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Pathophys final GI

QuestionAnswer
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