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Anatomy and Phyisology > HLTH 2501: disorders of the liver and pancreas > Flashcards

HLTH 2501: disorders of the liver and pancreas Flashcards

1
Q

what is the gallbladder commonly affected by?

A

formation of gallstones

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2
Q

colelithias

A

the formation of gallstones

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3
Q

gallstones

A

mass of solid material or calculi that form in the bile

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4
Q

cholecystitis

A

inflammation of the gallbladder and the cystic duct

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5
Q

cholangitis

A

inflammation related to the infection of bile duct

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6
Q

choledocholithias

A

obstruction by gallstones of the biliary tract

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7
Q

where do gallstones initially form?

A

the bile ducts, gallbladder, or the cystic duct

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8
Q

content found in gallstones

A

cholesterol, bile pigments, or mixed content including calcium salts

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9
Q

cholesterol stones

A

appear white or crystal

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10
Q

bilirubin stones

A

appear black

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11
Q

where are gallstones excreted?

A

the bile; small ones may pass through but large ones may obstruct the flow of bile, causing pain

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12
Q

why do gallstones form?

A

an excess of cholesterol and a deficit of bile salts; triggered or inflammation of infection which may form a calculus

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13
Q

infecting organisms for gallstones

A

usually are E coli

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14
Q

biliary colic

A

severe spasms of pain resulting from attempting to move the gallstone along

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15
Q

how might pancreatitis occur as a result of gallstones?

A

due to pancreatic secretions being backed up by gallstones

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16
Q

increased risk for gallstones

A

obesity, high cholesterol intake, multiparity (given birth to many children), and the use of oral contraceptives are risk for cholestrol gallstones; hemolytic anemia, alcoholic cirrhosis, or biliary tract infection are risk for bile gallstones

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17
Q

signs of gallstones

A

severe waves of pain in the URQ (radiate to the back and right shoulder), nausea, vomiting, and sometimes jaundice

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18
Q

when is gallstone pain triggered?

A

after a fatty meal

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19
Q

treatment for gallstones

A

laparoscopic surgery that removes the gallbladder and gallstones, shock wave therapy, or bile acids or drugs to break down the stone

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20
Q

2 other names for jaundice

A

icterus or hyperbilirubinemia

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21
Q

jaundice

A

yellowish colour of the skin that results from high levels of bilirubin in the blood

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22
Q

where does jaundice first appear?

A

in the sclera of the eyes

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23
Q

what is bilirubin a product of?

A

breakdown of RBCs

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24
Q

three disorders associated with jaundice

A

prehepatic jaundice, intrahepatic jaundice, and posthepatic jaundice

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25
Q

prehepatic jaundice

A

excessive destruction of RBCs; often a characteristic of hemolytic anemia or transfusion reactions; the liver is functional but cannot keep up with the additional bilirubin; common in newborns

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26
Q

intrahepatic jaundice

A

occurs in individuals with liver disease such as hepatitis or cirrhosis; a result of impaired uptake of bilirubin from the blood and decreased conjugation of it by the hepatocytes

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27
Q

posthepatic jaundice

A

caused by the obstruction of bile flow into the gallbladder or duodenum, as well as backup of bile into the blood

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28
Q

causes of posthepatic jaundice

A

congenital atresia of the bile ducts, obstruction by cholethiiass, inflammation of the liver, or tumors

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29
Q

unconjugated bilirubin

A

an indirect reading of serum levels and is elevated in prehepatic jaundice

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30
Q

conjugated bilirubin

A

associated with posthepatic jaundice

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31
Q

(non)conjugated bilirubin and intrahepatic jaundice

A

both are present due to inflammation or infection that impair hepatocyte function and obstruction of the bile canaliculi

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32
Q

stool of those with posthepatic jaundice

A

light coloured due to bile not entering the intestine because of obstruction

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33
Q

signs of posthepatic jaundice

A

irritation and pruritus due to bile salts entering the blood and tissues

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34
Q

treatment for jaundice

A

varies but can be phototherapy or UV light

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35
Q

hepatitis

A

the inflammation of the liver; causes hepatocyte function to be impaired, and in severe cases it causes inflammation and necrosis, impairing bile flow

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36
Q

hepatitis causes

A

fatty liver, an infection such as viral hepatitis, or chemical or drug toxicity

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37
Q

how many viral hepatitis infections are there?

A

A-E

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38
Q

two ways the liver cells are damaged

A

by direct action of the virus or via cell-mediated immune responses to the liver

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39
Q

biliary stasis

A

backup of bile into the blood and occurs with severe inflammation of the liver

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40
Q

general symptoms of hepatitis

A

necrosis, sometimes liver failure, scar tissue, and obstruction of bile flow

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41
Q

what types of hepatitis does chronic inflammation occur with?

A

B, C, and D; this is persistent inflammation and necrosis of the liver for more than six months

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42
Q

results of chronic liver inflammation

A

permanent liver damage (fibrosis) and cirrhosis; also an increased rate of hepatocellular cancer

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43
Q

fibrosis meaning

A

permanent liver damage

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44
Q

asymptomatic hepatitis’s

A

B, C, and D

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45
Q

how is hep A transmitted?

A

oral-fecal, often by contaminated water or shellfish

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46
Q

another name for hep A

A

infectious hepatitis

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47
Q

what is hep A caused by?

A

a small RNA virus called HAV

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48
Q

antibodies present in hep A

A

first IgM, then IgG

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49
Q

infection of hep A

A

acute and self-limiting; no carrier state

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50
Q

protection for hep A

A

vaccine and gamma globulin which provides a temporary protection to those just exposed

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51
Q

HIV and hep B

A

more than 50% of those with HIV also have hep B

52
Q

another name for hep B

A

serum hepatitis

53
Q

what is hep B caused by?

A

HBV, a partially double-stranded DNA virus called a Dane particle

54
Q

antigens in hep B

A

HBcAG, HBeAg, and HBsAg

55
Q

hep B incubation

A

has a long incubation period, making it easy to transmit

56
Q

how is hep B transmitted?

A

by infected blood; transfusions, intravenous infections, sexual transmission, placental, tattooing, and body piercings

57
Q

hep B protection

A

there is a vaccine for high risk groups and immune globulin as a temporary protection

58
Q

hep C virus

A

a single-stranded RNA virus

59
Q

what is hep C transmitted by

A

blood transufsions

60
Q

risk of hep C

A

increases the risk of hepatocellular carcinoma

61
Q

hep D virus

A

delta virus

62
Q

antibody for hep D

A

HBsAg

63
Q

hep D transmission

A

blood; high incidence in intravenous drug abusers

64
Q

hep D and other heps

A

hep D increases the severity of hep B infection

65
Q

hep E virus

A

a single-stranded RNA

66
Q

hep E spread

A

the oral-fecal route

67
Q

hep E common population

A

Asian and African countries, and pregnant women

68
Q

three stages of hepatitis

A

pericteric or prodromal, icteric or jaundice, and posticteric or recovery

69
Q

preicteric stage of hepatitis

A

insidious, with fatigue, anorexia, nausea, general muscle aching, fever, headache, and URQ discomfort

70
Q

serum levels during the preicteric stage

A

high levels of aspartate aminotransferase or alanine aminotransferase

71
Q

icteric stage of hepatitis

A

onset of jaundice (elevated bilirubin), biliary obstruction (light stool), dark urine, pruritic skin, tender and enlarged liver, mild aching pain, and prolonged blood clotting times

72
Q

in what hepatitis is the icteric stage longest?

A

hep B

73
Q

posticteric stage of hepatitis

A

reduction in signs; varies in length

74
Q

what two stages may follow the icteric stage?

A

recovery or chronic infection

75
Q

treatment for hepatitis viruses

A

gamma globulin may be helpful when given early in the infection course, a diet high in protein, carbs, and vitamins, and vaccines may prevent them

76
Q

how are hep B and C treated?

A

may be treated with interferon alpha and lamivudine to decrease viral replciation

77
Q

hepatotoxins

A

chemicals or drugs that may cause inflammation and necrosis in the liver; they may also cause an immune response

78
Q

hepatotoxic drugs

A

acetaminophen, halothane pehnothizaides, and tetracycline

79
Q

toxic hepatochemicals

A

carbon tetrachloride, toluene, or ethanol

80
Q

reye sydrome

A

occurs when aspirin is used in the presence of viral infections, causing toxic effects of the liver

81
Q

2 ways hepatocellular damage can occur

A

inflammation with necrosis or cholestasis

82
Q

cholestasis

A

obstructed flow of bilw

83
Q

cirrhosis

A

a disorder that occurs when there is progressive destruction of the liver tissue, leading to liver failure

84
Q

what is cirrhosis classified on?

A

the structural changes that take place; either micronodular or macronodular, or the cause of the disorder

85
Q

four categories of cirrhosis

A

alcoholic liver disease, biliary cirrhosis, postnecrotic cirrhosis, and metabolic

86
Q

alcoholic liver disease

A

the largest group of cirrhosis

87
Q

biliary cirrhosis

A

associated with immune disorders and those causing obstruction of bile flow

88
Q

postnecrotic cirrhosis

A

linked to chronic hepatitis or long-term exposure to toxic materials

89
Q

metabolic cirrhosis

A

caused by storage disorders such as hemochromatosis

90
Q

how is cirrhosis damaged diagnosed?

A

liver biopsy and serologic tests

91
Q

what does the liver look like in cirrhosis?

A

the liver is enlarged initially, but becomes small and shrunken as fibrosis proceeds

92
Q

another name for alcoholic liver disease

A

portal cirrhosis

93
Q

stages of alcoholic liver disease

A

accumulation of fat in liver cells occurs, causing fatty liver; then inflammation and cell necrosis occur, and fibrous tissue forms; then fibrotic tissue replaces normal tissue, altering the basic liver structure and changing the function

94
Q

results of cirrhosis

A

decreased removal of bilirubin, decreased bile production, impaired digestion, decreased production of blood clotting factors, impaired glucose metabolism, inadequate storage of iron and B12, decreased inactivation of hormones, and decreased removal of toxic substances

95
Q
A
96
Q

hepatic encephalopathy

A

impaired brain function due to liver dysfunction and is a result of altered blood chemistry; can cause confusion, convulsions, disordineation, personality and memory changes, and possibly a coma

97
Q

effects related to the obstruction of bile ducts

A

impaired digestion and absorption, jaundice, portal hypertension, congestion in the spleen that increases hemolysis, esophageal varices, and ascites

98
Q

esophageal varices

A

swollen veins surrounding the esophagus and is a result of increased pressure of blood due to obstruction of bile

99
Q

why does blood pressure increase with bile obstruction?

A

because the hepatic portal system is being blocked, aldosterone levels are increased, and albumin levels are decreased, lowering plasma osmotic pressure; causes ascites and esophageal varices

100
Q

initial signs of cirrhosis

A

fatigue, anorexia, weight loss, anemia, diarrhea, and dull aching pain in the URQ

101
Q

advanced signs of cirrhosis

A

ascites, edema, increased bruising, esophageal varices, jaundice, imbalance in sex hormones that leads to spider nevi, and these can lead to hemorrhage and circulatory shock

102
Q

cirrhosis and infections

A

skin and respiratory infections commonly develop due to excessive fluids in the tissues that interfere with the diffusion of nutrients

103
Q

treatment for cirrhosis

A

avoiding fatigue, avoiding exposure to infection, restrictions on protein and salt, along with high carb intake, diuretics, albumin transfers, ruptured esophageal treatment, and liver transplants

104
Q

tumors in the liver

A

are usually secondary tumors, although primary malignant ones may occur, but they are rare

105
Q

most common liver cancer

A

hepatocellular carcinoma which is common in cirrhotic livers

106
Q

what may liver tumors develop as a result of?

A

prolonged exposure to carcinogenic chemicals

107
Q

signs of liver cancer

A

usually mild but include anorexia, vomiting, fatigue, weight loss, hypertension, splenomegaly and hepatomegaly

108
Q

treatment for liver cancer

A

chemotherapy, and sometimes radiofrequency or lobectomy

109
Q

pancreatitis

A

an inflammation of the pancreas resulting from autodigestion of the tissue; can be acute or chronic

110
Q

why does autodigestion of the pancreas occur?

A

because of premature activation of the pancreatic proenzymes within the pancreas itself; more specifically, trypsinogen is converted into trypsin, which converts other proenzymes and chemicals into their active forms

111
Q

what enzymes digest the pancreatic tissue?

A

trypsin, protease amylase and protease lipase

112
Q

effects of pancreatitis

A

inflammation, bleeding, and necrosis

113
Q

what does the pancreas lack that makes it more susceptible to pancreatitis?

A

a fibrous capsule

114
Q

elastase

A

a protease that leads to hemorrhage in pancreatitis

115
Q

how are nearby tissues damaged in pancreatitis?

A

trypsin and other enzymes progress into surrounding tissues, as well as inflammatory chemicals such as cytokines and prostaglandins

116
Q

effects of pancreatitis

A

hypovolemia, circulatory collapse, severe pain, bacterial peritonitis, sepsis, adult respiratory distress syndrome, acute renal failure, and possibly death

117
Q

causes of pancreatitis

A

gallstones and alcohol abuse; gallstones obstruct the flow of bile and pancreatic secretions; alcohol stimulates an increased secretion of pancreatic enzymes

118
Q

sudden signs of acute pancreatitis

A

follows a large meal or large amount of alcohol; severe epigastric pain that radiates to the back, signs of shock (low BP, pallor, sweating, weak pulse), low-grade fever, and abdominal distention

119
Q

diagnostic tests for pancreatitis

A

high serum amylase and lipase levels; hypocalcemia as well due to calcium ions binds to fatty acids in necrotic areas

120
Q

treatment for pancreatitis

A

stopping all oral intake, treating shock and electrolyte balance, and analgesics (but not morphine)

121
Q

risk factor for pancreatic cancer

A

cigarette smoking, diett, and pancreatitis

122
Q

common neoplasm of pancreatic cancer

A

adencarcinoma

123
Q

pancreatic cancer effects

A

a tumour at the head of the pancreas causes obstruction of biliary and pancreatic flow, leading to weight loss and jaundice

124
Q

prognosis for pancreatic cancer

A

very poor as is metastases quickly and is not diagnosed early on

125
Q
A

Anatomy and Phyisology (94 decks)

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