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Clin Med I > Derm II > Flashcards

Derm II Flashcards

1
Q

Adolescent acne vs. Adult acne gender predilection

A

Adolescent - male

Adult - female

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2
Q

4 main factors of acne vulgaris

A
  1. Follicular hyperkeratinization
  2. Increased Sebum production
  3. Cutibacterium ances w/in follicle
  4. Inflammation

–> sebum is a growth medium for C. ances, Microcomedones are an anaerobic, lipid rich space for them, increased proliferation = increased inflammation

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3
Q

Closed comedone

A

Whitehead

-accumulation of sebum and keratinous material coverts a microcomedome into a closed comedome

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4
Q

Open comedome

A

Blackhead

  • the follicular oriface is opened w/ continued distension forming an open comedome
  • densely packed keratinocytes, oxidized lipids, and melanin all contribute to dark color
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5
Q

Acne vulgaris progression

A

Follicular rupture contributes to inflammatory lesions –> proinflammatory lipids and keratin are extruded into surrounding dermis –> worsened inflammation –> papules and nodules form

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6
Q

Most common endocrine disease associated w/ acne? What are some S/S

A

PCOS

-menstrual irregularity, insulin resistance, acne, hirsutism, ovarian cysts, acanthosis nigrans

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7
Q

What disease are androgens related to? How do they contribute?

A

Acne vulgaris

-stimulate the growth and secretory function of the sebaceous gland

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8
Q

Androgen production in adults vs. infants

A

adults - adrenal glands

infants - adrenal gland & testes in males, adrenal glands in females

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9
Q

A 6 mo. old presents with acne lesions, what is the cause? What should you advise the parents?

A
  • Elevated levels of androgens

- Androgen levels fall by age 1-2 and acne improves

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10
Q

A pts labs come back with elevated androgen levels, what conditions commonly present w/ Hyperandrogenism?

A
  • PCOS
  • Congenital adrenal hyperplasia
  • Adrenal or Ovarian tumors
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11
Q

How does insulin resistance affect acne

A
  • increases risk

- may increase androgen production and is associated w/ increased serum levels of insulin-like GF-1

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12
Q

Pt presents with acne lesions that are both closed and open, but not red or painful

-classify & stage

A

Comedonal acne –> non-inflammatory

Stage I (mild) - minor, no inflammation, black/whiteheads

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13
Q

Pt presents with acne lesions including papules & pustules that are red and inflammed

-classify & stage

A

Inflammatory acne

Stage II (moderate) - more blackheads, whiteheads, papules/pustules, slight inflammation, may progress from face

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14
Q

Extensive acne lesions that are highly inflammed and cause scarring

A

Nodular acne (cystic acne)

Stage III (Severe) - significant inflammation, severe papules/pustules, cystic nodules present, high risk for scarring and post-inflammatory hyperpigmentation

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15
Q

Female presents w/ persistent acne, irregular menstrual cycles & hirsutism

what test should you order?

A

PCOS –> endocrine testing for androgen levels

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16
Q

Treatments of acne vulgaris should target:

A

one of the 4 main contributors

  • follicular hyperkeratinization
  • increased sebum production
  • C. ances proliferation
  • Inflammation
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17
Q

Considerations for topical retinoids tx AV

A
  • once daily @ bedtime
  • local skin irritation, sun sesnitivity
  • Atralin - fish allergy
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18
Q

Considerations for topical combination products tx AV

A
  • once a day dosing
  • local skin irritation
  • may bleach hair/clothing
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19
Q

Considerations for oral abx tx AV

A
  • severe acne only, usually by specialist
  • avoid LT use
  • flare control
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20
Q

Pt presents w/ non-inflammatory open & closed comedones –> first line of tx after determining pt has a skin care routine

A
  • BP
    -Topical Retinoid
    or
    -Topical Combination Therapy (BP + abx, Retinoid + BP, or Retinoid + BP + abx)
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21
Q

Pt presents with slightly inflamed acne lesions with some papules and pustules –> 1st line of tx

A
  • Topical Combination Therapy (BP + abx, Retinoid + BP, or Retinoid + abx)
  • Oral abx + Topical Retinoid + BP
  • Oral abx + TR + BP + Topical abx
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22
Q

Pt presents with severely inflamed cystic acne lesions –> 1st line tx

A
  • Oral abx + Topical Combination Therapy (BP + abx, or Retinoid + BP + abx)
  • Oral Isotretinoin
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23
Q

For females w/ persistant inflammatory acne, what medications can we consider adding?

A

Oral contraceptives or Spironalactone

–> antiandrogenic

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24
Q

When prescribing a pt w/ acne vulgaris medication, what are important counceling points?

A
  • no cure –> improve outbreaks
  • may take 4 - 6 weeks to benefit
  • may get worse before it gets better
  • bleaching w/ BPO combo products
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25
Q

Who is most likely to develop rosacea?

A

-fair skinned, >30 y/o, women (men for phymatous)

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26
Q

prevalence of rosacea

A

1 - 10%

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27
Q

36 y/o female presents w/ persistent central erythema that gets worse when she drinks alcohol, she reports a stinging/burning sensation on the associated lesion. PE shows spidered vessels and roughness. How can you explain to this pt the pathogenesis of her disease?

A
  • Erythematotelangiectatic Rosacea
  • cause is unknown, related to: Immune dysfunction, Inflammatory responses to cutaneous microorganisms, UV damage, Vascular dysfunction
28
Q

Erythema congestivum

A
  • sxs of rosacea

- after exacerbation of facial redness, the return to baseline is slow

29
Q

Pt presents w/ papules and pustules on her cheeks and central face. PE shows inflammation that extends past the follicle and no presence of comedones. What should you council this pt to avoid?

A

Papulopustular rosacea

  • extreme temps, sun, hot beverages, spicy foods, EtOH, exercise, irritation from topical products, drugs (nicotinic acid, vasodilators)
  • also exacerbated by emotions
30
Q

54 year old male presents with thickened skin forming irregular contours on his nose & cheeks, what causes these contours to form?

A
  • Phymatous rosacea

- Tissue hypertrophy

31
Q

What is the risk for a patient with rosacea to develop ocular rosacea

A

> 50%

32
Q

How do you dx rosacea?

A
  • HPE

- no lab/serologic studies available

33
Q

Management of Erythematotelangiectatic Rosacea

A
  • 1st line: behavioral changes
  • 2nd line: laser and light based therapy
  • 3rd line: Alpha adrenergic agonists (topical –> Brimonidine gel, Oxymetazoline cream)
34
Q

Management of Papulopustular Rosacea

A
  • Topical Metronidazole cream/gel
  • Topical Azelaic acid cream/lotion/foam/gel
  • Topical Ivermectin cream
  • Oral Tetra, Doxy or Minocycline
  • Oral Isotretinoin
35
Q

Management of Ocular rosacea

A
  • lid scrubs, warm compress
  • Topical abx - Ilotycin ointment
  • Refer
36
Q

Management of Phymatous rosacea

A
  • Early dz: Oral Isotretinoin QD

- Late dz: Laser ablation or surgery

37
Q

Prevalence of Psoriasis (adults & peds)? Gender/Age predilection?

A
  • adults: 0.9 - 8.5% (55 - 79% = chronic plaque psoriasis)
  • peds: 0 - 2.1%
  • No gender predilection
  • peak onset: 30 - 39 yrs & 50 - 69 yrs
38
Q

Increased distance from the equator is associated w/ inc. rates of what disease

A

Psoriasis

39
Q

Psoriasis epidermis compared to normal epidermis shows:

A
  • increased epidermal stem cells
  • increased number of cells undergoing DNA synthesis
  • shortened cell cycle time of keratinocytes
  • decreased turnover time of the epidermis
40
Q

Pt presents w/ well demarcated, elevated erythematous plaques located symmetrically on her extensor elbows, knees and scalp. She reports the lesions are pruritic. Lesions have a silver scale appearance. What are two signs that are associated w/ this disease?

A
  • Chronic plaque psoriasis
  • Koebner phenomenon: development of skin disease in sites of skin trauma
  • Auspitz signs : visualization of pinpoint bleeding after removal of a scale overlying a psoriatic plaque
41
Q

22 y/o male presents w/ small papules and plaques (<1 cm) on his trunk and arms. Pt states these lesions appeared over the past 24 hours. Pt states he was last seen at his PCP 2 weeks ago for Streptococcal pharyngitis. Diagnosis? Who normally gets this?

A

Guttate Psoriasis

-children & young adults w/ no history of psoriasis

42
Q

Pt presents w/ acute onset of widespread erythema, scaling, and sheets of superficial pustules. What are you worried about? Causes?

A
  • Pustular Psoriasis
  • Life-threatening complications –> malaise, fever, diarrhea, leukocytosis & hypocalcemia
  • caused by pregnancy, infection, & withdrawal of oral GCs
43
Q

Erythrodermic Psoriasis presentation & consideration for management

A
  • can be acute or chronic
  • generalized erythema & scaling from head to toe
  • usually managed inpatent d/t high risk for infection & electrolyte abnormalities
44
Q

Pt presents w/ erythematous lesions w. no visible scaling distributed over her intertriginous areas –> why is this often misdiagnosed?

A
  • Inverse Psoriasis

- because there is often no visible scaling it can be misdiagnosed as a fungal or bacterial infxn

45
Q

Pt w/ Psoriatic arthritis comes in for an exam –> what manifestation are they at higher risk for ?

A

Nail Psoriasis –> most often Nail pitting

46
Q

How do we diagnose Psoriasis?

A
  • HPE: family hx (40% have 1st degree relative), characteristic plaques, Auspitz sign
  • Can do a 4mm punch biopsy to r/o other dz
  • No lab studies
47
Q

When taking a pt hx, what are some risk factors to watch for when considering a diagnosis of Psoriasis?

A
  • genetics (40% - 1st degree relative)
  • smoking
  • obesity (proinflammatory cytokines)
  • drugs (beta-blockers, Litium, antimalarials, NSAIDs, Tetracycline)
  • Strep pharangitis –> Guttate
  • HIV
  • Vitamin D deficiency (baseline lower levels)

-Exacerbations d/t Infections, EtOH, Stress

48
Q

Pathophysiology of Psoriasis

A
  • Complex, immune mediated
  • Hyperproliferation and abnormal differentiation of the Epidermis –> Scaling, Induration, & Erythema

–> no cure, manage sxs

49
Q

Mild-Moderate Psoriasis Management

A
  • Emollients
  • Topical Corticosteroids (Hydrocortisone, Triamcinolone, Flucinonide, Betamethasone diproprionate, Clobetasol)

ALTERNATIVES:

  • Tar-T/Gel
  • Vitamin D Analogs (Calcipotriol cream/foam, Calcitrol ointment, Tacalocitol)
  • Topical Retinoids (Tazarotene cream)
  • Anthralin shampoo
  • Tacrolimus (immunomodulator, good for large areas)
50
Q

Moderate-Severe Psoriasis Management (5 - 10% BSA affected)

A
  • Phototherapy
  • Excimer laser (higher doses of UVB but <10 treatments needed for results)
  • Systemic (MTX + Folic acid - 2-25 mg weekly, Cyclosporine [T-cell suppressor] - 2.5 - 5 mg/kg/day BID, Apremilast [PDE-4 Inhibitor] - 10-30 mg daily or BID)
  • Biologics (TNF-alpha inhibitors, IL-17 inhibitors, IL-23 and related cytokine inhibitors)
51
Q

Phototherapy in the Management of Moderate-Severe Psoriasis

A
  • good for widespread disease (>5% BSA)
  • UVB: +/- topical therapy –> near-erythema inducing dose 3/week until remission
  • Narrow band UVB: suberythemogenic dose, usually more effective & fewer doses req.
  • Photochemotherapy (PUVA): tx w/ oral or bath Psoralen followed by 2 hrs. UVA radiation –> 3x/week until remission, then 1-2x/week maintenance
52
Q

Hidradenitis Suppurativa is what kind of condition? AKA?

A
  • Chronic follicular occlusive skin condition

- Acne Inversa

53
Q

Prevalence of Hidradenitis Suppurativa? Who gets it? Distribution?

A

1 - 4%

  • African American Women
  • Onset ~ puberty - 40 y/o
  • Intertriginous areas (axilla, groin, perianal. inframammary)
54
Q

32 y/o African American pt presents w/ a single, painful, deep seated nodule in her axilla, pt states the last time this happened there were more than one painful lesion –> What stage is this? Management for this stage?

A
  • Hidradenitis Suppurativa
  • Hurley Stage I
  • Behavioral: avoid skin trauma, smoking cessation, weight management
  • Antiseptics: Chlorhexidine 1x/week
  • Emollients
  • Management of comorbidities
55
Q

What are the Hurley Stages

A
  • Hidradenitis Suppurativa
  • Stage I: abscess formation
  • Stage II: recurrent abscess formation w/ sinus tract formation & scarring
  • Stage III: diffuse involvement of multiple interconnected sinus tracts
56
Q

What is the pathophysiology for Hidradenitis Suppurativa?

A
  • Follicular occlusion –> rupture –> associated immune response
  • Ductal keratinocyte proliferation –> ductal plugging –> expansion –> rupture & release of contents –> immune response –> sinus tracts in skin
57
Q

Management of a patent classified as Hurley Stage II

A
  • Hidradenitis Suppurativa
  • Oral Tetracyclines for several months (Doxy - 100 mg BID, Tetra - 500 mg BID, Mino - 100 mg QD/BID)
  • Clindamycin 300 mg BID or Rifampin 600 mg QD
  • Oral Retinoids
  • Antiandronergic therapies (for females, BC, Spironolactone)
  • Punch biopsies of fresh lesions to prevent sinus tracts
58
Q

Management of a patent classified as Hurley Stage III

A
  • Hidradenitis Suppurativa
  • TNF-alpha Inhibitors (adalimumab, Infliximumab)
  • Systemic glucocorticoids (Prednisone)
  • Cyclosporine
  • Surgery
59
Q

Prevalence of Alopecia? Age/Gender predilection?

A
  • 1 in 1000, lifetime risk of 2%
  • 3rd decade of life, but can occur any time
  • No gender predilection
60
Q

Alopecia pathogenesis?

A
  • Autoimmune disease in which hair follicles in the growth phase (anagen) prematurely transitions to non-proliferative involution (catagen) and resting (telogen) phase
  • causes sudden hair shedding and inhibitor of regrowth + no permanent damage
  • T-cell mediated –> inappropriate trigger of immune response against follicular antigens
61
Q

Risk factors for Alopecia

A
  • Genetics (20% have first degree relative)
  • Severe stress
  • drugs and vaccinations
  • infections
  • vitamin D deficiency
62
Q

Diseases associated w/ Alopecia

A
  • **Thyroid Disease
  • Lupus
  • Vitiligo
  • Atopic dermatitis
  • Allergic rhinitis
  • Psoriasis
  • Down syndrome
  • Polyglandular autoimmune syndrome type I
63
Q

Pt presents w/ smooth, circular, discrete patches of complete hair loss that developed over the past 2-3 weeks. Pt states that the patches are pruritic and burn. What do you expect to see on PE? What lab test would you order?

A

Alopecia areata

  • exclamation point hair at margins
  • thyroid testing
  • if biopsy done (rare) - peribulbar lymphatic inflammatory infiltrates surrounding follicles (swarm of bees)
64
Q

Management of Alopecia

A

Limited hair loss (areara)
-Topical or Intralesional corticosteroids (Triamcinolone, Betamethasone diproprionate) –> Caution: skin atrophy, hypopigmentation

Extensive hair loss (totalis, universalis)
-Topical Immunotherapy (DPCP, SADBE, DNCB) –> 2% solution applied to desensitize pt, 1-2 weeks later 0.01% solution applied to area 1/week, slowly titrate up to 2% –> DC if no improvement by 6 mo.

2nd line: Minoxidil, Anthralin cream, Phototheraphy (PUVA)

Systemic Therapies: Oral GCs, Sulfasalazine, MTX, Cyclosporine, Biologics

65
Q

Clinical Course of Alopecia?

A
  • 50% w/ limited patchy hair loss recover spontaneously w/in a year
  • some progress to multiple episodes
  • 10% progress to alopecia totalis or univeralis
66
Q

What manifestation would you expect to see in alopecia totalis/universalis that is less common in alopecia areata

A
  • nail abnormalities –> Onyxhorrhexis (longitudinal nail fissuring)
  • 60% in severe disease
  • 10-20% in Areata

Clin Med I (4 decks)

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