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Exam 1 Year 3 > Skin > Flashcards

Skin Flashcards

1
Q

What is the function of the skin?

A

-Protective barrier
-Mechanical support - skeleton
-Prevents loss of moisture
-Reduces UV radiation - melanin
-Sensory organ - detect and protect environmental fators
-Body temp regulation
-Immune organ to detect infections
-Vitamin D Synthesis
-Excretes waste - sweat

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2
Q

How often do the epithelial cells in the epidermis replace?

A

Every 2-3 days

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3
Q

Do epithelial cells have a blood supply?

A

No

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4
Q

What cells are within the epidermis?

A

Langerhans dendritic cells, Keratinocyte, Corneocyte, CD8+ T Cells, Melanocytes

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5
Q

Describe the Dermis?

A

Has two layers.
Vascular rich layer with specialised nerve endings which detect pressure and temperature changes, there is glands within the dermis layer.

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6
Q

What is the papillary layer of the dermis?

A

-20% of it, vascular rich oxygen is released in the bottom layers to retain the nuclei, there is lots of connective tissue which is rich in collagen, there is more exchange of nutrients and oxygen.

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7
Q

What is the Reticular layer of the dermis?

A

The remainder of the dermis, this is a dense irregular connective tissue, rich in elastin, fibrin and lots of immune cells.

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8
Q

Describe the Hypodermis?

A

This layer is composed of adipose tissue which acts as a physical, thermal and energy store.

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9
Q

How is heat regulated within the skin?

A

Heat regulation uses subcutaneous fat and skin blood supply, this thickness depends on the whole body adiposity and needs little for skeletal and organ protection.

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10
Q

What do Keratinocyte’s do?

A

At the beginning they have a nucleus and at the top layer they become dead and flaky. When they are dead they flake off, these are enriched with lipids and Keratin, this secreted IL-1B, which is important in homeostasis and inflammation.

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11
Q

What do Merkel cells do?

A

These are attached to sensory neurons and respond to pressure, they can be found in different locations in the skin.

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12
Q

What do Melanocytes do?

A

These are found in the basal region and produce melanin and protect the skin from UV light.

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13
Q

What do Langerhan cells do?

A

Immune dendritic cells, which are within all layers of the epidermis and act by sampling bacteria and determining self vs non-self.

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14
Q

What is the skin like at the face?

A

High density of sebaceous glands, hair and eccrine glands and is exposed to the diagram - sebaceous!

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15
Q

What is the skin at the palms of the hands like?

A

Thick stratum corneum, hairless and high density of eccrine glands (dry)

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16
Q

What is the skin like at the Axilla (Armpits)

A

Apocrine glands are present, high density of hair, this is an occluded humid environment.

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17
Q

Where is the skin microbiome and simply what does it do?

A

There is lots of this on the skin, it protects use against disease but can exacerbate skin lesions, promote disease and delay wound healing. They interact with the host immune system (bi-directional), this can be affected by our lifestyle.

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18
Q

What does skin microbiome do?

A

1) Directly inhibits pathogen growth by occupying space and nutrients therefore pathogens have no space for food. They produce AMPs and bactericidal compounds to kill pathogens and inhibit the formation of S.Aureus biofilm formation.
2) Educate and prime adaptive immunity by local cytokine production epigenetically prime APCs to educate adaptive immunity and influence regulatory T cells in the epidermis.
3) Enhance host innate immunity which increases AMP production, decreases inflammation after injury and strengthens epidermal barriers.

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19
Q

A wound which is damage to the epithelium, heals rapidly through regeneration of epithelial cells and is not bleeding, what wound is this?

A

Superficial

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20
Q

A wound which is damage to the dermal layer, and there is vascular damage - is bleeding. What wound is this?

A

Partial thickness

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21
Q

A wound which involves subcutaneous fat and deeper tissues, takes a long time to heal and new connective tissue is required, also causes a scar to form, is what type of wound?

A

Full Thickness

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22
Q

What are the four stages of wound healing?

A

1) Bleeding
-Injury, -haemostasis blood clot forms to stop bleeding.
2) Inflammatory
-Stops infection, immune cells come in. New blood vessels are formed.
3) Proliferative
-More connective tissue to replace damaged tissue and close a wound, there is a new delicate epithelial layer
4) Remodelling
-Normal, decrease in immune cells and a vascular scar is formed

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23
Q

How many days is a wound in the inflammation phase?

A

1-10 days

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24
Q

What day is the wound in the cell proliferation and matrix deposition?

A

Day 3

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25
Q

What day is there Matrix remodelling?

A

Day 10-14
-After 1 month, the area is strengthened can take up to one year to fully repair

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26
Q

What cells are involved in the Inflammation state of wound healing?

A

Neutrophils, Macrophages make MMPs, ROS, Hydrogen peroxide, IL, TNF, VEGF, TGFb, FGFm PDGF - Proinflammatory cytokines made and growth factors

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27
Q

What cells are involved in the granulation and neo-angiogenesis stage of wound healing?

A

Fibroblasts, Macrophages, Endothelial cells, MMPs, Prolyl hydroxylase, IL, TNF, TGFb, VEGf, PDGF, KGF

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28
Q

What cells are involve in the re-epithelisation stage of wound healing?

A

Keretinocytes, MMPs, EGF, KGF

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29
Q

What cells are involved in the tissue remodelling stage of wound healing?

A

Fibroblasts, Collagen fibre cross-linking, MMPs, TGFb

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30
Q

What are the steps of Haemostasis? (stopping of blood flow)

A

1) Injury, blood seeps into the wound
2) Injured vessels contract - limiting blood supply
3) Coagulation cascade is activated by tissue factor, this limits blood loss
4) Clot formation and platelet aggregation
5) Platelets trapped in clot release PDGF, IGF, EGF, TGF-b, which attract and activate fibroblasts, macrophages and endothelial cells.
6) Also serotonin is released which increases vascular permeability - cells are relaxed and this allows immune cells into the area.

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31
Q

What happens in the early inflammatory phase?

A

-Complement system activated
-Neutrophils infiltrate into the area within 24-48 hours
-Diapedesis (blood to capillary) into the wound and phagocytosis of bacteria and foreign particles, with ROS and degrading enzymes - this prevents infection
-Dying cells are cleared by macrophages or extrusion to wound surface

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32
Q

What happens in the late inflammatory phase?

A

-Blood monocytes arrive and become macrophages within 48-72 hours.
*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 the wound within 72 hours and are involved in remodelling

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33
Q

What do fibroblasts do in the proliferative phase of wound healing?

A

Rebuild
-Produce fibronectin, hyaluronan, collagen, proteoglycans,
-Proliferate and construct new ECM

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34
Q

What does collagen do in the proliferative phase of wound healing?

A

Collagen synthesis - provides strength and integrity

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35
Q

What happens in angiogenesis in the proliferative phase of wound healing?

A

TGF beta and PDGF from platelets, TNF and bFGF from macrophages
-Capillary sprouts invade fibrin/fibronectin-rich wound clot and organise microvascular network

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36
Q

What does granulation tissue formation mean in the proliferative stage of wound healing?

A

Mainly proliferating fibroblasts, capillaries, macrophages in the matrix of collagen GAGs and fibronectin and tenascin.

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37
Q

What does epithelisation mean in the proliferative stage of wound healing?

A

-Single layer of epidermal cells migrate from wound edges to form a delicate covering, basal cells increase proliferation, new basement membrane.
-EGF stimulates epithelial mitogenesis and chemotaxis, bFGF and KGF stimulate proliferation

38
Q

What happens in the remodelling phase of wound healing?

A

Matrix matures and remodels
-Fibronectin and HA broken down
-Collagen bundles increase in diameter and strength
-Ongoing collagen synthesis and breakdown by TFG-b and MMPs
-Collagen becomes more organised and shrinks to bring wound margins closer together
-FIbroblasts and macrophages apoptose
-Capillary outgrowth halted and blood flow reduced
-Acellular, avascular scar results

39
Q

What happens when wounds don’t go back to normal?

A

Chronic wound and impaired healing, which is when inflammatory or proliferative stages of healing are disrupted.
-This can be because of disturbances in growth factors, too many cytokines, proteases and cells.
-The cells won’t leave the area

40
Q

What local factors can affect wound healing?

A

pressure, mechanic injury or trauma, infection or foreign substances, oedema, necrosis, topical agents, lack of oxygen delivery (Ischemia), desiccation and dehydration.

41
Q

What causes chronic wounds?

A

*neuropathy - DM/Spinal injury
*ischemia - atherosclerosis, PVD
*peripheral oedema - DVT/Varicose veins, renal/heart failure
*pressure - poor mobility
*other - connective tissue disorders

42
Q

What do chronic wounds look like?

A

-Necrotic and unhealthy tissue
-Excess exudate and slough
-Lack of adequate blood supply
-Absence of healthy granulation tissue
-Failure of re-epithelisation (keeps breaking)
-Cyclical or persistent pain
-Recurrent wound breakdown
-Clinical or sub-clinical infection

43
Q

How can neuron damage in a diabetic patient cause an ulcer?

A

1) Muscle atrophy –> Change in gait* –> New pressure distribution –> Ulcer –> Infection –> Gangrene –> Ischaemia –> Chronic ulcer
2) Bone changes –> deformed foot –> Change in gait*

44
Q

How can painless trauma cause diabetic ulcers?

A

Painless trauma –> ulcer –> Infection –> Gangrene –> Ischaemia –> Chronic ulcer

45
Q

How can your skin drying out cause diabetic ulcers, through the autonomic system?

A

Decreased sweating –> Dry skin with cracks –> Infection –> Gangrene –>Ischaemia –> Chronic ulcer

46
Q

What are the conditions which can cause dry, irritated and inflamed skin?

A

Eczema / Dermatitis

47
Q

I am a chronic disorder with flare ups and remissions, I may clear up for a long period of time. I am a type 4 allergic reaction. I often occur in patients which have asthma or hay fever, I commonly affect the knees, elbows, wrists, neck or face. I affect cheeks in infants, what am I?

A

Atopic Dermatitis

48
Q

What is in the Atopic Triad

A

Hay fever
Asthma
Atopic Dermatitis

49
Q

What gene has a defect with atopic eczema?

A

Filaggrin Gene - which maintains the skin barrier

50
Q

What is the MOA for Atopic Eczema?

A

1) Uptake of allergen by dendritic cells
2) MHC class 2 present and attracts Th1 cells,
3) Th2 now makes IgE a a switch occurs
4) IgE produced, travels in the blood via the B cell’s
5) Mediators of acute and chronic inflammation are released
6) Mast cell stimulation

51
Q

Pt A has the following symptoms:
Dry skin worsens with stress
Itching which can be severe at night
Red/Brown grey pathces which become thick
Broken skin
Often gets infected skin and sores which break the skin
What is the likely diagnosis?

A

Atopic Eczema

52
Q

How does Tacrolimus work?

A

Inhibits T-Cell response and prevents IL-4 secretion

53
Q

What type of allergic response is Allergic Contact Dermatitis?

A

Type 4

54
Q

What type of dermatitis has this MOA?
1) Allergen
2) Dendritic cells
3) T-cell lymph nodes
4) IgE class switching
5) Mast cell
6) Pro-inflammatory mediators
7) Cells in adaptive immune response are ON
8) Cytokines

A

Atopic dermatitis

55
Q

What type of dermatitis follows this MOA?
1) Irritant
2) Keratin sites affected
3) On and secreting pro inflammatory IL-1, IL-8, TNF - Dendritic cells (local response)
4) Vasodilation
5) Cell recruitment to skin (Neutrophils/lymphocytes)
6) Local inflammatory Innate response

A

Irritant contact dermatitis

56
Q

What type of dermatitis follows this MOA?
Adaptive and Innate

Adaptive
1) T-cells
2) T-regs
3)Mast cells and proinflammatory

Innate
1) Keratinocytes
2) Vasodilation and cell recruitment

A

Allergic contact dermatitis

57
Q

What condition is due to an overgrowth of Malassezia yeasts, and can trigger red, itchy inflamed rash on the scalp?

A

Seborrheic Dermatitis

58
Q

What shampoo can be used for the treatment of Seborrheic dermatitis in an adult?

A

-Ketoconazole, Zn pyrithione, Se sulfide (Anti-yeast)
-Steroid scalp lotions/mousses
-Topical milkd corticosteroids with salicylic acid
-Clotrimazole, Miconazole and nystatin
-Oral antifungals in extreme cases

59
Q

Pt N, Has a round oval blister with dry lesions, on the lower leg. What is this and what can be given to treat this?

A

Nummular (Discoid) Dermatitis
Treat with –> Emollients, steroids, antibiotics and phototherapy

60
Q

Pt SD has varicose veins, and is mildy overweight, they have fragile, thin, shiny inflamed itchy skin which is flaky, what is this likely to be?

A

Stasis dermatitis

61
Q

Pt DS, is 30 years old and has tiny itchy blisters on there hands and feet, which they found is worse when it is hot or they are stressed, what is this?

A

Dyshidrotic dermatitis

62
Q

I am a chronic autoimmune, inflammatory skin disease which has periods of remission and relapse, I can cause arthritis, what am I?

A

Psoriasis

63
Q

I am red, itchy, and form sore plaques with white or silvery scales which are well defined, what type of psoriasis am I?

A

Plaque psoriasis

64
Q

Pt B has lots of red tear drop spots across there back, they have recently been told they have strep throat, what is this?

A

Guttate

65
Q

Pt P, has small white and yellow filled blisters on there palms of hands and soles of feet, what type of dermatitis am I?

A

Pustular

66
Q

I affect the nails and can be often misunderstood for a fungal infection, I can cause nail discolouration, pitting, crumbling, cracking, splitting and nail detachment. What am I?

A

Nail Psoriasis

67
Q

How long do Keratinocytes take to shed in a patient with Psoriasis?

A

3-4 days

68
Q

What is the cycle of events which lead to psoriasis flare up?

A

1) Pt has genetic dispotition IL-23R/IL-12B or Stress
2) Keratinocyte cells become stressed
TWO paths occur
Path 1
1) Antimicrobial peptides IL-37
2) Release of DNA
3) Combines to make complexes Autoantigens
4) Not recognised by the immune system
5) The dendritic cells take up and present
6) IL-23 T-cells are ON
7) Th1 cells cause a response
8)IfG = dendritic and leukocytes are active
9) Inflammation chemokines
10) Allow macrophages in
-Clonal expansion
-Proinflamm production of EGF = hyperproliferation
=Increase in collagen
-Made very fast and cannot be shed off causing more neutrophils and more inflammation
Path 2
-Break and make pro-inflammatory cytokines –> Release DNA –> Activate dendritic cells –> Resulting in step 10!

69
Q

What medicines are vitamin D derivatives?

A

Calciprotriol, Tacalcitol, Calcitriol

70
Q

What type of mediation is a Vitamin A Derivative?

A

Acitretin

71
Q

What Anti-TNF are used for Psoriasis?

A

Infliximab, Adalimumab, Etanercept, Certolizumab

72
Q

What Anti-IL23 are used for Psoriasis?

A

Ustekinumab, Guselkumab, Rizankizumab, Tildrakizumab

73
Q

What Anti-IL17 are used for Psoriasis?

A

Secukinumab, Brodalumab, Ixekizumab

74
Q

What type of Psoriasis often causes arthritis?

A

Nail

75
Q

What JAK inhibitor is used for psoriatic arthritis?

A

Tofacitinib

76
Q

What anti-PDE4 is used for psoriatic arthritis?

A

Apremilast

77
Q

What are the signs of Melanoma?

A

Asymmetry
Border is irregular
Colour variation
Diameter more than 6mm
Evolving - changing shape, size, colour, lifting from skin, bleeding, itching, crusting

78
Q

What are warts caused by?

A

Hyman Papillomavirus

79
Q

Pt is young and has blisters and sores, on the nose and mouth, these leave a yellow/brown crust, what are they?

A

Impetigo - Non-bullous

80
Q

Pt has fluid-filled blisters that burst after a few days leaving a yellow crust, these are on the trunk of the patient, what is this?

A

Impetigo - Bullous

81
Q

What can cause a fungal infection?

A

Athletes foot
Ringworm
Contaminated floors
Nail infections

82
Q

What is the site of action for medicines applied to the skin?

A

Often lower layer of epidermis or dermis, so has to pass through lipid rich layers of epidermis

83
Q

What enhances absorption through skin in transdermal patches?

A

Skin glucocorticoid which has fatty acid esters

84
Q

What are the five target regions in dermatology?

A

1) Surface treatment - protective layer
2) Stratum Corneum - Epidermis layer
3) Skin Appendage
4) Viable Epidermis-Dermis
5) Systemic treatment - transdermal

85
Q

What are the advantages of transdermal skin patches?

A

-Avoids first pass metabolism
-Consistent site of absorption
-Constant drug input rate
-Can stop dose by removing patch

86
Q

Low amounts of drugs cross the skin meaning that most drugs delivered trans dermally are potent, and have a very low minimum effective concentration, True or False?

A

True

87
Q

What do retinoids do?

A

Vitamin A analogues
-Disturb vitamin A metabolism and disrupt skin homeostasis

88
Q

Tretinoin, isotretinoin, aliteretinoin, tazarotene, adapalene are all examples of what?

A

Vitamin A Analogues

89
Q

What is the MOA of Vitamin A Analogues?

A

Bind to RXR and RAR nuclear receptors in keratinocytes and sebaceous glands to decrease cell proliferation and sebum production. They have anti-inflammatory effects through pleiotropic actions on the immune system

90
Q

What class of drug is Calciriol?

A

Vitamin D Analogue

91
Q

What is the MOA of Vitamin D analogues?

A

Act via VDR to modulate gene transcription in keratinocytes, fibroblasts, Langerhan cells and sebaceous glands. They are anti-proliferative an pro-differentiative effects in keratinocytes.
-Inhibit T cell activation.

Exam 1 Year 3 (40 decks)

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