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Paediatrics STG > Paediatric Immunology > Flashcards

Paediatric Immunology Flashcards

1
Q

When should vaccines be postponed?

A

Vaccination should be postponed if acute illness; Minor infection without fever or systemic features is not contraindication

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2
Q

Which vaccines should not be given to immunocompromised patients?

A

Live Vaccines should not be given to immunocompromised patients – BCG, MMR, Varicella, Nasal Flu, Rotavirus

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3
Q

6in1 Vaccine

A

Diphtheria, Tetanus, Pertussis, HiB, Polio = DTaP/IPV/HiB/HepB) at 2, 3 and 4/12

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4
Q

Polio Vaccine

A 
Live polio (Sabin) no longer used due to risk of polio in the vaccinated patient and unvaccinated family members/immunocompromised
Can cause Asceptic Meningitis and Paralytic Poliomyelitis
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5
Q

Diphtheria

A

Local disease with membrane formation affecting Nose, Pharynx, Larynx or Systemic disease with Myocarditis and Neurological manifestations

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6
Q

Pertussis Vaccine

A

Whopping cough; Pregnant women now recommended to get dTaP/IPV from 20wks gestation

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7
Q

What other vaccines are given at 2,4 and `12 months

A

Pneumococcal Conjugate Vaccine (PCV13) and Meningococcal B

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8
Q

Which vaccines is given at 2 and 3 months

A

Rotavirus Oral Vaccine

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9
Q

What vaccines are given at 1year

A

Booster HiB and Meningococcus C

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10
Q

Which vaccine is given at 1 year and 3yr4months

A

MMR at 1yr and 3yr4mths

o MMR vaccine can cause mild form of disease 7-10/7 later

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11
Q

When is HPV vaccine given

A

HPV at girls aged between 12-13yrs,

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12
Q

Which vaccine is given from 14 years

A

Meningococcal ACWY at 14yrs

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13
Q

When is BCG given?

A

BCG given to newborns at high risk of TB infection

o Main value is prevention of Disseminated disease (E.g. Meningitis)

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14
Q

When HepB vaccine given?

A

Hep B at birth for babies born to HBsAg positive mothers; If born to highly-infectious HBeAg mothers, receive HB Ig at birth

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15
Q

When is varicella vaccine given?

A

May be given to siblings of at-risk children (E.g. Undergoing Chemotherapy)

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16
Q

Signs of Immunodeficiency

A

o Recurrent (proven) bacterial infections, Severe infections (Meningitis, Osteomyelitis, Pneumonia), Atypical/Unusually Severe/Chronic/Resistant disease, Unexpected pathogen, Severe long-lasting warts or generalised Molluscum contagiosum, Extensive Candidiasis, Complications following live vaccination, Abscesses, Diarrhoea

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17
Q

Primary Immunodeficiency

A

(Uncommon); Genetically determined defect of the Immune System
o Many are X-linked or Autosomal Recessive; FMHx might include consanguinity, unexplained death, especially of boys
o Considered in children with Severe, Prolonged, Unusual or Recurrent infections

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18
Q

Secondary Immunodeficiency

A

(More common); Disease or treatment related, such as Malignancy, Chemotherapy, Malnutrition, HIV infection, Immunosuppression, Splenectomy or Nephrotic Syndrome (Loss of immunoglobulins in the urine)

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19
Q

T Cell Defect Presentation

A

Severe, Unusual Viral and Fungal Infections E.g. Bronchiolitis, Diarrhoea, Oral Thrush, PCP, CMV Infection

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20
Q

T Cell Defects: Diseases

A
  • Severe Combined Immunodeficiency
  • HIV Infection
  • Wiskott-Aldrich; X-linked; Plus, Thrombocytopaenia and Eczema
  • DiGeorge Syndrome (Athymus)
  • Duncan Disease (X-linked Lymphoproliferative Disease)
  • Ataxia Telangiectasia
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21
Q

B Cell Defect Presentation

A

After Infancy, when maternal Ig wears off; Severe Bacterial infections (Ear, Sinus, Pulmonary, Skin), Recurrent diarrhoea, Pneumonia to Bronchiectasis

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22
Q

B Cell Defects Diseases

A
  • X-linked Agammaglobulinaemia (Bruton); Abnormal TK essential for B cell maturation
  • Common Variable Immunodeficiency – B-cell deficiency; risk of Autoimmune disorders and malignancy; Later onset than Bruton
  • Hyper IgM Syndrome – Class switching failure
  • Selective IgA Deficiency – Most common primary immune defect; Usually asymptomatic, but can cause recurrent ear, sinus and pulmonary infections
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23
Q

Neutrophil Defects: Presentation

A

Recurrent Bacterial Infections, Abscesses, Poor wound healing, Perianal and Periodontal infections; Invasive Fungal

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24
Q

Neutrophil Diseases

A

Chronic Granulomatous Disease – X-linked mostly but can also be AR; Failure to produce superoxide after phagocytosis
• Chediak-Higashi Syndrome – Failure of phagocytosis

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25
Q

Leukocyte Function Defects: Presentation

A

Delayed umbilical cord separation, Wound healing, Chronic skin ulcers

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26
Q

Leukocyte Function Defects: Diseases

A

Leukocyte Adhesion Defects – Inability for Neutrophils to migrate to sites of infection

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27
Q

Complement Defects: Presentation

A

Recurrent bacterial infections, SLE-like illness, Recurrent Encapsulated (Meningo, Pneumo, HiB)

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28
Q

Complement Defects: Disease

A
  • Early and Terminal Complement Component Deficiencies

* MBL Deficiency

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29
Q

Investigations into T Cell Defects

A

FBC, T cell subsets (CD3+ Total, CD4+ Helper, CD8+ Cytotoxic); T-cell proliferation in response to Mitogen

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30
Q

Investigations into B cell Defects

A

Ig levels (IgG, IgM, IgA, IgE), IgG subclasses (in children >2yrs), Specific antibody responses, Lymphocyte subsets

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31
Q

Investigation into SCID

A

Specific genetic/molecular tests

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32
Q

Investigation into Neutrophil Defects

A

FBC, Nitroblue-Tetrazolium Test, or newer assays for superoxide production (Abnormal in CGH), CD11b/CD18 expression in LAD, Chemotaxis tests

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33
Q

Investigation into Complement Defects

A

Tests for Classical and Alternative Complement Pathways, Assays for Complement proteins, MBL levels

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34
Q

Management of Primary Immunodeficiency: Antimicrobial Prophylaxis

A

Co-Trimoxazole to prevent PCP, Itraconazole/Fluconazole for other fungal infections for T and Neutrophil Defects; Antibiotics for B cell defects
Prompt treatment of infections; Longer courses, lower threshold for IV Abx

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35
Q

Management of Primary Immunodeficiency: Screening

A

Screening for End-organ disease e.g. HRCT for Bronchiectasis

36
Q

Management of Primary Immunodeficiency: Ig Replacement

A

For Ig Deficiencies; via CVC or Subcut

37
Q

Management of Primary Immunodeficiency: BMT and Gene Therapy

A

For SCID, CGD; Sibling donor, Matched unrelated or Parental transplant (Haploidentical)
Currently in development

38
Q

What is an allergy

A

Hypersensitivity Reaction initiated by Specific Immunological Mechanisms; IgE mediated (e.g. Peanut allergy) or non-IgE (e.g. Coeliac)

39
Q

What is hypersensitivity

A

Objectively reproducible response following exposure to defined stimuli at dose tolerated by most people

40
Q

What is atopy

A

Tendency to produce IgE in ordinary exposure to potential allergens
o Associated with Asthma, Allergic Rhinitis, Conjunctivitis, Eczema, Food Allergy

41
Q

Aetiology of allergy

A

Multigenetic; Polymorphisms or mutation can lead to susceptibility; Developing Immune system needs to be sensitized before response develops, which can be occult

42
Q

Common Allergens

A

o Common allergens include Aeroallergens (HDM, Pollen, Dander, Moulds), Ingestants (Cow’s Milk Protein, Nuts, Soya, Egg, Wheat etc), Insect stings, Drugs, Latex

43
Q

IgE Mediated Response

A

Early phase (release of Histamine and other Mast Cell Mediators) of Urticaria, Angioedema, Sneezing, Vomiting, Bronchospasm, Shock; followed by Late phase after 4-6hrs of Nasal congestion, Cough, Bronchospasm

44
Q

Hygiene Hypothesis

A

Lower risk of allergy in rural environments; Altered microbial ex posure in modern life possibly leading to increase in allergic disease

45
Q

The Allergic March

A

Eczema and Food Allergy usually in Infancy; Allergic Rhinitis, Conjunctivitis and Asthma in Preschool and Primary years; Asthma might follow

46
Q

Signs of Allergy

A

Mouth Breathing/Snoring/Sleep Apnoea, Pale swollen Turbinates, Hyperinflation, Atopic Eczema (Limb flexures), Allergic Conjunctivitis, Blue-green discolouration of lower eyelids

47
Q

Anaphylaxis

A

Severe, Life-threatening, Generalised or Systemic Hypersensitivity Reaction; Sudden onset, Progressive Life-threatening Airway, Breathing and Circulatory Arrest
o Skin, Mucosal signs of Urticaria, Angioedema
o 85% in children due to Food Allergy; IgE mediated reactions with cardiorespiratory compromise; Other causes are Insect stings, Drugs, Latex, Exercise, Aeroallergens
• Most occur in children under 5yrs age where food allergy is most prevalent
• Most deaths occur in adolescents with nut allergy

48
Q

Anaphylaxis: Long Term Management

A

Detailed strategies and training; Allergen avoidance, Treatment of Allergic Reactions, Adrenaline Auto-injectors; Preventative Allergen Immunotherapy

49
Q

Anaphylaxis ABCDE Assessment

A
  • ABCDE Stabilisation
  • Diagnosis – Acute onset Airway (Swelling, Hoarseness, Stridor), Breathing (Tachypnoea, Wheeze, Cyanosis, Desaturating), Circulation (Pale, Clammy, Hypotensive, Drowsy, Comatose)
50
Q

Emergency Management of Anaphylaxis

A

• Call for help; Sit up if difficulty breathing, Supine and Elevated legs if Hypotensive; Recovery position if unconscious; BLS/ALS resuscitation if needed
• IM Adrenaline 1:1000 IM
• Definitive Airway, High Flow O2, IV Fluids (20ml/kg Crystalloid), Chlorphenamine IM/slow IV, Hydrocortisone IM/slow IV, Salbutamol if wheeze
o Monitor SpO2, ECG, BP

51
Q

Food Allergy

A

Food allergy occurs due to pathological immune response against specific food protein; Mostly IgE-mediated

52
Q

Food Intolerance

A

Non-immunological hypersensitivity

Non-IgE food allergy occurs hours after ingestion and involves GI disturbances

53
Q

Food Allergy Presentations in Paediatrics

A

Food allergy most commonly primary, reacting to first exposure; Presentation variable
o Infants – Milk, Eggs and Peanut; Older Children – Peanut, Tree Nut, Fish, Shellfish
• Can also be secondary due to cross-reactivity between Proteins and Pollens (e.g. Apple and Birch Tree Pollens); also called Pollen Food Allergy Syndrome; Itchy mouth but not systemic

54
Q

Food Aversion

A

Refusal for Psychological or Behavioural Reasons

55
Q

IgE Mediated Food Allergy: Symptoms

A

Urticaria, Facial Swelling up to Anaphylaxis; Occurs 10-15 mins, up to 2hrs after ingestion

56
Q

Non IgE Mediated Food Intolerance: Symptoms

A

Diarrhoea, Vomiting, Abdominal Pain, Colic or Eczema might be present; Sometimes bloody stools due to Proctitis

57
Q

Food Protein Induced Enterocolitis Syndrome

A

Repetitive Vomiting leading to Shock

58
Q

Management of Food Allergy: Investigations

A

Clinical History, Skin Prick Testing and Specific IgE blood tests; Negative SP makes IgE mediated allergy unlikely;
For non-IgE; Endoscopy/Biopsy can identify Eosinophilic infiltrates
• Gold standard – Food exclusion followed by double-blind controlled incremental challenge

59
Q

Management of Food Allergy: Treatment

A

Avoidance of relevant foods, Paediatric dietitian advice, Education, Drug Management (Non-sedating Antihistamines, Adrenaline Auto-injector)

60
Q

Atopic Eczema

A

Dermatitis: With IgE antibodies to common allergens
FMHx; at least 50% develop other allergic diseases
o Filaggrin gene mutation identified as key genetic RF; Impairment of skin barrier function leading to Cutaneous sensitisation to allergens
o Up to 40% with Severe Eczema also have IgE-mediated Food Allergy

61
Q

Atopic Eczema: Stats

A

20% of children have Atopic Eczema; Usually presents in first year of life; Uncommon in first 2 months (C/f Infantile Seborrheic Dermatitis, which is not itchy)
• Mainly disease of childhood; 50% resolve by 12yrs, 75% by 16yrs

62
Q

Atopic Eczema: Diagnosis

A

Clinical diagnosis; If Severe, Atypical or associated with Unusual infections or Faltering growth, consider Immunodeficiency
o Pruritus is the main symptom; Atopic skin is usually dry; Lichenification occurs following prolonged scratching and rubbing

63
Q

Atopic Eczema: Ddx

A

Chickenpox, Allergy, Contact Dermatitis, Insect Bites, Scabies, Fungal Infections, Pityriasis Rosea

64
Q

Atopic Eczema: Exacerbations

A

Exacerbations can be caused by Infection, Allergen exposure, Environment (heat, humidity), Medication changes, Psychological stress or Idiopathic

65
Q

Atopic Eczema: Infections

A

Eczematous skin readily infected; Staph or Strep commonly; More Severe infections
o HSV Infection – Uncommon but spreads rapidly = Eczema Herpeticum
o Regional LNA is common; Resolves when the skin improves

66
Q

Management of Atopic Eczema: Irritant Avoidance

A

• Irritant Avoidance – Detergent, Clothing, Mittens and Nail clipping to reduce scratching, Allergens, where proven, should be avoided

67
Q

Management of Atopic Eczema: Treatments

A

Emollients – 2 or more times a day and after bath; Ointments of 50:50 White soft paraffin and Liquid paraffin; Preferable to cream if skin is very dry
• Topical Steroids – 1% Hydrocortisone applied 1-2 times daily if needed; Minimal use of moderately-potent steroids in Acute Exacerbations; Applied thinly and face avoided
o Excessive use can cause thinning of skin and systemic SE
• Immunomodulation (IL2 Inhibition) – Tacrolimus Ointment or Pimecrolimus cream if topical steroids not helpful; for children >2yrs
• Occlusive Bandages – Helpful if scratching and Lichenification is problem; can be medicated
• Antibiotics, Aciclovir, Antihistamines

68
Q

Management of Atopic Eczema: Dietary Elimination

A

Food allergy suspected if moderate or severe Eczema, especially if associated with GI dysmotility or growth faltering
o Most commonly egg or cow’s milk protein

69
Q

Infantile Haemangioma: What is it

A

• 1% of infants; Presents at or shortly after birth as single, red lumpy nodule that grows rapidly for first few months; May spontaneously resolve with good cosmesis, but take up to 7yrs
o Plastic surgery might be required to remove residual slack skin

70
Q

When does a haemangioma require treatment

A

Urgent treatment if – Interference with Feeding or Vision, Ulceration and Frequent Bleeding, Associated with High-output Cardiac Failure due to shunting, or consumption of platelets and clotting factors, causing life-threatening Haemorrhage (Kasabach-Merritt syndrome)

71
Q

Haemangioma Treatment

A

Treatment with Oral Propanolol (2mg/kg/day in 3 divided doses) rapidly shrinks lesions; High-dose Systemic Steroids, Vincristine or Embolisation for non-responding patients rarely

72
Q

Portwine Stain

A

Not true haemangioma; Abnormal dilation of dermal capillaries
• Presents as birth as flat, red macular area; Commonly found on face; Does not improve spontaneously and may thicken over time

73
Q

Sturge Weber Syndrome

A

Mark in distribution of Ophthalmic (CN V1), associated with underlying Meningeal Vascular Anomalies; can cause Epilepsy and Hemiplegia
o If involves skin near the eye, can lead to Glaucoma; Ophthalmic assessment required

74
Q

Port Wine Stain Treatments

A

Treatment with Tunable/Pulsed Dye Laser; Facial lesions respond best

75
Q

Nappy Rash: Causes

A

Common; Most commonly due to Irritant (Contact) Dermatitis

o Due to urine; Urea-splitting organisms increase alkalinity and likelihood of rash

76
Q

Nappy Rash: What does it look like

A

Irritant eruption covers convex surfaces; flexures are characteristically spared

77
Q

Nappy Rash: Treatment

A

Treat with mild Emollients while severe cases require mild Topical Steroids

78
Q

Nappy Rash: Ddx

A

Infantile Seborrhoeic Dermatitis, Candida Infection and Atopic Eczema

79
Q

Infantile Seborrhoeic Dermatitis

A

Eruption of unknown cause in first 3/12; Non-itchy (C/f Eczema); Scaly eruption followed by thick, yellow adherent layer; Resolves with Emollients, or if required steroids and antimicrobials can be used

80
Q

Candida

A

Erythematous, includes skin flexures, and may have satellite lesions; Topical antifungal agents

81
Q

Mongolian Blue Spots

A

Deep, blue-grey bruise-like area typically Sacrum or Back; Mistaken for NAI; Due to deep, Dermal Melanocytes; Common in Oriental children; Disappears by 7yrs

82
Q

Café Au Lait Spots

A

Pigment-producing Melanocytes; Multiple/large spots might be associated with NF1, McCune Albright Syndrome, Tuberous Sclerosis and Fanconi Syndrome

83
Q

Milia (Milk Spots)

A

Small follicular epidermal cysts (White pimples); Commonly found on face of infants; Spontaneously resolve without intervention

84
Q

Miliaria (Sweat Rash)

A

Small, Itchy Erythematous rash; Common in hot and humid conditions; Common in infants, due to underdeveloped Sweat glands

85
Q

Toxic Erythema of Newborn

A

Common, Transient Maculo-papular Rash in Newborns; Occasionally Pustular; Child is not toxic or unwell; Spontaneously resolve within days

86
Q

Acrodermatitis Enteropathica

A

Rare, Inherited Deficiency of Zn Absorption; Presents 4-6/52 after weaning; Erythematous sometimes Blistering rash; Might be associated with Photophobia, Diarrhoea or Alopecia; Rapidly responds to Zn supplementation

Paediatrics STG (17 decks)

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