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Flashcards in Immune Mediated Disorders Deck (54)
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0
Q

Type II hypersensitivity

-MOA, mediated by, examples

A

Cytotoxic allergy

MOA: IgM and IgG bind to the antigen, causing lysis by complement or phagocytosis

Mediated by antibodies and complement -> MAC

Examples: autoimmune hemolytic anemia, erythroblastosis fetalis, Goodpasture’s syndrome, rheumatic fever

1
Q

Type I hypersensitivity

-MOA, mediated by, examples

A

Anaphylactic and atopic hypersensitivity

MOA: Specific IgE antibodies against an antigen are bound to mast cells and basophils; when triggered, they cause release of vasoactive amines (histamine)

Rapid reaction (first and fast)
Antibody mediated

Examples: anaphylaxis, asthma, urticarial drug reactions, local wheal and flare

2
Q

Type III hypersensitivity subgroups

A

Serum sickness, immune complex, arthus reaction

3
Q

Immune complex

-MOA, examples

A

Antigen-antibody complex activates complement which attracts PMNs; these PMNs release lysosomal enzymes

Includes many glomerulonephritides and vasculitides ie PAN, immune complex glomerulonepritis, SLE, rheumatoid arthritis

4
Q

Serum sickness

-MOA, types and symptoms

A

Antibodies to foreign proteins are formed in around 5 days
Immune complexes then form and are deposited in membranes and lead to tissue damage 2/2 complement activation

Types: most serum sickness is now caused by drugs and not serum
-fever, urticaria, arthralgieas, proteinuria, LAD 5-10 days after antigen exposure

5
Q

Arthus reactions

-MOA and types

A

MOA: local reaction to antigen by preformed antibodies leading to vascular necrosis and thrombosis

This occurs rarely 4-12 hours after a vaccination

Causes hypersensitivity pneumonitis

6
Q

Type IV hypersensitivity

-MOA, types

A

MOA: this is a delayed hypersensitivity mediated by sensitized T lymphocytes; they encounter antigens and release lymphokines which activate macrophages
-cell mediated, THE ONLY ONE THAT IS

Examples: Tb skin test, transplant rejection, contact dermatitis

7
Q

Symptoms of atopic dermatitis

A

Pruritis leading to lichenification. Differs by age groups

Increases risk of bacterial (S aureus) and viral (HSV and molluscum) superinfection

8
Q

Atopic dermatitis in infants

-what kind of rash, where on body

A

Erythematous, edematous, weeping, pruritic papules and plaques present on the face, scalp, and extensor surfaces
Diaper area is usually spared

9
Q

Atopic dermatitis in children

-rash description and where

A

Dry, scaly, pruritic, excoriated papules and plaques in the flexural areas and neck

10
Q

Atopic dermatitis in adults

-presentation and where

A

Lichenification and dry, fissured skin
Flexural distribution
Often has hand or eyelid involvement

11
Q

Assocations with atopic dermatitis

A

Asthma and allergic rhinitis

12
Q

First line therapy for eczema

A
Aka atopic dermatitis
Topical corticosteroids = 1st line. DO NOT USE LONGER THAN 2-3 WEEKS
Topical immunomodulators (tacrolimus, pimecrolimus) for moderate to severe asthma in patients > 2 y/o
13
Q

Atopic dermatitis vs contact dermatitis

A

Eczema vs. type IV hypersensitivity (poison oak)

Eczema can be present in many places, usually as excoriations
Poison oak usually is present on contact surfaces and is weeping with erythematous papules and vesicles

14
Q

Erythema toxicum neonatorum

A

A rash that resembles eczema, present in neonates about 1-3 days after delivery
Red papules, pustules, and/or vesicles with surrounding erythematous halos
Eosinophilia in the pustules/vesicles
Benign rash that resolves in 1-2 weeks with no treatment

15
Q

Infant w/ hx of eczema treated w/ corticosteroids has new-onset rash and fever, showing grouped vesicles involving eczematous areas of the extremities and face. What is it and how to treat?

A

Eczema herpeticum
Superinfection of HSV on eczema
Medical emergency because HSV has a propensity to spread systemically
Tx w/ IV acyclovir

16
Q

Common contact dermatitis allergens

A

Poison oak, poison ivy, nickel, soaps/detergents/cosmetics, rubber products containing latex

17
Q

Treatment of contact dermatitis

A

Topical or systemic corticosteroids

Cool, wet compresses to soothe crusted lesion

18
Q

Types of dermatitis

A

Atopic dermatitis (eczema) vs. contact dermatitis (type IV hypersensitivity) vs. seborrheic dermatitis (Pityrosproum ovale (fungal) infection)

19
Q

Cause of seborrheic dermatitis

A

Pityrosporum ovale, usually in oily skin

20
Q

What diseases are associated with seborrheic dermatitis?

A

HIV and Parkinsons disease

21
Q

Appearance of seborrheic dermatitis in infants and children/adults

A

Infants: severe, red diaper rash. yellow scaling, erosions, and blisters. thick crust develops on scalp (cradle cap)

Children/adults: red, scaly patches around ears, eyebrows, nasolabial folds, midchest, scalp; less severe than in infants

22
Q

Treatment of seborrheic dermatitis

A

Selenium sulfide
Zinc pyrithion shamppos for the scalp
Topical antifungals
Topical corticosteroids for other areas in adults

23
Q

Psoriasis: what causes it and describe the rash

A

Cause: T cell mediated inflammatory dermatosis

Rash: erythematous plaques with silvery scales 2/2 dermal infalmmation and epidermal hyperplasia

Nails: pitting, oil spots, and onycholysis (lifting of the nail plate)

24
Q

Location of rash in psoriasis

A

Extensor surfaces (elbow, knee, scalp, lumbosacral regions)

25
Q

Rash that affects extensor surfaces is….?

Rash that affects flexor surfaces is….?

A

Psoriasis

Eczema (atopic dermatitis)

26
Q

Koebner’s phenomenon

A

Psoriatic lesions that are provoked by local irritation or by trauma

27
Q

Medications that can induce psoriasis

A

B-blockers, ACEi, lithium

28
Q

Dx of psoriasis

A

Clinical: Auspitz sign ie bleeding when scale is scraped
Biopsy: thickened epidermis elongated in rete ridges, absent granular cell layer, preservation of nuclei in the stratum corneum (parakeratosis), and a sterile neutrophilic infiltrate in the stratum corneum

29
Q

Munro’s microabscess

A

Biopsy finding in psoriasis: sterile neutrophilic infiltrate in the stratum corneum

30
Q

Tx of psoriasis

A

Topical steroids + keratolytic agents, tar OR
anthralin + UV therapy
MTX for severe cases
Vitamin A (retinoids) and Vitamin D3 analogs can be helpful

31
Q

What condition is associated with psoriasis?

A

Seronegative arthritis (psoriatic arthritis)

32
Q

What are urticara?

A

Hives: superficial, intense erythema and edema in a localized area
Type I hypersensitivity response: histamine and prostaglandin release

33
Q

Urticaria rash description

A

Elevated papule or plaque that is reddish or white and variable in size. These lesions are widespread and last a few hours

34
Q

Extracutaneous manifestation of hives

A
i.e. in severe allergic reactions
Tongue swelling and angioedema
Asthma
GI symptoms
Joint swelling
Fever
35
Q

Tx of urticaria

A

Systemic antihistamines

Anaphylaxis: IM epinephrine, IVF, antihistamines, airway maintenance

36
Q

Hospitalized patient who develops a cutaneous rash?

A

Likely a drug reaction. They can take many forms (all 4 types of hypersensitivities)

37
Q

Time-course of drug eruption

A

Reaction occurs 7-14 days after exposure
If a patient reacts within 1-2 days, that drug is probably not the causative agent
Relatively short-lived, disappears within 1-2 weeks after removal of the offending agent

38
Q

Description of typical drug eruption

A

Widespread, symmetrical, pruritic

39
Q

More widespread form of Stevens Johnson disease?

A

Toxic epidermal necrolysis
SJS < 10% of body surface area
TEN > 30% of body surface area

40
Q

Targetoid lesions are caused by?

A

Erythema multiforme
Erythematous macuels that become centrally clear and develop a blister
Usually affects palms and soles
a/w fever, myalgias, headaches, arthralgias

41
Q

Complication of erythema multiforme?

A

Stevens Johnson or toxic epidermal necrolysis

42
Q

Erythema nodosum description

A

Painful, erythematous nodules (paniculitis ie inflammation of subcutaneous adipose tissue) that appear on lower legs and slowly spread. They turn brown or gray, and p/w fever and joint pain
May have false VDRL

43
Q

Erythema nodosum triggers

A

Infection: Streptococcus, Cocci, Yersinia, Tb
Drug reactions: sulfonamides, various antibiotics, and OCPs
Chronic inflammatory diseases: sarcoid, Crohn’s disease, UC, Behcet disease

44
Q

Workup for erythema nodosum

A

ASO, PPD, CXR, small bowel series

Strep, Tb, Sarcoid, IBD

45
Q

Tense vs. flaccid blisters

A

Bullous pemphigoid vs. pemphigus vulgaris

46
Q

Nikolky’s sign

A

Sloughing off of skin with light rubbing

Present in Stevens Johnson, toxic epidermal necrolysis, pemphigus vulgaris

47
Q

Scalded skin syndrome vs. Stevens Johnson/TEN

A

Scalded skin: caused by Staph, usually affects children

SJ/TEN: caused by drugs, usually affects adults

48
Q

History of Stevens Johnson and TEN

A

Preceded by EM, flulike prodrome, skin tenderness, maculopapular drug rash, painful mouth lesions
Exam: severe mucosal erosions with widespread erythema, dusky red/purpuric macules or atypical targeoid lesions

49
Q

Biopsy results of Stevens Johnson vs. TEN

A

Stevens Johnson: degeneration of basal layer of epidermis

TEN: full-thickness eosinophilic epidermal necrosis

50
Q

Treatment of SJ and TEN

A

Treat like burn victims
Skin coverage, maintenance of fluid and electrolyte balance
Systemic corticosteroids in early disease

51
Q

Blistering skin conditions

A

Bullous pemphigoid vs. pemphigus vulgaris

52
Q

Bullous pemphigoid
-location of blisters, what antibodies, blister appearance, Nikolsky’s sign, mucosal involvement, patient age, associated medication triggers, mortality, diagnosis, treatment

A
Location: basement membrane zones
Abs: anti-bullous pemphigoid antigen
Blister appearance: firm, tense, stable blisters; preceded by urticaria
Nikolsky sign is negative
Mucosal involvement is rare
Age is usually > 60
Medication triggers: idiopathic
Mortality: rare and milder course
Diagnosis: clinical features, skin biopsy w/ immunofluorescence and/or ELISA
Treatment: prednisone
53
Q

Pemphigus vulgaris
-location of blisters, what antibodies, blister appearance, Nikolsky’s sign, mucosal involvement, patient age, associated medication triggers, mortality, diagnosis, treatment

A

Location: intraepidermal
Abs: anti-desmogelin (desmoglein is responsible for keratinocyte adhesion)
Appearance: erosions are more common (ie popped blisters) due to the lack of keratinocyte adherence; flaccid blisters
Nikolsky sign positive
Mucosal involvement is common
Age: 40-60
Medication triggers: ACEIs, penicillamine, phenobarbital, PCN
Mortality is possible
Dx: clinical features, skin biopsy w/ IF, and ELISA
Tx: high dose prednisone + IVIG/MMF/rituximab