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Internal Medicine > Skin > Flashcards

Skin Flashcards

1
Q

What are the features of Basal cell carcinoma?

A

Elevated or rolled border with central ulceration

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2
Q

How nodular BCC presents?

A

Pearly or translucent nodule with pink, red, or white color (nodular BCC)

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3
Q

How Superficial BCC presents?

A

Reddish patch or irritated area (superficial BCC)

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4
Q

Histological pattern of BCC

A

Invasive clusters of spindle cells surrounded by palisading basal cells

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5
Q

How to manage Low-risk BCC lesions on the trunk or extremities?

A

electro-dessication and curettage (ED&C).

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6
Q

How to manage Low-risk superficial BCC?

A

managed with topical therapy using either 5-fluorouracil or imiquimod.

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7
Q

How to t/m BCC on face?

A

Mohs micrographic surgery

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8
Q

How to manage Nodular BCC on the trunk or extremities?

A

standard surgical excision, typically with 3-5 mm margins.

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9
Q

Important point of BCC

A

Radiation therapy rarely used for pts who are unable to undergo surgery

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10
Q

What are the risk factors of SCC?

A

UV and ionizing radiation
Immunosuppression
Chronic scar or wound Or burn injuries

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11
Q

How SCC clinically present?

A

Scaly plaques / nodule

With or without hyperkeratosis Or ulceration

Neurologic sign with perineural invasion results paresthesias and numbness

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12
Q

Histological pattern of SCC

A

invasive cords of squamous cells with keratin pearls

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13
Q

How to confirmed SCC?

or excisional)

A

Skin biopsy (punch, shave or excisional)

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14
Q

How to manage Small or low-risk lesion SCC?

A

surgical excision or local destruction (e.g cryotherapy, electrodessication)

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15
Q

How to manage High risk lesion or lesion SCC located in cosmetically sensitive area?

A

Mohs micrographic surgery

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16
Q

How keratoacanthoma presents?

A

Rapidly growing, “volcano-like” nodule with a central keratotic plug.

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17
Q

How to treat keratoacanthoma?

A

May regress spontaneously, many are treated as well-differentiated squamous cell carcinomas.

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18
Q

What are the risk factors for the melanoma?

A

fair skin types,
h/o blistering sunburns,

prior personal or Fx H (>/=2 members) of melanoma

dysplastic nevus syndrome, atypical nevi and greater than 100 (>10 in one explanation) typical nevi.

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19
Q

What is the 1st step to approach melanoma?

A

excisional biopsy that removes the entire lesion with narrow margins and depth through the subcutaneous fat.

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20
Q

Important point of Melanoma

A

Don’t Perform shave biopsy—

won’t determine depth of tumor which is main prognostic factor

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21
Q

What are the signs of DELIBERATE SCALD INJURY ?

A

Linear demarcation with no splash marks
Doughnut pattern

Sparing of flexures creases (Zebra pattern)
Extensive burns to back and buttocks

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22
Q

How plaque psoriasis presents?

A

Most common well defined erythematous plaques with scales typically over extensor surface

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23
Q

How Guttate Psoriasis presents?

A

Erythematous macules with scaling typically following an acute strep infection

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24
Q

Triad of INTERTRIGO

A

Due to infection with Candida species
presents as well-defined, erythematous plaques with satellite vesicles or pustules in intertriginous

Occur at occluded parts of body viz axilla or groin

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25
Q

How to t/m Intertrigo?

A

Topical nystatin is used for Candidal skin infections

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26
Q

How tinea Capitis presents?

A

Scaly erythematous patch on scalp

Hair loss with residual black dot

With or without LAD seen in african american

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27
Q

How to dx tinea Capitis?

A

KOH examination of hair shaft to document spores

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28
Q

How to t/m Tinea Capitis?

A

Oral Griseofulvin as first line

Otherwise terbinafine / Itraconazole / fluconazole

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29
Q

What is the MCC type in US?

A

black dot tinea capitis—caused by Trichophyton tonsurans.

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30
Q

What are the risk factors for tinea Corporis?

A

Athletes who have skin to skin contact
Humid environment
Contact with infected animal

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31
Q

How tinea Corporis rash presents?

A

Scaly erythematous prurtic patch with centrifugal spread

Followed by central clearing with raised annular border

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32
Q

How to dx the Tinea Corporis?

A

clinical but skin scrapings and microscopic examination using KOH is confirmatory for atypical and refractory cases—> reveal the presence of hyphae.

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33
Q

How to t/m Tinea Corporis?

A

First line used of topical antifungal—>terbinafine / cotrimazole

2nd line as extensive oral meds—>Terbinafine / Griseofulvin

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34
Q

Name the organism which causes tinea Corporis

A

Trichophyton rubrum is the most frequent culprit

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35
Q

How Tinea Versicolor rash presents?

A

Hyper/Hypo pigment lesion on face if children Or Upper Extremity in adolescent and adult With Or without pruritus and fine scale

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36
Q

How to dx Tinea Versicolor?

A

KOH preparation shows hyphae and yeast cells in a spaghetti and meatballs pattern

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37
Q

How to t/m Tinea Versicolor?

A

Topical terbinafine / Ketoconazole Or Selenium sulfide

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38
Q

Triad of Seborrheic dermatitis

A

Erythematous plaques/ yellow Greasy scale on d/f parts of face, scalp, umbilicus and diaper area

Associated with Parkinson disease and HIV

T/m via topical antifungal agents Ketoconazole Or Selenium sulfide

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39
Q

Triad of Erythema NODOSUM

A

Subcutaneous fat cells inflammation present as red, tender discrete pretibial nodules

Multiple, tender, erythematous subcutaneous nodules/plaques on lower extremities—arthralgia and malaise can develop alongside nodule

Associated with Systematic disorder

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40
Q

Triad of Behcet syndrome

A

Recurrent painful ulcer in mouth and in Genital area
Thrombosis
Uveitis with Erythema NODOSUM

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41
Q

How to Dx Behcet syndrome?

A

Pethargy—>Exaggerated skin ulceration with minor trauma

Biopsy—> non specific vasculitis of different size vessels

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42
Q

Histopathologic findings of Pemphigus vulgaris

A 
Intra epidermal cleavage 
Detached kertinocytes (Acantholysis)
Tomestone cells along basal layer
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43
Q

Immunofluorescence finding of Pemphigus vulgaris

A

Netlike Or chicken wire pattern intra cellular IgG

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44
Q

How the SJS/TEN presents?

A

Prodromal symptoms like influenza

Rapid onset reddish macules / vesicles / bullae
Necrosis with sloughing of epidermis with mucosal involvement

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45
Q

Name the medication which could lead to SJS/TEN

A

Allopurinol
Anti epileptics / Abx like sulfonamides
NSAIDs
Sulfasalazine

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46
Q

Name the bugs which could lead to SJS/TEN

A

Mycoplasma pneumonia
Vaccination
Host VS graft disease

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47
Q

How to t/m SJS/TEN?

A

FLUID resuscitation

Wound care similar to that for burns and often done in burn unit

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48
Q

How to t/m Bullous pemphigoid?

A

High potency topical glucocorticoid (e.g. clobetasol)—1st line also effective against extensive disease

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49
Q

How the rashes of DERMATITIS HERPETIFORMIS presents?

A

Grouped and pruritic erythematous papules, vesicles, and bullae on the extensor surface of body like elbow

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50
Q

Skin biopsy—of Dermatitis herpetiformis

A

DH shows subepidermal microabscesses (blisters) at the tips of the dermal papillae

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51
Q

Name the medicine given in Dermatitis herpetiformis

A

Dapsone

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52
Q

How and where warfain induced skin necrosis?

A

breast / buttock, thighs / abdomen

pain Followed by bullae and skin necrosis

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53
Q

How the rashes of PORPHYRIA CUTANEA TARDA Present?

A

painless blisters with increased skin fragility on the dorsal surfaces of the hands,

facial hypertrichosis and hyperpigmentation.

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54
Q

How to manage PORPHYRIA CUTANEA TARDA ?

A

Phlebotomy or hydroxychloroquine may provide relief, as can interferon-alpha, in patients simultaneously infected with Hepatitis C virus.

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55
Q

Hyperkeratotic, hyperpigmented plaques with a classic velvety texture is feature of which skin condition?

A

ACANTHOSIS NIGRICANS

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56
Q

Triad Of Actinic keratosis

A

Occur on Sun exposed parts of body

Erythematous papules with a central scale due to hyperkeratosis. A “sandpaper-like” texture on palpation— typical.

T/m is fluorouracil cream

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57
Q

Name the other indication of fluorouracil cream besides actinic keratosis

A

Bowen disease

58
Q

How the rashes of Pityriasis Rosacea develop?

A

pink or brown scaly plaque with central clearing (crinkled, cigarette-paper like appearance) and a collarette of scale (herald patch)

followed by development of maculopapular rash classically in a “Christmas tree”

Occur on the trunk, neck or flexural surfaces of extremities

59
Q

Triad of ICHTHYOSIS VULGARIS (lizard skin)

A

hereditary or acquired and worse in winter

normal skin at birth with gradual progression to dry scaly skin—typical feature

skin is usually dry and rough with horny plates over the extensor surfaces of the limbs

60
Q

How the rashes of EXFOLIATIVE DERMATITIS (erythroderma) presents?

A

Widespread, scaly eruption of the skin

drug-induced, idiopathic, or secondary to an underlying dermatological or systemic disease

61
Q

Sun exposure topic

A

Read it from uworld

62
Q

How HIDRADENITIS SUPPURATIVA/ ACNE INVERSA occurs?

A

chronic inflammatory occlusion of folliculopilosebaceous units —> prevents keratinocytes from properly shedding from the follicular epithelium—> HS

63
Q

Triad of HIDRADENITIS SUPPURATIVA/ ACNE INVERSA

A

intertriginous areas and hair bearing area

solitary, painful, inflamed nodules which regress or Converts into abscess

usually made clinically without the need for biopsy or cultures.

64
Q

What are the complications of HIDRADENITIS SUPPURATIVA/ ACNE INVERSA?

A

Sinus tracts

Comedones

Scarring— Severe scarring can lead to dense, rope-like bands in the skin with strictures and lymphedema

65
Q

How to t/m keloid?

A

Symptomatic keloid treated with intralesional glucocorticoids

66
Q

Triad of DERMATOFIBROMA

A

Occurs lower extremities.

nontender & appear as discrete, firm, hyperpigmented nodules

dimpling in the center when the area is pinched (“dimple” or “buttonhole” sign) due to fibrous component

67
Q

How to t/m and dx the DERMATOFIBROMA?

A

Dx —-> made clinically based on the appearance of the lesion.

T/m—-> cryosurgery or shave excision is usually not required unless change in size color or symptomatic and cosmetics reasons

68
Q

Triad of Epidermal INCLUSION CYST/EPIDERMAL CYST

A

discrete benign nodule containing normal epidermis that produces keratin.

dome-shaped, firm, freely movable cyst or nodule with a central punctum (small, dilated, pore-like opening).

Larger and more inflamed lesions can have a thick, yellowish-white, cheesy, and malodorous discharge.

69
Q

How to manage Epidermal Inclusion cyst / Epidermal cyst?

A

usually resolve spontaneously but can often recur.

Excision is typically reserved for patients who desire removal of the lesion for cosmetic reasons.

Incision and drainage is usually needed for infected and fluctuant cysts that are painful and erythematous

70
Q

Important point of PRESSURE NECROSIS/DECUBITUS ULCER

A

Do not massage—as it will further damage skin overlying bony prominences

71
Q

Triad of PYODERMA GANGRENOSUM

A

Starts as inflammatory papule, pustule, vesicle, or nodule—> rapidly progresses to form expanding ulcer with a purulent base and ragged violaceous borders—painful

Dx with skin biopsy

T/m is steiod

72
Q

Triad of ECTHYMA GANGRENOSUM

A

Hemorrhagic nodule with surrounding erythema—>necrotic ulcer

Caused by P. aeruginosa

occurs in setting of profound neutropenia

73
Q

What is the main cause of sepsis on burns?

A

main causes are pneumonia and wound infections (from Staphylococcus aureus or Pseudomonas aeruginosa)

74
Q

Burn topic

Read it from skin chapter

A

Burn topic

Read it from skin chapter

75
Q

Name the medicine causing HTN Type 1

A

beta lactam drugs,
NM blocking agents,

quinolones
platinum containing chemotherapeutic agents and foreign proteins (e.g. chimeric proteins)

76
Q

How to manage type 1 HTN?

A

Urticarial and pruritus without systemic Sx: antihistamines discontinue offending drug and if Systemic give IM epi and steroids

77
Q

Name the COMMON DRUGS ASSOCIATED WITH PHOTOSENSITIVE REACTION

A

Tetracycline
Antipsychotic like chlorpromazine /prochlorperazine
Diuretics like lasix and thiazide
Amiodarone / Promethazine / piroxicam

78
Q

How drugs causing photo sensitive Rxn?

A

By producing oxidants

79
Q

How PHOTOALLERGIC REACTION occurs?

A

UV light alter the configuration of Topical (eg, sunscreens) and systemic medications—->induces a delayed hypersensitivity reaction.

80
Q

Name the condition which causes multiple skin tags

A

Insulin resistance

Pregnancy

Crohn disease (Perianal)

81
Q

Name the condition which shows explosive onset of multiple itchy Seborrheic keratosis

A

GIT malignancy

82
Q

Name the condition which shows Seborrheic Dermatitis

A

Parkinson disease

And

HIV infection

83
Q

Triad of Vitiligo

A

Autoimmune destruction of melanocytes

Depigmentation macules on acral areas and extensor surface

If limited topical steroids / If extensive and unresponsive—> oral steroids / topical calcineurin inhibitor and PUVA

84
Q

Skin condition which shows positive nikolsky sign

A

Pemphigus vulgaris

SJS / TEN

85
Q

Triad of PIEBALDISM

A

Inherited absence of melanocytes

Usually noticed at birth

Confined to head and trunk

86
Q

how Congenital dermal melanocytosis presents?

A

Neonate blue-grey macule on sacrum and buttocks.

Benign birthmarks fade spontaneously during 1st decade

87
Q

Name the types of Acne Vulgaris

A

Acne inflammatory
Acne comedones
Acne (cystic) nodular

88
Q

Triad of Acne comedones

A

Comdones on forehead / chin / nose

Progress to inflammatory pustules / Nodules

T/m retinoid / salicylic / glycolic acid and if fail, give benzoyl peroxide if inflammatory acne

89
Q

Triad of Inflammatory acne

A

Inflamed pustules / papule / Erythema

If mild—> topical retinoid + benzoyl peroxide
If moderate—> add topical ABx ( clindamycin/ erythomycin) and

And add oral ABx if severe

90
Q

Triad of Nodular cystic (acne)

A

Large nodules which appear cystic

Nodules change into sinus tract

If moderate give topical retinoid + benzoyl peroxide + topical ABx
If severe oral ABx and if unresponsive oral isotretinoin

91
Q

Important point of benzoyl peroxide

A

cause photosensitivity reaction Common S/E are irritation, contact dermatitis, dryness, erythema, peeling and stinging

92
Q

How STEROID-INDUCED ACNE OR STEROID INDUCED FOLLICULITIS presents?

A

Characterized by monomorphous pink papules on face, trunk and extremities

absence of comedones

93
Q

How acne Rosacea presents?

A

Papule and pustules on face With flushing
Dilated capillaries
Redness in conjunctivia and lid margin dilated vessel
Occur when body temperature increases

94
Q

How to t/m acne Rosacea?

A

Topical metronidazole for papulopustular type

Laser or Topical Brimonidine for Erythema telangiectasia

95
Q

How SEBACEOUS HYPERPLASIA presents?

A

small pale/yellow papules at the central face.

Lesions are stable in size and appearance

96
Q

Triad of SEBORRHEIC KERATOSIS

A

waxy, “stuck on,” warty, and well-circumscribed appearance.

Occur on face and trunk. But not occur on the palms and soles.

removal by snip/shave excision, cryosurgery, and electrodessication

97
Q

Triad of Atopic Dermatitis in children

A

Itchy red Scaly crusted lesion

Underlying allergic disorder

Topical emollient with or without steroid ointment

98
Q

Location of Atopic Dermatitis

A

Child / adult—-> lichenified plaques in flexural creases

In infants—–> Extensor surface / cheek / scalp / Trunk

99
Q

Name the complications due to Atopic Dermatitis

A 
Cellulitis/abscess 
Eczema herpeticum 
Impetigo 
Tinea Corporis
Molloscum contagiosum
100
Q

How Eczema Herpeticum presents?

A

Due to Atopic Dermatitis
Painful vesicular rash with punch out erosion & Hx crusting
Systemic acyclovir—>give asap

101
Q

Name the metals causing Allergic contact Dermatitis

A

nickel
chromium / cobalt, beryllium
zinc.

102
Q

Important point of allergic contact Dermatitis

A

Rash appears days after exposure

frequently form linear streaks where skin has brushed against plant leaves

103
Q

How the rash of uritricaria presents?

A

Well circumscribed raised reddish plaques

Lesions can be oval / round / serpiginous

104
Q

Important point of Uritricaria

A

Acute less than 6 wks
And
Chronic more than 6 wks

105
Q

Important point of Mast cell degranulation

A

If occurs in deeper layers—-> Angioedema with or without Uritricaria / typically presents as non-pitting and nonpruritic edematous swelling

If occurs in Superficial layers—-> pruritis and localized swelling in upper layers of skin

106
Q

Triad of Serum Sickness like condition

A

Prodromal Sxs with pain in joints / Uritricaria / no mucosal involvement

Occur after use of ABx like

Low complement with increased inflammatory markers

107
Q

Triad of Blue Nevi

A

Smooth-surfaced, dome-shaped melanocytic papules that develop from macules

tend to be less than 1cm in diameter

blue color due to the depth of the melanin in the skin.

108
Q

Important point

A

MELANOCYTIC NEVI follows the ABCDe rules

109
Q

How Nevus simplex presents?

A

Macular stain with salmon patch and stork bite /Angel kiss
Blanchable pink red patches occur at head and neck region
Fades away by 1-2 years of age but persist at back of neck

110
Q

How LENTIGO SIMPLEX presents?

A

characterized by a round or oval macule with even pigmentation
Due to intraepidermal melanocyte hyperplasia

111
Q

Important point of ACROCHORDON

A

Skin tag occurs in regions of body which causing friction

112
Q

Triad of SENILE PURPURA (solar or actinic purpura)

A

Due to loss of elastic fiber in perivascular CT
Seen in elderly using anticoagulants / steroids / NSAIDS
ecchymosis due to rupture of blood vessels

113
Q

Triad of STRAWBERRY (SUPERFICIAL INFANTILE) HEMANGIOMA

A

Composed of capillaries separated by connective tissue—superficial, well demarcated and lanch with pressure

grow rapidly during 1-2 yrs and then frequently regress spontaneously by age 5-8yrs

BB If complications

114
Q

Triad Of CHERRY ANGIOMA OR SENILE HEMANGIOMA

A

Seen in adults

sharply circumscribed areas of congested capillaries and post-capillary venules in the papillary dermis.

Dont regress spontaneously and may bleed if disrupted

115
Q

Triad of CAVERNOUS HEMANGIOMA OR CAVERNOUS MALFORMATIONS

A

Consist of dilated vascular spaces with thin-walled endothelial cells.

Cavernous hemangiomas of the brain and viscera are associated with von Hippel-Lindau disease

soft blue, compressible masses

116
Q

Triad of Pyogenic granuloma

A

small red papule that pedunculated or sessile shiny mass.
Grows rapidly over weeks / months

lip and oral mucosa and can bleed with minor trauma

117
Q

What are the d/f Neonatal rashes?

A

ERYTHEMA TOXICUM NEONATORUM
Neonatal HSV
Neonatal Varicella
SSSS

118
Q

Triad of ERYTHEMA TOXICUM NEONATORUM

A

Generalized reddish macules / papaules / pustules
No involvement of palms and soles
T/m is reassurance only

119
Q

Important point of Neonatal rashes

A

VSV and HSV both t/m with acyclovir

120
Q

HOW SSSS presents?

A

Neonatal rashes start with fever/ irritability / diffuse Erythema
Followed by blistering and exfoliation
T/m is vancomycin / nafcillin / oxacillin

121
Q

Triad of non Bullous Impetigo

A

Due to S.aureus / S.pyogenes
Painful non itching pustules
Honey crusted lesion without Prodromal Sxs

122
Q

Triad of Bullous Impetigo

A

Due to S.aureus
Flaccid bullae with yellow fluid without Prodromal Sxs
Collarette of scale at periphery of rupture lesions

123
Q

How to t/m Impetigo?

)

A

If limited —-> Topical ABx mupriocin

If extensive—-> Oral ABx (cephalexin / Dicloxacillin / clindamycin

124
Q

Triad of ERYSIPELAS

A

Prodromal Sxs early with superficial skin involvement
Raised, sharply demarcated margin is a classic feature.
T/m is Oral amoxicillin Or IV ceftriaxone

125
Q

Name the bacteria causing ERYSIPELAS

A

Strept pyogenes

126
Q

What are the risk factors of Cellulitis?

A

obesity / venous insufficiency
disruption of skin (e.g. Tinea pedis infection).
Chronic fungal foot infection can serve as a nidus of bacterial cellulitis

127
Q

Triad of Non purulent Cellulitis

A

S.pyogenes / MSSA with prodrome SxS later in course
Inflammation involve deep dermis & sub cutanous fat
Flat edges with poor demarcation

128
Q

Triad of Purulent Cellulitis

A

Due to MSSA / MRSA
Purulent drainage
Folliculitis—> furnucle—>Carbuncle (if multiple furnucle

129
Q

How to t/m Cellulitis?

A

If mild and without Systemic Sxs—->oral dicloxacillin

Severe Cellulitis with Systematic Sxs—-> IV nafcillin or cefazolin are DOC

In areas with high prevalence of MRSA, vancomycin can be used as 1st line agent.

Surgical Drainage if abscess Or necrotizing fasciitis

130
Q

Name the Bacteria causing Necrotizing fasciitis

A

Strep.pyogenes /Staphy aureus

C.perferingens

131
Q

Triad of Necrotizing fasciitis

A

Positive hx of trauma
Pain with Systematic Sxs
Erythema / Swelling / edema of Skin /Crepitus

132
Q

How to d/f polymyositis from Necrotizing fasciitis?

A

Polymyositis localise to only one muscle and without air on imaging
And
Necrotizing fasciitis is Generalized and with air on imaging

133
Q

How the patient of SSSS presents?

A

Start with Fever and Prodromal Sxs
Erythema starts on face and then Generalized
Superficial flaccid bullae with +ve Nikolsky sign
Scaling / desquamation /extensive exfoliation of skin continue for about 5 days

134
Q

Name the bacteria causing Scarlet Fever

A

group A β-hemolytic streptococcus that produce erythrogenic exotoxin

135
Q

How Scarlet Fever presents?

A

Pharyngitis with Prodromal Sxs
fine, pink blanching papular rash (rough, sandpaper like) initially
And desquamation begins in the face, progresses down the trunk and finally extends to hand and feet

136
Q

What is the characteristic of Scarlet Fever?

A

punctate or finely papular texture which is sometimes palpable, hence sandpaper like

Cheeks extremely red and area around moth appears pale—“circumoral pallor”

137
Q

How to t/m Scarlet Fever?

A 
penicillin V (drug of choice)
Erythromycin,clindamycin, and 1st  generation cephalosporins—good alternatives for penicillin allergic pts
138
Q

Triad of FELON

A

Due to needle INJURY and common in tailors

tense abscess (non-purulent vesicle in whitlow) and intense throbbing pain.

Incision and drainage with appropriate antibiotic (e.g cephalosporins) is the treatment of choice.

139
Q

Triad of CONDYLOMATA LATA

A

Due to Secondary syphilis
Flattened pink or gray velvety papules
Seen in mucous membranes and moist skin of the genital organs, perineum, and mouth

140
Q

Important point MOLLUSCUM CONTAGIOSUM

A

Do HIV testing if genelised rashes and hundred in number
Dx is clinical
Self limiting with 6 to 12 months otherwise curettage, cryotherapy, or topical agents (e.g. podophyllotoxins)

141
Q

Triad of CONDYLOMATA ACCUMINATA

A

anogenital warts

verrucous, papilliform, and either pink or skin-colored.

Usually Dx is clinical otherwise biopsy if atypical

142
Q

How to t/m CONDYLOMATA ACCUMINATA (anogenital warts)?

A

Chemical or physical agents (eg, trichloroacetic acid, podophyllin)

Immune therapy (eg, imiquimod)

Surgery (eg, cryosurgery, excision, laser treatment)

Internal Medicine (14 decks)

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