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Concepts in Pathology and Tissue Morphology > Skin Pathology > Flashcards

Skin Pathology Flashcards

1
Q

what is a macule

A

primary lesion; small flat (less than 1cm)

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2
Q

what is a patch

A

primary lesion; large flat (greater than 1 cm)

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3
Q

what is a papule

A

primary lesion; raised (smaller than 1 cm)

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4
Q

what is a plaque

A

primary lesion; raised (greater than 1 cm)

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5
Q

what is a vesicle

A

primary lesion; small, clear fluid filled (less than 1 cm)

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6
Q

what is a tumor/mass

A

primary lesion; raised, deep, and greater than 2 cm

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7
Q

what is a pustule

A

primary lesion; white fluid filled

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8
Q

what is a bulla

A

primary lesion; large, clear fluid filled (greater than 1 cm)

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9
Q

mechanism of papule or plaque formation

A

proliferation of cells in epidermis or superficial dermis

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10
Q

what is a nodule

A

primary lesion; usually greater than 1 cm, deep and palpable

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11
Q

mechanism of nodule formation

A

proliferation of cells into the mid-deep dermis or fat

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12
Q

erythematous means

A

red FROM inflammation

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13
Q

additional descriptors for primary lesions

A
  • color
  • size
  • texture
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14
Q

what is scale

A

secondary change; accumulated skin (stratum corneum)

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15
Q

what is crust

A

secondary change; died exudate: blood, serum, pus

scab

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16
Q

what is excoriation

A

secondary change; traumatized due to scratching

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17
Q

what is erosion

A

secondary change; depression with loss of epidermis (superficial)

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18
Q

what is ulceration

A

secondary change; depression with loss of epidermis and dermis (deeper than erosion)

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19
Q

what is fissure

A

secondary change; linear cleavage

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20
Q

what is lichenification

A

secondary change; thickening, accentuated skin line

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21
Q

what is atrophy

A

secondary change; depression, thinning, wrinkling

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22
Q

what is scar

A

secondary change; permanent fibrotic change

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23
Q

if something is vascular/vasculitic it will not

A

blanch with pressure

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24
Q

petechiae/petechial is a secondary descriptor. what does it mean

A

acute to subacute leakage of capillaries within skin; generally pinpoint to small

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25
Q

purpura/purpuric is a secondary descriptor. what does it mean

A

acute to subacute leakage of capillaries or small-larger vessels within skin; usually larger; may be palpable

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26
Q

ecchymotic is a secondary descriptor. what does it mean

A

subacute to chronic hemorrhage within skin; usually larger

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27
Q

examples of configuration

A 
•solitary
•discrete
•annular
•confluent/coalescent
•clustered/grouped
•linear
reticular (net-like)
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28
Q

what does the term acral mean in the context of distribution pattern

A

the most distal part (hands, feet, tip of nose)

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29
Q

how to describe skin findings

A

distribution, configuration, color/size primary lesion with +/- secondary change

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30
Q

causes of impetigo

A
  • staph aureus (more common)

* strep pyogenes

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31
Q

common location of impetigo

A

around mouth or perineum

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32
Q

description of impetigo

A

crusted, “glazed” eroded papule to plaque, peripheral rim of scale
uncommonly bullous -> blisters

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33
Q

impetigo can be tender or asymptomatic. how is it treated

A

topical or oral abx

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34
Q

impetigo is rarely biopsies, but what would be seen histologically

A

subcorneal neutrophils and scattered gram + cocci

usually doesn’t invade beyond epidermis

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35
Q

description of cellulitis

A
  • edematous, erythematous, warm, sometimes taut/shiny localized plaque
  • usually solitary
  • uncommonly blisters surface due to edema
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36
Q

cellulitis may be present with or without fever and other systemic sxs. what is the treatment

A
  • systemic abx (PO or IV)

* rest elevation

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37
Q

necrotizing fasciitis is usually deeper tissue injury than cellulitis. what usually causes it

A

anaerobic bacteria or group A strep pyogenes

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38
Q

description of necrotizing fasciitis

A

purple, dusky necrotic color +/- ulcers and bullae

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39
Q

necrotizing fasciitis is a surgical emergency and is associated with

A

severe, intense pain and systemic symptoms

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40
Q

In staph scalded skin syndrome, staph aureus produces

A

epidermolytic-toxin that causes cleavage/split within epidermis

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41
Q

what demographic is typically affected by SSSS, and why?

A
  • infants and younger kids b/c they have physiologically decreased renal function
  • also those who are immunocompromised
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42
Q

those affected by SSSS are usually febrile and have peeling that is accentuated at perioral areas and body folds. where is the most common primary infection?

A

nasopharynx

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43
Q

why is the area of primary infection important in staph scaled skin?

A

that is the area that must be cultured

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44
Q

SSSS doesn’t have any true mucosal involvement. what is the treatment?

A

systemic anti-staphylococcal abx (PO or IV)

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45
Q

histologically how could a biopsy of SSSS be differentiated from impetigo?

A

there are no organisms in the subcorneal blister of SSSS because it is a toxin-mediated effect

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46
Q

what are they cytopathic effect of herpes virus on keratinocytes?

A

the 3 Ms
•margination of chromatin
•multinucleation
•molding of nuclei (clumping together)

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47
Q

HSV1 more commonly affects

A

oral

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48
Q

HSV2 more commonly affects

A

genital

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49
Q

initial infection of HSV can range from

A

asymptomatic to fulminant stomatitis (rare)

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50
Q

Description of shingles (VZV) rash

A
  • dermatomal distribution disseminated papules, vesicles, plaques, bulla
  • itchy, painful
  • +/- systemic symptoms
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51
Q

concerning presentations of VZV

A
  • ophthalmic involvement -> possible blindness

* Ramsay-hunt syndrome -> facial palsy, ear pain

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52
Q

Histopathology of VZV

A

identical to HSV! 3Ms

Need PCR to discriminate between the 2

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53
Q

what are verruca and what the cause

A

warts; HPV

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54
Q

vulgaris verruca

A

common wart

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55
Q

condyloma acuminata

A

genital warts

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56
Q

histology of verruca vulgaris

A
  • papillomatous epidermal acanthosis
  • hyperkeratosis
  • hypergranulosis
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57
Q

what is molluscum contagiousum

A

in the pox virus category

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58
Q

description of molluscum contagiosum

A 
•dome-shaped papules with waxy surface
•single or multiple
•may be pruritic
•~5mm
"papule with central umbilication"
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59
Q

what is seen histologically in molluscum contagiosum

A

henderson-patterson bodies = accumulation of virus into brick-like structures

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60
Q

location of molluscum contagiosum lesions

A

trunk, face, axillae, genital area (STI)

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61
Q

how does molluscum contagiosum spread

A

with scratching

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62
Q

what are tinea

A

40+ species of fungi that “feed” on dead skin (dermatophyte infection)

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63
Q

species that cause tinea fall in which genera

A
  • tricophyton
  • microsporum
  • epidermophyton
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64
Q

what stain can be used for tinea

A

KOH stain the stratum corneum

*fungal culture if inconclusive

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65
Q

fungal forms of tinea can be difficult to see on HandE stain, but what might be identifiable?

A

altered cornified layer with intracorneal neutrophils

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66
Q

tinea pedis

A

athlete’s foot

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67
Q

tinea corporis

A

ringworm occurs anywhere on the body

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68
Q

tinea manuum

A

hand (usually left)

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69
Q

tinea cruris

A

jock itch

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70
Q

tinea capitis

A

scalp

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71
Q

tinea onychomycosis

A

nails

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72
Q

tinea versicolor (pityrosporum)

A

not technically tinea, b/c caused by yeas organism, but lumped in because similar presentation

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73
Q

bacterium that causes syphilis

A

treponema pallidum (spiral shaped bacteria)

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74
Q

primary syphilis infection (treponema pallidum)

A

solitary or multiple painless genital “chancres”

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75
Q

secondary syphilis infection (treponema pallidum)

A

rash and condyloma lata, systemic symptoms, moth-eaten alopecia

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76
Q

tertiary syphilis infection (treponema pallidum)

A

gummas (granumolas), aortitis, neurosyphilis, etc

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77
Q

congenital syphilis (treponema pallidum)

A

stillbirth, acral bullae/erosions, rhinitis, rhagades, deafness
*highly infectious

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78
Q

what is sarcoptes scabiei

A

the human itch mite

an arthropod that burrows under the skin and causes scabies

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79
Q

scabies infection occurs when

A

adult female sarcoptes scabiei burrows into the epidermis and lays eggs

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80
Q

transmission of scabies

A

close skin contact

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81
Q

description of scabies

A
  • usually exceedingly pruritic

* moth-eaten papules, burrows

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82
Q

what histologic prep may be useful in diagnosing scabies?

A

mineral oil prep

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83
Q

where does scabies infection occur

A
  • hands, feet, waistline/genitals

* infants may have atypical presentation

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84
Q

cutaneous infections caused by arthropod

A

scabies

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85
Q

cutaneous infections caused by bacteria

A

impetigo, cellulitis, SSSS

syphilis (treponema=spiral bacteria)

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86
Q

cutaneous infections caused by dermatohyte (fungus)

A

tinea

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87
Q

cutaneous infections caused by virus

A

HSV, VSV, molluscum contagiosum

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88
Q

subcutis is underneath the dermis and is also called

A

panniculus

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89
Q

stratum corneum

A
  • composed of dead, anucleated keratinocytes

* protects against environment and external pathogens

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90
Q

stratum lucidum is only normally found

A

•on thickened skin (palms and soles)

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91
Q

stratum granulosum (aka granular layer) have keratinocytes with heratohyalin granules that

A

are exocytosed to produce a water-proof barrier

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92
Q

stratum spinosum (aka spiny layer)

A
  • provided structural support

* home of langerhans cells

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93
Q

cellular junctions in stratum spinosum

A

desmosomes (have pairs), look like spines

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94
Q

stratum basale (basal layer)

A
  • connects epidermis to dermis

* home of melanocytes and stem cells

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95
Q

cellular junctions in stratum basale

A

hemidesmosome (no pairs)

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96
Q

merkle cells are somewhat of a mystery but serve the purpose of

A

group together to form a receptor for touch (sustained pressure/deep static touch)

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97
Q

melanocytes are derived from

A

neural crest

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98
Q

langerhans cells are located in stratum spinosum and act as

A
  • antigen presenting cells (APCs)

* mediators of immune response

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99
Q

langerhans cells contain

A

birbeck granules, which look like tennis rackets

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100
Q

what is found only in the dermis, and not the epidermis

A

blood vessels, lymphatics, and nerves

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101
Q

fibroblasts are the main cells of the dermis and produce

A

collagen, elastin, and ground substance

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102
Q

free nerve endings in the dermis have 2 kinds

A
  • c-type: small, slow, unmyelinated

* A delta type: small, fast, myelinated

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103
Q

meissner corpuscles sense what in dermis

A

light touch, vibration, and position

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104
Q

pacinian corpuscles sense what in dermis

A

vibration and pressure

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105
Q

ruffini corpuscles sense what in dermis

A

stretching, continuous pressure, proprioception

106
Q

merkle disks sense what in dermis

A

sustained pressure

107
Q

what kind of secretion occurs in sebaceous glands

A

holocrine

108
Q

where do sebaceous glands empty

A

into hair follicles; not directly onto skin

109
Q

where are sebaceous glands located

A

everywhere except palms and soles

110
Q

which sweat glands cause body odor

A

apocrine sweat glands

111
Q

where are apocrine sweat glands located?

A

axilla, areola, ear canal, eyelids, and anogenital area

112
Q

where are eccrine (merocrine) sweat glands located

A

everywhere except mucous membranes

113
Q

histologic comparison of apocrine and eccrine (merocrine) sweat glands

A
  • apocrine: more pink, larger ducts

* eccrine: more purple, more compact ducts

114
Q

where do apocrine and eccrine (merocrine) sweat glands empty

A

directly onto skin surface

115
Q

which sweat glands are important for thermoregulation?

A

eccrine (merocrine) sweat glands

116
Q

secretion of eccrine sweat glands regulated by

A

sympathetic nervous system

117
Q

secretion of sebaceous glands regulated by

A

primarily hormonal control

118
Q

orthokeratosis or hyperkeratosis is

A

thickened stratum corneum

119
Q

orthokeratosis/hyperkeratosis occurs where

A

palms/soles (naturally)

chronically rubbed/irritated skin

120
Q

parakeratosis is

A

dead cells within the stratum corneum that retain their nuclei

121
Q

clinical example of parakeratosis

A

psoriasis

122
Q

acanthosis is a protective mechanism. what occurs

A

thickened/elongated spinous layer

123
Q

clinical examples of acanthosis

A
  • psoriasis

* lichen planus

124
Q

acantholysis is

A

lysis of cells in the spinous layer

125
Q

clinical example of acantholysis

A

pemphigus

126
Q

psoriasis presents with

A
  • parakeratosis
  • acanthosis
  • neutrophils in stratum corneum
127
Q

what is a histiocyte

A

a macrophage in the skin

128
Q

eosinophils looks like “raspberries wearing sunglasses.” when they are in the skin, think

A

allergy!

129
Q

mast cells look like fried eggs. in the skin the can ___ and cause ___

A

degranulate -> itch

130
Q

plamsa cell histologic appearance

A

large, purple, peripheral nucleus

131
Q

acrochordon is

A

skin tag

132
Q

acanthosis nigricans presentation

A
  • hyperpignemted velvety plaque, looks dirty
  • +/- acrochordons
  • posterior neck fold, axillae most common
133
Q

what does acanthosis nigricans indicate

A

insulin resistance

134
Q

what is malignant acanthosis nigricans

A
  • in unusual locations and/or sudden onset
  • “tripe palms”
  • most common: gastric adenocarcinoma
  • less common: other adenocarcinoma
135
Q

what is the sign of leser-trelat

A
  • sudden onset numerous seborrheic keratosis
  • may be associated with malignant acanthosis nigricans
  • underlying malignancy usually aggressive
136
Q

what is dermatitis herpetiformis commonly associated with

A

celiac disease

137
Q

what is dermatitis herpetiformis

A

•autoimmune blistering disease

138
Q

what does dermatitis herpetiformis look like

A

extremely itchy papules/vesicles, particularly on extensor (sometimes only see erosion b/c scratching)

139
Q

what is required to diagnose dermatitis herpetiformis

A

biopsy and direct immunofluorescence (DIF) because it may resemble eczema

140
Q

what is the autoimmune reaction in dermatitis herpetiformis

A

IgA autoantibodies to:
•tissue transglutaminase
•epidermal transglutaminase
•gliadin

141
Q

HLA association with dermatitis herpetiformis

A

HLA DQ2 and HLA DQ8

142
Q

what is vitiligo

A

autoimmune attack on melanocytes

143
Q

what does vitiligo look like

A
  • depigmented macules and patches

* favors areas of trauma

144
Q

what can be helpful in diagnosing vitiligo

A

woods lamp (black light)

145
Q

difference between albinism and vitiligo

A

vitiligo -> melanocyte get attacked/killed

albinism -> melanocytes present, just don’t work

146
Q

what is a butterfly rash and what’s it associated with

A
  • red on the face and sparing nose and nasolabial folds

* systemic lupus erythematosus

147
Q

what is systemic lupus erythematosus (SLE)

A
  • chronic autoimmune inflammatory disease

* butterfly rash associated

148
Q

what will you see histologically in (SLE)

A
  • mucin = red scaly plaques
  • inflammatory cells eating keratinocytes -> premature death
  • red=dead
149
Q

what does subacute cutaneous lupus erythematosus (SCLE) look like

A
  • scaly erythematous plaques; annular/polycyclic, psoriasiform
  • favor photodistribution
  • highly sensitive to sun exposure
150
Q

what does discoid lupus erythemtosus look like

A
  • erythematous to violaceous scaly plaques
  • follicular plugging
  • hypo/hyperpigmentation
  • +/- scarring and atrophy
151
Q

dermatomyositis is considered a paraneoplastic process. what skin findings are there

A
  • heliotrope rash (eyelids)
  • gottrons papules (hands/elbows)
  • erythematous to dusky lilac patch-plaques, usually with minimal scale
152
Q

what is dermatomyositis

A

autoimmune inflammatory myopathy with characteristic skin findings

153
Q

most common malignancies found in those with dermatomyositis

A
  • ovarian
  • breast
  • melanoma
  • colon
  • non-hodgkins lymphoma
154
Q

what is erythema nodosum

A
  • hypersensitivity reaction usually limited to shins

* inflammation in the fat (panniculitis)

155
Q

findings in erythema nodosum

A
  • acute tender nodular eruptions

* giant cells in panniculus

156
Q

associations in erythema nodosum

A
  • infections
  • medications
  • pregnancy
  • systemic disease
157
Q

what is pyoderma gangernosum

A

uncommon neutrophilic disease

158
Q

presentation in pyoderma gangrenosum

A

scarring, painful deep ulers with “gun mettal” rolled or raggidy borders (necrotic)

159
Q

most common underlying association with pyoderma gangrenosum is

A

inflammatory bowel disease

160
Q

what is pathergy

A

new ulcers at the sites of skin trauma in pyoderma gangrenosum
*DONT debride

161
Q

what is cutaneous T-cell lymphona (aka mycosis fungoides)

A

lymphoproliferative disorder

162
Q

what is seen in cutaneous T-cell lymphoma

A
  • chronic, non-responsive erythamtous scaly plaques

* trunk and sun protected areas most common

163
Q

what is seborrheic keratosis

A

benign proliferation of keratinocytes that is common in older people. NO atypia or mitoses

164
Q

what is a prominent horn cyst

A

a keratin pearl that may be seen histologically in seborrheic keratosis

165
Q

characteristics of benign lesions in skin

A

symmetric, distinct border, homogenous color, smaller, stable/unchanging

166
Q

melanocytic nevi are described by which portions of the skin are involved. what are the subtypes

A
  • junctional - only in epidermis, flat
  • compounds - epidermis and dermis
  • intradermal - only dermis, raised
167
Q

ABCDEs of detecting melanoma

A

asymmetry, border, color, diameter, evolving

168
Q

what is the most common kind of melanoma

A

superficial spreading

169
Q

what subtype makes up majority of melanomas arising in dark skinned races

A

acral letiginous

170
Q

lentigo maligna is a melanoma usually seen on

A

usually face of older person with hx of lots of sun exposure

171
Q

what is pagetoid spread

A

upward intraepidermal spread of melanocytes

*sign of malignancy

172
Q

what histopathologic feature of melanoma is most important for prognosis

A

depth of invasion

173
Q

what is the most important/common mutation found in melanoma

A

BRAF V600E

174
Q

what is the most common type of skin cancer

A

basal cell carcinoma

175
Q

basal cell carcinomas occur in areas of sun exposed skin. what is the clinical presentation

A
  • pearly or shiny
  • papules with subastance
  • erosion/ulceration
  • bleed easily with minimal trauma
  • can be pigmented (look gray, blue, or black)
  • telangectasias (torturous blood vessels)
176
Q

histopathology of basal cell carcinoma

A

nests of basaloid cells with stromal clefting, palisading nuclei, and mucin

177
Q

basal cell carcinoma is the most common skin cancer. Classify its aggressivity

A

•locally aggressive, rarely metastasizes

178
Q

Actinic Keratosis is a premaligant condition that can present with

A

extensive, rough erythematous papules

179
Q

histopathology of actinic keratosis

A

SPA
•Solar elastosis (accumulation of elastin in dermis)
•parakeratosis (nucleated s. corneum)
•atypia of basal keratinocytes

180
Q

if untreated, 10% of actinic keratosis will progress to

A

squamous cell carcinoma

181
Q

histopathology of squamous cell carcinoma in situ (SCCIS)

A
  • atypical keratinocytes - full thickness of epidermis

* mitoses throughout epidermis

182
Q

presentation of SCCIS (bowens disease)

A
  • relatively well defined, localized
  • slightly scaly
  • thin (not indurated)
  • pink plaque
  • NO erosion, ulceration, or marked thickening
183
Q

histopathology of invasive squamous cell carcinoma

A
  • atypical keratinicytic proliferation
  • invades into dermis/subcutis
  • prominent keratin pearls
184
Q

what is the second most common skin cancer

A

squamous cell carcinoma

185
Q

which is more likely to metastasize squamous cell or basal cell carcinoma

A

squamous cell carcinoma

186
Q

pathogenesis of squamous cell carcinoma

A
  • most commonly exposure to UV light

* increased risk in immunosuppressed

187
Q

which UV is more prominent in sunburn

A

UVB - sunBurn

188
Q

which UV is more prominent in tanning and photoaging

A

UVA - tAnning and photoAging

189
Q

what is xeroderma pigmentosum

A
  • rare, autosomeal Recessive
  • deficient nucleotide excision repair pathway
  • risk for early onset skin cancer
190
Q

what mutation is associated with nevoid basal cell carcinoma syndrome (Gorlins)

A

PTCH mutation

191
Q

mutation associated with dysplastic nevus syndrome

A

CDKN2A genes

192
Q

what is dysplastic nevus syndromes

A

cutaneous condition with unusualy nevi and multiple inherited melanomas

193
Q

what is a pyogenic granuloma (aka lobular capillary hemangioma)

A

common benign vascular tumor

194
Q

what occurs in pygenic granuloma (aka lobular capillary hemangioma)

A
  • overgrowth of granulation tissue

* often following minor trauma or foreign body•

195
Q

location of pyogenic granuloma (aka lobular capillary hemangioma)

A

face or extremity (usually hands)

196
Q

description of pyogenic granuloma (aka lobular capillary hemangioma)

A
  • solitary, bright red, soft nodule
  • pedunculated (has stalk/stem)
  • 5-6 mm
  • friable surface
197
Q

location of infantile hemangioma (most common vascular tumor of infancy)

A
  • > 50% head/neck
  • 25% trunk
  • extremities
198
Q

timing of infantile hemangioma

A

several days to weeks after delivery

199
Q

what is a cherry angioma

A

benign vascular neoplasm in adults

200
Q

presentation of cherry angioma

A
  • multiple, small, dome-shaped discrete deep red papules
  • can bleed secondary to trauma
  • mocosa spared
201
Q

location of cherry angioma

A

trunk and upper arms

202
Q

glomus bodies are involved in thermoregulation, and are numerous in the fingers and toes. What is a glomus tumor

A
  • rare benign neoplasm from glomus body

* usually under nails, painful

203
Q

what is kaposi sarcoma

A
  • malignant vascular tumor

* usually seen in immunosuppressed or transplant patients

204
Q

what can be stained for in diagnosis of kaposi sarcoma

A

HHV-8 (human herpes virus)

205
Q

what is angiosarcoma

A
  • rare malignant neoplasm of sun damaged skin

* classic: older caucasian male scalp

206
Q

biopsy of seborrheic keratosis would show

A
  • horn cysts
  • string sign
  • no atypia
207
Q

What is bullous pemphigoid

A

autoimmune disorder with autoantibodies against hemidesmosomes
*remember Bullous=Below epidermis=hemidesmosome problem

208
Q

direct immunofluorescence for bullous pemphigoid shows

A

linear subepidermal deposition of IgG

209
Q

direct immunofluorescence for pmnphigus vularis would show

A

net like IgG fluorescence patterns

210
Q

what is the autoimmune reaction in pemphigus vulgaris

A

autoantibodies to components of desmosomes, namely desmogleins 1 and 3
-> intraepidermal blisters

211
Q

characterize the skin lesions in bullous pemphigoid

A

tense bullae and vesicles on normal to erythematous skin

212
Q

contrast presence or absence of oral/mucosal involvement in bullous pemphigoid and pemphigus vulgaris

A
  • no oral involvment in bullous pemphigus (or rare)

* pemphigus vulgaris does have oral involvement

213
Q

characterize skin lesions in pemphigus vulgaris

A

flacid bullae with erosions

214
Q

what is nikolsky’s sign

A

skin reddens, fluid collects underneath and skin rubs off leaving raw base
*happens in pemphigoid vulgaris

215
Q

when would you see tombstoning in histology

A

in pemphigus vulgaris

216
Q

age of patients with bullous pemphigus

A

older patients, usually 70 or older

217
Q

prognosis in pemphigus vulgaris

A

most patients die without treatment

218
Q

what is tombstoning

A

the tombstone appearance of the basal layer

*seen in pemphigus vulgaris

219
Q

what would you see histologically in bullous pemphigoid

A

eosinophilic infiltration and subepidermal blister (deep)

220
Q

what are urticarial eruptions

A
  • hives
  • Wheals with white-to-light-pink color centrally and peripheral erythema
  • worse with repeat exposure
221
Q

timing of urticaria

A
  • transient
  • 1 hive will last no longer than 48 hours
  • variable time of onset
222
Q

causes of urticaria

A
  • any drug exposure
  • viral infections
  • idiopathic
223
Q

what is a morbilliform eruption

A

“measles-like”

only true maculopapular rash

224
Q

timing of morbilliform eruption

A

usually starts 7-10 days after exposure

225
Q

causes of morbilliform eruption

A

common: penicillins, cephalosporings, other abx

can be viral infection, esp in kids

226
Q

what is erythema multiforme (“majore”)

A
  • self limited hypersensitivity syndrome
  • ~90% cause d by HSV1
  • “Major” if mucous membrane involvement
227
Q

what does the rash look like with erythema multiforme

A

targetoid eruptions that may or may not be bullous or crusty

228
Q

distinction of urticarial rash vs erythema multiforme

A
  • urticaria, central zone is normal skin

* erythema multiforme, central zone is damaged skin

229
Q

Stevens-johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a hypersensitivity disorder. which one predominated in children

A

stevens-johnson

230
Q

what are the most common medications associated with SJS/TEN?

A
  • anti-epileptics
  • sulfonamics
  • PCNs
  • Allopurinol
  • NSAIDs
231
Q

illnesses that can be associated with SJS/TEN

A

viruses

mycoplasma

232
Q

presentation of SJS/TEN

A
  • fever/malaise
  • mucosal pain/ swelling
  • photophobia
  • erythematous macular eruptions that can quickly evolve to vesicles/bullae
233
Q

what is seen histologically with SJS/TEN?

A

complete separation of epidermis from dermis

RED=DEAD

234
Q

what might cause earlier or later onset acne

A

androgen dysfunction or polycystic ovarian syndrome (PCOS)

235
Q

what is the acne pathogenesis

A
  1. pilosebaceous unit obstruction
  2. increased sebum production (hormonal influence at puberty)
  3. bacterial proliferation (prpionibacterium acnes)
  4. +/- inflammation
236
Q

what can trigger new acne in a post-pubertal person

A
  • anabolic steroids
  • corticosteroids
  • mood-stabilizing meds
  • protein supplementation
237
Q

stages of acne

A
  • open comedo -> black head
  • closed comedo -> whitehead
  • papule
  • pustule
238
Q

what are the more severe presentations of acne

A
  • acne conglobata
  • acne fulminans
  • multiple connecting sinuses/tracts
  • can have systemic symptoms
239
Q

what is acne excoriee

A

“factitial dermatitis”
•exogenous manipulation
•often in setting of anxiety, OCD or body dysmorphic issues

240
Q

what is postinflammatory dyspigmentation

A
  • increased melanin deposition within epidermis after inflammation
  • more common with darker skin types
241
Q

what is hidradenitis suppuitiva

A

chronic acneiform inflammatory condition that affects body folds with painful, draining sinuses

242
Q

folliculitis can be caused by exposure to what

A

hot tub -> pseudomonas

243
Q

what does folliculitis look like

A
  • follicularly centered papules or putules

* can be itchy/painful

244
Q

where do you find vellus hairs

A

fine hairs like on cheeks and forehead

245
Q

where do you find terminal hairs

A

axillary, pubic, scalp, bear, eyebrow

246
Q

what is glaborous skin

A

areas without hairs: palms + volar surface of fingers and soles

247
Q

which areas of follicles are more dependent on hormone singnalling?

A
  • frontal and vertex scalp (top of head)

* lateral face and jawline

248
Q

which areas of follicles are more independent of hormone signalling

A
  • occipital scalp

* central face and forehead

249
Q

on average, how many hairs do we normally shed per day

A

about 100

250
Q

what is the anagen phase of the hair follicle cycle (terminal scalp hair)

A
  • Anagen=Active; hair shaft growing

* 85-90% of scalp hairs in anagen phase at any time

251
Q

what is the catagen phase of hair follicle cycle (terminal scalp hair)

A
  • regression of the follicle (2-3 weeks)

* less than 1% of scalp follicles at any time

252
Q

what is the telogen phase of hair follicle cycle (terminal scalp hair)

A
  • resting phase, can be up to 3 months

* 10-15% of scalp follicles at any time

253
Q

what is the exogen phase of hair follicle cycle (terminal scalp hair)

A
  • shedding of hair shaft; early part of anagen phase as follicle starts to regenerate and grow new hair shaft
  • mechanical displacement of old hair shaft and protelytic process freeing shaft from follicle
254
Q

what is alopecia areata

A

localized (scalp) autoimmune phenomenon, can be associated with other autoimmune conditions (thyroid)

255
Q

what does alopecia areata look like

A

geometric, clean patterning, non scarring

256
Q

male pattern androgenetic apopecia can be associated with

A

•higher 5-alpha reducatase level, lower total testosterone, or higher free androgens

257
Q

what is trichotillomania

A

•hair pulling behavioral disorder on obsessive-compulsive spectrum. may have associated anxiety/depression

258
Q

what is Anagen effluvium

A
  • insult to hair follicle, impairing mitotic activity (ie chemo)
  • diffuse shedding of ACTIVELY GROWING hairs
259
Q

what is telogen effluvium

A
  • occurs with abrupt shift so all telogens are in phase

* diffuse shedding all at once of RESTING hairs

260
Q

what things might cause telogen effluvium

A

post-partum
stress
illness

Concepts in Pathology and Tissue Morphology (10 decks)

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