IntersessionW1L13 Diarrhoea and Malabsorption Flashcards

1
Q

How much fluid enters the GIT each day by oral ingestion?

A

2L

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2
Q

How much fluid is secreted by the stomach each day?

A

3L

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3
Q

Where is most fluid absorbed by GIT? How much is absorbed at this site?

A

Proximal SI, 7L.

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4
Q

What does the colon do? (main function)

A

Absorbs water- 1800ml. Standby area so you are not incontinent.

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5
Q

Where is Fe absorbed?

A

Proximal SI

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6
Q

How is B12 absorbed (steps)?

A
  1. Eat vitamin B12 from animal products—–
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7
Q

How is B12 absorbed (steps)?

A
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8
Q

What are the enzymes that break down carbohydrates?

A

Salivary amylases Pancreatic amylases Brush border enzymes

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9
Q

What are the enzymes that break down carbohydrates?

A

Salivary amylases Pancreatic amylases Brush border enzymes

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10
Q

What are the factors that break down proteins?

A

HCL, gastric pepsin, pancreatic proteases (peptidases)

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11
Q

What are the factors that break down fats?

A

Bile, pancreatic lipase

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12
Q

Define diarrhoea and chronic diarrhoea

A

abnormal liquidity of stool and stool > 200 g/day and number of movements > 3/day Considered chronic if persists > 4 weeks

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13
Q

What are the 4 mechanisms of diarrhoea?

A

osmotic, secretory, inflammatory & altered intestinal motility

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14
Q

How can you distinguish between large and small bowel diarrhoea?

A

Volume can indicate location and pathological mechanism e.g. large volume (> 750 mL/d) imply small bowel disease (and secretory diarrhoea); small volume stools are typical for colonic diseases and IBS

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15
Q

What is faecal elastase a test of?

A

Marker of exocrine pancreatic sufficiency

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16
Q

What is faecal calprotectin a marker of?

A

GI inflammation

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17
Q

What is a stool osmotic gap and what is it used for?

A

Used to distingish secretory and osmotic diarrhoe. It is calculated with the equation 290 − 2 * (stool Na + stool K). The 290 is the value of the stool osmolality. Low stool osmolic gap (100 mosm/kg) = osmotic diarrhoea. The reason for this is that secreted Na and K ions make up a greater percentage of the stool osmolality in secretory diarrhoea, whereas in osmotic diarrhoea, molecules such as unabsorbed carbohydrates are more significant contributors to stool osmolality. A normal gap is between 50 and 100 mosm/kg. High osmotic gap (>100 mosm/kg) causes of osmotic diarrhea include celiac sprue, chronic pancreatitis, lactase deficiency, lactulose, laxative use/abuse, and Whipple’s disease.

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18
Q

What is a stool osmotic gap? How do you calculate it? What do high and low gaps imply and why?

A

Used to distingish secretory and osmotic diarrhoe. It is calculated with the equation 290 − 2 * (stool Na + stool K). The 290 is the value of the stool osmolality. Low stool osmolic gap (100 mosm/kg) = osmotic diarrhoea. The reason for this is that secreted Na and K ions make up a greater percentage of the stool osmolality in secretory diarrhoea, whereas in osmotic diarrhoea, molecules such as unabsorbed carbohydrates are more significant contributors to stool osmolality. A normal gap is between 50 and 100 mosm/kg. High osmotic gap (>100 mosm/kg) causes of osmotic diarrhoea include celiac sprue, chronic pancreatitis, lactase deficiency, lactulose, laxative use/abuse, and Whipple’s disease.

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19
Q

SECRETORY diarrhoea: Caused by: Common causes: Stool volume: Stool osmotic gap: Effect of fasting: Stool leukocytes (WBC):

A

Due to active anion secretion from enterocytes Bacterial toxins (cholera, toxigenic E.coli), hormone secreting tumours (e.g. carcinoid, gastrinomas), laxative abuse, hyperthyroidism Stool volume > 1 litre/d, watery Normal osmolality (osmolar gap

20
Q

OSMOTIC diarrhoea: Caused by: Common causes: Stool volume: Stool osmotic gap: Effect of fasting: Stool leukocytes (WBC): H2/methane breath test:

A

Presence of excess unabsorbed substrates in gut lumen Fermentable carbohydrate malabsorption (FODMAPs) Stool volume typically 100) Stops with fasting Not present (normal faecal calprotectin) Increased breath hydrogen with malabsorption

21
Q

What is a stool osmotic gap and what is it used for?

A

Used to distingish secretory and osmotic diarrhoe. It is calculated with the equation 290 − 2 * (stool Na + stool K). The 290 is the value of the stool osmolality. Low stool osmolic gap (100 mosm/kg) = osmotic diarrhoea. The reason for this is that secreted Na and K ions make up a greater percentage of the stool osmolality in secretory diarrhoea, whereas in osmotic diarrhoea, molecules such as unabsorbed carbohydrates are more significant contributors to stool osmolality. A normal gap is between 50 and 100 mosm/kg. High osmotic gap (>100 mosm/kg) causes of osmotic diarrhea include celiac sprue, chronic pancreatitis, lactase deficiency, lactulose, laxative use/abuse, and Whipple’s disease. Low osmotic gap (

22
Q

What is a stool osmotic gap? How do you calculate it? What do high and low gaps imply and why?

A

Used to distingish secretory and osmotic diarrhoe. It is calculated with the equation 290 − 2 * (stool Na + stool K). The 290 is the value of the stool osmolality. Low stool osmolic gap (100 mosm/kg) = osmotic diarrhoea. The reason for this is that secreted Na and K ions make up a greater percentage of the stool osmolality in secretory diarrhoea, whereas in osmotic diarrhoea, molecules such as unabsorbed carbohydrates are more significant contributors to stool osmolality. A normal gap is between 50 and 100 mosm/kg. High osmotic gap (>100 mosm/kg) causes of osmotic diarrhoea include celiac sprue, chronic pancreatitis, lactase deficiency, lactulose, laxative use/abuse, and Whipple’s disease. Low osmotic gap (

23
Q

SECRETORY diarrhoea: Caused by: Common causes: Stool volume: Stool osmotic gap: Effect of fasting: Stool leukocytes (WBC):

A

Due to active anion secretion from enterocytes Bacterial toxins (cholera, toxigenic E.coli), hormone secreting tumours (e.g. carcinoid, gastrinomas), laxative abuse, hyperthyroidism Stool volume > 1 litre/d, watery Normal osmolality (osmolar gap

24
Q

INFLAMMATORY diarrhoea: Caused by: Common causes: Stool volume: Stool leukocytes and RBCs:

A

Altered membrane permeability →exudation of protein, blood, mucus Invasive bacteria (Shigella, Salmonella, Campylobacter, Clostridium difficile), Entamoeba histolytica, cytomegalovirus colitis, inflammatory bowel disease (IBD) Volume of faeces usually small Increased RBCs and leukocytes and red blood cells (elevated faecal calprotectin). Stools may contain visible (‘frank’) blood and be associated with urgency, tenesmus and constitutional upset e.g. fever

25
Q

What are is the mechanism and what are the causes (3) of rapid transit deranged motility diarrhoea?

A

Causes: Irritable bowel syndrome (IBS), thyrotoxicosis, diabetic neuropathy. Mechanism: Inadequate time for absorption of fluid (& nutrients)

26
Q

What are the 2 types of malabsorption syndromes?

A
  1. Intraluminal disorders (maldigestion) 2. Intramural disorders & transport (malabsorption)
27
Q

What are the 2 types of malabsorption syndromes?

A
  1. Intraluminal disorders (maldigestion) 2. Intramural disorders & transport (malabsorption)
28
Q

What are 4 categories of intraluminal maldigestion disorders?

A

Mechanical - Mixing disorders: eg: Post-gastrectomy Reduced nutrient availability: Co-factor deficiency e.g. pernicious anaemia Bacterial overgrowth (nutrient consumption) Defective nutrient hydrolysis (digestion): Pancreatic insufficiency e.g. chronic pancreatitis Reduced fat solubilisation (reduced bile salt concentration): Cholestasis, bacterial overgrowth

29
Q

What are 3 categories of intramural/ transport malabsorption disorders?

A

Inadequate absorptive surface: Intestinal resection or bypass due to disease Diffuse mucosal disease: Coeliac disease, Crohn’s disease, Giardia infection Brush border enzyme deficiency e.g. lactase Mucosal absorptive defects: lymphoma, lymphatic obstruction, radiation damage vascular problems

30
Q

What are 3 categories of intramural/ transport malabsorption disorders?

A

Inadequate absorptive surface: Intestinal resection or bypass due to disease Diffuse mucosal disease: Coeliac disease, Crohn’s disease, Giardia infection Brush border enzyme deficiency e.g. lactase Mucosal absorptive defects: lymphoma, lymphatic obstruction, radiation damage vascular problems

31
Q

What is the ddx (4) for clinical presentation is of bloody, mucousy diarrhoea with tenesmus? What category of diarrhoea do these all fall under?

A

This is usually due to an inflammatory mechanism Common causes are: 1. Infection (“dysentery”) e.g. Salmonella, Shigella, Yersinia, Entamoeba histolytica (amebiasis) and cytomegaloviral colitis 2. Inflammatory bowel disease 3. Ischaemic colitis 4. Radiation colitis

32
Q

What are the 2 types of IBD?

A

Crohn’s disease and ulcerative colitis

33
Q

What are the key histological features of Crohn’s disease/ where in the GIT are they found?

A

Can affect any part of digestive tract (gum to bum) Transmural distribution with skip lesions Focal inflammation ± noncaseating granulomas, deep fissuring + aphthous ulcerations, strictures Glands intact

34
Q

What are the key histological features of UC disease/ where in the GIT are they found?

A

Mucosal distribution, continuous disease (no skip lesions) Granulomas absent Gland destruction, crypt abscess Isolated to large bowel Always involves rectum, may progress proximally

35
Q

Outline the “Rome III” criteria for irritable bowel syndrome. What is the other thing you need to do when diagnosing IBS?

A

Rome III: • Symptoms for at least 3 months • Recurrent abdominal discomfort or pain associated with (2 or more of): –Improvement of symptoms with defecation –Change in stool appearance (form) –Change in stool frequency Also have to exclude other diagnoses.

36
Q

What are the red flags for someone presenting with an IBS-like picture (4)?

A

weight loss, rectal (PR) bleeding, nocturnal symptoms, and age >45

37
Q

What are the 2 antibodies tested for in coeliac disease?

A

transglutaminase (tTG-IgA) and gliadin (“deamidated gliadin peptides”, DGP-IgA and DGP-IgG).

38
Q

What are the diagnostic criteria for coeliac (2 main points):

A

i. demonstration of small bowel damage (villous atrophy, crypt hyperplasia and raised intra-epithelial lymphocytosis) whilst a person is consuming gluten, and ii. improvement in histology, serology and clinical picture following a gluten free diet

39
Q

Which 3 things could cause a false negative serology result for coeliac serology?

A

– Gluten free diet (especially if > 6 weeks) – IgA deficiency (seen in 3% of coeliac disease – that is why the total IgA level is measured or the IgG isotype of DGP assessed – Immunosuppression e.g. prednisolone

40
Q

WhICH 2 HLA alleles are associated with coeliac?

A

HLA-DQ2/8

41
Q

How common is IBS?

A

15-20% of western countries

42
Q

What is the key pathological mediator of IBS and how does it work? What are the two other important pathophys factors?

A

Serotonin (5-HT) a key mediator in IBS 1. disordered intestinal motility 2. altered perception of nociceptive stimuli (visceral hypersensitivity) 3. psychogenic factors 4. post-infectious component in some people

43
Q

What is the key pathological mediator of IBS and how does it work? What are the two other important pathophys factors?

A

Serotonin (5-HT) a key mediator in IBS 1. disordered intestinal motility 2. altered perception of nociceptive stimuli (visceral hypersensitivity) 3. psychogenic factors 4. post-infectious component in some people

44
Q

What is a common trigger for IBS?

A

FODMAP

45
Q

What are FODMAPs? What does it stand for?

A

• FODMAPs are poorly absorbed fermentable carbohydrates • Malabsorption of these sugars leads to fermentation by bacteria in the colon Ëhydrogen/methane gas leading to distention Ëosmotic diarrhoea Ëtriggering of IBS symptoms • A low FODMAP diet is now the 1st line treatment for IBS Fermentable oligosaccharides, disaccharides, monosaccharides and polyols.