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antibiotics/anti cancer > Antimicrobials, Anticancer, Antiviral > Flashcards

Antimicrobials, Anticancer, Antiviral Flashcards

1
Q

What are the side effects of erythromycin?

A

allergic cholestatic hepatitis,
thrombophlebitis,
inhibits hepatic cytochrome P-450–mediated metabolism of warfarin, phenytoin,

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2
Q

What are the groups of cell wall synthesis inhibitors? always bactericidal

A

these are the lactam antibiotics
penicillins, cephalosporins, imipenem/meropenem, aztreonam,

not a lactam:
vancomycin

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3
Q

What are the groups of bacterial protein synthesis inhibitors? bacteriostatic

A

aminoglycosides (BC-not BS)

tetracyclines, chloramphenicol, macrolides, streptogramins, linezolid, clindamycin

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4
Q

What are the groups that inhibit nucleic acid synthesis? BC

A

(flouro)quinolones, rifampin

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5
Q

What are the groups that inhibit folic acid synthesis? BC

A

sulfonamides, trimethoprim, pyrimethamine

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6
Q

Which cell wall synthesis inhibitor is not a lactam?

A

vancomycin

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7
Q

What is a lactam?

A

Square that is very unstable, makes the bonds very tense and likely to get ruptured;
the weakest bond in the structure is between the N-C , this is the site of resistance of B-lactamases produced by bacterias-cleave the ring!

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8
Q

What does the sulfur bond indicate in an antibiotic?

A

more lipid solubility and more prone to hypersensitivity reactions

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9
Q

How to all lactams work?

A
  1. Bind PBP (allow crosslinking of bacterial cell wall- transpeptidation)
  2. Inhibition of transpeptidation
  3. Prevent crosslinking of the bacterial cell wall
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10
Q

What is the primary resistance to lactams?

A
  1. Penicillinases
  2. Change of PBP structure (MRSA mechanism)
  3. Change of porins in the gram -ve bacterias (call wall made of peptidoglycan, periplasmic space which require porins to exchange foods between the outside and the inside) ex; Pseudomonas can change porin structure
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11
Q

What are the four groups of penicillins?

A
  1. Narrow spectrum: Penicillin G, Penicillin V (syphilis)
  2. Penicillinase resistant: methicillin, nafcillin, oxacillin, dicloxacillin ( only work against Staph. Aureus) –>MRSA

B lactamse sensitive, changed solubility to allow entrance to porin channels:

  1. Extended spectrum: amplicillin, amoxicillin ( Gram + rod and cocci; Strep, Listeria) (Gram -; E.coli, H.pylori, H,influenzae)
  2. Anti pseudomonal: carbenicillin, ticarcillin, piperacillin, azlocillin
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12
Q

What is the actual enzyme that separates Pseudomonas from others?

A

Oxidase +; green coloured sputum and green colour of skin in a burn patient; inhibits euk elongation factor 2 -> blocks translocation

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13
Q

What are the B-lactamase inhibitors?

A
  1. clavulanic acid
  2. sulbactam
  3. tazobactam
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14
Q

What is the trade name of amoxicillin + clavulanic acid?

A

Augmentin

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15
Q

Assuming that all antibiotics go through renal metabolism, what are the exceptions that do not?

A

Nafcillin and oxacillin are more lipid soluable and need lipid metabolism largely in the bile; they don’t require dosage adjustment in renally impaired

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16
Q

What is the side effects of penicillins?

A
  1. hypersensitivity - all types of HS
  2. diarrhea-the longer you take it, the more GI distress due to killing endogenous flora; ampicillin is the worst
    worry about superinfection with C.diff
  3. Jarisch-Herxheimer reaction- only see with penicillin; occurs in treatment of syphilis; if you use cell wall synthesis inhibitor and you break the structures, antigenic proteins are released into the blood- triggers immune response of fever, joint pain, swelling
    I knew it ! It was syphilis!

if patient is allergic to one penicillin, avoid all penicillins and use macrolides

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17
Q

Penicillin cross allergenicity with other classes of cell wall inhibitors?

A

Patient may have a 5-10% increased chance of having an allergy to cephalosporins if they have an allergy to penicillins

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18
Q

What are the mechanisms of action of cephalosporins?

A

Identical to penicillins -3

Modes of resistance- 3

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19
Q

What are the first generation cephalosporins?

A

Anything with a “ph”

cefazolin, cefadroxil, cephalexin

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20
Q

What is the contrast of cephalosporins to penicillins?

A
  1. Penicillins work mainly on gram +, whereas cephalosporins work on both gram + and some gram -
  2. Long duration of action than penicillins
    cefazolin: prophylaxis during surgery to prevent infections
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21
Q

What are the second generation cephalosporins?

A
  1. Better gram - coverage
  2. Cefuroxime can cross the BBB: meningitis
  3. Cefotitam
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22
Q

What are the third generation cephalosporns?

A

ceftriaxone, cefdinir, cefixime, cefotaxime, cefibuten

  1. empirical management of sepsis in the hospital
  2. empirical management of meningitis
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23
Q

Which bacteria do not respond to 3rd generation cephalosporins? LAME

A

L-Listeria (responds to penicllin, amoxicillin)
A-Atypicals (faulty cell wall and love to live intracellularily); mycoplasma and chalmydia it is better to use protein synthesis inhibitors
M-MRSA (use vancomycin)
E- enterococci (use amoxicllin or ampicillin)

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24
Q

What is the 4th gen cephalosporin?

A

B lactamase resistant

cefepime

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25
Q

What are the exceptions of cephalosporins that are not excreted by the kidney?

A

cefoparazone, ceftriaxone which are elimitated in the bile by liver metabolism which are more lipid soluable

cefoparazone cannot be used in meningitis but yet it is lipid soluable? wtf? -> for cefoparazone is too much of a good thing, you are highly protein bound when you are so highly lipid soluble and only a weak fraction crosses the BBB; too low concentrations achieved in the brain of your patient

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26
Q

What are the side effects of cephalosporins?

A
  1. hypersensitivity ( use macrolides instead !)
    always assume complete cross allergenicity between cephalosporins members
    only partial cross allergenicity between cephalosporins and penicillins

macrolides: gram +
aztreonam: only of it’s a gram - rod (Pseudomonas)

  1. GI distress, superinfection of C.diff
  2. Disulfiram like effect: cefoparazone
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27
Q

What is the mechanism of action of imipenem and meropenem?

A

similar to penicillins and cephalosporins
resistant to B-lactamases

empirical management of sepsis and meningitis

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28
Q

What bugs do imipenem and meropenem work on?

A

broad spectrum

most potent

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29
Q

What are two issues of imipenem that are not relevant of meropenem?

A

Imipenem:

  1. must be given with cilastatin coadministration- prevents patient’s kidneys from metabolizing the drug too quickly
  2. CNS effect: seizures ; half of patients will suffer when given imipenem;

these are not seen in meropenem

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30
Q

What are the side effects of imipenem and meropenem?

A
  1. GI distress. nephrotoxic
  2. drug fever-hypersensitivity
  3. CNS in imipenem
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31
Q

What is the mechanism of action of aztreonam?

A

same as penicillin and cephalosporins

resistant to B lactamses

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32
Q

What does aztreonam work against?

A

only active against gram - rods because the PBPs that it binds to are only found in the bacteria that are in the shape of a rod
no cross allergenicity with penicillins and cephalosporin

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33
Q

What is the mechanism of action of vancomycin?

A
  1. binds to D-ala D-ala muropentopeptide(different than binding to PBPs)
  2. blocks transglycosylation (elongation of peptidoglycan chains in the cell wall) it is not a process of crosslinking but a process of elongation
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34
Q

What do we use vancomycin for?

A

MRSA
enterococci- drink it because vancomycin is not absorbed well in the gut
2nd line agent for C.diff (metronidazole is first line)

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35
Q

Which drug blocks the P site on the ribosome to inhibit protein synthesis and prevent tRNA from binding to form the initiating complex?

A

The P site is the site of initiating protein synthesis; it is here the tRNA carries the first amino acid

it is inhibited by Aminoglycosides (class 1 of protein sythesis inhibitors)

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36
Q

Which drug binds to the A site on the ribosome to prevent elongation? (binding of tRNA to the A site to bring in the next aa to be incorporated into the protein)

A

Tetracycline binds to the 30S on the A binding site on the ribosome

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37
Q

Which drug inhibits peptidyl transferase to make the peptide bond?

A

Chloramphenicol

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38
Q

Which drug inhibits translocation of the ribosome (last step in protein synthesis)?

A

Macrolides and clindomycin

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39
Q

Are there any drugs that inhibit the incorporation of a stop codon? UGA UAA UAG?

A

No

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40
Q

How does Aminoglycoside work?

A

Prevents formation of the initiation complex by binding to the 30S subunit; linezolid also does this but it binds to the 50S subunit
only aminoglycoside causes misreading of the codon and incorporation of the wrong amino acid; this is why they are bactericidal whereas other protein synthesis inhibitors will be BS

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41
Q

How does Tetracycline work?

A

Prevents elongation by binding to the 30S subunit; and inhibiting amino acid incorporation at the A site
Dalfopristin/quinupristin also this way at the 50S subunit

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42
Q

What is Linezolid used for?

A

VRSE, VRE; alternatives are Dalfopristin/quinupristin

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43
Q

How does Chloramphenicol work?

A

Blocks peptidyl transferase at the 50S subunit

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44
Q

How do Macrolides and Clindomycin work?

A

Bind to ribosomal RNA at the 50S subunit and inhibit translocation

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45
Q

What is the mode of resistance to aminoglycosides?

A

need to get into bacteria to block protein synthesis by using O2 dependent uptake; anaerobes are resistant to aminoglycosides (chlostidium, actinomyces)

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46
Q

What do aminoglycosides work well on?

A

Gram - rods; used in combo with cell wall synthesis inhibitors such as penicillin and cephalosporin
Gram- : Pseudomonas Aeruginosa
Gram+: Enterococci

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47
Q

What are examples of aminoglycosides?

A

neomycin, amikacin, gentamicin, tobramycin, streptomycin

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48
Q

What is used for TB and bubonic plague?

A

streptomycin

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49
Q

What are the kinetics of aminoglycosides?

A

it is a sugar, so it is water soluble so it is polar and is metabolized through the kidney

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50
Q

What are the side effects of aminoglycosides?

A
  1. nephrotoxicity
  2. ototoxicity and deafness
  3. cause neuromuscular blockade-> decreased Ach release ; similar to botox toxin
  4. contact dermatitis in neomycin
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51
Q

What is the mode of resistance to aminoglycosides?

A

by bacterias producing conjugating enzymes; this production of enzymes causes the aminoglycosides to be eliminated faster and they cannot interact with the bacterias

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52
Q

How to tetracyclines work?

A

BS; prevent elongation at the 30S subunit

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53
Q

What do tetracyclines work against?

A

Atypical bacteria: Chlamydia, Mycoplasma
H.pylori in Gi ulcers
Ricketssia, Borellia, Brucella, Vibrio
doxycycline is the drug of choice in lyme disease

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54
Q

What are the tetracyclines?

A

demeclocycline(blocks ADH receptors- causes nephrogenic diabetes insipidus in those who use it) , minocycline (water soluble to interfere with bugs involved in gingivitis), doxycycline, tetracycline

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55
Q

What are the pharmokinetics for tetracycline?

A

kidney, doxycycline is more lipid soluble so it goes through the liver
chealation: chemicals that bind to ions such as Ca, Mg, and others that have positive charges; these drugs don’t get absorbed because they become ionized so don’t take tetracyclines with food
once in the body tetracycline looks for Ca to bind to; once in bone and teeth it is not an antibiotic anymore;

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56
Q

What are side effects of tetracyclines?

A
  1. tooth enamel dysplasia
  2. growth retardation in children
    CI: in children and pregnancy (teratogenic); would decrease bone formation
    3.phototoxic
  3. vestibular disfunction of balance in minocycline
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57
Q

What are three groups of drugs known for their phototoxicity?

A

Tetracyclines, Sulfonamides, Flouroquinolones

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58
Q

What is the mode of resistance to a tetracycline?

A

bacteria produce efflux pumps that push that drug outside of the cell; P-glycoprotein pumps tend to result in multi drug resistance

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59
Q

What is the mechanism of chloramphenicol?

A

Crosses BBB, liver metabolized, phenol rings confer lipid solubility of the drug;
BS drug that prevents peptidyltransferase
wide spectrum: sepsis, meningitis , H.influenzae meningitis

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60
Q

What are the side effects of chloramphenicol?

A
  1. dose dependent BMS; similar effects to anti cancer drugs which decreases WBC when you have an infection
  2. Gray Baby syndrome ; also displaces bilirubin from binding sites resulting in kernicterus
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61
Q

What are the modes of resistance to chloramphenicol?

A

changes of the bacterial peptidyltransferase

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62
Q

What is the mechanism of macrolides?

A

they inhibit cyP450 at 50S that block translocation

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63
Q

What are the macrolides used against?

A

Gram + cocci (not MRSA),
**Atypicals (chlamydia, mycoplasma,ureaplasma)
Legionella
Campylobacter jejuni
Mycobacterium avium intracellulare ( HIV patients)

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64
Q

What are the names of the macrolides? “THRO”

A

erythromycin, clarithromycin, azithromycin( more water soluble than others, and more safe in pregnancy), telithromycin

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65
Q

What are the primary side effects of macrolides?

A
  1. GI imbalances ( can stimulate motilin receptor; gut peptide that stimulates peristalsis)
  2. reversible deafness at high doses-ototoxic
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66
Q

What is so special about telithromycin?

A

very important for macrolide resistant strep. pneumoniae

lobar pneumoniae, meningitis, otitis media

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67
Q

What is the mode of resistance to macrolides?

A

The 50S is made of ribosomal RNA, the bases in ribosomal RNA get methylated by the bug, so the bacteria is making methyltransferases;
by methylating the rRNA the macrolides cannot recognize the binding sites

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68
Q

What is the mechanism of clindamycin?

A

blocks translocation, not a macrolide
Gram+ : Staph A.
anaerobic flora: bacteriodes fargilis, aspiration pneumoniaes
loves to go into the bone, and it is remains active in the bone
main cause of osteomyelitis is staph A-use clindamycin

on gram -ve bone infection: quinolones

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69
Q

What is a side effect of clindamycin?

A

Pseudomembranous colitis caused by C.diff,

use metronidazole to treat it, vancomycin as a backup

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70
Q

What is the mode of resistance to clindamycin?

A

It is the same as for macrolides;

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71
Q

What is the mechanism of linezolid?

A

identical to aminoglycosides

very toxic, BMS , drops platelets and causes severe bleeding

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72
Q

What are the streptogranins?

A

quinupristin/dalfopristin ; works like tetracycline but from 50S site, used in VRSA and VRE

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73
Q

What are the inhibitors of folic acid synthesis?

A

sulfonamides, trimethoprim, pyrimethamine, cotrimoxazole

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74
Q

What enzyme that is not found in the human body (only found in bacteria) that inhibits dihydropteroate synthetase?

A

sulfonamides-first step in folic acid synthesis

dont have to worry about them causing an issue with folic acid in the human body

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75
Q

What inhibits dihydrofolate reductase? (We also have this enzyme in the human body)

A

trimethoprim, pyrimethamine

(dihdrofolate->tetrahydrofolate): they will be associated with anti cancer side effects such as methotrexate

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76
Q

What three drugs cause DHFR inhibition?

A

trimethoprim, pyrimethamine, methotrexate

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77
Q

How are the folic acid inhibitors used?

A

Used in combination with DHFR inhibitors for syngery to decrease resistance, using sulfonamide alone is useless

78
Q

What does the combo of trimethoprim-sulfamethoxazole work against? (Bactram)

A

UTIs, Nocardia, Listeria (back up to moxicilllin), Gram + and Gram -, E.Coli, Shigella, Salmonella, H. Influenzae
BC
used for both prophylaxis and treatment of HIV opportunistic infections such as Pneumocystis jiroveci

79
Q

What does the combo of pyramethamine-sulfadiazene work against?

A

Protozoa: T.gondii
prophylaxis and suppression of T.gondii (in HIV)
toxoplasma is responsible for brain abscesses in HIV patients (rings )

80
Q

What is the pharmokinetics of sulfonamides?

A

hepatically acetylated, conjugates are renally excreted
ironically , conjugation in the liver this time causes the drug to be less soluble than the parent drug, so it precipitates in the kidney causing renal stones
-very high plasma protein binding-> kernicterus in neonates
-E.coli is a big target of sulfonamides

81
Q

What are the side effects of sulfonamides?

A
  1. HS (Sulfur); causes exfoliative dermatitis; Steven Johnson syndrome
  2. Hemolysis in G6PD deficiency; due to oxidizing! or oxidative free radicals
  3. Phototoxicity
82
Q

What are the side effects of trimethoprim and pyrimethamine?

A
  1. BMS (anti cancer like)

2. Enterocolitis

83
Q

What are the direct inhibitors of nucleic acid synthesis?

A

Quinolones, rifampin

84
Q

What are the names of the quinolones? “OXACIN”

A

ciprofloxacin, norfloxacin, ofloxacin, levofloxacin, moxifloxacin

85
Q

What is the mechanism of action of quinolones?

A

BC drugs interfere with DNA synthesis by blocking replication; by blocking topoisomerases II (DNA gyrase) which regulates DNA supercoiling ; can relax supercoils; it can also introduce negative supercoils which open the DNA and gene expression
quinolones block these processes
they also interfere with topoisomeraseIV (prevents sister chromatid from getting twisted at G2 and M phase)

86
Q

What bacteria are quinolones useful against?

A

UTIs, chlamydia, gonorrhea,
skin, soft tissue, and bone infections by Gram - bacteria
Shigella, Salmonella, E.coli, Campylobacter

87
Q

What are the pharmokinetics of quinolones?

A

iron and calcium limit their absorption ( don’t take with food)
eliminated by the kindey
distribute well in integuments (tendons, bones, soft tissue)-Topoisomerases are also used in human cells

88
Q

What are the side effects of quinolones?

A
  1. GI distress
  2. Phototoxicity
  3. Never use in pregnancy or children who haven’t finished their growth; tendonitis with potential tendon rupture (Achille’s tendon)
  4. CNS- seizures
  5. can increase the QT interval
89
Q

What is the rule for mycobacterial infections?

A

large combination therapy

90
Q

What are the primary anti tubercular drugs?

A

isoniazid, rifampin, ethambutol, pyrazinamide

91
Q

What are the mechanisms of action and resistance of isoniazid?

A

inhibits mycolic acid synthesis (cell wall inhibitor)
prodrug: required activation by catalse
high level resistance occurs when there is deletion of the catalse gene ( zero effect of isoniazid)

Need to treat TB for up to a year

92
Q

What are the side effects of isoniazid?

A
  1. Hepatitis ( increase aminotransferases; AST, ALT); cofactor of aminotransferases is vit B6
  2. B6 deficiency causing : neuritis(ammonia cannot be excreted without B6) and sideroblastic anemia
  3. SLE in slow acetylators
  4. percicpiates the G6P deficient patient into acute hemolysis
93
Q

What is the mechanism of action and resistance in rifampin?

A

inhibits DNA dependant RNA polymerase ( blocks transcription, nucleic acid synthesis inhibitor)
resistance is caused by changes in the enzyme

94
Q

What are the side effects of rifampin?

A
  1. Hepatitis
  2. Induction of P450
  3. Red-orange metabolites
95
Q

What is the mechanism of ethambutol?

A

cell wall synthesis inhibitor

96
Q

What are the side effects of ethambutol?

A
  1. Neurotoxicity: loss of green red colour
97
Q

What is the mechanism of action of pyrazinamide?

98
Q

What are the side effects of pyrazinamide?

A
  1. Hepatitis

2. Hyperuricemia

99
Q

What is the mechanism of streptomycin?

A

Protein synthesis inhibitor used as a second line treatment for TB
aminoglycoside

100
Q

What are the side effects of streptomycin?

A
  1. Deafness
  2. Ototoxicity: vestibular
  3. Neuromuscular blocker by decreasing Ach
101
Q

What is the main site of action of ‘‘fungins’’?

A

Inhibit synthesis of B-glucan which is part of the fungal cell wall

102
Q

Which drug works in the cell membrane?

A

polyenes: Amphotericin B and nystatin that interfere with ergosterol in the cell membrane

103
Q

Which group of drugs works on the ergosterol synthesis pathway itself?

A

Azoles: inhibit last step of ergosterol synthesis, 14A-demethylase
Terbinafine: inhibits squalene epoxidase

104
Q

What is the mechanism of action and mode of resistance of amphotericin B and nystatin?

A

interact with ergosterol; binds to ergosterol resulting in formation of pores in the fungal membrane causing FC activity
most resistance results from having low ergosterol content in the fungal membrane

105
Q

What does amphotericin B work against?

A

very potent and broad spectrum; very toxic
Aspergillus, Candida, Cryptococcus, Histoplasma, Mucor, Sporothrix
doesn’t cross BBB; but can administer intrathecally

106
Q

What is the mechanism of action of nystatin?

A

too toxic for systemic use so only used topically

Swish and swallow technique used for people that have oral and esophageal Candiditis; nystatin is not absorbed in the GI

107
Q

What are the side effects of amphotericin B?

A
  1. Infusion related: HS, a test dose is always advisable
  2. Dose dependent : nephrotoxicity; the most nephrotoxic drug
    use with flucytosine to minimize the toxicity; also use with lipsosomes to limit toxicity to help in the clearance and distribution of amphotericin B
108
Q

What is the mechanism of action and resistance of azoles?

A

FC; they block the synthesis of ergosterol; block 14A-demethylase
inhibit P450 enzyme; also interferes with our own steroid synthesis in humans;
resistance is due to P-glycoprotein efflux pumps

109
Q

What are the names of the azoles?

A

ketoconazle, fluconazole, itraconazole, voriconazole, clotrimazole, miconazole
all can be considered drug of choice in systemic fungal infections

110
Q

What are the uses of ketoconazole?

A

Paracoccidioides

backup for: Blastomyces, Histoplasma

111
Q

What are the uses of fluconazole?

A

used in immunosuppressed; Candida, Cryptococcus

only fluconazole crosses BBB

112
Q

What are the uses of itraconazole and voriconazole?

A

Aspergillus,

113
Q

What are the uses of clotrimazole and miconazole?

A

topically for Candida and dermatophyte infection

114
Q

What are the pharmokinetics of azoles?

A

orally; big advantage over amphotericin B
drug interactions: weak acids, antacids would decrease their absorption, eating helps with absorption ( more acid production with food)
inhibitors of P450

115
Q

What are the side effects of azoles?

A
  1. Decrease synthesis of steroids in humans; decrease levels of coritsol and testosterone; decrease libido and gynecomastia
  2. Drug interactions
116
Q

What is the mechanism of action of flucytosine?

A

Analog of cytosine; prodrug ->5FC
deaminated by a fungal deaminase to make 5FU

reistance develops by changing the deaminase

117
Q

What is the mechanism of 5FU ?

A

makes 5-Fd-UMP which inhibits thymidylate synthase; decrease in thymine affects DNA synthesis

resistance emerges rapidly when used alone; use with amphotericin B when you have severe Candidal or Cryptococcal infection

118
Q

What are the side effects of 5FU?

A
  1. Toxic bone marrow suppression
119
Q

What is the mechanism of action and side effects of Griseofulvin?

A

only active against dermatophytes; orally; only distributes where keratin is
disulfuram like reaction

120
Q

What is the mechanism of action and side effects of Terbinafine?

A

inhibits ergosterol synthesis, blocks squalene epoxidase against dermatophytes
Gi distress, rashes, hepatotoxicity

121
Q

What is the mechanism of caspofungin and micafungin?

A

cell wall synthesis inhibitors by blocking glucan synthesis
used primarily for invasive Candida and Aspergillus
HIV patients tolerate these drugs well!
GI side effects

122
Q

Which virus does enfuvirtide and maraviroc work on?

A

They work on HIV on the inital phases of the HIV infections of the cell

123
Q

Which drug is used for influenzae type of viruses?

A

amantadine

124
Q

Which drugs drugs work on preventing viral nucleic acid synthesis?

A

reverse transcriptase inhibitors, protease inhibitors, neuraminidase inhibitors(prophylaxis of influenzae)

125
Q

What is the mechanism of “ovir” drugs? ex: acyclovir

A

most of these drugs are prodrugs
require kinases to turn on since their nucleoside analogs
inserted into growing chain of RNA and DNA but they don’t have a 3’OH so they are chain terminators
work on DNA and RNA polymerases

126
Q

What is the mechanism of NNRTI and foscarnet?

A

block DNA and RNA polymerases but do not depend on kinsases to do their polymerase inhibition

127
Q

Which viruses contain TK (thymidine kinsase) to activate acyclovir?

A

HSV1, HSV2, VZV (narrow spectrum of activity)
nucleoside analogs can only work on replicating viruses (these viruses are dormant in the dorsal root ganglia but they can be reactivated during stress; if the virus is not replicating the drug cannot interfere with the virus)
so will never totally kill these viruses

128
Q

What are the side effects of acyclovir?

A
  1. required TK to be turned on, only in acively replicating cells, and these viruses don’t replicate in bone, so they are not hematotoxic
  2. IV acyclovir: to treat encephalitis so neurotoxicity is a side effect, nephrotoxicity
    make sure patient is hydrated
129
Q

What are newer analogs of acyclovir?

A

famciclovir and valacyclovir have a longer half life than acyclovir
never work on TK- strains because depend on TK to put on the first P

130
Q

What is the mechanism of ganciclovir? and drugs that aren’t acyclovir?

A

similar mechanism to acyclovir
the first Ption step may not always require a viral specific enzyme; once they are Pted anywhere in the human body and once they become nucleotide they will behave as anti cancer drugs and cause dose limiting hematotoxicity

131
Q

How does ganciclovir work in HSV and CMV?

A

thymydine kinase in HSV and VZV
but CMV doesn’t have TK it uses a UL97 which is a phosphotransferase to be turned on
it’ll find a kinase to do the job!

it inhibits viral DNA polymerases by being a chain terminator

132
Q

What are the side effects of ganciclovir?

A

f1. dose limiting BMS/hematotoxicity (like anti cancer drug) so it is used as prophylaxis and treatment of CMV (HIV patient)
2. mucositis (blisters in oral mucosa, gastroenteritis-similar to anti cancer drugs)
3. nephrotoxicity-maintain hydration in these patients

133
Q

What is the mechanism of resistance to ganciclovir?

A

similar to acyclovir;

having TK- strains or changes in TK

134
Q

What if you had an HIV patient who would not withstand ganciclovir because of bone marrow suppression?

A

because of immunosuppresion favouring opportunistic infection, we should use foscarnet;

135
Q

What is the mechanism of action of foscarnet?

A

it is not an anti metabolite so it is not a nucleoside analog; if it is not a nucleoside analog it blocks both RNA and DNA polymerases of viruses; it will never be inserted into the patients own DNA and not cause BMS; does not require TK

136
Q

What are the side effects of foscarnet?

A
  1. severely nephrotoxic that can cause acute tubular necrosis
  2. severe losses of Ca
  3. drug interaction with pentamidine (used to treat P.jiroveci; this drug doesn’t cause BMS) severe life threatening hypocalcemia when pentamidine and foscarnet are combined
137
Q

What is the main treatment of HIV infections?

A

reverse transcriptase inhibitors which are RNA dependent DNA polymerases; so these are nucleoside analogs exactly like acyclovir that get picked up by reverse transcriptase of HIV and block viral replication
(NRTIs)

138
Q

What are the 3 main properties of NRTIs?

A
  1. prodrugs: chain terminators; use nonspecific kinases to be turned on: BMS major issue
  2. used with protease inhibitors :synergy increases life expectancy, delays opportunistic infection occurance, increases CD4 count
  3. HAART: highly active anti retroviral therapy
139
Q

What are the 4 main points of NNRTIs?

A
  1. not prodrugs
  2. no myelosuppression
  3. synergistic with NRTIs and protease inhibitors
  4. nevirapine and efavirenz
140
Q

What is so special about the drug nevirapine? What are the side effects?

A

A single dose given at the time of delivery will decrease vertical transmission of HIV by 50% ! and this is as a single dose !

  1. induces P450 enzymes
  2. rash and hepatotoxicity (elevated liver enzymes)
141
Q

What is a major side effect of efavirenz?

A
  1. disrupts sleep cycle and dysphoric dreams ( aka nightmares)
142
Q

What is the mechanism of action of zidovudine? aka azidothymidine, ZDV, AZT

A

it is a chain terminator that is phosphorylated non specifically; it inhibits RT by competing with other T containing nucleotides and incorporates into viral DNA; this causes chain termination

143
Q

What is the mechanism of resistance to zidovudine?

A

Viral mutations in the gene that codes for RT

144
Q

What are the mechanisms of action to other NRTIs?

A

identical to zidovudine
all require metabolic activation to nucleotide forms that inhibit RT
only difference is what base analog they are that is inserted into the DNA

145
Q

What is the mechanism of resistance to NRTIs?

A

similar to zidovudine

there will never be complete cross resistance to NRTIs providing that they each represent different nucleotide analogs

146
Q

What are the side effects of zidovudine? AZT

A
  1. the most hematotoxic of all the NRTIs: major BMS
147
Q

What are the side effects of didanosine? DDI

A
  1. pancreatitis (major dose limiting side effect)

2. peripheral neuropathy

148
Q

What are the side effects of zalcitabine? DDC

A
  1. peripheral neuropathy (major dose limiting side effect)

2. pancreatitis

149
Q

What are the side effects of satvudine? D4T

A

T analog; so would compete with AZT (don’t combine similar nucleosides)
1. peripheral neuropathy ( major dose limiting )

150
Q

What are the side effects of lamivudine? 3TC

A
  1. least toxic and least potent of all of these drugs

active in hepatits B (only hepatitis virus that is a DNA virus)
emitricitabine is the newer form of lamivudine

151
Q

What are the names of the NRTIs? 7

A

zidovudine, stavudine, didanosine, tenofovir, lamivudine, emtricitabine, zalcitabine

152
Q

What are the names of NNRTIs? 3

A

nevirapine, delavirdine, efavirenz

153
Q

What are the names of PIs? (protease inhibitors)

A

ritonavir, saquinavir, indinavir, nelfinavir

154
Q

What is the mechanism of action of protease inhibitors? (PIs)

A

aspartate protease is the enzyme that is inhibited by PIs; (this is a viral enzyme that is needed to cleave the prodrug proteins in HIV and make the active ones)

this is similar to angiotensinagen being cleaved to angiotensin to make the active enzyme

155
Q

What is the mechanism of resistance to PIs?

A

point mutations in the gene of the aspartate protease enzyme

156
Q

What are the clinical uses of PIs?

A

indinavir and ritonavir are always used in combo with two NRTIs;
saquinavir is the least toxic HIV drug, most strains are resistant to it

157
Q

What are the side effects of PIs?

A
  1. nephrotoxicity: crystalluria with indinavir
  2. drug interactions: ritonavir, causes a nightmare when combined with other HIV drugs preventing opportunistic infections
  3. syndrome of disordered lipid and CHO metabolism causing central obesity and insulin resistance; this insulin resistance is less with atazanavir
158
Q

What are the names of the anti viral drugs used in the treatment of respiratory viral infections?

A

amantadine, oseltamovir, ribavirin, rimantadine, zanamivir

159
Q

What are the names of the anti viral drugs used in the treatment of hepatic viral infections?

A

interferon, lamirudine, adefovir, entecavir, telbivudine

160
Q

What are the anti viral drugs used in the treatment of herpes viral infections?

A

acyclovir, cidofovir, fomivirsen, foscarnet, ganciclovir, penciclovir and famciclovir

161
Q

What is the mechanism of action of amantadine? What are the side effects?

A

blocks attachment, penetration and uncoating of influenzae A virus
(these are the initial steps of the viral infection so they are only used in prophylaxis)

  1. atropine like peripheral effects
  2. livedo reticularis
162
Q

What are the mechanisms of action of zanamivir and oseltamivir? What are the side effects?

A

inhibit neuramidases of both influenzae A and B, prevents virus from leaving the cell and getting into the next cell
used for prophylaxis

ironically, the side effects are the same symptoms that the flu would give you
1. nasal irritation, fatigue, fever; which explains why very few people use these drugs

163
Q

What is the mechanism of action of ribavirin? What are the side effects?

A

rib: ribose-> nucleoside analog
inhibits viral RNA polymerase

  1. hematotoxic
164
Q

What is the only nucleoside analog devoid of hematotoxicity?

165
Q

What are the clinical uses in anti malarial therapy?

A

chloroquine work on red blood cell cycle

primaquine is used for the liver cycle

166
Q

What drugs are used in the treatment of malaria that is choloroquine resistant?

A

prophylaxis: mefloquine
treatment: quinine

167
Q

Which forms of malaria can be treated with just chloroquine ?

A

P. falciparum

P.malariae

168
Q

Which types of malaria should be treated with chloroquine + primaquine?

A

P. vivax
P. ovale
because these are the ones with relapses with dormant liver type

169
Q

What is the mechanism of action of artemether and artesunate (in chloroquine resistant forms of malaria)?

A

inhibit P.falciparum endoplasmic reticulum ATPase; which interferes with the metabolism of falciparum

170
Q

What are the side effects of the quinine family?

A
  1. muscarinic A antagonism; blurred vision, double vision, GI distress
  2. acute attack of hemolytic anemia if patient has G6P deficiency
171
Q

What are other antibiotics that cause a G6P deficient patient to go into an acute hemolytic attack?

A

sulfonamides

isoniaziid

172
Q

What are the drugs used for nemotode infections?

A

mebendazole; decreases glucose uptake in the worm preventing it from getting ATP; interferes with microtubular structure

pyrantel pamoate: nicotinic receptor agnoist that first results in muscle contraction thenparalysis; worm falls off the gut wall and gets excreted in the feces

173
Q

What are the drugs used in cestodes? (tapeworms)

A

praziquantel: increases Ca influx which causes spasm in the bug; vacuolization in the bug

may cause a little GI distress (evacuation of the normal parasite)

174
Q

Explain these two principles of anti cancer therapy:

  1. log kill hypothesis
  2. growth fraction
  3. cell cycle specificity
A
  1. anti cancer drugs kill a fixed percentage of cancer cells; not a fixed number
  2. cytotoxic drugs are more effective against tissues that have a high growth fraction; aka cells that are rapidly dividing such as bone marrow, hair, and the GI tract
  3. anti cancer drugs work on specific phases of the cell cycle in tumors with a high growth fraction; leukemia and lymphoma
    non cell cycle specific: both tumors with a high growth fraction and with a low growth fraction
175
Q

Which anti cancer drugs are S phase specific? aka Antimetabolite

A 
inhibit DNA synthesis
cytarabine (C)
6-mercaptopurine(P)
6-thioguanine(G)
methotrexate: inhibits DHFR
hydroxyurea
etoposide
5-FU (U)
176
Q

Which drug works in the G2 phase?

177
Q

Which drugs are M phase specific?

A

these are microtuble inhibitors that inhibit mitosis
vinblastine
vincristine
these above drugs inhibit polymerization of the micotubles

paclitaxel inhibits the depolymerization of the microtubules

178
Q

What drugs are non cell cycle specific? Go phase

A

Alkylating agents
Antitumor agents ( except bleomycin)
Nitrosureas (lomustine, carmustine): glioblastomas
Cisplatin

179
Q

What is the mechanism, use and side effects of cyclophosphamide?

A

alkylating agent: active form attacks guanine N7 dysfunctional DNA

non-Hodgkin, ovarian, breast cancer, neuroblastoma

BMS, mucositis, hemorrhagic cystitis (mesna traps acrolein which is protective)
acrolein is the toxic metabolite of cyclophosphamide

180
Q

What is the mechanism, use and side effects of cisplatin?

A

alkylating agent: cross links DNA strands

testicular, ovarian, bladder, lung cancer

doesn’t cause BMS, worst for nausea and vomiting
use ondansetron as an antiemetic
nephrotixic: use amifostine to protect the kidneys

181
Q

What is the mechanism, use and side effects of procarbazine?

A

alkylating agent:

Hodgkin

BMS, can cause secondary leukemia

182
Q

What is the mechanism, use and side effects of doxorubicin?

A

antibiotic: forms free radicals that cannot be detoxified in the cancer cells ( or the heart)

Hodgkin, breast, endometrial, lung, ovarian cancer

delayed CHF (dexrazoxane is the antidote)

183
Q

What is the mechanism and side effects of methotrexate?

A

antimetabolite: inhibits DHFR

BMS, mucositis, crystalluria
use leucovorin(folinic acid) to help rescue your own bone marrow
184
Q

What is the mechanism and side effects of 5-Fluorouracil?

A

Pyrimidine antimetabolite: inhibits thymidylate synthase

can be taken topically for BCC

BMS

185
Q

What is the mechanism and side effects of 6-Mercaptopurine?

A

Purine antimetabolite: activated by HGPF transferase
metabolized by XO and so is allopurinol; so co-administration or allopurinol and 6-mercaptopurine will cause increased plasma levels 6-mercaptopurine

186
Q

What is the mechanism and side effects of bleomycin?

A

complexes with Fe and O2: DNA scission

not BMS; pulmonary fibrosis

187
Q

What is the mechanism and side effects of vinblastine and vincristine?

A

Block microtubular polymerization

vinblastine: BMS
vincristine: neurotoxicity

188
Q

Which drugs do not cause BMS?

A

cisplatin
bleomycin
vincristine

189
Q

What is the mechanism of resistance to etoposide, methotrexate, vinca alkaloids?

A

decreased binding affinity to target enzymes; modify binding site on the topoisomerase II enzyme

190
Q

What is the mechanism of resistance methotrexate, alkylating agents, and dactinomycin?

A

increased P-glycoprotein efflux pumps resulting in decreased drug accumulation

antibiotics/anti cancer (1 decks)

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