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Pathology Block 10 > Dermatopathology > Flashcards

Dermatopathology Flashcards

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1
Q

Lesions with viral skin/mucosa infections

A

They are frequently transient, resolving on their own without therapy

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2
Q

Cutaneous viral infections are of greates concern in

A

Immunosuppressive individuals, as viral reactivation/dissemination can lead yo significant morbidity and mortality
-HIV, steroid use, organ transplant patient

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3
Q

Latency of viral skin infections

A

Many remain latent and can reactivate or not. Can still shed viral particles and not know it

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4
Q

Symptoms of molluscum contagiosum

A
  • Frequently asymptomatic

- umbilicated papules with pearly/waxy appearance, usually in clusters

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5
Q

What is the classical patten of molloscum contagiosum if there are symptoms

A

Umbilicated papules, with pearly/waxy appearance

-solid lesion, elevated with sunken centers

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6
Q

Why does molluscum contagiosum usually occur in clusters?

A

Because it spreads easy
Autoinnoculation
-usually in a Lila, anogenital folds, popliteal fossa

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7
Q

Epidemiology of molluscum contagiosum

A
  • children
  • sexually active
  • males >females
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8
Q

What family of virus is molluscum contagiosum

A

Poxvirus family

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9
Q

Sign of healing in molluscum contagiosum

A

Erythema (redness) around lesions

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10
Q

Primary concern with molluscum contagiosum

A
  • disfigurement (hyperpigmentation)

- transmission to sexual partners

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11
Q

Why is there hyperpigmentation when viral skin infections are healing

A

Constant inflammation, deposits melanin.

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12
Q

How long does molluscum contagiosum last

A

Self-limiting: body usually clears infection in 6 months (unless immunosuppressed)

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13
Q

Molluscum contagiosum in immunosuppressed patients

A

Diffuse lesions common

May appear in the conjunctiva, producing a unilateral conjunctivitis

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14
Q

Treatment for molluscum contagiosum

A
  • cryosurgery
  • curettage
  • electrodessication
  • topical antiviral
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15
Q

Do we always treat everyone who has molluscum contagiosum?

A

No, usually only in immunosuppressed

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16
Q

Were can you see HPV

A

Everywhere

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17
Q

What does HPV cause

A
  • subclinical infection (many dont know they have it)
  • clinical lesions
  • pre-malignant lesions, leading to some cancers
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18
Q

How many types of HPV are there ?

A 
>150
Common warts
Plantar warts
Flat warts 
Conjunctival papilloma 
Genital warts 
Carcinoma in situ (CIS) lesions and squamous cell carcinoma
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19
Q

Who is more likely to get verruca vulgaris

A

Very common esp amount school age children

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20
Q

Resolution of verruca vulgaris

A

Tend to resolve spontaneously, except in many adults and immunocompromised

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21
Q

How is verruca vulgaris transmitted

A

Skin to skin transmission, virus infects keratinocytes

Not dependent on fluid

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22
Q

Where are verrucae confined to

A

Epidermis, no “root” or “mother wart”

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23
Q

What is pathognomonic for warts

A

Black dots

-not in all warts, but can help distinguish from callus

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24
Q

clinical presentation of verrucae

A
  • black dots

- absence of fingerprint lines

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25
Predisposing factors in verrucae
Impaired immunity (HIV infection, transplant recipients, chemo) Pregnancy Occupation: handling raw meat and fish
26
Verrucae morphology
Infected keratinocytes-epidermal hyperplasia Hyperkeratosis Produces papules with plaque like coverings
27
What types of HPV clause conjunctival papilloma
6 and 11 - most often in fornix or palpebral conjunctica - pedunculated (not flat, very raised, sometimes on a stalk)
28
How is herpes simplex classically presented
As grouped vesicles with erythematous base
29
What are most HSV infections?
Atypical - subclinical lesions; or erosions, fissures - instead of classically presented grouped vesicles with erythematous base
30
Transmission of HSV
Can occur in the absence of symptoms | Skin to skin, skin to mucosa, or mucosa to skin
31
What percent of people are aware that they actually have HSV
10%
32
How does HSV infect
Virus replicates in epithelial cell, causing lysis and vesicle formation
33
HSV-1
Above neck
34
HSV-2
Below waist
35
Latency of HSV
Ascends peripheral sensory nerves and enters sensory or autonomic nerve root ganglia and remains latent -neurons can be infected in the absence of clinical lesions/symptoms
36
What is someone at risk for that has HSV
Risk of aseptic meningitis or recurrent sciatica
37
Recurrences in HSV
Can impact any region that is innervated by the infected sensory nerve (not limited to primary inoculation site) -genital inoculation may recur on buttocks or anus
38
How long is HSV infection
For life | -recurrences can happen at any time, even 81 years down the line)
39
Factors for recurrence of HSV
Occurs in 1/3rd of individuals with mouth lesions | -50% will have at least two recurrences annually
40
Triggers of HSV recurrence
Skin/mucosal irritation, menstruation, medications, other infections (colds), immunosuppression
41
How long do HSV lesions last
2-4 weeks
42
Signs and symptoms of HSV
- prodromal phase: tingling, pain, burning, sensation, itching - swelling - pain - fever - lymph nodes may enlarge
43
HSV sores
- erythematous papules | - vesicles fragile, rupturing easily, to form erosions
44
Most common site of primary infection of HSV
Mouth Anogenitalia Hands/fingers
45
HSV of fingers
Before "universal precautions", Herpetic Whitlow, resulting in painful infections of fingers and forearms. This would be something a dentist would get from working in a patients mouth who had HSV
46
Herpetic facial paralysis and HSV
Reactivation of geniculate ganglion infection implicated in pathognesis of indiopathic facial palsy (Bell's palsy). HSV-1 shedding detected in 40% of cases
47
Ocular infection of HSV
Recurrent dendritic keratitis is a major cause of corneal scarring and visual loss
48
Is recurrent dendritic keratitis from HSV due to HSV1 or HSV2
1, unless in neonate, then it would be 2
49
Ocular infections from HSV other than recurrent dendritic keratitis
- disciform - uveitis - blepharoconjunctivits
50
Treatment for HSV
Oral antiviral medications | Topical ointments not very helpful
51
Initial infection of varicella zoster
90% of cases in children <10 yo
52
Transmission of varicella zoster
Airborne droplets and direct contact with lesions - pts contagious before lesions appear - crusts not infectious
53
VZV infects what
Mucosa of upper respiratory tract/oropharynx, replicates in the mononuclear phagocyte system, and secondary viremia spreads to skin/mucous memebranes, it then spreads to sensory nerves
54
VZV reactivation
Pain and vesicular lesions develop after VZV reactivates (herpes zoster) - similar to HSV, ZVZ infections remain latent in nerve until reactivated by stress or immunosuppression - most patients >50
55
Where is VZV (herpes zoster) reactivation most common
In the trigeminal, cervical, thoracic, lumbar, or sacral dermatome
56
Prodrome and VZV
May be preceded by prodromal pain and/or itching
57
Herpes zoster ocular involvement
- Hutchinson sign (rash at nose tip) increased risk of ocular involvement - blepharoconjunctivitis - episcleritis - may also lead to facial palsy
58
Classic acute skin problems
Urticaria Eczema Erythema multiforme
59
Classic chronic inflammatory dermatoses
- psoriasis | - seborrheic dermatitis
60
Urticaria (hives) most common in
20-40 yo but seen in all ages
61
Symptom or urticaria
Wheals | -develop and fade within hours, but episodes may persist for months
62
Predisposed sites for urticaria
Trunk, distal extremities, ears
63
What causes the wheals in urticaria
Localized mast cell degranulation-dermal microvascualr permeability
64
IgE dependent urticaria
IgE Ab sensitized to antigen (food, pollen, etc) | Antigen-induced release of vasoactive mediators from mast cell granules
65
IgE independent urticaria
Some substances directly incite mast cell degranulation in some individuals -opiates, some abx, NSAIDS, cold
66
Cold urticaria
Holding ice cubes on the skin can also cause urticaria
67
Eczema features
Red, oozing, crusted lesions that develop with time into raised, scaling plaques
68
Types of eczema
``` Contact dermatitis Atopic dermatitis Drug related eczematous dermatitis Eczematous insect bite reaction Photo eczematous eruption Primary irritant dermatitis ```
69
Most famous example of this is poison ivy
Contact dermatitis
70
Is poison ivy contagious
The liquid in the vesicles is not, but the oils are
71
Antigen responsible for poison ivy, causing contact dermatitis
Urushiol
72
Skin reaction caused by furocoumarin chemicals (psoralens) in the plant and exposure to UV A sunlight
Phytodermatitis | -lime juice on the beach
73
How is edema in eczema distinguished from hives?
Eczema is in the epidermis: break and crust, thinner layer, more likely to rupture Hives are in the dermis, never breaks the skin -edema in stratum spinosum pushes keratinocytes apart-spongiosis

Pathology Block 10 (8 decks)

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