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MD2 GIT > Diarrhoea and Malabsorption > Flashcards

Diarrhoea and Malabsorption Flashcards

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1
Q

How much fluid enters the GIT each day?

A

9L

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2
Q

How much fluid is absorbed in the small intestine?

A

7L

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3
Q

How much fluid is absorbed in the colon?

A

1.8L

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4
Q

How much water can be absorbed in the colon?

A

4.5L

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5
Q

How much water leaves the GIT each day?

A

200mL

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6
Q

What enzymes are responsible for CHO breakdown?

A

Salivary amylases

Pancreatic amylases

Brush border enzymes

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7
Q

What factors/enzymes are responsible for protein breakdown?

A

HCl

Gastric pepsin

Pancreatic proteases (peptidases)

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8
Q

What factors are responsible for fat breakdown?

A

Bile

Pancreatic lipase

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9
Q

Define diarrhoea

A

Abnormal frequency and liquidity of stool >200g stool/day and >3 movements/day

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10
Q

When is diarrhoea considered chronic?

A

When it lasts >4 weeks

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11
Q

What location and pathological mechanisms does large volume diarrhoea suggest?

A

Small bowel disease

Secretory diarrhoea

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12
Q

What is small volume diarrhoea suggestive of?

A

Colonic diseases and IBS

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13
Q

List 4 tests routinely performed on faeces which could help diagnose the cause of diarrhoea

A

MCS

Faecal elastase

Faecal fat and microglobules

Calprotectin, lactoferrin (for IBD)

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14
Q

List 4 other tests less commonly used to help diagnose diarrhoea

A

Faecal electrolytes and osmolarity (look for stool osmotic gap)

C. difficile toxin

Faecal laxative screen

Faecal a1-antitrypsin

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15
Q

What is faecal elastase a marker of?

A

Exocrine pancreatic sufficiency

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16
Q

What laxatives are usually screened for?

A

Anthroquinones

Bisacodyl

Phenolphthalein

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17
Q

What is faecal a1-antitrypsin a marker of?

A

Protein-losing enteropathy

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18
Q

What other tests (non-faecal) may be indicated in the case of diarrhoea?

A

FBE

BGL

B12 and folate levels

Iron studies

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19
Q

What is the pathological mechanism of osmotic diarrhoea?

A

Presence of excess unabsorbed substrates in gut lumen

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20
Q

What is the most common cause of osmotic diarrhoea?

A

Fermentable CHO malabsorption (FODMAPs)

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21
Q

What is the typical stool volume in osmotic diarrhoea?

A

<1L

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22
Q

Describe the stool osmotic gap in osmotic diarrhoea

A

Increased (>100)

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23
Q

What findings would be expected on a H2/methane breath test in the case of osmotic diarrhoea?

A

Increased breath H with malabsorption

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24
Q

What is the pathological mechanism of secretory diarrhoea?

A

Active anion secretion from enterocytes

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25
Q

What are the most common causes of secretory diarrhoea?

A

Bacterial toxins (e.g. cholera, toxigenic E.coli)

Hormone-secreting tumours

Laxative abuse

Hyperthyroidism

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26
Q

Give 2 examples of hormone-secreting tumours which may cause secretory diarrhoea

A

Carcinoid tumours

Gastrinomas

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27
Q

What is the typical stool volume in secretory diarrhoea?

A

>1L/d, watery

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28
Q

Describe the stool osmotic gap in secretory diarrhoea

A

Normal osmolality (<100)

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29
Q

What is the effect of fasting on secretory diarrhoea?

A

Diarrhoea persists

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30
Q

Are stool leukocytes detected in secretory diarrhoea?

A

No

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31
Q

What is the pathological mechanism of inflammatory diarrhoea?

A

Altered membrane permeability leading to exudation of protein, blood and mucus

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32
Q

What are the 4 most common causes of inflammatory diarrhoea?

A

Invasive bacteria

Entamoeba histolytica

CMV colitis

IBD

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33
Q

Give 4 examples of bacteria which can cause inflammatory diarrhoea

A

Shigella

Salmonella

Campylobacter

C. difficile

34
Q

Describe the stool volume in inflammatory diarrhoea

A

Usually small

35
Q

Are stool leukocytes and RBCs detectable in inflammatory diarrhoea? What clinical features might accompany these findings?

A

Yes (may even be frank blood)

Associated with urgency, tenesmus and constitutional upset (including fever)

36
Q

List 3 conditions which may cause rapid transit of GI contents

A

IBS

Thyrotoxicosis

Diabetic neuropathy

37
Q

What is the mechanism of diarrhoea caused by slow transit of GI contents?

A

Bacterial overgrowth results in bacteria consuming nutrients in GIT and inactivation of bile salts NB Slow transit diarrhoea may be associated with malabsorption

38
Q

What pathologies may cause slow transit of GI contents?

A

Intestinal stasis due to strictures, blind loops, surgical procedures, etc

39
Q

What is the difference between maldigestion and malabsorption?

A

Maldigestion: intraluminal

Malabsorption: intramural and disorders of transport

40
Q

List 4 causes of maldigestion, giving specific examples of disease processes

A

Mechanical (mixing) disorders: post-gastrectomy (mixing disorder)

Reduced nutrient availability: co-factor deficiency (e.g. pernicious anaemia), bacterial overgrowth (nutrient consumption)

Defective nutrient hydrolysis (digestion): pancreatic insufficiency (e.g. in chronic pancreatitis)

Reduced fat solubilisation (reduced bile salt concentration): cholestasis, bacterial overgrowth

41
Q

Where is the most fluid from the GIT absorbed?

A

Small intestine

42
Q

Where is iron absorbed?

A

Mostly duodenum

43
Q

Where is vitamin B12 absorbed?

A

Terminal ileum (after binding to intrinsic factor)

44
Q

List 4 mechanisms causing diarrhoea

A

Osmotic

Secretory

Inflammatory

Altered intestinal motility

45
Q

What can be identified with an MCS?

A

Gram stain for bacteria

Examination for ova, cysts, parasites

Culture for pathogens WBCs (suggestive of colitis) and/or RBCs

46
Q

What is faecal calprotectin and lactoferrin indicative of?

A

GIT inflammation

47
Q

What is the effect of fasting on osmotic diarrhoea?

A

Stops

48
Q

Are stool leukocytes detectable in osmotic diarrhoea?

A

No

49
Q

Are there changes in the level of faecal calprotectin in osmotic diarrhoea?

A

No

50
Q

Are there changes in the level of faecal calprotectin in secretory diarrhoea?

A

No

51
Q

Are there changes in the level of faecal calprotectin in inflammatory diarrhoea?

A

Yes (elevated)

52
Q

List 3 causes of mucosal phase (malabsorption) and defective transport, giving examples of specific disease processes

A

Inadequate absorptive surface: intestinal resection or bypass due to disease (short gut syndrome)

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

53
Q

Brian, 42, presents with 3/12 of feeling unwell with loose stools 6-8 times/day (normally once every 1-2 days), often bloody with mucous mixed in, crampy abdominal pain prior to defecation, urgency and tenesmus, and occasional nocturnal diarrhoea

O/E: afebrile, looks tired and pale, abdominal examination unremarkable

What other Hx should you ask about?

A

Constitutional Sx

Recent travel or other context (e.g. exposure to “off” food)

SHx

PMHx

Rx

FHx of bowel pathology

54
Q

Brian, 42, presents with 3/12 of feeling unwell with loose stools 6-8 times/day (normally once every 1-2 days), often bloody with mucous mixed in, crampy abdominal pain prior to defecation, urgency and tenesmus, and occasional nocturnal diarrhoea

O/E: afebrile, looks tired and pale, abdominal examination unremarkable

Occasionally feverish, sleeping poorly, weight loss 2-3 kg in past 3/12

Recent travel: 6/12 ago holiday in Thailand but was not unwell there

SHx: lawyer, lives with partner Paul

PMHx: nil significant, non-smoker

No regular Rx (including OTC)

No significant FHx

DDx?

A

Clinical presentation is of bloody, mucousy diarrhoea with tenesmus, which usually has an inflammatory mechanism and of which common causes include:

Infection (dysentery; e.g. Salmonella, Shigella, Yersinia, Entamoeba histolytica - amoebiasis, CMV)

IBD

Ischaemic colitis

Radiation colitis

Other causes of bleeding per rectum include:

Haemorrhoids (“piles”)

Colorectal cancer

55
Q

Brian, 42, presents with 3/12 of feeling unwell with loose stools 6-8 times/day (normally once every 1-2 days), often bloody with mucous mixed in, crampy abdominal pain prior to defecation, urgency and tenesmus, and occasional nocturnal diarrhoea

O/E: afebrile, looks tired and pale, abdominal examination unremarkable

Occasionally feverish, sleeping poorly, weight loss 2-3 kg in past 3/12

Recent travel: 6/12 ago holiday in Thailand but was not unwell there

SHx: lawyer, lives with partner Paul

PMHx: nil significant, non-smoker

No regular Rx (including OTC)

No significant FHx

Initial Ix? Definitive Ix?

A

Faecal MCS

Faecal calprotectin

FBE

ESR, CRP

Nutritional studies (iron, B12/folate, vit D)

Definitive Ix: colonoscopy and colonic biopsy

56
Q

Brian, 42, presents with 3/12 of feeling unwell with loose stools 6-8 times/day (normally once every 1-2 days), often bloody with mucous mixed in, crampy abdominal pain prior to defecation, urgency and tenesmus, and occasional nocturnal diarrhoea

O/E: afebrile, looks tired and pale, abdominal examination unremarkable

Occasionally feverish, sleeping poorly, weight loss 2-3 kg in past 3/12

Faecal sample: unformed, mucoid and bloody, leucocytes and erythrocytes on direct examination (no Giardia cysts), C. dif toxin/rotavirus Ag/adenovirus Ag/norovirus by RTPCR all not detected, no Salmonella/Shigella/Campylobacter on culture

Faecal calprotectin >300 mcg/g (N 19.5-50) FBE: low Hb ESR 25, CRP 80 (both elevated)

Nutritional studies normal

Colonoscopy performed and colonic biopsies taken; interpret the results

A

Superficial ulceration with distorsion of crypts

Acute and chronic diffuse inflammatory infiltrate

Goblet cell depletion

Crypt abscesses

Lymphoid aggregates but no granulomas

57
Q

What is IBD?

A

Chronic inflammatory disorders of uncertain aetiology (genetics, environment, immune response are contribute)

Comprises of Crohn’s disease and ulcerative colitis (in some patients it is difficult to decide between the two diagnoses and so they are given the Dx of “indeterminate colitis”)

58
Q

Epidemiology of IBD

A
59
Q

Compare the features of UC and Crohn’s disease

A

UC: affects large bowel starting at rectum and proceeding proximally (i.e. no skip lesions), increased risk of colonic malignancy in longstanding UC

Crohn’s disease: focal transmural inflammation with fissures, ulcers and granulomas, and with healthy intestine between the lesions (skip lesions), can affect any part the gut from mouth (aphthous ulcers) to anus (most commonly terminal ileum and colon, extra-intestinal features include arthritis, uveitis and rashes

60
Q

Compare Sx of UC and Crohn’s disease

A

UC: frequent episodes of rectal bleeding, urgency and tenesmus often a feature of distal disease, other Sx include abdominal cramps, weight loss and fever in severe cases

Crohn’s: abdominal pain, diarrhoea, weight loss, fever, failure to thrive, disease progresses with relapses and remissions

61
Q

Compare the Mx of UC and Crohn’s disease

A

UC: 5-ASA compounds (sulphasalazine) and steroids, topical therapy (suppositories/enemas) used for distal disease, immunosuppressants used in severe or recurrent disease, surgery for severe or refractory cases (this is curative)

Crohn’s: steroids, 5-ASA compounds, immunosuppressants (e.g. azathioprine, methotrexate), biologicals (monoclonal Ab e.g. adalimumab), surgery (not curative - repeated surgeries can cause short gut syndrome)

62
Q

Mandy, 26, presents with ~10 year Hx of intermittent diarrhoea with bloating and flatulence, passing up to 2-5 bowel motions per day (erratic) but no blood and no weight loss

Stress, dairy products and some fruits make her Sx worse

Tried a gluten free diet on advice from friend and felt better

SHx: office manager, lives with partner

FHx: sister is “gluten intolerant”

PHx: depression

Rx: nil, non-smoker

O/E: anxious, afebrile, abdo examination normal

DDx?

A

IBS

Coeliac disease

Infection e.g. Giardia

IBD

63
Q

How is IBS diagnosed?

A

1) Typical clinical Hx: “Rome III” criteria

  • Sx for at least 3/12
  • Recurrent abdominal discomfort or pain associated with 2 or more of:
    • Improvement of Sx with defecation
    • Change in stool appearance (form)
    • Change in stool frequency

2) Exclude other Dx
* Presence of “red-flag” Sx or signs such as weight loss, PR bleeding, nocturnal Sx, age >45 should prompt further Ix before Dx of IBS is made

64
Q

How is coeliac disease Dx?

A

Screen for coeliac disease:

  • Blood test measuring tTG-IgA and DGP-IgA/-IgG (Abs to deamidated gliadin peptides)
    • DGP assay replaces older and less accurate anti-gliadin Abs (AGA-IgA/-IgG) test

If Abs are abnormally elevated, small bowel biopsy showing villous atrophy is required to confirm Dx

Current Dx criteria requires:

  • Demonstration of small bowel damage (villous atrophy, crypt hyperplasia, raised IELs) whilst a person is consuming gluten, and
  • Improvement in histology, serology and clinical picture following a gluten free diet
65
Q

How accurate is coeliac serology? What are the clinical implications?

A

tTG-IgA and DGP Ab assays have a sensitivity of ~90% (i.e. 10% of true coeliac Dx will not be detected using serology alone)

FPs can occur, so a Dx of coeliac disease is never made on the blood test alone (biopsy is required)

Accuracy of a Dx test is affected by pre-test probability

66
Q

What might cause false negative serology results?

A

Gluten free diet (esp if >6/52)

IgA deficiency (seen in ~3% of coeliac disease, which is why the total IgA level is measured or the IgG isotype of DGP assessed)

Immunosuppression e.g. prednisolone

67
Q

How can you test for coeliac disease if a person is already following a gluten free diet?

A

HLA-DQ2/8 gene test; seen in most (99.6%) patients with coeliac disease, so can be used to EXCLUDE coeliac

6 week gluten challenge (~4 serve gluten/day) followed by small bowel biopsy

68
Q

How can infection and IBD be excluded from a DDx?

A

Faecal assessment

Inflammatory markers

Gastroscopy and colonoscopy with biopsies may be required in some instances

69
Q

Mandy, 26, presents with ~10 year Hx of intermittent diarrhoea with bloating and flatulence, passing up to 2-5 bowel motions per day (erratic) but no blood and no weight loss

Stress, dairy products and some fruits make her Sx worse

Tried a gluten free diet on advice from friend and felt better

Ix?

A

FBE

Iron studies

ESR, CRP

TFTs

HLA-DQ2/8 genotyping

Faecal MCS and calprotectin

70
Q

Mandy, 26, presents with ~10 year Hx of intermittent diarrhoea with bloating and flatulence, passing up to 2-5 bowel motions per day (erratic) but no blood and no weight loss

FBE normal

Iron studies: low normal ferritin,

ESR normal, CRP normal

TFTs normal

HLA-DQ2/8 genotyping shows no genetic susceptibility for coeliac disease

Faeces: unformed, no leucocytes/erythrocytes/Giardia cysts, no C. diff toxin or growth, no rotavirus Ag/adenovirus Ag/norovirus by RTPCR, no Salmonella/Shigella/Campylobacter isolated

Faecal calprotectin: low

Dx?

A

IBS

71
Q

Describe the epidemiology of IBS

A

Common, affecting 15-20% of general population of Western countries

F>M

72
Q

Clinical presentation of IBS

A

Constipation-predominant, diarrhoea-predominant, pain-predominant or mixed pattern

73
Q

Describe the pathogenesis of IBS

A
  • 5HT is a key mediator
  • Disordered intestinal motility
  • Altered perception of nociceptive stimuli (visceral hypersensitivity)
  • Psychogenic factors
  • Post-infectious component in some people
  • “Stress” and small bowel bacterial overgrowth can be a trigger
  • Role of genetics unclear
74
Q

Why might foods like dairy, wheat and fruit trigger Sx in an IBS patient?

A

FODMAP (poorly absorbed fermentable CHOs) malabsorption is a common trigger for IBS

Malabsorption of these sugars leads to fermentation by bacteria in the colon, and hydrogen/methane gas production (causing distension), osmotic diarrhoea and triggering of other IBS Sx

Hydrogen/methane breath testing is available to test for lactose and fructose malabsorption

75
Q

Mx for IBS

A

Primarily aimed at alleviating Sx

Dietary modification: avoiding common food triggers (low FODMAP diet), avoiding caffeine, alcohol and smoking

Pharmacological therapies: probiotics, antispasmodics, antidiarrhoeals, laxatives, Abx (rifaximin) to treat bacterial overgrowth, ?increase or decrease fibre

Psychological therapies: relaxation, CBT, hypnotherapy

In the future, targeted treatments will become available that address the underlying ENS dysfunction (e.g. modify 5HT signalling)

76
Q

List the poorly absorbed fermentable CHOs, and their significant food sources

A
77
Q

Peter, 62, presents with 6/12 Hx of pale, smelly greasy stools which are difficult to flush, frequently feels bloated and nauseated after meals, more lethargic and has lost weight in past 6/12, denies drinking alcohol for past 2 years

PHx: HTN, ex-smoker, previous EtOH abuse, alcoholic pancreatitis 10 years ago and subsequent 2 episodes

O/E: bruises on arm, evidence of subcutaneous fat loss, several spider naevi on chest, abdominal examination normal, no hepatic flap or fetor

What features suggest malabsorption might be present and how can we confirm it?

A

Hx of steatorrhoea, lethargy, weight loss, examination findings of bruising, muscle wasting, weight loss

Ix: nutrient levels (Iron studies, B12/folate, vitamins), faecal assessment: increased faecal fat

78
Q

Peter, 62, presents with 6/12 Hx of pale, smelly greasy stools which are difficult to flush, frequently feels bloated and nauseated after meals, more lethargic and has lost weight in past 6/12, denies drinking alcohol for past 2 years

PHx: HTN, ex-smoker, previous EtOH abuse, alcoholic pancreatitis 10 years ago and subsequent 2 episodes

O/E: bruises on arm, evidence of subcutaneous fat loss, several spider naevi on chest, abdominal examination normal, no hepatic flap or fetor

What are potential causes for Peter’s malabsorption and how might they cause it?

A
  1. Defective nutrient hydrolysis (digestion): pancreatic insufficiency due to chronic pancreatitis or pancreatic cancer
  2. Reduced nutrient availability: poor oral intake (especially if still an alcoholic); bacterial overgrowth
  3. Reduced fat solubilisation (reduced bile salt concentration): cholestasis (failure of bile flow) due to underlying liver disease; bacterial overgrowth will inactivate bile salts
  4. Diffuse mucosal disease: e.g. coeliac disease, Giardia infection, brush border enzyme deficiency
  5. Mucosal absorptive defects: e.g. lymphoma, lymphatic obstruction
79
Q

Ix for pancreatic insufficiency

A

Imaging with CT scan (?chronic pancreatitis, ?cancer)

Faecal elastase level as marker of exocrine sufficiency

Empiric trial of pancreatic enzyme supplementation

Secretin stimulation test (rarely done)

80
Q

Ix for bacterial overgrowth

A

Hydrogen/methane breath test (assess for “early rise” in breath hydrogen due tofermentation in the small bowel)

Empiric trial of broad-spectrum antibiotics

81
Q

Ix for cholestasis/liver disease

A

Assess for underlying liver disease and alcoholic cirrhosis

LFTs, liver imaging (ultrasound), possibly biopsy

History of jaundice, dark urine and pale stools suggest extrahepatic cholestasis

Corroborate history of alcohol intake with family

82
Q

Describe the clinical approach to diarrhoea

A

MD2 GIT (14 decks)

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