s
What are the ribosome subunits for humans?
40s + 60s = 80s
What are the 2 ways we can target cancer cells using selectivity?
- variations inc ell growth behavior
2. increases susceptibility to apoptosis
What is the mechanism of action for 5-FU?
inhibits DNA synthesis in dividing cells by inhibiting thymidylate synthase, which is required for pyrimidine synthesis
Which NORMAL cells can be damaged by apoptosis from5-FU?
Those which rapidly divide normally: bone marrow, GI mucosa, hair (think cancer pt)
What do bacteriostatic drugs do?
They inhibit further bacterial growth but do not kill the current bacterial residents.
leaves them “in static”
What did Rihanna say when she was asked why she was working with Chris Brown again?
“Beats me.”
1 more: what do you call a mexican who had his car stolen?
Carlos
In what types of pts can you use bacteriostatic drugs?
immune COMPETENT because they rely on host systems to kill the left-over population.
What do bactericidal cells do?
KILL KILL KILL
What types of pts do u use bactericidal drugs in?
immnocompromised pts cuz thy cant clear the current infection.
Why cant u give tetracycline and PCN together?
PCN requires bacterial growth to work, but since tetracycline is a bacteriostatic drug, no bacteria will grow –> PCN is worthless
Why are PCN and aminoglycosides synergists?
PCN destroys the cell wall and aminoglycosides can get into the cell to wreck proteins.
What is the mech of action of aminoquinolones to treat malaria?
They inhbiit the alteration of heme by the parasite –> heme builds up –> kills parasite.
Why does ACV not kill host cells?
ACV needs viral kinases to activate it (viral polymerase)
What are the 3 Polymaerase inhibitors for viral infections?
Efavirenz, Acyclovir, Zidovudine
“PEAZ”
What are the 2 neuraminidase inhbitors (inhibit viral relase form cell)?
Oseltamivir, Zanzmivir
“-ivir”
Neuraminidase inhbiitors are good for treating what type of viral infection?
influenza
Why do most anti-cancer drugs not affect cancer cells in the G0 stage?
antineoplastic drugs target dividing cells, and since theyre in G0 and not dividing,they dont work.
How do taxanes and vinca alkaloids target microtubules?
they interfere with the spindle formation during M phase.
What do alkylating agents do to kill cancer cells?
they damage DNA and other macromolecules and are toxic to allphases int he cell cycle, including the M phase
What is the vertical transmission of bacterial resistance?
bacteria passe son resistance gene to daughter cell
What happens in the horizaontal transmission of bacterial drug resistance?
bacteriaacquires resistance by gaining geneticmaterialfrom other bacteria
What is conjugation?
bacteria sex. chromosomal/plasmid dDNA is transferred directly.
What is transduction?
viral stork. a phage transfers resistnace DNA from 1 bacteria to another.
What is transformation?
turkey baster. naked resistance DNA in environment is taken up by a bacteria.
Why can p-glycoproteins cause multidrug resistance?
P-glycoproteins are on the membrane of cells and actively pumps out antineoplastic drugs, so they cant work.
What i the most improtant cause of increased drug resistance in a population?
Over-prescribing antibiotics.
What are the 4 advantages to using multiple drugs in antimicrobial/neoplastic treatments?
- multiple ways to kill
- decreases resistance.
- reduces adverse effects cuz u can use lower doses
- many have antineoplastic drugs.
What does SMZ inhibit?
DHP synthase (which converts PABA to DHP)
What does TMP inhibit?
DHFR (which does DHF –>THF)
Why is TMP-SMZ given for UTI’s?
It’s excreted unchanged in the urine –> tx of UTI’s
What is the condition in which primethamine is the only effective agent?
toxoplasmosis
What drug is used when u give a lethaldose of methotrexate to kill cancer cells?
Leukovorin (folinic acid)
What is the mechanism of action of methotrxate (MTX)?
folate analogue to inhibit DHFR –> shortage of THF –> cessation of de novo purine/thymidylate –> cessation of DNA and RNA synthesis
What cells are suceptible to MTX attacks?
It attacks rapidlydividing cells, so bone marrow cells are susceptible.
