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Bio regulatory systems 2 > Dermatology > Flashcards

Dermatology Flashcards

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1
Q

What are the 2 major parts of the skin and where do they devolop from?

A

There are 2 major parts that arise from embryological elements: EPIDERMIS-originates from the ECTODERM DERMIS-arises from the MESODERM that comes into contact with inner surface of the epidermis

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2
Q

What is the mesoderm essential for ?

A

inducing differentiation of epidermal structures e.g hair follicles

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3
Q

Describe the stages of skin development?

A

1-Epidermis forms by week 4- single basal layer of CUBOIDAL cells 2-Secondary layer of squamos, non keratinising cuboidal cells(periderm) develops in week 5. This layer generatrs a white waxy protective substance 3-Week 11 onwards =basal layer of cuboidal cells(stratum germinavum) proliferates to form multilayered intermediate zone-> four more superficial strata 4-Spinosum(spinous), granulosum (granular), lucidum(only found on palms of the hand and soles of the feet) and corneum(horny) develop 5-week 10-17 Epidermal ridges protrude as troughs into developing dermis beneath neurovascular supply and develops into dermal papillae 6-weeks 9-13 developmetn of hair follicles in stratum germinativum and appearence of lanugo hair

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4
Q

What are melanocytes?

A

melanin-producing cells in the skin

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5
Q

Where are melanocytes derived form?

A

NEURAL CREST

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6
Q

Describe the progression of melanoblasts?

A

1-dervied from NEURAL CREST 2-differentiate into MELANOBLASTS 3-Migrate dorsally between week 6-8 to developing epidermis (and dermis) and hair follicles 4-By week 12-13, most melanoblast have reached destination and differentiated into melanocytes 5-Subset of meloblasts form melancyte stem cells in hair follicle bulge that replenish differentiated melanocytes

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7
Q

What is the difference between melanoblasts that migrate ventrially vs dorsally?

A

Those that migrate dorsally become melancytes Those that migrate ventrially become glial cells

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8
Q

Describe the regulation of melanocytes?

A

Regulated by MC1R (Melanocortin 1 receptor), a g-protein coupled receptior that regulates the quantity and quality of the melanins produced: -controlled by AGONISTS AND ANTAGONISTS -Agonists-alpha-melanocyte stimulating hormone (aMSH) and adrenocorticotrophic hormone(ACTH) activates the MCR1=MELANOGENIC CASCADE= synthesis of EUMELANIN(found in darker skin and hair) -Antagonist AGOUTI SIGNALLING PROTEIN (ASP) reverses these effects and elicit production of PHEOMELANIN(found in pale complexions and blonde hair) -ACTH can also upregulate(increase ) the expression of the MC1R gene

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9
Q

What does exposure to UV do to the skin?

A

-Increases expression of the transcription factor MITF and downstream melanogenic proteins including Pmel17, MART-1, YR, TRP1 and DCT=increas in melanin content -Increased PAR2 in KERATINCYTES=increases uptake and distribution of melanosomes( transport of melanin) by

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10
Q

What are keratincytes?

A

an epidermal cell which produces keratin.

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11
Q

What is the brief structure of the skin?

A

Epidermis-superficial layer(top) Basement membrane-deraml-epidermal junction Dermis: -under the epidermis -connective tissue Subcutaneous fat-below dermis

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12
Q

Describe the structure of the epidermis?

A

Composed of KERATINOCYTES predominantly Layers from bottom to to(progressive differentiation and flattening occur as you go up): -Basal Layer -Stratum spinosum -Stratum granulosm -Statum Lucidum(extra layer in palms and soles only) -Stratum corneum(no nuclei or organelles)

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13
Q

Where does cell division occur in the epidermis?

A

BASAL layer

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14
Q

How long does the cellular progression from the basal layer upwards take?

A

30 days but is accelerated in certain skin disease such as psoriasis

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15
Q

What does thee filamentous cytoskeleton of each keratinocyte comprise off?

A

-Actin containing microfilaments -Tubulin containing microtubules -Intermediate filaments containing keratin

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16
Q

What are the 5 roles of keratin?

A

-Structural properties -Cell signalling -Stress response -Apoptosis -Wound healing

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17
Q

What are desmosomes?

A

-Major adhesion complex in epidermis -Anchor keratin intermediate filaments to cell membrane and bridge adjacent keratinocytes -Allow cells to withstand trauma

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18
Q

What are the different cell junction between Keratinocytes and what are there functions?

A

GAP JUNCTIONs: - contain cluster of intercellular channels called connexons -directly form connections between cytoplasm of adjacent keratinocytes -essential for cell synchronisation, cell differentiation, cell growth, and metabolic conditions ADHERENS junction: -Transmembrane structures -Engage with actin skeleton and hold the actin fibres together TIGHT junctions: -Play a role in barrier integrity and cell polarity

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19
Q

What are the other 4 cell types in the epidermis?

A

MELANOCYTES: -Dendritic -Distribute melanin pigament(in melanosomes) to keratinocytes LANGERHAMS: -dendritic-for immune surveillance -antigen presenting cells MARKELL CELLS: -mechanisensory receptors MAST CELLS: -role in allergic reaction

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20
Q

Describe the basement membrane?

A

-under epidermal -made of proteins and glycoproteins including collage 4 and 7, laminin and integrins

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21
Q

What are the 2 functions of the basement membrane ?

A

-Cell migration -Cell adhesion

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22
Q

What is the structure of the dermis?

A

PAPILLARY DERMIS(UPPER): -Superficial -loose connective tissue -vascular RETICULAR DERMIS: -Deep -Dense connective tissue -Forms the bulk of the dermis -less vascular supply

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23
Q

What is the dermis made of?

A

-80-85% = type 1 and 3 collagen -Elastic fibres-2-4% (elastin and fibrilin) -Glycoproteins-facilitate cell adhesion and cell motility -Ground substance between the collagen and elastic tissue -made of glycosaminoglycan/proteoglycan

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24
Q

What is the primary cell found in the dermis?

A

FIBROBLASTS-synthesises connective tissue

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25
Q

What other cells are present in the dermis?

A

Histiocytes-immune cells Mast cells Neutrophils Lymphocytes Dermal dendritic cells

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26
Q

describe the vascular supply of the skin?

A

Blood supply-composed of deep and superficial vascular plexus that so not cross into the epidermis

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27
Q

What 2 tyoes of fibres innervate the skin?

A

senosory AUTONOMIC INNERVATION of the skin by: ADRENERGIC fibres-innervate ECCRINE and APOCRINE glands(sweat glands that secrete substances by emptying them into a hair follicle) CHOLINERGIC fibres- which innervate the ECCRINE glands in the skin(sweat glands that secrete through a duct onto skin surface)

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28
Q

What is a pilosebaceous unit?

A

Hair follicle

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29
Q

What muscles are found in the skin?

A

Arrector pili muscles/arteroles/shunts

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30
Q

How many afferent nerve fibres are in the skin?

A

One million

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31
Q

What is the structure of nerves in the skin?

A

BRANCHING NETWORK often occompanying blood vessels to form a MESHG OF INTERLACING NERVES in superficial dermis

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32
Q

Which body parts have more innervation?

A

Face, extremities and genetilia

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33
Q

How do afferent nerves terminate?

A

CORPUSCULAR encapsulated nerve ending receptors (dermis) FREE non-encapsulated receptors (epidermis)

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34
Q

What specific nerve receptors are in the dermis?

A

MEISSNERS CORPUSCLE: -encapsulated -unmyelinated -mechanoreceptors -senses low frequency stimulation at level of the DERMAL PAPILLA -most concentrated in thick hairless skin(finger pads and lips) RUFFINI CORPUSCULE: -Slow acting mechanoreceptor -sensitive to skin stretch -Deeper in the dermis -Spindle shaped -high density around the fingernails -Monitor the slippage of objects PACINIAN CORPUSCLE: -encapsulated -Rapidly adapting mechanoreceptor -Deep pressure and vibration -vibrational role in detecting surface textures -most concentrated in the hands and the feet

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35
Q

What are the receptors in the epidermis?

A

MERKEL RECEPTOR: -Non-encapsulated -Mechanoreceptor -Light and sustained touch/pressure detection -Oval shaped -In modified epidermal cells-stratum basale directly above the basement membrane -Most populous in fingertips -Also in palms, sores, oral and genital mucosa

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36
Q

What is the microbiome?

A

gentetic content of the microbioto-bacteria, fungi, and viruses

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37
Q

How much bacteria do we have on the skin?

A

1 million bacteria/cm2 skin

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38
Q

What are the predominant bacteria on the skin?

A

-Actinobacteria(including propionibacteria and corynebacteria) -Firmicutes(Clostridia and Bacilli strahylococcus), Bacteroidetes and proteobacteria

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39
Q

why does the composition of microbiota on each niche of the skin vary?

A

They have different environments

40
Q

What is the function of the microbiota?

A

-immune modulation and epithelial health -some bacteria are pro inflammatory -role in disease

41
Q

What are the 6 functions of the skin?

A

-Immunological barrier -Physical barrier -Thermoregulationn -Sensation -Metabolic functions -Aesthetic appearence

42
Q

What is Erithraderma?

A

A rash that effects 90% of the surface area of the skin0 this can lead to skin failure=at risk of infections, fluid loss, hyperthermia etc

43
Q

How do immune barrier of the skin work?

A

LANGERHAN CELLS are in the epidermis and have an equivalent in the dermis called DERMAL DENDRITIC CELLS These rapidly respond to microbial threats and contribute to immune tolerance They have a dense network with which potential invaders MUST interact

44
Q

What do Langerhan cells do?

A

-specialised to sense the environment -extend their dendrites through INTERCELLULAR TIGHT JUNCTIONS to sample the outermost layers of the skin=(Stateum corneum) -Interpret microenvironmental context -determine appropriate quality of immune -In absense of danger promote the expansion and activation of skin resident regulatory cells -When sense danger(PAMP)=rapid initiation of innate antimicrobial responses and induction of adaptive responses(T-cells)

45
Q

What carries out immune surveillance in the dermis?

A

-Tissue resident T-cells -Macrophages -Dendritic cells

46
Q

What are endogenous antibiotics in the skin?

A

-Keratinocyte dervied -e.g Cathelicidin and defensins -iinate immune defense against bacteria, viruses and fungi -They can be chemotactic meaning they can attract immune cells OR they can directly kill bacteria

47
Q

How does the skin act as a physical barrier to the environment ?

A

-CORNIFIED CELL ENVELOPE and STRATUM CORNEUM restrict water and protein loss from the skin (this could lead to high output cardiac failure and renal failure in extensive skin disease -SUBCUTANEOUS FAT has important roles in cushioning trauma -UV BARRIER -MELANIN in basal keratinocytes-protection against UV induced DNA damage

48
Q

How does the skin carry out thermoregualtion?

A

1-increases blood temp identified by central receptors in skin 2-hypothalumus recieves input and activates SNS responses 3-Vasodialation of peripheral vessels and skin arterioles tot ransfer more heart to the skin surface 4-Activation of eccrine glands to begin sweating 5-Heat leaves the body and blood temperature lowers

49
Q

What are the metabolic functions of the skin?

A

-Vitamin D synthesis -Subcutaneous fat- Calorie reserve -Hormone LEPTIN release-sregulates hunger and energy metabolism

50
Q

How much of the total body fat is in the skin?

A

80%

51
Q

What effect does the aesthetic appearance of the skin have on us?

A

-effects suicide risk -Psychosexual function

52
Q

What are the 6 functions of the hair?

A

-protection of the external factors -Sebum-lubricating properties -Apocrine sweat(gives of scents) -Thermoregulation(can make hair stand up or relax) -Social and sexual interaction -Role in injury as it contains Epithelial and melanocyte STEM CELLS that help in recovery

53
Q

What are the different types of hair?

A

TERMINAL HAIRS- scalp, eyebrows, and eyelashes VELLUS HAIRS-everywhere else except palm soles, mucosal region of the lips ans external genitalia

54
Q

What are the 3 major parts of the hair cycle?

A

ANAGEN(where new hair forms and grows) -85% of hair in this phase -Lasts 2-6 years CATAGEN(regressing phase) -Hair is shrinking -1% of hair in this phase -Lasts 3 weeks TELOGEN (resting phase) -no hair growing -10-15% in this phase -lasts 3 months -Then loss of old hair after this phase and the cycle restarts

55
Q

What is the structure of hair?

A

Skin contains PILOSEBACEOUS FOLLICLES (hair follicles) and sweat glands -Hair follicles =pockets of epithelium continuous with superficial epidermis -Hair follicles envelop a small papila of dermis at the base which contains a capillary loop, a nerve fibre and a mucopolysacharide rich stroma -ARRECTOR PILI(smooth muscle), allows the hair to stand up -HOLOCRINE SEBACEOUS GLANDS(OIL GLANDS)-open into the pilary canal ->in axilae follicles assossiated with apocrine glands

56
Q

What can cause acne?

A

Hyperactive HOLOCRINE SEBACEOUS GLANDS

57
Q

What are the 2 sections of the hair follicle?

A

INFUNDIBULUM- from the opening of the sebaceous gland to the surface of the skin ISTHMUS- between bottom the SEBACEOUS gland and insertion of the ARRECTOR PILI muscle

58
Q

What does the epithelium keratinisation of the hair begin with?

A

involves creating an epithelium without the granular layer- ‘trichilemmal keratinisation’

59
Q

What is the bulge?

A

-segment of the outer root sheath located at insertion of arrector pili muscle -Hair follicle STEM CELLS are here

60
Q

What happens to Stem cells in hair follicles?

A

Stem cells MIGRATE downwards to generate anagen hair follicle-> enter hair bulb matrix and proliferate and undergo terminal differentiation to form hair shaft and inner root sheath

61
Q

Where do bulge cells move?

A

upwards to replenish the subaceous gland and proliferate in response to wounding

62
Q

What are the 3 main parts of the hair follicle?

A

BULB: -contains the dermal papila and hair matrix -lower portion of the hair follicle OUTER ROOT SHEATH: -reservoir of stem cells originating from the bulge -extends along from hair bulb to infundibulum and epidermis INNER ROOT SHEATH: -guides shape of hair -encloses follicular dermal papilla, mucopoysaccharide rich stroma, nerve fibre and capillary loop

63
Q

What are the functions of the nail?

A

-Protect the underlying DISTAL PHALAX -COUNTERPRESSURE EFFECT to pulp, important for walking and tactile sensation -INCREASE DEXTERITY/ manipulation of small objects -enhance SENSORY DISCRIMINATION -Facilitate scratching or grooming

64
Q

What is the structure of the nail and describe?

A

NAIL PLATE: -final product of proliferation and differentiation of nail matrix keratinocytes -emerges from proximal nail fold -Grows at 1-3mm/month -Firmly attatched to nail bed -Detatches at hyponychium -lined laterally by lateral nail folds NAIL MATRIX: -produce nail plate -Lies under proximal nail fold, above bone of distal phalanx(connected by a tendon) -Lunula only visible proportion -final product of keratinocytes that have lost their nuclei and are completely filled by hard keratins -Also contains melanocytes

65
Q

What is Psoriasis?

A

chronic immune mediated skin disorder -arises from a polygenietic predisposition combined with environmental triggers e.g.trauma, infections or medications

66
Q

What is a common characteristic of Psoriasis?

A

Sharply demarcated, scaly erythematous plaques

67
Q

Where are the common sites of Psoriasis

A

-Scalp, elbows, knees -then nails, hand and feet and trunk

68
Q

What is the most common systemic manifestation

A

Psoriatic arthritis Is also assosiated with liver disorders and IBD and is a risk factor for coronary artery disease

69
Q

Describe the pathophysiology of Psorisis?

A

1-stress to a keratinocytes=release of DNA or RNA 2-DNA and RNA forms COMPLEXES with antimicrobial peptides (andogineous antibiotics) 3-these complexes induce cytokine(TNF-alpha, IL-1, IFN-alpha) production which activate dermal dendritic cells(dDCs) 4-dDCs migrate to the lymph nodes to promote T helper cell subsets(Th1, Th17, Th22) which release chemokines (cytokines that attract inflammatory cells) 5-this causes the migration of inflammatory cells including CD8s and Neutrophils into the skin 6-These signal for the keratinocytes to proliferate resulting in chronic PSORIATIC PLAQUE

70
Q

What are some of the clinical feature of Psoriasis?

A

Genital psoriasis Flexural Psoriasis-not as scaly Palmoplantar Psoriasis-only on soles of hands and feet Subungual hyperkeratosis-too much scale under the nail plate Salmon pink patches-pink stains on nail Oncholysis-raising of the nail characterised by pitting(dints) in nail

71
Q

If a patient with Psoriasis shows clinical features in nails why is this important?

A

At a much higher risk of developing Psoriatic arthritis

72
Q

What is flexural Psoriasis and how is this commonly presented?

A

These don’t involve chronic plaque Erythrpderma-red skin

73
Q

What is Guttate Psoriasis

A

Classic presentation following streptococcheal throat infection, less chronic spotty red dotes on body

74
Q

What are 3 types of Psoriasis?

A

Flexural Guttate chronic plaque

75
Q

How do you manage Psoriasis ?

A

Change lifestyle factors first: -alcohol(psoriasis can cause liver inflammation and the medicine used can also affect the liver) -smoking(aggravates it ) Dermatologist: to deal with skin symptoms Rheumatologist: -joint symptoms Phycologist: -Depression -Sleep disorders/fatigue -Personality traits/coping All 3 of these specialists can help with: -Pain -Quality of Life -Work diabiltiy Rheum and Dherm can both help with: -Physical functioning -Comorbid diseases Early recognition and treatment is best

76
Q

What is the therapeutic ladder?

A

Match severity with treatment

77
Q

What are topical therapies?

A

For not as severe Psoriasis: -Vitamin D analogues -Topical corticosteroids -Retanoids(vitamin A analogues) -Topical tacrolimus/pinecrolimus

78
Q

What is Phototherapy?

A

Used to treat Psoriasis which is spread over a large amount of the body: -Narrowband UVB -PUVA (psoralen+UVA)

79
Q

What drug can be given to manage Psoriasis?

A

SYSTEMIC IMMUNOSUPRESSANTS: -Methotrexate -Ciclosporin -Fumaric acid esters -Apremilast ADVANCED THERAPIES(used if other things don’t work): -Biologic agents ( can target cytokines) -JAK inhibitors(cytokine inhibitors)

80
Q

What is atopic eczema?

A

-chronic inflammatory condition that is very ITCHY -complex genetic disease with environmental influences

81
Q

When is the onset of atopic eczema?

A

infancy or early childhood

82
Q

What is atopic eczema assossiated with?

A

other atopic disorders e.g. asthma, rhinoconjuctivitis

83
Q

What is another word for eczema?

A

dermatitus

84
Q

What are the symptoms of atopic eczema in infants vs children/adults?

A

Infants: -inflammation of cheeks, scalp, and extensors Children/adults: -Flexural inflammation -lichenification in children and adults

85
Q

How can you treat atopic eczema?

A

-Daily emollients and anti-inflammatory therapy

86
Q

What are the different types of eczema?

A

-Atopic -Seborrhoiec(dandruff) -venous stasis -allergic contact -irritant contact

87
Q

Describe the pathophysiology of eczema?

A

BARRIER DEFECT: -Mutations in protein called FILAGGRIN which binds and aggregates keratin bundles and intermediate filaments to form cellular scaffold in corneocytes in superficial layer of the skin -reduced extracellular lipids in this layer of the skin and impaired ceramide production=INCREASED TRANSEPIDERMAL water loss and impaired PROTECTION against environmental irritant, microbes and allergens -This can all lead to inflammation IMMUNE DISREGUALTION also occurs: -patients have lots of STAPHYLOCOCCUS AUREUS that stimulate Th2 responses and subvert T-regulatory cells(which normally dampen immune response)

88
Q

What are the clinical features of atopic eczema in different ages?

A

INFANTS: erythematous, oedematous papule and plaques -blisters leaving erosions Older: -Flexoral distribution -Lichenification(thickening of skin and exaggeration of skin lines) -crusting -dipigmentation -excoriation -fissuring-painful cracks due to dryness -allergy to things e.g nickel and cobalt -Impetiginisation

89
Q

What is Impetiginisation?

A

-Gold crust -caused by STAPHYLOCOCCUS AUREUS usually but also stephlococcus

90
Q

What does venous stasis eczema look like?

A

-have oedema(excess of watery fluid collecting in the cavities or tissues of the body)

91
Q

What does Eczema herpeticum present as?

A

Lots of red dots on the skin -is an emergency because they can spread to internal organs including the brain

92
Q

How can you treat Eczema herpeticum

A

Systemic IV antivirals

93
Q

How is atopic eczema managed?

A

Most important thing to do is support the barrier function because that is what is lost Lifestyle: -EMOLLIENT mositurisers- to replace moisture in skin -Omission of soap- dries out skin Multidisciplinary team e.g. Clincial Nurse specialist involvement: - teach patients how to correctly application technique of moisturiser -Habit reversal-e.g.scratching Multidisciplinary team - due to it being a co-morbidity disease: -Psychology -Nursing -Dermitology -Allergy paediatricians -dietary aggrevators in children affect the condition(Type 1 allergen) -Patch testing-to look for allergens in adults(type 4 allergens)

94
Q

If atopic eczema of the nipple does not respond to treatment what do you do?

A

BIOPSY -because you have to rule out the possibility of it being Padget’s disease- a type of breast cancer which clinically presents the same

95
Q

There is also a therapeutic ladder for the management of eczema…describe?

A

TOPICAL THERAPIES: -Topical corticosteroids-correct potency for the correct site -Retinoids(hand dermatitis)(given orally) -Topical tacrolimus/ pinecromilus(unlike steroids they cant thin out the skin) Phototherapy: -Narrow UVB -PUVA(hand dermititis)

96
Q

What drugs are given to eczema patients?

A

Systemic immunosuppressents: -Methotrexate -Ciclosporin -Azathioprine -Mycophenolate mofetil Advanced therapies: -Biologics(anti-IL-4-alpha, anti-IL13) -JAK inhibitors

Bio regulatory systems 2 (15 decks)

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