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Gastro Flashcards

1
Q

What causes GORD?

A

Inappropriate relaxation of oesophagael sphincter

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2
Q

When does GOR become GORD?

A

After 12 months, if doesn’t resolve –> GORD (Gastrooesophagael Reflux Disease)

NOTE: GOR is due to functional immaturity

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3
Q

PACES: Important question to ask when considering diagnosis of GORD

A

IS THE CHILD GROWING? (ASK ABOUT RED BOOK) –> HEIGHT?WEIGHT

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4
Q

How does GORD present?

A

Vomiting
Refusal to feed / irritability
Aspiration
Chronic cough or wheeze
Slow weight gain

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5
Q

How is GORD typically diagnosed?

A

USUALLY A CLINICAL DIAGNOSIS

Can use:
(24h LOS pH monitoring)
(OGD)

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6
Q

What red flag sx would warrant a same day referral to a paediatrician in GORD?

A

Red flags (SAME DAY REFERRAL):
Haematemesis
Melaena
Dysphagia

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7
Q

What concerning features would warrant referral to a paediatrician in GORD?

A

Faltering growth
Unexplained distress
Unresponsive to medical therapy
Unexplained IDA

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8
Q

What complications would warrant a referral to a paediatrician in GORD?

A

Recurrent aspiration pneumonia
Dental erosion
Unexplained apnoea
Recurrent acute otitis media

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9
Q

PACES: What should be told to parents during GORD counselling?

A

Reassure (very common condition) –> may be frequent, less frequent with time, resolves by 12m

Note: no positional management – baby must sleep on back (risk of SIDS)

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10
Q

How does management vary in GORD?

A

If breast fed, or formula fed

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11
Q

How to manage GORD if breast-fed?

A

1st –> breastfeeding assessment
2nd –> consider trial of alginate for 1-2 weeks
3rd –> pharmacological*

*Pharmacological Management
4-week PPI/H2 antagonist trial
E.g. Omeprazole or Ranitidine

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12
Q

How to manage GORD if bottle-fed?

A

1st –> review feeding history
2nd –> trial smaller, more frequent feeds (aim for 150-180 mL/kg/day)
3rd –> trial of thickened formula (e.g. containing rice starch  Enfamil, Carabel)
4th –> trial of alginate (stop periodically to see if infant has recovered)
5th –> pharmacological*

*Pharmacological Management
4-week PPI/H2 antagonist trial
E.g. Omeprazole or Ranitidine

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13
Q

What causes pyloric stenosis?

A

Hypertrophy of pyloric muscle  gastric outlet obstruction

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14
Q

When does pyloric stenosis present?

A

Presents age 2-8 weeks

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15
Q

Which sex does pyloric stenosis present most often in?

A

4:1 (Male:Female)

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16
Q

PACES: What is important to get a description of in pyloric stenosis?

A

Contents of vomit (R/O bile, blood)
Description of vomiting:
“Does it go everywhere” vs drip down child’s chin

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17
Q

How does pyloric stenosis present?

A

Projectile Vomiting (non-bilious)
Hunger after vomiting
Failure to thrive

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18
Q

What is seen on examination in pyloric stenosis?

A

palpable ‘olive’ mass in RUQ
Visible peristalsis in upper abdomen

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19
Q

What investigations are done in pyloric stenosis?

A

Bloods
Blood Gas: hypochloraemic metabolic alkalosis
U&E: hyponatraemia and hypokalaemia

Imaging
Ultrasound

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20
Q

What is the management of pyloric stenosis?

A

Fluid resuscitation
Surgery: laparoscopic Ramstedt pyloromyotomy

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21
Q

Palpable ‘olive mass’

A

Pyloric stenosis

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22
Q

Hypochloraemic hypokalaemic metabolic acidosis on blood gas

A

Pyloric stenosis

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23
Q

Projectile non-bilious vomit

A

Pyloric stenosis

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24
Q

Target sign on USS

A

Pyloric Stenosis

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25
Q

Laparoscopic Ramstedy pyloromyotomy

A

Pyloric Stenosis

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26
Q

What is Oesophagael atresia?

A

malformation of oesophagus so it does not connect to stomach

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27
Q

What is tracheooesophagael fistula?

A

part of oesophagus joined to trachea

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28
Q

What is oesophgaeal atresia associated with?

A

Associations: polyhydramnios (no swallow), other developmental issues

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29
Q

What are VACTERL associations?

A

Set of conditions that can occur together:
Vertebral defects
Anal atresia
Cardiac defects
Tracheo‐Esophageal fistula
Renal malformations
Limb defects

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30
Q

How does oesophagael atresia present?

A

Excessive drooling
Choking
Failure to swallow or pass an NG tube

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31
Q

What investigations are done for oesophageal atresia?

A

Prenatal USS
NG tube placement +/- aspirate
Gastrograffin swallow (Gold-Standard)

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32
Q

Gold standard investigation for oesophagael atresia

A

Gastrograffin swallow

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33
Q

Oesophageal condition associated with polyhdramnios

A

Oesophageal atresia

NOTE: Also has VACTERL association: Vertebral defects, Anal atresia, Cardiac defects, Tracheo‐Esophageal fistula, Renal malformations, and Limb defects

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34
Q

How is Oesophagael atresia managed?

A

Surgical repair –> NICU for I&V
Before: Replogle tube (Drain saliva from oesophagus)

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35
Q

What must be done before surgical management of oesophagael atresia?

A

Replogle tube

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36
Q

What causes Intussusception?

A

Invagination of proximal bowel into distal component

NOTE: 95% ileum through to caecum through ileocecal valve

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37
Q

Cause of recurrent Intussusception

A

Meckel’s diverticulum

NOTE: If recurrent intussusception, consider investigating for a lead point
(e.g. Meckel’s diverticulum)

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38
Q

Risk Factors for Intussusception

A

Gastroenteritis (viral illness enlarging Peyer’s patches)
HSP
CF

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39
Q

Why can gastroenteritis cause intusussception?

A

Viral illness enlarging Peyer’s patches

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40
Q

How does intussusception present?

A

Abdominal pain
Vomit (may be bile stained)
Red-currant jelly stool (late sign)
Abdominal distension (+ sausage shaped mass RUQ)

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41
Q

What is a late sign of intussusception?

A

Red-currant jelly stool

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42
Q

Red current jelly stool

A

Intussusception

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43
Q

Sausage shaped mass in RUQ

A

Intussusception

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44
Q

First line Investigation for intussusception

A

Abdominal USS (Target mass)

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45
Q

Target mass on Abdominal USS

A

Intusussception

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46
Q

Investigations for intussusception

A

First line: Abdominal USS (Target mass)
Alternative: barium (or gastrograffin) enema

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47
Q

Management for intussusception

A

“Drip and suck:
1st line: rectal air insufflation
Otherwise: barium/gastrograffin enema
2nd line (perforation): surgical reduction + Broad-spectrum antibiotics

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48
Q

1st line management for intussusception

A

1st line: rectal air insufflation

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49
Q

What causes malrotation?

A

Congenital issue: intestines do not (fully) rotate and fixate in mesentery as usually expected

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50
Q

What can malrotation lead to?

A

bowel twisting and causing obstruction (volvulus)

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51
Q

What is malrotation (& volvulus) associated with?

A

exomphalos
congenital diaphragmatic hernia

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52
Q

How does malrotation (& volvulus) present?

A

Signs of bowel obstruction:
Abdominal pain and peritonism
Vomiting (bilious)
Constipation
Bloody stools

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53
Q

Investigations for malrotation (& volvulus)

A

Upper GI contrast study (assess patency)
USS

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54
Q

Management of malrotation (& volvulus)

A

Urgent laparotomy (Ladd’s procedure) - Untwist volvulus, remove necrotic bowel and place bowel in non-rotation position

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55
Q

Ladd’s procedure

A

Malrotation (& volvulus)

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56
Q

Cause of Hirchsprung’s Disease

A

Absence of ganglion cells from the myenteric (Auerbach) and submucosal (Meissner’s) plexuses

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57
Q

Most common location of hirchsprung’s disease

A

100% start in rectum, 75% spread proximally to rectosigmoid

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58
Q

RFs for hirchsprung

A

Down’s
MEN2a

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59
Q

PACES: what question to ask in Hirchsprung’s?

A

Did baby pass any stool in the first day of life?
“Dark, sticky/tarry stool”?

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60
Q

How does hirchsprung’s present?

A

Failure to pass meconium <24hrs
Abdominal distension
Bilious vomiting
Explosive passage of liquid/foul stools

NOTE: May present later in first few weeks of life with severe, life-threatening Hirschsprung enterocolitis (C. diff)

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61
Q

What may people with Hirchsprung’s present in first few weeks of life with?

A

severe, life-threatening Hirschsprung enterocolitis (C. diff)

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62
Q

What causes severe, life-threatening Hirschsprung enterocolitis?

A

C. Diff

NOTE: May present later in first few weeks of life

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63
Q

What severe, life-threatening infection may people with Hirchsprung’s present with?

A

Hirschsprung enterocolitis (caused by C. Diff)

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64
Q

What is a delayed clinical features of Hirchsprung?

A

Chronic constipation (delayed presentation)

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65
Q

Investigations for Hirchsprung’s

A

AXR (if obstruction)
Contrast (barium) enema: –> dilated distal segment + narrowed proximal segment
Definitive = suction-assisted full-thickness rectal biopsy: –> absence of ganglion cells, ACh +ve nerve trunks

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66
Q

Definitive investigation for Hirchsprung

A

Suction-assisted full thickness rectal biopsy (visualise the absence of the ganglion cells)

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67
Q

Management of Hirchsprung

A

Initial management = bowel irrigation
Followed by: Endorectal pull-through (colostomy followed by anastomosing normally innervated bowel)

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68
Q

Initial management of Hirchsprung

A

Bowel irrigation

Followed by: Endorectal pull-through (colostomy followed by anastomosing normally innervated bowel)

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69
Q

Definitive management of Hirchsprung

A

Endorectal pull-through (colostomy followed by anastomosing normally innervated bowel)

Preceded by: bowel irrigation

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70
Q

What causes meconium ileus?

A

Thick, sticky meconium that has a prolonged passing time

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71
Q

When should meconium have passed by?

A

Meconium usually passes within 24hrs of delivery, if not, there may be an ileus

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72
Q

Causes of delayed meconium passage

A

Meconium Ileus
Hirchsprung’s Disease

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73
Q

What is meconium ileus associated with?

A

Cystic Fibrosis (90%) and biliary atresia

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74
Q

What GI condition is cystic fibrosis associated with heavily?

A

meconium ileus

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75
Q

How may meconium ileus present?

A

Child may vomit meconium instead of passing it as stool

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76
Q

What test should be done if diagnosis of meconium ileus is suspected>

A

Heel prick test for CF

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77
Q

Management of meconium ileus

A

1st line = gastrografin enema (N-acetylcysteine can also be used)
2nd line = surgery

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78
Q

1st line management for meconium ileus

A

1st line = gastrografin enema (N-acetylcysteine can also be used)

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79
Q

What causes meckel’s diverticulum?

A

An ileal remnant of the vitello-intestinal duct containing ectopic gastric mucosa (i.e. can form gastric ulcers that bleed) or pancreatic tissue

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80
Q

What type of tissue is meckel’s diverticulum made from?

A

Ectopic gastric mucosa or pancreatic tissue

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81
Q

MASSIVE PAINLESS PR BLEED

A

Meckel’s diverticulum

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82
Q

How does meckel’s diverticulum usually present?

A

Mostly asymptomatic!
Painless massive PR bleeding
May present with intussusception, volvulus or diverticulitis

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83
Q

What GI condition may Meckel’s Diverticulum increase the recurrence of?

A

Intusussception

NOTE: Can be the lead point for intussusception, thereby presenting with intermittent abdominal pain and vomiting

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84
Q

Who is Meckel’s diverticulum more common in?

A

More common in boys (2:1)

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85
Q

Investigations for meckel’s diverticulum

A

Technetium scan (increased uptake by gastric mucosa)
Abdominal USS ± laparoscopy

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86
Q

1st line investigation for meckel’s diverticulum

A

Technetium scan can demonstrate increased uptake by ectopic gastric mucosa found within the diverticulum.

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87
Q

Management of Meckel’s Diverticulum

A

Only treat if symptomatic
Bleeding: excision (with blood transfusion if needed)
Obstruction: excision of diverticulum and lysis of adhesions
Perforation/peritonitis: excision or small bowel segmental resection with perioperative antibiotics

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88
Q

Treatment of Meckel’s if bleeding

A

Only treat if symptomatic
Bleeding: excision (with blood transfusion if needed)

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89
Q

Treatment of Meckel’s if osbtruction

A

Only treat if symptomatic
Obstruction: excision of diverticulum and lysis of adhesions

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90
Q

Treatment of Meckel’s if perforation/peritonitis

A

Only treat if symptomatic
Perforation/peritonitis: excision or small bowel segmental resection with perioperative antibiotics

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91
Q

RFs for oesophagael atresia

A

Trisomy 18 and 21

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92
Q

What may occur recurrently in oesophagael atresia?

A

Aspiration

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93
Q

What is a hernia?

A

Hernia = A bulging of an organ or tissue through an abnormal opening

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94
Q

Types of hernia

A

indirect/direct inguinal
umbilical
epigastric
femoral

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95
Q

PACES: Questions to ask if hernia

A

Duration of bulge/lump
Always present vs on standing or straining
Does it retract alone? Can they push it back in?
Any pain?
Constipation?

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96
Q

PACES: what are you trying to assess in a hernia history?

A

History is to assess for any signs of incarceration or strangulation

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97
Q

What type of hernia requires instant referral?

A

Femoral

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98
Q

Investigations for inguinal hernia

A

Clinical Diagnosis + examination

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99
Q

What should be checked on examination of inguinal hernia

A

EXAMINATION SHOULD BE BILATERAL

Painful vs painless
Cough impulse
Reducible (if not: incarceration)
Auscultation (bowel sounds?)

NEED TO ASSESS IF DIRECT VS INDIRECT

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100
Q

How to differentiate between direct and indirect inguinal hernias?

A

Direct vs indirect:
1.Locate deep inguinal ring (midway between ASIS and pubic tubercle).
2.Manually reduce hernia
3.Apply pressure over the deep inguinal ring and ask the patient to cough.
If reappears = direct; if not = indirect

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101
Q

Management of inguinal hernias

A

If incarcerated: emergency surgery
Non-incarcerated: elective repair
Open or laparoscopic

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102
Q

Management of incarcerated inguinal hernias

A

Emergency surgery

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103
Q

Management of non-incarcerated inguinal hernias

A

Non-incarcerated: elective repair
Open or laparoscopic

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104
Q

What anatomical structure do indirect inguinal hernias go through?

A

deep inguinal ring

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105
Q

How investigate femoral hernia?

A

Clinical diagnosis

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106
Q

How does femoral hernia compare to inguinal hernia?

A

Femoral = infero-lateral to public tubercle
Inguinal – supero-medial to pubic tubercle

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107
Q

Management of femoral hernias

A

All should be managed surgically – high risk of incarceration

NOTE: FEMORAL HERNIAS ARE AT MUCH HIGHER RISK OF INCARCERATION

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108
Q

Investigations for umbilical hernia

A

Clinical diagnosis

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109
Q

Management of umbilical hernia

A

Incarceration: attempt reduction and surgical repair
Non-incarcerated:
Large or symptomatic: elective surgical repair (age 2-3 years)
Small and asymptomatic: most self-resolve by age 5. If have not resolved, may consider elective repair.

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110
Q

Management of incarcerated umbilical hernia

A

Incarceration: attempt reduction and surgical repair

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111
Q

Management of non-incaracertaed umbilical hernia

A

Depends on size and symptoms

Large or symptomatic: elective surgical repair (age 2-3 years)
Small and asymptomatic: most self-resolve by age 5. If have not resolved, may consider elective repair.

112
Q

What type of hernia may self-resolve by the age of 5?

A

small and asymptomatic umbilical hernias

113
Q

What is constipation?

A

Infrequent passage of stools, often associated with abdominal discomfort.

114
Q

Risk factors for constipation

A

Dehydration
Toilet Anxiety
Hirschsprung Disease
Hypothyroidism
Coeliac Disease
Stress/emotional abuse

115
Q

PACES: What conditions do you need to rule out in constipation?

A

Hirschsprung Disease
Hypothyroidism
Coeliac Disease
Cystic Fibrosis

116
Q

PACES: What red flags should be ruled out in constipation?

A

Blood in stool
Weight loss

117
Q

Investigations for constipation

A

Clinical diagnosis (rule out secondary causes)
AXR (impaction)

118
Q

Clinical features of constipation

A

Abdominal pain
Difficult defecation
Soiling

119
Q

PACES: What questions should be asked to rule out social causes of constipation?

A

Enquire about diet and lifestyle
Enquire about home and school life

120
Q

What does management of constipation depend on

A

Presence of disimpaction:
If Faecal Impaction –> Disimpaction Regime
No Faecal Impaction –> Maintenance Regime

121
Q

How to manage constipation if faecal impaction?

A

Disimpaction regime:
Movicol Paediatric Plain (polyethylene glycol + electrolytes) - escalating dose for 2 weeks (followed by maintenance dose until regular bowel habit re-established)
Add stimulant laxative (e.g. Senna)

NOTE: If Movicol is not tolerated: a stimulant laxative (e.g. senna) can be used with lactulose or docusate (stool softeners)

122
Q

How to manage constipation if no faecal impaction?

A

Movicol with/without a stimulant laxative
Dose should be reduced over a period of months

123
Q

What management must always be given in constipation?

A

Lifestyle & Behaviour (ALWAYS GIVE):
Advise behavioural interventions (scheduled toileting, bowel habit diary, reward system)
Diet and lifestyle advice (adequate fluid intake)

124
Q

PACES: What advice should be given in constipation management?

A

Advice about establishing good toileting practices (e.g. positive reward schemes and regular toileting schedules)
Encourage good hydration and a balanced diet

125
Q

Where can Crohn’s affect?

A

Affects any part of the GI tract mouth to anus

126
Q

Where does Crohn’s most commonly affect?

A

distal ileum and proximal colon

127
Q

Does Crohn’s go through the layers of the mucosa?

A

Yes it is transmural

128
Q

What condition affects any part of the GI tract from mouth to anus?

A

Crohn’s

129
Q

What condition is transmural and most commonly affects the distal ileum and proximal colon

A

Crohn’s

130
Q

What social habit can make Crohn’s worse?

A

Smoking

NOTE: Makes UC better

131
Q

Presentation of Crohn’s

A

Abdominal pain, diarrhoea, weight loss
Fever, lethargy
Aphthous ulcers, perianal skin tags
Growth failure, delayed puberty
Uveitis, arthralgia, erythema nodosum
Complications: strictures and fistulae

132
Q

Extra-intestinal manifestations of Crohn’s

A

Aphthous ulcers
Perianal skin tags
Uveitis
Arthralgia
Erythema Nodosum

133
Q

Complications of crohn’s

A

strictures and fistulae

134
Q

Investigations for Crohn’s

A

Faecal calprotectin
FBC (including iron, B12 and folate), CRP and ESR

Upper GI and small bowel contrast scan
Colonoscopy and biopsy (cobblestones; non-caseating granulomas)

135
Q

Gold standard investigation for Crohn’s

A

Colonoscopy and biopsy (cobblestones; non-caseating granulomas)

NOTE: Unlikely to do this in a child

136
Q

What is seen on colonoscopy and biopsy of crohn’s?

A

cobblestones; non-caseating granulomas

137
Q

Cobblestones and non-caseating granulomas on biopsy

A

Crohn’s

138
Q

What does management of Crohn’s involve?

A

Inducing remission
Maintaining remission
Surgery for complications

139
Q

How is remission induced in Crohn’s?

A

Pharmacological management –> steroids (prednisolone)
Nutritional management –> effective in 85-100% patients (crohns.org)
Replace diet with whole protein modular diet – excessively liquid, for 6-8 weeks
May need NG if the child struggles to drink that much
Products are easily digested, provide all nutrients needed to replace lost weight

140
Q

How is remission maintained in Crohn’s

A

Aminosalicylates (e.g. mesalazine)
Immunosuppressive drugs (azathioprine, methotrexate, mercaptopurine)
Azathioprine cannot be given to people with a TPMT mutation
Must not have live vaccines
Must have pneumococcal and influenza vaccines
Anti-TNF antibodies in biologic therapies (e.g. infliximab

141
Q

What must be tested before giving azathioprine?

A

Presence of TPMT mutation

142
Q

What drug class must be avoided with azathioprine?

A

Xanthine oxidase inhibitors (e.g. allopurinol)

143
Q

What steroids are used in Crohn’s?

A

Prednisolone –> used to induce remission alongside nutritional management (whole protein modular diet)

144
Q

What aminosalicyclates are used to maintain remission in Crohn’s?

A

Mesalazine

Used alongside:
Immunosuppressive drugs (azathioprine, methotrexate, mercaptopurine)
Anti-TNF antibodies in biologic therapies (e.g. infliximab)

145
Q

What immunosuppressive drugs are used to maintain remission in Crohn’s?

A

azathioprine, methotrexate, mercaptopurine

Used alongside:
Aminosalicylates (e.g. mesalazine)
Anti-TNF antibodies in biologic therapies (e.g. infliximab)

146
Q

What biologic therapies are used to maintain remission in Crohn’s?

A

Infliximab (anti-TNF alpha)

Used alongside:
Aminosalicylates (e.g. mesalazine)
Immunosuppressive drugs (azathioprine, methotrexate, mercaptopurine)

147
Q

What do the biologic therapies in Crohn’s target?

A

Anti-TNF alpha antibodies in biologic therapies (e.g. infliximab

148
Q

When is surgery done for Crohn’s?

A

Surgery for complications: e.g. obstruction, fistula, abscess, severe localized disease

149
Q

What requires monitoring in medical management of Crohn’s?

A

biochemical measures (e.g. ferritin, B12, calcium and vitamin

150
Q

PACES: what support can be offered to those with Crohn’s?

A

Support: Crohn’s & Colitis UK (information leaflet and grants available)

151
Q

Where is affected in UC?

A

Partial thickness inflammation in a distal to proximal pattern

152
Q

Key features of UC

A

Crypt damage & ulceration

153
Q

What GI condition causes Crypt damage & ulceration?

A

UC

154
Q

What is UC associated with?

A

PSC, Toxic megacolon, enteric arthritis, haemorrhage, bowel cancer

155
Q

GI condition associated with PSC and toxic megacolon

A

UC

156
Q

How does UC present?

A

Classic presentation is rectal bleeding, diarrhoea, abdominal pain
Weight loss and growth failure
Erythema nodosum, arthritis

157
Q

Extra-intestinal manifestations of UC

A

Erythema nodosum, arthritis

158
Q

Investigations for UC

A

Endoscopy and histological features:
Confluent colitis extending from rectum proximally
Histology = mucosal inflammation/ulceration, crypt damage (abscesses, loss, architectural distortion)
Severity graded using:
Paediatric Ulcerative Colitis Activity Index (PUCAI) - N.B. be aware of coexistent depression
Truelove and Witts score

159
Q

What is seen on histology in UC?

A

mucosal inflammation/ulceration, crypt damage

160
Q

How is the severity of UC graded?

A

Paediatric Ulcerative Colitis Activity Index (PUCAI) - N.B. be aware of coexistent depression
Truelove and Witts score

161
Q

What psychiatric condition can co-exist with UC?

A

Depression

NOTE: Paediatric Ulcerative Colitis Activity Index (PUCAI)

162
Q

How is UC managed?

A

1st line: topical –> oral aminosalicylates – if no improvement 4 weeks after starting, move to oral, then 2nd line
Often used to maintain remission
Can use oral azathioprine or mercaptopurine if aminosalicylates insufficient
2nd line: topical –> oral corticosteroid (i.e. if aminosalicylates not tolerated/contraindicated)
Prednisolone
Beclomethasone
3rd line: oral tacrolimus
4th line: biological agents (infliximab, adalimumab and golimumab)
5th line (resistant disease) –> surgery (colectomy with ileostomy or ileojejunal pouch)

163
Q

what is 1st line management of UC?

A

topical –> oral aminosalicylates

NOTE: If no improvement after 4 weeks, try oral, before 2nd line –> topical –> oral immunosuppressants

164
Q

What is often used to maintain remission in UC?

A

aminosalicyclates

165
Q

What is 2nd line in UC?

A

2nd line: topical –> oral corticosteroid (i.e. if aminosalicylates not tolerated/contraindicated)
Prednisolone

166
Q

what is 3rd line in UC?

A

oral tacrolimus

Preceded by: topical+oral aminosalicyclates, topical+oral corticosteroids

167
Q

What biologic agents used in UC?

A

infliximab, adalimumab and golimumab

NOTE: 4th line after aminosalicyclates, corticosteroids and oral tacrolimus

168
Q

When is surgery used in UC?

A

Resistant disease

NOTE: after trialling oral aminosalicyclates, oral corticosteroids and oral tacrolimus and biologic agents

169
Q

What surgery is used in UC?

A

colectomy with ileostomy or ileojejunal pouch

170
Q

Management of severe fulminating disease in UC

A

IT IS AN EMERGENCY

MDT approach (medics and surgeons)
IV corticosteroids or ciclosporin and assess likelihood of needing surgery
Consider IV ciclosporin (if IV corticosteroids are contraindicated or ineffective)

171
Q

When is an MDT approach needed in UC?

A

SEVERE FULMINATING DISESE - MEDICAL EMERGENCY

172
Q

PACES: What support to offer in UC?

A

UC is associated with an increased risk of bowel cancer
Regular screening performed after 10 years of diagnosis
Support: Crohn’s and Colitis UK

173
Q

Crohn’s vs UC (table)

A
174
Q

What is the immune reaction against in coeliac?

A

Gliadin

175
Q

Genetic associations of coeliac

A

HLA DQ2 (95%) and DQ8 (80%) association

176
Q

How does coeliac present?

A

Malabsorption syndrome (failure to thrive, abdominal distension, bloating, irritability)
Malnutrition (check weight, height, BMI) –> wasted buttocks and distended abdomen
Pathogenomic = dermatitis herpetiformis (pruritic papulovesicular elbow/knee rash)

177
Q

What skin condition is pathognomonic for coeliac?

A

dermatitis herpetiformis (pruritic papulovesicular elbow/knee rash)

178
Q

Signs of malnutrition in coeliac

A

wasted buttocks and distended abdomen

179
Q

GI condition that causes dermatitis herpetiformis

A

Coeliac disease

180
Q

What does malabsorption syndrome present with in coeliac?

A

failure to thrive, abdominal distension, bloating, irritability

181
Q

How is coeliac investigated?

A

Serological diagnosis:
Most sensitive = IgA tissue transglutaminase (anti-tTG)
Less sensitive = IgA anti-endomysial cell antibodies (anti-EMA)
If IgA deficient  IgG DGP / Deiminated Gliadin Peptide
FBC and blood smear (iron deficient, vitamin B12/folate deficient, vitamin D deficient)
Confirmation of diagnosis (n.b. grading with the ‘Marsh’ system):
Older children / adults  OGD + jejunal biopsy (villous atrophy, crypt hyperplasia, ↑ IELs)

182
Q

What is the most sensitive serological test for coeliac?

A

Most sensitive = IgA tissue transglutaminase (anti-tTG)
Less sensitive = IgA anti-endomysial cell antibodies (anti-EMA)

NOTE: NEED TO TEST FOR IgA deficeincy

183
Q

What needs to be tested for before serological diagnosis of coeliac?

A

serum IgA levels

If IgA deficient  IgG DGP / Deiminated Gliadin Peptide

184
Q

What serological test is done if IgA deficient in coeliac?

A

IgG DGP / Deiminated Gliadin Peptide

185
Q

What deficiencies may be seen in coeliac?

A

Iron deficient, vitamin B12/folate deficient, vitamin D deficient

186
Q

Gold standard investigation for coeliac

A

Older children / adults  OGD + jejunal biopsy (villous atrophy, crypt hyperplasia, ↑ IELs)

187
Q

What findings may be found on blood film in coeliac?

A

hyposplenism –> target cells

188
Q

What is found on biopsy of coeliac?

A

villous atrophy, crypt hyperplasia, ↑ IELs

189
Q

villous atrophy, crypt hyperplasia, ↑ IELs on biopsy

A

Coeliac

190
Q

What is seen in coeliac disease if there is non-adherence to diet?

A

micronutrient deficiency (vitamin D, iron), osteoporosis, EATL, hyposplenism

191
Q

Management of coeliac

A

Remove all products containing wheat, rye and barley
MDT – dietician, child psychologist, school involvement, GP, gastroenterologist
Dietician referral (if problems with adhering to the diet) and annual (6-12m) review:
Regular checks of height & weight, r/v symptoms, diet, consider bloods
Support sources: Coeliac UK

192
Q

Most important management point in coeliac

A

REMOVAL OF TRIGGER

193
Q

PACES: What support to offer in coeliac?

A

Support sources: Coeliac UK

194
Q

What are the two types of cow’s milk protein allergy? When do they present?

A

Can be immediate (IgE mediated) or delayed (non-IgE mediated) – usually presents in first 3m of life in formula-fed children

195
Q

What type of cow’s milk protein allergy presents immediately?

A

IgE mediated

NOTE: Non-IgE mediated is delayed, usually presents in first 3m of life in formula-fed children

196
Q

What type of cow’s milk protein allergy has a delayed presentation?

A

Non-IgE mediated is delayed, usually presents in first 3m of life in formula-fed children

NOTE: IgE mediated presents immediately

197
Q

PACES: What is important to classify in cow’s milk protein allergy?

A

Classify the reaction – speed of onset (and relation to food), age of onset, severity, location, reproducibility, history

NOTE: take an atopic and feeding history too

198
Q

“3-month-old baby that vomits and has diarrhoea after every feed”

A

Cow’s milk protein allergy

199
Q

How does IgE mediated cow’s milk protein allergy present?

A

urticaria, angioedema, rash, erythema, nausea, D&V, colicky abdominal pain, sneezing, rhinorrhoea, congestion, cough, tightness, wheeze, ANAPHYLAXIS

200
Q

What type of cow’s milk protein allergy can anaphylaxis occur in?

A

IgE mediated

201
Q

How does non-IgE mediated cow’s milk protein allergy present?

A

erythema, atopic eczema, GORD, change in frequency of stools, blood/mucus in stools, abdominal pain, FTT, infantile colic, constipation, food aversion, pallor

202
Q

Investigations for cow’s milk protein allergy

A

Test 1: Skin prick allergy testing OR
Test 2: Measurement of specific IgE antibodies (RAST)

203
Q

When to refer to a specialist in cow’s milk protein allergy?

A

Faltering growth with ≥1 GI symptoms of allergy
≥1 acute systemic or severe delayed reactions
Severe atopic eczema
Persisting suspicion
Multiple allergies

204
Q

Management of cow’s milk protein allergy

A

1st  Trial cows’ milk elimination from diet for 2-6 weeks:
Breastfed Babies: mother to exclude cow’s milk protein from her diet
Consider prescribing daily supplement of 1g of calcium and 10 mcg of vitamin D
N.B. it takes 2-3 weeks to fully eliminate cow’s milk from breastmilk
Formula-fed Babies: replacement of cows’ milk-based formula with hypoallergenic infant formula (e.g. extensively hydrolysed formula or amino acid formula  if SEVERE: use amino-acid based formula)
Weaned infants/older children: exclude cows’ milk protein from their diet

2nd  Regularly monitor growth, nutritional counselling with a paediatric dietician

3rd  Re-evaluate tolerance to cows’ milk protein (every 6-12 months)  re-introduce cows’ milk protein into the diet  if tolerance is established, greater exposure of less processed milk is advised with ‘Milk Ladder’

205
Q

1st line management of cow’s milk protein allergy

A

Trial cows’ milk elimination from diet for 2-6 weeks:
Breastfed Babies: mother to exclude cow’s milk protein from her diet
Consider prescribing daily supplement of 1g of calcium and 10 mcg of vitamin D
N.B. it takes 2-3 weeks to fully eliminate cow’s milk from breastmilk
Formula-fed Babies: replacement of cows’ milk-based formula with hypoallergenic infant formula (e.g. extensively hydrolysed formula or amino acid formula  if SEVERE: use amino-acid based formula)
Weaned infants/older children: exclude cows’ milk protein from their diet

206
Q

Initial management of cow’s milk protein allergy

A

Trial cows’ milk elimination from diet for 2-6 weeks:

207
Q

How to manage breastfed babies with cow’s milk protein allergy?

A

Initially Trial cows’ milk elimination from diet for 2-6 weeks

Then Breastfed Babies: mother to exclude cow’s milk protein from her diet
Consider prescribing daily supplement of 1g of calcium and 10 mcg of vitamin D
N.B. it takes 2-3 weeks to fully eliminate cow’s milk from breastmilk

208
Q

How to manage formula fed babies with cow’s milk protein allergy?

A

Initially Trial cows’ milk elimination from diet for 2-6 weeks

Then Formula-fed Babies: replacement of cows’ milk-based formula with hypoallergenic infant formula (e.g. extensively hydrolysed formula or amino acid formula  if SEVERE: use amino-acid based formula)

209
Q

How to manage weaned infants/older children with cow’s milk protein allergy?

A

Initially Trial cows’ milk elimination from diet for 2-6 weeks

Then Weaned infants/older children: exclude cows’ milk protein from their diet

210
Q

What is the most common acuse of abdominal pain in childhood?

A

Appendicitis

NOTE: rare in <3 year old

211
Q

What is the most common cause of appendicitis in pre-school children?

A

Faecolith

212
Q

What is the most common cause of appendicitis post-preschool?

A

Perforation

213
Q

What cause of appendicitis can be seen on AXR?

A

Faecolith

214
Q

How does appendicitis present?

A

Anorexia, vomiting, nausea
umbilical–>RIF pain
Fever, tenderness, etc.

215
Q

Investigations for appendicitis

A

FBC, pregnancy test (if female)
Clinical (watchful waiting observation)
Consider USS if diagnostic uncertainty

216
Q

Mainstay of investigation for appendicitis

A

CLINICAL DIAGNOSIS

217
Q

When to consider USS in appendicitis

A

If diagnostic uncertainty

NOTE: APPENDICITIS IS PREDOMINANTLY A CLINICAL DIAGNOSIS

218
Q

Management of appendicitis

A

GAME:
G (Group & Save)
A (ABx IV)
M (MRSA screen)
E (Eat & drink – must be NBM)

THEN APPENDICECTOMY

219
Q

Who does mesenteric adenitis affect?

A

Mainly in children <15yo; recent viral/bacterial infection (including UTIs)

220
Q

What is usually the precursor to mesenteric adenitis?

A

Recent viral/bacterial infection (including UTIs)

221
Q

How does mesenteric adenitis present?

A

Abdominal pain – central or RIF
(Nausea ± diarrhoea)
↓ appetite

222
Q

Differential for appendicitis

A

Mesenteric adenitis –> May present with Nausea+Diarrhoea –> similar to appendicitis, hence bloods and USS can be used to differentiate

223
Q

What can be used to differentiate mesenteric adenitis from appendicitis?

A

Bloods to exclude appendicitis (bloods, urine MC&S, USS)

224
Q

How to confirm diagnosis of mesenteric adenitis

A

CLINICALLY

225
Q

Definitive diagnosis of mesenteric adenitis

A

Large mesenteric lymph nodes seen at laparoscopy (w/ normal appendix)

NOTE: Never done

226
Q

Management of mesenteric adenitis

A

Simple analgesia (symptoms usually resolve in a few days, maximum 2 weeks)
Safety net for increased pain or deterioration

227
Q

PACES: What to safety net for in mesenteric adenitis?

A

increased pain or deterioration

228
Q

What is the most common surgical emergency in newborn babies>

A

Necrotising enterocolitis

229
Q

Who does necrotising enterocolitis tend to affect?

A

Premature babies and LBW

230
Q

What does necrotising enterocolitis lead to?

A

Serious intestinal injury

231
Q

When does necrotising enterocolitis often begin?

A

After starting enteral feeding, occurs due to immature/fragile bowels

232
Q

How does necrotising enterocolitis present?

A

Early signs = biliary vomiting, feed intolerance
Abdomen distension
Blood-stained stool
Rapid deterioration and shock

233
Q

Early signs of necrotising enterocolitis

A

biliary vomiting, feed intolerance

234
Q

Investigations for necrotising enterocolitis

A

AXR – ‘gas cysts’ in bowel wall, distended loops of bowel with thickened walls
Blood cultures

235
Q

AXR findings for necrotising enterocolitis

A

‘gas cysts’ in bowel wall, distended loops of bowel with thickened walls

236
Q

AXR findings - ‘gas cysts’ in bowel wall, distended loops of bowel with thickened walls

A

Necrotising enterocolitis

237
Q

Management of necrotising enterocolitis

A

Bowel rest (NPO (stop oral feed) and switch to parenteral nutrition)
Broad-spectrum antibiotics (cefotaxime/tazocin and vancomycin)
Stage IA/IB (3 days), stage IIA (7-10 days), stage IIB, III (14 days)
Laparotomy (if perforated as seen on AXR)

238
Q

1st step in necrotising enterocolitis management

A

Bowel rest (NPO (stop oral feed) and switch to parenteral nutrition)

Followed by: Broad-spectrum antibiotics (cefotaxime/tazocin and vancomycin)

239
Q

Which broad spectrum ABs are used in necrotising enterocolitis management?

A

Cefotaxime/tazocin and vancomycin

NOTE: Preceded by Bowel rest (NPO (stop oral feed) and switch to parenteral nutrition)

240
Q

When is surgical management done in necrotising enterocolitis?

A

If perforation seen on AXR –> laparotomy

241
Q

Long term consequences of necrotising enterocolitis

A

Development of strictures
Malabsorption (if extensive bowel resection is necessary)

NOTE: (20% mortality/morbidity acutely)

242
Q

How do threadworms present?

A

Itchiness in anal/perianal region

243
Q

PACES: Important question to ask in threadworm history

A

Who is in the house (highly transmissible)

244
Q

Investigations for threadworms

A

Clinical
Stool sample (ova, cysts, parasites)

245
Q

Management of threadworms

A

Single dose of an anti-helminth (mebendazole) for the whole household
Repeat dose 2 weeks alter if infection persists
Rigorous hygiene for 2 weeks if on mebendazole or 6 weeks if using hygiene measures alone:
Hand washing
Cut fingernails regularly, avoid biting nails and scratching anus
Shower everyday, including perineal area, to remove eggs from skin
Change bed linin and nightwear daily for several days after treatment (don’t shake bedsheets)
Thoroughly dust and vacuum
Exclusion from school/nursery is NOT required
Children <6 months should be treated with hygiene measures alone for 6 weeks (seek advice from ID)
Treating all household contacts

246
Q

What medication should be given for threadworms?

A

Mebendazole (anti-helminth)

247
Q

Who should the medication be given to in threadworms?

A

Entire household –> mebendazole (anti-helminth)

248
Q

Is school exclusion required for threadworms?

A

NO EXCLUSION FROM SCHOOL/NURSERY IS NOT REQUIRED

249
Q

How long are hygiene measures required for in threadworm management?

A

Rigorous hygiene for 2 weeks if on mebendazole or 6 weeks if using hygiene measures alone:

250
Q

What is the commonest cause of loose stools in preschool kids?

A

Toddler’s diarrhoea

251
Q

Cause of toddler’s diarrhoea

A

Underlying maturational delay in intestinal mobility

252
Q

Presentation of toddler’s diarrhoea

A

Varying consistency stools (well-formed to explosive and loose ± presence of undigested vegetables in stool)

NOTE: Child is well and thriving (no precipitating dietary factors and normal examination)

253
Q

Investigations for toddler’s diarrhoea

A

CLINICAL DIAGNOSIS

254
Q

Management of toddler’s diarrhoea

A

Increased fibre and fat in diet (whole milk, yoghurts, cheeses)  relieve symptoms
Avoid fruit juice and squash

255
Q

What to avoid in toddler’s diarrhoea?

A

Avoid fruit juice and squash

256
Q

What is infantile colic?

A

Paroxysms of uncontrollable crying in an otherwise healthy infant.

257
Q

When does infantile colic typically resolve by?

A

3-12 months

258
Q

Presentation of infantile colic

A

manifests as random inconsolable crying and drawing up on the hands and feet

259
Q

PACES: Questions to ask in infantile colic

A

Clarify onset and duration of episodes
Clarify what happens in these episodes
Rule out any signs of illness
Check how parents are coping / support

260
Q

How is infantile colic diagnosed?

A

CLINICALLY

261
Q

Management of infantile colic

A

Soothe infant – hold with gentle motion, optimal winding technique, white noise
If persistent → consider cow’s milk protein allergy or reflux,  consider:
(1) 2-week trial of whey hydrolysate formula; followed by
(2) 2-week trial of anti-reflux treatment
Support:
Self-help support group www.cry-sis.org.uk for families with excessive crying or sleepless children
Get support from health visitor, family, friends and other parents

262
Q

What diagnoses to consider if infantile colic?

A

consider cow’s milk protein allergy or reflux
consider:
(1) 2-week trial of whey hydrolysate formula; followed by
(2) 2-week trial of anti-reflux treatment

263
Q

PACES: What support to offer for infantile colic?

A

Self-help support group www.cry-sis.org.uk for families with excessive crying or sleepless children
Get support from health visitor, family, friends and other parents

264
Q

What can be given as a trial medication for infantile colic?

A

Simeticone (anti-flatulant)

265
Q

random inconsolable crying and drawing up of the knees

A

Infantile Colic

266
Q

What is eosinophillic oesophogitis?

A

Inflammation of the oesophagus associated with activation of eosinophils within the oesophageal mucosa and submucosa.

267
Q

Risk factors for eosinophillic oesophagitis

A

Atopic conditions (asthma, hay fever, eczema)

268
Q

Clinical features of eosinophillic oesophagitis

A

dysphagia

269
Q

Investigations for eosinophiliic oesophogitis

A

Imaging:
OGD and biopsy (to identify eosinophilic infiltration)

270
Q

Management of eosinophilic oesophagitis

A

Oral Corticosteroids

271
Q

What is IBS?

A

Chronic condition characterised by abdominal discomfort and issues with intestinal motility (diarrhoea or constipation or both).

272
Q

what sex is IBS more common in?

A

Females

273
Q

RFs for IBS

A

Depression
Anxiety
Female Sex
Family History

274
Q

Presentation of IBS

A

Non-specific abdominal pain (often relieved by defecation)
Diarrhoea
Constipation
Bloating

275
Q

How to diagnose IBS?

A

Diagnosis of exclusion

276
Q

Management of IBS

A

Reassurance
Identify and attend to sources of stress and anxiety
Encourage fluid intake
FODMAP diet
Mebeverine (anti-spasmolytic)

277
Q
A

Paeds (14 decks)

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