Splenic flexure syndrome is a term sometimes used to describe bloating, muscle spasms of the colon, and upper abdominal discomfort thought to be caused by trapped gas at the splenic (as opposed to hepatic) flexure in the colon; the pain caused can be excruciating and debilitating, and may mimic that of a heart attack (because of the proximity of the splenic flexure to the diaphragm and referred pain from irritation to the diaphragmatic sensory nerves).

Some physicians classify splenic flexure syndrome as a type of IBS; others consider it a separate condition.

To minimise the risks associated with splenectomy, antibiotic and vaccination protocols have been established, but are often poorly adhered to by physicians and patients due to the complications resulting from antibiotic prophylaxis such as development of an overpopulation of Clostridium difficile in the intestinal tract.

Asplenia is a form of immunodeficiency, increasing the risk of sepsis from polysaccharide encapsulated bacteria, and can result in overwhelming post splenectomy infection (OPSI), often fatal within a few hours. In particular, patients are at risk from "Streptococcus pneumoniae", "Haemophilus influenzae", and meningococcus. The risk is elevated as much as 350–fold.

The risk to asplenic patients has been expressed as equivalent to an adult dying in a road traffic accident (in every 100 people without spleens, 1 to 5 would develop a severe infection per decade) (reference UK Splenectomy Trust Advice)—hence sensible precautions are advisable. Increased platelet counts can be seen in individuals without a functioning spleen.

The basic pathology is some kind of obstructive pathology in the portal, hepatic or splenic vein that causes obstruction of venous blood flow from the spleen towards the heart. The cause of such obstruction may be abnormalities present at birth (congenital) of certain veins, blood clots, or various underlying disorders causing inflammation and obstruction of veins (vascular obstruction) of the liver.

A 1998 review noted that life expectancy is usually normal, but that there have occasionally been reported neonatal deaths due to PCD. A 2016 longitudinal study followed 151 adults with PCD for a median of 7 years. Within that span, 7 persons died with a median age of 65.

Banti's syndrome (also known as Banti's disease), named for is Guido Banti., is a chronic congestive enlargement of the spleen resulting in premature destruction of the red blood cells by the spleen.

Biliary atresia seems to affect females slightly more often than males, and Asians and African Americans more often than Caucasians. It is common for only one child in a pair of twins or within the same family to have the condition. There seems to be no link to medications or immunizations given immediately before or during pregnancy. Diabetes during pregnancy particularly during the first trimester seems to predispose to a number of distinct congenital abnormalities in the infant such as sacral agenesis and the syndromic form of biliary atresia.

The exact incidence of ischemic colitis is difficult to estimate, as many patients with mild ischemia may not seek medical attention. Ischemic colitis is responsible for about 1 in 2000 hospital admissions, and is seen on about 1 in 100 endoscopies. Men and women are affected equally; ischemic colitis is a disease of the elderly, with more than 90% of cases occurring in people over the age of 60.

The exact causes are not known. It is not associated with a particular gene, but there is some evidence of recurrence in families.

Austrian syndrome is a medical condition first described by Robert Austrian in 1957. The classical triad consists of pneumonia, endocarditis, and meningitis, all caused by "Streptococcus pneumoniae". It is associated with alcoholism, due to the presence of hyposplenia (reduced splenic functioning), and can be seen in males between 40 and 60 years old.

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.

Asplenia is the absence of normal spleen function. It predisposes to some septicemia infections. Therefore, vaccination and antibiotic measures are essential in such cases. There are multiple causes:

- Some people congenitally completely lack a spleen, although this is rare.

- Sickle-cell disease can cause a functional asplenia (or autosplenectomy) by causing infarctions of the spleen during repeated sickle-cell crises.

- It may be removed surgically (known as a splenectomy), but this is rarely performed, as it carries a high risk of infection and other adverse effects. Indications include following abdominal injuries with rupture and hemorrhage of the spleen, or in the treatment of certain blood diseases (Idiopathic thrombocytopenic purpura, hereditary spherocytosis, etc.), certain forms of lymphoma or for the removal of splenic tumors or cysts.

Symptoms include an enlargement in the size of the spleen, or a change from the spleen's original position to another location, usually in either other parts of the abdomen or into the pelvis. This ability to move to other locations is commonly attributed to the spleen's pedicle being abnormally long.

Physical factors may cause ischuria, constipation, as well as numerous spleen-related diseases such as hypersplenism, thrombocytopenia, and lymphoma. Blocking of the arteries and torsion in the spleen can also result in abdominal pain or swelling. However, lack of visible symptoms — except in incidents of abdominal pain — makes the disease difficult for doctors to diagnose, though medical imaging techniques such as medical ultrasonography, magnetic resonance imaging, or computed tomography can be used to confirm its occurrence.

Wandering spleen is most commonly diagnosed in young children as well as women between the ages of 20 and 40. Even so, the disease is very rare and fewer than 500 occurrences of the disease have been reported as of 2005, of which around 148 (including both children and adult cases) were documented to have been from between 1960 and 1992. Less than 0.5% of all splenectomies, surgical removal of the spleen, are performed due to having this disorder.

Characteristics of the disorder include the loss, weakening, or malformation of the ligaments that help to keep the spleen located in the upper left part of the abdomen. Though not a genetic disease, wandering spleen is often found at birth. It can occur in adults as the result of injuries and other similar conditions that cause the ligaments to weaken, such as connective tissue disease or pregnancy. Wandering spleen (splenoptosis) predisposes the spleen to complications such as torsion, splenic infarction, pancreatic necrosis and rarely pseudocyst formation.

In 1992, the youngest case of the literature of torsion of wandering spleen at two days of birth was reported in Lebanon, by Dr Edouard Sayad.

Most patients with ischemic colitis recover fully, although the prognosis depends on the severity of the ischemia. Patients with pre-existing peripheral vascular disease or ischemia of the ascending (right) colon may be at increased risk for complications or death.

Non-gangrenous ischemic colitis, which comprises the vast majority of cases, is associated with a mortality rate of approximately 6%. However, the minority of patients who develop gangrene as a result of colonic ischemia have a mortality rate of 50-75% with surgical treatment; the mortality rate is almost 100% without surgical intervention.

Accessory pancreas is a rare condition in which small groups of pancreatic cells are separate from the pancreas. They may occur in the mesentery of the small intestine, the wall of the duodenum, the upper part of the jejunum, or more rarely, in the wall of the stomach, ileum, gallbladder or spleen. The condition was first described by Klob in 1859.

Accessory pancreas is a small cluster of pancreas cells detached from the pancreas and sometimes found in the wall of the stomach or intestines.

The causes of hemosuccus pancreaticus can be grouped into diseases of the pancreas and diseases of the vascular structures around the pancreas. Diseases of the pancreas include acute and chronic pancreatitis, pancreatic cancer, pancreatic duct stones, ruptured aneurysms of the splenic artery, and pseudoaneurysms of the splenic artery and hepatic artery. Pseudoaneurysms are complications of pancreatitis where a pseudocyst is formed, with one wall abutting an artery, usually the splenic artery. Should the arterial wall rupture, the pseudoaneurysm will hemorrhage into the pancreatic duct.

Rarely the bleeding is not channeled into the bowel from the main pancreatic duct (or "duct of Wirsung"), but rather comes from the accessory pancreatic duct (or "duct of Santorini"). The former is termed "Wirsungorrhage" and the latter is termed "Santorinirrhage". Bleeding from the duct of Santorini can be caused by pancreas divisum, a possible congenital cause of pancreatitis.

Many hypotheses have been raised for environmental factors contributing to the pathogenesis of ulcerative colitis. They include the following:

- Diet: as the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn's disease. Few studies have investigated such an association; one study showed no association of refined sugar on the prevalence of ulcerative colitis. High intake of unsaturated fat and vitamin B6 may enhance the risk of developing ulcerative colitis. Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages. Specifically, sulfur has been investigated as being involved in the etiology of ulcerative colitis, but this is controversial. Sulfur restricted diets have been investigated in patients with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the gut microbiota and mucosal sulfide detoxification in addition to the diet.

- Breastfeeding: Some reports of the protection of breastfeeding in the development of inflammatory bowel disease contradict each other. One Italian study showed a potential protective effect.

- One study of isotretinoin found a small increase in the rate of ulcerative colitis.

Treatment of hemosuccus pancreaticus depends on the source of the hemorrhage. If the bleeding is identified on angiography to be coming from a vessel that is small enough to occlude, embolization through angiography may stop the bleeding. Both coils in the end-artery and stents across the area of bleeding have been used to control the hemorrhage. However, the bleeding may be refractory to the embolization, which would necessitate surgery to remove the pancreas at the source of hemorrhage. Also, the cause of bleeding may be too diffuse to be treated with embolization (such as with pancreatitis or with pancreatic cancer). This may also require surgical therapy, and usually a distal pancreatectomy, or removal of the part of the pancreas from the area of bleeding to the tail, is required.

This can lead to a number of disease manifestations such as:

- Acute midgut volvulus

- Chronic midgut volvulus

- Acute duodenal obstruction

- Chronic duodenal obstruction

- Internal herniation

- Superior mesenteric artery syndrome

Pneumococcal septicemia, or whole-body infection caused by the "Streptococcus pneumoniae" bacteria, has been reported to cause autosplenectomy but is a very rare and poorly understood complication of the infection.

Gastric varices can present in two major ways. First, patients with cirrhosis may be enrolled in screening gastroscopy programs to detect esophageal varices. These evaluations may detect gastric varices that are asymptomatic. When gastric varices are symptomatic, however, they usually present acutely and dramatically with upper gastrointestinal bleeding. The symptoms can include vomiting blood, melena (passing black, tarry stools); or passing maroon stools or frank blood in the stools. Many people with bleeding gastric varices present in shock due to the profound loss of blood.

Secondly, patients with acute pancreatitis may present with gastric varices as a complication of a blood clot in the splenic vein. The splenic vein sits over the pancreas anatomically and inflammation or cancers of the pancreas may result in a blot clot forming in the splenic vein. As the short gastric veins of the fundus of the stomach drain into the splenic vein, thrombosis of the splenic vein will result in increased pressure and engorgement of the short veins, leading to varices in the fundus of the stomach.

Laboratory testing usually shows low red blood cell count and often a low platelet count. If cirrhosis is present, there may be coagulopathy manifested by a prolonged INR; both of these may worsen the bleeding from gastric varices.

In very rare cases, gastric varices are caused by splenic vein occlusion as a result of the mass effect of slow-growing pancreatic neuroendocrine tumors.

Treatment of accessory pancreas depends on the location and extent of the injured tissue. Surgery may be an option, or some physicians order prophylactic antibiotics.

Hemosuccus pancreaticus, also known as pseudohematobilia or Wirsungorrhage, is a rare cause of hemorrhage in the gastrointestinal tract. It is caused by a bleeding source in the pancreas, pancreatic duct, or structures adjacent to the pancreas, such as the splenic artery, that bleed into the pancreatic duct. Patients with hemosuccus may develop symptoms of gastrointestinal hemorrhage, such as blood in the stools, maroon stools, or melena. They may also develop abdominal pain. Hemosuccus pancreaticus is associated with pancreatitis, pancreatic cancer and aneurysms of the splenic artery. Angiography may be used to diagnose hemosuccus pancreaticus, where the celiac axis is injected to determine the blood vessel that is bleeding. Concomitant embolization of the end vessel may terminate the hemorrhage. Alternatively, a distal pancreatectomy may be required to stop the hemorrhage.

A genetic component to the etiology of ulcerative colitis can be hypothesized based on the following:

- Aggregation of ulcerative colitis in families.

- Identical twin concordance rate of 10% and dizygotic twin concordance rate of 3%

- Ethnic differences in incidence

- Genetic markers and linkages

Twelve regions of the genome may be linked to ulcerative colitis, including, in the order of their discovery, chromosomes 16, 12, 6, 14, 5, 19, 1, and 3, but none of these loci has been consistently shown to be at fault, suggesting that the disorder is influenced by multiple genes. For example, chromosome band 1p36 is one such region thought to be linked to inflammatory bowel disease.

Some of the putative regions encode transporter proteins such as OCTN1 and OCTN2. Other potential regions involve cell scaffolding proteins such as the MAGUK family. There may even be human leukocyte antigen associations at work. In fact, this linkage on chromosome 6 may be the most convincing and consistent of the genetic candidates.

Multiple autoimmune disorders have been recorded with the neurovisceral and cutaneous genetic porphyrias including ulcerative colitis, Crohn's disease, celiac disease, dermatitis herpetiformis, diabetes, systemic and discoid lupus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, Sjogren's disease and scleritis. Physicians should be on high alert for porphyrias in families with autoimmune disorders and care must be taken with the use of potential porphyrinogenic drugs, including sulfasalazine.