Hepatic Disorders PDF

**Chapter 43: Hepatic Disorders\ **Anatomy and physiology, pg. 3673 (will not be tested on this) - Liver is located in the right upper abdomen (RUQ) w/ 4 lobes. Blood circulation:Portal vein and hepatic artery; Hepatic vein. Hepatic duct **Metabolic functions/functions of the liver, pg....

**Chapter 43: Hepatic Disorders\ **Anatomy and physiology, pg. 3673 (will not be tested on this) - Liver is located in the right upper abdomen (RUQ) w/ 4 lobes. Blood circulation:Portal vein and hepatic artery; Hepatic vein. Hepatic duct **Metabolic functions/functions of the liver, pg. 3676** - **The liver plays a major role in the metabolism of glucose and the regulation of blood glucose concentration.** - Glucose metabolism: Glycogen and glycogenolysis (breakdown of glucose) - Ammonia conversion: liver converts the metabolically generated ammonia into urea and kidneys excretes it in the urine - **As the level increases, it can cause neuro problems & lead to coma** - Protein metabolism: albumin, clotting factors - People w/ liver issues will often times have bleeding issues - Fat metabolism: liver is active in fat metabolism; fatty acids can be broken down for the production of energy and ketone bodies - **Vitamin and iron storage: large amounts of A,B,D**, several B-complex vitamins; iron and copper are also stored in the liver - Bile formation: enterohepatic circulation - Bilirubin excretion: breakdown of RBC - If pt has lots of bilirubin, they'll present w/ jaundice \[skin, eyes, urine may be yellow/dark brown\] - Drug metabolism: Bioavailability and first-pass effect (PO Meds only) - **Bioavailability** is the fraction of the given medication that actually reaches the systemic circulation - The liver metabolizes many medications (barbs, opioids, sedatives, anesthetics, and amphetamines) **Assessment, pg. 3680** - Health Hx: Exposure to hepatotoxic substances or infectious agents, lifestyle behaviors - Occupation, exposures, sexual practices, alcohol use, medications (tylenol, ketoconazole, and valproic acid), hx of ETOH and IV drug use - Questions to ask: how much ETOH do they drink? Have you ever injected IV drugs/what drugs do you use? Are you promiscuous? - **Cirrhosis risk factors**: Men: ETOH intake of 60-80 g/day Women: ETOH intake of 40-60 g/day **Liver function tests: Table 43-1, pg. 3689** - **Ammonia** - **KNOW If high levels, give lactulose \[helps excrete excess ammonia\]** - Normal: 15-45 mcg/dL - **Need sitter if LOC is altered** - Direct/total bilirubin: Measures the ability of the liver to conjugate and excrete bilirubin - Total serum protein, Serum albumin; LDH - PT/INR increased in liver disease \[this means the blood is thin\] - PTT and INR may be prolonged in liver disease (book) - AST/ALT 2:1 ratio in damage - **AST**: 8--48 units per liter (U/L). AST signifies death of tissue - **ALT**: 7--55 U/L. ALT is released when there is liver damage - Elevation usually indicates liver disease - GGT, GGTP: Values are elevated in ETOH abuse and markers for biliary cholestasis - Cholesterol: Elevated in biliary obstruction - Liver biopsy (through needle aspiration), US, CT, MRI **Physical Assessment, pg. 3683** - Jaundice, malaise & weakness, pallor, muscle atrophy, petechiae, ecchymotic areas, palmar edema, slurred speech, neuro changes (assess their recall, memory, and abstract thinking ability), pruritus, abdominal pain and enlarged liver, N/V, ascites \[weigh them daily\], SOB \[need to sit up\], edema, spider angioma, asterixis (involuntary hand flapping) **Manifestations of hepatic dysfunction, pg. 3691:** **Jaundice \[don't have to differentiate b/t 3\]** - Clinically evident: bilirubin \> 2.5 mg/dL - Increased destruction of RBCs - Hemolytic - Increased destruction of RBCs (low H/H from this) - Bilirubin predominantly unconjugated - Typically symptom free unless prolonged - Hepatocellular - Damaged liver cells, bilirubin not cleared from blood - Various causes: anorexia, infections, chronic pancreatitis, medications - Obstructive - Extrahepatic (occlusion of bile duct from gallstones, tumors) or intrahepatic (thick bile from TCAs, Seizure meds, estrogens, abx) - Bile cant flow into the intestines, gets reabsorbed by liver into blood - Deep orange, foamy urine and clay colored stools - Hereditary hyperbilirubinemia - Gilbert Syndrome: familial disorder characterized by an increased level of conjugated bilirubin that causes jaundice - Dubin Johnson syndrome (will NOT be asked about this): chronic idiopathic jaundice **Portal HTN** - **The increased pressure throughout the portal venous system that results from obstruction of blood flow into and through the damaged liver** - Two major complications: Ascites and varices **Ascites, pg. 3694** - **KNOW S/S: Increased abdominal girth, rapid wt gain, SOB, distended neck veins, and fluid & electrolyte imbalances,** umbilical hernia - The failure of the liver to metabolize aldosterone increases Na and water retention by the kidney - Figure 43-5 (**do not need to memorize** this cycle, but NOTHING stops this cycle except a liver transplant) - **Medical Management** - Nutritional: negative Na balance to reduce fluid retention. low-Na (2-g Na diet) - Avoid: table salt, salty foods, salted butter, margarin and all canned/frozen food - **Pharmacologic: diuretics (spironolactone is the first line therapy).** May also use oral furosemide - Bed rest, paracentesis, Transjugular Intrahepatic Portosystemic Shunt (TIPS) \[DON'T MEMORIZE\] - **Surgical management**: Paracentesis - Pt should be sitting in upright position (high fowlers) - **KNOW Post-op procedures for paracentesis** - **KNOW If patient had a large volume paracentesis, they may need to receive albumin which reduces risk of circulatory and renal dysfunction; want to prevent fluid shift** - **Monitor vital signs during and pre/post procedure bc** large fluid shift can cause patient to go into shock - **Nursing management**: assess, educate, document I&O, abdominal girth, daily weight, monitor resp status, **labs** (**serum ammonia, AST/ALT, bilirubin, H/H**, creatinine and electrolyte levels to assess electrolyte balance) - **Chart 43-3 home care checklist**: - **Stop all alcohol intake \[including some meds\]** - Weigh daily, Refer them to AA - Need to identify s/s of early complications: hepatic encephalopathy - state time & date of follow-up, identify support system, educate on meds, diet needs to be low sodium & moderate protein, keep all medical appointments **Esophageal Varices, pg. 3702** - Enlarged veins in lower esophagus \[sometimes higher or in stomach\] d/t blood flow blocked in liver - S/sx: hematemesis, melena, general deterioration in mental or physical status, often has hx of ETOH abuse - shock s/s: cool clammy skin, hypotension, tachycardia - Endoscopy used to identify the bleeding site - Portal hypertension measurements, Lab tests (serum bilirubin, alkaline phosphatase, serum proteins) - Medical Management - IV volume expanders/blood transfusions. Nonsurgical management is preferred - **Meds** - **KNOW Octreotide (Sandostatin): vasoactive drug that's effective in decreasing bleeding from esophageal varices, and lacks the vasoconstrictive effects of vasopressin.** - **KNOW Considered the preferred treatment regimen for immediate control of variceal bleed** - **Nursing management: monitor for mild hypoglycemia and abdominal cramping** - Preventative meds: beta-blockers: propranolol or nadolol may also use nitrates - Balloon tamponade, Endoscopic Sclerotherapy, Endoscopic Variceal Ligation/Banding, TIPS - Surgical Management - Surgical Bypass procedures: Splenorenal and mesocaval shunts - Devascularization and Transection - Nursing Management for Esophageal Varices - Monitor VS Q4H, Monitor gastrointestinal secretions and output, Assess for GI bleeding - Don\'t let them do anything that causes friction in esophagus - Coughing, sucking on straw, smoking, alcohol, probably NPO (anything to disturb mucosa) - Assess nutritional and neurological status; Mouth Care, Alcohol withdrawals, Administer blood and vit K **Hepatic Encephalopathy & Coma, pg. 3718 PRIORITY PATIENT** - **Ammonia builds up as a result from profound liver failure/damage** - Ammonia enters brains & excites astrocyte cells which stimulate GABA. GABA causes **depression of CNS producing sleep** & behavioral patterns associated w/ hepatic encephalopathy \[book\] - Other reasons ammonia buildup: GI bleeding \[bleeding esophageal varices, chronic GI bleeding\], high protein diet, bacterial infection, or uremia, ingestion of ammonium salts, - **S/sx: Altered mental status, motor disturbances, mood swings,** asterixis, constructional apraxia, fector hepaticus (chronic bad breath due to liver failure) - **Early signs**: mental change and motor changes. Pt appears confused & unkempt & has alterations in mood & sleep patterns \[book\] - Assessment/Diagnostic - **Labs: draw serum ammonia for hepatic encephalopathy** - Psychometric tests - EEG: shows general slowing with amplitude of brain waves (need to monitor for seizures) - Medical Management - **Meds**: - **Lactulose (traps ammonia in the stool; given to reduce serum ammonia levels)** - Should have @ least 2-3 stools/day - The pt receiving lactulose is monitored closely for the development of watery diarrhea stools b/c it could indicate a medication overdose (book) - Antibiotics (prevents infection) - Avoid sedatives, tranquilizers, analgesics bc liver metabolizes these & if not metabolized, this will cause further sedation - Flumazenil (Romazicon) may be useful to wake them up - Rifaximin: antibiotic that lowers levels of ammonia - IV glucose to minimize protein breakdown, vitamins \[C, A, K, thiamine\], electrolytes - May need NG tube for med admin - Daily I&O and weight, VS Q4H - **KNOW Diet: Keep daily protein intake b/t 1.2 - 1.5 g/kg body weight per day (adequate protein)** - **Avoid protein restriction if possible (book)** - **Provide small, frequent meals and 3 small snacks per day in addition\ to a late-night snack before bed (book)** - Nursing Management - Prevent bleeding and infection - **Monitor respiratory status: Deep breathe and cough & position changes** - Monitor for complications - Constipation can precipitate encephalopathy. Monitor for neuro changes - Education - Diet: do not restrict protein in hepatic encephalopathy, low sodium (\