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Integuement > Anatomy? > Flashcards

Anatomy? Flashcards

1
Q

Describe skin anatomy

A
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2
Q

Describe the different kinds of UV light and their clinical significance:

  • wrinkles?
  • penetration?
  • Vit D synthesis?
  • tans?
  • burns?
A

UVC (<290 nm):

UVB (290-320): penetrates less, dierectly damages DNA, responsible for most of Vit D synthesis, the skin tanner

UVA (320-400): Penetrates most deeply, most damage is from damage to photosensitive things in cell which then directly damage DNA, the skin burner and wrinkler and sagger

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3
Q

What is the standard model of carcinogenesis in skin cancer? What kind of exposure are SSC and BCC linked with?

A
  1. Tumour induction (inital DNA damage- even low does of UVB can do this)
  2. Tumour promotion (usually multiple required)

SSC: long term UV exposure

BSC: intermittent bouts

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4
Q

What is melanin? Where is it produced? What are the different types? What are it’s functions?

A

Pigment that protects the skin from UV damage. Produced in melanosomes (tyrosinase) in melanocytes found in the stratum basale and transferred to adjacent keratinocytes (1 melanocyte can supplie 36 keratinocytes)

Eumelanin: most protective

Pheomelanin: less proctective, found in redheads

Functions:

  • protect from UV light
  • scavenge free radicals
  • neural development
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5
Q

What is the typical presentation of BCC? Do they metastasize?

A

Site: sun exposed areas, e.g. face

Appearance: erthematous nodule with telangiectasia, may have ulcer with rolled edge, pearly or translucent. Can be pigmented. Can also be superficial (as opposed to nodular)

Arises from keratinocytes in the stratum basale, are locally invasive, but don’t usually metastasize

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6
Q

What are the clinical features of SCC? Metastatic potential?

A

Derived from suprabasal keratinocytes

Where: Usually on areas of maximum sun exposure

Cause: prolonged UV exposure

Appearance: hard pink or white nodule, scaling

Has metastatic potential

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7
Q

What are the precursors to squamous cell carcinoma?

A

Actinic keratosis

SSC in-situ (Bowen’s disease

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8
Q

What are treatment options for actinic keratosis? Why does it need to be treated?

A
  1. cryotherapy
  2. topical 5-FU (pyrimidine suicide inhibitor)

~10% evolve into SCC if left untreated

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9
Q

What are treatment options for SCC and BCC and melanoma?

A

SCC

  • surgical excision
  • radiation

BCC

  • electrodissecation and curettage
  • simple excision
  • micrographic surgery (Mohs)
  • radiation therapy

Melanoma:

  • surgical, maybe with lymph node dissection
  • can try chemo if systemic, but poor response
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10
Q

What is Mohs surgery?

A

They remove the lesion with as narrow borders as possible, then look at the boders under the microscope to see if they are clear. If they aren’t, they remove a little more. all happens in the operating room.

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11
Q

What is a nevus, where does it come from and what is the typical evolution? What is an atypical nevus?

A

A nevus is a from sun-damaged melanocytes. A nevus is a nest of abnormally dividing melanocytes.

1) Junctional nevus (at the dermal-epidermal junction)
2) Compound nevus (in both)
3) Dermal nevus (entirely within dermis

An atypical nevus cannot evolve in the typical sequence to a dermal nevus so it has irregular edge and color and spreads sideways instead of down into the dermis. It is at high risk to progress to melanoma

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12
Q

What is the most significant risk factor for developing melanoma? What’s the most important prognostic factor of melanoma?

A

>100 nevi (risk 1:10 vs. 1:90)

tumous thickness- correlates with survival and metastasis potential

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13
Q

What are the ABCDE’s of melanoma?

A

Asymmetry

Border

Color

Diameter

Evolution

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14
Q

What are the types of melanoma?

A

Superficial spreading melanoma: when nevi become melanoma, it’s usually this

Nodular: develops without an obvious precursor lesion

Lentigo maligna melanoma: starts as brown patch, cells are along the dermal-epidermal junction, eventually nodule appears

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15
Q

What is SPF?

A

Sun-protective factor: the amount of time required to burn with the sunscreen on divided by the amount of time required to burn without the sunscreen.

Most of us only apply 1/3 of what is needed to acheive the lable spf….

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16
Q

What is the embryologic orgin of the dermis and epidermis?

A

epidermis: ectoderm (melanocytes are neural crest origin)
dermis: mesoderm

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17
Q

Describe the layers of the epidermis

A
  1. Stratum basale :single layer keratinocytes, melanocytes (have smaller darker nucleus and halo). attached to BM by hemidesmosomes
  2. Stratum spinosum: polygonal keratinocytes attached via desmosomes
  3. Stratum granulosum: flattened cells with keratohyaline granules
  4. Stratum corneum: coreneocytes- cells have lost nucleus and organelles
18
Q

How to tell keratinocytes and melanocytes apart on LM?

A

Keratinocytes: tonofilaments –>desmosomes

Melanocytes: melansomes (dark-skinned people have more melanosomes, not more melanocytes)..have smaller nucleus than basal keratinocytes and a halo (they are rigidly bound to neighboring cells like keratinocytes are)

19
Q

What are langerhans and Merkel cells (where are these most abundant)?

A

Langerhans: tissue dendritic cells. found in stratum spinosum. hard to see on LM. has Birbeck granules

Merkel: cells associated with free nerve endings- touch receptors. found in stratum basale and at the base of follicles. most abundant in acral skin

20
Q

What are the 3 mesenchymal layers of the skin?

A
  1. Papillary dermis: loose elastin and collagen
  2. Reticular dermis: thick collagen and ellastin
  3. Subcutis: lots of fat
21
Q

Describe blood and nerve supply to the skin

A

Superficial plexus: btw papillary and reticular

Deep plexus: btw reticular and subcutis

Glomus bodies are specialized arteriovenous shunts in the deep dermis. highest # in acral skin

Nerves mostly found in dermis

  • encapsulated: touch
  • free: temperature, pain
  • specialized: Meissner (in papillary dermis), Pacinian (in deep dermis/subcu)
22
Q

Structure of a pilosebaceous unit

A
23
Q

Differentiate apocrine, holocrine and merocrine (eccrine) secretion

A

Apo: a chunk of cell is secreted (an “apex”)

Holo: the whole cell is secreted, as in sebaceous glands

Merocrine: vesicles are released, as in sweat glands

24
Q

Differentiate apocrine and eccrine (merocrine) sweat glands

A

Apocrine: only found in groin, axilla, external ear (ceruminous glands), nipple, eyelid (Moll’s gland). empty into hair follicles. smelly sweat

Eccrine: release contents directly to skin (coil–>straight duct–> acrosyringium). straight portion is responsible for reabsorbing salt. coiled portion essentially releases an ultrafiltrate

25
Q
A
26
Q

What is a pilosebaceous unit?

A
  • hair follicle
  • arrector pili muscle
  • sebaceous gland
  • apocrine gland (when present)
27
Q

What is the fancy name for goose bumps?

A

Cutis anserina

28
Q
A
29
Q

What is the neural/hormonal control of apocrine, eccrine and sebaceous glands, arrector pili?

A

Eccrine: sweat…sympathetic cholinergic

Apocrine: smelly sweat….sympathetic adrenergic

Sebaceous: androgens/steroid hormones

Arrector pili: sympathetic cholinergic

30
Q

What kind of cells are found in the follicular bulge?

A

Stem cells

31
Q

Parts of the hair follicle

A
32
Q

What are hair growth phases?

A
  1. Anagen (3 yrs)
  2. Catagen (3 wks)
  3. Telogen (3 months)
33
Q

Avearage number of hair on the scalp and the number lost per day.

A

100 000, 100 lost per day

34
Q

What is female vs. male pattern baldness?

A

Women tend to lose hair up top, with hairline preserved. Men can lose hair in all sorts of ways, but the sides are usually preserved and the hairline usualy recedes

35
Q

Treatment of androgenetic alopecia

A

Finesteride (5alpha-reductase inhibitor- prevents conversion of TT to DHT)

Topical minoxidil

Hair transplant

36
Q

What is alopecia areata?

A

Autoimmune hair loss, usually occurs in oval patches anywhere on the body. 83% of cases resolve with no tx in 3 yrs, but can progress to Alopecia totalis, especially if in children with atopy. Classic finding is exclamation point hairs

37
Q

Two most common causes of tinea capitis in BC and how to diagnose

A

Microsporum cannis

Trichophyton tonsuras

Dx: scrapings–> KOH, Wood light exam, fungal culture

**can be inflammatory or non-inflammatory

38
Q

What is telogen effluvium, what causes it, what is the normal course?

A

Hairs are prematurly pushed into telogen

Triggers: parturition, febrile illness, stress, crash diets, drugs (metoprolol, anticoagulants, antithyroid drugs, sodium valproate)

Normal regrowth in 6 months

39
Q

Nail anatomy

A
40
Q

What are the features of acral skin?

A

no sebaceous glands/ pilosebaceous units

lots of eccrine glands

lots of merkel cells

lots of glomus bodies

41
Q

The single most common location for melanoma to occur in women is:

A

legs

42
Q

hyperkeratosis and acanthosis refer to what layers of the skin

A

stratum corneum and stratum spinosum

Integuement (2 decks)

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