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Osha 3a > Paeds GI > Flashcards

Paeds GI Flashcards

1
Q

What is Hirschprung’s?

A
  • congenital condition
  • nerve cells of myenteric plexus are absent in distal bowel and rectum
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2
Q

What is the myenteric plexus?

A
  • Auerbach’s plexus
  • enteric nervous system
  • brain of the gut
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3
Q

What is the pathophysiology of Hirschprung’s?

A
  • absence of PS ganglion cells
  • PS cells do not migrate down from higher in GI tract
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4
Q

What causes Hirschprung’s?

A
  • genetic
  • FHx inc chance
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5
Q

How does Hirschprung’s cause obstruction?

A
  • aganglionic colon
  • loss of movement of faeces
  • obstruction in bowel
  • proximal to obstruction: distention and fullness
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6
Q

How does Hirschprung’s present?

A
  • delay in passing meconium
  • chronic constipation since birth
  • abdo pain and distention
  • vomiting
  • poor weight gain and FTT
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7
Q

What syndromes is Hirschprung’s associated with?

A
  • Down’s
  • Neurofibromatosis
  • Waardenburg syndrome
  • multiple endocrine neoplasia type II
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8
Q

What is Hirschprung-Associated Enterecolitis?

A
  • inflammation and obstruction of intestine
  • occurs in 20% neonates w/ Hirschprung’s
  • presents 2-4 weeks after birth
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9
Q

How does hirschprung-associated enterocolitis present?

A
  • fever
  • abdo distention
  • (bloody) diarrhoea
  • sepsis features
  • can lead to toxic megacolon and bowel perf
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10
Q

How is hirschprung-associated enterocolitis managed?

A
  • urgent Abx
  • fluid resus
  • decompression of obstruction
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11
Q

How is Hirschprung’s investigated?

A
  • Abdo x-ray
  • rectal biopsy
  • histology showing absence of ganglionic cells
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12
Q

How is Hirschprung’s managed?

A
  • fluid resus if unwell
  • management of intestinal obstruction
  • surgical removal of aganglionic section
  • may be left with disturbances of function/incontinence
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13
Q

What is intussusception?

A
  • bowel invaginates into itself
  • thickens overall size and narrows lumen
  • obstructs passage of faeces
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14
Q

What is the epidemiology of intussusception?

A
  • infants 6mo - 2yrs
  • more common in boys
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15
Q

What conditions are associated with intussusception?

A
  • concurrent viral illness
  • HSP
  • cystic fibrosis
  • intestinal polyps
  • Meckel’s diverticulum
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16
Q

How does intussusception present?

A
  • severe, colicky abdo pain
  • pale, lethargic, unwell child
  • redcurrant jelly stool
  • sausage shaped RUQ mass
  • vomiting
  • intestinal obstruction
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17
Q

How is intussusception diagnosed?

A
  • USS
  • contrast enema
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18
Q

How is intussusception managed?

A
  • therapeutic enema
  • contrast/water/air pumped into colon to force normal position
  • surgical reduction
  • surgical resection if gangrenous
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19
Q

What are some complications of intussusception?

A
  • obstruction
  • gangrenous bowel
  • perforation
  • death
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20
Q

What is the pyloric sphincter?

A
  • ring of smooth muscle forming the canal between the stomach and duodenum
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21
Q

What is pyloric stenosis?

A
  • hypertrophy and narrowing of the pylorus
  • prevents food travelling to duodenum as normal
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22
Q

How does pyloric stenosis present?

A
  • projectile vomiting
  • thin pale baby
  • failure to thrive
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23
Q

Why is there projectile vomiting in pyloric stenosis?

A
  • peristalsis tries to push food into duodenum
  • ejects food into oesophagus and out of mouth
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24
Q

What is seen on examination of pyloric stenosis?

A
  • firm round mass in upper abdomen
  • feels like large olive
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25
Q

What is seen metabolically on investigation of pyloric stenosis?

A
  • hypochloric metabolic alkalosis
  • due to vomiting HCl acid
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26
Q

How is pyloric stenosis managed?

A
  • diagnosed by abdo USS
  • treatment: laparoscopic pyloromyotomy to widen canal
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27
Q

What is appendicitis and what is the epidemiology?

A
  • inflammation of the appendix
  • patients aged 10-20 yrs
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28
Q

What is the anatomy of the appendix?

A
  • small, thin tube arising from caecum, leads to dead end
  • located where 3 teniae coli meet
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29
Q

What is the pathophysiology behind appendicitis?

A
  • pathogens trapped due to obstruction where the appendix meets the bowel
  • trapped pathogens > infection + inflammation
  • can lead to gangrene and rupture > faeces and infectious material released into peritoneum
  • leads to peritonitis
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30
Q

What is the presentation of appendicitis?

A
  • central abdo pain > R iliac fossa
  • tenderness at McBurney’s point on palpation
  • loss of appetite
  • nausea and vomiting
  • guarding
  • rebound and percussion tenderness
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31
Q

What is Rovsing’s sign?

A
  • palpation of the LIF causes pain in the RIF
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32
Q

What is rebound tenderness?

A
  • increased pain when quickly releasing pressure
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33
Q

How is appendicitis diagnosed?

A
  • clinical presentation
  • raised inflammatory markers
  • CT/ultrasound
  • potential diagnostic laparoscopy
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34
Q

What are the key differential diagnoses of appendicitis?

A
  • ovarian cysts
  • Meckel’s diverticulum
  • ectopic pregnancy (hCG to exclude)
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35
Q

How is appendicitis managed?

A
  • appendectomy
  • laparoscopic surgery is ideal over open
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36
Q

What is biliary atresia?

A
  • congenital condition
  • bile duct is narrowed or absent
  • prevents excretion of conjugated bilirubin
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37
Q

How does biliary atresia present?

A
  • persistent jaundice
  • in term babies if >14 days
  • > 21 days in prem babies
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38
Q

How is biliary atresia investigated?

A
  • conjugated and unconjugated bilirubin levels
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39
Q

How is biliary atresia managed?

A
  • Kasai portoenterostomy
  • attaching section of small intestine to liver where bile duct normally attaches
  • or full liver transplant
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40
Q

What are the typical characteristics of Crohn’s (NESTS)

A
  • No blood or mucus
  • Entire GI tract (mainly ileum)
  • Skip lesions: unaffected areas between active disease
  • Terminal ileum (and proximal colon) most affected with transmural inflammation
  • Smoking is a risk factor
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41
Q

What are the characteristics of ulcerative colitis (CLOSE)?

A
  • continuous inflammation
  • limited to colon and rectum
  • only superficial mucosa affected
  • smoking is protective
  • excreted blood and mucus
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42
Q

How does IBD present?

A
  • diarrhoea
  • abdominal pain
  • passing blood
  • weight loss
  • anaemia
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43
Q

What are some extra-intestinal manifestations of IBD?

A
  • clubbing
  • erythema nodosum
  • inflammatory arthritis
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44
Q

What are some specific features of the presentation of ulcerative colitis?

A
  • blood and mucus with gradual onset of diarrhoea
  • bowel frequency related to severity of disease
  • crampy abdominal discomfort
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45
Q

How is IBD investigated?

A
  • bloods: anaemia, FBC, U&Es, cultures
  • CRP: inflammation and active disease
  • faecal calprotectin
  • endoscopy
  • imaging for complications
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46
Q

How is moderate UC managed medically?

A

inducing remission:
- 1st line: aminosalocylate (mesalazine)
- 2nd line: corticosteroids: prednisolone

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47
Q

How is severe UC managed medically?

A
  • hydrocortisone ± cyclosporin if severe
  • maintaining remission: sulfasalazine, mesalazine
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48
Q

How is UC managed surgically?

A
  • panproctocolectomy (colon removal)
  • permanent ileostomy or J-pouch
49
Q

How is Crohn’s managed medically?

A
  • inducing remission: steroids: prednisolone
  • hydrocortisone if severe
  • maintaining remission: azathioprine, methotrexate
50
Q

What is the surgical management of Crohn’s?

A
  • if only affecting distal ileum can be resected
  • surgery to treat strictures and fistulas
51
Q

What is the pathophysiology of IBD?

A
  • develops as a result of environmental trigger in genetically susceptible individual
  • bacteria or dietary antigens taken up by M cells, pass through gap between cells
  • picked up by antigen presenting cells causing secretion of pro-inflammatory cytokines
  • activates T cells leading to inflammation
52
Q

What is irritable bowel syndrome?

A
  • functional bowel disorder
  • symptoms resulting from abnormal functioning of bowel
  • due to disorders of gut motility or brain-gut axis
53
Q

What are the symptoms of IBS?

A
  • fluctuating bowel habit: alternating constipation and diarrhoea
  • abdominal pain relieved by defecation
  • bloating
  • chronic and exacerbated by stress
54
Q

How is IBS diagnosed?

A
  • exclusion: bloods, faecal calprotectin (IBD), anti-TTG (coeliac), colonoscopy
  • abdo pain + 2 symptoms
55
Q

How is IBS managed?

A
  • try exclusion diets
  • reduced processed food, caffeine and alcohol
  • regular small meals and fluid
  • loperamide for diarrhoea
  • laxatives for constipation
  • tricyclic antidepressants, SSRIs
56
Q

What is typical presentation of constipation?

A
  • <3 stools per week
  • hard or rabbit dropping stools
  • straining and painful passage
  • abdo pain
  • overflow soiling
  • retentive posturing
  • rectal bleeding
57
Q

What lifestyle factors cause constipation?

A
  • habitually not opening bowels
  • low fibre diet
  • poor fluid intake
  • sedentary lifestyle
  • psychosocial problems
58
Q

What is encopresis?

A
  • faecal incontinence
  • rectum loses sensation due to stretching
  • overflow soiling
59
Q

What is faecal impaction?

A
  • large hard stool blocking rectum
  • leading to desensitisation
60
Q

What are red flags of constipation in newborns and infants?

A
  • not passing meconium within 48hrs: CF, Hirschprung’s
  • vomiting: intestinal obstruction
61
Q

What physical exam findings are red flags in constipated children?

A
  • Abnormal anus or lower back/buttocks (spina bifida, cord lesion, abuse)
  • Neurological signs, especially in lower limbs (cerebral palsy, cord lesion)
62
Q

What systemic signs are red flags in constipated children?

A
  • Failure to thrive (coeliac, hypothyroidism, safeguarding)
  • Acute severe abdominal pain and bloating (obstruction, intussusception)
63
Q

How is constipation managed?

A
  • high fibre diet
  • hydration
  • laxatives: movicol
  • bowel diary
64
Q

What are complications of constipation?

A
  • pain
  • reduced sensation
  • fissures
  • haemorrhoids
  • overflow and soiling
65
Q

What is GORD?

A
  • reflux through lower oesophageal sphincter into throat and mouth
  • immaturity of sphincter in babies
66
Q

How does GORD present?

A
  • chronic cough
  • hoarse cry
  • distress after feeding
  • reluctance to feed
  • pneumonia
  • poor weight gain
67
Q

What systemic signs should raise concern in a vomiting child?

A
  • Respiratory symptoms (aspiration and infection)
  • Blood in the stools (gastroenteritis, cow’s milk)
  • Signs of infection (fever, lethargy)
  • Rash, angioedema, other signs of allergy (cow’s milk)
68
Q

What associated abdominal and neurological signs are concerning in a vomiting child?

A
  • Abdominal distention (obstruction)
  • Reduced consciousness
  • Bulging fontanelle
  • Neurological signs
    (meningitis, raised ICP)
69
Q

What are vomiting red flags?

A
  • Not keeping down any feed
  • Projectile or forceful vomiting
    (both pyloric stenosis or obstruction)
  • Bile-stained vomit
  • Haematemesis
    (peptic ulcer, oesophagitis, varices)
70
Q

How is GORD managed conservatively?

A
  • small, frequent meals
  • burping regularly
  • not over-feeding
  • keep baby upright
71
Q

How can GORD be managed medically?

A
  • gaviscon mixed with feeds
  • thickened milk or formula
  • PPIs
72
Q

What are causes of intestinal obstruction?

A
  • meconium ileus
  • Hirschprung’s
  • oesophageal atresia
  • duodenal atresia
  • intussusception
  • malrotation with volvulus
73
Q

How does intestinal obstruction present?

A
  • persistent, green, bilious vomiting
  • abdominal pain and distention
  • failure to pass wind or stools
  • high pitched, tinkling bowel sounds
74
Q

How is intestinal obstruction diagnosed?

A
  • abdominal xray
  • dilated bowel loops
  • absence of air in rectum
75
Q

How is intestinal obstruction managed?

A
  • paediatric surgical unit
  • nil by mouth
  • NG tube to drain stomach
  • IV fluids
76
Q

What is cow’s milk protein allergy and what is the epidemiology?

A
  • hypersensitivity to protein in cow’s milk
  • affecting <3 years old
  • usually outgrown by age 3
77
Q

What are the two types of cow’s milk protein allergy?

A
  • IgE mediated (within 2hrs)
  • Non-IgE mediated (slow over several days)
78
Q

What factors increase the risk of cow’s milk protein allergy?

A
  • formula feeding
  • FHx of atopic conditions
79
Q

What GI symptoms does cow’s milk protein allergy present with?

A
  • bloating and wind
  • abdo pain
  • diarrhoea
  • vomiting
80
Q

What general allergic symptoms does cow’s milk protein allergy present with?

A
  • urticarial rash
  • angio-oedema
  • cough/wheeze
  • sneezing
  • watery eyes
  • eczema
81
Q

How is cow’s milk protein allergy managed?

A
  • skin prick testing
  • avoiding cow’s milk
  • breast feeding mothers should avoid dairy
  • replace formula with hydrolysed formula
82
Q

What is the milk ladder?

A
  • every 6 months can be tried on first step of milk ladder
  • malted milk biscuits
  • slowly progress up ladder until develop symptoms
83
Q

What is cow’s milk intolerance?

A
  • presents with same GI features but no allergic features
  • outgrow by 2-3 years
  • after 1yr can be started on milk ladder
84
Q

What is acute gastritis?

A
  • inflammation of the stomach
  • presents with nausea and vomiting
85
Q

What is enteritis?

A
  • inflammation of intestines
  • presents with diarrhoea
86
Q

What is gastroenteritis?

A
  • inflammation from stomach to intestines
  • presents with nausea, vomiting, diarrhoea
87
Q

What are differentials for diarrhoea?

A
  • gastroenteritis
  • IBD
  • lactose intolerance
  • CF
  • IBS
  • coeliac
  • medication
88
Q

What are common causes of viral gastroenteritis?

A
  • rotavirus
  • norovirus
  • adenovirus
89
Q

Describe gastroenteritis caused by E. coli

A
  • spread through infected faeces, unwashed salad, contaminated water
90
Q

What toxin does E.coli produce and what are the symptoms?

A
  • produces shiga toxin
  • causes abdo cramps, bloody diarrhoea, vomiting
91
Q

What is haemolytic uraemic syndrome?

A
  • shiga toxin destroys blood cells
  • also caused by use of Abx
92
Q

Which bacteria commonly causes gastroenteritis?

A
  • E. coli
  • campylobacter jejuni
  • shigella
  • bacillus cereus
93
Q

What type of bacteria is campylobacter jejuni and how is it spread?

A
  • causes travellers diarrhoea
  • gram negative curved/spiral bacteria
  • raw/improperly cooked poultry, untreated water, unpasteurised milk
94
Q

What are the symptoms and treatment of campylobacter jejuni infection?

A
  • abdo cramps, bloody diarrhoea, vomiting, fever
  • azithromycin and ciprofloxacin
95
Q

How does shigella spread and what are the symptoms?

A
  • faeces contaminating drinking water, pools and food
  • abdo cramps, bloody diarrhoea, fever
  • shiga toxin > haemolytic uraemia syndrome
96
Q

What toxin does E. coli produce and what symptoms does this lead to?

A
  • shiga toxin
  • abdo cramps, bloody diarrhoea and vomiting
  • destroys blood cells > haemolytic uraemia syndrome
97
Q

How is salmonella spread and what are the symptoms?

A
  • raw eggs and poultry
  • water diarrhoea with mucus/blood, abdo pain and vomiting
98
Q

What type of bacteria is bacillus cereus and on what food is it produced?

A
  • gram positive rod
  • inadequately cooked food/food not immediately refrigerated
  • fried rice
99
Q

What toxin does bacillus cereus produce and what symptoms does it cause?

A
  • cereulide
  • abdo cramping, vomiting and water diarrhoea
100
Q

What is giardiasis, what are the symptoms and how is it treated?

A
  • Giardia lamblia is a microscopic parasite spread by faeco-oral transmission
  • can be asymptomatic or cause chronic diarrhoea
  • treated with metronidazole
101
Q

How is gastroenteritis managed?

A
  • barrier nursing
  • off school for 48hrs
  • MC&S
  • fluid challenge
102
Q

What treatment shouldn’t be given in gastroenteritis?

A
  • anti-diarrhoeal
  • antiemetic
  • Abx only when causative organism identified
103
Q

What complications might arise from gastroenteritis?

A
  • Lactose intolerance
  • Irritable bowel syndrome
  • Reactive arthritis
  • Guillain–Barré syndrome
104
Q

What is the pathophysiology behind coeliac disease?

A
  • T-cell mediated: auto-antibodies created in response to gluten exposure, targeting epithelial cells
  • anti-tissue transglutaminase and anti-endomysial (IgA)
  • affects small bowel, particularly jejunum, causing villus atrophy and malabsorption
105
Q

How does coeliac disease present?

A
  • failure to thrive
  • fatigue
  • diarrhoea
  • weigh loss
  • anaemia 2º to iron, B12, folate deficiency
  • dermatitis herpetiformis
106
Q

What neuro symptoms can coeliac disease cause?

A
  • peripheral neuropathy
  • cerebellar ataxia
  • epilepsy
107
Q

Which conditions is coeliac disease associated with?

A
  • T1DM
  • thyroid disease
  • autoimmune hepatitis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis
  • HLA-DQ2 gene
108
Q

Which auto-antibodies is coeliac disease associated with?

A
  • tissue transglutaminase (anti-TTG)
  • endomysial antibodies (EMAs)
  • deaminated gliadin peptides (anti-DGPs)
109
Q

How is coeliac disease investigated?

A
  • check total IgA to exclude IgA deficiency
  • raised anti-TTG
  • raised EMAs
110
Q

What is seen on endoscopy and intestinal biopsy?

A
  • crypt hypertrophy
  • villous atrophy
111
Q

How is coeliac disease managed?

A
  • lifelong gluten free diet
  • monitor coeliac antibodies
112
Q

What is Meckel’s diverticulum?

A
  • congenital abnormality of the GI tract
  • outpouching on anti-mesenteric border of ileum
113
Q

What causes Meckel’s diverticulum?

A
  • incomplete obliteration of the vitelline duct
114
Q

How does Meckel’s diverticulum present?

A
  • most remain asymptomatic
  • ectopic mucosa can cause inflammation and ulceration
  • resulting in painless dark red rectal bleeding
  • abdominal pain
  • intussusception
115
Q

What is the rule of 2s in Meckel’s diverticulum?

A
  • 2ft proximal to ileocaecal valve
  • 2in in length
  • 2 types of ectopic tissue: gastric and pancreatic
  • 2x more common in males
116
Q

What are differentials for Meckel’s diverticulum?

A
  • acute appendicitis: periumbilical pain, tenderness, vomiting
  • bowel obstruction (can cause)
  • gastroenteritis
  • peptic ulcer disease
117
Q

How is Meckel’s diverticulum investigated?

A
  • present acutely with bleeding or diverticulitis
  • CT scan
  • diagnostic laparoscopy
  • nuclear scintigraphy
118
Q

How is Meckel’s diverticulum managed?

A
  • urgent surgery
  • Meckel’s diverticulectomy
  • bowel resection if obstruction

Osha 3a (15 decks)

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