Do You Know These Skin Problems in Dermatology Flashcards

*Check Blood Cholesterol levels as xanthomas are associated with hyperlipidemia/LYMPHOPROLIFERATIVE DISORDERS.* Pt has tendinous xanthomas (yellow nodules composed of "lipid" laiden histiocytes in the dermis, these macrophages have FOAMY Cytoplasm which has lot's of TG,Phospholipids,Cholesterol, these macrophages can also be surrounded by inflammatory cells+ FIBROTIC stroma) while xanthelemas(Periorbital plaques/papules that are yellow because foam cells=lipid laden macrophages are lcoated in superficial dermis) usually aren't surrounded by fibrotic tissue,inflammation.also know:*Pale Xanthomas(linear lesions in skin folds that are strongly associated with Primary Billiary Cirrhosis)*Eruptive Xanthomas-Yellow papules which appear when plasma TG and Lipids increase)

*Desmosomes(Located in Statum Spinosum between Stratum granulosum and Statum Basale),Stem cells(in Startum Basale=DEEPEST layer of EPIDERMIS),Keratin(stratum Corneum-Outermost layer) are all located in EPICdermis.*Remember layers of epidermis from outside to inside:Corneum,Lucidum,Granulosum,Spinosum,Basale< after this layers of epidermis then comes Dermis(Blood vessels are located here) and after that Subcutaenous fat.

*Because cadherins(Calcium dependent adhesion proteins) is where Actin(Microfilament) Cytoskeletons of of cells attach and make up components of Adherent Junctions(bElt desmosome,Zonula Adherens) which normally would connect adjacent epithelial cells>Metastatic dissemination.*Don't confuse this Belt desmosomes with Spot desmosomes(Macula adherens) which provide structural support trough stabilization of INTERMEDIATE filament communications between cells.(In Pemhigus Vulgaris we have igG autoantibodies against Desmoglein3component of Desmosomes(MACULA ADHERENS) which is btw also a Cadherin protein, as we remember desmosomes are located in SPINOsum, thus this type of 2 hypersensitivity leads to destruction of epithelial junctions of these region )

*Tight junction also known as Zonula Occludens is composed of Cloudins and Occludins and prevents PARAcellular(In between cells) movement of solutes.*Gap junctions are basically Channels of Rapid Chemical/Electric communication in between cells trough Channel proteins: Connexons.

*Trough Integrins which are membrane proteins that can bind to laminin and collagen(type IV) in Basement membrane.

*Nikolsky Negative means that rubbing of the skin won't result in Exfoliation of outermost layer of the skin(Upper Epidermis won't separate from basal layer which is also part of epidermis, as vesicle is Subepidermal between basal layer and basement membrane).* +Sign makes sense in Pemphigus where Bullae are thin walled and rupture easily making shallow erosions with dried crust. Acantholysis(Separation of epidermal cells) here results in SUPRAbasal intraepidermal bullae(Due to destruction of Desmosomes between epithelial cells in Spinosum_layer), while in Bullous pemhigoid you have autoantibodies against HEMIdesmosomes which connect Keratin in Basal cells with Basement membrane underneath it, thus defect is in deeper layer and Subepidermal Nonacantholytic bullae has THICKER wall and is tense, thus superficial rubbing won't be able to exfoliate skin, robbin hood tells us that antibodies are directed against Type 17 collagen as a component of HEMIdesmosomes,on skin biopsy of Bullous Pemhigoid you would see separation of basement membrane from basal cells.*You would see Lineaar pattern of Immunofluorecence, + remember that TENSE bullae in Bullous pemhigoid contains eosinophils.(Complement activation with neutrophil recruitment is also involved in tissue damage)*Remember that Pemhigus vulgaris is MORE dangerous with potential for DEATH, due to MUCOSAL involvement and risk of infection(Blisters rupture easy so skin can't protect from pathogens)

*Desmosomes(Macula adherens,Spot desmosomes) use Desmoplakin and cytokeratin to provide structural support via Intermediate filament interactions, Desmosomes are located in Stratum SPINOSUM of epidermis, Desmoplakins communicate with cytokeratins in respective cells and themselves they come together to create junction between cells.*Autoantibodies agianst desmolgein component are mechanism of acantholysis in Pemhigus vulgaris, these autoandibosies create Fish net/reticular pattern of immunofluorescence = IgG surrounding keratinocytes.*Intraepithelial vesicles in PV are suprabasal, while basal cells resemble a row of tombstones.*As we have Suprabasal vesicles due to destruction of spinosum layer (located between basales and granulosum) there is + nikolsky sign(Outer epidermis separates from Basal layer with Minimal pressure).*THEY WANT YOU TO KNOW THAT PG INVOLVES ORAL MUCOSA(patient can present with Poor appetite due to dysphagia) and that it can be DEADLY without treatment(Corticosteroids,MTX,Azathioprine)

*Example of macules include:*Freckles(small flat brown marks arising on the face and other sun exposed areas,esp common in people with red-hair)*Labial Macule(flat dark well-circumscribed spot on lips)*Don't confuse macule with large birthmark(Congenital Nevus) which is basically macule which is larger than 1 cm) and is called PATCH.*Sattar realllllllly wants you to know the mechanism of Freckle(ephelides) is:increased number of melanosomes without altering Number of melanocytes, while Poppie wants you to contrast this with Increase in Number of MelanoCYTES in Solar Lentigo(Brown macules in elderly,Not precancerous and doesn't need treatment, don't confuse with Lentigo maligna melanoma).

*Papule, examples include Acne and Mole(Nevus).*If papule is larger than 1 cm in size it is plaque which is characteristic of psoriasis(Salmon-colored PLAQUE with silvery scales, check pic).*EY everyone knows that psoriasis loves elbows,knees,lumbosacral area, but it can also involve GLANS PENIS(Some uw action)*Note psoriasis has association with specific HLA(Cw-0602)+Poppie wants you to know that sudden onset of psoriasis is highly suggestive for HIV(so they might ask you for which ifnectious agent you should test them), he also wants you to know that Psoriasis commonly is preceded by Strep.pharyngitis.*While UW loves to show psoriatic plaques and ask you association with Joint deforming disease(Psoriatic arthritis) and its association with nail changes(thickening,crumbling,pitting, brown-yellow discoloration)

*Small fluid-containing blister < 1 cm is VESICLE.*Enveloped,DS,Linear,DNA virus which is known as VZV with primary infection it causes Chickenpox(Varicella-presents with multiple crops of lesions in various stages from vesicles to crusts) but VZV can remain latent in dorsal root ganglia and on reactivation(Stress,immunosupression) it can cause Shingles(Zoster, DERMATOMAL distribution of vesicles which manifest with pain/burning sensation,can be disseminated over other regions too).*Now Both chickenpox and Shingles are characterized by formation of VESICLES(small fluid-containing blister<1cm), rupture of vesicles>ulcers that crust in a few weeks and patient is contagious untill lesions are dry.*With VZV infections we have + Tzank smear(+for mutlinucleated giant cells in base of scrapped ulcer) with Eosinophilic Inclusion bodies in MULTINUCLEATED Giant Cells and keratinocytes on light microscope.*Leukocytoclastic vasculitis(Hypersensitivity angiitis)=Small vessel vasculitis along with dermal inflammatory infiltrate can be present (Some UW action :)

*Transient smooth papule/plaque which is itchy is known as wheal(Single unit of urticaria(Hives), often seen with type 1 hypersensitivity in response to allergen, IgE cross linking on mast cells Or DIRECT effect of drugs like Opiates>Degranulation of mast cells, characterized by SUPERFICIAL DERMAL EDEMA+LYMPHATIC CHANNEL DILATION+Excess TRANSUDATE(hypocellular,low protein) NO CHANGES in EPIDEMRIS.*UW also wants you to know that monocytes and eosinophils can be found immediately around dermal venules.

*Flaking of Stratum CORNEUM(Outermost layer of epidermis) is characteristic of scale.*Think of SCC,Eczema,Psoriasis(Silvery scales component)

*Honey-colored crusting is characteristic of impetigo Impetigo caused by strep.pyogenes(group A strep), know that baby has risk of developing Post Streptococcal glomerulonephritis(Contrast this with Rheumatic fever which only follows strep.pharyngitis)*Note: if impetigo is characterized by bullae(Large fluid containing blister>1cm), than causative agent is most likely S.aureus.*Impetigo is very contagious and can be transmitted trough skin contact or even by touching objects that came into contact with infected skin.

*Hyperkeratosis(Thickened Stratum Corneum with retention of nuclei in keratinocytes reflecting incomplete keratinization<normal process only in Mucous membranes)+Parakeratosis(Retention of Nuclei) with mitotic activity above basal layer +THINNING or ABSENCE of Stratum GRANULOSUM(layer between lucidum and spinosum), while spinosum layer gets thicker due to HYPERPLASIA(And can have Neutrophilic infiltrates)*CARDINAL SIGN:MUNRO Abscesses(Neutrophils from papillary dermis infiltrating Stratum corneum )+Elongation of rete ridges(which are epidermal thickenings that extend downward between dermal papillae)*Hyperkeratosis(thickening of stratum corneum)alone is characteristic of lot's of other conditions like Callus(callus would refer to thickened stratum corneum in response to mechanical forces, such as the hands of a carpenter working with tools, or the soles of the feet of a child going barefoot)*Sattar wants you to know PUVA combo(UVA + psoralen, Psoralen increases UVA absorbtion, while UVA will destruct proliferating keratinocytes and thus decrease Hyperkeratosis) can be used for treatment of psoriasis Corticosteroids(usually main treatment)and immune therapy can be used(As it is of autoimmune origin)

* Lichen planus is directly a result of hypergranulosis(Thickening of stratum granulosum)**LYMPHOCYTES at dermal-epidermal junction is common histologic finding.(Making sawtooth appearance)*Hep C has association with lichen planus.(So test them for hepatitis C virus)*usually lesions are self-limiting but chronic lesions can increase risk of SCC.*Lesions develop in areas of scratching(Koebner phenomenon)