Transcript DERMATOLOGY Vesicular Bullae, Acneform and Verrucous Lesions

PAC 03 DERMATOLOGY
Vesicular, Bullae, Acneiform Disease
By
Stacey Singer-Leshinsky R-PAC
Terms
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Vesicle:
Bullae: Fluid filled blister greater
than 100cm in diameter
Acneiform:
Vesicular Bullae
Bullous Pemphigoid
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Humoral and cellular response against
self-antigens BP 180, 230. These are
needed for dermo-epidermal cohesion.
Sub epidermal blister formation from
cascade of events
Vesicular Bullae
Bullous Pemphigoid
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Lesions usually appear on extremities
first then trunk. Flexor surfaces of
extremities.
Exacerbations/remissions.
Bullous Pemphigoid
History and Physical Exam
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Non Bullous phase: mild to
severe pruritus with excoriated,
eczematous, papular, urticarial
lesions
Bullous phase: Vesicles and
bullae on erythematous skin.
Filled with clear or blood tinged
fluid. Erode and crust.
Bullous Pemphigoid
Drug Induced
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Diuretics, analgetics, antibiotics
Drug acts as a trigger in patients with
genetic susceptibility by modifying
immune response
Bullous Phemphigoid
Diagnosis
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Clinical confirmed by
histopathology/immunopathology
Immunofluorescence studies reveal IgG
and/or C3 at dermal-epidermal junction
IgE in serum
Light microscopy of lesions reveals
eosinophils, neutrophils, lymphocytes
Bullous Phemphigoid
Differentials/Complications
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Differentials include erythema
multiforme, drug eruptions, dermatitis
herpetiformis
Complications
Bullous Pemphigoid
Treatment
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Systemic or Topical corticosteroids.
Immunosuppressive medications
Patients often go into a permanent
remission
Pemphigus Vulgaris
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IgG auto antibodies against cell surface
of keratinocytes. Results in acantholysis
and blister formation.
Found in middle age-elderly
Can be due to reaction to medications
50-70% of patients have mucosal
lesions
Pemphigus Vulgaris
Clinical manifestations
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Pain
Flaccid blister filled with clear
serous fluid
Blisters fragile.
Blisters rupture
Mucosal lesions can precede
cutaneous lesions.
Pemphigus Vulgaris
Diagnosis
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Nikolsky’s sign positive.
Asboe-Hansen sign: gentle pressure on
intact bulla forces fluid to spread under
the skin away from site of pressure.
Immunofluorescence
Tzanck smear: acantholytic cells
Pemphigus Vulgaris
Differentials/complications
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Differentials: Acute herpetic stomatitis,
aphthous stomatitis, erythema multiforme,
bullous lichen planus, bullous pemphigoid,
Complications
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Secondary infection
Dehydration
Often fatal unless treated with
immunosuppressive agents
Recurrent and relapsing
Pemphigus Vulgaris
Treatment
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Treat dehydration
GlucocorticoidsImmunosuppressive therapyAzathioprine, Methotrexate,
cyclophosphamide
Pilosebaceous Unit
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Sebaceous gland empties
into hair follicle.
Pilosebaceous unit opens
to surface.
Sebaceous gland produces
sebum.
Pilosebaceous Unit
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Amount of sebum produced
depends on size of gland, rate
of sebaceous cell proliferation
Large sebaceous glands
Sebum production related to
androgens
Sebaceous glands are rich in
staphyloccus epidermidis and
Propionibacterium.
Acne Vulgaris
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Primarily disorder of adolescence.
Affecting 40-50 million in USA.
Psychosocial and economic impact
Clinically characterized by comedones
and inflammatory lesions
Etiology: unknown.
Acne Vulgaris
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Androgens cause sebaceous glands to
overproduce sebum.
Bacteria secrete lipase which converts lipids
to fatty acids.
Hyperkeratinization in lining of follicle and
follicle plugging.
Papules, pustules, scarring result from
follicular rupture and inflammatory response
Acne Vulgaris
Clinical manifestations
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Non-inflammatory acne: open
and closed comedones. , open
comedones
Inflammatory acne: above
expands to form papules,
pustules, nodules and cysts of
varying severity. 1-5mm filled
with sterile pus.
Found on face, neck, shoulders
and upper trunk
Acne Vulgaris
Diagnosis/Differentials
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Hormone studies will rule
out other etiologies
Differential diagnosis to
include folliculitis, steroid
folliculitis
Complications to include
abscess formation and
severe infection
Scarring
Acne Vulgaris
Management
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ComedolyticsSebum suppressive medicationsantiandrogens include spironolactone, oral
contraceptives
Topical/Systemic antibiotics- emycin,
clindamycin
Benzoyl peroxideSevere Acne- Isotretinion(Accutane)- inhibits
sebaceous gland function and keratinization.
Rosacea
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Peaks in 30-40’s. Associated with
Parkinson’s, might be associated with
Helicobacter pylori or hair follicle mites
(Dermodex folliculorum)
Related to vascular hyper-activityRepeated episodes of dilation lead to
release of inflammatory mediators into
dermis.
Rosacea
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Involves nose, cheeks, forehead and
chin
Complain of reddening of face with
heat, hot fluids, spicy foods and ETOH
Rhinophyma caused by sebaceous
hyperplasia M>F
Blepharophyma
Metrophyma
Rosacea
Types
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Vascular Rosacea: Flushing
and persistent central facial
erythema with or without
telangiectasia.
Papulopustular rosacea:
central facial erythema with
transient papules and
pustules.
Rosacea
Types
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Sebaceous hyperplasia:
thickening skin, irregular
surface nodularities and
enlargement.
Ocular rosacea: Foreign body
sensation in eyes.
Photosensitivity, periorbital
edema, telangiectasia of
sclera.
Rosacea
Diagnosis/Differentials
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Diagnosis: Clinical diagnosis,
histopathological features
Differential diagnosis:
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Acne vulgarisPerioral dermatitis
Seborrheic dermatitis
Systemic Lupus Erythematosus
Rosacea
Management
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Avoid environmental and dietary triggers such
as heat/sun exposure, ETOH.
Topical MetronidazoleAzelaic acid cream.
Tetracycline- treats inflammation.
Retinoids- IsotretinoinClonidine
NO potent topical fluorinated steroids on face
Hidradenitis Suppurativa
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Skin infection that affects apocrine
gland bearing skin sites especially the
axillae and anogenital areas.
Characterized by recurrent boils and
draining sinus tracts with scarring.
Hidradenitis Suppurativa
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Risk factors include obesity, apocrine
duct obstruction, family history
Inflammatory condition originating in
the hair follicle. Follicle ruptures spilling
contents into surrounding dermis.
Hidradenitis Suppurativa
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Initially inflammatory nodules
and sterile abscesses in axillae,
groin, perianal areas. Then sinus
tracts and hypertrophic scars
develop.
Pain/foul odor
Erythematous abscess up to
2cm
Chronic and remitting
Hidradenitis Suppurativa
Diagnosis/Differentials
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Diagnosis:
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Bacterial cultures for antibiotic therapy
Differentials: Cellulitis, pilonidal cysts,
bacterial folliculitis
Complications:
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Squamous cell carcinoma
Hidradenitis Suppurativa
Management
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Might need incision and drainage if
large and painful.
Antibiotics such as tetracycline,
cephalosporin, clindamycin,
ciprofloxacin
Isotretinoin
Corticosteroids
Reduce friction and moisture.
Hypersensitivity Vasculitis
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Immune complex mediated
inflammation of small vessels such as
arterioles, capillaries, venules.
Occur as an exaggerated immune
response to a drug, infection or
autoantibodies
This leads to injury to vessel walls, and
so decreased function and blood flow.
Hypersensitivity Vasculitis
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Patients might report use of a new
drug, history of streptococcal infection
or collagen/vascular disease such as
lupus, Rheumatoid Arthritis
If not isolated then can have systemic
vascular involvement of kidneys,
muscles, joints, GI tract, peripheral
nerves
Hypersensitivity Vasculitis
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Palpable purpura 1-3mm in
diameter
Usually localized to lower
third of legs/ankles
Lesions are scattered,
discrete, confluent
Lesions can form papules
and ulcers due to lack of
blood supply
Hypersensitivity Vasculitis
Diagnosis
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Diagnosis: confirmed by skin biopsy
(vascular and perivascular infiltration of
broken up leukocytes)
Look for evidence of systemic disease
Hypersensitivity Vasculitis
Complications/Differentials
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Complications
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Systemic vascular involvement
Necrosis
Irreversible damage to kidneys
Differential diagnosis
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Thrombocytopenia purpura
Disseminated intravascular coagulation
Rocky Mountain Spotted Fever
Steven Johnson Syndrome
Hypersensitivity Vasculitis
Management
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Antibiotics
If skin involvement use colchicine or
Dapsone
If visceral involvement then use steroids
such as Prednisone combined with
Cytotoxic immunosuppressives
Folliculitis
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Common disorder with perifollicular pustules.
Etiology: staphylococcus aureus,
pseudomonas aeruginosa chemical irritation,
friction, perspiration, shaving, skin injury.
Follicle infiltrate of lymphocytes, neutrophils,
macrophages. Can lead to formation of
abscess.
Folliculitis
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Papule or pustule on
erythematous base
Asymptomatic, mild
discomfort or pruritic Favors
areas with terminal hair
Eye involvement:
Healing can lead to keloids
Folliculitis
Diagnosis/Differentials
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Diagnosis
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History and physical exam
Cultures, gram stains, KOH
Differentials
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Insect bites
Scabies
Rosacea
Tinea
Folliculitis
Management
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Wash area with antibacterial soaps
Topical and/or oral antibiotics (s.aureusoften resistant to pcn so use
dicloxacillin or cephalosporin or emycin
or clindamycin)
Pseudomonas
Antifungals/Antivirals
Xerosis
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Dry skin
Can be a natural occurrence sometimes
associated with aging , second to
contact dermatitis. Also exogenous
causes such as dry climate, excessive
exposure to water
Etiology:
Xerosis
Clinical Manifestations
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Pruritus
Involves back, abdomen, extremities
Dry rough, scaly skin
Cracking, fissuring
Xerosis
Diagnosis
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Diagnosis: histological findings
Differential Diagnosis: Eczema, contact
dermatitis, scabies
Xerosis
Management
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Moisturizing agents humectants (alpha
hydroxy acids- dry water from deeper
layers to skin surface), occlusives which
reduce water loss by epidermis
Example 1
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Prodrome of
erythematous skin prior
to bullae eruption
Pruritus weeks to
months prior to blister
eruption
Extremities first then
trunk
What is this? What do
immunofluorescence
studies reveal?
Treatment
Example 2
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Mucosal lesions
Flaccid blister on
normal or
erythematous skin.
Blisters rupture
leading to erosions
What sign is positive?
What happens if not
treated?
Treatment options:
Example 3
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Follicular
comedones with or
without
inflammatory
papules, pustules
and nodules
What is the cause
of this condition?
What is the
management?
Example 4
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Blood vessels dilate
easily and leakage of
inflammatory mediators
into dermis
Aggravated by what
medication
Describe the
appearance of the
lesion
Describe the
management
Example 5
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Chronic infection of
apocrine sweat
glands
Inflammatory red
hard raised nodules
in axilla, groin,
perineum
What is this?
What is the
management?
Example 6
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What is this?
What bacteria are
involved with this?
What is the
treatment of this?