Allergic and Immune-Mediated Disorders

Question 1

Pruritis leading to lichenification

Answer 1

Eczema (atopic dermatitis)

Question 2

History seen in eczema

Answer 2

Look for asthma, allergic rhinitis, family history of atopic disorders, onset before age 5, very rare to start after age 30

Can get thickened skin (lichenification) as adult

High IgE

Question 3

Tx for eczema

Answer 3

Withdraw offending agent. Topical steroids (sparingly - too much will cause skin atrophy) during flares.

Tacrolimus and pimecrolimus are T cell inhibiting agents that provide longer term control and help get patient off steroids. They come in topical form.

Antihistamines - mild gets nonsedating drugs (cetirizine, fexofenadine, loratadine). Severe gets hydroxyzine, diphenhydramine, doxepine*

ABx such as cephalexin, mupirocin, retapamulin when impetigo occurs

UV light for severe recalcitrant disease

Question 4

Skin care for atopic dermatitis

Answer 4

Stay moisturized; avoid bathing, soap, washcloths. Cotton is less irritating than wool.

Question 5

Type 1 hypersensitivity

Answer 5

Anaphylactic and atopic

Mechanism - antigen cross-links IgE on presensitized mast cells and basophils, triggering release of vasoactive amines like histamine. Rxn develops rapidly as a result of preformed antibody

First and Fast. Type 1, 2, and 3 are all antibody mediated.

Ex - anaphylaxis, asthma, urticarial drug reactions, local wheal and flare

Question 6

Type 2 hyper

Answer 6

Cytotoxic

Mechanism - IgM and IgG bind to antigen on an enemy cell, leading to lysis by complement or phagocytosis

Cy-2-toxic. Antibody and complement lead to MAC

Ex - autoimmune hemolytic anemia, erythroblastalis fetalis, Goodpasture, rheumatic fever

Question 7

Type 3 hyper

Answer 7

Immune complex
1) Mechanism - antigen-antibody complexes activate complement which attracts PMNs; PMNs release lysosomal enzymes.

2) Tricks - Imagine an immune complex as 3 things stuck together (antigen-antibody-complement). Includes many glomerulonephritides and vasculitides
3) Ex - polyarteritis nodosa, immune complex glomerulonephitis, SLE, RA

Serum Sickness
1) Mech - Antibodies to the foreign proteins are produced in about 5 days. Immune complexes form and are deposited in membranes where they lead to tissue damage by fixing complement

2) Tricks - Most serum sickness is now caused by drugs (not serum). Fever, urticaria, arthralgias, proteinuria, and LAD occur 5-10d after antigen exposure, More common than Arthus rxn.
3) Ex - Drug rxn

Arthus rxn
1) Mech - A local rxn to antigen by preformed antibodies characterized by vascular necrosis and thrombosis

2) Tricks - Arthus occurs rarely 4-12h after vaccination
3) Ex- hypersensitivity pnemonitis

Question 8

Type 4 hyper

Answer 8

Delayed (cell mediated)

Mech - Sensitized T cells encounter antigen and then release lymphokines (leading to macrophage activation)

4th and last - delayed. Cell mediated, not antibody mediated; therefore it is not transferable by serum

Ex - TB skin test, transplant rejection, contact dermatitis

Question 9

How can you establish causative allergen after acute phase rash has been treated in contact dermatitis?

Answer 9

Patch testing

Question 10

Contact dermatitis

Answer 10

type 4.

Dx is clinical - raised bumpy red lesion in shape of object that caused it. Poison oak/ivy

Tx is avoid triggers, topical diphenhydramine

Question 11

Seborrheic dermatitis (dandruff)

Answer 11

Can be caused by Pityrosporum ovale - a usually harmless yeast found in sebum and hair follicles. Predilection for areas with oily skin

Can present with cradle cap in infants

Dx - rule out psoriasis and contact dermatitis

Tx - selenium sulfide or zinc pyrithione shampoos for scalp. Topical antifungals and/or topical corticosteroids for other areas in adults. Cradle cap often resolves with routine bathing and application of emollients in infants

Question 12

Psoriasis

Answer 12

T cell mediated

Presentation - silvery, scaly plaques that are not itchy most of the time. Less than 10% have arthritis. Extensive disease is associated with depression*

Treatment

Local disease

1) Topical high potency steroids: fluocinonide, triamcinolone, betamethasone, clobetasol
2) Vit A and Vit D ointment help get patient off steroids. The Vit D agent is calcipotriene. Streroids cause skin atrophy bc they inhibit collagen formation and growth (steroids try to convert all amino acids to glucose for gluconeogenesis)
3) Coal tar preparation
4) Pimecrolimus and tacrolimus are used on more delicate areas such as face and penis. They are an alt to steroids and are less potentially deforming

Extensive disease

1) UV light
2) anti TNFa (etanercept, adalimumab, infliximab). These agents can be miraculous in efficacy for severe disease. Can reactivate TB tho. Screen with PPD prior to using.
3) Methotrexate - used last bc of adverse effects on liver and lung. Drug of last resort except in psoriatic arthritis.

Question 13

Auspitz sign

Answer 13

Bleeding when scale is scraped (psoriasis)

Question 14

Rash commonly involving extensor vs flexor surfaces?

Answer 14

Extensor - think psoriasis

Flexor - think atopic dermatitis

Question 15

Pityriasis Rosea

Answer 15

Looks like secondary syphilis but spares palms and soles

Starts out with single lesion (herald patch) then disseminates

Scaly, salmon colored

Dx - clinical. Rule out syphilis with RPR then tx with steroids

Question 16

What drugs commonly cause hypersensitivity reactions?

Answer 16

Drugs that cause hypersensitivity reactions of the skin are the same (generally) that cause hemolysis, interstitial nephritis, and often drug-induce thrombocytopenia (not heparin tho)

1) Penicillins
2) Sulfa drugs (thiazides, furosemide, sulfonylureas)
3) Allopurinol
4) Phenytoin
5) Lamotrigine
6) NSAIDs

Question 17

Severity of dif drug reaction types

Answer 17

Most severe - TEN. Steroids do NOT help. Treat with IVIG

SJS - Steroids prob dont work. IVIG used

EM - Prednisone may benefit some patients

Least severe - morbilliform rash - skin stays intact without mucous membrane involvement. No specific therapy

Question 18

EM and HSV

Answer 18

EM is often triggered by HSV infection of the lip. Other common triggers are drugs and mycoplasmal infections

Question 19

EM exam and history

Answer 19

1) Disease can occur on mucous membranes, where erosions are seen. Typically lesions start as red macules that become centrally clear and then develop a blister. Palms and soles are OFTEN affected (order RPR)
2) May be associated with systemic symptoms, including fever, myalgias, HA, and arthralgias
3) In minor form, disease uncomplicated and localized to skin. EM major can lead to TEN or SJS tho.

Question 20

Tx for EM

Answer 20

Symptomatic only. Systemic steroids are of no benefit.

Minor cases can be treated with antipyretics; major cases should be treated as burns

Question 21

Erythema Nodosum

Answer 21

A panniculitis (inflammatory process of the subq adipose tissue) whose triggers include infection (Strep, Coccidio, Yersinia, TB), drug reactions (sulfonamides, various ABx, OCPs), and chronic inflammatory diseases (sarcoid, Crohn, UC, Behcet’s)

History and exam

1) Painful, red nodules appear on patient’s lower legs and slowly spread turning brown or gray. Patients may present with fever and joint pain
2) Patients with EN may have false positive VDRL (just like SLE)

Dx

1) Clinical
2) Workup can include ASO titer, PPD test in high risk patients, CXR to rule out sarcoid, or a small bowel series to rule out IBD based on patient’s complaints

Tx - remove triggering factor and treat underlying disease where possible. NSAIDs can be used.

Question 22

Staph Scalded Skin Syndrome

Answer 22

SSSS seen in kids under 6 and has infectious etiology. Don’t confuse with SJS/TEN

Question 23

Bullous pemphigoid

Answer 23

1) Anatomic location of blisters - BM zone
2) Autoantibodies - Anti-bullous pemphoid antigen
3) Blister appearance - firm, stable blisters. May be preceded by urticaria
4) Nikolsky - neg
5) Mucosal involvement - rare
6) Patient age - usually greater than 60
7) Associated medication triggers - Generally idiopathic
8) Mortality - Rare and milder course
9) Dx - Clinical features, skin bx with IF and/or ELISA
10) Tx - Steroids (prednisone)

AI to hemidesmosomes down “bullow”

Thick walled blister. Linear IF. Blisters usually fluid filled.

Question 24

Pemphigus vulgaris

Answer 24

1) Anatomic location of blisters - intraepidermal
2) Autoantibodies - anti-desmosglein (responsible for keratinocyte adhesion)
3) Blister appearance - Erosions are more common than intact blisters owing to lack of keratinocyte adherence
4) Nikolsky - Pos
5) Mucosal involvement - common
6) Patient age -40-60
7) Associated medication triggers - ACEIs, penicillamine, phenobarbital, penicillin
8) Mortality - possible
9) Dx - same as for BP
10) Tx - High dose steroids (prednisone) plus immunotherapy (IVIG, MMF, Rituximab)

If will show antibodies everywhere there used to be desmosomes (basically everywhere). Will see tombstoning on bx.

The bad one is “vulgar”