Immunology 5: Inflammatory Dermatoses Flashcards
Recall the 5 layers of the epidermis
- Stratum corneum
- Stratum Lucidum
- Stratum granulosum
- Stratum spinosus
- Stratum basale
Describe the structure of the stratum corneum and describe the gene mutation common in eczema
Corneocytes surrounded by lipids.
Filagrin gene mutation common in eczema patients.
Describe the two types of sweat glands
- Apocrine- viscous sweat, located in axilla and groin, ‘smelly’
- Eccrine- less viscous secretions; highest density in palm and soles
List in order the cell differentiation in the epidermis
Basal cell —> Prickle cell –> Granular cell –> Keratin
Define atopy and give 3 examples
Tendency to develop hypersensitivity
Eczema, asthma and hay fever
Explain the atopic march phenomenon
Series of hypersensitivity conditions arise at different ages from atopic dermatitis (AD) and food allergy in infants to allergic rhinitis and asthma in children.
Describe the pathophysiology of eczema
Intrinsic factor lead to defective epidermal barrier and the presence of external factors (allergens, irritants and pathogens (staphylococcus)) trigger activation of CD4+ lymphocytes and the Th2 immune response acutely. Mast cell degranulation results in histamine release. Chronically activation of CD4+ and CD8+ lymphocytes and the Th1 immune response results in IFN-alpha production.
Where does atopic eczema affect infants in comparison to adults?
Infants- face, elbow and knees- areas they rub themselves
Adults- Flexion points
Describe the chronic appearance of eczema and state the clinical term for this
Skin looks thickened with extenuated skin markings= lichenification
State and describe some other types of eczema
Erythraderma- Eczema all over
Eczema hepeticum- herpes infection
Seborrhoeic- overgrowth of yeast and eczema- same as hair dandruff but around nasolabial folds and eyebrow region.
Allergic contact dermatitis- around the eye is common
Discoid- Legs and trunk. Often due to over washing and adults do not produce as much lipid.
Psoriasis clinical features
Inflamed skin (salmon pink and silver scales), scale and plaques
Histological features of psoriasis
Hyperkeratosis
Parakeratosis- corneocytes are nucleated
Acanthosis- thickened epidermis
Inflammation (Neutrophils in epidermis and lymphocytes in the dermis)
Causes of psoriasis
Genetic susceptibility and triggers including:
Stress; alcohol; drugs* and infections **
* Beta-blocker, anti-malarials, lithium
** Streptococal infections- removing tonsils can improve psoriasis in patients with recurrent tonsillitis
Describe some allergens that often result in hypersensitivity
Cosmetics; eye drops (with preservations) and hair dye (PPD) and some henna tattoos –> swelling and blistering
Nail features of psoriasis patients
- Subungal hyperkerotosis
- Dystrophic nail and cuticle loss
- Pitting
- Oncolysis- lifting off the nail bed
Describe psoriasis vulgaris on soles of feet
Well-demarcates, erythematous plaques with thick, yellowish scale and desquamation on sites of pressure arising on the plantar feet (similar lesions seen on palms). Very symmetrical deducible that the lesions are unlikely to be fungal or infection.
What is Guttate psoriasis and palmoplantar pustulosis
Occurs more in teenagers and young adults- little papules (2-3mm) and is exacerbated by streptococcal infections.
Psoriasis can just be affecting the hands and feet
Explain Generalised pustular psoriasis and what are some differentials for the presentation of this condition
Extensive involvement of the skin with pustules (three differentials: infection, adverse drug reaction or psoriasis). Pustules created by collections of neutrophils within the epidermis (yet no infection is present- STERILE). Patient will be very unwell- malaise, tachycardia and extensive inflammation.
Describe acne and some potential treatments
Build up of dead cells and sebum within hair follicles and sebaceous glands resulting in comedone formation (blackheads, whiteheads- closed comedones, papule, pustule and nodules)
Rupture of follicular canal and inflammation.
Tx: Sterilize skin; topical antibiotics (lipophilic- dissolves in sebum e.g erythromycin); OCP to reduce androgenic stimulation (Yasmin) and Isotretinoin (roaccutane).
Explain Bullous Pemphigoid and describe the treatment
Deep split in the skin caused by autoantibodies targeting the BPAg1 and BPAg2 proteins within the hemidesmosomes. Resulting in severely pruritic generalized eruption that consisted of urticarial, inflammatory plaques, papules, tense blisters (bullae) and crusted lesions. (can present as red areas).
Tx: long-term immunosuppresion
What is Epidermolysis bullosa?
Genetic defect in any one of the protein involved in basement membrane attachment. Resulting in splitting after any trauma. Degree of severity varies significantly.
Explain pemphigus vulgaris
Blisters exclusively arise in normal appearing skin (BP- shows tense blistering in enflamed areas). Intercellular connections between keratinocytes (stratum spinosus) are target by autoantigens (usually desmogleins in PV but could also be desmocollins).
Mortality <10% with Tx of oral steroids and systemic immunosuppression.
Rarer than BP but more likely to occur in Asians and 30/40s in comparison to BP 50/60s.
Immunofluorescent shows antibodies around keratinocytes.
