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Rush Advanced Pharmacology NSG
531 Exam 4 (Graded A+)
Ginseng - ANSWER taken for: Nervousness, Agitation, Insomnia, Diarrhea, Headaches, Heart Palpitation
Do not take with MAO inhibitors. Can alter affects with heart medications. Can increase the risk of bleeding when taken with blood clotting drugs CI: Neuro, Heart, MAO, bleeding, coag drugs
Ma Huang (Ephedra) - ANSWER Dangerously elevate blood pressure, stimulate heart rate, and CNS Associated with stroke, MI, and death Banned > 10 mg in U.S. with exception of traditional Asian medicine Metabolife Used for weight loss, allergies, asthma, bronchitis, fever, headache
arginine - ANSWER used for treatment of heart and blood vessel conditions including congestive heart failure (CHF), chest pain, high blood pressure, and coronary artery disease.
Don't use if: excess body acid high levels of potassium in the blood sickle cell anemia
heart attack within the last 30 days renal tubular acidosis decreased kidney function Don't use with nitro
pt. education for herbs and nutrients - ANSWER 1. herbs and nutrients have bioactive properties and have the same safety issues as drugs
- always consult a reliable source before adding
- consider when researching what are the credentials of the author of the website, what evidence is there to support their claims, are there any financial interests to influence the claims of the auther
biological basis of drug/herb/nutrient interactions - ANSWER absorption (changing pH or motility of the GI tract)
Distribution (displacing agents that are bound to plasma proteins
Biotransformation (inducing or inhibiting CYP450 enzymes)
receptor binding (competitive and noncompetitive antagonism
Gompertzian Kinetics - ANSWER Cancer cells lack of normal regulating factors leading to abnormal growth
You can go from 0 to 10^9 before symptoms This bounces because you go on and off of chemo That's why we do multiple rounds - so you initiate the next round of chemo before you get
non-cell cycle specific - it damages DNA
must be oxidized by p450 to be activated
chemotherapeutics: platinum analogs - ANSWER form intrastrand links between guanines
similar to alkylating agents
inhibit replication when you insert things into DNA that don't belong there
chemotherapeutics: Microtubule inhibitors - ANSWER inhibit microtubule polymerization
work during M phase
mitosis microtubules that form that help tear apart the daughter cell from the parent cell they assisst in the migration of DNA from one cell to the next
in order for them to form polymerization of the alpha and beta subunits need to take place
when the drug binds to the subunits they can't polymerize
chemotherapeutics: antibiotics - ANSWER doxorubicin - free radical generation
goes into cardiac cells, binds to DNA, and inhibits topoisomerase
one side effect is cardiomyopathy r/t doxorubicin toxicity
larger concentration of mitochondria in our cardiac myocytes because they are constantly at work
doxirubicin is biotransformed in the mitochondria - the byproduct is reactive oxygen species
because we have more mitochondria in cardiac cells we metabolize more doxirbicin so more oxygen species
chemotherapeutics: tumor specific antibodies - ANSWER monoclonal antibody - pembrolizumab treats melanoma cytotoxic T cells that provide an immune response against tumor cells first - recognition of the tumor cell antigen in association with the T cell receptor cytotoxic T cells have a receptor called PD1 - ligand is PDL1 - programmed death When PDL1 binds to PD1 inhibits the cytotoxic activity of the T cell - cancer cells have evolved to be able to turn off the body's defense pembrolizumab is going to bin to PD1 so that PDL1 cannot and the T cell is not inhibited
microtubule depolymerization inhibitor - ANSWER once the microtubules are constructed they also have to be torn down. if they remain intact then the cells get stuck together. they officially fall apart at the break down of the microtubules
mechanisms of quinolone resistance - ANSWER 1. gyrase and topoisomerase gene mutation
- alterations in efflux
- cell membrane alternations
- plasmid mediated resistance
Impact of gyrase and topoisomerase gene mutations? - ANSWER Will make quinolones not work well and will not be able to bind to an enzyme due to a mutation. Quinolones cannot inhibit.
Impact of alterations in efflux pumps in quinolones - ANSWER If bacteria increase expression of efflux pumps. The antibiotic may get into bacteria but it will be pumped right back out causing a decrease in the effectiveness of the antibiotic
impact of cell membrane alternations on quinolones - ANSWER Water soluble antibiotics such as quinolones gets in through porin channels. The bacteria can decrease the number or size of porins which will reduce antibiotic effectiveness.
Impact of plasmid mediated resistance - ANSWER Circular DNA that is not part of the chromosome. Can carry genese that make the bacteria resistant to drugs
bacterial resistance - ANSWER ability of bacteria to resist the action of antibiotics bacteria replicate very fast, mutations are seen in a much shorter period of time you can get mutations that will increase the number of efflux pumps that will pump the drug out bacterial membrane proteins need to be porous for the drug to get through - nonporous
Rush Advanced Pharmacology NSG 531 Exam 4 (Graded A+)Rush Advanced Pharmacology NSG 531 Exam 4 (Graded
are the ones that will survive antibiotics and replicate when you add a selective pressure such as an antibiotic any bacteria that has a genetic mutation is the kind that will grow out
RNA transcription - ANSWER bacteria duplicates the DNA then makes an mRNA copy of the DNA in order to get the blueprint for the new proteins that need to be synthesized to make the new bacteria DNA replication is the new dna that goes into the daughter cells RNA transcription is the blueprint to make the daughter cells polymerase is the bacterial enzyme that mediates
transcription inhibitors - ANSWER form a stable coplex with RNA polymerase and inhibit RNA synthesis if they are stuck to the RNA polymerase the polymerase cannot read the DNA and make the RNA copy example - rifampin
translation - ANSWER once the RNA is made it has to go to ribosomes who translate it and make proteins at the ribosome the mRNA is read and amino acids are synthesized into a polypeptide chain and all structures of the bacteria will eventually be synthesized from that chain
codons - ANSWER sequences of 3 nucleotides that read and the ribosome finds the appropriate tRNA that has a complimentary set of nucleotides to add to the peptide chain
30s unit - ANSWER samller unit that reads the codons and makes sure that the bacteria gets the correct tRNA bound to it
Rush Advanced Pharmacology NSG 531 Exam 4 (Graded A+)Rush Advanced Pharmacology NSG 531 Exam 4 (Graded
as you filter more, the vesicles full up and you get spillage into the cytoplasm of the proximal tubule cells when they get released they can act on the cell membrane and disrupt the phospholipid bilayer and cause kidney damage
aminoglycosides and the neuromuscular blockade - ANSWER can bind to calcium channels on the surface of presynaptic neurons and block them can act as calcium channel blockers in motor neurons which leads to a blockade because there is no release of Ach from influx of calcium in most extreme forms can have paralysis
resistance to aminoglycosides - ANSWER bacteria doesn't only have DNA in their nucleoids but also sitting in their cytoplasm. This DNA doesn't encode for structures and things that are necessary for survival but for things that are still important like enzymes these plasmid-encoded enzymes inactivate aminoglycosides through adenylation, acetylation, or phosphorylation the plasmids can then be spread from bacteria to bacteria bacterial cells interact through conjugation and the plasmids get spread very quickly so very quickly the bacterial population can convert from being antibiotic sensitive to resistant.
tetracyclines - ANSWER bind to 30s and block tRNA binding to mRNA which interrupts peptide elongation
macrolides - ANSWER bind to 50s and prevent the formation of peptide bonds between amino acids and prevent exit of nascent proteins from ribosomes into the cytoplasm where they would undergo cleavage, packaging to make them ready to be put together to make new cells
Rush Advanced Pharmacology NSG 531 Exam 4 (Graded A+)Rush Advanced Pharmacology NSG 531 Exam 4 (Graded
drugs that work at the ribosome level are not very selective - greater concern for adverse effects
Describe the difference between gram positive and gram negative - ANSWER positive - you have a lipid bilaryer that is normal, then on top of it you have a cell wall that is made up of peptidoglycens - sugar peptides on top of that layer there is nothing - more water soluble purple dye gets through
negative is the same but the peptidoglycen layer is theinner and then on top there is another plasma membrane - this one has a lot of lipopolysaccarides embedded so the dye cannot penetrate it - not very water soluble
drugs that have to get through gram negative have to go through the extra layer
Steps of peptidoglycan synthesis - ANSWER 1. monomer synthesis
- polymerization
- cross-linking
Inhibitors of monomer synthesis - ANSWER Fosfomycin - inhibits enzyme that links protein (peptido) to sugar complexes (glycan) Bacitracin - inhibits dephosphoryilation step in monomer synthesis
inhibitors of monomer polymerization - ANSWER vancomycin - prevents monomer chain elongation so it binds to the monomer at the point of attachment to the next monomer and prevents elongation can cause red man syndrome
Rush Advanced Pharmacology NSG 531 Exam 4 (Graded A+)Rush Advanced Pharmacology NSG 531 Exam 4 (Graded
beta lactamase that will keep the drug from binding to the receptor to inhibit cross linking
fungal ergosterol synthesis inhibitors - ANSWER azoles bind to and inhibit a fungal p450 enzyme involved in ergosterol synthesis can also bind to human enzymes resistance d/t p450 mutations or upregulation of drug efflux pumps there is a good chance that you are going to inhibit cholesterol synthesis which is a precursor for streroids so in men you might see gynocomastia or impotence
fungal membrane stability inhibitors - ANSWER polyenes - bind to ergosterol and create cell membrane pores that will likely kill the fungal cell liposomal delivery of amphotericin reduces AEs
MOA of amphotericin B - ANSWER Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes. leading to cell death because disruption in solutes
How does liposomal amphotericin reduce toxicity? - ANSWER works locally - delivered in liposome that is broken down by macrophages macrophages are at site of infection so when the liposome gets to the site of the infection it is broken down
Inhibitors of fungal cell wall synthesis - ANSWER echinocandins fungal cell walls composed of proteins, chitins, and beta-glucans inhibit enzyme involved in beta-glucan synthesis leads to cell death
Rush Advanced Pharmacology NSG 531 Exam 4 (Graded A+)Rush Advanced Pharmacology NSG 531 Exam 4 (Graded
How do viruses infect humans? - ANSWER viruses can't replicate on their own, they need a host cell to use their machinery for their own replication look a lot like human cells because they use the human cell to replicate it is harder to give antivirals because they may end up having toxic effects on human cells to stop viruses you need to give drugs that unfortunately stop human cell machinery because that is what fuels the replication of the virus
virus binds to a cell surface postbinding the virus gets in the vesicles of the cytopasm then you get uncoding of the capsid of the virus that contains dna/RNA gets incorporated into the host cell dna and can use the host cell to replicate then they are delivered to the host cell membrane and branch off
virus needs the hydrogen ion inside to cause disruption and release of genetic material - it is pumped in by M2 protein
Tamiflu MOA - ANSWER neuraminidase inhibitor to prevent release of virus from host cell (stop spread of virus)
works later in the viral life cycle virus has already uncoded and gone into the human host cell and is ready to bud off. works at the site of neuraminidase that cleaves off the virus to bud and replicate
acyclovir MOA - ANSWER has to be phosphorylated to work against viruses the HSV has a specific kinase that will convert it into acyclovir phosphate then triphosphate that is the active drug so it is not active unless in the presence of herpes
Rush Advanced Pharmacology NSG 531 Exam 4 (Graded A+)Rush Advanced Pharmacology NSG 531 Exam 4 (Graded
