Gastrointestinal Disease Flashcards

1
Q

What are the key differences between the adult and child GI tract?

A
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2
Q

What systemic diseases commonly haave gastro-intestinal manifestations?

A
  • diabetes ie DKA → acute abdo pain
  • sickle-cell + Henoch-Schoenlein disease → acute abdo pain
  • migraine → vomiting + abdo pain
  • raised ICP → vomiting
  • septicaemia + meningitis → mimics gastroenteritis
  • cystic fibrosis → pancreatic insufficiency
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3
Q

Why are children vulnerable to malnutrition?

A
  • low nutritional stores of fat + protein
  • growth creating high nutritional demands
  • brain growing rapidly during first 2yrs of life + is vulnerable to energy deprivation
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4
Q

Why are children at particular risk of dehydration?

A
  • greater surface area to volume ratio → greater insensible water loss
  • inability to gain access to fluids when thirsty
  • higher basal fluid requirement (10-20% of body weight per day)
  • immature renal reabsorption process
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5
Q

What is the difference between gastro-oesophageal reflux (GOR) and gastro-oeseophageal reflux disease (GORD)?

A
  • GOR is the effortless passage of gastric contents into the oesophagus +/- regurgitation and vomiting, it is a normal physiological occurrence especially common in infants
  • GORD refers to either the symptomatic regurgitation of gastric contents into the oesophagus or GOR w/ complications, GORD commonly presents in infancy w/ a prevalence of 4.3% at 6 months old
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6
Q

What is the aetiology behind gastro-oesophageal reflux?

A
  • laxity of LOS → in infants it is partly due to immaturity of the LOS, symptoms improve as the sphincter tone increases, a more solid diet is introduced + child spends more time in an upright posture
  • food allergy or intolerance
  • foregut intestinal dysmotility associated w/ gut inflammation or neurological disorder
  • increased gastric pressure → due to a more distal intestinal obstruction, obesity or chronic respiratory disorders
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7
Q

It is important and can be challenging to distinguish between GOR and GORD in infants. Frequent, effortless regurgitation of feeds is normal and there is no reliable investigation to distinguish between the two.

What are clinical features of GORD?

A
  • persistent/recurrent regurgitation, particularly after meals
  • feeding difficulties, food refusal +/- crying/irritability post feeds
  • arching of back + neck in infants
  • resp symptoms, such as coughing + wheezing
  • sore throat + hoarseness
  • apnoeic/bradycardic episodes
  • heartburn/chest pain
  • faltering growth

O/E check for: hydration, malnutrition, abnormalities indicating a differential diagnosis, assess growth charts

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8
Q

For GORD diagnosis, it is important to take a full feeding history - what should be involved?

A
  • check position, attachment, technique, duration, frequency + type of milk
  • calculate the volume of milk being given as babies can be over-fed + therefore have gastric over-distension
  • ask about frequency + estimated volume of vomits
  • find out the relationship of symptoms to feeds
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9
Q

What is the difference between possetting, vomiting and gastro-oesophageal reflux?

A
  • Posseting refers to bringing up small amounts of milk after a feed (often on burping). It causes no pain or discomfort and is no cause for concern if the baby is happy, feeds well and fains weight. It usually settles at around 5 months when the baby is sitting
  • Vomiting is active, forceful contractions through the GIT to bring up stomach contents (could be more solid in nature)
  • GOR is when milk or stomach acid may only be regurgitated as far as the oesophagus or throat. This form of reflux does cause the baby discomfort and there is usually disruption of feeding, and possibly sleeping patterns. Baby may cry during or after a feed, pull off the breast, arch his back, become rigid, writhe, kick or throw out his arms.
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10
Q

GORD in older children may be identified w/ a typical history and physical examination. In challenging or complicated GORD, further investigations can aid understanding the cause and severity of the disease.

What investigations can be done?

A
  • Bloods → FBC, U+Es, ABG
  • pH impedance study → measures pH as well as non-acid reflux in oesophagus by placing probe in stomach, benefits infants on milk feeds w/ non-acidic reflux that won’t be detected on “pH” but will on “impedance”
  • Endoscopy → upper GI endoscopy + biopsies
  • Oseophageal + antroduodenal manometry
  • Abdo USS
  • Barium contrast study
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11
Q

Effortless regurgitation in otherwise well infants is common. Approximately 40% of infants will experience this and no intervention is necessary. Symptoms should have started in the first 2 months of life and usually improves with age until they are 1 years old. Reassurance is key.

What is the conservative and medical management for GORD in children?

A
  • optimise position by raising the cot base at the head end by 30 degrees
  • avoid over-feeding + consider smaller, more frequent meals
  • use feed thickeners
  • ensure adequate nutrition w/ regular monitoring of weight
  • for babies w/ suspected GORD:
    • if breastfed → 1-2wk trial of an antacid (eg. gaviscon infant)
    • if formula-fedsee image of stepwise approach
    • if above doesn’t work → 4wk trial of ranitidine or omeprazole
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12
Q

If symptoms persist for GORD after medical treatment, what is the surgical management?

A
  • Nissen’s fundoplication (uses top of stomach to strengthen LOS) may be considered in:
    • older infants
    • children w/ severe GORD unresponsive to med therapy
    • children who have previously suffered or are at increased risk of ‘life-threatening’ events like aspiration pneumonia and apnoea
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13
Q

What are the differentials for acute abdominal pain, of medical nature?

A
  • infant colic
  • constipation
  • mesenteric adenitis
  • gastroenteritis
  • hepatitis
  • UTI
  • DKA
  • sickle cell
  • lower lobe pneumonia
  • henoch-schoeinlein purpura
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14
Q

What are the differentials for acute abdominal pain, of surgical nature?

A
  • appendicitis
  • intussusception (intestinal obstruction)
  • ovarian or testicular torsion
  • strangulated inguinal hernia
  • volvulus
  • inflamed meckel’s diverticulum
  • peritonitis
  • trauma
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15
Q

What are differentials for recurrent abdominal pain?

A
  • usually functional
  • UTI
  • obstructive uropathy
  • food intolerance
  • IBD
  • ulcer
  • malrotation
  • pancreatitis
  • coeliac disease
  • CF
  • porphyria
  • lead poisoning
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16
Q

Upon taking a thorough history of the presenting complaint, what clinical features may be present in an acute abdomen?

A
  • babies - screaming + drawing up of legs
  • pain lasting for >4 hrs → significant
  • nature: consistent, colicky, intermittent
  • vomiting: bile or blood stained
  • diarrhoea → blood in infant suggests intussusception, older child IBD
  • anorexia: normal appetite → sign of wellbeing
  • fever implies infection → eg. UTI, mesenteric adenitis, appendicitis
  • urination: pain → UTI
  • symptoms of LRTI → pneumonia
  • rash → HSP
  • look at hernial orifices
  • look at genitalia
  • check hip joints
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17
Q

What investigations can be done for the acute abdomen?

A
  • bloods → FBC + WBC (bacterial infection), sickling test, U+Es, glucose
  • urinanalysis → glucose, ketones, infection
  • AXR → constipation, renal calculi, obstruction
  • USS → obstructive uropathy, appendix mass, intussusception
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18
Q

What is mesenteric adenitis?

A
  • often accompanied by URTI w/ cervical lymphadenopathy
  • second most common cause of RLQ pain after appendicits
  • definitive diagnosis can only be made during a laparotomy or laparoscopy if enlarged mesenteric lymph nodes + normal appendix is seen
  • resolves in 24-48hrs
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19
Q

Describe the features of acute appendicitis

A
  • central abdo pain moves to right iliac fossa over a period of hours
  • pain is aggravated by movement
  • anorexia; vomiting; colickly pain; fever; guarding @ McBurney’s point
  • if perforated, there will be generalised guarding + fluid resuscitation and intravenous antibiotics must be given before appendicectomy
20
Q

What is intussusception?

A
  • invagination of proximal segment of bowel into another more distal part
  • occurs most commonly in infants aged between 2 months - 2 years
  • majority of cases occurring before the first b’day
  • males at higher risk (3:2)
  • most cases are idiopathic, condiiton is more common in winter + spring suggesting a link to viral infections (gastro, resp infections)
  • in up to 10% cases, a pathological lead point found → meckel’s, Peutz-Jeghers polyps + small bowel lymphoma
21
Q

The most common type of intussusception occurs in the terminal ileum + passes through the ileocaecal valve. This usually draws the mesentery of the small bowel into the intussusception an venous congestion ensues. Soon after, arterial occluson occurs leading to ischaemia, necrosis + perforation.

What are the clinical features of intussusception?

A
  • Abdominal pain → sudden, colickly, severe bouts that occur every 10-20mins. Pain usually associated w/ drawing up legs + screaming
  • Lethargy/irritability betwen waves of pain
  • Pallor → particularly associated w/ pain
  • Vomiting
  • Redcurrant jelly stool → mixture of blood + mucus
  • O/E → weak, dehydrated, tachycardic, lethargic, sausage-shaped mass in RUQ, abdo distension, frank peritonitis, sepsis
22
Q

What investigations can be done for intussusception?

A
  • blood tests → inflammation, electrolyte derangement, dehydration + significant bleeding
  • ULTRASOUNDgold standard
    • classic sign is the “target sign” (or doughnut sign) on transverse section
    • represents two concentric lumina of bowel
    • an AXR may reveal features of small bowel obstruction
23
Q

What is the management for intussusception?

A
  • appropriate fluid resuscitation should occur prior to any intervention as children will have huge third space losses of fluid
  • IV abx (broad spec eg co-amoxiclav)
  • pneumatic reduction enema performed:
    • catheter inserted into rectum of child + air insufflated under fluoroscopic screening
    • pressure generated by air, in most cases, is sufficient to achieve a complete reduction
  • those failing enema/highly distended abdo/peritonitic → urgent laparotomy
    • right transverse incision made + manual reduction done
    • in some bowel too oedematous or non-viable → resection + end-to-end anastomosis
  • following successful air reductin enema, fluids reintroduced after 12-24hrs and pts discharged 48hrs later
24
Q

First-born male babies are more 4 times more likely to have pyloric stenosis. What are the clinical features of pyloric stenosis?

A
  • present w/ non-bilious vomiting that commences between 3-6wks of age, post-feeding
  • vomiting is projectile + associated w/ haematemesis 2o to oeseophagitis
  • prolonged vomiting leads to:
    • lethargy
    • weight loss (or failure to gain) despite being hungry baby
    • constipation
  • O/E:
    • infants appear thin, but hungry + may be dehydrated
    • occasionally visible gastric peristalsis can be seen
    • a palpable pyloric tumour (olive-shaped mass) in the epigastrium or RUQ is diagnostic of condition but difficult to feel
      • if unsure, a “test feed” should be done by offering infant dextrose water → relaxes abdo muscles + allows deeper palpation, stimulating pylorus to contract
25
Q

Pyloric stenosis is characterised by gradual thickening of the pyloric muscle, which eventually results in complete gastric outlet obstruction.

What is the pathophysiology of this in regards to prolonged vomiting?

A
  • electrolyte + water loss → hypochloraemic, hypokalaemic metabolic alkalosis
  • hypovolaemia → increase in aldosterone → inc renal absorption of sodium + water
  • results in paradoxical loss of hydrogen ions
  • alkalosis worsened by renal absorption of bicarbonate
  • potassium ion fluctuations also seen: both hypokalaemia + hyperkalaemia
  • severity of hypovolaemia + electrolyte abnormalities directly proportional to length of symptoms prior to presentation
26
Q

What investigations should be done for pyloric stenosis?

A
  • blood gashypochloraemic, hypokalaemic metabolic alkalosis
  • ultrasound abdomen:
    • pyloric muscle thickness >4 mm and pyloric canal length >17 mm meet the diagnostic criteria for full-term infants
  • if USS inconclusive → contrast studies: “string sign”
27
Q

What is the management of pyloric stenosis?

A
  • MEDICAL:
    • preoperative rehydration + correction of electrolyte imbalances
    • NG tube allows stomach to be decompressed, losses to be measured + losses to be replaced accurately (oral feeds stopped)
  • SURGICAL:
    • ramstedt’s pyloromyotomy → performed via RUQ or supraumbilical incision, incision made along length of pyloric swelling down to mucosa
28
Q

Coeliac disease is a primarily digestive disorder. It is estimated to be the most common genetically related food intolerance. It is a life-long gluten-sensitive autoimmune disease of the small intestine.

What is the pathophysiology of coeliac disease?

A

Coeliac disease has a complex pathogenesis that is not yet fully understood. It results from a combination of immunological responses to an environmental factor (gliadin) and genetic factors (HLA-DQ2/DQ8). Infant feeding practices, viral infections and gut bacteria may also play a role in developing coeliac disease.

In simple words, when the body’s immune system overreacts to gluten in food, the reaction damages the villi that line the small intestine. Villi help to absorb vitamins, minerals and nutrients. When villi are damaged malabsorption occurs.

Coeliac disease is considered a T cell-mediated immune disorder. The main characteristics are development of inflammatory anti-gluten CD4 T cell response, anti-gluten antibodies, autoantibodies against tissue transglutaminase, endomysium (connective tissue surrounding intestinal muscle) and the activation of intraepithelial lymphocytes. All of these result in epithelial cell destruction and villous atrophy.

29
Q

What are the gastrointestinal clinical features of coeliac disease?

A
  • unintentional weight loss
  • fatigue
  • chronic diarrhoea or constipation
  • flatulence
  • pale stools
  • severe recurrent abdominal pain
  • anorexia
  • mouth ulcers
  • vomiting
30
Q

Apart from the classical gastrointestinal symptoms what are a variety of extra-intestinal symptoms in coeliac disease?

A
  • dermatitis herpetiformis
  • dental enamel hypoplasia
  • osteoporosis
  • delayed puberty
  • short stature
  • iron-def anaemia (resistant to oral Fe)
  • liver + biliary tract disease
  • arthritis
  • peripheral neuropathy, epilepsy, ataxia
31
Q

What investigations are done for coeliac disease?

A
  • FBC, LFTs
  • iron studies, vit b12, folate
  • U+Es, bone profile, magnesium
  • tissue transglutaminase antibody (tTGA) then IgA endomysial antibodies (EMA)
    • pt needs to have included gluten-containing foods in diet over prev 6 weeks
    • if +ve serology → referred to endoscopy + intestinal biopsy
    • if -ve serology → IgA serology to check for IgA deficiency (may mask positive test)
  • upper GI endoscopy (gold std) → histological findings include atrophic villi + crypt hyperplasia
32
Q

What is the management for coeliac disease?

A
  • strict gluten free diet (lifelong) → refer to dietician
  • lifelong annual follow up:
    • check adherence to gluten free diet
    • ensuring adequate nutrition + growth
    • osteoporosis screening w/ DEXA scan should be carried out every 3yrs
    • assessment of psychological wellbeing
33
Q

What are the features of a congenital diaphragmatic hernia?

A
  • normally a left-sided herniation of abdominal contents through posterolateral foramen of diaphragm
  • heart will be displaced to the right
  • there will be poor air entry in left side of chest
  • diagnosis made on plain film xray after birth or antenatal USS
  • newborns may have RDS or show failure to respond to resuscitation
  • NG tube passed down + suction is done to prevent distension of intrathoracic bowel
  • after stabilisation → hernia surgically repaired
  • surgical correction attempted when foetus is 22-24wks gestation in utero to prevent death from lung hypoplasia, however it can precipitate pre-term delivery
34
Q

What are features of an umbilical hernia?

A
  • present as reducible, painless bulge at umbilicus
  • distress + crying cause increase in protrusion
  • common in afro-caribbean infants
  • infants w/ incarcerated hernias present w/ painful irreducible lumps that can change colour + when strangulated associated w/ vomiting or constipation
  • no treatment usually requires since it self-resolves in 2-3yrs
35
Q

What are the features of an inguinal hernia?

A
  • more common in boys, prem babies + those w/ FHx
  • majority are indirect + due to a patent process vaginalis
  • intermittent swelling in groin or scrotum
  • hardness, tenderness + vomiting in a previously reducible hernia are signs of trapped bowel within sac
  • this can lead to strangulation - more common in young infants
  • surgery should be delayed for 24-48hrs to allow oedema to resolve unless evidence of bowel entrapment ini which case it should be done urgently
  • sedation, analgesia + expert manipulation may allow reduction before surgery
36
Q

Why are hernias managed differently in children than adults?

A
  • urgent surgery required for:
    • diaphragmatic hernia since the compromised resp system may be fatal
    • inguinal hernia since strangulation is more likely to occur in young infants
  • some may be left to correct themselves:
    • umbilical hernia as it may resolve in 2-3yrs
37
Q

Hirschprung’s disease affects 1 in 5000 births w/ a male preponderance. Approximately 10-20% cases are familial and 15% of children w/ HD have trisomy 21.

What is the pathophysiology of Hirschprung’s disease?

A
  • congenital absence of ganglion cells in the nerve plexuses that innervate the GI tract
    • absent in the submucosal + intermyenteric plexuses
  • distal segment appears aganglionic on histological examination
  • transition zone is hypoganglionic
  • proximal segment will appear normally ganglionated
  • disease is believed to be caused by failure in the development of tissue derived from the neural crest
  • normally, ganglia act as final common path for both sympathetic and parasympathetic influences
  • their absence produces uncoordinated contractions of the affected bowel
  • spasm, lack of propulsive peristalsis, and mass contraction of the aganglionic segment noted, in addition to the lack of relaxation of the bowel and the spasm of the internal sphincter
38
Q

What are the clinical features of Hirschprung’s?

A
  • failure to pass meconium in first 24-48hrs of life
  • abdominal distension
  • bilious vomiting
  • explosive passage of liquid + foul stools (particularly caused by PR)
  • fever
  • failure to thrive (as manifestation of chronic moderate enterocolitis)
39
Q

What are the relevant investigations for Hirschprung’s disease?

A
  • plain abdo x-ray → air-fluid levels present; dilated colon
  • contrast enema → contracted distal bowel + dilated prox bowel
  • rectal biopsy (gold std)
40
Q

What is the management for Hirschprung’s?

A
  • bowels need to be adequately decompressed → achieved using regular rectal washouts, or, if needed, by formation of a colostomy or ileostomy
  • next step is surgery → remove aganglionic segment + join the normal ganglionic bowel to the internal anal sphincter
41
Q

25% of IBD presents in childhood.

What is the prevalence of Crohn’s and UC?

A
  • Crohn’s is 55-140 / 100,000
  • UC is 160-240 / 100,000
42
Q

IBD usually presents in adolescence and early adulthood. IBD in children generally has a more extensive + rapidly progressing course. Children often present acutely, but at presentation patients often report long-standing symptoms.

What is the presentation of IBD?

A

For BOTH:

  • incrased freq of bowel movements
  • abdo pain
  • weight loss
  • n+v
  • faltered growth
  • delayed puberty
  • reduced appetite
  • malaise/fatigue
  • sweats
  • clinical signs: fever, tachycardia, dehydration, pallor
43
Q

What investigations can be done for IBD?

A
  • bloods → FBC, coag, ESR, CRP, U+Es, LFTs, coeliac
  • stool + urine → MC+S, faecal calprotectin
  • imaging + biopsies → AXR, ACT, upper/lower GI endoscopy (gold):
    • CD → cobble stone appearance, wall thickening, fissures
    • UC → pseudopolyps, ulcerations
44
Q

What is the treatment for IBD?

A
45
Q

Summarise the key differences between Crohn’s and UC

A