1. Cirrhosis
By: Renee Alta

2. What is Cirrhosis?
Cirrhosis is a condition that causes irreversible scarring of the liver. As scar tissue replaces normal tissue, blood flow through your liver is affected. This makes it increasingly difficult for your liver to carry out essential functions, such as detoxifying harmful substances, purifying your blood and manufacturing vital nutrients.

3. What does the liver do? Synthesize Bile and bile salts
Synthesize Proteins
Phagocytosis
Dextoxification
Metabolism of Carbohydrates
Metabolism of Protein
Metabolism of Fats
Excretion
Storage

4. The Liver
Healthy Liver
Cirrhotic Liver

5. Types of Cirrhosis Alcoholic Cirrhosis Postnecrotic Cirrhosis
Primary Biliary Cirrhosis
Secondary Biliary Cirrhosis
Cardiac Cirrhosis
Alcoholic Cirrhosis
history of chronic ingestion of alcohol
Postnecrotic Cirrhosis
viral hepatitis, expossure to hepatoxins, or infections
Primary Biliary Cirrhosis
Destruction of the bile ducts
Secondary Biliary Ducts
Obstructions caused by gallstones, a tumor, or biliary atresia
Cardiac Cirrhosis
long standing, severe right-sided, heart failure in patients with cor pulmonale

6. What happens to the body with liver cirrhosis?
Portal hypertension is an increased venous pressure in the portal circulation caused by compression in the portal or hepatic vascular system.
Increased pressure causes ASCITES.
If fluid leaves the adrenal cortex will increase the secretion of aldosterone. Aldosterone is the hormone that signals for the retention of sodium and water.

7. Signs & Symptoms Hypocomastia Liver size Splenomegaly Ascites
Spider Angiomata
Palmar Erythema
Nail Changes
Muehtrcke’s Nails
Terry’s Nails
Clubbing
Hypertrophic osteoarthropathy
Dupuytren’s Contracture
Gynecomastia
Hypocomastia
Liver size
Splenomegaly
Ascites
Caput Medusa
Cruveilhier_Baumgarten
Feta Hepaticus
Jaundice
Asterixis
Spider angiomata. Vascular lesions consisting of central arteriole surrounded by many smaller vessels due to an increase in estradiol.
Palmar erythema. Exaggerations of normal speckled mottling of the palm, due to altered sex hormone metabolism.
Nail changes.
Muehrcke's nails --- paired horizontal bands separated by normal color due to hypoalbuminemia
Terry's nails --- proximal two thirds of the nail plate appears white with distal one-third red, also due to hypoalbuminemia
Clubbing. Angle between the nail plate and proximal nail fold > 180 degrees
Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long bones that can cause considerable pain.
Dupuytren's contracture. Thickening and shortening of palmar fascia that leads to flexion deformities of the fingers. Thought to be due to fibroblastic proliferation and disorderly collagen deposition. It is relatively common (33% of patients).
Gynecomastia. Benign proliferation of glandular tissue of male breasts presenting with a rubbery or firm mass extending concentrically from the nipples. This is due to increased estradiol and can occur up to 66% of patients.
Hypogonadism. Manifested as impotence, infertility, loss of sexual drive, and testicular atrophy due to primary gonadal injury or suppression of hypothalamic or pituitary function.
Liver size. Can be enlarged, normal, or shrunken.
Splenomegaly. Due to congestion of the red pulp as a result of portal hypertension
Ascites. Accumulation of fluid in the peritoneal cavity giving rise to flank dullness (needs about 1500 mL to detect flank dullness).
Caput medusa. In portal hypertension, the umbilical vein may open. Blood from the portal venous system may be shunted through the periumbilical veins into the umbilical vein and ultimately to the abdominal wall veins, manifesting as caput medusa.
Cruveilhier-Baumgarten murmur. Venous hum heard in epigastric region due to collateral connections between portal system and the remnant of the umbilical vein in portal hypertension.
Fetor hepaticus. Sweet pungent smell in breath due to increased dimethylsulphide due to severe portal-systemic shunting.
Jaundice. Yellow discoloring of the skin, eye, and mucus membranes due to increased bilirubin (at least 2-3 mg/dL). Urine may also appear dark.
Asterixis. Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in patients with hepatic encephalopathy.
Other. weakness, fatigue, anorexia, weight loss

8. Muehrcke’s Nail
Terry’s Nail

10. Diagnostic Tests
The gold standard for diagnosis of cirrhosis is a liver biopsy, through a percutaneous, transjugular, laparoscopic, or fine-needle approach.

11. Lab Findings
Aminotransferases -- AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferases do not preclude cirrhosis.
Alkaline phosphatase -- Usually slightly elevated.
GGT -- Correlates with AP levels. Typically much higher in chronic liver disease from alcohol.
Bilirubin -- May elevate as cirrhosis progresses.
Albumin -- Levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver
Prothrombin time -- Increases since the liver synthesizes clotting factors.

12. Lab Findings Cont’d
Globulins -- Increased due to shunting of bacterial antigens away from the liver to lymphoid tissue.
Serum sodium -- Hyponatremia due to inability to excrete free water resulting from high levels of ADH.
Thrombocytopenia -- Due to both congestive splenomegaly
Leukopenia and neutropenia -- Due to splenomegaly with splenic margination.
Coagulation defects -- The liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.

13. Medical Management
Antiemetics such as Finergen to control nausea or vomitting
Benadryl or Dramamine may be given for the pruritis
Compazine, Vistraril and Atarax are CONTRAINDICATED in severe liver dysfunction.

14. Nursing Interventions
Check vital signs every 4 hours and more so if a hemorrhage is present
Monitor for GI hemorrhage as evidence by hematemesis, melena, anxiety and restlessness
Sodium Restrictions
Lotion to relieve the pruritis
Monitor I&O
Measure abdominal girth and weigh daily