Pathophysiology Flashcards
Psoriasis pathophysiology?
genetic component
1) Keratinocytes under stress (intiated by trauma/drugs/unknown allergen) lead to activation of dermal dendrites
2) Dermal dendrites activate T helper cells
4) T helper cells release growth factors (TNFa), adhesion molecules and other cytokines which propel inflammation and epidermal turnover
Psoriasis presentation?
Epidermal cell turnover increased (silvery scales)
Granular layer absent
Affects extensor surfaces
itchy - bleed
thinning epidermal over blood vessels, multiple bleeding pts
Well demarcated papulo-squamous red scaly plaques
Eczema?
Impairment of skin barrier function due to mutations in fillagrin gene (fillagrin holds keratin filaments together.)
This leads to stressed keratinocytes, which attract dermal dendritic cells (Ag presenting, chemokine releasers), and therefore T cells. Immune response intiated.
Defective barrier allows access/sensitization to allergens and promotes bacterial colonisation
Eczema presentation?
Red inflamed patches
Flexor surfaces
common children
Hyperkeratosis
Increased thickness of keratin layer
Parakeratosis
Persistence of nuclei in the keratin layer
Acanthosis
Increased thickness of prickle cell layer
Basic biochemistry of porphyrias?
Porphyrias deposit in skin, energy from sun absorbed.
Porphyria moves deeper into the skin and can intiate a secondary reaction and inflammatory immune response.
Photoallergy is also known as - , it is a form of - - -
photodermatitis,
allergic contact dermatitis
Phototoxcitiy does not involve the - -. It is a - induced skin reaction.
immune system, chemically
Erythropoetic protophoryia usually presents in - and most cases are -. Clinical presentation involves - - - and - within few mins exposure to sun.
childhood
congenital (inborn metabolic defects)
pruritus, erythema, swelling and pain
Porphyria cutanea tarda typical clinical presentation involves - and - as well as -pigmentation, -trichosis and solar -
Blister, fragility Hyperpigmentation Hypertrichosis Solar urticaria morphoea which is localised (patches on skin) scleroderma (hard bits of skin)
Acute intermittent porphyria presents with acute -, as well as peripheral neuropathy syndromes such as – syndrome, and - multiplex.
abdomen
gullian barre
mononeuritis
psychosis
Lesion is
Lesion is traumatic or pathogic loss of normal tissue continuity, structure or function
Rash is
temporary eruption of skin
Flat lesions called?
Macule is flat spot <1cm
Patch >1cm
Raised lesions called
Nodule if >0.5cm
Papule if <0.5cm
Plaque is
ELEVATED edges and flatter surface >1cm
Wheal is
localised skin edema, compressible
Lichenification
thickened leathery roughening of skin caused by scratching
Blisters are
Circumscribed elevations f skin caused by fluid under or within epidermis
Pustules are
sircumscribed elevations of skin -pus filled
Vesicles are
<1cm blister
Bullae are
> 1cm blister
Erosion is
loss of superficial epidermis, surface moist but does not bleed
Ulcer is
Skin defect where there is loss of epidermis and papillary layer of dermis - may extend to subcutaneous tissue
Callus is?
Hyperkeratotic plaque of skin develops because of pressure or friction
Purpura is
reddening of skin due to extraversion of blood - doesn’t blanche
Petechia
small (1-2mm) area of purpura
Cyst is?
Nodule containg semi-solid material
Onycholyisis is?
seperation of nail plate from nail bed
Alopecia?
loss of hair
Hypertrichosis
general excess growth (hair, nails etc)
Hirsutes?
excess growth in male pattern (i.e. beard in women)
Enzyme deficient in acute intermittent porphyria?
PBG Deaminase (high up metabolic pathway)
Enzyme deficient in porphyria cutanea tarda?
Uroporphyrinogen Decarboxylase (middle metabolic pathway)
Enzyme deficient in erythropoietic protoporphyria?
Ferrochelatase (bottom of metabolic pathway)
Discoid eczema is?
well defined, erythematus and scaly “discs” of eczema
Often atopic
Diagnostic criteria for eczema?
Itch plus 3+ of: Visible flexural rash* History of flexural rash* Personal history of atopy (or first degree relative if under 4 yo) Generally dry skin Onset before age 2 years
Immunopathology of contact allergic dermatitis?
Langerhans cell in epidermis processes antigen
antigen is then presented to Th cells
Sensitised T cells proliferate epidermis and cause damage = spongiosis
Contact allergic dermatitis is inflammation in contact with an?
allergen
Irritant contact dermatitis is inflammation in response to?
non-specific physical irritation rather than a specific allergic reaction
e.g. soap, detergent, nappy
difficult to distinguish from allergic ?
Atopic eczema is caused by?
Genetic & environmental factors resulting in inflammation
itching,not sleeping, affects whole family w kids
Chronic changes of atopic eczema?
Lichenification
Excoriation – erosion brought about by scratching
Secondary infection – high carriage Staph A, erosions good carrier bacteria
Eczema herpeticum is caused by? Presents as?
Herpes simplex virus
monomorphic punched out lesions
fecer
Stasis eczema is secondary to?
hydrostatic pressure
oedema
red cell extravasation
What is “cradle cap”?
Seborrhoeic dermatitis
Pompholyx eczema is characterised by?
Spongiotic vesicles
Photosensitive eczema is in response to sun exposure t/f
t
What is a chronic leg ulcer?
open lesion between the knee and ankle joint that remains unhealed for at least 4 weeks.
60-80% of leg ulcers are arterial in nature
F
60-80% of leg ulcers are VENOUS in nature
Features of arterial ulcers? FEED P
Full thickness defect
Embolic “showering” on the toes
Extremities
Diabetics
Punched out appearance
Features of venous ulcers? VVERD
Varicose veins Varying depths Exudative and painful Recurrent Distal leg and ankle
