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YA - Interactive seminars/University lectures > GI - Diarrhoea & malabsorption > Flashcards

GI - Diarrhoea & malabsorption Flashcards

1
Q

Define diarrhoea

  • volume

- frequency

A

Stool > 200 g/day and number of movements > 3/day

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2
Q

What are the mechanisms that cause diarrhoea?

A

osmotic, secretory, inflammatory & altered intestinal motility (can occur in combination)

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3
Q

What (2) are small volume stools typical of?

A

colonic diseases and IBS

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4
Q

What (2) are large volume (>750ml/d) stools typical of?

A

small bowel disease and secretory diarrhoea

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5
Q

What tests on faeces could help establish the mechanism or diagnosis for diarrhoea?

A
  • MCS of stool
  • Faecal electrolytes & osmolarity
  • faecal fat
  • faecal elastase
  • C. difficile toxin
  • faecal calprotectin
  • faecal laxative screen
  • faecal alpha-1 antitrypsin
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6
Q

What does Faecal elastase indicate?

A

Presence of faecal elastase = marker of exocrine pancreatic sufficiency

Hence lack of = insufficiency

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7
Q

What does Faecal calprotectin indicate?

A

marker of gastrointestinal inflammation

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8
Q

What does Faecal laxative screen indicate?

A

anthroquinones, bisacodyl, phenolphthalein

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9
Q

What does Faecal alpha-1 antitrypsin screen indicate?

A

marker of protein losing enteropathy

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10
Q

Describe osmotic diarrhoea

  • cause
  • stool volume
  • stool osmotic gap
  • effect of fasting
  • stool leukocytes
  • H2/methane breath test
A
  • Presence of excess unabsorbed substrates in gut lumen
  • Common cause: Fermentable carbohydrate malabsorption (FODMAPs)
  • Stool volume typically 100)
  • Stops with fasting
  • Not present (normal faecal calprotectin)
  • Increased breath hydrogen with malabsorption
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11
Q

Describe secretory diarrhoea

  • cause
  • stool volume
  • stool osmotic gap
  • effect of fasting
  • stool leukocytes
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
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12
Q

Describe inflammatory diarrhoea

  • cause
  • stool volume
  • stool leukocytes
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 red blood cells and leukocytes (elevated faecal calprotectin). Stools may contain visible (‘frank’) blood and be associated with urgency, tenesmus and constitutional upset e.g. fever
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13
Q

Describe rapid transit as a cause of diarrhoea

  • mechanism
  • causes
A

Inadequate time for absorption of fluid (& nutrients)

Irritable bowel syndrome (IBS), thyrotoxicosis, diabetic neuropathy

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14
Q

Describe slow transit as a cause of diarrhoea

  • mechanism
  • causes
A

Bacterial overgrowth -> nutrient consumption -> bile salt inactivation (unable to solubilise micelles

Intestinal stasis due to anatomical defects (strictures, blind loops, surgical procedures)

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15
Q

List (4) classes of causes of luminal phase maldigestion

A
  1. Mechanical - Mixing disorders
    - Post-gastrectomy
  2. Reduced nutrient availability
    - Co-factor deficiency e.g. pernicious anaemia
    - Bacterial overgrowth (nutrient consumption)
  3. Defective nutrient hydrolysis (digestion)
    - Pancreatic insufficiency e.g. chronic pancreatitis
  4. Reduced fat solubilisation (reduced bile salt concentration)
    - Cholestasis, bacterial overgrowth
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16
Q

List (3) classes of causes of mucosal phase maldigestion & defective transport

A
  1. Inadequate absorptive surface
    - Intestinal resection or bypass due to disease
  2. Diffuse mucosal disease
    - Coeliac disease, Crohn’s disease, Giardia infection
    - Brush border enzyme deficiency e.g. lactase
  3. Mucosal absorptive defects
    - lymphoma, lymphatic obstruction, radiation damage
    - vascular problems
17
Q

42yo male
Three months of feeling unwell
Loose-stools, 6-8 times a day (normally once every 1-2 days)
Often bloody with mucous mixed in
Crampy abdominal pain prior to defecation
Urgency and tenesmus
Occasional nocturnal diarrhoea

Afebrile. Looks tired. Pale.
Abdominal examination: unremarkable

Constitutional symptoms: Feeling lethargic & sleeping poorly, occasionally “feverish”; weight loss 2-3 kg in past 3 months
Recent travel: 6 months ago holiday in Thailand. Was not unwell there.
Social History: Lawyer, lives with partner Paul

Mechanism of diarrhoea? DDx?

A

The clinical presentation is of bloody, mucousy diarrhoea with tenesmus 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
18
Q

How do you confirm the diagnosis of IBD?

A

colonoscopy and colonic biopsies

19
Q

Describe what you’d see on colonoscopy & colonic biopsy of UC

A
  • superficial ulceration with distortion of crypts
  • acute and chronic diffuse inflammatory infiltrate
  • goblet cell depletion
  • crypt abscesses
  • lymphoid aggregates but no granulomas
20
Q

Rx of ulcerative colitis

A

–5-ASA compounds (sulphasalazine) and steroids.
–Topical therapy (suppositories/enemas) used for distal disease.
–Immunosupressants used in severe or recurrent disease
–Surgery for severe or refractory cases (this is curative)

21
Q

Rx of Crohn’s disease

A

Steroids, 5-ASA compounds, immunosupressants (e.g. azathioprine, methotrexate), biologicals (monoclonal Ab), surgery

22
Q

26yo female
~ 10 year history of intermittent diarrhoea with bloating & flatulence
Up to 2-5 bowel motions per day (erratic), no blood
No weight loss
Stress, dairy products and some fruits make her symptoms worse
She tried a gluten free diet on advice of a friend and felt better.
SHx: Office manager, lives with partner
FHx: Sister is “gluten intolerant”
PHx: Depression
Meds: Nil. Non-smoker.

DDx?

A
  1. Irritable bowel syndrome
  2. Coeliac disease
  3. Infection such as Giardia
  4. Inflammatory bowel disease
23
Q

How do you diagnose irritable bowel syndrome?

A 
1. Typical clinical Hx
“Rome III” criteria
•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
  1. Exclude other Dx
    Presence of “red-flag” symptoms or signs such as weight loss, rectal (PR) bleeding, nocturnal symptoms, and age >45 should prompt further investigation before a diagnosis of IBS is made
24
Q

How do you diagnose coeliac disease? (c.f. screen)

A
  1. demonstration of small bowel damage (villous atrophy, crypt hyperplasia and raised intra-epithelial lymphocytosis) whilst a person is consuming gluten, and
  2. improvement in histology, serology and clinical picture following a gluten free diet
25
Q

How do you screen for coeliac disease?

A

–blood test measuring antibodies to transglutaminase (tTG-IgA) and gliadin (“deamidated gliadin peptides”, DGP-IgA and DGP-IgG).

–The DGP assay replaces the older and less accurate anti-gliadin antibodies (AGA-IgA, AGA-IgG) test.

If antibodies are abnormally elevated (positive), a small bowel biopsy showing villous atrophy is required to confirm the diagnosis

26
Q

What (3) might cause false negative serology results in Coeliac disease screening?

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

27
Q

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

A

HLA-DQ2/8 gene test. This is seen in most (99.6%) patients with coeliac disease. If negative, it can be used to exclude coeliac disease.

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

28
Q

How can you exclude infection and inflammatory bowel disease?

A
  • Faecal assessment
  • Inflammatory markers
  • Gastroscopy and colonoscopy with biopsies may be required in some instances
29
Q

(4) pathogenesis of irritable bowel syndrome

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

“Stress” and small bowel bacterial overgrowth can be a trigger
Role of genetics is unclear

30
Q

Rx of IBS

A

•Dietary modification

  • Avoiding common food triggers – FODMAPs
  • Avoiding caffeine, alcohol, smoking

•Pharmacological therapies

  • Probiotics
  • Antispasmodics, antidiarrhoeals, laxatives
  • Antibiotics (Rifaximin) to treat bacterial overgrowth
  • ? Increase fibre ? Decrease fibre

•Psychological therapies
-Relaxation, cognitive behaviour therapy, hypnotherapy

31
Q

62yo male
6 month history of pale, smelly, greasy stools, difficult to flush
Frequently feels bloated and nauseated after meals. More lethargic and has lost 15 kg weight in past 6 months. Denies drinking alcohol for the past 2 years

PHx:

  1. Hypertension
  2. Ex-smoker.
  3. Heavy drinker in the past
  4. Alcoholic pancreatitis 10 years ago, subsequent two recurrent episodes

O/E: Bruises on arm. Evidence of subcutaneous fat loss. Several spider naevi on chest. Abdominal exam normal. No hepatic flap or fetor

DDx?

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
32
Q

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

A
  • History of steatorrhoea, lethargy, weight loss
  • Examination findings of bruising, muscle wasting, weight loss

Confirm it by:
•Nutrient levels (Iron studies, B₁₂, folate, vitamins)
•Faecal assessment: Increased faecal fat

33
Q

Differing clinical picture associated with peritonitis

  • red
  • grey
  • white
A

–Red: vasodilated, warm peripheries, flushed (bacterial peritonitis)
–Grey: shutdown, clammy, sweaty (chemical peritonitis/severe pancreatitis/MI/PE)
–White – pale, shut down, cold peripheries (haemorrhagic shock)

YA - Interactive seminars/University lectures (87 decks)

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