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Dermatology > Miscellaneous Disorders > Flashcards

Miscellaneous Disorders Flashcards

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Dermatology Board Prep flashcards
1
Q

What is the etiology of acanthosis nigricans?

A

Unknown
Stimulation of insulin-like growth factor receptors and tyrosine kinase receptors on keratinocytes and fibroblasts

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2
Q

Which population is more likely to get acanthosis nigricans?

A

African Americans (25x more than white)

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3
Q

What are the 8 types of acanthosis nigricans?

A

Obesity
Malignancy
Drug induced
Syndromic
Acral: elbows, knees, knuckles (putting pressure on elbows/knees)
Unilateral: nevoid (epidermal nevus)
Benign: rare autosomal dominant type
Mixed

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4
Q

What causes obesity related acanthosis nigricans?

A

Diabetes
Insulin resistance
High BMI
Metabolic syndrome
PCOS

If seen in non obese patient raises suspicion for malignancy

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5
Q

What is the MC cause of malignancy acanthosis nigricans?

A

gastric carcinoma

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6
Q

Appearance of acanthosis nigricans?

A

symmetric dark brown hyperpigmented plaques with a velvety, verrucous, or papillomatous appearance typically in neck folds
Sometimes inguinal, inframammary, ac, and popliteal fossae, elbows, periumbilical

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7
Q

where is acanthosis nigricans rarely located?

A

knuckles, palms, soles, eyelids, periorally, near mucosal surfaces, or generalized
Oral mucosa and lip lesions have thickening and papillation and usually lack hyperpigmentation

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8
Q

If you see a rare location of acanthosis nigricans, what should you be concerned for?

A

Malignancy

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9
Q

Tests for acanthosis nigricans?

A

H&P: obesity, DM, masculinization, weight loss, lymphadenopathy, or organomegaly, BMI
Skin biopsy diagnostic but rarely needed
Check A1C or fasting plasma insulin and glucose to r/o diabetes related
plasma testosterone and dehydroepiandrosterone sulfate test in women with signs of hyperandrogenism to r/o PCOS

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10
Q

Management of AN?

A

Multidisciplinary including specialists in endocrinology, oncology, psych (can cause issues with body image), and nutrition depending on underlying cause

Treat underlying condition
Topical retinoids and/or vitamin D analogs to help with appearance
Refer to GI for endoscopy if suspicion of malignancy

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11
Q

What is a pressure injury?

A

Breakdown of skin and underlying tissue resulting from unrelieved soft tissue pressure between bony prominence and external surface

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12
Q

Pathophysiology of pressure injury

A

Non-relieving pressure/shearing forces –> decreased blood flow —> cell death

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13
Q

Etiology of pressure injury

A

Impaired mobility (MC)
Contractures/spasticity
Impaired sensation
aging skin
incontinence/fistula
malnutrition
hypoproteinemia

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14
Q

Location of pressure injury

A

Sacrum/hip: ischial tuberosity, trochanter, sacrum
lower extremity: malleolar, heel patellar pretibial
can occur anywhere with pressure

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15
Q

What population mc has pressure injury

A

hospitalized patients

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16
Q

clinical findings of pressure injury

A

Inspection can be deceiving to untrained eye and wound wider at base
May require pain meds for adequate exam

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17
Q

Staging of pressure injuries

A

NPUAP staging for initial evaluation and diagnosis and for description and documentation purposes only
not for evaluation of wound progression
stage doesn’t change wiht healing

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18
Q

stage 1 pressure injury

A

intact skin
non-blanchable hyperemia
blanchable erythema, skin firmness, change in sensation or temp may precede stage 1 injury

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19
Q

stage 2 pressure injury

A

intact blister or loss of epidermis with exposed dermis
subcutaneous tissue is not visible

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20
Q

stage 3 pressure injruy

A

full thickness skin loss with exposed subcutaneous tissue/adipose
no fascia, muscle, tendon, ligament, cartilage or bone visible
granulation tissue

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21
Q

management of pressure injury

A

optimize nutrition (nutritionist if needed): increase protein and caloric intake and supplement parenterally as needed
redistribute pressure: reposition every 2hrs or sooner, head elevated <30 degrees, massage prone areas during repositioning, work on remobilization if possible
Clean skin with mild cleansing agents and keep dry
pain control
antimicrobial therapy if indicated

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22
Q

local wound care of pressure injury

A

Stage I: cover with transparent film for protection
Stage II: transparent or hydrocolloid dressing, hydrocolloid dressing CI in active infection
Stage III/IV: debridement

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23
Q

course and prognosis of pressure injury

A

with app treatment
stage 1&II heal in 1-2 weeks
stage III & IV heal in 6-12 weeks

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24
Q

what is hidradenitis suppurativa?

A

chronic suppurative disease of the apocrine gland bearing skin areas: axillae, inguinocrural, and anogenital regions; scalp

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25
Q

epidemiology of hidradenitis suppurativa

A

females >males
onset beginning at puberty

predisposing factors: (primarily high BMI and smokers)
occlusive dressing
trauma
obesity
smoking
host defense defects
hormones
genetics

26
Q

symptoms hidradenitis suppurativa

A

history of recurrent painful suppurative lesions which heal leaving scars

27
Q

physical exam of hs

A

open comedones
nodules with sinus tracts
abscesses
scarring
sinus tracts

28
Q

complications of hidradenitis suppurativa

A

secondary infection
fistulas to urethra, bladder, and/or rectum
chronic inflammatory reactions: anemia, proteinsemia, hypoproteinemia, amyloidosis, interstitial keratitis, and renal disease

29
Q

Management goals of hs

A

decrease length and symptoms of breakout
get rid of scars and tunnels
prevent new breakouts

30
Q

management overview of hs

A

combination of:
intralesional glucocorticoids
oral antibiotics
isotretinoin
biologics (humira)
surgery

31
Q

immediate treatment of hs lesions

A

intralesional steroid followed by I&D abscesses
oral antibiotics: B-lactamase PCN, cephalosporins, augmentin, clindamycin
oral steroids to manage pain/inflammation

32
Q

medical treatment for recurrent hs lesions

A

antibiotics plus retinoid
systemic biologics: reserved for treatment-resistant

33
Q

surgical treatment of hs

A

small excision of chronic recurrent, fibrotic nodules, or sinus tracts
complete excision of lesions with wide margins: if chronic recurrent lesions, may require skin grafts
address psychological complications too!

34
Q

lifestyle modifications for hs

A

local ordinary hygiene
weight reduction in patients who are obese (skin on skin friction can flare)
antiseptic agents
application of warm compresses with burrow solution
wearing of loose-fitting clothing
laser hair removal
smoking cessation

35
Q

what is photosensitivity?

A

Abnormal response to light, usually sunlight, with varying occurance and duration

36
Q

3 types of acute photosensitivity

A

sunburn type response
rash
urticarial

37
Q

sunburn type response

A

skin changes simulating normal sunburn such as in phototoxic reactions to drugs or phytophotodermatitis

38
Q

rash response

A

macules, papules, or plques, similar to eczematous dermatitis

39
Q

urticarial response

A

typical for solar urticaria

40
Q

chronic photosensitivity

A

chronic repeated sun exposures over time result in polymorphic skin changes that have been termed dermatoheliosis or photoaging

41
Q

clinical presentation of photosensitivity from acute sunburn

A
42
Q

physical exam of acute sunburn

A

confluent bright red erythema on sun-exposed areas
sharply marginated at border
develops after 6 hours and peaks at 24

43
Q

management of acute sunburn

A

topical: cool, wet dressings and topical glucocorticoids, aloe vera
systemic: NSAIDs
severe sunburn: bedrest and oral fluids, toxic patients may require hospitalization for IV fluids

44
Q

prevention of photosensitivity

A

SPT 1/II avoid sun exposure between 10 AM and 2 PM
Adequate sunscreen use and proper reapplication
clothing- UV screening cloth garments

45
Q

what is drug/chemical induced photosensitivity

A

adverse reaction of skin due to interaction between UVR with chemical or drug

46
Q

2 types of drug/chemical induced photosensitivity

A

phototoxic reactions: photochemical

47
Q

what is xerosis?

A

dry skin or asteatosis
rough, dry skin texture with fine scale and occasionally fine fissuring

48
Q

what is xerosis associated with?

A

disease status
low humidity
frequent bathing
harsh soaps
ichthyoses
atopic dermatitis
hypothyroidism
down syndrome
renal failure
malnutrition
hIV
lymphoma
liver disease

49
Q

incidence of xerosis increases with —–

A

age
nearly all over the age of 60

50
Q

look for what in xerosis

A

dry, dull, rough skin with fine bran-like scales that flake off easily
in more advanced stages, stratum corneum may begin to exhibit a polygonal pattern of superficial cracks and fissures with erythema
MC on lower extremities, trunk, dorsal hands, usually sparing head

51
Q

diagnostic pearls for xerosis

A

inquire about bathing habits
hot water, frequent or prolonged bathing, and use of

52
Q

best tests for xerosis

A

clinical diangosis
systemic cause: thyroid, renal

53
Q

management of xerosis

A

bathing in tepid water
gently patting instead of fully drying skin
immediate application of moisturizing cream to damp skin following bathing

54
Q

what can patients use for xerosis?

A

mild soap substitutes: dove, tone, purpose, cetaphil
liberal use of emollients and humectants
ointments such as petroleum jelly or aquaphor
humidifiers
topical agents containing urea, lactic acid, ammonium lactate or alpha hydroxy acids beneficial but can be irritating

55
Q

what is ichthyosis vulgaris?

A

common, autosomal dominant inherited condition of abnormal cornification
altered profilaggerin expressing
leads to scaling and desquamation
often seen in association with atopic dermatitis

56
Q

when is ichthyosis vulgaris more prominent?

A

winter and climates with low humidity
childhood between 3 and 12 months of age and alleviates in intensity by adulthood
no known race or sex predilection
hydration, lubrication, keratolytics

57
Q

rare ichthyosis variant

A

develops in adulthood

58
Q

look for in ichthyosis

A

dry, fine scaling skin forming netwok of polygonal fish skin like scale
most apparent on extensor surfaces

59
Q

consider wht in males with ichtyosis?

A

X-linked ichthyosis with darker scale and in popliteal and AC fossae

60
Q

best test for ichthyosis

A

clinical
skin biopsy characteristic
mutational analysis and steroid sulfatase activity if hereditary ichthyosis indicated

61
Q

management of ichthyosis

A

emollients
bath oils
non-drying soaps or non-soap cleansers
soaking skin and mechanically exfoliating
humidification of environment

62
Q

therapy for ichthyosis

A

moisturizer once dailuy
keratolytics

Dermatology (12 decks)

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