Derm

Question 1

mechanism of action of Terbinafine

Answer 1

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

Question 2

Chediak-Higashi syndrome

Answer 2

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

Question 3

what is the Asboe-Hansen sign

Answer 3

when the bullae of pemphigus vulgaris spread laterally when pressure is applied on top

Question 4

what is the Nikolsky sign

Answer 4

when new blisters may form with gentle traction or rubbing like with pemphigus vulgaris

not seen with bullous pemphigoid

Question 5

xeroderma pigmentosum

Answer 5

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

Question 6

enzyme deficient in xeroderma pigmentosum

Answer 6

UV-specific endonuclease–> enzyme used to repaired thymine dimers caused by UR rays (damaged DNA)

Question 7

vitamin D analogs can be used to treat psoriasis–> how?

Answer 7

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

Question 8

androgenetic alopecia

Answer 8

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

Question 9

what is urticaria

Answer 9

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

Question 10

what is acantholysis

Answer 10

loss of cohesion between kertinocytes in the epidermis–> found in the pemphigus family of disorders

Question 11

what is acanthosis

Answer 11

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

Question 12

victamin C deficiency will lead to failure in forming what?

Answer 12

collagen–> gingival swelling/bleeding, petechiae, ecchymosies, poor wound healing, perifolluclar hemorrhages, and coiled (corkscrew) hair

Question 13

why do you need vitamin C in production of collagen

Answer 13

act as cofactor for post-translational modification that happens int he RER

Question 14

healing by primary vs secondary intention

Answer 14

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

Question 15

keloids is due to what

Answer 15

excessive collagen formation during the remodeling phase of wound healing

Question 16

what are accessory nipples due to

Answer 16

failure of involution of the mammary ridge

Question 17

what is photoaging

Answer 17

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

Question 18

what is actinic keratoses

Answer 18

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

Question 19

Ehlers- Danlos syndrome

Answer 19

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

Question 20

Stewart-Treves syndrome

Answer 20

cutaneous angiosarcoma

risk factor: chronic lymphedema

Question 21

exocrine glands

Answer 21

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)

Question 22

4 major components of acne formation

Answer 22

• 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

Question 23

erythema multiforme

Answer 23

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)

Question 24

3 phases of wound healing

Answer 24

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

Question 25

what role does transforming growth factor-beta plays on wound healing

Answer 25

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

Question 26

complications of psoriasis

Answer 26

psoriatic arthritis, nail pitting, and uvetis

Question 27

how to differentiate between tuberculoid leprosy and lepromatous leprosy

Answer 27

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)

Question 28

mutation that is seen in 40-60% of patients with melanoma

Answer 28

BRAF V600E mutation

BRAF= protein kinase involved in activation of signaling pathways for melanocyte proliferation

treat with vemurafenib: potent inhibitor of mutated BRAF

Question 29

what skin disease is associated with celiac disease?

Answer 29

dermatitis herpetiformis-erythematous pruritic papules, vesicles, and vullae that appear bilaterally and symmetrically on extensor surfaces

treat with gluten-free diet

Question 30

pellagra

Answer 30

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

Question 31

primary effector cells in contact dermatitis

Answer 31

cytotoxic CD8+ T cells or CD+ TH1 cells

if urushiol-induced contact dermatitis (poison ivy, poison oak, and poison sumac), the CD8+ T cells

Question 32

junctional nevus

Answer 32

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

Question 33

compound nevus

Answer 33

aggregates of nevus cells extend into dermis

raised papules with uniform bown to tan pigmentation

Question 34

intradermal nevus

Answer 34

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

Question 35

viral-dependent nucleoside analog antiviral drugs

Answer 35

acyclovir, valacyclovir, famciclovir, and ganciclovir

require both viral and cellular kinases for conversion to their active nucleoside triphosphate form

Question 36

nucleotide analog antiviral drugs

Answer 36

cidofovir and tenofovir

nucleoside monophosphate that requires only cellular kinases for activation

Question 37

atopic dermatitis (eczema)

Answer 37

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

Question 38

what do you see on ligh microscopy of varicella zoster virus (VZV)

Answer 38

intranuclear inclusions in keratinocytes and multinucleated giant cells (positive Tzanck smear)

Question 39

what do you see on skin biopsy of varicella zoster virus

Answer 39

acantholysis (loss of intercellular connections) of keratinoctes and intraepidermal vesicles

Question 40

what can trigger IgE-independent mast cell degranulation

Answer 40

usually medications such as opioids, radiocontrast agents, and some antibiotics (eg, vancomycin)

symptoms: diffuse itching and pain, bronchospasm, and localized swelling urticaria)

Question 41

glomangioma

Answer 41

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)

Question 42

role of glomus body:

Answer 42

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