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Yr 3 - December lectures 2018 > Allergy and allergic disease > Flashcards

Allergy and allergic disease Flashcards

1
Q

What are the different types of type 1 allergies?

A

aeroallergy
- hay fever, allergic asthma, atopic dermatitis
food allergy
drug allergy
venom allergy
the way a person reacts can be very different

mediated by IgE antibodies

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2
Q

What is the prevalence of allergies and how did they impact people’s lives?

A

1: 3
- QoL
- concentration
- performance - work, exams, school
- socialisation
- diet
- sleeping/snoring
- anxiety

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3
Q

Why has there been an increase in allergy?

A

no single factor explains the rise - combo of genetic and environmental
Hygiene hypothesis - all too clean now => lack of exposure to germs, skews Th1 cell response to a Th2 cell response

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4
Q

What are the key characteristics of type 1 allergies and their Tx?

A

IgE mediated

  • immediate - within minutes of exposure - rapid mast cell degranulation
  • life-threatening

Tx- avoidance, antihistamine, adrenaline, steroids

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5
Q

What are the key characteristics of type 4 allergies and their Tx?

A

T cell mediated
> 4 hours, often a day or 2 after antigen exposure
Tx = avoidance, steroids
much less severe than type 1

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6
Q

What is the process of developing a type 1 allergy?

A

1) allergen exposure
2) sensitization => can’t have a reaction on 1st exposure
3) specific IgE production
4) Re-exposre to allergen = acute allergic response
5) Long-term exposure leads to chronic inflammation or tolerance e.g. chronic asthmas - scarring and remodeling - can desensitize by giving them a higher dose than normal exposure in environment

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7
Q

What are the molecules involved in type 1 allergy and what happens?

A

antigen activates IgE (antibody class that can stimulate allergy cells)

  • high affinity receptor on mass cell that cross link the antigen and IgE
  • allergy cell that releases substances that cause allergic symptoms
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8
Q

What are the mast cell mediators and what do they cause?

A

histamine, prostaglandin, leukotrienes, PAF, tryptase

  • vasodilation (erythema)
  • vascular permeability (swelling)
  • heart rate, cardiac contraction - hypotension
  • glandular secretion - IL13 release
  • bronchoconstriction
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9
Q

What are some examples of how mild and severe allergic diseases vary?

A

Mild

  • hay fever - mild intermittent nose itching
  • eczema - mild itching of skin
  • asthma - intermittent wheeze
  • food allergy - mild oral itching

Severe

  • persistent nasal blockage, asthma periorbital swelling
  • fatal bronchospasm
  • fatal anaphylaxis
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10
Q

What is hay fever?

A

allergic rhinitis

  • allergic response to aeroallergens (pollen, dust mites)
  • effects barrier areas: - resp tract and eyes (mucosal surfaces)
  • rhinorea = watery eyes
  • affects 20% pop
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11
Q

What are the nasal and eye symptoms of hay fever?

A

Nasal - itching, rhinorrhoea, sneezing

eyes- allergic conjunctivitis, tears, itching, redness

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12
Q

Why is it important to discuss when pts get hay fever?

A

it can help to identify what causes their hay fever
- e.g. tree pollen tends to be high in spring, grass pollen tends to be higher in early/mid summer, fungal spores tend to higher mid/late summer

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13
Q

What tests are available to support history?

A

serum specific IgE - helpful to back up history but sensitivity and specificity only 60-80%, false positives (atopic dermatitis)
total IgE - guide, helps interpret ssIgE
Skin prick tests = more sensitive than ssIgE

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14
Q

What happens in skin prick tests and what do they rely on?

A

relies on IgE mediated local reaction
- gives immediate answer
itchy, doesn’t really hurt
results within 20 mins

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15
Q

What are some examples of unproven allergy tests and what are the problems with them?

A

hair analysis, pulse test, cytotoxic food testing, ELISA/ACT

- a lot of these are actually for intolerances and therefore are not that helpful

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16
Q

How easy is it avoid allergens?

A

animal dander is straightforward= don’t have pets
grass, dust mites, moulds are much more difficult
therefore if you can’t avoid them you need to treat them

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17
Q

How is mild intermittent rhinitis treated?

A

allergen avoidance
douching
nasal or oral antihistamine = nasal sprays need to taken properly, head all the way forward to be effective

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18
Q

How is mild-moderate intermittent or persistent rhinitis treated?

A

regular treatment
nasal steroids and nasal or oral antihistamine
pre-medicate before season (if appropriate)

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19
Q

What additional therapies can be added on if you are still suffering from rhinitis?

A

ipratropium, increase antihistamine dose, short term course of oral steroids, immunotherapy

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20
Q

What are some of the potential reasons for treatment failure?

A 
compliance 
not taking the treatment properly 
not taking it due to side effects 
try different device 
pre-season medication may be necessary = generally more effective if you stop inflammation happening in the first place
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21
Q

What happens in allergic asthma?

A

one of the phenotypes of asthma
symptoms worse on exposure to allergen but also complex late phase responses due to inflammation
direct bronchospasm
reversible bronchial hyper-reactivity due to smooth muscle contraction

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22
Q

How are rhinitis and asthma linked?

A

concept of one airway
- 80% of asthmatics have rhinitis
- 20-50% of patients with rhinitis have asthma
allergic rhinitis is an important independent risk factor for asthma

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23
Q

What are the treatment approaches for asthma?

A

avoid triggers
stabilise mast cells - sodium chromoglycate = more useful in children
treat the inflammation = steroids, LTRA (montelukast)
relieve bronchospasm - beta2 agonists

24
Q

What is atopic dermitits/eczema and what are some risks associated with it?

A

allergic skin disease and immunodeficiency and chronic inflammation
more complex response to allergen than hay fever or asthma
very high IgE but allergen is not usually identified
T cells and infection with S aureus important = if barrier is broken more likely to come into contact with immune cells
often underlying genetic defect in barrier defense

25
What genetic defect is thought to be involved in asthma?
filaggrin - structural protein in the keratinocyte layer - only discovered about 10 years ago 70% of atopic dermatitis
26
What are the treatments for eczema?
avoid the allergen and prevent scratching prevent barrier defense breakdown (moisturizers deluxe) - the key treatment is moisturisation treat the infection - antibiotic creams treat the chronic inflammation = steroids
27
What does being atopic mean?
allergic to one allergen then more likely to be allergic to another allergen
28
What is a key factor in food allergies and what is important to ask in the history?
patients usually tell you what the food is take food allergies seriously as they can be life-threatening Hx - temporal relationship - consistent relationship = every time they eat that food - mouth itching/swelling/hives/angiodema - can come at any age
29
What do we know about food intolerances?
pathogenesis is not fully understood Non-IgE mediated often a threshold and can tolerate varying amounts of food unpredictable non-life threatening but distressing abdominal discomfort, bloating, vomiting, nausea, diarrhea, headache, feeling unwell no reliable diagnostic tests except avoidance reintroduction diets can be difficult to distinguish from IBS
30
How are food allergies managed?
``` avoidance antihistamines adrenalin mx plan medical alert medical notes ```
31
Why is drug allergy terminology confusing ?
terminology is used freely resulting in confusion to patients and physicians - 1:10 people that come into hospital think they are penicillin allergic but <1 in 10 actually are poorly documented - risk to patient - may have a severe reaction, prevented from potentially helpful abx many patients then won't get 1st line Tx so they end up staying in hospital longer
32
What are the common characteristics of an immediate drug reaction and how long do they take?
less than an hour - urticaria/angioedma - vomiting/diarrhoea - high pulse rate - low blood pressure - wheeze - hoarse voice / stridor - confusion / loss of consciousness
33
What are the common characteristics of an delayed drug reaction and how long do they take?
over an hour - sometimes it can difficult to know if it is the drug or not - variety of rashes - itching - unexplained fever - GI upset - Arthralgia - Myalgia
34
What are idiosyncratic reactions?
unpredictable drug reactions: - steven johnsons syndrome - toxic epidermal necrolysis - hemolysis severe and life threatening managed in the burns unit and the drug is never given again
35
What are some idiosyncratic symptoms?
``` high fevers exfoliating rash mucous membrane involvement hematological problems liver problems ```
36
What are side effects to drug allergies?
reactions that occur when taking a drug at the normal dose reactions may range from mild to severe - so may be able to tolerate not everyone gets the same side effects factors such as your genes, other medications and illness may increase the likelihood of side effects
37
What is the most common drug reaction?
penicillin - responsible for 26% of fatal drug reactions and 11% of all fatal anaphylaxis only 10-20% of individuals who believe to have it are truly allergic - it is worth referring certain groups for testing
38
What documentation needs to be noted for drug reactions?
abx at time of reaction: drug, date, commenced, time to reaction from starting dose concomitant medications especially antihistamines and steroids - can modulate immune response previous reaction hx - same as this reaction? describe details of reaction and often helpful to photograph visible symptoms
39
What management processes should be carried out following severe reactions?
allergy/severe reaction should be clearly documented in every set of notes - lack of linking between hospitals and GPs contact GP to update their records advise pt to wear a medical alert bracelet / carry advice card provide and train pt with an adrenalin auto-injector
40
What investigations are carried out for drug reactions?
medical illustration to document any visible reaction measure tryptase at 2 hours and 24 hours post reaction a FBC to look for eosinophilia, hemolytic anaemia and platelets U&E and LFTs to assess renal and liver function ssIgE blood tests for some drugs (6-8 weeks later) = pen V, amoxicillin, cefalexin, ciprofloxacin
41
What is anaphylaxis?
a severe, life threatening generalized or systemic hypersensitivity reaction follows exposure to an allergen to which the patient has been previously sensitized results following allergen stimulated IgE mediated mast cell degranulation
42
What isn't anaphylaxis?
chronic spontaneous urticaria (hives) - relatively common breakthrough itching and rash onset often slower than allergy often slower to resolve
43
What are exacerbating factors of anaphylaxis?
``` thyroid function and antibodies physical stress emotional stress aspirin urticarial vasculitis ```
44
What factors make anaphylaxis easier to recognize?
``` rapidly developing symptoms life threatening compromise: - airway - breathing - circulation usually associated with skin changes ```
45
What are the "timing" characteristics of anaphylaxis?
symptoms almost invariably begin within 60 mins later onset generally less severe symptoms and more likely a different diagnosis 1 in 5 reactions may be biphasic in nature - 2 episodes occurring 1-8 hours apart - this is why patients are admitted for 5-6 hours (mast cells are able to refill)
46
What is the ABC approach to anaphylaxis?
``` Airway problem - hoarse voice/stridor - swelling of tongue / throat Breathing problems - increased RR - wheeze - cyanosis (late, bad) / resp arrest Circulation - hypotension - tachycardia - myocardial ischemia / cardiac arrest ```
47
What neurological and skin/mucosal symptoms are associated with anaphylaxis?
``` neurological = confusion, agitation, loss of consciousness, impending doom skin/mucosa = erythema, urticaria, angioedema ```
48
How common is anaphylaxis and what is the prognosis?
incidence increased 7 fold over last 20 years approx 20 deaths in UK / year prognosis is good, only fatal in 1% but its worse if you have pre-existing asthma
49
What are some common causes of anaphylaxis?
``` drugs - abx, anesthetic agents, RCM foods - nuts, shellfish, fish, milk insect stings latex idiopathic ```
50
What is the pathophysiology of anaphylaxis?
1) sensitization 2) antigen binds specific IgE 3) cross links receptor on mast cell 4) release of preformed mediators 5) increased synthesis of mediators
51
What are the differential diagnoses of anaphylaxis?
``` syncope/faint anxiety induced hyperventilation hypotension due to MI, Blood loss, sepsis scombroid poisoning mastocytosis = too many mast cells = measure baseline tryptase carcinoid syndrome vocal cord dysfunction chronic urticaria and angiodema exercise induced ```
52
/What is the acute management of suspected anaphylaxis?
medical emergency - ABCDE approach - adrenalin is life saving- delay in admin or incorrect admin is life threatening need to use big enough needle = IM 0.5 mls - repeat at 5 mins if no improvement IV only if in monitored situation (ITU) high flow oxygen placed in comfortable condition fluids - 500-1000 ml challenge bronchodilator therapy
53
What does adrenalin do?
increase peripheral vasoconstriction increase peripheral vascular resistance increase BP and coronary artery perfusion decrease vascular permeability and angiodema bronchodilation reduce inflammatory mediator release
54
What is done to prevent a biphasic reaction?
corticosteroids - 200mg hydrocortisone IV, 40mg oral | antihistamines 10g chlorphenicamine IV or IM
55
When do you check tryptase levels?
as soon as possible 2 hours after symptoms started baseline - ask GP
56
Following discharge what management is done?
3 day course of steroid/antihistamine consider adrenalin auto-injector or replacing existing prescription teach how to use auto-injector refer to allergy clinic
57
Who are the high risk patients that are likely to need adrenalin auto-injectors?
asthma reaction to trace allergen repeated exposure likely e.g. healthcare worker and latex lives in remote setting

Yr 3 - December lectures 2018 (15 decks)

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