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NURS 2514 > 7 - The Liver, Pancreas, + Gallbladder > Flashcards

7 - The Liver, Pancreas, + Gallbladder Flashcards

1
Q

Bilirubin

A

A pigment derived from the breakdown of aged RBCs

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2
Q

Hepatotoxic

A

Damaging or destructive to liver cells

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3
Q

ERCP

A

Endoscopic retrograde cholangiopancreatography; procedure usedto diagnose diseases of the glalbladder, biliary system, pancreas, + liver

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4
Q

Steatorrhea

A

Passage of large amts of fat as bulky, fatty, frothy, foul-smelling, yellow-grey, greasy stools w putty-like consistency; results from the failure to digest + absorb fat

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5
Q

Jaundice [icterus]

A

a condition resulting from an abnormal elevation of blood bilirubin; as a result there is a yellowish discoloration to the skin + sclera of the eye

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6
Q

Ascites

A

Accumulation of fluid in the peritoneal or abdominal cavity; occurs in the later stages of cirrhosis

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7
Q

Encephalopathy

A

Damage or disease that affects the brain

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8
Q

Varices

A

Enlarged, swollen veins

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9
Q

Asterixis

A

Liver flap - flapping tremors commonly affecting the arms + hands; manifestation of hepatic encephalopathy

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10
Q

Fetor hepaticus

A

Musty, sweet odour of the pt’s breath resulting from the accumulation of digestive byproducts that the liver is unable to degrade; smells like a freshly opened corpse

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11
Q

Portal hypertension

A

Hypertension characterized by increased venous presure in the portal circulation as well as by splenomegaly, large collateral veins, ascites, systemic hypertension, and esophageal varices

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12
Q

Spider angiomas

A

Small, dilated blood vessels of the skin that have a bright-red center and spider-like branches

Occur on the nose, cheeks, upper trunk, neck, + shoulders

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13
Q

Palmar erythema

A

Skin condition in which the palms of both hands become red; associated with many forms of liver disease

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14
Q

NAFLD [nonalcoholic fatty liver disease]

A

Spectrum of disease that ranges from simple fatty liver that causes no hepatic inflammation to severe liver scarring

Characterized by accumulation of fat in hepatocytes not associated w alcohol

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15
Q

NASH [nonalcoholic steatohepatitis]

A

Condition characterized by the accumulation of fat in the liver cells, causing inflammation and liver cell injury

Occurs in people who drink little or no alcohol

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16
Q

Cullen’s sign

A

Superficial edema + bruising in the subcut fatty tissue around the umbilicus

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17
Q

Grey-Turner’s sign

A

Bruising of the flanks; may occur in conjunction w Cullen’s sign

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18
Q

Chvostek’s sign

A

Twitching of the facial muscles in response to tapping over the area of the facial nerve just anterior to the ear

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19
Q

Trousseau’s sign

A

Carpopedal spasm caused by inflation ofthe BP cuff to a level above systolic pressure for 3 mins

Looks like: adduction of the thumb, flexion of metacarpophalangeal joints, extension of the interphalangeal joints, and flexion of the wrist

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20
Q

Murphy’s sign

A

Elicited in pts w acute cholecystitis by asking the pt to take in and hold a deep breath while palpating the right subcostal area - if pain occurs on inspiration [when the inflamed gallbladder comes into contact w the examiner’s hand], Murphy’s sign is positive

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21
Q

Cholecystitis

A

Inflammed gallbladder

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22
Q

What is the hepatic portal system?

A

The hepatic portal system is a series of veins that carry blood from the capillaries of the stomach, intestine, spleen, and pancreas to capillaries in the liver.

Blood from the GI tract is drained by the superior + inferior mesenteric veins and then drained into the hepatic portal vein –> liver.

Detoxified blood from the liver drains into the hepatic veins and into the IVC [back to the heart]

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23
Q

What is the function of the Hepatic Portal System?

A

Its main function is to deliver de-oxygenated blood to the liver to be detoxified further before it returns to the heart.

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24
Q

What 2 types of blood does the liver receive from the superior + inferior mesenteric veins?

A

The liver receives both arterial + portal venous blood

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25
Q

What are the functions of the liver?

A
  • produce bile salts
  • excrete bilirubin in bile
  • destroy bacteria in the portal blood
  • maintain blood glucose levels
  • produce urea
  • produce FAs, triglycerides, cholesterol, and lipoproteins
  • metabolize drugs, hormones, + toxins
  • produce clotting proteins, albumin, angiotensin, and IGF
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26
Q

When and where is bilirubin formed in the body?

A

Bilirubin is formed during the breakdown of hemoglobin which occurs w/in the macrophages in the spleen and liver sinusoids

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27
Q

How is bilirubin excreted from the liver?

A

When blirubin reaches the liver sinusoids it is transported into the hepatocytes

The liver then makes bilirubin water-soluble by conjugating bilirubin to glucaronic acid in the SER of the hepatocytes

Conjugated [water-soluble / direct] bilirubin can now be excreted in the bile

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28
Q

What is another name for unconjugated bilirubin? (aka not water soluble)

A

indirect or free bilirubin

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29
Q

Identify the 3 types of jaundice

A
  1. pre-hepatic jaundice
  2. hepatic [hepatocellular] jaundice
  3. post-hepatic [cholestatic] jaundice
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30
Q

Define:

  • pre-hepatic jaundice
  • hepatic [hepatocellular] jaundice
  • post-hepatic [cholestratic] jaundice
A
  • pre-hepatic jaundice: caused by excessive RBC destruction
  • hepatic [hepatocellular] jaundice: caused by impaired uptake or conjugation of bilirubin
  • post-hepatic [cholestratic] jaundice: occurs when bile flow is obstructed at any point between the liver + duodenum [also called obstructive jaundice]
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31
Q

What are the typical causes of pre-heptic jaundice?

A
  • hemolytic transfusion rxn
  • sickle cell anemia
  • autoimmune / acquired hemolysis
  • hemolytic disease of the newborn
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32
Q

What is pre-hepatic jaundice characterized by?

A

Characterized by:

  • indirect [free] hyperbilirubinemia
  • no bilirubin in the urine
  • decreased hematocrit
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33
Q

Describe hyperbilirubinemia of the neonate

A

In the first 2-3 days of life, 60% of infants become jaundiced due to the breakdown of fetal hemoglovin + an immature liver. It usually resolves itself w/in a week

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34
Q

When does jaundice more serious in infants? What are the potential causes? How do we treat it?

A

More serious if jaundice occurs at birth or after 1 week of life.

Potential causes are breast-feeding, hemolytic disease of the newborn, hypoxia, infection, + albumin-binding drugs

Treated w phytotherapy or exchange transfusion

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35
Q

What is kernicterus?

A

Neurological disorder in which unconjugated bilirubin passes the BBB; often occurs in more serious cases of fetal hyperbilirubinemia

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36
Q

What are the most common causes of hepatocellular jaundice?

A

hepatitis [inflammation or infection] + cirrhosis are the most common causes

cellular dysfunction results in impaired conjugation of bilirubin and edema interferes w bile secretion

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37
Q

What is hepatocellular jaundice characterized by?

A

characterized by:
- unconjugated + conjugated hyperbilirubinemia

  • increased amts of water-soluble [conjugated] bilirubin in the urea; making it dark in colour
  • elevated amts of liver-specific enzymes in the blood such as AST + ALT
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38
Q

What is Gilbert’s Disease?

A

Genetic liver disorder in which its enzymes do not properly process bilirubin and therefore conjugate it less often

Causes a slight elevation in unconjugated bilirubin and is considered mostly harmless

39
Q

What are the most common causes of post-hepatic jaundice?

A

Most common causes are bile duct strictures, gallstones, and tumors

40
Q

What is post-hepatic jaundice characterized by?

A

Characterized by:

  • elevated conjugated bilirubin in the blood [unconjugated bilirubin is usually elevated but can be normal]
  • elevated blood cholesterol
  • dark coloured urine [due to increased conjugated bilirubin]
  • pale coloured feces + steatorrhea [by decreased urobilinogen + stercobilin]
  • accumulation of bile salts in the blood and depositing in the skin [pruritis]
  • vitamin K deficiency
41
Q

What is cholelithiasis?

A

Gallstone formation.

Occurs when solutes in the bile become so concentrated that they no longer stay in solution.

42
Q

What do most gallstones consist of?

A

Most gallstones consist of cholesterol w or w/o calcium deposits; occasionally consist of bilirubin

43
Q

What are the 2 categories of risk factors for gallstone formation?

A
  • altered bile composition

- impaired gallbladder mobility

44
Q

What are other risk factors for gallstone formation?

A
  • age 50 in women, age 60 in men
  • prior pregnancies
  • diabetes
  • dyslipidemia, obesity, rapid weight loss
45
Q

What is the most common clinical manifestation of cholelithiasis? What are the potential consequences of this manfestation?

A

Cholecystitis [inflamed gallbladder]; but most gallstones are asymptomatic

An inflamed gallbladder can become infected, necrotic, and may even rupture which would result in peritonitis.

46
Q

What are the symptoms of gallstones?

A
  • range from mild abdominal pain + nausea to severe URQ, epigastric, or lower back pain
47
Q

What are the potential consequences if the bile duct becomes obstructed by a gallstone? What if the stone fails to clear the sphincter and blocks the pancreatic duct?

A
  • obstructive jaundice + cholangitis [inflammation or infection of the bile duct]
  • if the stone fails to clear the sphincter it may cause pancreatitis
48
Q

How do we typically treat symptomatic cholelithiasis?

A

Cholecystectomy

49
Q

Why is obstructive jaundice a clinical manifestation caused by obstructed bile flow?

A

Due to no bile flow into the duodenum

50
Q

Why is dark amber urine which foams when shaken a clinical manifestation caused by obstructed bile flow?

A

Soluble bilirubin gets in the urine

51
Q

Why is an absence of urobilinogen a clinical manifestation caused by obstructed bile flow?

A

No bilirubin reaches the small intestine to be converted to urobilinogen

52
Q

Why are clay-coloured stools a clinical manifestation of obstructed bile flow?

A

Due to the blockage of the flow of bile salts out of the liver

53
Q

Why is pruritis a clinical manifestation of obstruction of bile flow?

A

Bile salts are deposited into skin tissues

54
Q

Why is intolerance of fatty foods leading to nausea, a sensation of fullness, and anorexia a clinical manifestation of obstructed bile flow?

A

Due to the lack of bile in the SI for fat digestion

55
Q

Why is bleeding tendencies a clinical manifestation of obstructed bile flow?

A

Lack of / decreased absorption of vitamin K resulting in decreased production of prothrombin

56
Q

Why is steatorrhea a clinical manifestation of obstructed bile flow?

A

No bile salts in the duodenum which prevents fat emulsion + digestion

57
Q

What is viral hepatitis?

A

Inflammation of the liver due to a viral infection

58
Q

Identify the 3 most common viral agents that cause hepatitis

A 
hep a (HAV)
hep b (HBV)
hep c (HCV)
59
Q

Identify 6 other viral agents that cause hepatitis

A
  • hep D
  • epstein-barr
  • cytomegalovirus
  • herpes simplex
  • rubella
  • yellow fever
60
Q

Identify the 2 ways in which viral infections can cause liver cell damage.

A

1) direct toxic effect on hepatocytes

2) immune-mediated cell death

61
Q

Describe hepatitis A in terms of:

  • the viral agent that causes it
  • method of transmission
  • incubation period length
  • if it can have carriers or not
  • the populations it most commonly effects
  • how it attacks hepatocytes
  • immunity + treatment options
A
  • viral agent HAV
  • oral-fecal transmission
  • incubation period 2-6 weeks
  • no carriers
  • most commonly affects children, young adults, and care-givers
  • multiplies w/in + kills hepatocytes; usually a benign + self-limiting process, but fatalities can occur
  • following recovery, IgGs persist in the blood providing immunity; vaccine available
62
Q

Describe hepatitis B in terms of:

  • the viral agent that causes it
  • method of transmission
  • incubation period length
  • if it can have carriers / chronic cases or not
  • drug therapy
  • prevention
A
  • HBV
  • transmitted through contaminated blood + body fluids, also thru birth + maternally
  • 2-3 months
  • can have carriers + chronic cases
  • treated w interferon, nucleoside + nucleotide analogues
  • vaccination + passive immunity available
63
Q

Compare acute + chronic hepatitis B in terms of survival rate

A
  • most people survive the initial acute hepatitis (1% develop fulminant liver failure resulting in death)
  • 10% of adults and 80% of infants develop lifelong chronic hepatitis and ultimately cirrhosis
64
Q

How much does HBV increase the risk of liver cancer?

A

x 300

65
Q

Describe Hepatitis C in terms of:

  • viral agent that causes it
  • method of transmission
  • incubation period length
  • whether it can have carriers / chronic cases
  • treatment options
A
  • HCV
  • blood + body fluids [but not as virulent as hep B]
  • 6-9 weeks
  • can have carriers + chronic cases
  • only half of people infected develop acute hepatitis, and 50% of these cases progress to chronic hepatitis
  • no vaccine currently available; interferon therapy useful for some cases
66
Q

Why is hepatitis D virus considered to be an “incomplete” virus?

How is it treated?

A
  • incomplete virus b/c it is unable to make its own surface protein
  • “borrows” capsule protein from HBV - therefore only a person infected w HBV can contract HDV
  • infection frequently results in fulminant hepatic failure
  • no vaccine is available but vaccination against HBV prevents HDV in unexposed people
67
Q

What is nonalcoholic fatty liver disease characterized by?

A

Characterized by hepatic steatosis [accumulation of fat in the liver] not associated w other causes such as viral hepatitis, autoimmune disease, or alcohol.

Often associated w obesity + type 2 diabetes, carries an icnreased CV risk.

68
Q

Describe toxic and drug-induced hepatitis in terms of the agents that cause it and when liver necrosis most often occurs

A

Agents that produce toxic hepatitis are generally systemic poisons [such as carbon tetrachloride + gold compounds]; or those that are converted in the liver to toxic metabolites such as acetaminophen + alcohol

Liver necrosis generally occurs w/in 2-3 days of acute exposure to a toxic substance

69
Q

What is chronic hepatitis?

A

Liver inflammation persisting for > 6 mo

70
Q

Identify the 2 most common causes of chronic hepatitis

A

1) chronic viral hepatitis (HBV = 10%, HCV = 60%)

2) alcoholism (30%)

71
Q

What are the potential consequences of chronic hepatitis?

A

Can result in continued hepatocyte destruction, irreversible fibrous alterations in the liver architecture, and ultimatelt lead to cirrhosis.

72
Q

What is cirrhosis of the liver? What is the leading cause?

A

Cirrhosis is an irreversible distortion in liver architecture resulting in extensive fibrosis and hepatocyte dysfunction.

The extensive fibrosis results in icnreased resistance to blood flow and ultimately leads to portal hypertension.

The leading cause is alcohol abuse

73
Q

What are the major manifestations of liver cirrhosis associated with portal hypertension?

A

esophageal varices –> hematemesis or melena

gastropathy –> melena

splenomegaly

dilated abdominal veins

ascites

rectal varices [hemorrhoids]

74
Q

Whar are the major manifestations of liver cirrhosis associated with liver cell failure?

A

coma

fetor hepaticus

spider nevi

gynecomastia

jaundice

ascites

loss of pubic hair

testicular atrophy

liver flap

bleeding tendency due to decreased prothrombin

blood loss anemia

ankle edema

75
Q

Describe edema + ascites as a result of both portal hypertension and liver cell failure. What causes it to develop?

A

Develops due to:

  • portal hypertension + liver cell failure
  • hepatorenal syndrome
76
Q

Describe varicosities + splenomegaly + thrombocytopenia as a result of portal hypertension

A

Portal hypertensino can cause blood to back-up into the spleen, leading to splenomegaly and thrombocytopenia

Portal hypertension also stimulates bypass channels to be formed via anastomosis. This causes varices - commonly in the esophagus, rectum, and abdominal veins

esophageal varicosities commonly rupture creating a life-threatening GI bleed that is complicated by thrombocytopenia + coagulopathy

77
Q

describe jaundice as a manifestation of cirrhosis

A

hepatic jaundice can occur due to hepatocyte damage and intrahepatic cholestasis

78
Q

describe infections as a manifestation of cirrhosis

A

portal-systemic shunts allow ingested bacteria to bypass the liver

79
Q

describe hormonal imbalances as a manifestation of cirrhosis

A

– impaired breakdown of steroid hormones can cause water + Na+ retention, testicular atrophy, gynecomastia, amenorrhea, spider nervi, + abnormal hair growth

80
Q

describe coagulopathy + anemia as a manifestation of cirrhosis

A

impaired clotting factor synthesis, vitamin K deficiency and / or thrombocytopenia can lead to bleeding disorders and blood loss anemia

81
Q

describe encephalopathy as a manifestation of cirrhosis

A

disturbed CNS function can occur when urea production is impaired and ammonia accumulates in the blood; can be worsened o lead to coma following a large meal high in protein or a GI bleed [treated w Lactulose]

82
Q

describe drug toxicity as a manifestation of cirrhosis

A

impaired hepatocyte function can result in impaired clearance of drugs due to diminished conjugation or cytochrome P450 activity; can cause elevated levels of drugs or metabolites in the blood and can have toxic effects

83
Q

define pancreatitis

A

inflammation of the exocrine pancreas - characterized by intrapancreatic activation and releae of destructive pancreatic enzymes

84
Q

identify the 3 most common causes of pancreatitis

A
  1. alcohol abuse
  2. cholelithiasis
  3. severe hyperlipidemia
85
Q

why is alcohol abuse a common cause of pancreaitis?

A

accounts for 65% of all cases; usually precipitated by an episode of heavy drinking

ethanol may have a direct toxic effect on pancreatic cells; or may cause decreased muscle tone in the sphincter of oddi leading to reflux of duodenal contents into the pancreatic duct

86
Q

why is cholelithiasis a common cause of pancreatitis?

A

occurs when a gallstone fails to clear the sphincter of ODDi + obstructs the pancreatic duct

87
Q

describe severe pain as a manifestation of pancreatitis. what causes it?

A

deep epigastric pain that radiates to the back –> caused by inflammation, enzymatic breakdown of pancreatic tissue, + stimulation of peritoneal nerve endings

88
Q

describe hemorrhage, shock, + fever as a manifestation of pancreatitis

A

o enzymatic destruction of blood vessels leads to hemorrhage and shock [hypovolemic + neurogenic]
o lactic acidosis can ensue
o inflammatory cells release pyrogens + cause fever

89
Q

describe hyperamylasemia + hyperlipasemia as a manifestation of pancreatitis

A

o destruction of pancreatic cells releases enzymes amylase + lipase into the interstitial space and is picked up by blood – this has very important diagnostic value

90
Q

describe hypocalcemia as a manifestation of pancreatitis

A

o release of pancreatic lipase into the interstitial fluid results in the breakdown of mesenteric adipose tissue and release of free fatty acids
o these FAs can bind to free calcium and can lead to hypocalcemia
 manifestations:
• tetany
• prolonged QT interval w risk of VT
• convulsions

91
Q

describe hyperglycemia as a manifestation of pancreatitis

A

o inflammation of pancreatic B cells can prevent insulin release and lead to hyperglycemia
o ketoacidosis also common
o pancreatitis can cause diabetes mellitus if 70% of B cells are destroyed

92
Q

describe pulmonary complications as a manifestation of pancreatitis

A

o pancreatic inflammation and release of proteolytic enzymes can result in pleural effusion and pulmonary edema
o release of pancreatic phospholipase can destroy alveolar surfactant and hypotension can lead to “shock lung” or acute resp distress syndrome (ARDS)

93
Q

describe hyperkalemia as a manifestation of pancreatitis

A

o caused by tissue necrosis and acidosis

o hypokalemia is common following fluid repletion and correction of acidosis

94
Q

describe peritonitis as a manifestation of pancreatitis

A

o activated digestive enzymes irritate the peritoneum

NURS 2514 (10 decks)

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