pharm 3B: topical ABX + anti-TB Flashcards

1
Q

what is the MOA for bacitracin?

A

it clogs the channels and prevents intracellular proteins from going from cell to intracellular space

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2
Q

what is the spectrum/pharmacokinetics/ s/e for bacitracin?

what is bacitracin often combined with?

A

spectrum - KILLS GRAM POSTIVES

pharmacokinetis - topically for derm, opthalmically

often combined with neomycin or polymyxin

S/E: nephrotoxicity if given systemically

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3
Q

what is the two polymyxin bacterias and what is the MOA?

A
  1. colistin (polymyxin E) and polymxin B

MOA - the abx kills the hydrophobic and hydrophillic compoentns of the bacteria cell wall and casuesing its destruction

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4
Q

what is the spectrum and pharmaokineitcs and S/E for polymyxin?

A

KILLS GRAM NEGATIVES

given topically, often combined w bacitracin

S/E: polymyxin E is nephrotoxicity when given IV so dont give it with other nephrotoxici drugs like vancomycin

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5
Q

what is mupirocin MOA, spectrum and pharmokinetics?

A

MOA - inhibits bacterial tRNA syntheases so it cannot make new proteins

kills MOST - AND +

given topically for skin infections and lesions

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6
Q

what are the two cell walls for mycobacterium and what is the importance?

A
  1. mycolic acid - it has 90C atoms in the molecules and its a waxy cell wall
  2. arabinogalacton - stabzlies the mycolic acid and cell wall
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7
Q

whats so imp about the arabinogalactan cell wall?

A

its part of the mycobacterium
- the arabinogalactan cell wall has arbinosyl transferase III
- this enzyme syntehsizes arabinogalactan
- since mycobacteria has a thick wall it protects the BUG FROM degradation

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8
Q

what happens when theres a TB in your body?

A
  1. TB will enter the alveolus and macrophages will engulf it
  2. normally macrophaes will shuttle it to lysosome to get it kills but bc the mycobacteria has this thick wall it prevents it from being hydrolyzed by the macophages
  3. the WAXY cell also inhibits + stops enzymes that porduces the molecules in the first place
  4. it also stops the macrophages from releases enzymes that helps w degradation
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9
Q

how is a granuloa formed with TB infection?

A
  1. since the bug cannot be killed, the immune system WALLS off the infection and forms a granuloma
  2. the macrophages with the TB will go under activation and is now called **epitheloid cell **
  3. some of the activated macrophages will fuse tg to form the CORE of ganuloma
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10
Q

what happens around the granuloma in the lungs for TB?

A
  1. since now we have a macrophage with latent TB in, the fiberglass secretes fibrotic tissues to WALL OFF the entire area of infection since the bug cannot be killed
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11
Q

how is caseous necrosis formed?

A
  • overtime TB will secret TB TOXINS and it will kill the macrophages
  • it will then kill the alveolar cells and when it kils the macriophages it will form a **caseous necrosis **
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12
Q

how many bugs live in the a TB granulmona?

A

107-109

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13
Q

what is milliary tB?

A

when it spreads to other orgran, skeletal and musucles

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14
Q

what is methy methacrylate balls?

A

they used this to tx TB in the 20th centry, they would put the balls in the upper lobe lung to have it collaspe to to prevent the spread of the DZ

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15
Q

what rx would u use for 4 month tx for TB?

A

RIP
rifampam, isoniazid, pyramizide

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16
Q

what type of rx happens with the TB test?

A

hypersensitvity TYPE 4 RX

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17
Q

explain if TB test is >5, >10, >15?

A

> 5 = immunocomprised ppl, HIV ppl, fibrotic changes should get TX

> 10 - iv drug users, hospital people, children exposed, immigrants - needs tx

> 15 - everyone like u doesnt need tx

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18
Q

what is the MOA for rifamycins and how does the bacteria become resisitant?

A
  • it inhibits the beta subunit of the BACTERIAL RNA polymerase –> prevents the RNA from making protein
  • the bacteria become reisistacne by mutating the beta subunit so that rifamycin cannot bind to it
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19
Q

what does rifamycin kill?

A
  • TB, other mycobacterias
  • gram +
    gram -
20
Q

what is the pharmokinetics for rifamycin?

A

it was a STRONG CYP INDUCER through heptatic metabolism so be careful with other drugs ,

main one: HIV drugs

very little in the kidney

21
Q

what are the S/E to rifamycin?

A
  1. orange color discoloration
  2. rash fever flu sx
  3. hepato toxic - liver failure can happen
  4. GRAVID - AVOID
  5. hypersensitivty - can lead to hematuria or hemolysis
  6. DRUG DRUG INTERACTION
    rifampin > rifapentine > rifabutin
    really bad for HIV medications
22
Q

what is INH?

A

INH is isoNICOTINYLhydrazide which is an isoniaid PRODRUG that is taken up by mycobacteria when given

23
Q

what is the MOA for isonizaid ?

A

MOA - mycobacteira takes up isoniazid and in the bacteria there is KATG enzyme that changes the isonaizid pro drug into active drug

this allows iso to bind to NAD and NADH
NAD binding - allows to inhibit mycolic acid
NADH binding allows it to inhibit dihydrofolate reductase so it cannot make any more DNA

24
Q

what is the resisitane for isoniazid?

A

the bacteria is able to mutate KATG so that iso cannot turn into its active form

25
what is the pharmacokinetic for isonizid ? what is the metabolites?
it is prone to hepatic metabolism - it has major and minor metabolites 1. N-acetyl isonizaid - MAJOR metabolite 2. Actylhydrazine - minor metabolite
26
explain the metabolites for isoniazid? which is the heptotoxic one?
the major metabolite (N-acetyl-isonizid) minor metabolite - acetylhydrazine IS HEPATOTOXIC!! - theres slow and fast metabolism
27
exaplin the slow and fast metbaolism groups for isonizaid?
SLOW - scandinavians, jews, blacks so more drugs will build up in the blood since its slow and u have more S/E FAST - japanese! - more drugs will be pulled out of the blood, lowering the concentration so for this you would need to redose to get to the therputic window
28
what are the S/E for isonizid?
1. LIVER - HEPATITIS -some people will have hepatoxic which can leave to mutilobar hepatic necrosis :( *anyone who is a slow acetlyayor w undelying liver dz can get this so monitor liver enzyems 2. neurpathy - so suppliement iso with pyridxine B6 3. FAMOUS - LUPUS LIKE SYNDROME
29
30
31
what are the S/E to pyrazinamide?
1. GOUT - so normally we have the OAT 2 receptors that will take up uric acid and excrete it in the urine BUT pyrazinamide INHIBITS the OAT2 receptors and keeps the uric acid in the blood - it ALSO reabsorbs the uric acid in the blood via the URAT1 receptor so alot of pt will get hyperuremia and grout 2. arthalgia - due to uric acid build up ? 3.. GRAVID - AVOID 4. LIVER - can lead to hepatoxicity
32
what is the MOA and resisitance for ethambutol ?
ehtambutol disrupts the cell wall formation, it inhibits the arabinosyl transferase 3 which helps make the mycolic cell wall. if u inhibit that, the cell will becomes unstable resistnace --> bacteria will mutate the gene that codes for the arabinosyl transferse 3
33
what is the pharmaokinitcs and S/E for ehtmabutol?
kinetics - MAINLY RENAL so be careful and lil liver S/E - GI, gout famous - optic neurtisis it accumualtes in the cooper and zine in optioc nerve so ppl cant distingue between red and green
34
which drug clogs channel/pores and prevents intracellualr protein from going to the intracellualr spoace?
bacitracin
35
which drug destroys the amiphathic compoentns of bacterial cell wall?
polymxins
36
which drugs inhibits tRNA synthesis?
mupirocin
37
which drug inhibits RNA polymerase ?
rifamycin
38
which drug has an organe disocloration
rifamycin
39
which drug is a potent CYP inducer?
rifamycin
40
which drug gets converted via KATG enzyme to do its thing ?
isoniazid
41
which drug has neuprahty as one of the s/e? how do u tx?
isonaizid , tx w B6 pyridoxine
42
which drugs has a lupus like syndrome?
isonaizid
43
which drug inhibits the FA synthesis and NAD metabolism?
pyrazinamid
44
which drug has s/e of grout and arthralgia?
pyrazinamide
45
which drug inhibits the arabinosyl trnasfgerse to disrupt the cell wall formation?
ehtambutol
46
which drug has optic nerutiis as a s/e?
ethambutol