Your SlideShare is downloading. ×
0
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Cirrhosis
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Cirrhosis

1,620

Published on

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
1,620
On Slideshare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
102
Comments
0
Likes
0
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  1. GI: Cirrhosis Marnie Quick, RN, MSN, CNRN
  2. Normal Liver
  3. Label:
  4. Answers from previous slide  A. Liver  B. Hepatic vein- blood from liver  C. Hepatic artery- oxygenated blood to liver  D. Portal vein- partly O2 blood to liver  E. Common bile duct  F. Stomach  G. Cystic duct  H. Gallbladder
  5. Liver
  6.  Symptoms of liver failure appear when 80% liver destroyed  Liver can regenerate itself if adequate nutrition and no alcohol
  7. Liver functions  1. Metabolic functions  CHO- liver removes glucose from blood, stores it as glycogen, breaks it down to release glucose PRN  Protein- converts ammonia to urea**  Protein (food/blood) is 1st broken down by bacteria in GI to form ammonia. Ammonia to liver which converts to urea.  Fat- ketogenesis. (see next slide- bile)  Steriod- aldosterone metabolism (liver damage= inc levels aldosterone causing Na & H2O retention)
  8. 2. Bile synthesis & secretion- Bile aids digestion/absorption fats in small intestine. Indirect bilirubin broken down & excreted stool 3. Storage- Vitamin A, all B’s, D, E, and K 4. Regulates blood coagulation**-Forms prothrombin, fibrinogen, heparin If decrease Vit K & fibrinogen= increase fibrinolysis, & decrease platelets> hemorrhage 5. Detoxification** -Rids body of endogenous waste- drugs, bacteria, etc 6. Heat production 7. Phagocyte action- breakdown old RBC, WBC, bacteria
  9. Cirrhosis of the liver: Etiology/pathophysiology  End stage of chronic liver disease  Functional liver tissue destroyed and replaced by fibrous scar tissue  Metabolic functions are lost; blood and bile flow in liver is disrupted, portal hypertension develops  Types: Alcoholic/nutritional (common); biliary (chronic biliary obstruction); postnecrotic (hepatitis B or C; toxic substances); cardiac
  10. Stages of alcohol-induced liver damage
  11. Cirrhosis
  12. Alcoholic/nutritional cirrhosis  Most common cause of cirrhosis with resultant lack of nutrition  Stage 1: metabolic changes affect fatty metabolism, fat accumulates in liver. In this stage abstinence from alcohol could allow liver to heal  Stage 2: With continued use of alcohol, inflammatory cells infiltrate the liver causing necrosis, fibrosis and destruction of liver  Stage 3: regenerative nodules form- liver shrinks
  13. Cirrhosis of liver: Complication & treatment Portal hypertension  Fibrous connective tissue in liver disrupt blood and bile flow. Portal and hepatic veins become compressed.  With backup of blood have acites, splenomegaly, peripheral edema, increase blood cell destruction- anemia, low WBC and low platelets  Treatment: medication to control hypertension, diuretics to decrease fluid retention/acites and TIPS procedure to increase blood flow
  14. TIPS procedure- Note shunt that will divert blood- relieving hypertension & esophegeal varcies
  15. Cirrhosis: complication & treatment Esophageal varices  As a result of portal hypertension, veins in esophagus, rectum and abdomen become engorged/congested resulting in esophageal and gastric varices (major concern- can bleed out)  60% esophageal varices occur with cirrhosis  Treat-  Medications: vasopressin (control bleeding), beta blockers (prevent bleeding), blood replace, Vit K  Surgery: shunt (TIPS), ligation varices, banding  Sengstaken-Blakemeore tube (tamponade bleeding)
  16. Esophageal varices
  17. Sengstaken Blackmore tube: Inflate gastric balloon; Esophageal balloon; and third one to aspirate stomach
  18. Cirrhosis: Complications and treatment Splenomegaly, acites and peripheral edema  Spleen enlarges from blood shunted from portal hypertension. Blood cells destroyed  As liver impairment of synthesis of albumin occurs have accumulation plasma-rich fluid in abd cavity- ascites (abd distention & wt gain)  Treat ascites- diuretics (aldactone), paracentesis, diet (hi CHO, low fat, low Na
  19. Ascites with dilated veins
  20. Ascites
  21. Cirrhosis: Complications & treatment Hepatic encephalopathy  Protein (from food or blood in GI) is broken down (with the aid of bacteria) in GI to ammonia  Liver then converts ammonia to urea and is excreted by kidneys  With liver failure have accumulation of ammonia in blood. Ammonia then enters brain and interferes with function of brain- encephalopathy
  22. Hepatic encephalopathy-- continued  Stages: 1. personality changes, irritability 2. hyperreflexia (liver flap-asterixis) violent/abusive behavior 3. coma  Treat:  Enemas decrease ammonia absorption  Lactulose- a laxative that decreases ammonia by decreasing the bacteria in bowel that normally converts protein to ammonia. Causes 3-4 stools/day  Neomycin- intestinal antiseptic to decrease bacteria  Decrease protein intake
  23. Asterixis- liver flap
  24. Liver Failure
  25. Cirrhosis: Therapeutic intervention  Diagnostic tests-  Liver function test ALT, AST- not as high as hepatitis;  CBC platelets (anemia, thrombocytopenia)  Coagulation studies (lack Vit K- prolonged PT)  Bilirubin (elevated); ammonia (elevated)  Serum albumin (hypoalbuminemia)  Abdominal ultrasound (liver size/nodular, ascitis)  Esophagoscopy- varices  Liver biopsy(p 590) not done if bleeding time elevated
  26. Liver biopsy
  27. Cirrhosis Therapeutic Interventions cont  Medications:  Avoid *drugs metabolized by the liver and drugs toxic to liver- sedatives, hynotics, actaminophen, and alcohol.  Diuretics to reduce ascites  Lactulose (laxative) and neomycin (antibiotic) to dec ammonia- hepatic encephalopathy  Vit K to reduce risk bleeding  Beta-blockers to prevent esophegeal varices from rebleeding  Ferrous sulfate and folic acid to treat anemia  Antacids decrease acute gastritis
  28. Cirrhosis: Therapeutic interventions cont  Dietary and fluid  Restricted fluid/Na intake based on response to diuretic therapy, urine output and electrolyte values  Hi calories; Hi CHO; low fat  Surgery  Surgery to treat complications  Liver transplant (Lewis p 1087)
  29. Liver transplant
  30. Cirrhosis: Nursing Assessment specific to Cirrhosis  Health history  Current symptoms, altered bowel; excess bleeding; abdominal distention; jaundice; pruritus; history liver or gallbladder disease; alchohol history  Physical assessment  VS; mental status, color skin; peripheral pulses and edema; abd assessment; bowel sounds; abd girth; tenderness and liver size
  31. Cirrhosis: Pertinent Nursing problems/Care  Health promotion  Patient family teaching guides  Acute intervention  Ambulatory home care  Imbalance nutrition less than body reequirements  Dysfunctional family process: alcoholism  Excess fluid volume  Potential complication: hemorrhage; hepatic encephalopathy

×