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Nsg 234: Concept of Clotting; Exemplar of Liver Disease
Terms in this set (43)
Functions of the liver
1. synthesis of bile salts and secretion of bile; bile secretion is the main digestive function
2. Synthesis of plasma proteins (plasma in the blood vital to maintain blood volume= homeostasis)
3. Keeps interstitial fluid in the blood vessels
4. Temporary storage for blood in general circulation, glycogen and fat soluble vitamins (A,D,E,K, et B12)
5. Detoxification of drugs and other substances (site of metabolism for most drugs)
6. Excretion of bilirubin, cholesterol, and drugs.
7. Causes changes in sexual characteristics (men= gynecomastia, women= amenorrhea)
8. Metabolism of CHO, fats et protein
What does bile do?
Where does bile flow?
through the common bile duct to the duodenum
What are Kupffer cells?
cells that phagocytose bacteria and other substances
What is hepatitis?
diffuse inflammation of the liver
What causes hepatitis?
1. Viral Infections, such as Epstein-Barr, Cytomegalovirus, Herpes, Coxsackievirus, et Rubella.
2. Toxic Reactions from ETOH, Methyldopa, INH, Arsenicals, Oral contraception, *Tylenol
3. Inherited disorders, such as Wilson's disease, Hemochromatosis (too much blood volume), Glycogen Storage Disease, Fanconi's Syndrome.
4. Other causes: Sarcoidosis, Graft vs. Host Disease, Chronic Inflammatory Bowel, Jejunoileal Bypass, DM
Hepatitis can lead to what?
What are the 2 different types of hepatitis?
Pathophysiology of hepatitis
Inflammation of liver (normal pattern disturbed); interrupts the blood supply to liver, causing necrosis and breakdown of cells. Over time, the damaged liver cells are removed from the body by immune system and replaced with healthy liver cells
Signs and symptoms of hepatitis
Vary greatly: Asymptomatic, to liver failure, to hepatic encephalopathy.
Generalized flu-like sx, such as malaise, aching muscles, HA, abd. pain, nausea, constipation, fatigue, photophobia, lassitude, chills, dyspepsia, diarrhea, pruritis d/t bile salt build-up
Assessment findings from hepatitis
enlarged liver, enlarged lymph nodes, weight loss, rhinitis, jaundice, dark amber urine (d/t bilirubin), clay colored stool (floaters, foul smelling d/t fats not being digested), pruritis
Medical management of hepatitis
No specific tx, treat the symptoms. Prevent transmission. Treat dehydration. Vitamins B complex and Vitamin K. Avoid ALL unnecessary medications. Bed rest. No ETOH, small frequent meals that are low fat, high CHO, trim nails d/t pruritis. Reposition q2h. Hospitalization d/t bilirubin > 10dL, prolonged PT.
Cirrhosis of the liver
Liver disease combinded with this is the 8th leading cause of death in the US. Insidious, chronic degenerative disease. Liver damage not reversible but can be stopped or delayed.
Pathology of liver cirrhosis
scar tissue replaces healthy tissue- blocking blood flow through the organ, rendering it unable to function.
What drug is the most common cause of drug induced liver damage?
Causes of liver cirrhosis
Any chronic liver disease.
Excessive ETOH consumption.
Non-alcohol fatty liver disease.
Exposure to hepatoxins
Primary biliary cirrhosis more common in females (destruction of bile ducts)
Cardiac cirrhosis: hepatic damage resulting from long standing right sided heart failure.
How is Hep C transmitted?
via needlesticks, blood transfusions, IV drug use, straws (cocaine); Baby Boomer generation
How is Hep B transmitted?
via contaminated serum-transfusions, contaminated instruments, needlesticks, IV drug use, dialysis, contact with body fluids from infected persons
Progression of Liver Destruction
3. Fibrotic regeneration
4. Hepatic insufficiency
Results of altered liver function
-Decreased ability to synthesize albumin (fluid accumulates in legs, abdomen)
- Slows or stops production of clotting factors, causing bleeding tendencies, bruising
- Portal HTN: compression or occlusion of the portal vascular system- usually irreversible. Causes ascites in conjunction with hypoalbuminemia and hyperaldosteronism
reduced synthesis of protein and the leaking of existing protein. Protein in blood acts as an absorber- "attracts" fluid back into the vessels
Early clinical manifestations of cirrhosis
Onset insidious (not sudden or abrupt). Enlarged liver-abdominal pain. RUQ discomfort, under the ribs. Malaise. GI disturbances. Indigestion. Change in bowel habits. N/V. Dyspepsia. Decreased Hgb, fever, weight loss and jaundice.
Late clinical manifestations of cirrhosis
Jaundice, esophageal varicies, ascites, hepatomegaly, splenomegaly, hemorrhoids, peripheral edema, peripheral neuropathy, asterixis (hand flapping), changes in mental status, spiderangiomas, anemia,
coagulation disorders, palmar erythema (from estrogen), sexual characteristic changes
Lab results for liver cirrhosis
Elevated bilirubin, abnormal electrolytes, abnormal liver enzymes, decreased serum albumin, abnormal CBC, hypoglycemia, elevated prothrombin time, elevated serum ammonia
Diagnostic testing for liver cirrhosis
ERCP, esophagoscopy, barium swallow, liver scan, liver bx, U/S, paracentesis
Treatment of liver cirrhosis
Identify the cause.
Management of ascites, respiratory compromise or abdominal pain.
Support- prevent further liver damage. Eliminate ETOH, hepatotoxins, exposure to environmental chemicals.
Diuretics (assess dehydration, electrolyte imbal., decreased renal function)
Diet for liver cirrhosis
Avoid fluid retention- reduce sodium.
Low fat, low sodium
may have restricted protein nutritional state.
High carbs, high calorie.
Additional vitamins K, C, folic acid
What dietary considerations are made for impending liver failure?
Proteins and fluids are restricted. Protein metabolism results in elevated ammonia levels, which increases the risk of encephalopathy
Procedure for paracentesis
Have pt empty bladder. Position to the side of the bed or High Fowler's. Fluid removed slowly 30-90 minutes to prevent syncope and hypotension. Post procedure, assess dressing, hypovolemia, electrolyte imbalances, bleeding
shunts peritoneal fluid from abdominal cavity into the SVC
Complications of the LeVeen Shunt
CHF, leakage of fluid, infection, peritonitis, septicemia, shunt thrombosis
varicose veins in the lower end of the esophagus, causes portal HTN. Can rupture with increased abd. venous pressure. Diagnosed with endoscopy. If rupture, life threatening. Maintain airway. Give vasopressin to control or stop bleeding. Use Sengstaken-Blakemore tube to control bleeding.
Treatment of esophageal varicies
NPO-HOB 30-45 degrees. Iced isotonic solution. Endoscopic sclerotherapy, will have NG tube passed into the esophagus to suction saliva that can't drain into the stomach
Symptoms of hepatic encephalopathy
inappropriate behavior; disorientation; asterixis; twitching of extremities; progression to stupor and coma
Treatment of hepatic encephalopathy
Prevent further liver damage.
Lactulose PO to decrease production of ammonia
Neomycin inhibits protein synthesis, decreasing ammonia production.
Meds metabolized in the liver are avoided
Nursing interventions for hepatic encephalopathy
VS, strict I&O, weight daily, assess for hemorrhage (restlessness, anxiety, hematemesis, melana)
Carcinoma of liver
Liver CA, primary site is rare. Mets to lungs common. Usually a metastatic site- vascularity. Associated with patients with hx of hep B or C.
Diagnostic tests for liver CA
Liver scan, hepatic arteriography, cholangiopancreatography, ERCP, liver bx, AFP
What is an ERCP?
ERCP is short for endoscopic retrograde cholangiopancreatography. It is a procedure that looks at the bile ducts. It is done through an endoscope. Bile ducts are the tubes that carry bile from the liver to the gallbladder and small intestine.
Symptoms of liver CA
similar to early stages cirrhosis (enlarged liver, RUQ discomfort under ribs, malaise)
Treatment of liver CA
Dissect out CA.
Usually has poor response to chemo.
Prognosis of liver CA
Rapid growth. Death usually 4-7 months. Usually develop hepatic encephalopathy and GI bleeds. Liver transplants for patients with localized disease.
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