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Semester 3 Revision > Integ1 > Flashcards

Integ1 Flashcards

1
Q

What are the functions of skin?

A
  • barrier
  • homeostasis
  • insulation
  • sensation
  • vitamin D production
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2
Q

What are the three basic layers of the skin?

A
  • thin epidermis
  • thicker dermis
  • subcutis
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3
Q

What is the stratum basale?

A

the layer at the base

these are the stem cells that proliferate - they divide, pushing upwards.

It takes 10-14 days to go from stem cells to flattened top cells.

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4
Q

What is the stratum spinosum?

A

the spiny layer

There are lots of desmosomes which act as plates to hold the cytoskeletons of two cells tighter, making it strong and a good barrier. These cells get flatter and flatter towards the top.

A friction blister occurs due to damage in the stratum spinosum layer. Initially, fluid builds up due to burst cells, and later some transudate.

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5
Q

What is the stratum granulosum?

A

the granular layer

the cells are very flat in this layer. There are keratohyalin granules (keratin precursor) and lamellar bodies (lipids)

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6
Q

What is the stratum corneum?

A

the horny layer

contains keratin-packed enucleated cells –> NB soft keratin (nails)

lipids from lamellar bodies act as mortar, holding the cells packed with keratin together.

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7
Q

What is the stratum lucidum?

A

the clear layer

this layer is only found in thick skin. it contains immature keratin (eleidin).

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8
Q

What is there within the epidermis?

A
  • melanocytes
  • langerhans cells
  • merkel cells
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9
Q

What are melanocytes?

A
  • pigmentation
  • in stratum basalis
  • every shade of hair and skin is just a mix of two melanins (think of vitiligo)
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10
Q

What are langerhans cells?

A
  • immune cells
  • antigen presenting cells
  • in stratum spinosum
  • when it goes wrong it can cause eczema - attacks the wrong cells
  • protection against microorganisms
  • small, pale cells in non-basal layers of skin
  • they are dendritic cells - have branching cytoplasmic processes
  • they are antigen presenting cells and form a network in the epidermis - part of the immune system
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11
Q

What are merkel cells?

A
  • sensory
  • associated with nerve endings
  • in stratum basalis
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12
Q

What are examples of appendages?

A

HAIR FOLLICLES: erector pili muscle
SWEAT GLANDS: eccrine and apocrine
SEBACEOUS GLANDS: holocrine

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13
Q

What kind of glands are there?

A

MEROCRINE: exocytosis
APOCRINE: clinch bits off themselves
HOLOCRINE: apoptosis/explode

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14
Q

What can vitamin D deficiency result in?

A

Children: rickets
Adults: osteomalacia

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15
Q

What is meant by integument?

A

means the skin, hair and nails. it is the interface between the body and the environment - thus is subject to a wide range of insults/stresses

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16
Q

What is the importance of keratin in protection and adaptation?

A

–> cell flow in the epidermis

Stratum corneum: cornfield keratinocytes lose nuclei, continuing to move distally
Daughter cells move distally through the epidermis while differentiating into mature keratinocytes - making lots of the tough, waterproof protein keratin
Basal layer: first cell layer, containing dividing stem cells

Nail is also made of keratinocytes, and is full on keratin. Horns and hoofs are also keratin(-ocytes).

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17
Q

What can extensive epidermal damage lead to?

A
  • dehydration and shock
  • infection
  • heat loss and hypothermia
  • protein loss, electrolyte imbalance, high-output cardiac failure, renal failure
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18
Q

What does the skin act as a barrier to/protect against?

A
  • irradiation and UV light
  • physical trauma
  • microbes
  • allergens
  • irritants
  • heat
  • cold
  • infections
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19
Q

What does epidermal melanin do?

A

UV protection
the colour of human skin is due mainly to melanin (dark skin) and haemoglobin (light skin)
much normal genetic variation in the amount of melanin (>12 genes known)
melanin protects against DNA damage and this skin cancer, especially in dark skin, incidence only 8-10% that of white people

melanin is made by melanocytes - cells in basal epidermal layer, with dendrites that feed pigment to keratinocytes

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20
Q

What happens during tanning?

A
  • melanocytes increase activity - they make and transmit more melanin
  • the signal for this works through DNA damage by uv
  • gives some protection against uv
  • additional protection by skin thickening in response to uv
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21
Q

What is lichenification?

A

more extreme form of hyperkeratosis - reaction to excessive rubbing or scratching/skin conditions

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22
Q

What is sunburn?

A

sunburn is a radiation burn causing blisters, inflammation and cell death (severe dna damage).

if you have ever been sunburnt it increases your risk of skin cancer

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23
Q

What are naevi?

A

MOLES
singular: naevus
benign proliferation of melanocytes
many of large naevi = risk factor for melanoma skin cancer

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24
Q

What are ephelides?

A

FRECKLES
involve a genetic component
also linked to red/fair hair
sun exposed areas

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25
Q

What are visual cues of solar lentigos?

A

liver spots, age spots, age related

26
Q

What is solar keratoses?

A

dysplastic growth of keratinocytes

27
Q

What are the two types of carcinoma?

A
  • squamous cell carcinoma

- basal cell carcinoma

28
Q

Why is UV good?

A

UV is needed for vitamin D production in skin.

UV radiotherapy is used for skin conditions such as vitiligo and psoriasis

29
Q

What is irritant contact dermatitis?

A
  • occurs when too much exposure to a substance
  • can still use it, but reduce amount
  • people vary in sensitivity
  • common
  • any of redness, itching, swelling, blistering and/or scaling
30
Q

What is allergic contact dermatitis?

A
  • allergy to something that contact skin - immune system involved
  • tiny amount may be sufficient
  • relatively uncommon
  • varies greatly between people. may develop after long or short use
  • any of redness, itching, swelling, blistering and/or weeping
31
Q

What are examples of microbes?

A
  • fungi
  • bacteria
  • viruses
32
Q

What is paronychia?

A

nail fold infection - fungal or bacterial

fungal example: tine wapitis, scalp ringworm
virus example: HPV warts

Portal of entry: microbes can enter breach in epidermis (e.g. streptococcus in cellulitis)

Impaired immunity predisposes to infection, e.g. HIV and viral warts, eczema herpeticum or herpes (cold sore) virus infecting eczema

33
Q

What is eczema?

A

An inflammatory process affecting the skin and due to various factors, both internal and external.

Interchangeable with the term ‘dermatitis’.

34
Q

What is atopic eczema?

A

The most common form, affects 15% of the population. In children the majority of onset is

35
Q

What is the histology of atopic eczema?

A

ACUTE STAGE: oedema of the epidermis (spongiosis), intraepidermal vesicles form, which coalesce/form blisters/rupture

CHRONIC STAGE: los of vesicles, epidermis thickens; stratum spinosum-acanthosis, stratum corneum-hyperkeratosis

36
Q

What are symptoms of infantile atopic eczema?

A
  • widespread dry red scaly skin
  • can be weeping
  • often cheeks are first area affected
  • nappy area spared - moisture effect
37
Q

What are the symptoms of atopic eczema in toddlers/school age children?

A
  • more localised (flexural) and thickened, leathery (lichenified) lesions
  • scratch marks
  • elbows, knees, eyelids, ear creases, neck, scalp
38
Q

What are the symptoms of atopic eczema in adults?

A
  • commonly persistent localised eczema
  • recurrent secondary staphylococcal infection
  • major factor for irritant contact dermatitis, particularly hands
39
Q

What is the treatment of atopic eczema?

A
  • trigger avoidance
  • break the itch-scratch-itch cycle
  • regular emollients (moisturisers)
    (consistency regulated to oil/water content –> lotion (oil in higher water content preparation), cream (oil in lower water content preparation), ointment (oil-based preparation))
  • soap substitutes - aqueous cream, emulsifying ointment, dermal 500 (with antimicrobial)
  • bath preparations (oilatum, balneum, dermal 600)
  • intermitted topical steroids:
    1% hydrocortisons (mild)
    eumovate (moderate)
    betnovate, elocon (potent)
  • other: topical calcineurin inhibitors (tacrolimus), oral antibiotics, antihistamines
40
Q

When should someone be referred to a dermatologist in the case of atopic eczema?

A
  • diagnostic uncertainty
  • severe eczema or poor response to topical therapy for consideration of: UV phototherapy, systemic treatment - cyclosporin, methotrexate, azathioprine
41
Q

What are possible complications of atopic eczema?

A
  • bacterial co-infection - impetiginisation
  • viral co-infection - eczema herpeticum
  • post-inflammatory hypo pigmentation/hyperpigmentation
  • scarring
  • striae/skin atrophy from steroid use
  • depression/psychosocial impact
42
Q

What is psoriasis?

A

a common (1-2% of the population) chronic inflammatory disorder. It has focal, well-maintained, inflamed, oedematous plaques covered with silvery-white scale. Psoriasis can affect any age and there is no significant male/female difference.

The distribution of psoriasis comes in a variety of shapes and sizes. It is symmetrical and appears on extensor surfaces, sacrum, scalp, ears, palms, soles. There are environmental, genetic and immunologic factors.

43
Q

What is the histology of psoriasis?

A
  • disordered maturation of keratinocytes and reduced epidermal transit time from 30 days to 6 days
  • leads to hyperprolifertion and thickening of the epidermis
44
Q

What is the treatment of psoriasis?

A
  • topical
  • emollients
  • topical steroids
  • coal tar
  • salicylic acid
  • vitamin D analogues (calcipqotriol - dovonex)
  • combination of above - diprosalix, dovobet)
  • dithranol
45
Q

What would you refer a psoriasis case to a dermatologist for?

A

PHYSICAL: UV phototherapy
SYSTEMICS: ciclosporin, methotrexate, acitretin
BIOLOGICS: monoclonal antibodies against TNF - ethanercept (Enbrel), infliximab (remicade) and adalimumab (humira), monoclonal antibody against IL-12 and IL-23 - urstekinumab (stellar), must meet specific criteria based on disease severity and impairment of quality of life, and failure of other systemics

46
Q

What is acne vulgaris?

A
  • Affects the areas of skin with the densest population of sebaceous follicles
  • Over-activity of polo-sebaceous units secondary to hormonal stimulation
  • Hyper proliferation of follicular epidermis with subsequent follicle plugging
  • Presence and activity of Propionibacterium acnes with the above setting
47
Q

What is the treatment of acne vulgaris?

A
  • topical retinoids (adapalene, tretinoin)
  • topical antibodies(dalacin-T, zineryt)
  • benzoyl peroxide (Duac)
  • oral antibodies (erythromycin, oxytetracycline, lymecycline)
  • oral contraceptive pill (Dianette)

Referral to specialist dermatologist for consideration of Isotretinoin (Roaccutane):

  • systemic retinoid
  • works against all contributing factors
  • teratogenic - two forms of contraception, monthly pregnancy tests
  • other side effects: dry lips and skin, myalgia, hair thinning, depression
  • base line FBC, LFTs and lipids
48
Q

What is impetigo?

A
  • most common bacterial skin infection in children; bacterial skin infection with staphylococcus aureus ± streptococcus pyogenes
  • begins with a single erythematous macule which rapidly evolves into vesicle or pustule then ruptures
  • exudate dried to fold classic golden crust
  • if mild and localised - topical Fucidin
  • if extensive - oral Flucloxacillin
49
Q

What are viral warts?

A
  • growths caused by infection with HPV (>70 subtypes)
  • spread by direct or indirect contact - swimming pools, biting fingernails, shaving
  • incubation ranges from a few weeks to over a year
  • contagious but low risk of spread
  • treatment: nil/self-resolving, duct tape, salicylic acid, cryotherapy
50
Q

What is tinea?

A
  • the most common organism is the dermatophyte trichophyton rubrum
  • clue is history - short history, very itchy
  • slowly enlarging, annular, scaly, erythematous plaque with well-defined edge and central clearing
  • under microscopy - hyphae visible
51
Q

What is the treatment of tinea?

A
  • topical azalea (eg clotrimazole) or allylamine (eg terbinafine) for two weeks
  • systemic therapy may be indicated if extensive, immunosuppression, resistance to topical therapy
  • nails; terbinafine for 6 weeks (fingernails) or 3-4 months (toenails)
  • monitoring for adverse effects and drug interactions
52
Q

What is actinic keratosis?

A
  • common sun-induced scaly or hyperkeratotic lesion, which has the potential to become malignant
  • affects 23% of the UK population >60 years
  • consequences of cumulative long-term sun exposure, so incidence increases with age
  • also risk in long-term phototherapy (e.g. psoriasis) and immunosuppressed patients
  • genetic factors/skin type important
53
Q

What is the treatment for actinic keratosis?

A

Largely managed in the community

Treatment:

  • observation
  • emollients
  • cryotherapy
  • 5-fluorouracil cream (Efudix), imiquimod cream (Aldara), Diclofenac gel (Solaraze)

Should be referred to a dermatologist if:

  • diagnostic uncertainty
  • suggestion of transformation into SCC (under 2ww) - e.g. growth, pain, bleeding
54
Q

What is the histology of actinic keratosis?

A
  • abnormality confined to epidermis only
  • clusters of atypical keratinocytes at lower layer of epidermis
  • once this involves full thickness of epidermis = Bowen’s
55
Q

What is squamous cell carcinoma?

A
  • the result of cumulative sun exposure, so incidence increases with age
  • sun-exposed sites - dorsum of hands, forearms, ears, upper face, lower lip
  • arise de novo or from AK/bowens
  • also site of chronic inflammation e.g. chronic leg ulcer
  • refer immediately under 2ww for surgical intervention
56
Q

What is the histology of squamous cell carcinoma?

A
  • invasion of islands of typical squamous cells into the dermis
  • classed as well, moderately, or poorly differentiated
  • assessment of how significantly the tumour cells differ from normal keratinocytes
  • lips and ears have a higher rate of metastasis to lymph nodes
57
Q

What is basal cell carcinoma?

A
  • slow growing skin malignancy also known as a ‘rodent-ulcer’
  • head and neck most common
  • shiny, translucent, nodule with a rolled-edge, telangiectasia, central depression or ulceration
58
Q

What is the histology of basal cell carcinoma?

A

nests of basiloid tumour cells, palisading of cells at periphery

59
Q

What is the treatment of basal cell carcinoma?

A
  • routine dermatology referral (not 2ww)
  • treatment usually by excision
  • GP follow up, education regarding sun awareness and skin surveillance
60
Q

What are suspicious pigmented lesions?

A
  • think about risk factors
  • counsel about risk
  • at risk groups: educate about sun awareness, skin surveillance…
Asymmetry
Border irregularity
Colour variation
Diameter >6mm - and persistent growth
Extra features - itching, bleeding

Other suspicious features: bleeding without trauma, new nodularity, new pigmentation or unexplained destruction of a nail, new pigmentation on the lips or mucous membranes

61
Q

What is melanoma?

A
  • over 12,000 new cases in 2010 (rate doubled in past 20 years)
  • second most common cancer in the 15-34 year age group
  • most common on the trunk (males) and legs (females)
  • types: nodular, superficial spreading, lentigo maligna, acial lentiginous
  • all suspicious lesions should be referred under the 2 week wait rule
62
Q

What is the histology of melanoma?

A
  • varies depending on melanoma subtype
  • atypical melanocytes arranged singly or in nests
  • invasion into the dermis and subcutaneous fat
  • depth of invasion is major prognostic indicator (breslow thickness)

Semester 3 Revision (7 decks)

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