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A TO REVISE - PHASE 3A > PAEDS - GI/LIVER TO DO > Flashcards

PAEDS - GI/LIVER TO DO Flashcards

1
Q

IBD
What is the clinical presentation of Crohn’s disease?

A
  • Abdominal pain (RLQ), diarrhoea (often non-bloody) + weight loss
  • Failure to thrive
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2
Q

IBD
What is the clinical presentation of Ulcerative colitis?

A
  • PR bleeding (+ mucus), diarrhoea + colicky pain (LLQ)
  • Tenesmus and urgency too
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3
Q

IBD
What extra-intestinal features are seen in…

i) Crohn’s disease?
ii) Ulcerative colitis?
iii) Both?

A

i) Perianal disease = skin tags, anal fissures, abscesses + fistulas, strictures, obstruction
ii) primary sclerosing cholangitis
iii) Arthritis, erythema nodosum, pyoderma gangrenosum, uveitis + episcleritis, finger clubbing

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4
Q

IBD
What are some initial investigations for IBD?

A
  • FBC (microcytic anaemia, raised WCC + platelets)
  • U+Es
  • Low albumin (malabsorb)
  • Raised ESR/CRP
  • Stool MC&S
  • Faecal calprotectin released by intestines when inflamed (useful screening)
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5
Q

IBD
What is the medical management of Crohn’s disease?

A
  • Whole protein modular enteral feed for 6–8w can induce remission
  • Flares = PO prednisolone or IV hydrocortisone
  • Remission = azathioprine, methotrexate or mercaptopurine
  • Biologics (remission) = infliximab, adalimumab
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6
Q

IBD
How do you induce remission in Ulcerative colitis?

A
  • Mild-mod = 1st line topical (rectal) aminosalicylate (5-ASA, mesalazine), add PO if remission not achieved or extensive disease, 2nd line = PO prednisolone
  • Severe = 1st line IV hydrocortisone, 2nd line IV ciclosporin
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7
Q

IBD
How do you maintain remission in Ulcerative colitis?
What should be cautioned?

A
  • PO/PR mesalazine, azathioprine or mercaptopurine
  • Mesalazine can cause acute pancreatitis
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8
Q

IBD
What is the surgical management of Ulcerative colitis?

A
  • Panproctocolectomy = curative as removes disease
  • Pt left with permanent ileostomy or ileo-anal anastomosis (J-pouch) where ileum folded back on itself + fashioned into large pouch that functions as a rectum as it attaches to anus
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9
Q

COELIAC DISEASE
What is the aetiology of coeliac disease?

A
  • Genetics = HLA-DQ2 + HLA-DQ8
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10
Q

COELIAC DISEASE
What is the clinical presentation of coeliac disease?

A
  • Abnormal stools (smelly, diarrhoea, floating)
  • Abdo pain, distension + buttock wasting
  • Failure to thrive, weight loss, fatigue
  • Dermatitis herpetiformis = itchy blistering skin rash, often on abdo
  • Nutrient deficiencies (B12, folate, Fe)
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11
Q

COELIAC DISEASE
What are the characteristic features seen on small intestinal biopsy?

A
  • Villous atrophy
  • Crypt hyperplasia
  • Increased intraepithelial lymphocytes
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12
Q

COELIAC DISEASE
What are some complications of coeliac disease?

A
  • Anaemias
  • Osteoporosis
  • Lymphoma (EATL)
  • Hyposplenism
  • Lactose intolerance
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13
Q

HIRSCHSPRUNG’S DISEASE
What is a complication of Hirschsprung’s disease?

A
  • Hirschsprung-associated enterocolitis (HAEC) = inflammation + obstruction of intestine, sometimes due to C. difficile
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14
Q

HIRSCHSPRUNG’S DISEASE
How does hirschsprung associated enterocolitis (HAEC) present?

A
  • 2-4w after birth = fever, abdo distension, diarrhoea (bloody) + signs of sepsis
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15
Q

PYLORIC STENOSIS
What are some investigations for pyloric stenosis?

A
  • Test feed = visible gastric peristalsis
  • Hyponatraemic, hypokalaemic + hypochloraemic metabolic alkalosis
  • USS = Dx, visualises thickened pylorus
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16
Q

PYLORIC STENOSIS
What is the management of pyloric stenosis?

A
  • Correct fluid + electrolyte disturbances (0.45% saline, 5% dextrose + K+ supplements) before any surgery
  • Laparoscopic Ramstedt’s pyloromyotomy
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17
Q

ABDOMINAL PAIN
What are some causes of acute abdominal pain?

A
  • Surgical = appendicitis, intussusception, Meckel’s, malrotation, mesenteric adenitis
  • Boys = exclude testicular torsion + strangulated inguinal hernia
  • Medical = UTI, DKA, HSP, lower lobe pneumonia
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18
Q

ABDOMINAL PAIN
What are some causes of recurrent abdominal pain?

A
  • No structural cause in >90%
  • GI = IBS, abdominal migraine, coeliac
  • Gynae = ovarian cysts, PID, Mittelschmerz (ovulation pain)
  • Hepatobiliary = hepatitis, gallstones, UTI
  • Psychosocial = bullying, abuse, stress
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19
Q

APPENDICITIS
What are the signs of appendicitis?

A
  • Low grade fever
  • Abdominal pain aggravated by movement
  • RIF tenderness + guarding (McBurney’s point)
  • Rebound + percussion tenderness (precipitated by cough, jump)
  • Rovsing’s sign = LIF pressure causes RIF pain
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20
Q

INTUSSUSCEPTION
What is intussusception and where does it most commonly affect?

A
  • Bowel telescopes (invaginates) into itself (proximal bowel into distal segment)
  • Commonly ileocaecal valve (ileum>caecum)
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21
Q

INTUSSUSCEPTION
What are some signs of intussusception?

A
  • RUQ ‘sausaged-shaped’ mass
  • Redcurrant jelly stool as blood + mucus in stool
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22
Q

MECKEL’S DIVERTICULUM
What is Meckel’s diverticulum?

A
  • Ileal remnant of the vitello-intestinal duct which contains ectopic gastric mucosa or pancreatic tissue
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23
Q

CONSTIPATION
What are some features of constipation?

A
  • Hard or like rabbit droppings (type 1)
  • May have PR bleed if hard
  • Waxing + waning of pain with stool passage
  • Retentive posturing
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24
Q

CONSTIPATION
What are some causes of constipation?

A
  • Usually idiopathic
  • Meds (opiates)
  • LDs
  • Hypothyroidism
  • Hypercalcaemia
  • Poor diet (dehydration, low fibre)
  • Occasionally forceful potty training
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25
Q

CONSTIPATION
What are some red flags in constipation?

A
  • Delayed passage of meconium = Hirschsprung’s, CF
  • Failure to thrive = hypothyroid, coeliac
  • Abnormal lower limb neurology = lumbosacral pathology
  • Perianal bruising or multiple fissures = ?abuse
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26
Q

CONSTIPATION
What investigations might you do in constipation?

A
  • Abdo exam may reveal palpable faecal mass
  • PR examination only by an expert
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27
Q

CONSTIPATION
What are some complications of constipation?

A
  • Acquired megacolon
  • Anal fissures
  • Soiling + behavioural problems
  • Child may avoid defecating due to pain > constipation + overflow diarrhoea
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28
Q

CONSTIPATION
What is the medical management of constipation?

A
  • 1st = macrogol (osmotic) laxative like polyethylene glycol + electrolytes (Movicol)
  • 2nd = lactulose (osmotic) if movicol is not tolerated +/- stimulant e.g. Senna
  • 3rd = consider enema ± sedation or specialist manual evacuation
  • Continue for several weeks after regular bowel habit then gradual dose reduction
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29
Q

GORD
What are the investigations for GORD?

A
  • Usually clinical but if atypical Hx, complications or failed Tx…
    – 24h oesophageal pH monitoring
    – Endoscopy + biopsy to identify oesophagitis
    – Contrast studies like barium meal
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30
Q

GORD
What are some complications of GORD?

A
  • Failure to thrive from severe vomiting
  • Oesophagitis = haematemesis, discomfort on feeding or heartburn, Fe anaemia
  • Aspiration > recurrent pneumonia, cough/wheeze
  • Sandifer syndrome = dystonic neck posturing (torticollis)
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31
Q

GORD
What is the management of uncomplicated GORD?

A
  • Small + frequent meals, do not over feed
  • Regular burping to help milk settle
  • Keep baby upright after feeds
  • Trial thickening agents like Nestargel or add Gaviscon to feeds (not at same time)
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32
Q

GORD
What is the management of more significant GORD?

A
  • Acid suppression = H2 receptor antagonists (ranitidine) or PPI (omeprazole)
  • Surgical Mx (fundoplication) if complications, unresponsive to intensive medical treatment or oesophageal strictures
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33
Q

GASTROENTERITIS
What is the difference in gastroenteritis in developing and developed countries?

A
  • Developing = causes thousands of deaths, mostly bacteria from contaminated food
  • Developed = mostly viral, infants susceptible to dehydration
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34
Q

GASTROENTERITIS
What are 5 bacteria that can cause gastroenteritis?

A
  • Campylobacter jejuni
  • E. coli
  • Shigella
  • Salmonella
  • Bacillus cereus
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35
Q

GASTROENTERITIS
What is the management of campylobacter jejuni?

A
  • Abx considered after isolating organism where pts have severe symptoms or other risk factors
  • Azithromycin or ciprofloxacin
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36
Q

GASTROENTERITIS
What E. coli strain is important to be aware of in terms of gastroenteritis?
How is it spread?
How does it present?

A
  • E. coli 0157 as produces the Shiga toxin
  • Contact with infected faeces, unwashed salads or contaminated water
  • Abdominal cramps, bloody diarrhoea + vomiting
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37
Q

GASTROENTERITIS
What is a complication of E. coli 0157?

A
  • Destroys blood cells + can lead to haemolytic uraemic syndrome
  • Abx increase this risk so avoid
38
Q

GASTROENTERITIS
How is Shigella spread?
How does it present?
Complication?

A
  • Faeces contaminating drinking water, swimming pools + food
  • Bloody diarrhoea, abdominal cramps + fever
  • Shiga toxin > HUS
39
Q

GASTROENTERITIS
How is Salmonella spread?
How does it present?

A
  • Raw eggs, poultry
  • Watery diarrhoea ± mucus or blood
40
Q

GASTROENTERITIS
What is Bacillus Cereus?
How does it present?

A
  • Gram +ve rod spread through inadequately cooked food, grows well on food, classically undercooked or reheated rice
  • Produces toxin (cereulide) > abdominal cramping + vomiting soon after ingestion, reaches intestines + different toxin causes watery diarrhoea, resolves within 24h
41
Q

GASTROENTERITIS
What are signs of clinical shock?

A
  • Pale/mottled
  • Hypotension
  • Prolonged CRT
  • Cold
  • Decreased GCS
  • Sunken fontanelle
  • Weak pulses
  • Anuria
42
Q

GASTROENTERITIS
What is the management of gastroenteritis with clinical dehydration?

A
  • 50ml/kg low osmolarity oral rehydration solution (Dioralyte) in addition to maintenance fluid,
  • may need NG tube if unable to drink or vomiting
43
Q

BILIARY ATRESIA
What is the clinical presentation of biliary atresia?

A
  • Prolonged jaundice >2w
  • Pale stools + dark urine (obstructive pattern)
  • Failure to thrive
  • Hepatosplenomegaly
44
Q

BILIARY ATRESIA
What are the investigations for biliary atresia?

A
  • Serum split bilirubin = conjugated elevated
  • USS abdo gold standard for Dx, laparotomy confirms
45
Q

BILIARY ATRESIA
What is the management of biliary atresia?

A
  • Kasai portoenterostomy (attach section of small intestine to opening of liver where bile duct attaches)
  • Some will need full liver transplant
  • Success decreases with age so early Dx crucial
46
Q

NEONATAL HEPATITIS
What are some investigations for neonatal hepatitis syndrome?

A
  • Deranged LFTs with raised unconjugated + conjugated bilirubin
  • Liver biopsy = multinucleated giant cells + Rosette formation
47
Q

NEONATAL HEPATITIS
What are 4 main causes of neonatal hepatitis?

A
  • Congenital infection
  • Alpha-1-antitrypsin (A1AT) deficiency
  • Galactosaemia
  • Wilson’s disease
48
Q

NEONATAL HEPATITIS
What is galactosaemia?

A
  • Deficiency of galactose-1-phosphate uridyltransferase (GALT) involved in galactose metabolism (lactose breaks down into galactose)
49
Q

NEONATAL HEPATITIS
What are the complications of galactosaemia?

A
  • Rapidly fatal course with shock, DIC + haemorrhage due to gram -ve sepsis
  • Liver failure, cataracts + Developmental delay if untreated
50
Q

NEONATAL HEPATITIS
What is the management of galactosaemia?

A
  • Stop cow’s milk, breastfeeding C/I
  • Dairy-free diet
  • IV fluids
51
Q

NEONATAL HEPATITIS
How does Wilson’s disease present?

A

Sx of copper accumulation

  • Eyes (Kayser-Fleischer rings)
  • Brain (Parkinsonism + psychosis)
  • Kidneys (vit D resistant rickets)
  • Liver (jaundice)
52
Q

FAILURE TO THRIVE
What are the different categories of causes for failure to thrive?

A
  • Inadequate calorie intake (most common)
  • Malabsorption
  • Inadequate retention
  • Increased calorie requirements
53
Q

FAILURE TO THRIVE
What is marasmus?

A
  • Severe protein malnutrition
  • Weight for height >3 standard deviations below the median
  • Wasted, wrinkly appearance due to severe protein-energy malnutrition
54
Q

FAILURE TO THRIVE
How is failure to thrive defined by height?

A
  • Mild = fall across 2 centile lines on growth chart
  • Severe = fall across 3 centile lines on growth chart
55
Q

FAILURE TO THRIVE
How does NICE define faltering growth in children by weight?

A
  • ≥1 centile spaces if birth weight was <9th centile
  • ≥2 centile spaces if birth weight was 9th–91st centile
  • ≥3 centile spaces if birth weight was >91st centile
  • Current weight is below 2nd centile for age, regardless of birth weight
56
Q

FAILURE TO THRIVE
What are some investigations for failure to thrive?

A
  • Serial measurements on growth charts for Dx
  • Full Hx + examination
  • Measure height + weight > BMI (if >2y)
  • Calculate mid-parental height
  • Food diary
  • Urine dipstick for UTI + coeliac screen (anti-TTG) for 1st line investigations
57
Q

CMPA
What is the clinical presentation of cows milk protein allergy (CMPA)?

A
  • Apparent when weaned from breast > formula milk or food with milk
  • GI = bloating + wind, abdo pain, D+V, failure to thrive
  • Allergic = urticaria, cough, wheeze, sneezing, itching
  • Anaphylaxis + angioedema is rare
58
Q

KWASHIOKOR
what are the clinical features?

A
  • growth retardation
  • diarrhoea
  • anorexia
  • oedema - defining characteristic
  • skin/hair depigmentation
  • abdominal distension with fatty liver
59
Q

KWASHIOKOR
what are the investigations?

A

bloods - FBC, U+E, serum protein, urine dipstick
- hypoalbuminaemia
- normo/microcytic anaemia
- low calcium, magnesium, phosphate and glucose

60
Q

MARASMUS
what is it?

A

a type of protein-energy malnutrition caused by a severe energy (calories) deficiency

61
Q

MARASMUS
what are the clinical features?

A
  • height is relatively preserved compared to weight
  • wasted appearance
  • muscle atrophy
  • listless
  • diarrhoea
  • constipation
62
Q

HERNIA
what are the most common types of hernia that affect children?

A

indirect inguinal hernia - caused by an opening in the abdominal wall that is present at birth
umbilical hernia

63
Q

HERNIA
what are the risk factors for developing a hernia?

A
  • premature, underweight babies
  • male gender
  • family history
  • medical conditions - undescended testes, CF
  • African descent
64
Q

CHOLEDOCHAL CYST
How may it present?

A
  • Cholestatic jaundice
  • abdominal mass
  • pain in RUQ
  • nausea and vomiting
  • fever
65
Q

CHOLEDOCHAL CYST
what are the investigations?

A

can be detected on ultrasound before the child is born

after the baby is born, the parent’s may notice lump in RUQ, the following tests are then done:
- CT scan
- cholangiography

66
Q

CHOLEDOCHAL CYST
What are the complications?

A
  • Cholangitis
  • small risk of malignancy
67
Q

CHOLEDOCHAL CYST
what are the different types?

A

Type 1 - cyst of extrahepatic bile duct (most common)
Type 2 - abnormal pouch/sac opening from duct
Type 3 - cyst inside the wall of the duodenum
Type 4 - cysts on both intrahepatic and extrahepatic bile ducts

68
Q

LIVER FAILURE
what are the causes?

A
  • chronic hepatitis
  • biliary tree disease
  • toxin induced
  • A1AT deficiency
  • autoimmune hepatitis
  • wilson’s disease
  • CF
  • budd-chiari syndrome
  • primary sclerosing cholangitis
69
Q

IBD
Are granulomas found in Crohn’s disease?

A

Yes - it is granulomatous

70
Q

IBD
Are goblet cells present in Crohn’s disease?

A

Yes

71
Q

IBD
What is the histology of Crohn’s disease?

A

Non-caseating epithelioid cell granulomata

72
Q

IBD
Which layer of the GI tract is affected by ulcerative colitis?

A

Only the mucosa

73
Q

IBD
what is the histology of ulcerative colitis?

A
  • Increased crypt abscesses,
  • pseudopolyps,
  • ulcers
74
Q

COELIAC DISEASE
What is the pathophysiology?

A

Autoimmune response to alpha-gliadin portion of protein gluten causes inflammation in small intestine (particularly jejunum)

75
Q

CONSTIPATION
What is encopresis?

A

Involuntary soiling

76
Q

GORD
When can it become problematic?

A

Problematic = chronic cough, hoarse cry, distress after feeding + reluctance to feed, failure to thrive

77
Q

GASTROENTERITIS
What is the most common cause?

A
  • Viral rotavirus in paeds,
  • norovirus in adults
78
Q

GASTROENTERITIS
What are some risk factors?

A
  • Poor hygiene,
  • immunocompromised,
  • poorly cooked foods
79
Q

GASTROENTERITIS
what is the management for shigella infection?

A

severe = azithromycin or ciprofloxacin

80
Q

GASTROENTERITIS
what is the management for shigella infection?

A

severe = azithromycin or ciprofloxacin

81
Q

GASTROENTERITIS
How is shock managed in gastroenteritis?

A

Rapid IVI (0.9% NaCl 20ml/kg), repeat if necessary, Abx if septicaemia

82
Q

BILIARY ATRESIA
What genetic mutation is biliary atresia associated with?

A

Associated with CFC1 gene mutations

83
Q

NEONATAL HEPATITIS
How does it present?

A
  • Intruterine growth restriction (IUGR),
  • hepatosplenomegaly at birth,
  • failure to thrive
  • dark urine
84
Q

NEONATAL HEPATITIS
What is the cause of A1AT deficiency?

A

AR on chromosome 14

85
Q

NEONATAL HEPATITIS
What is the presentation of A1AT deficiency?

A
  • Prolonged neonatal jaundice (cholestasis), worse on breast feeding,
  • can have (prolonged) bleeding due to vitamin K deficiency,
  • COPD
86
Q

NEONATAL HEPATITIS
What is the management for A1AT deficiency?

A
  • ?Transplantation
  • Never smoke
87
Q

NEONATAL HEPATITIS
How does galactosaemia present?

A
  • Poor feeding,
  • vomiting,
  • jaundice + hepatomegaly when fed milk
88
Q

NEONATAL HEPATITIS
What are the genetics for Wilson’s disease?

A

AR on chromosome 13

89
Q

FAILURE TO THRIVE
What are some causes of inability to process nutrients properly?

A
  • T1DM,
  • inborn errors of metabolism
90
Q

CMPA
What is cow’s milk protein allergy (CMPA) associated with?

A
  • More common in formula fed babies
  • those with personal or FHx of atopy
91
Q

NEONATAL HEPATITIS
What is the management of Wilson’s disease?

A

Penicillamine for copper chelation

A TO REVISE - PHASE 3A (16 decks)

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