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My Phase 3a Revision > PAEDS - GI/LIVER > Flashcards

PAEDS - GI/LIVER Flashcards

1
Q

MALABSORPTION
What is malabsorption?

A
  • Disorders affecting digestion or absorption of nutrients
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2
Q

MALABSORPTION
How does it present?

A

It manifests as:
– Abnormal stools (difficult to flush, offensive odour)
– Failure to thrive or poor growth
– Nutrient deficiencies (Fe anaemia, B12 deficiency)

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3
Q

MALABSORPTION
What are some causes of malabsorption?

A
  • Small intestine disease = coeliac
  • Exocrine pancreas dysfunction = CF
  • Cholestatic liver disease, biliary atresia
  • Short bowel syndrome (NEC, bowel removal)
  • Loss of terminal ileum function (resection, Crohn’s, absent bile acid)
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4
Q

IBD
What is inflammatory bowel disease (IBD)?

A
  • Umbrella term for Crohn’s disease + ulcerative colitis
  • Relapsing-remitting conditions involving inflammation of walls in the GI tract
  • Result of environmental triggers in a genetically predisposed individual
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5
Q

IBD
Where does Crohn’s disease tend to affect?

A
  • Mouth>anus,
  • spares rectum,
  • favours terminal ileum
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6
Q

IBD
Which layer of the GI tract is affected by Crohn’s disease?

A

It is transmural - it affects all the layers

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7
Q

IBD
Is the inflammation in Crohn’s disease continuous?

A

No - there are skip lesions

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8
Q

IBD
Are granulomas found in Crohn’s disease?

A

Yes - it is granulomatous

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9
Q

IBD
What is the effect of smoking on Crohn’s disease?

A

It is a risk factor

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10
Q

IBD
Are goblet cells present in Crohn’s disease?

A

Yes

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11
Q

IBD
What is the histology of Crohn’s disease?

A

Non-caseating epithelioid cell granulomata

Transmural inflammation
Goblet cells
Granulomas

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12
Q

IBD
Where is affected by ulcerative colitis?

A

Colon only (never further than ileocaecal valve), starts at rectum

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13
Q

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

A

Only the mucosa

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14
Q

IBD
Is the inflammation in ulcerative colitis continuous?

A

Yes - the whole colon is affected

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15
Q

IBD
Is granulomatous inflammation found in ulcerative colitis?

A

No

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16
Q

IBD
What is the effect of smoking on ulcerative colitis?

A

It is protective

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17
Q

IBD
Are goblet cells present in ulcerative colitis?

A

There is depletion of goblet cells

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18
Q

IBD
what is the histology of ulcerative colitis?

A
  • Increased crypt abscesses,
  • pseudopolyps,
  • ulcers
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19
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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20
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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21
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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22
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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23
Q

IBD
What test is diagnostic for IBD?
What would it show?
What other investigation might you do?

A
  • Colonoscopy with biopsy (histology)
  • Crohn’s = small bowel narrowing, fissuring or thickened bowel wall, cobblestone appearance
  • UC = visible ulcers
  • Further imaging (USS, CT or MRI) to look at complications of Crohn’s
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24
Q

IBD
How do you treat flares of crohns disease?

A

PO prednisolone or IV hydrocortisone

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25
Q

IBD
How do you induce remission in crohns disease?

A

1st line = steroids (e.g. oral prednisolone or IV hydrocortisone).

If steroids alone don’t work, consider adding immunosuppressant medication under specialist guidance:

Azathioprine
Mercaptopurine
Methotrexate
Infliximab
Adalimumab

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26
Q

IBD
How do you maintain remission in crohns disease?

A

1st line = Azathioprine or Mercaptopurine

Alternatives:
Methotrexate
Infliximab
Adalimumab

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27
Q

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

A
  • Surgical resection of distal ileum if only affected area
  • Treat strictures + fistulas secondary to Crohn’s
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28
Q

IBD
How do you induce remission in Ulcerative colitis?

A

Mild to moderate disease
- 1st line = aminosalicylate (e.g. mesalazine oral or rectal)
- 2nd line = corticosteroids (e.g. prednisolone)

Severe disease
- 1st line = IV corticosteroids (e.g. hydrocortisone)
- 2nd line = IV ciclosporin

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29
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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30
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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31
Q

COELIAC DISEASE
What is coeliac disease?

A
  • Gluten-sensitive enteropathy
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32
Q

COELIAC DISEASE
What is the pathophysiology?

A

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

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33
Q

COELIAC DISEASE
What is the consequence of the autoimmune response in coeliac disease?

A
  • Autoantibodies in response to gluten exposure target epithelial cells of intestine > inflammation + atrophy of the intestinal villi > malabsorption of nutrients
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34
Q

COELIAC DISEASE
What is the aetiology of coeliac disease?

A
  • Genetics = HLA-DQ2 + HLA-DQ8
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35
Q

COELIAC DISEASE
What conditions is coeliac disease associated with?

A
  • T1DM,
  • thyroid,
  • Down’s syndrome,
  • FHx = test for it
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36
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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37
Q

COELIAC DISEASE
What are the investigations for coeliac disease?

A
  • Pt must be on gluten-containing diet to be accurate
  • Raised antibodies (IgA), useful to monitor disease too – anti-tissue transglutaminase (TTG = first choice), anti-endomysial
  • Endoscopic small intestinal biopsy = gold standard
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38
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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39
Q

COELIAC DISEASE
What are some complications of coeliac disease?

A
  • Anaemias
  • Osteoporosis
  • Lymphoma (EATL)
  • Hyposplenism
  • Lactose intolerance
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40
Q

COELIAC DISEASE
What is the management of coeliac disease?

A
  • Lifelong gluten free diet = curative, supervised by dietician
  • May have gluten challenge later in life if Dx at <2y to ensure still intolerant
  • PCV vaccine with booster every 5y due to hyposplenism
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41
Q

HIRSCHSPRUNG’S DISEASE
What is Hirschsprung’s disease?

A
  • Absence of ganglionic cells from myenteric (Auerbach’s) plexus of large bowel resulting in narrow, contracted section of bowel > large bowel obstruction
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42
Q

HIRSCHSPRUNG’S DISEASE
Where is most affected by Hirschsprung’s disease?
What is it associated with

A
  • 75% confined to rectosigmoid
  • Commonly ileum moves into the caecum via the ileocaecal valve
  • M»F, Down’s syndrome
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43
Q

HIRSCHSPRUNG’S DISEASE
What is the clinical presentation of Hirschsprung’s disease?

A
  • Failure or delay to pass meconium within 24h
  • Abdo pain, distension + later bile (green) stained vomit = obstruction
  • Chronic constipation + failure to thrive
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44
Q

HIRSCHSPRUNG’S DISEASE
What are some investigations for Hirschsprung’s disease?

A
  • PR exam = narrow segment + withdrawal causes flow of liquid stool + flatus
  • AXR with barium contrast = dilated loops of bowel with fluid level
  • Suction rectal biopsy = DIAGNOSTIC showing absence of ganglionic cells
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45
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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46
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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47
Q

HIRSCHSPRUNG’S DISEASE
What is a complication of Hirschsprung associated enterocolitis (HAEC)?

A

Toxic megacolon + perforation = life-threatening

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48
Q

HIRSCHSPRUNG’S DISEASE
How is Hirschsprung associated enterocolitis (HAEC) managed?

A

Urgent Abx, fluid resus + decompression of obstructed bowel

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49
Q

HIRSCHSPRUNG’S DISEASE
What is the management of Hirschsprung’s disease?

A
  • Bowel irrigation as initial management so meconium can pass
  • Surgical resection of aganglionic section of bowel = anorectal pullthrough (anastomosing innervated bowel>anus)
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50
Q

PYLORIC STENOSIS
What is pyloric stenosis?
What is the epidemiology?

A
  • Hypertrophy of the pyloric (circular) muscle causing gastric outlet obstruction
  • Presents 2–7w, M>F 4:1, particularly first-borns
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51
Q

PYLORIC STENOSIS
What is the clinical presentation of pyloric stenosis?

A
  • Projectile vomiting (no bile) due to powerful peristalsis AFTER feeds
  • Hunger after vomiting until dehydration > loss of interest
  • Failure to thrive
  • Palpable abdominal ‘olive’ mass in RUQ (hypertrophic muscle of pylorus)
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52
Q

PYLORIC STENOSIS
What are some investigations for pyloric stenosis?

A
  • Test feed = visible gastric peristalsis
  • Hyponatraemic, hypokalaemic + hypochloraemic metabolic acidosis
  • USS = Dx, visualises thickened pylorus
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53
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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54
Q

PYLORIC STENOSIS
What is Ramstedt’s pyloromyotomy?
What is the after care?

A
  • Incision into smooth muscle of pylorus to widen canal
  • Can feed 6h after
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55
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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56
Q

ABDOMINAL PAIN
What is recurrent abdominal pain?

A
  • Recurrent pain sufficient to interrupt normal activities + lasting ≥3m
  • Often functional abnormalities of gut motility or enteral neurones = IBS, abdominal migraine or functional dyspepsia
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57
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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58
Q

ABDOMINAL PAIN
What are some red flags in recurrent abdominal pain for organic disease?

A
  • Epigastric pain at night, haematemesis = duodenal ulcer
  • Vomiting = pancreatitis
  • Jaundice = liver disease
  • Dysuria, secondary enuresis = UTI
  • Bilious vomiting + abdo distension = malrotation
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59
Q

ABDOMINAL PAIN
What are some investigations for abdominal pain?

A
  • Guided by clinical features, urine MC&S essential
  • Endoscopy if dyspeptic
  • Colonoscopy if any PR bleeding
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60
Q

ABDOMINAL PAIN
How can abdominal pain be managed?

A
  • Encourage parents to not ask about or focus on pain
  • Distract child with other interests + activities
  • Advice about sleep, regular balanced meals, exercise etc
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61
Q

APPENDICITIS
What is appendicitis?

A
  • Commonest cause of surgical abdominal pain, very uncommon in <3y
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62
Q

APPENDICITIS
What is the pathophysiology of appendicitis?

A
  • Obstruction of the appendix lumen (faecolith) causing inflammation + infection of the appendix wall
  • This makes it liable to perforation which can be rapid as omentum less developed so fails to surround the appendix + then peritonitis
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63
Q

APPENDICITIS
What are the symptoms of appendicitis?

A
  • Classic central, colicky abdominal pain which localises to RIF from localised peritoneal inflammation
  • Anorexia
  • Minimal vomiting
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64
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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65
Q

APPENDICITIS
What are some investigations for appendicitis?

A
  • FBC (raised WCC), CRP raised
  • Faecoliths can be see in AXR
  • USS to exclude gynae pathology
  • Gold standard = CT abdomen esp if uncertain
  • -ve tests but clinical suspicion = diagnostic laparoscopy
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66
Q

APPENDICITIS
What is the management of appendicitis?

A
  • ?Perforation = fluid resus + prophylactic IV Abx before surgery
  • Appendicectomy (often diagnostic laparoscopy, may be delayed if stable)
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67
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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68
Q

INTUSSUSCEPTION
What is the epidemiology?

A
  • Most common cause of intestinal obstruction in infants 2m–2y, M>F
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69
Q

INTUSSUSCEPTION
What are some symptoms of intussusception?

A
  • Severe paroxysmal abdominal colic pain + food refusal
  • Child becomes pale + draws up legs during episodes of pain (colic), screaming
  • Vomiting (bilious), abdominal distension + shock
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70
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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71
Q

INTUSSUSCEPTION
What are the investigations for intussusception?

A
  • USS #1 choice, shows ‘target sign’
  • AXR shows distended small bowel + no gas distally in large bowel
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72
Q

INTUSSUSCEPTION
What is the management of intussusception?

A
  • Aggressive IV fluid resus
  • Reduction via air enema (air insufflation) by radiologist (risk of perf)
  • Caution as risk of gangrenous bowel + perf so laparotomy if air enema fails
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73
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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74
Q

MECKEL’S DIVERTICULUM
What are some features of Meckel’s diverticulum?

A

Rule of 2s –

  • 2% population
  • 2 feet from ileocaecal valve
  • 2 inches
  • 2 types of tissue
  • 2y/o
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75
Q

MECKEL’S DIVERTICULUM
What is the clinical presentation of Meckel’s diverticulum?

A
  • Severe, painless, dark red PR bleeding
  • May present with intussusception, volvulus or diverticulitis (mimics appendicitis)
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76
Q

MECKEL’S DIVERTICULUM
What are the investigations for Meckel’s diverticulum?

A
  • Technetium scan will demonstrate increased uptake by ectopic gastric mucosa
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77
Q

MECKEL’S DIVERTICULUM
What is the management of Meckel’s diverticulum?

A

Surgical resection, may need transfusion if severe haemorrhage

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78
Q

IBS
What is irritable bowel syndrome (IBS)?

A
  • Associated with altered gastrointestinal motility + an abnormal sensation of intra-abdominal events
  • Can be exacerbated by psychosocial factors like stress + anxiety
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79
Q

IBS
How does IBS present?

A
  • Abdo pain often worse before or relieved by defecation
  • Intermittent explosive, loose or mucous stools + constipations
  • Bloating
  • Feeling of incomplete defecation
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80
Q

IBS
How is IBS diagnosed?

A
  • By exclusion (FBC, CRP/ESR, coeliac screen, faecal calprotectin + MC&S)
  • Dietician involvement with possibility of excluding foods if they aggravate Sx
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81
Q

IBS
What is the management of IBS?

A
  • Constipation = good water + fibre intake, physical activity, PRN laxatives
  • Diarrhoea = avoid alcohol + caffeine, try bulking agent ± anti-motility such as loperamide after each loose stool
  • Anti-spasmodic for pain like mebeverine or hyoscine butylbromide (Buscopan)
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82
Q

CONSTIPATION
What is constipation?

A
  • Infrequent passage of dry, hardened faeces often accompanied by straining or pain, by definition <3 complete stools per week
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83
Q

CONSTIPATION
What is encopresis?

A

Involuntary soiling

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84
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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85
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
86
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
87
Q

CONSTIPATION
What investigations might you do in constipation?

A
  • Abdo exam may reveal palpable faecal mass
  • PR examination only by an expert
88
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
89
Q

CONSTIPATION
What is the process of constipation and overflow diarrhoea?

A
  • Prolonged faecal status = resorption of fluids = increase in size + consistency
  • This leads to rectal stretching + reduced sensation > overflow + soiling (very smelly)
90
Q

CONSTIPATION
What conservative management is given for constipation?

A
  • Balanced diet with adequate fibre + sufficient fluids
  • Toilet train to sit on toilet after mealtimes
  • Star charts reward
  • Use these in combination with medical management
91
Q

CONSTIPATION
What is the medical management of constipation?

A
  • 1st = macrogol (osmotic) laxative like polyethylene glycol + electrolytes (Movicol)
  • 2nd = stimulant laxative if no effect like Senna, bisocodyl ± osmotic laxative (lactulose) or stool softener (docusate) if hard stools
  • 3rd = consider enema ± sedation or specialist manual evacuation
  • Continue for several weeks after regular bowel habit then gradual dose reduction
92
Q

GOR
What is gastro-oesophageal reflux (GOR)?
What are some risk factors?

A
  • Involuntary passage of gastric contents into the oesophagus due to inappropriate relaxation of the lower oesophageal sphincter, often due to functional immaturity
  • Preterm delivery, neuro disorders (cerebral palsy)
93
Q

GORD
What is the clinical presentation of GORD?

A
  • Recurrent regurgitation or vomiting but normal weight gain
94
Q

GORD
When can it become problematic?

A

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

95
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
96
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)
97
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)
98
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
99
Q

GASTROENTERITIS
What is gastroenteritis?

A
  • Inflammation of the stomach and intestines with diarrhoea, nausea + vomiting
100
Q

GASTROENTERITIS
What is the most common cause?

A
  • Viral rotavirus in paeds,
  • norovirus in adults
101
Q

GASTROENTERITIS
What are some risk factors?

A
  • Poor hygiene,
  • immunocompromised,
  • poorly cooked foods
102
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
103
Q

GASTROENTERITIS
What is the clinical presentation of gastroenteritis?

A
  • Diarrhoea = change in consistency of stools to loose/liquid ± increase in frequency of passing stools (acute if <2w, often lasts 5–7d)
  • Vomiting (1–3d), abdominal cramps
  • Bloody diarrhoea associated with bacterial infection
104
Q

GASTROENTERITIS
What are 5 bacteria that can cause gastroenteritis?

A
  • Campylobacter jejuni
  • E. coli
  • Shigella
  • Salmonella
  • Bacillus cereus
105
Q

GASTROENTERITIS
What is campylobacter jejuni?
How is it spread?
How does it present?

A
  • # 1 bacterial cause worldwide, gram negative curved/spiral bacteria
  • Raw/poorly cooked poultry, untreated water, unpasteurised milk
  • Abdominal cramps, bloody diarrhoea, vomiting + fever
106
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
107
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
108
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
109
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
110
Q

GASTROENTERITIS
what is the management for shigella infection?

A

severe = azithromycin or ciprofloxacin

111
Q

GASTROENTERITIS
How is Salmonella spread?
How does it present?

A
  • Raw eggs, poultry
  • Watery diarrhoea ± mucus or blood
112
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
113
Q

GASTROENTERITIS
What are the main investigations for gastroenteritis?

A
  • Assess for dehydration as main concern
  • FBC, CRP/ESR, U+Es
  • ?Stool MC&S (electron microscopy if viral) if blood in stool, immunocompromised, travel Hx, not improved in a week
114
Q

GASTROENTERITIS
What are signs of clinical dehydration?

A
  • Sunken eyes
  • Reduced skin turgor
  • Lethargic
  • Tachycardia, tachypnoea
  • Dry mucous membranes
  • Appears unwell
  • Oliguria
115
Q

GASTROENTERITIS
What are signs of clinical shock?

A
  • Pale/mottled
  • Hypotension
  • Prolonged CRT
  • Cold
  • Decreased GCS
  • Sunken fontanelle
  • Weak pulses
  • Anuria
116
Q

GASTROENTERITIS
what is the management for shigella infection?

A

severe = azithromycin or ciprofloxacin

117
Q

GASTROENTERITIS
What are some complications of gastroenteritis?

A
  • Isonatraemic + hyponatraemic dehydration
  • Hypernatraemic dehydration
  • Post-infective lactose intolerance (remove lactose + slowly reintroduce)
  • Guillain-Barré
  • Dehydration #1 cause of death
118
Q

GASTROENTERITIS
What is isonatraemic dehydration?

A
  • Water loss + Na+ loss are proportional
119
Q

GASTROENTERITIS
What is hyponatraemic dehydration?

A
  • Child with diarrhoea drinks large quantities of water, Na+ loss greater than water so fall in plasma Na+
    – Fluid shifts from ECF>ICF + can result in convulsions
120
Q

GASTROENTERITIS
What is hypernatraemic dehydration?

A
  • Water loss exceeds Na+ loss + fluid shifts from ICF>ECF (rare)
121
Q

GASTROENTERITIS
How does hypernatraemic dehydration present?

A

Jittery movements,
increased muscle tone,
hyperreflexia,
convulsions,
drowsiness/coma

122
Q

GASTROENTERITIS
How is hypernatraemic dehydration managed?

A

Slow rehydration over 48h

123
Q

GASTROENTERITIS
What are the general measures of managing gastroenteritis?

A
  • Isolation if in hospital with barrier nursing as spreads easily
  • School isolation until Sx settled for 48h
  • Continue feeds (not solids)
  • Encourage PO fluids
  • Discourage fruit juices + carbonated drinks
  • Mx at home if can keep fluid down
124
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
125
Q

GASTROENTERITIS
How is shock managed in gastroenteritis?

A

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

126
Q

TODDLER’S DIARRHOEA
What is Toddler’s diarrhoea?
How common is it?

A
  • Chronic non-specific diarrhoea
  • Commonest cause of persistent loose stools in pre-school children
127
Q

TODDLER’S DIARRHOEA
What causes it?

A

Likely maturational delay in intestinal motility

128
Q

TODDLER’S DIARRHOEA
What is the clinical presentation of Toddler’s diarrhoea?

A
  • Stools vary in consistency (well-formed>explosive + loose)
  • Presence of undigested vegetables common = ‘peas + carrots diarrhoea’
129
Q

TODDLER’S DIARRHOEA
What is the management of Toddler’s diarrhoea?

A
  • Most outgrow by age 5 but may be delay in reaching faecal continence
  • Ensure adequate fat to slow gut transit + fibre, avoid fresh fruit juice
130
Q

BILIARY ATRESIA
What is biliary atresia?

A
  • Congenital condition where section of bile duct either narrowed or absent
  • Results in cholestasis as bile cannot be transported from liver>bowel so increase in conjugated bilirubin
131
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
132
Q

BILIARY ATRESIA
What are the investigations for biliary atresia?

A
  • Serum split bilirubin = conjugated elevated
  • USS abdo gold standard for Dx, laparotomy confirms
133
Q

BILIARY ATRESIA
What genetic mutation is biliary atresia associated with?

A

Associated with CFC1 gene mutations

134
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
135
Q

CHOLEDOCHAL CYST
What is a choledochal cyst?

A

Cystic dilatations of extrahepatic or intrahepatic biliary system
It is a congenital anomaly

136
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

137
Q

CHOLEDOCHAL CYST
How may it present?

A
  • Cholestatic jaundice
  • abdominal mass
  • pain in RUQ
  • nausea and vomiting
  • fever
138
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

139
Q

CHOLEDOCHAL CYST
What are the complications?

A
  • Cholangitis
  • small risk of malignancy
140
Q

CHOLEDOCHAL CYST
What is the management?

A

Surgical cyst excision

141
Q

NEONATAL HEPATITIS
What is neonatal hepatitis syndrome?

A
  • Prolonged neonatal jaundice + hepatic inflammation
142
Q

NEONATAL HEPATITIS
How does it present?

A
  • Intruterine growth restriction (IUGR),
  • hepatosplenomegaly at birth,
  • failure to thrive
  • dark urine
143
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
144
Q

NEONATAL HEPATITIS
What are 4 main causes of neonatal hepatitis?

A
  • Congenital infection
  • Alpha-1-antitrypsin (A1AT) deficiency
  • Galactosaemia
  • Wilson’s disease
145
Q

NEONATAL HEPATITIS
What is A1AT deficiency?

A
  • Deficiency of protease A1AT which inhibits neutrophil elastase + protects tissues
146
Q

NEONATAL HEPATITIS
What is the cause of A1AT deficiency?

A

AR on chromosome 14

147
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
148
Q

NEONATAL HEPATITIS
How do you diagnose A1AT deficiency?

A
  • Serum A1AT concentration
149
Q

NEONATAL HEPATITIS
What is the management for A1AT deficiency?

A
  • ?Transplantation
  • Never smoke
150
Q

NEONATAL HEPATITIS
What is galactosaemia?

A
  • Deficiency of galactose-1-phosphate uridyltransferase (GALT) involved in galactose metabolism (lactose breaks down into galactose)
151
Q

NEONATAL HEPATITIS
How does galactosaemia present?

A
  • Poor feeding,
  • vomiting,
  • jaundice + hepatomegaly when fed milk
152
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
153
Q

NEONATAL HEPATITIS
What is the management of galactosaemia?

A
  • Stop cow’s milk, breastfeeding C/I
  • Dairy-free diet
  • IV fluids
154
Q

NEONATAL HEPATITIS
What is Wilson’s disease?

A
  • Reduced synthesis of caeruloplasmin (normally binds to copper + allows it to be excreted with bile)
155
Q

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

A

AR on chromosome 13

156
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)
157
Q

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

A
  • 24h urine copper assay (high),
  • serum caeruloplasmin (low)
158
Q

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

A

Penicillamine for copper chelation

159
Q

FAILURE TO THRIVE
What is failure to thrive?

A
  • Failure to gain adequate weight or achieve adequate growth at a normal rate during infancy or childhood
  • Descriptive term (aka faltering growth)
160
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
161
Q

FAILURE TO THRIVE
What are some causes of inadequate calorie intake?

A
  • Impaired suck/swallow (cleft palate, neuro-motor dysfunction, CP)
  • Inadequate availability of food (socioeconomic deprivation)
  • Neglect
  • Maternal depression
162
Q

FAILURE TO THRIVE
What are some causes of malabsorption?

A
  • Cystic fibrosis
  • Cow’s milk protein intolerance
  • Coeliac disease
  • IBD
  • Short gut syndrome
163
Q

FAILURE TO THRIVE
What are some causes of inadequate retention?

A
  • Vomiting (GORD, pyloric stenosis),
  • gastroenteritis
164
Q

FAILURE TO THRIVE
What are some causes of increased calorie requirements?

A
  • Chronic illness (CHD, CKD, CF, HIV),
  • hyperthyroidism,
  • cancer
165
Q

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

A
  • T1DM,
  • inborn errors of metabolism
166
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
167
Q

FAILURE TO THRIVE
What is kwashiorkor?

A
  • Severe protein malnutrition
  • Generalised oedema
  • Sparse + depigmented hair
  • Skin rash
  • Angular stomatitis
  • Distended abdomen
  • Hepatomegaly + diarrhoea
168
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
169
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
170
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
171
Q

FAILURE TO THRIVE
What would you ask about in a failure to thrive history + examination?

A
  • Pregnancy, birth, developmental + social Hx
  • Feeding or eating Hx (breast/bottle, times, volume, frequency)
  • Observe feeding
  • Mum’s physical + mental health
  • Parent-child interactions
172
Q

FAILURE TO THRIVE
What might BMI tell you?
Any other investigations to perform?

A
  • <2nd centile = ?undernutrition or small build, <0.4th centile = likely undernutrition > assessment + intervention
  • Specific underlying cause if suspected (CRP/ESR, U+Es, LFTs, TFTs)
173
Q

FAILURE TO THRIVE
What is the MDT management approach for failure to thrive?

A
  • Health visitor (parental support if inorganic)
  • Dietician may suggest nutritional supplement drinks or add energy dense foods, encourage regular structured mealtimes + Snacks
  • Community paediatrician
  • SALT if impaired suck or swallow
174
Q

FAILURE TO THRIVE
When would hospital admission be required?

A
  • Severe failure to thrive + require active refeeding
  • Can use this time to observe + improve method of feeding if needed
175
Q

FAILURE TO THRIVE
What is the last line consideration in failure to thrive?

A
  • Enteral tube feeding
  • Must have clear goals + defined end point
  • Only used if serious concerns about weight gain + other interventions tried
176
Q

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

A
  • Affects children <3y where there’s hypersensitivity to protein in cow’s milk,
  • most outgrow by age 3,
  • IgE and non-IgE types
177
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
178
Q

CMPA
How does cows milk protein allergy (CMPA) differ from lactose intolerance?

A
  • Lactose is a sugar
  • Explosive watery stools, abdo distension, flatulence + audible bowel sounds
179
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
180
Q

CMPA
How does cows milk protein allergy (CMPA) differ to cow’s milk intolerance?

A
  • cows milk intolerance is not an allergic reaction (mild-mod delayed reactions) so does not involve immune system
  • Same GI Sx but not allergic features
  • Infants may be able to tolerate some cow’s milk just with Sx, same Mx
181
Q

CMPA
What are the investigations for cows milk protein allergy (CMPA)?

A
  • IgE mediated = skin prick tests + RAST for cow’s milk protein
  • Gold standard if doubt = elimination diet under dietician supervision
182
Q

CMPA
What is the management for cows milk protein allergy (CMPA)?

A
  • Breastfeeding mothers should avoid dairy
  • Replace formula with extensive hydrolysed formula
  • Amino acid-based formula if severe or no response to eHF
  • Food challenge may be performed in hospital setting
183
Q

CMPA
How do hydrolysed and amino acid-based formulas work?

A
  • Proteins broken down so they no longer trigger an immune response
184
Q

CMPA
How should allergic attacks be managed in cows milk protein allergy (CMPA)?

A
  • Antihistamines or IM adrenaline (EpiPen) if severe reactions
185
Q

FOOD ALLERGIES
What food allergies present in children?

A
  • Infants = milk, egg, peanut
  • Older children = peanut, fish + shellfish
186
Q

FOOD ALLERGIES
What are the different types of food allergy?

A
  • IgE mediated = urticaria, angioedema, wheeze
  • Non-IgE = D+V, failure to thrive, abdo pain
187
Q

FOOD ALLERGIES
What is a food intolerance?

A

Non-immunological hypersensitivity reaction to food

188
Q

KWASHIOKOR
what is it?

A

it is a type of protein-energy malnutrition caused by a severe deficinecy pf protein/amino acids

189
Q

KWASHIOKOR
what are the clinical features?

A
  • growth retardation
  • diarrhoea
  • anorexia
  • oedema - defining characteristic
  • skin/hair depigmentation
  • abdominal distension with fatty liver
190
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

191
Q

MARASMUS
what is it?

A

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

192
Q

MARASMUS
what are the clinical features?

A
  • height is relatively preserved compared to weight
  • wasted appearance
  • muscle atrophy
  • listless
  • diarrhoea
  • constipation
193
Q

MARASMUS
what are the investigations?

A
  • bloods - FBC, U+Es
  • stool MC+S for intestinal ova, cysts and parasites
194
Q

KWASHIOKOR
what is the management?

A

ready-to-use therapeutic food (RUTF)
antibiotics

milk-based liquid food followed by RUTF if severe (complicated)

195
Q

MARASMUS
what is the management?

A

correct dehydration and electrolyte imbalance
treat underlying infection/parasitic infections
treat causative disease
orally refeed slowly - watch for refeeding syndrome

196
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

197
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
198
Q

HERNIA
what is the clinical presentation?

A
  • lump or swelling near the groin/belly button
  • pain or tenderness around the groin/lower belly
  • unexplained crying or fussiness
  • visible bulge that gets bigger during straining, crying or coughing
199
Q

HERNIA
what is the treatment for umbilical hernias?

A

small = 85% will close without surgery
large/stays open past 2yrs = surgery

200
Q

HERNIA
what is the treatment for indirect inguinal hernias?

A

require surgery to reduce the hernia

201
Q

HERNIA
what are the complications of hernias?

A

strangulation/incarceration - there is 30% chance of testicular infarction due to pressure on gonadal vessels

202
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
203
Q

LIVER FAILURE
what is the clinical presentation?

A
  • jaundice (not always present)
  • GI haemorrhage
  • pruritis
  • FTT
  • anaemia
  • enlarged hard liver
  • non-tender splenomegaly
  • hepatic stigmata e.g. spider naevi
  • peripheral oedema and/or ascites
  • nutritional disorders
  • developmental delay
  • chronic encephalopathy
204
Q

LIVER FAILURE
what are the investigations?

A
  • BLOODS
    - FBC = low WCC, low Hb (if GI bleed), low platelets
    - LFT = normal/low bilirubin, raised AST/ALT
    - coagulation = increased prothrombin time (PTT)
    - glucose = normal/low
    - U+Es, viral serology, IgG, complement, autoimmune antibodies
  • METABOLIC STUDIES
    - sweat test = CF
    - serum/urinary copper = Wilson’s disease
  • ABDOMINAL ULTRASOUND
  • LIVER BIOPSY
  • UPPER GI ENDOSCOPY
205
Q

LIVER FAILURE
what is the management?

A
  • treat the underlying cause + give nutritional support
  • lower protein, increased energy, higher carb diet
  • vitamin supplementation (ADEK)
  • fluid restriction for ascites (alternatively use spironolactone)
  • liver transplantation
206
Q

LIVER FAILURE
what is the prognosis?

A

there is up to 50% mortality without liver transplant

207
Q

INFANT COLIC
what is it?

A

The term is used to describe a symptom complex that occurs in the first few months of life

208
Q

INFANT COLIC
What is the epidemiology?

A

It occurs in up to 40% of babies
It typically occurs in few few weeks of life and resolves by 4 months

209
Q

INFANT COLIC
What is the clinical presentation?

A

Paroxysmal inconsolable crying or screaming
Often accompanied by drawing up of the knees
Passage of excessive wind several times per day, particularly in the evening

210
Q

INFANT COLIC
what is the risk of this condition?

A

It is very frustrating for parents
It may precipitate non-accidental injury in infants already at risk

211
Q

INFANT COLIC
what is the cause?

A

Unknown but thought to be gastrointestinal
If severe and persistent it may be due to cow’s milk protein allergy or GORD

212
Q

INFANT COLIC
What is the management?

A

Support and reassurance
If severe an empirical 2-week trial of a whey hydrolysate formula followed by a trial of anti-reflux treatment may be considered.

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