Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.

Anorectal varices are the dilation of collateral submucosal vessels due to backflow in the veins of the rectum. Typically this occurs due to portal hypertension which shunts venous blood from the portal system through the portosystemic anastomosis present at this site into the systemic venous system. This can also occur in the oesophagus, causing oesophageal varices, and at the level of the umbilicus, causing caput medusae. Between 44% and 78% of patients with portal hypertension get anorectal varices.

Unlike oesophageal varices, rectal varices are less prone to bleeding, are less serious when a bleed does occur, and are easier to treat because of the more accessible location.

Typically, treatment consists of addressing the underlying portal hypertension. Some treatments include portosystemic shunting, ligation, and under-running suturing. Insertion of a transjugular intrahepatic portosystemic shunt (TIPS) has been shown to alleviate varices caused by portal hypertension. Successful treatment of portal hypertension that subsequently reduces anorectal varices provides a confirmation of the initial diagnosis, allowing for a distinction between varices and hemorrhoids, which would not have been alleviated by reduction of portal hypertension.

In ideal circumstances, patients with known varices should receive treatment to reduce their risk of bleeding. The non-selective β-blockers (e.g., propranolol, timolol or nadolol) and nitrates (e.g., isosorbide mononitrate (IMN) have been evaluated for secondary prophylaxis. Non-selective β-blockers (but not cardioselective β-blockers like atenolol) are preferred because they decrease both cardiac output by β blockade and splanchnic blood flow by blocking vasodilating β receptors at splanchnic vasculature. The effectiveness of this treatment has been shown by a number of different studies.

However, non-selective β-blockers do not prevent the "formation" of esophageal varices.

When medical contraindications to beta-blockers exist, such as significant reactive airway disease, then treatment with prophylactic endoscopic variceal ligation is often performed.

Congestion of the mucosa in other parts of the gastrointestinal tract can also be seen in portal hypertension. When the condition involves the colon, it is termed "portal hypertensive colopathy".

The incidence of anal fissures is around 1 in 350 adults. They occur equally commonly in men and women and most often occur in adults aged 15 to 40.

Intestinal varices are dilated submucosal veins in the intestine.

One treatment includes a transjugular intrahepatic portosystemic shunt.

Portal hypertensive gastropathy can also be treated with endoscopic treatment delivered through a fibre-optic camera into the stomach. Argon plasma coagulation and electrocautery have both been used to stop bleeding from ectatic vessels, and to attempt to obliterate the vessels, but have limited utility if the disease is diffuse.

Transjugular intrahepatic portosystemic shunt procedures, or TIPS involve decompressing the portal vein by shunting a portal venule to a lower pressure systemic venule, under guidance with fluoroscopy. Since it treats the root cause of portal hypertension gastropathy, it has been putatively used for the condition. The literature reports suggest both regression of portal hypertensive gastropathy on endoscopic images and improvement in bleeding after TIPS.

Finally, cryotherapy involves the use of pressurized carbon dioxide administered through the endoscope to freeze and destroy tissue in a focal area. It is being studied for the treatment of portal hypertensive gastropathy.

A varix (pl. varices) is an abnormally dilated vessel with a tortuous course. Varices usually occur in the venous system, but may also occur in arterial or lymphatic vessels.

Examples of varices include:

- Varicose veins, large tortuous veins usually found on legs

- Sublingual varices

- Esophageal varices, commonly stemming from cirrhosis of the liver, also known as oesophageal varicose

- Gastric varices, commonly stemming from cirrhosis of the liver

- Intestinal varices

- Scrotal varices

- Vulvar varices

- Pelvic varices

- Vesical varices, varicose veins associated with the urinary bladder

- Rectal varices, which can be similar to external haemorrhoids

For adults, the following may help prevent anal fissures:

- Avoiding straining when defecating. This includes treating and preventing constipation by eating food rich in dietary fiber, drinking enough water, occasional use of a stool softener, and avoiding constipating agents. Similarly, prompt treatment of diarrhea may reduce anal strain.

- Careful anal hygiene after defecation, including using soft toilet paper and cleaning with water, plus the use of sanitary wipes.

- In cases of pre-existing or suspected fissure, use of a lubricating ointment (It is important to note that hemorrhoid ointment is contraindicated because it constricts small blood vessels, thus causes a decrease in blood flow, which prevents healing.)

In infants, frequent diaper change can prevent anal fissure. As constipation can be a cause, making sure the infant is drinking enough fluids (i.e. breastmilk, proper ratios when mixing formulas) is beneficial. In infants, once an anal fissure has occurred, addressing underlying causes is usually enough to ensure healing occurs.

Gastric varices are dilated submucosal veins in the stomach, which can be a life-threatening cause of bleeding in the upper gastrointestinal tract. They are most commonly found in patients with portal hypertension, or elevated pressure in the portal vein system, which may be a complication of cirrhosis. Gastric varices may also be found in patients with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow. The latter may be a complication of acute pancreatitis, pancreatic cancer, or other abdominal tumours, as well as hepatitis C. Gastric varices and associated bleeding are a potential complication of schistosomiasis resulting from portal hypertension.

Patients with bleeding gastric varices can present with bloody vomiting (hematemesis), dark, tarry stools (melena), or rectal bleeding. The bleeding may be brisk, and patients may soon develop shock. Treatment of gastric varices can include injection of the varices with cyanoacrylate glue, or a radiological procedure to decrease the pressure in the portal vein, termed transjugular intrahepatic portosystemic shunt or TIPS. Treatment with intravenous octreotide is also useful to shunt blood flow away from the stomach's circulation. More aggressive treatment including splenectomy (or surgical removal of the spleen) or liver transplantation may be required in some cases.

Initial treatment of bleeding from gastric varices focuses on resuscitation, much as with esophageal varices. This includes administration of fluids, blood products, and antibiotics.

The results from the only two randomized trials comparing band ligation vs cyanoacrylate suggests that endoscopic injection of cyanoacrylate, known as gastric variceal obliteration or GVO is superior to band ligation in preventing rebleeding rates. Cyanoacrylate, a common component in 'super glue' is often mixed 1:1 with lipiodol to prevent polymerization in the endoscopy delivery optics, and to show on radiographic imaging. GVO is usually performed in specialized therapeutic endoscopy centers. Complications include sepsis, embolization of glue, and obstruction from polymerization in the lumen of the stomach.

Other techniques for refractory bleeding include:

- Transjugular intrahepatic portosystemic shunts (TIPS)

- Balloon occluded retrograde transvenous obliteration techniques (BORTO)

- Gastric variceal ligation, although this modality is falling out of favour

- Intra-gastric balloon tamponade as a bridge to further therapy

- a caveat is that a larger balloon is required to occupy the fundus of the stomach where gastric varices commonly occur

- Liver transplantation

A number of preventative measures are recommended, including avoiding straining while attempting to defecate, avoiding constipation and diarrhea either by eating a high-fiber diet and drinking plenty of fluid or by taking fiber supplements, and getting sufficient exercise. Spending less time attempting to defecate, avoiding reading while on the toilet, and losing weight for overweight persons and avoiding heavy lifting are also recommended.

It is difficult to determine how common hemorrhoids are as many people with the condition do not see a healthcare provider. However, symptomatic hemorrhoids are thought to affect at least 50% of the US population at some time during their lives, and around 5% of the population is affected at any given time. Both sexes experience about the same incidence of the condition, with rates peaking between 45 and 65 years. They are more common in Caucasians and those of higher socioeconomic status.

Long-term outcomes are generally good, though some people may have recurrent symptomatic episodes. Only a small proportion of persons end up needing surgery.

This may occur when there is a large mass of feces in the rectum (fecal loading), which may become hardened (fecal impaction). Liquid stool elements are able to pass around the obstruction, leading to incontinence. Megarectum (enlarged rectal volume) and rectal hyposensitivity are associated with overflow incontinence. Hospitalized patients and care home residents may develop FI via this mechanism, possibly a result of lack of mobility, reduced alertness, constipating effect of medication and/or dehydration.

Rectovestibular fistula is the most common defect of the rectum and anal canal in females.

Liquid stool is more difficult to control than formed, solid stool. Hence, FI can be exacerbated by diarrhea. Some consider diarrhea to be the most common aggravating factor. Orlistat is an anti-obesity (weight loss) drug that blocks the absorption of fats. This may give side effects of FI, diarrhea and steatorrhea.

There are 2 schools of thought regarding the nature of internal intussusception, viz: whether it is a primary phenomenon, or secondary to (a consequence of) another condition.

Some believe that it represents the initial form of a progressive spectrum of disorders the extreme of which is external rectal prolapse. The intermediary stages would be gradually increasing sizes of intussusception. The folding section of rectum can cause repeated trauma to the mucosa, and can cause solitary rectal ulcer syndrome. However, internal intussusception rarely progresses to external rectal prolapse.

Others argue that the majority of patients appear to have rectal intussusception as a consequence of obstructed defecation rather than a cause, possibly related to excessive straining in patients with obstructed defecation. Patients with other causes of obstructed defecation (outlet obstruction) like anismus also tend to have higher incidence of internal intussusception. Enteroceles are coexistent in 11% of patients with internal intussusception. Symptoms of internal intussusception overlap with those of rectocele, indeed the 2 conditions can occur together.

Patients with solitary rectal ulcer syndrome combined with internal intussusception (as 94% of SRUS patients have) were shown to have altered rectal wall biomechanics compared to patients with internal intussusception alone. The presumed mechanism of the obstructed defecation is by telescoping of the intussusceptum, occluding the rectal lumen during attempted defecation. One study analysed resected rectal wall specimens in patients with obstructed defecation associated with rectal intussusception undergoing stapled trans-anal rectal resection. They reported abnormalities of the enteric nervous system and estrogen receptors. One study concluded that intussusception of the anterior rectal wall shares the same cause as rectocele, namely deficient recto-vaginal ligamentous support.

The precise cause is unknown, and has been much debated. In 1912 Moschcowitzl proposed that rectal prolapse was a sliding hernia through a pelvic fascial defect.

This theory was based on the observation that rectal prolapse patients have a mobile and unsupported pelvic floor, and a hernia sac of peritoneum from the Pouch of Douglas and rectal wall can be seen. Other adjacent structures can sometimes be seen in addition to the rectal prolapse. Although a pouch of Douglas hernia, originating in the cul de sac of Douglas, may protrude from the anus (via the anterior rectal wall), this is a different situation from rectal prolapse.

Shortly after the invention of defecography, In 1968 Broden and Snellman used cinedefecography to show that rectal prolapse begins as a circumferential intussusception of the rectum, which slowly increases over time. The leading edge of the intussusceptum may be located at 6–8 cm or at 15–18 cm from the anal verge. This proved an older theory from the 18th century by John Hunter and Albrecht von Haller that this condition is essentially a full-thickness rectal intussusception, beginning about 3 inches above the dentate line and protruding externally.

Since most patients with rectal prolapse have a long history of constipation, it is thought that prolonged, excessive and repetitive straining during defecation may predispose to rectal prolapse. Since rectal prolapse itself causes functional obstruction, more straining may result from a small prolapse, with increasing damage to the anatomy. This excessive straining may be due to predisposing pelvic floor dysfunction (e.g. obstructed defecation) and anatomical factors:

- Abnormally low descent of the peritoneum covering the anterior rectal wall

- poor posterior rectal fixation, resulting in loss of posterior fixation of the rectum to the sacral curve

- loss of the normal horizontal position of the rectum with lengthening (redundant rectosigmoid) and downward displacement of the sigmoid and rectum

- long rectal mesentery

- a deep cul-de-sac

- levator diastasis

- a patulous, weak anal sphincter

Some authors question whether these abnormalities are the cause, or secondary to the prolapse. Other predisposing factors/associated conditions include:

- pregnancy (although 35% of women who develop rectal prolapse are nulliparous (have never given birth)

- previous surgery (30-50% of females with the condition underwent previous gynecological surgery)

- pelvic neuropathies and neurological disease

- high gastrointestinal helminth loads (e.g. Whipworm)

- COPD

- cystic fibrosis

The association with uterine prolapse (10-25%) and cystocele (35%) may suggest that there is some underlying abnormality of the pelvic floor that affects multiple pelvic organs. Proximal bilateral pudendal neuropathy has been demonstrated in patients with rectal prolapse who have fecal incontinence. This finding was shown to be absent in healthy subjects, and may be the cause of denervation-related atrophy of the external anal sphincter. Some authors suggest that pudendal nerve damage is the cause for pelvic floor and anal sphincter weakening, and may be the underlying cause of a spectrum of pelvic floor disorders.

Sphincter function in rectal prolapse is almost always reduced. This may be the result of direct sphincter injury by chronic stretching of the prolapsing rectum. Alternatively, the intussuscepting rectum may lead to chronic stimulation of the rectoanal inhibitory reflex (RAIR - contraction of the external anal sphincter in response to stool in the rectum). The RAIR was shown to be absent or blunted. Squeeze (maximum voluntary contraction) pressures may be effected as well as the resting tone. This is most likely a denervation injury to the external anal sphincter.

The assumed mechanism of fecal incontinence in rectal prolapse is by the chronic stretch and trauma to the anal sphincters and the presence of a direct conduit (the intussusceptum) connecting rectum to the external environment which is not guarded by the sphincters.

The assumed mechanism of obstructed defecation is by disruption to the rectum and anal canal's ability to contract and fully evacuate rectal contents. The intussusceptum itself may mechanically obstruct the rectoanal lumen, creating a blockage that straining, anismus and colonic dysmotility exacerbate.

Some believe that internal rectal intussusception represents the initial form of a progressive spectrum of disorders the extreme of which is external rectal prolapse. The intermediary stages would be gradually increasing sizes of intussusception. However, internal intussusception rarely progresses to external rectal prolapse. The factors that result in a patient progressing from internal intussusception to a full thickness rectal prolapse remain unknown. Defecography studies demonstrated that degrees of internal intussusception are present in 40% of asymptomatic subjects, raising the possibility that it represents a normal variant in some, and may predispose patients to develop symptoms, or exacerbate other problems.

Anal warts are irregular, verrucous lesions caused by human papilloma virus. Anal warts are usually transmitted by unprotected, anoreceptive intercourse. Anal warts may be asymptomatic, or may cause rectal discharge, anal wetness, rectal bleeding, and pruritus ani. Lesions can also occur within the anal canal, where they are more likely to create symptoms.

Proctitis is inflammation of the anal canal and the distal of the rectum.

Proctitis has many causes, such as infections or intercourse.

Tuberculosis proctitis can create a mucous discharge.

Anorectal anomalies are medical problems affecting the structure of the anus and rectum. A person with an anorectal problem would have some sort of deformative feature of the anus or rectum, collectively known as an anorectal malformation.

Examples of anorectal anomalies include:

- Anal stenosis

- Imperforate anus

- Proctitis

- Anal bleeding

- Anal fistula

- Anal cancer

- Anal itching

- Hemorrhoid (piles)

The prognosis for non-ischemic cases of SBO is good with mortality rates of 3–5%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%.

Cases of SBO related to cancer are more complicated and require additional intervention to address the malignancy, recurrence, and metastasis, and thus are associated with poorer prognosis.

All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery. More than 90% of patients also form adhesions after major abdominal surgery.

Common consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility.

Several definitions have been offered:

- "Absence of normal relaxation of pelvic floor muscles during defecation, resulting in rectal outlet obstruction".

- "Malfunction (a focal dystonia) of the external anal sphincter and puborectalis muscle during defecation".

- "[...] failure of [the external anal sphincter and puborectalis] muscle[s] to relax, resulting in maintenance of the anorectal angle and the difficulty with initiating and completing bowel movements".

- "[...] failure of relaxation (or paradoxic contraction) of the puborectalis muscle sling during defaecation, attempted defaecation or straining."

Esophageal diseases can derive from congenital conditions, or they can be acquired later in life.

Many people experience a burning sensation in their chest occasionally, caused by stomach acids refluxing into the esophagus, normally called heartburn. Extended exposure to heartburn may erode the lining of the esophagus, leading potentially to Barrett's esophagus which is associated with an increased risk of adenocarcinoma most commonly found in the distal one-third of the esophagus.

Some people also experience a sensation known as globus esophagus, where it feels as if a ball is lodged in the lower part of the esophagus.

The following are additional diseases and conditions that affect the esophagus:

- Achalasia

- Acute esophageal necrosis

- Barrett's esophagus

- Boerhaave syndrome

- Caustic injury to the esophagus

- Chagas disease

- Diffuse esophageal spasm

- Esophageal atresia and Tracheoesophageal fistula

- Esophageal cancer

- Esophageal dysphagia

- Esophageal varices

- Esophageal web

- Esophagitis

- GERD

- Hiatus hernia

- Jackhammer esophagus (hypercontractile peristalsis)

- Killian–Jamieson diverticulum

- Mallory-Weiss syndrome

- Neurogenic dysphagia

- Nutcracker esophagus

- Schatzki's ring

- Zenker's Diverticulum