Exam 4- Gastrointestinal Flashcards
Hepatocytes
Metabolize nutrients, detoxify chemicals, secrete bile, synthesize albumin and clotting factors, and other functions.
Synthesize the primary bile acids from cholesterol.
Kupffer cells
Remove bacteria and foreign particles from blood in the hepatic sinusoids.
Pancreatic acinar cells
Secrete digestive enzymes.
Bile
Produced in liver. Slightly alkaline. Secreted by hepatocytes into the canaliculi, which empty into the bile ducts.
Choleretic agent stimulates liver to release bile.
Peristalsis
Waves of sequential relaxations and contractions of the gastrointestinal muscles.
Caused by stretching of the esophagus or intestine by bolus of food.
Gastric emptying
Delayed by fatty foods and hypertonic gastric contents. And cholecystokinin.
Stimulated by gastrin.
Intestinal brush border
Collection of microvilli.
Enzymes in the border hydrolyze oligopeptides.
Small intestine
Supplied primarily by the superior mesenteric artery.
The 3 segments are the duodenum, jejunum, and ileum.
Absorbs most of the water that enters the gi tract.
Sugars absorbed primarily in the initial portions.
Pancreatic proteases
Secretes in inactive form.
Pancreatic amylases
Secreted in active form. Digests carbohydrates.
Gastrointestinal changes with age
Gastrointestinal motility tends to decrease.
Liver blood flow and enzyme activity decrease.
LFTs remain normal in an older adult without overt liver disease.
Gastric acid
Increased by histamine, gastrin, vagal stimulation, and caffeine.
Decreased by cholecystokinin and sympathetic stimulation.
Esophagus
Upper 1/3 has striated muscle.
Lower 1/3 had smooth muscle.
Peritoneum
Visceral layer covers the abdominal organs.
Parietal layer extends along the abdominal wall.
Pepsin
Gastric enzyme that digests proteins.
Only functions in an acidic environment.
Celiac artery
Supply most of the blood to the stomach.
Superior mesenteric artery
Provides most of the circulation to the small intestine.
Villi
The functional units of the intestine.
Each one has a capillary at the center known as the lacteal, which is important in absorption of fat molecules.
Excretion in the intestines happen at the tops of the villi.
Round ligament
Remnant of the umbilical vein.
Enteric nervous system
Lies within the gastrointestinal tract and consists of neurons of the submucosal plexus, the myenteric plexus, and the subserosal plexus.
Pyloric valve
Valve between the stomach and duodenum.
Chief cells
Gastric cells that secrete pesinogin
Parietal cells
Gastric cells that secrete hydrochloric acid.
Cephalic phase
Phase of gastric acid secretion acid secretion involving anticipation and swallowing.
Sphincter of Oddi
Sphincter through which bile enters the intestine.
GERD
Reflux of acid and pepsin from the stomach to the esophagus that causes esophagitis.
Decreased resting tone of the lower esophageal sphincter. Symptoms include heartburn and chronic cough.
Acute mesenteric ischemia
The damaged intestinal mucosal I cannot produce enough mucus to protect itself from digestive enzymes. Bacteria invade the necrotic intestinal wall, eventually causing peritonitis.
Visceral obesity
Associated with a greater risk for metabolic syndrome, type 2 diabetes, and cardiovascular complications. Resistance to leptin and decreased production of adiponectin contribute to the influences of obesity.
Ascites
Involves the combination of portal hypertension and vasodilation. I sightings can be complicated by bacterial peritonitis.
Hepatitis A infection
Transmitted by fecal oral, sexual, and parenteral routes. Acute. Cannot be a carrier.
Hepatitis B infection
Transmitted by parenteral and sexual routes. Acute or chronic. Can be a carrier.
Hepatitis C infection
Transmitted by parenteral route. Candy acute or chronic. Can be a carrier.
Hepatitis D infection
Transmitted by parenteral, fecal oral, or sexual route. Chronic. Can be a carrier.
Depends on hepatitis B in order to replicate.
Hepatitis E
Transmitted by fecal oral route. Acute. I cannot be a carrier.
NERD
Nonerosive reflux disease.
Similar to GERD but with no signs of esophagitis.
Type A chronic gastritis
Caused by autoimmune damage primarily in the gastric fundus.
Type B chronic gastritis
Caused by nonimmune mechanisms such as H pylori, chronic ETOH and NSAID use, and occurs primarily in the antrum of the stomach.
Maldigestion
Failure of the chemical process of breaking down nutrients that take place in the intestinal lumen or at the brush border.
Malabsorption
The failure of the intestinal mucosa to transport the digested nutrients into the blood and lymph.
Orexins
Molecules that stimulate eating.
Anorexins
Molecules that inhibit eating.
Short-term starvation
The body responds with glycogenolysis and glyconeogenesis with only a small amount of protein catabolism.
Long-term starvation
The body responds with lipolysis and eventually proteolysis, which can cause death.
Alcoholic cirrhosis
Damage begins with the hepatocytes.
Biliary cirrhosis
Damage begins in the bile caniculi and bile ducts.
Zollinger-Ellison Syndrome
Gastrin-secreting tumor that causes gastric and duodenal ulcers, gastroesophageal reflux with AP, and diarrhea.
Lactase deficiency
absence of an enzyme causes bloating, crampy pain, diarrhea, and flatulence after ingesting milk.
Cholestatic jaundice
Increased bilirubin, predominantly conjugated, in the blood due to obstruction of the common bile duct.
Dumping syndrome
Clinical manifestations including increased pulse, hypotension, weakness, pallor, sweating, and dizziness following a partial gastrectomy or pyloroplasty. Occurs about 20 minutes after eating. Rapid gastric emptying and creation of a high osmotic gradient within the small intestine cause a sudden shift of fluid from the vascular compartment to the intestinal lumen. Usually managed very well with dietary management: frequent small meals; no fluid during meals; high protein, low carbs.
Rapid gastric emptying of hypertonic chyme after bariatric surgery, causing tachycardia, hypotension, pallor, diaphoresis, cramping m, naive, and diarrhea.
Diverticulitis
Inflammation of saclike outpouchings that are continuous with the GI tract lumen.
Diverticulosis
Asymptomatic presence of saclike outpouchings that are continuous with the GI tract lumen.
Irritable bowel syndrome
A functional gastrointestinal disorder characterized by abdominal pain and altered bowel habits.
Acute liver failure
Necrosis of liver cells without preexisting liver disease or cirrhosis, often due to acetaminophen OD.
Refeeding Syndrome
Rapid provision of nutrients after starvation, causing severe phosphatemia and other electrolyte imbalances that may be fatal.
Hepatocellular jaundice
Increased bilirubin, both conjugated and unconjugated, in the blood due to failure of liver cells to conjugate bilirubin and of bilirubin to pass from liver to intestine.
Achalasia
Functional dysphagia cause led by loss of esophageal interaction.
Hiatal hernia
Protrusion of the upper part of the stomach through the diaphragm and into the thorax. Most common type is sliding. Not associated with gerd
Peptic ulcers
Gastric and duodenal ulcers.
Risk factors: H pylori and NSAIDs
Obesity
BMI that exceeds 30 kg/m2
Macrophages that infiltrate adipose tissue secrete pro inflammatory cytokines.
Acute pancreatitis
Primary diagnostic marker is elevated serum lipase.
Chronic pancreatitis
May be autoimmune or associated with chronic alcohol abuse.
Cholecystitis
Occurs when a gallstone lodges in the cystic duct. The most common type of gallstone is made of cholesterol.
Fatty liver
Associated with chronic use of alcohol or with obesity. Although fatty liver is asymptomatic, person to have it may develop steatohepatitis add may progress to cirrhosis, liver failure, or liver cancer.
Crohn’s disease
Family history is more common. Lesions are located on the entire G.I. tract with small and large most common, skip lesions. Lesions involve the entire thickness of the intestinal wall. Fistulas, abscesses, near lumen with obstruction, recurrent episodes of diarrhea are all common. Blood in stools is less common. Patients have remission and exacerbation.
Ulcerative colitis
Family history is less common. Lesions are in the rectum and colon and our continuous. Nature of lesions involve me postal layer only. Fistulas abscesses near lumen in recurrent episodes of diarrhea are rare. Blood in stools are common. Remission and exacerbations.
Alcoholic hepatitis
I
Bowel obstructions
Bowel Obstruction: the most common occurring small intestinal obstruction is related to adhesions account for 50% to 70% of small bowel obstructions.
Small bowel obstructions usually presents early with abdominal distention. If the obstruction is at the pylorus or high in the small intestine, metabolic alkalosis develops initially as a result of excessive loss of hydrogen ions that normally would be reabsorbed from the gastric juice. In prolonged intestinal obstruction the lack of circulation produces lactic acid (decreased tissue perfusion) thus metabolic acidosis.
Leptin resistance
Hi levels of leptin in obesity that are ineffective at decreasing appetite and increasing energy expenditure. It disrupts hypodermic satiety signaling, promotes over eating, and excessive weight gain.
Leptin
Acts on the hypothalamus to suppress appetite and regulates body weight. Low leptin levels stimulate food intake and reduce energy expenditure.
