Derm Flashcards
mechanism of action of Terbinafine
inhibits synthesis of ergosterol of the fungal membrane by inhibiting the enzyme squalene epoxidase
drug tends to accumulate in skin and its appendages, and its side effects are mild by the topical route
Chediak-Higashi syndrome
autosomal recessive syndrome of neutrophil phagosome lysosome fusion that results in neurologic abnormalities, partial albinism, and an immunodeficiency caused by defective neutrophil function
neuro defects: nystagmus, peripheral and cranial neuropathies
what is the Asboe-Hansen sign
when the bullae of pemphigus vulgaris spread laterally when pressure is applied on top
what is the Nikolsky sign
when new blisters may form with gentle traction or rubbing like with pemphigus vulgaris
not seen with bullous pemphigoid
xeroderma pigmentosum
rare autosomal recessive disorder that occurs due to defective nucleotide excision repair of DNA damaged by UV light
leads to accumulation of abnormal pyrimidiine nucleotides and other carcinogenic adducts
skin= normal at birth, but present during the first year of life with severe sun sensitivity affecting affecting light-exposed areas, especially the face
skin shows atrophy, telangiectasias (spider veins), and intermingling areas of hypo-and hyperpigmentation due to chronic UV damage–> melanoma and squamous and basal cell carcinoma develop early like at 5-6 yo
enzyme deficient in xeroderma pigmentosum
UV-specific endonuclease–> enzyme used to repaired thymine dimers caused by UR rays (damaged DNA)
vitamin D analogs can be used to treat psoriasis–> how?
bind to vitamin D receptor and inhibit keratinocyte proliferation and stimulate keratinocyte differentiation
also inhibit T cell proliferation and other inflammatory mediators
ex) calcipotriene, calcitriol, and tacalcitol
androgenetic alopecia
hair loss primarily at the anterior scalp and vertex
polygenic inheritance
dihydrotestosterone (DHT)= primary pathogenic factor
treat with 5-alpha-reductase inhibitors (eg, finasteride) to decrease conversion of testosterone to DHT
what is urticaria
hives
pruritic, raised, erythematous plaque (wheals)
due to increased permeability of the microvasculature–> edema of superficial dermis
IgE-mediated degranulation of mast cells and also non-IgE-mediated degranulation or mast cell-independent mechanisms
what is acantholysis
loss of cohesion between kertinocytes in the epidermis–> found in the pemphigus family of disorders
what is acanthosis
diffuse increase in thickness of the stratum spinosum (prickle cell layer) between the granular cell layer and basal layer of the epidermis
ex) psoriasis, seborrheic dermatitis (“stuck-on cysts), and acanthosis nigricans
victamin C deficiency will lead to failure in forming what?
collagen–> gingival swelling/bleeding, petechiae, ecchymosies, poor wound healing, perifolluclar hemorrhages, and coiled (corkscrew) hair
why do you need vitamin C in production of collagen
act as cofactor for post-translational modification that happens int he RER
healing by primary vs secondary intention
primary: surgical closure of well-approximated wound edges, which decreases the likelihood of significant scarring
secondary: (spontaneous healing) lead to scarring and prolonged remodeling as the wound edges are not well approximated
keloids is due to what
excessive collagen formation during the remodeling phase of wound healing
what are accessory nipples due to
failure of involution of the mammary ridge
what is photoaging
product of excess exposure to UVA wavelengths
characterized by epidermal atrophy with flattening of rete ridges
decreased collagen fibril production and increased degradation of collagen and elastin in the dermis
what is actinic keratoses
most commonly present as erythematous papules with overlying whitish scale
“felt more than seen” and have rough, sandpaper-like texture on palpation
due to excessive sun exposure but with genetically predisposed people age 40-60
considered as a premalignant condition
Ehlers- Danlos syndrome
hereditary disorders involving a defect in collagen synthesis (type III collagen- classical type; type V collagen- vascular type))
hypermobile joints, overelastic skin, and fragile tissue susceptible to bruising, wounds, and hemarthrosis
associated with berry and aortic aneurysms
Stewart-Treves syndrome
cutaneous angiosarcoma
risk factor: chronic lymphedema
exocrine glands
merocrine: secrete via exocytosis (salivary, eccrine sweat, and apocrine sweat)
apocrine: secrete via membrane-bound vesicles (mammary glands)
holocrine: cell lysis releases entire contents of the cytoplasm and cell membrane (sebaceous and meibomian glands)
4 major components of acne formation
- keratinization of hair follicle with formation of a keratin plug that blocks release of sebum
- hypertrophy of sebaceous glands with excess sebum production
- colonization of glands with Propionibacterium acnes
- bacterial hydrolysis of triglycerides in sebum and release of inflammatory fatty acids
erythema multiforme
acute inflammatory disorder that involve skin
characterized by erythematous papules the evolve into target lesions
associated with infections (herpes simplex virus and mycoplasma) and medications (sulfonamides)
3 phases of wound healing
1) inflammatory phase: formation of fibrin clot that results in hemostasis. Cytokines released by activated platelets and damaged cells–> migration of neutrophils (within the first 24 hours) and macrophages (2-3 days later) to damaged area
2) proliferative phase: 3-5 days after injury. Fibroblasts and endothelial vascular cells proliferate to form connective tissue and blood vessels (neovascularization)
3) maturation phase: fibrosis (scar formation) and starts during the second week after injury. active fibroblasts synthesize collagen, elastin, and other components of the connective tissue matrix
what role does transforming growth factor-beta plays on wound healing
critical for fibroblast migration, proliferation, and connective tissue synthesis
responsible for hypertrophic/keloid scarring and fibrosis of the lung, liver, and kidney if there is increased activity of this growth factor
complications of psoriasis
psoriatic arthritis, nail pitting, and uvetis
how to differentiate between tuberculoid leprosy and lepromatous leprosy
tuberculoid: exhibit a strong CD4+ TH1 cell-mediated immune response to Mycobacterium leprae so lepromin skin test will be positive
lepromatous: lepromin skin test will be negative due to their weak TH1 cell-mediated immune response (this form can be lethal) (with the lion facies)
mutation that is seen in 40-60% of patients with melanoma
BRAF V600E mutation
BRAF= protein kinase involved in activation of signaling pathways for melanocyte proliferation
treat with vemurafenib: potent inhibitor of mutated BRAF
what skin disease is associated with celiac disease?
dermatitis herpetiformis-erythematous pruritic papules, vesicles, and vullae that appear bilaterally and symmetrically on extensor surfaces
treat with gluten-free diet
pellagra
secondary to vitamin B3 (niacin) deficiency–> needed for NAD and NADP, which are cofactors for many dehydrogenase and reductase enzymes
characterized by photosensitive dermatitis, diarrhea, and dementia
primary effector cells in contact dermatitis
cytotoxic CD8+ T cells or CD+ TH1 cells
if urushiol-induced contact dermatitis (poison ivy, poison oak, and poison sumac), the CD8+ T cells
junctional nevus
aggregates of nevus cells limited of the dermoepidermal junction
flat, black-to brown-pigmented macules with darker coloration in the center than the periphery and preserved skin markings
compound nevus
aggregates of nevus cells extend into dermis
raised papules with uniform bown to tan pigmentation
intradermal nevus
older lesions in which the epidermal nests of nevus cells have been lost
remaining dermal nevus cells lose tyrosinase activity and produce little to no pigment
skin-to-tan-colored, dome-shaped, and sometimes pedunculated
viral-dependent nucleoside analog antiviral drugs
acyclovir, valacyclovir, famciclovir, and ganciclovir
require both viral and cellular kinases for conversion to their active nucleoside triphosphate form
nucleotide analog antiviral drugs
cidofovir and tenofovir
nucleoside monophosphate that requires only cellular kinases for activation
atopic dermatitis (eczema)
chronic inflammatory skin disorder of childhood
pruritus and erythematous, weeping/crusted papules and plaques that occur in response to certain enviro antigens
associated with other atopic diseases such as allergic rhinitis and asthma
what do you see on ligh microscopy of varicella zoster virus (VZV)
intranuclear inclusions in keratinocytes and multinucleated giant cells (positive Tzanck smear)
what do you see on skin biopsy of varicella zoster virus
acantholysis (loss of intercellular connections) of keratinoctes and intraepidermal vesicles
what can trigger IgE-independent mast cell degranulation
usually medications such as opioids, radiocontrast agents, and some antibiotics (eg, vancomycin)
symptoms: diffuse itching and pain, bronchospasm, and localized swelling urticaria)
glomangioma
tumor of the modified smooth muscle cells of a glomus body (numerous small, encapsulated neurovascular organs found in the dermis of the nail bed, the pads of fingers and toes, and the ears)
role of glomus body:
shunt blood away from the skin surface in cold temperatures in order to prevent heat loss
direct blood flow to skin surface in hot environments to facilitate dissipation of heat
