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Dermatology > Posters- week 1 derm > Flashcards

Posters- week 1 derm Flashcards

(107 cards)

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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
What investigations would you do into allergy?
``` History RAST- looks for specific IgE Skin prick or prick prick testing Challenge test Serum mast cell tryptase (during anaphylaxis) ```
26
Advantages of skin prick test
Cheap and quick Very small chance of anaphylaxis (1/3000) Sensitive and specific
27
Challenge test
Only used if skin prick and prick prick test are negative. involves gradual introduction of antigen.
28
Management of allergy
``` Allergen avoidance Corticosteroids (anti inflammatory) Mast cell stabilisers (sodium cromoglycate) Immunotherapy Adrenaline for anaphylaxis ```
29
Dosage of adrenaline in anaphylaxis
300ug in adults | 150 in children
30
Describe type 4 allergy
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.
31
Investigations into type 4 allergy
Patch testing- allergens put in special chambers and are applied to the patients back for 48 hours)
32
Drugs can get across the stratum corneum. T or F.
F- drugs have to bypass the stratum corneum.
33
What is the stratum corneum
The top layer of dead keratinocytes.
34
Why do drugs need to penetrate the stratum corneum?
They won't have an effect without this.
35
What is rate of absorption denoted by?
Ficks law
36
What is Ficks law?
J (flux/rate of absorption)= KpCy Kp= permeability co-efficient Cy= Concentration of drug in vehicle
37
What does the permeability co-efficient encompass?
Partition co-efficient, diffusion co-efficient and the length of the diffusion pathway.
38
Why is the permeability co-efficient important clinically?
Because the partition co-efficient and the diffusion co-efficient change depending on which vehicle the drug is in.
39
What is the stratum corneum model often referred to as?
Brick and mortar model.
40
How can you make a drug more soluble?
Include excipients e.g. propylene glycol
41
How else can you make a drug more effective?
Reduce the barrier function of the stratum corneum by hydrating the skin by occlusion.
42
Describe transdermal delivery
Drug is incorporated into an adhesive patch and applied to the epidermis. Drug release is partially controlled by a drug release membrane.
43
Which drugs are suitable for transdermal delivery
Low molecular weight Moderately lipophilic Potent Relatively short half life.
44
What is irritatant contact dermatitis
Non immunological process | Contact with agents that abrade, irritate or traumatise the skin.
45
Macule
Small flat lesion, change in colour (<10mm)
46
Papule
Small, elevated lesion that can be felt or palpated (<10mm)
47
Plaque
Palpable lesion >10mm that are elevated or depressed
48
Nodule
Firm papule or lesions that extend into the dermis or subcutaneous tissue.
49
Vesicles
Small, clear fluid filled vesicles <10mm
50
Bullae
Clear fluid filled blisters >10mm
51
Pustules
Vesicles containing pus.
52
Atrophy
Thinning of the skin
53
Purpura
Large area of haemorrhage that may be palpable
54
Petechiae
Small haemorrhage
55
Ulcers
Loss of epidermis and at least part of the dermis
56
Erosions
Open areas of the skin from loss of the epidermis.
57
Porphyrias
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
Name some porphyrias
Severe congenital porphyrias Acute attack porphyrias Blistering and fragility skin porphyrias Phototoxic skin porphyrias
59
What do all porphyrias have in common?
All give sensitivity to sunlight exposure.
60
Porphyria cutanea tarda (PCT) presentation
``` Blistering Fragility Hyperpigmentation Solar urticaria (urticaria on exposure to UV) Hypertrichosis- excessive hair growth Morphoea- painless discoloured patches. ```
61
Investigations into PCT
Wood lamps (shows up differently on these)
62
Management of PCT
Decide underlying cause e.g. alcohol, viral hepatitis, oestrogen, haemachromatosis and treat this cause
63
Presentation of erythropoietic protoporphyria (EPP)
Generally presents in childhood Skin becomes very painful (itching and burning) May cause swelling
64
What is EPP
Deficiency of enzyme which normally confers protoporphyrin to haem by adding iron to it.
65
Investigations into EPP
Quantitive RBC porphyrins Flurocytes (patients relatives) Transaminases
66
Management of EPP
Genetic counselling | Visible light photoprotection
67
What should you consider in your differential of acute intermittent porphyria
Acute abdomen Mononeuritis multiplex Gullian Barre syndrome Pyschoses.
68
How would you manage a drug eruption
Stop drug Topical steroids Antihistamines Report
69
Type 1 hypersensitivity in response to drugs presentation
Urticaria and blistering rash
70
Type 2 hypersensitivity reaction in response to drugs presentation
Cytotoxic reaction | Pemphigus and pemphigoid
71
Type 3 hypersensitivity reaction in response to drugs presentation
Often vasculitic type rash
72
Type 4 hypersensitivity reaction in response to drugs presentation
Erythema/rash
73
Exathematous drug eruptions
90% of drug eruptions Usually mild and self limiting Widespread, symmetrically distributed rash sparing the mucous membranes. Priuritis and mild fever are common.
74
When would you think an exanthematous drug reaction is severe?
``` Involves mucous membranes Facial oedema and erythema Fever Blisters, purpura, necrosis Wheezing/ SOB Lymphadenopathy ```
75
Fixed drug eruptions presentation
Round/ovoid plaques Red and painful Involves the hands, genitalia, lips and occasionally the oral mucosa.
76
Pustular/bullous drug eruptions
Acne- in response to glucocorticosteroids Androgens- therapeutic Acute generalised exanthematous pustulosis (AGEP)- rare, caused by antibiotics and calcium channel blockers.
77
What is virulence
Capacity of a microbe to cause damage to a host
78
What does a microbe need to be to become highly virulent
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
What makes up the epidermis (cell arrangement)
Stratified squamous epithelium
80
4 layers of the epidermis from superficial to deep
Keratin Granular Prickle cell Basal
81
Cells that make up the epidermis
Keratinocytes Melanocytes Merkel cells Langerhan cells
82
Function of the keratin layer
Forms waterproof barrier | Also known as the stratum corneum,
83
What makes up the granular layer
Alive keratinocytes 2-3 layers Contains keratinohylin and structural filagrin and involucrin proteins High lipid content
84
What makes up the prickle cell layer
Large polyhedral cells | Lots of desmosomes connected by intermediate filaments
85
What makes up the basal layer
Usually one cell thick. | Lots of intermediate filaments
86
The basal layer isn't metabolically active. T or F
F- the basal layer is highly metabolically active.
87
Describe keratinocytes
Building blocks of tough fibrous protein keratin
88
Describe melanocytes
Pigment producing dendritic cells- synthesis melanin.
89
Where are melanocytes present
In the basal layer and above
90
What do melanocytes do?
Convert tyrosine to melanin pigment
91
eumelanin
Brown or black melanin pigment
92
Phaeomelanin
Red or yellow melanin pigment
93
Describe langerhan cells
Immune cells that ingest pathogens | Antigen presenting cells
94
Where were langerhan cells made and where do they live now?
Made in the bone marrow. Now in the prickle cell layer.
95
Describe merkel cells
Sit between keratinocytes and nerve fibres | Combine with nerve endings to create a sensory receptor for touch.
96
Where are Merkel cells found?
Basal layer
97
Describe the three phases of growth of a hair follicle
Anagen- growing phase Catagen- Involuting Telogen-resting phase
98
Which muscle moves the hair follicle
Arrector pilli muscle
99
What makes up the dermis
Fibres Ground substance Blood vessels, lymphatics, nerves Cells- fibroblasts, macrophages, mast cells, langerhan cells and lymphocytes
100
Fibroblasts function in the dermis
Secrete collagen
101
Macrophages function in the dermis
Antigen presentation
102
Sensor for pressure
Pacinian
103
Sensor for vibration
Meissners
104
Three types of glands in the skin
Sebaceous Apocrine Eccrine
105
Sebaceous glands
Widely distributed Hormone sensitive Produce sebum, squalene, wax esters, triglycerides and FFA
106
Apocrine glands
Develops as part of the pilosebaceous unit Found in the axilla and perineum Androgen dependent- produce oily fluid
107
Eccrine glands
Sweat glands Sympathetic cholinergic nerve supply Stimulated by mental, thermal and gustatory

Dermatology (21 decks)

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