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Block 6; Week 2-Michelle > Hunter-Type I Hypersensitivity > Flashcards

Hunter-Type I Hypersensitivity Flashcards

1
Q

Give some examples of secondary immunodeficiency.

A

HIV
malnutrition
immunosuppressant drugs

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2
Q

What are 2 names for when the immune system goes from being the hero to being the bad guy? What are some examples of this?

A

immunopathology & hypersensitivity diseases

Ex: allergy, rejection of a grafted organ, autoimmunity

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3
Q

T/F There is immunopathology even when a healthy immune system is attacking a bad pathogen.

A

True. B/c when you attack a bad pathogen you get some collateral damage. This is acceptable immunopathology. With bad immunopathology–>the attack & collateral damage becomes the primary damage.

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4
Q

What percentage of Americans have an allergy? What is an allergy?

A

50% of Americans have an allergy.

Allergy: unwanted response of your immune system to innocuous materials. Ex: pollen is not dangerous.

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5
Q

What is more concerning & why–have an allergy to cats or an autoimmune disorder?

A

Autoimmune is more concerning!! You can get rid of your cat, but not your liver!

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6
Q

T/F The immune system can recognize every form of cancer.

A

False. It can only recognize some forms of cancer.

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7
Q

T/F If you have an autoimmune disease…with proper treatment you can return to self tolerance.

A

FALSE. You can never return. perhaps one day you will be able to with gene therapy.

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8
Q

There are ___ types of hypersensitivity reactions according to the ________ classification.

A

4 types

Coombs-Gell

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9
Q

What is Type I Hypersensitivity? Which immune reagent activates it?

A

Allergies!

IgE mediated

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10
Q

What type of antigen do you usu see in Type 1 reactions?

A

soluble antigens

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11
Q

What is the effector mechanism in Type 1 reactions?

A

mast cell activation

also eosinophil activation

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12
Q

What are some examples of Type 1 reactions?

A

allergic rhinitis, allergic asthma, atopic eczema, systemic anaphylaxis, some drug allergies

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13
Q

T/F Some types of Type 1 reactions are autoimmune by nature.

A

FALSE. They are all created by extrinsic things. No autoimmune.

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14
Q

Which immune reactant is involved in Type II hypersensitivities? What types of reactions are these?

A

IgG mediated

autoimmune…responds to things on our own cell surface receptors & ECM etc. Antibodies made against self tissue.

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15
Q

What is the immune reactant involved in Type III hypersensitivities? What types of reactions are these?

A

IgG mediated

immune complexes formed (antibody-antigen)

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16
Q

What is the immune reactant involved in Type IV hypersensitivities? What types of reactions are these?

A

involves T cells (Th1, Th2, CTL)

do their thing & cause some tissue damage in the process, some autoimmune & some extrinsic

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17
Q

What is another name for an allergy?

A

immediate hypersensitivity

Note: allergies have both immediate & delayed effects

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18
Q

What is an example of a delayed hypersensitivity?

A

TB…when you get the PPD test–you have to check hours later for the reaction.

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19
Q

What is the nature of the antigens in Type I reactions?

A

they are small & soluble antigens

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20
Q

What is found in the granules of mast cells that are activated in a Type I Hypersensitivity reaction?

A

they contain lots of mediators for attack

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21
Q

What was the Type I mechanism originally made to do?

A

attack metazoan parasites. Like worms. Now, they react to innocuous things.
Esp: IgE mediated killing of worms by eosinophils
**worms release things that prompt the reaction

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22
Q

What were the mast cells of the Type I response originally intended to do?

A

expel parasites
think of the effects of histamine: rapid contraction of the gut, explosive diarrhea, projectile vomiting–moves worms out of the gut.
**this comes with cross-linking anti-parasite IgEs on mast cells

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23
Q

What is a schistosome?

A

these are worms found in your blood

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24
Q

What are some inhaled materials that could potentially be the extrinsic allergens of Type I hypersensitivity?

A

plant pollen
dander of domesticated animals
mold spores
feces of very small animals–such as house dust mites

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25
Q

What are some injected materials that could potentially be the extrinsic allergens of Type I hypersensitivity?

A

insect venoms
vaccines
drugs
therapeutic proteins

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26
Q

What are some ingested materials that could potentially be the extrinsic allergens of Type I hypersensitivity?

A

food

orally administered drugs

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27
Q

An allergen gets to the surface of mucosa. It crosses the mucosa. It comes in contact with a _____ cell. What happens next?

A

dendritic cell

  • *confused with a metazoan parasite so a cytokine soup is released.
  • *this makes the immature effector T cell differentiate into Th2 cell. This helper cell activates a B cell that has a receptor for the allergen.
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28
Q

What are the substances that make up the cytokine soup that forces the Th2 pathway?

A

IL-4, IL-5, IL-9, IL-13

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29
Q

If you don’t go down the Th2 pathway…what is the other option? Describe this.

A

Th1 pathway.
This is NOT an allergic response.
This pathway is favored in the presence of IFN gamma, IL-12

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30
Q

T/F Allergens can be proteins, carbs, nucleotides.

A

False. THey are proteins. Then after being chewed up by an APC, a peptide is presented on the MHCII molecule.

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31
Q

T/F Any person who is exposed to an allergen will become allergic to it. Why or why not?

A

False. B/c you have to have the genetic code for the MHCII molecule that recognizes that allergen. You will of course have a T cell that will recognize it no matter what. This applies to autoimmune disease as well–MHCII is the culprit.

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32
Q

T/F Less than 1 microgram/year of ragweed pollen is enough to produce an extended allergic response.

A

True! Crazy.

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33
Q

B cells present allergen peptides on MHC Class II to CD4 TH2 cells that produce cytokines like IL-4 and express CD40L. Then IL-4/IL-4R & CD40L/CD40 costimulatory signaling activates what & promotes what?

A

activates the B cell
promotes isotype switching to IgE
**Note: Get allergen, get Th2…get cytokine release w/ T & B cell interaction–>helps with isotope switching.

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34
Q

What is the order of the antibody classes produced? First 3…

A

First: IgM
Second: IgG
Third: IgE

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35
Q

What would happen if the isotope switching didn’t get all the way to IgE, but stopped at IgG?

A

it would actually be protective. This is immunotherapy.

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36
Q

What quality does IgE have that the other Igs don’t have?

A

it is cytophilic.

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37
Q

What are the typical levels of IgE in blood plasma? How does this compare to IgM & IgG levels?

A

IgE levels: 0.1-0.4 micrograms/dL

IgG & IgM levels are much higher.

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38
Q

What is an example of a time when IgE levels would be super elevated in blood plasma?

A

**when there is a severe allergic response

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39
Q

One of the more minor reasons that IgE levels are lower in the plasma (in a misleading way) is that they are bound to which cells? Via which receptor?

A

Bound to mast cells, basophils, eosinophils
via FcepisilonRI
Note: eosinophils only express this receptor when activated, the other 2 cells always express it.

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40
Q

What happens with a person’s first exposure to an antigen?

A

You are exposed & have no allergic response at first. The pollen interacts with an APC. T cells deviate in the Th2 direction. T cells come in contact with B cells of the lymph node. IL-4 drives B cells to produce IgE. This IgE binds to mast cells.

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41
Q

What happens with a person’s second exposure to an antigen?

A

there is an acute release of the mast cell contents. Allergic rhinitis-hay fever.

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42
Q

T/F The whole concept of first exposure & second exposure is an example of delayed hypersensitivity.

A

FALSE. Nope.

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43
Q

Where are mast cells found? Which of these mast cells have access to IgE that is produced?

A

Mast cells are found basically everywhere (skin, mucosa, b.v lining)! They all have access. This is why you can have an allergic response to an allergen in your nose & a skin test (allergen on skin).

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44
Q

Review: how does the IgE attach to the mast cell?

A

FCeRI receptor

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45
Q

Describe how the second exposure leads to mast cell degranulation.

A

Allergen cross links IgE on mast cells. Once it reaches a threshold of stimulation, the mast cell will be signaled intracellularly to release its contents via exocytosis. This involves gene transcription of actin filaments etc.

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46
Q

What types of things are contained in the mast cell granules?

A 
Vasoactive amines:  histamine
Proteases:  chymase, tryptase
Prostaglandins:  PGD2
Leukotrienes:  LTC4
Cytokines:  TNF-a
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47
Q

There are 3 pathways that are activated via intracellular signaling in the mast cell. What is their timeframe?

A
  1. happens in minutes; granules
  2. happens in minutes to hours
  3. happens in hours
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48
Q

Describe the 1st pathway in more detail.

A

Pathway #1: Granules contains lots of things, including vasoactive amines & proteases. Causes vascular dilation, smooth muscle contraction, & tissue damage.

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49
Q

Describe the 2nd pathway in more detail.

A

Pathway #2: Enzymatic modification of arachidonic acid. Lipid mediators are formed. Release of prostaglandins & leukotrienes. Causes vascular dilation & smooth muscle contraction. Note: same effect as pathway #1 but on a different time scale.

50
Q

Describe the 3rd pathway in more detail.

A

Pathway #3: Transcriptional activation of cytokine genes. Cytokines, including TNFalpha are released. Inflammation & leukocyte recruitment ensue.

51
Q

Mast cell activation has different effects on different tissues. What is its effect on the GI tract?

A

increased fluid secretion, increased peristalsis

expulsion of the GI tract (diarrhea, vomiting)

52
Q

Mast cell activation has different effects on different tissues. What is its effect on the eyes, nasal passages & airways?

A 
decreased diameter 
increased mucus secretions
congestion & blockage of airways
wheezing, coughing, phlegm
swelling & mucus secretions in the nasal passages.
53
Q

Mast cell activation has different effects on different tissues. What is its effect on the blood vessels?

A

increased blood flow, vessel permeability
increased fluid in tissues & flow to lymph nodes
increased cells & proteins in tissues
increased effector response in tissues
potential hypotension & anaphylactic shock

54
Q

If you have laryngeal edema…how vast is the mast cell activation?

A

we have a systemic issue!

55
Q

T/F The dose & route of allergen administration determines the IgE mediated allergic reaction.

A

TRUE

56
Q

Which allergens have the potential to cause systemic anaphylaxis? What is the route of entry & the response?

A

Allergens: drug, serum, venoms, food
Route: IV (or absorption into blood)
Result: edema, increased vascular permeability, laryngeal edema, circulatory collapse, death

57
Q

What is urticaria?

A

increased vascular permeability

58
Q

What causes acute urticaria, wheal & flare or hives? Which route? What are the results?

A

Allergen: animal hair, insect bites, allergy testing
Route: through skin–>systemic
Results: local increase in blood flow & permeability

59
Q

What causes seasonal rhino conjunctivitis or hay fever? Which route? What are the results?

A

Allergens: pollens (ragweed, trees, grasses), dust-mite feces
Route: inhalation
Results: Edema of nasal mucosa, sneezing

60
Q

What causes asthma? Which route? What are the results?

A

Allergens: cat dander, pollen, dust-mite feces
Route: inhalation
Results: bronchial constriction, increased mucus production, airway inflammation

61
Q

Which allergens often cause food allergy? Which route? Results?

A

Allergens: tree nuts, shellfish, peanuts, milk, eggs, fish, soy, wheat
Route: Oral
Results: vomiting, diarrhea, pruritis (itching), urticaria (hives), anaphylaxis

62
Q

What happens in systemic anaphylaxis?

A

laryngeal edema, bronchoconstriction, peripheral dilation (lower BP). You can’t breathe & you have no BP.

63
Q

T/F Skin testing at an allergist’s office could NEVER be dangerous.

A

False. even the small doses of a skin test could become systemic. That is why allergists have a vial of epinephrine next to them at all times.

64
Q

if you deliver a high dose of an allergen intravenously–>what is the likely reaction?

A

general release of histamine, systemic anaphylaxis

65
Q

If you deliver a low dose of allergen subcutaneously–what is the likely reaction?

A

local release of histamine

wheal & flare

66
Q

If you deliver a low dose of an allergen via inhalation–>what is the likely reaction?

A

allergic rhinitis
increased mucus production
nasal irritation
asthma (due to mucus & bronchial constriction)

67
Q

If you deliver an allergen via ingestion…what is the likely reaction?

A

contraction of intestinal smooth muscle–>vomiting
outflow of fluid into the gut–diarrhea
urticaria or anaphylaxis via systemic diffusion of the antigen

68
Q

Where are house dust mites?

A

Um…everywhere!! Also, year round.

69
Q

What is the scientific name for house dust mites? What is the irritating part?

A

dermatophagoides pteronyssimus

they eat skin cells & give out fecal pellet with the enzyme der p1.

70
Q

What does der p1 do that is not so awesome?

A

it acts on occludin–>gets thru epithelial tight jcns. ONce it gets across the mucosa of the resp tract…it comes into contact with a dendritic cell. Get plasma cells making antibodies. Second time of exposure get mast cell degranulation.

71
Q

What percentage of North Americans are allergic to house dust mite feces?

A

20%

72
Q

Who might display eosinophilia? Which percentage of WBCs are normal for eosinophils & elevated?

A

Normally: 1-3% of WBCs are eosinophils.
Eosinophilia: like 30%!
This is the case for people with worms in their belly or people with constant allergies.

73
Q

Which growth factor is produced by people with allergies that leads to such high levels of eosinophils?

A

IL-5…goes to the bone marrow & prompts the production of eosinophils from the myeloid line

74
Q

What are eotaxins 1 & 2 (CCL11)? What is their fcn?

A
  • *they are chemokines, chemo-attractant molecules

* *they recruit eosinophils to the right site

75
Q

So…a rando eosinophil chillin’ in the blood…does it have Fc3RI?

A

Nope! It isn’t activated. When it is activated…it will have cytophilic IgE

76
Q

Which is a natural born killing machine: mast cell or eosinophil?

A

EOSINOPHIL!!

Its products are super potent & tightly regulated (including its enzymes & leukotrienes)

77
Q

Asthma has both an acute & chronic component. Describe the acute component.

A

Allergen gets into the lungs & arms the mast cells. Second time the allergen comes into the lungs, the mast cells release their granules. You get increased mucus secretion & smooth muscle contraction. This gives some airway obstruction. The THF alpha released by the mast cells increases vascular permeability & you get Th2 cells.

78
Q

Asthma has both an acute & chronic component. Describe the chronic component.

A

Th2 cells release IL-5 & Eotaxins. Thru this release recruitment of eosinophils happens. They release crazy killing substances after they express FC3RI & bind to IgE. So many bad killing substances are released that there is airway remodeling (healing by second intention).
If you get a ton of fibrosis you will eventually have COPD perhaps.

79
Q

What is airway hyper reactivity & why can this be dangerous?

A

this is more neurogenic. Ex: kid w/ asthma goes out into the cold air & experiences bronchoconstriction.

80
Q

Most allergic reactions have both an early & late phase reaction. What is the timeline of this? What is involved in each reaction?

A

Early Reaction: 30 min, vasodilation, congestion, & edema

Late Reaction: 8 hrs, inflammatory infiltrate rich in eosinophils, neutrophils, T cells

81
Q

Describe the complete process of type I hypersensitivity.

A

Allergen crosses the mucosal lining.
Interacts with a dendritic cell.
Dendritic cell releases cytokines.
The Cytokines prompt Th2 deviation.
A costimulatory signal or 3rd signal activates the T cell.
B cell recognizes the antigen.
Th2 helps the B cell to differentiate into a plasma cell
Cytokines present encourage B cell to isotype switch to producing IgE.
Antibodies bind onto the mast cell via FC3RI
Next exposure to the allergen, the mast cell degranulates.
Get an inflammatory response.
Get an immediate & late phase reaction.

82
Q

What is atopy? What percentage of Americans exhibit this?

A

tendency to make exaggerated IgE responses

50% of Americans

83
Q

Which genetic factors favor atopy?

A

Certain MHCII, FC3RI, TH2 cytokine genes.

Note: NOT T cell & B cell genes b/c those can recognize anything! It is an issue of the genes & products listed above.

84
Q

What are the environmental factors that favor atopy?

A

exposure to certain microbial pathogens favors a Th1 deviation. Not an allergic reaction. Maybe Americans are too hygienic, not enough exposure to things when we are young. Th2 deviation more natural.

85
Q

Where is the MHC locus found & on which chromosome?

A

found on 6p21

86
Q

With skin tests, what are 2 important controls to have?

A

A negative control–saline. What no rxn looks like.

A positive control-histamine. What a rxn looks like.

87
Q

What is the proper name of antihistamines? What do they do?

A

diphenhydramine HCl
block histamine H1 receptors
**decreases vascular permeability
**inhibits itching of unmyelinated nerves

88
Q

What is acute asthma treated with?

A

inhaled bronchodilators
beta receptors adrenergic agonists
albuterol
**relaxes bronchial smooth muscle

89
Q

What’s the deal with singulair? What does it treat & how?

A

treats asthma & seasonal allergies

  • *cysteinyl leukotriene receptor antagonists
  • *blocks leukotrienes D4, C4, E4, inhibits bronchoconstriction
90
Q

What are anaphylactic reactions treated with?

A

epinephrine (adrenaline)

  • *Relaxes bronchial smooth muscle, constricts vascular smooth muscle; reforms endothelial tight junctions
  • *has a few side effects on the heart & the brain, but it is a miracle drug!
91
Q

How is chronic inflammation treated?

A

systemic & topical corticosteroids

  • *methylprednisolone
  • *inhibits transcription of many pro-inflammatory genes by blocking NF-kappa beta
  • *blocks the prostaglandin-leukotriene pathway
92
Q

A 25-year-old male is brought by ambulance to the emergency department after collapsing at a restaurant. His history is significant for peanut allergy. Physical exam reveals a blood pressure of 60/30 mm Hg. He has cold, clammy skin, diffuse urticaria, dyspnea, and wheezing. What drug is best to rapidly reverse the man’s symptoms?

A.  	Inhaled b-agonist
B.  	Intravenous b-blocker
C.  	Intravenous methylprednisolone
D.	Oral diphenhydramine
E.	Parenteral epinephrine
F.	Oral Monteleukast
A

E. Parenteral epinephrine

93
Q

T/F With allergies, we can really only treat the symptoms.

A

True.

94
Q

What does omalizumab do?

A

these are anti-IgE antibodies
they bind to the IgE Fc region of mast cells so that IgE can’t bind there!
reduces allergy symptoms

95
Q

What’s the deal with desensitization therapy?

A

this involves injections of a specific antigen
regulatory T cells are inducted
it prevents the Th2 response

96
Q

What do lipoxygenase inhibitors do?

A

inhibit synthesis of specific mediators

97
Q

Describe desensitization therapy in detail.

A

goal is to shift the allergen response from IgE to IgG (from Th2 to Th1).
when more allergen injected intradermally–you get more production of IgG
when the allergen is present in life, the IgG binds all of it up & there is no cross-linking of IgE.
t regulatory cells are also produced that secrete IL-10 & TGF beta & promotes isotype switching to IgG

98
Q

A 5-month-old boy is brought to your office by his mother who is concerned about her son’s intermittent, pruritic rashes. She reports that the rashes started when her son was about 3 months-old and were initially concentrated on his cheeks and around his mouth. Since that time, the rashes seem to come and go and now also intermittently affect his trunk and extremities. He frequently scratches the affected areas. She has treated the condition with various “baby lotions” and is uncertain whether these help. Other than the rash, the boy appears healthy and meeting developmental milestones. Vital signs are within normal limits. His father has a history of asthma. Cutaneous examination reveals symmetric, ill-defined, brightly erythematous, scaling, pink patches on his cheeks and similar, although milder, patches on his trunk and extremities. One of the patches appears to be infected, and Gram stain of an aspirate reveals Staphylococcus aureus.
What does this child likely have?

A

atopic dermatitis aka eczema

**common, lifetime prevalence of 17%

99
Q

How did this child get a staph infection if they have eczema?

A

Staph is a common colonist of our skin. If the kid was scratching…he probably infected himself with the staph.

100
Q

T/F Eczema can be lethal.

A

False.

101
Q

If a child has eczema, what other issues might they also have?

A
  • *often atopic (allergies)
  • *other immunoregulatory abnormalities
  • *Elevated Serum IgE
  • *Eosinophilia
  • *Elevated Serum Th2 cytokines
102
Q

What is the treatment for eczema?

A

avoidance of the irritant
lotions to maintain a healthy epidermis
topical corticosteroids

103
Q

A 10-year-old boy is brought to the ER by his parents with difficulty breathing. They report that he was stung by a honey bee. The stinger is still embedded in the boy’s arm. His vitals include a heart rate of 110, respirations 40, and blood pressure of 90/40. An mild anaphylactic response is diagnosed and the boy is injected with epinephrine IM. The stinger is quickly removed to prevent further envenomization. After 20 minutes his vital signs have improved markedly. He is observed for 6 hours, then discharged home with instructions to see an allergist.
How common is it for something like this to happen? What are some things that you can use for diagnosis?

A

anaphylaxis from insect stings happens in 3% of adults & 1% of children
**can be fatal
**25% of adults are sensitized to venom
Diagnosis: Venom skin tests and venom-specific IgE immunoassays

104
Q

What are some treatment options for people with anaphylaxis from insect stings?

A

IM injection of Epi (better than IV, subcu useless)
allergy consultation
venom immunotherapy

105
Q

Why is it important to remove the stinger in this case?

A

b/c it keeps pumping venom into the poor kid!!

106
Q

What are some examples of IgE mediated hypersensitivity reactions?

A
  • anaphylaxis from beta lactam antibiotics
  • halthane hepatitis
  • hypotension from protamine
  • dermatitis from sulfonamides
  • serum sickness from phenytoin or cofactor
  • hypotension after succinycholine
  • quinine-induced thrombocytopenia
  • phenolphthalein-induced fixed drug eruption
  • cis-platinum-associated urticaria
107
Q

What is haptenation?

A

this is when penicillin attaches to another molecule, maybe a protein thru lysine acylation & forms a hapten-carrier complex
**when haptenation happens, it is possible that a drug-specific immune response will ensue

108
Q

What is the chemical structure in penicillin & in other beta lactam antibiotics that allows for haptenation to happen? What is the clinical significance of this?

A

beta lactam ring

  • *it is inherently unstable
  • *this is found in penicillins, cephalosporins, carbapenems, monobactams
  • *an allergic cross rxn can occur with any of these & perhaps anaphylaxis. Be careful what you give your patient!
109
Q

Describe in detail the reaction to penicillin.

A

**Self proteins can be tagged with the penicilloyl hapten (multi-haptens)
**When taken up in the presence of a “danger signal” (infection), penicilloyl-peptides in certain MHC II molecules can activate CD4 T cells
**This CD4 T cell can interact with a penicilloyl-specific B cell, and IgE anti-penicilloyl antibodies are made
**The cytophilic IgE antibodies can arm mast cells, which can degranulate when exposed to proteins tagged with the penicilloyl hapten
Anaphylaxis!

110
Q

What is the greatest foreign antigenic load that a human body experiences?

A

FOOD!

111
Q

T/F Most people develop tolerance to food allergens.

A

True.

112
Q

What percentage of people struggle with food allergies? How much has the incidence of peanut allergy changed in the Western countriest? What is the proven treatment?

A

8% of children under 5 yo
3.5% of the general population
**peanut allergy has tripled in Western countries in the past decade
Treatment: avoidance of the food allergen

113
Q

PATIENT HISTORY: John was healthy until the age of 22 months, when he developed swollen lips while eating cookies containing peanut butter. The symptoms disappeared in about an hr. A month later, while eating the same type of cookies, he started to vomit, became hoarse, had great difficulty in breathing, started to wheeze and developed a swollen face. He was taken immediately to the emergency room, and on the way he became lethargic and lost consciousness.
CLINICAL FINDINGS: On arrival at the hospital, his blood pressure was catastrophically low at 40/0 mmHg (normal 80/60 mmHg). Pulse was 185 bpm (normal 80-90 bpm), and respiratory rate was 76 per min (normal 20 per min). His breathing was very labored. An anaphylactic reaction was diagnosed.
What should the treatment be?

A

TREATMENT: John was immediately given an intramuscular injection of 0.15 mL of a 1:1000 dilution of epinephrine. An intravenous solution of physiologic saline was started and he was given 25 mg of the anti-histamine Benadryl (diphenhydramine HCl) and 25 mg of the anti-inflammatory corticosteroid Solu-Medrol (methylprednisolone) intravenously. A blood sample was taken to test for histamine and the enzyme tryptase.

114
Q

Then…Within minutes of the epinephrine injection, John’s hoarseness improved, the wheezing diminished and his breathing became less labored. His blood pressure rose to 50/30 mmHg, pulse decreased to 145 bpm and his breathing to 61 per min. However, 30 min later, the hoarseness and wheezing got worse again and his blood pressure dropped to 40/20 mmHg, pulse increased to 170 and respiratory rate to 70.
What should be done for John now?

A

John was given another injection of epinephrine and was made to inhale an aerosolized solution (5 mg/mL) of the b2-adrenergic agent albuterol. This treatment was repeated once more at 30 min. One hr later the child was fully responsive, his blood pressure, pulse, and respirations were 70/50, 116, and 46 respectively. John was admitted to the hospital for further observation. Treatment with Benadryl (25 mg) and Solu-Medrol (1 mg/kg) intravenously every 6 hr was continued for 24 hr, by which time the facial swelling had subsided and his vital signs were normal. He had stopped wheezing and his chest was clear on auscultation.

115
Q

What should be done with follow up for this patient?

A

FOLLOW-UP: John was taken off all medication and observed for another 12 hr. He remained well and was discharged home. His parents were instructed to avoid giving him food containing peanuts in any form. They were referred to an allergist, and John tested positive for peanut allergy by skin test and radioallergosorbent test (RAST). A Medi-Alert bracelet indicating John’s allergy to peanuts was ordered, and his parents were given an Epi-Pen (syringe pre-filled with epinephrine) to keep at home or while traveling in case John developed another anaphylactic reaction.

116
Q

Why did John have a mild response to the peanut butter cookies at first?

A

Sensitization the first one or two times someone is exposed to an allergen.

117
Q

Why was John hoarse & wheezing?

A

Hoarse: laryngeal edema
Wheezing: bronchoconstriction (trying to get air out)

118
Q

Why was John first treated with epinephrine in the ER?

A

to achieve bronchodilation

119
Q

What other drug in the epinephrine family was given to John?

A

Albuterol

120
Q

What was John given a blood test for histamine & tryptase?

A

b/c mast cells would release histamine & tryptase…can theoretically show what kind of a reaction happened.

121
Q

Skin testing for peanuts was not done in the hospital immediately after John recovered. Why?

A

Taxyphylaxis. The mast cells hadn’t recovered yet. The skin test was irrelevant.

Block 6; Week 2-Michelle (8 decks)

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