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formative 3b > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

what are the three core symptoms of ADHD?

A

inattention impulsivity hyperactivity

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2
Q

symptoms of inattention

A

easily distracted often appears not to be listening has difficulty sustaining attention during activities avoids or dislikes tasks requiring sustained attention forgetfulness disorganised loses important items

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3
Q

symptoms of hyperactivity

A

squirms and fidgets cannot remain seated runs or climbs excessively in inappropriate situations talks excessively cannot perform leisure activities quietly

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4
Q

symptoms of impulsivity

A

blurts out answers before question is finished has difficulty waiting turn interrupts or intrudes on others

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5
Q

how common is ADHD in school age children

A

4-7%

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6
Q

what is the male to female ratio of adhd in children and adults

A

childhood - M:F = 4:1 adulthood - M:F = 1:1

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7
Q

affect of adhd on mortality

A

untreated adhd has twice the childhood mortality than no adhd

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8
Q

ADHD crossover with developmental disorders

A

13% mental retardation 47% developmental coordination disorder 40% reading/writing disorder

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9
Q

ADHD crossover with psychiatric disorders

A

7% aspergers 33% tic disorders 60% oppositional defiant disorder

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10
Q

comment on thee pathophysiology of ADHD

A

Cortical maturation happens in the same order – from the back of the head to the front – but in ADHD it happens about 3-5 years later

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11
Q

how is a child assessed for ADHD

A

symptoms may not be present in highly structured environments where there are interesting activities like the assessment itself. therefore home videos or testimonials from those involved in the child’s care/education can be important.

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12
Q

proposed etiologies of ADHD

A

neuroanatomic/neurochemical CNS insults genetic origins (as hereditary as height) environmental factors

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13
Q

management of adhd

A

education adhd parenting programme school support and liason medical (methylphenidate, atomexetine or lisdexamfetamine)

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14
Q

what is the prevalence of ASD

A

1%

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15
Q

what is the m:f for asd

A

4:1

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16
Q

what are the three realms of asd

A

communication social interaction poor behaviour and imagination rigidity

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17
Q

what’s the asd thing where they repeat speech called

A

echolalia

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18
Q

asd management

A

education and information asd parenting workshops school liason and support manage comorbidity

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19
Q

types of anaemia common in paediatrics

A

iron deficiency haemolytic - membrane/enzyme/immune haemoglobinopathies aplasia

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20
Q

thrombocytopenias in paeds

A

immune - ITP neonatal alloimmune marrow failure

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21
Q

clotting factor disorders in paeds

A

haemoglobinopathies hypercoagulable states

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22
Q

haematopoiesis in children

A

at birth basically all bones are actively haematopoietic and in childhood it becomes central bone (vertebrae, sternum, ribs and pelvis)

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23
Q

causes of severe anaemia at birth

A

haemolytic disease of the newborn (erythroblastosis fatalis) bleeding (umbilical cord or internal haemorrhage)

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24
Q

signs and symptoms of erythroblastosis fatalis

A

severe anaemia compensatory hyperplasia of blood forming organs (spleen and liver)

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25
Q

treatment of erythroblastosis fatalis

A

prevention of sensitization with Rh immune globulin IU transfusion of affected fetus

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26
Q

what is the physiologic anaemia of newborns

A

normal drop in Hb from birth which reaches a nadir at 2 months

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27
Q

what causes physiologic anaemia of the newborn

A

decreaseed rbc production plasma dilution due to increasing blood volume neonatal rbcs have a shorter lifespan

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28
Q

describe the switch from HbF to HbA

A

from birth HbF decreases about 3% per week at 6 months it represents only 2% of total Hb

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29
Q

what is anaemia of prematurity

A

low birth weight infants have a poor erythropoietin response and this means the protein in breast milk may not be sufficient for hematopoiesis

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30
Q

signs of anaemia of prematurity

A

apnoea failure to thrive pallor decreased activity tachycardia

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31
Q

what are the 4 functional areas of the developmental assessment

A

1) gross motor 2) vision and fine motor 3) hearing speech and language 4) social, emotional and behavioural

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32
Q

what median age do they raise their heads 40 degrees in prone

A

6-8 weeks

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33
Q

what is the limit age for head control

A

4 months

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34
Q

what is the limit age for sitting upright without support

A

9 months

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35
Q

what median age for crawling

A

8-9 months

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36
Q

what is the limit age for pulling to stand

A

12 months

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37
Q

what median age walking independently

A

12 months

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38
Q

what is the limit age for walking independently

A

18 months

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39
Q

what median age fixing and following

A

6 weeks

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40
Q

what is the limit age for fixing and following

A

3 months

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41
Q

what median age for reaching for toys

A

4 months

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42
Q

what is the limit age for reaching for toys

A

6 months

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43
Q

what median age for palmar grasp

A

4-6 months

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44
Q

what median age for transferring from hand to hand

A

7 months

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45
Q

what is the limit age for transferring from hand to hand

A

9 months

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46
Q

what is the limit age for mature pincer grip

A

12 months

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47
Q

what median age for mature pincer grip

A

10 months

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48
Q

what is the median age for drawing line without demonstration

A

2 years

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49
Q

what median age for drawing circle without demonstration

A

3 years

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50
Q

what median age for drawing a cross without demonstration

A

3.5 years

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51
Q

what median age for drawing a square without demonstration

A

4

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52
Q

what median age for drawing a triangle without demonstration

A

5

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53
Q

what adjustment do you make for the drawing ages if you give them a demonstration

A

reduce by 6 months if they are copying you

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54
Q

how many bricks can they stack at 18 months

A

3

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55
Q

how many bricks can they stack at 2 yrs

A

6

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56
Q

how many bricks can they stack at 2.5

A

8

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57
Q

what is the limit age for a polysyllabic babble

A

7 months

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58
Q

what is the median age for being able to say 2-3 words other than mamma and dada

A

12 months old

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59
Q

what is the median age for 6-10 words other than mama and dada

A

18 months

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60
Q

what is the limit age for holding a spoon and getting food safely to mouth

A

18 months

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61
Q

what is the limit age for joining 2 words to make simple phrases

A

2 years

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62
Q

what is the limit age for making 3 word sentences

A

2.5 years

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63
Q

what is the limit age for being able to say 6 words with meaning (i.e. not mama or dada)

A

18 months

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64
Q

what is the limit age for smiling responsively

A

8 weeks

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65
Q

what median age for symbolic play

A

18-24 months

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66
Q

what is the limit age for symbolic play

A

2-2.5 years

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67
Q

what is the median age to be dry by day

A

2 years

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68
Q

what is the limit age to have fear of strangers

A

10 months

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69
Q

what is the median age for interactive play to begin evolving

A

2.5-3 years

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70
Q

what is the limit age for interactive play

A

3-3.5 years

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71
Q

how should you adjust the developmental assessment if a child is born pre-term

A

calculate their age from the expected date of their delivery this correction is no longer required after about 2 years of age

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72
Q

what is the normal range of Hb for a neonate

A

<140g/L

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73
Q

what is the normal range of Hb for a child aged 1 month to 12 months

A

<100g/L

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74
Q

what is the normal range of Hb for a child aged between 1 year and 12 years of age

A

Hb less than 110g/L

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75
Q

three broadest causes of anaemia

A

1) impaired red cell production 2) increased red cell destruction 3) blood loss

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76
Q

two different types of impaired red cell production

A

1) red cell aplasia 2) ineffective erythropoiesis

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77
Q

three causes of red cell aplasia

A

1) congenital (diamond blackfan anaemia) 2) transient erythroblastopenia of childhood (TEC) 3) parvovirus B19 infection

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78
Q

5 causes of ineffective erythropoiesis

A

1) iron deficiency 2) folic acid deficiency 3) chronic inflammation 4) chronic renal failure 5) lead poisoning

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79
Q

4 types of haemolytic disorder and an example of each

A

1) membranopathies e.g. hereditary spherocytosis 2) enzymopathies e.g. G6PD deficiency 3) hamoglobinopathies e.g. alpha and beta thalassaemias as well as sickle cell disease 4) immune e.g. haemolytic disease of the newborn

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80
Q

draw the flow diagram of simple diagnostic approach to anaemia in children

A
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81
Q

what are the diagnostic clues that the cause of anaemia is ineffective erythropoiesis

A
  • normal or high reticulocyte count
  • abnormal MCV
    • low in iron deficiency
    • high in folic acid deficiency
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82
Q

anaemia is often asymptomatic before Hb drops below

A

70g/L

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83
Q

management of iron deficiency anaemia

A

oral iron supplementation with nifarexx or sytron

this should be continued until Hb is normal and then a further 3 months

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84
Q

how quickly should Hb inrease on oral iron supplementation and what might it mean if it is not increasing at that rate

A
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85
Q

what is diamond blackfan anaemia

A

it is congenital red cell aplasia

caused by specific mutation

can present at birth but typically at 2-3 months age

treatment is with oral steroids

if steroid unresponsive then they can have monthly red cell transfusions

stem cell transplant is also an option down the line

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86
Q

what is transient erythroblastopenia of childhood

A
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87
Q

what can parvovirus B19 infection cause

A

it can cause red cell aplasia in children with inherited haemolytic anaemias not in healthy children

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88
Q

what are the diagnostic clues in red cell aplasia

A

normal bilirubin

negative coombs test

absent reticulocytes

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89
Q

how many times can bone marrow increase production of red cells in order to compensate haemolysis

A

8 times

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90
Q

what are the main causes of haemolytic anaemias in children

A
  • immune haemolytic anaemias are uncommon so the main causes are the intrinsic abnormalities of the red cells
    • membranopathies - e.g. heredetary spherocytosis
    • haemoglobinopathies - e.g alpha or beta thalassaemias or sickle cell disease
    • enzymopathies - e.g. Glucose-6-phosphate dehydrogenase deficiency
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91
Q

how common is hereditary spherocytosis

A

1/5000 live births

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92
Q

what is the inheritance pattern of hereditary spherocytosis

A

AD inheritance

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93
Q

what is the brief pathophys of hereditary spherocytosis

A
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94
Q

what is the presentation of hereditary spherocytosis

A

affected individuals could be asymptomatic

presentation is very variable

jaundice - could be severe in first few days of life, could be intermittent throughout childhood

anaemia - may be mild but could worsen transiently during infections

mild to moderate splenomegaly

aplastic crisis - very rare caused by parvovirus B19 infection

gallstones due to increased bilirubin infection

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95
Q

diagnosis of hereditary spherocytosis

A

blood film

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96
Q

treatment for hereditary spherocytosis

A

mostly mild so only treatment is oral folic acid supplementation

splenectomy if there is poor growth or severe anaemia

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97
Q

how many people worldwide does G6PD deficiency affect worldwide

A

100 million people worldwide

10-20% prevalence in people from central africa, the med, the middle east and the far east

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98
Q

what is the inheritance pattern of G6PD deficiency

A

x linked recessive so predominantly seen in males

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99
Q

what is the pathophys of G6PD deficiency

A

G6PD is the rate limiting enzyme in the pathway that prevents oxidative damage to red cells

so the cells are vulnerable to oxidative damage caused by certain drugs, infection and fava beans

100
Q

G6PD deficiency presentation

A

neonatal jaundice

fever

malaise

abdominal pain

passage of dark urine

101
Q

management of G6PD deficiency

A

patients need advice on spotting signs of acute haemolysis

patients should be given a list of drugs, chemicals and foods to avoid

transfusion is rarely required, even in acute haemolysis

102
Q

which haemoglobinopathies are delayed until after 6 months of age and why

A

sickle cell and beta thalassaemias are delayed to 6 months of life because this is when HbF is decreased to non-functional levels

sickle cell and beta thalassaemia affect the beta globin gene

HbF does not require beta globin but it does require alpha globin so this is why alpha thalassaemias present at birth

103
Q

how common is sickle cell disease

A

1/2000 live births

104
Q

what is the sickle cell mutation

A

mutation in codon 6 of the beta globin gene that changes a glutamine to a valine

105
Q

what is the inheritance pattern of sickle cell

A

autosomal recessive

106
Q

what is the pathophys of sickle cell

A

HbS polymerises to rigid tubular spiral bodies with reduced lifespan

they can be trapped in microcirculation causing vaso-occlusion and ischaemia

this is exacerbated by low oxygen concentration, dehydration or cold

variation in disease severity is caused by either co-inheritance with other haemoglobinopathies or by genetic variation in the levels of HbF

107
Q

describe the anaemia of sickle cell

A

all have moderate anaemia with clinically detectable jaundice from chronic haemolysis

108
Q

describe the susceptibility to infection in sickle cell disease

A
  • marked susceptibility to encapsulated organisms
    • pneumococci
    • haemophilus influenzae
  • increased incidence of osteomyelitis caused by salmonella and other organisms
  • the susceptibility to infection is caused by chronic microinfarction in the spleen causing hyposplenism
  • the risk of overwhelming sepsis is highest in early childhood
109
Q

describe the different types of painful crisis

A
  • common mode of presentation in late infancy is hand foot syndrome
    • dactylitis with swelling and pain of the fingers and or feet from vaso occlusion
  • bones of limbs and spine are most common sites
  • most serious type of painful crisis is acute chest syndrome which can lead to severe hypoxia and the need for mechanical ventilation and emergeny transfusion
110
Q

precipitants for painful crisis in sickle cell

A

exposure to cold

dehydration

excessive exercise

stress

hypoxia

infection

111
Q

causes of acute anaemia in sickle cell

A
  • haemolytic crises - sometimes associated with infection
  • aplastic crises - Hb may fall precipitously
    • parvovirus B19 infection causes complete although transient cessation of red blood cell production
  • sequestration crises - sudden splenic or hepatic enlargement, abdominal pain and circulatory collapse from accumulation of sickled cells in spleen
112
Q

long term problems associated with sickle cell

A
  • short stature and delayed puberty
  • stroke and cognitive problems
    • 1/10 have stroke
    • 2/10 develop more subtle neurological damage
  • adenotonsillar hypotrophy
    • may cause sleep apnoea which could lead to nocturnal hypoxaemia, preciptiating a vaso-occlusive crisis
  • cardiac enlargement from chronic anaemia
  • heart failure from chronic anaemia
113
Q

prophylaxis in sickle cell

A
  • immunisations including
    • pneumococcal
    • haemophilus
    • influenzae type B
    • meningococcal infection
  • once daily oral folic acid
  • daily oral penicillin
  • avoid exposure to precipitants
114
Q

treatment of acute sickle cell crisis

A

oral and iv analgesia

infection should be treated with Abx

oxygen should be given if sats drop

exchange transfusion for acute chest syndrome, stroke and priapism

115
Q

treatment for chronic problems

A

children with repeat admissions may benefit from hydroxycarbamide which works to increase HbF

bone marrow transplant for the most severely affected

116
Q

hydroxycarbamide side effect

A

white blood cell suppression

117
Q

sickle cell mortality during childhood

A

3% - usually due to bacterial infection

118
Q

describe the difference between the two types of beta thalassaemia

A
  • Beta thalassaemia major
    • HbA cannot be produced at all because the mutations are so severe
  • Beta thalassaemia minor
    • small amounts of HbA and/or larger amounts of HbF can be produced due to the nature of the mutations
    • this leads to milder disease
119
Q

clinical features of beta thalassaemia major

A
  • severe anaemia which is transfusion dependent from 3-6 months of age
  • jaundice
  • faltering growth
  • extramedullary haemopoiesis is prevented with regular transfusions
    • without them you get hepatosplenomegaly and maxillary overgrowth with skull bossing
120
Q

managment of beta thalassaemia

A
  • monthly red cell transfusions for life
  • maintain Hb concentration above 100g/L in order to reduce growth failure
121
Q

what are the risks of repeated blood transfusion

A
  • chronic iron overload which if untreated causes:
    • cardiac failure
    • liver cirrhosis
    • diabetes
    • infertility
    • growth failure
122
Q

how many alpha globin genes are there

A

4

123
Q

what is alpha thalassaemia major and how does it present?

A
  • this is where there is deletion of all 4 alpha globin genes so HbA cannot be produced
  • presents with
    • fetal hydrops
    • fatal in utero or within hours of delivery
    • only survivable with monthly intrauterine transfusions until delivery followed by lifelong monthly transfusions after birth
124
Q

what if 3 alpha globin genes are mutated

A

it’s called HbH disease and children have mild/moderate anaemia but occasional patients are transfusion dependent

125
Q

what if one or two alpha globin genes is mutated

A

usually asymptomatic with mild or absent anaemia

126
Q

what is the iron requirement of a child

A

1mg/kg/day

127
Q

diagnostic clues for iron deficiency anaemia

A
128
Q

what is aplastic anaemia

A

it is aka bone marrow failure

it is a reduction or absence of the three main lineages in the bone marrow leading to pancytopenia

129
Q

what are the acquired causes of aplastic anaemia

A

hepatitis viruses

drugs such as those used in chemo

toxxins such as benzene glue

130
Q

what is the clinical presentation of aplastic anaemia

A

anaemia - reduced red cells

infection - reduced white cells

bruising - thrombocytopenia

131
Q

name two inherited aplastic anaemias and which one is more common

A

fanconi anaemia - most common one

shwachman diamond syndrome

132
Q

what is the presentation of fanconi anaemia

A
  • children have congenital abnormalities which may be spotted at birth
    • short stature
    • abnormal radii and thumbs
    • renal malformations
    • micropthalmia
  • signs of bone marrow failure don’t normally become apparent until the age of 5 or 6
    *
133
Q

what is the difinitive treatment for fanconi anaemia

A

bone marrow transplant

134
Q

which clotting factors does prothrombin time measure the activity of

A

activity of factors II, V, VII and X

135
Q

which clotting factors does activated partial thromboplastin time measure the activity of

A

II, V, VIII, IX, X, XI and XII

136
Q

how common is haemophilia A, what is the inheritance pattern and which clotting factor is deficient

A

haemophilia A is FVIII deficiency, it is 1/5000 male births and it is X linked recessive

137
Q

which clotting factor is affected by haemophilia B, what is the inheritance pattern and how common is it

A

1/30,000 male births, it is factor IX deficiency and it is X linked recessive

138
Q

draw the table on haemophilia A that includes columns for factor VIII level, severity and bleeding tendancy

A
139
Q

what are the two most common situations surrounding presentation of haemophilia

A

40% is in neonatal period with intracranial haemorrhage, bleeding post-circumcision or prolonged oozing from heel prick

most of majority present around 1 yr of age with walking and crawling progressing

140
Q

most common bleeding sites of haemophilia

A

into joints or muscles

141
Q

what is the management for haemophilia

A
  • recombinant factor VIII for haemophilia A
  • recombinant factor IX for haemophilia B
  • give these clotting factors whenever there is bleeding
  • mild haemophilia A can be given desmopressin which stimulates endogenous release of FVIII and vWF
  • desmopressin doesn’t work for haemophilia B
142
Q

what are the two major roles of vWF

A

facilitates platelet adhesion to damaged endothelium

acts are the carrier protein for FVIII, protecting it from clearance

143
Q

what is the most common subtype of vWD, when does it most commonly present and what are the clinical features

A

subtype 1 is most common and it is mild so may not be diagnosed until puberty (e.g. with menorrhagia) or adulthood

144
Q

management of vWD

A

type 1 can be treated with desmopressin

more severe types have to be treated with plasma derived FVIII as recombinant contains no vWF and desmopressin is ineffective

145
Q

name 4 acquired disorders of coagulation

A

haemorrhagic disease of the newborn due to vitamin K deficiency

liver disease

immune thrombocytopenia

disseminated intravascular coagulation

146
Q

what platelet count constitutes thrombocytopenia

A

<150x109/L

147
Q

what is the most common cause of thrombocytopenia in childhood

A

Immune thrombocytopenia (ITP)

aka

immune thrombocytopenic purpura

148
Q

what causes ITP

A

destruction of circulating platelets by IgG antibodies

149
Q

clinical features of ITP in children

A

most common between ages of 2 and 10

1-2 weeks after viral infection

short history of days to weeks

can cause mucoas bleeding such as epistaxis

profuse bleeding is rare despite platelets sometimes getting v low

150
Q

what is important about the diagnosis of ITP

A

if they have any abnormal clinical features other than the thrombocytopenia they need to be investigated for ALL or aplastic anaemia with a bone marrow examintion

SLE could also be a differential

but if there are no other abnormal clinical features and it fits ITP clinical picture properly then it’s what it is

151
Q

how often is ITP in children acute and how often is it chronic

A

in 80% of cases it is acute, benign and self-limiting

in 20% of cases it is chronic, lasting more than 6 months

152
Q

what is the treatment for acute ITP

A
  • Most can be treated at home unless there is evidence of severe bleeding
  • Treatment options are
    • Oral prednisolone
    • IV anti-D
    • IV Ig
  • All of the above have bad side effects and need monitoring
153
Q

what is the treatment for chronic ITP

A

supportive

rituximab (anti-B lymphocyte) can be used for those that have recurrent bleeding episodes

154
Q

causes of DIC

A

Severe sepsis or other shock due to circulatory collapse

extensive tissue damage due to tissue damage

155
Q

what are the features of DIC

A
  • bruising
  • purpura
  • haemorrhage
  • thrombocytopenia
  • prolonged PT
  • prolonged APPT
  • low fibrinogen
  • raised fibrinogen depletion products
  • raised D-dimer
156
Q

treatment for DIC

A

treat underlying cause and support with FFP

157
Q

thrombosis in children is ______ and pretty much always caused by a _______ _______

A

thrombosis in children is rare and pretty much always caused by a hypercoagulable state

158
Q
  1. types of congenital thrombophilia
A
  1. protein C or S (natural anti-coagulants) deficiency
  2. antithrombin deficiency
  3. factor V leiden mutation - it is malformed and resistant to degradation
  4. prothrombin gene mutation which is associated with very high levels of prothrombin in the blood
159
Q

6 acquired hypercoagulable states

A
  1. catheter-related thrombosis
  2. DIC
  3. hypernatraemia
  4. malignancy
  5. SLE
  6. persistent antiphospholipid syndrome
160
Q

what must you do in every child presenting with a thrombotic event

A
  • not miss an inherited cause so do the following investigations
    • assays for protein C and S
    • PCR for factor V leiden mutation
    • PCT for prothrombin gene mutation
161
Q

write as much as you can from the child with petechiae diagram

A
162
Q

what is classed as a fever in a child

A

anything over 37 C

163
Q

red flag symptoms suggesting serious illness in children

A
  • fever over 38 if aged less than 3 months
  • fever over 39 if 3 months to 6 months
  • pale, mottled or cyanosed colour
  • neck stiffness
  • reduced consciousness
  • bulging fontanelle
  • status epilepticus
  • focal neurological signs
  • seizures
  • significant respiratory distres
  • bile stained vomiting
  • severe dehydration or shock
164
Q
A
165
Q

what are the empirical abx if they’re less than 1 month old

A

perenteral cefotaxime with ampicillin added to cover listeria

166
Q

what are the empirical abx if they’re over one month of age

A

high dose ceftriaxone

167
Q

what should be included in the septic screen

A
  • blood cultures
  • FBC including differential white cell count
  • acute phase reactants
  • urinalysis and urine MC&S
  • consider if indicated
    • CXR
    • LP
    • rapid antigen screen on blood/CSF
    • meningococcal and pneumococcal PCR on blood/CSF samples
    • PCR for viruses in CSF
168
Q

is it more common for bacteria or viruses to cause meningitis

A

viruses are more common

169
Q

does bacterial or viral meningitis typically have more severe problems

A

bacterial

170
Q

what is the mortality of bacterial meningitis

A

5-10%

171
Q

what proportion of bacterial meningitis is in children under 16

A

80%

172
Q

what percentage of survivors of meningitis are left with neurological impairment

A

>10%

173
Q

organisms most likely to cause bacterial meningitis in neonates to 3 months old

A

group b streptococcus

escerichia coli

listeria monocytogenes

174
Q

most common bacteria causing meningitis in 1 month old to 6 years old

A

neisseria meningitides

streptococcus pneumoniae

haemophilus influenzae

175
Q

most common organisms causing bacterial meningitis in children over 6 years old

A

neisseria meningitides

streptococcus pneumoniae

176
Q

which bacteria causes lowest probability of long-term sequelae

A

neisseria meningitides which causes meningococcal septicaemia causes few neurological sequelae despite being able to kill in a number of hours

177
Q

differentials for heads stiffness

A

tonsillitis and cervical lymphadenopathy

178
Q

findings on examination of bacterial meningitis

A

fever

purpuric rash

neck stiffness

bulging fontanelle in infants

opisthotonus

positive brudzinski

positive kernig

signs of shock

focal neurological signs

altered consciousness levels

papilloedema

179
Q

what is a positive brudzinski sign

A

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

seen in meningitis

180
Q

what is a positive kernig sign

A

with the child lying supine and with the hips and knees flexed there is back pain on extension of the knees

indicates meningitis

181
Q

what are the contraindications for lumbar puncture

A
  • cardiorespiratory instability
  • focal neurological signs
  • signs of raised ICP
    • high BP
    • coma
    • low heart rate
    • papilloedema
  • coagulopathy
  • thrombocytopenia
  • local infection at site of LP
  • if it causes undue delay in starting abx
182
Q

draw the table for LP interpretation with the rows named normal, bacterial meningitis, viral meningitis, tuberculosis meningitis and encephalitis and the columns named appearance, white blood cells, protein, glucose

A
183
Q

managment of bacterial meningitis

A

IM Benzylpenicillin while awaiting transfer to secondary care

IV ceftriaxone once in hospital

supportive care

184
Q

cerebral complications of meningitis

A

hearing impairment

local cerebral infarction can result in epilepsy

hydrocephalus from impaired resorption of CSF - ventricular shunt may be required

cerebral abscess

185
Q

what protection do you give the household contacts of someone who has had bacterial meningitis

A

meningococcal meningitis - rifampicin or ciprofloxacin to all household contacts

group C meningococcal meningitis should be vaccinated with meningococcal group C vaccine

186
Q

how do you diagnose viral meningitis

A

by PCR of CSF, stool, urine, np aspirate and throat swabs

187
Q

what are two differences between meningitis and encephalitis in presentation

A

encephalitis can be insidious

encephalitis often includes behaviour change

188
Q

which organisms is impetigo caused by

A

s.aureus or group A strep

189
Q

what are the most common organisms causing encephalitis

A
  • Enteroviruses
  • Influenza viruses
  • Herpesviruses
    • HSV
    • VZV
    • HHV-6
190
Q

management of encephalitis

A
  • All children with encephalitis should be treated with high dose IV acyclovir since it is safe and HSV encephalitis is very dangerous and destructive
  • PCR of CSF to determine if it’s HSV
  • If it’s HSV encephalitis then CT/MRI may show focal damage often to the temporal lobe
191
Q

what causes toxic shock syndrome

A

staphylococcus aureus and group A streptococci can produce toxins that act as super antigens

192
Q

characteristics of TSS

A

fever over 39C

hypotension

diffuse erythematous maculopapular rash

193
Q

what do you see 1-2 weeks after onset of symptoms in toxic shock syndrome

A

desquamation of the palms, soles, fingers and toes

194
Q

which systems can TSS affect

A
  • mucousitis of the conjunctival oral mucosa and genital mucosa
  • GI dysfunction - d&v
  • renal impairment
  • liver impairment
  • clotting abnormalities and thrombocytopenia
  • CNS - altered consciousness
195
Q

management of TSS

A
  • surgical debridement of infection site
  • ceftriaxone with clindamycin
    • clindamycin works to inhibit production of the toxin by the bacteria
  • IV Ig can be given to neutralise the antigen
196
Q

which organisms may cause necrotising fasciitis

A

S.aureus or group A strep

197
Q

what is the danger with necrotising fasciitis

A

the area involved spreads rapidly and abx are not enough to treat

ITU is usually required due to systemic illness

IV abx are given but surgical debridement is also necessary

IVIg may also be given

198
Q

who does impetigo most commonly occur in

A

infants and young children

it is more common in children with pre-existing skin conditions such as atopic eczema

199
Q

what do the lesions look like in impetigo

A

usually on face, neck and hands

begin maculr, become papular and even bullous

characteristic honey coloured crusty lesions

200
Q

what is the treatment for impetigo

A

flucloxacillin

201
Q

what organisms cause periorbital cellulitis and what is the treatment

A

s.aureus and group A strep

treatment is with IV ceftriaxone to rapidly prevent posterior spread

202
Q

what is nikolsky sign and what does it indicate

A

areas of epidermis seperate on gentle pressure

it indicates staphylococcal scalded skin syndrome

203
Q

what is scalded skin syndrome

A

staphylococcal toxin causes exfoliative separation of the epidermal skin

mainly affects infants and young children

fever and malaise followed by widespread erythema and tenderness of the skin

204
Q

what is the treatment for scalded skin syndrome

A

IV anti-staph abx like flucloxacillin

analgesia and monitoring of fluid balance is also needed

205
Q

name all 8 human herpesviruses

A

HSV-1

HSV-2

EBV

CMV

VZV

HHV-6

HHV-7

HHV-8

206
Q

What is eczema herpeticum

A

it is an emergency

it is widespreasd vesicular legions caused by HSV1 or HSV2

it happens on eczematous skin

can be complicated by secondary bacterial infection which may result in septicaemia

207
Q

what are the complications from chicken pox

A
  • these are rare but serious
    • secondary bacterial infection
      • fever will settly but recur a few days later
    • encephalitis
    • purpura fulminans
    • in the immunocompromised host infection may result in severe progressive disseminated disease which has a mortality of up to 20%
    • generalised encephalitis
    • aseptic meningitis
208
Q
A
209
Q

treatment for chickenpox

A
210
Q

what is median incubation period for chickenpox

A

14 days

211
Q

describe the typical vesicular rash in chickenpox

A

50-500 lesions

start on head and trunk and then progress to the peripheries

up to one week of papules, vesicles, pustules

itchy

if new lesions appear beyond 10 days it suggests defective cellular immunity

212
Q

which cells does epstein barr virus have a particular tropism for?

A

B lymphocytes and the epithelial cells of the oropharynx

213
Q

clinical features of epstein barr virus

A

fever

malaise

tonsillitis/pharyngitis

diffuse lymphadenopathy

prominant cervical lymph node swelling

splenomegaly

hepatomegaly

214
Q

diagnosis of EBV is supported by

A

atypically large T lymphocytes seen on blood film

positive monospot test

serology

215
Q

how long does infectious mononucleosis normally last?

and what is the treatment

A

1-3 months

treatment is symptomatic until they resolve

where the airway is compromised corticosteroids may be considered

216
Q

what is the danger with cmv

A

subclinical infection in normal hosts

most people infected by adult age

can cause morbidity to the immunocompromised and to the developing foetus

217
Q

what do HHV6 and HHV7 do?

A
  • closely related and have similar presentations
  • HHV6 is more prevalent
  • classically cause
    • exanthema subitem aka roseola infantum
      • high fever and malaise for a few days
      • generalised maculopapular rash which appears as the fever wanes
  • can be fever without rash or can be subclinical
  • clinically similar picture to rubella or measles
218
Q

what is common slip up with HHV6 and HHV7

A

Occasionally what happens is the infant is seen by a doctor in the early stages of the illness and is prescribed antibiotics and when a rash appears it is erroneously attributed to allergic reaction to the drug

219
Q

What are the 4 syndromes that human parvovirus B19 can cause

A
  • asymptomatic - 65% adults have antibodies
  • erythema infectiosum aka slapped cheek syndrome
    • viraemic phase of fever, malaise, headache and myalgia
    • followed by characteristic rash on cheek
220
Q

what is hand foot and mouth disease

A

painful vesicular lesions on hands, feet and mouth and sometimes buttocks

systemic features generally mild

subsides within a few days

caused by coxsackie virus

221
Q

which type of viruses are the most common cause of viral meningitis in high income countries

A

enteroviruses

222
Q

complications of measles

A
  • respiratory
    • pneumonia
    • secondary bacterial infection
    • otitis media
    • tracheitis
  • neurological
    • febrile seizures
    • EEG abnormalities
    • encephalitis
    • subacute sclerosing panencephalitis (sspe)
  • other
    • diarrhoea
    • hepatitis
    • appendiciitis
    • corneal ulceration
    • myocarditis
223
Q

how frequently does SSPE occur and what is it

A

it is a complication of measles where 7 years after infection, 1/100,000 cases lose neurological function and progress to dementia and death over several years

224
Q

how frequently does encephalitis occur as a consequence of measles

A

1/5000 cases

225
Q

which time of year does mumps occur

A

spring and winter

226
Q

how is mumps spread

A

droplets

227
Q

what is the usual disease course of mumps

A
  • incubation period of 15-24 days
  • 30% of cases are subclinical
  • onset is with fever, malaise and parotisis
  • fever disappears within 3-4 days
  • infectious for 7 days following parotid swelling
228
Q

complications of mumps

A
  • hearing loss - usually unilateral and transient
  • meningitis/encephalitis
  • orchitis - usually unilateral and while sperm count may drop, infertility is rare
229
Q

what is rubella like and are there any complications

A
  • usually mild
  • low grade fever if at all
  • maculopapular rash is first sign of infection
    • starts on face but spreads centrifugally
  • rash fades over 3-5 days
  • complications are reare
    • arthritis
    • encephalitis
    • thrombocytopenia
    • myocarditis
  • the real danger is with congenital rubella syndrome so it should be confirmed by serology if there is risk of exposure to a non-immune pregnant woman
230
Q

9 non-infectious causes of prolonged fever

A
  • systemic onset juvenile idiopathic arthritis
  • systemic lupus erythematosus
  • vasculitis including kawasaki
  • IBD
  • sarcoidosis
  • malignancy
  • macrophage activation syndromes
    • lymphophagocytic lymphohistiocytosis
  • drug fever
  • FII
231
Q

what age does kawasaki mainly affect

A

6 months to 4 years of age with a peak at the end of the first year of life

232
Q

diagnosis of kawasaki

A
  • clinical diagnosis
  • based on fever of 5 days and 4 of the following
    • non-purulent conjunctivitis
    • red mucous membranes
    • cervical lymphadenopathy
    • rash
    • red and oedematous palms and soles
    • peeling of fingers and toes
  • in infants they may have an incomplete clinical picture so have a high index of suspicion
233
Q

what are children with kawasaki like

A

they are strikingly miserable and this isn’t improved with oral anti-pyretic agents

234
Q

what are the bloods like in kawasaki

A

they have high inflammatory markers and a platelet count that rises in the second week of illness

235
Q

what is the management of kawasaki

A

they need IV Ig and aspirin

they need an echo at 6 weeks

236
Q

what’s the feared complication and the mortality of kawasaki

A
  • coronary arteries affected in 1/3 of affected children –> aneurysms
  • mortality is 1-2%
237
Q

how would you diagnose active TB in children

A

diagnosis in children is even harder than in adults

clinical features are non-specific

sputum samples are unobtainable in children under 8

since they swallow their sputum, gastric washings on three consecutive mornings can be used to identify M.tuberculosis

238
Q

what are the microbiological techniques used to identify TB

A
  • Staining techniques are for acid fast bacilli using Ziehl Neelsen stains
239
Q

what is the treatment for TB

A
  • triple or quadruple therapy with
    • rifampicin
    • isoniazid
    • pyrazinamide
    • ethambutol
  • this is decreased to rifampicin and isoniazid after 2 months
  • total treatment is usually for 6 months
240
Q

vomiting child red flag symptoms and what they indicate

A
  • bile stained vomit - intestinal obstruction
  • haematemesis - peptic ulceration, gastritis, oesophageal varices
  • projectile vomiting - pyloric stenosis
  • abdominal pain on movement - surgical abdomen e.g. appendicitis
  • blood in the stool - intussesception, gastroenteritis
  • severe dehydration - DKA, severe gastroenteritis, systemic infection
  • headache or seizures - raised ICP
  • failure to thrive - GORD, coeliac
241
Q
A
242
Q

what is a chronic cough in children

A

>3 weeks

243
Q

‘barking cough’ is characteristic of _____

A

croup

244
Q
A
245
Q
A
246
Q
A
247
Q
A

formative 3b (18 decks)

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