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Fall17-Pharmacology > Block 4 > Flashcards

Block 4 Flashcards

1
Q

What is MIC?

A

Minimum inhibitory concentration

This is the lowest concentration of antibiotic that inhibits bacterial growth after 24 hours in a specific growth medium - if you remove the antibiotic the organism will grow

*stops replication but does NOT kill it

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2
Q

What is MBC?

A

Minimum bactricidal concentration

Lowest concentration of antibiotic that prevents growth on an antibiotic free subculture - kills 99.9% of bacteria

After replated on anti-biotic free medium, there is no growth - bacteria are dead

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3
Q

What is the basic principle of routine antibiotic testing?

A

Start with narrow spectrum drugs, if nothing dies, then move broader and broader

Narrow to broad

*when TREATING, go broad to narrow

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4
Q

What are bactericidal antibiotics?

A

Most antibiotics are bactericidal

Kills bacteria

Effective in innummocompromised individuals

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5
Q

What are bacteristatic antibiotics? Also give their names

A

Inhibit the growth of organisms but do NOT kill them

You need a very good immune system

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6
Q

What is antibiotic synergy? What are 2 examples of this?

A

When 2 antibiotics are given together provide a greater outcome than either of them alone

Ex. Aminoglycosides + Penicillins
Ampicillin + Gentamicin
Ex. TMP + SMX
Trimethoprim + Sulfonamide

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7
Q

In immunocompetent individuals, what is the infectious agent?

A

External

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8
Q

In immunocompromised individuals, what is the infectious agent?

A

Internal

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9
Q

What are the 3 drugs that do NOT need to be adjusted in renal failure? Why?

A

They are excreted by liver routes instead of kidneys

Ceftriaxone
Doxycycline
Metronidazole

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10
Q

What are the 4 types of beta-Lactams?

A

Penicillins
Cephalosporins
Cabapenems
Aztreonam (monobactam)

They all have a four member ring

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11
Q

What are the 2 cell wall drugs that are NON beta lactams?

A

Vancomycin

Bacitracin

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12
Q

What are BLIs? Beta lactamase inhibitors

A

They allow the beta lactam antibiotics to remain alive and kill the bacteria

Without them, bacteria produce beta lactamase which cleaves the ring structure and inactivates beta lactam drugs

Clavulanic acid

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13
Q

What is the name of the natural penicillin?

A

Penicillin G

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14
Q

What is the anitstaphylococcal penicillin?

A

Nafcillin

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15
Q

What is the amino penicillin?

A

Amoxicillin

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16
Q

What is the antipseudomonal penicillin?

A

Piperacillin

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17
Q

What is the MOA of penicillins?

A

Bactericidal

Inactivate penicillin binding proteins (PBPs) involved in the synthesis of the bacterial cell wall

Pens block the transpeptidase reaction to prevent the crosslinks essential for cell wall integrity

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18
Q

What are PBPs?

A

They are transpeptidase enzymes

They catalyze cross-linkages between the peptidoglycan chains

Blocked by penicillins to prevent the cross linking for cell wall integrity

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19
Q

Is the transpeptidase the earlier step or the later step in cell wall synthesis?

A

Later!

This is the gluing and strengthening phase

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20
Q

What is the earlier step in cell wall synthesis? What drug targets this?

A

Transglycosylase - laying down components for cell wall

Vancomycin

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21
Q

What in gram negative bacteria do drugs use to enter?

A

Porins!

This is how Gram - bacteria build resistance

They modify their porins so the drugs can no longer enter

Gram positives don’t have an outer membrane so they don’t have porins

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22
Q

What is the only type of bacteria that vancomysin can kill?

A

Gram +

B/c it is too big to enter the gram - porins

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23
Q

What are the only beta lactam drugs NOT cleaved by beta lactamase enzyme?

A

Antistaphs - Nafcillin

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24
Q

What is the MOA of beta lactamase inhibitors? What is the the BLI called?

A

Irreversibly binds to beta lactamase enzyme so it can’t degrade the drug

Clavulanic acid

*synergy with amoxicillin

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25
Q

How do bacteria build a resistance to penicillins?

A

Naturally - if they lack a cell wall

Acquired - transfer of beta lactamase to bacteria

  • decrease porin size so drug can’t reach PBPs
  • modify PBPs so drug can’t bind
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26
Q

What are the side effects of penicillins?

A

Hypersensitivity - MOST important - rash, anaphylaxis
*may have cross-allergic reactions that occur from all beta lactam drugs due to similar structure

GI issues - diarrhea

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27
Q

What are the penicillins from most narrow to most broad?

A

Antistaphs - nafcillin
Pen G
Aminopens - Amoxicillin
Antipseudomonals - Piperacillin

*all pens kill gram + but as you go down the list add more and more gram -

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28
Q

What are cephalosporins?

A

Very similar to penicillins

Have the same MOA but are slightly more resistant to degradation by beta lactamases

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29
Q

What is the 1st generation cephalosporin?

A

Cephalexin

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30
Q

What is the 2nd generation cephalosporin?

A

Cefaclor

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31
Q

What is the 3rd generation cephalosporin?

A

Cefotaxime

Ceftriaxone

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32
Q

What is the 4th generation cephalosporin?

A

Cefepime

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33
Q

What is the 5th/other generation cephalosporin?

A

Ceftaroline

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34
Q

What is the MOA for cephalosporins?

A 
Bactericidal
Inactivate PBPs (transpeptidase) to prevent crosslinkage formation
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35
Q

What generation of cephalosporins is the only one to adequately get into the CSF?

A

3rd generation!

Think meningitis treatment

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36
Q

What is a contraindication for meningitis and ceftriaxone?

A

Can’t use ceftriaxone in neonates! May cause biliary obstruction

Use cefotaxime instead

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37
Q

What are side effects to cephalosporins?

A

Hypersensitivity - a lot off cross allergies with pens

*if people have a mild rash to pens, try cephalosporins but if they have anaphylaxis to pens, avoid all beta lactams altogether

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38
Q

What is the only cephalosporin that can kill MRSA?

A

Ceftaroline! 5th gen/other

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39
Q

Which cephalosporin is used for surgical prophylaxis?

A

1st generation - cephalexin

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40
Q

Which cephalosporin is used for surgical prophysix of anaerobes such as bacteroides?

A

1nd gen - cefaclor

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41
Q

Which cephalosporin is used for meningitis or gonorrhea?

A

3rd gen - cefotaxime, ceftriaxone (if not neonate)

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42
Q

Which cephalosporin is used for hospital acquired infections but is overkill for community acquired infections?

A

4th gen - cefepime

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43
Q

Which ceph is best for Gram +, which is best for Gram -?

A

1st is best for +

4th is best for -

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44
Q

What is the carbapenem?

A

Imipenem

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45
Q

What is side effects of imipenem?

A

Hypersensitivity and seizures in patients with renal dysfunction - if kidney function goes down and you don’t adjust dose this could also happen

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46
Q

What is the MOA of carbapenems?

A

Broadest spectrum Beta lactam - kill almost everything

Same as penicillins - binds to PBPs

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47
Q

What does imipenem need to be combined wiht?

A

Cilastatin - it protects imipenem from being cleaved and forming a nephrotoxic metabolite

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48
Q

What are monobactams?

A

Aztreonam

It only has one ring which means no cross allergies with penicillins! *key difference

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49
Q

What is MOA for Monobactams?

A

Same as other beta lactams

Resistant to most beta lactamases

Binds to PBPs

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50
Q

What is the other cell wall drug that is NOT a beta lactam?

A

Vancomycin

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51
Q

What is the MOA for vancomycin?

A

Prevents peptidoglycan elongation by binding to D-Ala-D-Ala terminal and inhibiting transglycosylase

Earlier step than beta lactams

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52
Q

What is the use for vancomycin?

A

Drug of choice for hospital acquired MRSA

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53
Q

What are vancomycin side effects?

A

Red man syndrome - histamine mediated flushing of face, neck and upper torso and hypotension

NOT an allergy just infused too quickly - must infuse for at least 1 hour

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54
Q

What is bacitracin?f

A

Similar to vancomycin but used topically for gram + bacteria

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55
Q

What are polymixyins?

A

Used topically for gram - bacteria

Combined with bacitracin for Neosporin

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56
Q

This is the smaller subunit of the ribosome?

A

30s

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57
Q

This is the larger subunit of the ribosome?

A

50S

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58
Q

What are tetracyclines? What is the drug name?

A

Consist of 4 fused rings

Doxycycline

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59
Q

What is the MOA for tetracyclines?

A

BacterioSTATIC

Bind to 30S subunit, block access of tRNA to ribosome at the A site - so it stops the docking step

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60
Q

What is the use for tetracyclines?

A

Broad spectrum antibiotics

Drug of choice for rickettsia (rocky Mtn spotted fever) and borrelia (Lyme disease) - from ticks

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61
Q

How is resistance accomplished by tetracyclines?

A

Mg++ dependent active efflux of the drug by the protein TetA

Bacteria have a pump that gets rid of the drug as soon as it gets in

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62
Q

What should you avoid when taking tetracyclines?

A

Dairy and antacids

B/c tetracyclines chelate with metals (Ca+, mg+, and aluminum)

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63
Q

What are side effects of tetracyclines?

A

Gastric discomfort

Effects of calcified tissue - drugs go where there is lots of Ca+ - may stunt growth in children

Photoxicity - rash to sun exposed skin

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64
Q

What is the aminoglycoside drug?

A

Gentamicin

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65
Q

What is the MOA for amiinoglycosides?

A

Bactericidal

Enter cell with oxygen transporter - NEED oxygen to work

Binds to 30s to interfere with initiation complex - causes misreading of code - inhibits translocation of tRNA from A site to P site

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66
Q

What is the use for aminoglycosides?

A

Against gram - bacteria

Synergy with penicillins!

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67
Q

What is the resistance of aminoglycosides?

A

Enzyme mediated inactivation of the drug

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68
Q

What are the side effects of aminoglycosides?

A

Nephrotoxicity - mild renal impairment to severe with therapy longer than 5 days

Ototoxicity - balance and hearing issues after 5 days
*particular issue with patient also receiving loop diuretics (furosemide)

Neuromuscular paralysis - occurs only at very high doses and can cause respiratory paralysis - blocks ACh release like Botox

Very toxic - basically never use alone anymore, just for synergy

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69
Q

What are the 2 30 S drugs?

A

Tetracyclines (doxycycline)

Aminoglycosides (gentamicin)

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70
Q

What are the 2 50S drugs?

A

Macrolides (erythromycin, clarithromycin, azithromycin)

Clindamycin

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71
Q

What are the 3 macrolides?

A

Erythromycin
Clarithromycin
Azithromycin

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72
Q

What is the MOA for macrolides?

A

BacterioSTATIC

Bind to 50S to inhibit translocation (no A site to P site movement of tRNA)

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73
Q

What are some uses for macrolides?

A

For patients with allergies to beta lactams

Community acquired pneumonia and legionella, chlalmydophila, and mycoplasma

Mycobacterium Avium (aka MAC)

Chlamydia trachomatis - STD

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74
Q

How is resistance built to macrolides?

A

Binding site has been methylated

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75
Q

Side effects of macrolides?

A

GI distress - actually commonly used to increase GI motility in diabetics (gastroparesis) by stimulating motilin receptors

Teratogenic

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76
Q

Which macrolides are P450 inhibitors?

A

Erythromycin and clarithromycin

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77
Q

Which is the most popular macrolides?

A

Azithromycin

Does NOT affect P450 and doesn’t have any drug interactions

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78
Q

What is the MOA for clindamycin?

A

Binds to 50s and inhibits translocation

Use for bacteroides

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79
Q

What are the side effects of clindamycin?

A

Superinfection of C. Difficile - causes pseudomembranous colitis - signs include fever, cramping, abdominal pain, and diarrhea

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80
Q

What are antifolates?

A

Disrupt the synthesis of purine and pyrimidines

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81
Q

What are the 2 antifolate drugs?

A

Sulfonamides

TMP-SMX

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82
Q

What is the MOA for sulfonamides?

A

BacterioSTATIC

Compete with PABA for dihydropteroate synthase (early step) to prevent bacterial folic acid synthesis

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83
Q

What is the use for sulfonamides?

A

Generally limited but topically in the eye for conjunctivitis and infections of the cornea

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84
Q

How is resistance built to sulfonamides?

A

Increase PABA synthesis to try to out compete antifolate drugs

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85
Q

What are the side effects to sulfonamides?

A

Hypersensitivity - rash, angioedema, Stevens-Johnson syndrome (bleeding and crusty lips)

Cross allergies with diuretics

86
Q

What is the MOA of Trimethoprim alone?

A

Competitively inhibits dihydrofolate reductase (later step)

87
Q

What is the MOA of TMP/SMX?

A

Inhibits dihydrofolate reductase and works synergistically to prevent the formation of tetrahydofolic acid

88
Q

What is the clinical use of TMP/SMX?

A

Uncomplicated UTIs!!

Also community acquired MRSA
Pneumocystis jiroveci pneumonia (PCP)

89
Q

What are side affects to TMP-SMX?

A

Bone marrow suppression - can’t make DNA without folate
-commonly seen as anemia

Allergic skin reaction in elderly and HIV patients

90
Q

What are the 2 misc/DNA antibiotics?

A

Metronidazole

Fluoroquinoles

91
Q

What is the MOA for metronidazole?

A

Prodrug metabolized by ferredoxin that interacts with DNA once in active form

Bactericidal

92
Q

What is the use for metronidazole?

A

Anaerobes and parasites

Bacteroides
Clostridium
Trachomonas
Entamoeba 
Giardia
Gardnerella
93
Q

What are side effects of metronidazole?

A

Gi upset
Metallic taste in mouth
Disulfiram effect if taken with alcohol - very sick blocks alcohol metabolism - hangover symptoms

94
Q

What is the MOA for fluoroquinolones?

A

Gram - organisms

Inhibits DNA gyrase so there is no relaxation of supercoils

Binds to both enzyme and DNA to prevent

Bactericidal

95
Q

What are the uses for fluroroquinolones?

A

Gram - infections

Kill most gram -

3rd and 4th gen kill gram +

96
Q

What are the generations of fluoroquinolones?

A

2nd - ciprofloxacin
3rd - levofloxacin
4th - gemifloxacin

97
Q

What infections do we use fluoroquinolones for?

A

UTIs - most common alternative to TMP-SMX
Gram - infections
Community acquired pneumonia (3rd and 4th gen only)

98
Q

What is the resistance to FQs?

A

Mutation of bacterial DNA gyrase

99
Q

Side effects of FQs?

A

Tendinitis and tendon rupture

Phototoxicity

Avoid interactions with antacids (Mg/Al) or iron and zinc due to chelation

100
Q

What is another option for UTIs?

A

Nitrofuantoin

101
Q

What is the MOA for Nitrofuantoin?

A

Prodrug metabolized to a form that I hits various enzymes and damages DNA

Bactericidal

No resistance

Turns urine brown and causes GI upset, and pulmonary effects with chronic treatment

102
Q

What are common targets for drugs in HIV?

A

Stopping the entry of virus - fusion inhibitors

Stopping the enzyme of the virus - reverse transcriptase inhibitors, integrate inhibitors

Stopping the budding of new parts of the HIV virus - protease inhibitors

103
Q

What is a nucleotide?

A

DNA base plus a sugar and 3 phosphates

104
Q

What is a nucleoside?

A

DNA base plus a sugar with no phosphates

105
Q

What are the Nucleoside Reverse transcriptase inhibitors (NRTIs) drugs?

A

Zidovudine
Lamivudine
Emtricitabine

106
Q

What is the MOA for NRTIs?

A

Must be phosphorylated to the 5’ by the HOST kinases

The active phosphorylated form terminated DNA elongation and competes with natural deoxynucleotides for reverse transcriptase

107
Q

What are side effects of NRTIs?

A

Bone marrow suppression (zidovudine)

The other 2 are the least toxic NRTIs

*always use 2 NRTIs together but can’t use lamivudine and emtricitabine together b/c they are both built off cytosine and they will compete against each other

108
Q

What are nucleotide reverse transcriptase inhibitors (NtRTI)?

A

Tenofovir (TDF)

109
Q

What is the MOA of NtRTI?

A

Has a single phophate and must be furhter phosphorylated to the active form

Use - in combat with NRTI

110
Q

What are the side effects of NtRTI?

A

None - well tolerated

Preferred combination is tenofovir coformulated with emtricitabine due to overall efficacy, low toxicity and convenience

111
Q

What is the NNRTI drug?

A

Efavirenz

112
Q

What is the MOA of NNRTIs?

A

These are already active, NOT a prodrug

Binds to reverse transcriptase at an allosteric site to inhibit it resulting in inactivation of the enzyme

113
Q

What are side effects of NNRTIs?

A

CNS effects (vivid dreams)

114
Q

What are PIs? What is the drug?

A

Protease inhibitors

Ritonavir

115
Q

What is the MOA of PIs?

A

Inhibit HIV protease which is an enzyme that produces mature infectious virions

116
Q

What are the side effects of PIs?

A

Lipid and carb metabolism issues causes central adiposity (fat distribution around waist) and insulin resistance (hyperglycemia)

They are p450 inhibitors! Other drugs work better at a lower dose b/c it blocks metabolism

117
Q

What are the 2 fusion inhibitors?

A

Enfuvirtide

Maraviroc

118
Q

What is the MOA of enfuvirtide?

A

Blocks gp41 protein on t-cell surface to prevent viral entry

119
Q

What is MOA of maraviroc?

A

Blocks CCR5 protein on t-cell surface to prevent viral entry

120
Q

What is the integrase inhibitor drug?

A

Raltegravir

121
Q

What is the MOA of raltegravir?

A

Inhibits the HIV integrase enzyme which normally integrates the viral genetic material into human chromosomes

122
Q

What is the treatment strategy for someone with HIV?

A

2 NRTIs + 1-2 PIs OR 1 NNRTI OR Raltegravir

123
Q

What is the treatment strategy for someone who does NOT have HIV but are at high-risk for exposure to it?

A

Combo of Tenofovir + Emtricitabine

124
Q

How are patients with HIV evaluated to see if therapy is working?

A

By monitoring CD4 counts at a 3 month intervals

125
Q

What kind of drug is Acyclovir?

A

Antiherpes drug

126
Q

What is the MOA for Acyclovir?

A

It is a prodrug - it needs 3 phosphates to become active

1 phosphate comes from herpes virus via thymidine kinase

2 phosphates must come from host

*compare to HIV, all 3 must come from host

127
Q

What does it mean if the herpes virus is a TK negative strain?

A

It doesn’t have thymidine kinase which is the enzyme that provides the 1st phosphate

Most -ovir drugs will not work in TK neg strains!
-Cidofovir is the only one that will work in TK neg strains

128
Q

What is Cidofovir?

A

Herpes drug that is a prodrug but activated by all host phosphates!

It doesn’t get any from thymidine kinase

It is the only -ovir drug to work in TK- strains

129
Q

What is Ganciclovir?

A

Same as acyclovir but is used for Cytomegalovirus (CMV) retinitis

This only occurs in VERY immunosuppressed patients

130
Q

What are side effects of Ganciclovir?

A

Bone marrow suppression is major toxicity

131
Q

What is Foscarnet?

A

For herpes, CMV retinitis, acyclovir resistant herpes, herpes zoster

NOT a prodrug! NO phosphorylation

132
Q

What is the MOA of foscarnet?

A

Not a prodrug so needs no phosphates

Selectively inhibits the pyrophosphate binding site on virus DNA polymerase and reverse transcriptase

Also works in TK- strains of herpes

133
Q

What are side effects of Foscarnet?

A

Nephrotoxicity (targets kidneys)

134
Q

What is Oseltamivir used for?

A

Influenza A and B

135
Q

What is the MOA of oseltamivir?

A

Block neuraminidase to inhibit budding and release of virus from cells

136
Q

What is the most important drug used for Tuberculosis?

A

Isoniazid (INH)

Used ONLY for TB

137
Q

What is the MOA for Isoniazid (INH)?

A

Targets the enzyme that assembles the mycolic acids into the outer layer of the mycobacteria

138
Q

How is resistance built to isoniazid?

A

Due to deletion of the gene that encodes for catalase (enzyme that activates isoniazid)

It’s a prodrug activated by bacterial catalase

The organism just deletes the catalase gene so the drug never goes active

139
Q

What are side effects of isoniazid?

A 
Peripheral neuritis (pins and needles in arms and legs) 
-this is cured by giving Vit B6!

Hepatotoxicity caused by toxic metabolite

140
Q

What is the MOA of rifampin?

A

Inhibits bacterial DNA and RNA polymerase which blocks transcription

P450 inducer - metabolizes drugs faster so they are less effective

141
Q

What are side effects of Rifampin?

A

Urine and feces turn orange

Tears stain contact lenses orange

Acute renal failure, anemia

142
Q

What is pyrazinamide?

A

Used only for TB

MOA unknown

143
Q

What are side effects of TB?

A

Hyperuricemia

144
Q

What other drugs also cause hyperuricemia like pyrazinamide?

A

Loops and thiazide diuretics

They are weak acids competing with urticaria acid at the PCT

145
Q

What is Ethambutol used for?

A

Just for TB

146
Q

What are the side effects of Ethambutol?

A

Optic neuritis
Decreased VA
Retinal damage with prolonged use
Hyperuricemia

May also have red-green color blindness

147
Q

What is streptomycin used for in TB?

A

This is only a backup drug!

It is an aminoglycoside (30s) so it has major side effects

148
Q

What are the side effects of Streptomycin?

A

Ototoxicity
Nephrotoxicity
Neuromuscular paralysis

149
Q

What is the treatment regimen for TB?

A

Initiation phase: 4 drugs for 2 months
-isoniazid + rifampin + pyrazinamide + ethambutol

Continuation phase: 2 drugs for 4 months
-isoniazid + rifampin

150
Q

What is the prevention regimen for TB?

A

Isoniazid (first choice) taken for 9 months either daily or 2/week

Rifampin (alternative) taken for 4-9 months either daily or 2/week

*always only take one drug at a time

151
Q

What are the common drugs for treatment of MAC?

A

Rifabutin - most common for treatment

Also could use azithromycin or clarithromycin

152
Q

What is the MOA of rifabutin?

A

Inhibits DNA dependent RNA polymerase to block transcription

153
Q

What are the nematodes?

A

River blindness
Pinworm
Roundworm

154
Q

What is the most common helm in this infection in the US?

A

Enterobiasis (pinworms)

White worms visible in stool

155
Q

What is the 2nd most common parasite in the US?

A

Ascariasis (roundworms)

156
Q

What is the major cause of blindness in Africa?

A

Onchocerciasis (river blindness)

157
Q

What are the drugs for treatment of nematodes?

A

Albendazole
Mebendazole
Pyrantel pamoate
Ivermectin

158
Q

What is the MOA of albendazole and mebendazole?

A

Inhibition of microtubel synthesis and blockage of glucose uptake in the worm

It can’t undergo mitosis

159
Q

This is the drug of choice for Pinworms but also roundworms and hookworms?

A

Albendazole

Mebendazole

160
Q

What is the mechanism of pyrantel pamoate?

A

This stimulates the nicotinic receptors present at the neuromuscular junction resulting is spastic paralysis of the worm (works just like succinylcholine

161
Q

This is the drug of choice for roundworms, hookworms, and pinworms?

A

Pyrantel pamoate

162
Q

What is the MOA of Ivermectin?

A

GABA agonist to cause hyperpolarization of nerve and muscle cells and death of worm?

163
Q

This is the drug of choice for onchocerciasis (river blindness)?

A

Ivermectin

164
Q

What are the side effects of ivermectin?

A

Rashes and joint pain

Treat with antihistamines and NSAIDS

165
Q

What are trematodes?

A

Flukes

166
Q

What are cestodes?

A

Tapeworms

167
Q

What is the drug of choice for trematodes and cestodes? (Tapeworms and flukes)

A

Praziquantel

168
Q

What is the MOA of praziquantel?

A

Increases membrane permeability to Ca+ causing muscle contraction then paralysis of the worm

169
Q

What are superficial fungal infections?

A

Vuvovaginal candidiasis

Dermatophytoses (skin or nail)

170
Q

What are invasive fungal infections?

A

Cryptococcoisis (causes meningitis)
Candida
Aspergillus

171
Q

What is amphotericin B used for?

A

Very serious Systemic fungal infections

Cryptococcus neoformans (meningitis)

172
Q

What is the MOA of Amphotericin B?

A

Binds to ergosterol in fungal cell membrane to form pores causing it to leak and die

DONT use this drug unless very critical condition

173
Q

What are side effects of amphotericin B?

A

Very damaging to kidneys
Flushing and muscle spasms during IV infusion due to histamine (just like vancomycin)

Dose limiting decrease in GFR, renal tubular acidosis

Bone marrow suppression

174
Q

What is the MOA for Flucytosine (5-FC)?

A

It enters fungus, then is converted to 5-FU then to 5-FdUMP which inhibits thymidylate synthase and DNA synthesis - b/c cant make thymine

175
Q

What is the only time flucytosine is used?

A

Only in combination with Amphotericin B for cryptococcus neoformans!

176
Q

What is the only example of fungal synergy?

A

Amphotericin B and Flucytosine

177
Q

What are the -conazole antifungal drugs?

A

Fluconazole

Voriconazole

178
Q

What is the MOA for the -conazole drugs?

A

Inhibit the synthesis of ergosterol by blocking the enzyme C-14 alpha-demethylase (P450 enzyme)

179
Q

What are side effects of -conazole?

A

Drug interactions due to p450 inhibitor

Affects the synthesis of cortisol and androgens

180
Q

This is the drug of choice in esophageal, oral, and vaginal candiditis

Also used for cryptococcal meningitis
It is the only conazole to penetrate the CNS

A

Fluconazole

181
Q

This is the drug of choice for invasive aspergillosis and some fluconazole resistant organisms?

A

Voriconazole

182
Q

What is another name for the drug echinocandins?

A

Caspofungin

“-fungins”

183
Q

What is the MOA for caspofungin?

A

Inhibits the synthesis of beta 1,2 glucan which is a component of fungus cell walls

184
Q

What is caspofungin used for?

A

Candida and aspergillus

185
Q

What are side effects of caspofungin?

A

Fever, chills, rash, and flushing due to histamine release

186
Q

What are the 2 drugs for systemic superficial fungal infections?

A

Griseofulvin

Terbinafine

187
Q

What is the MOA for griseofulvin?

A

Old - very rarely used

Disrupts the mitotic spindle and inhibits mitosis

188
Q

What is the NOA of terbinafine?

A

This is the NEWER and more effective drug (compared to griseofulvin)

Inhibits the enzyme squalene epoxidase, which normally converts squalene to squalene expoxide. But without it, squalene accumulates and is toxic

This is the early step in ergosterol synthesis

189
Q

What is terbinafine used for?

A

Very effective in dermatophytic infections, specifically nail infections

190
Q

What is the most common target in fungal treatment?

A

Ergosterol

191
Q

Which drug is the early step in ergosterol synthesis? How does it work?

A

Terbinafine

It inhibits squalene eposidase

192
Q

Which drug is the late step in ergosterol synthesis? How does it work?

A

Fluconazole

Inhibits 14-alpha-demethylase

193
Q

Which drug binds directly to ergosterol to inhibit ergosterol synthesis?

A

Amphotericin B

194
Q

Which drug inhibits ergosterol synthesis but does it at the cell wall NOT the cell membrane?

A

Caspofungin

195
Q

What are the 2 types of malaria?

A

P. Falciparum (15% more serious)

P. Vivax (80%)

196
Q

What are the drugs for malaria treatment?

A

The -quins

197
Q

What is the MOA for chloroquine?

A

Blood schizonticide - intracellular heme accumulation is toxic to the parasite

198
Q

Chloroquine is the drug of choice for?

A

Only P. Vivax

199
Q

What are side effects of chloroquine?

A

Cinchonism - hearing and vision issues after prolonged use

200
Q

What is the MOA for quinine?

A

Blood schizonticide

201
Q

What is the use for quinine?

A

P. Falciparum

Usually given with doxycycline

202
Q

What are the side effects of quinine?

A

Cinchonism, blurred vision, tinnitus

203
Q

What is the use for mefloquine?

A

Only use this when you can’t use chloroquine or quinine

For p. Falciparum

204
Q

What is the MOA of primaquine?

A

This is the only TISSUE schizonticide

Forms quinine metabolites that cause oxidative stress

205
Q

What is primaquine used for?

A

Liver stages of P vivax

206
Q

What is the drug of choice for giardiasis?

A

Metronidazole

Prodrug activated by ferredoxin

Metallic tase in mouth, disulfiram like effects if taken with alcohol

207
Q

What protozoan causes giardiasis?

A

Giardia lamblia

208
Q

What Protozoa is amebiasis caused by?

A

E. Histolytica

209
Q

What is the drug of choice for e. Histolytica (amebiasis)?

A

Metronidazole

210
Q

What does the organism toxoplasma Gondii cause?

A

Toxoplasmosis

211
Q

What is the drug of choice for toxoplasmosis?

A

Pyrimethamine + sulfadiazine

Antifolate drugs - similar to TMP-SMX

Fall17-Pharmacology (4 decks)

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