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Skin > Antifungals/Antihistamines > Flashcards

Antifungals/Antihistamines Flashcards

1
Q

What are major differences between fungi and bacteria?

A
  1. cell membrane has ergosterol in fungi

2. cell wall contains beta-glucan in fungi

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2
Q

Superficial fungal infection

A

Cutaneous surfaces (common), subcutaneous, mucous membrane surfaces

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3
Q

Systemic fungal infection

A

Internal organs (cause pneumonia and can disseminate), difficult to treat, often life-threatening

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4
Q

What are fungal infections harder to treat than bacterial?

A

Fungal organisms grow slowly, infections often occur in poorly perfused tissues, and usually requires prolonged treatment

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5
Q

Systemic drugs for systemic infections

A

Azoles

Amphotericin B

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6
Q

Oral systemic drugs for mucocutaneous infections

A

Terbinafine

Griseofulvin

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7
Q

Topical drugs

A

Topical azoles
Topical amphotericin B
Nystatin
Topical terbinafine

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8
Q

Griseofulvin mechanism

A

Deposits in newly forming skin where it binds to keratin, protecting skin from new infection (prevents microtubule function)

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9
Q

Griseofulvin clinical use

A

Tinea capitis and glabrous (nonhairy) skin (e.g. nail)

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10
Q

Griseofulvin side effects

A
  • Incidence of serious reactions is low
  • GI upset (diarrhea, epigastric distress, bleeding, nausea, vomiting)
  • Hepatotoxicity (rare)
  • Photosensitivity
  • Drug-drug interactions
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11
Q

Drug-drug interaction of griseofulvin

A

-Induces hepatic CYP450 enzymes, thereby increasing the rate of metabolism of other drugs (substrates of CYPs) such as warfarin, anti-epileptics (e.g., phenytoin), theophylline, oral contraceptives (OCPs), etc.

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12
Q

Terbinafine mechanism

A
  • inhibits enzyme squalene epoxidase (fungal enzyme), further inhibiting ergosterol synthesis
  • membrane damage and leaky
  • accumulation of squalene which is toxic to fungal cells
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13
Q

Terbinafine clinical use

A
  • Fungicidal
  • oral or topical
  • DOC for tinea unguium (nail) and capitis
    • oral
    • high cure rate
    • prolonged therapy
    • more effective than griseofulvin or azoles
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14
Q

Terbinafine side effects

A
  • Well tolerated with rare side effects
  • Low incidence of GI distress, headache, rash, hepatotoxicity, neutropenia, hypersensitivity
  • Pregnancy Category B (no evidence of drug risks in humans) - recommended therapy for onychomycosis be postponed until after pregnancy
  • no significant drug-drug interactions
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15
Q

Systemic azoles

A

Ketoconazole (older), fluconazole, itraconazole, voriconazole

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16
Q

Topical azoles

A

Clotrimazole, miconazole, ketoconazole

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17
Q

Azoles MOA

A
  • Azoles inhibit the synthesis of erogsterol from lanosterol via inhibition of 14-a-demethylase, a CYP450 enzyme (CYP51A1)
  • Decreasing ergosterol leads to membrane damage and leaky, also leads to accumulation of squalene
  • Some azoles also inhibit other human CYP450 enzymes thus causing side effects
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18
Q

Azoles clinical use and general side effects

A

Clinical use:
-Used in both superficial and systemic infections. Broad spectrum of action including Candida spp., Cryptococcus neoformans, endemic mycoses (blastomycosis, coccidioidomycosis, histoplasmosis), dermatophytes, even Aspergillus infections.
Side effects:
-Relatively nontoxic. Can cause minor GI upset, abnormalities in liver enzymes, hepatitis
-Prone to drug-drug interactions because they inhibit human CYP450 enzymes

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19
Q

Ketoconazole clinical use

A
  • Dermatophytosis, mucocutaneous candidiasis, tinea versicolor, seborrheic dermatitis (topical use)
  • Not for systemic use (due to its narrow therapeutic index and side effects)
  • Has been largely replaced by fluconazole and itraconazole for antifungal treatment, except using in Cushing’s syndrome (off-label use)
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20
Q

Off-label use of ketoconazole

A
  • “Off-label use” means use the drug for a condition other than that for which it has been officially approved.
  • Ketoconazole inhibits adrenal steroidogenesis (mechanism discussed in next slide), thus is used in
    • Cushing’s syndrome (decrease glucocorticoid production)
    • Prostate cancer (decrease androgen production)
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21
Q

Ketoconazole side effects

A
  • Potent CYP450 inhibition
  • Inhibits adrenal steroidogenesis causing adrenal insufficiency (related symptoms: gynecomastia, impotence, decreased libido, abnormal menstruation)
  • Hepatotoxicity
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22
Q

How does ketoconazole inhibit adrenal steroidogenesis? (MOA)

A
  • Inhibits CYP450 enzymes critical in adrenal steroid synthesis
  • Binds to steroid receptors as an antagonist
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23
Q

Compared to ketoconazole, other azoles…

A
  • Have same mechanism
  • Used more frequently with better activity, less toxicity
  • Less effect on CYP450
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24
Q

Clinical use of fluconazole

A

Cryptococcal meningitis (good CSF penetration), mucocutaneous candidiasis

25
Q

Clinical use of itraconazole

A

Dimorphic fungi including Histoplasma, Blastomyces, Coccidioides immitis, Sporothrix

26
Q

Clinical use of voriconazole

A

Candida spp., dimorphic fungi, Aspergillus spp.

27
Q

Polyenes MOA

A

preferentially bind to ergosterol (unique to fungi), forming pores in membrane, causing leaky membranes and disrupting osmotic integrity (Polyenes form Pores)

28
Q

Amphotericin B clinical use

A
  • Broad spectrum activity
  • DOC for most severe and/or life-threatening infections, systemic fungal infections (severe fungal pneumonia, severe cryptococcal meningitis (intrathecally for fungal meningitis), severe or rapidly progressing histoplasmosis, blastomycosis, coccidioidomycosis)
  • Topical use for Candida albicans infection (ineffective against dermatophytosis)
29
Q

Amphotericin B immediate toxicity side effects

A
  • Shake and Bake (fever/chills), muscle spasms, vomiting, headache, hypotension
  • prevention: slow infusion or decrease dose
  • Treated by drugs [e.g, antipyretics (reduce fever), antihistamine (reduce allergy), meperidine (reduce pain), corticosteroids (reduce allergy and pain)
30
Q

Amphotericin B cumulative toxicity side effects

A
  • Renal toxicity (caused by: constriction of afferent arterioles and renal tubular damage caused by disruption of membrane permeability)
  • Can cause renal tubular acidosis and renal wasting of K and Mg
31
Q

Nystatin clinical use

A
  • Topical only
  • cutaneous, mucocutaneous, and oral infections normally caused by Candida spp.
    • swish for oral
    • topical for diaper rash or vaginal
32
Q

Nystatin side effects

A

Not absorbed from GI tract, skin, or vagina, thus has little toxicity

33
Q

Primary DOC for tinea unguium; alternative?

A

Terbinafine; itraconazole, fluconazole

34
Q

Primary DOC for tinea capitis? Alternative?

A

Terbinafine or griseofulvin; itraconazole, fluconazole

35
Q

Primary DOC for tinea corporis, tinea cruris, tinea pedis? Alternative?

A

Topical azoles (clotrimazole, miconazole); terbinafine, fluconazole, itraconazole

36
Q

DOC for tinea versicolor

A

Topical azoles (lesions have a tendency to recur), fluconazole or itraconazole (for recurrences), or selenium sulfide shampoo

37
Q

Urticaria (hives, welts, or wheals)

A

Episodic inflammatory, allergic reaction in a localized area of skin; majority of cases are acute, not chronic; possible mechanisms: IgE mediated, non-IgE-mediated, autoimmune, idiopathic; vascular reaction in the upper dermis (pruritic, edematous, erythematous lesions)

38
Q

H1 receptor

A
  • Gq
  • Found on: smooth muscle, endothelium, and CNS
  • Activation: (mediated through C-nerve fibers)
    • Vasodilation
    • Separation of endothelial cells
    • Itching (pruritus)
    • Bronchoconstriction
    • Primary receptor involved in allergic rhinitis symptoms and motion sickness
39
Q

Antihistamines 1st gen

A

Diphenhydramine (oral, topical, parenteral)
Dimenhydrinate (oral)
Promethazine (oral)

40
Q

Antihistamines 2nd gen

A

Fexofenadine
Loratadine
Cetirizine
ALL ORAL

41
Q

Topical steroids

A

Clobetasol (super high potency)
Betamethasone (super high, high, low potency)
Hydrocortisone (low-medium potency)

42
Q

Antihistamines

A
  • Inverse agonists (not an antagonist)
  • Block the physiological effects of histamine by selectively acting on receptors to prevent histamine from stimulating the receptor and inducing the common effects observed during an allergic reaction:
    • redness, edema, itching
    • allergy headache
    • breathing difficulty
  • Anticholinergic
    • Drying effect that reduces nasal, salivary, and lacrimal gland secretions (runny nose, tearing, and itching eyes)
43
Q

Antihistamine clinical usage

A 
Allergic reactions
Allergic rhinitis, hay fever, common cold
Allergic conjunctivitis
Angioedema (allergic)
Antiemetic
Insect bite reactions
Sedation (1st generation)
Urticaria
44
Q

1st gen characteristics

A
  • Older, traditional antihistamines
  • Work both peripherally and centrally
    • Lipid soluble - CNS penetration and effects
    • Sedation and performance impairment is a primary concern with 1st generation
  • Have anticholinergic effects, making them more effective than nonsedating agents in some cases
45
Q

1st gen adverse effects

A

Sedation/drowsiness (gives effect of BAC of .05-.1)

46
Q

Potential benefit of sedation in 1st gens

A
  • decrease central itch perception

- helps patients sleep

47
Q

Anticholinergic effects of 1st gens

A 
Dry mouth
Difficulty urinating
Constipation
Glaucoma exacerbation
Tachycardia
Blurred vision
Confusion, etc.
48
Q

2nd gen characteristics

A
  • developed to eliminate unwanted side effects (less lipophilic, does not readily cross BBB)
  • similar relief with few side effects
  • work peripherally (fewer CNS side effects)
  • longer duration of action (better compliance)
  • shown to improve quality of life
49
Q

2nd gen side effects

A
  • Drowsiness (less)
  • fatigue
  • dry mouth
50
Q

Topical steroids MOA

A

Anti-inflammatory

  • Suppress production of
    • Cytokines
    • Prostaglandins
    • Leukotrienes
  • decrease release of proinflammatory mediators
  • Stabilizes lysosomal membranes
    • Prevents catabolic enzyme release from neutrophils
  • Causes vasoconstriction and decreases capillary permeability
51
Q

Super high potency used…

A
  • for severe dermatoses over nonfacial/nonintertriginous areas
    • e.g., psoriasis, severe atopic dermatitis, severe contact dermatitis
  • Especially useful over areas that tend to resist topical steroid penetration due to the thick stratum corneum (e.g., palms, etc.)
52
Q

Medium to high potency

A

Appropriate for mild to moderate nonfacial/nonintertriginous dermatoses

53
Q

Low to medium potency

A
  • Trunk, arms, legs
  • Consider when large areas are treated
    • Possible systemic absorption
54
Q

Low potency

A
  • Thin-skinned, sensitive areas

- Axillae, groin, perianal, breast folds, face, eyelids

55
Q

Absorption depends on nature of lesions

A

High: atopic and exfoliative dermatitis
Low: hyperkeratinized and plaque forming lesions

56
Q

Occlusion can enhance topical corticosteroid potency by as much as….

A

100-fold

57
Q

Topical steroids adverse effects

A 
Skin atrophy, striae 
Telangiectasia, purpura 
Perioral dermatitis, rosacea 
Tachyphylaxis or rebound 
Hypopigmentation
Systemic absorption (uncommon) 
Contact dermatitis - reaction to preservatives and additives is also common with prolonged use
58
Q

Minimizing risks of topical steroids

A

Avoid high potency steroids on flexures, face, or genitals
Be cautious when using steroids on face
Avoid high potency steroids in children
Avoid use of occlusion for long periods

59
Q

Skin atrophy can have visible…

A

telangiectasia, hypopigmentation, and prominence of underlying veins

Skin (9 decks)

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