6. 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
8. Symptoms of liver
failure appear when
80% liver destroyed
Liver can regenerate
itself if adequate
nutrition and no
alcohol
9. 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)
10. 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
11.
12. 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
16. 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
17.
18. 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
19. TIPS procedure- Note shunt that will divert
blood- relieving hypertension & esophegeal
varcies
20. 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)
25. 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
28. 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
29. 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
35. 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
36. 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)
38. 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
39. 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