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Paediatrics > Allergies, immunodeficiency and infection > Flashcards

Allergies, immunodeficiency and infection Flashcards

1
Q

Epidemiology of allergies in children

A
  • Very common, 1/2 children have at least 1 type of allergy
  • Affects boys > girls
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2
Q

Cause of allergy in children

A
  • Children who have a parent with an allergy are more likely to have one themselves
  • Hygiene hypothesis: children exposed to fewer allergens are more likely to become sensitised and develop allergies
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3
Q

Two main types of allergic reaction

A

1. IgE mediated allergic reactions occur immediately when the body recognises an allergen. Body produces large numbers of antibodies which act against the specific allergen – binding of the allergen to the antibodies bound to mast cells causes the mast cells to degranulate and release histamine

  • Clinical features include immediate sneezing, rhinorrhoea, red and itchy eyes, wheeze, cough and urticaria rash

2. Non-IgE mediated reactions are not immediate, this makes it difficult to associate the symptoms with exposure to a specific allergen. The pathophysiology of non-IgE mediated allergic reactions is unclear

  • Often take around 48hrs to appear
  • Clinical features are non-specific and do not occur immediately after exposure, symptoms may include diarrhoea, dry and itchy skin or a chronically blocked nose
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4
Q

Diagnosis of allergy

A
  • Can be diagnosed clinically without the need for invasive tests if the symptoms occur after exposure.
  • Diary can be used to document exposure to potential allergens and any symptoms experienced
  • Skin prick testing is used to identify allergens,
    • Allergens in liquid form are applied to the skin and the skin below is superficially scratched and if a reaction develops within 15 minutes of exposure and allergy is confirmed
      • Important not to take antihistamines for a few days before this test because it could affect the result
      • Not helpful to measure total levels of IgE because this is non-specific as they may be raised in conditions such as asthma which is related to allergy but is not the same thing
  • Blood tests can be carried out to measure the number of specific IgE antibodies present for a particular allergen e.g. IgE against peanuts or tree pollen
  • Useful when skin prick testing isn’t available but is less sensitive than skin prick testing
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5
Q

Management of allergy

A
  • Avoid allergen
  • Symptomatic relief using anti-histamines
  • EpiPen adrenaline devices given to all children with nut allergies and those who presented with anaphylaxis symptoms as well as those on inhaled steroids for asthma and have food allergies
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6
Q

What are the common allergic diseases?

A
  • Allergic rhinitis
  • Asthma
  • Eczema
  • Food allergy
  • Venom allergy
  • Drug allergy
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7
Q

What is allergic rhinitis?

A

Inflammation of the nasal mucosa following immune reaction to an allergen, usually an allergen in the air

  • Common types of air allergen
    • Seasonal (hay fever): grass pollen, tree pollen, weeds, fungal spores
    • Perennial (all year round): house dust mite faeces, animal hair, mould
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8
Q

Clinical features of allergic rhinitis

A
  • Sneezing, rhinorrhoea – occurs due to nasal inflammation
  • Child may also have red, itchy, watery eyes and other clinical features of atopy
  • Nasal speculum examination findings
    • Pale blue, enlarged nasal turbinates with a clear, watery discharge, inflamed mucosa, nasal polyps
  • Allergic shiners: dark patches under eyes associated with itchy eyes and rubbing eyes
  • Mouth open to allow breathing with chronically blocked nose
  • Patches of eczema on flexures
  • Excoriation
  • Many children with allergic rhinitis also have eczema and asthma - if the child has these 3 conditions they are said to have atopy and are described as atopic
  • If nasal polyps are found in a child it may prompt the consideration of cystic fibrosis as they are associated with allergy and nasal polyps
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9
Q

Management of allergic rhinitis

A
  • Avoid allergen - although this can be tricky
  • Topical nasal corticosteroids, antihistamines and decongestants are used
  • If severe, regular use of oral steroids or allergen immunotherapy is given to suppress the immune system
    • This is usually reserved for times it is needed most e.g. when child is taking exams
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10
Q

Symptoms of IgE mediated food allergy

A
  • Occur within 60mins of ingestion
  • Swelling of the face
  • Urticaria
  • Vomiting
  • Wheeze and cough
  • Anaphylaxis
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11
Q

Symptoms of non-IgE mediated food allergy

A
  • Occurs 24hrs-days after ingestion
  • Vomiting, diarrhoea
  • Abdominal cramps
  • Malabsorption or poor weight gain
  • Eczema
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12
Q

Can children with egg allergy receive the flu vaccine?

A

Not the standard one, it is grown in fertilised hen eggs so they are given an egg-free flu vaccine

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13
Q

Is peanut allergy IgE or non IgE mediated?

A
  • IgE mediated, symptoms occur immediately after ingestion
  • Affects 1 in 50 children
  • Symptoms
    • Rash, lips swelling, itchy throat, vomiting, diarrhoea
    • Anaphylaxis can occur if reaction is severe
  • Diagnosis
    • Based on hx
  • Management
    • Avoidance of ingestion and other types of exposure to nuts
    • Use of antihistamines if exposed
    • EpiPen
    • Peanut allergies tend to be life-long
    • 10% children grow out of tree nut allergy
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14
Q

Is cow’s milk protein allergy IgE or non-IgE mediated?

A

Does not fit into either category

  • An allergy to one or more proteins in cows milk
  • 60% cases = IgE mediated
  • 40% cases = non-IgE mediated
    • Cows milk protein allergy is the most commonly recognised non-IgE mediated food allergy
  • Affects 5% of neonates and infants
  • Ingestion of milk, either breast or formula causes an immediate IgE reaction or a delayed non-IgE reaction
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15
Q

Symptoms of cow’s milk protein allergy

A

Colic, diarrhoea, mucous in stool, eczema, FTT

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16
Q

Diagnosis of cow’s milk protein allergy

A
  • IgE mediated: skin prick testing or serum milk IgE levels
  • Non-IgE mediated: clinical diagnosis
  • Trial of hypo-allergenic formula or a dairy-free diet for the mother if baby is breast-fed
    • If symptoms improve this confirms the diagnosis and avoidance of cows milk should be avoided
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17
Q

Management of cow’s milk protein allergy

A
  • Initial avoidance of dairy
  • Reintroduced around 9-12 months under the supervision of a dietician, stopped if symptoms recur
  • 50% cases non-IgE mediated allergy resolve by 1 year and 90% by 3 years
  • 50-60% cases IgE mediated allergy resolve by 5 years
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18
Q

Differences between IgE and non-IgE mediated allergic reactions

A

IgE:

Mast cells degranulate, release histamine, immediate reaction, itchy, sneezing, rhinorrhoea, bronchospasm, flushing

Non-IgE:

T-cell mediated, eosinophils cause inflammatory infiltrate, late phase reaction, nasal blockage

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19
Q

Primary vs secondary immunodeficiency

A
  • Primary = genetic problem with the immune system underlies the susceptibility to infection
  • Secondary = immune system is impaired due to other cause
20
Q

What is primary immunodeficiency?

A
  • Suspected when there s a hx of SPUR: severe, persistent, unusual or recurrent infections
  • Epidemiology and aetiology
    • >200 primary immunodeficiencies exist but they are uncommon
    • Affect 1 in 10,000
    • 80% of cases diagnosed before age of 20
    • Do not present until 6 months because maternal antibodies are still circulating up to this time
    • Specific immunodeficiencies are associated with specific syndromes e.g. DiGeorge’s syndrome, Job’s syndrome and Wiskott-Aldrich syndrome
21
Q

Clinical features of primary immunodeficiency

A
  • Frequent, mild infections – up to 12 viral infections per year
  • Primary immunodeficiency is suspected when a child presents with multiple infections in close succession, these are more severe than a normal childhood infection for example a child with sepsis or meningitis
  • Infections are often severe enough to warrant treatment with IV antibiotics
  • A child presenting with more than two infections separated by time at the same anatomical site for example recurrent urinary tract infections might raise suspicion of a structural abnormality
22
Q

Management of primary immunodeficiency

A
  • This depends on the underlying cause of immunodeficiency and is guided by an immunologist
  • Patients will often be given prophylactic antibiotics to prevent infection and if infection does occur they are given antibiotics for a longer period of time and often require IV administration
  • IV immunoglobulins are given as replacement therapy in children with congenital agammaglobulinaemia and hypogammaglobulinaemia
    • Either a deficiency or total lack of IgG in the blood
  • In severe cases bone marrow transplant is needed
  • Prognosis is variable and depends on the severity of the immunodeficiency
23
Q

What is DiGeorge’s syndrome?

A
  • Also known as congenital thymic aplasia, a congenital syndrome that affects 1/4000 children
  • A genetic defect leads to a defect in the embryological development of the third and fourth pharyngeal pouches. This results in the absence of the thymus gland and the development of abnormal parathyroid glands
  • Thymus = site of T-cell maturation so absence of thymus = immunodeficiency
  • The abnormal development of the parathyroid glands leads to hypocalcaemia and hypoparathyroidism
  • Also associated with cleft palate, congenital heart abnormality and 90% have learning difficulties
  • CATCH 22 - DiGeorge’s syndrome
    • C: Cardiac abnoramlities
    • A: Abnormal facies
    • T: Thymic asplasia
    • C: Cleft palate
    • H: Hypocalcaemia and hypoparathyroidism
    • 22: Chromosome 22 deletion
24
Q

What is secondary immunodeficiency?

A
  • Diagnosed when a disease or condition impairs the functioning of the immune system
  • Causes of secondary immunodeficiency
    • Chemotherapy, leukaemia or lymphoma, HIV, malnutrition, nephrotic syndrome
  • Presentation is the same in primary deficiency but diagnosis can be reached more quickly if the child is known to have a condition which is known to impair the immune system
  • Secondary immunodeficiency is usually reversed once the underlying cause is addressed for example when chemotherapy ends and prognosis depends on the cause of the deficiency
25
Q

What is exanthem?

A

Widespread skin rash

26
Q

What is enanthem?

A

Rash on the mucous membranes

27
Q

How does measles spread?

A

Respiratory droplets

28
Q

How soon after infection do symptoms of measles present?

A
  • Symptoms occur around 10 days after infection
    • Characteristic of a measles infection is a very miserable child because they feel so unwell
29
Q

Four phases of measles infection

A
  1. Incubation period which lasts for 10 days and is asymptomatic
  2. Prodrome phase includes fever, malaise, anorexia, conjunctivitis and Koplik’s spots (these are a viral enanthem of measles, clustered, white lesions on the insides of the patient’s cheeks - these are detected in 50–70% of patients and resemble grains of salt on a red background)
  3. Rash face occurs on day five and includes a maculopapular, blanching rash with lymphadenopathy, high fever and pharyngitis
  4. Recovery phase occurs around daytime however a cough come persist for two weeks
30
Q

How is measles infection confirmed?

A

Presence of anti-measles antibodies in the saliva

31
Q

Management of measles

A

Supportive

Serious complications:

  1. Pulmonary complications: bronchopneumonia
  2. Neurological complications: encephalitis, acute disseminated encephalomyelitis
  3. Eyes: keratitis and corneal ulceration
  4. GI: hepatitis, mesenteric lymphadenitis, appendicitis, gastroenteritis, diarrhoea
  5. Cardiac: myocarditis and pericarditis
  6. Immunosuppression leading to severe secondary infections
32
Q

Clinical features of rubella

A

Pyrexia, arthralgia, coryza – these occur around 14 days after infection

  • A maculopapular rash can also develop typically starting on the face before spreading to the trunk and limbs and covers the whole body within 24 hours. The rash usually resolves within three days
33
Q

Congenital rubella syndrome

A

Can occur if a woman contracts rubella during pregnancy particularly during the first trimester.

This can cause miscarriage or stillbirth and a baby born with congenital rubella will have severe birth defects such as congenital heart disease, hearing impairment, cataracts and developmental delay.

A presenting sign is the blueberry muffin rash

34
Q

Which childhood infection is associated with infertility?

A

Mumps

Can cause testicular swelling

35
Q

Are MMR notifiable diseases?

A

Yes

36
Q

4 stages of chickenpox infection

A
  1. Incubation period lasting 10–21 days
  2. Prodrome period lasting for 24 hours featuring fever, malaise, pharyngitis and a loss of appetite
  3. Exanthem which last for several days and is characterised by a generalised, pruritic, vesicular rash
  4. Evolving phase which lasts for around four days or less involves the crusting of lesions, crusts will usually fall off by 2 weeks
37
Q

When are children with chickenpox contagious?

A
  • Children are contagious from two days before the rash appears until the lesions have crusted over
38
Q

Management of chicken pox

A
  • For most patients treatment is symptomatic and includes antihistamines to help relieve the itching
  • Children who have an impaired immune system will be given anti-viral medication to help prevent severe infection as complications can be very serious:
  • Severe infections can lead to cellulitis, necrotising fasciitis, pneumonitis, meningitis, diarrhoea, hepatitis, pharyngitis and congenital anomalies if contracted during gestation
    • If chickenpox are contracted during the first trimester baby can have scarred limbs, microcephaly and ocular damage
    • If chickenpox are contracted near to terminate baby they may be born with severe neonatal infection
  • Once the initial infection is over the varicella-zoster virus remains dormant in the dorsal root ganglia and if the patient becomes immunosuppressed later in childhood or adult life the virus can be reactivated and cause shingles
39
Q

What is glandular fever?

A

Disease caused by the Epstein-Barr virus, 20% of children contracted particularly in teenage years – it is transmitted through contact with infected saliva

40
Q

Clinical features of glandular fever

A

Malaise, headache, mild fever followed by tonsillitis, pharyngitis, cervical lymph node enlargement, high grade fever and fatigue

  • Not all patients will be symptomatic
  • Other features include a petechial rash on the palate and periorbital oedema, mild hepatitis occurs in 90% of patients and splenomegaly and 50% of patients
41
Q

Diagnosis and management of glandular fever

A
  • Diagnosis is clinical but it can be confirmed by the presence of EBV antibodies in the serum or a blood film showing atypical lymphocytes
  • Management of glandular fever
    • Treatment is supportive and symptoms resolve in around two weeks but the fatigue can last for months
    • Splenic rupture is rare but is a known complication therefore patients are advised to avoid contact sports for a month after infection
42
Q

What type of herpes infection causes blisters around/ inside the mouth?

A

HSV1

43
Q

Clinical features of herpes simplex virus 1 infection

A
  • General malaise followed by inflammation of the mouth and gums followed by small vesicles that rupture and leave painful ulcers

Children affected by herpetic gingivostomatitis can be very unsettled, they may not want to eat or drink and are therefore at risk of dehydration

44
Q

Diagnosis and management of herpes simplex virus type 1

A
  • Diagnosis is based on clinical appearance but can be confirmed via PCR of the vescicular fluid which will show the present of the HSV1 DNA
  • Management is symptomatic including analgesia and fluids

Herpes simplex virus is associated with many other infections apart from herpetic gingivostomatitis and can affect various organ systems

45
Q

What is subacute sclerosing panencephalitis?

A

This is a degenerative disease of the central nervous system that present 7–10 years after measles infection even if the patient appears to have fully recovered from the illness. It occurs due to an abnormal immune response and is divided into four stages. Symptoms include myoclonus with massive myoclonic jerks and pathognomonic changes on the EEG. Patients end up in a continuous vegetative state which may last for several years and culminates in death

  • This occurs in one in 100,000 cases of measles
46
Q
A

Paediatrics (19 decks)

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