Pharmacology of Respiratory Disease Flashcards Preview

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Flashcards in Pharmacology of Respiratory Disease Deck (29):
1

Tx of blastomyces

Itraconazole or ketoconazole

NOT fluconazole or amphotericin

DO NOT combine with antacids...need low pH to dissolve the capsule

2

MOA of amphotericin

Inhibiton of ergosterol

3

Itraconazole MOA

Inhibition of lanosterol demthylase

4

Progression to meningeal dz

Itraconzaole shifted to amphotericin

5

Itera nad keto distribution

Both highly protein bound but fluconzole cors BBB readily

6

Pregnancy and azoles

p450s

steroid hormones

7

Coccidiomces

Amphotericin is the mainstay of tx

8

How would tx of coccidio be changed if student was also taking acyclovir

Kidney toxicity through two different mechansis ms

9

Aspergillosis

Voriconazole is new SOA compared to amphotericin

If pt is getting cyclophosphamide...then need to adjust dose because it could inhibt p450 and block activation of cyclo

10

If aspergilosis therapies fail

Then caspfungin (echinocandins) can be added to voriconazole

11

Tx of histo

Itraconzaole...can't use amphotericin if kidney problems

12

Fluconazole activity and pharm
Itraconzsole

Flu - yeasts yes, molds no...good CSF

Itra-
borader spectrum, poor availabiloty...good for histo...long T1/2

13

VOriconazole activity and pharm

Asp yes, mucor no

Side effects (vision, neuron, rash)

P450 sub and inhibitor

14

Itraconzole and ovoriconazole uptake

Effected by food

Flu - NOT

15

Mucor tx

Amphotericin B

Voriconazole and fluconoizole NOT

16

LP drugs

Isonizaid
Rifampin
Pyrazinamide
Ethambutol

Needs to be treated for about 6 months...this is because waxy coat that makes it difficult

17

Isonizaid

Prophylactially and for HIV infected patients

Interferes with synthesis of mycolic acid

Pro-drug converted by mycobacterial catalase (KatG)...adds specificty

18

Resistance to isonizid

Mutations to enoyl reductase

Mutations in KatG

Mutations in other virulence genes

19

PKs isoniazid

Well absorbed

Slow acetylation - dose adjusemnt reuirement in most white

If patients has slow acetylation, then you need to decrease the dose

20

Toxicity of ison

Neuritis, heptotoxicty

This could be problem in TB population because of alcohol problems/hepatitis

21

Rifmapin

Targets RNA polymerase

Resistance through mutations in the target

22

Rfimapin toxicty

Hepatotoxicty

Orange secretions and urine

23

Rifmapin interactions

P450 inducer

24

Pyrazinamide MOA

Unknown

Inhibits mycolic acid biosynthesis

Pro-drug converted by pyrazinamidase...mutations are resistacne

Hepatitis is main toxocity

25

Ethambutol MOA

UNknown...interferes with mito rep

Well-tolerated

Optic neuritis

26

Why is hepatoxocity important

Why is bacteirocidal for divding and bacteriostatic for dormant important

When to discontnue

IMportant if they have heptitis or other liver dz

Means tx means to be given longer bc over time some will break out

Side effects do not warrant disconitnuing

27

MDR resistance

Resitance to isoniazid and rifampin (poor adherence)

If MDR, then tx with pyrazinamide, ehtambutol, and ethionamide for 24 months

28

Ethionamide

Prodrug

Inhibits enoyl reductase (similar to isoni) but different mechanism

GI probs

Inhibits mycolic acid synthesis

29

Practial considerations of TB therapy

Neuritis, orange, hepato, P450

Adding ethionamide introduces GI and hypotension