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Dermatology > Posters- week 1 derm > Flashcards

Posters- week 1 derm Flashcards

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1
Q

4 factors that contribute to the skin as an immunological organ

A

Keratin layer
Immune cells (keratinocytes and langerhan cells)
Chemical signals (chemokines and cytokines)
Genetics

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2
Q

What is the role of keratinocytes?

A

Sense pathogens via cell surface receptors
Help mediate the immune response
Produce antimicrobial peptides
Produce cytokines

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3
Q

What is the role of Langerhan cells

A

Dendritic cells
Antigen presenting cells- present antigen to effector T cells
Produce cytokines and chemokines

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4
Q

Healthy skin contains a large number of T cells. T or F

A

True

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5
Q

Which type of T cells are present in the epidermis and then the dermis

A

Epidermis- CD8 +

Dermis- CD4 and CD8+

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6
Q

What is the role of helper T cells?

A

Release chemical mediators

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7
Q

What is the role of cytotoxic T cells

A

Kill directly

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8
Q

Class 1 major histocompatibility complex

A

Found on almost all cells. Present antigen to cytotoxic T cells

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9
Q

Class 2 major histocompatibility complex

A

Found on antigen presenting cells and T helper cells.

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10
Q

Types of cells that exist in the dermis

A 
Dermal dendritic cells
Plasmacytoid dendritic cells
Mast cells
Macrophages 
Neutrophils
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11
Q

Plasmacytoid dendritic cells role

A
  • produce IFN alpha- found in diseased skin
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12
Q

Dermal dendritic cells role

A

involved in antigen presentation and secreting chemokines

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13
Q

Quick immunology of psoriasis

A

Mix between genetics and the environment. The keratinocytes are under stress the plasmacytoid dendritic cells release IFN alpha. The T cells then arrive and this stimulates keratinocyte proliferation.
‘Wound that keeps healing’

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14
Q

Quick immunology of eczema

A

Develop sensitisation to allergen and mast cells mass degranulate to produce an inflammatory response.

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15
Q

Describe a type 1 hypersensitivity reaction

A

IgE mediated

Mast cells bind to IgE releasing inflammatory mediators

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16
Q

Describe a type 2 hypersensitivity reaction

A

IgG mediated

Antibody is directed against cell surface antigens-causing cell destruction.

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17
Q

Describe a type 3 hypersensitivity reaction

A

Immune complex mediated

Antigen-antibody complexes are deposited. This activates complement causing inflammation.

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18
Q

Describe a type 4 hypersensitivity reaction

A

Cell mediated

Sensitised T helper cells release cytokines that activate macrophages causing direct cell damage.

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19
Q

Example of type 1 HS reaction

A

Allergy e.g. hay fever

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20
Q

Example of a type 2 HS reaction

A

Blood transfusion

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21
Q

Example of a type 3 HS reaction

A

Glomerular nephritis

Necrotising fasciitis

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22
Q

Example of a type 4 HS reaction

A

Graft rejection.

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23
Q

Describe the process of someones immune system when they are exposed to nuts.

A

Nut exposure
Dendritic cells present the antigen to T helper cells. They then present it to B cells which produce nut specific IgE.
If these then attach to mast cells you get mass degranulation.

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24
Q

Clinical presentation of allergy

A

Anaphylaxis
Angioedema- localised swelling of subcutaneous tissue
Urticaria- red itchy rash, ‘wheals and hives’. Appear within one hour of exposure
Wheezing

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25
Q

What investigations would you do into allergy?

A 
History
RAST- looks for specific IgE
Skin prick or prick prick testing
Challenge test
Serum mast cell tryptase (during anaphylaxis)
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26
Q

Advantages of skin prick test

A

Cheap and quick
Very small chance of anaphylaxis (1/3000)
Sensitive and specific

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27
Q

Challenge test

A

Only used if skin prick and prick prick test are negative. involves gradual introduction of antigen.

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28
Q

Management of allergy

A 
Allergen avoidance
Corticosteroids (anti inflammatory)
Mast cell stabilisers (sodium cromoglycate)
Immunotherapy
Adrenaline for anaphylaxis
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29
Q

Dosage of adrenaline in anaphylaxis

A

300ug in adults

150 in children

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30
Q

Describe type 4 allergy

A

It is a delayed hypersensitivity reaction.
Haptens (a small molecule that can bind to proteins eliciting the production of antibodies) activate the innate immune system.
Dendritic cells present the antigen to T cells
T cells kill haptens and cause inflammation.

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31
Q

Investigations into type 4 allergy

A

Patch testing- allergens put in special chambers and are applied to the patients back for 48 hours)

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32
Q

Drugs can get across the stratum corneum. T or F.

A

F- drugs have to bypass the stratum corneum.

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33
Q

What is the stratum corneum

A

The top layer of dead keratinocytes.

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34
Q

Why do drugs need to penetrate the stratum corneum?

A

They won’t have an effect without this.

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35
Q

What is rate of absorption denoted by?

A

Ficks law

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36
Q

What is Ficks law?

A

J (flux/rate of absorption)= KpCy
Kp= permeability co-efficient
Cy= Concentration of drug in vehicle

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37
Q

What does the permeability co-efficient encompass?

A

Partition co-efficient, diffusion co-efficient and the length of the diffusion pathway.

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38
Q

Why is the permeability co-efficient important clinically?

A

Because the partition co-efficient and the diffusion co-efficient change depending on which vehicle the drug is in.

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39
Q

What is the stratum corneum model often referred to as?

A

Brick and mortar model.

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40
Q

How can you make a drug more soluble?

A

Include excipients e.g. propylene glycol

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41
Q

How else can you make a drug more effective?

A

Reduce the barrier function of the stratum corneum by hydrating the skin by occlusion.

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42
Q

Describe transdermal delivery

A

Drug is incorporated into an adhesive patch and applied to the epidermis. Drug release is partially controlled by a drug release membrane.

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43
Q

Which drugs are suitable for transdermal delivery

A

Low molecular weight
Moderately lipophilic
Potent
Relatively short half life.

44
Q

What is irritatant contact dermatitis

A

Non immunological process

Contact with agents that abrade, irritate or traumatise the skin.

45
Q

Macule

A

Small flat lesion, change in colour (<10mm)

46
Q

Papule

A

Small, elevated lesion that can be felt or palpated (<10mm)

47
Q

Plaque

A

Palpable lesion >10mm that are elevated or depressed

48
Q

Nodule

A

Firm papule or lesions that extend into the dermis or subcutaneous tissue.

49
Q

Vesicles

A

Small, clear fluid filled vesicles <10mm

50
Q

Bullae

A

Clear fluid filled blisters >10mm

51
Q

Pustules

A

Vesicles containing pus.

52
Q

Atrophy

A

Thinning of the skin

53
Q

Purpura

A

Large area of haemorrhage that may be palpable

54
Q

Petechiae

A

Small haemorrhage

55
Q

Ulcers

A

Loss of epidermis and at least part of the dermis

56
Q

Erosions

A

Open areas of the skin from loss of the epidermis.

57
Q

Porphyrias

A

A group of disorders that result from a build of natural chemicals that produce porphyrin in the body. These are essential for the function of haemoglobin.

58
Q

Name some porphyrias

A

Severe congenital porphyrias
Acute attack porphyrias
Blistering and fragility skin porphyrias
Phototoxic skin porphyrias

59
Q

What do all porphyrias have in common?

A

All give sensitivity to sunlight exposure.

60
Q

Porphyria cutanea tarda (PCT) presentation

A 
Blistering
Fragility
Hyperpigmentation
Solar urticaria (urticaria on exposure to UV)
Hypertrichosis- excessive hair growth
Morphoea- painless discoloured patches.
61
Q

Investigations into PCT

A

Wood lamps (shows up differently on these)

62
Q

Management of PCT

A

Decide underlying cause e.g. alcohol, viral hepatitis, oestrogen, haemachromatosis
and treat this cause

63
Q

Presentation of erythropoietic protoporphyria (EPP)

A

Generally presents in childhood
Skin becomes very painful (itching and burning)
May cause swelling

64
Q

What is EPP

A

Deficiency of enzyme which normally confers protoporphyrin to haem by adding iron to it.

65
Q

Investigations into EPP

A

Quantitive RBC porphyrins
Flurocytes (patients relatives)
Transaminases

66
Q

Management of EPP

A

Genetic counselling

Visible light photoprotection

67
Q

What should you consider in your differential of acute intermittent porphyria

A

Acute abdomen
Mononeuritis multiplex
Gullian Barre syndrome
Pyschoses.

68
Q

How would you manage a drug eruption

A

Stop drug
Topical steroids
Antihistamines
Report

69
Q

Type 1 hypersensitivity in response to drugs presentation

A

Urticaria and blistering rash

70
Q

Type 2 hypersensitivity reaction in response to drugs presentation

A

Cytotoxic reaction

Pemphigus and pemphigoid

71
Q

Type 3 hypersensitivity reaction in response to drugs presentation

A

Often vasculitic type rash

72
Q

Type 4 hypersensitivity reaction in response to drugs presentation

A

Erythema/rash

73
Q

Exathematous drug eruptions

A

90% of drug eruptions
Usually mild and self limiting
Widespread, symmetrically distributed rash sparing the mucous membranes. Priuritis and mild fever are common.

74
Q

When would you think an exanthematous drug reaction is severe?

A 
Involves mucous membranes
Facial oedema and erythema
Fever
Blisters, purpura, necrosis
Wheezing/ SOB
Lymphadenopathy
75
Q

Fixed drug eruptions presentation

A

Round/ovoid plaques
Red and painful
Involves the hands, genitalia, lips and occasionally the oral mucosa.

76
Q

Pustular/bullous drug eruptions

A

Acne- in response to glucocorticosteroids
Androgens- therapeutic
Acute generalised exanthematous pustulosis (AGEP)- rare, caused by antibiotics and calcium channel blockers.

77
Q

What is virulence

A

Capacity of a microbe to cause damage to a host

78
Q

What does a microbe need to be to become highly virulent

A

Adhesin- able to bind to the host
Invasin- enables the organism to invade host tissues
Impedin- enables organism to avoid host defence mechanisms
Agressin- causes damage to the host directly
Modulin- induces damage indirectly

79
Q

What makes up the epidermis (cell arrangement)

A

Stratified squamous epithelium

80
Q

4 layers of the epidermis from superficial to deep

A

Keratin
Granular
Prickle cell
Basal

81
Q

Cells that make up the epidermis

A

Keratinocytes
Melanocytes
Merkel cells
Langerhan cells

82
Q

Function of the keratin layer

A

Forms waterproof barrier

Also known as the stratum corneum,

83
Q

What makes up the granular layer

A

Alive keratinocytes
2-3 layers
Contains keratinohylin and structural filagrin and involucrin proteins
High lipid content

84
Q

What makes up the prickle cell layer

A

Large polyhedral cells

Lots of desmosomes connected by intermediate filaments

85
Q

What makes up the basal layer

A

Usually one cell thick.

Lots of intermediate filaments

86
Q

The basal layer isn’t metabolically active. T or F

A

F- the basal layer is highly metabolically active.

87
Q

Describe keratinocytes

A

Building blocks of tough fibrous protein keratin

88
Q

Describe melanocytes

A

Pigment producing dendritic cells- synthesis melanin.

89
Q

Where are melanocytes present

A

In the basal layer and above

90
Q

What do melanocytes do?

A

Convert tyrosine to melanin pigment

91
Q

eumelanin

A

Brown or black melanin pigment

92
Q

Phaeomelanin

A

Red or yellow melanin pigment

93
Q

Describe langerhan cells

A

Immune cells that ingest pathogens

Antigen presenting cells

94
Q

Where were langerhan cells made and where do they live now?

A

Made in the bone marrow. Now in the prickle cell layer.

95
Q

Describe merkel cells

A

Sit between keratinocytes and nerve fibres

Combine with nerve endings to create a sensory receptor for touch.

96
Q

Where are Merkel cells found?

A

Basal layer

97
Q

Describe the three phases of growth of a hair follicle

A

Anagen- growing phase
Catagen- Involuting
Telogen-resting phase

98
Q

Which muscle moves the hair follicle

A

Arrector pilli muscle

99
Q

What makes up the dermis

A

Fibres
Ground substance
Blood vessels, lymphatics, nerves
Cells- fibroblasts, macrophages, mast cells, langerhan cells and lymphocytes

100
Q

Fibroblasts function in the dermis

A

Secrete collagen

101
Q

Macrophages function in the dermis

A

Antigen presentation

102
Q

Sensor for pressure

A

Pacinian

103
Q

Sensor for vibration

A

Meissners

104
Q

Three types of glands in the skin

A

Sebaceous
Apocrine
Eccrine

105
Q

Sebaceous glands

A

Widely distributed
Hormone sensitive
Produce sebum, squalene, wax esters, triglycerides and FFA

106
Q

Apocrine glands

A

Develops as part of the pilosebaceous unit
Found in the axilla and perineum
Androgen dependent- produce oily fluid

107
Q

Eccrine glands

A

Sweat glands
Sympathetic cholinergic nerve supply
Stimulated by mental, thermal and gustatory

Dermatology (21 decks)

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