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Liver Disorders
| Term | Definition |
|---|---|
| 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
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