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Liver Disorders

TermDefinition
Liver Largest vital organ. 3rd most important organ. Performs>400 essential functions 1. Digests 2. Nutrition 3. Metabolism 4. Clotting
Cirrhosis Extensive scarring of the liver usually d/t chronic inflammation/ necrosis. **Cirrhosis= decreased albumin
Pathophysiology of Cirrhosis destruction of hepatcytes->Cirrhosis-> Hepatomegaly (early)-> Atrophy (late)
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)
Cirrhosis complications Portal hypertension- may back flow into spleen . May cause ascites & varices.
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
Cirrhosis Complications Esophageal/ gastric varices- bleeding or rupture = medical emergency
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!!!
Cirrhosis complications- Jaundice r/t hepatocellular dz or intra-hepatic obstruction. Results in yellowing and itching.
Cirrhosis complications: Hepatorenal syndrome Poor prognosis. Death common. Oliguria, increased BUN & creatinine, increased urine osmolarity.
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.
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.
Hepatic encephalopathy Nutrition Cirrhosis: high carb & protein, mod. fat. H.E.: moderate protein & fat, w/ simple carbs.
Drug therapy for hepatic encephalopathy 1. Limit opioid-difficult to metabolize. 2. Lactulose to help excrete ammonia. Monitor hypokalemia & dehydration.
Assessment for Hepatic Encephalopathy Asterixis (muscle flapping) Fetor hepaticus (liver breath) *both are signs of worsening encephalopathy.
High Risk of hepatic encephalopathy high protein diet infections hypovolemia hypokalemia constipation GI bleed drugs
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)
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
Cirrhosis Abdominal Assessment daily weights is the best indicator for fluid retention
Lab values for Cirrhosis Increased: AST, ALT, LDH, Alk Phos, Bilirubin, PT/INR Decreased: Protein, Albumin, platelet
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.
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
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.
Cirrhosis Non-Surgical Management Paracentesis Comfort measures Fluid electrolytes
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.
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.
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.
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.
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.
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)
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.
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.
Hepatitis Clinical Manifestations Abdominal pain/RUQ W/ light palp. Jaundiced sclera Arthralgia/ Myalgia Fever Lethargy/Malaise N/V Pruritis
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
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
Hepatitis Interventions 1. GOAL: Rest liver, promote cellular regeneration & prevent complications. 2. Diet: high carb & cal w/ mod. fat & protein.
Hep B drugs Tenofivir (1stline), Interferon, Adefovidipivoxil, Lamivudine. *Report any muscle weakness. These drugs cause myopathy.
Hep C drugs Combo therapy Interferon + ribavirin (women of childbearing age must agree to contraception)
Fatty Liver=Steatohepatitis Accumulation of fats in and around hepatic cells.
Hepatic abscess Uncommon. High mortality rate.
Liver trauma Commonly injured d/t size. Lacerations, avulsions(tears), crushes. Often caused by steering wheel. May cause hemorrhagic shock.
Liver trauma CM RUQ pain Guarding Increase abd. pain exaggerated by deep breathing & referred to R shoulder.
Liver Cancer One of the most common tumors in the world. (Increased rates w/Hep C) #1 sx RUQ discomfort
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
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.
Liver Transplant complications Monitor for : tachycardia; fever; flank pain; RUQ pain; decreased bile pigment & volume; increased: jaundice, AST, ALT, Alk phos, PT INR
Created by: egb76au