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Paediatrics > GI > Flashcards

GI Flashcards

1
Q

Red flag conditions for bile stained vomit

A

Intestinal obstruction

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2
Q

Red flag conditions for haematemesis

A

oesophagitis
Peptic ulceration
Oral or nasal bleeding
oesophageal variceal bleeding

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3
Q

Red flag conditions for projectile vomiting

A

pyloric stenosis

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4
Q

Red flag conditions for vomiting at end of paroxysmal coughing

A

Whooping cough

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5
Q

Red flag conditions for abdo tenderness

A

surgical abdomen

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6
Q

Red flag conditions for abdo distention

A

intestinal obstruction
strangulated inguinal hernia

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7
Q

Red flag conditions for hepatosplenomegaly

A

chronic liver disease, inborn error of metabolism

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8
Q

Red flag conditions for blood in stool

A

intussusception
bacterial gastroenteritis

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9
Q

Red flag conditions for severe dehydration or shock

A

severe gastroenteritis
systemic infection
diabetic ketoacidosis

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10
Q

Red flag conditions for bulging fontanelle or seizures

A

raised ICP

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11
Q

Red flag conditions for faltering growth

A

GORD
Coeliac

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12
Q

Posseting

A

small amounts of milk that often accompany the return of swallowed air

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13
Q

Vomiting

A

forceful ejection of gastric contents

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14
Q

Causes of vomiting in infants

A

GORD
Feeding problems
Infections
Food allergy or intolerance
Eosinophillic oesophagitis
Intestinal obstruction
Inborn errors of metabolism
Congenital adrenal hyperplasia
renal failure

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15
Q

Causes of vomiting in preschool children

A

Gastroenteritis
Infection
Appendicitis
Intestinal obstruction
Raised ICP
Coeliac disease
Renal failure
Inborn errors of metabolism
Torsion of testes

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16
Q

Causes of vomiting in school age children and above

A

Gastroenteritis
Infection
Peptic ulceration and H.pylori
Appendicitis
Migrane
Raised ICP
Coeliac disease
Renal failure
Diabetic ketoacidosis
Alcohol or dug ingestion
Cyclical vomiting syndrome
Bulimia or anorexia
Pregnancy
Torsion of testes.

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17
Q

GORD

A

involuntary passage of gastric contents into oesophagus
Common in pregnancy

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18
Q

Contributions to GORD

A

liquid diet
Horizontal posture
Short intrabdominal length of oesophagus

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19
Q

Resolution of spontaneous GORD

A

Within 12 months
Probably due to maturation of LOS, upright posture and more solids in diet

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20
Q

RF GORD

A

Children with cerebral palsy or other neurodevelopmental disorders

Preterm infants - bronchopulmonary dysplasia

Surgery - oesophageal atresia or diaphragmatic hernia

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21
Q

Complications of GORD

A

Faltering growth
Oesophagitis
Recurrent pulmonary aspiration
Dystonic neck posturing (sandier syndrome)
Apparent life threatening events.

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22
Q

Ix GORD

A

Clinical

Failure to respond to treatment -
24 hour pH monitoring
24 hour impedance monitoring
Endoscopy with oesophageal biopsies to identify oesophagitis or other causes

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23
Q

Management of uncomplicated GORD

A

Parental reassurance
adding inert thickening agents
smaller and more frequent feeds

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24
Q

Management significant GORD

A

Acid suppression - hydrogen receptor antagonists ranitidine or PPI omeprazole

Nissen fundoplication in which funds of stomach wrapped around the intrabdominal oesophagus - for those unresponsive medical management or intensive medical treatment.

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25
Q

Pyloric stenosis

A

hypertrophy of the pyloric muscle causing gastric outlet obstruction.
Presents 2-8 weeks of age.
More common in boys

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26
Q

Clinical features of pyloric stenosis

A

Vomiting, which increases in frequency and forcefulness over time, ultimately becoming projectile

Hunger after vomiting until dehydration leads to loss of interest in feeding

Weight loss if presentation is delayed

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27
Q

Ix and examination pyloric stenosis

A

Test feed
- Gastric peristalsis may be seen as a wave from left to right abdomen

Pyloric mass - olive size - usually palpable in RUQ.

If stomach overdistended with air - emptied by nasogastric tube to allow palpation

USS

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28
Q

Management Pyloric stenosis

A

Correct any fluid and electrolyte disturbances with IV fluids

Pyloromyotomy - division of hypertrophied muscle down to, but not including mucosa.

Fed within 6 hours and discharged within 2 days

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29
Q

Common causes of sudden onset crying

A

UTI
Middle ear or meningeal infection
Pain from unrecognised fracture
Oesophagitis
Torsion of testes
Severe nappy rash
Constipation
Eruption of teeth

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29
Q

Features of Infant colic

A

paroxysmal inconsolable crying or screaming
accompanied by drawing up of knees and passage of excessive flatus several times a day

40% of babies
Occurs in first few weeks of life and resolves gradually from 3-12 months

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30
Q

Surgical causes of acute abdo pain

A

Appendicitis
Intestinal obstruction
Inguinal hernia
Peritonitis
Inflamed mocked diverticulum
Pancreatitis
Trauma

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31
Q

Medical causes of abdo pain

A

UTI
HSP
Diabetic ketoacidosis
Sickle cell
Hepatitis
IBD
Constipation
Psychological
Lead poisoning
Acute porphyria (rare)

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32
Q

Extraabdominal causes of acute abdominal pain

A

URTI
Lower lobe pneumonia
Torsion of the testes
Hip and spine

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33
Q

Signs and Symptoms of acute appendicitis

A

Anorexia
Vomiting
Abdominal pain - central and colicky but then localising to the right iliac fossa

Fever
Persistent tenderness with guarding in the right iliac fossa (Mcburneys)

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34
Q

Ix and treatment of Acute appendicitis

A

Thickened non compressible appendix with increased blood flow - USS

Appendicectomy

If no palpable mass in RIF and no signs of generalised peritonitis - IV abx and waiting several weeks

Potential laparotomy if no other explained symptoms

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35
Q

Complicated appendicitis

A

presence of appendix mass
abscess
perforation

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36
Q

Non specific abdominal pain

A

Pain that resolves in 24-48 hours

Often accompanied by URTI with cervical lymphadenopathy

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37
Q

Intussusception

A

Invagination of proximal bowel into a distal segment
Commonly involves ileum passing into caecum through ileocaecal valve

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38
Q

Epidemiology of intussusception

A

Common cause of intestinal obstruction
Peak age 3 months - 2 years

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39
Q

Complication Intussusception

A

Stretching and constriction of mesentery resulting in venous obstruction, causing engorgement and bleeding from bowel mucosa, fluid loss and bowel perforation, peritonitis and gut necrosis.

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40
Q

Presentation Intussusception

A

Paroxysmal, severe colicky pain with pallor - especially around the mouth, draws up legs

May refuse feeds, vomit which may become bile stained

Sausage shaped mass - often palpable in abdo

Passage of redcurrant jelly stool

Abdominal distension and shock

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41
Q

Management of intussusception

A

IV fluid resuscitation likely to be required immediately as often pooling of fluid in gut leading to hypovolaemic shock

Unless signs of peritonitis, reduction of it by rectal air insufflation. Only when child has been resuscitated

When peritonitis present or recurrence or all else fails - surgery

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42
Q

Ix intussusception

A

X-ray = Distended small bowel and absence of gas in the distal colon or rectum.

Abdo USS - confirm diagnosis, donut sign.

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43
Q

Meckel diverticulum

A

Remenant of Vitelli-intestinal duct - contains ectopic gastric mucosa or pancreatic tissue.

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44
Q

Signs and Symptoms of meckel diverticulum

A

Asymptomatic
Severe rectal bleeding
Acute reduction in haemoglobin

Intussusception, volvulus or diverticulitis

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45
Q

Ix and management meckel diverticulum

A

Technetium scan - increased ectopic gastric mucosa

Surgical resection

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46
Q

Malrotation

A

During rotation of the small bowel in metal life
If mesentery is not fixed at the duodenojejunal flexure or in the ileocaecal region - leads to:

Its base is shorter than normal and is predisposed to volvulus.

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47
Q

Two presentations of malrotation

A

Obstruction or Obstruction with a compromised blood supply

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48
Q

Complications of malrotation

A

Dark green vomiting leading to upper GI contrast studies revealing vascular compromise - urgent laparotomy needed

Leads to volvulus occurring and the superior mesenteric arterial blood supply to the small intestine and proximal large intestine is compromised and unless corrected will lead to infarction of areas

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49
Q

Management of malrotation

A

Operation - volvulus is untwisted - duodenum mobilised and the bowl placed in the non-rotated position with the duodenojejunal flexure on the right and the caecum and appendix on the left.

Malrotation not corrected but mesentery broadened.

Appendix generally removed to avoid diagnostic confusion for appendicitis

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50
Q

Ix of recurrent abdominal pain

A

Urine microscopy and culture
Abdo USS
Coeliac antibodies
thyroid function test
Other investigations only if clinically indicated

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51
Q

Causes of recurrent abdominal pain

A

IBS
Constipation
Non-ulcer dyspepsia
Abdominal migraine
Gastritis or peptic ulceration
Eosinophillic oesophagitis
IBD
Malrotation

Dysmenorrhoea
Ovarian cysts
Pelvic inflammatory disease

Psychosocial

Hepatitis
Gall stones
Pancreatitis

UTI
PUJ obstruction

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52
Q

Signs and symptoms that suggest organic disease of recurrent abdominal pain

A

Epigastric pain at night
Haematemesis
Diarrhoea
Weight loss
Growth failure
Vomiting
Dysuria
Jaudice
Biliary vomiting and abdominal distension

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53
Q

Abdominal migraine

A

Abdominal pain in addition to headaches and in some cases abdo pain predominates
No fhx
Long periods of no symptoms and then a shorter period of 12-48h with symptoms and non-specific abdominal pain and pallor

Treatment is anti migraine medication

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54
Q

Irritable bowel syndrome

A

Altered GI mobility and an abnormal sensation of intra abdominal events

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55
Q

Symptoms of IBS

A

Non specific abdominal pain - often peri umbilical and may be worse before or relieved by defaecation

explosive, loose or mucous stools
Bloating
Feeling of incomplete defection
Constipation

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56
Q

Bacterial cause of duodenal ulcers

A

H.pylori

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56
Q

treatment of peptic ulceration

A

PPI - omeprazole and then eradication therapy of amoxicillin and metronidazole or clarithromycin

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57
Q

Functional dyspepsia

A

Suspected peptic ulceration with endoscopy and no abnormalities - functional dyspepsia

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58
Q

Differences in symptoms of functional dyspepsia vs peptic ulceration

A

Functional has more general non-specific symptoms
Early satiety
Bloating
Postprandial vomiting
Delayed gastric emptying

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59
Q

Eosinophilic oesophagitis

A

Inflammatory condition affecting oesophagus caused by activation of eosinophils within the mucosa and submucosa.

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60
Q

Presentation eosinophilic oesophagitis

A

Vomiting
Discomfort on swallowing
Bolus dysphagia

More common in children with atopy

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61
Q

Disagnosis eosinophilic oesophagitis

A

endoscopy

Macroscopic - linear furrows and trachealisation of the oesophagus

Micro - eosinophilic infiltration

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62
Q

Treatment eosinophilic oesophagitis

A

swallowed corticosteroids - fluticasone or viscous budesonide

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63
Q

most frequent cause of gastroenteritis

A

Rotavirus

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64
Q

How to tell if gastroenteritis is bacterial and what bacteria is most common

A

Blood in stools
Campylobacter jejuni

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65
Q

Symptoms of shigella gastroenteritis

A

blood and pus in stool
Pain
Tenesmus
Fever

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66
Q

Symptoms of cholera and e.coli infection gastroenteritis

A

profuse, rapidly dehydrating diarrhoea

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67
Q

Complication of gastroenteritis

A

Dehydration leading to shock

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68
Q

RF Inc risk of dehydration

A

Infants <6months or LBW
Passed 6+ diarrhoea stools in last 24 hours
Vomited 3+ times in last 24h
Unable to tolerate extra fluids
Malnutrition

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69
Q

Why are infants more susceptible to dehydration

A

Greater surface area to weight ratio leading to greater insensible water losses.

Have higher basal fluid requirements and immature renal tubular reabsorption

Unable to obtain fluids themselves when thirsty

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70
Q

Most accurate method of measuring dehydration

A

Degree of weight loss during illness.
No clinically detectable dehydration = <5% loss
Clinically detectable 5-10%
Shock >10%

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71
Q

Isonatraemic dehydration

A

losses of sodium and water are proportional and plasma sodium remains within normal range

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72
Q

Hyponatraemic dehydration

A

Greater net loss of sodium than water leading to a fall in plasma sodium

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73
Q

Complications of hyponatraemic dehydration

A

Shift of water from extracellular to intracellular compartments and inc in intracellular volume leads to inc in brain volume which may result in seizures.
Marked extracellular depletion leads to greater degree of shock per unit of water loss.

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74
Q

Hypernatraemic dehydration

A

water loss exceeds relative sodium loss and plasma sodium concentration increases

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75
Q

How does hypernatraemic dehydration happen

A

high insensible water loss - fever, hot or dry environment
or from profuse low sodium diarrhoea

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76
Q

Signs of extracellular fluid depletion

A

depression of the fontanelle
Reduced tissue elasticity
Sunken eyes

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77
Q

Complication of hypernatraemic dehydration

A

water drawn out of brain and leads to cerebral shrinkage.

Lead to jittery movements, inc muscle tone hyperreflexia and altered consciousness. Seizures and multiple small cerebral haemorrhages

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78
Q

Ix gastroenteritis

A

Stool culture if child appears septic, blood or mucus in stool or child is immunocompromised.

May also be required if foreign travel recent and not improved by day 7

Plasma electrolytes, urea, creatinine and glucose should be checked if IV fluids required

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79
Q

Management gastroenteritis

A

Abx if bacterial

Oral rehydration

IV fluid for shock or deterioration or persistent vomiting

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80
Q

Why does diarrhoea resolve with oral rehydration solution

A

Large amounts sodium excreted in intestine but nearly all reabsorbed.

Sodium is allied to absorption of glucose. Sodium then actively pumped from epithelial cells into circulation via Na/K adenosine triphosphatase, creating electrochemical gradient water moves down.

If oral solution contains both glucose and sodium, passive water absorption is increased. Works even if inflammation in gut

Does not solve the infective organism, but keeps child hydrated and healthy until it passes.

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81
Q

Antidiarrhoeal drugs - loperamide and lomotil and antiemitics in gastroenteritis

A

Should not be used because:
- Ineffective
- May prolong secretion of bacteria in stools
- Associated with side effects
- Unnecessary costs
- Focus attention away from oral rehydration

82
Q

Abx in gastroenteritis

A

Not routinely used even in bacterial cases unless
Only in suspected or confirmed sepsis, extra intestinal spread of bacterial infection , for salmonella - if aged under 6 months, in malnourished or immunocompromised or for specific bacterial or protozoal infections

83
Q

Treatment following diarrhoea

A

nutritional intake increased
May be associated with zinc deficiency and supplementation may be helpful as treatment and prophylaxis.

84
Q

Postgastroenteritis syndrome

A

introduction of normal diet results in return of watery diarrhoea and oral rehydration should be restarted.

85
Q

Manifestations of digestion or absorption disorder

A

Abnormal stools
Poor weight gain or faltering growth
Specific nutrient deficiencies

86
Q

Coeliac disease

A

enteropathy in which the gliadin fraction of gluten and other related protamines in wheat barley and rye provoke a damaging immunological response in the proximal small intestinal mucosa

87
Q

Pathophysiology coeliac

A

Migration of absorptive cells moving up villi - enterocytes - from the crypts is increased but is insufficient to compensate for increased cell loss from villous tips.

Villi become progressively shorter and absent. - leaving a flat mucosa

88
Q

Presentation of coeliac

A

profound malabsorption syndrome at 8-24 months

Faltering growth
Abdominal distension
Buttock wasting
Abnormal stools
General irritability.

More likely to present less acutely in later childhood

89
Q

Clinical features coeliac

A

Mild-non-specific GI symptoms
Anaemia
growth faltering

90
Q

RF coeliac

A

T1DM
Autoimmune thyroid disease
Down syndrome
1st degree relatives of individuals known with coeliac

91
Q

Ix of coeliac

A

SI biopsy - increased intraepithelial lymphocytes and a variable degree of villous atrophy and crept hypertrophy

Screening tests - Anti-tTg and EMA - IgA and endomysial antibodies

92
Q

Management of coeliac

A

All products containing wheat, rye and barley are removed from diet
Supervision from dietician

If first diagnosis doubtful then tested again later in life.

Gluten free diet adhered to for life

93
Q

Complications of non adherence to gluten diet

A

micronutrient deficiency
osteopenia
inc risk bowel malignancy especially small bowel lymphoma

94
Q

Chronic non-specific diarrhoea - toddler diarrhoea

A

preschool children

Stools are of varying consistency

Undigested veg in stools is common

May result in undiagnosed coeliac, or excessive ingestion of fruit juice - especially apple juice

Temporary cows milk allergy following gastroenteritis

Most commonly - dysmotility of the gut - form of IBS and fast-transit diarrhoea

Almost always improves with age

95
Q

IBD causes

A

genetics
Gut microbiome
Mucosal immunity
Autoimmune diseases

96
Q

What condition is more common that UC

A

Crohns

97
Q

Difference between crohns and UC

A

Any part of GI tract

Uc - inflammation confined to colon

98
Q

Presentation crohns

A

Growth failure
Puberty delayed
Abdo pain.
Diarrhoea
Weight loss
Fever
Lethargy
Oral lesions
Uveitis
Arthralgia
Erythema nodosum

99
Q

Why is there delay in crohns diagnosis

A

Mistaken for psych problems or anorexia nervosa

100
Q

Pathophysiology Crohns

A

transmural, focal, subacute or chronic inflammatory disease

Most commonly affecting the distal ileum and proximal colon.

Initially acutely inflamed, thickened bowel.
Next - strictures of the bowel and fistulae may develop between adjacent loops of bowel, between bowel and skin or to other organs.

101
Q

Diagnosis of crohns

A

endoscopic or histological findings on biopsy

upper GI endoscopy, ileocolonoscopy and small bowel imaging are required

Histology - presence of non-caveating epitheliliod cell granulomata

Small bowel imaging - narrowing, fissuring, mucosal irregularities and bowel wall thickening

102
Q

Acute presentation remission in crohns

A

diet replaced by whole protein modular feeds - for 6-8 weeks

Systemic steroids are required if ineffective

103
Q

How to prevent relapse crohns

A

immunosuppressant medication - azathioprine, mercaptopurine or methotrexate

Anti-tumour necrosis agents - infliximab, adalimumab if other treatments have failed

Growth failure correction - long term supplemental enteral nutrition - often with overnight nasogastric or gastrostomy

Surgery - complications

104
Q

UC

A

recurrent inflammatory and ulcerating disease involving the mucosa of the colon.

105
Q

presentation of UC

A

rectal bleeding
diarrhoea
Colicky pain
Weight loss
Growth failure

106
Q

Diagnosis UC

A

endoscopy - confluent colitis extending from rectum proximally for a variable length.
Histology - mucosal inflammation, crypt damage and ulceration

Small bowel imaging - check that extra-colonic inflammation suggestive of crohns is not present.

107
Q

Difference in UC in adults to children

A

adults - limited to distal colon,

Children - pancolitis

108
Q

Mild disease UC treatment

A

aminosalicylates - mesalazine are used for induction and maintenance.

109
Q

Management of UC confined to the rectum and sigmoid colon (rare in children)

A

topical steroids

109
Q

Severe UC treatment

A

systemic steroids for acute exacerbations and immunomodulatory therapy - azathioprine alone to maintain remission or in combination with Low dose corticosteroid therapy

110
Q

If all other medication fails UC

A

Infliximab or ciclosporin - biological therapies

Surgery - colectomy with an ileostomy or ileorectal pouch

Severe fulminating disease - IV fluid and steroids

111
Q

Average no stools in infancy

A

4x a day up until first year and then average two per day

Breastfed children may not pass stool for several days and be entirely healthy

112
Q

Constipation definition

A

infrequent passage of dry, hardened faeces - accompanied by straining or pain and bleeding associated with hard stools.

May be abdominal pain, which waxes and wanes with passage of stool or overflow soiling

113
Q

RF constipation

A

dehydration or reduced fluid intake
Anal fissure causing pain
Problems with toilet training
Refusal and and anxieties about opening bowels at school or unfamiliar situations

114
Q

Examination constipation

A

well child
normal growth
abdomen is soft
abdominal distention normal for age

Soft fecal mass may sometimes be palpable in lower abdomen

115
Q

Underlying causes constipation

A

Hirschsprung disease
lower spinal cod problems
anorectal abnormalities
hypothyroidism
coeliac disease
hypercalcaemia

116
Q

red flag symptoms of constipation

A

Failure to pass meconium within 24 hours of life - Hirschsprung disease

Faltering growth

Gross abdominal distention - Hirschsprung

Abnormal lower limb neurology or deformity - Lumbosacral pathology

Sacral dimple above natal cleft or over spine - spina bifida occulta

Abnormal appearance / position / latency of anus

Perianal bruising or multiple fissures - sexual abuse

Perianal fistulae, abscess or fissures - perianal crohns

117
Q

Treatment mild constipation

A

polyethylene glycol 3350 + electrolytes

+ or - stimulant laxative - sodium picosulphate or Senna

IF GOOD RESPONSE

Laxative therapy as seen above for minimum 6 months

118
Q

Treatment of impaction constipation

A

polyethylene glycol 3350 + electrolytes disimpaction regime - escalating dose over 1-2 weeks

If good response move forward to normal mild constipation therapy

If INADEQUATE RESPONSE
Add stimulant laxative

119
Q

Complications of long standing constipation

A

rectum becomes overdistended
Subsequent loss of feeling to defecate
Involuntary soiling - contractions of the full rectum inhibit internal sphincter leading to overflow

120
Q

Lifestyle advise for chronic constipation

A

NO dietary interventions proven helpful

No fibre inc intake - may make stools larger

Normal fluid and balanced diet

Child encourage to sit on toilet after meals to utilise physiological gastrocolic reflex and improve likelihood of successful defecation

121
Q

Hirschsprung disease

A

Absence of ganglion cells from myenteric and submucosal plexuses of part of the large bowel - resulting in a narrow contracted segment which extends from the rectum for a variable distance proximally ending in a normally innervated and dilated colon

122
Q

Most common lesion area in HD

A

Rectosigmoid

123
Q

Presentation of Hirschsprung disease

A

neonatal period
Intestinal obstruction by failure to pass meconium within first 24 hours life
Abdominal distention and bile stained vomitingDi

124
Q

Ix Hirschsprung disease

A

Rectal exam - narrowed segment and withdrawal of the examining finger often releases a gust of liquid stool and flatus

Absence of ganglion cells with presence of large acetylcholinesterase positive nerve trunks on a suction renal biopsy

Anorectal manometry or barium studies - surgeon idea of length of ganglionic segment

125
Q

Presentation of severe life threatening Hirschsprung

A

chronic constipation
Abdo distention and without soiling
Growth failure

126
Q

Management Hirschsprung

A

Surgical - initial colonstomy followed by anatomising normally innervated bowel to anus.

127
Q

Marasmus

A

Malnutrition

128
Q

Kwashiorkor

A

Malnutrition specific to protein deficiency

129
Q

Prominent feature of liver disorders in children

A

Prolonged neonatal jaundice (> 14 days if term and >3 weeks if preterm)

130
Q

Signs and symptoms of hepatic dysfunction

A

Encephalopathy
Jaundice
Epistaxis
Varices with portal hypertension
Spider naevi
Muscle wasting from malnutrition
Bruising and petechiae
Splenomegaly with portal hypertension
Hyperslenism
Hepatorenal failure
Palmar erythema
Clubbing
Loss of fat stores secondary to malnutrition
Ascites
Hypotonia
Peripheral neuropathy
Rickets secondary to Vit D deficiency

131
Q

Causes of prolonged unconjugated jaundice

A

Breastmilk jaundice
Infection
Haemolytic anaemia
Hypothyroidism
High GI obstruction
Crigler-najjar syndrome

132
Q

Causes of conjugated persistent neonatal jaundice

A

Bile duct obstruction - biliary atresia and choledochal cyst

Neonatal hepatitis syndrome - Congenital infection
- Inborn errors
- a1-antitrypsin deficiency
- Galactosaemia
- Tyrosinaemia

Intrahepatic biliary hypoplasia
- Alagille syndrome

133
Q

Biliary atresia

A

Progressive fibrosis and obliteration of the extrahepaoc and intrahepatic biliary tree.

134
Q

Complications of biliary atresia

A

Chronic liver failure and death within 2 years

135
Q

Presentation of biliary atresia

A

Mild jaundice and pale stools. Normal birthweight but faltering growth.
Hepatomegaly and splenomegaly develops due to portal hypertension

136
Q

Ix biliary atresia

A

Inc conjugated bilirubin and abnormal LFT

Fasting abdo USS - contracted or absent gallbladder

Cholangiogram - ERCP - fails to outline normal biliary tree.

Liver biopsy - neonatal hepatitis with features of extra hepatic biliary obstruction

136
Q

Treatment of biliary atresia

A

Palliative surgery with a kauai hepatoportoenterostomy (where a loop of jejunum is anastomosed to the cut surface of porta hepatitis) which bypasses the fibrotic ducts and facilitates drainage of bile from remaining patent ductules.

Nutrition and fat soluble vitamin supplementation.

Liver transplant if previous surgery fails.

137
Q

Choledochal cysts

A

Cystic dilations of the extra hepatic biliary system.

138
Q

Signs and symptoms and Ix of choledochal cysts

A

Neonatal jaundice or in older children with abdo pain, palpable mass or cholangitis.
USS or MRCP - cysts present

139
Q

Treatment choledochal cysts

A

Surgical excision of the cyst with a roux-en-y anastomosis of the biliary duct.

140
Q

Neonatal hepatitis syndrome

A

Prolonged neonatal jaundice and hepatic inflammation
Babies may have LBW and faltering growth.
Liver biopsy - giant cell hepatitis.

141
Q

Alagille syndrome

A

Rare autosomal dominent condition.- characteristic triangle facies, skeletal abnormalities, congenital heart disease, renal tubular disorders and defects in the eye.

May be cholestatic with severe pruritis and faltering growth.

Identifying gene mutation confirms diagnosis and treatment is to provide nutrition and fat soluble vitamins.

Small number will require transplantation.

141
Q

Clinical presentation progressive familial intrahepatic cholestasis

A

Jaundice
Intense pruritis
Faltering growth
Rickets
Diarrhoea
Hearing loss
Gallstones in older children

142
Q

Diagnosis and treatment of progressive familial intrahepatic cholestasis

A

Identifying mutations in bile salt transport genes.
Treatment nutritional support and fat soluble vitamins.

143
Q

Types of neonatal metabolic liver disease

A

A1-antitrypsin deficiency
Galactosaemia

143
Q

Pathophysiology A1 antitrypsin deficiency

A

Autosomal recessive disorder
There are many phenotypes of the protease inhibitor which are coded on chromosome 14 with liver disease primarily with PiZZ
Abnormal folding of the protease a1 antitrypsin is associated with the accumulation of the protein within the hepatocytes and hence liver disease in infancy and childhood.

144
Q

Presentations of a1 antitrypsin deficiency

A
  • Prolonged neonatal jaundice
  • Bleeding due to vit k deficiency
  • Hepatomegaly
  • Splenomegaly with cirrhosis and portal hypertension
145
Q

Diagnosis of a1 antitrypsin deficiency

A
  • Estimating level of antitrypsin in the plasma and identifying protein phenotype.
146
Q

Galactosaemia

A

Infants develop poor feeding, vomiting, jaundice and hepatomegaly when fed milk.
Liver failure, cataracts and developmental delay

147
Q

Acute complication of galactosaemia

A

Shock
Haemorrhage
Disseminated intravascular coagulation often due to gram negative sepsis

148
Q

Ix galactosaemia

A

Galactose - a reducing substance in the urine.
Measuring the enzyme galactose-1-phosphate-uridyl transferase in red cells.
Recent blood transfusion may mask the diagnosis.

149
Q

Management of galactosaemia

A

galactose free diet

150
Q

Features of hepatitis in children

A

nausea
Vomiting
Abdominal pain
Lethargy
Jaundice
Large tender liver

Liver transaminases are markedly elevated
Normal coagulation

151
Q

Hep A

A

RNA virus which is spread by faecal-oral transmission

Vaccinations in endemic areas

May be asymptomatic but have mild illness and recover both clinically and biochemically within 2-4 weeks.

152
Q

Diagnosis and treatment Hep A

A

detecting IgM antibody to virus.
No treatment and no evidence that bed rest or change of diet is effective.

Close contacts vaccinated within 2 weeks of the onset of illness.

153
Q

HBV

A

DNA virus
Africa and far east
Cause of acute and chronic liver failure

Perinatal transmission from carrier mothers or horizontal spread within families
Inoculation from infected blood via transfusion, needles or renal dialysis
Sexual transmission

154
Q

Symptoms, Management and Ix of HBV

A

Asymptomatic but 90% chronic carriers.
Majority resolve spontaneously
1-2% develop fulminant hepatic failure

Diagnosis - detecting HBV antigens and antibodies. IgM antibodies to the core antigen are positive in acute infection.
Hep B surface antigen HBsAg denotes ongoing infectivity

No treatment.

155
Q

Chronic HBV

A

Some progress
Risk of hepatocellular carcinoma

Interferon or pegylated interferon treatment helpful in 30-50% children

Oral antiviral therapy - lamivudine and adefovir

Newer drugs ? - entecavir, tenofovir and telbivudine.

156
Q

Prevention Hep B

A

antenatal screening for HBsAg.
Babies of HBV mothers should receive course of hep B vaccination
Hep B immunoglobulin if mother is also HBeAg positive

157
Q

HCV

A

RNA virus
High among IV drug users
vertical transmission is most common in children.

Risk of cirrhosis or hepatocellular carcinoma

158
Q

Treatment HCV

A

Combination of pegylated interferon and ribavirin.

Oral antivirals - sofobuvir

No treatment before 3YO as may resolve spontaneously after vertical transmission

159
Q

HDV

A

Defective RNA depending on HBV for replication
Occurs as confection
Cirrhosis develops in 50-70% of those with HDV

160
Q

HEV + HEV in pregnancy

A

RNA
Enterally transmitted but usually in contaminated water
Mild and self limiting
Transmitted by blood transfusion, infected pork
In pregnant women - fulminant hepatic failure with a high mortality rate.

161
Q

Fulminant hepatitis - Acute liver failure

A

Development of hepatitis necrosis with subsequent loss of liver function

162
Q

Presentation of acute liver failure

A

within hours or weeks with
jaundice
encephalopathy
coagulopathy
hypoglycaemia
electrolyte disturbance

Alternate periods of irritability and confusion with drowsiness

Older children - aggressive and unusually difficult

163
Q

Complications of acute liver failure

A

cerebral oedema
haemorrhage
sepsis
pancreatitis

164
Q

Diagnosis of ALF

A

Bilirubin normal in early stages

Transaminases are greatly elevated
ALP inc
Coagulation abnormal
Plasma ammonia elevated

EEG - acute hepatic encephalopathy
CT - Cerebral oedema

165
Q

Management ALF

A

Maintaining blood glucose with IV dextrose
Preventing sepsis - broad spec abx
Preventing haemorrhage - IV Vit K and H2 blocking drugs or PPI
Prevent cerebral oedema by fluid restriction and mannitol diuresis

166
Q

Causes of ALF in children <2

A

Infection - herpes simplex
Metabolic disease
Seronegative hepatitis
Drug induced
Neonatal haemochromatosis

167
Q

Causes of ALF in children >2

A

Seronegative hepatitis
Paracetamol overdose
Mitochondrial disease
Wilson disease
Autoimmune hepatitis

168
Q

Causes of chronic liver failure in older children

A

Postviral Hep B and C
Autoimmune hep and sclerosis cholangitis
Drug induced - NSAIDS
CF
Wilson
Fibropolycystic liver disease
NAFLD
A1-antitrypsin deficiency

169
Q

Liver complications of CF

A

hepatic steatosis
Protein energy malnutrition or micronutrient deficiencies
Thick tenacious bile with abnormal bile acid concentration leading to progressive biliary fibroids

Liver histology - fatty liver, focal biliary fibroids, or focal nodular cirrhosis.

170
Q

Treatment of liver complications with CF

A

endoscopic treatment of varies and nutritional therapy
Ursodeoxycholic acid
Liver transplantation

171
Q

Wilson disease

A

reduced synthesis of caeruloplasmin (copper binding protein) and defective excretion of copper in the bile which leads to an accumulation of copper in the brain, liver, kidney and cornea

172
Q

Presentation of Wilsons disease

A

Liver problems

Acute hepatitis
Fulminant hepatitis
Cirrhosis
Portal hypertension
Vit D resistent rickets
Renal tubular dysfunction

Kayser-fleischer rings not seen before 7 YO

Second decade - Incoordination, tremor, dysarthria

173
Q

Ix Wilsons

A

Low serum caeruloplasmin and copper

Urinary copper excretion increased
Further inc after administering chelating agent penicillamine

Elevated hepatic copper on liver biopsy or identification of gene mutation - diagnosis confirmed

174
Q

Treatment wilson

A

Penicillamine or Trientine - promote urinary copper excretion reducing hepatic and CVS copper

Zinc - reduce copper absorption

Pyridoxine - prevent peripheral neuropathy

Liver transplant considered for end stage liver disease or ALF

175
Q

Congenital hepatic fibrosis and complications

A

Children over 2
Hepatosplenomegaly, abdominal distention and portal hypertension

Complications:
portal hypertension with varicose and recurrent cholangitis.

176
Q

Ix and management Congenital hepatic fibrosis

A

Differs from cirrhosis in that LFT are normal in the early stages

Liver histology shows large bands of hepatic fibrosis containing abnormal bile ductules

Liver transplant

177
Q

NAFLD progression

A

Steatosis to steatohepatitis to fibrosis, cirrhosis and end stage liver failure

178
Q

Symptoms NAFLD

A

Asymptomatic
Vague RUQ pain or lethargy

Incidental finding of echogenic liver on USS or mildly elevated transaminases carried out for some other reason.

Liver biopsy - marked steatosis with or without inflammation or fibrosis

179
Q

Treatment NAFLD

A

Weight loss through diet and exercise

180
Q

Fat soluble vitamins and complications of deficiency

A

K - bleeding diathesis, including intracranial bleeding

A - Retinal changed in infants and night blindness in older children

E - Peripheral neuropathy, haemolysis and ataxia

D - rickets and fractures

181
Q

Treatment pruritis

A

Loose cotton clothing and avoiding overheating
Keep nails short
Moisturising the skin with emollients

Medication

Phenobarbital - stim bile flow

Cholestryamine - bile salt resin to absorb bile salt

Ursodeoxycholic acid - oral bile acid to solubilise the bile

Rifampicin - enzyme inducer

182
Q

Treatment fat malabsorption

A

medium chain triglyceride containing milk if children are persistently cholestatic as it does not require bile micelles for absorption

183
Q

Presentation of hepatic encephalopathy

A

Infants - irritability and sleepiness
Older - abnormalities in mood, sleep rhythm, intellectual performance, and behaviour

Plasma ammonia may be elevated and EEG always abnormal

Oral lactulose and a non absorbable oral abx - rifaximin - will help reduce the ammonia by lowering colonic pH and increasing gut transit time.

184
Q

Cirrhosis

A

extensive fibrosis with regenerative nodules
Secondary to hepatocellular disease or chronic bile duct obstruction

185
Q

Pathophysiology cirrhosis

A

diminished hepatic function and portal hypertension, with splenomegaly, varies and ascites.

186
Q

Signs of cirrhosis

A

May be asymptomatic if liver function is okay

Jaundice
Palmar and plantar erythema
telangiectasia
spider nave
malnutrition
Hypotonia
Dilated abdominal veins and splenomegaly

187
Q

Ix cirrhosis

A

screening for known causes of liver disease

Upper GI endoscopy to detect the presence of oesophageal varicose and or erosive gastritis

Abdo USS - may show a shrunken liver and splenomegaly with gastric and oesophageal varices

Liver biopsy - May identify aetiology if can be done around the fibrosis.

188
Q

Oesophageal varices

A

consequence of portal hypertension and may develop rapidly

Upper GI endoscopy

Treatment - blood transfusions and H2 blockers - ranitidine or omeprazole.

189
Q

Treatment oesophageal varies if bleeding persists

A

octreotide infusion, vasopressin analogues, endoscopic band ligation or sclerotherapy

190
Q

Treatment ascites

A

sodium and fluid restriction and diuretics

191
Q

Indications of transplantation in chronic liver failure

A

Severe malnutrition unresponsive to intensive nutritional therapy
Complications refractory to medical management
Failure of growth and development
Poor quality of life.

192
Q

Pyloric stenosis Summary

A

Progressive hypertrophy of the pyloric sphincter causing gastric outlet obstruction

Epidemiology
- Much more common in boys
- Affects 1 in 500
- Family history
- First borns

Clinical Presentation
- Presents 4-6 weeks of age
- Non bilious, forceful, projectile vomiting after every feed approx 30 mins
- Will continue to feed despite vomiting
- Weight loss
- Dehydration
- Constipation
- Visible peristalsis
- Palpable olive sized pyloric mass felt

Investigations
- Test feed with NG tube and empty stomach to feel for visible peristalsis and olive
shaped mass
- USS - Hypertrophy of the muscle
- Blood gas - Hypochloremic, Hypokalemic Metabolic Alkalosis (loss of hydrogen
and chloride ions due to vomiting gastric contents)

Management
- Correct metabolic imbalances - NaCl
- Fluid bolus for hypovolemia
- NG tube and aspiration of the stomach
- Ramstedt’s Pyloromyotomy - feeding can commence 6 hours after procedure

193
Q

Hirschsprung’s disease summary

A

Nerve cells of the myenteric plexus are absent in the distal bowel and rectum, specifically the parasympathetic ganglionic cells resulting in lack of peristalsis.

Epidemiology
- 90% present in the neonatal period
- Average age of presentation: 2 days
- Males
- Down’s syndrome

Pathophysiology
Short segment is the most common type where the disease is confined to the rectosigmoid part of the colon
- Ganglion cells of the submucosal plexus aren’t present
- Failure of peristalsis and bowel movements causing obstruction
- Can lead to bacterial build up and enterocolitis (inflammation) and sepsis

Clinical Presentation
1. Failure to pass meconium (within 48 hours of birth)
2. Abdominal distention
3. Bilious vomiting
- Palpable faecal mass in the left lower abdomen
- Empty rectal vault

Investigations
Rectal suction biopsy to test for ganglionic cells in anyone who has:
- Delayed passage of meconium
- Constipation in the first few weeks
- Chronic abdominal distention
- Positive family history
- Faltering growth
Contrast Enema - Shows short transition zone between proximal and distal colon and a small rectal diameter

Management
IV Abx
Bowel decompression
NG tube
Surgery is definitive treatment: Swenson, Soave, Dunhamel pull through surgery

194
Q

Malrotation and Volvulus

A

Twisting loop of bowel leading to intestinal obstruction
- Generally presents in the first month of life

Clinical Presentation
- Abdominal pain
- Bilious vomiting
- Caecum at the midline
- Reflux symptoms

Investigations
- Barium enema
- Abdominal X-ray with contrast to look for obstruction (dilated stomach and
proximal small bowel - double bubble sign)

Treatment
Emergency surgical repair

195
Q

Intusucception summary

A
  • One piece of the bowel telescopes inside another leading to ischaemia and bowel obstruction
  • Most common in the distal ileum at the ileocecal junction

Epidemiology
- 3 months to 3 years
- Most commonly < 1
- Most common cause of obstruction in neonates

Risk factors
- CF
- Meckel’s diverticulum
- HSP
- Rotavirus vaccine > 23 weeks

Clinical Presentation
- Colic abdominal pain
- Pallor
- Sausage shaped mass palpable in the RUQ
- Redcurrant jelly stools, often late in presentation
- Abdominal distention
- Shock
- Peritonitis: Guarding, rigidity,pyrexia

Investigations
USS: target shaped mass
Abdominal X Ray: Distended small bowel, absence of gas in the large bowel

Treatment
Medical emergency
IV fluids
Air Enema using USS to stretch the walls of the bowel and reduce the intussusception -> if this is unsuccessful then surgery to repair manually
If perforation and peritonitis, broad spec Abx e.g Gentamicin

196
Q

Necrotising enterocolitis summary

A
  • Acute inflammatory disease affecting preterm neonates leading to bowel necrosis and multi system organ failure

Epidemiology
- Low birth weight (1500g)
- Most common surgical emergency in neonates
- Commonly presents in the first 2 weeks of life
- Prematurity
- Abx therapy > 10 days
- Genetic

Presentation
New feed intolerance
- Vomiting (+ bile)
- Fresh blood in stools
- Abdominal distention
- Reduced bowel sounds
- Palpable abdominal mass
- Visible intestinal loops
- Sepsis

Investigations
- Bloods: thrombocytopenia, neutropenia
- Cultures
- Blood gas: acidotic
- USS: Air in the portal system, ascites, perforation
- Xray:
1.Rigler’s sign: both sides of the bowel are visible due to gas in the peritoneal cavity
2. Dilated bowel loops
3. Distended bowel
4. Thickened bowel wall
5. Air outlining falciform ligament

Management
- Nil by mouth
- Bowel decompression by NG tube
- IV Cefotaxime
- Surgery to remove necrotic bowel

197
Q

Meckels Diverticulum Summary

A

Congenital diverticulum of the small intestine containing ileal, gastric and pancreatic mucosa
- Occurs in 2% of the population
- Is 2cm from the ileocecal valve
- Supplied by the omphalomesenteric artery
- Risk of peptic ulceration

Clinical Presentation
- Abdominal pain
- Rectal bleeding in children age 1-2 years
- Obstruction due to intussusception and volvulus

Management
- Removal if symptomatic (resection)

198
Q

Biliary Atresia Summary

A

Obstruction of the biliary tree due to sclerosis of the bile duct, reducing bile flow

Epidemiology
- Females
- Neonatal cholestasis 2-8 weeks
- Associated with CMV
- Congenital malformations

Pathophysiology
- Type 1: Common duct is obliterated
- Type 2: Atresia of the cystic duct in the porta hepatis
- Type 3: Most common atresia of the right and left ducts at the level of the porta
hepatis

Clinical Presentation
- Jaundice post 2 weeks
- Dark urine
- Pale stools
- Appetite disturbance
- Hepatosplenomegaly
- Abnormal growth
- Duodenal atresia - presents in the first 24 hours of life and more common in trisomy
21

Investigations
- Serum bilirubin: conjugated bilirubin high
- LFTs raised
- Alpha 1 antitrypsin to rule out deficiency
- Sweat test to rule out CF
- USS to look for structural abnormalities

Management
- Surgical dissection of the abnormalities: Kasai procedure - Abx

Complications
- Cirrhosis and HCC
- Progressive liver disease

199
Q

Neonatal Jaundice Summary

A
  • Caused by hyperbilirubinemia

Pathophysiology
1. Physiological
- Breakdown of in-utero Hb
- Immature liver cannot break down high bilirubin concentrations
- Starts 2-3 days of life, peak at day 5, usually resolves by 14 days

  1. Pathological Jaundice
    - Onset less than 24 hours is pathological
    - G6PD deficiency
    - Spherocytosis
  2. Prolonged Jaundice
    - Jaundice > 14 days in term infants and 21 days in preterm
    - Biliary atresia
    - Hypothyroidism
    - Breast milk jaundice resolves 1.5-4 months
    - UTI/Infection

Aetiology
- Prematurity
- Small for dates
- Previous sibling with neonatal jaundice

Clinical Presentation
- Colour
- Drowsiness
- Signs of infection

Investigations
- TCB can be used over 35 weeks gestations -> measures bilirubin in the skin
- Serum bilirubin if TCB cannot be used
- Total and conjugated bilirubin
- Coombs test
- Infection screen

Management
- Treatment threshold graphs for specific gestation
- Phototherapy will be used for those above threshold
- Those below the threshold should have levels rechecked within 24 hours
- Repeat bilirubin 4-6 hours after commencing phototherapy and 6-12 hourly once
levels stabilise
- Stop phototherapy once over 50umol/L from the treatment line
- Recheck bilirubin 12-18 hours after stopping
- Exchange transfusion

200
Q

Constipation Summary

A

An extremely common condition affecting children characterised by decreased frequency, increased harness of the stool and painful defecation.
- Most cases of constipation are idiopathic however it is important to think about secondary causes.

Secondary causes
- Hirschprung’s disease
- Cystic fibrosis
- Hypothyroidism
- Spinal cord lesions
- Sexual abuse
- Intestinal obstruction
- Cows milk intolerance

Clinical Presentation
- Less than 3 stools a week
- Hard stools that are difficult to pass
- Rabbit dropping stools
- Straining and painful passages of stools
- Abdominal pain
- Overflow soiling caused by faecal impaction
- Palpable hard stools in the abdomen

Management
- Idiopathic constipation can be diagnosed clinically, once red flags have been considered.
- Correction of any reversible contributors e.g. high fibre diet, good hydration
- Laxatives: Movicol is first line
- Disimpaction regimen may be needed with high dose of laxatives at first followed by
half the disimpaction dose as maintenance
- Encouragement of visiting the toilet to reduce withholding.

Paediatrics (17 decks)

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