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Phase 3a > Paediatrics- GI + Liver > Flashcards

Paediatrics- GI + Liver Flashcards

1
Q

What are the differences between ‘Posseting’, ‘Regurgitation’, and ‘Vomiting’?

A

Posseting is the small amounts of milk that accompany the return of swallowed air (wind)- happens in nearly all babies

Regurgitation describes larger, more frequent losses and may indicate GORD

Vomiting is forceful ejection of gastric contents

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2
Q

What are the causes of vomiting in children?

A

1) Gastro-oesophageal reflux
2) Feeding problems
3) Infection (GE, urinary tract, meningitis, pertussis, resp tract etc.)
4) Food allergy/intolerance
5) Intestinal obstruction (pyloric stenosis etc.)
6) Inborn errors of metabolism
7) Congenital adrenal hyperplasia
8) Renal failure

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3
Q

What are the causes of vomiting in preschool children?

A

1) GE
2) Infection (meningitis, pertussis, resp tract, urinary tract etc.)
3) Appendicitis
4) Intestinal obstruction
5) Raised ICP
6) Coeliac
7) Renal failure
8) Inborn errors of metabolism
9) Testicular torsion

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4
Q

What are the causes of vomiting in school age and adolescent children?

A

1) GE + Infection (pyelonephritis, septicaemia)
2) Peptic ulcer + H. Pylori infection
3) Appendicitis
4) Migraine
5) Raised ICP
6) Coeliac disease
7) Renal failure
8) Diabetic ketoacidosis
9) Alcohol/drug ingestion or meds
10) Cyclical vomiting syndrome
11) Bulimia/anorexia nervosa
12) Pregnancy
13) Testicular torsion

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5
Q

What are the red flags in the vomiting child?

A

1) Bile-stained vomit (obstruction)
2) Haematemesis (ulcer)
3) Projectile vomiting (pyloric stenosis)
4) Vomiting at end of cough (whooping cough)
5) Abdominal tenderness/pain on movement
6) Hepatosplenomegaly (chronic liver disease, metabolism problems)
7) Blood in stool (infection, obstruction)
8) Severe dehydration/shock (severe GE, systemic infection, ketoacidosis)
9) Bulging fontanelle/seizures (raised ICP)
10) Faltering growth (GORD, coeliac)

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6
Q

Gastro-oesophageal reflux is more common in what type of children?

A

1) Cerebral palsy or other neurodevelopmental disorders
2) Preterm infants (esp. bronchopulmonary dysplasia)
3) Following surgery for oesophageal atresia or diaphragmatic hernia

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7
Q

What are the complications of gastro-oesophageal reflux?

A

1) Faltering growth
2) Oesophagitis
3) Recurrent pulmonary aspiration
4) Dystonic neck posturing (Sandifer syndrome)
5) Apparent life-threatening events

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8
Q

How is gastro-oesophageal reflux investigated?

A

Usually clinically diagnosed- investigations indicated if atypical history, complications, or failure to respond to treatment

1) 24 hour oesophageal monitoring
2) 24 hour impedance monitoring
3) Endoscopy with oesophageal biopsies

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9
Q

How is gastro-oesophageal reflux managed?

A

Uncomplicated: good prognosis, managed by parental reassurance, thickening agents to feeds, making feeds smaller + more frequent

Significant reflux: ranitidine or omeprazole

Complicated + doesn’t respond to treatment/oesophageal stricture: Nissen fundoplication

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10
Q

What is pyloric stenosis?

A

Hypertrophy of the pyloric muscle causing gastric outlet obstruction. It presents at 2-8 weeks of age. More common in boys.

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11
Q

What is the presentation of pyloric stenosis?

A

Vomiting- increases in frequency/forcefulness until projectile

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

Weight loss (if delayed presentation)

Hypochloraemic metabolic alkalosis w/ a low plasma sodium + potassium

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12
Q

How is pyloric stenosis diagnosed?

A

1) Test feed: give milk feed, gastric peristalsis is seen moving from left to right across abdomen. Pyloric mass feels like an olive and is usually palpable in the RUQ
2) USS to confirm diagnosis if in doubt

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13
Q

How is pyloric stenosis managed?

A

1) Correct fluid + electrolyte imbalance with IV fluids

2) Pyloromyotomy (division of hypertrophied pyloric muscle down to the mucosa)

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14
Q

Name some extra-abdominal causes of acute abdominal pain:

A

1) URTI
2) Lower lobe pneumonia
3) Testicular torsion
4) Hip and spine

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15
Q

Name some intra-abdominal (medical) causes of acute abdominal pain:

A

1) GE
2) Urinary tract (UTI etc.)
3) Henoch-Schonlein purpura
4) Diabetic ketoacidosis
5) Sickle cell disease
6) Hepatitis
7) IBD
8) Constipation
9) Recurrent abdominal pain of childhood
10) Gynaecological
11) other (psychological, lead poisoning, acute porphyria)
12) Non-specific abdominal pain

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16
Q

Name some intra-abdominal (surgical) causes of acute abdominal pain:

A

1) Acute appendicitis
2) Intestinal obstruction
3) Inguinal hernia
4) Peritonitis
5) Inflamed Meckel diverticulum
6) Pancreatitis)
7) Trauma

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17
Q

What are the symptoms of acute appendicitis?

A

1) Anorexia
2) Vomiting
3) Abdominal pain (initially central + colicky –> localises to the RIF

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18
Q

What are the signs of acute appendicitis?

A

1) Flushed face with oral fetor
2) Low grade fever
3) Abdominal pain aggravated by movement)
4) Persistent tenderness with guarding in the RIF (McBurney’s point)
5) If retrocaecal there may be no guarding. If pelvic there may be few abdominal signs

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19
Q

How is acute appendicitis investigated?

A

1) Diagnosis made by repeat observation and clinical review. Avoid delay and unnecessary laparotomy.
2) USS- may support clinical diagnosis and demonstrate complications (perforation, abscess etc.).

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20
Q

How is acute appendicitis managed?

A

Uncomplicated: appendicectomy

Perforation: fluid resus + IV antibiotics given prior to laparotomy

Palpable mass w/ no signs of generalised peritonitis: IV antibiotics with surgery a few weeks later. If symptoms progress, do laparotomy

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21
Q

What is non-specific abdominal pain and mesenteric adenitis?

A

NSAP: abdominal pain which resolves in 24-48 hours.

Mesenteric adenitis: diagnosed in children who have large mesenteric nodes on laproscopy and whose appendix is normal.

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22
Q

How do you distinguish between non-specific abdominal pain and appendicitis?

A

The pain is less severe than appendicitis

Tenderness in the RIF is variable

Often accompanied with an URTI with cervical lymphadenopathy

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23
Q

What is intussusception and where does it normally happen?

A

Invagination of proximal bowel into a distal segment

Most commonly involves ileum passing into the caecum through the ileocaecal valve

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24
Q

When does intussusception tend to present?

A

Peak presentation is between 3 months and 2 years of age

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25
Q

What are the complications of intussusception?

A

Stretching and constriction of the mesentery –> results in venous obstruction –> causes engorgement and bleeding from the bowel mucosa, fluid loss, and subsequently bowel perforation, peritonitis, and gut necrosis

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26
Q

How does intussusception present?

A

1) Redcurrant jelly stool comprising blood stained mucus (CHARACTERISTIC)
2) Paroxysmal, severe colicky pain with pallor (becoming increasingly lethargic)
3) Sausage-shaped mass (often palpable in abdomen)
4) Abdominal distension and shock

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27
Q

How is intussusception investigated?

A

1) X-ray of abdomen: distended small bowel and absence of gas in distal colon or rectum
2) Abdominal USS: useful to confirm diagnosis and check response to treatment

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28
Q

How is intussuception managed?

A

1) Immediate IV fluid resus
2) If no signs of peritonitis: reduction of the intussusception by rectal air insufflation
3) If this fails, surgery is required

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29
Q

What is Meckel Diverticulum?

A

An ileal remnant of the vitello-intestinal duct which contains ectopic gastric mucosa or pancreatic tissue

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30
Q

What is the presentation of Meckel Diverticulum?

A

1) Most are asymptomatic
2) May present with severe rectal bleeding (neither bright red nor true melaena)
3) Other forms of presentation include intussusception, volvulus, or diverticulitis

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31
Q

How is Meckel Diverticulum investigated?

A

1) Usually an acute reduction in haemoglobin

2) A technetium scan will demonstrate increased uptake by ectopic gastric mucosa (in 70% of cases)

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32
Q

How is Meckel Diverticulum managed?

A

Surgical resection

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33
Q

What is the pathology of malrotation?

A

During rotation of the small bowel in foetal life, if the mesentery is not fixed at the duodenojejunal flexure or in the ileocaecal region its base is shorter than normal and is predisposed to volvulus

Ladd bands are peritoneal bands which may cross the duodenum, often anteriorly. They obstruct the duodenum or volvulus

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34
Q

What are the two ways in which malrotation presents?

A

Obstruction

Obstruction with a compromised blood supply: emergency

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35
Q

What are the presenting features of malrotation?

A

Bilious vomiting (often first few days of life)

Abdominal pain and tenderness (from peritonitis or ischaemic bowel)

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36
Q

How is malrotation investigated?

A

Urgent upper GI contrast study to assess intestinal rotation (always do when bilious vomiting)

If compromised blood supply: urgent laparotomy

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37
Q

How is malrotation treated?

A

Urgent surgical correction

Appendix is generally removed to avoid diagnostic confusion

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38
Q

What is the definition of recurrent abdominal pain?

A

Pain sufficient to interrupt normal activities that lasts over 3 months

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39
Q

How does recurrent abdominal pain present?

A

Characteristic peri-umbilical pain

Children are otherwise entirely well

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40
Q

What are the causes of recurrent abdominal pain?

A

IBS, Constipation, dyspepsia, abdominal migraine, gastric/peptic ulceration, eosinophilic oesophagitis, IBD, malrotation

Gynaecological

Psychological

Hepatobiliary (hepatitis, gallstones, pancreatitis)

Urinary tract (UTI, PUJ obstruction)

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41
Q

How is recurrent abdominal pain managed/investigated?

A

1) Full history + thorough examination (check growth)
2) Urine microscopy and culture
3) USS to exclude gallstones and PUJ obstruction
4) Coeliac antibodies and TFTs

42
Q

What is the prognosis of recurrent abdominal pain?

A

50%: rapidly become free of symptoms

25%: symptoms take months to resolve

25%: symptoms continue or return in adulthood as migraine, IBS, or functional dyspepsia

43
Q

Abdominal Migraine: Definition

A

Often associated with abdominal pain in addition to headaches, and in some children the abdominal pain predominates

44
Q

Abdominal Migraine: Epidemiology

A

Usually a personal or FH of migraine

45
Q

Abdominal Migraine: Presentation

A

Characteristic history with long periods of no symptoms and then a shorter period (12-48 hours) of non-specific abdominal pain and pallor, with or without vomiting

The attacks of pain are midline, associated with abdominal pain and facial pallor

46
Q

Abdominal Migraine: Management

A

Treatment with anti-migraine medication may be beneficial if the problem causes school absence

47
Q

IBS: Pathology

A

Associated with altered GI motility and an abnormal sensation of intra-abdominal events

Symptoms may be precipitated by a GI infection

Often a positive FH

48
Q

IBS: Presentation

A

Non-specific abdominal pain, may be worse before or relieved by defecation

Explosive, loose, or mucus stools

Bloating

Feeling of incomplete defecation

Constipation (often alternating with normal or loose stools)

49
Q

Peptic ulceration/Gastritis/Functional Dyspepsia: Causes

A

H. Pylori infection is a strong predisposing factor

50
Q

Peptic ulceration/Gastritis/Functional Dyspepsia: Presentation

A

Ulcers: epigastric pain that wakes them up at night, and radiates to the back

Gastritis: abdominal pain + nausea

Functional Dyspepsia: peptic ulcer symptoms + early satiety, bloating, post-prandial vomiting, delayed gastric emptying

51
Q

Peptic ulceration/Gastritis/Functional Dyspepsia: Investigations

A

1) Gastric antral biopsies (H. Pylori produces urease)
2) 13C breath test
3) Stool antigen may be positive for H.Pylori

52
Q

Peptic ulceration/Gastritis/Functional Dyspepsia: Management

A

Peptic ulceration: PPI (omeprazole) + clarithromycin/metronidazole + amoxicillin.

If they fail to respond do upper GI endscopy

If normal, then functional dyspepsia is diagnosed (some children respond to a hypoallergenic diet)

53
Q

Eosinophilic Oesophagitis: Definition

A

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

54
Q

Eosinophilic Oesophagitis: Presentation

A

1) Vomiting
2) Discomfort on swallowing
3) Bolus dysphagia (food ‘sticks’ in the upper chest)

55
Q

Eosinophilic Oesophagitis: Investigations

A

Endoscopy

56
Q

Eosinophilic Oesophagitis: Management

A

Oral corticosteroids (fluticasone or viscous budesonide)

57
Q

Gastroenteritis: Causes

A

Virus: rotavirus (also adenovirus, norovirus, coronavirus)

Bacterial (less common- blood in stool): campylobacter jejuni, shigella, salmonella, cholera, enterotoxigenic E.Coli)

Protozoan parasite (giardia, cryptosporidium

58
Q

How is degree of dehydration assessed and what are the degrees?

A

Body weight

1) No clinically detectable dehydration (<5% loss of body weight)
2) Clinical dehydration (5-10% loss of body weight)
3) Shock (>10% loss of body weight)

59
Q

What is post-gastroenteritis syndrome?

A

Following an episode of GE, the introduction of a normal diet causes a return of watery diarrhoea –> Return to the use of ORT

60
Q

In what 3 ways do disorders affecting digestion or absorption of nutrients present?

A

1) Abnormal stools
2) Poor weight gain/faltering growth
3) Specific nutrient deficiencies (single or combination)

61
Q

Coeliac Disease: Pathology

A

1) An enteropathy in which the gliadin fraction of gluten provokes a damaging immunological response in the proximal small intestinal mucosa
2) As a result, enterocytes start moving up the villi at a higher rate but it isn’t enough to compensate for increased cell loss from villous tips
3) Villi become progressively shortened and then absent, leaving a flat villi

62
Q

Coeliac Disease: Presentation

A

1) Faltering growth
2) Abdominal distension
3) Buttock wasting
4) Abnormal stools
5) General irritability

Other (anaemia, short stature, mild + non-specific GI symptoms)

63
Q

Coeliac Disease: Investigations

A

1) Serology (IgA tissue transglutaminase and endomysial antibodies)
2) Endoscopy w/ biopsy: confirmation depends on mucosal changes (increased intraepithelial lymphocytes, villous atrophy and crypt hypertrophy, with catch-up growth on gluten withdrawal)

64
Q

Coeliac Disease: Management

A

Gluten-free diet

65
Q

Other than coeliac disease, name 6 other (uncommon) causes of nutrient malabsorption:

A

1) Short bowel syndrome
2) Exocrine pancreatic dysfunction (CF)
3) Small-intestinal mucosal disease
4) Lymphatic leakage or obstruction
5) Loss of terminal ileal function (Crohn’s)
6) Cholestatic liver disease or biliary atresia

66
Q

What is the most common cause of persistent loose stools in preschool children?

A

Chronic Non-specific Diarrhoea (previously known as Toddler diarrhoea)

67
Q

Crohn’s Disease: How does it present in children and adolescents?

A

1) General ill health (fever, lethargy, weight loss)
2) Growth failure
3) Delayed puberty
4) Classic presentation: abdominal pain, diarrhoea, weight loss
5) Extra-intestinal manifestation: oral lesions (or perianal skin tags), uveitis, arthralgia, erythema nodusum

68
Q

Crohn’s Disease: How is it investigated?

A

Endoscopy with biopsy (non-caseating epithelioid granulomata)

May also have raised ESR, CRP, platelet count

May have iron deficiency anaemia and low serum albumin

69
Q

Crohn’s Disease: How is it managed?

A

1) Remission is induced with nutritional therapy or steroids
2) Relapse: immunosuppressants (azathioprine, mercaptopurine, or methotrexate). Anti-TNF (infliximab or adalimumab)
3) Surgery for complications

70
Q

Ulcerative colitis: presentation

A

1) Rectal bleeding, diarrhoea, and colicky pain
2) Weight loss and growth failure (less common than Crohn’s)
3) Extraintestinal (erythema nodusum, arthritis)

71
Q

Ulcerative colitis: diagnosis

A

1) endoscopy w/ biopsy (mucusal inflammation, crypt damage
2) exclude infection
3) small bowel imaging to check that extra-colonic inflammation suggestive of Crohn’s is not present

72
Q

Ulcerative colitis: management

A

Mild disease: aminosalicylates (balsalazide and mesalazine)

More aggressive disease: systemic steroids for exacerbations and immunomodulatory therapy (azathioprine) to maintain remission

Surgery for severe disease

73
Q

Name 7 causes of constipation

A

1) Idiopathic
2) Hirschsprung disease
3) Lower spinal cord problems
4) Anorectal abnormalities
5) Hypothyroidism
6) Coeliac disease
7) Hypercalcaemia

74
Q

What is the presentation of constipation in children?

A

1) Abdominal pain, which changes with passage of stool or overflow soiling
2) Constipation may be precipitated by dehydration or anal fissure
3) Older children: problems with toilet training, anxieties about opening bowels in unfamiliar toilets
4) Soft faecal mass in lower abdomen on examination

75
Q

What are the red flags of constipation in children?

A

1) Failure to pass meconium in first 24 hours (Hirschsprung)
2) Faltering growth/growth failure (hypothyroid/coeliac)
3) Abdominal distension
4) Abnormal lower limb neurology or deformity
5) Sacral dimple over natal cleft (spina bifida occulta)
6) Abnormal appearance/position/patency of anus (anormal anorectal anatomy)
7) Signs of sexual abuse
8) Perianal fistulae, abscesses, or fissures

76
Q

How is constipation investigated?

A

History and clinical findings (do not do DRE)

77
Q

What can occur in longstanding constipation and how should this be explained to the child and parents?

A

The rectum becomes distended, with a loss of the need to defecate. Involuntary soiling may occur as contractions of the full rectum inhibit the internal sphincter, leading to overflow.

Explain that the soiling is involuntary and that recovery of normal rectum size and sensation can be achieved but may take a long time

78
Q

What is the general aim of constipation management?

A

Evacuate the overloaded rectum completely. This is done using a disimpaction regime of stool softeners, followed by maintenance treatment to unsure ongoing regular pain-free defecation.

79
Q

What is Hirschsprung Disease?

A

The absence of ganglion cells from the large bowel, resulting in a narrow contracted segment. The abnormal bowel extends from the rectum proximally, ending in a normally innervated, dilated colon

80
Q

Hirschsprung Disease: Presentation

A

1) Usually presents in neonatal period
2) Intestinal obstruction with failure to pass meconium in first 24 hours
3) Followed by abdominal distension and bile-stained vomiting
4) Rectal exam: narrow segment, withdrawal of finger releases gush of liquid stool and flatus
5) In later childhood: profound chronic constipation, abdominal distension, growth failure

81
Q

Hirschsprung Disease: Diagnosis

A

Suction rectal biopsy is diagnostic (demonstrates absence of ganglion cells and presence of large, acetylcholinesterase-positive nerve trunks

82
Q

Hirschsprung Disease: Management

A

Surgical: initial colostomy followed by anastomosing normally innervated bowel to the anus

83
Q

What is the most common presentation of liver disease in the neonatal period?

A

Prolonged (persistent) neonatal jaundice

84
Q

At what point is physiological jaundice in newborns considered prolonged?

A

If the jaundice doesn’t subside after 2 weeks (3 if premature)

85
Q

Why must prolonged neonatal jaundice be investigated promptly?

A

To distinguish between unconjugated hyperbilirubinaemia (resolves spontaneously) and conjugated (sign of liver disease)

86
Q

What are the causes of prolonged neonatal jaundice?

A

Unconjugated: breastmilk jaundice, infection (UTI), haemolytic anaemia, hypothyroidism, Crigler-Najjar syndrome

Conjugated: bile duct obstruction (biliary atresia, choledochal cyst), neonatal hepatitis syndrome, intrahepatic biliary hypoplasia

87
Q

What is the characteristic appearance of prolonged neonatal jaundice?

A

Raised conjugated bilirubin (>20) accompanied by:

1) Pale stools
2) Dark urine
3) Bleeding tendency
4) Failure to thrive

88
Q

What is biliary atresia?

A

Progressive fibrosis and obliteration of the extrahepatic and intrahepatic biliary tree

Leads to chronic liver failure and death within 2 years unless treated

89
Q

What is the presentation of biliary atresia?

A

1) Mild jaundice
2) Pale stools (increasingly pale as disease progresses)
3) Normal birthweight followed by faltering growth
4) Hepatomegaly initially, then splenomegaly due to portal hypertension

90
Q

How is biliary atresia investigated?

A

1) ERCP is diagnostic
2) Raised conjugated bilirubin
3) Fasting abdominal USS: may show contracted or absent gallbladder
4) Liver biopsy: extrahepatic biliary obstruction
5) LFTs abnormal but of little value to diagnosis

91
Q

How is biliary atresia managed?

A

1) Kasai hepatoportoenterostomy
2) If surgery fails: liver transplant

(nutrition and fat-soluble vitamin supplementation is essential)

92
Q

Choledochal cysts: pathology

A

cystic dilatations of the extrahepatic biliary system

93
Q

Choledochal cysts: presentation

A

Abdominal pain, palpable mass, jaundice, or cholangitis

94
Q

Choledochal cysts: investigations and management

A

Investigate: USS or MRCP
Manage: surgical removal of cyst

95
Q

Neonatal hepatitis syndrome: pathology

A

Prolonged neonatal jaundice and hepatic inflammation

96
Q

Neonatal hepatitis: presentation

A

1) Low birthweight + faltering growth

2) Jaundice may be severe

97
Q

A1AT Deficiency: pathology

A

Inherited autosomal recessive disorder –> accumulation of protein in hepatocytes –> lack of circulating A1AT results in emphysema in adults

98
Q

A1AT Deficiency: presentation

A

1) Prolonged neonatal jaundice
2) Bleeding (vit K deficiency)
3) Hepatosplenomegaly

99
Q

A1AT Deficiency: Investigation and management

A

Investigation: estimating the level of A1AT in plasma and identify protein phenotype

Management: 50% good prognosis, rest develop liver disease and may require transplant

100
Q

What are the clinical features of acute viral hepatitis?

A

1) Nausea and vomiting
2) Abdominal pain
3) Lethargy
4) Jaundice
5) Large, tender liver

Phase 3a (7 decks)

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