Brainscape's Knowledge GenomeTM

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


See full index

4th Year > Paeds - Gastroenterology (textbook) > Flashcards

Paeds - Gastroenterology (textbook) Flashcards

1
Q

What are some “red flag” clinical features in a vomiting child?

A
  • Bilious vomiting = intestinal obstruction
  • Haematemesis = oesophagitis, peptic ulcer, oral/nasal bleeding, oesophageal variceal bleeding
  • Projectile up to 2 months old = pyloric stenosis
  • vomiting after paroxysmal coughing = whooping cough (pertussis)
  • Abdo pain/ tenderness
  • Abdo distension = obstruction, strangulated inguinal hernia
  • Hepatosplenomegaly = CLD, inborn error of metabolism
  • Blood in stool = bac gastroenteritis, Cows Milk Protein Allergy
  • Severe dehydration/shock = severe gastroenteritis, systemic infection (eg. UTI, meningitis), DKA
  • Bulging fontanelle/ seizures = Raised ICP
  • Faltering growth = GORD, Coeliac, etc
  • Chronic diarrhoea = cows milk protein allergy
  • With or At risk of atopy = CMPA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is GORD common in infancy?

A

It is the involuntary passage of gastric contents into the oesophagus.

Caused in infants by inappropriate relaxation of the LOS as a result of functional immaturity, predominantly fluid diet, mainly horizontal posture, and short intra-abdo length of oesophagus.

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

What are some complications children with GORD can experience?

A
  • faltering growth from severe vomiting
  • oesophagitis (haematemesis, discomfort on feeding, heartburn, iron deficiency anaemia)
  • Recurrent pulmonary aspiration (recurrent pneumonia, cough or wheeze, apnoea in preterm infants)
  • Dystonic neck posturing (Sandifer syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How would you investigate GORD in children?

A
  • 24 hour oesophageal pH monitioring to quantify degree of acid reflux
  • Endoscopy with oesophageal biopsies to exclude other causes eg. oesophagitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How would you decide who to refer with suspected GORD in children?

A

Refer for same day admission:

  • haematemesis
  • Melaena
  • Dysphagia

Refer for speciliast asessment

  • faltering growth
  • unexplained distress
  • GORD symptoms not responding to medical treatment
  • unexplained iron deficiency anaemia
  • No improvement in regurg after 1 year of age
  • Suspected Sandifer’s syndrome (episodic torticollis + neck extension and rotation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How would you manage a child with GORD

A
  • breastfed infants = trial 1-2 week alginate therapy like Gaviscon
    • then trial 4 weeks of PPI (omeprazole) or Histamine-2 Receptor Antagonist (Oral Ranitidine)
  • formula fed infants =
    • 1st = reduce the vol of feeds if they are excessive
    • 2nd = trial 1-2 weeks of smaller more freq feeds
    • 3rd = trial 1-2 weeks of feed thickeners like pre-thickened formula or adding thickener (Carobel)
    • 4th = trial 1-2 weeks of alginate therapy added to formula
    • 5th = trial 4 weeks of PPI or H2RA
  • Children 1-2 years old = trial 4 weeks PPI or H2RA

Surgical = for complications unresponsive to medications or oesophgeal strictures

  • Nissen Fundoplication either lap or abdo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is pyloric stenosis?

A

Hypertorphy of the pyloric muscle, causing gastric outlet obstruction

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

How would pyloric stenosis present? (clinical and exam)

A

Clinical features

  • hypochloraemic hypokalaemic metabolic alkalosis as a result of vomiting
  • Vomiting which increases in freq and forcefulness over time, eventually projectile
  • Hunger after vomiting until dehydration results in loss of interest in feeding
  • weight loss
  • not bilious

Exam

  • Test feed is given to allow examination
    • Gastric peristalsis from left to right across abdo
    • Pyloric mass (feels like an olive) can be palpated in RUQ
    • classical “scaphoid abdomen” due to weightloss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How would you manage pyloric stenosis?

A

Try investigating with an USS or Barium Meal.

Correct fluids and electrolyte disturbance with IV fluids

Definitive treatment = pyloromyotomy

Post op = child can be fed within 6 hours, discharged within 2 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some features that would make you think - abdominal migraine?

A
  • Recurrent abdo pain
  • abdo pain in addition to headaches (abdo pain can predominate)
  • midline pain + vomiting + facial pallor
  • fhx migraines
  • anti-migraine medication can benefit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How would you test for HPylori?

A
  • Urea (13C) breath test
    • Do not test within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug.
  • Stool Helicobacter Antigen Test
  • Serology tests
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How would you manage peptic ulceration in children?

A
  • PPI (eg. omeprazole)
  • If investigations indicate H Pylori infection give eradication therapy:
    • amoxicillin + metronidazole OR clarithromycin for 1 week

If unresponsive to treatment, do an upper GI endoscopy.

If normal, diagnose functional dyspepsia.

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

What is the typical clinical picture of gastroenteritis?

A
  • sudden change to loose or watery stools
  • vomiting
  • contact with person with D/V or recent travel abroad
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some common causes of gastroenteritis?

(Infective vomiting and diarrhoea)

A
  • Commonly rotavirus, adenovirus, norovirus, etc.
  • Bacterial suggested by blood in stools
    • Campylobacter jejuni = severe abdo pain
    • Shigella or salmonella = blood and pus in stool, pain, tenesmus. Shigella has high fever
    • Cholera or EColi = profuse diarrhoea
  • Parasite = Giardia or Cryptosporidium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the biggest danger in gastroenteritis and why are infants at risk

A

DEHYDRATION leading to shock

  • Red flag symptoms to identify progression to shock =
    • appears unwell, unresponsive, lethargic, sunken eyes, tahcycardia, tachypnoea, Reduced skin turgor
  • infants have greater surface area to weight ratio
  • higher basal fluid requirements
  • immature renal tubular reabsorption
  • unable to obtain fluids for themselves when thirsty

Give FLUIDS!!!!! but beware of hypernatraemic dehydration

(go slow or pontine myelinolysis)

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

What is coeliac disease?

A

Gliadin fraction of gluten provokes a damaging immunological response in the proximal small intestinal mucosa.

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

What is the classical presentation of coeliac disease?

A

Either Profound malabsorptive syndrome at 8-24 months of age after introduction of wheat containing weaning foods

  • poor growth
  • abdo distension
  • buttock wasting
  • abnormal stools

OR less acutely later in childhood

  • non specific GI symptoms
  • anaemia (iron/ folate deficiency)
  • poor growth
  • typically 1st degree relative with coeliac
  • at risk kids are screened (T1DM, Autoimmune thyroid disease, Down syndrome)
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How would you investigate coeliac disease

A
  • anti-tTG (Immunoglobulin A tissue transglutaminase antibodies) serological screening
  • anti-EMA (anti-endomysial antibodies)
  • Usually if these 2 are strongly positive, biopsy may be unnecessary and a gluten free diet can just be trialled
  • Otherwise jejunal biopsy (while on gluten diet) is gold standard
  • Check IgA levels
  • Mucosal changes on s intestinal biopsy performed in endoscopy
    • increased intraepithelial lymphocytes
    • variable degree of villous atrophy and crypt hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some clinical features of Crohns disease in kids?

A
  • growth failure, delayed puberty
  • Classical presentatiln = Abdo pain + Diarrhoea + Weight loss
  • Extraintestinal = oral lesions, perianal skin tags, uveitis, arthralgia, erythema nodosum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Crohns disease?

A
  • Transmural inflammation
  • commonly affects distal ileum and proximal colon
  • strictures of the bowel and fistulae can form between adjacent loops of bowel, skin, organs, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is Crohns disease investigated and diagnosed?

A
  • Upper GI endoscopy
  • Ileocolonoscopy
  • Small bowel imaging
    • narrowing, fissuring, mucosal irregularities, bowel wall thickening
  • Histology = non-caseating epithelioid cell granulomata
  • CRP and ESR can be raised in active inflammation
  • Serum ferritin, vit B12, folate, vit D can be low due to malabsorption
  • Coeliac serology to rule it out
  • Stool Microscopy and Culture to rule out infective gastroenteritis
  • Faecal calprotectin (raised in IBD. IBS has normal values)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How would you manage Crohns disease?

A

Induce Remission:

  • nutritional therapy for 6-8 weeks
    • normal diet replaced with whole protein modular feeds (polymeric diet)
  • Systemic steroids (eg. prednisolone) if ineffective

Maintain Remission:

  • immunosuppressants like azathioprine, mercaptopurine or methotrexate
  • can trial antitumour necrosis factor agents like infliximab or adalimumab
  • Supplemental enteral nutrition (eg. overnight NG or gastrostomy feeds) to correct growth failure
  • Surgery for complications eg. obstruction, fistulae, abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Ulcerative Colitis?

A
  • inflammatory and ulcerating disease involving the mucosa of the colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a typical clinical presentation of UC?

A
  • Rectal Bleeding + Diarrhoea + Colicky pain
  • weight loss and growth failure less freq than Crohns
  • Extra-intestinal = erythema nodosum and arthritis
25
Q

How would you diagnose UC?

A
  • Endoscopy (Upper GI and ileocolonoscopy)
  • Histological = mucosal inflammation, crypt damage (abscess, loss, cryptitis), ulceration
26
Q

How would you manage UC?

A

Mild

  • aminosalicylates (eg. mesalazine) for induction and maintenance

confined to Rectum and sigmoid colon

  • topical steroids eg. budesonide

Aggressive or extensive disease

  • systemic steroids (eg. prednisolone) for acute exacerbations
  • immunomodulators (eg azathioprine) to maintain remission
    • can combine with low dose corticosteroids
  • Trial Infliximab or Ciclosporin for resistant disease

Surgery for severe fulminating disease

Regular colonoscopic screening after 10 years from diagnosis due to increased incidence of adenocarcinoma of the colon

27
Q

What are some red flag symptoms for a child that presents with constipation?

A
  • Failure to mass meconium within first 24 hours = Hirschsprung
  • Faltering growth = HypoThyroid, coeliac, etc
  • Abdo distension = Hirschsprung, GI dysmotility
  • Abnormal lower limb neurology or deformity (eg urinary incontinence) = Lumbosacral pathology
  • Abnormal anorectal anatomy
  • Perianal bruising or multiple fissures = sexual abuse
  • Perianal fistulae, abscess, fissures = perianal crohns disease
    *
28
Q

How would you generally manage constipation in a child?

A
  • encourage good toileting habits, bowel habit diary, use of encouragement and rewards systems
  • ensure adequate oral fluid intake
  • lifestyle = high fibre, daily physical activity
  • Coeliac screen and TFTs

Treat Impaction

  • Oral laxative regimen and review in 1 week
    • 1st line = Macragol
    • If unresponsive in 2 weeks, add stimulant laxative (eg. Senna or sodium picosulphate)

If impaction is treated or not present

  • Maintenance laxative treatment
    • 1st line = Macragol
    • Add Stimulant laxative like senna if constipation persists

SE = if diarrhoea occurs, reduce laxatives as prolonged diarrhoea can cause hypokalaemia.

Ensure child has easy access to toilet as disimapction can initially increase symptoms of soiling and abdo pain.

29
Q

What are some common surgical causes of acute abdominal pain?

A
  • acute appendicitis
  • intestinal obstruction eg. intussusception
  • Inguinal hernia
  • Peritonitis
  • Inflamed Meckel Diverticulum
  • Pancreatitis
  • Trauma
30
Q

What is biliary atresia?

A

It is when there is progressive fibrosis and obliteration of the extrahepatic and intrahepatic biliary tree.

31
Q

How would biliary atresia present?

A
  • mild jaundice
  • pale stools (become paler as disease progresses)
  • normal birthweight followed by faltering growth
  • Hepatomegaly often present initially
  • Splenomegaly develops due to portal HTN
  • Eventual Chronic Liver Failure and death within 2 years
32
Q

How would you investigate biliary atresia?

A
  • abnormal LFTs with raised conjugated bilirubin
  • Fasting abdo US may show contracted or absent Gallbladder
  • Confirmed with cholangiogram (Endoscopic Retrograde Cholangiopancreatography or Operative)
    • will fail to outline a normal biliary tree
  • Liver biopsy initally shows neonatal hepatitis
    • features of extrahepatic biliary obstruction will develop
33
Q

How would you treat biliary atresia?

A
  • Palliative surgery = Kasai Hepatoportoenterostomy
    • if unsuccessful, consider liver transplant
  • Nutrition and fat soluble vitamin supplementation
34
Q

How would an acute viral hepatitis present?

A
  • nausea, vomiting
  • abdo pain
  • lethargy
  • jaundice sometimes
  • large tender liver
  • 30% have splenomegaly
  • LFTs elevated
  • Normal coagulation
35
Q

How would you diagnose Hepatitis A?

A

Detection of the IgM antibody to the virus

36
Q

How is hepatitis B spread?

A
  • perinatal transmission from carrier mothers
  • inoculation with infected blood via blood transfusion, needlestick injuries, renal dialysis
  • sexually transmitted among adults through body fluids
37
Q

How would you test for Hep B?

A
  • HBV antigens and antibodies
  • anti-HBc are positive in acute infection (these are the IgM antibodies)
  • HbsAg (Hepatitis B surface antigen) are positive in ongoing infectivity
38
Q

How would you manage Chronic Hep B and prevent the spread?

A

30%-50% asymptomatic carrier children will develop chronic HBV liver disease, which progresses to cirrhosis in 10%.

(monitor risk of hepatocellular carcinoma with AFP and Liver US)

  • Symptom control in adults
    • paracetamol/ ibuprofen for pain relief
    • metoclopramide or cyclizine for nausea in mild liver impairment
    • chlorphenamine or ursodeoxycolic acid for itch

Management

  • Interferon or pegylated interferon
  • Or oral antivirals eg. lamivudine and adefovir

Prevention of spread

  • antenatal screening for HBsAg in all pregnant women
  • All babies from HbsAg +ve women are given Hep B Vaccine
    • also give Hep B Immunoglobulin if mother is also HBeAg +ve
  • Vaccinate other members of the family too
39
Q

How is Hep C Spread?

A
  • Post-transfusion hepatitis from donor blood before 1991
  • Intravenous Drug Users
  • Vertical Transmission most common cause to children
40
Q

How would you manage Hep C?

(Almost always chronic carriers, rarely an acute infection)

A
  • Combination of pegylated interferon and ribavirin
  • Monitor for cirrhosis and hepatocellular carcinoma risk
41
Q

How does hepatitis D work?

A

Hep D is a defective RNA virus that needs Hep B virus for replication.

Only occurs in coinfection with Hep B or can cause an acute exacerbation in someone with a chronic hep B infection.

Chronic HDV has a 70% chance of developing to cirrhosis

42
Q

How is Hep E transmitted?

A
  • enterally transmitted, usually by contaminated water
  • known to be transmitted by blood transfusion or eating infected pork
43
Q

How does acute liver failure happen in kids?

A
  • development of massive hepatic necrosis and loss of liver function
    • Can present within hours-weeks with jaundice, encephalopathy, coagulopathy, hypoglycaemia, electorlyte disturbance
    • mostly due to metabolic or infective conditions.
  • can also have hepatic encephalopathy
    • early signs = periods of irritability, confusion, drowsiness
44
Q

What are some common causes of acute liver failure in children below and above 2 years old?

A

Below 2 years old

  • infection eg. herpes simplex
  • Metabolic disease (Galactosemia, Fatty Acid Oxidation Defect, Tyrosinemia etc)
  • Seronegative hepatitis
  • Drug induced
  • Neonatal haemochromatosis

Above 2 years old

  • Seronegative hepatitis
  • Paracetamol overdose
  • Mitochondrial disease
  • Wilsons Disease
  • Autoimmune hepatitis
45
Q

How would you diagnose acute liver failure in children?

A
  • Transaminases are hugely elevated (10-100x)
  • Alkaline Phosphatase is increased
  • Coagulation is abnormal
  • Plasma ammonia is elevated
  • EEG can show hepatic encephalopathy
  • CT can show cerebral oedema (a complication)
    • other complications = haemorrhage from gastritis or coagulopathy, sepsis, pancreatitis
46
Q

How would you manage acute liver failure?

A
  • early referral to national paediatric liver centre
  • Stabilise the child prior to transfer
    • IV dextrose to maintain blood glucose >4mmol/L
    • Broad spec antibiotics to prevent sepsis
    • IV Vitamin K to prevent haemorrhage
    • H2 blockers or PPIs to prevent haemorrhage from GI tract
    • Fluid restriction to prevent cerebral oedema
    • Mannitol diuresis if oedema develops
47
Q

What are some common causes of chronic liver disease in older children?

A
  • Postviral Hepatitis B or C
  • Autoimmune hepatitis (and sclerosing cholangitis)
  • Non alcoholic fatty liver disease
  • Drug induced liver disease (NSAIDs)
  • Cystic Fibrosis
  • a1-antitrypsin deficiency
  • Fibropolycystic liver disease
  • Wilsons disease should always be excluded
48
Q

How would autoimmune hepatitis (and sclerosing cholangitis) present, be diagnosed, and be treated?

A

Presentation

  • acute hepatitis/ fulminant hepatic failure/ CLD with autoimmune features (skin rash, arthritis, haemolytic anaemia, nephritis)

Diagnosis

  • elevated total protein (= inflammation or infection like hep)
  • hypergammaglobulinaemia (= commonly seen in CLD)
    • best diagnostic marker for AIH is elevated levels of serum immunoglobulin G (IgG)
  • positive autoantibodies (eg. ANA)
  • low serum complement (low levels of C4)

Management

  • AIH = Prednisolone and azathioprine
  • Sclerosing cholangitis = ursodeosycholic acid
49
Q

What is Wilsons disease and how does it present?

A
  • autosomal recessive disorder
  • reduced synthesis of caeruloplasmin (copper binding protein)
  • defective excretion of copper in bile = accumulation of copper in liver, brain, kidney, cornea

Presentation

  • childhood = hepatic presentation eg. acute hepatitis, fulminant hepatitis, cirrhosis, portal HTN
  • >7 years old Copper accumulation in cornea (Kayser-Fleischer rings)
  • >20 years old = neuropsychiatric features (mood change, behaviour change, extrapyramidal signs eg. incoordination, tremor, dysarthria)
  • Renal tubular dysfunction
  • Vit D resistant rickets
  • Haemolytic anaemia
50
Q

How would you diagnose and manage Wilsons disease?

A

Investigations

  • low serum caeruloplasmin and copper
  • Urinary copper excretion is increased (further increases after adminstering penicillamine)
  • Diagnostic = elevated hepatic copper on liver biopsy OR identification of gene mutation

Management

  • Penicillamine or trientine (promote urinary copper excretion)
  • Zinc reduces copper absorption
  • Pyridoxine prevents peripheral neuropathy
51
Q

How would you generally manage the complications of chronic liver disease?

A
  • Fat malabsorption
    • Fat soluble vitamins (K, A, E, D) should be given orally
  • Protein malnutrition due to poor intake & high catabolic rate of diseased liver
    • do not restrict protein intake unless child is encephalopathic
  • Severe Pruritus is associated with cholestasis
    • loose cotton clothing, avoid overheating, keep nails short
    • moisturising skin with emollients
    • Drugs =
      • phenobarbital to stimulate bile flow
      • Cholestyramine to absorb bile salts
      • Ursodeoxycholic acid
      • Rifampicin

​

  • Encephalopathy
    • oral lactulose can help reduce ammonia
52
Q

What is cirrhosis?

A

Extensive fibrosis with regenerative nodules.
Results in diminished hepatic function and portal HTN with splenomegaly, varices, ascites.

53
Q

What are some signs of cirrhosis and why may it not be obvious until later?

A

Sometimes in compensated cirrhosis children may be asymptomatic if liver function is adequate.

Eventually due to increasing cirrhosis, deteriorating liver function and increasing portal HTN become obvious.

Physical signs:

  • jaundice
  • palmar/ plantar erythema
  • telangiectasia
  • spider naevi
  • malnutrition
  • hypotonia
  • dilated abdo veins and splenomegaly suggest portal HTN
  • liver can be shrunken and impalpable
54
Q

How would you investigate cirrhosis?

A
  • screening for known causes
  • upper GI endoscopy to detect oesophageal varices or erosive gastritis
  • Abdo US = shrunken liver and splenomegaly with gastric and oesophageal varices
  • Liver biopsy can indicate aetiology eg. copper storage
  • LFTs (elevated AST and ALP, plasma albumin falls, prothrombin time becomes prolonged)
55
Q

Pathophysiology of oesophageal varices and how you manage them.

A
  • consequence of portal HTN
  • Diagnosis = gastrointestinal endoscopy

Management

  • acute bleeding = blood transfusions, H2 blockers (eg. ranitidine) or omeprazole
  • persistent bleeding = octreotide infusion, vasopressin analogues, endoscopic band ligation, sclerotherapy
  • Surgery = portacaval shunts are a temporary measure while considering liver transplantation
56
Q

How would you manage ascites in cirrhosis?

A
  • sodium and fluid restriction
  • Diuretics
  • Refractory ascites = try albumin infusions or paracentesis
57
Q

What is spontaneous bacterial peritonitis what would you do?

A
  • an infection of the ascitic fluid that cannot be attributed to any intra-abdo, ongoing, inflammatory, or surgically correctable condition
  • Suspect it in undiagnosed fever, abdo pain, tenderness, vomiting, altered mental status, GI bleeding, unexplained deterioration in hepatic/renal function
  • Do a diagnostic paracentesis
  • Defined as an ascitic fluid absolute neutrophil count >250cells/mm3
  • Treat with broad spectrum antibiotics
58
Q

A kid comes in with a rash, low grade fever, and abdo pain. He has bloody diarrhoea and swollen painful joints.

He has a hx of a past strep infection.

What do you suspect?

A

Henoch-Schonlein Purpura

  • it is a small vessel vasculitis
  • typically post streptococcal infection eg. Group A Strep, EBV
  • Starts with a low grade fever and abdo pain, then purpuric rash.
  • Can have blood diarrhoea and swollen painful joints
  • The rash is macular but progresses to papaulae in the classic buttock and back of leg location
  • Renal involvement
59
Q

How would a congenital diaphragmatic hernia present?

A

Herniation of abdo viscera into chest due to incomplete formation of diaphragm

  • scaphoid abdo due to herniation of abdo contents into cleft
  • classical concave abdo appearance
  • dyspnoea and tachypnoea
  • reduced breath sounds bilaterally due to pulmonary hypoplasia and compression of lungs due to abdo contents

Most common is the L sided posterolateral Bochdalek hernia

4th Year (17 decks)

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