NUR 2063 NURSING PATHOPHYSIOLOGY
STUDY NOTES
, 1
▪ complications: peptic ulcer; gastric cancer; hemorrhage
▪ h. pylori: most common cause of chronic gastritis
▪ bacteria embeds in mucous layer; activates toxins & enzymes that cause inflammation
▪ genetic vulnerability & lifestyle behaviors (smoking, stress) may increase susceptible
▪ other causes: organisms through food/water contamination, lt nsaid use, excess alcohol
use, severe stress, autoimmune conditions
▪ manifestations of gi bleeding: indigestion; heart burn, epigastric pain; abdominal
cramping, n/v; anorexia, fever; malaise, hematemesis, dark, tarry stools = ulceration &
bleeding
• gi tract disorders o
peptic ulcer disease
▪ duodenal: most commonly associated with excess acid or h.pylori infections, typically
present with epigastric pain relieved by food
▪ gastric: less frequent; more deadly, typically associated with malignancy and nsaids, pain
worsens with food
▪ symptoms
▪ curling’s ulcer from what: associated with burns
▪ cushing’s ulcer from what: associated with head injuries
▪ complications of ulcers: gi hemorrhage; obstruction; perforation; peritonitis
▪ manifestations: epigastric or abdominal pain, abdominal cramping, heartburn; indigestion,
n/v
▪ diagnosis: same as gastritis
▪ treatment: same as for gastritis, surgical repair may be necessary for perforated or
bleeding ulcers, prevention is crucial – may need prophylactic medications (ex: acid-
reducers) for at-risk clients
o gallbladder disorders
▪ cholelithiasis: gallbladder stones
▪ cholecystitis: inflammation or infection in the biliary system caused by calculi
▪ manifestations: biliary colic; abdominal distension; n/v; jaundice; fever; leukocytosis
▪ diagnosis: h & p; abdominal xray; gallbladder us; laparoscopy
▪ treatments: low-fat diet, medications to dissolve calculi, antibiotic therapy, ng tube with
intermittent sxn, lithotripsy, choledochostomy, laparoscopic surgery
o liver disorders
▪ hepatitis – infectious: a, b, c, d, e vs. noninfectious: giant cell hepatitis, ischemic hepatitis,
non-alcoholic fatty liver hepatitis, autoimmune hepatitis, toxic & drug-induced hepatitis,
alcoholic hepatitis
▪ transmission of viral hepatitis: if it’s a vowel, it comes from the bowel. all others are
blood
▪ define: acute: proceeds through 4 stages—asymptomatic stage then 3 symptomatic stages
chronic: characterized by continued liver disease > 6 months
▪ symptom severity and disease progression vary by degree of liver damage
, 2
▪ can quickly deteriorate with declining liver integrity fulminant: uncommon, rapidly
progressing form that can quickly lead to
▪ liver failure, hepatic encephalopathy, or death within 3 wks
• diagnosis: h & p, serum hepatitis profile, liver enzymes, clotting studies, liver
biopsy, abdominal us
• treatment for viral hepatitis: treat with interferon & antiviral mediations
▪ cirrhosis
• common causes: hepatitis and all factors that can lead to hepatitis, hep c and
chronic alcohol abuse most common cause in u.s.
• what happens to liver: leads to fibrosis, nodule formation, impaired blood flow,
and bile obstruction liver failure
• manifestations: portal hypertension, varicosities, bleeding –slow or severe,
muscle wasting, bile accumulation, clay-colored stools, dark urine, ulcers/gi
bleeding, encephalopathy, spontaneous bacterial peritonitis
• diagnosis: h & p; liver biopsy; abdominal xray; liver enzymes; egd; clotting
studies; stool exam for occult blood
• treatments: avoid alcohol, drugs, hepatotoxic meds, nutritional imbalances
usually treated with tpn; metabolic dysfunction corrected, bile-acid binding
agents can aid bile excretion
• hepatic encephalopathy
o pancreatitis
▪ causes: cholelithiasis, alcohol abuse, biliary dysfunction, hepatotoxic drugs, metabolic
disorders, trauma, renal failure, endocrine disorders, pancreatic tumors, penetrating
peptic ulcer
▪ what happens to the pancreas in the disorder? pancreatic enzymes to leak into the
pancreatic tissue and initiate autodigestion - -results in edema, vascular damage,
hemorrhage & necrosis
▪ acute pancreatitis importance & complications: medical emergency, acute respiratory
distress syndrome (ards), dm, infection, shock, disseminated intravascular coagulation
(dic), renal failure, malnutrition, pancreatic cancer, pseudocyst, abscess
• manifestations: sudden and severe,
upper abdominal pain that radiates to
the back, worsens after eating,
somewhat relieved by leaning forward
or pulling knees to chest, n/v, mild
jaundice, low-grade fever, bp and pulse
changes
▪ chronic pancreatitis manifestations: usually insidious, upper abdominal pain, indigestion,
losing weight without trying, steatorrhea, constipation, flatulence
▪ pancreatitis diagnosis: h & p, serum amylase & lipase, serum calcium level, cbc, liver
enzymes, serum bilirubin level, abg, stool analysis (lipid & trypsin levels), abdominal
xray, ct/mri, abdominal us, ercp (endoscopic retrograde cholangiopancreatography)
▪ treatment: fasting; administer iv nutrition; gradually advance diet from clears as
tolerated to low fat, pancreatic enzyme supplements when diet resumed, maintain
STUDY NOTES
, 1
▪ complications: peptic ulcer; gastric cancer; hemorrhage
▪ h. pylori: most common cause of chronic gastritis
▪ bacteria embeds in mucous layer; activates toxins & enzymes that cause inflammation
▪ genetic vulnerability & lifestyle behaviors (smoking, stress) may increase susceptible
▪ other causes: organisms through food/water contamination, lt nsaid use, excess alcohol
use, severe stress, autoimmune conditions
▪ manifestations of gi bleeding: indigestion; heart burn, epigastric pain; abdominal
cramping, n/v; anorexia, fever; malaise, hematemesis, dark, tarry stools = ulceration &
bleeding
• gi tract disorders o
peptic ulcer disease
▪ duodenal: most commonly associated with excess acid or h.pylori infections, typically
present with epigastric pain relieved by food
▪ gastric: less frequent; more deadly, typically associated with malignancy and nsaids, pain
worsens with food
▪ symptoms
▪ curling’s ulcer from what: associated with burns
▪ cushing’s ulcer from what: associated with head injuries
▪ complications of ulcers: gi hemorrhage; obstruction; perforation; peritonitis
▪ manifestations: epigastric or abdominal pain, abdominal cramping, heartburn; indigestion,
n/v
▪ diagnosis: same as gastritis
▪ treatment: same as for gastritis, surgical repair may be necessary for perforated or
bleeding ulcers, prevention is crucial – may need prophylactic medications (ex: acid-
reducers) for at-risk clients
o gallbladder disorders
▪ cholelithiasis: gallbladder stones
▪ cholecystitis: inflammation or infection in the biliary system caused by calculi
▪ manifestations: biliary colic; abdominal distension; n/v; jaundice; fever; leukocytosis
▪ diagnosis: h & p; abdominal xray; gallbladder us; laparoscopy
▪ treatments: low-fat diet, medications to dissolve calculi, antibiotic therapy, ng tube with
intermittent sxn, lithotripsy, choledochostomy, laparoscopic surgery
o liver disorders
▪ hepatitis – infectious: a, b, c, d, e vs. noninfectious: giant cell hepatitis, ischemic hepatitis,
non-alcoholic fatty liver hepatitis, autoimmune hepatitis, toxic & drug-induced hepatitis,
alcoholic hepatitis
▪ transmission of viral hepatitis: if it’s a vowel, it comes from the bowel. all others are
blood
▪ define: acute: proceeds through 4 stages—asymptomatic stage then 3 symptomatic stages
chronic: characterized by continued liver disease > 6 months
▪ symptom severity and disease progression vary by degree of liver damage
, 2
▪ can quickly deteriorate with declining liver integrity fulminant: uncommon, rapidly
progressing form that can quickly lead to
▪ liver failure, hepatic encephalopathy, or death within 3 wks
• diagnosis: h & p, serum hepatitis profile, liver enzymes, clotting studies, liver
biopsy, abdominal us
• treatment for viral hepatitis: treat with interferon & antiviral mediations
▪ cirrhosis
• common causes: hepatitis and all factors that can lead to hepatitis, hep c and
chronic alcohol abuse most common cause in u.s.
• what happens to liver: leads to fibrosis, nodule formation, impaired blood flow,
and bile obstruction liver failure
• manifestations: portal hypertension, varicosities, bleeding –slow or severe,
muscle wasting, bile accumulation, clay-colored stools, dark urine, ulcers/gi
bleeding, encephalopathy, spontaneous bacterial peritonitis
• diagnosis: h & p; liver biopsy; abdominal xray; liver enzymes; egd; clotting
studies; stool exam for occult blood
• treatments: avoid alcohol, drugs, hepatotoxic meds, nutritional imbalances
usually treated with tpn; metabolic dysfunction corrected, bile-acid binding
agents can aid bile excretion
• hepatic encephalopathy
o pancreatitis
▪ causes: cholelithiasis, alcohol abuse, biliary dysfunction, hepatotoxic drugs, metabolic
disorders, trauma, renal failure, endocrine disorders, pancreatic tumors, penetrating
peptic ulcer
▪ what happens to the pancreas in the disorder? pancreatic enzymes to leak into the
pancreatic tissue and initiate autodigestion - -results in edema, vascular damage,
hemorrhage & necrosis
▪ acute pancreatitis importance & complications: medical emergency, acute respiratory
distress syndrome (ards), dm, infection, shock, disseminated intravascular coagulation
(dic), renal failure, malnutrition, pancreatic cancer, pseudocyst, abscess
• manifestations: sudden and severe,
upper abdominal pain that radiates to
the back, worsens after eating,
somewhat relieved by leaning forward
or pulling knees to chest, n/v, mild
jaundice, low-grade fever, bp and pulse
changes
▪ chronic pancreatitis manifestations: usually insidious, upper abdominal pain, indigestion,
losing weight without trying, steatorrhea, constipation, flatulence
▪ pancreatitis diagnosis: h & p, serum amylase & lipase, serum calcium level, cbc, liver
enzymes, serum bilirubin level, abg, stool analysis (lipid & trypsin levels), abdominal
xray, ct/mri, abdominal us, ercp (endoscopic retrograde cholangiopancreatography)
▪ treatment: fasting; administer iv nutrition; gradually advance diet from clears as
tolerated to low fat, pancreatic enzyme supplements when diet resumed, maintain
