Gi tract

Bacteria produce acid which erode enamel and damage dentin.

reach the pulp inside the tooth, causing inflammation (pulpitis)

Saliva

can progress to periodontal disease, where the infection spreads to the tissues supporting the teeth. This leads to the formation of small infection pockets between the teeth and gums, causing teeth to become loose and potentially fall out.

-Leukoplakia – white lesions -Erythroplakia-depressed red lesions frequently -Oral cancers readily metastasize – many nearby LN in head and neck (associated with smokers and drinkers) -

Esophageal sphinster dysfuncition

two types 1) Achalasia: Sphinter fails to open 2) Incompetent cardiac sphincter (Stays open and causes reflux).

1)Reflux Esophagitis: Irritation/ inflammation of esophagus lining due to constant acid exposure= can increase the risk of asthma. 2)Ulcers and Scarring: The lining of the esophagus can get damaged and develop ulcers, leading to scar tissue that can make the esophagus narrower. 3)Barrett Esophagus: The normal squamous cells in the esophagus change into a different type (columnar cells), which can increase the risk of developing esophageal cancer.

1)Carcinoma (Esophageal Cancer) What happens: A tumor can develop anywhere in the esophagus, narrowing its passage (lumen) and growing into surrounding tissues. 2)Food Impaction(not swallow well)/Stricture (Narrowing) 3)Hiatal Hernia/rings:Part of the stomach pushes up through the diaphragm into the chest, which can press on the esophagus and cause blockages or symptoms of reflux.

occurs when forceful retching or vomiting (often from excess alcohol intake or conditions like bulimia) causes tears in the lining of the esophagus.

involving a complete rupture (full-thickness tear) of the esophagus. (life threatning)

inflammation of the lining of the stomach nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX) enzyme: Aspirin, ibuprofen, naproxen COX-1: Promotes synthesis of prostaglandin that protects gastric mucosa COX-2: Promotes synthesis of prostaglandin that mediates inflammation

gram-negative bacteria that lives on the surface of the stomach lining. H. pylori produces urease, which turns urea into ammonia. The ammonia neutralizes stomach acid, helping the bacteria survive. It also breaks down the stomach’s protective mucus, making the stomach more vulnerable to damage.

-Chronic gastritis,Increased cancer risk , Peptic ulcers.

Common Acute Enteritis caused by Rotavirus and Norovirus (highly contageous) self-limiting (goes away on its own)

body can’t digest lactose becuase lack of enzyme, Unabsorbed lactose in increases osomotic pressure which pulls water into the bowl. Bacteria in the colon ferment the unabsorbed lactose, producing lactic acid and gas

T cells, attacks the small intestine when gluten is consumed, causing inflammation. This inflammation increases the risk of intestinal cancer over time. Also the vili shrink over time which causes malabsorption and diarrhea

crampy abdominal discomfort.Diagnosis made by exclusion – no structural or biochemical anomalies

Increased C. Diff and GI infection -evidence that the appendix plays a role in the immune system. Removing it has been linked to a higher risk of gastrointestinal (GI) infections.

The appendix’s narrow opening can get blocked by fecal material. This blockage causes poor drainage, leading to a buildup of pressure inside the appendix.

two major types of IBD 1) crohns disease:the entire bowel wall becomes inflamed. THICKNING of bowl wall. 2)Ulcerative colitis: affects the colon and rectum, with inflammation of only the inner lining of the bowel. inner lining inflamation

Broad-spectrum antibiotics destroy normal intestinal bacteria, allowing the growth of Clostridium difficile (C. diff),

High intestinal obstruction :Small intestines low intestinal obstruction:large intestine

bands of connective tissue that form in the abdomen, often after surgery. leading to an obstruction (blockage) in the bowel near where the adhesion forms.