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3a paeds > Paeds Derm + Infectious Disease + Allergy > Flashcards

Paeds Derm + Infectious Disease + Allergy Flashcards

1
Q

How is sepsis risk calculated

A

quick SOFA score

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2
Q

what is quick SOFA score

A

≥ 22 breaths/min RR
<15 GCS
≤ 100 mm Hg. sys

also coagulation (platelets) liver (bilirubin) and renal (creatine)

score of >2/3 = risk

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3
Q

What is the traffic light system for assessment of children under 5 with fever in children

A

green (low risk), amber (intermediate risk) or red (high risk)

  • color -> normal v. cyanosis
  • activity –> alert v. absent & appears ill
  • respiratory -> >40-50 RR v. red = >60 RR/ grunting
  • circulation and hydration -> normal skin and moist membranes v. tachycardia dry membranes and poor skin turgor, cap refil >3sec
  • other -> fever >5 days under 3 months, non blanching rash, seizures
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4
Q

What is action for low risk in assessment of children under 5 with fever in children

A

Child can be managed at home with appropriate care advice, including when to seek further help

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5
Q

What is action for moderate risk in assessment of children under 5 with fever in children

A
  • F2F assessment to judge admission or not
  • provide parents with a safety net or refer to a paediatric specialist for further assessment
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6
Q

What is action for severe risk in assessment of children under 5 with fever in children

A

urgent admission

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7
Q

What are signs of sepsis

A
  • Deranged physical observations
  • Prolonged capillary refill time (CRT)
  • Fever or hypothermia
  • Deranged behaviour
  • Poor feeding
  • Inconsolable or high pitched crying
  • High pitched or weak cry
  • Reduced consciousness
  • Reduced body tone (floppy)
  • Skin colour changes (cyanosis, mottled pale or ashen)
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8
Q

What is the immediate management for sepsis

A
  • Give oxygen if the patient has evidence of shock or oxygen saturations are below 94%
  • Obtain IV access (cannulation)
  • Blood tests, including a FBC, U&E, CRP, clotting screen (INR), blood gas for lactate and acidosis
  • Blood cultures, ideally before giving antibiotics
  • Urine dipstick and laboratory testing for culture and sensitivities
  • Antibiotics according to local guidelines. They should be given within 1 hour of presentation.
  • IV fluids. 20ml/kg IV bolus of normal saline if the lactate is above 2 mmol/L or there is shock. This may be repeated.
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9
Q

What investigations can be ordered for sepsis

A
  • Chest xray if pneumonia is suspected
  • Abdominal and pelvic ultrasound if intra-abdominal infection is suspected
  • Lumbar puncture if meningitis is suspected
  • Meningococcal PCR blood test if meningococcal disease is suspected
  • Serum cortisol if adrenal crisis is suspected
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10
Q

What is septic shock

A

when sepsis has lead to cardiovascular dysfunction.

The arterial blood pressure falls, resulting in organ hypo-perfusion.

This leads to a rise in blood lactate as the organs begin anaerobic respiration.

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11
Q

What is management if IV fluid boluses fail to improve the blood pressure and lactate level in children w septic shock

A

escalated to ICU + give inotropes (noradrenalin) to stimulate the cardiovascular system and improve blood pressure and tissue perfusion.

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12
Q

What is Kawasaki’s

A

Medium vessel vasculitis

6m - 5yr M, AfroCarbb/Asian

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13
Q

How does Kawasaki’s present

A
  • persistent high fever (above 39ºC) for more than 5 days.
  • strawberry tongue
  • widespread erythematous maculopapular rash and desquamation on feet and hands
  • conjunctivitis
  • cervical lymphadenopathy
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14
Q

How is Kawasaki’s investigated

A

FBC -> anaemia, leukocytosis and thrombocytosis
LFT -> hypoalbuminemia and elevated liver enzymes
Inflammatory markers -> ^ESR
Urinalysis -> ^WCC
Echocardiogram

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15
Q

What is the disease course of Kawasaki’s

A

Acute Phase
Subacute Phase
Convalescent stage

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16
Q

What is the Acute Phase of Kawasaki’s

A

The child is most unwell with the fever, rash and lymphadenopathy. This lasts 1 – 2 weeks.

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17
Q

What is the Subacute Phase of Kawasaki’s

A

The acute symptoms settle, the desquamation and arthralgia occur and there is a risk of coronary artery aneurysms forming. This lasts 2 – 4 weeks.

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18
Q

What is the Convalescent Phase of Kawasaki’s

A

remaining symptoms settle, the blood tests slowly return to normal and the coronary aneurysms may regress. This last 2 – 4 weeks.

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19
Q

How is Kawasaki’s managed

A
  • High dose aspirin to reduce the risk of thrombosis
  • IV immunoglobulins to reduce the risk of coronary artery aneurysms
  • Echo
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20
Q

what is a complication of Kawasaki’s

A

coronary artery aneurysms

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21
Q

Why is aspirin usually avoided in children

A

risk of Reye’s syndrome.

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22
Q

What is Inactivated vaccines

A

giving a killed version of the pathogen
cannot cause an infection
are safe for immunocompromised patients

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23
Q

give an example of Inactivated vaccines

A

Polio - salk version
Flu vaccine
Hepatitis A
Rabies

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24
Q

what is Subunit and conjugate vaccines

A

only contain parts of the organism used to stimulate an immune response
cannot cause infection
are safe for immunocompromised patients.

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25
Q

give an example of Subunit and conjugate vaccines

A

Pneumococcus
Meningococcus
Hepatitis B
Pertussis (whooping cough)
Haemophilus influenza type B
Human papillomavirus (HPV)
Shingles (herpes-zoster virus)

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26
Q

what is a Live attenuated vaccines

A

contain a weakened version of the pathogen.

They are still capable of causing infection, particularly in immunocompromised patients.

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27
Q

give an example of Live attenuated vaccines

A
  • Measles, mumps and rubella vaccine: contains all three weakened viruses
  • BCG: contains a weakened version of tuberculosis
  • Chickenpox: contains a weakened varicella-zoster virus
  • Nasal influenza vaccine (not the injection)
  • Rotavirus vaccine
  • Typhoid
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28
Q

what are toxin vaccines

A

contain a toxin that is normally produced by a pathogen.

They cause immunity to the toxin and not the pathogen itself

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29
Q

given an example of a toxin vaccine

A

diphtheria
tetanus

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30
Q

What vaccines are given at 8 weeks

A

6 in 1 vaccine (diphtheria, tetanus, pertussis, polio, haemophilus influenzae type B (Hib) and hepatitis B)
Meningococcal type B
Rotavirus (oral vaccine)

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31
Q

what is in the 6 in 1

A
  • diphtheria
  • tetanus
  • pertussis
  • polio
  • haemophilus influenzae type B (Hib)
  • hepatitis B

‘Parents Will Immunise Toddlers Because Death’

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32
Q

what vaccines are given at 12 weeks

A

6 in 1 vaccine (again)
Pneumococcal (13 different serotypes)
Rotavirus (again)

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33
Q

what vaccines are given at 16 weeks

A

6 in 1 vaccine (3/3)
Meningococcal type B (2/3)

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34
Q

what vaccines are given at 1 year

A

2 in 1 (haemophilus influenza type B and meningococcal type C)
Pneumococcal (again)
MMR vaccine (measles, mumps and rubella)
Meningococcal type B (again)

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35
Q

what vaccines are at 3 years 4 months

A

4 in 1 (diphtheria, tetanus, pertussis and polio)
MMR vaccine (again)

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36
Q

what is in the 4 in 1

A

diphtheria, tetanus, pertussis and polio

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37
Q

what vaccine is given at 12-13 years

A

Human papillomavirus (HPV) vaccine (2 doses given 6 to 24 months apart)

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38
Q

what vaccine is given at 14 years

A

3 in 1 (tetanus, diphtheria and polio)
Meningococcal groups A, C, W and Y

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39
Q

what is in the 3 in 1

A

tetanus, diphtheria and polio

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40
Q

what strains of HPV cause genital warts

A

6 and 11

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41
Q

what strains of HPV cause cervical cancer

A

16 and 18

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42
Q

what is chickenpox

A

caused by primary infection with varicella zoster virus

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43
Q

what is shingles

A

reactivation of the dormant virus in dorsal root ganglion

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44
Q

how does chickenpox present

A

fever initially
itchy, rash starting on head/trunk before spreading. Initially macular then papular then vesicular
systemic upset is usually mild

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45
Q

when does chickenpox infectivity continue til

A

infectivity continues until all the lesions are dry and have crusted over

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46
Q

what are complications of chickenpox

A

common - secondary bacterial infection of the lesions –> group A streptococcal

rare:
pneumonia
encephalitis (cerebellar involvement may be seen)
disseminated haemorrhagic chickenpox
arthritis, nephritis and pancreatitis may very rarely be seen

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47
Q

what is 1st disease

A

Measles

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48
Q

what is 2nd disease

A

Scarlet Fever

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49
Q

what is 3rd disease

A

Rubella (AKA German Measles)

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50
Q

what is 4th disease

A

Dukes’ Disease

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51
Q

what is 5th disease

A

Parvovirus B19

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52
Q

what is 6th disease

A

Roseola Infantum

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53
Q

what is measles

A

caused by the measles virus. It is highly contagious via respiratory droplets.

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54
Q

how does measles present

A

Koplik spots - spots inside the mouth (pathognomonic)
erythematous, maculopapular rash with flat lesions starts on face behind ears after fever then spreads to rest of body

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55
Q

how is measles managed

A

self resolving after 7 – 10 days of symptoms.

Children should be isolated until 4 days from onset of rash

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56
Q

what are notifiable diseases

A

Measles
Scarlet Fever
Rubella (AKA German Measles)

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57
Q

what are complications of measles

A

Otitis media
Pneumonia
Diarrhoea
Dehydration
Encephalitis
Meningitis
Hearing loss
Vision loss
Death

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58
Q

what is scarlet fever

A

caused by an exotoxin produced by the streptococcus pyogenes (group A strep) bacteria

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59
Q

how does scarlet fever present

A

red-pink, blotchy, macular rash with rough “sandpaper” skin starts on trunk and spreads

Fever: typically lasts 24 to 48 hours
Lethargy
Flushed face
Sore throat
Strawberry tongue
Cervical lymphadenopathy

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60
Q

how is scarlet fever managed

A

phenoxymethylpenicillin (penicillin V) for 10 days.

Children should be kept off school until 24 hours after starting antibiotics.

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61
Q

what other conditions are associated with group a strep infection

A

Post-streptococcal glomerulonephritis rheumatic fever

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62
Q

what is rubella

A

caused by the togavirus virus
highly contagious
spread by respiratory droplets

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63
Q

how does rubella present

A

milder erythematous macular rash compared with measles
starts on face spreads to body
mild fever, joint pain and a sore throat
lymphadenopathy

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64
Q

how is rubella managed

A

supportive and the condition is self limiting
Children should stay off school for at least 5 days after the rash appears.
Children should avoid pregnant women.

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65
Q

what are complications of rubella

A

arthritis
thrombocytopaenia
encephalitis
myocarditis

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66
Q

what can rubella in pregnancy lead to

A

congenital rubella syndrome, which is a triad of

  • deafness
  • blindness
  • congenital heart disease.
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67
Q

what is Parvovirus B19

A

caused by the parvovirus B19

also known as fifth disease, slapped cheek syndrome and erythema infectiosum

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68
Q

how does Parvovirus B19 present

A

starts with mild fever, coryza and non-specific viral symptoms such as muscle aches and lethargy

After 2 – 5 days the rash appears quite rapidly as a diffuse bright red rash on both cheeks, as though they have “slapped cheeks

few days later a reticular (net-like) mildly erythematous rash affecting the trunk and limbs appears that can be raised and itchy.

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69
Q

how is parovirus b19 managed

A

self limiting and the rash and symptoms usually fade over 1 – 2 week

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70
Q

when is parovirus b19 infectious

A

infectious prior to the rash forming, but once the rash has formed they are no longer infectious and do not need to stay off school.

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71
Q

who is at risk of parovirus b19 complucations

A

mmunocompromised patients, pregnant women and patients with haematological conditions such as sickle cell anaemia, thalassaemia, hereditary spherocytosis and haemolytic anaemia

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72
Q

what are complications of parovirus b19

A

Aplastic anaemia
Encephalitis or meningitis
Pregnancy complications including fetal death
Rarely hepatitis, myocarditis or nephritis

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73
Q

what is Roseola Infantum caused by

A

human herpesvirus 6 (HHV-6) and less frequently by human herpesvirus 7 (HHV-7).

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74
Q

what is main complication of Roseola Infantum

A

febrile convulsions

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75
Q

how does Roseola Infantum present

A

3-5 day high fever followed by a 2 day maculopapular rash which starts on the chest and spreads to the limbs.

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76
Q

what is Staphylococcal Scalded Skin Syndrome

A

caused by a type of staphylococcus aureus bacteria that produces epidermolytic toxins –> protease enzymes that break down the proteins that hold skin cells together.

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77
Q

how does SSSS present

A

generalised patches of erythema on the skin
formation of fluid filled blisters called bullae
burst & leave very sore, erythematous skin below

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78
Q

what is Nikolsky sign

A

very gentle rubbing of the skin causes it to peel away.

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79
Q

what are complications of SSSS

A

untreated lead to sepsis and potentially death.

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80
Q

How is SSSS managed

A

admission and treatment with IV antibiotics.

Fluid and electrolyte balance

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81
Q

What is whooping cough

A

upper respiratory tract infection caused by Bordetella pertussis (a gram negative bacteria).

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82
Q

how does whooping cough present

A

starts with mild coryzal symptoms, a low grade fever and possibly a mild dry cough.

More severe coughing fits start after a week or more

large, loud inspiratory whoop when the coughing ends

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83
Q

what is a paroxysmal cough

A

Coughing fits are severe and keep building until the patient is completely out of breath.

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84
Q

how is whooping cough diagnosed

A

within 2-3 weeks = nasopharyngeal or nasal swab with PCR testing or bacterial culture

more than 2 weeks = anti-pertussis toxin immunoglobulin G.

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85
Q

how is whooping cough managed

A

notifiable disease
supportive care
within first 3 weeks = Macrolide antibiotics such as azithromycin, erythromycin and clarithromycin
close contacts = prophylactic antibiotics

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86
Q

what is a complication if whoopung cough

A

bronchiectasis.

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87
Q

what is TB

A

infectious disease caused by Mycobacterium tuberculosis, a small rod-shaped bacteria (a bacillus)

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88
Q

what stain is used for M. tuberculosis and what does it look like

A

Zeihl-Neelsen stain, which turns them bright red against a blue background.

acid fast bacilli

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89
Q

what are the 4 possible outcomes of TB disease course

A
  • Immediate clearance of the bacteria (in most cases)
  • Primary active tuberculosis (active infection after exposure)
  • Latent tuberculosis (presence of the bacteria without being symptomatic or contagious)
  • Secondary tuberculosis (reactivation of latent tuberculosis to active infection)
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90
Q

what is miliary tuberculosis

A

When the immune system cannot control the infection, disseminated and severe disease can develop

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91
Q

what happens in latent TB

A

the immune system encapsulates the bacteria and stops the progression of the disease.

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92
Q

what is secondary TB

A

When latent tuberculosis reactivates, and an infection develops, usually due to immunosuppression

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93
Q

what is MC site of TB infection

A

lungs

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94
Q

What are Extrapulmonary tuberculosis sites

A

Lymph nodes
Pleura
Central nervous system
Pericardium
Gastrointestinal system
Genitourinary system
Bones and joints
Skin (cutaneous tuberculosis)

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95
Q

what is a cold abscess

A

firm, painless abscess caused by tuberculosis usually in neck

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96
Q

what are RF for TB

A
  • Close contact with active tuberculosis (e.g., a household member)
  • Immigrants from areas with high tuberculosis prevalence
  • People with relatives or close contacts from countries with a high rate of TB
  • Immunocompromised (e.g., HIV or immunosuppressant medications)
  • Malnutrition, homelessness, drug users, smokers and alcoholics
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97
Q

WHat is the vaccine for TB

A

Bacillus Calmette–Guérin (BCG)

live attenuated (weakened) Mycobacterium bovis bacteria (close relative)

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98
Q

who is TB vax offered to

A

increased risk of TB, such as those from areas of high TB prevalence, with close contact with TB (e.g., family members) and healthcare workers

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99
Q

how does TB present

A

Cough
Haemoptysis (coughing up blood)
Lethargy
Fever or night sweats
Weight loss
Lymphadenopathy
Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)
Spinal pain in spinal tuberculosis (also known as Pott’s disease of the spine)

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100
Q

what are the two tests for an immune response to TB cause by previous infection, latent or actiev TB

A

Mantoux test
Interferon‑gamma release assay (IGRA)

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101
Q

what investigations can support TB diagnosis

A

Chest x-ray
Cultures

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102
Q

what is Mantoux test

A

injecting tuberculin into the intradermal space on the forearm.

infection creates a bleb under skin

induration of skin measured 5mm or more = positive test

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103
Q

what is Interferon-Gamma Release Assays

A

mixing a blood sample with antigens from the M. tuberculosis bacteria.

positive result is when interferon-gamma is released during the test.

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104
Q

what does primary TB show on XRay

A

patchy consolidation, pleural effusions and hilar lymphadenopathy.

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105
Q

what does Reactivated TB show on XRay

A

patchy or nodular consolidation with cavitation (gas-filled spaces), typically in the upper zones.

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106
Q

what does Disseminated miliary TB show on XRay

A

appearance of millet seeds uniformly distributed across the lung fields.

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107
Q

what are ways to collect TB culture sample

A

Sputum cultures (3 separate sputum samples are collected)
Mycobacterium blood cultures (require special blood culture bottle)
Lymph node aspiration or biopsy
Sputum induction with nebulised hypertonic saline
Bronchoscopy and bronchoalveolar lavage (saline is used to wash the airways and collect a sample)

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108
Q

how is latent TB treated

A

Isoniazid and rifampicin for 3 months
or
Isoniazid for 6 months

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109
Q

how is active TB treated

A

R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months

110
Q

what is co prescribed with RIPE for TB

A

pyridoxine or vitamin B6.

111
Q

what is SE of Rifampicin

A
  • Red/orange discolouration of secretions, such as urine and tears.
  • It is a potent inducer of the cytochrome P450 enzymes and reduces the effects of drugs metabolised by this system
112
Q

What is SE of Isoniazid

A

can cause peripheral neuropathy

113
Q

what is SE of Pyrazinamide

A

hyperuricaemia (high uric acid levels), resulting in gout and kidney stones.

114
Q

WHat is SE of Ethambutol

A

colour blindness and reduced visual acuity.

115
Q

what TB drug is NOT associated with hepatotoxicity

A

Ethambutol <3

116
Q

what is HIV

A

human immunodeficiency virus

117
Q

what is AIDS

A

acquired immunodeficiency syndrome
end stage HIV

118
Q

what type of virus is HIV

A

RNA retrovirus

119
Q

what is the pathophysiology of HIV

A

virus enters and destroys the CD4 T helper cells.

initial seroconversion flu

120
Q

what are AIDs defining illnesses

A

Kaposi’s sarcoma
Pneumocystis jirovecii pneumonia (PCP)
Cytomegalovirus infection
Candidiasis (oesophageal or bronchial)
Lymphomas
Tuberculosis

121
Q

how is HIv spread

A
  • Unprotected anal, vaginal or oral sexual activity
  • Mother to child at any stage of pregnancy, birth or breastfeeding. This is referred to as vertical transmission.
  • Mucous membrane, blood or open wound exposure to infected blood or bodily fluids.

passed on through blood, semen, vaginal fluid, anal mucus and breast milk,

122
Q

When is a normal vaginal delivery recommended for HIV + women

A

viral load < 50 copies / ml

123
Q

When is a Caesarean section considered for HIV + women

A

> 50 copies copies / ml and in all women with > 400 copies / ml

124
Q

what medication is given during. c section is viral load unknown of HIV + mother or >10000 coplies/ml

A

IV zidovudine

125
Q

What Prophylaxis treatment may be given to the baby when HIV + mother viral load is < 50 copies per ml

A

zidovudine for 4 weeks

126
Q

What Prophylaxis treatment may be given to the baby when HIV + mother viral load is >50 copies per ml

A

zidovudine, lamivudine and nevirapine for 4 weeks

127
Q

when is breastfeeding recommended for mothers with HIV

A

never

128
Q

what are two options for HIV testing

A

HIV antibody screen
HIV viral load

129
Q

what is HIV antibody screen:

A

tests whether the immune system has created antibodies due to exposure to the HIV virus

standard screening

can give false positive

130
Q

what is HIV viral load

A

tests directly for viruses in the blood

never be falsely positive

131
Q

what can cause false positive in hiv antibody tets

A

can be positive in infants who do not have HIV for up to 18 months of age. This is due to maternal antibodies that have crossed the placenta during pregnancy.

132
Q

when is HIv tested

A

Babies to HIV positive parents
When immunodeficiency is suspected, for example where there are unusual, severe or frequent infections
Young people who are sexually active can be offered testing if there are concerns
Risk factors such as needle stick injuries, sexual abuse or IV drug use

133
Q

how is HIV managed

A
  • Antiretroviral therapy (ART) to suppress the HIV infection
  • Normal childhood vaccines, avoiding or delaying live vaccines if severely immunosuppressed.
  • Prophylactic co-trimoxazole (Septrin) for children with low CD4 counts, to protect against pneumocystis jirovecii pneumonia (PCP)
  • Treatment of opportunistic infections
134
Q

what is the aim of antiretroviral therapy (ART)

A

chieve a normal CD4 count and undetectable viral load.

135
Q

what should paediatric HIV multidisciplinary team be involved in

A

Regular follow up to monitor growth and development
Dietician input for nutritional support when required
Parental education about the condition
Disclosing the diagnosis to the child is often delayed until they are mature enough
Psychological support
Specific sex education in relation to HIV when appropriate

136
Q

what is Meningitis

A

inflammation of the meninges. The meninges are the lining of the brain and spinal cord

137
Q

what is Neisseria meningitidis

A

gram-negative diplococcus bacteria

commonly known as meningococcus

138
Q

what is Meningococcal septicaemia

A

meningococcus bacterial infection in the bloodstream.

139
Q

what does non-blanching rash in Meningitis indicate

A

the infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages

140
Q

what is Meningococcal meningitis

A

the bacteria is infecting the meninges and the cerebrospinal fluid around the brain and spinal cord

141
Q

what are the MC causes of bacterial meningitis in children and adults

A

Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus).

142
Q

what is the MC cause of meningitis in neonates

A

group B strep (GBS).

143
Q

how does meningitis present

A

fever, neck stiffness, vomiting, headache, photophobia, altered consciousness and seizures
non-blanching rash

144
Q

how do neonates and babies present with meningitis

A

non-specific signs and symptoms, such as hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanell

145
Q

when does NICE recommen a LP as investigation in children

A
  • Under 1 month presenting with fever
  • 1 to 3 months with fever and are unwell
  • Under 1 year with unexplained fever and other features of serious illness
146
Q

what is kernig test

A

lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees

meningitis = spinal pain or resistance to movement.

147
Q

what is Brudzinski’s test

A

ying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest.

meningitis = patient to involuntarily flex their hips and knees.

148
Q

how is meningitis managed in the community

A

IM benzylpenicillin

149
Q

how is meningitis managed in the hospital

A

Under 3 months – cefotaxime plus amoxicillin (for listeria)
Above 3 months – ceftriaxone

150
Q

how is meningitis investigated

A

blood culture
lumpar puncture
meningococcal PCR
Viral PCR

151
Q

what prophylaxis is given for meningitis

A

single dose of ciprofloxacin

close contact within 7 days of symptoms

152
Q

what are common viral causes of meningitis

A

herpes simplex virus (HSV), enterovirus and varicella zoster virus (VZV)

153
Q

how is viral meningitis treated

A

Aciclovir

154
Q

what are the LP results for bacterial meningitis

A

Appearance - cloudy
Protein - high
Glucose - low
White Cell Count - high neutrophils
Culture - bacteria

155
Q

what are the LP results for viral meningitis

A

Appearance - clear
Protein - mild raised or normal
Glucose -normal
White Cell Count - high lymphocytes
Culture - negative

156
Q

what are complications of meningitis

A

Hearing loss is a key complication
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Cerebral palsy, with focal neurological deficits such as limb weakness or spasticity

157
Q

at what level is a LP taken at

A

L3 – L4

158
Q

what are LP sample tested for

A

bacterial culture, viral PCR, cell count, protein and glucose

159
Q

what is given in addition to Abx to reduce frequency and severity of hearing and neurological loss

A

Dexamethasone is given 4 times daily for 4 days to children over 3 months

160
Q

what is Encephalitis

A

inflammation of the brain. This can be the result of infective or non-infective causes.

non infective = autoimmune

161
Q

what is MC cause of Encephalitis in children

A

herpes simple type 1 (HSV-1) from cold sores.

162
Q

what is MC cause of Encephalitis in neonates

A

herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth.

163
Q

what are other viral causes of Encephalitis

A

varicella zoster virus (VZV) -> chickenpox
cytomegalovirus -> immunodeficiency
Epstein-Barr virus -> infectious mononucleosis
enterovirus
adenovirus
influenza virus.

164
Q

how does Encephalitis present

A

Altered consciousness
Altered cognition
Unusual behaviour
Acute onset of focal neurological symptoms
Acute onset of focal seizures
Fever

165
Q

how are children with suspected Encephalitis investigated

A

Lumbar puncture -> cell count, protein and glucose levels, Gram stain, bacterial culture, viral PCR testing
MRI scan
EEG recording
HIV testing

166
Q

when is LP CI

A

GCS below 9, haemodynamically unstable, active seizures or post-ictal.

167
Q

how is herpes simplex virus (HSV) and varicella zoster virus (VZV) encephalitis treated

A

Aciclovir

168
Q

how is cytomegalovirus (CMV) encephalitis treated

A

Ganciclovir

169
Q

what is performed before stopping antivirals for encephalitis

A

Repeat lumbar puncture

Followup, support and rehabilitation is required after encephalitis

170
Q

what are complications of encephalitis

A

Lasting fatigue and prolonged recovery
Change in personality or mood
Changes to memory and cognition
Learning disability
Headaches
Chronic pain
Movement disorders
Sensory disturbance
Seizures
Hormonal imbalance

171
Q

what is Impetigo

A

superficial bacterial skin infection, usually caused by the staphylococcus aureus bacteria

Impetigo is contagious and children should be kept off school during the infection.

172
Q

how is Impetigo classified

A

non-bullous or bullous.

173
Q

what is non bullous Impetigo

A

typically occurs around the nose or mouth.

The exudate from the lesions dries to form a “golden crust”

rarely causes systemic symptoms

174
Q

how is localised non bullous Impetigo treated

A

1st line antiseptic cream (hydrogen peroxide 1% cream)

175
Q

how is wide spread non bullous Impetigo treated

A
  • oral flucloxacillin
  • oral erythromycin if penicillin-allergic
176
Q

what is advice to stop spread of Impetigo

A

not touching or scratching the lesions, hand hygiene and avoiding sharing face towels and cutlery

off school until all the lesions have healed or they have been treated with antibiotics for at least 48 hours

177
Q

what is Bullous impetigo

A

staphylococcus aureus bacteria produce epidermolytic toxins that break down skin cells causing fluid filled vesicles to form grow and cause golden crust to form

+ systemic symtoms - feverish and generally unwell

178
Q

who is Bullous impetigo most commin

A

neonates and children under 2 years

179
Q

how is Bullous impetigo investigated

A

Swabs of the vesicles can confirm the diagnosis, bacteria and antibiotic sensitivities.

180
Q

what can severe bullous impetigo infection lead to

A

staphylococcus scalded skin syndrome.

181
Q

how is bullous impetigo treated

A

oral or IV flucloxacillin

182
Q

what are complications of impetigo

A

Cellulitis if the infection gets deeper in the skin
Sepsis
Scarring
Post streptococcal glomerulonephritis
Staphylococcus scalded skin syndrome
Scarlet fever

183
Q

what is 1st line treatment for mild to moderate Oral candidiasis

A

Topical antifungals:
Nystatin suspension
Miconazole gel

184
Q

what is 1st line treatment for severe Oral candidiasis

A

Oral fluconazole

185
Q

what are Rf for Oral candidiasis

A

DM
denture use
inhaled ICS
immunicompromised

186
Q

what is Hand, foot and mouth disease caused by

A

coxsackie A virus

187
Q

how does Hand, foot and mouth disease present

A

starts with typical viral upper respiratory tract symptoms such as tiredness, sore throat, dry cough and raised temperatur

1-2 days later small mouth ulcers appear, followed by blistering red spots across the body

Painful mouth ulcers, particularly on the tongue are also a key feature

188
Q

how is how does Hand, foot and mouth disease managed

A

no treatment for hand, foot and mouth disease.

Management is supportive, with adequate fluid intake and simple analgesia such as paracetamol if required

189
Q

what are complications of Hand, foot and mouth disease

A

Dehydration
Bacterial superinfection
Encephalitis

190
Q

how long should it take for Hand, foot and mouth disease to resolve

A

esolve spontaneously without treatment after a week to 10 days

191
Q

what is an allergy

A

hypersensitivity of the immune system to allergens.

192
Q

what are allergens

A

proteins that the immune system recognises as foreign and potential harmful, leading to an allergic immune response

193
Q

what are antigens

A

proteins that can be recognised by the immune system.

194
Q

what is atopy

A

predisposition to having hypersensitivity reactions to allergens

195
Q

what are atopic conditions

A

eczema, asthma, hayfever, allergic rhinitis and food allergies.

196
Q

what is the leading theory on orugin of allergies

A

skin sensitisation theory

197
Q

what is skin sensitisation theory

A

two main contributors to a child developing an allergy to a food:

  1. There is a break in the infant’s skin (from eczema or a skin infection) that allows allergens, such as peanut proteins, from the environment to cross the skin and react with the immune system.
  2. The child does not have contact with that allergen from the gastrointestinal tract, and there is an absence of GI exposure to the allergen.
198
Q

what conditions are a result of hypersensitivity reactions

A

Asthma
Atopic eczema
Allergic rhinitis
Hayfever
Food allergies
Animal allergies

199
Q

what is type 1 Coombs and Gell classification

A

Antigen reacts with IgE bound to mast cells

200
Q

Give an example of a type 1 Coombs and Gell classification

A

Anaphylaxis
Atopy (e.g. asthma, eczema and hayfever)

201
Q

what is type 2 Coombs and Gell classification

A

IgG or IgM binds to antigen on cell surface and activate the complement system

202
Q

Give an example of a type 2 Coombs and Gell classification

A

haemolytic disease of the newborn
ITP
Pernicious anaemia
Goodpastures

203
Q

what is type 3 Coombs and Gell classification

A

Free antigen and antibody (IgG, IgA) combine and accumulate and cause damage to local tissues.

204
Q

Give an example of a type 3 Coombs and Gell classification

A

systemic lupus erythematosus (SLE)
Post-streptococcal glomerulonephritis
Henoch-Schönlein purpura (HSP)

205
Q

what is type 4 Coombs and Gell classification

A

hypersensitivity T-cell mediated

206
Q

Give an example of a type 4 Coombs and Gell classification

A

MS
TB
Guillain-Barre syndrome
organ transplant rejection

207
Q

what are 3 ways of test for allergy

A

Skin prick testing
RAST testing, which involves blood tests for total and specific immunoglobulin E (IgE)
Food challenge testing

208
Q

which allergy tests are unreliable and misleading

A

Skin prick testing and RAST testing assess sensitisation and not allergy.

= makes the unreliable and misleading

209
Q

what is the gold standard investigation for diagnosing allergy

A

Foot challenge testing

210
Q

what is Skin Prick Testing

A
  1. A drop of each allergen solution is placed at marked points along the patch of skin, along with a water control and a histamine control.
  2. A fresh needle is used to make a tiny break in the skin at the site of each allergen.
  3. After 15 minutes, the size of the wheals to each allergen are assessed and compared to the controls.
211
Q

what is patch testing

A

most helpful in determining an allergic contact dermatitis in response to a specific allergen NOT food allergies

  1. A patch containing the allergen is placed on the patient’s skin. The patch can either contain a specific allergen, or a grid of lots of allergens as a screening tool.
  2. After 2 – 3 days the skin reaction to the patch is assessed.
212
Q

what is RAST testing

A

measures the total and allergen specific IgE quantities in the patient’s blood sample.

213
Q

what is food challenge

A

child is gradually given increasing quantities of an allergen to assess the reaction, starting with almost non-existent quantities diluted further in other foods, for example mixing a small amount of peanut into a bar of chocolate.

214
Q

how are allergies managed

A
  • Establishing the correct allergen is essential
  • Avoidance of that allergen
  • Avoiding foods that trigger reactions
  • Regular hoovering and changing sheets and pillows in patients that are allergic to house dust mites
  • Staying in doors when the pollen count is high
  • Prophylactic antihistamines are useful when contact is inevitable, for example hayfever and allergic rhinitis
  • Patients at risk of anaphylactic reactions should be given an adrenalin auto-injector
215
Q

what is immunotherapy for allergies

A

gradually exposing the patients to allergens over months with the aim of reducing their reaction to certain foods or allergens.

216
Q

what is the management of allergies follwoing exposure

A
  • Antihistamines (e.g. cetirizine)
  • Steroids (e.g. oral prednisolone, topical hydrocortisone or IV hydrocortisone)
  • Intramuscular adrenalin in anaphylaxis
217
Q

what is Allergic rhinitis

A

IgE-mediated type 1 hypersensitivity reaction.
Environmental allergens cause an allergic inflammatory response in the nasal mucosa

218
Q

when can Allergic rhinitis occur

A

Seasonal, for example hay fever
Perennial (year round), for example house dust mite allergy
Occupational, associated with the school or work environment

219
Q

how does Allergic rhinitis present

A

Runny, blocked and itchy nose
Sneezing
Itchy, red and swollen eyes

220
Q

how is Allergic rhinitis investigated

A

diagnosis usually history
Skin prick testing - pollen, animals and house dust mite allergy

221
Q

what can trigger Allergic rhinitis

A
  • Tree pollen or grass allergy
  • House dust mites and pets
  • Pets can
  • Other allergens lead to symptoms after exposure (e.g. mould)
222
Q

what are Non-sedating antihistamines for Allergic rhinitis

A

cetirizine, loratadine and fexofenadine

223
Q

what are sedating antihistamines for Allergic rhinitis

A

chlorphenamine (Piriton) and promethazine

224
Q

what are nasal corticosteroid sprays for Allergic rhinitis

A

fluticasone and mometasone

225
Q

what is Anaphylaxis

A

life-threatening medical emergency
severe type 1 hypersensitivity reaction

226
Q

what is the pathophysiology of Anaphylaxis

A
  • Immunoglobulin E (IgE) stimulates mast cells to rapidly release histamine and other pro-inflammatory chemicals.
  • This is called mast cell degranulation.
  • This causes a rapid onset of symptoms, with airway, breathing and/or circulation compromise
227
Q

what are the rapid onset of allergic symptoms

A

Urticaria
Itching
Angio-oedema, with swelling around lips and eyes
Abdominal pain

228
Q

what additional symptoms indicate anaphylaxis

A

Shortness of breath
Wheeze
Swelling of the larynx, causing stridor
Tachycardia
Lightheadedness
Collapse

229
Q

how is anaphylaxis initially assessed

A

A – Airway: Secure the airway
B – Breathing: Provide oxygen if required. Salbutamol can help with wheezing.
C – Circulation: Provide an IV bolus of fluids
D – Disability: Lie the patient flat to improve cerebral perfusion
E – Exposure: Look for flushing, urticaria and angio-oedema

230
Q

how is anaphylaxis treated

A

Intramuscular adrenalin, repeated after 5 minutes if required

Antihistamines, such as oral chlorphenamine or cetirizine

231
Q

how is anaphylaxis managed after the event

A
  • admitted to watch for biphasic reactions (2nd anaphylactic reaction after successful treatment of the first)
  • serum mast cell tryptase within 6 hours of the event.

Education and follow-up of the family and child is essential

  • how to avoid allergens and how to spot the signs of anaphylaxis
  • trained in basic life support
  • how to use an adrenalin auto-injector.
232
Q

what are Indications for an Adrenalin Auto-Injector

A

given to all children and adolescents with anaphylactic reactions.

children with generalised allergic reactions (without anaphylaxis) with certain risk factors
- Asthma requiring inhaled steroids
- Poor access to medical treatment
- Adolescents
- Nut or insect sting allergies
- Significant co-morbidities, such as cardiovascular disease

233
Q

how is an Adrenalin Auto-Injector used

A
  1. Prepare the device by removing the safety cap on the non-needle end
  2. Grip the device with the needle end pointing downwards.
  3. Administer the injection by firmly jabbing the device into the outer portion of the mid thigh until the device clicks.
  4. Remove the device and gently massage the area for 10 seconds.
  5. Phone an emergency ambulance. A second dose may be given (with a new pen) after 5 mins
234
Q

how is Anaphylaxis confirmed

A

measuring the serum mast cell tryptase within 6 hours of the event

235
Q

when is tryptase released

A

during mast cell degranulation

236
Q

what is Urticaria

A

hives
small itchy lumps that appear on the skin

may be associated with a patchy erythematous rash

localized or widespread

237
Q

what is the pathophysiology of Urticaria

A

caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin.

allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.

238
Q

what causes acute urticaria

A

Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications
Viral infections
Insect bites
Dermatographism (rubbing of the skin)

239
Q

what is acute urticaria

A

typically triggered by something that stimulates the mast cells to release histamine.

240
Q

what is chronic urticaria

A

autoimmune condition, where autoantibodies target mast cells and trigger them to release histamines and other chemicals.

241
Q

what is Chronic idiopathic urticaria

A

recurrent episodes of chronic urticaria without a clear underlying cause or trigger.

242
Q

what can trigger Chronic inducible urticaria

A

Sunlight
Temperature change
Exercise
Strong emotions
Hot or cold weather
Pressure (dermatographism)

243
Q

what is Autoimmune urticaria

A

chronic urticaria associated with an underlying autoimmune condition, such as systemic lupus erythematosus.

244
Q

how is urticaria managed

A

Antihistamines
chronic 1st = Fexofenadine
Oral steroids for severe flares

245
Q

what specialist treatment can be considered for severe urticaria

A

Anti-leukotrienes such as montelukast
Omalizumab, which targets IgE
Cyclosporin

246
Q

what is Eczema

A

chronic atopic condition caused by defects in the normal continuity of the skin barrier, leading to inflammation in the skin

247
Q

how does Eczema present

A

presents in infancy with dry, red, itchy and sore patches of skin over the flexor surfaces (the inside of elbows and knees) and on the face and neck

248
Q

how is Eczema maintained

A

emollients

avoid activities that break down the skin barrier, such as bathing in hot water, scratching or scrubbing their skin and using soaps and body washes that remove the natural oils in the skin

249
Q

how are Eczema flares treated

A

thicker emollients, topical steroids, “wet wraps” (covering affected areas in a thick emollient and applying a wrap to keep moisture locked in overnight) and treating any complications such as bacterial or viral infections.

250
Q

what are specialist treatments in severe eczema

A
  • zinc impregnated bandages
  • topical tacrolimus
  • phototherapy
  • systemic immunosuppressants, such as oral corticosteroids, methotrexate and azathioprine.
251
Q

what are Thin cream Emollients

A

E45
Diprobase cream
Oilatum cream
Aveeno cream
Cetraben cream
Epaderm cream

252
Q

what are thick greasy Emollients

A

50:50 ointment (50% liquid paraffin)
Hydromol ointment
Diprobase ointment
Cetraben ointment
Epaderm ointment

253
Q

what is the steroid ladder for eczema

A

Mild: Hydrocortisone 0.5%, 1% and 2.5%
Moderate: Eumovate (clobetasone butyrate 0.05%)
Potent: Betnovate (betamethasone 0.1%)
Very potent: Dermovate (clobetasol propionate 0.05%)

254
Q

what is the general steroid rule for eczema

A

use the weakest steroid for the shortest period required to get the skin under control.

The thicker the skin, the stronger the steroid required.

255
Q

how are bacterial infections in eczema managed

A

MC organism = staphylococcus aureus

Tx = flucloxacillin

256
Q

what is Stevens-Johnson Syndrome

A

disproportional immune response causes epidermal necrosis, resulting in blistering and shedding of the top layer of skin

257
Q

what medication can cause Stevens-Johnson Syndrome

A

Anti-epileptics
Antibiotics
Allopurinol
NSAIDs

258
Q

what infections can cause Stevens-Johnson Syndrome

A

Herpes simplex
Mycoplasma pneumonia
Cytomegalovirus
HIV

259
Q

How does Stevens-Johnson Syndrome present

A
  • start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin
  • develop a purple or red rash that spreads across the skin and starts to blister.
  • blistering skin breaks away and shed leaving raw skin
260
Q

how is Stevens-Johnson Syndrome managed

A

medical emergency
supportive care

Tx = steroids, immunoglobulins and immunosuppressant

261
Q

what condition is similar to Stevens-Johnson Syndrome but covers larger part of body

A

toxic Epidermal Necrolysis

262
Q

what are complications of Stevens-Johnson Syndrome

A

Secondary infection
Permanent skin damage
Visual complications:

263
Q

what do B cells do

A

responsible for producing antibodies

specific immunity

264
Q

what is selective Immunoglobulin A Deficiency

A

MC immunoglobulin deficiency

IgA = LOW
IgG = normal
IgM = normal

265
Q

where is IgA present

A

secretions of the mucous membranes, such as saliva, respiratory tract secretions, GI tract secretions, tears and sweat.

protects against opportunistic infections

266
Q

when is it important to test for total immunoglobulin A levels

A

in coeliac disease

267
Q

what is Common Variable Immunodeficiency

A

caused by a genetic mutation in the genes coding for components of B cell

unable to develop immunity to infections or vaccination

IgG = LOW
IgA = LOW
IgM = normal

268
Q

how does Common Variable Immunodeficiency present

A

recurrent respiratory tract infections, typically leading to chronic lung disease over time.

269
Q

what conditions are patients with Common Variable Immunodeficiency prone to

A

rheumatoid arthritis, and cancers such as non-Hodgkins lymphoma

270
Q

how are Common Variable Immunodeficiency managed

A

regular immunoglobulin infusions

271
Q

what is X-linked Agammaglobulinaemia

A

X-linked recessive condition

results in abnormal B cell development and deficiency in all classes of immunoglobulins.

3a paeds (12 decks)

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