GiI Disorders Flashcards
What are risk factors for GI disorders
PREVIOUS ABDOMINAL SURGERY OR TRAUMA
Family History
Chronic Laxative Use/alcohol/tobacco use
Long term GI conditions (ulcerative colitis can predispose one to colorectal cancer)
Barium Swallow (upper GI)
examines upper GI under fluoroscopy performed after the client drinks barium sulfate
Abstain from foods and fluids prior to test
Post Procedure- laxative; 6-8 glasses of water a day for 2 days; monitor for passage of chalky white stool
**don’t want barium to stay in you; if it does it will get hard and stiffen and body can’t expel it
Barium enema (lower GI)
fluoroscopic and radiographic exam of the lg intestine
pre procedure - laxatives to get everything out of systems and a liquid diet 1 day in advance
post procedure - increased fluid intake for 2 days; mild laxatives to get rid of barium
Gastroscopy
insertion of a scope through the esophagus and into the stomach and upper portion of small intestine - looks at the lining to see if any bleeding, mass, tumors etc.
**must have gag reflex return before they can start eating agian
Sigmoidoscopy
endoscopic visualization of the sigmoid colon (go in through the butt)
Colonoscopy
GOLD STANDARD
up through the rectum - examine the lining of the Large intestine
Want to make sure that it’s cleaned out (laxatives)
Best procedure because if they see a poll up they can remove them
Gall bladder Studies
HIDA Scan
Ultrasound
CT scan
Cholangiography
HIDA scan
radioactive material is injected into vein and taken up by the gallbladder (want to see if ti’s taken up to know how well it’s functioning)
Cholangiography
percutaneous or endosopic
scope goes down through the esophagus and into the gall bladder rather than the stomach - shoot dye into it to show the bile ducts and can shoot dye into the pancreas to see pancreas and liver function
Liver Biopsy
a needle is inserted through the abdominal wall to the liver to obtain a tissue sample for microscopic examination
**make sure that the b4 the procedure is done that the person is able to clot; want to know this bc the liver produces coagulation factors
Can place client on right side for 1-2 hours to decrease risk of hemorrhage and to put pressure to stop the liver from bleeding
Paracentesis
transabdominal removal of fluid from the peritoneal cavity
to examine electrolytes, RBCs, WBCs, bacteria and viruses
** Want to measure abdominal girth to make sure you didn’t puncture anything when you went in (look for hematuria)
Dry sterile dressing
Stool Specimens
examining stool for the presence of occult blood; take the tongue depressor and smash stool on 2 card; flip it over and put stool on other card (2 sep specimens); sent to the lab where they put hydrogen peroxide on it
Liver and Pancreas Tests include
Alkaline Phosphatase Prothrombin Time (PT) Serum Ammonia Liver Enzymes (AST and ALT) Cholesterol Bilirubin
Alkaline Phosphatase
released during liver damage or biliary obstruction (damage = increased value)
Prothrombin Time
time it takes body to clot; if liver damage = decreased PT
Serum Ammonia
Assesses the ability of the liver to dominate protein by products; if Liver failure = ammonium levels rise
Liver Enzymes
Aspartate Aminotransferase (AST) Alanine Aminotransferase (ALT)
these are the 2 most common enzymes and they are important for liver function tests
Cholesterol tests
tell us whats going on with the pancreas - increase can indicate pancreatitis or biliary obstruction
Bilirubin
Increase indicates liver damage or biliary obstruction Biliary Direct (conjugated) Biliary Indirect (unconjugated) ** 2 different stages in making bile
Amylase and Lipase
Elevations indicated pancreatitis
*** We will draw these two enzymes
What are some s/sx of common GI disorders
Anorexia and Nausea
Vomiting (protective function)
Hematemesis (blood vomit
Hematochezia (passage of red blood in stool)
Melena (black tarry fatty stool)
Occult - must be detected by chemical testing and usually caused by gastritis, ulcer, or lesions on the small intestine
Hematemesis
vomiting up blood
may be red = person probably bleeding from stomach/esophagus
may be coffee color = old blood from below
Esophageal Diverticulum and it’s s/sx
out pouching of the esophageal wall leading to the retention of food
s/sx gurgling, belching, coughing, foul smelling breath
Mallory-Weiss Syndrome
Longitudinal tears in the esophagus
Associated with chronic alcoholism or severe vomiting
Infection may lead to an ulcer or mediastinitis (inflammation of the tissues of the mid chest)
What is GERD (Gastroesophageal Reflux)
Backward movement of gastric contents into the esophagus resulting in heartburn possibly d/t weak/incompetant lower esophageal sphincter
***THE SEVERITY OF THE HEARTBURN IS NOT INDICATIVE OF THE EXTENT OF THE MUCOSAL INJURY
Pain can radiate to throat, shoulder, or back and can also produce respiratory problems (wheezing, cough, hoarseness)
What can Chronic GERD result in
strictures (from scarring = spasm, and edema) OR
Barrett’s esophagus (squamous epithelial cells replaced by columnar and high risk for esophageal cancer)
How do you treat GERD
Avoid large meals Decrease alcohol use and NO smoking Sit up while eating and don't resume the recumbent position until several hours after meals Sleep with head elevated If overweight - lose some weight
What are the 2 major causes of Gastric Irritation and Ulcer Formation
Aspirin or NSAIDS (irritate mucosal lining in stomach)
H. pylori infection (loves acid environments in the stomach)
What are the types of Gastritis and what do they do
Acute = TRANSIENT inflammation of the gastric mucosa
bacterial endotoxins, alcohol, and ASA) ex. too much alcohol or ate something that was bad
Chronic = CHANGES in inflammation that is characterized by the absence of grossly visible erosions; leads to atrophy of the glandular epithelium of the stomach (ex. H. pylori, chemical gastropathy) **This is lower level damage
What are 2 other names for Acute and Chronic Gastritis
Acute = EROSIVE CHRONIC = INVASIVE
How do you detect H. pylori infection
Measure the Carbon in the breath (C urea breath test)
Stool antigen test
Endoscopic biopsy for urease testing
Blood tests to obtain serologic titers of H. pylori antibodies
What is Peptic Ulcer Disease
ulceration of the stomach, pylorus, or duodenum (portions must be accessible to gastric secretions)
Erosion may extend through the muscle to the peritoneum
Most common peptic are GASTRIC and DUODENAL
Gastric ulcers
ulceration of the mucosal lining that extends to the submucosal layer of the stomach
**PAIN starts right after you eat d/t digestive enzymes irrigating the area
Predisposing factors of gastric ulcers
use of steroids, NSAIDS, alcohol and hx of gastritis or H. pylori infection
How do you assess gastric ulcers
gnawing, sharp pain in left midepigastric region 1-2 hours after eating
Nausea and vomiting
Hematemesis
Duodenal Ulcers
break in the mucosa of the duodenum (same as gastric except in the duodenum)
What are predisposing factors of duodenal ulcers
steroids, NSAIDS, alcohol, caffiene, stress, H. pylori
How do you assess duodenal ulcers?
Burning pain in the midepigastric area 2-4 hours after eating and during the night
Melena
**PAIN IS OFTEN RELIEVED BY EATING - d/t acids and digestive enzymes working on the food rather than your ulcer
Complications of Peptic Ulcers?
Hemorrhage
Obstruction - d/t edema, spasm, or contraction of scar tissue that interferes with passage of gastric contents through the pylorus
Perforation - ulcer erodes through all the layers of the stomach/duodenum
Risk factors for Stress Ulcers
Trauma Burns Sepsis Liver failure Major surgical procedures
**Body physiologically stressed from all of these and can develop an ulcer.
Zollinger-Ellison Syndrome
body is making too much acid typically d/t gastrin secreting tumor (in pancreas or submucosa of stomach)
2/3 are malignant
Assessment = diarrhea, impaired fat digestion, elevated serum gastrin, decreased intestinal pH
**typically in ppl with lots of gastric ulcers
Gastric Cancer Assessment
abnormal, malignant growth of stomach
anorexia weight loss palpabe mass ascites anemia/fatigue
Risk Factors for Gastric Cancer
Genetics/hx of Gastric Ulcers Carcinogenic factors in the diet (very charred foods) High starch and salty diet Smoking and alcohol Gastric adenomas or polyps
Vit B12 deficiency
inadequate intake of bit B12 or lack of absorption of ingested B12 (no intrinsic factor to absorb it)
What is a result of Vit B12 deficiency
Pernicious anemia (bc no intrinsic factor for intestinal absorption of B12) ** can lead to neurological issues
Vit B12 Assessment
severe pallor
fatigue
SMOOTH BEEFY RED TONGUE
paresthesias of the hands and feet
Dumping Syndrome
rapid emptying of the gastric contents into the small intestine
Assessment of Dumping Syndrome
**symptoms occur 30 min after eating nausea and vomiting abdominal cramping tachycardia perspiration weakness and dizziness diarrhea
Irritable Bowel Syndrome (IBS)
FUNCTIONAL disorder (more common in women than men)
persistent symptoms of abdominal pain
altered bowel function with complaints of flatulence/bloatedness
Constipation and/or diarrhea
possibly d/t anxiety, depression or stress
What are the 2 types Irritable Bowel Disease (IBD)
Crohn's (affects any part of the GI tract) Ulcerative colitis (only affects the colon)
Crohn’s Disease (aka Regional Enteritis)
can affect any area from the mouth to the anus (typically adolescents or people who smoke)
*often occurs in the terminal ileum and it LEADS TO thickening and scarring
narrowed lumen
fistulas
ulcerations
abscessess
Assessment of Crohn’s disease
Fever cramplike pain after meals (recurrent) abdominal distention electrolyte imbalances weight loss
Ulcerative Colitis
confined to the colon and is STRUCTURAL
inflammatory disease that results in poor absorption of nutrients
Begins in rectum and spreads upward to cecum
Edemouys colic may develop bleeding lesions = scarring/scar tissue = loss of elasticity and can’t absorb nutrients
***remissions and exacerbations
Assessment of Ulcerative Colitis
VITAMIN K DEFICIENCY (bleeding ulcers and now can't clot so bleed more) Bloody diarrhea abdominal tenderness and cramping electrolyte imbalances weight loss
***COULD RESULT IN COLON CANCER
What are the 2 most common bacterial infections in the intestine?
Protozoal?
Clostridium Difficile Colitis (D-diff)
E.coli
E. histolytica (contaminated H2O)
Diverticulosis
Outpounches/herniations of the intestinal mucosa (mainly sigmoid colon)
Diverticulitis
when one of the out pouching areas becomes inflamed/painful
possibly d/t lowe fiber/genetic weakness
Assessment of diverticulitis
Left lower quadrant abdominal pain (pain increases with coughing, straining or lifting) Elevated teamp nausea/vomiting abdominal distention and tenderness palpable tender RECTAL mass
Hemorrhoids
dilated varicose veins in the anal canal
can be internal, external, or prolapsed (internal and then spill out)
caused by portly HTN, straining, irritation, and increased venous/abdominal pressure
Appendicitis
inflammation of the appendix - becomes inflamed and can rupture = spilling everything into the peritoneum
Peritonitis
SERIOUS surgical emergency
inflammation of the peritoneum (sterile area)
abdominal distention and pain (very firm “surgical” abdomen)
pallor and right guarding of abdomen
Causes of Peritonitis
Ruptured appendix
Perforated peptic ulcer or diverticulum
Abdominal trauma/sounds
Types of diarrhea
Large Volume - H2O pulled into GI tract very fast d/t infection/lactose deficiency (osmotic) or organism secreting toxins (secretory
Small Volume = Inflammatory bowel disease, infections, irritable colon **peristaltic activity is faster
Four causes of diarrhea
Increased secretion of electrolytes and water in bowel lumen
Increased osmotic load within intestine = water retention in bowel of lumen
Inflammation
Altered intestinal motility = rapid transit times
Increased Secretion diarrhea
WATERY STOOL:
cholera toxin
clostridium
carcinoid syndrome
Increased osmotic load
BULKY GREASY STOOL:
SORBITOL INGESTION (sugar free candy)
Lactose deficiency
Dumping syndrome
Inflammation diarrhea
BLOODY STOOL W OR W/O LEUKOCYTES
Ulcerative colitis
Crohn’s disease
Invasive microbial gastroenteritis
Altered intestinal motility diarrhea
Thyrotoxicosis
IBS
Neurologic disease (DM)
Common causes of Constipation
Failure to respond to the urge to defecate
Low fiber in diet
Not taking in enough fluids
Inactivity/Bedrest
Mechanical Bowel Obstruction
Volvulus - twisting
Adhesions - sticking of tubes together
Intussusception - part of intestines slides into adjacent parts of the intestines
Incarcerated inguinal hernia - area of intestines slides through a weaker area and causes an obstruction
Intestinal Obstruction
Can develop ischemia d/t blockage and O2 can’t even get through
Abdominal distention
Loss of fluids and electrolytes (hypokalemia)
Can lead to strangulation, gangrenous changes, and perforation of the bowel
Increased pressure = necrosis
Assessment of Intestinal Obstruction
ABSOLUTE CONSTIPATION - nothing is getting through
Pain
Abdominal distention
visible peristalsis
Celiac Disease
Immune disorder triggered by ingestion of grains (wheat, barley, rye)
Inappropriate response of T cells (go wild and attack)
Can impair absorption bc you can lose the absorptive villi to the point where you can’t absorb anymore
The small intestine thickens so nutrients can’t get across (malabsoprtion)
Celiac in babies
Failure to thrive
Diarrhea
Abdominal distention
Symptoms of Malabsorption
Steatorrhea
Weight Loss and Abdominal Distension
Diarrhea/Constipation
Bloating/Cramps/Abdominal Pain
Intestinal Tumors
s/sx usually all over the place
malignant lesions in bowel wall or polyps in colon/rectum
Metastasis occurs via lymphatics
Colorectal Cancer
2nd in cancer mortalitiy
Prevention = screening early
Incidence rises after age 40 and significally increases after age 55
Etiology of Colorectal Cancer
mainly from pre-existing benign adenomatous polyps that undergo malignant transformation (hence why they are removed in colonoscopy)
Confined to the mucosa, but may progress to the submucosa and adjacent tissue
Invasive = spreads to lymph nodes
Adenomas
neoplastic lesions of glandular epithelium that display abnormal cellular differentiation and vary in size and shape (tubular, tubulovillous, villous)
Risk Factors of Colorectal Cancer
Hx of adenomatous polyps IBD (ulcerative > risk) Family hx of colon cancer High fat diet or Low fiber or both ***Use of ASA may lower incidence
Advanced Sx of Colorectal Cancer
GI bleeding (occult or anemia) Change in bowel habits = NARROW CALIBER STOOL Anorexia/Weight loss Mass may be found on external palpation or Digital Rectal Exam
Screening for Colorectal Cancer
Stool Occult Blood Tests
Xray with barium
DRE
colonoscopy
