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Management of GI and Endocrine Conditions > Lecture 8 - Diarrhoea and Constipation > Flashcards

Lecture 8 - Diarrhoea and Constipation Flashcards

1
Q

What is diarrhoea?

A

Increased liquidity of the stool and/or increased loose or liquid stool frequency (>3 times a day)

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2
Q

Classifications of diarrhoea?

A

acute (<14 days)
persistent (>14 days)
chronic (>30 days)

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3
Q

How many people a year suffer from one or more episodes of acute diarrhoea?

A

1 billion

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4
Q

What % of acute cases are caused by infectious agents?

A

90%

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5
Q

what are the two catagories of diarrhoea?

A

Inflammatory and non-inflammatory

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6
Q

What is inflammatory diarrhoea?

A

Presence of an inflammatory process (can be due to viral, bacterial or parasitic infection, radiation injury or inflammatory bowel disease

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7
Q

Symptoms of inflammatory diarrhoea?

A

mucoid and bloody stool, tenesmus, fever, crampy abdominal pain

small frequent bowel movements

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8
Q

Histology of GI tract in inflammatory diarrhoea?

A

abnormal

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9
Q

What is diarrhoea the main cause of?

A

death or disability in the world today

death is due to decreased blood volume

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10
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

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11
Q

Symptoms of non-inflammatory diarrhoea?

A

No tenesmus, blood in the stool, fever or faecal leucocytes

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12
Q

Histology of GI tract in non-inflammatory diarrhoea?

A

Preserved

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13
Q

2 types of non-inflammatory diarrhoea?

A

Osmotic diarrhoea and secretory diarrhoea

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14
Q

Osmotic diarrhoea?

A

Presence of unabsorbed or poorly absorbed solute (eg Mg2+, mannitol and sortbitol - these promote water into the GI tract)

due to maldigestion or malabsorption

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15
Q

Stool volume of osmotic diarrhoea?

A

Small (compared to secretory diarrhoea)

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16
Q

Osmotic diarrhoea stops due to?

A

Stops or improves with fasting

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17
Q

Secretory diarrhoea?

A

altered transport of ions across the mucosa

increased secretion and decreased absorption of fluids

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18
Q

Secretory diarrhoea does not improve with?

A

Fasting

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19
Q

What is maldigestion?

A

when there is impaired digestion of nutrients in the GI lumen or the border of the mucosal epithelial cells

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20
Q

What is the most common cause of acute diarrhoea?

A

Infectious agents such as bacteria, viruses and parasites/protozoa

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21
Q

Bacteria causing diarrhoea?

A

E. coli, campylobacter, salmonella, C difficile, listeria, vibrio cholerae

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22
Q

E coli?

A

most common in developing countries, also a common cause of travellers diarrhoea

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23
Q

Campylobacter?

A

comes from contaminated poultry in developed countries

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24
Q

Salmonella?

A

ingestion of contaminated poultry (eggs and milk products)

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25
Q

C difficile?

A

one of the most common HAI, frequent cause of morbidity and mortality among older hospitalised patients

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26
Q

Viruses that cause diarrhoea?

A

Rotavirus, norovirus, adenovirus, astrovirus

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27
Q

Rotavirus?

A

leading cause of viral gastroenteritis and diarrhoeal deaths worldwide

it is vaccine preventable and causes diarrhoea that results in volume decrease

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28
Q

Norovirus?

A

major cause of epidemic gastroenteritis

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29
Q

Parasites/protozoa that cause diarrhoea?

A

Entamoeba histoltica, giardia lamblia, cryptosporidium

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30
Q

E. histoltica?

A

40-50 million develop colitis or extraintestinal disease annually

~40,000 deaths
is asymptomatic

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31
Q

Giardia lamblia?

A

causes epidemic and sporadic diseases, important cause of water and food borne diarrhoea

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32
Q

Cryptosporidium

A

has become more prevalent with increase of HIV and increased use of immunosuppressants in transplant patients

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33
Q

What is the most common non-infectious cause of diarrhoea?

A

medication

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34
Q

What % of adverse drug reactions does diarrhoea account for?

A

~10%

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35
Q

CV drugs that cause diarrhoea?

A

digoxin, quinidine, propranolol, ACE inhibitors

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36
Q

GI drugs that cause diarrhoea?

A

antacids (magnesium salts), laxatives, H2 antagonists

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37
Q

Endocrine system drugs that cause diarrhoea?

A

oral hypoglycaemic agents, thyroxine

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38
Q

Antibacterials that cause diarrhoea?

A

amoxicillin, cephalosporins, erythromycin

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39
Q

What type of diarrhoea do most drugs cause?

A

secretory

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40
Q

What are the 4 main processes of the GI tract?

A

digestion, absorption, secretion and motility

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41
Q

How much fluid enters GI tract every day?

A

Normally ~10L

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42
Q

How much fluid is reabsorbed?

A

~99%, 0.1ml is excreted normally

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43
Q

What is the major site of reabsorption?

A

the small intestine

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44
Q

What is diarrhoea caused by?

A

a decreased absorption of fluids and/or increased secretion of fluid

can also be caused by an increase in bowel motility

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45
Q

What does water follow?

A

the movement of electrolytes and glucose

follows the osmotic gradient

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46
Q

What do epithelial cells do?

A

form a boundary between the external environment and internal environment

they also transport material across cells

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47
Q

What is absorption?

A

transporting material from the lumen to the internal environment

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48
Q

What is secretion?

A

process of transporting material from the internal environment to the lumen

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49
Q

What are enterocytes?

A

the intestinal absorption cells

they are similar to columnar epithelial cells

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50
Q

Where are enterocytes found?

A

all the way along the large and small intestine, they are the most abundant cell in the GI tract

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51
Q

What do microvilli do?

A

increase the surface area for digestion and transport of molecules from the lumen

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52
Q

What membrane faces the GI lumen?

A

apical membrane

53
Q

What membrane faces the interstitial fluid?

A

the basolateral membrane

54
Q

Why is transport across enterocytes possible?

A

the membrane on one side has different transport systems to the membrane on the other side, meaning that they are polarised cells

55
Q

Give examples of mechanisms that can cause diarrhoea?

A

increased Cl- secretion

reduced Na+ absorption

increased paracellular permeability

reduced Cl- absorption

reduced H2O absorption

reduced Na+ and glucose absorption

56
Q

How does water move across cell membranes?

A

It is not actively transported

active transport of sodium results in a decrease concentration of sodium on one side the the epithelial later and an increase on the other side, these changes are accompanied by changes in water concentration, which causes water to move by osmosis

57
Q

What diarrhoea does vibrio cholerae cause?

A

acute diarrhoea that does not cause enteritis

58
Q

What does adenelyl cyclase do?

A

converts ATP to cAMP

59
Q

what does an increase in cAMP in the cell do?

A

activates protein kinases

it also inhibits the Na+/H+ exchanger, which prevents absorption of sodium from the GI lumen (attracts water to the GI lumen)

60
Q

What does the use of antibacterials cause?

A

a distruption of normal intestinal microflora and proliferation of opportunistic pathogens (C difficile)

61
Q

What does C difficile produce?

A

2 different toxins

62
Q

What % of cases of drug induced diarrhoea are due to antibacterials?

A

~25%

63
Q

What % does C difficile account for?

A

> 20% of antibacterial associated diarrhoea and almost all causes of pseudomembranous colitis

64
Q

What is the disease spectrum of antibacterial associated diarrhoea?

A

from benign to pseudomembranous colitis

most frequently it is benign, appearing within the first days of treatment and disappearing when treatment is stopped

65
Q

What else can antibacterials cause?

A

impaired fermentation of poorly absorbed carbohydrate and/or reduced production of short chain fatty acids - resulting in diarrhoea

66
Q

Frequency of diarrhoea caused by antibiotics?

A

~40%

67
Q

What does reduction in intestinal transit time cause?

A

inadequate absorption of nutrients

68
Q

What do drugs with cholinergic activity do?

A

mimic the parasympathetic effects of acetylcholine by directly acting on the acetylcholine receptors on smooth muscle cells

69
Q

How does pilocarpine work?

A

Has cholinergic activity
(usually used for dry mouth)

excites smooth muscle cells in the GI tract causing an increase in the motility and leading to diarrhoea as an adverse effect

70
Q

Drugs with anticholinesterase activity?

A

Donepezil (for Alzheimer’s disease)

drug prevents the breakdown of acetylcholine, allowing it to accumulate in the synaptic and neuromuscular junctions, prolonging its effect

this enhances contractile effects and produces diarrhoea in up to 14% of patients

71
Q

Drug treatment of diarrhoea?

A

antimotility drugs such as loperamide

these prolong the duration of intestinal transit by binding to opioid receptors in the GI trat

72
Q

when to use antimotility drugs?

A

in uncomplicated acute diarrhoea in adults, not good for use in young children

73
Q

What is important in all forms of acute diarrhoea?

A

fluid and electrolyte replacement

74
Q

Symptomatic treatment of diarrhoea?

A

diet and oral rehydration therapy

75
Q

Treatment of severe diarrhoea?

A

hospitalisation may be necessary for parenteral rehydration therapy and correction of hypokalaemia

76
Q

How does most diarrhoea resolve?

A

Most are self limiting and resolve themselves without treatment

77
Q

What does diphenoxylate work on?

A

Mu opioid receptors on neuronal varicosities

78
Q

What does diphenoxylate cause?

A

a decrease in acetylcholine release, which results in a decrease in peristaltic activity and increased segmental contraction

79
Q

How is diphenoxylate usually provided?

A

as a mixture with atropine (co-phenotrope)

80
Q

What is codeine phosphate used for?

A

symptomatic relief of chronic diarrhoea

POM medicine

81
Q

Mechanism of codeine phosphate ?

A

similar to that of diphenoxylate

82
Q

Adverse effects of opiates?

A

rebound constipation

higher doses can have CNS effects

prolonged use can lead to opioid dependence

83
Q

What side effects can patients taking medication that contains atropine experience?

A

nausea and dry mouth

84
Q

What receptors does racecadotril activate?

A

delta opioid receptors

85
Q

What does activation of delta opioid receptors cause?

A

decreased cAMP, causing a decrease secretion of Cl-, and therefore decreased secretion of water

86
Q

What are the endogenous activator of delta opioid receptors?

A

enkephalins

87
Q

What is racecadotril metabolised to?

A

Thoirphan

88
Q

What is thiorphan?

A

an enkephalinase inhibitor (prevents the breakdown of enkephalins)

89
Q

What does thiorphan cause?

A

enkephalins to be present for longer and stimulate delta opioid receptors, causing a longer inhibitory effects on the chloride ion channels and iproves diarrhoea

90
Q

What does racecadotril act as?

A

an anti-secretory drug and is less likely to cause rebound constipation

91
Q

What is constipation?

A

it is a symptom rather than a disease itself

a heterogenous disorder

92
Q

What do patients with constipation report?

A

One of more of -

fewer than 3 bowel movements per week

straining

lumpy or hard stools

sensation of anorectal obstruction

sensation of incomplete defaecation

manual manoeuvring required to defaecate

93
Q

What causes primary constipation?

A

intrinsic defects in colonic function

94
Q

Subtypes of primary constipation?

A

normal transit constipation

slow transit constipation

pelvic floor dysfunction

irritable bowel syndrome with constipation

95
Q

Normal transit constipation?

A

most common subtype, stool passes through the colon at a normal rate but patient finds it difficult to evacuate the bowels

96
Q

Slow transit constipation?

A

decreased frequency, decreased urgency or straining

more common in females - have impaired phasic colonic motility

97
Q

Pelvic floor dysfunction?

A

patients report prolonged/excessive straining, feeling of incomplete evacuation, difficult meals to evacuate

98
Q

irritable bowel syndrome?

A

many reasons - genetic, environmental, psychological

99
Q

Secondary constipation?

A

medications, metabolic disorders (hypercalcaemia, hypothyroidism), endocrine disorders, psychiatric (anxiety, depression, spinal cord diseases)

100
Q

Drugs causing constipation?

A

drugs with anticholinergic activity, opioids, drugs effecting electrolytes, laxative misuse

101
Q

Drugs with anticholinergic activity?

A

antidepressants, antihistamines, antimuscarinics, antipsychotics, antiparkinsonian agents

lead to a decreased motility which results in constipation

102
Q

Antimuscarinics have …?

A

an inhibitory effect on the GI tract

103
Q

Opioids causing constipation?

A

mechanism of action to treat diarrhoea will cause constipation by suppressing peristalsis, raise sphincter tone which delays passage time of faeces through GI tract

104
Q

What does a delayed passage time through GI tract cause?

A

increased absorption of water and electrolytes

105
Q

What does laxative misuse lead to?

A

atonic colon

106
Q

Treatment of constipation

A

Laxatives

drug treatment is commonly used in constipation associated with IBS and chronic idiopathic constipation

107
Q

Osmotic laxatives?

A

drawing fluid into the body or retaining fluid

macrogols, saline purgatives (milk of magnesium)

can take up to 48 hours to work

108
Q

Stimulant laxatives?

A

increase motility and can cause stomach cramps

should be avoided if there is intestinal obstruction

excessive use can cause diarrhoea

rapid acting (8-12 hours)

109
Q

Examples of stimulant laxatives?

A

glycerol and senna

110
Q

Bulk forming laxatives?

A

Increase faecal mass which stimulated peristalsis

good for patients with hard stools and adequate fluid must be maintained to avoid intestinal obstruction

111
Q

Examples of bulk forming laxatives?

A

methylcellulose, isphagula husk

112
Q

Faecal softeners?

A

liquid paraffin

113
Q

What is linaclotide?

A

14 amino acid synthetic peptide

114
Q

What does linaclotide activate?

A

guanylate cyclase C (GC-C)

115
Q

What does activation of GC-C cause?

A

increase cGMP and activation of PKG

116
Q

what does increase cGMP and activation of PKG cause?

A

phosphorylation on Cl- channel, resulting in increased efflux of Cl- (and water)

117
Q

What is GC-C?

A

a membrane protein which is also an enzyme

located on the apical membrane of the enterocytes

118
Q

What is use of linaclotide restricted to?

A

restricted to use in patients with moderate to severe IBS with constipation who have not responded to other suitable treatments

119
Q

How is linaclotide taken?

A

it is orally active

120
Q

What is lubiprostone?

A

member of a class of agents called prostones

121
Q

What are prostones derived from?

A

functional fatty acids that occur naturally

122
Q

What does lubiprostone activate?

A

it directly activates the Cl- channel (CIC-2)

123
Q

What happens upon activation of the Cl- channel

A

there is an efflux of Cl- into the GI lumen, which water follows

this relieves symptoms of constipation

124
Q

What does drawing water into the GI lumen do?

A

helps facilitate movement of the stool to the colon

125
Q

What is lubiprostone used to treat?

A

chronic idiopathic constipation in the adult population

126
Q

What else might lubiprostone do?

A

restore mucosal barrier function

127
Q

What are the adverse effects of linaclotide and lubiprostone?

A

They are generally well tolerated

diarrhoea
nausea
vomiting
abdominal pain

128
Q

What has lubiprostone not been approved for?

A

SMC has not approved it for treatment of chronic idiopathic constipation (due to cost/benefit analysis)

Management of GI and Endocrine Conditions (24 decks)

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