Dermatology #1 Flashcards

1
Q

What are the four main pathophysiology factors of acne vulgaris?

A

1) follicular hyperkeratinization
2) increased sebum production
3) Propionibacterium acne overgrowth (bacteria)
4) inflammatory response

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2
Q

What stimulates sebum production with acne vulgaris?

A

Androgens

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3
Q

Clinical manifestations of acne vulgaris

A
  • Often occur in areas with sebaceous glands (chest, back, face, upper arms)
  • Open comedones: blackheads (incomplete blockage)
  • Closed comedones: whiteheads (complete blockage)
  • Inflammatory: papules or pustules surrounded by inflammation
  • Nodular or cystic: often heals with scarring
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4
Q

Explain the different severity levels of acne vulgaris (mild, moderate, and severe)

A

Mild: comedones, small amounts of papules/pustules
Moderate: comedones, larger amount of papules/pustules
Severe: nodular or cystic acne

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5
Q

Management of the three severities of acne vulgaris

A
  • Mild: Topical (Azelaic acid, salicylic acid, benzoyl peroxide, retinoids. Tretinoin or topical ABX such as Clindamycin or Erythromycin)
  • Moderate: As above + Oral ABX (Minocycline or Doxycycline). Spironolactone
  • Severe: Oral Isotretinoin
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6
Q

What is the most effective medication for acne vulgaris and why?

A

Isotretinoin

-Affects all 4 pathophysiologic mechanisms of acne

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7
Q

Name 5 side effects of isotretinoin

A
  • Dry skin and lips
  • Highly teratogenic: must obtain at least 2 pregnancy tests prior to starting treatment and commit to 2 forms of contraception. Must sign up for iPledge. Monthly pregnancy tests before refills.
  • Increased triglycerides and cholesterol
  • Photosensitivity
  • Worsening of Diabetes Mellitus
  • Headache
  • Fatigue
  • Visual Changes
  • Premature closure of long bones
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8
Q

Risk factors for acne rosacea

A
  • Women

- 30-50 years old

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9
Q

What is acne rosacea?

A

Disease of pilosebaceous units associated with increased activity of capillaries, leading to telangiectasias and flushing secondary to vasodilation

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10
Q

Triggers of acne rosacea

A
Alcohol
Hot or cold weather
Hot drinks
Hot baths
Spicy foods
Sun exposure
Medications

(HEAT RELATED)

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11
Q

Symptoms of acne rosacea

A
  • Acne-like rash (papulopustules)
  • Centrofacial erythema
  • Facial flushing
  • Telangiectasias
  • Skin coarsening with burning and stinging
  • Red eyes
  • Later, lymphedema, hyperplasia, and telangiectasias develop
  • Rhinophyma (red, enlarged nose), otophyma (ear), gnathophyma (chin), metophyma (forehead), and blearophyma (eyelid)
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12
Q

Although a ______ is the definitive diagnostic for acne rosacea, it is rarely done.

A

Biopsy

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13
Q

Treatment for acne rosacea

A
  • Lifestyle modifications: limit triggers, avoid irritants
  • Topical metronidazole (first-line), Sodium sulfacetamide, erythromycin
  • Oral ABX (Tetracycline, Minocycline, or Doxycycline if fail topical treatments)
  • Oral isotretinoin if failed other treatments or severe
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14
Q

For the facial erythema of acne rosacea, what is a specific treatment/medication that can be given?

A

Topical Brimonidine

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15
Q

Risk factors for folliculitis

A
  • Men
  • Prolonged use of ABX
  • Topical corticosteroids
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16
Q

MCC of folliculitis

A

Staph Aureus

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17
Q

MCC of hot tub-related folliculitis

A

Pseudomonas aeruginosa

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18
Q

Noninfectious folliculitis is common in what types of jobs?

A

People working hot, oil environments such as engine workers, on ships, machinists, or working in a hot, dirty environment
-Occlusion, perspiration, skin rubbing against tight clothing

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19
Q

Symptoms of folliculitis

A
  • Singular or clusters of erythematous papules or pustules on hair bearing skin
  • Not painful, but pruritic
  • Abscesses may form at the site of severe folliculitis
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20
Q

Treatment for folliculitis

A
  • Gentle cleansing with antibacterial soap and mild compresses
  • Topical Mupirocin, Clindamycin, Erythromycin, or Benzoyl peroxide
  • Oral ABX for severe: Cephalexin or Dicloxacillin
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21
Q

Treatment for hot tub folliculitis

A

usually resolves without treatment (severe cases may be treated with an oral fluoroquinolone such as Ciprofloxacin, Moxifloxacin)

22
Q

What is Erythema Multiforme?

A

-Type IV hypersensitivity reaction of the skin following infections of medication exposure

23
Q

MC infection that causes Erythema Multiforme

A
  • Herpes Simplex Virus

- Mycoplasma sp is another common cause in children

24
Q

Medications that cause Erythema Multiforme

A

-Sulfa drugs, beta-lactams, Phenytoin, Phenobarbital, Allupurinol

25
Q

Explain the lesions in Erythema Multiforme

A

Target lesions that have 1) a dusky central area or blister, 2) surrounded by a pale ring of edema and 3) an erythematous halo on the extreme periphery
-Most common on extremities and trunk

26
Q

Other symptoms of Erythema Multiforme

A
  • Negative Nikolsky sign: no epidermal detachment. Often febrile.
  • Minor: target lesions with no mucosal involvement
  • Major: target lesions head –> centrally + mucosal membrane involvement (oral, genital, ocular). No epidermal detachment still.
27
Q

What are the two types of Erythema Multiforme and how do they differ?

A
  • Minor: no mucosal involvement

- Major: mucosal involvement

28
Q

Treatment for Erythema Multiforme

A
  • Symptomatic: discontinue offending agent, antihistamines, skin care. Diphenhydramine + Lidocaine mouth wash for oral lesions
  • Systemic corticosteroids if severe. Oral Acyclovir if HSV related.
29
Q

What are Steven-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)?

A

Severe mucocutaneous reactions characterized by detachment of the epidermis and extensive necrosis

30
Q

What is the difference between SJS and TEN?

A

SJS: sloughing involving < 10% of body surface involvement
TEN: sloughing involving > 30% of body surface involvement

31
Q

Risk Factors/Causes of SJS/TEN

A
  • Medications (MCC): Sulfa drugs, Anticonvulsants, Lamotrigine, Allopurinol, NSAIDS, antipsychotics, antibiotics
  • Sulfa drugs: Bactrim, Glyburides
32
Q

Symptoms of SJS and TEN

A
  • Prodrome of fever, URI followed by widespread flaccid bullae beginning at trunk/face
  • Pruritic target lesions (erythematous macule with purpuric centers) and involvement of at least 1 mucous membrane
  • Positive Nikolsky sign (epidermal detachment)
  • Ocular involvement common (uveitis, corneal ulceration)
33
Q

Treatment for SJS/TEN

A
  • Prompt discontinuation of causative agent
  • Supportive therapy: treat like severe burns (burn unit admission, pain control, prompt withdrawal of offending medications, fluid and electrolyte replacement, wound care)
34
Q

Alopecia Areata is commonly associated with

A

Other autoimmune disorders: thyroid disease, Addison’s disease, etc.

35
Q

Exam findings of Alopecia Areata

A
  • Exclamation point hairs: short hairs broken off a few mm from the scalp. Tapering near the proximal hair shaft.
  • Nail abnormalities: pitting, trachyonychia (roughening of the nail plate)
  • Smooth, discrete, circular patches of complete hair loss that develop over a few weeks
36
Q

What gives a definitive diagnosis of alopecia areata?

A

-Punch biopsy

37
Q

Treatment for alopecia areata

A
  • Local: intralesional corticosteroids

- Extenstive: topical corticosteroids

38
Q

What is alopecia totalis and alopecia universalis?

A

Totalis: complete scalp hair loss
Universalis: complete hair loss on scalp and body, including eyelashes

39
Q

What is androgenetic alopecia?

A

Genetically predetermined loss of terminal hairs on scalp in a pattern. Most common type of hair loss in men and women.

40
Q

What is the key androgen that leads to hair loss in androgenetic alopecia

A

Dihydrotestosterone (DHT)

41
Q

Activation of DHT does what in androgenetic alopecia?

A

Shortens the anagen (growth phase) in the normal hair growth cycle
-Pathologic specimen show decreased anagen to telogen ratio

42
Q

Symptoms of androgenetic alopecia

A
  • Hair thinning and non scarring hair loss
  • -In males, it begins as bitemporal thinning of frontal scalp then involves vertex
  • -In females, thinning of hair between frontal and vertex of scalp without affecting frontal hairline
43
Q

Treatment for androgenetic alopecia

A
  • Topical Minoxidil: Requires 4-6 month trial and must be used indefinitely
  • Oral Finasteride
  • Hair transplant
44
Q

Mechanism of action of Minoxidil

A

-Widens blood vessels, allowing more blood, oxygen, and nutrients to promote the anagen (growth phase)

45
Q

Finasteride, a 5-alpha reductase type 2 inhibitor, has a MOA of

A

-androgen inhibitor (inhibits the conversion of testosterone to dihydrotestosterone)

46
Q

What are some adverse effects of Finasteride?

A

Decreased libido, sexual or ejaculatory dysfunction, increased risk of prostate cancer
-Category X

47
Q

Explain the Rule of 9’s (Anterior/Posterior)

A

Anterior

  • Head: 4.5%
  • Torso: 9%
  • Belly: 9%
  • Genital: 1%
  • Arm: 4.5%
  • Leg: 9%

Posterior:

  • Head: 4.5%
  • Torso: 9%
  • Lower Back: 9%
  • Arm: 4.5%
  • Leg: 9%
48
Q

What is considered a “minor burn” in adults and children/old?

A

Adults: < 10% TBSA
Children/Old: < 5% TBSA
–Must be isolated injury
–Must NOT involve face, hands, perineum, feet
-Must NOT cross major joints or circumferential.

49
Q

What is considered a MAJOR burn in adults and children/old?

A

Adults: > 25% TBSA
Children/Old: > 20% TBSA
-Burns involving: face, perineum, hands, feet
-Burns crossing major joints, circumferential

50
Q

What is the rule of 9’s chart that is used (the specific name of it)?

A

Lund-Browder Chart (most specific)