Metabolism Flashcards

Liver disorders, inflammation, hepatitis, cirrhosis.

1
Q
  • What does the liver do?
A

Metabolizes bilirubin (byproduct of the destruction of old RBCs).

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2
Q
  • What happens when RBCs die?
A

Iron is recycled and stored as ferritin.

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3
Q
  • What is hepatic encephalopathy?
A

Decreased in detoxification reactions. Ammonia from breakdown can cause encephalopathy.

Liver can’t filter out and detoxify the ammonia.

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4
Q
  • When the liver cannot filter out and detoxify the ammonia, this causes?
A

Encephalopathy, altered LOC, seizures, coma, death.

Encourage patient to monitor protein by cutting it down.

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5
Q
  • What will decreased protein production and decreased oncotic pressure lead to?
A

Ascites.

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6
Q
  • Decrease in protein production can decrease?
A

Clotting factor production, increasing the risk of bleeding.

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7
Q
  • What causes hemolytic jaundice?
A

Bilirubin from the breakdown of RBCs.

Excessive hemolysis of RBCs or absorption of hematoma.

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8
Q
  • Leading cause of cirrhosis?
A

Alcoholism.

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9
Q
  • Thrombosis can cause?
A

Portal hypertension and is a pre hepatic problem.

Occurs before it gets to the liver.

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10
Q

What is portal hypertension?

A

High blood pressure in the portal vein system.

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11
Q

What is the portal vein system composed of?

A

The portal vein, its branches and its tributaries.

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12
Q

Elevation of hepatic venous pressure gradient?

A

> 55 mmHg.

(Normal is 3).

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13
Q
  • What can be caused by portal hypertension?
A

Varicose veins, vomiting, anything that causes pressure in the body (vomiting, valsalva maneuver, pushing during labor), or any increase in pressure can cause bleeding and the varices to bleed.

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14
Q
  • What are varicose veins?
A

They are distended neck veins caused by portal hypertension. More commonly in esophageal varicose.

Pressure can cause the varicose to start bleeding which can become a problem.

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15
Q
  • AST & ALT determine?
A

How much alcohol is in the system.

You would not expect to see AST & ALT in very end stage liver failure.

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16
Q

Why would AST & ALT not be elevated in very end stage liver failure?

A

Hepatocytes are no longer being produced.

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17
Q

Three phases in viral hepatitis?

A
  1. Viral replication.
  2. Prodromal.
  3. Icteric phase.
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18
Q
  • Signs and symptoms of icteric phase?
A

Most commonly jaundice, enlarged liver, and dark urine.

Pale colored stool, in addition to the predominant GI symptoms from malaise, patients become icteric and may develop upper quadrant pain with hepatomegaly.

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19
Q

Significance of viral hepatitis?

A

Varies with the individual, as well as with the specific causative virus.

Some patients may be entirely symptomatic or mildly symptomatic at presentation.

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20
Q
  • Cause of elevated prothrombin time?
A

Lack of synthesis of clotting factors that may occur in liver disease.

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21
Q

Prothrombin time is more often associated with?

A

Acute liver disease.

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22
Q

Decrease in albumin is associated with?

A

Chronic liver disease.

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23
Q

What are the 5 types of hepatitis?

A

A, B, C, D, and E.

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24
Q
  • Hepatitis A transmitted by?
A

Fecal-oral route (feces, bile, sera of infected people).

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25
* Hepatitis B transmitted by?
Infected blood, body fluids, or contaminated needles.
26
* Hepatitis C transmitted by?
Implicated in infections related to IV drug use.
27
* Hepatitis D transmitted by?
Same as Hepatitis B. Infected blood, body fluids, or contaminated needles.
28
* Hepatitis E transmitted by?
The same as Hepatitis A. Fecal-oral route.
29
* How else is Hepatitis B transmitted by?
Maternal transmission if the mother is infected during the 3rd trimester.
30
* The worst types of Hepatitis to get are?
Hepatitis B and C because patients with hepatitis B go into chronic hepatitis.
31
* Can Hepatitis A become a chronic illness?
No.
32
* Most common symptom of Hepatitis A?
Fever.
33
What can help prevent transmission and development of Hepatitis B?
Hepatitis B vaccine.
34
* Hepatitis D cannot be obtained without?
Hepatitis B.
35
* Hepatitis D + B.
Hepatitis D and B go together. You can have Hepatitis B as a standalone disease, but D will always occur along with Hepatitis B.
36
* Complications of Hepatitis D?
Fulminant hepatitis, cirrhosis.
37
* Complications of Hepatitis B?
Chronic necrosis, encephalopathy, and organ failure.
38
* Hepatitis C increases the risk for?
Hepatocellular carcinoma.
39
What is hepatitis?
Inflammation of the liver?
40
What causes hepatitis?
Infections (usually viral), alcohol, medications (acetaminophen, anti-seizure agents, and antibiotics, or autoimmune disease.
41
Characteristics of hepatitis?
Can be acute, chronic, or fulminant. Can be active or nonactive.
42
During non-viral hepatitis?
Not contagious, and the person usually recovers.
43
A person with non-viral hepatitis may develop?
Liver failure, liver cancer, or cirrhosis.
44
What can hepatitis result in?
Hepatic cell destruction, necrosis, autolysis, hyperplasia, and scarring.
45
Characteristics of viral hepatitis?
Contagious, usually recover in time with no residual damage.
46
Advancing age and comobidity in persons with viral hepatitis can cause?
Increase likelihood for development of liver failure, liver cancer, or cirrhosis.
47
Hepatitis A risk factors?
Crowded, unsanitary conditions. Food and water contamination.
48
What is Hepatorenal Syndrome?
Renail failure demonstrating oliguria, sodium and water retention, hypotension, and peripheral vasodilation.
49
Hepatorenal Syndrome is caused by?
Advanced liver disease.
50
Another word for Jaundice is?
Icterus.
51
Obstructive jaundice consists of?
1. Extrahepatic obstruction. | 2. Intrahepatic obstruction.
52
Hemolytic jaundice consists of?
1. Prehepatic jaundice. | 2. Excessive hemolysis of RBCs or absorption of a hematoma.
53
What is hepatic encephalopathy?
A neurologic syndrome of impaired cognitive function, flapping tremor, and EEG changes.
54
When does hepatic encephalopathy develop?
It develops rapidly during fulminant hepatitis or slowly during chronic liver disease?
55
Varices consists of?
Lower esophagus, stomach, and rectum.
56
Consequences of portal hypertension?
1. Varices 2. Splenomegaly 3. Ascites 4. Hepatic encephalopathy 5. Systemic hypertension
57
Factors affecting metabolism?
1. Endocrine System | 2. Hepatic System
58
Purpose of endocrine system?
Production, synthesis, and release of hormones.
59
The liver metabolizes?
Carbs, proteins, fats, meds (to prepare them for excretion).
60
The liver synthesizes?
Glucose, protein, cholesterol, triglycerides, and clotting factors.
61
The liver stores and releases?
Glucose, fats, and micronutrients.
62
The liver detoxifies?
Blood of potentially harmful chemicals.
63
The liver maintains?
Intravascular fluid volume.
64
The liver produces?
Bile
65
The liver inactivates and prepares?
Hormones for excretion.
66
The liver removes?
Damaged or old RBCs.
67
Why does the liver removes damaged or old RBCs?
So that it can recycle iron and protein.
68
The liver serves as?
A blood reservoir.
69
The liver converts?
Fatty acids to ketones.
70
What is portal hypertension?
Abnormally high blood pressure in the portal venous system.
71
Portal hypertension is caused by?
Resistance to portal blood flow.
72
The 3 types of portal hypertension are?
1. Prehepatic. 2. Intrahepatic. 3. Posthepatic.
73
What are the liver disorders?
1. Portal hypertension 2. Hepatic encephalopathy 3. Jaundice
74
Can a person live without a liver?
No.
75
Can the liver regenerate?
To an extent.
76
50% to 80% of hepatitis C cases result in?
Chronic hepatitis.
77
Hepatitis C is responsible for most cases of?
Post-transfusion hepatitis.
78
Hepatitis G is transmitted by?
Hepatitis G has been recently discovered and is transmitted parentally and sexually.
79
What is an acute infection?
Liver damage.
80
In acute infection, liver damage is mediated by?
1. Cytotoxic cytokines. | 2. Natural killer cells.
81
Liver cell damage in acute infection results in?
Hepatic cell necrosis.
82
Acute infection inflames?
The periportal areas that may interrupt bile flow.
83
Acute infection causes proliferation and enlargement of?
Kupffer cells.
84
What forms inflammation?
Antigen-antibody complexes.
85
Systemic effects of inflammation?
Rash, angioedema, arthritis, fever, malaise, glomerulonephritis, vasculitis.
86
Sequence of Hepatitis?
1. Incubation phase. 2. Prodromal (preicteric) phase. 3. Icteric phase. 4. Recovery phase.
87
Fuliminant hepatitis results from?
Impairment or necrosis of hepatocytes.
88
What is chronic active hepatitis?
Persistant symptoms.
89
What are the 2 types of hepatitis that can form?
1. Chronic active hepatitis. | 2. Fulminant hepatitis.
90
What is cirrhosis?
Chronic, progressive, irreversible, diffuse damage to the liver.
91
Cirrhosis results in?
Decreased liver function.
92
Most common etiology for cirrhosis?
Hepatitis.
93
How long does cirrhosis take to develop?
Up to 40 years.
94
The problem with removing the underlying cause of cirrhosis?
Cirrhosis can still develop.
95
Cirrhosis leads to?
Fibrosis, nodule formation, impaired blood flow, and bile obstruction that can result in liver failure.
96
The 2 types of cirrhosis?
1. Alcoholic. | 2. BIliary (bile canaliculi)
97
What is Alcoholic Cirrhosis?
Oxidation of alcohol which damages hepatocytes.
98
Where does Biliary Cirrhosis begins?
Bile cannaliculi and ducts.
99
Primary biliary cirrhosis?
Autoimmune.
100
Secondary biliary cirrhosis?
Obstruction.
101
* Systolic pressure in hepatorenal syndrome?
< 100 mmHg
102
* Signs and symptoms of hepatorenal syndrome?
Anorexia, weakness, and fatigue.
103
* Renal failure is a complication of advanced liver disease caused by?
1. Portal hypertension 2. Alcoholic cirrhosis 3. Portal hypotension 4. Peripheral vasodilation
104
Maternal transmission of infected mother during third trimester?
Puts newborns at risk by 80-90%.
105
Maternal transmission of infected mother in the first trimester?
10%
106
* Alcoholic Cirrhosis can cause?
Fatty liver, which is reversible.
107
* Important result in hepatitis?
Necrosis.
108
* Obstructive Jaundice Pathway?
1. Obstructive jaundice. 2. Bile duct obstruction. 3. Light colored stools. 4. Conjugated bilirubin accumulated in liver and enters blood stream. 5. Excreted in urine which causes urine to be dark. 6. Deposited in tissues which causes person to be jaundiced.
109
What happens to the cells in hepatic encephalopathy?
Cells in the nervous system are vulnerable to neurotoxins absorbed from the GI tract. Circulate to the brain because of liver dysfunction.
110
* Ascites Pathway?
1. Increased capillary permeability. 2. Loss of plasma. 3. Ascites.
111
* Hepatits A Prevalence?
40%
112
* Hepatitis B Prevalence?
5%
113
Hepatitis C Prevalence?
20% | 50% Chronic