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Phase 3A > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Most common cause of pneumonia in newborns

A

group B streptococcus from mothers genital tract

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2
Q

most common cause of pneumonia in infants

A

RSV

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3
Q

most common causes of pneumonia in children > 5

A

Mycoplasma pneumoniae, streptococcus pneumoniae and chlamydia pneumoniae

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4
Q

what vaccines in the childhood immunisation protect from pneumonia

A

6 in 1 vaccines (haemophilus influenzae B)

Pneumococcal PCV vaccine (streptococcus pneumoniae)

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5
Q

most important examination finding in pneumonia for paeds

A

tachypnoea

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6
Q

antibiotic management of pneumonia in paediatrics

A

 New-born: broad spectrum IV antibiotics
 Older infants: oral amoxicillin, broad spectrum antibiotics e.g. co-amoxiclav if unresponsive
 Child > 5: amoxicillin or an oral macrolide e.g. erythromycin

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7
Q

main symptoms of croup

A

hoarse cry and barking cough

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8
Q

main causative organism in croup

A

parainfluenza viruses 1 - 4

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9
Q

peak age incidence in croup

A

2 years old

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10
Q

first line management of croup

A

150mcg/kg oral dexamethasone; single dose

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11
Q

list the 9 causes of wheeze in children

A 
- viral induced wheeze
o	Atopic asthma (IgE mediated)
o	Non atopic asthma 
o	Recurrent aspiration of feeds 
o	Inhaled foreign body 
o	Cystic fibrosus 
o	Recurrent anaphylaxis of child with food allergies 
o	Congenital abnormality of lungs, airway or heart 
o	Idiopathic
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12
Q

what should you not do in a child with epiglotittis

A

lie them down or use tongue depressor as it can cause total airway obstruction

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13
Q

key symptoms of epiglottitis

A 
acute onset 
unwell looking child 
sat upright, immobile, mouth open 
painful to speak and swallow (muffled voice, hoarse cry)
soft stridor
high temperature
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14
Q

peak incidence of bronchiolitis

A

3 - 6 months

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15
Q

most common causative pathogen of bronchiolitis

A

RSV

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16
Q

presentation of bronchiolitis (main symptoms)

A

preceded by coryzal symptoms
persistent cough
tachypnoea and chest recession
fine inspiratory crackles and wheeze

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17
Q

differential diagnosis for bronchiolitis

A 
viral wheeze (esp. if no crackles)
pneumonia (esp. if temperature above 39)
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18
Q

risk factors for bronchiolitis

A

premature birth + bronchopulmonary dysplasia
chronic lung disease e.g. CF
congenital heart disease
severe combined immunodeficiency syndrome

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19
Q

Prevention of bronchiolitis

A

monoclonal RSV antibody to those at high risk

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20
Q

cystic fibrosis epidemiology

A

1 in 2500 caucasian live births

1 in 25 carriers

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21
Q

cystic fibrosis pathophysiology

A

mutation in CFTR gene leads to defects in protein and abnormal ion transport. Chloride ions are not pumped out into secretions so water is not drawn in and secretions are viscous

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22
Q

presentation of CF in newborns

A

screening

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23
Q

presentation of CF in infants

A 
meconium ileus in neonatal period
prolonged neonatal jaundice
failure to thrive 
malabsorption and steatorrhea 
recurrent chest infections
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24
Q

presentation of CF in young children

A

bronchiectasis
nasal polyps
sinusitis
rectal prolapse

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25
Q

presentation of CF in older children and adolescence

A 
allergic bronchopulmonary aspergillosis 
diabetes mellitus 
cirrhosis and portal hypertension 
distal intestinal obstruction
pneumothorax or recurrent haemoptysis
infertility in males
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26
Q

diagnosis of CF is done through which test

A

sweat test: chloride ions > 60mmol/L on 2 occasions

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27
Q

Management of CF

A

multidisciplinary
annual reviews, look at FEV1 to monitor progression
respiratory: prophylactic and rescue antibiotics, physiotherapy, nebulised hypertonic saline
nutritional: high calorie, fat soluble vitamins, oral enteric coated pancreatic replacement therapy
psychological management

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28
Q

kawasaki disease peak incidence

A

second half of the first year of life

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29
Q

Presentation of kawasaki disease

A

Fever for 5 or more days + 4 of the following 5

  • bilateral dry conjunctivitis
  • inflammation of the lips, mouth or tongue
  • non-vesicular rash
  • erythrma, swelling or desquamation to skin extremities
  • cervical lymphadenopathy
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30
Q

Medical Management of kawasaki disease and dose

A

IVIG: 2g/kg in a single infusion over 12 hours

aspirin

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31
Q

what follow up treatment is required for kawasaki disease and why

A

Echocardiogram to look for cardiac artery aneurysms

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32
Q

common causes of bacterial meningitis in neonates

A

group b strep
E. coli
listeria monocytogenes

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33
Q

common causes of bacterial meningitis in infants and chilldren

A

Neisseria meningitidis, streptococcus pneumoniae, HiB

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34
Q

Common presenting features for meningitis

A 
unwell child 
non-blanching petechial/purpuric rash 
neck stiffness
bulging fontanelle in infants 
photophobia 
altered mental state 
kernig's and brudzinski's signs
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35
Q

investigations for suspected meningitis

A

LP - CSF analysis
Also: full blood count, CXR, Urine dipstick + culture, blood culture U+E (septic screen)
Others: glucose, blood gases, coagulation screen, whole blood PCR for N.meningitidis

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36
Q

management of meningitis overview

A

supportive treatment: antipyretics, antiemetics, fluids
antibiotics
treat complications

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37
Q

Management of bacterial meningitis

A

Primary care: IM/IV benzylpenicillin (<1 300mg, 1-9: 600mg; 10+:1200mg)

Dexamethasone if over 3 months

blind antibiotic: IV ceftriaxone (cefotaxime + amoxicillin if under 3 months)

Specific antibiotic regimen depending on pathogen

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38
Q

antibiotic management of meningococcal meningitis

A

IV ceftriaxone for at least 7 days; prophylactic ciprofloxacin or rifampicin for close contacts

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39
Q

most common type of leukaemia in children

A

acute lymphoblastic leukaemia

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40
Q

peak presentation of ALL

A

age 2 - 5

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41
Q

signs and symptoms of ALL

A

general: malaise, anorexia
bone marrow infiltration: anaemia - pallor, lethargy; recurrent infections; bruising; bone pain
reticulo-endothelial infiltration: hepatoslenomegaly, lymphadenopathy, superior mediastinal obstruction
other organ involvement: CNS - vomiting, nerve palsies, headache; testicular enlargement

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42
Q

ALL investigations

A

FBC, blood smear, bone marrow examination

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43
Q

ALL management

A
  1. correct anaemia, infections, low platelet count
  2. remission induction: 4 weeks of combination chemotherapy
  3. consolidation + CNS protection
  4. interim maintenance
  5. delayed intensification
  6. continued maintenance
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44
Q

ALL relapse management

A

high dose chemotherapy, total body irradiation, bone marrow transplant

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45
Q

poor prognostic ALL markers

A 
age less than 1 or more than 10
being male 
high WCC load: >50x10^9
MLL rearrangement, translocation 4,11; hypodiploidy <44
persistence after initial chemotherapy 
high minimal residual disease assessment
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46
Q

Types of paediatric brain tumours

A

astrocytoma: benign to highly malignant (glioblastoma multiforme)
medulloblastoma, ependymoma
brainstem glioma
craniopharyngioma: benign, (Rathke’s pouch)

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47
Q

clinical features of a brain tumour

A

raised intracranial pressure: headache, vomiting, behaviour and personality, seizures, visual disturbance, papilloedema

focal neuroligical signs

spinal: back pain, peripheral weakness, bladder and bowel dysfunction

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48
Q

which investigations should you perform and avoid in brain tumours

A

MRI

avoid LP if signs of ICP

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49
Q

management and late effects of brain tumours

A

surgery, chemotherapy/radiotherapy

late effects: neurological disability, endocrine and growth problems

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50
Q

neuroblastoma definition

A

cancer arising from neural crest tissue in adrenal glands and sympathetic chain

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51
Q

clinical features of neuroblastoma

A

weight loss, abdominal mass, hepatomegaly, bone pain, limp

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52
Q

symptoms of asthma

A

wheeze, chest tightness, shortness of breath, cough

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53
Q

drugs used in the management of asthma

A

bronchodilators: SABA (salbutamol), LABA (salmeterol), anticholinergic bronchodilators (ipratropium bromide)
inhaled corticosteroids: preventers
other therapies: leukotrine receptor antagonist, theophylline, oral prednisolone, anti IgE: omalizumab

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54
Q

step 1 of asthma management

A

SABA prn

consider ipratropium bromide in young children

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55
Q

step 2 of asthma management

A

add inhaled steroid

consider montelukast in under 5s if not tolerated

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56
Q

step 3 of asthma management

A

> 5: LABA, monteleukast or theophylline if no response

<5 montelukast

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57
Q

stage 4 of asthma management

A

> 5 increase to maximum dose of steroids

<5 refer to paediatrics

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58
Q

stage 5 of asthma management

A

paediatric referral
daily oral steroid use
immunosuppressant or immunomodulation

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59
Q

features of an innocent murmur

A 
asymptomatic 
soft 
systolic 
left sternal edge 
normal heart sounds, no thrills or radiation
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60
Q

types of left to right shunt and their %

A

ventricular septal defect 30%
atrial septal defect 7%
persistent ductus arteriosis 12%

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61
Q

types of right to left shunts and %

A

tetralogy of Fallot 5%

Transposition of the GA 5%

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62
Q

types of asymptomatic obstructive outflow %

A

pulmonary stenosis 7%

aortic stenosis 5%

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63
Q

types of symptomatic obstructive outflow

A

coarctation of the aorta 5%

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64
Q

types of common mixing heart defects

A

atrioventricular septal defect 2%

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65
Q

which heart defects are associated with Down’s syndrome

A

ventricular septal defect

atrioventricular septal defect

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66
Q

which heart defects are associated with Turner’s syndrome

A

coarctation of the aorta

aortic stenosis

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67
Q

which heart defects are associated with foetal alcohol syndrome

A

VSD, ASD, TOF

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68
Q

which heart defects are associated with maternal rubella or warfarin therapy

A

PDA, pulmonary stenosis

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69
Q

which heart defects are associated with William’s syndrome

A

pulmonary stenosis

aortic stenosis

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70
Q

which heart defects are associated with Noonan’s syndrome

A

AVSD, PS

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71
Q

VSD murmur

A

loud pansystolic at lower left sternal edge

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72
Q

PDA murmur

A

continuous murmur in left clavivle

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73
Q

ASD murmur

A

ejection systolic, upper left sternal edge

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74
Q

TOF murmur

A

harsh ejection systolic murmur at left sternal edge

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75
Q

PS murmur

A

 Ejection systolic murmur at upper left sternal edge

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76
Q

AS murmur

A

 Ejection systolic murmur maximal at upper right sternal edge –> neck

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77
Q

when do most cases of GORD resolve by

A

12 months

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78
Q

what are complications of GORD

A

failure to thrive from severe vomiting
oesophagitis leading to haematemesis, heartburn or anaemia
recurrent pulmonary aspiration –> recurrent pneumonia, cough, wheeze or apnoea in preterms
dystonic neck posturing (sandifer syndrome)

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79
Q

common presentation of GORD

A

regurgitation and vomiting

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80
Q

risk factors for severe GORD

A

cerebral palsy or other neurodevelopmental disorders

preterm infants (+brunchopulmonary dysplasia)

following oesophageal atresia or diaphragmatic hernia

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81
Q

investigations for gord

A

normally clinical

24hr oesophageal pH monitoring, endoscopy

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82
Q

management of gord

A

parental reassurance + thickening agents + head prone position 30degrees after feeds

significant gord: H2 receptor antagonists e.g. ranitidine or PPI e.g. omeprazole

surgical management for severe non-responsive cases

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83
Q

what is pyloric stenosis

A

hypertrophy of pyloric muscle causing gastric outlet obstruction

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84
Q

when does pyloric stenosis present

A

between 2 weeks and 7 weeks

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85
Q

risk factors for pyloric stenosis

A

being male

maternal family history

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86
Q

clinical features of pyloric stenosis

A

projectile vomiting, weight loss,

signs: visible gastric peristalsis, palpable mass (‘olive’ RUQ), dehydration

hyponatraemic, hypochloraemic, hypokalaemic metabolic acidosis

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87
Q

investigations for pyloric stenosis

A

test feed

USS

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88
Q

management of pyloric stenosis

A

rehydrate + restore electrolyte imbalance

surgery

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89
Q

what is colic

A

set of symptoms such as aroxysmal crying/screaming, knee up-drawing and excessive flatus
usually resolves by age 4

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90
Q

DD for colic

A

GORD, cow’s milk intolerance

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91
Q

causes of acute abdominal pain

A

surgical: appendicitis, obstruction, inguinal hernia, peritonitis, inflamed meckel diverticulum, pancreatitis, trauma
medical: gastroenteritis, UTI, henoch-schonlein purpura, DKA, constipation, hepatitis, IBD

extra abdominal: URTI, lower lobe pneumonia, testicular torsion, hip + spine

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92
Q

signs and symptoms of appendicitis

A

symptoms: anorexia, vomiting, pain
signs: flushed face, low grade fever, pain aggravated by movement, persistent tenderness + guarding (faecoliths in preschool children)

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93
Q

investigations in appendicitis

A

repeated observation and clinical review every few hours
WCC or organisms in urine
USS: thickened incompressible appendix with increased blood flow

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94
Q

management of uncomplicated appendicitis

A

appendicectomy

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95
Q

what are the features of complicated appendicitis

A

presence of mass, abscess or perforation

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96
Q

management of complicated appendicitis

A

fluid resuscitation, IV antibiotics before surgery

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97
Q

what is intussusception

A

invagination of proximal bowel into a distal segment

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98
Q

common area of intusussception

A

ileum to caecum through ileocaecal valve

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99
Q

peak age of presentation for intusussception

A

2 months and 2 years

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100
Q

what are complications of intusussception

A

venous obstruction –> bleeding from bowel mucosa, fluid loss, perforation, peritonitis and gut necrosis

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101
Q

presentation of intusussception

A

paroxysmal severe colicky pain, child becomes pale and draws up legs

refuse feeds, vomits (bile stained)

sausage shaped mass in abdomen

redcurrant jelly stools

abdominal distension and shock

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102
Q

investigations for intusussception

A

abdominal XR: distended small bowel, absence of gas in distal colon/rectum
USS

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103
Q

management

A

IV fluid resuscitation
rectal air insufflation if no signs of peritonitis
surgery

104
Q

what is Meckel diverticulum and what is the prevalence

A

ileal remnant of vitello-intestinal duct, contains ectopic gastric mucosa or pancreatic tissue

2%

105
Q

presentation of Meckel diverticulum

A

asymptomatic
severe rectal bleeding that’s neither bright red or malaena
other: intusussception, volvulus, diverticulitis

106
Q

investigations for meckel diverticulum

A

technetium scan

107
Q

treatment of Meckel diverticulum

A

surgical resection

108
Q

presentation of malrotation

A

bilous vomiting due to ladds bands across the duodenum or volvulus usually within 1st 3 days of life

abdominal pain and tenderness from peritonitis

109
Q

investigations for malrotation

A

upper GI contrast study

110
Q

treatment for malrotation

A

urgent surgical correction

111
Q

IBS symptoms/presentation

A

positive family history
associated with stress, anxiety/GI infection

abdominal pain relieved by defecation
bloating 
explosive, loose or mucousy stools 
feeling of incomplete defecation
constipation
112
Q

what is hirschsprung disease

A

absence of ganglion cells from myenteric and submucosal plexus part of the large bowel resulting in a narrow contracted segment. extends from rectum

113
Q

presentation of hirschsprung’s disease

A

failure to pass meconium within 24hrs
abdominal distension
bile stained vomiting
rectal examination: narrowed segment, withdrawal –> gush of liquid stool and flatus

later childhood: chronic constipation, abdominal distension, growth failure

114
Q

complication of hirschsprung disease

A

hirschsprung enterocolitis

due to clostridium difficile infection

115
Q

diagnostic investigation of hirschsprung disease

A

suction rectal biopsy: absence of ganglion cells + large acetylcholinesterase + nerve trunks

116
Q

management of hirschsprung disease

A

surgical: colostomy followed by anastomosing innervated bowel to anus

117
Q

red flag symptoms in a child with constipation

A 
failure to pass meconium in 24hrs
failure to thrive
gross abdominal distension
abnormal lower limb neurology
sacral dimple over natal cleft
abnormality of anus 
perianal bruising or multiple fissures 
perianal fistulae, abscess or fistulae
118
Q

what is constipation

A

infrequent passage of dry hardened faeces accompanied by straining or pain

119
Q

causes of constipation

A

secondary to other diseases e.g. hirschsprungs, hypothyroidism etc.
dehydration/reduced fluid intake
toilet training problems

120
Q

management of chronic constipation

A
  1. evacuate rectum: stool softeners (macrogol laxative e.g. movicol)/osmotic laxative if not toterated; 2nd line stimulant laxative; 3rd line: enema, manual excavation under GA
  2. maintenance treatment: movicol (polyethylene glycol)

dietary interventions
psychological/behavioural

121
Q

presentation of Toddler’s diarrhoea

A

loose stools of varying consistency + undigested vegetables

122
Q

prognosis of toddler’s diarrhoea

A

outgrow symtoms by 5 but may have delayed faecal continence

123
Q

management of toddler’s diarrhoea

A

ensure diet contains enough fat and fibre

avoid excessive consumption of fresh fruit juice

124
Q

presentation of crohn’s disease

A

abdominal pain, diarrhoea, weight loss

growth failure + delayed puberty

fever + lethargy

oral lesions, perianal skin tags, uveitis, arthralgia, erythema nodosum

125
Q

investigations for crohn’s

A

raised inflamatory markers: platelet count, ESR, CRP
iron deficency anaemia, low albumin

diagnosis: endoscopic biopsy

126
Q

pathophysiology of crohn’s

A

transmural, commonly affects distal ileum and proximal colon

initially: acutely inflamed, thickened bowel
subsequently: strictures of bowel + fistula

histology: non-caseating epitheliod cell granulomata

127
Q

management of crohn’s

A

remission induction: nutritional therapy for 6 - 8 weeks (polymeric diet); 2nd line: systemic steroids

remission: immunosupressants -e.g. azathioprine, methotrexate; anti-tumour necrosis factor agents e.g. infliximab

long term supplemental enteral nutrition e.g. overnight NG feeds to correct growth failure

surgery for complications

128
Q

presentation of ulcerative colitis

A

rectal bleeding, diarrhoea + colicky pain

extra-intestinal: erythema nodosum + arthritis

129
Q

diagnostic infection of UC

A

endoscopy + exclude infective colitis

small bowel imaging to exclude Crohns

130
Q

pathophysiology of UC

A

inflammation of mucosa starting from rectum and moving proximally; 90% have pan-colitis

histology: mucosal inflammation, crypt damage and ulceration

131
Q

management of UC

A

Mild disease: aminosalycates (e.g. balsalazide) for remission induction + maintenance
topical steroids if confined to rectum + sigmoid colon

Aggressive disease: systemic steroids for exacerbation azathioprine for maintenance

severe fulminating disease: IV fluids + steroids; ciclosporin; colectomy (toxic megacolon complications)

132
Q

complications of UC

A

toxic megacolon

adenocarcinoma: regular colonoscopic screening after 10 years of diagnosis

133
Q

presentation of diaphragmatic hernia

A

failure to respond to resuscitation or respiratory distress

134
Q

prevalence of diaphragmatic hernia

A

1 in 4000 births

135
Q

signs of diaphragmatic hernia

A

displaced apex beat and heart sounds to right side of chest, poor air entry in left chest

136
Q

complications of diaphragmatic hernia

A

pneumothorax on vigorous resuscitation attempts

pulmonary hypoplasia

137
Q

diagnostic investigation

A

x-ray chest abdomen

138
Q

management

A

NG tube + suction

surgical repair once stabilised

139
Q

what is neonatal hepatitis syndrome

A

prolonged neonatal jaundice and hepatic inflammation

140
Q

causes of neonatal hepatitis syndrome

A 
congenital infection
inborn errors of metabolism 
alpha1-antitrypsin deficiency 
type 1 tyrosinaemia 
galactosaemia
cystic fibrosis 
intestinal failure associated liver disease
progressive familial intrahepatic cholestasis 
error of bile synthesis
141
Q

symptoms of neonatal hepatitis syndrome

A

IUGR

hepatosplenomegaly at birth

142
Q

what is biliary atresia

A

progressive disease in which there is destruction or absence of the extrahepatic biliary tree and intrahepatic biliary ducts

143
Q

what is wilson disease

A

autosomal recessive disorder
defective excretion of copper leading to accumulation of copper in liver, brain, kidney and cornea (Kayser-Fleischer rings)

144
Q

treatment of wilson disease

A

penicillamine, zinc, pyridoxine

145
Q

causes of acute liver failure in children

A

paracetamol overdose

viral hepatitis: A, B, C

146
Q

investigative findings of liver failure

A

elevated transaminase and alkaline phosphotase and ammonia, abnormal coagulation

EEG: acute hepatic encephalopathy

CT: cerebral oedema

147
Q

management of liver failure

A

maintain blood glucose
prevent sepsis with antibiotics and anti fungals
IV fresh frozen plasma and vitamin K to prevent haemorrhage

148
Q

biliary atresia presentation

A

normal birthweight –> failure to thrive
jaundice
pale stools and dark urine
hepatosplenomegaly

149
Q

diagnostic investigation for biliary atresia

A

laparoscopic cholangiography

150
Q

treatment of biliary atresia

A

surgical bypass of fibrotic ducts

liver transplants

151
Q

what are choledochal cysts and what is their management

A

cystic dilations of extrahepatic biliary system

surgical excision of cyst

152
Q

what is marasmus

A

severe protein energy malnutrition leading to a weight <70% for height

153
Q

what is kwashiorkor

A

severe protein deficiency + oedema

also: flaky skin rash, angular stomatitis, diarrhoea, hypothermia, hypotension, bradycardia, distended abdomen and hepatomegaly

154
Q

causes of failure to thrive

A

inadequate intake: non organic (e.g. maternal depression), organic (e.g. cleft palette, LoA)

inadequate retention: vomiting

malabsorption: CF

failure to utilise nutrients e.g. T21

increased requirements: chronic infection, CF, thyrotoxicosis

155
Q

most common cause of gastroenteritis

A

rotavirus

campylobacter jejuni

other
shigella: high fever, blood, pus, tenesmus

cholera + ecoli: dehydration

156
Q

children at higher risk of dehydration with gastroenteritis

A

infants < 6 months/ low birthweight
more than 5 diarrhoeal stools in 24 hrs
vomited 3+ in 24hrs
unable to tolerate feeds

157
Q

what is clinical dehydration

A

5 - 10% loss of body weight

158
Q

what is post-gastroenteritis syndrome

A

temporary lactulose intolerance; non absorbed sugar in stools

159
Q

what is coeliac disease

A

immune response against gliadin leading to proximal small intestine damage

160
Q

presentation of coeliac disease

A

abdominal distension, buttocks wasting, abnormal stools, failure to thrive, irritability, anaemia

161
Q

histological findings in coeliac disease

A

intraepithelial lymphocytes
crypt hypertrophy
villous atrophy

162
Q

management

A

dietary changes

gluten challenge in later childhood

163
Q

what is cerebral palsy

A

non progressive disturbances in the developing foetal or infant brain causing motor impairment

164
Q

causes of cerebral palsy

A

80% antenatal: vascular occlusion, genetic syndromes, infection

10% hypoxic ischaemic injury during delivery

10% postnatal e.g. preterm infants with periventricular leucomalacia secondary to severe intraventricular haemorrhage. Also: meningitis/encephalopathy, NAI/trauma, hypoglycaemia, hyperbilirubinaemia

165
Q

possible investigations for cerebral palsy

A

MRI

166
Q

Presentation of CP

A

abnormal limb/trunk posture + delayed motor milestones

slowed head growth

feeding difficulties

abnormal gait

hand preference before 12 months

167
Q

Gross motor function classification system

A

used in CP functional assessment

  1. walks without limitations
  2. walks with limitations
  3. walks using hand held mobility device
  4. self mobility with limitations
  5. transported in manual wheel chair
168
Q

classification of CP and regions involved

A

spastic: motor cortex
dyskinetic: basal ganglia
ataxic: cerebellum

169
Q

types of spastic CP

A

hemiplegia
paraplegia
quadraplegia

170
Q

features of spastic CP

A

hypertonia/spasticity , brisk reflexes, extensor plantar responses

tip toe walk, scissor gait

171
Q

symptoms of dyskinetic CP

A

chorea: dance like movements
dystonia: contraction of agonist and antagonist muscles = twisting appearance

floppiness, poor trunk control

172
Q

features of ataxic CP

A

hypotonia, delayed motor development, poor balance, ataxic gait, intention tremor, in-coordinate movement

173
Q

pathogenic aetiology of UTI

A 
e.coli 
klebsiella 
proteus: boys>girls; alkaline urine
pseudomonas: ~ structural abnormality
strep faecalis
174
Q

risk factors for UTI

A

incomplete bladder emptying (infrequent voiding, neuropathic bladder, obstruction, vesicoureteric reflux)

175
Q

atypical UTI

A 
seriously ill or septicaemia 
poor urine flow 
abdominal or bladder mass
raised creatinine 
failure to respond to suitable antibiotics in 48hrs 
non-ecoli
176
Q

investigations for UTI under 6 months

A 
urine dipstick (>3)
clean catch urine sample for microscopy and culture

USS during acute infection if atypical or recurrent or 6 weeks otherwise

DMSA dimercaptosuccinic acid 4 - 6 months after in atypical or recurrent

MCUG micturating cystourethrogram if USS abnormal, atypical or recurrant

177
Q

investigations if 6months - 3 years UTI

A

typical: no further investigations
atypical: USS acute; DMSA 6 months; recurrent USS in 6 weeks, DMSA

178
Q

investigations UTI 3y+

A

typical: none
atypical: acute USS
recurrent: 6 month USS; DMSA

179
Q

what do USS show in UTI

A

renal size, outline, congenital abnormalitis, renal calculi, hydronephrosis

180
Q

what does MCUG show in UTI

A

reflux

181
Q

what does DMSA show in UTI

A

renal parenchymal defects

182
Q

management of UTI

A

7 - 10 days antibiotics if uper UTI

3 days in lower UTI

183
Q

risk factors for recurrence in UTI

A

<6months
female
VUR grade 3 - 5

184
Q

complication of UTI

A

renal scarring

hypertension

185
Q

symptoms of severe asthma

A
  • To breathless to talk or feed
  • Use of accessory neck muscles
  • SPO2 <92%
  • Tachypnoea and tachycardia
  • Peak flow <50% predicted
186
Q

features of life-threatening asthma

A
  • Silent chest
  • Poor respiratory effort
  • Altered consciousness
  • Cyanosis
  • Oxygen saturations < 92%
  • Peak flow < 33%
187
Q

management of moderate asthma exacerbation

A
  • SABA via spacer; 2 – 4 puffs
  • Increase by 2 puffs every 2 minutes to 10 puffs if required
  • Consider oral prednisolone
  • Reassess within 1h
188
Q

immediate management of severe/life-threatening asthma

A

Oxygen via face mask/ nasal prongs to achieve normal saturations

189
Q

management of severe asthma

A

10 puffs of SABA via spacer or nebuliser

oral prednisolone or IV hydrocortisone

nebulised ipratropium bromide if response is poor

repeat bronchodilators every 20-30mins prn

190
Q

management of life threatening asthma

A

nebulised SABA + ipratropium bromide
IV hydrocortisone
consider HDU/PICU
repeat bronchodilators every 30mins

191
Q

management of responding asthma after exacerbation

A
  • Continue bronchodilators 1 – 4 h prn
  • Discharge when stable on 4h treatment
  • Continue oral prednisolone for up to 3 days
192
Q

management of asthma attack not responding to treatment

A

• Transfer to HDU or PICU and consider CXR and blood gases
• IV salbutamol or aminophylline (caution if already receiving theophyllines)
o ECG and electrolyte monitoring
o IV aminophylline – loading dose over 20 minutes followed by continuous infusion. SE: seizures, severe vomiting + fatal cardiac arrythmias (Omit loading dose if already on theophylline)
• Consider bolus of IV magnesium sulphate

193
Q

important factors when discharging a patient after acute asthma attack

A

patient education
review medication and inhaler technique
personalised action plan
arrange follow up

194
Q

3 signs of shaken baby syndrome

A

subdural haemorrhage
retinal haemorrhage
encephalopathy

195
Q

what are the 3 types of child abuse

A

neglect
physical abuse
sexual abuse

196
Q

what are features that should make you consider neglect

A

severe and persistent infestations

parents who administer essential prescribed treatment /follow up etc

failure to dress child in suitable clothing

animal bite on inadequately supervised child

197
Q

features where you should suspect neglect

A

failure to seek medical advice leading to compromised child’s health

child who is persistently smelly and dirty

198
Q

features where you should consider sexual abuse

A

persistent dysuria or anogenital discomfort without medical explanation

gaping anus

pregnancy/STI in 13-15 year old

199
Q

features where you should suspect sexual abuse

A

persistent or recurrent genital or anal symptoms + behavioural change

anal fissure + constipation with no Crohn’s

STI in under 12

200
Q

features where you should consider physical abuse

A

serious or unusual injury with unsuitable explanation

201
Q

features where you should suspect physical child abuse

A

bruising, lacerations or burns on an immobile child

retinal haemorrhage

multiple fractures with different ages, evidence of occult fractures

202
Q

possible presentation of childhood abuse

A

bruising
fractures: particularly metaphyseal, posterior rib fractures or multiple fractures at different stages of healing
torn frenulum: e.g. from forcing a bottle into a child’s mouth
burns or scalds
failure to thrive
sexually transmitted infections e.g. Chlamydia, Gonorrhoea, Trichomonas

203
Q

factors which point towards child abuse

A

story inconsistent with injuries
repeated attendances at A&E departments
late presentation
child with a frightened, withdrawn appearance - ‘frozen watchfulness’

204
Q

immediate complications of meningitis

A 
septic shock 
coma 
raised ICP
cerebral oedema
seizures
septic arthritis 
pericardial effusions
205
Q

other complications of meningitis

A

subdural effusions
syndrome of inappropriate ADH secretion
sensorineural hearing loss

206
Q

preventative measures for meningitis

A

vaccination: Hib, meningococcus group B and C
meningococcus ACWY

intrapartum group B strep + antibiotic prophylaxis

207
Q

aetiology and causative pathogens for encephalitis

A

direct invasion by neurotoxic virus
post infectious encephalopathy
slow virus infection

enterovirus, respiratory virus, HSV

208
Q

encephalitis presentation

A

fever, altered consciousness, behavioural changes and seizures

209
Q

encephalitis management

A

high dose IV acyclovir until HSV is excluded

proven HSV: 3 weeks treatment

210
Q

clinical features of measles

A

cough, conjunctivitis, coryza
Koplik’s spots
rash: maculopapular, downwards from ears, becomes confluent
high temperature

211
Q

complications of measles

A

otitis media
encephalitis
subacute sclerosing panencephalitis

212
Q

management of measles

A
  • Symptomatic
  • Isolate admitted children
  • Antiviral drug ribavirin in immunocompromised patients
213
Q

clinical features of chicken pox

A

o Lesions start on head and trunk –> peripheries
o Appear as crops of papules and vesicles with surrounding erythema –> pustules –> crusts
o New lesions appear at different times for up to 1 week (new lesions after 10 days suggestive of defective cellular immunity)
o Itching + scratching may cause permanent scar formation or secondary infection

214
Q

complications of chicken pox

A

o Secondary bacteria infection: e.g. staphylococci or group A streptococci –> toxic shock syndrome, necrotising fasciitis
o CNS: cerebellitis, generalised encephalitis, aseptic meningitis
o Immunocompromised: haemorrhagic lesions, pneumonitis, progressive and disseminated infection, disseminated intravascular coagulation

215
Q

management of chicken pox

A

immunocompromised/adults: oral valaciclovir

HVZ IG following contact in immunosuppressed

216
Q

clinical features of mumps

A

fever, malaise, parotitis

217
Q

complications of mumps

A

transient hearing loss
viral meningitis + encephalitis
orchitis in post pubertal males

218
Q

features of rubella

A

low grade fever
maculopapular rash from face to entire body
suboccipital and post auricular lymphadenopathey

219
Q

complications of rubella

A

o Arthritis, encephalitis, thrombocytopenia and myocarditis

220
Q

diphteira microscopic features

A

cornybacterium diphtheriae Gram-positive, aerobic, non-motile, rod shaped bacterium

221
Q

management of diptheria

A

erythromycin + close contacts prophylactic

immunisation

222
Q

presentation of diptheria

A

nasal discharge (watery  purulent  blood stained), enlarged cervical lymph nodes, membranous pharyngitis + respiratory obstruction; vesicular or pustular rash in lower legs, feet and hands; cardiomyopathy or myocarditis

223
Q

scalded skin syndrome causative organism

A

staphylococcus aureus

releases a toxin that causes separation of epidermal skin through the granular cell layers

224
Q

scalded skin syndrome differential diagnosis

A

Toxic epidermal necrolitis

225
Q

scalded skin syndrome rash

A

vesicular
bulbous
pustular

226
Q

presentation of SSS

A

fever + malaise
generalised erythema + skin tenderness

large superficial blisters commonly affecting the flexures–> Nikolsky sign positive

227
Q

management of SSS

A

fluid balance
analgesia
flucloxacillin

228
Q

whooping cough causative organism

A

bordella pertussis

229
Q

clinical features of whopping gough

A

o 1 week of coryza (catarrhal phase)  spasmodic cough + inspiratory whoop or apnoea in infants (paroxysmal phase)
o Cough is worse at night  vomiting, epistaxis and subconjunctival haemorrhage
o Child may go red or blue in face
o Symptoms may last for 3 – 6 weeks
o Convalescent phase: can last for months

230
Q

management of whooping cough

A

azithromycin in ist 21 days

exclusion from school for 48hrs

231
Q

features of TB on a CXR

A

hilar lymphadenopathy
Ghon complex
consolidation

232
Q

investigations for TB

A

gastric washings to visualise acid fast bacilli

Mantoux test

Interferon gamma release assay

CXR

233
Q

management of TB

A

Rifampicin: GI, red urine
isoniazid: peripheral neuropathy (weekly pyridoxine)
Pyrazinamide: joint pains
Ethambutol: visual impairment

TB meningitis: dexamethasone

BCG immunisation, contact tracing

234
Q

clinical features of HIV

A

o Asymptomatic: routine screening
o Mild immunosuppression: lymphadenopathy or parotitis
o Moderate immunosuppression: recurrent bacterial infection, candidiasis, chronic diarrhoea and lymphocytic interstitial pneumonitis
o Severe AIDs: opportunistic infections (e.g. pneumocystis carinii pneumonia), severe failure to thrive, encephalopathy, malignancy

235
Q

investigations for HIV

A

PCR HIV DNA/ antibodies

236
Q

treatment of HIV

A

ART, PCP prophylaxis, co-trimoxazole

avoid BCG,
consider hep A, B and VZR vaccinations

237
Q

coxsackie’s disease/ hand foot and mouth disease

A

coxcackie virus

o Painful vesicular lesions on hands, feet, mouth and tongue and buttocks; mild systemic features

238
Q

scarlet fever causative organism

A

• Group A streptococci: streptococcus pyogenes

239
Q

management of scarlet fever

A

penicillin V or azithromycin for 10 days; return to school after 24hrs of antibiotics

240
Q

characteristic features of scarlet fever

A

sandpaper rash

strawberry tongue

241
Q

toxic shock syndrome presentation

A 
o	Fever > 39C
o	Hypotension
o	Diffuse erythematous macular rash
o	Organ dysfunction:
	Mucositis: oral, conjunctival and genital 
	Vomiting/ diarrhoea 
	Renal and liver impairment 
	Clotting abnormalities and thrombocytopenia 
	Altered consciousness
242
Q

causative organisms for toxic shock syndrome

A

• Staphylococcus aureus and group A streptococci

243
Q

management of toxic shock syndrome

A

intensive care to manage shock
surgical debridement
cefrtiaxone + clindamycin (switches off toxin production)
IVIG to neutralise circulating toxins

244
Q

candida infection risk factors

A 
hot weather 
infrequent nappy changes 
corticosteroid or antibiotic 
poor hygiene 
immunodeficiency
245
Q

impetigo causative organism

A

staphylococcus/streptococcus

246
Q

impetigo presentation

A

vesicular, bullous, pustular rash which ruptures and produces honey crusted lesions

lesions on face, neck and hands

247
Q

management of impetigo

A

o Mild cases: topical antibiotics e.g. mupirocin
o Severe: systemic antibiotics e.g. flucloxacillin or co-amoxiclav
o Avoid nursery or school until lesions are dry
o Nasal carriage eradication: nasal cram with mupirocin or chlorhexidine and neomycin

248
Q

slapped cheek syndrome rash

and causative organism

A

maculopapular

parvovirus B19

249
Q

presentation of slapped cheek syndrome

A

Fever, malaise, headache + myalgia –> facial rash a week later (slapped cheek) –> lace like rash on trunk + limbs

250
Q

complication of slapped cheek syndrome

A

aplastic crisis

251
Q

tropical fevers and their management

A

malaria: quinine
typhoid: azithromycin
dengue fever
gastroenteritis

252
Q

classification of immune deficiency

A

primary: intrinsic defect of immune system
(X-linked or autosomal recessive)

secondary: caused by another disease or treatment e.g. infection, malignancy, immunosuppressive therapy

253
Q

presentation of immune deficiency

A 
recurrent bacterial infections
severe infections
atypical presentation of infections/failure to respond to infections
opportunistic infections
failure to thrive

(SPUR: severe, prolonged, unusual, recurent)

254
Q

categories of primary immune deficiency

A

T-cell defects: severe combined immunodeficiency, ataxia telangectasia, DiGeorge, Wiskott-Aldrich

B-cell defects
Neutrophil defects
leukocyte function defects
complement defects

255
Q

treatment of primary immune deficiency

A

Antibiotic / antiviral prophylaxis
Prompt treatment of infections
Replacement immunoglobulin
Bone marrow transplant

256
Q

investigations for primary immune deficiency

A

FBC : low total WBC, neutrophil or lymphocytes
Total Ig GAM +/-E
Responses to routine immunisations
Lymphocyte subsets: numbers of T and B cells
Lymphocyte function

Phase 3A (9 decks)

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