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Pathophysiology: Test 4 > The Liver > Flashcards

The Liver Flashcards

0
Q

Portal Hypertension

A
  1. Abnormally high BP in the portal venous system
  2. Normal pressure is 3mm Hg
  3. Portal HTN is an increase to at least 10 mm Hg.
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1
Q

Liver Disease

-Life Threatening Complications

A
  1. Portal Hypertension
  2. Ascites
  3. Hepatic encephalopathy
  4. Jaundice
  5. Hepato-renal Syndrome
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2
Q

Portal Hypertension

-Caused by?

A
  1. Caused by disorders that obstruct or impede blood flow through any component of the portal venous system or vena cava
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3
Q

Portal Hypertension

-Intra-hepatic Causes

A
  1. Results from vascular remodeling w/ shunts, thrombosis, inflammation, or fibrosis of the sinusoids
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4
Q

Portal Hypertension

-Intra-Hepatic Examples

A

Occurs in:

  1. CIRRHOSIS**
  2. Viral hepatitis
  3. Schistosomiasis (parasitic infection)
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5
Q

Portal Hypertension

-Post-Hepatic Causes

A
  1. Occur from hepatic vein THROMBOSIS or cardiac disorders that impair the pumping ability of the RIGHT HEART
    - Right Sided HF
    - Cardiomyopathy
    - Constrictive pericarditis
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6
Q

Portal Hypertension

-Most Common Cause

A
  1. Fibrosis & Obstruction caused by cirrhosis of the liver
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7
Q

Long-Term effects of Portal Hypertension

A
  1. Varices
  2. Splenomegaly
  3. Ascites
  4. Hepatic encephalopathy
  5. Hepatopulmonary syndrome
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8
Q

Portal Hypertension

-Pre-hepatic Causes

A
  1. Thrombosis before circulation reaches the liver
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9
Q

Varices

A
  1. Distended, tortuous, collateral veins

2. Rupture of varices can cause life-threatening hemorrhage

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10
Q

Splenomegaly

A
  1. Enlargement of the spleen caused by increased pressure in the splenic vein, which branches from the portal vein.
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11
Q

Congestive Splenomegaly

-Most Common Symptom

A
  1. Thrombocytopenia is the most common symptom of congestive splenomegaly
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12
Q

Caput Medusae

A
  1. Prominent superficial abdominal veins seen on a patient w/ cirrhosis and portal hypertension
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13
Q

Hepatopulmonary Syndrome

A
  1. Vasodilation, intrapulmonary shunting & hypoxia
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14
Q

Portopulmonary Hypertension

A
  1. Pulmonary vasoconstriction and vascular remodeling
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15
Q

Liver Dx and Portal HTN

-Complications

A
  1. Hepatopulmonary syndrome
  2. Portopulmonary HTN
    - Both are complications of liver dx and portal HTN
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16
Q

Portal Hypertension

-Most common Manifestation

A
  1. Vomiting of blood (hematemesis) from bleeding esophageal varices is the most common clinical manifestation of portal HTN
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17
Q

Esophageal Varices

-What Happens when they Rupture?

A
  1. Causes hemorrhage
  2. Voluminous vomiting of dark-colored blood
  3. Usually painless
  4. Rupture is caused by combination of erosion by gastric acid and elevated venous pressure
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18
Q

Portal Hypertension

-Diagnoses

A
  1. Portal HTN is often dx at the time of variceal bleeding
  2. Dx is confirmed by endoscopy and evaluation of portal venous pressure
  3. Pt usually has hx of jaundice, hepatitis, or alcoholism
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19
Q

Ascites

A
  1. Accumulation of fluid in the peritoneal cavity

2. Traps body fluid in a ‘third space’

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20
Q

Third Spacing

A
  1. Accumulation of body fluid in a space where it does not normally collect
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21
Q

Ascites

-Most Common Cause?

A
  1. Cirrhosis is the most common cause of ascites
  2. Also Caused by:
    - HF
    - Constrictive pericarditis
    - Abdominal malignancies
    - Nephrotic syndrome
    - Malnutrition
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22
Q

Ascites

-Factors that contribute to development

A
  1. Decreased synthesis of albumin by the liver & fluid retention
  2. Portal HTN
  3. Hydrostatic pressure exceeding capillary osmotic pressure
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23
Q

Ascites

-Clinical Manifestations

A
  1. Weight gain
  2. Abdominal distention / increased abdominal girth
  3. Dyspnea by decreasing lung capacity
  4. RR increases and individual assumes semi-fowler position
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24
Q

Ascites

-Bacterial Peritonitis

A
  1. 10% of individuals with ascites develop bacterial peritonitis
  2. Causes:
    - Fever & Chills
    - Abdominal pain
    - Decreased bowel sounds & cloudy ascitic fluid
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25
Q

Hepatic Encephalopathy

A
  1. Complex neurologic syndrome characterized by impaired cerebral function, flapping tremor (asterixis), and electroencephalogram (EEG) changes.
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26
Q

Hepatic Encephalopathy

-Development of the syndrome?

A
  1. Hepatic encephalopathy develops rapidly during acute fulminant hepatitis
  2. Develops slowly during the course of chronic liver disease and the development of portal HTN
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27
Q

Hepatic Encephalopathy

-Pathophysiology

A
  1. Collateral vessels develop that shunt blood around liver to the systemic circulation
  2. Absorbed toxins from the GI tract are permitted to accumulate and circulate freely to the brain
  3. Accumulated toxins alter cerebral energy metabolism, interfere w/ neurotransmission, and cause edema
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28
Q

Hepatic Encephalopathy

-Most Hazardous Substances??

A
  1. End products of intestinal protein digestion, particularly AMMONIA, which cannot be converted to urea by the diseased liver.
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29
Q

Factors that Precipitate Hepatic Encephalopathy

A
  1. Infection
  2. Hemorrhage
  3. Electrolyte imbalance (including zine deficiency)
  4. Use of sedatives and analgesics
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30
Q

Hepatic Encephalopathy

-Initial Manifestations

A
  1. Subtle changes in personality
  2. Memory loss
  3. Irritability & lethargy
  4. Sleep disturbances
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31
Q

Hepatic Encephalopathy

-Late Manifestations

A
  1. Confusion
  2. Flapping tremor of the hands (asterixis)
  3. Stupor
  4. Convulsions
  5. Coma & Death from Liver failure
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32
Q

Hepatic Encephalopathy

-1st step in Treatment

A
  1. Correction of fluid and electrolyte imbalance

2. Withdrawal of depressant drugs metabolized by the liver

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33
Q

Hepatic Encephalopathy

-Lactulose?

A
  1. Administered to prevent AMMONIA absorption in the colon
34
Q

Jaundice

A
  1. Yellow or greenish pigmentation of the skin caused by hyperbilirubinemia (plasma bilirubin concentrations > 2.5 to 3.0 mg/dl
35
Q

Jaundice

-Caused by?

A
  1. Post-hepatic obstruction to bile flow
  2. Intra-hepatic obstruction
  3. Pre-Hepatic excess production of unconjugated bilirubin
    - excessive hemolysis of RBC’s
36
Q

Jaundice in Newborns

-Caused By?

A
  1. Caused by impaired bilirubin uptake and conjugation
37
Q

Obstructive Jaundice

-Caused by?

A
  1. Obstructive Jaundice can result from extra-hepatic (post-hepatic) or intra-hepatic obstruction
38
Q

Extra-Hepatic (Post-hepatic) Obstructive Jaundice

-Caused by?

A
  1. Develops if the common bile duct is occluded w/:
    - Gallstone
    - Tumor
    - Inflammation
39
Q

Intra-Hepatic Obstructive Jaundice

-Caused by?

A
  1. Disturbances in hepatocyte function and obstruction of bile canaliculi
40
Q

Pre-hepatic Jaundice

A
  1. Also referred to as hemolytic Jaundice

2. Caused by excessive hemolysis (destruction) of RBC’s

41
Q

Jaundice

-Clinical Manifestation

A
  1. If there is a complete obstruction of bile flow from the liver to the duodenum, the patient will have light-colored (clay colored) stools.
42
Q

Viral or Bacterial Caused Jaundice

-Clinical Manifestations

A
  1. Fever, chills, and pain

Ex. Viral Hepatitis

43
Q

Where to first spot Jaundice?

A
  1. Yellow discoloration may first occur in the sclera of the eye and then progress to the skin as bilirubin attaches to elastic fibers
44
Q

Hepato-renal Syndrome

A
  1. Functional renal failure that develops as a complication of advanced liver disease
45
Q

Hepato-renal Syndrome

-How is the Renal Failure caused?

A
  1. Renal failure is caused by:
    -Portal HTN and other circulatory alterations associated w/ advanced liver disease, such as alcoholic cirrhosis or fulminant hepatitis w/ portal HTN and functional renal failure including oliguria, sodium and water retention, hypotension, and peripheral vasodilation
    PG 919
46
Q

Hepato-Renal Syndrome

-Manifestations

A
  1. May be gradual or acute
    - Oliguria
    - Jaundice
    - Ascites
    - GI bleeding
47
Q

What does Elevated Prothrombin Time Mean??

A
  1. Elevated prothrombin time due to lack of synthesis of clotting factors may occur in liver disease
48
Q

Elevated Prothrombin time

-Associated with?

A
  1. Elevated prothrombin time is more associated with ACUTE LIVER DISEASE
49
Q

Decrease in Albumin

-Associated with?

A
  1. Decrease in albumin is generally associated with chronic liver disease
50
Q

Viral Hepatitis

-Hepatitis A Transmission

A
  1. Fecal-Oral

2. 40% of world’s population

51
Q

Viral Hepatitis

-Hepatitis A Clinical Manifestations

A
  1. Acute viral hepatitis
    - fever, jaundice, and a painful enlarged liver
  2. 1% develop fulminant hepatitis
  3. NEVER becomes chronic
52
Q

Viral Hepatitis

-Hepatitis B Transmission

A
  1. Blood transfusion
  2. Needle sticks
  3. Sexual
  4. Across the placenta
53
Q

Viral Hepatitis

-Hepatitis B Clinical Manifestations

A
  1. Acute viral hepatitis
  2. Fulminant hepatitis
    - severe acute hepatitis w/ rapid destruction of the liver
  3. Chronic hepatitis 10%
54
Q

Viral Hepatitis

-Hepatitis B Complications

A
  1. Primary hepatocellular carcinoma

2. Cirrhosis

55
Q

Viral Hepatitis

-Hepatitis C Transmission

A
  1. Blood transfusion
  2. Needle sticks
  3. Sexual
  4. Across the placenta
56
Q

Viral Hepatitis

-Clinical Manifestations

A
  1. Acute viral hepatitis
  2. 50% will get chronic hepatitis
  3. 20% will develop cirrhosis
  4. Increase risk of developing primary Hepatocellular carcinoma
57
Q

Viral Hepatitis

-Hepatitis C Statistic and Treatment

A
  1. Immunoglobulins & Interferon

2. Hepatitis C lives on dry surfaces for 30 days

58
Q

Viral Hepatitis

-Hepatitis D Transmission

A
  1. Blood Transfusion
  2. Needle sticks
  3. Sexual
  4. Across the placenta
59
Q

Viral Hepatitis

-Hepatitis D Clinical Manifestations

A
  1. Coinfection:
    - HBV and HDV are acquired at the same time
    - Cause an acute hepatitis
60
Q

Viral Hepatitis

-Hepatitis D Complications

A
  1. Fulminant hepatitis

2. Cirrhosis

61
Q

Cirrhosis

-Complications

A
  1. Portal Hypertension
    - Right-sided HF
    - Esophageal Varices
    - Varicose Veins
  2. Ascites
  3. Encephalopathy/Coma
  4. Hepatorenal syndrome
62
Q

Acute Fulminating Hepatitis

A
  1. Associated with Hepatitis B
  2. Characterized by massive hepatic necrosis
  3. Causes severe encephalopathy
    - manifested as confusion, stupor & coma
63
Q

Clinical Hepatitis

-Prodromal Phase

A
  1. Begins 2 weeks after exposure & ends with the appearance of Jaundice
  2. Marked as:
    - fatigue, anorexia, malaise, N/V, headache, hyperalgia, cough, low-grade fever
  3. Infection is highly transmissible during prodromal phase
64
Q

Clinical Hepatitis

-Icteric Phase

A
  1. Begins 1-2 weeks after prodromal phase
  2. Lasts 2 to 6 weeks
  3. Acute Phase of illness
65
Q

Clinical Hepatitis

-Icteric Phase Manifestations

A
  1. Jaundice
  2. Dark Urine
  3. Clay-colored stool
  4. Liver is enlarged, smooth, and tender and percussion causes liver pain.
66
Q

Clinical Hepatitis

-Recovery Phase

A
  1. Begins w/ resolution of jaundice (6-8 weeks after exposure)
  2. Symptoms diminish but the liver remains enlarged and tender
  3. Liver function returns to normal 2-12 weeks after the onset of jaundice.
67
Q

Chronic Hepatitis

A
  1. Persistence of clinical manifestations and liver inflammation after acute stages of HBV & HCV infection
  2. Liver function tests remain abnormal for > 6 months
    - HepB surface antigen persists
  3. Predisposes to cirrhosis and primary hepatocellular carcinoma
68
Q

Chronic Hepatitis

-Extra-hepatic Manifestations

A
  1. Arthralgias
  2. Fatigue
  3. Neurologic & renal symptoms
69
Q

Leading Cause of Liver Failure in US?

A
  1. Acetaminophen overdose is the leading cause of liver failure in the United States
70
Q

Hepatic Encephalopaty

-Clinical Manifestations

A
  1. Lethargy
  2. Altered motor function
  3. Coma
    - Manifestations are R/T cerebral edema, ischemia, & brain stem herniation
71
Q

Cirrhosis

A
  1. Irreversible inflammatory, fibrotic liver disease and is a leading cause of death in the US
72
Q

Alcoholic Fatty Liver

A
  1. Mildest form of alcoholic liver disease
  2. Can be caused by relatively small amounts of alcohol
  3. May be asymptomatic
  4. Reversible w/ cessation of drinking
73
Q

Alcoholic Steatohepatitis

A
  1. Precursor of cirrhosis characterized by:

- Inflammation, degeneration, & necrosis of hepatocytes and infiltration of neutrophils and lymphocytes

74
Q

The Liver: Review

-What vitamins are stored in liver?

A
  1. The liver stores fat-soluble vitamins

- A, E, D, & K

75
Q

The Liver: Review

-Everything that the liver does?

A
  1. Produces Bile
  2. Stores Fat-soluble Vitamins
  3. Metabolizes bilirubin
  4. Synthesizes plasma proteins
  5. Synthesizes prothrombin, fibrinogen, and clotting factors
  6. Stores and releases glucose
  7. Stores Iron as ferritin
76
Q

The Liver: Review

-Bilirubin?

A
  1. The liver metabolizes bilirubin

- bilirubin is a byproduct of the lysis of old RBC’s

77
Q

The Liver: Review

-Albumin?

A
  1. The liver synthesizes plasma proteins (albumin) to maintain plasma Oncotic pressure
78
Q

The Liver: Review

-How does the liver Decrease bleeding?

A
  1. The liver synthesizes prothrombin, fibrinogen, and clotting factors
79
Q

Pt’s with Liver Failure

-What is the treatment when they are unable to coagulate correctly?

A
  1. Use Fresh Frozen Plasma
80
Q

The Liver: Review

-Glucose

A
  1. The liver stores and releases glucose

- Helps maintain blood sugar LONG-TERM

81
Q

The Liver: Review

-Iron

A
  1. The liver stores iron as ferritin

- Problem w/ oxygen carrying capacity if liver is damaged

82
Q

The Liver: Review

-Alcohol & Drug Metabolism

A
  1. The liver detoxifies alcohol and certain drugs

Pathophysiology: Test 4 (9 decks)

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