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Gastroenterology > Normal function and Malabsorption > Flashcards

Normal function and Malabsorption Flashcards

1
Q

What are the 3 regions of the primitive gut tube that gives rise to the organic of the GI tract?

A

Foregut
- pharynx to proximal of duodenum
- includes the liver, gall bladder and pancreas
Midgut
- distal half of duodenum to proximal 2/3 of transverse colon
Hindgut:
- distal 1/3 of transverse colon to rectum
- includes urogenital sinus

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2
Q

The persistence of Vitelline duct results in what condition?

A

Merkel’s diverticulum

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3
Q

What protein is required for the normal formation of enteral ganglia?

A 
RET protein (receptor tyrosine kinase) 
- mutations of this results in Hirschsprung's disease
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4
Q

What are parietal cells?

A

Epithelial cells that secrete hydrochloric acid, found in the gastric glands in funds and cardia of stomach

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5
Q

What controls the secretion of HCl?

A

Cephalic phase

  • sight / taste / smell of food triggers this phase
  • postganglionic cholinergic fibres of vagus nerve releases acetylcholine / serotonin which then stimulate mast cells to produce histamine
  • ~30% total HCl released

Gastric phase

  • food ingestion / astral dilation / intragastric protein / pH > 3 stimulate secretion of gastrin from antrum of stomach and results in increased acid production
  • ~50-60%

Intestinal phase

  • chyme arriving at duodenum results initially increases acid secretion then it inhibits it by stimulating sympathetic neurone and increasing duodenal enteroendocrine cells to release secretin and cholecystokinin
  • reduces gastric mobility too
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6
Q

What does the gastric chief cells secrete?

A

Pepsinogen and gastric lipase

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7
Q

What does sucrose (disaccharides) get hydrolysed to?

A

Glucose and fructose

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8
Q

What does lactose (disaccharides) get hydrolysed to?

A

Glucose and galactose

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9
Q

What are fat soluble vitamins?

A

Vitamin A, D, E and K

  • dependent on micellar solubilisation (i.e adequate bile production)
  • vit A and D require hydrolysis by pancreatic enzymes before absorption
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10
Q

What is the most sensitive test for carbohydrate malabsorption?

A

Breath Hydrogen testing

  • released by fermentation of unabsorbed carbohydrate in the colon by intestinal bacterial flora
  • most common indication: lactose malabsorption
  • also used for sucrose / fructose malabsorption
  • screening for intestinal bacterial overgrowth
  • useful for measuring intestinal transit time
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11
Q

What is the preferred method of assessing protein-losing enteropathy in children?

A

Alpha-1 antitrypsin clearance

  • compare serum level and level from stools (24hr collection)
  • clearance value can then be calculated
    • alpha-1 antitrypsin is similar molecular weight to albumin and resistant to digestion in GI tract**
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12
Q

What are the chances of first degree relatives having Coeliac’s disease?

A

10% in 1st degree
30-40% in HLA identical siblings
60-70% concordance in identical twins

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13
Q

What is the chance that someone has coeliac’s disease if HLA D2 / D8 are negative?

A

Very very low!

Only 1% of people of coeliac’s disease will have negative HLA DQ2 or DQ8

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14
Q

What is coeliac disease?

A

Autoimmune (T-cell immune response) disease resulting in enteropathy

  • Essential immunological event is blinding of gliadin by HLADQ2 molecule for antigen presentation to TH1 cells
  • i.e type IV hypersensitivity
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15
Q

What is abetalipoproteinaemia?

A

Rare, autosomal recessive disorder that results in lack of apolipoprotein B so TAG’s can’t be packaged into chylomicrons –> low VLDL and LDL’s in blood

  • results in severe malabsorption from birth
  • FTT
  • assoc with peripheral neuropathy from Vit E deficiency, intellectual impairment and cerebella ataxia
  • atypical retinitis pigmentosa from adolescence

Rickets may be unusual initial px caused by steatorrhoea induced calcium losses and vit D deficiency

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16
Q

What is cystinuria?

A

Relative common, autosomal recessive disease, characterized by high concentrations of the amino acid cysteine in the urine, leading to the formation of cystine stones.

  • dx must be excluded in anyone with renal stones
  • check urinary cystine
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17
Q

What is glucose-galactose malabsorption?

A

Rare, autosomal recessive disease due to defect in sodium-glucose cotransporter gene (SGLT1) resulting in osmotic diarrhoea from birth and can cause death from dehydration.
Glycosuria often present even though BSL low.
Stools are acidic / positive for reducing substance
Breath hydrogen test positive
Manage by restricting glucose and galactose, fructose is safe

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18
Q

What’s the most common cause of malabsorption in children?

A

Lactase deficiency

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19
Q

What is intestinal lymphangiectasia?

A

Protein losing enteropathy due to dilation of intestinal lymphatic vessels.
Elevated Faecal alpha-1-antitripysin level will be consistent with protein losing enteropathy
Small bowel biopsy is diagnostic

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20
Q

What causes intestinal lymphangiectasia?

A

Primary
- assoc with turners and noonans
Secondary
- Chronic R) heart failure, constrictive pericarditis
- disturbance to lymphatic system from surgery / obstruction from malrotation or retroperitoneal tutor

21
Q

What are the symptoms / signs of intestinal lymphagiectasia?

A

Steatorrhoea
Low alb and generalised oedema
Recurrent infections due to low IgG and lymphocytopenia (leakage of lymphocytes into gut)
Chylous ascites

22
Q

What is microvillus inclusion disease?

A

Rare malabsorption disorder that seems to be inherited in an AR pattern.
Most common cause of persistent diarrhoea (intractable watery) that begins in neonatal period.
Pathology includes
- Villous atrophy
- crypt hypoplasia
- microvillus inclusions in enterocytes and coloncytes
Managed to octreotide (somatostatin analogue) to reduce volume of stools
Needs lifelong TPN / intestinal transplant

23
Q

What is tufting enteropathy?

A

AR disorder resulting in intestinal epithelial dysplasia
- symptomatic with watery diarrhoea
- present in first few weeks (not like microvillus inclusion disease where it is present immediately after birth
Found in middle eastern population - esp island of Gozo in Malta
Needs lifelong TPN / intestinal transplantation

24
Q

What is the energy of fat / protein / carbohydrate?

A

Fat 10kcal/g
Protein 4kcal/g
CHO 4kcal/g

25
Q

What is absorbed in the duodenum and the proximal jejunum?

A

Calcium, magnesium, phosphorous, iron and folic acid

26
Q

What is absorbed in the proximal 100-200cm of small bowel?

A

Carbohydrate, protein, water soluble vitamin

27
Q

What is absorbed throughout small intestines?

A

Monoglycerides, fatty cards and MCT

28
Q

What is absorbed in the distal ileum?

A

Vitamin B12 and bile acids

29
Q

What is absorbed in the colon?

A

Water and electrolytes

30
Q

Why does renal stones occur with malabsorption?

A

When there is large amounts of unabsorbed fat available, calcium binds to fat instead of oxalate. Increased oxalate is then absorbed and excreted in renal tract

31
Q

How to test for fat absorption?

A

Fat balance studies (not diagnostic)
Done over 3 days and have to measure fat intake also to calculate % with below formula
- [fat intake - (faecal fat losses / fat intake] x 100
Useful in monitoring enzyme replacement therapy in CF

32
Q

What investigations are available for exocrine pancreatic function?

A

Faecal elastase

  • stable endoprotease unaffected by exogenous pancreatic enzymes
  • Does lack full differentiation between primary exocrine pancreatic insufficiency vs exocrine pancreatic dysfunction secondary to intestinal villous atrophy (reduced pancreoenzyme / cholecystokinin secretin leading to pancreatic insufficiency)
  • false positive in acute diarrhoea

Serum tyrinsinogen

  • raised in CF early in life then gradually falls
  • Levels in shwachman-diamond syndrome is low
33
Q

What will the histology of coeliac disease look like?

A

Loss of absorptive villi
Hyperplasia of crypts
Presence of lymphocytes

injury greatest in proximal small bowel

34
Q

What are the differential diagnoses for intestinal villi atrophy?

A 
Small intestinal lymphoma 
Crohns
Eosinophilic gastroenteritis 
Giardia
Tropical sprue 
Whipple disease
35
Q

What is tropical sprue?

A

Major cause of malabsorption / endemic in South India, Phillipines, Islands in Caribbean
Follows outbreak of acute diarrhoea illness and improves with antibiotics
Sx: fever / malaise / followed by watery diarrhoea then 1 week later, sx resolves then develops anorexia / chronic absorption
O/e: glossitis, stomatitis, cheilosis, night blindness, oedema
To prevent occurrence: 6m therapy with oral folic acid and tetracyclines or sulphonamides

36
Q

What is whipple disease?

A

Chronic systemic infectious disorder secondary to Tropheryma whippelii (gram positive bacterium) which can be cultured from a lymph node in involved tissue
Presents with diarrhoea / abdo pain / weight loss / joint pain
Associated with malabsorption / lymphadenopathy / skin increased pigment and neurological changes

37
Q

What % of small bowel loss will result in malabsorption?

A

50%

NB: typical length of small bowel

  • neonate: 200-300cm
  • adult: 600-800cm
38
Q

What are the causes of malabsorption in short gut syndrome?

A 
Reduced surface area 
Rapid transit
Suboptimal bowel function 
Acide hypersécrétion 
Bile acid deficiency 
Bacterial overgrowth - injury intestinal mucousa further
39
Q

What are the clinical features of short gut syndrome?

A

FTT
Steatorrhoea
Hyponatraemia, hypokalaemia
Acidosis with anions gap in absence of elevated serum lactate (bacterial overgrowth can cause malabsorption and metabolic acidosis secondary to bacterial production of D-lactate which can’t be metabolised by humans and not measured by lab)

40
Q

What is the prognosis of short gut syndrome?

A

Can usually come off TPN
- >25cm small bowel and intact ileocecal valve
- >40cm w/o IC valve
(ileocecal valve resection results in greater tendency to bacterial overgrowth and subsequent mucosal damage)

Small bowel bacterial overgrowth has been associated with prolonged dependence on TPN

41
Q

What are complications of short gut syndrome?

A 
FTT 
Water / sodium depletion 
Nutrient deficiencies 
Renal stones 
Gallstones 
Liver disease
Late VB12 deficiency 
D-lactic acidosis
42
Q

What are the differences between fat globules and fat crystals?

A

Fat globules = problem with digestion (problem with pancreatic enzymes or bile salts)
Fat crystals = problem with absorption = (mucosal abnormality)

43
Q

What are the differentials for malabsorption?

A

Can be divided into:

  • Lumen
  • Cell related: Reduced integrity of mucosa, Enzyme deficiency, Transport defects, Substrate overload, Immune related, Altered secretory function
  • Lymphatics
  • Structural
44
Q

What are luminal causes of malabsorption?

A 
Exocrine pancreatic insufficiency 
- CF
- Schwachman-Diamond syndrome 
- Johansson-Blizzard syndrome 
- Chronic pancreatitis 
Bile acid disorder 
- Chronic cholestasis 
- Terminal ileum resection 
- Bacterial overgrowth 
- Primary bile acid malabsorption
45
Q

What are the causes of reduced integrity of mucosa that can lead to malabsorption?

A
  • infection / post-infection
  • cow’s milk intolerance
  • coeliac disease
  • IBD
  • Tufting enteropathy
46
Q

What are causes of enzyme deficiency that can lead to malabsorption?

A

Lactase deficiency
Sucrase-isomaltase deficiency
- primary disaccharide deficiency **sucrose is not a reducing sugar so is clingiest negative unless you add HCl
Hereditary fructose intolerance
- primary monosaccharide issue secondary to deficiency in 1, 6 bisphonate aldolase
- early clinical manifestation resembles galactossaemia w jaundice, hepatomegaly, vomiting, lethargy, irritabliliy and convulsions
Enterokinase deficiency
- Trypsinogen can’t turn into trypsin and in turn, can’t active other proteases or cleave cocolipase –> collapse
- presents really unwell in early infancy with severe diarrhoea and FTT
- Treat with pancreatic enzyme replacement

47
Q

What are transport defects that can cause malabsorption?

A

Glucose-galactose malabsorption

  • Abnormality in the Na-glucose co-transporter
  • affects GIT > renal
  • positive reducing sugars
  • can result in low BSL / dehydration
  • treat with fructose based formula
Chloride-losing diarrhoea 
- severe watery diarrhoea 
- presents with alkalosis, hypochloraemia, hypokalaemia 
- potentially fatal 
Sodium diarrhoea 
- Na/H exchanger defect 
- met acidosis, hypoNa 
- associated with polyhydramnios 
Acrodermatitis enteropathica

Amino acid transport defects

  • Hartnup disease (malabsorption of neutral amino acid including tryptophan which is a precursor for serotonin, melatonin, niacin; symptomatic with photosensitive pellagra-like rash, headaches, cerebellar ataxia, dev. delay, diarrhoea)
  • Methionine malabsorption (purple, red-brown coloured urine with cabbage odour; symptoms include white hair, near signs, diarrhoea)
  • Blue-diaper syndrome (malabsorption of tryptophan and results in bluish discolouration in nappy)

Abetalipoproteinaemia
Microvillus inclusion disease

48
Q

What are immune-related causes for malabsorption?

A

Autoimmune enteropathy
CVI / AIDS / IgA deficiency
Eosinophilic gastroenteropathy

Gastroenterology (5 decks)

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