ch 13 Flashcards
Overview of the Liver
Largest gland in the body (~1400-1800 g)
Hepatocytes form ~80% mass, crucial to:
Detoxification of drugs and vits and hormones
metabolism of AA + ammonium
biochemical oxidative reaction
> 500 known functions (see Nelms Table 16.1)
“Secretory gland” (i.e. bile)
Huge functional reserve
~80-90% liver cells must be injured before
s/s of physiological dysfunction appear
Remarkable regenerative capacity
Blood Circulation To and From the Liver
Liver receives blood from:
Hepatic artery
Arterial blood that provides the livers o2 supply
Hepatic portal vein- venous blood drains from the digestive tract to the liver for nutrient processing/storage
Blood leaves the liver from:
Hepatic vein
Bile
Yellow/green fluid composed of:
Cholesterol, bile acids (salts), bilirubin, water, K, Na, bicarbonate, copper and other metals
Produced in the Liver__________
Stored in the gallbladder________
Emulsifying agent
Decreases surface tension and allows intestinal agitation to break up fat globules
Bile salts aid in absorption of fatty acids, monoglycerides, cholesterol, and other lipids by forming micelles that are soluble in chyme
Acute liver failure:
large proportion of hepatocytes are destroyed; often self-limiting (i.e. resolve in time with treatment, i.e. acute heptatis; obviously if get to certain state, may require liver transplant)
acute hepatitis, shock liver, acute liver failure
acute on chronic liver failure
Chronic liver failure
defined by increased inflammation, infiltration of lymphocytes, plasma cells and hepatocyte apoptosis; will review each of the phases (fibrosis, cirrhosis etc in a couple slides)
fatty liver, steatosis
fibrosis
cirrhosis
hepatocellular carcinoma
Compensated liver disease:
Decompensated l
a person will not have symptoms related to their cirrhosis
iver disease: a person will present with symptomatic complications related to liver disease/cirrhosis (jaundice, ascites, HE, esophageal varices etc).
k
causes of liver disease
toxins: alcohol, meds
metabolic causes: obesity, wilsons disease
infection: viral hep a, s, c,e, bacterial - tuberculosis
immune mediated:autoimmune, primary biliary cirrhosis
other: carcinoma
Primary biliarycholangitis (PBC), also known asprimary biliary cirrhosis,
is an autoimmune disease of the liver. It results from a slow, progressive destruction of the small bile ducts of the liver, causing bile and other toxins to build up in the liver, a condition called cholestasis.
Primary sclerosing cholangitis(PSC)
) is a chronic liver disease characterized by a progressive course of cholestasis with inflammation and fibrosis of the intrahepatic and extrahepatic bile ducts. The underlying cause of the inflammation is believed to be autoimmunity.
Amyloidosis
is a rare disease that occurs when a substance called amyloid builds up in your organs. Amyloid is an abnormal protein that is produced in your bone marrow and can be deposited in any tissue or organ.
Progression of Chronic Liver Disease
goes from normal liver to early cirrhosis to cirrhosis to wither a liver transplant or hepatocellular carcinoma
if the removal of the underlysing cause it taken away at early cirrohosis - the liver can go back to normal- if cirrhosis cannot iprove but can maintain
what are the primary causes of liver disease
alcohol, obesity, viral hep
Key Laboratory Parameters
“Liver function tests” / “liver panel” Enzymes: ALP, ALT, AST, GGT, LDH Proteins: Albumin, Total protein Clotting studies: PTT, INR Ammonia (present in blood in ionized form NH4) Bilirubin Total (unconjugated) Direct (conjugated)
Jaundice (Icterus)
Yellowish tint to body tissues
Eyes: Icteric sclerae
↑bilirubin
↑ RBC destruction
↓ bilirubin uptake / ↓ liver function
Bile duct obstruction
Pruritis
Itchy skin. ? Related to ↑bilirubin
Portal Hypertension
Elevated blood pressure in the hepatic vein
Blood flow forced backward, causing veins to enlarge
Primary symptoms/complications:
Ascites
Esophageal varices
Hepatic encephalopathy
Ascites
alterations is systemic hemodynamics and build up of pressure causes fluid leaking into abdominal space.
(also why peripheral edema occurs, along with decreased albumin resulted in decreased oncotic pressure in blood vessels resulting in leaky vessels and fluid shifting in interstitial space)
How do they think ascites could impact nutrition/diet:
Full full quickly; anorexia, poor intake
Possible Fluid and Na restrictions (more on this later)
Physical observation muscle wasting! Ribs, clavicle, arms
Use of PEG tubes in pt’s with ascites: mortality has been shown to be high and thus is not recommended.
Treatments:
of ascites
Paracentesis (protein also removed as part of fluid) – several litres can be removed at once (4L ascitic fluid has ~40-80g protein)
TIPS (transjugular intrahepatic portosystemic shunt) – surgical procedure where a shunt is placed such that blood flow is rerouted through the liver to the hepatic vein to decrease pressure.
DSRS (distal spenlorenal shunt) – splenic vein is disconnected from the portal vein and
(Esophageal) Varices
Low-pressure veins in esophagus (and upper stomach) that become distended from increased pressure d/t portal HTN
Use of Feeding Tubes in Patients with Chronic Liver Disease
Non-bleeding esophageal varices
Use of nasoenteric tubes (NG, NJ):
Risk low that placement of soft-tipped, fine-bore tube will precipitate variceal hemorrhage
Actively bleeding esophageal varices
Advise holding EN for 48-72h post-banding
Critically ill: Sengstaken-Blakemore Tube
No nasoenteric access
If suspected prolonged NPO, high malnutrition risk PN
Hepatic Encephalopathy (HE)
Syndrome of impaired mental status and abnormal neuromuscular function resulting from liver failure
S/S
Changes in mental status and personality
Mild confusion Lethargy/disorientation Somnolent but arousable Coma
Neuromuscular changes
Contributing factors: Degree of liver failure Diversion of portal blood through venous systemic circulation Bleeding from varices Exogenous factors (i.e. sepsis)
Pathogenesis of HE
Ammonia is key neurotoxin Colon: major site of NH3 production Healthy liver NH4 urea, excreted by kidney Diseased liver NH4 bypasses liver metabolism and accumulates in systemic circulation NH4 metabolized at extrahepatic sites (i.e. SM and brain) to glutamine NH4 passes blood brain barrier Accumulates in brain
Plasma NH4 Levels
Often used in clinical setting as diagnostic tool for HE
BUT: Poor correlation b/w NH4 levels & HE
Plasma NH4 levels not required to make a diagnosis or helpful in monitoring effectiveness of NH4 lowering therapies
Primary Treatments
Aimed at reducing circulating ammonia (NH3)
Lactulose Non-absorbable disaccharide Stimulates passage of NH3 from body tissues into gut lumen Inhibits intestinal NH3 production Side effects?
Antibiotics
Decrease colonic concentration of bacteria that can produce NH3
