Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Paediatrics > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

How does Hirschsprung disease present?

A

It usually presents with bilious vomiting, abdominal distension, constipation and failure to pass meconium in the first 48 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is Hirschsprung disease more common in boys or girls?

A

Hirschsprung disease is a congenital bowel disease, which is five times more likely to occur in boys than girls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a common complication of viral gastroenteritis?

A

Transient lactose intolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Symptoms of necrotising enterocolitis?

A

Necrotising enterocolitis is one of the leading causes of death among premature infants.

Initial symptoms can include feeding intolerance, abdominal distension and bloody stools, which can quickly progress to abdominal discolouration, perforation and peritonitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diagnostic investigation for nectrotising enterocolitis?

A

Abdo X-ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How to manage suspected mild-moderate cow’s milk protein intolerance?

A

a extensive hydrolysed formula should be tried

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Hirschsprungs disease

A

Congen absence of ganglia in distal colon

Parasympathetic neuroblasts fail to migrate from neural crest to distal colon, development failure of PNS Auerbach + Meissner plexuses, uncoordinated peristalsis

Aganglionic section does not relax, causing it to become constricted > loss of movement of faeces and obstruction in bowel

M>F, down’s syndrome, neurofibromatosis, Waardenburg syndrome, MEN II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Features of Hirschsprungs disease

A 
Delayed passage of meconium (>48hrs)
Abdo distension 
Vomiting
Poor weight gain, FTT
Older children: constipation, abdo distension

Hirschsprung-associated enterocolitis - presents within 2-4 weeks of birth with fever, abdominal distention, diarrhoea (often with blood) and features of sepsis. Life threatening and can lead to toxic megacolon and bowel perforation. Requires Abx, fluid resuscitation and decompression of obstructed bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Complications of Hirschsprungs disease

A 
Functional obstruction, megacolon 
GI perf 
Bleeding 
Ulcers 
Entercolitis 
Short gut syndrome after surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Investigations for Hirschsprungs disease

A

PR: tight sphincter + explosive discharge of stool + gas
Rectal suction/ biopsy: aganglionic Stain for acetylcholinesterase + nerve XS.
AXR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Management of Hirschsprungs disease

A 
Initially rectal washouts/ irrigation, 
Fluid resuscitation and management of obstruction 
Excision of aganglionic segment
Colostomy, 
Anorectal pull through procedure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is oesophageal atresia and trachea-oesophageal fistula?

A

a birth defect in which part of a baby’s esophagus (the tube that connects the mouth to the stomach) does not develop properly

often happens along with another birth defect called a tracheo-oesophageal fistula, which is a connection between the lower part of the oesophagus and the windpipe (trachea).

common in babies with mothers with polyhdramnios

also more common in babies who have problems with kidney, heart and spine development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Features of oesophageal atresia and trachea-oesophageal fistula?

A

Prenatal: polyhydramnios = can’t swallow, small/ absent stomach bubble

Postnatal: resp distress, aspirating after feeds cough/ choke when fed (regurg of food/ cyanotic during feeding), vomiting

Persistent salivation/ drooling of frothy saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications of oesophageal atresia and trachea-oesophageal fistula?

A

Recurrent resp infections

LT GORD (poor motility)/ strictures = due to scar tissue not growing/functioning as well

Tracheomalacia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diagnosis of oesophageal atresia and trachea-oesophageal fistula?

A

Inability to pass Ryles/NGT – XR shows coiling in oesophagus. Avoid contrast imaging

CXR: if stomach bubble suggest fistula, air filled pouch at level of 3rd thoracic vertebra.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Management of oesophageal atresia and trachea-oesophageal fistula?

A

NBM
Continuous oesoph pouch suction using replogle tube.
1° surgical repair in 1st 24hrs. Longer gap may not allow, gastromy tube necessary to allow enteral feeding
Elongation of oesophagus via Foker technique, colon interposition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is congenital diaphragmatic hernia?

A

Diaphragm defect, herniation of abdo contents into chest, pul hypoplasia + HTN, poor surfactant production

usually represents a failure of the pleuroperitoneal canal to close completely

Left sided posterolat Bochdalek: 85%, failure of fusion of septum transversum with pleuroperitoneal membrane

Morgani: <5%, failure of fusion of septum transversum, ant with sternum + ribs. R sided

1 in 2000 newborns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Features of congenital diaphragmatic hernia?

A

Difficult resus at birth
Resp distress ↑RR, nasal flaring, cyanosis, grunting intercostal retractions
Barrel chest, scaphoid abdo (concave ant abdo wall)
Bowel sounds in 1 hemithorax, displaced heart to R, no BS on affected side
pH <7.3 + cyanosis
Possible syndromic dysmorphism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Complications of congenital diaphragmatic hernia?

A

Bowel complications: obstruction, strangulation, incarceration, ileus, ulceration, perforation
Only 50% survive due to pul hypoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Diagnosis of congenital diaphragmatic hernia?

A

Prenatal USS: fluid filled stomach/ bowel in thorax, peristalsis in chest, oesophageal compression >polyhydramnios.

CXR: abdo contents, air/fluid filled bowel + poorly aerated lung.

NG tube inserted + chest radiograph seen in thorax.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Management of congenital diaphragmatic hernia?

A

Prenatal: fetal tracheal obstruction by balloon, encourage lung growth, pushing out other viscera.

Postnatal: intubation at birth, ventilation, ECMO, NGT to decompress bowels

Surfactant

Facemask ventilation CI > pushes air into gut

Surgery: ↓ of hernial contents, closure of defect. 24-48hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is imperforate anus?

A

No anal opening: membranous covering to complex cloacal malformations. Can involve muscles, nerves, GUT + spine

VACTERL

The rectum or the colon may be connected to the vagina or the bladder by a tunnel (fistula

RF: trisomy 13, 18 + 21, paternal smoking, maternal obesity + DM

8-12 wks gest. Impaired septation + cloacal membrane short in dorsal part, hindgut retains attached to sinus urogenitalis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Features of imperforate anus?

A

Fails to have bowel movement within 24hrs.

Abdo distension

Meconium may emerge from fistula in perineum or urethra

Urine: look for meconium

Fistula to GU tract if stool noted coming out of urethra or vagina instead of anus

Girls: post fourchette fistula
Boys: post urethral fistula - may pass meconium in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Investigations for imperforate anus?

A

Look for other abnormalities

USS: help estimate distance between rectal pouch + perineum

Seen on exam.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Management of imperforate anus?

A

Surgery

Hydration, avoidance of sepsis

NG tube for stomach decompression, avoid vomiting + aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is midgut malrotation?

A

a defect in the normal embryonic rotation of the gut, which causes an abdominal obstruction that presents acutely or with chronic intermittent gastrointestinal symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Features of midgut malrotation?

A

Bilious V if volvulus

Obstruction in infancy, insidious onset in older children (intermittent Sx)

Normally RUQ, severe, sudden onset

Blood PR: mid-gut necrosis, urgent surgical decompression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Complications of midgut malrotation?

A 
Volvulus 
Obstruction 
Hernia 
Malnutrition 
Ischaemic/ necrotic bowel
Omphalocele
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Diagnosis and management of midgut malrotation?

A

Upper GI contrast: R sided, inf or medial duodenum. Volvulus: bird beak, corkscrew.

CT abdo: if midgut volvulus upper GI series 1st. No oral contrast beyond duodenum (volvulus), no contrast in SMA (volvulus with ischaemia), transportation of SMA/V (malrotation), R sided duodenum

Ladd procedure: surgical detorsion of bowel, division of ladd bands (peritoneal tissue, attach cecum to retroperitoneum in RLQ), widening small intestine mesentery, appendectomy, reorientation of small bowel

Laparotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is gastroschisis?

A

a birth defect where there is a hole in the abdominal wall beside the belly button - no peritoneal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

RF of gastroschisis?

A

mother young age, teratogenic substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Features of gastroschisis?

A

Fetal: asymptomatic
Birth: difficulty passing stool/feeding
Small defect in abdo wall, herniated organs exposed to air.
Most common R side, usually small intestine, stomach, liver, may also protrude

Intestinal inflam due to IU exposure to amniotic fluid
Malabsorption
Infarction due to compressed BV
Infection

U USS, MRI
↑ AFP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Management of gastroschisis?

A

Fatal if untreated

Abx

IV fluid/nutrients

Cling film covered to prevent loss of fluid

Surgical repositioning into abdo cavity, closure of defect, multiple surgeries

Vaginal delivery may be attempted, newborns go to theatre ASAP eg within 4 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is omphalocele and exomphalos?

A

a birth defect of the abdominal (belly) wall. The infant’s intestines, liver, or other organs stick outside of the belly through the belly button. The organs are covered in a thin, nearly transparent sac that hardly ever is open or broken.

exomphalos involves a stronger covering of the hernia (with fascia and skin), whereas omphalocele involves a weaker covering of only a thin membrane.

Associated with: trisomy 13 18 21 Beckwith-Wiedemann syndrome

RF: alcohol/tobacco during pregnancy, SSRIs, obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Complications of omphalocele and exomphalos?

A

Abdo cavity malformation
Volvulus
Ischaemic bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Diagnosis and management of omphalocele and exomphalos?

A

IU USS
↑ AFP
Amniocentesis

C-section to ↓ risk of sac rupture
Surgical repositioning of protruding organs
Gradually to give time to expand, if done when no space = compartment syn, if VC obstruction, ↓return to heart, hypotension, death. Sac allowed to granulate, epithelise over wks/ mnths. When can fit, sac removed abdo closed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is pyloric stenosis?

A

hypertrophy of the circular muscles of the pylorus, narrows pyloric canal

incidence 4 per 1000 live births

M>F (4:1)

10-15% infants have FHx

first-borns are more commonly affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Features of pyloric stenosis?

A

‘projectile’ non-bilious, vomiting, typically 30 minutes after a feed

constipation and dehydration may also be present. hungry baby

a palpable mass may be present in the upper abdomen. Visible peristaltic waves L>R

hypochloraemic, hypokalaemic alkalosis due to persistent vomiting

FTT/ weight loss
↓wet nappies, dry mucous membranes, flat/depressed fontanelles > severe volume depletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Diagnosis and management of pyloric stenosis?

A

USS

Ramstedt pyloromyotomy

Electrolyte replacement + IV fluid

Wide bore NG tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is intestinal atresia?

A

used to describe a complete blockage or obstruction anywhere in the intestine

Congen malformation, closed/ absent part of intestine

Duodenal: failure in duodenal vacuolisation to re-establish duodenal passageway after duodenal epithelium prolifs + full duodenal obstruction. Associated with down’s

Non-duodenal: IU ischaemic injury, apple peel appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Features of intestinal atresia?

A

Bilious vomiting
Abdo pain
Malnutrition

Stomach/duodenum distension (accumulated AF has nowhere to go)
Polyhydramnios, fetus swallows less due to intestinal obstruction
Intestinal perf, pneumoperitoneum, meconium peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Diagnosis and management of intestinal atresia?

A

Prenatal USS: 3rd trim. Obstruction. Duodenal (dilated fluid filled stomach adjacent to dilated duodenum). Non-duodenal: dilated fluid filled bowel Polyhydramnios.

Post-natal x-ray: duodenal (double bubble sign), non-duodenal (dilated bowel, air filled fluid levels proximal to obstruction).

Gastric decompression: removal of fluid from stomach
IV fluid compensation
Surgical reattachment of functional portions of intestines. Duodenal intestinal atresia > duodenoduodenostomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is infantile colic?

A

a benign, self-limited process in which a healthy infant has paroxysms of inconsolable crying. The standard diagnostic criteria—known as the “rule of three”—is crying more than three hours per day, more than three days per week, for longer than three weeks.

Drawing up knees
Passage of XS flatus

> 40% in 1st few mnths of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Management of infantile colic?

A

Benign condition
Resolves
If not consider GORD/ milk free formula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is recurrent abdominal pain in children?

A

defined as at least three episodes of pain that occur over at least three months and affect the child’s ability to perform normal activities

most often considered functional (non-organic) abdominal pain.

However an organic cause is found in 5-10% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Risk factors for recurrent abdominal pain in children?

A

F>M, parenteral anxiety, illness in sibling, ADHD, bullied, child abuse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Types of recurrent abdominal pain in children?

A

IBS: abdo pain, improved with defecation, change in stool

Functional dyspepsia: 2+ mnth postprandial fullness after ordinary sized meals, several times per wk, upper abdo bloating, XS blenching

Functional abdo pain: 4X a mnth for last 2mnths episodic or continuous, not attributed to other med condition.

Functional abdo pain syndrome: as above + other body pains, impacts ADLs, somatic Sx eg headache, limb pain or diff sleeping.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Features of recurrent abdominal pain in children?

A

Peri-umbilical, poorly localised.

No other GI Sx

School absence + anxiety

Headache, joint pain, V+N, anorexia, excessive gas, altered bowels

Abdo migraine: paroxysmal eps of intense, acute periumbilical pain 1hr+, intervening periods of normal health wks to mnths, interferes with normal activity, 2+ of: anorexia, N/V, headache, photophobia, pallor. 2X in last 12 mnth.Tx: pzitofen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Alarming features in recurrent abdominal pain?

A 
Involuntary WL
Falling of growth centiles 
GI blood loss 
Sig vomiting 
Chronic severe diarrhoea 
Unexplained fever
Persistent RUQ/RLQ pain
FHx of IBD
Pallor, jaundice, guarding, rebound tenderness, altered bowel sounds, palpable mass 
Joint inflam
Oral/perianal lesions
Skin rashes 
Delayed puberty
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Diagnosis of recurrent abdominal pain?

A 
Rule out CD/IBD gynae causes
Coeliac serology: IgA
FBC/haemantics: IBD/coeliac 
CRP
Faecal calprotectin 
H pylori
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Management of recurrent abdominal pain?

A

Identify + remove things that reinforce Sx eg time off school with access to TV + treats
Encouraged to attend school even if in pain
Avoid excessive investigations
Dietary interventions + probiotics, fibre, low FODMAP. If IBS
CBT

52
Q

What is neuroblastoma?

A

a cancer that starts in certain very early forms of nerve cells, most often found in an embryo or fetus

Malig, neuroendocrine tumour. Neural crest cells of adrenal medulla, paraganglia (carotid bodies), SNS

Secretes catecholamines

Undiff: small blue round cells, contains nerve fibers (neuropil)

Poorly diff: displays diff + undiff characteristics

Differentiated: surrounded by myelin AKA Schwannian stroma, better prognosis

53
Q

Features of neuroblastoma?

A

Median onset 18 months, some disappear, others present w mets ± DVT

Palpable abdo mass

Abdo distension

Pallor, ↓weight, sweating fatigue, ↓appetite

Fussiness

Bone pain, limp

Paraplegia

Hepatomegaly

Proptosis

SVC syndrome: dyspnoea, facial swelling, cough, distended neck/ chest veins, oedema of upper extremities.

54
Q

Complications of neuroblastoma?

A

Mass effect: Horner’s, SCC, constipation

Bone mets

Skull base #: battle, racoon eyes

Myelosuppression: anaemia, leukopenia, thrombocytopaenia

SCC: loss of bowel/ bladder function, lower extremity weakness

Intractable secretory diarrhoea: VIP secretion.

55
Q

Diagnosis of neuroblastoma?

A

Urine catecholamine

Biopsy

↑urinary vanillylmandelic acid + homovanillic acid

Calcification on AXR

CT: renal mass/mass adjacent to spinal nerve roots

USS: heterogenous internal vascularity, areas of necrosis or calcifications

FBC: pancytopenia
↑Cr:Ur + LFTs, LDH

56
Q

Treatment of neuroblastoma?

A

Specialist referral

Chemotherapy (carboplatin, etopside, cyclophosphamide + doxorubicin)

Surgery

Radiotherapy

57
Q

What is intussusception?

A

describes the invagination of one portion of bowel into the lumen of the adjacent bowel, most commonly around the ileo-caecal region.

usually affects infants between 6-18 months old. Boys are affected twice as often as girls

Post infection lymphoid hyperplasia (Peyer’s patch)

Meckel’s diverticulum (lead point)

58
Q

RF’s for intussusception?

A

<24 mnths, Hx of intestinal malrotation/intussusception, intussusception in sibling, M>F, nephrotic syndrome.

59
Q

Features of intussusception?

A

paroxysmal abdominal colic pain

during paroxysm the infant will characteristically draw their knees up and turn pale

vomiting

bloodstained stool - ‘red-currant jelly’ - is a late sign

sausage-shaped mass in the right upper quadrant

60
Q

Complications of intussusception?

A 
Peritonitis 
Sepsis 
Obstruction 
Volvulus 
Intestinal tearing
61
Q

Investigations for intussusception?

A

Sausage like abdo mass
USS (1st line), XR, CT: telescoped intestine, bull’s eye/target like mass/image, obstruction.
May be felt on PR

62
Q

Management of intussusception?

A

the majority of children can be treated with reduction by air insufflation under radiological control, which is now widely used first-line compared to the traditional barium enema

if this fails, or the child has signs of peritonitis, surgery is performed > free telescoped intestine clear obstruction, remove necrotic tissue

63
Q

Causes of appendicitis?

A

Intraluminal stasis, mucus secreted into lumen, ↑luminal pressure. Appendix swells.

Obstruction: lymphoid follicle hyperplasia, fecalith, FB, pinworm, tumour, infection

XS bacteria multiplication behind obstruction. Immune response, pus accumulates, parietal peritoneum irritation

RF: 10-30, M, FH, CF

64
Q

Features of appendicitis in children?

A

Abdo pain: umbilical, then McBurney’s point

N/V/D/C/ fever/anorexia

Rovsing’s: LLQ palpated leads to RLQ pain

Psoas sign: pain on extending hip if retrocaecal appendix

↑HR

Furry tongue

Lying still, pain worse on breathing, moving

RT, guarding

Preschool: D/V, sometimes no abdo pain, may have abdo mass + collections. Perf rapid as omentum thin.

uncommon in children under 4 years old but in this group often presents with perforation

65
Q

Complications of appendicitis?

A 
Appendiceal a, doesn’t reach end of appendix, pressure compresses capill, ischaemia, necrosis. Cell wall weaker, rupture. Peritonitis  
Periappendiceal abscess
Subhrenic abscess
Pylephlebitis 
Portal venous thrombosis 
Sepsis
66
Q

Diagnosis of appendicitis?

A

CT contrast: 🡩appendix diameter + wall enhancement. Pus spillage, abscess

USS: visible, dilated appendix, noncompressible, 🡩blood flow in appendix wall, appendicolith, RIF fluid collection.

Neutrophilic leucocytosis more important than ↑CRP in kids. ↑serum BR: perf

Urinalysis - exclude pregnancy in girls, renal colic, UTI

67
Q

Management of appendicitis?

A

ABx (metronidazole)

Appendecotomy

Abscess drainage

IV fluids, NBM

Perf > abdo lavage.

If constipated + suspect appendicitis, avoid taking laxatives/enema. May cause rupture.

If child appears well, sit forward unsupported + hop, appendicitis unlikely.

68
Q

RF’s for GORD?

A

RF: premies, FH, obesity, hiatus hernia, repaired congen diaphragmatic hernia, repaired oesophageal atresia, neurodisability (CP)

40% of infants regurg their feeds, so is degree of overlap with normal physiology

69
Q

Features of GORD?

A

Typically <8wks

Vomiting/ regurg following feeds

Distress: crying, lifting legs, arching back, coughing

70
Q

Complications of GORD?

A

Reflux oesophagitis

Recurrent aspiration pneumonia

Recurrent OM

Dental erosion

Apnoea, SIDS

Resolves in 90% before 1 y/o ↑length of oesophagus, ↑tone of LOS, upright position + weaning

71
Q

Treatment of GORD in infants?

A

Gaviscon infant – dual sachets

Thickened formula

Head position in feeds >30°, head up

Unexplained feeding diff, distressed, faltering growth: PPI, prokinetics, fundoplication

72
Q

What is necrotising enterocolitis?

A

one of the leading causes of death among premature infants

Acute neonatal intestinal necrosis, serious acute inflam response to insult.

Immature epithelial cells > enteral feed in premie

M>F, LBW, premie, comorbidities affecting gut perfusion (CHD, IUGR, sepsis), mechanical ventilation, 5 min APGAR <7, formula fed, hypoxia, infection (Abx promote floral changes)

73
Q

Features of necrotising enterocolitis?

A

> 90% within 10 days of life, triad; bilious vomit, abdo distension, altered bowel habit, bloody stool

Feeding intolerance,

Lethargy

Apnoea + dyspnoea

Temp instability

Abdo discolouration

Mucosal sloughing

PR bleed

74
Q

Diagnosis of necrotising enterocolitis?

A

Abdo XR - dilated bowel loops, bowel wall oedema, pneumatosis intestinal, portal venous gas, pneumoperiotoneum, Rigler sign (air inside and outside bowel wall), football sign (air outlining falciform ligament)

Blood + stool culture

FBC: thrombocytopenia,

Clotting, U+Es

Blood gas + lactate

75
Q

Complications of necrotising enterocolitis?

A

Bowel perforation
DIC
Peritonitis
Shock

76
Q

Management of necrotising enterocolitis?

A

Supportive initially for non-perf, IVI, discontinuation of enteral feeds, NBM, total gut rest, TPN

IV broad spectrum Abx after cultures taken

Laparotomy + resection in perf

Analgesia

Low threshold for intubation

77
Q

Summary of mesenteric adenitis?

A

Inflamed LN in mesentery
Follows recent viral infection

Similar to appendicitis
Not as localised
Lower fever, no vomiting

Resolves within 48hr
Clinical diagnsosis

No Tx

78
Q

What is Meckel’s diverticulum?

A 
a congenital diverticulum of the small intestine. It is a remnant of the omphalomesenteric duct (also called the vitellointestinal duct) and contains ectopic ileal, gastric or pancreatic mucosa.
.
Rule of 2s
occurs in 2% of the population
is 2 feet from the ileocaecal valve
is 2 inches long
symptomatic presentation <2 y/o
2 types of ectopic mucosa - pancreatic, gastric

arterial supply: omphalomesenteric artery.

normally obliterated wk5-6 pregnancy

79
Q

Features of Meckel’s diverticulum?

A

abdominal pain mimicking appendicitis

rectal bleeding - Meckel’s diverticulum is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years

intestinal obstruction - secondary to an omphalomesenteric band (most commonly), volvulus and intussusception

80
Q

Investigation for Meckel’s diverticulum?

A

USS

if the child is haemodynamically stable with less severe or intermittent bleeding then a ‘Meckel’s scan’ should be considered - uses 99m technetium pertechnetate, which has an affinity for gastric mucosa

mesenteric arteriography may also be used in more severe cases e.g. transfusion is required

AXR

FBC

81
Q

Management of Meckel’s diverticulum?

A

removal if narrow neck or symptomatic

options are between wedge excision or formal small bowel resection and anastomosis

82
Q

What is biliary atresia?

A

involving either obliteration or discontinuity within the extrahepatic biliary system, which results in an obstruction in the flow of bile

neonatal presentation of cholestasis in the first few weeks of life.

infectious agents(CMV), congenital malformations and retained toxins within the bile are all contributing factors

Associations - cardiac malformations, polysplenia +/- situs inversus, premies

F>M

1 - Proximal ducts patent, CBD obliterated
2 - Atresia of cystic duct + cystic structures in porta hepatis
3 - Atresia of L + R duct to level of porta hepatis, >90% of case

83
Q

Features of biliary atresia?

A

Neonatal cholestasis in 1st few wks of life.

Jaundice

FTT

Dark urine > CBR

Fatty pale stools

Hepatosplenomegaly, ascites

Malnutrition > poor growth

Irritability

Appetite + growth disturbance

Cardiac murmurs if associated cardiac abnormalities present

84
Q

Investigations for biliary atresia?

A

Serum bilirubin including differentiation into conjugated and total bilirubin: Total bilirubin may be normal, whereas conjugated bilirubin is abnormally high

Liver function tests (LFTs) including serum bile acids and aminotransferases are usually raised but cannot differentiate between biliary atresia and other causes of neonatal cholestasis

Serum alpha 1-antitrypsin: Deficiency may be a cause of neonatal cholestasis

Sweat chloride test: Cystic fibrosis often involves the biliary tract

Ultrasound of the biliary tree and liver: May show distension and tract abnormalities

HIDA scan - rules out if contrast in intestine

Percutaneous liver biopsy with intraoperative cholangioscopy

85
Q

Management of biliary atresia?

A

Surgical intervention is the only definitive treatment for biliary atresia: Intervention may include dissection of the abnormalities into distinct ducts and anastomosis creation

Kasai procedure - portoenterostomy = excision of extrahepatic BD remnants + GB. May require liver transplant at 1-2 y/o. Bypass fibrotic ducts connect liver to SI

Surgical cholangiogram - surgical exploration

Medical intervention includes antibiotic coverage and bile acid enhancers following surgery

Ursodeoxycholic acid

Nutritional therapy - fat soluble vitamins

86
Q

Complications and prognosis of biliary atresia?

A

Comp’s:
Unsuccessful anastomosis formation
Progressive liver disease
Cirrhosis with eventual hepatocellular carcinoma

Prognosis:
Prognosis is good if surgery is successful
In cases where surgery fails, liver transplantation may be required in the first two years of life

87
Q

Summary of neonatal hepatitis?

A

Various causes
Infection from mother (CMV, rubella, hep A, B or C)

Jaundice at 1-2 mnths of age, not gaining weight, hepatosplenomegaly

In contrast to BA where develop issues, often born with IUGR/ hepatomegaly

88
Q

What is coeliac disease?

A

Enteropathy induced by gluten

Strongly associated with HLA-DQ2 + HLA-DQ8

Associated with other AI disorders, Down’s + Turner’s

89
Q

Features of coeliac disease?

A

Diarrhoea, anorexia, abdo distension, pain

Can present at any age > signs less obvious in older children

Anaemia: ↓folate/ferritin

Malabsorption + malnutrition

Faltering growth

FTT

Lymphoma if continuous inflammation.

90
Q

Investigations for coeliac disease?

A

↑IgA anti-TTG + endomysial IG. Must eat gluten for 6 wks prior

Measure IgA as if def then not good test: anti-gliadin IG instead. ↓reliability if < 18 mnths

Small bowel biopsy in duodenum usually > villous atrophy, crypt hyperplasia. Eat gluten or can’t see.

91
Q

Management of coeliac disease?

A

MDT approach

Dietician input, gluten free diet, some gluten free food can be prescribed

Explain to them that no gluten = no disease.

92
Q

Causes of malnutrition in children?

A

CD, CF, worms, IBD bacterial overgrowth, eosinophilic gastroenteritis.

93
Q

Marasmus vs Kwashiorkor malnutrition?

A

Marasmus: more common, old man (thin, flaccid skin, prominent bones, alert, irritable, distended abdo). Protein + carb starvation.
Kwashiorkor: ↑mortality, bilat pitting oedema, apathy, anorexia. Skin/ hair depigmentation, fragility. Distended abdo. Mostly protein starvation

94
Q

Sx of malnutrition?

A

Weak immune system
Bleeding gums

Acute: ↓wght:ht or mid upper arm circumference
Chronic: ↓ht for age, shunting

95
Q

Management of malnutrition?

A

Re-education

In developed countries > neglect

Gradual increases, high protein diet + vitamins. Make sure to avoid refeeding syndrome

96
Q

What is Rickets?

A

Mineral def prevents normal mineral deposition, slows growth + bone age retarded - mostly vit D and calcium

Nutritional: northern latitude, dark skin, ↓sun, maternal def, ↓Ca, P, vit D (exclusive BF, dairy free diets), prolonged TPN in infancy without Ca supplement.

Malabsorption: CD, CF, (pancreatic) cholestatic LD.

Defective production: CLD, faconi syndrome (renal loss), renal phosphate wasting, renal tubular disorders, x-linked hypophosphatemia, McCune- Albright syndrome.

Meds: loop diuretics, corticosteroids > Ca + P def. phenytoin cause target organ resistance to calcitriol.

97
Q

Sx of Rickets?

A

Ping-pong ball skull (craniotabes) > by pressing firmly on post parietal bones

Bowed legs

Rachitic rosary: bead like thickenings on chest wall expansion of costochondral junctions

Harrison sulcus: horizontal depression on lower chest, attachment of shortened ribs

Tender/swollen joints

Delayed walking, waddling gait

Frontal bossing due to soft skull. Delayed

FTT

98
Q

Investigations and management of Rickets?

A

↓Ca = ↑PTH
↓P, ↑ALP
Low vit D
Most common <2 + teen = rapid growth periods
Only in growing children, in adults, osteomalacia.

Tx - vit D, Ca supplements

99
Q

Summary of Fe def anaemia in children?

A

Inadequate intake, non-modified cow’s milk (not formula)
Parasite in LEDCs

Angular cheilitis: inflam corner of mouth
Koilonychia: thin, concave nails
Tachycardia

Pica: ED, eating non-food substances e.g. soil, ice for >1 mnth
Flow murmur

100
Q

Summary of vit C deficiency?

A

Water soluble vit
Function: antioxidant, collagen synthesis, facilitates iron absorption, cofactor for norepinephrine synthesis.

Scurvy: defective collagen synthesis, capillary fragility (gum bleeding, epistaxis, haematuria), poor wound healing
General malaise

Gingivitis, loose teeth

101
Q

Summary of Vit A (retinol) deficiency?

A

Fat soluble vit
Converted to retinal, visual pigment, important in epithelial cell differentiation

Night blindness

102
Q

Summary of vit B3 (niacin) deficiency?

A

Water soluble vit
Precursor to NAD+ + NADP+, essential metabolic role in cells

Pellagra, dermatitis, diarrhoea, dementia

103
Q

Obesity in children?

A

Overnutrition accelerates linear growth + puberty

If short + obese search for an endogenous cause

Under exercise, diet

Endogenous: Cushing’s, hypothyroid, GH def, Prader-Willi, Down’s,

Asian children: 4X more likely to be obese than white children

F>M

104
Q

Sx of obesity in children?

A

> 98th is obese (>91st is overweight)

Obese children usually above 50th centile for height

Psychological consequences: poor self-esteem, bullying

Orthopaedic: slipped upper femoral epiphyses, Blount’s disease(development abnormality of tibia bowing of legs), pain

Sleep apnoea

Benign IC HTN

T2DM, HTN + IHD

105
Q

Investigations and management of obesity in children?

A

> 12 just normal BMI, before this is adjusted for age/sex

If >91st centile consider tailored clinical intervention, if >98th centile assess for comorbidities

Healthier eating, ↑ activity – aim to maintain weight so can grow into it

106
Q

Constipation and soiling (encopresis) in children?

A

Faecoliths: hard faeces that has been calcified

No identifiable cause > idiopathic constipation, 90%

Dehydration, ↓fibre, meds (opiates), over-enthusiastic potty training, hypothyroid, Hirschsprung’s, ↑Ca, neurological, LD.

Functional: fissures, scared to go, exacerbate problem, overflow + soil themselves

Dx where constipation common: down’s, CP, SG

mean of 3 times per day for infants under 6 months old to once a day after 3 years of age.

107
Q

Sx of constipation and soiling (encopresis) in children?

A

↓freq, passage of hard stools may be large with straining + pain. Sometimes blood.

Overflow soiling: very loose, smelly, passed without sensation or awareness

108
Q

Diagnosis of constipation in children?

A

Suggested by 2 or more of the following:

Children < 1 year:
Fewer than 3 complete stools per week (type 3 or 4 on Bristol Stool Form Scale) (this does not apply to exclusively breastfed babies after 6 weeks
of age)
Hard large stool
'Rabbit droppings' (type 1)
Distress on passing stool
Bleeding associated with hard stool
Straining
Previous episode(s) of constipation
Previous or current anal fissure

Children > 1 yr:
Fewer than 3 complete stools per week (type 3 or 4)
Overflow soiling (commonly very loose, very smelly, stool passed without sensation)
‘Rabbit droppings’ (type 1)
Large, infrequent stools that can block the toilet
Poor appetite that improves with passage of large stool
Waxing and waning of abdominal pain with passage of stool
Evidence of retentive posturing: typical straight-legged, tiptoed, back arching
posture
Straining
Anal pain
Previous episode(s) of constipation
Previous or current anal fissure
Painful bowel movements and bleeding associated with hard stools

109
Q

Red flags for constipation?

A

Reported from birth or first few weeks of life

Passage of meconium > 48 hrs

Ribbon stools

Faltering growth - amber flag

Previously unknown or undiagnosed weakness in legs, locomotor delay

Abdo distension

Amber flag: Disclosure or evidence that raises concerns over possibility of child maltreatment

110
Q

Signs indicating idiopathic constipation?

A

Starts after a few weeks of life
Obvious precipitating factors coinciding with the start of symptoms: fissure, change of diet, timing of potty/toilet training or acute events such as infections, moving house, starting nursery/school, fears and phobias, major change in family, taking medicines

Passage of meconium <48 hrs

Growth generally well, weight and height within normal limits, fit and active

No neurological problems in legs, normal locomotor development

Diet - Changes in infant formula, weaning, insufficient fluid intake or poor diet

111
Q

Features of faecal impaction?

A

symptoms of severe constipation

overflow soiling

faecal mass palpable in the abdomen (digital rectal examination should only be carried out by a specialist)

112
Q

Management of faecal impaction?

A

polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment

add a stimulant laxative (Senna) if Movicol Paediatric Plain does not lead to disimpaction after 2 weeks

substitute a stimulant laxative singly or in combination with an osmotic laxative such as lactulose if Movicol Paediatric Plain is not tolerated

inform families that disimpaction treatment can initially increase symptoms of soiling and abdominal pain

113
Q

Management of constipation in children?

A

first-line: Movicol Paediatric Plain

add a stimulant laxative if no response

substitute a stimulant laxative if Movicol Paediatric Plain is not tolerated. Add another laxative such as lactulose or docusate if stools are hard

continue medication at maintenance dose for several weeks after regular bowel habit is established, then reduce the dose gradually

do not use dietary interventions alone as first-line treatment although ensure the child is having adequate fluid and fibre intake

consider regular toileting and non-punitive behavioural interventions

for all children consider asking the Health Visitor or Paediatric Continence Advisor to help support the parents.

114
Q

Management of constipation in infants?

A

Infants not yet weaned (usually < 6 months)
bottle-fed infants: give extra water in between feeds. Try gentle abdominal massage and bicycling the infant’s legs

breast-fed infants: constipation is unusual and organic causes should be considered

Infants who have or are being weaned
offer extra water, diluted fruit juice and fruits
if not effective consider adding lactulose

115
Q

Causes of diarrhoea in children?

A

Normal for BF to have loose, pasty stools

Acute: 3+ partially formed/ loose stools per day <14 days. Common cause of gastroenteritis is rotavirus

Dysentery: loose stools, blood, mucus, pyrexia, abdo cramps

Causes: CD, Abx, LI, Toddler’s diarrhoea, IBS, chronic bowl infection, IBD, food allergy + intolerance, small intestinal bacterial overgrowth, malig, cows mil intolerance, post-GE LI, cholestatic LD, CF, hyperthyroid, short bowel syndrome.

116
Q

Sx of diarrhoea in children?

A

NICE suggest that typically:
diarrhoea usually lasts for 5-7 days and stops within 2 weeks
vomiting usually lasts for 1-2 days and stops within 3 days

Dehydration - Appears to be unwell or deteriorating
Decreased urine output
Skin colour unchanged
Warm extremities
Altered responsiveness (for example, irritable, lethargic)
Sunken eyes
Dry mucous membranes
Tachycardia
Tachypnoea
Normal peripheral pulses
Normal capillary refill time
Reduced skin turgor
Normal blood pressure
Clinical shock - Decreased level of consciousness
Cold extremities
Pale or mottled skin
Tachycardia
Tachypnoea
Weak peripheral pulses
Prolonged capillary refill time
Hypotension

Secretory: ↓absorption/ ↑secretion. Stool watery, even if fasting
Osmotic: ↑in osmotic load in gut lumen, watery, acidic + for ↓substances
Motility: ↑: thyrotoxicosis, IBS. ↓: pseudo-obstruction, intussusception.
Inflam: bloody diarrhoea, salmonella, shigella, campylobacter, rotavirus, IBD, coeliac, HUS

117
Q

Children at risk of dehydration?

A

children younger than 1 year, especially those younger than 6 months

infants who were of low birth weight

children who have passed six or more diarrhoeal stools in the past 24 hours

children who have vomited three times or more in the past 24 hours

children who have not been offered or have not been able to tolerate supplementary fluids before presentation

infants who have stopped breastfeeding during the illness

children with signs of malnutrition

Not clinically detectable = <5% weight
Detectable = 5-10% weight loss
Shock = >10%

118
Q

Features of hypernatraemic dehydration?

A 
jittery movements
increased muscle tone
hyperreflexia
convulsions
drowsiness or coma
119
Q

Diagnosis of diarrhoea in children?

A

NICE suggest doing a stool culture in the following situations:
you suspect septicaemia or
there is blood and/or mucus in the stool or
the child is immunocompromised

You should consider doing a stool culture if:
the child has recently been abroad or
the diarrhoea has not improved by day 7 or
you are uncertain about the diagnosis of gastroenteritis

120
Q

Management of diarrhoea in children?

A

If clinical shock is suspected children should be admitted for intravenous rehydration.

For children with no evidence of dehydration
continue breastfeeding and other milk feeds
encourage fluid intake
discourage fruit juices and carbonated drinks

If dehydration is suspected:
give 50 ml/kg low osmolarity oral rehydration solution (ORS) solution over 4 hours, plus ORS solution for maintenance, often and in small amounts

continue breastfeeding

consider supplementing with usual fluids (including milk feeds or water, but not fruit juices or carbonated drinks)

Return to school/ childcare facility 48hrs after last episode

121
Q

Causes of chronic diarrhoea in infants?

A

most common cause in the developed world is cows’ milk intolerance

toddler diarrhoea: stools vary in consistency, often contain undigested food

coeliac disease

post-gastroenteritis lactose intolerance

122
Q

Summary of toddler’s diarrhoea?

A

Chronic non-specific diarrhoea
Commonest cause of persistent loose stools in children of pre-school age, most grow out by 5, faecal continence delayed in some. Probably maturinal delay of intestines = intestinal hurry.

Stools varying consistency, well-formed > diarrhoea
Undigested veg in stool common = ‘peas + carrots’ diarrhoea
No other Sx, no FTT

Tx - ↑consumption of fat/↓ fruit juices (fructose) helps

123
Q

Summary of encopresis?

A

Often functional, overflow due to withholding faces (fear), or constipation.
Fear of toilets, punitive potty training. Neurodevelopmental.
M>F

Repeated voluntary/ involuntary passage of faeces in inappropriate places.
>4y/o normal bowel control expected

60-90% will become continent within a year.

Reassure: address stress + review toilet training.
At least once a month 3 months in a row.

Daily laxative: stool softeners: 1g/kg/day polyethylene glycol
Behav therapy: encourage toilet usage, normalise bowel movements
Dietary: avoid constipating foods, hydration, ↑fibre, fibre tablets

124
Q

Causes of enuresis?

A

Causes: genetic, environment, stress, FH, M>F, development delay, constipation, faecal impaction, psychiatric comorbidities

1°: toilet training never mastered. Delayed maturation of bladder’s innervation or generalised development delay. Stress + excessively relaxed/ strict training.

2°: dryness achieved for at 6 mnths then lost. Stress (e.g. starting new school). IDDM, UTI, constipation, psychological or family issues.

125
Q

Sx of enuresis?

A

Repeated voluntary/ involuntary passage of urine in inappropriate places, >5y/o

Diurnal enuresis: F>M

Nocturnal: bed wetting, M>F

Majority of children achieve continence by 3-4 y/o

126
Q

Diagnosis and management of enuresis?

A

2X per week > 3 consecutive months affects life
Assess pattern + arrange renal USS with bladder capacity for daytime wetting/dysfunction voiding
Review toilet training
Possible underlying causes/triggers - constipation, DM, UTI if recent onset

Tx:
Enuresis alarm - sensor pads
Desmopressin - short-term control or alarm not effective
Star charts: given for agreed behav eg using toilet before sleep not dry nights. 
Oxybutynin 
Therapy 
Reassure: common, nobody at fault
Fluid restriction before bed
Double voiding

Paediatrics (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions