March 23 - Dermatology Flashcards
Three types of exocrine glands
- Merocrine
- secrete via exocytosis, in which vacuole fuses with plasma membrane
- salivary galnds, eccrine and apocrine sweat gland - Apocrine
- secrete via membrane-bound vesicles that pinch from cell
- mammary glands - Holocrine glands
- cell lysis releases entire contents of cell
- sebaceous glands, meibomian glands of eyelid
Foreign body retetntion
Retained foreign body such as a stitch can elicit a granulomatous reasponse with a tender papule, nodule, plaque. Develops over days to weeks.
Steps of collagen synthesis
Nucleus
- Pre-pro-alpha chains made
- Signal sequence directs chain to rough ER
ER
- Signal sequence cleaved generating pro-alpha chains
- Proline and lysine hydroxylation (vit C dependent)
- Certain hydroxylysines glycosylated
- Pro-alpha chains assemble into procollagen triple helix
- Procollagen transferred to Golgi and secreted into ECM
ECM
- Procollagen peptidases cleave terminal ends
- Collagen molecules spontaneously assemble into fibrils
- Lysyl oxidase covalently crosslinks fibers to stabilize the,
Defects in Ehelers danlos vs osteogenesis imperfecta
Ehlers danlos: defect in procollagen peptidase such that terminal propeptides can’t be cleaved. Results in soluble collagen that can’t crosslink.
Osteogenesis imperfecta: decreased quantity and/or quality of type I collagen
tRNA structure
Anticodon loop: binds codon on mRNA
Acceptor stem
- 3’ end and 5’ end base pair to form the acceptor stem
- 3’ end is amino acid attachment site. Undergoes post-transcriptional modifictation to add CCA to end
D loop: dihydrouridine residues
T loop: ribothymidine, pseudouridine, and cytidine residues
mRNA splicing
Spliceosomes (snRNP complexes) remove introns with GU at 5’ end and AG at 3’ end
Tuberculoid vs lepromatous leprosy
Tuberculoid
- positive skin test
- cell mediated Th1 resopnse with production of IL-2, IFN-gamma, and IL-12
- mild disease with low bacterial load
Lepromatous
- negative skin test
- humoral Th2 response with production of IL-4, IL-5, IL-10, and high antibody levels
- severe disease with high bacterial load - can get positive blood cultures
Different types of bruising
Petechiae:
Telangiectasia
Small dilations of superficial capillaries or venules. Blanches
Lentigines
Small tan or brown macules seen on sun exposed skin
Acrochordon
Skin tag, seen in areas of friction
Cavernous hemangioma
Dilated vascular spaces with thin-walled endothelial cells. Soft blue, compressible masses up to a few cm in diameter. Seen in skin, deep tissue, mucosa, viscera. Brain adn skin ones associated with VHL syndrome.
Cystic hygromas
Lymphatic cysts lined by epithelium. Associated with turner and down syndrome
Terbinafine: use and MOA
Use: dermatophyte infections
MOA: inhibits squalene epoxidase, leading to inhibition of ergosterol synthesis
Caspofungin:MOA
Echinocandin that blocks synthesis of beta-D-glucan in candida and Aspergillus cell walls
Griseofulvin: MOA and use
MOA: binds polymerized MTs, disrupting mitotic spindle
Use: accumulates in skin so used to treat dermatophyte infection
Process of wound healing
- Inflammatory phase: fibrin clot allows for hemostasis. Cytokine release calls in PMNs and macrophages.
- Proliferative phase: 3-5 days after injury. Fibroblasts and endothelial vascular cells proliferate causing neovascularization. Fibroblast migration and proliferation driven by platelet-derived growth factor and TGF-beta. Epithelial cells proliferate and secrete basement membrane.
- Maturation phase: fibrosis and scar formation. Fibroblasts secrete collagen, elastin, and other connective tissues.
TGF-beta
- stimulates fibroblasts, connective tissue synthesis, and ECM remodeling
- decreases during maturation pahse to limit collagenous scar formation
- overexpression is associated with hypertrophic scar formation
Interferon-beta
- antiviral cytokine
- decreases inflammatory cell movement across the BBB and so has a role in treatment of MS
Complication of chronic lymphedema
Risk of cutaneous angiosarcoma down the road. Presents as firm violaceous nodules. Poor prognosis because usually widespread at time of diagnosis. Infiltration of dermis with slit-like abnormal vascular spaces
IgE-independent mast cell activation
Associated with opioids, radiocontrast agents, vancomycin. Presents with diffuse itching and pain, bronchospasm, swelling shortly after starting one of those drugs. Medicine activates PKA and IP3 kinase leading to release of mediators
Acantholysis and acanthosis
Acantholysis: loss of adhesion beween keratinocytes in epidermis. Seen in pemphigus disorders
Acanthosis: increased thickness of stratum spinosum, seen in psoriasis, seborrheic dermatitis, acanthosis nigricans
Erythema multiforme
Acute inflammatory disorder. Erythematous round papules that evolve into target lesions with dusky central area, pale ring, and erythematous halo. Mediated by CD8+ cells. Most often associated with infection, esp HSV and mycoplasma. Can also be seen with sulfonamides, malignancy, collagen vascular disease
VZV on microscopy
Intranuclear inclusions in keratinocytes. Multinucleated giant cells. Biopsy shows acantholysis
Xanthelasma
Cutaneous lesion, commonly on eyelid, that contains lipid laden macrophages. Seen in hyperlipidemia and chronic cholestatic disease
Actinic keratosis
Erythematous papules with whitish scale. Rough sandpaper like texture
Niacin
Essential component of NAD and NADP. Obtained in diet and synthesized from tryptophan endogenously
Psoriasis: pathophysiology and treatment
Pathophys: Hyperproliferation of keratinocytes. Inflammation of epidermis and dermis leading to epidermal thickening and scaling. Can be itchy or asymptomatic and itching leads to bleeding. Typcially on extensor surfaces which distinguishes from fungal infections which are in areas of increased moisture
Treatment: Topical vit D analogues (calcipotriene, calcitriol) which activates vit D receptor and inhiit keratinocyte proliferation. Topical steroids. Second line is methotrexate or oral retinoid
Melanocytic nevi: phases
Benign lesion with round, uniforn, mitotically quiescent melanocytes. Mature through three phases:
1) junctional nevus: cells at dermal-epidermal junction. Flat and brown to black.
2) compound nevus: aggregates extend into dermis, raised tan to brown papules
3) intra-dermal nevus: older lesions in which epidermal nests lost. Lose tyrosinase activity so stop making pigment. Skin colored-tan and dome shaped.
Seborrheic keratosis pathology
Hyperpigmented, well circumscribed, dull surface. Stuck on appearance. Keratin-containing cysts and hyperkeratosis.
Breast cancer skin dimpling
Indicates suspensory ligament involvement
Discoid lupus erythematous
Thick, scaly, discoid plaques on unexposed skin. Can result in scarring
Lichen planus
Polygonal, planar, pruritic, purple palques. May have fine white lines (Wickhams striae) on plaque surface
Tinea versicolor
Hypo or hyperpigmented or erythematous macules on upper body due to malassezia infection of stratum corneum. Diagnosed by KOH prep
