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High Acuity > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What is the largest solid organ in the body?

A

Liver

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2
Q

How fast and what kind of blood enters the liver?

A

Arterial (hepatic artery) and venous (portal vein) blood enters the liver at 1800 ml/min

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3
Q

What is the functional unit of the liver?

A

Hepatic lobules (there are 8)

When you break the liver down into sections/functional units you get lobules- contain rows of hepatic cells (hepatocytes) arranged around a central vein

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4
Q

Explain blood flow through the liver

A
  1. Receives oxygenated blood from hepatic artery branching off aorta
  2. Receives deoxygenated blood from portal vein from stomach, intestines, spleen and pancreas TO the liver. The blood, though deoxygenated, is containing newly absorbed nutrients, drugs and other organisms from the GI tract. Is detoxified and purified in the liver before entering the inferior vena cava and returning to the heart
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5
Q

What locations does the portal vein carry blood from?

A

stomach, spleen, pancreas, and intestines

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6
Q

What % of cardiac output flows through the liver?

A
  • Receives 1800ml/min
  • Normal CO = 5-6L/min
  • Approx 30%
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7
Q

Hepatobiliary Functions (10)

A
  1. Phagocytosis/Immune
  2. Bilirubin Metabolism
  3. Production/processing of cholesterol
  4. Biotransformation/Detoxification
  5. Bile production, metabolism, excretion
  6. Enzyme synthesis and activation
  7. Protein Synthesis
  8. Metabolic functions
  9. Blood volume reservoir
  10. Filtering
  11. Blood clotting
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8
Q

How does the liver function in cholesterol?

A

Produces LDL and HDL

Rids of it through bile

Cholesterol = precursor to hormones and vitamin D

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9
Q

Function of bile

A

a fluid that is made and released by the liver and stored in the gallbladder. Bile helps with digestion. It breaks down fats into fatty acids, which can be taken into the body by the digestive tract.

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10
Q

What enzymes are synthesized/activated in the liver

A

Copper, zinc, magnesium, iron, vitamin A, D, E, K, B12

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11
Q

What proteins are synthesized in the liver and their function?

A

Blood clothing (prothrombin)

Cholesterol transport (lipoproteins)

Immune functions (globulins)

Oncotic pressure (albumin)

Copper bioavailability

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12
Q

Explain bilirubin metabolism

A
  1. hemolysis reveals heme group
  2. heme group broken down into unconjugated (insoluble) bilirubin and is attached to albumin and sent to liver
  3. Liver conjugates (makes soluble) bilirubin by combining it with glucuronic acid
  4. Can now be excreted into bile through biliary system and emptied into small intestine
  5. Converted into urobilinogen in small intestine (gives stool its dark color), some also excreted in urine
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13
Q

5 Metabolic Functions of Liver

A
  1. Fat, carbohydrate, protein metabolism
  2. Vitamin absorption and iron storage
    * Fat soluble: ADEK (bile necessary for absorption)
    * Water soluble: group b and c
  3. Produces bile for fat digestion
  4. Converts ammonia (product of protein breakdown – toxic) to urea for excretion by kidneys
  5. Gluconeogenesis- glycogen converted as needed by body
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14
Q

How does the liver function as a blood volume reservoir?

A
  • Alters circulating blood volume
  • Expands and compresses fluid as needed, up to 1 liter
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15
Q

How does the liver act as a filter?

A

Purifies blood returning from intestines of bacteria & other toxic substances

**Kupffer’s cells ** “garbage collector/macrophages in hepatic lobules

breakdown old RBC’s, hemoglobin (bilirubin) WBC’s and other cellular material before return to IVC

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16
Q

How does liver function in blood clotting?

A
  • Synthesizes vitamin K from intestines
  • Produces clotting factors
  • Produces fibrinogen
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17
Q

Define acute hepatic failure

A

a patient with no pre-existing history that develops rapidly with encephalopathy and increased INR

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18
Q

Causes of ALF

A
  • Acetaminophen OD
  • Drug Induced Injury
  • Viral Hepatitis
  • Autoimmune
  • Ischemia
  • Wilson’s Disease
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19
Q

Explain hepatitis

A

Widespread inflammation and infection of liver cells

  1. Liver enlarges after exposure to cause (usually virus)
  2. Becomes congested with inflammatory cells and fluid (RUQ pain)
  3. Inflammation interferes with blood flow to lobules causing edema to bile channels resulting in obstructive jaundice
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20
Q

At what point does hepatitis become chronic

A

When inflammation lasts longer than 6months

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21
Q

Which hepatitis are associated with cirrhosis and cancer

A

B, C, D

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22
Q

What is cirrhosis?

A

Final stage of chronic liver disease

“Extensive, irreversible scarring of the liver, usually caused by a chronic reaction to hepatic inflammation and necrosis”

Develops slowly; progressive, prolonged destruction of liver

Widespread fibrotic (scarred) bands of connective tissue that change the liver’s anatomy and physiology

Tissue becomes nodular and blocks bile ducts and normal blood flow; obstructions

Normal tissue replaced with fibrous tissue > decreased functional liver cells

Over time, liver shrinks and gets harder

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23
Q

Result of liver cirrhosis:

A

Cellular necrosis occurs, causing inability to complete functions:

  1. Inability to conjugate bilirubin
  2. Inability to detoxify substances
  3. Inability to produce clotting factors and albumin
  4. Inability to convert ammonia to urea
  5. Inability to regulate glucose
  6. Inability to purify blood
  7. Inability to regulate blood volume
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24
Q

9 Complications of Cirrhosis

A
  • Portal HTN
  • Esophageal varices
  • Ascites
  • Biliary obstruction
  • Jaundice
  • Bleeding
  • Hepato-renal syndrome
  • Infections
  • Hepatic encephalopathy
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25
Q

What is portal HTN?

A

Complication of cirrhosis

Persistent increase in pressure in the portal vein
* Increased resistance or obstruction (blockage) of blood flow within the portal venous system

Resistance to blood flow through liver  causes backward pressure
* Seeks collateral channels to get around the high-pressure area

26
Q

Result of portal HTN

A
  1. Collateral Channels to get around high pressure areas = varices
  2. Blood back flows into spleen (splenomegaly)
  3. Esophagus, stomach, intestines, abdomen, rectal veins dilate
27
Q

What can relieve portal HTN?

A

TIPS procedure (Transjugular intrahepatic portosystemic shunt)

28
Q

Gastro/Esophageal Varices

A

Due to portal HTN, blood backing up from the liver enters esophageal and gastric veins

Fragile, thin-walled esophageal veins become distended & tortuous from increased pressure; prone to rupture

Most often in distal esophagus; can also be stomach and rectum

Increase in pressure (coughing, vomiting, straining) can cause the varices to rupture

Can also occur spontaneously

29
Q

Management of Bleeding Esophageal Varices

A
  1. ABCs
  2. Drug Therapy
    - octreotide (sandostatin)
    > Inhibit glucagon, results in vasodilation of splanchnic circulation
    - vasopressin
    > Selectively decreases blood supply to varices
    - nitroglycerin
    > Vasodilating
    - beta blockers
    > propranolol- REDUCES pressure
  3. Correction
    - shunts
    - endoscopic therapy (cauterization and clipping)
    - sengstaken blakemore tube
30
Q

Why is caput medusae?

A

Dilated abdominal veins

Portal HTN causes backflow of blood into superficial veins connected to portal system

31
Q

Explain patho of ascites

A

Abnormal collection of free fluid in peritoneal cavity

  1. increased hydrostatic pressure from portal HTN
  2. decreased albumin = decreased osmotic pressure = fluid shift from vasculature into abdomen
  3. plasma proteins in peritoneal fluid = decreased circulating plasma protein
32
Q

Hepatobiliary Obstruction

A

Blockage in bile duct

  1. decreased liver bile production = decreased absorption of fat soluble vitamins (including k)
    > risk for bleeding
  2. Jaundice caused by:
    > hepatocellular disease (can’t conjugate)

> obstruction (edeman, fibrosis, scarring of duct)

33
Q

2 Main Causes of Infection Associated with Liver Failure

A
  1. Loss of Kupffer Cells (macrophages in lobules)
  2. Spontaneous Bacterial Peritonitis
    Bacteria typically from the bowel migrate through bowel wall and lymphatic system into ascitic fluid (= infected ascitic fluid)

Cues: malaise, fever, chills, abdominal pain

Confirmed with paracentesis

34
Q

Cause of hepatic encephalopathy

A

Caused by toxic levels of circulating ammonia which cross the blood-brain barrier

Usually, the liver converts ammonia to urea for excretion in urine

Failing liver is unable to convert ammonia to urea– toxicity develops

35
Q

Factors that worsen hepatic encephalopathy:

A
  • Infection (SBP)
  • Elevated protein intake (increases production of ammonia)
  • Hypovolemia/hyponatremia
  • Hypokalemia
  • Diuretic usage
  • GI bleeding
  • Constipation (large protein load in the intestines)
  • Drug toxicity (esp. opioids, analgesics, sedatives, illicit drugs)
  • TIPS procedure
36
Q

Cues of Hepatic Encephalopathy

A

Neurotoxic effects of ammonia
1. Neuropsychiatric manifestation
2. Abnormal transmission of nerve impulses; asterixis

asterixis, clonus, seizures, + Babinski, musty breath, manifestation of liver disease: ascites, jaundice, caput medusae

37
Q

Grading System of Mental Status with hepatic encephalopathy

A

1: lack of awareness, anxiety, shortened attention span

2: lethargy, personality changes, inappropriate behaviour, minimal space/time disorientation

3: stuporous but responsive to verbal stimuli, gross disorientation

4: coma

38
Q

What is hepatorenal syndrome?

A

Caused by portal hypertension

  1. No structural abnormality of kidney
  2. splanchnic and systemic vasodilation + decreased arterial volume reduces renal perfusion, decreasing renal function
  3. results in renal failure (oliguria, azotemia, increased urine/serum osmolality)
39
Q

History indicative of liver failure

A
  • Diet and eating patterns - Fatty liver disease
  • Exposure to chemical toxins
  • Needlestick injury; tattoos
  • Blood transfusions
  • Military or prison
  • Potential hepatitis transmission
  • Occupation: health worker, police officer, firefighter, paramedic, etc.
  • Greater incidence of exposure
  • Sexual history and orientation
  • Social habits ETOH
  • Illicit drug use (cocaine, needlestick)
40
Q

Onset of cirrhosis

A

Usually have slow onset

Compensated cirrhosis  may have no symptoms

Uncompensated/advanced/end-stage-liver failure  evidence of lack of many liver functions (GI bleed, jaundice, ascites, etc.)

41
Q

Early signs and symptoms of liver cirrhosis

A

can be vague and non-specific
* Fatigue
* Significant change in weight
* GI symptoms (N/V, anorexia)
* Abdominal pain/liver tenderness

42
Q

Liver enzymes of patient with cirrhosis

A
  • ALT, AST, GGT
  • Enzyme elevation indicates damage to hepatocytes
  • Isoenzymes (LDH) most specific
43
Q

Bilirubin levels of patient with cirrhosis

A
  • Elevated level indicates hepatic dysfunction
  • Liver isn’t conjugating bilirubin
44
Q

Serum ammonia levels of patient with cirrhosis

A
  • Elevated in liver dysfunction
  • Inability to detoxify and excrete
  • Monitor often
45
Q

Albumin levels of patient with cirrhosis

A

May decrease
> Liver’s role in production

46
Q

Coagulation studies of patient with cirrhosis

A

Liver produces prothrombin, vitamin K, other clotting factors
* PT/INR will go UP
* PTT may potentially go up
 Longer to clot

47
Q

Glucose levels of patient with cirrhosis

A

Inability to breakdown glycogen

BG can drop

48
Q

CBC of patient with cirrhosis

A

May have low RBC, HGB, Hct, platelets

Due to portal HTN causing spleen to hold these cells/take out of circulation

Iron may be low due to liver’s inability to store

49
Q

What is bilirubin and explain conjugation

A

End-product of hemoglobin degradation

Fat-soluble (unconjugated= not converted by liver “pre- hepatic”)

Water-soluble (conjugated= converted by liver for excretion)

50
Q

6 Priorities of Liver Disease

A

1, Risk for bleeding

  1. Fluid/Volume Deficit/excess
  2. Acute confusion
  3. Activity intolerance with ascites
  4. Malnutrition
  5. Risk for infection
51
Q

Why is fluid volume deficit/excess priority for liver disease?

A
  •  Hypovolemia and edema/ascites at the same time
  • Fluid not staying in right spot
  • Lack of oncotic pressure
  • Intravascularly hypovolemic with fluid in interstitial spaces
52
Q

Management of hemorrhage in liver failure

A

Preventative = Non-selective B-blocker– propranolol

Vitamin K supplementation

Octreotide = reduces blood flow (vasoconstriction), reducing portal pressure; reduces GI blood flow

Fresh frozen plasma, platelets

53
Q

Management of SBP in liver failure

A

Antibiotics (*Metronidazole)

54
Q

Management of HE in liver failure

A

Moderate amount of protein (limit; reduce ammonia) and fatty foods and simple carbohydrates

Lactulose (binds to ammonia for excretion)

Anti-infective (neomycin, metronidazole)

Reduces buildup of other toxins in brain contributing to toxicity

Monitoring neuro status, ICP

55
Q

Management of hypoglycemia in liver failure

A

Administer IV dextrose

Liver not breaking down glycogen

Can also see hyperglycemia if body isn’t creating glycogen

56
Q

Management of Ascites in liver failure

A

Diuretics

Sodium restriction, fluid restriction; daily weights

Paracentesis

Albumin before diuretics to pull fluid out

Folic acid/folate

57
Q

7 Diagnostics/Procedures for Liver Failure

A
  1. Liver biopsy
  2. Liver ultrasound
  3. EGD/ERCP
  4. Paracentesis (Drain ascites)
  5. Endoscopic variceal ligation
  6. TIPS: portal HTN shunting
  7. Transplant
58
Q

Problems associated with TIPS procedure

A
  • Shunt to help bypass, improving backflow
  • Blood bypasses most of liver’s filtration… toxins build up
  • Prophylactic lactulose; dietary modification
59
Q

What electrolyte abnormalities may accompany ascites?

A

Low electrolytes - hyponatremia, hypokalemia, hypocalcemia

60
Q
A

High Acuity (20 decks)

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