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Year 5 > Paediatrics 2 > Flashcards

Paediatrics 2 Flashcards

1
Q

What are the 4 most common paediatric malignancies?

A 
Leukaemia/lymphoma 
Brain tumours 
Neuroblastoma
Wilm's tumour 
Bone tumours
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2
Q

What is a Wilm’s tumour?

A

A rare kidney cancer that primarily affects children

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3
Q

How do brain tumours present?

A 
Raised ICP - early morning headache, vomiting, papilloedema
Focal seizures 
Neurological signs 
Endocrine disturbance 
Raised OFC
Developmental delay/regression
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4
Q

What investigations should be done if a brain tumour is suspected?

A 
CT or MRI 
Tumour biopsy 
Tumour markers 
Endocrine screen 
CSF cytology and tumour markers
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5
Q

What are the most common malignant bone tumours in children?

A

Osteosarcoma

Ewing’s sarcoma

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6
Q

How do bone tumours present?

A 
Often delayed 
Persistent nocturnal pain 
Swelling 
Deformity 
Pathological fractures 
Systemic symptoms - fever, weight loss
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7
Q

How is Ewing’s sarcoma treated?

A

Chemotherapy
Surgery
Autologous stem cell transplant
Radiotherapy

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8
Q

How is osteosarcoma treated?

A

Chemotherapy

Surgery

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9
Q

Why is long term follow up required for patients treated for bone tumours?

A

Significant toxicity associated with treatment

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10
Q

What are the common malignant causes of an abdominal mass?

A 
Neuroblastoma 
Wilm's tumour
Hepatoblastoma
Lymphoma
Germ cell tumour 
Soft tissue tumour
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11
Q

What are blueberry muffin skin nodules associated with?

A

Neuroblastoma

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12
Q

What investigation should be done if neuroblastoma is suspected?

A

Urinary catecholamines

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13
Q

What malignancy causes leucocoria?

A

Retinoblastoma

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14
Q

What malignancy causes a bitemporal hemianopia?

A

Craniopharyngioma

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15
Q

What are children receiving chemotherapy at increased risk of?

A

Neutropenic sepsis

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16
Q

What is tumour lysis syndrome?

A

Breakdown of malignant cells results in hyperuricaemia, hyperkalaemia, hypophosphataemia and hypocalcaemia, causing AKI, seizures, arrhythmia and death if left untreated

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17
Q

When is tumour lysis syndrome most likely to occur?

A

During induction chemotherapy

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18
Q

How is tumour lysis syndrome managed?

A 
Regular observation and monitoring
U&Es and bone profile
IV fluids 
Xanthine oxidase inhibitor (allopurinol)
Manage hyperkalaemia 
Renal dialysis
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19
Q

What are the early and late effects of chemotherapy?

A

Early - marrow suppression, temporary hair loss, nausea and vomiting, renal impairment
Late - cardiac toxicity, infertility, risk of secondary malignancy

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20
Q

Give an example of passive immunisation

A 
Normal immunoglobulin (IV/subcutaneous)
Specific antibodies (e.g. varicella zoster IgG)
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21
Q

Give an example of active immunisation

A

Foreign antigen stimulates a host immune response
Live attenuated vaccines
Inactivated vaccines

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22
Q

Give 2 examples of live attenuated vaccines

A 
BCG
MMR 
Rotavirus 
Influenza 
Oral polio
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23
Q

Give 2 examples of inactivated vaccines

A 
Polio 
Trivalent influenza 
Diphtheria and tetanus
Pertussis 
HPV
MenB
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24
Q

What is the major difference in immune response between children and adults in regards to vaccination?

A

Polysaccharide antigens do not stimulate an effective and lasting immune response in children < 2
Polysaccharide blocks opsonisation, preventing phagocytosis and subsequent antigen presentation to T-cells in association with MCH by APCs. The immune response is therefore largely T-cell independent and relies on the formation of antibody by B-cells.

Infants have low numbers of/immature B cells, and without T-cell activation may produce only small numbers of short-lived antibodies.

To induce T-cell responses the polysaccharide antigen of pathogenic microbes can be linked to a carrier protein (e.g. tetanus or diphtheria toxoid), to which the child reacts.

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25
Q

Give 2 examples of conjugates vaccines

A

Hib
Group C meningococcus
Pneumococcal
Group ACWY meningococcal

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26
Q

What immune protection is offered by the placenta, covering babies up to 2 months?

A

IgG

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27
Q

Why are booster vaccinations needed?

A

Live vaccine produce long lasting immunity after 1 or 2 doses but inactivated vaccines need several doses

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28
Q

What is the main contraindication to vaccination?

A

Confirmed anaphylaxis to previous vaccine with same antigens or other vaccine components (e.g. neomycin/streptomycin)

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29
Q

In what population is the yellow fever vaccine contraindicated?

A

Those with a confirmed anaphylaxic reaction to egg

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30
Q

In whom are live vaccines contraindicated?

A

Immunosuppressed

Primary immunodeficiency, chemo/radio therapy in last 6 months, bone marrow transplant treatment in last 12 months, high dose steroids until 3 months without, immunosuppressant medication in last 6 months
HIV (no BCG but may have MMR)

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31
Q

How long should there be between live vaccine administration?

A

3 weeks

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32
Q

How long should vaccination be postponed for if a patient has received immunoglobulin?

A

3 months

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33
Q

What is subacute sclerosing panencephalitis?

A

Very rare, but fatal disease of the central nervous system that results from a measles virus infection acquired earlier in life
SSPE generally develops 7 to 10 years after a person has measles, even though the person seems to have fully recovered from the illness

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34
Q

What is the incubation and infectivity period for measles?

A

7-14 days

1-2 days before symptoms to 4 days after rash

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35
Q

What are the clinical features of measles?

A

3-5 days prodrome of fever, coryza, cough, conjunctivitis and Koplik’s spots
Maculopapular rash starts behind ears and migrates to face/trunk/limbs
Associated cervical lymphadenopathy and fever

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36
Q

What are the complications of measles?

A 
Otitis media 
Lymphadenitis 
Interstitial pneumonitis 
Secondary bacterial bronchopneumonia
Myocarditis 
Post-infectious demyelinating encephalomyelitis 
SSPE
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37
Q

What is the incubation and infectivity period for chicken pox?

A

14-21 days

2 days before and 5 days after rash

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38
Q

What are the clinical features of chicken pox?

A

48 hours of fever, malaise, headache and abdominal pain

Itchy crops of erythematous macules -> papules -> vesicles of serous fluid

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39
Q

What are the complications of chicken pox?

A 
Secondary bacterial infection (Group A strep, S.aureus)
Pneumonia
Encephalitis
Progressive disseminated varicella 
Cerebellar ataxia 
Thrombocytopenia 
Purpura fulminans 
Post-infectious encephalitis
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40
Q

How is zaricella zoster prevented?

A

Vaccination for high-risk patients

Post-exposure prophylaxis with varicella zoster immunoglobulin (IVIG) if immunocompromised

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41
Q

What is the incubation and infectivity period for mumps?

A

14-21 days

1-2 days prior to 9 days after parotid swelling

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42
Q

What are the clinical features of mumps?

A

Prodrome - fever, anorexia, headache

Painful uni/bilateral salivary +/- submandibular gland swelling

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43
Q

What are the complications of mumps?

A 
Meningoencephalitis
Deafness
Orchitis 
Epididymitis
Pancreatitis 
Nephritis
Myocarditis 
Arthritis
Thyroiditis
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44
Q

What is the incubation and infectivity period for parvovirus B19?

A

4-14 days

Not infectious once rash appears

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45
Q

What is parvovirus B19 also known as?

A

Erythema infectiosum
Slapped cheek
Fifth’s disease

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46
Q

What are the clinical features of parvovirus B19?

A

Prodrome - low grade fever, malaise
Maculopapular spots on cheeks which coalesce to give slapped cheek appearance
Fine lacy rash extends to trunk and limbs
Associated arthralgia and arthritis
Lasts 2-30 days

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47
Q

What are the complications of parvovirus B19?

A

Aplastic crisis in sickle cell/thalassaemia/immunocompromised

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48
Q

What is the incubation and infectivity period for rubella?

A

14-21 days

1-2 days before to 7 days after rash appears

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49
Q

What are the clinical features of rubella?

A

Prodrome - coryza, tender cervical lymphadenopathy
Fine maculopapular rash on face and spreads to trunk
Arthralgia and palatal petechiae

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50
Q

What are the complications of rubella?

A

Encephalitis
Thrombocytopaenia
Congenital rubella syndrome

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51
Q

What is the incubation and infectivity period for HHV6?

A

7-14 days

Until fever subsides

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52
Q

What is HHV6 also known as?

A

Human herpes virus 6
Roseola infantum
Sixth disease

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53
Q

What are the clinical features of HHV6?

A

Sudden onset high fever with mild coryza which resolves on day 3-4 and maculopapular rash appears on trunk and limbs for 1-2 days

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54
Q

What are the complications of HHV6?

A

Febrile convulsions in 6-18 month olds

Encephalitis

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55
Q

What is the incubation and infectivity period for pertussis?

A

7-14 days

Whilst coughing during catarrhal phase

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56
Q

What are the clinical features of pertussis?

A

Catarrhal phase - low grade fever, coryza, conjunctivitis for 1-2 weeks
Paroxysmal phase - severe cough +/- whoop, vomiting, cyanosis, apnoea for 2-8 weeks
Convalescent phase - cough subsides over weeks/months

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57
Q

What are the complications of pertussis?

A 
Apnoea 
Secondary bacterial pneumonia 
Weight loss 
Bronchiectasis
Otitis media
Seizures 
Encephalopathy 
Subconjunctival/subarachnoid/intraventricular haemorrhage
Umbilical/inguinal hernia
Ruptured diaphragm
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58
Q

How is pertussis diagnosed?

A

Nasal swab for PCR testing and culture

Associated lymphocytosis

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59
Q

How is pertussis treated?

A

Supportive

Macrolides

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60
Q

Give 4 causes of meningitis

A 
Bacterial
Viral 
Fungal 
Parasitic
Malignancy 
Immune-mediated
Drugs
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61
Q

What are the 2 most common causative bacterial organisms in meningitis in children?

A

Neisseria meningitidis
Streptococcus pneumoniae

Haemophilus influenzae
TB
Group B strep

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62
Q

What is the most common cause of viral meningitis in children?

A

Enterovirus

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63
Q

What is the most common cause of bacterial meningitis in neonates?

A

Group B streptococcus

Listeria monocytogenes
E.coli

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64
Q

How does bacterial meningitis present?

A 
Fever
Headache
Nausea and vomiting 
Neck stiffness 
Photophobia 
Lethargy
Decreased level of consciousness
Seizures 
Positive Kernig's sign and Brudzinski sign
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65
Q

What is Kernig’s sign?

A

Positive when flexing the thigh at the hip and knee to 90 degree angles, and subsequently extending the knee is painful (leading to resistance)

This may indicate subarachnoid haemorrhage or meningitis

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66
Q

What is Brudzinski’s sign?

A

Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed

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67
Q

Give 4 ways in which an infant may present with bacterial meningitis

A 
Unexplained fever 
Lethargy 
High pitched/irritable cry 
Cannot be soothed by parents 
Poor feeding 
Apnoeic/cyanotic attacks 
Posturing 
Seizures 
Bulging fontanelle
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68
Q

How is bacterial meningitis diagnosed?

A

LP

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69
Q

What are the contraindications to LP?

A

Cardiovascular compromise
Signs of increased ICP (herniation risk)
Abnormal clotting/low platelets (subdural/epidural haematoma)
Skin infection at site

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70
Q

Give 4 signs of increased ICP

A 
GCS <9/drop of 3 or more 
Bradycardia and HTN 
Focal neurological signs 
Abnormal posturing
Unequal/dilated/poorly responsive pupils 
Papilloedema 
Abnormal doll's eye movements
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71
Q

What will CSF analysis reveal in suspected meningitis?

A

WCC >5 (>20 neonates) - polymorphs = bacterial, lymphocytes = viral
Elevated protein and decreased glucose = bacterial or TB
Organisms may be seen on staining
PCR for pneumococcus/meningococcus/Hib/HSV/ZVZ/enterovirus

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72
Q

What is the empirical treatment for suspected bacterial meningitis?

A

IV cefotaxime
(+ amoxicillin and gentamicin if <6 weeks)
(+ dexamethasone if >3 months and no purpura)

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73
Q

What is the definitive treatment for Neisseria meningitidis meningitis?

A

7 days IV cefotaxime/ceftriaxone

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74
Q

What is the definitive treatment for Streptococcus pneumoniae meningitis?

A

14 days IV cefotaxime/ceftriaxone

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75
Q

What are the complications of meningitis?

A 
Hydrocephalus
Deafness (Hib)
Neuromotor disorders 
Seizures 
Visual disorders
Speech and language disorders 
Learning difficulties
Behavioural problems
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76
Q

What is the difference between septicaemia and sepsis?

A

Septicaemia - infection of the blood stream

Sepis - systemic inflammatory response to infection

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77
Q

What is sepsis syndrome/severe sepsis?

A

When sepsis is associated with hypoperfusion resulting in organ dysfunction which can lead to septic shock and multiple organ failure

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78
Q

What is the pathophysiology of meningococcal sepsis?

A

Capillary leak
Coagulopathy
Myocardial depression
Metabolic derangement

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79
Q

How does meningococcal bacteraemia present?

A

Fever
Petechial/purpuric rash
Relatively well child who rapidly deteriorates

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80
Q

What are the features of septic shock?

A 
Difficulty breathing
Tachycardia 
Hypotension 
Cool extremities 
Leg pain 
CRT >2 secs 
Decreased conscious level 
Moribund
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81
Q

How is septic shock managed?

A

High flow oxygen 15L via facemask with reservoir bag
IV fluid bolus of 20ml/kg of 0.9% saline; repeat once if needed, then consult PICU
IV cefotaxime 50mg/kg
Correct any metabolic derangements and coagulopathy

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82
Q

What are the 5 F’s of abdominal distension?

A 
Fat
Fluid
Faeces
Flatus
Foetus
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83
Q

Give 2 scars that might be present on abdominal examination of a nephrology patient

A

Nephrectomy - hockeystick at flank

Renal transplant - LIF

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84
Q

Give 3 renal causes of a unilateral mass on abdominal examination

A 
Multicystic kidney
Compensatory hypertrophy 
Obstructed hydronephrosis 
Wilms tumour
Renal vein thrombosis
Neuroblastoma
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85
Q

Give 3 renal causes of a bilateral mass on abdominal examination

A

AR/AD polycystic kidney disease
Tuberous sclerosis
Renal vein thrombosis

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86
Q

Give 3 urinary tract abnormalities

A 
Absent kidney/s 
Multicystic dysplastic kidney 
Duplex 
Horseshoe/pelvic kidney
Obstruction
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87
Q

What is Potter’s syndrome?

A

Describes the typical physical appearance caused by pressure in utero due to oligohydramnios, classically due to bilateral renal agenesis

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88
Q

What is a duplex kidney and what are its complications?

A

2 ureters
Upper - obstructs, associated with ureterocele
Lower - reflux (VUR)

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89
Q

Give 2 points of the urinary system which commonly obstruct

A

Posterior urethral valves - bladder hypertrophy, hydronephrosis, renal failure
VUJ
PUJ

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90
Q

Give 2 causes of oedema in children

A

HF
Nephrotic syndrome
Liver failure
Malnutrition

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91
Q

Give 3 pathological causes of proteinuria

A

Glomerular - sclerosis, nephritis, nephrotic syndrome, familial haematuria
Tubular
Physiological stress - exercise, cold, febrile, HF

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92
Q

Define nephrotic syndrome

A

Proteinuria (>1g/m2/day),
Hypoalbuminaemia (<25 g/l)
Oedema

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93
Q

What test can be used to diagnose nephrotic syndrome?

A

Protein to creatinine ratio from one early morning urine sample
Normal <20 mg/mmol
Nephrotic >150 mg/mmol

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94
Q

What type of patient is at higher risk of nephrotic syndrome?

A

Asian (x6) boys (2:1)

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95
Q

How is nephrotic syndrome classified?

A

Idiopathic - minimal change disease, focal segmental glomerulosclerosis
Secondary - HSP, SLE
Congenital

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96
Q

Give 3 investigations for nephrotic syndrome

A

Bloods - FBC, U&Es, LFT’s, C3/C4, Varicella status and ASOT
Urine - protein creatinine ratio, culture
BP

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97
Q

Give 2 complications of nephrotic syndrome

A

Hypovolaemia
Thrombosis
Infection
Hypertension

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98
Q

How is nephrotic syndrome treated?

A

Prednisolone - high dose and then reduce
20% albumin and furosemide - hypovolaemia/oedema
Pneumococcal vaccination
Penicillin prophylaxis
Salt/fluid restriction

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99
Q

What percentage of patients with nephrotic syndrome will have a relapse?

A

60-70%

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100
Q

Give 5 non-glomerular causes of haematuria

A 
Infection 
Trauma 
Stones 
Sickle cell
Coagulopathy/bleeding disorder
Renal vein thrombosis
Tumour 
Structural abnormality 
Munchausen by proxy
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101
Q

Give 2 glomerular causes of haematuria

A

Acute/chronic glomerulonephritis
IgA nephropathy
Familial nephritis

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102
Q

Give 3 things to find out about while taking a history for haematuria

A 
Pain 
Timing 
Trauma 
Recent URTI
Rash 
Medications 
FH renal disease or deafness
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103
Q

Give 4 investigations for haematuria

A

Bloods - FBC, coagulation, U&Es, ASOT, ANF, complement
Urine - MC&S, oxalate, calcium, phosphate and urate levels, calcium creatine ratio
AXR, renal USS, +/- renal biopsy

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104
Q

How is hypertension defined in children?

A

BP persistently >95th% for age and gender/height

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105
Q

Give 5 causes of hypertension

A 
Renal parenchymal disease
Renovascular 
Renal tumours
Coarctation of the aorta
Phaeochromocytoma
Neuroblastoma
Congenital adrenal hyperplasia 
Cushing's 
Hyperthyroidism
Essential HTN
Obesity 
Drugs - steroids, stimulants, recreational, liquorice
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106
Q

Give 5 first line investigations for hypertension

A

Bloods - FBC, U&Es, creatinine, albumin, bicarbonate, calcium, phosphate, LFTs, plasma renin activity, aldosterone, plasma catecholamines
Urine - urinalysis, urine microscopy and culture, urinary protein to creatinine ratio, urinary catecholamines
Imaging - renal USS with Doppler flow of the renal vessels, echo, ECG, CXR, DMSA

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107
Q

What is a DMSA scan?

A

Radionuclide scan that uses di mercapto succinic acid (DMSA) in assessing renal morphology, structure and function

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108
Q

How can end organ damage be assessed in hypertension?

A

Echo
Fundoscopy
Urinalysis for proteinuria

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109
Q

How is hypertensive crisis treated?

A

Labetalol/sodium nitroprusside infusion

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110
Q

What can be caused by UTI in presence of VUR?

A

Scarring of the kidneys

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111
Q

Give 3 causes of UTI

A 
Infrequent voiding 
Vulvitis
Hurried micturition 
Constipation 
VUR 
Neuropathic bladder
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112
Q

What is the most causative organism in UTI?

A

E.coli (85%)

Proteus (boys)
Staphylococcus 
Klebsiella
Enterococcus 
Pseudomonas (structural)
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113
Q

What are the symptoms of a UTI in an infant and older child?

A

Infant - fever, vomiting, lethargy, irritability, poor feeding, failure to thrive, sepsis, shock
Older - frequency, dysuria, changes in continence, abdominal pain, loin tenderness, fever, malaise, vomiting, haematuria

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114
Q

What investigations should be done in suspected UTI?

A

Urinalysis
Urgent urine culture and microscopy if <3 months
MSSU
Imaging

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115
Q

How does the imaging required for UTI differ depending on age?

A

<6 months - USS in 6 weeks (acute if recurrent/atypical); DMSA and MCUG 4-6 months after infection if recurrent/atypical
>6 months - atypical need acute USS and DMSA at 4-6m; recurrent need USS at 6w and DMSA at 4-6m

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116
Q

What are most UTIs resistant to?

A

Amoxicillin

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117
Q

How can recurrence of UTI be prevented?

A

Fluids
Prevention/treatment of constipation
Complete bladder emptying
Good perineal hygiene (girls)

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118
Q

Give 3 methods of urine collection in babies/children

A

Clean catch - unable to do MSSU (too young)
MSSU - mid-stream, gold standard
CSU - catheter
SPA - suprapubic aspiration
Urine bags - not sterile, can be used to measure volume

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119
Q

Define acute renal failure

A

Sudden reduction in renal function

Oliguria <0.5ml/kg/hr

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120
Q

Give a pre-renal, renal and post-renal cause of acute renal failure

A

Pre - hypovolaemia, HF
Renal - HUS, ATN, GN, NSAIDs
Post - urinary obstruction

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121
Q

What are the 5 indications for dialysis?

A 
Severe volume overload
Severe hyperkalaemia
Symptomatic uraemia
Severe metabolic acidosis
Removal of toxins

AEIOU - acidosis, electrolyte imbalances, ingestion, overload (volume), and uraemia

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122
Q

What is a renal USS good for?

A

General idea of renal anatomy (size, shape, symmetry and position of kidneys and tracts)
Vascular perfusion by Doppler
Screening tool

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123
Q

What is a DMSA scan good for?

A

Static scan to delineate divided function of kidneys
Identifies scars
Needs to be done at least 3 months after UTI

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124
Q

What is a DTPA scan good for?

A 
Dynamic scan allows assessment of drainage and obstruction
Micturating cystourethrogram (MCUG) - looking for vesicoureteric reflux, bladder outline, and the presence of posterior urethral valves
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125
Q

What is an AXR good for (renal)?

A

Stones

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126
Q

Define diabetes mellitus

A

Metabolic disorder of multiple aetiology characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both.

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127
Q

What is the pathophysiology of type 1 diabetes?

A

Autoimmune beta cell destruction, leading to absolute insulin deficiency

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128
Q

What is the pathophysiology of type 2 diabetes?

A

Non-autoimmune, multifactorial condition with insulin resistance and/or relative deficiency

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129
Q

What does ‘walking wounded’ mean?

A

Presentation of 70% Glasgow paediatric new-diagnoses - patient walks into hospital with absent/minimal dehydration and acidosis

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130
Q

Give 5 signs/symptoms of diabetes

A 
Thirst
Weight loss
Polydipsia
Dehydration 
Polyuria
Nocturia
Nocturnal enuresis
Lethargy 
Behavioural change 
Infection (balanitis, candidiasis)
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131
Q

Give 5 signs/symptoms of ketoacidosis

A 
Ketotic breath
Dehydration 
Laboured breathing - Kussmaul's
Nausea/vomiting 
Abdominal pain 
Headache
Irritability 
Confusion
Unrousable 
Features of cerebral oedema - sunken eyes, reduced skin turgor, CRT >2 secs, cool peripheries, tachycardia, hypotension
Raised ICP/altered consciousness
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132
Q

Name 4 types of diabetes

A 
Type 1
Type 2
MODY
Disease related - CF, haemochromatosis, acromegaly, Cushing's
Steroid induced 
Syndromal - Trisomy 21, Prader-Willi
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133
Q

Name 2 types of insulin regimen

A

Twice daily - rarely used, inflexible, simple
Split evening - young children
Basal bolus - flexible, correction doses

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134
Q

What are correction and ketone doses?

A

Correction - rapid acting insulin to lower high BG if > 8mmol/l and ketosis minimal; dependent on blood glucose
Ketone - rapid acting insulin to clear moderate/large ketosis if BG > 14 mmol/l; independent of blood glucose

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135
Q

Give 3 methods of insulin administration

A

Subcutaneous fat injection (pen & needle device or (rarely) syringe)
Subcutaneous fat infusion (via “insulin pump”)
Intravenous infusion (ketoacidosis or while fasting (+ IV dextrose))
Other - islet cell transplant, implanted pump

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136
Q

Give 3 causes of ketosis/ketoacidosis

A 
Lack of awareness
Delay of diagnosis 
Infection 
Trauma
Insulin pen/pump failure 
Insulin omission (accidental/deliberate)
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137
Q

How is ketoacidosis investigated?

A

Glucose, U&E, Blood Gas ([H+], [HCO3-], UA (ketosis)

Other - Osmolality; consider Septic screen (blood, urine, etc.)

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138
Q

How is ketoacidosis managed?

A 
Managed in HDU/ITU
A-E assessment 
IV fluids - rehydrate slowly 
IV insulin - syringe driver 
IV K+ - once shock is corrected 
Monitoring - BP, ECG, neuro
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139
Q

What are the complications of ketoacidosis?

A

Cerebral oedema
Arrhythmia
Renal failure

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140
Q

How is cerebral oedema secondary to ketoacidosis managed?

A 
Exclude hypoglycaemia 
Restrict fluid 
Mannitol 
Ventilate
CT
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141
Q

What are the signs/symptoms of hypoglycaemia?

A

Mild neuroglycopenia - feeling faint, hunger, headache, confusion
Autonomic symptoms - pallor, sweating, nausea, tachycardia
Severe neuroglycopenia - slurred speech, seizure, coma, death

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142
Q

How is hypoglycaemia treated in the outpatient setting?

A

Rapid-acting oral glucose, followed by slower-acting carbohydrate
“GlucaGel” oral glucose gel (if can tolerate oral intake)
IM Glucagon injection, anterior thigh (if unconscious, fitting)

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143
Q

How is hypoglycaemia treated in the inpatient setting?

A

Oral glucose if conscious and able to take orally

IV dextrose bolus +/- infusion (if unconscious, persistent low BG)

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144
Q

Why do diabetics need additional management when ill?

A

Immune response impaired in those with T1DM
Metabolic stress causes catabolism and hormone release
May cause relative insulin deficiency and increased insulin requirement
Causes hyperglycaemia with ketosis/ketoacidosis

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145
Q

How does acute epiglottitis present?

A

3-7 year old
Drooling and stridor
Toxic within a few hours

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146
Q

What should be avoided in a child presenting with epiglottitis and why?

A

Visualisation of epiglottis or distressing the child (e.g. cannulation)
May precipitate respiratory arrest

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147
Q

How should epiglottitis be managed?

A

ITU
Intubation
Humidified air/oxygen
IV chloramphenicol/ampicillin

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148
Q

What is the differential diagnosis for epiglottitis?

A

Foreign body
Retropharyngeal abscess
Diphtheria
Croup

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149
Q

How does croup present?

A 
Age 6 months - 3 years 
May have preceding coryzal symptoms 
Inspiratory stridor 
Wheeze
Mild fever and fatigue
Barking cough
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150
Q

How is croup managed?

A

Humidified air/oxygen

No antibiotics

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151
Q

Give 5 causes of acute respiratory failure

A

Central - head injury, drugs, convulsion, infection
Airway - acute epiglottitis, foreign body
Parenchymal - pneumonia, bronchiolitis, asthma
Chest wall - polio, trauma

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152
Q

How does acute respiratory failure present?

A

Restless, agitated from hypoxia, cyanosis, silent chest not moving sufficient air
Blood gases - low PaO2 and/or rising CO2 on oxygen

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153
Q

How is acute respiratory failure managed?

A

Secure airway - bag valve mask, intubation, assisted ventilation
Deal with primary cause

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154
Q

How does acute bronchiolitis present?

A 
6 weeks - 6 months old 
Preceding coryzal symptoms 3-5 days prior
Progressive cough
Wheeze
Difficulty feeding 
Similar signs to asthma 
Fine inspiratory crepitations
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155
Q

What causes bronchiolitis?

A

Respiratory syncytial virus

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156
Q

How is bronchiolitis managed?

A

Oxygen
Suction of secretions
Tube feeding/IV fluids if unable to tolerate oral
Antibiotics if bacterial infection suspected

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157
Q

What is the prognosis of bronchiolitis?

A

May recur

Third develop asthma in later life

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158
Q

How does acute asthma present?

A 
>1 year old 
Expiratory wheeze
Difficulty speaking 
Extended head 
Flared nostrils 
Increased AP chest diameter 
Accessory muscle use 
Tachycardia
Cyanosis
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159
Q

How is acute asthma managed?

A 
Oxygen 
Nebulised salbutamol and ipratropium bromide 
Oral prednisolone 
IV theophylline 
Monitor
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160
Q

What type of pneumonia is more common in pre-school children?

A

Bronchopneumonia (as opposed to lobar pneumonia)

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161
Q

How does pneumonia present?

A

Babies - ill, grey, cyanosed, increased WOB and RR, febrile convulsion
Children - can mimic acute appendicitis, upper respiratory rattle

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162
Q

What investigations should be done for pneumonia?

A 
CXR
Bloods - Hb, FBC 
Throat swab
Blood culture 
Mantoux (if severe)
Sweat test (if recurrent or staph)
163
Q

How is pneumonia managed?

A 
Suction of secretions 
PT
Oxygen 
NG/IV feeds 
Antibiotics - ampicillin/penicillin and gentamicin (sick) +/- flucloxacillin (staph)
164
Q

Give 3 symptoms which may indicate cardiac failure

A 
Lethargy 
Feeding problems/breathless on feeding 
Sweating
Failure to thrive 
Recent excessive weight gain/oedema 
Blue attacks
Precipitated or exacerbated by illness
165
Q

Give 2 signs which may indicate cardiac failure

A

Tachycardia
Tachypnoea
Hepatomegaly
Femoral pulse changes

166
Q

How is cardiac failure managed?

A 
Position - sitting/incline, head up 
Diuretic (e.g. furosemide)
Digoxin 
Oxygen 
Morphine 
Treat cause
167
Q

In what condition is digoxin contraindicated?

A

Tetralogy of Fallot

168
Q

How should burns and scalds be managed immediately at home?

A

Strip off soaked clothing
Immerse in cold running water
Cover area in clean dry sheet/towel/dressing

169
Q

How should burns and scalds be managed in hospital?

A 
Airway - soot in nostrils, wheeze
IV access
Analgesia - IV morphine 
Plasma expanders if >10% surface affected to prevent shock/renal failure 
Blood transfusion for full thickness
Weight
Check Hb for anaemia 
Monitor closely for renal failure
170
Q

How is % burn calculated in children?

A

Head 18%, legs 13%, arms 8%, trunk 18%

Child’s palm = 1%

171
Q

What is the difference between superficial and superficial dermal burns?

A

Superficial - sunburn, no blisters

Superficial dermal - good blood supply, blistered

172
Q

How do deep dermal and full thickness burns differ?

A

Deep dermal - altered sensation but not painless, may have blisters, well demarcated, speckled appearance
Full thickness - painless, white/brown, dry

173
Q

What % cut offs are important clinically in regards to burns?

A

> 3% need referral
Full thickness >1% need to be seen
10% needs IV fluids
30% needs ICU

174
Q

How is isotonic dehydration quantified in children?

A

As percentage loss of body weight
5% = mild = 50ml/kg
10% = moderate = 100ml/kg
15% = severe = 150ml/kg

175
Q

Give 2 symptoms/signs of mild dehydration

A

Lethargic
Loss of skin turgor
Dry mouth
Slack fontanelle

176
Q

Give 2 symptoms/signs of moderate dehydration

A 
Tachycardia 
Tachypnoea
Sunken fontanelle 
Sunken eyes 
Mottled skin 
Oliguria
177
Q

Give 2 symptoms/signs of severe hydration

A

Shock
Coma
Hypotension

178
Q

How are fluid boluses calculated in children?

A

20ml/kg

179
Q

How should oral rehydration solution be administered?

A

5-10ml every 1-5 minutes (to replace deficit in 6 hours)

180
Q

How might meningitis present?

A 
Gastroenteritis
Irritable cry 
Coma
Convulsion
Apnoea
Bulging fontanelle
Head retraction and resistance to flexion 
Otitis media 
Purpura
181
Q

What investigations should be done for meningitis?

A

LP for CSF cells, Gram stain and glucose
Bacteriology
Hb, WBC, U&Es, blood glucose
Chest x-ray

182
Q

How is meningitis treated?

A

Neonate - probably e.coli/GBS = benzylpenicillin and chloramphenicol
>3 months - probably H.influenzae/meningococcus/pneumococcus = ampicillin and chloramphenicol

183
Q

Give 4 important complications of meningitis

A 
Convulsions
Cerebral oedema 
Subdural effusion 
Hydrocephalus 
Hyponatraemia (inappropriate ADH) 
Deafness 
Fever (rises after initial fall)
Mental handicap 
Cerebral palsy 
Epilepsy
184
Q

What early symptoms may indicate osteomyelitis/septic arthritis?

A

Reluctance to use a limb
Local swelling
Local tenderness

185
Q

How are osteomyelitis/septic arthritis treated?

A

IV antibiotics - flucloxacillin and ampicillin
Immobilise the limb
Monitor

186
Q

When is surgery indicated for osteomyelitis/septic arthritis?

A

Infants - immediately for septic hip

Older children - poor response to treatment after 24 hours

187
Q

Give 4 symptoms of UTI

A 
Dysuria
Frequency 
Haematuria
Foul smelling urine 
Bedwetting 
Abdominal pain 
Pyrexia of unknown origin 
Malaise 
Not feeding
188
Q

What investigations should be done for UTI?

A

BP
Hb, WBC, U&Es, serum creatinine, urine and blood culture
Ultrasound
Radio isotope studies for scarring, pelvi-ureteric obstruction and ureteral reflux, duplex collecting systems, bladder diverticuli/obstruction

189
Q

What bacteria are most commonly implicated in UTI?

A

<1 year = E.coli

> 1 year = E.coli, proteus

190
Q

Give 4 symptoms/signs of DKA

A 
Polydipsia/polyuria for days or weeks
Weight loss
Dehydration
Vomiting
Abdominal pain,  Infection associated
Coma
191
Q

How is severe DKA managed?

A

0.9% saline
K+ supplementation
Insulin bolus and then IV infusion until glucose falls to 15mmol/L
Then give dextrose instead of saline and insulin every 4-6 hours

192
Q

How is poisoning managed immediately at home?

A

Induce vomiting with fingers (unless volatile hydrocarbons, caustics or the child is unconscious)

193
Q

How is poisoning managed in hospital?

A

Establish what has been taken, in what volume, when and how
Induce vomiting with 15ml syrup of ipecac and water, repeat if no result after 20 mins/gastric lavage if unconscious
Give specific antidotes

194
Q

What is the antidote for paracetamol poisoning?

A

Acetyl cysteine/methionine

195
Q

What is the antidote for TCA or theophylline poisoning?

A

Activated charcoal

196
Q

What is the antidote for opiate poisoning?

A

Naloxone

197
Q

What is the antidote for alcohol poisoning?

A

Glucose (hypoglycaemia can be severe)

198
Q

How should pyrexia be investigated?

A

Infection screen - blood culture, urine culture +/- lumbar puncture, Hb, WBC, ESR, chest x-ray

199
Q

How are seizures managed?

A

Keep child safe

Give diazepam IV or rectal -> paraldehyde if no response after 10 minutes

200
Q

How are infantile spasms treated?

A

ACTH/corticosteroids

Benzodiazepines

201
Q

How is a petit mal seizure treated?

A

Ethosuximide

Sodium valproate

202
Q

How is temporal lobe/focal epilepsy treated?

A

Carbamazepine

Phenytoin

203
Q

What is sudden infant death syndrome?

A

Sudden and unexpected death of an apparently normal 1 month-1 year old after which a properly performed autopsy fails to reveal a major cause of death

204
Q

What are the risk factors for SIDS?

A

Male
Low birth weight
Winter
Adverse social/domestic conditions

205
Q

How should SIDS be managed?

A

Attempt resuscitation if appropriate
Inform parents cot death is likely
Offer holding the baby
Inform GP, health visitor and social services
Procurator Fiscal and police will investigate
Emphasise routine nature of inquiries and remove blame from parents/carers
Suppress lactation if breastfeeding

206
Q

What is non-accidental injury?

A

Where abuse is inflicted or knowingly not prevented by person(s) caring for a child and signs are present of physical injury and/or neglect, drug administration, failure to thrive, emotional or sexual abuse

207
Q

What factors may make you consider NAI?

A

Injuries inconsistent with explanation
Delay in seeking help
Medical advice sought for many minor injuries
Young, single parent
Known to social services
Handicapped child
Physical signs of neglect/abuse - bruising of different ages, black eyes, torn frenulum, retinal detachment/bleeds, genital bruising, withdrawn, drugged, burns/scalds, fractures

208
Q

What gene mutation is associated with eczema?

A

Filaggrin

209
Q

How can the skin barrier be improved in eczema?

A

Bathing without soap

Liberal and frequent emollients

210
Q

What are the main areas of management for eczema?

A

Improve skin barrier
Avoid irritants
Reduce itching
Topical steroids

211
Q

How can itching be improved in eczema?

A

Sedative anti-histamines
Cotton clothing
Scratch mitts
Keep nails short

212
Q

What steroids regimen is suitable for eczema of the body?

A

Medium potency for 7 days for flares and 2-3 times weekly for chronic patches
Increase to potent steroid if suboptimal response

213
Q

What steroids regimen is suitable for eczema of the face?

A

1% hydrocortisone safe for daily use (eyelids 3 times weekly only)
Short 3 day course of moderate steroids for flares

214
Q

How does irritant contact napkin dermatitis occur?

A

Moisture and friction disrupt skin barrier and allow irritants from urine/faeces to penetrate

215
Q

Give 3 features of irritant contact napkin dermatitis

A

Can be associated with candida and bacterial overgrowth
Glazed erythema
Sparing of skin folds
Can ulcerate if left untreated/diarrhoea occurs
Wrinkled scaly appearance during resolution

216
Q

How is irritant contact napkin dermatitis treated?

A 
Frequent nappy changes 
Avoid soap/wipes
Greasy zinc-based emollient 
Topical steroid/antifungal cream if very inflamed
Anti-yeast if candida infection
217
Q

How does candida associated with irritant contact napkin dermatitis present?

A

Satellite papules and pustules which spread to flexures

218
Q

Give 3 features of vulvitis

A

Pre-pubertal girls
Localised eczema
Atopic children
Itch, erythema, discharge, stinging passing urine

219
Q

Why is candidiasis not a probable differential in young girls?

A

pH of vulval skin before puberty does not support candidal overgrowth

220
Q

How is vulvitis managed?

A

Cotton underwear
Avoid tights and soap/wipes
Greasy zinc-based emollient
Topical steroid cream if very inflamed

221
Q

How is lick lip dermatitis managed?

A

Greasy emollient

Topical steroid with anti-yeast when red

222
Q

How does pityriasis alba present?

A 
Hypopigmentation 
Dry rough skin on cheeks of atopic children 
4-12 year olds 
Coloured skin
Patchy and poorly demarcated
223
Q

How is pityriasis alba managed?

A

Emollients

Sunscreen (prevent surrounding skin tanning which makes it more obvious)

224
Q

Give 3 features of juvenile plantar dermatosis

A 
Affects anterior plantar surface 
Predominantly boys
Onset 4-7 years, resolves with puberty 
Main trigger is sweating 
Worse in winter 
Erythema, hyperkeratosis and fissuring
225
Q

How is juvenile plantar dermatosis treated?

A

Avoid occlusive footwear/synthetic socks
Aluminium hydrochloride powder can reduce sweating
Emollients and topical steroids

226
Q

What area should be carefully managed if affected by HSV skin infection and why?

A

Periorbital

Check eyes for corneal involvement as it can cause scarring

227
Q

What organism commonly causes impetigo?

A

Staphylococcus aureus

228
Q

How does impetigo present?

A

Annular erythematous lesions with honey coloured crust

May become bullous if epidermis is exfoliated by staph

229
Q

How is impetigo managed?

A

Reduce spread
Topical antiseptic
Topical/oral antibiotics (flucloxacillin)

230
Q

How does molluscum contagiosum present?

A

Small pearly umbilicated papules

231
Q

What causes molluscum contagiosum?

A

DNA pox virus

232
Q

How is molluscum contagiosum treated?

A

Usually resolve spontaneously
Topical antiseptics to avoid infection
Can be physically/chemically irritated to clear

233
Q

How does scabies present in children?

A

Extremely itchy rash
Burrows may be seen on the soles of the feet
Nodules may be seen in warm/moist areas (e.g. axilla, groin)

234
Q

What organisms cause tinea capitis?

A

Trichophyton tonsurans

Microsporum canis

235
Q

How does tinea capitis present?

A

Diffuse scale/patchy alopecia with black dots (broken hairs) or widespread pustules with associated lymphadenopathy

236
Q

How is tinea capitis managed?

A

Terbinafine (unlicensed)

Ketoconazole shampoo prevents spread to other children

237
Q

Give 4 common dermatological conditions seen in newborns

A 
Sebaceous hyperplasia
Milia
Miliaria
Naevus flammeus
Mongolion/blue spot 
Congenital melanocytic naevi
Haemangiomas
Capillary malformations/port wine stain
Urticaria
238
Q

What causes sebaceous hyperplasia, what does it look like and how is it managed?

A

Hypertrophy of sebaceous glands due to maternal androgens
Yellow/white pinpoint lesions clustered around the nose
Resolves spontaneously in 4-6 weeks

239
Q

What is milia, what does it look like and how is it managed?

A

Epidermal inclusion cysts
Discrete white/yellow papules on chin/cheeks/forehead/mouth/genitalia
Spontaneously resolve in few weeks

240
Q

What are the 2 types of miliaria, what do they look like and what is their cause?

A

Crystalina - clear vesicles which may wipe away; superficial duct obstruction and trapping of sweat
Rubra - erythematous papules/pustules over head/neck/trunk; deep obstruction of sweat ducts

241
Q

What is a naevus flammeus and where does it most commonly occur?

A

Capillary vascular malformation

Nape of neck (persist)/face (fade)

242
Q

What causes the blue colour of Mongolion spots and when do they resolve?

A

Deep dermal melanocytes

Resolve within 4 years

243
Q

Give 3 features of congenital melanocytic naevi

A

Macular area of pigmentation
Colour varies from light brown to near black
Scalp lesions may disappear with time and overlying hair may be hyperpigemented/thicker

244
Q

What are the complications of congenital melanocytic naevi?

A

Risk of melanoma in very large naevi >25cm is 5-14%

Naevi overlying spine or skull may be associated with neurological pathology

245
Q

How are congenital melanocytic naevi managed?

A

Cover and sunscreen
Monitoring advice
Can excise if monitoring difficult or cosmetically visible

246
Q

Why might dermabrasion/cutterage in first few weeks of life be counterintuitive?

A

Theoretically by reducing the melanocytic load it could reduce the risk of malignant transformation but by leaving only the deeper melanocytes it may mask the appearance of melanoma

247
Q

Give 2 features of epidermal naevi

A

Linear plaques of warty pigmented skin along Blaschko’s lines
Become darker and more verrucous with age
May be uni/bilateral

248
Q

What are Blaschko’s lines?

A

Lines of normal cell development in the skin

249
Q

Give 3 features of sebaceous naevi

A

Predominantly on scalp and face
Usually flat and pale at birth with waxy smooth surface
Can darken and become verrucous over time, especially behind ears
May develop into secondary tumours after puberty
Most are benign

250
Q

How are sebaceous naevi managed?

A

Excise for cosmesis

CO2 resurfacing laser and dermabrasion can be used to flatten but scarring and recurrence common

251
Q

How are vascular anomalies classified?

A

Vasclar tumours - infantile haemangioma

Vascular malformation - fast flow, slow flow, combined

252
Q

Name 2 infantile haemangiomas

A

Kaposiform haemangioendothelioma (HE)
Tufted angioma (TA)
Rapidly involuting congenital haemangioma (RICH )
Non-involuting congenital haemangioma (NICH)

253
Q

Name a fast flow, slow flow and combined vascular malformation

A

Fast - arterial, arteriovenous fistula, arterial venous malformation
Slow - venous, lymphatic, capillary
Combined - CLM, CVM, CLVM, LVM, CAVM,

254
Q

What are the risk factors for infantile haemangiomas?

A

Female
Preterm
Low birth weight
Twin pregnancies

255
Q

How do infantile haemangiomas present?

A

Within first 6 weeks
Preceded by bruising/telangiectasia/pallor
Superficial, deep or mixed
Grow rapidly for 6 week to 6 months and then very slowly involute

256
Q

How do infantile haemangiomas involute?

A

Darkening of superficial redness
Slow breaking up of colour starting from the centre
Softening and flattening of deep component
Deep component need fibrofatty tissue/lax skin surgically removed

257
Q

Give 2 features of segmental haemangiomas

A

Large
Plaques
Associated with underlying visceral lesions/abnormalities related to their location

258
Q

What are the complications of segmental haemangiomas and how are they treated?

A

Ulceration - beta-blocker (3 months)
Infection - antibiotics
Bleeding - pressure for 10-15 minutes
Obstruction of visual axis or airway - beta-blocker (12-18 months)

259
Q

Give 2 features of capillary malformations/port wine stain

A

Present at birth
Size remains constant
Occur anywhere on the body
Bright red initially, violaceous with time

260
Q

What should be considered if a port wine stain overlies the V1 distribution of the facial nerve?

A

Sturge Weber syndrome - neurological and ocular complications

261
Q

What is Klippel-Trenaunay syndrome?

A

Capillary malformation associated with lymphatic and venous malformation
Limb overgrowth may occur

262
Q

Give 4 triggers for urticaria

A 
Infection 
Infestation - worms 
Injection - drugs, blood, vaccination
Ingestion - drugs, food 
Inhalation - pollen, mould
263
Q

Over what duration is urticaria classed as being acute?

A

<6-8 weeks

264
Q

How is urticaria managed?

A

Chlorpheniramine (and antihistamine if >6 months)

265
Q

How much fluid/milk do neonates need per day?

A

150 ml/kg/day

266
Q

How are fluids prescribed in children?

A

421 rule
First 10kg = 4ml/kg/hr
Next 10kg = 2ml/kg/hr
Rest = 1ml/kg/hr

267
Q

What are the daily requirements for Na, Cl and K?

A

Na 2-4 mmol/kg/day
Cl 2-4 mmol/kg/day
K 1-2 mmol/kg/day

268
Q

Give 3 important features to ask about when a baby presents with vomiting

A 
Bilious 
Projectile
Feeding 
Weight gain
Fever
Rash
269
Q

How do oz of milk equate with mls?

A

1 oz = 30mls

270
Q

Give 4 causes of a vomiting baby

A 
Overfeeding 
Posseting
GORD
Pyloric stenosis 
Obstruction
271
Q

At what age does pyloric stenosis present and what factors make it more likely?

A

2-6 weeks

Male, FH

272
Q

How does pyloric stenosis present?

A 
Rapidly progressive projectile vomiting
Soon after feeds 
No bile 
Hungry baby 
Acute weight loss 
Dehydration 
Hypochloraemic hypokalaemic metabolic alkalosis
273
Q

How is pyloric stenosis diagnosed and managed?

A

Diagnosis - test feed (visible peristalsis and palpable olive in RUQ), USS
Management - correct electrolyte imbalance, pyloromyotomy

274
Q

Give 3 causes of bilious vomiting in a baby

A 
Malrotation +/- volvulus
Necrotising enterocolitis 
Atresia
Hirschsprungs 
Meconium ileus/plug
275
Q

What causes malrotation?

A

Failure of intestinal rotation (270 degrees) and fixation which should occur at week 4-12 of gestation

276
Q

What is the most common abnormality with malrotation?

A

Caecum lies close to DJ flexure resulting in abnormally narrow midgut mesentery which is liable to twist (volvulus)

277
Q

How does malrotation present?

A

Early - collapse and acidosis due to intestinal infarction

Late - bile stained vomit and distension

278
Q

How is malrotation diagnosed and managed?

A

Barium contrast studies

Resuscitation and laparotomy

279
Q

What is necrotising enterocolitis?

A

Acute inflammatory disease occurring in the intestines of premature infants which can lead to necrosis of the bowel

280
Q

How does necrotising enterocolitis present?

A 
Abdominal distension
Blood in stool 
Feeding intolerance 
Vomiting (bilious)
Pyrexia
281
Q

How is necrotising enterocolitis managed?

A

Conservative - stop feeds, give IV fluids and antibiotics

Needs surgery if severe - bowel resection and stoma formation

282
Q

What is intestinal atresia?

A

Congenital malformation resulting in narrowing/absence of a segment of intestine

283
Q

What is the most common site for intestinal atresia?

A

Ileum and jejunum

284
Q

What condition is associated with duodenal atresia?

A

Down’s syndrome

285
Q

Give 3 features of Hirschsprungs

A

Aganglionic section of bowel
Starts at anus and progresses upwards
Causes bowel obstruction
Often presents with delayed passage of meconium
Can present late with distension, constipation, failure to thrive and obstruction

286
Q

Give 3 things to ask about in acute abdomen

A 
SOCRATES pain
Urinary/bowel symptoms 
LMP in girls 
Last meal 
DH and allergies
287
Q

Give 3 differentials for acute abdomen in children

A 
Acute appendicitis
Mesenteric adenitis
Constipation
Gastroenteritis
UTI
288
Q

Give 3 features of acute appendicitis on abdominal x-ray

A

Scoliosis due to pain
Faecolith
Absent right psoas shadow
Intraperitoneal gas indicating perforation
Abnormal caecal gas or small bowel dilatation

289
Q

What is intussusception?

A

Full thickness invagination of proximal into distal bowl

Telescoping

290
Q

Where does intussusception most commonly occur and why?

A

Ileo-colic

Enlarged Peyer’s patches due to viral illness/Meckel’s diverticulum

291
Q

Give 2 conditions associated with intussusception in older children

A

HSP
Lymphoma
CF

292
Q

What is the classic triad of intussusception symptoms?

A

Severe intermittent abdominal pain
Redcurrant jelly stools
Vomiting

293
Q

What imaging modalities are available for intussusception, what do they show and which is better?

A

Abdominal x-ray - absence of air and soft tissue density in ascending colon
Abdominal USS* - target lesion/doughnut sign

294
Q

How is intussusception diagnosed and managed?

A

Contrast enema can do both

May need surgery

295
Q

What is a hernia?

A

Protrusion of a viscus/part of a viscus into a cavity where it should not lie

296
Q

How are incarcerated hernias managed?

A

Resuscitate
Reduce
Repair

297
Q

What are the risk factors of hernias in neonates?

A

Male
Premature
LBW

298
Q

What is a hydrocele?

A

Fluid in the scrotum due to a patent processus vaginalis

299
Q

Give 2 features of a hydrocele

A 
Noticed with systemic illness
Can have a blue hue 
Can get above it on examination 
Transilluminates 
Most resolve spontaneously in first year of life
300
Q

What is the management pathway for undescended testes?

A

Detected at baby check/8 week check –> referred as outpatient to surgeon –> surgical correction before first birthday

301
Q

Give 3 causes of an acute scrotum

A

Testicular torsion
Torsion of the appendage (hydatid of Morgagni)
Epididymo-orchitis
Hydrocele (rarely painful)
Idopathic scrotal oedema (rarely painful)

302
Q

What is the difference in pain of testicular torsion, appendage torsion and epididymo-orchitis?

A

TT - sudden, severe
AT - gradual over 2-3 days
EO - gradual, less severe

303
Q

What is the difference in examination of testicular torsion, appendage torsion and epididymo-orchitis?

A

TT - high riding, swollen, hard, red, tender
AT - localised to upper scrotum, blue spot, hydrocele
EO - swelling, red, oedema

304
Q

What are the 2 peaks of age for testicular torsion?

A

0-2 and 10-15 years

305
Q

At what fluid resuscitation requirement following trauma should a surgeon be called?

A

> 40ml/kg

306
Q

Give 3 anatomical features of children which need to be considered in trauma situations

A 
Small body size 
Large surface area 
Relatively large head 
Compliant elastic skeleton 
Airway differences (small cavity, large tongue, short trachea, <6m are nose breathers)
307
Q

What are the 5 principles of a primary survey?

A

Airway and C-spine
Breathing – look listen feel; administer O2
Circulation; HR BP CRT; IV access, bloods
Disability – GCS (modified) /AVPU
Exposure - remember hypothermia and glucose

308
Q

How can a child’s weight be estimated for calculation of fluid/drug doses?

A

Weight = (age + 4) x 2

Weight at birth average 3.5kg, 6 months 7.5kg and 1 year 10kg, gain 2kg a year after that

309
Q

Give 3 features to ask about when a child presents with head injury

A 
Mechanism 
Vomiting 
LOC
Amnesia
Other injuries 
NAI
310
Q

Give 3 things to check on examination when a child presents with head injury

A 
GCS/AVPU
HR and BP
Head examination - boggy haematoma 
Signs of skull fracture 
Neurological examination
311
Q

Give 6 indications for head CT on head injury in children

A

Witnessed loss of consciousness >5 minutes
Amnesia (antegrade or retrograde) >5 minutes
Abnormal drowsiness
≥3 Discrete episodes of vomiting
Clinical suspicion of non-accidental injury
Post-traumatic seizure (no PMH of epilepsy)
GCS <14 in emergency room (Paediatric GCS <15 if aged <1)
Suspected open or depressed skull fracture or tense fontanelle
Signs of base of skull fracture
Focal neurological deficit
Aged <1 - bruise, swelling or laceration on head >5 cm
Dangerous mechanism of injury (high-speed RTA, fall from >3 m, high-speed projectile)

312
Q

Define amblyopia

A

Poor vision in a structurally normal eye

E.g. if image from one eye is clearer, the brain will switch off the other blurrier eye and cause visual loss

313
Q

By what age is most visual development complete?

A

7 years

314
Q

Give 2 causes of amblyopia

A

Reduced view through eye - ptosis, cataract
Unequal focus - one eye more long/short sighted (anisometropia)
Misalignment of eyes - squint

315
Q

How is amblyopia treated?

A

Occluding patch over stronger eye

Atropine eye drops

316
Q

What are the 2 types of squint?

A

Inwards/esotropia/convergent

Outwards/exotropia/divergent

317
Q

What is an important differentials to consider for squint?

A

Eye movement syndromes

Cranial nerve palsies

318
Q

How is a squint managed?

A

Glasses (correct long-sightedness)

319
Q

How do you know if a squint is fully or partially accommodative?

A

Fully - will correct fully with glasses

Partially - only partially corrected with glasses

320
Q

Give 2 causes of leukocoria

A 
Cataract
Retinoblastoma 
Retinal detachment 
Toxoplasmosis 
Uveitis
321
Q

What may be seen on examination of the eye in NF1?

A

Lisch nodules

322
Q

What may be seen on examination of the eye in albinism?

A

Iris transillumination

323
Q

What may be seen on examination of the eye in Marfan’s syndrome?

A

Dislocated lens

324
Q

What may be seen on examination of the eye in JIA?

A

Anterior uveitis

325
Q

What is nasolacrimal duct obstruction?

A

Incomplete canalisation of the duct causing a sticky watery eye in the absence of conjunctivitis; resolves by 1 year

326
Q

What is the most common type of permanent deafness?

A

Sensorineural

327
Q

How are neonates screened for deafness?

A

Auditory brainstem response (ABR) screening

328
Q

Give 3 acquired causes of deafness

A

Prenatal - toxoplasma, rubella, CMV
Perinatal - hypoxia, kernicterus, aminoglycoside antibiotics
Postnatal - meningitis, head injury, ototoxic drugs (e.g. cisplatin, antibiotics)

329
Q

Give 2 congenital causes of deafness

A

Syndromic - Usher’s, Pendred’s, branchio-oto-renal, Jervell and Lange-Nielsen, Stickler’s
Non-syndromic - AR mutation in connexin 26 gap junction protein gene

330
Q

How is deafness managed?

A

Cochlear implantation

331
Q

What condition can cause a transient conductive deafness?

A

Otitis media with effusion (glue ear)

332
Q

When is glue ear considered pathological?

A

Mucus fluid present for >3 months

333
Q

How does the tympanic membrane look on examination in otitis media with effusion?

A

Dull
Retracted
Yellow/grey colour

334
Q

How does conductive hearing impairment due to OME present?

A

Speech delay

335
Q

How is hearing investigated in OME?

A

Audiometry - excludes sensorineural

Tympanometry - fluid pressure

336
Q

How is OME managed?

A

Watch and wait
Grommet insertion
Removal of adenoids

337
Q

What are the signs/symptoms of tonsillitis?

A 
Prolonged sore throat 
Tonsillar exudate 
Fever
Cervical lymphadenopathy 
Malaise
338
Q

When is tonsillectomy advised for tonsillitis?

A

5 episodes per year over 2 years or 7 episodes in 1 year

339
Q

What is the most common cause of nasal obstruction in pre-school children and what are its associations?

A

Physiological hypertrophy of adenoids

Snoring and green rhinorrhoea

340
Q

When do adenoids spontaneously shrink?

A

6 years old

341
Q

How is nasal obstruction due to adenoids managed?

A

Saline nasal douches

Adenoidectomy (severe)

342
Q

What is the most common cause of nasal obstruction in school children and what are its associations?

A

Allergic rhinitis

Sneezing and clear rhinorrhoea

343
Q

How is allergic rhinitis managed?

A

Topical nasal steroid spray

Oral non-sedating antihistamine

344
Q

What is the most important thing to ask in the history of nasal obstruction?

A

Sleep quality

345
Q

What can cause obstructive sleep apnoea in children aged 2-7?

A

Physiological hypertrophy of tonsils and adenoids

346
Q

How can OSA be diagnosed?

A

Sleep studies - overnight pulse oximetry/12 channel polysomnography

347
Q

Give 3 points to ask about in a sleep history when OSA is suspected

A 
Sleep quality 
Snoring 
Breath holding during sleep 
Waking during the night 
Restless/sweaty at night
348
Q

Give 3 causes of chronic stridor

A

Laryngomalacia (benign, self-limiting)
Subglottic stenosis
Airway haemangioma
Tracheal stenosis

349
Q

How is the cause of chronic stridor established?

A

Airway endoscopy

350
Q

Give 2 causes of lumps/bumps in the head and neck area

A

Branchial lesions
Thyroglossal cysts
Dermoids

351
Q

What is the most common cause of cervical lymphadenopathy?

A

Reactive lymphoid hyperplasia (infection)

352
Q

What 2 types of cancer are common in the head and neck of children?

A

Lymphoma

Rhabdomyosarcoma

353
Q

From what sources can information be gathered when carrying out a psychiatric assessment?

A 
Interview parents/carers
FH, PMH, PH
Interview and observe child 
Other assessments - community paediatrics, psychologist, SLT, OT
Educational attainment
354
Q

What contextual factors should be taken into account for psychiatric assessment?

A 
Ability of parent to meet child's needs 
Parental mental health 
Child's relationships with other family members
Child's home environment 
Major life events
355
Q

What are the 2 main groups of mental disorder a child may present with? Give examples

A

Internalising/emotional behaviour disorder (e.g. phobias, OCD, depression, psychosomatic complaints)
Externalising/disruptive behaviour disorder (e.g. ADHD, conduct disorder, oppositional defiant disorder)

356
Q

What are the biopsychosocial features of ADHD?

A

Restlessness, overactivity, inattentiveness, impulsivity
Poor self-esteem, low mood, learning difficulties
Poor peer and family relationships

357
Q

How can ADHD be managed?

A

Stimulant (methylphenidate) or non-stimulant medication
Therapy - individual, family
Clubs/activities

358
Q

How is ADHD diagnosed?

A

Careful evaluation of full history and observation

Features must occur in >1 setting

359
Q

What is conduct disorder?

A

Group of behavioural problems where a child is aggressive (verbal or physical), antisocial and defiant to a much greater degree than expected for their age

360
Q

What are the features of conduct disorder?

A

Violation of rights of others and social norms
Fighting and physical cruelty (people and animals)
Destructiveness (usually of property)
Lying and stealing
Violation of rules (e.g. truancy, running away from home)

361
Q

What is the relevance of age in conduct disorder?

A

<10 years old = early onset conduct disorder

>10 years old = adolescent onset conduct disorder

362
Q

What are the risk factors for conduct disorder?

A

Genetic - parent with antisocial personality disorder/who had CD
Individual - difficult temperament
Physical - problems processing social information/cues (e.g. disability, brain injury)
Environmental - family/parenting problems, deprived area
Emotional - depression, isolation

363
Q

How are conduct disorders managed?

A

Group based parent training/education programmes

CBT

364
Q

What is reactive attachment disorder (RAD)?

A

Hypersensitive to changes in their environmental circumstances due to their adverse early life experiences

365
Q

What are the features of RAD?

A

Lack of emotional responsiveness
Fearfulness and hypervigilance
Aggressive or defiant behaviour
Inhibition or hesitancy in social interactions
Disinhibition or inappropriate familiarity or closeness with strangers
RAD may be accompanying disorder of a child who shows a failure to thrive

366
Q

What is the most common type of mental health disorder in children?

A

Anxiety disorders

367
Q

What is PANDAS?

A

Paediatric autoimmune neuropsychiatric disorders associated with strep (A infection) - can cause OCD which presents suddenly

368
Q

Give 7 signs/symptoms of depression in children

A

Appearing unhappy much of the time
Outbursts of shouting, crying or unexplained irritability
Having poor self-esteem, guilt or recurrent feelings of worthlessness
Loss of interest/lack of pleasure in enjoyable activities
Suicidal thoughts
Spending a lot of time in bed but sleeping badly and experiencing early morning awakening
Major changes in weight and appetite
Headaches, stomach aches, tiredness and other vague physical complaints that appear to have no obvious cause.

369
Q

When is medication used to treat depression in children?

A

Severe cases

370
Q

Give 3 conditions associated with autism spectrum disorder

A 
Depression
Anxiety disorders (social, OCD) ADHD
Learning disability
Epilepsy
GI (IBS)
Tourette’s 
Genetic disorders
371
Q

What is the ASD triad of impairment?

A

Social interaction
Social communication
Stereotyped behaviour/sensory sensitivites/restricted interests

372
Q

What is the difference between autism and Asperger’s syndrome?

A

Asperger’s syndrome - IQ is at least average and there was no language delay in early childhood
Autism - IQ can be anywhere on the scale and there is a history of language delay

373
Q

How is ASD managed?

A 
Behavioural interventions
SLT
Appropriate schooling
OT
Medication for anxiety/aggression
Education
374
Q

What are tics?

A

Tics are sudden, involuntary, non-rhythmic motor movements or vocal productions which are purposeless, happen rapidly and are often repetitive in nature

375
Q

What types of tics exist?

A

Simple motor - blinking, twitching
Complex motor - facial grimace and head twist
Simple vocal - grunt, cough
Complex vocal - full words/sentences

376
Q

What is Tourette’s?

A

Combined vocal and motor tic disorder that can often persist into adult life

377
Q

Give 2 behaviours occurring in anorexia nervosa

A 
Intense fear of weight gain
Obsession with eating
Weighs self repeatedly
State they are overweight and exercise excessively
Counts or portions food carefully and may only eat certain foods
Increased consumption of liquids
Rigid meal or eating rituals
May refuse to eat in front of others
378
Q

What are the physical signs/symptoms of anorexia?

A

Weight loss
Cessation of growth/arrested pubertal development
Osteopenia
Lanugo body hair, brittle nails and hair, dry skin
Constipation/abdominal discomfort

379
Q

What biopsychosocial developmental changes occur in early adolescence?

A

Bio - males (testicular enlargement), females (breast buds, pubic hair development)
Psych - concrete thinking, moral concepts, awareness of sexual identity
Soc - emotional separation from parents, peer identification, exploratory behaviours

380
Q

What biopsychosocial developmental changes occur in mid adolescence?

A

Bio - males (sperm production, voice breaks, growth spurt), girls (menarche, change in body shape)
Psych - abstract thinking, believe they are immortal, increasing verbal dexterity, fervent ideology
Soc - continuing parental separation, heterosexual peer interest, early vocational plans

381
Q

What biopsychosocial developmental changes occur in late adolescence?

A

Bio - males (continued growth in height)
Psych - complex abstract thinking, increased impulse control, development of personal identity
Soc - social autonomy, develop intimate relationships, develop financial independence

382
Q

What tool should be used to take a history from an adolescent?

A 
HEADS
H - home life
E - education
A - activities
D - drinking, driving, drugs 
S - sex, smoking, suicide
383
Q

What is the sequence of puberty in females?

A

Breast development (8-12 years) -> pubic hair growth -> rapid growth spurt -> menarche (2.5 years after puberty starts)

384
Q

What is the sequence of puberty in males?

A

Testicular enlargement -> pubic hair growth (10-14 years) -> height spurt (1.5 years after puberty starts)

385
Q

Define delayed puberty

A

Absence of pubertal development by age 14 in girls and 15 in boys
More common and benign in boys

386
Q

Give 2 causes of delayed puberty

A 
Constitutional delay 
Hypogonadotrophic hypogonadism (Crohn's, CF, anorexia, intracranial tumour, panhypopituitarism)
Hypergonadotrophic hypogonadism (Turner/Klinefelter syndrome, trauma, chemotherapy, torsion)
387
Q

How is delayed puberty assessed?

A

Male - pubertal staging, growth parameters, exclude chronic systemic disease
Female - pubertal staging, growth parameters, karyotype, thyroid hormone, sex hormones

388
Q

How is delayed puberty managed?

A

Reassurance
Male - oxandrolone/low dose testosterone
Female - oestradiol

389
Q

Give 2 concerning features when considering sexual health of adolescents

A 
Age <13 years 
Power imbalance 
Coercion
Substance misuse 
Risk
390
Q

Give 2 risk factors for STIs in adolescents

A

Avoidance of barrier contraception
Multiple partners
Mental illness
Substance misuse

391
Q

Give 2 risk factors for substance misuse in adolescents

A 
Conduct disorder 
Poor parenting 
Early experience of substance misuse 
Peer group pressure 
Poor social environment
392
Q

Give 2 negative effects of chronic illness in adolescents

A 
Constitutional delay in growth/puberty 
Negative self-image 
Low mood
Poor school attainment 
Poor peer development
393
Q

How can transition from paediatric to adolescent services be optimised?

A 
Inform adolescent and parents early 
Run specific teenage clinic
Involve GP to maintain continuity 
Encourage adolescent to take charge 
Support and educate parents to allow adolescent to take over
394
Q

In what situation would it be necessary to administer a drug by IM injection (which is usually avoided where possible due to pain)?

A

Benzylpenicillin should be given IM by GP in suspected meningococcal sepsis

395
Q

Other than according to age and weight, how else can medications doses be prescribed?

A

Body surface area (e.g. aciclovir) using Boyd equation (back of BNF)

396
Q

How does drug absorption differ in babies?

A

Gastric and bile acid secretion and intestinal motility are reduced in babies which affects bioavailability especially of acidic drugs

397
Q

How does drug distribution differ in young children?

A

Higher percentage body weight is water and there is reduced plasma protein binding due to low albumin so higher doses of water soluble drugs are needed

398
Q

How does drug metabolism differ in babies?

A 
Immature liver enzymes 
Conjugation reactions (e.g. oxidation) are not developed until 1 year (limits drugs which can be used before 1 year)
399
Q

How does drug metabolism differ in children 1-12 years old?

A

Faster than adults until 2 years and then slowly declines

May need to increase dose or frequency for drugs which undergo hepatic metabolism

400
Q

How does drug excretion differ in babies and children?

A

Increased half-lives of renally excreted drugs; renal function complete at 6-8 months

401
Q

Under what circumstances does a man have parental rights?

A

If they are listed on the birth certificate

If they are married to the child’s mother

402
Q

Who has parental rights in a same sex partnership?

A

Both if they were civil partners at time of conception

If not, they can apply for parental responsibility

403
Q

At what age would a young person be considered unable to consent to sex and therefore it be considered statutory rape?

A

13 years of age

Year 5 (10 decks)

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