Gastroenterology Flashcards

1
Q

What is colic? Describe the different symptoms of colic
What age of children does it usually occur in?
What commonly is a differential?
What is essential in it’s treatment?

A

Continual crying in a baby - inconsolable/difficult to comfort. Crying is often high pitched/screeching
More common in the afternoon or evening (but not always)
Baby may bend knees up towards chest and tighten fists
Passage of excessive flatus
Usually occurs in babies aged up to 3 or max 6 months of age
Commonly a differential is gastrointestinal problems
Essential in treatment is support of parents as is can often be very frustrating and worrying for parents. It may precipitate non-accidental injury in infants already at risk

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2
Q

What is the definition of constipation?

A

Infrequent passage of dry, hardened faeces often accompanied by straining or pain and bleeding associated with hard stools

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3
Q

What other symptoms may be associated with constipation in children?

A

Abdominal pain

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4
Q

Usually, what is the reason for the development of constipation (think of lifestyle rather than diagnosis)

A
Decreased fluid intake
Dehydration
Anal fissure (causes pain so they don't want to go)
Problems with toilet training
Anxieties over using unfamiliar toilet
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5
Q

How does Hirschsprung’s disease present? What time frame?

A

Usually presents as failure to pass meconium in first 24 hours of life

Presentation:

  • Constipation
  • Abdominal distention
  • Bile-stained vomiting

Can present later in life with growth failure

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6
Q

What is a complication of long standing constipation? Why?

A

Distention of the rectum leading to loss of sensation which leads to involuntary soiling
This occurs because the rectum becomes over distended, leading to decreased sensation of the need to defecate.
Involuntary soiling subsequently occurs because contractions of the full rectum inhibit the internal sphincter, leading to overflow
This may present on a AXR as severe faecal loading

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7
Q

What is the treatment for faecal impaction in children?

A

Disimpaction regime:

Stool softeners (commonly movicol paeds plan) for 1-2 weeks or until the impaction resolves FOLLOWED BY...
maintenance treatment to ensure ongoing, regular pain free defecation (target is 1 large soft stool/day). The medication should be continued at the maintenance dose for several weeks after regular bowl habit it established, then the dose reduced gradually

If movicol paediatric plain doesn’t lead to disimpaction after 2 weeks a stimulant laxative should be given

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8
Q

How is involuntary soiling in children treated?

A

Involuntary soiling is commonly due to faecal loading in the rectum. You carry out disimpaction regime followed by regular laxatives. Encouragement by family and health professionals is essential as relapse is common and psychological support is sometimes required

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9
Q

Which test is diagnostic of Hirschsprung’s disease?

A

Rectal biopsy is the diagnostic test (tissue is diagnosed under the microscope for the absence of ganglionic cells).

This may also be combined with a barium enema or anorectal manometry

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10
Q

What is the most common causative organism of gastroenteritis in the UK?

A

Rotavirus

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11
Q

What are some bacterial causes of gastroenteritis?
How may each present?
How common is bacterial gastroenteritis in the UK?

A

Campylobacter - SEVERE abdominal pain
Shigella - blood, pus, fever, tenesmus
Chloera and E.coli - quickly dehydrating diarrhoea

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12
Q

What protozoal organisms can cause gastroenteritis?

A

Giardia

Cryptosporidium

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13
Q

Clinically assessing dehydration in children is difficult - what is the most accurate measure?

A

Change in weight
This can, however, be difficult f the child has not recently been weighed or if you are unsure whether they were wearing clothes when they were weighed

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14
Q

What signs may be seen on examination of a patient with clinical dehydration?
What percentage of body weight are the likely to have lost?

A

Eyes - sunken, Tachycardia, Tachypnoea, decreased urine output, irritable, dry mucous membranes, looks ill or deteriorating, reduced skin turgor
5-10%

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15
Q

What signs may be seen on examination of a patient with shock?
What percentage of body weight are they likely to have lost?

A

Hypotension, tachycardia, tachypnoea, decreased cap refill, cold peripheries, pale in colour or mottled rash, decreased urine output, sunken eyes, may be unconscious, looks ill or deteriorating, reduced skin turgot
Usually >10%

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16
Q

Explain how hyponatraemic dehydration may arise.
What are the complications of hyponatraemic dehydration?
In what circumstances does it most commonly occur?

A

If a child is drinking a lot of water then they net loss of sodium is more than the loss of water. This leads to a shift of water from extracellular to intracellular compartments. This can cause the brain to swell (cerebral oedema) and can lead to seizures.
It occurs more commonly in underdeveloped countries where children are more likely to be malnourished

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17
Q

What is hypernatraemic dehydration?
When does it arise?
What are the complications?
How may it present?

A

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18
Q

When is a stool culture indicated in the investigation of gastroenteritis?

A
If there are signs of sepsis
If the patient has blood or mucus in their stool
If diarrhoea has not improved by day 7
If they are questioning the diagnosis
If the child is immunocompromised
If there has been recent foreign travel
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19
Q

When are antibiotics indicated in gastroenteritis?

A
  1. If there is suspected or confirmed sepsis
  2. Extra-intestinal spread of bacterial infection
  3. Salmonella gastroenteritis if aged under 6 months
  4. Malnourished/immunocompromised children
  5. Specific bacterial or protozoal infections
    If antibiotics are started a blood culture should be taken first
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20
Q

What is the mainstay of management of gastroenteritis?

A

Prevention or correction of dehydration
This may be done via oral rehydration solution and encouraging fluid intake or in the cases where patients are continually vomiting/deteriorating/in shock IV fluids

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21
Q

What is the most likely cause is a child presents with projective vomiting in the first few weeks of life?

A

Pyloric stenosis

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22
Q

What is gastro-oesophageal reflux?
What is it caused by in infants?
What other factors contribute to GOR in infants?

A

Involuntary passage of stomach contents into the oesophagus
In infants it is caused by an functional immaturity of the lower sphincter combined with that fact that infants spend a lot of time horizontally, mainly have liquid diet and also have a short intra-abdominal length.

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23
Q

By what age does most GOR resolve by?

What is this thought to be due to?

A

Usually resolves by the age of 12 months

This is thought to be due to maturation of the lower sphincter, increased solid diet and more time sitting up

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24
Q

When is gastro-oesophageal reflux termed gastro-oesophageal reflux disease?

A

When there are complications e.g:
Faltering growth (failure to thrive) due to severe vomiting
Oesophagitis (which may present as haematemesis)Recurrent pulmonary aspiration resulting in recurrent pneumonia, cough or wheeze or apnoea in preterm infants
Dystonic neck posturing (Sandifer syndrome)
Life threatening events

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25
Q

Which children is gastro-oesophageal reflux DISEASE more common in?

A
  • Children with cerebral palsy or other neuro-developmental disorders
  • Preterm infants (especially those with bronchopulmonary dysplasia)
  • Following surgery for oesophageal atresia or diaphragmatic hernia
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26
Q

When may investigations be indicated for GOR?

What investigations?

A

If the child is suffering from complications
Investigations include:
- 24 hour pH monitoring
- 24 hour impedence monitoring
- Endoscopy with oesophageal biopsies (to look for oesophagitis)

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27
Q

How is uncomplicated GOR managed?

A

Adding thickening agents to foods and changing feeds to more frequent, smaller feeds
General advise e.g advise regarding position during feeds - 30 degree head-up
Ensure infant is not being overfed (as per their weight)
Trial of alginate therapy (gavison). (Alginates should not be used at the same time as thickening agents)

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28
Q

When is GOR considered to be significant?

How is significant GOR managed?

A

Considered to be significant if the child has feeding difficulties, distressed behaviour or faltering growth

It is managed with food thickeners etc (same as uncomplicated GOR) but medications can also be added onto this. This may include H2 antagonists (ranitidine) or PPI (omeprazole)

29
Q

If medical treatment for GOR is not successful what are the next steps that should be taken?

A

Investigations should be carried out to look into allergy to cow’s milk protein
Surgery is reserved for children with complications unresponsive to intensive medical treatment - e.g fundoplication

30
Q

Why is jaundice so common?

A

For 3 main reasons:

  • There is a high Hb level at birth due to red cell breakdown
  • Infant red blood cells have a shorter life span (90 days)
  • Hepatic bilirubin metabolism is less efficient in the first few days of life
31
Q

Why is neonatal important to identify and treat?

A

Because it may be a sign of another disorder e.g haemolytic anaemia, infection, inborn error of metabolism, liver disease

Also, it can lead to serious complications including kernicterus

32
Q

What is kernicterus?
Why does it occur? (think cellular level)
What are some clinical signs?

A

It is when unconjugated bilirubin is deposited in the basal ganglia and brainstem nuclei
It occurs because the levels of unconjugated bilirubin exceeds the albumin binding capacity of bilirubin in the blood. The free bilirubin is fat soluble so it can cross the blood brain barrier
Clinical signs vary - may be lethargy and poor feeding or increased muscle tone, seizures and coma.

33
Q

What level of bilirubin causes babies to become clinically jaundiced?

A

> 80micromol/L

34
Q

If the onset of jaundice is less than 24 hours what is the most likely cause?

A

A haemolytic cause or congenital infection.
Haeolytic causes include:
- Rhesus disease of the newborn
- ABO incompatibility
- G6PD deficiency
- Spherocytosis
If the cause is congenital infection the bilirubin will be conjugated and they will have other abnormal clinical signs e.g growth restriction, hepatosplenomegaly and thrombocytopenic purpura

35
Q

What is haemoglobin broken down to become?
What are the properties of this breakdown product?
What is the normal process continuing on from the breakdown product?

A

It is broken down into unconjugated bilirubin.
Unconjugated bilirubin is fat soluble - not water soluble.
From here the unconjugated bilirubin bound to albumin is taken up by the liver and converted into conjugated bilirubin
Conjugated bilirubin is water soluble and is excreted in bile and then into the gut
In the gut it is converted into stercobilinogen and urobilinogen

36
Q

What are some of the causes of jaundice that present between 2 days - 2 weeks?

A
Physiological jaundice
Breast milk jaundice
Dehydration
Infection
(May be haemolytic causes)
(Crigler-Najjar)
37
Q

What is ABO incompatibility?

How can it be investigated?

A

When group O women have an IgG anti-A-Haemolysin in their blood which can cross the placenta and haemolyse the red blood cells of a group A infant
It can be investigated with the coombs test

38
Q

What is phototherapy?
Over what time period is it given?
What advise is given to mothers regarding their babies over this time?

A

Light from the blue-green band of the visible spectrum converts unconjugated bilirubin into a harmless water-soluble pigment
Give over periods of 6-8 hours
The mother is advised to bottle feed the baby over this time so as to decrease the time that the baby is not under the light

39
Q

What is exchange transfusion?

When is it given?

A

It is given if the bilirubin rises to levels that are potentially dangerous.
It is rarely done
Babies blood is replaced with donor blood. Usually twice the infant’s blood volume (2x90ml) is replaced.

40
Q

What is jaundice which occurs in babies >2 weeks (or 3 weeks preterm) otherwise named?

A

Persistent/prolonged neonatal jaundice

41
Q

What are some of the cause of jaundice in babies >2 weeks of age?
What is the difference in presentation of conjugated vs unconjugated bilirubinaemia?

A

Unconjugated:
Breast milk jaundice
Infection
Congenital hypothyroidism

Conjugated:
Neonatal hepatitis syndrome
Biliary atresia
Symptoms include: baby passing dark urine and unpigmented pale stools. Hepatosplenomegaly and poor weight gain are other clinical signs that may be present.

42
Q

What is breast milk jaundice?

A

It is common - it affects up to 15% of healthy breast fed infants. The jaundice gradually fades and disappears by 4-5 weeks of age
It is benign unconjugated hyperbilirubinaemia
It is thought to be due to a complex steroid in breast milk which inhibits the hepatic enzyme but no definitive cause has been identified

43
Q

What symptoms or signs may a child with Hirschsprung’s disease presenting in later life present with?

A

Delayed passage of meconium (passage >48 hours)

Treatment of chronic treatment-resistant constipation

44
Q

What investigations may be suggestive of Hirschsprung’s disease? What is the definitive investigation?

A

May be suggested on abdominal x-ray, abdominal US and contrast enema.
Some sections of the bowel may look very dilated and the affected section narrow

However, definitive diagnosis is with rectal biopsy

45
Q

How does pyloric stenosis typically present?

A

With projectile non bile stained vomiting at 4-6 weeks

46
Q

What is a common cause of chronic diarrhoea post gastroenteritis?
How is it treated?

A

Post-gastroenteritis lactose intolerance is a common complication of viral gastroenteritis
Treatment = removal of lactose from the diet for a few months followed by gradual reintroduction

47
Q

What is intussusception?

A

Invagination of proximal bowel into a distal segment

48
Q

In what age group of children does intussusception commonly present?
What is intussusception a common cause of?

A

3 months-2 years

It is a common cause of bowel obstruction

49
Q

What is a complication of intussusception?

A

Stretching and constriction of the mesentery
This results in venous obstruction causing engorgement and bleeding
This can lead to fluid loss, bowel perforation, peritonitis and gut necrosis

50
Q

What are some different presentations of intussusception?

A
  1. Paroxysmal, severe colicky pain with pallor
  2. Refusal of feeds and vomiting. Vomit may be bile stained depending on the level of the intussusception
  3. Sausage shaped mass, often palpable in the abdomen
  4. Passage of characteristic red-currant jelly stool (comprised of blood stained mucus)
  5. Abdominal distention and shock
51
Q

What is the treatment of intussusception of the bowel?

A

IV fluid resuscitation

Reduction of intussusception

52
Q

There are 2 different types of reduction of intussusception. What are they and when would you choose one over another?

A
  1. Via rectal air insufflation (carried out after the child has been resuscitated)
  2. Through surgery. This is if rectal air insufflation is unsuccessful or if peritonitis is present
53
Q

What is mesenteric adenitis?

How may it present?

A

Inflamed lymph nodes within the mesentery
It can cause similar symptoms to appendicitis and can be difficult to distinguish between the 2
Often follows a recent viral infection and needs no treatment

54
Q

How may conditions affecting the digestion or absorption of nutrients manifest?

A

Abnormal stools
Failure the thrive/Poor weight gain
Symptoms of specific nutrient deficiencies

55
Q

What is coeliac disease?

A

It is an auto-immune disease affecting the small intestine. It is caused my inflammation secondary to gluten exposure.

56
Q

What happens on the cellular level with coeliac disease?

A

There is villous atrophy - villi become progressive shorter secondary to an immunological response to gluten. This leaves flat mucosa

57
Q

What is the typical presentation of coeliac disease? At what age?

A

Typical presentation - failure to thrive, constipation/diarrhoea, irritability
It commonly presents in children aged 8-24 months

58
Q

Which children are at increased risk of developing coeliac disease? (think about the conditions in which you screen for coeliacs)

A

T1DM
Autoimmune thyroid disease
Down’s syndrome

59
Q

What is the screening test for coeliac disease?

A

anti tTG, EMA (endomysial antibodies)

60
Q

How is diagnosis of coeliac disease confirmed? What findings are found?

A

Small intestinal biopsy
Increased number of intraepithelial lymphocytes, villous atrophy

They need to be eating wheat at the time in order to mount a response

Positive serology IgA for anti endomyseal and anti TTG antibodies

Resolution of symptoms on gluten free diet AND catch up growth

61
Q

What food items contain gluten and there for must be excluded from the diet in coeliac disease?

A

Barley
Wheat
Rye

62
Q

What type of laxative is movicol?

A

An osmotic laxative

63
Q

What type of dietary advice can be given to children with chronic constipation?

A

Increase fruit and vegetable intake (except from bananas)
Increase weetabix intake - avoid porridge
Increased fluid intake
Increase exercise

64
Q

What is the pathophysiology behind hirschprung’s disease?

A

Pathophysiology = absence of parasympathetic ganglion cells from the myenteric and submucosal plexuses of part of the large bowel (usually the rectum, may extend to colon) resulting in a narrow, contracted segment

65
Q

What may be noticed on PR examination of a patient with hirschprung’s disease?

A

A narrowed segment noticed on PR examination

Withdrawal of the examining finger often releases a gush of liquid stool and flatus

66
Q

What is the treatment of hirschprung’s disease?

A

Management
- Initially - rectal washouts
THEN
- Surgical: usually involves an initial colostomy followed by anastomosing normally innervated bowel to the anus.

67
Q

What are some complications of Hirschprung’s disease?

A

Perforation
Hirschprung’s enterocolitis
Megacolon
Bowel obstruction

68
Q

What is hirschprung’s enterocolitis?

How does it present?

A
Proximal colonic dilatation secondary to obstruction
WITH
Thinning of the colonic wall 
Bacterial overgrowth
Translocation of gut bacteria

Presents with fever, abdominal distension and bloody diarrhoea. Shock and death can follow rapidly