Vesiculobolous lesions

Question 1

Herpes Simplex Infection

Answer 1

primary infection is the initial systemic infection, and secondary is the localized reactivation in a previously infected person. an immunocompromised host may develop severe secondary disease.
control of symptoms not cure is the goal, as the virus stays latent in the nerves
the virus spreads through exposure to body fluids

Question 2

Herpes simplex infection progression

Answer 2

primary infection affects the skin, vermilion, and the oral mucous membranes, on any mucosal surface
Secondary lesions are confined to the lips, hard palate, and gingiva, healing in 1-2 weeks.
in immunodeficient patients secondary HSV1 results in significant pain and discomfort, can be chronic, destructive, and extensive.
Herpetic whitlow is an infection of the fingers through a break in the skin integrity. They form vesicles or pustules that eventually become ulcers

Question 3

Herpes simplex virus Histology

Answer 3

intraepithelial vesicles containing exudate, inflammatory cells, and characteristic virus-infected epithelial cells are seen
Virus-infected keratinocytes contain one or more homogenous, glassy nuclear inclusions that can be found on cytologic preparations.

Question 4

Herpes simplex virus differential

Answer 4

streptococcal pharyngitis (does not involve the lips or perioral tissues, and vessicles do not precede ulcers)
erythema multiforme (ulcers are larger, usually without a vesicular stage, and are less likely to affect the gingiva)
acute necrotizing ulcerative gingivitis (lesions are more limited to the gingiva, not preceded by vesicles)
Apthos stomatitis (usually multiple lesions, neurologic prodrome (tingling), vesicles preceding ulcers, and palatal and gingival location are indicative of HSV, and apthae are almost exclusively on nonkeratinized mucosa)

Question 5

Herpes simplex diagnosis

Answer 5

Tzanck smear
Serology
viral culture
immunohistochemistry
PCR testing

Question 6

Herpes simplex virus treatment

Answer 6

if no later than 48-72 hours prior to symptoms, then Acyclovir 5% ointment
5X/day topicaly
systemic acyclovir 400mg TID can be used for primary infections (usually HSV2)
for immunosupressed patients prophylactic acyclovir may be needed.
in HIV patients IV acyclovir may be needed

Question 7

Varicella Zoster pathogenesis

Answer 7

transmitted through direct contact by contaminated droplets from skin lesions
the virus proliferates within macrophages over a 2 week incubation period
host defenses are overcome, and systemic signs and symptoms develop.
It can reside asymptomatically int eh sensory ganglia

Question 8

Varicella Zoster clinical features

Answer 8

fever, chills, malaise, and headache accompany rash primarily in the trunk, head and neck
the rash becomes a vesicular eruption that forms pustules, and eventually ulcerates.
Secondary bacterial infections are common, and may result in scar formation.

Question 9

Herpes Zoster

Answer 9

occurs through the branches of the nerves
can inovlve the trigeminal nerve, and resuts in unilateral oral, facial ,r occular lesions
remission usually occurs in several weeks

Question 10

Varacella Zoster Histopathology

Answer 10

same as HSV
virus infected epithelial cells have homogenous nuclei representing viral products
multinucleation of infected cells is typical
Acantholytic vesicles break down and ulcerate

Question 11

Varicella Zoster Differential

Answer 11

diagnosed by history of exposure, and type/distribution of lesions.
DD: primary HSV infection
hand-foot and mouth disease

Question 12

Varicella Zoster treatment

Answer 12

Supportive therapy is indicated
for immunocompromised patients, anti-viral therapies are warranted, including systemic acyclovir, vidarabine, and interferon.
Corticosteriods are contraindicated

Question 13

hand-foot-and-mouth disease etiology

Answer 13

Coxsacki virus
transmitted through direct contact with nasal secretions
predilection for mucous membranes of the mouth (buccal mucosa and tongue) and cutaneous regions of the hands and feet

Question 14

hand-foot-and mouth clinical features

Answer 14

resolves spontaneously in 1-2 weeks
usually occurs in children younger than 5
The lesions progress to a vesicular state, then become ulcerated, then encrusted lesions without later scarring

Question 15

hand-foot-and-mouth histopathology

Answer 15

the vesicles are found in the epithelium due to obligate viral replication in keratinocytes
as keratinocytes are destroyed the vesicle enlarges and becomes filled with proteinaceous debris and inflammatory cells

Question 16

hand-foot-and-mouth differential

Answer 16

primary herpetic gingivostomatitis
varicella Zoster

Question 17

hand-foot-and-mouth treatment

Answer 17

no specific treatment, only of symptoms
bicarbonate mouth rinses may help

Question 18

measles etiology

Answer 18

spread by airborne droplets
rash consists of pinpoint elevations over the soft palate that coalesce with involvement of the pharynx with bright erythema

Question 19

measles clinical features

Answer 19

the lesion spots of the buccal mucosa are known as Kiplik’s spots
complications of the virus include encephalitis and thrombocytopenic purpura

Question 20

Measles Histopathology

Answer 20

infected epithelial cells which become necrotic, overlie an inflamed connective tissue that contains dilated vascular channels and a focal inflammatory response

Question 21

measles differential diagnosis

Answer 21

prodromal symptoms, Koplik’s spots, and rash in unvaccinated individuals is sufficient evidence, but laboratory testing can confirm virus

Question 22

Pemphigus Vulgaris etiology

Answer 22

mucocutaneous disease characterized by intraepihtelial blister formation from a loss of intercellular keratinocyte adhesion
Produces epithelial cell separation (acantholysis)
circulating autoantibodies of IgG reat against composnents of epithelial desmosome-tonofilament complexes
the extent of epithelial cell separation is proportional to teh titer of circulating pemphigus antibodies

Question 23

pemphigus vulgaris clinical features

Answer 23

painful ulcers preceded by flaccid and short lived intraoral vesicles and bullae
Bullae rapidly rupture following their fomration ,eaving a red, painful ulcerated base with a friable epithelial border
lesions range from small apthos like lesions to large irregular map-like lesions
can occur with other autoimmune diseases such as myasthenia gravis, lupus erythematosus, rheumatoid arthritis, Hashimoto’s thyroiditis, thyroma, Sjogrens syndrome

Question 24

pemphigus vulgaris histopathology

Answer 24

interepithelial clefting iwth keratinocyte acantholysis
loss of desmosomal attachment of tonofilaments, resulting in free floating Tzanck cells
the basal layer remains attached to the basement membrane

direct immunofluorescent testing can diagnose, where a sample is tested for circulating antibodies of IgG type.

Question 25

pemphigus vulgaris differential

Answer 25

mucous membrane pemphigoid
erythema multiforme
erosive lichen planus
paraneoplastic pemphigus
apthos ulcers

Question 26

pemphigus vulgaris treatment

Answer 26

systemic corticosteroids
these medications do have their own associated long term morbidity
topical corticosteroids can be used judiciously, but long term use does have complications, and antifungal therapy may be needed

Question 27

Mucous membrane pemphigoid etiology

Answer 27

autoimmune process with unknown stimulus or etiology
deposits of immunoglobulins and compliment in teh basement zone.
targers include laminin 332

Question 28

Mucous Membrane Pemphigoid clinical features

Answer 28

other mucosal sites affected are conjunctiva, nasopharynx, larynx, esophagus, and ano-genital region
Oral lesions typically rpesent as superficial ulcers, Bullae are not always observed, blisters are fragile and short lived
THe lesions are chronic and persistant, and may scar

Question 29

Mucous Membrane Pemphigoid histopathology

Answer 29

subepithelial clefting disorder without acantholysis. few lymphocytes are seen initially but the infiltrate becomes more dense and mixed over time

Question 30

Mucous Membrane Pemphigoid differential

Answer 30

pemphigus vulgaris
erosive lichen planus
if lesion only in attached gingiva
atropic lichen planis
linear IgA disease
discoid lupus erythematosus
contact allergy

Question 31

Mucous membrane Pemphigoid treatment

Answer 31

Corticosteroids are typically used to control. Prednisone for moderate to severe disease, topical steroids for mild disease and maintenance
Note the possible appearance of ocular disease, so ophthalmic evaluation is important

Question 32

Bullous Pemphigoid etiology

Answer 32

closely related to mucous membrane pemphigoid, but titers of circulating autoantibodies to the basement membrane zone antigens are detectable.
lesions cannot be differentiated from mucous membrane pemphigoid

Question 33

Bullous Pemphigoid histopathology

Answer 33

the lesions are similar to mucous membrane pemphigoid
the basement membrane is cleaved at the level of the lamina lucida

Question 34

Bullous Pemphigoid treatment

Answer 34

systemic corticosteroids are typically used to control this disease

Question 35

Epidermolysis Bullosa Etiology

Answer 35

a general term for about 20 genetic or hereditary variety of diseases
characterise are formation of blisters
IgG deposits are commonly found in sub-basement membrane tissues and Type 7 collagen

Question 36

Epidermolysis Bullosa clinical features

Answer 36

bulla formation from minor trauma
blisters may be widespread and severe, and may result in scarring and atrophy
Oral lesions are common in the recessive forms of disease and uncommon in the acquired form

Question 37

Epidermolysis Bullosa treatment

Answer 37

avoidance of trauma, supportive measures, and chemotherapeutic agents such as corticosteroids, vitamin E, phenytoin, retinoids, dapsone, immunosupressive agents