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PEADS > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

causes of constipation

A

Acute: dehydration, inadequate fibre intake, bowel obstruction, congenital malformation (atresia), cows milk protein allergy
Chronic: functional constipation, withholding, medications, Hirschsprung’s disease

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2
Q

assessment of child with constipation

A

History: stool consistency, frequency, meconium, associated symptoms? vomiting, signs of infection, any pattern with eating. dietary and medication history important.
examination: plot growth, abdominal exam for hard masses, may need anorectal exam to look for fissures.

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3
Q

Management of constipation

A

increase fibre intake, increase fluid intake.

movicol - can use for 3-6 months, at a stimulant laxative if movicol not working after 2 weeks.

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4
Q

prevalence of soiling

A

3% of children between 4-5, 2% of children between 5-6, 0.1% of those above 10.

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5
Q

causes of soiling/encopresis

A

Developmental: developmental or neurological delay, never learnt to use the toilet
Behavioural: stress, fear
Biological: anal fissure, overflow, severe UC or chrons.

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6
Q

Causes of gastroenteritis

A

most common cause: rotavirus.

other causes: norovirus, shigella (from E.coli), campylobacter, salmonella.

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7
Q

Presentation of gastroenteritis

A

low grade fever and loss of appetite, and vomiting, which will precede the diarrhoea.

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8
Q

investigations for gastroenteritis

A

assess dehydration status

only if prolong or ?bacterial cause do stool culture

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9
Q

Management for gastroenteritis? School exclusion? how long should it last for?

A

fluids -increase intake, ORS, if infant encourage breastfeeding, discourage sugary fruit juice.
no school for 48hrs after the last episode
should recover from 7 days, can last for 2 weeks

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10
Q

what is secondary lactose intolerance?

A

enterocytes in the gut have enzyme lactase, they are lost with D/V and so due to their damage can have secondary lactose intolerance after infection. can last a few months, usually recover.

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11
Q

what causes haemolytic uraemic syndrome?

A

a complication of the shiga toxin, which is produced by some strains of E.coli.

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12
Q

what is the presentation of haemolytic ureamic syndrome?

A

clinically unwell, pale, bruises.

triad of acute renal failure, thrombocytopenia and haemolytic anaemia

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13
Q

GORD vs Posseting

A

GORD: non-forceful regurgitation of gastric contents into oesophagus due to an incompetent sphincter.
posseting: non forceful quantities of milk post feed - normal!

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14
Q

Presentation of GORD

A

can be asymptomatic. recurrent regurgitation, small amounts of vomiting, feeding problems, failure to thrive.
could present with apnoea, cough, or an aspiration pneumonia

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15
Q

Assessment of vomiting baby

A

review feeding routine and volumes
history: colour of vomit, quantity, when it occurs, how often. Growth, feeding and birth history. associated symptoms, (fever, diarrhoea, irritability, melena).
examination: abdominal palpation, hydration status.
Investigations; Ph study for GORD, upper GI study if suspetedmalrotation, bloods: U&Es, blood gas

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16
Q

Management of GORD

A

reassurance - most resolve by 10 months. change feeds to smaller and more frequent.
PPI can be used if indicated.
NG feeds if faltering growth.
surgery if not resolving - Nissen fundoplication.

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17
Q

presentation of gastroenteritis caused by adenovirus

A

cough and cold followed by D/V.

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18
Q

Differentials of a vomiting child

A

GORD, gastroenteritis, overfeeding, pyloric stenosis, malrotation with volvulus,, bowel obstruction, duodenal atresia, systemic infection, intersusseption, paralytic ileus

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19
Q

RED flags for vomiting presentation

A

Bile stained vomit, blood in vomit, drowsiness, signs of dehydration, flattening of growth curve.

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20
Q

electrolyte imbalances commonly seen with dehyration

A

matabolic alkalosis. look at the sodium, potassium, glucose and chloride

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21
Q

Fluid bolus for shock management

A

20ml/kg of 0.9% saline STAT

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22
Q

Fluids used for maintenance

A

0.9% saline with 5% dextrose
100ml for first 10kg
50ml for next 10 kgs
20mls per kg after that.

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23
Q

management for replacing fluid losses

A
  1. if shocked give fluid bolus STAT
  2. start maintenance fluids
  3. replace losses by adding fluid deficit (will be given as a % of dehydration).
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24
Q

causes of acute abdominal pain

A

appendicitis, gastroenteritis, mesenteric adenitis, obstruction, malrotation volvulus, IBD, intersusseption, Henoch-schonlein purpura.
Renal: UTI, hydroneohrosis renal caliculi
other: torsion, ovarian cysts

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25
Q

causes or recurrent abdominal pain

A

peptic ulcer, oesophagitis, IBD, constipation, pancreatitis, PID, dysmenorrhoea, stress.

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26
Q

appendicitits: presentation, investigations, management

A

Presentation: pain moving to RIF, N/V, low grade fever, localised tenderness, Rovsings sign (palpation on LLQ increases pain in RLQ)
Investigations: abdominal USS, Bloods (FBC, U&Es, CRP, group and save), urinalysis.
Management: laposcopic emergency surgery, with fluids and analgesia

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27
Q

pathophysiology of coeliac disease

A

multigenic disorder, a reaction to the gliadin and glutenins protiens in gluten which causes villous atrophy. this leads to malabsorpition, diarrhoea and poor gowth.

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28
Q

presentation of coeliac disease

A

non specific inflammation. failure to thrive, diarrhoea, vomiting, distended abdomen, muscle wasting, excessive bruising, finger clubbing.

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29
Q

investigations for coeliac disease

A

antibody testing: serum tissue transglutimine type 2, total IA.
jejunal biopsy - villous atrophy and crypt hyperplasia
Bloods: FBC, LFTs, (elevated transaminases)
stool sample

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30
Q

complications of coeliac disease

A

nutritional deficiencies
increased risk of bowel cancer and GI lymphoma
dermatitis herpetiformis (pruritic itchy skin rash)
neurological complications at peripheral neuropathy, cerebella ataxia)

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31
Q

ingulinal hernia: direct vs indirect

A

direct: through the weakness in the posterior wall of the inguinal canal, running inferior and medial to the epigastric vessels - RARE in children
indirect: through the internal inguinal ring, running lateral to the inguinal vessels (COMMON in children)

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32
Q

risk factors for inguinal hernia

A

PTB, undescended testes, FH, CF, hip dysplasia, congenital abnormalities

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33
Q

presentation of an inguinal hernia

A

small swelling in the groin or larger swelling in the scrotum. more noticeable when child is straining/coughing/crying.
smooth, soft, painless. more common on RHS.

34
Q

complications of irreducible inguinal hernias

A

strangulation - leading to infarction and loss of the testes.

35
Q

what is intussusception?

A

when one part of the bowel overlaps inside another part, most commonly occurring in the terminal ileum.

36
Q

when doe intussusception commonly occur?

A

under 2 years, between 3mo and 6years. most common cause of bowel obstruction in this age group

37
Q

causes of intussusception

A

viral infection - payers patches inflammation causing the blockage which can move.
meckles diverticulum, polps, lymphoma, tumours, CF, HSP.

38
Q

presentation of intussusception

A 
paroxysmal pain - colicky severe pain then child sleeps
bilious vomiting
red-current jelly stool
abdominal mass in RUQ
pale, dehydrated child.
39
Q

management and investigations of suspected intussusception

A

A-E approach

investigations: FBC, U&Es, Abo XR, USS (will show target sign)
management: IV fluids, analgesia, antibiotics. emergency surgical intervention or air enema to push bowel back to normal (risk of perforation)

40
Q

signs of abdominal XR an USS for intussusception

A

XR: round edge of intersusseption with contrast against the lucent lumen of the bowel, air in the bowel
USS: target sign, looks like a Pseudokidney.

41
Q

three initial management steps for GORD

A

1) feeding advise, positional advice
2) feeding thickeners
3) acid blockers (PPI) or motility agents (erythromycin and domperidone)

42
Q

Most common cause of constipation in a child

A

functional - due to dehydration of low fibre intake

43
Q

treatment for faecal impaction

A

top down treatment - movicol at a high dose.

2nd line is an enema

44
Q

Causes of jaundice in children

A

Pre hepatic: haemolysis, - sickle cell, haemolytic disease of the newborn, gilberts syndorme
Hepatic: hepatitis, alpha 1 antitrypsin
post hepatic: obstruction of biliary tree, CF.

45
Q

what is conjugated vs unconjugated bilirubin?

A

conjugated: soluble, metabolised bilirubin (hepatic and post-hepatic causes)
unconjugated: insoluble, pre-hepatic causes of jaundice

46
Q

Jaundice history key points

A

when did it start? how long? ever happened before? BINDS?
associated symptoms: malaise, puritus, dark urine, steatorrhea, abdominal tenderness, signs of anaemia - tiredness, breathlessness, pallor

47
Q

complications of jaundice

A

failure to thrive, kernecitus (bilirubin excess in the CNS)

48
Q

Blood results seen in jaundice: LFTs

A

Low Hb
excess bilirubin
ALP raised
liver enzymes raised

49
Q

what is mesenteric adenitis? how common is it?

A

enlargement of intraabdominal lymph nodes, causing abdominal pain.
most common cause of abdominal pain in children under15.
due to viral or bacterial infection

50
Q

management of mesenteric adenitis

A

self limiting, will resolve within a few days - 2 weeks.

supportive treatments - fluids, analgesia.

51
Q

presentation of pyloric stenosis, history and examination findings.

A

projectile non-bilious vomiting, 30 mins after feeding. usually starts within 2 weeks of life.
O/E: faltering growth, dehydration, infrequent bowel movements, stomach peristalsis can be seen as well as a lump n RUQ.

52
Q

blood gas of pyloric stenosis

A

hypokalaemia, hypochloraemic alkalosis

53
Q

investigation for pyloric stenosis

A

test feed.
Bloods: U&Es or VBG - lo k, Na and Cl with a alkalosis.
abdominal XR or USS: hyperinflated stomach

54
Q

where do you see the double buble sign?

A

on an abdominal XR id there is duodenal atresia - showing air before and after te connection.

55
Q

management for pyloric stenosis

A

Fluid correction , empty stomach with NG.

Surgical management - Ramstad’s pyloromyomotomy)

56
Q

presentation of testicular torsion

A

sudden onset of scrotal or abdominal pain.
unilateral red, swollen, oedematous scrotum. absent ceremstric reflex. lifting the testes increases pain
associated with N/V

57
Q

who gets testicular torsion?

A

neonates or adolescents, peak age is 12. most commonly on the LHS

58
Q

two types of testicular torsion? what causes them?

A

intravaginal - rotation within the tunica vaginalis, lack of normal fixation

extravaginal - neonates, just below the inguinal canal, occurs before testes are fixed

59
Q

investigations and management of testicular torsion

A

A-E approach. Medical emergency

investigations: USS doppler to visualise blood flow. Urinalysis to exclude UTI and epididymitis
management: analgesia. emergency surgery within 8 hrs to preserve testes.

60
Q

prevalence and risk factors for undescended testes/cryptorchidism

A

Occurs in 1/300 boys. Usually unilateral.

risk factors: PTB, LBW, FH, SGA, congenital adrenal hyperplasia, prader willi, kalmans syndromes.

61
Q

Management of undescended testes

A
  • If present at birth - review at 6 weeks to see if they have descend. Then review again at 3 months.
  • If still present at 3 months, will need surgery (gold standard) preferably before 6 months, definitely before 18 months
  • Alternatively can use hCG or GnRH if it is a low undescended tests, to avoid surgery.
62
Q

What is biliary atresia? how does it present?

A

inflammation of the extrahepatic bile ducts, causing them to be blocked. three types.
presentation: prolonged neonatal jaundice, obstructive jaundice (dark urine, pale stools after a normal meconium), splenomegaly, failure to thrive

63
Q

LFTS in biliary atresia

A

elevated conjugated bilirubin, elevated transaminases, elevated bile acids and GGT.

64
Q

Management of Biliary atresia

A

Medical: ursodeoxycholic acid (used to trat gallstones and blockages) to encourage bile flow, vitamin supplementation, prophylactic AbX, nutritional support
surgical: only definitive treatment, dissection of abnormalities and anatsamosis creation.

65
Q

causes of biliary atresia

A

congenital: glutathione S transferase deficiency
acquired: autoimmune inflammation, due to viral infection, occurs soon after birth.

66
Q

Presentation of hepatitis

A

N/C, jaundice, (conjugated), abdominal tenderness, fever, myalgia, puritus.

67
Q

investigations and management of hepatitis

A

Investigations: Bloods - LFTs, U&Es, Coagulation, FBC.
viral serology.
liver USS, may need liver biopsy.
Management: supportive treatment, flids, analgesia, may need prophylactic abx. antivirals

68
Q

causes of hepatitis

A

Hep ABCDE, MV, EBV, ESV, VZV, rubella, adenovirus, enterovirus, paravirus, autoimmune

69
Q

Presentation of Hirschprung’s disease

A

Neonates: failure to pass meconium, repeated vomiting.
older children: chronic constipation, soiling, abdominal pain, poor growth.
could present with acute infection - entercolitis.

70
Q

pathophysiology of Hirschprung’s

A

absence of parasympathetic ganglions in the submucosa of rectum and colon. segments are unable to relax, leading toa functional obstruction.

71
Q

Management of hirschrung’s

A

surgery to remove effected segment.

treat bowel obstruction/infections. IV fluids, NBM, prophylactic Abx.

72
Q

investigations for IBD

A

faecal calprotien.

endoscopy or colonoscopy.

73
Q

management for IBD

A

diet:

medical: corticosteroids, immunosuppressants, aminosalicylates (eg mezalazine for UC)
surgical: resection of inflammation

74
Q

presentation and risk factors of toddlers diarrhoea

A

foul smelling loose stool with undigested food within. more common with high sugar diet, high fibre and water intake, low fat diet. child is otherwise well and growing normally

75
Q

management of toddlers diarrhoea

A

plot height and weight. reassurance to parents (common benign condition, due to fast transit through the GI system), cut down fruit juices, normalise feeding patters, limit water intake and high fibre foods.

76
Q

how does malrotation and volvulus occur

A

malrotaion of the midgut during development (no twisting, mesentry I not attached to the gut in the correct place). due to no mesentry attatchment, the gut is prone to twisting on itself ( a volvulus)

77
Q

presentation of volvulus

A

bilious vomit, FFT, feeding intolerance, constipation, may have bloody stools, intermittent apnoea.
can present collapsd and acutely unwell.

78
Q

investigations with bilious vomiting

A

A-E approach. volvulus until proven otherwise
Bloods: FBC, U&Es
Imaging: Upper GI study, abdo XR

79
Q

what are the findings in a upper GI study and an abdo XR with malrotation and volvulus

A

upper GI study: corkscrew appearance of the jejunum

abdo XR: can show partial obstruction with the double bubble sign

80
Q

management of malrotation and volvulus

A

A-E assessment. stabilisation

emergency surgery, Ladds procedure

81
Q

how to calculate % fluid deficit

A

if 10% deficit - need an extra 100mls/kg

if 5% deficit - need an extra 50mls/kg

PEADS (6 decks)

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