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Skin Flashcards

1
Q

What is the most common cause of rubber contact derm?

A

The accelerators in rubber

  • benzothiazoles
  • carba chemicals
  • thiurams
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2
Q

contact derm common veg culprits

A

onions, garlic, tomato and carrot in this order

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3
Q

what is the culprit of poison ivy and mgmt when it occurs

A
  1. uroshiol
  2. presents with a linear pattern of blistering
  3. wash immediately with cold water to degrade the uroshiol
  4. treatment with topical steroids and anti histamines
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4
Q

contact irritants of eyelids (4)

A
  1. nickel
  2. nail products: tosylamide, formaldehyde, and methyl methacrylate
  3. hair products: PPD (paraphenylenediamine), CAPB (cocomindopropyl)
  4. cosmetic procedures: parabens
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5
Q

what specific stains do you request in a biopsy for uritcaria?

A
  1. routine hematoxylin and eosin staining

2. IIF with michel’s media, DIF

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6
Q

Name 4 bullous skin diseases

A
  1. pemphigus vulgaris – flaccid bullae of non inflamed skin, targets are desmoglein and desmosomes 1,3
  2. bullous pemphigus - tense bullae on urticaria with pruritus, targeted by bp180
  3. dermatitis herpetiformis - small bullae on extensor surfaces due to celiac disease
  4. linear IgA bullous dermatosis - tense bullae like BP
  5. chronic bullous disease of childhood - tense bullae
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7
Q

what are the major and minor criteria of cutaneous mastocytosis?

A

Major - typical skin lesions of mastocytosis associated with dariers sign (UP/ Maculopapular cut. mastocytosis/ diffuse cut mast/ solitary mastocytoma)

Minor
- increased mast cells in biopsy of skin, KIT mut in lesional tissue

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8
Q

advantage of SPT over Immunoassays

A

greater sensitivity
wider selection of allergens
immediately available results
less time and reagent expense per test

Immunoassays:
lack of risk for allergic reaction
results not affected by drugs
results not affected by condition of skin
Greater patient convenience
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9
Q

Ecallantide approval and dosing

A

approved in US for > 12 years old

30 mg SC

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10
Q

Icatibant (Firazyr)
approval
dosage

A

Bradykinin receptor antagonist
approved for 2+
20 mg SC peds
30 mg SC adults

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11
Q

Berinert and Cinryze

A

berinet approved in CAN for acute tx - 20 IU/kg IV ages 3- 16

Cinryze approved in CAN for long term tx - 1000 IU q3-4 days IV

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12
Q

Adverse events assocaited with Berinert and Cinryze

A

(pC1inh)
thrombosis
anaphylaxis
transmission of infectious agent (theoretical)

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13
Q

Haegarda indications

A

prevention of HAE

  1. Peds > 8 years old
  2. Geri 65-72 year old
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14
Q

CI to Haegarda

A
  • hypersensitivity reactions like anaphylaxis to any C1 esterase inhibitor products
    or to any ingredient in the formulation
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15
Q

Haegarda dosing

A

60 IU/kg Q3-4 days

max dose is 10,000 IU which is 20 ml injection SC

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16
Q

stepwise approach to treatment of CSU (2018 CSACI)

A
  1. anti histamines
  2. increase AH 4 fold
  3. add Omalizumab 150 mg or 300 mg SC
  4. add Cyclosporin 3-5 mg/kg

** can trial LTRA for 2-4 weeks prior to Omalizumab and Cyclosporin, data is lacking in efficacy

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17
Q

HUVS diagnostic criteria

A

major: urticaria > 6 months and hypocomplemtemia

minor: 2 of
1. arthralgia
2. dermal venulitis
3. uveitis/ episcleritis
4. mild GN
5. recurrent abdominal pain
6. positive C1q with a suppressed C1q level

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18
Q

What features would you see on imaging of hypersensitivity pneumonitis

A
  1. upper lobar ground glass opacites
  2. centralobular nodular opacties
  3. air trapping
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19
Q

what invx would you order for hypersensitivity pneumonitis

A
  1. HRCT with inspiratory and expiratory images
  2. sIgE to possible culprit
  3. PFTs
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20
Q

Name 3 types of latex reactions, the mechanism and agent

A
  1. Anaphylaxis - IgE Mediated - Hev B 1
  2. Contact dermatitis - T cell mediated - thiuram or carbonate
  3. Irritant reactions - irritant mechanism - no allergen
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21
Q

what is the target for tac

A

FK binding protein

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22
Q

what is the target for sirolimus

A

mTor binding

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23
Q

what cytokine is needed for T cell proliferation?

A

IL-2

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24
Q

Name 3 drugs that interact with the effect of Epinephrine

A
  1. TCAs prolong the effect of Epi
  2. BB decrease the effect of Epi
  3. MOAs block the metabolism of Epi
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25
Q

Name the 3 receptors that Epi acts on and mechanism

A

a1 - vasoconstriction and increases PVR
b1- ionotropic and chronotropic effects that increase CO
b2- decreased mediator release from mast cells and basophils, bronchodilation and increased vasodilation

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26
Q

What are the two categories of RCM reactions

A
  1. Chemotoxic - nephrotoxicity, neurotoxicity

2. Hypersensitivity - IgE Mediated and Non Ige Mediated

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27
Q

Biggest RF for RCM reaction

A
  1. Previous RCM reaction
28
Q

DDX for recurrent anaphylaxis

A
  1. Idiopathic anaphylaxis
  2. mastocytosis
  3. pheochromocytoma
  4. carcinoid tumour
  5. MCAS
29
Q

4 mediators of anaphylaxis

A
  1. PAF
  2. Cysteinyl leukotrines
  3. Prostaglandin D2
  4. NO
  5. Histamine
  6. Tryptase
30
Q

What mediator is the best predictor of anaphylaxis

A

PAF (Peter Vadas NEJM 2008)

Tryptase also correlates with severity mostly in food allergy

31
Q

What is the mechanism of Frey’s Syndrome?

A
  • damage to the sympathetic nerves of the parotid gland (birth trauma, tumour, toxins)
  • eating results in flushing and sweating bc of regeneration of nerves to the sweat glands
32
Q

Treatment of rhinitis medicamentosa

A
  1. d/c medication

2. short course of PO steroids or INCS

33
Q

Yellow fever cause of rxns

A

Egg

34
Q

Varicella cause of rxns

A

gelatin

35
Q

Hepatitis cause of rxns

A

yeast

36
Q

Tetanus cause of rxns

A

latex

37
Q

Dtap cause of rxns

A

milk

38
Q

histology in UV (Direct IF, and routine histological examination)

A
  1. fragmentation of leukocytes
  2. fibrin deposition
  3. neutrophilic infiltration
39
Q

CSU histology

A
  • interstitial edema with perivascular mixed infiltrate
  • CD4 T cells
  • absences of neutrophils
40
Q

treatment of UV

A
  1. AH
  2. NSAIDs for arthralgias
  3. Steroids for moderate disease
  4. Other DMARDS - MMF, Methotrexate, azathioprine, cyclosporin used for refractory disease
41
Q

Ice cube negative cold urticaria

A
  • cold induced cholinergic urticaria
  • systemic cold urticaria
  • cold dependant dermatographism
  • FCAS
42
Q

Ice cub positive urticaria

A
  • idiopathic
  • secondary diseases - cryoglobulinemia, paroxysmal cold hemoglobinuria
  • delayed cold urticaria
  • localized cold urticaria
  • cold reflex urticaria
43
Q

diseases with urticaria or that present with hives and angioedema

A
  • UV
  • CAPS - FCAS, MWS, NOMID
  • Gleich’s syndrome (episodic angioedema and eosinophilia)
  • Wells syndrome ( granuloma dermatitis, with eosinophilia and eosinophilic cellulitis)
44
Q

what tests should you do for inducible urticaria?

A
  • cold provocation test

- CBC , ESR, CRP to rule out other diseases esp infections

45
Q

UAS7 Score

A

0 - none
1 - mild less than 20 wheals/ 24 hours
2 - moderation 20-50 wheals/ 24 hours
3 - intense > 50 wheals/ 24 hours or large confluent areas of wheals

score of 16 or higher considered severe over 7 days

46
Q

clinical feautres of SJS/ TENS - the triad

A
  1. mucous membrane erosions
  2. target lesions
  3. epidermol necrosis w detachement (nikolskys sign)
47
Q

treatment of SJS/TENS

A
  1. admit to hospital
  2. determine disease severity using SCORTEN score, a score of > 2 needs ICU
  3. supportive care - optho, fluids, antibx
  4. steroids
  5. IVIG - controversial - inhibits fas-fas ligand apoptosis
48
Q

pathogenesis of SJS

A
  • drug specific cytotoxic T cells kill keratinocytes directly and indirectly through recruitment of other cells
  • key mediator of cell death is granulysin produced by cytokines
  • others include perforin, fas ligand, granzyme
49
Q

FDA suggests screening which population before the start of aromatic anti convulsants? and why?

A
  • south asian population

- screen for HLA B15:02 bc risk of SJS/ TEN

50
Q

AGEP feautures

A
  1. pustulosis
  2. fever
  3. neutrophilia
51
Q

what is gleich syndrome

A
  • episodes of angioedema, weight gain and eosinophilia
52
Q

schnitzler syndrome

A

IgM monoclonal paraprotein with non pruritic urticaria

53
Q

HAE mutation

A

SERPING1

AD but also de novo in 25% of cases

54
Q

what is the normal role of C1 INH

A
  1. inhibits complement C1r, C1s, and MASP
  2. inhibits kalikrein and coag factors XI and XII
  3. fibrinolytic system- tissue plasminogen activator
55
Q

pathogenesis of factor XII HAE

A
  • mutation causes activation and facilitates activation of kininogen and bradykinin
56
Q

mgmt of HAE

A
  1. acute attacks
    - action plan for nearby ED
    - ABCs
    - Berinert 20 units/kg IV over 10 minutes, 2nd dose at 2 hrs if needed
    - Icatibant 30 mg SC slow infusion, max 3 doses in 24 hrs
    - Ecallantide (not avail in CAN)
    - FFP (second line)
    - treat pain for GI attacks
    - treat dehydration
  2. chronic care
    - identify triggers and avoid
    - education - involve pts with orgs
    - medic alert bracelet
    - avoid ACEi and OCP
    - discuss px meds
  3. Prophylactic Meds
    - > 2 episodes a month
    - Haegarda 60 U/kg SC Q3-4 days
    - Cinryze c1inh
    - Androgens: danazol
    - anti fibrinolytics
57
Q

pregnant with HAE

A
  • treat with C1 inh most clinical experience with this

for BF too

58
Q

surgery prep with HAE

A
  1. give C1 INH 1000-2000 U
  2. alternative: danazol 10mg/kg/day 5 days prior and 2 days after
  3. alternative: TXA 5 days prior and 2 -5 days after
59
Q

two theories of AA

A
  1. anti C1inh aa created by B lymphocyte clones, leading to depletion of C1inh
  2. neoplastic lymphoid tissue cause activation of the complement pathway which depletes C1inh
60
Q

3 differences between HAE and AA

A
  1. AA age on onset is older > 40 (HAE usually before age 20)
  2. AA mostly involves face and not GI or extremities
  3. AA has less erythema marginatum than HAE
61
Q

3 classifications of HES

A
  1. primary or neoplastic
  2. secondary or reactive
  3. idiopathic
62
Q

HES treatments

A
  1. Steroids
  2. Imatinib
  3. Hydroxyurea
  4. INF-a
63
Q

difference between mHES and lHES

A

myeloid HES

  • HSM
  • leukocytosis immature form
  • increase serum B12 and tryptase conc
  • anemia and thrombocytopenia
  • cardiac
  • less steroid sensitive
  • more aggressive clinical phenotype
  • SM

lymphoid HES

  • increase IL5
  • increase sIgE
  • polyclonal hyperpigmentation
  • itching and eczema
  • urticaria and angioedema
  • steroid sensitive
  • T cell phenotype subsets
  • approx 25% of HES pts
64
Q

which mutational testing for HAE should be done when HAE-nl-C1inh is suspected?

A
  • plasminogen- angiopoetin -1
  • Factor XII
  • kinogen
65
Q

diagnostic criteria for HAE

A
  1. recurrent attacks of angioedema in the absence of urticaria, and no use of medications that cause angioedema
  2. low C1inh level or function
  3. low C4 (during an attack or at baseline)
  4. age <40

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