Inflammation Dermatoses Flashcards
(24 cards)
Basic microanatomy of the skin?
From bottom, up:
• subcutaneous tissue (hypodermis) –> dermis –> epidermis
What makes up the skin: • sweat gland • sebaceous gland • hair follicle • blood vessels
Skin histology?
Stratum cornea Epidermis Papillary dermis Reticular dermis Hypodermis
(onenote!)
What are some important cells found in the stratum basale?
- Merkel cells
- Melanocytes
- Dividing keratinocytes
What is the differentiation bathways of a keratinocyte?
- Basal cell
- Prickle cell
- Granular cell
- Keratin
Explain the stratum corneum?
- Important barrier function of the skin
- Defects lead to eczema
- Composed of corneocytes (differentiates keratinocytes) with lipids in betw. each of them
What are the 4 types of eczema?
(1) Atopic
(2) Seborrhoeic
(3) Discoid
(4) Allergic contant
Explain Atopic Eczema
Atopic – “the tendency to develop hypersensitivity”
• includes eczema, hay fever & asthma
Very common, itchy skin condition with onset from first 6 months of life
• many grow out of it
Explain the cause of atopic eczema?
Cause – defective barrier of skin
Filagrin (an epidermal protein) gene mutation in ~10% of patients
• Palmar hyperlinearity is a sign of the mutation
Defective barrier then allows entry of irritants, allergens & pathogens which then cause inflammation
Explain Seborrhoeic Eczema
Common skin condition affecting babies and adults but is NOT itchy.
Associated with an overgrowth of malassezia (species of yeast on the skin that causes inflammation)
• the rash has a distinctive distribution involving – nasolabial folds, eyebrows, scalp, central chest, axilla and groin
What is Discoid Eczema?
Occurs in small discrete discs
Define Psoriasis
Common inflammatory dermatoses usually starting in teens or 40s/50s
Histology of psoriasis?
From top to bottom: • Hyperkeratosis • Parakeratosis • Acanthosis • Inflammation • Dilate blood vessels
Types of psoriasis?
- Chronic plaque
- Guttate
- Palmoplantar pustulosis
- Generalised pustular psoriasis (same as above, just EVERYWHERE)
Cause of psoriasis and possible triggers?
Genetic susceptibility
• many genes are implicated including PSOR1
Envrionmental causes
Triggers may include:
• infections, drugs & stress
Pathophysiology of psoriasis?
T-lymphocytes move out of blood vessels into the dermis
• initiate release of cytokines (e.g. TNFa)
• the epidermis thickens in response (produces more keratinocytes)
Neutrophils infiltrate the epidermis
AND
lymphocytes infiltrate the dermis.
Pathophysiology of Acne?
Disease of the pilosebaceous unit of the skin
Acne pathogenesis?
Multifactorial:
o Hyperkeratinisation of the epidermis in the infundibulum of hair follicles
• accumulation of dead keratinocytes in the lumen of the hair follicle
o Increase sebum production stimulated by androgens
o Proliferation of Propionibacterium acnes within pilosebaceous unit
o Rupture of inflamed pilosebaceous unit –> further inflammation of surrounding skin
Clinical features of acne?
• Open (blackhead) / closed (whitehead) COMEDONES
- Papules
- Pustules
- Nodules
- Scars on face, chest & back
What is Bullous Pemphigoid?
A.I bullous inflammatory condition most common in the elderly
Clinical features of Bullous Pemphigoid?
Intense pruritus followed by development of TENSE blisters on an erythematous background of skin or mucous membrane
• e.g. epidermolysis bullosa
Pathogenesis of Bullous Pemphigoid?
IgG auto-Abs agaisnt the BM antigens BP180 (T17 collagen) or BP230
• result in cleavage of skin at the dermo-epidermal junction, leading to sub-epidermal blisters
Define Pemphigus Vulgaris?
Uncommon A.I bullous inflammatory disease
Most common in middle-ages people
Clinical features of Pemphigus Vulgaris?
FLACCID blisters
which break easily leaving
• erosions & crusted lesions
Pathogenesis of Pemphigus Vulgaris?
IgG auto-Abs to epidermal cell-surface proteins desmogleins 1 & 3
- loss of cell-cell adhesion (acantholysis) within the epidermis
- causes flaccid blisters in the skin OR mucous membrane
