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Phase 3a Emily > Paediatrics 1 (Cardio, GI, Neuro, Psych, Onco, MSK, Neonatal) > Flashcards

Paediatrics 1 (Cardio, GI, Neuro, Psych, Onco, MSK, Neonatal) Flashcards

1
Q

Investigation: Fever in baby

A
  • blood culture
  • urine dip is not sensitive enough in under 3 months old
  • send for urine microscopy
  • WBC
  • FBC
  • U+Es
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2
Q

What condition should be checked for in febrile babies?

A

Meningitis
- weak blood brain barrier
- sample CSF

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3
Q

Management: febrile baby

A

Broad spectrum antibiotics
- cefotaxine or ceftriaxone and amoxicillin

(until culture come back)

Admit babies under 3 months with a fever > may need IV antibiotics

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4
Q

What is the most common cause of UTI?

A

E.coli

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5
Q

What antibiotic is used to treat E.coli UTIs in children?

A

IV cefuroxime
(once meningitis ruled out - doesn’t reach the blood brain barrier)

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6
Q

What investigation should be completed with a baby under 6 months old with a UTI?

A

Renal tract USS
- recurrent infections can cause scarring that can lead to long term renal problems

(or recurrent UTIs in older children)

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7
Q

What needs to be ruled out in a fitting child with a fever?

A

CNS infection
- might need an LP

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8
Q

What can be a cause of ineffective antibiotic treatment?

A

Some bacteria has Extended Spectrum Beta-lactamase producer

  • resistant to all penicillins and cephalosporins
  • change to meropenem
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9
Q

Presentation: meningitis

A
  • Temperature
  • Semi-comatose
  • Purple rash on skin
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10
Q

Management: meningitis

A

ASAP
(before any investigations)

Bacterial meningitis or meningococcal sepsis:

  1. First line intravenous cefotaxime
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11
Q

Investigations: meningitis

A
  • blood cultures
  • EDTA (acid) blood for PCR
  • Lumbar Puncture CSF = might delay if concerns about clotting and raised intracranial pressure

notify Public health

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12
Q

What bacteria causes meningitis?

A

Neisseria meningitidis
- gram negative diplococci

group B streptococcus

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13
Q

What are contraindications to a lumbar puncture?

A
  • Findings of increased intracranial pressure
  • bleeding diathesis
  • cardiopulmonary instability
  • soft tissue infection at the puncture site
  • shock
  • respiratory insufficiency
  • suspected meningococcal
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14
Q

What is a complication of meningitis that causes petechial haemorrhages to develop on the trunk?

A

Waterhouse - Friderichsen syndrome

  • petechial haemorrhages
  • rapidly stops oxygen saturations
  • severely hypotensive
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15
Q

What conditions should be noticed to public health?

A
  • all meningitis
  • all invasive meningococcal
  • all encephalitis
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16
Q

Presentation: pneumonia

A
  • short of breath
  • pyrexial
  • miserable
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17
Q

Investigations: pneumonia

A
  • sputum culture or nose/ throat swab
  • CXR = RLL change
  • blood culture
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18
Q

What is the main cause of pneumonia?

A

Streptococcus penumoniae
- Gram positive cocci in pairs

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19
Q

Management: pneumonia

A

IV benzylpenicillin
PO amoxicillin

  • if not improving check if child has developed an empyema in the pleural space = CXR
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20
Q

Define: prematurity

A
  • under 37 weeks
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21
Q

At what gestation is resuscitation of a baby allowed?

A

from 22 weeks

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22
Q

management: premature rupture of membranes

A
  • antibiotics e.g. Erythromycin for 10 days
  • steroids
  • IV MgSO4 = neuroprotection
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23
Q

What is a main problem in premature babies?

A

lungs are not fully formed

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24
Q

When is surfactant and alveoli produced in a foetus?

A
  • surfactant = retained in type 2 pneumocystis (allow lungs to stretch and reduce surface tension)
  • alveoli = absent at 24 weeks then exponential increase towards term
    (from type 1 pneumocytes)
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25
Q

How does steroids help with lung development in a foetus?

A

Steroids trigger type 2 pneumocytes to release surfactant

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26
Q

Presentation: chronic lung disease of prematurity

A
  • Reduced lung volume
  • Reduced alveolar surface area
  • Diffusion defect
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27
Q

Presentation: apnoea of prematurity

A
  • brain stem not fully myelinated fully until 32 to 34 weeks
  • not signal from brain stem to breathe
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28
Q

Management: apnoea of prematurity

A

Physical:
- NCPAP
- Stimulation

Drugs
- phosphodiesterase inhibitors e.g. sildenafil (helps with pulmonary hypotension)
- caffeine

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29
Q

what is the cause of ventricular haemorrhage in premature babies?

A
  • sometimes spontaneously bleeds
  • worry about blood loss
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30
Q

Define: Cystic periventricular leukomalacia

A
  • brain injury most common in premature babies
  • the white matter (Leuko) surrounding the ventricles of the brain is deprived of blood and oxygen leading to softening (malaria)
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31
Q

What cause periventricular leukomalacia?

A

If the blood supply to an area of the brain is stopped or reduces, this causes tissue damage

  • uterine infections
  • early RoM
  • premature
    babies
  • ventricular haemorrhage
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32
Q

What are the benefits of breastfeeding for the infant?

A

Less Infection:
Diarrhoea, Otitis media, Respiratory Syncytical Virus, Respiratory Infections, Enhanced Vaccine Response

Less immune driven/allergic disease:
Wheezing, Childhood cancer, Eczema, Hodgkin’s disease, Multiple sclerosis, Crohn’s disease, Diabetes mellitus, Enhanced immunologic development

  • Reduces risk of NEC
  • Reduced Reduced SIDS
  • Reduced Gastroesophageal Reflux
  • Lower risk of Childhood Inguinal Hernia
  • Higher IQ
  • Better Cognitive Development
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33
Q

What are the maternal benefits of breastfeeding?

A

Reduces cancer risk for:
Breast, Uterine, Ovarian, Endometrial

Improved health with less:
Post partum haemorrhage, postnatal depression, Decrease insulin requirements in diabetics, Osteoporosis later in life, Less child abuse

Promotes postpartum weight loss
Optimum child spacing
Less food expense
Less medical expense
More ecological
Delays fertility

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34
Q

What are the causes of unconjugated and conjugated jaundice?

A
  • haemolysis,
  • prematurity,
  • sepsis,
  • dehydration,
  • hypothyroid,
  • metabolic disease

Conjugated:
prolonged parenteral nutrition, NEC, sepsis, metabolic, anatomical problems

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35
Q

How to treat neonatal jaundice?

A

Unconjugated = high levels cause kernicterus (so need to treat)

High levels treated by phototherapy (blue light, 450nm) or exchange transfusions

jaundice lasting more than 3 weeks needs investigation

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36
Q

Define: Necrotising enterocolitis

A

acute inflammatory disease leading to bowel necrosis in premature neonates

  • intestinal disease that affects premature or very low weight birth infants
  • causes intestinal tissue to die
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37
Q

What is the cause of necrotising enterocolitis?

A
  • Very low birth weight or very premature
  • Formula feeds (it is less common in babies fed by breast milk feeds)
  • Respiratory distress and assisted ventilation
  • Sepsis
  • Patient ductus arteriosus and other congenital heart disease
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38
Q

Presentation: necrotising enterocolitis

A

premature neonates
- Intolerance to feeds
- Vomiting, particularly with green bile
- Generally unwell
- Distended, tender abdomen
- Absent bowel sounds
- Blood in stools

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39
Q

Investigations: necrotising enterocolitis

A

blood tests
- Full blood count = thrombocytopenia and neutropenia
- CRP = inflammation
- Capillary blood gas = metabolic acidosis
- Blood culture = sepsis

Abdo x-ray
- dilated loops of bowel
- bowel wall oedema
- pneumatosis intestinalis = gas in bowel wall
- pneumoperitoneum = free gas in peritoneal cavity + perforation

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40
Q

Management: necrotising enterocolitis

A
  • nil by mouth
  • IV fluids, total parenteral nutrition and antibiotics
  • surgical emergency
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41
Q

What are the complications of necrotising enterocolitis?

A

Perforation and peritonitis
Sepsis
Death
Strictures
Abscess formation
Recurrence
Long term stoma
Short bowel syndrome after surgery

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42
Q

how does prematurity affect immunity?

A

Last 3 months of gestation active IgG transfer
- the more premature you are, the less of this you get
- cell mediated immunity is less active

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43
Q

Define: retinopathy of prematurity

A
  • too much oxygen given = hyperopic insult
  • arrest of normal vascular growth
  • fibrous ridge forms
  • vascular proliferation

cause:
- retinal haemorrhages
- retinal detachment
- blindness

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44
Q

Management: retinopathy

A

Laser therapy
- to reduce growth of abnormal blood vessels

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45
Q

What are the main symptoms of ADHD?

A

1) inattention,
2) hyperactivity
3) impulsivity.

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46
Q

What are the types of ADHD?

A

three categories of ADHD:
- predominantly inattentive type;
- predominantly hyperactive-impulsive type; and
- combined type.

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47
Q

What is the diagnosis of ADHD?

A

<17 years

6/9 Inattentive
6/9 Hyperactive/ Impulsive symptoms

Present before 12 years
Developmentally inappropriate
Several symptoms in 2 or more settings
Clear evidence symptoms interfere/reduce quality of social/academic/occupational function

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48
Q

Presentation: ADHD

A

Very short attention span
Quickly moving from one activity to another
Quickly losing interest in a task and not being able to persist with challenging tasks
Constantly moving or fidgeting
Impulsive behaviour
Disruptive or rule breaking

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49
Q

Management: ADHD

A
  1. detailed assessment by specialist
  2. establish healthy diet and exercise
  3. Medication (central nervous system stimulants)
    - Methylphenidate ‘Ritalin’ (CNS stimulant)
    - Dexamfetamine (stimulant)
    - Atomoxetine (SNRI, increase norepinephrine)
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50
Q

What are some medications for ADHD?

A

-Methylphenidate ‘Ritalin’
Dexamfetamine
Atomoxetine

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51
Q

What are some side effects of ADHD medication?

A
  • headache, insomnia, loss of appetite, stomach ache, dry mouth, nausea
  • Can stunt growth
  • Need to Monitor weight, height and BP
  • Methyphenidate is Not recommended to take during pregnancy
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52
Q

What groups are at higher prevalence of ADHD?

A

Preterm
LAC
ODD/CD
Mood Disorders (Anxiety/ Depression)
Close family members with ADHD
Epilepsy
Neurodevelopmental Conditions
Mental Health
Substance Use Disorder
Youth Justice/ Adult Criminal Justice System
Acquired Brain Injury

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53
Q

How do ADHD symptoms present differently in girls to boys?

A

harder to recognise in girls

  • daydreaming
  • more chatty
  • better at masking it in public/school
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54
Q

Define: Autism

A
  • genetically based neurological variant of cognition, communication, motivation and interests
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55
Q

How to diagnose autism?

A

To reach the threshold of a diagnosis, patients must meet all criteria A and at least 2 of B in the presence of C,D and E.

A) Persistent deficits in social communication and social interaction
B) Restricted, repetitive patterns of behaviour, interests, or activities

C) Symptoms must be present in the early developmental period
D) Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning.
E) These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay.

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56
Q

What does category A for autism diagnosis include?

A
  • social-emotional reciprocity = info dumping, direct answers to questions, abstract language
  • non-verbal communicative behaviours for social interaction
  • developing, maintaining and understand relationships
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57
Q

What is included in category B for autism?

A

Need 2 out of 4

  1. stereotyped or repetitive motor movements, use of objects or speech
  2. highly restricted, fixated interests that are abnormal in intensity or focus
  3. preference for sameness, and strong adherence to routines, or ritualised patterns of verbal or non-verbal behaviour
  4. hyper or hypo-reactivity to sensory input
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58
Q

What are included in category C for a autism diagnosis?

A

not acquired, (e.g.not TBI or anxiety/mood disorder etc).

Can be hard if childhood trauma, attachment.

Acknowledgement that might not present until demand exceeds capacity

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59
Q

What are included in category D for a autism diagnosis?

A

significant impairment (adults are usually diagnosed at a period of breaking point)

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60
Q

What are included in category E for a autism diagnosis?

A

not better explained by something else

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61
Q

What are factors for an increased risk of autism?

A

A sibling with autism.
Birth defects associated with central nervous system malformation and/or dysfunction, including cerebral palsy.
Gestational age less than 35 weeks.
Parental schizophrenia-like psychosis or affective disorder.
Maternal use of sodium valproate in pregnancy.
A learning (intellectual) disability.
Attention deficit hyperactivity disorder.
Neonatal encephalopathy or epileptic encephalopathy, including infantile spasms.
Chromosomal disorders such as Down’s syndrome.
Genetic disorders such as fragile X.
Muscular dystrophy.
Neurofibromatosis.
Tuberous sclerosis.

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62
Q

Define: ALL

A

Acute lymphoblastic leukaemia (ALL)
- affects one of the lymphocyte precursor cells
- acute proliferation of a single type of lymphocyte, usually B-lymphocytes.
- Excessive accumulation of these cells replaces the other cell types in the bone marrow, leading to pancytopenia.

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63
Q

Presentation: paediatric malignant disease

A

Localised mass
- Lymphadenopathy
- Organomegaly
- Soft tissue or bony mass

Problems from disseminated disease
- Bone marrow infiltration

Problems from localised mass
- Airway obstruction from lymphadenopathy

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64
Q

What symptoms are present in bone marrow malignant disease?

A

fever = reduced WBCs
fatigue = anaemia (RBCs)
easy bruising = reduced platelets
Bone pain

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65
Q

Presentation: Acute lymphoblastic leukaemia

A

Fever
Fatigue
Frequent infections
Lymphadenopathy
Hepatomegaly and/or splenomegaly
Anaemia
Bruising,petechiae
Bone or joint pain

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66
Q

What are the specific features of ALL?

A
  • MC in children
  • associated with Down’s syndrome
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67
Q

Investigations: ALL

A

Blood film
Serum chemistry
CXR
Bone marrow aspirate
Lumbar puncture

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68
Q

Management: ALL

A
  1. Chemotherapy – 5 phases
    - Induction, Consolidation, Interim maintenance
    - Delayed intensification, Maintenance
  2. Haemopoietic stem cell transplantation
    - High risk patients in first remission
    - Relapsed patients
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69
Q

Presentation: CNS tumours

A

Headache = often worse lying down
Vomiting = especially early morning
Papilloedema
Squint
Nystagmus
Ataxia (for kids they lose skills e.g. revert back to crawling)
Personality or behaviour change

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70
Q

When to scan headaches?

A

If also papilloedema, decreased acuity, visual loss

If also other neurological signs (or they develop)
If recurrent and/or early morning

If associated with vomiting
if persistent, more frequent, preceded by headache

If also have short stature / decelerated linear growth

If have symptoms of diabetes insipidus

If age < 3 years

If child has neurofibromatosis (NF1)

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71
Q

Management: CNS tumours

A
  1. Surgery
    Resection (can only do in certain parts of the brain)
    VP shunt
  2. Chemotherapy
    Single agent
    Combination treatment
  3. Radiotherapy
    For malignant tumours in older children
    Whole brain not used in very young
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72
Q

What are the causes of lymphadenopathy?

A

Mostly due to self limiting benign cause

Other causes:
HIV infection
Auto immune conditions
Storage disorders
Malignancy

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73
Q

When to biopsy in lymphadenopathy?

A
  • Enlarging node without clear infective cause
  • Persistently enlarged node
  • Unusual site e.g. supraclavicular
  • If have associated symptoms and signs
  • Fever, weight loss, enlarged liver/spleen
  • If CXR abnormal
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74
Q

Management: paediatric lymphoma therapy

A
  1. Chemotherapy
    Determined by histology and stage
  2. Radiotherapy
    Hodgkin’s – to residual bulk disease
    NHL - rarely
  3. Surgery – mainly limited to biopsy
  4. High dose therapy mainly for relapse
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75
Q

Presentation: abdominal mass

A

mass
Pain,
haematuria,
constipation,
hypertension,
weight loss

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76
Q

Investigation: abdominal mass

A
  • CT scans
  • biopsy
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77
Q

What are the differential diagnosis for abdominal mass?

A

Hepatoblastoma
Wilms tumour
Neuroblastoma
Lymphoma/leukaemia
Sarcoma
Constipation
Enlarged kidneys – polycystic disease

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78
Q

Presentation: neuroblastoma

A

proptosis = can appear like orbital cellulitis

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79
Q

Management: neuroblastoma

A
  1. Surgery
    Primary - if resectable
    Following chemotherapy
  2. Chemotherapy
    Type determined by stage and biology
    High dose with HPSC - high risk groups
  3. Radiotherapy
    Mainly for high risk group or at relapse
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80
Q

Management: Wilms tumour

A
  1. Chemotherapy
    Prior to surgery
    Following surgery
  2. Surgery
    Nephrectomy
    Partial nephrectomy if bilateral
  3. Radiotherapy
    If residual abdominal or pulmonary disease
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81
Q

What are the causes of retinoblastoma?

A
  • RB1 gene on chromosome 13
  • familial 40% vs sporadic
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82
Q

presentation: retinoblastoma

A

leukocoria – loss of red reflex (also called cat’s eye)
Strabismus
pain or redness around the eye
poor vision or change in child’s vision

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83
Q

Management: retinoblastomablastoma

A

Treatment may include one or more of the following:
chemotherapy
radiation therapy
laser therapy
phototherapy
thermal therapy
cryotherapy
surgery - enucleation of eye

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84
Q

Limping child: history + examination

A
  • trauma
  • duration, onset
  • swelling, bruising, erythema
  • listen to parents
  • soles of feet
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85
Q

What are the types of limp?

A
  • antalgic
  • trendelenberg = waddling
  • vaulting or circumduction = leg length discrepancy
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86
Q

Investigations: limping child

A

Bloods: FBC, ESR, CRP, blood culture

X-rays: remember the joint above and below (BONE)

USS: Good for infection (SOFT TISSUE)

(MRI)

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87
Q

What are the features of transient synovitis/irritable hip?

A
  • commonest cause of hip pain in kids
  • commonly 4-8yrs
  • can affect any major joint
  • non-specific inflammation= thought to be related to viral infection
  • improve 24-48 hr and resolve 1-2 weeks
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88
Q

Presentation: transient synovitis

A

occurs within a few weeks of a viral illness

  • limp
  • refusal to weight bear
  • groin or hip pain
  • mild low grade temperature

they should be otherwise well

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89
Q

Management: transient synovitis

A
  • analgesia
  • exclude septic arthritis
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90
Q

Define: Septic arthritis

A
  • intra-articular infection (inside a joint)
  • <2yrs
  • 35% hip 35% knee
  • acute pain
  • systemic symptoms
  • flexion abduction and external rotation
  • fever, look unwell
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91
Q

Presentation: septic arthritis

A

only affects a single joint
Hot, red, swollen and painful joint
Refusing to weight bear
Stiffness and reduced range of motion
Systemic symptoms such as fever, lethargy and sepsis

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92
Q

What are the main causes of septic arthritis?

A

mechanism: direct, haematogenous, extension from adjacent bone (osteomyelitis)

Staph aureus MC

Neisseria gonorrhoea (gonococcus) in sexually active teenagers
Group A streptococcus (Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)

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93
Q

Management: Septic arthritis

A
  • require admission to hospital
  • joint aspiration
  • send sample for gram staining, crystal microscopy, culture and antibiotic sensitivities
  • empirical IV antibiotics until sensitivity known for 3 to 6 weeks
  • may require surgical drainage and washout of joint
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94
Q

What is the Kocher criteria?

A

used for septic arthritis

NEWT
non- weight bearing
ESR>40
WCC>12
Temp>38.5

4/4 = 99% of septic arthritis

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95
Q

What are the features of Osteomyelitis?

A
  • infection of the bone and bone marrow
  • mean age 6.5yrs
  • more common <10yrs due to the blood supply to the metaphysis
  • association with (minor) trauma
  • NB. often have frequent presentation before diagnosis
  • less likely to have systemic upset
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96
Q

What are the risk factors for osteomyelitis?

A

Open bone fracture
Orthopaedic surgery
Immunocompromised
Sickle cell anaemia
HIV
Tuberculosis

boys <10 yrs

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97
Q

Presentation: osteomyelitis

A

can be acutely unwell or more subtle

Refusing to use the limb or weight bear
Pain
Swelling
Tenderness
They may be afebrile, or may have a low grade fever.

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98
Q

Investigations: osteomyelitis

A
  • x-rays = can be normal, blurry outline
  • MRI - better
  • blood tests = raised CRP and ESR and WBCs
  • blood culture
  • bone marrow aspiration or bone biopsy
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99
Q

Management: osteomyelitis

A

prolonged antibiotics
- may require surgery fro drainage and debridement of the infected bone

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100
Q

What are the red flags for non-accidental injury?

A

Any bruising in an infant <4-6m

Injury location (ears, neck, frenulum, cheek)

Any fracture in a non-ambulant child

Unexplained delays in presentation

Multiple presentations

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101
Q

what is developmental dysplasia of the hip (DDH)?

A
  • Abnormal growth/development of the hip joint
  • When the ball does not sit and load the socket, the ball and socket do not grow/mould correctly
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102
Q

What are the risk factors for DDH?

A

Breech presentation
Female
Family history
First baby
Packagaing disorders

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103
Q

Management: DDH

A
  • Can resolve over time without intervention
  • Pavlik harness can be used in <6 months old]
  • Older children may need surgery
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104
Q

What are the main clinical findings in DDH?

A

Red flags on examination
1. Leg length difference (Galeazzi test)
2. Trendelenberg gait

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105
Q

Investigation: DDH

A

Usually picked up on NIPE Exam with Barlow (dislocate) and Ortolani (relocate) tests

B before O, dislocate then relocate

  • Ultrasound for <4.5 months
  • X-ray for >4.5 months

(all breech babies from 36 weeks need scan even if fixed to cephalic with ECV)

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106
Q

What is Legg- Calve-Perthes?

A
  • idiopathic avascular necrosis of the proximal femur in children
  • 4-8 yrs
  • male:female 5:1
  • usually asymmetrical
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107
Q

What is slipped upper femoral epiphysis (SUFE)?

A
  • head of the femur is displaced along the growth plate
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108
Q

Define: Slipped upper femoral epiphysis

A

Rare hip condition where the femoral head epiphysis is displaced posteroinferiorly

Much more common in males between the age of 8-15

More common in obese children

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109
Q

Management: Perthes disease

A
  • Initial management is conservative by maintaining position and alignment in the joint with bed rest, analgesia and casts
  • If <6 years of age, observation is usually sufficient
  • Older children may need surgery and physio
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110
Q

Investigations: Perthes

A

Plain X-ray: Widening of the joint space initially then decreased femoral head size

Technetium bone scar/MRI if normal X-ray and symptoms persisting

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111
Q

Presentation: SUFE

A
  • hip, groin, thigh or knee pain
  • externally rotated gait (more comfortable for patient)
  • restricted range of hip movement
  • painful limp
  • restricted movement in the hip
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112
Q

What are the aetiology of SUFE?

A

Male
obese
12-13 yrs
due to rapid periods of growth

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113
Q

Investigations: SUFE

A

X-ray first

Blood tests are normal, particularly inflammatory markers used to exclude other causes of joint pain

Technetium bone scan
CT scan
MRI scan

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114
Q

management: SUFE

A

Surgery
is required to return the femoral head to the correct position and fix it in place to prevent it slipping further.

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115
Q

What are the red flags for bone tumours?

A

Night pain
Pain that doesn’t go after treatment/as expected
Lump in the soft tissues or bone
(Weight loss/other systemic symptoms)

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116
Q

What are the features of bone tumours on x-ray?

A
  • bone destruction/hole in th ebone
  • soft tissue swelling
  • periosteal reaction
  • new bone formation
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117
Q

What spinal conditions cause a limp?

A

Spinal tumours
Spinal cord problems
Nerve root compression

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118
Q

What changes occur to foetal circulation when baby is delivered?

A

Pulmonary resistance falls allowing more blood into the lungs
- foramen ovale closes
- ductus ateriosis closes
- aortic pressure rise due to clamping of umbilical arteries

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119
Q

What are the 3 categories of congenital heart disease?

A
  1. holes/connections
  2. narrowings
  3. complex (mixed)

other categories
- duct dependent/non-duct dependent
- cyanotic/acyanotic

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120
Q

What are the features of ventricular septal defect?

A
  • most common congenital defect
  • L to R shunt causes increased blood flow to lungs, symptoms when PVR falls
  • Pan systolic murmur, LLSE
  • tachypnoea, poor feeding, failure to thrive
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121
Q

What are the features of Atrial septal defect?

A
  • 2nd most common
  • L to R shunt (acyanotic)
  • atria are low pressure chambers, so only get symptoms later in life in early adulthood
  • fixed splitting S2, pulmonary flow murmur (Not ASD murmur as not high enough pressure to hear)
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122
Q

What are the features of Atrioventricular septal defect?

A
  • common defect in Trisomy 21 (Down syndrome)
  • can lead to pulmonary vascular disease
  • will not close spontaneously = needs surgery
  • poor feeding, failure to thrive, tachypnoea
  • active precordium, thrill, gallop, rhythm
  • hepatomegaly, oedema
  • murmur rises from valvular regurgitation rather than septal defects
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123
Q

What are the features of Patent ductus arteriosus?

A
  • usually preterm babies (prostaglandins E higher in preterm infants)
  • poor feeding, failure to thrive, tachypnoea
  • active precordium, thrill, gallop, rhythm
  • classical continuous machinery murmur in pulmonary area ‘bounding pulse’ (in diastolic and systolic phase)
  • hepatomegaly, oedema
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124
Q

Management: ASDs

A
  • only surgery on large defects or if failing to thrive
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125
Q

Management: VSD and PDS

A

If failing to thrive
- increase calories, nasogastric feeds
- diuretics
- surgical closure

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126
Q

What are the types of congenital heart defects with stenosis/narrowing?

A
  • coarctation of aorta
  • aortic stenosis
  • pulmonary stenosis
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127
Q

Aortic Stenosis

A
  • critical AS > acute presentation with shock collapse in newborns
  • reduced stroke volume (reduced blood flow to the body)
  • symptoms: reduced exercise tolerance, poor feeding, syncope
  • signs: femoral, thrill, ejection, systolic murmur loudest in aortic area, radiating to carotids
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128
Q

Pulmonary stenosis

A
  • ejection systolic murmur in the left upper sternal edge
  • murmur often radiates to the back especially if the pulmonary branches are stenosed
  • right ventricular heave
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129
Q

Coarctation of aorta

A
  • critical anomaly, need surgery
  • impaired perfusion to the body
  • present = after a week of age (as PDA still open helping with blood flow but once closed baby presents with collapse)
  • pre and post ductal difference in saturations (only if PDA open)
  • 4 limb BP, discrepancy between upper and lower limb BP
  • older children murmur over back (after collaterals develop)
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130
Q

Management: coarctation of aorta

A

in critical cases
- prostaglandin E = used to keep ductus arteriosus open while waiting for surgery
- surgery = correct coarctation and to ligate the ductus arteriosus

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131
Q

Management: obstructive lesions

A
  • keep PDA open with prostaglandins
  • surgical = balloon valvoplasty or surgical repair
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132
Q

What are the 2 Cyanotic heart conditions?

A
  • transposition of great arteries
  • tetralogy of fallot’s
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133
Q

Transposition of great arteries

A
  • aorta and pulmonary artery have swapped
  • this circulation is not compatible with life (foramen open in foetus so can survive in the uterus)
  • cyanosis
  • acidosis
  • collapse/death
  • emergency cardiac surgery = septosotmy, start prostaglandins
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134
Q

What are the 4 features of tetralogy of fallot?

A
  1. ventricular septal defect
  2. Pulmonary stenosis
  3. overriding of aorta
  4. right ventricle has thickened muscle RVH
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135
Q

Presentation: tetralogy of fallot

A

depends on severity of RVOT narrowing
- may be cyanotic or pink
- murmur
- normal pulses
- poor feeding
- respiratory distress

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136
Q

Management: tetralogy of fallot

A

RVOT/ductal stent implantation

Primary surgical repair

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137
Q

Fallot spells

A

Right ventricle muscle goes into spasm preventing blood from flowing to the lungs
- baby becomes blue
- R to L shunting
- short and self resolving

Management:
- propanolol/morphine

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138
Q

What syndromes are associated with congenital heart defects?

A
  • trisomy 21 = AVSD, TOF, VSD (all get cardiac screening)
  • Turner’s (females, webbed neck) = coarctation of aorta, AS, aortic dissection later in life, bicuspid aortic valve
  • Williams syndrome (chromosome 7) = supravalvular AS, PA stenosis

Di George
- interrupted aortic arch
- truncus arteriosis
- TOF
- VSD
- PDA

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139
Q

What is Eisenmenger syndrome?

A

when blood flows from the right side of the heart to the left across a structural heart lesions, bypassing the lungs

  • develop after 1-2 yrs with large shunts
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140
Q

What are the examination findings for Eisenmenger syndrome?

A

Right ventricular heave: the right ventricle contracts forcefully against increased pressure in the lungs

Loud P2: loud second heart sound due to forceful shutting of the pulmonary valve

Raised JVP

Peripheral oedema

murmur depending on the location of septal defect

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141
Q

Management: eisenmenger syndrome

A
  1. oxygen
  2. treatment for pulmonary hypertension = sildenafil
  3. treatment of arrhythmias
  4. treatment of polycythaemia with venesection
  5. preventions and treatment of thrombosis with anticoagulation
  6. prevention of infective endocarditis using prophylactic antibiotics
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142
Q

Define: infective endocarditis

A

infection of the endothelium of the heart valves

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143
Q

What are the risk factors for infective endocarditis?

A

MC with congenital cardiac disease

Intravenous drug use
Structural heart pathology (see below)
Chronic kidney disease (particularly on dialysis)
Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
History of infective endocarditis

Structural pathology can increase the risk of endocarditis:

Valvular heart disease
Congenital heart disease
Hypertrophic cardiomyopathy
Prosthetic heart valves
Implantable cardiac devices (e.g., pacemakers)

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144
Q

What are the features of infective endocarditis?

A
  • fever
  • heart murmur
  • splenomegaly
  • petechiae
  • Osler’s nodes
  • laneway lesions
    splinter haemorrhages
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145
Q

investigations: infective endocarditis

A

Blood cultures and echo

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146
Q

What is the criteria for infective endocarditis?

A

Modified Duke’s criteria

Major
- typical microorganism on 2 separate blood cultures
- evidence of endocardial involvement

minor
- predisposition
- fever >38
- vascular phenomena
- immunologica phenomena
- micro and bloods that don’t meet major criteria

1 major + 3 minor
5 minor

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147
Q

Management: IE

A

IV broad spectrum antibiotics 4-6 weeks

surgery
- if due to valve pathology
- large vegetation’s or abscesses
- not responding to antibiotics

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148
Q

Define: Faltering growth

A

Failure to gain adequate weight or achieve adequate growth during infancy or early childhood.

  • a significant interruption in the expected rate of growth compared with other children of similar age and sex during early childhood.
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149
Q

What are the thresholds of concern about faltering growth in infants and children?

A

a fall across 1 or more weight centile spaces, if birth weight was below the 9th centile.

a fall across 2 or more weight centile spaces, if birth weight was between the 9th and 91st centiles.

a fall across 3 or more weight centile spaces, if birth weight was above the 91st centile.

when current weight is below the 2nd centile for age, whatever the birth weight.

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150
Q

How to monitor weight for different age groups?

A
  • daily if less than 1 month old
  • weekly between 1–6 months old
  • fortnightly between 6–12 months
  • monthly from 1 year of age
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151
Q

What to do if infants in the early days of life lose more than 10% of their brith weight?

A
  1. perform a clinical assessment
  2. take a detailed history to assess feeding
  3. consider direct observation of feeding
  4. perform further investigations only if they are indicated based on the clinical assessment
  5. provide feeding support (by a person with appropriate training and expertise).
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152
Q

What should you be concerned about linear growth when looking at BMIs?

A

In a child over 2 years of age determine the BMI centile:

BMI< 2nd centile this may reflect either undernutrition or a small build

BMI < 0.4th centile probable undernutrition that needs assessment and intervention

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153
Q

What are the medical risk factors for faltering growth?

A

Congenital anomalies (cerebral palsy, autism, trisomy 21)
Developmental delay
Gastroesophageal reflux
Low birth weight (<2.500g)
Poor oral health, dental caries
Prematurity (<37w)
Tongue-tie (controversial)

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154
Q

What are the psychosocial risk factors for faltering growth?

A

Disordered feeding techniques
Family stressors
Parental or family history of abuse/violence
Poor parenting skills
Postpartum depression
Poverty

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155
Q

How to assess a child with faltering growth?

A
  • Perform a clinical, developmental and social assessment
  • Take a detailed feeding or eating history
  • Consider direct observation of feeding or meal times

Refer if symptoms indicate an underlying disorder

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156
Q

What examinations can be found in a child with faltering growth?

A

Dysmorphic appearance (genetic abnormality)
Oedema (renal, liver disease)
Hair color/texture change )(zinc deficiency)
Heart murmur (anatomic cardiac defect)
Hepatomegaly (infection, chronic illness, malnutrition)
Mental status change (cerebral palsy, poor social bonding)
Poor parent- child interaction (depression, social stress)
Rash, skin changes, bruising (HIV infection, abuse)
Respiratory compromise (CF)
Wasting (cerebral palsy, cancer)

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157
Q

What 4 main physiological factors affect weight gain?

A

Not enough in
Not absorbed
Too much used up
Abnormal central control of growth/appetite

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158
Q

What can cause faltering growth in milk-fed infants?

A

ineffective suckling in breastfed infants
ineffective bottle feeding
feeding patterns or routines being used
the feeding environment
feeding aversion
parent/carer–infant interactions
physical disorders that affect feeding

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159
Q

When is enteral tube feeding used for faltering growth?

A

If there are serious concerns about weight gain.

An appropriate specialist multidisciplinary
assessment for possible causes and contributory
factors has been completed.

Other interventions have been tried without improvement.

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160
Q

What can cause inadequate nutrient absorption?

A

Anemia (iron deficiency)
Biliary atresia
Coeliac disease
Chronic GI conditions (infections, IBS)
Cystic fibrosis
Inborn errors of metabolisms
Milk protein allergy
Pancreatic cholestatic conditions

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161
Q

What are the antibodies of coeliac disease?

A
  1. Tissue transglutaminase antibodies (anti-TTG)
  2. Endomysial antibodies (EMAs)
  3. Deaminated gliadin peptides antibodies (anti-DGPs)
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162
Q

Presentation: coeliac disease

A

often asymptomatic so low threshold to test

Failure to thrive in young children
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen

all new type 1 diagnosis are tested for coeliac disease (often linked)

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163
Q

Investiagtions: coeliac disease

A
  • antibody test:
  • check total immunoglobulin A levels to exclude IgA deficiency
  • raised anti-TTG antibodies
  • raised anti-endomysial antibodies
  • serological test after gluten free first for 6 weeks
  • Upper Gi endoscopy and small bowel biopsy
  • crypt hypertrophy
  • villous atrophy
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164
Q

Management: coeliac disease

A

Gluten free diet

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Perfectly
165
Q

What are the complications of untreated coeliac disease?

A

Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL) of the intestine
Non-Hodgkin lymphoma (NHL)
Small bowel adenocarcinoma (rare)

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166
Q

What are the features and treatment of Giardia?

A

Only 20% pick up rate on immediate stool examination

May last for years: foreign travel not necessary

Giardia stool ELISA

Practically: treat empirically with metronidazole 15mg/kg 3x a day for 7 days

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167
Q

What are the 2 types of cow’s milk allergy?

A
  1. IgE mediated
    - angiooedema
    - pruritus
    - colicky abdominal pain
    - vomiting and diarrhoea
    - acute urticaria
  2. Non-IgE mediated
    - GOR
    - loose or frequent stools
    - blood/mucus in stools
    - ado pain
    - food refusal/aversion
    - perinatal redness
    - pallor or tiredness
    - faltering growth
    - atopic eczema
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168
Q

Presentation: Cow’s milk allergy

A
  • vomiting
  • asthma
  • swelling of the lips or eyelids
  • wheezing and coughing
  • iron deficiency anaemia
  • refusal to feed
  • blood in poop
  • diarrhoea
  • skin rash
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169
Q

Management: Cow’s milk allergy

A
  • no investigations, diagnosis made on clinical findings = skin prick testing
  • put on diary free diet for 3 weeks and see if effective
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170
Q

What would cause increased metabolism leading to faltering growth?

A

Chronic infections (HIV, tuberculosis)
Chronic lung disease of prematurity
Congenital heart disease
Hyperthyroidism
Inflammatory conditions (e.g. asthma, IBD)
Malignancy
Renal failure

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171
Q

What can cause abornomal growth control?

A
  • GH
  • thyroid
  • psychosocial influcence

rare

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172
Q

Define: avoidant or restrictive food intake disorder (ARFID)

A
  • significant weight loss
  • nutritional deficiencies (such as iron deficiency anemia)
  • a dependence on nutritional supplements, (i.e., oral or enteral formulas), to meet energy requirements without an underlying condition necessitating this
  • significant interference with day-to-day functioning due to the inability to eat appropriately.
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173
Q

What are the challenges to management of faltering growth?

A

Faltering growth is complex and often multifactorial and a
specific underlying cause may not be identified.

Children may undergo excessively frequent monitoring or
unnecessary investigations looking for an underlying disorder.

Parents may feel blamed for their child’s slow weight gain,
whereas neglect is an uncommon cause of faltering growth.

Healthcare professionals should remain alert to the possibility of safeguarding concern, but should be sensitive to the emotional impact of caring for a child with faltering growth.

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174
Q

What should always be ruled out in assessing children with faltering growth?

A
  • urinary tract infection
  • coeliac disease, if the diet has included gluten-containing foods
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175
Q

Presentation: Infantile spasms

A

aka West syndrome

  • spasms consist of a sudden stiffening. often the arms fling out as the knees pull up and the body bends forward
  • may cry or after seizure
  • lasts 1-2 seconds. and occur close together in a series
  • happen most often just after waking up (rare during sleep)
  • skin changes, dysmorphism
176
Q

What causes infantile spasms?

A
  • structural change in brain e.g. brain infection, hypoxia, dysplasia
  • Tuberous sclerosis (growths present in brain) MC
177
Q

Investigations: infantile spasms

A
  • History and see
  • Classical EEG- hypsarrythmia
  • Developmental delay/regressing
178
Q

Management: Infantile spasms

A

Vigabatrin
+/- Prednisolone

179
Q

Define: Sleep myoclonus

A
  • benign
  • jerking movements when asleep
  • growing well

No treatment

180
Q

What are febrile convulsions?

A

A type of seizure that occurs in children with a high fever (usually after viral infection)
- children aged 6 months to 5 yrs

181
Q

What are the 2 types of febrile convulsions?

A
  1. simple febrile convulsions = generalised, tonic clonic seizures that last 15 mins and occur only once
  2. Complex febrile convulsions = consist of partial or focal seizures, last more than 15 mins or occurs multiple times during the same febrile illnes
182
Q

How do you diagnose febrile convulsions?

A

Child around 18months presenting with a seizure during a high fever
(once seizure is finished, he acts normal and well again)

Good GCS

rule out other diagnoses e.g. epilepsy, meningitis, intracranial space occupying lesion, trauma

rule out riggers = normal shaking with a fever or delirius

183
Q

Management: febrile convulsion

A
  1. manage source of infection and control fever with analgesia
  2. if complex give parents advice on how to deal with seizures
184
Q

What are the features of Reflex anoxic seizure?

A
  • Triggered by pain or strong emotion
  • goes stiff and then starts jerking
  • Results in decreased perfusion to brain
  • Work up includes ECG (?arrhythmia) and EEG (normal)
  • can happen at any age

Prognosis- Most will grow out of it

185
Q

What are the features of Juvenile myoclonic epilepsy?

A
  • myoclonic jerks
  • absence seizures = become clumsy as LoC for a second
  • worse when tired
186
Q

Treatment: juvenile myoclonic epilepsy

A

Sodium valproate
(now need 2 neurologist to sign before prescribing)

NOT carbamazepine
(focal seizures respond well to it)

187
Q

What are the features and investigations for Faints/syncope?

A
  • ask what they were doing
  • eaten food and dehydrated
  • completely aware after
  • last for 30s, LOC

Investigations
- ECG
- BP lying and standing
- rule out family history

188
Q

What are the features of Absence seizures?

A
  • vacant, daydreaming episodes
  • induced by hyperventilation (signifies its epilepsy)
  • last 30s
  • behavioural arrest, when aware again will go back to what they were doing
  • MC in childhood
189
Q

treatment: absence seizures

A

ethosuximide (zarontin)

190
Q

What does an EEG show for an absence seizure?

A

3Hz spike and wave discharges

191
Q

Define: status epilepticus

A

A seizure that lasts for more than 5 mins

192
Q

What is the protocol for status epilepticus?

A
  1. ABCDE
  2. 5 mins: Benzodiazepine (midazolam buccal, lorazepam IV, diazepam PR)
  3. 10mins later: Further benzodiazepine e.g. IV lorazepam
  4. Prepare PR paraldehyde
  5. Prepare phenytoin
  6. Call for senior support
  7. 10mins later: IV phenytoin
193
Q

What is the complication of status epilepticus?

A

airway is shut off in seizure

After 30 mins will start developing irreversible changes to brain

194
Q

What are the 4 categories for child abuse?

A
  • physical abuse
  • sexual abuse
  • emotional abuse
  • neglect
195
Q

What are the risk factors for child abuse?

A

Parental:
Lack of support
Generational effect
Deprivation
Mental health problems
Learning difficulty
Alcohol and substance misuse
Domestic violence
ACEs- adverse childhood experiences

Child:
Difficult to care for
Preterm
Disabled

196
Q

How do children who’ve been abused present?

A

Disclosure

Injury observed e.g. At school

Found incidentally when attending for other reason

Injury presented with or without explanation.

197
Q

What are the types of injuries that present with child abuse?

A

Superficial:
Bruises (age is important, if they can’t walk yet why do they have bruises?)
Scratches
Marks from implements (Patterned injuries)

Burns and scalds

Fractures
Multiple
long bones, ribs, metaphyseal

Internal Organ Damage
Abdominal
Intracranial

198
Q

What are the consequences of a shaken baby?

A

Cerebral Hypoxia*

Subdural haematoma*

Rib fractures

Retinal haemorrhages*

May have other fractures, torn frenulum, bruises etc.

199
Q

How does sexual abuse present?

A

Disclosure or allegation

Behaviour change:
Sexualised
Indicative of distress

Physical symptoms:
Bleeding
Discharge
Soreness
Wetting or soiling
STI
Pregnancy

200
Q

What do persistence of primitive reflexes in a infant indicate?

A

Upper motor neuron abnormality

201
Q

Define: cerebral palsy

A

permanent neurological problems resulting from damage to the brain around the time of brith

  • non progressive
  • variation in severity anf symptoms
202
Q

What are the causes of cerebral palsy?

A

Antenatal:

Maternal infections
Trauma during pregnancy

Perinatal:

Birth asphyxia
Pre-term birth

Postnatal:

Meningitis
Severe neonatal jaundice
Head injury

203
Q

What are the types of cerebral palsy?

A
  • Spastic: hypertonia (increased tone) and reduced function resulting from damage to upper motor neurones
  • Dyskinetic: problems controlling muscle tone, with hypertonia and hypotonia, causing athetoid movements and oro-motor problems. This is the result of damage to the basal ganglia.
  • Ataxic: problems with coordinated movement resulting from damage to the cerebellum
  • Mixed: a mix of spastic, dyskinetic and/or ataxic features
204
Q

What are the patters of spastic cerebral palsy?

A

Monoplegia: one limb affected

Hemiplegia: one side of the body affected

Diplegia: four limbs are affects, but mostly the legs

Quadriplegia: four limbs are affected more severely, often with seizures, speech disturbance and other impairments

205
Q

Presentation: cerebral palsy

A

Might have hypoxic-ischaemic encephalopathy first

Become more evident during development:
- Failure to meet milestones
- Increased or decreased tone, generally or in specific limbs
- Hand preference below 18 months is a key sign to remember for exams
- Problems with coordination, speech or walking
- Feeding or swallowing problems
- Learning difficulties

206
Q

What types of gait is present in cerebral palsy?

A

hemiplegic or diplegia gait

  • due to increased muscle tone and spascitiy in the legs
  • leg will be extended with plantar flexion of the feet and toes (swing leg in a semicircle around them)
207
Q

What are the complications of cerebral palsy?

A

Learning disability
Epilepsy
Kyphoscoliosis
Muscle contractures
Hearing and visual impairment
Gastro-oesophageal reflux

208
Q

Management: cerebral palsy

A

permanent condition

  • physiotherapy
  • occupational therapy = support with getting dressed, washing, cooking
  • speech and language therapy
  • dieticians = peg feeding
  • orthopaedic surgeons = to release contractors or lengthen tendons

medications
- muscle relaxants e.g. baclofen
- anti-epileptic drugs = seizures
- glycopyrronium bromide = excessive drooling

209
Q

Define: syncope

A

event of temporarily losing consciousness due to a disruption of blood flow to the brain, often leading to a fall

  • problem with autonomic nervous system regulating blood flow to the brain
210
Q

What are the signs and symptoms of syncope?

A

Patients often remember the event and can recall how they felt prior to fainting.

This is called the prodrome, and involves feeling:

Hot or clammy
Sweaty
Heavy
Dizzy or lightheaded
Vision going blurry or dark
Headache

loss of consciousness,
fall over
ditching, shaking

211
Q

What are the primary and secondary causes of syncope?

A

Primary syncope (simple fainting):

Dehydration
Missed meals
Extended standing in a warm environment, such as a school assembly
A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood

Secondary causes:

Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
Valvular heart disease
Hypertrophic obstructive cardiomyopathy

212
Q

What are the differences between syncope and epilepsy?

A

syncope
- prolonged upright position before event + lightheadedness + sweating + blurred vision
- reduced tone

213
Q

Define: disability

A

someone who has a physical or
mental impairment that results in a marked, pervasive limitation of activity

214
Q

Define: impairment

A

an abnormality or loss of function

215
Q

What are the types of impairments?

A
  • Physical
    E.g. cerebral palsy, brain injury, neuromuscular disorders, musculoskeletal conditions-ABI
  • Sensory Impairments
    = Hearing and visual impairments
  • Learning e.g. low IQ
  • Neurodevelopmental disorders E.g.ADHD,Autism -
  • Emotional/Behavioral
    E.g. Depression Conduct disorder, attachment disorder D
216
Q

What are the 3 things to assess in disabilities?

A
  1. functioning
  2. activity
  3. their ability to participate
217
Q

What are the 6 domains of functioning included in WHODAS?

A

World health organisation disability assessment schedule

  • Cognition – understanding & communicating
  • Mobility– moving & getting around
  • Self-care–hygiene,dressing,eating&stayingalone
  • Social– interacting with other people
  • Lifeactivities–domesticresponsibilities,leisure,work&school
  • Participation– joining in community activities
218
Q

What are factors that affect children with learning disabilities?

A
  • Disabled children are more likely to live in poverty
  • Parents are more likely to be unemployed
  • Higher rates of mental health needs
  • Poorer physical health and lower life expectancy
219
Q

Define + 3 main factors: quality of life

A

The degree to which a person enjoys the important possibilities of his/her life.

  • Being –who one is
  • Belonging –how one fits into the environment
  • Becoming –How to have purposeful activities in order to achieve ones goals
220
Q

What are 3 ages that diagnosis for vomiting changes?

A

6 hrs - neonates

6 weeks

6 months

likely differential diagnosis changes with each

221
Q

What are the causes of vomiting in neonates?

A
  • GORD (reflux)n= yellow/milky
  • overfeeding = milky
  • duodenal atresia/stenosis
  • sepsis
  • malrotation =
222
Q

investigations: sepsis

A

Bloods = FBC, U+Es, CRP, blood gas = lactate
Blood culture
Lumbar puncture = for meningitis
Urine dip = UTI

223
Q

Define: malrotation and volvulus

A

bowel has herniated into umbilicus
and then has not rotated correctly when goes back into the abdomen

  • reduced surface area so easier for bowel to twist on blood supply
  • then bowel can infarct
224
Q

Investigations: malrotation

A

green vomiting >

barium meal
- x-ray

needs diagnosis within 6 hrs to prevent infarction of bowels

225
Q

What is the cause of vomiting in infants?

A
  • overfeeding
  • GORD
  • sepsis
  • pyloric stenosis
226
Q

Define: pyloric stenosis

A

ring of smooth muscle the forms the canal between the stomach and the duodenum.

Hypertrophy (thickening) and narrowing of the pylorus is called pyloric stenosis.

This prevents food traveling from the stomach to the duodenum as normal.

after feeding, peristalsis in the stomach tries to push food into duodenum and becomes so powerful that it ejects the food in the oesophagus and out the mouth

227
Q

Presentation: Pyloric stenosis

A
  • projectile vomiting
  • failing to thrive
  • firm, round mass found I upper abdomen
  • 4-6 weeks old
228
Q

Investigations: pyloric stenosis

A

blood gas analysis
- hypochloric metabolic alkalosis (as vomiting HCL form stomach)
- low potassium (excrete potassium)

Abdo USS
(then resuscitate baby by giving them fluids)

229
Q

Management: pyloric stenosis

A

laparoscopic pyloromyotomy
(known as “Ramstedt’s operation“)
- incision in smooth muscle of pylorus to widen the canal

230
Q

Define: intussusception

A

bowel telescopes into itself, folding inwards
- thickens the overall size of the bowel and narrows lumen leading to obstruction of faeces

  • mC 6-12 months old
    due to start weaning > stimulate GI immune system > Peyers patch enlarge as challenges lots of immune cells > peristalsis cause preyers patches to get caught
231
Q

Presentation: intussusception

A

Severe, colicky abdominal pain

Pale, lethargic and unwell child

“Redcurrant jelly stool” = blood coming from iscahemic bowel caught

Right upper quadrant mass on palpation. This is described as “sausage-shaped” = feeling when bowel has folded

Vomiting = milky then green

Intestinal obstruction

232
Q

Causes: intussusception

A

Most idiopathic
ileocolic
anatomical lead point

associated with CF and Meckel’s diverticulum

233
Q

Investigations: intussusception

A

USS
- doughnut shape/ target shaped mass

Abdominal X-ray
- distended small bowel with absence of gas in the large bowel

234
Q

Management: intussusception

A

Air/water/contrast enema 90% = pushes folded bowel out of the bowel and into the normal position

surgical reduction

Recur

235
Q

What are the complications of intussusception?

A

Obstruction
Gangrenous bowel
Perforation
Death

236
Q

Define: acute abdominal pain

A

less than 7 days
duration
sudden onset severe

237
Q

What are the most common surgical causes of acute abdominal pain in children?

A
  1. non-specific abdomen pain
  2. appendicitis
  3. ovarian pathology = ovarian torsion, cysts
  4. intussusception
  5. Merkel’s diverticulum
238
Q

What are 5 non-surgical causes of acute abdominal pain?

A
  1. UTI
  2. gastroenteritis
  3. constipation
  4. pancreatitis = gallstones
  5. right sided pneumonia
239
Q

What are the red flags for serious abdominal pain?

A

Persistent or bilious vomiting
Severe chronic diarrhoea
Fever
Rectal bleeding
Weight loss or faltering growth
Dysphagia (difficulty swallowing)
Nighttime pain
Abdominal tenderness

240
Q

What is guarding?

A

Abdominal wall muscles tense up in response to pain or inflammation inside the abdomen

voluntary
or involuntary (signifies inflammation in peritoneum causing overlaying muscles to go into spasm > surgery)

241
Q

Investigations: acute abdo pain

A
  • urine dip = exclude UTI
  • FBC, CRP
  • U+E
  • USS abdo
242
Q

What is a abdominal migraine?

A

children sometimes get this before developing traditional migraines as they get older

  • central abdo pain lasting more than 1 hr
  • examination will be normal
  • associated with = nausea, vomiting, anorexia, pallor, headache, photophobia, aura
243
Q

Management: abdominal migraine

A

acute attacks
- low stimulus environments
- paracetamol
- ibuprofen
- sumatriptan

preventative
- Pizotifen, a serotonin agonist
- Propranolol, a non-selective beta blocker
- Cyproheptadine, an antihistamine
- Flunarazine, a calcium channel blocker

244
Q

Define: appendicitis

A

inflammation of the appendix
- infection gets trapped in the appendix by obstruction

245
Q

Presentation: appendicitis

A

MAGNET
migration of pain to RIF
anorexia (LOA)
guarding
nausea (not much vomit)
elevated temp
tenderness in RIF

acute onset
Rovsing’s sign
Rebound tenderness
percussion tenderness

246
Q

Diagnosis: appendicitis

A
  • clinical presentation
  • inflammatory markers
  • CT scan
  • USS in females to exclude gynae
  • diagnostic laparoscopy
247
Q

Management: appendicits

A

appendicectomy
- laparoscopic better than laparotomy

248
Q

Complication sof appendicetomy

A

Bleeding, infection, pain and scars
Damage to bowel, bladder or other organs
Removal of a normal appendix
Anaesthetic risks
Venous thromboembolism (deep vein thrombosis or pulmonary embolism)

249
Q

Define: Self harm

A

act with intent to hurt themselves

  • no intention to kill self
  • associated with suicidal ideas therefore check
250
Q

Define: suicide attempt

A

act with intent to kill self

includes overdose, attempted hanging

intention includes desire to be dead

(its what the intent was, even if the act did not/would not kill them)

251
Q

What are the causes of self harm?

A

-depression
bullying
sexual abuse
family/friend conflict
subculture (self-harm)
drugs and alcohol misuse

252
Q

What are the factors that increase the risk of completed suicide?

A

presence of psychiatric disorder
previous suicide attempt
alcohol or substance misuse

253
Q

What needs to be checked in an assessment of a suicidal attempt?

A

Circumstances eg alone, did they tell anyone
Planned or impulsive
Left letter
Continuing ideas
What would stop a further episode
hope for the Future

254
Q

Management: depression

A

Mild depression = watchful waits advice, lifestyle changes

Moderate to severe:
- referral to CAMHS
- establish diagnosis
- psychological therapy = CBT
- 1st line = Fluoxetine
- 2nd = sertraline + citalopram
- continue medication until 6 months after remission

255
Q

Define: anorexia nervosa

A

the person feel they are overweight despite evidence of normal or low body weight
- involves restricting calorie intake with the intention of losing weight

(no longer BMI criteria)

256
Q

What are the risk factors of anorexia?

A
  • low self esteem
  • complex family dynamics
  • bereavement
  • pressure of education
  • social pressure
  • genetic risk
  • abuse
  • perfectionist/obsessive personality traits
  • co-morbidities - gender dysphoria, depression, anxiety, OCD, ASD, attachment disorder
257
Q

What are the features of anorexia nervosa?

A

Excessive weight loss
Amenorrhoea
Lanugo hair is fine, soft hair across most of the body
Hypokalaemia
Hypotension
Hypothermia
Changes in mood, anxiety and depression
Solitude

Cardiac complications include arrhythmia, cardiac atrophy and sudden cardiac death.

258
Q

How to diagnose anorexia

A

weight loss is self induced by avoidance of ‘fattening foods’

1 or more
- self induced vomiting
- self induced purging
- excessive exercise
- use of appetite suppressants and/or diuretics

body image distortion

259
Q

Define: bulimia nervosa

A

recurrent episodes of binge eating:
- eating within any 2hr period an amount of food that most would not eat
- a feeling that line one cannot stop eating

The period of purging by induced vomiting or taking laxatives to prevent the calories being absorbed

can have normal body weight

260
Q

What are the features of bulimia?

A
  • Alkalosis, due to vomiting hydrochloric acid from the stomach
  • Hypokalaemia
  • Erosion of teeth
  • Swollen salivary glands
  • Mouth ulcers
  • Gastro-oesophageal reflux and irritation
  • Calluses on the knuckles where they have been scraped across the teeth. This is called Russell’s sign.
261
Q

Management: bulimia nervosa

A

Guided self-help
- monitor what eating
- make realistic meal plans

CBT - BN

family therapy

antidepressants e.g. fluoxetine

262
Q

What are the features of a binge eating disorder?

A
  1. eating in discrete period of time, that is defo larger that most people would eat
  2. lack of control over eating and marked distress
  3. at least 3 of:
    - eating more rapidly than normal
    - eating until feeling uncomfortably full

once a week for 3 months

Usually overweight

263
Q

Management: binge eating disorder

A
  • weight control
  • guided self help
  • CBT
  • meal plan
  • work not riggers
  • change negative feelings about body
264
Q

Define: avoidance restricted food intake disorder

A
  1. An eating or feeling disturbance manifested by persistent failure to meet appropriate nutritional and/ or energy needs associated with one or more
    - sig weight loss
    - sig nutri def
    - dependence on enteral feeding
    - marked interference with psychosocial functioning

(e.g. maybe only eats beige food or certain textures)

not better explained by lack or food

265
Q

What other conditions or thinking is linked with ARFID?

A
  • linked with high rates of autism
  • often GI problems like reflux or vomiting
  • might be a sensory issue or a fear of choking/vomiting
  • linked with anxiety, OCD and ADHD
  • not interested in food so genuinely forget to eat
266
Q

what are some other eating disorders?

A

Orthorexia - eating helpfully that goes too far
body dysmorphic disorder
Diabulimia = people with diabetes
Pica = eating things that aren’t food
Bigorexia = people who don’t think they are big/muscly enough

267
Q

What are the short and long term problems of anorexia?

A

short term
- malnutrition
- weight loss
- dry skin
- atria loss
- dizziness/fainting
weakness
- low BP
Low body temp

long term
- severe dehydration
- cardiac problems
- infertility
- fragile bones = stops releasing oestrogen so can’t lay down good bones especially if in teen years
- depression, anxiety
- risk of relapse post recovery

268
Q

What is the effect of eating disorder on family?

A
  • guilt, blame
  • anxiety, confusion
  • shrinking of social/family life
  • future plans on hold
  • lives reorganised
269
Q

MAnagement: anorexia

A
  • if medically unstable need to be admitted for stabilisation and re-feeding admission

after discharge:
- continue meal plan
- follow up with community EDS
- follow up in medical/physical health monitoring clinics
- or transfer to tier 4 bed for further intense treatment

(always get to a healthy weight before starting next steps)

270
Q

What are the 4 phases of Family Based Treatment?

A
  1. acknowledge starvation, focus on referring and control given to parents
  2. continued focus on weight gain, starting to shift responsibility from parent to young person
  3. weight maintenance, focus on family relationships, develop family strengths (may start family therapy)
  4. relapse prevention
271
Q

Define: Juvenile Idiopathic Arthritis

A

Onset before 16th birthday

Persistent joint swelling lasting at least 6 weeks with no identified underlying cause

272
Q

What are the 5 key subtypes of Juvenile Idiopathic arthritis?

A
  1. Systemic JIA
  2. Polyarticular JIA
  3. Oligoarticular JIA
  4. Enthesitis related arthritis
  5. Juvenile psoriatic arthritis
273
Q

What are the 3 key features of juvenile idiopathic arthritis (JIA)?

A
  • joint pain
  • swelling
  • stiffness
274
Q

What are the features of systemic JIA?

A

Still’s disease

Subtle salmon-pink rash
High swinging fevers
Enlarged lymph nodes
Weight loss
Joint inflammation and pain
Splenomegaly
Muscle pain
Pleuritis and pericarditis

275
Q

What would investigations show for systemic JIA?

A

Antinuclear antibodies + rheumatoid factor = negative

inflammatory markers
- CRP, ESR, platelets and serum ferritin = raised

276
Q

What is a key complication of systemic JIA?

A

Macrophage activation syndrome
- severe activation of the immune system
- acutely unwell child with disseminated intravascular coagulation DIC, anaemia, thrombocytopenia, bleeding, and non-blanching rash

LOW ESR

277
Q

What are the key non-infective differentials when a child presents with a fever for more than 5 days?

A
  1. Kawasaki disease
  2. Still’s disease
  3. Rheumatic fever
  4. Leukaemia
278
Q

What are the features of polyarticular JIA?

A
  • idiopathic inflammatory arthritis in 5 joints or more
  • symmetrical
  • minimal systemic symptoms = can be mild fever, anaemia and reduced growth
  • normally rheumatoid factor negative

(equivalent to rheumatoid arthritis in adults)

279
Q

What are the features of Oligoarticular JIA?

A

AKA pauciarticular JIA
- involves 4 joints or less
- usually only affects single joint
- larger joints e.g. ankle or knee
- more common in girls under 6yrs
- no systemic symptoms
- inflammatory markers normal or mildly elevated

280
Q

What is a key feature/complication of oligoarticular JIA?

A

Anterior uveitis

281
Q

What are the features of Enthesitis-Related Arthritis?

A
  • paediatric version of seronegative spondyloarthropathy = HLA B27 gene
  • inflammation where the tendon inserts into the muscle

MC in males >6 yrs

282
Q

Investigations: Enthesitis Related arthritis

A

MRI scan
- but cannot distinguish between an enthesitis due to stress or an autoimmune process.

HLA-B27 testing

ANA and RF = negative

prone to anterior uveitis = seen by ophthalmologist

283
Q

What are the features of juvenile psoriatic arthritis?

A
  • seronegative inflammatory arthritis associated with psoriasis
  • symmetrical polyarthritis affecting the small joints
284
Q

What are the signs of juvenile psoriatic arthritis on examination?

A
  • Plaques of psoriasis on the skin
  • Pitting of the nails (nail pitting)
  • Onycholysis, separation of the nail from the nail bed
  • Dactylitis, inflammation of the full finger
  • Enthesitis, inflammation of the entheses, which are the points of insertion of tendons into bone
285
Q

Management: juvenile idiopathic arthritis

A

Specialist paediatric rheumatologist

  • NSAIDs e.g. ibuprofen
  • Steroids = either oral, intramuscular or intra-artricular in oligoarthritis
  • Disease modifying anti-rheumatic drugs (DMARDs) e.g. methotrexate, sulfasalazine and leflunomide
  • Biologic therapy = tumour necrosis factor inhibitors etanercept, infliximab and adalimumab
286
Q

Define: osteogenesis imperfecta

A
  • genetic condition
  • results in brittle bones that are prone to fractures
  • mutations affect formation of collagen
287
Q

Presentation: osteogenesis imperfecta

A
  • Hypermobility
  • *Blue / grey sclera (the “whites” of the eyes)
  • Triangular face
  • Short stature
  • Deafness from early adulthood
  • Dental problems, particularly with formation of teeth
  • Bone deformities, such as bowed legs and scoliosis
  • Joint and bone pain
288
Q

Investigations: osteogenesis imperfecta

A

clinical diagnosis

x-rays
Genetic testing but no routinely done

289
Q

Management: osteogenesis imperfecta

A
  • bisphosphates = increase bone density
  • vitamin D supplementation = prevent deficiency
290
Q

Define: Rickets

A

condition affecting children where there is defective bone mineralisation causing ‘soft’ and deformed bones

291
Q

What are the causes of Ricketts?

A
  • deficiency in vitamin D or calcium

a rare from caused by genetic defects resulting in low phosphate in the blood
= hereditary hypophosphataemic rickets

292
Q

What is the pathophysiology of rickets?

A
  1. vitamin D is a hormone created from cholesterol by the skin in response to UV radiation
  2. malabsorption disorders reduce the amount of vit D absorbed
  3. vitamin D is essential in calcium and phosphate absorption from the intestines and kidneys
  4. reduced calcium and phosphate in the blood means less in bones = defective bone mineralisation
  5. low calcium causes a secondary hyperparathyroidism as the parathyroid gland tries to raised calcium level by secreting parathyroid hormone so increased reabsorption of calcium from the bones
293
Q

Presentation: Rickets

A

Lethargy
Bone pain
Swollen wrists
Bone deformity
Poor growth
Dental problems
Muscle weakness
Pathological or abnormal fractures

294
Q

What bone deformities occur in rickets?

A
  • Bowing of the legs = where the legs curve outwards
  • Knock knees = the legs curve inwards
  • Rachitic rosary = the ends of the ribs expand at the costochondral junctions, causing lumps along the chest
  • Craniotabes = which is a soft skull, with delayed closure of the sutures and frontal bossing
  • Delayed teeth with under-development of the enamel
295
Q

Investigations: rickets

A

Serum 25-hydroxyvitamin D = <25 is vit D deficient

X-ray = for diagnosis

Serum calcium may be low
Serum phosphate may be low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high

296
Q

What other tests done to rule out conditions for rickets?

A

Full blood count and ferritin, for iron deficiency anaemia

Inflammatory markers such as ESR and CRP, for inflammatory conditions

Kidney function tests, for kidney disease

Liver function tests, for liver pathology

Thyroid function tests, for hypothyroidism

Malabsorption screen such as anti-TTG antibodies, for coeliac disease

Autoimmune and rheumatoid tests, for inflammatory autoimmune conditions

297
Q

management: rickets

A

Prevention
- breastfed babies receive less vit D as it is included in formula
(breastfeeding women and all children should take vit D supplement)

Treatment
- vitamin D e.g. ergocalciferol
- calcium

298
Q

Define: transient synovitis

A

irritable hip

299
Q

Define: Osgood-Schlatter disease

A
  • caused by inflammation at the tibial tuberosity where the patella ligament inserts
  • common cause of anterior knee pain in adolescents
  • unilateral
300
Q

Pathophysiology: Osgood-Schlatters disease

A

patella tendon inserts into tibial tuberosity (epiphyseal plate)

stress from running, jumping etc. result in inflammation on tibial epiphyseal plate

(rare complication) multiple small avulsion fractures where patella ligament pulls away tiny pieces of the bone

causing growth of tibial tuberosity

initially this lump is tender due to inflammation but as the bone heals and inflammation settles it becomes hard and non-tender

301
Q

Presentation: Osgood Schlatter

A

Visible or palpable hard and tender lump at the tibial tuberosity
Pain in the anterior aspect of the knee
The pain is exacerbated by physical activity, kneeling and on extension of the knee

302
Q

Management: Osgood- schlatter

A

reducing the pain and inflammation.

Reduction in physical activity
Ice
NSAIDS (ibuprofen) for symptomatic relief
Physio

Symptoms will fully resolve over time. The patient is usually left with a hard boney lump on their knee.

303
Q

What is the definition of regurgitation, rumination and possetting?

A

Regurgitation: effortless expulsion of gastric contents (healthy infants and older children who eat in excess)

Rumination: frequent regurgitation of ingested food (largely behavioural)

Possetting – small volume vomits during or between feeds in otherwise well child

304
Q

What are the common cubes of vomiting in neonatal 0-2 days?

A

-Duodenal or other intestinal atresia
-TEF (types A/C)

305
Q

What is the common cause of vomiting in newborns (3 days -1 month)?

A

-Gastroenteritis
-Pyloric stenosis
-Malrotation +/- volvulus
-TEF (types B/D/H)
-Necrotizing enterocolitis
-Milk protein intolerance
-CAH
-IEM

306
Q

What are the common causes of vomiting in infants (1 -36 months)?

A

-Gastroenteritis
-UTI, pyelonephritis
-GER
-GERD
-Ingestion
-Intussusception
-Milk protein intolerance

307
Q

What are the common causes of vomiting in a child (36 maths - 12 yrs)?

A

-Gastroenteritis
-UTI
-DKA
-Increased intracranial pressure
-Eosinophilic esophagitis
-Appendicitis
-Ingestion
-Post-tussive vomiting

308
Q

What are the common causes of vomiting in adolescents (12-18yrs)?

A

-Gastroenteritis
-Appendicitis
-DKA
-Increased intracranial pressure
-Eosinophilic esophagitis
-Bulimia nervosa
-Pregnancy
-Post-tussive vomiting

309
Q

Define: GORD/GOR

A

Gastrooesophageal reflux
- the passage of gastric contents into the oesophagus
- with or without regurgitation or vomiting

GORD
- the presence of troublesome symptoms and/ or complications of persistent GOR

310
Q

Presentation: GOR

A

Often babies reflux after larger feeds but is a problem if it causes them distress

Chronic cough
Hoarse cry
Distress, crying or unsettled after feeding
Reluctance to feed
Pneumonia
Poor weight gain
Heartburn
acid regurgitation
epigastric pain

311
Q

What are the red flags of vomiting?

A
  • Not keeping down any feed (pyloric stenosis or intestinal obstruction)
  • Projectile or forceful vomiting (pyloric stenosis or intestinal obstruction)
  • Bile stained vomit (intestinal obstruction)
  • Haematemesis or melaena (peptic ulcer, oesophagitis or varices)
  • Abdominal distention (intestinal obstruction)
  • Reduced consciousness, bulging fontanelle or neurological signs (meningitis or raised intracranial pressure)
  • Respiratory symptoms (aspiration and infection)
  • Blood in the stools (gastroenteritis or cows milk protein allergy)
  • Signs of infection (pneumonia, UTI, tonsillitis, otitis or meningitis)
  • Rash, angioedema and other signs of allergy (cows milk protein allergy)
  • Apnoeas are a concerning feature and may indicate serious underlying pathology and need urgent assessment
312
Q

Management: GOR/GORD

A
  • Small, frequent meals
  • Burping regularly to help milk settle
  • Not over-feeding
  • Keep the baby upright after feeding (i.e. not lying flat)

More problematic cases can justify treatment with:

  • Gaviscon mixed with feeds
  • Thickened milk or formula (specific anti-reflux formulas are available)
  • Proton pump inhibitors (e.g., omeprazole)

Surgery - fundoplication

313
Q

Investigations: GORD

A
  • pH
  • Barium swallow and meal then endoscopy
  • PPI test
314
Q

What is Sandifer’s syndrome?

A

rare condition causing brief episodes of abnormal movements associated with GOR in infants

  • Torticollis = forceful contractions of the neck muscles causing twisting of neck
  • Dystonia = abnormal muscle contractions causing twisting movements, arching of the back or unusual postures

usually resolves

315
Q
A
316
Q

What is the ROME III criteria of functional constipation?

A
  • Two or fewer defecations per week
  • At least 1 episode of faecal incontinence per week
  • Retentive posturing or stool retention.
  • Painful or hard bowel movements
  • Presence of a large faecal mass in the rectum
  • Large diameter stools that may obstruct the toilet
317
Q

What are the red flags of constipation?

A
  • Delayed passage of meconium (within 48 hrs of birth)
  • Fever, Vomiting, Bloody Diarrhea
  • Failure to thrive
  • Tight, empty rectum with presence of palpable abdominal faecal mass
  • Abnormal anus (anal stenosis, IBD or sexual abuse)
  • abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
  • Abnormal neurological exam
  • acute severe abdo pain + bloating (obstruction/intussusception)
318
Q

What is encopresis?

A

means faecal incontinence

not pathological until 4 yrs old
- usually a sign of chronic constipation where the rectum becomes stretched and looses sensation
- large hard stools remain in the rectum and only loose stools are able to leak out > soiling

319
Q

What are some other causes of encopresis?

A

Spina bifida
Hirschprung’s disease
Cerebral palsy
Learning disability
Psychosocial stress
Abuse

320
Q

What lifestyle factors contribute to constipation?

A
  • Habitually not opening the bowels
  • Low fibre diet
  • Poor fluid intake and dehydration
  • Sedentary lifestyle
  • Psychosocial problems such as a difficult home or school environment (always keep safeguarding in mind)
321
Q

What is a complication of constipation?

A

desensitisation of the rectum
- if a habit is developed of not opening the bowels
- they loose the sensation
- start to retain faeces causing faecal impaction
- rectum stretched over time and becomes further desensitised

322
Q

Management: constipation

A
  1. Correct any reversible contributing factors, recommend a high fibre diet and good hydration
  2. Start laxatives (movicol is first line) - keep going LT and slowly wean off until normal bowel habit
  3. Faecal impaction may require a disimpaction regimen with high doses of laxatives at first
  4. Encourage and praise visiting the toilet. This could involve scheduling visits, a bowel diary and star charts.
323
Q

What are the different types of medications for constipation?

A

Softener: lactulose, liquid paraffin
Bulking agent: Fybogel
Non-absorbed laxative irrigative: Movicol
Stimulant: Senna, Dulcolax
Enema
Anal fissure: anaesthetic cream +/- vasodilator

324
Q

Define: gastroenteritis

A

inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea

325
Q

What is the differential diagnosis of diarrhoea?

A

Infection (gastroenteritis)
Inflammatory bowel disease
Lactose intolerance
Coeliac disease
Cystic fibrosis = steatorrhoea
Toddler’s diarrhoea
Irritable bowel syndrome
Medications (e.g. antibiotics)

326
Q

What are the causes of gastroenteritis?

A

MC - viral

Rotavirus and norovirus MC

  • E.coli = some strains, produces Shiga toxin
  • Campylobacter jejune = travellers diarrhoea
  • Shigella = contaminated drinking water, pools or food
  • salmonella
  • giardiasis = microscopic parasite, faecal-oral transmission
327
Q

Management: gastroenteritis

A
  1. isolate to prevent spread
    (stay off school until 48 hrs after symptoms resolved)
  2. faeces tested for microscopy to establish antibiotic sensitivities
  3. ensure hydrated = fluid challenge
  4. slowly introduce food
  5. Antidiarrhoeal (loperamide) and antiemetics (metoclopramide) NOT RECOMMENDED
  6. antibiotics only given in patients at risk of complications once causative organism confirmed
328
Q

What are post- gastroenteritis complications?

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome

329
Q

What are the features of Crohn’s disease?

A

(crows NESTS)

N – No blood or mucus (these are less common in Crohns.)
E – Entire GI tract
S – “Skip lesions” on endoscopy
T – Terminal ileum most affected and Transmural (full thickness) inflammation
S – Smoking is a risk factor (don’t set the nest on fire)

Crohn’s is also associated with weight loss, strictures and fistulas.

330
Q

What are the features of ulcerative colitis?

A

U – C – CLOSEUP

C – Continuous inflammation
L – Limited to colon and rectum
O – Only superficial mucosa affected
S – Smoking is protective
E – Excrete blood and mucus
U – Use aminosalicylates
P – Primary sclerosing cholangitis

331
Q

Presentation: IBD different to adults

A
  • poor growth
  • delayed puberty
  • reduced final adult height
  • Catch up growth
  • persistent poor growth - only sign of disease activity
332
Q

Investigations: IBD

A

Blood tests
- anaemia
- infection
- thyroid
- kidney
- liver function
- CRP

Faecal calprotectin - inflamed bowels

Endoscopy = gold standard

Imaging = USS, CT and MRI for complications e.g. fistulas, abscesses and strictures

333
Q

Management: Crohn’s

A

Inducing remission
1. steroids e.g. oral prednisolone or IV hydrocortisone
2. alternative = azathioprine, methotrexate, mercaptopurine

Maintaining remission
1. azathioprine or mercaptopurine
2. alternative = methotrexate, infliximab, adalimumab

Surgery
- if only affect distal ileum
- to treat strictures and fistulas

334
Q

Management: UC

A
  1. Inducing remission
    Mild to moderate disease

First line: aminosalicylate (e.g. mesalazine oral or rectal)
Second line: corticosteroids (e.g. prednisolone)

Severe disease

First line: IV corticosteroids (e.g. hydrocortisone)
Second line: IV ciclosporin

  1. Maintaining Remission

Aminosalicylate (e.g. mesalazine oral or rectal)
Azathioprine
Mercaptopurine

  1. Surgery
    - removing colon and rectum will remove the disease
    - ileostomy or oleo-anal anastomosis (J-pouch)
335
Q

Define: Biliary atresia

A

Congenital condition where a section of the bile duct is either narrowed or absent
- results in cholestasis (bile cannot be transported from the liver to the bowel)
- conjugated bilirubin excreted in the bile

336
Q

Presentation: biliary atresia

A
  • persistent jaundice from birth till >14 days in term babies and 21 days in premature babies
337
Q

Investigations: biliary atresia

A
  • check conjugated and unconjugated bilirubin levels
338
Q

management: biliary atresia

A

Surgery
- kasai portoenterostomy = attaching a section of small intestine to the opening of the liver where the bile duct normally attaches

often a full liver transplant needed in future

339
Q

Define: Hirschsprung’s disease

A

Congenital condition where nerve cells of the myenteric plexus (Auerbach’s plexus) are absent in the distal bowel and rectum
- responsible for stimulating peristalsis of large bowel
- the section of the colon without innervation becomes aganglionic and does not relax > constricts
- proximal to the obstruction the bowel becomes distended and full

340
Q

What are the associations with Hirschsprung’s?

A
  • family history of hirschsprung’s
  • Downs syndrome
  • neurofibromatosis
  • Waardenburg syndrome = a genetic condition causing pale blue eyes, hearing loss and patches of white skin/hair
  • multiple endocrine neoplasia type II
341
Q

Presentation: Hirschsprung’s

A

Delay in passing meconium (more than 24 hours)
Chronic constipation since birth
Abdominal pain and distention
Vomiting
Poor weight gain and failure to thrive

342
Q

What is Hirschsprung-associated Enterocolitis?

A

Inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s disease.
- within 2-4 weeks of birth
- fever, abdominal distension, diarrhoea
- life threatening > toxic megacolon, perforation of the bowel

343
Q

Investigation: Hirschsprung’s

A
  • Abdominal x-ray = diagnose intestinal obstruction
  • Rectal biopsy = absence of ganglionic cells
344
Q

Management: Hirschsprung’s

A
  1. fluid resuscitation
  2. manage intestinal obstruction
  3. IV antibiotici in HAEC
  4. Definitive = surgical removal of the ganglionic section of bowel
    (most will then a live a normal life and may have LT disturbances in bowel function)
345
Q

Define: Meckel’s diverticulum

A

A malformation of the distal ileum that occurs in around 2% of the population
- usually asymptomatic + does not require treatment
- it can bleed, become inflamed, rupture or cause a volvulus or intussusception

346
Q

Define: marasmus

A

A severe undernutrition
- a deficiency in all the macronutrients that body requires to function

347
Q

Define: Kwashiorkor

A

A deficiency in protein predominantly

348
Q

Presentation: Marasmus vs kwashiorkor

A

Marasmus
- wasted, shrivelled appearance

kwashiorkor
- oedema
- swelling with fluid in abdomen and face

349
Q

What happens to the body in marasmus disease?

A

When the body is deprived of energy from food, it begins to feed on its own tissue
- first adipose fat tissue and then muscle
- reduced functions to conserve energy = low HR, low BP, low body temp
- children stunted in growth

350
Q

What are the main causes of marasmus?

A

The main causes affecting all ages include:

Poverty and food scarcity.
Wasting diseases such as AIDS.
Infections that cause chronic diarrhea.
Anorexia.

Additional causes affecting children include:

Inadequate breastfeeding or early weaning of infants.
Child abuse/neglect.

Additional causes affecting adults include:

Dementia.
Elder abuse/neglect.

351
Q

Presentation: marasmus

A

Visible wasting of fat and muscle.
Prominent skeleton.
Head appears large for the body.
Face may appear old and wizened.
Dry, loose skin (skin atrophy).
Dry, brittle hair or hair loss.
Sunken fontanelles in infants.
Lethargy, apathy and weakness.
Weight loss of more than 40%.
BMI below 16.

352
Q

Management: marasmus

A
  1. Rehydration and stabilisation
    - keep warm
  2. nutritional rehabilitation
    - slowly to prevent referring syndrome
  3. Follow up and prevention
353
Q

What are the causes of kwashiorkor disease?

A
  • diet of mostly carbohydrates
  • kwashiorkor = in ghana ‘the sickness the baby gets when the new baby comes’ > rapidly weaning the toddler off breastfeeding to feed the new baby
  • lack of dietary antioxidants
  • parasites and infectious diseases e.g. measles, malaria, HIV
354
Q

Presentation: Kwashiorkor

A
  • oedema
  • ascites
  • hair loss
  • dermatitis
  • enlarged liver
  • depleted muscle mass but retained subcutaneous fat
  • dehydration
  • loss of appetite
  • stunted growth in children
355
Q

Management: kwashiorkor

A
  1. treat/prevent hypoglycaemia
  2. treat/prevent hypothermia
  3. treat/prevent dehydration
  4. correct electrolyte imbalances
  5. treat/prevent infection
  6. correct micronutrient deficiencies
  7. start cautious feeding
  8. achieve catch up growth
  9. provide sensory stimulation and emotional support
  10. prepare for follow-up after recovery
356
Q

Define: choledochal cysts

A

aka biliary cysts
- congenital
- swellings in your bile duct
- usually found in young children but can be diagnosed in adults

357
Q

What are the 5 types of choledochal cysts?

A

type 1
- a cyst in the bile duct outside your liver
- MC

type 2
- a cyst that develops as a sac and comes off the side of the bile duct outside your liver

type 3
- a cyst at the end of the bile duct, outside your liver, where it joins your intestines
- choledochocele

type 4
- cysts in the bile ducts inside and outside your liver
- like type 1 they are caused by the tubes swelling up

type 5
- Carol disease

358
Q

Presentation: choledochal cysts

A
  • abdo pain
  • bloating
  • oedema
  • jaundice
  • pale coloured poo
359
Q

Investigations: choledochal cyst

A
  • 20 week USS
  • blood test = LFTs
  • USS
  • ERCP
360
Q

Management: choledochal cysts

A

Surgery
- key hole for cysts outside the liver
- ERCP for type 3 cysts
- surgery for cysts inside your liver

361
Q

What causes liver failure in children?

A
  • viruses e.g. HSV, EBV, CMV, hepatitis
  • inherited metabolic disorders
  • toxins e.g. rat poison, insect killer, weed killer
  • medications e.g. erythromycin, caloric acid, acetaminophen
  • autoimmune hepatitis
  • low blood flow to the liver
362
Q

Presentation: liver failure

A
  • fatigue
  • nausea or vomiting
  • loss of appetite
  • abdominal pain
  • dark urine
  • jaundice
  • itching
  • ascites
  • eventual brain problems
363
Q

Investigations: liver failure

A
  • high bilirubin levels > jaundice
  • high liver enzyme levels
  • problems with blood clotting
  • signs of encephalopathy
364
Q

Management: liver failure

A
  • watch + wait = often viruses will resolve
  • medicines = antibiotics, diuretics, BP drugs
  • liver transplant
365
Q

Define: Colic

A

Frequent, prolonged and intense crying in a healthy infant
- peak at 6 weeks old till 3/4 months

366
Q

Presentation: colic

A

car for more than 3hrs a day, 3 days a week for at least 1 week but are otherwise healthy

  • intense crying for no reason
  • extreme fussiness
  • predictable timing e.g. more in evening
  • facial discolouring
  • body tension
367
Q

What are the causes of colic?

A

Unknown
- digestive system not fully developed
- imbalance of healthy bacteria in the digestive tract
- food allergies or intolerances
- overfeeding, underfeeding
- early form of childhood migraine

368
Q

What causes the need for neonatal resuscitation?

A
  • labour causes hypoxia
  • babies have a large surface area to weight ratio and get cold easily
  • born wet so lose heat rapidly
  • born through meconium so may this in their mouth or airway
369
Q

What are the principles of neonatal resuscitation?

A
  1. warm the baby
    - dry
    - under heat lamp
    - < 28 weeks place in plastic bag
  2. calculate APGAR score
    - done at 1, 5 and 10 mins
  3. Stimulate breathing
    - stimulate to prompt breathing
  4. Inflation breaths
    - 2 cycles of 5 inflation breaths
    - then 30s of ventilation breaths
  5. chest compressions
370
Q

What does the APGAR score measure?

A

out of 10
lowest score = 0

Appearance
Pulse
Grimmace (response to stimulation)
Activity
Respiration

371
Q

What are the risk factors for neonatal sepsis?

A

Vaginal GBS colonisation
GBS sepsis in a previous baby
Maternal sepsis, chorioamnionitis or fever > 38ºC
Prematurity (less than 37 weeks)
Early (premature) rupture of membrane
Prolonged rupture of membranes (PROM)

372
Q

What are the red flags for neonatal?

A
  • Confirmed or suspected sepsis in the mother
  • Signs of shock
  • Seizures
  • Term baby needing mechanical ventilation
  • Respiratory distress starting more than 4 hours after birth
  • Presumed sepsis in another baby in a multiple pregnancy
373
Q

Management: neonatal sepsis

A
  • 1 RF or clinical features = monitor for at least 12 hrs
  • 2 or more RF or clinical features = start antibiotics
  • start antibiotics = if any red flag
  • antibiotics would be given within 1 hr of decision to start them
  • blood cultures taken before antibiotics given
  • perform a LP if infection strongly suspected or meningitis

antibiotics = benzylpenicillin and gentamycin

374
Q

Define: hypoxic ischaemic encephalopathy

A

occurs due to hypoxia during birth
- lack of oxygen with restriction of blood flow to the brain causing malfunctioning of the brain

375
Q

What are the causes of HIE?

A

Anything that leads to asphyxia (deprivation of oxygen) to the brain

  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord = causing compression of the cord during birth
  • Nuchal cord = where the cord is wrapped around the neck of the baby
376
Q

What are 3 grades for hypoxic ischaemic encephalopathy?

A

Mild
- poor feeding = irritable
- resolves within 24 hrs
- normal prognosis

moderate
- poor feeding = lethargic, hypotonic, seizures
- weeks to resolve
- up to 40% develop cerebral palsy

Severe
- reduced consciousness, apnoeas, flaccid, reduced/absent reflexes
- up to 50% mortality
- up to 90% develop cerebral palsy

377
Q

Management: HIE

A
  • supportive care
  • neonatal resuscitation and optimal ventilation
  • therapeutic hypothermia = helps protect brain from hypoxic injury
378
Q

Define: meconium aspiration syndrome

A

varying spectrum of respiratory distress in neonates born through meconium stained liquor

  • meconium is in feats intestinal tract and if released into amniotic fluid can enter respiratory tract and stimulate an inflammatory response through cytokine release
379
Q

What are the clinical features of meconium aspiration?

A
  • meconium stained liquor
  • respiratory distress at or shortly following birth
  • increased oxygen requirements
  • respiratory distress
380
Q

Investigations: meconium aspiration

A

bloods = FBC, CRP and blood cultures
(raised WBCs,)

CXR = hyperinflation, patchy opacification and consolidation

381
Q

Management: meconium aspiration syndrome

A

Preventative
- prevent intrapartum foetal hypoxia and postdates gestation

post delivery
- oropharyngeal suctioning
- admitted to neonatal unit
- supportive = oxygen therapy, CPAP
- antibiotics started while waiting for blood cultures

382
Q

Define: bronchopulmonary dysplasia

A

a form of chronic lung disease that affects newborns, most often premature babies that need oxygen therapy

  • the lungs and airways are damaged causing tissue destruction in the tiny air sacs of the lung
383
Q

What is the cause of bronchopulmonary dysplasia?

A

damaged to lungs from:
- mechanical ventilation
- long term use of oxygen

(especially susceptible in premature babies lungs)

384
Q

Presentation: bronchopulmonary dysplasia

A
  • Rapid breathing
  • Labored breathing (drawing in of the lower chest while breathing in)
  • Wheezing (a soft whistling sound as the baby breathes out)
  • The need for continued oxygen therapy after the gestational age of 36 weeks
  • Difficulty feeding
  • Repeated lung infections that may require hospitalization
385
Q

Management: bronchopulmonary dysplasia

A

no cure

  • diuretics = help decrease fluid in and around alveoli
  • bronchodilators = relax the muscles around the air passages
  • cortiosteroids = reduce inflammation > decreasing amount of mucus
  • viral immunisation = increased risk for resp tract infections
  • cardiac medications = relax blood vessels to reduce strain on heart

symptoms usually raced by 2/3 yrs old
- should still have regular checkups to prevent future lung problems

386
Q

Define: gastroschisis

A

abdominal wall defect that occurs when the intestines develop outside the abdomen and are open to the air when the child is born
- don’t know the cause

387
Q

Management: gastroschisis

A

many are born prematurely at 35 weeks or induced at 37 weeks

  1. wrapped exposed intestines in a types of lying film to reduced the amount of fluid and body heat loss, and protect from further damage
  2. surgery = put back in abdomen (sometimes done in stages ) and sewn up
  3. ICU = mesh sac over intestines and use gravity to move intestines back inside abdomen
388
Q

Define: oesophageal atresia

A

the upper part of the oesophagus doesn’t connect with the lower oesophagus and stomach

  • associated with trachea-oesophageal fistula = air passes from trachea into stomach and stomach acid to pass into the lungs
389
Q

What are the risk factors for oesophageal atresia?

A
  • polyhydraminos
  • ## more common in babies who have problems with development of kidneys, heart and spine too
390
Q

investigations: oesophageal atresia

A

Check ability to swallow

pass thin feeding tube down to see if it reaches stomach

CXR

391
Q

Management: oesophageal atresia

A

surgery
- closes off fistula
- sew together upper and lower oesophagus

after surgery
- antibiotics
- ventilator
-tube to drain fluid in chest
- oxygen
- pain medication

392
Q

Define: bowel atresia

A

when the jejunum or ileum are not completely connected or blocked

393
Q

Investigations: small bowel atresia

A

USS
- polyhydaminos

Not passing meconium when born

X-ray = shows blockage
Contrast CT
enema

394
Q

Management: small bowel atresia

A

surgery
- repairs the atresia

395
Q

What are the risk factors for neonatal hypoglycaemia?

A
  • intrauterine growth restriction in term infants
  • premature babies
  • maternal diabetes
  • macrocosmic babies
  • infants of mothers taking beta blockers
  • hypothermia
  • hypoxia
396
Q

Presentation: neonatal hypoglycaemia

A

first 48 hours of life

Hypotonia
Lethargy (excessive sleepiness with or without abnormal tone)
Poor feeding
Hypothermia
Apnoea
Irritability
Pallor
Tachypnoea
Tachycardia or bradycardia
Seizures
Abnormal feeding behaviour (not waking for feeds, not sucking effectively, appearing unsettled and demanding very frequent feeds especially after a period of feeding well)

397
Q

Management: neonatal hypoglycaemia

A
  1. offer additional feed - observe breastfeed and ensure good attachment
  2. administer dose of 40% buccal glucose 200mg/kg
  3. check blood glucose
  4. continue to establish breastfeeding
  5. IV access - 2.5ml/kg glucose bolus IV
  6. recheck blood glucose after 30mins
  7. if below <2 give another bolus
398
Q

What are the 4 domains of child development?

A
  1. Gross motor.
  2. Fine motor and vision.
  3. Speech, language and hearing.
  4. Social interaction and self care skills.
399
Q

What are some developmental milestones for fine motor and vision?

A

4 months
- Grasp an object
Uses both hands reaches for things, and brings things to mouth**

12 months
scribbles with a crayon,

3 years
Tower of multiple cubes

400
Q

What are the developmental milestones for gross motor function? 3 months to 9 months

A

3m: lifts head on tummy.
6m: chest up with arm support, can sit unsupported.
8m: crawling.
9m: pulls to stand.

401
Q

What are the developmental milestones for gross motor function? 12 months to five years

A

12m: walking.
2 years: walking up stairs.
3 years: jumping.
4 years: hopping.
5 years: rides a bike.

402
Q

What are the developmental milestones for speech, language and hearing?

A

3m: laughs and squeals.
9m: can make sounds such as ‘dada’ and ‘mama’.
12m: can say one word.
2 years: can form short sentences and name body parts.
3 years: speech is mainly understandable.
4 years: knows colours and can count.
5 years: knows the meaning of words.

403
Q

Give some developmental milestones for social and self care, 6 weeks to 12 months

A

6 weeks
Smiles spontaneously

6 months
Finger feeds

9 months
Waves bye – bye

12 months
Uses spoon/fork

404
Q

Give some developmental milestones for social and self care 2 -4 years

A

2 years - can take some clothes off, play w toys, but not sharing, “parallel play” w others

3-4 years can learn to play, take turns, dress themselves mostly

405
Q

Give two examples of concerning child development with regards to gross motor function.

A

Not sitting by 12 months.
Not walking by 18 months

406
Q

Give an example of concerning child development with regards to fine motor function.

A

Hand preference before 18 months.

407
Q

Give two speech and language examples that may suggest concerning child development.

A
  1. Not smiling by 3 months - blindness? ASD?
  2. No clear words by 18 months - ASD? Language problems?
408
Q

Give two examples of concerning child development with regards to social development.

A
  1. No response to carers interactions by 8 weeks.
  2. No interest in playing by 3 years.
409
Q

Give some examples of conditions that cause global development delay (child displaying slow development in all developmental domains, Gross motor, fine motor, speach and language, social skills)

A

Down’s syndrome
Fragile X syndrome
Fetal alcohol syndrome
Rett syndrome
Metabolic disorders

410
Q

Give some examples of conditions that cause gross motor delay

A

A delay that is specific to the gross motor domain may indicate underlying:

Cerebral palsy
Ataxia
Myopathy
Spina bifida
Visual impairment

411
Q

Give some examples of conditions that cause fine motor delay

A

A delay that is specific to the fine motor domain may indicate underlying:

Dyspraxia
Cerebral palsy
Muscular dystrophy
Visual impairment
Congenital ataxia (rare)

412
Q

Give some examples of conditions that cause language delay

A

Specific social circumstances, for example exposure to multiple languages or siblings that do all the talking

Hearing impairment
Learning disability
Neglect
Autism
Cerebral palsy

413
Q

Give some examples of conditions that cause Personal and social delay

A

Emotional and social neglect
Parenting issues
Autism

414
Q

What is are neuroblastoma tumours?

A

Tumours arising from neural crest tissue in the adrenal medulla and sympathetic nervous system.

415
Q

Give 2 signs of a neuroblastoma tumour.

A
  1. Abdominal mass - often crosses the midline and envelopes major vessels and lymph nodes.
  2. Symptoms of metastases e.g. bone pain, weight loss, pallor, limp, hepatomegaly.
416
Q

Describe the treatment for a neuroblastoma malignancy

A

Surgery - localised primaries can often be cured with surgery alone.

Chemotherapy - can be given before and/or after surgery to control disease.

Radiotherapy for high risk groups.

417
Q

What is a hepatoblastoma?

A

Hepatoblastoma is a malignant liver cancer occurring in infants and children and composed of tissue resembling fetal liver cells, mature liver cells, or bile duct cells

418
Q

What is a discoid meniscus?

A

congenital anomaly of the knee found in 3% of the population, typically affecting lateral meniscus

discoid meniscus is thickened and has a fuller crescent shape and does not taper as much towards the center of the joint and is shaped like a disc.

419
Q

What can having a discoid meniscus lead to ? What is the best way to diagnose it?

A
  • thickness of meniscus
  • diminished blood supply
  • weak capsular attachment
    –> more prone to tears

x- ray = rules out bony pathology
MRI = tp visualise discoid meniscus

420
Q

Outline what happens in scoliosis

A

Condition that causes a lateral curvature of the spine

This leads to bending of the spine and poor posture, even lead to cardiorespiratory failure

421
Q

What are some symptoms of scoliosis?

A

Symptoms:

– Pain in the shoulders and back

– Restrictive lung disease

– Limited mobility

– Uneven hips, arms or leg lengths

– Constipation due to tightening up of the bowel contents

422
Q

What is the management of scolisis?

A

– If minor –>can self-resolve

– If severe –> may require bracing and physiotherapy, else surgery is needed

423
Q

What is Torticollis? What causes it?

A

This is known as wry neck and is defined by an abnormal, asymmetrical head position

– It is due to excessive contraction of the sternocleidomastoid which pulls the ear to ipsilateral shoulder and the face to the other side.

Congenital torticollis:
– Birth trauma
– Also can be due to a sternocleidomastoid tumour

Acquired:

– Due to muscle spasm (most common)
– Also due to ENT infections, antipsychotics

424
Q

What is the treatment for torticollis

A

– Physical therapy like stretching helps and it usually self-resolves within a few days

– If unresolving, surgery may be required

425
Q

What are the common neonatal infections that make up the TORCH acryonym? When is transmission most likely?

A

TORCH infection –

  • Toxoplasmosis,
  • Other (syphilis, varicella-zoster, parvovirus B19),
  • Rubella,
  • Cytomegalovirus,
  • Herpes

As a rule, the likelihood of transmission to a fetus is greatest when primary maternal infection occurs.

426
Q

What are some features/consequences of toxoplasmosis infection?

A

There is a classic triad of features in congenital toxoplasmosis:

Hydrocephalus
Intracranial Calcifications (calcium deposits in the brain)
Chorioretinitis (inflammation of the choroid and retina of eye)

427
Q

What are some features of Congenital cytomegalovirus?

A

The features of congenital CMV are:

Fetal growth restriction
Microcephaly
Hearing loss
Vision loss
Learning disability
Seizures

428
Q

What can a listeria infection do to a foetus? What are some key signs of it?

A
  • bacteremia = mild, influenza like illness in mother and pass to foetus via placenta
  • maternal infection may cause spontanous abortion, preterm delivery, or fetal/neonatal sepsis

signs
- meconium staining of amniotic fluid
- widespread rash
- septicaemia
- pneumonia
- meningitis

429
Q

Treatment: listeria

A

IV Amoxicillin and Gentamicin.

430
Q

What is the most common cause of Encephalitis, in
a) Children
b) Neonates

A

In children the most common cause is herpes simple type 1 (HSV-1) from cold sores.

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

431
Q

What are some investigations for Encephalitis?

A
  • Lumbar puncture = sending cerebrospinal fluid for viral PCR testing
  • CT scan = if a lumbar puncture is contraindicated
  • MRI scan = after the lumbar puncture to visualise the brain in detail
  • EEG recording = can be helpful in mild or ambiguous symptoms but is not always routinely required
  • Swabs of other areas can help establish the causative organism, such as throat and vesicle swabs
  • HIV testing = is recommended in all patients with encephalitis

Contraindications to a lumbar puncture include a GCS below 9, haemodynamically unstable, active seizures or post-ictal.

432
Q

What is the management for encephalitis?

A

Aciclovir = HSV and VZV
Ganciclovir = cytomegalovirus

Repeat Lumbar puncture to check treatment is successful

433
Q

What is cleft lip? What is cleft palate, and what can it lead to?

A

Cleft lip is a congenital condition where there is a split or open section of the upper lip

Cleft palate is where a defect exists in the hard or soft palate at the roof of the mouth.
- This leaves an opening between the mouth and the nasal cavity.
- Cleft lip and cleft palate can occur together or on their own.

434
Q

What are some complications of cleft lip/palate?

A
  • problems with:
  • feeding
  • swallowing
  • speech
  • affect bonding between mum and child
  • social outcast
435
Q

Managment: cleft lip/palate

A
  • ensure baby can eat using specially shaped bottles and teats
  • surgery
    = cleft lip performed at 3 months
    = cleft palate done at 6-12 months
436
Q
A

Phase 3a Emily (8 decks)

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