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 |