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MSK II: Test 1 > Skin Path Buzzin > Flashcards

Skin Path Buzzin Flashcards

1
Q

excoriation

A

Traumatic lesion breaking the epidermis and causing a raw linear area (i.e., deep scratch); often self-induced

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2
Q

lichenification

A

Thickened and rough skin (similar to lichen on a rock); usually the result of repeated rubbing

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3
Q

macule/patch

A

Circumscribed flat lesion distinguished from surrounding skin by color.
Macule 5 mm (or >1 cm in some texts)

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4
Q

Onycholysis

A

speration of nail plate from nail bed

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5
Q

Papule/

Nodule

A

Elevated dome-shaped or flat-topped lesion.
Papule < 5 mm
Nodule >5 mm

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6
Q

plaque

A

Elevated flat-topped lesion, usually greater than 5 mm across (may be caused by coalescent papules

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7
Q

scale

A

Dry, horny, platelike excrescence; usually the result of imperfect cornification

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8
Q

blisters?

A

Blister = Any fluid-filled raised lesion

Vesicle 5 mm

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9
Q

wheal

A

itchy, , transient, elevated lesion with variable blanching and erythema formed as the result of dermal edema

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10
Q

acantholysis

A

Loss of intercellular cohesion between keratinocytes = SC falling off and floating around

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11
Q

acanthosis

A

Diffuse epidermal hyperplasia = thickening of epidermis

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12
Q

dyskeratosis

A

Abnormal, premature keratinization within cells below the stratum granulosum = see keratin layer doesn’t lose nucleus at the surface

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13
Q

exocytosis

A

Infiltration of the epidermis by inflammatory cells

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14
Q

hydropic swelling

A

Intracellular edema of keratinocytes, often seen in viral infections = swelling of the cell

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15
Q

hypergranulosis

A

Hyperplasia of the stratum granulosum, often due to intense rubbing

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16
Q

hyperkaratosis

A

Thickening of the stratum corneum, often associated with a qualitative abnormality of the keratin

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17
Q

lentiginous

A

A linear pattern of melanocyte proliferation within the epidermal basal cell layer

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18
Q

papillomatosis

A

Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae = lots of little bumps

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19
Q

parakeratosis

A

Keratinization with retained nuclei in the stratum corneum. On mucous membranes, parakeratosis is normal

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20
Q

spongiosis

A

intercellular edema of epidermis - b/w cells

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21
Q

ulceration

A

Discontinuity of the skin showing complete loss of the epidermis revealing dermis or subcutis

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22
Q

vacuolization

A

Formation of vacuoles within or adjacent to cells; often refers to basal cell-basement membrane zone area = space inside of cell that’s clear

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23
Q

Fibroepithelial Polyp (FEP):

A

skin tags, squamous papilloma

  • Occur in individuals usually age 30 or greater and particularly in obese individuals
  • Associated with areas of rubbing by clothing; collar of neck or groin
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24
Q

epithelial inclusion cyst

A

• Also known as:
– epithelial cyst
– follicular cyst
– wen
– Common
• Caused by obstruction of hair follicle above infundibulum near where hair shaft extends beyond skin surface
• Filled with keratinous debris (i.e., not a sebaceous cyst) and lined by squamous epithelium with a granular cell layer
• If ruptured (trauma), provoke a chronic inflammatory reaction with granuloma elicited by the extravasated keratin (foreign body giant cell reaction) – can be very smelly!

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25
Q

seborrheic keratosis

A

proliferation of epidermal basal cells
“postage stamp”

FGFR3

round, flat and elevated

clinically appear as “pore like ostea filled with keratin”

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26
Q

acanthosis nigricans

A

hyperpigmentation at flexural regions

epidermal hyperplasia of stratum spinosum

20% occur d/t underlying ADCA

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27
Q

adnexal neoplasms

A

• Arise from the ductal and glandular epithelial cells of the three major adnexal groups (sweat glands & ducts; hair-bulb germinal epithelium and sebaceous glands; apocrine glands and ducts)

•	Benign adnexal tumors are:
–	Symmetrical
–	Small (less than 1 cm)
–	Superficial
–	Vertical in orientation
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28
Q

cowden syndrome

A

multiple thicoepithelioma (hair follicle) w/ dominant inheritance

PTEN mutation

see benign follicular appendage tumors; hamartomatous colon polyps, internal ADCA, cerebellar gangliocytoma

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29
Q

Muire-torre syndrome

A

sebaceous adenomas with association colorectal malignancy

MSH2/MLH1 mutation

sebaveous adenoma, sebaceous carcinoma, visceral malignancy

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30
Q

Turban tumor

A

massive confluent cylindromas around forehead and scalp

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31
Q

benign fibrous histiocytoma

A

= dermatofibroma

  • Tan-brown papules which are usually small (less than 1.0 cm) and may occasionally be tender
  • More common name is dermatofibroma
  • histologically see fibrous lesions w/ prominent collagen bundles and fibroblastic cells
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32
Q

suntan

A

increased melanin production in epidermis d/t increased melanosomes

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33
Q

melasma

A

“mask of pregnancy”

• Occurs: increased pigmentation d/t hyperestrogenism
– During pregnancy
– In women taking oral contraceptives
– At menopause

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34
Q

solar lentigo

A

as opposed to suntan, see actual small increase in melanocytes and also increased melanin production

= “sun spots”

benign, but “lentigo maligna” is term used for things arising in sun exposed areas

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35
Q

vitiligo

A

skin depigmentation thats transient

associated with: diabetes, hyperTH, melanoma, industrial chemicals

Also associated with Addison’s, alopecia, PA, IBD, and polyendocrine syndrome – CD 8 T cells.

Always look for adrenal and thyroid disease!!!

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36
Q

melanocytic nevi

A

NRAS and BRAF mutations

benign

= normal mole

junctional: small flat lesion, dermoepidermal junction
compound: raised dome, intraepidermal nests + dermal cells
intradermal: smooth raised dome/ d/t overlying dermis being stretched - just found in dermal layer

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37
Q

dysplastic nevus syndrome

A

sporadic change in a nevus - one is very little problem, but multiple nevi can develop into melanoma more likely

see dark spots/moles all over back

see nests at tips of rete ridges that are “bridged” and have “fibroplasia”

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38
Q

lentigo maligna

A

malig. melanoma from sun exposed areas

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39
Q

malignant melanoma

A

superficial spread = horizontal

nodular spread = vertical phase

usually arise as an isolated lesion, but 10% arise from melanocytic nevus

mets early: LNs, liver, lungs, brain

risks:
- fair skin
- peeling before age 20

mutations:
- nevus have NRAS and BRAF
- to become melanoma, se p16 or CDK4/6 mutation

survival based on mets, and also on thickness 92% survival <1mm

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40
Q

solar elastosis

A

(“Sailor “ or “Farmer” skin):

Permanent, incremental damage to reticular collagen (elastosis) with loss of texture (leathery skin) and wrinkling

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41
Q

actinic (solar) keratosis

A
  • Actinic keratosis is a precancerous skin condition- feels like “sandpaper”
  • Present on common sun-exposed areas of skin such as scalp, face and dorsum of forearms and hands.

1/1000 continue to SCC

• Appear as erythematous, reddish-brown macules or minimally elevated papules with overlying scales.

located in the epidermis, if you get rid of the epidermal layer, get rid of the tumor

can develop” cutaneous horn”

Progression to full-thickness nuclear atypia, with or without the presence of superficial epidermal maturation, heralds the development of squamous cell carcinoma in situ. (note see that there are nuclei in the keratin layer)

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42
Q

Squamous cell carcinoma

A

malignant proliferation of epidermal keratinocytes which has the potential for metastasis to regional nodes or distant sites, if not sun related. The malignant keratinocyte proliferation has penetrated the dermal-epidermal junction basement membrane and entered the dermis.
– Bowen disease = SCC in situ

long term sun exposure = increased risk of SCC

Major Clinical Characteristics of SCC
• Areas of greatest cumulative sun exposure
• Early invasive SCC is usually a small, firm, skin-colored or erythematous nodule with indistinct margins.
• The surface may be granular, and bleed easily.
• The surface may be smooth, verrucous or papillomatous.
• Older SCCs are larger, invasive, and central area of the tumor on the skin surface may be ulcerated.
• Mortality quite low for SCC of skin

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43
Q

keratocanthoma

A
  • Rapidly growing (days-weeks) neoplasm; occurs on sun-exposed areas (face, hands) of older adults (men more than women)
  • Often involutes and clears spontaneously within 3 to 4 months
  • Histologically is SCC; now termed “Squamous cell carcinoma, Keratoacanthoma type” – like “grade 1 SCC of the skin”
  • just need to resect these clinically
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44
Q

BCC

A

• Definition: Basal cell carcinoma (BCC) consists of several types of skin neoplasm originating from the basal regenerative epithelium of the epidermis that seldom - virtually never – metastasize.

most common!

always assoc. w/ sun exposure

  • can become a “rodent ulcer”
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45
Q

Gorlin syndrome

A

Nevoid BCC syndrome

  • autosomal dominant disorder
  • multiple basal cell carcinomas before age 20
  • pits of the palms and soles
  • odontogenic keratocysts
  • medulloblastomas: brain tumors
  • ovarian fibromas

Genetics of BCC :
- sonic hedgehog binds patch gene and allows for patch to release smoothen à increased GLI1 à increased replication
if there is defect in Patch or smoothen – then its dissociated and smoothen is always turning on GLI1

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46
Q

nodular BCC

A
  • Traditional or “classic” appearance of BCC
  • Dome-shaped, pearly papule or nodule
  • Prominent surface dilated dermal vessels (telangiectasia)
  • Easily treated by excision if not large; may become quite large if neglected
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47
Q

sclerosing BCC

A
  • Important clinical and pathologic type
  • Occurs predominately on face
  • “Rodent Ulcer”: Typically yellowish-white or pearly white, indurated plaque that may retract below plane of skin surface (leading to the designation rodent ulcer)
  • Poorly defined margins (edge of lesion)
  • Difficult to excise, high recurrence rate and may disfigure
  • Reason MOHS surgery was invented (take tumor out without removing a lot of skin)
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48
Q

superficial BCC

A
  • Multifocal erythematous, scaly plaque; elevated rolled edges.
  • Occurs non-sun exposed skin sites on proximal limbs or trunk
  • Multifocal growth pattern localized to dermal-epidermal junction
  • Easily excised; do not become locally invasive or metastasize, but part of a “field defect” and therefore recur.
  • May be confused clinically with melanoma, if pigmented
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49
Q

bednar tumor

A

pigmented variant of Dermatofibrosarcoma Protuberans

– Malignant superficial fibroblastic neoplasm (fibrosarcoma of skin)
– Locally aggressive but rarely metastasizes

The tumor usually presents as a flesh-colored fibrotic nodule on sectioning. B, The lesion often infiltrates the subcutis in a manner reminiscent of “Swiss cheese” to aficionados. C, A characteristic storiform (swirling) alignment of spindled cells is apparent.

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50
Q

Mycosis fungoides

A

cutaneous T cell lymphoma
- see inflammation of atypical lymphocytes underneath the epidermis: erythemaouts patches, pruritis, lymphadenopathy

may see “sezary cells” detected in the blood

  • CD4+ T-cell lymphoma of the skin (CLA, CCR4 & CCR10)
  • Aggressive neoplasm with median survival 8-9 years (M>F)
    • erythematous patches/plaques present on trunk, usually over 5cm in diameter
    • pruritis is common complaint

progression: premycotic, patch, plaque, tumor

PAS+ stain with CD4+ T cells in epidermis

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51
Q

sezary syndrome

A

cutaneous T cell lymphoma where skin shows generalized exfoliative erythroderma/dermatitis

scaling/erythema over most of body

itching, malaise, fever, chills, w/l

redness and scaling of skin >30%

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52
Q

icthyosis

A

scaling - looks like fish skin

  • genetic abnormality leading to hyperkaratosis
  • look for malignancy in LNs!
  • worrisome when comes up suddenly
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53
Q

acute urticaria

A

hives often Mast cell-dependent and IgE-dependent

• All types can cause fatalities
– Systemic anaphylaxis
– Laryngeal edema
– Treat with antihistamines, subcutaneous epinephrine and IM injection corticosteroids (or with known C1 inhibitor deficiency use C1 inhibitor (C1-INH) concentrates, kallikrein inhibitor or fresh-frozen plasma)

• Classic skin lesion: Abrupt appearance of a wheal (always multiple) and area of wheal is intensely pruritic.
– Wheal: Transient edematous erythematous plaque secondary to an acute allergic reaction seen in hives (Urticaria)
– Bulla: Larger fluid-filled lesion (e.g., friction blister)

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54
Q

Eczema

A

Spongiotic Dermatitis – looks red and oozy
• Generalized term: numerous pathologic and clinical conditions: previous referred to “Chronic Dermatitis” or included collectively as “Spongiotic Dermatitis” because of common denominator of epidermal edema with prominent lymphocytes in dermis and epidermis
• spongiosis = intracellular edema
• Most commonly encountered in pediatric age groups
• Common denominator is acute onset of red, papulovesicular lesions (“boiling over” appearance) which may ooze or crust
• Usually driven by T cell mediated type IV hypersensitivity inflammation
• Acute lesions may evolve into raised, scaling plaques

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55
Q

type I HST?

A

IgE mediated = allergy

= anaphylaxis, wheels,

56
Q

type II HST?

A

IgM or IgG mediated (i.e. autoimmune)
- antibody binds to antigen on target cell

  • RHD
  • Goodpasture’s
  • Grave’s
  • Myasthenia Gravis
57
Q

type III HST?

A

IgG binds to soluble antigen –> circulating immune complex

  • serum sickness
  • RA
  • post-strep pneumococcus
  • SLE
58
Q

type IV HST?

A
  • T cell mediated “delayed type” cell mediated immune response
  • contact dermatitis
  • chronic transplant rejection
59
Q

erythema multiforme

A

“target lesions”
• Hypersensitivity (CD8+ cytotoxic T cells) reaction to drugs, infections, malignancy, collagen vascular disorders
– Infections: Herpes simplex, deep fungal (Histoplasmosis), Salmonella typii, Leprosy
– Drugs: Antibiotics, Salicylates, Anti-malarials
– “Multiforme” because of wide variety of clinical appearances in addition to characteristic “target” lesions (red-pale-red)
– Other skin disorders have targetoid lesions but not the classic red-pale-red pattern
• Severe, systemic febrile form with mucosal involvement: Stevens-Johnson syndrome
• Toxic epidermal necrolysis is form with diffuse necrosis and sloughing of skin and mucosae (emergency situation – skin is like burn patient)

erythema minor - most often d/t herpes simplex
erythema major - most often d/t drugs

60
Q

seborrheic dermatitis

A

“dandruff” = dry scales and underlying erythema - seen on scalp, face, back, glabella (upper eyebrow)

  • Chronic “dermatitis” more common than Psoriasis (5% of population)
  • Involves skin regions with high density of sebaceous glands (oil or sebum production)

• Infection with superficial yeast (Malassezia furfur) may play important role since condition is improved by use of topical antifungal agents

  • often seen in hostpitalized patients with acute illness

** can be associated with parkinson’s disease!!! slow soft speech, swallowing, seborrheic dermatotis!

61
Q

acute vs. chronic inflammatory conditions?

A

acute:
urticaria, eczema, erythema multiforme

chronic: 
seborrheic dermatitis
psoriasis
LSC
lichen planus
discoid lupus erythematosus
rosacea
62
Q

psoriasis

A

“AI disease” → results in plaques: silvery scales on bright red well demarcated plaques (knees, elbow, scalp)
• Chronic skin condition affects 1-2% of the US population
• Clinical association with arthritis
• Affects skin of elbows, knees, scalp, = EXTENSOR AREAS!!!!

Koebner phenomenon – trauma can induce psoriatic lesions – irritated skin sets of psoratic lesion

  • Typical lesion: well-demarcated, pink- to salmon plaque
  • Many different clinical presentations
  • HLA-Cw*0602 association – increased CD4+TH1 sensitized cells set off other T-cells causing increased cytokines leading to epidermal proliferation.

tx: phototherapy - UV rays help it
- topical corticosteroids

associated with: MI, metabolic syndrome, IBD, depression, nail pits, koebner reaction, arthritis, +ASOT

63
Q

LSC

A

Lichen Simplex Chronicus: chronic scratching!
• From chronic rubbing or scratching
• If nodular = Prurigo nodularis
• seen in nervous people
• see neoplasia of the epidermis
- see skin lines, well circumscribed and scaly plaque

64
Q

civatte bodies

A

lichen planus

65
Q

wickhan striae

A

lichen planus

66
Q

lichen planus

A

: inflammation – see bandlike infiltrate of lymphocytes

pruritic, purple planar, papular - more often seen in oriental populations

  • see wickam striae in mouth!
  • Self-limiting chronic inflammatory condition of skin and mucous membranes (oral cavity)
  • Usually resolves spontaneously 1-2 years after onset, but may persist for years in oral cavity
  • Multiple plaques that are symmetrically distributed, particularly on extremities, often on wrists and elbows and on the glans penis, + Koebner phenomenon

** note: commonly assoc. w/ hep c, UC, vitiligo and MG — cell mediated immune response of u/k origin

67
Q

Discoid Lupus Erythematosus:

A

• Localized cutaneous manifestation of Systemic Lupus Erythematosus (SLE) with no associated systemic manifestations

Excessive sun exposure may trigger cutaneous lesions or exacerbate them
– “butterfly rash”

REMEMBER:

  • SLE type III HST, d/t ANA Abs directed against nuclear antigens, that result in immune complex formation
  • linked with HLA-DQ
  • see Antigen-Ab complexes stuck at the basement membrane: IgG and antigen along with complement C3 get stuck at the basal layer
  • see : malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis (pleuritis, pericarditis), renal dysfunction, nseizures, hemolytic anemia
68
Q

rosacea

A

see erythema and telangiectasias

flush easily

dfft. from acne b/c of neurovascular componenet and no comedones

69
Q

bullous diseases

A 
•	Common Friction Blister
–	Intraepidermal blister usually just beneath the stratum granulosum with scant  or no inflammation in papillary dermis.
•	Immune-Mediated 
–	Pemphigus Group of Diseases
–	Bullous Pemphigoid
–	Dermatitis Herpetiformis
•	Genetic-Congenital
–	Epidermolysis Bullosa- inherited defects in collagen, laminin, etc leading to several disorders with weak skin and blistering
–	Porphyrias
70
Q

subcorneal blister?

A

pemphigus follaceous

more benign course; involves face, scalp, chest and back and spares mucous membranes
– Epidemic form occurs in South America (fogo salvagem)

autoAbs against Dsg1 only (most superficial) - leads to subcorneal blisters

71
Q

suprabasilar/intraepidermal blister

A

under epidermis, but above the BM

= pemphigus vulgaris

autoAbs against DSg1 and Dsg3 - cause blisters in the deep suprabasal epidermis

produce reticular “fishnet” like pattern

72
Q

subepidermal blister

A

entire epidermis seperates from dermis

= bullous pemphigoid

autoAbs bind BPAG2 (component of hemidesmosomes, leading to blister formation) at level of basement membrane

  • more resistant to rpture, look more like friction blister
  • see linear deposition of C’ along dermo-epidermal junction
73
Q

Dermatitis Herpetiformis:

A

– IgA to gliadin attacks reticulin in dermal papillae fibrils
– Rare skin bullous disorder
o Major association with Celiac Disease (Sprue, gluten- sensitive enteropathy)
o anti-gliadin antibodies cross-react with reticulin in the anchoring fibrils in dermal papillae
o Intensely pruritic plaques and vesicles
o located on extensor surfaces, elbows, knees, upper back and buttocks
• Note: Selective deposition of IgA autoantibody at the tips of dermal papillae is characteristic

74
Q

erythema nodosum

A

panniculitis - painful red nodules w/out ulceration on anterior aspects of legs
- seen with drug exposure or inflammatory bowel disease

** strep infection is the most common cause *** 2nd most common is BCP’s

– Acute septal inflammation associated with infection by many agents [(e.g. Beta-strep, TB, sarcoidosis, inflammatory bowel disease, malignancies and drugs (e.g. sulfonamides , oral contraceptives)]

Erythema nodosum is a form of panniculitis characterised by tender red nodules, 1–10 cm, associated with systemic symptoms including fever, malaise, and joint pain. Nodules may become bluish-purple, yellowing, and green, and subside over a period of 2–6 weeks without ulcerating or scarring.

erythema induratum seen from TB: posterior surfaces of legs, may ulcerate

75
Q

verruca vulgaris

A

warts

etiology - often d/t HPV virus

76
Q

molluscum contagiosum

A

poxvirus

long incubation time, younger age group, umbilicated lesion, transmitted through contact

77
Q

impetigo

A

= superficial blisters w/ purulent material that rupture easily w/ “honey colored crust”

** very contagious

** often gram + : most commonly caused by staph aureus, though historically seen with beta strep infections

78
Q

different tinea infections

A

– Tinea capitis: scalp in children
– Tinea corporis (“ringworm”): trunk and extremities in all ages but more in children
– Tinea cruris: inguinal skin adjacent to genitalia, obese men in hot weather
– Tinea pedis (athlete’s foot): feet (between toes)
– Tinea barbae: beard area in men
– Onychomycosis: fungal infection of nail beds
– Tinea versicolor: this one is not named by a location and is a yeast (Malassezia furfur) infection (not a dermatophyte with hyphae, unlike the others)

79
Q

tinea versicolor

A

a yeast skin (Malassezia furfur) infection (not a dermatophyte with hyphae, unlike the others)

would see pseudohyphae

80
Q

epidermolysis bullosa

A
  • genetic abnormalites in structural proteins keratin 14 or 5 –> lead to bulla forming that are massive!!! suprabasalar lesion
81
Q

porphyrias

A

AD inheritence = non inflammatory blisters d/t sun

  • hypertrichosis and skin fragility
  • assoc. w/ liver disease and elevated urinary porphyrins

defects in heme synth, leads to increased intermediates causing urticaria and supepidermal vesicles (esp. in sun exposure)

82
Q

atopic dermatitis

A

insect, light, drug, allergen, food allergy

  • eos are prominent in inflamm.along with IgE
  • humoral mediation - responds well to steroids
  • pruritic, exudative, or lichenified eruption on face, neck trunk, wrists, hands
  • onset often in children, rare after age 30
  • flexural areas are common

note: often linked with staph - staph makes biofilm –> causing a rash that itches

83
Q

allergic contact dermatitis

A

topically applied antigens

  • t-cell mediated
  • won’t respond well to steroids
  • no inflamm. until second exposure

ex: poison ivy, nickel, jewelry

84
Q

primary irritant dermatitis

A
  • d/t chemicals
  • no prior exposure necessary
  • necrosis and ulceration w/ neutrophil response
85
Q

NF1

A

NF1/neurofibromin gene

see neurofibromas, optic nerve gliomas, cafe au lait spots

86
Q

NF2

A

NF2/merlin gene mutation

see neurofibromas, bilateral acoustic neuromas, CNS gliomas, cataracts

87
Q

pityriasis rosea

A

oval, fawn-colored scaly eruption following cleavage lines of trunk - “christmas tree pattern”

common, mild inflamm. disease more common in females

d/t HHV 6 and 7

itching is mild and common

center of lesions have “cigarette paper” appearance - thin red scale around the outside, with clearing in the middle

“herald patch” - larger lesion that is usually seen before other lesions

NOTE: must rule out syphilis, with RPR - esp. if pregnant!

88
Q

tinea corporis

A

“body ringworm”
- ring-shaped lesions with advancing scaly border, central clearing or scaly patches

often on trunk

ddx via culture/scrapings

trichophyton rubrum is most common pathogen

89
Q

scaling of palms, soles, in between toes and fingers

A

think tinea pedis/manuum

90
Q

bowen disease

A

intraepidermal SCC

91
Q

folliculitis

A

itching and burning in hairy areas - pustules in hair follcicles

frequently caused by staph infections

“hot tub follcilitis” = pseudomonas aeruginosa

92
Q

milaria

A

“heat rash”

burning, itching, small vesicles, usually on trunk in hot moist climates

93
Q

steven johnson syndrome

A

erythema multiforme major where <10% BSA skin loss

caused by toxicity - often d/t sulfonamides, NSAIDs, allopurinol, antivonculscants

94
Q

toxic epidermal necrolysis

A

see erythema multiforme major, TEN where there is >30% BSA skin loss

caused by toxicity - often d/t sulfonamides, NSAIDs, allopurinol, antivonculscants

must be tx like a burn patient

95
Q

erythema migrans

A

think lyme disease - gradual expansion of red target

96
Q

erysipelas

A

= an infectious erythema

edematous, spreading, hot erythematous region, pain chills, fever,

cellulitis d/t Beta-hemolytic strep

97
Q

cellulitis

A

edematous, expanding, erythematous warm laque often involving lower leg

pain, chills, fever, may cause sepsis

Beta-hemolytic strep or staph aureus

leukocytosis is present throughout

98
Q

kaposi sarcoma

A

Herpes Type 8

endemic in young black men in Africa

red/purple plaques or nodules on cutaneous or mucosa surfaces

seen in pts. with HIV/AIDS

99
Q

scabies

A

generalized severe itching, burrows, especially on finger webs/wrist creases

red papules or nodules on scrotum and penil glands is pathognomonic

= “seven year itch”

100
Q

pediculosis

A

pruritis with excoriation, nits on hair shafts, lice in skin/clothes

“crabs” or body lice — due to the pubic louse

101
Q

do darrow’s slide show

A

do it NOW.

102
Q

where does melanoma most often mets to?

A

liver. (shows elevated alk phos)

other places: LNs, lungs, brain

103
Q

“the itch that rashes”

A

rash starts with pruritis –> rash = a type of atopic dermatitis, IgE mediated (seen at flexion of fossa, face, dorsal feet)

most often d/t staph - forms biofilm over the skin

Staphylococcal biofilm which block sweat glands. Toll-like receptor 2 is the protein that is involved in the innate immune system, which is activated in areas where there are blocked sweat ducts in cases of eczema.

treatment:
Current management for eczema includes the use of steroids to reduce inflammation and enhance the body’s ability to fight the bacteria. Patients should be instructed to be wary of soap, hot water, scrubbing, and clothing that can aggravate itching, scratching, and peeling. Oil rather than water-based moisturizers are recommended. Products containing dyes, perfumes, or peanuts should be avoided.

104
Q

Job’s disease/ Hyper IgE syndrome

A

problem with phagocytic function- see recurrent staph absessess

  • eczema + neutrophil problem

Job’s disease: white cells can’t get where they need to d/t no integrin CD11/CD18 - thus there are high WBC’s but recurrent bacterial infections = hyper IgE syndrome

  • they present with atopic dermatitis and recurrent infections
  • increased IL-4 –> results in increased TH2 response –> stimulates IL4, ** IL-5, –> production of B cells –> plasma cells (IgE)
  • see decreased TH1 and CD8+ cells

case: An 8 year old child has a history of staphylococcal abscesses, a prior episode of pneumonia with pneumatoceles, high IgE levels,
eosinophilia, and rash as shown. He has lost none of his teeth. The primary problem in this patient is:

105
Q

wiskott-aldrich

A

see eczema with combined immunodeficiency: this is a combined B and T cell immunodeficiency disorder

106
Q

This 60 y/o male complains of dry itching skin with circular coin shaped lesions found in the winter. He bathes nightly. This is which eczema.

A

nummular eczema

107
Q

drugs that can produce psoriasis?

A

stopping corticosteroids

Certain drugs can also produce psoriasis,
ie beta blockers, lithium, interferon, etc.

Flare up may be an HIV marker

108
Q

koebner phenomenon

A

scratch skin and rash will break out where you scratch

  • its more common for this to be associated with poison ivy
  • almost like the itch that rashes
109
Q

nail pitting, fungal looking nails, oil spots

A

think psoriasis

110
Q

fungal infection that extends to the nail junction?

A

marker for immunodeficiency - think AIDS

trichophyton rubrum should be superficial and distal

111
Q

dull yellow fluoresence under wood’s light

A

malassezia furfur = a genus of fungi that can cause hypopigmentation

“scraping show” - spaghetti/meatballs

can cause tinea versicolor - “sun fungus” that causes hypo or hyperpigmentation that is increased with sunlight - looks like small spots

Tinea versicolor = worsens with Cushings, malnutrition or immunosuppression

112
Q

spaghetti and meatball

A

malassezia furfur, tinea versicolor

113
Q

steroid acne

A

steroid dermatitis = small, firm follicular papules on the forehead, cheeks, and chest. They appear as pinkish maculopapular rash without any comedones or cyst

steroid acne is the same condition as malassezia folliculitis and is due to proliferation of malassezia yeasts (also known as pityrosporum).

114
Q

pink florescence under wood’s lamp

A

cornebacterium

Bacterial infection in skin flexures due to erythrasma (Corynebacterium minutissimum)

115
Q

green fluorescence under wood’s lamp

A

Cat ringworm Microsporum canis

116
Q

porphyria cutanea tarda

A

hepatic uroporphyrinogen decarboxylase deficiency: disorder results from low levels of the enzyme responsible for the fifth step in heme production.

  • see blistering of the skin, is a chronic condition and can result in chronic liver prolbmes, cirrhosis and inflammation and hepatic fibrosis
  • void wine colored urine d/t increased uroporphyrin I enzyme
  • see elevated ALT, hep C infection, photosensitivity

yields a pink fluorescence under Wood lamp (black light) radiation

117
Q

b/l pneumonia w/ bullous myringitis (inflammation of TM) and dry cough,along with erythema multiforme

A

mycoplasma pneumonia

118
Q

drugs causing SJS/TEN

A

West:

  1. oxicam NSAIDs***, ie perioxicam (Feldene)
  2. sulfas

East:

  1. carbamazepine (Tegretol) – HLA - B*1502
  2. allopurinol – HLA - B*5801

if from west think NSAIDs, if from east don’t give tegretol or allopurinol!!! (antiseizure drugs)

SJS works through FasR death receptor - drugs activate this pathway –> self breakdown

119
Q

sharp demarcation of inflammation/rash

A

think strep = ‘st. anthony’s fire”

120
Q

organism responsible for necrotizing cellulitis/ fascitis - associated with colon, gyn, or lymphoreticular malignancies.

A

Clostridium septicum - see “gas gangrene”

for some reason malignincies result in growth of C. septicum

Infections are typically seen in settings of trauma, surgery, malignancy, skin infections/burns, and septic abortions.

121
Q

pt with rash after spending day in spa

A

pseudomonas aeruginosa

122
Q

skin infection that feathers out around a central lesion - not sharp borders

A

think staph aureus or MRSA

123
Q

what to worry about what with child w/ impetigo?

A

group A strep infection - can cause glomerulonephritis - child has puffy face d/t fluid retention and hematuria

124
Q

what causes rosacea?

A

demodex mite or may be d/t intestinal bacterial overgrowth

see rinofina - large scarred nose

worry about Keratopathy. Corneal melting!
Corneal vascularization and thinning.
Associated with PD.

many have SIBO(small intestinal bacterial overgrowth) ad respond to rifamixin

see telangiectasias but no comedones

125
Q

parkinson’s

A

think seborrheic dermatitis and malssezia furfur

126
Q

complications of ioxides scapularis lyme disease?

A

Stage I: Flu syndrome with rash (ECM)

Stage II: Dissemination: heart, joints, nerves and skin (heart block, Bell’s palsy, migratory arthralgias, ECM)

Stage III: Late: joints and CNS and PNS (oligoarthritis, encephalitis/memory loss
- sleep disturbances, neuropathies/paresthesias)

127
Q

“fifth’s disease”

A

slap cheek, reticulated rash that looks like giraffee

caused by parvovirus B19

Fifth disease starts with a low-grade fever, headache, rash, and cold-like symptoms, such as a runny or stuffy nose. These symptoms pass, then a few days later the rash appears. The bright red rash most commonly appears in the face, particularly the cheeks. This is a defining symptom of the infection in children (hence the name “slapped cheek disease”).

This ssDNA virus can also produce the glove and stocking purpuric syndrome. The mother may also develop a small joint arthritis resembling RA.

** worry about mom b/c can cause aplastic anemia

128
Q

blueberry muffin baby, deafness, hematopoiesis, malaise, polyarthritis - see dark blue spots

A

congenital rubella syndrome = “german measles”

blueberry spots d/t extramedullary hematopoisis

The syndrome (CRS) follows intrauterine infection by the rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects- It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anemia and hepatitis.

129
Q

This patient developed this rash on her forehead that is spreading
centifugally. She also has the
bluish white spots in the mouth
with fever, conjunctivitis, coryza, and cough.

A

rubeola virus = regular measels

problem if develops panencephalitis when older!

koplik spots = small red based lesions with blue white centers in mouth

130
Q

levamisole

A

used to cut cocaine - causes arteritis and plugs up vesicles

131
Q

see bubble fingers d/t?

A

caused by PDF/VEGF –> neoangiogenesis –> subperiosteal new bone formation

seen in lung cancer, lung infections, CF, cirrhosis, graves disease

132
Q

DRESS syndrome

A

Drug Rash with Eosinophilia and Systemic Syndrome = DRESS

  1. 2-6 weeks after start of a new medicine
  2. Progression from acral edema to generalized rash to pinpoint pustules and desquamation
  3. Lymphadenopathy, hepatomegaly and abnormal LFTs
  4. An IL5 disease.

see progression from desquamation –> lymphadenopathy –> hepatomegaly and liver problems

type IV reaction d/t HHV6 induced CD8 T cell response

133
Q

poison ivy is what response

A

T cell response with macrophage activation

Type IVa Gell-Combs

134
Q

acquired C1 esterase deficiency

A

anyone with B cell lymphoma/leukemia forms antibodies, if you form Abs you tend to form them for C1 esterase, if C’ is activated you can’t shut it off and get angioedema, because you have formed Abs aainst C1 esterase

Angioedema: 
- Cause: Bradykinin
- Screen with C4 for
 angioedema
- Decreased CI level points to acquired C1 esterase deficiency rather than the hereditary type (It’s new and the body can’t keep up!)

hopefully won’t be on test…

135
Q

urticaria >24 hours

A

means that its chronic = urticarial vasculitis

136
Q

photosensitive pt. with RO/SSA antibody?

A

= subacute cutaneous lupus

  • skin lesions that are scaly and evolve as polycyclic annular lesions or psoriasiform plaques
  • lesions look annular and serpentine
  • can be deficiency of the 2nd component of complement
  • child could be born with heart block!!!

MSK II: Test 1 (7 decks)

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