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Dermatology pharm > Leprosy > Flashcards

Leprosy Flashcards

multi drug Tx; MOA; Sx of dapsone syndrome; elim/ dose mod in dysfxn; neurologic/teratogenic/immuno suppressive actions

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Dermatology Board Prep flashcards
1
Q

What drugs are given to patients that cannot tolerate clofazimine?

A

clarithromycin; minocycline; ofloxacin

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2
Q

What is the standard Tx for tuberculoid leprosy?

A

dapsone and rifampicin for 12 months then D/C therapy

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3
Q

Standard Tx for lepromatous leprosy?

A

Dapsone, rifampicin, clofazimine for 24 months then D/C therapy

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4
Q

What is an inactive metabolite of dapsone metabolism?

A

hydroxylamine (potent oxidant)

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5
Q

What will the production of hydroxylamine cause?

A

methemoglobinemia and hemolysis

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6
Q

Dapsone interaction with rifampin will lead to what?

A

increased toxicity

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7
Q

dapsone interaction with cimetidine and omeprazole will cause what?

A

decrease in toxicity

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8
Q

dapsone and trimethoprim lead to what?

A

increased in serum levels of both drugs

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9
Q

How is dapsone eliminated?

A

renal (renal fxn important)

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10
Q

What does the interaction of probenecid and dapsone have with elimination?

A

decreases clearance with renal tubular secretion

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11
Q

What are the MOAs of dapsone?

A

1) folate antagonsist producing bacteriostatic effect; 2) inhibitor of 2nd msg path involved in neutrophil chemotaxis

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12
Q

What can dapsone syndrome lead to?

A

hemolysis; methemoglobinemia; hepatitis; cholestatic jaundice; peripheral neuropathy; severe hypoalbuminemia; psychosis; leukopenia; agranulocytosis

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13
Q

How does dapsone syndrome clinically present?

A

maculopapular or exfoliative rash confined to either upper limbs or forehead

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14
Q

What are the sequence of Sx associated with dapsone syndrome?

A

dermatitis; LAD along post. border of SCM; hepatitis

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15
Q

What are the clinical indications for dapsone?

A

acne vulgaris; dermatitis herpetiformis; leprosy

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16
Q

What is the MOA of rifampin?

A

inhibits bacterial and mycobacterial RNA synthesis via DNA dep RNA polymerase

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17
Q

What type of cells are susceptible to rifampin?

A

rapidly and slowly dividing organisms

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18
Q

What is the distribution of rifampin?

A

widely and crosses inflamed meninges; placenta; breast milk

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19
Q

metabolism of rifampin

A

hepatic (recirculates in entero-hepatic)

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20
Q

elimination of rifampin

A

hepatic

21
Q

Rifampin Effects on CYP

A

INDUCER of CYP with multiple DDI

22
Q

CYP3A induction by rifampin is variable and affected how?

A

tissue/intracellular concentration of agonists (P-gp efflux); genetic variations of P450

23
Q

What is a sometimes fatal ADE associated with rifampin?

A

transient increases in hepatic enzymes and severe hepatotoxicity

24
Q

What patients should be monitored while taking rifampin?

A

diabetics

25
Q

What are side affects that can scare the patient taking rifampin?

A

discolor of bodily fluids

26
Q

Therapy intervals are not less than 2x weekly and may present how?

A

hemolysis; hemoglobinuria; hematuria; renal tox

27
Q

MOA for clofazimine

A

preferential binding to mycobacterial guanine in DNA (non-intercalator)

28
Q

How does clofazimine improve leprosy?

A

progressive, dose dep anti-inflam & immunosuppressive

29
Q

What can clofazimine treat?

A

reversal rxns and erythema nodosum leprosum

30
Q

What is significant about the duration and make up of clofazimine?

A

highly lipophilic so months of persistence => fat and RES system

31
Q

clofazimine elimination

A

hepatic => jaundice and hepatitis

32
Q

What are alarming ADEs associated with clofazimine?

A

staining of body; body fluids; suckling infant => depression can result

33
Q

How may clofazimine look like a GI disturbance?

A

black or tarry feces

34
Q

What must always be monitored in patients taking clofazimine?

A

CBC and platelets

35
Q

What is the MOA of clarithromycin?

A

inhibits 50S ribosomal sub unit

36
Q

clarithromycin static or cidal

A

cidal

37
Q

clarithromycin and pregnancy

A

C

38
Q

MOA of minocycline

A

inhibits 30S ribosomal subunit

39
Q

minocylcine static or cidal

A

cidal

40
Q

ofloxacin MOA

A

inhibits bacterial DNA gyrase

41
Q

ofloxacin static or cidal

A

cidal

42
Q

pregnancy and minocycline

A

D

43
Q

pregnancy and ofloxacin

A

C

44
Q

Resistance to oxfloxacin, minocycline or clarithromycin

A

rare

45
Q

ADEs are associated with oxfloxacin, minocycline and clarithromycin. What are considered type 1 rxns? tx for type 1?

A

red patchy skin lesions; erythema; swollen hands/feet; joint pain
Tx: corticosteroids

46
Q

What are considered type 2 rxns? Tx for type 2

A

erythema nodosum leprosum with sudden eruption of painful nodules and neuritis
Tx: corticosteroids; clofazimine; thalidomide

47
Q

MOA of thalidomide

A

inhibits NFkB mediated transcriptional upregulation and TNF-a production => block leukocyte migration

48
Q

What are serious ADEs associated with thalidomide?

A

teratogen; somnolence > rash > headache; rare peripheral neuropathy

49
Q

Thalidomide and HIV patients

A

increase in plasma HIV viral load so must be monitored

Dermatology pharm (10 decks)

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