NUR2063: Essentials of Pathophysiology Exam 2 Blueprint- STUDY GUIDE

Essentials of Pathophysiology (NUR 2063) – Exam 2 blueprint 1

NUR2063: Essentials of Pathophysiology Exam 2 Blueprint
GI disorders

• Dysphagia Difficulty swallowing o Causes Nero disease: Parkinson’s,
dementias, muscular dystrophy, Huntington’s, ALS, MN, Guillain Barre
Syndrome. Other: Congenital issues/cerebral palsy, Esophageal stenosis,
esophageal diverticula, tumors, stroke, achalasia
• Vomiting – why and consequences Why: protect against substance, reverse
peristalsis, increase intracranial pressure, severe pain. Consequences: lead to
fluid, electrolyte, pH imbalance, aspiration o Emesis types and why the emesis
would be a problem Hematemesis: blood in vomit (protein),
Yellow/green: presence of bile. Deep brown: fecal matter. Undigested food o
Treatment of vomiting disorders Antiemetic med., fluid replacement, correct electrolyte
imbalance, restore acid-base
• Esophageal disorders o Hiatal hernia Stomach section protrudes through
diaphragm
 Causes: Weakening of diaphragm muscle, trauma, congenital defects.
 Manifestation: Indigestion; heartburn; frequent belching; nausea; chest pain; strictures;
dysphagia; and soft abdominal mass
 diagnosis: H & P; barium swallow; upper GI Xrays; EGD ,
 treatment: eat small meals, sleep elevated, antacid
o GERD
 Causes: Certain foods: chocolate, caffeine, carbonated beverages, citrus fruit,
tomatoes, spicy or fatty foods, peppermint
 Alcohol consumption; nicotine
 Hiatal hernia
 Obesity; pregnancy
 Certain medications – such as corticosteroids; beta blockers; calcium-channel blockers;
anticholinergics
 NG intubation
 Delayed gastric emptying
 Manifestations: Heartburn, Epigastric pain, Dysphagia, Dry cough, Laryngitis
Pharyngitis, Food regurgitation, Sensation of lump in throat
 Diagnosis: H & P; barium swallow; EGD; esophageal pH monitoring
 Treatments: Avoid triggers; avoid restrictive clothing
 Eat small frequent meals; high Fowler’s positioning, Weight loss; stress reduction;
Antacids; acid reducing agent; mucosal barrier agents, Herbal therapies (licorice,
chamomile), Surgery
 Complications : Esophagitis; strictures; ulcerations; esophageal cancer; chronic
pulmonary disease
o Gastritis/gastroenteritis
 Acute: Can be mild, transient irritation or can be severe ulceration with hemorrhage

,Essentials of Pathophysiology (NUR 2063) – Exam 2 blueprint 2
 Usually develops suddenly
 Likely to also have nausea & epigastric pain

 Chronic: Develops gradually
 May be asymptomatic but usually accompanied by dull epigastric pain and a sensation
of fullness after minimal intake
 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:
acidreducers) 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

, Essentials of Pathophysiology (NUR 2063) – Exam 2 blueprint 3
 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
 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