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370.3: Hepatic Disorders Flashcards

1
Q

What are the 2 sources of blood to the liver?

A
  1. Hepatic artery (500mL/min)
  2. Hepatic Portal Vein (1000mL/min)
    = partially oxygenated
    = connects back with inferior vena cava after filtering blood
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2
Q

What are the functions of the liver?

A
  1. Blood filtration + detox
  2. RBC production in fetus
  3. Synthesis + storage of amino acids, glycogen, blood proteins (albumin, fibrinogen, globulin, Heparin, clotting factors), vitamins (A, B, D, E, K), minerals, and fats
  4. Formation/excretion of bile
  5. Blood glucose regulation
  6. Hormone synthesis (ex. Angiotensin)
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3
Q

What is the pathophysiology pathway of injury on the liver?

A
  1. Injury (virus, obesity, alcohol, drugs)
  2. Hepatitis
    1. A. Inflammation
    2. B. Apoptosis
    3. C. Fibrosis. ⤴️ back to inflammation
  3. Cirrhosis (fibrosis + scar tissue)
  4. Hepatocellular Carcinoma
  5. Liver failure
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4
Q

What are EARLY clinical manifestations of liver dysfunction?

A

Early:

  1. Fatigue
  2. Weight changes
  3. GI disturbances
  4. Dull pain in RUQ/epigastrium
  5. FEVER
  6. Malaise
  7. Enlarged liver + spleen
  8. Pruritus
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5
Q

What are LATE clinical manifestations of liver dysfunction?

A

Late:

  1. Jaundice
  2. Skin lesions (spider angiomas, palmar erythema)
  3. Hematologic problema
  4. Endocrine disturbances
  5. Peripheral neuropathy
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6
Q

Why do skin lesions, such as spider angiomas and palmar erythema, present in liver dysfunction?

A

Theory caused by high levels of estrogen:

  1. Produces arterial vasodilation
  2. Liver detoxifies estrogen from blood
  3. Can be toxic
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7
Q

What are manifestations of Liver Disease?

A
  1. Portal hypertension
  2. Ascities
  3. Hepatic-encephalopathy
  4. Jaundice
  5. Hepatorenal Syndrome
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8
Q

What are the presentations of Portal Hypertension?

A
  1. Portal hypertension = 10 mmHg or greater (normal = 3 mmHg)
  2. Swelling, inflammation, fibrosis, scarring of liver
  3. Thrombosis
  4. Resistance in inferior vena cave = R CHF, myopathy
  5. Blood takes collateral channels = esophagus, anterior abdominal wall, rectum
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9
Q

What are consequences of portal hypertension?

A
  1. Varices (inc intersplenic pressure, 1/3 platelets stored can inc)
  2. Splenomegaly
  3. Ascites
  4. Hepatic encephalopathy (d/t toxic ammonia buildup)
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10
Q

Esophageal varices

A
  1. Collateral circulation develops in lower esophagus
  2. Most common symptom of portal hypertension is vomiting blood from bleeding esophageal varices
  3. Portal pressure >10% takes 4 years to develop varices
  4. More likely to rupture at Bottun, more reflux and acidity
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11
Q

What are symptoms of hepatic encephalopathy?

A
  1. Impaired cognition
  2. Asterixis (flapping hands)
  3. EEG changes
  4. Personality changes
  5. Confusion, memory loss
  6. Stupor, coma, death
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12
Q

What is the pathophysiology of hepatic encephalopathy?

A

Poor liver function permits neurotoxins and other harmful substances absorbe from GI tract to circulate to brain
(ex. AMMONIA)

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13
Q

What levels of bilirubin cause Jaundice?

A

Bilirubin > 2.5 - 3 mg/dL

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14
Q

What are the 3 types of Jaundice?

A
  1. Hemolytic
  2. Obstructive
  3. Hepatocellular
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15
Q

Hemolytic Jaundice

A

Excessive destruction of RBCs

  1. Mismatched blood transfusion
  2. Sickle Cell Disease
  3. Fetal/maternal mismatch
  4. Hemolytic anemia
  5. Severe infection
  6. Toxins
  7. Immune response
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16
Q

Obstructive Jaundice

A

Blockage in the passage of conjugated bilirubin (water soluble) from the liver to the intestine.

  1. Gallstone/tumour obstruction of bile duct
  2. Obstruction of bile flow through liver
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17
Q

Hepatocellular Jaundice

A

Failure of liver cells to conjugate bilirubin and of bilirubin to pass from liver to intestine.

  1. Hepatitis
  2. Biliary cirrhosis
  3. Physiological changes
  4. Baby Jaundice
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18
Q

How are where does bilirubin get conjugated?

A
  1. Bilirubin passes from blood cells to liver
  2. Albumin needed to transfer
  3. Liver conjugates bilirubin into water-soluble molecule
  4. Passes through bile duct into intestines
  5. Urobilinogen formed by bacteria in gut
  6. Excreted as STERCOBILIN in feces
    OR
  7. Reabsorbed by kidneys and excreted as UROBILIN in urine
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19
Q

Where is one place a nurse can see Jaundice on every patient?

A

Sclera of eyes

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20
Q

What is the hematological mechanism of Jaundice?

A
  1. Excessive lysis of RBCs
  2. Hepatocytes Connor conjugate + excrete bilirubin as rapidly as formed
  3. Bilirubin enters bloodstream
  4. UNCONJUGATED HYPERBILIRUBINEMIA
  5. Jaundice (bilirubin deposits in tissues)
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21
Q

What is the mechanism of intraheptic obstructive Jaundice?

A
  1. Hepatocellular damage/obstruction of bile canaliculi
  2. Decreased liver ability to excrete bilirubin
  3. Conjugated and UNCONJUGATED HYPERBILIRUBINEMIA
  4. Jaundice (bilirubin deposits in tissue)
22
Q

What is the mechanism of extraheptic obstructive Jaundice?

A
  1. Bile duct obstruction (CHOLESTASIS)
  2. Conjugated bilirubin accumulates in liver and enters blood stream
  3. Light-coloured stools (dec bile)
  4. CONJUGATED HYPERBILIRUBINEMIA
  5. Increased secretion of bilirubin in urine
  6. Jaundice (bilirubin deposits in tissue)
23
Q

Hepatorenal Syndrome (HRS)

A

Renal failure associated with liver failure

  1. Hypovolemia
  2. Hypotension
  3. Decreased renal blood flow
  4. Intestinal vasoconstriction
  5. Decreased GFR
  6. Decreased urine output
24
Q

What is the route of transmission for Hepatitis A?

A
  1. Fecal-Irak

2. Parenteral (rare)

25
Q

What is the route of transmission for Hepatitis B?

A
  1. Parenteral
  2. Sexual
  3. Perinatally
26
Q

What is the route of transmission for Hepatitis C?

A

Parenteral only

27
Q

What is the route of transmission for Hepatitis D?

A
  1. Parenteral

2. Sexual

28
Q

What is the route of transmission for Hepatitis E?

A

Fecal-oral

29
Q

Which Hepatitis viruses are can be chronic?

A
  1. Hep B (adults <5%, preschool: 25%, neonates: 90%)
  2. Hep C (70-80%)
  3. Hep D
30
Q

Which hepatitis viruses can be prevented by immunization?

A
  1. Hep A
  2. Hep B
  3. Hep D* (because needs Hep B to survive)
31
Q

What is the prophylaxis for Hepatitis A?

A
  1. Immunization before and after exposure
    (for travel)

Havrix: 2 doses IM

Twinrix: HAV + HBV @ 0-, 1-, and 6-months

32
Q

What is the prophylaxis for Hepatitis B?

A

Immunization before and after exposure
(Common routine vaccine)

Hep B Immune globulin (HBIg) = within 48 hrs of exposure

Twinrix = HAV + HBV @ 0-, 1-, and 6-months

33
Q

What is the prophylaxis for Hepatitis C?

A
  1. Blood donor screening

2. Risk behaviour modification (harm reduction, safe injection supplied, etc)

34
Q

What is the prophylaxis for Hepatitis D?

A

Immunization for Hep B (HBV) prevents HDV due to HDV dependent on HBV for replication

35
Q

What is the prophylaxis for Hepatitis E?

A

Ensure safe drinking water

No vaccine

36
Q

What is the pathophysiology of Hepatitis?

A
  1. Acute infections
  2. Liver damage mediated by:
    Cytotoxic cytokines
    Natural killer cells
  3. Results in hepatic cell necrosis
  4. Inflammation of periportal areas may interrupt bile flow
  5. CHOLESTASIS May occur

➡️ liver cells can regenerate if rested and no complications

37
Q

What are systemic effects of the activation of antigen-antibody complex activation from Hepatitis?

A
  1. Rash
  2. Angioedema
  3. Arthritis
  4. FEVER
  5. Malaise
  6. Cryoglobulinemia
  7. Glomerulonephritis
  8. Vasculitis
38
Q

What are the stages of hepatitis disease progression?

A
  1. Incubation Phase
  2. Prodronal (preicteric) phase (Pre-Jaundice)
  3. Acute (Interic/anticteric) Phase (Jaundice)
  4. Convalescent/Recovery Phase
    OR
  5. Chronic active hepatitis
39
Q

Fulminant Hepatitis

A

From impairment or necrosis of hepatocytes

40
Q

Acute Hepatic Failure

A

Ex. Acetaminophen overdose

4 grams in 24hrs for healthy adults

41
Q

What are clinical manifestations of the Prodromal (Preicteric) Phase is hepatits?

A
  1. Flu-like symptoms
  2. General malaise
  3. Fatigue
  4. Body aches, headache
  5. GI symptoms - n/v, diarrhea, abd discomfort
  6. Low grade FEVER, Chills
42
Q

What are clinical manifestations of the Acute Phase is Hepatits?

A

(1 - 4months) MAX INFECTIVITY PERIOD

  1. ICTERIC or ANICTERIC (Jaundice vs. No jaundice)
  2. Anorexia (weight loss)
  3. Abdominal discomfort
  4. Hepatomegaly + tender liver
  5. Lymphadenopathy
  6. Splenomegaly
  7. Dark urine (bilirubin)
  8. Clay-coloured stool
  9. Pruritus with Jaundice (bile salts itchy)
  10. Fever subsided when Jaundice occurs
43
Q

What are clinical manifestations of the Convalescent Phase is Hepatits?

A

(Weeks - months)

  1. Malaise
  2. Easily fatigability

Almost all cases of Hep A are resolved

44
Q

What is the pathophysiology of Cirrhosis?

A
  1. Hepatocytes are destroyed and portal HTN develops
  2. Liver cells attempt to regenerate
  3. Functional live tissue is destroyed
  4. Liver scars
  5. New fibrous connective tissue (NODULES) distorts liver’s normal structure
  6. Impedes blood flow
45
Q

Alcoholic Cirrhosis

A

Oxidation of alcohol damages hepatocytes

46
Q

Biliary Cirrhosis

A

Cirrhosis begins in bile canaliculi and ducts.

Primary = autoimmune 
Secondary = obstruction
47
Q

Postnecrotic Cirrhosis

A

Caused by viruses, drugs, or other toxins. May also be caused by autoimmune destruction.

48
Q

What is the pathophysiology of Alcoholic Cirrhosis?

A

Fat accumulates in liver. Liver hepatocytes cannot break down fat cells.
Increased lipogenesis and decreased fatty acid oxidation by hepatocytes.
Derangement of the lobular architecture by necrosis and fibrosis with obstruction of biliary and vascular channels.

49
Q

What are the major complications of cirrhosis?

A
  1. Portal hypertension
  2. Variceal bleeding
  3. Ascites
  4. Spontaneous bacterial peritonitis
  5. Hepatorenal Syndrome
  6. Hepatic encephalopathy
50
Q

Hypoalbuminemia

A

Decreased colloidal oncotic pressure

51
Q

Hyperaldosteronism

A

Increased sodium absorption due to accumulation of serious fluid in peritoneum from Cirrhosis

52
Q

What 4 factors lead to ascites?

A
  1. Hypoproteinemia
  2. Increased capillary permeability
  3. Portal hypertension
  4. Increased sodium and water retention

Nursing - Bloomberg (52 decks)

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