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CMT > Vesicular Dermatoses > Flashcards

Vesicular Dermatoses Flashcards

1
Q

Herpes Simplex 1

transmitted how?

A
  • viral transmission
  • contaminated saliva
  • infected body secretions
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2
Q

Herpes Simplex 1

Pathophys

A
  1. direct contact at mucosal or skin sites
  2. viral entry into upper dermis until it reaches sensory & autonomic nerve endings
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3
Q

Herpes Simplex 1

clinical presentation of primary infection

2 components

A
  1. most commonly asx
  2. can cause tonsil pharyngitis or gingivostomatitis
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4
Q

Herpes Simplex 1

clinical presentation of recurrent infection

2 components

A
  1. prodromal sx w/in 24 hrs of viral reactivation
  2. development of grouped vesicles on erythematous base
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5
Q

Herpes Simplex 1

dx

A

PCR (most sensitive & specific)

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6
Q

Herpes Simplex 1

tx

A

valacyclovir 2g BID x1d

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7
Q

Herpes Simplex 2

affects what % of the population?

A

approx 25%

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8
Q

Herpes Simplex 2

pathophys

A
  1. sexually transmitted via direct contact
  2. viral entry into upper dermis until it reaches sensory and autonomic nerve endings
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9
Q

Herpes Simplex 2

clinical presentation

4 components

A
  1. prodrome sx
  2. painful genital ulcers
  3. vesicles which evolve to pustules
  4. (+/-) inguinal LAD
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10
Q

Herpes Simplex 2

describe the vesicles

3 components

A
  1. multiple, shallow, tender, grouped
  2. 2-4mm in size
  3. erythemtous base
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11
Q

Herpes Simplex 2

how do the vesicles progress?

A
  1. vesicles
  2. vesicle pustules, erosions, or alterations
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12
Q

Herpes Simplex 2

dx

A
  • PCR (most sens/spec)
  • Tzanck smear (classic, but not specific)
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13
Q

Herpes Simplex 2

what will you see on Tzanck smear?

A

multi-nucleated giant cells

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14
Q

Herpes Simplex 2

tx options

A
  1. acyclovir
  2. valacyclovir
  3. famciclovir
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15
Q

Herpes Zoster

reactivation of what?

A

latent varicella zoster virus infection

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16
Q

Herpes Zoster

where does the virus lie dormant?

A
  • dorsal root ganglia
  • terminal ganglia
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17
Q

Herpes Zoster

clinical presentation of prodrome

4

A
  • fever
  • malaise
  • sensory changes
  • rash
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18
Q

Herpes Zoster

clinical presentation of rash

5 components

A
  1. unilateral
  2. vesicular dermatomal eruption
  3. painful, grouped vesicles
  4. erythematous base
  5. does not cross midline
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19
Q

Herpes Zoster

clinical manifestation

2- PPP for boards

A
  • thoracic and lumbar roots most commonly affected
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20
Q

Herpes Zoster

dx

A

usually clinical
PCR as needed

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21
Q

Herpes Zoster

Tx

A
  • valacyclovir, acyclovir, famiciclovir w/in 72 hrs of sx onset
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22
Q

Herpes Zoster

education to provide to pts on infectiousness

A

no longer infectious once lesions crust over

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23
Q

Herpes Zoster

prophylaxis for immunocompromised pts

A

VZV immune globulin

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24
Q

Herpes Zoster

prevention

A
  • Shingrix vax
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25
Q

Herpes Zoster

when to refer to opthalmology?

A

zoster on face/eyes

26
Q

Herpes Zoster

what does Shingrix vax reduce the risk of?

A

postherpetic neuralgia

27
Q

Atopic Dermatitis

  1. rash due to what?
  2. susceptible to what?
  3. leading to what?
A
  1. defective skin barrier
  2. drying
  3. pruritis, inflammation
28
Q

Atopic Dermatitis

atopic triad?

A
  1. eczema
  2. allergic rhinitis
  3. asthma
29
Q

Atopic Dermatitis

triggers

4

A
  1. heat
  2. perspiration
  3. allergens
  4. contact irritants
30
Q

Atopic Dermatitis

pathophys

A

disruption of skin barrier due to filaggrin gene mutation and disordered immune response

31
Q

Atopic Dermatitis

dx

A

clinical

32
Q

Atopic Dermatitis

hallmark components of presentation

2

A

pruritis
xerosis

33
Q

Atopic Dermatitis

clinical maifestations of rash

A
  1. erythematous
  2. scaly
  3. ill-defined papules or plaques
34
Q

Atopic Dermatitis

describe nummular clinical presentation

A
  • sharply-defined discoid or circular coin-shaped lesions
  • on hands, feet, extensor surfaces
35
Q

Atopic Dermatitis

tx

mild/mod disease

A
  1. topical corticosteroids w/ emollient
  2. antihistamines for itching
36
Q

Atopic Dermatitis

tx

moderate/severe disease

A

dupliumab

37
Q

Contact Dermatitis

pathophys of irritant rxn

A

nonummunologic rxn, immediate

38
Q

Contact Dermatitis

pathophys of allerng rxn

A

typer 4 hypersensitivity rxn
develops over time

39
Q

Contact Dermatitis

causes of irritant rxn

3

A
  1. chemicals
  2. alcohol
  3. creams/lotions
40
Q

Contact Dermatitis

common causes of allergen rxn

5

A
  1. nickel/metals
  2. poison ivy
  3. chemicals
  4. detergent
  5. cleaners
41
Q

Contact Dermatitis

dx

A

clinical

42
Q

Contact Dermatitis

what testing may be helpful to reduce potential allergens

A

patch testing

43
Q

Contact Dermatitis

clinical presentations

A
  • erythematous papules or vesicles
  • linear or geometric distribution
  • associated w/ local pruritis, stinging, burning
44
Q

Contact Dermatitis

tx

A

avoid the irritant
topical corticosteroids + general measures

45
Q

Contact Dermatitis

general measures for tx

A
  • cool compress
  • oatmeal bath
  • skin emollients
46
Q

Contact Dermatitis

tx for severe/extensive disease

A

1- day prednisone taper

47
Q

Dyshidrotic Eczema/Pompholyx

most commonly affects who?

A

young adults

48
Q

Dyshidrotic Eczema/Pompholyx

triggers

4

A
  1. sweating
  2. emotional stress
  3. warm/humid weather
  4. metals
49
Q

Dyshidrotic Eczema/Pompholyx

clinical manifestation

A
  1. sudden onset of pruritic “tapioca like” small, tense vesicles
  2. on hands, palms, or fingers
50
Q

Dyshidrotic Eczema/Pompholyx

how does rash progress?

A
  • desiccation
  • desquamation
  • papules
  • scaling
  • lichenification
51
Q

Dyshidrotic Eczema/Pompholyx

dx

A

clinical

52
Q

Dyshidrotic Eczema/Pompholyx

tx

mild, severe

A
  • mild/moderate: topical corticosteroid ointment
  • severe: PO corticosteroids, potent topical corticosteroid
53
Q

Dyshidrotic Eczema/Pompholyx

general measures

4

A
  • lukewarm water
  • fragrence free & sensitive skin produces
  • gloves during household chores
  • use emollients
54
Q

Impetigo

commonly found in who?

A

children

55
Q

Impetigo

risk factors

5

A
  1. poor personal hygiene
  2. poverty
  3. crowding
  4. warm/humid weather
  5. skin trauma
56
Q

Impetigo

3 classifications

A
  1. Non-bullous
  2. Bullous
  3. Ecthyma
57
Q

Impetigo

describe non-bullous presentation

5 components

A
  • most common type
  • typically caused by S. aureus
  • papules, vesicles, pustules w/ weeping
  • progress to: honey color, golden crust
  • primarily on face & arms
58
Q

Impetigo

describe bullous clinical presentation

3 components

A
  • commonly caused by S. aureus
  • vesicles form large bulla rapidly which rupture
  • ruptured bulla develop a thin, varnish-like curst
59
Q

Impetigo

ecthyma clinical presentation

3 components

A
  • ulcerative pyoderma
  • group a strep
  • rare
60
Q

Impetigo

dx

A

clinical

61
Q

Impetigo

tx

mild vs severe

A
  1. mupirocin (TID, 10d)
  2. extensive: cephalexin, dicloxacillin
62
Q

Impetigo

complications

2

A
  1. cellulitis
  2. acute glomerulonephritis

CMT (72 decks)

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