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Pathology Block 10 > Dermatopathology > Flashcards

Dermatopathology Flashcards

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
Q

Predisposing factors in verrucae

A

Impaired immunity (HIV infection, transplant recipients, chemo)
Pregnancy
Occupation: handling raw meat and fish

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26
Q

Verrucae morphology

A

Infected keratinocytes-epidermal hyperplasia

Hyperkeratosis
Produces papules with plaque like coverings

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27
Q

What types of HPV clause conjunctival papilloma

A

6 and 11

  • most often in fornix or palpebral conjunctica
  • pedunculated (not flat, very raised, sometimes on a stalk)
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28
Q

How is herpes simplex classically presented

A

As grouped vesicles with erythematous base

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29
Q

What are most HSV infections?

A

Atypical

  • subclinical lesions; or erosions, fissures
  • instead of classically presented grouped vesicles with erythematous base
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30
Q

Transmission of HSV

A

Can occur in the absence of symptoms

Skin to skin, skin to mucosa, or mucosa to skin

31
Q

What percent of people are aware that they actually have HSV

32
Q

How does HSV infect

A

Virus replicates in epithelial cell, causing lysis and vesicle formation

33
Q

HSV-1

A

Above neck

34
Q

HSV-2

A

Below waist

35
Q

Latency of HSV

A

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
Q

What is someone at risk for that has HSV

A

Risk of aseptic meningitis or recurrent sciatica

37
Q

Recurrences in HSV

A

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
Q

How long is HSV infection

A

For life

-recurrences can happen at any time, even 81 years down the line)

39
Q

Factors for recurrence of HSV

A

Occurs in 1/3rd of individuals with mouth lesions

-50% will have at least two recurrences annually

40
Q

Triggers of HSV recurrence

A

Skin/mucosal irritation, menstruation, medications, other infections (colds), immunosuppression

41
Q

How long do HSV lesions last

42
Q

Signs and symptoms of HSV

A
  • prodromal phase: tingling, pain, burning, sensation, itching
  • swelling
  • pain
  • fever
  • lymph nodes may enlarge
43
Q

HSV sores

A
  • erythematous papules

- vesicles fragile, rupturing easily, to form erosions

44
Q

Most common site of primary infection of HSV

A

Mouth
Anogenitalia
Hands/fingers

45
Q

HSV of fingers

A

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
Q

Herpetic facial paralysis and HSV

A

Reactivation of geniculate ganglion infection implicated in pathognesis of indiopathic facial palsy (Bell’s palsy). HSV-1 shedding detected in 40% of cases

47
Q

Ocular infection of HSV

A

Recurrent dendritic keratitis is a major cause of corneal scarring and visual loss

48
Q

Is recurrent dendritic keratitis from HSV due to HSV1 or HSV2

A

1, unless in neonate, then it would be 2

49
Q

Ocular infections from HSV other than recurrent dendritic keratitis

A
  • disciform
  • uveitis
  • blepharoconjunctivits
50
Q

Treatment for HSV

A

Oral antiviral medications

Topical ointments not very helpful

51
Q

Initial infection of varicella zoster

A

90% of cases in children <10 yo

52
Q

Transmission of varicella zoster

A

Airborne droplets and direct contact with lesions

  • pts contagious before lesions appear
  • crusts not infectious
53
Q

VZV infects what

A

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
Q

VZV reactivation

A

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
Q

Where is VZV (herpes zoster) reactivation most common

A

In the trigeminal, cervical, thoracic, lumbar, or sacral dermatome

56
Q

Prodrome and VZV

A

May be preceded by prodromal pain and/or itching

57
Q

Herpes zoster ocular involvement

A
  • Hutchinson sign (rash at nose tip) increased risk of ocular involvement
  • blepharoconjunctivitis
  • episcleritis
  • may also lead to facial palsy
58
Q

Classic acute skin problems

A

Urticaria
Eczema
Erythema multiforme

59
Q

Classic chronic inflammatory dermatoses

A
  • psoriasis

- seborrheic dermatitis

60
Q

Urticaria (hives) most common in

A

20-40 yo but seen in all ages

61
Q

Symptom or urticaria

A

Wheals

-develop and fade within hours, but episodes may persist for months

62
Q

Predisposed sites for urticaria

A

Trunk, distal extremities, ears

63
Q

What causes the wheals in urticaria

A

Localized mast cell degranulation-dermal microvascualr permeability

64
Q

IgE dependent urticaria

A

IgE Ab sensitized to antigen (food, pollen, etc)

Antigen-induced release of vasoactive mediators from mast cell granules

65
Q

IgE independent urticaria

A

Some substances directly incite mast cell degranulation in some individuals
-opiates, some abx, NSAIDS, cold

66
Q

Cold urticaria

A

Holding ice cubes on the skin can also cause urticaria

67
Q

Eczema features

A

Red, oozing, crusted lesions that develop with time into raised, scaling plaques

68
Q

Types of eczema

A 
Contact dermatitis 
Atopic dermatitis 
Drug related eczematous dermatitis 
Eczematous insect bite reaction 
Photo eczematous eruption 
Primary irritant dermatitis
69
Q

Most famous example of this is poison ivy

A

Contact dermatitis

70
Q

Is poison ivy contagious

A

The liquid in the vesicles is not, but the oils are

71
Q

Antigen responsible for poison ivy, causing contact dermatitis

72
Q

Skin reaction caused by furocoumarin chemicals (psoralens) in the plant and exposure to UV A sunlight

A

Phytodermatitis

-lime juice on the beach

73
Q

How is edema in eczema distinguished from hives?

A

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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