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Pharmacology drew > winter 3 > Flashcards

winter 3 Flashcards

1
Q

Sulfonamides MOA

Trimethoprim MOA

A
  • sulfonamide MOA- inhibit dihydropteroate synthase stoping conversion of PABA–> dihydropteroic acid,
  • TMP MOA- a diaminopyrimidine- inhibits DHFR enzyme stopping DHF-> THF, 100,000x more sensativte to bacteria DHFRf
  • both stop folate production, and inhibiting DNA production
  • each is static on own but tidal when used together, 1:5 TRI to SMX ratio-> 1:20 ration in serum
  • Sulfonamides penetrate in to most body fluids, and can cross into CNS and cross the placenta, TMP penetrates CNS better b/c lipophilicity
  • t1/2 both = 10-12 hr, tmp excreted in urine-> dose adjust in renal disease
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2
Q

Sulfonamide and Trimethoprim adverse effects

A
  • sulfonamide low solubility–> crystal urea(prevent with 1200ml output/day), redox potential-> hemolytic anemia in G-6PD deficiency pts
  • anti folate drugs in general-> can lead to anemia from bone marrow suppression (esp in aids/cancer pts)
  • both-skin hypersensitivity(^ inHIV pts), NV and GI distress
  • allergy also to other sulfa drugs( sulfonureas, diuretics, and diazoxide)
  • TRI- hyperK(via blocking Na abs in distal nephron), inhibit human folate in malnurished pts
  • PREGNANCY- category D- early in preg-> inhibit human DHFR, late preg can displace bilirubin-> neurotoxic kernicterus, in milk-> don’t use in G-6PD infant nursing
  • but use in preg when benefit>risk - P. jirovecii pneumo treat/prophylax and toxoplasma prophylaxis
  • displace phenytoin, warfarin, sulfonylureas
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3
Q

Sulfonamide and Trimethoprim USES

A
  • lower UTI- TRi penetrates prostate, G- like E. coli, proteus, klebsiella, enterobacter, morganella
  • RESP pathogens- strep pneumo, h flu, moraxella, P. jirovecii, high rate of pneumococcal resistance
  • GI- E coli, salmonella, VIbrio cholera, NOT for shigella

_some MRSA are sensitive to it

-Listeria, yersinia pestis, nocardia, Toxoplasma gondii, pneumocystis

  • resistance mutations to DHFR or dihydropteroate synthase, Pseudomonas use efflux pumps, Bacteroides, MTB, Treponema palladium, Campylobacter, penicillin resistant pneumococcus, rickettsiae
  • enterococcus faecalis is auxotrophic for folic acid
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4
Q

Silver Sulfoadiazine

A
  • also mafenide, and sulfacetamide
  • standard treatment for the infection of burns because of the very little absorption into the body and limiting the toxicities,
  • ophthalmological ointments for chlamydia trachoma conjunctivitis
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5
Q

aminoglycosides pharmacokinetics

A
  • MOA- inhibit bacterial protein synthesis bind to 30S unit
  • polar drugs effecting pharmicokinetics–> poor oral absorption, whole dose out in feces, so give IV(30-60 min drip) or IM
  • dont penetrate cell well, little entrance into eye or CNS
  • form complex w/ b lactam ABx-> administer separately
  • cross G- outer membrane thru poron, cross inner membrane via O2 dependent active transport(not effective in low pH and anderobic infections), B lactase enhance transport–> synergistic killing effect
  • NOT metabolized, cleared via filtration, dose adjust in renal failure(t.5 in healthy=2-3, in renal disease 24-48 hrs)
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6
Q

aminoglycosides pharmacodynamics

A
  • inhibit bacterial protein synthesis by irreversibly binding to 30S subunit, and are bactericidal(dose dependent)
  • blocks initiation of protein synthesis
  • blocks movement of ribosome-> breakup of 70S subunit
  • mRNA misreading-> mutant proteins that kill the cell( even at [ ] below MIC
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7
Q

aminoglycosides toxicities

A

-Ototoxic CNVIII damage(acumulate in the endo and perilymph-> distraction of vestibular and cochlear hair cells) strepto>amika=genta=tobra, ^ risk w/loop diuretics and vancomycin, in elderly, dehydrate, and long term use

  • tinnitus-> hearing loss (Amika, Kana, netil,Neo)
  • Vestibular tox->vertigo ataxia,loss of balance, Genta,strepto, tobra
  • NEPHROTOXICITY-in prox tubule and is reversible, monitor w/ creatinine serum level every 2-3 day, Genta, tobra, neo
  • ^ risk w/^ doses, coda w/ vanco or cephalosporin, prexisting renal fail, elderly and dehydtrate pts
  • NEUROmuscular blockade-weakness and resp paralysis, blockage of Ach release and post synapse activity, treat w/ Ach as inhibitor (neostigmine/edrophonium) and IV Ca
  • drug levels routinly obtained in pts b/c of ^ toxic effects
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8
Q

Bacterial resistance to aminoglycosides

A
  • production of bacterial enzymes that phosphorylate, adenylate, or acetylate the drugs-> not allowing binding to the 30S subunit, on plasmid and spread via conjugation
  • problem in hospital setting
  • Amikacin, netilmicin are most resistant to these enzymes, these are useful in gentamicin resistant G- bacteria
  • important in entercoccal endocarditis
  • inability to penetrate the cell wall(less problem clin) , mutation in the 30S subunit to decrease binding
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9
Q

antibacterial spectrum of aminoglycosides

A
  • USED TO TREAT SYSTEMIC INFECTIONS FROM G- ENTERICS (SPESIS)
  • IN COMBO W/CELL WALL INHIBITORS TO TREAT BACTERIAL ENDOCARDITIS
  • G+ baceria- limited activity alone, used in combo w/ ABx that inhibit cell wall synthesis to have synergistic effects,
  • good for S. aureus and epidermidis, Strep pneuma and pyogenes are highly resistant, Genta and strepta use w penicillin and amoxicillin for synergistic effect on enterococci and viridens group strep
  • G- Bacteria-best activity against G- enterics, E coli Klebsiella pneumo, Proteus

–Genta Tobra, Netil, Amikacin have Pseudomonas activity

  • NOT ACTIVE AGAINST ANAEROBES(b/c transported in tobacteria via O2 dependent manner)
  • no fungal or virus
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10
Q

streptomycin

A

aminoglycoside

  • inhibit bacterial protein synthesis by irreversibly binding to 30S subunit
  • less G- activity b/c of resistance->limited colin use
  • uses- in combo w/ penicillin for Bacterial endocarditis (gentamicin is preferred but some resistant to it are sensitive to street), 2nd line in combo for MDR MTB,yersinia and francisella IM in combo w/ tetracycline
  • adverse RXN- allergic skin rash, pain at injection, OTOTOXICITY, irreversible associated w/ vertigo and loss of balance, in pts using for >2wks, defenses of child if used in preg
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11
Q

Gentamicin

A

aminoglycoside
-inhibit bacterial protein synthesis by irreversibly binding to 30S subunit

-first choice b/c of low cost

-USE- G- infections from Pseudomonas, enterobacter, klebsiella, serratia
UTI in combo w/ B lactam ABx(initial broad spec coverage) switched to less tox ABx if susceptible infection(TMP-SMX), G- pneumoniaI as initial empirical therapy HAP(Not for CAP)

  • in combo w/ penicillin for bacterial endocarditis(better than amika or tobra),
  • G- sepsis, for pseudomonas use genta in combo w/ ticarcillin or piperacillin(anti pseudomonal penicillins)
  • adverse effects- nephrotox and ototox( trough [>2ug/ml]
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12
Q

Tobramycin

A

aminoglycoside
-inhibit bacterial protein synthesis by irreversibly binding to 30S subunit,

  • same spec of activity as gentamicin
  • better pseudomonal coverage than gentamicin and use in sepsis, osteomyelitis and pneumonia from this bug
  • orphan drug status for pseudomonal bronchopulm infections in Cistic fibrosis pts
  • less effective against enterococci, E faecium
  • TOX- nephrotoxicity and ototoxicity
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13
Q

Amikacin

A

aminoglycoside

  • inhibit bacterial protein synthesis by irreversibly binding to 30S subunit, derivative of kanamycin
  • broadest spectrum of the aminoglycosides b/c resistant to the enzymes that inhibit genta and tobra
  • G- bacteria- proteus, pseudomonas, enterobacter, serratia
  • bad against G+ bacteria, but does have activity against streptomycin resistant MTB
  • USES-serious nosocomial G- infections resistant to genta and tobra, should NOT be used in endocarditis
  • TOX- nephro and ototoxicity( oto is more common
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14
Q

Fluoroquinolones drugs, MOA, kinetics

A

Ciprofloxacin
levofloxacin
moxifloxacin

  • target and inhibit bacterial DNA gyrase and topoisomerase IV, these enzymes fix supercoiling that occurs in DNA replication-> inhibition of replication(cidal), gyrase more in G- and topoisomerase more in G+
  • addition of Fluorine improved lipid solubility, accumulation in bacteria, and affinity for DNA
  • good oral abs, inhibited by poly cations(Ca, Mg, Al, Fe, Zn) supplements
  • wide distribution to exceed serum [ ] in Mphage, PMN, kidney, urine, prostate, lung, stool, bile
  • not used in CNS infection, t1/2 mostly 3-10 hrs
  • cleared by renal mech–> dose adjust
  • moxifloxacin met in liver-> caution in liver fail
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15
Q

Fluoroquinolone Theraputic uses

A
  • target and inhibit bacterial DNA gyrase and topoisomerase IV, these enzymes fix supercoiling that occurs in DNA replication-> inhibition of replication(cidal)
  • UTI and prostatitis(e coli most common for both), useful in Chlamydia and haemophilus ducreyi chancre
  • no use- N. gonorrhea(ceftriaxone instead) or trepomona palladium, preg category C
  • diarrheas from Salmonella, shigella, and e coli
  • only class w/ oral form for pseudomonas(cipro)
  • levo and moxi(resp fluoros) to treat CAP, cipro
  • bone joint and soft tissue infections, osteomyelitis and diabetes foot infections
  • M. avium in AIDS pts, francisella and anthrax
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16
Q

Ciprofloxacin

A
  • fluoroquinolone
  • UTI and prostatitis( coli most common for both), useful in Chlamydia and haemophilus ducreyi chancre
  • oral dose pseudomonas in cistic fibrosis pts
  • diarrheas from Salmonella, shigella, and e coli
  • bone joint and soft tissue infections, osteomyelitis and diabetes foot infections
  • M. avium in AIDS pts, francisella and anthrax
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17
Q

levofloxacin

A

respiratory fluoroquinolone-target and inhibit bacterial DNA gyrase and topoisomerase IV, these enzymes fix supercoiling that occurs in DNA replication-> inhibition of replication(cidal)

  • pneumonia causeing- s. pyogenes S aureus, mycoplasm, and legionella, prominent( but not 1st line)role in CAP,
  • UTI and prostatitis( coli most common for both), useful in Chlamydia and haemophilus ducreyi chancre
  • diarrheas from Salmonella, shigella, and e coli
  • bone joint and soft tissue infections, osteomyelitis and diabetes foot infections
  • M. avium in AIDS pts, francisella and anthrax
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18
Q

moxifloxacin

A

respiratory fluoroquinolone-target and inhibit bacterial DNA gyrase and topoisomerase IV, these enzymes fix supercoiling that occurs in DNA replication-> inhibition of replication(cidal)

  • pneumonia causeing- s. pyogenes S aureus, mycoplasm, and legionella, prominent( but not 1st line)role in CAP,
  • reported w/ high rate of adverse effects
  • BEST CHOICE of class for anaerobics for complicated intra abdominal infections on par w/ pipercillin/amox
  • UTI and prostatitis( coli most common for both), useful in Chlamydia and haemophilus ducreyi chancre
  • diarrheas from Salmonella, shigella, and e coli
  • bone joint and soft tissue infections, osteomyelitis and diabetes foot infections
  • M. avium in AIDS pts, francisella and anthrax
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19
Q

resistance to fluoroquinolone

A

-develop quickly and confers resistance to all

  • most rapid from plasmid factors,
  • quinolone resistance proteins(Qnr)- protect bacterial gyrase
  • aminoglycoside acetyltrasnferase can act on cipro conferring resistance to both
  • 3rd plasmid- efflux pumps
  • chromosomal pont mutations to binding site
  • cross resistance is common- enterobacter and klebsiella resistant to both quinolone and B lactase
  • no use in MRSA-resistance is wide spread
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20
Q

Fluoroquinolone adverse effect and interactions

A
  • most serious-QT prolongation, hypoglycemia, immune hemolytic anemia, hepato tox, photo tox,
  • moxifolxacin - reported w/ high rate of adverse effects
  • GI-are most common-NVD, most common cause of C difficile, an especially toxic strain
  • 10% CNS- headache, dizzy, other like hallucination or seizure are rare- caused by displacing GABA from receptor, enhanced by theophylline or NSAIDS
  • black box 1- achilles tendon rupture in elderly, steroid pts, and organ transplants
  • blackbox 2-exacerbation of myasthenia gravis
  • category C preg- meta acidosis and hemolytic anemia
  • rash 2%,
  • caution w/ QT prolonging drugs-SRI, TRIcyclic AD, diuretics, anti psychotics
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21
Q

Vancomycin

A
  • Inhibits Bacterial cell wall synthesis
  • poor oral abs, IV arm
  • wide distribution and penetrates CNS w/ inflammed meninges, 90% renal excretion, dose adjust in failure
  • MOA- binds to D-alanyl-D-alanine of peptidoglycan pentapeptide-> inhibit PG formation and is bactericidal
  • resistance via alteration cell wall precursors so vance can’t bind as well, ex: DaDa replaced w/D-alanyl-D lactase/serine
  • USE- G+ bac, active against MSSA and MRSA, s epidermitis, strep, corny bacteria, C dif and C. perfringes
  • G- bac: NO ACTIVITY
  • anaerobes: only clostridium- not used against others
  • clinical- serious staph infections(sepsis and endocarditis), G+ in pts allergic to penicillins and cephalosporons( enterococcus endocarditis-vanco w/aminoglcosides), dhrea from C diff and GI bugs, staph meningitis w/3rd cephalo
  • tox-ototox and nephrotox(rare) more common in combo w/ ahminoglycosides, RED MAN- arm to fast-> His release
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22
Q

Clindamycin

A
  • MOA- binds to 50S subunit and inhibits protein synthesis
  • well abs orally, t.5=2.9 metabolized and excreted mostly in bile, dose adjust in hepatic failure- Bacterio static
  • widely distributed inbody, not in CNS even w/ inflammation of meninges, GOOD entry into Abscesses
  • resistance- mutation to 50S subunit to prevent binding, methylase modification of binding site, enzymatic inhibition of ABx, bugs resistant to clindamycin are also resistant to erythromycin
  • USES- G+ bac- most staph aureus strains(some MRSA), s. pneuma, but ENTEROCOCCI are resistant, NO G- USE, active against G+ and G- anaerobes, including b. fragilis and C. perfringens
  • used to treat abscesses( not in brain), prophylactic use for dental procedures prevent endocarditis, alternative to cephalosporins and penicillin allergic pts, P, Jiroveci and toxo in AIDS pts
  • tox-ND, skin rash, pseudomembranous colitis- C dif
23
Q

Nitrofurantoin

A
  • MOA- not well understood- reduced forms damage DNA, static and cidal
  • rapid oral abs, rapid met and excretion by filtration and renal secretion(not used in renal fail) so fast that systemic effects not seen, more active at urine ph of 5.5- administer with acidifying agent
  • Uses-many G- and G+, pseudomonas and proteus are resistant
  • clinical-used to treat UTI and prophylaxis of frequent UTI, Ecoli resistant to TMP-SMA and Fluroquinolones
  • Tox- GI upset=anorexia NV, rare hemolytic anemia, headache, demylination, pulm fibrosis, shronic hepatitis (rare but serious), contraindicated in renal failure cautious in preg
24
Q

Polymyxin B sulfate

A
  • cidal Abx by interacting with cell membrane phospholipids and disrupting cell membrane permeability and causing leakage of intracellular components
  • resistance from inability to pass through cell wall
  • restricted to susceptible G- bac. enterobacter, ecoli, klebsiella, h flu, acinetobacter, pseudomonas
  • topical treat of eye, skin, MM, ear wound and burn infections, IV therapy for drug resistant G- pneumonia, IV or IM for G- septicemia and UTI, Intra thecal for Meningitis, combo w/ neomycin to irregate bladder to prevent infection from indwelling catheters
  • TOX-neurotoxicity, nephrotoxicity, reserve use to when less toxic Abx are no longer available for use
25
Q

Metronidazole

A
  • MOA-reduction of drug to compounds that bind to intracell macromolecules, bactericidal effect
  • a nitroimidazole, good oral abs,IV, rectal or topical vag gel
  • Mide distrubution include CNS and abscesses, met in live excrete via kidney
  • not good for G+or G- aerobes, GOOD ACTIVITY against anaerobes including clindamycin resistant B. fragilis
  • CLIN-anaerobic infections (soft tissue, brain abscess, intra AB, pelvic inflame) pseudomembranous colitis from C diff, H pylori
  • TOX-carcinogenic potential, present intreats milk and crosses placenta->NO USE in PREG, disulfiram like interaction w/ EtOH
26
Q

Bacitracin

A
  • inhibits cell wall formation via inhibiting lipids that carry PG to the site of cell wall formation, no cross resistance
  • ophthalmic and dermatologic ointment( not used parenteral b/c nephrotox)
  • similar activity to PCN, activity to G+ cocci and rods, and G- Neisseria, H flu, and spirochete treponema palladium
  • USES-topical wounds to eradicate mixed microbes, eye infections
  • TOX-SERIOUS nephrotox w/ parenteral use-> renal failure due to tubular and glomerular necrosis, rare hypersensitivity from topical use
27
Q

Quinupristin/dalfopristin

A
  • Streptogamin ABx combo- Q is group B, D is group A
  • MOA- like macrolides- inhibit protein synthesis by binding to 50S subunit, each binds to different site on subunit
  • resistance- modification of Q bind site, enzyme destruction or efflux of D
  • IV for bacteremia and life threat vanco resistant entercoccus faecium and complicated skin infections from s aureus and s progenies
  • activity to MRSA and MSSA, PSSP and PRSP
  • used when E faecium, strep or staph infections resistant to other ABx, or allergy to other ABx
  • erethyma/pain at injection site, arthralgia/myalgia, CYP3A4 inhibition
28
Q

Linezolid

A
  • MOA-binding 50S subunit-> prevent 70S initiation complex
  • oral and parenteral adm
  • cidal to strep static to many others
  • resistance- entero and streptococci via point mutation at 23S rRNA of 50S subunit
  • spec activity-vanco resistant E. Facacium,HAP/CAP from S. aureus and PSSP, skin infection from MRSA and MR S pyogenes
  • TOX-NVD, Thrombocytopenia-monitor platelet count in treatment >2 weeks, reversible inhibitor to monoamine oxidase( co adm w/ tyramine foods-> HTN), avoid in PKU pts, can lead to C diff
29
Q

Daptomycin

A
  • [ ]dependent killing effect by binding and depolarizing cell membranes-> loss of Mem potential->K efflux->death
  • use only IV, t.5=8-9 hrs, 80% excreted in urine-> dose adjust if creatine clear is below 30
  • cidal for aerobic, facultative , and anaerobic G+
  • skin and skin structure infection s from MSSA MRSA, hemolytic strep , and vanco resistance B faecalis
30
Q

first line drugs for TB

A

Isoniazid
Ethambutol
Rifampin
pyrazinamide

31
Q

drugs for treating leprosy

A

Dapsone
Clofazimine
rifampin

32
Q

principles of TB therapy

A
  • therapy must consist of 2 or more drugs that Tb is sensitive to
  • treatment must continue 3-6 months after sputum becomes negative
  • drugs work only during replication, TB obligate aerobe, effected by the pH of its environment
  • recommended 6 months of INH, rifampin, and pyrazinamide ( 1st 2 mo) and INH and rifampin for final 4
  • resistance- 3 variables, history of prior anti TB therapy, country of origin , and duration of residence in US
  • single drug therapy is only in preventative therapy, INH for 9 months( also 2mo of combo rifampin and pyrazinamide)
33
Q

short course chemotherapy for TB

A

6-9 months in US
- initial phase of INH, rifampin, pyrazinamide, and ethambutol daily for 2 months

-continuous phase- INH and rifampin (daily, 2x/wk, or 3x/wk) for 4 months

34
Q

goal of leprosy chemotherapy

A

broad objectives

  1. render the pt noninfectious
  2. prevent further bacterial multiplication
  3. avoid or treat reactions
  • paucibacillary treatment- Sulfone Sensative- dapsone(3-5y), rifampin(6mo), SR- clofazimine and rifampin
  • multibacillary- SS-dapsone(10y-indefinate) rifampin(3y), SR-clofazimine(indefinate) rifampin(3y)
35
Q

INH- Isoniazid

A
  • hydrazide of isonicotinic acid
  • interferes w/ mycolic acid biosynthesis, bactericidal in rapidly dividing bacteria
  • excreted in the urine w/in 24hrs as acetylated or hydrolyzed nisonicotinic acid(slow android acylators)
  • Adverse rxn- peripheral neuropathy from increased excretion of pyridoxine
  • Hepatitis- Major effect more communion the slow acetylators, pts should be monitored peridically serum transaminase levels
36
Q

Rifampin

A
  • derivative of rifamycin B, for TB and leprosy
  • inihbits bacterial RNA synthesis- binding to B subunit of DNA dependant RNA polymerase, does not inhibit mammalian RNA Polymerase
  • resistance w/ mono therapy, met in liver and excrete in urine(33%) and bile (66%)
  • inhbits most G+ and some G-, most active during cell multiplication
  • ADVERSE RXN- GI disturbance, NV , hepatitis, red-orange color in urine salivia and sweat w/long term use
  • Potent activator of P450 system-> decreased t1/2 of many drugs
37
Q

Ethambutol

A

-MOA- unknown- inhibits incorporation of mycolic acid into the mycobacterium cell wall, rapid abs from GI tract

  • Adverse RXN- MOST SIG- dose related ocular toxicity, reversible vision changes -> retrobulbar neuritis and loss of green red discrimination
  • should be stopped immediately
  • oral adm w/ rifampin and INH in TB chemotherapy
38
Q

Pyrazinamide

A

-pyrazine analogue of nicotinamide

  • MOA- unknown-exhibits bactericidal activity at acidic pH, hydralized to pyrazinoic acid which has anti TB activity
  • good GI abs
  • adverse RXN- hepatotox is main SE, all pts treated w/ this should have LFT before beginning and throughout treat
  • nongouty polyarthralgia- drug causes hyperuricemia
  • important in short term multi drug therapy of TB
39
Q

Clofazimine

A
  • red colored compound
  • MOA- binding of drug to mycobacterial DNA to inhibit growth, cidal for M. leprosy
  • Very long t.5=70days, slowly excreted in urine
  • TOX- discoloration of the skin- first reddish-> mahogany brown, will clear after discontinuation
  • GI- most serious effects- NVD at higher doses

-used for lepromatous leprosy

40
Q

Dapsone

A

-sulfone analogue of p-aminobenzoic acid

  • MOA- inhibits folic acid synthesis (similar to sulfonamides by inhibiting dihydropteroate synthase)
  • bacteriostatic for M leprae, T.5=10-50 hours, acetylated inlayer and excreted in urine

-TOX-usually mild, but can cause hemolytic anemia(CBC should be performed frequently), methemoglobinemia, sulfone syndrome- exacerbation of lepromatous leprosy

41
Q

Agents that block attachment and penetration

A

Gamma globulin

42
Q

amantadine

A

blocks viral penetration and uncoating

only specific for influenza A

43
Q

Sulfasalazine

A
  • not well absorbed form GI
  • Used in ulcerative colitis and IBD, b/c converted to 5- ASA and sulfapyridine to have an anti inflammatory effect and immune modulating properties
  • sulfapyridine IS absorbed and causes hemolysis in G6-PD
44
Q

Amphotericin B

A

antifungal therapy for sub Q and systemic mycosis
-creates pores in membranes causeing leaking and death of fungus

-SE-nephrotoxicity( increased w/ conccurrent treatment of aminos or cyclosporons), anemia due to decreased production of EPO

  • systemic fungal infections iv or intrathecal, superficial from candidia
  • protozoa infections
45
Q

Ketoconazole

A

imidazole

antifungal therapy for sub Q and systemic mycosis

  • inhibit 14 a demethylase-> buildup of 14 a methyl sterols(lanosterol)->impairing membrane bound enzymes systems, and permeability of fungal membrane
  • fungistatic at low [ ] and tidal at higher [ ]
  • endocrinological abnormalities- inhibition of steroid synthesis, inhibit of P450 enzymes
46
Q

Miconazole

A

imidazole

antifungal therapy for sub Q and systemic mycosis

–inhibit 14 a demethylase-> buildup of 14 a methyl sterols(lanosterol)->impairing membrane bound enzymes systems, and permeability of fungal membrane

-low tox w/ oral iv or intrathecal arm

47
Q

Fluconazole

A

triazole
antifungal therapy for sub Q and systemic mycosis

–inhibit 14 a demethylase-> buildup of 14 a methyl sterols(lanosterol)->impairing membrane bound enzymes systems, and permeability of fungal membrane

  • 25-30 hr halflife-> once daily dosing ,increses concentration of drugs met by P450 enzymes
  • low tox, no effect on pts plasma level of test or response to ACTH
48
Q

Itraconazole

A

triazole
-antifungal therapy for sub Q and systemic mycosis

–inhibit 14 a demethylase-> buildup of 14 a methyl sterols(lanosterol)->impairing membrane bound enzymes systems, and permeability of fungal membrane

  • 30 hr t1/2, increses concentration of drugs met by P450 enzymes
  • low tox, nausea, heart burn , headache
49
Q

drugs to treat systemic mycosis

A 
Amphotericin B
Ketoconazole
Miconazole 
Fluconazole 
Itraconazole
50
Q

Griseofulvin

A

MOA- disrupts the cells mitotic spindle structure , arresting cell in metaphase

-SE- CNS headache
GI- epigastric pain, NVD
Hypersensitivity- rare
precaution:periodic assessment of renal hepatic and hematopoietic function should be performed

-used in treatment of dermatophytes , not for tinea versicolor or candidia

51
Q

Nystatin

A
  • binds to sterols in fungal cell membranes-> resulting in membrane not acting as a selective barrier-> loss of K and other cell contents
  • SE_ very rare w topical use, hypersensitivity rare
  • too toxic for parenteral use
  • used mainly for cutaneous, mucocutaneous, and oral cavity candidal infections
52
Q

Tolnaftate

A

inihibts squalene monooxygesase ->build up of squalene and changes in membrane properties

_low tox
- main use is dermatophytes

53
Q

Terbinafine HCl

A

inihibts squalene monooxygesase ->build up of squalene and changes in membrane properties

  • low tox
  • main use is dermatophytes
54
Q

Caspofungin

A
  • echinocandins antifungal
  • MOA- inhibits the synthesis of B 1-3 D-glucan( essential component of fungal walls

SE-rach fever, phlebitis at injection site, NV fluching

-use in treating invasive aspergillosis and esophageal candidiasis in PTS REFRACTORY TO OTHER ANTIFUNGAL MEDICATIONS

Pharmacology drew (9 decks)

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