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Hemolytic
jaundice CAUSES- increased breakdown of RBCs (blood transfusions, sickle cell crisis) Hepatocellular jaundice CAUSES-damage in liver hepatocytes so billirubin leaks from out Obstructive jaundice-obstruction in liver or biliary duct
What
is Jaundice?
Yellowish
skin color resulting from increased bilirubin Some form of alteration in a persons normal metabolism or obstruction in hepatic or biliary duct. Its a symptom not a disease Bilirubin is either unconjugated (indirect) or conjugate (direct
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Fig. 44-1
What
does Jaundice look like in the body? Dark urine secondary to excess bilirubin being excreted by kidneys Stools will be light or clay colored. Pruritus (dry skin) due to bile salts beneath the skin.
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Etiology
Hepatitis A-G
Clinical manifestations: no s/s, acute phase include malaise, anorexia, n/v, RUQ pain, hepatomegaly, Lymph involvement
Viral
Hepatitis Hepatitis
drug users.
Inflammation
of liver tissue Cytotocic cytokines and killer cells cause lysis of infected hepatocytes. Liver can regenerate with time if no complications.
Incubation
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Collaborative care Drug therapy Chronic hepatitis B -Interferon Nucleoside analogs Chronic hepatitis C Prevention Hepatitis A Hepatitis B Hepatitis C
Studies:
GGT
Serum/urinary
bilirubin Prothrombin time (PT) prolonged because of decreased absorption of vitamin K in intestine with decreased production of prothrombin by liver.
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Nutritional High
Therapy
calorie, high protein, high carbohydrate, low fat diets with vitamin supplements
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Nursing Nursing
assessment? diagnoses?
Planning?
ASSESSMENT: Passed
history of hemophilla, exposure, food or water contamination, transfusion before 1992, IV drug use, etc. Miss use of acetaminophen, other toxic drugs to liver cells. Functional lifestyle, relationships, ETOH, weightloss, RUQ pain.
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Objective: Nursing
physical exam
Diagnosis: imbalanced nutrition, activity intolerance ineffective therapeutic regimen mang. (f/u care
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What
are some ways a nurse can implement care for a patient with Viral Hepatitis?
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One
of the leading public health concerns. Only definitive way to distinguish forms of hepatitis is presence of antigens and antigenic subtyples Nurses could teach prevention Understand the types of Hepatitis Types A and B can be prevented and treated Type C-no vaccine
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Nursing implementation
Health promotion
Hepatitis A Hepatitis B Hepatitis C
Acute intervention
Jaundice Rest Ambulatory and home care
Evaluation
Control
Hepatitis C
Standard Precautions
Autoimmune
hepatitis Wilsons disease Hemochromatosis Primary biliary cirrhosis Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis
Clinical manifestations and diagnostic
Autoimmune Chronic
Hepatitis
inflammation of liver of unknown cause. Elevated liver enzymes without viral antigens (no A, B, C, etc. Thought to be caused by environmental factors or genetics Treated with corticosteroids and immunosuppressive agents.
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Wilsons
Disease
Neurologic
Disease in the presence of chronic liver disease Diagnosic findings: KayserFleischer rings (brownish red colored rings in the cornea) seen in eye exam. Higher levels of Copper levels Treatment is eliminating Copper in active disease.
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Hemochromatosis Caused
(HH)
by the increased and inappropriate absorption of dietary iron. untreated damage to organs
If
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Primary
S/S-Pruritus,
diarrhea of pale stools, hepatomegaly. Unclear of etiology: genetic and environmental factors such as chemical exposure and infection. 95% if those diagnosed are women Treatment-suppress ongoing liver damage with Actigall.
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liver cells. Liver tries to regenerate New cells are abnormal due to scarring and fibrous tissue Resulting in abnormal blood vessel and bile duct functioning
Alcoholic Large
Cirrhosis-
intake of ETOH causes accumulation of fat in the liver in scarring and impaired functioning
Resulting
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Postnecrotic Resulting
Cirrhosis:
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Biliary
Cirrhosis:
Chronic
Fibrotic
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Cardiac
Cirrhosis:
Resulting
from severe right sided heart failure, pericarditis and tricuspid insufficiency.
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What
would be some of the early signs and symptoms we would see with Cirrhosis?
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GI
symptoms: anorexia, nausea, vomiting, change in bowel patterns (liver is having difficulty metabolizing carbs, fats, proteins). Dull heavy pain in right upper quadrant, epigastric area. Enlarged liver and spleen
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Later
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Jaundice Skin
lesions (livers inability to metabolize steroid hormones) Problems: anemia, coagulation disorders, thrombocytopenia. problems-liver metabolizes normally (estrogen, testosterone
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Hematologic
Endocrine
Fig. 44-4
Fig. 44-6
Complications
esophageal and gastric varices Peripheral edema and ascites Hepatic encephalopathy Hepatorenal syndrome
Portal
HypertensionCompression and Destruction of the portal veins. What do you think happens as a result of decreased blood flow?
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Answers:
Increased Ascites Systemic
venous pressure
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Fig. 44-8
Esophageal
Varices As a result of tortuous veins at the lower end of the esophagus. Little elastic tissue-fragile Varies are responsible for 80% variceal hemorrhage BLEEDING VARIES LIFE THREATENING COMPLICATION OF CIRRHOSIS.
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Esophageal
Varices
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Sengstaken-Blakemore
Tube
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Ascites
Peripheral edema results from Portal Hypertension, occurring in ankles and presacral area. Ascites is serous fluid in peritoneal or abdominal cavity. HTN moves protein to lymph space.
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measure reserved to help with breathing Peritoneovenous Shunt-reinfusion of ascitic fluid into venous system.
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Peritoneovenous Reinfusion
Shunt
Tube that runs from the peritoneum under the SQ tissue into the jugular vein or superior vena cava
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Fig. 44-9
Fig. 44-11
Nursing
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History Health
patterns r/t: chronic ETOH, weight loss, n/v, anorexia, dark urine, bowel changes, easy bruising, change is skin color, dull pain in RUQ or epigastric, sexual dysfunction Skin changes, abdominal girth size, foul breath, enlarged liver, speen.
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What
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nutrition
skin integrity
fluid volume
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Planning: Decrease
discomfort Prevent complications Return to active living when possible Prevention in relation to causes: ETOH, exposure to viral causes.
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Hepatic
Encephalopathy Neuropsychiatric complication of liver damage. Ammonia enters systemic circulation Crosses the blood brain barrier
S/S-confusion, agitation, slurred speech, respiratory changes, reflex changes. CLASSIC SIGN: Asterixis
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How
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Asterixis When
(flapping tremors)
asked to hold hand and arms stretched out.the patient can not hold this position shows flexion and extension of the hands.
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What
might be the focus of nursing care for patients with Hepatic Encephalopathy?
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Provide Assist
a safe environment
with monitoring and measures to reduce ammonia levels Neuro checks Give medications as ordered such as laxatives to decrease ammonia levels by excretion.
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Pancreatitis Inflammatory
pancreas.
process of the
Common
causes: biliary tract disease in women, alcoholism in men. Less common: trauma, viral, after surgical procedures
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Pathogenic Body
mechanisms:
Injury
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What
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Left
upper quadrant pain, could be midepigastric pain. Sudden onset: severe, steady, constant pain Flushing of the skin, dyspnea, n/v, tachycardia, Guarding of the abdomen Decreased bowel sounds Ileus
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What
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Monitoring
frequently.
Respiratory distress, lung sounds (retroperitoneal fluid raises the diaphragm) Monitoring electrolytes
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NPO status with possible NG tube Mental status changes Pain management
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