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GIT summary
Physiology (PS140)
جامعة طرابلس
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By: Mohimen Faraj
Oral cavity
-Inflammation: mouth-> stomatitis 1)Aphthous stomatitis "canker sore""unknown" -single or multiple, common, self Limited. -mostly in children (2 decades) · Caused by: Stress, fever, IBD, Celiac disease · Cause Ulcer -superficial erosion -Lateral tongue, foor month, Bucolabial mucosa 2)Herpetic Stomatitis (cold sore, Fever blisters) Blisters—-> “vesicle filled with clear fluid”—>Rupture form ulcer. -caused by HSV Dormant -Activated by change in temperature, Immune suppression Change in T by (fever. cold, URTI,Trauma) 3)Oral candidiasis. normally in month—> Activates by Immune suppression white pseudomembrane "thrush, moniliasis"--can be Remove by Tongue depressant unlike Leukoplakia Activated by: Diabetics, Anemia, AB Glucocorticoias, AIDS, Cancer. Complication -> 1Extension to Esophagus 2 Blood stream infection "Life threatening"
Sites of oral cancer: 1) ventral surface of tongue 2) floor of mouth 3) lower lip Morphology : 1) white to Gray circumscribed thickening 2) exophytic pattern 3) Endophytic pattern Most common malignancy. Microscopic : form well, differentiated keratin”Cell nests” to anaplastic dysplasia. Spread: lymphatic because it’s carcinoma Treatment: surgery and radiotherapy
Salivary glands
Inflammation of saliva gland —> sialadenitis.
- traumatic: mucocele rupture of duct and release of saliva into tissue
- viral: mumps RNA virus affect parotid gland “enlarged”
Types 1) childhood limited manifestation.
- adult may cause pancreatitis and sterility. Prevented by MMR vaccine.
- bacterial: staph aureus, strep viridans After gland obstruction Retrograde movement of bacteria, after dehydration Please note that bacteria causes abscess while virus cause necrosis without abscess
Autoimmune sialadenitis “Sjogren syndrome” Destruction of both salivary gland and lacrimal gland Causing xerostomia, keratoconjuctivitis. Teeth decay, Damage to eye.
Salivary gland tumors
M = F. 6th to 7th decade. 80% in parotid gland—> 60% pleomorphic adenoma “Mixed” 20% in submandibular gland —> 50% benign.
- pleomorphic adenoma: Painless mass at the angle of jaw. Silent for years, require adequate resection “2experts, wide margin” While doing resection, be careful, it may damage facial nerve Morphology: encapsulated,heterogenous “epithelium,mesenchyme”
- Warthin tumor “papillary cyst Adenoma, lymphomatosum”
Benign tumor in Parotid the gland
Capsulated tumor in: 1 Smokers
2 Radiation
Two types: 1) epithelial
- lymphoid Malignant transformation Is rare
- Mucoepidermoid carcinoma common primary malignant tumor due to radiation It could be squamous, mucous or intermediate cell Classified by grade low, intermediate high.
clinical
- Dysphasia, nocturnal regurgitation, food aspiration
- Squamous cell carcinoma
- Bird beak X ray 2)Hiatal hernia Segment of stomach protrude above the diaphragm Reflex ~> heartburn ~> esophagitis ~> ulceration ~> bleeding. Causes: congenital ~> muscle diaphragm defect Acquired ~> 1)muscle degradation with age
- increase in intra-abdominal pressure, pregnancy, tumor.
- obese people Types of hernia
- axial sliding 95% “Bell shape” still bounded by diaphragm
- non axial “para esophageal” Rolling. 5%
3)Laceration “ Mallory Weiss syndrome”
Longitudinal tear due to severe vomiting by “alcohol or bulimia”
Mostly superficial
Boehaave syndrome: Transmural rupture rare, and catastrophic
4)Varices
Tortious, dilation and engorged veins in submucosa
Caused by: 1) liver cirrhosis
- portal vein thrombosis
- hepatic vein thrombosis
Esophagitis
Chemical ~> more common in children Infection ~> more common in adult, mostly“fungal,viral”bacterial is rare.
reflux esophagitis “GERD” ~> 1) Acid in stomach
- Zollinger Ellison syndrome
- Hiatal hernia
- Obesity
- Pregnancy
- Diabetic
candida, HSV, CMV.
ingestion of corrosive and irritating substance.
radiation, and chemotherapy
gastric intubation Morphology: depend on causative, agent, duration, and severity. Microscopic: eosinophil “ more than 20 per zone”~> eosinophilic Neutrophil. “ intraepithelial= severe” Basal zone hyperplasia Elongation of lamina propria papillae Clinical ~> heartburn, dysphagia, and chest pain. Complication ~> Bleeding Stricture Barrett esophagus “Intestinal”—>1)Columnar metaplasia
goblet cells Morphology: salmon, velvety patch Complication: ulcer, stricture, invasive adenocarcinoma.
congenital pyloric stenosis
diaphragmatic hernia Herniation of stomach into thorax by diaphragmatic defect
gastric heterotopia Gastric mucosa in esophagus or small intestine, may cause ulcer
Gastritis : Inflammation of gastric mucosa
Acute> anywhere
Chronic> Antrum H. pylori 90%
Body auto immune 10%
Gastric defense: Mucus HCO3 alkaline pH
Tight junctions
Blood flow maintained by PG
Acute gastritis : Acute transient inflammation with hemorrhage
Caused by: NSID
Stress “ trauma, burn, surgery” hypovolemia
Alcohol and smoking
Chemotherapy
Pathogenesis: Increase acid secretion
Decrease in bicarbonate
Decrease in mucus
Decrease in blood flow
Morphology: local erosion “ acute erosive hemorrhagic gastritis”
Clinical features: Pain “epigastric”,nausea, vomiting.
Hematemesis or melana
####### Chronic gastritis
Antrum mucosal inflammation causes: 1) metaplasia “ intestinal”
2) atrophy
Caused by: 1) H. pylori > non-invasive bacteria “S shape” on lumen
Features: flagella for movement
Adhesion to mucus cells
Urease> increase in ammonia> acid reflex
Toxin “CAG A” causes ulcers and cancer
Morphology ~> lymphocyte + plasma cells
“If + neutrophil>Acute on chronic” “Active chronic”
Intestinal metaplasia ~> replace gastric with columnar and goblet
May lead to intestinal adenocarcinoma
Diagnosis: urea breath test
Treatment: AB, proton pump inhibitors.
Auto immune gastritis
Ab For parietal cells>Hypo or Achlorohydra> pernicious anemia
Decrease in acidity increase in G cell activity “Hypergastronemia”
May lead to carcinoid tumor or intestinal adenocarcinoma
Morphology ~> body, fundus~~> Thin mucosa
Loss of rugal folds
Inflammation “ lymphocyte, MQ”
Damage partial, peptic cell.
Microscopic: 1st layer: necrotic debris
2nd layer: inflammation
3rd layer: granulation tissue
4th layer: fibrosis
Clinical >1) gastric> pain with food > vomiting, hematemesis.
2) duodenum> food relieve pain, no vomiting, Melena.
Complication: 1) hematemesis
2) perforation>Gastric ~~> peritonitis
Duodenal ~~> peritonitis>pancreatitis
3) fibrosis> hourglass pyloric stenosis
Duodenal stenosis
4) duodenal diverticulum> fibrosis with traction
Treatment: 1) H. pylori~> AB
2) proton pump inhibitors
3) H+ receptor antagonist
Gastric tumors
Polyps: 1) hyperplastic Small, multiple, sessile. Non-malignant unless it’s above 1 cm. Cystically dilated gland with hyperplastic mucosa 2) Fundic gland Small, multiple, sessile. Nonmalignant transformation Cystically dilated gland with parietal and chief cells. 3) Adenomatous Single, small or large, sessile or peduniculated. Malignant transformation Adenoma with or without dysplasia
Gastric tumors
Carcinoma: 5th most common cancer Mostly due to geographic distribution: Japan, Chile.
- Intestinal type
- Above 50 male
- Precursor lesion
- Ulcerative exophytic Unique causes: H pylori, APC.
- Diffuse type
- below 50 female
- No precursor
- Infiltrative Pathogenesis: H. pylori~> intestinal by “CAG A” Diet ~> 1) nitrate, nitrate. 2) smoked, salted food, chili peppers. 3) lack of fruits and vegetables. Geographic ~> Japan Blood group A Premalignant ~> 1) polyps 2) chronic ulcer 3) stump carcinoma Genetic ~> E-Cadherin for adhesion in diffusion APC In intestinal type Morphology: Microscopic: Intestinal ~> neoplastic adenocarcinoma Diffuse ~> gastric type mucus “Mucin” ~> singet ing Spread: early ~> mucosa, and submucosa. Late ~> below mucosa into muscular propria.
GIT summary
Course: Physiology (PS140)
University: جامعة طرابلس
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