Hepato-Billiary Disorders

Functions of the liver

-production of bile (emulsify fat)

-elimination of bilirubin

-metabolism of steroid proteins

-drug metabolism

-carbohydrate and fat metabolism (conversion of lipids to ketones)

-synthesis of plasma proteins (albumin)

-synthesis of clotting factors

-conversion of ammonia to urea

-phagocytosis from Kupffer cells

Bilirubin

Waste product from the breakdown of hemoglobin.

jaundince

-yellowish discoloration of skin

-abnormal bilirubin metabolism

-in darker skin tone check sclera and palate

normal bilirubin metabolism

1. hemoglobin breakdown makes unconjugated/indirect bilirubin

2. conjugated in liver by enzymes

3. conjugated bilirubin is secreted in bile

4. Bile enters the intestines and is secreted through stool

5. conjugated bilirubin is converted to urobilinogen by bacteria in gut

6. some urobilinogen is re-absorbed in gut but mostly excreted in urine

3 types of jaundice

hemolytic, hepatocellular, obstructive

hemolytic jaundice

-liver is working but RBC's being broken down (hemolysis) in larger quantities (ex: sickle cell crisis, transfusion reaction)

-only increased unconjugated

Hepatocellular jaundice

-damage to liver and damaged liver cells release conjugated bilirubin

-can also increase unconjugated if enough cells damaged

-ex: hepatitis, cirrosis, liver cancer

-both are increased

Cholestatic jaundice

-obstruction of bile flow

-elevation in conjugated only (bc liver is working)

-ex: hepatitis, cirrohsis, gall stones

-NO urobillinogen in urine

hemolytic jaundice lab findings

-elevated indirect bilirubin

-urine bilirubin negative

hepatocellular jaundice lab findings

-elevated indirect and direct bilirubin

-elevated urine bilirubin

-elevated urobilinogen

cholestatic jaundice lab findings

-elevated mostly direct bilirubin

-elevated urine bilirubin

-negative urobilinogen

Alanine aminotransferase (ALT) and Aspartate Aminotransferase (AST)

liver enzymes that show liver damage, released from dead hepatocytes, LOW levels normal

Hepatotoxins

-damage results primarily from toxic metabolites

-ex: alcohol, tylenol, aminodarone (anti-arrythmatic), TB drugs

hepatitis

Inflammation of the liver, usually caused by a viral infection, that causes fever, loss of appetite, jaundice, fatigue, and altered liver function.

viral hepatitis patho

-damage results from a viral destruction of hepatocytes and immune response to infection

-lysis of hepatocytes

-inflammation leads to cholestasis (blockage in bile channels)

Hepatitis A

-fecal oral (contaminated food/water)

-vaccine preventable (2 shots)

-not chronic

pre-icteric phase

malaise, headache, low grade fever, arthralgias (joint stiffness)

icteric phase

jaundice, dark urine (bilirubin), clay colored stool (bile), pruritis (itchy), nausea, abdominal pain, hepatomegaly

Post-icteric phase

jaundice resolves, hepatomegaly and fatigue slowly resolve (complications rare for Hep. A)

Hepatitis A treatment

rest, hydration, nutrition, teach infection control, avoid alcohol and other hepatotoxins

Hepatits B

-blood borne (STD, needle sharing, perinatal)

-vaccine preventable (3 shots)

-chronic (5-10% of cases)

-antibodies given for exposure

hepatits B immune globulin (HBIG)

given within 1 week of exposure if not vaccinated, PASSIVE IMMUNITY

Hepatits B complications

-fulminant hepatitis (rapid liver decline)

-chronic hepatits (risk of cirrhosis or cancer)

Hepatitis C

-blood borne, needle sharing, STD, transfusion before 1992

-NOT vaccine preventable

-chronic

Anti-HAV IgM

positive = currently or recently infected with Hepatitis A

Anti-HAV IgG

positive = immunity to Hep. A that was naturally or vaccine/passively accquired

HBsAg (Hepatitis B surface antigen)

positive = active Hep. B infection

Anti-HBs (Hepatitis B surface antibody)

positive = immunity to Hep. B from infection or vaccine

Anti-HCV

only shows EXPOSURE to Hep. C, we do not know if infected

HCV RNA

positive = actively infected (shows active load)

Chronic hepatitis

-remains + for more than 6 months

-treat w/ antivirals

-monitor for cirrhosis or cancer (liver biopsy)

-protect from further damage (vaccinate, no toxins)

Cirrhosis

-chronic progressive destruction of liver cells with fibrosis (scar tissue)

-results in obstruction of bile and vascular flow (decreased liver function)

-causes: alcoholism, chronic hepatitis, non-alcoholic steatohepatits/NASH, post necrotic tissue

Non-alcoholic steatohepatitis (NASH)

more severe form of Nonalcoholic fatty liver disease where fat buildup in the liver causes inflammation and liver cell damage without alcohol use

early signs of cirrhosis

-Vague GI symptoms (Anorexia, dyspepsia, nausea)

-Hepatomegaly

later signs of cirrhosis

-jaundice

-portal hypertension

-ascites (fluid in belly)

-thrombocytopenia (low platelet count)

-clotting dysfunction

-gynecomastia (male breast enlargement)

-increased aldosterone (liver supposed to breakdown it)

-dark urine (bilirubin)

-clay colored stools

portal circulation

blood from the gut goes to the liver to be detoxified before it goes to the vena cava

portal hypertension patho

-Most commonly caused by Cirrhosis

-Liver becomes scarred and stiff

-Blood can't flow easily through the liver

-Pressure builds backward into the portal system

Splenomegaly

enlargement of the spleen, causes thrombocytopenia (low platelet) bc the enlarged spleen traps and destroys the platelets

impact of portal hypertension

-esophageal varices

-contributes to ascites

-splenomegaly (causes thrombocytopenia)

-hemorrhoids

esophageal varices

-enlarged veins at base of esophagus

-result of portal HTN

-bleeding varices = life threatening hemorrhage

-risk of bleeding increased with elevated intra-abdominal pressure (coughing, vomiting, straining at stool)

esophageal varices treatments

-endoscopy with ligation or sclerosis

-Non-selective beta blocker Propranolol (Inderal®) to lower pressure in portal system

-TIPS procedure

-Avoid NSAIDS or ASA

TIPS procedure

-Transjugular intrahepatic portal-systemic shunt

-lowers portal pressure in portal HTN by redirecting blood flow from portal vein to hepatic vein

-increases risk of encephalopathy (ammonia) bc blood cannot be detoxified by liver

Ascites

-abnormal accumulation of fluid in the abdomen

-causes are portal hypertension, hypoalbuminemia from loss of oncotic pressure, hyperaldosteronism, excessive ADH secretion

ascites clinical effects

-difficulty breathing, keep pt in semi fowlers

-decreased intravascular volume

-hypokalemia (bc of excessive aldosterone)

-abd. pressure or pain

-pressure on diaphragm

-risk of spontaneous bacterial peritonitis (SBP) from growth in excess fluid in abdomen

Ascites management

-Low sodium diet.

-Diuretics - Spironolactone (Aldactone®).

-Management of fluid/electrolyte balance.

-Maintain nutritional intake.

-Vitamin supplementation.

-Abstain from alcohol.

-Paracentesis.

-TIPS (to relieve pressure from portal HTN)

Spironolactone

potassium sparing diuretic

ascites nursing care

-Position for comfort

-Daily weights

-Abdominal girth measurements (around umbillicus)

-Assess fluid/electrolyte status

-Patient education

paracentesis nursing care

Consent, encourage client to void, vital signs, measure abdominal girth, and weight the patient

Coaugulopathy

-impaired clotting due to thrombocytopenia (splenomegaly) decreased clotting factor synthesis

-manage with platelet transfusions or fresh frozen plasma (FFP)

PT/INR

-measures liver function

-shoes that liver is synthesizing clotting factors

-normal is 0.9-1.1 (high = dysfunctional liver)

Hepatic encephalopathy

-brain dysfunction

-liver is not converting ammonia to urea to be excreted by kidneys

-shows change in mental status (ranges from lethargy to confusion to coma)

-asterixis or "liver flap" from wrist shaking

factors that worsen hepatic encephalopathy

-dehydration (ammonia more concentrated)

-constipation (longer in system)

-GI bleed (blood has protein)

-infection

-cerebral depressants

-TIPS procedure (blood isn't detoxified in liver)

Hepatic encephalopathy treatment

-lactulose (laxative) to trap ammonia in gut and excrete via stool

-high carb and controlled protein diet

-rifaximin (antibiotic that decreases bacteria in gut)

-monitor ammonia (15-45 ug/dl)

-neuro assessment, fluid/electrolyte, manage diarrhea)

cirrhosis labs

-normal or elevated AST/ALT

-PT/INR increased (shows liver not making clotting factors)

- decreased platelets (bc of splenomegaly)

-low albumin

liver cancer

-primary hepatocellular cancer less common, usually is metastatic

-dx: CT, MRI of abdomen, alpha-feta protein tumor marker, liver biopsy

-palliative chemo

liver transplant

-options for localized liver cancer, cirrhosis, fulminant hepatitis, toxic hepatitis

-needs match

-post-op immunosuppressants

Cholelithiasis (gall stones)

-Composed of cholesterol

-Risk factors

--Female

--Fertile (multiparous)

--Fair (Caucasian)

--Forty

--Fat (obese)

--Rapid Weight Loss

-Can be asymptomatic

biliary colic

-caused when cystic duct transiently obstructed by a gall stone

-pain is sharp, RUQ, radiated to shoulder

-occurs after eating fatty foods

-pain lasts 1-5 hrs

Cholecystitis

-inflammation of the gallbladder; usually associated with obstructing gallstones

-s/s: RUQ pain radiating to right shoulder, fever, jaundince, murphy's sign

-complications: abscess, pancreatitis, cholangitis, gangrene of gallbladder, sepsis

Murphy's sign

pain with palpation of the RUQ during inspiration, indicative of cholecystitis

Cholecystitis workup

-ultrasound

-HIDA scan (nuclear medicine test)

-ERCP of biliary tree

-WBC elevation

-AST, ALT, and bilirubin may be elevated due to obstruction

-amylase and lipase elevated if pancreatitis

Cholecystitis Treatment

-antibiotics

-pain meds

-IV fluids

-ERCP to remove common bile duct stones

-cholecystectomy (laparoscopic or open)