Liver disfunction

Nursing diagnosis

-ACTIVITY INTOLERANCE RELATED TO FATIGUE, ETC. -ALTERED NUTRITIONAL STATUS RELATED TO GASTRITIS, DECREASED GI MOTILITY, AND ANOREXIA -IMPAIRED SKIN INTEGRITY RELATED TO EDEMA, JAUNDICE, AND COMPROMISED IMMUNOLOGIC STATUS -HIGH RISK FOR INJURY RELATED TO ALTERED CLOTTING MECHANISMS AND PORTAL HYPERTENSION -ALTERED THOUGHT PROCESSES RELATED TO DETERIORATION OF LIVER FUNCTION AND EVEVATION OF AMMONIA LEVEL

CIRRHOSIS-PATHOPHYSIOLOGY

-ALCOHOL MAJOR CAUSATIVE FACTOR - MALNUTRITION -EXPOSURE TO CERTAIN CHEMICALS -2X MORE MEN THAN WOMEN -CIRRHOSIS IS CHARACTERIZED BY WIDESPREAD FIBROTIC (SCARRED) BANDS OF CONNECTIVE TISSUE THAT CHANGE THE LIVER'S NORMAL MAKEUP. -INFLAMMATION CAUSED BY EITHER TOXINS OR DISEASE RESULTS IN EXTENSIVE DEGENERATION AND DESTRUCTION OF HEPATOCYTES (LIVER CELLS). -AS CIRRHOSIS DEVELOPS, THE TISSUE BECOMES NODULAR

ASCITES AND GASTROESOPHAGEAL VARICES

-ASCITES IS THE COLLECTION OF FREE FLUID WITHIN THE PERITONEAL CAVITY CAUSED BY INCREASED HYDROSTATIC PRESSURE FROM PORTAL HYPERTENSION -MASSIVE ASCITES MAY CAUSE RENAL VASOCONSTRICTION, TRIGGERING THE RENIN-ANGIOTENSIN SYSTEM. -THIS RESULTS IN SODIUM AND WATER RETENTION, WHICH INCREASES HYDROSTATIC PRESSURE AND THE VASCULAR VOLUME AND LEADS TO MORE ASCITES.

albumin and total protein

-Albumin - measures the main protein made by the liver; the level can be affected by liver and kidney function and by decreased production or increased loss. -Total protein (TP) - measures albumin and all other proteins in blood, including antibodies made to help fight off infections

AST and bilirubin

-Aspartate aminotransferase (AST) - an enzyme found in the liver and a few other organs, particularly the heart and other muscles in the body -Bilirubin - two different tests of bilirubin often used together (especially if a person has jaundice): total bilirubin measures all the bilirubin in the blood; direct bilirubin measures a form that is conjugated (combined with another compound) in the liver.

Hepatic cirrhosis

-CIRRHOSIS IS EXTENSIVE, IRREVERSIBLE SCARRING OF THE LIVER, USUALLY CAUSED BY A CHRONIC REACTION TO HEPATIC INFLAMMATION AND NECROSIS -THE DISEASE TYPICALLY DEVELOPS SLOWLY AND HAS A PROGRESSIVE, PROLONGED, DESTRUCTIVE COURSE RESULTING IN END-STAGE LIVER DISEASE. -THE MOST COMMON CAUSES FOR CIRRHOSIS IN THE UNITED STATES ARE CHRONIC ALCOHOLISM, CHRONIC VIRAL HEPATITIS, NONALCOHOLIC STEATOHEPATITIS (NASH), BILE DUCT DISEASE, AND GENETIC DISEASES

BLEEDING ESOPHAGEAL VARICES PATHOPHYSIOLOGY AND CLINICAL MANIFESTATIONS

-DILATED, TORTUOUS VEINS IN THE SUBMUCOSAL LAYERS OF THE LOWER ESOPHAGUS OR UPPER STOMACH. -CAUSED BY PORTAL HYPERTENSION -LIFE-THREATENING, CAN RESULT IN HEMORRHAGIC SHOCK, INCREASED NITROGEN LOAD, " ENCEPHALOPATHY -MELENA -HEMATEMESIS

Biliary cirrhosis manifestations (early and later)

-EARLY: LIVER LARGE, FATTY, FIRM, SHARP PALPABLE EDGE -ABDOMINAL PAIN -LATER: LIVER $ IN SIZE AND PALPATED EDGE IS NODULAR -CHRONIC DYSPEPSIA -CONSTIPATION OR DIARRHEA

BLEEDING ESOPHAGEAL VARICES ASSESSMENT

-ENDOSCOPY -BARIUM SWALLOW -ULTRASOUND -CT SCAN -ANGIOGRAPHY -LABORATORYTESTS

bile

-FORMED BY HEPATOCYTES AND COLLECTED IN THE CANALICULI AND BILE DUCTS. -COMPOSED MAINLY OF WATER, ELECTROLYTES, LECITHIN, FATTY ACIDS, CHOLESTEROL, BILIRUBIN, AND BILE SALTS. -BILE SALTS ARE SYNTHESIZED BY THE HEPATOCYTES FROM CHOLESTEROL. NEEDED FOR THE EMULSIFICATION OF FATS, THEN REABSORBED

HEREDITARY HYPERBILIRUBINEMIA

-GILBERT'S SYNDROME -DUBIN-JOHNSON SYNDROME -ROTOR'S SYNDROME

cirrhosis clinical manifestations

-GRADUAL WEIGHT LOSS -ASCITES -VARICES -SPLENOMEGALY -SPIDER TELANGIECTASIS -PROMINENT DISTENDED ABDOMINAL VEINS -PLASMA ALBUMIN DECREASED -INCREASED ALDOSTERONE -CLOTTING PROBLEMS -ANEMIA -NEUROLOGIC CHANGES

GGT and LD

-Gamma-glutamyl transferase (GGT) - another enzyme found mainly in liver cells -Lactate dehydrogenase (LD) - an enzyme released with cell damage; found in cells throughout the body

nursing interventions (liver dysfunction? slide 57)

-HAVE PATIENT VOID -OBSERVE FOR VASCULAR COLLAPSE -MONITOR VITAL SIGNS -DOCUMENT -SHUNTS- *PERITONEOVENOUS: LeVEEN SHUNT AND DENVER SHUNT *TRANSVENOUS PERCUTANEOUS PORTA CAVAL SHUNT: TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS) OR TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC STENT SHUNTING (TIPSS) -SURGERY -FEVER -SEDATIVES, TRANQUILIZERS, NARCOTICS

HEPATIC ENCEPHALOPATHY

-HEPATIC ENCEPHALOPATHY (ALSO CALLED PORTAL-SYSTEMIC ENCEPHALOPATHY [PSE]) IS A COMPLEX COGNITIVE SYNDROME THAT RESULTS FROM LIVER FAILURE AND CIRRHOSIS. -PATIENTS REPORT SLEEP DISTURBANCE, MOOD DISTURBANCE, MENTAL STATUS CHANGES, AND SPEECH PROBLEMS EARLY AS THIS COMPLICATION BEGINS. -HEPATIC ENCEPHALOPATHY MAY BE REVERSIBLE WITH EARLY INTERVENTION. -LATER NEUROLOGIC SYMPTOMS INCLUDE AN ALTERED LEVEL OF CONSCIOUSNESS, IMPAIRED THINKING PROCESSES, AND NEUROMUSCULAR PROBLEMS. -HEPATIC ENCEPHALOPATHY MAY DEVELOP SLOWLY IN PATIENTS WITH CHRONIC LIVER DISEASE AND GO UNDETECTED UNTIL THE LATE STAGES. -SYMPTOMS DEVELOP RAPIDLY IN ACUTE LIVER DYSFUNCTION.

hepatocellular jaundice (liver dysfunction manifestation)

-HEPATOCELLULAR JAUNDICE - INABILITY OF THE DISEASED LIVER CELLS TO CLEAR NORMAL AMOUNTS OF BILIRUBIN FROM THE BLOOD (HEPATITIS, YELLOW FEVER, DRUG OR CHEMICAL TOXICITY). -PATIENTS MAY BE MILDLY OR SEVERELY ILL: ANOREXIA, NAUSEA, MALAISE, WEIGHT LOSS -SERUM BILIRUBIN, URINE UROBILINOGEN, SGOT(AST), SGPT (ALT) MAY BE ELEVATED.

FACTORS THAT MAY LEAD TO HEPATIC ENCEPHALOPATHY IN PATIENTS WITH CIRRHOSIS INCLUDE:

-HIGH-PROTEIN DIET -INFECTION -HYPOVOLEMIA (DECREASED FLUID VOLUME) -HYPOKALEMIA (DECREASED SERUM POTASSIUM) -CONSTIPATION -GI BLEEDING (CAUSES A LARGE PROTEIN LOAD IN THE INTESTINES) -DRUGS (E.G., HYPNOTICS, OPIOIDS, SEDATIVES, ANALGESICS, DIURETICS, ILLICIT DRUGS)

BILIARY OBSTRUCTION

-IN PATIENTS WITH CIRRHOSIS, THE PRODUCTION OF BILE IN THE LIVER IS DECREASED. -THIS PREVENTS THE ABSORPTION OF FAT-SOLUBLE VITAMINS (E.G., VITAMIN K). -WITHOUT VITAMIN K, CLOTTING FACTORS II, VII, IX, AND X ARE NOT PRODUCED IN SUFFICIENT QUANTITIES AND THE PATIENT IS SUSCEPTIBLE TO BLEEDING AND EASY BRUISING. -SOME PATIENTS HAVE A GENETIC PREDISPOSITION TO OBSTRUCTION OF THE BILE DUCT THAT LEADS TO BILIARY CIRRHOSIS — USUALLY FROM GALLBLADDER DISEASE OR AN AUTOIMMUNE FORM OF THE DISEASE CALLED PRIMARY BILIARY CIRRHOSIS (PBC). -JAUNDICE (YELLOWISH COLORATION OF THE SKIN) IN PATIENTS WITH CIRRHOSIS IS CAUSED BY ONE OF TWO MECHANISMS: HEPATOCELLULAR DISEASE OR INTRAHEPATIC OBSTRUCTION

Liver dysfunction manifestation

-JAUNDICE -ABNORMALITIES OF CHO, PROTEIN, AND FAT METABOLISM -INCREASED SERUM AMMONIA LEVEL -INCREASED PORTAL VEIN PRESSURE (ASCITES, ESOPHAGEAL VARICES) -BLEEDING -ENDOCRINE ABNORMALITIES -HEPATIC COMA -LIVER FUNCTION TESTS -OVER 70% OF LIVER MAY BE DAMAGED BEFORE LFT'S BECOME ABNORMAL -CLINICAL MANIFESTATIONS ALSO INCLUDE JAUNDICE -HEMOLYTIC JAUNDICE - THE RESULT OF AN INCREASED DESTRUCTION OF RED BLOOD CELLS (TRANSFUSION REACTIONS, PHYSIOLOGIC JAUNDICE, ETC).

BLEEDING ESOPHAGEAL VARICES MAY RESULT FROM

-LIFTING HEAVY OBJECTS -STRAINING AT STOOLS -SNEEZING -COUGHING -VOMITING -ESOPHAGITIS -DRUGS THAT ERODE ESOPHAGEAL MUCOSA

Hepatic coma assessment and clinical manifestations

-MINOR MENTAL CHANGES AND MOTOR DISTURBANCES -DIFFICULT TO AWAKEN -ASTERIXIS (FLAPPING TREMORS OF THE HANDS) -EEG CHANGES -FETOR HEPATICUS (BREATH ODOR OF MOWED GRASS, ACETONE, OR OLD WINE) -GROSS' DISTURBANCES OF CONSCIOUSNESS -COMA, CONVULSIONS -ABOUT 35% OF PATIENTS WITH CIRRHOSIS DIE IN HEPATIC COMA

ALP

45 to 115 U/L

Total protein.

6.3 to 7.9 g/dL

ALT

7 to 55 units per liter (U/L)

AST

8 to 48 U/L

GGT (gamma glutamyl transferase)

9 to 48 U/L

PT

9.5 to 13.8 seconds

CONTROLLING FLUID RETENTION AND ASCITES

-NUTRITIONAL CONTROL--GOAL IS A NEGATIVE SODIUM BALANCE TO REDUCE FLUID RETENTION -DIURETICS--LASIX, EDECRIN, ALDACTONE; OBSERVE FOR ELECTROLYTE DISTURBANCES AND ALTERED SKIN INTEGRITY

Gastrointestinal Function Tests

-Normal blood test results for typical liver function tests include: -ALT. 7 to 55 units per liter (U/L) -AST. 8 to 48 U/L -ALP. 45 to 115 U/L -Albumin. 3.5 to 5.0 grams per deciliter (g/dL) -Total protein. 6.3 to 7.9 g/dL -Bilirubin. 0.1 to 1.2 milligrams per deciliter (mg/dL) -GGT. 9 to 48 U/L -LD. 122 to 222 U/L -PT. 9.5 to 13.8 seconds

obstructive jaundice (liver dysfunction manifestation)

-OBSTRUCTIVE JAUNDICE - BILE DUCT OCCLUSION BY GALLSTONE, INFLAMMATORY PROCESS, TUMOR, PRESSURE FROM AN ENLARGED ORGAN, MAY BE INTRAHEPATIC. BILE BACKS UP INTO THE LIVER SUBSTANCE, IS REABSORBED INTO THE BLOOD AND CARRIED THROUGHOUT THE BODY -IT IS EXCRETED IN THE URINE (BRIGHT ORANGE OR DARK AMBER, FOAMY), DECREASED IN, THE STOOL (LIGHT, OR CLAY-COLORED). -PRURITUS, DYSPEPSIA, # BILIRUBIN AND ALKALINE PHOSPHATASE.

BLEEDING ESOPHAGEAL VARICES

-OCCURS IN ABOUT 1/3 OF PATIENTS WITH CIRRHOSIS AND VARICES -MORTALITY RATE FROM 1st EPISODE IS 40-50%

SPONTANEOUS BACTERIAL PERITONITIS (SBP)

-PATIENTS WITH CIRRHOSIS AND ASCITES MAY DEVELOP ACUTE SPONTANEOUS BACTERIAL PERITONITIS (SBP). -THOSE WHO ARE PARTICULARLY SUSCEPTIBLE ARE PATIENTS WITH VERY ADVANCED LIVER DISEASE. -THIS MAY BE THE RESULT OF LOW CONCENTRATIONS OF PROTEINS; PROTEINS NORMALLY PROVIDE SOME PROTECTION AGAINST BACTERIA. -THE BACTERIA RESPONSIBLE FOR SBP ARE TYPICALLY FROM THE BOWEL AND REACH THE ASCITIC FLUID AFTER MIGRATING THROUGH THE BOWEL WALL AND TRANSVERSING THE LYMPHATICS. -CLINICAL MANIFESTATIONS VARY BUT MAY INCLUDE FEVER, CHILLS, AND ABDOMINAL PAIN AND TENDERNESS.

Portal hypertension

-PORTAL HYPERTENSION, A PERSISTENT INCREASE IN PRESSURE WITHIN THE PORTAL VEIN GREATER THAN 5 MM HG, IS A MAJOR COMPLICATION OF CIRRHOSIS -IT RESULTS FROM INCREASED RESISTANCE TO OR OBSTRUCTION (BLOCKAGE) OF THE FLOW OF BLOOD THROUGH THE PORTAL VEIN AND ITS BRANCHES. -BLOOD FLOW BACKS INTO THE SPLEEN, CAUSING SPLENOMEGALY (SPLEEN ENLARGEMENT). -VEINS IN THE ESOPHAGUS, STOMACH, INTESTINES, ABDOMEN, AND RECTUM BECOME DILATED. -PORTAL HYPERTENSION CAN RESULT IN ASCITES (EXCESSIVE ABDOMINAL [PERITONEAL] FLUID), ESOPHAGEAL VARICES (DISTENDED VEINS), PROMINENT ABDOMINAL VEINS (CAPUT MEDUSAE), AND HEMORRHOIDS.

PT, AFP, autoimmune antibodies

-Prothrombin time (PT) - the liver produces proteins involved in the clotting (coagulation) of blood; the PT measures clotting function and, if abnormal, may indicate liver damage. -Alpha-feto protein (AFP) - associated with regeneration or proliferation of liver cell -Autoimmune antibodies (e.g., ANA, SMA, anti-LKM-1) - associated with autoimmune hepatitis

Paracentesis

-REMOVAL OF FLUID FROM THE PERITONEAL CAVITY -PRIMARILY FOR DIAGNOSTIC REASONS--TREATMENT OF MASSIVE ASCITES RESISTANT TO OTHER THERAPY, AND AS A PRELUDE TO OTHER PROCEDURES.

Nursing interventions (?? slide 110)

-REST -IMPROVED NUTRITIONAL STATUS -SKIN CARE -PREVENTION OF BLEEDING -IMPROVED MENTAL FXN -PATIENT EDUCATION AND HOME HEALTH CARE

Hepatic coma

-RESULTS, FROM THE ACCUMULATION OF AMMONIA AND OTHER TOXIC METABOLITES IN THE BLOOD

HEPATORENAL SYNDROME (HRS)

-THE DEVELOPMENT OF HEPATORENAL SYNDROME (HRS) INDICATES A POOR PROGNOSIS FOR THE PATIENT WITH LIVER FAILURE. -IT IS OFTEN THE CAUSE OF DEATH IN THESE PATIENTS. -HRS OFTEN OCCURS AFTER CLINICAL DETERIORATION FROM GI BLEEDING OR THE ONSET OF HEPATIC ENCEPHALOPATHY.

Implications of cirrhosis

-THE LOSS OF HEPATIC FUNCTION CONTRIBUTES TO THE DEVELOPMENT OF METABOLIC ABNORMALITIES. -HEPATIC CELL DAMAGE MAY LEAD TO THESE COMMON COMPLICATIONS: >PORTAL HYPERTENSION >ASCITES AND ESOPHAGEAL VARICES >COAGULATION DEFECTS >JAUNDICE >PORTAL-SYSTEMIC ENCEPHALOPATHY (PSE) WITH HEPATIC COMA >HEPATORENAL SYNDROME >SPONTANEOUS BACTERIAL PERITONITIS

HEPATIC COMA AGGRAVATING AND PRECIPITATING FACTORS

-increased AMMONIA LEVELS -decreased DIURESIS -DEHYDRATION -INFECTIONS

BILIARY OBSTRUCTION (continued...)

...-HEPATOCELLULAR JAUNDICE DEVELOPS BECAUSE THE LIVER CELLS CANNOT EFFECTIVELY EXCRETE BILIRUBIN. -THIS DECREASED EXCRETION RESULTS IN EXCESSIVE CIRCULATING BILIRUBIN LEVELS. -INTRAHEPATIC OBSTRUCTIVE JAUNDICE RESULTS FROM EDEMA, FIBROSIS, OR SCARRING OF THE HEPATIC BILE CHANNELS AND BILE DUCTS, WHICH INTERFERES WITH NORMAL BILE AND BILIRUBIN EXCRETION. -PATIENTS WITH JAUNDICE OFTEN REPORT PRURITUS (ITCHING).

SPONTANEOUS BACTERIAL PERITONITIS (SBP) (continued...)

...-HOWEVER, MANIFESTATIONS CAN ALSO BE MINIMAL WITH ONLY MILD SYMPTOMS IN THE ABSENCE OF FEVER. WORSENING ENCEPHALOPATHY AND INCREASED JAUNDICE MAY ALSO BE PRESENT WITHOUT ABDOMINAL SYMPTOMS -THE DIAGNOSIS OF SBP IS MADE WHEN A SAMPLE OF ASCITIC FLUID IS OBTAINED BY PARACENTESIS FOR CELL COUNTS AND CULTURE. -AN ASCITIC FLUID LEUKOCYTE COUNT OF MORE THAN 250 POLYMORPHONUCLEAR (PMN) LEUKOCYTES MAY INDICATE THE NEED FOR TREATMENT.

ASCITES AND GASTROESOPHAGEAL VARICES (continued...)

.... -AS A RESULT OF PORTAL HYPERTENSION, THE BLOOD BACKS UP FROM THE LIVER AND ENTERS THE ESOPHAGEAL AND GASTRIC VEINS. -ESOPHAGEAL VARICES OCCUR WHEN FRAGILE, THIN-WALLED ESOPHAGEAL VEINS BECOME DISTENDED AND TORTUOUS FROM INCREASED PRESSURE. VARICES OCCUR MOST OFTEN IN THE DISTAL ESOPHAGUS BUT CAN BE PRESENT ALSO IN THE STOMACH AND RECTUM -BLEEDING ESOPHAGEAL VARICES IS A LIFE-THREATENING MEDICAL EMERGENCY. -THE BLEEDING MAY BE EITHER HEMATEMESIS (VOMITING BLOOD) OR MELENA (BLACK, TARRY STOOLS). -LOSS OF CONSCIOUSNESS MAY OCCUR BEFORE ANY OBSERVED BLEEDING.

CIRRHOSIS - PATHOPHYSIOLOGY (continued...)

..... -THESE NODULES CAN BLOCK BILE DUCTS AND NORMAL BLOOD FLOW THROUGHOUT THE LIVER. -IMPAIRMENTS IN BLOOD AND LYMPH FLOW RESULT FROM COMPRESSION CAUSED BY EXCESSIVE FIBROUS TISSUE. -IN EARLY DISEASE, THE LIVER IS USUALLY ENLARGED, FIRM, AND HARD. -AS THE PATHOLOGIC PROCESS CONTINUES, THE LIVER SHRINKS IN SIZE, RESULTING IN DECREASED LIVER FUNCTION, WHICH CAN OCCUR IN WEEKS TO YEARS. -SOME PATIENTS WITH CIRRHOSIS HAVE NO SYMPTOMS UNTIL SERIOUS COMPLICATIONS OCCUR. -THE IMPAIRED LIVER FUNCTION RESULTS IN ELEVATED SERUM LIVER ENZYMES (PAGANA & PAGANA, 2014). CIRRHOSIS OF THE LIVER CAN BE DIVIDED INTO SEVERAL COMMON TYPES, DEPENDING ON THE CAUSE OF THE DISEASE

ASCITES AND GASTROESOPHAGEAL VARICES (continued 2...)

......-PATIENTS WITH PORTAL HYPERTENSION MAY ALSO HAVE PORTAL HYPERTENSIVE GASTROPATHY. -THIS COMPLICATION CAN OCCUR WITH OR WITHOUT ESOPHAGEAL VARICES. SLOW GASTRIC MUCOSAL BLEEDING OCCURS, WHICH MAY RESULT IN CHRONIC SLOW BLOOD LOSS, OCCULT-POSITIVE STOOLS, AND ANEMIA -SPLENOMEGALY (ENLARGED SPLEEN) RESULTS FROM THE BACKUP OF BLOOD INTO THE SPLEEN. -THE ENLARGED SPLEEN DESTROYS PLATELETS, CAUSING THROMBOCYTOPENIA (LOW SERUM PLATELET COUNT) AND INCREASED RISK FOR BLEEDING. -THROMBOCYTOPENIA IS OFTEN THE FIRST CLINICAL SIGN THAT A PATIENT HAS LIVER DYSFUNCTION...........

Bilirubin

0.1 to 1.2 milligrams per deciliter (mg/dL)

LD

122 to 222 U/L

Albumin.

3.5 to 5.0 grams per deciliter (g/dL)

When a complete assessment of this patient is performed, what other manifestations would the nurse expect? (Select all that apply.) A.Muscle twitching B.Dry skin with rash C.Personality changes D.Peripheral dependent edema E.Ecchymosis, spider angiomas

Answer: B, D, E Rationale: Personality changes and muscle twitching are findings that may be seen when the patient with cirrhosis develops portal-systemic encephalopathy. Additional manifestations that may be found on assessment include palmar erythema, clubbing of fingernails, and fixed flexion of fingers.

The patient tells the nurse that once he is discharged to home, he has no intention to stop drinking alcohol. What is the appropriate nursing response? A."Why do you continue to drink?" B."It's your choice to drink or not to drink." C."Does it frighten you to consider quitting?" D."If you continue to drink, you are going to die."

Answer: C Rationale: Asking the patient about quitting allows him to express his feelings about drinking. Response A demands an answer and is nontherapeutic. Response B does not give recognition to the problem of drinking. Response D gives advice as opposed to listening to the patient's concerns.

Which assessment finding requires immediate nursing intervention in a patient with severe ascites? A.Confusion B.Temperature 38.2º C C.Tachycardia, rate 110 beats/min D.Shallow respirations, rate 32 breaths/min

Answer: D Rationale: Ascites can increase abdominal distention, which interferes with lung expansion and compromises ventilation and oxygenation. Risk for infection, fluid displacement, and confusion are also assessment variables requiring monitoring in a patient with ascites.

The nurse is providing teaching for a client scheduled for a paracentesis. Which statement by the client indicates the teaching has been successful? A."I must not use the bathroom prior to the procedure." B."I will lie on my stomach while the procedure is performed." C."I will not be allowed to eat or drink anything the night before surgery." D."The physician will likely remove 2 to 3 liters of fluid from my abdomen."

Answer: D Rationale: The client should void before the procedure to prevent injury to the bladder. The client will lie in bed with the head of the bed elevated during the procedure.

BILIARY CIRRHOSIS

BILIARY CIRRHOSIS -ALSO CALLED CHOLESTATIC -CAUSED BY CHRONIC BILIARY OBSTRUCTION OR AUTOIMMUNE DISEASE. -PERICHOLANGITIC, PERILOBULAR SCARRING

ALT and ALP

Alanine aminotransferase (ALT) - an enzyme mainly found in the liver; the best test for detecting hepatitis. Alkaline phosphatase (ALP) - an enzyme related to the bile ducts but also produced by the bones, intestines, and during pregnancy by the placenta (afterbirth); often increased when bile ducts are blocked.

What is a primary reason for a higher incidence of liver cancer in the United States? A.Incidence of hepatitis C B.Incidence of HIV infection C.Incidence of illicit drug use D.Increased Asian population

Answer: A Rationale: In the United States and worldwide, the incidence of liver cancer is increasing because there is an increase in cases of hepatitis C (HCV). Liver cancer tumors are most often seen in regions of Asia and the Mediterranean area. Worldwide the disease kills about 1 million people each year and affects Vietnamese men more than any other group. Black and Hispanic populations have twice the rate of the disease as Euro-Americans, and older adults are affected more than other age-groups (Rossi et al., 2010).

Which intervention will the nurse include in the plan of care for a client with severe liver disease? A. Encourage the client to eat a low-protein, high-carbohydrate diet. B. Administer Kayexalate enemas. C. Instruct the client to eat a high-protein, low-carbohydrate diet. D. Teach the client to participate in frequent, vigorous physical activities

Answer: A Rationale: The client with severe liver disease should eat a diet high in carbohydrates and calories with moderate amounts of fat and protein. Kayexalate enemas and frequent, vigorous physical activities should be avoided.

A 55-year-old patient with a history of alcohol abuse spanning 10 years has been diagnosed with cirrhosis. The patient will be undergoing abdominal paracentesis on the medical unit today. Which assessment finding would alert the nurse that the paracentesis has been successful? A.Decrease in post-procedure weight B.No residual obtained during procedure C.Substantial decrease in blood pressure D.Immediate sensation of a need to urinate

Answer: A Rationale: Weight should decrease as fluid is drained from the abdominal cavity. A substantial decrease in blood pressure can indicate shock. Residual should be obtained during the procedure. The patient should not feel a sensation or need to urinate, because a primary safety measure is to have the patient void right before the procedure to avoid injury to the bladder during the procedure.

A client previously diagnosed with liver cirrhosis visits the medical clinic. What assessment findings does the nurse expect in this client? Select all that apply. A. Ecchymosis B. Soft abdomen C. Moist, clammy skin D. Jaundice E. Ankle edema F. Fever

Answer: A, D, E Rationale: Clients with advanced cirrhosis often have symptoms such as gastrointestinal (GI) bleeding, jaundice, ascites, and spontaneous bruising. They may also have dry skin, rashes, purpuric lesions (e.g., petechiae), warm and bright red palms of the hands, vascular lesions (spider angiomas), and peripheral dependent edema of the extremities and sacrum

What is the priority nursing intervention in the management of a patient with decompensated cirrhosis? A.Limiting protein intake B.Managing nausea and vomiting C.Monitoring fluid intake and output D.Elevating the head of bed >30 degrees

Answer: B Rationale: Decompensated cirrhosis has multiple complications. However, bleeding esophageal varices can present a life-threatening emergency. Preventing nausea and vomiting is an important intervention in the management of esophageal varices. Monitoring protein, fluid balance, and patient positioning are also important interventions in the care of the patient with end-stage liver disease.

The patient's assessment reveals yellowish coloration of skin and sclerae. Which laboratory values would the nurse anticipate? A.Increased urine bilirubin, decreased direct bilirubin B.Increased direct bilirubin, increased indirect bilirubin C.Decreased direct bilirubin, increased indirect bilirubin D.Increased direct bilirubin, decreased indirect bilirubin

Answer: B Rationale: When a patient's skin is jaundiced, laboratory values of indirect and direct bilirubin are increased. Urine bilirubin is also increased. Urobilinogen in stool is normal to decreased, but in urine it is normal to increased.

liver dysfunction causes

CAUSED BY: INFECTIOUS AGENTS ANOXIA METABOLIC DISORDERS TOXINS DRUGS NUTRITIONAL DEFICIENCIES STATES OF HYPERSENSITIVITY

liver cellular components

CELLULAR COMPONENTS: ¨HEPATOCYTES- filter the blood ¨KUPFFER CELLS- clean blood from debris and bacteria (like macrophages)

Complications of cirrhosis

COMMON PROBLEMS AND COMPLICATIONS ASSOCIATED WITH HEPATIC CIRRHOSIS DEPEND ON THE AMOUNT OF DAMAGE SUSTAINED BY THE LIVER. IN COMPENSATED CIRRHOSIS, THE LIVER IS SCARRED BUT CAN STILL PERFORM ESSENTIAL FUNCTIONS WITHOUT CAUSING MAJOR SYMPTOMS. IN DECOMPENSATED CIRRHOSIS, LIVER FUNCTION IS IMPAIRED WITH OBVIOUS MANIFESTATIONS OF LIVER FAILURE.

ASCITES

DECREASED INTRAVASCULAR VOLUME -> RENIN RELEASED BY THE KIDNEYS -> increased ALDOSTERONE -> RETENTION OF NA+ & H2O -> ATTEMPT TO increase VASCULAR VOLUME -> LEADS TO FURTHER ASCITES

glycogenesis

GLUCOSE IS CONVERTED INTO GLYCOGEN THROUGH THE PROCESS OF ____

Common bile duct

HEPATIC DUCT FROM THE LIVER AND CYSTIC DUCT FROM THE GALLBLADDER FORM THE _____

Liver

LARGEST GLAND IN THE BODY AND CAN BE CONSIDERED A CHEMICAL FACTORY THAT MANUFACTURES, STORES, ALTERS, AND EXCRETES A LARGE NUMBER OF SUBSTANCES INVOLVED IN METABOLISM. -RUQ behind the ribs -4 lobes -2 blood sources (75% portal vein, 25% hepatic artery) -venous drainage from liver through hepatic vein

liver dysfunction pathophysiology

LIVER DYSFUNCTION RESULTS FROM DAMAGE TO THE LIVER PARENCHYMAL CELLS DIRECTLY OR INDIRECTLY RESULTS IN REPLACEMENT OF GLYCOGEN BY LIPIDS PRODUCING FATTY INFILTRATION WITH OR WITHOUT NECROSIS (SHRUNKEN, FIBROTIC LIVER)

Bilirubin excretion

PIGMENT DERIVED FROM THE BREAKDOWN OF HEMOGLOBIN, CARRIED IN BILE TO DUODENUM, CONVERTED INTO UROBILINOGEN AND EXCRETED IW THE URINE AND FECES.... erythrocyte get destroyed every 120 days or 3 months. where urine and feces get its color

POSTNECROTIC CIRRHOSIS

POSTNECROTIC CIRRHOSIS -CAUSED BY VIRAL HEPATITIS (SPECIALLY HEPATITIS C), AND CERTAIN DRUGS OR OTHER TOXINS -BROAD BANDS OF SCAR TISSUE

Canaliculi

SMALLEST BILE DUCTS ARE CALLED ____ AND ARE LOCATED BETWEEN THE LOBULES OF THE LIVER

Stage I hepatic encephalopathy

STAGE I -SUBTLE MANIFESTATIONS THAT MAY NOT BE RECOGNIZED IMMEDIATELY -PERSONALITY CHANGES -BEHAVIOR CHANGES (AGITATION, BELLIGERENCE) -EMOTIONAL LABILITY (EUPHORIA, DEPRESSION) -IMPAIRED THINKING -INABILITY TO CONCENTRATE -FATIGUE, DROWSINESS -SLURRED OR SLOWED SPEECH -SLEEP PATTERN DISTURBANCES

Stage II hepatic encephalopathy

STAGE II -CONTINUING MENTAL CHANGES -MENTAL CONFUSION -DISORIENTATION TO TIME, PLACE, OR PERSON -ASTERIXIS (HAND FLAPPING)

Stage III hepatic encephalopathy

STAGE III -PROGRESSIVE DETERIORATION -MARKED MENTAL CONFUSION -STUPOROUS, DROWSY BUT AROUSABLE -ABNORMAL ELECTROENCEPHALOGRAM TRACING -MUSCLE TWITCHING -HYPERREFLEXIA -ASTERIXIS (HAND FLAPPING)

Stage IV hepatic encephalopathy

STAGE IV -UNRESPONSIVENESS, LEADING TO DEATH IN MOST PATIENTS PROGRESSING TO THIS STAGE -UNAROUSABLE, OBTUNDED -USUALLY NO RESPONSE TO PAINFUL STIMULUS -NO ASTERIXIS -BABINSKI'S SIGN -MUSCLE RIGIDITY -FETOR HEPATICUS (CHARACTERISTIC LIVER BREATH—MUSTY, SWEET ODOR) SEIZURES

BLEEDING ESOPHAGEAL VARICES?? SURGICAL BYPASS PROCEDURES

SURGICAL BYPASS PROCEDURES -PORTACAVAL ANASTOMOSIS -SPLENORENAL SHUNT -MESOCAVAL SHUNT -DEVASCULARIZATION AND TRANSECTION

Esophageal varices treatment

Sengstaken-Blakemore tube in place for the emergency treatment of hemorrhage from esophageal varices. The tube has three openings for (1) gastric aspiration, (2) inflating the esophageal balloon, and (3) inflating the gastric balloon. The esophageal balloon is inflated to a pressure of 20 to 40 mm Hg (monitored by attachment to a gauge or a sphygmomanometer) that compresses the esophageal veins. The gastric balloon, inflated with 250 cc of air, applies pressure to the fundal veins when slight traction is applied.

gluconeogenesis

___ RESULTS IN THE FORMATION OF GLUCOSE FROM SUSTANCES THAT ARE NOT CARBOHYDRATES (I.E; PROTEINS)

glycogenolysis

____ IS THE BIOCHEMICAL BREAKDOWN OF GLYCOGEN TO GLUCOSE

hepatic cirrhosis common causes

• ALCOHOLIC LIVER DISEASE • VIRAL HEPATITIS • AUTOIMMUNE HEPATITIS • STEATOHEPATITIS (FROM FATTY LIVER) • DRUGS AND CHEMICAL TOXINS • GALLBLADDER DISEASE • METABOLIC/GENETIC CAUSES • CARDIOVASCULAR DISEASE

management (liver dysfunction? slide 58)

ASSESS FREQUENTLY: -I & 0, BODY WEIGHT DAILY -VS q4h -ASSESS LUNGS -SERUM AMMONIA DAILY -PROTEIN INTAKE $. -NEOMYCIN -MONITOR ELECTROLYTES -USUALLY NO SEDATIVES, ETC. -LACTULOSE

LAENNEC'S PORTAL CIRRHOSIS.

LAENNEC'S PORTAL CIRRHOSIS. -CAUSED BY CHRONIC ALCOHOLISM OR NUTRITIONAL DEFICIENCIES) -SCAR TISSUE CHARACTERISTICALLY SURROUNDS THE PORTAL AREAS

BLEEDING ESOPHAGEAL VARICES MANAGEMENT

NONSURGICAL MANAGEMENT -PHARMACOLOGIC THERAPY: -VASOPRESSIN (PITRESSIN): CAUSES CONSTRICTION OF THE SPLANCHNIC ARTERIAL BED. MAY BE USED WITH NITROGLYCERIN. -SOMATOSTATIN: RESULTS IN $ BLEEDING WITHOUT VASOCONSTRICTIVE EFFECTS -INDERAL: REDUCES CARDIAC OUTPUT, USUALLY USED IN CONJUNCTION WITH SCLEROTHERAPY OR BALLOON TAMPONADE: SENGSTAKEN-BLAKEMORE TUBE, INJECTION SCLEROTHERAPY

HEPATORENAL SYNDROME (HRS) Manifestations

THIS SYNDROME IS MANIFESTED BY: -A SUDDEN DECREASE IN URINARY FLOW (<500 ML/24 HR) (OLIGURIA) -ELEVATED BLOOD UREA NITROGEN (BUN) AND CREATININE LEVELS WITH ABNORMALLY DECREASED URINE SODIUM EXCRETION ¨INCREASED URINE OSMOLARITY

PORTAL HYPERTENSION AND ASCITES

TWO MAJOR SEQUELAE OF PORTAL HYPERTENSION: FORMATION OF ESOPHAGEAL, GASTRIC, AND HEMORRHOIDAL VARICES.

Esophageal varices

esophageal varices is caused by cirrhosis

Metabolic functions of liver

glycogenesis, glycogenolysis, gluconeogenesis -SYNTHESIZES ALMOST ALL OF THE PLASMA PROTEINS, BLOOD CLOTTING FACTORS, SPECIFIC TRANSPORT PROTEINS, AND MOST OF PLASMA LIPOPROTEINS -ACTIVE IN FAT METABOLISM -STORAGE OF VITAMINS A, B12, D, K, AND SEVERAL OTHER B COMPLEX VITAMINS -DRUG METABOLISM (CONJUGATION)