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First Aid, UWorld sets > gen pharm + anti-micro > Flashcards

gen pharm + anti-micro Flashcards

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1
Q

which antibacterial drugs work by inhibiting the 30S sub-unit of protein synthesis

A

aminoglycosides “-mycin, -micin” : gentamicin, paromycin, neomycin

tetracycline, doxycycline, minocycline, tigecycline

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2
Q

which antibacterial drugs work by inhibiting the 50S sub-unit of protein synthesis

A

chloramphenicol
macrolides: clindamycin, erythromycin, azithromycin, clarithromycin
linezolid

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3
Q

which antibacterials inhibit DNA methylation via x folic acid

A

sulfonamides (SMX, sulfadiozine, sulfisoxazole)
trimethoprim

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4
Q

what antibacterials inhibit DNA topoisomerase I and IV (DNA gyrase)

A

flouroquinolones (__-floxacin)

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5
Q

which antibac inhibits RNA polymerase –> x mRNA synthesis

A

rifampin

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6
Q

which antibac inhibits DNA synthesis

A

metronidazole

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7
Q

which antibac drug class inhibits cell wall synnthesis via binding PBP

which are beta lactam sensitive and which are not

A

penicillins - BL sensitive

(alterations in PBP will require dif subtypes of penicillin)

cephalosporins- not BL sensitive

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8
Q

which antibac drugs function via beta lactamase inhibition

A

CAST: Clavulanic acid, Avibactam, Sulbactam, Tazobactam

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9
Q

name the neuramindase inhibitors

what is their MOA and which virus are they used against

A

zanamivir, oseltamivir = x influenza A+B

stop the release progeny of the virus from the human cell = x virion release

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10
Q

name the nucleic acid synthesis antivirals: what process do they inhibit

A

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

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11
Q

MOA of

amantadine

rimantadine

A

antivirals, function to inhibit uncoating of viral genetic material in the infected human cell

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12
Q

what is the MOA of interferon-alpha antviral trx

which viruses is it used against

A

xxprotein synthesis by binding the PKR protein on the human cell surface

use against HBV and HCV

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13
Q

which antivirals function as protease inhibitors in the CD4 cells: what process is disrupted do their action

A

xproteolytic processing –> inability for CD4 cells to release processed viral proteins

“__-navir”

atazanavir

darunavir

fosamprenavir

indinavir

lopinavir

ritonavir

saquinavir

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14
Q

which antivirals inhibit DNA integrase? what process does this disrupt?

A

xDNA integrase = virus is unable to integrate its genes into the CD4 cell’s DNA ==> no viral proteins made

=”__-gravir”

dolutegravir

elvitegravir

raltegravir

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15
Q

which antiviral drug classes inhbit reverse transcriptase ? what process does this prohibit?

A

= 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

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16
Q

which two antiviral drugs inhibit virus fusion to CD4 cells?

what are their mechanismS of action

A

maraviroc = no attachment to the cell

enfuvirtide= no penetration of the virus through the cell membrane

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17
Q

what is the MOA +drug class of

  • bethanechol
  • carbachol,
  • neostigmine
  • tobucuranine
  • succinylcholine
  • pralidoxime
  • bupivacaine/lidocaine
A
  • 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
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18
Q

trx of malaria, w MOA

-specify when changes are made in the regimen

A

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

-

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19
Q

down syndrome is associated with what bone marrow neoplasm?

A

trisomy 21 + ALL

ALL= in children = inc lymphoblasts in BM, with pancytopenia + bruising

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20
Q

what are the age ranges in

  • ALL
  • CLL

_AML

_CML

A
  • ALL = child
  • CLL= adult > 60
  • AML= adult thru 65ish
  • CML= adult 45-85
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21
Q

what functions does collagen play in the body

A

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

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22
Q

hydroxyurea is used to trx what

MOA

AE

A

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

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23
Q

cetuximab

indication

MOA

AE

A

stage IV colorectal CA (∝ w KRAS), head and neck CA

MOA= mab against EGFR

AE=rash, elevated LFTs, diarrhea

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24
Q

imatinib

indication

MOA

AE

A

-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

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25
rituximab ## Footnote 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
26
name the two SERMS ## Footnote 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
27
trastuzumab ## Footnote indications MOA AE
= HER2 (+) breast CA, gastric CA =MOA= anti-HER2 mab--\> inhibit cell signalling, inc cytotoxicity against HER2 cells AE= dilated cardiomyopathy,
28
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
29
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= **_P_**revent **_A_** **_P_**ainful **_F_**lare\*\* ****_A_**llopurinol** * 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) ****_P_**robenecid** * 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 ****_P_**egloticase** * 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 ****_F_**ebuxostat** * xanthine oxidase inhibitor
30
what drug is often used to close a patent ductus arteriosus
indomethacin= NSAID (non-selective) - block prostaglandin synthesis
31
acetominophen has slighly different indications than NSAIDs bc it is not \_\_\_
not anti-inflammatory only analgesic (pain) and antipyretic (N/V)
32
describe the dose dependent effect of ASA on inflammation
ASA is antiinflammatory only at high doses!
33
Kawasaki ds: clin presentation high dosees of what drug can mitigate some of the sx?
=most common vasculiits seen in children mucosal erythema, rash, conjunctivits, + cervical lymphadenopathy high dose ASA bc becomes anti-inflammatory
34
differentiate between the physiologic role of COX1 and COX2
COX1 = constituitively expressed * inc thromboxan A2 --\> vasoconstriction, platelet aggregation * inc prostoglandins --\> inc uterine tone, gastroprotective * (PGE1 is a prostacyclin mediator--\> actually dec vascular tone.. COX1= baseline mediator) COX 2= expressed during inflammatory states, in vascular endothelial and sm M cells * inc prostacyclin --\> vasodilation and inc in vascular permeability, inc pain sensitivity, and cause fever
35
what is the function of phospholipase A2
in response to injury --\> inc intracellular Ca --\> activate PLA2- PLA2 will release arachadonic acid from the membrane so that it can be broken down by COX OR liposygenase to make TXA2/prostacyclines/prostaglandins OR leukotrienes, respectively
36
what are the 5 main antidiarrheal agents and their MOAs
37
what is the clinical hx associated w chronic schistosomiasis infection what is the trx and MOA of the trx?
hx: - recurrent hematuria w abd pain, but will self-resolve for months before returning - initial presentation will have dysuria, but afterwards just hematuria on and off - inguinal lymphadenopathy trx= praziquantel * x membrane permeability of the parasite --\> vacuolization * inc permeability of Ca ions --\> paralysis of the parasite --\> inc exposure to immune cells
38
clin features of serotonin syndrome what mood stabilizing drug, when given w SSRIs, can cause serotonin syndrome? what abx has properties similar to that class of mood stabilizers, and thus can cause serotonin syndrome as well?? what substance of abuse can cause serotonin syndrome in someone on a serotonergic med
SS= * AMS= anxiety, agitation, delirium * autonomic dysregulation: diaphoresis, HTN, tachy, hyperthermia, vomiting, diarrhea * NMSK hyperactivity: tremor, myoclonus, hyperreflexia \*\*MAO-inhibitors linezolid (trx G+, esp vancomycin resistant enterococcus and MRSA) \*can also happen w SSRI/SNRI not tapered off, give w TCAs, -MDMA!!
39
how are monoclonal antibodies metabolized in the body how does dosage need to be altered given hepatic or renal ds
mAbs are NOT removed hepatic or renally removal = * target oriented: they are internalized by the cells that have the Ag that is their target * nonspecific clearance: taken up by reticuloendothelial macrophages or vascular endothelial cells
40
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)
41
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
42
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
43
trx of C. Dif
oral vancomycin = inhibit cell wall synthesis = _bacteriostatic_ or oral fidaxomicin = inhibit sigma unit of RNA polymerase (--\> xprotein synthesis --\> cell death =_bactericidal_)
44
mechanism of clearance of metformin metformin can cause lactic acidosis in what pts especially
renal pts w heart failure or renal failure
45
what is the pharmalogic trx of prostate CA and MOA
prostate CA is hormonally responsive to Testosterone -testosterone is controlled by PULSATILE GnRH release * give **buserelin** = GnRH agonist : bc its constant, it will eventually lower the level of T released * but for the first few weeks, the level of T might go up (bc you're giving a GnRH agonist) so at first, co-admin with **bicalutimide** = block T effect on tumor cells
46
compare and contrast antihistamines first generation vs second generation * when would you use second gen over first?
* first gen antihistamines * =hydroxazine, promethazine, chlorpheniramine, diphenhydramine * AE: * muscurinic= blurry vision, delierium, urine retention, constipation, can worsen glaucoma * alpha adrenergic= postural dizziness, falls * serotanergic= appetitie stimulation + weight gain * pretty contra-indicated in the elderly * bc of the above AE * + are lipophilic and can cross BBB--\> neuro sx (sedation, cognitive sx) * second gen antihistamines * loratidine, cetirizine * minimal AE, NO cross BBB bc not lipophilic * better preferred, esp in eldery
47
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
48
what are the 5 classes of anti-emetic drugs
* anticholinergics * antihistamine * dopamine receptor receptor * 5-HT3 receptor antagosit * NK1 receptor anatgonist
49
* 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)
50
how does CKD change phosphate levels what meds are given to remedy this + MOA
CKD --\> hyperPh phosphate binders * calcium carbonate/acetate * (non-Ca containing) = sevelamer, lanthanum * nonabsorbable, anion exchange resin * bind intestinal phosphate to reduce systemic absorption
51
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** -
52
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
53
what are the mechanisms of resistance to the following classes of drugs * penicillin * vancomycin * quinolones * aminoglycosides * tetracyclines * rifamycins
54
what are the specific AE/toxicities seen with the following chemo drugs * anthracyclines (who are they?) * bleomycin * cisplatin * cyclophosphamide * paclitaxel * vincristin/vinblastine
55
equations for half life maintence dose loading dose
56
57
58
who are the fibrinolytic agents when are they indicated, and what is their MOA
59
60
intracellular MOA of nitroglycerin
61
62
63
two ways that beta blockers lower BP
b1 inhibiition on the heart--\> dec contractility inhibit production of renin
64
what is the pathogenesis of migraine pain and the MOA of the abortive drug to trx migraines at onset
65
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67
68
69
DRESS = **D**rug **R**eaction with **E**osinophilia and **S**ystemic **S**x
70
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
71
how does Amiodarone affect the sinus rate? which antiarrhythmics increase the PR segment
72
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
73
treatment for essential tremors MOA AE associated with the class of drugs
\*b2 worsening of obstructive lung ds ~ worsening asthma, etc\*\*
74
what drugs (and MOA) can be used to treat M hyperspasticity/hyperreflexia
75
most beneficial drug for ischemia induced ventricular arrhythmias
76

First Aid, UWorld sets (15 decks)

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