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Pathophys final GI
| Question | Answer |
|---|---|
| alimentary canal- GI | the whole passage along which food passes through the body from mouth to anus. It includes the esophagus, stomach, and intestines. |
| esophagus | Diaphragmatic Hiatus, Upper Esophageal Sphincter, Lower Esophageal Sphincter; Voluntary and involuntary phases of swallowing (medulla and ANS roles)- innervation by vagal nerve |
| stomach | Pyloric Valve; connect throat to stomach |
| small intestine | Duodenum, Jejunum, Ileum, Ileocecal Valve; between stomach and large intestine; Continued digestion and break-down nutrients; Absorption of carbs, proteins, fats, nutrients/vitamins (portal circ) |
| large intestine | Ascending Colon, Transverse Colon, Descending Colon, Sigmoid Colon, Rectum, Anus |
| accessory organs of GI | Salivary Glands, Pancreas, Liver, Gallbladder |
| control of GI system and motility/sphincter tone | |
| Mouth | Oral cavity Function/Role in digestion- chew, taste Saliva- Salivary Glands- Submandibular, Sublingual, Parotid Water, mucus, Na, bicarb, CL, K, ptyalin- Neutralizes acid and bacteria, Moistens/bulks, IgA= immune protection, Carb digestion initiated |
| esophagus | Stretch receptors- transmits impulses for swallowing to medulla and can stimulate muscular contrax b/c ↑ bolus or ↓ transmission of food. LES tone- changes w/ hormonal stim- Nonadrenergic, noncholinergic vagal stimulation; Progesterone, secretin, glucag |
| Hiatal Hernia | the protrusion of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm. Risks- hemorrhage, obstruction, strangulation |
| GERD | chronic symptoms or mucosal damage produced by the abnormal reflux of stomach acid to the esophagus. A typical symptom is heartburn. Manifestations- excessive back-flow of gastric contents into esophagus |
| Barrette's esophagus | Dysplasia of lining of esophageal mucosa; attempt at healing esophageal mucosa, but squamous mucosa replaced with columnar epithelium resembling intestine or stomach and these cells can be seen as precancerous as this is a precursor to esophageal CA |
| stomach- hormones/ neurotransmitters | increased activity- eating, parasympathetic n.s., gastrin, histamine, acetylcholine, aggression/hostility decreased activity- somatostatin, secretin, sympathetic n.s., bad odors/tastes, emotions |
| Gastric Juice | Components- mucus + acid (HCL) + K + Na + enzymes + hormones + intrinsic factor + gastroferrin Functions- digestion |
| Gastric Acid | Parietal cells- Hydrolysis of H20; H+ and CL- → HCL from parietal cells to stomach lumen Functions- Dissolve food, Bacteriocidal, Pepsinogen (from chief cells) → pepsin protein break-down |
| Stomach | Gastroferrin- facilitates iron absorption in small intestine Intrinsic Factor- binds B12 for absorption in small intestine |
| Mucosal Barrier | Impermeable to acid = protective barrier Prostaglandins stimulate mucus production |
| PUD | Gastric, duodenal, or esophageal ulcer; H. pylori, stress, increased HCL sitmulation/production, rare tumors with gastrin secretion; Gastrin/acid-pepsin, decreased resistance of mucosa |
| Small intestine- villi/microvilli | Functions- enzyme secretion/nutrient absorption; Replacement every 4-7 days Risks if decreased villi- decreased absorption, diarrhea and malnutrition, B12 deficiency, starvation, cytotoxic drugs, radiation, etc |
| Small intestine | Arterial- Gastroduodenal artery; Superior Mesenteric artery Venous- Superior mesenteric vein → Splenic Vein → Portal System Lymph- Drain into thoracic duct |
| basic building blocks of food | Carbs →disaccharides and monosaccharides- Move to veins and portal circulation Proteins → amino acids and peptides- Move to veins and portal circulation Fats → fatty acids and monoglycerides- Move to lymph system and eventually circulation and liver |
| Large intestine | Fluid and electrolyte absorption (epithelial cells)- diffusion, active transport, aldosterone Mucus production for lubrication and passage of stool Final stool formation |
| Feces | Defecation reflex- Internal anal sphincter = autonomic nervous system/reflex control; External anal sphincter = voluntary/conscious control of cerebral cortex Control of anal sphincters |
| Normal intestinal flora- when does it harm | Proliferation or overgrowth of bacteria; Perforation of the intestine; Contamination of neighboring structures |
| Liver | Bile production; Clotting Factors- Vitamin K’s role- Fat (and Vit K) will not be absorbed without appropriate bile salts/bile from liver, many clotting factors require Vitamin K for their formation; stores- blood, vitamins, minerals |
| Liver functions cont'd | Nutrient metabolism/distribution- fats, proteins, carbs; Detoxification- Chemicals, foreign molecules, hormones; ↓accumulation, ↓adverse affects, ↑excretion; May produce toxins as end result |
| Bile | Function- Emulsification and absorption of fats in intestine; Components- Bile salts, cholesterol, bilirubin, electrolytes, water; Stored in gallbladder |
| bilirubin | bile pigment; excreted- Converted to urobilinogen → urine and feces |
| portal circulation | Carry/contain- Collects blood from capillaries in visceral structures of abdomen; Functions- Allows reabsorption of bile salts, metabolism of nutrients, detoxification |
| Fats | Role- Lacteals (lymph) → liver (triglycerides) → energy and lipoproteins; Risks- too much cholesterol |
| Proteins | Amino acids → ketoacids- Ammonia waste; Plasma proteins- Albumin |
| Carbs | Control of BG; Gluconeogenesis- can also convert amino acids and glycerol to glucose in times of need; Glyconeogenesis- Stores glucose in times of hyperglycemia, stores as glycogen |
| Hepatitis | inflammation of the hepatocytes r/t virus; chronic associated with hepatocellular carcimoma and liver failure. B and C also associated with acute fulminating hepatic necrosis. Cause- dirty needles. Contact with infection |
| Jaundice | hyperbilirubinemia secondary to increased hemolysis of RBCs or obstruction of the bile duct or liver cells → yellow-green pigment to skin. |
| Ascites | accumulation of fluid in peritoneal cavity; decreases with restoration of liver fxn |
| enchepalopathy | liver dysfunction allows toxins to circulate freely to brain (ammonia, which was byproduct of protein digestion) most harmful; confusion, irritability, memory changes, stupor, tremor, coma |
| cirrhosis | irreversible inflammatory dz of liver- disrupts structure and function of liver with fibrosis and hardening; Slow progression of cell death and inflammation |
| Gallbladder | stores and concentrates bile |
| Cholelithiasis | Gallstone formation (from aggregates of bile) |
| Cholecystitis | Inflammation of the gallbladder or cystic duct as a result of gallstone obstruction and blockage of the flow of bile into and out of the gallbladder and the resulting inflammation; Risks: ischemia. Necrosis, perforation Pancreas |
| Pancreas | Functions (exocrine AND endocrine)- neutralize chyme, digestion enzymes, ↑ secretion w/ PSNS/vagal stim, secretin release, cholecystokinin, acetylcholine ↓ secretion w/ sympathetic n.s. stimulation, vasoconstriction, increased activated enzymes |
| pancreas enzymes | Amylase, Lipase, Trypsin Trypsin inhibitor’s role- deactivates enzymes while in pancreas Enterokinase’s role- in duodenal mucosa, activates pancreatic enzymes in duodenum; Purpose of alkaloid fluid- buffer |
| Pancreatitis | Inflammation of pancreas, obstruction of outflow of enzymes |
| Gastritis | Inflammation of the stomach (gastric) mucosa Edema, hyperemia, superficial erosion; Decreased gastric juice production at inflammation |
| constipation | infrequent defecation, hard stools, stool retention; change from normal causes- ignore urge, meds, disorders/obstruction complications- chronic constipation, incontinence, megacolon, impaction, hemorrhoids, fissures, perforation, ↑ arterial pressure, UT |
| diarhhea | Increased frequency of and amount of stool with altered consistency (acute vs. chronic) Risks dehydration and hypokalemia especially |
| malabsorption | Inability of digestive system to absorb 1 or more of major vitamins, minerals, and nutrients Risks- Malnutrition, wgt loss, nutrient deficiency, dehydration |
| IBS- dx of exclusion | an extremely rare dx, often unresponsive to therapy, the diagnosis of which is seriously considered only when all other possible–potentially treatable conditions–eg 'growing pains' or idiopathic midline granuloma, have been completely excluded |
| IBS | Alteration in BMs- diarrhea, constipation, or mixed |
| Appendicitis | Definition- Inflammation and edema of appendix; Cause- kinked or occluded by fecal material, tumor, or foreign body; Risks- can become easily obstructed and very vulnerable to infection |
| Diverticular Disease | herniation of colon mucosal layers thru muscular wall → pockets Cause- genetics, ↓ muscle strength, ↑ intraluminal pressure, low colon vol |
| Diverticular Disease (cont'd) | Sxs- perforation, spasticity of colon wall, abscess, peritonitis, and erosion of vessel walls → hemorrhage Risks- inflammation, infection, perforation, obstruction |
| difference b/n IBS & IBD | IBS- no inflammation, functional disorder, a syndrome or collection of symptoms; IBD- chronic, autoimmune, inflammatory diseases IBD risks- weight loss, nutritional deficiencies, electrolyte imbalance |
| Chron's (IBD) | Inflammation of GI tract, thru all layers; Anywhere, ususally distal ileum; Patches of edema, thickening, inflammation → ulceration, fistula, fissure, abscess → thickened, fibrotic bowel wall, narrowed intestinal lumen |
| UC | Recurrent ulceration and inflammation of mucosa of colon/rectum; Multiple, diffuse, confluent ulcerations with shedding of colonic epithelium, bleeding, abscesses |
| Mechanical Obstruction (Intestinal Obstruction) | Intraluminal obstruction or a mural obstruction from pressure on the intestinal wall; ex- polypoid tumors, stenosis, stricture, adhesions, hernias |
| Functional Obstruction | Intestinal musculature cannot propel the contents along the bowel; ex- muscular dystrophy, temporary secondary manipulation of bowel during surgery |
| 4 general types of intestinal obstruction | Herniation Intussusception- shortening of bowel casued by movement of 1 segment into another Volvulus- twisting of bowel with resulting edema Constriction Adhesions- scar tissue Risks- electrolyte imbalance, infection, jaundice, perforation |
| Cancer types | Esophageal; Gastric (Stomach); Colon; Rectal; Pancreatic; Liver |
| Esophageal CA risk factors | Increased/recurrent reflux (ulceration and metaplasia), changes in structure and function of esophagus that permit food and fluid to remain in esophagus delayed time, chronic exposure to irritants (tobacco, alcohol), obesity, inadequate nutrition |
| Gastric (stomach CA) risk factors | genetics, male gender, Japan/Iceland, H pylori infection, heavily salted/cured foods, low vegetable/fruit intake, tobacco, alcohol |
| colon/rectal CA risk factors | increased age, high fat diet with decreased fiber, alcohol, smoking, obesity, family hx, low physical activity levels, ulcerative colitis |
| Pancreatic CA risk factors | largely unknown, smoking, dietary factors, obesity, DM, chronic pancreatitis |
| Liver CA risk factors | chronic hepatitis (B or C), cirrhosis, dietary exposure to particular fungi |
| Barretts Esophagus | abnormal change (metaplasia) in the cells of the inferior portion of the esophagus |
| Polyps | Abnormal growth of tissue projecting from a mucous membrane; invasive- if it penetrates muscularis mucosae and enters the submucosal layer; colonoscopy needed if adenomatous |
Created by:
sccrgrl159
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