Dermatology Flashcards
What type of lesions will blanch under pressure?
Erythematous
What is the size of the following lesions: Macule, Patch, Papule, Plaque, Vesicle, and Bulla?
<0.5cm, >0.5cm, <0.5cm, >0.5cm, <0.5cm, and >0.5cm
Which of the following lesions are non-palpable and which are palpable?
Macule and Patch=non-palpable
Papule and Plaque=palpable
What type of primary lesion will not blanch under pressure and why?
Purpuric legions: petechia, purpura, and ecchymosis. Won’t blanch due to extravasation of red blood cells (ruptured or leaky blood vessels).
What are the sizes of the purpuric lesions and are they palpable or non-palpable?
petechia <0.3mm, purpura 3-9mm, and ecchymosis >1cm. They can be either.
What is the most common dermatitis in the USA?
Eczema (atopic dermatitis)
What is the atopic march triad?
atopic dermatitis, asthma, and allergic rhinitis.
What percentage of children with atopic dermatitis will develop asthma and what percentage will develop allergic rhinitis?
50% and 75%
What type of skin condition is due to mutation in filaggrin gene leading to defect in skin barrier (“leaky” skin leading to water loss); also, low number of beta defensins leading to infections (S. aureus)?
Atopic dermatitis
What is lichenification?
(thickening of the skin and an increase in skin markings) normally from repeated scratching.
What’s the effect on the innate immunity (epidermal barrier) in atopic dermatitis?
Water loss and increased penetration.
What causes xerosis (water loss) and increased penetration in atopic dermatitis?
xerosis=skin barrier is compromised which leads to transepidermal water loss which causes dry skin. It’s worsened by sweating, stress, and prolonged hot showers or bath which further strips the skin of its natural oils.
Increased penetration= defective/compromised skin causes more penetration of allergens and irritants like detergents, dust mites, and hard water which leads to itching (pruritus) and potential skin infection.
In what way is adaptive immunity affected in atopic dermatitis?
There is an increased number of T helper type 2 (TH-2) cells and elevated levels of Immunoglobulin E (IgE), which are indicative of a skewed adaptive immune response.
This immune dysregulation leads to inflammation in the form of papules and patches and can cause intercellular edema known as spongiosis, which results in the formation of vesicles (small blisters).
IL-13 is a cytokine that is known to contribute to the itch experienced in atopic dermatitis.
What cytokine contributes to itchiness in atopic dermatitis?
IL-13
What are the physical manifestations of atopic dermatitis?
Scratching due to intense itchiness causes vesicle to rupture leading to excoriations (scratches or abrasions), oozing of fluid, crusting, and dry scales forming on skin.
Which bacteria is associated with changing the skin microbiome in atopic dermatitis?
Staphylococcus aureus Colonization due to its release of toxins.
How does chronic lesions like plaque arise in atopic dermatitis?
arise from resolution of acute flares which causes excess keratin to accumulate and hyperplasia (thickening) of the epidermis and dermis which overtime leads to lichenification which is the thickening of the skin with pronounced lines and margins.
How does atopic dermatitis present clinically in infants?
widely distributed xerosis (dry/scaly), erythematous patches with exudation and small excoriations (also in face, scalp; cheeks & forehead especially; diaper area is spared).
How does atopic dermatitis present clinically in toddlers (ages >/=1)?
rash becomes more localized (face/neck/extensor surfaces).
How does atopic dermatitis present clinically in children (ages 3-12)?
rash in flexor surfaces (wrists, elbows, ankles, and knees). Eczematous and exudative lesions, lichenification (thickening of skin); excoriations and crusting.
How does atopic dermatitis present clinically in adults (beyond puberty)?
widespread lichenification & xerosis; some have brown macular ring around neck (amyloid deposition); lesions in flexural surfaces (anti-cubital & popliteal fossae).
What is contact dermatitis and what causes it?
Inflammatory eczematous disease caused by chemicals or metal ions.
What skin condition is subdivided into allergic and irritant forms?
Contact dermatitis
What only produces innate immune response and produce toxic effects without inducing a T-cell response
Contact irritants (Examples: direct chemical injury to the skin from hand soap (healthcare providers), hydrofluoric acid exposure (chemical plant) that cause contact dermatitis aka irritant contact dermatitis.
What are allergens and what do they do in contact dermatitis?
They are chemicals that modify proteins; haptens (small particles that bind to protiens to create antibody effect) induce innate & adaptive immune responses
Which skin condition produces (type IV hypersensitivity; delayed [happens 48-72 hrs after exposure).
Contact dermatitis
What are some common causes of allergic contact dermatitis?
Paraphenylenediamine: Found in hair dyes, it can cause reactions on the scalp, face, and ears.
Poison Ivy: Contains urushiol, a potent allergen that can cause severe skin reactions.
Neomycin and Bacitracin: Commonly found in topical antibiotics, they can cause reactions especially in areas of skin breakdown such as stasis dermatitis and leg ulcers.
Topical Neomycin and Corticosteroids: These can cause reactions when used in the ear to treat otitis externa.
Nickel: A metal commonly found in artificial jewelry and coins, and it is the most common cause of allergic contact dermatitis.
What is the most common cause of atopic dermatitis?
Nickel
What form of contact dermatitis is caused by release of proinflammatory cytokines from keratinocytes in response to chemical stimuli causing skin barrier disruption and further cytokine release?
[irritant contact dermatitis]
What are the 2 stages in allergic contact dermatitis?
Sensitization and Elicitation
What does the sensitization stage and elicitation stage of allergic contact dermatitis entail?
Sensitization: Dendritic cells in skin take the allergen to the lymph nodes and present it to the helper T-cells there which activates the allergen specific cytotoxic T-cell.
Elicitation: Upon re-exposure to the allergen causes a more vigorous response activating the cytotoxic T-cells which damages tissue causing the symptoms of dermatitis.
What is an immediate Type 1 hypersensitivity reaction, IgE mediated, and may progress to anaphylaxis or angioedema (normally swelling around eyes, mouth etc.)?
Contact Urticaria (hives at site of contact with allergen)
Which Immunoglobulin is associated with allergies?
IgE antibodies
What are the most common symptoms of contact dermatitis?
burning, itching, stinging, soreness, and pain (at the beginning).
Which symptom is more common in allergic contact dermatitis?
Pruritus
How does acute phase of contact dermatitis present clinically?
erythema, edema, oozing,crusting, tenderness, vesicles or pustules.
What phase of contact dermatitis presents clinically as crusts, scales, and hyperpigmentation? acute, subacute, or chronic?
Subacute phase
How does chronic phase of contact dermatitis present?
Lichenification
Which appears and peaks sooner and improves faster, irritant or allergic contact dermatitis?
Irritant
What is a Chronic proliferative and inflammatory skin condition (may have systemic manifestations; eyes, joints, depression)?
Psoriasis
What induces Psoriasis lesions?
Trauma (mechanical [friction or pressure], chemical [irritants], and radiations [sunburn)
secondary inducers: psychological stress, alcohol, smoking, obesity, and hypocalcemia
What worsens Psoriasis lesions?
chloroquine [used for malaria and autoimmune condition], lithium [used for bipolar], beta-blockers [used for high blood pressure], steroids, and NSAIDs
What skin condition improves during summer season but worsens in winter seasons?
Psoriasis
Summer provides Vitamin D and antiinflammatory effects from sunlight
What does type 1 and type 2 Psoriasis invove?
Type 1: This type is associated with a positive family history, typically affects individuals younger than 40, and is associated with the HLA-Cw6 gene.
Type 2: This type has no family history, usually affects individuals older than 40, and is not associated with the HLA-Cw6 gene.
What influences and exacerbates Psoriasis?
Drugs (NSAIDs, lithium, beta-blockers); inflammatory bowel disease, smoking, alcohol, obesity, diet, changing seasons, humidity, HLA Cw6.
What skin conditions involves regulatory T-cell defect leading to inflammation in the dermis due to TH-17 immune response which then causes T-cells, dendritic cells, macrophages to migrate to epidermis via IL-8 which attract immune cells to sites of inflammation?
Psoriasis
What causes the silver scales and thickened skin commonly seen in Psoriasis?
Keratinocytes proliferate increasedly causing silver appearance and accumulates in excess causing thickened skin.
What is the most common type of Psoriasis?
Plaque Psoriasis (80-90%)
What is Plaque Psoriasis?
well defined erythematous plaques with silvery scales over scalp, extensor surfaces (knees, elbows, lumbosacral region). May produce blepharitis, conjunctivitis, and corneal dryness.
What can blepharitis lead to?
Blepharitis may lead to cicatricial trichiasis (eyelashes grow wrong direction like inward) and ectropion (lower eye lid droops away from eye and turns outward).
What is the auspitz sign and which skin condition is it associated with?
pinpoint bleeding on removal of plaque scales.
Plaque Psoriasis
What is the Koebner sign and what skin condition is it associated with?
psoriasis lesions appear at sites of trauma (cuts, sutures, etc.).
Which skin condition is common in children after upper respiratory tract infection (Streptococcus). Involves Erythematous & scaly papules (droplet pattern) in trunk and back.
Guttate Psoriasis
Which condition is associated with hypocalcemia; sterile pustules (small non-infectious pus-filled lesions (palms and soles; may be in whole body).
Pustular Psoriasis
What is Inverse Psoriasis and what areas of the body does it affect?
smooth, erythematous, sharply demarcated patches in intertriginous areas (groins, armpits, intergluteal, inframammary region). Moist and macerated skin; may have fissures (painful, malodorous, pruritic). Affects flexor or intertriginous areas.
What results in exacerbation of unstable plaque psoriasis after abrupt withdrawal of systemic steroids. Presents with severe itching, swelling, and pain and widespread inflammation, erythema, and exfoliation of more than 90% of skin?
Erythrodermic Psoriasis
What related to Psoriasis is associated with skin and nail psoriasis (pitting, oil spots, subungual hyperkeratosis, and dystrophy). Affects joints of fingers and toes leading to sausage-shaped swelling of fingers and toes (dactylitis). Also affects hips, knees, spine (spondylitis) and sacroiliac joints (sacroiliitis)?
Psoriatic arthritis (30%)
What are some complications of Psoriasis?
impaired skin barrier ( due to infection or dehydration), increased cutaneous vasodilation and circulation, or high output heart failure (treated as emergency).
What is Parakeratosis?
Retention of nuclei in stratum corneum.
What is Acanthosis?
Greatly thickened epidermis with elongations into the dermis.
What type of Psoriasis presents clinically with erythematous scaly plaques on the trunk and extensor surfaces of the limbs.
Psoriasis Vulgaris
What are 2 types of pustular psoriasis and how do they present?
C: generalized pustular psoriasis.
D: pustular psoriasis localized to the soles of the feet.
This variant typically affects the palms of the hands as well; hence, psoriasis pustulosa palmoplantaris.
What type of Psoriasis affects the folds of the skin (axillary, intergluteal, inframammary, and genital involvement)?
Inverse Psoriasis. E and F pic
What is a clinical presenting of psoriasis on nails and on reddened skin?
Onycholysis (nail separating from nail bed) and Erythrodermic Psoriasis (red rash, rare)
Erythrodermic Psoriasis pic
Psoriasis presentation pic
What is an uncommon inflammatory condition that manifests with characteristic pruritic (severe and insatiable) lesions on wrists, ankles, and mucous membranes.
Unknown etiology; more common in females and it is associated with hepatitis C (especially when mucous membranes are involved)?
Lichen planus
What skin conditions is 5 times more likely to test positive for hepatitis C?
Lichen planus
What are the 6 P’s of Lichen Planus lesions clinical presentation?
Lesions are pruritic, planar, polygonal, purple, plaques, and papules.
May have vesicles or bullae and produce scarring alopecia.
Nails may be dystrophic.
What is the mucosal clinical presentation of Lichen Planus?
white, lacy, reticulated patches in oral mucosa = diagnostic of lichen planus (known as Wickham striae).
What is Wickham Striae and what skin condition is it associated with?
fine, white, lacy, reticulated patches/lines in oral mucosa = diagnostic of lichen planus (known as Wickham striae).
What skin condition progresses from oral lesions to squamous cell carcinoma in <5% of cases?
Lichen Planus
Why is Lichen Planus called a T-cell-mediated autoimmune disease?
T-cells that are normally to protect from pathogens mistakenly target and destroy body’s own cells.
In Lichen Planus, how does exogenous agent (virus, drug, or contact allergen) affect body’s own cells?
alters epidermal self-antigens leading to activation of CD8+ T cells (cytotoxic T-cell). Protein on surface of body’s own cells are altered making it look foreign to immune system.
In Lichen Planus, why do cytotoxic T-cells attack basal keratinocyte in epidermis?
cross reactivity where immune system can’t distinguish between normal and altered self-antigens/cells.
What are some agents that can trigger Lichen Planus?
Metals used in dental restoration: Mercury, copper, and gold used in dental fillings and crowns can sometimes provoke an immune response, leading to autoimmune reactions.
Drugs: Certain medications, such as antimalarials, ACE inhibitors (ACEIs), thiazide diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), quinidine, beta-blockers, and tumor necrosis factor (TNF)-alpha inhibitors, have been implicated in triggering autoimmune responses, potentially by altering self-antigens or affecting immune regulation.
What are some common treatments for Psoriasis or Lichen Planus?
topical corticosteroids, vitamin D analogs, and retinoids
What is a common, acute, mucocutaneous disease with classic target-shaped lesions in a symmetric distribution.
Affects young people (18 - 30 years old)?
Erythema Multiforme
What triggers cell destruction in the hypersensitive skin reaction called erythema multiforme?
Fragments of herpes simplex virus remaining in keratinocytes after infection subsides are recognized and targeted by cytotoxic T-cells who believe them to be still infected/abnormal.
What are the most common viral/bacterial causes of erythema multiforme?
Herpes simplex (HSV-1>HSV-2), Mycoplasma pneumonia (respiratory infection)
Less common causes: drugs (sulfonamides, β-lactams [antibiotic], phenytoin [anticonvulsant], vaccines).
What is the name of a type of Erythema Multiforme (EM) that occurs in patients with Systemic Lupus Erythematosus (SLE)?
Rowell Syndrome
It is characterized by a specific set of symptoms, including EM-like lesions, positive lupus erythematosus tests, and speckled pattern of antinuclear antibodies.
What skin disorder is the following a description of?
Skin lesions: raised (papular), target lesions with multiple rings and dusky center (in contrast to annular lesions of urticaria). Lesions are asymptomatic (some may be itchy).
Erythema Multiforme
What are the most common site of erythema multiforme?
palms/soles, backs of hands and feet, extensor aspects of forearms and legs.
May involve mucous membranes.
May have systemic signs.
What is a Negative Nikolsky sign and which skin disorder exhibits it?
Negative Nikolsky sign (rubbing of skin does not cause sloughing – splitting of epidermis from dermis).
Erythema Multiforme
What are the 3 concentric zones of an erythema multiforme lesion from inner to outer ring?
Center is dusky/dark and can be crust/vesicle (blistered), next is surrounding pale pink or erythematous zone, next is peripheral red/dark ring.
Which skin disorders are flatter, more tender, and ALWAYS involve mucous membrane with +Nikolsky sign compared to Erythema Multiforme?
Steven’s Johnson Syndrome (SJS) or Toxic Epidermal Necrolysis (TEN)
What is Steven Johnson syndrome/toxic epidermal necrolysis? and how do you classify them separately?
Spectrum of severe, febrile, blistering diseases of the skin and mucous membranes with skin detachment.
Classification:
SJS: < 10% of body surface area
TEN: > 30% of body surface area (high mortality).
SJS/TEN overlap: 10-30% of body surface area
Which skin disorder is mainly triggered by drugs such as penicillin, sulfonamides, phenytoin, carbamazepine, lamotrigine, NSAIDs?
Etiology: penicillin, sulfonamides, phenytoin, carbamazepine, lamotrigine, NSAIDs.
Less common cause: infections (Mycoplasma pneumoniae).
How does widespread blistering and skin detachment occur in Steven Johnson syndrome/toxic epidermal necrolysis?
Drugs are metabolized but body fails to clear the metabolites properly so they form a complex with proteins in keratinocytes that the immune system recognizes as foreign. The cytotoxic T-cells then mistakenly attack the body’s own keratinocytes leading to widespread blistering and skin detachment.
What presents with Very painful skin (vs in EM, very mild), systemic signs (fever, dehydration, hypotension) that starts within 1 to 3 weeks after initiating an offending drug?
Steven Johnson syndrome/toxic epidermal necrolysis?
Which skin disorder involves Prodromal period [period between appearance of initial symptoms and full development of rash or fever] with malaise, fever, headache, cough, and keratoconjunctivitis, followed by atypical target lesions that suddenly appear on the face, neck, and upper trunk.
Steven Johnson Syndrome/toxic epidermal necrolysis
Which skin disorder involves Lesions coalescing into large flaccid bullae, and sloughing over a period of 1 to 3 days.
Nails and eyebrows may be lost along with epithelium?
Steven Johnson Syndrome/toxic epidermal necrolysis