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MDCM626 > EXAM > Flashcards

EXAM Flashcards

1
Q

Most conazoles?

Which one doesnt?

A
  • Lengthen QTc
  • But Isavuconazole shortens
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2
Q

Amphotericin B

Spectrum?

Cidal or static?

Toxicity?

A
  • Broad
  • Both
  • Very toxic
    • Nephrotoxic
    • Thrombophlebitis (vein clot causes inflammation)
    • Fever, shaking, chills, hypotension
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3
Q

Echinocandins

General special properties?

administration?

Metabolism and Excretion?

A
  • The target is so unique that you dont see toxicity with these drugs
  • Peptide makes it poorly bioavailable
  • Target mutations are common –>relapse is common
  • There are no drug interactions

INJECTION

  • Slow metabolism
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4
Q

Conazole

MOA

A
  • Block synthesis at a later step than Allylamines
  • Blocking P450 resposible for oxidating Lanosterol
  • This causes leakage
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5
Q

Pyrazinamide (PZN)

Static or cidal?

DMPK

MOA?

3 things

Toxicity?

Resistance?

A
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6
Q

Amphotericin spectrum?

A

Broad pretty much everything.

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7
Q

Second line agents cycloserine and p-aminosalicylic acid (PAS)

Cycloserine MOA, resistance, spectrum

Pamino- Inhibits?, Resistance?

A
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8
Q

Rifampin

Color?

Sensitive to?

MOA?

Static or Cidal?

Spectrum?

Resistance?

A
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9
Q

Second line Capreomycin

MOA

static or cidal?

Admin?

Resistance?

Toxicity?

A
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10
Q

First line treatment of TB needs to do what?

A
  • Block the synthesis of Mycolic Acid and arabinogalactans
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11
Q

WHat other interactions do conazoles have?

Oral bioavailability increases when?

A
  • P-glycoprotein transporters - Mostly the biggers ones
  • Increases with increase in acid (isaconazole and posaconazole)
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12
Q

Topical and Supository Conazoles?

A
  • Clotrimazole
  • Econazole
  • Butoconazole
  • Very lipophilic not good for systemic
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13
Q

Bedaquiline (TMC-207)

MOA?

Treatment?

A
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14
Q

Liposomal targeting of Fungal cell wall?

Selectivity

Role of Liposomes

Toxicities of AmBisome?

A
  • Mammalian have no cell wall
  • Attracts to the fungal cell wall - targeting agent
  • This makes the drug less nephrotoxic because there is less interaction, renal toxicity can still be seen
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15
Q

Echinocandins MOA?

A

Interferes with the synthesis of the fungal cell wall

blocks 1,3-B-glucan synthase that converts UDP-glucose to B-D glucan

Ruptures the cell wall

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16
Q

Major coverage and uses of echinocandins (fungins)

A
  • Narrow spectrum
  • Candidal infections that are resistant to azoles
  • Apergillus infections
  • Less common
    • Esophageal candidiasis
    • Prophylactically in patients undergoing hematopoietic stem cell transplant
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17
Q

Ethionamide

A
  • Similar MOA to INH (mycolic acid synthesis inhibition)
  • Only effective against mycobacterium
  • Resistance is fast
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18
Q

Amphotericin B

Binding to ergosterol?

A
  • Cation
  • Greasy portions bind to each other
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19
Q

Echinocandins resistance?

A
  • Mutation of synthase and/or upregulation of other cell wall components.
20
Q

Mechanism of action of PZN

A
  • Mechanism of action of pyrazinamide (PZA). PZA enters the bacilli by passive diffusion and is then converted by the nicotinamidase PncA into pyrazinoic acid (POA). POA exits the cell by passive diffusion, as well as by an efflux mechanism, which is not yet well characterized. In their revised mechanism, Zhang and co‐workers show that POA binds RpsA and blocks trans‐translation. Note: for simplicity, only the inner membrane of the mycobacterial cell envelope is depicted.
21
Q

INH is a ____ that gets converted by ____ then it can inhibit ___

Resistance is common with?

A
  • Prodrug that eventually gets coverted by KatG then it can inhibit INHa
  • Mutations in both of these sites pose problems
22
Q

What are the echinocandins

A

Caspofungin, Anidulafungin, Micafungin

They are all very similar dont need to know specifics within class

23
Q

Allylamines?
What do they do?

Cidal or static?

What is their problem?

A

Inhibit the conversion of squalene to squalene epoxide

Step in Sterol biosynthesis

Effectively block downstream conversion of lanosterol and ergosterol–> Malfunction

Static or cidal depends on the species

Causes build up of squalene

  1. Membrane tension, faulty membrane
  2. Build up of squalene

Problem very greasy not good systemically and first pass is an issue.

Not orally available mostly topical use

24
Q

WHat are the Non-Allylamines squalene epoxidase inhibitors?

A
  • Butenafine - Broader spectrum
  • Tolnaftate - Non-prescription preparations for decades.
  • Topically used greasy
25
Q

Isoniazide (INH)

DMPK: Administration?

Distributes on an empty?

Toxicity?

MOA?

Resistance?

A
26
Q

Conazole Resistance and Main interaction with drugs and P450?

A
  • Target modification and efflux - This whole thing occurs much more slowly than bacteria
  • Interaction with Heme of P450 and Azole nitrogen lone pair.
27
Q

Coverage of conazoles

Yeast (Candida)

Mold (Asperigillus, Fusarium, Zygomycetes)

A
  • Yeast all- Fluconazole, Itraconazole, Voriconazole, Posaconazole)
  • Asperigillus- Itra, Vori, Posa
  • Fusarium- Vori and Posa
  • Zygo- Posa
28
Q

How resistant is Restistant TB?

TB

MDR TB

Definition and second line

XDR TB

A
29
Q

Amphotericin B

Solubility?

What is it?

Preparation?

A

Polyene macrolide no bacteria effect

Amphoteric: Acidic carboxyl nd basic primary amino functional groups

Poor water solubility

Prep using emulsifying agents and liposomes

30
Q

Clinical properties of Rifampin

Usage

Prophylactic usage?

Toxicities?

Interactions?

A
31
Q

Name the Allylamines?

A

Naftifine

Terbinafine (topical and pill)- One example of one that can be used systemically

32
Q

What are the broad spectrum conazoles?

A

Vori, Isavu, Posa

33
Q

What is the general trend with conazoles in terms of spectrum?

A

Spectrum increases as you go from:

  • Fluconazole (No molds)
  • Itraconazole
  • Voriconazole
  • Isavuconazole
  • Posaconazole (Broad and best)
34
Q

Second line and alternative therapies for TB

A
  • Unique second line
    • Ethionamide, Cycloserine, PAS, Capremycin, Bedquiline
  • Antibiotic classes already discussed
    • FQs (levo, oflo, Moxi)
    • AGs (kanamycin, amikacin, streptomycin)
    • COmbo therapy needs (INH, Pyrazinamide, ethambutol)
35
Q

Difference between Human and Fungal cells

A

Sterol they have ergosterol instead of cholesterol

36
Q

Rifabutin and Rifaximin?

___ Macrolides?

Treatment of?

Rifaximin absorption admin, treats, alternative for?

A
37
Q

Standard TB Tx

TB exists in 3 portions:

Six month treatment (___)

7 points

Rationale for Therapeutic Combos

Multiple Targets?

Resistance

Toxicities

A
  • At cell wall mycolic acid and arabanogalactan layer, transcription and translation
  • High levels of resistance 3 to 4 durgs to overcome this
  • Puts stress on the liver
38
Q

TB drugs in development

A
39
Q

Ethambutol

Only used for?

Static or Cidal?

MOA?

Resistance?

DMPK?

Major Toxicity?

A
40
Q

Properties of Rifampin?

DMPK

Metabolism

Excretion?

A
41
Q

Conazoles

What do they do?

A

Ergosterol biosynth inhibitors

Azole group think inhbition of CYP450s

42
Q

Schematic Diagram of Mycobacterial Cell wall

Or at least the parts that are targeted for TB

8 parts

A
43
Q

Antifungal coverage chart

A
44
Q

Conazole P450 interactions

3 points to know?

Mechanism of Human P450 interactions?

A
  • All have 3A4
  • Voriconazole has the most
  • Isavu and Posa have the fewest
45
Q

Fungin Coverage?

A
  • Good with yeast but variable efficacy with everything else

MDCM626 (26 decks)

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