NG+ NUR 144 - WEEK 3 - BILIARY & EXOCRINE PANCREAS Flashcards

(20 cards)

1
Q

Describe exocrine functions of the Pancreas

What are the products?
Where are they collected?
What is it stimulated by?

A

(Endocrine = into bloodstream, exocrine = external ducts of body)

  1. Exocrine productions:
    - High alkaline secretion (d/t high sodium bicarb) which neutralizes highly acidic stomach acid in the duodenum
    - Amylase: digests carbs
    - Trypsin: digests proteins
    - Lipase: Digests fats
  2. Exocrine secretions are collected in pancreatic duct
  3. GI tract hormones stimulate this secretion
    - Hormone Secretin: Major stimulus for increase bicarb secretion
    - Hormone Cholecystokinin (CCK): Major stimulus for digestive enzyme secretion
    - Vagus nerve
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2
Q

Describe bile

A

Bile - Produced by the liver hepatocytes, aids in digestion of fats; also neutralizes stomach acid in duodenum (d/t it containing high amounts of bicarb)

  • When in the gallbladder between meals, a large amount of water is drawn out of the bile. This makes bile in the gallbladder 5x-10x more concentrated than what’s created by the hepatocytes
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3
Q

Describe Gallblader

A

Storage unit for bile, holds roughly 30-50 mL. Attaches to duodenum

Bile release is stimulated by Cholecystokinin which is produced & released by the small intestine

Bile - Produced by the liver, aids in digestion of fats; also neutralizes stomach acid in duodenum (d/t it containing high amounts of bicarb)

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4
Q

Describe the Bile Ducts

A

Common hepatic duct connects liver/hepatocytes which creates bile to the Cystic Duct and Common Bile Duct.

Bile flows from liver/hepatocytes down Common hepatic Duct –> Cystic Duct for storage –> Common Bile Duct for secretion into duodenum

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5
Q

What is the Sphincter of Oddi?

A

Controls secretion of bile and pancreatic enzymes, where the common bile duct and pancreatic duct merge

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6
Q

Lab Tests / Diagnostic Tools for Biliary System Dysfunction

A
  • Pancreatic Enzymes: (Amylase, Lipase)
  • LFT (Liver Function Test): AFT, ALT,
  • Bilirubin (direct and indirect):
  • Ultrasound
  • Computed Telemetry (CT)
  • Magnetic Resonance Imagery (MRI)
  • Endoscopy
  • ERCP
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7
Q

Describe Cholecystitis

What is it
What causes it
S/S

A

Inflammation of the gallbladder; can be acute or chronic
Secondary infection of bile may occur, may lead to empyema (buildup of pus)

Cause:
- Usually Calculous cholecystitis = i.e. “gallstone obstructs bile flow and compresses blood vessels”

  • If Acalculous (no gallstones) cause may be: bile stasis, high bile viscosity, torsion

S/S: Pain-tenderness of upper right abdomen may radiate to midsternal or right shoulder, nausea, vomiting

Complication: Gangrene (necrosis), perforation, infection

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8
Q

Describe Cholelithiasis

What is it
What causes it
S/S
Complications

A

Stones that form in gallbladder; can be chronic or acute

Cause: Excess bilirubin OR cholesterol

s/s: discomfort d/t inflammation & contractile spasms, digestive issues d/t inadequate bile

Complication: Necrosis or rupture d/t untreated swelling/distention; digestive problems d/t reduced/absent bile

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9
Q

Two Types of Cholelithiasis:

Describe Pigment Type:
What is it?
Risk factors?

A

Small dark stones of bilirubin and calcium salts; 10%-25% of cases
Cholelithiasis may lead to cholecystitis

  • Look for dark colored urine & grayish colored feces

Risk factors
- Cirrhosis
- Hemolysis; “Excess breakdown of RBCs = excess bilirubin”
- Biliary tract infection

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10
Q

Two Types of Cholelithiasis

Describe Cholesterol Type:
What is it?
Risk factors?
s/s?

A

Usually green/white/yellow; roughly 75% of cases
Cholelithiasis may lead to cholecystitis

” Decreased bile acid synthesis + increased cholesterol synthesis in the liver = leads to bile saturated w/ cholesterol “

LDL: causes atherosclerosis
HDL: Carries cholesterol to liver

Risk Factors:
- Cystic Fibrosis
- Estrogen therapy
- Diabetes
- Fatty diet, hypocholesteremia (high cholesterol in the blood)
- Sedentary lifestyle

s/s: RUQ pain (esp. after fatty meal), fullness, abdominal distention, biliary colic (pain d/t gallstone)

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11
Q

Medical Management of Cholelithiasis

A
  • ERCP
  • Dietary management

Medication: Ursodeoxycholic Acid
Laparoscopic: Cholecystectomy

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12
Q

Nursing interventions for the biliary system

A

Post surgery, assess for:
- Loss of appetite
- Vomiting
- Pain
- Distention

Post-Surgery goals:
- Pain relief
- Intact skin
- Improved biliary drainage

Post-Surgery Interventions:
- Low Fowlers
- NPO / NG Tube
- Care of biliary drainage system
- Pain management

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13
Q

Describe Acute Pancreatitis

What it is
What Causes it
S/S

A

Inflammation of the pancreas
- Acute: Obstruction of pancreatic duct & backed up enzymes

Cause:
- Cholelithiasis, alcohol abuse

S/S:
- Acute: Autodigestion (Digestive enzymes breakdown its own tissues), and inflammation of pancreas

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14
Q

Interstitial Pancreatitis vs. Necrotizing Pancreatitis

A

Both are Acute Pancreatitis

Interstitial Pancreatitis:
Pancreas becomes swollen d/t inflammation
- Majority of patients
- Minimal organ dysfunction; normal function returns in 6 months
- Risk for: hypovolemic shock, sepsis

Necrotizing pancreatitis:
Pancreas’ enzymes digests itself (enzymes get activated early
- Damage to local blood vessels; bleeding and thrombosis
- Severe, resistant to treatment, rapidly fatal
- Necrosis in pancreas, or surrounding tissue
- Can be sterile or infected

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15
Q

S/S, assessment for acute pancreatitis

A
  • Severe abdominal pain, worsens after meals
  • Distended & rigid abdomen
  • Nausea / vomiting
  • Fever
  • Jaundice
  • Ill appearance
  • Hypoactive bowel
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16
Q

Diagnosis of pancreatitis

A
  • Hx of upper abominal pain
  • Serum amylase or lipase levels = 3x upper limit
  • Abnormal imaging (CT, MRI, ultrasound)
17
Q

Treatment for pancreatitis

A
  • Initially, NPO
  • Then, Enteral feeding
  • NG suctioning to relieve nausea/vomiting, distention
  • Analgesia
  • Removal of blockage
18
Q

Describe Chronic Pancreatitis

What is it
What causes it
S/S

A

Inflammatory disorder with destruction of pancreases
Pancreatic cells are replaced by fibrous tissue (scarring i.e. dead cells) = leads to obstruction of pancreatic/bile ducts, atrophy of duct epithelium

Cause:
- Excess alcohol consumption
- Malnutrition

Assessment-S/S:
- Upper abdominal and back pain
- Vomiting
- Weight loss, anorexia
- Frothy, frequent, foul stools
- Calcium stones in ducts

19
Q

Medical Management of Chronic Pancreatitis

A
  • Prevent acute attacks, pain management
  • Nonsurgical: Endoscopy (stone removal, widen structures with stents, drain cysts)
  • Surgical: Pancreatojejunostomy (Drainage of pancreatic secretions into jejunum)
20
Q

True/False:

Patients with acute pancreatitis require a high-carbohydrate, low-protein, and low-fat diet.​

A

True​

Rationale: In patients with acute pancreatitis, a high-carbohydrate, low-protein, and low-fat diet increases caloric intake without stimulating pancreatic secretions beyond the ability of the pancreas to respond.