gen pharm + anti-micro Flashcards
which antibacterial drugs work by inhibiting the 30S sub-unit of protein synthesis
aminoglycosides “-mycin, -micin” : gentamicin, paromycin, neomycin
tetracycline, doxycycline, minocycline, tigecycline
which antibacterial drugs work by inhibiting the 50S sub-unit of protein synthesis
chloramphenicol
macrolides: clindamycin, erythromycin, azithromycin, clarithromycin
linezolid
which antibacterials inhibit DNA methylation via x folic acid
sulfonamides (SMX, sulfadiozine, sulfisoxazole)
trimethoprim
what antibacterials inhibit DNA topoisomerase I and IV (DNA gyrase)
flouroquinolones (__-floxacin)
which antibac inhibits RNA polymerase –> x mRNA synthesis
rifampin
which antibac inhibits DNA synthesis
metronidazole
which antibac drug class inhibits cell wall synnthesis via binding PBP
which are beta lactam sensitive and which are not
penicillins - BL sensitive
(alterations in PBP will require dif subtypes of penicillin)
cephalosporins- not BL sensitive
which antibac drugs function via beta lactamase inhibition
CAST: Clavulanic acid, Avibactam, Sulbactam, Tazobactam
name the neuramindase inhibitors
what is their MOA and which virus are they used against
zanamivir, oseltamivir = x influenza A+B
stop the release progeny of the virus from the human cell = x virion release
name the nucleic acid synthesis antivirals: what process do they inhibit
xreplication of viral DNA in the human cell
guanosine analogs
acyclovir = HSV and Varicella
ganciclovir = CMV
anti-viral DNA polymerase inhibitors
cidofavir: HSV
foscarnet: CMV
guanine nucleotide synthesis
ribavirin = RSV, HCV
MOA of
amantadine
rimantadine
antivirals, function to inhibit uncoating of viral genetic material in the infected human cell
what is the MOA of interferon-alpha antviral trx
which viruses is it used against
xxprotein synthesis by binding the PKR protein on the human cell surface
use against HBV and HCV
which antivirals function as protease inhibitors in the CD4 cells: what process is disrupted do their action
xproteolytic processing –> inability for CD4 cells to release processed viral proteins
“__-navir”
atazanavir
darunavir
fosamprenavir
indinavir
lopinavir
ritonavir
saquinavir
which antivirals inhibit DNA integrase? what process does this disrupt?
xDNA integrase = virus is unable to integrate its genes into the CD4 cell’s DNA ==> no viral proteins made
=”__-gravir”
dolutegravir
elvitegravir
raltegravir
which antiviral drug classes inhbit reverse transcriptase ? what process does this prohibit?
= x unable to turn viral RNA into DNA –> won’y be able to be inserted into CD4 cell DNA for transcription& translation
NRTIs (nucleoside RT inhibit) = inhib the GATC
=abacavir
didanosine
emtricitabine
lamivudine
stavudine
tenofovir
zidovudine
NNRTIs (inhib a dif part of RT)
=delavirdine
efavirenz
nevirapine
which two antiviral drugs inhibit virus fusion to CD4 cells?
what are their mechanismS of action
maraviroc = no attachment to the cell
enfuvirtide= no penetration of the virus through the cell membrane
what is the MOA +drug class of
- bethanechol
- carbachol,
- neostigmine
- tobucuranine
- succinylcholine
- pralidoxime
- bupivacaine/lidocaine
- bethanechol = direct agonist on muscurinic receptors = a cholimimetic (+methacholine, pilocarpine)
- carbachol = a cholimimetic direct agonists on muscurinic and nicotinic receptors
- neostigmine= AchE inhbiitors (indirect cholimimetics)
+pyridostigmine, physostigmine (reverse atropine OD)
- directly binds the Ach receptor at the NMSK and blocks it, causing flaccid paralysis (M rigidity)=systemic
- tobucuranine: inhibit depol nAchR at the NMJ plate
+pancuronium, cisatracurium
- reversible by neostigmine
- succinylcholine: depol nAchR (nAchR agonist) that is also used as an NMSK blocker
- pralidoxime: regenerate AchE at mAchR and nAchR
- REVERSE the cholinergic block of succinylcholine, neostigmine…
- bupivacaine/lidocaine
- bind the Na/K ATPase on nerve cells to prevent depolarization
- =LOCAL anesthetic effect
trx of malaria, w MOA
-specify when changes are made in the regimen
chloroquine = block heme polymerse in Plasmodium
- if life-threatening: IV quinidine or artesunate
- if P. vivax or P. ovale = add primaquine
= will kill the hypnozoites of those strains
*as opposed to P. falciparum, P. malariae
-
down syndrome is associated with what bone marrow neoplasm?
trisomy 21 + ALL
ALL= in children = inc lymphoblasts in BM, with pancytopenia + bruising
what are the age ranges in
- ALL
- CLL
_AML
_CML
- ALL = child
- CLL= adult > 60
- AML= adult thru 65ish
- CML= adult 45-85
what functions does collagen play in the body
T1: strengthens bones, skin, dentin, fascia, cornia, late wound repair (makes up scars)
-holds hair follicles and teeth in place
T2= cartllage
T3= reticulin = in BVs, uterus, fetal tissue, granulation tissue
T4: basement membrane, basal lamina, lens
hydroxyurea is used to trx what
MOA
AE
sickle cell ds, polycythemia vera
**2nd line in CML, bc imatinib direclty affects the Philadelphia chromosome**
MOA= stop S phase DNA Synthesis
AE= severe myelosuppression, megaloblastic anemia
cetuximab
indication
MOA
AE
stage IV colorectal CA (∝ w KRAS), head and neck CA
MOA= mab against EGFR
AE=rash, elevated LFTs, diarrhea
imatinib
indication
MOA
AE
-CML (!!), GI stromal tumors
MOA= tyrosine kinase inhibi of
CML: bcr-abl fusion on Philidelphia chromosome t(9;22)
GIST: c-kit protein
AE= fluid retenion
rituximab
indication
MOA
AE
indication:
NHL, CLL, Immune thrombocytopenic purpura (ITP), RA, Thrombotic thrombocytopenic purpura (TTP), autoimmune hemolytic anemia
MOA:
anti-CD20 mab (on msot B cells)
AE:
inc risk of progressive, multifocal leukoencephalopathy
name the two SERMS
MOA
indications
AE
tamoxifen
- breast CA trx + prevention
- AE= in risk endometrial CA, inc risk DVT/PE/hot flashes
raloxifene
- prevention of breast CA and osteoporosis
- +antagonist of estrogen-R in endometrium, inc risk of DVT/PE/hot flashes
MOA= selective estrogen receptor modulators,
antagonist in breast, agonist in bone
-block estrogen binding to ER+ CA cells
trastuzumab
indications
MOA
AE
= HER2 (+) breast CA, gastric CA
=MOA= anti-HER2 mab–> inhibit cell signalling, inc cytotoxicity against HER2 cells
AE= dilated cardiomyopathy,
SLE
- sx/lab findings/ clin presentation
- common causes of death
- how can SLE complicated pregnancy/fetus
SLE:
RASH_OR_PAIN
R: malar/discoid rash
A: arthritis (nonerosive)
S: serositis = pericarditis, pleuritis, Libman Sacks Endocardiits (non-bac thrombi on undersurface of mital or aortic valve)
H: hematologic ds - normocytic+normochromic anemia, thrombocytopenia (∝ ITP), neutropenia, lymphocytopenia
O: oral/nasopharyngeal ulcers - often painless
R: renal ds =membranoproliferative nephropathy T2, diffuse proliferative GN (granular type), RPGN
P: photosensitivity
A: antinuclear Ab = antidsDNA and antiSmith + anti-phospholipid Ab
I : immune ds
N: neurologic sx (seizures, psychosis)
COD=
renal ds >>> infections, accelerated Coronary A Ds
-Anti-Smith (+) pregnancy –> neonatal lupus
=congenital heart block, periorbital/diffuse rash, transaminitis, cytopenias at birth
acute vs chronic trx of gout
drug names: MOA + AE
ACUTE GOUT
NSAIDS
- (esp indomethacin), will act as anti-inflammatory at the joint
- in high doses will prevent uric acid reabsorb and in low doses will prevent uric acid excreteion (beware of low dose ASA given to pts w hx of chronic gout)
GLUCOCORTICOIDS
- (esp prednisone)
colchicine
- bind and stabilize tubulin to xpolymerization –> xnø chemotoxis+degranulation
CHRONIC GOUT
**Drugs= Prevent A Painful Flare**
Allopurinol
- competitive inhib of xanthine oxidase
- 1st line in all pt, regardless of under excreter or over producer
- v helpful in preventing tumor lysis syndrome in lymphomas and leukemias
- also use in Lesch-Nyhan= Xlinked ds∝hyperuricemia, presents w skin pick+lip biting)
- will inc concentration of azathioprine (+other drugs)–> toxicity
- AE= toxic necrolysis, rash, steven johnson, DRESS syndrome (2-4 wks later–> fever, gen lymphadenopathy, facial edema, diffuse morbiliform skin rash)
Probenecid
- x reabsorbtion of urin acid in PT
- can also be used to prevent excretion of penicillin and inc drug half-life
- AE= can precipitate uric acid calculi
Pegloticase
- recombinant uricase catalyzing uric acid to allantoin, a more water soluble produce
- AE= can cause inc hemolysis in G6PD deficiency (presents w bite cells) : anaphylaxis in sign population
Febuxostat
- xanthine oxidase inhibitor
what drug is often used to close a patent ductus arteriosus
indomethacin= NSAID (non-selective) - block prostaglandin synthesis
what are the 5 main antidiarrheal agents and their MOAs
what steps of folate metabolism do methotrexate and 5-FU inhibit
lead to what metabolite accumulation
methotrexate –> build up DHT
- (dihydrofolate polyglutamate)
5-FU –> build up THF
- (tetrahydrofolate)
anti-androgen medications can be helpful to trx what diagnosis?
what are the different meds used and what is their MOA?
BPH
(finasteride can also help w alopecia)
PDE-5 inhibitors used in erectile dysfunction but TIDALIFIL is the only one that can also be used for BPH
- LH release from anterior pituitary
- GnRH agonist (leuprolide)
- x testosterone synthesis
- ketoconazole, spironolactone
- x T–> DHT(–>estrogen) in periphery
- finasteride (5 alpha reductase inhibitor)
- androgen receptor inhibition
- flutamide, spironolactone, cyproterone
what is the MOA difference in MTX and 5-FU
both inhibit steps in the folic acid–>DNA pathway
- MTX
- folic acid analog: inhibit dihydrofolate reductase
- prevents reduction of folic acid to tetrahydrofolate
- 5-FU
- a pyrimidine analog: inhibit thymidilate synthetase
- prevent creation of thymidine needed to make THF
mycophenolate
- clinical use
- MOA
mycophenolate
- immunosuppressant: used in organ transplant, v useful bc specifically targets lymphoblastic proliferation ds
- MOA= inhibits de novo purine synthesis
- inhibit inosine monophosphate (IMP–>GMP) guanisine monophosphate conversion
- = no purine synthesis
- this is esp good for lymphocytic proliferation bc… lymphocytes don’t have a purine salvage pathway so they have to make it all de novo…. so v vulnerable to mycophenolate
what are the 5 classes of anti-emetic drugs
- anticholinergics
- antihistamine
- dopamine receptor receptor
- 5-HT3 receptor antagosit
- NK1 receptor anatgonist
- at what part of the renal tubule does ACE-I cause change
- what is the tubular diuretic class of choice for patients with heart failure (fluid overload)
- what is the tubular diuretic class of choice for patients with HTN
- what is the tubular diuretic class of choice for patients with severe L ventricular systolic heart dysfunction
- efferect arteriole leaving the glomerulus –> dilate it
- (systemic vasodilation to reduce BP –> AE of dec GFR is why its contraindicated in renal fail patients)
- decompensated heart failure = loop diuretic
- huge natriuretic effect, v quick
- HTN = thiazide
- LVsystolic heart dysfunction =
- collecting tubule drugs aka K sparing drugs
- ALD inhibitors (spirinolactone, eplerenone) > Na-channel inhibitors (amiloride, triamterene)
a bimodal distribution of INH metabolism, as shown below, is explained by differences in what process within the population
what would be the difference if this graph was for azothioprine/ 6-MCP
difference in speed of acetylation
- INH is metabolised via acetylation in the liver
- slow acetylators (shaded) will have the original drug accumulate in the plasma for a lil longer before it is metabolized
slow acetylators will show up in the metabolization of
- INH, dapsone, procainamide, hydralazine
- azothioprine/ 6-MCP ~ methylation
-
mnemonic for
- the antibiotic drugs and where they each work about the resistance
- 30S vs 50S
- antipseudomonal drugs
THE ANTI-BACTERIAL RESISTANCE
- the APA was penicillinase sensitive, but now is a new DON of resistance against the PGP cell wall
- APA= amoxicillin, penicillin G+V, ampicillin = penicillinase-senstiive penicillins
- DON= dicloxacillin, oxacillin, nafcillin = penicillinase resistance penicillins
-
Free Radicals flood the Metro, make ‘dem unstable
- metronidazole= x DNA integrity via free radicals
- I Am R.P Oly
- Rifampin = only drug that xRNA polymerase
- we’ll fight the PGP wall with out Rockets, our pens, and our sit-ins and we’ll stand wise As Trees
- rockets= cephalosporins
- pens= carbapenems
- sit-ins= penicillins
- “as trees”= azteronam
- we’ll backtrack the vans of bricks to stop wall synthesis
- bactracin + vancomycin = x bacterial wall synthesis
- 3 meth pimps and the sulfa bride will hoard all the folate to stop ‘dey meth flow
- trimethoprim and sulfanomides = x DNA methylation via x folic acid synthesis
- Flox of ppl to Dixie’s Gyros to cut off ‘dey food supply
- flouroquinolones (-floxacin) and Nalidixic Acid = xDNA gyrase (cut open DNA)
30S vs 50S
-
x 30S: Gently Step To-emBrace And-Kiss, a New Cycle begins My-Kin
- gentamicin, streptomycin, tobramycin, amikicin, neomycin and the “-cyclin”s
-
x50S: keep my Big House Pristine, with chlorine pools and straight lineZ, to ACE-my see-ins
- “-pristin”s, chloremphenicol, linzolid, ampicillin, amoxicillin, erythromycin
- Mona Lisa doesn’t like the piper’s tics, they ARE-SILLY
- antipseudomonasl= pipercillin and ticarcillin
what are the mechanisms of resistance to the following classes of drugs
- penicillin
- vancomycin
- quinolones
- aminoglycosides
- tetracyclines
- rifamycins
what are the specific AE/toxicities seen with the following chemo drugs
- anthracyclines (who are they?)
- bleomycin
- cisplatin
- cyclophosphamide
- paclitaxel
- vincristin/vinblastine
equations for
half life
maintence dose
loading dose
who are the fibrinolytic agents
when are they indicated, and what is their MOA
intracellular MOA of nitroglycerin
two ways that beta blockers lower BP
b1 inhibiition on the heart–> dec contractility
inhibit production of renin
what is the pathogenesis of migraine pain and the MOA of the abortive drug to trx migraines at onset
DRESS = Drug Reaction with Eosinophilia and Systemic Sx
pt with a-fib can be given what drugs
IC, class 3, class 4 (nondihydropyridine CCB= verampamil and deltiazem), class 2
change in E = change in K (increase repol) –> PUSH T WAVE FORWARD –> QT PROLONGATION
how does Amiodarone affect the sinus rate?
which antiarrhythmics increase the PR segment
phsyiologic mechanism of Digoxin
what arrhythmias is it indicated for
mechanism of clearance
renally cleared : need dose adjusment for older ppl bc of age related dec in renal clearence
treatment for essential tremors
MOA
AE associated with the class of drugs
*b2 worsening of obstructive lung ds ~ worsening asthma, etc**
what drugs (and MOA) can be used to treat M hyperspasticity/hyperreflexia
most beneficial drug for ischemia induced ventricular arrhythmias
