HEPATIC DISORDERS - PowerPoint Presentation

Slide1

HEPATIC DISORDERS

NUR – 224Slide2

LEARNING OUTCOMES

Explain liver function tests.

Relate jaundice, portal hypertension, ascites, varices, nutritional deficiencies to the pathophysiology of the liver.

Use the nursing process as the framework for the care of the patient with cirrhosis of the liverSlide3

LIVER

Largest gland in the body /complex organ

Located on the right side of the abdomen – anterior to the stomach

Highly vascular organ

Circulation of blood to the liver is of major importance.

Multiple metabolic and regulatory functionsSlide4

ESSENTIAL FUNCTIONS

Secretes bile

Stores fat-soluble vitamins (A, B,D, and several B- complex vitamins)

Metabolizes medication – barbiturates, opioids, sedatives, amphetamines, anesthetics

Active in fat/protein metabolism.

Releases glucose during times of hypoglycemia

Takes up glucose during times of hyperglycemia and stores it as glycogen or converts it to fat

Store iron as ferritin – which is released as needed for the production of RBC’s

Converts ammonia to ureaSlide5

DIAGNOSTIC STUDIES

Liver Function test

Liver biopsySlide6

LIVER BIOPSY

Performed to r/o metastatic cancer, detect cyst, or cirrhosis of the liver

Considered minor surgery

Results of coagulation test – PTT, PT, platelet count

Signed consent

Withhold any anticoagulants, ibuprofen, ASA – for a week prior to the procedure

Food/fluids withheld 4-6 hours before the procedure

Void prior to the procedureSlide7

LIVER BIOPSY

Post procedure

Client lies on the right side, immobile for several hours

Avoid coughing and straining

Monitor vital signs

Avoid heavy lifting, strenuous activity for 1 week Slide8

COMMON MANIFESTATIONS OF LIVER DISORDERS

Jaundice

Ascites

Portal hypertension

Esophageal varices

Hepatic encephalopathySlide9

Jaundice

Disrupted metabolism/excretion of bilirubin

accumulates in the tissues --jaundice

yellow staining of the body tissues

First noticeable in the sclera of the eyes, then the skin

Concentration of bilirubin in the blood is abnormally increased

Types

Hemolytic

Hepatocellular

ObstructiveSlide10

Portal Hypertension

Impaired/obstruction blood flow through the liver increases pressure in the portal venous system

drains into the GI system, spleen and surface veins of the abdomen.

Leads to:

ascites

esophageal varicesSlide11

Ascites

Accumulation of serous fluid in the peritoneal/abdominal cavity

Contributing factors

portal hypertension, increase flow of hepatic lymph system, and

hyperaldosteronism

.

Common manifestation of cirrhosis

Large amounts albumin-rich fluid fills the peritoneal cavity (12-15 L)

Slide12

Manifestations of Ascites

Abdominal distention

Rapid weight gain

Signs of dehydration

Decrease in urine output

HypokalemiaSlide13

Treatment of Ascites

Sodium restriction

Diuretics

Fluid removal -

paracentesis

Bedrest

Shunt procedures –

transjugular

intrahepatic

portosystemic

shunt (TIPS)Slide14

Esophageal Varices

Develop on a majority of patients with cirrhosis

Dilated, tortuous vessels that develop at the lower end of the esophagus

Enlarged and swollen

 as a result

portal hypertension

Are responsible for

approx

80% of

variceal

hemorrhagesSlide15

Bleeding Esophageal Varices

Life threatening and led to shock

Varices rupture and bleed in response to ulceration and irritation

Contributing factors

Clinical manifestations – hematemesis, melena,

hx

of alcohol abuse, s/s of shock may be present

Diagnostic findings - endoscopySlide16

Treatment of Bleeding Varices

Treatment of shock

Oxygen

IV fluids with electrolytes

Vasopressin, somatostatin,

octreotide

Beta-blocker agents

Balloon tamponade

Endoscopic therapiesSlide17

TreatmentSlide18

TreatmentSlide19

Nursing Management

Monitor patient condition

 physical, emotional and cognitive status

Assess nutritional and neurologic status – increase ammonia levels  drowsiness, confusion

Monitor tube care and GI suction

Oral care

Quiet calm environmentSlide20

Hepatic Encephalopathy

Impaired consciousness and mental status

 accumulation of toxic waste products in the blood  blood bypasses the congested liver

Ammonia is considered the major etiologic factor in the development of encephalopathy.

Life threatening complication of liver disease

Associated with portal hypertension and the shunting of blood from the portal venous into the systemic circulation

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Hepatic Encephalopathy

Onset insidious

Clinical manifestations

early symptoms – minor mental changes/motor disturbances

late symptoms – incomprehensible speech, marked confusion

Asterixis

Apraxia

Fetor hepaticusSlide22
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Management Hepatic Encephalopathy

Eliminate precipitating factors

Administer lactulose as ordered

Assess neurologic status frequently

Monitor mental status

Administer antibiotics

Discontinue sedatives, analgesics and tranquilizers

Prevent development of respiratory complicationsSlide24

Cirrhosis

Chronic progressive disease

Normal liver tissue is replaced by fibrous liver tissue

 that disrupts the structure and function of the liver

12

th

leading cause of death in the US

Death rate is twice as high in men than women

Native American men have the highest incidence and mortality rate from cirrhosisSlide25

Pathophysiology

Functional tissue is destroyed and replaced by fibrous tissue.

Hepatocytes and liver lobules are destroyed , metabolic function of the liver is lost.

Fibrous connective tissue forms



constructive bands that disrupt blood and bile flow within the liver lobules

Blood no longer flows freely through the liver to the IVC

Restricted blood flow

 portal hypertension, increased pressure in the portal systemSlide26
Slide27

Cirrhosis

Types

alcoholic – end result of alcoholic liver disease

postnecrotic

– results from chronic hepatitis B or C,

NAFLD

biliary – retained bile damages and destroys liver cellsSlide28

Clinical Manifestations

Onset insidious

Early signs

Dull aching pain – epigastric area/RUQ

Weight loss, weakness,

Bowel function disrupted – diarrhea/constipation

Late signs

Impaired metabolism

 bleeding, ascites, jaundice, neurological changes,

splenomeagly

GI varices, edema, vitamin deficiency, and anemiaSlide29

Assessment & Diagnostic Findings

Liver function tests

Coagulation studies

Serum electrolytes

Serum ammonia levels

CBC with platelets

Abdominal ultra sound

Liver biopsySlide30

Collaborative Care

Medications

Fluid

Management/Nutrition Slide31

Nursing Process

Excess Fluid Volume

Risk for Bleeding

Impaired

Skin Integrity

Risk for Acute ConfusionSlide32

Practice Alert

Monitor for signs of impaired renal function

 oliguria, central edema and increase in serum

Crt

/BUN.

Closely monitor patient who have GI bleeding  assess for signs of hepatic encephalopathy.

Monitor the respiratory status of the patient with a Blakemore/Minnesota tube.