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Liver Disorders

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Term
Definition
Liver   Largest vital organ. 3rd most important organ. Performs>400 essential functions 1. Digests 2. Nutrition 3. Metabolism 4. Clotting  
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Cirrhosis   Extensive scarring of the liver usually d/t chronic inflammation/ necrosis. **Cirrhosis= decreased albumin  
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Pathophysiology of Cirrhosis   destruction of hepatcytes->Cirrhosis-> Hepatomegaly (early)-> Atrophy (late)  
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Types of Cirrhosis   1. Laennec's (alcoholism) 2. Postnecrotic (hepatitis/drugs/ chemicals) (Hep C #1 cause in US) 3. Biliary (chronic obstruction from gallbladder dz or autoimmune)  
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Cirrhosis complications   Portal hypertension- may back flow into spleen . May cause ascites & varices.  
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Cirrhosis complications: Ascites related to Portal HTN   1. Increased pressure causes fluid to collect in pertioneal cavity. --> 2. Decreased osmotic pressure d/t albumin leaking out of peritoneal area & decreased albumin production from impaired liver cells.---> 3. Massive ascites caues renal vasoconstrictio  
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Cirrhosis Complications   Esophageal/ gastric varices- bleeding or rupture = medical emergency  
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Cirrhosis complications   1. Coagulation defects- dec. bile=inability to absorb K (needed for factors II, VII, IX,X) 2. Spenomegaly- destruction of platelets (thrombocytopenia) 3. Increased risk of bleeding!!!  
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Cirrhosis complications- Jaundice   r/t hepatocellular dz or intra-hepatic obstruction. Results in yellowing and itching.  
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Cirrhosis complications: Hepatorenal syndrome   Poor prognosis. Death common. Oliguria, increased BUN & creatinine, increased urine osmolarity.  
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Cirrhosis complications: helaptic encephalopathy   aka Portal-systemic encephalopathy. Toxins not broken down->metabolic abnormalities (ie Inc. GABA & ammonia) **ammonia & the brain don't get along.  
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Potential for hepatic encephalopathy   R/t toxins not cleared by the liver=Ammonia. Protein breakdown releases ammonia->liver unable to convert ammonia to less toxic form-> ammonia carried to brain via circulatory system. Goal: reduce ammonia levels.  
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Hepatic encephalopathy Nutrition   Cirrhosis: high carb & protein, mod. fat. H.E.: moderate protein & fat, w/ simple carbs.  
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Drug therapy for hepatic encephalopathy   1. Limit opioid-difficult to metabolize. 2. Lactulose to help excrete ammonia. Monitor hypokalemia & dehydration.  
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Assessment for Hepatic Encephalopathy   Asterixis (muscle flapping) Fetor hepaticus (liver breath) *both are signs of worsening encephalopathy.  
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High Risk of hepatic encephalopathy   high protein diet infections hypovolemia hypokalemia constipation GI bleed drugs  
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Cirrhosis Clinical Manifestations- Early stage   Fatigue significant change in weight. GI symptoms Abd. pain & liver tenderness pruritis **often asymptomatic; &incidenal finding with routine labs (abnormal LFTs &/or thrombocytopenia)  
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Cirrhosis- CM- Late stages   1. Jaundice & icterus (sclera) 2. Dry skin 3. Rashes 4. Petechiae, or ecchymosis (lesions) 5. Warm, bright red palms 6. Spider angiomas 7. Peripheral dependent edema of extremities & sacrum. 8. Ascites  
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Cirrhosis Abdominal Assessment   daily weights is the best indicator for fluid retention  
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Lab values for Cirrhosis   Increased: AST, ALT, LDH, Alk Phos, Bilirubin, PT/INR Decreased: Protein, Albumin, platelet  
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More Cirrhosis lab values   Dilutional Hyponatremia (d/t RAAS) H&H might be low. WBC might be low. Ammonia might be high. Creatinine might be high.  
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Cirrhosis Problem List   Risk for Bleeding Risk for Imbalanced Nutrition Impaired breathing pattern Potential for drug toxicity Potential for hepatorenal syndrom Potential for hyponatremia Potential for hypokalemia Fluid volume excess  
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Nutrition & Drug management for cirrhosis   Nutrition: LOW SODIUM, vitamin supplements (thiamin, folate, MVI) Drug: Diuretics (monitor for dec. K & Na); non-selective beta blockers; antibiotics.  
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Cirrhosis Non-Surgical Management   Paracentesis Comfort measures Fluid electrolytes  
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Prevent/Manage Hemorrhage w/ Cirrhosis   Pre-Bleed: Slow the HR w/ Beta Blockers. Bleed: Find the source! Sclerotherapy, banding, TIPS, esophogastric balloon tampanode, IV octreotide or Vasopressin, Rapid blood transfusion.  
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Action Alert for Cirrhosis   Avoid alcohol and drugs:prevents further scarring, allows liver to heal, prevents gastric/esophogeal irritation, reduces incidence of bleeding, prevents other life-threatening complications.  
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Hepatitis   1. Widespread viral inflammation of liver cells. 2. Post-exposure: Liver enlarged &congested w/ inflammatory cells= RUQ pain. 3. After dz progresses: lobular patterns become distorted r/t widespresd inflammation, necrosis, & regeneration.  
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Hep A   1. Similar to viral syndrome. Often unrecognized. 2. Spread via fecal-oral route. 3. Destroyed by bleach & temp 195 F 4. Vaccine available. 5. Get IV G shot after exposure.  
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Hep B   1. Spread by unprotected sex, needles. 2. Sx occur 25-180 days post exposure. 3. Most adults recover & dev. immunity. 4. Carrierscan have chronic hepatitis & risk for cirrhosis/liver cancer. 5. Vaccine available.  
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Hepatitis C   1. Spread by sharing needles/blood exposure. 2. Incubation 21-140 days. 3. Asymptomatic for years. 4. NO VACCINE 5. Damage is done over decades. 6. Leading cause for transplant (new liver gets infected)  
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Hep D   1. Spread by parenteral routs but can thru sexual activity. 2. Incubation 14-56 days 3. * Must have Hep B to get Hep D.  
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Hep E   1. In areas where waterborne epidemic & travelers who visit there. (Not in US). 2.Fecal-Oral route 3. Resembles Hep A 4. Incubation 15-64 days.  
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Hepatitis Clinical Manifestations   Abdominal pain/RUQ W/ light palp. Jaundiced sclera Arthralgia/ Myalgia Fever Lethargy/Malaise N/V Pruritis  
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Hep Lab assessment   Increased: AST, ALT, Alk Phos, Bilirubin. Urine bilirubin present. Hep A= Anti-HAV Hep B= hep B antigen-antibody & detectable viral count  
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Hep lab assessment continued   1. Hep B: if >6 mo w/ HBsAG=carrier or chronic hepatitis. 2. Hep C: ELISA is initial screening 3. Hep D: anti-HDV 4. Hep E: anti-HEV  
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Hepatitis Interventions   1. GOAL: Rest liver, promote cellular regeneration & prevent complications. 2. Diet: high carb & cal w/ mod. fat & protein.  
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Hep B drugs   Tenofivir (1stline), Interferon, Adefovidipivoxil, Lamivudine. *Report any muscle weakness. These drugs cause myopathy.  
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Hep C drugs   Combo therapy Interferon + ribavirin (women of childbearing age must agree to contraception)  
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Fatty Liver=Steatohepatitis   Accumulation of fats in and around hepatic cells.  
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Hepatic abscess   Uncommon. High mortality rate.  
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Liver trauma   Commonly injured d/t size. Lacerations, avulsions(tears), crushes. Often caused by steering wheel. May cause hemorrhagic shock.  
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Liver trauma CM   RUQ pain Guarding Increase abd. pain exaggerated by deep breathing & referred to R shoulder.  
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Liver Cancer   One of the most common tumors in the world. (Increased rates w/Hep C) #1 sx RUQ discomfort  
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Liver Cancer treatment   Surgery: lobe resection-5 yr survival rate. NO RADIATION Hepatic artery embolization Ablation- heats CA cells to kill them. Chemo- not as affective Liver transplant End-of-life care/ hospice  
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Liver transplant   1.Only in end-stage liver dz, primary malignant neoplasm. 2. If you abuse your liver-you're not a candidate. 3.Donated liver is moved to surgery center in cooled saline solution that preserves it for up to 8 hours.  
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Liver Transplant complications   Monitor for : tachycardia; fever; flank pain; RUQ pain; decreased bile pigment & volume; increased: jaundice, AST, ALT, Alk phos, PT INR  
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