GI Flashcards
Pancreatitis signs and symptoms
- Pain increases with eating
- Abdominal distention/ascites (losing protein rich fluids like enzymes and blood into the abdomen) → ascites
- Abdominal mass-swollen pancreas
- Rigid board-like abdomen (guarding or bleeding) > peritonitis
- Bruising around umbilical area Culling sign; flank area Gray Turner’s sign.
- Fever (inflammation)
- N/V
- Jaundice
- Hypotension = bleeding or ascites
Patho pancreatitis
- Pathophysiology:
a. The pancreas has two separate functions:
1) Endocrine-insulin
2) Exocrine-digestive enzymes
b. Two types of pancreatitis:
1) Acute: #1 cause = alcohol
#2 cause = gallbladder disease
2) Chronic: #1 cause = alcohol
Pancreatitis diagnosis and labs
Normal Lab Values Amylase: 45-200 U/L (dye) Lipase: 0-110 U/L AST=8-40 U/L ALT= 10-30 U/L Hemoglobin: Male: 14-18 g/dl Female: 12-16 g/dl Hematocrit: Male: 40-54% Female: 38-47% a. Serum lipase and amylase increase b. WBCs increase c. Blood sugar increases d. ALT, AST-liver enzymes increases e. PT, PTT longer f. Serum bilirubin increased g. H/H (Hemoglobin & Hematocrit) up or down • down if bleeding, up if dehydrated
Pancreatitis treatment
***Pancreas client = Keep stomach empty and dry.
a. Goal: Control pain
1) Decrease gastric secretions (NPO, NGT to suction, bed rest) • Want the stomach empty and dry
2) Pain Medications:
• PCA narcotics morphine sulfate(Morphine®), hydromorphone
(Dilaudid®)
• Fentanyl patches(Duragesic®)
3) steroids to decrease inflammation
4) Anticholinergics, dry up
• Benztropine (Cogentin®), Diphenoxylate/Atropine (Lonox®)
5) Pantoprazole (Protonix®) (proton pump inhibitor)
6) Ranitidine HCI (Zantac®), Famotidine (Pepcid®) (H2 receptor antagonist)
7) Antacids
8) Maintain fluid and electrolyte balance
9) Maintain nutritional status → ease into a diet
10) Insulin WHY?
• pancrease not producing enough
• steroids increase sugar
• TPN
11) Daily weights
12) Eliminate alcohol
13) Refer to AA if this is the cause
Cirrhosis patho
TESTING STRATEGY
If your liver is sick your #1 concern = Bleeding.
Never give Tylenol to liver people.
- Liver detoxifies the body.
- Helps your blood to clot
- The liver helps to metabolize (break down) medications
- The liver synthesizes/makes albumin
- Pathophysiology:
• Liver cells are destroyed and are replaced with connective/scar tissue→ alters the circulation within the liver→ the BP in the liver goes up, this is called portal HTN
Cirrhosis S/S
a. Firm, nodular liver
b. Abdominal pain – liver capsule has stretched c. Chronic dyspepsia(GI upset)
d. Change in bowel habits
e. Ascites
f. Splenomegaly
g. Decreased serum albumin (unexplained swelling, check albumin)
h. Increaded ALT & AST
I. Anemia from bleeding
j. Can progress to hepatic encephalopathy/coma build up of ammonia (also caused by rye syndrome and Tylenol overdose)
TESTING STRATEGY
When spleen is enlarged the immune system is involved.
Cirrhosis dx
a. Ultrasound
b. CT, MRI
c. Liver biopsy
• Clotting studies pre- PT and PTT
• Vital signs pre-procedure
• position supine, r arm behind head
• Exhale and hold breath for few seconds
Why? To get the diaphragm out of the way.
• Post: Lie on R side
Vital signs, worried about hemorrhage
Cirrhosis treatment
a. Antacids, vitamins, diuretics
b. No more alcohol (don’t need more damage)
c. I&O and daily weights
d. Rest
e. Prevent bleeding(bleeding precautions)
f. Measure abdominal girth for ascites
g. Paracentesis:
• Removal of fluid from the peritoneal cavity (ascites)
• Have client void
• Position sitting up so that fluid settles
• Vital signs for shock
h. Monitor jaundice – good skin care
i. Avoid narcotics- liver can’t metabolize drugs well when it’s sick
j. Diet:
• Decrease protein
• Low Na diet
TESTING STRATEGY
Anytime you are pulling fluids→ worry about throwing them into shock.
If you give liver client narcotics it’s the same thing as double dosing them.
Let’s Get Normal Straight First!
Protein→ Breaks down to ammonia→ The Liver converts ammonia to urea→ Kidneys excrete the urea
Hepatic coma
Patho
a. When you eat protein, it transforms into ammonia, and the liver converts it to urea. Urea can be excreted through the kidneys without difficulty.
b. When the liver becomes impaired then it can’t make this conversion, so what chemical builds up in the blood? Ammonia
c. What does this chemical do to the LOC? Decreases
Hepatic coma
S/S
A. Minor mental changes/motor problems
b. Difficult to awaken
c. Asterixis hand tremors, handwriting changes d. Reflexes will decrease
e. EEG slow
f What is Fetor? Breath smells like ammonia.
g. Anything that increases the ammonia level will aggravate the problem.
h. Liver people tend to be GI bleeders.
Hepatic coma treatment
a. Lactulose (Lactulax®, Duphalac®) (decreases serum ammonia)
b. Cleansing enemas-get fat out of GI tract
c. Decrease protein in the diet
d. Monitor serum ammonia daily
Bleeding Esophageal varices
- Pathophysiology:
a. High BP in the liver (portal HTN) forces collateral circulation to form.
• This circulation forms in 3 different places→ stomach, esophagus, rectum
b. When you see an alcoholic client that is GI bleeding it is usually esophageal
varices.
• Usually no problem until it ruptures - Tx:
a. Replace blood
b. VS
c. CVP
d. Oxygen (any time someone is anemic, Oxygen is needed)
e. Octreotide(Sandostatin®)lowers BP in the liver.
f. Sengstaken- Blakemore Tube
• What is the purpose? To hold pressure on bleeding varice
g. Cleansing enema to get rid of blood
h. Lactulose (Neo-Fradin®) (decreases ammonia)
i. Saline lavage to get blood out of stomach
EVL: Esophageal Variceal Ligation
Also an option. In this procedure a rubber- band like Ligature is slipped over the varices via an endoscope, necrosis results and the varices eventually slough off.
Peptic ulcers
pathophysiology and signs and symptoms
- Pathophysiology:
a. Common cause of GI bleeding
b. Can be in the esophagus, stomach, duodenum
c. Mainly in males
d. Erosion is present - S/S:
a. Burning pain usually on the mid-epigastric area/back
b. Heartburn (dyspepsia)
Peptic ulcers diagnosis
a. Gastroscopy (EGD, endoscopy):
1) NPO preop
2) Sedated
3) NPO until gag reflex returns
4) Watch for perforation by watching for pain,bleeding, or trouble swallowing.
Upper GI:
1) Looks at the esophagus and stomach with dye
2) NPO past midnight
3) No smoking, chewing gum, or mints. Remove the nicotine patch, too.
• Smoking increases stomach motility which will affect the test.
• Smoking increases stomach secretions.
Peptic ulcers treatment
Tx:
a. Medications:
1) Antacids: Liquids (to coat stomach) • Take when stomach is empty and at bedtime – when stomach is empty
acid can get on ulcer… take antacid to protect ulcer.
2) Proton Pump Inhibitors: (decrease acid secretions)
• Omeprazole (Prilosec®), Lansoprazole (Prevacid®), Pantoprazole (Protonix®), Esomeprazole (Nexium®)
3) H2 antagonist: Ranitidine (Zantac®), Famotidine (Pepcid®)
• GI Cocktail (donnatal, viscous lidocaine, Mylanta II®)
• Antibiotics for H. Pylori: Clarithromycin (Biaxin®), Amoxicillin (Amoxil®), Tetracycline (Panmycin®), Metronidazole (Flagyl®)
• Sucralfate (Carafate®): forms a barrier over the wound so acid can’t get on the ulcer.
b. Client Teaching:
• Decrease stress
• Stop smoking
• Eat what you can tolerate; avoid temperature extremes and extra spicy foods; avoid caffeine (irritant).
• Need to be followed for one year
