Drugs for fungal infections, head lice, hyperhidrosis, hair growth and pigmentation - Sweatman Flashcards

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1
Q

what is the unique, significnat adverse effect of ketoconazole use that were the subject of a recent FDA article?

A

Adrenal insufficiency - ketoconazoles ability to disrupt steroid synthesis

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2
Q

what are 2 common adverse effects shared by all azoles

A

Hepatotoxicity

Drug-drug interactions via CYP interactions

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3
Q

what are 3 BBW associated with Itraconazole use? Why does it carry these?

A

Heart Failure
Ventricular dysfunction
Co-administration with drugs (CYP)
Itraconazole produces negative inotropic effects on the heart

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4
Q

Are azoles safe in pregnancy?

A

no

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5
Q

Are azoles safe in breast feeding?

A

no - potential of the drug to pass to infant

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6
Q

which azoles produce QT prolongation?

A

Fluconazole, Psoaconazole, Voriconazole

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7
Q

Which azole are you worried about visual disturbances due to optic neuritis?

A

Voriconazole

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8
Q

Which azole are you worried about photosensitization of skin?

A

Voriconazole

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9
Q

which azole must be administered with a full meal for adequate bioavailability?

A

Posaconazole

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10
Q

This is a potential test question
You have a pt that has a fungal infection and renal failure - what azole can you not give, or at least need to dose adjust?

A

Fluconazole

most azoles are extensively hepatically metabolized, but fluconazole is metabolized and eliinated renally

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11
Q

which azoles have access to CSF?

A

Fluconazole and Voriconazole

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12
Q

What is the MOA of Griseofulvin?

A

binds microtubules, disrupts the mitotic spindle - thus inhibits fungal growth

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13
Q

what is the effect of Griseofulvin on CYP?

A

it is a CYP3A4 inducer (azoles are inhibitors)

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14
Q

is Griseofulvin safe in pregnancy?

A

no

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15
Q

What drug allergy in a pt would make you not want to give Griseofulvin?

A

Penicillin allergy

commonality in structure with Beta lactams

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16
Q

What is the MOA of Terbinafine and Naftifine (allylamines)?

A

inhibit squalene epoxidase, a step in ergosterol synthesis

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17
Q

is terbinafine safe in pregnancy?

A

yes

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18
Q

what precautions do you need to take with Terbinafine?

A

CBCs and LFTs

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19
Q

what is an important point about the allylamines and azoles in combination therapy?

A

both classes work to block ergosterol incorporation into fungal cell walls - there is no gain in combining the two classes

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20
Q

what is the route of delivery for Ciclopirox and Amorolfine?

A

TOPICAL ONLY

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21
Q

for review only, what is the MOA of azoles? what enzyme do they inhibit?

A

inhibit the cytochrome P450 enzyme sterol 14 demethylase

blocks production of ergosterol

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22
Q

for review only, what is the MOA of capsofungin (and Echinocandin)

A

inhibits 1,3-B-glucan synthase

results in disruption of cell wall integrity

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23
Q

for review only, what is the MOA of amphotericin B?

A

binds ergosterol and creates pores in the fungal cell membrane

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24
Q

what is the general mechanism used to treat hyperhidrosis?

A

anti-cholinergics

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25
Q

from the CNS, what causes activation of Eccrine (thermoregulatory) sweat glands?

A

sympathetic innervation with Ach as neurotransmitter, rather than customary NE
(the nerves innervating eccrine, or thermoregulatory, sweat glands are sympathetic cholinergic nerves, this is unique)

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26
Q

so an M2 student has sweaty armpits in anticipation of being pimped by Sweatman in class (eh, eh?) what is the post-synaptic neuro-effector receptor responsible for the sweating?

A

Muscarinic M2

the nerves innervating eccrine, or thermoregulatory, sweat glands are sympathetic cholinergic nerves, this is unique

27
Q

what are the affects of cholinergic agonists or AchE inhibitors? what is the pneumonic?

A
DUMBBELS 
Diarrhea
Urination
Miosis/muscle weakness
Bronchorrhea
Bradycardia
Emesis
Lacrimation 
Salivation/sweating
28
Q

what is first line treatment for hyperhidrosis (i.e. early stages)

A

start with general antiperspirants, such as aluminum chloride

29
Q

what is second line treatment for hyperhidrosis (i.e. no response to antiperspirants)?

A

botulinum toxin

30
Q

what is the treatment modality (3rd line) used for hyperhidrosis if there is no response to botulinum toxin?

A

systemic anticholinergics

or surgery with sympathectomy

31
Q

what is the MOA of Aluminum Chloride

A

short-term occlusion of eccrine and apocrine sweat gland ducts

32
Q

What is the MOA of botulinum toxin

A

cleaves SNARE proteins, prevents fusion of vesicle containing Ach and the presynaptic membrane - prevents Ach release into the cleft

33
Q

what is a rare but impt BBW associated wiht Botulinum Toxin

A

systemic botulism is rare, but reported

34
Q

for systemic anti-muscarinic therapy used for the treatment of hyperhidrosis, what type of drugs and what drug names do we want to choose, and why

A

we want to choose drugs that cannot cross the BBB, so as to not cause anti-muscarinic sedation and delirium
need quaternary ammonium compounds
glycopyrrolate, propantheline

35
Q

what drugs can you use to diminish the central emotionally impacted sympathetic causation of sweating

A

propranolol (beta blocker) or clonidine (a2 agonist)

36
Q

what are the two general divisions of head lice treatment types?

A

chemical and physical

37
Q

in general, what is the effect of chemical methods to treat head lice

A

result in paralysis of louse and result in its demise from dehydration

38
Q

in general, what is the effect of physical methods to treat head lice

A

suffocation of the little shits

39
Q

Malathion - MOA and what does it treat?

A

AchE inhibitor

Chemical method to treat head lice

40
Q

What should you admin in the event that Malathion is ingested (instead of applied topically, as indicated)

A

use atropine

muscarinic antagonist to help reduce the Ach overstimulation caused by Malathion

41
Q

Permethrin - MOA and what does it treat?

A

blocks volt gated Na channels - slows and stops nervous system activity
chemical method to treat head lice
(also first line for scabies)

42
Q

Ivermectin - MOA and what does it treat?

A

binds glutamate receptors gating chloride - leads to hyperpolarization of cell
also may act as agonist for GABA
used to treat head lice, and is a broad spectrum antiparasitic agent

43
Q

In broad generalities, what is your approach to treatment of head lice? what all do you need to eradicate and how many treatments?

A

more than one treatment may be necessary in order to eradicate all adult and nit louse

44
Q

What is the mechanism of resistance by lice to the chemical agents?

A

typical mechanisms common to other drugs
decreased concentration at target, increased rate of inactivation / removal, point mutations in targets
i.e. knock down resistance from point mutations in targets like the volt gate sodium channel (permethrin target)

45
Q

What is dimethicone? what is it used to treat? what is its MOA?

A

a mechanical (physical) methd of lice treatment
it is a silicon based polymer that lubricates hair and aids in removal of lice and nits
and causes suffocation of lice

46
Q

what is Air Alle, what is it used to treat?

A

mechanical treatment of hair lice, application of heat causes dehydration of louse leads to death

47
Q

what drug treats hair conditions by inhibiting 5-alpha dihydrotestosterone production?

A

Finasteride (propecia)

48
Q

what drug used for the treatment of hair conditions requires activation by UV light

A

Methoxsalen

49
Q

What drugs block the production of melanin when used to treat hair conditions?

A

hydroquinone, Tretinoin

50
Q

what is the danger of the practice of scalp cooling? (used to prevent alpecia following CTX)

A

preservation of scalp micrometastases

51
Q

what is the MOA of minoxidil?

A

it is a potent oral vasodilator - mechanism of topical application leading to hypertrichosis is unknown

52
Q

you are thinking about prescribing Finasteride (propecia) to somebody with alopecia; what herbal supplement do you need to ask them if they are taking, because it acts by a similar mechanism as finasteride

A

Saw Palmetto - used for BPH

53
Q

what is a potential, debilitating side effect of Finasteride or saw palmetto?

A

sexual dysfunction / infertility

54
Q

what is Eflornithine used to treat?

A

topical drug to reduce unwanted female facial hair growth

55
Q

What is the MOA of Eflornithine used to treat unwanted female facial hair

A

inhibits ornithine decarboxylase - a mandatory step in polyamine production - causes decreased cell division and differentiation

56
Q

what else, besides unwanted female facial hair growth, can Eflornithine be used to treat?

A

given IV, is trypanostatic - employed in tx of sleeping sickness

57
Q

what 3 drug regimen is used in the treatment of melasma, or facial skin darkening caused by hormonal changes, prgnancy, OCs or HRT?

A

Fluocinolone, Hydroquinone, Tretinoin

58
Q

what is the MOA of Fluocinolone? (part of 3 drug regimen to treat melasma)

A

anti-inflammatory corticosteroid

59
Q

what is the MOA of Hydroquinone? (part of 3 drug regimen for melasma)

A

inhibits melanin formation, blocking melanocyte enzymatic oxidation of tyrosine to DOPA

60
Q

what is the MOA of tretinoin? (part of 3 drug regimen for melasma?)

A

modulates skin growth and pigmentation

it is a retinoid, so it just does retinoid things

61
Q

when on the 3 drug regimen for melasma Fluocinolone, Hydroquinone, Tretinoin, what do pts need to be cautioned about

A

increased sensitivity to UV, protection is necessary

62
Q

What is the MOA of Methoxsalen? used to treat a number of different skin conditions

A

activated by exposure to UV light

conjugation and cross-linking of DNA - cell death

63
Q

in cases of CTX induced alopecia, regrowth often occurs, via stem cells located where in the hair follicle

A

stem cells located in the bulge

64
Q

what is the mechanism of CTX induced hair loss

A

apoptotic cell death, a result of dec BCL2, and inc Bax and p53