PAC 03 DERMATOLOGY Vesicular, Bullae, Acneiform Disease - PowerPoint PPT Presentation

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PAC 03 DERMATOLOGY Vesicular, Bullae, Acneiform Disease

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Title: PAC 03 DERMATOLOGY Vesicular, Bullae, Acneiform Disease


1
PAC 03 DERMATOLOGYVesicular, Bullae, Acneiform
Disease
  • By
  • Stacey Singer-Leshinsky R-PAC

2
Terms
  • Vesicle
  • Bullae Fluid filled blister greater than 100cm
    in diameter
  • Acneiform

3
Vesicular BullaeBullous Pemphigoid
  • 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

4
Vesicular BullaeBullous Pemphigoid
  • Lesions usually appear on extremities first then
    trunk. Flexor surfaces of extremities.
  • Exacerbations/remissions.

5
Bullous PemphigoidHistory and Physical Exam
  • 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.

6
Bullous PemphigoidDrug Induced
  • Diuretics, analgetics, antibiotics
  • Drug acts as a trigger in patients with genetic
    susceptibility by modifying immune response

7
Bullous PhemphigoidDiagnosis
  • Clinical confirmed by histopathology/immunopatholo
    gy
  • Immunofluorescence studies reveal IgG and/or C3
    at dermal-epidermal junction
  • IgE in serum
  • Light microscopy of lesions reveals eosinophils,
    neutrophils, lymphocytes

8
Bullous PhemphigoidDifferentials/Complications
  • Differentials include erythema multiforme, drug
    eruptions, dermatitis herpetiformis
  • Complications

9
Bullous PemphigoidTreatment
  • Systemic or Topical corticosteroids.
  • Immunosuppressive medications
  • Patients often go into a permanent remission

10
Pemphigus Vulgaris
  • 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

11
Pemphigus VulgarisClinical manifestations
  • Pain
  • Flaccid blister filled with clear serous fluid
  • Blisters fragile.
  • Blisters rupture
  • Mucosal lesions can precede cutaneous lesions.

12
Pemphigus VulgarisDiagnosis
  • Nikolskys 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

13
Pemphigus VulgarisDifferentials/complications
  • Differentials Acute herpetic stomatitis,
    aphthous stomatitis, erythema multiforme, bullous
    lichen planus, bullous pemphigoid,
  • Complications
  • Secondary infection
  • Dehydration
  • Often fatal unless treated with immunosuppressive
    agents
  • Recurrent and relapsing

14
Pemphigus VulgarisTreatment
  • Treat dehydration
  • Glucocorticoids-
  • Immunosuppressive therapy- Azathioprine,
    Methotrexate, cyclophosphamide

15
Pilosebaceous Unit
  • Sebaceous gland empties into hair follicle.
  • Pilosebaceous unit opens to surface.
  • Sebaceous gland produces sebum.

16
Pilosebaceous Unit
  • 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.

17
Acne Vulgaris
  • Primarily disorder of adolescence. Affecting
    40-50 million in USA.
  • Psychosocial and economic impact
  • Clinically characterized by comedones and
    inflammatory lesions
  • Etiology unknown.

18
Acne Vulgaris
  • 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

19
Acne VulgarisClinical manifestations
  • 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

20
Acne VulgarisDiagnosis/Differentials
  • Hormone studies will rule out other etiologies
  • Differential diagnosis to include folliculitis,
    steroid folliculitis
  • Complications to include abscess formation and
    severe infection
  • Scarring

21
Acne VulgarisManagement
  • Comedolytics-
  • Sebum suppressive medications- antiandrogens
    include spironolactone, oral contraceptives
  • Topical/Systemic antibiotics- emycin, clindamycin
  • Benzoyl peroxide-
  • Severe Acne- Isotretinion(Accutane)- inhibits
    sebaceous gland function and keratinization.

22
Rosacea
  • Peaks in 30-40s. Associated with Parkinsons,
    might be associated with Helicobacter pylori or
    hair follicle mites (Dermodex folliculorum)
  • Related to vascular hyper-activity-Repeated
    episodes of dilation lead to release of
    inflammatory mediators into dermis.

23
Rosacea
  • Involves nose, cheeks, forehead and chin
  • Complain of reddening of face with heat, hot
    fluids, spicy foods and ETOH
  • Rhinophyma caused by sebaceous hyperplasia MgtF
  • Blepharophyma
  • Metrophyma

24
RosaceaTypes
  • Vascular Rosacea Flushing and persistent central
    facial erythema with or without telangiectasia.
  • Papulopustular rosacea central facial erythema
    with transient papules and pustules.

25
RosaceaTypes
  • Sebaceous hyperplasia thickening skin, irregular
    surface nodularities and enlargement.
  • Ocular rosacea Foreign body sensation in eyes.
    Photosensitivity, periorbital edema,
    telangiectasia of sclera.

26
RosaceaDiagnosis/Differentials
  • Diagnosis Clinical diagnosis, histopathological
    features
  • Differential diagnosis
  • Acne vulgaris-
  • Perioral dermatitis
  • Seborrheic dermatitis
  • Systemic Lupus Erythematosus

27
RosaceaManagement
  • Avoid environmental and dietary triggers such as
    heat/sun exposure, ETOH.
  • Topical Metronidazole-
  • Azelaic acid cream.
  • Tetracycline- treats inflammation.
  • Retinoids- Isotretinoin-
  • Clonidine
  • NO potent topical fluorinated steroids on face

28
Hidradenitis Suppurativa
  • 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.

29
Hidradenitis Suppurativa
  • Risk factors include obesity, apocrine duct
    obstruction, family history
  • Inflammatory condition originating in the hair
    follicle. Follicle ruptures spilling contents
    into surrounding dermis.

30
Hidradenitis Suppurativa
  • 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

31
Hidradenitis SuppurativaDiagnosis/Differentials
  • Diagnosis
  • Bacterial cultures for antibiotic therapy
  • Differentials Cellulitis, pilonidal cysts,
    bacterial folliculitis
  • Complications
  • Squamous cell carcinoma

32
Hidradenitis SuppurativaManagement
  • Might need incision and drainage if large and
    painful.
  • Antibiotics such as tetracycline, cephalosporin,
    clindamycin, ciprofloxacin
  • Isotretinoin
  • Corticosteroids
  • Reduce friction and moisture.

33
Hypersensitivity Vasculitis
  • 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.

34
Hypersensitivity Vasculitis
  • 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

35
Hypersensitivity Vasculitis
  • 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

36

Hypersensitivity Vasculitis Diagnosis
  • Diagnosis confirmed by skin biopsy (vascular and
    perivascular infiltration of broken up
    leukocytes)
  • Look for evidence of systemic disease

37
Hypersensitivity VasculitisComplications/Differe
ntials
  • Complications
  • Systemic vascular involvement
  • Necrosis
  • Irreversible damage to kidneys
  • Differential diagnosis
  • Thrombocytopenia purpura
  • Disseminated intravascular coagulation
  • Rocky Mountain Spotted Fever
  • Steven Johnson Syndrome

38
Hypersensitivity VasculitisManagement
  • Antibiotics
  • If skin involvement use colchicine or Dapsone
  • If visceral involvement then use steroids such as
    Prednisone combined with Cytotoxic
    immunosuppressives

39
Folliculitis
  • 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.

40
Folliculitis
  • Papule or pustule on erythematous base
  • Asymptomatic, mild discomfort or pruritic Favors
    areas with terminal hair
  • Eye involvement
  • Healing can lead to keloids

41
FolliculitisDiagnosis/Differentials
  • Diagnosis
  • History and physical exam
  • Cultures, gram stains, KOH
  • Differentials
  • Insect bites
  • Scabies
  • Rosacea
  • Tinea

42
FolliculitisManagement
  • Wash area with antibacterial soaps
  • Topical and/or oral antibiotics (s.aureus-often
    resistant to pcn so use dicloxacillin or
    cephalosporin or emycin or clindamycin)
  • Pseudomonas
  • Antifungals/Antivirals

43
Xerosis
  • 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

44
XerosisClinical Manifestations
  • Pruritus
  • Involves back, abdomen, extremities
  • Dry rough, scaly skin
  • Cracking, fissuring

45
XerosisDiagnosis
  • Diagnosis histological findings
  • Differential Diagnosis Eczema, contact
    dermatitis, scabies

46
XerosisManagement
  • Moisturizing agents humectants (alpha hydroxy
    acids- dry water from deeper layers to skin
    surface), occlusives which reduce water loss by
    epidermis

47
Example 1
  • 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

48
Example 2
  • 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

49
Example 3
  • Follicular comedones with or without inflammatory
    papules, pustules and nodules
  • What is the cause of this condition?
  • What is the management?

50
Example 4
  • Blood vessels dilate easily and leakage of
    inflammatory mediators into dermis
  • Aggravated by what medication
  • Describe the appearance of the lesion
  • Describe the management

51
Example 5
  • Chronic infection of apocrine sweat glands
  • Inflammatory red hard raised nodules in axilla,
    groin, perineum
  • What is this?
  • What is the management?

52
Example 6
  • What is this?
  • What bacteria are involved with this?
  • What is the treatment of this?
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