week 4- skin Flashcards

1
Q

o What is weight and area of the skin? Function?

A

o Weighs an average of 4 lbs, covers 2 sq m

o Barrier, excretory functions

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2
Q

o What are the layers of the skin, and what’s they incude?

A

o Epidermis: Basement membrane
o Dermis: Appendages; Blood vessels and nerve endings
o Subcutaneous/Hypodermis layer: Appendages; Fat layer

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3
Q

What may be the cause of a skin lesion?

A

 Infection; Infestations; Sun; Autoimmune; Allergy; Internal disease; Cancer- either skin or internal; Environmental; Iatrogenic; Congenital; Hormonal; Nutritional Deficiency; Emotional

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4
Q

o What questions should you ask for Hx with a skin lesion?

A
  1. Where is the lesion/rash located?
  2. When did it first appear?
  3. Has it spread or changed locations?
  4. Is there any sensation associated with it?
  5. Has the appearance changed?
  6. Does anything make it worse or better?
  7. Does anyone else around you have it?
  8. Recent travel?
  9. Change in exposures?
  10. Have you treated it with anything?
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5
Q

What is some additional hx info to gather about a skin lesion?

A

o History of atopy (atopic dermatitis/eczema)
o Occupational, household and other skin exposures (contact dermatitis)
o Sunlight and/or radiation exposure (benign or malignant skin tumors, lupus, polymorphous light eruption)
o General health, systemic disease (diabetes/Candida/tinea, celiac disease/ dermatitis herpetiformis, hep C/ cryoglobulinemia, IBD/pyoderma gangrenosum, many internal diseases/erythema nodosum)
o All medications including OTC, herbs, etc
o Travel history (Lyme, skin infections)

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6
Q

o What should you get from ROS, FH, SH?

A

o ROS: Organ involvement; Concomitant symptoms (fever, chest pain, GI)
o FH: Atopy, Autoimmune, Malignancy; Anyone else have it?
o SH: Sexual history (syphilis, gonorrhea, warts, herpes)

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7
Q

o How should you do PE of sken lesion?

A
o	Adequate light
o	Examine all skin areas, including mucus membranes
o	Palpate the lesion(s)
o	Skin scraping
o	Hair, scalp, nails: Wood’s lamp
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8
Q

o what is the atopic triad?

A

o Allergies, eczema, asthma

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9
Q

o What is a macule? Papule? Plaque?

A
  • Macule: flat, usu less than 10 mm, variable shape, nonpalpable color change
  • Papule: elevated, palpable; less than 10 mm
  • Plaque: elevated plateau-like lesion greater than 10 mm; superficial;
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10
Q

What is a nodule? Vesicle? Bullae?

A
  • Nodule: firm papule, palpable, extends into dermis or subQ tissue; Tumors: large nodules more than 10 mm
  • Vesicle: fluid-filled blister less than 10 mm
  • Bullae: vesicles larger than 10 mm
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11
Q

What is a pustule? Urticaria? Scale?

A
  • Pustule: elevated lesion containing pus
  • Urticaria (wheals or hives): transient elevated lesion due to localized edema
  • Scale: accumulation of epithelium; dry, whitish
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12
Q

What is crust? Erosion? Excoriation?

A
  • Crust: dried pus, blood or serous exudate on the surface usually due to broken pustules or vesicles
  • Erosion: loss of epidermis.
  • Excoriation: linear erosion, usu caused by scratching
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13
Q

What is an ulcer? Petechiae? Purpura?

A
  • Ulcer: deeper erosions involving the dermis; bleed and scar
  • Petechiae: small non-blanchable punctuate foci of hemorrhage
  • Purpura: Larger area or hemorrhage, mb palpable; Large areas are bruises or ecchymosis
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14
Q

What is atrophy? Scar? Telangiectasia?

A
  • Atrophy: paper thin wrinkled and dry-appearing skin
  • Scar: fibrous tissue replacement after injury
  • Telangiectasia: dilated superficial blood vessels
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15
Q

What is secondary morphology/cobnfiguration of skin lesions? Examples?

A
  • shape of single lesion or cluster of lesions:
  • Linear
  • Annular – rings with central clearing
  • Nummular – circular
  • Target – rings with central duskiness
  • Serpiginous – fungal and parasitic infections
  • Reticulated - lacy pattern
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16
Q

• What may be the texture of a skin lesion?

A
  • Verrucous – irregular surface
  • Lichenification: epidermal thickening with accentuation of skin lines due to chronic irritation
  • Induration: dermal thickening; skin feels hard and rough
  • Umbilicated: with a central indentation
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17
Q

What may be the location and distribution of a skin lesion?

A
  • Single versus multiple lesions
  • Presence on particular body parts may be significant
  • Random versus patterned distribution
  • Symmetric or asymmetric distribution
  • Sun-exposed areas versus not
  • Crosses midline?
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18
Q

What are the colors of skin lesions, and what they indicate?

A
  • Red (Erythema); increased blood flow to the skin
  • Orange: hypercarotenemia
  • Yellow: jaundice, heavy metal poisoning, myxedema, uremia
  • Green: in fingernails, suggests pseudomonas
  • Violet: darkening cutaneous hemorrhage, vasculitis
  • Gray/blue skin: cyanosis, metal deposits
  • Black: melanocytic lesions, infection, arterial insufficiency
  • White: tinea, Pityriasis alba, vitiligo
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19
Q

What are some other clinical signs of skin lesions?

A
  • Dermatographism – urticaria after stroking the skin
  • Diascopy: pressure to indicate blanching (hemorrhagic lesions don’t blanch, inflammatory lesions do)
  • Darier’s sign – stroking lesions causes intense and sudden erythema and wheal formation
  • Nikolsky’s sign – bullae formation and erosion following gentle traction pressure
  • Auspitz’ sign – pinpoint bleeding after removal of plaques
  • Koebner’s phenomenon – development of lesions within areas of trauma
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20
Q

When are diagnostic tests used in skin lesions? What tests?

A
  • Indicated when diagnosis is not obvious with history and physical alone
  • Microscopic examination (biopsy): for suspected malignancies, unknown lesions that persist= Punch or shave
  • Cultures: fungal, bacterial, viral
  • Patch test for allergies
  • KOH test: fungus
  • Gram stain
  • PCR
  • Skin scraping for scabies, fungus
  • Immunofluorescence, serology
  • Wood’s lamp: UV light for fungi
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21
Q

• What is Pruritis?

A

o Itching is stimulated by chemical and physical stimulation of cutaneous nerve endings. Stimulus may be external or internal. Several mediators of itching exist: histamine, kallekrein, and various peptidases.

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22
Q

• What may you find on hx for pruritis? What testing may be done?

A

o History: must include drug and occupational/hobby exposures
o Testing: biopsy, CBC, liver, kidney, thyroid function, evaluation for underlying malignancy, immunoglobulins

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23
Q

• What is cause of pruritis?

A

o Dry skin most common cause

o Itching may occur with or without an associated skin eruption, which may help determine the cause.

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24
Q

• What is urticaria? 2 types? Etiology?

A

o Migratory, erythematous pruritic plaques. Mostly involves release of histamine
o Acute vs Chronic: >6 weeks duration?
o Etiology: viral/bacterial infection, IgE allergy, medications esp NSAIDS. Rare- autoimmune dz, malignancy,

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25
Q

• What can you find on hx for urticaria? What PE? What tests?

A

o History: duration, triggers, frequency, concomitant sxs (GI). Always ask about resp system. Also – use of drugs, travel and family history
o PE: Complete examination of skin, sign of infections or systemic disease.
o Testing: CBC, Immunoglobulins to foods, ANA or thyroid studies may be appropriate. Biopsy if uncertain.

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26
Q

• What are the acne and related disorders?

A

o Acne vulgaris; rosacea;

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27
Q

• What is acne vulgaris? Causes?

A

o Obstruction of the pilosebaceous unit presenting with comedones (white/blackheads), papules, pustules, inflamed nodules, superficial pus filled cysts and sometimes deep purulent sacs.
o Causes: androgen stimulus, sebum, bacteria interaction, drug induction, diet (milk, sugar, bromine)

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28
Q

• What is epidemiology of acne vulgaris? Where is it distributed on skin? Ssx?

A

o Age: Puberty - age ~35.
o Gender: M>F
o Distribution: Face, chest, back, upper arms
o S/Sxs: comedones, papules, pustules, nodules, cysts (actually very rare).

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29
Q

• How is acne vulgaris diagnosed? What labs may be done?

A

o Dx by H & P: comedones and often several stages of lesions. Grade by severity (mild = 5 cysts or >125 lesions)
o Labs: Serum total/free testosterone w/DHT, FSH, LH, DHEA-S. Bacterial and fungal cultures can be done to r/o infectious folliculitis

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30
Q

• What is ddx of acne vulgaris?

A

o rosacea (no comedones), perioral dermatitis, drug eruptions, folliculitis (yeast or bacterial, keratosis pilaris, Pseudofolliculitis barbae and acne keloidalis nuchae (in African Americans)

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31
Q

• what is rosacea? Causes?

A

o chronic inflammatory disorder characterized by facial flushing, telangiectasias, erythema, papules, pustules, and possibly rhinophyma.
o Causes: “Idiopathic” although pts have a higher infection rates of H. Pylori and small intestinal bacterial overgrowth (SIBO)

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32
Q

• What is epidemiology of rosacea? Where is it distributed on skin?

A

o Ages 30-60, fair complexions, and blushers.

o Distribution: Most on the central area of the face and scalp

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33
Q

What may you find in hx of a pt with rosacea?

A

o increased susceptibility to recurrent flushing reactions that may be provoked by a variety of stimuli including hot or spicy foods, drinking alcohol, temperature extremes, and emotional reactions.
o may have eye involvement such as foreign body sensation and burning, telangiectasia and irregularity of lid margins, meibomian gland dysfunction (posterior blepharitis), keratitis, conjunctivitis, and episcleritis

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34
Q

what are ssx of rosacea (stages)?

A

o “Pre-rosacea”
o Vascular phase
o Inflammatory phase-papules, pustules, nodules and cysts present
o Late-stage/rhinophyma

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35
Q

• What are the criteria for diagnosis of rosacea?

A

o one or more of the following primary features: flushing (transient erythema), Nontransient erythem, Papules and pustules, Telangiectasia and one or more of the following secondary features: Burning or stinging, Plaque, Dry appearance, Edema, Ocular manifestation, Peripheral location, Phymatous changes

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36
Q

• what is ddx for rosacea?

A

o SLE, discoid lupus, acne vulgaris, drug eruptions, granulomas, perioral derm, infectious folliculitis, seborrheic dermatitis, carcinoid, chronic topical glucocorticoids

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37
Q

• What are the bullous skin disorders?

A

o Bullous pemphigoid; dermatitis Herpetiformis; pemphigus vulgaris

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38
Q

• What s bullous pemphigoid? Causes?

A

o Chronic pruritic bullous eruptions. Uncommon

o Autoimmune, drug induced from furosemide, captopril and NSAIDS

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39
Q

• What are ssx of bullous pemphigoid?

A

o prodromal phase mb with pruritic eczematous, papular, or urticaria-like skin lesions that become tense bullae, negative Nikolsky’s sign, may see urticaria early that turns dusky annular lesions. Bullae form on top of erythematous plaques and rupture in about 1 week leaving an eroded base. Pruritis common.

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40
Q

• Where is bulous pemphigoid found on body? Epidemiology? Associated with?

A

o Distribution: trunk, lower legs, extremity flexures, and axillary and inguinal folds
o Age >60
o Associated with dementia, Parkinson’s disease, and unipolar or bipolar

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41
Q

• How is bullous pemphigoid diagnosed?

A

o H & P, skin biopsy (from edge of intact blister) shows subepidermal bulla with infiltrate of eosinophils- direct immunofluorescence (Gold Standard) of skin shows IgG and/or C3 in a linear band in basement membrane, serum antibody titers- Anti-BP180 antibodies. Biopsy must be done to dx

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42
Q

• What is ddx for bullous pemphigoid?

A

o pemphigus vulgaris, dermatitis herpetiformis, erythema multiforme, drug eruptions

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43
Q

• what is dermatitis Herpetiformis? Causes? Ssx?

A

o Autoimmune, chronic, recurring, intensely itchy, with symmetrical groups of inflamed vesicles, papules and hives.
o Causes: Autoimmune, celiac dz (asx)-often gluten can cause major sxs
o SSX: Burning, severe stinging and itching, and last for weeks to years.

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44
Q

• What is distribution of DH? Epidemiology?

A

o Distribution: Symmetrical extensor aspects, sacrum, base of head or generalized.
o Age 20-50
o Gender male:female 2:1

45
Q

• How is DH diagnosed?

A

o H & P, skin biopsy of lesion and adjacent normal skin, shows subepidermal clefting and papillary dermal tips w/neutrophils and eosinophils. Direct immunofluorenscence is gold stand for dx. IgA deposition. Labs- TTG (tissue trans-glutaminase), anti-endomysial Ab, jejunal bx for celiac dz

46
Q

• What is DH associated with? Ddx?

A

o Associated with celiac and thyroid disorders

o DDX: pemphigus, bullous pemphigoid, dermatitis, herpes, insect bites, scabies

47
Q

• What is pemphigus vulgaris? Cause? Ssx?

A

o potentially fatal blistering disease. Rare
o Causes: Autoimmune
o Ssx: Flaccid bullae, various sizes, on the skin and mucus membranes. Skin shears off easily, leaving painful erosions. Nikolsky’s sign.

48
Q

• What is distribution of pemphigus vulgaris? Epidemiology?

A

o Distribution: Oral lesions often precede skin lesions in 50-70%, then found on groin, scalp, abd, back, upper legs, axilla and umbilicus.
o Age >60, F>M
o Incidence highest in Ashkenazi Jews

49
Q

• How is PV diagnosed? Is it an emergency?

A

o By H & P and biopsy. Biopsy shows intraepidermal bulla or separation of epidermal cells, eosinophil infiltrate, IgG, complement C3. Immunofluorescence from edge of fresh lesion and adjacent normal area. Serum anti-Dsg 3 and anti-Dsg 1 Ab- titers relate to dz activity. Nikolsky’s sign present.
o Hospitalization almost universally required. 15% mortality rate

50
Q

• What is ddx of PV?

A

o Herpes simplex and zoster, bullous pemphigoid, canker sores, paraneoplastic pemphigus (must do bx to exclude)

51
Q

• What are the cornification disorders? How are they diagnosed?

A

o Calluses and corns; ichthyosis; keratosis pilaris

o Diagnose all with H & P.

52
Q

• What are calluses and corns?

A

o epidermal thickening from pressure or friction; feet and toes
o Calluses: usu asymptomatic, intact skin lines
o Corns: mb painful with pressure, yellowish core when pared, interrupts skin lines

53
Q

• What is ichthyosis? Inherited?

A

o Scaling and flaking of skin, a range of types
o Inherited ichthyoses: Autosomal Dominant and X-linked. excessive accumulation of scales on skin. Resembles cracked pavement. Accentuated palmar creases

54
Q

• What is age, distribution, dx, and ddx for ichthyosis?

A

o Age- improves and can resolve with age
o Distribution: shins, outer arms most common.
o No biopsy needed for dx
o DDx- dry skin, acquired ichthyosis (related to infection or systemic disease, sudden onset

55
Q

• What is keratosis pilaris? Causes?

A

o keratinization disorder where horny plugs fill the openings of the hair follicles
o Causes: Nutritional deficiency, genetic

56
Q

• What are ssx of keratosis pilaris? Age? Atopy?

A

o keratotic follicular papules on lateral aspects of the upper arms, thighs and buttocks. On the face in children (can be confused with acne). Skin feels rough like sandpaper.
o Age: usually worse in children and resolved or improves with adulthood
o More common in atopy

57
Q

• What are the types of dermatitis?

A

o Atopic derm; contact derm; lichen simplex chronicus; nummular derm; seborrheic derm; stasis derm

58
Q

• What is atopic dermatitis? Causes?

A

o Immune-mediated skin inflammation, with typically a genetic component.
o Causes: genetic component (Atopy), food and environmental allergies; Aggravated by dry skin, wool, sweating, allergens, tight clothing, emotional stress, nutritional deficiency, SIBO

59
Q

• What are ssx of AD?

A

o red, weeping, crusted lesions on face, spread to neck, extremities, abdomen, flexor surfaces of elbow and knee, buttocks, neck, hands. Pruritic (intense), lichenification. May have palmar hyperlinearity, keratosis pilaris, hand/foot involvement, cheilitis, increased susceptibility to cutaneous infections

60
Q

• what is age distribution of AD?

A

o begins very young- distribution changes
o Infantile phase (2months-2year) cheeks, perioral, scalp, extensor tops of feet and elbows with exudates
o Childhood phase (2-12) flexural surfaces, lichenification
o Adult phase (12-adult) flexural, hands, upper eyelids or patchy and diffuse over whole body

61
Q

• How is AD diagnoses? Ddx?

A

o H & P. culture and sensitivity if infection is suspected. Eosinophilia can occur. Food allergy/sensitivity testing- especially in children, vitamin D, GI assessment (dysbiosis, 3hr lactulose breath test for methane, hydrogen)
o DDX: seborrheic derm, contact derm, nummular derm, Candida, scabies, tinea

62
Q

• What is contact dermatitis? Cause?

A

o Acute inflammation of skin caused by irritants or allergens
o Cause: exposure

63
Q

• What are the 2 types of contact dermatitis?

A

o Irritant contact derm: Chemicals, soap, acids, alkaline chemicals, oils, water, woods dust, fiberglass or body fluids.
o Allergic contact derm: Hypersensitivity reaction with an initial sensitization, then reaction on re-exposure. Drugs (this is big! Neomycin, bacitracin, hydrocortisone), latex, metals, cosmetics, lotion, sunscreen, nail polish, or fragrances. Also poison ivy, oak, sumac are types.

64
Q

• What are ssx of ICD and ACD?

A

o ICD: hands often affected, both the dorsal and palmar surfaces. Around mouth of chronic lip lickers. Erythema, dryness, painful cracking or fissuring. Acute may have papules with weeping and edema, chronic may have lichenification, excoriations and scaling.
o ACD is intensely pruritic. Mild erythema to hemorrhage, vesiculization and ulceration.

65
Q

• How is CD diagnosed? Dx?

A

o H & P (including occupation, hobbies, household duties, travel, topical exposures). Patch testing when ACD doesn’t respond to treatment
o DDX: seborrheic derm, atopic derm, nummular derm, tinea

66
Q

• What is lichen simplex chronicus? Aka? Ssx?

A

o chronic pruritis that causes an extreme scratch-itch-scratch cycle without demonstrable cause.
o Aka neurodermatitis
o Ssx: pruritis, dry scaling skin, hyperpigmentation, erythematous, violaceous, lichenified plaques in irregular shapes. Most common areas are back of neck, wrists, ankles and pubic region, usually not present on back, abd, face or upper legs

67
Q

• How is lichen simplex chronicus diagnosed? Ddx?

A

o H & P, KOH wet mount (to differentiate from tinea), biopsy, patch testing to identify role of allergens
o DDX: tinea, lichen planus, psoriasis

68
Q

• What is nummular dermatitis? Epidem? Cause?

A

o Inflammation of the skin in a coin-shaped pattern.
o Mostly mid-aged pts with dry skin.
o Idiopathic, often with no hx of eczema, gradual onset. M>F

69
Q

• What are ssx of nummulus dermatitis?

A

o exceedingly pruritic, inflamed coin shaped lesions, vesicular, crusting and scaling, as well as pruritic. Extensor surfaces, buttocks and trunk. Often begins on the legs. 1-50 lesions can be present

70
Q

• how is ND diagnosed? Ddx?

A

o H & P, patch testing can be positive, culture can reveal Staph aureus, biopsy, KOH wet mount
o DDX: Psoriasis, Tinea corporis, cutaneous T Cell lymphoma scabies, seborrheic dermatitis, fungus, Paget’s disease when on the breast.

71
Q

• What is seborrheic dermatitis? Causes?

A

o Inflammation of skin in high-density areas of sebaceous glands (scalp, eyebrows, eyelids, face)
o Causes- speculated that Malazzezia fungi may play a role, nutritional deficiency

72
Q

• What are ssx of seborrheic dermatitis?

A

o gradual onset, well demarcated erythematous plaques with greasy-looking, yellowish scales distributed on areas rich in sebaceous glands such as the scalp, the external ear, the center of the face, eyebrows, axillae, nasolabial folds, the upper part of the trunk, and the intertriginous areas (axilla, inside elbow/knee, buttocks). May see papules. No hair loss. Cradle cap in newborns.

73
Q

• What ages are SD seen? Susceptibility?

A

o Biphasic incidence 2-12 months then during adolescence and adulthood, that peaks between 30-50. M>F
o Increased susceptibility in HIV+(may be presenting sign), Parkinson’s and the use of neuroleptic medications

74
Q

• How is SD diagnosed? Ddx?

A

o H & P, KOH and fungal culture may be indicated

o DDX: atopic dermatitis, contact dermatitis, psoriasis (may overlap), tinea, cutaneous lupus, rosacea

75
Q

• What is stasis dermatitis? Ssx?

A

o Persistent dermatitis of the lower legs, especially the ankle, secondary to chronic venous insufficiency
o S/Sxs: Brown pigmentation over time, bronze. Often edema and petechiae. Then erythema, fissured, dry or weeping, crusting. Pruritic. May see varicosities, and cellulitis. Often develop stasis ulcers that do not heal, and may penetrate to the bone. Pt complains of heaviness/aching in leg that is agg by walking/standing. Legs are often swollen at the end of the day. Secondary infxn with Staph aureus is common.

76
Q

• Hx of Stasis derm? Diagnosed? Ddx?

A

o Hx may include DVT, surgery, trauma or ulceration
o Diagnosis: H & P. venous studies, ankle brachial index, if DVT hx should check protein S, C, factor V Leiden, fibrinogen, and homocystiene levels
o DDX: cellulitis, contact dermatitis, tinea

77
Q

• What conditions have acute effects from sunlight? Chronic?

A

o Acute: Polymorphous light eruption

o Chronic: aging, actinic keratosis; skin CAs

78
Q

• What is polymorphous light eruption? Ssx? Types of lesions?

A

o An idiopathic, recurrent photodermatitis that occurs after sun exposure
o Ssx: lesions appear 2hrs-5days after sun exposure. Burning, itching, erythema to exposed skin. Lesions persist 7-10 days
o 3 types of lesions: papular, plaque or papulovesicular.

79
Q

• What is epidemiology of polymorphous light eruption? Diagnosed? Ddx?

A

o all ages, all races, all genders although most common in young F
o Diagnosis: H &P. ANA, anti-dsDNA, anti-SSB to distinguish from SLE
o DDX: SLE, photodrug rxn, porphyria tarda, solar urticaria

80
Q

• What are the aging chronic effects of sunlight?

A

o chronic exposure produces fine and coarse wrinkles, rough leathery texture, mottled hyperpigmentation, and telangiectasia

81
Q

• what is actinic keratosis? Ssx?

A

o precancerous neoplasm due to UV exposure
o ssx: Rough scaling macule, papule or plaque; 1-10 mm; reddish/pink, ill-marginated with rough scale, with time develop a thin, adherent transparent scale- this becomes thicker and more yellow over time and forms horns

82
Q

• what is distribution of AK? Epidem? Dx? Ddx?

A

o Distribution: face, lips, backs of hand, shoulders, legs (think sun)
o Age: increases with age, usu in blondes or red-heads with light skin (skin type I and II)
o Diagnosis: biopsy to distinguish from squamous cell carcinoma
o DDX: seborrheic keratosis, squamous cell carcinoma

83
Q

• What pop are sun-caused skin CAs most common in?

A

light-skinned people extensively exposed to sunlight as children.

84
Q

What are the psoriasis and scaling dzs?

A

o Psoriasis; Pityriasis rosea; lichen planus

85
Q

• What is psoriasis? Cause? Ssx? Systemic?

A

o chronic recurring inflammation of epidermis and dermis with increased epidermal proliferation resulting in scaling. Immune mediated.
o Cause: genetics, environmental triggers, infection, physical or psychological stress, and medications. Smoking, obesity (adipokines?) and HIV predispose
o Ssx: dry, sharply demarcated, erythematous papules and plaques topped with silvery scales. May itch but usually asx. Limited or systemic. Better in the summer.
o May see systemic signs of arthritis, fever, chills, and deformed nails (pitting). Comes and goes.

86
Q

• What are the 7 different types of psoriasis?

A

o Plaque psoriasis (classic)
o Guttate psoriasis (sudden appearance of many papules on the trunk as w/Strep A or steroid withdrawl)
o Pustular psoriasis(small pustules on palms and soles)
o Inverse psoriasis (found on flexor surfaces and intertriginous areas)
o Nail psoriasis
o Generalized Pustular (generalized pustules w/fever-emergency)
o Erythrodermic psoriasis (total body redness with chills and skin pain-emergency)

87
Q

• What is the distribution of psoriasis? Epidem?

A

o Distribution: Scalp, extensor surfaces, buttocks, and back but may also be seen in the nails, eyebrows, axilla, umbilicus and anogenital region.
o Age: Biphasic 20 -30 and 50-60. M=F

88
Q

• How is psoriasis diagnosed? Ddx?

A

o H & P, Auspitz sign. Biopsy rarely necessary but will see thickening of epidermis.
o DDX: seborrheic dermatitis, eczema, pityriasis rosea, tinea capitus, squamous cell carcinoma, dermatophytoses, cutaneous lupus, dermatitis, lichen simplex chronicus

89
Q

• What is Pityriasis rosea? Causes? Ssx?

A

o acute, self limited, mild inflammatory, scaling skin disease.
o Causes: possibly reactivation of HHV-7, or primary infxn with HHV-6, -8 or H1N1 flu
o Ssx: Prodrome of headache, malaise, and pharyngitis may occur in some cases, but except for itching, usually asx. Oval, minimally elevated scaling papules and plaques. “Herald” patch. “Christmas tree” distribution. Can persist for months.

90
Q

• For PR, Age, distribution, dx, ddx?

A

o Age: young adults
o Distribution: trunk
o Diagnosis: by examination.
o DDX: tinea corporis, tinea versicolor, drug eruptions, psoriasis, syphilis

91
Q

• What is lichen planus? Causes?

A

o Recurrent itching, inflammation with small, discrete angular papules that can coalesce. Uncommon
o Cause: unknown, Hep C may play a role

92
Q

• What are ssx of lichen planus?

A

o Papules are 2-4 mm, with angular borders, and a violet color. Oral lesions. May see severe itching. Abrupt or gradual onset, with symmetrical distribution on flexor surfaces, trunk, genitals, Koebner phenomenon (skin lesions appear at sites of injury). “purple, polygonal pruritic papules”. New lesions are pink/white but change to the PPPP, surface shows lacy reticulated pattern of whitish lines. Lesions that persist become thicker and dark red.

93
Q

• Epidem of lichen planus? Distribution?

A

o Age: >5. F>M

o Distribution: ankles, wrists, pubic region, lips, mouth. Uncommon on trunk, upper legs, face and head

94
Q

• How is lichen planus diagnosed? Ddx?

A

o Diagnosis: by examination, biopsy- accumulation of PMN’s and T-cell mediated cytotoxic rxn against basal cell keratinocytes. Antibodies to Hepatitis C are detected in 16% of cutaneous LP and 30% with mucosal involvement.
o DDX: leukoplakia, candidiasis, herpes stomatitis, carcinoma, aphthous ulcers, erythema multiforme, psoriasis, discoid lupus, drug eruptions

95
Q

• What are the hypersensitivity and inflammatory skin disorder?

A

o Drug eruptions, erythema multiforme, erythema nododum,

96
Q

• What are drug eruptions? Causes?

A

o Drug eruptions: a common condition that is immune mediated

o Causes: most common drugs are penicillin, sulfonamides, quinidine but almost any drug can induce

97
Q

• What are the types of drug eruptions?

A

o Exanthems; urticartia; pustular; fixed drug eruptions

98
Q

• What is cause of exanthems? Ssx? Distribution? Age? Hx?

A

o Most common. Antibiotics cause. Mildly pruritic measles-like (morbilliform) rash, macules or papules. Symmetric distribution almost always on trunk and extremities. Can occur on palms/soles/mucus membranes. Age- not common in infants- all other ages equal. Hx should include EBV, CMV for amoxicillin.

99
Q

• What is cause of urticaria drug eruptions? Ssx?

A

o common and IgE-mediated. Antibiotics often cause. Also non IgE mediated- NSAIDS often cause. Pruritis, burning of palm/soles. May also have systemic sx such as flushing, fatigue, numbness of tongue, bronchospasm, N/V, palpitations, hypotension.

100
Q

• What is pustular drug eruptions?

A

o ‘acne’ on arms and legs.

101
Q

• What is fixed drug eruptions? Ssx? Causes?

A

o Fixed drug eruptions: circular and recurring at same site. Can also be generalized. Erythematous patch, plaque, bulla or erosion. Occurs within hours of ingestion. Many classes of drugs implicated.

102
Q

• What may be the pigementations of drug eruptions?

A

o gray, brown, black, orange, blue.

Many drugs and they are all different as to which color change they can induce

103
Q

How are drug eruptions diagnosed? Ddx?

A

o Hx &P. CBC-eosinophils

o DDx- too many to list.

104
Q

• What is erythema multiforme? Causes?

A

o inflammatory reaction characterized by “target” lesions

o Causes: drugs(many), infections (HSV or mycoplasma), immunization, autoimmune dz, malignancy or unknown

105
Q

• What are major and minor erythema multiforme?

A

o Major: w/ mucosal involvement (ano genital, oral, ocular).
o Minor w/out mucosal involvement.

106
Q

• What are ssx of erythema multiforme?

A

o onset 3-5 days, often resolved in 2 weeks. Can recur. erythema, edema, bullous lesions, of sudden onset mainly on face and extremities. Symmetrical annular lesions, bulls-eye, target, or iris forms. Pruritic, painful and sometimes see systemic symptoms like fever, weakness, malaise. Can be mild to very severe

107
Q

• what is distribution of erythema multiforme? Epidem?

A

o Distribution: dorsal/palmar hands, soles, forearms, feet, face, elbows, knees, penis and vulva, mucus membranes.
o Age: 50% F

108
Q

• How is erythema multiforme diagnosed? Ddx?

A

o Hx &P. biopsy is non-specific but will show PMN infiltrate, edema. HSV serology/PCR, M. pneumonia serology/PCR
o DDX: urticaria, drug eruptions, bullous pemphigoid, pemphigus, dermatitis herpetiformis, aphthous stomatitis, herpes stomatitis