121 terms

Patho 3- Chapter 39

a lack of a desire to eat despite physiologic stimuli that would normally produce hunger
-forceful emptying of the stomach and intestinal contents (chyme) through the mouth
-common symptoms are hypersalivation, tachycardia, sweating and tachypnea
vomiting reflex
-intestinal, vagal, or sympathetic stimuli initiate the vomiting reflex, including the presence of ipecac or copper salts in the duodenum
-severe pain and activation of chemoreceptor trigger zone in the medulla.
-5-hydroxytryptamine (sertonin)/ these receptor antagonist are effective antiemetics to treat n/v.
-subjective experience that is associated with a number of conditions
-nausea and retching usually precede vomiting
-nonproductive vomiting
-the upper esophageal sphincter is not open
projectile vomiting
-spontaneous vomiting that does not follow nausea or retching
-caused by direct stimulation of the vomiting center by neurologic lesions (ex. tumors, aneurysms) involving the brain stem
-infrequent or difficult defecation
-decrease in the number of bowel movements per week, hard stools, and difficult evacuation
-normal could be 2-3/day to 1 per week
pathophysiology of constipation
-neurogenic disorders, functional or mechanical conditions, low residue diet, sedentary lifestyle, excessive use of antacids and opiates, changes in bowel habits.
-use of anticholinergic would block the parasympathetic impulses in the GI tract, thereby impairing motility
-neurogenic disorders of the large intestines in which neurotransmitters are altered or neural pathways are absent or degenerated (Hirschsprung disease, pelvic hiatal hernia, MS, spinal cord trauma, CVA)
Hirschsprung disease
-aka congenital megacolon
-the absence of ganglion cells in the myenteric plexus of large intestines. constipation at birth.
functional/mechanical constipation
-muscle weakness or pain d/t surgery can impair or inhibit defecation
-abdominal muscles are often use to increase intraabdominal pressure to evacuate the stool
-lesions of the anus, fistulae, inflamed hemorrhoids make defecation painful
-increased frequency of bowel movements
-increased volume, fluidity, weight of the feces
-three of more days is considered abnormal
osmotic diarrhea
-nonabsorbable substance in the intestine draws water into the lumen by osmosis.
-causes large volume diarrhea
-lactase deficiency is the most common cause of osmotic diarrhea and loss of pancreatic enzymes can be a contributing factor
-ingestion of sorbitol (nonabsorbable sugar) would have the same effect
secretory diarrhea
-d/t excessive mucosal secretion of chloride or bicarb rich fluid or inhibition of net sodium absorption
-most causes are bacterial enterotoxins (cholera or strains of E coli) and neoplasms that stimulate intestinal secretions
small volume diarrhea
-caused by inflammation of intestines
-ex. ulcerative colitis or crohn disease
-could be bloody
motility diarrhea
-caused by resection of the small intestine, surgical bypass of an area of the intestine or fistula formation
-food is not mixed properly, and there is impaired digestion and increased motility
abdominal pain
-a symptom of a number of gastrointestinal disorders and is usually associated with tissue injury
-abd organs aren't sensitive to mechanical stimuli, cutting, tearing or crushing
-sensitive to stretching and rapid distention; activates nerve endings in hollow and solid structures
-capsules surrounding organs contain pain fibers that are stimulated by stretching
parietal (somatic) pain
-arises from parietal peritoneum
-more localized intense pain
-pain corresponds to the skin dermatomes (T6-L1)
-pain tends to be lateralized
Visceral Pain
-arises from stimuli acting on an abdominal organ
-felt near the midline in the epigastrium, midab or lower abd
-pain is poorly localized, dull and difficult to describe
-example: pain arising from stomach as sensation of fullness, cramping, or gnawing in midepigastric region
Referred Pain
-visceral pain felt at some distance from a diseased or an affected organ
-tissues share a central afferent pathway with the affected organ
-example: gallbladder pain referred to back
Upper gastrointestinal bleeding
-esophagus, stomach, or duodenum
-causes: PUD, varices, Mallory-Weiss tear
Mallory-Weiss tear
-esophageal gastric juice from severe retching or cancer
Lower gastrointestinal bleeding
-below the ligament of Treitz, or bleeding from the jejunum, ileum, colon, or rectum
-Causes: polyps, IBD, diverticulosis, cancer, vascular ectasias (dilations) or hemorrhoids
vomit of blood
frank bleeding from rectum
dark, tarry stools
occult bleeding
can only be detected by guaiac testing the stool or vomit for the presence of blood
difficulty swallowing
dysphagia d/t mechanical (anatomic) obstructions
-Intrinsic: wall of esophageal lumen (tumor, strictures, diverticular herniations/outpouchings)
-Extrinsic: outside the esophageal lumen (narrow the esophagus by pressing inward: tumor)
dysphagia d/t functional (motor) obstructions
-caused by neural or muscular disorders that interfere with voluntary swallowing or peristalsis
-ex: CVAs, parkinson dz
-denervation of smooth muscle in the middle and lower esophagus
-decrease in the number of myenteric ganglion cells and atrophy of smooth muscle cells (loss of LES tone)
-decrease muscle tone and peristaltic function prevent food from entering the stomach, causing esophageal distention
-reflux of chyme from the stomach to the esophagus
-conditions that increase abdominal pressure can contribute to GERD (vomiting, cough, lift or bend)
-hiatal hernia and delayed gastric emptying (gastric/duodenal ulcers) can increase reflux and esophagitis
-ulcers cause strictures that narrow the pylorus
reflux esophagitis
-if GERD causes inflammation of the esophagus
-severity depends on the composition of contents, the length of time in contact w/esophagus mucosa and epithelial resistance to acid
consequences of GERD
-fibrosis, basal cell hyperplasia and elongation of papillae
-precancerous lesions (Barret esophagus) can be a long term consequence
Manifestations of GERD
-heartburn, regurgitation of acidic chyme, and upper abdominal pain within 1 hour of eating
Hiatal Hernia
-diaphragmatic hernia, protrusion of the upper part of the stomach through the diaphragm into the thorax
Sliding (direct) hiatal hernia
-90% most common
-the stomach slides into the thoracic cavity through the esophageal hiatus (opening for the esophagus and vagus nerves)
-reduced when standing but exacerbated by increased intraabdominal pressure
-associated w/GERD and esophagitis bc diminishes resting pressure of the LES
Paraesophageal (rolling) hiatal hernia
-herniation of the greater curvature of the stomach through a secondary opening in the diaphragm
-entire stomach could pass through the opening into the thorax
-reflux is uncommon
-the portion above the diaphragm causes congestion of mucosal blood and leads to gastritis and ulcers
-it can strangulate
pyloric obstruction
-blocking or narrowing of the opening between the stomach and the duodenum
-can be acquired or congenital
-manifestations: epigastric pain & fullness, n/v (undigested food w/no bile), succussion splash
-prolonged obstructions lead to malnutrition, dehydration and extreme debilitation
acquired pyloric obstruction
-usually caused by PUD or carcinoma near the pylorus
-duodenal ulcers are more likely than gastric ulcers to obstruct the pylorus
-ulceration can cause obstruction by inflammation, edema, fibrosis or scarring
intestinal obstruction and ileus
-any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing lesion (ileus)
-ileus is an obstruction of the intestines
simple obstruction
-mechanical blockage of the lumen by lesion (adhesions most common)
-accumulation of fluid and gas inside lumen proximal to obstruction
-severe electrolyte and fluid disturbances (dehydration)
functional obstruction
-failure of motility (paralytic ileus)
small intestine obstruction
-if above the pylorus or high in the small intestines (metabolic alkalosis develops initially from excessive loss of hydrogen ions that would be reabsorbed from gastric juice)
-if obstruction is lower in the intestines, metabolic acidosis is more likely b/c bicarbonate from pancreatic secretion and bile cannot be reabsorbed
large bowel obstruction
-consequences are r/t the competence of the ileocecal valve
-ischemia can occur when the intraluminal pressure exceeds capillary pressure in the lumen
-inflammatory disorder of the gastric mucosa usually affecting the fundus or antrum or both
acute gastritis
-injury of the protective mucosal barrier by drugs, chemicals, or H. pylori infections
-drugs (prostaglandin inhibitors which decrease mucus secretion)
chronic gastritis
-usually in elders with thinning and degeneration of the stomach wall with atrophy of gastric epithelium
Chronic fundal (immune) gastritis
-most severe form of gastritis
-can result in gastric atrophy and decreased secretion of hydrochloric acid, pepsinogen and intrinsic factor
-loss of chief cells and parietal cells d/t autoimmunity to these cells
Chronic antral gastritis
-most common type
-not associated with impaired secretion of gastric atrophy
-causes: ETOH, tobacco, NSAIDS, H. Pylori
Peptic Ulcer Disease
-a break or ulceration in the protective mucosal lining of the lower esophagus, stomach or duodenum
-such breaks expose submucosal areas to gastric secretions and autodigestion
-acute and chronic ulcers
Superficial Peptic Ulcers
-erosions because they erode the mucosa but do not penetrate the muscularis mucosae
Deep Peptic Ulcers
-true ulcers b/c they extend through the muscularis mucosae and damage blood vessels causing hemorrhage or perforation
duodenal ulcers
-most common type of peptic ulcer
-tend to develop in younger persons and those with type O blood
-present w/chronic intermittent pain in the epigastric area. Begins 30 min to 2 hrs post prandial, when stomach is empty
-pain is relieved with rapid ingestion of food or antacids "pain-food-relief" pattern
developmental factors for duodenal ulcers
-H. pylori infection (toxins and enzymes that promote inflammation and ulceration)
-hypersecretion of stomach acid and pepsin and inadequate secretion of bicarbonate by the duodenal mucosa
-use of NSAIDS which inhibit prostaglandin
-high gastrin levels
-acid production by cigarette smoking
Gastric Ulcer
-tend to develop in the antral region of the stomach, adjacent to the acid-secreting mucosa of the body
-not as common
-55-65 yo
-primary defect is an increased mucosal permeability to hydrogen ions
-gastric secretions tend to be normal or less than normal
-increased cancer risk, usually chronic, pain occurs AFTER eating
Stress Ulcer
-a peptic ulcer that is related to severe illness, neural injury or systemic trauma
-multiple sites of ulceration within the stomach or duodenum
-decreased mucosal blood flow is an important contributing event in stress ulcer formation
-bleeding may be slight
-ischemic, curling and cushing
Ischemic stress ulcer
-develops within hours of an event such as hemorrhage, trauma, severe burns, CHF, sepsis
-anything that decreases mucosal blood flow can cause ischemia
Curling Stress Ulcers
-ulcers that develop as a result of a burn injury
Cushing Stress Ulcer
-stress ulcer associated with severe head trauma or brain surgery
postgastrectomy syndromes
-group of signs and symptoms that occur after gastric resection
-caused by changes in motor and control functions of the stomach and upper small intestines
Dumping Syndrome
-the rapid emptying (10-20 min) of chyme from a surgically created, residual stomach into the small intestine
-clinical complication of partial gastrectomy or pyloroplasty surgery
-a high osmotic gradient within the small intestine cause a sudden shift of fluid from the vascular compartment to the intestinal lumen; rapid distention produces fullness, n/v/d
-loss of gastric capacity, loss of emptying control and loss of feedback control by the duodenum wen it is removed
-1-2 hrs after eating
Malabsorption Syndromes
-pancreatic insufficiency
-lactase deficiency
-bile salt deficiency
-fat soluble vitamin deficiences
-failure of the chemical processes of digestion that take place in the intestinal lumen or at the brush border of the intestinal lumen
-frequently occurs w/malabsorption
-failure of the intestinal mucosa to absorb digested nutrients
Pancreatic Insufficiency
-insufficient pancreatic enzyme production
-causes include pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis
-fat maldigestion is the main problem, so pt. will exhibit fatty stools and weight loss
lactase deficiency
-inability to break down lactose into monosaccharides and therefore prevent lactose digestion and monosaccharide absorption
-fermentation of lactose by bacteria causes gas and osmotic diarrhea
bile salt deficiency
-conjugated bile salts needed to emulsify and absorb fats aren't present
-can result from liver disease and bile obstructions
-poor intestinal absorption of lipids causes fatty stools (steatorrhea), diarrhea, and loss of fat soluble vitamins (A, D, E, K)
Fat soluble vitamin deficiencies
-Vit A (night blindness)
-Vit D (decreased calcium absorption, bone pain, osteoporosis, fractures)
-Vit K (prolonged prothrombin time, purpura, and petechiae)
-Vit E
Inflammatory Bowel Disease
-chronic relapsing inflammatory bowel disorders of unknown orgin
-genetics, alteration of epithelial barrie functions, immune reactions to intestinal flora, abnormal T cell responses
Ulcerative Colitis
-Chronic inflammatory disease that causes ulceration of the colonic mucosa
-extends proximally FROM RECTUM TO COLON
-lesions of UC are limited to the mucosa
-inflammation begins at the base of crypts of lieberkuhn in the Large intestine w/infiltration of neutrophils, lymphocytes, plasma cells, macrophages, eosinophils and mast cells
-20-40 yo
-causes: infectious, immunological, dietary, genetic
Sx of UC
-diarrhea (10-20/day), bloody/watery stools, cramping, tenesmus, purulent mucus is common in stools
-abscess formation can occur at crypts
-necrosis and ragged ulceration of the mucosa
-edema and thickening of the muscularis may narrow lumen of the colon
-increases risk of colon cancer
Crohn Disease
-granulomatous colitis, ileocolitis, or regional enteritis
-idiopathic inflammatory disorder; effects any part of digestive tract from MOUTH TO ANUS
-distal small intestine and proximal large colon are most commonly affected
-inflammation can affect some haustral segments but not others creating "skipped lesion" pattern
Crohn Disease specifics
-"skip lesions"
-"cobblestone" pattern
-transmural (entire intestinal wall involved)
-granulomas, fistulas, and abscesses are common
-anemia may result
-risk for malignancy
-herniations (saclike outpouchings) of mucosa through the muscle layers of the coon wall, especially the sigmoid colon
-usually occur at weak points in the colon wall, usually where arteries penetrate the tunica muscularis to nourish the mucosal layer
-asymptomatic diverticular disease
-unknown cause but associated with decreased fiber and increase intracolonic pressure
-the inflammatory stage of diverticulosis
-usually over 60 yo
-usually in developed countries where diet consists of refined foods
-can cause abscess formation or perionitis
-LLQ tenderness if abscess over diverticula occurs
-inflammation of the vermiform appendix
-most common surgical emergency of the abdomen
-most 20-30 yo
-various things may cause increase in intraluminal pressure which decreases mucosal blood flow and the appendix becomes hypoxic; mucosa ulcerates, promoting bacterial invasion w/further inflammation and edema. gangrene develops followed by perforation.
signs/sx of appendicitis
-epigastric/periumbilical and RLQ pain
-rebound tenderness
-n/x, anorexia, fever
-most serious complication is peritonitis
Vascular Insufficiency
-blood supply to the stomach and intestines (3 branches of abdominal aorta
-celia axis, superior and inferior mesenteric arteries
-2 of 3 must be compromised to cause ischemia
-increase in body fat mass
-body fat index >30
-major cause of morbidity, death and increased health care costs
-risk factor for many diseases and conditions
Portal Hypertension
-abnormally high blood pressure in the portal venous system due to resistance to portal blood flow
-normal is 3mmHg, if >10 mmHg portal HTN
-caused by obstruction of any component of the portal venous system or vena cava (portal veins, sinusoids, hepatic veins)
-most common cause of portal HTN is obstruction caused by cirrhosis of liver
Prehepatic Portal HTN
-caused by thrombosis or narrowing of the portal vein
Intrahepatic portal HTN
-results from thrombosis, inflammation, or fibrois of the sinusoids from causes like: cirrosis, viral hepatitis, schistosmiasis (parasitic infx)
Posthepatic portal HTN
-occur from heptaic vein thrombosis or cardiac disorders (right heart failure) or constrictive pericarditis
Portal hypertension pathology
-high pressure portal veins causes collateral vessels to open between the portal veins and the systemic veins, in which blood pressure is considerably lower
-the collateral veins develop in the esophagus, anterior abdominal wall and rectum.
-consequence of portal HTN
-distended, torturous collateral veins
-appear in the lower esophagus, stomach and rectum
-s/s: bleeding, anemia, melena
-consequence of portal HTN
-increased pressure in splenic vein
-thrombocytopenia can occur and increase risk for bleeding
-consequence of portal HTN
-accumulation of fluid in the peritoneal cavity d/t hydrostatic pressure changes
-increase pressure in the mesenteric tributaries of the portal vein forces water out of these vessels into the peritoneal cavity
hepatic encephalopathy
-consequence of portal HTN
-a neurologic syndrome of impaired cognitive function, flapping tremor (asterixis) and EEG changes
-condition develops rapidly during fulminant hepatitis or slowly during chronic liver disease
-cells in the NS are vulnerable to neurotoxins (ammonia) absorbed from the GI tract that, due to liver dysfunction, circulate to the brain
source of ammonia in hepatic encephalopathy
-end products of intestinal protein digestion
-digested blood leaking from ruptured varies
-ammonia-forming bacteria in the colon
Jaundice (icterus)
-caused by hyperbilirubinemia
Extrahepatic Obstruction
-type of obstructive jaundice
-develops if the common bile duct is occluded by a stone, tumor, compression, edema, pancreatitis
-because the duct is obstructed, the bilirubin is conjugated by hepatocytes but cannot flow to the duodenum
-water soluble conjugated bilirubin ends up in the urine, not in the stool
-stools also lack urobilinogen because bile is not available for conversion to urobilinogen
Intrahepatic Obstruction
-type of obstructive jaundice
-involves disturbances in hepatocyte function and obstruction of bile canaliculi
-increase in (direct) conjugated and (indirect) unconjugated bilirubin
-the stool may be normal in color
Hemolytic Jaundice
-prehepatic jaundice: destruction of heme component which increases the level of unconjugated bilirubin in the blood. This causes jaundice. It is not water soluble to it is NOT excreted in the urine.
-excessive hemolysis of red blood cells or absorption of a hematoma
Gilbert Disease
-metabolic defect that impairs the uptake or conjugation of unconjugated bilirubin in the liver with no other symptoms of liver disease
Viral Hepatitis
-systemic viral disease that primarily affects the liver
Hepatitis A
-can be found in the feces, bile, and sera of infected individuals
-usually transmitted by fecal-oral route
-risk factors: crowded, unsanitary conditions, food and water contamination
Hepatitis B
-transmitted through contact with infected blood, body fluids, or contaminated needles
-maternal transmission can occur if the mother is infected during the third trimester
-the vaccine prevents transmission and development of hepatitis B; which makes it a cure to cancer
Hepatitis C
-responsible for most cases of post-transfusion hepatitis
-implicated in infections related to IV drug use
Hepatitis D
-depends on hepatitis B for replication
Hepatitis E
-fecal-oral transmission
-developing countries
Hepatitis G
-recently discovered
-parentally and sexually transmitted
-irreversible inflammatory disease that disrupts liver function and even structure
-decreased hepatic function due to nodular and fibrotic tissue synthesis (fibrosis)
-biliary channels become obstructed and cause portal HTN. Due to the HTN, blood can be shunted away from the liver, and a hypoxic necrosis develops
Cirrhosis d/t Alcohol
-the oxidation of alcohol damages hepatocytes
Cirrhosis & Biliary (bile canaliculi)
-cirrhosis begins in the bile canaliculi and ducts
-primary biliary cirrhosis (autoimmune)
-secondary biliary cirrhosis (obstruction)
Postnecrotic Cirrhosis
-consequence of chronic liver disease
-obstruction or inflammation of the gallbladder
-the most common cause of gallbladder problems
-gallstone formation
-Types: cholesterol (most common) and pigmented (cirrhosis)
-risks: obesity, middle age, female, Native American ancestry, and gallbladder, pancreas or ileal disease
Gallstones (cholelithiasis)
-cholesterol stones form in the bile that is supersaturated with cholesterol
-manifestations: epigastric and RUQ pain that radiates to mid upper back. Intolerance to fatty foods. Vague symptoms
-Biliary colic can occur from lodging of gallstones in cystic or common duct
-pancreatitis can occur
bile supersaturated w/cholesterol theories
-enzyme defect that increases cholesterol synthesis
-decreased secretion of bile acids to emulsify fats
-decreased resorption of bile acids from the ileum
-gallbladder smooth muscle hypomotility and stasis
-genetic predisposition
genetic predisposition
-combination of any or all of the above
-acute or chronic
-most caused by lodging of stone in the cystic duct
-gallbladder becomes distended and inflamed
-pressure against the wall of GB causes decrease blood flow.
-ischemia, necrosis, and perforation of the GB are possible
-s/s: fever, leukocytosis, rebound tenderness, guarding
-inflammation of the pancreas and more common in 50-60 yo
-associated w/several other clinical disorders (ETOH, cholelithiasis, PUD, trauma, hyperlipidemia)
-caused by an injury or damage to pancreatic cells and ducts, causing a leakage of pancreatic enzymes into the pancreatic tissue
-these enzymes cause autodigestion of pancreatic tissue and leak into the bloodstream to cause injury to blood vessels and other organs
Acute Pancreatitis (acute hemorrhagic pancreatitis)
-usually mild and caused by ETOH and biliary tract obstruction.
-most likely that pancreatic acinar cells are damaged, permitting leakage of pancreatic enzymes into pancreatic tissue
-bile reflux can occur if the common bile duct is occluded with a stone
-the activated proteolases break down tissue and cell membranes (edema, hemorrhage, necrosis, fibrosis)
manifestations of acute pancreatitis
-epigastric and midabdominal pain radiating to the back
-fever and leukocytosis
-hypotension and hypovolemia (enzymes and increased permeability)
-characterized by an increase in a pts serum amylase level, lipase also increases
-if hemorrhagic pancreatitis, flank pain or periumbilical ecchymosis= poor diagnosis
Chronic Pancreatitis
-structural and functional impairment
-related to chronic alcohol abuse
-fibrosis, strictures, continued inflammation, and pancreatic cysts are common
Esophageal Cancer
-ETOH, tobacco, esophagitis (Barret)
Stomach Cancer
-H. Pylori, salty food, food additives (nitrates) pickled/salted, low fruits/vegs
Colon and Rectum Cancer
-2nd most common cause of cancer death
-Familial polyposis, high fat, low fiber, low calcium
Liver Cancer
-usualy be metastatic spread
-risk factors for primary liver CA or Hep B, C, D, inconjunction with cirrhosis
-heavy smoking/ETOH use
Gallbladder Cancer
-most are metastatic spread
-if primary then usually associated with chronic cholecystitis and cholelithiasis
Pancreas Cancer
-risk rises with age
-mortality is nearly 100%
-smoking is a risk factor