functions of the liver

each hepatic lobule is made of

hepatocytes, kupffer cells (phagocytic activity and toxin removal), a&v blood flow, bile flow

liver major fxns

Peter Drinks So Much

Produce ABCs

Detox (kupffer cells)

Store (glycogen for times of need)

Metabolism

albumin

attracts water into the vascular system. its a plasma protein that binds to water, calcium, and drugs, and transports them into the blood

liver failure = NO albumin → ascites, edema

bile

helps excrete cholesterol and digests food and fat in the small intestine → energy

liver failure = NO bile → inc cholesterol in blood

what is bile made of

conjugated bilirubin, cholesterol, water, bile salts

clotting factors

produced in the liver

liver failure = no clotting factors → bleeding and bruising

how do we know if we have enough clotting factors?

prothrombin time (PT) and partial thromboplastin time (PTT) labs

glucose → glycogen

gluconeogenesis

glycogen → glucose

glycolysis

expected lab values with liver impairment

albumin - LOW

bilirubin - HIGH

cholesterol - HIGH

PT, PTT, INR - HIGH

ammonia - HIGH

jaundice

yellow discolaration of skin, resulting from a change in normal bili met or disruption of the flow of bile into the hepatic or biliary duct systems.

if conjugated bili cannot pass into the intestines from the liver bc of obcsturction or inflammation of the bile ducts, the stool will be clay colored

bilirubin

product of the breakdown of old RBCs

binds to albumin and is transferred to the liver → bile

unconjugated bili

combines w glucouronic acid in the liver to become conjugated

conjugated

water soluble, excreted in bile via GI

hemolytic jaundice

inc hgb bkdn

liver cant keep up with hemolysis

inc in uncon bili

what causes hemolytic jaundice

• blood transfusion rxns

• hemolytic anemia

  • sickle cell crisis

hepatocellular jaundice

damage and dysfxn of liver

• liver cannot take up, conjugate or excrete bili

• hepatocytes leak con bili

• inc in serum uncon and con bili

  • the liver loses the capacity to take up bili from blood or to con or excrete it

what causes hepatocellular jaundice

• cirrhosis

• hepatitis

• liver cancer

obstructive jaundice

obstruction of the flow of bile through the liver or biliary duct

normal uncon bili

HIGH con bili

dec in urine and fecal bilirubinogen

• clay colored stools w complete obstruction

what causes obstructive jaundice

gall stones

biliary strictures

pancreatic cancer

primary sclerosing cholangitis

hepatitis

inflammation of the hepatocytes, destroying it and liver

acute - full resolution and regeneration

chronic - results in cirrhosis

hep a

oral fecal

vaccine

hep b

blood, sex

vaccine

hep c

blood, no vaccine, 90% curable w meds

nursing mgmt of hepatitis

•Maintain food and fluid intake adequate to meet nutritional needs

•Avoid alcohol and other hepatotoxic agents

•Show gradual increase in activity tolerance

•Perform daily activities with scheduled rest periods

cirrhosis of the liver

scarring of liver tx

• unsuccessful regeneration of cells

• impedes vascularization and bile flow

• effectively disrupts all processes of the liver

end stage of liver disease

cirrhosis pathophysiology

liver inflammation → necrosis → scarring/fibrosis

liver necrosis → alteration in fxn → liver failure → hepatic encephalopathy → hepatic coma → death

• scarring → vascular obstruction → portal HTN

portal HTN

liver structural changes → obstruction of BF in/out of liver → inc pressure within the livers circulatory system

leads to:

• splenomegaly

• large collateral veins

• ascites

• esophageal and gastric varices

ascites

serous fluid in the peritoneal or abdominal cavity

• signs of dehydration

• hypokalemia due to excessive loss of K caused by hyperaldosteronism

ascites caused by

portal HTN and low albumin

• liver cant produce albumin

• hypoalbuminemia → dec colloidal oncotic pressure

ascites management

sodium restriction (2g/day), diuretics, paracentesis

paracentesis

treatment for ascites

have pt void before so you dont puncture bladder

high fowlers

monitor for hypovolemia and electrolyte imbalances

esophageal and gastric varices

tortuous and enlarged veins at lower end of esophagus

fragile, do not tolerate high pressure = bleeds easily

ruptured esophageal varices are the most life threatening complication of cirrhosis and a med emergency

beta blocker to reduce bleeding risk

manage airway!

EGD w ligation (banding/clipping)

balloon tamponade

mechanical comp of varices

TIPS

transjugular intrahepatic portosystemic shunt

portal HTN treatment

• shunt connects the portal vein (in) to the hepatic vein (out)

• bypasses the liver

last resort treatment as it does not improve liver fxn and makes labs worse

hepatic encephalopathy

build up of ammonia in blood, which is neurotoxic

CM of hepatic encephalopathy

cuckoo town

asterixis “flapping tremors”

apraxia - impairments in writing/drawing

fector hepaticus - musty, sweet odor of breath

lactulose

drug that traps ammonia in the gut, reduces ammonia formation in the intestines

removed via stool (laxative effect)