March 23 - Dermatology Flashcards

1
Q

Three types of exocrine glands

A
  1. Merocrine
    - secrete via exocytosis, in which vacuole fuses with plasma membrane
    - salivary galnds, eccrine and apocrine sweat gland
  2. Apocrine
    - secrete via membrane-bound vesicles that pinch from cell
    - mammary glands
  3. Holocrine glands
    - cell lysis releases entire contents of cell
    - sebaceous glands, meibomian glands of eyelid
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2
Q

Foreign body retetntion

A

Retained foreign body such as a stitch can elicit a granulomatous reasponse with a tender papule, nodule, plaque. Develops over days to weeks.

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3
Q

Steps of collagen synthesis

A

Nucleus

  1. Pre-pro-alpha chains made
  2. Signal sequence directs chain to rough ER

ER

  1. Signal sequence cleaved generating pro-alpha chains
  2. Proline and lysine hydroxylation (vit C dependent)
  3. Certain hydroxylysines glycosylated
  4. Pro-alpha chains assemble into procollagen triple helix
  5. Procollagen transferred to Golgi and secreted into ECM

ECM

  1. Procollagen peptidases cleave terminal ends
  2. Collagen molecules spontaneously assemble into fibrils
  3. Lysyl oxidase covalently crosslinks fibers to stabilize the,
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4
Q

Defects in Ehelers danlos vs osteogenesis imperfecta

A

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

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5
Q

tRNA structure

A

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

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6
Q

mRNA splicing

A

Spliceosomes (snRNP complexes) remove introns with GU at 5’ end and AG at 3’ end

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7
Q

Tuberculoid vs lepromatous leprosy

A

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
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8
Q

Different types of bruising

A

Petechiae:

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9
Q

Telangiectasia

A

Small dilations of superficial capillaries or venules. Blanches

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10
Q

Lentigines

A

Small tan or brown macules seen on sun exposed skin

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11
Q

Acrochordon

A

Skin tag, seen in areas of friction

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12
Q

Cavernous hemangioma

A

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.

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13
Q

Cystic hygromas

A

Lymphatic cysts lined by epithelium. Associated with turner and down syndrome

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14
Q

Terbinafine: use and MOA

A

Use: dermatophyte infections
MOA: inhibits squalene epoxidase, leading to inhibition of ergosterol synthesis

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15
Q

Caspofungin:MOA

A

Echinocandin that blocks synthesis of beta-D-glucan in candida and Aspergillus cell walls

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16
Q

Griseofulvin: MOA and use

A

MOA: binds polymerized MTs, disrupting mitotic spindle
Use: accumulates in skin so used to treat dermatophyte infection

17
Q

Process of wound healing

A
  1. Inflammatory phase: fibrin clot allows for hemostasis. Cytokine release calls in PMNs and macrophages.
  2. 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.
  3. Maturation phase: fibrosis and scar formation. Fibroblasts secrete collagen, elastin, and other connective tissues.
18
Q

TGF-beta

A
  • stimulates fibroblasts, connective tissue synthesis, and ECM remodeling
  • decreases during maturation pahse to limit collagenous scar formation
  • overexpression is associated with hypertrophic scar formation
19
Q

Interferon-beta

A
  • antiviral cytokine

- decreases inflammatory cell movement across the BBB and so has a role in treatment of MS

20
Q

Complication of chronic lymphedema

A

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

21
Q

IgE-independent mast cell activation

A

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

22
Q

Acantholysis and acanthosis

A

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

23
Q

Erythema multiforme

A

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

24
Q

VZV on microscopy

A

Intranuclear inclusions in keratinocytes. Multinucleated giant cells. Biopsy shows acantholysis

25
Q

Xanthelasma

A

Cutaneous lesion, commonly on eyelid, that contains lipid laden macrophages. Seen in hyperlipidemia and chronic cholestatic disease

26
Q

Actinic keratosis

A

Erythematous papules with whitish scale. Rough sandpaper like texture

27
Q

Niacin

A

Essential component of NAD and NADP. Obtained in diet and synthesized from tryptophan endogenously

28
Q

Psoriasis: pathophysiology and treatment

A

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

29
Q

Melanocytic nevi: phases

A

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.

30
Q

Seborrheic keratosis pathology

A

Hyperpigmented, well circumscribed, dull surface. Stuck on appearance. Keratin-containing cysts and hyperkeratosis.

31
Q

Breast cancer skin dimpling

A

Indicates suspensory ligament involvement

32
Q

Discoid lupus erythematous

A

Thick, scaly, discoid plaques on unexposed skin. Can result in scarring

33
Q

Lichen planus

A

Polygonal, planar, pruritic, purple palques. May have fine white lines (Wickhams striae) on plaque surface

34
Q

Tinea versicolor

A

Hypo or hyperpigmented or erythematous macules on upper body due to malassezia infection of stratum corneum. Diagnosed by KOH prep