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Pathological genetics > Tumor Epithelium lecture 19 > Flashcards

Tumor Epithelium lecture 19 Flashcards

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1
Q

Normal histology and function of the skin

A
  • Protective barrier ( Fluid loss, mechanical injury, and micro-organisms )
  • Sensation: Touch, temperature, pressure, and pain
  • Termoregilation
  • Control evaporation
  • Storage : lipids and water
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2
Q

Classification of skin layers

A

Upper surface: Epidermis (contains squamous cells and melanocytes)
Middle layer: Dermis (Contains blood vessels hair follicles and nerves, it is the connective tissue )
Lower layer: Hypodermis (contains nerves and larger blood vessels )

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3
Q

Discuss the squamous papilloma

A
  • Common benign cutaneous lesions

* The most common is a viral wart

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4
Q

Discuss the histology of squamous papilloma

A
  • Hyperkeratosis
  • papollomatosis
  • Acanthosis( think)
  • elongated rete ridges
  • koilocytosis
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5
Q

Discuss the histology of squamous papilloma

> Squamous Tumors

A
  • Hyperkeratosis
  • papollomatosis
  • Acanthosis( think)
  • elongated rete ridges
  • koilocytosis
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6
Q

Discuss the solar (actinic keratosis)

> ST

A

*It is due to chronic exposure to the sun
*More common in light-skinned individuals
*

Clinically you will see hyperkeratosis, tan/brown lesions and may form cutaneous horns

*may regress, remain unstable, or undergo malignant transformation

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7
Q

Discuss the histology of solar (Actinic ) keratosis

ST

A
  • Defining features (epidermal dysplasia (mild, moderate/severe)
  • Hyperkeratosis, parakeratosis, and solar elastosis (sun damage )
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8
Q

Discuss Bowen’s disease and its sites

A

> Carcinoma in-situ
Full-thickness epidermal dysplasia
HPV implicated

> Sites

  • skin: Bowen’s disease
  • Vulval intraepithelial neoplasm
  • Glans: Erythroplasia of queyrat
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9
Q

Discuss the squamous cell carcinoma Aetiology

A

> Commonly secondary to basal cell carcinoma
Often arises from pre-existing dysplasia eg solar keratosis but can arise de novo

1.Chronic sun exposure( most important) 
2Chronic ulceration (marjolin's ulcers) or scarring 
3.ionising radiation 
4.albinism ,xeroderma pigmentatosum 
5. chemicals  arsenic ,tar
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10
Q

What are the clinical manifestations of squamous cell carcinoma

A

> Raised, rolled, everted edges
often central ulcerations
Usually locally aggressive
and cured by excision

Recurrence :

  • twice as the frequency of BCC
  • Risk factor for recurrence include incompletion and aggressive histological patterns
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11
Q

Discuss the metastasis of the SCC

A
  • uncommon
  • deoendent on clinical setting :0,5%in sun-damaged skin vs % in marjolins ulcer
  • Usually to regional lymphoma nodes
  • pulmonary metastasis is uncommon
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12
Q

Discuss the histology of SCC

A
  • Invasion beyond the basement membrane into underlying dermis
  • Comprises nest of malignant squamous cells
  • Intercellular bridges ,abundant eosinophilic cytoplasm
  • keratin formation
  • mitotic activity
  • may have dysplasia of the overlying epidermis with or without ulceration
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13
Q

discuss the Seborrhoeic keratosis (AKA seborrhoeic wart / basal cell papilloma )

A

*It is common among middle-aged individuals
*Benign
*Arises spontaneously in the trunk, extremities, head, and neck
*Round, flat, dark plaques with a velvety granular surface
*has a stuck-on appearance
*

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14
Q

Discuss the seborrhoeic keratosis histology

A
  • Exophytic and sharply demarcated
  • Basaloid cells: small with dark nuclei and scanty cytoplasm
  • Variable melanin pigmentation
  • Exuberant keratin production
  • Horn cysts
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15
Q

Discuss the BCC

A
  • Due to UV exposure
  • most common malignant tumor
  • Usually elderly caucasian patients (in more sunny areas ,patients are often younger )
  • Mainly on the face and it cured by adequate excision
  • Locally aggressive but almost never metastasis
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16
Q

t/f: BCC are common malignant tumors

A

true

17
Q

BCC clinical presentation

A
  • nodule

* ulcer (rodent ulcer )

18
Q

Tumors of melanocytes classification

A

> Benign

  • melanocytic naevus
  • Blue naevus

> Pre-malignant
*Dysplastic naevus

> Malignant
*Melanoma

19
Q

Discuss the melanocytic naevi

A

> Benign
Commonly referred to as moles
Nests of bland melanocytes
Usually acquired but some are congenital
*Malignant transformation is rare eg giant congenital melanocytic naevus

20
Q

What are the 3 types of reflect progression monocytic naevi

A
  • Junctional
  • Compound
  • intradermal
21
Q

Dysplastic Naevi

A
  • Sporadic or familial
  • Larger and more irregular than benign naevi
  • The neoplastic melanocytes are larger and more atypical
  • May have fusion of the rete ridges or spindled melanocytes

*Significance : whilte americans : 0,6% lifetime risk of melanocyte and increases10 10% if dysplastic naevi are present

22
Q

Discuss melanoma

A
  • Malignant tumours of melanocytes
  • Currently no effective chemotherapy
  • Incidence is increasing
  • *Rare in children except for giant congenital naevus
23
Q

True or false: Melanoma only occur in cutaneous sites

A

*May arise in non-false; cutaneous sites eg eyes,

anus, meninges, and mouth

24
Q

What are the predisposing factors to melanoma

A
  • UV light / radiation
  • Albinism
  • Xeroderma pigmentosum
  • Dysplastic naevus syndrom
  • Gaint congenital naevus

> More common in light-skinned people (especially red hair and freckles )

> common sites : lower leg in females and trunk and back in males

> Rare in dark-skinned races except in acral sites eg palms and soles

25
Q

Melanoma clinical clues

ABCDEUS

A
  • Asymmetry
  • Border irregularities
  • Colour variegation
  • Diameter >6mm
  • Evolving lesion
  • Ulceration
  • Satelites lesions
26
Q

List 4 types of melanoma

A

> Lentigo maligna melanoma
*older men and face ,indolent

> Sperficial spreading melanoma
*Most common due to sun-exposed skin

> Acral lentiginous melanoma
*Common in black patients on their palms ,hands and soles and it is not related to sun exposure

> Nodular melanoma
*Vertical growth

27
Q

List the growth phases of the melanomas

A

> Lentigo maligna superficial spreading and acral lentiginous: Radial growth phase that is horizontal growth within the dremin and lacks the capacity to metastasis and amicable to curative excision

> Nodular melanoma: Vertical growth phase with dermal invasion and exponential risk of metastasis with depth

28
Q

What is the prognosis of melanoma

A

> Correlates with depth

  • Breslow’s tumor thickness
  • Clark’s level of tumor invasion

> Others :

  • Ulceration
  • Mitoses
  • Necrosis

> Spread via lymphatics and blood stream which contributes to prognosis

29
Q

t/f: Breslow’s tumor thickness tells us that the thinner the tumor the more the likelihood of metastasis

A

Fales, the Breslow tumor thickness tells us that the thicker the tumor the more the likelihood of survival

Tumor thickness / correlation
*< 0,76mm /metastasis rare ,potentially curable

  • 0,76-1,5mm : metastases in 25%
  • > 1,5mm :metastases in 75%
30
Q

List the Clarks levels

relates with which structure is involved

5 years survival decreases as the Clark level increases

A
  1. Epidermis only
  2. Into papillary dermis
  3. Junction between papillary and reticular dermis
  4. Into reticular dermis
  5. Into subcutaneous tissue
31
Q

Summary

A

The Breslow’s thickness correlates with the Clark levels

Skin tumours are common
Can arise from any of the cells making up the skin
Most important: basal cells, squamous cells, and melanocytes
Range from benign to highly malignant
Most are due to sun exposure
Most can be cured with surgery if detected early

Pathological genetics (13 decks)

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