Dermatology Topic Reviews Flashcards
(162 cards)
1
Q
DSM criteria for trichotillomania?
A
visible hair loss from pulling
mounting tension prior to pulling
release of tension after hair pulling (gratification)
absence of hallucinations, delusions or inflammatory skin condition
this disorder has overlap with OCD
2
Q
how does trichotillomania present?
A
compulsive hair pulling
usually at crown of head, can be eyebrows/eyelashes
irreg bald patch with broken hairs at various lengths
note broken hairs
3
Q
complication of trichotillomania?
A
hemorrhage, crusting, and chronic folliculitis
Trichophagy, resulting in trichobezoars
Long-term repeated trauma –> irreversible damage and permanent alopecia
4
Q
treatment of trichotillomania?
A
behavioural interventions
if dx with OCD: add clomipramine or SSRI
N-Acetylcysteine can be helpful
5
Q
Acne in 1- 7 year olds - next steps?
A
Always pathological until proven otherwise!
think endocrine –> assess for precocious puberty, virilization, growth
6
Q
treatment of mild acne?
A
Retinoid or benzoyl peroxide
retinoid = best for comedones
benzoyl peroxide = best for inflammation and bacteria
7
Q
treatment of moderate acne?
A
3mo of TOPICAL combination
Either of:
- Benzoyl peroxide + retinoid OR antibiotic
- Retinoid + antibiotic (Clindamycin or Dapsone)
Consider adding oral doxycycline, OCP or spironolactone
(never oral as monotherapy)
8
Q
treatment of severe acne?
A
Topical Combo + Oral
Benzoyl peroxide + retinoid OR antibiotic
AND
oral doxycycline or minocycline, OCP or spironolactone
Consider Isotretinoin if severe scarring acne or refractory acne
9
Q
You have decided to treat a patient’s severe acne with Isotretinoin . How long should they try it for?
A
6 months
10
Q
what monitoring needs to be done for a patient on Isotretinoin for their acne?
A
LFT and lipids
ensure female patients are on contraception and aware of teratogenicity - avoid conception during and 1 month post treatment
11
Q
side effects of Isotretinoin?
A
pseudotumour cerebri
teratogenic
elevated blood lipids and liver enzymes
night blindness
mucocutaneous dryness
myalgia
arthritis
12
Q
mechanism of action of isotretinoin?
A
only acne treatment that inhibits all 4 pathogenic factors of acne
- decr inflam
- decrease bacteria (cutibacterium acnes) colonization
- repair keratinization
- reduce sebum production by sebaceous glands
13
Q
what is atopic dermatitis?
A
eczema
=inherited, chronic, relapsing, pruritic skin condition with inflammation (dermatitic lesions) + xerosis (dry skin)
14
Q
age of onset of atopic dermatitis?
A
50% dx <1yrs old
30% dx 1-5 yrs old
dermatitis onset at >5yrs is unlikely to be eczema
15
Q
distribution of eczema of infants vs children vs adolescents/adults?
A
Infants = extensors
>2yrs = flexural predominance
antecubital /popliteal fossa at any age
Sparing of groin and axillary regions in all ages
16
Q
list the 6 diagnostic criteria of atopic dermatitis and how many do you need to make the diagnosis?
A
3 of the following:
Pruritus
Early age of onset (<5yrs)
Typical morphology and distribution
Chronically relapsing course
Xerosis (dry skin)
Personal or family history of atopy
17
Q
list some mimickers of eczema
A
immunodeficiency (Wiskott-Aldrich, Hyper IgE syndrome, SCID)
always think of immunodeficiency if “severe atopic dermatitis”
zinc deficiency
seborrheic dermatitis
contact dermatitis
psoriasis
scabies
dermatomyositis
18
Q
What are “red flags” in eczema?
A
Red Flags for Immunodeficiency – Wiskott–Aldrich syndrome, Hyper IgE Syndrome, SCID
- Neonatal severe “eczema”
- Poor response to appropriate treatment
- Lack typical distribution for age
- Recurrent/severe infections
- FTT
- Hepato-splenomegaly
- Dysmorphic features
- Chronic Diarrhea
19
Q
Non-pharmacologic treatment of eczema?
A
daily bath with unscented soap for <10min, pat dry and immediately apply emolient after bath.
Wear cotton
Hypoallergenic detergents
20
Q
pharmacologic treatment of eczema?
A
Topical corticosteroid ointment
Face and folds = mild potency eg. 1% hydrocortisone
Body = moderate potency eg. 0.05% betamethasone valerate
Topical Calcineurin inhibitors (pimecrolimus, tacrolimus) 2x/wk if >2yrs and failed steroids
Topical Crisaborole (PDE-4 inhibitor) ointment BID if >2yrs
21
Q
Complications of eczema?
A
Secondary impetigo
Eczema Herpeticum
Warts
Molluscum
22
Q
pathogen causing impetigo?
A
staph aureus (less commonly strep)
23
Q
diagnosis of secondary impetigo in a child with atopic dermatitis?
A
Clinical dx (swabs not that helpful bc kids often colonized with staph aures, but consider MRSA swab if RF)
lesions that progress from papules -> vesicles -> pustules -> honey -colored crusts on face/extremities
often preceded by abrasion, insect bite, chickenpox, scabies, burns
24
Q
Treatment of secondary impetigo in a child with atopic dermatitis?
A
PO cephalexin x 7 days
IV if unwell, unable to tolerate po abx or severe AD flare
25
Presentation of eczema herpeticum?
Punched out monomorphic lesions, all the same size.
Intact vesicles rarely seen due to scratching.
26
diagnosis of eczema herpeticum?
Clinical diagnosis - need to make it quickly as this is a "dermatological emergency"
- swab for HSV PCR for confirmation
27
Treatment of eczema herpeticum?
dermatologic emergency!
PO Acyclovir x 7-10d
IV acyclovir if <1 yrs, fever, systemic sx, poor oral intake or severe
If V1 involvement - optho consult!
28
what do you do?
this is eczema herpeticum involving the V1 reason
start acyclovir ASAP and OPTHO consult!!
29
What is this?
Herpetic Whitlow due to deep HSV infection
30
What is the etiology of herpetic whitlow?
HINT: there is a bimodal age peak distribution
Two peaks of occurrence:
HSV-1: HSV infection of child’s fingertip (specifically infection of paronychia) due to child’s fingers in caregivers mouth that has cold sore (HSV-1 infection).
HSV-2: HSV-2 infection of teens fingertip (specifically infection of paronychia) due to exposure to active HSV-2 lesions / genital secretions
31
Herpetic Whitlow is due to an HSV infection of the paronychia under the thicker fingerpad skin. What is the clinical features /presentation of Herpetic Whitlow?
HINT:
- Onset of rash after exposure
- Skin change
- Other features
Onset
- 2-7days after exposure
Skin Changes:
- Erythematous, tenderness of fingertip with deep seated grouped/coalescing vesicles/pustules clustered on distal phalanx, vesicles rarely rupture (as finger skin is quite thick).
Other features:
+/- regional lymphadenopathy or lymphangitis
+/- neuralgia
32
Herpetic Whitlow is due to an HSV infection of the paronychia under the thicker fingerpad skin. Treatment for herpetic whitlow?
PO Acyclovir
(can help with alleviation of pain + more rapid healing)
33
This child has sensitivity to gluten, what is this rash likely due to?
Dermatitis Herpetiformis (DH) is a type of rash that is found in individuals with gluten-sensitive enteropathy (aka celiac disease). Majority of individuals with DH are asymptomatic or have minimal gastrointestinal symptoms.
34
What type of rash occurs in a patient with dermatitis herpatiformis (DH) and what location would it commonly be found?
Rash:
SYMMETRIC, grouped, small, tense, ERYTHEMATOUS, stinging, intensely PRURITIC papules and vesicles.
Rash eruption is pleomorphic (can have erythematous, urticarial, papular, vesicular, and bullous lesions
Location:
- Knees, elbows, shoulders, buttocks, forehead, and scalp;
- Mucous membranes spared.
+/- Hemorrhagic lesions (palms, soles)
35
Dermatitis Herpetiformis is a rash that occurs in individuals with gluten sensitive enteropathy (aka Celiac disease). What is the pathophysiology of this rash?
IgA antibodies (most commonly (70-90%) an Ab to smooth muscle endomysium) are directed at epidermal transglutaminase (transglutaminase 3).
36
How do you diagnose dematitis herpetiformis?
Direct Immunofluorescence (diagnostic for DH): Demonstrates presence of granular IgA in dermal papillary tips
AND Need to pursue Jejunal biopsy to diagnose likely underlying celiac disease because cutaneous manifestations may precede malabsorption.
Helpful Tests:
+/- Skin Biopsy: Subepidermal blisters composed predominantly of neutrophils are found in dermal papillae.
+/- HLA positivity: Usually express HLA-DQ2 (+) (90% of patients).
37
Patient has celiac disease and develops Dermatitis Herpetiformis (DH). Treatment for DH?
Gluten-free diet (response within weeks-months).
+/- PO Dapsone (indicated for intense pruritus)
38
Treatment of subcutaneous fat necrosis of the newborn?
lesions are self-limited
if fluctuant lesion, needle aspiration to prevent rupture and subsequent scarring
monitor for hypercalcemia for first few months of life
treat hypercalcemia with hydration and furosemide, limit Ca + Vit D intake, and steroids (per Nelson's). Pamidronate if severe
39
Pathophys of psoriasis
Inflammatory autoimmune related disease characterized by inflammation and keratinocyte proliferation
Characteristic Pathology: parakeratosis, acanthosis, elongated rete ridges, neutrophilic infiltrate in the epidermis
40
what is this?
subcutaneous fat necrosis of the newborn
41
Which age group does pityriasis versicolor occur in?
ADOLESCENCE
Do not consider this diagnosis (especially not on the exam) in any other age group
42
Clinical presentation of psoriasis?
Lesions common on extensors, can be pruritic but not always
Presents in the first 2 decades of life in ~ 30% of affected individuals
Red, well-defined, scaly papules/plaques with irregular boarders
1/3 have family history
43
What is pityriasis versicolor
Proliferation of Malassezia (normal skin flora)
Discrete and coalescent ovoid papules and plaques with fine scale
Hypopigmented, pink, red, tan
Seborrheic areas --> forehead, temple, neck, upper back, chest, arms
Mildly pruritic
44
What is this?
pityriasis versicolor
45
Treatment of pityriasis versicolor?
Topical antifungals
Topical antifungal shampoo (apply shampoo to the skin and leave overnight)
Can use oral antifungal if severe but NOT oral terbinafine
46
What is post-inflammatory hypopigmentation?
Hypopigmented lesions that are poorly demarcated and have NO scale
Occur after previous inflammation
eg mosquito bites
acne
allergic reactions
dermatitis
other trauma
Improves with time, no treatment needed
Sun protection / SPF shortens duration
47
What is pityriasis alba? What are features that distinguish it from other hypopigmented lesions?
"light eczema"
Can be associated with eczema
Often happens in the SUMMERTIME (this has come up in question stems)
Hypopigmented, poorly marginated, with fine white scale
Common on the FACE (rather than trunk or limbs)
Treat with 1% hydrocortisone x 5-7 days
48
What is the Koebner phenomenon
Psoriatic lesions are induced in areas of local trauma
eg scratching leads to linear lesions
This can also occur in vitiligo (depigmented lesions can occur at sites of trauma eg eye rubbing --> eyelids become depigmented)
49
Describe the lesions associated with psoriasis
Red, well-defined, scaly papules/plaques with irregular boarders
Often scale appears silver
50
What is guttate pattern psoriasis?
Many tiny small papules <1cm
Common sites include trunk, face, proximal portions of limbs
Occurs after GAS infection
--> consider treating with Penicillin x 10 days
Treatment does NOT alter the course of psoriasis but is only for treatment of the GAS infection
Guttate pattern psoriasis is the only type of psoriasis that might occur only once --> otherwise psoriasis is usually chronic relapsing / remitting
51
What increased risks / comorbidities are associated with psoriasis
Obesity
Metabolic syndrome
Cardiovascular disease
T2DM
HTN
IBD
Celiac
Stroke
Psoriatic arthritis
Depression
Eating disorders
Suicidal ideation
52
What triggers are most common for psoriasis?
Sun exposure (in about 10% of pts)
Obesity
Smoking
Excessive alcohol
Stressful event
Medications: beta blockers, NSAIDs
53
What annual screening is indicated in psoriasis?
Yearly screening:
Wt check (start age 2)
BP (start age 3)
Depression/anxiety
Arthritis
Uveitis if psoriatic arthritis
Lipids → 9-11yo, 17-21yo if obese at diagnosis
If overweight
fasting glucose if risk factors age 10+ every 3 years
ALT if risk factors age 9-11, if normal repeat q2-3 years
If obese
fasting glucose age 10+ every 3 years
Screening lipids at diagnosis
ALT age 9-11 (sooner if severe obesity), if normal rpt q2-3 years
54
Treatment for psoriasis?
1st line - Topical Steroids/TCI’s
– TCI or Mod-High Potency topical steroid on body
– Low Potency topical steroid or TCI - face and folds
* Other topical tx:
– Topical Calcipotriol (vitamin D analog)
– Topical steroids/vitamin D analog combination topical
– Topical Retinoid
– Topical steroids/retinoid combination topical
Systemic therapy (mod-severe psoriasis)
– Phototherapy
– Methotrexate
– Acitretin - Oral Retinoid
– Biological Agents
* Etanercept
* Ustekinumab
* Ixekizumab
* Secukinumab
55
what is this?
Erythema toxicum (RC photo)
56
what is this?
Erythema toxicum (Another RC photo)
57
Treatment and outcomes for LCH?
Prognosis is much better for single-system disease than for multisystem disease
Single system disease --> usually self limited, may require low dose radiation or corticosteroid injections
Multi system disease --> aggressive chemotherapy and worse outcomes, has associated neurodegenerative syndrome that can occur
58
what is this?
Erythema toxicum (third RC photo)
59
What is pityriasis rosea?
Can be a reaction to many different viruses
Starts with herald patch (annular plaque with scale with central clearing)
Days to weeks later, develops generalized erythematous plaques/papules with mild pruritus. "Christmas tree" pattern.
May have viral prodrome. Resolves over 6 weeks to 3 months.
Can try topical corticosteroid if severe but usually no treatment
60
what is this?
Transient Neonatal Pustular Melanosis
61
How does erythema toxicum present?
first few days of life
50% of newborns
Irregular (blotchy) red macules/papules
62
What is the differential diagnosis for congenital melanocytic nevi?
Congenital melanocytic nevi
Dermal melanocytosis
Cafe au lait macules
Smooth muscle harmatomas
63
Which congenital melanocytic nevi are associated with leptomeningeal melanocytosis (neurocutaneous melanocytosis)?
Giant congenital melanocytic nevi
> 40cm in diameter or >5% of body surface
Patients with this giant nevus need MRI within 6 months of birth to look for leptomeningeal melanosis --> 30% will have this and still be asymptomatic
64
What is the presumed pathophysiology of vitiligo?
Acquired macular depigmentation disorder associated with the destruction of melanocytes due to complex interaction of environmental, genetic, and immunologic factors. Anti-melanocyte Abs (present in up to 80%) thought to be cytotoxic to melanocytes.
65
Vitiligo can be associated with various syndromes. What syndrome is known for VITILIGO + UVEITIS + DYSACUSIA (hearing sensitivity) + MENINGOENCEPHALITIS
Vogt-Koyangi-Harada Syndrome
66
There are two types of vitiligo
(1) Dermatomal/Segmental vs
(2) Nondermatomal/Nonsegmental
What type of vitiligo is more common in children?
Nondermatomal/Nonsegmental is more common in children (50% present before age 20yrs)
67
Nondermatomal/Nonsegmental is more common in children (50% present before age 20yrs). What is the typical presentation?
- Nondermatomal / nonsegmental sharply demarkated distribution of progressive depigmentation with lifelong flareups.
- No scale overlying the depigmentation
- +/- Koebner phenomenon (hypopigmentation occurs in areas of trauma / friction)
- +/- hair depigmentation (at later stages)
- +/- halo neus formation
Commonly have a personal or FHx of autoimmunity
68
What conditions commonly occur with a diagnosis of pediatric vitiligo?
Autoimmunity occurs in 20% of children with vitiligo
Most commonly HASHIMOTOS, ADDISONS, T1DM, pernicious anemia, hypoparathyroidism, psoriasis, SLE, polyglandular autoimmune syndrome with selective IgA deficiency, alopecia areata.
69
What is the treatment for pediatric vitiligo?
STRONG TOPICAL STEROIDS
+/- calcineurin inhibitor (tacrolimus or pimecrolimus)
+/- UV-B light therapy (if extensive involvement)
Minimize sun exposure to depigmented areas
70
what is this?
Miliaria = heat rash
71
Consideration of involvement of plastics for burns
Full thickness (NON blanching) only heal by wound contraction - consider for skin grafting
If not healed within 2 weeks > Plastics/Burn center
72
Definition of minor burns
Superficial or partial thickness AND <10% BSA
Superficial partial thickness burns blister
73
Acute management of minor burns
- early cooling within 30 min to prevent further injury (cool running water)
- consider tetanus
- de-roof blisters over joints or are very large, remainder leave. Should be debrided once ruptured.
- analgesia
-sterile non-adherent bandage, daily dressing changes with topical antimicrobial if de-roofed - mepilex Ag, silver dressing, bacitran, silvadene
- fluid management using parkland for TBSA >10%
74
Burn severity differentiation
Superficial (1st degree) - level of epidermis, pain, erythema for 48-72 hours
Partial thickness (second degree) - superficial dermis or deep dermis layer - blisters, extreme pain (can have schar with or without pain depending how deep) Heals 7-14 days
Full thickness (third degree) - subcutaneous tissue level, leathery eschar and WILL NOT heal. Painless, non-blanching
75
Rule of 9's for BSA
>9y - rule of 9s
<9 - legs rule of 7s, head 18% anterior and posterior each.
76
Criteria for referral to burn center
Extent: partial thickness burn > 10% TBSA, any full thickness burn
Location: burns on the face, neck, hands, feed, perineum, major joints, circumferential burns
Type: chemical, electrical
Associated with: smoke inhalation, head injury, trauma/fractures, pre existing medical condition that could complicate management
Social Situation: infants and young children, abuse, self-inflicted, psychological issue
77
parkland formula for burns
4ml * weight (kg) * TBSA
1st 8 hours = 50%
2nd 16 hours = 50%
If <30kg, maintenance fluid with dextrose should be added on top of parkland formula. Avoid K+.
78
Acute management of moderate to severe burns
- evaluate and treat for resppiratory compromise - consider early intubation
- gases, carboxyhemoglobin, CXR - FiO2 100% for potential smoke inhalation.
- fluid management with parkland
- analgesia with tylenol/NSAIDS/oral ir IV morphine, fentanyl
- psychological support - family and child to help reintegrate into home environment and PTSD
79
What is this rash?
Scabies
80
Scabies transmission
direct skin to skin contact - cause by a mite (Sarcoptes scabei)
clothing, bed linen, hats
81
groups with increased risk of scabies
Indigenous
Young, elderly
Immunocompromised
Developmentally delayed
Associated with poverty, overcrowding, malnutrition, reduced access to health care
82
clinical manifestations of scabies
- burrows, erythematous papules, pruritis worse at night
- wrist, elbow, armpiut flexures, genitals, breasts - burows
- risk of secondary bacterial infections
- crusted scabies - hyperinfestation which is rare usually immunocompromised
83
Investigations for scabies
Clinical diagnosis
Can do skin scraping, burrow ink test or dermatoscopy if unclear dx
84
Treatment scabies for all ages
Permethrin 5% cream MOST effective
Infants - treat WHOLE body (head to toe)
Children and adolescents - neck to toes
Leave on overnight and was in AM x7d
- re-treat 1 week later
- treat ALL household contacts
all bed linen and clothing should be laundered in hot water
Suphur approved <3 months and pregnancy but smells awful
85
When can kids return to school after scabies infection?
Child may return to child care or school the day after completing the initial treatment series
86
What is the most common trigger for erythema multiforme?
HSV - usually WITHOUT mucositis
87
Medications that can cause erythema multiforme
Less commonly (10%)
Barbitruates
NSAIDs
Penicillins, sulphonamides, nitrofurantoin
AEDs
88
Name this lesion
Erythema multiforme
Target lesion - dusky center with blister or crusting
89
Describe cutaneous lesions in Erythema multiforme
initially macules -> papules -> plaques
- central area darkens and develops blistering or crusting
- target lesions
-polymorphous rash with lesions at different stages
- few to hundred of skin lesions in 24h period
90
Clinical presentation of erythema multiforme
- Few to hundreds of skin lesions in a 24 hour period
- Usually asymptomatic rash, but can itch and burn sometimes
- RARE prodromal symptoms
- can have mucous membrane involvement (primarily oral) but less common than RIME
91
Management of erythema multiforme
Supportive
If concerns for HSV - may need Acyclovir or azithromycin if Mycoplasma
92
RIME clinical presentation
>/= 2 mucosal surfaces (often hemorrhagic crusting of lips, erosions on tongue and buccal mucosa, anogenital lesions, purulent conjunctivitis)
infectious prodrome
limited skin involvement (less confluent, absence of acral target lesions, absence of epidermal detachment in TENs).
93
proposed diagnostic criteria for RIME
- Mucocutaneous eruption with <10 % BSA involvement
- Involvement of 2+ mucosal sites
- Presence of a few vesiculobullous lesions or scattered, atypical, targetoid lesions
- Clinical and laboratory evidence of M. pneumoniae infection
94
Organisms other than mycoplasma that can cause RIME
chlamydia pneumoniae, ERV, FluB, HMPV, paraflu, HSV
95
Management of RIME
Mouth washes
Foley catheter
Empirici abx (Azithro)
Analgesia
Ophthalmology consult (often for placement of amniotic membranes and management of conjunctivitis)
Etanercept + Steroid
96
What is the difference between a hordeolum (stye) and chalazion?
Hordeolum - "H"urts - painful, sudden onset usually from infection, erythematous eyelid
Chalazion - "C"hills - non-infectious gland occlusion that is "C"hronic. Firm lump, slow-growing. Painless.
97
Management of hordeolum
Warm compresses to lids
Daily baby shampoo and scrub with cloth
Can use topical abx if purulent drainage
persists x4-6 weeks
98
what is this?
Miliaria = heat rash
rash is from blocked sweat ducks
tx = cooler environment and loose clothing
99
What does
100
how does Transient Neonatal Pustular Melanosis present?
present at birth
pustules, scale collarette
NON-erythematous
(unlike 24-72hr onset and erythematous base for erythema toxicum)
Resolves in a few days, Self limited
101
102
103
What is this lesion?
incontinentia pigmenti
104
Clinical features of incontinentia pigmenti
Skin: alopecia, nail ridging and pitting
Dental: late dentition, hypodontia, conical teeth, malocclusion, impaction
CNS: seizures, intellectual disability, hemiplegia, hemiparesis, spasticity, microcephaly
Ocular: microphthalmus, strabismus, optic nerve atrophy, cataracts
105
Inheritance pattern of incontinentia pigmenti
X-linked dominant
106
stage of progression of incontinentia pigmenti lesions
stage 1 - linear vesicles on red base (spares face and respects midline)
stage 2 - verrucous, hyperkeratosis
stage 3 - hyperpigmentation
stage 4 - hypopigmentation
107
What is the difference from SJS and TEN?
SJS <10% of TBSA
SJS-TEN 10-30% of TBSA
TEN > 30% TBSA
108
Clinical presentation of SJS/TEN
>/= 2 or more mucosal surfaces with systemic involvement USUALLY after exposure to drugs, less commonly infectious
109
dermatological progression of SJS and TEn
erythematous macules that rapidly develop central necrosis to form vesicles and bullae
110
Common drugs that can trigger SJS/TEN
Anti-epileptic meds (phenytoin i.e.), sulfonamides, penicillin, NSAIDS
111
What is Nikolsky sign?
denudation of the skin with gentle tangential pressure ONLY in signs of erythema
112
Pathophysiology of SJS/TEN
Drug-specific T-cell mediated reaction with HLA activation of CD8+ T cell receptors (drug specific) and release of cytotoxic proteins resulting in epidermal necrolysis.
113
Management of SJS/TEN
Mostly supportive and symptomatic treatment - complications can be life threatening
In drug eruption:
- IVIG (0.75-1g/kg/d x3d)
- Steroids (controversial)
- antibiotic therapy - azithro if suspect mycoplasma - consider cephalosporins if suspected 2ndary bacterial infection
114
What is this bright red perianal rash from?
Perianal infectious dermatitis
115
Treatment of perianal infectious dermatitis
7d course of cefuroxime (20mg/kg/d divided BID) with topical mupirocin 2-3x/d
116
Progression of infestation of lice
live close to the scalp surface - on first infestation, sensitatization takes 4-6 weeks then itching
117
Treatment recommendations for lice in kids
- >2mos old - permethrin 1% (high resistance) and pyrethrin recommended
- 2 applications 7-10 days appart
If does not eradicate live lice, consider administering a full treatment course using a medication from another class
118
Does itching indicate re-infection after completion of lice treatment?
No - post-treatment itching, burning, mild rash are COMMON as side effect from insectiside therapy - topical steroids or antihistamine can provide relief
119
Return to school policy for lice in kids
Send to school immediately! Do not exclude from school or daycare. Avoid head-to-head activities (i.e. helmets, hats)
120
What is this lesion suggestive of?
Alopecia areata
121
Pathophysiology of alopecia areata
T-cell driven autoimmune disorder producing non-scarring, sharply defined areas of hair loss
122
Clinical presentation of alopecia areata
Rapid or complete hair loss in round or oval patches on the scalp, eyebrows, eyelashes - skin below is NORMAL
common 'exclamation hairs'
Atopy and nail changes associated
123
Common autoimmune diseases associated with alopecia areata
Hashimoto's thyroiditis >> Addison disease, Pernicious anemia, Ulcerative colitis, Myasthenia gravis, Vitiligo
124
Management of alopecia areata
if no spontaneous resolution (usually 6-12 months, but common recurrences)
treatments control not cure:
- potent topical or mid-potent injected steroids - tramicinolone
- wigs
- counselling
- disease education
125
What is this lesion associated with?
Tinea Capitis (Ringworm)
126
What is a kerion?
Inflammatory form of tinea capitis with hypersensitivity reaction against dermatophyte
Boggy inflamed granulomatous abscess
127
Treatment of kerion
Systemic antifungal therapy - terbinafine, fluconazole i.e.
Oral steroids are equivocal so not recommended.
128
Findings associated with Alopecia Areata
Atopy and nail changes (pits, longitudinal striations and leukonycia)
Autoimmune diseases eg Hashimotos thyroiditis, Addisons disease, pernicious anemia, ulcerative colitis and vitiligo
129
Management of Alopecia Areata
Spontaneous resolution in 6-12 months
Treatment CONTROLS but does not CURE - potent topical or mid-potent injected steroid
Screen for autoimmune disease
130
Features of a superficial burn
Damage to the epidermis only. Presents with redness, pain, no blisters. Heals in 3-5 days
131
Features of a superficial partial thickness burn
Damage to the epidermis and part of the dermis. Presents with redness, pain, moist, blisters. Heals in 2 weeks
132
Features of a deep partial thickness burn
Damage to the epidermis and > 50% of the dermis. Presents with pale, dry, less tender, speckled appearance. Often needs grafting
133
Features of a full thickness burn
Damage to subcutaneous tissue. Presents with pale, charred, leathery appearance, non-tender. Most needs grafting
134
Acute management of a burn
Cover with sterile bandage
early cooling
tetanus (for a dirty wound)
analgesia
135
Indications for intubation in burns
Carbonaceous sputum
singed nasal hairs
soort in airway
hoarse voice
136
Criteria for Referral to Burn Centre
Extent: partial thickness burn > 10% TBSA, any full thickness burn
Location: burns on the face, neck, hands, feed, perineum, major joints, circumferential burns
Type: chemical, electrical
Associated with: smoke inhalation, head injury, trauma/fractures, pre existing medical condition that could complicate management
Social Situation: infants and young children, abuse, self-inflicted, psychological issue
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Estimation of BSA for fluid management in burns
Age > 9: rule of 9s
Age < 9: palm = 10% BSA
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What rash presents with “Punched out” erosions and vesicles on background of dermatitis, monomorphous?
Eczema Herpticum
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Most common pathogen for superinfection of Eczema Herpticum
Staph Aureus
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Management of Eczema Herpticum
If unwell, <1 year, poor fluid intake, severe: admit and treat with IV acyclovir
If well, localized, good fluid intake, good f/u: oral acyclovir x 7-10 days
If V1 are involved, consult ophtho
Admit to hospital if < 2 years
Add antibiotics if necessary
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3 types of pustules in neonatal pustular melanosis
Pustules with no erythema
Ruptured pustules with peripheral scale
Hyperpigmented macules
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Findings on pustule smear in neonatal pustular melanosis
PMNS (neutrophils)
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rash present at birth with 1- to 2-mm vesicopustules or ruptured pustules that disappear in 24 to 48 hours, leaving pigmented macules with a collarette of scale
Transient Neonatal Pustular Melanosis
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Small hypopigmented depressed scars occurring in areas of minor trauma presents in sun exposed areas
Pseudoporphyria
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Medication associated with Pseudoporphyria
NSAID - specifically Naproxen
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Triad of Sturge-Weber Syndrome
1. facial capillary malformation (port wine stain or nevus flammeus)
2. ipsilateral vascular anomaly in the brain (leptomeningeal hemangioma)
3. ocular hemangioma and glaucoma
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Neurologic features of Sturge-Weber Syndrome
Seizure - presents in the first year of life but rarely in the first month
Hemiparesis
Stroke like episodes
developmental delay and intellectual disability later in childhood
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MRI findings in Sturge-Weber Syndrome
white matter abnormalities are common due to chronic hypoxia
atrophy noted ipsilateral to the leptomeningeal capillary malformation
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Management of Sturge-Weber Syndrome
seizure control- pre-symptomatic treatment in high risk babies may prevent or delay seizure onset
headache relief
prevention of stroke like episodes
Ophthalmological evaluation for glaucoma with regular intraocular pressure measurements
laser therapy for cutaneous malformations
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Non-scaring, sharply defined area of hair loss
Alopecia Areata
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Clinical presentation of perianal infectious dermatitis
Rectal pain, burning inside anus during defection, blood streaked stools, pruritis
Rash - superficial, erythematous, well marginated, nonindurated and confluent from anus outwards. Tends to be bright red, moist, and tender to touch.
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What are the major risk factors for neurocutaneous melanocytosis (leptomeningeal melanocytosis)?
Giant congenital melanocytic nevus, location on the head or midline on the trunk, >20 “satellite” lesions
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What is neurocutaneous melanocytosis (leptomeningeal melanocytosis)?
Proliferation of melanocytes within the CNS
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rare but serious complication of subcutaneous fat necrosis of the newborn?
hypercalcemia
presents at 1-2 mo of life with lethargy, poor feeding, vomiting, FTT, irritability, seizures, short QT or renal failure
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how does subcutaneous fat necrosis of the newborn present?
red/violaceous sharply demarcated plaque or nodule on cheeks, bum, back, thighs, upper arms
calcium deposits in the lesions which can rupture and drain liquid
heal with or without atrophy
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when does subcutaneous fat necrosis of the newborn typically present?
at birth or within first 4 weeks of life in term infants
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Which conditions are associated with subcutaneous fat necrosis of the newborn?
HIE - both from the ischemic injury itself (from maternal preeclampsia, birth trauma, asphyxia) and from whole body cooling
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Which antibiotic do we use to treat skin abscess and for which duration?
PO Septra x 7 days
covers MSSA and MRSA
IV if systemically unwell
if <1mo = IV vancomycin, or outpt PO clindamycin if abscess <1cm and well
if significant cellulitis = add cephalexin to cover GAS pending cultures
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indications for empiric antibiotics of skin abscess?
vast majority of MSSA/MRSA skin abscesses resolve postdrainage WITHOUT antibiotics
Empiric Antibiotics for 7 days if:
- <3mo
- Significant cellulitis
- >48hr no improvement
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treatment of skin abscess?
ALL abscesses are drained and pus cultured
vast majority of MSSA/MRSA skin abscesses resolve postdrainage without antibiotics
know indications for abx (diff flashcard)
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risk factors for community acquired MRSA skin abscesses?
skin abrasion
contaminated items and surfaces
close skin to skin contact
crowded living conditions
poor hygiene
Aboriginal populations, athletes, daycare attendees, military recruits, IV drug users, MSM, prisoners
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Which pathogens typically cause abscesses in children, particularly the buttocks and lower limbs?
MSSA and MRSA
