Exam 5 Flashcards

(70 cards)

1
Q

Treatment for liver CA:

A
  • transplant if dz is local (rigorous screening)
  • poor prognosis if metastasized. Death due to:
    ^ encephalopathy
    ^ GI bleed r/t low clotting factors
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2
Q

Diagnostics for liver CA:

A

CT/MRI to look for lesions

Biopsy (needleguided) to test lesions for CA cells

Serum alpha fetoprotein (AFP) - elevated levels in 60% of patients… it’s a tumor marker, high levels indicate CA

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3
Q

What is the #1 and #2 causes of liver CA?

A

Cirrhosis from chronic Hepatitis C is #1

Alcoholic cirrhosis is #2

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4
Q

If someone presents with the following symptoms, what may they indicate?

  • Hepatomegaly
  • Jaundice
  • Peripheral edema
  • Ascites
  • Dull, epigastric pain
  • Anorexia, N/V
A

Possibly liver cancer.

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5
Q

What are some functions of the liver?

A
  • Produces bile. Bile helps carry away waste (bilirubin) and helps breakdown fats in the small intestine.
  • It metabolizes proteins, carbohydrates, and steroids (the major site for cortisol metabolism).
  • Clears the blood of drugs and other harmful substances
  • Produces proteins for blood plasma (albumin, fibrinogens)
  • Regulates blood clotting
  • Produces cholesterol and special proteins to help carry fats through the body
  • Stores and releases glucose
  • Processes hemoglobin for its iron (stores iron), this process produces bilirubin… which the liver conjugates with a sugar group so it can be secreted with the bile in the stool and urine.
  • Converts harmful ammonia into an amino acid (glutamine) and a chemical compound (urea).
  • Produces immune factors and removes bacteria from the blood stream. Kupffer cells.
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6
Q

What are the main causes of acute liver failure?

A
  • Acetaminophen OD or with alcohol abuse
  • Hep B is 2nd most common cause
  • NSAIDs, isoniazid (TB abx), and sulfa drugs are other causes.
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7
Q

If a patient has clinical manifestations of the following, what may this indicate?

  • Rapid onset of sever liver dysfunction
  • Decrease in mental responsiveness
  • Jaundice
  • Ascites
  • Coagulation abnormalities
A

Acute liver failure.

Other possible signs:

  • Low BG
  • Cerebral edema
  • Renal failure r/t dehydration r/t fluid shift
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8
Q

In what type of patient would we be monitoring their hemodynamic status, liver enzymes, glucose, and CBC?

A

Acute liver failure…

  • Hemodynamic: clotting factors (bleeding)
  • Liver enzymes: AST and ALT are elevated with hepatic inflammation/injury
  • Glucose: Can be unpredictable
  • CBC for immune, clotting factors, etc.
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9
Q

Why would we want to perform neuro assessments, utilize safety precautions, avoid sedatives and consider oral/skin care with patients in acute liver failure?

A

Neuro - VERY important to monitor for progression… hepatic encephalopathy, cerebral edema.

Safety - Seizure precautions, altered mental status

Sedatives - Can exacerbate lethargy and precipitate encephalopathy/coma.

Skin/oral care - sedentary, “out of it,” excessive sleeping… probably not taking care of their teeth… skin breakdown r/t immobility.

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10
Q

Where is the bruising seen on the abdomen with Cullen’s sign? (d/t acute pancreatitis)

A

Around the naval.

Ecchymoses to periumbilical area.

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11
Q

Gallbladder disease is the number one cause of what in women?

A

Pancreatitis.
Pancreatitis is most chronic in the middle-aged.

Other causes: smoking, hypertriglyceridemia, post-procedure.

Some procedures such as ERCP can cause pancreatitis.
Also, post surgery on: pancreas, stomach, duodenum, biliary tract.

African Americans are 3x more likely to get.

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12
Q

What is the most common cause of pancreatitis in men?

A

Chronic alcohol intake.

Other causes: smoking, hypertriglyceridemia, post-procedure/surgery.

Some procedures such as ERCP can cause pancreatitis.
Also, post surgery on: pancreas, stomach, duodenum, biliary tract.

African Americans are 3x more likely to get.

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13
Q

Pathophysiology of pancreatitis:

  1. Injury to pancreatic cells (from gallbladder or irritants such as alcohol/smoking).
  2. Activation of pancreatic enzymes (from the injury)
  3. Auto-digestion of pancreas by the enzymes.
A

Don’t need to memorize the enzymes but…

  • Trypsin
  • Elastase
  • Phospholipase A/ Lipase
  • Kallikrein
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14
Q

Which classification of acute pancreatitis (mild/severe) is described as “edematous” or “interstitial?”

A

Mild pancreatitis.

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15
Q

Where is the ecchymosis seen on the abdomen with Grey Turner’s sign? (d/t acute pancreatitis)

A

Bruising is seen on the flank.

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16
Q

Which classification of pancreatitis is described as:

  • having endocrine and exocrine dysfunction
  • necrosis, organ failure, sepsis
  • 25% mortality rate
A

Severe pancreatitis, aka Necrotizing Pancreatitis.

Mortality rate r/t fluid shifts, hemorrhaging, leading to shock.

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17
Q

What may the following indicate?

  • LUQ, mid-epigastrum pain
  • Low-grade fever
  • Hypotension/tachycardia
  • Jaundice: especially if r/t anything with the gallbladder.
A

Acute pancreatitis

Other signs/symptoms:

  • Pain worsens when laying in the recumbant position
  • Pain can radiate to the back, can be deep and severe, can be continuous, can be worse with eating, and may experience tenderness with muscle guarding.
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18
Q

If a patient presents with the following, what might it be?

  • Severe, continuous, pain in the back
  • Pain worsens with eating
  • Pain worsens while on their side
A

Could be acute pancreatitis.

Normal clinical manifestations:

  • LUQ, mid-epigastrum pain
  • Low-grade fever
  • Hypotension/tachycardia
  • Jaundice: especially if r/t anything with the gallbladder.

Other:

  • Pain worsens when laying in the recumbant position
  • Pain can radiate to the back, can be deep and severe, can be continuous, can be worse with eating, and may experience tenderness with muscle guarding.
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19
Q

Patient presents with the following:

  • Bowel sounds are hypoactive or absent
  • Lungs have crackles
  • Intravascular damage: blood exudate spilling out into the abdominal cavity.

What might these indicate?

A

Acute pancreatitis.

Grey Turner’s sign: ecchymoses to flank are

Cullen’s sign: ecchymoses to periumbilical area.

Due to the fluid shifts and hemorrhaging = shock.

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20
Q

Pseudocysts and abscesses are local complications of what?

A

Acute pancreatitis.

Pseudocysts: collection of fluid, pancreatic enzymes, tissue debris and inflammation exudate surrounded by a wall.

Abscess: collection of pus from extensive necrosis of pancreas.

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21
Q

When a patient is experiencing abdominal pain, anorexia, N/V, and has a palpable mass, what might this indicate?

A

A pseudocyst. This is a local complication of acute pancreatitis.

The palpable mass is the pseudocyst which is a collection of fluid, pancreatic enzymes, tissue debris, and exudate that is walled off.

** They usually resolve but MAY perforate, causing peritonitis (possibly life-threatening).

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22
Q

What is the treatment for a pancreatic abscess?

A

Needs prompt surgery to drain it and prevent sepsis.

If not tx’d, can get infected or perforate into adjacent organs… sepsis is a life-threatening complication.

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23
Q

Acute pancreatitis can have systemic effects, especially on the pulmonary and cardiovascular system d/t the fluid shifts and pancreatic enzymes circulating through the lymph system. What are some common systemic manifestations?

hint: 4 our pulmonary, 3 are “hypo, hypo, clot”…

A
  • Pleural effusion
  • Atelectasis (Complete/partial collapse of a lung or lobe of a lung)
  • Pneumonia
  • ARDS (acute respiratory distress syndrome)
  • Hypotension
  • Hypocalcemia = tetany
  • Clotting disorders = DIC (disseminated intravascular coagulation)
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24
Q

What are the diagnostic studies done with acute pancreatitis?

A

1 - Pancreatic enzyme levels will be very high (amylase and lipase are noted)

  • Calcium levels will be low (not sure why)
  • Abdominal ultrasound
  • X-ray will show lung changes/fluid
  • Contrast-enhanced CT scan will show pseudocyst vs abscess
  • Endoscopic retrograde cholangiopancreatography (ERCP) is used to if the the gallbladder is involved. This test may also cause pancreatitis. =(
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25
Acute pancreatitis treatment and collaborative care... | Always start with conservative measures first. What are some of these?
* Aggressive hydration - to clean/flush exudate * Pain management - morphine IVP: extreme pain * Decrease pancreatic stimulation: NPO, NGTube ~~drugs: PPI's to slow secretions, Atropine is an anticholinergic antispasmodic that in high doses decreases GI/GU motility and decrease secretions. * Watch for ARDS (respiratory failure) * Watch for tetany (hypocalcemia) * If all else fails = surgery
26
Which sign of tetany is demonstrated with the blood pressure cuff?
Trousseau's Sign. Note: sounds like "true" and this is the more definitive sign for hypocalcemia... it is more sensitive and specific, present in 94% of patients with hypocalcemia and only 1% of people with normal calcium levels. The other sign, Chvostek's sign, is not as accurate: only 1/3 of patients with hypocalcemia have positive C's sign AND is also present in 10% of those with normal Ca levels. This sign is demonstrated with the tapping over the facial nerve, making a muscle twitch in the face.
27
If conservative treatment is unsuccessful then surgery is performed on acute pancreatitis. What are some other indications for surgical intervention?
- Gallstones (for those that have pancreatitis d/t gallbladder dz) - Cholecystectomy (gallbladder removal may be needed for some patients) - An uncertain diagnosis (if labs, s/s, are not conclusive, may need to "go in" to see what's going on) - Necrotic fluid (need to go in to drain this bc this complication can be very dangerous - sepsis, etc.)
28
What things do we need to consider with pancreatitis in regards to nutritional therapy?
- NPO status initially (to decrease stimulation) - Enteral vs TPN is determined by severity of case - Monitor triglycerides if IV lipids are given - Small, frequent high-carb feedings to decrease stimulation of the exocrine function of the pancreas. - NO alcohol (irritant) - Supplemental fat-soluble vitamins further down the road of recovery... r/t gallbladder and bile
29
Chronic pancreatitis is a continuous, prolonged, inflammatory and fibrosing process of the pancreas over a long period of time.
The pancreas is slowly destroyed and replaced with fibrotic tissue, strictures, and calcifications. This can occur after acute pancreatitis. If fibrosis is from injury then it also called scarring. Strictures: narrowing
30
Chronic pancreatitis has two types: 1. Chronic Obstructive: r/t gallstones or CA 2. Chronic Nonobstructive: r/t inflammation or sclerosis What is the pathophysiology behind these causes?
1. a) Gallstones cause inflammation of the sphincter of Oddi (also hepatopancreatic sphincter, is a muscular valve that controls the flow of digestive juices (bile and pancreatic juice) through the ampulla of Vater into the second part of the duodenum) b) CA of ampulla of Vater, duodenum, pancreas cause obstructions 2. Inflammation and sclerosis in the head of pancreas or pancreatic duct caused by alcohol abuse.
31
What are the differences in clinical manifestations between acute and chronic pancreatitis?
Not much difference. Both present with: -- Abdominal pain/tenderness in the same areas (LUQ and mid-epigastrum) -- Heavy, burning pain not relieved by food/antacids (pancreatic spasms) -- Recurrent over time (this is different from acute) this can occur over months/years... then patients may begin showing signs of malabsorption and weight loss. - Jaundice, and/or steatorrhea may be seen, depending on the specific cause of the pancreatitis.
32
What are the diagnostics run for suspicion of chronic pancreatitis?
#1 is elevated amylase and lipase enzymes (just like acute) Serum bilirubin/ alkaline phosphatase = these indicate liver function ERCP/ MRCP and/or CT = all used to figure out what is going on Stool samples if clay-colored or steatorrhea.
33
What is the treatment for chronic pancreatitis?
Same as acute care... * Analgesics: morphine or fentanyl transdermal patch (Duragesic). * Bland diet, low-fat, small, frequent meals (decreases stimulation) * NO smoking * NO alcohol * NO caffeine * Pancreatic enzyme replacement if pancreas is showing signs of insufficiency * Bile salts help with the absorption of fat-soluble vitamins and digestion of fats. * Insulin or oral hypoglycemic agents * Acid-neutralizing and acid-inhibiting drugs (PPIs) help decrease pancreatic stimulation * Antidepressants r/t chronic nature of dz * If all else fails... surgery
34
When is surgery indicated for chronic pancreatitis?
- When biliary disease is present or if obstruction or pseudocyst develops - To divert bile flow or relieve ductal obstruction - Choledochojejunostomy: anastomosis of the common bile duct to the jejunum, performed to relieve symptoms of biliary obstruction and restore continuity to the biliary tract - Roux-en-Y pancreatojejunostomy: attaching the pancreas to the jejunom so that pancreatic secretions may still enter (minus the section they removed).
35
What nursing education needs to be addressed r/t chronic pancreatitis?
Long-term therapy... - Dietary control - Pancreatic enzymes - Diabetes education (BG all over r/t panc dysfunction) - Avoidance of alcohol
36
What is bile good for? Where does it enter the duodenum?
Emulsifies fat and helps with its digestion... also helps with the absorption of KADE vitamins. At the ampulla of Vater (first part of sm intestine)
37
What is the most common cause of gallbladder disease?
Cholelithiasis: Gallstones This is the most common disorder of the biliary system. The stones can get lodged in the neck, cystic duct, or common bile duct.
38
What do we call the inflammation of the gallbladder?
Cholecystitis This is usually associated with cholelithiasis (gallstones), the build-up of the stones cause disruption and obstruction of the flow of bile... or with sludge.
39
What are some other risk factors for gallbladder disease? Other than sedentary lifestyle, multiparity, and obesity?
* Female * Age 40+ * Estrogen therapy: r/t the increased cholesterol production from the estrogen. (menopause, birth control) * Genetics/Ethnicity: Asian and African American
40
The cause of gallstones is unknown but they seem to develop when the balance of cholesterol, bile salts, and calcium are altered. What are some factors that could lead to this imbalance?
- Infection - Alteration in metabolism of cholesterol - Immobility - Pregnancy - Inflammatory or obstructive lesions of the biliary system that cause a decrease in bile flow. These can all lead to stasis of bile which is high in lipids and becomes "sludge." This condition leads to stone formation.
41
Stones may remain in the gallbladder or may migrate to the cystic or common bile duct. This migration causes excruciating pain. They may lodge in ducts and produce an obstruction. What are some clinical manifestations of cholelithiasis?
It varies from severe s/s to asymptomatic... * Pain is more severe when stones are migrating or obstructing -- Pain is steady and excruciating (from spasms aka biliary colic) -- Tachycardia, diaphoresis -- Pain may radiate to the RT shoulder/scapula -- Tenderness in RUQ -- Pain occurs 3-6 hours after a high-fat meal or when patient lays down
42
Sources of fatty foods:
Fatty meats and fish (mackerel, herring, salmon) Cheese Nuts/Seeds Butter Chocolate Avocado
43
What is acalculous cholecystitis? Who is at risk?
An inflammatory disease of the gallbladder without evidence of gallstones or cystic duct obstruction. It is a severe illness that is a complication of various other medical or surgical conditions. An acute attack will damage the mucous lining or entire gallbladder. - Older adults who are critically ill - Prolonged imobility - Prolonged TPN - Those who've had bacteria travel to the gallbladder
44
What are the clinical manifestations of chronic cholecystitis?
- Fat intolerance - Dyspepsia (indigestion) - Heartburn - Flatulence Inflammation: - Increased WBC (leukocytosis) - Fever Physical Exam: - RUQ tenderness - Abdominal rigidity - Referred pain to RT shoulder/scapula
45
What are the clinical manifestations of a complete obstruction r/t gallbladder?
* Jaundice (bilirubin is conjugated with bile and excreted in stools/urine) * Dark amber urine r/t increased bilirubin in urine * Clay-colored stools r/t decreased bilirubin in stool * Pruritis r/t increased bile salt in the skin * Intolerance of fatty foods r/t lack of bile in intestine = steatorrhea * Bleeding tendencies r/t decrease in KADE vitamins absorbed from bile not helping... K is needed in prothrombin clotting factor.
46
What are some complications of cholecystitis, besides fistulas, biliary cirrhosis, and pancreatitis?
* Gangrenous cholecystitis * Subphrenic abscess: an accumulation of infected fluid between the diaphragm, liver, and spleen. * Cholangitis: a serious infection of the liver's bile ducts * Gallbladder rupture: leads to peritonitis (life-threatening) * Choledocholithiasis: gallstones in the bile duct
47
What are the diagnostic studies r/t cholecystitis (procedures and labs)?
-- Ultrasonography -- ERCP to visualize stones and ducts (risk of pancreatitis from this procedure) -- Percutaneous transheptatic cholangiography: needle into the gallbladder, duct is injected with contrast. - - Lab tests: * Elevated WBC * Elevated serum bilirubin level * Elevated urinary bilirubin level * Elevated liver enzyme levels (ALT, AST, alkaline phosphatase) * Elevated serum amylase level = pancreatic involvement
48
Treatment options for cholelithiasis depends on the stage of the disease, what is the conservative treatment?
* IV fluids * NPO * NG tube (to prevent gallbladder stimulation) * Pain medication * Nausea medication * KADE supplementation * Atropine (antispasmotic, anticholinergic) * Possibly abx if secondary infection * Bile salts may be used to mimic bile
49
Once gallstones become symptomatic what does this indicate???
Cholecystectomy: surgical removal of the gallbladder. It is a common treatment of symptomatic gallstones and other gallbladder conditions.
50
When is an ERCP with sphincterotomy procedure used?
When there is only one stone and/or is easily retrieved (in a "basket"). This procedure allows visualization, dilation of the sphincter of Oddi, placement of stents, an endoscope passed to the duodenum then stone removal or allowed to pass in stool.
51
Treatment options for cholelithiasis? There's really only one (besides the ERCP with sphincterotomy):
Extracorporeal shock-wave lithotripsy (ESWL). If stones can't be removed via endoscope, this is a high-energy shock wave that attempts to disintegrate stones. It takes 1-2 hours and is used in conjunction with bile acids to help break up the stones even further.
52
What are some treatment options for cholecystitis?
- PAIN control: Morphine, NSAIDs (Toradol), Anticholinergic (Atropine - INFECTION control: abx, cholecystectostomy - FandE BALANCE: NG tube if severe N/V, NPO, bile salts to help with digestion Also CHOLESTYRAMINE which lowers cholesterol levels and treats severe itching caused by liver dz.
53
What is the surgical treatment options for cholecystitis?
** Laparoscopic cholecystectomy. This is the treatment of choice for gallbladder disease. It is the removal of the gallbladder through 1-4 puncture holes (quick and easy). Minimal post-operative pain. Able to resume normal activities, including work, within 1 week. Few complications (and up to 4 lap sites to monitor).
54
Nursing management considerations with laparoscopic cholecystectomy?
- Monitor for complications - Patient comfort: * May experience referred pain to shoulder from the CO2 that was pumped into body during procedure. * Perform deep breathing, ambulation, analgesia - Clear liquids then advance as tolerated (on solid = start with low fat and smaller meals) - Discharge the same day.
55
As FYI there is another form of cholecystectomy that is not as common anymore, it's the open cholecystectomy and is the gallbladder removal through the subcostal incision...
A T-tube is inserted into the common bile duct to allow for drainage, it ensures patency of the duct and excess bile to drain.
56
Is gallbladder cancer common?
No. It is usually considered secondary. Primary is very uncommon. Adenocarcinomas are a glandular CA. There's a relationship between chronic cholecystitis and cholelithiasis and development of CA This is more common in women (maybe because gallbladder dz is more common in women?).
57
Early symptoms of gallbladder CA are insidious and similar to those of cholecystitis and cholelithiasis. The late symptoms are usually those of biliary obstruction. It is therefore usually not detected until it is advanced. What are the diagnostics and staging with this CA?
* EUS: endoscopic ultrasound * Transabdominal ultrasonography * CT: computed tomography * MRI: magnetic resonance imaging * MRCP: magnetic resonance cholangiopancreatography ~~Gallbladder CA can only be cured if found early.~~
58
How do we treat gallbladder cancer?
-- Endoscopic stent is placed in the biliary tree to reduce jaundice. -- Just like other CA's... Radiation and chemotherapy -- Poor prognosis if not found early
59
What is the nursing management for gallbladder CA?
Supportive. Nutrition Hydration Skin care Pain relief
60
Esophageal CA is mostly adenocarcinomas (from the glands lining the esophagus). It is similar to CA's of the stomach and small intestine. The cause is unknown, however, the incidence increases with age and men are at greater risk than women. What are some other risk factors?
+ Smoking (doubles chances) + Alcohol + Obesity + Barrett's Metaplasia (chronic GERD) + Achalasia (absent peristalsis in 2/3 of esophagus, from nerve damage)
61
What clinical manifestations can you expect to find with esophageal cancer?
** Advanced disease by s/s appear -- Progressive dysphagia occurs (difficulty swallowing), first with meat, later with soft foods and liquids. -- Pain is a late symptom but can be found substernal, epigastric, and back (radiated) that worsens with swallowing. -- Weight loss -- Sore throat, choking, hoarseness (if tumor is in upper 1/3 of esophagus) -- Esophageal regurgitation. May be blood tinged, indicating narrowing of the esophagus. * Most tumors are located in the mid to lower portion of the esophagus.
62
What are some common complications with esophageal cancer?
- Hemorrhage r/t erosion of mucosa. It can erode all the way to the aorta. - Fistulas: to the lung or trachea - Obstruction: if the tumor is large enough - Metastasis: Commonly spread to the lung and liver through the lymph system.
63
Common diagnostics for esophageal cancer: - Endoscopy with biopsy (for dx) - Barium swallow (to ID narrowing at tumor site) and what other two?
1. CT/ MRI to ID metastasis | 2. Bronchoscopy - may be necessary to detect involvement of the lung
64
Treatment for esophageal CA is based on location and metastasis. What are some common treatment options?
Late diagnosis = poor prognosis Best treatment involves the combination of the following 3: -- Surgery to remove some of the esophagus. Post-op tx... TPN or J-tube feedings, swallowing study -- Photodynamic/ laser therapy to oblate areas of the esophageal mucosa -- Radiation and chemo to slow dz progression
65
Nursing considerations regarding esophageal CA?
#1 Respiratory status and patent airway (duh) Ensure patient is able to swallow B4 oral fluids (swallow study) Patient positioned in HIGH fowlers if able to eat Tube feeding tolerance, slowly increase the amount so they can develop a tolerance Pain relief r/t esophageal dissection.
66
What type of cancer is stomach cancer? What type of diet is associated with this CA?
Adenocarcinoma. It's r/t injury to the mucus lining (H. pylori, autoimmune disorders, NSAIDs, tobacco) High risk diet: smoked meats, salted fish/meats, pickled vegetables. Conversly, diets rich in whole grains and veggies = low risk of stomach CA
67
Stomach CA typically spreads to adjacent organs before it is diagnosed, what are some clinical manifestations you may see?
- Weight loss, early satiety, indigestion, abdominal pain, anemia (possibly from chronic blood loss r/t lesion of mucosa, possibly from pernicious anemia r/t malabsorption of vit B-12) - Weakness, fatigue, SOB, OB positive stool, ascites (poor prognosis).
68
What would we be trying to diagnose with an endoscopy and biopsy, CT/PET scans, and labs (HandH, liver enzymes, and OB in stool)?
Stomach CA Endoscopy and biopsy for definitive diagnosis. CT/PET scans to determine metastasis and staging Lab tests: - H and H (hemoglobin and hematocrit to check for anemia - Liver enzymes (ALT, AST) will reveal if the liver is involved - You'll see an increase in amylase if pancreas involved - OB (occult blood) in stools from bleeding
69
What is the typical treatment for stomach CA?
* Surgery to remove the tumor and removal of the stomach up to normal tissue, maybe a total gastrectomy (anastomize the esophagus to jejunum). * Lesions in the fundus require a total gastrectomy. * Chemo and radiation to slow dz progression. After a gastrectomy you need to pay close attention to fluid intake and dumping syndrome. After this procedure they may lose significant weight, need vitamins C, D, K, and B-complex bc these are usually absorbed in the duodenum.
70
Upper GI bleeding is from which three areas?
1. Esophageal 2. Stomach 3. Duodenum