Week 1 Flashcards
Atopic Dermatitis (Eczema)
“The itch that rashes”; we have is a breakdown of normal skin barrier, leading to water loss/dryness
Major features: Pruritus, Rash on face and/or extensors in infants and young children, Lichenification in flexural areas in older children, Tendency toward chronic or chronically relapsing dermatitis, Personal or family history of atopic disease: asthma, allergic rhinitis, atopic dermatitis
Clinical Findings: Acute skin lesions are characterized by intensely pruritic, erythematous papules associated with excoriation, vesicles over erythematous skin, and serous exudate, lesions are symmetrical
Pathophys: AD is a highly pruritic inflammatory skin disease that results from complex interactions between genetic susceptibility genes resulting in a defective skin barrier, defects in the innate immune system, and heightened immunologic responses to allergens and microbial antigens.
Differentials: Allergic reaction, Psoriasis
Tinea Capitis
Dermatophyte infection of hair and scalp
Clinical Findings: pruritic, painful, scaly plaques on scalp with broken hairs, numerous pustules, diffuse erythema, crusting, and scale
Treatment: Griseofulvin and itraconazole
Mild to moderate acne
Clinical Findings: Erythema, pustules, closed and open comodomes
Pathogenesis: first step: ducts become blocked with oil from puberty
- DHT (dihydrotestosterone/androgens) goes up, follicles become blocked from increased sebum production
- Keratinocytes - hyperproliferation of the epidermal layer and the keratin increases plugging of the pore, and you end up getting a microcomodome
○ Follicular epidermal hyperproliferation of keratinocytes (excess keratin production and it gets sticky and clogs pore); then you get excess sebum production because of that pesky androgen
- 2nd thing that happens: microcomodomes continue to grow, more keratin, more sebum, bacteria get in and causes a hot mess!
○ As they grow, you get more inflammation and they can rupture and cause even more inflammation
Treatment: low sugar diet, benzoyl peroxide, salicylic acid
Pathogenesis of acne and how do hormones cause acne?
The pathogenesis of acne is multifaceted, but four basic steps have been identified. These key elements (Fig. 80-1) are: (1) follicular epidermal hyperproliferation, (2) excess sebum production, (3) inflammation, and (4) the presence and activity of Propionibacterium acnes. Each of these processes are interrelated and under hormonal and immune influence.
Increase in androgen causes follicular epidermal hyperproliferation causing overgrowth of keratin causing increase in sebum causing blockage of pores. Increased sebum causes continued growth of keratin causing increase in inflammation causing ruptured comedo which releases the sebum and causes increase in proliferation of p.acnes
Non-RX treatment for Atopic Dermatitis
-skin hydration (take warm 10 min baths to hydrate skin, then use moisturizer to lock in hydration–use oil based) -identifying allergen (allergy testing) -avoiding allergen and substances that could cause irritation (use fragrance free, dye free, sensitive skin products)
Alternative treatment for Atopic Dermatitis
-coal tar: anti-itch, anti-inflammation -lactic acid: add moisture -phototherapy: sunlight -probiotics: lactus bacilluc -chinese herbs: anti-itch -oral omega 3: add moisture -peanuts: introduce early
Meds to stop scratch-itch cycle
- Antihistamines can be used secondary to any histamines that don’t cross the blood-brain barrier
- Corticosteroids, Topical
- High potency steroids are for acute
- Lower potency steroids used for chronic situations
Allergic reaction to a medication
Adverse cutaneous drug eruptions (Table 251-3) are a potential complication of nearly all medications. They can be immunologically mediated or nonimmunologic. Nonimmunologic reactions can be due to enzyme deficiencies, cumulative ingestion, photosensitivity, or topical irritants. Risk factors may include age, gender, dose, and the type of medication.
Cutaneous drug eruptions can mimic almost any other skin disease. Most reactions occur within 1 to 3 weeks of exposure, but hypersensitivity reactions may take longer to develop, so obtain a careful drug history when evaluating any type of rash.18 Patients may have taken the drug in the past without any problems.
The most common presentation is the morbilliform exanthem (Figure 251-19). Diffuse, symmetric, pruritic, erythematous macules and papules appear first on the trunk and then spread to the extremities. The initial eruption is usually within 7 to 14 days of exposure, usually resolves within 2 weeks after discontinuation
An allergic reaction to the antibiotic:
§ Pruritic, diffuse rash, macules, papules, itchiness, start in trunk area
§ You know that this isn’t a viral rash because the rash is itchy
What else could it be?
○ Measles, rubella, pustular psoriasis
Moderate Rosacea
- Exacerbated by Sun exposure, alcohol, and stressors—> commonly associated with Rosacea
- Papules, puss-filled–> also characteristic of Rosacea
• Fixed centrofacial erythema in a characteristic pattern that may periodically intensify
• Phymatous changes
• Major features of rosacea (2 or more major features may be considered diagnostic)
• Flushing
• Papules and pustules
• Telangiectasia
• Ocular manifestations
• Ocular rosacea occurs in up to 50% of patients with cutaneous disease. It presents with redness, chronic irritation or foreign body sensation, and blepharitis
• History and physical examination are the primary diagnostic tools for rosacea2
• Treatment is targeted to clinical feature(s) of rosacea present in the individual patient
• Brimonidine (an α₂ agonist) is effective for overall reduction of erythema. Laser and intense pulsed light therapies are effective in reducing telangiectasias
Topical agents (ie, azelaic acid, metronidazole, ivermectin) are recommended for papulopustular disease. Subantimicrobial dose oral doxycycline (40 mg) can be added to a topical treatment if needed. Low-dose oral isotretinoin is a third line treatment
Differentials: • Could also be carcinoid syndrome, migraines, brain tumor, acne, other autoimmune conditions like lupus
Pityriasis rosea
Characteristics: typical primary plaque and secondary papulovesicles • Christmas tree pattern • Usually has a primary/larger plaque (Harrold patch) that "spreads" into the Christmas tree pattern • Can be caused by viruses (Herpes) • Papulosquamous rash • Asymptomatic • In teens • Lasts a few weeks
Clinical Findings: Classically, but not invariably, the onset of the disease is ‘heralded’ by a single round or ovoid flesh-colored or pink scaly patch of variable size ( Fig. 16.14A ). The patch may appear anywhere on the body and exhibit central clearing with a raised border. The herald patch is followed in days to weeks by an eruption of smaller, variably sized, macules, papules and scaly patches ( Fig. 16.14B ). Four main distributions have been described in children: central (face and trunk), peripheral (arms and legs), inverse (axillary and inguinal) and diffuse. 56 Lesions on the trunk arise within Langer’s skin cleavage lines and impart the appearance of a ‘Christmas tree’ pattern.
Differentials: Secondary syphilis, tinea corporis, dermatitis, psoriasis, drug reaction
