Unit 2: Chapter 38 Flashcards

(52 cards)

1
Q

Liver

A

Larges visceral organ in body
1.3 kg
Located below the diaphragm
Recieves 25% of resting cardiac output
Major exocrine function: bile secretion

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2
Q

Lobules

A

Functional unit of the liver
50,000 to 100,000.
Each is organized around a central vein that empties into the hepatic veins and from there to vena cava.

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3
Q

Metabolic Function of the Liver

A

Produces bile, metabolizes hormones and drugs; synthesizes proteins, glucose, and clotting factors; stores vitamins and minerals; changes ammonia produced by deamination of amino acids to urea; and converts fatty acids to ketones. The liver also degrades excess nutrients and converts them into substances essential to the body.
Metabolizing drugs and hormones

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4
Q

Cholestatsis

A

Cholestasis represents a decrease in bile flow through the intrahepatic canaliculi and a reduction in secretion of water, bilirubin, and bile acids by the hepatocytes. As a result, the materials normally transferred to the bile, including bilirubin, cholesterol, and bile acids, accumulate in the blood.

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5
Q

Cholestasis: 2 Main Causes

A

The condition may be caused by intrinsic liver disease: intrahepatic cholestasis, or by obstruction of the large bile ducts: extrahepatic cholestasis.

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6
Q

Pruritis

A

Most common presenting symptom in people with cholestasi realted to an elevation in plasma bio acids

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7
Q

Bilirubin

A

final product of the breakdown of heme contained in aged red blood cells.
Substance that gives bile its color.

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8
Q

Bilirubin Process of Degradation

A

The hemoglobin from the red blood cell is broken down to form biliverdin, which is rapidly converted to free bilirubin (insoluble in plasma).
Transported in the blood attached to plasma albumin. Even bound to albumin, this bilirubin is still called free bilirubin, to distinguish it from conjugated bilirubin. As it passes through the liver, free bilirubin is absorbed through the hepatocytes’ cell membrane and released from its albumin carrier molecule. Inside the hepatocytes, free bilirubin is converted to conjugated bilirubin, making it soluble in bile. Conjugated bilirubin is secreted as a constituent of bile, and in this form it passes through the bile ducts into the small intestine.

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9
Q

Normal Serum Bilirubin

A

1.5 mg/dL

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10
Q

Jaundice

A

Yellowish discoloration of the skin and deep tissues results from abnormally high levels of bilirubin in the blood.
Occurs when there is an imbalance between the synthesis of bilirubin and the clearance of bilirubin.
Becomes evident when the serum bilirubin levels rise above 2 to 2.5 mg/dL (34.2 to 42.8 μmol).
The eye is the first structure that it can be detected.

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11
Q

5 Major Causes of Jaundice

A
  1. excessive destruction of red blood cells
  2. impaired uptake of bilirubin by the liver cells
  3. decreased conjugation of bilirubin
  4. obstruction of bile flow in the canaliculi of the hepatic lobules or in the intrahepatic or extrahepatic bile ducts
  5. excessive extrahepatic production of bilirubin
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12
Q

Viral Hepatitis

A

Refers to inflammation of the liver caused by hepatotropic viruses that primarily affect liver cells or hepatocytes, autoimmune mechanisms, or reactions to drugs and toxins, or are secondary to other systemic disorders.

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13
Q

Known Hepatotropic VIrsues that cause Hepatitis

A

hepatitis A virus (HAV), hepatitis B virus (HBV), the hepatitis B–associated delta virus (HDV), hepatitis C virus (HCV), and hepatitis E virus (HEV). Although all of these viruses cause acute hepatitis, they differ in the mode of transmission and incubation period; mechanism, degree, and chronicity of liver damage; and ability to evolve to a carrier state.

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14
Q

Viral Hepatitis Manifestations

A

can be divided into three phases:
1. the prodromal or preicterus period
2. the icterus period
3. the recovery period.

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15
Q

Manifestations of Prodromal Period

A

Vary from abrupt to insidious, with general malaise, myalgia, arthralgia, easy fatigability, and anorexia.
Gastrointestinal symptoms such as nausea, vomiting, and diarrhea or constipation may also occur.

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16
Q

Manifestations of the Icterus Phase

A

If it occurs, usually follows the prodromal phase by 7 to 14 days.
People have tenderness around the area of the liver, mild weight loss, and spider angiomas.
Approximately 80% of people with acute Hepatitis C do not have any symptoms.

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17
Q

Manifestations of The Recovery Phsae

A

Characterized by an increased sense of well-being, return of appetite, and disappearance of jaundice.

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18
Q

Hepatitis A

A

caused by the HAV, a small, unenveloped, single-stranded ribonucleic acid (RNA) virus. Fecal oral route contraction.
It usually is a benign, self-limited disease, although it can cause acute fulminant hepatitis and death or need for transplantation in 0.15% to 0.2% of cases.

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19
Q

Hepatitis A Manifestations

A

Usually is abrupt and includes fever, malaise, nausea, anorexia, abdominal discomfort, dark urine, and jaundice.
The presentation of symptoms is dependent on age, with the severity of symptoms increasing in older age groups

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20
Q

Hepatitis A Serology

A

Antibodies HAV appear early
IGM appear during the 1st week and decline over 3 to 4 months.
Peak levels of IgG occur after 1 months and may persist for life

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21
Q

Hepatitis A Treatment

A

Immunization is available for international travel

22
Q

Hepatitis B

A

Caused by the HBV, a double-stranded deoxyribonucleic acid (DNA) virus.34 The complete virion, also called a Dane particle, consists of an outer envelope and an inner nucleocapsid that contains HBV DNA and DNA polymerase.
Can produce both acute and chronic hep, cirrhosis, hep D.
Transmission: infected blood or serum, body secretions

23
Q

Hepatitis B Serology

A

Three well-defined antigens are associated with the virus: a core antigen, HBcAg, which is contained in the nucleocapsid; a longer polypeptide transcript with precore and core regions, designated HBeAg; and a surface antigen, HBsAg, which is found in the outer envelope of the virus.

24
Q

Hepatitis C

A

HCV is a single-stranded RNA virus, with properties similar to those of the flaviviruses, a genus of the family of Flaviviridae that includes yellow fever and St. Louis encephalitis viruses.
The virus is genetically unstable, which leads to multiple genotypes and subtypes.

25
Hepatitis C Manifestations
incubation period for HCV infection ranges from 2 to 26 weeks (average, 6 to 12 weeks). Most children and adults who acquire the infection usually are asymptomatic. Jaundice is uncommon, and only 10% of symptomatic adults have jaundice.54 These symptoms usually last for 2 to 12 weeks.
26
Hep C Serology
antibody and viral tests are available for detecting the presence of HCV infection. False-negative results can occur in immunocompromised people and early in the course of the disease before antibodies develop.
27
Hepatitis D
Of the Deltaviridae family, is the sole RNA virus of the genus. is an incomplete virus, in that it requires the assistance of HBV to replicate. It can cause acute or chronic hepatitis. Infection depends on concomitant infection with HBV, specifically the presence of HBsAg.33 Acute hepatitis D occurs in two forms: co-primary infection that occurs simultaneously with acute hepatitis B and a superinfection in which hepatitis D is imposed on chronic hepatitis B infection.
28
Hepatitis E
An unenveloped, single-stranded RNA virus. It is transmitted by the fecal–oral route and causes manifestations of acute hepatitis that are similar to those of hepatitis A. Genotype 3 of the virus has been linked to chronic HEV infection
29
Chronic Viral Hepatitis
Defined as chronic inflammation reaction of the liver of more than 3-6 months duration Characterized by persistently elevated serum aminotransferase levels and characteristic histologic findings on liver biopsy.
30
Chronic Viral Hepatitis Manifestations
Most common symptoms: fatigue, malaise, loss of appetite, and occasional bouts of jaundice. Elevation of serum aminotransferase concentrations depends on the level of disease activity.
31
Cirrhosis
represents the end-stage chronic liver disease, in which much of the functional liver tissue has been replaced by fibrous tissue. Usually is associated with alcoholism Can develop in other disorders: viral hepatitis, toxic reactions to drugs and chemicals, biliary obstruction, and NAFLD.
32
Cirrhosis and Metabolic Disorders
Accompanies metabolic disorders that cause the deposition of mineral int he liver 1. Hemochromatosis (iron deposition) 2. Wilson disease (copper deposition)
33
Cirrhosis Characterization
characterized by diffuse fibrosis and conversion of normal liver architecture into nodules containing proliferating hepatocytes encircled by fibrosis. The formation of nodules, which vary in size from very small (<3 mm, micronodules) to large (several centimeters, macronodules), represents a balance between regenerative activity and constrictive scarring.
34
Cirrhosis Manifestation
Asymptomatic hepatomegaly to hepatic failure There are no symptoms until the disease is far advanced. The most common is weight loss (sometimes masked by ascites), weakness, and anorexia. Diarrhea +/- consitpation Hepatomegaly and jaundice Abdominal pain because of liver enlargement or stretching of the Glisson capsule. This pain is located in the epigastric area or in the upper right quadrant and is described as dull, aching, and causing a sensation of fullness.
35
Portal Hypertension
is characterized by increased resistance to flow in the portal venous system and sustained portal vein pressure.
36
Portal Hypertension Causes
caused by a variety of conditions that increase resistance to hepatic blood flow, including prehepatic, posthepatic, and intrahepatic obstructions
37
Splenomegaly
spleen enlarges progressively in portal hypertension because of shunting of blood into the splenic vein. The enlarged spleen often gives rise to sequestering of significant numbers of blood elements and development of a syndrome known as hypersplenism.
38
Hypersplenism
characterized by a decrease in the lifespan of all the formed elements of the blood and a subsequent decrease in their numbers, leading to anemia, thrombocytopenia, and leukopenia.
39
Liver Failure
Most severe clinical consequence of liver disease is hepatic failure. It may result from sudden and massive liver destruction, as in fulminant hepatitis, or be the result of progressive damage to the liver, as occurs in alcoholic cirrhosis.
40
Liver Failure Manifestations
Reflect the various synthesis, storage, metabolic, and elimination functions of the liver. Fetor hepaticus refers to a characteristic musty, sweetish odor of the breath in the person in advanced liver failure, resulting from the metabolic by-products of the intestinal bacteria.
41
Hepatic Encephalopathy
Refers to the totality of central nervous system manifestations of liver failure. Characterized by neural disturbances ranging from a lack of mental alertness to confusion, coma, and convulsions. Early sign of hepatic encephalopathy is a flapping tremor called asterixis. Suspected neurotoxin: ammonia
42
Hepatobiliary System
consists of: Gallbladder Left and right hepatic ducts, which come together to form the common hepatic duct; Cystic duct, which extends to the gallbladder Common bile duct, which is formed by the union of the common hepatic duct and cystic duct.
43
Cholelithiasis
Or gallstones is caused by precipitation of substances contained in bile, mainly cholesterol and bilirubin. 80%: cholesterol 20% mucin glycoproteins
44
2 Factors that Contribute to Gallstone Formation
1. abnormalities in the composition of bile (particularly increased cholesterol) Due to obesity 2. stasis of bile
45
Cholelithiasis Manifestations
People with gallstones have no symptoms. Symptoms occur when they obstruct bile flow or cause inflammation. Small stones (i.e., <8 mm in diameter) pass into the common duct, producing symptoms of indigestion and biliary colic. Larger stones are more likely to obstruct flow and cause jaundice. Pain of biliary colic is located in the upper right quadrant or epigastric area and may be referred to the upper back, the right shoulder, or midscapular region.
46
47
Acute Pancreatitis
Represents a reversible inflammatory process of the pancreatic acini brought about by premature activation of pancreatic enzymes. Disease process may be limited to pancreatic tissue, it also can involve peripancreatic tissues or those of more distant organs.
48
Pancreatitis Pathogenesis
Involves the autodigestion of pancreatic tissue by inappropriately activated pancreatic enzymes. Thought to begin with the activation of trypsin. Once activated, trypsin can then activate a variety of digestive enzymes that cause pancreatic injury, resulting in an intense inflammatory response.
49
Pancreatitis Manifestations
Range from mild with minimal organ dysfunction to severe and life-threatening. 20% of people with acute pancreatitis have a severe course. Abdominal pain is a cardinal manifestatation, located in the epigastric or periumbilical region and may radiate to the back, chest, or flank areas. Other include fever, tachycardia, hypotension, severe abdominal tenderness, respiratory distress, and abdominal distension.
50
Cancer of the Pancreas
most common: adenocarcinoma 85% Unknown cause. Occur early in younger than 50 years. Moist significant factor: smoking
51
Cancer of the Pancreas Manifestation
Early stage has no symptoms but spreads quickly making it difficult to detect. adenocarcinomas of the ductal epithelium, and symptoms are primarily caused by mass effect rather than disruption of exocrine or endocrine function. manifestationss depend on the size and location of the tumor as well as its metastasis. Pain, jaundice, and weight loss are classic presentation. The most common pain is a dull epigastric pain often accompanied by back pain, often worse in the supine position, and relieved by sitting forward.
52
Pathways of Lipid Metabolism
Occur mainly in the liver including the oxidation of free fatty acids to keto acids that supply energy for other body functions; synthesis of cholesterol, phospholipids, and lipoproteins; and formation of triglycerides from carbohydrates and proteins. Liver cant use all CoA formed so its converted to ace to acetic acid used for energy.