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PaedsY5 Gastro > Gastro A-C > Flashcards

Gastro A-C Flashcards

1
Q

What is Anorectal malformations (ARM)?

A

Wide spectrum of disorders affecting the distal anus and rectum, with or without involvement of the genitourinary tract.

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2
Q

What is the background of Anorectal malformations (ARM)?

A

1/5k live births.

Wide spectrum of disorders. Mild forms have a bowel outlet via a fistula in the perineal region. Severe forms have bowel outlet in the genitourinary tract region in males, or genital tract in females. Associated with other anomalies in 60%: VACTERL, CHARGE, MURCS, OEIS, Trisomy 13/18/22, Hirschprungs, vertebral/sacral abnormalities.

Wingspread classification: by the relation of the fistula or pouch to levator muscle complex (low/intermediate/high)

Krickenbeck classification:

· Major group (wither with presence of fistula – perineal /rectourethral/ prostatic/ bulbar/ retrovescical/ vestibular. There may be no fistula, and colaca or anal stenosis).

· Minor group (pouch colon, rectal atresia/stenosis, rectovaginal fistula, H fistula and others).

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3
Q

What are the history/ exam findings of Anorectal malformations (ARM)?

A

Clinical examination by surgeon to classify the type in 90%. Associated abnormalities.

Specific for low lesions: prominent midline skin bridge (bucket handle), subepithelial midline raphe fistula, rectovestibular fistula, anal membrane. A flat perineum (absence of gluteal fold and anal dimple) may indicate absence of perineum muscle and therefore high ARM.

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4
Q

What investigations do you do for Anorectal malformations (ARM)?

A

General: Screning for other abnormalities: CXR, ECHO, RUSS, Karyotype, USS for hydrometytrocolpos/spinal abnormalities, sacral XR, urinalysis.

Specific: Prone cross table lateral XR with specific marker for perineum (air column to marker <1cm low lesion, >1cm colostomy). High pressur distal colostography.

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5
Q

What is the management of Anorectal malformations (ARM)?

A

Medical (neonatal): REsuscitaiton, abnormalities screening, NBM, IVI, Abx, transfer to paediatric surgery centre. Observe? Passage of meconium through fistula/GUT.

Surgical (neonatal): Severe: primary diverting colostomy. Low: cutback anoplasty/limited PSARP. Rectovestibular fistula dilation.

Surgical (definite): Posterior sagittal anorectoplasty (PSARP) with separate colostomy closure.

Post surgical bowel management programmes inducing enemas, laxatives and dietary advice.

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6
Q

What are the complications and prognosis of Anorectal malformations (ARM)?

A

Most common functional disorder is constipation. Urinary and fecal incontinence may occur due to poorly developed spinal outflow.

Generally good, Low ARM has less complications than high.

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7
Q

What is Acute appendicitis?

A

Acute inflammation of the vermiform appendix

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8
Q

What is the background of Acute appendicitis?

A

Most common cause of acute abdomen in children, 4/1k children. Usually >5y.

Obstruction of appendiceal lumen by faecolith -> contraction -> muscle decrease venous drain and arterial supply -> fail to relax -> necrosis -> peritonitis.

Related to poor fibre intake, increased fecal viscosity, and bowel transit time.

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9
Q

What are the history/ exam findings of Acute appendicitis?

A

Large variation in clinical picture, Classically colic pain from umbilicus to RIF. Constant with peritoneal inflammation and more with movement. Anorexia, vomiting, constipation and diahrrea. Fever (low grade)

General: tachycardia, pyrexia, not moving

Abdominal exam: rebound tenderness, guarding with palpation in RIF (McBurney’s point). Rosving’s sign (RIF pain reproduced with palpation of LIF). There may be pain in breathing and coughing.

Rectal exam: should only be preformed by most senior doctor, only if diagnosis in doubt. Tenderness against anterior abdominal wall.

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10
Q

What investigations do you do for Acute appendicitis?

A

General: clinical diagnosis

Bloods: increased WCC, CRP/ESR, U&E if vomiting.

Utine: MCS if UTI is DDx.

Radiology: plain XR may show dilated loops of bowel proximal to appendix. Not necessary to preform.

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11
Q

What is the management of Acute appendicitis?

A

Traditional open surgical approach (Lanz incision) or laprescopically. Washout essential if complicated by perforation.

Conservative: with confirmed appendiceal abscess that responds to IV abx. Interval appendicectomy offered.

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12
Q

What are the complications and prognosis of Acute appendicitis?

A

Perforation very common in children <3, but very uncommon in children >10. Abscess formation, wound infection, abdominal abscess, low fertility in girls if complicated, obstructions, adhesions.

Usually excellent prognosis

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13
Q

What is Coeliac disease?

A

A lifelong gluten induced enteropathy of the small bowel resulting in malabsorption and inflammation, which resolves completely upon gluten withdrawal

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14
Q

What is the background of Coeliac disease?

A

1% positive in the UK.

Sensitivity to the a-gliadin component of gluten protein. Immunological reaction to this component leads to mucosal damage.

Associated with HLA DQ2 or DQ8.

Pathology: Macro - subtotal villous atrophy of proximal SI, flattened mucosa. Micro – inflammatory infiltrate, crypt hyperplasia, atrophy.

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15
Q

What are the history/ exam findings of Coeliac disease?

A

Classic history of constipation, abdominal pain, weight loss, failure to thrive, steatorrhea, fatigue, irritability.

Many children will have no abnormal findings.

General: miserable, pale, anaemic, irritable, clubbing, uttock wating, pot belly appearance, distension, delayed puberty.

Dermatitis herpetiformis: causing itchy blisters on elbows, knees, face, buttocks.

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16
Q

What investigations do you do for Coeliac disease?

A

Serological testing offered in any individual with AI thyroid disease, dermatitis herpetiformis, IBS, T1DM and first degree relatives.

Serology: check IgA level as 2% will be deficient. Abx directed against tTga, or anti EMA antibodies.

Bloods: low Hb, high MCV (B12 def) low Ca and albumin if severe.

Jejunal biopsy: gold standard for diagnosis, shows subtotal villous atrophy and crypt hyperplasia.

Gluten challenge can confirm.

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17
Q

What is the management of Coeliac disease?

A

Prevention: breastfeeding while weaning onto wheat may be protective.

Nutritional advice: complete avoidance required. Strict diet. Iron supplements.

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18
Q

What are the complications and prognosis of Coeliac disease?

A

With adherence to diet, fine.

Osteoporosis, higher chance of leukemia, secondary lactose intolerane due to damage to brush border, bacterial overgrowth, social morbidity, decreased fertility, weight gain after dx.

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19
Q

What is Constipation?

A

Delay or difficulty in defecation, for over two weeks or enough to cause considerable distress.

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20
Q

What is the background of Constipation?

A

Very common – 3-5% and 35% gastro clinic presentations.

Functional: 90-95%. Due to vicious cycle of retention, pain on defecation, more retention. -> retention leads to pain, and eventually leads to decreased sensory input. Chronic retention then also leads to dilation of rectum, muscle weakness, and reabsorption of more water from stools leading to harder and harder stool.

Slow transit constipation STC: poor prognosis, refractory to medical management.

Nutritional: coeliac, CMPA, intolerance, low fibre diet.

Organic (rare) due to GI abnormalities: Hirschprungs, neuromuscular disease, spinal disease, anal atresia or abnormalities, hypothyroidism, cerebral palsy.

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21
Q

What are the history/ exam findings of Constipation?

A

Pain, difficulty passing stool, may have diahrrea.

Take history of diet, social setting, stress factors, birth. Delayed meconium passing (>24h) is common in Hirschprungs.

General: abdominal distension and pain, presence of stool.

DRE: location of anus, tone, anal wink, presence of stools in passage, presence of anal fussires, fistulae etc.

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22
Q

What investigations do you do for Constipation?

A

Radiology not helpful

Anorectal manometry: to measure pressures in bowel and anus

Radionuclear transit scintiography: to identify causes of slow colonic transit.

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23
Q

What is the management of Constipation?

A

General: evacuation of stools, education of emptying, regular routine.

Medical: lidocaine gel if fissure, dietary changes, exercise etc

Hurschprungs: ENdorectal pullthrough, with placement antegrade continence enema.

Other: ?transcutanous electrical stimulation

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24
Q

What are the complications and prognosis of Constipation?

A

Fecal overload, encopresis, peritonitis, overflow incontinence, behavioral difficulty.

50% recoverin 1y and 65% in 2y. Remainder require laxative therapy.

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25
Q

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

A

Immune hypersentivitiy reaction to cows milk.

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26
Q

What is the background of Cow’s milk protein allergy (CMPA)?

A

2.5% at 1y.

Related to parental atopy. Reaction to cows milk proteins, either whey or casein (80%). Children often also suffer from atopic eczema and other allergies.

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27
Q

What are the history/ exam findings of Cow’s milk protein allergy (CMPA)?

A

Symptoms within the first five weeks of introducing cow’s milk. Divided into immediate IgE, Mixed IgE and non IgE, and Delayed Non IgE

· Immediate IgE (1h)

o Skin – flush, itch, urticarial, angioedema

o Resp: wheeze, angioedema, cough, bronchospasm

o CVS: tachycardia and hypotension

o GI: vomiting, diahrrea, abdominal pain

o Pathophysiology: exposure to food in a sensitized individual leads to mass degranulation of PG/LKT from Mast cells, activated by IgE cross binding.

· Mixed IgE and Non IgE (2-12h)

o Skin: atopic eczema

o GI: eosinophilic oesophagitis (leading to reflux, food aversion, dysphagia) proctolitis (bloody stools in otherwise well child)

· Delayed non IgE (12+h)

o GI: food protein induced enterocolitis, FPIES – presents with vomiting and possibly diahrrea, shock and metabolic acidosis. Failure to thrive, constipation.

o Pathology: food protein taken up by APCs, presented to T cells. Th2 interact with B cells and produce allergic cytokines leading to inflammation

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28
Q

What investigations do you do for Cow’s milk protein allergy (CMPA)?

A

IgE mediated: skin prick tests and specific IgE (95% positive) Gold standard is a double blind, placebo food trial.

Non IgE mediated: no good diagnostic criteria other than exclusion trials. Blood may show signs of malabsorption (low Hb, low Alb).

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29
Q

What is the management of Cow’s milk protein allergy (CMPA)?

A

Prevention: breastfeeding up until 4 months can be protective, especially in families with atopy. Maternal avoidance of dairy may be required. If no breastfeeding, hypoallergenic formulas essential.

Avoidance: all mammalian dairy products. Replace cows milk with either extensively hydrolised formulas EHF, or with Amino acid formulas. If those still cause problem, rice/soya/pea milk may be given fortified with calcium.

NB: soya milk has high cross allergenicity in children therefore often not an option.

Reintroduction: may be attempted in children who can tolerate traces of milk over 6-12m.

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30
Q

What are the complications and prognosis of Cow’s milk protein allergy (CMPA)?

A

Anaphylaxis risk, failure to thrive, malabsorption, electrolyte disturbances from vomiting, existence of other allergies and therefore asthma.

IgE mediated, 1/3 resolve by 2y, ½ by 3, and 2/3 by 4. Non IgE, 90% by 3y.

High risk of eczema developing, and allergic asthma / rhinitis.

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31
Q

What is an anal fissure?

A

• This is a split in the skin of the distal anal canal characterised by pain on defecation
and rectal bleeding

32
Q

What is the aetiology and epidemiology of an anal fissure?

A

• Usually develop as a side effect of constipation → the anal sphincter stretches to let
hard faeces pass causing tissue around it to tear

33
Q

What are the S/S of anal fissures?

A

Severe pain on defecation (‘like passing broken glass’)
• Fresh red blood passed on stool/on wiping
• Start to heal after passing stool but can re-open when child next defecates

34
Q

What investigations do you do for an anal fissure?

A

History/ Exam

35
Q

What is the management of an anal fissure?

A

Treatment aims to soften the stool to allow tissue to heal
o Change in diet
o Laxatives
• Can also use a warm bath and creams to sooth the area

36
Q

What is biliary atresia?

A

A progressive, idiopathic, necroinflammatory process that can involve a segment or the entire
extrahepatic biliary tree

37
Q

What is the pathophysiology of biliary atresia?

A

o There is progressive fibrosis and obliteration of the extrahepatic and intrahepatic
biliary tree
o The hepatic or common bile duct is obliterated or discontinuous for a portion between
the porta hepatis and the duodenum
o This destruction/deformity of the bile duct leads to obstruction to bile flow
o The pressure in the duct proximal to the obstruction builds up
o Eventually, bile pushes through the tight
junctions of epithelial cells lining the ducts
and leaks into the circulation → hence
increase in conjugated bilirubin in blood
and jaundice symptoms

38
Q

What are the RFs for biliary atresia?

A 
o Viral infection/toxin exposure
o Defects in embryological development
o Genetic predisposition
o Defects in antenatal circulation
o Immune or autoimmune dysregulation
39
Q

What are the types of biliary atresia?

A

o Type 1: proximal ducts are patent, but common duct is obliterated
o Type 2: atresia of cystic duct and cystic structures are found in porta hepatis
o Type 3: atresia of left and right ducts to the level of the porta hepatis (>90%)

40
Q

What are the clinical features of biliary atresia?

A
  • Presents in first few weeks of life
  • Mild jaundice extending > 2 weeks
  • Pale stools (colour may fluctuate but becomes increasingly pale as the disease progresses)
  • Dark urine
  • Normal birthweight followed by faltering growth
  • Hepatomegaly often present at first
  • Splenomegaly develops due to portal hypertension
41
Q

What are the investigations for biliary atresia?

A

Must exclude biliary atresia in a baby with jaundice persisting beyond 14 days of age or
if conjugated bilirubin is > 17.1umol/L
• Serum total and conjugated bilirubin: total bilirubin may be normal, conjugated bilirubin >
17.1 umol/L
• Newborn screen (for galactosaemia, thyroid dysfunction, cystic fibrosis, metabolic diseases
etc)
• Prothrombin time: usually normal

• FBC: in advanced disease, low platelets and low WCC
• LFTs: high GGT
• Fasting abdominal ultrasound: may show a contracted or absent gallbladder, may be normal
• Coomb’s test: negative
• Serum alpha 1-antitrypsin
• Diagnosis is confirmed via a cholangiogram (ERCP – endoscopic retrograde
cholangiopancreatography) or operatively
o Liver biopsy: bands of fibrous tissue with bile duct proliferation

42
Q

What is the management of biliary atresia?

A

• Surgery: KASAI HEPATOPORTOENTEROSTOMY
o A loop of jejunum is anastomosed to the cut surface
of the porta hepatis
o This bypasses the fibrotic ducts and facilitates
drainage of bile from any remaining patent ductules
o +/- ursodeoxycholic acid (may facilitate bile flow)
o Early surgery increases success rate: 80% clear
jaundice if performed before 60 days
• Even with successful clearance of jaundice, disease
progresses in most and can lead to cholangitis and cirrhosis
with portal hypertension
• Requires nutrition, fat-soluble vitamin supplementation,
antibiotic prophylaxis (trimethoprim/sulfamethoxazole) for
first year of life
• If Kasai unsuccessful or if end-stage liver disease → liver
transplantation

43
Q

What is a cleft palate?

A

Results from failure of fusion of the palatine

44
Q

What is a cleft lip?

A

o Results from failure of fusion of the frontonasal and maxillary processes
o May be unilateral or bilateral

45
Q

What are the causes of cleft palate/ lip?

A

May be a part of a syndrome e.g. chromosomal disorders

o Some are associated with maternal anticonvulsant therapy

46
Q

What is the management of a cleft palate/ lip?

A

o Surgical repair
▪ Cleft lip: 3 months
▪ Cleft palate: 6-12 months
o May make feeding difficult esp if bottle-fed → may need special teats and feeding
devices
o Secretory otitis and acute otitis media is common

47
Q

What is acute liver failure (ALF)?

A

• Acute liver failure in children is the development of massive hepatic necrosis with subsequent
loss of liver function +/- hepatic encephalopathy
• Uncommon
• High mortality

48
Q

What are the causes of acute liver failure in <2 yo?

A 
▪ Infection (most common herpes simplex)
▪ Metabolic disease
▪ Seronegative hepatitis
▪ Drug-induced
▪ Neonatal haemochromatosis
49
Q

What are the causes of acute liver failure in >2yo?

A 
▪ Seronegative hepatitis
▪ Paracetamol overdose
▪ Mitochondrial disease
▪ Wilson disease
▪ Autoimmune hepatitis
50
Q

What are the complications of ALF?

A

o Cerebral oedema
o Haemorrhage from gastritis or coagulopathy
o Sepsis
o Pancreatitis

51
Q

What are the clinical features of ALF?

A
  • May present with hours or weeks
  • Jaundice
• Encephalopathy
o Irritability
o Confusion
o Drowsiness
o Older children may be aggressive
  • Coagulopathy (INR > 1.5)
  • Hypoglycaemia
  • Electrolyte disturbances
52
Q

What investigations would you do in ALF?

A

• LFTs
o Bilirubin may be normal in early stages
o Transaminases greatly elevated (10-100x normal)
o High ALP
o Abnormal coagulation

  • High plasma ammonia
  • Monitor acid-base balance, blood glucose and coagulation
  • EEG: acute hepatic encephalopathy
  • CT: may show cerebral oedema
53
Q

What is the management of ALF?

A

• Early referral to a national paediatric liver centre
• Steps to stabilise the child:
o Maintaining blood glucose (> 4 mmol/L) with IV dextrose
o Preventing sepsis with broad-spectrum antibiotics and antifungals
o Preventing haemorrhage with IV vitamin K and H2 antagonists/PPIs
o Prevent cerebral oedema by fluid restriction and mannitol diuresis

TREAT CAUSE

54
Q

What are poor prognostic markers in ALF?

A 
o Shrinking liver
o Rising bilirubin
o Falling transaminases
o Worsening coagulopathy
o Coma
55
Q

What is obesity?

A

Obesity is a condition of excessive body fat or adiposity that exceeds healthy limits.

A BMI between the 85th and 94th percentiles is defined as overweight, and a BMI ≥95th percentile is defined as obesity. Severe obesity is defined as BMI of 120% of the 95th percentile.

56
Q

What is the epidemiology of obesity?

A

NHANES data from 2017 to 2018 showed that 13.4% of 2- to 5-year-olds, 20.3% of children aged 6 to 11 years, and 21.2% of people aged 12 to 19 years were obese.

57
Q

What are causes for obesity?

A 
Syndromic
Genetic
Environmental/ Behavioural
In utero environment
Drug related (e.g. steroids)
58
Q

What are the complications of obesity?

A 
Adulthood obesity
T2DM
Cardiac disease
NAFLD/ metabolic syndrome
Hypertension
PCOS
59
Q

What is the management of childhood obesity?

A

Lifestyle advice

Manage co-morbidities

60
Q

What are the causes of neonatal jaundice <24hrs?

A

Rhesus haemolytic disease (Rare due to Anti D, hydrops, hepatosplenomegaly, rapid jaundice),

ABO incompatibility (DAT +ve, Mainly Gp O, less severe jaundice, no hepatosplenomegaly, normal/low Hb)

G6PD deficiency (X linked rec, fava beans, moth balls, stress and COCP)

Spherocytosis (DAT+ve),

Congenital infection (CMV/ rubella/ HSV)

neonates with cephalohaematoma might become jaundiced

61
Q

What are the causes of neonatal jaundice 1-14 days?

A

Rhesus haemolytic disease (Rare due to Anti D, hydrops, hepatosplenomegaly, rapid jaundice),

ABO incompatibility (DAT +ve, Mainly Gp O, less severe jaundice, no hepatosplenomegaly, normal/low Hb)

G6PD deficiency (X linked rec, fava beans, moth balls, stress and COCP)

Spherocytosis (DAT+ve),

Congenital infection (CMV/ rubella/ HSV)

neonates with cephalohaematoma might become jaundiced

62
Q

What are the causes of prolonged jaundice (>14 days term or 21 days pre term)?

A

Sepsis

Metabolic: Hypothyroid/ pituitarism, galactosaemia

Usually Guthrie

May be syndromic

GI: Biliary atresia, choledochal cyst

Presentation: dark urine, pale stools, failure to thrive, hepatomegaly

63
Q

What are the risk factor for jaundice?

A

Exclusively breastfed,

gestational age <38 weeks, LBW, small for dates,

previous sibling needing phototherapy,

visible jaundice within 24 hrs of life,

infant of diabetic mother

64
Q

What is the management of jaundice?

A

Phototherapy graph threshold:

Above Initiate Tx

Below:

> 50 mmol/L below, clinically well with no RFs for neonatal jaundice do not routinely repeat level

<50 mmol/L below, clinically well, repeat level within 18 hours (RFs present) to 24 hours (no RFs present)

After phototherapy initiated:

Repeat 4-6 hrs after starting -> then 12 hrly once stable

Stop when >50 mmol/L above line

Check rebound 12-18 hrs after stopping

65
Q

What would you screen in prolonged jaundice?

A

Conjugated/ Serum BR

FBC

Blood film

Group and save

DAT

Urine MCS + reducing substances

Metabolic screen

TFTs

66
Q

How do you measure BR in children?

A

If <35 weeks gestation = serum BR

If <24hrs old = serum BR

If >24 hrs old = transcutaneous bilirubinometer -> if >250 mmol/L do a serum BR

67
Q

How do you treat jaundice?

A

Exchange transfusion = red line on graph

Simultaneous exchange of baby’s blood with donated blood or plasma

Performed via umbilical artery/ vein

Indications: Signs of acute bilirubin encephalopathy or the level/ rate of rise >8.5 mmol/l/hr

IVIG

Adjunct in rhesus haemolytic disease/ ABO incompatability

68
Q

What is hypermetropia and how is it corrected?

A

o MOST COMMON refractive error

o Can be corrected using convex lenses

69
Q

What is vasovagal syncope?

A

Neurally mediated reflex syncope (NMRS) refers to a group of related conditions or scenarios in which symptomatic hypotension occurs as a result of neural reflex vasodilation and/or bradycardia. Vasovagal syncope (VS) refers to a particular type of NMRS also known as the common faint.

70
Q

What are the causes of vasovagal syncope?

A

In susceptible people, vasovagal syncope may be triggered by prolonged periods of upright posture; relative dehydration; excessively warm, closed-in environments; or extreme emotions. Common places for these events are churches, restaurants, and long queues.

71
Q

How do you diagnose vasovagal syncope?

A

Hx- trigger, dizziness, nausea, pallor
ECG
Hb, glucose, cardiac enzymes, Ddimer, cortisol, urea/ serum creatinine

72
Q

What is the management of vasovagal syncope?

A

Education and trigger avoidance

Volume expansion if necessary

73
Q

What is a migraine?

A

A headache type can be with or without aura

74
Q

What is a migraine without aura?

A

o 90% of migraines
o Headache is often bilateral but can be unilateral
o Characteristically pulsatile over the temporal or frontal area
o Often accompanied by GI disturbance (e.g. nausea, vomiting, abdominal
pain)
o Photophobia and phonophobia
o Aggravated by physical activity and relieved by sleep

75
Q

What is a migraine with aura?

A

o 10% of migraines
o Headache is preceded by an aura (visual, sensory or motor)
o Aura can occur without a headache
o Common auras include visual disturbances:
▪ Negative phenomena - hemianopia, scotoma (small areas of visual
loss)
▪ Positive phenomena - fortification of spectra (zigzag lines)
o Rarely, it may cause unilateral sensory or motor symptoms
(e.g. hemiplegic migraine)
o Attacks usually last a few hours
o Children will prefer to lie down in a quiet, dark room
o Migraines have a genetic predisposition
o Bouts can be triggered by disturbances of inherent biorhythms (e.g

76
Q

What are the uncommon migraines?

A

o Familial hemiplegic migraine: caused by calcium channel defect, dominant
inheritance
o Sporadic hemiplegic migraine
o Basilar-type migraine (vomiting with nystagmus and/or cerebellar signs)
o Periodic syndromes (often precursors of
migraine)
▪ Cyclical vomiting
▪ Abdominal migraine
▪ Benign paroxysmal vertigo of childhood

77
Q

What is myotonic dystrophy?

A

a type of MD that can develop at any age; life expectancy isn’t always affected, but people with a severe form of myotonic dystrophy may have shortened lives

PaedsY5 Gastro (5 decks)

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