Constipation

Today we are going to discuss a very common condition that I’m sure most of us have experienced at one point in our lives; so it’s going to be a topic that is very relatable. And it’s about POO! So it will relatable and awkward as well! Without further ado, let’s dive into the enemy of mankind and what many people view as the bane of their existence: constipation!

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And on to today's topic:

Constipation is the passage of infrequent or hard stools with straining. “Infrequent” is defined as < 3 times/week, and “hard” is defined as stools with water content < 50ml. As mentioned previously, it is a very common condition, increasing in prevalence with age and affecting more females than males. Having said that, constipation is less common in Africa and India, where stool weight is 3~4 times greater than Western countries.

Constipation can have many different causes. The most common one is idiopathic, attributed to colon dysmotility—but this is very difficult to quantify. Other organic causes include medication side effects (narcotics, antidepressants), intestinal obstruction, left sided colon cancer (consider in older populations), and fecal impaction. Metabolic causes such as diabetes mellitus, hypothyroidism, hypercalcemia, hypokalemia, and uremia can also result in constipation, as do neurological causes such as intestinal pseudo-obstruction, Parkinson’s disease, and multiple sclerosis. Some collagen vascular diseases (e.g. scleroderma) can cause constipation; and painful anal conditions (e.g. fissures) can definitely cause constipation too.

Mnemonic for causes of constipation: DOPED

Drugs

Obstruction

Pain

Endocrine dysfunction

Depression

Clinical presentation of constipation can be very similar to that of IBS. The stool is firm, difficult to expel, and passed with straining. There is associated abdominal pain that is relieved by flatulence and defecation. Other symptoms include tenesmus, abdominal distention, overflow diarrhea, and infrequent bowel movements.

If constipation is the only symptoms, the underlying disease can be very difficult to find; the only test recommended by American Gastroenterology Association (2013) would be CBC—to exclude any sinister, systemic conditions. However, TSH, calcium, and glucose levels can also be helpful, as is an abdominal X-ray. If the constipation is associated with rectal bleeding, weight loss, or anemia, visualization of the colon through colonoscopy or CT colonography would be indicated.

For constipation that is refractory to treatment, colon transit time can be measured by having the patient ingest radio-opaque markers then taking a series of abdominal X-rays. The normal time is around 70 hours. If the colon transit time test result is indeed normal, then the patient has a misperception of normal defecation (IBS). If the result is prolonged throughout, the patient has “colonic inertia” (infrequent bowel movements with gas/bloating, often occurring in youth). If the result shows outlet obstruction, it could be that the patient is unable to coordinate pelvic muscles to empty rectum, causing straining. This tends to occur in old age, and often stool will be found in rectum on digital exam.

Treatment (in order of increasing potency):

·      Dietary fiber

o   Useful in mild/moderate constipation

o   Aim for 30g daily, increasing dosage slowly

·      Surface-acting agents (to soften and lubricate stools)

o   Docusate salts

o   Mineral oils

·      Osmotic agents (effective in 2~3 days)

o   Lactulose

o   Sorbitol

o   Magnesium salts

o   Lactitol

o   Polyethylene glycol 3350

·      Cathartics/stimulants (effective in 24 hours)

o   Castor oil

o   Senna (avoid prolonged use to prevent melanosis coli)

o   Bisacodyl

·      Enemas and suppositories

o   Saline

o   Phosphate

o   Glycerin

o   Bisacodyl

·      Prokinetic agents

o   Prucalopride

·      Linaclotide—increases water secretion into the intestinal lumen.

Irritable Bowel Syndrom

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On to today's topic:

Irritable bowel syndrome is a diagnosis that is being handed out much more readily these days, and it is often featured/referenced in pop culture (usually in a comical way). But what is IBS exactly? It is much more real and severe than you think! So this week let’s find out more about this mysterious disease.

To start off, irritable bowel syndrome is a form of functional bowel disease (which means that although the organs seem normal, there are still signs that something is wrong). Irritable bowel is more than a label for unexplained GIT symptoms because although many investigations come back normal (indicating normal anatomy), there is often abnormal motility. It can also be associated with abnormal perception of intestinal activity as well; however while psychological stress may increase IBS symptoms, it probably does not cause IBS. IBS affects 20% of North Americans, more so females than males; and the onset of symptoms usually start in young adulthood.

There are four types of IBS: IBS with diarrhea, IBS with constipation, IBS with mixed type (involving both diarrhea and constipation), and IBS un-typed (insufficient abnormality in stool to fit into any one category).

IBS is essentially a syndrome of pain.

Things that are definitely NOT IBS:

1.     Pain NOT relieved by passing of stools

2.     Patient waking up at night due to pain

3.     Blood in the stools

4.     White blood cells in stools

5.     Fever

6.     Weight loss

7.     Anemia

8.     Abnormal gross findings on flexible sigmoidoscopy

Physical examination should be normal in IBS patients. If history is consistent with Rome III criteria with no alarm features (see list above), and no family history of IBS or colorectal cancer, then limited investigations are required. The investigations aim to rule out diseases which mimic IBS (see list below), especially coeliac disease and inflammatory bowel disease; investigations can be limited to CBC, inflammatory markers (ESR, CRP), and coeliac serology. If available, fecal calprotectin is likely more reliable test to rule out inflammatory bowel disease. TSH and stool cultures can be considered based on clinical circumstances. Consider colonoscopy if alarm features present, family history of IBD, or age > 50 years.

IBS mimickers:

1.     Enteric infections e.g. Giardia

2.     Lactose intolerance (watch for osmotic ion gap)

3.     Crohn’s disease

4.     Coeliac disease

5.     Drug-induced (e.g. laxative)

6.     Diet-induced (e.g. caffeine)

Treatment includes reassurance, explanation, and support for the patient; aim for realistic goals. Lifestyle changes include relaxation therapy, biofeedback, hypnosis, stress reduction, and exercise. A diet that is low in fat and high in fiber can help with symptoms such as pain, bloating, and irregular bowel movements—of these, pain is most difficult to control. No therapeutic agent is consistently effective for IBS; so all medications are to treat symptoms as necessary.

Symptom-guided treatment

·      Pain predominant

o   Antispasmodic medication (such as hyoscine, pinaverium, trimebutine) before meals (low evidence).

o   Tricyclic antidepressants, selective serotonin reuptake inhibitors (moderate evidence).

·      IBS with diarrhea

o   Loperamide (Imodium)

o   Diphenoxylate (Lomotil)

o   Cholestyramine

·      IBS with constipation

o   Linaclotide

o   Osmotic or other laxative

80% of patients will improve over time, despite intermittent episodes of symptoms. Most will have normal life expectancy.

Coeliac Disease

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Onto today's topic:

While eating gluten-free can be just a lifestyle choice, for those with coeliac disease it is not a choice but a necessity. Now, perhaps with the combination of advanced medicine, wheat consumption, and migratory patterns, the diagnosis and worldwide distribution of coeliac disease is on the rise. So let’s get to know one of the most common genetic diseases: coeliac disease.

Essentially coeliac disease is an abnormality of the small intestine mucosa due to a reaction to gluten, a protein found in cereals. As mentioned previously, it is a genetic disease; HLA-DQ2 (chromosome 6) is found in 80~90% of patients compared with 20% in the general population. Coeliac disease can also be associated with HLA-DQ8 (up to 40% of Caucasians carry the HLA alleles but will never develop the disease.) When gluten is digested, it is broken down into gliadin, which is the toxic factor to those with coeliac disease—the body attacks the gliadin and in the process damages its own villi; interestingly, unlike other autoimmune diseases, coeliac disease is the only autoimmune disease in which the antigen is actually recognized. However, like other autoimmune diseases, when you get one, you tend to get more than one—coeliac disease is associated with other autoimmune diseases, especially Sjogren’s disease and thyroid disease.

Once thought to be a disease only affecting Caucasians, coeliac disease is now diagnosed worldwide. It is more commonly found in women. Family histories reveal that 10~15% of first-degree relatives will also be affected. Coeliac disease can present any time from infancy (when cereals introduced—peak presentation) to the elderly; it can lay dormant until triggered by certain events (immigration or sickness or other).

A classic presentation of coeliac disease would be the combination of diarrhea, weight loss, anemia, symptoms of vitamin/mineral deficiency, and failure to thrive in infants. More common current presentations include bloating, gas, and iron deficiency. The symptoms improve when gluten is eliminated from the diet and deteriorate when gluten is reintroduced. Because the disease is usually more severe in the proximal bowel, iron, calcium, and folic acid deficiency is more common (as these are absorbed proximally) than B12 deficiency (absorbed in ileum). Coeliac disease can be associated with non-GIT conditions such as dermatitis herpetiformis skin eruptions (large vesicles with yellow liquid), epilepsy, myopathy, depression, paranoia, infertility, bone fractures, or metabolic bone disease.

The golden standard of diagnosis is small bowel mucosal biopsy (usually from duodenum) showing increased intraepithelial lymphocytes (earliest pathologic finding), crypt hyperplasia, and villous atrophy (which can also be seen in small bowel overgrowth, Crohn’s disease, lymphoma, Giardia, and HIV); however, serological tests can also be performed. Serum anti-tTG (tissue transglutaminase) antibody, IgA, is 90~98% sensitive, 94~97% specific. IgA deficient patients have false-negative anti-tTG; therefore, measure serum IgA concomitantly via serum quantitative protein electrophoresis and incorporate serum testing tTG and/or DGP (deamidated gliadin peptide) IgG in IgA deficiencies. There will be evidence of malabsorption; these can be either localized or generalized, such as steatorrhea, low levels of ferritin/iron saturation, iron, calcium, albumin, cholesterol, carotene, and vitamin B12. Consider CT enterography to visualize small bowel to rule out lymphoma.

Gluten-free diets should not be started before serological tests and biopsy. Gluten is found in barley, rye, some oats, and wheat (mnemonic BROW) and should be avoided in the patient’s diet; however, sometimes oats are allowed if it is grown in soil without cross-contamination by other grains. Rice and corn flour are acceptable. Supplementary of iron, folate, and other vitamins/minerals should be added as necessary. If there is a poor response to diet change, consider alternate diagnosis, concurrent disease (e.g. microscopic colitis, pancreatic insufficiency), development of intestinal (enteropathy-associated T-cell) lymphoma (symptoms include abdominal pain, weight loss, and palpable mass), or development of diffuse intestinal ulceration, characterized by aberrant intraepithelial T-cell population (precursor to lymphoma).

Coeliac disease is associated with increased risk of lymphoma, carcinoma (e.g. small bowel and colon; small increase compared with general population), and autoimmune diseases. The risk of lymphoma may be lowered by gluten-free diet.

Inflammatory Bowel Disease Part 2

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This week we continue to explore inflammatory bowel disease:

Ulcerative colitis is defined as an inflammatory disease affecting colonic mucosa anywhere from the rectum (ALWAYS involved) to the cecum, causing anything from proctitis (rectum-only) to pancolitis (entire colon); inflammation limited to rectum or left colon is more common than pancolitis. On colonoscopy, the inflammation seen is diffuse, continuous, and confined to the mucosa. The incidence of ulcerative colitis is 2~10/100,000 and prevalence is 35~100/100,000. This makes it more common than Crohn’s disease. Two-thirds of patients have disease onset by age 30, with a second peak after age 50; like Crohn’s disease, the distribution is equal between male and female patients. There is a small hereditary contribution—15% of cases have 1^st degree relative with disease. Risk is LESS in smokers.

The hallmark clinical feature of ulcerative colitis is rectal bleeding. Diarrhea can also be present, as well as abdominal cramps/pain (especially with defecation), tenesmus, urgency, and incontinence; systemic symptoms include fever, anorexia, weight loss, and fatigue. The severity of the colonic inflammation correlates with the symptoms (e.g. stool volume, amount of blood in stool). Patients with ulcerative colitis present with characteristic exacerbations and remissions; 5% of cases are fulminant.

Although there is no single confirmatory test, sigmoidoscopy with mucosal biopsy is often sufficient for diagnosis, but a colonoscopy would be helpful in determining the extent of disease (but contraindicated in severe exacerbation). CT colonography (formerly barium enema) can be done if colonoscopy not possible. Stool culture and microscopy and C. Difficile toxin assay should be done to exclude infectious causes.

The mainstay of treatment is 5-ASA derivatives (suppository and enema form in acute treatment; oral form can be used in maintaining remission) and corticosteroids (IV for acute disease; suppositories/enemas/topical applications can be used for disease distal to splenic flexure) for mild to moderate disease; the use of 5-ASA medications such as sulfasalazine or mesalamine may decrease rate of colorectal cancer. Immunosuppressants (e.g. 6-MP) and biologics (e.g. infliximab) are used in hospitalized patients with severe ulcerative colitis; biologics can also be used for outpatients with moderate to severe disease, particularly those that are steroid-unresponsive or steroid-dependent. Azathioprine can also be used in those who are steroid-dependent, but they are most commonly used to maintain remission while corticosteroids are being withdrawn; when given together with biologics, azathioprine increases the efficacy of biologics and decreases the likelihood of tolerance to biologics (around 10% chance/year). Diet change is of little value in decreasing inflammation but may alleviate symptoms. Anti-diarrheal medications are generally not used in ulcerative colitis. When all else fails, colectomy is a curative option; bowel continuity can be restored with ileal pouch-anal anastomosis (IPAA). Other indications of colectomy include toxic megacolon, uncontrollable bleeding, pre-cancerous changes detected by endoscopy/colonoscopy/biopsy, overt malignancy, or inability to taper corticosteroids.

Complications of ulcerative colitis are similar to that of Crohn’s disease, except that there are more liver problems involved in ulcerative colitis (especially primary sclerosing cholangitis in men). There is a greater risk of colorectal cancer in ulcerative colitis; the risk increases with duration and extent of disease and also increases with active mucosal inflammation and development of sclerosing cholangitis. Thusly, regular colonoscopy and biopsy in pancolitis of ≥ 8 years is indicated. Toxic megacolon (traverse colon diameter > 6cm on abdominal x-ray) with immediate danger of perforation is also a major complication! This is lethal and requires immediate treatment using steroids +/- surgery.

A comprehensive list of complications of ulcerative colitis is as follows:

Urinary calculi

Liver problems

Cholelithiasis

Epithelial problems

Retardation of growth/sexual maturation

Arthralgia

Thrombophlebitis

Iatrogenic complications

Vitamin deficiencies

Eye problems

Colorectal cancer

Obstruction

Leakage (perforation)

Iron deficiency

Toxic megacolon

Inanition (wasting)

Strictures

In patients with only proctitis, the disease usually runs a benign course. However, most patients present in chronic relapse pattern. More colonic involvement in the first year of onset correlates with increased severity of attacks and increased colectomy rate. Post colectomy most patients can have normal life expectancy.

The biggest difference between Crohn’s disease and ulcerative colitis is that Crohn’s disease can affect any part of the GIT where as ulcerative colitis is limited to the large intestines.

And as promised... the bonus chart of extra-intestinal manifestations of IBD!