Liver, Biliary, and Pancreatic Disorders Flashcards
1
Q
right lobe of the liver is separated from the right lung and pleura by the
A
right dome of the diaphragm
2
Q
80% of the blood to the liver comes from the
A
portal veins
3
Q
20% of the blood (oxygen-rich) to the liver comes from the
A
hepatic artery
4
Q
hepatic artery supplies liver with
A
oxygenated blood
5
Q
portal vein drains the viscera (abdomen and spleen) and delivers blood to
A
the liver
6
Q
central veins in the liver join to form the _________ which drains into the inferior vena cava
A
hepatic vein
7
Q
small bile ducts throughout the liver join to form the ________ which carries bile formed in the liver and other secretions
A
hepatic duct
8
Q
the cystic duct comes from the gallbladder to release bile and combines with the hepatic duct to then form the _________ which empties into the small intestine
A
common bile duct
9
Q
Functions of the liver
A
Glucose Metabolism
Protein Metabolism
Fat Metabolism
Conversion of Ammonia
Bile Formation
Bilirubin Excretion
Drug Metabolism
Vitamin and Iron Storage
10
Q
The liver stores what vitamins?
A
vitamins A,D,E,K, and B12
11
Q
up to ___% of the liver can be damaged before you see a change in lab values
A
70%
12
Q
Portal Vein brings glucose to liver to
A
store as glycogen
13
Q
When the liver converts glycogen to glucose when needed
A
Glycogenolysis
14
Q
glucose synthesized from non-carbs (proteins or lactate)
A
Gluconeogenesis
15
Q
The liver breaks down fatty acids for production of energy into
A
ketone bodies and cholesterol/lipids
16
Q
the liver synthesizes which plasma proteins?
A
albumin, clotting factors, fibrinogen
17
Q
Vit K is required for
A
clotting factor synthesis
18
Q
provides colloidal osmotic pressure within vascular system
A
Albumin
19
Q
Vit K needs ____ to be absorbed
A
bile
20
Q
Prothrombin cannot be made without
A
Vit K
21
Q
Function of bile
A
to digest fats
22
Q
Function of Kupffer cells :
A
Remove bacteria, debris , RBC
23
Q
formed by hepatocytes, collected in bile ducts
A
Bile
24
Q
Made of water, electrolytes, fatty acids, cholesterol, bilirubin, bile salts
A
bile
25
Pigment from breakdown of hemoglobin
bilirubin
26
Colors feces brown
bilirubin
27
A byproduct of gluconeogenesis that is converted to urea then excreted in urine (also a byproduct of bleeding)
Ammonia
28
the liver metabolizes these hormones
estrogen and aldosterone
29
refers to black stools that occur as a result of gastrointestinal bleeding.
Melena
30
A neurological disorder that causes a person to lose motor control of certain areas of the body.
Asterixis
31
Liver function tests:
specific to liver, elevated with liver disease;
hepatitis, cirrhosis
ALT (alanine aminotransferase)
32
Liver function tests:
increased with damage to the heart, liver,
muscle, kidney
AST (aspartate aminotransferase)
33
Liver function tests:
increased with alcohol abuse
GGT (gamma glutamyl transferase)
34
Liver function tests:
found in bones, liver and intestines (an increase is seen with biliary obstruction w/o bone disease)
ALP ((alkaline phosphatase)
35
cholestasis
bile is stasis
36
Liver function tests:
elevated in ischemic hepatitis
LDH
37
chemical elevated in liver failure
Ammonia
38
Elevated if bile duct obstruction, decreased in parenchymal liver disease
Cholesterol
39
For biopsy coagulation studies, must have consent and have
patient void prior
40
Post-Op biopsy care:
Right side position for 2-4 hours, apply pressure dressing
41
Stages of liver damage:
stage 1
healthy liver
42
Stages of liver damage:
stage 2 (reversible)
fatty liver
43
Stages of liver damage:
stage 3 (thickening/hardening)
liver fibrosis
44
Stages of liver damage:
stage 4
cirrhosis
45
Replacement of normal liver tissue with fibrosis/scar tissue
cirrhosis
46
Type of cirrhosis:
chronic alcoholism, most common cirrhosis
Alcoholic
47
Type of cirrhosis:
scarring after viral hepatitis
Post necrotic
48
Type of cirrhosis:
scarring to liver around the bile ducts, less common cirrhosis
Biliary
49
Type of cirrhosis:
from Right sided heart failure
Cardiac
50
80% of patients diagnosed _________ remain asymptomatic for the next 10 years (may have vague symptoms only)
compensate
51
Early signs of compensate are subtle:
GI, anorexia, nausea, vomiting , changes in bowel
52
symptoms advanced from portal HTN
Decompensated
53
Late signs of decompensate:
Portal Hypertension, ascites, edema, varices, encephalopathy
54
Late cirrhosis
decompensated
55
Scarred liver cells can not process the blood returning from GI, blood backs up in these organs causing high pressure
Portal Hypertension
56
Obstruction of venous blood flow through liver – increased capillary pressure
Increased intravascular volume
Decreased production of albumin
-FLUIDS SHIFT into PERITONEAL CAVITY
Liver can’t metabolize aldosterone – kidneys then retain Sodium and H2O
ASCITES
57
Collateral blood vessels -
Esophagus, stomach, lower rectum (hemorrhoids) develop new blood vessels to drain blood
VARICES
58
Blood with ammonia can not be metabolized in liver – gets circulated
Hepatic encephalopathy (in brain)
Shunting of blood
59
The obstructed spleen from the portal HTN: thrombocytopenia/anemia
Splenomegaly
60
keeps fluid where it belongs
albumin
61
spleen destroys
platelets and RBC's
62
large veins on abdomen
caput medusae
63
Nursing interventions for Cirrhosis Patients
high carb, limited protein, low sodium diet
Smaller more frequent meals
Assess: abdominal percussion
Daily weights
64
Treating Ascites
Spironolactone
Fluid restrictions
Sodium Restrictions
Albumin
Daily weights, measure abdominal girth
Assess rate and effectiveness of respirations
65
blocks aldosterone and spares potassium
Spironolactone
66
keep fluid in intracellular space
Albumin
67
In ascites, respiratory issues are caused by
large abdomen
68
Catheter inserted to drain fluid
Often will give Albumin after procedure
Have patient void prior
Have patient sitting up in chair/bed
PARACENTESIS
69
Stent inserted from portal vein to hepatic to decrease pressure / divert blood
TIPS
70
TIPS
Transjugular Intrahepatic Portosystemic Shunt
71
The nurse assess pt with ascites. VSS BP: 128/78, P: 118, RR 28, Temp 98.9 Pulse ox 89% on room air. What is first thing to do?
a. Assess heart sounds
b. Prepare for paracentesis
c. Raise HOB
d. Assess lung sounds
c. Raise HOB
72
Life threatening condition from dilated, thin walled veins in submucosa of lower esophagus
Esophageal Varices
73
due to portal HTN - may rupture when chemically or mechanically irritated or when pressure is increased due to sneezing, coughing, Valsalva maneuver or excessive exercise
Esophageal Varices
74
Bleeding esophageal varies is an
EMERGENCY
75
Same process of esophageal varices causes veins in rectum to bulge
hemorrhoids
76
Medication that constricts esophageal veins to stop bleeding
Octreotide
77
Med given ASAP, before endoscopy
octreotide
78
med injected to cause inflammation & sclerosis
Endoscopic Sclerotherapy
79
after endoscopy, Pt remains NPO after until
return of GAG reflex
80
NGT with balloon inflated in esophagus to stop bleeding
Sengstaken Blakemore Tube
81
Risks of balloon tamponade
Tube dislodges, airway obstruction, (cut port for balloon to deflate ASAP)
82
Esophageal Varices is a risk factor for any patient admitted with
advanced cirrhosis
83
Hepatic Encephalopathy =
END STATE CIRRHOSIS
84
Portal HTN shunting of unfiltered blood (ammonia) to circulation
Hepatic Encephalopathy
85
Causes of high ammonia in hepatic encephalopathy:
GI bleeding (varices, melena) increase levels of Ammonia
High Protein diet, bacterial infection
Hypokalemia & alkalosis
86
Signs & Symptoms of hepatic encephalopathy:
Mental changes, motor disturbance, asterixis
Sleep….to COMA
87
Hepatic Encephalopathy Treatment
Lactulose
Antibiotic (neomycin)
Diet : monitored protein, high carb
88
laxative that traps and expels ammonia in feces (enema or oral)
Lactulose
89
Hepatic Encephalopathy can be reversible if
treated promptly
90
The nurse is giving lactulose to patient with hepatic encephalopathy. What effect should be seen
a. Increase urine output
b. Impaired level of consciousness
c. Increased bowel movements
d. Nausea and vomiting
c. Increased bowel movements
91
jaundice is seen with serum bilirubin levels
> 2.0 mg/dL
92
Type of Jaundice:
increase in destruction of RBC pigments in blood, cannot be excreted fast enough. Not
dangerous unless it gets very high
hemolytic
93
Type of Jaundice:
occlusion of the bile duct, can be intra or extrahepatic. Bilirubin cannot flow into the
intestines and “backs up” and is then reabsorbed into the blood
obstructive
94
Type of Jaundice:
seen with damaged liver cells that cannot clear bilirubin - seen with alcoholic damage and with medications that can cause hepatotoxicity
hepatocellular
95
Bile can’t flow into intestines causing
clay colored stool
96
Excess bile yellows skin/sclera and urine becomes
orange & frothy
97
Icteric
yellow sclera
98
Prolonged Jaundice predisposes pt to
stones and CNS damage
99
Manifestations of Liver Disease:
Edema from
hypalbuminemia
100
Manifestations of Liver Disease:
Thrombocytopenia causing
large spleen
101
Manifestations of Liver Disease:
Vitamin Deficiency
Vit A, D, E, K, Thiamin
102
Manifestations of Liver Disease:
Large belly BUT
Malnourished
103
Manifestations of Liver Disease:
Pruritus from retention of bile salts from
biliary obstruction / cholestasis
104
Manifestations of Liver Disease:
Gynecomastia, amenorrhea, testicular atrophy from
liver’s inability to metabolize hormones
105
Manifestations of Liver Disease:
Elevated Respiratory rate r/t
ascites
106
Common virus with symptoms similar to mono
Cytomegalovirus
107
Hepatitis by mode of transmission:
fecal/oral route; poor sanitation, person to person contact
- waterborne/foodborne
Hep A
108
Hepatitis by mode of transmission:
- by intimate contact with carriers or those w/acute disease; sexual and oral-oral contact
- perinatal transmission from mothers to infants
Hep B
109
Hepatitis by mode of transmission:
transfusion of blood and blood products; exposure to contaminated blood through equipment or drug paraphernalia
Hep C
110
Hepatitis by mode of transmission:
Contact with infected blood (occurs only in people already infected with Hep B)
Hep D
111
Hepatitis by mode of transmission:
Eating contaminated food or drink. Dangerous to pregnant women
Hep E
112
HCV antibodies testing basic info
If test is reactive its is most likely positive and RNA test is needed. both test confirm diagnosis
113
the 3 hepatitis antigens
surface antigen
E antigen
Core antigen
114
Blood born Heps
B/D and C
115
Food borne Heps
A and E
116
Liver cancer is usually caused by
another cancer in the body
117
Primary liver cancer is usually caused by
Hep B, C or cirrhosis
118
Hepatic Encephalopathy assessment requires
neuro checks
119
Bile made in liver travels via the common hepatic duct to the
common bile duct to the duodenum
120
Not all bile goes straight to the common bile duct, some is stored in
GB via the cystic duct
121
Liver makes up to ___cc of bile daily
700cc
122
GB can hold _____cc of bile
30-50cc
123
What does the gallbladder do?
Digest fats via the bile salts and cholesterol
Alkalize intestinal contents to aide in digestion
124
Inflammation of GB
Cholecystitis
125
90% of Acute cholecystitis from
Stones
126
Calculous in common duct:
choledocholithiasis
127
Calculous (stone) in GB:
cholelithiasis
128
GB condition caused by burns, severe trauma, major surgery, obstruction of cystic duct, or bacterial
Acalculous
129
More common in women older than 40, multiparous, increase weight
Chronic Cholecystitis
130
Older person with cholecystitis and comorbidities may have no symptoms until
septic
131
stone blocks bile flow – GB distends becomes inflamed and infected. Fever, possible palpable mass
Acute Cholecystitis
132
after heavy meal GB contracts b/c can not release bile – the GB can become gangrene!!
Biliary colic
133
tenderness in RUQ on deep inspiration or when GB palpated
Murphy’s sign
134
Vitamin Deficiency with cholelithiasis why??
Can not absorb fat sol vitamins w/o BILE!
135
Diagnostic test where tube goes down toward the duodenum then curves up into gallbladder
ERCP - Endoscopic Retrograde cholangiopancreatography
136
Can treat confirmed choledocholithiasis- CBD stone can be extracted with
ERCP
137
80% of patients with acute GB inflammation will achieve remission with:
IV Fluids
NG suction
Pain relievers * treat pain!!!
Antibiotic
Rest
138
Medication – For non obstructing stones taken for up to a year
UDCA (Agtigall)
139
Non surgical GB stone treatment:
Laser pulse directed under endoscopy/fluoroscopic guidance directly to stone
Intracorporeal Lithotripsy
140
Non surgical GB stone treatment:
Shock waves directed at gallstones to fragment stones. Fragmented stones are then either spontaneously passed or removed via endoscope.
ESWL - Extracorporeal Shock Wave Lithotripsy:
