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Medical Journal Article (1996) - Glossary of Terms

hungerbound posted this article on Laxative Abuse. I'm just taking apart some of the more medical terms so you may understand the article better. Some of the words I take apart may sound stupid to the more learned people here, but bear with me.

Italics: text from article
Bold: words to be taken apart
Normal: defined words.



Laxative abuse is an uncommon but clinically important cause of chronic diarrhea, a condition often associated with other gastrointestinal symptoms, as well as with disturbances in electrolyte and acid-base balance. A high index of suspicion, a detailed history, and the detection of laxative in stool and/or urine will establish the diagnosis once routine laboratory, endoscopic, and radiologic investigations have excluded common causes of chronic diarrhea. Confirmation of the diagnosis may rule out the need for more extensive, invasive, and costly investigations. However, management is frequently difficult owing to the laxative abuser's complex underlying psychopathology.

Electrolytes: ions in your body such as sodium (Na+), potassium (K+), chloride (Cl-) [main ones] that are required by your cells to regulate your nervous activities. Sodium regulates your brain, potassium your heart, chloride your body's acid-base balance.

Acid-base balance: your bodies normal balance of acids and bases. No duh, right? For example, your stomach is very acidic, your skin is slightly basic, etc. Basically, it's an equilibrium. Not balanced, it could mean your body goes downhill.

Endoscopic: gastroscopies, colonoscopies. Checking our your stomach or your intestines respectively.

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Introduction

Laxatives are viewed as harmless drugs by western society and are freely available for self-medication. If taken on an occasional basis they produce few unwanted side effects. However, ease of access to laxatives renders them liable to abuse, and chronic administration may produce severe physical, psychological, social, or financial complications. Because of the low profile and general acceptability of the drugs, laxative abuse is often unsuspected and hence undetected. This review aims to raise awareness of the diagnosis of laxative abuse, especially in the context of the differential diagnosis of chronic diarrhea.


Types of Laxative Abuse

Patients who take laxatives in amounts exceeding the recommended dose fall into two broad categories - those who habitually abuse laxatives and those who abuse them surreptitiously.

Habitual Laxative Abuse

Habitual laxative abusers are usually middle-aged or elderly people who begin to use these drugs for a variety of reasons. These include distorted perceptions about "normal bowel habit" as well as increased constipation associated with poor diet, decreased mobility, or concomitant drug therapy. Patients become established in a cycle of constipation, which may be exacerbated by drug-induced hypokalemia. This results in the use of increasing doses of laxatives, which becomes difficult to interrupt. These patients often do not realize they are doing anything out of the ordinary and may only admit to laxative ingestion when questioned directly.


Normal bowel habit: up to every 3 days IS normal. It all depends on your routine. However, elderly people have this notion that if they don't go every day, they are not normal. Then they abuse laxatives to the point where their bowels no longer work without them.

Drug-induced hypokalemia: Drug induced low potassium levels. Hypokalemia usually occurs when someone has a burn, or when they've been vomiting or having diarrhea and are therefore losing a lot of fluid. Diuretics obviously make you use a lot of fluid, so that's the drug that induces this.

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Surreptitious Laxative Abuse

Laxatives may be abused surreptitiously, as for instance in patients with anorexia and bulimia nervosa, two conditions where distorted body image and a morbid fear of obesity lead to inappropriate weight loss. Patients with anorexia severely restrict their food intake, whereas patients with bulimia nervosa exhibit a binge/starvation pattern of behavior. Both groups may use other methods of weight control, such as vomiting, excessive exercise, and the use of diuretics. Laxative abuse is practiced in the belief that increasing intestinal transit will impair nutrient absorption; laxatives are also used for the weight-reducing effects of dehydration. Purging behavior (i.e. the desire to take laxatives) in anorexia and bulimia nervosa has been shown to be associated with a past history of sexual abuse, and an eating disorder associated with laxative abuse has a poorer prognosis than an eating disorder without that association (1). Laxative abuse has also been used as a weight-control device by athletes, such as wrestlers, who are required to fulfill certain body-weight criteria before being allowed to participate in competitive events (2).

Factitious diarrhea is another manifestation of surreptitious laxative abuse (3). This self- mutilating condition usually presents as chronic diarrhea. Laxative abuse has been found to account for 3.57% of cases of diarrhea of unknown origin (4, 5). Patients with this disorder exhibit certain common features. They are predominantly female (6, 7) and often associated with the medical profession (8), which enables them to disguise the cause of their illness more effectively. Their medical history may be extensive and include multiple negative investigations and even explorative or corrective surgery. Attempts to treat misdiagnosed factitious diarrhea with intestinal resection and ileostomy, and even partial pancreatic resection, have been reported (9). These patients are remarkable for their inappropriate affect and lack of concern in the face of seemingly horrific symptoms and equally unpleasant investigations (10). This emotional dissociation from physical problems appears in part to be related to the positive gain of sympathy and attention brought on by the illness, as well as to the escape it brings from the pressures of everyday life. However, abuse of laxatives is not simply a deliberate attempt to induce such emotional support because patients deny the abuse to themselves (11). This denial persists even after the patient is confronted with positive evidence of his or her laxative abuse.


Factitious diarrhea: usually associated with Munchausen's Disease [pretending your children are constantly sick to seek further attention]. Basically these people continue to abuse laxatives in order to make themselves constantly sick to seek further attention.

Intestinal resection: also known as "small bowel resection". It's a little hard to imagine, but basically part of your small bowel or small intestine is disease or completely clogged with hardened feces and it has to be removed.

Ileostomy: Put into place after the intestinal resection. Basically, since your small bowel is removed, you can no longer have a bowel movement through your rectum and anus so you have to do it through your abdominal wall. They bring the end of the small intestine (the ileum) through the abdominal wall and form a "stoma" which is this little cherry-looking thing poking thru the stomach. They attach a bag called a colostomy bag in which the feces fills.

Partial pancreatic resection: Removal of part of the pancreas.

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Nonspecific Complications of Laxative Abuse

Gastrointestinal Effects

The most common symptom of laxative abuse is diarrhea. Laxatives that are abused generally induce a marked osmotic or secretory diarrhea resulting in a stool frequency that may reach 20 motions per day. There are no distinguishing features to differentiate this type of diarrhea from other pathologies. There may be nocturnal diarrhea, as seen in inflammatory bowel disease, and the patient may report blood in the stools, which complicates the diagnostic process. Diarrhea is often associated with cramping abdominal pain, and rectal pain may accompany defecation. The discomfort appears to be related to the increase in stool volume and a direct effect of the laxative on intestinal motility. There may be nausea, vomiting, and weight loss (although not necessarily as a direct effect of the laxative). Potassium is the predominant electrolyte in stool water at a concentration of 7090 mmol/l. Sodium and chloride are present at lower concentrations (3040 and 15 mmol/l, respectively). As daily fecal water loss is normally 100 ml or less, electrolyte losses in the normal stool are small. In patients abusing laxatives, fecal electrolyte losses can be extremely high and can cause severe metabolic disturbances.


Osmotic diarrhea: occurs when unabsorbed solutes remain in the bowel where they retain water. Usually occurs due to slow absorption rates.

Secretory diarrhea: occurs when the small and large bowel secrete more electrolytes and water than they absorb.

Fecal electrolyte losses: mainly the potassium loss. Huge K+ losses related to fluid loss.

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Dehydration and Sodium Depletion

As stool volume increases, the concentration of sodium in the feces increases until, at a daily output of 3 l, the sodium concentration approaches that of plasma. Large amounts of sodium may be lost, but hyponatremia is rare because of the concomitant loss of water. The resulting clinical picture is one of dehydration with hypotension, tachycardia, postural dizziness, and syncope. Chronic deficiency of sodium and water leads to increased renin secretion and secondary hyperaldosteronism. This may occasionally become autonomous and has been reported as pseudo-Bartter's syndrome, in which hyperreninemia persists after laxative withdrawal and renal biopsy specimens show hyperplasia of the juxtaglomerular apparatus (12).


Hypotension: decreased blood pressure

Tachycardia: increased heart rate

Postural dizziness: aka postural/orthostatic hypotension. Decrease in blood pressure when sitting or standing. Common in anoretics.

Syncope: pronounced sin-ko-pee. Sudden loss of consciousness or fainting caused by a drop in blood pressure.

Increased renin secretion: released by the kidney to raise blood pressure in the body when needed [such as in the case of low blood pressure, etc].

Secondary hyperaldosteronism: aldosterone is a hormone secreted by the adrenal cortex that regulates salt and water balance in the body; secondary hyperaldosteronism is usually caused by hyponatremia [low sodium levels related to laxative/diuretic abuse], hypovolemia [loss of fluid volume in the body], hypertension.

Pseudo-Bartter's syndrome: potassium wasting.

Hyperreninemia: increased production of blood related to an increase in renin secretion.

Renal biopsy specimens: basically, going into the kidney, and taking out a piece of the tissue for analysis.

Hyperplasia of the juxtaglomerular apparatus: an abnormal increase in the number of cells in a part of the kidney that controls renin release; consequent enlargement occurs.

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Hypokalemia

Patients who abuse laxatives lose excessive amounts of potassium in their stool and through the renal effects of secondary hyperaldosteronism. Hypokalemia may present as generalized muscle weakness and lassitude in up to 60% of these patients (6). More profound levels of hypokalemia may be life-threatening, resulting in cardiac arrhythmias, in skeletal muscle paralysis, or in rhabdomyolysis, renal impairment, and nerve palsies. Hypokalemia is an important indicator of the presence of laxative abuse and its incipient complications, but total body potassium content may be significantly reduced in the presence of normokalemia.


Lassitude: feelings of weariness, or diminished energy

Cardiac arrhythmias: irregular heart rates

Rhabdomyolysis: breakdown of muscle fibres resulting in release of muscle fibre content into the circulation. Most of these fibres are really toxic and can result in kidney damage.

Renal impairment: failure of the renal system to work, i.e. lack of water reabsorption or lack of urine output.

Nerve palsies: e.g. Bell's palsy - nerves don't shoot off messages to the brain, thus the muscles in the body don't work, and like in the case of Bell's palsy, your face droops.

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Disturbance of Acid-Base Balance

Chronic diarrhea induced by laxative abuse results in a hypochloremic metabolic alkalosis. Severe hypokalemia increases renal ammoniagenesis(13) and promotes bicarbonate reabsorption in the renal tubule. Potassium depletion also impairs the function of the intestinal mucosa so that chloride resorption is inhibited and hydrogen ion secretion is enhanced (14).


Hypochloremic metabolic alkalosis: decrease blood chloride levels that cause the body to go into a alkalotic (basic, not-acidic) state.

Renal ammoniagenesis: creation of ammonia by renal system related to not getting rid of urine in the kidneys.

Bicarbonate reabsorption: reabsorption of the body of bicarbonate (a base) which can led to a further state of alkalosis.

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Divalent Cation Disturbance

Chronic laxative abuse may produce hypocalcemia and hypomagnesemia resulting in tetany, particularly if the patient is alkalotic. Hypermagnesemia may occur where magnesium-containing laxatives have been taken in excess, leading to quadriparesis and neuromuscular junction defects. Low plasma zinc levels have been detected, especially where laxative abuse is associated with anorexia.


Hypocalcemia: decreased calcium levels, usually related to renal failure, malabsorption, or alkalosis.

Hypomagnesemia: decreased magnesium levels, usually related to malnutrition, malabsorption, or chronic renal disease.

Tetany: abnormal condition characterised by periodic painful muscular spasms and tremors, related to improper of calcium metabolism.

Alkalotic: basic, not-acidic

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Renal Failure

Severe impairment of renal function may occur occasionally in patients abusing laxatives. Renal function is reduced by a combination of severe hypokalemia, volume depletion, rhabdomyolysis, hyperuricemia, stones, and the direct nephrotoxic effects of some laxatives that cause renal tubular damage in high doses. The metabolic effects of laxative abuse are often complicated by the simultaneous use of diuretics, vomiting, and starvation. This leads to a scenario of "metabolic madness" (12) with a myriad of abnormalities. The picture may not improve immediately following laxative withdrawal. Metabolic abnormalities may occasionally persist with continued kaliuresis, chloruresis, and hyperreninemia, which appears to have become autonomous.


Hyperuricemia: increased urea levels in the blood, usually related to malnutrition, or malabsorption.

Nephrotoxic effects: poisoning of the kidney

Kaliuresis: excretion of potassium in the urine in excessive amounts

Chloruresis: excretion of chloride in the urine in excessive amounts

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Iatrogenic and Social Complications

The diagnosis of factitious diarrhea is often carefully disguised by the patient who is subjected to multiple investigations and a variety of therapies. These may in themselves give rise to complications such as steroid-induced side effects or adhesions after exploratory laparotomy. In-patient assessment and expensive investigations also have resource implications for the health care supplier. Laxative-induced chronic illness puts a strain on interpersonal relationships, which may subsequently break down. Employment may be jeopardized, as well as insurance, with other social implications. The deterioration of the patient's circumstances may reinforce the benefits of illness produced by laxative abuse.


Exploratory laparotomy: surgical incision through the abdominal wall.

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Specific Complications of Laxative Abuse

Laxatives commonly abused fall into three main categories diphenolic laxatives (e.g. phenolphthalein, bisacodyl, and oxyphenisatin), anthraquinones (e.g. senna glycosides and danthron), and osmotic laxatives (e.g. sodium or magnesium sulphate). Only diphenolic laxatives and anthraquinones produce specific side effects.


Diphenolic laxatives: acts directly on the intestine by increasing its motor activity; increases water in the colon.

Anthraquinones: stimulates peristalsis by action on the nerve fibres of the stomach and intestines; softens feces by increasing water and electrolytes in the large intestine.

Osmotic laxatives: increases osmotic pressure; draws fluid into the colon.

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Diphenolic Laxatives

Long-term administration of diphenolic laxatives is toxic to the gastrointestinal tract. These agents damage the small intestinal mucosa, and bisacodyl at a concentration of 2 mg/100 ml has been shown to disturb cytoplasmic and nuclear structure within rat small-intestinal enterocytes (15). Diphenolic laxative abuse may result in malabsorption with mild steatorrhea and deficiency in fat-soluble vitamins, osteomalacia with pseudofractures, and inhibition of carbohydrate absorption (16).

Diphenolic laxatives also have adverse effects on the colon. They induce mild, nonspecific inflammatory changes of the colonic mucosa and at high doses enhance epithelial cell proliferation throughout the rat intestinal tract (17). Chronic abuse over many years may cause partially reversible or irreversible damage to the colon. The colon becomes dilated and distensible and on radiologic examination is seen to have decreased or absent haustrations with a gaping ileocecal valve and pseudostrictures. Histology of the affected bowel reveals loss of colonic myenteric neurons, atrophy of smooth muscle, and sometimes increased submucosal fat, fibrosis, and hypertrophy of the muscularis mucosae. This condition, widely known as the cathartic colon, has been seen less frequently over the past two decades, which presumably reflects a change in the types of stimulant laxatives being ingested.

Hepatotoxicity, manifesting as a chronic active hepatitis-like picture, has resulted in the withdrawal of oxyphenisatin, and phenolphthalein has been associated with fixed drug eruptions (18).

Anthraquinones

The gastrointestinal side effects of anthraquinones are similar to those described for the diphenolic laxatives. In some patients, prolonged ingestion of anthraquinones also results in the production of melanosis coli, a brown-black pigmentation of the sigmoid and rectal mucosa seen during large bowel endoscopy. The pigment is lipofuscin, formed by the incorporation of damaged organelles into the lysosomes of macrophages, and these macrophages are found in the lamina propria, extending into the submucosa in severe cases. Melanosis coli is significant only as an indicator of prolonged ingestion of anthraquinones.

There is some debate as to whether anthraquinone ingestion is a risk factor for colorectal cancer. In a prospective endoscopic study of 1095 patients, Siegers et al (19) found that the incidence of melanosis coli (which was judged to equate with chronic anthraquinone ingestion) was 6.9% in patients with no other endoscopic abnormality, but this increased to 9.8% in those with adenomas and to 18.6% for patients with colonic carcinoma. From these data they calculated a relative risk of 3.04 (1.18, 4.90; 95% confidence interval) for colorectal cancer in patients abusing anthraquinone laxatives. However, the large population-based Melbourne Colorectal Cancer Study found no evidence that prolonged use of any type of laxative influenced the incidence or prognosis of colorectal cancer in the community (20).

Nongastrointestinal complications of prolonged anthraquinone use include contact dermatitis, hepatotoxicity (with danthron), and reversible finger clubbing and skin pigmentation (with senna).

Assessment and Management of Laxative Abuse

Common causes of chronic diarrhea can be excluded by a combination of stool and plasma analysis, gastrointestinal endoscopy, and radiologic investigation. Laxative abuse accounts for 3.57% (4, 5) of remaining cases of "diarrhea of unknown origin" and should be excluded before embarking on costly and invasive investigations. The most important factor in making the diagnosis of laxative abuse is a high index of suspicion on the part of the clinician. An important feature of this condition is denial, and proof of its existence must be obtained before attempting to manage the patient. This may require a chaperoned search of a patient's possessions without his or her consent, which is usually justified despite the ethical and legal issues raised by such a course of action. If laxative tablets are found they should be counted and replaced. If a recount a few days later shows a decrease in supplies, this provides further, indirect evidence of their consumption. Confrontation of patients with the diagnosis of laxative abuse produces a variety of reactions including denial, admission with indifference, acceptance and abstinence, or even attempted suicide. Patients often continue to take laxatives after discovery because of an internal block against reality, and thus only limited success of treatment can be achieved. Therapy should concentrate on symptomatic treatment of complications with replacement of depleted vitamins, nutrients, and minerals. Psychiatric help may be attempted but is often unsuccessful in the face of continued denial of the condition. A major benefit of identifying the patient with laxative abuse is that repetition or instigation of potentially harmful investigations and therapies can be avoided.




I've done most of it; if you need more, just comment and I'll add to what I've already done.

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