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MSS Weeks 3-5 > Neoplastic Disorders, Infectious Disorders, Cutaneous signs of systemic Conditions > Flashcards

Neoplastic Disorders, Infectious Disorders, Cutaneous signs of systemic Conditions Flashcards

1
Q

What bacterial infections of the skin did we talk about?

A

Impetigo

Staphylococcal scalded skin syndrome

Cellulitis (Deep pyogenic infection)

Erysipelas

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2
Q

What viral infections of the skin did we talk about?

A

Verrucae (Warts), Human papilloma virus

Condyloma accuminatum

Herpes Simplex Virus (HSV-1/HSV-2)

Varicella Zoster Virus (Chicken pox/Shingles)

Molluscum contagiosum

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3
Q

What arthropod reactions of the skin did we talk about?

A

Scabies (Sarcoptes scabiei)

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4
Q

What fungal infections of the skin did we talk about?

A

Superficial fungus (Dermatophytosis) (Tinea)

Tinea versicolor

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5
Q

What epidermal, melanocytic, lymphoid neoplasms of the skin did we talk about?

A

Epidermal:

Sebhorrheic Keratosis

Actinic Keratosis

Squamous Cell Carcinoma

Keratoacanthoma

Basal Cell Carcinoma

Melanocytic Tumors:

Acquired and Congenital Melanocytic Nevi

Sporadic and Familial Dysplastic Nevi

Melanoma

Skin Lymphomas

Mycosis Fungoides

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6
Q

What is Impetigo?

With whom is it seen?

What causes it?

How does it present?

Where does it present?

A

Common superficial bacterial skin infection that is highly infectious.

Mostly seen in childhood or immunocomp adults

Staph aureus most common (Strep pyogenes less)

Small vesicles burst and replaced by thick yellowish crust (Honey colored)

Mouth, nose, extremities most commonly affected.

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7
Q
A

Impetigo

Histo: Spongiotic epidermis with neutrophilic infiltrate

Clinical: Honey colored thick yelloish dirty crust with margin of erethema

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8
Q

What is Staphylococcal Scalded Skin Syndrome?

In whom is it seen?

What causes it?

Clinical presentation?

Where is it clinically present?

What is it associated with?

A

Toxin-mediated type of exfoliative dermatitis causing intraepidermal splitting through the granular layer

Seen in infant and children

Caused by 2 exotoxins, ET-A and ET-B (Epidermolytic Toxin) from Toxigenic strains of Staph aureus

Sudden onset of skin tinderness and macular eruption followed by development of large flaccid bullae.

Face, neck, trunk, axillae, groin. MUCOUS NOT INVOLVED

Though rarely in adults, associated with renal disease/inability to clear the toxin and may result in fatal staphylococcal septicemia

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9
Q
A

Staphylococcal Scalded Skin Syndrome

Histological: Subcorneal splitting of the epidermis, a few acantholytic cells and sparse neutrophils present within blister

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10
Q

What is cellulitis (Deep pyogenic infection)?

Where is it common on the body?

What causes it?

What is the clinical presentation?

A

Diffuse inflammation of the connective tissues of the skin and/or the deeper soft tissues

More common on legs

Beta-hemolytic streptococci and/or coagulase positive staphylococci

Expanding area of erythema (tender)

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11
Q
A

Cellulitis (Deep pyogenic infection)

Histologically: In both cellulitis and erysipelas there is marked dermal edema and lymphatic dilatation. Also diffuse infiltrate of neutrophils accentuated around blood vessels

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12
Q

What is Erysipelas?

How does it clinically present?

Where does it commonly clinically present?

What organism commonly causes it?

A

Distinctive type of cellulitis, a bacterial skin infection involving upper dermis (Superficial cutaneous lymphatics)

Sharply outlined edematous erythematous tender and painful plaques

More common on lower exptremities and in elderly

S. pyogenes is most common

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13
Q
A

Erysipelas

Histologically: In both cellulitis and erysipelas there is marked dermal edema and lymphatic dilatation. Also diffuse infiltrate of neutrophils accentuated around blood vessels

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14
Q

What causes Verrucae (warts)?

What is the result of warts?

What are the different types of Verruca?

What are the different types of HPV?

What is the pathology?

A

Human Papilloma Virus (DNA virus)

Self limited, regressing spontaneously w/in 6mo-2yr

Verruca Vulgaris (hands commonly)/Verruca plana (face or dorsal surface of hands)/Verruca plantaris/Verruca palmaris

Low and High risk HPV (verruca caused by low-risk)

Verrucous epidermal hyperplasia/Koilocytosis of upper layer of epidermis/Keratohyaline granules and intracytopasmic aggreg

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15
Q
A

Verruca (warts)

Verrucous epidermal hyperplasia

Koilocytosis (cytoplasmic vacuolization) of the upper layer of epidermis

Infected cells show keratohyaline granules and intracytoplasmic aggregates

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16
Q

What is Condyloma Accuminatum?

What other HPV types are of note and why?

Clinical presentation?

A

Sexually transmitted disease caused by HPV 6 and 11

High risk HPV types 16, 18, 31, 33 may increase risk for cancer

Single or multiple papular lesions that are pearly, filiform, fungating, cauliflower, or plaquelike

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17
Q
A

Condylomata acuminata

Histologically: characterized by marked acanthosis with a broad rounded exophytic growth. Surface of the lesion is hyperkeratotic parakeratotic

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18
Q

What is Varicella-zoster virus and what does it cause?

What causes it?

Pathology of Varicella

Pathology of Shingles

A

DNA Herpesvirus (lipid-enveloped DS) that causes Chickenpox and Shingles

HSV-1 (common in childhood, lips) and HSV-2 (genitalia, sexually transmit)

Varicella spreads through respiratory route. Rash progresses from macules to vesicles to pustules.

Shingles is recurrence of VZV in adulthood. Unilateral dermatomal distribution in thorax and lumbar

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19
Q
A

Herpes Simplex and VZV show same histologic changes

Acantholysis of epidermis

Multinucleated keratinocytes with intranuclear inclusions (Cowdry Type A inclusions)

Perineurial and intraneurial inflammation

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20
Q

What is a Tzank Smear

A

Rapid cytological diagnosis done by making a smear from the base of a freshly opened stain ( of HSV) and staining it with Giemsa stain.

Not as sensitive

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21
Q

What is Molluscum contagiosum?

Where is it seen?

Pathology?

A

Cutaneous infection caused by large brick shaped DNA poxvirus

Children acquire from close contact (eyelids, face, axilla) and immunocompromised patients (HIV). Penis vulva groin as STD

Pathology: Inverted nodule “crater-like”/Eosinophilic cytoplasmic bodies (Molluscum bodies or Henderson-Patterson bodies)

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22
Q
A

Molluscum Contagiosum

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23
Q

What is Scabies and how is it spread?

How does it present and where and when?

A

Contagious caused by the mite Sarcpotes Scabiei, transmitted via prolonged direct human contact and rarely by fomites

Presents as extremely pruritic papulovesicular eruption

Fingers/penis/umbilicus/waistband/axilla/hands

Erupts 4 wks after infestation

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24
Q
A

Scabies

Fertilized female deposits eggs in burrows in the epidermis. Extend at shallow angle through stratum corneium an dmay reach deeper epidermis.

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25
Q

What is tinea/dermatophytosis?

What are the 3 genera?

How does it present?

What test would you use to identify?

What are the different tineas?

A

Very common superficial cutaneous infections by fungus

Microsprum/Epidermophyton/Trichophyton

Scaly, erythematous plaques, annular

KOH prep rapid test to find branching septate hyphae

Tinea capitis (scalp)

Tinea corporis (trunk/back)

Tinea barbae (beard)

Tinea cruris (groin)

Tinea pedis (feet)

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26
Q
A

Tinea

Histologically: variable. Presence of sandwich sign (hyphae sandwiched between normal basket weave stratum corneum and a lower layer of stratum corneum with eitehr orthokeratotic or parakeratosis)

PERIODIC ACID SCHIFF (PAS) STAIN CAN REVEAL THE FUNGUS

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27
Q

What is Tinea versicolor?

Where is it common?

What causes it?

How is it presented?

A

A common superficial fungal infection.

Tropical climates and in summer months

Malassezia globosa

Multiple irregular areas of hypo or hyperpigmentation which are CIRCULAR AND MACULAR

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28
Q
A

Tinea versicolor

Histologically: Stratum corneum contains round budding yeasts and short septated hyphae imparting spaghetti and meatballs appearance.

Seen clearly in H&E and PAS preparations

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29
Q

What are Seborrheic keratoses?

Where are they commonly found on the body?

What causes it?

What is a condition involving multiple of these and what is it assoc with

A

Pigmented papules and plaques with “stuck on” appearance (warty)

Common on face, trunk, and upper extremities

Harbor activating mutations in fibroblast growth factor FGF receptor 3

Leser Trelat sign, associated with internal malignancies (stomach cancer)

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30
Q
A

Seborrheic Keratosis

Histologically: Hyperkeratotic, papillomatous, verrucous epidermis.

Presence of horn and pseudo horn cysts is characteristic

Variable melanin pigmentation accounting for brown coloration

31
Q

What is Actinic Keratosis?

From what is it thought to arise?

How does it present?

A

Solar/senile keratosis

A result of chronic sun damage

Presents as Erythematous yellow/brown scaly lesions

32
Q
A

Actinic keratinosis

Histoogically: Cytologic atypia of the basal layer of the epidermis. Corneal layer is thickened with retained nuclei (parakeratosis). Dermis contains thickened blue-gray elastic fibers (solar elastosis) the result of chronic sun damage.

33
Q

What is Squamous Cell Carcinoma?

How does it present?

How do invasive lesions present?

What is the most common cause and other factors?

What % in situ develop invasive component and of these what have metastatic potential?

A

Common neoplasm in older people

Sharply defined red scaly plaque

Invasive tend to be nodular and may ulcerate

UVB most common. Others: ulcers, old burn scars, HPV, radiation, arsenic, immunosupp

5% invasive component. 30% of these w/metastatic potential

34
Q
A

Squamous Cell Carcinoma in Situ

Histologically: Full thickness dysplasia, involving entire epidermis. Disorganization of the epidermal architecture, loss of maturation, and lack of polarity of cells.

35
Q
A

Invasive squamous cell carcinoma

36
Q

What are Keratoacanthomas?

How does it present?

Why is it treated?

A

Variant of SCC

Solitary flesh colored nodule w/ a CENTRAL KERATIN PLUG

Causes extensive local destruction

37
Q
A

Keratoacanthoma

HIstologically: Exophytic lesions w/ invaginating mass of keratinizing well diff squamous epithelium at the sides and bottom o the lesion

Epithelium is characterized by well differentiated pale staining eosinophilic glassy cytoplasm showing striking tendency towards keratinization

38
Q

What is basal cell carcinoma?

Does it metastasize?

What is it assoc w pathwise?

Presentation?

A

Most common human cancer secondary to chronic sun exposure. Locally destructive, slow growing tumor rarely metastasizes.

Metastasizes in immunocompromised

Dysreg of sonic hedgehog or PTCH pathway

Pearly papules w/ prominent dilated subepidermal blood vessels (telangiectasia)

39
Q
A

Basal Cell Carcinoma

Histologically: characteristic clefting artifact b/w tumor nodules and stroma

40
Q

What are melanocytic nevi?

What kinds are there?

What kinds are there histologically?

A

Seen in epidermis

Increase w sun exposure (acquired) and Present at birth (congenital)

Histologically: Junctional/Compound/Intradermal

41
Q

What is dysplastic nevus syndrome?

How is the familial variant inherited?

What are the differences between Sporadic form and Familial form?

How does it present typewise?

A

Patients tend to develop large number of dysplastic nevi (80 or more)

Autosomal dominant disease with incomplete penetrance and is assoc w/ mutations of the CDKN2A gene

Sporadic has 2-10 dysplastic moles vs. hundreds for familial

and

lifetime risk of melanoma is 10% in sporadic, 100% in familial

Junctional or compound NOT INTRADERMAL

42
Q

At what age and body location is Melanoma typically found?

Melanoma risk factors?

A

Adulthood. Men on back and women on legs

Factors: Sunlight exposure at early age is most important. Fair complexion/older age/dysplastic nevus/history of melanoma/Xeroderma pigmentosum

43
Q

what are the ABCDEs of melanoma?

What are the growth phases for Melanoma

What is the most important predictor of metastatic disease?

What are the thicknesses that rarely metastasize vs. greater potential to?

A

Asymmetry/Borders uneven/Color heterogeneity/Diameter >6mm/Evolution or change

Early phase/Radial Growth phase/Vertical Growth phase

Depth of invasion (Breslow thickness) is the most important predictor of metastatic disease

Tumors < 1mm rare… >1.7mm potential

44
Q

What are other indicators of metastatic potential (other than the most important factor of depth of invasion) for melanoma?

Where can metastases involve?

A

Ulceration, mitotic rate, angioinvasion

Metastases involve not only regional lymph nodes, but liver lungs brain, any other site.

45
Q

What types of Melanoma are there?

A

Superficial spreading type- Most common, commonly in back and extremities

Nodular type- NO radial growth phase directly invading dermis. poor prognosis.

Lentigo maligna type- Commonly in head and neck area.

Acral Lentiginous type-Located on palm sole or beneath nail. Common in African Americans.

46
Q

What is Mycosis Fungoides

How does it present?

What are the phases it goes through?

What syndrome is assoc?

A

A skin lymphoma, most common CTCL

Non-specific erythrodermic rash, progressing over time

Phases of patch, plaque, and nodules

Sezary syndrome is the blood involvement of T-cell lymphoma

47
Q
A

Mycosis fungoides

48
Q

What are the different skin conditions seen in diabetes mellitus?

A

Diabetic dermopathy: Lower legs/Atrophic, pink and hyperpigmented macules and plaques

Bullous diabeticorum: Acral, lower legs and lower arms. Tense blisters.

Necrobiosis lipoidica: Yellow atrophic plaques/shins/telangiectasia/multiple and bilateral/ulcerate esp in males

Acanthosis nigracans: Common in Type II DM. Marker for insulin resistance. Velvety hyperpigmented thickening of the skin. Also seen in other locations and skin tags. (AN 1- Familial/AN 2- Malignancy/AN 3- obesity insulin resistance and endocrinopathy assoc)

Other: Tinea/Candidiasis/Cellulitis/MRSA infections/Neuropathic ulcers

49
Q

What are characteristics of Hyperthyroidism?

A

Fine, velvety, smooth skin
Warm and moist due to increased sweating
Hyperpigmentation – localized or generalized
Pruritus
Hair: Fine, thin hair
Mild, diffuse alopecia
Nails: Onycholysis (nail lifts off bed)

50
Q

What are characteristics of Hypothyroidism?

A

Dry, rough, coarse skin
Cold and pale skin
Yellow discoloration from carotenemia
Thick scale on feet (keratoderma)
Generalized boggy and edematous skin (myxedema): rare
Hair: Dull, coarse, brittle, slow growing
Alopecia of the lateral third of the eyebrows
Nails: Thin, brittle, slow growing

51
Q

What do people with Hyperthyroidism AND Grave’s disease have?

A

Pretibial myxedema:

Cutaneous infiltration of skin of shins with MUCIN

Peau d’orange, skin colored to brown red, firm

Can occur during Grave’s or following treatment of same

52
Q

What is Addison’s disease?

What are the skin manifestations?

A

Primary adrenocortical insufficiency (Autoimmune)

Hyperpigmentation (MSH like effect of ACTH)

Striae of nails

Mucosal pigmentation

Loss of ambisexual hair in post pubertal women

Fibrosis and calcification of the cartilage (ear) rare

53
Q

What is Cushing’s syndrome?

Symptoms?

A

Overproduction of Cortisol by adrenal gland

Moon facies

Buffalo hump

Truncal obesity

Spindly limbs

STriae distensae

Easy bruisability

Slow wound healing

Acne/hirsutism

54
Q

What is Lupus Erythematosus?

What are the ARA criteria of SLE (systemic Lupus Erythematosus)? (Skin related and Multisystem)

A

Multisystem disorder that can have subsets of cutaneous lupus (3)

Malar (cheek) erythema/Discoid (chronic/thick) lesions/Oral ulcers/Photosensitivity

Arthritis/serositis/Nephropathy/CNS disorder/Hematologic disorder/Immunologic

55
Q

What are the risk factors for Systemic Lupus Erythematosus

A

Female>male 6:1

Young>old

African american/dark skin>Caucasian

56
Q

What is the marker for Acute Cutaneous Lupus Erythematosus?

What is the marker for Chronic cutaneous (discoid) Lupus Erythematosus?

What is the marker for Subacute cutaneous Lupus Erythematosus?

A

Butterfly rash (malar rash). Resolves in quickly in hrs to days w/out scarring. Brought on by sun but not always. Marker for Acute.

Discoid lupus top of head, cheek, and ear has scarring lesions

Polycyclic annular rash on back or arms found in Subacute cutaneous.

57
Q

What is Neonatal lupus?

A

Mother’s antibodies cross placenta.

58
Q

What is dermatomyositis?

What are the markers?

Why is having dermatomyositis concerning?

A

Inflammation of skin and muscle

Heliotrope rash. violet colored rash of upper eyelids

Photosensitive poikiloderma (Pigment altered skin thing and blood vessels)

Gottron’s papules (Characteristic flattop pink papules over extensor knuckles)

Nailfold capillary changes

Assoc with cancer in adults 10-50% (OVARIAN represented)

59
Q

What is the skin manifestation of sarcoidosis?

When does cutaneous disease occur in sarcoidosis?

What is the cutaneous presentation of sarcoidosis?

A

Non-caseating granulomas (not a lot of lymphocytes around it) is characteristic in organs

Onset of disease is when cutaneous occurs

Periorbital granulomatous papules.

Diascopy reveals brow/red color.

Brown red papules and plaque/lesions can be small papules or larger plaques/A great pretender (looks like a lot of things)

60
Q

What is diascopy?

A

Use glass slide and press down. Can reveal red brown of sarcoidosis. Can also reveal purpura

61
Q

What is Lofgren’s syndrome?

A

A sarcoidosis syndrome charcterized by

Hilar adenopathy

Erythema nodosum

Fever

(Iritis, arthritis)

62
Q

What is Porphyria Cutanea Tarda?

What does it present with?

A

Accumulation of porphyrins.

Caused by defective uroporphyrin decarboxylase which breaks down heme groups. Caused by liver disease or autosomal mutation.

Present with vesicles that heal with scarring on sun exposed areas particuarly on hands and face.

Hairgrowth of face

63
Q

What cutaneous manifestation occurs with IBS?

A

Pyoderma gangrenosum

a sterile rapid ulceration necrosis of the skin caused by neutrophilic infiltration.

Also assoc with other diseases.

64
Q

What is Dermatitis Herpetiformis

How does it present and Where does it occur?

Best Treatment?

A

Consequence of gluten sensitivity. Immune reaction in the small bowel which alters the mucosa, leading to antibody formation, leading to antibodies entering blood and attach to skin. Anti transglutaminase antibodies causing dermatitis herpetiformis

Little vesicles like herpes, super itchy. Presenting on extensor surfaces.

Avoid gluten. AFter 3 mo, ab levesl decrease mucosa of gut normalizes and symptoms of Dermatitis herpetiformis abate. Dapsone is effective treatment for relief of DH itchiness. But does not affect gut or autoantibodies.

65
Q

What are the cutaneous reaction patterns we talked about?

A

Urticaria

Exanthematous Drug Eruptions/Morbilliform drug rashes

Drug reaction with Eosinophilia and systemic symptoms (DRESS)

Erythema Multiforme (EM)

Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

Vasculitis

Leukocytoclastic Vasculitis

Henoch-Schonlein Purpura

66
Q

How does Urticaria present?

How is it happening?

Cause?

Treatment?

A

Pink edematous papules and plaques

Lesions are migratory and individual lesions last less than 24 hr

Angioedema and anaphylactic shock are the other forms of anaphylaxis

Caused by IgE mediated immediated hypersensitivity

Most common identified cause is Upper Respiratory Infection

Treat w/ oral antihistamines (nonsedating w/sedating H1 antihistimines)

67
Q

Exanthematous drug eruptions/Morbiliform drug rashes mediated by?

How does it present?

When does it present?

Treatment?

A

Type IV (delayed) hypersensitivity

Monomorphic (individual lesions look similar to one another) macules and thin papules start on face and trunk then spread to extremities

2-14 days after drug initiation onset.

Spontaneously resolve over 1-2 wks (treatment is supportive for pruritis with topical corticosteroids and oral antihistamines)

68
Q

DRESS (drug reaction w/ eosinophilia and systemic symptoms) resembles what but why is it different?

How is it presented?

Most common site of systemic involvement?

Treatment?

A

Resembles Exanthematous drug eruptions but commonly associated with fever

Facial edema, enlarged lymph nodes, arthralgias may be present

Liver is most common site of systemic involvement.

Drug discontinuation imperative. Systemic corticosteroids required to treat.

69
Q

Erythema multiforme was similar to what?

Clinical presentation hallmark finding?

Tissue involvement?

Triggers?

Treatment?

A

Thought to be similar to SJS and TEN but now thought distinct

Target lesions characterized by 3 or more color zones and a dusky red or purple center as hallmar finding.

Ocular oral genital mucosa involvement

Infectious triggers for 90%, drugs 10%

Symptomatic treatment for pruritis or pain sufficient, systemic corticosteroids for severe disease

70
Q

SJS (Stevens-Johnson syndrome) and Toxic epidermal necrolysis (TEN) presentation?

Difference between the spectrum of SJS/SJS TENOverlap/TEN

Tissue involvement?

Triggers?

Mortality?

Treatment?

A

Prodrome of fever, malaise, Upper respiratory symptoms before onset of cutaneous lesions.

Painful red patches evolve to bullae and areas of necrosis

Epidermal detachment <10%, 10-30%, >30% body surface area involvement

ANY MUCOSAL SURFACE may be involved (oral, conjuctiva, genital, GI)

Allopurinol, NSAID, sulfa, anticonvulsants, antibiotics implicated.

Mortality primarily from sepsis. Prompt discontinuation required. Support including IV immunoglobulin maybe

71
Q

What is vasculitis?

A

Inflammation and destruction of blood vessels.Most cutaneous vasculitis is small vessel vasculitis with inflammation centered around arterioles and venules in the dermis.

72
Q

LCV (Leukocytoclastic Vasculitis), what is it?

Common causes?

Hallmark cutaneous finding? Where is it?

Difference from urticaria?

Other findings?

A

Small vessel vasculitis of skin when neutrophils are predominant inflammatory cell seen on biopsy.

Common causes: infections (upper resp./Group A streptococal/hep b/hep c/HIV)/drug hypersensitivity (antibiotics)

Palpable purpura are the hallmark cutaneous finding, more commonly on legs

Lesions last longer than 24 hrs, unlike urticaria

Other findigns: nodules, ulceration, livedo reticularis (purple lacy netlike pattern)

73
Q

What is Henoch-Schlonlein purpura (HSP)?

Diagnosis?

Triggers?

Hallmark?

Treatment?

A

Small vessel vasculitis predominantly affecting children

A leukocytoclastic vasculitis seen on biopsy but IgA immune complexes are a more specific finding when direct immunofluorescence is performed.

Triggered by infections, typically group A Streptococcal infection and other upper respiratory infections

Palpable purpra on the skin, especially buttocks and lower extremities are the main physical finding.

Self-limited and resolves over course of 2-4 wks

MSS Weeks 3-5 (22 decks)

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