CNUR 204 NEWEST ACTUAL EXAM WITH COMPLETE
QUESTIONS WITH ANSWERS/ VERIFIED/GRADED A+/
GUARANTEED PASS
Subjective data for GI
-HPI (history of present illness)-including OPQRSTUV
-PMHx (past medical history)
-GI related questions
-Appetite; N&V; dysphagia; bowel habits; food intake; food
intolerance...
-Family history
-Medications
-Psycho-social history
-Use of alcohol & tobacco
-Any stressful events, look at chart- -Lab values & recent
diagnostics : any significance related to the current situation
-Other notes (consultation reports...)
Jaundice (icterus)
•Hyperbilirubinemia
-Alteration in normal bilirubin metabolism/flow
•Symptom rather than a disease
•Yellowish discoloration of body tissues- Mucosal membrane
may show jaundice
-Appears on the sclera & skin
Page 1 of 335
,•Usually appears when serum bilirubin level is higher than 34
mcmol/L (twice the normal upper limit)
Jaundice is usually first observed in the sclera and later in the
skin, types can overlap- Pre-hepatic Jaundice
Occurs with an increase in bilirubin; over production of
unconjugated bilirubin (i.e., hemolysis)- can occur with
incorrect blood transfusions, sickle cell anemia
Hepatic Jaundice
Caused by inability to take up bilirubin by the liver due to
damaged liver cells (cirrhosis; hepatitis; hepatocellular
carcinoma)- damage to liver
Post-hepatic Jaundice (or cholestatic)
Failure for bile to reach the duodenum due to obstruction of
bile flow
Intrahepatic obstructions (i.e., fibrosis or swelling of the liver's
canaliculi/bile ducts from hepatitis, cirrhosis)
Extrahepatic obstructions (i.e., obstruction of common bile
duct from gallstones; pancreatic cancer..)
A & P of Bilirubin
Bilirubin is not water soluble- sticks to albumin to get to liver
(unconjugated)- still not water soluble, needs to conjugate so
it is water soluble and can be excreted in the bile (metabolize
fat for digestion), serobilirubin- brown colour to feces, some
urobiliogen can be excreted in the kidneys
Page 2 of 335
,Liver, gallbladder, pancreas
Liver produces bile, goes into gall bladder, and common bile
duct, enzyme comes out of pancreatic duct and mixes in
duodenum for digestion
Bile may not be able to go through- post hepatic jaundice
Hepatitis
•Involves widespread Inflammation of liver tissue
•During acute infection:
-Mediated by cytotoxic cytokines & natural killer cells- cause
lysis of infected hepatocytes-liver cell necrosis
-Inflammation interrupt bile flow- cholestasis-liver cell
damage
•With no complications, liver cells can regenerate with
complete recovery
•With massive liver cell loss, may progress to chronic hepatitis
and cause further complications (e.g., chronic hepatitis leading
to cirrhosis), -The most common cause of hepatitis is a viral
infection
-Hepatitis A, B, C, D, E virus
-Cytomegalovirus
-Epstein-Barr virus
-Herpes virus
-Coxsackie virus
-Rubella virus
Page 3 of 335
, -Other possible causes
§Drugs (alcohol)
§Chemicals
§Autoimmune liver disease
§Metabolic disorders
§Genetic abnormalities, •Depending on the stage/types of the
liver condition & other disorders
•No symptoms in individuals with immunosuppressed
condition
•30% of patients with HBV are asymptomatic.
•80% of patients with acute HCV will be asymptomatic, HAV has
symptoms
Extent of burns
•Total body surface area (TBSA) affected by burn (Lund-
Browder chart- more precise and accurate & Rule of nines
chart- initital assessment)
•Patchy burns (e.g., irregular/odd shaped) can be estimated
using patient's hand as 1% TBSA, superficial partial thickness
burns not measured by TBSA
•Online tools & App are available for TBSA estimation
•First degree burns, equivalent to a sunburn are not included
when TBSA burned is calculated.
•The Lund browder chart is considered more accurate because
the patient's age, in proportion to relative body are size, is
taken into account. The rule of nines which is easy to
Page 4 of 335
QUESTIONS WITH ANSWERS/ VERIFIED/GRADED A+/
GUARANTEED PASS
Subjective data for GI
-HPI (history of present illness)-including OPQRSTUV
-PMHx (past medical history)
-GI related questions
-Appetite; N&V; dysphagia; bowel habits; food intake; food
intolerance...
-Family history
-Medications
-Psycho-social history
-Use of alcohol & tobacco
-Any stressful events, look at chart- -Lab values & recent
diagnostics : any significance related to the current situation
-Other notes (consultation reports...)
Jaundice (icterus)
•Hyperbilirubinemia
-Alteration in normal bilirubin metabolism/flow
•Symptom rather than a disease
•Yellowish discoloration of body tissues- Mucosal membrane
may show jaundice
-Appears on the sclera & skin
Page 1 of 335
,•Usually appears when serum bilirubin level is higher than 34
mcmol/L (twice the normal upper limit)
Jaundice is usually first observed in the sclera and later in the
skin, types can overlap- Pre-hepatic Jaundice
Occurs with an increase in bilirubin; over production of
unconjugated bilirubin (i.e., hemolysis)- can occur with
incorrect blood transfusions, sickle cell anemia
Hepatic Jaundice
Caused by inability to take up bilirubin by the liver due to
damaged liver cells (cirrhosis; hepatitis; hepatocellular
carcinoma)- damage to liver
Post-hepatic Jaundice (or cholestatic)
Failure for bile to reach the duodenum due to obstruction of
bile flow
Intrahepatic obstructions (i.e., fibrosis or swelling of the liver's
canaliculi/bile ducts from hepatitis, cirrhosis)
Extrahepatic obstructions (i.e., obstruction of common bile
duct from gallstones; pancreatic cancer..)
A & P of Bilirubin
Bilirubin is not water soluble- sticks to albumin to get to liver
(unconjugated)- still not water soluble, needs to conjugate so
it is water soluble and can be excreted in the bile (metabolize
fat for digestion), serobilirubin- brown colour to feces, some
urobiliogen can be excreted in the kidneys
Page 2 of 335
,Liver, gallbladder, pancreas
Liver produces bile, goes into gall bladder, and common bile
duct, enzyme comes out of pancreatic duct and mixes in
duodenum for digestion
Bile may not be able to go through- post hepatic jaundice
Hepatitis
•Involves widespread Inflammation of liver tissue
•During acute infection:
-Mediated by cytotoxic cytokines & natural killer cells- cause
lysis of infected hepatocytes-liver cell necrosis
-Inflammation interrupt bile flow- cholestasis-liver cell
damage
•With no complications, liver cells can regenerate with
complete recovery
•With massive liver cell loss, may progress to chronic hepatitis
and cause further complications (e.g., chronic hepatitis leading
to cirrhosis), -The most common cause of hepatitis is a viral
infection
-Hepatitis A, B, C, D, E virus
-Cytomegalovirus
-Epstein-Barr virus
-Herpes virus
-Coxsackie virus
-Rubella virus
Page 3 of 335
, -Other possible causes
§Drugs (alcohol)
§Chemicals
§Autoimmune liver disease
§Metabolic disorders
§Genetic abnormalities, •Depending on the stage/types of the
liver condition & other disorders
•No symptoms in individuals with immunosuppressed
condition
•30% of patients with HBV are asymptomatic.
•80% of patients with acute HCV will be asymptomatic, HAV has
symptoms
Extent of burns
•Total body surface area (TBSA) affected by burn (Lund-
Browder chart- more precise and accurate & Rule of nines
chart- initital assessment)
•Patchy burns (e.g., irregular/odd shaped) can be estimated
using patient's hand as 1% TBSA, superficial partial thickness
burns not measured by TBSA
•Online tools & App are available for TBSA estimation
•First degree burns, equivalent to a sunburn are not included
when TBSA burned is calculated.
•The Lund browder chart is considered more accurate because
the patient's age, in proportion to relative body are size, is
taken into account. The rule of nines which is easy to
Page 4 of 335
