week 7-skin Flashcards

1
Q

what is acne? treated

A

Very common
• Characterised by blackheads and whiteheads and pustules
• Mostly affects face, the upper part of the chest, and the back
where most sebaceous follicles
• Severe acne is inflammatory, but acne can also manifest in
non-inflammatory forms
• Lesions are caused by excess oil and dead skin cells clogging
up follicles – Propionibacterium acnae grow, triggering
inflammation and pus
• In adolescence, acne is usually caused by an increase in
testosterone, which accrues during puberty
• Acne scars are the result of inflammation within the dermis
brought on by acne (1 in 5 sufferers have scarring)
• Benzoyl peroxide, antiseptics, antibiotics, hormonal
treatments, retinoids

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2
Q

what are 3 main skin cancers?

A

Basal cell carcinoma
• Squamous cell carcinoma
• Malignant melanoma

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3
Q

what is basal cell cacinoma?

A

Slow-growing and locally invasive tumours
• 4 times more common than other skin cancers
• Caused by UV exposure and proliferation of basal
keratinocytes
• Commonly on head and neck
• Morbidity related to local tissue invasion and
destructions
• Imiquimod cream treatment

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4
Q

what is squamous cell carnioma?

A

• Malignant invasive proliferation of epidermal
keratinocytes
• Second most common skin cancer
• More common in men and the elderly
• Caused by UV exposure
• Common in white skin that burns easily
• Also caused by topical carcinogens – arsenic, or
chronic immunosuppression
• With treatment overall remission rate is 90%

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5
Q

what is maligant melanoma?

A

Malignant proliferation of melanocytes
• Incidence and mortality are increasing
• Highest incidence in Australia and New Zealand
• Caused by UV exposure
• Mortality rate of 25%
• ‘Limited’ treatment options
- recent high-profile successes of immune system
modulation

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6
Q

what ares some risk factors for melanoma?

A
UV	exposure	
Intense	short	exposure	in	
childhood	
Fair	skin	
Red	and	blonde	hair	
Blue	eyes	
Difficulty	to	tan	
Freckles	
Benign	naevi/dysplastic	
naevi
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7
Q

what are some signs of melanoma?

A
A	Asymmetry	
B	Border	is	irregular	
C	Colour	variegation	
D	Diameter	(>6	mm)	
E	Evolving	–	any	change	
size,	shape,	colour	
elevation	
bleeding,	itching	
crusting
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8
Q

what actually happens causing melanoma?

A
  • in the epidermis you have melanocytes in the basal layer
  • when we get proliferation of them they can turninto beign moles
  • but soemtiemes they grow our of controland you get dysplastic nevus
  • overtime youll get radio growth phase they grow in epidermal layer
  • they they exoand into dermal layer then evenually become metastatic melanoma and reach bood vessles and can move to otther to form metatsisis
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9
Q

what can affect the survival of the melanaoma?

A

the thickness more than 4mm 5years survival is 37-50%

less than 1mm 5 year survial is 95-100%

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10
Q

what is treatment for melanoma?

A
• Surgery	
– Simple	or	wide	
– Sentinel	node	biopsy	
• Chemotherapy	
– Dacarbazine	iv	infusion	or	Temozolomide	oral	
– Taxanes	(docetaxel,	paclitaxel)	and	platinum	agents	
– Targeted	therapy	
• Interferon	alpha	2b	
• IL2	
• Ipilimumab	(anti-CTLA4)	
• Anti-BRAF	
• Anti-PD1
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11
Q

what is warts and verrucas?

A

• Caused by human papillomavirus – causes excess keratin
production on epidermis
• Virus can spread through close skin to skin contact,
contaminated objects eg towels, shoes, communal
changing areas, more likely to spread if skin wet, soft and in
contact with rough surface
• Clear up after about 2 years
• Salicylic acid containing creams , gels and paints
• Cryosurgery
Genital warts - very common, sexually transmitted
• Months or even years to develop after HPV infection
• Liquids and creams, eg Imiquimod, a topical cream that
stimulates the immune system to fight papillomavirus by
encouraging interferon production
• Keratolysis and cryosurgery

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12
Q

what is impetigo?

A

• Common highly contagious skin infection causing sores
and blisters – often Streptoccocus/Staphylococcus
infections
• 2 types –
– Non-bullous – most common - nose and mouth, sores
quickly burst – leave yellow-brown crust
– Bullous – trunk, fluid-filled blisters that burst after few
days – leave yellow crust
• Very common in young -1/35 children in UK aged 0-4
• Topical antibiotics, stay away from other people.
• Severe cases – systemic antibiotics (eg. Flucloxacillin).

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13
Q

what are fungal infections?

A

• Several types of infections eg dermatophytes and yeasts,
result in inflammation
• Fungi invade and grow in dead keratin
• Dermatophytes
– Athletes foot –
• Ringworm growing between toes
• Itchy flaky red skin
• Contaminated floors
– Nail infections – usually toenails – start from edge to base
– Ringworm – body, scalp, groin
• Small areas treated with topical application of imidazoles
(2%)
• Severe cases with systemic antifungal agents (griseofulvin, itraconazole)
• Immunocompromised patients (Candida and Aspergillus).

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14
Q

what is vitiligo?

A

Also called leucoderma
• Loss of skin colour in patches – discoloured
areas usually get bigger with time
• Affects any part of the body, hair and inside
the mouth but more often around eyes,
nostrils, mouth, navel, knees and elbows
• Melanocytes die or stop functioning leading
to loss of melanin
• Affects people of all races and all skin types
• 95% develop it before age 40
• Not contagious or life threatening and not
linked to cancer
• No cure
• 3 Types
– Focal, Segmental, Generalised

• Aetiology
– Autoimmune component
– 30% of patients have a family history
– 15-24% have autoimmune disease
– Immune system attacking its own melanocytes
– Triggers – stress, skin damage, hormonal changes, chemical
exposure (phenol) , liver/renal disease
• Pathogenesis
– Autoimmune component
– Body makes autoantibodies to tyrosine hydroxylase in nonsegmental vitiligo
– Increase in ROS production also in mitochondria of affected cells

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15
Q

what is Psoriasis?

A
Chronic	autoimmune,	inflammatory	skin	
disease	with	periods	of	remission	and	
relapse	
• Affects	2-3%	UK	population	
• Equally	in	men	and	women,	any	age	
• Peaks	in	late	teens-early	30s	and	50-60	
• Normal	skin	cells	produced	faster	than	
they	are	shed	resulting	in	itchy,	skin	
lesions/plaques	–	pink/red	with	white	
scales,	variety	of	shapes	and	sizes		–	can	
split	–	painful	
• Can	develop	psoriatic	arthritis
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16
Q

whats plaque psoriasis?

A

Most common
• Alone or in combination with other type(s)
• Red, itchy, sore plaques with white or silvery
scales – well demarcated
• Occurs anywhere on body – usually different
type if on palms or soles or where skin
touches skin

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17
Q

what is the aetiology of psorosis?

A

• Genetic predisposition
– Complex inheritance but 1/4 children of affected
parent
– Several susceptibility loci
• Keratinocytes normally take 3-4 weeks from
basal layer to shedding – 3-4 days in psoriasis
• Inflammatory cells increased in all layers
• Trigger often outside event – eg throat infection
(streptococcal) , stress or injury to skin, virus (HIV
or HPV) or withdrawal of corticosteroids

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18
Q

what is the treatment for psorosis?

A

• Unique to each individual
• Topical treatments
– Moisturisers and emollients
– Vitamin D derivatives (calcipotriol, tacalcitol, calcitriol)
– Topical steroids (eumovate, betnovate, dermovate),
– Dovobet (betamethasone and Vit D derivative)
– Coal Tar preps – scalp
– Dithranol – for well-defined plaques not on sensitive
areas
– Calcineurin inhibitors
• Phototherapy
• Systemic treatments
– Immunosuppressants – methotrexate and ciclosporin
– Vitamin A derivative (Acitretin)
– Apremilast – inhibits phosphodiesterase 4
– Dimethyl fumarate – activates Nrf2
– Anti-TNF (infliximab, adalimumab, etanercept, certolizumab)
– Anti-IL23 (ustekinumab (anti-Il12/Il23), guselkumab, rizankizumab, tildrakizumab)
– Anti-IL17/IL17A (secukinumab, brodalumab, ixekizumab)

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19
Q

what is psoriatic arthritis? and treatment

A
• Inflammatory	joint	disease	affecting	both	joints	
(eg	knees,	hands	and	feet)	and	tendons	(eg	heel	
and	lower	back)	
• Relapsing	and	remitting	
• Generally	occurs	after	skin	lesions		
• Not	linked	to	severity	of	psoriasis	
• Joints	become	tender,	swollen	and	stiff	–	worse	
in	morning	and	ease	with	exercise	
• Inflammation	of	tendons	without	joints	
• Often	associated	with	nail	psoriasis		
Treatment	of	psoriatic	arthritis	
• Painkillers	
• NSAIDs	–	ibuprofen,	diclofenac,	COX-2	
inhibitors	
• Corticosteroids	
• DMARDS	– leflunomide
• Biologicals		
– Anti-TNF	– adalimumab,	etanercept,	certolizumab
– Apremilast –	anti-PDE4	
– Tofacitinib –	JAK	inhibitor
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20
Q

what is the aetiology for atopic eczema?

A

Genetic predisposition – atopic families
• Defects in the skin barrier – repair and maintain
• Lack of anti-microbial peptides
• Defect in the filaggrin gene - important for maintaining
the skin barrier – in most eczema patients
• Abnormalities in the normal inflammatory and allergy
responses
• Barrier defects makes the skin in affected patients
much more susceptible to infection and to irritation
and allows allergy-inducing substances to enter the
skin, causing itch and inflammation

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21
Q

whats the clinical features of atopic eczema?

A

Often age-specific
– Flexural eczema in children
– Hand eczema in adults
• Dry skin
• Itching, may be severe, especially at night
• Red to brownish grey patches on affected areas
become lichenified
• Raw, sensitive, swollen skin from scratching
• Skin infections and sores can occur when
scratching breaks the skin

22
Q

whats the treatment for eczema?

A

• Emollients
• Topical corticosteroids
• Antibiotics if eczema infected
• Phototherapy
• Systemic corticosteroids
• Topical calcineurin inhibitors (TCIs) – pimecrolimus and
tacrolimus
• Immunosuppressants – ciclosporine, azathioprine
• Dupilimumab – mAb inhibiting IL4/IL13 signaling
• Alitretinoin – for chronic hand eczema refractory to
steroids (retinoid)

23
Q

whats allergic contcat dermatisi?

A

– Majority of occupational skin disorders
– Type IV hypersensitivity reaction
– Over time of exposure , immune response builds up
– Nickel, rubber, perfumes, preservatives in cosmetics, dyes
– Diagnosis by patch testing

24
Q

whats the treatment for coontcat dermatisis?

A
• Avoid	irritants	and	allergens	
• Emollients	
• Topical	corticosteroids	
• Oral	corticosteroids	
• Alitretinoin	for	chronic	hand	contact	
dermatitis	refractory	to	steroids		(retinoid)
25
what is seborrhoeic dermatitis and treat,ment?
``` • Infants aged 3-8 months • Yellow, waxy scales on the scalp, thick and difficult to remove • Pink flaky patches on forehead, eyebrows, behind ears, nappy area • Due to developing sebum glands ``` • Infants – Emollients or mineral oils (for scalp) – Topical steroids with antifungal (for body) • Adults – Shampoos with ketoconazole, Zn pyrithione, Se sulfide (anti-yeast) – Steroid scalp lotions/mousses – Topical mild corticosteroids with salicylic acid (for scalp) – Topical mild corticosteroids with anti-yeast – creams/ ointments (clotrimazole, miconazole and nystatin) – Oral antifungals (severe cases)
26
what is a wound?
break in the epithelial integrity of the skin – may affect deeper layers even to bone
27
what are the diff types of wounds?
``` • Superficial – Damage to epithelium – Heals rapidly through regeneration of epithelial cells • Partial thickness – Involves dermal layer – Vascular damage • Full thickness – Involves subcutaneous fat and deeper – Longest time to heal – new connective tissue required – Contraction during healing ```
28
what are the 4 main stages of wound healing?
- bleeding - inflammation - proliferative - remodeling
29
what happens during wound healing
- injury to the skin leading to bleeding where a blot clot from to stop the bleeding - inflammation occurs to stop infection occurring so lots of immune cells come into the area and encourage new vessels - proliferation= making more connective tissue and pull the wound closed formed a new epidermal - remodelling to bring it back to normal decrease immune cells there
30
what are the cells and mediators involved in acute wound healing
- durining inflammation= neutrophils and macrophage they ll produce MMP ROS,IL,PDGF - GRANULATION=fibroblasts, macrophages, endotheial cels TNF,IL - Re-epithelialisation= keratinocytes, MMP, KGF, EGF - Tissue remodelling= fibroblasts, collagen , MMPs, TGf3
31
how does haemostatsis occur during would healing?
• Microvascular injury – blood seeps into wound • Injured vessels contract • Coagulation cascade activated by tissue factor • Clot formation and platelet aggregation • Platelets trapped in clot release PDGF, IGF, EGF, TGF-β which attract and activate fibroblasts, macrophages and endothelial cells • Also release serotonin, which increases vascular permeability
32
what is the early inflammatory phase?
• Activation of complement • Infiltration of neutrophils within 24-48h • Diapedesis into wound and phagocytosis of bacteria and foreign particles, with ROS and degrading enzymes – prevent infection • Dying cells cleared by macrophages or extrusion to wound surface
33
what is the late inflammatory phase?
• Blood monocytes arrive and become macrophages (48-72 hr) – key cell type for repair – cytokines and growth factors to recruit fibroblasts, keratinocytes and endothelial cells to repair damage – Collagenases to degrade tissue – Poor wound healing when inadequate monocytes/ macrophages • Lymphocytes enter wound (>72hr) and are involved in remodelling
34
what is the proliferative phase?
Fibroblast migration – produce fibronectin, hyaluronan, collagen, proteoglycans – Proliferate and construct new ECM • Collagen synthesis – strength and integrity • Angiogenesis – TGF beta and PDGF from platelets, TNF and bFGF from macrophages – Capillary sprouts invade fibrin/fibronectin-rich wound clot and organise microvascular network • Granulation tissue formation – Mainly proliferating fibroblasts, capillaries ,macrophages in matrix of collagen GAGs and fibronectin and tenascin • Epithelialisation – single layer of epidermal cells migrate from wound edges to form delicate covering, basal cells increase proliferation, new basement membrane – EGF stimulates epithelial mitogenesis and chemotaxis, bFGF and KGF stimulate proliferation
35
what is the remodelling phase?
• Matrix matures and remodels – Fibronectin and HA broken down – Collagen bundles increase in diameter and strength (80% of strength of original) – Ongoing collagen synthesis and breakdown by TGFbeta and MMPs – Collagen becomes more organised and shrink to bring wound margins closer together – Fibroblasts and macrophages apoptose – Capillary outgrowth halted and blood flow reduced – Acellular, avascular scar results
36
what are some local factors affecting wound healing?
* Pressure * Mechanical injury/Trauma * Infection/Foreign substances * Oedema * Necrosis * Topical agents * Lack of oxygen delivery (Ischemia) * Desiccation and dehydration
37
what are some systemic factors affecting wound healing?
``` Old age • Obesity • Chronic diseases eg diabetes, anemia • Connective tissue disorders • Immunosuppression • Smoking • Malnutrition • Vascular insufficiency • Stress • Radiation or chemotherapy ```
38
what are some causes of chronic wounds?
• Neuropathy – Diabetes mellitus, Spinal injuries • Ischemia – Atherosclerosis, PVD, Microangiopathy (DM) • Peripheral oedema – DVT, Varicose veins, renal or cardiac failure • Pressure – Poor mobility, spinal cord injuries, dementia, diabetes mellitus, old age, terminal illness • Other – Connective tissue disorders leading to vasculitis, Systemic diseases, malignancy, smoking, drugs such as corticosteroids and hydroxyurea
39
what are some clinical features of chronic wounds?
* Presence of necrotic and unhealthy tissue * Excess exudate and slough * Lack of adequate blood supply * Absence of healthy granulation tissue * Failure of re-epithelialisation * Cyclical or persistent pain * Recurrent wound breakdown * Clinical or sub-clinical infection
40
what is thr funcion of the skin?
* Protective barrier – physical and chemical * Involved in mechanical support * Prevents loss of moisture * Reduces harmful effects of uv radiation * Sensory organ – touch, temperature, pressure etc * Helps regulate body temperature * Immune organ to detect infections * Involved in production of vitamin D * Excretion of waste products
41
what is the anatomy of the skin?
epidermis>dermis>hypodermis
42
what are the major epidermis cell types?
``` Keratinocytes – Main cell type – Numerous layers – Stem cells • Merkel cells – Pressure, attached to nerves – Different locations in skin • Melanocytes – Melanin, protect from uv – Basal region • Langerhans cells – Immune - Dendritic cells – All layers of epidermis • T cells – CD8 positive ```
43
what are keratinocytes?
``` -theres stem cells in the stratum basale that Stem cells – self renew Rapidly proliferate – Responsible for replenishing tissue Differentiate into different cells -10-20µm 15-25 flattened, stacked hexagonal cornified cells (corneocytes) -Cells have died and lost nuclei Enriched lipids and keratin ```
44
how is the red oigment and brownpigment made in our skin?
- tyosinne is metabolised to dopa and then todopaquinone through tyrosinase - in the presense of cystein dopaquinen becomes pheomelanins that are the red pigment that people with freckles and red hair have more of - but dopaquinine can be metabolised to eventually for eumelanins that are the blackand brown pigemnt shown in darker skin
45
what is the dermis?
``` Middle skin layer, 1-6mm fibrous and elastic tissue. Made of connective tissue Supportive and cushioning tissue composed mainly of collagen (70%), elastin and fibrillin • Immune cells – several types • Number of structures found – Nerve endings – Blood vessels – Lymph vessels – Piloerector muscles – Hair follicles – Sweat glands – Sebaceous glands ```
46
what occurs in the subcutaneous tissue (hypodermis)?
Subcutaneous fat layer acts as a: – Mechanical protector – Thermal insulator – Energy store Heat regulation uses subcutaneous fat pad (hypodermis) and skin blood supply Thickness depends on whole body adiposity but need a minimal amount for skeletal and organ protection
47
what is the skin appendages?
where • Sweat glands • Oil glands • Hairs and follicles • Nails
48
what occurs to cause inflammation of the skin?
• Signal-mediated response to cellular insult by: – Infectious agents • Bacteria, Fungi, Viruses, Parasites etc – Toxins • Chemical, Radiation, UV, Biological etc – Physical stresses • Mechanical, Burns, Trauma, etc • Protective response – ultimate goal to remove initial cause of injury and consequences of injury – the necrotic cells and tissues
49
what is the skin microbiome?
``` • 1cm2 human skin contains up to 1b microorganisms – bacteria, fungi, viruses, mites • Beneficial – Protect against disease • Detrimental – Exacerbate skin lesions – Promote disease – Delay wound healing • Interact with host immune system – Bi-directional • Affected by lifestyles ```
50
how can there be a change in skin due to microbes?
- chnage in amount due to n the skin due to infection of long term antibiotic use or over growth - leads to inflammation in the skin producing proinflammatory cytokines which can damage the barrier to the skin allowing the immune system to infiltrate, disrupt physical barrier and microbes can infilitrate
51
how can there be a chnage to the skin due host biology?
-if they have a chronic illness like diabtete or wounds -chnages the microbl community that can be taken over by pathogens and they penearte to sterile tissues leading to inflammation leading to breakdown of barrier, impaired wound healing