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pH of Stomach
1.5-3.5, rises when food enters
Where Are Nutrients Absorbed in the Body
Small Intestines
churn and turns food into chyme
receives digestive enzymes from pancrease and liver
which part of body absorps water and electrolytes
large intestine
and produce/absorbs vitamins
Liver Function
- Produce bile, albumin, and cholesterol
- Metabolizes drugs
- Produces clotting factors
- Converts glucose to glycogen
- Converts ammonia to urea
- Metabolizes bilirubin in the breakdown of RBCs
Complications of TPN
Infection risk(change bag and tubing every 24 hrs), fluid overload, hyper or hypoglycemia *check BG every 4-6 hours)
GIVE CENTRAL LINE hard on veins (check for air embolisim)
what to do if you run put pf TPN
run D10w at the same rate to prevent hypoglycemia
Antidiarrheals
Loperamide, Diphenoxylate, Bismuth Subsalicylate
Famotidine Nursing Considerations
- Can be given with meals
- Monitor CBC and kidney function
- Separate from other drugs when possible
Omeprazole Nursing Considerations
- Administer 30-60 mins before meal
- Report black, tarry stools
Sucralfate Nursing Consideration
- Take on empty stomach
- Don't give within 30 mins of antacids
- Can decrease the bioavailability of warfarin, digoxin, phenytoin, levothyroxine, and several classes of antibiotics
If Residual on NG Tube is greater than 500, What Happens
Call the doctor and hold feeding
high risk for aspiration
when tp empty ostomy
when it is 1/3-1/2 full
change pouch ever 3-5 days
Blakemore Tube
Used to stop bleeding on esophageal varices
For Blakemore Tube, what is important to keep at bedside
Must keep a pair of scissors at bedside to deflate the gastric balloon
Esophageal Varices
Dilated submucosal veins in the esophagus
Causes of Esophageal Varices
Liver disease and alcoholism
GERD Risk Factors
Conditions that increase abdominal pressure: vomiting, coughing, lifting, bending, or obesity
Treatment for GERD
Sit upright after eating, small frequent meals, H2 blockers, PPIs
Barrett's Esophagus
A condition that occurs when the cells in the epithelial tissue of the esophagus are damaged by chronic acid exposure
Gastritis is associated with
Helicobacter pylori, NSAIDs
increase stress and alc can also cause this
Gastric Ulcer Symptoms
Pain 1-2 hours after meal, abdominal pain aggravated by eating, vomiting, weight loss, hematemesis if hemorrhage occurs
Treatment for Gastric Ulcer
Treat H. pylori infection(aBX), reduce acid with PPIs and H2 blockers
Duodenal Ulcer Symptoms
-Pain 2-4 hrs after meals
-Eating makes it feel better
-Melena if hemorrhage occurs
Weight gain
EXACT CAUSES AND TX OF GASTRIC ULCERS
H2 RECEPTOR BLOCKERS
drugs and nursing consideration
-tidine
FOMATIDINE CIMETIDINE NIZATIDINE
block acid production
monitor CBC and kidney function, can be given with meals, only take small doses for short period of time cuz abrupt disocntinouation can cause rebound, can affect drug metabolisim (not used with phenytoin and warfrim)
proton pump inhibitors
"-prazole"
(Omeprazole, Lansoprazole, Rabeprazole sodium, Esomeprazole)
give 30-60 minutes before meal
REPORT BLACK TARRY STOOL(can cause GI bleed)
antacid
drug that neutralizes stomach acid
Sucrafate
gi protectant
give on empthy stomach (1 hr before or 2 hours after)
avoid giving with antacid
monitor blood sugar (contains sucrose)
give separate from warfarin dig and phenytoin and antibiotics to avoid reduced bioavalibility
contains aluminum (can impair kidney function)
Crohn's Disease Location
Inflammation and erosion of the ileum and anywhere throughout the GI tract
Skip lesions
Ulcerative Colitis Risk Factors
Jewish descent 20-40 years
Ulcerative Colitis Location
Only in colon, continuous
large instestine
chrons/ uc assessment
rebound tewnderness
cramping
diarreah after eating
vomiting
dehydration
recal bleed
bloody tool
fever
chrons/ uc tx
high fiber food
avoid hot and cold food
aoid smooking
antidiarreah
antibiotics
steroids
surgery (ileostomy. colonsotmy)
stool of someone has colonostomy or ileostomy
colonostomy - formed stool (UC)
ileostomy - small instetine is affected so watery stool (chrons)
Diverticula
Herniation of mucosa through layers of the colon wall
Diverticulosis
Asymptomatic diverticular disease
Diverticulitis
Inflammatory stage of diverticulosis
Causes of Diverticulosis
Decreased fiber
Abnormal neuromuscular function
Alterations in intestinal mobility
Older than 60
Assessment of Diverticulitis
Rebound tenderness, cramping, diarrhea, vomiting, dehydration, weight loss, rectal bleeding, bloody stools, anemia, fever
Treatment of Diverticulosis
Low fiber diet, avoid cold or hot foods, no smoking, antidiarrheals, antibiotics, steroids, in severe cases may end up surgically removing the affected portion of the intestines
Intestinal Obstruction
Any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal mobility in the absence of an obstructive lesion
Small Intestinal Obstruction Clinical Manifestation
Colicky pain caused by intestinal distension, followed by nausea and vomiting
Large Intestine Obstruction
Hypogastric pain and abdominal distension
Appendicitis Pain
Begins as dull, steady periumbilical pain over 4-6 hours; pain progresses and localizes to right lower quadrant; sudden relief of pain is bad
McBurney's Point
Pain in right lower quadrant with appendicitis
Pre-op Appendicitis
No heat - this can aggravate inflamed appendix and cause rupture; position right side, low fowlers for comfort
Post-op Appendicitis Treatment
IV fluids, IV antibiotics, pain management, NPO until return of bowel sounds, wound care
Number One Cause of Pancreatitis
Alcoholism
What Is Pancreatitis
Digestive enzymes of the pancreas autodigest
Assessment of Pancreatitis
Pain that increases with eating, abdominal distension, ascites, abdominal mass, rigid abdomen, fever, jaundice, hypotension
Cullen's Sign
Ecchymosis in umbilical area, seen with pancreatitis
Grey Turner's Sign
Bruising in flank area (lower back area) in pancreatitis
Pancreatitis Nursing Interventions
PANCREAS: Pain control (morphine or dilaudid), antispasmodic drugs to reduce gut motility, NPO/NGT suction, TPN, calcium replacement due to hypocalcemia, replace fluids and electrolytes (fluid shift), elevated enzymes (check amylase and lipase), antibiotics with fever, steroids-corticosteroids for acute attacks
Cholelithiasis Caused By
Hardened deposits of bile in the gallbladder; Causes: Hyperlipidemia, hyperbilirubinemia
Cholelithiasis Assessment Findings
Sudden, sharp RUQ pain; Pain continues to get worse, can radiate to back and between the shoulder blade or right shoulder, gets worse at night or after a fatty meal, nausea, vomiting
Treatment for Cholelithiasis
Cholecystectomy
Cholecystitis
Inflammation of the gallbladder
Clinical Manifestations of Cholecystitis
Fever, leukocytosis, rebound tenderness, and abdominal muscle guarding
Treatment of Cholecystitis
Pain control, replacement of fluids and electrolytes, fasting, antibiotic administration
Hepatitis Can Progress To
Cirrhosis or hepatic encephalopathy
can notice this by elevation in ammonia because the liver is not able to convert it to urea
rx for hepatic encephalopathy
high protein diet
hypovolemia hypokalemia
infection
gi bleed
drugs
constipation
Hep A Transmission
Fecal oral
Prevention of Hep A
Vaccine, sanitation + hygiene
Treatment of Hep A
Supportive
Hepatitises with Risk of Chronic Infection
B, C, D
Hepatitis B Transmission
Contact with infected body fluids such as blood, semen, vaginal fluids
Prevention of Hep B
Vaccine, blood screening, improved hygiene
Treatment of Hep B
Acute - Supportive, Chronic - Antiviral therapy with/without interferon
Hep C Transmission
Contact with infected body fluids (IV drug use, non-sterilized medical equipment)
Hep C Prevention
Blood screening, sterile needles for injection
Hep C Treatment
No specific treatment available, usually self-limiting
Hep D Transmission
Contact with infected body fluids
Hep E Transmission
Oral-fecal
Hep E Prevention
Hygiene and sanitation
Hep E Treatment
Supportive
Hepatic Encephalopathy
Protein in diet is broken into ammonia. When there is damage in the liver due to hepatitis, the ammonia builds up instead of being converted to urea. These increased ammonia levels can cause a hepatic coma.
Assessment Findings of Hepatic Encephalopathy
Change in LOC, asterix (tremor in hand), fetor, sleep, mood, and speech problems
tx hepatic encephalopathy
lactulose (allows ammonia to be excetred)
antibiotics (rifazmin or neomycin)
decrease fluid retensiosn (k sparing dirtic)
avoid cns depressants
Treatment for Hepatic Coma
Neomycin or rifaximin (reduces bacterial production of ammonia), lactulose, potassium-sparing diuretic
Drugs to Avoid with Hepatic Coma
Benzodiazepines and opioids
Cirrhosis
Chronic disease of the liver marked by degeneration of cells, inflammation, and fibrous thickening
Cirrhosis Assessment
Palpable firm liver, ascites, edema, abdominal pain, bloating, dyspepsia, poor appetite, spider angioma, jaundice, decreased albumin, increased liver enzymes
Liver Damage Leads to What Risk
Bleeding risk because the liver produces clotting factors
Treatment of Cirrhosis
Antacids, vitamins, diuretics, paracentesis, skin care, strict I and Os, daily weights, bleeding precautions
Diet for Cirrhosis
Low protein, low sodium
Drug Doses to Be Careful with for Liver Failure
Narcotics and acetaminophen
hepatic Steatosis
accumulation of fat in the liver cells
Ascites
accumulation of fluid in the peritoneal cavity
Hepatorenal Syndrome
progressive kidney failure in individuals with severe liver disease
Hepatopulmonary Syndrome
presence of pulmonary vascular dilatations in individuals with liver disease
Hepatocellular Carcinoma
primary malignancy of the liver