Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the mechanisms that cause diarrhoea?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What (2) are small volume stools typical of?

A

colonic diseases and IBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

small bowel disease and secretory diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does Faecal elastase indicate?

A

Presence of faecal elastase = marker of exocrine pancreatic sufficiency

Hence lack of = insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does Faecal calprotectin indicate?

A

marker of gastrointestinal inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does Faecal laxative screen indicate?

A

anthroquinones, bisacodyl, phenolphthalein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does Faecal alpha-1 antitrypsin screen indicate?

A

marker of protein losing enteropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions