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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
What does Parcinian corpuscle do? What does it look like histologically?
Deep touch, vibration, pressure
26
What happens when arrector pilli (smooth muscle, innervates by sympathetic NS) contracts?
- “goosebumps” | - squeeze sebaceous gland —> sebum secretion
27
Hair follicle stem cells, sebaceous and apocrine glands are __dermal.
Ectodermal
28
Dermal papillae & inner and outer sheaths (hair) are ___dermal.
Mesodermal
29
What causes loss of skin elasticity?
Elastin fibres atrophy with age
30
Where can we find eccrine glands?
Pretty much everywhere in thick & thin skin | - more common in palms of hands & soles of foot
31
What are the ducts and secretory acini of eccrine glands lined with?
Ducts - simple to stratified cuboidal cells, narrow lumen Secretory portion - lined with cuboidal / low columnar cells
32
Where can we find myoepithelial cells? What is it?
Eccrine glands (sit between secretory acini and basement membrane) + Apocrine glands (Smaller, flatter nuclei) Isolated contractile cells Lots of it in breast tissue
33
Can you find myoepithelial cells in ducts?
NO. It’s absent in ducts! ONLY present in secretory portion!
34
Sebaceous glands normally associate with hair follicles. True of false?
True
35
There’s NO lumen in sebaceous glands. True or false?
True.
36
Where can we find apocrine glands?
Axilla, pubic region, breast, eyelid
37
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?
Biggest lumen: apocrine gland! (Sebaceous have no lumen) Only active at puberty: apocrine gland Both apocrine & sebaceous associate with hair follicle
38
Breast and ear wax glands are modified apocrine sweat glands. True or false?
True
39
How many different layers are there in hair follicle?
3. Infundibulum (upper) Isthmus (middle) Bulb & supra bulb (lower)
40
What is the outermost covering of hair follicle lined by?
External root sheath
41
Why is malignant melanoma the most serious skin cancer?
Metastasise early! Cause a number of deaths even in young people
42
What are the risk factors for melanoma?
- 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
What are the ABCDE criteria for malignant melanoma?
``` A - asymmetry B - border irregularity C - colour (varied shades) D - diameter (>6mm) E - evolution (if the lesion has changed / is growing) ```
44
How many different clinical types are there for melanoma? And what are they?
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
What treatment options are available for melanoma?
BRAF inhibitors - vemurafenib | [induces G1 arrest]
46
What are the pre-malignant cutaneous lesions ?
- actinic keratoses - Bowen’s disease - keratoacanthoma - familial atypical multiple mole melanoma (FAMM) - giant congenital melanocytic naevi - lentigo maligna
47
What is lentigo maligna?
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
What is keratoacanthoma?
Rapidly growing epidermal tumours that develop central necrosis + ulceration
49
What are the major and minor criteria for Glasgow seven-point checklist for melanoma?
Major criteria: - change in size - change in shape - change in colour Minor criteria: - diameter >6mm - inflammation - oozing / bleeding - mild itch / altered sensation
50
What are the 2 growth patterns of tumour dev in melanoma?
Radial + vertical Radial = cancer 1st tries to grow within the epidermis (laterally) Vertical = when radial growth finishes —> grow down and invade into dermis
51
Explain ugly duckling rule.
Melanoma is usually the ‘odd one out’!
52
What is a dermoscope? What’s it used for?
A light source with magnification. - to see lesions more accurately
53
What is someone’s 5 year survival rate based on TNM classification if he has stage I melanoma? What about stage IV melanoma?
Stage I - 90% Stage IV - 20% *stage II - 80% stage III - 50%
54
Based on Breslow thickness of tumour, what is the recurrence of melanoma?
<0.76 mm thick = low risk 0.76 - 1.5 mm thick = medium risk >1.5 mm thick = high risk
55
What is Breslow thickness? Is it a better prognostic tool than Clark level?
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
How many types of skin neoplasms are there? What are they?
2. 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
What are the phototoxic meds that increase photo-toxicity, leading to skin cancer?
Azathioprine, mercaptopurine (immunosuppressor) Thiazides diuretics Voriconazole (antifungal)
58
What is epidermolysis bullosa ?
- 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
What is the relationship between organ transplant recipients and skin cancer?
Massive increase in incidence in keratinocytes cancers!
60
What is a blue naevi?
An acquired asymptomatic blue-grey mole caused by a deeper proliferation of melanocytes in mid-dermis
61
What is spitz naevus?
Occurs mainly in children / YA | Rapidly growing solitary, nodular naevi
62
What is the new therapy for advanced melanoma?
BRAF/MEKi combination therapy
63
What are the genetic factors that predispose someone to getting skin cancer?
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
What is the immunotherapy used to treat melanoma? And why?
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
Cold vs hot tumours
Cold tumour = tumour cells + immune-suppressing cells Hot tumour = tumour cells + T cells + other cancer fighters (may not be active but are there)
66
What is Bortezomib?
Protease inhibitor - induces G2 arrest in melanoma cells BTZ-treated cells are also quickly phagocytosis by macrophages
67
What are different closure options for skin cancer surgery?
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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