liver

portal vein

75% of blood to liver is from here. nutrient rich and oxygen poor

hepatic artery

25% of blood to liver is from here. nutrient poor and oxygen rich

functions of the liver

1. Glucose, protein, fat, drug metabolism

2. Ammonia conversion

3. Vitamin and iron storage

4. Bile formation

5. Bilirubin excretion

carcinoembryonic antigen

used to identify cancer. the presence of this antigen indicates cancer

prothrombin time

clotting time may be prolonged

pigment studies

reflect the livers ability to break down and excrete bili

cholesterol

elevated in biliary obstruction but decreased in liver disease that affects liver cells

amonia

liver converts ammonia to urea so ammonia level increases

why cant enzyme activity alone determine liver function

More than 70% of the liver may be damaged before changes become abnormal and although liver function is usually measured by enzyme activity, this alone cannot determine liver function.

serum aminotransferases

indicators of injury to the liver cells, useful in detecting hepatitis

ALT

levels increase primarily in liver disorders; used to monitor the course of hepatitis, cirrhosis, the effects of treatments that may be toxic to the liver

AST

not specific to liver diseases however levels of AST may be increased in cirrhosis, hepatitis, and liver cancer

GGT

levels are associated with cholestasis; alcoholic liver disease

diagnostic tests

liver biopsy- a needle is inserted into the abdominal wall and tissue is aspirated for analysis. complications are bleeding and bile peritonitis so if the patient has abnormal coagulation studies or ascites dont do it

after a liver biopsy

• Right side with a pillow for 2-3 hours for compression

• Avoid coughing or straining

• Vital sign protocol

• Dressing

• Avoid heavy lifting for 1 week

causes of liver dysfunction

• Acetaminophen    overdose

• Prescription medications

• Herbal supplements

• Hepatitis and other viruses

• ETOH

• Toxins

• Autoimmune disease

• Diseases of the   veins in the liver

• Metabolic disease

• Cancer

s/s of liver dysfunction

• Pallor 

• Jaundice

• Muscle atrophy

• Edema

• Vitamin deficiencies

• Skin excoriation r/t itching

• Petechiae 

• Ecchymotic areas

• Spider angiomas

• Palmar erythema

• Males: gynecomastia, testicular hypertrophy

• Neuro changes: cognition, tremors, asterixis, weakness, slurred speech

• Unstable blood glucose

child pugh classification

predicts the outcome of patients with liver disease. higher the score the poorer the prognosis

types of jaundice

1. Hemolytic- increased destruction of rbcs so cant excrete bilirubin as fast as its formed

2. Hepatocellular- liver cells are damaged so cant clear bilirubin

3. Obstructive- occlusion of bile duct from gallstone

4. Hereditary- from an inherited disorder like gilbert syndrome

s/s hepatocellular jaundice

• Mild or severely ill

• Lack of appetite, nausea or vomiting, weight loss

• Malaise, fatigue, weakness

• Headache, chills, fever, infection 

s/s of obstructive jaundice

• Dark orange-brown urine, clay-colored stools

• Dyspepsia and intolerance of fats, impaired digestion

• Pruritus

consequences of liver dysfunction

ascites, esophageal varices, hepatic encephalopathy, hepatic coma

portal hypertension

• Often associated with cirrhosis

• Major consequences include ascites 

   and varices

• Splenomegaly & thrombocytopenia

ascites

Shift of fluid into peritoneal cavity

ascites diagnostic findings

percussion- there will be shifting dullness as fluid moves from one position to another, flank edema, fluid wave

major ascites complication

spontaneous bacterial peritonitis

ascites manifestation

fever, malaise, worsening liver function

hepatorenal syndrome

if ascites is untreated or very aggressive. form of renal failure without pathological changes to the kidney

ascites medical mangement

low sodium diet- watch out for salt subs bc they have ammonia

diuretics

bed rest

paracentesis

TIPS

pracentesis

removal of fluid from a peritoneal cavity done through a puncture or small surgical incision through the abdominal wall

before paracentesis

consent, void, vitals, weight and abdominal girth

during paracentesis

as upriught as possible, vitals, s/s of hypovolemia

after paracentesis

s/s hypovolemia, weight and abdomen girth, measure describe document fluid collected, assess puncture site for drainage, neuro status, limit activity, fluid electrolyte replacement (albumin)

TIPS

decreases portal hypertension which is thought to contribute to ascites

peritoneovenous shunts

Drains peritoneal fluid from the peritoneum into veins, usually the internal jugular vein or the superior vena cava

ascites education

• Rationale for low sodium diet, bed rest

• Medications (diuretics)

• Major complication (spontaneous bacterial peritonitis)

• Paracentesis & TIPS

ascites monitoring

• Abdominal girth q shift

• Daily weight

• Strict intake and output

• Fluid and electrolyte balance 

• Respiratory status

• S/S of encephalopathy

most common ascites cause

cirrhosis

main contributor of ascites

portal hypertension

first line of treatment for ascites

sodium restricted diet and aldactane→ lasix→ paracentesis→ tips→ liver transplant

varices manifestations

hematemesis, melena, general deterioration, s/s shock

varices diagnostics

endoscopy to find bleeding site, CT barium swallow, angiography

cause of bleeding esophageal varices

portal hypertension

bleeding varices treatments

ICU admit/transfer, Balloon tamponade, Vasopressin, Sclerotherapy, Banding, TIPS

hepatic encephalopathy

occurs with profound liver failure. not physical but neuropsychiatric manifestations. caused from ammonia increasing and portosystemic shunting

things that precipitate encephalopathy

gi bleeding, high protein diet, bacterial infections, renal failure

constructional apraxia

sign of hepatic encephalopathy. inability to produce simple figures in 2 or 3 dimensions

viral hepatitis

a systemic viral infection in which necrosis and inflammation of liver cells produce a characteristic cluster of clinical, biochemical and cellular changes

hepatatis A

has 2 phases. thee first phase is before jaundice and the second one is once jaundice sets in. spread by poor hand hygiene. fecal to oral

hepatitis A incubation period

between 2 and 6 weeks and can last 4 to 8 weeks

hepatitis A manifestations

mild flu-like symptoms, low-grade fever, anorexia, later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen

managing hep A

prevention by good handwashing and vaccine, bed rest during acute stage, nutritional support

hepatitis B

Transmitted through blood, saliva, semen, and vaginal secretions; sexually transmitted; transmitted to infant at the time of birth. A major worldwide cause of cirrhosis and liver cancer. usually chronic

hepatitis B incubation period

1 to 6 months

hep b manifestations

insidious and variable; similar to HAV, loss of appetite, dyspepsia, abdominal pain, generalized aching, malaise, and weakness. jaundice may or may not be evident

managing hep B

• Medications for chronic hepatitis type B include alpha interferon and antiviral agents: entecavir (ETV) and tenofovir (TDF)

• Bed rest and nutritional support

• Vaccine: for persons at high risk, routine vaccination of infants

• Passive immunization for those exposed

• Standard precautions and infection control measures

• Screening of blood and blood products

hepatitis C

• Transmitted by blood and sexual contract, including needle sticks and sharing of needles

• The most common bloodborne infection

• A cause of one third of cases of liver cancer and the most common reason for liver transplant

hepatitis C incubation period

15 to 160 days

hepatitis C manifestations

Symptoms are usually mild, Chronic carrier state frequently occurs

management of hep C

• Antiviral medications

• Alcohol potentiates disease; medications that effect the liver should be avoided

• Prevention: public health programs to decrease needle sharing among drug users

• Screening of blood supply

• Safety needles for health care workers

hepatitis D

• Only persons with hepatitis B are at risk

• Blood and sexual contact transmission

• Use of IV or injection drugs, patients undergoing hemodialysis, and recipients of multiple blood transfusions

• Likely to develop fulminant liver failure or chronic active hepatitis and cirrhosis

hep D incubation period

between 30 and 150 days

hep D treatment

Interferon alfa is the only licensed drug available in the treatment for HDV infection

hepatitis E

• Transmitted by fecal–oral route, contaminated water

• Incubation period: 15 to 65 days

• Resembles hepatitis A; self-limiting, abrupt onset, not chronic

• Prevention: good hygiene, handwashing

non viral hepatitis

• Inflammation of the liver r/t hepatotoxins

  • Toxic hepatitis

  • Drug-induced hepatitis

toxic hepatitis

• Ingestion of hepatotoxic chemical

• Fever, extreme physical weakness, hematemesis, vascular collapse

• Delirium, seizures, coma

drug induced hepatitis

• Ingestion of hepatotoxic chemical

• Abrupt onset: chills, fever, rash, pruritus, arthralgia, anorexia and nausea

• Jaundice, dark urine, enlarged & tender liver

most common cause of acute liver failure

drug induced hepatitis and the overdose of acetaminophen is the leading cause of the drug induced hepatitis

toxic vs drug induced hepatitis

• Both have a better prognosis if identified early and the hepatotoxin is removed otherwise recovery is unlikely

• Toxic hepatitis resembles viral hepatitis; so patient history is important

• For both of these situations, treatment options are limited because there are few antidotes

fulminant hepatic failure

the clinical syndrome of sudden and severely impaired liver function in a previously healthy person. patient becomes jaundice and progresses to encephalopathy within 7 to 72 days. most common reason is viral hepatitis. usually need liver transplant

fulminant hepatic failure interventions

find root cause, icu, antidote, plasma exchange, prostaglandin therapy, intracranial monitoring, mannitol, liver transplant

cirrhosis

the irreversible scarring of the liver which disrupts the structure and function of the liver

compensated cirrhosis

mild fever, spider hemangiomas, palmar erythema, unexplained nosebleed, ankle edema, indigestion, flatulent dyspepsia, abdominal pain, firm enlarged liver, splenomegaly

decompensated cirrhosis

ascites, jaundice, weakness, muscle wasting, weight loss, mild fever, clubbing of fingers, purpura, spontaneous bruising, nosebleeds, hypotension, sparse body hair, white nails, gonadal atrophy

cirrhosis complications

Hepatorenal syndrome- decrease in renal function related to liver disease

Hepatopulmonary syndrome

primary liver tumors

Associated with hepatitis B and C, Hepatocellular carcinoma (HCC)

liver metastasis

Few cancers originate in the liver, Frequent site of metastatic cancer

liver cancer manifestations

• Dull persistent pain, RUQ, back, or epigastrium

• Weight loss, anemia, anorexia, weakness

• Jaundice, bile ducts occluded, ascites, or obstructed portal veins

liver cancer diagnostic findings

• Early signs: liver pain (RUQ, epigastric, back)

• Weight loss, anorexia, anemia

• Enlarged liver (jaundice, ascites)

liver cancer labs

• Serum bilirubin ↑

• Serum alkaline phosphatase ↑

• AST, GGT, lactic dehydrogenase ↑

• Leukocytosis, erythrocytosis, hypercalcemia, hypoglycemia, hypercholesterolemia

percutaneous biliary drainage

Catheter inserted under fluoroscopy to bypass obstructed biliary ducts (palliative, not curative)

liver transplant indications

irreversible advanced chronic liver disease, fulminant

liver transplants and immunosuppression

success depends on immunosuppression