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Pathophysiology
Anal fissure
Anal fistula
Hemorrhoid
Rectal prolapse
Diverticulosis and diverticulitis
Crohn disease
Microscopic colitis
Ulcerative colitis
Irritable bowel syndrome
Ischemic colitis
Small bowel ischemia and infarction
Bowel obstruction
Gallstone ileus
Intestinal adhesions
Volvulus
Colorectal polyps
Familial adenomatous polyposis
Gardner syndrome
Juvenile polyposis syndrome
Peutz-Jeghers syndrome
Lactose intolerance
Alcohol-induced liver disease
Alpha 1-antitrypsin deficiency
Autoimmune hepatitis
Benign liver tumors
Budd-Chiari syndrome
Cholestatic liver disease
Cirrhosis
Hemochromatosis
Hepatic encephalopathy
Hepatitis
Hepatitis A and Hepatitis E virus
Hepatitis B and Hepatitis D virus
Hepatitis C virus
Jaundice
Neonatal hepatitis
Non-alcoholic fatty liver disease
Portal hypertension
Primary biliary cirrhosis
Primary sclerosing cholangitis
Reye syndrome
Wilson disease
Adenovirus
Bacillus cereus (Food poisoning)
Campylobacter jejuni
Clostridium difficile (Pseudomembranous colitis)
Clostridium perfringens
Cryptosporidium
Cytomegalovirus
Entamoeba histolytica (Amebiasis)
Escherichia coli
Giardia lamblia
Norovirus
Rotavirus
Salmonella (non-typhoidal)
Shigella
Staphylococcus aureus
Vibrio cholerae (Cholera)
Yersinia enterocolitica
Arsenic poisoning
Cyanide poisoning
Ethylene glycol poisoning
Lead poisoning
Mercury poisoning
Methemoglobinemia
Neuroleptic malignant syndrome
Paracetamol toxicity
Serotonin syndrome
Appendicitis: Pathology review
Cirrhosis: Pathology review
Colorectal polyps and cancer: Pathology review
Congenital gastrointestinal disorders: Pathology review
Disorders of amino acid metabolism: Pathology review
Disorders of carbohydrate metabolism: Pathology review
Diverticular disease: Pathology review
Environmental and chemical toxicities: Pathology review
Esophageal disorders: Pathology review
Fat-soluble vitamin deficiency and toxicity: Pathology review
Gallbladder disorders: Pathology review
Gastrointestinal bleeding: Pathology review
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Inflammatory bowel disease: Pathology review
Jaundice: Pathology review
Malabsorption syndromes: Pathology review
Medication overdoses and toxicities: Pathology review
Neuroendocrine tumors of the gastrointestinal system: Pathology review
Pancreatitis: Pathology review
Viral hepatitis: Pathology review
Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review
Benign tumors are masses of cells that can’t invade neighboring tissues or organs, and therefore are usually defined as non-cancerous.
Benign liver tumors are actually pretty common, and typically don't cause any serious complications, and there are three major types: cavernous hemangiomas, focal nodular hyperplasias, and hepatocellular adenomas.
Cavernous hemangiomas are the most common form and are these masses or swelling of the endothelial cells in blood vessels of the liver that, when we check it out on histology, they form these huge vascular spaces that sort of look like a system of caves.
In other words, instead of blood flowing through a tube, the blood goes into a giant cavern with endothelial cells randomly sprinkled throughout.
Although these vascular spaces look huge on histology, most patients have relatively small lesions, usually less than about 1.5 cm, and therefore don’t have any symptoms; in more rare cases, with larger lesions, patients may develop symptoms and in very rare cases, experience rupture and intraperitoneal bleeding.
Finding and diagnosing these hemangiomas can be done through several imaging techniques like ultrasound, CT scans, and MRI.
The second most common type of benign liver tumor is a focal nodular hyperplasia, or FNH.
These are like these localized (focal) aggregates (nodular) of rapidly reproducing liver cells (hyperplasia).
FNH is actually the most common non-blood vessel-related benign tumor in the liver and are seen slightly more in women than men, but can happen at any age.
Basically this is a loosely used term to describe when nodules or aggregations of seemingly benign hepatocytes are found in the liver.
Ultimately, we don’t really know why these form, but it’s thought that they could be a response to vascular injury of some kind that leads the hepatocytes to ramp up reproduction and form these aggregates of cells.
Another reason it’s thought to be a result of vascular injury is that there’s almost always an abnormally large blood vessel in the center, with smaller branches radiating out into the periphery.
And further supporting the injury hypothesis, is that there’s almost always a characteristic gross finding of centralized fibrous scar tissue produced by stellate cells.
On histology you’ll often see this fibrous tissue as well, sometimes called fibrous septae, which means wall or separation.
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