Gastrointestinal Flashcards
Pancreatitis: Pathophysiology
Auto digestion of the pancreas. Pancreas has two seperate functions - Endocrine (Insulin) and Exocrine (Digestive Enzymes). There is acute and chronic pancreatitis - mostly caused by alcoholism.
There are a lot of enzymes in the pancreas! They are usually inactive in a healthy person. In the case of an alcoholic, it creates alot of scar tissue/gallstone that occludes and stops enzymes from escaping. Then they begin to digest the pancreas.
Pancreatitis: Signs and Symptoms/Diagnosis
Different degrees of severity.
Pain increases with eating
Abdominal distention/ascites because they are losing protein rich fluids like blood and enzymes into the abdomen
Abdominal mass - Swollen pancreas
RIGID BOARD LIKE ABDOMEN with guarding or bleeding- there is damage to the blood vessels because of the enzymes. Bleeding can lead to peritonitis.
Bruising around umbilical area (Cullen’s Sign) and flank area ( Grey Turners sign)
Fever ( inflammation)
N/V
Jaundice
Hypotension = because of bleeding or Ascites
Diagnosis Serum Lipase is REALLY UP WBC UP Blood Sugar UP ( Damages insulin) ALT, AST UP (Jaundice) PT, aPtt is longer ( Risk for bleeding and CLOTS) Bilirubin UP Hb/Hct Down or UP ( Can be down because of bleeding) and UP because of Not enough volume/dehydration/concentrated blood
Pancreatitis Treatment
Goal: Control Pain
Decrease Gastric Secretions ( NPO, NGT to suction, bed rest) - You want the stomach empty and dry
PCA narcotics, morphine, dilaudid and fentanyl
Steroids: Will decreases inflammation - but can cause diabetes or Cushings in the long term
Anti-cholinergics ( Dry up the stomach)
Benztropine, Atropine
GI protectants:
Panto, Rantidine, Antacids
Maintain Fluid and electrolyte imbalances
Maintain nutritional status (Ease into diet)
INSULIN: Because there is no insulin production, there is uncontrolled blood glucose due to steroids, TPN is packed with glucose
Daily Weights
Eliminate alcohol
Refer to AA
4 Major Functions of the Liver
Detoxifying the body
Helps your blood to clot
Uncontrolled Blood Glucose due to steroids
TPN is packed with Glucose
Cirrhosis: Pathophysiology/ Signs & Symptoms
Liver cells are destroyed and are replaced with scar tissue which alters the circulation of the liver. This causes the BP in the liver to go up, causing portal hypertension.
Firm, Nodular Liver Abdominal pain - Capsule has stretched Chronic dyspepsia ( GI upset) Change in bowel Habits Ascites Splenomegaly ( When the spleen is enlarged, the immune system is invovled) Decreased Serum Albumin Increased ALT and AST Anemia ( Risk for bleeding) Can progress to hepatic encephalopathy/ coma (Build up of Ammonia causes toxicity/sedation and coma)
Cirrhosis: Diagnosis & Treatment
Ultrasound, CT, MRI
Liver Biopsy - potential for hemorrhage
Clotting studies and vitals completed pre-procedure
Client is positioned at the edge of the bed, arm extended above head
Exhale and hold breath to get the diaphragm out of the way
Post procedure, Lie on right side with a towel roll over the puncture site. Worry about low BP and increased pulse.
Treatment
Antacids, vitamins, diuretics
No more alcohol
I&O and Daily weight
Rest
PREVENT BLEEDING (BLEEDing PRECAUTIONS)
Measure abd. girth –> Changes in girth indicate fluid loss
Monitor for jaundice - good skin care
Avoid NARCOTICS - the liver cannot metabolize drugs well when it is sick
Diet - Decrease protein (because protein increases ammonia, thus decreasing LOC) and low sodium for the ascites
Paracentesis
Removal of fluid from the peritoneal cavity ( ascites).
Have the client void - an empty bladder means less chance of puncturing
Sit client up to facilitate drainage
Vital signs
ANY TIME YOU PULL FLuiDS you can throw someone into shock
Protein breakdown
Protein breaks down into AMMONIA and the LIVER converts AMMONiA into UREA which is excreted by the kidneys
Hepatic Coma: Patho/Signs & Symptoms/Treatment
When you eat protein, it breaks down into ammonia and the liver converts it to Urea. Urea can be excreted through the kidneys without difficulty. When the liver becomes impaired, it can’t make this conversion.
Urea then builds up in the blood and LOC decreases
Minor Mental changes/motor problems Diffucult to rouse Asterixis - Tremor of the hand Handwriting changes Reflexes will decrease EEG slow FETOR - stinky ammonia breath Anything that will increase the ammonia level will aggravate the problem Liver people tend to be GI bleeders
Treatment Lactulose (decreases serum ammonia) Cleansing enemas (get blood out of the GI. Blood breaks down into ammonia) Decreased Protein in diet Monitor serum ammonia
Bleeding Esophageal Varices Patho/Treatment
Patho : High Blood pressure in the liver forces new circulation to form, such as in the stomach, esophagus and rectum. When you see an alcoholic client that is GI bleeding, it is usually esophageal varices. There isn’t a problem until it ruptures. Pt will be coughing up red blood. Could also have delirium tremens from being alcoholic.
Treatment
Replace blood/fluid
VS
CVP
Oxygen ( anytime some one is HYPOXIC, oxygen is needed)
Octreotide (Lowers BP in the liver, Prevents fistulas/constipation and vasoconstrictors other areas)
Balloon Tamponade
Cleansing enema to clear out the blood
Lactulose to decrease ammonia
Saline lavage to get blood out of the esophagus
Serotonin Blocker Antiemetics : Ondansetron (Zofran), Granisetron (Kytril), Dolasetron, Netupitan/ palonosetron (Akymzeo)
Common Uses:
Post-op nausea and vomiting, Chemotherapy
Contraindications: Hypersensitivity
Torsades de
pointes
PO/IV Interactions: Use with apomorphine can lead to unconsciousness, hypotension. Do NOT use together. Decrease ondansetron effect with rifampin, phenytoin.
moA: Suppress nausea and vomiting by blocking the serotonin receptors in the afferent vagal nerve terminals in the upper GI tract.
Advantages: Do not block the dopamine receptors;
therefore, they do not cause extrapyramidal
symptoms as do the phenothiazine
antiemetics.
Side Effects: Headache Diarrhea Dizziness Fatigue
Adverse Effects:
Transient elevation of AST and ALT.
Bronchospasm
Interventions:
Monitor ECG for QT prolongation in clients with cardiac disease or
receiving other medications that prolong QT.
Education:
Report diarrhea, constipation, rash, changes in respirations.
Antacids: Magnesium carbonate (Gaviscon), Magnesium hydroxide (Milk of Magnesia), Calcium Carbonate (Tums)
Common uses: Heartburn Gastritis Peptic Ulcer disease GERD Indigestion Prophylaxis with burns Hypomagnesemia
Contraindications: Renal failure
PO Interactions: Risk of side effects of anticoagulants. Blocks absorption of other medications when given simultaneously
MoA: Antacids work by counteracting or neutralizing the acid in the stomach. The neutralization makes the stomach contents less corrosive.
Side Effects:
Diarrhea
Loss of appetite
Adverse: Hives Itching Dyspnea Tightness in chest Edema of face, mouth, tongue Hypermagnesemia
Interventions:
Give either 30 minutes before or 1 hour after other medications to
prevent decreased absorption and effectiveness of medications
Education:
Take with or without food. Follow with a full glass (240 mL)
water or other liquid.
Balloon Tamponade
Sengstaken-Blakemore Tube is a type of balloon tamponade tube
It is an infrequently used emergency procedure that may be used to stabilize clients with severe hemorrhage. It should not be used for more than 12 hours. Many of the safety implications for the tube can be applied to other oropharynyx or naso pharynx tubes.
To hold pressure on the bleeding varices.
Assess if tube placement is moving or altered. It could occlude the airway because the balloon is inflated. Deflate balloon/cut tube to restablish airway. ACT QUICKLY.
Peptic Ulcers: Patho/S&S/Diagnosis
Classification:
Gastric ulcers: Malnourished, pain is usually 30 mins to 1 hour after meals - food doesn’t help but vomiting does - they vomit blood and have decreased weight
Duodenal Ulcers: Well nourished; night time pain is common and occurs 2 - 3 hours after meals, Food helps and there is blood in the stools
Common Cause of GI bleeding, It can be in the esophagus or in the stomach or duodenum. Erosion is present.
Burning Pain usually in the mid epigastric area/back and heart burn
Gastroscopy NPO pre-procedure Sedated NPO until gag reflex returns Watch for perforation by watching for pain/distention, bleeding or if they are having trouble swallowing
Upper GI
Looks at the esophagus and stomach with dye
NPO past midnight
No smoking, chewing gum or mints. Remove the nicotine patch too.
Smoking increases stomach motility, which will affect the test and it also increase stomach secretions which increases the chance of aspiration
Peptic Ulcers: Treatment/Teaching
Medications:
Antacids: Liquid to coat the stomach. Take when the stomach is empty and at bedtime. When the stomach is empty, acid can get onto the ulcer so take antacids to protect the ulcer.
PPI: Decrease the acid secretions.
H2 Antagonist: Rantinidine.
GI cocktails
Antibiotics for H.Pylori: Clarithromycin, amoxicillin, tetracycline and metronidazole
Sulcrafate forms a barrier over the wound to protect the ulcer from acid
Teaching: Decrease Acid Stop Smoking Eat what you can tolerate; Avoid temp extremes and extra spicy foods, avoid caffeine Need to be followed for one year
Hiatal Hernia: Patho/S&S/Treatment
Hole in diaphragm = stomach is where it shouldn’t be
Main cause is a large abdomen - Lots of intrabdominal pressure. Can also be caused by cogenital abnormalities, trauma and straining
LOTS OF REFLUX
Heartburn, Pain after eating, regurgitation, Dysphagia (difficulty swallowing)
Treatment: (Keep the stomach down) Small frequent meals Sit up 1 hour after meals HOB up Surgery Teach lifestyle and healthy diet
