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Objective 6

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Objective 6. Discuss the pathophysiology, symptoms, d/dx and investigations of diarrhoea and
constipation.
Diarrhoea is the passage of >250g of liquid stool per day, it can be a sign of infection, malabsorption
or osmotic and secretory diarrhoea, if it is bloody it may be a sign of infarction or dysentery (bloody
with mucous stool, sign of infection). It can also occur in the small and large bowel.
Diarrhoea can be caused by:
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mucosal atrophy in the small intestine with loss of the villi and concurrent loss of the brush
border disaccharidases.
Problems with cell mediated immunity which predispose patients to parasitic infection of
the bowel.
Loss of lactase, a disaccharidase, which causes problems when dairy products are
consumed.
Types of diarrheal diseases:
1. Acute (<3 weeks)
2. Chronic (>4 weeks)
These are further subdivided into:
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Invasive
Osmotic- excessive amounts of solutes retained in the intestinal lumen, as water is not
absorbed, diarrhoea will result. Osmotic diarrhoea is usually as a result of ingestion of poorly
absorbed substrates for e.g. carbohydrate or divalent ions such as mannitol or sorbitol,
Epson salt MgSo4 and some antacids MgOH2 and malabsorption, commonly carbs such as
lactose. Osmotic diarrhoea stops if the patient stops consuming the poorly absorbed solute
or fasts for a certain period.
Secretory- caused when secretion of water into the intestinal lumen exceeds absorption.
Will not resolve after a 2-3 day fast.
Malabsorption
Test used to diagnose diarrheal diseases:
a) Faecal smear for leucocytes (invasive diarrhoea)
b) Calculation of stool osmotic gap (SOG) [2 * (random stool Na++ random stool K+}, where
300mOsm/kg = normal plasma osmolality levels, osmotic gap < 50mOsm/kg = secretory
diarrhoea (characterised by a loss of isotonic fluid e.g. on cholera) indicating that the
diarrheal fluid POsm approximates the normal POsm and an osmotic gap > 100 mOsm/kg =
osmotic diarrhoea (e.g. in lactase deficiency (a common genetic defect in Native Americans,
Asians, and Africans. Colonic anaerobes degrade undigested lactose into lactic acid and H2
gas leading to abdominal distention with explosive diarrhoea), or due to certain laxatives)
indicating a hypotonic loss of stool caused by the presence of osmotically active
substances.
Malabsorption: this is chronic diarrhoea with increased faecal excretions of fat (steatorrhea).
Concurrent deficiencies of fat- soluble vitamins, minerals, carbohydrates and proteins are commonly
present.
Diarrhoea associated with deranged motility.
Disorder in motility can accelerate the transit time and decrease the absorption of water and
nutrients resulting in diarrhoea even of the absorptive process was proceeding properly.
Constipation
This is a symptom generally defined as when bowel movements occur three or fewer times a week
and are difficult to pass. It is due to reduced colonic motility and can be caused by a lack of fibre
intake, immobility drugs that reduce transit time (antidepressants, antacids with Aluminium or
Calcium, antihistamines, diuretics and anti -Parkinson drugs) and depression.
It is also associated with small bowel disease and presents as colicky pain (which is a sharp localised
gastrointestinal or urinary pain that can arise abruptly and tends to come and go in spasm like
waves) accompanied by constipation and the inability to pass gas.
If left unrecognized, it can develop into sequelae such as anorectal disorders.
If a patient experiences at least two of the following symptom over a 6 month period, it can be
deemed constipation:
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fewer than three spontaneous bowel movements per week
Straining for more than 25% of defecation attempts
Lumpy or hard stools for at least 25% of defecation attempts
Sensation of anorectal obstruction or blockage for at least 25% of defecation attempts
Sensation of incomplete defecation for at least 25% of defecation attempts
Manual maneuvering required to defecate for at least 25% of defecation attempts
Also the patient must rarely have loose stools present without use of a laxative and must not meet
Rome IV criteria for IBS.
Other symptoms of constipation are:
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Abdominal bloating
Pain on defecation
Rectal bleeding
Spurious diarrhoea
Low back pain
Feeling of incomplete evacuation
Digital extraction
Tenesmus
Enema retention
The following signs and symptoms, if present, are grounds for particular concern:
 Rectal bleeding
 Abdominal pain (suggestive of possible IBS with constipation [IBS-C])
 Inability to pass flatus
 Vomiting
Constipation is diagnosed by:
 Rectal and perineal examination
 Imaging studies to rule out process that may cause colonic ileus, sources of sepsis or intraabdominal problems in patients with leucocytosis or other systemic intra-abdominal
processes, or to determine the cause of chronic constipation.
 Lower GI endoscopy, colonic transit study, defecography, anorectal manometry, surface anal
EMG and balloon expulsion testing.
Management
 Initially treatment may be manual disimpaction and transrectal enemas
 Dietary changes (increase fibre and fluid intake and decreased ,milk products, coffee, tea,
alcohol)and exercise rather than laxatives, enemas and suppositories.
 Bulk forming medications e.g. psyllium
 Emollient stool softeners e.g. docusate
 Rapidly acting lubricants e.g. mineral oil
 Prokinetics e.g. tegaserod
 Stimulant laxatives e.g. senna
 Prucalopride
 Lubiprostone
 Linaclotide
 Mu opioid receptor antagonists.
Constipation may originate from within the colon and rectum or externally via the following
processes:
 Colon obstruction
 Slow colonic motility
 Outlet obstruction (anatomical or functional) Anatomic outlet obstruction may derive from
intussusception of the anterior wall of the rectum on straining, rectal prolapse, and
rectocele; functional outlet obstruction may derive from puborectalis or external sphincter
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spasm when bearing down, short-segment Hirschsprung disease, and damage to the
pudendal nerve, typically related to chronic straining or vaginal delivery
Hirschsprung disease in children
Chagas disease
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