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130 Cards in this Set
- Front
- Back
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fundus cells
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Oxyntic Glands
Mucous neck cells Parietal cells Chief cells ECL cells |
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antrum cells
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pyloric glands
Mucous cells G cells |
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parietal cell function
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Make acid
Kill microorganism Cleaves pepsinogen to pepsin Activates pepsin at pH<4 Intrinsic factor Binds vitamin B12 – only essential for life function of stomach B12 is liberated from dietary proteins by pepsin and acid B12 binds to salivary/gastric R factor and carries to small intestine Pancreatic enzymes cleaves R factor, and intrinsic factor binds in small intestine B12-IF complex binds to ileal receptor Pernicious Anemia – autoimmune gastritis against IF or parietal cells Mucus damage and gland destruction leads to achlorhydria and vitB12 deficiency Gastritis then metaplasia then dysplasia then carcinoma |
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chief cell function
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Chief Cells
Make pepsinogen Cleaved by HCL, needs pH<4 |
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ECL cell function
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ECL cell – enterochromaffin Like Cell
Makes histamine Stimulates parietal cell to secrete HCL Release – when stimulated by gastrin or vagus, inhibited by somatostatin |
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G cell function
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G Cells – gastrin cells
Make gastrin Stimulates ECL cells to release histamine which stimulates oxyntic glands to make HCL and pepsinogen Trophic effect – parietal cells and ECL cell mass Release of gastrin – stimulated by gastric distention and amino acids Inhibited by somatostatin and gastric acid |
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D cell function
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D cells
Release somatostatin Inhibites histamine, gastrin, and HCL release Stimulated to be released by acid, CCK, gastrin Inhibited by vagus |
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cephalic phase
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(1)Cephalic phase – vagus nerve
Sight, smell, taste of food stimulates vagus Vagus increases acid production by parietal, ECL, G cell, and blocks D cells pH low – get inhibition of acid production |
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gastric phase
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(2) Gastric phase
Mediated by gastric distention and amino acid/peptides Mechanoreceptors and stimulation of G cells |
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intestinal phase
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(3)Intestinal Phase
Inhibition – acid in duodenum inhibits vaso-vagal reflexes Duodenum releases secretin that block g cell release of gastrin Fat and protein in duodenum stimulate release of CCK which inhibit acid secretion |
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H. pylori
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lives in mucus layer
Has ability to produce urease Neutralizes area around itself cagA and vacA genes – induce chronic gastritis through cytotoxins and bacterial LPS inflamed gastric mucosa produces less mucus/bicarb, hindering protection leads to intestinal metaplasia, then dysplasia, then carcinoma gastric adenocarcinoma MALT lymphoma |
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H pylori dx
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Dx.
Serology Urea breath test Stool antigen assay Biopsy urease test (CLO) Histology Culture difficult |
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h pylori tx
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Tx.
Antibiotics + PPI Very difficult |
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NSAIDs and peptic ulcer
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Inhibit COX
COX1 – constitutive isoform Produces prostacyclin – cytoprotective in gastric mucosa COX2 – inducible isoform Induced by inflammation, cytokines Prostaglandins – increased blood flow, stimulate secretion of mucus and bicarbonate, increased mucosal cell restitution, inhibit acid secretion NSAID effect: Decrease blood flow, mucus production, bicarb production, increased acid COX1 inhibiters – more likely to cause ulcers COX2 selective better Celecoxib |
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stress and peptic ulcer
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Stress (physiologic, not psychologic)
Only in extremely sick patients Trauma, burns, head injuries, ventilator patients Related to alpha adrenergic mediated decrease in mucosal blood flow Ischemia of mucosal blood flow – less mucus, less bicarbonate |
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gastrinoma and peptic ulcer
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Gastrinoma – Zollinger-Ellison Syndrome
Endocrine tumors of duodenum or pancreas Of G cells Dramatic gastrin production drives acid production that overwhelms normal defense dx. serum gastrin level tx. Surgical resection |
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tx of peptic ulcer
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Acid reduction
Acetylcholine – ACh, vagatomy Histamine – H2 receptor antagonists Cimetidine Ranitidine Famotidine nizatidine Gastrin – antrectomy PPI Omeprazole Lansoprazole Dexlansoprazole Rabeprazole Esomeprazole Mucosal Protection: not commonly used Misoprostol Synthetic prostaglandin increases mucus/bicarbonate production and decreases acid production Sucralfate Adheres to ulcer base, forming protective barrier Blocks pepsin activity |
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histamine antagonists
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Histamine – H2 receptor antagonists
Cimetidine Ranitidine Famotidine nizatidine |
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PPIs
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PPI
Omeprazole Lansoprazole Dexlansoprazole Rabeprazole Esomeprazole |
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mucosal protection agents
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Misoprostol
Synthetic prostaglandin increases mucus/bicarbonate production and decreases acid production Sucralfate Adheres to ulcer base, forming protective barrier Blocks pepsin activity |
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sphincters of esophagus
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Sphincter – upper
Lower end of pharynx Inferior constrictor Cricopharyngeus Proximal esophagus Lower sphincter Mostly inner layer of circular muscle Also part of diaphragm |
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innervation of esophagus
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Innervation – vagus
Striated – mediated by Ach Smooth – mediated Ach and NOS |
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swallowing and esophagus
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Swallowing:
(1)pharyngeal phase Food reaches pharynx, swallowing center activated activating CN 5,7,9,10,12 Tongue raises, nasal airway closes, epiglottis closes, UES relaxes, pharyngeal muscles contract (2)Esophageal phase Vagal afferent nerves activates, peristalsis begins and activation of myeneteric plexses, LES relaxes, peristalsis proceeds |
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oropharyngeal dysphagia
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Oropharyngeal Dysphagia – transfer problem
Can’t initiate swallowing or can’t move from striated to smooth muscle (pharyngeal phase problem) Etiology – Zenker’s Diverticulum, cricopharyngeal bar, webs, tumors CNS problems - strokes Neurologic - parkinsons Myopathy – myasthenia gravis |
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esophageal dysphagia
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Esophageal Dysphagia – food bolus stops
Doesn’t make it past smooth muscle section of esophagus Dx – barium esophagram Esophagoscopy Esophageal manometry Etiology – (a) mechanical rings, webs, tumors, peptic stricture, infections, Schatzki ring – constriction in esophagus Peptic stricture – results from acid reflux causes stricture in esophagus (b) inflammatory |
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eosinophilic esophagitis
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Eosinophilic Esophagitis
Solid food dysphagia and food impactions Lots of eosinophils in esophagus (>15 on high field) No evidence of GERD and don’t respond to PPIs well M>>F Associated with other allergic responses – asthma, rhinitis Young adults Have multiple lines of rings or proximal stenosis or linear furrows Therapy – Acid suppression Elimination diets Topical steroids – swallowed fluticason or budesonide |
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odynophagia
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painful swallowing
Odynophagia – painful swallowing Infectious esophagitis Candida most common White exudates, pseudohyphae, budding yeast Viral or idiopathic |
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achalasia
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Achalasia – most common
Esophagus does not relax Failure of LES to relax with swallowing + loss of peristalsis Age range 25-60 yo M=F Elevated LES pressure Symptoms – dysphagia, regurgitation, chest pain, weight loss |
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pathophysiology of achalasia and tx
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Pathophysiology –
Myenteric plexus: ACh – contractile NOS/VIP – relax Damage to NOS/VIP nerves, resulting in unopposed ACh nerves with sustained contraction Need NOS for proper peristalsis Tx. Drugs – botox Pneumatic dilation – large balloon forces dilation of LES Myotomy – surgery |
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GER vs GERD
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GER – gastroesophageal reflux – effortless movement of stomach contents into esophagus
GERD – GER with disease GER causes symptoms and or injury to esophagus |
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GER/GERD pathology and symptoms
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Pathology – acid, pepsin, bile into esophagus
Acid primary mediator Mucosal defenses are overwhelmed Symptoms – heart burn (pyrosis) Regurgitation Dysphagia Respiratory symptoms Chest pain |
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mechanism of reflux in GER/GERD
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Mechanisms of reflux
Transient LES relaxation Hypotensive lower esophageal sphincter Anatomic disruption of GE junction – hiatal hernia |
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dx of GERD
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Dx.
Symptoms Response to empirical trial of acid suppression Endoscopy 24 hr pH monitoring |
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complications of GERD
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Complications of GERD
Ulcer Stricture Barrett’s esophagus – change in esophageal mucosa Normal squamous with metaplasia to columnar Risk factor to become adenocarcinoma Chronic inflammation leads to metaplasia then dysplasia and carcinoma No proven therapy Need to begin screening Adenocarcinoma |
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Tx of GERD
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Tx.
Lifestyle modifications Antacids H2 receptor antagonists PPI – work on parietal cells More effective in relieving heartburn and healing esophageal damage Antireflux surgery Repair hiatal hernia, tighten diaphragm, immobilize fundus of stomach |
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Esophageal cancer types
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Squamous cell decreasing in US
Adenocarcinomas is increasingly more common 5 year survival is very poor |
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SCC
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More common in Asia
No gender difference In US – AA males Risk Factors: Alcohol and tobacco known risk factors Associations – achalasia – LES doesn’t relax Lye ingestion |
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Adenocarcinoma
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Adenocarcinoma
Caucausian>AA M>F Most arise from Barret’s Metaplasia Risk factors: Unrelated to alcohol Related to obesity Smoking GERD |
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Barret's
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risk to become adenocarcinoma
Barret’s – risk of becoming cancer is actually very small But larger than general population Must be on surveillance therapy |
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Clinical presentation of esophageal cancer
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Clinical Presentation:
Location SCC proximal ACC distal, GE junction Dysphagia Odynophagia SCC – vocal cord paralysis |
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Dx of esophageal cancer and Tx
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Dx
Virchow’s nodes Barium swallow, EGD, EUS, PET Tx Stage dependent Poor survival Surgery with chemo/radiation |
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Gastric cancer
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Asia, men most common
H. pylori Benign gastric ulcer disease Pathology – in Japan there is early pre-cancerous lesion Presentation: Weight loss Abdominal pain Signs of obstruction if large tumor |
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dx of gastric cancer and surgery
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Dx.
Endoscopy with biopsy Barium studies Tx surgery |
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gastric carcinoid
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Gastric Carcinoid
Asymptomatic Low prevalence Risk factors – pernicious anemia Chronic atrophic gastritis Hypergastrinemia with ECL hyperplasia Good prognosis |
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gastrointestinal stromal tumor (GIST)
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Gastrointestinal Stromal Tumor (GIST)
Mesenchymal tumors Most commonly in Stomach Slow growing tumors, usually asymptomatic until large Gain of function – ckit mutations Proto-oncogene growth factor receptor Dx. EGD Tx. Surgery |
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MALT
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MALT
H. pylori associated Tumors of the small bowel Most common metastatic from other cancers Presentation – nonspecific Often advanced disease by time they have symptoms |
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acute vs chronic pancreatitis
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Acute pancreatitis – an acute inflammatory process of the pancreas which has ht potential to return to normal
Chronic pancreatitis – irreversible chronic inflammatory process characterized by fibrosis and loss of endocrine and exocrine elements of gland Usually get from repeated acute pancreatitis episodes But, can go straight from normal to chronic pancreatitis from necrosis |
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mechanism of pancreatitis
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Molecular mechanism for acute:
Idiopathic Protection from pancreatitis Highly toxic enzymes (trypsin) are contained and usually secreted in inactive forms Low extracellular ionized Ca Alpha-antrypsin Alkaline pH When these fail, get pancreatitis (1)blockage of secretion (2)fusion of lysosome and zymogen granules |
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tx of pancreatitis
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Volume Replace in severe acute pancreatitis
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complications of pancreatitis
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Complications – due to inflammatory cytokines
IL, NO, TNF-alpha |
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symptoms of pancreatitis
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Symptoms:
Epigastric pain that radiates to the back Tender/rigid abdomen Hypomobility Nausea and vomiting Fever Tachycardia Elevated serum AML and serum lipase Lipase – more specific for pancreatitis |
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causes of acute pancreatitis
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Causes of Acute Pancreatitis:
Gallstones – most common cause 90-95% related to microlithiasis Alcohol - Drugs Trauma Structural Autoimmune Genetic |
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gall stones and pancreatitis
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(1)Gall stones:
Opie’s theory: Gallstone lodged in ampulla of vater – causes back up ERCP – study in endoscopy lab Can put a cannuli in bile duct Pull stones out |
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alcohol and pancreatitis
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(2)Alcohol:
10-20 years of abuse |
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drugs and pancreatitis
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(3)Drug induced:
>300 drugs reported cause Idiosyncratic, not dose related |
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metabolic and pancreatitis
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(4)Metabolic:
Hypercalcemia – almost always due to hyperaparathyriodism Increasing incidence of milk-alkali syndrome from Calcium containing antiacids Hypertriglyceridemia Very high amount needed (>1000) |
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structural and pancreatitis
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(5)Structural – pancreas divisum
Failed fusion of pancreas, can have multiple ducts Predisposes to pancreatitis |
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colon cancer epidemiology and risk factors
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3 cause of death for male and female
10% of all cancer deaths Highest incidence: Caucasians Much higher in North America Risk factors: Age biggest risk Over 50 Family hx Inflammatory bowel disease Most sporadic mutations Healthcare disparity – Caucasians get more screening than AA |
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pathogenesis of colon cancer
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Germline mutation – sperm/ovum mutations
Somatic mutations – during development of tissue Oncogene – normally drive growth, but mutated cause cancer Tumor suppressor genes – inhibit growth Mismatch repair genes – repaid DNA Microsatellite instability – repeated errors indicator that MMR are not working |
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specific mutations in colon cancer
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K-ras
Most frequent mutation of the ras oncogene Leaves growth “switch” on Adenomatous Polyposis Coli (APC) gene Tumor suppressor gene is deactivated P53 gene Tumor suppressor gene is deactivated |
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stepwise progression of colon cancer
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(1)APC gene mutated or MMR – dysplastic tissue
(2)k-ras mutated - adenoma (3)p53 mutation – carcinoma Timeline: 10 year progression from adenoma to carcinoma |
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colon cancer syndromes
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(1)familial adenomatous polyposis (FAP)
(2)hereditary nonpolyposis colorectal cancer (3)peutz-jegher's syndrome |
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Familial Adenomatous Polyposis (FAP)
variants |
Variants – gardner’s syndrome
Associated with extra-gastroinestinal tumors Osteomas, cutaneous tumors, desmoids tumors Turcot’ s syndrome Associated with brain tumors Medulloblastoma glioma |
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Familial adenomatous polyposis (FAP) genetics
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Autosomal dominant
Germline APC gene Thousands of polyps develop in colon in 2nd decade Also get duodenal carcinoma 100% have by age 45 |
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familial adenomatous polyposis (FAP) tx
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Tx – protocolectomy (remove rectum and colon)
And iliostomy |
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Hereditary Nonpolyposis colorectal cancer (HNPCC)
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Autosomal dominant
Germline mutations in DNA MMR gene More rapid adenoma carcinoma sequence Average of onset = 48 Predominance of Right side colon Synchronous and metachronous cancers are common Extra-colonic tumors Uterus Tx - coloectomy |
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Peutz-Jegher's Syndrome
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Autosomal dominant
Multiple pigmented spots on lips and buccal mucosa Associated with hamartomas Small bowel, colon, stomach Typically present 3rd decade of life Intussusceptions, obstruction, bleeding Benign tumors that can change into carcinoma |
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clinical presentation of colorectal cancer
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Abdominal pain – 40%
Rectal bleeding or melena – 40% Change in bowel habit – 40% Weakness – 20% Anemia alone – 10% Right colon – tend to present with blood loss Left colon – tend to present with pain, altered BM Pain – worse prognosis |
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test for dx of colon cancer
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Colonoscopy – best
Allows for biopsy Best sensitivity and specificity Barium enema – 50% sensitivity CT – poor sensitivity for intraluminal lesions Good for detecting metastases CT colongraphy – positive results still require colonoscopy |
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staging of colorectal cancer
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Staging: guides prognosis and treatment
0 and 1 – endoscopy resection all that is needed 2-3 need surgery Lymph nodes involved - chemotherapy 4 – depends on functional status Surgery of metastases can actually help |
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screening for colorectal cancer
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Begin at age of 50
Fecal occult blood – 1 year interval Sigmoidoscopy – 5 year interval CT colonography – 5 years Colonoscopy – 10 year interval Preferred method for patients at increased risk Family hx – start age 40 Personal of adenoma Personal hx of colon Personal hx of ulcerative colitis |
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Inflammatory bowel disease spectrum
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Ulcerative colitis
Crohns Indeterminate |
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inflammatory bowel disease epidemiology
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Distribution – more developed nations
North America in particular Affects all races Age of onset – age 20 for UC and crohn’s Diagnosed throughout life though F=M |
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etiology of inflammatory bowel disease
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Genetic component
Crohn’s has stronger genetic correlation Environmental trigger Immune disregulation as end result Over active immune response |
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ulcerative colitis presentation/symptoms
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Bloody diarrhea
Abdominal cramping Tenesmus – painful BM Weight loss Systemic symptoms Extraintestinal manifestations |
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ulcerative colitis clinical findings
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Clinically: Starts at rectum and goes proximally
Pancolitis – entire colon Distal – left sided Diffuse inflammation No blood vessels No sharp folds Edematous Mucu-pus Natural Course: Relapse and remission Intermittent course most common |
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complications of ulcerative colitis
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Complications:
Toxic Dilation Bleeding Cancer – after about 20 years of UC |
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crohn's disease symptoms
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Diarrhea
Abdominal pain If colon involved – bloody If just small – pain and diarrhea Weight loss Fever Perianal disease Extraintestinal manifestations Ileocolitis – most common presentation 25% - involve colon only |
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clinical presentations of crohn's
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Clinically:
Patchy – skip lesions Transmural Cobble stoning Natural Hx Relapse and remission |
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complications of crohn's
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Complications:
Require surgery very common Obstruction, constriction Fistulae Abscess Surgery is not curative |
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inflammatory bowel disease extraintestinal manifestations
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Skin disorders –
erythema nodosum – red nodules on shin Pyoderma gangrenosum Joint disorders Peripheral arthritis Sacroilitis Ankylosing spondylitis Ocular disorders Hepatobiliary Gallstones in crohns Sclerosing cholangitis Renal Renal stones – crohns Oral ulcers |
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tx for inflammatory bowel disease
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(1)aminosalicylates
(2)steroids (3)immunomodulators (4)biologics (5)surgery |
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aminosalicylates
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(1)Aminosalicylates: 5ASA first line therapy
Use: UC or mild crohns |
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steroids
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(2)Steroids
Prednisone, budesoinide Bad side effects Use budesoinide to help with terminal ileum and right colon Low systemic levels Good for crohn’s |
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immunomodulators
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(3)Immunomodulators
Azathioprine, methotrexate Non responsive UC and Crohns More risks |
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biologics
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(4)Biologics
Anti-TNF therapy Infliximab, adalimumab, certolizumab |
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ulcerative colitis therapy
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UC therapy:
First line: 5ASA Steroids for bad flares Severe: IV steroids IV infliximab IV cyclosporine |
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crohn's disease treatment
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Mild to moderate
Oral aminosalicylates Budesonide Moderate to severe Prednisone short course Immunomodulators good for maintenance therapy only Azathioprine Methotrexate Anti-TNF therapy – good for quick response Infliximab Certolizumab Adalimumab |
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anti-TNF therapy for crohns
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Anti-TNF therapy – good for quick response
Infliximab Certolizumab Adalimumab |
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indications for surgery
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UC:
Bad hemorrhage Toxicity Suspected cancer Crohns Strictures Fistulae Perforations Perianal disease Failed medical response |
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etiology of hepatocellular carcinoma (HCC)
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Chronic liver diseases
HBV HCV Most arise in setting of cirrhosis US – fatty liver HCV More commonly seen in areas where HBV is Subsarah Africa and asia Primary tumor of liver |
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clinical manifestations of hepatocellular carcinoma (HCC)
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Clinical features
Cirrhosis masks weight loss, malaise, abdominal pain, hepatomegaly Serum alpha fetoprotein elevated 50-70% of patients |
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Tx for hepatocellular carcinoma (HCC)
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Tx – surgery
Screening test Imaging studies: Ultrasound every 6 months-12 months Blood tests Alpha-fetoprotein every 6 months |
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hepatobiliary malignancies presentation
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Hepatobiliary malignancies
Presentation – Jaundice! |
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gallbladder carcinoma risk factors
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Risk factors
Female >50yo Gallstone >40 years of age Chronic cholecystitis Calcified GB Fat, fertile, female, forty |
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tx for gallbladder carcinoma
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Tx
Surgery – for cure Palliation – ERCP for obstruction to help drain |
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cholangiocarcinoma risk factors and pathology
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Damage to ducts in liver in setting of IBD
Risk factors Primary sclerosing cholangitis (PSC) Associated inflammatory bowel disease Pathology – adenocarcinoma |
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cholangiocarcinoma presentation and dx
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Presentation – cholestasis, jaundice, pruritus (itching), weight loss
Hepatomegaly dx. – labs show obstructive pattern billirubin, ALT are levated elevated CA19-9 imaging – US dilated intrahepatic or extrahepatic duct, no mass CT – dilated ducts, no mass ERCP – detect level of stricture |
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ampullary carcinoma risk factors
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Ampullary Carcinoma
Risk factors Familial polyposis Ampullary adenoma |
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ampullary carcinoma presentation
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Presentation
Cholestatic jaundice Pruritus Intermittent bleeding Cholangitis Pancreatitis Obstructive LFTs |
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ampullary carcinoma dx and therapy
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Dx – CT or US – dilated ducts
ERCp – usually diagnostic Biopsies or brushings Therapy Surgical resection possible |
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pancreatic cancer presentation
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Poor survival
At presentation, advanced disease Back pain Pruritus Onset of diabetes Anorexia Recent pancreatitis Trousseau’s – migratory thrombophlebitis |
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dx of pancreatic cancer
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Dx – CT see tumors >3cm
EUS effective for smaller tumors |
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risk factors for pancreatic cancer
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Risk factors:
Smoking Chronic pancreatitis Juevinile onset of DM Recent diabetes |
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pathology for pancreatic cancer
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Pathology
Ductular cells most commonly Adenocarcinoma most common Head most common |
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presentation for pancreatic cancer
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Presentation
Pain, nausea, vomiting, anorexia, weight loss, jaundice Mass – palpable distended gall bladder |
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tx for pancreatic cancer
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Tx – surgery
Criteria – no extrapancreatic disease No tumor extension into celiac or sma |
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cystic neoplasms of pancreas
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(1)serous cystadenoma
(2)intraductal papillary mucinous neoplasm (3)mucinous cystadenoma/carcinoma |
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serous cystadenoma of pancreas
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Cystic neoplasms of pancreas
(a)Serous cystadenoma Benign Elderly women Large lesions, multiloculated |
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intraductal papillary mucinous neoplasm of pancreas
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Cystic neoplasms of pancreas
(b)intraductal papillary mucinous neoplasm Premalignant Elderly men Pancreatic duct obstruction |
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mucinous cystadenoma/carcinoma of pancreas
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Cystic neoplasms of pancreas
(c)mucinous cystadenoma/carcinoma 40-60 yo Unilobular or multilobular Should be resected Benign but patients are symptomatic |
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pancreatic neuroendocrine tumors
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(islet cell tumors)
Functional vs non-functional Distinguish by hormone they produce All endocrine tumors appear similar histologically Malignancy based on presence of local invasion Solid tumor in pancreas Good prognosis |
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splanchnic circulation blood consumption and response to acute blood loss
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¼ of cardiac output at rest
Can increase to consume 40-50% Response to acute blood loss: Peripheral vasoconstriction Diminished CO Decreased urine Orthostatic hypotension |
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hematemesis definition
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Hematemesis
Vomiting of blood Based on how long blood as been in stomach color: Bright red – reactive hemorrhage Bright red with clots – mixture Coffee grounds – older blood |
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melena definition
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Melena:
Black, tarry, sticky, pungent Digested blood that has passed through GI tract |
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hematochezia definition
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Hematochezia
Passing of bloody stools Usually mixture of bright red (or maroon) blood and clots |
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causes of upper GI blood loos
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(1)ulcerative or erosive disease - most common
(2)esophagitis (3)portal hypertension (4)AVM (5)traumatic or post procedure (6) tumors |
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ulcerative or erosive disease and blood loss
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Peptic ulcer
Gastric>duodenal Drugs Infectious |
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esophagitis and blood loss
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Esophagitis
Reflux – acid induced |
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AVM and blood loss
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AVM
Can form anywhere in GI tract GAVE – linear streaks of AVMs Dieulafoy’s lesion – bleeding with no ulcer |
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traumatic or post procedure blood loss
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Traumatic or post procedure
Mallory-Weiss tear – tear in GE junction from retching |
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lower GI causes of blood loss
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(1)diverticulosis - most common
(2)neoplasms (3)colitis (4) angiodysplasia (5)post polypectomy bleeding |
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diverituclosis and lower GI blood loss
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Diverticulosis – most common
Herniation of colonic mucosa and submucosa in weak areas of muscularis Usually at site of vessel Prevalence increases with age L>>right side, but right side bleeds more often |
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colitis and lower GI blood loss
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Diverticulosis – most common
Herniation of colonic mucosa and submucosa in weak areas of muscularis Usually at site of vessel Prevalence increases with age L>>right side, but right side bleeds more often |
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angiodysplasia and blood loss
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Angiodysplasia – dilated, tortuous submucosal vessels (usually veins) that can rupture
More common in elderly |
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post polypectomy and lower GI blood loss
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Post polypectomy bleeding – recent procedure
Bleeding after cauter-induced ulcer base |
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management of acute GI blood loss
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Resucitation:
First thing to do Establish good vasculature access Initiate fluids Consider intubation for airway protection if necessary |
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therapy for blood loss
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(1)PPIs
PPIs Decreases rebleeding rate, decreases hospital stay, and transfusion requirement Use IV at beginning with endoscopy (1)inject epinephrine (2) contact coagulation (3) clips (4)noncontact thermal therapy APC probe or superficial coagulation |
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noncontact thermal therapy for GI bleeding
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Noncontact thermal therapy
APC probe – superficial coagulation For angiodysplasia and GAVE |
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occult GI bleeding etiologies
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cancers
ulcer disease |
