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Gastrointestinal system
Biliary atresia
Crigler-Najjar syndrome
Dubin-Johnson syndrome
Gilbert's syndrome
Rotor syndrome
Acute cholecystitis
Ascending cholangitis
Biliary colic
Cholangiocarcinoma
Chronic cholecystitis
Gallbladder cancer
Gallstone ileus
Gallstones
Alcohol-induced liver disease
Alpha 1-antitrypsin deficiency
Autoimmune hepatitis
Benign liver tumors
Budd-Chiari syndrome
Cholestatic liver disease
Cirrhosis
Hemochromatosis
Hepatic encephalopathy
Hepatitis
Hepatocellular adenoma
Hepatocellular carcinoma
Jaundice
Neonatal hepatitis
Non-alcoholic fatty liver disease
Portal hypertension
Primary biliary cirrhosis
Primary sclerosing cholangitis
Reye syndrome
Wilson disease
Pancreatic neuroendocrine neoplasms
Zollinger-Ellison syndrome
Acute pancreatitis
Chronic pancreatitis
Pancreatic cancer
Pancreatic pseudocyst
Bowel obstruction
Gallstone ileus
Intestinal adhesions
Volvulus
Colorectal cancer
Colorectal polyps
Familial adenomatous polyposis
Gardner syndrome
Juvenile polyposis syndrome
Peutz-Jeghers syndrome
Gastroschisis
Hirschsprung disease
Imperforate anus
Intestinal atresia
Intestinal malrotation
Intussusception
Meckel diverticulum
Necrotizing enterocolitis
Omphalocele
Abdominal hernias
Femoral hernia
Inguinal hernia
Crohn disease
Microscopic colitis
Ulcerative colitis
Ischemic colitis
Small bowel ischemia and infarction
Celiac disease
Lactose intolerance
Protein losing enteropathy
Short bowel syndrome (NORD)
Small bowel bacterial overgrowth syndrome
Tropical sprue
Whipple's disease
Carcinoid syndrome
Appendicitis
Diverticulosis and diverticulitis
Gastroenteritis
Irritable bowel syndrome
Anal fissure
Anal fistula
Hemorrhoid
Rectal prolapse
Cleft lip and palate
Congenital diaphragmatic hernia
Esophageal web
Pyloric stenosis
Tracheoesophageal fistula
Achalasia
Barrett esophagus
Boerhaave syndrome
Diffuse esophageal spasm
Eosinophilic esophagitis (NORD)
Esophageal cancer
Gastroesophageal reflux disease (GERD)
Mallory-Weiss syndrome
Plummer-Vinson syndrome
Zenker diverticulum
Cyclic vomiting syndrome
Gastric cancer
Gastric dumping syndrome
Gastritis
Gastroenteritis
Gastroparesis
Peptic ulcer
Aphthous ulcers
Dental abscess
Dental caries disease
Gingivitis and periodontitis
Ludwig angina
Oral cancer
Oral candidiasis
Parotitis
Sialadenitis
Temporomandibular joint dysfunction
Warthin tumor
Appendicitis: Pathology review
Cirrhosis: Pathology review
Colorectal polyps and cancer: Pathology review
Congenital gastrointestinal disorders: Pathology review
Diverticular disease: Pathology review
Esophageal disorders: 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
Neuroendocrine tumors of the gastrointestinal system: Pathology review
Pancreatitis: Pathology review
Viral hepatitis: Pathology review
Everyone who has ever had a pimple has had an abscess, even though they’re tiny, they’re still abscesses.
An abscess forms when normal tissue, like the gingiva or gums and teeth for example, is split apart and that new space is invaded by nearby pathogens like bacteria.
In a healthy mouth, normal or commensal bacteria thrive but don’t cause disease.
However, any cut or break in the mucosa is an invitation for bacteria to dive in and multiply, causing an infection.
When that happens, the immune system typically responds and a battle ensues with the result being pus - a mixture of bacteria, immune cells, and dead tissue.
So, in response to an injury, cells release small chemicals called cytokines, like tumor necrosis factor, interleukin-1, interleukin-6, interleukin-8, and interleukin-17, and these attract nearby immune cells.
It’s kinda like yelling for help and being heard by the nearby police.
In addition, the cytokines also dilate nearby capillaries and make them leaky - which brings more blood to the site, and allows immune cells that do show up, to easily slip out of the blood and into the tissue.
The first immune cells at the scene are neutrophils, and they release chemicals and enzymes that kill themselves and the bacteria they swallow up, creating a pool of dead bacteria and cells.
This is a specific type of acute inflammatory response called suppurative inflammation, which simply means that pus is created in the process.
From a macroscopic view, this is sometimes referred to a liquefactive necrosis, because the area of dead tissue turns to liquid.
Initially the dead tissue is intermixed with healthy tissue, but over time it can coalesce into a single area.
And around this pool of pus, a wall of fibrinogen - starts to harden into a barrier.
Occasionally sheets of fibrin form septations, creating loculations or pockets of pus within the abscess itself...kinda like an abscess within an abscess...
Even though the pus is largely dead material, there are still plenty of live bacteria within the pus, which makes it highly infectious if it gets spread from one place to another.
There are a few different types of dental abscesses.
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