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1mrcpch fop and tas > Infection, Immunology and Allergy > Flashcards

Infection, Immunology and Allergy Flashcards

1
Q

What is the overall mortality of bacterial meningitis?

A

5-10%

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2
Q

What percentage of survivors from bacterial meningitis are left with long term neurological impairment?

A

10%

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3
Q

What are the most common organisms which cause bacterial meningitis in under 3month olds?

A

GBS
E.coli
Listeria

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4
Q

What are the most common organisms which cause bacterial meningitis in over 3month olds?

A

Neisseria meningitides
Strep. pneumoniae

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5
Q

What is the Brudzinsk sign?

A

Flexion of the neck with the child supine causes flexion of knees and hips

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6
Q

What is the Kernig sign?

A

If child lying supine, with hips and knees flexed, there is pain on extension of the knee

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7
Q

What are the contraindications to LP?

A

Cardiorespiratory instability
Focal neurological signs
Signs of raised ICP
Coagulopathy
Thrombocytopenia
Local infection at site of LP
If it will cause delay in abx

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8
Q

In a CSF sample for meningitis, what colour would the fluid be in a bacterial infection?

A

Turbid

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9
Q

In a CSF sample for meningitis, what colour would the fluid be in a TB infection?

A

Turpid/clear/viscous

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9
Q

In a CSF sample for meningitis, what would be expected to be found on the cell count for a bacterial infection?

A

Very increased WCC, mainly polymorphs

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10
Q

In a CSF sample for meningitis, what colour would the fluid be in a viral infection?

A

Clear

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10
Q

In a CSF sample for meningitis, what colour would the fluid be in a viral encephalitis infection?

A

Clear

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11
Q

In a CSF sample for meningitis, what would be expected to be found on the CSF protein level for a viral infection?

A

Normal or protein +

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11
Q

In a CSF sample for meningitis, what would be expected to be found on the cell count for a viral encephalitis infection?

A

Normal/increased lymphocytes

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11
Q

In a CSF sample for meningitis, what would be expected to be found on the cell count for a viral infection?

A

Increased WCC, lymphocytes

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11
Q

In a CSF sample for meningitis, what would be expected to be found on the cell count for a TB infection?

A

Increased WCC, lymphocytes

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12
Q

In a CSF sample for meningitis, what would be expected to be found on the CSF protein level for a TB infection?

A

Protein +++

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12
Q

In a CSF sample for meningitis, what would be expected to be found on the CSF protein level for a bacterial infection?

A

Protein ++

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13
Q

In a CSF sample for meningitis, what would be expected to be found on the CSF protein level for a viral encephalitis infection?

A

Normal or protein +

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14
Q

In a CSF sample for meningitis, what would be expected to be found on the CSF glucose level for a bacterial infection?

A

Glucose –

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15
Q

In a CSF sample for meningitis, what would be expected to be found on the CSF glucose level for a viral infection?

A

Normal or glucose -

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16
Q

In a CSF sample for meningitis, what would be expected to be found on the CSF glucose level for a TB infection?

A

Glucose —

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17
Q

In a CSF sample for meningitis, what would be expected to be found on the CSF glucose level for a viral encephalitis infection?

A

Normal or glucose -

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18
Q

What are the potential complications from meningeal infection?

A

Hearing impairment
Local vasculitis
Local cerebral infacrtion
Subdural effusion
Hydrocephalus
Cerebral abscess

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19
Q

What prophylaxis is given to close contacts of a person with proven meningitis?

A

Ciprofloxacin to close contacts
In cases of A,C,W or Y infections, close contacts should be offered vaccination

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20
Q

What are the common pathogens causing viral meningitis?

A

Enterovirus
Parechovirus
EBV
Adenovirus
Mumps

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21
Q

What are the most common infectious causes of encephalitis in the UK>

A

Enteroviruses
Respiratory viruses
HSV
HHVs

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21
Q

What is the treatment for HSV encephalitis?

A

3 weeks of IV aciclovir

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22
Q

What is the prognosis for HSV encephalitis?

A

Untreated, mortality is >70%
Those who survive tend to have long term neurological sequelae

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23
Q

In HSV encephalitis, on doing a CT/MRI brain what may be seen other than typical signs encephalitis?

A

Focal changes in the temporal lobe(s)

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23
Q

Which organisms typically cause necrotising fasciitis?

A

Staph aureus or GAS
Can be synergistic anaerobes

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23
Q

Which organisms are responsible for causing toxic shock syndrome?

A

Staph aureus
GAS

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24
Q

What is the typical presentation in TSS?

A

Fever >39degrees
Hypotension
Diffuse, erythematous, macular rash

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25
Q

What is the evidence of organ dysfunction in TSS?

A

GI dysfunction
Renal or liver impairment
Deranged clotting and thrombocytopenia
Altered consciousness

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25
Q

In TSS what happens to the skin around 1-2weeks following acute infection?

A

Desquamation of palms, soles, fingers and toes

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26
Q

What is the significance of a PVL toxin in TSS and how does this differ the usual course of the disease?

A

Can cause necrotising fasciitis and necrotising haemorrhagic pneumonia both of which increase mortality rate
Leads to a procoagulant state to venous thromboses more likely to occur

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26
Q

How is TSS treated?

A

Usually with ceftriaxone and clindamycin
Debridement of areas of infection
IVIG may be needed to neutralise toxin
Usually needs managing in an PICU setting

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27
Q

How does necrotising fasciitis typically present?

A

Rapidly advancing, highly painful areas of tissue necrosis and systemic illness

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28
Q

How is necrotising fasciitis managed?

A

IV antibiotics
Surgical debridement
IVIG may be used

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29
Q

How does the rash in meningococcal infection usually appear?

A

Non-blanching
Irregular
May have necrotic centre
Typically lesions are larger than 5mm

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30
Q

What types of infection does strep pneumoniae often cause in children?

A

Pharyngitis
OM
Conjunctivitis
Sinusitis
Invasive infection

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31
Q

What antibiotic should be given prophylactically to immunocompromised or at risk children to prevent strep pneumoniae infection?

A

Penicillin

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32
Q

Which organism causes scarlet fever?

A

GAS

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33
Q

How does the rash in scarlet fever typically present?

A

Diffuse, erythematous, maculo-papular rash with a sandpaper texture
Usually appears on face, trunk and limbs

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34
Q

What are the typical oral findings in scarlet fever?

A

Circumoral pallor
Tongue initially white but desquamates to become a strawberry tongue

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34
Q

What is the treatment for scarlet fever?

A

10 days or PenV or erythromycin

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34
Q

How is periorbital cellulitis managed?

A

IV abx e.g. ceftriaxone to prevent spread to orbital tissues

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35
Q

How does the typical rash in impetigo present?

A

Lesions on face, neck and hands which are initially erythematous macules which then blister and then rupture to leave honey-crusted lesions

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35
Q

What oraganisms cause impetigo?

A

Usually staph aureus but may be strep

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36
Q

What is the treatment for impetigo?

A

Topical or oral abx (flucloxacillin) depending on severity

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36
Q

What is a boil?

A

Infection of hair follicle or sweat gland

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37
Q

What organism usually causes boils?

A

Staph aureus

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37
Q

What is the treatment for boils?

A

Swab lesion
Systemic abx
Occasionally I&D

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38
Q

How does periorbital cellulitis usually present?

A

Fever with erythema, tenderness and oedema of eyelid or other skin adjacent to eye
All anterior to orbital septum

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38
Q

How does orbital cellulitis present?

A

Proptosis
Painful or limited ocular movements
Potential decline in visual acuity

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39
Q

How does staphylococcal scalded skin syndrome present?

A

Fever and malaise
Purulent crusting and localised infection followed by widespread erythema and tenderness of the skin

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40
Q

What is the treatment of SSSS?

A

ABX IV
Analgesia
Careful fluid balance and rehydration

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41
Q

At what level does the skin separate in SSSS?

A

Epidermis

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42
Q

Do SSSS lesions cause scarring?

A

No

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43
Q

What is Nikolsky sign?

A

Areas of epidermis separate on gentle pressure

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44
Q

What conditions is HHV 8 associated with?

A

Kaposi sarcoma

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45
Q

What kind of lesion is HSV1 typically associated with?

A

lip and skin lesions

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46
Q

What kind of lesion is HSV2 typically associated with?

A

genital lesions

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47
Q

What is the treatment for HSV infections?

A

Aciclovir

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47
Q

How do gingivostomatitis HSV lesions typically present?

A

Usually from 10months to 3years
Vesicular lesions on lips, gums, anterior surface of tongue and hard palate which often progress to extensive and painful ulceration

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48
Q

Which pathogen causes cold sores?

A

HSV

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48
Q

How does eczema herpeticum present?

A

Widespread, ‘punched-out’ vesicular lesions on eczematous skin

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49
Q

What is a herpetic Whitlow?

A

Painful, erythematous, oedematous white pustules at the site of broken skin, esp fingers

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49
Q

How is eczema herpeticum managed?

A

IV aciclovir

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50
Q

How does HSV eye disease present?

A

Blepharitis or conjunctivitis usual
Can extend to cornea causing dendritic ulcers
Needs urgent ophthalmological assessment

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50
Q

What are the clinical features of chickenpox?

A

Fever
Rash
Itching and scratching may cause scarring and secondary bacterial infection

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51
Q

What does the typical rash look like in chickenpox?

A

50-500 lesions start on head and trunk and progress to limbs
Appear as crops of papules and vesicles with surrounding erythema
Then become pustules
Then crust over and heal

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52
Q

What are the complications of VZV infection?

A

Secondary bacterial infection - usually staph or strep
CNS infection
Purpura fulminans

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52
Q

What treatment is given to immunocompromised individuals for uncomplicated chickenpox?

A

IV aciclovir, switched to oral valaciclovir when safe

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53
Q

What treatment is given to immunocompetent individuals for uncomplicated chickenpox?

A

Calamine lotion for itching
Antivirals not recommended

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53
Q

How does EBV infection typically present?

A

Fever
Malaise
Tonsillitis/Pharyngitis
Lymphadenopathy

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54
Q

What treatment is given to immunocompromised individuals for close contact with VZV infection?

A

IVIG

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55
Q

How does shingles present?

A

Vesicular eruption in a dermatomal pattern - usually on torso

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55
Q

How is EBV diagnosed?

A

Atypical lymphocytes on blood film
Positive monospot test

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56
Q

How does CMV present in an immunocompetent individual?

A

Usually asymptomatic or a mild EBV-like syndrome

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56
Q

How may CMV present in an immunocompromised individual?

A

Retinitis
Pneumonitis
Bone marrow failure
Encephalitis
Hepatitis
Oesophagitis
Enterocolitis

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56
Q

How is CMV treated?

A

IV ganciclovir or oral valganciclovir/foscarnetor/cidofovir

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56
Q

What are the less common symptoms of EBV infection?

A

Petechiae on soft palate
Hepatomegaly - 10%
Splenomegaly - 50%
Maculopapular rash - 5%
Jaundice

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56
Q

What disease does HHV 6 and 7 usually cause?

A

Roseola Infantum

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56
Q

How does Roseola Infantum usually present?

A

High fever and malaise for a few days
Followed by generalised macular rash as fever subsides

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57
Q

What condition does parvovirus B19 typically cause?

A

Erythema Infectiosum aka Fifth disease aka Slapped cheek syndrome

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57
Q

How does slapped cheek syndrome typically present?

A

Fever, malaise, headache and myalgia
Followed by a rash on the face which spreads to the trunk and limbs (maculopapular ‘lace-like’)

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57
Q

What is the most serious complication of parvovirus B19 infection?

A

Aplastic crisis
Occurs more often in those with haemolytic disease or immunocompromised

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57
Q

How does hand foot and mouth disease typically present?

A

Painful vesicular lesions on hands, feet, mouth and often buttocks

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58
Q

Which organism causes hand foot and mouth disease typically?

A

Enteroviruses

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58
Q

What virus is the most common cause of viral meningitis in the UK?

A

Enterovirus

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59
Q

What is pleurodynia also known as?

A

Bornholm disease

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59
Q

Which organism is responsible for Bornholm disease?

A

Enterovirus

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59
Q

How does pleurodynia usually present?

A

Acute illness with fever, pleuritic chest pain and muscle tenderness

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60
Q

What can enterovirus D68 rarely cause?

A

Acute flaccid myelitis

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60
Q

What organism causes eczema coxsackium?

A

Enterovirus

60
Q

How does eczema coxsackium present?

A

vesicles, bullae and erosions

60
Q

How is influenza treated for children who are hospitalised?

A

Osteltamivir or zanamivir

60
Q

What are koplik spots?

A

White spots on buccal mucosa

60
Q

How does measles typically present?

A

Fever
Conjunctivitis and coryza
Cough
Rash
Koplik spots

61
Q

What is the mortality for measles encephalitis?

A

15%

61
Q

How does mumps typically present?

A

Fever, malaise and parotitis

61
Q

How does the rash in measles typically present?

A

Discrete maculopapular rash which later becomes blotchy and confluent
Typically starts behind ear and spreads downwards to rest of body

62
Q

What is the prevalence of CNS involvement in mumps?

A

Lymphocytes in CSF in 50%
Meningitis in 10%
Encephalitis in 1 in 5000

62
Q

In how many cases of measles does measles encephalitis occur?

A

1 in 5000

62
Q

How does measles encephalitis typically present?

A

Headache, lethargy and irritability leading to seizures and coma

62
Q

What are the long term sequelae of measles encephalitis?

A

40% survivors will have some or all of:
Seizures
Deafness
Hemiplegia
Severe LD

63
Q

What viral condition can sometimes cause orchitis?

A

Mumps

63
Q

What is the treatment of measles?

A

Mainly supportive
Isolate form others
Ribavirin if immunocompromised
Vitamin A in low-income countries

63
Q

What is the risk of developing SSPE following measles infection

A

1 in 100000 cases

63
Q

Which condition does subacute sclerosing panencephalitis (SSPE) occur after?

A

Measles

63
Q

How long after measles infection does SSPE occur?

A

7 years

64
Q

How does SSPE present?

A

Loss of neurological function which leads to dementia and death over several years

64
Q

What age group does Kawasaki disease most commonly affect?

A

6months - 4years

64
Q

How does rubella typically present?

A

Mild prodrome with low-grade fever
Maculopapular rash starting on face then spreads to cover whole body
Lymphadenopathy is prominent

64
Q

Which ethnic group is more prone to Kawasaki disease?

A

Japanese
Black-Caribbeans

65
Q

Kawasaki disease can be diagnosed clinically by the presence of fever for 5 days and presence of 4 of 5 other features. what are these other features?

A

Bilateral non-purulent conjunctivitis
Erythema and cracking of lips, strawberry tongue +/- erythema of oral mucosa
Cervical lymphadenopathy
Maculopapular rash
Erythema and oedema of hands and feet in acute phase or peeling of skin in subacute phase

65
Q

What blood findings would be expected in Kawasaki disease?

A

Raised WCC, CRP, ESR and platelets

65
Q

What proportion of children with Kawasaki disease have coronary artery involvement?

A

1/3

66
Q

What are the coronary artery issues in Kawasaki disease?

A

Coronary artery aneurysms
Narrowing of vessels which can lead to ischaemia and sudden death

66
Q

What treatment is given in Kawasaki disease?

A

IVIG
Aspirin

66
Q

What is the mortality rate in Kawasaki disease primarily due to coronary artery disease?

A

0.5%

66
Q

What are the presenting features or PIMS?

A

Persistent fever
Evidence of inflammation
Single or multi-organ failure
GI symptoms, rash and conjunctivitis common

67
Q

What is the cardiac involvement in PIMS?

A

Myocarditis
Coronary artery abnormalities
Valve involvement
Pericardial effusion

67
Q

How is PIMS treated?

A

IVIG
Low dose aspirin
Corticosteroids

67
Q

What increases the risk of TB transmission?

A

Close proximity
Large infectious load in index case
Underlying immunodeficiency

68
Q

What are the symptoms of primary TB infection?

A

Local and regional lymphadenopathy
Systemic symptoms:
Fever
Anorexia and weight loss
Cough

CXR changes - hilar lymphadenopathy

68
Q

What percentage of children are asymptomatic with primary TB infection?

A

50% neonates
90% older children

68
Q

What percentage of children with TB have pulmonary TB?

A

75%

68
Q

How is TB diagnosed?

A

Gastric washings or induced sputum from 3 separate mornings examined for acid-fast bacilli and culture
Mantoux test also done (>5mm is a +ve result)
IGRA also useful

69
Q

What is the treatment for TB?

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
All of the above for 2 months, then reduced to just rifampicin and isoniazid
Total treatment for uncomplicated disease is for 6 months

69
Q

What are the typical symptoms of malaria?

A

Fever
D&V
Flu-like Sx
Jaundice
Anaemia
Thrombocytopenia

69
Q

How is malaria diagnosed?

A

Thick blood film diagnoses condition and thin blood film confirms species

70
Q

How does typhoid infection present?

A

Worsening fever
Headaches
Cough
Abdominal pains
Anorexia
Malaise
Myalgia
Occasionally splenomegaly, bradycardia and rose coloured spots

70
Q

How is plasmodium falciparum infection treated?

A

Quinine or artemisinin based formulation

70
Q

What are the serious complications of typhoid?

A

GI perforation
Myocarditis
Hepatitis
Nephritis

71
Q

What is the treatment for typhoid?

A

Co-trimoxazole and chloramphenicol/ampicillin
If drug resistance then 3rd gen. cephalosporin or azithromycin may be needed

71
Q

How does Dengue fever typically present?

A

Erythematous rash, myalgia, arthralgia and high fever

71
Q

Where does Dengue fever commonly occur?

A

Tropics

72
Q

Where is Chikungunya commonly found?

A

Endemic in parts of Africa, Asia and India

73
Q

How does Chikungunya typically present?

A

Fever
Arthritis
Arthralgia

73
Q

Where is the Zika virus commonly found?

A

Transmitted by aedes mosquitoes in Central and South America and the Caribbean

73
Q

How does zika virus commonly present?

A

Fever
Rash
Conjunctivitis
Arthralgia

74
Q

How does the zika virus affect pregnant women?

A

Causes fetal microcephaly and other brain abnormalities

74
Q

What causes lyme disease?

A

Borrelia Burgdorferi transmitted via ticks

74
Q

Describe the lesion associated with lyme disease infection?

A

Erythematous macule at the site of lesion enlarged to cause typical “target” lesion aka erythema migrans

75
Q

How does early lyme disease present?

A

Fever
Headache
Malaise
Myalgia
Arthralgia
Lymphadenopathy

75
Q

How does late lyme disease present?

A

Neurological:
- fluctuating fatigue
- meningoencephalitis
- peripheral, central or autonomic neuropathies
Cardiac:
- myocarditis
- heart block
MSK:
- brief migratory arthritis
- acute asymmetrical mono or oligoarthritis or large joints

75
Q

How is lyme disease diagnosed?

A

Clinically and lyme serology

76
Q

What is the treatment of lyme disease in those <8y/o

A

Amoxicillin

77
Q

What is the treatment of lyme disease in those >8y/o

A

Doxycycline

77
Q

What are examples of live attenuated vaccines?

A

MMR
Rotavirus
BCG

77
Q

What are examples of inactivated vaccines?

A

Polio
Influenza

78
Q

What are examples of subunit vaccines?

A

Diphtheria
Pneumococcal
HPV
HBV

79
Q

What vaccines are routinely given in the UK at 2 months?

A

6 in 1
Rotavirus
Meningococcal B

79
Q

What is included in the 6 in 1 vaccine?

A

Diphtheria
Tetanus
Pertussis
Polio
H. influenzae B
Hepatitis B

79
Q

What vaccines are routinely given in the UK at 3 months?

A

6 in 1
Rotavirus
Pneumococcal conjugate vaccine (PCV)

80
Q

What vaccines are routinely given in the UK at 4 months?

A

6 in 1
MenB

80
Q

What vaccines are routinely given in the UK at 12 months?

A

PCV
MenB
HiB/MenC
MMR

80
Q

What vaccines are routinely given in the UK at 2-7 years?

A

Influenza seasonal vaccine

80
Q

What vaccines are routinely given in the UK at 3 years and 4 months?

A

MMR
4 in 1 (Diphtheria, tetanus, pertussis, polio)

81
Q

What vaccines are routinely given in the UK at 12-13 years?

A

HPV

81
Q

What vaccines are routinely given in the UK at 14 years?

A

Men ACWY
3 in 1 (diphtheria, pertussis, polio)

81
Q

What are the contraindications of immunisation?

A

Postponed if acute infection
Live vaccines should not be given to immunocompromised patients
Anaphylaxis to previous dose

82
Q

In immunodeficiency how do T-cell defects typically present?

A

Severe and/or unusual viral and fungal infections
Faltering growth in the first months of life
PCP or disseminated/severe CMV

82
Q

Is SCID a T-cell or B-cell immunodeficiency?

A

Can affect both

82
Q

What is SCID?

A

A heterogenous group of inherited disorders of profoundly defective cellular and humoral immunity

82
Q

What triad of features is typical of Wiskott-Aldrich syndrome?

A

Immunodeficiency
Thrombocytopenia
Eczema

83
Q

What is Duncan disease and how does it present?

A

X-linked proliferative disease
Inability to generate a normal response to EBV
Patients either succumb to initial infection or develop secondary lymphoma

83
Q

What is ataxia telangiectasia and how does it present?

A

Defect in DNA repair
Increased risk of lymphoma
Cerebellar ataxia and developmental delay

83
Q

In immunodeficiency how do B-cell defects present?

A

Severe bacterial infections especially ear, sinus, pulmonary and skin
Recurrent diarrhoea
Faltering growth

83
Q

What are some types of B-cell defects?

A

X-linked agammaglobulinaemia
Common variable immune deficiency (CVID)
Hyper IgM syndrome
Selective IgA deficiency

84
Q

In immunodeficiency how do neutrophil defects present?

A

Recurrent bacterial defects - abscesses, poor wound healing, perianal disease, periodontal infections and invasive fungal infections
Diarrhoea and faltering growth
Granulomas from chronic inflammation

85
Q

What is an example of neutrophil defect disease?

A

Chronic granulomatous disease

86
Q

How is chronic granulomatous disease inherited?

A

Mostly x-linked recessive but some AR

87
Q

In immunodeficiency how do leukocyte function defects present?

A

Delayed separation of umbilical cord
Delayed wound healing
Chronic skin ulcers
Deep-seated infections

88
Q

What is the basic pathophysiology of leukocyte adhesion deficiency?

A

Deficiency of neutrophil surface adhesion molecules CD15a
Leads to inability of neutrophils to migrate to sites of infection/inflammation

89
Q

What is the basic pathophysiology of chronic granulomatous disease?

A

Neutrophils fail to produce superoxide after phagocytosis of microorganisms

89
Q

What is an example of a leukocyte function defect?

A

Leukocyte adhesion deficiency

90
Q

In immunodeficiency how do complement defects present?

A

Recurrent bacterial infections
SLE-like illness
Recurrent meningococcal, pneumococcal and H.influenzae infections

90
Q

What are some examples of complement defect disorders?

A

Early complement component deficiency
Terminal complement component deficiency
Mannase-binding lectin (NBL) deficiency

91
Q

What investigations should be done for T-cell defects?

A

FBC
Lymphocyte subsets

92
Q

What investigations should be done for neutrophil defects?

A

FBC
NBT (nitroblue tetrazolium test) - abnormal in chronic granulomatous disease
Tests for leukocyte adhesion deficiency
Tests for chemotaxis

92
Q

What investigations should be done for B-cell defects?

A

Immunoglobulins
IgG subclasses
Lymphocyte subsets
Specific antibody responses

93
Q

What investigations should be done for complement defects?

A

Tests of classical and alternative complement pathways
MBL levels
Assays for individual complement proteins

93
Q

What is the antibiotic prophylaxis of T-cell and neutrophil defects?

A

Co-trimoxazole to prevent PCP
Itraconazole/fluconazole to prevent fungal infections

93
Q

What is the antibiotic prophylaxis of B-cell defects?

A

Azithromycin to prevent recurrent bacterial infections

93
Q

Other than prophylactic antibiotics what are the other treatments for immunodeficiency?

A

Screening for end organ disease
Immunoglobulin replacement therapy
Bone marrow Tx
Gene therapy

94
Q

What are the symptoms of non-IgE mediated allergy?

A

D&V
Abdo pain
Faltering growth

94
Q

What tests can be done in suspected allergy?

A

Skin prick tests
IgE blood tests
Spirometry and lung function tests
Allergy challenge

94
Q

What happens in the late phases of an IgE mediated allergic reaction?

A

Nasal congestion in the upper airway, cough and bronchospasm in the lower airway

95
Q

What happens in the early phases of an IgE mediated allergic reaction?

A

Urticaria, angioedema, sneezing, vomiting, bronchospasm and/or cardiovascular shock
Caused by release of histamine and other mediators from mast cells

95
Q

How does eosinophilic oesophagitis present?

A

Persistent vomiting and swallowing difficulty in young children
Difficulty swallowing and food impaction in older children

96
Q

What gene mutations are a risk factor for development of atopic eczema?

A

Fillagrin gene mutations

97
Q

At what stage is urticaria considered chronic?

A

6 weeks

98
Q

How is chronic urticaria managed?

A

Non-sedating antihistamines
Refractory disease may need omalizumab

99
Q

What does a child with Chediak-Higashi syndrome typically look like?

A

Pale with red hair

100
Q

How is Chediak-Higashi syndrome inherited?

A

AR

101
Q

What is the prognosis for Chediak-Higashi syndrome?

A

Often fatal in childhood

102
Q

After erythema migrans, what is the next most common symptom in lyme disease?

A

Neurological disorders - facial nerve palsy is most common

103
Q

What are the neurological symptoms in lyme disease?

A

Facial nerve palsies
Meningitis
Encephalitis
Peripheral mononeuritis
Lymphocytic meningoradiculitis

104
Q

What are the cardiac symptoms in lyme disease?

A

Myopericarditis
Heart block (1st degree)

105
Q

What are lymhocytomas and where do they typically present?

A

Bluish-red nodules infiltrated with lymphocytes
Typically on earlobe or nipple

106
Q

How is SCID usually inherited?

A

AR
May be de novo

107
Q

In SCID what would be seen on the lymphocyte count?

A

Lymphopenia <2.5-3

107
Q

In SCID what would the CXR show?

A

Absent thymic shadow

108
Q

In SCID what would be seen on checking immunoglobulin levels?

A

Low IgG, IgM and IgA

109
Q

If an individual with SCID needs a blood transfusion what additional precautions should be taken?

A

Blood should be CMV -ve and irradiated

110
Q

What may precipitate hereditary angioedema?

A

Trauma
Stress
Menstruation
ACEIs
OCPs

111
Q

What are the GI symptoms of Omenn syndrome?

A

Chronic diarrhoea
Protein loss leading to generalised oedema

111
Q

What are the skin symptoms of Omenn syndrome?

A

Generalised erythroderma with thickened and leathery skin and alopecia

112
Q

What is Omenn syndrome?

A

Exaggerated inflammatory response by oligoclonal T-cells

112
Q

What are the reticuloendothelial symptoms of Omenn syndrome?

A

Lymphadenopathy
Hepatosplenomegaly

112
Q

What protein is behind the symptoms in hereditary angioedema?

A

C1 esterase inhibitor
Type 1 is a deficiency
Type 2 is a defective version

113
Q

What proteins are deficient in Omenn syndrome?

A

RAG1 and RAG2

113
Q

How is hereditary angioedema inherited?

A

AR

113
Q

What would screening tests show in hereditary angioedema type 1?

A

C1INH functional level decreased
C1INH antigenic level reduced
C4 low

114
Q

How does hereditary angioedema present?

A

Episodic attacks of angioedema
Abdo pain common due to GI mucosal oedema

114
Q

Which type of hereditary angioedema is most common?

A

Type 1 - 85% of cases

115
Q

How are hereditary angioedema attacks prevented?

A

Antifibrinolytics
- epsilon amino caproic acid
- TXA
Purified C1INH from human plasma
Landelumab

115
Q

What would screening tests show in hereditary angioedema type 2?

A

C1INH functional level decreased
C4 low

116
Q

How are acute attacks of hereditary angioedema managed?

A

C1INH IV
Ecallantide
Icantibant

117
Q

How is Wiskott-Aldrich syndrome inherited?

A

X-linked recessive

117
Q

What type of bacteria causes gonorrhoea?

A

Gram negative coccus

117
Q

What mutation causes Wiskott-Aldrich syndrome?

A

WAS gene on x-chromosome p11.22-11.23

117
Q

What mediates a type I hypersensitivity reaction?

A

Immediate reaction mediated by IgE antibodies

117
Q

What mediates a type II hypersensitivity reaction?

A

IgG or IgM mediated cytotoxic reaction occurring over hours to days

117
Q

Give examples of type I hypersensitivity reactions.

A

Allergy
Anaphylaxis
Atopic disease

118
Q

Give examples of type II hypersensitivity reactions.

A

Haemolytic disease of the newborn
AI haemolytic anaemia
Goodpastures

119
Q

What mediates a type III hypersensitivity reaction?

A

Antibody-antigen complex mediated occurring over several hours, to days to weeks

120
Q

Give examples of a type III hypersensitivity reaction.

A

RA
SLE
Post-streptococcal GN

121
Q

What mediates a type IV hypersensitivity reaction?

A

T-cell mediated occuring 24-72hours after exposure

122
Q

Give examples of a type IV hypersensitivity reaction.

A

Dermatitis
Mantoux testing

123
Q

What infection is a major cause of SNHL in young children?

A

CMV

124
Q

How does symptomatic congenital CMV present?

A

Blueberry muffin rash
Symmetrical IUGR
Congenital cataracts
Jaundice
Petechiae
Hepatosplenomegaly
Microcephaly
Unexplained ventriculomegaly
Hearing loss
DD

125
Q

How does acquired CMV present?

A

Pneumonia
Colitis
Retinitis
Encephalitis

126
Q

How is CMV treated?

A

Ganciclovir or valganciclovir in severe infections

127
Q
A

1mrcpch fop and tas (11 decks)

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