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Anatomy and Function of the Liver: Bile Production, Cirrhosis, and Liver Diseases, Schemes and Mind Maps of Nursing

An in-depth exploration of the liver's structure, functions, and common diseases, with a focus on bile production and cirrhosis. Learn about the roles of hepatocytes, bile, and the digestive and metabolic functions of the liver.

What you will learn

  • What are the main functions of the liver?
  • What causes cirrhosis and how does it affect liver function?
  • How does the liver produce and process bile?
  • What are the common causes and symptoms of liver diseases?
  • How is liver function assessed through laboratory tests?

Typology: Schemes and Mind Maps

2021/2022

Uploaded on 09/27/2022

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Liver Disease
Let’s Review the Liver!
Anatomy
Largest internal organ in the body
Divided into right and left lobes (right is largest and is further divided into caudate and quadrate lobes)
Within the lobes are smaller units called lobules which consist of hepatocytes (liver cells)
The hepatocytes are the functional cells of the liver, the remaining mass is made up of Kupffer cells, stellate cells,
endothelial cells, blood vessels, bile duct cells and supporting structures.
Hepatic Blood Supply
Obtains dual blood supply from the portal vein and hepatic artery...this is very unique! A vein is located between
two capillary beds. The hepatic vein collects blood from capillaries in visceral structures located in the abdomen
and empties it into the liver.
The liver gets approximately 1500 ml of blood/minute. This comes out to 13% of total body blood supply. The
hepatic artery supplies 25% (around 300 ml/min), and the portal vein supplies 75% (around 1050 ml./min).
Because the portal vein supplies most of the blood supply, you can imagine why it’s so devastating when that vein
gets backed up...lots and lots of blood with no where to go (except back into the portal system).
The hepatic vein empties into the inferior vena cava
The liver stores 450 ml of blood due to pressure differences between the hepatic vein and the vena cava.
In CHF, blood backs up and accumulates in the liver. That can’t be good!
Hepatic portal vein takes all the flow from other vessels....it there are problems it’s going to back up to all these
other organs. (see slide, it’s the blue veins)
Our biggest concern is with cirrhosis or fatty liver, and we can’t get blood flow to go back out through the hepatic
vein and on through the system.
Digestive Role
Produces bile (main fxn). Bile emulsifies fats and stimulates peristalsis (more on bile below)
Conveys bile from the gallbladder (where bile is stored) until it enters the duodenum at the Sphincter of Oddi
through the common bile duct
Processes and stores fats, carbohydrates and proteins
Processes and stores vitamins and minerals (fat-soluble vitamins A,D,E,K, B12, copper and iron...iron is in the
form of ferritin). Vit A is necessary for retinal fxn and epithelial cellular growth; Vit B-12 is necessary for DNA
synthesis, normal RBCs and nerve fxn (Pernicious anemia is d/t a lack of Vit B-12); Vit K is necessary for clotting.
Synthesizes cholesterol
Produces triglycerides
What is bile?
Bile is an alkaline fluid composed of cholesterol, phospholipids, bile salts, bile pigments (bilirubin), proteins and
electrolytes. The liver produces 600-1200 ml of bile a day 97% of which is water). It flows through the canaliculi, into the
common bile duct, goes through the Sphinctor of Oddi and empties into
the duodenum. Bile is stored in the gallbladder, where it is concentrated,
and discharged into the duodenum when fatty chyme enters from the
stomach. The function of bile is to emulsify fats, facilitating their digestion
in the small intestine by pancreatic lipase. It is also necessary for
transport of cholesterol via fatty acids and the transport of fat soluble
vitamins (ADEK). Bile also stimulates peristalsis. 94% of the bile salts
that go into the intestines is reabsorpbed into the portal circulation for
recycling.
Metabolism Role (carbohydrates, fats and proteins)
Carbohydrates
production of glucose from proteins and fats
Liver pg 1 of 12
Terms To Know
Glycogenesis = formation of glycogen from glucose
Lipogenesis = formation of fat from CHO
Glycogenolysis = breaking down of glycogen
Gluconeogenesis = AA + glycerol + lactic acid = glucose
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Download Anatomy and Function of the Liver: Bile Production, Cirrhosis, and Liver Diseases and more Schemes and Mind Maps Nursing in PDF only on Docsity!

Liver Disease Let’s Review the Liver! Anatomy

  • Largest internal organ in the body
  • Divided into right and left lobes (right is largest and is further divided into caudate and quadrate lobes)
  • Within the lobes are smaller units called lobules which consist of hepatocytes (liver cells)
  • The hepatocytes are the functional cells of the liver, the remaining mass is made up of Kupffer cells, stellate cells, endothelial cells, blood vessels, bile duct cells and supporting structures. Hepatic Blood Supply
  • Obtains dual blood supply from the portal vein and hepatic artery...this is very unique! A vein is located between two capillary beds. The hepatic vein collects blood from capillaries in visceral structures located in the abdomen and empties it into the liver.
  • The liver gets approximately 1500 ml of blood/minute. This comes out to 13% of total body blood supply. The hepatic artery supplies 25% (around 300 ml/min), and the portal vein supplies 75% (around 1050 ml./min). Because the portal vein supplies most of the blood supply, you can imagine why it’s so devastating when that vein gets backed up...lots and lots of blood with no where to go (except back into the portal system).
  • The hepatic vein empties into the inferior vena cava
  • The liver stores 450 ml of blood due to pressure differences between the hepatic vein and the vena cava.
  • In CHF, blood backs up and accumulates in the liver. That can’t be good!
  • Hepatic portal vein takes all the flow from other vessels....it there are problems it’s going to back up to all these other organs. (see slide, it’s the blue veins)
  • Our biggest concern is with cirrhosis or fatty liver, and we can’t get blood flow to go back out through the hepatic vein and on through the system. Digestive Role
  • Produces bile (main fxn). Bile emulsifies fats and stimulates peristalsis (more on bile below)
  • Conveys bile from the gallbladder (where bile is stored) until it enters the duodenum at the Sphincter of Oddi through the common bile duct
  • Processes and stores fats, carbohydrates and proteins
  • Processes and stores vitamins and minerals (fat-soluble vitamins A,D,E,K, B12, copper and iron...iron is in the form of ferritin). Vit A is necessary for retinal fxn and epithelial cellular growth; Vit B-12 is necessary for DNA synthesis, normal RBCs and nerve fxn (Pernicious anemia is d/t a lack of Vit B-12); Vit K is necessary for clotting.
  • Synthesizes cholesterol
  • Produces triglycerides What is bile? Bile is an alkaline fluid composed of cholesterol, phospholipids, bile salts, bile pigments (bilirubin), proteins and electrolytes. The liver produces 600-1200 ml of bile a day 97% of which is water). It flows through the canaliculi, into the common bile duct, goes through the Sphinctor of Oddi and empties into the duodenum. Bile is stored in the gallbladder, where it is concentrated, and discharged into the duodenum when fatty chyme enters from the stomach. The function of bile is to emulsify fats, facilitating their digestion in the small intestine by pancreatic lipase. It is also necessary for transport of cholesterol via fatty acids and the transport of fat soluble vitamins (ADEK). Bile also stimulates peristalsis. 94% of the bile salts that go into the intestines is reabsorpbed into the portal circulation for recycling. Metabolism Role (carbohydrates, fats and proteins)
  • Carbohydrates
  • production of glucose from proteins and fats Terms To Know Glycogenesis = formation of glycogen from glucose Lipogenesis = formation of fat from CHO Glycogenolysis = breaking down of glycogen Gluconeogenesis = AA + glycerol + lactic acid = glucose
  • results in glycogen storage
  • Helps maintain normal blood glucose levels through glycogenesis, lipogenesis, glycogenolysis and gluconeogenesis.
  • Protein (will affect diet teaching for patient, also very important!)
  • breakdowns dietary proteins
  • albumin synthesis (keeps oncotic pressure high, controls fluid/electrolyte balance...leads to ascites)
  • formation of urea from ammonia (you make a lot of waste products, specifically ammonia. It is the liver’s job to turn ammonia to urea so you can pee it out. Too much ammonia and the pt will have severe neurological defects and look like they are in a coma. Need ammonia labs!, electrolytes)
  • synthesis of clotting factors (want to look at PT, PTT, PLT, fibrinogen levels, H&H)
  • Fats
  • Dietary triglycerides are metabolized by the liver into fatty acids that are used for: oxidation and energy production; metabolized to ketones; synthesis of cholesterol and phospholipids; formation of triglycerides from dietary lipids, cho and proteins; formation of lipoproteins (triglyceride + protein + cholesterol + phospholipid); the fatty acids released from adipose tissues are used by the liver for the same purposes
  • Metabolizes hormones such as mineralocorticoids, glucocorticoids and sex hormones (see detoxification) Excretory Role
  • Excretes bile
  • Excretes cholesterol
  • Converts ammonia to urea
  • Detoxifies drugs, hormones and other foreign substances (more on this below) Detoxification The liver detoxifies ammonia, which is produced in the gut by bacteria after de-amination of ingested high protein foods or GI bleeds. It is produced in the liver from de-amination of amino acids (NH3). Ammonia is HIGHLY TOXIC to body tissues, especially neurons! It is converted by the liver into urea that is excreted through the kidneys. With liver disease, urea synthesis is often depressed. This leads to increased ammonia levels and decreased BUN. 80-90% of alcohol is detoxed by the liver...so be kind to your liver and don’t drink so much! Hormones are also detoxified by the liver. (is detoxified a word?) This involves de-amination of insuin and glucagon; de- iodination of thyroxin and triiodothyronine; glucocorticoids are transformed to water soluble form; ADH and aldosterone detoxification; estrogen and androgen detoxification. Drugs are also a biggie. Dr. Brady listed amphetamines, many sedatives, and barbituates except for phenobarbital and barbital (not sure if she meant these are detoxed by liver, or these drugs damage liver?) Hematologic Role
  • Stores blood! In case of rt-side heart failure or valvular problems, excess blood can be sored in the liver. In the case of hemorrhage, the liver can release blood (approx 450 ml) to maintain circulatory volume)
  • Synthesizes all but two clotting factors and synthesizes bilirubin (discussed elsewhere in more detail) What is bilirubin anyway? When RBCs break down they are pulled out of circulation by macrophages at the cellular level and by the spleen, liver and bone marrow at the organ level. The amino acids and iron are recycled and put back into the bone marrow for construction of new RBCs. The heme group of the old falling-apart RBC does not go to the bone marrow for recycling. Instead, it is converted to bilirubin and transported to the liver where it is incorporated into bile. Some of this goes to the digestive system to be excreted in feces, and some goes in the blood stream so it can travel to the kidneys and be excreted in the urine. What do bilirubin levels mean?
  • Total bilirubin: high levels warrant more testing
  • Unconjugated /indirect: high levels indicate large hemolysis or problems with intrahepatic cells
  • Conjugated/direct: high levels indicate problems with the bile flow, suggestive for biliary tract obstruction

Nursing Responsibilities/Patient Teaching with Tests/Interventions

  • Ultrasound/CT/MRI: Big issue is that they have to go FLAT into the scanner. Worry about breathing! Make sure you have a portalbe pulse ox on them, and portable oxygen on while in scanner. MRI takes 45 minutes. Also make sure they can follow directions (may not be able to d/t ammonia issues) to hold breath when they need to. Most scanners cannot handle over 300 pounds...so what do you do? They do ultrasound, x-ray instead.
  • Liver Biopsy: Very concerned about bleeding...watch H&H, watch vitals. Stop any aspirin or Plavix 7 days prior, no alcohol for a week prior, for 2 weeks after should not be doing any lifting, no driving for 24 hours after, watch the dressing for signs of bleeding. Position on right side for 1-2 hours on BR to put pressure on the liver.
  • Endoscopy: Big issues are NPO prior, consent, conscious sedation...so watch airway during recovery.
  • Paracentisis: Only remove up to 1 L at a time. The most determining factor in the use of paracentesis is respiratory distress. When a large amount of protein-rich fluid is removed, fluid will shift between the intravascular space and the interstitial tissue causing hypovolemia...this is the major factor that determines the rate at which the fluid can safely be removed (may be over several hours). Tell pt they may experience pain or pressure at site. - Nursing interventions for paracentesis (just the non-obvious ones): take baseline vitals including weight and abdominal girth, have the client void prior to the procedure (or put in a Foley), explain that local anesthetics used at the site, administer sedation if ordered, position client sitting with legs dangling and arms resting on bedside table or supine (depends on tolerance). - After the procedure (just the non-obvious ones): maintain pressure at needle-insertion site for several minutes, re-do vitals and compare, monitor temp q 4 for 48 hours, give IV fluids or albumin as ordered, place pt on unaffected side for 1-2 hours after, document what the fluid looked like and how much. - If the site continues to leak, apply dry sterile gauze and change as often as necessary. - Diuretics may be prescribed to control fluid volume, may need K supplements as a result. Monitor K and -lytes. - Lab tests afterward are: albumin, protein, glucose, amylase, BUN, creatinine - To prevent hypovolemia: slow drainage, administration of plasma expanders (albumin); monitor for signs (tachyC, hypoT, pallor, diaphoresis, dizziness) - Bladder perforation is rare but possible; symptoms are hematuria, low or no urine output, suprapubic pain/ distention, symptoms of cystitis, fever; if suspected, call the MD! - Peritonitis can occur d./t injury to intestines from needle insertion; symptoms include sharp, constant abdominal pain, fever, nausea, vomiting and diminished or absent bowel sounds; if suspected, call the MD!
  • Angiography and portal pressure measurements: The pt is usually under sedation, and to go through angiography they have a groin site so watch for bleeding there.

Lab Test of Liver Function AST 0-35 units/L Liver, skeletal & heart muscle. ↑ with INFLAMMATION; not specific for liver ALT 4-36 units/L shows parenchymal inflammation; SPECIFIC for liver GGT (alcohol) 8-38 units/L liver cells and kidney fxn; ↑ with alcohol-related problems ALP 20-80 ALKALINE PHOSPHATASE; ↑ with obstruction LDH 100-190 units/L heart, kidneys, liver, skeletal, RBCs, brain and lungs Ammonia 80-110 units/L byproduct of metabolism that is normally converted to urea by liver. when high you will have a change in LOC, shaking (asterixis); will be ↑ Cholesterol < 200 mg ↓ or ↑ in severe hepatocellular disease Phospholipid 150-250 mg/dL Albumin 3.5-5 /dL ↓ in liver disease (cirrhosis, alcoholism, hepatitis) BUN 8-22 ↓ with severe liver disease; BUN & Cr ↑ with hepatorenal syndrome PT 11-12.5 seconds ↑ with liver dysfunction PTT 68-82 seconds ↑ with severe liver disease / Cirrhosis PLT 130-400 either ↓ or WNL but poor quality; d/t storage in spleen and distribution with portal hypertension...they get squished and misshapen. Bili Total 0.3-1 mg/dL ↑ in liver disease Direct Bili 0.1 -0.3 mg/dL CONJUGATED; ↑ with obstruction of ducts Indirect Bili 0.2 - 0.8 mg/dL UNCONJUGATED; ↑ d/t reduced parenchymal surface and hemolysis Urine Bili 0 - 0.2 mg/dL ↑ in hepatocellar disorders and bilariy track obstruction Urobilinogen 0.3 - 3.5 mg/dL ↑ in hepatocellar disorders and bilariy track obstruction Fecal urobilinogen 75 - 275 EU/100g Na/K decrease or increase Glucose 70-110 mg/dL ↑ with pancreatic obstruction; ↓ with severe liver disease H & H ↓ d/t severe anemia and hemorrhage

The Table of Hepatitis

Factor Transmission incubation severity Prevent/Vac.

Hep. A Fecal – oral

Carrier state

30 days low Hygiene

Hep A vac

Hep. B Blood born

Body fluids

Unprotected sex

Drugs & Needles

Health workers

Carrier state

12-14Wk May be fatal Hygiene/Univ perca/

HepBVac

Hep. C

Blood born

Body fluids

Unprotected sex

Drugs & Needles

Health workers

Carrier state

6-7 Wk Chronic hep Univ Per. HCV

interferon

Hep. D

Blood born

Body fluids

Unprotected sex

Drugs & Needles

Health workers

Carrier state

Same as Hep. B Co-infect with

hep.B. risk for

carcinoma

Univ Perc Hygiene

Hep B vaccine

Hep. E Fecal – oral Asia

Africa, India & Mexico

40 days Self limiting risk

increase in

pregnancy

Hygiene sanitation

Hep. F Rare & difficult to diagnose due to lack of testing methodsRare & difficult to diagnose due to lack of testing methodsRare & difficult to diagnose due to lack of testing methodsRare & difficult to diagnose due to lack of testing methods

Hep. G percutaneous - No liver disease Hygiene

Serologic Markers and Antibodies for Hepatitis

  • Serologic markers^ identify presence of virus (HAV,HBsAg, Anti-HBc IgM, HCV,HDV, HEV)
    • Serum HBsAg for longer that 6month => chronic hepatitis or carrier.
  • Hepatitis anti-body^ serum testing serum:^ Anti-HAV, HBsAb, Anti-HCV, Anti-HDV, Anti-HEV.
    • Presence of HBsAb indicates immunity to HBV either from recovery of Hep.B or successful immunity. Medical and Nursing Management of Hepatitis
  • Reduce fatigue (pace nursing activities, rest periods, short but frequent activity)
  • Maintain nutritional and fluid balance (follow I/O, albumin levels, low protein diet, CHOs, small frequent meals)
  • Reduce effects of hepatitis
  • Antiemetics, antihistamines, vitamin K, bile acid sequestrants (Cholysteramine... it binds up bile salts and reduces itchiness, immune globulin (not as common now, using more Interferon), vaccines for other Heps
  • Medications to avoid (chloropromazine, aspirin, acetaminophen, phenothiazine and many sedatives) Sedatives tend to last longer in these pts. Jaundice Management
  • Medical management
  • Determine cause of jaundice
  • Reduce pruritis and maintain skin integrity
  • Oral cholestyramine resin bind salts in GI*
  • Antihistamines*
  • Phenobarbital enhance bile flow (not seen a lot)
  • Nursing management
  • Impaired Skin Integrity, disturbed body image, ineffective health maintenance Jaundice usually clears once you resolve the underlying condition. Usually takes 4-6 weeks.

Complications of Hepatitis

  • Fulminant hepatitis progression of liver necrotic process. Major complications...
    • Jaundice
    • Hepatic encephalopathy occurs b/c of high ammonia levels, decreased LOC, changes in comprehension, don’t know where they are, can go to full coma. Can give mds to bind that up (Lactulose)
    • Ascites: pt may need paracentesis, or give albumin/lasix
  • Chronic hepatitis liver inflammation (drug dosages will need to be adjusted)
    • Chronic active hepatitis B, C are most common ones that cause thsi problem
    • B superimposed with D
  • Chronic carrier state (develop carcinoma)
  • Aplastic anemia a rare complication of hep. (has to deal with the whole problem of not being able to store vitamins normally, esp B-12... and Vit K synthesis) Chronic Hepatitis
  • Chronic hepatitis is liver inflammation > 3- 6 months
  • Chronic active hepatitis (B 5%) & (C 50-70%)
  • B superimposed with D
  • Elevation of AST & ALT > 6 months
  • Drugs & toxins methyldopa, nitrofurantoin, amiodarone & izoniazid
  • Autoimmune following hep. A, Epstein Barr or Measles infections.
  • Metabolic disorders (alcoholic hep.) Liver Cirrhosis Cirrhosis is a chronic progressive disease characterized by widespread fibrosis (scarring) of the liver and nodular formation. In cirrhosis, the normal flow of blood, bile and hepatic metabolites is altered by fibrosis. The pt will have high uncongugated levels and back-up in portal hepatic vein. It is the 10th, leading cause of death in the US. Note that 45% of cases are alcohol related, which means most of the cases are not due to alcohol. Don’t be all judgy with your patients! Though cirrhosis can be life threatening, it can be controlled if discovered early. Cirrhosis Classification by cause
  • Alcoholic or Laennec’s or Micro-nodular (more common in men, most common form in North America)
  • Post-necrotic (macro-nodular or toxin induced, also malaria-treatment drugs)
  • World-wide cirrhosis; more common in in women; causes = chronic viral Hep B/C/D, tyelonol, Isoniazide
  • Biliary (bile duct obstruction, bile stasis and hepatic fibrosis)
  • Primary = disordered immune response damages bile ducts resulting in intrahepatic obstruction
  • Secondary = partial or complete obstruction of the bile duct from gallstones, strictures, pacreatitis, tumors
  • Cardiac (results from prolonged right-side heart failure or constrictive pericarditis) Caput Medusae Caput Medusae is a plexus of dilated veins around the umbilicus. It is seen in patients with portal hypertension that is usually a result of cirrhosis. Medical Management The main goal with cirrhosis is to treat underlying cause…
  • Modify medication doses and trend liver labs of ALT AST Albumin
  • Diet changes (low protein diet to decrease production of ammonia)
  • Monitor for complications
  • GI bleed
  • Renal failure
  • Prevent infection Mortality from hepatitis complications increase with age, especially people over 60 (approaches 90%) A client with liver disease should avoid: Acetaminophen!
  • Fluids/Blood
  • Sclerotherapy (ligate or clip?)
  • Transjugular intrahepatic portosystemic shunt (TIPS)
  • Vasopressin
  • Beta-adrenergic-blocking agents ( propranolol= inderal, metoprolol=lopressor, or nadolol = Corgard.
  • Balloon tamponade (see picture at right) The lecture had various photographs of different esophageal problems which I didn’t use here because they kind of all looked the same to me. The Portacaval Shunt is a procedure to decrease the risk of bleeding. As you can see from the picture, the portal vein is redirected straight into the SVC. This releases the pressure of portal hypertension since some of the blood is now going straight into the SVC and bypassing that high-pressure area. The drawback is that the blood doesn’t get cleaned in the liver like it’s supposed to. A person with this type of shunt will take a long time to metabolize drugs. Another procedure that is done (but not very common) is a LeVeen peritoneovenous shunt. It moves fluid from the peritoneal cavity into the SVC. Liver Failure (leads to...)
  • Hematologic disorders
  • Endocrine disorders
  • Skin disorders
  • Hepatorenal syndrome
  • Hepatic encephalopathy Hepatorenal Syndrome (a type of Liver Failure)
  • Advanced liver failure with ascites^ →^ decrease renal perfusion^ →^ renal failure
  • Progressive azotemia (elevated waste products)
  • Increased serum Cr. Levels
  • Oliguria and urine Na < 10mEq/L
  • Azotemia & elevated levels of Ammonia^ →^ hepatic encephalopathy^ →^ coma.
  • Pts will not respond to diuretic therapy for ascites Hepatic Encephalopathy: Medical Management
  • Identify and treat cause
  • Reduce nitrogenous waste in blood
  • Reduce bacteria in colon
  • Maintain fluid volume balance Liver Failure Management Medications (KNOW THESE MEDS!)
  • Diuretics (Spironalactone, Lasix)
  • Folic acid, thiamine, vitamins, minerals
  • Albumin (increases oncotic pressure to reduce ascites)
  • Lactulose (reduces blood ammonia levels)
  • Neomycin
  • Octreotide (used to decrease flow to blood vessels in GI system, helps to control GI bleed)
  • IV infusion to stop internal hemorrhage and lower splanchic blood flow
  • Bolus: 100 mcg
  • Infusion: 10 mcg/hr Liver Failure Management
  • Eliminating alcohol intake is very very important!
  • Monitor for signs of bleeding (teach patient about bleeding precautions also)
  • Preventing infection
  • Providing sufficient carbohydrate & calories to prevent protein break down (low protein diet!)
  • Correcting fluid & electrolyte imbalance...particularly hypokalemia
  • Decrease GI NH4 (ammonia) by controlling protein intake and administering lactulose to bind ammonia.
  • Liver transplant may be the only effective treatment Black, Joyce M., and Jane Hokanson Hawks. Medical-Surgical Nursing: Clinical Management for Positive Outcomes - Single Volume (Medical Surgical Nursing- 1 Vol (Black/Luckmann)). St. Louis: Saunders, 2009. Print. Brady, D. (2009). Liver Disease Advanced Med/Surg. Lecture conducted from CSU Sacramento, Sacramento. Deglin, Judith Hopfer, and April Hazard Vallerand. Davis's Drug Guide for Nurses, with Resource Kit CD-ROM (Davis's Drug Guide for Nurses). Philadelphia: F A Davis Co, 2009. Print. Medical-Surgical Nursing Made Incredibly Easy! (Incredibly Easy! Series). Philadelphia: Lippincott Williams & Wilkins, 2008. Print. Nettina, Sandra M. Lippincott Manual of Nursing Practice. Philadelphia: Lippincott Williams & Wilkins, 2006. Print Springhouse. Pathophysiology Made Incredibly Easy! (Incredibly Easy! Series). Philadelphia: Lippincott Williams & Wilkins,
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