follicular, hair, nails, xanthomas

muehreckes nails

-Double white transverse bands in the nail bed -Problem with vasculature in the nail bed, therefore they do not "grow out" with nail plate -Blanch with pressure -Associated with hypoalbuminemia -Eg: Nephrotic syndrome, Cirrhosis, Protein Losing Enteropathy

causes of onycholysis

-Psoriasis -Hyperthyroidism -Infection (onychomycosis, etc.) -Trauma -Overzealous manicure -Prolonged immersion of nails in water -Leukemia or lymphoma -Diabetes -Drugs (tetracyclines, OCP, etc.)

onycholysis

-Separation of nail plate from nail bed -Distal to Proximal

beaus lines

-Transverse ridging due to growth arrest of proximal nail matrix - INDENTION in nail

mees lines

-Transverse white bands in the nail plate -Discoloration grows out with growing nail -Associated with heavy metal toxicity (esp. Arsenic)

normal hair growth timeline

Anagen: active growth phase, 85% of hairs, ~ 3 years Catagen: transitional phase, 0-5%, ~3 weeks Telogen: resting phase, 10-15% of hairs, ~3 mo

female pattern baldness

Diffuse central thinning of the crown. Frontal hairline less affected. "Christmas tree" thinning everywhere

male pattern baldness

Gradual loss of hair from the vertex and fronto-temporal regions

Pseudofolliculitis barbae

Most common in beard area of male patients with tightly curled hair Hair shaft re-enters dermis and inflammation Inflammatory papules and pustules and firm papules and keloidal scars razon bumps- beard of tighly curled haired, AA, causes a foreign body reaction

follicular occlusion syndrome tetrad

all of the above +pilonidal sinus

treatment of pseudofolliculitis barbae

education, discontinue close shaving Warm compresses, topical steroids (low potency), antibiotics, retinoids- mediate cell turn over Laser hair removal, topical eflornithine (VANIQA) low potency steroids

tenindous xanthomas

firm smooth nodular deposits on tendons or ligaments - achilles tendon high ldl and idl

follicular occlusion syndrome

group of disease in which hail follicle becomes blocked and then rupture resulting in inflammatory skin disorders

clubbing

increased curvature of the nail plate in the longitudnal and transverse plantes

telgogen effluvium course

may take up to a year to recover but will grow back and reassure that baldness does not occur

causes of clubbing

nLung cancer nNSCLC >> Mesothelioma >> SCLC nInterstitial lung disease nComplicated TB, Lung abscess, Empyema nBronchiectasis, CF nChronic hypoxia nCongenital cyanotic heart disease nSubacute Endocardititis nAtrial myxoma nMalabsorption nIBD nCirrhosis nGraves' disease nAka: Thyroid Acropachy nNOT COPD!

traction alopecia

prolonged tension on the hair from braiding, rolling may scar damage follicle or cause permenant hair loss

treatment of alopecia areata

steroids time immunotherby methotrexate+ toacitinib

whats associated with beaus lines

temporailly acute systemic stress severe illness chemo

lovibonds angle

the angle at which the proximal nail fold meets the nail plate, normally less than 180 degrees when viewed from the side. In clubbing is it >180.

tuberous xanthomas

• Orange-yellow papules or nodules • Over areas of pressure (joints, extensors) • High LDL/IDL

follicular occlusion syndrome triad

•Acne conglobata •Dissecting cellulitis of the scalp •Hidradenitis suppurativa

disorders of hair growth

•Alopecia Areata •Telogen Effluvium •Anagen Effluvium •Androgenetic Alopecia •Trichotillomania •Traction Alopecia

alopecia areata variants

•Alopecia totalis: total loss of scalp hair •Alopecia universalis: total loss of scalp + body hair

hidradenitis suppurativa tx

•Antibiotics •Retinoids •Steroids topically •Surgery •Humira anti tnf in ra and psoarisis •Weight Loss, Stop smoking must cut out the skin to cure

treatment of dissecting cellulitis of the scalp

•Antibiotics •Topical, intralesional, and systemic steroids •I&D •Isotretinoin, Dapsone, Humira •Excision w/skin grafting •Radiation

splinterhemorrhages

•Can be seen in endocarditis •May also see Osler's nodes, Janeway lesions, & LCV •Most often just due to trauma

hidrarenitis suppurativa

•Chronic destructive inflammatory d/o of follicular occlusion in apocrine gland-bearing regions + terminal hairs- trapping, rupture and inflammation •Axillae •Inframammary •Groin •Buttocks •Waistband •Inner thighs • •Leads to trapping of follicular contents, rupture, and inflammation -> abscesses, nodules, scars, sinus tracking, superinfection •MC in women, African-American descent

dissecting cellulitis of the scalp

•Chronic, suppurative dz of the scalp •Starts as firm scalp nodules in the mid-posterior vertex, developing into interconnecting boggy fluctuant ridges with scarring alopecia •MC in young adult AA men cellulitic plaques all over the scalp infected as well, chronic process, difficult to treat, tends to occur

Koilonycha

•Concave curvature of the nails •aka "spoon nails" •Associations •Iron deficiency anemia •Polycythemia vera •Plummer-Vinson syndrome

favre racouchot syndrome

•Disorder related to chronic sun exposure •Formation of small cysts, open comedones, most commonly on the periocular region, temples, and extending to the cheeks •MC in elderly, white men and heavy smoking •Treatment: sun protection, acne regimen

anagen effluvium

•Follow cancer chemotherapy •Attacks rapidly dividing cells in the anagen phase •Occurs 1-2 weeks after chemotherapy •90% of hair is lost •Can affect all body hair •Usually not permanent

telogen effluvium

•High percentage (>25%) of hairs enter the telogen phase, resulting in excessive shedding 3 months later normally 15% of hair but get an instul to all in telogen phase so after 3 months then they shed so a quarter or hair shed all at once

xanthomas

•Irregular yellow patches or nodules •Represent abnormal accumulation/deposition of lipids in the skin, tendons, fascia, and periosteum •Mainly TGs or cholesterol •Some are indicative of underlying lipid metabolism disorders, either a genetic disorder or secondary to another disease process •Some occur in the setting of normal blood lipid levels

acne keloidalis nuchae

•Keloid-like papules and plaques which progress to scarring alopecia •Posterior neck/occipital scalp of AAM keloiding acne on back of neck

trichotillomania

•Neurotic practice of plucking or breaking the hair from the scalp or eyebrows •Usually in girls under 10, subject to psychosocial stressors •Can see broken hairs in bizarre, irregular patches or scarring of the follicles •May be permanent

alopecia areta

•Rapid non-scarring hair loss in round + oval patches •Look for "exclamation point" hair that are easy to pull out •An autoimmune attack on the hair follicle by T cells •Association with other autoimmune diseases not scarring or inflammatory, tapered and easily pulled out •Common locations: scalp, beard, eyebrows, eyelashes

eruptive xanthomas

•Red to yellow papules on extensor surfaces, buttocks •Associated with high TG levels > 3000-4000

treatment of acne kelodalis

•Remove friction (head gear, shirts etc) •No close shaving •Topical tretinoin and mid to high potency corticosteroid •Intra lesional steroids •Topical/systemic antibiotics •Surgical excision

causes of acne keloidalis nuchae

•Similar to PFB? •Friction •Chronic low grade folliculitis? •Autoimmune process?

Prognosis of Alopecia Areata

•Spontaneous recovery possible within 1 year •Can progress to become widespread and permanent •Childhood onset has poorer prognosis

what causes telogen effluvium

•Surgery •Childbirth •Severe infection •Drugs (vit A, retinoids, anti-thyroid) •Crash dieting

treatment of androgenetic alopecia

•Topical minoxidil (Rogaine) •Finasteride (Propecia): 5-alpha reductase inhibitor decrease DHT which reduces hair loss •Spironolactone: aldosterone antagonist •Hair transplant take from the back of the head and sprinkle on top to keep that hair permantly •Platelet rich plasma blood from yourself spun and take out rbc and have clear liquid and inject back into the scalp

terrys nails

•Whitening of the proximal 2/3 of the nail plate with sparing of the distal third •Most commonly associated with liver failure, cirrhosis chronic renal failure

treatment of xanthomas

•Work-up to rule out any underlying or associated disorders •Full lipid profile •If indicated: CBC, LFTs, SPEP, UPEP, bone marrow biopsy, genetic testing, stress test •Lifestyle modifications •HMG-CoA reductase inhibitors (statins) •Fibric acid derivatives •Bile acid binding resins •Nicotinic acid •Probucol •Cosmetic removal:dermabrasion, ablative lasers, excision, electrocautery + dessication

types of xanthromas

•Xanthelasma •Eruptive xanthomas •Tuberous xanthomas •Tendinous xanthomas •Plane xanthomas

xanthelasma

•Yellowish thin plaques that occur near the inner canthus of the eylid, upper lid, or lower lid •Up to 50% may be normolipemic

half and half nails

•aka Lindsay's nails •Whitening of the proximal half of the nail plate with sparing of the distal half •Associated with chronic renal failure

androgenetic alopecia

•aka male-pattern or female-pattern hair loss •Genetically determined sensitivity of scalp hair follicles to adult levels of androgens •Strong genetic predisposition, polygenic inheritance •More follicles in telogen phase, lengthening of telogen phase, progressive miniaturization of the hair follicles, telogen phase last longer and hair follicles decrease in size, can be permenant when loss of hair follicles

causes of xanthomas

•dysfunctional or def lipoprotein lipase, apolipoprotein CII, impaired insulin activity, obesity, DM, alcoholics, retinoids, protease inhibitors, olanzapine