derm Flashcards
Name the primary lesion.

Macula
This is a small spot that is not palpable & that is < 1 cm.
What is a macula?
What is a large spot that is not palpable & that is > 1 cm
A patch
Name the primary lesion.

Patch
What is a small superficial bump that is elevated & that is < 1 cm?
Papule
Name the primary lesion.

Papule
Name the primary lesion.

Plaque
What is a large superficial bump that is elevated & > 1 cm
Plaque
Name the primary lesion.

Nodule
What is a small bump with a significant deep component & is < 1 cm
Nodule
Name the primary lesion.

Tumour
What is a large bump with a significant deep component & is > 1 cm
Tumour
Name the primary lesion.

Vesicle
What is a small fluid-filled bubble that is usually superficial & that is < 0.5 cm
Vescile
Name the primary lesion.

Bulla(e)
What is a large fluid-filled bubble that is superficial or deep & that is > 0.5 cm
Bulla(e)
Name the primary lesion.

Pustule
What is pus containing bubble often categorized according to whether or not they are related to hair follicles
Pustule
Follicular pustule rash that is superficial, and generally multiple follicles
Folliculitis
Follicular pustule rash that is a deeper form of folliculitis.
Furuncle
A deeper follicular pustular rash that involves multiple follicles coalescing
Carbuncle
What may a nonfollicular pustule rash indicate, as opposed to a follicular rash.
Indicates systemic infection as opposed to local.
Name the primary lesion.

Cyst
What is a primary lesion?
Lesions that appear as a direct result of the pathologic process.
What is a secondary lesion?
Lesions that appear as a result of alteration or evolution of a primary lesion (e.g. rubbing, scratching, necrosis)
Name the secondary lesion.

Scale
What lesion is the accumulation or excess shedding of the stratum corneum?
Scale
What does a scale indicate?
It indicates that there is epidermal infolvment, specifically epidermal inflammation: i.e. psoriasis, tinea, eczema
Name the secondary lesion.

Crust.
What is a crust?
Crust is dried exudate (ie. blood, serum, pus) on the skin surface
Name the secondary lesion.

Excoriation
What is excoriation?
Excoriation is a loss of skin due to scratching or picking
Name the secondary lesion.

Lichenification
What is lichenification?
Lichenification is an increase in skin lines & creases from chronic rubbing
Name the secondary lesion.

Maceration
What is maceration?
Maceration is raw, wet tissue
Name the secondary lesion.

Fissure
What is a fissure?
A linear crack in the skin - often painful
Name the secondary lesion.

Erosion
What is an erosion?
An erosion is a superficial open wound with loss of epidermis or mucosa only
Name the secondary lesion.

Ulcer
What is an ulcer?
An ulcer is a deep open wound with partial or complete loss of the dermis or submucosa
Name the distinct lesion.

Wheal (Hive)
What is a wheal or hive?
A wheal or hive describes a short lived (< 24 hours), edematous, well circumscribed papule or plaque seen in urticaria
Name the distinct lesion.

Burrow.
What is a burrow.
A burrow is a small threadlike curvilinear papule that is virtually pathognomonic of scabies
Name the distinct lesion.

Comedome
Name the distinct lesion.

Atrophy
Name the distinct lesion.

Keloid
Distinguish keloid from hypertrophic scar.
A keloid overgrows the original wound boundaries and is chronic in nature
A hypertrophic scar on the other hand does not overgrow the wound boundaries
Name the distinct lesion.

Fibrosis / Sclerois
Name the distinct lesion.

Petechiae.
What does petechia, purpura, and ecchymosis describe?
Petechiae or purpura or ecchymosis describes red blood cells that are outside the vessel walls & areas are nonblanchable
Name the distinct lesion.

Telangiectasis
What is telangiectasis?
Telangiectasis describes dilated superficial dermal vessels
Name the distinct lesion.

Milium
What is a milium?
A milium is a small superficial cyst containing keratin (usually
What distinct lesion is striae an example of?
Atropy
Describe the lesions colour.

Erythematous
Describe the lesions colour.

Violaceous / Purpuric
Describe the lesions colour.

Blue-Grey
Describe the lesion’s colour.

Variegated - brown, blue-grey, black, hypopigmented.
Describe the lesion’s colour.

Hypopigmented
Describe the lesion’s colour.

Depigmented
Describe the lesion’s colour.

Yellow
Describe the lesion’s margin.

Well circumscribed, well demarcated
Describe the lesion’s margin.

Poorly circumscribed, poorly demarcated.
Describe the lesion’s shape.

Polygonal
Describe the lesion’s shape.

Targetoid. (e.g. erythema multiforme)
Describe the lesion’s shape.

Umbilicated (e.g. molluscum contagiosum)
Describe the lesion’ shape.

Serpiginous
Describe the lesion’s shape.

Verrucous
Descrie the lesion’s configuration.

Linear
Describe the lesion’s configuration.

Annular (forming a ring)
Describe the lesion’s configuration.

Arcuate (curved like a bow)
Describe the lesion’s configuration.

Polycyclic
Describe the lesion’s configuration.

Grouped
Describe the lesion’s configuration.

Zosteriform - Dermatomal
Describe the lesion’s configuration.

Reticulate (lacy-like pattern)
Name the 8 histological components of skin.
- Epidermis - epithelial layer (ectodermal origin)
- Dermis - CT layer (mesodermal origin)H
- Hair
- Sebaceous glands
- Sweat glands
- Vessels
- Nerves
- Hypodermis
Name the four physiological functions of the skin.
- Protection
- UV light shield
- injury
- dehydration
- microorganisms
- Sensation
- touch
- pressure
- pain
- temperature
- Thermoregulation
- insulation against heat loss
- heat loss by sweat and blood flow
- Metabolic
- energy storage
- Vit D syntehsis
The epidermal / dermal junction is irregular. What two regions interdigitate?
Dermal Papillae with epidermal Rete Ridges.

What kind of epithelium is the epidermis composed of?
Stratified, keratinizing squamous epithelium.
What are the four morphologic layers of the epidermis?
- Stratum basale
- Stratum spinosum
- Stratum granulosum
- Stratum corneum
Which layer of the epidermis is described as a single layer of mitotically active cuboidal cells?
Stratum basale.
Which layer of epidermis is described as an anucleate layer composed mostly of protein.
Stratum corneum.
Which layer of epidermis is described as the main living layer consisting of large polyhedral cells.
Stratum spinosum
Which layer of epidermis is described as 1-3 cells thick containing large keratohyaline granules.
Stratum granulosum.
What is the function of Stratum Corneum?
Main diffusion barrier.
In what layer of the epidermis do the cells flatten?
Stratum granulosum.
In what epidermal layer does most cellular maturation occur?
Stratum spinosum
What is the function of the Stratum basale?
Replicating immortal cells that give rise to other keratinocytes.
Name the four cell types within the epidermis
- Keratinocytes
- Melanoctyes
- Langerhans cells
- Merkel cells
Which epidermal cell relies on this structure to hold tightly to each other, and a hemi-desmosome to the basement membrane.

Keratinocyte.
Which epidermal cell is of neural crest origin?
Melanocyte
Which epidermal cell’s function is main melanin storage?
Keratinocyte
Which epidermal cell synthesizes melanosomes?
Melanocytes
Melanin is produces by the action of what enzyme?
Tyrosinase
(tyrosine –> DOPA –> dopaquinone –> melanin)
Which epidermal cell contains Birbeck granules, which are tennis racquet-shaped on EM?
Langerhans cells
What is the main function of Langerhans cells?
Antigen presenting cells
What epidermal layer are Langerhans cells located?
Spinous layer
Where in the epidermis are Merkel cells located?
Basal epidermis and hair follicle.
Which epidermal cell contains Neurosecretory granules?
Merkel cell
What is the main function of Merkel cells?
Sensory touch receptors
What are the two layers of dermis?
Papillary dermis and Reticular dermis
Which layer of dermis is immediately beneath epidermis?
Papillary dermis
What is the papillary layer of dermis made of?
What is the reticular dermis made of?
Thick type I collagen bundles, and thick elastic fibers
What is responsible for facial wrinkles?
Loss of elastic fibers in the papillary dermis
What layer in skin is responsible for thermal insulation?
Subcutis or Hypodermis composed of adipocytes
What structure separtes the papillary and reticular dermis?
Superficial dermal capillary plexus.
What structure is preset at the dermal subcutaneous junction?
Deep cutaneous plexus of larger vessels
Which four skin appendages form the pilosebacous unit?
- Hair follicle
- Sebacous gland
- Apocrine gland
- Arrector pili muscle
Lable the image.

- Hair shaft
- Follicular infudibulum
- Arrector pili muscle
- Follicular isthmus
- Follicular Bulge
- Hair Bulb
- Sebacous gland
- Eccrine gland
What is cutis anserina?
Goose bumps
What is described as the deepest of the hair follicle, with the appearance of basaloid epithelium and mesenchyme?
Hair bulb
What is the function of hair bulb?
Synthesize hair.
What is the bundle of spindle cells that attaches to the follicle at the bulge?
Arrector pili muscle?
What is the function of the Arector pili muscle?
Cutis anserina (goose bumps)
What is the function of the follicular bulge?
Stem cell reservoir
What is the superficial part of the hair follicle, above the opening of the sebaceous duct, called?
Follicular ifundibulum
What is the short section of hair follicle between the opening of the sebaceous duct and follicular bulge called?
Follicular isthmus
What kind of secretion do sebaceous glands undergo?
Holocrine (lysis of secretory cells)
What kind of secretion do apocrine glands undergo?
Apocrine (pinching off one end of the secretory cell)
What kind of secretion do Eccrine glands undergo?
Merocrine (secretion that is discharged without major damage to the secretory cells)
Which dermal gland appears as multivacuolated lipid laden cells?
Sebaceous
Which dermal gland appears as apical snouts
Apocrine
Which dermal gland appears with a tightly coiled intraepidermal duct
Eccrine
What is the function of the sebaceous gland
Lubricate hair
What is the function of the apocrine gland?
Scent glands in other mammals (pheromone?)
What is the function of the eccrine gland?
Temperature regulation - sweat
Which dermal gland is only found in the skin of the axilla, groin, genitalia, nipple and external ear and eyelid?
Apocrine
What is the tightly coiled intraepidermal duct of the eccrine gland called?
Acrosyringium
Which dermal gland does not connect with the surface via the follicular ostium, but rather connects directly with the epidermal surface?
Eccrine
What is the main product of sebaceous glands?
Sebum
What is the primary systemic control of sebum production?
Steroid hormones
What is the primary systemic control of eccrine glands?
Cholinergic sympathetic nerves
What is the primary systemic control of apocrine glands?
Adrenergic Sympathetic Nerves
What skin appendage is described as multilayered, onion-like structures?
Pacinian corpuscle
Where is a Pacinian corpuscle located?
Deep reticular dermis & subcutis adjacent to nerves
What is the function of Pacinian corpuscle?
Pressure and vibration receptors
What skin appendage is described as a rugby ball standing on its tip consisting of horizontally stacked fibers and spindle shaped nuclei?
Meissner’s corpuscle
Where is a Meissner’s corpuscle located?
Papillary dermis
What is the function of Meissner’s corpuscle?
Touch receptors
What skin appendage is described as one or more layers of uniform cuboidal cells arranged around a blood vessel in the deep reticular dermis?
Glomus body
What is the functio of a glomus body?
Regulate body temperature by controlling flow through direct arteriovenous shunts / anastomoses
Are hair follicles absent or present in thick skin?
Absent
Are specialized nerve end organs absent or present in thick skin?
Present
Are specialized nerve end organs absent or present in thin skin?
Absent
Are hair follicles absent or present in thin skin?
Present
Where is the highest density of eccrine glands?
Thick skin
Where are sebaceous glands absent?
Thick skin
Which form of UV does not reach earth’s surface significantly due to the ozone layer?
ultraviolet C
Which form of UV is the most carcinogenic band that reaches earth in significant quantity
ultraviolet B
Which form of UV directly damages DNA by causing strand breaks and nucleotide dimerization?
ultraviolet B
Which form of UV mainly produces vitamin D?
ultraviolet B
Which form of UV damages DNA indirectly by activating photosensitizers within the cell?
ultraviolet A
Which form of UV is a weak carcinogen by itself?
ultraviolet A
Which form of UV is an important cause of skin wrinkling?
ultraviolet A
Which kind(s) of skin carcinoma is associated with even low doses of UVB and childhood exposure increasing risk?
BCC and melanoma
Which kind(s) of skin carcinoma is associated with a cumulation of UV light based on large amount of exposure, as in outdoor workers, and active sport participants.
SCC
What are the two types of melanin, and which one - found commonly is in all racial groups - and more protective, as opposed to being found in red-heads.
Eumelanin & Phaeomelanin
Eumelanin
What is the most common type of skin cancer, that is locally invasive and rarely metastatic?
BCC
Which skin canner manifests most comony as a translucent nodule/plaque with telangiectasia, or later as an ulcer with a raised rolled edge?
BCC

Which skin cancer can have a slcerosing variant, and pigmented in darker skinned individuals?
BCC

What are the four treatment options for BCC?
- electrodessication and curettage
- simple surgical excision
- micrographic surgery
- radiation therapy
What is the precursor lesion - pink, scaling patch, limited to epidermis - that precedes SCC?
Actinic keratosis

What are the two treatment options for actinic keratoses?
- liquid nitrogen cryotherapy
- topical 5-Fluorouracil
Which skin cancer manifests as a clinically hard pink or white nodule, often surrounded by typical scaling, and can have systemic spread, particularly to lymph nodes?
SCC

Which skin cancer can present intraorally as leukoplakia?
SCC

What are the 2 treatment options for SCC?
- surgical excision
- radiation therapy
What are the four ways that damaged melanocytes can manifest and what is there related malignancy?
- freckles (not malignant)
- nevi (not malignant - predicts melanoma risk)
- atypical nevi (pre-malignant)
- melanoma (malignant)
What lesion is the result of an increased number / nest of melanocytes due to cell division?
Nevi
What are the thre types of nevi, based on location?
- Junctional (dermal-epidermal junctional)
- Compound (epidermis and dermis)
- Dermal (entirely within dermis)
What is the most significant predictor of melanoma risk?
Number of common Nevi (>100 nevi suggest melanoma risk of at least 1 in 10 - vs. 1:90)
Define atypical nevi
Subset of nevi showing variation in edge and color, due to variable melanin production
What are the ABCD’s of melanoma?
Asymmetry
Border
Color
Diameter
Describe superficial spreading melanomas.
When nevi become melanomas.
Considerable variation in edge and color, like a very severely atypical nevus

Describe nodular melanoma
Arises without obvious percursor lesion, rather than increasingly abnormal nevi

Describe lentigo maligna melanoma.
Arises from expanding brown patch (lentigo maligna) from abnormal melanocytes extending along dermal-epidermal junction -often for years- similar etiology to SCC, 10% of melanomas.

What is the primary treatment for melanoma?
Surgical management excised with 1-3 cm margin
What does the risk of melanoma systemic spread correlate with?
Tumor thickness
What is the indication for chemotherapy in melanoma and what is the prognosis?
Systemic involement, but response rate is low. 5-year survival with reginal lymph node - 60%, with distant metastes - 16%
What is the definition of SPF?
Sun protective factor - the amount of light required to burn with sunscreen on divided by the amount without the sunscreen
From the described pathology, name the condition:

(1) Inflammation in & around the hair follicles
(2) Excess collagen
(3) Plugging of the hair follicle by keratin
Acne
From the described pathology, name the condition:

(1) Enlargement & pleomorphism of keratinocytes
(2) Sharply demarcated column of compact hyperkeratosis & parakeratosis
(3) Confinement of proliferation to epidermis
(4) Dermal inflammatory cells
Actinic Keratosis
From the described pathology, name the condition:

(1) Peripheral palisading
(2) Rim of mucin
(3) Dermal nests of basaloid cells
(4) Intact epidermis
Basal Cell Carcinoma
From the described pathology, name the condition:
- dermal eosinophils
- subepidermal cleft, with fluid accumulation
Bullous Pemphigoid
From the described pathology, name the condition:

(1) Langerhans cells in the epidermis
(2) Lymphocytes in the epidermis
(3) Spongiosis
(4) Hyperkeratosis & parakeratosis
(5) Elongated rete ridges
(6) Lymphocytes surrounding dermal vessels
Eczema
From the described pathology, name the condition:

(1) Nodule of dermal blood vessels
Hemangioma
From the described pathology, name the condition:

(1) Necrosis of epidermal cells, sloughing
(2) Multinucleated keratinocyte
(3) Dermal inflammation
Herpes Simplex, Varicella - Zoster
From the described pathology, name the condition:

(1) Band-like infiltrate of lymphocytes at the dermoepidermal junction
(2) Hypergranulosis
(3) Necrotic basal keratinocytes
(4) Hyperkeratosis
Lichen Planus
From the described pathology, name the condition:

(1) Symmetry
(2) Nested pale slightly pigmented cells in the dermis
Melanocytic nevus
From the described pathology, name the condition:

(1) Upward spread of pale cells above the basal layer of the epidermis
(2) Asymmetry
(3) Nested cells with pale slightly pigmented cytoplasm at the dermoepidermal junction
(4) Dermal inflammation
(5) Singly dispersed pale cells
Melanoma
From the described pathology, name the condition:

(1) Suprabasal, intraepidermal bullae
(2) Superficial perivascular inflammatory infiltrate
(3) “Tombstoning” of basal keratinocytes
(4) Normal stratum corneum with basketweave appearance
(5) Acantholysis
Pemphigus vulgaris
From the described pathology, name the condition:

(1) Patchy epidermal spongioses & lymphocytes
(2) Lymphocytes surrounding dermal vessels
(3) Extravasated red blood cells
(4) Patchy hyperkeratosis & parakeratosis
Pityriasis rosea
From the described pathology, name the condition:

(1) Hyperkeratosis without parakeratosis
(2) Few inflammatory cells in the epidermis
(3) Numerous yeast & plump hyphae
Pityriasis versicolor / Tinea versicolor
From the described pathology, name the condition:

(1) Hyperkeratosis & parakeratosis
(2) Neutrophils in the epidermis
(3) Thinning of the epidermis overlying the dermal papillae
(4) Vessels close to the epidermis
(5) Elongated rete ridges
Psoriasis
From the described pathology, name the condition:

(1) Telangiectases
(2) Inflammation in & around the hair follicles
Rosacea
From the described pathology, name the condition:

(1) Domed superficial aspect
(2) Melanin within tumour keratinocytes
(3) Sharply demarcated epidermal thickening
(4) “Cysts” containing keratin
Seborrheic keratosis
From the described pathology, name the condition:

(1) Penetration of tumour epithelium into dermis
(2) Enlargement & pleomorphism of keratinocytes with abundant eosinophilic cytoplasm
(3) Hyperkeratosis
Squamous Cell carcinoma
From the described pathology, name the condition:

(1) Sparse fine branching hyphae
(2) Numerous inflammatory cells in the epidermis
(3) Hyperkeratosis & parakeratosis
Tinea Corporis
From the described pathology, name the condition:

(1) Serum in the stratum corneum
(2) Hyperkeratosis & parakeratosis
(3) Coarse keratohyaline granules & perinuclear vacuolation
(4) Papillomatosis
Verruca Vulgaris
From the described pathology, name the condition:

(1) Intact epidermis
(2) Dermal proliferation of cells with round & angulated nuclei
(3) Thick collagen fibers
(4) Hemosiderin pigment
(5) Hemorrhage
Dermatofibroma
What is the desribed method of specifmen aquisition:
Contains the full thickness of dermis, but not ideal for diagnosing melanoma
Punch biopsy
What is the desribed method of specifmen aquisition:
Ideal for the one-step diagnosis and therapy of skin tumours
Excisional biopsy
What is the desribed method of specifmen aquisition:
Results in a less consipicous scar than other biopsy methods
Shave biopsy
What is the desribed method of specifmen aquisition:
Used specifically to obtain evidence of intraepidermal infections
Scrapings
What is the desribed method of specifmen aquisition:
Most frequently combined with electrosurger
Curettage
Name the five cardinal morpologic features of psoriasis.
- Plaque, raised lesions
- Well circumscribed margins
- Bright salmon red colour
- Silvery scale
- Symmetric distribution

What lesion sites are common in psoriasis?
Extensor surfaces (elbows, knees)
Scalp, retroauricular, and ears
Palms and soles
Umbilicus
Glans Penis
Lumbar
Shins
Supragluteal
Nails - pitting, onycholysis
Describe guttate psoriasis.
acute extensive eruption of small psoriatic papules over trunk and proximal extremities; usually in association with group A streptococcal infections, and may recur with each reinfection
Describe inverse psoriasis
psoriasis occurring within flexural sites (i.e. axillae, groin, gluteal fold) will usually lack scale, and have a bright red, moist, macerated appearance
Describe pustular psoriasis.
can be generalized (von Zumbusch) or localized (usually to the palms or soles); generalized pustular psoriasis is associated with fever, leukocytosis and can be life-threatening
Describe erythrodermic psoriasis.
the entire body is affected and is red and scaly; prominent systemic complications
Describe the pathology of psoriasis.
- psoriasis is a chronic immunologic disease of the skin characterized by profound cutaneous inflammation and epidermal hyperproliferation
- in psoriasis, it takes 3-4 days for a keratinocyte to transit from the basal layer to the surface where it is shed
- key role for Th1 cells
What phenomenon is seen, and what disease is it associated with?
Koebner phenomenon
Psoriasis aggragavation by tattoo
Describe Psoriatic Arthritis
5-10% of patients with psoriasis will have psoriatic arthritis; seronegative (RF), association with HLA-B27
- asymmetric peripheral joint involvement (most common)
- symmetric peripheral joint involvement (resembles rheumatoid arthritis)
- axial disease (resembles ankylosing spondylitis)
- arthritis mutilans (uncommon)
What are some of the systemic complications of generalized pustular or erythrodermic psoriasis?
- fever, weight loss
- congestive heart failure (due to increased cutaneous blood flow)
- fluid/electrolyte imbalance
- hypoalbuminemia, low iron, hyperuricemia
What are the topical treatments used in psoriasis?
Glucocorticoids
Tars
Calcipotrial (Vit D derivative)
Anthralin
Taxarotene (retionoid, Vit A derivative)
Salicyclic acid
Calciurin inhibitor
What systemic therapy is used in psoriasis?
Methotrexate
Acitretin (oral retinoid)
Cyclosporine
Phototherapy (UVB or Psoralen UVA)
What is the intensely prurit inflammatory skin disorder Atopic dermatitis or “eczema” associated with?
Asthma, hayfever, allergic conjunctivitis
Describe the pathogensis of Atopic dermatitis “eczema”
- cutaneous inflammation mediated by Th2 cells (type 2 helper T cells producing Il-4 and IL-5)
- elevated serum levels of IgE
- impaired cutaneous barrier function (increased transepidermal water loss leads to dry skin)
- skin colonization and infection by Staphylococcus aureus (the toxins of which may serve as superantigens to promote cutaneous inflammation)
- diet factors rarely important
Descibe the clinical symptoms and basic morphology of Atopic dermatitis “eczema”
- pruritus is usually the most outstanding clinical feature
- depending on the acuity of the skin disease there can be:
- ill-defined erythema
- tiny coalescing edematous papules or papulovesicles
- excoriations
- crusting (if secondarily infected)
- xerosis (or dry, scaly skin)
- depending on the acuity of the skin disease there can be:
- lichenification
What are the 3 phases of atopic dermatitis “eczema” and what are their clinical features?
- Infantile
- facial, extensor distribution
- Childhood
- tendency to xerosis
- flexural distribution
- more lichenification and excoriations
- Adult
- improves with age, may remit
- may primarily affect hands
What is the treatment for atopic dermatitis “eczema”?
- Avoid irritating factors
- Aggressive restoration of the cutaneous permeability barrier with bland emollients and moisturizers
- Topical glucocorticoids (creams or ointments)
- Topical immunomodulators (tacrolimus, pimecrolimus)
- Topical or systemic anti-staphylococcal antibiotics
- Oral antihistamines
What is allergic contact dermatitis?
type IV hypersensitivity to an allergen in contact with the skin (e.g. nickel allergy, poison ivy)
What is irritant contact dermatitis?
contact of the skin with something that primarily causes direct local irritation
Describe the pathogenesis of Seborrheic Dermatitis
Involves sebum production and Pityrosporum fungus
(fungus is lipophilic yeast that thrives on lipids in sebum - scaling and inflammation may be due to host reponse to increased fungi on skin)
What are the clinical features of Seborrheic Dermatitis in adults
- Dandruff
- Ill-defined erythema
- Greasy-appearing scale
- Face distribution (glabella, eyelids, eybrows, nasolabial folds, nose, mustache/beard, ears)
- Trunk (presternal, umbilicus)
What are the clinical features of Seborrheic Dermatitis in infants?
What are the associated disorders with seborrheic dermatitis?
Parkinson’s disease (and other neurologic disorders) - due to immobility of facial muscles
HIV infection - get a more resistant disease
Name this greasy, scaly, erythematous lesion.
Seborrheic dermatitis
What is a mild, common, self-limited eruption, that may be due to herpesvirus?
Pityriasis rosea
Describe the clinical course of pityriasis rosea?
Evolves over 6-8 weeks, primarily in adolescents and young adults in spring and fall
- herald “Patch” - solitary 2-6cm scaly plaque
- eruption of multiple pauples with fine “collarette” scaling along rim of lesion
- “T shirt and shorts”distribution
- Pruritis variable
- Recurrance uncommon
What are the mimickers of Pityriasis rosea?
Secondary syphilis
Drug eruptions
What is te treatment of Seborrheic dermatitis?
What are the five clinical features of lichen planus?
- Papules (2-5mm)
- Pruritus (intense)
- Purple
- Polygonal
- Planer (flat-toppped)
- Also may sow scale-like fine white lines on surface (Wickham’s striae)
Where is the typical distribution of lichen planus lesions?
Flexor wrists and forearms, neck, thighs, shins, lumbar back, genitalia
Oral lesions common (with lacy white reticular lesions on buccal mucosa most common, may also become ulcerated)
What is Dr. Lui’s #1 Rule?
What are four common and distinctive drug reaction patterns?
- Urticaria
- Maculopapular / exanthematous / morbilliform (measles-like)
- Erythema multiform (target lesions, mucosal infolvement)
- Fixed drug eruption (localized plaques that recur at the same body site every time the patient is exposed to the offending systemic drug)
What are the Skin infections that cause Vesicular and Vesicobullous Eruptions?
- Herpes Simplex
- Varicella
- Herpes Zoster
- Impetigo
- Bullous insect bite reaction
- Primary skin bullous disorder (eg. pemphigus)
What are the clinical features of Herpes Simplex I and II
Grouped vesicles on an erythematous base
Most of adult population has been exposed
Virus can be shed without visible lesions
Persist in sensory ganglia leading to recurrent infections
Precipitated by UV, menses, fever, URTI, immunodeficiency
HSV-1 predominatly Labialis distribution
HSV-2 predominantly Urogenital distribution
What are the clinical features of Varicella?
“Dewdrop on rose petal” distribution
Initially papules, which become vesiscles, which crust over
Christmas tree distribution due to hematogenous spread
Test with viral culture, Tzanck smear, or skin biopsy
What are the clinical features of Herpes Zoster?
Prodrome of neuritic pain (days-weeks)
Acute vesicles then crusted papules
Unilateral dermatomal distribution
Grouped vesicles on erythematous base
Viral culture, Tzanck smear, or skin biopsy
What are the identical histological changes seen in herpes simplex, varicella, and zoster on skin biopsy?
Tzanck smear shows multinucleated keratinocytes or acantholytic keratinocytes
What are the clinical features of nonbullous impetigo?
- Scaling honey crusted lesions
- Group A Strep, or Staph aureus
- Supericial infection
What are the clinical features of bullous impetigo?
- vesicles and bullae
- clear or slightly yellow fluid
- shallow erosions form if bullae break
- caused by Staph aureus
What are the clinical features of arthropod bites?
Grouped papeuls or vesicles
Multiple, close together bites “breakfast, lunch, dinner”
Pruritic / urticarial, painful papules
causes: mites, ticks, spiders, centipedes, millipedes, mosquitoes, black flies, sand flies, bedbugs, ants, bees, wasps, hornets, fleas
What are the clinical features of bedbugs?
Erythematous papules, vesicles, nodules
Bugs are red-brown colour size of a ladybug
Nocturnal
Bites on body and head and neck area
What are the infectious causes of follicular eruptions?
- Pityrosporum folliculitis
- Pseudomonas folliculitis
- Staphylococcal follicultis
- Acne
How do you differentiate follicular eruptions?
- hot tub exposure
- distribution
- presence of comodones, pauples, nodules and cysts (acne)
- level of inflammation (pityrosporum has less)
- KOH and cultures
What are the clinical features of Pityrosporum folliculitis?
Monomorphous papules
Sweaty individual
KOH positive
What are the clinical features of Pseudomonas folliculitis?
Hot tub exposure
Other proximal individuals affected
Inlammatory follicular-based papules and pustules
Culture positive
Self-limited
What are the clinical features of staphylococcal folliculitis?
Inflammatory pustules
Gram stain and culture positive
What is the infectious and inflammatory differential for annular and scaling eruptions?
- Tinea corporis
- Tinea versicolour
- Secondary syphilis
- Psoriasis
- Nummular eczema
How do you diagnose a scaling eruption? (4)
- Scrape scaling edge for KOH and culture
- Distribution – psoriasis symmetrical and extensor surfaces
- Tinea versicolour non-inflammatory brown and white scaling patches
- Tinea corporis few lesions with central clearing
What are the clinical features of tinea corporis?
AKA ringworm
Annular scaling edge (ring-like)
Well demarcated plaque with central clearing
Single or multiple lesions
Assymetrical
Scrape edge for KOH and culture
Caused by Trichophyton rubrum and Microsporum canis
What are the clinical features of Tinea versicolor, aka “pityriasis versicolor”
Well marginated round scaling brown or light macules
Common in young adults
risk factors: warm and humid climate, oil skin, hyperhidrosis
Psoitive KOH
Microscopy - scale + “spaghetti and meatballs” spores and hyphae
Malassezia furfur or Pityrosporum versicolor
What are the clinical features of Secondary syphilis?
Widespread red-brown scaling papules
Involvement of palms and soles
2-6 months after primary infection
First eruption is macular, then papulosquamous, pustular, or acneiform
Condylomata lata - flat-topped papules in most areas (mouth and ano-genital)
Treponema pallidum
Dx with serology, or skin biopsy
What are the infectious causes of papular eruptions? (3)
- Verruca
- Molluscum contagiosum
- Insect bites
How do you differentiate papules?
- Central punctum + pearly apperance = molluscum
- Often surrounding eczema = molluscum
- Dull surface + capillary loops = verruca
- Minimally elevated = verruca plana
- Pruritic + grouped, also vesicular = insect bites
What are te clinical features of Verruca vulgaris?
Firm, hyperkartotitc papules with clefted surface and vegetations
Red or brown dots caused by thrombosed capillary loops
HPV
Skin to skin transmittion
Breaks in stratum corneum to facilitate epidermal infection
Risk factors: immunocompromise, meat handlers
What are the clinical features of Molluscum contagiosum?
Skin coloured umbilicated papules
Gentle pressure causes the central keratotic plug to extrude
Mollusca undergoing spontaneous regression may have an erthematous halo
Caused by a pox virus
Spread through skin to skin contact
Common in children and sexually active adults
Also seen in HIV
What are the infectious and inflammtory causes of eczematous and pruritic eruptions? (4)
Scabies
Louse infestation
Insect bites
Eczema
How do you differentiate pruritic eruptions? (4)
- Scabies = burrows or nodules
- Louse = no primary lesion
- Insect bites = grouped
- Atopic dermatitis = past history dry skin, hyper-linear palms, flexural dist.
What are the clinical features of scabies
Widespread eruption
Nocturnal prurities
Due to hypersensitivy to mite Sarcoptes scabiei (can take 6 weeks post-exposure to develop)
Burrows: Serpiginous track with spot at end, scrape for Dx
Nodules: Red-brown nodules in axillary area and groin
Dx - mite, eggs, feces on microscopy, biopsy
Norwegian scabies - scabies in immunocomprosied, highly contagious, requires repeated treatment
What are the clinical features of louse? AKA Pediculosis Corporis
Eczematous eruption
No primary lesions
Secondary infection common
Seen in crowded conditions, poverty
Etiology: pediculosis humanus humanus
Transmit infections: trench fever and epidemic typhus
Louse: look in seams of clothing for louse and nits
What is the differential for scalp eruptions? (4)
- Tinea capitis
- Head lice
- Psoriasis
- Seborrheic dermatitis
How do you differentiate scalp eruptions?
- Pruritic? lice, nits or live louse confirm (nits adhere to hair shaft)
- Tinea? KOH and culture of scale and hair
- Well-marginated plaque erythematous = Psoriasis
- Yellowish scale = seborrheic dermatitis
What are te clinical features of Tinea capitis?
Infection of hair
Risk factors: contact with infected person, animal, fomites
Dx: Wood’s lamp exam: Microsporum display bright green fluorescence. KOH and cultures – scrape scale and some hairs
What is a tinea capitis infection outside the hair shaft called and how will it present?
Ectothrix - partial alopecia with broken hair shafts
Microsporum spp.
What is a tinea capitis infection within the hair shaft called and how will it present?
Endothrix
Black dot tinea capitis
hair breaks off near surface
Trichophyton spp.
How will Kerion tinea capitis present?
Inflammtory mass with boggy plaques
What are the clinical features of Pediculosis Capitis?
Scalp pruritis
Head lice and nits may be isible
Bite reactions - eczema, excoriation, lichenification
Pediculosis humanus capitisI
Transmitted via shared hats, brushes, head to head
What are the infectious / inflammatory causes of intertrigo (body folds)? (4)
- Tinea cruris
- Candida
- Erythrasma
- Inverse psoriasis
How do you differentiate causes of intertrigro? (4)
- Scaling edge, feet involvement = tinea
- Inflammatory with satellite pustules = candida
- no scale, psoriasis elsewhere, recurrent = inverse psoriasis
- brick red / coral red, fluorescence wit Wood’s light = erythrasma
What are the clinical features of Tinea Cruris?
Well marginated scaling red plaques with central clearing
Papules and pustules may be present at margins
Inguinal region and on thighs
T. rubrum, T. mentagrophytes
Risk factors: warm weather, obesity, tight clothing, topical steroid use, male, tinea pedis or tinea unguium
KOH show hyphae
What are the clinical features of Candida intertrigo?
Erythematous plaques with satellite papules and pustules
Found in moist environment
Risk factors: immunocompromised, topical steroid use, diabetic
Dx: Swab for gram stain and culture
What are the clinical features of Erythrasma?
Sharply marginated patch
Prediliction for folds – toe web spaces, groin, axillae, intergluteal, inframammary Etiology: Corynebacterium minutissimum Epidemiology: adults, humid weather, obesity, tight clothes Dx: coral red fluorescence on Wood’s light, bacterial culture positive for C. minutissimum, absence of fungi on KOH
What are the clinical manifestations of Staph aureus? (8)
- Impetigo
- Ecthyma (ulcerative pyoderma of the skin - deeper from of impetigo extending into dermis)
- Cellulitis
- Folliculitis
- Foruncles (boils)
- Carbuncles
- Abscesses
- Staphylococcal Scalded skin
What are the clinical features of cellulitis?
Skin infection extending into subcu. tissue
Painful firm area of erythema
Malaise, fever, chills may be present
May form bullae or undergo necrosis with epidermal sloughing
Common causes: Adults: Staph aureus, GAS, Children: Hib, Staph aureus, GAS
Ddx: DVT, stasis dermatitis, contact dermatitis, erysipelas
Risk factors: interdigital tinea, IVDU if arm, operative wound site
Diagnosis: clinical, wound cultures if exudative,
What are the clinical features of furuncles (boils)?
Follicular infection spreads and involves the tissue around the hair follicle
Firm erythematous nodule (early)
Fluctuant erythematous nodule (later)
Very tender/painful
Sites: face, neck, axilla, buttocks, perineum, thighs
Course: red, tender nodule points → ruptures
What are the clinical features of carbuncles?
Form as several furuncles connect subcutaneously
larger and deeper than furuncles
Sites: hair bearing skin, prefer back of the neck in males
Lesions drain through multiple sites to the skin surface
Diabetes predisposes to carbuncles
What are the clinical features of abscesses?
Form when furuncles/carbuncles not treated adequately
Subcutaneous tissue liquefies, forms granulomatous “pus pocket”
Signs: tender, swollen areas of reddened skin, hot and tender to touch
Can progress via hematogenous or lymphatic spread → ultimately seed other end organs
Sepsis, pneumonia, arthritis, osteomyelitis and endocarditis can subsequently develop
What are the clinical manifestations of HPV? (5)
- flat warts
- plantar warts
- verruca vulgaris
- periungal warts
- condylomata
What are the clinical features of flat warts?
Verruca plana
Sharply defined flat skin coloured or brown papules; 1-2 mm thick
Ddx: seborrheic keratoses, skin tags
Hard to treat
Spread by shaving
What are the clinical features of plantar warts?
Note multiple capillary loops – these distinguish warts from callus
Plantar warts are very common
Often acquired at swimming pool
Mosaic plantar warts
What are the clinical features of condylomata?
Perianal condylomata due to HPV
Transmission primarily sexual
Etiology HPV 6 & 11 > 16, 18, 31, 35
HPV types 16, 18, 31, 35 associated with carcinoma
HPV vaccine should decrease incidence of infection
Ddx condylomata lata of secondary syphilis, seborrheic keratoses, skin tags
Diagnosis is clinical, biopsy can differentiate if clinically difficult
What are the clinical manifestations of Tinea? (4)
- Tinea corporis
- Tinea capitis
- Tinea pedis
- Tinea unguium
What are the clinical features of Tinea Unguium?
Thick yellow dystrophic toenails or fingernails
Toenails more often involved
Genetic predisposition
Often associated tinea pedis
Etiology: T. rubrum most common
DDx: psoriasis, traumatic changes
Dx: scrape under toenail for KOH and culture
What are the clinical features of Tinea pedis?
Interdigital type: area has scaling, maceration and fissures. Often between 4th and 5th toes
Moccasin type: well marginated erythema with fine scale and hyperkeratosis Inflammatory or bullous type: vesicles filled with clear fluid Transmitted by walking barefoot on contaminated ground esp. swimming pool Etiology: Trichophyton, Microsporum, Epidermophyton Dx: hyphae on KOH, culture + for dermatophyte DDx: erythrasma, psoriasis, eczema
What lesion sites are common in psoriasis?
Extensor surfaces (elbows, knees)
Scalp, retroauricular, and ears
Palms and soles
Umbilicus
Glans Penis
Lumbar
Shins
Supragluteal
Nails - pitting, onycholysis
Describe guttate psoriasis.
acute extensive eruption of small psoriatic papules over trunk and proximal extremities; usually in association with group A streptococcal infections, and may recur with each reinfection

Describe inverse psoriasis
psoriasis occurring within flexural sites (i.e. axillae, groin, gluteal fold) will usually lack scale, and have a bright red, moist, macerated appearance

Describe pustular psoriasis.
can be generalized (von Zumbusch) or localized (usually to the palms or soles); generalized pustular psoriasis is associated with fever, leukocytosis and can be life-threatening

Describe erythrodermic psoriasis.
the entire body is affected and is red and scaly; prominent systemic complications

Describe the pathology of psoriasis.
- psoriasis is a chronic immunologic disease of the skin characterized by profound cutaneous inflammation and epidermal hyperproliferation
- in psoriasis, it takes 3-4 days for a keratinocyte to transit from the basal layer to the surface where it is shed
- key role for Th1 cells
What phenomenon is seen, and what disease is it associated with?

Koebner phenomenon
Psoriasis aggragavation by tattoo
Describe Psoriatic Arthritis
5-10% of patients with psoriasis will have psoriatic arthritis; seronegative (RF), association with HLA-B27
- asymmetric peripheral joint involvement (most common)
- symmetric peripheral joint involvement (resembles rheumatoid arthritis)
- axial disease (resembles ankylosing spondylitis)
- arthritis mutilans (uncommon)
What are some of the systemic complications of generalized pustular or erythrodermic psoriasis?
- fever, weight loss
- congestive heart failure (due to increased cutaneous blood flow)
- fluid/electrolyte imbalance
- hypoalbuminemia, low iron, hyperuricemia
What are the topical treatments used in psoriasis?
Glucocorticoids
Tars
Calcipotrial (Vit D derivative)
Anthralin
Taxarotene (retionoid, Vit A derivative)
Salicyclic acid
Calciurin inhibitor
What systemic therapy is used in psoriasis?
Methotrexate
Acitretin (oral retinoid)
Cyclosporine
Phototherapy (UVB or Psoralen UVA)
What is the intensely prurit inflammatory skin disorder Atopic dermatitis or “eczema” associated with?
Asthma, hayfever, allergic conjunctivitis
Describe the pathogensis of Atopic dermatitis “eczema”
- cutaneous inflammation mediated by Th2 cells (type 2 helper T cells producing Il-4 and IL-5)
- elevated serum levels of IgE
- impaired cutaneous barrier function (increased transepidermal water loss leads to dry skin)
- skin colonization and infection by Staphylococcus aureus (the toxins of which may serve as superantigens to promote cutaneous inflammation)
- diet factors rarely important
Descibe the clinical symptoms and basic morphology of Atopic dermatitis “eczema”
- pruritus is usually the most outstanding clinical feature
- depending on the acuity of the skin disease there can be:
- ill-defined erythema
- tiny coalescing edematous papules or papulovesicles
- excoriations
- crusting (if secondarily infected)
- xerosis (or dry, scaly skin)
- depending on the acuity of the skin disease there can be:
- lichenification

What are the 3 phases of atopic dermatitis “eczema” and what are their clinical features?
- Infantile
- facial, extensor distribution
- Childhood
- tendency to xerosis
- flexural distribution
- more lichenification and excoriations
- Adult
- improves with age, may remit
- may primarily affect hands
What is the treatment for atopic dermatitis “eczema”?
- Avoid irritating factors
- Aggressive restoration of the cutaneous permeability barrier with bland emollients and moisturizers
- Topical glucocorticoids (creams or ointments)
- Topical immunomodulators (tacrolimus, pimecrolimus)
- Topical or systemic anti-staphylococcal antibiotics
- Oral antihistamines
What is allergic contact dermatitis?
type IV hypersensitivity to an allergen in contact with the skin (e.g. nickel allergy, poison ivy)
What is irritant contact dermatitis?
contact of the skin with something that primarily causes direct local irritation
Describe the pathogenesis of Seborrheic Dermatitis
Involves sebum production and Pityrosporum fungus
(fungus is lipophilic yeast that thrives on lipids in sebum - scaling and inflammation may be due to host reponse to increased fungi on skin)
What are the clinical features of Seborrheic Dermatitis in adults
- Dandruff
- Ill-defined erythema
- Greasy-appearing scale
- Face distribution (glabella, eyelids, eybrows, nasolabial folds, nose, mustache/beard, ears)
- Trunk (presternal, umbilicus)
What are the clinical features of Seborrheic Dermatitis in infants?
What are the associated disorders with seborrheic dermatitis?
Parkinson’s disease (and other neurologic disorders) - due to immobility of facial muscles
HIV infection - get a more resistant disease
Name this greasy, scaly, erythematous lesion.

Seborrheic dermatitis
What is a mild, common, self-limited eruption, that may be due to herpesvirus?
Pityriasis rosea
Describe the clinical course of pityriasis rosea?
Evolves over 6-8 weeks, primarily in adolescents and young adults in spring and fall
- herald “Patch” - solitary 2-6cm scaly plaque
- eruption of multiple pauples with fine “collarette” scaling along rim of lesion
- “T shirt and shorts”distribution
- Pruritis variable
- Recurrance uncommon

What are the mimickers of Pityriasis rosea?
Secondary syphilis
Drug eruptions
What is te treatment of Seborrheic dermatitis?
What are the five clinical features of lichen planus?
- Papules (2-5mm)
- Pruritus (intense)
- Purple
- Polygonal
- Planer (flat-toppped)
- Also may sow scale-like fine white lines on surface (Wickham’s striae)

Where is the typical distribution of lichen planus lesions?
Flexor wrists and forearms, neck, thighs, shins, lumbar back, genitalia
Oral lesions common (with lacy white reticular lesions on buccal mucosa most common, may also become ulcerated)
What is Dr. Lui’s #1 Rule?
What are four common and distinctive drug reaction patterns?
- Urticaria
- Maculopapular / exanthematous / morbilliform (measles-like)
- Erythema multiform (target lesions, mucosal infolvement)
- Fixed drug eruption (localized plaques that recur at the same body site every time the patient is exposed to the offending systemic drug)

What are the Skin infections that cause Vesicular and Vesicobullous Eruptions?
- Herpes Simplex
- Varicella
- Herpes Zoster
- Impetigo
- Bullous insect bite reaction
- Primary skin bullous disorder (eg. pemphigus)
What are the clinical features of Herpes Simplex I and II
Grouped vesicles on an erythematous base
Most of adult population has been exposed
Virus can be shed without visible lesions
Persist in sensory ganglia leading to recurrent infections
Precipitated by UV, menses, fever, URTI, immunodeficiency
HSV-1 predominatly Labialis distribution
HSV-2 predominantly Urogenital distribution

What are the clinical features of Varicella?
“Dewdrop on rose petal” distribution
Initially papules, which become vesiscles, which crust over
Christmas tree distribution due to hematogenous spread
Test with viral culture, Tzanck smear, or skin biopsy
What are the clinical features of Herpes Zoster?
Prodrome of neuritic pain (days-weeks)
Acute vesicles then crusted papules
Unilateral dermatomal distribution
Grouped vesicles on erythematous base
Viral culture, Tzanck smear, or skin biopsy
What are the identical histological changes seen in herpes simplex, varicella, and zoster on skin biopsy?
Tzanck smear shows multinucleated keratinocytes or acantholytic keratinocytes

What are the clinical features of nonbullous impetigo?
- Scaling honey crusted lesions
- Group A Strep, or Staph aureus
- Supericial infection

What are the clinical features of bullous impetigo?
- vesicles and bullae
- clear or slightly yellow fluid
- shallow erosions form if bullae break
- caused by Staph aureus

What are the clinical features of arthropod bites?
Grouped papeuls or vesicles
Multiple, close together bites “breakfast, lunch, dinner”
Pruritic / urticarial, painful papules
causes: mites, ticks, spiders, centipedes, millipedes, mosquitoes, black flies, sand flies, bedbugs, ants, bees, wasps, hornets, fleas
What are the clinical features of bedbugs?
Erythematous papules, vesicles, nodules
Bugs are red-brown colour size of a ladybug
Nocturnal
Bites on body and head and neck area
What are the infectious causes of follicular eruptions?
- Pityrosporum folliculitis
- Pseudomonas folliculitis
- Staphylococcal follicultis
- Acne
How do you differentiate follicular eruptions?
- hot tub exposure
- distribution
- presence of comodones, pauples, nodules and cysts (acne)
- level of inflammation (pityrosporum has less)
- KOH and cultures
What are the clinical features of Pityrosporum folliculitis?
Monomorphous papules
Sweaty individual
KOH positive

What are the clinical features of Pseudomonas folliculitis?
Hot tub exposure
Other proximal individuals affected
Inlammatory follicular-based papules and pustules
Culture positive
Self-limited

What are the clinical features of staphylococcal folliculitis?
Inflammatory pustules
Gram stain and culture positive

What is the infectious and inflammatory differential for annular and scaling eruptions?
- Tinea corporis
- Tinea versicolour
- Secondary syphilis
- Psoriasis
- Nummular eczema
How do you diagnose a scaling eruption? (4)
- Scrape scaling edge for KOH and culture
- Distribution – psoriasis symmetrical and extensor surfaces
- Tinea versicolour non-inflammatory brown and white scaling patches
- Tinea corporis few lesions with central clearing
What are the clinical features of tinea corporis?
AKA ringworm
Annular scaling edge (ring-like)
Well demarcated plaque with central clearing
Single or multiple lesions
Assymetrical
Scrape edge for KOH and culture
Caused by Trichophyton rubrum and Microsporum canis

What are the clinical features of Tinea versicolor, aka “pityriasis versicolor”
Well marginated round scaling brown or light macules
Common in young adults
risk factors: warm and humid climate, oil skin, hyperhidrosis
Psoitive KOH
Microscopy - scale + “spaghetti and meatballs” spores and hyphae
Malassezia furfur or Pityrosporum versicolor

What are the clinical features of Secondary syphilis?
Widespread red-brown scaling papules
Involvement of palms and soles
2-6 months after primary infection
First eruption is macular, then papulosquamous, pustular, or acneiform
Condylomata lata - flat-topped papules in most areas (mouth and ano-genital)
Treponema pallidum
Dx with serology, or skin biopsy

What are the infectious causes of papular eruptions? (3)
- Verruca
- Molluscum contagiosum
- Insect bites
How do you differentiate papules?
- Central punctum + pearly apperance = molluscum
- Often surrounding eczema = molluscum
- Dull surface + capillary loops = verruca
- Minimally elevated = verruca plana
- Pruritic + grouped, also vesicular = insect bites
What are te clinical features of Verruca vulgaris?
Firm, hyperkartotitc papules with clefted surface and vegetations
Red or brown dots caused by thrombosed capillary loops
HPV
Skin to skin transmittion
Breaks in stratum corneum to facilitate epidermal infection
Risk factors: immunocompromise, meat handlers

What are the clinical features of Molluscum contagiosum?
Skin coloured umbilicated papules
Gentle pressure causes the central keratotic plug to extrude
Mollusca undergoing spontaneous regression may have an erthematous halo
Caused by a pox virus
Spread through skin to skin contact
Common in children and sexually active adults
Also seen in HIV

What are the infectious and inflammtory causes of eczematous and pruritic eruptions? (4)
Scabies
Louse infestation
Insect bites
Eczema
How do you differentiate pruritic eruptions? (4)
- Scabies = burrows or nodules
- Louse = no primary lesion
- Insect bites = grouped
- Atopic dermatitis = past history dry skin, hyper-linear palms, flexural dist.
What are the clinical features of scabies
Widespread eruption
Nocturnal prurities
Due to hypersensitivy to mite Sarcoptes scabiei (can take 6 weeks post-exposure to develop)
Burrows: Serpiginous track with spot at end, scrape for Dx
Nodules: Red-brown nodules in axillary area and groin
Dx - mite, eggs, feces on microscopy, biopsy
Norwegian scabies - scabies in immunocomprosied, highly contagious, requires repeated treatment

What are the clinical features of louse? AKA Pediculosis Corporis
Eczematous eruption
No primary lesions
Secondary infection common
Seen in crowded conditions, poverty
Etiology: pediculosis humanus humanus
Transmit infections: trench fever and epidemic typhus
Louse: look in seams of clothing for louse and nits

What is the differential for scalp eruptions? (4)
- Tinea capitis
- Head lice
- Psoriasis
- Seborrheic dermatitis
How do you differentiate scalp eruptions?
- Pruritic? lice, nits or live louse confirm (nits adhere to hair shaft)
- Tinea? KOH and culture of scale and hair
- Well-marginated plaque erythematous = Psoriasis
- Yellowish scale = seborrheic dermatitis
What are te clinical features of Tinea capitis?
Infection of hair
Risk factors: contact with infected person, animal, fomites
Dx: Wood’s lamp exam: Microsporum display bright green fluorescence. KOH and cultures – scrape scale and some hairs

What is a tinea capitis infection outside the hair shaft called and how will it present?
Ectothrix - partial alopecia with broken hair shafts
Microsporum spp.
What is a tinea capitis infection within the hair shaft called and how will it present?
Endothrix
Black dot tinea capitis
hair breaks off near surface
Trichophyton spp.
How will Kerion tinea capitis present?
Inflammtory mass with boggy plaques
What are the clinical features of Pediculosis Capitis?
Scalp pruritis
Head lice and nits may be isible
Bite reactions - eczema, excoriation, lichenification
Pediculosis humanus capitisI
Transmitted via shared hats, brushes, head to head

What are the infectious / inflammatory causes of intertrigo (body folds)? (4)
- Tinea cruris
- Candida
- Erythrasma
- Inverse psoriasis
How do you differentiate causes of intertrigro? (4)
- Scaling edge, feet involvement = tinea
- Inflammatory with satellite pustules = candida
- no scale, psoriasis elsewhere, recurrent = inverse psoriasis
- brick red / coral red, fluorescence wit Wood’s light = erythrasma
What are the clinical features of Tinea Cruris?
Well marginated scaling red plaques with central clearing
Papules and pustules may be present at margins
Inguinal region and on thighs
T. rubrum, T. mentagrophytes
Risk factors: warm weather, obesity, tight clothing, topical steroid use, male, tinea pedis or tinea unguium
KOH show hyphae

What are the clinical features of Candida intertrigo?
Erythematous plaques with satellite papules and pustules
Found in moist environment
Risk factors: immunocompromised, topical steroid use, diabetic
Dx: Swab for gram stain and culture

What are the clinical features of Erythrasma?
Sharply marginated patch
Prediliction for folds – toe web spaces, groin, axillae, intergluteal, inframammary
Etiology: Corynebacterium minutissimum
Epidemiology: adults, humid weather, obesity, tight clothes
Dx: coral red fluorescence on Wood’s light, bacterial culture positive for C. minutissimum, absence of fungi on KOH

What are the clinical manifestations of Staph aureus? (8)
- Impetigo
- Ecthyma (ulcerative pyoderma of the skin - deeper from of impetigo extending into dermis)
- Cellulitis
- Folliculitis
- Foruncles (boils)
- Carbuncles
- Abscesses
- Staphylococcal Scalded skin
What are the clinical features of cellulitis?
Skin infection extending into subcu. tissue
Painful firm area of erythema
Malaise, fever, chills may be present
May form bullae or undergo necrosis with epidermal sloughing
Common causes: Adults: Staph aureus, GAS, Children: Hib, Staph aureus, GAS
Ddx: DVT, stasis dermatitis, contact dermatitis, erysipelas
Risk factors: interdigital tinea, IVDU if arm, operative wound site
Diagnosis: clinical, wound cultures if exudative,

What are the clinical features of furuncles (boils)?
Follicular infection spreads and involves the tissue around the hair follicle
Firm erythematous nodule (early)
Fluctuant erythematous nodule (later)
Very tender/painful
Sites: face, neck, axilla, buttocks, perineum, thighs
Course: red, tender nodule points → ruptures

What are the clinical features of carbuncles?
Form as several furuncles connect subcutaneously
larger and deeper than furuncles
Sites: hair bearing skin, prefer back of the neck in males
Lesions drain through multiple sites to the skin surface
Diabetes predisposes to carbuncles

What are the clinical features of abscesses?
Form when furuncles/carbuncles not treated adequately
Subcutaneous tissue liquefies, forms granulomatous “pus pocket”
Signs: tender, swollen areas of reddened skin, hot and tender to touch
Can progress via hematogenous or lymphatic spread → ultimately seed other end organs
Sepsis, pneumonia, arthritis, osteomyelitis and endocarditis can subsequently develop

What are the clinical manifestations of HPV? (5)
- flat warts
- plantar warts
- verruca vulgaris
- periungal warts
- condylomata
What are the clinical features of flat warts?
Verruca plana
Sharply defined flat skin coloured or brown papules; 1-2 mm thick
Ddx: seborrheic keratoses, skin tags
Hard to treat
Spread by shaving

What are the clinical features of plantar warts?
Note multiple capillary loops – these distinguish warts from callus
Plantar warts are very common
Often acquired at swimming pool
Mosaic plantar warts

What are the clinical features of condylomata?
Perianal condylomata due to HPV
Transmission primarily sexual
Etiology HPV 6 & 11 > 16, 18, 31, 35
HPV types 16, 18, 31, 35 associated with carcinoma
HPV vaccine should decrease incidence of infection
Ddx condylomata lata of secondary syphilis, seborrheic keratoses, skin tags
Diagnosis is clinical, biopsy can differentiate if clinically difficult

What are the clinical manifestations of Tinea? (4)
- Tinea corporis
- Tinea capitis
- Tinea pedis
- Tinea unguium
What are the clinical features of Tinea Unguium?
Thick yellow dystrophic toenails or fingernails
Toenails more often involved
Genetic predisposition
Often associated tinea pedis
Etiology: T. rubrum most common
DDx: psoriasis, traumatic changes
Dx: scrape under toenail for KOH and culture

What are the clinical features of Tinea pedis?
Interdigital type: area has scaling, maceration and fissures. Often between 4th and 5th toes
Moccasin type: well marginated erythema with fine scale and hyperkeratosis
Inflammatory or bullous type: vesicles filled with clear fluid
Transmitted by walking barefoot on contaminated ground esp. swimming pool
Etiology: Trichophyton, Microsporum, Epidermophyton
Dx: hyphae on KOH, culture + for dermatophyte
DDx: erythrasma, psoriasis, eczema

What is the following definition referring to?
Chronic inflammatory conditions involving the pilosebacious units of the skin
Acneiform disorder
What are the three types of pilosebacious units and what kind of hair are they associated with?
- Terminal follicles
- Long hairs (scalp)
- Vellus follicles
- Miniature hairs (arm)
- Sebaceous follicoles
- No visible hair (most on face)
What is the main type of follicle involved in acneiform disorders?
Sebaceous
How is sebum produced by sebaceous glands?
Holocrine secretion - glandular cells degenerate and become secreted material
What is the composition of sebum?
Triglyceride, cholesterol and cholesterol esters, wax esters and squalene.
Minor Ig A secretion role.
What is the physiological function of sebum in humans?
No known function.
Possibly - hydration, antimicrobial, anti-oxidant
What are the regulators of sebum production?
Androgens - increase production (peak levels at puberty)
Retinoids - inhibit sebum production, trigger sebocyte apoptosis
What is the key definitive characteristic of acne vulgaris?
Presence of comodones
Define comodone
Engorged follicular ostium - plugged hair follicles - by dead keratinocytes and sebum
What are the four features of pathogenesis of Acne Vulgaris?
- Abnormal follicular keratinization
- “Over production” of sebum
- Over-growth of follicular bacterium, specifically Proprionibacterium acnes
- Inflammation
List some common misconceptions about acne pathogenesis.
“Acne is worsened by chocolate and fatty foods.”
“Acne is caused by dirt and can be washed away.”
“Acne is due to poor hygiene.”
“Acne does not usually require treatment”
“Acne is caused by stress.”
What are some proven acne exacerbaters (Hormonal, Meds, Hygiene, Diet)?
Hormonal - prementsrual flare, exogenous, endogenous excess syndromes
Medications - lithium, barbiturates, corticosteroids, environmental toxins
Hygiene - digital pressure, excessive cleaning, oily cosmetics, mechanical friction
Diet - excessive milk consumption
Describe primary and secondary lesions of acne.
Primary
closed comodones (white heads) and open comodones (black heads) develop into inflammatory lesions
- papules
- pustules
- cysts
- nodules
Secondary
- Scars
- Post-inflammatory hyperpigmentation
Define mild acne (for management purposes)
Mostly comedones
Few inflammatory lesions
No scars
Define moderate acne (for management purposes)
Comedones
Numerous papules and pustles
Some scarring
No cysts or nodules
Define severe acne (for management purposes)
Presence of cysts or nodules
Or
Papulo-pustular acne with significant scarring
Describe the four treatment approaches to mild acne
- Hygienic advice:
- gentle cleansing BID
- avoid comedogenic face products,
- salicylic acid and/or benzoyl peroxide based skin wash
- Treating comedones
- topical retinoic acid creams or gels
- surgical extraction
- Reducing sebum production
- topical retinoic acids
- Decrease bacterial overgrowth
- topical antibiotics
- topical benzoyl peroxide
- Topical azelaic acid
Describe the six management approaches to moderate acne.
- Gentle skin cleansing (as per mild)
- Topical
- antibiotics and anti-inflamm.
- Systemic antibiotics
- Tetracyclines
- Avoid erythromycin, clindamycin
- Systemic hormonal therapies
- low dose estrogen plus
- antiandrogen or 3rd gen. progestins
- Systemic isotretinoin (Acutane)
- Intra-lesional steroid injection (watch for dermal atrophy)
Describe the three management approaches to severe acne.
- Limited role for topical
- Systemic anti-inflamm. antibiotics (tetracyclines)
- Systemic isotretinoin - most effective
What is the MOA of Isotretinoin (acutane)
Inibits sebum production
causes sebaceous gland atrophy
What are the transient side effects of Isotretinoin?
Teratogen
Depressive symptoms (controversial)
Dry skin
Decreased night vision
Arthralgia
Hyper-triglyceridemia
Elevated LFTs
Photosensitivy
Alopecia
What are the considerations to starting systemic isotretinoin?
Informed consent
Contraceptive
Lab monitoring of ALT, fasting trigs, b-HCG
Stop tetracycline
Lipophilic - take with biggest meal
Manage xerosis, cheilitis
What is the MOA of topical retinoic acids?
Comedolytic by improving desquamation of dead keratinocytes
Onset slow, therefore longterm
Can cause irritation and skin peeling
What is the following definition referring to?
A cutaneous vascular and inflammatory disorder characterized by chronic facial flushing and erythema
Rosacea
What are the epidemiologic trends of Rosacea?
More common in Caucasions than blacks and asians
More common in women
While the pathogenesis is largely unknown, give some hypothetical factors.
- genetic predisposition
- microvascular dilatation
- demodex flooculorum mites
- UV light
- Temp. shifts
- topical steroids
- alcohol
What is the pathology of Rosacea?
Dilated capillaries
perifollicular inflammation
What are the 5 clinical classifications of Rosacea?
- pre-rosacea
- subtype 1 - erythematotelangiectatic
- subtype 2 - papulopustular
- subtype 3 - phymatous
- subtype 4 - ocular
What are the clinical features of Pre-rosacea?
“Blusher and flusher”
Transient erythema
most do not progress to clinical rosacea
What are the clinical features of subtype 1 erythematotelangiectatic rosacea
Dilated capillaries
fixed facial erythema
What are the five clinical features of subtype 2 papulo-pustular rosacea
- central facial erythema
- pustules
- papules
- fixed edema
- no comedones
What is the clinical feature of phymatous rosacea
Hypertrophic changes of protuding structures
Nose - rhinophyma
Chin - gnathophyma
Eyelids - blepharophyma
Ears - otophyma
Forehead - metophyma
What are the six clinical features of Ocular Rosacea?
- foreign body sensation
- burning or stinging, drynes, itching
- photophobia
- conjunctival telangiectasias
- periocular erythema
- possible keratitis and blindness
What are the treatment principles for Pre-rosacea
No effective Tx
Avoid triggers (sun protection, cold compresses)
What are the treatment principles for Erythematotelangectatic Rosacea
Erythema - no effective therapy, oral tetracyclines (mild to moderate), laser or intense pulsed light (moderate)
Telangectasia - vascular laser surgery, or intense pulse light
What is the MOA of vascular laser and other light devices in Rosacea treatment?
Obliterates uperficial blood vessels
What are the treatment principles for papulo-pustular rosacea
Topical therapies (anti-inflammatory?)
- metronidazole
- azelaic acid
Oral therapies (suppressive)
- tetracyclines
- isotretinoin (lower dose)
What are the treatment principles for phymatous rosacea?
- Oral tetracyclines
- Oral isotretinoin
- Surgical reconstruction
- CO2 laser
- Electric surgery
- Reconstructive plastic surgery
What are the treatment principles for Ocular Rosacea?
Topical steroid solutions
Oral tetracyclines
What are the three childhood acne variants?
- Nonatal - resolve spontaneously
- Infantile - resolve spontaneously
- Early onset acne vulgaris - may be associated with precocious puberty, treat acne
What do these three highly inflammatory, nodular-cystic, interconnecting tract forming, scarring variants represent?
- Acne conglobata
- Dissecting cellulitis of the scalp
- Hidradenitis suppurativa (axillae, groin, perianal)
Follicular Occlusion Triad
What are the treatment principles for Follicular Occlusion Triad?
Systemic antibiotics
Systemic isotretinoin
Surgical debridement / drainage
What are the clinical features of Acne Fulminans
Acute febrile ulcerative acne
Young males
Sudden onset of papules, pustules on chest, back, and shoulders
Feber, arthralgias, anorexia, leukocytosis, focal lytic bone lesions
Treat with systemic isotretinoin
What are the clinical features of Acne excoriee
Mild background acne
Self-inflicted excoriations
Therapy - supportive to stop excoriation
What are the clinical features of Rosacea Conglobata
Similar to acne conglobata - except adult women
treat with systemic isotretinoin and prednisone
What are the clinical features of steroid rosacea
Inflammatory papules and erythema associated with burning sensation following steroid use
Stop steroid
Treat with systemic tetracyclines
What are the clinical features of Perioral dermatitis?
Typically females of childbearing age
Red papulopustules, no telangiectasia, no vasomotor flushing
Invovles nasolabial folds, perioral, periocular
Treat wit systemic tetracyclines