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clinical medicine > Vesicular Bullae & Desquamation > Flashcards

Vesicular Bullae & Desquamation Flashcards

0
Q

What age does bullous pemphigoid normally appear?

A

after 65 years

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1
Q

What is bullous pemphigoid?

A

A chronic, autoimmune, inflammatory, subepidermal, blistering disease
Autoantibodies attach to the skin basement membranes and activate inflammation

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2
Q

How long does bullous pemphigoid last?

A

persists from months to years, with remissions and exacerbations
it is relatively uncommon

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3
Q

What is the most common form of bullous pemphigoid?

A

generalized bullous form

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4
Q

What are the clinical features of bullous pemphigoid?

A

generalized bullous form: tense bullae arise on any part of skin surface, most commonly in flexural areas

  • can occur after other chronic inflammatory conditions, such as lichen planus and psoriasis
  • acute/subacute onset
  • intense pruritus
  • lesions may our intra-orally (NOT common)
  • lesions heal without scarring
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5
Q

What is the “workup” for bullous pemphigoid?

A
  • Indirect immunofluorescence
  • Skin biopsy–from edge of blister + specimen for direct immunofluorescence (must be taken from normal looking peri-lesional skin, highlights deposits of antibodies)
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6
Q

What is the treatment for bullous pemphigoid?

A
  • GOAL; decrease blister formation
  • topical steroids
  • oral steroids
  • oral antibiotics (tetracyclines)
  • immunosuppresives: methotrexate, dapsone, imuran
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7
Q

What is Erythema multiforme (EM)?

A

-acute, self-limited, recurring skin condition, inflammatory
-type IV hypersensitivity reaction
-resolves 2-3 weeks, can be recurrent
-symmetric erythematous skin lesions
-TARGET LESIONS-clear with erythematous rings
MAJOR AND MINOR TYPE

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8
Q

Where does EM occur?

A

extensor surfaces, palms, soles, mucous membranes

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9
Q

What are precipitating factors of EM?

A

-herpes simplex virus most common cause
(herpes associated erythema multiforme minor)
-epstein-barr virus

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10
Q

How is the diagnosis for EM made?

A

physical and history

biopsy to rule out DDx

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11
Q

What are the DDx of EM?

A

bullous pemphigoid, contact (irritant & allergic) derm, drug eruptions, SJS, TEN

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12
Q

What is the treatment of EM?

A

Treat HSV infection–suppressive dosing for recurrent flares

-most important treatment is symptomatic treatment; oral antihistamines, soothing mouthwashes

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13
Q

What characterizes Stevens Johnson Syndrome (SJS)?

A
  • blisters
  • epidermal detachment
  • epidermal necrosis
  • involves skin + mucous membranes
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14
Q

How much of BSA does SJS affect?

A

<10%

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15
Q

What are the causes of SJS?

A
  • infection
  • meds: NSAIDS, Anti Gout, Psychoepileptics, ABX (antibiotic)
  • Malignancy
  • Idiopathic (disease with unknown origin)
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16
Q

What are the prodromal (early) symptoms of SJS?

A
  • productive cough
  • headache
  • malaise
  • arthralgias
17
Q

What are clinical features of SJS?

A
  • mucocutaneous onset: mouth, esophagus, genital
  • nonpruritic
  • rash can being as macules–>papules, vesicles, bullae, urticarial plaques, or confluent erythema
  • Center of lesions: vesicular, purpuric (red/purple discoloration), or necrotic
  • Lesions can become bullous and rupture–secondary infection of skin
18
Q

What are ocular symptoms of SJS?

A

red eye, tearing, dry eye, pain, blepharospasm, itching, grittiness, heavy eyelid, foreign body sensation, decreased vision, burn sensation, photophobia, diplopia
–painful to chew/swallow

19
Q

What signs may be noted upon examination (SJS) ?

A
  • fever (consider systemic infection)
  • orthostasis
  • tachycardia
  • hypotension
  • altered level of consciousness
  • epistaxis
  • conjunctivitis
  • corneal ulcerations
  • erosive vulvovaginitis or balanitis
  • seizures
  • coma
20
Q

How is SJS diagnosed?

A

biopsy

21
Q

What is the treatment for SJS?

A
  • care in burn unit or ICU– no specific treatment; treat symptomatically
  • eliminate offending drug
  • fluid/electrolyte resuscitation
  • wet dressings on skin
  • nutritional support–parenteral nutrition
  • ophthalmology consult
  • pain control
  • treat secondary infections
22
Q

What is the prognosis for SJS?

A

mortality determined by extent of skin sloughing!!!

  • 1-5%
  • depends on age, comorbidity, & reepithelialization usually complete in 3 weeks
23
Q

What are long-term complications related to ocular problems in SJS?

A
  • photophobia
  • blurred vision
  • water eyes
24
Q

What are the defining characteristics of Toxic Epidermal Necrolysis?

A
  • widespread erythema, necrosis, bullous detachment of the epidermis and mucous membranes
  • massive exfoliation–>sepsis–>death
  • potentially life-threatening disorder
25
Q

How much BSA is affected in TEN?

A

30%

26
Q

What is the etiology of TEN?

A
  • medications most common:
  • antibiotics, NSAIDS, anticonvulsants
  • occurs within 1-3 wks of therapy initiation and not after 8 wks
27
Q

What are the clinical features of TEN?

A
  • vital signs: hypotension secondary to hypovolemia (decreased blood volume), tachycardia
  • skin lesions begin symmetrically on face & thorax then spread to entire body
  • influenzalike prodrome: malaise, fever, rash, cough, arthralgia, myalgia, rhinitis, headache, anorexia, nausea, vomiting (prodrome lasts from 1 day to 3 weeks)
28
Q

What area is spared in TEN?

A

scalp

29
Q

What does the “rash” look like in TEN?

A

poorly defined
erythematous macular rash
purpuric (red/purple) center

30
Q

What happens to the rash in TEN over a period of days?

A

rash comes together to form flaccid blisters and sheetlike epidermal detachment, predominately on torso and face

31
Q

What are ocular manifestations of TEN?

A

-acute conjunctivitis, corneal erosions, ulcers

32
Q

What mucosal surfaces that can be involved in TEN?

A

esophagus, intestinal tract, respiratory epithelium

-bronchial epithelial sloughing may result in dyspnea (shortness of breath) and hypoxemia

33
Q

What precedes skin erosions in TEN?

A

mucous membrane erosions (90% of cases)–precede skin erosions by 1-3 days
-also pain at site of skin lesion

34
Q

When does reepithelialization occur in TEN? How long do peak symptoms last?

A

1-3 weeks reepithelialization

2-3 days peak symptoms

35
Q

What is the diagnostic study to confirm dx in TEN?

A

biopsy, but history and physical will determine dx

36
Q

What is the “sign” that occurs when slight lateral pressure is put on the epidermal surface, resulting in epidermal surface easily separating in TEN?

A

Nikolsky sign

37
Q

What is the treatment for TEN?

A
  • remove offending drug
  • patient should be cared for in burn unit or ICU
  • fluid and electrolyte resuscitation
  • temperature regulation
  • monitor respiratory states (O2, intubation)
  • nutritional support-parenteral feedings
  • pain control
  • infection precautions
  • skin dressings
38
Q

What are complications of TEN?

A

ocular, skin scarring, pigment changes, nail loss, esophageal strictures, chronic oral and genital erosions

39
Q

What is the treatment for TEN?

A

consults, ophthalmology, plastics, IM, hospitalist

40
Q

What is the prognosis for TEN?

A

mortality rates range from 10-70%, but AVERAGE is 25-50%

depends on extent of involvement, age, comorbid conditions, cause of death attributed to sepsis and multi organ filure

clinical medicine (12 decks)

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