Unit 3 - Chapter 42 Alterations of digestive fx Flashcards
Common clinical manifestations of many GI d/o
- Anorexia (loss of appetite)
- vomting
- constipation
- diarrhea
- abdominal pain
- GI bleed
Vomiting
- forceful emptyig of stomach effected by GI contraction and reverse peristalsis of esophagus
- PRECEDED by nausea and retching with the exception for projectile vomiting (associated with direct stimulation of vomiting center in the brain)
Primary constipation
Three categories
1) functional - associated w/ low residue, low fluid diet
2) slow transit - related to impaired colonic motor fx
3) pelvic floor dyssynergia-anismus (pelvic floor dysfunction that makes it hard to poop l/t chronic constipation (located near bottom of bowel and bladder // behind pubic bone)
Secondary constipation
- neurogenic disease (These typically result from brain injuries due to stroke, trauma, brain tumors, or progressive neurological diseases (for example, Parkinson disease, Alzheimer’s dementia, ALS, or primary progressive aphasia)
- drugs that decrease intestinal motility (lomotil or diphenoxylate + atropine, treats diarrhea)
- endocrine or metabolic disroders
- or obstruction
Diarrhea
- d/t excessive fluid drawn into intestinal lumen by osmosis (osmotic diarrhea)
- excessive secretions of fluids by intestinal mucosa (secretory diarrhea)
- excessive GI motility (motility diarrhea)
Abdominal pain
- caused by strecthing, inflammation, or ischemia
- can originate in peritoneum (parietal pain - lining the cavity of abdomen) or organ themselves (visceral pain or in the viseceral peritoneum)
- visceral pain is often referred to the “back”
GI bleeding
- upper or lower tract
manifestations
* hematemesis (vomiting of blood)
* melena (dark, tarry stools)
* hematochezia (frank bleeding from the rectum)
* Occult bleeding (GI bleeding not visible to patient or physician) – can only be detected by testing stools or vomitus for presence of blood
Dysphagia
- difficulty swallowing
- or perception of obstruction during swallowing
- can be d/t mechanical or functional obstruction of the esophagus
- functional obstruction means… an impairment of esophageal motility
Achalasia
- form of functional dyshpagia d/t loss of esophageal (t-10 to t-10) innervation or relaxation of lower esophageal sphincter
Gastroesophageal reflux
- regurgitation of chyme from stomach into esophagus causing esophagitis from repeated exposure to acids, enzymes, or bile salts in the regurgitated gastric contents
Hiatal hernia
- protrusion of upper part of stomach thorugh hiatus (esophageal opening in diaphragm) at the gastroesophageal junction
1) sliding (gastroesophageal junction (GEJ), which is defined as the point where the distal esophagus joins the proximal stomach, is pushed out towards hiatus or diaphragm
2) paraesophageal (only part of stomach pushes out of diaphragm or muscle wall)
3) mixed – GEJ and part of stomach go out diaphragm)
gastroparesis
delayed gastric emptying in absence of mechanical gastric outlet obstruction
pyloric obstruction
- narrowing or blockage of pylorus (opening between stomach and duodenum)
- d/t cogenital defect, inflammation, scarring 2ndary to gastric ulcer or tumor growth
intestinal obstuction
- occur in small or large intestine and prevents normal mvmt of chyme through intestinal tract
- USUALLY mechanical; caused by torsion, herniation (weakened abdominal wall), or tumor
- functional reason ===> paralytic ileus (condition in which the muscles of the intestines do not allow food to pass through, resulting in a blocked intestine. Paralytic ileus may be caused by surgery, inflammation, and certain drugs.)
Consequences of intestinal obstruction?
- fluid and electrolyte loss, hypovolemia, shock, intestinal necrosis, perforation of intestinal wall
Gastritis
- acute or chronic inflammation of gastric mucosa
causes:
1. regurgitation of bile (Bile reflux occurs when bile — a digestive liquid produced in your liver — backs up (refluxes) into your stomach and, in some cases, into the tube that connects your mouth and stomach (esophagus). Bile reflux may accompany the reflux of stomach acid (gastric acid) into your esophagus.)
2. use of antiinflammatory drugs or alcohol
3. h. pylori infection (H. pylori bacteria are usually passed from person to person through direct contact with saliva, vomit or stool. H. pylori may also be spread through contaminated food or water. The exact way H. pylori bacteria causes gastritis or a peptic ulcer in some people is still unknown.)
4. systemic diseases
Chronic fundal gastritis
- top portion of stomach (uppermost)
- rare, associated with autoantibodies to parietal cells (cell of stomach wall that secrete gastric acid) and intrinsic factor
- l/t gastric atrophy and pernicious aenemia (diminishment in dietary vitamin B12 (cobalamin) absorption, resulting in B12 deficiency and subsequent megaloblastic anemia. It affects people of all ages worldwide, particularly those over 60)
Chronic antral gastritis
- most common gastritis
- d/t h pylori and NSAIDs (NSAIDs work by stopping the production of prostaglandins (which promote inflammation, pain, and fever), they do this do this by blocking cyclooxygenases (COX) enzymes. These enzymes produce prostaglandins, yet they also protect your stomach and intestinal lining. This is why NSAIDs can damage your gut.)
==== prostagladins found in gastric mucosa and gastric juice ==
alkaline reflux gastritis
- stomach inflammation d/t reflux of bile and pancreatic secretions from the duodenum into the stomach;
- these substances disrupt mucosal barrier and cause inflammation
peptic ulcer
three types of ulcers: duodenal, gastric, and stress
1) duodenal (most common peptic ulcer) associated with inc numbers of parietal cells (acid secreting) in stomach, elevated gastrin (hormone that stimulates secretion of gastric juice and is secreted into bloodstream by the stomach wall in response to presence of food), and rapid gastric emptying (Rapid gastric emptying is a condition in which food moves too quickly from your stomach to your duodenum)
* pain occurs when stomach is empty
* relieved with food and antacids
* these tend to heal spontaneously and recur frequently
2) gastric ulcers (develop near parietal cells, usually antrum before “pylorus” where it opens up to duodenum) + tend to be chronic
* gastric secretions tend to be normal or decreased while pain may occur after eating
3) stress ulcer – acute form of peptic ulcer associated with severe illness or extensive trauma
* ischemic stress ulcer comes from severe illness, systemic trauma, neural injury, burns (curling ulcer)
* ulceration (break on surface of organ) => mucosal damage d/t ishcemia (decreaed blood flow to gastric mucosa)
* cushing ulcer – stress ulcer caused by head trauma ==> ulceration follows hypersecretion of hydrochloric acid (in stomach juice) d/t overstimulation of vagal nuclei
These ulcers are most commonly seen as a complication of a severe burn. This can limit blood flow to your stomach and cause the mucous lining of the stomach to wear away. Curling’s ulcers can also appear in other parts of your gastrointestinal (GI) tract near your stomach, such as the duodenum.
Zollinger-ellison syndrome
- associated w/
1) gastrinoma (neuroendocrine tumors characterized by the secretion of gastrin with resultant excessive gastric acid production causing severe peptic ulcer disease and diarrhea, a combination referred to as the Zollinger-Ellison syndrome)
2) chronic secretion of gastric acid
3) gastric and duodenal ulcers
Postgastrectomy syndromes
- group of s/s that happen after gastric resection
- usually for tx of peptic ulcer, gastric carcinoma, bariatric surgery for obesity
- characterized by:
1) lowered tolerance for large meals
2) rapid emptying of food into small intestine or dumping
3) abdominal cramping
4) lightheadness after eating + increased HR + sharp drops in blood sugar levels
Dumping syndrome
- malabsorption by rapid emptying of hypertonic chyme from surgical residual stomach into small intestine
- CAUSING osmostic shift of fluid from vascular compartment to intestinal lumen, which causes decrease in PLASMA volume
Malabsorption syndrome
- impaired digestion or absorption of nutrients
1) Pancreatic insufficiency - can cause poor absorption d/t lower amounts of enzymes that digest protein, carbohydrates, and fats into components that can be absorbed by intestine
2) Deficient lactase production —- brush border of small intestine (microvilli) inhibits breakdown of lactose l/t stopped lactose absorption and causing osmotic diarrhea
3) Bile salt deficiency — l/t poor fat absorption (such as fat solube vitamins) and causing steatorrhea (fatty stools).
* can be d/t decreased seceretion of bile, excessive bacterial deconjugation of bile (manipulate bile production as signaling?), or impaired reabsorption of bile salts d/t ileal disease (last part of small intestine)
Ulcerative colitis
- inflammatory bowel disease
- causes ulceration, abscess formation
- necrosis of colonic and rectal mucosa
s/s
* cramping pain
* bleeding
* frequent diarrhea
* dehydration
* weight loss
- course of frequent remissions and exacerbations is common
Ulcerative colitis begins in the rectum and may extend proximally in a contiguous fashion without intervening patches of normal bowel.
- Symptoms are intermittent episodes of abdominal cramping and bloody diarrhea.
- Complications include fulminant colitis, which may lead to perforation; long-term, the risk of colon cancer is increased.
- Treat mild to moderate disease with 5-ASA by rectum and, for proximal disease, by mouth.
- Treat extensive disease with high-dose corticosteroids, immunomodulator therapy (eg, azathioprine, 6-mercaptopurine), biologics (eg, infliximab, vedolizumab), tofacitinib, or ozanimod.
- Treat fulminant disease with high-dose IV corticosteroids or cyclosporine and antibiotics (eg, metronidazole, ciprofloxacin) or infliximab; colectomy may be required. [Toxic colitis or fulminant colitis occurs when transmural extension of ulceration results in localized ileus and peritonitis. Within hours to days, the colon loses muscular tone and begins to dilate ——— Toxic colitis is a medical emergency that usually occurs spontaneously in the course of very severe colitis but is sometimes precipitated by opioid or anticholinergic antidiarrheal drugs. Colonic perforation may occur, which increases mortality significantly.]
About one third of patients with extensive ulcerative colitis ultimately require surgery.
Crohn disease
- similar to ulcerative colitis but affects entire GI tract, including small + large intestine (Ulcerative colitis is usually only in the innermost lining of the large intestine (colon) and rectum)
- ulceration tends to involve all layers of lumen
- skip lesion fissues (unhealthy then healthy – along intestinal tract) + granulomas (tiny cluster of white blood cells and other tissue that can be found in the lungs, head, skin or other parts of the body in some people) are characteristic of this disease
- abdominal tenderness, nonbloody diarrhea, weight loss
Crohn disease typically affects the ileum and/or colon but spares the rectum (which is invariably affected in ulcerative colitis).
- Intermittent areas of diseased bowel are sharply demarcated from adjacent normal bowel (called skip areas).
- Symptoms primarily involve episodic diarrhea and abdominal pain; gastrointestinal bleeding is rare.
- Complications include abdominal abscesses and enterocutaneous fistulas.
- Treat mild to moderate disease with 5-aminosalicylic acid (mesalamine) and/or antibiotics (eg, metronidazole, ciprofloxacin, rifaximin).
- Treat severe disease with corticosteroids and sometimes immunomodulators (eg, azathioprine) or biologics (eg, infliximab, vedolizumab, ustekinumab).
About 70% of patients ultimately require an operation, typically for recurrent intestinal obstruction, intractable fistulas, or abscesses.
