NURS 6501 Module 3 Knowledge Check Quiz

Question 1

A 45-year-old male comes to the clinic with a chief complaint of epigastric abdominal pain that has persisted for 2 weeks. He describes the pain as burning, non-radiating and is worse after meals. He denies nausea, vomiting, weight loss or obvious bleeding. He admits to bloating and frequent belching.

PMH-+ for osteoarthritis, seasonal allergies with frequent sinusitis infections.

Meds-Zyrtec 10 mg PO daily and takes it year-round, ibuprofen 400-600 mg po prn pain

Family Hx-non contributory

Social history-recently divorced and expressed concern at how expensive it is to support 2 homes. Works as a manager at a local tire and auto company. He has 25 pack/year history of smoking, drinks 2-3 beers/day, and drinks 5-6 cups of coffee per day. He denies illicit drug use, vaping or unprotected sexual encounters.

Breath test in the office revealed + urease.

The healthcare provider suspects the client has peptic ulcer disease.

1 of 2 Questions: What factors may have contributed to the development of PUD?

Correct Answer: Stress secondary to divorce and financial situation, cigarette smoking, alcohol consumption, use of NSAIDS, excess coffee consumption, +H Pylori test

Question 2

PMH-+ for osteoarthritis, seasonal allergies with frequent sinusitis infections.

Meds-Zyrtec 10 mg po daily and takes it year-round, ibuprofen 400-600 mg po prn pain

Family Hx-non contributary

Breath test in the office revealed + urease.

The healthcare provider suspects the client has peptic ulcer disease.

2 of 2 Questions: How do these factors contribute to the formation of peptic ulcers?

Correct Answer: Chronic use of NSAIDS causes suppresses of mucosal prostaglandin and direct irritative topical effect. High gastrin level and excessive gastric acid production © 2020 Walden University 2 often seen in Zollinger-Ellison syndrome which can caused by gastrinoma. Smoking impairs healing by vasoconstriction. H Pylori causes gastritis and interferes with mucosa

Question 3

A 36-year-old morbidly obese female comes to the office with a chief complaint of “burning in my chest and a funny taste in my mouth”. The symptoms have been present for years but patient states she had been treating the symptoms with antacid tablets which helped until the last 4 or 5 weeks. She never saw a healthcare provider for that. She says the symptoms get worse at night when she is lying down and has had to sleep with 2 pillows. She says she has started coughing at night which has been interfering with her sleep. She denies palpitations, shortness of breath, or nausea.

PMH-HTN, venous stasis ulcers, irritable bowel syndrome, osteoarthritis of knees, morbid obesity (BMI 48 kg/m²)

Family history-non contributary

Medications-amlodipine 10 mg po qd, dicyclomine 20 mg po, ibuprofen 600 mg po q 6 hr prn

Social hx- 15 pack/year history of smoking, occasional alcohol use, denies vaping

The health care provider diagnoses the patient with gastroesophageal reflux disease (GERD).

Question: The client asks the APRN what causes GERD. What is the APRN’s best response?

Correct Answer: GERD manifestations result directly from gastric acid reflux into the esophagus. Pyrosis, the classic symptom, is a substernal burning sensation typically described as heartburn. It may be accompanied by regurgitation, particularly in someone who has recently eaten. The lower esophageal sphincter (LES) relaxes due to certain medications (calcium channel blockers), hiatal hernia, and obesity allows stomach contents to enter the lower esophagus causing inflammation and possibly erosion of the esophagus.

Question 4

A 34-year-old construction worker presents to his Primary Care Provider (PCP) with a chief complaint of passing foul smelling dark, tarry stools. He stated the first episode occurred last week, but it was only a small amount after he had eaten a dinner of beets and beef. The episode today was accompanied by nausea, sweating, and weakness. He states he has had some mid epigastric pain for several weeks and has been taking OTC antacids. The most likely diagnosis is upper GI bleed which won’t be confirmed until further endoscopic procedures are performed.

Question: What factors can contribute to an upper GI bleed?

UGI bleeds can be caused by Peptic ulcer disease (PUD) which remains the most common cause of UGIB. Esophageal bleeding from a Mallory-Weiss tea.

Question 5

A 64-year-old steel worker presents to his Primary Care Provider (PCP) with a chief complaint of passing bright red blood when he had a bowel movement that morning. He stated the first episode occurred last week, but it was only a small amount after he had eaten a dinner of beets and beef. The episode today was accompanied by nausea, sweating, and weakness. He states he has had some left lower quadrant pain for several weeks but described it as “coming and going”. He says he has had a fever and abdominal cramps that have worsened this morning. The likely diagnosis is lower GI bleed secondary to diverticulitis.

Question: What can cause diverticulitis in the lower GI tract?

Correct Answer: Diverticulitis is defined as an inflammation of one or more diverticula. Fecal material or undigested food particles may collect in a diverticula causing obstruction. The obstruction can cause vascular compromise. Increased intraluminal pressure or food particles cause erosion of the diverticular wall, resulting in inflammation, localized necrosis, and perforation.

Question 6

Question: How does cirrhosis cause portal hypertension?

Correct Answer: Portal hypertension results from an increase in resistance or blood flow in the portal venous system. In cirrhosis, the most common cause of portal hypertension is the formation of scar tissue and regenerative nodules that lead to an increase in intrahepatic vascular resistance and, consequently, portal pressure. Hepatitis and the resultant inflammation and subsequent scarring also contributes to portal hypertension. Chronic right sided heart failure can also cause portal hypertension due to the increase in preload that the right ventricle cannot pump effectively

Question 7

A 48-year-old man presents to his gastroenterologist for increasing abdominal girth and increasing jaundice. He has a long history of alcoholic cirrhosis and has multiple admissions for encephalopathy and GI bleeding from esophageal varices. He has been diagnosed with portal hypertension. The increased abdominal girth has been progressive, and he says it is getting hard to breathe. The APRN reviews his last laboratory data and notes that the total protein is 4.6 gm/dl and the albumin is 2.9 g/dl. Upon exam, he has icteric sclera, jaundice, and abdominal spider angiomas. There is a significant fluid wave when percussed. The APRN tells the patient that he has ascites.

Question: Discuss how ascites develops as a result of portal hypertension.

Correct Answer: There are several theories that contribute to ascites. In the underfilling theory, the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a subsequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention. The overflow theory postulates that increased portal pressure, along with decreased serum albumin, cause capillary hydrostatic pressure to exceed capillary oncotic pressure, pushing transudative fluid into the peritoneal cavity

Question 8

A 45-year-old man with known alcoholic cirrhosis, portal hypertension, and ascites is brought to the ED by his family due to increasing confusion. The family states that he had been stumbling for several days but had not fallen. The family also noted that he had been “flapping his hands” as well. Labs in the ED reveal Hgb 9.4 g/dl, Hct 28.0 %, ammonia (NH₃) level is 159 μmol/L. The APRN informs the family that the patient has developed hepatic encephalopathy (HE).

Question: Explain how hepatic encephalopathy develops in patients with cirrhosis of the liver.

Correct Answer: HE develops from a combination of biochemical alterations that affect neurotransmissions. Liver disfunction and collateral vessels that shunt blood around the liver. This allows neurotoxins and other harmful substances that are absorbed from the GI track to accumulate and circle freely to the brain. The substances include inflammatory cytokines, short-chain fatty acids, serotonin, tryptophan and false neurotransmitters. The most harmful substances are the end products of protein digestion, especially ammonia (NH3) that cannot be converted to urea by a diseased liver. The blood that is digested from leaking or ruptured vessels add to the amount of ammonia in the gut. Ammonia that reaches the brain is metabolized into glutamine which causes changes in osmotic disturbances and alterations in cerebral blood flow causing cerebral edema.

Question 9

A 65-year-old man with a history of atrial fibrillation presents to his PCP’s office 2 months after suffering from a myocardial infarction.  He declined anticoagulation due to fear he would bleed to death. He has had sudden-onset, moderately severe diffuse abdominal pain that began 18 hours ago. He has been vomiting, and he has had several episodes of diarrhea, the last of which was bloody. He has a fever of 100.9 ˚ F. CBC reveals WBC of 15,000/mm^3.

Question: What is the most likely mechanism behind his current symptoms?

Correct Answer: Thrombosis of the superior mesenteric artery, whether due to thrombotic or embolic origin, causes a sudden decrease or interruption in the primary blood flow to most of the small bowel as well as the ascending colon. This disruption leads © 2020 Walden University 6 to malperfusion of the involved end organ leading to ischemia and, ultimately, infarction. Elderly patients are at risk due to atherosclerosis which lead to thrombus formation. Embolic origins usually arise from cardiac arrythmias, usually atrial fibrillation, which leads to pooling of the blood in the atria.

Question 10

A 46-year-old Caucasian female presents to the PCP’s office with a chief complaint of severe, intermittent right upper quadrant pain for the last 3 days. The pain is described as sharp and has occurred after eating french fries and cheeseburgers and radiates to her right shoulder. She has had a few episodes of vomiting “green stuff”. States had fever and chills last night which precipitated her trip to the office. She also had some dark orange urine, but she thought she was dehydrated. Physical exam: slightly obese female with icteric sclera as well as generalized jaundice. Temp 101˚F, pulse 108, respirations 18. Abdominal exam revealed rounded abdomen with slightly hypoactive bowel sounds. + rebound tenderness on palpation of right upper quadrant. No tenderness or rebound in epigastrium or other quadrants. Labs demonstrate elevated WBC, elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Serum bilirubin (indirect) 2.5 mg/dl. Abdominal ultrasound demonstrated enlarged gall bladder, dilated common bile duct and multiple stones in the bile duct. The APRN diagnoses the patient with acute cholecystitis and refers her to the ED for further treatment.

Question 1 of 2: Describe how gallstones are formed and why they caused the symptoms that the patient presented with.

Correct Answer: Gallstones are formed from impaired metabolism of cholesterol, bilirubin, and bile acids. Gallstones are always composed of cholesterol, unconjugated bilirubin, bilirubin salts, fatty acids, calcium carbonates and phosphates and mucin glycoproteins. Gallstones form in bile that is supersaturated and can begin the process of cholesterol crystal formation. More crystals aggregate thus enlarging and forming stones. These stones may lie dormant or start to move down the cystic or common bile duct. These stones can cause biliary stasis, bacterial infections, biliary parasites.

Question 11

Question 2 of 2: Explain how the patient became jaundiced.

Correct Answer: In extrahepatic jaundice, the common bile duct is obstructed, usually by gallstones, tumor or inflammation. The bilirubin conjugated by the hepatocytes cannot flow through the obstructed common bile duct into the duodenum. It begins to accumulate in the liver and enters the bloodstream, causing hyperbilirubinemia and jaundice.

Question 12

Ruth is a 49-year-old office worker who presents to the clinic with a chief complaint of abdominal pain x 2 days. The pain has significantly increased over the past 6 hours and is now accompanied by nausea and vomiting. The pain is described as “sharp and boring” in mid epigastrum and radiates to the back. Ruth admits to a long history of alcohol use, and often drinks up to a fifth of vodka every day.

Physical Exam:

Temp 102.2F, BP 90/60, respirations 22. Pulse Oximetry 92% on room air.

General: thin, pale white female in obvious pain and leaning forward. Moving around on exam table and unable to sit quietly.

CV-tachycardic. RRR without gallops, rubs, clicks or murmurs

Resp-decreased breath sounds in both bases with poor inspiratory effort

Abd- epigastric guarding with tenderness. No rebound tenderness. Negative Cullen’s and + Turner’s signs observed. Hypoactive bowel sounds x 2 upper quadrants, and no bowel sounds heard in both lower quadrants.

The APRN makes a tentative diagnosis of acute pancreatitis based on history and physical exam and has the patient transferred to the ER where laboratory and radiographic exams reveal acute pancreatitis.

Question: Explain how pancreatitis develops and the role alcohol played in this patient’s case.

Correct Answer: The pancreatic acinar cells metabolize ethanol with the generation of toxic metabolites that injure pancreatic acinar cells, causing release of active enzymes. This causes formation of protein plugs in the pancreatic ducts and spasm of the sphincter of Oddi which result in obstruction. The destruction leads to intrapancreatic release of activated enzymes, autodigestion, inflammation and pancreatitis. © 2020 Walden University 8 Inflammation of the pancreas leads to systemic effects that are associated with moderately and severely acute pancreatitis. Proinflammatory cytokines and vasoactive peptides are released into the blood stream. There is activation of leukocytes, injury to vessel wall and coagulation abnormalities with development of vasodilation and shock.

Question 13

A 23-year-old bisexual man with a history of intravenous drug abuse presents to the clinic with a chief complaint of fever, fatigue, loss of appetite, nausea, vomiting, abdominal pain, and dark urine. He says the symptoms started about a month ago and have gotten steadily worse. He admits to reusing needles and had unprotected sexual relations with a man “a couple months ago”.

PMH-noncontributory.

Social/family history-works occasionally as a night clerk in a hotel. Parents without illnesses. Admits to bisexual sexual relations and intravenous heroin use. He has refused drug rehabilitation. 3 year/pack history of tobacco but denies vaping.

Physical exam unremarkable except for palpable liver edge 2 fingerbreadths below costal margin. No ascites or jaundice appreciated.

The APRN suspects the patient has Hepatitis B given the strong history of risk factors. She orders a hepatitis panel which was positive for acute Hepatitis B.

Question: What are the important hepatitis markers that indicated the patient had acute hepatitis B

Correct Answer: When looking at any hepatitis panel, it is important to remember that Ag=antigen=acute phase of infection and Ab=antibody=past or chronic phase

In Hepatitis B, there are 3 antigens: Surface-+ for acute infection: Core-IgM antiHBc indicates acute infection & IgG anti-HBc remains + for life: e indicates current infectivity-HBeAg

Hepatitis B surface antigen (HBsAg)- the presence of HBsAg indicates that the person is infectious. It can be detected in high levels in serum during acute or chronic HBV infection.

Hepatitis B surface antibody (anti-HBs): The presence of anti-HBs generally indicates recovery and immunity from HBV infection. Anti-HBs also develops in a person who has been successfully vaccinated against hepatitis B.

Total hepatitis B core antibody (anti-HBc): Appears at the onset of symptoms in acute hepatitis B and remains for life.

IgM antibody to hepatitis B core antigen (IgM anti-HBc): Positivity indicates recent and infection with HBV (≤6 months)

Hepatitis B e antigen (HBeAg): The presence of HBeAg indicates that the virus is replicating

Question 14

Hannah is a 19-year-old college sophomore who came to Student Health with a chief complaint of lower abdominal pain. She says the pain has been present for 2 months and she has had multiple episodes of diarrhea alternating with constipation, and anorexia. She says she has lost about 10 pounds in these 2 months without dieting. The abdominal pain has gotten worse in the last 2 hours, but she thought she had “the GI bug” like other students at her Synagogue had.

Physical exam-noncontributory except for the abdomen which was lightly distended with no visible masses. Normoactive BS x 4. Diffuse tenderness throughout but increased pain on deep palpation LUQ & LLQ. Slight guarding but no rebound tenderness or rigidity.

Rectal-tight anal sphincter and patient grimacing in pain during exam. Slightly + guaiac stool.

Based on her history and current symptoms, the APN arranges for a consult with a gastroenterologist who diagnoses Hannah with ulcerative colitis (UC).

Question: How does ulcerative colitis develop in a susceptible person?

Correct Answer: It is thought to occur in individuals with genetic predispositions, environmental risk factors, and the immune system. Several genes likely play a role; their products, when combined with environmental factors and dysfunctional immunity, can lead to UC. In normal patients’ colonic mucosa, phagocytic cells do not respond to the normal flora. In patients with inflammatory bowel disease, these phagocytes may begin to respond to gut flora, secreting proinflammatory cytokines that activate a certain population of T cells. This results in mucosal inflammation and damage. Ulcerative colitis (UC) is usually limited to the colon, but in severe cases, may involve the entire colon up to the cecum. Typically, inflammation begins at the rectum and continuously involves all or part of the colon. The lesions are limited to the mucosa, are not transmural, and do not involve skip lesions. It is a disease with many active and dormant periods and many patients can be managed with medications. Other patients have disease that is so fulminant that it causes damage to the epithelial mucosal barrier with leaks of fluid in the gut, which can lead to peritonitis.

Question 15

A 64-year-old woman with long standing coronary artery disease presents to the clinic with lower extremity swelling, abdominal distension, and shortness of breath. Patient states she has a 30-pound weight gain in 6 weeks and is now requiring 3 pillows to sleep.

On physical exam the patient is a well-developed, well-nourished female exhibiting signs of respiratory distress with use of accessory muscles. Blood pressure 150/80, pulse 105, respirations 28 and labored. Body weight 89 kg. HEENT was unremarkable. Cardiac exam had an S1, S2 and S3 without S4 or murmur. Respiratory exam was positive for bilateral rales 1/2 up both lung fields. Abdomen was enlarged with a positive fluid wave. Lower extremities were remarkable for 3+ pitting edema.

Laboratory data was significant for an increase in K+ from 3.4 mmol/l to 6.1 mmol/l in 2 weeks, BUN increased from 18 mg/dl to 104 mg/dl, and creatinine increased from 0.8 mg/dl to 6.9 mg/dl.

CXR revealed congestive heart failure. The APRN calls the cardiologist on call who admits the patient to the hospital and orders a nephrology consult.

She was diagnosed with exacerbation of congestive heart failure (CHF) and acute kidney injury (AKI).

Question: What type of acute kidney injury does the patient have and what factors contributed to this diagnosis?

Correct Answer: The patient has pre-renal AKI most likely secondary to decreased cardiac output from CHF. Glomerular pressure depends primarily on renal blood flow (RBF) and is controlled by the combined resistances of renal afferent and efferent arterioles. Decreased renal blood flow causes hypoxia of the cells. Volume loss, which results in decreased renal blow flow can be caused by sepsis, hemorrhage, decreased cardiac output, sequestration of fluids in severe burns, multiple organ dysfunction, renal vasoconstriction (caused by nonsteroidal anti-inflammatory drugs or radiographic contrast materials), renal artery stenosis, or kidney edema that restricts renal arterial blood flow. Initially, during periods of hypoperfusion, autoregulatory mechanisms maintain glomerular filtration rate (GFR) at a relatively constant level through afferent arteriolar dilation and efferent arteriolar vasoconstriction. The GFR eventually declines due to decreases in filtration pressure. Prolonged decreases in blood volume or blood pressure results in cellular injury, acute tubular necrosis, and apoptosis, or acute interstitial necrosis, which is a severe form of AKI.

Question 16

The APRN is giving a pathophysiology lecture to APRN students on renal blood flow, related hormones, and glomerular filtration rate.

Question: What would be the most important concept of glomerular filtration rate that the APRN should address?

Correct Answer: Renal blood flow (RBF) and glomerular filtration are important aspects of maintaining normal kidney functions. A delicate balance exists between renal blood flow and the glomerular filtration rate as changes in one may affect the other.  The kidneys receive approximately 20-25% of the cardiac output (CO) which is about equal to 1000- 1200 cc/minute. With normal blood pressure and hematocrit, about 700 cc of the blood flowing through the kidney is plasma. The filtration of the plasma per unit of time is called the glomerular filtration rate. The GFR is directly related to the perfusion pressure in the glomerular capillaries.

Question 17

The APRN is giving a pathophysiology lecture to APRN students on renal blood flow, glomerular filtration rate, autoregulation, and related hormone factors regulating renal blood flow

Question: What would be the most important concept of autoregulation that the APRN should address?

Correct Answer: There are two mechanisms by which this occurs. The first is called the myogenic mechanism. During the increased stretch, the renal afferent arterioles contract to decrease GFR. The second mechanism is called the tubuloglomerular feedback. Increased renal arterial pressure increases the delivery of fluid and sodium to the distal nephron where the macula densa is located. It senses the flow and sodium concentration. ATP is released and calcium increases in granular and smooth muscle cells of the afferent arteriole. This causes arteriole constriction and decreased renin release. This overall process helps decrease GFR and maintain it in a limited range, albeit slightly higher than baseline.

Question 18

The APRN is giving a pathophysiology lecture to APRN students on renal blood flow, glomerular filtration rate, autoregulation, and related hormone factors regulating renal blood flow

Question: What would be the most important concept of hormonal regulation that the APRN should address?

Correct Answer: Hormonal regulation of renal blood flow involves the renin-angiotensionaldosterone system. During periods of renal hypoperfusion (e.g., hypotension, hypovolemia), hyponatremia or increased sympathetic tone causes the kidneys to release renin which is produced in the juxtaglomerular apparatus. Renin converts angiotensinogen (produced in the liver) to angiotensin I. That is followed by the conversion of angiotensin I to angiotensin II through angiotensin-converting enzyme, which is mostly produced in the lungs. Angiotensin II acts as a strong vasoconstrictor and induces the secretion of aldosterone by the adrenal cortex. Aldosterone increases renal reabsorption of sodium (and water) and augments the excretion of potassium and protons, which increases extracellular fluid and blood pressure.

Question 19

A 28-year-old female comes to the clinic with a chief complaint of right flank pain, urinary frequency, and foul-smelling urine. The symptoms have been present for 3 days but this morning, the patient states she had a fever of 101 F and thought she should get it checked out. Physical exam noncontributory with the exception of right costovertebral angle (CVA) tenderness upon percussion. Urine dipstick shows + blood, + bacteria and + white blood cells. Renal ultrasound reveals right staghorn renal calculus and the patient was diagnosed with acute pyelonephritis.

Question: How does a renal calculi calculus contribute to acute pyelonephritis?

Correct Answer: Urinary tract obstruction caused by something such as a kidney stone can lead to acute pyelonephritis. An outflow obstruction of urine can lead to incomplete emptying and urinary stasis which causes bacteria to multiply without being flushed out. The usual organism that causes acute pyelonephritis is e. coli.

Question 20

Mr. Kent is a 45-year-old African American male with a history of Type 2 diabetes, hypertension, and hyperlipidemia. His renal function has slowly decreased over the past 4 years and his nephrologist has told him that his GFR has decreased to 15cc ml/min and will soon need renal dialysis for chronic renal failure.

Question: How does chronic renal failure develop?

Correct Answer: There are multiple complex factors that contribute to CKD and include the interactions of many cells, cytokines and structural alterations. Two main factors that are recognized to progress renal disease are proteinuria and angiotension II activity. Glomerular hyperfiltration and increased glomerular capillary permeability lead to proteinuria. Proteinuria contributes to tubular injury by accumulating in the interstitial spaces and activating complement proteins and other mediators and cells, such as macrophages, that promote inflammation and eventually fibrosis. As glomerular function decreases, angiotension II increases which promotes glomerular hypertension and hyperfiltration caused by efferent arteriole vasoconstriction. The process progresses until there is expression of growth factors that may cause tubulointerstitial fibrosis and scarring, thus reducing renal function further

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NURS 6501 Module 3 Knowledge Check Quiz

NURS 6501 Module 3 Knowledge Check Quiz

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