Chapter 38 Health Alt Flashcards
Clinical Manifestations of Gastrointestinal Dysfunction: Part 1 Anorexia
-Anorexia
->A lack of a desire to eat despite physiologic stimuli that would normally produce hunger
->Associated with nausea, abdominal pain, diarrhea, psychological stress, and weight loss
->Side effects of drugs, cancer, heart disease, renal disease, & liver disease
Clinical Manifestations of Gastrointestinal Dysfunction: Part 2 Vomiting
-Vomiting (emesis)
->The forceful emptying of the stomach and intestinal contents through the mouth
->Several types of stimuli initiate the vomiting reflex
->The common symptoms of vomiting are hypersalivation and tachycardia
->Nausea: subjective experience that is associated with a number of conditions
->Retching: nonproductive vomiting
->Projectile vomiting: Spontaneous vomiting that does not follow nausea or retching
Clinical Manifestations of Gastrointestinal Dysfunction: Part 3 Constipation
-Constipation
->Defined as infrequent or difficult defecation. can’t take a shit.
->Primary condition
->Normal transit (functional): involves a normal rate of stool passage but difficulty with stool evacuation.
->Slow transit: involves impaired colonic motor activity, with infrequent bowel movements, straining to defecate, mild abdominal distention, and palpable stool in the sigmoid colon.
->Pelvic floor or outlet dysfunction
->Secondary condition
->Caused by many different factors such as diet, medications, various disorders, aging
->Clinical Manifestations:
->Straining with defecation
->Hard stools
->Sensation of incomplete emptying
->Manual maneuvers to facilitate stool evacuation
->Fewer than three bowel movements per week
Clinical Manifestations of Gastrointestinal Dysfunction: Part 4 Diarrhea
-Diarrhea
->Presence of loose, watery stools
->Acute or persistent: Acute diarrhea is more than three loose stools developing within 24 hours & lasting less than 14 days. Persistent diarrhea lasts longer than 14 to 30 days, and chronic diarrhea lasts longer than 4 weeks.
->Large-volume diarrhea
->Caused by excessive amounts of water or secretions or both in the intestines
->Small-volume diarrhea
->Volume of feces is not increased, usually results from excessive intestinal motility
-Major mechanisms of diarrhea
->Osmotic diarrhea: A nonabsorbable substance in the intestine draws excess water into the intestine and increases stool weight and volume, producing large-volume diarrhea. Causes include lactase and pancreatic enzyme deficiency; excessive ingestion of synthetic, nonabsorbable sugars; full-strength tube-feeding formulas; or dumping syndrome associated with gastric resection.
->Secretory diarrhea: Excessive mucosal secretion of fluid and electrolytes produces large-volume diarrhea. Infectious causes include viruses (e.g., rotavirus), bacterial enterotoxins (e.g.,Escherichia coliandVibrio cholerae), exotoxins from overgrowth ofClostridium difficileafter antibiotic therapy, or small bowel bacterial overgrowth.
->Motility diarrhea: caused by resection of the small intestine (short bowel syndrome), surgical bypass of an area of the intestine, fistula formation between loops of intestine, irritable bowel syndrome–diarrhea predominant, diabetic neuropathy, hyperthyroidism, and laxative abuse. Excessive motility decreases transit time and the opportunity for fluid absorption, resulting in diarrhea.
-Systemic effects
->Dehydration
->Electrolyte imbalance
->Weight loss
-Associated with malabsorption syndromes
-Treated with fluid restoration, antimotility or water-absorbent medications, treatment of causal factors
Clinical Manifestations of Gastrointestinal Dysfunction: Part 5 Abdominal Pain
-Abdominal pain
->Mechanical, inflammatory, or ischemic
->Usually associated with tissue injury and inflammation
->Parietal pain: Parietal pain,from the parietal peritoneum, is more localized and intense than visceral pain, which arises from the organs themselves. Parietal pain lateralizes because, at any particular point, the parietal peritoneum is innervated from only one side of the nervous system.
->Visceral pain: Visceral painarises from a stimulus (distention, inflammation, ischemia) acting on an abdominal organ. Inflammatory mediators associated with chronic low-grade inflammation can cause pain hypersensitivity. The pain is usually poorly localized, diffuse, or vague with a radiating pattern because nerve endings in abdominal organs are sparse and multisegmented.
->Referred pain: Referred painis visceral pain felt at some distance from a diseased or affected organ. It is usually well localized and is felt in the skin dermatomes or deeper tissues that share a central afferent pathway with the affected organ. For example, acute cholecystitis may have pain referred to the right shoulder or scapula.
Clinical Manifestations of Gastrointestinal Dysfunction: Part 6 Gastrointestinal Bleeding
-Gastrointestinal bleeding
->Upper gastrointestinal bleeding in the
->Esophagus, stomach, or duodenum (caused by bleeding varices (varicose veins) in the esophagus, peptic ulcers, arteriovenous malformations, or a Mallory-Weiss tear at the esophageal-gastric junction caused by severe retching.)
->Lower gastrointestinal bleeding
->Jejunum, ileum, colon, or rectum (caused by polyps, diverticulitis, inflammatory disease, cancer, or hemorrhoids.)
->Occult bleeding (usually caused by slow, chronic blood loss that is not obvious and results in iron deficiency anemia as ironstores in the bone marrow are slowly depleted.)
->Physiologic response depends on rate and amount of blood loss
->Hematochezia: bright red stools
->Melena: black or tarry stools
Disorders of Motility: Part 1 Dysphagia
-Dysphagia
->Difficulty swallowing
->Mechanical obstructions (Intrinsic obstructions originate in the wall of the esophageal lumen (esophageal dysphagia) and include tumors, strictures, and diverticular herniations (outpouchings). Extrinsic mechanical obstructions originate outside the esophageal lumen and narrow the esophagus by pressing inward on the esophageal wall. The most common cause of extrinsic mechanical obstruction is tumor.)
->Functional disorders (caused by neural or muscular disorders that interfere with voluntary swallowing or peristalsis.)
->Achalasia
->Related to loss of inhibitory neurons in the myenteric plexus with smooth muscle atrophy in the middle and lower portions of the esophagus;
Disorders of Motility: Part 2 Gastrointestinal Reflux Disease (GERD)
-Gastroesophageal reflux disease (GERD)
->Reflux of acid and pepsin from the stomach to the esophagus that causes esophagitis
->Resting tone of the LES tends to be lower than normal
->Conditions that increase abdominal pressure or delay gastric emptying can contribute to the development of reflux esophagitis
->Gastroesophageal reflux that doesn’t cause symptoms is known asphysiologic reflux.
->Innonerosive reflux disease (NERD),individuals have symptoms of reflux disease but no visible or minimal esophageal mucosal injury (functional heartburn).
->Delayed gastric emptying can contribute to reflux esophagitis by (1) lengthening the period during which reflux is possible and (2) increasing gastric acid content.
->Disorders that delay emptying include gastroparesis; gastric or duodenal ulcers, which can cause pyloric edema; and strictures that narrow the pylorus.
Disorders of Motility: Part 3 Hiatal Hernia
-Hiatal hernia
->Diaphragmatic hernia with protrusion of the upper part of the stomach through the diaphragm and into the thorax
->Sliding hiatal hernia (type 1; most common): The proximal portion of the stomach moves into the thoracic cavity through the esophageal hiatus, an opening in the diaphragm for the esophagus and vagus nerves.
->Paraesophageal hiatal hernia (type 2): The herniation of the greater curvature of the stomach through a secondary opening in the diaphragm alongside the esophagus.
->Mixed hiatal hernia (type 3; less common): ls a combination of sliding and paraesophageal hiatal hernias. It tends to occur in conjunction with several other diseases, including reflux esophagitis, peptic ulcer, cholecystitis (gallbladder inflammation), cholelithiasis (gallstones), chronic pancreatitis, and diverticulosis.
->Conservative treatment
Disorders of Motility: Part 4 Gastroparesis
-Gastroparesis
->Delayed gastric emptying in the absence of mechanical gastric outlet obstruction
->Associated with diabetes mellitus, surgical vagotomy, or fundoplication
->Symptoms include nausea, vomiting, abdominal pain, and postprandial fullness or bloating
Disorders of Motility: Part 5 Pyloric Obstruction
-Pyloric obstruction
->The blocking or narrowing of the opening between the stomach and the duodenum
->Can be acquired or congenital
->Manifestations
->Epigastric pain and fullness
->Nausea and vomiting
->Succussion splash (Rolling or jarring of the abdomen produces a sloshing sound called thesuccussion splash)
->With a prolonged obstruction, malnutrition, dehydration, and extreme debilitation
->Usually conservative management
Disorders of Motility: Part 6 Intestinal Obstruction
-Intestinal obstruction
->An intestinal obstruction is any condition that prevents the flow of chyme through the intestinal lumen
->Simple obstruction
->Mechanical blockage of the lumen by a lesion
->Functional obstruction (paralytic ileus)
->Failure of intestinal motility
->Often occurs after intestinal or abdominal surgery, pancreatitis, or hypokalemia
->Acute obstructions usually have mechanical causes, such as adhesions or hernias.
->Chronic or partial obstructions are more often associated with tumors or inflammatory disorders, particularly of the large intestine.
->Postoperative paralytic ileus results from inhibitory neural reflexes associated with inflammatory mediators, and the influence of exogenous (i.e., meperidine or morphine) and endogenous opioids (endorphins) that affect the entire GI tract.
-Signs of small intestinal obstruction
->Colicky pains (caused by intestinal distention)
->Nausea and vomiting
-Signs of large intestine obstruction
->Hypogastric pain and abdominal distention
Dysphagia Clinical Manifestations
-Manifestations
->Stabbing pain at the level of obstruction
->Discomfort after swallowing
->Regurgitation of undigested food
->Unpleasant taste sensation
->Vomiting
->Aspiration
->Weight loss
Symptoms managed by eating small meals slowly, taking fluid with meals, and sleeping with the head elevated to prevent regurgitation and aspiration
Gastroesophageal reflux disease (GERD) Clinical Manifestations
-Manifestations
->Heartburn
->Acid regurgitation
->Dysphagia
->Chronic cough
->Asthma attacks
->Laryngitis
->Upper abdominal pain within 1 hour of eating
-Proton pump inhibitors are the agents of choice for controlling symptoms and healing esophagitis
Gastritis
-Inflammatory disorder of the gastric mucosa
-Acute gastritis
->Caused by injury of the protective mucosal barrier
->NSAIDs (e.g., ibuprofen, naproxen & aspirin) cause gastritis because they inhibit prostaglandin synthesis, which normally stimulates the secretion of mucus. Alcohol, histamine, digitalis, and metabolic disorders, such as uremia, are contributing factors.H. pylori–associated acute gastritis causes inflammation, increased gastric secretion in antral gastritis, decreased gastric secretion in fundal gastritis, pain, nausea, and vomiting.
->Clinical manifestations of acute gastritis can include vague abdominal discomfort, epigastric tenderness, andbleeding. Healing usually occurs spontaneously within a few days.
-Chronic gastritis
->Chronic fundal gastritis (type A, immune): rare; associated with loss of T-cell tolerance and development of autoantibodies to acid-secreting parietal cells. The gastric mucosa degenerates extensively in the fundus of the stomach, leading to gastric atrophy.
->Chronic antral gastritis (type B, nonimmune): generally involves the antrum only and is more common than fundal gastritis. It is caused byH. pyloribacteria, and it also is associated with use of NSAIDs, alcohol, and smoking.
-Symptoms vague
->Anorexia, fullness, nausea, vomiting, epigastric pain
