Derm I, II, III Flashcards
What 4 cells compose the epidermis?
which is the main cell, describe its development and what could occur if there was a problem with proper development
What are the layers of the epidermins?
- major differences between thin and thick skin*
- describe appearance of the major layers*
CELLS:
1. Keratinocytes (mainly) - matures through a process of desquamatization where they rise vertically from the basal layer (undifferentiated) to the cornified layer (fully differentiated) over 25 days. shorter periods of maturation seen during imflammatory conditions; keratin production also changes as the cell matures. Disordred maturation causes skin thickening due to lack of desquamation.
2. Melanocytes
3. Langerhan’s cells
4. Merkel cells
LAYERS: outer to innermost
Stratum Corneum - extra thick in thick skin; basket weave look
Stratum lucidum - only found on thick skin (palms and soles of feet), thin and bright
Stratum Granulosum -
Stratum Spinosum - thickest layer
Stratum Basale - containing rete ridges, increasing surface area of connection between the epidermis and dermis; basal layer, lower most layer connecting epidermis to dermins via hemidesmesomes
–Cancel Lab Get Some Beer–
Define:
Hyperkeratosis
Thickening of stratum CORNEUM
Define:
Parakeratosis
flattened, keratinocyte nuclei within the stratum corneum, where nuclei are not normally present
= when the keratinocytes retain their nuclei in the S. Corneum
Define:
Orthokeratosis
Hyperkeratosisi of ANUCLEAR keratinocytes within the stratum corneum
so its hyperkeratosis WITHOUTH parakeratosis
Define:
Acanthosis
Thickened STRATUM SPINOSUM
Define:
Acatholysis
Loss of cohesion btw keratinocytes d/t dissolution of intercellular connections.
Keratinocytes separate and round up (versus in spongiosis, where keratinocyets strech and elongate)
Define:
Dyskeratosis
Abnormally or prematurely cornified (keratinized) keratinocytes in the epidermis that stain pink on H&E
Define:
Spongiosis
Intercellular edema btw keratinocytes
Edema may cause keratinocytes to become elongated and stretched, hallmark eczema
Define:
Papillomatosis
Irregular undulation of epidermal surface
What is…
Dermal atrophy?
Decreased thickness of the DERMIS
What is…
Edema?
Accumulation of interstitial fluid
(edema may cause keratinocytes to become elongated and stretched, hallamrk of eczema / interceullular edema btw keratinocytes = spongiosis)
What is…
Solar elastosis?
Accumulation of basophilic (grey/blue) material in the UPPER DERMIS d/t SUN DAMAGE
What is…
Hyalinization?
Accumulation of dense, eosinophilic (stains pink/red) aceullar material
What is…
Sclerosis
Hyalinzed collagen with decreased fibroblasts
What is…
mucin?
DERMAL mucin contains ACID MUCOPOLYSACCHARIDE and stains PALE BLUE, smudgey, threadlike or granular on H%E
What is…
a wheal?
Transiet papule/plaque
What is…
papule ?
elevated skin lesion < 1 cm
What is…
Macule?
Flat discoloration < 1 cm
What is…
a patch?
Macule > 1 cm
What is a plaque?
papule > 1cm
What is excoriation?
Small superficial defect involving the EPIDERMIS and PAPILLARY DERMIS
Results from localized trauma like picker or scratching
What is an ulcer?
loss of EPIDERMID and DERMIS (and sometimes deeper tissue)
What is Icaythosis?
How is it diagnosed?
How is it aquired?
What are the different types (4)
Disorder of Desquamatization
Defective desquamatization that leads to a build up of COMPACTED SCALE –
Mostly hereditary disorders that appear at birth
DX: clinical presentation
Types:
Icathyosis vulgaris - autosomal dominant or acquired, DRY, scaly skin; often described as fish scales; defect in the FLG gene, which synthesizes the microfilament filaggrin. More prominent during winter and TX - heavy duty moisturizers, usually creams and oinments over lotions. NOT in a baby (could be acquired). Orthokeratosis (thickening of the cornified layer) with loss of granular layer (hyperkeratosis withouth parakeratosis)
Lamellar ichathyosis: Autosomal recessive. presents with severe, thick plates of scale that almost resemble reptile scales and PRESENT AT BIRTH. Mostly @ hands, soles and flexures. associated with a mutation in keratinocyte transglutaminase
X-linked Icathyosis: more brownish and scaly eruptions in MALES, usually early in childhood. flexural creases usually involved. Associated with deficiency in STS gene which makes steroid sulfatase
Congenital Icathyosiform Erythroderma: autosomal recessive
LXVC - icathyosis types
What are the 4 BENIGN/Nonmalignant Epithelial/epidermal Neoplasms?
Seborrheic keratosis
Acanthosis nigricans
Fibroepithelial Polyp/ achrocordon / skin tag
Epidermal inclusions cysts/ Wen
Seborrheic Keratosis (SK)
Where are they located/ where are they NOT seen?
General population you can see SK in?
Histologically what can be seen?
Any important associations?
epidermal papillomatosis, acathosis and horn cyst formation
“stuck- on” waxy appearaning brown papules or plaques
anywhere on the skin EXCEPT PALMS and SOLES
Generally patients > 30 y/o growth of aging; seldom in young pts
Histo: hyperkeratosis, epidermal acanthosis (thickening of S. spinosis), composed of uniform small keratinocytes with a FLAT BASE “string sign” and keratin filled “horn cells” – frequent melanin pigment present
*string sign lets us know its benign*
Leser-Trelat Sign- multiple (hundreds) may be seen as part of a paraneopastic syndrome in patients with metastatic cancer
Acanthosis Nigricans:
How coudl you tell SK from AN?
Patient population?
Associations?
Clinically presents as a velvety, papillomatous, hyperpigmented plaques
Common on the back of the neck or axilla
Could be seen in all age pateints
Histo: lots of papillomatosis, hyperkeratosis, NO acanthosis, NO horn cyst (in comaprision to SK)
Associated with insulin resistance and malignancy
Compare and contrast SK and AN.
Clinical appearance
Age onset
Histo
Associations
SK: Roudish, flat, coin-like waxy plaques with velvety surface. Appears everywhere except palms and soles. Usually seen in middle age people and above - aging. Histologically, acathotic hyperkeratosis, horn cysts, increased melanin. Associated with leser-trelat sign, paraneoplastic syndrome / malignancy
AN: Velvety patches that could be seen everywhere but most prominent on the back of the neck and axilla. See in any age. Histologically - epidermal papillomatosis, with increased melanin but NO acanthosis and NO horn cells. Associated with obesity, endocrine issue or hereditary in children and bening. In middle age and above, could be malignant
Fibroepithelial Polyp?
what is the common name for fibroepithelial polyp?
where are they usually seen?
What are they composed of?
Skin tag or acrochordon
BENIGN polypoid growths most common at sites of RUBBING/FRICTION
Composed of fibroblasts and collagen with vessels covered with normal or acanthotic epidermis
Inside the polp - adipose tissue and vessels creating the pulp
Epidermal inclusion Cysts / Wen:
What’s the misnomer associated with Wen?
NOT an epidermal neoplasm
Follicular cysts composed of hte infundibular portion of the hair follicle which is similar to epidermis, with the exception of a LOSS of RETE PEGS.
Makes keratin (like epidermis) and thus appears as a kertain filled cystic structure lined by epidermis.
Most do NOT communicate with the epidermis and are therefore DERMAL based nodules
What are Pre-Malignant and Malignat Epidermal Neoplasms (3)
Actinic Keratosis (AK)
Squamous Cell Carcinoma (SCC)
Basal Cell Carcinoma (BCC)
Actinic Keratosis:
Clinical presenation:
Typical patient:
What causes AKs?
Histo:
Tx?
Actinic Keratosis:
- Clinical presenation:*scaly erythematous papule/plaque located on sun-damaged skin; poorly demarcated, and esp located on face, balding scalp, posterior neck and dorsal upper extremity. Feel rough and “gritty” and may be difficult to see
- Typical patient:* increasingly common with age, esp with sun-damaged skin
What causes AKs? UV radiation but ionizing radiation, arsenic or polycyclic hydrocarbon exposure could also cause them
PRECURSOR OF SCC, third most comon dermatological dx
Histo: basal layer ATYPIA with overlying parakeratosis alternating with orthoparakeratosis = FLAG SIGN (alternating pink/blue), SOLAR elastosis
Tx? Cryotherapy or topical chemotherapeutics to prevent progression to SCC
Squamous Cell Carcinoma:
Clinical Presentation-
Population commonly presenting with SCC-
Microscopic Presenation-
Causes-
Clinical Pres: Generally erythematous, scaly papules / plaques with ill-defined borders (may be confused with AKs)
Population: sun-exposed sites (head and neck) region of older individuals, esp MALES. Hyperkeratosis, ulceration or crustin gmay be found on its surface, and sx such as itching, pain and bleeding may also be seen
Microscopic Pres: SCC show proliferation of pleomorphic keratinocytes confied to the epidermis (SCC in situ) or extending into the dermis (invasive)
Causes- AK is a precursor of SCC although it can develop de novo. Most common cause is exposure to UV light with TP53 mutations, often see at pyrimidine dimers (=driving force behind SCC via two hit hypothesis). Xeroderma pigmentosum, extra susceptible. Activating mutations n HRAS, loss of function mutations in Notch receptors, immunosupression (specifically HPV 5 and 8), industrial, chronic wounds, burn scars, arsenic, ionizing radiation
Histology of SCC:
Islands of atypical squamous cells (pinkish)/atypical keratinocytes extending from epidermins into the dermins (if invading) with an uneven base
Individual cells have a glassy eosinophlic cytoplasm, with large nuclei. MItotic figures and kertain pearls are also seen (with retained nucelus
Normal spinous layer is increased
various degrees of differentiation could be seen; increasing malignancy show less demarcation btw the tumor masses and teh stroma, greater atypia, less keratinization and loss of intraceullar bridges
other histologic variants include acatholytic, adenosquamous, spindle cell, verrucous and desmoplastic SCC
What is bowen’s disease?
Histology:
Clinical presentation:
Tx:
SCC in situ – confied to the epidermis (NO invasion to dermis)
Histology: full thickness atypia, basal layer sparing (EYELINER SIGN), may show skip areas but involved follicles (in contrast to AKs), NO invasion into the dermis (in contrast to SCC) - no blebbing – no atyoical signs in the lower levesl; otherwise, atypical full thickness, disorganization across layers
Clincally a plaque like lesion
Won’t regress, needs to be excised
Bowenoid Papulosis?
Histological features?
Causes?
Tx?
SCC IN SITU
Similar histological appearance as bowen’s disease
HPV induced, located on the genitals!
esp HPV 5 and 8
Frequently multiple papules
May spontaneous regress or progress
Major difference is that this is HPV driven and CAN REGRESS
Basal Cell Carcinoma:
Appearance:
Risk Factors:
Epidemilogy
Appearance: Pearly, pink papule with overlying telangiectasia
Risk Factors: older individuals at sun exposed sites, fair skin, men (2:1), family history of skin cancer, immunsuppressed, radiation therapy, genetic syndromes - DNA mismatch repair sydromes (xeroderma pigmentosa, nevoid BCC syndrome)
PTCH gene mutations - 30%, regulates the hedgehog pathway, could be genetically acquired (Gorlin Syndrome)
P53 mutations 40-60%
Epidemiology: Most COMMON invasive cancer in humans
Gorlin Syndrome
Genetic inhertance:
Feature:
Associations (3):
Affected gene and mode of transmisison
Nevoid Basal Cell Carcinoma
Autosomal Dominant
Multiple BCC before the age of 20
accompanied by medulloblastomas, meningioma, ovarian fibromas, odontogenic keratocyts, skeletal defects (macrocephaly, hypertelorism, frontalparieta bossing, spina bifida or rib abnormality…)
PTCH gene on chromosome 9q22.3
“2 hit” hypothesis
Histology of BCC:
Comes from the basal layer
Blue tumor
peripheral palisading“picket fence”
Retraction artifact (due to how the neoplasm separates from the rest of the layers)
Nodular type - islands of basaloid cells in the dermis
Treatment of SCC (4)
Only 5% are malignant; most are excised
1) excision for low risk SCC (less than 2 cm in diameter, well differentiated)
2) Mohs micographic surgery
3) Radiation therapy (in combi with other modalities for aggressive, recurrent or large inoperable tumors)
4) Cryotherapy (for small, superficial or low-risk lesions)
What are Melanocytic Neoplasms (3)
Lentigos
Melanocytic Nevi
Melanoma
[True/False] Melanocytes are brown with melanin?
Where are they derived from? What is their function
FALSE!
Melanocytes are clearish cells in the BASAL layer with dark nuclei
@ a ratio of 1:10
Derived from neuroectoderm
Fxn: make melanin pigment using enz tyrosinase
They are smaller hyperchromatic with clearish cells - they don’t hold their pigment but pass it to their neighbor, agulated nuclei on the basal layer
- Dark skin indviduals don’t have more melanocytes but rather the melanocytes are just more active thus make more melanin.*
- Albinism is a disease in which melanocytes are unable to produce melainin because they lake the enzyme tyrosinase and thus have very high rates of skin cancer (don’t have melanin to protect from the UV radiation)*
What are benign proliferations of melanocytes?
Lentigos and nevi
Lentigo = small, oval tan-brown, located in mucous membranes at any age; flat lesion
melanocytic hyperplasia along basal layer (difficult to appreciate)
Two types: solar lentigines (liver spots, age spots) and simple lentigines
Melanocytic Nevi: tan to bronw macules and papules.
Common type: junctional (epidermal), compound (both epi and derma), and intradermal (dermal) - nests of melanocytes
Dysplastic Nevi: single and cytologically atypical melanocyte, in addition to nests with architectural atypia
What are malignant transformation of melanocytes?
Melanoma
