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Sarah Paeds > Gastro/Liver > Flashcards

Gastro/Liver Flashcards

1
Q

GI CF management

A

Monitoring appetite, stools and GORD
Replace pancreatic enzymes (e.g. pancreatin, CREON)
+ PPI to improve alkaline environment for pancreatin to do its thing

Nutrition - increased caloric intake (150%) - consider overnight feed by gastrotomy
Vitamins ADEK

Ursodeoxycholic acid (improve bile flow)

Ranitidine/omeprazole to help with GORD symptoms

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2
Q

Four gastro causes of recurrent abdominal pain

A 
IBD
IBS
Gastritis/dyspepsia 
Abdominal migraine 
(Recurrent abdominal pain (RAP))
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3
Q

IBS mx

A

Diet and lifestyle modification (avoiding triggers, stress coping strategies)

Antispasmodic (e.g. Buscopan)

If mainly diarrhoea: Antidiarrhoeals (e.g. loperamide)

If mainly constipation: Laxatives

TCA/SSRI

CBT/hypnotherapy

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4
Q

Conservative measures IBS

A

Diet and lifestyle modidication
CBT
Hypnotherapy

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5
Q

Which type of GI ulcers are more common in children?

A

Duodenal

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6
Q

How is H.pylori diagnosed?

A

C13 breath test, stool antigen

Gastric antral biopsy

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7
Q

Mx acute gastritis

A

Endoscopy +/- blood transfusion

Lansoprazole

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8
Q

Mx chronic gastritis. Next steps if failure to respond

A

If H.pylori - triple therapy:

  • PPI
  • Clari
  • Amox

If fail to respond = upper GI endoscopy

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9
Q

Dyspepsia with normal biopsy

A

Functional dyspepsia

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10
Q

Where is the pain loated in abdominal migraines?

A

Central, midline

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11
Q

Presentation abdominal migraine

A

Central pain
Vomiting
Pallor

Associated with headache migraines

Personal/FHx migraines

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12
Q

What percentage of IBD patients prsent in childhood?

A

25%

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13
Q

What is recurrent abdominal pain defined as?

A

More than three months of abdominal pain sufficient to disrupt normal activities

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14
Q

Non gastro causes of recurrent abdo pain

A

Urinary (UTI)
Gynae (dysmenorrhoea, PID, cysts)
Psychosocial (RAP)
Hepatobiliary (hepatitis, stones, pancreatitis)

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15
Q

Commonly affected areas in Crohn’s

A

Distal ileum to proximal colon

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16
Q

Presentation of Crohn’s

A

Bloody diarrhoea
Abdo pain
Weight loss

Pallor
FTT

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17
Q

Clinical features of Crohn’s (+ SIGNS)

A

Bloody diarrhoea
Abdo pain
Weight loss

Pallor
FTT

Erythema nodosum 
Fissures 
Fistulae 
Tags 
Ulcers
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18
Q

Investigations for Crohn’s

A

Bloods (raised CRP/ESR, low Hb, low albumin)

Small bowel biopsy w/ histology (non-caseating epthelioid cell granulomata)

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19
Q

Management of Crohn’s

A

Conservative: stop smoking

Medical:

  • Steroids - budenoside (induce and maintain remission)
  • Immunosuppressants: azathioprine/methotrexate
  • Biologics - infliximab (with abx)

Nutritional support. Enteral supportive feed if necessary.
Ca, VitD, B12, ferritin

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20
Q

Presentation of UC

A
  • Bloodu, mucous diarrhoea
  • Abdo pain (colicky)

Weight loss
Growth failure
Erythema nodosum
Clubbing

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21
Q

Ix for UC

A

Bloods

Colonic biopsy - crypt damage and abscesses in the mucosa

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22
Q

How is the severity of UC assessed?

A

Paediatric Ulcerative Colitis Activity Index

Higher score = increased severity

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23
Q

Mx of UC (mild/mod/severe/steroid dependent)

A 
Mild - mesalazine (induce and maintain remission). 
Oral pred if relapse 
Mod - Oral pred for 2-4 weeks then taper 
Mesalazine 
Severe - MEDICAL EMERGENCY. 
IV methylprednisolone 
Parenteral nutrition 
Surgery

Steroid dependent - infliximab

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24
Q

Features of malabsorptive disease

A

FTT / poor growth
Abnormal stools
Specific nutrient deficiencies

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25
Q

Four examples conditions resulting in malabsorption

A

Coeliac
Biliary atresia
Pancreatic exocrine dysfx (e.g. CF)
Short bowel syndrome

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26
Q

Presentation of coeliac

A 
Poor growth/FTT 
Buttock wasting 
Abnormal/offensive/fatty stools 
Abdominal distension
General irritability
Pallor

Rash - dermatitis herpetiformis

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27
Q

Age of presentation coeliac

A

8-24 months

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28
Q

Pathophysiology of coeliac

A

Non-IgE reaction against gliadin protein in gluten.

Immune response in the mucosa of the proximal small intestine

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29
Q

Which part of the bowel is most affected in coeliac?

A

Proximal small bowel (mucosa)

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30
Q

Which other conditions is coeliac associated with (and should children with coeliac be screened for)?

A

T1DM
Hypothyroid
Down’s

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31
Q

Ix for suspected coeliac

A

Bloods (anti-TTG Abs, Endomysial antibodies) - in some cases these are now sufficient for diagnosis

Small bowel (jejunum) biopsy - villous blunting, crypst hyperplasia

Removal of gluten = catch up growth

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32
Q

Mx of coeliac

A

MDT

Remove gluten from diet (with dietary advice from dietician)

Calcium, vitaminD, iron

Regular monitoring of height, weight, development

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33
Q

How can coeliac patients’ diets be checked?

A

Serology

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34
Q

Complications of coeliac disease

A

Malnutrition
EATL lymphoma
Osteoporosis

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35
Q

Causes of diarrhoea

A 
Gastroenteritis 
Toddler's diarrhoea 
IBD 
Coeliac 
IBS 
Medications 
Food allergy/intolerance
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36
Q

Commonest cause persistent loose stoolin preschool children

A

Toddler’s diarrhoea

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37
Q

Presentation toddler’s diarrhoea

A

Persistent loose stool
Undigested veg
Varying consistency

Child is otherwise WELL AND THRIVING

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38
Q

Pathophysiology of toddler’s diarrhoea

A

Underlying delay in intestinal maturity

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39
Q

Complication of toddler’s diarrhoea

A

Achieving faecal continence may be delayed

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40
Q

Mx toddler’s diarrhoea

A

More fat and fibre in diet to slow gut transit

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41
Q

Causes of constipation in infants

A 
Hirschsprung's 
Atresia 
Hypothyroid 
Hypocalcaemia 
Anorectal abnormalities
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42
Q

Causes of constipation in children

A

Dehydration
Poor diet
Toilet training issues
Stress

Hypothyroid
Hypocalcaemia

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43
Q

Constipation presentation

A

Infrequent passage hard, dry faeces
Accompanied by straining/pain

Palpable abdo mass

May have overflow diarrhoea

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44
Q

Red flag symptoms associated with constipation

A

Neuro signs - SCC/SOL
FTT
Gross distension
Anal sx - sexual abuse?

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45
Q

Constipation mx

A

Movicol (osmotic)
Diet
Increased fluid

Behavioural interventions - regular toileting, reward system, bowel habit diary

CBT
Family therapy

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46
Q

Four types of laxative

A

Osmotic - movicol
Stimulant - senna
Bulk-forming - fybogel
Stool softener - docusate sodium

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47
Q

Features of overflow diarrhoea

A

Faecal incontinence

Foul smelling diarrhoea

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48
Q

Mx anal fissure

A

Increase fibre
Increase fluids

Stool softeners (e.g. docusate sodium)

Topical GTN intra-anally
Analgesia

Anal hygiene
AVOID stool withhoding

If not healed after 2 weeks, come back

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49
Q

Causes vomiting in a neonate

A 
Hirschsprung's 
Pyloric stenosis 
Allergy 
Atresia 
Sepsis 
CAH
Overfeeding
Meconium plug 
Intussusception 
Malrotation/volvulus 
GORD
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50
Q

Pathophysiology of Hirschsprung’s

A

Absence of myenteric plexus in rectum –> colon

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51
Q

Presentation of Hirschsprung’s

A

Failure to pass meconium in first 48 hours of life
Gross abdominal distension
Eventually bilious vomiting

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52
Q

Mx Hirschsprung’s

A

Bowel irrigation

Surgical - colostomy followed by anorectal pull through: anastamoses of normally innervated bowel to anus

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53
Q

Complications Hirschsprung’s

A

Acute enterocolitis (15%)

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54
Q

Is Hirschsprung’s more common in males or females?

A

Males (4:1)

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55
Q

Presentation of pyloric stenosis

A

Projectile vomiting
HUNGER (will keep attempting to feed until they are dehydration when they will no longer attempt)
Weight loss

  • Peristalsis across abdomen
  • Mass RUQ
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56
Q

Age of presentation pyloric stenosis

A

2-7 weeks

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57
Q

Which infants more commonly get pyloric stenosis

A

Males
(Particularly first born)
Maternal GDM

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58
Q

Pathophysiology of pyloric stenosis

A

Hypertrophy of pyloric muscle = gastric outlet obstruction

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59
Q

Ix for pyloric stenosis

A

Gas (often metabolic alkalosis)
- Hypochloraemic, Hyponatraemic, Hypokalaemic

USS

60
Q

What acid-base disturbance occurs as a result of pyloric stenosis?

A

Metabolic alkalosis

61
Q

Mx pyloric stenosis

A

IV fluid resuscitation (severe dehydration)

  • 1.5x maintenance with dextrose and saline
  • Add potassium once urine output is adequate

Surgery - Ramstedt pyloromyotomy - dividing hypertrophied muscle (not mucosa)

62
Q

What must be done before surgery to correct pyloric stenosis?

A

IV fluid resuscitation and electrolye balancing

63
Q

Presentation duodenal atresia

A

Persistent bile stained vomit
Meconium may be passed, but then with subsequent delay
Abdominal distension

64
Q

Which genetic abnormality is duodenal atresia associated with?

A

Down’s syndrome

65
Q

Do higher or lower lesions present earlier in duodenal atresia?

A

Higher

66
Q

Mx duodenal atresia

A 
NBM
D&S (NGT)
IV fluid resuscitation
Surgery 
\+/- abx
67
Q

Intrauterine trachy-oesophageal fistulae

A

Polyhydramnios

68
Q

Presentation of trachy-oesophageal fistulae

A

Persistent drooling
Vomiting
Aspiration

69
Q

Which multi-system syndrome are trache-oesophageal fistulae associated with?

A

VACTERL

Vertebrae 
Anal atresia 
Cardiac 
Trache-oEsophageal fistula
Renal 
Limb
70
Q

Risk factors for GORD (young infants)

A

Short oesophagus
Horizontal posture
Fluid diet

71
Q

Complications of GORD

A

FTT
Recurrent aspiration
Oesophagitis – IDA
Sandiser syndrome - dystonic neck posture

72
Q

When do most GORDs resolve spontaneously by?

A

1 year

73
Q

Ix GORD

A

24hr pH monitoring
Endoscopy
(USS to rule out pyloric stenosis, atresia)

74
Q

Mx GORD

A

REASSURE
Consider (breast feeding) assessment

1) Mechanical/conservative - vertical position when feeding, winding. Feeds little and often. Thicken feeds.
2) Baby gaviscon / alginate therapy
3) PPI trial
4) Enteral feeding / Nissen fundoplication if FTT

75
Q

Pathophysiology of intussusception

A

Invagination of proximal bowel into distal bowel causes obstruction

76
Q

Where does intussusception often take place

A

Ileo-caecal valve

77
Q

Age of presentation of intusussception

A

3mos - 2 years

78
Q

What is the commonest cause of GI obstruction after the neonatal period?

A

Intussusception

79
Q

Complications of intussusception?

A

Engorgement
Bleeding
Ischaemic bowel – enterocolitis

80
Q

Presentation of intussusception

A 
Paroxysmal, severe colicky pain
Pallor, increasingly lethargic
Bile stained vomit 
Refusal of feeds 
Sausage-shaped palpable mass on abdomen 
REDCURRANT JELLY STOOL
81
Q

What diagnosis is redcurrant jelly stool indicative of?

A

Intussusception

82
Q

Ix intussusception

A

USS: target lesion
AXR: distended small bowel loops. Absence of gas in distal colon
Bloods: shock

83
Q

Mx intussusception

A

ABCDE
(IVI and NG tube aspiration)

AIR INSUFFLATION

Broad spec abx - clindamycin + gentamicin

Surgery if insufflation fails

84
Q

When is air insufflation not appropriate in treating intussusception?

A

If there are signs of peritonitis, perforation, hypovolaemic shock

85
Q

Percentage of children with Meckel’s diverticulum

A

2%

86
Q

Presentation of Meckel’s diverticulum

A

Severe PR bleed - not bright red nor malaena

intussusception/malrotation

87
Q

Mx Meckel’s diverticulum

A

Surgical excision
Adhesion lysis
+/- bowel resection

88
Q

What is a Meckel’s diverticulum?

A

Ileal remnant of vitello-intestinal duct

89
Q

Presentation of malrotation

A

Intestinal obstruction with reduced blood supply - bile stained vomit, distended abdomen

90
Q

Age of presentation malrotation

A

Usually first 1-3 days of life

91
Q

Ix malrotation

A

Upper GI contrast study

92
Q

Mx malrotation if evidence of vascular compromise

A

Emergency laparotomy

93
Q

Mx malrotation

A

Surgery: Ladd procedure - detort bowel, divide, Ladd bands

Normally also remove appendix to avoid future confusion

Abx: cefalozin

94
Q

Appendicitis presentation

A

Abdo pain (starting umbilical, localise to RIF)
Anorexia
Vomiting

Oral fetor
Low grade fever

McBurney’s/Rovsing’s signs

95
Q

Ix appendicitis

A

Bloods (raised WCC, CRP)
BC
USS - inflammed, thickened. Increased blood flow on dopplers.

96
Q

Mx appendicitis

A

SURGERY

NBM
IVI fluid resuscitation

Abx: cefalozin

97
Q

Mx mesenteric adenitis

A

Self resolving

98
Q

Presentation mesenteric adenitis

A

Non specific abdo pain

Often accompanied by URTI and cervical lymphadenopathy

99
Q

Commonest viral cause of gastroenteritis

A

Rotavirus

100
Q

Ix gastroenteritis

A

Bloods
BC
Stool sample

Monitor weight loss

101
Q

Ix post gastroenteritis syndrome

A

Positive clinitest

102
Q

Post gastroenteritis syndrome

A

Temporary lactose intolerance

103
Q

Mx gastroenteritis

A

Fluid replacement

104
Q

Presentation of hepA

A

Mild illness - lethargy, some nausea, malaise

105
Q

Management of hepA

A

Notify HPU

Supportive (for pain, nausea, itch)
Close contacts should be vaccinated within 2 weeks of illness starting

106
Q

How is hepB transmitted?

A 
Vertical from mother 
Horizontal from families 
Blood products 
Needlestick injuries 
Renal dialysis 
(Sexual transmission in adults)
107
Q

Mx of acute hepatitis B

A

Notify HPU

Supportive
Anti-virals e.g. tenofovir disoproxil

108
Q

Mx of chronic hep B

A

Notify HPU

Supportive
Anti-virals - interferon, tenofovir disoproxil

109
Q

What % of asymptomatic carriers develop chronic HBV infection?

A

30-50%

110
Q

How cna hepB be prevented?

A

Antenatal screening
Antiviral therapy for HBsAg positive mothers

HepB vaccine for infants born to HBsAg positive mothers
+ immunoglobulin if mother is HBeAg positive

111
Q

Commonest hepatitis C infection

A

Chronic carrier

112
Q

% of chronic hepC carriers who go onto have HCC/cirrhosis

A

20-25%

113
Q

Treatment chronic hepC

A

Notify HPU

S/c peg interferon and ribavarin

114
Q

Commonest causes of acute liver failure, including three most common

A
  • PARACETAMOL OD
  • NON-A TO G HEPATITIS
  • METABOLIC
  • Hep ABC
  • AI hep
  • Other poisons
115
Q

Pathophysiology of acute liver failure

A

Massive hepatic necrosis = reduced liver function +/- encephalopathy

116
Q

Presentation of acute liver failure

A

Jaundice
Bleeding
Hypoglycaemia
Electrolyte disturbances

Encephalopathy

  • Irritability/confusion/drowsiness
  • Aggressive/difficult behaviour
117
Q

Complications of acute liver failure

A 
Hepatic encephalopathy 
Cerebral oedema 
Bleeding 
Sepsis 
Pancreatitis
118
Q

Mx of acute liver failure (think of liver fx)

A 
Hypoglycaemia - IV dextrose 
Haemorrhage - IV vit K, cryo, FFP 
Oedema - fluid restriction/mannitol diuresis 
Sepsis risk - broad spec abx
Gastritis - PPI/H2 antagonist 
Transplant
119
Q

Which features are suggestive of a poor prognosis in acute liver failure?

A

Shrinking liver
Rising BR with falling transaminases
Worsening coagulopathy
Coma

120
Q

Causes of chronic liver disease

A 
Chronic hepatitis (B,C, AI, PSC, drugs)
Wilson's 
alpha1-antitrypsin
CF
Neonatal liver disease 
Bile duct lesions
121
Q

Which drugs particularly can predispose to chronic liver failure?

A

Nitrofurantoin

NSAIDs

122
Q

Commonest causes of chronic liver disease

A

Hep B C

AI hep

123
Q

Presentation of chronic liver failure

A

Lethargy
Malnutrition
Insidious hepatosplenomegaly

124
Q

Age of presentation AI hepatitis

A

7-10 years

125
Q

Is AI hepatitis more common in boys or girls?

A

Girls

126
Q

Presentation of AI hepatitis

A

Lethargy, malnutrition
Liver signs
+ other AI signs - rash, arthralgia, haemolytic anaemic, nephritis

127
Q

Investigations for AI hepatitis

A

Bloods: hypergammaglobulinaemia (IgG>20)
+ve autoantibodies
Reduced serum C4
Histology

128
Q

Mx of AI hepatitis

A

Prednisolone
Azathioprine

If PSC: ursodeoxycholic acid

129
Q

Mx of PSC

A

Ursodeoxycholic acid

130
Q

Wilson’s mode of inheritance

A

AR

131
Q

Pathophysiology of Wilson’s

A

Reduced copper excretion in bile, reduced caeruloplasmin = copper deposits in liver, brain, kidney, cornea

132
Q

Ix Wilson’s disease

A

Urinary copper excretion (particularly raised after chelation)

133
Q

Mx Wilson’s disease

A

Zinc - reduces copper absoprtion in intestine
Trientine - increases copper excretion in urine
Pyridoxine - vitB6 prevents peripheral neuropathy

134
Q

Mx of NAFLD

A

Weight loss - diet, exercise, bariatric surgery
Treat underlying insulin resistance
Vitamin E

135
Q

Mx of cirrhosis/portal HTN (think ascites)

A

Na/fluid restriction
Diuretics
HAS/clotting factors
Paracentesis

NUTRITIONAL SUPPORT

136
Q

What nutritional support to patients with cirrhosis need?

A

Vits ADEK

Increased calories

137
Q

Management for encephalopathy

A

Supportive
Aim to reduce nitrogenous load – protein restricted diet,
lactulose

138
Q

Why might intussusception occur after a febrile illness?

A

Enlarged Peyer’s patches acting as the lead point for intussusception

139
Q

What may be the cause of recurrent intussusception ?

A

Pathological lead point, e.g. Meckel’s diverticulum

140
Q

Should CF children have increased or reduced caloric intake?

A

Increased (150%)

141
Q

HLA associated with coeliac?

A

HLA DQ8

142
Q

What happens if you remove the gluten from the diet of a child with FTT caused by coeliac?

A

Catch up growth

143
Q

Why is increased fat diet recommended in toddler’s diarrhoea?

A

Slow gut transit

144
Q

What should be monitored in a child with gastroenteritis?

A

Weight loss (dehydration)

145
Q

Features of post- gastroenteritis syndrome?

A

Temporary lactose intolerance

+ve clinitest

146
Q

Normal hepB immunisation schedule

A

8/12/16 weeks

147
Q

HepB immunisation schedule if infected mother (HBsAg +ve)

A

4/12/16 weeks
AND
Birth, 4 weeks, 1 year

Sarah Paeds (20 decks)

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