1
Q
How many functions is the liver responsible for?
A
Over 400! Therefore any dysfunction to the liver will cause diffuse and serious complications
2
Q
What can liver failure result from?
A
- Viral hepatitis
- Cirrhosis
- Damage d/t drugs or alcohol
3
Q
Describe the blood supply of the liver:
A
- Liver made of two major lobes and then subdivided into smaller lobes
- Liver receives large amounts of blood via the hepatic artery (one to each lobe), supplying ~25% of blood to liver. Portal vein branches from stomach, spleen and intestines supply ~75% of blood for filtering.
- Hepatic vein returns filtered blood to inferior vena cava
4
Q
Describe the anatomy of the liver:
A
- Organized into lobules (hexagonal shapes)
- Each lobule contains several liver cells (hepatocytes), with a central vein in the middle of each lobule that branches off
- Branched veins connects to more bile ducts, hepatic veins and arteries on corners of hexagon
- Essentially the liver receives +++ blood supply for filtering this way!
5
Q
What are some of the physiological functions of the liver?
A
- Carbohydrate metabolism
- Maintenance of blood glucose (stores excess as glycogen; synthesize glucose from amino acids; release during fasting)
- Lipid metabolism (synthesis of cholesterol, lipoproteins; formation of triglycerides from carbs or proteins)
- Protein synthesis and degradation (plasma proteins, fibrinogen, coagulation factors, albumin, binding and transport of hormones and bilirubin)
- Conversion of ammonia to urea (the byproduct of metabolic liver reactions)
- Storing nutrients and vitamins (e.g. Vitamin A, D, K)
- Metabolism of drugs
- Production of bile salts and eliminating bilirubin
- Metabolism of steroid hormones
- Filtration of blood and removal of bacteria via Kupffer cells
6
Q
How does albumin work?
A
Contributes to plasma colloidal osmotic pressure
7
Q
What is ammonia? How is it made?
A
- By-product of metabolic reactions in the liver
- During deamination process (removal of amino groups from amino acids), conversion of amino acids to ketoacids and ammonia occurs
- Also in intestines d/t conversion of ammonia
8
Q
Why is ammonia harmful?
A
Toxic to tissues, especially neurons, so it requires quick removal from the body. typically removed from blood by liver and converted into urea, which is a safer form that can be easily excreted by the kidneys,
9
Q
What is alcoholic cirrhosis?
A
- Condition resulting from permanent damage or scarring to liver leading to blocked blood flow and prevention of normal metabolic and regulatory processes
- Diffuse fibrosis of liver into nodules that vary in size d/t imbalance regeneration and constrictive scarring
- Liver attempts to reorganize and repair itself after injury, but process is disorganized and leads to fibrosis
- Fibrosis is constrictive and disrupts flow of vascular and biliary duct systems
- Disorganization = poor cellular nutrition and hypoxia, causing further decreased liver functioning
10
Q
Why is alcohol a cause of cirrhosis?
A
- Liver responsible for metabolism of alcohol
- Metabolic end-products of conversion have multiple toxic effects to liver cells and their function; forces reorganization and functional changes
- Alcoholism can also cause malnutrition, which is bad for the liver
11
Q
What are common manifestations of cirrhosis?
A
- Weight loss, masked by ascites
- Weakness
- Anorexia
- Diarrhea
- Hepatomegaly (d/t structural changes)
- Abdominal pain d/t hepatomegaly and ascites - dull, aching, sensation of fullness
- Portal hypertension
- Splenomegaly (build up of blood d/t portal hypertension)
- Ascites **
- Bleeding d/t decreased clotting factors (thrombocytopenia)
- Anemia d/t splenomegaly
- Spider angiomas (increased circulation of estrogen makes more visible)
- Palmar erythema
- Improper drug action and increased sensitivity to adverse effects
- Endocrine disturbances (gynecomastia in men)
12
Q
What is the connection between liver failure and thrombocytopenia?
A
- Responsible for production of prothrombin and other factors essential for blood clotting
- Strongest indicator of cirrhosis *
13
Q
What happens when the liver fails to metabolize aldosterone?
A
- Aldosterone plays a role in water regulation
- Liver unable to metabolize, so high rates remain in the body
- Hyperaldosteronism with subsequent sodium retention = water retention and K+ loss = increased fluid retention
- Increased sodium re-absorption by renal tubules = increase in anti diuretic hormone = additional water retention = decreased blood flow and GFR
14
Q
What is portal hypertension?
A
- Increased resistance to flow in the portal venous system with increased pressure
- Can be d/t pre, post or intra origins
- Cirrhosis causes intrahepatic portal HTN d/t tissue changes and increased resistance in blood flow
- Increased pressure and dilation of venous channels behind obstruction = opening of collateral channels to connect portal circulation with systemic venous circulation = ascites, splenomegaly and esophageal varices
15
Q
What is ascites? What causes it?
A
- Late-stage manifestation of liver failure; an accumulation of fluid in the peritoneal cavity (evident ~500 cc of fluid)
- Increase in hydro-static pressure d/t portal hypertension
- Salt and water retention by kidneys
- Decreased osmotic pressure r/t impaired albumin syntehsis
- When portal pressure changes, proteins shifts from blood vessels to larger pores into lymph space = lymph unable to carry off such a high amount of fluid and proteins = leaking through liver capsule into cavity occurs = osmotic pressure of proteins pull fluid into cavity
16
Q
What is hepatic encephalopathy?
A
- A terminal complication of liver failure, indicating that ammonia cannot be detoxed by liver and is now crossing the BBB to produce neurotoxic manifestations
- Occurs when blood shunted past liver via collateral anastomoses or when liver unable to convert to urea
17
Q
What are other causes of hepatic encephalopathy?
A
- GI hemmorhage
- Constipation
- Hypokalemia/volemia
- Infection
- Cerebral depressants
- Metabolic alkalosis
- Paracentesis
- Dehydation
- Increased metabolism
- Uremia (kidney failure)
Essentially, it can occur in any condition that causes ammonia to enter systemic circulation without detoxification by the damaged liver
18
Q
How is hepatic encephalopathy graded?
A
EARLY STAGES, GRADES 0-1: euphoria; depression; apathy; irritability; memory loss; confusion; yawning; drowsiness; insomnia; and agitation.
GRADES 2 AND 3: slow and slurred speech; impaired judgement; slow and deep respiration’s; hiccups; hyperactive reflexes; positive Babinski reflex.
GRADE 4: Coma; disorientation; asterixis (flapping of hands); hyperventilation; hypothermia; grimacing and gasping reflexes
19
Q
Describe jaundice as it relates to liver failure:
A
- A common and late manifestation of failure d/t obstruction (e.g. structural changes have obstructed the biliary tract to gall bladder and pancreas)
- Build up of free bilirubin (breakdown of old RBC’s) in blood stream
- Becomes clinically evident when levels reach 2 to 2.5 mg/dL (normally 0.1 to 1.2)
- Due to either pre, intra or post hepatic causes. Hepatitis and cirrhosis are most common causes of intrahepatic jaundice, as there is interference with all phases of bilirubin metabolism (uptake, conjugation, excretion)
20
Q
Describe how bilirubin is converted:
A
RBC degraded > hemoglobin converted down to heme and globin > Heme forms biliverdin > biliverdin converted to free bilirubin, in plasma and bound to albumin > conjugated by hepatocytes (released from albumin) > product becomes soluble in bile > passes though bile ducts into small intestine > converted into new substance and re-absorbed through portal circulation or excreted in feces
21
Q
What else can cause jaundice?
A
- Excessive destruction of RBC’s
- Impaired uptake of bilirubin by liver cells
- Decreased conjugation of bilirubin
- Obstruction of file flow in the canaliculi of hepatic lobules
22
Q
Why might these patients experience pruritus?
A
- Obstruction of biliary tract can cause irritation
- Bile salt buildup under the skin
- Urea/ammonia buildup likely to deposit to skin and mucous membranes
23
Q
What are the general treatment goals for individuals with liver failure?
A
- Care aimed at preventing or treating complications
- Helping individuals with alcoholism
- Prevention of infection
- Providing sufficient amounts of carbs and calories to prevent protein breakdown (will worsen hep. encephalopathy). Also advocate for low fat.
- Correction of fluid and electrolyte imbalances
- Decreasing ammonia production in GI tract (lactulose, controlling protein intake)
- Assessment of low blood levels (e.g. thrombocytopenia)
- Conserving energy (AAT, modify activity and rest schedule)
- Monitor for bleeding r/t esophageal varices, especially if n/v has become a problem
- Liver transplant remains the only effective treatment; there is no specific therapy that can treat cirrhosis!
24
Q
Describe liver function tests (aka. liver panel) and their relevance to liver failure:
A
- Liver function tests (serum levels of liver enzymes) assess injury to liver cells, livers ability to synthesize proteins and extent of liver damage. Measures amount of enzymes found in the blood stream.
- Elevated usually indicates injury earlier than other indicators
- ALT and AST key enzymes, likely to demonstrate parallel rises
- Also evaluates ALP, albumin, total protein and total and direct bilirubin
- Prothrombin is also a useful lab, but may not be under a common LFT panel
25
What are other causes of altered LFT's?
- Auto-immune hepatitis (attacks liver)
- Fatty liver
- Inherited liver diseases
- Liver tumors
- Heart failure
26
What does ALT do?
This enzyme metabolizes amino acids and makes proteins
27
What does AST do?
Enzyme that metabolizes amino acids and making/processing proteins, found in liver, heart, muscles and kidneys
28
What does ALP do?
- Enzyme also found in other body areas, so hi levels may be due damage elsewhere in the body (e.g. hyperthyroidism)
- Metabolizes phosphorus
29
Describe a typical PPT:
- 10-15 seconds (measures time it takes for a fibrin clot to form)
- Will be increased with liver disease d/t altered production of factors
- Without Vitamin K coagulation is also impaired because there are vitamin K dependent clotting factors
30
What are additional diagnostics that would be performed for these patients?
- History and physical examination
- Liver function tests and enzyme measurements
- Liver biopsy
- Endoscopy
- Liver UC
- CT/MRI
- Electrolytes/CBC
- Testing of stool for occult blood
31
How do we treat esophageal and gastric varices?
- Drugs (e.g. BB, vasopressin, statins)
- Band ligation
- Balloon tamponade
- Surgical shunting procedure
32
When are we likely to see surgery?
- Emergency placement of shunts (e.g. attempt to relieve some portal hypertension)
- Liver transplant
33
How do we treat ascites?
- Restriction of sodium
- Diuretics, using different types that work on different parts of the nephron to have the best results
- K+ supplements since already predisposed to hypokalemia (n/v, lasix, loss via the aldosterone complex)
- Large volume paracentesis to promote comfort, especially with pulmonary compromise
- Evaluate for infection, as ascites increases risk of peritonitis
- Record daily I&O, body weight, and ongoing assessment of location and severity of edema
34
What diuretics are likely to be used to treat ascites?
- Lasix and Spironolactone
| - Spironolactone is K+ sparing and acts as an antagonist to aldosterone
35
How does lactulose help treat encephalopathy?
- Binds with excess amounts of ammonia so it can leave the body in feces
- Changes the pH and discourages bacterial growth and release of ammonia in intestines
- Focus with this patient is to maintain a safe environment while experiencing symptoms, assess responsiveness, monitor fluid and electrolyte imbalances, acid-base imbalances, and sensory and motor abnormalities
36
How do we treat jaundice?
- A stent may be placed to keep bile duct open
- Medications to relieve pruritus (e.g. cholestryamine, a bile acid sequestrate)
- Provide baking soda baths and lotions with antihistamines and calamine
- Thorough skin assessment and care
- Thorough oral care
- Observe urine and stool for progression (alterations)
37
What health promotion do we do with liver failure patients?
- Prevention and treatment of cirrhosis
- Promote adequate nutrition
- Identify and treat underlying disease (e.g. heart failure)
- Vaccinations for Hep A and B
- Avoid sleeping pills or sedatives
- Avoid aspirin, NSAID's, etc. to prevent bleeding and renal complications
- Teach signs of infection for early tx
- Surveillance of live cancer
- Provision of community supports (e.g. if patient is alcoholic, recommend AA)
- Teach signs of compensation (e.g. abdominal swelling, black stool)
38
What are common nursing diagnoses?
- Imbalanced nutrition: less than body requirements r/t anorexia, impaired use and storage of nutrients, and nausea
- Impaired skin integrity r/t edema, ascites and pruritus
- Ineffective breathing pattern r/t pressure on diaphragm and reduce long volume secondary to ascites
- Risk for injury r/t diminished sensory perception secondary o peripheral neuropathy
- Risk for infection r/t increased susceptibility to environmental pathogens
- Hepatic encephalopathy r/t inability of liver to detox toxins
- Hemorrhage r/t bleeding tendency secondary to altered clotting factors and rupture of esophageal or gastric varices
N304
flashcards
Decks in class (16)
# Cards
-
Palliative Part 131
-
Palliative Part 225
-
Symptom Management40
-
Integrative Therapies42
-
Medication Management in the Elderly13
-
Elder Abuse25
-
Multiple Injuries27
-
AKI/CKD24
-
Burns23
-
HIV/AIDS: Part 1, Epidemiology to Treatment45
-
HIV/AIDS: Part 2, Treatment as Prevention to Precautions26
-
Ovarian Cancer Case Study19
-
Liver Failure Case Study38
-
Spinal Cord Injuries68
-
Interprofessional Communication18
-
Palliative Care Panel18
