Constipation, Diarrhea, and Other Diseases - 1 (1) PDF

**[CONSTIPATION, DIARRHOEA, IBS, DIVERTICULAR DISEASE, STOMAS, EXOCRINE PANCREATIC INSUFFICIENCY. ]** **[CONSTIPATION. ]** [The functions of the large intestine and formation of faeces. ] Food passes from the small intestine and passes along caecum, colon and into rectum by peristalsis. Water and...

**[CONSTIPATION, DIARRHOEA, IBS, DIVERTICULAR DISEASE, STOMAS, EXOCRINE PANCREATIC INSUFFICIENCY. ]** **[CONSTIPATION. ]** [The functions of the large intestine and formation of faeces. ] Food passes from the small intestine and passes along caecum, colon and into rectum by peristalsis. Water and salts are absorbed which causes the drying of the stools and if there is excess drying of the stools, it can cause constipation. The role of bacteria in the intestine and the whole GI tract is. - Fermenting non-digestible polysaccharides, some metabolites absorbed. - Produce vitamin K and biotin (vit B7) which can be absorbed. - Produce gases from undigested polysaccharides. - Essential for development of caecum and lymphatics. Faeces itself is stored in the rectum until there is an urge for defecation. Stools get hard when stored in the rectum for longer than normal since a lot of water is absorbed from it. **Constipation**: is the passage of hard stools less frequently than the patient's own normal pattern. This is entirely dependent on the patient as other people will have a normal pattern different than others. Constipation itself is a symptom and not a disease, it could be a side effect of a medication or another disease but it's not a disease. It is characterized by the difficulty in opening the bowel and typically we look at patients, going less than three (3) per week, straining to open bowels more than 25% of occasions and patient experiencing hard or pellet-like stool on more than 25% of occasions. Chronic constipation is defined as if in the previous 6 months the patient has experienced any of the symptoms mentioned above for greater than 3 months which is 50% of the last 6 months. It is common and affects all age groups; 1 in 7 adults experience it, 1 n 5 older people experience it, 1 in 3 children, it is more common in women than men, late pregnancy and people taking regular medicines because some medicines can cause constipation. [Aetiology of constipation] - Age: very young and very elderly patients are more at risk. - Diet; low fibre diet, high animal fat intake, inadequate fluid intake, high caffeine intake and high alcohol intake. - Poor bowel habits: ignoring the urge to defaecate so we advise to never ignore the call to stool. - Imaginary constipation: eg in an adult who doesn't eat as much as they used to and hence does not go that much now but still thinks they should be going more frequently. - Can be a side effect of many medications; antacids (AL and Ca salts), antispasmodics, antidepressants (amitriptyline, doxepin), iron tablets (ferrous sulphate), diuretics, painkillers (codeine, morphine), ca channel blockers (diltiazem, verapamil), ACE inhibitors (enalapril, lisinopril), anticholinergic (hyoscine, tolterodine), ulcer healing (lansoprazole, omeprazole) and antipsychotics. - Laxative abuse - Irritable bowel syndrome - Intestinal obstruction: scarring from IBD, diverticulitis of post-surgery, adhesions, intestinal cancers, abdominal hernia, gallstones wedged in intestine, volvulus, foreign bodies, intussusception, haemorrhoids, fissures. - Other diseases causing constipation; diabetic autonomic neuropathy, spinal cord injury or tumours, cerebrovascular accident, multiple sclerosis, Parkinson's disease, connective tissue disorders and Hirschsprung's disease. - Mechanical problems of the anus and the rectum; rectal relapse. - Poor thyroid function - Lead poisoning - Pregnancy - Travel - Immobility. Diagnosis - First look at the patient's medical history - Then look at history of symptoms; what are the normal patterns of defecation, any other symptoms, frequency and consistency, faecal impaction, incontinence, how long/intense are the symptoms? And the impact it has on daily life. - Medications - Changes in diet and lifestyle: change jobs, holidays, and diet Constipation in children. Prevalent if 5-30% of children and mostly the cause is unknown in children but frequently is put down in a change in their diet if they move from breast milk because breast milk can be a laxative and in addition as they start to consume new semi solids this can have an impact on their GI system which can contribute to the development of constipation in children. The symptoms will typically be infrequent bowel activity, they will have foul smelling wind and stools, excess of flatulence and irregular stool texture, abdominal pain distention and discomfort. In older patients, the main cause is the GI losing its elasticity and some patients have lack of motility and this can cause it. Poor diet and it can be a side effect of many medications. [Summary]. - Constipation is a symptom, not a disease. - It affects a high percentage of the population. - Many factors can cause constipation. - When constipation has been confirmed appropriate steps need to be taken to manage the problem.. Lifestyle and dietary changes.. Short course of laxatives. Goals of constipation Management. 1. Achieve an individual's normal frequency of defecation. 2. Establishing regular, comfortable defecation. 3. Preventing laxative dependence. 4. Relieving discomfort. Faecal loading is a generalised term for the buildup of faecal matter within the colon whiles impaction is when it has stayed there for a longer period and hence the body has had a lot of time to reabsorb the water from it which results in a hard dry material which the patient cannot get rid of. Hard stools are seen mostly in impaction whiles low stools are mostly seen in loading. For hard stools which are mainly of the faecal impaction, the guidelines say we should give a high dose oral macrogol which is an osmotic laxative which will draw water into the stool making it easier for the body to eject it. If after 48 hours, there is no improvement then we can move to a stimulant like senna or bisacodyl and we aim to get a movement of the bowel in about 12 hours. If still no improvement, then we can move to the next step where we consider moving to a glycerol alone or adding it to a bisacodyl suppository and we expect to get a response early with these. If the response is still inadequate, then we can move to a sodium phosphate (a powerful potent osmotic laxative) or arachis oil retention enema which is going to improve the symptoms of the patient. For a soft stool which is mostly a symptom of faecal loading, the first step is to use a stimulant laxative like senna or bisacodyl and if unsuccessful then we can consider moving to docusate which is also an osmotic laxative with a stimulant effect also or a sodium citrate mini enema which is also an osmotic laxative. [Patients with opioid induced constipation]. According to the guidelines, for patients on opioids, we do not suggest bulk forming laxatives, and this is because for bulk forming laxatives, they increase faecal mass and hence they stimulate peristalsis in the colon, but opioids are known to cause contraction of the bowel and hence there is an antagonistic effect, so we avoid bulk forming laxatives like fibrogel. For a patient who is on opioids, the first line is to give osmotic laxatives like docusate or macrogols which makes the stools much softer and easier to excrete and adding a stimulant laxative like senna which are going to act directly on the bowel and stimulate peristalsis which allows the bowel to overcome the activity of the opioid on the bowel. If the patient has been unsuccessful of the pure laxatives used, then we can consider switching to the new ones like naloxegol which is a peripherally acting mu-opioid receptor antagonist (PAMORA). We can give good lifestyle advice patients like increased physical activity which can cause bowel movement and increase the fluid intake to at least 2L per day. Note that if the patient is having increased physical activity, then the water intake should increase accordingly. We can also advice high fibre diet (patient should aim for at least 30g of fibre per day). [Pregnancy and breastfeeding]. The first line is to offer a bulk forming laxative and depending on the response of the patient, wither add in or switch to osmotic laxative then we can then consider a short course of a stimulant such as Senna (never do this close to term, only prescribed, NOT OTC because it can stimulate labour contractions. Then we can move to glycerol suppository. [Children]. The first line is to offer a macrogol (pediatric version) and negotiated and nonpunitive behavioural interventions suited to persons stage of development. The second line of treatment is a stimulant laxative or if the first line is not tolerated then you switch to a stimulant laxative. The third line is to add lactulose (or another softening laxative) if macrogol not tolerated. Continue at maintenance dose (which may be for several months). Some paediatric macrogol products are not licensed for children under 2(such as Cosmo Col paediatric) informed and documented verbal consent recommended for prescriber). Suppositories and enemas not recommended for routine use in primary care. Laxatives may be needed for several months (to overcome the learned behaviour). [Bulk Forming laxatives].  The take home message is that for the bulk forming laxatives, we advise patients not to take this just before bed and this is because during the night time there is little or no activity of the stimulation of the bowel and when you take bulk forming laxatives, it stimulates the bowel by increasing the volume of the stool which means it has an opposite effect to what the normal thing is. The patient must have a good fluid intake because bulk forming laxatives will draw fluid into the stools and also takes longer for it to have an effect, 2-3 days for effect. [Osmotic laxatives]. A close-up of a product list Description automatically generated Macrogols vary in terms of their sodium content and hence it is important to check. Lactulose does not cross the gut wall, so it has no effect on body's sugar levels. Magnesium hydroxide (milk of magnesia) can be abused, and this is because it empties the stools quite quickly and hence a lot of patients can abuse them. [Suppositories and enemas]. They are mostly used for quick action and are not the preferred options for a lot of patients and hence when giving this, it is worth counselling patients on the reason that these are for fast actions and sometimes the time wait in the oral medications may mean the constipation may get worse and may require hospital admission.  Also, it is worth letting patients know that there is an arachis oil enema which contains peanut oil and hence make sure the patients are not allergic to the peanut before you sell it. [Stimulant laxatives]. They are normally short-term use as they can cause almost a lazy bowel. They are different from the osmotic and the bulk forming laxatives as they work directly on the bowels and that is how they exert their effect by promoting peristalsis. A close-up of a prescription Description automatically generated [Prucalopride]. (brand name: Resolor) It is a 5HT4-receptor agonist with prokinetic properties which means it promotes GI motility. It should be prescribed by clinicians who are specialist in chronic constipation and after careful consideration. It mostly comes in 2mg tablets once daily but there are 1mg tablets as well. The normal dose is 2mg once daily. The treatment will be reviewed and if the patient has had no response after 4 weeks, then the medication will be discontinued. The common side effects are headache and GI disturbances. It should be known that increasing the dose if this medication does not actually improve the response and hence the maximum dose should only be 2mg. It takes 1-2 weeks for effect and the treatment will be reviewed after 4 weeks. The other medication that is worth mentioning is linaclotide. [The pharmacology of bulk forming laxatives]. The bulk forming laxatives are mostly of plant origin which includes non-digestible polysaccharides like cellulose and other components. The mechanism depends on the type of medication but typically the polysaccharides increase osmolality in gut when broken down, causing water retention and as there is water retention in the GIT, it expands and softens the stools which in turn makes stools bulkier and hence distend the colon. As the colon distends it promotes peristalsis via the stimulation of the colonic mucosal receptors/ stretch receptors which then leads to the release of acetylcholine which drives parasympathetic response as well as it can also bind directly to the m3 and m2 receptor subtypes of acetylcholine which increases the peristalsis of the bowel. Also, it creates mucus layer in intestinal lining, facilitating defecation.  Image [The pharmacology of osmotic laxatives]. The osmotic laxatives are poorly absorbed and so they act as osmotic agents and increase water retention in the gut lumen. As hyperosmolar agents, they are absorbed into stool by osmosis which then makes the stools softer and softer stools are easier to pass. Many of the osmotic laxatives contain Mg2+ (magnesium) and magnesium triggers the release of cholecystokinin (CCK) which increases the intestinal secretions and colonic motility. This decreases the transit time through the gut.  [The pharmacology of stimulant laxatives]. The stimulant laxatives stimulate a local reflexes of myenteric nerve plexus of the gut and this irritate the nerve endings in the wall of the intestine. This causes a motor effect on gut all which increases propulsion. Their secondary effect is increasing secretion of water into the bowel which increases gut motility and decreases transit time. Image [Senna pharmacology]. It is an anthraquinone laxative which combine sugars to form glycosides. Glycosides are molecules where sugar is attached to a functional group via glycosidic bond. Glycoside bond is hydrolysed in the gut by the colonic bacteria to release irritant anthracene glycoside derivatives, specifically sennosides A and B. They are also absorbed and have direct action on myenteric nerve plexus which increases smooth muscle activity and hence increases peristalsis. Also, they increase PGE2 secretion which increases gut motility and reduce colonic water retention. [The pharmacology of stool softeners or emollient laxatives]. Some of them work as surface wetting agents/surfactants (e.g., Docusate). This causes a reduced surface tension allows water/fats to penetrate stool which results in the softening of stools, making it easier to pass. Docusate also has some stimulant activity. Arachis oil and paraffin creates a barrier between stool and intestinal wall. This eases the passage of stool through intestine. Paraffin no longer popular due to concerns over carcinogenicity.  [The pharmacology of other agents]. PAMORAs are competitive antagonists at intestinal mu-opioid receptors. They prevent opioid activation of intestinal mu-opioid receptors. Targeting underlying opioid induced side effects ie reduced GI motility, hypertonicity, increased fluid absorption which then results in normal propulsion and peristalsis. Prucalopride is a 5HT4 receptor agonist. 5HT4 receptors are present in GI tract especially myenteric plexus. When the 5HT-4 receptors are activated, they result in the release of acetylcholine (Ach) which then causes an increase in the rest and digest/ parasympathetic drive and in all increases peristalsis and propulsion. [Responding to symptoms]. A person in a suit Description automatically generated [In summary]. - We been through the guidelines. - Discussed lifestyle advice. - Considered specific patient groups. - Focused on specific counselling for each drug classes. - Discussed OTC use. **[DIARRHOEA]**. Diarrhoea is a change in the normal bowel habit of an individual which leads to increased frequency of bowel movements and the passage of soft and watery stools. There may be accompanying colicky pain. This is because, in some cases, there may be increased smooth muscle contractions and production of some gases which in itself can lead to this colicky pain. Diarrhoea is a symptom and not a disease. [Acute diarrhoea]: This is the abrupt onset of \> 3 loose stools/day and lasts no longer than 14 days. Mainly caused by a dietary insult. Example alcohol or spicy foods. There may be a bacterial or viral cause relating to this. In majority of cases, acute diarrhoea resolves within 2 -- 3 days without a specific treatment. [Chronic Diarrhoea]: Here there is a pathological cause and may last for about more than 14 days. Chronic diarrhoea is possibly due to a flare up of previously diagnosed conditions such as IBS. In chronic diarrhoea, mostly there is the need for investigation. [How common is diarrhoea? ] It is much more to quantify as the condition itself is self-limiting and in most cases, people don't report it. - [Children under 5]: In children under 5, acute gastroenteritis is the most common. 1 -- 3 bouts per year. - [Adults]: Just under 1 episode per year. 22% of these are food related. There is also the possibility of traveller's diarrhoea. [Mortality and Morbidity]. Mortality in terms of acute diarrhoea is on a decline mainly since, there are some management systems (ORS) which are used to mainly counteract the effects of diarrhoea (dehydration). It should be noted that diarrhoea is the 2^nd^ highest cause of childhood mortality. Age and nutritional status are the most important host factors in determining the severity and duration of the condition. NB: The younger the child, the higher the risk for severe, life -- threatening dehydration. [Pathophysiology of diarrhoea]. In general, diarrhoea is caused by the change in the balance between secretion and absorption of water and electrolytes. This can be due to two possible factors. - Osmotic force that drives water into the GUT lumen example after ingestion of nonabsorbable sugars (manotol, zylotol or sorbitol) or there could be an underlying condition such pancreatic insufficiencies etc., that renders the ability to digest sugars impossible thereby causing them to be nonabsorbable. It is important to note that this is proportional to the intake of sugars meaning, the more the nonabsorbable sugars are consumed, the more the diarrhoea will occur. Due to this correlation, this form of diarrhoea is responsive to fasting. - There could be enterocytes which are actively secreting fluid example enterotoxin-induced diarrhoea. It should be noted that in this form of diarrhoea, it is unresponsive to fasting. Here, the ion transporters are activated by example bacteria resulting in pathogens. - Invading the enterocytes OR. - Producing enterotoxins which damage cells OR. - Inducing cytokine secretion to produce prostaglandins which stimulate secretion. [Mechanism of diarrhoea]. a. Bacteria causing diarrhoea. Bacteria causing diarrhoea comes in two main ways. i. [Invasive]: Here, the bacteria are directly attacking the mucosal cells which causes the diarrhoea. Here, there may be the presence of blood and pus in stools. The patient may also present with a fever. Example of bacteria causing this will include: Shigella, salmonella, Yersinia, Enteroinvasive E coli. ii. [Non -- invasive]: here the bacteria are not directly damaging the gut but rather, they produce enterotoxins that disrupts secretion. Here the patient may present with watery diarrhoea. Example of bacteria causing this include S aureus, B cereus, C perfingens, Enterotoxigenic E coli. b. Virally induced diarrhoea. In terms of virally induced diarrhoea, the mechanism is not fully understood. Enterocytes become secretory resulting in watery diarrhoea. [Diagnosis]. In terms of diagnosis, a lot of things may be looked at. - [Symptoms]: Are there any accompanying symptoms such as fever, temperature, blood or pus in stool etc., rapid onset of the diarrhoea, is there any absence of stool formation. - [Trigger factors]: Are there the possibility of consuming any bad or unusual food, alcohol intake, drugs or even ingesting contaminated water. - [Time /intensity]: Dehydration in major risk groups. - [Faecal studies]: Identification of the pathogen. - Serum albumin. - Faecal alpha 1 antitrypsin. - Intestinal biopsy. [Common causes of diarrhoea]. - [Infants]: infectious gastroenteritis, toddlers, diarrhoea, food intolerance, coeliac disease. - [School age children]: Infectious gastroenteritis, Drugs (Antibiotics). - [Adults]: Infectious gastroenteritis, IBS, IBD, drugs, XS alcohol and spicy food, coeliac disease. - [Older people]: Infectious gastroenteritis, large bowel cancer, faecal impaction, drugs, ischaemic colitis. [Microorganisms causing diarrhoea]. Children \< 5 years. - Rotavirus most common: Onset 12 -- 48 hours. Adults. - Campylobacter (onset 2 -- 5 days) most common, followed by rotavirus. Other causes. - E coli (1 -- 6 days), Salmonella (12 -- 24 hours), Shigella (1 -- 7 days), Clostridium difficile (usually starts during AB therapy), Clostridium perfringens (12- 18 hours), Bacillus cereus (1 -- 16 hours), Staphlococcus aureaus (1-7 hours). [Examples of drugs that can induce diarrhoea]. Antibiotics -- most common is the broad-spectrum ones. Laxatives. Metformin. Ferrous sulphate (iron). NSAIDs. Colestyramine. Antacids -- Mg salts. Beta blockers. Digoxin. Misoprostol. [Preventing diarrhoea]. Good hygiene. Mainly wash hands. - After visiting the toilet. - Before touching food. - After gardening. - After playing with pets. - Between handling raw and cooked food. **[IRITABLE BOWEL SYNDROME (IBS).]** [Epidemiology]. The onset of IBS is most common in the ages of 20 -- 30 years. It is 2X more common in females when compared to males. IBS is estimated to affect about 10 -- 20% of the population. It should be noted that this figure may be underestimated as most patients who present with IBS self-treat themselves and do not report symptoms. There is about 2X the risk of IBS among 1^st^ degree relatives. NB: There is lack of reliable prevalence data. [Aetiology of IBS]. In terms of the aetiology, the exact cause is unknown. However, it is thought that food intolerances (e.g., lactose/gluten) are precursors to IBS. When looking at IBS, there are no lesions present. That is the gut is not damaged / diseased. - Post infective bowel dysfunction, gut hypersensitivity, altered colonic motility, and heightened pain sensation, stress is all implicated. In terms of post infective bowel syndrome, it could be that a patient may have this infection and then clears it. After clearing it, the patient may present with symptoms of IBS. It is thought that 1 in 6 patients with IBS are because of post infective bowel syndrome. [Pathophysiology of IBS]. In terms of IBS, the gut is structurally normal. This means it is termed as functional GI disorder. Due to this normal structural of the gut, IBS is not detectable in terms of pathology when standard tests are used. NB: It should be noted that blood tests/stool samples/colonoscopy may be used to rule out other conditions à Mainly thinking about the differential diagnosis. - Functional conditions such as IBS requires symptoms management. [Symptoms]. - Abdominal cramping. - Diarrhoea/constipation/alternating. - Flatulence. - Bloating. - Urgency to defecate. In addition to these, the patient may also experience. - Acid indigestion. - Nausea. - Lethargy. - Eating may worsen symptoms. - Passing mucus in stools. [Diagnosis]. In terms of diagnosis there need to be abdominal pain for at least 6 months. This abdominal pain needs to be relieved by defecation OR increased/decreased bowel frequency or stool form. Plus at least 2 of the following. - Abdominal bloating/distention. - Altered passage of stool (straining, urgency, incomplete evacuation). - Worsened by eating. - Passing mucus. In secondary care: the Rome IV criteria are sometimes used. Abdominal pain needs to be present at least 1 day per week in the last 3 months. In addition to this, symptom should have begun at least 6 months prior. Alongside this, more than 2 of the following should be present. - Related to defecation. - Change in stool frequency. - Change in stool form. [IBS Classification (Rome IV criteria).] According to the Rome IV criteria, a patient with IBS symptoms may be classified into 4 different categories based on their stool characteristics using the Bristol stool chart. Attached below is the Bristol stool chart. n. [IBS-C]: A patient with IBS and predominantly constipation symptoms. Here, if more than 25% of stools are type 1 OR 2 and less than 25% are types 6 OR 7. o. IBS-D: A patient with IBS and predominantly diarrhoea symptoms. Here, if more than 25% of the stools are type 6 OR 7 and less than 25% of the stool are types 1 OR 2. p. IBS-M (IBS-Mix). Here if more than 25%of the stool are type 1 OR 2 and more than 25% of the stool are type 6 OR 7. q. IBS-U(IBS unclassified). Here, if a person has IBS but the bowel habits can\'t be categorized as above. [Treatments of IBS]. - Antispasmodic drugs. - Antidepressants. - Laxatives. - Loperamide. - Linaclotide. - [Antispasmodics]: These medications are preferably to be used as they are direct acting smooth muscle relaxants. They include. a. Alverine citrate 60 -- 120 mg up to TDS. b. Mebeverine 135 mg TDS (to be taken 20 mins before food) OR 200 mg BD for the MR preparation. c. Peppermint oil capsules, 1 -- 2 capsules up to TDS. Other antispasmodics that may be used are hyoscine butyl bromide and Dicycloverine but with these they tend to have a lot of antimuscarinic effects. All antispasmodics are contraindicated in intestinal obstruction or paralytic ileus. [Pharmacology of antispasmodics]. The exact mechanism of action of Mebeverine is unknown. It specifically acts on the smooth muscle cells. It blocks the voltage gated sodium channels. This prevents the build-up of intracellular calcium. This reduces the symptoms of colonic hypermotility. - [Antidepressants]: The use of antidepressants in IBS is unlicensed and will only be used for people with IBS pain. It is mainly used for people who usually do not respond to typical treatments. - Doses given are lower than what may be seen for mental health uses. First line: Tricyclic antidepressants (TCA) à mainly amitriptyline at a starting dose of 10 mg at night to be increased to a maximum dose of 30 mg at night. Second line: SSRIs à Sertraline, citalopram, fluoxetine. It should be noted that the BSG do not specify one of these SSRIs to be used as first choice mainly due to their off label in IBS. They do have some pain modulatory effects/peripheral effects on the GI function. It is important to counsel patients as they may be shocked when reading the PIL. - [Laxatives]: For patients with IBS -- C laxatives may be used. Laxatives from any class may be used except lactulose. This is because, lactulose may increase gas production which in turn may worsen the symptom of IBS. - The dose of laxative should be titrated against the symptoms of IBS. NB: Is important to avoid prolonged use of stimulant laxative use. - [Loperamide]: When a patient has IBS -- D, then loperamide may be used. It is important to note that, P/GSL version of loperamide can be used for acute diarrhoea in IBS but only for patients \> 18 years old. This is different from the management of acute diarrhoea without IBS which is licensed for patients \> 12 years. This important distinction is supposed to be made. The patient should have been diagnosed with IBS. It is only recommended for attacks lasting up to 48 hours. Patients should be referred if this is longer. Can be used for up to a maximum of 2 weeks if individual bouts are less than 48 hours. - [Linaclotide]: Is recommended for patients with moderate to severe IBS-C in adults. Is important that for patients to be eligible to use linaclotide, they should have had the IBS-C for at least 12 months. Linaclotide should only be used if maximum tolerated doses of laxatives haven't helped. 290 mcg once daily is supposed to be used 30 minutes before food. Avoid linaclotide in patients with GI obstruction as they have laxative effect which is not good. Also, should be avoided in IBD. [Pharmacology of Linaclotide]. Linaclotide is a Guanylate cyclase-c (GC-C) agonist. The activation of GC-C activation leads to increased production of cyclic guanosine monophosphate (cGMP). Increased cGMP stimulates the cystic fibrosis transmembrane conductance regulator (CFTR) ion channel. CFTR ion channel increases the secretion of chloride and bicarbonate into the intestinal lumen. This leads to increased GI transit. [Red flag referral criteria]. - Unintentional weight loss. - Unexplained rectal bleeding. - Family history of bowel/ovarian cancer. - Loose stools for \> 6 weeks in patients \> 60 years old. - Anaemia. - Elevated inflammatory markers. - Abdominal/rectal masses. **[DIVERTICULITIS]**. Diverticular disease is defined as the presence of diverticula (plural is diverticulum). Diverticula are basically pouching protruding outwards from the large intestinal wall. They can also be small mucosal herniations protruding through the intestinal layers and smooth muscle. - [Diverticulosis]: This is a condition of uninflamed diverticula. This is basically the presence of diverticula in the large intestine of the patient. This condition is basically asymptomatic. - [Diverticular disease]: Here the patient has diverticular and has basically become symptomatic. - [Diverticulitis]: This is a condition where there is the presence of one or more inflamed diverticula which has become infected. [Epidemiology. ] Diverticular disease is very common particularly in industrialised countries. It is thought that westernisation increases the incidence of the condition. It is mainly due to lack of fibre which is found in the food eaten by these westernised countries. Prevalence: In terms of the prevalence, diverticular disease is similar in males and females. It mainly increases with age. It is mostly rare in people aged \< 40 years. About 1/3 people over the age of 65 years, 65% people over the age of 85 years will have diverticular disease. NB: About 80 -- 85% of patients will remain asymptomatic. The condition may only be unveiled when the patient goes for another condition check and finds out of this. It is known that about approximately 5% of patients with diverticulosis will develop diverticulitis. 15 -- 25% of patients with diverticulitis may develop complications which will require surgery. Mortality of the condition is associated with these. - Abscess formation. - Intestinal rupture. - Fistulas (inflammation/abscess causing passageway à linking two sites of the Gut together where is not supposed to be). - Peritonitis (inflammation or infection of the lining abdominal wall and organs in abdomen). - Massive bleeding. Developing these complications are much more common in patients who are immunocompromised, on anti-inflammatories or have sever co-morbidities. [Aetiology]. In terms of aetiology, the causative agents are unknown. However, it is related to. Increased intraluminal pressure and weakening of the muscle wall thought to be a primary cause. Abnormal colonic activity. Defective muscular structure. Changes in collagen structure example aging. Factors thought to be involved. - Genetics: Left-sided diverticula predominate in the west (sigmoid colon) and right-sided predominate in Asians. - Dietary factors: associated with a low fibre diet and constipation and obesity. [Pathogenesis. ] In terms of the pathogenesis, it is mainly the colonic muscular hypertrophy which results in narrowing of the lumen and formation of small chambers with high pressure and subsequent diverticula. - In terms of diverticulitis: faecal material or undigested food collect in the diverticula and cause obstruction. Mucus secretion and normal bacteria overgrowth lead to the formation of distention of diverticula. This results in vascular compromise and perforations. Increase in intraluminal pressure and stuck food particles may also damage diverticula wall thereby resulting in inflammation and necrosis and perforation. Recurrent attacks lead to scar tissue formation and lumen narrowing. [Diverticulosis management]. In patients with diverticulosis, they are basically asymptomatic. As such, there is no need for follow ups. Is important to. a. Advise the patient to maintain a healthy balanced diet especially high in fibre. b. Maintain an adequate fluid intake. c. If the patient tends to be overweight, advise the patient about the benefits of weight loss, exercise and smoke cessation to prevent the progression of the condition. d. If the patient is constipated, the offer a bulk forming laxative. [Diverticular disease]. In this condition, patients may present with an intermittent pain in the lower left quadrant (with constipation, diarrhoea, rectal bleeds). Abdominal pain will be worsened by eating and often relieved upon the passing of stool or wind. The patient may also present with flatulence. There could also be the lower left quadrant tenderness on palpitations. In the Asian population, the symptoms will normally present in the right side. There can also be overlapping symptoms with other conditions such as IBS. NB: In diverticula disease, there is no systemic symptoms present. [Management]. Patient needs to be advised to be taking high fibre food. Bran supplements/bulk-forming laxatives. Also, lifestyle advice as per diverticulosis. Antispasmodics when colic example: Alverne, Mebeverine, peppermint oil etc. Importantly, patients should be told to avoid NSAID. Also, anti-motility drugs that slow the transit time example codeine and loperamide should not be used. This is because, there is risk of diverticular perforation. [Diverticulitis]. In terms of diverticulitis, there is a constant lower left abdominal pain with: - Fever. - Sudden bowel change. - Blood/mucus in stools. - Lower left quadrant tenderness. - Palpable abdominal mass/distention. - Malaise. - Nausea and vomiting. - Increased WBC, if bleeding occurs there could be increased platelets, anaemia, and increased CRP. [Management]. In terms of the management, it is important to refer any patient who is. - over the age 65 years. - Presence of co-morbidities/immunosuppressed. - Can't take oral antibiotics at home. - Dehydrated or at risk of dehydration, can't rehydrate sufficiently from home. - Uncontrollable abdominal pain plus signs of complicated acute diverticulitis. Signs of complicated acute diverticulitis: this will include intra-abdominal abscess which will be detected upon examination. Diverticular haemorrhage which could manifest itself as blood in stools. Peritonitis which will present itself as rigidity/guarding upon examination. Stricture which could present itself as reduced GI motility, constipation and cramping. Fistula formation which can be detected by faecaluria, pneumaturia (bubbles present in the urine), passing faeces through the vagina. Intestinal obstruction with the symptoms being cramping, absolute constipation and distention. There may be sepsis which presented as increase in respiration, increase in heart rate, decrease in systolic BP, no urine output, skin discoloration, cognitive impairment. [Management of acute diverticulitis]. - [A patient with acute diverticulitis and is not systemically well (but does not need admission)] à Co-amoxiclav 500/125 TDS for 5 days (Cefalexin if patient is penicillin allergic) + metronidazole 400 mg TDS for 5 days OR. Trimethoprim 200 mg BD for 5 days + metronidazole 400 mg TDS for 5 days. - [Patients who have acute diverticulitis and are systemic well] à Consider no antibiotics strategy mainly due to antimicrobial stewardship. Encourage the use analgesia such as paracetamol and is important to avoid NSAIDs and opioids. The patient is encouraged to re-present if the symptoms worsen. **[STOMA]**. This is an opening in front of the abdomen which is surgically created either on the bowel or bladder. Mainly to enable the elimination of contents. [Indications]. Diseases. - Inflammatory Bowel Disease (IBD). - Diverticular disease. - Cancer of the Large intestine. Volvulus à Which is twisted bowel. Perforation of the colon. Toxic Megacolon. Colonic Polyps. These above conditions are essentially capable of disrupting the intestine of the patient which will then mean they may require a stoma to enable the elimination of waste from the body. [Types of Stomas]. [Colostomy] à This is a stoma which has been surgically inserted in the colon. [Ileostomy] à A stoma that has been inserted at the site of the ileum. [Urostomy] à This is stoma that is used to remove urine. 1. [COLOSTOMY]. This is the most type of stoma where it is attached to the large intestine. Mainly end colostomy and this could be attached to the. a. [Descending colon] à This means the stool will be firmer. This is because, the body has had enough time to remove the water contents found in the stool by the time it reaches the descending colon thereby accounting for the firmer stools. b. [Ascending or transverse:] Here, there will be fluid stool. This is because there will be less time spent in the colon which means less water will be reabsorbed from the stool. NB: It should be noted that, colostomy may be permanent or temporary depending on the condition to which the patient may need it. [COLOSTOMY BAGS]. Generally, this is a closed bag which is usually disposable. Normally to be changed once or twice a day. This bag is opaque/beige and is more discrete. - Normally use a one- or two-piece system. [One piece system]: Here, the pouch or the bag itself is already attached to the base plate. The base plate is the contact point for the bag to the skin. [Two-piece system]: Here, the base plate is separate from the stoma pouch. The base plate is attached to the skin and the stoma pouch is then attached to the base plate. Here, the base plate may be changed every 3 -- 7 days. 2. [ILEOSTOMY]. This is where the end of the small intestine becomes a stoma. Mainly seen in patients whose large intestine has been removed. It should be noted that, due to the large intestine being removed, the content is the stoma will be generally fluid. This is because the content will have had a reduced opportunity to even form the stool proper and reabsorption of water. [ILEOSTOMY BAGS]. Generally drainable bags which are sometime reusable mainly depending on whether it is an integrated clip or a no closure system. The ileostomy bag can also be a one-piece system or a two-piece system. 3. One piece system. As already mentioned, in the one-piece system the base plate is directly attached to the pouch. 4. Two-piece system Here the base plate separates from the pouch. In ileostomy bags, they may come as integrated clip or a no closure system. If it is an integrated clip system, then it can be reusable, and this means the patient may change this every 3 -- 5 days. If it is closure system, then this will be non-reusable. 5. [UROSTOMY]. This is formed following bladder removal. The output that is seen her is urine. The correct term used is Conduit Urinary Diversion. Here. - Small piece of bowel connected to the ureters. - Acts as a channel for urine. It should be noted that urostomy is not reversible and there is continuous flow. [UROSTOMY BAGS]. There are many different urostomy bags available. These can also be a one-piece system or a two-piece system. 6. One-piece system. 7. Two-piece system. With these urostomy bags, there is a tap outlet which needs changing every 1 -- 3 days. Special stoma nurse is involved in this. In most cases, there is also a night drainage bag which can be used at home whiles the patient is sleeping. The drainage bag is connected to the tap outlet which then drains into the night drainage bag. NIGHT DRAINAGE BAG [OTHER ITEMS AVAILABLE]. Adhesives. Adhesive removers. Deodorants. Skin fillers and protectives. Stoma caps. [Psychosocial dimensions] [COMMON PROBLEMS. ] **[PANCREATIC EXOCRINE INSUFFICIENCY. ]** [Causes of exocrine pancreatic insufficiency]. Ultimately, this is the lack of pancreatic enzymes (amylase, lipase and protease) being secreted into the duodenum. Some other underlying causes of lack of digestive enzymes include. - [Pancreatic resection]: Surgical removal of the pancreas which may be due to a whole load of reasons. This means there will be lack of digestive enzymes being produced. - [Pancreatitis]: Inflammation of the pancreas and this can affect the secretion of the pancreas. A key example is diabetes. Here, there could be atrophies of the pancreas due to lack of insulin. Diabetes is also inflammatory, and this can lead to pancreatic inflammation. - [Coeliac disease]: This may need to pancreatic fibrosis, fewer secretory granules. - [Pancreatic tumour]: This may lead to a blockage of the pancreatic duct. - [Cystic fibrosis]: Here, the pancreatic duct may become blocked with mucus. [Symptoms of Exocrine pancreatic insufficiency]. There is where we see an overlap of symptoms with other conditions. - Macronutrients (fats, carbohydrates, protein) are undigested. - Malnutrition, lack of energy, low blood levels of fat-soluble vitamins (ADEK) - In children this can lead to the lack of growth rates (weight loss in adults) - Low blood levels of zinc selenium-can show up as reduced immune function, poor wound healing, thyroid function. - General signs of malnutrition can present lethargy, depression, poor concentration, muscle loss, dry skin, brittle nails etc. More of the physical presentations from the inability to digest macronutrients properly are; - Diarrhoea and this are where overlap with other symptoms is mostly seen. This is because of the patient's inability to release the enzymes needed to digest the food, the food is partially digested and is seen as diarrhoea. - Cramping/bloating/flatulence; This is because of the food being partially digested but the body still undergoes peristalsis because it wants to remove the food and keep stuff going, this is what results in the cramping as the food are not properly digested. Also, since the food is not properly digested it results in bloating and if there is bloating then there is wind production and hence flatulence. - Steatorrhea (Fatty, foul-smelling stools, usually light in colour) some patients will describe it as a stool which floats but it is a fatty smelling stool coming about because of a poorly digested food. The aim of the treatment is to give a pancreatic enzyme replacement (amylase, lipase, protease) - Pancrex V - Creon - Nutrizym 22 - Pancrease HL These are different forms of pancreatin with amylase, lipase and protease that helps patient\'s breakdown and digest their food. The dose will be tailored to the meal that the patient had. Higher doses are for main meals and lower doses are for snack. Physical symptoms should be eased because their food is digested properly, they should experience less cramping, less flatulence and less bloating. Also, the presentation of their stools should improve as their food is being digested well. The clinical manifestations such as lethargy, muscle loss, low blood levels of fat-soluble vitamins and nutrients should also improve. Again, because the food are digested properly and the micronutrinets are actually being given the chance to through and utilised by the body then the muscle weakness should improve and also the body should get enough energy.