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NUNP543 > FINAL - Derm > Flashcards

FINAL - Derm Flashcards

1
Q

Describe the epidemiology of rosacea.

A

-usually 30- 50 years (can occur in children)
-genetic factors (celtic, northern european), more common in fair skin
-F>M

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2
Q

What is the pathophysiology of rosacea?

A

Cause unknown- involves genetic factors, skin sensitivity, and triggers.
-Innate immunity activated
-Vascular hyperactivity
-Inflammation

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3
Q

Triggers for rosacea?

A

Hot food and drinks, spicy food, red wine, alcohol, sunlight, harsh skin care

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4
Q

Time course of rosacea?

A

Chronic and fluctuating condition

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5
Q

Describe the signs and symptoms of rosacea.

A

-Characterized by redness, telangiectasia, flushing, blushing (vascular component), and inflammatory papules and pustules
-Central facial erythema (centrofacial distribution- forehead, cheeks, nose, around the eyes)
-No comedones

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6
Q

What are some ocular manifestations of rosacea?

A

-blepharitis and conjunctivitis
-gritty, burning, itchy eyes
-lacrimation

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7
Q

What is rhinophyma?

A

-Bulbous nose due to chronic inflammation
-Irreversible skin thickening
-More common in M

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8
Q

How to diagnose rosacea? Ddx?

A

Clinical diagnosis
-Presence of 1+ of primary features: flushing, erythema, papules and pustules, telangiectasia
-May include 1+ secondary feature: burning or stinging, dry appearance, edema, phymatous changes, ocular manifestations, peripheral location.

Ddx- acne vulgaris, seborrheic dermatitis, perioral dermatitis, contact dermatitis

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9
Q

Non pharm management of rosacea?

A

-Avoid triggers (hot food and drinks, spicy food, red wine, sunlight)
-Wear sunscreen
-Green based cosmetics can mask redness
-Avoid harsh skincare
-Photodynamic therapy

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10
Q

T/F Corticosteroids are first line for rosacea

A

FALSE avoid corticosteroids

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11
Q

Pharm management of rosacea?

A

Tx usually only if pustules
-Topical (metronidazole) or systemic (tetracycline, erythromycin)
-If chronic and relapsing, referal to derm for oral isotretinoin

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12
Q

Describe epidemiology and risk factors for acne vulgaris.

A

-85% of adolescents and young adults (9- 24 years; peak prevalence/ severity during puberty)
* Preteens: comdeonal lesions
* Teenage: inflammatory lesions
-Most common skin conditions seen by health care providers in Canada
-Risk factors: genetic predisposition, white> black/ Hispanic/ Asian, excessive face washing, local skin occlusion, conditions with hormonal imbalance, medications (lithium, phenytoin, steroids, androgens, etc.), oily cosmetics, ointments, emotional stress, local occlusion of pores

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13
Q

What are endogenous (internal/ host factors) that contribute to acne?

A
  • Hormones (androgen excess, changes in estrogen/ progesterone during menses, stressed induced cortisol release)
  • Skin microflora balance
  • Sebum overproduction
  • Skin hyperkeratinization
  • Pro-inflammatory pathways
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14
Q

What are exogenous (extenal) factors that can contribute to acne?

A
  • Medications/ drugs (progestin only contraceptives, isoniazid, phenytoin, steroids, lithium)
  • Chemical (ptrolium)
  • Oily/ waxy hair products and cosmetics
  • Over zelous facial cleansing
  • Local skin occlusion from sports gear
  • Excessive perspiration
  • Diet (high glycemic index, high dairy intake)
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15
Q

Briefly describe patho of acne vulgaris

A

-Hyperkeratinization leads to pilosebaceous follicle plugging, comedone formation
-Sebum over production leads to over proliferaction of c. acnes
-This leads to inflammation and immune response

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16
Q

When does acne vulgaris tend to resolve

A

By third decade after birth

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17
Q

Signs and symptoms of acne vulgaris?

A

-Acne lesions primarily affect the face (central facial areas, T zone (forehead, nose, chin), as well as areas of body dense in sebaceous glands (neck, chest, shoulders, back)
-Comedones
* Open (black heads- small, dome shaped, open orifice containing dark central material (oxidized fatty acids, not dirt)
* Closed (white heads- small, flesh colored, no surrounding erythema (plugged sebaceous follicle)
-Inflammatory lesions
* Pustules (superficial epidermal layer)
* Papules (lower dermal layer/ deeper- more severe inflammatory reaction, scarring may result)
* Nodules or cyst (supperative inflammatory lesions located in deep dermis; assoc with most severe form of acne.

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18
Q

Is acne in pre- pubescent kids abnormal?

A

If >1, yes! Concern for precocious puberty, hormone secreting tumours

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19
Q

Describe/ differentiate mild, moderate, and severe acne.

A

Mild- comedones, few papules/ pustules, no scarring
Moderate- comedones, papules and pustules (may or may not have scarring)
Severe- Nodules, cysts, severe scarring

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20
Q

Non pharm recommendations for acne vulgaris?

A

Avoid excess skin care, avoid stress ,avoid scrubs/ toners, use oil free make up, dont touch/ squeeze/ pick, wash face once daily (no more than BID) with water and soap less cleanser, avoid sunlight, use non comodegenic moisturizers, evidence limited for diet.

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21
Q

Describe step up therapy for acne

A

1) General measures
2) Topical BPO, topical retinoids
3) Add topical antibiotics (if papulopustular/ inflammatory)
4) Step up options include oral antibiotics, combined OCP
5) Isotretinoin (systemic)

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22
Q

Can your patient use BPO and topical retinoids in addition to isotretinoin?

A

Avoid, increased drying effect

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23
Q

What topical antibiotics are used for mild- mod acne?

A

o Clindamycin
o Erythromycin
o Dapsone

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24
Q

What oral antibiotics are used for moderate acne? Describe common AE

A

o Tetracycline and derivatives are first line (CI <8, active pregnancy, DI isotretinoin)
o Azithromycin, TMP-SMX, amoxicillin, cephalexin generally less effective.
o AE: candida infection, GI upset, photosensitivity

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25
Q

T/F IUDs are good for acne

A

F- at least for hormonal- unopposed progestin leads to acne, hirsutism

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26
Q

Describe teaching and monitoring for accutane.

A
  • Influences all aspects of acne formation.
  • Strongest and most effective acne tx, can provide long term remission
  • First line for severe (nodulocystic) acne
  • Many side effects and potential AE
    o Skin dryness, GI upset, myalgia and joint pain, fatigue, HA, hematuria, hematologic abnormalities, elevated triglycerides
    o VERY teratogenic*** 2 negative preg tests separated by 1 month, 2 forms active birth control. Unsafe in lactation
    o Baseline CBC, LFTs, lipid panel and ongoing monitoring (i.e., Toronto Notes suggests q1-2 weeks until lipid/ LFT response is stabilized)
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27
Q

What is psoriasis?

A

-Chronic inflammatory skin condition
-Comes in many types- plaque, guttate, pustular, erythrodermic, inverse

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28
Q

Describe epidemiology and risk factors of plaque psoriasis

A

1.5-2% of people
M=F
Peak of onset: bimodal (20-30, 50-60)
Polygenic inheritance- 8% with one affected parent, 41% with both parents affected
Risk factors: smoking, obesity, alcohol, drugs, infections, physical trauma (Koebner phenomenon- appearance of new lesions on skin secondary to trauma)

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29
Q

Describe patho pf psoriasis

A

Not fully understood, genetic and immunologic factors.
* Skin infiltrated by activated T cells, which stimulate proliferation of keratinocytes. Dysregulated keratinocyte turnover leads to formation of thick plaques.
* Epidermal hyperplasia; epidermal cells fail to secrete lipids which results in flaky and scaly skin

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30
Q

Clinical course of psoriasis?

A

Chronic, unpredictable, multi-system, many comorbidities (i.e., arthritis, ocular), often poor QOL (depression),
Guttate has best prognosis.

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31
Q

How is psoriasis diagnosed?

A

Clinical diagnosis
Biopsy if abnormal
Genetic testing not used
(Up To DatE)

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32
Q

Ddx for psoriasis?

A

Atopic dermatitis, mycosis fungoides, cutaneous T cell lymphoma, seborrheic dermatitis, tinea, nummular dermatitis, lichen planus

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33
Q

Describe the classic clinical presentation of plaque psoriasis

A

-Well circumscribed, sharply defined
-Erythematous papules/ plaques
-Silvery white coarse scales
-Auspitz sign (pinpoint bleeding when scale removed)
-Common sites include scalp, EXTENSOR surfaces (elbows, knees), trunk (esp. buttocks, gluteal cleft), nails, pressure areas (recall- koebner phenomenon- lesions form at site of trauma)

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34
Q

Treatment for mild plaque psoriasis?

A

Mild= <3% of body surface area
-Topical steroids +/- topical vitamin D analogue
-Emollients
-Possible phototherapy

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35
Q

Treatment for moderate to severe plaque psoriasis (3-10% of body surface area; >10% BSA )

A

-Phototherapy
-Systemic or biologic therapy depending on patient hx/ comorbidities methotrexate, biologic immune modifying agents, cyclosporine)
-Topical steroids, topical vit D3

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36
Q

What is guttate psoriasis?

A

Discrete, scattered salmon-pink small scaling papules (<1cm)

-Rain drop shaped
-Sites: diffuse, usually on trunk and legs, sparing palms and soles
-Often occurs before/ after streptococcal pharyngitis

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37
Q

Treatment for guttate psoriasis?

A

UVB phototherapy, sunlight, lubricants, topical steroids

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38
Q

Describe the clinical presentation of pustular psoriasis

A

Sudden onset of diffuse erythematous macules and papules which evolve rapidly into pustules, can be painful. These can desquamate.
-lesions are non- infectious
-May be generalized or localized
-Patient usually has a history of psoriasis; may occur with sudden withdrawal from steroid therapy
-Patient appears toxic

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39
Q

T/F pustular psoriasis can be life threatening

A

True

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40
Q

Treatment for pustular psoriasis?

A

Methotrexate, cyclosporine, acitretin, UV, biologics

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41
Q

Describe the clinical presentation for erythrodermic psoriasis.

A

Generalized erythema (>90% of BSA) with fine desquamative scale on surface
-Associated signs and symptoms: arthralgia, swelling, pruritus, pain, dehydration, electrolyte imbalance
-Aggravating factors: lithium, β-blockers, NSAIDs, antimalarials, phototoxic reaction, infection
-Increased risk infection

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42
Q

Treatment for erythrodermic psoriasis?

A

-Potentially life-threatening, requires immediate medical care
-IV fuids, monitor fuids and electrolytes, may require hospitalization
-Treat underlying aggravating condition, sun avoidance
-Cyclosporine, acitretin, methotrexate, UV, biologics

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43
Q

Describe the clinical presentation of inverse psoriasis.

A

Erythematous plaques on flexural surfaces such as axillae, inframammary folds, gluteal fold, inguinal folds (affects intertriginous areas)
-Lesions may be macerated

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44
Q

Treatment for inverse psoriasis?

A

-Low potency topical corticosteroids
-Topical vitamin D analogues (e.g. calcipotriene, calcitriol)
-Topical calcineurin inhibitors (e.g. tacrolimus, pimecrolimus)

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45
Q

What percentage of patients with psoriasis also suffer from psoriatic arthritis?

A

20-30%

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46
Q

T/ F Psoriatic patients with nail or scalp involvement are at a higher risk for developing psoriatic arthritis

A

True

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47
Q

How does psoriatic arthritis present?

A

Different patterns- can affect DIPS, be symmetrical or asymmetrical, destructive, or cause sacroillitis and spondylitis
-Peripheral arthritis, axial disease, enthesitis (inflammation at insertion of tendons/ ligaments, i.e., achilles, plantar fascia), dactylitis (diffuse sausage swelling of digit), skin and nail (pitting, splinter emorrages) disease
-Non specific lab findings

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48
Q

Treatment of psoriatic arthritis?

A

-Imaging (XR)
-NSAIDs
-Local glucocorticoid injection into entheses can be beneficial, but has not been systematically evaluated (do not inject achilles- associated with rupture)
-Referral to rheumatology (possible TNF, interleukin, or other agents, DMARDs, methotrexate)
-Surgery for severe destruction

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49
Q

Why do we use emollients in psoriasis?

A

Increase barrier function, hydration; reduce fissure formation

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50
Q

Tar is a possible treatment option for psoriasis. Why?

A

inhibits DNA synthesis, increases cell turnover
however, has poor long term compliance

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51
Q

What is the function of topical corticosteroids in psoriasis?

A

Reduce scaling, redness, and thickness; use appropriate potency steroid based on area and severity of psoriasis

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52
Q

Why do we use topical vit D analogues in psoriasis?

A

Reduces keratinocyte hyperproliferation

53
Q

Methotrexate is sometimes used in psoriasis that does not adequately respond to topical therapy. What are some AE?

A

Bone marrow toxicity
Hepatic cirrohsis
Teratogenic

54
Q

What are the most common types of eczematous dermatoses?

A

Seborrheic dermatitis

Atopic dermatitis

Contact dermatitis

Stasis dermatitis

Asteototic dermatitis

55
Q

What are the clinical features of seborrheic dermatitis?

A

Seborrheic dermatitis presents with erythematous, scaly patches located in areas with a high density of sebaceous glands:

*Lateral sides of the nose and the nasolabial folds

*Eyebrows and glabella

*Retroauricular folds

*Scalp

Less commonly involved are the chest, upper back, and axillae

56
Q

Atopic dermatitis (eczema) is a chronic, pruritic, inflammatory skin disease that occurs most frequently in children but also affects adults.

The hallmarks of atopic dermatitis are dry skin, severe pruritus, and cutaneous hyperreactivity to various environmental stimuli.

The clinical presentation varies with age in which ways?

A

●Infants and toddlers (<2 years) - atopic dermatitis presents with pruritic, red, weeping or scaly, and crusted lesions on the extensor surfaces of limbs and on the trunk, face, and scalp.
Older children and adolescents – atopic dermatitis typically presents with lichenified plaques in a flexural distribution, especially of the antecubital and popliteal fossae, volar aspect of the wrists, ankles, and neck.

●Adults – atopic dermatitis is usually more localized, with predominant lichenification, but exudative forms can also be seen; chronic hand eczema, facial dermatitis, and eyelid eczema are also frequently seen in adults.

57
Q

What is stasis dermatitis?

A

Stasis dermatitis, or stasis eczema, is a common, inflammatory dermatosis of the lower extremities occurring in patients with chronic venous insufficiency.

It typically presents with erythematous, scaling, and eczematous patches or plaques on chronically edematous legs.

Acute forms may present with severely inflamed, weeping plaques, vesiculation, and crusting, often with bacterial superinfection.

58
Q

What is asteatotic dermatitis?

A

A common type of pruritic dermatitis that typically occurs on the lower extremities of older individuals with dry skin.

Its incidence peaks during cold winter months.

Water loss from the stratum corneum due to age-related skin barrier impairment is believed to be a key pathogenetic factor.

59
Q

Causative organisms of impetigo?

A

Staphylococcus aureus &/or Streptococcus pyogenes

60
Q

Which is the most common skin cancer?

A

Basal cell carcinoma.

61
Q

Basal cell carcinoma is known to quickly metastasize.

True or false?

A

False, it rarely mets but it can of course.

62
Q

Risk factors for basal cell carcinoma?

A

Advanced age (more common)

M>F

Fair skin, eyes, hair, easily sunburns

Cumulative ultraviolet light exposure (sun, tanning beds)

Weak link with photosensitizing drugs (ie. thiazides) or food (citrus products)

Chronic arsenic exposure

Immunosuppression

Smoking

HPV, multiple nevi

Family hx, certain inherited skin syndromes

63
Q

Clinical features of impetigo

A
  • acute purulent infection which appears vesicular; progresses to golden yellow “honey-crusted” lesions
    surrounded by erythema
  • can present with bullae
64
Q

Common locations for impetigo on the body?

A
  • common sites: face (nares, perioral), arms, legs, and buttocks
65
Q

Who is most likely to get impetigo?

A

preschool and young adults living in crowded conditions, poor hygiene, neglected minor trauma

66
Q

Treatment of impetigo

When do we use systemic tx?

A

remove crusts, use saline compresses, and topical antiseptic soaks BID

  • topical antibiotics (e.g. mupirocin 2% or fusidic acid 2%
  • Topical antibiotic therapy is considered the treatment of choice for patients with uncomplicated impetigo localized to 2 or 3 small areas.
  • systemic antibiotics for more extensive or severe lesions, systemic symptoms, failure of topical tx, immunocompromised (e.g. cloxacillin or cephalexin for 7-10 d)
67
Q

Impetigo is highly contagious!
Precautions to take to limit spread?

A

careful attention to hygiene.

Wash hands frequently
Use antiseptics for bathing
Hot wash clothing, bedding, towels
Avoid sharing clothing and towels

cleaning minor wounds with soap and water can help prevent infection.

68
Q

Typical basal cell carcinoma skin findings?

A

Slowly growing plaque or nodule

Skin coloured, pink or pigmented

Varies in size from a few mms to several cms in diameter

Spontaneous bleeding or ulceration

69
Q

What are the 2 kinds of impetigo?

A

nonbullous (70% of cases) and bullous (30% of cases).

  • Bullous involves the vesicles turning into large bullae that rupture after 3-5 days
70
Q

T/F Impetigo generally resolves on its own in 2-3 weeks but has high risk of scarring

A

False! Typically without scarring

71
Q

Is impetigo painful or itchy?

A

Nonbullous may be tender and slightly itchy

Bullous slight itchy but not painful.

72
Q

How does impetigo relate to existing skin conditions?

A

develops at sites where skin is broken due to minor trauma or pre-existing skin condition, e.g., atopic dermatitis, contact dermatitis, insect bite, abrasion, scabies.

Less commonly: can occur on healthy, intact skin.

73
Q

When are impetigo lesions no longer infectious?

A

No longer infectious once ALL lesions have dried and crusted or 48 h after starting antibiotic therapy

74
Q

How is basal cell carcinoma diagnosed?

A

BCC is diagnosed clinically by the presence of a slowly enlarging skin lesion with typical appearance.

The diagnosis and histological subtype is usually confirmed pathologically by a diagnostic biopsy or following excision.

Some typical superficial BCCs on trunk and limbs are clinically diagnosed and have non-surgical treatment without histology.

75
Q

About 50% of people with basal cell carcinoma develop a second presentation within _____ years.

A

3

76
Q

Clinical features of Nodular basal cell carcinoma?

A

-Most common type of facial BCC

-Shiny or pearly nodule with a smooth surface

-May have central depression or ulceration, so its edges appear rolled

-Blood vessels cross its surface

-Cystic variant is soft, with jelly-like contents

-Micronodular, microcystic and infiltrative types are potentially aggressive subtypes

77
Q

What are the 6 P’s of lichen planus?

A

Purple
Pruritic
Polygonal
Peripheral
Papules
Penis (i.e. mucosa)

78
Q

Patho of lichen planus

A

Immune-mediated, antigen unknown
* lymphocyte activation leads to keratinocyte apoptosis

79
Q

Clinical features of superficial basal cell carcinoma?

A

-Most common type in younger adults

-Most common type on upper trunk and shoulders

-Slightly scaly, irregular plaque

-Thin, translucent rolled border

-Multiple microerosions

80
Q

Common sites of lichen planus

A

wrists, nails, scalp, mucous membranes in 60% (mouth, vulva, glans)

81
Q

Distribution of lesions in lichen planus

A

symmetrical and bilateral

82
Q

Clinical features of morphoeic basal cell carcinoma?

A

-Usually found in mid-facial sites

-Waxy, scar-like plaque with indistinct borders

-Wide and deep subclinical extension

-May infiltrate cutaneous nerves (perineural spread)

-Also known as morpheic, morphoeiform or sclerosing BCC

83
Q

What is pathognomonic for lichen planus?

A

Wickham’s striae

reticulate white-grey lines over surface; pathognomonic but may not be present

84
Q

Describe the lesions in lichen planus

A

*acute or chronic infammation of skin or mucous membranes
* morphology: pruritic, well-demarcated, violaceous, polygonal, fat-topped papules

mucous membrane lesions: lacy, whitish reticular network, milky-white plaques/papules;

nails: longitudinal ridging; pterygium formation, complete dystrophy

  • scalp: scarring alopecia with perifollicular hyperkeratosis and erythema
85
Q

What am I describing?

-Very common keratotic lesions with malignant potential
- Lesions most commonly found in sun-exposed areas of elderly folks with hx of significant sun exposure
-Yellow or pigmented, sharp, tightly adherent scales
-Considered precursor to BCC or SCC

A

Actinic keratosis

86
Q

Dose lichen planus resolve spontaneously?

A

Yes but can take weeks, months, years…

87
Q

Treatment of lichen planus

A
  • topical or intralesional corticosteroids
  • short courses of oral prednisone (rarely)
  • phototherapy, oral retinoids, or systemic immunosuppressants (e.g. azathioprine, methotrexate,
    cyclosporine) for extensive or recalcitrant cases
88
Q

Ringworm is caused by?

A

Tinea infections

89
Q

Tinea is caused by dermatophytes. What are dermatophytes?

A

superficial fungal infections caused by dermatophytes; a group of fungi that infect keratinized tissues, such as the skin, hair, and nails.

90
Q

Tinea corporis usual distribution (where on the body)

A

Usually the smooth and hairless (glabrous) areas of the trunk or limbs (excluding the face, hands, feet and groin)

known as Tinea faciei if it occurs on a nonbearded area of the face.

91
Q

Describe the lesions of tinea corporis

A

Typically round, erythematous (more likely on lighter skin) or hyperpigmented (more likely on darker skin) patch; scaly with a clearing central portion and a raised vesicular border that advances circumferentially outward

92
Q

Risk factors for tinea corporis (and tinea in general)?

A

Athletes in sports with skin-to-skin contact, such as wrestling, where it is called tinea corporis gladiatorum​[14]

Direct or indirect contact (via fomite) with infected person or animal

Moist conditions including occlusive clothing, humid climates

Impaired immunity states (e.g., diabetes, HIV infection, chemotherapy)

Genetic predisposition

93
Q

What is jock itch?

A

Tinea cruris

94
Q

Describe distribution of tinea cruris

A

Symmetrical, involving the groin area (medial and upper parts of the thigh and the pubic area). Occasionally the anal cleft is affected.

**Unlike yeast infections, the scrotum and penis are usually spared.

95
Q

Is tinea cruris typically itchy?

A

Yes

96
Q

What time of the year is tinea cruris most common?
How does it get into the groin?

A

Summer

Individuals with an infection on the feet, which is spread to the groin while putting on underwear

97
Q

Tinea curirs, corporis, capitus are NOT YEAST infections. What infections are caused by yeast?

A

Pityriasis Versicolor (aka Tinea Versicolor)

Cutaneous Candidiasis, oral thrush (most often caused by candida albicans)

98
Q

Describe tinea capitus

What does it affect?
Describe most common lesions

A

Affects scalp hair follicles and adjacent skin.

Lesions:
“Black dot tinea capitis” (most common): annular patch of itchy, scaling skin and hair loss. Hairs may break off flush with the scalp surface, and debris in the follicle formerly occupied by hair appears as black dots.

Can also get a grey form that is contracted by cats and dogs

In some patients, a hypersensitivity response may lead to development of a boggy inflammatory mass called a kerion that can result in scarring and permanent hair loss.

99
Q

Topical abx available for tinea infections?

A

Topical pharmacologic options available for the treatment of dermatophyte skin infections include:

ciclopirox, clotrimazole, ketoconazole, miconazole, terbinafine, tolnaftate and undecylenic acid.

There is limited evidence upon which to base selection of one antifungal over another. A systematic review found low-quality evidence that the topical azoles, terbinafine and ciclopirox achieve comparable clinical and mycological cure rates (all have an NNT of 2), but treatment duration is shorter with terbinafine.​[19] Terbinafine treatment for 1 week has produced similar cure rates to those reported for azole treatment for 4 weeks
(as per CPS)

100
Q

T/F dermatophyte infections can be treated with nystatin

A

False - Nystatin is ineffective in the treatment of dermatophytosi

101
Q

Actinic cheilitis is a sun-induced keratinocyte found on the ________ ______. It can be clinically subtle but behave aggressively, progressing to ____________.

It presents with erythema and ________.

A

lower lip

SCC

scaling

102
Q

Risk factors for tinea capitus?

A

Age: primarily affects children

In North America, children of African-American descent are more commonly affected than other groups​[b]

Low socioeconomic and crowded environments

Direct or indirect contact (via fomite) with infected person or animal

Moist conditions including occlusive clothing, humid climates

Impaired immunity states (e.g., diabetes, HIV infection, chemotherapy)

103
Q

Where are the most common sites to find squamous cell carcinoma?

Which population is it seen in the most?

A

Most commonly found on the face, neck, head or hands of elderly patients.

104
Q

General nonpharm tx of fungal infections

A

Keep skin clean and dry to discourage fungal proliferation:
bathe daily

avoid excessive rubbing with towels

an electric hair dryer on the cool setting may be helpful to thoroughly dry the skin

using cool water compresses (1 minute on, 1 minute off) for 15–20 minutes 3 times daily may help to keep the area dry through evaporation; the affected area should be air dried afterwards

Wear loose-fitting clothing made of fabrics that allow adequate ventilation and are moisture-wicking, if possible.

Additional measures for dermatophyte infections:
Prevent spread of the infection by avoiding direct or indirect contact (via fomites such as personal items, shedded hairs, clothing, bedding) with an infected person or animal and laundering clothing and linens of the infected person separately from those of other family members

105
Q

Topical antifungals are effective for which kinds of tinea?

A

Corporis & cruris, manuum (on hands)

106
Q

Which kinds of tinea require systemic tx?

A

Tinea barbae and tinea capitis - topical antifungals do not adequately penetrate the hair follicles.

107
Q

How does SCC differ from SCC in-situ?

A

In SCC in-situ, the malignant cells are confined to the tissue of origin (the epidermis) and have not grown beyond the epidermis.

108
Q

What is Bowen’s disease?

A

Another term for SCC in-situ.

109
Q

What are the clinical features of SCC?

A

Cutaneous SCCs present as enlarging scaly or crusted lumps. They usually arise within pre-existing actinic keratosis or intraepidermal carcinoma (SCC in-situ).

They grow over weeks to months
They may ulcerate
They are often tender or painful
Located on sun-exposed sites, particularly the face, lips, ears, hands, forearms and lower legs
Size varies from a few millimetres to several centimetres in diameter.

110
Q

What are the distinct clinical types of invasive SCC?

A

Cutaneous horn — the horn is due to excessive production of keratin

Keratoacanthoma (KA) — a rapidly growing keratinising nodule that may resolve without treatment

Carcinoma cuniculatum (‘verrucous carcinoma’), a slow-growing, warty tumour on the sole of the foot

Marjolin ulcer - a cutaneous SCC that has developed in a scar or chronic ulcer

111
Q

The typical time frame for SCC to move from cutaneous to regional lymph node is ___________.

A

2-3 years

112
Q

The treatment of primary SCC is:

A

Wide local incision with histological confirmation of the margins.

Mohs micrographic surgery may be useful for sites where tissure sparing is desired

Radiation therapy may be considered.

113
Q

Does SCC found on the lip, ear, or scalp tend to be more or less aggressive than other sites?

A

More aggressive, tend to mets to regional lymph nodes and beyond.

114
Q

You suspect your patient has patches of eczema and you presribe topical steroid cream. When there is no therapeutic response, what differential diagnosis are you most suspicious for? Suspicious of?

A

Bowen’s disease - SCC in-situ.

The lesions have well defined borders and can closely resemble psoriasis, chronic eczema, and seborrheic keratosis.

115
Q

ABCDE of malignant melanoma recognition?

A

A - asymmetry

B - border irregularity

C - colour variegation

D - diameter > 6mm

E - evolution of lesion

116
Q

Over 90% of melanomas develop within a pre-existing nevus.

True or false?

A
117
Q

Should you biopsy a lesion you think might be melanoma?

A

Nope. Refer!! If you don’t get all the margins you can make it angry and vengeful.

118
Q

How often should you be reassessing a patient with a hx of melanoma?

A

Every 3 months, as per derm text.

119
Q

What are the ABCDEFs of subungual (under the nail) hematomas?

A

●Age - African Americans, Asians, and Native Americans

●Brown to black band

●Change in the nail band

●Digit most commonly involved (great toe and thumb)

●Extension of the pigment onto the proximal and/or lateral nail fold

●Family or personal history of melanoma

120
Q

What is the other name for urticaria?

A

Hives

121
Q

Describe a urticarial lesion

A

intensely pruritic circumscribed, raised erythematous plaque, often with central pallor. Morphology and size vary
Develop over minutes to hours and resolve in hours to one day without residual markings.

122
Q

What are possible triggers for urticaria?

A

a drug, food, insect sting or infection
In many cases no specific cause is found, particularly when the condition persists for weeks or months

123
Q

What are important components of taking a history of a patient with urticaria?

A

Exclusion of possible anaphylaxis
Identification of a trigger
Determination if any S/S suggesting urticarial vasculitis or an underlying systemic disorder.

124
Q

Would you do any diagnostics for urticaria?

A

Usually not indicated unless symptoms persist. May include CBC, urinalysis, ESR, LFTs

125
Q

What are some differentials for urticaria?

A

insect bites, atopic dermatitis, contact dermatitis, morbilliform drug eruptions, bullous pemphigoid, erythema multiforme minor, and plant-related dermatoses (eg, poison ivy)

126
Q

Treatment for urticaria?

A

In mild, new-onset urticaria, treat with non-sedating H1 antihistamine alone. Some patients require higher doses (ex. cetirizine 10mg BID)

If low risk for anti-cholinergic side effects, can recommend a sedating H1 antihistamine at bedtime and non-sedating in the morning

127
Q

What might you try if your patient has persistent urticaria despite H1 antihistamine?

A

Can add a brief course of oral glucocorticoids - prednisone 30-60 mg daily.

128
Q

What is the time course of urticaria?

A

2/3 resolve in a few days - a few weeks
Those than continue beyond 6 weeks are continued chronic.
Referral to allergy or derm specialist may be indicated for patients with persistent/difficult to control symptoms

NUNP543 (11 decks)

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