Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Musculoskeletal and Skin > Neoplastic Study Guide > Flashcards

Neoplastic Study Guide Flashcards

1
Q

Keratinocytes

A

held together via desmosomes (tight junctions)
 Produce keratin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Keratinocytes

A

held together via desmosomes (tight junctions)
 Produce keratin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Melanocytes

A

produce melanin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Langerhans cells

A

involved in immune response

  • dendrocytes function similarly in the dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

macule

A

flat lesion ≤ 5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

patch

A

flat lesion > 5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

papule

A

elevated lesion ≤ 5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

plaque

A

elevated lesion >5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

scale

A

dry, plate-like lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

excoriation

A

traumatic break in the epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

lichenification

A

thickened, rough skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pustule

A

discrete, pus-filled, raised lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

vesicle

A

fluid filled, raised lesion ≤ 5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

bulla

A

fluid filled, raised lesion > 5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

wheal

A

itchy, elevated lesion with variable blanching and erythema; transient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

onycholysis

A

separation of the nail plate from the nail bed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

acanthosis

A

diffuse epidermal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

dyskeratosis

A

abnormal premature kertinization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

erosion

A

discontinuity of the skin with incomplete loss of the epidermis

20
Q

ulceration

A

discontinuity of the skin with complete loss of the epidermis

21
Q

exocytosis

A

infiltration of the epidermis by inflammatory cells

22
Q

hydropic change

A

intracellular edema

23
Q

spongiosis

A

intercellular edema

24
Q

parakertosis

A

retention of nuclei in uppermost layers of the epidermis

25
Q

ephelis

A

freckles - most common pigmented lesions of childhood

particularly common in light-skinned ppl

often appear after sure exposure

once present, fade and darken in a cyclic pattern during winter and summer

26
Q

lentigo

A

aka age spots

small tan-brown macula’s or patches

do not darken upon exposure to sunlight

27
Q

melanocytic nevi

A

aka moles, common benign neoplasms

acquired melanocytes nevi- most common type

tan-brown to black, uniform pigmented

well-defined round borders

nests of round melanocytes with uniform nuclei - inconspicuous nucleoli, little to no mitotic activity

grow in nests along the dermoepidermal junction (junctional nevus)

grow in the dermis and dermoepidermal junction - compound nevus

grow only in the dermis -intradermal nevus

at the deepest point in there dermis the cells become less rounded and start to grow in fascicles that resemble neural tissue- neurotization, implies maturation/growth of nevus cells

28
Q

congenital nevus

A

present at birth or nearly infancy

no associated with sun exposure

have irregular borders

may be hair bearing

similar to acquired nevi on histology but grow along adnexal structure such as hair follicles

29
Q

dysplastic nevus

A

grossly and histology abnormal

may give rise to melanoma

larger than benign nevi

irregular borders

variability in pigmentation

can e seen in both sun exposed and non sun exposed areas

nests of enlarged nevus cells that fuse along the dermoepidermal junction - individual nuclei are enlarged and hyper chromatic with irregular borders

30
Q

melanoma

A

strongly linked to acquired mutations caused by UV radiation in sunlight

vast majority arise in skin- other sites include oral mucosa, angogential mucosa, esophagus, meninges, uvea of eye

31
Q

mutations of melanoma

A

p16 and p14 lead to increased melancytic proliferation due to loss of cell cycle control

p16 mutation prevent RB from arresting cells in the G1 phase of the cell cycle leading to uncontrolled cell growth

p14 mutations enhance p53 activity leading to uncontrolled cell growth

32
Q

Other melanoma mutation

A

BRAF mutations are seen in 40-50% of melanomas, ucontrolled cell proliferation

TERT promoter mutations turn on telomerase- prevent cell senescence

33
Q

clinical warning signs of melanoma

A

A - asymmetry

B- irregular borders

C- color changes

D- increasing diameter

E- evolution over time

34
Q

melanoma radial growth

A

horizontal spread within the epidermal and superficial dermis

35
Q

melanoma vertical growth

A

tumor cells invade deeper into the dermis

Breslow depth - depth of invasion of melanoma measured from granular of epidermis to deepest point of invasion- measured mircroscopically , most important prognostic factor

36
Q

histology of melanoma

A

individual cells are larger than those seen in benign nevi

 Enlarged nuclei with irregular borde Characteristic prominent, cherry red nucleolus

 Cells grow singly and in nests along the dermoepidermal junction (lentiginous
growth) and extend down into the dermis
 There is no evidence of maturation/neurotization as malignant cells
extend into the dermis

37
Q

favorable prognostic indicators (melanoma)

A

thinner Breslow depth, less mitotic activity, brisk tumor infiltrating lymphocyte response

38
Q

poor prognostic indicators (melanoma)

A

ulceration, lymph node metastases (even with few cells)

39
Q

Seborrheic keratosis

A

common in middle aged older individuals

o Arise spontaneously

o Activating mutations in FGFR3 are thought to drive growth

o Leser-Trelat sign – sudden appearance of large numbers of seborrheic keratoses
 Paraneoplastic syndrome associated with GI malignancies

o Round, flat, waxy plaques
 Often appear “stuck on”

o Sheets of small basal epithelial cells with exuberant keratin production
Pseudohorn cysts – invaginations of epithelium with abundant laminated
keratin

40
Q

Actinic Keratosis

A

scaly erythematous lesion seen in sun damaged skin

Tan-brown, red, or flesh colored with a rough consistency

o Dysplastic cells are present in the lowermost layers of the epidermis

o Parakeratosis is seen in the superficial epidermis

o Associated solar elastosis
 Thickened, blue-grey elastic fibers  Result of sun damage

o May progress to squamous cell carcinoma

41
Q

Squamous cell carcinoma (SCC) of the skin

A

related to DNA damage induced by exposure to UV light

Tumor incidence is proportional to the degree of lifetime sun exposure

o Other patients at particular risk for SCC: chronic immunosuppression, industrial
carcinogens, chronic ulcers, draining osteomyelitis, old burn scars, arsenic, ionizing
radiation, tobacco

o DNA damage caused by UV radiation (sun exposure) gives keratinocytes increased
susceptibility to infection with and transformation by oncogenic viruses such as human papillomavirus (HPV), particularly HPV types 16 and 18 o High incidence of TP53 mutations
 p53 is not able to arrest the cells in G1 phase of the cell cycle for repair of DNA
damage or elimination via apoptosis
 DNA damage induced by UV radiation is passed on to daughter cells

o SCC in situ – atypical cells are confined to the epidermis  Grossly appear as sharply defined, red, scaly plaques

o Invasive SCC – lesions become nodular with variable keratin production  May ulcerate

o Well differentiated tumors consist of atypical squamous cells with enlarged,
hyperchromatic nuclei

Large areas of keratinization
 May be swirls of keratin – “keratin pearls”

o As tumors become more poorly differentiated the tumor cells become larger and more
irregularly shaped
 Less and less keratinization may be present

42
Q

Basal cell carcinoma

A

Slow growing tumors

o Rarely metastasize

o Nevoid basal cell carcinoma syndrome (aka Gorlin syndrome)
 Germline mutations of PTCH gene
 Uncontrolled cell growth and survival

o Pearly papules with prominent telangiectasias  Advanced lesions may ulcerate
 Superficial BCCs may present as an erythematous, scaly, plaque

o Tumor cells resemble normal basal cells of the epidermis
 Polygonal with enlarged, hyperchromatic nuclei  Grow in nests/clusters that can extend along the epidermal surface or deep
down into the dermis  Cells at the periphery of the clusters show peripheral palisading  Stromal clefting – stroma retracts from islands of tumor cells
 Artifact of processing  Fairly specific for BCC

43
Q

dermatofibroma

A

aka benign fibrous histocytoma

firm tan brown papule

benign spindle cells

44
Q

dermatofibrosarcoma protuberans (DFSP)

A

well differentiated fibrosarcoma of the skin

slow growing but locally agressive

characteristic translocation t(17:22)

firm nodule that my ulcerate

storiform patter of fibroblasts

45
Q

mycosis fungoides

A

lymphoma of CD4 T cells that presents in the skin

patch, plaque and nodular stages

Sezary-Lutzner cell with characteristic hyperconvoluted/ceribriform nucleus

Musculoskeletal and Skin (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions