Sunday, July 26, 2009
Sunday, May 10, 2009
Monday, April 27, 2009
LIVER AND PORTAL HYPERTENSION
Liver and Portal Hypertension
Afroz Lakhani, RN,BScN
Pathophysiology 2009
Liver
The liver is the largest organ in the body, normally weighing about 1 to 2.3kg (although this can increase to over 10kg in chronic cirrhosis). The liver is the main organ of metabolism and energy production; its other main functions include:
Bile production
Storage of iron, vitamins and trace elements
Detoxification
Conversion of waste products for excretion by the kidneys
Functions of Liver
Carbohydrate metabolism: Maintains plasma glucose levels. Post-meal when glucose levels rise, glucose with the influence of insulin is converted to glycogen for storage.
When glucose levels falls, the hormone glucagon stimulates glycogen into glucose again. That’s how our glucose levels stays in normal range.
Fat metabolism: Excess dietary carbs or protein will store as fat. (under the skin, around kidneys)
Digested fat convert triglycerides for energy and storage.
Protein metabolism:
Deamination of amino acids: a)Nitrogenous portion is removed to form into urea, excreted into urine.
b) nucleic acids breaks down to uric acidsurine.
Transamination: removal of nitrogenous portion of amino acids and attaches to carb moleculenon-essential amino acids.
Synthesis of plasma proteins and most blood clotting factors from amino acids.
Portal Circulation
The liver is unusual has a double blood supply; the right and left hepatic arteries carry oxygenated blood to the liver, and the portal vein carries venous blood from the GI tract to the liver.
Portal vein enters the liver, the blood drains into the hepatic sinusoids, where it is screened by specialized macrophages (Kupffer cells) to remove any pathogens that manage to get past the GI defenses. The plasma is filtered through the endothelial lining of the sinusoids and bathes the hepatocytes; these cells contain vast numbers of enzymes capable of breaking down and metabolizing most of what has been absorbed.
The portal venous blood contains allof the products of digestion absorbed from the GI tract, so all useful and non-useful products are processed in the liver before being either released back into the hepatic veins which join the inferior vena cava just inferior to the diaphragm, or stored in the liver for later use.
Liver Cirrhosis
Scarring of the Liver
Cx: alcoholism, viral hepatitis, toxic reaction to drugs, biliary obstruction
S/S: wt loss, anorexia, weakness, hepatomegaly, jaundice, abdominal pain (stretching of Glisson’s cap)
Pathophysiology Liver Cirrhosis
Portal Hypertension
Obstructed blood flow through the damaged liver results in increased blood pressure (portal hypertension) throughout the portal venous system.
Pressure normally 3mm Hg;
portal HTN at least 10 mmHg
Cx: thrombosis, inflammation, fibrosis of sinusoids, viral hepatitis, cardiac disorders, most common is cirrhosis of liver.
Long term PHTN can lead to Ascites, Varices, Splenomegaly, Hepatic encephalopathy.
Ascites
Pathophysiology
PHTN and decreased serum albumin capillary hydrostatic pressure to exceed capillary osmotic pressure and causes fluid into peritoneal cavity.
The failure of the liver to metabolize aldosterone increases sodium and water retention by the kidney.
Loss of fluid into the peritoneal space causes further sodium and water retention by the kidney in an effort to maintain the vascular fluid volume.
Treatment
No salt diet
Diuretics: Spironolactone (Aldactone), an aldosterone blocking agent.
Ammonium chloride and acetazolamide are contraindicated because of the possibility of precipitating hepatic coma.
Bed rest
Paracentesis
Insertion of a peritoneovenous shunt to redirect ascitic fluid from the peritoneal cavity into the systemic circulation.
Caput medusae is the appearance of distended and engorged paraumbilical veins which are seen radiating from the umbilicus across the abdomen to join systemic veins
Esophageal Varices
Are extremely dilated sub-mucosal veins in the esophagus.
Bleeding or hemorrhage from esophageal varices occurs in approximately one third of patients with cirrhosis and varices.
The mortality rate resulting from the first bleeding episode is 45% to 50%;
It is one of the major causes of death in patients with cirrhosis
Pathophysiology EV
Increased obstruction of the portal vein causes venous blood from the intestinal tract and spleen seeks an outlet through collateral circulation (new pathways of return to the right atrium).
The effect is increased pressure, particularly in the vessels in the of the lower esophagus and upper part of the stomach.
These collateral vessels are not very elastic but rather are tortuous and fragile and bleed easily.
Treatment:
Prevent hemorrhage
Straight to ICU
potential hypovolemia
Oxygen
Intravenous fluids with electrolyte
Blood transfusion
Strict I/O
vasopressin, vasopressin with nitroglycerin, somatostatin, balloon tamponade, TPSS (transhepatic portosystemic shunt), transhepatic catheter embolization, shunt surgery, gastric stapling and sclerotherapy
Splenomegaly
an enlargement of the spleen.
Caused by increased pressure in the splenic vein, which branches from the portal vein.
Hepatic Encephalopathy
CNS totality
Lack of mental alertness, confusion, coma, convulsions.
Flapping tremor called asterixis (liver flap)
Memory loss
Pathophysiology HEn
Ammonium ion produced in the intestinal tract, abundance in colon by bacterial degradation of luminal proteins and amino acids.
Normally: Ammonium ion diffuse into portal blood, transported to the liver, where they converted to urea.
When the blood from intestines bypass the liver, ammonia is not converted to urea, and ammonia moves directly into general circulation then to cerebral circulation thus hepatic encephalopathy occurs.
Treatment
No big protein diet
Prevent GI bleeding
No narcotics or tranquilizers
Nonabsorbable antibiotic like neomycin (to eradicate bacteria from the colon)
Lactulose (acts in Large intestine, low ph)
References:
Carpenito, J.L. (2002). Nursing diagnosis: Application to clinical practice (9th edition) Philadelphia: Lippincott.
Huether & McCane. (2000). Understanding Pathophysiology (2nd edition) Mosby
Illustrated manual of Nursing Practice (2002). 3rd edition. Springhouse
Kozier & Erb. (2008). Fundamentals of Nursing (8th edition) New Jersy: Pearson.
Porth.(2005). Pathophysiology (7th edition) Lippincott
Ross and Wilson. (2006). Anatomy and physiology (10th edition) Churchill Livingstone
Afroz Lakhani, RN,BScN
Pathophysiology 2009
Liver
The liver is the largest organ in the body, normally weighing about 1 to 2.3kg (although this can increase to over 10kg in chronic cirrhosis). The liver is the main organ of metabolism and energy production; its other main functions include:
Bile production
Storage of iron, vitamins and trace elements
Detoxification
Conversion of waste products for excretion by the kidneys
Functions of Liver
Carbohydrate metabolism: Maintains plasma glucose levels. Post-meal when glucose levels rise, glucose with the influence of insulin is converted to glycogen for storage.
When glucose levels falls, the hormone glucagon stimulates glycogen into glucose again. That’s how our glucose levels stays in normal range.
Fat metabolism: Excess dietary carbs or protein will store as fat. (under the skin, around kidneys)
Digested fat convert triglycerides for energy and storage.
Protein metabolism:
Deamination of amino acids: a)Nitrogenous portion is removed to form into urea, excreted into urine.
b) nucleic acids breaks down to uric acidsurine.
Transamination: removal of nitrogenous portion of amino acids and attaches to carb moleculenon-essential amino acids.
Synthesis of plasma proteins and most blood clotting factors from amino acids.
Portal Circulation
The liver is unusual has a double blood supply; the right and left hepatic arteries carry oxygenated blood to the liver, and the portal vein carries venous blood from the GI tract to the liver.
Portal vein enters the liver, the blood drains into the hepatic sinusoids, where it is screened by specialized macrophages (Kupffer cells) to remove any pathogens that manage to get past the GI defenses. The plasma is filtered through the endothelial lining of the sinusoids and bathes the hepatocytes; these cells contain vast numbers of enzymes capable of breaking down and metabolizing most of what has been absorbed.
The portal venous blood contains allof the products of digestion absorbed from the GI tract, so all useful and non-useful products are processed in the liver before being either released back into the hepatic veins which join the inferior vena cava just inferior to the diaphragm, or stored in the liver for later use.
Liver Cirrhosis
Scarring of the Liver
Cx: alcoholism, viral hepatitis, toxic reaction to drugs, biliary obstruction
S/S: wt loss, anorexia, weakness, hepatomegaly, jaundice, abdominal pain (stretching of Glisson’s cap)
Pathophysiology Liver Cirrhosis
Portal Hypertension
Obstructed blood flow through the damaged liver results in increased blood pressure (portal hypertension) throughout the portal venous system.
Pressure normally 3mm Hg;
portal HTN at least 10 mmHg
Cx: thrombosis, inflammation, fibrosis of sinusoids, viral hepatitis, cardiac disorders, most common is cirrhosis of liver.
Long term PHTN can lead to Ascites, Varices, Splenomegaly, Hepatic encephalopathy.
Ascites
Pathophysiology
PHTN and decreased serum albumin capillary hydrostatic pressure to exceed capillary osmotic pressure and causes fluid into peritoneal cavity.
The failure of the liver to metabolize aldosterone increases sodium and water retention by the kidney.
Loss of fluid into the peritoneal space causes further sodium and water retention by the kidney in an effort to maintain the vascular fluid volume.
Treatment
No salt diet
Diuretics: Spironolactone (Aldactone), an aldosterone blocking agent.
Ammonium chloride and acetazolamide are contraindicated because of the possibility of precipitating hepatic coma.
Bed rest
Paracentesis
Insertion of a peritoneovenous shunt to redirect ascitic fluid from the peritoneal cavity into the systemic circulation.
Caput medusae is the appearance of distended and engorged paraumbilical veins which are seen radiating from the umbilicus across the abdomen to join systemic veins
Esophageal Varices
Are extremely dilated sub-mucosal veins in the esophagus.
Bleeding or hemorrhage from esophageal varices occurs in approximately one third of patients with cirrhosis and varices.
The mortality rate resulting from the first bleeding episode is 45% to 50%;
It is one of the major causes of death in patients with cirrhosis
Pathophysiology EV
Increased obstruction of the portal vein causes venous blood from the intestinal tract and spleen seeks an outlet through collateral circulation (new pathways of return to the right atrium).
The effect is increased pressure, particularly in the vessels in the of the lower esophagus and upper part of the stomach.
These collateral vessels are not very elastic but rather are tortuous and fragile and bleed easily.
Treatment:
Prevent hemorrhage
Straight to ICU
potential hypovolemia
Oxygen
Intravenous fluids with electrolyte
Blood transfusion
Strict I/O
vasopressin, vasopressin with nitroglycerin, somatostatin, balloon tamponade, TPSS (transhepatic portosystemic shunt), transhepatic catheter embolization, shunt surgery, gastric stapling and sclerotherapy
Splenomegaly
an enlargement of the spleen.
Caused by increased pressure in the splenic vein, which branches from the portal vein.
Hepatic Encephalopathy
CNS totality
Lack of mental alertness, confusion, coma, convulsions.
Flapping tremor called asterixis (liver flap)
Memory loss
Pathophysiology HEn
Ammonium ion produced in the intestinal tract, abundance in colon by bacterial degradation of luminal proteins and amino acids.
Normally: Ammonium ion diffuse into portal blood, transported to the liver, where they converted to urea.
When the blood from intestines bypass the liver, ammonia is not converted to urea, and ammonia moves directly into general circulation then to cerebral circulation thus hepatic encephalopathy occurs.
Treatment
No big protein diet
Prevent GI bleeding
No narcotics or tranquilizers
Nonabsorbable antibiotic like neomycin (to eradicate bacteria from the colon)
Lactulose (acts in Large intestine, low ph)
References:
Carpenito, J.L. (2002). Nursing diagnosis: Application to clinical practice (9th edition) Philadelphia: Lippincott.
Huether & McCane. (2000). Understanding Pathophysiology (2nd edition) Mosby
Illustrated manual of Nursing Practice (2002). 3rd edition. Springhouse
Kozier & Erb. (2008). Fundamentals of Nursing (8th edition) New Jersy: Pearson.
Porth.(2005). Pathophysiology (7th edition) Lippincott
Ross and Wilson. (2006). Anatomy and physiology (10th edition) Churchill Livingstone
Tuesday, February 10, 2009
Management of conditions affecting GI and accessory organs of digestion
Afroz Lakhani, RN,BScN
Quick Review of GI A&P
"alimentary canal"
all organs through which food passes (mouth to anus)
Accessory Structures
1. assist in digestion
2. includes teeth, salivary glands, liver, gall bladder, pancreas
Layers of GI Tract
Esophagus
Passage about 10 inches long, lined with a mucous membrane.
Function is to complete the act of swallowing.
The involuntary movement of material down the esophagus is carried out by the process known as peristalsis, which is the wavelike action produced by contraction of the muscular wall. This is the method by which food is moved throughout the alimentary canal.
Stomach
• four major secretory cells:
• chief cells: pepsinogen activation by low pH to form pepsin , is a protease for protein digestion
• parietal cells : HCl secretion enhanced by histamine via H2 receptors
Tagamet blocks H2 histamine receptors to inhibit HCl secretion
intrinsic factor binds to and allows B12 absorption in intestines
• G-cell : secretes gastrin hormone
activates gastric juice secretion & gastric smooth muscle “churning” , activates gastroileal reflex which moves chyme from ileum to colon
• mucus cell :protective role of mucus against acids and digestive enzymes
• pyloric sphincter regulates entry into the duodenum
• chyme is liquified digested material
Small Intestine
• 22 ft long
• divided into three continuous parts: duodenum, jejunum, and ileum.
• Most of the absorption of food takes place in the small intestine, villi
• receives digestive juices from three accessory organs of digestion: the pancreas, liver, and gallbladder
Large intestine
• 5 ft long
• Cecum, appendix , ascending, transverse, descending colon , sigmoid colon, rectum
• The main function is the recovery of water and electrolytes from the mass of undigested food it receives from the small intestine. As this mass passes through the colon, water is absorbed and returned to the tissues. Waste materials, or feces, become more solid as they are pushed along by peristaltic movements.
• Constipation is caused by delay in movement of intestinal contents and removal of too much water from them.
• Diarrhea results when movement of the intestinal contents is so rapid that not enough water is removed
Diagnostic Procedures
• Upper GI studies (barium swallow)
Examination of the upper GI tract under fluoroscopy after patient drinks barium sulfate.
Pre : NPO midnight
Post: Instruct for increased oral fluids to help pass the barium.
Monitor stools for passage of barium. Stools should appear chalky white in color.
Lower GI tract study (barium enema)
Fluoroscopic and radiographic examination of large intestine after rectal instillation of barium sulfate
Pre: low residue diet 1 or 2 days prior,
clear liquid and laxative evening before,
NPO midnight, cleansing enema morning of test.
Post: Increase oral fluids to pass barium, mild laxative, monitor stools, report absence of bowel movement more than 2 days.
Gastric analysis:
Aspirate gastric contents thru NG tube for the analysis of acidity, appearance, volume.
4 Upper GI fiberoscopy: ( EGD)
5 Anoscopy, proctoscopy, and sigmoidoscopy:
6 Fiberoptic colonoscopy:
7 Cholecystography: to detect gall stones, and assess ability to fill, concentrate , contract and empty.
Pre: no allergies to iodine or seafood, NPO, anaphylactic shock symptoms.
Post: dysuria is common cause contrast agent excreted in urine, fatty meal to pass contrast agent.
8 Paracentesis: Transabdominal removal of fluid from the peritoneal cavity.
Pre: Consent, void prior procedure, measure ab girth, wt, upright or fowler’s position.
Post: v/s, dry sterile dressing and monitor bleeding, ab girth, look for hematuria, hypovolemia.
9 Liver biopsy:
Pre:consent, must ck prothombin time, partial thromboplastin time, platelet.
Post: site bleeding, peritonitis, bedrest, place patient on the rt side with a pillow under the coastal margin to decrease the risk of hemorrhage, avoid coughing, straining, no heavy weights for one week.
Assessment
Dietary History:
The number of meals ate per day.
Meal times.
Food restrictions or special diets followed.
Changes in appetite. Increased? Decreased? No appetite?
What foods, if any, have been eliminated from the diet? Why? What foods are not well tolerated?
Alterations in taste.
Medications used. Dosage and frequency.
Assessment contd…
Bowel pattern history: Frequency of bowel movements. Use of laxatives and/or enemas. Changes in bowel habits. Stool Description (color, consistency, any blood)
any complaints??
Nausea. Frequency? Duration? Associated with meals? Relieved by?
Vomiting. Frequency? Character of emesis? Relieved by?
Heartburn/indigestion. Frequency? Duration? Associated with specific foods? Relieved by?
Gas (belching and flatus). Frequency? Associated with specific foods? Relieved by?
Pain. Location? Frequency? Duration? Character of the pain?
Weight loss. How much? In what time period?
Assessment
Inspect skin for color, abnormalities, contour, abdomen for distention.
Auscultate bowel sounds, normal 5-30/min or every 5-15 secs in all quadrants.
Listen at least 5 minutes in each quadrant to be certain for any absence.
Stool test
Stool samples can be examined on the ward and in the laboratory to determine the presence of substances that aid in diagnosis. For example:
color, consistency, and amount of stool. The presence of unseen blood (occult)
In the laboratory, tests can be performed to determine the presence of fat, urobilinogen, ova, parasites, bacteria, and other substances.
Small, dry, hard stools may indicate constipation or fecal impaction.
Diarrhea may indicate fecal impaction or fecal mass, or it may be the result of a disease process (such as colitis or diverticulitis) or a bacterial infection (such as dysentery)..
Black, tarry stools may be the result of upper GI bleeding, iron supplements, or diet selection (eating black licorice, for example).
Reddish colored stools may be the result of bleeding in the lower GI tract or diet selection (eating carrots or beets).
Gastroesophageal Reflux (GER)
Back flow of gastric and duodenal contents into the esophagus.
Cx: incompetent lower esophageal sphincter, pyloric stenosis or motility disorder. May mimic heart attack.
Pathophysiology Gastritis
In gastritis, the gastric mucous membrane becomes edematous
and hyperemic (congested with fluid and blood) and undergoes
superficial erosion . It secretes a scanty amount of gastric juice, containing very little acid but much mucus. Superficial ulceration may occur and can lead to hemorrhage.
Gastritis
Stomach or gastric mucosa inflammation.
Acute: Contaminated food, irritating (spicy), over use of aspirin, excess alcohol
Abdominal discomfort, headache, anorexia, n/v, hicupping
Chronic: benign or malignant ulcers or H pylori, medications, caused by autoimmune diseases, smoking or reflux.
Anorexia, heartburn, belching, vit B12 def, sour taste
PUD
An ulceration in the mucosal wall of the stomach, pylorus, duodenum or esophagus.
Gastric and duodenal are common
Predisposing factors: Stress, smoking, use of steroids, NSAIDs, alcohol, gastritis, family hx, infection with H-pylori.
Complication: hemorrhage, perforation, pyloric obstruction.
Assessment: Gnawing, sharp pain LT of midepigastric 1 0r 2 hrs after eating.
Implementation: v/s, signs of bleeding, Meds
Pathophysiology Irritable Bowel Syndrome IBS results from a functional disorder of intestinal motility.
The change in motility may be related to the neurologic regulatory system, infection or irritation, or a vascular or metabolic disturbance.
The peristaltic waves are affected at specific segments of the intestine and in the intensity with which they propel the fecal matter forward. There is no evidence of inflammation or tissue changes in the intestinal mucosa.
IBS contd…
S/S:
constipation, diarrhea, or a combination of both. Pain, bloating, and abdominal distention often accompany
The abdominal pain is sometimes precipitated by eating and is frequently relieved by defecation.
Mngt: aimed at relieving abdominal pain, controlling the diarrhea or constipation, and reducing stress.
Restriction and then gradual reintroduction of foods that are possibly
irritating may help determine what types of food are acting as irritants
(eg, beans, caffeinated products, fried foods, alcohol, spicy
foods).
A healthy, high-fiber diet to help control the diarrhea and constipation.
Exercise to reducing anxiety and increasing intestinal motility.
APPENDICITIS Pathophysiology
The appendix becomes inflamed and edematous as a result of either becoming kinked or occluded by a fecalith (ie, hardened mass of stool), tumor, or foreign body.
The inflammatory process increases intraluminal pressure, initiating a progressively severe, generalized or upper abdominal pain that becomes localized in the right lower quadrant of the abdomen within a few hours.
Eventually, the inflamed appendix fills with pus.
Appendectomy (ie, surgical removal of the appendix) is performed as soon as possible to decrease the risk of perforation.
Nursing Management:
Goals : relieving pain, preventing fluid volume deficit, reducing anxiety, eliminating infection , disruption of the GI tract, maintaining skin integrity, and attaining optimal nutrition.
The nurse prepares the patient for surgery, which includes an
intravenous infusion to replace fluid loss and antibiotic therapy to prevent infection.
An enema is not administered because it can lead to perforation.
After surgery, the nurse places the patient in a semi-Fowler
position. This position reduces the tension on the incision and abdominal organs, helping to reduce pain.
An opioid, morphine sulfate, is prescribed to relieve pain.
When tolerated oral fluids are administered.
Any patient who was dehydrated before surgery receives intravenous fluids.
Food is provided as desired and tolerated on the day of surgery.
COLOSTOMY:
A colostomy is a surgically created, artificial opening (stoma) into the colon through the abdomen. It may be temporary or permanent.
A temporary colostomy is normally made for diversion of fecal material. Fecal diversion is utilized in order to rest a portion of the colon following intestinal surgery, in preparation for further surgery, or in cases of severe inflammatory disease (such as diverticulitis).
A permanent colostomy serves as an artificial anus for the remainder of the patient's life. This procedure is done in conjunction with the removal of the lower bowel and rectum. Although there is no sphincter muscle control at the stoma, bowel movements may be controlled by a daily routine that encompasses diet, physical activity, and colostomy irrigation. Consistency of the bowel movements generally depends upon the location of the colostomy, but can be manipulated by the patient's choice of diet.
Colostomy Irrigation
Irrigation should be done at the same time each day in order to establish regularity of bowel evacuation. Unless contraindicated or otherwise ordered by the physician, it is best to establish a routine of daily irrigation in accordance with the patient's former bowel habits. For example, if the patient has always moved his bowels after breakfast, establish the irrigation routine for that time, rather than some other arbitrary schedule.
Ileostomy:
An ileostomy is a surgically created, artificial opening (stoma) into the small bowel (ileus) through the abdomen. The stoma is located low on the abdomen (lower quadrants.) Most ileostomies are performed because of inflammatory bowel disease.
An ileostomy may be temporary or permanent. If temporary, the bowel is left intact. In a permanent ileostomy, the colon is removed.
Unlike a colostomy, an ileostomy cannot be regulated. The fecal contents of the ileum are fluid, and drain continuously. For this reason, an ileostomy patient must always wear an appliance.
Dietary considerations (ileostomy)
Most physicians do not recommend dietary restrictions once the patient has recovered from surgery and is released from the hospital. However, foods that cause discomfort, gas, or diarrhea should be omitted.
Hard to digest foods should be avoided if they cause discomfort. Examples are celery, popcorn, berries, and high-fiber foods.
Odor-causing foods include cabbage, onions, fish, and eggs. These foods should be tested individually to determine if they can be tolerated.
Spinach, parsley, yogurt, and buttermilk act as deodorizers on the intestinal tract.
All foods ingested will normally pass through the ileostomy within 4-6 hours.
Afroz Lakhani, RN,BScN
Quick Review of GI A&P
"alimentary canal"
all organs through which food passes (mouth to anus)
Accessory Structures
1. assist in digestion
2. includes teeth, salivary glands, liver, gall bladder, pancreas
Layers of GI Tract
Esophagus
Passage about 10 inches long, lined with a mucous membrane.
Function is to complete the act of swallowing.
The involuntary movement of material down the esophagus is carried out by the process known as peristalsis, which is the wavelike action produced by contraction of the muscular wall. This is the method by which food is moved throughout the alimentary canal.
Stomach
• four major secretory cells:
• chief cells: pepsinogen activation by low pH to form pepsin , is a protease for protein digestion
• parietal cells : HCl secretion enhanced by histamine via H2 receptors
Tagamet blocks H2 histamine receptors to inhibit HCl secretion
intrinsic factor binds to and allows B12 absorption in intestines
• G-cell : secretes gastrin hormone
activates gastric juice secretion & gastric smooth muscle “churning” , activates gastroileal reflex which moves chyme from ileum to colon
• mucus cell :protective role of mucus against acids and digestive enzymes
• pyloric sphincter regulates entry into the duodenum
• chyme is liquified digested material
Small Intestine
• 22 ft long
• divided into three continuous parts: duodenum, jejunum, and ileum.
• Most of the absorption of food takes place in the small intestine, villi
• receives digestive juices from three accessory organs of digestion: the pancreas, liver, and gallbladder
Large intestine
• 5 ft long
• Cecum, appendix , ascending, transverse, descending colon , sigmoid colon, rectum
• The main function is the recovery of water and electrolytes from the mass of undigested food it receives from the small intestine. As this mass passes through the colon, water is absorbed and returned to the tissues. Waste materials, or feces, become more solid as they are pushed along by peristaltic movements.
• Constipation is caused by delay in movement of intestinal contents and removal of too much water from them.
• Diarrhea results when movement of the intestinal contents is so rapid that not enough water is removed
Diagnostic Procedures
• Upper GI studies (barium swallow)
Examination of the upper GI tract under fluoroscopy after patient drinks barium sulfate.
Pre : NPO midnight
Post: Instruct for increased oral fluids to help pass the barium.
Monitor stools for passage of barium. Stools should appear chalky white in color.
Lower GI tract study (barium enema)
Fluoroscopic and radiographic examination of large intestine after rectal instillation of barium sulfate
Pre: low residue diet 1 or 2 days prior,
clear liquid and laxative evening before,
NPO midnight, cleansing enema morning of test.
Post: Increase oral fluids to pass barium, mild laxative, monitor stools, report absence of bowel movement more than 2 days.
Gastric analysis:
Aspirate gastric contents thru NG tube for the analysis of acidity, appearance, volume.
4 Upper GI fiberoscopy: ( EGD)
5 Anoscopy, proctoscopy, and sigmoidoscopy:
6 Fiberoptic colonoscopy:
7 Cholecystography: to detect gall stones, and assess ability to fill, concentrate , contract and empty.
Pre: no allergies to iodine or seafood, NPO, anaphylactic shock symptoms.
Post: dysuria is common cause contrast agent excreted in urine, fatty meal to pass contrast agent.
8 Paracentesis: Transabdominal removal of fluid from the peritoneal cavity.
Pre: Consent, void prior procedure, measure ab girth, wt, upright or fowler’s position.
Post: v/s, dry sterile dressing and monitor bleeding, ab girth, look for hematuria, hypovolemia.
9 Liver biopsy:
Pre:consent, must ck prothombin time, partial thromboplastin time, platelet.
Post: site bleeding, peritonitis, bedrest, place patient on the rt side with a pillow under the coastal margin to decrease the risk of hemorrhage, avoid coughing, straining, no heavy weights for one week.
Assessment
Dietary History:
The number of meals ate per day.
Meal times.
Food restrictions or special diets followed.
Changes in appetite. Increased? Decreased? No appetite?
What foods, if any, have been eliminated from the diet? Why? What foods are not well tolerated?
Alterations in taste.
Medications used. Dosage and frequency.
Assessment contd…
Bowel pattern history: Frequency of bowel movements. Use of laxatives and/or enemas. Changes in bowel habits. Stool Description (color, consistency, any blood)
any complaints??
Nausea. Frequency? Duration? Associated with meals? Relieved by?
Vomiting. Frequency? Character of emesis? Relieved by?
Heartburn/indigestion. Frequency? Duration? Associated with specific foods? Relieved by?
Gas (belching and flatus). Frequency? Associated with specific foods? Relieved by?
Pain. Location? Frequency? Duration? Character of the pain?
Weight loss. How much? In what time period?
Assessment
Inspect skin for color, abnormalities, contour, abdomen for distention.
Auscultate bowel sounds, normal 5-30/min or every 5-15 secs in all quadrants.
Listen at least 5 minutes in each quadrant to be certain for any absence.
Stool test
Stool samples can be examined on the ward and in the laboratory to determine the presence of substances that aid in diagnosis. For example:
color, consistency, and amount of stool. The presence of unseen blood (occult)
In the laboratory, tests can be performed to determine the presence of fat, urobilinogen, ova, parasites, bacteria, and other substances.
Small, dry, hard stools may indicate constipation or fecal impaction.
Diarrhea may indicate fecal impaction or fecal mass, or it may be the result of a disease process (such as colitis or diverticulitis) or a bacterial infection (such as dysentery)..
Black, tarry stools may be the result of upper GI bleeding, iron supplements, or diet selection (eating black licorice, for example).
Reddish colored stools may be the result of bleeding in the lower GI tract or diet selection (eating carrots or beets).
Gastroesophageal Reflux (GER)
Back flow of gastric and duodenal contents into the esophagus.
Cx: incompetent lower esophageal sphincter, pyloric stenosis or motility disorder. May mimic heart attack.
Pathophysiology Gastritis
In gastritis, the gastric mucous membrane becomes edematous
and hyperemic (congested with fluid and blood) and undergoes
superficial erosion . It secretes a scanty amount of gastric juice, containing very little acid but much mucus. Superficial ulceration may occur and can lead to hemorrhage.
Gastritis
Stomach or gastric mucosa inflammation.
Acute: Contaminated food, irritating (spicy), over use of aspirin, excess alcohol
Abdominal discomfort, headache, anorexia, n/v, hicupping
Chronic: benign or malignant ulcers or H pylori, medications, caused by autoimmune diseases, smoking or reflux.
Anorexia, heartburn, belching, vit B12 def, sour taste
PUD
An ulceration in the mucosal wall of the stomach, pylorus, duodenum or esophagus.
Gastric and duodenal are common
Predisposing factors: Stress, smoking, use of steroids, NSAIDs, alcohol, gastritis, family hx, infection with H-pylori.
Complication: hemorrhage, perforation, pyloric obstruction.
Assessment: Gnawing, sharp pain LT of midepigastric 1 0r 2 hrs after eating.
Implementation: v/s, signs of bleeding, Meds
Pathophysiology Irritable Bowel Syndrome IBS results from a functional disorder of intestinal motility.
The change in motility may be related to the neurologic regulatory system, infection or irritation, or a vascular or metabolic disturbance.
The peristaltic waves are affected at specific segments of the intestine and in the intensity with which they propel the fecal matter forward. There is no evidence of inflammation or tissue changes in the intestinal mucosa.
IBS contd…
S/S:
constipation, diarrhea, or a combination of both. Pain, bloating, and abdominal distention often accompany
The abdominal pain is sometimes precipitated by eating and is frequently relieved by defecation.
Mngt: aimed at relieving abdominal pain, controlling the diarrhea or constipation, and reducing stress.
Restriction and then gradual reintroduction of foods that are possibly
irritating may help determine what types of food are acting as irritants
(eg, beans, caffeinated products, fried foods, alcohol, spicy
foods).
A healthy, high-fiber diet to help control the diarrhea and constipation.
Exercise to reducing anxiety and increasing intestinal motility.
APPENDICITIS Pathophysiology
The appendix becomes inflamed and edematous as a result of either becoming kinked or occluded by a fecalith (ie, hardened mass of stool), tumor, or foreign body.
The inflammatory process increases intraluminal pressure, initiating a progressively severe, generalized or upper abdominal pain that becomes localized in the right lower quadrant of the abdomen within a few hours.
Eventually, the inflamed appendix fills with pus.
Appendectomy (ie, surgical removal of the appendix) is performed as soon as possible to decrease the risk of perforation.
Nursing Management:
Goals : relieving pain, preventing fluid volume deficit, reducing anxiety, eliminating infection , disruption of the GI tract, maintaining skin integrity, and attaining optimal nutrition.
The nurse prepares the patient for surgery, which includes an
intravenous infusion to replace fluid loss and antibiotic therapy to prevent infection.
An enema is not administered because it can lead to perforation.
After surgery, the nurse places the patient in a semi-Fowler
position. This position reduces the tension on the incision and abdominal organs, helping to reduce pain.
An opioid, morphine sulfate, is prescribed to relieve pain.
When tolerated oral fluids are administered.
Any patient who was dehydrated before surgery receives intravenous fluids.
Food is provided as desired and tolerated on the day of surgery.
COLOSTOMY:
A colostomy is a surgically created, artificial opening (stoma) into the colon through the abdomen. It may be temporary or permanent.
A temporary colostomy is normally made for diversion of fecal material. Fecal diversion is utilized in order to rest a portion of the colon following intestinal surgery, in preparation for further surgery, or in cases of severe inflammatory disease (such as diverticulitis).
A permanent colostomy serves as an artificial anus for the remainder of the patient's life. This procedure is done in conjunction with the removal of the lower bowel and rectum. Although there is no sphincter muscle control at the stoma, bowel movements may be controlled by a daily routine that encompasses diet, physical activity, and colostomy irrigation. Consistency of the bowel movements generally depends upon the location of the colostomy, but can be manipulated by the patient's choice of diet.
Colostomy Irrigation
Irrigation should be done at the same time each day in order to establish regularity of bowel evacuation. Unless contraindicated or otherwise ordered by the physician, it is best to establish a routine of daily irrigation in accordance with the patient's former bowel habits. For example, if the patient has always moved his bowels after breakfast, establish the irrigation routine for that time, rather than some other arbitrary schedule.
Ileostomy:
An ileostomy is a surgically created, artificial opening (stoma) into the small bowel (ileus) through the abdomen. The stoma is located low on the abdomen (lower quadrants.) Most ileostomies are performed because of inflammatory bowel disease.
An ileostomy may be temporary or permanent. If temporary, the bowel is left intact. In a permanent ileostomy, the colon is removed.
Unlike a colostomy, an ileostomy cannot be regulated. The fecal contents of the ileum are fluid, and drain continuously. For this reason, an ileostomy patient must always wear an appliance.
Dietary considerations (ileostomy)
Most physicians do not recommend dietary restrictions once the patient has recovered from surgery and is released from the hospital. However, foods that cause discomfort, gas, or diarrhea should be omitted.
Hard to digest foods should be avoided if they cause discomfort. Examples are celery, popcorn, berries, and high-fiber foods.
Odor-causing foods include cabbage, onions, fish, and eggs. These foods should be tested individually to determine if they can be tolerated.
Spinach, parsley, yogurt, and buttermilk act as deodorizers on the intestinal tract.
All foods ingested will normally pass through the ileostomy within 4-6 hours.
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