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D & T exam 2 > Dermatopathology 3 > Flashcards

Dermatopathology 3 Flashcards

1
Q

Pemphigus vulagris what happens

A

IgG autoantibodies against desmogleins 1 and 3 in desomosomes in suprabasal deep epidermis and mucosal epithelium

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2
Q

what is Nikolsky sign and what are Pemphigus vulgaris tests results

A

pressure on blister causes lateral spread of lesion

- positive

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3
Q

where do 80-90% of pemphigus vulgaris begin

A

oral lesions

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4
Q

what forms the roof of the blister for pemphigus vulagris

A

stratum corneum

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5
Q

what happens in pemphigus foliaceus

A

autoantibodies against Dsg1 alone

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6
Q

histo for pemphigus

A

row of tombstomes
acantholysis
net like pattern of intracellular IgG deposists

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7
Q

what does pemphigus vegetans look like

A

large, moist, verrucous, plaques rather than blisters

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8
Q

common lesion site for pemphigus vegetans

A

oral lesions

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9
Q

what other disorder is pemphigus vegetans related to

A

ulcerative colitis

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10
Q

what country is pemphigus foliaceus found

A

Brazil

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11
Q

what happens in bullous Pemphigoid

A

autoantibodies bind BPAg1 and BPAg2 ( only one causing blister) in hemidesosome

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12
Q

At what layer of the skin does bullous Pemphigoid form a blister

A

lamina lucida of the basement membrane

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13
Q

age groups of pemphigus and Bullous Pemphigoid

A

P: 30-50
BP: elderly

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14
Q

target antigen for pemphigus and Bullous Pemphigoid

A

P: demoglein 1 and 3
BP: BPAg1 and BPAg2 in hemidesmosomes

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15
Q

Blister ( bulla) pemphigus and Bullous Pemphigoid

A

P: suprabasal, ancantholytic, positive Nikosky sign
BP: subepidermal, nonacantholytic, sturdy

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16
Q

oral mucosa for pemphigus and Bullous Pemphigoid

A

P: many early lesions
BP: few after cutaneous lesions

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17
Q

what happens in Dermatitis Herpetiformis

A

IgA autoantibodies to transglutaminases bind to TG in gut and cross-react with reticulin in fibrils in skin

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18
Q

what is the onset and gender of Dermatitis Herpetiformis

A

20-60

males

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19
Q

clinical presentation of Dermatitis Herpetifromis

A

symmetrically grouped lesions

-papules and plaques progressing to vesicles and bullae

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20
Q

For Dermatitis Herpetiformis what other disease is present and what is used to show this

A

Gluten senstive

small bowel biopsy

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21
Q

Histo feature for Dermatitis Herpetiformis

A

subepidermal blister

microabscesses at dermal papillae

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22
Q

what is epidermolysis bullosa

A

group of disorders caused by inherited defects ( 10 genes) in proteins that lend stability to skin

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23
Q

when do symptoms of Epidermolysis bullosa occur

A

at or soon after birth

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24
Q

Name 4 types of Epidermolysis Bullosa

A

simplex
junctional
dystrophic
non-Herlitz junctional

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25
Q

Simplex type

A

mutations in gene encoding keratin 14 or 5 ( form keratin fiber)
- basal cell layer defect

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26
Q

Junctional type

A

blisters formed from separation lamina lucida

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27
Q

Dystrophic types

A

blisters below lamina densa, from defect in collagen VII

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28
Q

Non-Herlitz Junctional

A

defect in laminin Vbeta3

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29
Q

histo for Epidermolysis Bullosa? similiar to what?

A

fibrin deposition in floor of blister cavity

- bullous pehphigoid

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30
Q

what happens in prophyria cutanea tarda

A 
uroporphyrinogen decarboxylase (UROD) deficiency 
- excessive accumulation of porphyrins
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31
Q

who is prone for Prophyria cutanea tarda

A

30-50 yrs

  • females on OCP
  • alcohol
  • hep C
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32
Q

what are the types of Porphyria cutanea tarda

A

Type I: acquired

type II: autosomal dominant, deficient in RBC and fibroblasts

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33
Q

what does Porphyria cutanea tarda do to skin

A

make it photosenstivie

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34
Q

what does Porphyria cutanea tarda do to face

A

hypertrichosis ( hairy face)

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35
Q

how does one diagnose Porphyria cutanea tarda

A

uroprophryin in urine

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36
Q

what 3 things must be avoided for porphyria cutanea tarda

A

alcohol
estrogens
fungicides

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37
Q

histo for porphyria cutanea tarda

A

subepidermal vesiculation

  • protuberance of rigid dermal papillae into blister cavity( festooning
  • thickening of walls of superficial dermal vessels
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38
Q

what happens in acne vulgaris

A

obstruction of sebaceous follicles by sebum

-promotes proliferation of propionibacterium acnes ( anaerobe)

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39
Q

what do obstructive acne look like

A

closed
whiteheads
flesh colored dome

40
Q

what do inflammatory acne look like

A

papules/pustules to nodules to cysts

41
Q

Risk factors for Acne vulgaris

A 
male
puberty 
Cushing 
oily complexion
androgen excess
42
Q

what are 4 components of acne vulgaris

A
  1. keratinization of lower portion of follicular infundibulum
    - development of keratin plug, block outflow of sebum
  2. hypertrophy of sebaceous gland
  3. lipase-synthesizing bacteria ( propionibacterium acnes_ colonizing upper hair follicle
  4. inflammation of follicle
    - release of cytoxic and chemotactic factors
43
Q

Acne Rosacea what is it

A

chornic inflammatory disorder that affects blood vessels and pilosebaceous units

44
Q

4 stages of acne rosacea

A
  1. flushing
  2. persistent erthyema and telangiectasias
  3. pustules and papules
  4. Rhinophyma
45
Q

what is rhinophyma

A

skin on nose becomes thick and greasy, hyperplasia of sebaceous glands, connective tissue and vasculature

46
Q

what areas of the face are impacted with acne rosaceae

A

nose and cheeks including nasolabial folds

47
Q

histo for rosacea

A

perfollicular infiltrate of lymphocytes

48
Q

Panniculitis

A

inflammation of lobules or connective tissue septa separating fat lobules

49
Q

what is Erythema nodosum

A

inflammatory reaction of connective tissue septa separating fat lubules

50
Q

gender of who gets it more for Erythema nodosum

A

females

51
Q

clinical for Erythema nodosum

A

red, painful, elevated nodules, poorly circumscribed

52
Q

where is erythema nodosum usually ocur

A

anterior aspect of tibial

53
Q

what are some crazy things that cause Erythema nodosum

A 
strep 
pregnancy 
OCP
syphilis 
TB
54
Q

histo erythema nodosum

A

widening of septa from fibrin, edema, and neutrophilic infiltrate

55
Q

what is warts

A

infection of epidermal cells with human papilloma virus

56
Q

who usuallly gets warts

A

children and young adults

57
Q

who are warts transmitted

A

skin to skin

58
Q

in warts, intralesional borwn-black dots are pathognomonic and represesent what

A

thrombosed vessels

59
Q

scientific name for common wart

A

Verruca vulgaris

60
Q

scientific name for flat wart?

location

A

verruca plana

-chin, dorsum of hand, legs

61
Q

scientific name for war on foot? what can cause this

A

Verruca platnaris

HPV1

62
Q

Condyloma acuminatum

A

anogenital wart

63
Q

what causes Condyloma acuminatum

A

most common STD, HPV6 and 11

64
Q

hist for warts

A

Church spire

65
Q

who usually gets Molluscum contagiosum

A

viral infection in kids and sexually active adults

66
Q

what causes Molluscum contagiosum

A

poxvirus

67
Q

how is Molluscum contagiosum transmitted

A

skin to skin

68
Q

clinical representation of Molluscum contagiosum

A

asymptomatic smooth, dome-shaped papules with central umbilication

69
Q

hist for Mollluscum contagiosum

A

Molluscum bodies in stratum corneum and granulosum

70
Q

what is impetigo

A

superficial bacterial infection of skin

71
Q

what are the two forms of impetigo

A

nonbullous and bullous

72
Q

what is the most common form of impetigo

A

nonbullous

73
Q

what is the most common cause of impetigo

A

Staph aureus

74
Q

histo for impetigo

A

neutrophils beneath stratum corneum

75
Q

Sacabies how long in incubation

A

1 month

76
Q

scabies is infection with

A

Sarcoptes scabiei

77
Q

where does scabies usually occur

A

finger webs, wrists, and penis

78
Q

the egg and feces causes what reaction to the body

A

type IV hypersensitivity

- extremem itching at night

79
Q

how does one confirm scabies

A

scraping burrow with scalpel

look under microscope

80
Q

what is Xanthelasma ( Xanthoma)

A

collection of macrophages containing lipid droplets

81
Q

Mongolian spots clinical picture

A

single-gray-blue lesion over lumbosacral area

82
Q

who usually gets Mongolian spots

A

Asian and Native Americans

83
Q

what goes wrong in Mongolain spots

A

melanocytes located in dermis instead of epidermis

84
Q

what is cherry angioma

A

bright red, domed, vascualar lesions on trunk

- increase with age

85
Q

what is the most common tumor of infancy

A

Hemangioma of infancy

86
Q

what is Hemangioma of infancy? what does it look like

A

benign hyperplastic blood vessels,

- blanchable bright red to deep purple lesions

87
Q

over time what happens to hemangioma of infancy

A

regressses

88
Q

when do you treat hemangioma of infancy

A

do not treat until ulcerates or blocks ears, eyes, larynx

89
Q

what are the 3 phases of hair devleopment

A

anagen
catagen
telogen

90
Q

what is alopecia

A

common cause of hair loss in adults

91
Q

Xeroderma pigmentosum how is it inherited?

A

Autosomal recessive

92
Q

Xerdomera pigmentosum

A

decrease ability to repair DNA following UV damage

93
Q

timeline of Xeroderma pigmentusm

A

1st year of life: scaling
later: atrophy
5-6 yeras: squamous and basal cell cancer

94
Q

Chediak-Higashi syndrome

A

immunodiciency due to defect in neutrophil phagosome lysosome fusions
-abonormal giant lysosomal inclusions visible on peripheral blood smear

95
Q

Wiskott-Aldrich Syndrome

A 
X-linked
immunodeficiency 
Exzema
thrombocytopenia
B and T lymphocyte disorder
96
Q

albinsim

A

melanocytes normal in number and location

  • production of melanin defective
  • due to complete absence of tyrosinase

D & T exam 2 (27 decks)

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