Allergies Flashcards
What is atopy
Personal or familial tendency to become sensitised and produce IgE antibodies to low doses of allergens and as a consequence develop sx of an allergic disease, eg asthma, rhinitis, hay fever, eczema, food allergens etc
Approach to allergies
Description of symptoms: itchiness, redness, swelling, sneezing, coughing, wheezing
Site of manifestations
Hx of presenting sx
Age of onset , severity, duration,timing, pattern, triggers, ass/sx, response to tx
Management of allergies (4 Pillars of allergy management)
Education
Trigger avoidance
Pharmacotherapy
Allergy immunotherapy
How do we make the dx of allergic rhinitis
2 or more sx for more than an hour per day for more than 2 weeks
Sx: runny nose, itchiness and sneezing
Clinical fx of allergic rhinitis
Dennie-Morgan lines (wrinkles under eyes)
Allergic shiner (darkness under eye)
Transverse nasal crease
Dental malocclusion
Mouth breathing
Pale, swollen, with lots of thin watery mucous Turbinate (nasal canal)
Tx of allergic rhinitis
- Primary anti-inflammatory
Intranasal corticosteroids
Leukotriene receptor amtagonists
Sodium cromoglygate - Block release modulators
Antihistamines
Anticholinergics - Work on physical basis
Decongestants
Which immunotherapy agents would you give to a child with allergic rhinitis
Sublingual immunotherapy
Subcutaneous immunotherapy
What are the 3 patterns of anaphylaxis
Uniphasic: short lived episode, resolves completely within 2hours
Biphasic (20%): first episode which may seem resolves, 8-24 hours later another episode or wave of symptoms more severe than first episode
Protracted (rare): personal remains symptomatic for hours to days
What is Alpha gal syndrome
People with alpha gal syndrome react after eating red meat.
Due to the galactose alpha 1,3 galactose.
Onset is delayed by 2-5 hours after eating red meat because antigen is absorbed via lymphatics, on,y enteric enteric circulation after some time
Alpha gal is highly concentrated in meat like liver, heart and kidney.
Tick bites can also cause cross sensitisation, new onset allergy in adults may be due to this.
How is Radiocontrast media anaphylaxis mediated
Acute onset is caused by mast cell activation via IgE
Delayed, 3hrs to 5days is due to Tcell mediated hypersensitivity reaction
Can prophylactic medications be used to prevent anaphylaxis
e.g antihistamine and corticosteroids
No, worsens attack or prognosis
Which cells must be activated to mediate anaphylaxis
Mast cells and basophils
What sensitivity components directly activate mast cells rather than IgE for anaphylaxis (What are the non immunological causes of anaphylaxis)
RadioContrast media
Exercise induced anaphylaxis
Alcohol
Temperature eg cold exposure or heat
NSAIDs
What investigations can you do to dx anaphylaxis
It is a clinical dx, no special investigations required
however ,
1. IgE sensitisation can be seen in skin or blood test
2. Serial monitoring of tryptase levels, taken at onset of sx, 1 or 2hours later and at resolution of sx. A change from baseline of >2 ng/g has 90% Sensitivity for detecting anaphylaxis
How is the dx of asthma made
- Detailed hx (patterns of sx, exacerbations, exposures, development and tx of disease and if reversed sx immediately with bronchodilator)
- Thorough exam (hyperinflation, barrel chest, prolonged expiration and hoovers sign, wheezing, incr work of breathing)
- Demonstrating lower airway reversibility (1. Peak flow expiratory flow rate- PEFR, from 5y/o, 15% or more improvement after bronchodilator indicates positive response. 2. Spirometry, which is a lung fx test to assess lung volume air flow on insp and exp, FVC, FEV, FEF)
-To make dx of asthma, flow volume loops must show reduced FEV1, normal FVC and reduced FEV1 to FVC ratio.
Classify asthma meds according to Relievers and controllers
Relievers
1. SABA eg salbutamol
2. Ipratroprium bromide
3. Steroids
Controllers
1. Inhaled corticosteroids eg beclomethasone
2. LABA eg salmeterol, Formoterol
3. Leukotriene receptor antagonist
4. LAMA-Long acting antimuscarinics
5. Theophylline
What is the most effective asthma controller medication
ICS
Outline step by step management of asthma
A- SABA (CAT<10) CAT is asthma control test (Ipratropium bromide can be added to SABA in moderate or severe attacks)
B- low ICS or LABA (CAT>/=10) (never use LABA alone as reliever, use with ICS with steroid)
C- ICS (Inhaled Corticosteroids) +LABA or LAMA
D- ICS + LABA and/or LAMA
Leukotriene receptor antagonist for pt unable or unwilling to take ICS, can be used as monotherapy for mild asthma, mild asthma with exercise induced components, aspirin sensitive asthma, and tx allergic reactions rhinitis concomitant with asthma.
Step 1
Reliever: SABA
Controller: None (but can consider low dose ICS)
Step 2
Reliever: SABA
Controller: Low dose ICS (Alternative is Leukotriene Receptor antagonist OR low dose Theophylline)
Step 3
Reliever: SABA or low dose ICS or Formoterol
Controller: Low dose ICS or LABA (Alternative is mid/high dose ICS OR low dose ICS with LRA or Theophylline)
Step 4
Reliever: SABA or low dose ICS or Formoterol
Controller: Med/high dose ICs or LABA (Alternative is to add tiotropium, OR high dose ICS with LRA or Theophylline)
Step5
Reliever: SABA or low dose ICS or Formoterol
Controller: Refer for additional on tx eg anti IgE
(alternative: Add tiotroprium Or Add low dose ICS)
Causes of angioedema
Drug induced
Hereditary
Non histaminergic angioedema
What is the Asthma predictive index (minor and major criteria) for dx asthma
Early frequent wheezing plus (any 1 major or 2 minor: )
Major
-Parental asthma
-Atopic dermatitis
Minor
-wheezing apart from during colds
-Eosinophils (>4%)
-Allergic rhinitis
How to classify asthma severity (for tx purposes)
Stage 1: sx less than 2 a month
Stage 2: sx 2 or more a month
Stage 3: sx on most days a week or waking up at night once a week or more
Stage 4: daily sx, waking up at night and low lung functions
Stages are phases of tx you give lol
Side effects of ICS
Easy bruising
Oral candidate
Decreased bone mineral density (reduced growth)
WHat is the difference between adults, children and infantile atopic dermatitis
Infantile
-involves face and trunk
-cheeks and chin, spares area around nose ans eyes
-usually acute appearance, knees may be involved with crawling
Childhood
-involves flex tyres, neck, hands, wrist
-acute, subacute and chronic lesions
-May have discoid or mummular lesions
ADULT ATOPIC DERMATITIS
Involvement as per childhood AD
Perineal, peri-orbital and prominent hand involvement
Lichenification may be well established
Discuss pharmacological management of Atopic dermatitis
Tx according to severity, different tx used at different times (eg when skin is clear, during flare up, during healing)
Step 1: Dry skin only
-skin hydration, avoidance of triggers/irritants, identify and address the triggers
Step 2: Mild to Moderate Atopic dermatitis
-Low-mild potency topical Corticosteroids (TCS) and/or Topical Calcineurin inhibitors (TCIs)
Step 3: Moderate to Severe AD
-Mild to high potency TCS and or TCIs
Step 4: Severe AD, Recalcitrant
-Systemic therapy or UV therapy
-Mild to High potency TCS and or TCI
Common infections in AD
Staph aureus
Candida
HSV
Molluscum Contagiuosum Virus
Less common: scabies, Malassezia species
What systemic anti-inflammatory therapy can be used for AD and what are the complications of each
Methotrexate (slow onset)- hepatotoxic and teratogenic
Cyclosporine (quick onset)- BP and renal failure
Azathiprine (slow onset)- acute GI and haematological abnormalities
Oral steroids (quick onset)- cataracts, osteoporosis, short height
Mycophenilate mofetil (slow onset)- GI and haematological. Teratogenic.
