9 - Geriatric Skin Disorders Flashcards
Normal skin aging
o Chronological = physiologic alteration in skin function
o Photoaging = secondary to UV exposure
Decrease in skin lipids with againg leads to
dryness
Decreased cell replacement with againg leads to
roughness, delayed healing
Decreased DNA repair with againg leads to
increased malignancies
Fragmentation of collagen and elastin with againg leads to
Wrinkles, increase in ulcers
Reduced connective tissue support of blood vessels with againg leads to
increased purpura
Decreased sensation with againg leads to
Increased injury
Impaired thermoregulation with againg leads to
vulnerability to heat and cold
Reduced function of subcutaneous glands with againg leads to
decreased lipids
Reduced function of sweat glands with againg leads to
risk of overheating
Decrease in Langerhans cells with againg leads to
Delayed healing and increase in infection
Reduced subcutaneous fat with againg leads to
increased risk of injury
Flatteneing of DE junction with againg leads to
increase risk of skin tears and listers
Reduced linear nail growth with againg leads to
Onychogryphosis, longitudinal striations, brittle nails
Decreased melanocytes with aging leads to
Increase in malignancies
A patient asks you why their nails are so brittle and why they are susceptible to skin tears when bumped. Your response includes:
o Brittleness is due to the longer time it takes for nails to grow
o Brittleness is due decrease in skin lipids
o Skin tears are due to decreased number of Langerhans’ cells
o Skin tears are due to decreased number of melanocytes
o Skin tears are due to flattening of the DE junction
o Brittleness is due to the longer time it takes for nails to grow
o Skin tears are due to flattening of the DE junction
Extrinsic changes due to UV light
- Pruritus
- Spider veins
- Age “spots”
- Easy bruising and skin breaks
- Increase in malignancy
Decubitus ulcer
- Occur over bony prominences
- Pressure over time leads to ischemia and tissue damage
- Stages (according to NPUAP)
o I - non-blanchable erythema
o II - necrosis with superficial to partial thickness skin loss
o III - necrosis with full-thickness skin loss to fascia
o IV - extensive necrosis into muscle and bone - Treatment
o Frequent change of position
o Use of air, gel, water mattresses
o Keep ulcer dry
o Nutritional consult
o Infection control measures
Xerosis
- Cause
o Due to decrease in lipids combined with impaired epidermal barrier function (greater loss of water from skin) - Symptoms
o Dryness leads to pruritus, rough and scaly skin
o Exacerbated by soap, hot water, low humidity - Similar (synonymous?) to asteatotic eczema
- Treatment
o Moisturizers with urea, lactic acid, petrolatum, lanolin
o Can add low potency steroid ointment (1 % hydrocortisone)
o Apply after bath Best time to apply either type of moisturizer is after a bath
o Hasten moisturizing by applying Saran wrap® over area, cover w/ sock at night - NOTE: there are numerous treatments out there because patients respond differently and there is no way to tell which ones
o Hydrophobic = ointment/Vaseline physically trap water in the skin
o Hydrophilic = lactic acid, urea, etc. draw water up to the epidermis to increase moisture - When you have SERIOUS xerosis skin is breaking/bleeding down to the dermis, use 40% urea (costs $60 for a jar)
Pruritus
with resultant excoriations
- Most commonly caused by xerosis and leads to local excoriations
- Due to increased touch and pain thresholds and/or systemic disorders (“PHILL”)
o P = polycythemia vera
o H = HIV
o I = iron deficiency anemia
o L = liver and renal dysfunction
o L = lymphoma - Treatment
o topical steroid ointments
o topical Benadryl® (with or without calamine lotion)
o topical lidocaine
o topical NSAID’s and moisturizers
Stasis dermatitis
- Symptoms
o Dermatitis may be weepy, dry, scaly, or lichenified - Cause
o Venous hypertension leads to inflammatory reaction accompanied by leukocyte activation and release of red cells into tissue
o This breaks down into hemosiderin depositions - Treatment
o Compression dressings w/ or w/o Unna boot® to treat underlying skin condition
Bacterial infection
- Cause
o Usually caused by Staph and Strep species (gram positive)
o Due to alteration in skin architecture (loss of Langerhans’ cells) and loss of barrier function caused by physical factors (e.g., venous stasis) - Cellulitis
o Infection of subcutaneous fat
o Deeper than erysipelas and does not have a distinct border - Erysipelas
o Infection of dermis and upper subcutaneous tissue - Treatment
o Without open wound, topical treatment ineffective-need oral antibiotics
o Usually PCN (but may have resistant staph infection), cephalosporin, clindamycin
Herpes zoster
- Cause
o Due to impaired immune function
o After recovery from chickenpox at young age, varicella zoster virus becomes latent in dorsal root ganglia, and reactivated with decline in immunity - Symptoms
o Follows dermatome and very painful
o Pain usually precedes onset of vesicular lesions and may last for months to years after disappearance of lesions (post-herpetic neuralgia) - Treatment
o Oral acyclovir® and local wound therapy
o Oral prednisone not recommended
o Topical lidocaine
o Zoster vaccine (Zostavax™) used for prevention only (effective 60% of the time)
Herpes simplex
- Types
o Occurs as two types (1 and 2) with 1 being more common and usually occurs around the mouth (type 2 occurs in the genitalia) - Symptoms
o After it infects skin it can remain latent in the nerve cell ganglia proximal to site of infection
o In immune-compromised host, blisters form and then eventually ulcers with serpiginous borders
o Abrupt onset, fever and malaise present before blisters-not as painful as zoster - Diagnosis via Tzanck smear
o The vesicle should be unroofed aseptically.
o Using a sterile instrument, the floor of the newly produced ulcer can then be scraped. The obtained material can be spread on a glass microscope slide and then dried and fixed for staining.
o Staining can be performed with a Papanicolaou smear stain or, alternatively, whatever is available will suffice (eg, Gram, Giemsa, or Wright stain).
o A positive result is the finding of multinucleate giant cells. - Treatment
o Nucleoside analogs (Acyclovir®) and local wound therapy