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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
Q

TCS ADVERSE EFFECTS
* What are the systemic symptoms? (6)

A
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26
Q

TOPICAL CALCINEURIN INHIBITORS
* What is the MOA (3)?

A
  • 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)
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27
Q

TOPICAL CALCINEURIN INHIBITORS
* Indictions (2)?

A
  • Moderate to severe atopic dermatitis
  • Patients ≥ 2 years
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28
Q

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?

A

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

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29
Q
  • What are the two topical calcineurin inhibitors?
  • What is important about them?
  • What are the preparations?
A
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30
Q

Antihistamines:
* Histamine released from what?
* What happens when histamine binds to H1 receptors?
* What happens when histamine binds to H2 receptors?

A
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31
Q

How does antihistamine work?

A
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32
Q

What are the indications for first gen antihistamine? (7)

A
  • Allergies
  • Motion sickness
  • Vertigo
  • Sedation
  • Insomnia
  • Cold symptoms
  • EPS treatment

maces vi

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33
Q

First gen antihistamine:
* Does it cross the BBB?
* What receptors do they affect?

A

Yes
* Antiemetic
* Histamine
* Acetylcholine receptor blockage

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34
Q

What are the SE of first gen antihistamines?

A
  • Cholinergic - anticholinergic (Mad hatter)
  • Alpha adrenergic – hypotension
  • Serotonergic – increased appetite

Mad hatter: fever, dry mucous mem, flushing, blurred vision (mydriasis), Hallcuninations, sedation and tachycardia

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35
Q

What are the first gen antihistamines examples (8)?

A
  • 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

  • Diphen – insomnia
  • Prometh, mecli, dimen = n/v associated with motion sickness
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36
Q

What is the class/indication of 2nd gen antihistamine?

A
  • Allergies only
  • H1 selective
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37
Q

2nd gen antihistamine:
* Does it cross BBB?
* What are the SE?

A
  • No
  • Less SE
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38
Q

What are the 2nd gen histamine drugs (5)?

A
  • Cetirizine (Zyrtec)
  • Levocetirizine (Xyzal)
  • Loratadine (Claritin)
  • Desloratadine (Clarinex)
  • Fexofenadine (Allegra)

-irizine or -adine

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39
Q

What are humectant, emollients and occlusive?

A
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40
Q

Humectant:
* What happens to skin?
* What skin type to use it on?
* what are examples?

A
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41
Q

emollient:
* What happens to skin?
* What skin type to use it on?
* what are examples?

A
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42
Q

Occlusive:
* What happens to skin?
* What skin type to use it on?
* what are examples?

A
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43
Q

What are the different eczematous rash?

A
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44
Q

ATOPIC DERMATITIS (ECZEMA)
* What type of condition?
* What type of rxn?
* What is the pathophysiology?

A
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45
Q

ECZEMA PATTERNS
* What type of rash?
* What areas of body?
* Worsens when?

A
  • Dry, itchy rash see
  • Flexor surfaces (elbows, wrists, knees)
  • Face, hands, feet
  • Worsens when exposed to allergens
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46
Q

Atopic dermatitis:
* What are the treatment goals?

A
  • Provide symptom relief
  • Control atopic dermatitis
  • Identify and reduce triggers
  • Prevent exacerbations
  • Minimize treatment adverse effects
  • Treat secondary skin infections->MC Staphylococcus
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47
Q

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?

A
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48
Q
  • What is the first line pharmacologic therapy for atopic derminitis?
  • What are the directions?
A

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

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49
Q

What is second line, systemic and toher agents for atopic derm?

A

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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50
Q
A
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51
Q

Contact dermatitis:
* What type of reaction?
* What type of rash? What are the two types of CD?

A
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52
Q

What are causes of irritant contact and allergic contact dermtitis?

A
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53
Q

Contact dermatitis - treatment
* What is first line?
* What is second line?

A
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54
Q

CONTACT DERMATITIS - TREATMENT
* What do you use for acute and weeping?

A
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55
Q

ECZEMATOUS DERMATITIS

What are the nonpharmacologic txt for nummular dermatitis?

A
  • Reduce skin dryness
  • Moisturize 1-2 times daily
  • Reduce irritants
  • Non soap cleansers
  • House humidification
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56
Q

What is first line pharm for nummular dermatitis?

A

High or ultra-high potency TCS x 2 to 4 weeks

2nd line: Triamcinolone lesion injection Phototherapy

57
Q

What are the non-pharm txt of Dyshidrosis?

A
  • 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
Q

What is the first line pharm txt of Dyshidrosis?

A
  • High or ultra-high potency TCS x 4 weeks
  • Ointments preferred; not often tolerated

D/t this being thick skin

2nd: Systemic corticosteroids-> Prednisone 40 to 60 mg PO x 1 week, followed by taper

59
Q

What is the nonpharm txt of Perioral dermatitis?

A

Zero therapy
* Elimination of corticosteroids
* Non soap cleansers
* Reduce irritants (make-up, sunscreen)

60
Q

What is the first line thearpy of perioral dermatitis?

A
  • Erythromycin 2% topical gel x 4 to 8 weeks
  • Metronidazole topical gel, lotion, cream x 8 weeks
  • Pimecrolimus / tacrolimus topical x 4 weeks
61
Q

Seborrheic Dermatitis:
* Requires what?
* Associate with what?
* What are mc areas?
* What is mild and severe types?

A
  • 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
Q

What is the treatment and SE of dandruff and facial seborrheic dematitis

63
Q

Cradle cap:
* Subset of what?
* When is onset?
* What type of condition?
* What are the characterisitcs?

A
  • 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
Q

What is the txt of cradle cap?

A
  • Application of baby oil or petroleum
  • Scale removal
  • Washing with baby shampoo
65
Q

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
Q

What is DRESS syndrome?

A

Drug reaction with eosinophilia and systemic symptoms

67
Q

What is the txt for exanthematous drug eruptions?

68
Q

What drugs can cause exanthematous drug eruptions?

69
Q

What drugs can cause photosensitivity?

70
Q

Lichen Planus:
* What type of disease?
* What does it affect?
* Associated with what?

A

Immune-mediated
* Skin, nails, mucous membranes
* Including oral cavity, genitalia
* Association with Hepatitis C

71
Q

What is the first line and 2nd line txt of lichen planus?

72
Q

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
Q

What is the txt of pityrasis rosea?

A

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
Q

Psoriasis:
* What type of disease? What is the pathophysiology of this?

A

Autoimmune disorder
* Immune response does not turn off
* Increased levels of cytokines
* Abnormal and excessive proliferation of keratinocytes
* Keratin growth > sloughing

75
Q

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
Q

Psoriasis:
* Treatment depends on what?
* What is the mc type?
* Therapies are aimed at what?

A

Treatment depends on type and severity
* MC: limited (mild) – 80%
* Therapies aimed at decreasing symptoms and
keratinocyte proliferation

77
Q

Psoriasis general txt:
* What should all patients be doing?
* Mild dx?
* Moderate to severe dx?

A
  • All patients -> nonpharmacologic
  • Mild dx = topical therapy
  • Moderate to severe dx = systemic therapy
78
Q

Psoriasis txt:
* What are the nonpharm and pharm txts?

A

Nonpharmacologic pharmd
* Stress reduction
* Moisturizers
* sunscreen

Pharmacologic
* Topical therapies: TCS, vitamin D analogs, retinoids
* Phototherapy
* Systemic therapies
* Steroids, monoclonal antibodies

79
Q

What is mild, moderate and severe psoriasis?

80
Q

Vitamin D analogs:
* What are the different ones?
* What is the MOA?
* What are the SE?

81
Q

Retinoids and anthralin:
* What are the different ones?
* What is the MOA?
* What are the SE?

82
Q

PHOTOTHERAPY-UVB
* Interferes with what?
* Decreases what?
* Type of therapy?

A
  • ­ Interferes with protein and nucleic acid synthesis
  • ­ Decreased epidermal keratinocyte proliferation
  • ­ Monotherapy or to increase efficacy of topical agents (coal tar, anthralin)
83
Q

PHOTOTHERAPY-ADRs
* What is it for?
* Risk of what?
* What protection is needed?

A
  • ­ Erythema, pruritus, xerosis, hyperpigmentation, blistering
  • ­ Theoretical risk of skin cancer
  • ­ Eye protection needed
84
Q

PHOTOTHERAPY- (P)UVA
* Similar MOA as what?
* Dermal penetration may do what?
* Given with what?
* effective?

A
  • Similar MOA as UVB
  • ­ Dermal penetration may decrease inflammation
  • ­ Given with psoralens (photosensitizer) to increase efficacy
  • Most effective but difficult to find
85
Q

ADRs:
* What is it used for?
* Increased risk of what?
* CI in who?
* What is needed?

A
  • 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
Q

What is the txt flow for mild to moderate psoriasis?

87
Q

What is the txt flow for mod to severe psoriasis?

88
Q

Systemic therapies of psoriasis:
* What are the first lines of nonbiologic agents?
* What are the first lines of biologic agents (when systemic therapies fail)?

A

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
Q

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?

A

Increase infection risk = ALL

90
Q

Cyclosporine:
* What is the MOA?
* What are teh SE?
* What do you need to monitor?

A

Increase infection risk = ALL

91
Q

Acitretin:
* What is the MOA?
* What is the CI?

A

Increase infection risk = ALL

92
Q

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
Q

Erythema Multiforme:
* What type of reaction is this?
* What happens in results?
* What are the most common triggers?

94
Q

What is erythema multiforme minor and major?

95
Q

EM treatment?

A
  • Rapid onset – 24 to 48 hours
  • Lasts for 48 hours…..begins to resolv
96
Q

What are the drugs that can cause SJS?

A

SATAN – sulfa, allopurinol, tetracylines, anticonvulsants, NSAIDS
* Anticonvulsants: lamotrigine, phenytoin, carbamazepine, phenobarbital

99
Q

Acne:
* What is increased (2)?
* What is colonized?
* Release what?

A
  1. Increased follicular keratinization
  2. Increased sebum production by sebaceous gland ( increase androgens)
  3. Cutibacterium acnes follicular colonization
  4. Release of inflammatory mediators
100
Q

Acne-Classification
* What is noninflammatory and inflammatory?

101
Q

Treatment of acne:
* Most critical target is what?
* Elimination of what?
* What are the goals?

A
  • 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
Q

What are the nonpharm therapy acne?

103
Q

What is the pharm flow chart of acne?

104
Q

Select topical agents for acne:
* Benzyol peroxide: MOA, ADRs, comments

105
Q

Select topical agents of ance-> topical retinoids
* What are the topical?
* What is the MOA?
* ADRs?
* What are the comments (CI)?

106
Q

Clindamycin 1% and erythromycin:
* What is the MOA?
* What are the ADRs? (only Clindamycin)
* What are the comments? (only Clindamycin)

108
Q

ISOTRETINOIN
* What type of derivative?
* Works on what?

109
Q

Isotretinoin:
* What is the dosing?
* What is the max dose?
* Multiple brand names and generic?

110
Q

Isotretinoin:
* What needs to happen since it is teratogenic?
* What do you need to caution with its/

111
Q

What are the adverse effects of isotretinoin?

112
Q
  • What do you need to monitor with isotretinoin?
  • What happens in pregnacy?
113
Q

Hormonal agents for acne:
* What are the the different ones and their MOA?

A

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
Q

What are the SE of Spironolactone?

115
Q

Fill in for the txt of acne

116
Q

Rosacea:
* What type of skin disease?
* What is the rash?
* Face usually appears as what?
* What is often present?

A
  • 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
Q

Rosacea txt for flushing and redness:
* What is first line, second line and the pharmcotherapy options?

118
Q

Treatment of rosacea-> Papules/pustules
* What is the txt for mild to moderate?

119
Q

Treatment of rosacea-> Papules/pustules
* What is the txt for moderate to severe?

120
Q

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
Q

Mupurocin (bactroban)-Cream/ointment
* What is the MOA?
* What are the indications?
* What is the dosing?
* What are the adverse rxns?

122
Q

What are teh ABCDE?

123
Q

What is the premalignant cutaneous lesion?

A

Actinic keratosis

124
Q

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
Q

Actinic keratosis
* What are the lesion directed therapies?

A

Isolated lesion:
* Cryotherapy (MC)
* Curettage / shave
* Surgery

Mild therapies only

126
Q

AK TREATMENTS
* What are the field directed therapies?
* What are the topical medicine therapies?

127
Q

Fill in for the topical txt of AK

128
Q

Fill in for AK topical treatments?

129
Q

Label

130
Q

GENERAL NEOPLASM TREATMENT OPTIONS
* What are the five different options?

131
Q

Basal cell carcinoma
* What are the characteritics?

132
Q

What are the characteristics of low risk and high risk recurrance with BCC? What is the first line of each?

133
Q

Squamous cell carcinoma:
* What are the characteritics?

134
Q

What are the characteristics of low risk and high risk recurrance with SCC? What is the first line of each?

135
Q

melanoma:
* Involes what?
* May or may not originate from waht?
* Rapidly _
* Cure rates are lower when? (2)

136
Q

Fill in for melanoma

137
Q

Melanoma txt:
* What is mainstay?
* When is LN biopsy recommended?
* What is mainstay for unresectable or residual disease?›

138
Q

Fill in for melanoma

Pharmacology (14 decks)

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