dermatology1.2 Flashcards
Penetration of Topical Medication through Stratum Corneum
The outermost layer of the skin, the stratum corneum, acts as the primary barrier to percutaneous absorption of topical medications. The stratum corneum is usually described as a ‘brick and mortar’ structure, where keratinocytes represent the bricks and intercellular lipids acting as the mortar. To be effective, topical medications need to gain entry into the skin and reach the site of action in desired concentrations. Typically, the site of topical medication action is the epidermis or the dermis. Medications gain access to sites of action through three primary mechanisms. First, the medications can move across the stratum corneum by passive diffusion. Second, the agents can be transported through channels or pores within a lacunar system in the stratum corneum. Finally, the medications may be transported via appendageal structures, such as sweat glands or hair follicles.
Factors Influencing Absorption of Topical Medications
Drug formulations for topical medications consist of an active ingredient in a vehicle base. Factors that influence effective percutaneous absorption of topical medications can be categorized into (a) drug factors and (b) patient factors. Drug factors affecting percutaneous absorption include: Active drug concentration, Composition of the vehicle, Molecular size of the drug or prodrug, and Lipophilicity of the drug. Patient factors affecting percutaneous absorption of topical medications include: Presence of barrier disruption, Anatomic location (including thickness of the stratum corneum), Skin hydration, and Occlusion.
Affect of composition of vehicle and active drug concentration on drug absorption
Studies have shown that, given the same vehicle, cutaneous absorption is directly proportional to the concentration of the active ingredient in the medication. However, given the same concentration of the active ingredient, cutaneous absorption can differ when the ingredient is embedded in different vehicles.
Affect of molecular size of the drug on absorption
Molecular size of the drug affects its absorption at the site of action. When absorbed through passive diffusion, molecules need to traverse a tortuous path through the intercellular lipid domains, or the “mortar”. Typically, the diffusion of a compound is inversely proportional to the molecular size of the drug.
Affect of liphophilicity of the drug on drug absorption
Because stratum corneum contains a mixture of lipids that includes ceramides, cholesterol and fatty acids, lipophilic topical agents are more likely to permeate the skin than hydrophilic agents.
Affect of skin hydration on drug absorption
Skin hydration affects percutaneous absorption in important ways, sometimes by several folds. Occlusion of the skin often leads to markedly increased skin hydration. Therefore, active ingredients that are delivered in the form of an ointment, tape, or to the skin folds, reach much higher concentrations because occlusion prevents loss of medication by evaporation, friction, or exfoliation.
Affect of anatomic location on drug absorption
Percutaneous absorption of topical medications is also related to anatomic location. In general absorption is lower in anatomic regions where the stratum corneum is thicker, such as the palms and soles. In contrast, percutaneous absorption is higher in areas where the stratum corneum is thinner, such as the eyelids and scrotum.
Classification of Vehicles
The art of using topical medications often revolves around selecting the appropriate vehicle. Overall, the choice of selecting the appropriate vehicle is as important as selecting the concentration or the active ingredient. Ointments: Water in oil emulsion. Creams: Oil in water emulsion. Gels: Semisolid emulsion in alcohol base. Lotions/Solutions: Powder in water (some oil in water). Foams: pressurized collections of gaseous bubbles in a matrix of liquid film
Ointments
Active ingredients delivered in an ointment vehicle have strong potency. Ointments are hydrating, with very low sensitization risk or irritation risk. Body sites most amenable to ointment use are non-intertreginous sites. It’s best to avoid using ointments on face, hands, and groin. Despite of their many therapeutic advantages, some patients dislike greasiness of ointments. Patient education is necessary as ointments may stain clothing.
Creams
Active ingredients delivered in a cream vehicle have moderate potency. Creams offer some hydration, but they are not as hydrating as ointments. Creams have a significant sensitization risk and a low irritation risk. Virtually all body sites can be amenable to application of cream-based topical agents. Avoid using cream in sites with maceration. There is a high rate of acceptance by patients.
Gels
Active ingredients delivered in a gel vehicle have strong potency. Gels are drying. Gels carry a significant sensitization risk and a relatively high irritation risk. Sites most amenable to gel application are oral mucosal surfaces and the scalp. Avoid applying gels on fissures, erosions, or macerated regions. Patient preference for gels is variable.
Lotions/Solutions
Active ingredients delivered in a lotion or solution vehicle have relatively low potency. Lotions and solutions tend to be variably drying. Lotions and solutions have a significant sensitization risk and moderate irritation risk. Sites most amenable to lotion or solution application are scalp and intertriginous areas. Avoid using lotion or solution on fissures or erosions. There is a relatively high rate of patient acceptance for lotions and solutions.
Foams
Foam vehicles are a relatively newer type of vehicle for topical agents, and I will discuss them relatively more extensively here. The foam matrix is stable at room temperature but readily melts at body temperature. After the foam is applied to the skin, the volatile components (such as alcohol and water) quickly evaporate, leaving behind lipid and polar components containing supersaturated active ingredients to interact with lipids of the stratum corneum. These supersaturated solutions enable maximal delivery of active ingredients into the skin. Interestingly, alcohol, a component of the foam matrix, may play a role in altering the stratum corneum’s barrier properties and lead to improved penetration of the active ingredient. Active ingredients delivered in a foam vehicle have strong potency. Foams are quick- drying, stain-free, and leave almost no residue. Sites most amenable to foam application are hair-bearing areas. Avoid applying gels on fissures or erosions. Patient preference for foam is quite high.
Considerations for Selecting an Appropriate Vehicle
When selecting an appropriate vehicle, three factors are of particular importance: anatomic location, contact allergy/sensitization, and irritancy. As explained in the above text, some vehicles are more appropriate for certain body sites than others. For example, for hair bearing regions, the clinician should consider choosing a solution or foam vehicle over ointment. Various water-based vehicles, such as creams, lotions, and solutions, contain preservatives that may increase the risk of contact allergy and sensitization. These preservatives include known allergens such as parabens and formalin releasers. Irritancy is most notably associated with high concentrations of propylene glycol, other types of alcohols, and certain acidic vehicle ingredients. For example, avoid using formulations containing alcohol or salicylates on extensively fissured, eroded, or macerated areas, which can lead to stinging and burning.
FTU (Fingertip Unit)
1 FTU is the amount of ointment dispensed from a 5 mm diameter nozzle that is applied to the distal third of the index finger, from the crease under the distal interphalangeal joint to the fingertip. 1 FTU=0.5 g
Few other Useful Quantities of Application
1 gram of cream covers approximately 10 cm x 10cm area of skin. 1 gram of ointment spreads 10% further than the same amount of cream. Approximately 20 g are necessary to treat the entire body of an adult man, or roughly 280 g per week if the medication were applied twice daily for 1 week. Quantities of ointment to dispense in children differ according to age due to different body surface areas.
Molecular Mechanism of Action of Glucocorticosteroids
Binding of glucocorticosteroids to their receptors, which are located in the cytoplasm of most cells in the body. Upon binding by glucocorticosteroids, the release of 90 kDa heat shock protein occurs, and subseuqent nuclear localization signals facilitate translocation of the glucocorticoid receptor complex into the nucleus. In the nucleus, the glucocorticoid receptor forms a dimer, which binds to the glucocorticoid response element of the promoter region of steroid-responsive genes. This binding is associated with the following downstream molecular events:
Downstream molecular events from glucocorticosteroids binding to its receptor
Alteration of transcription rate, messenger RNA production, and protein synthesis of associated with various inflammatory pathways. The glucocorticoid receptor interacts with other transcription factors that play a role in the inflammatory response and their coactivator molecules, including cAMP response element binding protein (CREB)-binding protein. Inhibition of nuclear factor-κB pathway, whch leads to reduction in transcription of genes that play a significant role in chronic inflammation, including genes for many cytokines, adhesion molecules, inflammatory enzymes, and growth factors. The glucocorticoid receptor interacts with activating protein 1 (AP-1) (AP-1 is a collective term for the heterodimeric transcription factor composed of c-jun, c-fos and activating transcription factor), which controls transcription of growth factor and cytokine genes. Glucocorticosteroids inhibit TNF-α, granulocyte–macrophage colony-stimulating factor, and several interleukins (e.g. IL-1, IL-2, IL-6, IL-8). Cyclooxygenase and adhesion molecules such as intercellular adhesion molecule- 1 and E-selectin are also inhibited.
General Classification of Topical Steroids
A large numbers of topical glucocorticosteroid medications are available in a wide range of potency. In general, seven classes have been proposed based on potency. The superpotent topical glucocorticosteroids belong to class 1, and the very low-potency topical glucocorticosteroids belong to class 7. These classes were developed based on vasoconstrictor assays. The vehicle can greatly influence the percutaneous absorption and efficacy of the some glucocorticosteroids.
Hydrocortisone 2.5% (cream or ointment)
“The Gentle Touch.” Hydrocortisone 2.5% (cream or ointment) belongs to class 7, the lowest potency class. It is efficacious for mild eczema in children and adults and for treating inflammatory dermatoses involving anatomic regions such as the face, intertriginous areas, or groin, where mid to high-potency topical steroids may be contraindicated.
Triamcinolone Acetonide 0.1% (cream or ointment)
“The Almost All-Purpose Weapon.” Triamcinolone acetonide is affordable and readily available in many different tube sizes (and even in 1 pound jar!). Triamcinolone 0.1% cream or ointment belongs to class 4, or a mid-potency class of topical steroids. Triamcinolone 0.1% is effective against most moderate spongiotic dermatoses (including eczematous dermatitis, atopic dermatitis, allergic contact dermatitis, arthropod bites, id reactions, drug reactions) involving the trunk and extremities. Long-term use of triamcinolone is not recommended for facial, intertriginous, and groin lesions.
Clobetasol Propionate 0.05% (cream or ointment)
“Hercules.” Clobetasol propionate 0.05% cream or ointment belongs to Class 1 of topical steroids, and it is considered one of the most potent topical steroids. Clobetasol is best used in acute eruptions that necessitate relatively rapid amelioration, such as contact dermatitis or acute drug eruptions. Clobetasol should be avoided on the face, intertriginous areas, or the groin, where the skin is relatively thin. Longer-term use of clobetasol requires monitoring of development of adverse effects.
General Considerations for Selecting a Topical Steroid
When selecting an appropriate topical steroid for clinical use, the practitioner should take into account severity of the condition, location of the lesion, and need for hydration or drying effect. Furthermore, the clinician should be aware of the potential for sensitization or irritation of certain types of vehicles. Due to the occlusive nature of an ointment vehicle, the same active glucocorticosteroid ingredient in an ointment vehicle will often be more potent than the same ingredient in a cream, lotion, or solution vehicle. This is because the ointment vehicle enhances hydration of the stratum corneum, which leads to improved penetration of the medication. In general, potent or superpotent topical steroids should be avoided for use on the face, skin folds (axillary and intertriginous folds), and groin areas due to the risk of epidermal atrophy and potential for steroid-induced rosacea/perioral dermatitis on the face.
Adverse Effects of Topical Glucocorticosteroids
The use of topical corticosteroids has been associated with a number of side effects. In general, more potent topical steroids are associated with greater adverse effects. The most common adverse effect is skin atrophy, and this is most commonly associated with long- term use of potent to super-potent topical steroids. Skin atrophy may manifest as shiny, thin skin, telangiectasia, and striae formation. Areas with baseline relatively thin epidermis such as face and intertriginous areas are more susceptible to developing skin atrophy compared to other areas of the body. Extensive and long-term use of potent or super-potent topical steroids have been associated with systemic side effects due to increased systemic absorption of percutaneously delivered active ingredient. Potential systemic side effects include adrenal suppression, Cushing’s syndrome, and growth retardation in children. For example, psoriasis and atopic dermatitis patients may require longer-term use of potent topical steroids to cover larger body surface areas than other dermatologic patient populations. Systemic adverse effects of topical steroids are particularly relevant to these populations. Currently, the AAD guideline for maximum use of class I topical steroids is to not exceed 50 grams per week.
Seborrheic Dermatitis
A more severe form of common dandruff that can affect the scalp, face and even upper torso. Seen with Parkinson’s, after head trauma, HIV(New onset severe), chronic neurologic conditions such as cerebral palsy
Neurofibromas
a benign nerve sheath tumor in the peripheral nervous system. Usually found in individuals with neurofibromatosis type I (NF1), an autosomal dominant genetically inherited disease, they can result in a range of symptoms from physical disfiguration and pain to cognitive disability. skin, pink or tan to brown colored soft, rubbery, compressible papules. Neurofibromatosis (Types 1-7+) I – other skin/external findings include axillary freckling, café-au-lait spots (6+), Lisch nodules on the iris, macrocephaly, short stature, plexiform neurofibromas (bag of worms); chromosome 17, neurofibromin 1 gene. OK to see a few with no other criteria with no significance
Angiofibromas
small, reddish brown or even flesh-colored, smooth, shiny, 0.1- to 0.3cm papules present over the sides of the nose and the medial portions of the cheeks. They contain fibrous tissue. Findings include tuberous Sclerosis Complex – Adenoma sebaceum (Angiofibroma), facial, multiple, also: Shagreen patch, Ash leaf spots (hypomelanotic macules), forehead plaques, Koenen’s tumors (periungual fibromas) and may have poliosis and increased café-au-lait spots; caused by either TSC 1 – hamartin or TSC 2 – Tuberin mutations
Tuberous sclerosis complex
a genetic disorder characterized by the growth of numerous noncancerous (benign) tumors in many parts of the body. These tumors can occur in the skin, brain, kidneys, and other organs, in some cases leading to significant health problems.
Dermatologic associated findings of diabetes mellitus (DM)
includes acanthosis nigricans, biabetic bullae, diabetic cheiroarthropathy, diabetic dermopathy, disseminated granuloma annulare, necrobiosis lipoidica, and neuropathic leg ulcers.
Acanthosis nigricans
velvety hyperpigmentation of the intertriginous areas and, less often, extensor surfaces. Commonly associated with insulin resistance. Most of the patients are obese. More common in darkly pigmented individuals.
Acral dry gangrene
necrosis of the fingertips or toes. Due to vascular disease in larger vessels.
Acral erythema
erysipelas-like erythema of the hands and/or feet. May be due to small vessel occlusive disease with compensatory hyperemia.
Carotenemia
diffuse orange- yellow skin color, seen in 10% of diabetics. Related to an increase in serum carotene level.
Diabetic bullae (bullous diabeticorum)
tense non-inflammatory bullae on the lower extremities. Unknown pathogenesis.
Diabetic cheiroarthropathy
Thickened skin and limited joint mobility of the hands and fingers, leading to flexion contractures (starting with the fifth digit and progressing radially) and an inability to approximate the palmer surfaces of the hands and fingers (prayer sign). Postulated to result from increased glycosylation of collagen in the skin. Associated with retinopathy, nephropathy, and duration (but not control) of the DM.
Diabetic dermopathy
brown atrophic macules and patches on the legs. Possible precipitated by trauma.
Disseminated granuloma annulare
erythematous annular lesions composed of papules. There ais controversy about the exact relationship of disseminated granuloma annulare and DM.
Eruptive xanthomas
red-yellow papules that appear over a period of weeks to months. Associated with elevated serum triglycerides in patients with poorly controlled diabetes. Control of the DM results in a disappearance of the xanthomas.
Hemochromatosis
bronzing of the skin due to an increase in melanin rather than iron. Excess of iron sotres associated with cirrhosis and cardiac dysfunction as well as DM. due to mutations in HFE, most commonly C282Y. also a risk factor for porphyria cutanea tarda.
Necrobiosis lipoidica
yellow atrophic patches, most often on the shins. An erythematous rim may indicate activity at the border. Ulceration is common and often healing is prolonged. Intralesional triamcinolone, aspirin, dipyridamole and/or pentoxyfylline are possibly helpful. Not all patients have DM.
Neuropathic leg ulcers
non-painful ulcerations at sites of pressure most commonly on the foot; a keratotic rim is characteristic. Associated with sensory neuropathy.
Perforating disorders
e.g. perforating folliculitis. Keratotic papules, often in a perifollicular location. Occurs primarily in African- American diabetic patients on dialysis.
Rubeosis
chronic, flushed appearance of the face, neck and upper extremities. Improved by dietary diabetic control. Flares with vasodilator therapies.
Scleredema (adultorum of Buschke)
erythematous induration of the upper back and nape due to glycosaminoglycan deposition. Unknown etiology. No relationship to control of the DM.
Dermatologic manifestations of hyperthyroidism
fine, velvety, smooth skin. Warm and moist due to increased sweating. Hyperpigmentation (localized or generalized), pruritus (itching), pretibial myxedema (a waxy, discolored induration of the skin), thyroid acropachy (subperiosteal new bone formation), urticaria (hives), dermatographism (the skin becomes raised and inflamed when stroked, scratched, rubbed, and sometimes even slapped), increased incidence of vitiligo (the loss of skin color in blotches), fine, thin, mild and diffuse alopecia, increased incidence of alopecia areata (an autoimmune disease in which hair is lost from some or all areas of the body), onycholysis, koilonychias (thin nails which have lost their convexity, becoming flat or even concave in shape), and clubbing from thyroid acropachy.
Dermatologic manifestations of Hypothyroidism
Dry skin, brittle nails, sparse hair, carotenenia (orange color), delayed wound healing, puffy eyelids, thickened lips, madarosis (loss of lateral 3rd of eyebrow), xanthomas and effect on stature and musculoskeletal development based on age of inset
Dermatologic manifestations of Addison’s Disease
Increased pigmentation (from increased ACTH, with MSH-like effect) including diffusely on skin, palmar creases, sites of trauma, skin folds, mucous membranes, nipples, darker nevi, hair and nails
Dermatologic manifestations of Cushing’s Syndrome
Due to effect of fat distribution: Round face, moon facies, “buffalo hump”, increased fat in arms, legs and waistline. Due to atrophy: diffuse skin thinning, increased bruising(ecchymosis and purpura), striae, delayed wound healing. Other skin findings: Hirsutism, steroid acne (monomorphic on face and upper torso), increased susceptibility to yeasts and fungus on skin
Dermatologic manifestations of Ehlers-Danlos
an inherited connective tissue disorder. Skin findings include increased joint and skin elasticity, poor wound healing with “fish mouth” and “cigarette paper” scars, increased ecchymoses. Cardiac significance: In Classic and Hypermobility types (I–III) there is aortic root dilation, mitral and tricuspid valve regurgitation or prolapse, while in Vascular type (IV) there is increased risk of arterial aneurysms, dissection and rupture, while in Cardiac Valvular type there are valvular abnormalities
Dermatologic manifestations of Endocarditis
Skin findings include splinter hemorrhages, purpura, nail fold changes, Janeway lesions, Osler’s nodes
Dermatologic manifestations of Primary Systemic Amyloidosis
skin findings include pinch purpura (classic tape rip bruise), clear papules, macroglossia, waxy skin. Cardiac significance: unexplained congestive heart failure, conduction abnormalities and cardiomegaly
Myxoma syndromes
Carney complex and its subsets LAMB syndrome and NAME syndrome are autosomal dominant conditions comprising myxomas of the heart and skin, hyperpigmentation of the skin (lentiginosis), and endocrine overactivity
Dermatologic manifestations of Myxoma syndromes including LAMB, NAME, Carney
Skin findings show cutaneous myxomas, increased lentigines and blue nevi. Cardiac significance is atrial myxomas that can obstruct valve function causing CHF, pulmonary edema or embolize
Posterior fossa malformations–hemangiomas–arterial anomalies–cardiac defects–eye abnormalities–sternal cleft and supraumbilical raphe syndrome (PHACES Syndrome)
a cutaneous condition characterized by multiple congenital abnormalities.
Dermatologic manifestations of PHACES Syndrome
will have large hemangioma of face and neck. Cardiac findings include aortic coarctation, atrial and ventricular septal defects and abnormal cervical and vertebral arteries
Dermatologic manifestations of Marfan’s syndrome
Habitus, decreased subcutaneous fat. Cardiac findings of dilation and dissection of the ascending aorta, mitral valve prolapse and regurgitation
Dermatologic manifestations of Cutis laxa
a group of rare connective tissue disorders in which the skin becomes inelastic and hangs loosely in folds. Shar pei like skin. Cardiac abnormalities include aortic dilation and rupture, pulmonary artery stenosis and right-sided heart failure
Dermatologic manifestations of Sarcoidosis
a disease involving abnormal collections of inflammatory cells (granulomas) that can form as nodules in multiple organs. The granulomas are most often located in the lungs or its associated lymph nodes, but any organ can be affected. Skin findings can be protean including hyperpigmented plaques, erosive and ulcerated plaques, granulomatous reactions in tattoos. X-ray will classical show hilar lymphadenopathy and commonly develop pulmonary fibrosis. Also, renal stones, uveitis, hepatosplenomegaly and other systemic symptoms
Dermatologic manifestations of characterised by hardening (sclero) of the skin (derma).
In the more severe form, it also affects internal organs. Skin findings of thickened skin over fingers and hands, skin tightening around mouth, Raynaud’s. Commonly develop pulmonary hypertension, however pericarditis has poor prognosis
Dermatologic manifestations of Tuberculosis
scrofuloderma on neck, lupus vulgaris, tuberculoid reactions, cutaneous TB lesions when disseminated. Lung infection with cavitary lesions or unilateral hilar lymphadenopathy
Dermatologic manifestations of ANCA positive conditions
Churg-Strauss will have nodules, hive like lesions and palpable purpura/vasculitic lesions with asthma like symptoms. Wegener’s granulomatosis (now called Granulomatosis with polyangiitis or GPA) shows vasculitis, granulomatous nodules, ulcers and pyoderma gangrenosum appearing lesions with cavitating lung lesions and pulmonary vasculitis
Dermatologic manifestations of Viral Hepatitis, C and B
Flaviviridae family, single stranded RNA, 6 genotypes with 6 genotypes and 1a and 1b causing 75% of US infections. Other associations: Autoimmune thyroiditis (most common associated autoimmune disorder), non-Hodgkin’s B cell lymphoma association, pulmonary fibrosis, aplastic anemia, autoimmune thrombocytopenic purpura, peripheral neuropathies and joint pain(10+% will have findings). Also associated with Small vessel vasculitis (B,C), Cryoglobulinemic vasculitis (C»B), Urticarial vasculitis (B,C), Polyarteritis nodosa (classic – B, cutaneous – C), Livedo reticularis (C), Urticaria (B,C), Porphyria cutanea tarda (B,C), Pruritus (B,C), Lichen planus – particularly erosive oral disease (C), more in Europe, Sarcoidosis (following therapy with interferon and/or ribavirin) (C>B), Necrolytic acral erythema (C), Gianotti–Crosti syndrome (B>C), more in Europe, Erythema multiforme (B,C), and Erythema nodosum (B>C)
Dermatologic manifestations of Porphyria Cutanea Tarda
skin findings classically are blistering lesions on dorsal hands with sun exposure, hypertrichosis and atrophic scars with milia forming. Associated with hepatitis as listed above (up to 82% in one study). Due to deficiency in uroporhyrinogen decarboxylase. Treated often with serial phlebotomy to decrease iron load
Osler-Weber-Rendu
an inherited disorder of the blood vessels that can cause excessive bleeding. GI bleed, telangiectatic lesions on lips, tongue, finger tips
Gardner’s Syndrome
an autosomal dominant form of polyposis characterized by the presence of multiple polyps in the colon together with tumors outside the colon. 100% cancer risk, multiple epidermoid cysts in almost all, desmoid tumors, fibromas, lipomas, osteomas of mandible/maxilla, impacted teeth, supernumerary teeth, dental cysts, and early tooth loss
Cronkhite-Canada
a rare syndrome characterised by multiple polyps of the digestive tract. polyps, malabsorption, lower cancer risk, rapid and complete hair loss, freckling on extremities and nail changes
Muir-Torre Syndrome
a rare hereditary, autosomal dominant cancer syndrome. polyps, GI/breast/uterine/laryngeal cancer, NHL, sebaceous neoplasms on the skin and multiple keratoacanthoma type of squamous cell carcinoma
Cowden’s
a rare autosomal dominant inherited disorder characterized by multiple tumor-like growths called hamartomas and an increased risk of certain forms of cancer. Polyps and breast and thyroid cancer risk, trichilemmomas on face(small skin colored papules), sclerotic fibromas, lipomas, acral keratosis
Peutz-Jeghers
an autosomal dominant genetic disease characterized by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa (melanosis). polyps, GI bleed and intussusception, testicular/breast/ovary/pancreatic/gallbladder cancer risk, shows freckling around mouth, on lips and mucosa from young age
Pyoderma Gangrenosum
a condition that causes tissue to become necrotic, causing deep ulcers that usually occur on the legs. When they occur, they can lead to chronic wounds. Punched out ulcers that can rapidly enlarge. Associated with inflammatory bowel disease as much as 30% of the time. Never debride, will only enlarge. Can have internal PG lesions in organs
Dyslipidemias
an abnormal amount of lipids (e.g. cholesterol and/or fat) in the blood. Type IIa, increased LDL shows web space xanthoma. Type III, increased IDL, shows palmar crease xanthomas. Xanthoma types: Tuberous–larger, over joints, types 2, 3 and 4; Tendinous–over tendons, types 2 and 3; Eruptive–multiple, small, larger flat or extensor surface, less specific, seen in types 1, 3, 4 and 5, but other systemic causes also (hypothyroid, chronic renal failure, diabetes and more); Plana–Seen with types 2 and 3, but also systemic disease like multiple myeloma, biliary cirrhosis, other gammopathies; usually around eyes, but also neck and upper torso; Xanthelasma around eyes: 50%notassociatedwith dyslipidemia and not usually affected by control of disease when present
xanthoma
is a deposition of yellowish cholesterol-rich material that can appear anywhere in the body in various disease states.
Dermatologic manifestations of Vitamin A deficiencies
Phrynoderma or toad skin, diffuse xerosis and xerophthalmia, Bitot’s spots (eyes), increase mortality with measles
Dermatologic manifestations of Vitamin D deficiencies
hair loss only sign, “deficiency” is area of debate but even complete photoprotection does not lead to deficiency without other factors
Dermatologic manifestations of Vitamin K deficiencies
bruising, purpura, increased bleeding
Dermatologic manifestations of B1/Thiamine deficiencies
Beri Beri, glossitis, glossodynia, edema
Dermatologic manifestations of B2/Riboflavin deficiencies
Oral-ocular-genital syndrome. Findings include: Angular cheilitis (inflammation of one, or more commonly both, of the corners of the mouth), Depapillated glossitis, Magenta tongue (purplish red coloration of the tongue, with edema and flattening of the filiform papillae, occurring in riboflavin deficiency), Seborrheic-like dermatitis around nose (scaly, flaky, itchy, and red skin), Genital dermatitis (scrotal dermatitis sparing midline and extending to thighs), Conjuctivitis/ Photophobia and blepharitis (chronic inflammation of the eyelid, generally the part where eyelashes grow), Anemia, mental retardation, and EKG changes.
