Liver Disease Flashcards
What is the largest solid organ in the body?
Liver
How fast and what kind of blood enters the liver?
Arterial (hepatic artery) and venous (portal vein) blood enters the liver at 1800 ml/min
What is the functional unit of the liver?
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
Explain blood flow through the liver
- Receives oxygenated blood from hepatic artery branching off aorta
- 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
What locations does the portal vein carry blood from?
stomach, spleen, pancreas, and intestines
What % of cardiac output flows through the liver?
- Receives 1800ml/min
- Normal CO = 5-6L/min
- Approx 30%
Hepatobiliary Functions (10)
- Phagocytosis/Immune
- Bilirubin Metabolism
- Production/processing of cholesterol
- Biotransformation/Detoxification
- Bile production, metabolism, excretion
- Enzyme synthesis and activation
- Protein Synthesis
- Metabolic functions
- Blood volume reservoir
- Filtering
- Blood clotting
How does the liver function in cholesterol?
Produces LDL and HDL
Rids of it through bile
Cholesterol = precursor to hormones and vitamin D
Function of bile
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.
What enzymes are synthesized/activated in the liver
Copper, zinc, magnesium, iron, vitamin A, D, E, K, B12
What proteins are synthesized in the liver and their function?
Blood clothing (prothrombin)
Cholesterol transport (lipoproteins)
Immune functions (globulins)
Oncotic pressure (albumin)
Copper bioavailability
Explain bilirubin metabolism
- hemolysis reveals heme group
- heme group broken down into unconjugated (insoluble) bilirubin and is attached to albumin and sent to liver
- Liver conjugates (makes soluble) bilirubin by combining it with glucuronic acid
- Can now be excreted into bile through biliary system and emptied into small intestine
- Converted into urobilinogen in small intestine (gives stool its dark color), some also excreted in urine
5 Metabolic Functions of Liver
- Fat, carbohydrate, protein metabolism
- Vitamin absorption and iron storage
* Fat soluble: ADEK (bile necessary for absorption)
* Water soluble: group b and c - Produces bile for fat digestion
- Converts ammonia (product of protein breakdown – toxic) to urea for excretion by kidneys
- Gluconeogenesis- glycogen converted as needed by body
How does the liver function as a blood volume reservoir?
- Alters circulating blood volume
- Expands and compresses fluid as needed, up to 1 liter
How does the liver act as a filter?
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
How does liver function in blood clotting?
- Synthesizes vitamin K from intestines
- Produces clotting factors
- Produces fibrinogen
Define acute hepatic failure
a patient with no pre-existing history that develops rapidly with encephalopathy and increased INR
Causes of ALF
- Acetaminophen OD
- Drug Induced Injury
- Viral Hepatitis
- Autoimmune
- Ischemia
- Wilson’s Disease
Explain hepatitis
Widespread inflammation and infection of liver cells
- Liver enlarges after exposure to cause (usually virus)
- Becomes congested with inflammatory cells and fluid (RUQ pain)
- Inflammation interferes with blood flow to lobules causing edema to bile channels resulting in obstructive jaundice
At what point does hepatitis become chronic
When inflammation lasts longer than 6months
Which hepatitis are associated with cirrhosis and cancer
B, C, D
What is cirrhosis?
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
Result of liver cirrhosis:
Cellular necrosis occurs, causing inability to complete functions:
- Inability to conjugate bilirubin
- Inability to detoxify substances
- Inability to produce clotting factors and albumin
- Inability to convert ammonia to urea
- Inability to regulate glucose
- Inability to purify blood
- Inability to regulate blood volume
9 Complications of Cirrhosis
- Portal HTN
- Esophageal varices
- Ascites
- Biliary obstruction
- Jaundice
- Bleeding
- Hepato-renal syndrome
- Infections
- Hepatic encephalopathy
What is portal HTN?
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
Result of portal HTN
- Collateral Channels to get around high pressure areas = varices
- Blood back flows into spleen (splenomegaly)
- Esophagus, stomach, intestines, abdomen, rectal veins dilate
What can relieve portal HTN?
TIPS procedure (Transjugular intrahepatic portosystemic shunt)
Gastro/Esophageal Varices
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
Management of Bleeding Esophageal Varices
- ABCs
- 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 - Correction
- shunts
- endoscopic therapy (cauterization and clipping)
- sengstaken blakemore tube
Why is caput medusae?
Dilated abdominal veins
Portal HTN causes backflow of blood into superficial veins connected to portal system
Explain patho of ascites
Abnormal collection of free fluid in peritoneal cavity
- increased hydrostatic pressure from portal HTN
- decreased albumin = decreased osmotic pressure = fluid shift from vasculature into abdomen
- plasma proteins in peritoneal fluid = decreased circulating plasma protein
Hepatobiliary Obstruction
Blockage in bile duct
- decreased liver bile production = decreased absorption of fat soluble vitamins (including k)
> risk for bleeding - Jaundice caused by:
> hepatocellular disease (can’t conjugate)
> obstruction (edeman, fibrosis, scarring of duct)
2 Main Causes of Infection Associated with Liver Failure
- Loss of Kupffer Cells (macrophages in lobules)
- 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
Cause of hepatic encephalopathy
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
Factors that worsen hepatic encephalopathy:
- 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
Cues of Hepatic Encephalopathy
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
Grading System of Mental Status with hepatic encephalopathy
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
What is hepatorenal syndrome?
Caused by portal hypertension
- No structural abnormality of kidney
- splanchnic and systemic vasodilation + decreased arterial volume reduces renal perfusion, decreasing renal function
- results in renal failure (oliguria, azotemia, increased urine/serum osmolality)
History indicative of liver failure
- 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)
Onset of cirrhosis
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.)
Early signs and symptoms of liver cirrhosis
can be vague and non-specific
* Fatigue
* Significant change in weight
* GI symptoms (N/V, anorexia)
* Abdominal pain/liver tenderness
Liver enzymes of patient with cirrhosis
- ALT, AST, GGT
- Enzyme elevation indicates damage to hepatocytes
- Isoenzymes (LDH) most specific
Bilirubin levels of patient with cirrhosis
- Elevated level indicates hepatic dysfunction
- Liver isn’t conjugating bilirubin
Serum ammonia levels of patient with cirrhosis
- Elevated in liver dysfunction
- Inability to detoxify and excrete
- Monitor often
Albumin levels of patient with cirrhosis
May decrease
> Liver’s role in production
Coagulation studies of patient with cirrhosis
Liver produces prothrombin, vitamin K, other clotting factors
* PT/INR will go UP
* PTT may potentially go up
Longer to clot
Glucose levels of patient with cirrhosis
Inability to breakdown glycogen
BG can drop
CBC of patient with cirrhosis
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
What is bilirubin and explain conjugation
End-product of hemoglobin degradation
Fat-soluble (unconjugated= not converted by liver “pre- hepatic”)
Water-soluble (conjugated= converted by liver for excretion)
6 Priorities of Liver Disease
1, Risk for bleeding
- Fluid/Volume Deficit/excess
- Acute confusion
- Activity intolerance with ascites
- Malnutrition
- Risk for infection
Why is fluid volume deficit/excess priority for liver disease?
- 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
Management of hemorrhage in liver failure
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
Management of SBP in liver failure
Antibiotics (*Metronidazole)
Management of HE in liver failure
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
Management of hypoglycemia in liver failure
Administer IV dextrose
Liver not breaking down glycogen
Can also see hyperglycemia if body isn’t creating glycogen
Management of Ascites in liver failure
Diuretics
Sodium restriction, fluid restriction; daily weights
Paracentesis
Albumin before diuretics to pull fluid out
Folic acid/folate
7 Diagnostics/Procedures for Liver Failure
- Liver biopsy
- Liver ultrasound
- EGD/ERCP
- Paracentesis (Drain ascites)
- Endoscopic variceal ligation
- TIPS: portal HTN shunting
- Transplant
Problems associated with TIPS procedure
- Shunt to help bypass, improving backflow
- Blood bypasses most of liver’s filtration… toxins build up
- Prophylactic lactulose; dietary modification
What electrolyte abnormalities may accompany ascites?
Low electrolytes - hyponatremia, hypokalemia, hypocalcemia
