GI Tract Pathology 

Pre-Knlowge of GI Tract

• the diaphragm separates the esoágues from the stomach
• parietal cells produce HCl and KCl (gastric acid) and excrete it in gastric glands
• What happens when someone vomits for days?   * hypochloremic (hyper chloride) in blood   * lower pH in the stomach
• PAS staining   * Staines the lining of the mucus → polysaccharides
• Bolus moves passively and actively through the esophagus( peristaltic movement)
• Different squinters in GI tract
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Functions and Characteristics of the GI tract

• %%Small intestines%% → absorption of carbohydrates, fats, minerals, proteins, water, and vitamins.
• %%Colon%%: absorption of water and electrolytes   * Peyers patches →patches of immune cells that are found in ilium that detect and respond to foreign substances   * most bacteria found( digest found + ferment food)
• %%Appendix%%: stores immune cells

*Villi: finger-like projections on the surface of the mucosa that increase the surface area for nutrient absorption to the lymphatic system and capillaries

→ they also have mussels to move bolus muscles

**Crypts: small tube-like structures that are located in the lining of the small intestine and the large intestine, produce digestive juices + harbor stem cells for epithelial lining

***Goblet cells: goblet cells secrete mucus that protects the mucosa from damage

**** Squamous cells: are flat and often found in barrier tissues

***** Columnar cells: are taller and typically found in tissues with secretory or absorptive functions.

Pathology of esophagus

• %%Heartburn%%   * normally prevented by the angle of the stomach and lower esophageal sphincter(LES)   * gastroesophageal reflux disease→ Barret disease of the esophagus (damaged and replaced by abnormal cells. This is usually caused by long-term acid reflux and is a risk factor for developing esophageal cancer)
• %%Eosinophilic esophagitis%%   * allergy in the esophagus and a lot of eosinophils → rectaion to what pathogen is unclear maybe food
• %%IBD%%:
• 
• ==Two types of IBD== (systematic disease) → due to a genetic defect, all leukocytes attack microbes and food   * the peak of onset 20 and 60 → 25% of all IBD start in childhood !!!   * symptoms come in waves and increase over a lifetime   * loss of tolerance**   * impairment of mucosal defense   * epithelial barrier defects   * Environmental factors:     * The earlier the onset, the more genetic the IBD   * Crohn’s disease     * vomiting   * Ulcerative colitis     * only concerns the colon → a lot of rectal symptoms that crawl upwards   * (difficult to diagnose because they look so similar (diarrhea with blood+ cramping + fever), but they are very different to treat     * red blood → inflammation colon     * black blood → small intestine     *
• ==Things that are specific to each disease==   * $Crohn’s$     * the disease can skip passages in the colon and cause inflammation → patchy inflammation     * Fistulas: abnormal passageways that form between different parts of the body       * → transmural ( tears through the tissue of them muscle) inflammation → feces can end up in urine     * granulomas: clusters of cells that form when the body's immune system attempts to contain and eliminate foreign substances or bacteria     * muscle hypertrophy     * cobblestone appearance     * fat wrapping     * serological marker: ASCA
• @@Ulcerative colitis@@   * crypt distortions   * always originates in the rectum and then moves up until half of the colon or the entire colon     * serological markers: pANCA     * ulceration within the mucosa     * in children it does not have to start in rectum       *
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• {{Manifestation of IBD{{   * code in the lymph node that triggers an intestine attack   * you can only have skin irritation and no intestine → due to gene alteration   * because innate immune system is not working( NOD 2 intracellular bacterial receptor) there is an overload of B and T cells → underlying explanation of IBD
• **Tolerance in immunology   * there is recognition of everything in our body by the immune system; in a normal state, there is a tolerant state; however, in IBD there is a loss of accepting new things   * inflammation vs. tolerance ( too much aggressive inflammatory cells or too few protective cells)
• }}Treatment options}}   * take out the colon in colitis to decrease inflammation →; however, inflammation will always stay because you can’t take out return   * in crohns you can’t take out the colon because inflammation will continue in small intestines   * steroids   * targeted immunosuppression for specific immune cells

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