Chapter 34 - Other Vesiculobullous Diseases Flashcards

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.

A

True

17
Q

Can a small vessel vasculitis produce bullous lesions?

A

Yes

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.

A

True

20
Q

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

A

Flea bites

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
Q

If PUVA-induced acrobullous dermatosis occurs, should PUVA therapy be stopped?

A

No, there’s in no need to interrupt PUVA therapy

26
Q

What is bullosis diabeticorum usually associated with?

A

Diabetes mellitus (type 1 or 2), with peripheral neuropathy, retinopathy or nephropathy

27
Q

Which anatomical locations are most commonly affected by bullosis diabeticorum (in decreasing order)?

A

Feet, lower legs, hands, forearms

28
Q

What is the treatment for bullosis diabeticorum?

A

Spontaneous healing in 2-6wks. Treat as any blister (eg. aspirate, de-roof, prevent infection)

29
Q

What are coma blisters usually associated with?

A

Coma, neurologic diseases, blisters in 2-3d usually at pressure sites

30
Q

What are predisposing factors of friciton blisters?

A

Poor fitting shoes, heat, sweat

31
Q

What are the 8 different types of bullous drug eruptions?

A

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
Q

Who are more likely to develop bullous insect bite reactions?

A

Children, those with chronic lymphocytic leukemia

33
Q

What % of BSA involvement is commonly found in patients who develop delayed postburn blisters?

A

30%

34
Q

When do delayed postburn/postgraft blisters develop?

A

2-3 days or weeks after complete healing

35
Q

What are some risk factors for development of edema blisters?

A

Elderly, immobile, anasarca, whenever there is acute exacerbation of chronic edema

36
Q

What is the pathogenesis of PUVA induced acrobullous dermatosis?

A

Chronic PUVA induced weakening of the epidermal-dermal cohesion + friction/trauma, usually on distal limbs