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CSI year 2 > Case 11 Diarrhoea > Flashcards

Case 11 Diarrhoea Flashcards

1
Q
  • What is diarrhoea defined as?
A

3 or more losse or liquid stools per 24 hours and or/

Stools that are more frequent than what is normal for the individual lasting <14 days and or/

Stool weight greater than 200g/da

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2
Q
  • How would you classify acute, persistent or chronic diarrhoea?
A

Acute - ≤14 days

Persistent - >14 days

Chronic - >4 weeks

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3
Q
  • What are the 3 main pathologies underlying diarrhoea in general?
A

Decreased absorption

Increased secretion of fluid and electrolytes

Increase in bowel motility

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4
Q
  • What are the 3 types of infection that inflammatory diarrhoea can be due to?
  • What happens during inflammatory bowel disease
A

Bacterial, Viral, Parasitic

less water is absorbed

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5
Q
  • How would you describe the stool of inflammatory diarrhoea?
A

Mucoid and bloody stool

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6
Q
  • What are 3 of the symptoms of inflammatory diarrhoea?
A

Tenesmus- the feeling that you need to pass stools, even though your bowels are already empty

Fever

Severe crampy abdominal pain

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7
Q
  • Describe the volume and frequency of bowel movements in infectious inflammatory diarrhoea
A

Small in volume

Frequent in bowel movements

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8
Q
  • Does infectious inflammatory diarrhoea result in volume depletion in adults and how does this differ with children or older adults?
A

It does not usually result in volume depletion in adults

May do so in children or older adults - dehydration

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9
Q
  • In inflammatory diarrhoea, would you see leukocytes in the stool?
A

Yes

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10
Q
  • Would a test for faecal occult blood be positive in inflammatory diarrhoea?
A

May be positive

Reset for faecal leukocytes is plagued by a high rate of false-negative results leading to low sensitivity but a positive test is very informative

This is a lab test used to check stool samples for hidden (occult) blood which may indicate colon cancer or polyps in the colon or rectum - though not all cancers or polyps bleed

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11
Q
  • What are the causes of inflammatory diarrhoea?
A

Salmonella

Shigella

Yersina

Campylobacter

Enteroinvasive E.Coli

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12
Q
  • How would you describe the volume and frequency of stool in non-inflammatory diarrhoea?
  • Two types of Non-inflammatory diarrhoea
A

Watery, large-volume, frequent stool (>10 to 20 per day)

secretory

osmotic

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13
Q
  • Would you have volume depletion with non-inflammatory diarrhoea?
A

Possible due to high volume and frequency of bowel movements

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14
Q
  • Is there tenesmus, blood in the stool, fever or faecal leukocytes in non-inflammatory diarrhoea?
  • Is the GI architecture preserved in non-inflammatory diarrhoea?
A

No

Yes

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15
Q
  • What is the pathophysiology of secretory diarrhoea?
A

Altered transport of ions across the mucosa, which results in increased secretion and decreased absorption of fluids and electrolytes from the GI tract, especially in the small intestine

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16
Q
  • Would secretory diarrhoea decrease by fasting?
A

No, because there is decreased absorption of ions alongside continuous secretion of ions, so fasting would still mean that there is secretion occurring

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17
Q
  • Why do enterotoxins cause secretory diarrhoea?
A

Increased chloride permeability leads to leakage into the lumen followed by Na+ and H20 movement. (more secretion)

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18
Q
  • Give examples of enterotoxins that would cause secretory diarrhoea?
A

Enterotoxins: these can be from infection such as Vibrio cholera, Staphylococcus aureus, enterotoxigenic E. coli. And possibly HIV and rotavirus.

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19
Q
  • Give examples of Hormonal agents that would cause secretory diarrhoea?
A

Vaso-active intestinal peptide - prevents Na+, Cl- and water absorption from the intestines

Small-cell cancer of the lung

Neuroblastoma - secretes vaso-active intestinal peptide

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20
Q
  • What are some other causes of secretory diarrhoea?
A

Laxative use- Draws water into the gut or causes muscle of the intestine to contract

Intestinal resection- Bile acid malabsorption is mild and compensatory increase in hepatic synthesis of bile acids is sufficient to restore their secretion; the increased passage of bile acids into the colon causes diarrhoea

Bile salts and fatty acids- Bile acids in large bowel cause abnormally high levels of water and salts to get into the large bowel from the bloodstream

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21
Q
  • How would you describe the stool volume in osmotic diarrhoea compared to that in secretory diarrhoea?
  • Does osmotic diarrhoea improve with fasting?
A

small

yes

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22
Q

Is secretory diarrhoea also seen in chronic diarrhoea with coeliac sprue, collagenous colitis, hyperthyroidism and carcinoid tumours?

A

Yes

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23
Q
  • What occurs during osmotic diarrhoea?
A

Results from presence of unabsorbed or poorly absorbed solute (Mg, sorbitol and mannitol) in the intestinal tract causing an increased secretion of liquids into the gut lumen

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24
Q
  • What does measuring stool electrolytes of osmotic diarrhoea show?
A

Increased osmotic gap (>50) but the test has very limited practical value

osmotic gap- a measurement of the difference in solute types between serum and faeces

Stool (normal or diarrhoea) is always isosmotic (260 to 290 mOsml/L)

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25
Q
  • Osmotic diarrhoea can be subdivided into:
A

Maldigestion

Malabsorption

26
Q
  • What is maldigestion?
A

Impaired digestion of nutrients within the intestinal lumen or at the brush border of the membrane of mucosal epithelial cells

27
Q
  • What two main things is maldigestion seen in?
A

Pancreatic exocrine insufficiency and lactase deficiency

28
Q
  • How does pancreatic exocrine insufficiency cause diarrhoea?
A

Lack of pancreatic enzymes (amylase, proteases, lipases) to digest proteins and amylase

so lack of Na+/Glucose co-transport and Amino Acid/Na+ co-transport

so Na+ remains in the lumen, drawing water from capillaries into the lumen paracellularly

29
Q
  • How does lactase deficiency cause diarrhoea?
A

Inability to digest lactose

so less glucose can be absorbed from lumen to the enterocyte via the Na+/Glucose co-transporter

Na+ remains in the lumen, drawing water from capillaries into lumen paracellularly.

Also decreased galactose as lactose is not broken down into glucose and galactose

30
Q
  • What is malabsorption?
  • What can it be seen in?
A

Impaired absorption of nutrients

small bowel bacterial overgrowth

in mesenteric ischaemia

post bowel resection (short bowel syndrome)

mucosal disease (coeliac disease).

31
Q
  • Why would malabsorption be seen in bowel bacterial overgrowth?
A

Bile salts which are normally needed to digest fats are broken down by excess bacteria in SI resulting in incomplete digestion of fats and diarrhoea

Also physically blocks the apical side of enterocytes leading to blocked ion uptake transporters

32
Q
  • Describe why you would see malabsorption in mesenteric ischaemia, post bowel resection and coeliac disease (mucosal disease) respectively?
A

Mesenteric ischaemia - lack of blood flow to mesenteries supplying the intestines causes lack of absorption of small intestine.

Post-bowel resection - removal of walls of intestines used to absorb food products

Coeliac disease - autoimmune attack of gut tissues by immune system when gluten is consumed so there is a lack of ion uptake transporters

33
Q
  • What causes secretory diarrhea?
A

chloride channel is switched on

cholera toxin

laxatives

In intestinal brush border cells raised cyclic AMP levels result in increased secretion of chloride ions, leading to fluid accumulation in the gut.

34
Q
  • How does water get secreted back into the lumen of the small intestine when the gut is empty eg. You have not eaten yet?
A

Cl- enters lumen from enteroctye via Cl- transporter protein

Na+ follows via the paracellular (between cells through the tight junctions) route from the capillaries into the lumen

Water then follows the Na+ via the paracellular route from the capillaries into the lumen

35
Q
  • When the gut is full, how is water absorbed from the small intestine?
A

All the ion transporters in the apical side of the enterocyte will transport ions from the lumen to the enterocyte

Cl- is then transported basolaterally from enterocyte to the capillaries (opposite to when water needed to be secreted)

Na+K+ATPase transports Na+ into the capillaries from the enterocyte after it was taken from lumen to enterocyte

Na+ Increases plasma osmolality causing water to be absorbed from lumen to capillary paracellularly

36
Q
  • What are the transporters responsible for transporting Na+ from the lumen into the enterocyte?
A

Amino/Na+ co-transporter

Na+/Glucose co-transporter

Na+/H+ antiporter

37
Q
  • Drug intervention for inflammatory diarrhoea
A

anti-inflammatory drugs (steroids)

if you stick conjugate onto steroid, you can reduce its ability to absorb across the plasma membrane. Makes it stomach resistant

very powerful, however may not go to your target area

38
Q
  • Drug for secretory diarrhoea
A

drugs targeting ion channels-either Na/glucose co-transporter (SGLT1), or blockage of Cl channel, so water cant go in.

39
Q
  • Maldigestion treatment
A

probiotics (supplement gut bacteria)

enzyme supplementation (coating to protect it from the stomach)

gene therapy

not eat certain foods

gene therapy-targeting right cells, immune response

40
Q
  • malabsorption treatment
A

gene therapy

41
Q
  • What is oral-rehydration therapy?
A

Solution of Na+, K+ and Glucose administered orally

SGLT-1 takes up Glucose and Na+ from lumen to enterocytes and then these are taken up from here into the capillaries

Water absorbed from the lumen to the capillaries paracellularly

42
Q
  • Is bloating, mucus in stool and alternating constipation and diarrhoea seen in IBS or IBD?
  • Is abdominal pain, faecal urgency and fatigue seen in IBS or IBD?
  • Is weight loss, fever and blood in stool seen in IBS or IBD?
A

IBS

Both

IBD

43
Q
  • What are the organic cause of diarrhoea-investigations you should do
A

FBC- look for anaemia and signs of inflammation/infection

Urea and electrolytes- check renal function and electrolyte status

CRP- Look for infection/inflammation

Extra Blood tests- LFT, TFT, ferritin / Vitamin B12, folate, coeliac serology (tissue transglutaminase antibody)

44
Q
  • What are the main differences in presentation between ulcerative colitis and Crohn´s disease.
A

Ulcerative-decrease in goblet cells number, neutrophil driven, only affects the mucosa. continuous ulcers (pseudopolyps)

affects colon and rectum

Crohn´s-increase in goblet cells, macrophage driven, affects all layers (muscularis propia), non continuous cobblestone appearance

most commonly affectsthe colon and the last part of the small intestine (ileum).

45
Q

what are the most common causes of acute and persistent diarrhoea

A

infections, travellers diarrhoea, and side effects of medicines.

46
Q

What are causes of chronic diarrhoea that is not infection.

A

Disorders of thepancreas(e.g. chronic pancreatitis, pancreatic enzyme deficiencies, cystic fibrosis)

Intestinal disorders (e.g. colitis, Crohn’s Disease, irritable bowel syndrome)

Medications (e.g. antibiotics, laxatives)

47
Q
  • What is the first-line treatment for Crohn’s disease
A

glucocorticoids (predniselone, desonide)

48
Q
  • Other medical treatment for Crohn’s disease (other drugs you may add)
A

Methotrexate (immunosuppresant)

monoclonal antibodies (targets TNF, Infliximab)

49
Q
  • When is Surgery needed?
  • Non-pharmacological methods of treating Crohn’s
A

Strictures appear- bowel narrows due to inflammation
lesions in gut wall- gut content passes into the peritoneum

Dietary triggers, smoking cessation

50
Q

What are the main symptoms of Crohn’s disease

A
  • The main symptoms are:
    • diarrhoea
    • stomach aches and cramps
    • blood in your poo
    • tiredness (fatigue)
    • weight loss
51
Q

What are the main causes of Crohn’s disease

A

Causes of Crohn’s disease
- your genes
- a problem with the immune system (the body’s defence against infection) that causes it to attack the digestive system
- smoking
- a previous stomach bug
- an abnormal balance of gut bacteria

52
Q

What are the potential environmental triggers of Crohn’s disease.

A

Associated environmental factors may include any of the following:

  • Substances from something you’ve eaten
  • Microbes such as bacteria or viruses
  • Cigarette smoke
53
Q
  • what are the gastroenterologist tests to diagnose Crohns:
A
  • acolonoscopy
  • abiopsy
  • an MRI scan orCT scan
54
Q
  • What are the main treatments for Crohn’s
A
  • Treatment
    • Steroids
    • Liquid diet
    • Immunosuppressants
    • Biological medicines
    • Surgery
55
Q

What are the five main considerations when living with Crohn’s

A

Pharmacy medicines-anti-inflammatory painkillers like[ibuprofen] can make some people’s symptoms worse

vaccinations

pregnancy-some Crohn’s disease medicines can harm an unborn baby

contraception -Ask your GP or care team about the best contraception to use because some types, such as the pill, may not work as well as usual if you have Crohn’s disease.

cancer screening

56
Q

How can NSAIDs make the symptoms of Crohn’s worse

A

NSAIDs cancause inflammation and worsen bleeding in the small intestine

they also cause the digestive system to lose some of its normal protective substances so canpromote ulcers by disrupting the mucus that coats the stomach lining

57
Q

What stool tests are required to work out the cause of diarrhoea.

A

Stool tests- microbiology, ova and cysts. faecal calprotectin- key to tell difference between IBS and IBD. IBD has inflammation but IBS doesn’t.

58
Q

What are two conditions that fall under IBD

A

Crohn’s disease and ulcerative colitis

59
Q

What is the difference in cause between Crohn’s and ulcerative Colitis

A

Crohn’s: the immune system mistakes bacteria in the colon, which aid digestion, as harmful, leading to the colon and terminal ileum becoming inflamed.

Ulcerative: body is infected by a bacteria or virus, but even after infection is cleared, the inflammatory response does not stop. anitbodies are formed against colonic epithelial proteins

60
Q

what is the osmolar gap

A

the osmolarity gap is what part of the serum/faecal osmolarity that Na+, Glucose and K+ are not responsible for

61
Q
  • Why would the faecal osmolar gap be larger than the serum osmolar gap?
A

There are a lot more ions in the intestines composing the osmolarity

Faecal osmolarity gap above 50 is normal

62
Q
  • A faecal osmolar gap BELOW what would you suspect secretory diarrhoea?
A

50

Because enterocytes expel electrolytes into the lumen and so the contribution of Na+, K+ and glucose to osmolarity should increase, so the osmolarity gap decreases

CSI year 2 (8 decks)

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