Liver study guide course. # 6 PDF

Preview

Summary

Hepatic disorders: Structure & FunctionWhat am I❖ The largest gland of the body. ❖ Located in the right upper abdomen. ❖ Very vascular. ❖ Receives blood from the GI tract via the portal vein and the hepatic artery.Lobes❖ Glisson's capsule: A layer of connective tissue surrounding the liver a...

Description

Hepatic disorders: Structure & Function

6-1

Changes with older Age

Functions What am I ❖ ❖ ❖ ❖

The largest gland of the body. Located in the right upper abdomen. Very vascular. Receives blood from the GI tract via the portal vein and the hepatic artery.

❖

❖

❖

Glucose metabolism Ammonia conversion Protein metabolism Fat metabolism Vitamin and iron storage Drug metabolism Bile formation Bilirubin excretion Clotting factors Blood filtering

❖ ❖ ❖ ❖

Liver decreases in size and weight. Decreased hepatic flow. Decreased ability to metabolize drugs. Increased risk of gallstones. More frequent and severe complications of biliary tract disease.

M: Metabolism of glucose. R: Regulation of clotting factors.

Lobes ❖

❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

Glisson's capsule: A layer of connective tissue surrounding the liver and ensheathing the hepatic artery, portal vein, and bile ducts within the liver. Caudate lobe: A lobe of the liver bounded on the right by the inferior vena cava, on the left by the fissure of the ductus venosus, and connected with the right lobe by a narrow prolongation. Quadrate lobe: Is an area of the liver situated on the under surface of the medial segment left lobe (Couinaud segment IVb), bounded in front by the anterior margin of the liver; behind by the porta hepatis; on the right, by the fossa for the gall-bladder; and on the left, by the fossa for the umbilical vein.

L: Let s food become energy by breaking down fats and proteins. I: Iron storage. V: Vitamin storage. E: Excretion of bilirubin . R: Removes toxins and filters bacteria.

Hepatic circulation One hepatic artery carries nutrient poor, oxygen rich blood through the hepatic circulatory system. One portal vein flows through the hepatic circulatory system carrying nutrient rich, oxygen poor blood. Blood flows from the abdominal organs which pass through the portal vein. Then into the sinusoids of the liver, and into the hepatic vein before returning to the heart from the inferior vena cava. The hepatic artery provides 30 to 40% of the oxygen to the liver, while only accounting for 25% of the total liver blood flow. The rest comes from the partially deoxygenated blood from the portal vein which makes up about 75% of liver blood flow. The liver consumes about 20% of the total body oxygen when at rest. That is why the total liver blood flow is quite high, at about one litre a minute and up to two litres a minute. This pathway permits the liver to process and to detoxify substances entering the body from the gastrointestinal tract.

Hepatic dysfunctions & manifestations Dysfunctions: ❖ Acute or chronic cirrhosis of the liver ❖ Malnutrition from alcoholism ❖ Infection ❖ Anorexia ❖ Metabolic disorders ❖ Nutritional deficits ❖ Hypersensitivity states Manifestations: ❖ Jaundice ❖ Portal hypertension ❖ Acities ❖ Varices ❖ Hepatic Encephalopathy ❖ Coma ❖ Nutritional deficits

Manifestations of liver dysfunction ❖ ❖ ❖

❖ ❖

❖ ❖

www.SimpleNursing.com

Pallor often seen with chronic illness and jaundice. The skin, mucosa, and sclerae are inspected for jaundice, Extremities are assessed for muscle atrophy, edema, and skin excoriation secondary to scratching. Petechiae or ecchymotic areas (bruises), spider angiomas), and palmar erythema. The male patient is assessed for unilateral or bilateral gynecomastia and testicular atrophy due to hormonal changes. Cognitive status (recall, memory, abstract thinking) and neurologic status are assessed. General tremor, asterixis, weakness, and slurred 6-1 speech.

jaundice Assessment

6-2

What am i? Yellow or green tinged sclera and skin caused by elevated bilirubin levels.

❖ ❖

Types Hemolytic jaundice: Occurs as a result of hemolysis (an accelerated breakdown of red blood cells) leading to an increase in production of bilirubin. Usually a result of a hemolytic transfusion reaction. Hepatocellular jaundice: Occurs as a result of liver disease or injury. There is an inability of the liver to remove normal amounts of bilirubin from the blood. Obstructive jaundice: Occurs when the essential flow of bile to the intestine is blocked and remains in the bloodstream. Hereditary hyperbilirubinemia: Increased serum bilirubin levels resulting from hereditary issues such as Gilbert’s syndrome. There is no hemolysis.

❖

Labs

Hemolytic: Usually asymptomatic. Hepatocellular: Mild or severe illness, lack of appetite, nausea, malaise, fatigue weakness and weight loss, headache chills and fever if the cause is infectious. Obstructive: Light gray or clay colored stool, intense itching, dyspepsia, and intolerance to fatty foods.

❖ ❖ ❖

AST and ALT elevation GGT elevation Increased serum bilirubin

Treatments Jaundice itself requires no treatment in adults, if itching becomes an issue, the HCP may prescribe cholestyramine 2 to 8 g po bid. However, cholestyramine is ineffective in patients with complete biliary obstruction.

Patho If the flow of bile is impeded or if there is excess destruction of red blood cells as a consequence of liver disease or bile ducts obstruction causes an increase in serum bilirubin. When serum bilirubin levels become abnormally elevated all of the tissues in the body will turn yellow or green.

Interventions ❖

Causes ❖

Increased production

❖

Decreased hepatic uptake

❖

Decreased conjugation

❖

Dysfunction of hepatocytes (hepatocellular dysfunction)

❖

Slowing of bile egress from the liver (intrahepatic cholestasis)

❖

Obstruction of extrahepatic bile flow

Interventions are associated with the cause of the jaundice.

Education ❖ ❖ ❖ ❖ ❖ ❖ ❖

Educate the client on treatment regimen. Causes of jaundice. Long term jaundice can cause pigment stones, CNS dysfunction and brain stem injury. Signs and symptoms of jaundice. Encourage smoking and alcohol cessation if appropriate. Encourage proper diet. Encourage your client to keep up with their appointments and lab work studies.

(extrahepatic cholestasis)

6-2 www.Simplenursing.com

6-3

Hepatic dysfunctions & manifestations Dysfunctions

Acute or chronic cirrhosis of the liver ❖

❖ ❖

Most common cause is malnutrition from alcohol abuse. Chronic cirrhosis is most common. Replaces stored glycogen with lipids causing inflammation and fibrotic tissue.

Anoxia

Fatty liver ❖

❖ ❖ ❖

❖ ❖ ❖

An accumulation of fat in and around the liver cells. Risks include: Diabetes High cholesterol Alcohol abuse

❖ ❖

Hypoxic liver. Increased liver enzymes. Caused by right sided HF in older adults. Caused by decreased cardiac output. Blood will back up into the liver and the GI tract causing ascites and Edema.

Manifestations Jaundice Hemolytic jaundice: Occurs as a result of hemolysis (an accelerated breakdown of red blood cells) leading to an increase in production of bilirubin. Usually a result of a hemolytic transfusion reaction. Hepatocellular jaundice: Occurs as a result of liver disease or injury. May be mildly or severely ill and express a lack of appetite. Obstructive jaundice : Occurs when the essential flow of bile to the intestine is blocked and remains in the bloodstream.

Portal Hypertension Portal hypertension is an increase in the blood pressure within a system of veins called the portal venous system.

Esophageal varices Esophageal varices develop when normal blood flow to the liver is blocked by a clot or scar tissue in the liver. To go around the blockages, blood flows into smaller blood vessels that aren't designed to carry large volumes of blood. The vessels can leak blood or even rupture, causing life-threatening bleeding.

Ascites Ascites is a gastroenterological term for an accumulation of fluid in the peritoneal cavity that exceeds 25 mL.

Hepatic encephalopathy Hepatic encephalopathy is a syndrome observed in patients with cirrhosis. Hepatic encephalopathy is defined as a spectrum of neuropsychiatric abnormalities in patients with liver dysfunction, after exclusion of brain disease.

Misc. Coma Nutritional deficits

6-3 www.SimpleNursing.com

Portal hypertension

6-4

Assessment ❖ ❖ ❖

What am i? The portal venous system is a low pressure system of circulation with a pressure gradient of about 5 mmHg. When the portal venous system is obstructed or stenosed it causes a rise in portal pressure causing portal hypertension.

❖

Varices Ascites Thrombocytopenia: Early indicator of liver dysfunction. Splenomegaly

Labs CBC: Will show low platelets. Hemoccult: Will yield a positive result if bleeding occurs in the GI tract. H&H: Will be low, showing anemia.

Results in ❖

Patho

❖

Obstruction of portal blood flow, such as cirrhosis or portal vein thrombosis. In liver cirrhosis, increased intrahepatic vascular resistance to the portal flow elevates portal pressure and leads to portal hypertension.

❖ ❖

Ascites: Fluid build up in the abdomen. Esophageal varices: Varicose veins in the throat. Splenomegaly : Enlarged spleen. Portal hypertensive gastrophy: Chronic slow bleeding in the GI tract.

Causes ❖ ❖ ❖ ❖

Blood clots in the portal vein. Blockage of the veins that carry blood from the liver to the heart. Focal nodular hyperplasia usually seen in HIV. Parasitic infection, schistosomiasis.

Interventions ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

Elevate the head of the bed to minimize SOB. Restrict sodium intake. Administer diuretics. Monitor intake and output. Weigh the client daily. Monitor LOC. Administer blood products if indicated. Monitor prothrombin time and coagulation studies. Administer Vitamin K if indicated. Administer lactulose if indicated. Avoid opioids, sedatives, and barbituates. Educate the client on the importance of alcohol cessation.

6-4 www.SimpleNursing.com

6-5

Ascites Assessment ❖

What am i? Albumin rich fluid build up in the abdomen of 25 mL or more, caused by portal hypertension resulting in increased capillary pressure and obstruction of venous blood flow.

❖ ❖ ❖ ❖ ❖ ❖

Swollen, rounded abdomen, bulging flanks in the supine position Striae Weight gain Shortness of breath Distended veins Umbilical hernia Electrolyte and fluid imbalances, hypovolemia

Nursing interventions ❖ ❖ ❖ ❖ ❖ ❖ ❖

F: Fluid and electrolyte imbalances L: Large swollen abdomen U: Umbilical hernia Portal hypertension leads to vasodilation, I: Intense stretch marks D: Distended veins which causes a decrease in effective S: Shortness of breath arterial blood volume. As the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This causes overflow of albumin rich fluid into the peritoneal cavity.

Patho

Daily weights. Strict intake and output monitoring. Daily abdominal girth measurements. Monitor respiratory status. Monitor serum ammonia, creatinine, and electrolyte levels. Monitor client's response to therapy. Monitor for signs of encephalopathy. When potassium is decreased ammonia is increased causing encephalopathy.

Complications

Spontaneous bacterial peritonitis

Education ❖

Causes ❖ ❖

❖ ❖ ❖

❖ ❖

Vasodilation of splanchnic circulation. Changes in the ability to metabolize aldosterone which increases fluid retention. Decreased albumin synthesis. Decreased serum osmotic pressure. Movement of albumin into the peritoneal cavity, causing a decrease in circulating protein. Pericarditis. Endocrine disorders.

Manifestations: Rigid board like abdomen, low grade fever, decreased appetite, changes in mental status.

❖ ❖ ❖

Assessment: Assess bowel sounds, palpate abdomen. Treatments : Fluoroquinolones Ciprofloxacin and Levofloxacin.

❖

❖

Educate the client on the plan of treatment. Avoid alcohol intake. Importance of adhering to a low sodium diet. Take their medications as ordered. State the importance of daily weights, more than 2kg a day is too much loss. Discuss the importance of avoiding NSAIDS, cough mixtures containing alcohol, antibiotics or antacids that contain salts.

Treatments ❖ ❖ ❖ ❖

❖ ❖

Dietary restrictions: 2g sodium per day restriction, no salt substitutes because they contain potassium and ammonia. Bed rest: Semi fowlers. Diuretics: Spironolactone to prevent potassium loss. Lasix may be used cautiously to avoid sodium depletion. Paracentesis: removal of excess abdominal fluid under sterile conditions. Can take up to 4 L of fluid a day.have the client void prior to procedure, obtain baseline vitals, labs, weight and abdominal girth. Monitor for shock, bleeding, hematuria. Send fluid to the lab. Apply sterile dressing and monitor vitals. Transjugular Intrahepatic Portosystemic Shunt: Cannula is threaded into the portal vein to reduce portal HTN. Administer salt poor albumin. www.SimpleNursing.com

6-5

Esophageal varices Assessment

6-6

What am i ? A plumbing backup in the portal venous system, manifested by fragile tortuous veins that are prone to rupture and cause massive bleeding. Occurs in about ⅓ of clients with cirrhosis. First bleeding episode has a 30-50% mortality rate. These veins can spontaneously bust. Bleeding varices are an emergency. Goal of treatment is to control the bleeding.

❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

Hematemesis Melena bloody diarrhea General deterioration Shock Ascites Jaundice Hypotension Hepatomegaly, splenomegaly Dilated abdominal veins (caput medusa)

B: BP decrease from shock, hypotension L: Lots of bloody vomit E: Extra fluid in the abdomen (ascites) E: Extra bilirubin (jaundice) D: Dilated abdominal veins E: Excess blood in the stool (melena) R: Really big organs (hepatomegaly, splenomegaly)

Patho When a significant increase in the blood flow through the portal vein occurs there is a further contribution to portal hypertension. Esophageal varices appear and may bleed when the HVPG exceeds 12 mm Hg.

❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

❖ ❖ ❖

Severe liver scarring (cirrhosis). Hepatitis infection. Alcoholic liver disease. Fatty liver disease. Bile duct disorder called primary biliary cirrhosis Cirrhosis. Increased abdominal pressure can cause rupture. Chest trauma can cause rupture. Salicylates can cause rupture. Acid reflux can cause rupture.

Serum ammonia: Will increase if there is bleeding in the GI tract. Ast & ALT: Will be elevated due to liver dysfunction. H&H: Will be low from blood loss. Hepatic Portography & celiac angiography. Usually done in the OR.

Interventions ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

Causes ❖

LABs & Diagnostics ❖

❖ ❖ ❖ ❖

Monitor vitals. Elevate the head of the bed. Monitor for orthostatic hypotension. Monitor lung sounds. Administer 02. Administer IV fluids. Monitor hemoglobin,hematocrit and coagulation factors. Instruct the client to avoid strenuous activities. Initiate parenteral nutrition if rest of the esophagus is ordered. Gastric suction. Frequent oral hygiene. Initiate Vitamin K therapy to promote clotting.

Treatments ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

Treat for shock by administering blood products and fluids with volume expanders at a good pace, not too fast. Administer electrolytes Vasopressin: Causes vasoconstriction to the coronary arteries and cause a cardiac event, give this with nitroglycerin. This is not the first line treatment because of the cardiac contraindications. Somatostatin and octreotide drips: Diminish blood flow to the portal system. Nitroglycerin with vasopressin: To reduce coronary vasoconstriction. Beta blockers: Propranolol and nadolol to decrease portal pressure. Used in combination with other medications. Sengstaken-blakemore tube: Tube that puts pressure on the varices and temporarily stop the bleeding. Do not leave the client alone. Sclerotherapy: Sclerosing agents are used to scar up the vessel to prevent further rupture or bleeding. Ligation: Put a band on the area. This can cause esophageal stricture, dysphagia, and chest pain.

www.SimpleNursing.com

6-6

Hepatic encephalopathy

6-7

What am i? A life threatening complication of liver disease that occurs in severe liver failure. Usually there are no signs of the illness, but neuropsychological testing may show abnormalities. Survival rate after a first episode is 40% at 1 year. Patients usually end up on the transplant list.

Causes ❖

❖ ❖ ❖ ❖ ❖ ❖ ❖

Caused by severe liver failure. Associated with portal hypertension. Can improve with recovery of liver function. Excess diuresis. Dehydration. Infection. Surgery. Fever. Sedatives, tranquilizers, analgesics, potassium losing diuretics.

Labs & Diagnostics

Assessment CNS: Mental status changes, confusion, sleepiness during the day, patient may lapse into coma or have seizures. EEG changes. MS: Asterixis “liver flap” usually seen in stage 2 encephalopathy. Hyperactive DTRs in early stages, flaccidity in late stages. MISC: Fetor hepaticus. A: Asterixis. M: Mental status changes. M: Muscle flaccidity (late). O: Out of it during the day. N: Nightwalkers (awake at night). I: Initiate seizure precautions (they may seize). A: Ammonia levels will be high causing fetor hepaticus.

❖

❖

❖

❖

❖

Accumulation of ammonia and other toxic metabolites in the blood.

Interventions

Hepatic insufficiency may result in encephalopathy due to a diseased liver that is unable to detoxify toxic by products of metabolism. Porto systemic shunting where collateral vessels are developed as a result of portal hypertension allows toxic substances extracted from the liver into the systemic circulation. Ammonia is considered the main factor in the development of hepatic encephalopathy. Ammonia enters the brain and excites benzodiazepine receptors causing CNS depression; which produce the sleep and behavior patterns noted in hepatic encephalopathy. Ammonia from digestion of dietary and blood proteins in the GI tract. Increases in ammonia from these sources can cause GI bleeding (including varices).

States of Hepatic Encephalopathy ❖

❖

Treatment is aimed at eliminating precipitating causes and minimizing potential complications. Lactulose: Reduces serum ammonia by trapping and expelling it in feces. 2-3 soft stools a day is indicative the lactulose is having a therapeutic effect. IV Glucose: Minimize protein breakdown. Vitamins: To correct deficits and electrolyte imbalances.

Complications ❖

❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

❖

Treatments ❖

❖

Patho ❖

EEG: Shows generalized slowing of brain waves. Ammonia: Elevated ammonia levels.

Stage 1: Normal LOC, periods of lethargy and euphoria. Reversal of day and night sleep. Asterixis, impaired writing and ability to draw figures. Stage 2: Increased drowsiness, disorientation, inappropriate behavior, mood swings, agitation. Asterixis, increased DTR’s , rigidity of extremities. Stage 3: Comatose, may not respond to painful stimuli. Absence of asterixis, absence of DTR, flaccidity of extremities.

❖ ❖