Exam 4 Study Guide
Alterations in Metabolism
Gallbladder:
Function is the concentration and storage of bile
Cystic duct connects to the hepatic duct, forming the common bile duct.
Bile:
Is made up of water, electrolytes, and organic solutes.
It has low protein content, contains bile acids, pigment, cholesterol, and
phospholipids.
Formed in the liver, then modified and stored in the gallbladder and bile ducts
before secretion into the intestinal tract.
Aid in digestion of lipids.
Disorders of the Gallbladder
Cholelithiasis and Cholecystitis
Clinical Manifestations determine if acute or chronic.
Acute Cholecystitis
Patho/Etiology:
o Acute inflammation of gallbladder wall, and/or sphincter of Oddi
Causes:
Stasis of bile – Bile is trapped and can lead to stones
Increased saturation of bile with cholesterol (most common cause)
Nucleation - Cholesterol crystals aggregate together and form
stones
Hypomotility and stasis allow stone growth.
Obstruction of cystic duct is present in almost all patients.
Cholelithiasis (90% of the time)
Bacterial infection may be present (Sepsis Risk septic shock)
Acalculous (without a stone) – after major surgery, trauma, or
burn-related injury. TPN is a common cofactor. – Gangrene can
develop more rapidly than with a stone - At risk for abscess.
Continued presence of gallstones promotes these inflammatory changes
in the gallbladder wall
, S/Sx:
o Pain, tenderness, and rigidity of the RUQ that may radiate to the mid-
epigastric area or right shoulder and is associated with nausea, vomiting, and
the usual signs of acute inflammation.
o Severe RUQ pain that radiates to the back. Abdominal tenderness and fever;
cholelithiasis is present in 90% of cases. Bacterial infection accompanies acute
episode.
Diagnosis:
o Leukocytosis, elevated bilirubin and serum transaminases
o Ultrasound of abdomen
o Hepatobiliary nuclear scintigraphy
o CT & MRI
o ERCP – risk of perforation and pancreatitis
Left Untreated- may lead to gangrene of the gallbladder wall with rupture
peritonitis, septic shock, abscess (empyema), and fistulas (between gallbladder and
GI tract).
Treatment:
o Depends on severity of symptoms
o Surgeons like to let a hot gallbladder cool down first
o Broad-spectrum antibiotics
o Laparoscopic or open Cholecystectomy – Definitive treatment
o Chemodissolution
o ESWL (lithotripsy)
o Pain management
80% achieve remission with rest, IVF, NG suction, analgesia, and antibiotic agents.
Cholelithiasis (or gallstones)
o Supersaturation of bile with Cholesterol
o Become more prevalent with age
o Patho: 2 types composed of 1. Pigment and 2. Cholesterol.
Cholesterol stones account for 75% of stones
Are 2-3x more prevalent in women.
Black Pigment stones are associated with cirrhosis or hemolysis
, Brown Pigment stones are more common in developing countries from
parasites.
Risk Factors:
o High spinal cord injuries, TPN, prolonged fasting or rapid weight loss, and
pregnancy, oral contraceptives, obesity, diabetes, and octreotide .
o Female/Fair/Fat/Forty
o Most susceptible are Native Americans, White Europeans, and Asians, with the
lowest risk.
o In children, usually associated with cystic fibrosis or sickle cell
S/Sx’s:
o Often asymptomatic
o Mild GI Symptoms
o Epigastric Fullness
o Right Upper Quadrant Pain
Diagnosis
o Ultrasound
o Nuclear imaging studies (HIDA Scan)
o CT
o MRI
o Endoscopy (ERCP)
Chronic Cholecystitis
o Patho/Etiology
Persistent irritation/inflammation to gallbladder wall from cholelithiasis
Causes fibrosis and thickening r/t continued presence of gallstones.
Diabetes and obesity are predisposing factors.
Untreated – increased risk of cancer; sepsis
Can lead to calcified or porcelain gallbladder (from scarring) or biliary
sepsis, associated with higher risk of cancer.
o S/Sx: Same as acute
o Diagnosis: Same as acute
Chronic Cholelithiasis
o Patho/Etiology:
Incidence r/t age, gender, and variety of medical issues
, Gallstones are developed by
Supersaturation of bile with cholesterol
Nucleation of crystals
Hypomotility allowing stone growth
o S/SX:
Can be asymptomatic
Intermittent Biliary colic (persistent epigastric or RUQ pain that can
radiate to the back, accompanied by N/V, sweating, and
flatus/belching/blaoting lasting several hours. Caused by obstruction of
the cystic duct by a gallstone, rarely from spasm of the sphincter of Oddi.
Precipitated by a meal or occurs spontaneously
Pain increases steadily for 15 minutes and persists for an hour – slowly
decreases
Related fatty food intolerance
“Patient may think they are having a heart attack.”
Fever
Palpable mass
Nausea and vomiting after eating a heavy meal
Restlessness
Jaundice
Dark colored urine – from excretion of bile pigments.
Stool color greyish or clay-like (lack of bile pigments)
Vitamin A, D, E, & K deficiency – obstructed bile flow interferes with
absorption.
o Complications
Peritonitis
Gangrene
Post-procedure – bleeding, sepsis
Empyema
Pancreatitis
o Diagnosis
Abdominal X-Ray
Ultrasonography/Ultrasound - fastest and easiest test for abd RUQ pain
and sweating
Alterations in Metabolism
Gallbladder:
Function is the concentration and storage of bile
Cystic duct connects to the hepatic duct, forming the common bile duct.
Bile:
Is made up of water, electrolytes, and organic solutes.
It has low protein content, contains bile acids, pigment, cholesterol, and
phospholipids.
Formed in the liver, then modified and stored in the gallbladder and bile ducts
before secretion into the intestinal tract.
Aid in digestion of lipids.
Disorders of the Gallbladder
Cholelithiasis and Cholecystitis
Clinical Manifestations determine if acute or chronic.
Acute Cholecystitis
Patho/Etiology:
o Acute inflammation of gallbladder wall, and/or sphincter of Oddi
Causes:
Stasis of bile – Bile is trapped and can lead to stones
Increased saturation of bile with cholesterol (most common cause)
Nucleation - Cholesterol crystals aggregate together and form
stones
Hypomotility and stasis allow stone growth.
Obstruction of cystic duct is present in almost all patients.
Cholelithiasis (90% of the time)
Bacterial infection may be present (Sepsis Risk septic shock)
Acalculous (without a stone) – after major surgery, trauma, or
burn-related injury. TPN is a common cofactor. – Gangrene can
develop more rapidly than with a stone - At risk for abscess.
Continued presence of gallstones promotes these inflammatory changes
in the gallbladder wall
, S/Sx:
o Pain, tenderness, and rigidity of the RUQ that may radiate to the mid-
epigastric area or right shoulder and is associated with nausea, vomiting, and
the usual signs of acute inflammation.
o Severe RUQ pain that radiates to the back. Abdominal tenderness and fever;
cholelithiasis is present in 90% of cases. Bacterial infection accompanies acute
episode.
Diagnosis:
o Leukocytosis, elevated bilirubin and serum transaminases
o Ultrasound of abdomen
o Hepatobiliary nuclear scintigraphy
o CT & MRI
o ERCP – risk of perforation and pancreatitis
Left Untreated- may lead to gangrene of the gallbladder wall with rupture
peritonitis, septic shock, abscess (empyema), and fistulas (between gallbladder and
GI tract).
Treatment:
o Depends on severity of symptoms
o Surgeons like to let a hot gallbladder cool down first
o Broad-spectrum antibiotics
o Laparoscopic or open Cholecystectomy – Definitive treatment
o Chemodissolution
o ESWL (lithotripsy)
o Pain management
80% achieve remission with rest, IVF, NG suction, analgesia, and antibiotic agents.
Cholelithiasis (or gallstones)
o Supersaturation of bile with Cholesterol
o Become more prevalent with age
o Patho: 2 types composed of 1. Pigment and 2. Cholesterol.
Cholesterol stones account for 75% of stones
Are 2-3x more prevalent in women.
Black Pigment stones are associated with cirrhosis or hemolysis
, Brown Pigment stones are more common in developing countries from
parasites.
Risk Factors:
o High spinal cord injuries, TPN, prolonged fasting or rapid weight loss, and
pregnancy, oral contraceptives, obesity, diabetes, and octreotide .
o Female/Fair/Fat/Forty
o Most susceptible are Native Americans, White Europeans, and Asians, with the
lowest risk.
o In children, usually associated with cystic fibrosis or sickle cell
S/Sx’s:
o Often asymptomatic
o Mild GI Symptoms
o Epigastric Fullness
o Right Upper Quadrant Pain
Diagnosis
o Ultrasound
o Nuclear imaging studies (HIDA Scan)
o CT
o MRI
o Endoscopy (ERCP)
Chronic Cholecystitis
o Patho/Etiology
Persistent irritation/inflammation to gallbladder wall from cholelithiasis
Causes fibrosis and thickening r/t continued presence of gallstones.
Diabetes and obesity are predisposing factors.
Untreated – increased risk of cancer; sepsis
Can lead to calcified or porcelain gallbladder (from scarring) or biliary
sepsis, associated with higher risk of cancer.
o S/Sx: Same as acute
o Diagnosis: Same as acute
Chronic Cholelithiasis
o Patho/Etiology:
Incidence r/t age, gender, and variety of medical issues
, Gallstones are developed by
Supersaturation of bile with cholesterol
Nucleation of crystals
Hypomotility allowing stone growth
o S/SX:
Can be asymptomatic
Intermittent Biliary colic (persistent epigastric or RUQ pain that can
radiate to the back, accompanied by N/V, sweating, and
flatus/belching/blaoting lasting several hours. Caused by obstruction of
the cystic duct by a gallstone, rarely from spasm of the sphincter of Oddi.
Precipitated by a meal or occurs spontaneously
Pain increases steadily for 15 minutes and persists for an hour – slowly
decreases
Related fatty food intolerance
“Patient may think they are having a heart attack.”
Fever
Palpable mass
Nausea and vomiting after eating a heavy meal
Restlessness
Jaundice
Dark colored urine – from excretion of bile pigments.
Stool color greyish or clay-like (lack of bile pigments)
Vitamin A, D, E, & K deficiency – obstructed bile flow interferes with
absorption.
o Complications
Peritonitis
Gangrene
Post-procedure – bleeding, sepsis
Empyema
Pancreatitis
o Diagnosis
Abdominal X-Ray
Ultrasonography/Ultrasound - fastest and easiest test for abd RUQ pain
and sweating
