W07 - PAEDS: Allergies (Paeds); Paed Nephrology; Paed Sx; Paed Urology Flashcards
Describe the pathophysiological mechanisms of IgE mediated allergy
Histamine , Tryptase, Hydrolase
Later biphasic reaction: Secreted inflammatory mediators – Prostaglandins, Leukotrienes, PAF, Cytokines
HISTAMINE:
Bronchial smooth muscle contraction
Vasodilation
Separation of endothelial cells (responsible for hives)
Pain and itching
TRIGGERS:
Food
Environmental Allergen
Drug
Sting / Bite
Idiopathic
Recognise the presenting features suggestive of IgE medicated food allergy and be able to elicit an allergy focussed history
Mild/moderate
Severe: +airway, bronchispasm, hypoT
Formulate and justify a diagnosis of IgE Mediated allergy
- previous reactions
- atopy
- FHx
- Response to Tx
- Co-existing asthma? - bronchospasm exacerbation
Be able to identify and select appropriate investigations to aid diagnosis of suspected food allergy
SKIN PRICK TESTING
- strong negative predictor
SPECIFIC IgE
- no risk of reaction,
- unreliable in eczema
- delay
ORAL FOOD CHALLENGE
GOLD STANDARD
daycase procedure, double blind controlled.
Identify and describe the management for the prevention and treatment of food allergy
Avoidance of triggers
H1- Antihistamine (2nd or 3rd generation)
- PYRITON
- CHLORPHENAMINE
(1st gen sedating)
(2nd or 3rd are non-sedating)
High Dose Antihistamines +/- second antihistamine
Leukotriene Antagonist
Corticosteroids (3-5 days)
Tranexamic Acid
Anti IgE Monoclonal antibody (Omalizumab) in children over 7 years of age
Hereditary angioedema
C4 and C1 Esterase Inhibitor Dysfunction
Signs of anaphylaxis
Laryngeal Oedema
Hypotension/collapse
Bronchospasm
Feeling of impending doom
Onset usually in minutes
- onset around 60mins, faster = worse prognosis
- 20% have biphasic reaction 1-8 hrs later therefore need steroids and hospital admission
RF for anaphylaxis
Asthma (poorly controlled)
Stress
Exercise
Viral infection
Alcohol
Mgmt for Anaphylaxis
EPIPEN
Adult 0.3mg / 0.5mg, Junior 0.15mg
Education on use home/school
1st line treatment of anaphylaxis
Early use is associated with better outcomes
Potential interaction with B-blockers and tricyclics
ACTIONS:
Reverses peripheral vasodilation
Increases peripheral vascular resistance
Improves BP and coronary perfusion
Decreases angiooedema
Causes bronchodilation
Decreases release of inflammatory mediators
- hx of severe reaction, trace amounts
- cvd, resp, co-existing asthma comorbidities
Food Allergies
RF: existing allergies, atopy
Peanut:
> avoid
> immuno rx?, Palforzia
Egg:
67% grow out of it by 5yo
> promote re-introduction, egg ladder
Milk:
D&V, confusion, infants = histamine
D&V, eczema, bloating bleeding, irritability = non-histamine, non-IgE MOST COMMON
Fruit & Veg Allergy
Oral Allergy Syndrome
Cross reactivity of tree/plant pollens and foods
Causes mainly oral symptoms - itching, mouth swelling, tongue discomfort etc…
Birch - kiwi, apple, pear, nectarines
Alder - celery, pear, apple, cherry
Ragweed - watermelon, banana, cucumber
NEPHROTIC SYNDROME in paeds
*proteinuria, intravascular depletion,
* glomerular disease
* Interaction between lymphocytes (T and B cells) and podocytes
- hypoalbuminemia = oedema
- frothy urine
- minimal change most prevalent
- followed by Focal segmental glomerulosclerosis (FSGS)
> PREDNISOLONE
!cushings
Investigating glomerular disease
i. DIPSTIC
ii. PROTEIN:CREATININE
iii. 24hr urine (gold standard)
NEPHRITIC SYNDROME in paeds
- haematuria, intravascular overload
- glomerular disease
- fluid overload, JVP, oedema
- increased creatinine
- hyponatremia, hyperk.
Acquired Glomreulopathy in paeds
PODOCYTE implicated in Minimal Change Disease
BASEMENT MEMBRANE implicated in Post Infectious Glomerulonephritis
ENDOTHELIAL CELL implicated in PIGN, Haemolkytic Uremic Syndrome
MESANGIAL CELL implicated in
IgA Vasculitis
* common in children
+STEROID RESISTANT NEPHROTIC SYNDROME: genetic factor, podocyte loss, progressive inflammation and sclerosis
Congenital Glomerulopathy
*rare, layer involved
PODOCYTE DYSFUNCTION
BASEMENT MEMBRANE PROTEIN DYSFUNCTION
ENDOTHELIAL VASCULAR DYSFUNCTION
Considerations for steroid therapy in paeds
Behaviour
Mood lability
Sleep disturbance
*infection risk: varicella status, pneumococcal vax, abx prophylaxis
Acute post-infectious glomerulonephritis
Group Strep A, beta hemolytic
throat, skin
- ag mimicry produces Ab-Ag complexes = TYPE 3 HYPERSENSITIVITY
= AKI
*self-limiting
* bacterial culture!
> Abx
Support renal functions
Diuretics
IgA Nephropathy
Most common glomerulonephritis
1-2 days after URTI
Usually older children and adults
Recurrent macroscopic haematuria
Chronic microscopic haematuria
Varying degree of proteinuria
- biopsy confirms: IgA, IgG, C3 deposits
> ACEi - mild disease, proteinuria
imm suppr.
Mesangial Deposits of IgA, IgG, and C3 on immunostaining are suggestive of which glomerular disease?
IgA Nephropathy
HSP IgA Vasculitis
HENOCH SCHONLEIN PURPURA
* VASCULITIS (most common childhood vasculitis): palpable purpura
+ abdo pain
+ renal involvement
+ arthritis
+ BIOPSY
5-15yrs
associated with sensitivity vs nephrotic/nephritic IgAN, but still nephritic in picture
post viral trigger or drug trigger
4-6w duration
> symptomtic
glucocorticoid rx: improve GI involvement
imm suppr.
LT hypertension and proteinuria screening
PSGN Vs IgAN
Latency
Imm complexes in PSGN biopsy
* both nephritic
In addition, PSGN classically presents with hypocomplementemia, and if the patient undergoes a renal biopsy there is evidence of an immune complex-mediated process. In contrast, IgA Nephropathy shows normal serologic values (though IgA levels may be elevated in about a third of patients) and the renal biopsy will show mesangial IgA deposition.
One of the most important distinctions can be made in taking a good history: In PSGN, glomerulonephritis typically does not set in until several weeks after the initial infection. In contrast, IgA Nephropathy may present with so-called “synpharyngitic glomerulonephritis”–pharyngitis and glomerulonephritis at the same time.
AKI Hallmarks & Approach
hallmarks:
Anuria/oliguria (<0.5ml/kg/hr) - havent pissed for more than 8hrs
Hypertension with fluid overload
Rapid rise in plasma creatinine - 1.5x+ rise
injury resulting in retention and failure to filter
> MONITOR: BP, urine, wt
MAINTAIN: hydration, electrolytes, balance
MINIMISE: drugs
Pre-Renal AKI Causes
Perfusion
