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Test 2 Flashcards

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Dermatology Board Prep flashcards
1
Q

clinical presentation and tx for Mycobacterium marinum?

A

Mycobacterium marinum
Severe fish-tank granuloma w/sporotrichoid distribution pattern
Tx: Clarithromycin/Rifampin + ethambutol

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2
Q

Clinical presentation of Microsporum canis, and the txs?

A

Microsporum canis:
Tinea corporis, use topical terbinafine
Tinea capitis, use oral terbinafine

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3
Q

What are 2 cutaneous MRSA presentations, and their txs?

A

MRSA
Impetigo, use topical mucipiron
Curbuncle, use TMP/SMX or (a Lincosamide)

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4
Q

What are the scalp layers?

A 
S = skin
C = dense Connective tissue
A = Aponeurotic (occipitofrontalis m)
L = Loose connective tissue
P = Pericranium
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5
Q

What’s innervation for scalp?

A

CN V1-3 anteriorly

C2-3 posteriorly

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6
Q

What’s vascular for scalp?

A

Supratrochlear and Supraorbital arteries from Ophthalmic artery from Internal Carotid
External carotid’s superficial temporal, posterior auricular, and occipital

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7
Q

Describe major hair cycle phases

A 
Hair cycle:
Anagen growth
Catagen = regression
Telogen = rest
Exogen = ejection from follicle
Kenogen = no hair in follicle
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8
Q

Differentiate vellus and terminal hair?

A

· Most follicles produce vellus hair: fine (<0.03 mm,) short, non-pigmented, rapidly-cycling.
· Eyebrow, scalp, and eyelash follicles produce terminal hair: course (>0.06 mm,) long, pigmented, slowly-cycling.
· Lanugohairs are fine and long, and are formed in the fetus at 20 weeks’ gestation. They are normally shed before birth, but may be seen in premature babies.
· During puberty, vellus hairs in the genital areas and axilla are stimulated to become terminal hairs

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9
Q

Compare Exogen during Anagen w/exogen in Telogen

A

Exogen during Anagen = normal

Exogen during Telogen = longer period of Kenogen

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10
Q

What are 6 stages of Anagen?

A

Anagen:
1-5 Proanagen: proliferation of hair generating in dermal pipilla
6 Metanagen: full hair unit produced w/epithelial hair bulb around dermal papilla

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11
Q

What occurs during Catagen? how long does it last?

A

Catagen:
Hair follicle involutes, goes through apoptosis-driven regression, shrinks to 1/6 of its diameter in Anagen, and moves up towards surface
Club hair forms w/brush-like base to anchor hair fiber in Telogen follicle
Lasts few weeks

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12
Q

What occurs during Telogen

A

Telogen:

no melanocytes, layer of epithelial cells forms over dormant dermal papilla

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13
Q

What occurs during Exogen?

A

Exogen:
proteolytic cleaving of hair fiber shaft
Technically this is occurring in early Anagen

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14
Q

What protein occurs just before Anagen? and where?

A

WNT proteins appear just before Anagen in hair follicle bulb

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15
Q

Differentiate Psoriasis and Seborrheic dermatitis

A

Psoriasis = beyond hairline, silver scale on erythematous base, asymptomatic, Auspitz sign

Seborrheic dermatitis = chronic inflammation where sebaceous glands dense (scalp, forehead, eyebrows, lash line, nasolabial folds, beard postauricular), yellow greasy crust, Malassezia furfur

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16
Q

Differentiate Nevus sebaceous, Pilar cyst

A

Nevus sebaceous = hamartomatous lesion of sebaceous gland, usually found in newborns, velvety yellow/orange/tan plaque, hairless, benign but 10% transform to BCC

Pilar cyst = keratin arising from hair follicle, multiple/firm/mobile/slow growing SubQ nodules up to 5cm

Both on scalp

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17
Q

Differentiate Epidermoid cyst and Lipoma

A

Epidermoid cyst = usually trunk, can be scrotal/face/neck proliferation of EPIdermal cells within DERMIS, a keratin plug, looks like pore, ruptured smelly cottage cheese-like

Lipoma = trunk and extremities, can be scalp, painless/rubbery/mobile

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18
Q

Differentiate Epidermoid from Pilar cyst?

A

Epidermal cysts are usually trunk, epidermal cells in dermis, causing keratin plug that looks like pore, and smelly cottage cheese inside

Pilar cysts are on scalp, multiple/firm/mobile/slow growing, keratin arising from follicle

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19
Q

Describe inheritance pattern of androgenetic alopecia, and what’s the 1 gene that contributes the most to it?
How to tx? MOA?

A

Androgen receptors are X-linked, esp PAX1 (paired box 1) gene is implicated
Tx: Minoxidil, direct vasodilator

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20
Q

Describe Telogen Effluvium hx, PE findings, tx?

A

Telogen effluvium =
stress response triggers up to 50% of hair to pass into Telogen phase
PE: diffuse shedding/thinning 2-4mo after stress event, when new hairs begin to gow
Tx: reassurance

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21
Q

Describe Alopecia Areata, what are the associated conditions and subtypes?

A

Alopecia areata:
Spontaneous tart/end to smooth round areas completely devoid of hair
Assoc w/autoimmune diseases
PE finding = exclamation point hairs

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22
Q

Differentiate Traction alopecia from Trichotillomania?

A

Traction alopecia = hair loss d/t styling aka white people tryna dread
Trichotillomania = hair loss d/t nervous compulsions of pulling out hair, and loss can become permanent

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23
Q

Compare mechanism and causative agents for Anagen vs Telogen effluvium

A

Anagen effluvium: reversible impaired mitotic ability causing hair loss when they’re in Anagen… XRT, chemo, ANTIMITOTICS (etoposide, teniposide), or ANTITUMOR ABX (doxorubicin, daunorubicin)
Telogen effluvium: meds that start hair loss 2-4mo after, by inducing Telogen… OCPs, lithium, anticoagulants, valproic acid, heavy metals, colchicine, cimetidine

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24
Q

How does Lupus manifest on scalp?

Dx?

A

SLE can manifest as scarring alopecia in well-circumscribed erythematous patches w/follicular hyperkeratosis/plugging
Once starts, is permanent
Bx is diagnostic

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25
Q

What’s mechanism for Acne Keloidalis nuchae? tx?

A

Acne Keloidalis nuchae… is not Acne or Keloids!
AA 15-24yo M athletes w/irritated follicles when hairs cute short, causing papules, pustules, hair loss, and granuloma formation
Tx: stop close shaving, friction, and styling products
Use Abx + topical steroid + retinoids if necessary

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26
Q

What’s typical presentation of dissecting cellulitis?

A

Dissecting Cellulitis:

Painful pustules, nodules connected by infected sinus tracts draining blood or pus, leading to allopecia

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27
Q

what’s pathophysiology of allopecia areata?

A 
Loss of immune privilege leads to:
	– Peribulbar inflammation
	– Oligoclonal T lymphocytes
	– Aberrant expression of HLA class I antigens
	– Activation of CD8+ T lymphocytes
	– Secretion of IFN-γ
		○ Maybe introduced from an infection
	– Up-regulation of HLA class II antigens, Activation of CD4+ T lymphocytes, and CD4+ Th1 lymphocytes provide help to CD8+ lymphocytes which cause damage
**CD8 mediated response though
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28
Q

Differentiate immunopathogenic mechanisms responsible for allopecia areata and primary cicatrical alopecia

A

Allopecia areata = Th1 mediated d/t loss of immune privilege, so autoimmune diesease
Primary cicatrical alopecia = Th17 and inflammation mediated

Both end up having CD8 Tcells activate

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29
Q

differentiate the 3 types of tinia capitis?

A

Tinia capitis: (progressively worse)
Black dots are broken off hairs
kerion are painful, inflamed nodules that drain pus
favus are extensive alopecia, atrophy, scarring, YELLOW adherent crusts

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30
Q

what are the asexual conidia of the 3 dermatophytes?

A

Epidermophyton: thin walled, 2-4cell macroconidia
Microsporum: spindle-shaped, thick walled, 8-15celled
Trichophyton: broad hyphae w/microconidia growing at 90 degree angles

31
Q

What are 2 most common bacterial agents of scalp folliculitis

A

Usually Staph aureus or P acnes cause scalp folliculitis

unless it’s fungal, then t’s Deramtophytes

32
Q

What are 3 types of cells in nail matrix?

A

Nail matrix = Langerhans, melanocytes, and keratinocytes

33
Q

What usually causes the follow nail colors?
Blue
Brown/Black
yellow

A 
Blue = usually hypoxia or vasoconstriction, but can be d/t drugs like Minocycline, if only Lunula think Wilson's disease
Black/brown = melanoychia, caused by nevus in nail bed, can be melanoma
Yellow = usually elderly, can be lymphedema or pulmonary disease
34
Q

How do the following present? significance?
Splinter hemorrhage?
Subungual hematoma?

A

Splinter hemorrhages = sign of Infective Endocarditis! +Roth spots in macula, Osler nodes on fingers, Janeway lesions on palms/soles
Subungual hematoma = super painful traumatic hematoma under nail, needs acute puncture for relief, bc old wounds already coagulated

35
Q

How do the following present? significance?
half and half nails?
Mee’s lines?
Beau’s lines?

A

Half and half nails = prox white, dist brown/red nails, indicated liver disease if line is straight (Terry’s nails) or renal disease if wavy
Mee’s lines = multiple transverse white lines d/t arsenic poisoning or severe illness
Beau’s lines = transverse depressions in nails d/t severe illness or disease that causes nails to stop growing, then as they regrow the groove forms

36
Q

How do the following present? significance?
Onycholysis?
Onychoschizia?
Onychogryphosis?

A 
Onycholysis = nail plate separating from nail bed
Onychoschizia = thing/brittle nails that split distally, foten d/t repeated wetting and drying, can be seen in thyroid dz
Onychogryphosis = hypertrophy and excessive curving of nails, elderly claw nails or d/t hypoperfusion, DM, or neglect
37
Q

How do the following present? significance?
Clubbing?
Koilonychias?
Paronychia?

A 
Clubbing = pulmonary, cardiac, GI, or malignancies
Koilonychias = spoon nails d/t iron deficiency
Paronychia = acute/chronic infection of tissue surrounding nail
38
Q

What are 2 types of Leukonychia, and differentiate

A

Leukonychia = white spots
Leukonychia striata = usually d/t trauma like vigorous manicuring, can be spontaneous
Leukoncyhia totalis = can be hereditary or acquired in hypoalbuminemia and other severe systemic diseases

39
Q

define Uritcaria

A

Urticaria = hives, well circumscribed, raised, erythematous w/central pallor, may coalesce, typically disappears over a few hrs

40
Q

define xerosis?

A

Xerosis = dry skin

41
Q

Cause of atopic dermatitis?

differentiate atopic dermatitis in infants vs kids vs adults

A

Atopic dermatitis = eczema, d/t mutations in Fillagrin

infants: face, scalp, extensors
kids: flexors, eyelids, neckline, Dennie-Morgan lines pronounced infraorbital fold d/t edema
adults: flexors, eyelids, neckline

42
Q

what are tx options for atopic dermatitis, and why?

A

atopic dermatitis tx options

  • avoid irritants, sweating, use antihistamines and
  • corticosteroids
  • immunomodulators (Tacrolimus, Pecrolimus)
  • PUVA
  • Methotrexate, Cyclosporine, or Azathioprine if severe disease
43
Q

what are systemic causes of pruritus?

A

Systemic causes of pruritis:
○ Hodgkin’s lymphoma (legs especially pruritic),Non-Hodgkin’s lymphoma, Cutaneous T Cell Lymphoma
○ Polycythemia Vera (aquagenic)
○ ESRD
○ hyper/hypothyroidism
○ diabetes
○ dz causing bile stasis (primary biliary cirrhosis, viral hep, cholestasis of pregnancy, sclerosing cholangitis, drug induced cholestasis)
○ infections like HIV, *eosinophilic folliculitis

44
Q

what are common neurogenic causes of pruritis?

A 
Neurogenic causes of pruritis:
Brachioradial pruritis
Notalgia paresthetica = chronic sensory neuropathy, usually upper back just inf to scapula
Peripheral neuropathy
Post-herpetic neuralgia
45
Q

what are common psychiatric causes of pruritis?

A

Psychogenic causes of pruritis:

Psychogenic excoriation = skin picking disorder

46
Q

What is hyperkeratosis pilaris?

A

Hyperkeratosis pilaris = thickened/keratinized skin around follicles on posterior-lateral UEs usually, puberty problem usually disappears in adulthood
tx: exfoliation and lotion

47
Q

Differentiate acute vs chronic Urticaria

A

acute urticaria <6w

chronic urticraia >6w

48
Q

What’s pathophysiology behind Urticaria?

A

Urticaria: mediated by mast and basophils that release Histamine
causes pruritis, vasodilation, and edema in epidermis

49
Q

What are most common tx for Urticaria?

A
  • 2/3 of acute urticaria resolves spontaneously
  • H1 antihistamines, use 2nd gen (cetrizine, loratadine, fexofenadine) over 1st gen (phenylnephrine)
  • H2 antihistamines (ranitidine, nizatidine, famotidine, cimetidine) usually used for GERD but maybe more effective for acute urticaria than H1
  • glucocorticoids
50
Q

What is Pediculosis?

What is Sarcoptes?

A 
Pediculosis = lice 
Sarcoptes = scabies, most common infestation worldwide
51
Q

What 3 bacteria can Pediculosis transmit?

A

Pediculosis carries

1) Rickettsia prowazekii
2) Bartonella
3) Borrelia

52
Q

What is the super bad form of Sarcoptes called?

A

Crusted = Hyperkeratotic = Norwegian scabies

53
Q

What are 2 drug tx for Sarcoptes?

A

Sarcoptes (Scabies) Tx:
Permethrin cream for immunocompetent
Ivermectin for immunocompromised w/Norweigan/crusted scabies

54
Q

Why isn’t Lindane usually used for Sarcoptes or Pediculosis tx?

A

Lindane has serious CNS ADEs that easily occur w/percutaneous absorption

55
Q

why does fluid resuscitation need to be aggressive but monitored carefully?

A

Bc excess can cause infection, Acute Respiratory Distress Syndrome (ARDS), abdominal compartment syndrome, or death

Edema: capillaries increase permeability -> systemic capillary leaks -> severe protein loss -> localized and generalized edema w/o HTN

Shock: zones of Coagulation, Stasis, and Hyperemia will occur -> Ischemia + Hyperemia (excess blood) + inflammation cascade

56
Q

What can happen during burn shock? (hypovolemia, distribution, and cardiogenic shock)

A

Burn shock:
Hypovolemia d/t fluid loss to outside AND into cells AND into interstitium
Distributive d/t vasodilation, moving fluid away from organs that need it
Cardiogenic d/t decreases in preload and contractility, and increase in afterload

57
Q

What kind of AKI can occur w/burns?

A

burn AKI:
early phase = hypovolemia w/low cardiac output and systemic vasoconstriction (less common w/fluid resuscitation)
late phase = sepsis, multiorgan failure, fluid shifts, myocardial depression… Abdominal compartment syndrome pressure compresses renal vein and decreases GFR… stress hormones, inflammatory mediators, and nephrotoxins damage

58
Q

What type of hypermetabolic state is assoc w/burns?

A

Hypermetabolic burn state
Ebb: first 48hrs hypometabolic state, decreased cardiac output, metabolism, O2 consumption
Flow: can last up to 1yr after burn, hypermetabolic state, increased cardiac output up 2x, insulin resistance, increased lipid/protein consumption leading to higher resting energy expenditure, reduced bone mineralization, linear growth, muscle, and immune response

59
Q

What are 2 types of ionizing radiation? how do they damage DNA?

A

Particulate (alpha, beta, neutrons) directly ionize
-alpha and neutrons cause tissue damage
-Beta cause Burns
Electromagnetic (gamma, xrays, photos) indirectly ionize
-gamma causes local injury and acute radiation syndrome

60
Q

Define acute radiation syndrome

A

Acute radiation syndrome:
prodrome 0-2d = GI sxs
latent 2-20d = asymptomatic
manifestation 21-60d = anemia, infection, bleeding, diarrhea, hypovolemia, electrolyte disturbances, cerebral edema, mental deterioration, CV collapse

61
Q

what’s usual time course of sxs and tx involved in acute radiation syndrome?

A

Prodrome 0-2d
Latent 2-20d
Manifestation 21-60d

62
Q

which layer of skin do you find sebaceous glands?

A

Sebaceous glands are in Connective Tissue sheath surrounding hair follicle

63
Q

What are the 3 parts of skin called around the nail?
1-overlying nail root
2-keratinized free edge
3-under free end

A

1 Nail fold overlies nail root
2 Eponychium is keratinized free edge
3 Hyponychium is under nail’s free end

64
Q

what classifies a burn as 3rd degree?

A

3rd degree burns have transmural necrosis and fibrin exudation

65
Q

What are hallmark characteristics of CO poisoning?

A

CO poisoning =
bright cherry-red blood
fingernail beds also bright red
soot in airways if CO source was fire

66
Q

What happens w/direct lightening strikes? w/indirect?

A

Direct lightening strike causes Cardiopulmonary arrest

Side-flash hit causes clothing tearing and electrical burns

67
Q

Describe histology of psoriasis (Epidermis, Dermis)

A

Psoriasis
Epidermis = hyperkeratosis, parakeratosis (retains nuclei in stratum corneum), acanthosis (stratum spinosum thickening), elongation of rete ridges, dermal papillae
Neutrophils migrate into Epidermis, forming Munro Abscesses
Dermis super vascularized -> Auspitz sign

68
Q

Which mutation’s seen in all benign nevi (melanoma)?
Which mutations are most often seen in cutaneous melanoma?
Which mutation’s seen in all invasive melanomas?

A

Benign nevi = BRAF-V600E
Cutaneous melanoma = BRAF and NRAS
invasive melanoma = CDKN2A

69
Q

How do you classify Melanomas subtypes?

A

Melanoma:
Junctional = dermal epidermal junction
Compound = at dermal-epidermal junction AND in dermis
Intradermal = dermis only

70
Q

What do you see histologically for Squamous Cell Carcinoma?

A

SCC = well differentiated, atypical keratinocytes that’re slightly enlarged w/abundant amounts of cytoplasm, “pearls”

71
Q

Describe Basal Cell Carcinoma’s appearance?

A

BCC = pearly nodules w/telangectasia, made of uniform basaloid nests in dermis

72
Q

What are common complications of SLE?

A 
SLE:
butterfly/malar rash
Discoid lupus
Pleuritis
Pericarditis
(seizures/psychosis, endo/myocarditis, hemolytic anemia, leukopenia, thrombocytopenia, glomerulonephritis, nonerosive arthritis, LAD)
73
Q

Which 2 drugs are ovicidal and which 3 are not for Sarcoptes?

A

Ovicidal
1 Ivermectin
2 Spinosad

non-Ovicidal
1 Permethrin/myrethrin
2 Malation = organophosphate
3 benzyl alcohol

Derm (2 decks)

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