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Pathophysiology > Other acquired abdominal disorders > Flashcards

Other acquired abdominal disorders Flashcards

1
Q

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

A
  • 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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2
Q

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

A
  • 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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3
Q

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

A
  • 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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4
Q

What are the causes of GI bleeding in adolescents?

A
  • 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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5
Q

What is 99m Tc-dimercaptosuccinic acid used for?

A
  • 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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6
Q

What is 99m Tc-mercaptoacetyltriglycine?

A
  • 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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7
Q

What is Diethylenetriamine penta-acetic acid?

A
  • 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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8
Q

What is hydroxyiminiodiacetic acid?

A
  • 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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9
Q

What is di-isopropyl iminodiacetic acid?

A
  • 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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10
Q

What is Tc 99m sodium pertechnetate?

A
  • 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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11
Q

What is metaiodobenzylguanidine?

A
  • 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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12
Q

What is FDG PET and how does it work?

A
  • 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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13
Q

What are the functions of the spleen?

What is OPSI?

A
  • 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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14
Q

Describe the histopathology of isolated juvenile polyps

A
  • 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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15
Q

What is the proposed pathogenesis of juvenile polyps?

A
  • 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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16
Q

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

A
  • 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
17
Q

What is Gardner Syndrome?

A
  • 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.
18
Q

What is Turcot Syndrome?

A
  • Turcot syndrome refers to colonic familial adenomatous polyposis AND extracolonic tumours.
    • Glioblastoma
    • Medulloblastoma
    • Ependymomas
    • Thyroid carcinomas
19
Q

How would you classify the juvenile polyposis syndromes?

A
  • 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
20
Q

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

A
  1. Hamartomatous polyps - 80%
  2. Lymphoid polyps - 15%
  3. Adenomatous polyps - 3%
21
Q

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

A
  • Isolated/Non-syndromic biliary atresia (80-85%)
  • Syndromic (10-20%) - biliary atresia splenic malformation syndrome
  • Cystic biliary atresia
  • CMV associated biliary atresia
22
Q

What are the 3 pathological subtypes of isolated biliary atresia?

A
  • 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.
23
Q

What are the theories of the pathogenesis of biliary atresia?

A
  • 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.
24
Q

What are 5 post operative complications in biliary atresia?

A
  • 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)
25
Q

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

A
  • 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.
26
Q

Name 5 common causes of paediatric pancreatitis (6 classes)

A
  • 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
27
Q

Describe 3 types of pancreatic disease in the newborn period.

A
  • 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.
28
Q

Name 3 pancreatic tumours

A
  • 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
29
Q

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

A
  • 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.
30
Q

Describe the Todani classification

A
  • 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.
31
Q

Which choledochal cysts are congenital and which are acquired?

A
  • 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.
32
Q

What factors contribute to rectal prolapse in children?

A
  • 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
33
Q

Give examples of primary intussusception and secondary intussusception

A
  • 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
34
Q

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

A
  • 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

Pathophysiology (7 decks)

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