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SMS Week 3 > Acute Inflammatory Dermatoses > Flashcards

Acute Inflammatory Dermatoses Flashcards

1
Q

What are the 5 forms of acute inflammatory dermatoses? (the first is comined)

A
  1. Urticaria and angioedema
  2. Erythema Multiform (minor and major)
  3. Stevens Johnson Syndrome
  4. Toxic Epidermal Necrolysis
  5. Fixed Drug Eruption
  6. Panniculitis (erythema nodosum and erythema induratum)
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2
Q

What acute inflammatory dermatosis occurs in the dermis only?

A

urticaria

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3
Q

WHat 3 (only 1 in a way) acute inflammatory dermatoses occur in botht he epidermis and dermis?

A

erythema multiforme

SJS

TEN

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4
Q

What acute inflammatory dermatosis forms in the epidermis only?

A

fixed drug eruption

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5
Q

What acute inflammatory dermatosis occurs in the subcutaneous tissue?

A

panniculitis

(erythema nodosum and erythema induratum)

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6
Q

What is the morphology for urticaria?

A

Usually erythematous papules called wheals

they’re typically transient - individual wheels only last less than 24 hours

often pruritic

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7
Q

What is the main underlying issue in urticaria that causes the wheal?

A

IgE mediated histamine release causing dermal edema

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8
Q

What is angioedema?

A

It’s deep dermal and subQ swelling that is often painful

It’s a more severe component of urticaria

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9
Q

WHen is angioedema considered an emergency?

A

with laryngeal involvment

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10
Q

How is angioedema related to why we rather give antibiotic orally instead of IV?

A

IV anti iotic are more likely to cause laygneal angioedema

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11
Q

What are some important questions to ask when you see a patient with urticaria and/or angioedema?

A
  1. hx of allergies
  2. recent travel
  3. recent infection
  4. occupational exposures
  5. new meds
  6. new ingestion of goods
  7. exposure to new physical stimuli (soaps, dogs, etc.)
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12
Q

Where does angioedema most often occur?

A

lips

eyes

groin

palms/soles

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13
Q

What will blood work show to be increase in urticaria?

A

eosinophils, lymphocytes, polymorpholeukocytes

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14
Q

How do acute and chronic urticaria differ?

A

Acute lasts less than 6 weeks and is usually a type 1 IgE mediated event

Chronic lasts more than 6 weeks and the cause is often unknown (requires long term therapy)

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15
Q

What are the 3 general causes of immune urticaria?

What are the 3 general causes of non=immune urticaria?

A

immune: Type 1 IgE mediated, auto-immune, infectious

Non-immune: physical urticarias, direct mass cell degranulation, foods containing high levels of histamine.

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16
Q

What are some common cases of IgE mediated immune urticaria?

A

Foods (shellfish, fish, peanuts, tree nuts, eggs, milk ,soy and wheat)

latex

bee stings and the like

Meds (penicillin, cephalosporin, sulfa)

Aeroallergens (dust mites, pollen, mold, dander)

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17
Q

What are the general steps for an IgE mediated allergy?

A
  1. Sensitization: production of IgE by B cells in response to T cell cytokine secretion
  2. Binding of the IgE to mast cells or basophils
  3. Re-introduction of antigen
  4. Crosslinking of obund IgE
  5. Mast cell activation
  6. release of mediators like histamine, leukotrienes, cytokines, and enzymes
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18
Q

What are three different forms of autoimmune urticaria?

A

Hashimoto’s immune thyroiditis

Systemic lupus

Vasculitis

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19
Q

What are 4 vrises that can cause urticaria related to the immune reponse to infection?

A

CMV

EBV, HIV

HEP A, B, and C

also parasitic, fungal or bacterial

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20
Q

WHat are some examples of physical urticarias (non-immune)?

A
  1. solar
  2. cholinergic (sweating and heat)
  3. Cold urticaria
  4. Dermographism
  5. Aquagenic
  6. VIbratory angioedema
  7. Pressure urticaria (butt hurts fater sitting)
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21
Q

What are some things that can cause direct mast cell dedgrantulation that is NON-IMMUNE (aka can happen without previous desensitization)?

A

Narcotics lik MS and codeine

Aspirin

NSAIDS

Contrast

Dextran

ACE inhibitors

Vancomycin (remember “red man” syndrome?)

22
Q

What are some foods that contain high levels of histamine and can thus cause non-immune urticaria?

A

strawberries, tomatoes, shrimp, lobster, cheese, spinach, and eggplant

23
Q

What are the general treatments for urticaria?

A
  1. avoid what caused it (and avoid extreme temperatures, eercise and alcohol - cause vasodilation)
  2. Antihistamines (non-sedating H1 blockers) for acute urticaria
24
Q

What are 4 first like non-sedating H2 blockers?

A

Cetrizine (zyrtec)

Fexofenadine (Allegra D)

Desloratadine (Clarinex)

Loratidine (Claritin)

25
Q

What are 3 second-string antihistamines for urticaria (sedating)?

A

Hydroxyzine (Atarax)

Diphenhydramine (Benadryl)

Cyproheptadine (Periactin)

26
Q

What is the last report option for urticaria?

A

Oral corticosteroid like prednisone

27
Q

What is the prevantative medication we give to patients with a hx of severe type 1 IgE mediated reactions?

A

the EpiPen

28
Q

What does erythema multiforme look like?

A

It’s an iris-shaped lesion with erythima in the periphery, sometimes central clearing, and often a vesicle in the center.

Often several occur at one time

It’s a reaction pattern of blood vessels in the dermia

29
Q

Where on the body does erythema multiforme usually occur?

A

extremities (esp palms and soles) and mucous membranes

30
Q

Who does erythema multiforme most often occur in?

A

50% are under 20 years of age and it’s more frequent in males

31
Q

What drugs are often responsible for erythema multiforme?

A

sulfonamides

phenytoine

barbiturates

phylbutazone

penicillin

allopurinol

32
Q

What are two infections that can cause erythema multiforme?

A

HSV and mycoplasma pneumoniae

33
Q

What is the difference between EM minor and EM major?

A

EM minor is the mild form involving 1 or less than 1 mucosal site (major cuase is post herpes simplex infection with onset of rash at day 10)

EM major is severe with extensive skin and mucous membrane involvement. THIS IS STEVENS JOHNSON SYNDROME.It’s usually due to drugs and after mycoplasma pneumoniae infection.

34
Q

How can you differentiate EM from urticaria?

A

EM is fixed while wheals are more transient

EM doesn’t usually itch

35
Q

What happens in Stevens Johnson Syndrome?

A

It’s basically really severe EM major

You get a severe hypersensitivity reaction, first with fever, malaise an d arthralgias days after starting a drug

This proceeds to skin tenderness and erythema of the skin/mucosa

This is followed by a painful morbilliform rash that becomes confluent and then bullous and exfoliative.

You get extensive cutaneous and mucosa epidermial necrosis and sloughing

very serious - potentially life threatening.

36
Q

What are the criteria to consider something SJS beyond just EM Major?

A

It has to involved 2+ muscosal membranes and less than 10% epidermal detachment

37
Q

Stevens Johnson syndrome overlaps with what condition? WHat criteria are there for that diagnosis?

A

Toxic Epidermal Necrolysis

This needs 2+ mucosal memrbane and 30% epiermal detachment

(this is why they overlap - in the 10-30% epidermal detachment range)

38
Q

WHen are SJ/TEN more common in the lifespand? Gender difference?

A

over 40 years

equal sex incidence

39
Q

What are 3 risk factors for developing SJS/TEN?

A

1 systemic lupus erythematosis

HLA-B12

HIV

40
Q

What is the leading cuasative factor for SJS/TEN?

A

DRUGS!

Especially in TEN - 80% associated with drugs.

The time from first drug exposure to symptoms is about 1-3 weeks

41
Q

What is the therapy for SJS/TEN?

A
  1. diagnose early and stop med
  2. admit to ICU or burn unit
  3. IVF
  4. Systemic glucocorticoids
  5. High dose Immunoglobulins for TEN
  6. Debridement of only frankly necrotic skin
  7. Deal with complications
42
Q

How does SJS/TEN kill people?

A

sepsis (secondary infeciton)

GI hemorrhage (ulcers due to stress)

dehydration

43
Q

What does a fixed drug eruption look like?

A

a localized sharply demarcated erythematous patch that will itch, burn, or be asymptomatic

44
Q

Where are gixed drug eruptions usually located?

A

face and genitals

45
Q

What is the mechanism behind fixed drug eruptions? WHat’s the treatment?

A

mechanism is unknonw, but probably immune.

Just eliminate the offending drug and it will most likely go away (may leave a hyperpigmented area)

46
Q

In what layer does Panniculitis occur?

What doe sit look like?

A

In the subcutaneous tissue

erythematous or violaceous nodule in the SG fat which progresses and is decribed as lobular or septal depending on where it began

47
Q

Wat are the two types of panniculitis we’re concerned about?

A

erythema nodosum

erythema induratum

48
Q

Describe erythema nodosum.

A

erythematous tender noculdes typically located on anterior shins of young women

49
Q

What are common triggers of erythema nodosum?

Treatment?

A

Infectios with strep, TB or gunal

Oral contraceptives, sulfa meds, NSAIDS

autoimmen (IBD, Sarcoid)

Treatment is just rest, ice and pain control

50
Q

Describe erythema induratum.

A

Tender RED nodules

Also called lobular panniculitis and vasculitis

Usually on the posterior legs of middle aged women

This will sometimes be chronic - recurrent subcutaneous nodules with plaques and ulceration

51
Q

What infection is erythema induratum associated with?

A

TB

52
Q
A

SMS Week 3 (11 decks)

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