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Pediatrics- Noelle > Allergy/ immunology > Flashcards

Allergy/ immunology Flashcards

1
Q

By what route should you administer epinephrine for anaphylaxis

A

IM

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2
Q

How often can IM epinephrine be given for anaphylaxis?

A

every 5 to 15 minutes

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3
Q

what is the dose of IM epinephrine

A

0.01 mg/kg to max of 0.5mg

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4
Q

why is subcutaneous epinephrine not recommended for anaphylaxis

A

causes local vasoconstriction which may inhibit absorption

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5
Q

when should you consider IV epinephrine

A

repeated doses of IM epi (typically after 3 doses)

persistent hypotension despite fluid boluses

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6
Q

patients on beta blockers may be resistant to epinephrine, what medication should you consider?

A

glucagon

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7
Q

what are 5 second line agents for anaphylaxis

A
  1. salbutamol
  2. nebulizer epinephrine
  3. H1- antihistamines
  4. H2- ranitidine
  5. corticosteroids
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8
Q

what is the risk of having a biphasic reaction

A

5-20%

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9
Q

when do most biphasic reactions occur

A

4-6h but can occur up to 72 hours

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10
Q

name 3 factors that increase your risk of having a biphasic reaction

A

more than one dose of epinephrine
delayed administration of epinephrine
severe symptoms at presentation

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11
Q

what are the 3 most common causes of anaphylaxis in children

A

food
venom
medications

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12
Q

what is required at discharge for a pt with anaphylaxis

A 
epipen
referral to allergist
anaphylaxis action plan
medical alert bracelet
avoid trigger
consider 3 day course of antihistamines and corticosteroids
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13
Q

what are the most common food allergies (8)

A 
milk
egg
peanuts
tree nuts
shell fish
fish
wheat
soy
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14
Q

what are the advantages of a skin prick test (4)

A

results within 15 minutes
more sensitive then serum specific IgE
cost effective
high negative predictive value

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15
Q

what are the disadvantages of a skin prick test (4)

A

false positives (up to 50%)
affected by the use of antihistamines and corticosteroids
cannot perform if skin disease at the skin
risk of systemic reaction (although low)

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16
Q

what are the advantages of serum specific IgE (3)

A

not affected by antihistamines and corticosteroids
no risk of systemic reaction
can be performed if the patient has skin disease

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17
Q

what are the disadvantages of serum specific IgE (3)

A

false positives if elevated total IgE
more expensive then skin prick test
less sensitive compared to skin prick test

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18
Q

what percentage of children outgrow cows milk protein and egg allergy? peanuts?

A

80% of children outgrow cow’s milk protein and egg allergy

20 % of children outgrow peanut allergy

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19
Q

how should you manage someone with food allergy

A 
Avoidance of responsible food
Oral immunotherapy offered in some centers
Epinephrine auto-injector
Anaphylaxis action plan
Medical identification device
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20
Q

what conditions do we use immunotherapy for? (4)

A

venom allergy
allergic rhinitis
allergic asthma
atopic dermatitis with aeroallergen sensitivity

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21
Q

what is the typical injection schedule for immunotherapy

A

weekly injections for 6 months (build up phase) followed

by monthly injection for 5 years (maintenance phase)

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22
Q

What is cross reactivity between penicillin and

cephalosporins?

A

2%

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23
Q

what is the dose for epipen jr and the weight we use it for

A

0.15mg

10-25kg

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24
Q

what is the dose for epipen and the weight we use it for

A

0.3mg

>25kg

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25
Q

what are the 3 receptors that epinephrine works on

A

a1
b1
b2

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26
Q

What is the first line treatment for chronic urticaria

A

standard dosing non sedating second generation antihistamine

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27
Q

what is the second line treatment for chronic urticaria

A

increase the dose of non sedating second generation antihistamine 4 fold

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28
Q

what is the third line treatment for chronic urticaria

A

montelukast, cyclosporin, omalizumab, short dose of steroids (not more then 10 days)

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29
Q

what is the first line treatment for hereditary angioedema? second line?

A

C1 inhibitor concentrate

FFP

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30
Q

A child has received IVIG in the course of their treatment. How long should you wait before giving them vaccines to ensure adequate response?

A

8-11 months

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31
Q

what are the advantages of second generation antihistamines

A 
less sedating
faster onset
once daily dosing
less anticholinergic effect
fewer drug interactions (do not significantly interact with cytochrome p450 system)
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32
Q

what is the mutation associated with hyper IgM syndrome

A

mutation in CD40 ligand (on x-chromosome)

important for cross talk between t and b cells

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33
Q

what are the laboratory features for hyper IgM syndrome

A 
elevated IgM
low IgA
low IgG
normal T and B cell numbers
50% have neutropenia
poor antibody responses to vaccines
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34
Q

what is the treatment for hyper IgM syndrome

A

PJP prophylaxis
IVIG
HSCT- for immunodeficiency and to prevent malignancy

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35
Q

what type of infections are seen with Hyper IgM syndrome? what liver problems? malignancy?

A

Bacterial infections in 1st year of life
Opportunistic: PJP, Cryptococcus

Autoimmunity
• Cytopenias, arthritis, inflammatory bowel disease

Liver disease
• Sclerosing cholangitis
• Chronic hepatitis

Malignancy (lymphoma) later in life

36
Q

what is Cartilage Hair Hypoplasia?

A

Short-limbed dwarfism and combined

immune deficiency

37
Q

what is the clinical presentation of someone with cartilage hair hypoplasia

A 
Short pudgy hands
hyper-extensible joints
sparse light hair
Hirschsprung’s disease (in some)
immunodeficiency (range from SCID to almost normal)
38
Q

what type of immunodeficiency is IRAK4 Deficiency

A

innate immunodeficiency

39
Q

what is Chronic Mucocutaneous Candidiasis

A

Persistent Candida infection in skin, nails & mucous membranes

40
Q

what type of donor is required for Hematopoietic stem cell transplantation

A

HLA matched donor- ideally a sibling

Alternatively HLA-matched unrelated donor or cord donors

41
Q

what are some adverse effects of IVIG

A

Risk of transmission of blood-borne infections
• Headache, myalgias, fevers, chills
• Aseptic meningitis, anaphylaxis, hemolytic anemia
• Thrombosis, renal complications

42
Q

which PID are inherited in an autosomal dominant fashion (5)

A
  • Hereditary angioedema (C1 inhibitor)
  • Hyper IgE syndrome (STAT3)
  • DiGeorge syndrome (22q11 microdeletion)
  • Autoimmune lymphoproliferative syndrome (Fas)
  • Chronic mucocutaneous candidiasis (STAT1)
43
Q

which PID are inherited in an x-linked recessive fashion (8)

A

X-linked agammaglobulinemia (BTK)
X-linked SCID (IL2Rγ)
Hyper IgM syndrome (CD40 ligand)
Wiskott-Aldrich syndrome (WAS)
X-linked lymphoproliferative disease (SH2D1A)
IPEX (FoxP3)
X-linked chronic granulomatous disease (gp91phox)
X-linked dyskeratosis congenita (dyskerin)

44
Q

what does IPEX stand for

A

Immune Dysregulation
• Infections not typically significant feature
Polyendocrinopathy
•Neonatal or infantile insulin dependent diabetes
Enteropathy
•Severe colitis
X-Linked

45
Q

what is the mutation associated with IPEX

A

Mutations in FoxP3: defect in regulatory T

cells

46
Q

what infection is seen with X-Linked Lymphoproliferative Disease

A

Selective inability to respond to EBV infection
75% develop severe/fatal infectious mononucleosis with
hepatic necrosis & bone marrow failure

47
Q

List 3 Diseases of Immune Dysregulation

A
  • Autoimmune Lymphoproliferative Syndrome (ALPS)
  • IPEX
  • X-linked lympophoproliferative disease (XLP)
48
Q

what are symptoms of allergic rhinitis

A 
nasal congestion
rhinorrhea (clear and bilateral)
sneezing 
postnasal drip (cough, throat clearing)
ocular itch
49
Q

what are some physical exam findings for allergic rhinitis

A 
allergic shiners
dennie Morgan lines
allergic salute (horizontal line on nose)
open mouth
enlarged pale nasal turbintes
cobblestonning in posterior oral pharynx
50
Q

what are the treatment options for allergic rhinitis

A

allergen avoidance
intranasal corticosteroids (mometasone, fluticasone, ciclesonide)
second generation antihistamine (cetirtizine, loratadine)
leukotriene receptor antagonist (montelukast)
immunotherapy

51
Q

type 1 hypersensitivity reactions are mediated by what cells

A

IgE mediated

52
Q

how do you diagnose a penicillin allergy?

A

skin prick test (to major and minor determinants- 20 percent are due to minor determinants)
graded oral challenge

53
Q

how do you treat acute graft versus host disease

A

Acute GVHD is usually treated with glucocorticoids; about 40-50% of patients show a complete response to steroids.

54
Q

what are the manifestations of acute graft versus host disease

A

erythematous maculopapular rash
persistent anorexia
vomiting and/or diarrhea
liver disease with increased serum levels of bilirubin, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase

55
Q

what are the two types of GVHD

A

acute GVHD- within 3 months

chronic GVHD- after 3 months

56
Q

what are the manifestations of chronic graft versus host

A

Scleroderma-like, skin, joints, eyes, lungs, bone marrow, gut

57
Q

if you are ordering IgG, IgM, IgA, IgE what must you order with it?

A

have to do albumin and total protein

58
Q

if you are worried about T cell deficiency what must you rule out?

A

HIV

59
Q

what is the long term treatment for hereditary angioedema

A 
education on trigger avoidance (trauma, early and prompt recognition and treatment of oral/dental infection, meds (estrogens, ACE))
medical alert bracelet
written plan for acute attacks
hepB vaccine (incase they need blood products in the future)
long term prophylaxis: 
       c1 inhibitor concentrate
      androgens
      antifibrinloytics (TA)
60
Q

what is the difference in body surface area for SJS versus TEN

A

SJS<10%
TEN >30%
Tx= supportive

61
Q

what is the rash that is seen with erythema multiforme?

A

target lesions

can sometimes have mucosal membrane involvement

62
Q

what are the symptoms of serum sickness

A 
Rash
arthralgia / arthritis 
renal disease
fever
low complement
63
Q

what is the treatment for serum sickness

A

Discontinue medication
NSAIDS, analgesics
Steroids, plasmapheresis for severe cases

64
Q

what is the difference between serum sickness and serum sickness like?

A

there is NO renal disease

normal complement

65
Q

serum sickness like is often caused by what two antibiotics

A

cefaclor

penicillin

66
Q

How do patients with egg allergy get MMR, influenza vaccine and yellow fever?

A

¤ MMR vaccine: receive as single dose
¤ Inactivated influenza vaccine: receive as single dose with post vaccination monitoring same as any other vaccine
¤ Live attenuated influenza vaccine: receive as single dose
with post vaccination monitoring same as any other vaccine
¤ Yellow fever: requires skin testing with vaccine prior to
administration

67
Q

what are some causes of acute urticaria?

A 
food
meds
NSAIDS
lasix
venom

infection
idiopathic

68
Q

what are some causes of chronic urticaria?

A 
cold
heat
exercise
water
solar
cholinergic
vibration
dermatographism
idiopathic
69
Q

how do patients with pollen food allergy syndrome present?

A

Oropharyngeal pruritus with ingestion of uncooked fruits, vegetables, spices, peanuts and tree nuts

70
Q

what should a patient do if they have pollen food allergy syndrome?

A

Isolated oropharyngeal symptoms should avoid the raw foods but can have cooked foods

Systemic reactions should avoid all forms of the food and carry epinephrine auto-injector

71
Q

what are the symptoms of DRESS (drug rash with eosinophilia and systemic symptoms)? what is the onset after drug?

A 
Onset 1 - 8 weeks of drug exposure
Rash
eosinophilia
hepatic dysfunction
fever
facial angioedema
lymphadenopathy
72
Q

what is the treatment for poison ivy dermatitis?

A

mid potency topical steroid for 2-3 weeks

73
Q

what is the name for poison ivy and what is it caused by?

A

Rhus dermatitis (poison ivy, poison sumac, poison oak), a response to the plant allergen urushiol,

74
Q

what is an example of a type 1 hypersensitivity reaction and what is the effector cell?

A

IgE

anaphylaxis

75
Q

what is an example of type 3 hypersensitivity reaction and what is the effector cell?

A

immune complexes (antigen-antibody)- IgG or IgM
serum sickness
serum sickness like
SLE

76
Q

what is an example of type 4 hypersensitivity reaction and what is the effector cell

A 
T cell mediated (lymphocytes)
contact dermatitis
TB skin test
SJS
DRESS
77
Q

what is the only immunoglobulin that crosses the placenta?

A

IgG

78
Q

what is the innate immune system and what are 4 defensive barriers?

A

it is the first line defence to an intruding pathogen

  1. anatomic (skin, mucous membrane)
  2. physiologic (pH, temperature, chemical)
  3. Phagocytic (Neutrophils, monocytes, macrophages)
  4. inflammation
79
Q

High tryptase can indicate what?

A

systemic mastocytosis

80
Q

Acute graft versus host affects what 3 things?

A

skin, liver, GI tract

81
Q

what are two common causes of erythema multiforme

A

HSV

Mycoplasma

82
Q

what two medication classes cause SJS/TEN

A

sulfonamides

anticonvulsants

83
Q

what class of medication is associated with DRESS

A

anticonvulsants

84
Q

what causes hereditary angioedema

A

C1 esterase inhibitor deficiency

tx: C1 inhibitor (blood product)

85
Q

what is an example of Type 2 hypersensitivity reaction

A

rh hemolytic disease of the newborn

86
Q

what is the criteria for anaphylaxis?

A

Acute onset of an illness (minutes - hours) with involvement of the skin, mucosal tissue or both and at least one of the following:
Respiratory compromise
Reduced BP or associated symptoms of end-organ dysfunction

Two or more of the following that occur rapidly after exposure to a likely allergen for that patient:
Involvement of the skin-mucosal tissue
Respiratory compromise
Reduced BP or associated symptoms of end-organ dysfunction
Persistent gastrointestinal symptoms (eg, crampy abdominal pain or vomiting)

Reduced BP after exposure to a known allergen for that patient (minutes to hours)
Infants and children: low systolic BP (age specific) or greater than 30% decrease in systolic BP*

Pediatrics- Noelle (28 decks)

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