Other acquired abdominal disorders Flashcards by Ben Wagstaff

What are the causes of GI bleeding in a newborn (<1 month of age)?

Upper GI:
- Common
  - Swallowed maternal blood (can test by APT test - mix vomit with 1% sodium hydroxide - maternal blood will turn brown).
  - Oesophagitis
  - Gastritis (usually stress related, exacerbated by prematurity, mechanical ventilation) - 20% in NICU
  - Cows milk allergy
- Uncommon
  - Coagulopathy
  - Haemorrhagic disease of the newborn (lack of vitamin K).
  - Sepsis
Lower GI:
- Common
  - Anal fissure (most common cause in first 2 years of life).
  - NEC
  - Malrotation with volvulus
  - Hirschsprung associated enterocolitis
- Uncommon
  - Thrombocytopaenia
  - Vascular malformation (haemangioma, haemangiomatosis).

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What are the causes of GI bleeding in an infant (1 month to 2years)?

Upper GI
- Common
  - Oesophagitis
  - Gastritis
  - Gastrostomy/tube trauma
- Uncommon
  - Foreign body
  - NSAID
  - Pyloric stenosis/repeated vomiting.
Lower GI
- Common
  - Anal fissure
  - Meckel diverticulum
  - Intussusception
  - Lymphonodular hyperpleasia
  - Infectious diarrhoea
  - Allergic proctocolitis
  - Eosinophilic gastroenteropathy
- Uncommon
  - Thrombocytopaenia
  - Foreign body
  - Intestinal duplication
  - Gangrenous bowel

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What are the causes of GI bleeding in children aged 2-12yrs?

Upper GI:
- Common
  - Oesophagitis
  - Gastritis
- Uncommon
  - Foreign body
  - Vascular malformations
Lower GI:
- Common
  - Polyps
    - Juvenile/retention polyps (common between 3 and 5 years of age).
    - Bleeding occurs when - the rate of growth of the polyp exceeds the blood supply - sloughs off stalk, OR when polyp injured in passage of stool
  - Lymphonodular hypoplasia
  - Meckel Diverticulum
  - Infectious diarrhoea
  - Anal fissure
  - Eosinophilic gastroenteropathy
  - Inflammatory bowel disease
- Uncommon
  - Henoch-Schonlein Purpura
  - Haemolytic uraemic syndrome (Associated with verocytotoxin producing - E Coli → bloody diarrhoea)
  - Vascular malformations
    - Klippel-Trenaunay Syndrome
    - Rendu-Osler-Weber syndome
    - Proteus
  - Chemotherapy

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What are the causes of GI bleeding in adolescents?

Upper GI
- Common
  - Oesophageal or gastric varices
  - Peptic ulcer (H pylori)
  - Gastrostomy tube trauma
  - Gastritis/Oesophagitis
- Uncommon
  - Chemo
  - NSAIDs
  - Mallory-Weiss tear
  - Eosinophilic gastroenteropathy
Lower GI
- Common
  - Infectious diarrhoea
  - Anal fissure
  - Eosinophilic gastroenteropathy
  - Inflammatory bowel disease
- Uncommon
  - HSP
  - Chemo

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What is 99m Tc-dimercaptosuccinic acid used for?

99m Tc-dimercaptosuccinic acid (DMSA) is the radioisotope used in the DMSA (static renal scintigraphy)
- DMSA is a marker of renal perfusion and function, as well as focal areas of dysfunction/reduced uptake = scarring (gives no indication of drainage as there is minimal excretion in the urine).
  - Binds to proximal tubules at renal cortex.
- To be accurate, must be performed 4-6 weeks post birth (as renal function too immature prior).

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What is 99m Tc-mercaptoacetyltriglycine?

99m Tc-mercatoacetyltriglycine (MAG3) is a radioisotope used in dynamic renal scintigraphy.
- MAG3 assesses both renal function and excretion/drainage.
  - Differential function of kidneys
  - Drainage from collecting system and renal pelvis.
    - Limitation:
      - Doesn’t give GFR (DTPA) and less accurate for function (DMSA)
      - Doesn’t account for focal scarring (DMSA)
- MAG3 is absorbed by the proximal tubules and actively secreted in the distal part of the proximal tubule.

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What is Diethylenetriamine penta-acetic acid?

Diethylenetriamine penta-acetic acid (DTPA) is a radioisotope used in dynamic renal scintigraphy.
- Gives assessment of renal function (differential) and drainage.
- Removed from blood by glomerular filtration (can give accurate GFR)
- Limitations:
  - Less accurate that MAG3 for younger children (reduced GFR/extraction rate).

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What is hydroxyiminiodiacetic acid?

Hydroxyiminiodiacetic acid (HIDA) is a radioisotope used in hepatobiliary scintigraphy.
- HIDA is taken up by hepatocytes and secreted into biliary system.
  - Uses:
    - Biliary atresia - HIDA is quickly taken up by hepatocytes but there is no evidence of excretion at 24 hours.
    - Cholelithiasis/GB dyskinesia - assesses effectiveness of GB contraction and drainage.
  - Limitations:
    - Significant false positive rate in BA due to delayed uptake or excretion.

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What is di-isopropyl iminodiacetic acid?

Di-isopropyl iminodiacetic acid (DISIDA) is a radioisotope used in hepatobiliary scintigraphy.
- Taken up by hepatocytes, secreted into biliary system.
  - Similar uses to HIDA.

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What is Tc 99m sodium pertechnetate?

99m Tc-pertechnetate is the radio-isotope used in Meckel’s scan.
- Taken up by parietal cells in gastric mucosa.
  - Useful in localising Meckel diverticulum because see uptake outside the stomach.
  - Limitation:
    - Not all Meckel diverticulum have ectopic gastric mucosa.

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What is metaiodobenzylguanidine?

Metaiodobenzyguanidine (MIBG) is the radioisotope used in diagnosis and treatment of neuroblastoma.
- MIBG is a noradrenaline analogue bound to radioactive iodine.
  - Transported to, stored in the chromatin cells (in the same way as noradrenaline).
- Uses:
  - Diagnostic
    - Taken up by neuroblastoma - allows for localisation of the tumour
  - Therapeutic
    - Higher doses of radioactive iodine can be attached to the MIBG → absorbed by the tumour → directed, localised therapy of high dose radiation.

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What is FDG PET and how does it work?

FDG = fluorinated analogue of glucose
PET = positron emission tomography
- Radioactive tracer isotope combined with biological/carrier molecule such as a glucose analogue (FDG).
- Absorbed by tissues with high metabolic rate.
- Tracer released positively charged ‘positron’ that collide with electrons to release gamma rays (photons) which are collected and analysed by the PET scanner.
Used in tumour diagnosis, localisation, staging, monitoring and screening for recurrence.

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What are the functions of the spleen?

What is OPSI?

Spleen composed of white pulp and red pulp.
- White pulp - composed of lymphocytes and macrophages arranged around a central artery,
  - Antigen presentation -
    - Macrophages and dendritic cells (antigen presenting cells) come in contact with T cells in white pulp.
    - T-cells become activated by the antigen and travel to the follicle whereby B-cells convert to plasma cells and begin making antibodies to combat the antigen (IgG or IgM)
  - Viral infection
    - Virus enters the white pulp via the central arteriole.
    - Virus comes into contact with the follicular B cells which activate them OR macrophages which then present to B cells.
    - B cells become plasma cells and begin making antibodies to combat the virus,
- Red pulp
  - Cords of Billroth are full of macrophages.
  - RBCs enter the red pulp via central arteriole, and then enter venous sinuses by passing through slits between endothelial cells.
    - Old or deformed RBCs are unable to pass through slits and instead become phagocytosed by surrounding macrophages.
  - Opsonised pathogens are destroyed by macrophages in the red pulp.

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Describe the histopathology of isolated juvenile polyps

Isolated juvenile polyps (juvenile retention polyps, inflammatory polyps, cystic polyps) = 80% of paediatric polyps.
- Hamartomas, benign.
  - Surface is single layer of epithelium
  - Main body of polyp consists of dilated, cystic epithelial tubules lined by normal colonic epithelium. Embedded in a lamina propria and and abundant loose, vascular fibrous storm.
  - Often heavily infiltrated with leucocytes
  - NO MITOTIC FIGURES
- Thought to occur as a structural rearrangement of the mucosa secondary to an inflammatory process.

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What is the proposed pathogenesis of juvenile polyps?

Rearrangement of the colonic mucosa secondary to an inflammatory process.
- Inflammation/ulceration of the mucosa
- Obstruction of colonic glands within mucosa
- Proliferation of obstructed glands → branch and dilated to form cystic structure.
- Cystic structure elevates mucosa as it dilates.
- Causes further ulceration, inflammation and formation of granulation tissue.
- Continues to occur until polyp formed.
  - Peristalsis pushes polyp downstream, elongating the stalk of polyp.

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What is familial adenomatous polyposis? What gene is involved? What tumours are associated?

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FAP refers to a condition associated with the deletion of the adenomatous polyposis coli (APC) gene.
- Causes hundreds to thousands of adenomatous polyps in the colon.
- Defined as > 100 visible polyps within the large intestine.
  - Associated with:
    - Colorectal cancer (100% by age 39)
    - Papillary thyroid cancer
    - Stomach
    - Hepatobiliary cancers

What is Gardner Syndrome?

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Gardner syndrome refers to findings of familial adenomatous polyposis (APC gene deletion) and extracolonic findings.
- Extensive GI polyps
- Osteomas (mainly craniofacial and associated with dental abnormalities)
- Sebaceous/epidermoid cysts on legs, face, scalp and arms.
- Lipomas and fibromas
- Desmoid tumours of the abdominal wall and mesentery of the small bowel (20%)
  - Desmoid tumours are the leading cause of death in patients who have had prophylactic colectomy.
Autosomal dominant inheritance.

What is Turcot Syndrome?

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Turcot syndrome refers to colonic familial adenomatous polyposis AND extracolonic tumours.
- Glioblastoma
- Medulloblastoma
- Ependymomas
- Thyroid carcinomas

How would you classify the juvenile polyposis syndromes?

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Juvenile polyposis syndromes are associated with hamartomatous polyps. They can be divided by age.
- 0-3 months:
  - Diffuse juvenile polyposis of infancy.
    - Presents in the first few months of life with diarrhoea, rectal bleeding, intussusception, protein losing enteropathy.
- 6 months to 5 years:
  - Diffuse juvenile polyposis
    - Presents between 6 months and 5 years - mild rectal bleeding, prolapse, intussusception and protein losing enteropathy.
- 5yrs to 15yrs:
  - Juvenile polyposis coli
    - Presents with bright red rectal bleeding, anaemia, rectal prolapse.
    - Polyps are usually in the distal colon and rectum.
    - Usually associated with cleft palate, malrotation, polydactyly and abnormalities of the heart and cranium

What are the three classifications of GI polyps in children, and what is their frequency?

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Hamartomatous polyps - 80%
Lymphoid polyps - 15%
Adenomatous polyps - 3%

What are the four types of biliary atresia (clinical classification)

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Isolated/Non-syndromic biliary atresia (80-85%)
Syndromic (10-20%) - biliary atresia splenic malformation syndrome
Cystic biliary atresia
CMV associated biliary atresia

What are the 3 pathological subtypes of isolated biliary atresia?

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Type I: Atresia of CBD only
Type IIa: Atresia of common hepatic duct only
Type IIb: Atresia of CBD and common hepatic ducts
Type III: Atresia of all extra-hepatic ducts extending into the port.

What are the theories of the pathogenesis of biliary atresia?

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Pathogenesis is likely multifactorial.
- Viral - reovirus 3, CMV, EBV exposure in utero thought to contribute.
- Autoimmune - higher levels of HLA-B12 antigen in babies with BA (immune mediated damage to biliary epithelial cells and hepatocytes by cytotoxic T cells/inflammatory cytokines).
- Genetic - likely accounts for syndromic BA. CFC1 gene implicated in some.
- Embryological - abnormalities in ductal plate remodelling.

What are 5 post operative complications in biliary atresia?

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Cholangitis
Portal hypertension (intrahepatic changes → biliary cirrhosis → portal hypertension)
Cirrhosis (disease progression)
Hepatopulmonary syndrome (diffuse intrapulmonary shunting as a result of vaso-active compounds from portal circulation not being deactivated by liver).
Intrahepatic bile lake cysts - associated with bile stasis, bacterial colonisation and recurrent cholangitis.
Malignancy (cirrhosis → HCC or cholangiocarcinoma)

What risk factors/conditions are associated with cholelithiasis? What are the two most common types of stones?

* _Risk factors_: * Obesity * Haemolytic anaemias (sickle cell disease, hereditary spherocytosis, thalassaemia) * Cystic fibrosis * Prolonged TPN/short gut syndrome * Mast cell activation * Familial hypercholesterolaemia * _Cholesterol stones_ - most common - supersaturation of bile by excess cholesterol. * _Pigmented stones_ - associated with haemolytic anaemias.

Name 5 common causes of paediatric pancreatitis (6 classes)

* _Viral illness_: coxsackie, mumps, rubella * _Trauma_ * _Ductal anomalies (up to 33% of pediatric pancreatitis)_ * Pancreaticobiliary malunion * Pancreas divisum * Choledochal cyst * Choledocholithiasis * _Drugs (25% of pediatric pancreatitis)_ * Azathioprine * Tetracyclines * _Metabolic_ * Hypertriglyceridaemia * _Systemic illness_ * Cystic fibrosis * Reyes Syndrome * Kawasaki disease

Describe 3 types of pancreatic disease in the newborn period.

* _Pancreatic insufficiency (exocrine)_ - associated with cystic fibrosis. * _Congenital hyperinsulinism (permanent)_ * Genetic mutation resulting in abnormal K+ channels in pancreatic beta cells → continuous unregulated insulin secretion → hypoglycaemia. * _Hyperinsulinaemic hypoglycaemia (transient)_ * As seen with Beckwith-Wiedemann, maternal diabetes, IUGR, birth asphyxia.

Name 3 pancreatic tumours

* **_Neuroendocrine tumours_** * _Insulinomas_ (most common) * 10% malignant * Whipple triad - fasting hypoglycaemia, symptoms of hypoglycaemia, relief with glucose. * May be associated with MEN1 * _Gastrinomas_ * Primary source of foetal gastrin is the pancreas, gastric antrum takes over after birth. * Frequently malignant. * **_Pancreatic exocrine tumours_** * _Pancreaticoblastoma_ (most common) * Due to persistence of embryonic pancreatic progenitor cells beyond 8/40 gestation. * _Acinar cell carcinoma_

Name 3 anatomical variations of the pancreas and how they contribute to disease (4)

* _Annular pancreas (1 per 20000)_ * Errors in rotation of the ventral bud or fusion of the accessory duct → annular pancreas. * Associated with duodenal stenosis and duodenal atresia. * _Pancreas divisum_ * Failed fusion of the accessory and pancreatic ducts → main pancreatic duct drains via minor papilla. * Associated with both acute and chronic pancreatitis * _Pancreaticobiliary malunion_ * Long common channel, reflux of bile into pancreas → chemical inflammatory process → pancreatitis * _Congenital short pancreas_ * Associated with polysplenia * Deficiency of tissue in the pancreatic body and tail secondary to agenesis of the dorsal pancreatic bud.

Describe the Todani classification

* Type I are the most common. * 90% of all choledochal cysts are either Type I or Type Iva. * Type V = Caroli disease * Segmental saccular dilatation of the intrahepatic bile ducts.

Which choledochal cysts are congenital and which are acquired?

* Congenital cysts appear to develop as a result of a prenatal structural defect in the bile duct (fewer ganglion cells on histopath) * Acquired cysts occur secondary to an abnormally long pancreaticobiliary common channel (pancreaticobiliary malunion). * Long channel allows reflux of proteolytic pancreatic enzymes into biliary tree → epithelial and mural damage → dilatation. * Likely Type I and Type IV.

What factors contribute to rectal prolapse in children?

* Rectal prolapse caused by a combination of factors: * **Weakness of the pelvic levator musculature** * Doesn't improved with time. * Straining on the toilet weakens pelvic floor. * **Loose attachment of the rectal submucosa to the underlying muscularis** * Usually improves with time. * _Associated with_: * _Cystic fibrosis_ (20% of rectal prolapse in children \< 3yrs associated with CF) * Increased abdominal pressure associated with coughing → weakens levator * Inspissated stools → constipation → further damage to pelvic floor. * _Spina bifida_ * Paralysis of levator ani + raised intra-abdominal pressure → prolapse. * _Iatrogenic_ * Anorectal malformations - usually mucosa only. * Hirschsprung Disease * _Connective tissue disorders_ * Loose attachments between submucosa and muscularis → prolapse

Give examples of primary intussusception and secondary intussusception

* _Primary intussusception_ = idiopathic - 2months to 2yrs * Often associated with viral illness (respiratory or gastroenteritis) * High rates of lymphatic tissue in distal ileum and appendix can become enlarged (lymphoid hyperplasia) → gripping/lead point. * Rotavirus and adenovirus are implicated in up to 50% of cases. * _Secondary intussusception_ = pathological lead point = children \<2months or \>3years. * Meckel diverticulum * Polyp * Peutz-Jehger * Juvenile polyps or polyposis syndrome * Inflammatory lesion * HSP - IgA deposition and oedema. * Duplication * Lymphoma * Cystic fibrosis

What is recurrent abdominal pain of childhood? What are differential diagnoses?

* Recurrent abdominal pain of childhood refers to \> 3 episodes of abdominal pain over at least 3 months. * Functional (non-organic) in 90-95% of children * Abdominal migraine * Irritable bowel syndrome * Functional dyspepsia * Chronic constipation * Organic in 5-10% * Coeliac disease * Constipation * Gastritis * GORD

Other acquired abdominal disorders Flashcards

(34 cards)