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csi (phase 1b) > case 11 - diarrhoea > Flashcards

case 11 - diarrhoea Flashcards

1
Q

what is diarrhoea?

A

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 weight greater than 200 g/day

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2
Q

what are the three classifications of diarrhoea?

A

acute (≤14 days)
persistent (>14 days)
chronic (>4 weeks)

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3
Q

what is acute diarrhoea?

A

lasting less than or equal to 14 days

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4
Q

what is persistent diarrhoea?

A

lasting longer than 14 days

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5
Q

what is chronic diarrhoea?

A

lasting longer than 4 weeks

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6
Q

how much fluid enters the GI tract every day?

A

approx 10 litres in one day

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7
Q

what are the constituents of the fluid that enters the GI tract every day?

A

ingested food and drink

secretions from salivary glands, stomach, pancreas, bile duct and duodenum

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8
Q

how much of the fluid entering the GI tract is reabsorbed and how much is excreted?

A

99% reabsorbed = 9.9 litres

1% excreted (in the faeces) = 0.1 litres

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9
Q

where does the majority of reabsorption take place in the GI tract?

A

small intestine

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10
Q

what happens in the GI tract as a result of diarrhoea?

A

reduced reabsorption of fluid

increased secretions of fluid and electrolytes

increased bowel motility

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11
Q

what are the two classifications of diarrhoea?

A

inflammatory and non-inflammatory diarrhoea

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12
Q

what are the classifications and sub-classifications of diarrhoea?

A

inflammatory and non-inflammatory

inflammatory = infectious OR non-infectious

non-inflammatory = secretory or osmotic

osmotic = malabsorption or maldigestion

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13
Q

what are some infectious causes of inflammatory diarrhoea?

A

bacterial, viral or parasitic infection

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14
Q

what are some non-infectious causes of inflammatory diarrhoea?

A

(inflammation due to) bowel ischaemia, radiation injury or inflammatory bowel disease

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15
Q

what symptoms does inflammatory diarrhoea present with?

A

mucoid or bloody stool

tenesmus

sever crampy abdominal pain

fever

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16
Q

define tenesmus

A

continual or recurrent inclination to empty the bowels

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17
Q

what is the most common cause of infectious inflammatory diarrhoea?

A

bacterial infection (Campylobacter, Salmonella, Shigella, E. coli C. difficile)

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18
Q

who is affected by viral inflammatory diarrhoea most commonly?

A

children who attend day care centres

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19
Q

who is affected by protozoa/parasitic inflammatory diarrhoea most commonly?

A

people in developing countries (get acute diarrhoea as a result)

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20
Q

what does infectious inflammatory diarrhoea usually look like?

A

small in volume, but frequent bowel movements

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21
Q

why does infectious inflammatory diarrhoea not usually result in volume depletion?

A

small in volume, but frequent bowel movements

can result in volume depletion in children/young adults

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22
Q

what will a stool test for infectious inflammatory diarrhoea show?

A

high leukocytes (but false-negatives common)

faecal occult blood

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23
Q

what does non-inflammatory diarrhoea look like?

A

watery, large volumes and frequent stool (10-20 per day)

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24
Q

why does non-inflammatory diarrhoea usually result in volume depletion?

A

usually larger volumes and watery so increased fluid loss

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25
Q

which type of diarrhoea is usually associated with volume depletion and why?

A

non-inflammatory diarrhoea as it is watery and large in volume whereas inflammatory diarrhoea is smaller in volume

(both have frequent bowel movements)

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26
Q

what are the symptoms of non-inflammatory diarrhoea?

A

large volumes of water stool + cramping

no tenesmus/blood in stool/fever/faecal leukocytes

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27
Q

compare the symptoms of inflammatory and non-inflammatory diarrhoea

A

inflammatory diarrhoea presents w tenesmus, mucoid and bloody stool, fever and abdominal cramps whereas non-inflammatory diarrhoea only presents w abdominal cramps

inflammatory = small volumes, frequent

non-inflammatory = large volumes, watery stool, frequent

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28
Q

compare the histology of the GI tract in inflammatory and non-inflammatory diarrhoea

A

histology of the GI tract is abnormal in inflammatory diarrhoea but is preserved in non-inflammatory diarrhoea

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29
Q

what are the two categories of non-inflammatory diarrhoea?

A

secretory and osmotic

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30
Q

how do the stool test results differ for the two types of diarrhoea?

A

blood in stool and faecal leukocytes present = inflammatory

NO blood in stool and faecal leukocytes absent = non-inflammatory

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31
Q

why does secretory diarrhoea occur?

A

altered transport of ions across the mucosa

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32
Q

how does secretory diarrhoea occur?

A

altered transport of ions across the mucosa

SO increased secretion and less reabsorption of ions of fluid and electrolytes

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33
Q

how are the types of non-inflammatory diarrhoea affected by fasting?

A

secretory diarrhoea does not decrease by fasting

osmotic diarrhoea usually improves/stops on fasting

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34
Q

what are some causes of secretory diarrhoea?

A

enterotoxins (cholera, S. aureus, E. coli)

hormonal agents (neuroblastoma, small cell cancer of lung, vasoactive intestinal peptide)

laxative use

intestinal resection

bile salts, fatty acids

coeliac sprue, collagenous colitis, hyperthyroidism, carcinoid tumours (= chronic diarrhoea)

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35
Q

why does osmotic diarrhoea occur?

A

due to the presence of unabsorbed/poorly absorbed solute in the GI tract

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36
Q

how does osmotic diarrhoea occur?

A

due to the presence of unabsorbed/poorly absorbed solute in the GI tract

= increased secretion of liquids into the gut lume

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37
Q

what happens if you measure stool electrolytes in osmotic diarrhoea?

A

increased osmotic gap

but not significant as stool always isoosmotic - 260-290 mOsml/L

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38
Q

what are the two categories of osmotic diarrhoea?

A

malabsoprtion and maldigestion

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39
Q

what is malabsoprtion diarrhoea?

A

a type of non-inflammatory, osmotic diarrhoea

diarrhoea due to impaired absorption of nutrients across the gut lumen

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40
Q

what is maldigestion diarrhoea?

A

a type of non-inflammatory, osmotic diarrhoea

diarrhoea due to impaired digestion of nutrients within intestinal lumen or at the brush border membrane of mucosal epithelial cells

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41
Q

what are the causes of malabsorption diarrhoea?

A

mesenteric ischaemia, short bowel syndrome (post a bowel resection), mucosal disease (coeliac disease)

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42
Q

what are the causes of maldigestion diarrhoea?

A

pancreatic exocrine insufficiency, lastase deficiency

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43
Q

what are the broad causes of diarrhoea?

A

infection of the bowel

inflammation of the bowel

irritation of the bowel

increased bowel motility

secretion of water into the bowel

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44
Q

why does inflammatory diarrhoea cause mucoid stool?

A

layer of mucus lines and protects the inside of your colon

layer gets damaged due to inflammation so more mucus in stool

+ overactivity of mucus-secreting goblet cells

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45
Q

what is the function of the small intestine?

A

to absorb digested nutrients

to reabsorb 90 % of the water in the GI tract

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46
Q

what is the function of the large intestine?

A

to hold and prepare faeces (containing undigested food, dead
cells, dead bacteria) for egestion from the body.

to reabsorb the remaining 10% of the water in variable amounts

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47
Q

how does water re-enter enterocytes from the lumen?

A

via osmosis from an area of high water potential to an area of low water potential

via aquaporins

48
Q

explain how inflammatory diarrhoea occurs

A

viral/bacterial infection (infectious) OR radiation injury, bowel ischaemia, IBD (non-infectious) etc

inflammatory response damages epithelial lining and impairs enterocyte function

so absorption of nutrients and WATER impaired

49
Q

explain how secretory diarrhoea occurs

A

enterocyte functioning is impaired

instead of retaining the solutes that will allow water absorption, they secrete them into the lumen so water remains in lumen

(if sufficiently low water potential is generated, water from inside the enterocyte side also enters the lumen)

50
Q

explain how osmotic diarrhoea occurs

A

enterocytes and their functioning is intact however due to the presence of solutes in the lumen, an sufficiently strong water potential cannot be established

51
Q

explain how malabsorption diarrhoea occurs

A

a digested solute present in the lumen is not absorbed into the enterocyte and remains within the intestinal lumen and decreases water potential

52
Q

explain how maldigestion diarrhoea occurs

A

enterocytes and their functioning is intact

molecules that should have been digested are not and at they cannot therefore be absorbed, they remain in the intestinal lumen and decrease water potential

53
Q

how does cholera cause secretory diarrhoea?

A

cholera enterotoxin interferes w the transport of ions across the intestinal lumen as chloride secretion is increased and so the osmotic balance is disrupted so water remains inside the lumen

54
Q

give an example of maldigestion diarrhoea

A

lactose intolerance (i.e. lactase deficiency)

also pancreatic exocrine insufficiency

55
Q

give an example of malabsorption diarrhoea

A

sorbitol in prunes is not absorbed = laxative effect

56
Q

which ion is specifically responsible for the ionic imbalance in secretory diarrhoea?

A

chloride ions (secreted into the lumen)

57
Q

why is volume depletion a medical emergency?

A

larger volumes of water are lost causing dehydration which impairs the preservation of blood volume and blood pressure risking hypoperfusion

58
Q

how is volume depletion managed?

A

oral rehydration therapy

59
Q

why is it important to preserve blood volume?

A

sufficient volume = sufficient pressure to perfuse the organs effectively = prevent circulatory collapse and shock

60
Q

what is oral rehydration solution?

A

oral rehydration salts (sodium chloride, potassium chloride, sugars etc) dissolved in water

61
Q

how does oral rehydration solution work?

A

using the SGLT1 transport protein found on the brush border of enterocytes

high enough concentrations of sodium and glucose will activate SGLT1 so two sodium molecules and one glucose are transported into the enterocyte

solutes transported into te blood via transport proteins, decreasing water potential of blood

water follows solute movement into blood, down the water potential gradient, via aquaporins

62
Q

name five cell types present in the gut epithelium

A 
enterocytes
goblet cells
Paneth cells
enteroendocrine cells
stem cells
63
Q

what is the function of enterocytes?

A

absorption of solutes and water

64
Q

what is the function of goblet cells?

A

mucus secretion to facilitate passage of material through bowel

65
Q

what is the function of Paneth cells?

A

secretion of antimicrobial peptides and immunomodulating proteins

66
Q

what is the function of enteroendocrine cells?

A

secrete hormones to influence gut motility

67
Q

what is the function of stem cells in the gut epithelium?

A

continuously replenish the surface epithelium

68
Q

why does secretory diarrhoea not improve with fasting?

A

pumps will secrete solutes into the intestinal lumen and so pathogenesis is not affected by food you eat

69
Q

why does osmotic diarrhoea improve with fasting?

A

digestion of solutes is impaired and so osmotic imbalance increases and can worsen based on the foods you eat (more solutes are being taken into GI tract)

70
Q

differentiate between IBS and IBD

A

IBS = disorder of the gastrointestinal (GI) tract

IBD = inflammation or destruction of the bowel wall = can lead to sores and narrowing of the intestines.

71
Q

which symptoms overlap between IBS and IBD?

A

abdominal pain, faecal urgency and fatigue

72
Q

which features are exclusive to IBS and do not appear in IBD?

A

alternating constipation and diarrhoea, mucoid stool, abdominal bloating

73
Q

what is important to remember about an IBS diagnosis?

A

IBS is a diagnosis of exclusion - rule out majority of possible causes before diagnosing IBS

(i.e. patients suspected of having IBS should be check for UC or CD first)

74
Q

which features are exclusive to IBD and do not appear in IBS?

A

weight loss, fever, blood in stool

75
Q

what are the top differentials for patients that present with chronic diarrhoea?

A

Crohn’s disease OR ulcerative colitis (IBD)

76
Q

list some basic investigations to carry out on a patient that presents with chronic diarrhoea

A

blood tests = FBC, CRP, ESR, LFTs, ferritin, TFTs, vitamin B12 anf folate, U+E

stool tests = faecal calprotectin, serology (microbiology, culture, ova and cysts)

77
Q

why is a FBC done to investigate chronic diarrhoea?

A

to look for anaemia (of chronic disease) and signs of inflammation/infection

78
Q

why are CRP and ESR done to investigate chronic diarrhoea?

A

markers of inflammation

CRP = non-specific marker of inflammation

79
Q

why are U+E done to investigate chronic diarrhoea?

A

to check renal function and electrolyte status

80
Q

why are LFTs done to investigate chronic diarrhoea?

A

liver responds to inflammation by causing hypoalbuminaemia = acute inflammation

+ surrogate marker for malnutrition (frequently seen in IBD patients)

81
Q

why is a ferritin test done to investigate chronic diarrhoea?

A

liver responds to inflammation by sequestering iron from the bloodstream that can further cell damage during inflammation (by partaking in free-radical driven reactions)

so inflammation = high stored iron = high ferritin

82
Q

why is a faecal calprotectin test done to investigate chronic diarrhoea?

A

surrogate marker of inflammation specifically in the bowel

indicative of migration of neutrophils to the intestinal mucosa

83
Q

why are serological investigations (microbiology, ova/cysts) done to investigate chronic diarrhoea?

A

to check for coeliac disease and infective causes

coeliac serology - will present with tissue glutaminase antibody

microbiology - bacterial infection

ova, cysts - parasitic infection

84
Q

why are TFTs done to investigate chronic diarrhoea?

A

hyperthyroidism can also cause diarrhoea (increased gut motility)

  • also caused by hypothyroidism -
85
Q

why are vitamin B12 and folate tests done to investigate chronic diarrhoea?

A

can be due to OR can cause the diarrhoea

86
Q

how are ova and cysts tested for in suspected chronic diarrhoea?

A

three specimens two days apart

as ova and cysts are shed intermittently

87
Q

what are some shared features of CD and UC?

A

chronic inflammation of the GI tract

in genetically predisposed patients

triggered by dysbiosis

symptoms - diarrhoea, tiredness (inflammation is energy consumptive), weight loss (poor absorption of nutrients)

88
Q

define dysbiosis

A

dysregulation of the gut flora

89
Q

what is Crohn’s disease?

A

a chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the GI tract

90
Q

what causes Crohn’s disease?

A

inappropriate immune response against the normal gut flora in a genetically susceptible individual

91
Q

what two factors can exacerbate Crohn’s disease?

A

smoking increases risk of CD

NSAIDs can exacerbate CD

92
Q

what are examples of some NSAIDs?

A

don’t give NSAIDs to Crohn’s patients

ibuprofen, neproxene, diclofenac, indomethacin, high dose aspirin

93
Q

what is ulcerative colitis and what causes it?

A

aberrant immune response in which antibodies are formed against colonic epithelial proteins

94
Q

what are the layers of the GI tract?

A

mucosa, submucosa, muscularis propia, serosa

95
Q

compare the gut layers affected in CD and UC

A

in CD = transmural (all gut layers affected)

in UC = limited to mucosa (rarely, submucosa can be affected)

96
Q

compare the regions affected in CD and UC

A

in CD = entire GI tract affected, in patches

in UC = limited to colon, but always includes rectum

97
Q

compare the pattern of disease in CD and UC

A

in CD = patchy, ‘skip’ lesions

in UC = continuous (in colon)

98
Q

compare the macroscopic findings in CD and UC

A

in CD = cobblestone appearance, strictures, fat creeping (increased risk of fistulas)

in UC = pseudopolyps

99
Q

compare the microscopic findings in CD and UC

A

in CD = non-caseating granulomas, increased goblet cell

in UC = crypt abscesses, decreased goblet cells

100
Q

what causes the patchy ‘skip’ lesions in CD?

A

in CD, the patches of inflammation (i.e. granulomas in specific areas) are interspersed between bits of completely normal mucosa

101
Q

what causes the cobblestone appearance in CD?

A

the patches of inflammation are interspersed between bits of completely normal mucosa = cobblestone appearance

(i.e. granulomas form only in specific areas)

102
Q

what causes the fat creeping in CD?

A

form as a mechanical plug for transmural ulcers to prevent pathogenic bacteria exiting the lumen

(but unclear why the fat continues to advance after this)

103
Q

what causes the strictures in CD?

A

due to repeating cycles of inflammation in isolated sections of bowel

104
Q

what causes the formation of pseudopolyps in UC?

A

benign complication of active colitis - due to mucosal loss

105
Q

what are non-caseating granulomas?

A

granulomas that are not typically cheese-like

cluster of white blood cells that will enclose the pathogenic material separating it from the healthy tissue

106
Q

what are crypt abscesses and why do they form?

A

commonly seen in UC

when crypt structure is affected causing crypt atrophy, crypt loss or crypt branching = impaired ability to remove pathogens that get stuck in this region = abscess formation

107
Q

differentiate between pseudopolyps and polyps

A

polyps have an increased cancer risk associated w them (hyperplasia of mucous membrane causing growth of tissue)

pseudopolyps are a benign overgrowth of

108
Q

compare the flare pattern of CD and UC

A

in CD = continuous symptoms

in UC = relapsing-remitting symptoms

109
Q

what is a functional disorder?

A

cannot detect any abnormalities on blood tests or imaging but symptoms are present

110
Q

how is Crohn’s disease treated acutely?

A

corticosteroids - to induce remission and settle the symptoms

111
Q

how is Crohn’s disease treated in the long term medically?

A

azithroprine - targets purine needed for replication of immune cells

biologics - infliximab works on TNF-alpha to dampen down the immune response and counter granuloma formation

surgery - NOT a cure but treats fistulas and strictures that form

(smoking cessation + avoiding trigger foods = non-medical treatment)

112
Q

how does azithroprine work?

A

targets the purine needed for replication of immune cells

113
Q

how does infliximab work?

A

works on TNF-alpha to dampen the immune response and counter granuloma formation

114
Q

how does smoking affect CD as opposed to UC?

A

in CD = increases risk

in UC = apparent protective effect?

115
Q

what is one extraintestinal manifestation of CD?

A

aphthous ulcers

csi (phase 1b) (8 decks)

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