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5th (Final year) > Paeds > Flashcards

Paeds Flashcards

1
Q

What is Ipratropium (atrovent)?

A

Muscarinic antagonist used for bronchodilation

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2
Q

Differences in Bronchiolitis and Viral induced Wheeze?

A

Both present with cough, coryza, wheeze and possibly some respiratory distress

  1. Brochiolitis does not respond to inhalers, viral wheeze does
  2. Most children under the age of 1 will have bronchiolitis
  3. Resp distress in viral induced wheeze is caused by bronchospasm induced by the viral infection. In Bronciolitis it is caused by the large numbers of secretions in the airways.
  4. Viral induced wheeze will cause resp distress over a short space of time, bronchiolitis will cause a slow progression to respiratory distress
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3
Q

What is a macular rash, a vesicular rash, a papular rash and a pustular rash?

A

Macular:
- change in colour of the skin - normally associated with erythema

Vesicular:
- Clear fluid filled blisters

Papular:
- Solid raised lesion

Pustular:
- Pus filled blisters

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4
Q

What does coryzal mean?

A

Cold-like symptoms of the upper respiratory tract snotty inflamamtion of nasal passages

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5
Q

What is brittle bone disease?

A

Oteogenesis imperfecta

Group of genetic disorders affecting bone development (8 types)

Lack of type 1 collagen production

Types vary from mild symptoms to life threatening ones

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6
Q

What is Duchenne’s muscular dystrophy?

A

X-linked recessive disorder

Lack of protein dystrophin

Normally present at about 5 years old

Chair at about 8

Life expectancy is avg. 25 years

Progressive muscle weakness, often originally affecting proximal muscles of shoulder and thigh

Also affects smooth muscle - Respiratory failure is ultimate cause of death.

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7
Q

What is tuberous sclerosis?

A

Genetic condition that causes benign tumours to form, these are usually present from birth.

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8
Q

What is Montelukast?

A

Leukotriene receptor antagonist for treatment of asthma.

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9
Q

What are CPAP and BiPAP

A

Both create positive pressure to keep the airways open (usually used when sleeping e.g. in muscular dystrophy)

CPAP is continuous
BiPAP has two pressure settings - one for inhalation and one for exhalation.

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10
Q

What is kawasaki syndrome?

A

Rare Vasculitis

Range of symptoms, as described by a japanese doctor - it can be sub acute, acute and convalescent. Fever, red palms, strawberry tongue, lymphadenopathy

Treated with aspirin and antibodies

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11
Q

Triad of symptoms in autism?

A

Lack of:

  1. Social and emotional communication
  2. Imagination/flexibility of thought - activities and interests
  3. Social and emotional interaction
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12
Q

Types of symptoms in autism?

A

Social interaction:
- Appears unresponsive
- Absent/unusual eye contact and expressions
- Does not spontaneously share interest and enjoyment
- Does not make friends

Social communication:
- Unusual/repetitive language
- Delayed/impoverished language development
- Does not initiate/maintain

Activities & Interests:
- Pre-occupation with narrow interests
- Unusual/repetitive gestures & actions
- Rigid routines

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13
Q

Normal baby weight?

A

2.7-4.1kg

6-9lbs

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14
Q

Verbal development stages?

A

1 year - one word
2 years - phrases
3 years - sentences

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15
Q

Causes of clubbing?

A

Bronchiectasis (CF)
Fibronising alveolitis
cyanotic congenital heart disease
IBD

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16
Q

4 T’s in relation to diabetes?

A

Tired
Thin
Thirsty
Toilet

Fatigue
Weight loss
Polydipsia
Polyuria

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17
Q

Prevalence of childhood diabetes?

A

1 in 400 children

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18
Q

Main risk factors of children with diabetes at time of presentation?

A

Younger children

Fmaily Hx (1st degree relative)

Lower SES

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19
Q

Normal range of fasting blood glucose (for kids)

A

6.1-7.8

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20
Q

Brief description of DKA?

A

Essentially it’s a lack of insulin (why it’s type 1) this causes two main things:

  1. Increased release of glucose production from glycogen - spilling over into the urine, taking Na and K and extra water with it leading to polyuria, polydipsia and dehydration.
  2. Body uses fat as an alternative source of fuel - to protect the metabolically active brain. This forms ketones in large quantities which lowers the blood pH and induced metabolic acidosis.
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21
Q

What percentage O2 do you use for acutely unwell children?

A

100% - don’t fuck about.

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22
Q

Complications associated with DKA?

A

Hyperglycaemia

Hypokalaemia

Cerebral oedema

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23
Q

DKA treatment?

A

SLOW insulin infusion
Fluid resus - Normal saline w/ K+

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24
Q

Treatment of cerebral oedema?

A

Sit child up
High conc saline
Intubation

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25
Q

Signs of Cerebral oedema?

A

Biggest one - headache

Tachycardia/HTN

Also:
- Nausea
- Vomiting
- Reduced consciousness

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26
Q

DO you give child with DKA water?

A

No - will most likely just vomit it up and this increases risk of aspiration - may even put in NG tube.

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27
Q

What is Alport syndrome?

A

Genetic condition affecting children, rare. Characterised by glomerulonephritis, end-stage kidney disease and hearing loss. Type IV collagen is affected.

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28
Q

Investigations in children with possible epilepsy?

A

EEG
Bloods - magnesium

ECG - rule out cardiac cause e.g. long-QT syndrome
Brain imagining

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29
Q

Two types of absence epilepsy?

A

Childhood absence epilepsy - short fits, grow out if

Juvenile absence epilepsy - longer fits, probably won’t grow out of.

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30
Q

Types of epileptic seizures in childhood/generally?

A

Generalised:

Absence - transient loss of consciousness, with abrupt onset and termination, normally unaccompanied by motor phenomena apart from some increase in muscle tone and eyelid flickering.

Myoclonic seizures - Repetitive jerking movements of the limbs neck or trunk

Tonic seizures - generalised increase in tone

Tonic-Clonic - classic symptoms of a rigid tonic phase followed by rhythmic jerking movements, may also be accompanied by loss of continence, followed by deep sleep.

Atonic seizures - jerk followed by transient loss of muscle tone.

Focal
- Frontal - motor
- Temporal - auditory, smell or taste
- Occipital - visual
- Parietal - altered sensation (contralateral)

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31
Q

In what type of infection do lymphocytes fall and neutrophils rise?

A

Bacterial.

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32
Q

What are some of the possible causes of abdo masses in CF children?

A

Fibrosing colonopathy - right colon (RIF)

Hepatosplenomegaly

Constipation - LIF

Gastrostomy tube.

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33
Q

What is hypospadias?

A

Urethral orifice is not in the usual position - different grades.

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34
Q

What is rhesus incompatibility and how does it affect the neonate?

A

Antibodies to rhesus D antigens have developed.

Mother is Rh Negative and baby is positive then the mother may produce antibodies against the babies RhD antigens (on RBCs). Has to be second baby.

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35
Q

How many babies become jaundiced? What causes this around 24hrs?

A

Roughly 50% of babies are visually jaundiced.

Prehepatic - excessive breakdown of red cells (haemolysis)

Hepatic - abnormality in liver function (neonatal hepatitis)

Posthepatic - absent or bile duct atresia, causes conjugated hyperbilirubinaemia

Why is it important?

Unconjugated bilirubin deposited in the brain (basal ganglia and brainstem nuclei) may cause irreversible neurological damage - kernicterus

Normal physiological jaundice (>24hrs - weeks):
- Marked physiological release of haemoglobin from the breakdown of red cells due to high haemoglobin conc at brith
- Liver does not function as well.

<24hrs may also be a sign of another disorder:
- Haemolytic anaemia
- Infection
- Inborn error of metabolism
- Liver disease

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36
Q

Haemolytic disorders of the newborn?

A

Rhesus haemolytic disease
- Antibodies to rhesus D antigens have developed. Now mostly treated antenatally - low haemoglobin, hepatosplenomegaly, jaundice. Coombs test is positive.

ABO incompatibility
- Some group O women have IgG anti-A-Haemolysin in their blood, bad for group A infants. Group B infants also at risk. Hepatosplenomegaly is not usually present. Coombs test (detects antibody on red cells) is positive.

G6PD (gluc. 6 dehydrogenase deficiency.
- mainly in non-caucasian backgrounds. Mostly affects males

Spherocytosis
- Rare genetic disorder, Family history is present.

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37
Q

At what time of onset is jaundice worrying?

A

Before 24hrs - haemolytic disorder or infection.

After 2 weeks - breast milk jaundice, biliary atresia

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38
Q

Signs of respiratory distress in the infant?

A

Head bobbing
Nasal flaring
Grunting
Recession (4 types)
Tachopnoea (>60 RR)
Cyanosis

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39
Q

Why do you feed small quantities slowly and early to neonates?

A

To avoid Necrotising enterocolitis (NEC)

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40
Q

Normal neonatal obs?

A

HR <170

<60 RR

BP - depends on gestation and age

Sys: ranges from 48-72 roughly
Dia: ranges from 25-50
Mean - above corrected gestation is normal

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41
Q

What is necrotizing enterocolitis?

A

Bowel becomes inflamed and necrosis occurs. Caused by bowel iscaemia and bacterial infection.

Seen within the first few weeks of life.

Early signs include feed intolerance and vomiting and bilious aspirates. Abdo becomes distended and stool can be blood stained.

Can induce shock, and can lead to bowel perforation.

Stop feed and give broad spectrum antibiotics, start Parenteral nutrition. Mechanical ventilation and circulatory support may be needed.

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42
Q

Normal ABG ranges?

A

pH: 7.35-7.45
pCO2: 4.7-6.0
pO2: 11-13
Bicarb: 22-26
BE: -2 to +2

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43
Q

Difference in type 1 and 2 resp failure?

A

Type 1: low O2 with no Co2 diff
- V/Q mismatch:
- Normal perfusion and reduced ventilation e.g.pulmonary oedema
- Normal ventilation and reduced perfusion e.g. Pulmonary embolus

Type 2: both O2 and CO2 are affected O2 is low, CO2 is high.
- alveolar hypoventilation

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44
Q

Causes of Hyponatraemia?

A

Fluid status:
- Low volume/Normal volume/High Volume

Low volume:
- D&V

Normal volume, conc. Urine:
- SIADH

Normal volume, dilute urine:
- adrenal insufficiency, Hypothyroidism, too much water

High volume:
- HF
- Liver failure
- Kidney failure

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45
Q

Causes of loose stools in a child?

A

IBD
IBS (less likely)
Long term infection
Diet - too much fibre
Addison’s

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46
Q

Symptoms to ask if loose stools is presenting complaint?

A

Blood/mucus in stool
Consistency
Colour of poo
Weight loss
Abdo pain
Intolerance to anything
Coeliac?
Difficult to flush away
Smelly

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47
Q

What does fetal calpotectin test for?

A

Sensitive for IBD, not specific though

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48
Q

Types of spina bifida?

A

Occulta - most common, vertebrae don’t properly form, doesn’t usually cause issues

Meningocele - meninges push out, will need surgery, outcomes aren’t too bad.

Myelomeningocele - most severe, spinal canal is actually open.

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49
Q

What is Hirschprungs disease?

A

Congenital megacolon

Part/all of the large intestine has no nerve supply, causes blockage.

Treated surgically by removing that bit of bowel.

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50
Q

What is congenital adrenal hyperplasia?

A

Collection of autosomal recessive genetic conditions that interfere with the production of steroids from cholesterol by the adrenal glands. Either results in excess or insufficient sex hormones.

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51
Q

Differential diagnoses for widening of the mediastinum?

A

Lymphoma
Thymus
Vascular anomalies

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52
Q

What is HSP (Henoch-Schonleine-purpura), what are it’s clinical features?

A

IgA vasculitis

Affects skin, mucous membranes of 3-13yr olds (ish), more common in boys, usually after respiratory infection.

Classic symptomatic triad of
1. Purpura, skin rash
2. Arthritis
3. Abdo pain

Can also get periarticular oedema and glomerulonephritis

Clinical diagnosis based on combination of symptoms.

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53
Q

Hep B problem in children?

A

In children it can lead to chronic hep b infection (90% of children with hep b)

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54
Q

What is the retic count, in neonates?

A

The reticulocyte (“retic”) count is the percent of RBCs that contain nucleic acid (also called “reticulated” cells), The retic count is used to assess whether the marrow is producing more RBCs than in the normal steady state.

High in haemolytic disease
Low in congenital anaemia

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55
Q

What is magnesium sulphate used for?

A

Bronchodilator in children

Prevent eclampsia in pregnancy

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56
Q

What is a pyeloplasty?

A

Operation to remove a blockage from one of the ureters.

Stent is put in and later removed.

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57
Q

Causes of hyponatraemia in neonates?

A

Administration of hypotonic fluids during the delivery.

Renal failure

Infection

Gi fluid loss

Adrenal insufficiency

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58
Q

Anatomical terms for a clear fluid filled area superficially on skin?

A

Vesicle - smallest <5mm
Bulla - >5mm

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59
Q

Anatomical terms for a change in surface colour without elevation or depression?

A

Small (<5mm) - macula
Larger (>5mm) - patch

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60
Q

Different anatomical terms for raised solid elevation of skin with no visible fluid?

A

Papule - <5mm
Plaque - larger confluence of papules >1cm

Nodule - similar to a papule (<5mm) but deeper in the dermis.
Tumour - >5mm nodule

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61
Q

What is purpura? What is it called if it’s smaller?

A

Non-blanching superficial, caused by broken blood vessels measuring 3-10mm

Petechiae is the same but smaller than 3mm.

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62
Q

Causes of jaundice >24hrs?

A

Physiological jaundice
- normal jaundice, caused by liver not working as well, and high levels of fetal haemoglobin breakdown.

Breast milk jaundice
- unconjugated bilirubin, normal

Dehydration
- in some infants IV fluids are needed. Caused by lack of bilirubin excretion?

Infection

BILIARY ATRESIA

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63
Q

Jaundice metabolism?

A

Haemoglobin breakdown to form unconjugated bilirubin.

Unconjugated bilirubin is conjugated in the liver

All of this conjugated bilirubin is excreted into the bowel. In the bowel bacteria form urobilinogen (some of this circulates back to the liver and some to the kidneys (where it is excreted in the urine)

Urobilinogen in the bowel is further processed to form stercobilinogen - darker colour in the stool.

Light stools - hepatic blockage (no stercobilinogen in stool)

dark urine/stool - extra urobilinogen in urine - haemolysis

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64
Q

What is neonatal erythema toxicum?

A

Normal baby rash - will pass,

central yellow plaque with a halo of erythema

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65
Q

What does the TORCH screen include

A

T- Toxoplasmosis
O- Other - syphilis
R- Rubella
C- CMV
H- Herpes

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66
Q

Measles rash and signs?

A

Koplik spots - appear as white spots in teh mouth before the rash does.

Rash consists of confluenced macula (and sometimes papular) widespread - starts on the head/nech then spreads to rest of body.

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67
Q

Complications from chickenpox?

A

Ataxia from cerebellitis

Encephalitis

Rheumatitis

GI involvement

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68
Q

What is impetigo? what does it look like?

A

Superficial skin bacterial infection caused most commonly by Staph A (but also strep & MRSA)

Crusty yellow lesions of face arm and legs - may be painful/itchy

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69
Q

Common causative organisms of abscesses?

A

Staph and Strep

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70
Q

What is ichthyosis?

A

Family of rare genetic skin disorders, dry thickened scaly skin.

Linked to metabolic syndromes such as T2DM and PCOS - have to screen.

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71
Q

What is aminophylline?

A

Methylxanthine, give via infusion - bronchodilator

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72
Q

What is clenil?

A

Beclomethasone

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73
Q

Principles of the UN statement on the rights of the child?

A

Right to survival

Right to health and healthcare

Right to develop to the fullest

Right to full participation in family, social and cultural life

Right to freedom from violence

In the UK the 1989 and 2004 children act legislates for these rights

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74
Q

Definition of abuse and neglect?

A

Maltreatment of a child by inflicting harm or failing to act to prevent harm…

In a family/institutional/community setting…

By those known/not known to them…

by an adult or child

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75
Q

Categories of abuse?

A

Physical abuse

Sexual abuse

Neglect

Emotional abuse

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76
Q

Definition of physical abuse?

A

Any physical harm to a child, including when a parent or carer fabricates the symptoms of illness, or causes illness

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77
Q

Definition of sexual abuse?

A

Forcing or enticing a child to participate in sexual activities, whether they are aware of what is happening or not.

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78
Q

Definition of neglect?

A

Persistent failure to meet a childs physical or emotional needs, likely to result in the serious impairment of the childs health or development

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79
Q

Definition of emotional abuse?

A

Persistent emotional maltreatment of a child, such that it impairs the childs emotional development.

Domestic violence for example.

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80
Q

How many 18-24 year olds report some kind of abuse?

A

11%

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81
Q

Toxic trio that potentially increase the risk of abuse

A

Domestic abuse

Alcohol/drug misuse

Mental illness

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82
Q

What should you do if you are concerned about a child?

A

Record full details of presenting incident, your concerns and observations

Listen to child and put them first

Seek advice from a senior

Consider who else might be involved, siblings?

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83
Q

What type of immunity do vaccines produce?

A

Active immunity

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84
Q

What can vaccines be made up of?

A

Inactivated or attenuated live organism

Secreted products

Components of cell walls

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85
Q

What is the childhood immunisation schedule?

A

2 months:
- DTaP
- IPV
- Hib
- PCV
- Men B
- Rotavirus

3 months
- DTaP
- IPV
- Hib
- Rotavirus

4 months
- DTaP
- IPV
- Hib
- PCV
- Men B

12 months
- Hib
- Men C
- MMR
- PCV
- Men B

2-7 years
- Influenza

3.5 - 4 years
- DTap
- IPV
- MMR

Girls 12/13
- HPV

14 Years
- TdIPV
- MenACWY

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86
Q

Aims of herd immunity?

A
  • Reduce sources of infection
  • Those who cannot be immunised will still benefit
  • May eliminate disease
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87
Q

Contraindications for vaccinating a child?

A

For inactivated vaccines true anaphylaxis is the only contraindication

Severe allergic reactions, stable neurological conditions, local or general reactions are all not contraindications

Live vaccines
- High dose steroids
- Immunosuppressive treatment
- hypogammaglobulinaemia
- Pregnant
- Had a live vaccine in previous 3 weeks

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88
Q

Which vaccines are inactivated

A

Pertussis
Polio
Tetanus
Diptheria
Pneumococcus

Primary response - IgM then IgG
There’s a primary course then a booster

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89
Q

Which vaccines are live?

A

MMR
Varicella
Influenza
Yellow fever
BCG

May see mild form of disease

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90
Q

Four main things in a 6 week health check?

A

Physical exam

Review of development

Give health promotion advice

Opportunity for parent to express concern

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91
Q

What are you checking for in the physical exam in the 6 week baby check?

A

Congenital heart disease

Developmental dysplasia of the hip

Congenital cataracts

Undescended testes

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92
Q

How would you check for congenital heart disease in teh 6 week check?

A

Look for cyanosis, ventricular heave, respiratory distress, and tachypnoea; a respiratory rate persistently over 55 is suspicious.

Feel for apex beat and assess whether displaced.

Listen for murmurs. Innocent murmurs are common and are typified by low intensity, localised to a small area of precordium and in the absence of other symptoms or signs. All murmurs should be referred to a specialist for assessment.

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93
Q

How would you check for developmental dysplasia of the hip (in the 6 week check)?

A

leg-leg length discrepancy

Asymmetry of leg creases

Barlow and Ortolani tests
- Barlow: press both thighs posteriorly looking to see if femoral head dislocates
- Ortolani: looking to see if femoral head pops back in

If abnormality should have USS

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94
Q

Eye exam in the 6 week check?

A

Examine external eyes (one eye bigger may indicate glaucoma)

Check for normal red reflex

Check for FH, ask if parents have any worries

Any abnormalities should be treated as urgent referral, abnormal red-reflex should be same day

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95
Q

How would you assess the development of the baby in the 6 week check?

A

Review feeding and weight gain

Check growth chart

Review vision and hearing

Most will be spontaneously smiling, and making a variety of sounds e.g. coos

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96
Q

What health promotion discussions should you have in the 6 week check?

A

Immunisations

Breast feeding, check tongue tie

SIDS
- No smoking
- Sleep on back (but have tummy time)
- Don’t sleep on same bed/sofa together
- Avoid overheating
- Breast feed

Could ask about maternal depression

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97
Q

Common physical signs of abuse?

A

Abnormal bruising

Cuts and scratches

Bite marks

Unconscious or fitting (shaken baby)

Subtle signs such as sky away from touch, not want to get changed for PE, afraid to go home.

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98
Q

What would constitute abnormal bruising?

A
  • <1 year (as not walking)
  • Disproportionate to reason given
  • Multiple sites or clusters
  • Look like a hand, stick, tooth, belt
  • Non bony part of the body or face e.g. eyes, ears, cheek, back, abdomen
  • Ankles or hands
  • On neck
  • Delay in presentation
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99
Q

Childs behaviour that may suggest sexual abuse?

A

Anxious about going to a particular place or seeing a particular person.

Sudden mood swings, or aggressiveness

Displays over-sexualised behaviour or inappropriate knowledge for their age

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100
Q

Who is the usual suspect for sexual abuse?

A

Usually the abuser is a family member or someone known to the child, such as a family friend. For teenagers it is commonly a boyfriend or girlfriend. Child sex abusers can come from any professional, racial or religious background, and can be male or female.

Older children may abuse younger children.

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101
Q

4 areas of early development

A

Gross motor

Vision and fine motor

Hearing, speech and language

Social, emotional and behavioural

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102
Q

When do you stop correcting for prematurity?

A

At 2 years post-natal

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103
Q

Rough guide to gross motor development 12 months up until 3 years?

A

6-8 weeks
- Moves head side to side when prone
- developing head control

6-8 months
- sits briefly
- rolls (both ways)
- starts to crawl

12 months
- walks unsteadily

18 months
- squats to pick things up off the floor
- Runs
- Walks well

2 years
- Kicks ball
- Climbs stairs 2 feet at a time

2.5 years
- Running well

3
- Jumps with both feet
- Stairs 1 foot at a time

4-5
- Stands on one foot
- Throws and catches

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104
Q

Fine motor/vision rough guide from 14 months to 4 years?

A

6-8 weeks
- grasp reflex
- hands lightly closed

6-8 months
- Palmar grasp
- Object from hand to hand
- Reaches for toys

12 months
- Mature grasp
- Gives objects away

18 months
- Linear scribble
- Tower of three

2 years
- Tower of six
- Circular scribble

2.5
- Tower of eight

3 years
- Circle
- Bridge

4 years
- Square
- Steps after demonstration
- Man with head, legs and trunk

5 years
- Triangle
- Person with 6 body parts
- fork and spoon

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105
Q

Rough guide to communication and hearing 12 months to 3.5 years?

A

6-8 weeks
- Coos and gurgles
- Watches mums face
- Startled by loud noises
- Cries when hungry or uncomfortable

6-8 months
- Turns to mum
- laughs aloud

12 months
- can say single words, probably two or three in vocab

18 months
- Can point
- 6-10 words, knows two areas of the body

20-24 months
- Simple phrases using two or more words

2.5 - 3 years
- Talks all the time in 3-4 word sentences

4-5 years
- Speech grammatically correct
- Nursery rhymes
- Name and age

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106
Q

Rough guide to social, emotional and behaviour development?

A

6-8 weeks
- Smiles
- follows people with eyes

6-8 months
- Takes everything to mouth
- Plays with rattle
- Looks at self in mirror

12 months
- Holds spoon, puts to mouth
- waves bye-bye
- Demonstrates affection

18 months
- Symbolic play beginning
- Uses a spoon

24 months
- Dry by day
- Pull some clothes off
- Toddler tantrums
- No awareness of danger

3 years
- Turn taking
- Vivid interactive play with others
- Names friend

4-5 years
- Dresses and undresses
- Complex games
- Comforts others
- independent toileting

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107
Q

What are learning disabilities and learning difficulties?

A

Learning disabilities is the general condition of arrested development, resulting in the impairment of skills manifest during the developmental period.

Learning difficulties applies to a specific area of difficulty e.g. dyslexia or dyscalculia

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108
Q

Different grades of learning disabilities?

A

Mild (IQ 50-69)

Moderate (35 - 49)

Severe (20-34)

Profound (<20)

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109
Q

Learning difficulty causes?

A

Prenatal
- Genetic abnormalities
- Intrauterine abnormalities
- Intrauterine insults

Perinatal
- Prematurity
- Severe asphyxia
- meningitis

Postnatal
- Infection
- Trauma
- Lead poisoning
- Malnutrition
- Neglect

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110
Q

What is neurodisability?

A

Group of congital or acquired disorders including impairment to the brain or neuromuscular system, affecting: Movement, Cognition, Hearing or vision, communication and emotion/behaviour

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111
Q

General structure to an assessment of development?

A

History
- Parents concerns
- Is there a barrier to learning?
- Is there a useful diagnosis to be made?

Reports
- Nursery
- School
- physio
- SALT

Observation and informal development
- may be different to testing situation

Formal evaluation
- Schedule of growing skills
- Griffiths (toys)
- Bayley infant development scales
- Hammersmith infant neurological examination

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112
Q

Clinical signs in a neuro-developmental assessment?

A

Patterns of growth

Dysmorphic features

Neurocutaneous stigmata

CNS abnormalities
- Tone
- Wasting
- reflexes

CVS abnormalities

Visual abnormalities

Hearing abnormalities
- Ask parents
- Check tests were done as newborn

Patterns of mobility
- dexterity
- hand dominance

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113
Q

Causes of abnormal development (broadly)?

A

Neglect of physical and psychological needs

Ill health

Neurodevelopmental disorder

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114
Q

Causes of abnormal development (broadly)?

A

Neglect of physical and psychological needs

Ill health

Neurodevelopmental disorder

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115
Q

When does global developmental delay normally present?

A

Within the first two years

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116
Q

Causes of abnormal motor development?

A

Central motor
- Cerebal palsy

Congenital myopathy/primary muscle disease

Spina bifida

Global developmental delay
- Syndromes
- Unidentified cause

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117
Q

If a child showed hand dominance or asymmetry of motor skills within the first year is this okay?

A

No, hand dominance isn’t present until 1-2 years, and this may suggest a underlying hemiplegia

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118
Q

When is the limit age of walking?

When might this be less worrying?

A

> 18 months

If the child shows the variants of bottom shuffling or commando crawling this may be normal.

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119
Q

What is cerebal palsy?

A

An abnormality of movement or posture caused by disturbances in the developing fetal or infant brain.

Used up until about 2 years old then would call it acquired brain injury

Often accompanied by disturbances of
- cognition
- communication
- perception
- sensation
- behaviour
- seizure disorder

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120
Q

What are the causes of cerebral palsy

A

80% antenatal
- Vascular occlusion
- Cortical migration disorders
- Structural maldevelopment

Genetic syndromes

Infection

10% due to hypoxic injuries at delivery

About 10% postnatal
- CNS infection
- Head trauma
- Hypoglycaemia
- Hyperbilirubinaemia
- Hydrocephalus

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121
Q

Early features of cerebral palsy?

A

Abnormal limb/trunk posture and tone

Feeding difficulties

Abnormal gait

Asymmetric hand function

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122
Q

Types of cerebral palsy?

A

Spastic
- UMN
- Increased limb tone

Dyskinetic
- involuntary, uncontrolled movements

Ataxic
- hypotonia and poor balance

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123
Q

Causes of speech and language abnormalities?

A

Hearing loss

GDD

Anatomical problem e.g. cleft palate

Environmental deprivation

Normal variant

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124
Q

What type of neuro-developmental deal would downs cause?

A

Global developmental delay

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125
Q

When does autism present?

A

2-4 years

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126
Q

Management of autism spectrum disorder?

A

Applied behavioural analysis is the only intervention really shown to work

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127
Q

What is development co-ordination disorder or dyspraxia?

A

Disorder of motor planning and/or execution, without any findings on a neurological examination, a disorder if higher cognitive functions it is the inability to execute a planned series of actions.

Difficulties can present as:
- Handwriting
- Dressing (buttons etc)
- Cutting up food
- poorly established laterality
- copying and drawing
- Messy eating

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128
Q

What is dyslexia?

A

Disorder of reading skills disproportionate to the child’s IQ, need to include vision and hearing assessment.

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129
Q

Causes of in-toeing in children?

A

Metatarsus varus
- passively correctable
- no treatment required

Medial tibial torsion
- toddlers
- self corrects in 5 years

Persistent anteversion of the femoral neck
- usually self corrects by 8
- if persistent can do femoral osteotomy

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130
Q

Types of muscular dystrophy?

A

Duchenne

Becker

Congenital

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131
Q

Inheritance pattern of duchenne muscular dystrophy?

A

X-linked recessive

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132
Q

Brief summary of the pathophysiology of duchenne’s?

A

Abnormality in coding for the dystrophin protein. Leads to malformation of muscle fibres.

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133
Q

What blood result is high in duchennes muscular dystrophy?

A

CPK

creatine phosphokinase

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134
Q

When are duchenne’s patients normally first noticed?

A

5.5 years

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135
Q

Presentation of duchenne’s?

A

Waddling gait

+/- language delay

Pseudohypertrophy of calves

Clumsier and slower than peers

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136
Q

Progression of duchennes?

A

Present 5-6 years

In a wheelchair by 10-14

Respiratory failure and associated cardiomyopathy

Life expectancy is late 20s

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137
Q

Management of duchenne’s muscular dystrophy?

A

Physio
- Appropriate exercises to maintain muscle power and delay the onset of scolios

Contractures, particularly at the ankles should be prevented by passive stretching and wearing of splints

Later CPAP may be required, or NIPPV

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138
Q

Brief differences in becker muscular dystrophy?

A

Some functional dystrophin is still produced, similar features to duchenne’s, but will progress slower (age of onset is 11 y/o), life expectancy is 40 or normal

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139
Q

Features of congenital muscular dystrophy?

A

Recessively inherited heterogenous group of disorders.

Normally presents at birth with weakness, hypotonia or contractures

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140
Q

How common is down syndrome in the UK?

A

1 in 1000 births

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141
Q

Most common form of inheritance for down syndrome?

A

Non-dysjunction

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142
Q

What is non-dysjunction?

A

Error at meiosis (sex cell production producing haploid cells.

Chromosome 21 from the parent cell does not divide producing one gamete with two 21’s and one with none.

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143
Q

How can down syndrome otherwise be inherited (not non-dysjunction)?

A

Translocation
- 21 is joined onto another chromosome (normally 14)
- Can produce carriers

Mosaicism
- Some cells trisomy some not

144
Q

How is down syndrome screened for antenatally?

A

Combined test offered at 10-14 weeks
- PAPP-A
- Nuchal translucency scan
- β-hCG

145
Q

Facial features of down syndrome postnatally? (10)

A

Round face with flat nasal bridge

Upslanted palpebral fissures

Epicanthic folds

Brushfield spots in iris

Small mouth and protruding tongue

Small, low-set ears

Flat occiput and third fontanelle.

Short neck

146
Q

Other (non-facial) symptoms of down syndrome?

A

Single palmar crease

incurved 5th finger

wide gap between Big and 2nd toe

147
Q

Features of turners syndrome?

A

Short stature

Webbed neck

Low set ears

Broad chest

148
Q

Features of edwards syndrome?

A

Microcephaly

Prominent occiput

Narrow palpebral fissures

Cleft lip/palate

Low set ears

149
Q

Features of fetal alcohol syndrome?

A

Smooth philtrum

Thin upper lip

Small palpebral fissures

Single palmar crease

150
Q

Complications associated with downs?

A

Cardiovascular complications
VSD.
ASD
PDA
Aortic Coarctation
MVP
Tetralogy of Fallot

Duodenal atresia

Hirschprungs disease

151
Q

usual age for presentation of diabetes in children?

A

above 10, between 10-14 yrs normally

152
Q

Adverse health outcomes for children with diabetes?

A

Reduced life expectancy
- 20 years in T1DM
- 10 years in T2DM

Increased risk of stroke and MI

Renal failure

Blindness

Stillbirth/miscarriage/congenital malformations

153
Q

Findings on urine dipstick in childhood type 1 diabetes?

A

Glycosuria, ketonuria (can be normal if not glycosuria, in diabetes may be indicative of DKA.

154
Q

Treatment for T1DM in kids?

A

Fast acting insulin
- novorapid

Slow acting insulin
- Glargine

Mixed

Basal bolus regime
- Long acting at night
- Short acting

Mixed regime
- two injections 10 hours apart

155
Q

Hypoglycaemia blood glucose in a patient on insulin?

A

<4mmol/L (<2.7mmol/L in others)

156
Q

What would you tell a child to look out for in hypoglycaemia?

A

Sweating

Fatigue

Feeling dizzy

157
Q

Is it common to be in DKA when presenting for T1DM as a kid?

A

Yes, 2/3 kids are at presentation.

158
Q

DKA presentation?

A

Polyuria
Polydipsia
Breathless
Tired
Weight loss
N&V
Headache
Ketotic breath
Shock
Drowsy
Abdo pain
Constipation

159
Q

What type of acid base disturbance would DKA cause?

A

Metabolic acidosis, (N&V, Dehydration?)

160
Q

Three stages of paediatric growth?

A

Infant (0-2)
- rapid growth
- nutrition deoendent

Childhood (2-puberty)
- Steady growth
- Hormone dependent

Pubertal growth
- Rapid linear growth
- Depends on pubertal hormones and GH
- Start of puberty in girls
- End of puberty in boys

161
Q

When should you refer a child for poor growth?

A

Short for parents height (mid-parental height)

Height velocity is below that for age

Crossed >2 centiles up or down

Height <0.4th centile

162
Q

Average age of puberty in girls and boys?

A

10.5 - girls

14 - boys

163
Q

What age is precocious puberty in boys and girls?

A

<8 in girls
<9 in boys

164
Q

What age is pubertal delay in boys and girls?

A

> 13 in girls
15 in boys

165
Q

What is arrested puberty for boys and girls?

A

Time to complete puberty is too long

Girls should complete in 4 years

Boys should complete in 6 years

166
Q

Type of conditions that can cause abnormal growth and development?

A

Chromosomal abnormalities
Malnutrition - poor intake or malabsorption
Chronic ill health
Iatrogenic
Psychological & emotional factors
Skeletal abnormalities
Syndromes
Hormones

167
Q

How would coeliac disease present in terms of growth and development?

A

Abdo distention

Discrepancy between parental and child’s height

Drop in weight following weaning

168
Q

If a kid is fat and tall what’s most likely the diagnosis?

A

Exogenous obesity

169
Q

If a kid is short and fat what’s the most likely diagnosis?

A

Endocrine disorder

170
Q

How might hypothyroidism present in childhood?

A

Short stature - thyroxine is important for growth

Might be cold

Dryness of the skin and hair, coarsening of the facial features, constipation and a slow pulse rate all occur in children but tend to be relatively late features.

171
Q

In terms of growth and development how might turners present?

A

Pubertal delay and short stature.

172
Q

Ddx if a girl of 5 y/o started developing pubic hair?

A

Increased adrenal hormone secretion
Precocious puberty
Premature Adrenarche (normal variant)

173
Q

Chromosomal abnormalities associated with abnormal growth?

A

Downs - short

Klinefelters - XXY, boys may grow more quickly

Turners - short/no puberty

174
Q

Nutritional disorders causing abnormal growth?

A

GORD - feeding aversion

Coeliac - short

IBD

Pancreatic insufficiency - CF

175
Q

Most common skeletal abnormality causing poor growth?

A

Achondroplasia

176
Q

Genetic syndromes associated with short stature?

A

Noonans - cardiac and developmental delay

Williams - elfin appearance, warm and bubbly, short stature and cardiac defects

Russel-silver syndrome - poor growth

177
Q

Hormonal problems resulting in abnormal growth?

A

Hypothyroidism - short and fat

GH deficiency - short and slightly chubby

Hypopituitarism - short

178
Q

What can affect GH?

A

Stress
Poor sleep
Malnutrition
SOL in pituitary

179
Q

What investigation would you want to do in precocious puberty?

A

Image pituitaries

180
Q

If a kid is gillick competent can they refuse consent given on behalf of them?

A

No - can only give consent

181
Q

What are you checking for in a newborn infant assessment?

A

Birth weight - centile & age plotted

Posture & movements

Head circumference

Fontanelles
- if tense and no crying need to exclude hydrocephalus

Face
- genetic abnormalities

Pale
- check anaemia

Jaundice
- <24 hrs is abnormal (haemolysis)

Red reflex
- cataracts
- retinoblastoma

Palate
- cleft

RR, auscultate heart

Abdo masses

Femoral pulse
- coarctation of the aorta

Genitalia and anus
- check wee and poo

Muscle tone

Back & spine

Hips
- the two tests (barlow and ortolani)

182
Q

What is hypoxic ischaemic encephalopathy?

A

ischaemic injury occurring perinatally at the time of labour or delivery resulting in brain damage.

183
Q

Common causes of hypoxic ischaemic ancephalopathy/

A

Excessive/prolonged contractions (hyperstimulation?)

Cord compression (shoulder dystocia & prolapse)

Hypo/hypertension

IUGR/anaemia

Failure to breathe

184
Q

What causes RDS in neonates?

A

Surfactant deficiency

185
Q

Management of neonatal jaundice?

A

Phototherapy
- blue-green light converts unconjugated bilirubin into a harmless water soluble pigment

Exchange transfusion
- at higher levels of bilirubin
- blood from art line or umbilical vein is removed, and replaced with donor blood.

186
Q

Signs of respiratory distress syndrome in the newborn?

A

Same as normal respiratory distress:
- Head bobbing
- Nasal flaring
- Grunting
- Recession (4 types)
- Tachopnoea (>60 RR)
- Cyanosis

187
Q

Presentation of IVH in the newborn?

A

Intraventricular haemorrhage

Symptoms:
- Diminished/absent Moro reflex.
- Poor muscle tone.
- Sleepiness.
- Lethargy.
- Apnoea.

Signs:
- The fontanelle may be tense and bulging with severe IVH.
- Neurological depression may progress to coma.

In mild forms there may be no clinical signs, or there may be alternating symptomatic and asymptomatic periods.

188
Q

Management of IVH in the newborn

A

Intraventricular haemorrhage

Management is initially mainly supportive and may include the correction of anaemia, acidosis and hypotension. Ventilatory support may also be required for some who deteriorate acutely.

Fluid/volume replacement:

  • Packed red blood cells or fresh frozen plasma for anaemia and shock.
  • Sodium bicarbonate infusion (carefully) for metabolic acidosis.
189
Q

What is the APGAR score how do you calculate it?

A

(named after it’s creator)

A - appearance

P - Pulse (>100 N)

G - Grimace (movements)

A - Activity (Strong/weak)

R - Respiration (cry/no cry)

0 is nothing

1 is something

2 is normal

190
Q

What is transient tachypnoea of the newborn?

A

A self-limiting period of respiratory distress most often seen in term babies following pre-labour Caesarean Section. It is thought to be due to delayed absorption of lung fluid and may require oxygen therapy.

191
Q

What is meconium aspiration?

A

It is not uncommon for infants to pass meconium before delivery. In rare instances the infant may aspirate meconium stained liquor, this occurs when a hypoxic infant begins to gasp in utero. Pulmonary vasodilatation is delayed and results in Persistent Pulmonary Hypertension which can make an infant very unwell.

192
Q

Why do we give vit k to babies?

A

To prevent haemorrhagic disease of the newborn - deficiency in factors II, VII, IX, X1

193
Q

What is cephalohaematoma in the newborn?

A

Subperiosteal haematoma (can’t cross suture line) resolves over weeks, may exacerbate jaundice

194
Q

What is a caput in the newborn?

A

Oedema and bruising usually associated with a ventousse delivery, resolves in a few days and can cross suture lines

195
Q

Benefits of breast feeding?

A

Nutrition, protection from disease, development, allergy, autoimmune, reduced obesity and long term health.

196
Q

General advice regarding the continuation of breast feeding and the administration of bottle fed milk?

A

Breast feeding is the gold standard; the World Health Organisation recommends that infants should be exclusively breast fed until 6 months of age

Solids should not be introduced before 4 months

Bottles for formula milk must be sterilised and milk made up according to instructions with boiled water

197
Q

Causes of prolonged jaundice

A

Most commonly breast milk jaundice

Although must rule out biliary atresia
- pale stools
- dark urine

198
Q

Infants at risk of GBS infection?

A

Premature

If the mother is colonised with Group B strep or has previously had a child with Group B strep infection

There is evidence of maternal infection (pyrexia or elevated CRP)

There is prolonged rupture of membranes

Evidence of fetal distress

199
Q

Four infections mothers are screened for?

A

hepatitis B, HIV, syphilis and susceptibility to rubella

200
Q

When is the blood spot screening performed, what is it testing for?

A

PKU

Congenital Hypothyroidism

Sickle cell disease

MCADD

CF

Isovaleric acidaemia

Maple syrup urine disease

Homocystinuria

Glutaric Aciduria type 1(GA1)

201
Q

What type of bilirubin crosses the BBB?

A

Unconjugated bilirubin, this occurs in kernicterus

202
Q

What does the ductus arteriosus do antenatally? What is the problem in PDA?

A

Shunts blood from the pulmonary artery to the aorta.

In PDA this means there is less volume of blood in the aorta

203
Q

Presentation of PDA in a premature infant?

A

Classical signs are usually absent

May be systolic murmur in left sternal edge

Bounding peripheral pulses

Hyperactive precordium (can see it moving)

Tachycardia with or without gallop rhythm

204
Q

Investigations for suspected PDA?

A

Echocardiogram

205
Q

Management of PDA in the preterm infant?

A

Possible NSAIDS

?indomethacin

Conservative

Surgical closure
- may be associated with increased morbidity

206
Q

Presentation of NEC in the prem baby?

A

Abdominal distension with increasing gastric aspirates.

Altered stool pattern.

Bloody mucoid stool and bilious vomiting.

Decreased bowel sounds with erythema of the abdomen.

Palpable abdominal mass or ascites.

Associated features are bradycardia, lethargy, shock, apnoea, respiratory distress, temperature instability.

207
Q

Investigations for NEC?

A

Bloods - FBC and blood gas, serial CRPs

Abdo XRAY confirms findings/not

208
Q

Management of NEC?

A

Nil by mouth

TPN, IV fluids and Abx

surgery inc. bowel follow through can be performed

209
Q

Most common cause of ambiguous genitalia in newborns?

A

Congenital adrenal hyperplasia

210
Q

Diagnosis of hirschsprungs disease?

A

Rectal biopsy

211
Q

Presentation of hirschsprungs disease?

A

Delayed passage of meconium (> 2 days after birth), abdominal distension and bilious vomiting. May have distended abdomen, and bowel movements not working otherwise - visible waves of peristalsis.

212
Q

Causative organism in scarlet fever?

A

Group A haemolytic streptococci

213
Q

How do left to right shunts commonly present?

A

Breathless

214
Q

How to right to left shunts commonly present?

A

Blue

215
Q

inheritance pattern of haemophilia?

A

X-linked recessive

216
Q

Causes of left to right shunts?

A

VSD
PDA
ASD

217
Q

Causes of right to left shunts?

A

Tetralogy of fallot
Transposition of the great arteries

218
Q

Innocent murmurs?

A

The S’s

aSymptomatic patient
Soft blowing murmur
Systolic only
left Sternal edge

219
Q

ASD presentation?

A

None (common)
Recurrent chest infections / wheeze
Arrhythmias

Ejection systolic murmur on upper left sternal edge

220
Q

Management of ASD?

A

Correction by 3-5 years of age in ASDs that are significant enough to cause right ventricle dilatation

221
Q

Presentation of a VSD?

A

Small:
- asymptomatic

  • Loud pansystolic murmur left lower sternal edge

CXR, ECG will be normal

Echo will show defect

Large:
- HF, breathlessness, recurrent chest infections

Tachypnoea, tachycardia, hepatomegaly
Active precordium
Pansystolic murmur

CXR
- cardiomegaly
- Enlarged pulmonary arteries
- Pulmonary oedema

ECG
- Biventricular hypertrophy

Echo
- shows defect

222
Q

VSD management?

A

Small may manage conservatively

First line is increased calorific density of feeding – orally if they can tolerate it, and if they can’t manage oral feeds can supplement with NG feeds.

Don’t give fluids – more volume, more work – exacerbate the problem

Manage HF:
- Diuretics
- Captopril ACEI

Digoxin (but not really)

223
Q

What is a PDA (in a term infant)?

A

When the PDA has not closed 1 month after EDD

224
Q

PDA clinical features?

A

Continuous murmur beneath the left clavicle

Wider pulse pressure - collapsing or bounding pulse

Large PDA may cause HF & pulmonary hypertension

CXR and ECG normally normal

225
Q

Management of PDA >1month

A

Close it with coil or occlusion device

226
Q

Four features of tetralogy of fallot?

A

Large VSD

Overriding aorta

Subpulmonary stenosis

RV Hypertrophy

227
Q

Presentation of tetralogy of fallot?

A

severe cyanosis

hypercyanotic spells

squatting on exercise

Clubbing

Loud ejection systolic

228
Q

Management of tetralogy of fallot?

A

Neonates
- prostin to keep ductus arteriosus open

Surgically
- shunt
- RVOT stent (more common now)

if less severe can perfom surgery 3-6 months

in attack:
- On shoulder with calming
- Otherwise give O2 and morphine +/- intravenous propranolol.

229
Q

What are AVSDs most commonly associated with?

A

Trisomy 21

230
Q

Common genetic abnormality associated with fallots?

A

22q 11 deletion

231
Q

What is coarctation of the aorta?

A

Narrowing of the aortic arch

232
Q

Clinical findings in coarctation?

A

Hypertension in upper vasculature - arm

233
Q

Treatment of coarctation?

A

Prostin to maintain ductus arteriosus and supply lower half of body

Then surgery in first few weeks to correct

If narrowing is less, may present late
- Notching on CXR
- Absent femorals
- HTN upper body

234
Q

Management in transposition of arteries/

A

Prostin to keep ductus arteriosus open

Sugical operation called balloon atrial septostomy - shunt in atrium

Later (2 weeks) do arterial switch proceadure

235
Q

What Is HLH in children how do they present and how do you manange?

A

Hypoplastic left heart - very rare

Pesent dueing antenatal screening usually or at birth will be very sick with no peripheral pulses

Need to do norwood proceadure

236
Q

What is aortic stenosis in newborns?

A

Aortic valve leaflets are fused together can present with other abnormalities such as coarctation of the aorta

237
Q

How does aortic stenosis in newborns present?

A

Asymptomatic murmur, ejection systolic (upper right sternal edge)

Carotid thrill

Ejection click

238
Q

Management of aortic valve stenosis?

A

Monitor early to assess when to intervene then balloon valvotomy, less complicated when older.

If problems such as intolerance to exercise may have to do younger, will probably eventually need to replace aortic valve

239
Q

Interval symptoms in asthma?

A

Night time cough

Wheeze on exertion

240
Q

Diagnosis of asthma in children, 3 cardinal symptoms?

A

Breathlessness
Wheeze
Cough

241
Q

What might asthma show on spirometry?

A

15% improvement on reversibility

242
Q

Treatment of asthma?

A

Preventers
- ICS
- LABA
- Leukotriene receptor antagonist

Relievers
- SABA
- Ipratropium bromide

Start with SABA,
then ICS
then LABA/Leukotriene
then more steroid

243
Q

Genetic abnormality in CF and inheritance pattern?

A

ABnormality in the CFTR chloride channel on chromosome 7 causing thick mucus secretions

1 in 20 people are carriers

Autosomal recessive

244
Q

How does CF present?

A

20% at birth with bowel obstruction (meconium ileus)

Older
- cough
- recurrent infection
- fatty light stool (pancreatic insufficiency)
- failure to thrive

245
Q

CF management?

A

Physiotherapy (at least twice a day)

High calorie diet

Pancreatic enzyme supplements

Psychological input

246
Q

Bronchiolitis management?

A

Supportive, O2 therapy,
High flow
CPAP
Ventilation

NG, IV fluids if needed

247
Q

Bronchiolitis presentation?

A

Couple of days of coryzal illness (longer than VIW)

Irritability, feeding difficulty

Cough, wheeze (expiratory) , crackles

248
Q

Croup (upper airway obstruction) presentation?

A

Stridor

Barking cough

Hoarse voice

<38.5

don’t look toxic

249
Q

Persistent upper airway obstruction (with stridor) most likely caused by what?

A

Laryngomalacia

250
Q

What does laryngomalacia look like?

A

Omega shaped deformity of the epiglottis

251
Q

most common cause of croup?

A

Parainfluenza virus

252
Q

Croup management?

A

Don’t look at throat

Keep child calm

Oxygen and hydration

Dexamethasone steroid orally

Nebulised budesonide

Nebulised adrenaline

Intubate

253
Q

Croup management?

A

Don’t look at throat

Keep child calm

Oxygen and hydration

Dexamethasone steroid orally

Nebulised budesonide

Nebulised adrenaline

Intubate

254
Q

How can you (maybe) differentiate between viral and bacterial pneumonia?

A

Viral:
- more common in infants
- fever <38.5

Bacterial
- Fever >38.5
- Any age
- Resp rate >50

255
Q

Presentation of pneumonia in children?

A

Fever
Tachopneoa
Cough

O/E:
- Dullness
- Reduced air entry
- Bronchial breathing

256
Q

Investigations and management of kids with pneumonia?

A

Investigations:
- sputum analysis
- bloods
- blood culture
- CXR
- URINE PNEUMOCOCCAL ANTIGEN

Tx
- Oxygen
- Physio if collapse (of lung)
- Abx

If empyema then chest drain and urokinase enzyme

257
Q

What is whooping cough, how does it present, how do you treat?

A

Highly contagious infection caused by pertussis

Week of coryzal symptoms then spasmodic cough with inspiratory whoop

258
Q

Viral induced wheeze in children treatment?

A

Bronchodilators and steroids as well as supportive care.

259
Q

Recurrent cough Ddx in children?

A

Series of respiratory tract infections

Asthma

CF

Reflux

Foreign body

TB

Habit

260
Q

How many Obstructive sleep apnoea present in children?

A

Loud snoring
Witnessed apnoeas (stopped breathing)
Restless and disturbed sleep

Can cause daytime sleepiness leading to learning and behavioural problems

261
Q

What is obstructive sleep apnoea normally caused by?

A

Adenotonsillar hypertrophy

262
Q

Key investigation for sleep apnoea on children?

A

overnight pulse oximetry, however normal oximetry doesn’t exclude the condition and may have to do polysomnography

263
Q

General Ddx for vomiting?

A

Reflux

Feeding issues

Infection
- Gastro/elsewhere

Intolerances

Obstruction

Metabolism

CAH

Renal failure

Appendicitis

Raised ICP

Coeliac disease

Migraine

Anorexia

Pregnancy

Testicular torsion

264
Q

When does reflux (GORD) normally resolve in children?

A

By 12 months, normally by 6 months.

265
Q

Complications of reflux in children?

A

Failure to thrive

Oesophagitis
- haemetemesis
- Iron deficiency anaemia

Pulmonary aspiration

Apparent life-threatening events

266
Q

What is colic in kids?

A

Colic is a frequent crying in a baby who appears to be otherwise healthy and well fed. It occurs in 1 in 5 babies and affects male and female infants equally

Usually begins within the first few weeks of life resolving by 4-6 months. Crying tends to be worst in the late afternoon or evening and usually lasts for several hours.

During episodes the baby’s face may become flushed, and they may clench their fists, draw their knees up to their tummy, or arch their back.

Linked to reflux and migraines.

267
Q

What causes reflux in babies?

A

Liquid diet

Immature lower oesophageal sphincter

Predominantly lying down

Short distance from mouth to stomach

268
Q

Reflux management?

A

Conservative (depends on severity)
- Don’t worry
- Sit up
- Thicken feed.

Medical:
- Ranitidine (5HT anatag)
- PPI

269
Q

How does cows milk protein allergy present?

A

Atopic eczema
Gastro-Oesophageal Reflux Disease
Chronic Gastro-intestinal symptoms, including chronic constipation

270
Q

How would pyloric stenosis present?

A

Around 3 weeks

Worsening vomits with feeds, progressing to projectile vomiting, non-bilious with undigested milk.

Mallory-Weiss tear may lead to blood in vomit.

Weight loss, dehydration, reduced urine output and even shock. Infants may become jaundiced; resolves with treatment.

Hypochloraemic Metabolic Alkalosis

Persistent vomiting leads to a loss of hydrogen and chloride ions, leading to a Hypochloraemic Metabolic Alkalosis. There is increased reabsorption of Bicarbonate in the kidneys whilst passive Na reabsorption is hindered by chloride loss; active reabsorption is done at the expense of Potassium ions which, along with vomiting losses, leads to Hypokalaemia (this may initially be concealed due to a potassium shift from extracellular fluids).

271
Q

Pyloric stenosis management?

A

Initial management includes placing the child nil by mouth and correcting the dehydration and electrolyte imbalance. The child can then go to surgery for a Pyloromyotomy - a laparoscopic procedure where the thickened muscle is cut to allow widening of the stomach outlet. The infant is usually able to feed within 6 hours and makes a full recovery with no ill effects.

272
Q

Test for cows milk protein allergy?

A

• Take it away for 3-4 weeks
• AND
• GIVE IT BACK!!!!!!!!!!!

273
Q

Overflow constipation management?

A

Movicol first line with escalating regime

Then add stimulant laxative

Add lactulose if hard stools

continue treatment for a few weeks after regular habit established and taper down slowly

274
Q

What do you need to check with constipation?

A

Leg weakness/delay gross motor development (spinal abnormality)

Constipation from birth

Faltering growth

275
Q

What investigations are available for coeliac disease, when would you perform them?

A

TTG and total IgA are first line serological tests. MUST be done whilst the patient is eating gluten.

Definitive diagnosis is a biopsy - needs to be done whilst on gluten - shows subtotal villous atrophy

276
Q

Features of crohns disease?

A

Diarrhoea

Abdo pain

Oral ulceration

Rectal bleeding

Anal tags, fissure and fistulae

Weight loss

Poor growth and delayed puberty

277
Q

Features of ulcerative colitis?

A

RECTAL BLEEDING

PASSAGE OF MUCUS

DIARRHOEA

URGENCY

ABDOMINAL PAIN

POOR GROWTH &DELAYED
PUBERTY

278
Q

Manifestations of IBD outside the bowel?

A

JOINTS: Arthritis can occur, leading to painful swollen
joints e.g.knees hips ,ankles.

SKIN : “Erythema Nodosum”- red painful lumps on the
lower legs ,shins and occasionally the arms.

EYES : “Iritis” - inflammation of the iris. “Episcleritis”-
inflammation of the eyeball.

LIVER : Inflammation and scarring of the liver and bile
ducts.

279
Q

Difference pathophysiologically between Crohns and UC?

A

UC:

  • Affects colon only
  • Diffuse progression from rectum upwards
  • Mucosal involvement
  • Histology – crypt abscesses / pseudopoyps

Crohns

  • Can affect anywhere along the GI tract – pan enteric
  • Skip lesion
  • Transmural involvement
  • Histology – granulomas/ cobble stone appearances
280
Q

Confirmation of IBD diagnosis?

A

Upper and lower colonoscopy with biopsy.

281
Q

Big risk in UC?

A

Toxic megacolon

282
Q

Toxic megacolon management?

A
  1. IV fluids and NBM
  2. IV antibiotics
  3. IV steroids
  4. Blood transfusion if necessary
  5. Urgent surgical review (N.B. emergency colectomy has a mortality of 10%, but perforation has a mortality of 33%)
283
Q

What is toxic megacolon?

A

Toxic megacolon is an acute form of colonic distension.

It is characterized by a very dilated colon (megacolon), accompanied by abdominal distension (bloating), and sometimes fever, abdominal pain, or shock.

284
Q

What is toddler’s diarrhoea?

A

Toddler’s diarrhoea typically occurs in the second year of life and is associated with undigested food such as peas and carrots in the stools. The child is well and growing normally. It is thought to relate to a rapid intestinal transit time. It resolves by the age of 4 years.

285
Q

What is intussusception?

A

Describes the invagination of the proximal bowel into the distal segment - commonly ileum into caecum at the ileocaecal valve

286
Q

When does intussusception usually occur?

A

3 months to 2 years

287
Q

Complications in intussusception?

A

Venous obstruction causing engorgement, bleeding and bowel perforation

288
Q

Presentation of intussusception?

A

Paroxysmal severe colicky pain and pallor

May refuse feeds, vomit - may be bilious

Redcurrent jelly stool

Sausage shaped mass in abdomen

289
Q

Management of intussusception?

A

IV fluid resus

Rectal air insufflation - by a radiologist

Surgically if the air fails

290
Q

Abdominal migraine presentation?

A

Periodic pain, can be in the midline assoc. with vomiting and facial pallor

Headache is normally present too, but not necessarily

291
Q

Gastroenteritis pathogens?

A

Most common - rotavirus (up to 60%)

Others:
- adenovirus
- norovirus
- coronavirus
- astrovirus

Bacteria are less common, may have blood in the stool
- Campylobacter jejuni
- Shigella and salmonella - blood and pus
- Cholera and e. coli - profuse rapidly dehydrating

292
Q

groups of children at risk of dehydration with respect to gastroenteritis?

A

<6 months or born with low birth weight

> 6 diarrhoeal stools in prev. 24 hrs

> 3 vomits in previous 24 hours

Not tolerating fluids

Malnourished

293
Q

Signs of dehydration in children?

A

Decreased conscious level

Sunken fontanelle

Dry mucous membranes

Sunken eyes

Tckypnoea

prolonged cap refill

Tchycardia

Pale skin

Hypotension

Weight loss

Cold extremities

Reduced tissue turgor

294
Q

Management of gastroenteritis?

A

May get stool sample if in shock

Hypernatraemic dehydration is hard to manage:
- Oral rehydration solution
IV fluids (if shock) - need to measure plasma sodium, and if hypernatraemic then slow infusion, over 48 hours.

Antibiotics if there is sepsis

295
Q

Gastroenteritis presentation?

A

D & V, may be evidence of infection such as contact with an infected person or travel abroad.

296
Q

What amount of ORS do you give in management of dehydration?

A

50 ml/kg over 4 hours

297
Q

How do you correct fluid deficit (in IV fluids) in kids - not maintenance?

A

100ml/kg if shocked

50ml/kg if not shocked

0.9% saline or normal saline with 5% dex

298
Q

most common pathogens causing UTIs in children?

A

E coli - almost all
Klebsiella
Proteus species

299
Q

Risk factors for UTIs?

A

Constipation
- incomplete voiding, urinary stasis

Voiding dysfuntion
- Sit on heel in girls, pinch penis in boys, so that they don’t have to go to the loo, may not empty properly urinary stasis again.

Anatomic anomoly
-PUJ (Pelviureteric junction obstruction)
- others

Neuropathic
- spina bifida

1 year fairly common - not potty trained, need basic hygiene advice perhaps

> 6 months more common in girls
<6 month more common in boys

300
Q

Presentation of UTI?

A

Preverbal (<3 months)
- fever
- vomiting
- lethargy
- irritability
- poor feeding
- tenderness

> 3 months (if verbal )
- dysuria
- frequency
- abdo/loin tenderness
- dysfunctional voiding

301
Q

Management of UTI?

A

Really ill - pyelonephritis
- Analgesic
- fluids
- IV abx

Well child
- Abx
- ?analgesia

302
Q

Types of enuresis

A

Primary nocturnal enuresis

Daytime enuresis (normally with night)

Secondary enuresis

303
Q

What is daytime enuresis?

A

lack of bladder control during the day in a child over 3-55 years

304
Q

What can cause daytime enuresis?

A

Lack of attention to bladder sensation, normal or developmental or psychogenic

Detrusor instability

Bladder neck weakness

Neuropathic bladder

UTI

Constipation

Ectopic ureter

305
Q

Management (inc. investigations in daytime enuresis?

A

Examination to rule out neuropathic bladder

Urine sample for microscopy to exclude UTI

USS of bladder

urodynamics

Can use star reward charts, bladder training and pelvic floor exercises if neuropathic bladder or anomaly excluded

306
Q

What is secondary enuresis?

A

Loss of previously achieved urinary continence

307
Q

Causes of secondary enuresis?

A

Emotional upset (most common)

UTI

Polyuria from diabetes or CKD

308
Q

management of secondary enuresis (inc. management)?

A

Test urine sample for infection, glycosuria and proteinuria

USS of renal tract

Assess urinary osmolality of early morning sample to assess urinary concentrating ability

309
Q

Causes of proteinuria?

A

Orthostatic proteinuria
- when standing up, will resolve

Glomerular abnormalities

Increased glomerular filtration pressure

Reduced renal mass

HTN

Tubular proteinuria

310
Q

Clinical features of nephrotic syndrome?

A

Protein in urine so low plasma albumin resulting in oedema (periorbital, scrotal, vulval, leg and ankle)

May have ascites

May have breathing difficulties resulting in breathlessness

311
Q

Complications of nephrotic syndrome?

A

infection
- peritonitis
- cellulitis

Hypovolaemia

VTE - PE

Acute renal failure

protein depletion

312
Q

Most common cause of nephrotic syndrome in kids

A

Minimal change glomerulonephritis. Epithelial cell foot processes fuse

313
Q

What is steroid sensitive nephrotic syndrome? What are the features that suggest this?

A

When the nephrotic syndrome is treatable with steroids, normally:

Between 1-10years
No macroscopic haematuria
Normal BP
Normal complement
Normal renal function

314
Q

Management of nephrotic syndrome

A

Normally try steroids

Try to use steroid sparing agents as many will relapse and steroid over use can cause all kinds of shit

Prevent complications:

Maintain hydration
- Don’t restrict fluids (unless must)
- IV albumin
- Caution with diuretics

Minimise oedema
- Low salt

Prevent infection
- Imms

If they have lots of relapses then will need steroids long term

315
Q

If the urine is brown or red what is the haematuria likely caused by?

A

Brown - glomerular

Red - LUTI

316
Q

Most common cause of haematuria?

A

UTI

317
Q

Causes of acute nephritis in children?

A

Post infective (strep)
- doesn’t last long, prognosis is good

Vasculitis e.g. HSP

IgA nephropathy

318
Q

Features of acute nephritis in children?

A

Decreased urine output and volume overload

Hypertension

Oedema

Haematuria and proteinuria

319
Q

Management of acute nephritis in children?

A

Manage fluid and electrolyte balance, diuretics when necessary.

320
Q

Definition of HTN in kids?

A

Blood pressure above the 95th centile for height, age and sex

321
Q

Presentation of HTN in kids?

A

Vomiting, headaches facial palsy, retinopathy, convulsions or proteinuria.

322
Q

Causes of hypertension in kids?

A

Renal
Polycystic kidneys, tumours, parenchymal disease

Coarctation of the aorta

Catecholamine excess
- Phaeochromocytoma

Endocrine
- CAH
- Cushings
- Hyperthyroidism

Essential HTN

323
Q

Meningococcal septicaemia most likely causative organism?

A

Neisseria meningitidis - gram negative

324
Q

Presentation of bacterial meningitis and of meningococcal septicaemia?

A

Different conditions, bacterial meningitis, does often present with sepsis though:

Bacterial meningitis
- Fever
- Headache
- Stiff neck, bulging fontanelle, photophobia
- Altered mental state
- Non-blanching rash

Shock

Seizures, focal neurological signs

Meningococcal septicaemia without meningitis probably wouldn’t have the classic stiff neck/photophobia/bulging fontanelle

325
Q

Red flags of SOL in kids?

A

Visual field deficits
Cranial nerve abnormalities

Headache worse on lying down, wakes kid up associated with morning nausea or vomiting

Abnormal gait
Torticolitis (tilting of the head)
Growth failure
papilloedema (late)
Cranial bruits
Personality change

326
Q

Three main divisions of headache in kids?

A

Primary
- Migraine
- Tension
- Cluster
- Cough/exertional

Secondary
- Due to SOL or raised ICP

Trigeminal or other neuralgia

327
Q

What is the most common migraine in kids?

A

Migraine without aura (90%)

328
Q

Features of migraine without aura in kids? How does migraine with aura differ?

A

1-72hrs

Commonly bilateral, may be unilateral though

Pulsatile, normally over temporal or frontal area

Photophobia/phonophobia

GI symptoms such as nausea, vomiting, abdo pain

Aggravated by physical activity

Aura obviously also has aura, this may be visual sensory or motor and positive or negative symptoms

329
Q

Management of headaches (primary)?

A

Rescue
- Analgesia (paracetamol and NSAIDS)
- Antiemetics
- 5HT agonists

Prophylaxis
- Pizofen (5HT antagonists)
- Beta-blockers
- Sodium channel blockers

Psychosocial support

330
Q

Most likely pathogen to cause encephalitis in children?

A

Herpes simplex - it is usually viral

331
Q

Presentation of encephalitis?

A

Most patients with viral encephalitis present with the symptoms of meningitis (fever, headache, neck stiffness, vomiting) followed by altered consciousness, convulsions, and sometimes focal neurological signs, signs of raised intracranial pressure, or psychiatric symptoms. There may be an association with a history of infection elsewhere in the body.

332
Q

BDZ in status epilepticus in children?

A

Rectal diazepam

333
Q

How do you calculate maintenance fluids in kids?

A

first 10kg - 1 Litre (100ml/kg)

10-20kg - 500ml (50ml/kg)

20-80kg 20ml per kg

334
Q

What is neurofibromatosis type 1 and type 2?

A

Genetic disorder causing lesions to the skin, nervous system and skeleton

Type 1
- More common
- Genetic inheritance - autosomal dominant
- cafe au lait spots
- increased risk of developing benign and malignant tumours

Type 2
- less common
- presents in adolescence
- Central CNS tumours e.g. vestibular schwannoma

335
Q

Diagnostic criteria for NF1 diagnosis?

A

Need two or more of these:

Six or more cafe au lait spots >5mm (>15mm after puberty)

Axillary freckles

> 1 neurofibroma

optic glioma

Lisch nodule (Iris haemotoma)

Sphenoid dysplasia

First degree realtive

336
Q

What is tuberous sclerosis?

A

genetic disorder resulting in the growth of benign tunours around the body, may have neurocutaneous and systemic lesions

337
Q

What is haemophilia, what are the types, inheritance pattern and features?

A

Haemopilia A and B, X-linked recessive disorders

In A there is factor 8 deficiency and is more common

B is factor 9 deficiency, less common

2/3rd of patients have family history, 1/3rd don’t as can be a de novo mutation.

Can range from mild to severe deficiency:
- severe would have recurrent spontaneous bleeding into joints and muscles - would lead to bad arthritis

normally present <1 year, can lead to intraventricular haemorrhage in neonates and bleeding episodes (into joints and stuff when starting to walk)

338
Q

Management of Haemophilia?

A

Replace the lost factor (8 in A, 9 in B), prophylactic therapy normally begins at 2-3 years.

339
Q

What is ITP?

A

Immune thrombocytopenic purpura
- lack of circulating platelets leading to bleeding

Normally occurs in children following viral infection or immunisation and is self-limiting in 6-8 weeks.

Can cause bleeding and purpura

340
Q

Management of sickle cell disease?

A

Full imms and antibiotic prophylaxis (due to increased risk of infection) throughout childhood.

Supportive in acute event

Hydroxyurea may predict in children who are struggling

341
Q

Clinical manifestations of Sickle cell disease?

A

Anaemia, chronic and acute

Infection

Painful crisis

Priaprism - needs to be treated promptly

Splenomegaly

Other long term issues

342
Q

Main causes of iron deficiency in children?

A

Main:
- Inadequate intake (may be because still breast fed >6 months)
- Malabsorption
- Blood loss

Other disorders such as:
- Sickle cell
- Thalassaemias
- G6PD deficiency, spherocitosis
- Haemophilias

343
Q

Most common cancer in children? how o you differentiate ALL and AML

A

ALL

AML and ALL are diferentiated morphologically

344
Q

Leukaemia presentation, features and management?

A

2-5 years, normally insidious over a few weeks, but can be v rapid.

General:
Malaise, anorexia

Bone marrow infiltration
- Anaemia - pallor, lethargy
- Netropaenia - infection
- thrombocytopaenia - bruising, petechiae
- bone pain

hepatosplenomegaly, lymphadenopathy

Other:
- CNS - headache. vomiting

Testicular enlargement

345
Q

Types of lymphoma in childhood?

A

Hodkin and non-hodgkin

hodgkin is painless lymphadenopathy, non is mediastinal mass, prognosis is good with combined chemotherapy

346
Q

What is CVID?

A

B cell issue

umbrella diagnosis in that it encompasses a group of genetic disorders which result primarily in hypogammaglobulinaemia or failure of antibody production

Presents with recurrent infection

347
Q

What is anaphylaxis and how do you manage it?

A

Severe rapid onset immunological reaction that threatens ABC

Normally IgE mediated reaction to food allergy, asthma is a. risk factor.

ABCDE approach

High flow O2

Adrenaline IM:
>12 500mg (0.5ml of 1 in 1000)
6-12 0.3ml
<6 0.15ml

Fluid and steroids

348
Q

Orbital cellutitis and periorbital cellulitis differences and management?

A

Periorbital cellulitis is not in the obit yet, it presents with erythema, tenderness and oedema of the eyelid, it may follow local trauma. Needs prompt Iv antibiotics to prevent it spreading to the orbit and becoming orbital cellulitis.

Orbital cellulitis is an emergency, there is proptosis, painful and limited ocular movement and reduced visual acuity. It may be complicated by meningitis, cavernous sinus thrombosis or abscess formation.

349
Q

Chickenpox presentation and management?

A

Varicella zoster infection, normally happens by 5 years

Pyrexia
Headache and malaise
Vesicles for 3-5 days - papule, vesicle, pustule and crust
Can be very itchy, less so in younger kids

Not a problem in younger kids but much more of a problem in older adults if they haven’t had it. Just general supportive management, can use antihistamine and paracetamol

350
Q

What is slapped cheek disease? Presentation and management?

A

Fith disease or parovirus infection or erythema infectiosum.

Coryzal symptoms at first

then free from symptoms for 7-10 days

Then slapped cheek rash

About 1-4 days after the facial rash appears, an erythematous macular rash develops on the extremities, mainly on the extensor surfaces. disappears after 3-21 days.

351
Q

What is hand foot and mouth disease, how does it present and how is it managed?

A

Viral illness which commonly causes lesions involving the mouth, hands and feet.

Can affect other areas such as genitalia and buttocks.

Coxsackievirus A16 (CA16) and enterovirus 71 (EV71)

Prodrome such as low grade fever, malaise and loss of apetite

Lesions begin in mouth, macular that progress to ulcers, then skin lesions

Self-limiting

Management is supportive, assure it is not foot and mouth disease in animals. Paracetamol, soft diet and analgesics.

May rarely have complications such as meningitis or encephalitis, infection from open sores, cardiorespiratory failure.

352
Q

What is JIA?

A

Juvenile idiopathic arthritis (JIA) is defined as joint inflammation presenting in children under the age of 16 years and persisting for at least six weeks, with other causes excluded.

Lots of different types, can cause fever, is not infective in origin.

353
Q

What is malrotation and volvulus?

A

A volvulus is a complete twisting of a loop of intestine around its mesenteric attachment site. This can occur at various locations of the gastrointestinal (GI) tract, including the stomach, small intestine, caecum, transverse colon and sigmoid colon.

Midgut malrotation refers to twisting of the entire midgut about the axis of the superior mesenteric artery (SMA).

Bilious vomiting is key, malrotation may lead to volvulus, which is pretty bad

Volvulus may present with abdo mass, distention and pain - urgent care needed, surgical correction.

354
Q

Appendicitis presentation?

A

RIF (may start periumbilical) pain, worse on movement is key, nausea vomiting and anorexia.

Rebound tenderness

355
Q

What causes roseola infantum?

A

Human Herpes virus 6

356
Q

Most likely cause of nephrotic syndrome in children/young adults?

A

Minimal change disease

5th (Final year) (34 decks)

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