inflammatory dermatosis

Question 1

summarise the microanatomy of the skin

Answer 1

epidermis on top attached to BM

then dermis - made of collagen, elastin, glycosaminoglycans, bv, nerves and appendigeal strutures (hair follicles, sweat and sebaceous glands)

then subcutaneous tissue

Question 2

describe the non-hair baring skin

Answer 2

stratum cornea

epidermis

papillary dermis

reticular dermis

hypodermis

(fibroblasts involved in production of collagen, elastin and GAGs; inflammatory cells; bv; nerves)

Question 3

histology of hair-baring skin

Answer 3

sebaceous glands - lunricate the hair

see hair shafts and follicles and bulbs

2 types of sweat glands

• apocrine - mainly in axillan groins- make viscous sweat that is smelly after degredation by bacteria
• ecrine glands

Question 4

cells and their location in the epidermis *

Answer 4

langerhans cells - apc within epidermis

melanocytes - on bm

merkel cells - sensation - on bm

keratinocyte - in epidermis

Question 5

describe the structure of the epidermis and the keratinocytes through it *

Answer 5

at stratum basale have dividing keratinocytes (stem cells) - they differentiate as they move up the epidermis - and they make keratin

at stratum spinosum have connections between keratinocytes

at stratum granulosum - have keratin-hyalin granules

stratum lucidum

stratum corneum - flattened keratinocytes that have lost nucleus and are filled with keratin

Question 6

melanocytes - histology

Answer 6

with H and E stain, they are vacuolated

Question 7

describe the structure and function of the striatum corneum *

Answer 7

made of keratocytes and a glue - glue is made of lipids and proteins

this is a very important barrier layer - defect predispose to eczema and therefore other atopic conditions, and allow infections and irritants to enter the skin

filigrin is a protein in the glue - gene mutation of this is common in eczema

Question 8

what is atopy *

Answer 8

the tendancy to develop hypersensitivity/allergy

Question 9

what are the atopic diseases *

Answer 9

eczema - relapsing-remitting - have as baby and grow out of it/continuous - problem is the skin barrier ie stratum corneum allowing ingress of allergens and irritants

asthma

hayfever

Question 10

describe the atopic march *

Answer 10

develop a series of atopic conditions at different stages in life

pt 1st has eczema - this dies down by yr1/2

but then get food allergy - because food goes on the skin on face that has eczema so hasnt developed properly = increased sensitisation to it

then get asthma and rhinitis - sensitisation to house dust mites etc through the skin with eczema

Question 11

describe the pathophysiology of atopic eczema *

Answer 11

intrinsic factors leading to defects at the skin barrier eg filagrin gene mutation, combined with extrinsic factors ie penetration of exogenous agents - allergens (HDM), irritants (detergants), pathogens (staph coccus)

lead to immune reponse and recruitment of inflammatory cells - mast cells degranulation releasing histamine

get acute ectopic eczema - activation of CD4+ T cells and Th2 immune response

if goes on longer - chronic - activation of CD4 and CD8 T cells - and Th1 immune response

Question 12

describe palmar hyperlinearity *

Answer 12

it is a clinical sign of filigrin mutation

large proportion of people with eczema have these mutations - if have it = likly to develop eczema

the lines on hand are more prominant

Question 13

describe infantile ectopic eczema *

Answer 13

sore

crusty

inflammed and eroded

not immediately around the mouth

in areas where baby can rub themselves against what sleeping on - face, elbows and knees

baby will be irritable, distressed and not sleeping properly

Question 14

common sites of eczema outbreaks in children *

Answer 14

scalp

neck

hand

feet

Question 15

common sites of eczema in adults *

Answer 15

where there are flexures

face

Question 16

describe eczema with lichenification (chronic changes) *

Answer 16

less red

more lichenified - skin look like they have thickened with more obvious skin markings - excoriation (scratch marks)

cut off between eczema and normal skin not clear

Question 17

describe severe eczema *

Answer 17

can be all over - erythroderma

pt is febrile, unwell, may need hospitalisation

Question 18

describe eczema herperticum *

Answer 18

the barrier problem predisposes pt to staph aures infection - acts as a super ag and makes eczema worse

also suseptible to herpes virus ie cold sore spread all over area of inflammed skin - begins as vesicles then punched out ulcer

Question 19

treatment of eczema herpeticum

Answer 19

acyclovir

topical corticosteroid

Question 20

describe seborrhoeic eczema *

Answer 20

dandruff

combination of overgrowth of yeast and eczema

flare in stress

greesy and scaley

on nasolabral fold, elbow, chest and back

Question 21

treatment of seborrhoeic eczema

Answer 21

antifungal cream

shampoo

topical steroid

Question 22

describe allergic contact dermititis *

Answer 22

against specific ag

atopic eczema predisposis contact dermitis but can have dermititis without AE

sensitised to: cosmetics, eyedrops with preservatives, hair dye/henna (PPD in it), fragrances, rubber, nickle allergies

get blistering and swelling

Question 23

describe discoid eczema *

Answer 23

can be related to ectopic asthma but not necessarily

disc like patch on leg and trunk

related to dryness - people who overwash

adults dont produce as much lipid in skin so more likely to get this

Question 24

treatment of discoid eczema

Answer 24

avoid soap

moisturise

mild topical steroid

Question 25

describe psoriasis \*

Answer 25

plaque legion - scaley and pink well defined areas have erythrodermis have underlying genetic suseptibility - many genes are involved - so if enough genetic load develops or you are genetically suseptible and have triggers you can get psoriasis triggers include stress, alcohol, drug (B blockers, anti-malaria and lithium), smoking, stapholycoccal infections - if have repeated staph infections causing psoriasis can remove tonsils to improve it

Question 26

pathophysiology of psoriasis \*

Answer 26

over-proliferation of keratin cells they move up the epidermis and shed when immature and still have nuclei

Question 27

histology of psoriasis \*

Answer 27

hyperkeratosis - thick keratin layer, have nuclei parakeratosis - corneocytes shouldnt have nuceli but they do acanthosis - thick epidermis inflammation - recruitment of inflammartory cells - neutrophils in epidermis, lymphocytes in dermis dilated bv - redness

Question 28

common locations for psoriasis \*

Answer 28

extensor surfaces - elbows, buttocks, knee nails trunk face armpit groin and genitals

Question 29

descibe psoriasis soles \*

Answer 29

symettrical so inflammatory rather than infection

Question 30

nail effects in psoriasis \*

Answer 30

build up of debris under nail dystrophic nail (roughening of nail plate) loss of cuticle - normally seal of proximal nail pole to plate - this has gone = bacteria and fungi enter- get secondary infection onycholysis - nail plate has lifted off pitting

Question 31

describe guttate psoriasis \*

Answer 31

in teenagers and young adults - 20/30yrs papules 2-3mm pink and scaly exacerbated by streptococcus infections raindrop papules

Question 32

describe plantopalmar pustulosis \*

Answer 32

can have plaques in othe regions, but mainly just on hands and feet differnet genes involved than in other forms of psoriasis triggered by stress, smoking and obesity

Question 33

describe generalised pustular psoriasis \*

Answer 33

extreme involvement of the skin with pustules neutrophils in epidermis coagulate to form pustules - they are superficial and sterile there is a lot of inflammation pt has high HR, is toxic, febrile and needs immunosuppression

Question 34

summarise acne \*

Answer 34

it is a disorder of the pilosebaceous unit common in children and young adult

Question 35

describe acne formation \*

Answer 35

have genetic predisposition occurs at puberty and when antigenic stimultation pore/hair follicle opens - build of debris - forms comedone (blackhead/white head) this causes a build up behind it that gets colonised by probionibacteria acnes (bacteria) and others hair follicle swells and becomes inflammed - may burst - pus goes into surrounding demis = more inflammatory reaction

Question 36

clinical features of acne \*

Answer 36

whitehead - comedone with skin covering blackhead - open comedone papule - small inflammatory legion, red pustule - pus nodule - bigger inflammatory lump scarring combination of all features ay same to,e

Question 37

treatment of acne

Answer 37

things to steralise skin - benym peroxide isotretinoin/reoaccutane - SE of depression oral contraceptive - reduces testosterone contraceptive pills like yasmin have direct anti-androgenic effect oral erythromycin, tetracyclin topical AB - erythromycin/clarithromycin - lipophilic so dissolve into sebum and kill bacteria and have direct anti-inflammatory effect

Question 38

describe bullus pemphigoid \*

Answer 38

blistering split in skin is deeper the basement membrane zone is a connection between epidermis derived from ectoderm, and dermis derived from mesoderm - they are stuck together by proteins and proteins in basement membrane zone stick BM to itself these proteins are a target of auto AB/ can be mutated BPAg1 and BPAg2 are targets of autoAb of B cells - cause inflammatory reaction and splitting just above the bm

Question 39

describe epidermolysis bullosa \*

Answer 39

genetic condition - defect in protein in basement membrane zone cause splitting of skin after minor trauma if minor might present later eg in military boots blister easily however many die yound

Question 40

describe patholgy of bullus pemphigoid \*

Answer 40

autoAb to BPAg1/2 cause blister with inflammatory cells below present at 60-70rs tense blisters (bullae) severe blistering seen all over the body can be red areas with occaisional blistering w/o treatment get infection and sepsis so die get better with steroids to suppress Ab formation and immunosuppression for long time

Question 41

describe pempigus vulgaris \*

Answer 41

blisters are superficial autoAb against connections between kertatinocytes again in stratum spinosum eg desmogleins and desmocollins the split is within the epidermis present as flaccid blisters - easily broken severe and all over body rarer then pemphigoid - more common in asian than caucasian treat with oral steroid (suppress the Ab), and systemic immunosuppresive high mortality w/o treatment - 80-90%, \<10% with treatment