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SKIN Flashcards

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1
Q

Where can we find muco-cutaneous junction?

A

Mouth, nostrils

  • skin has to become continuous with mucous membrane lining —> muco-cutaneous junction (epithelium becomes non-keratinising)
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2
Q

Does hairless skin have sebaceous / apocrine glands ?

A

NO.

Hairless skin is usually thick skin

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3
Q

What is the general function of keratin, keratohyalin granules and lamellar bodies?

A

Protect against mechanical damage & dehydration

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4
Q

What happens to skin of premature babies? When’s epidermal maturation completed?

A

Skin barrier function won’t be good during 1st week of life,

Epidermal maturation completed by 34 weeks of gestation

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5
Q

What is epidermis mainly composed of?

A

Keratinocytes

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6
Q

Where do keratinocytes originate from?

A

Proliferating basal layer

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7
Q

What do keratinocytes synthesise and secrete?

A

Synthesise keratin filaments + desmosomal proteins - they make up “cytoskeleton”, giving cell strength + cohesion

Secrete antimicrobial peptides, cytokines in response to tissue injury

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8
Q

What are the function of lamellar bodies?

A

Secrete lipid & lipid hydrolases - to form water-tight intercellular lipid bilateral

Produce filaggin in stratum corneum - hold moisture

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9
Q

What happens in someone with filaggrin deficiency?

A

‘Leaky’ skin that loses water & allows entry of allergens that trigger an immunological response

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10
Q

What are the consequences of loss of function mutations in filaggrin gene?

A
  • Dry, scaly skin
  • Ichthyosis vulgaris - autosomal dominant disorder causing dry scaly skin
  • Major risk factor for ectopic eczema & associated allergies
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11
Q

What would lead to shedding of skin (desquamation)?

A

Changes in lipid metabolism + protease activity in outermost layer

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12
Q

Where do melanocytes originate from, and what are their functions?

A

*Originate from NCC!

Synthesise pigment melanin (transferred to surrounding keratinocytes to give protection against UV)

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13
Q

What are the functions of Langerhan’s cells?

A

Dendritic cells derived from bone marrow

- play role in antigen presentation & immunoregulation

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14
Q

Which skin layer is Merkel cells found in?

A

Basal layer

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15
Q

Where can you find Merkel cells? What role do they play?

A

numerous on fingertips, oral cavity
Also found on erectile tissue, foot

Play a role in sensation

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16
Q

What can be found in dermis?

A

Collagen & elastin fibres

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17
Q

How many layers are there in dermis?

A
  1. Superficial papillary layer
    Reticular layer (thicker)
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18
Q

What happens to skin since there’s over-distension / stretching in pregnancy / obesity?

A

Collagen bundles rupture (in reticular layer) —> stretch marks —> abdominal striae

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19
Q

What parts of the dermis have smooth muscle fibres? And why?

A

Nipples, penis, scrotum

  • contract and ripple skin
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20
Q

What is panniculus carnosus? Where can we find it?

A

Muscle sheet
- present in face, neck, around scrotum
Moves skin

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21
Q

What is Ruffini corpuscle?

A

Slow-adapting mechanoreceptors

- detect continuous pressure

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22
Q

Where can we find Krause end bulb?

A

In conjunctiva, mucous membrane of lips + tongue

*formed by expansion of CT sheath

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23
Q

Where can we find Meissner’s corpuscle? (Incl. Skin layer) What does it do?

A

Located in dermis, inside dermal papilla

  • light & discriminatory touch
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24
Q

What are the layers of epidermis (stratified squamous) from surface to base?

A

Come let’s get sun burned:

Stratum Corneum (keratin) 
Stratum Lucidum (most prominent in palms + soles)
Stratum Granulosum
Stratum Spinosum (desmosomes) 
Stratum Basale (stem cell site)
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25
Q

What does Parcinian corpuscle do? What does it look like histologically?

A

Deep touch, vibration, pressure

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26
Q

What happens when arrector pilli (smooth muscle, innervates by sympathetic NS) contracts?

A
  • “goosebumps”

- squeeze sebaceous gland —> sebum secretion

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27
Q

Hair follicle stem cells, sebaceous and apocrine glands are __dermal.

A

Ectodermal

28
Q

Dermal papillae & inner and outer sheaths (hair) are ___dermal.

A

Mesodermal

29
Q

What causes loss of skin elasticity?

A

Elastin fibres atrophy with age

30
Q

Where can we find eccrine glands?

A

Pretty much everywhere in thick & thin skin

- more common in palms of hands & soles of foot

31
Q

What are the ducts and secretory acini of eccrine glands lined with?

A

Ducts - simple to stratified cuboidal cells, narrow lumen

Secretory portion - lined with cuboidal / low columnar cells

32
Q

Where can we find myoepithelial cells? What is it?

A

Eccrine glands (sit between secretory acini and basement membrane)

+

Apocrine glands

(Smaller, flatter nuclei)
Isolated contractile cells
Lots of it in breast tissue

33
Q

Can you find myoepithelial cells in ducts?

A

NO. It’s absent in ducts! ONLY present in secretory portion!

34
Q

Sebaceous glands normally associate with hair follicles. True of false?

A

True

35
Q

There’s NO lumen in sebaceous glands. True or false?

A

True.

36
Q

Where can we find apocrine glands?

A

Axilla, pubic region, breast, eyelid

37
Q

Which of the following glands - eccrine, apocrine and sebaceous, have the biggest lumen?
Which one is only active at puberty?
Which one(s) associate with hair follicle?

A

Biggest lumen: apocrine gland! (Sebaceous have no lumen)

Only active at puberty: apocrine gland

Both apocrine & sebaceous associate with hair follicle

38
Q

Breast and ear wax glands are modified apocrine sweat glands. True or false?

A

True

39
Q

How many different layers are there in hair follicle?

A

Infundibulum (upper)
Isthmus (middle)
Bulb & supra bulb (lower)

40
Q

What is the outermost covering of hair follicle lined by?

A

External root sheath

41
Q

Why is malignant melanoma the most serious skin cancer?

A

Metastasise early! Cause a number of deaths even in young people

42
Q

What are the risk factors for melanoma?

A
  • fam history of melanoma
  • freckles / red hair
  • no. Of melanocytic naevi (>50)
  • fair skin that burns easily
  • immunosuppression
  • atypical mole syndrome
  • giant congenital melanocytic naevi
  • lentigo maligna
43
Q

What are the ABCDE criteria for malignant melanoma?

A 
A - asymmetry 
B - border irregularity 
C - colour (varied shades) 
D - diameter (>6mm)
E - evolution (if the lesion has changed / is growing)
44
Q

How many different clinical types are there for melanoma? And what are they?

A

4 clinical types:

  1. Lentigo maligna melanoma
    - patch of lentigo maligna that develops a papule / nodule —> signalling invasive tumour
    - precursor lesion of melanoma
    - atypical pigmented macular lesions
    - seen in ELDERLY patients esp. FACE
  2. Superficial spreading malignant melanoma
    - most common
    - large, flat, irregularly pigmented lesion that grows laterally before vertical invasion develops
  3. Nodular malignant melanoma
    - MOST AGGRESSIVE type
    - presents as rapidly growing pigmented nodule (raised) which bleeds / ulcerates
  4. Acral lentiginous malignant melanoma
    - arise as pigmented lesions on palm / sole / under nail
    - usually present late
    - more commonly in dark-skinned / Asians
    - may not be related to sun exposure
45
Q

What treatment options are available for melanoma?

A

BRAF inhibitors - vemurafenib

[induces G1 arrest]

46
Q

What are the pre-malignant cutaneous lesions ?

A
  • actinic keratoses
  • Bowen’s disease
  • keratoacanthoma
  • familial atypical multiple mole melanoma (FAMM)
  • giant congenital melanocytic naevi
  • lentigo maligna
47
Q

What is lentigo maligna?

A

Slow-growing macular area of pigmentation seen in elderly people, common on face!

*aka Hutchison’s Melanotic freckle (HMF)
- precursor lesion of melanoma!
If invasive component develops (i.e. malignant transformation) —> known as lentigo maligna melanoma

48
Q

What is keratoacanthoma?

A

Rapidly growing epidermal tumours that develop central necrosis + ulceration

49
Q

What are the major and minor criteria for Glasgow seven-point checklist for melanoma?

A

Major criteria:

  • change in size
  • change in shape
  • change in colour

Minor criteria:

  • diameter >6mm
  • inflammation
  • oozing / bleeding
  • mild itch / altered sensation
50
Q

What are the 2 growth patterns of tumour dev in melanoma?

A

Radial + vertical

Radial = cancer 1st tries to grow within the epidermis (laterally)

Vertical = when radial growth finishes —> grow down and invade into dermis

51
Q

Explain ugly duckling rule.

A

Melanoma is usually the ‘odd one out’!

52
Q

What is a dermoscope? What’s it used for?

A

A light source with magnification.

  • to see lesions more accurately
53
Q

What is someone’s 5 year survival rate based on TNM classification if he has stage I melanoma? What about stage IV melanoma?

A

Stage I - 90%
Stage IV - 20%

*stage II - 80%
stage III - 50%

54
Q

Based on Breslow thickness of tumour, what is the recurrence of melanoma?

A

<0.76 mm thick = low risk
0.76 - 1.5 mm thick = medium risk
>1.5 mm thick = high risk

55
Q

What is Breslow thickness? Is it a better prognostic tool than Clark level?

A

Measurement of depth of melanoma from epidermis down thru to the deepest point of the rumour

Thicker = greater chance it has metastasised

*better prognostic tool compared to Clark

56
Q

How many types of skin neoplasms are there? What are they?

A

Melanocytic neoplasms (benign + malignant)

  • freckles
  • acquired melanocytic naevus
  • dysplastic naevus
  • lentigo maligna
  • melanoma

Non-melanocytic neoplasms (arise from keratinocytes)

  • seborrheic keratosis
  • actinic keratosis
  • SCC
  • BCC
57
Q

What are the phototoxic meds that increase photo-toxicity, leading to skin cancer?

A

Azathioprine, mercaptopurine (immunosuppressor)

Thiazides diuretics

Voriconazole (antifungal)

58
Q

What is epidermolysis bullosa ?

A
  • genetic
  • kids that don’t have collage 7 at basal layer of kin —> loss of dermal-epidermal adherence —> skin fragility —> multiple wounds but over time these wounds give rise to SCC
59
Q

What is the relationship between organ transplant recipients and skin cancer?

A

Massive increase in incidence in keratinocytes cancers!

60
Q

What is a blue naevi?

A

An acquired asymptomatic blue-grey mole caused by a deeper proliferation of melanocytes in mid-dermis

61
Q

What is spitz naevus?

A

Occurs mainly in children / YA

Rapidly growing solitary, nodular naevi

62
Q

What is the new therapy for advanced melanoma?

A

BRAF/MEKi combination therapy

63
Q

What are the genetic factors that predispose someone to getting skin cancer?

A

Loss of DNA repair ability
- DNA repair system defect: Xeroderma pigmentosum
—> severe sunburn for minimal exposure from birth, early freckling before 2 yo, skin cancer from 5-7 yo

Loss of TSG
- Gorlin syndrome
—> multiple BCC before 20 yo

64
Q

What is the immunotherapy used to treat melanoma? And why?

A

Combined nivolumab (PD-1 antagonist) + ipilimumab (CTLA4 antagonist)

  • by far the best
  • PD-1 —> responsible for inhibiting T cell action on melanoma cells
  • CTLA4 inhibitor —> increase immune activity
65
Q

Cold vs hot tumours

A

Cold tumour = tumour cells + immune-suppressing cells

Hot tumour = tumour cells + T cells + other cancer fighters (may not be active but are there)

66
Q

What is Bortezomib?

A

Protease inhibitor
- induces G2 arrest in melanoma cells

BTZ-treated cells are also quickly phagocytosis by macrophages

67
Q

What are different closure options for skin cancer surgery?

A

P - primary (side to side / curvilinear)
I - secondary intention
G - full thickness skin graft FTSG / split thickness skin graft STSG
C - composite cartilage graft / combination closure / interpolation flaps
A - advancement flap (defined by linear movement: unilateral A-L / bilateral A-T)
R - rotation flap (defined by arcuate movement)
T - transposition flap (transpose - up & over adjacent skin / structures)
S - island pedicle flaps (no cutaneous attachment e.g. nasal - based on subcutaneous / myocutaneous tissue)

Clinical Science (8 decks)

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