Chapter 34 - Other Vesiculobullous Diseases Flashcards

(36 cards)

1
Q

Do the blisters of bullosis diabeticorum occur on the background of normal or inflammed skin?

A

They appear on normal-appearing skin

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2
Q

What type of diabetes has bullosis diabeticorum been associated with?

A

Both type 1 and type 2 diabetes

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3
Q

Do the blisters of bullosis diabeticorum occur slowly or rapidly?

A

Rapidly, often developing “overnight”

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4
Q

Is DIF generally positive or negative in bullosis diabeticorum?

A

Usually negative (although deposits of IgM and C3 can sometimes occur in dermal blood vessels)

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5
Q

How long does it usually take for blisters of bullosis diabeticorum to heal?

A

Between 2-6 weeks (they heal spontaneously)

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6
Q

Do coma blisters usually occur at sites of pressure or at sites without pressure?

A

Sites of pressure

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7
Q

What is the most commonly implicated drug-induced coma with coma blisters (i.e. the specific drug involved)?

A

Barbiturates, although other drug-induced comas have been implicated (e.g. opiods), as well as non-drug-induced comas (e.g. infection, CVAs, etc.)

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8
Q

Does a patient have to be in a coma to develop coma blisters?

A

No, they can occur in patients that are chronically immobilized or have neurologic diseases

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9
Q

What is the classic histologic finding associated with coma blisters, other than subepidermal blisters?

A

Eccrine coil necrosis (presumably due to drugs excreted through the eccrine coil)

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10
Q

Do coma blisters heal spontaneously?

A

Yes, within 1-2 weeks if the patient survives

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11
Q

Will DIF be positive or negative in biopsies of coma blisters?

A

Negative

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12
Q

Where is the histologic level of the split in friction blisters?

A

Just below the stratum granulosum

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13
Q

Does moist or dry skin provide higher frictional forces?

A

Moist skin does, thus it’s more prone to friction blisters than dry skin

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14
Q

If a friction blister contains blood-tinged fluid, should you reconsider your diagnosis?

A

Not necessarily; friction blisters often contain serosanguinous fluid

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15
Q

True or false: it’s appropriate to fully de-roof a friction blister.

A

False; this increases the risk of infection; it’s best to create a small “window” to avoid fluid reaccumulation, leaving the remainder of the blister roof to act as a physiologic dressing

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16
Q

True or false: some drug eruptions can present as blistering eruptions.

17
Q

Can a small vessel vasculitis produce bullous lesions?

18
Q

In which two patient populations are bullous insect bites most common?

A

In children and in adults with CLL

19
Q

True or false: both humoral (type I, IgE-mediated) and cell-mediated (type IV, delayed hypersensitivity) immunity are involved in the response to insect bites.

20
Q

Which type of insect bite is most likely to produce a bullous reaction (i.e. what type of insect)?

21
Q

Can insect bites ever be pustular?

A

Yes, for example the bites of fire ants can be pustular

22
Q

Histologically, flame figures are occasionally seen on biopsies of insect bites (particularly in patients with CLL). What are flame figures?

A

Eosinophilic granules that have covered collagen fibers

23
Q

With respect to delayed postburn/postgraft blisters, is it just the burned/grafted skin that’s affected? Or can the adjacent normal skin also be affected?

A

It’s only the burned/grafted skin that’s affected

24
Q

What are blisters that occur in the context of chronic lymphedema called?

A

Edema blisters

25
If PUVA-induced acrobullous dermatosis occurs, should PUVA therapy be stopped?
No, there's in no need to interrupt PUVA therapy
26
What is bullosis diabeticorum usually associated with?
Diabetes mellitus (type 1 or 2), with peripheral neuropathy, retinopathy or nephropathy
27
Which anatomical locations are most commonly affected by bullosis diabeticorum (in decreasing order)?
Feet, lower legs, hands, forearms
28
What is the treatment for bullosis diabeticorum?
Spontaneous healing in 2-6wks. Treat as any blister (eg. aspirate, de-roof, prevent infection)
29
What are coma blisters usually associated with?
Coma, neurologic diseases, blisters in 2-3d usually at pressure sites
30
What are predisposing factors of friciton blisters?
Poor fitting shoes, heat, sweat
31
What are the 8 different types of bullous drug eruptions?
1) Fixed drug eruption, 2) SJS/TEN, 3) LABD/pemphigus/BP, 4) pseudoporphyria, 5) AGEP, 6) phototoxicity, 7) bromoderma/iododerma, 8) palmar plantar erythrodysesthesia
32
Who are more likely to develop bullous insect bite reactions?
Children, those with chronic lymphocytic leukemia
33
What % of BSA involvement is commonly found in patients who develop delayed postburn blisters?
30%
34
When do delayed postburn/postgraft blisters develop?
2-3 days or weeks after complete healing
35
What are some risk factors for development of edema blisters?
Elderly, immobile, anasarca, whenever there is acute exacerbation of chronic edema
36
What is the pathogenesis of PUVA induced acrobullous dermatosis?
Chronic PUVA induced weakening of the epidermal-dermal cohesion + friction/trauma, usually on distal limbs