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Pharmacology > Lecture 5 (Derm)- Exam 3 > Flashcards

Lecture 5 (Derm)- Exam 3 Flashcards

1
Q

Steroids:
* Endogenous steroids produced where?
* Steroids released when?
* What effects?

A
  • Endogenous steroids produced in the adrenal gland (MC cortisol)
  • Released in response to stress and inflammation
  • Anti-inflammatory and immunosuppressive effects
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2
Q

What is the MOA of steroids? (cytokines and mediators)

A

Inhibit the production of inflammatory cytokines
* Bind to glucocorticoid receptors inside cells
* Bind to sites on DNA
* Down regulate cytokine production

Inhibit the production of inflammatory mediators
* Inhibit phospholipase A2
* Prevents the production of arachidonic acid
* Decreasing prostaglandins, leukotrienes, thromboxane

Immunosuppression

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3
Q

Steroids effects:
* What do they suppress?

A

Suppress inflammatory response to all noxious stimuli
* Pathogens
* Chemical / physical
* Immune mediated / hypersensitivity

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4
Q

How does steroids reduce inflammation? (4)

A

Reduce inflammation by DECREASING:
* Cytokine production – including various interleukins, tumor necrosis factor alpha
* Recruitment of WBCs and monocytes to sites of inflammation (neutrophil demargination)
* Lymphocyte, monocytes, basophil, eosinophil, mast cell production / function-> T-lymphocyte activity
* Production of prostaglandins, bradykinins, leukotrienes (inhibition of phospholipase A2)

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5
Q

T/F: Steroids corrects the underlaying cause of disease

A

False

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6
Q

What are the short term steroids effects? (6)

A
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7
Q

What are the long term steroids effects? (8)

A
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8
Q

What are the different vehicles of topical corticosteroids?

A
  • ­ Ointments
  • ­ Creams
  • ­ Lotions
  • ­ Gels
  • ­ Foams
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9
Q

TCS:
* What does it decrease?
* How is it anti-inflammatory?
* Vasoconstrictor or VD?
* Decreases what molecules?
* Anti_
* Inhibits what?
* Immunosuppressive or immunopotent?

A
  • Decrease burning or itching
  • Anti-inflammatory->Decrease production of pro-inflammatory genes
  • Vasoconstrictive of perperial vessels
  • Decreases prostaglandin and leukotriene synthesis
  • Antimitotic
  • Inhibits cell proliferation and collagen synthesis
  • Immunosuppressive
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10
Q

What is the MOA of TCS?

A
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11
Q

Topical bases
* Penetrations increases with what?
* What also increases penetrations?

A
  • Penetration increased with moisture->Apply after shower or bath
  • Plastic dressings increase penetration
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12
Q

Ointments:
* What are the properties? (3)
* What are the uses/comments (3)

A

Properties:
* Potency high
* High lubrication
* Occlusive (help keep moisture in)

Uses/comments:
* Very dry to thick, hyperkeratotic lesions
* Avoid in areas with hair
* Greasy = poor satisfaction/ compliance

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13
Q

Cream:
* What are the properties? (4)
* What are the uses/comments (2)

A

Properties:
* Lower potency
* (drug: drug)
* Less occlusive
* Drying effects

Uses/Comments:
* Vanish in skin – more appealing
* More often contain preservatives (Sensitivity to skin)

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14
Q

Lotions/gel:
* What are the properties? (1)
* What are the uses/comments (3)

A

Properties:
* Least occlusive or greasy

Uses/comments:
* Lotions-contain alcohol; drying for oozing lesions
* Good for areas with hair

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15
Q

Shampoos, foams, mouses
* What are the properties? (1)
* What are the uses/comments (2)

A

properties
* least effective vehicle

Uses/comments:
* Easy to apply
* good for areas with hair

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16
Q

How are the steroid potency classes determined? How many classes are there?

A

Determined by vasoconstriction / blanching test
* Seven classes

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17
Q

Steroid potency classes:
* Group one: Potency level, what type of disease, how long, areas of skin?

A

Group 1 = highest potency (ultra, super)
* Severe disease
* Short duration (3 weeks)-> then stop, small areas
* Not face, groin, axilla
* Not under occlusion

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18
Q

Steroid potency classes:
* Group seven: Potency level, safety level, how long, what areas of the body?

A

Group 7 = lowest potency
* Safest
* Long-term (3 months), large areas
* Face, thin skin
* Children

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19
Q

What happens when you have chronic administrations of steroids? (4)

A
  • Tolerance, tachyphylaxis
  • Taper off to prevent rebound symptoms then go to next bullet point
  • Off x 1 week
  • Resume at maintenance dosing (BIW) after tapering
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20
Q

Topical Steroid dosing?

A
  • Once or twice daily
  • Fingertip unit = 0.5 grams
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21
Q
A

BET PROB FLU

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22
Q

list drug and percent

A
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23
Q

List drugs and percent

A
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24
Q

TCS ADVERSE EFFECTS
* What are the local effect? (9)

A
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25
TCS ADVERSE EFFECTS * What are the systemic symptoms? (6)
26
TOPICAL CALCINEURIN INHIBITORS * What is the MOA (3)?
* Bind calcineurin and inhibit the production of nuclear factor of activated T-cells (NFAT) * NFAT necessary for T-cell production of cytokines * No production of cytokines (IL2, etc)
27
TOPICAL CALCINEURIN INHIBITORS * Indictions (2)?
* Moderate to severe atopic dermatitis * Patients ≥ 2 years
28
TOPICAL CALCINEURIN INHIBITORS * Improved benefit when? * Safe for what? * What are the BBW (2)? * What is the adverse reactions? * What education do you give to your patient?
Improved benefit when added to TCS Safe for sensitive areas BBW: * Increased risk of non-melanomatous skin cancers and lymphoma * Weak evidence Adverse reactions: Local burning sensation Education - sunscreen
29
* What are the two topical calcineurin inhibitors? * What is important about them? * What are the preparations?
30
Antihistamines: * Histamine released from what? * What happens when histamine binds to H1 receptors? * What happens when histamine binds to H2 receptors?
31
How does antihistamine work?
32
What are the indications for first gen antihistamine? (7)
* Allergies * Motion sickness * Vertigo * Sedation * Insomnia * Cold symptoms * EPS treatment | maces vi
33
First gen antihistamine: * Does it cross the BBB? * What receptors do they affect?
Yes * Antiemetic * Histamine * Acetylcholine receptor blockage
34
What are the SE of first gen antihistamines?
* Cholinergic - anticholinergic (Mad hatter) * Alpha adrenergic – hypotension * Serotonergic – increased appetite ## Footnote Mad hatter: fever, dry mucous mem, flushing, blurred vision (mydriasis), Hallcuninations, sedation and tachycardia
35
What are the first gen antihistamines examples (8)?
* Brompheniramine * Chlorpheniramine * Cyproheptadine (Periactin)-> not really allergic but serotoninic * Diphenhydramine (Benadryl) * Hydroxyzine hcl / pamoate (Atarax)-> good for anti-itch * Promethazine (Phenergan)->serotoninic * Meclizine (Antivert) * Dimenhydrinate (Dramamine)-> motion sickness ## Footnote * Diphen – insomnia * Prometh, mecli, dimen = n/v associated with motion sickness
36
What is the class/indication of 2nd gen antihistamine?
* Allergies only * H1 selective
37
2nd gen antihistamine: * Does it cross BBB? * What are the SE?
* No * Less SE
38
What are the 2nd gen histamine drugs (5)?
* Cetirizine (Zyrtec) * Levocetirizine (Xyzal) * Loratadine (Claritin) * Desloratadine (Clarinex) * Fexofenadine (Allegra) | -irizine or -adine
39
What are humectant, emollients and occlusive?
40
Humectant: * What happens to skin? * What skin type to use it on? * what are examples?
41
emollient: * What happens to skin? * What skin type to use it on? * what are examples?
42
Occlusive: * What happens to skin? * What skin type to use it on? * what are examples?
43
What are the different eczematous rash?
44
ATOPIC DERMATITIS (ECZEMA) * What type of condition? * What type of rxn? * What is the pathophysiology?
45
ECZEMA PATTERNS * What type of rash? * What areas of body? * Worsens when?
* Dry, itchy rash see * Flexor surfaces (elbows, wrists, knees) * Face, hands, feet * Worsens when exposed to allergens
46
Atopic dermatitis: * What are the treatment goals?
* Provide symptom relief * Control atopic dermatitis * Identify and reduce triggers * Prevent exacerbations * Minimize treatment adverse effects * Treat secondary skin infections->MC Staphylococcus
47
Nonpharmacologic therapies for atopic dermatitis: * What should the pt throughout the day? * What should help with hydration? * Use what? What are the characteritics? (3) * Apply what? * Keep what short? * What type of fabrics? * Consider what? * body temp?
48
* What is the first line pharmacologic therapy for atopic derminitis? * What are the directions?
TCS: * ­ Reactive therapy for mild disease * ­ Proactive therapy for moderate to severe disease-> ­ Long-term anti-inflammatory therapy – usually 2 days per week * ­ Potency should match disease severity and location * Taper to avoid withdrawal rebound
49
What is second line, systemic and toher agents for atopic derm?
Calcineurin inhibitors second-line * Steroid failure or steroid sparing Other agents: * Coal tar * PDE – 4 inhibitors * Phototherapy Systemic therapies: * Rarely indicated * Corticosteroids generally not recommended-> Very short term (< 1 week) for severe flare / disease * Antibiotics for superinfections
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51
Contact dermatitis: * What type of reaction? * What type of rash? What are the two types of CD?
52
What are causes of irritant contact and allergic contact dermtitis?
53
Contact dermatitis - treatment * What is first line? * What is second line?
54
CONTACT DERMATITIS - TREATMENT * What do you use for acute and weeping?
55
# ECZEMATOUS DERMATITIS What are the nonpharmacologic txt for nummular dermatitis?
* Reduce skin dryness * Moisturize 1-2 times daily * Reduce irritants * Non soap cleansers * House humidification
56
What is first line pharm for nummular dermatitis?
High or ultra-high potency TCS x 2 to 4 weeks ## Footnote 2nd line: Triamcinolone lesion injection Phototherapy
57
What are the non-pharm txt of Dyshidrosis?
* Non soap cleansers * Dry hands well after washing * Wear gloves for specific tasks * Emollients * Avoid irritants * Burrow’s solution or witch hazel * Draining large lesions
58
What is the first line pharm txt of Dyshidrosis?
* High or ultra-high potency TCS x 4 weeks * Ointments preferred; not often tolerated | D/t this being thick skin ## Footnote 2nd: Systemic corticosteroids-> Prednisone 40 to 60 mg PO x 1 week, followed by taper
59
What is the nonpharm txt of Perioral dermatitis?
Zero therapy * Elimination of corticosteroids * Non soap cleansers * Reduce irritants (make-up, sunscreen)
60
What is the first line thearpy of perioral dermatitis?
* Erythromycin 2% topical gel x 4 to 8 weeks * Metronidazole topical gel, lotion, cream x 8 weeks * Pimecrolimus / tacrolimus topical x 4 weeks
61
Seborrheic Dermatitis: * Requires what? * Associate with what? * What are mc areas? * What is mild and severe types?
* Mild, chronic, relapsing * Requires sebaceous glands but not disease of them * Associated with Malassezia colonization * MC involves face and scalp * Mild – diffuse scaliness without underlying erythema (dandruff) * More severe – patchy orange to salmon-colored plaques with yellowish, **greasy scales**
62
What is the treatment and SE of dandruff and facial seborrheic dematitis
63
Cradle cap: * Subset of what? * When is onset? * What type of condition? * What are the characterisitcs?
* **Subset of infantile seborrheic dermatitis (ISD)** * Onset: third week and first couple months of life * Self-limiting, chronic non-inflammatory scaling skin condition * Erythematous plaques with greasy-appearing yellowish scale located on the scalp
64
What is the txt of cradle cap?
* Application of baby oil or petroleum * Scale removal * Washing with baby shampoo
65
Exanthematous drug eruption: * What type of rash? * How long after medicaition initiation? * What type of rn? * What are the s/s of more severe disease?
66
What is DRESS syndrome?
Drug reaction with eosinophilia and systemic symptoms
67
What is the txt for exanthematous drug eruptions?
68
What drugs can cause exanthematous drug eruptions?
69
What drugs can cause photosensitivity?
70
Lichen Planus: * What type of disease? * What does it affect? * Associated with what?
Immune-mediated * Skin, nails, mucous membranes * Including oral cavity, genitalia * Association with Hepatitis C
71
What is the first line and 2nd line txt of lichen planus?
72
PITYRIASIS ROSEA * What type of disease? * What type of rash? * What may be there? * Asymptomatic execpt what? * What will 50-90% patients have? * What is the rast pattten?
73
What is the txt of pityrasis rosea?
Spontaneous resolution occurs in 2 to 3 months Symptomatic treatment includes: * Medium potency corticosteroids as needed for itching * Systemic antihistamines * Topical antipruritic agents: Pramoxine (local anesthetic) and Menthol * **Topical antihistamines generally not effective**
74
Psoriasis: * What type of disease? What is the pathophysiology of this?
Autoimmune disorder * Immune response does not turn off * Increased levels of cytokines * Abnormal and excessive proliferation of keratinocytes * Keratin growth > sloughing
75
What are the two substypes of psoriasis do you we need to know? What are there symptoms and what areas of the body do they affect?
76
Psoriasis: * Treatment depends on what? * What is the mc type? * Therapies are aimed at what?
Treatment depends on type and severity * MC: limited (mild) – 80% * Therapies aimed at decreasing symptoms and keratinocyte proliferation
77
Psoriasis general txt: * What should all patients be doing? * Mild dx? * Moderate to severe dx?
* All patients -> nonpharmacologic * Mild dx = topical therapy * Moderate to severe dx = systemic therapy
78
Psoriasis txt: * What are the nonpharm and pharm txts?
Nonpharmacologic pharmd * Stress reduction * Moisturizers * sunscreen Pharmacologic * Topical therapies: TCS, vitamin D analogs, retinoids * Phototherapy * Systemic therapies * Steroids, monoclonal antibodies
79
What is mild, moderate and severe psoriasis?
80
Vitamin D analogs: * What are the different ones? * What is the MOA? * What are the SE?
81
Retinoids and anthralin: * What are the different ones? * What is the MOA? * What are the SE?
82
PHOTOTHERAPY-UVB * Interferes with what? * Decreases what? * Type of therapy?
* ­ Interferes with protein and nucleic acid synthesis * ­ Decreased epidermal keratinocyte proliferation * ­ Monotherapy or to increase efficacy of topical agents (coal tar, anthralin)
83
PHOTOTHERAPY-ADRs * What is it for? * Risk of what? * What protection is needed?
* ­ Erythema, pruritus, xerosis, hyperpigmentation, blistering * ­ Theoretical risk of skin cancer * ­ Eye protection needed
84
PHOTOTHERAPY- (P)UVA * Similar MOA as what? * Dermal penetration may do what? * Given with what? * effective?
* Similar MOA as UVB * ­ Dermal penetration may decrease inflammation * ­ Given with psoralens (photosensitizer) to increase efficacy * Most effective but difficult to find
85
ADRs: * What is it used for? * Increased risk of what? * CI in who? * What is needed?
* Erythema, pruritus, xerosis, hyperpigmentation, blistering * Increased risk of squamous cell carcinoma * **CI in patients with history of melanoma or multiple nonmelanoma skin cancers** * Eye protection needed
86
What is the txt flow for mild to moderate psoriasis?
87
What is the txt flow for mod to severe psoriasis?
88
Systemic therapies of psoriasis: * What are the first lines of nonbiologic agents? * What are the first lines of biologic agents (when systemic therapies fail)?
Nonbiologic agents * Acitretin – oral retinoid * Cyclosporine – oral calcineurin inhibitor * Methotrexate – oral/SQ antimetabolite * Tofacitinib – oral Janus kinas inhibitor Biologic agents * Ustekinumab (Stelara) – plaque psoriasis * IL-12/IL-23 inhibitor * Adalimumab (Humara) – psoriatic arthritis * TNF-α inhibitor
89
Methotrexate (MTX) * What is the MOA? * how does it compare to cyclosporine? * What is the CI? * What are the SE? * What do you need to monitor?
## Footnote Increase infection risk = ALL
90
Cyclosporine: * What is the MOA? * What are teh SE? * What do you need to monitor?
## Footnote Increase infection risk = ALL
91
Acitretin: * What is the MOA? * What is the CI?
## Footnote Increase infection risk = ALL
92
biologic systemic therapy * Increased risk of what? * What do you need to screen your patients for? * What do you need to give your patients? * Monitor patient closely for what? * Infusion reaction common what?
93
Erythema Multiforme: * What type of reaction is this? * What happens in results? * What are the most common triggers?
94
What is erythema multiforme minor and major?
95
EM treatment?
* Rapid onset – 24 to 48 hours * Lasts for 48 hours…..begins to resolv
96
What are the drugs that can cause SJS?
**SATAN** – sulfa, allopurinol, tetracylines, anticonvulsants, NSAIDS * Anticonvulsants: lamotrigine, phenytoin, carbamazepine, phenobarbital
97
98
99
Acne: * What is increased (2)? * What is colonized? * Release what?
1. Increased follicular keratinization 2. Increased sebum production by sebaceous gland ( increase androgens) 3. Cutibacterium acnes follicular colonization 4. Release of inflammatory mediators
100
Acne-Classification * What is noninflammatory and inflammatory?
101
Treatment of acne: * Most critical target is what? * Elimination of what? * What are the goals?
* Most critical target is microcomedone * Elimination of follicular occlusion will stop the acne cascade Goals * Alleviation of symptoms * Reduce the size and number of lesions * Limit duration and reoccurrence of lesions * Prevent scarring / pigmentation changes * Improve appearance
102
What are the nonpharm therapy acne?
103
What is the pharm flow chart of acne?
104
Select topical agents for acne: * Benzyol peroxide: MOA, ADRs, comments
105
Select topical agents of ance-> topical retinoids * What are the topical? * What is the MOA? * ADRs? * What are the comments (CI)?
106
Clindamycin 1% and erythromycin: * What is the MOA? * What are the ADRs? (only Clindamycin) * What are the comments? (only Clindamycin)
107
108
ISOTRETINOIN * What type of derivative? * Works on what?
109
Isotretinoin: * What is the dosing? * What is the max dose? * Multiple brand names and generic?
110
Isotretinoin: * What needs to happen since it is teratogenic? * What do you need to caution with its/
111
What are the adverse effects of isotretinoin?
112
* What do you need to monitor with isotretinoin? * What happens in pregnacy?
113
Hormonal agents for acne: * What are the the different ones and their MOA?
Combination oral contraceptives (maybe used alone or in combo) * Antiandrogenic * Decrease ovary androgen production * Increase sex-hormone-binding globulin * Binds free testosterone Spironolactone: * Antiandrogen * Recommended by **AAD for select women**
114
What are the SE of Spironolactone?
115
Fill in for the txt of acne
116
Rosacea: * What type of skin disease? * What is the rash? * Face usually appears as what? * What is often present?
* Chronic inflammatory skin disease * Pathophysiology poorly understood * Scattered small inflammatory papulopustules and sometimes nodules occurring cheeks, chin, forehead, glabella and nose * Face usually appears red or flushed * Telangiectasia are often present
117
Rosacea txt for flushing and redness: * What is first line, second line and the pharmcotherapy options?
118
Treatment of rosacea-> Papules/pustules * What is the txt for mild to moderate?
119
Treatment of rosacea-> Papules/pustules * What is the txt for moderate to severe?
120
Folliculitis: * What is folliculits? * What may casue folliculitis? * Usually what? * What is used for hot packs? * Avoid what? * What is recommmended if limited area without resoltion?
121
Mupurocin (bactroban)-Cream/ointment * What is the MOA? * What are the indications? * What is the dosing? * What are the adverse rxns?
122
What are teh ABCDE?
123
What is the premalignant cutaneous lesion?
Actinic keratosis
124
Actinic keratosis * What is it also called? * what is the patho? * What is it associated with? * What does the rash look like? * May evolve into what?
125
Actinic keratosis * What are the lesion directed therapies?
Isolated lesion: * Cryotherapy (MC) * Curettage / shave * Surgery | Mild therapies only
126
AK TREATMENTS * What are the field directed therapies? * What are the topical medicine therapies?
127
Fill in for the topical txt of AK
128
Fill in for AK topical treatments?
129
Label
130
GENERAL NEOPLASM TREATMENT OPTIONS * What are the five different options?
131
Basal cell carcinoma * What are the characteritics?
132
What are the characteristics of low risk and high risk recurrance with BCC? What is the first line of each?
133
Squamous cell carcinoma: * What are the characteritics?
134
What are the characteristics of low risk and high risk recurrance with SCC? What is the first line of each?
135
melanoma: * Involes what? * May or may not originate from waht? * Rapidly _ * Cure rates are lower when? (2)
136
Fill in for melanoma
137
Melanoma txt: * What is mainstay? * When is LN biopsy recommended? * What is mainstay for unresectable or residual disease?›
138
Fill in for melanoma

Pharmacology (14 decks)

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