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pharm > other ABX note exam 3 lecture 2 > Flashcards

other ABX note exam 3 lecture 2 Flashcards

1
Q

what is the ribosome made out of ? what unit is it based on ?

A

30S + 50S = 70S
sheburg unit which measures sedimentation rate

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2
Q

what does the 50s unit contain and the 30s unit

A

50s = 5S and 23S rRNA with 34 proteins
30s = 16S with 21 proteins

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3
Q

what are the 6 aminoglycosides and its improtance?

A

SNK-GTA
1. streptomycin - give IM, 1st drug islated from strep grizz
2. neomycin - PO good to wipe out gut floor
3. kanamycin - IV
4. genetmicin IV - came from microsporiporia
5. tobramycin - IV
6. amikacin - semi synthetic of kanamycin

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4
Q

what is the MOA of aminoglycoside ?

A

binds to 30s subunit esp on the 16s

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5
Q

how does aminoglysocide work?

A

it STOPS THE TRANSCRIPTION OF PROTEIN = BACTERIAL STATIC= death

unlike PCN which directly kills the bacteria

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6
Q

what is the pharmacokinites for aminoglycoside ?

A
  • given IM PO IV
  • renal excretion mainly builds up in the renal cortex and endo/perilym of ear
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7
Q

what is the MOR of aminoglycoside?

A
  1. bacterai will make enzymes that will inactivate aminoglycoside
  2. or bacteria will find ways to prevetn aminoglycoside from getting INTO the cell so it cant pentrate
  3. FAMOUS; BACTERIA WILL MUTATE 30S
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8
Q

what drug does aminoglycoside work well w when killing a bacteria?

A
  • Works well w PCN bc PCN breaks through the cell wall then you can deliver the aminoglycoside
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9
Q

what are the S/E for aminoglyocosides?

A
  1. high dose can cuase ototoxicity and nephrotiocity so make sure u dont give it w other drugs that can cause that too
  2. ototoxciity: neomycin, kana, amikan
    - strepto and genta = vestibular damange
  3. nephrotoxicity = neomycin, tobramycin, gentimicin
  4. curae like effect = dont give to someone w NM dz like MS or parkinson dz
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10
Q

where did tetracylcine come from?

A

streptomycin auerofaciens

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11
Q

what are the 4 tetracylcine?

A

doxy
minoxcline
tigecylcine
demeclocylcine

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12
Q

what is the MOA for doxy?

A

binds to 30S on the A site to prevetn transctiption

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13
Q

what should u be careful when giving someone doxy?

A

becareful of the ion intake they take: CA MG FE ZN
this can impair the doxy absorption

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14
Q

what is the pharmacokinetics for tetracylcine ? where can doxy accumalte in the body?

A
  • PO - be careful for ions MG CA FE ZN
  • IV
  • it can accumalt in the liver, bone, teeth spleen :(
  • bad for babies it can go to their teeth
  • excreted in the BILE!!!!!!!
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15
Q

what is the MOR for doxy?

A

same thing, it can modfiy the 30s, enzymes for inactivation, or imapir drug from going into cell

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16
Q

what are the S/E for doxy?

A
  1. GI upset- casue C.diff
  2. photosenxifity - can casue reddness
  3. change normal flora
  4. nephrotoxicity - only if given w dureitics
  5. vestibulotoxicity - ONYL MINOCYLCINE.

AVOID IN GRAVID - can casue discoloration dysplasia and growth of fetal bone teeth

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17
Q

what is the MOA of macrolides?

A

binds to 50S and stops the elongation of peptide chaine

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18
Q

what are the three macrolides?

A

erythro, clarithro, azithro

19
Q

what are the pharmacokinetics/ MOR for macolides?

A
  • give IV and PO good distruction
  • heptaic (E and C)
  • billiary (E and A)
  • renal (c)

MOR- esterase breaks up the drug, 50s modifcation

20
Q

what is the S/E of macrolids?

A
  1. GI upset FAMOUS! thought to bind to motelin receptor in gut and cause peristalsis
  2. arrthymia - Q-T long Vtachj
  3. hepatic issues
  4. Drug to drug interactions P450 inhibitor, bad for warfarin
  5. digoxin interaction - macrolides wipes out the gut so digoxin i nthe blood more
21
Q

which rx interacts w digonxin and casues bad s/e?

A

macrolides

22
Q

whcih drugs is a CYP450 inhibtior?

A

macrolides

23
Q

which drug can builkd up in bone

A

doxy

24
Q

what is the moa of clinda?

A

same as macrolides, binds to 50S and stops peptide growth

25
Q

what is the pharmakinietcs for clinda and the MOR and S/E?

A

kinetics - IV PO, good tissue peneration, H and B and R excretion jsut like macrolides
MOR - same as macrolides. theres cross resisitnact so if resisitant to macorlide then resis to clinda

S/E
- GI, RAsh, heptic function
- ***neutropnea, pseudomembranouse colitis **= it can casue Cdiff overgrowth!!!

26
Q

which drug can casue pseudomembranous colitis?

A

clinda

27
Q

what is the MOA for cloramphenicol?

A

it binds to 50S like macrolides

28
Q

what is the S/E for chloramphenicol?

A
  1. aplastic anemia - wipe off everything in bone marrow
  2. gray baby syndrome - can fuck up the ETC in baby, leading to organ fialure and grey color
29
Q

when should linezolid be used?

A

it should be last resort due to developement of resistance

30
Q

what is the MOA and pharmacokineitcs for linezolid?

A

MOA - binds to 50s 23s so ribosome is not formed
kinetics- IV PO 100% bioav unlike vanco

  • heptatic and renal excretion so be careufl w renal dz
31
Q

what are the S/E for linezolid?

A
  1. thrombocytopenia - can wipe out platletes and casue anemia
  2. serotonin syndrom - build uip serotonin esp w SSRI
  3. optic and peripheral nerupahty - eye probs if on for 1 month
32
Q

What are the 5 fluroquinilone abx and what is the MOA?

A

LMNOC
levofloxacin
moxifloxacin
norfloxciain
oflaxocin
ciproflocin

MOA - inhbits the topo 3 which unwinds DNA so transcirtion/replication is preveneted
it also inhibits topo 4 which prevents DNA from seperating

33
Q

what are the s/e for fluroquinilone?

A
  • GI
  • arrthymia - QT longation
    FAMOUS- CARTILOGUS TENDONITIS - can decrease sysntehsisi of collagen and lead to tendontisis and tendon rupture
  • M/C in acl ruptures and marathon runners, or those immunosuprised or thspoe taking steriods or age
  • CANNOT GIVE FOR PREGNANY
34
Q

what is the pharmacokineitcs for fluro?

A

JUST LIKE DOXY, you cannot give it if youre taking dairy products or antacids or iron supplements

excreted renal

35
Q

who made the first sulfaonamide ABX claled prontosil?

A

DOMAGK

36
Q

who made trimethoprim ABX?

A

HITCHENS

37
Q

what is the MOA of sulfonamide?

A
  • normally bacteria uses PABA to make dihydrofolic acid via dihydropteroate synthase and will make tetra acidvia dihydroflate reducatase

SULFAMIDE ABX will inhbit the first enzyme dihydropteroate so the bacteria cannot make dna

38
Q

what is the MOA for trimethprim?

A

trimehtpriun inhibits the 2nd enzyme called dihydroflate reducase preventing it to make tetra acid

39
Q

what is the S/E for TMP SMX?

A
  1. hypersensitivty derm –> will ccasue rash and peeling of skin called steven johnson syndrome
  2. GI - duh
  3. trimethorprim component will cause megaloblastic anemia since it only affects bacterial cell so if someone was b12 defiencet this will happen
  4. sulfonamide component will casue acute hemolytic anemia
  5. GRAVID - safe 1st trimester but unsure later –> will casue bilibrum buildup in brain irreversle damage = kernicterus
40
Q

what is the MOR of TMP-SMX?

A
  1. incresae production of PAVA to overcome inhibtion duh
  2. active efflux pump
    3.. mutate the dihydro enzmye so sulfa abx cannot bind
41
Q

what is the MOA for nitrofurantonin?

A

the bacteria takes up nitro and activates the drug
- drug turns into ROSA which will go into the bacerteria and kill the DNA

so dumb for the bacteria to eat it lol

42
Q

what is the S/E and pharmokinetics for nitro?

A

taken PO

S/E
1. hemolytics anemia
2. pneumonitis/intersitial pul fibrosis - ROS can casue fibrosis
3. neurological - HA, vertigo, dizzy usually reversible but if someone has parathesia or motor defeict then its not due to demylenation
4. heptasisi - be careful w advance liver dz

43
Q

what is the MOA for fosfomycin ?

A

remember NAM which is needed to make bacteria cell wall?
well the enzyme that makes this is phophoenolpyruvate syntehase and fosfomycin inhbits that so cell wall NOT MADE!!

44
Q

what is the kinetics for fosfomycin?

A

given IV MDR in house sometimes if bacteria is resisince to everything

pharm (13 decks)

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