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ABSN NUR 326 > Week 4: Gallbladder, Pancreas, and Liver > Flashcards

Week 4: Gallbladder, Pancreas, and Liver Flashcards

1
Q

What is cholelithiasis?

A

stones in the gallbladder

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2
Q

Etiology of cholelithiasis?

A

unkown

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3
Q

Risk factors for cholelithiasis

A

female, estrogen, obesity, sedentary, diet and family hx

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4
Q

What is bile’s function?

A

help digest lipids and transport waste products

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5
Q

Components of bile?

A

bilirubin, cholesterol, bile salts, water, protein and calcium

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6
Q

Pathogenesis of cholelithiasis?

A

bile stasis—->super saturation with cholesterol—-> precipitation—> stones remain in the gallbladder or migrate through the ducts

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7
Q

Cholelithiasis manifestations?

A

sometimes silent, biliary colic ( steady severe pain, RUQ may radiate to R shoulder)

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8
Q

Obstructed bile flow manifestation?

A

jaundice, dark foamy urine, clay stools, steatorrhea (oily stool), puritis, intolerance of fatty foods, and bleeding tendencies

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9
Q

Cause for Jaundice symptoms with an obstructed bile flow?

A

bile cannot flow into duodenum leading to a high bilirubin

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10
Q

Cause for dark amber urine with an obstructed bile flow?

A

soluble bilirubin in the urine

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11
Q

Cause for clay colored stools with an obstructed bile flow?

A

bilirubin does not reach small intestine to be converted into urbilinogen

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12
Q

Cause for steatorrhea (oily stools) with an obstructed bile flow?

A

no bile salts in duodenum preventing fat digestion

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13
Q

Cause for puritis with an obstructed bile flow

A

deposit of bile salts into skin tissue

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14
Q

Cause for intolerance to fatty foods due to an obstructed bile flow

A

No bile in small intestine to help with fat digestion

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15
Q

Cause for bleeding tendencies with an obstructed bile flow

A

decreased absorption of vitamin K

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16
Q

What is cholecystitis?

A

Inflammation of gallbladder

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17
Q

Reasons for cholecystitis

A

GALLSTONES, prolonged immobility or fasting, bacterial infection, receiving TPN, DM

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18
Q

What happens to the gallbladder during cholecystitis?

A

edematous, hyperemic, distended abdomen, and over time scarring and decreased function will occur

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19
Q

S/S of cholecystitis

A

Cholic pain, fever, N/V, restlessness, diaphoresis

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20
Q

Lab values associated with cholecystitis

A

increased bilirubin, liver enzymes and WBC
If obstruction is low enough increases amylase

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21
Q

Pharmacotherapy for gallbladder problems?

A

analgesic (ketorolac), antiemetic, anticholinergics, and bile acids (rarely used)

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22
Q

What is pancreatits?

A

inflammation of the pancreas

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23
Q

Risk factors for pancreatitis

A

middle age, African Americans

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24
Q

Etiology of pancreatits

A

biliary tract disease (women), ETOH abuse (men)

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25
Q

S/S of pancreatits

A

LUQ or epigastric pain, sudden onset that may radiate towards their back, N/V, fever. cyanosis or green coloring on the abdomen

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26
Q

Labs associated with pancreatitis

A

increases amylase, lipase, glucose and WBC

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27
Q

Complications of acute pancreatitis

A

pseudocyst, abcess, pulmonary complications, hypotension, tetany bc of hypoCa, increased risk for clotting

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28
Q

What is a pseudocyst?

A

a fluid filled cavity that surrounds the outside of the pancreas

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29
Q

S/S of a pseudocyst

A

similar to pancreatitis, but also a palpable epigastric mass

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30
Q

What is a pancreatic abscess?

A

a large fluid filled cavity inside the pancreas that may result in extensive necrosis in the pancreas

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31
Q

What is chronic pancreatitis

A

inflammation in the pancreas that persists over weeks-months

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32
Q

Main etiology for chronic pancreatitis

A

ETHOH abuse (~50% of alcoholics)

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33
Q

What happens to the pancreas during chronic pancreatitis?

A

destruction of tissue (necrosis), scar tissue (fibrosis), loss of pancreatic enzyme and insulin

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34
Q

S/S of chronic pancreatitis

A

signs of dysfunction after acute attack, chronic pain, DM, malabsorption of fat, and weight loss

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35
Q

Drug therapy for pancreatits

A

morphine (pain), dicyclomine (antispasmodic), antacids and H2-receptor antagonists (decrease secretion of pancreatic enzyme),PANCRELIPASE (replacement therapy for pancreatic enzyme), and insulin (if DM occurs)

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36
Q

What is the major functions of the liver?

A
  1. metabolism and storage of FAT, CHO, vitamins and minerals,
  2. blood volume reservoir
  3. blood filter
  4. blood clotting factors
  5. drug metabolism and detoxification
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37
Q

What is portal circulation?

A

when the stomach, intestine, spleen and pancreas bring blood to the liver

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38
Q

Where does the blood enter the liver?

A

portal vein

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39
Q

What is the first pass effect?

A

When a drug’s bioavailability decreases due to being metabolized in the liver before it can be systemically circulated

40
Q

What are Liver Function Test (LFT)

A

liver enzymes (AST, ALT, Alk Phos), Bilirubin (conjugated and unconjugated) serum Ammonia, protein, albumin and prothrombin time

41
Q

Normal lab value for ALT

A

5-35

42
Q

Normal lab value for AST

A

0-35

43
Q

Normal lab value for Alk Phos

A

29-90

44
Q

Normal lab value for total bilirubin

A

0.1-1.2

45
Q

Normal lab value for conjugated (direct) bilirubin

A

0.1-0.3

46
Q

Normal lab value for unconjugated (indirect) bilirubin

A

0.1-1.0

47
Q

Normal lab value for serum Ammonia

A

15-45

48
Q

Normal lab value for serum protein

A

6.0-8.3

49
Q

Normal lab value for serum albumin

A

3.5-5.0

50
Q

Normal lab value for prothrombin time

A

10-13

51
Q

What causes jaundice?

A

an increase level of bilirubin in the blood. Usually visible when total bilirubin is 2.0-2.5

52
Q

Reasons for elevated indirect or unconjugated bilirubin

A

bilirubin overproduction OR impaired liver function

53
Q

What are the 3 classes of jaundice?

A

hemolytic, hepatocellular, and obstructive

54
Q

Reason for elevated direct or conjugated bilirubin

A

liver is working but cannot get bilirubin out (e.g obstruction due to gallstones)

55
Q

What causes hemolytic jaundice?

A

increased breakdown of RBC, causing an increase in bilibrubin

56
Q

What causes hepatocellular jaundice?

A

liver isn’t working, so bilirubin is not filtered out of the blood

57
Q

What causes obstructive jaundice?

A

decreased or obstructive flow of bile, typically from a gallstone

58
Q

Strains of hepatitis?

A

COMMON: Hep A, B and C (HAV, HAB, and HAC) RARE: Epstein-Barr and cytomegalovirus

59
Q

S/S of hepatitis in the prodromal phase?

A

2wks after exposure–> fatigue, anorexia, malaise, N/V, hyperalgesia (extreme response to pain), cough, low grade fever, and HIGHLY transmissible

60
Q

S/S of hepatitis in icteric phase?

A

jaundice, dark urine, clay colored stools, enlarged liver, tenderness on palpation, fatigue, and increasing abdominal pain

61
Q

S/S of hepatitis in the recovery phase

A

resolution of jaundice, symptoms begin to diminish, but liver may remain enlarged/tender

62
Q

Complications associated with hepatitis

A

chronic hepatitis, liver cirrhosis, liver cancer, and acute liver failure

63
Q

How can HepA be transmitted?

A

fecal-oral, parental, sexual. Typically caused my unsanitary food service workers

64
Q

HepA S/S

A

acute onset w/ fever, mild severity, does NOT lead to chronic hepatitis

65
Q

Ways to prevent HepA

A

hand hygiene and HepA vaccine

66
Q

Ways HepB can be transmitted

A

parental, sexual. Common with IV drug use and unprotected sex

67
Q

S/S of HepB

A

insidious onset, severe disease that may develop into chronic hepatitis

68
Q

How to prevent Hep B

A

HBV vaccine, safe sex, and hand hygiene

69
Q

How can HepC be transmitted

A

parental and sexual. Extremely common with IV drug use and unsafe sex bc NO vaccine

70
Q

S/S of HepC

A

insidious onset, mild-severe symptoms, ~80% develop into chronic

71
Q

How to prevent HepC

A

NO vaccine, blood screenings, hygeine

72
Q

Complication of HepC

A

hepatocellular carcinoma (will need a transplant)

73
Q

Dose and timing of HepA vaccine?

A

2 doses 6 months apart

74
Q

Who is recommended to receive the HepA vaccine?

A

all children starting at 6 months and special high risk populations

75
Q

Dose and timing of HepB vaccine?

A

3 doses 4 months apart

76
Q

Who is recommended to receive the HepB vaccine?

A

All infants beginning as newborns

77
Q

Who will receive drug treatment for HepB

A

high risk patients, elevated AST levels, hepatic inflammation and those with advanced fibrosis

78
Q

Disadvantages of pharm for HepB

A

prolonged therapy, costs, s/e and high relapse rate

79
Q

What is liver cirrhosis (scarring)

A

irreversible, inflammatory, fibrotic liver disease that changes structurally due to injury (typically alcohol or virus)

80
Q

What does chaotic fibrosis lead to?

A

obstructive biliary channels and blood flow, causing the pt to be jaundice and have portal hypertension

81
Q

What are common causes for cirrhosis of the liver?

A

Hep B&C, excessive alcohol intake, idiopathic, and non-alcoholic fatty liver disease (NASH or NALFD)

82
Q

What are the stages of alcoholism and liver disease?

A

alcoholic fatty liver, alcoholic steatohepatitis, and alcoholic cirrhosis

83
Q

What stages of alcoholism and liver disease is the damage reversible?

A

alcoholic fatty liver

84
Q

What stages associated with alcoholism and liver disease is the damage irreversible?

A

alcoholic steatohepatitis and alcoholic cirrhosis

85
Q

What are early manifestations of cirrhosis?

A

N/V, anorexia, flatulence, change in bowel habits, fever, weight loss, and palpable liver

86
Q

What are late manifestations of cirrhosis?

A

jaundice, peripheral edema, decreased albumin and PT, ascites, skin lesions, hematologic problems (anemia, bleeding), endocrine problems, varicies, and encephalopathy

87
Q

What is portal hypertension?

A

the build of pressure at the portal vein caused by resistance of blood flow from intestines, stomach, and pancreas. Damage done is irreversible

88
Q

What is hepatic encephalopathy?

A

when the liver is failing to rid the body of toxins and those toxins build up in the brain causing mental status changes (typically ammonia).

89
Q

What is acute liver failure?

A

NOT cirrhosis!! necrotic and inflammed hepatocytes, typically caused from a tylenol overdose or after a viral hepatitis

90
Q

Why would someone with liver failure take lactulose?

A

because it decreases ammonia levels which decreases the odds of hepatic encephalopathy

91
Q

MOA of lactulose

A

converts ammonia to ammonium

92
Q

What considerations need to be made when giving lactulose?

A

make sure that the pt is not experiencing hypokalemia, as it has similar s/e to hepatic encephalopathy

93
Q

MOA for rifaximin

A

inhibits bacteria RNA synthesis by binding to bacterial DNA

94
Q

s/e of rifaximin

A

peripheral edema, nausea, ascites, fatigue, pruritis, rash, abd pain, and anemia

95
Q

What complication is associated with rifaximin?

A

C. diff

96
Q

Indications for taking rifaximin

A

to prevent hepatic encephalopathy

ABSN NUR 326 (10 decks)

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