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Y2 - CSI > Lucy Allen > Flashcards

Lucy Allen Flashcards

1
Q

What does the introduction video reveal about Lucy Allen?

A

Last 6 months - travelling around indonesia, Phillipines and Australia

Started new job 6 weeks ago

Persistent diarrhoea for the last 10 days

Has a temperature

Mildly dehydrated

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2
Q

What does Lucy’s patient persona say about her?

A

Enjoys playing 5 a side football in the weekends

Loves to collect souvenirs from overseas trips

Loves her cactus garden

Loves to travel around the world

Finding it difficult to sleep lately

Lost 7kg since most recent trip overseas (i.e. 6 months ago)

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3
Q

What does Lucy Allen talk about in the case video?

A

Terrible diarrhoea - been there for 6 weeks, but gotten a lot worse over the weekend

Tummy pain

3-4 times a day for a month, last 2-3 days like 8x a day

Overnight too - particularly the last few days

Loose poo - brown, watery, occasionally blood on the tissue (From wiping, not actual faeces)

Indonesia and then the Philippines for 10 weeks, 2 months ago

Did not have these symptoms overseas, except once has a bout of diarrhoea for 2 days over something she ate

No nausea or vomiting

Poorer appetite

Pain comes and goes - most on left upper quadrant

Pain does not change with opening bowels

Lost about 7kg since she got back

Very tired, no energy atm

On the contraceptive pill

Adopted - no FH

Drink on weekends, drink occasionally with friends after work

Smoke 5 a day

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4
Q

What is diarrhoea? How is it clinically defined?

A

Defined as the passage of:

Three or more loose 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 weigh greater than 200 g/day
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5
Q

What are the 3 types of diarrhoea based on duration?

A

Acute (≤14 days)
Persistent (>14 days)
Chronic (>4 weeks)

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6
Q

What is the basic pathophysiology of diarrhoea?

A

Normally approximately 10L of fluid + secretions (from the salivary glands, stomach, pancreas, bile ducts, and duodenum) enter the GI tract every day

The small intestine = major site for re-absorption

Overall, about 99% of the fluid is re-absorbed, leaving 0.1 litre to be excreted in the faeces

Diarrhoea = factors interfere with normal process = decreased reabsorption or increased secretion of fluid and electrolytes, or increase in bowel motility

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7
Q

What two categories can diarrhoea be divided into pathophysiologically?

A

Inflammatory diarrhoea

Non-inflammatory diarrhoea

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8
Q

What is inflammatory diarrhoea? What can it be caused by?

A

Inflammatory process present - can be due to bacterial, viral, or parasitic infection, or may develop early in the course of bowel ischaemia, radiation injury, or inflammatory bowel disease

May also be called infectious diarrhoea

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9
Q

What are the symptoms of inflammatory diarrhoea?

A

Associated with - mucoid and bloody stool, tenesmus, fever, and severe crampy abdominal pain

Infectious inflammatory diarrhoea = small in volume, with frequent bowel movements (so does not result in volume depletion in adults, but may do so in children or older adults)

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10
Q

What is the most common cause of infectious diarrhoea?

A

In the US = bacterial infection: mainly Campylobacter, Salmonella, Shigella, Escherichia coli, or Clostridium difficile

Viruses = more common among children who attend day care centres

Protozoa and parasites are common causes of acute diarrhoea in developing countries

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11
Q

What is likely to show up in the examinations, tests and histology reports in a patient with inflammatory diarrhoea?

A

Examination of the stool may show leukocytes, and tests for faecal occult blood may be positive

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

Histology of the GI tract is abnormal in inflammatory diarrhoea

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12
Q

What is non-inflammatory diarrhoea?

A

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

Volume depletion is possible due to high volume and frequency of bowel movements

No tenesmus (cramping rectal pain), blood in the stool, fever, or faecal leukocytes

Histologically the GI architecture is preserved

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13
Q

What are the 2 further subdivisions of non-inflammatory diarrhoea?

A

Secretory diarrhoea

Osmotic diarrhoea

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14
Q

What is secretory diarrhoea?

What does not alleviate secretory diarrhoea?

A

Altered transport of ions across the mucosa = increased secretion and decreased absorption of fluids and electrolytes from the GI tract, esp. in the small intestine.

Secretory diarrhoea tends not to decrease by fasting

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15
Q

What are some causes of secretory diarrhoea?

A

Enterotoxins = can be from infections e.g. Vibrio cholerae, Staphylococcus aureus, enterotoxigenic E coli, and possibly HIV and rotavirus

Hormonal agents = vaso-active intestinal peptide, small-cell cancer of the lung, and neuroblastoma

Laxative use, intestinal resection, bile salts, and fatty acids

It is also seen in chronic diarrhoea with coeliac sprue, collagenous colitis, hyperthyroidism, and carcinoid tumours

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16
Q

What is osmotic diarrhoea?

How does it differ from secretory diarrhoea in terms of alleviating factors?

A

Stool volume is relatively small (compared with secretory diarrhoea), and diarrhoea improves or stops with fasting

Results from presence of unabsorbed / poorly absorbed solute (magnesium, sorbitol, and mannitol) in the GI tract that causes an increased secretion of liquids into the gut lumen

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17
Q

What test may be done to see if a patient has osmotic diarrhoea?

Why is this test limited in a practical setting?

A

Measuring stool electrolytes shows an increased osmotic gap (>50), but the test has very limited practical value

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

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18
Q

What are the 2 subdivisions of osmotic diarrhoea?

A

Maldigestion and Malabsorption

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19
Q

What are the characteristics of maldigestion and malabsorption?

A

Maldigestion = impaired digestion of nutrients within the intestinal lumen or at the brush border membrane of mucosal epithelial cells; can be seen in pancreatic exocrine insufficiency and lactase deficiency

Issue with the breakdown of the nutrients in the lumen for it to be absorbed (e.g. lactose intolerance)

Malabsorption = impaired absorption of nutrients; can be seen in small bowel bacterial overgrowth, in mesenteric ischaemia, post bowel resection (short bowel syndrome), and in mucosal disease (coeliac disease)

Issue with the movement of the nutrient from the lumen to the enterocytes

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20
Q

Are the fluids that enter the digestive system only the ones we drink?

How much fluid is lost in the faeces?

What happens to the fluid that is not excreted?

A

1-2 litres = fluids we drink/ day
6-7 litres = entering via secretions/ day

So overall 10 - 11 L fluids go through our digestive tract a day

And 0.1L lost in faeces

Gets absorbed via the walls of the small and large intestine

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21
Q

How are fluids reabsorbed in the lumen of the digestive tract?

A

Enterocytes and permeable molecules can travel across the lumen into the enterocyte

First the permeable nutrients travel into the enterocytes

The nutrients are pushed in the bloodstream in exchange for solutes using a pump

The solutes accumulate in the enterocyte

This creates an osmotic gradient allowing water to follow into the enterocyte to be reabsorbed

This is how 99% of the fluids are reabsorbed

[look up bio notes]

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22
Q

So what happens in diarrhoea?

A

Issue with membrane that prevents uptake of the nutrients (and so fluids) into the enterocytes
Or
Increased fluid secretion into the lumen

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23
Q

What are the issues between the lumen and the enterocyte for each type of diarrhoea?

A

Inflammatory Diarrhoea

  • exodation of serum and blood
  • inflammation damages the enterocyte membrane, nutrients are lost to the lumen (affects osmotic gradient) = fluid left in the lumen

Non-inflammatory Diarrhoea:

Secretory diarrhoea

  • Error with the ion channels, whilst solutes are supposed to only stay on the enterocyte side, but now the
  • Cl channel activated in cholera = solute in the lumen = fluid held by the solutes in the lumen

Osmotic diarrhoea:
Maldigestion
- Lack of digestion of nutrients = nutrients remain in the lumen = fluid held in the lumen

Malabsorption
- Solutes not absorbed by enterocytes e.g. prunes, sorbitol (sugar alcohol) = water is retained in lumen

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24
Q

What happens in inflammatory diarrhoea (enterocytes)?

A

Destruction of the epithelium due to inflammation

Enterocytes cannot absorb fluids

Excess fluid in lumen

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25
Q

What happens in secretory diarrhoea (enterocytes)?

A

Ion channels become wrongly activated so solutes moves into the lumen

E.g. Cholera - chloride channel on enterocyte membrane becomes activates

Fluid follows the chloride

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26
Q

What happens in maldigestion diarrhoea (enterocytes)?

A

Solutes are not able to digest

Products remain in lumen - high solute concentration

Fluid moves to lumen

E.g. lactose intolerance

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27
Q

What happens in malabsorption diarrhoea (enterocytes)?

A

Solutes not absorbed by enterocytes

E.g. prunes

Sorbitol is not absorbed by enterocytes

Water is retained

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28
Q

What drug could help inflammatory?

A

Anti-cytokines e.g. Anti-TNF

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29
Q

What drug could help secretory?

A

Block dysregulated channel

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30
Q

What drug could help maldigestion?

A

Enzyme replacement to facilitate reabsorption

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31
Q

What drug would you design for each type of diarrhoea?

A

Inflammatory = something that reduces inflammation e.g. steroids

Secretory = antagonist to fight the molecule that is activating the ion channels

Maldigestion = give the enzyme that is missing

Malabsorption = a drug that kills the parasite

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32
Q

What is the treatment for diarrhoea in the short term (acutely)?

A

ORS - oral rehydration salts

Sodium glucose linked transporter 1 channel (SGLT1)

ORS gives a ratio of 1 glucose to 2 Na+

SGLT1 pick up the Na+ ions into the enterocytes, solute is now inside the enterocyte so fluid moves down the osmotic gradient into the enterocytes as well

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33
Q

Why does diarrhoea kill?

A

Dehydration

ORS essential especially in children

34
Q

Lucy has presented with chronic diarrhoea

What are the 2 causes for chronic diarrhoea?

A

Functional = e.g. IBS

Organic = everything else (all other causes) e.g. IBD = structural change that can be seen and measured

35
Q

What is IBS?

A

Functional cause of diarrhoea

No known structural changes

Symptoms are unexplained

Non-progressive and will not kill patient

36
Q

Divide the following the symptoms in terms of functional and organic causes?

A

Functional (e.g. IBS):
Mucus in stool
Abdominal bloating
Alternating constipation and diarrhoea

Organic (e.g. IBD):
Fever
Blood in stool
Weight loss

Both:
Fatigue
Abdominal pain
Faecal urgency

37
Q

How can blood on stool be divided into 2 separate symptoms and what do they indicate?

A

Blood on the toilet paper VS blood actually mixed into the stool

Blood on toilet paper = more benign causes e.g. haemorrhoids

Blood in actual stool = symptom of IBD

38
Q

Looking at the Venn diagram, what is the likely cause of Lucy’s chronic diarrhoea?

A

Organic cause

e.g. IBD, coeliac disease, lactose intolerance, bowel cancer etc.

39
Q

What was found upon Lucy’s abdo examination?

A

Soft abdomen
Tenderness particulary in LLQ
No masses

40
Q

What investigations would you do next to determine the exact organic cause of Lucy’s chronic diarrhoea and why?

A
  1. FBC - look for signs of infection / inflammation and anaemia
  2. Urea and electrolytes - check renal function and electrolyte status
  3. CRP - look for infection/inflammation
  4. Stool sample test - check for parasites, bacteria (microbiology, ova and cysts)
  5. Antibody assay - for coeliac disease
  6. LFT - liver function tests, also get albumin levels in this so low albumin = low something or malnourishment
  7. Thyroid function test - hyperthyroidism = diarrhoea esp. autoimmune thyroid conditions common in young females
  8. Blood test for ferritin / Vit B12, folate
  9. Stool test - for faecal calproctectin = surrogate marker for inflammation in the bowel = indicator of migration of neutrophils int he intestinal mucosa (cannot tell you source or cause of inflammation - raised in IBD, colon cancer, etc.)
41
Q

x

A

x

42
Q

x

A

x

43
Q

Why bother with a stool sample if the GP has already checked?`

A

Need 3 samples 2 days apart as ova and cysts shed intermittently

So could have been none present in the sample given to the GP

44
Q

All investigations normal except - raised WCC, raised CRP and elevated faecal calprotectin

What are the top differentials for Lucy Allen?

A

Investigation results suggest inflammation

Differentials narrow to IBD or colon cancer

In a young women, IBD most likely

45
Q

What should be done next?

A

Refer to gastro unit

Here colonoscopy can take place - conducted by a specialist

46
Q

The colonoscopy and histopathology report shows:

Non continuous areas of linear ulcers with cobblestone appearance are seen extending from the caecum through to the splenic flexure. When examined under a microscope, changes are seen in the mucosa, submucosa and muscularis propria. Numerous non caseating granulomas and increased goblet cells noted

What is Ms Allen’s diagnosis and why?

A

IBD - likely Crohn’s

Due to:
Non-continuous areas of abnormality / inflammation
Caecum –> splenic flexure = location
Non-caseating granulomas - collections of neutrophils
Deep ulcerations
Cobblestone appearance
Changes in the mucosa, submucosa and muscularis propria

47
Q

How do UC and Crohn’s differ?

A

IBD = non-continuous and can affect any part of the GI tract from the mouth to the anus; non-caseating granulomas; cobblestone appearance due to long ulcers that go deep into the bowel; affects all layers of the bowel - transmural disease; deep transmural affect = fistula (hollow tube)

Ulcerative colitis (UC) = continuous, starting from the rectum and does NOT extend beyond the large bowel (although in severe cases is may affect small bowel due to backwash); pseudopolyps (raised areas give the appearance of polyps) due to cycle of inflammation and scarring; changes confined to mucosa (and in severe cases = submucosa); lack of fistulas but higher predisposition to colon cancer due to affecting only mucosa and submucosa

48
Q

What treatments can be offered for Crohn’s disease for Lucy Allen?

Conservative
Medical
Surgical

A

Conservative:
Smoothies - replace malnutrition
Diet
Psychological therapies - mental support for socially embarrassing symptoms (difficult to fit into social life)
Patient support groups - meet others with same condition as them
Smoking cessation

Medical:
Acute phase = corticosteroids to induce remission of disease (settle symptoms)
Steroids are not prescribed for life due to long term side effects
Long-term = azothiprine or biologics
Biological medications - synthesised antibodies, interleukins, etc. e.g. infliximab

Surgical:
Resection of the affected areas - most patients with Crohn’s require this due to fistulas

49
Q

Why does smoking worsen Crohn’s but help ulcerative colitis?

A

Causes small areas of infarction in the gut in Crohn’s

Dampen down immune response in UC

50
Q

Does UC and Crohn’s have the same treatment?

A

No, because for UC, inflammation always starts at rectum and proceeds in a continuous fashion - so UC patients can be given local treatments rather than systemic (rectal ointments / medications)

51
Q

What are some complications of UC?

A

High predisposition to Colon Cancer

52
Q

At what age does Crohn’s present?

How does Crohn’s present clinically?

A

Affects people of all ages - symptoms usually start in childhood or early adulthood.

The main symptoms are:

    diarrhoea
    stomach aches and cramps
    blood in your poo
    tiredness (fatigue)
    weight loss

Symptoms may be constant, or come and go (‘come’ = flare up)

53
Q

When should you see the GP regarding Crohn’s?

A

Blood in your poo
Diarrhoea for more than 7 days
Frequent stomach aches or cramps
Lost weight for no reason, or your child’s not growing as fast as you’d expect

54
Q

What are the main treatments for Crohn’s?

A

Medicines to reduce inflammation in the digestive system – usually steroid tablets

Medicines to stop the inflammation coming back – either tablets or injections

Surgery to remove a small part of the digestive system – sometimes this may be a better treatment option than medicines

55
Q

Where can you get support for living with Crohn’s?

A

CoNtrolled symptoms = normal life

Unpredictability of flare ups can affect social life
Support is available from your care team and organisations like Crohn’s and Colitis UK if you need it

56
Q

What causes Crohn’s disease?

A

your genes – you’re more likely to get it if a close family member has it

a problem with the immune system

smoking

a previous stomach bug

an abnormal balance of gut bacteria

57
Q

What are the other symptoms of Crohn’s?

A 
a high temperature
feeling and being sick
joint pains
sore, red eyes
patches of painful, red and swollen skin – usually on the legs
mouth ulcers
children grow more slow than usual
58
Q

What would your GP ask you about?

A

your symptoms
your diet
if you’ve been abroad recently – you might have an infection
any medicines you’re taking
if you have a family history of Crohn’s disease

59
Q

What investigations might your GP do?

A

feel and examine your tummy
take a sample of blood
ask you to provide a poo (stool) sample

60
Q

What investigations might a specialist do?

A

Colonoscopy
Biopsy
MRI/CT Scan

61
Q

How can steroids help with Crohn’s?

A

can relieve symptoms by reducing inflammation in your digestive system – they usually start to work in a few days or weeks

are usually taken as tablets once a day – sometimes they’re given as injections

may be needed for a couple of months – do not stop taking them without getting medical advice

62
Q

What are the side effects of steroids?

A 
weight gain
indigestion
problems sleeping
an increased risk of infections
slower growth in children
63
Q

What can be helpful in children and young adults?

A

Liquid diet
Drinks containing all the nutrients
Avoids the risk of slower growth that happens with steroids

64
Q

What is a liquid diet?

A

liquid diet (enteral nutrition)

involves having special drinks that contain all the nutrients you need, instead of your usual diet, for a few weeks

65
Q

What are the side effects of enteral nutrition?

A

Diarrhoea
Constipation
Nausea

66
Q

What immunosuppressants might be taken with Crohn’s?

A

azathioprine, mercaptopurine and methotrexate

67
Q

What can immunosuppressants do in Crohn’s?

A

can relieve symptoms if steroids on their own are not working

can be used as a long-term treatment to help stop symptoms coming back

are usually taken as a tablet once a day, but sometimes they’re given as injections

may be needed for several months or years

68
Q

What are the side effects of Immunosuppressants?

A

feeling and being sick, increased risk of infections and liver problems

69
Q

What biological medicines are used in Crohn’s?

A

adalimumab, infliximab, vedolizumab and ustekinumab

70
Q

What can biological medicines do in Crohn’s?

A

can relieve symptoms if other medicines are not working

can be used as a long-term treatment to help stop symptoms coming back

are given by injection or a drip into a vein every 2 to 8 weeks

may be needed for several months or years

71
Q

What are the side effects of biological medications?

A

increased risk of infections and a reaction to the medicine leading to itching, joint pain and a high temperature

72
Q

When might surgery be recommended?

A

the benefits outweigh the risks or that medicines are unlikely to work

73
Q

What does a resection involve?

A
  1. Making small cuts in your tummy (keyhole surgery).
  2. Removing a small inflamed section of bowel.
  3. Stitching the healthy parts of bowel together
74
Q

What might you need to careful about with Crohn’s?

A

Triggers

e.g. certain foods
pharmacy medicines

75
Q

What’s the deal with Crohn’s and vaccinations?

A

Flub jab yearly

Avoid live vaccines e.g. MMR

76
Q

What might be more difficult during a flare up?

A

Getting pregnant

77
Q

What might not work as well when you have Crohn’s?

A

Some contraceptives

e.g. the Pill

78
Q

What are possible complications of Crohn’s?

A

Damage to bowel e.g. scarring, narrowing, ulcers, fistulas

Difficulty absorbing nutrients - osteoporosis, iron deficiency anaemia

Bowel cancer

79
Q

How does the risk of bowel cancer change with Crohn’s?

A

after 10 years the risk is about 1 in 50
after 20 years the risk is about 1 in 10
after 30 years the risk is about 1 in 5

80
Q

What should people with Crohn’s do?

A

Have regular colonoscopies

Y2 - CSI (8 decks)

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