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Pathophysiology - Dermatology > Pediatric Dermatology > Flashcards

Pediatric Dermatology Flashcards

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1
Q

Why is measles very contagious?

A

It is airborne contagious, and can be transmitted 4 days before rash onset to 4 days after rash onset

Can survive on fomites for up to 2 hours

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2
Q

What is the prodrome of measles and how does the rash spread? What’s the morphology of the rash?

A

Prodrome: 4 C’s
Cough, Coryza, Conjunctivitis, Koplik’s spots

Rash starts on forehead and spreads towards feet, becoming confluent (dress in sketchy with falling rubies). It is genuinely a maculopapular rash

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3
Q

What is one thing that should always be given to treat measles and why?

A

Vitamin A - it is significantly reduced early in exanthem. Children treated with Vitamin A recover more rapidly from pneumonia and diarrhea, lower morbidity and mortality.

Think of the vitamin A partyhat in sketchy

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4
Q

What is the pattern of the rubella exanthem? What other symptoms are associated? What is the oral finding?

A

Typically an occipital or postauricular lymphadenopathy

Associated with pinpoint macules starting on face spreading all the way down the body, unlikely to become confluent (vs measles).

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5
Q

What is the enanthem of rubella?

A

Forchheimer’s spots - soft palate petechiae

An enanthem is a rash inside the body

Exanthem is a rash on the external surface of the body

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6
Q

What adults typically get manifestations of rubella, and what are they?

A

Typically women. Transient polyarthritis particulary affecting phalangeal joints and knees.

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7
Q

What is the triad of Rubella which affects children?

A
  1. Patent ductus arteriosus
  2. Congenital cataracts
  3. Blueberry muffin rash - due to extramedullary hematopoiesis
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8
Q

What virus causes erythema infectiosum? How do children vs adolescents present differently?

A

Parvovirus B19 (fifth disease)

Children - slapped cheap rash which waxes and wanes, children are NOT viremic at presentation

Adolescents - papular-purpuric gloves and socks syndrome! - they ARE viremic at presentation

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9
Q

What are the two phases of erythema infectiosum following the slapped-cheek phase?

A
  1. Net-like erythema - fishnet-like erythematous eruption begins on extremities 2 days after slapped cheek rash, extending to trunk and buttocks, fading within two weeks
  2. Recurrence phase - rash may fade and reappear over next 2-3 weeks.
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10
Q

What are the feared complications of parvovirus B19 and should children be excluded from school?

A
  1. Transient aplastic crisis in Sickle Cell patients
  2. Hydrops fetalis in pregnancy

Children should not be excluded from school since they are not viremic

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11
Q

Is roseola common? What virus is the cause? How is it spread?

A

HHV-6 = Rose-6-ola

Extremely common, 80% of children seroconvert in first year of life

Virus remains latent in monocytes, macrophages, CD4+ T cells and salivary glands
-> spread through saliva from mother to child

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12
Q

What rash is characteristic of roseola? Name that rash.

A

Think Rose-6-o-Later

Exanthem subitum - 6th disease

HHV-6 causes a macular rash which spreads LATER than the fever (4 days later). First there is a high fever then a diffuse macular rash once the fever has subsided which often spares the face

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13
Q

What type of rash is measles said to cause?

A

“Morbilliform” - literally meaning measles-like

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14
Q

What are the three main toxic erythemas?

A
  1. Scarlet fever
  2. Staphylococcal Scalded Skin Syndrome
  3. Mucocutaneous lymph node syndrome (Kawasaki disease) -> toxin unknown
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15
Q

What is the clinical presentation of all toxic erythemas? One of these is inconsistent with the three syndromes.

A
  1. Fever
  2. Sandpaper-like rash where skin turns red, and will ultimately desquamate
  3. Mucous membranes are involved (exception: Staphylococcal Scalded Skin Syndrome).
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16
Q

What is the significance of mucous membranes not being involved in SSSS?

A

It is the only toxic erythema which does not cause oral mucositis
-> Kawasaki and Scarlet Fever will cause STRAWBERRY TONGUEs.

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17
Q

What is the triad of Scarlet Fever?

A

Think of the guy eating a strawberry in sketchy, with a neckerchief, and painting a gingerbread man.

  1. Strawberry tongue
  2. Strept pharyngitis
  3. Diffuse rash which typically spares the face
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18
Q

Describe the rash of scarlet fever and how it heals? What are the linear petechial streaks it is associated with and where are they found?

A

Fine, erythematous papules around the body healing via desquamation

Linear petechial streaks: Pastia’s lines - seen in axillary, antecubital, and inguinal areas

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19
Q

How does a strawberry tongue typically progress? What toxins mediate the progression of this disease in scarlet fever?

A

Oral enanthem -> white tongue coating

4-5 days later, white coating is sloughed off and leaves classic red strawberry tongue / beefy red tongue

Streptococcal pyrogenic exotoxins (erythrogenic toxins) - SpeA-C

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20
Q

What is bullous impetigo, and what is the cause of the systemic form of this disease?

A

Bullous impetigo is the localized form of SSSS, which in this case you would be able to culture S. aureus locally

Systemic form is SSSS, and is caused by toxins circulating throughout body distant from site of infection.
-> Staphylococcal exfoliative toxins cause INTRAepidermal splitting by cleaveage of desmoglein 1 in desmosomes

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21
Q

What pathology does SSSS cause? Is Nikolsky sign positive or negative?

A

Causes flaccid bullae since it’s intraepidermal. Nikolsky sign will by positive, like pemphigus vulgaris (pressing on the skin can create blisters due to circulating toxin which cleaves desmosomes)

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22
Q

How should you diagnose and treat SSSS? Will children be bacteremic?

A

Should culture specimens from nose, throat, umbilicus in neonates, and any obviously infected areas to check for MRSA, then treat based on antibiotic susceptibility.

Patient may need to be admitted to burn unit, give aggressive fluid replacement

Skin and blood culture is often negative in children

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23
Q

What is the major cause of Toxic Shock Syndrome now, and what will the rash look like? What will happen to blood pressure?

A

Usually seen more now with post-operative patients (especially following rhinoplasties, “nasal packing” with tampons to control bleeding, pg 131). Used to be caused by vaginal tampons.

Generalized erythroderma over large body surface area, with desquamation especially of palms and soles 1-2 weeks after onset.

Severe hypotension occurs due to systemic cytokine release.

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24
Q

What labs are commonly elevated in TSS?

A

ALT, AST, and bilirubin -> end-organ liver damage.

Also causes renal failure (elevated BUN), and acute ischemic encephalopathies

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25
Q

What is the other name for Kawasaki disease and who tends to get it? What is the characteristic ocular finding? What type of disease is it?

A

Mucocutaneous lymph node syndrome

Tends to occur in children <4 years old, especially Asians

Ocular finding - conjunctival injection WITHOUT purulent discharge

Multisystem vasculitis

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26
Q

What is the mnemonic for Kawasaki disease?

A

CRASH and burn (your Kawasaki motorcycle)

Conjunctival injection
Rash - (toxic erythema of some kind)
Adenopathy - cervical nodes
Strawberry tongue
Hand-foot changes -> erythematous rash (think of holding the motorcycle with your hands and feet as in pathoma)

burn - Fever

27
Q

What are the hand and foot changes of Kawasaki disease?

A

Palms and soles become red, with hands and feet developing a non-pitting edema (due to vasculitis).

10-14 days after fever, the skin peels off in sheets, beginning in fingernails and progressing down palms and soles.

28
Q

What are the possible cardiac symptoms of Kawasaki disease?

A

Acute - arrhythmias due to myocarditis

Subacute - aneurysm formation in medium-sized arteries, especially coronary arteries. Acute thrombi can also form.

Chronic - persistent scarring and risk of thrombus formation, death from MI or aneurysm rupture is possible.

29
Q

What are the lab findings and treatment of Kawasakii disease?

A

Leukocytosis with left shift (indicating acute inflammation or infection of some kind)

treatment is aspirin and IVIg

30
Q

What is the cause of hand, foot, and mouth disease and how do most rashes start?

A

Due to Coxsackie A virus

Most rashes start in the mouth (enanthem) with aphthous-ulcer-like erosions on soft palate

31
Q

What are the cutaneous symptoms of hand-foot-mouth disease (HFMD) and are they pruritic?

A

Oval-shaped vesicles on PALMS and SOLES (look like footballs), but can also appear on buttocks sometimes.

They are very pruritic in adults but not often in children

32
Q

How can herpangina be told apart from aphthous stomatitis?

A

Herpangina lesions (oral lesions of HFMD) are more uniform and usually smaller

33
Q

How can HFMD be told apart from herpes and varicella?

A

Herpes - tend to appear in clusters, but can do PCR to confirm

Varicella - Vesicles last longer and always crust over

For both, you can do a Tzank smear to check for multinucleated giant cells

34
Q

WHat condition of the nails may follow hand foot and mouth disease?

A

Beau’s lines (transverse ridging) with possible shedding (onychomadesis)

35
Q

What is diaper dermatitis and what causes it? What areas are spared?

A

Irritant contact dermatitis due to urine &/or fecal contact

Causes:

  • Acidic environment of urine
  • Basic environment of feces
  • Proteolytic enzymes in stool as well as irritant soaps / powders

Areas spared: creases (not touched by poop)

36
Q

When should diaper candidiasis be suspected?

A

Whenever a diaper rash fails to respond to usual therapeutic measures. Often occurs following systemic antibiotic therapy

37
Q

What does a diaper candidiasis look like?

A

Widespread, BEEFY erythema, with raised edges, and pinpoint pustulovesicular satellite lesions (vesicles around the outside of the rash).

38
Q

What is the treatment for candidiasis and main focus during this time?

A

Identify etiology, and keep skin dry, protected, and free of infection (can easily become secondarily infection).

Topical antifungals must be used: i.e. nystatin, clotrimazole

39
Q

What is the cause of neonatal cephalic pustolosis (NCP) and how is it differentiated from infantile acne?

A

Maternal hormones stimulate sebaceous gland proliferation, allowing Malassezia to proliferate
-> differentiated from infantile acne because of its absence of comedones (only pustules).

40
Q

What is the benign, self-limiting rash which is very common in newborns called, and what is your main concern?

A

Erythema Toxicum Neonatorum (ETN)

Main concern is distinguishing from other pustular conditions (i.e. bacterial, fungal, viral), because no treatment is required

41
Q

What is the morphology of the rash in ETN? What type of baby is it typically found on?

A

Typically in full term healthy infants

Rash is not present at birth, and starts at 3-4 days of age as blotchy macules which develop into papules and pustules which can coalesce into large pink patches filled with these

42
Q

Where do the lesions typically appear in ETN and what will be seen on histology?

A

Lesions typically occur on face, trunk, and proximal extremities

Palms and soles are NOT affected (vs congenital syphilis)

HIstology - numerous eosinophils -> can give rise to peripheral eosinophilia

43
Q

What is Transient Neonatal Pustular Melanosis? What will be left over when they resolve?

A

Superficial pustular lesions which easily rupture, occurring especially in dark-skinned individuals

When they resolve, hyperpigmented macules will remain

44
Q

What will histology of transient neonatal pustular melanosis show? (vs. erythema toxicum neonatorum)

A

Histology shows neutrophils.

eosinophils in ETN

45
Q

Who gets Lichen Sclerosus et Atrophicus (LSA) and what is it?

A

90% in females, occurs in both children and older adults

It is sharply defined, pink-to white papules which coalesce into porcelain-like plaques, with atrophy as disease progresses

46
Q

Are the lesions of LSA itchy? What pattern do they typically create?

A

They are very pruritic. Typically involve the anogenital area forming an hourglass / figure eight appearance around both the vagina and the anus

47
Q

What can happen if males get LSA in their dorsal glans penis, and what is the treatment for LSA overall?

A

Males can get phimosis (tightening of foreskin)

Treatment: superpotent topical steroids

48
Q

What is the difference between a congenital vascular tumor and vascular malformation? Give an example of each

A

Vascular tumor -> characterized by endothelial proliferation
Example: strawberry hemangioma

Vascular malformation -> characterized by anomalous blood vessels but normal endothelial turnover
Example: port wine stain

49
Q

What are the three phases in the natural history of infantile (strawberry) hemangiomas?

A
  1. Rapid growth phase for 6-18 months, starting within first month of life
  2. Plateau phase
  3. Involution phase - slow regression, average of 5 years to involution.
50
Q

Who tends to get strawberry hemangiomas and how can you tell if they’re superficial vs deep?

A

Typically occur in females born prematurely

Superficial - more red, vessels more obvious

Deep - appears with a bluish hue to the skin

51
Q

What immunohistochemical stain can be used for infantile hemangiomas?

A

GLUT-1 -> stains endothelial cells in hemangiomas as well as placental tissues

52
Q

What complications are associated with hemangiomas in a beard distribution?

A

Airway obstruction -> look out for stridor, need an endoscopy for definitive diagnosis

53
Q

If you have multiple c cutaneous hemangiomas, which places should you check for visceral involvement?

A

Liver
GI tract - can cause significant bleeding
Brain

Typically done with ultrasound

54
Q

What is the first-line treatment for infantile hemangiomas these days?

A

Beta-blockers, i.e. propanolol or timolol

-> thought to induce vasoconstriction and inhibit vasculogenesis in these lesions

55
Q

What is the most common vascular lesion of infancy? Does it follow a dermatomal distribution?

A

Salmon patch / nevus simplex

  • > a cutaneous vascular malformation
  • > does NOT follow a dermatomal distribution
56
Q

What is an Angel’s kiss vs a Stork bite?

A

Angel’s kiss - nevus simplex of forehead / eyelid which usually fades by 1 year

Stork bite - Nevus simplex of the back of the neck, does not fade, often covered by hair not known about in adults

57
Q

How do Port-Wine Stains change as you age? How does this relate to their treatment?

A

Growth is proportional to child’s growth

Appears at birth as flat red-to-purple patch.

Throughout life, will become more papular, simulating a cobblestone appear
-> reason why you want to treat early with pulsed dye laser

58
Q

Are PWS’s typically unilateral or bilateral? What do they follow? What is the other name for these?

A

Typically unilateral, tend to follow a dermatomal pattern, i.e. a particular branch of the trigeminal nerve if on the face (vs salmon patches)

PWS is also called Nevus Flammeus

59
Q

What does a PWS of the face vs back typically mean?

A

Face - Could be associated with Sturge-Weber syndrome (encephalotrigeminal angiomatosis)

Back - May be associated with an underlying spinal cord AV malformation

60
Q

What is the cause of Sturge-Weber syndrome and what is typically found on the face?

A

Sporadic, congenital condition due to somatic mosaicism of GNAQ gene.

Typically, a PWS in the V1/V2 distribution is seen

61
Q

What is seen in the brain of patients with Sturge-Weber syndrome?

A

Leptomeningeal angioma -> due to abnormal blood vessels in brain

Tram-track calcifications - seen on CT scan due to calcified damage of blood vessels in pia mater on the gyri, ipsilateral to PWS (typically occipital region)

62
Q

What are the neurological consequences of what is seen in the brain in Sturge-Weber syndrome?

A

Seizures starting in the first year of life -> intractable epilepsy

Mental retardation

63
Q

What are the possible ocular consequences of Sturge-Weber?

A

Glaucoma - can develop in early or late childhood due to hemangiomas in V1 distribution increasing intraocular pressure

Buphthalmos (referring to enlargement of eyeballs common in bovines) - marked enlargement of eye which is congenital (due to glaucoma) -> pediatric emergency that could lead to blindness

64
Q

What is the mnemonic for Sturge-Weber?

A

STURGE

Sporadic Stain
Tram-track calcifications
Unilateral
Retardation
Glaucoma, GNAQ gene
Epilepsy

Pathophysiology - Dermatology (14 decks)

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