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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
Q

What genetic defect is thought to be involved in asthma?

A

filaggrin - structural protein in the keratinocyte layer - only discovered about 10 years ago
70% of atopic dermatitis

26
Q

What are the treatments for eczema?

A

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
Q

What does being atopic mean?

A

allergic to one allergen then more likely to be allergic to another allergen

28
Q

What is a key factor in food allergies and what is important to ask in the history?

A

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
Q

What do we know about food intolerances?

A

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
Q

How are food allergies managed?

A 
avoidance
antihistamines
adrenalin
mx plan
medical alert 
medical notes
31
Q

Why is drug allergy terminology confusing ?

A

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
Q

What are the common characteristics of an immediate drug reaction and how long do they take?

A

less than an hour

  • urticaria/angioedma
  • vomiting/diarrhoea
  • high pulse rate
  • low blood pressure
  • wheeze
  • hoarse voice / stridor
  • confusion / loss of consciousness
33
Q

What are the common characteristics of an delayed drug reaction and how long do they take?

A

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
Q

What are idiosyncratic reactions?

A

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
Q

What are some idiosyncratic symptoms?

A 
high fevers 
exfoliating rash 
mucous membrane involvement 
hematological problems
liver problems
36
Q

What are side effects to drug allergies?

A

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
Q

What is the most common drug reaction?

A

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
Q

What documentation needs to be noted for drug reactions?

A

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
Q

What management processes should be carried out following severe reactions?

A

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
Q

What investigations are carried out for drug reactions?

A

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
Q

What is anaphylaxis?

A

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
Q

What isn’t anaphylaxis?

A

chronic spontaneous urticaria (hives) - relatively common
breakthrough itching and rash
onset often slower than allergy
often slower to resolve

43
Q

What are exacerbating factors of anaphylaxis?

A 
thyroid function and antibodies
physical stress 
emotional stress
aspirin 
urticarial vasculitis
44
Q

What factors make anaphylaxis easier to recognize?

A 
rapidly developing symptoms 
life threatening compromise:
- airway 
- breathing 
- circulation 
usually associated with skin changes
45
Q

What are the “timing” characteristics of anaphylaxis?

A

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
Q

What is the ABC approach to anaphylaxis?

A 
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
Q

What neurological and skin/mucosal symptoms are associated with anaphylaxis?

A 
neurological = confusion, agitation, loss of consciousness, impending doom 
skin/mucosa = erythema, urticaria, angioedema
48
Q

How common is anaphylaxis and what is the prognosis?

A

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
Q

What are some common causes of anaphylaxis?

A 
drugs - abx, anesthetic agents, RCM
foods - nuts, shellfish, fish, milk
insect stings
latex
idiopathic
50
Q

What is the pathophysiology of anaphylaxis?

A

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
Q

What are the differential diagnoses of anaphylaxis?

A 
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
Q

/What is the acute management of suspected anaphylaxis?

A

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
Q

What does adrenalin do?

A

increase peripheral vasoconstriction
increase peripheral vascular resistance
increase BP and coronary artery perfusion
decrease vascular permeability and angiodema
bronchodilation
reduce inflammatory mediator release

54
Q

What is done to prevent a biphasic reaction?

A

corticosteroids - 200mg hydrocortisone IV, 40mg oral

antihistamines 10g chlorphenicamine IV or IM

55
Q

When do you check tryptase levels?

A

as soon as possible
2 hours after symptoms started
baseline - ask GP

56
Q

Following discharge what management is done?

A

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
Q

Who are the high risk patients that are likely to need adrenalin auto-injectors?

A

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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