Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018
CHOLELITHIASIS
Disorder of the Biliary Tract. Cholelithiasis involves the presence of gallstones, which
are concretions that form in the biliary tract, usually in the gallbladder. Gallstones are
“fatty stones” formed by the buildup of cholesterol. The cause is unknown. A blockage in
the common bile duct affects the liver, as it prevents the release of bile. A blockage
farther down from here affects the pancreas.
RISK FACTORS:
MEDICATIONS:
SIGNS & SYMPTOMS: 1. Female
1. Anticholinergics
Asymptomatic until the stones start 2. >40 years of age
2. Antispasmodics
moving through the ducts. 3. Sedentary lifestyle
3. Antiemetics
1. Abdominal pain (often radiates) 4. Obesity
2. Cramping (constant pain) 5. Genetics
3. N & V 4. Diaphoretic LAB FINDINGS: 1. Increased Liver Enzymes 2. Increased WBC
r/t Inflammation of the gallbladder 3. Increased serum amalyze if the pancreas is
involved 4. Increased bilirubin?
5. Restlessness 6. Fever 7. Indigestion 8. Food intolerance 9. Obstructive jaundice
TREATMENTS
DO: 1. Give Pain medications 2. Give medications to treat N/V 3. Control infection 4.
Maintain fluid & electrolyte imbalance 5. Replace fat soluble vitamins (A,D,E,K) 6. NG
inserted on suction to remove fluid if PATIENT TEACHING: 1. Low fat diet when person
can eat, avoid
whole fat dairy products, foods, pastries, gravies, nuts
distention is present 7. Removal of Gallbladder 8. NPO with gastric decompression if
nausea and vomiting is severe
DIAGNOSTIC TOOLS: Ultrasound ERCP: Endoscopic retrograde
cholangiopancreatography 1. ASSESSMENTS:
COMPLICATIONS: 1. ABCs
1. Pancreatitis 2. Initial assessment: Objective &
Subjective data 3. Pain Assessment 4. Vital Signs
2. Biliary cirrhosis 3. Fistulas 4. Rupture of gall bladder & peritonitis 5. Gangrenous
gall bladder
Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018
CHOLECYSTITIS
Disorder of the Biliary Tract. Cholecystitis is inflammation of the gallbladder, a small
organ near the liver that plays a part in digesting food. Normally, fluid called bile passes
,out of the gallbladder on its way to the small intestine. If the flow of bile is blocked, it
builds up inside the gallbladder, causing swelling, pain, and possible infection.
CAUSES: Stones lodged into neck of gall bladder or cystic duct or acalculous cystitis
RISK FACTORS: 6. Surgery 7. Immobility 8. Recent TPN 9. Diabetes Mellitus 10.
Elderly 11. Women 12. Burns 13. Trauma 14. Bacterial infections (E.
coli) 15. Cancer
LAB FINDINGS: 1. Increased Liver Enzymes 2. Increased WBC r/t Inflammation of the
gallbladder 3. Increased serum amalyze if the pancreas is involved 4. Increased
bilirubin? 16.
TREATMENTS
DO: 1. Control pain 2. Control infection 3. Maintain fluid and electrolyte balance 4. NPO
with gastric decompression if
nausea and vomiting is severe 5. Replace fat soluble vitamins: A D E K
and bile salts 6. Anticholinergics, antispasmodics 7. Low fat diet when person can eat,
avoid whole fat dairy products foods, pastries, gravies, nuts 8.
MEDICATIONS:
SIGNS & SYMPTOMS: 1. Anticholinergics
1. burning to stomach 2. Antispasmodics 2. Distention
3. Restlessness 4. Tenderness to abdomen on palpation
COMPLICATIONS: 6. Pancreatitis 7. Biliary cirrhosis 8. Fistulas 9. Rupture of gall
bladder & peritonitis 10. Gangrenous gall bladder
ASSESSMENTS: 1. ABCs 2. Objective & Subjective data 3. Pain Assessment 4. Vital
Signs
DIAGNOSTIC TOOLS/PROCEDURES: 1. Ultrasound: hard to determine if there were
stones if looked at after the fact. 2. ERCP: special scope to study bio duct to
visualize what’s happening. Assessing the drainage routes to make sure everything is
flowing. If there is a stone, sometimes they can remove it 3. Extracorporeal shock wave
lithotripsy
(ESWL) used to break up stones 4. Cholecystectomy: removal of gallbladder 5.
Choledocholithotomy- incision into bile duct
& removal of stones 6.
Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018 HEPATITIS
PATHO
Inflammation of liver that results in damage or necrosis of hepatocytes, blockage of
bile flow. Acute phase < 6 months in duration can end with liver failure or death. Most
common cause of hepatitis is viral Other: drug induced, abdominal trauma, or an
autoimmune process
,Toxic & Drug Induced Hepatitis: 1. Hepatitis D 1. Incomplete virus 2.
Similar to viral 2. Treatment is Needs B- transmitted thru
supportive 3. Usually quick recovery 4. blood. 3. No current vaccine
First 6 months 5. Overdose of Tylenol:
life threatening situation 6. Liver Hepatitis E 1. Similar to A 2. Fecal-oral
cleanses route 3. No vaccine 4.
Hepatitis A 1. Low incidence 2. PHASES: 1. Preicteric/prodromal
Common in children 3. Vaccine phase
available 4. Fecal/oral HAV: Maximum infectivity from 1-21
Hepatitis B 1. Most prevalent 2. Blood days HBV: can be infective for years
& fluids 3. Causes acute & chronic 4. People may be asymptomatic, or have
Vaccine available 5. Can live on flu like symptoms: Malaise, headache,
intimate surfaces for up to 7 low grade fever, arthralgia's (joint pain),
Hepatitis B 1. Most prevalent 2. Blood skin rashes On examination:
& fluids 3. Causes acute & chronic 4. hepatomegaly, splenomegaly,
Vaccine available 5. Can live on lymphadenopathy
intimate surfaces for up to 7
days. 2. Icteric phase “CHARACTERIZED
Hepatitis C 1. common cause of liver BY JAUNDICE”
t/p 2. blood & fluids 3. Often Lasts from 2-4 weeks Urine may be
asymptomatic 4. Causes chronic dark amber, stools light or clay colored
diseases 5. No vaccine Pruritus: secretion of bile salts in skin
Hepatitis C 1. common cause of liver When jaundice occurs... Fatigue,
t/p 2. blood & fluids 3. Often Weight loss, Liver is enlarged and
asymptomatic 4. Causes chronic tenderness
diseases 5. No vaccine
Hepatitis C 1. common cause of liver 3. Posticteric/convalescent phase
t/p 2. blood & fluids 3. Often Jaundice disappears. can last from
asymptomatic 4. Causes chronic weeks to months. Disappearance of
diseases 5. No vaccine jaundice does not mean person has
recovered Major complaint is malaise
and patient is easily fatigued
Hepatomegaly lasts for several weeks,
Hepatitis G 1. Usually seen with B or C the spleen starts to return to normal
2. Found in blood donor size The spleen is enlarged r/t to
inflamed liver which backs up blood and
goes into spleen
Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018 HEPATITIS
Inflammation of liver that results in damage or necrosis of hepatocytes, blockage of
bile flow. Acute phase < 6 months in duration can end with liver failure or death. Most
, common cause of hepatitis is viral Other: drug induced, abdominal trauma, or an
autoimmune process
RISK FACTORS: 1. recent incarceration 2. Sex (males 2X more likely) 3. Age 4. IV
drug user 5. Overcrowded housing 6. Low education level 7. Low income
CAUSES: 1. IV drug use 2. Recent exposure to the
virus
SIGNS & SYMPTOMS: 1. N/V/D 2. RUQ pain 3. Diminished senses 4. Headaches 5.
General malaise 6. Weight loss
NURSING ASSESSMENT: 1. Assess subjective Data, objective data
S&S of Hepatitis 2. Blood work monitored. 3. COAGs studies: aptt, INR 4. Liver function
tests 5. Ammonia levels
MEDICATIONS: - Pegasys (sub-Q) - Ribavirin (PO) - Victrelis (PO) **To treat the HEP
virus** - Anti-emetics - Diphenhydramine COMPLICATIONS:
DIAGNOSTIC TOOLS: HEP A: can cause hepatic failure, but not chronic hepatitis
1. Recent/previous health history HEP B: can cause hepatic failure, or chronic hepatitis
or Fibrosis
2. Physical Assessment of liver
3. Viral Studies HEP C: can become chronic, progress to cirrhosis, and cause
4. PCR assay (HCV RNA) hepatocellular carcinoma
COLLABORATIVE PATIENT TEACHING:
& PATIENT TEACHING: 1. Minimal high risk activities
1. Rest important to assist liver in regenerating 2. Medication compliance
2. Watch patient for bleeding 3. Rest!
3. High calorie high protein, high carb, low fat diet, 4. When to seek medical attention
small frequent meals 5. Get Hepatitis Vaccine, encourage
4. Avoid: alcohol and drugs detoxified in liver hand hygiene
5. Avoid NSAIDs (Advil, Aspirin) 6. Supportive therapy: anti-emetics, diphenhydramine
LAB VALUES: 1. Liver Function 2. COAGS: apt, INR 3. Ammonia levels
Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018 CIRRHOSIS OF
THE LIVER
The liver is injured or inflamed and hepatocytes are damaged. Produces fibrosis or scar
tissue and nodules. Scar tissue builds up causing nodules that occur inside and out.
These nodules can impede blood flow. Occurs in 40-60 year olds.
CAUSES: A. PRIMARY: Alcoholism, Hepatitis B. SECONDARY: Obesity, genetics,
medications, toxins/infections, malnutrition
CLINICAL MANIFESTATIONS: Gastrointestinal: 1. Anorexia, N/V/D, Constipation,
RUQ pain,
weight loss, Dyspepsia, flatulence 2. Splenomegaly 3. Ascites (fluid in abdomen)
Cardiovascular/Neurological: 1. Tachycardia and overall vasodilation 2. Decreased
SVR 3. hepatic encephalopathy 4. peripheral neuropathy
CHOLELITHIASIS
Disorder of the Biliary Tract. Cholelithiasis involves the presence of gallstones, which
are concretions that form in the biliary tract, usually in the gallbladder. Gallstones are
“fatty stones” formed by the buildup of cholesterol. The cause is unknown. A blockage in
the common bile duct affects the liver, as it prevents the release of bile. A blockage
farther down from here affects the pancreas.
RISK FACTORS:
MEDICATIONS:
SIGNS & SYMPTOMS: 1. Female
1. Anticholinergics
Asymptomatic until the stones start 2. >40 years of age
2. Antispasmodics
moving through the ducts. 3. Sedentary lifestyle
3. Antiemetics
1. Abdominal pain (often radiates) 4. Obesity
2. Cramping (constant pain) 5. Genetics
3. N & V 4. Diaphoretic LAB FINDINGS: 1. Increased Liver Enzymes 2. Increased WBC
r/t Inflammation of the gallbladder 3. Increased serum amalyze if the pancreas is
involved 4. Increased bilirubin?
5. Restlessness 6. Fever 7. Indigestion 8. Food intolerance 9. Obstructive jaundice
TREATMENTS
DO: 1. Give Pain medications 2. Give medications to treat N/V 3. Control infection 4.
Maintain fluid & electrolyte imbalance 5. Replace fat soluble vitamins (A,D,E,K) 6. NG
inserted on suction to remove fluid if PATIENT TEACHING: 1. Low fat diet when person
can eat, avoid
whole fat dairy products, foods, pastries, gravies, nuts
distention is present 7. Removal of Gallbladder 8. NPO with gastric decompression if
nausea and vomiting is severe
DIAGNOSTIC TOOLS: Ultrasound ERCP: Endoscopic retrograde
cholangiopancreatography 1. ASSESSMENTS:
COMPLICATIONS: 1. ABCs
1. Pancreatitis 2. Initial assessment: Objective &
Subjective data 3. Pain Assessment 4. Vital Signs
2. Biliary cirrhosis 3. Fistulas 4. Rupture of gall bladder & peritonitis 5. Gangrenous
gall bladder
Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018
CHOLECYSTITIS
Disorder of the Biliary Tract. Cholecystitis is inflammation of the gallbladder, a small
organ near the liver that plays a part in digesting food. Normally, fluid called bile passes
,out of the gallbladder on its way to the small intestine. If the flow of bile is blocked, it
builds up inside the gallbladder, causing swelling, pain, and possible infection.
CAUSES: Stones lodged into neck of gall bladder or cystic duct or acalculous cystitis
RISK FACTORS: 6. Surgery 7. Immobility 8. Recent TPN 9. Diabetes Mellitus 10.
Elderly 11. Women 12. Burns 13. Trauma 14. Bacterial infections (E.
coli) 15. Cancer
LAB FINDINGS: 1. Increased Liver Enzymes 2. Increased WBC r/t Inflammation of the
gallbladder 3. Increased serum amalyze if the pancreas is involved 4. Increased
bilirubin? 16.
TREATMENTS
DO: 1. Control pain 2. Control infection 3. Maintain fluid and electrolyte balance 4. NPO
with gastric decompression if
nausea and vomiting is severe 5. Replace fat soluble vitamins: A D E K
and bile salts 6. Anticholinergics, antispasmodics 7. Low fat diet when person can eat,
avoid whole fat dairy products foods, pastries, gravies, nuts 8.
MEDICATIONS:
SIGNS & SYMPTOMS: 1. Anticholinergics
1. burning to stomach 2. Antispasmodics 2. Distention
3. Restlessness 4. Tenderness to abdomen on palpation
COMPLICATIONS: 6. Pancreatitis 7. Biliary cirrhosis 8. Fistulas 9. Rupture of gall
bladder & peritonitis 10. Gangrenous gall bladder
ASSESSMENTS: 1. ABCs 2. Objective & Subjective data 3. Pain Assessment 4. Vital
Signs
DIAGNOSTIC TOOLS/PROCEDURES: 1. Ultrasound: hard to determine if there were
stones if looked at after the fact. 2. ERCP: special scope to study bio duct to
visualize what’s happening. Assessing the drainage routes to make sure everything is
flowing. If there is a stone, sometimes they can remove it 3. Extracorporeal shock wave
lithotripsy
(ESWL) used to break up stones 4. Cholecystectomy: removal of gallbladder 5.
Choledocholithotomy- incision into bile duct
& removal of stones 6.
Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018 HEPATITIS
PATHO
Inflammation of liver that results in damage or necrosis of hepatocytes, blockage of
bile flow. Acute phase < 6 months in duration can end with liver failure or death. Most
common cause of hepatitis is viral Other: drug induced, abdominal trauma, or an
autoimmune process
,Toxic & Drug Induced Hepatitis: 1. Hepatitis D 1. Incomplete virus 2.
Similar to viral 2. Treatment is Needs B- transmitted thru
supportive 3. Usually quick recovery 4. blood. 3. No current vaccine
First 6 months 5. Overdose of Tylenol:
life threatening situation 6. Liver Hepatitis E 1. Similar to A 2. Fecal-oral
cleanses route 3. No vaccine 4.
Hepatitis A 1. Low incidence 2. PHASES: 1. Preicteric/prodromal
Common in children 3. Vaccine phase
available 4. Fecal/oral HAV: Maximum infectivity from 1-21
Hepatitis B 1. Most prevalent 2. Blood days HBV: can be infective for years
& fluids 3. Causes acute & chronic 4. People may be asymptomatic, or have
Vaccine available 5. Can live on flu like symptoms: Malaise, headache,
intimate surfaces for up to 7 low grade fever, arthralgia's (joint pain),
Hepatitis B 1. Most prevalent 2. Blood skin rashes On examination:
& fluids 3. Causes acute & chronic 4. hepatomegaly, splenomegaly,
Vaccine available 5. Can live on lymphadenopathy
intimate surfaces for up to 7
days. 2. Icteric phase “CHARACTERIZED
Hepatitis C 1. common cause of liver BY JAUNDICE”
t/p 2. blood & fluids 3. Often Lasts from 2-4 weeks Urine may be
asymptomatic 4. Causes chronic dark amber, stools light or clay colored
diseases 5. No vaccine Pruritus: secretion of bile salts in skin
Hepatitis C 1. common cause of liver When jaundice occurs... Fatigue,
t/p 2. blood & fluids 3. Often Weight loss, Liver is enlarged and
asymptomatic 4. Causes chronic tenderness
diseases 5. No vaccine
Hepatitis C 1. common cause of liver 3. Posticteric/convalescent phase
t/p 2. blood & fluids 3. Often Jaundice disappears. can last from
asymptomatic 4. Causes chronic weeks to months. Disappearance of
diseases 5. No vaccine jaundice does not mean person has
recovered Major complaint is malaise
and patient is easily fatigued
Hepatomegaly lasts for several weeks,
Hepatitis G 1. Usually seen with B or C the spleen starts to return to normal
2. Found in blood donor size The spleen is enlarged r/t to
inflamed liver which backs up blood and
goes into spleen
Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018 HEPATITIS
Inflammation of liver that results in damage or necrosis of hepatocytes, blockage of
bile flow. Acute phase < 6 months in duration can end with liver failure or death. Most
, common cause of hepatitis is viral Other: drug induced, abdominal trauma, or an
autoimmune process
RISK FACTORS: 1. recent incarceration 2. Sex (males 2X more likely) 3. Age 4. IV
drug user 5. Overcrowded housing 6. Low education level 7. Low income
CAUSES: 1. IV drug use 2. Recent exposure to the
virus
SIGNS & SYMPTOMS: 1. N/V/D 2. RUQ pain 3. Diminished senses 4. Headaches 5.
General malaise 6. Weight loss
NURSING ASSESSMENT: 1. Assess subjective Data, objective data
S&S of Hepatitis 2. Blood work monitored. 3. COAGs studies: aptt, INR 4. Liver function
tests 5. Ammonia levels
MEDICATIONS: - Pegasys (sub-Q) - Ribavirin (PO) - Victrelis (PO) **To treat the HEP
virus** - Anti-emetics - Diphenhydramine COMPLICATIONS:
DIAGNOSTIC TOOLS: HEP A: can cause hepatic failure, but not chronic hepatitis
1. Recent/previous health history HEP B: can cause hepatic failure, or chronic hepatitis
or Fibrosis
2. Physical Assessment of liver
3. Viral Studies HEP C: can become chronic, progress to cirrhosis, and cause
4. PCR assay (HCV RNA) hepatocellular carcinoma
COLLABORATIVE PATIENT TEACHING:
& PATIENT TEACHING: 1. Minimal high risk activities
1. Rest important to assist liver in regenerating 2. Medication compliance
2. Watch patient for bleeding 3. Rest!
3. High calorie high protein, high carb, low fat diet, 4. When to seek medical attention
small frequent meals 5. Get Hepatitis Vaccine, encourage
4. Avoid: alcohol and drugs detoxified in liver hand hygiene
5. Avoid NSAIDs (Advil, Aspirin) 6. Supportive therapy: anti-emetics, diphenhydramine
LAB VALUES: 1. Liver Function 2. COAGS: apt, INR 3. Ammonia levels
Megan Seiferling – SCBScN Program CNUR 204 OSCE PREP 2018 CIRRHOSIS OF
THE LIVER
The liver is injured or inflamed and hepatocytes are damaged. Produces fibrosis or scar
tissue and nodules. Scar tissue builds up causing nodules that occur inside and out.
These nodules can impede blood flow. Occurs in 40-60 year olds.
CAUSES: A. PRIMARY: Alcoholism, Hepatitis B. SECONDARY: Obesity, genetics,
medications, toxins/infections, malnutrition
CLINICAL MANIFESTATIONS: Gastrointestinal: 1. Anorexia, N/V/D, Constipation,
RUQ pain,
weight loss, Dyspepsia, flatulence 2. Splenomegaly 3. Ascites (fluid in abdomen)
Cardiovascular/Neurological: 1. Tachycardia and overall vasodilation 2. Decreased
SVR 3. hepatic encephalopathy 4. peripheral neuropathy
