Which of the following medications would the nurse question for a client with acute pancreatitis?

4. Patient with severe acute pancreatitis who has inspiratory crackles at the lung bases
Patients with acute pancreatitis can develop respiratory complications including pleural effusions, atelectasis, and ARDS. These complications are often due to activated pancreatic enzymes and cytokines that are released from the pancreas into the circulation and cause focal or systemic inflammation. ARDS is the most severe form of these complications and can rapidly progress to respiratory failure within a few hours. Therefore, the presence of inspiratory crackles in this patient could indicate early ARDS and needs to be assessed further for progression.
Fine crackles are a series of distinct, discontinuous, and high-pitched snapping sounds usually heard on inspiration. The sound originates as small atelectatic bronchioles quickly reinflate and can be expected in patients who have undergone abdominal surgery due to shallow breathing related to pain. Although the presence of fine crackles requires treatment, this is not the priority assessment.
Rhonchi are continuous, low-pitched wheezes usually heard on expiration that sound like moaning or snoring. The sound originates from air moving through large airways (bronchi_ filled with mucus secretions are are expected in patients with chronic bronchitis. Although they require treatment, this is not the priority assessment.
The lung under the pleural efusion is compressed, and the breath sounds are decreased/absent if auscultated over the area; this is an expected finding. Until the pleural effusion is treated with diuretics or thoracentesis, these findings will remain unchanged.

1, 2, 4, 5
A client with cirrhosis may experience pruritus (itching) due to buildup of bile salts beneath the skin. Clients with cirrhosis are also at an increased risk for skin breakdown due to the development of edema, which increases skin fragility and impedes wound healing, and the loss of muscle and fat tissue from pressure points (eg, heels, sacrum).

The nurse encourages the client to cut the nails short, wear cotton gloves, and wear long-sleeved shirts to avoid injury to the skin from scratching (Options 2 and 5). Other comfort measures include baking soda baths; calamine lotion; and cool, wet cloths, which cool and soothe irritated skin (Options 1 and 4).

Cholestyramine (Questran) may be prescribed to increase the excretion of bile salts in feces, thereby decreasing pruritus. It is packaged in powdered form, must be mixed with food (applesauce) or juice (apple juice), and should be given 1 hour after all other medications.

(Option 3) Temperature extremes (eg, hot baths/showers) may intensify pruritus. The nurse should instruct the client to bathe with tepid water until the pruritus has subsided.

4
Hypomagnesemia, a low blood magnesium level (normal 1.5-2.5 mEq/L [0.75-1.25 mmol/L]), is associated with alcohol abuse due to poor absorption, inadequate nutritional intake, and increased losses via the gastrointestinal and renal systems. It is associated with 2 major issues:

Ventricular arrhythmias (torsades de pointes): This is the most serious concern (priority).
Neuromuscular excitability: Manifestations of low magnesium, similar to those found in hypocalcemia and demonstrated by neuromuscular excitability, include tremors, hyperactive reflexes, positive Trousseau and Chvostek signs, and seizures.
(Option 1) Constipation and polyuria indicate hypercalcemia. Calcium has a diuretic effect.

(Option 2) Increased thirst with dry mucous membranes indicates hypernatremia.

(Option 3) Hypokalemia results in muscle weakness/paralysis and soft, flabby muscles. Paralytic ileus (abdominal distension, decreased bowel sounds) is also common with hypokalemia. However, the most serious complication is cardiac arrhythmias.

2, 3, 5
Hyperosmolar hyperglycemic state is a serious complication usually associated with type 2 diabetes. With this condition, clients are able to produce enough insulin to prevent diabetic ketoacidosis but not enough to prevent extreme hyperglycemia, osmotic diuresis, and extracellular fluid deficit. Because some insulin is produced, blood glucose rises slowly and symptoms may not be recognized until hyperglycemia is extreme, often >600 mg/dL (33.3 mmol/L). This eventually causes neurological manifestations such as blurry vision, lethargy, obtundation, and progression to coma. Because some insulin is present, symptoms associated with ketones and acidosis, such as Kussmaul respirations (hyperventilation) and abdominal pain, are typically absent (Options 1 and 4).

2, 3, 4
Cirrhosis, the end stage of many chronic liver diseases, is characterized by diffuse hepatic fibrosis with replacement of the normal architecture by regenerative nodules. The resulting structural changes alter blood flow through the liver and decrease the liver's functionality.

Elevated bilirubin (jaundice) results from functional derangement of liver cells and compression of bile ducts by nodules. The liver has a decreased ability to conjugate and excrete bilirubin (Option 3).

Most coagulation factors are produced in the liver. A cirrhotic liver cannot produce the factors essential for blood clotting. As a result, coagulation studies (prothrombin time [PT]/International Normalized Ratio [INR] and activated partial thromboplastin time [aPTT]) are usually elevated (Option 4).

Ammonia from intestinal deamination of amino acids normally goes to the liver and is converted to urea and excreted by the kidney. This does not happen in cirrhosis. Instead, the ammonia level rises as the cirrhosis progresses; ammonia crosses the blood-brain barrier and results in hepatic encephalopathy (Option 2).

(Options 1 and 5) Albumin holds water inside the blood vessels. In cirrhosis, the liver is unable to synthesize albumin (protein), so hypoalbuminemia would be expected. This is the primary reason that fluid leaks out of vascular spaces into interstitial spaces (eg, edema, ascites). The kidneys perceive this as low perfusion and try to reabsorb (conserve) both sodium and water. The large amount of water in the body results in a dilutional effect (low sodium).

3, 4, 5
Paracentesis is performed to remove excess fluid from the abdominal cavity or to provide a specimen of ascitic fluid for diagnostic testing. Paracentesis is not a permanent solution for resolving ascites and is performed only if the client is experiencing impaired breathing or pain due to ascites.

Nursing actions include:
Explain the procedure, sensations, and expected results
Instruct the client to void to prevent puncturing the bladder
Assess the client's abdominal girth, weight, and vital signs
Place the client in high Fowler's position and remain with the client during the procedure
After the procedure, assess and bandage the puncture site and reassess client weight, girth, and vital signs
(Option 1) NPO status is not required for this procedure. Paracentesis is often performed at the bedside or an HCP's office with only a local anesthetic.

(Option 2) Informed consent can be obtained only by an HCP. The nurse can witness informed consent verifying that it is given voluntarily, the signature is authentic, and the client appears competent to consent.

4
The client is exhibiting signs and symptoms (eg, fever, chills, nausea) of septicemia (blood infection). Other findings include a subnormal body temperature instead of fever, hypotension, tachycardia, decreased urine output, and confusion. Although CVCs are warranted to provide important treatment for many clients, they are often a source of infection that can lead to sepsis and septic shock.

It is most important to obtain a culture and sensitivity first so that the specific pathogen can be identified prior to starting antibiotics. Identification of the specific pathogen and the antibiotics to which it is sensitive will allow the health care provider (HCP) to determine the best antibiotic for treatment. If the culture is obtained after antibiotic administration, the results will be altered. In addition to obtaining blood cultures x 2, it is standard procedure to cut off the tip of the discontinued CVC and send it to the lab to ensure it is the source of the septicemia.

Broad-spectrum antibiotics are often prescribed after cultures are obtained to begin treatment and prevent progression to septic shock (Option 1).

(Option 2) It is important to document this occurrence in the client's medical record and to follow hospital protocol for reporting infections. However, implementation of client care is a priority.

(Option 3) Ondansetron may be administered for nausea symptoms. However, treatment of the cause is the most effective way to reduce symptoms; it is a life-saving measure and therefore the priority.

Catheter occlusion is the most common complication of central venous access devices. Kinked tubing, catheter malposition, medication precipitate, or thrombus can occlude the lumen, preventing the ability to flush or aspirate blood.

The nurse should first assess for mechanical, nonthrombotic problems by:

Repositioning the client (eg, head, arm) as the catheter tip may be resting against a vessel wall (Option 4)
Assessing IV tubing for clamps, kinks, and precipitate
The nurse should then attempt to flush the device again. If the occlusion remains, the nurse should not flush against resistance as applying force may damage the catheter or dislodge a thrombus. Instead, the nurse should contact the health care provider (HCP), who may prescribe medication (ie, alteplase) to dissolve a thrombus or fibrin sheath.

(Option 1) Most needleless connector manufacturers recommend flushing with normal saline. Some facilities may use heparinized saline flushes; the nurse should follow HCP prescriptions and institution guidelines. Heparin flushes should be at the lowest acceptable dose (eg, 10 units/mL) to prevent heparin-induced thrombocytopenia.

(Option 2) Flushing with a syringe smaller than 10 mL causes increased intraluminal pressure and may damage the catheter.

(Option 3) The nurse should rule out a mechanical problem before notifying the HCP.

2, 4, 5
Metabolic acidosis is due to an increase in the production or retention of acid or the depletion of bicarbonate via the kidneys or gastrointestinal (GI) tract. In metabolic acidosis there is a decrease in pH (<7.35) and HCO3- (<22 mEq [22 mmol/L]).

Common causes of metabolic acidosis include:

GI bicarbonate losses (eg, diarrhea) (Option 2)
Ketoacidosis (eg, diabetes, alcoholism, starvation)
Lactic acidosis (eg, sepsis, hypoperfusion) (Option 4)
Renal failure (eg, hemodialysis with inaccessible arteriovenous shunt) (Option 5)
Salicylate toxicity
(Option 1) A client with claustrophobia who was stuck in an elevator is at risk for an anxiety attack, which leads to hyperventilation and respiratory alkalosis (pH >7.45, PaCO2 <35 mm Hg [4.66 kPa]).

(Option 3) A client with excessive vomiting is at risk for metabolic alkalosis due to loss of stomach acid.

1
Clients with chronic kidney disease (CKD) have decreased glomerular filtration, resulting in retention of fluid, potassium, and phosphorus. Fluid retention is initially treated with sodium restriction and diuretic therapy. Dietary adjustments should also be made to reduce serum potassium and phosphorus.

Laboratory values are key to determining allowable foods. Dairy products (eg, milk, yogurt) and certain fruits (eg, bananas, oranges, coconuts, watermelons, and avocados) contain high potassium levels. Dairy products also contain high phosphorus levels.

Examples of allowable foods for CKD clients include apples, pears, grapes, pineapple, blackberries, blueberries, and plums.

(Option 2) Avocados are high in potassium; the chips may be high in sodium.

(Options 3 and 4) Pudding and yogurt contain dairy products and are high in phosphorous and potassium. Oranges are high in potassium.

Educational objective:
The diet for a client with chronic kidney disease may need to be restricted in fluids, sodium, potassium, and phosphorus. Dairy products (eg, milk, yogurt) and certain fruits (eg, bananas, oranges, coconuts, watermelons, and avocados) contain high potassium levels. Dairy products are also high in phosphorus.

3, 4, 5
The creation of an AVF for hemodialysis access involves an anastomosis between an artery and a vein (usually the cephalic or basilic vein). The fistula permits the arterial blood to flow through the vein, causing the vein to become larger in diameter and the walls to thicken, enabling blood to flow at high pressures. After the AVF is placed, it takes 2-4 months for it to mature to accommodate the repeated venipunctures necessary for hemodialysis access.

The major complications of an AVF are infection (especially in end-stage kidney disease and diabetes), stenosis, thrombosis, and hemorrhage. Clients are taught the following preventive interventions:

Report numbness or tingling of the extremity to the HCP to prevent neuromuscular damage (Option 1)
Do not allow anyone (other than dialysis personnel) to draw blood or take blood pressure measurements on the extremity to prevent thrombosis (Option 2)
Avoid wearing restrictive clothing or jewelry to prevent thrombosis
Do not use the arm with vascular access to carry heavy objects (more than 5 lb [2.26 kg]); however, exercises to increase strength could include squeezing a soft ball or sponge several times a day (Option 3)
Check the function of the vascular access several times a day by feeling for vibration to assess for patency, stenosis, and clotting (Option 4)
Do not sleep on the arm with vascular access or use creams or lotions on the site (Option 5)
Monitor for signs of infection and bleeding after dialysis and report immediately
Keep the site clean to help prevent infection

2
Nephrotic syndrome, an autoimmune disease, affects children age 2-7 and is characterized by increased permeability of the glomerulus to proteins (eg, albumin, immunoglobulins, natural anticoagulants). Loss of albumin in urine leads to hypoalbuminemia; this causes decreased plasma oncotic pressure, which allows fluid to leak out of the vascular spaces. Reduced plasma volume (hypovolemia) activates kidneys to retain salt and water (renin-angiontensin-aldosterone system). Clients will have generalized edema, weight gain, loss of appetite (from ascites), and decreased urine output. Loss of immunoglobulins makes children susceptible to infection. Treatment typically includes:

Corticosteroids and other immunosuppressants (eg, cyclosporine)
Loss of appetite management by making foods fun and attractive
Infection prevention (eg, limiting social interaction until the child is better) (Option 2)
(Option 1) A regular diet without added salt is prescribed to prevent edema while in remission. More stringent sodium restrictions are necessary when symptoms are present.

(Option 3) Fluid restriction is needed in severe cases of edema.

(Option 4) There is a high risk for recurrence after recovery, and relapses may occur several times per year. The parent/caregiver should test daily for proteinuria, weigh the child weekly, and keep a diary of results. Early detection and treatment improve the course of the illness.

4
Peritoneal dialysis (PD) is a process that uses the abdominal lining (peritoneum) as a semipermeable membrane to dialyze a client whose kidneys are not functioning properly. A catheter is placed in the peritoneal cavity for infusing dialysate (dialysis fluid). Dialysate is infused into the cavity and then the tubing is clamped to allow the fluid to dwell for a specified period. After the specified dwell time, the catheter is unclamped and the fluid (effluent) drains out via gravity. Waste products and electrolytes cross the membrane into the dialysate during the dwell time with the aid of added osmotic agents.

Peritonitis, an infection of the peritoneal cavity, is a major concern with PD. There is also a risk for infection at the catheter exit site, which can lead to peritonitis if untreated. Using sterile technique when spiking and attaching bags of dialysate fluid to the client's catheter is a priority to prevent contamination and decrease the incidence of infection. Any signs of developing complications (eg, cloudy effluent, low-grade fever, redness or tenderness of the exit site) should be reported to the health care provider.

(Option 1) The catheter drainage bag is placed below the level of the abdomen to aid gravity in fluid outflow (effluent). The placement is important but not the highest priority.

(Option 2) The client is typically placed in Fowler's or semi-Fowler's position to utilize gravity. If the outflow becomes sluggish, the client can be turned from side to side to increase flow. The positioning is important but not a priority.

(Option 3) Cloudy effluent indicates infection, bloody effluent indicates possible perforation, and brown effluent indicates suspected bowel perforation. Therefore, documenting the effluent characteristics is important but not a priority over sterile technique (prevention).

3
In CF, unusually thick mucus obstructs the pancreatic ducts, preventing pancreatic enzymes (amylase, trypsin, and lipase) from reaching the small intestine. The result is malabsorption of carbohydrates, fats, and proteins; the inability to absorb fat-soluble vitamins (A, D, E, and K) is of particular concern. Gastrointestinal signs and symptoms of CF include flatulence, abdominal cramping, ongoing diarrhea, and/or steatorrhea.

Nutritional therapy includes the administration pancreatic enzyme supplements with or just before every meal or snack (Option 2). These enzymes are enteric-coated beads designed to dissolve only in an alkaline environment similar to that of the small intestine. They must not be mixed with a substance that would cause them to dissolve prior to reaching the jejunum. Capsule contents may be sprinkled on applesauce, yogurt, or acidic, soft, room-temperature foods with pH <4.5. Capsules should be swallowed whole and not crushed or chewed; chewing the capsules could cause irritation of the oral mucosa. Excessive intake of pancreatic enzymes can result in fibrosing colonopathy (Option 1).

(Option 4) This is a true statement; some children have difficulty taking a whole capsule. Capsule contents can be sprinkled in acidic substances such as applesauce. Capsules should not be taken with milk as they can cause it to curdle.

2, 4, 5
In a client with cirrhosis and ascites, discomfort is often due to pressure of the fluid on the surrounding organs. Shortness of breath occurs due to the upward pressure exerted by the abdominal ascites on the diaphragm, which restricts lung expansion.

Positioning the client in semi-Fowler or Fowler position can promote comfort, as this position can reduce the pressure on the diaphragm (Option 2). In semi-Fowler position, the head of the bed is elevated 30-45 degrees; in Fowler position, elevation is 45-60 degrees. Side-lying with the head elevated can also be a position of comfort for the client with ascites as it allows the heavy, enlarged abdomen to rest on the bed, reducing pressure on internal organs and allowing for relaxation.

Meticulous skin care is a priority due to the increased susceptibility of skin breakdown from edema, ascites, and pruritus. It is important to use a specialty mattress and implement a turning schedule of every 2 hours (Option 4).

A distraction can take the client's mind off the current symptoms and may also help promote comfort in many different situations. Some of these distractions include listening to music, watching television, playing video games, or taking part in hobbies (Option 5).

(Option 1) This client has ascites and peripheral edema; higher levels of fluid or sodium intake can worsen these conditions.

(Option 3) In Trendelenburg position, the bed is tilted with the head lower than the legs. This position is contraindicated in the client with ascites, as it may exacerbate shortness of breath by causing the abdominal ascites to push upward on the diaphragm, restricting lung expansion.

2, 3, 5
ALT and AST are the enzymes released when hepatic cells are injured (hepatitis). There are smaller amounts in the cardiac, renal, and skeletal tissues, but ALT/AST are used to diagnose hepatic disorders. Besides viral hepatitis, liver injury can occur with excessive chronic alcohol intake (Option 3), some over-the-counter medications (eg, acetaminophen), and certain herbal and dietary supplements (Option 5). IV illicit drug use increases the risk for hepatitis B and C infection (Option 2).

(Option 1) Black tarry stool (melena) is an expected finding from a gastrointestinal bleed (from the digested blood). Melena can be seen in clients with gastric or esophageal varices, which are often complications of hepatic disease (eg, cirrhosis). However, melena is not an etiology of liver injury.

(Option 4) Immunizations do not cause liver damage. It is possible to get a small elevation with an intramuscular injection, but not values this high.

4
Hypomagnesemia, a low blood magnesium level (normal 1.5-2.5 mEq/L [0.75-1.25 mmol/L]), is associated with alcohol abuse due to poor absorption, inadequate nutritional intake, and increased losses via the gastrointestinal and renal systems. It is associated with 2 major issues:

Ventricular arrhythmias (torsades de pointes): This is the most serious concern (priority).
Neuromuscular excitability: Manifestations of low magnesium, similar to those found in hypocalcemia and demonstrated by neuromuscular excitability, include tremors, hyperactive reflexes, positive Trousseau and Chvostek signs, and seizures.
(Option 1) Constipation and polyuria indicate hypercalcemia. Calcium has a diuretic effect.

(Option 2) Increased thirst with dry mucous membranes indicates hypernatremia.

(Option 3) Hypokalemia results in muscle weakness/paralysis and soft, flabby muscles. Paralytic ileus (abdominal distension, decreased bowel sounds) is also common with hypokalemia. However, the most serious complication is cardiac arrhythmias.

2
Total parenteral nutrition (TPN) is administered via a central venous catheter to meet the nutritional needs (eg, glucose, amino acids, vitamins, minerals) of clients who cannot digest nutrients via the gastrointestinal tract. The nurse should hang 10% dextrose in water at the same infusion rate of 75 mL/hr until the new bag arrives. If the 20% dextrose solution is temporarily replaced with an infusion lacking dextrose (eg, normal saline, lactated Ringer's [LR]), the pancreas will continue to produce insulin in response to the residual glucose, which may cause hypoglycemia (Option 2).

(Option 1) The infusion of 0.9% saline solution without dextrose can lead to hypoglycemia. Rapid infusion (150 mL/hr) of the hypertonic TPN solution can increase the risk for fluid overload and hyperglycemia. The nurse should never increase the rate of central TPN to make up for volume lost during previous hours.

(Option 3) Dextran in saline solution is a colloid used to expand intravascular volume in clients with hypovolemia. It can cause fluid overload and so is not an appropriate action.

(Option 4) LR contains electrolytes but no glucose; hypoglycemia may result.

Educational objective:
Abrupt cessation of central total parenteral nutrition (TPN), which usually contains 20%-50% dextrose, increases the risk for hypoglycemia, as the pancreas will continue to produce insulin in response to the residual glucose. When TPN is discontinued, the infusion rate is gradually reduced and then replaced with a solution containing dextrose.

1, 3, 5
Viral hepatitis is a disease of the liver characterized by inflammation, necrosis, and cirrhosis. One of the most common viral strains that causes hepatitis is hepatitis B. The transmission of hepatitis B is primarily through contact with blood, semen, and vaginal secretions (mnemonic: B for body fluids), commonly through unprotected sexual intercourse and intravenous illicit drug use (Options 1, 3, and 5). Infants born to infected mothers are also at risk for vertical transmission of hepatitis B. Although kissing, sneezing, sharing drinks/utensils, and breastfeeding are not known routes of transmission, hepatitis B could possibly be transmitted through saliva entering the bloodstream via sharing a toothbrush or receiving a bite.

Hepatitis B has an insidious onset of illness, and clients may be asymptomatic carriers. Early symptoms are often nonspecific (eg, malaise, nausea, vomiting, abdominal pain). Hepatitis B may produce jaundice, weight loss, clay-colored stools, and thrombocytopenia in late stages of illness. An effective vaccine is widely available for hepatitis B.

(Option 2) The transmission of hepatitis A occurs through the fecal-oral route via poor hand hygiene and improper food handling. Therefore, this infection is seen primarily in developing countries. Hepatitis B is not transmitted through feces.

(Option 4) Urine is not known to be a mode of transmission for any form of hepatitis.

Educational objective:
The transmission of hepatitis B occurs through parenteral or sexual contact with body fluids such as blood, semen, or vaginal secretions (mnemonic: B for body fluids).

1, 2, 3, 5
Inflammation of the liver is present in acute viral hepatitis. Liver functions (eg, detoxifying the blood, manufacturing bile for lipid digestion) are disrupted, leading to signs and symptoms in various body systems. These include the digestive (eg, nausea, vomiting, anorexia, right upper-quadrant tenderness), urinary (eg, dark-colored urine), musculoskeletal (eg, fatigue, arthralgia, myalgia), and integumentary (eg, pruritus, jaundice) systems.

Nursing interventions for the acute phase of hepatitis focus on resting the liver and providing nutrition for healing:

Rest
Alternate periods of rest and activity (Option 3)
Avoid alcohol and other drugs that increase liver metabolism (Option 5)
Medications (eg, appetite stimulants, antipruritics, analgesics) should be used cautiously to allow hepatocytes to heal. Antiemetics can be used to prevent nausea (Option 1).
Nutrition
Encourage small, frequent meals to decrease nausea. Anorexia is lowest in the morning; promote eating a larger breakfast (Option 2).
Provide oral care and avoid extremes in food temperature to increase appetite
Drink adequate amounts of fluid (2500-3000 mL/day) and encourage a diet high in carbohydrates and calories
(Option 4) Clients with acute hepatitis should eat a diet high in calories and carbohydrates while decreasing fat and protein consumption. The liver produces bile, which aids in lipid digestion. A high-protein diet produces more ammonia and other toxic substances and the inflamed liver may not detoxify these well. Moderation of fat and protein intake allows the liver to rest.

Educational objective:
Acute viral hepatitis is treated with supportive measures, including rest (alternate activity and rest), avoiding alcohol and hepatotoxic medications, and adequate nutrition (increase calories and carbohydrates; eat small, frequent meals). Clients should reduce their consumption of fats and proteins, which increase liver metabolism.

1, 2
Hepatic encephalopathy (HE) is a frequent complication of liver cirrhosis. Precipitating factors include hypokalemia, constipation, gastrointestinal hemorrhage, and infection. It results from accumulation of ammonia and other toxic substances in blood.

Clinical manifestations of HE range from sleep disturbances (early) to lethargy and coma. Mental status is altered, and clients are not oriented to time, place, or person (Option 1). A characteristic clinical finding of HE is presence of asterixis (flapping tremors of the hands). It is assessed by having the client extend the arms and dorsiflex the wrists (Option 2). Another sign is fetor hepaticus (musty, sweet odor of the breath) from accumulated digestive byproducts.

(Option 3) Spider angiomas (eg, small, dilated blood vessels with bright red centers), gynecomastia, testicular atrophy, and palmar erythema are expected findings in cirrhosis due to altered metabolism of hormone in the liver.

(Option 4) Jaundice occurs when bilirubin is 2-3 times the normal value. Jaundice can occur in hepatitis and tends to worsen in cirrhosis due to increasing functional derangement. It is not related specifically to encephalopathy.

(Option 5) Amylase and lipase are enzymes from pancreatic tissue. Alanine aminotransferase and aspartate aminotransferase are liver enzymes. They would be elevated with hepatitis and are not unique to cirrhosis or HE. Elevated ammonia levels would be more specific to cirrhosis.

Educational objective:
HE manifests with sleep disturbances, altered mental status, and lethargy. Asterixis and elevated ammonia are characteristic of HE.

D. Hypercalcemia
Major Takeaway
Acute pancreatitis is most commonly caused by alcohol use or gallstones. Other risk factors for acute pancreatitis include hypercalcemia and hypertriglyceridemia.

Main Explanation
This patient has acute pancreatitis, which is likely to be secondary to hypercalcemia due to hyperparathyroidism. Commonly, patients report acute upper abdominal pain that radiates to the back. These symptoms may persist for days. Diagnostically, serum amylase and lipase concentrations rise within 4-8 hours of onset more than three times the upper limit of normal.

The two most common causes of acute pancreatitis are gallstones and alcoholism. Other common causes of acute pancreatitis include hypertriglyceridemia, hypercalcemia (as in this patient), trauma, steroid use, endoscopic retrograde cholangiopancreatography, and drugs such as 6-mercaptopurines, aminosalicylates, valproic acid, and pentamidine.

Mnemonic: GET SMASHED. This stands for Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hyperlipidemia, ERCP,and Drugs.

A. Alanine aminotransferase (ALT)

Major Takeaway
Cirrhosis is characterized by fibrosis and disruption of normal liver architecture. ALT is believed to be more specific than AST in diagnosing hepatic pathology.

Main Explanation
Cirrhosis of the liver is characterized by fibrosis and disruption of normal liver architecture. It is among the top 10 causes of death in the western world. Common causes of cirrhosis are alcohol abuse, chronic infection, autoimmune hepatitis, biliary disease, and iron overload. Pathogenesis includes the replacement of type IV collagen in the perisinusoidal space (space of Disse) with type I and III collagen. Sinusoids in liver vasculature are lost, leading to decreased solute exchange and increased portal blood pressure. Liver enzymes, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase, are released from damaged hepatocytes and consequently elevated in serum. ALT is found mainly in the cytosol of hepatocytes and in very low levels in other tissues. Therefore, ALT is more specific than other liver enzymes in diagnosing hepatic injury.

A. Aspartate aminotransferase of 120 U/L and alanine aminotransferase of 60 U/L

Major Takeaway
Alcoholic hepatitis is inflammation of the liver that results in elevated aspartate aminotransferase and alanine aminotransferase levels. They are classically elevated in a 2:1 ratio.

Main Explanation
Alcoholic hepatitis is a progressive inflammatory liver condition secondary to excessive alcohol intake. Patients with symptomatic or acute alcoholic hepatitis are generally characterized by nonspecific symptoms such as nausea, malaise, and a low-grade fever. Complications of underlying cirrhosis can be observed and include variceal bleeding, encephalopathy, or ascites. Variceal bleeding can lead to the presence of melanotic stools. Physical examination may show tachycardia, fever, hepatomegaly, and mild right upper quadrant tenderness due to the inflammatory process in the liver. Symptoms of chronic liver disease or alcohol withdrawal may also be present.

The diagnosis of alcoholic hepatitis requires a history of alcohol use, symptoms, and physical examination findings consistent with the disease, and laboratory studies revealing elevated liver enzymes. In alcoholic hepatitis, aspartate aminotransferase concentration is elevated relative to alanine amino aspartate - classically by a degree of 2:1 AST:ALT. Other laboratory studies may reveal a neutrophilic leukocytosis, anemia, and thrombocytosis. However, thrombocytopenia is also possible from bone marrow suppression or portal hypertension causing splenic sequestration. Patients with mild alcoholic hepatitis have a good prognosis with the cessation of alcohol. Patients with hepatic encephalopathy; however, have as high as a 50% chance of early death within 30 days of presentation.

B. Biliary atresia

Major Takeaway
Neonates with biliary atresia initially are characterized by jaundice anytime between birth and eight weeks of age and is unlikely to appear later. Other signs can include acholic stools, dark urine, increased conjugated bilirubin, and increases in serum aminotransferases.

Main Explanation
Atresia is a condition in which a passage in the body is abnormally closed or absent. Biliary atresia (BA) is a progressive disease of the extrahepatic biliary tree that is characterized by biliary obstruction in the neonatal period. Most infants with biliary atresia are born at full term, have a normal birth weight, and initially thrive and seem normal and healthy. Patients with biliary atresia initially are characterized by jaundice anytime between birth and eight weeks of age and is unlikely to appear later. Other symptoms and signs can include acholic stools, dark urine, increased conjugated bilirubin, and mild or moderate increases in serum aminotransferases.

Diagnosis of BA is made with a series of imaging, lab tests, and liver biopsy to exclude other causes of cholestasis in the neonate. Ultrasound imaging may show triangular cord sign, which is highly suggestive of biliary atresia. The sign represents the fibrous ductal remnant of the extrahepatic bile duct in biliary atresia. Confirmed BA is treated with a hepatoportoenterostomy, a procedure in which a roux-en-Y loop of bowel is created and directly anastomosed to the hilum of the liver. The biliary remnant and portal fibrous plate are removed during surgery

A 65-year-old man with a history of alcoholic cirrhosis and ascites comes to the emergency department because of 7 days of worsening confusion and impaired memory. For the past 2 days, he has been increasingly agitated at night and spends a large portion of the daytime asleep. He denies diarrhea, melena, hematemesis, impaired balance, and double vision. He takes no medications. His temperature is 37.7°C (100°F), pulse is 90/min, respirations are 16/min, and blood pressure is 130/74 mm Hg. Abdominal examination shows a tender, distended abdomen with shifting dullness. The rest of the examination and a computed tomography scan of the head show no other abnormalities. Urinalysis and fecal occult blood test show no abnormalities. Serum laboratory results are shown below:

Ethanol: 0.0 mg/dL
Leukocytes: 8,500/mm3
Total bilirubin: 0.9 mg/dL
AST: 75 U/L
ALT: 62 U/L
Phosphatase (alkaline): 87 U/L

Which of the following is the most appropriate diagnosis?

A. Alzheimer dementia
B. Hepatic encephalopathy
C. Intracranial hemorrhage
D. Urinary tract infection
E. Wernicke encephalopathy

Which of the drug of choice for pain controls the patient with acute pancreatitis?

What would the nurse note as typical findings on the assessment of client with acute pancreatitis?

Which of the following medications is used to treat acute pancreatitis with necrosis and infection?

Which medication is administered to a patient with acute pancreatitis to decrease gastric acid secretion?