Nurs 6501 advanced pathophysiology midterm quizlet
Nurs 6501 advanced pathophysiology midterm questions and answers
Nurs 6501 advanced pathophysiology midterm questions
Nurs 6501 advanced pathophysiology midterm answers
Nurs 6501 advanced pathophysiology midterm answer key
nurs 6501 midterm exam 2023
advanced pathophysiology midterm exam walden university quizlet
nurs 6501 midterm exam quizlet
A runner has depleted all the oxygen available for muscle energy. Which of the following will facilitate his continued muscle performance?
Answer: Anaerobic glycolysis
What causes the rapid change in the resting membrane potential that initiates an action potential?
Answer: Sodium gates open, and sodium rushes into the cell, changing the membrane potential from negative to positive.
A 12-year-old male is diagnosed with Klinefelter syndrome. His karyotype would reveal which of the following?
Answer: XXY
A nurse is reviewing the pedigree chart. When checking for a proband, what is the nurse looking for?
Answer: The person who is first diagnosed with a genetic disease
An aide asks the nurse why people who have neurofibromatosis will show varying degrees of the disease. Which genetic principle should the nurse explain to the aide?
Answer: Expressivity
In teaching a patient with cirrhosis, which information should the nurse include regarding cholesterol?
Answer: Cholesterol decreases the membrane fluidity of the erythrocyte, which reduces its ability to carry oxygen.
When a patient asks what causes cystic fibrosis, how should the nurse respond? Cystic fibrosis is caused by an _____ gene
Answer: Autosomal recessive
How are potassium and sodium transported across plasma membranes?
Answer: By adenosine triphosphate enzyme (ATPase)
The nurse would be correct in identifying the predominant extracellular cation as:
Answer: Sodium
The early dilation (swelling) of the cell’s endoplasmic reticulum results in:
Answer: Reduced protein synthesis
What principle should the nurse remember when trying to distinguish aging from diseases?
Answer: It is difficult to tell the difference because both processes are believed to result from cell injury.
What is the diagnosis of a 13-year-old female who has a karyotype that reveals an absent homologous X chromosome with only a single X chromosome present? Her features include a short stature, widely spaced nipples, reduced carrying angle at the elbow, and sparse body hair.
Answer: Turner syndrome
A eukaryotic cell is undergoing DNA replication. In which region of the cell would most of the genetic information be contained?
Answer: Nucleolus
The nurse is teaching staff about the most common cause of Down syndrome. What is the nurse describing?
Answer: Maternal nondisjunction
A 50-year-old male was recently diagnosed with Huntington disease. Transmission of this disease is associated with:
Answer: Delayed age of onset
A patient wants to know the risk factors for Down syndrome. What is the nurse’s best response?
Answer: Pregnancy in women over age 35
What is the role of cytokines in cell reproduction?
Answer: Provide growth factor for tissue growth and development
A newborn male is diagnosed with albinism based on skin, eye, and hair appearance. Which finding will support this diagnosis?
Answer: Inability to convert tyrosine to DOPA (3,4 dihydroxyphenylalanine)
Sodium and water accumulation in an injured cell are a direct result of:
Answer: Decreased ATP production
A nurse is reading a chart and sees the term oncotic pressure. The nurse recalls that oncotic pressure (colloid osmotic pressure) is determined by:
Answer: Plasma proteins
The ion transporter that moves Na + and Ca 2+ simultaneously in the same direction is an example of which of the following types of transport?
Answer: Symport
A 20-year-old pregnant female gives birth to a stillborn child. Autopsy reveals that the fetus has 92 chromosomes. What term may be on the autopsy report to describe this condition?
Answer: Tetraploidy
Why is potassium able to diffuse easily in and out of cells?
Answer: Because the resting plasma membrane is more permeable to potassium
Hypothyroidism
A disorder caused by a thyroid gland that is slower and less productive than normal, does not produce enough T3 and T4
T3, T4, TSH
Diagnosing hypo/hyperthyroidism T3/T4 = thyroid. TSH = Pituitary.
T3/T4 abnormality = problem with THYROID.
T3/T4 normal + TSH abnormal = Secondary thyroid problem
If too much T3/T4, then TSH will be down. Vice Versa.
calcium
parathyroid glands responsible for regulating ___ levels.
metabolism, temperature
Thyroid produces hormones T3, T4, and plays big role in __, ___ regulation and growth and development
iodine
Brain cannot make T3 and T4 without ___
slows
hypothyroidism everything ___.
stimulates sympathetic nervous system, drowsy, lethargic
constipated, food move slows, weight gain
body temp increases
Hyperthyroidism
excessive activity of the thyroid gland: increased levels of T3, T4 and TSH
loss
Hyperthyroidism:
burning calories at an excessive rate
weight ___
stimulates sympathetic nervous system: alert, quick reflexes, increased HR & BP (fight or flight response_
Heat intolerance: increased body temp
Active GI: diarrhea
anterior pituitary gland
the anterior part of the pituitary gland; an endocrine gland whose secretions are controlled by the hypothalamic hormones
produces thyroid stimulating hormone (TSH)
Cushing’s disease
(Remember: UP, UP, UP, DOWN, UP)
HYPERnatremia,
HYPERtension,
INCREASED blood volume,
HYPOkalemia,
HYPERglycemia
adrenal cortex
outer section of each adrenal gland; secretes cortisol, aldosterone, and sex hormones
Aldosterone
Hormone that stimulates the kidney to retain sodium ions and water to regulate BP via angiotensin-aldosterone system, retention of sodium and secretes potassium
cortisol
stress hormone released by the adrenal cortex helps the body deal with stress such as illness or injury
increases blood glucose
breaks down fats, proteins, carbs
electrolyte regulations
Negative feedback
Hypothalamus releases CRH corticotropin releasing hormone –> pituitary gland releases ATCH adrenocorticotropic hormone –> adrenal cortex to release cortisol
increased
Cushings disease has ___ secretion of cortisol
decreased
Addison’s disease has __ secretion of cortisol and aldosterone
Need to ADD some steroids
syndrome
Cushing ___ is when an outside cause results in too much production of cortisol, like treatment with steroids
disease
Cushings ___ is when an internal issue is causing over production of cortisol
autoimmune
Addison’s disease is typically an ____ disorder where the body is attacking the adrenal cortex on top of the adrenal gland
Cushing’s
___ symptoms:
skin fragile
truncal obesity, small
extremities with striae on them
excessive hair
“moon face”
buffalo hump
females –> no menstruation
males–> ED
hyperglycemia d/t high cortisol
Addison’s
___ symptoms:
brownish hyperpigmentation of skin
diarrhea, nausea
hyponatremia d/t low aldosterone levels –> hyperkalemia
hypoglycemia d/t low cortisol
low bp, risk for vascular collapse going into shock
Anti-diuretic hormone
aka Vasopressin
ADH is a hormone made by the hypothalamus in the brain and stored in the posterior pituitary gland. It tells your kidneys how much water to conserve.
ADH constantly regulates and balances the amount of water in your blood.
increase
SIADH will have ___ in antidiuretic hormone
decrease
Diabetes insipidus will have a __ in ADH
posterior pituitary gland
stores and secretes ADH
after hypothalamus produces ADH
Pheochromocytoma
a benign tumor of the adrenal medulla that causes the gland to secrete catecholamines (epinephrine, norpinephrine, dopamine, and dopa) leading to high BP, headache, sweating and symptoms of a panic attack.
diabetic ketoacidosis
acidity of the blood caused by the presence of ketone bodies produced when the body is unable to burn sugar; thus, it must burn fat (triglycerides and amino acids instead of glucose) for energy
hyperglycemia
hyperketonemia
metabolic acidosis
occurs mostly in type 1 diabetes mellitus
cerebral, coma
DKA causes nausea, vomiting, and abd pain and can progress to __ edema, __ and death
deficiency
DKA: hyperglycemia d/t insulin ___ causes an osmotic diuresis leading to marked urinary losses of water and electrolytes
urinary excretion of ketones leads to additional loss of sodium and potassium
inflammation
Pericarditis is ___ of the pericardium, often with fluid accumulation in the pericardial space (pericardial effusion)
cardiac tamponade
acute compression of the heart caused by fluid accumulation in the pericardial cavity–> impairs cardiac filling leading to low cardiac output.
infective endocarditis
inflammation of endothelium that lines heart and cardiac valves. most commonly damages mitral valve, then aortic and tricuspid valves. commonly caused by bacteria that are normally present in the body. can also occur after an invasive medical or dental procedure. symptoms: valvular dysfunction, may affect organ systems, chest pain, CHF, clubbing, meningitis, low back pain, arthralgia, arthritis
myocarditis
inflammation of the myocardium with necrosis of cardiac myocytes
biopsy shows inflammatory infiltrate of the myocardium with lymphocytes, neutrophils, eosinophils, and granulomas
direct cardiomyocyte injury cased by an infectious or other cardiotoxic agent OR myocardial injury caused by an autoimmune reaction to an infectious or cardiotoxic agent
aortic regurgitation
(aortic insufficiency) incompetent aortic valve that allows backward flow of blood from the aorta into left ventricle during diastole
aortic stenosis
calcification of aortic valve cusps that restricts forward flow of blood during systole
narrowing of the aortic valve, obstructing blood flow from the left ventricle to the ascending aorta during systole
mitral regurgitation
mitral insufficiency; incompetent mitral valve allows regurgitation of blood from the left ventricle back into left atrium during systole
mitral stenosis
narrowing of the mitral valve orifice that impedes blood flow from the left atrium to the left vetricle
mitral valve prolapse
Improper closure of the valve between the heart’s upper and lower left chambers.
billowing of mitral valve leaflets into the left atrium during systole
pulmonic regurgitation
pulmonic insufficiency; backflow of blood through incompetent pulmonic valve into the right ventricle
causes blood from from the pulmonary artery into the right ventricle during diastole
pulmonic stenosis
narrowing of the opening and valvular area between the pulmonary artery and right ventricle
narrowing of the pulmonary outflow tract causing obstruction of blood flow from the right ventricle to the pulmonary artery during systole
deep vein thrombosis
blood clot forms in a large vein, usually in a lower limb d/t impaired venous return, endothelial injury or hypercoagulability
thrombi
__ consist of thrombin, fibrin, and red blood cells with few platelets and without treatment can travel to the lungs causing PE
Hypertension
high blood pressure sustained SBP >130
BP= cardiac output x total peripheral vascular resistance (TPR)
HTN leads to ↑ CO, ↑ TPR
A runner has depleted all the oxygen available for muscle energy. Which of the following will facilitate his continued muscle performance?
Answer: Anaerobic glycolysis
What causes the rapid change in the resting membrane potential that initiates an action potential?
Answer: Sodium gates open, and sodium rushes into the cell, changing the membrane potential from negative to positive.
A 12-year-old male is diagnosed with Klinefelter syndrome. His karyotype would reveal which of the following?
Answer: XXY
A nurse is reviewing the pedigree chart. When checking for a proband, what is the nurse looking for?
Answer: The person who is first diagnosed with a genetic disease
An aide asks the nurse why people who have neurofibromatosis will show varying degrees of the disease. Which genetic principle should the nurse explain to the aide?
Answer: Expressivity
In teaching a patient with cirrhosis, which information should the nurse include regarding cholesterol?
Answer: Cholesterol decreases the membrane fluidity of the erythrocyte, which reduces its ability to carry oxygen.
A 15-year-old female is diagnosed with Prader-Willi syndrome. This condition is an example of:
Answer: Gene imprinting
When a patient asks what causes cystic fibrosis, how should the nurse respond? Cystic fibrosis is caused by an _____ gene
Answer: Autosomal recessive
How are potassium and sodium transported across plasma membranes?
Answer: By adenosine triphosphate enzyme (ATPase)
The nurse would be correct in identifying the predominant extracellular cation as:
Answer: Sodium
The early dilation (swelling) of the cell’s endoplasmic reticulum results in:
Answer: Reduced protein synthesis
What principle should the nurse remember when trying to distinguish aging from diseases?
Answer: It is difficult to tell the difference because both processes are believed to result from cell injury.
What is the diagnosis of a 13-year-old female who has a karyotype that reveals an absent homologous X chromosome with only a single X chromosome present? Her features include a short stature, widely spaced nipples, reduced carrying angle at the elbow, and sparse body hair.
Answer: Turner syndrome
A eukaryotic cell is undergoing DNA replication. In which region of the cell would most of the genetic information be contained?
Answer: Nucleolus
The nurse is teaching staff about the most common cause of Down syndrome. What is the nurse describing?
Answer: Maternal nondisjunction
A 50-year-old male was recently diagnosed with Huntington disease. Transmission of this disease is associated with:
Answer: Delayed age of onset
A patient wants to know the risk factors for Down syndrome. What is the nurse’s best response?
Answer: Pregnancy in women over age 35
What is the role of cytokines in cell reproduction?
Answer: Provide growth factor for tissue growth and development
A newborn male is diagnosed with albinism based on skin, eye, and hair appearance. Which finding will support this diagnosis?
Answer: Inability to convert tyrosine to DOPA (3,4 dihydroxyphenylalanine)
Sodium and water accumulation in an injured cell are a direct result of:
Answer: Decreased ATP production
A nurse is reading a chart and sees the term oncotic pressure. The nurse recalls that oncotic pressure (colloid osmotic pressure) is determined by:
Answer: Plasma proteins
The ion transporter that moves Na + and Ca 2+ simultaneously in the same direction is an example of which of the following types of transport?
Answer: Symport
0 out of 1 points
A patient has severe mental retardation caused by a deletion of part of chromosome 5. What genetic disorder will the nurse see documented in the chart?
Answer: Cri du chat syndrome
A 20-year-old pregnant female gives birth to a stillborn child. Autopsy reveals that the fetus has 92 chromosomes. What term may be on the autopsy report to describe this condition?
Answer: Tetraploidy
Why is potassium able to diffuse easily in and out of cells?
Answer: Because the resting plasma membrane is more permeable to potassium
Why is HDL considered good cholesterol?
It’s able to remove cholesterol from artery plaques and recycle it back to the liver.
Why is HDL consider good cholesterol
HDL is considered good cholesterol because it collects excess cholesterol in the body cells and transports it to the liver where it is excreted. HDL carries 20 to 25% of total plasma cholesterol.
Explain the role inflammation has in the development of atherosclerosis
Inflammation in the heart muscle caused by chronic inflammatory processes leads to mitochondrial damage that results in an increased free radical production that further activates the chronic inflammatory vicious cycle
Explain the role inflammation has in the development of atherosclerosis
Activated mast cells recruit inflammatory cells that provoke plaque formation and lead to atherosclerosis. Chronic inflammatory infiltrates occupy layers of arteries were stable plaques are formed and associated with atherosclerosis.
Explain the role inflammation has in the development of atherosclerosis
Additionally active inflammation involves a thinning at the fibrous Of atherosclerotic plaque which predisposes vulnerable plaque to rupture.
Why does the APRN recognize as the result of the pleural friction rub?
The inflammation of the pericardium due to either the underlying autoimmune disease or a post viral syndrome causes roughening of the pericardium. This causes the classic rug which can be best heard at the Apex of the heart and left sternal border.
Explain how a positive strep test has caused the patient’s symptoms
Rheumatic heart disease RHD only develops after a pharyngeal infection with group a beta hemolytic streptococcus. It is an abnormal response to humoral and cell mediated response to M proteins. Inflammation causes proliferative and exudative lesions in connective tissue.
Explain how a positive strep test has caused the patient’s symptoms
Inflammation causes scarring of the valve tissue. Inflammation usually affects the endocardium which contains the valves. Endocardial inflammation causes swelling of leaflets in the valves.
Describe the factors that could have contributed to the development of a DVT in this patient and explain how each of the factors could cause DVT
Virchow’s Triad caused damage to the walls of the vessels. Injury to the intimal layer of the vessel, antiplatelet substances such as nitric oxide and prostacyclin, along with the expression of collagen on the vessel wall, causes adherence to the platelets to the vessel wall.
Describe the factors that could have contributed to the development of a DVT in this patient and explain how each of the factors could cause DVT
Platelets become activated, then aggregate, forming clots. Venous stasis is a result of obesity, patients advanced age, and inability to perform physical therapy therapy.
Explain why large pulmonary embolus interferes with oxygenation
The embolus lodges somewhere in the pulmonary circulation and causes a ventilation/perfusion mismatch V/Q. Ventilation perfusion mismatch or V/Q defects are defects in total long ventilation perfusion ratio.
Explain why large pulmonary embolus interferes with oxygenation
It is a condition in which one or more areas of the lung receive oxygen but no blood flow, or they receive blood flow but no oxygen due to obstruction somewhere in the pulmonary circulation. This causes a decreased area for oxygen exchange.
Explain why a large pulmonary embolism causes right ventricular strain
The V/Q mismatch causes release of neurohumeral substances and inflammatory mediators that cause vasoconstriction of the pulmonary vasculature further impeding oxygenation.
Explain why a large pulmonary embolism causes right ventricular strain
Hemodynamically this vasoconstriction results in pulmonary hypertension, making it difficult for the right ventricle to pump blood.
Explain why a large pulmonary embolism causes right ventricular strain
The V/Q mismatch also creates decreased production of surfactant causing atelectasis that further decreases surface area available for oxygen exchange.
Explain early asthmatic responses in the cells responsible for the responses
When there is an initial airway exposure to an antigen, an innate and adaptive immune response is initiated.
Explain early asthmatic responses in the cells responsible for the responses
Cells that can initiate the inflammation of the bronchial mucosa and hyperresonance of the airways include Dedrick cells, T-helper 2 cells, lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, and basophils.
Explain early asthmatic responses in the cells responsible for the responses
Early asthmatic response is a phase of bronchospasm that peaks at about 30 minutes and usually resolves after about 3 hours.
Explain late asthmatic responses in the cells responsible for the responses
Late asthmatic responses are mediated by earlier exposure in early phase that causes a latent release of inflammatory mediators. These mediators, leukotrienes and prostaglandin D, cause bronchospasm, edema, and mucus secretions that obstruct airflow.
Explain late asthmatic responses in the cells responsible for the responses
Airway obstruction creates resistance to airflow and causes air trapping. Continued air trapping increases intrapleural and alveolar gas pressure, decreases ventilation and perfusion leading to uneven and variable ventilation/perfusion in the lung.
Explain the pathophysiology of emphysema and how it relates to COPD
Emphysema is a disease of the airways that causes permanent enlargement of the gas exchange airways. It is accompanied by destruction of the alveolar walls and does not appear to be fibrotic.
Explain the pathophysiology of emphysema and how it relates to COPD
Chronic exposure to irritants recruit neutrophils, macrophages, and lymphocytes to the lung resulting in progressive damage from inflammatory oxidative stress.
Explain the pathophysiology of emphysema and how it relates to COPD
Emphysema is characterized by destruction of alveoli leading to decrease surface area for gas exchange that causes significant ventilation/perfusion mismatch.
Explain the pathophysiology of chronic bronchitis and how it relates to COPD
Chronic bronchitis is caused by inhalation of irritants that promote bronchial inflammation. This inflammation causes bronchial Edema, increase in the size and number of mucus glands and goblet cells, smooth muscle hyper trophy with fibrosis and narrowing of the airway.
Explain the pathophysiology of chronic bronchitis and how it relates to COPD
Increased secretions of thick mucus that patient cannot cough up due to impairment of ciliary function.
Explain the pathophysiology of chronic bronchitis and how it relates to COPD
As disease progresses, the smaller airways are involved as well as the large airways. These airways, due to hyper trophy, cause narrowing of smooth muscle and obstruct airflow, especially during expiration. The obstruction can lead to VQ mismatches.
Patient was hypoxic as evidence by the low PaO2. Explain the pathological processes that caused this patient’s hypoxemia
Arterial hypoxemia early in acute pneumococcal pneumonia is principally caused by persistence of pulmonary artery blood flow to the consolidated lung resulting in an intrapulmonary shunt, and by ventilation perfusion mismatch later.
Patient was hypoxic as evidence by the low PaO2. Explain the pathological processes that caused this patient’s hypoxemia
Release of mediators cause widespread inflammation of the bronchial structures, especially the alveolar capillary membrane. The alveoli collapse due to an inactivation of surfactant and the alveoli fill with exudate, decreasing surface area for gas exchange.
Explain why patients with COPD are at risk for malnutrition
Many of the patients with severe COPD are lean, and frequently in a malnourished and under nourished state, which is characterized by loss of fat free body mass causing muscle wasting.
Explain why patients with COPD are at risk for malnutrition
The muscle wasting in COPD not only leads to decrease skeletal muscle function associated with reduce exercise capacity but it also is a major determinant of mortality in COPD.
Explain why patients with COPD are at risk for malnutrition
Patients with COPD require a low carbohydrate diet as increased CHO can lead to hypercapnia as the end products of CHO metabolism are CO2 and H2O.
What factors may have contributed to the development of PUD
Stress secondary to divorce and financial situations, cigarette smoking, alcohol consumption, use of NSAIDs, excess coffee consumption, positive h pylori test
How do these factors contribute to the formation of peptic ulcer’s
Chronic use of NSAIDs causes suppression of mucosal prostaglandin and a direct irritative topical effect. High gastrin level and excessive gastric acid production is often seen in Zollinger-Ellison syndrome which can be caused by gastrinoma.
How do these factors contribute to the formation of peptic ulcer’s
Smoking impairs healing by vasoconstriction. H pylori causes gastritis and interferes with mucosa
What causes GERD?
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.
What causes GERD?
The lower esophageal sphincter (LESS) relaxes due to certain medications (calcium channel blockers), hiatal hernia, and obesity allows stomach contents into the lower esophagus causing inflammation and possibly erosion of the esophagus
What factors can contribute to an upper G.I. bleed
Upper G.I. bleeds can be caused by peptic ulcer disease (PUD) which remains the most common cause of you UGIB. Esophageal bleeding from a Mallory-wise tear
What can cause diverticulitis in the lower G.I. tract
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.
What can cause diverticulitis in the lower G.I. tract
Increased intraluminal pressure or food particles cause erosion of the diverticular wall, resulting in inflammation, localized necrosis, and perforation.
How does cirrhosis cause portal hypertension
Portal hypertension results from an increase in resistance or blood flow in the portal venous system.
How does cirrhosis cause portal hypertension
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.
How does cirrhosis cause portal hypertension
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
Discuss how ascites develops as a result of portal hypertension
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 to the portal hypertension and a subsequent decrease in effective circulating blood volume.
Discuss how ascites develops as a result of portal hypertension
This underfilling theory activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention.
Discuss how ascites develops as a result of portal hypertension
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
Overflow theory of ascites
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
Underfilling theory of ascites
the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed to the portal hypertension and a subsequent decrease in effective circulating blood volume.
Underfilling theory of ascites
This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention.
Explain how hepatic encephalopathy develops in patients with cirrhosis of the liver
Hepatic encephalopathy develops from a combination of biochemical alterations that affect neurotransmissions. Liver dysfunction and collateral vessels that shunt blood around the liver.
Explain how hepatic encephalopathy develops in patients with cirrhosis of the liver
This allows neurotoxins and other harmful substances that are absorbed from the G.I. track to accumulate and circle freely to the brain.
Explain how hepatic encephalopathy develops in patients with cirrhosis of the liver
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.
Explain how hepatic encephalopathy develops in patients with cirrhosis of the 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.
A 65-year-old male with a history of a fib has had sudden onset abdominal pain. He has been vomiting, had several episodes of diarrhea, the last of which was bloody. He has a fever of 100.9. CBC reveals white blood cell count of 15,000. What is most likely the mechanism behind his current symptoms
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.
A 65-year-old male with a history of a fib has had sudden onset abdominal pain. He has been vomiting, had several episodes of diarrhea, the last of which was bloody. He has a fever of 100.9. CBC reveals white blood cell count of 15,000. What is most likely the mechanism behind his current symptoms
This disruption leads to malperfusion of the involved end organ leading to ischemia and ultimately infarction.
A 65-year-old male with a history of a fib has had sudden onset abdominal pain. He has been vomiting, had several episodes of diarrhea, the last of which was bloody. He has a fever of 100.9. CBC reveals white blood cell count of 15,000. What is most likely the mechanism behind his current symptoms
Elderly patients are at risk due to atherosclerosis which lead to thrombus formation. Embolic origins usually arise from cardiac arrhythmias usually a fib which leads to pooling of the blood in the atria
Describe how gallstones of formed and why they caused the symptoms that the patient presented with
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 carbonate and phosphates and mucin glycoproteins.
Describe how gallstones of formed and why they caused the symptoms that the patient presented with
Gallstones form in bile that is super saturated and can begin the process of cholesterol crystal formation. More crystals aggregate thus enlarging and forming stones.
Describe how gallstones of formed and why they caused the symptoms that the patient presented with
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
Explain how the patient became jaundiced
In extrahepatic jaundice, the common bile duct is obstructed, usually by gallstones, tumor, or inflammation.
Explain how the patient became jaundiced
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
Explain how pancreatitis develops and the role alcohol played in the patient’s case
The pancreatic acinar cells metabolize ethanol with the generation of toxic metabolites the injure pancreatic acinar cells causing release of active enzymes. This causes formation of protein plugs in the pancreatic ducts in spasm of the sphincter of Oddi which result in obstruction.
Explain how pancreatitis develops and the role alcohol played in the patient’s case
The destruction leads to intra-pancreatic release of activated enzymes, auto digestion, inflammation, and pancreatitis. Inflammation of the pancreas leads to systemic effects that are associated with moderately and severely acute pancreatitis.
Explain how pancreatitis develops and the role alcohol played in the patient’s case
Pro inflammatory cytokines and vasoactive peptides are released into the bloodstream. There is activation of leukocytes, injury to vessel wall, and coagulation abnormalities with development of vasodilation and shock
What are the important hepatitis markers that indicated the patient had acute hepatitis B
When looking at any hepatitis panel it is important to remember that Ag = antigen = acute phase of infection. And. Ab = antibody = part of chronic phase.
What are the important hepatitis markers that indicated the patient had acute hepatitis B
In hepatitis B, there are three antigens: surface positive for acute infection: core-IgM antiHBc indicates acute infection and IgG antiHBc remains positive for life: E indicates current infectivity- HBeAg.
Ag
Antigen, acute phase of infection
Ab
Antibody, past or chronic phase of infection
HBsAg (hepatitis B surface antigen)
Indicates that the person is infectious. It can be detected in high levels in serum during acute or chronic HBV infection
Anti-HBs (hepatitis B surface antibody)
Indicates recovery and immunity from HBV infection. anti-HBs also develops in a person who has been successfully vaccinated against hepatitis B
Anti-HBc
Appears at the onset of symptoms in acute hepatitis B and remains for life
IgM anti-HBc (IgM antibody to hepatitis B core antigen)
Positively indicates recent infection with HPV of six months or less
HBeAg (hepatitis B e antigen)
Indicates that the virus is replicating
How does ulcerative colitis develop in a susceptible person
Ulcerative colitis is thought to occur and individuals with genetic predisposition’s, 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 ulcerative colitis.
How does ulcerative colitis develop in a susceptible person
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 a gut flora, secreting pro inflammatory cytokines that activate a certain population of T cells.
How does ulcerative colitis develop in a susceptible person
This results in mucosal inflammation and damage. Ulcerative colitis is usually limited to the colon, but in severe cases may involve the entire colon up to the cecum.
How does ulcerative colitis develop in a susceptible person
Typically inflammation begins at the rectum and continuously involves all are part of the colon. The lesions are limited to the mucosa and are not transmural, and do not involve Skip lesions.
How does ulcerative colitis develop in a susceptible person
It is a disease with many active in 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 that leaks fluid in the gut, which can lead to peritonitis
What type of acute kidney injury does the patient have and what factors contributed to this diagnosis
The patient has pre-renal acute kidney injury (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 resistance is of renal afferent and efferent arterioles.
What type of acute kidney injury does the patient have and what factors contributed to this diagnosis
Decrease RBF causes hypoxia of the cells.
What type of acute kidney injury does the patient have and what factors contributed to this diagnosis
Volume loss, results in decreased RBF caused by sepsis, hemorrhage, decreased cardiac output, sequestration of fluids in severe burns, multiple organ dysfunction, renal vasoconstriction by NSAIDs or radiographic contrast, renal artery stenosis, or kidney edema that restricts RBF.
What type of acute kidney injury does the patient have and what factors contributed to this diagnosis
Initially during periods of hypo perfusion auto regulatory mechanisms maintain glomerular filtration rate (GFR) at a relatively constant level through afferent arteriolar dilation and efferent arteriolar vasoconstriction.
What type of acute kidney injury does the patient have and what factors contributed to this diagnosis
The GFR eventually declines due to decreased infiltration pressure. prolonged decreases in blood volume or blood pressure result in cellular injury, acute tubular necrosis, and apoptosis, or acute interstitial necrosis, which is a severe form of AKI
What would be the most important concept of glomerular filtration rate (GFR) that the APRN should address
RBF and GFR are important aspects of maintaining normal kidney functions. A delicate balance exist between RBF and GFR as changes in one may affect the other. The kidneys receive approximately 20 to 25% of the cardiac output (CO) which is about equal to 1000 to 1200 cc/minute.
What would be the most important concept of glomerular filtration rate (GFR) that the APRN should address
With normal blood pressure and hematocrit, about 700 cc (mL) of blood flowing through the kidney is plasma. The filtration of the plasma per unit of time is called the GFR. the GFR is directly related to the perfusion pressure in the glomerular capillaries
What would be the most important concept of autoregulation that the APRN should address
There are two mechanisms by which this occurs the first is called the myogenic mechanism. During the increase stretch, the renal afferent arterioles contract to decrease GFR.
What would be the most important concept of autoregulation that the APRN should address
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 of sodium concentration.
What would be the most important concept of autoregulation that the APRN should address
ATP is released and calcium increases in granular and smooth muscle cells of the afferent arteriole.
What would be the most important concept of autoregulation that the APRN should address
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
myogenic mechanism of autoregulation
During the increase stretch, the renal afferent arterioles contract to decrease GFR.
tubuloglomerular feedback of autoregulation
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 of sodium concentration.
tubuloglomerular feedback of autoregulation
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
What would be the most important concept of hormonal regulation that the APRN should address
Hormonal regulation of RBF involves the renin-angiotensinaldosterone system. During periods of renal hypo perfusion (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.
What would be the most important concept of hormonal regulation that the APRN should address
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.
What would be the most important concept of hormonal regulation that the APRN should address
Aldosterone increases renal reabsorption of sodium (and water) and augments excretion of potassium and protons which increases extracellular fluid and blood pressure
How does renal calculi calculus contribute to acute pyelonephritis
Urinary tract obstruction caused by something such as a kidney stone can lead to acute pyelonephritis.
How does renal calculi calculus contribute to acute pyelonephritis
And 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.
How does chronic renal failure develop?
There are multiple complex factors that contribute to CKD and include the interactions of many cells, cytokines, and structural alterations.
How does chronic renal failure develop?
Two main factors that are recognized to progress renal disease are proteinuria and angiotensin II activity. Glomerular hyper filtration and increase glomerular capillary permeability lead to proteinuria.
How does chronic renal failure develop?
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.
How does chronic renal failure develop?
As glomerular function decreases, angiotensin II increases which promotes glomerular hypertension and hyper filtration caused by efferent arteriole vasoconstriction.
How does chronic renal failure develop?
The process progresses until there is expression of growth factors that may cause tubulointerstitial fibrosis and scarring, thus reducing renal function further
Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH
Syndrome of inappropriate anti-diuretic hormone (SIADH) is a disorder characterized by excessive anti-diuretic hormone (ADH) production in the body without physiological stimuli to trigger its release.
Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH
ADH is necessary for the kidneys to regulate fluids but excess ADH can lead to hypervolemia, hypotonic hyponatremia, Edema, weight gain, and G.I. upset.
Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH
As sodium levels drop, symptoms of lethargy, confusion, muscle twitching, seizures, and neurological damage may present. The patient’s history of diabetes and treatment with metformin leads to an increased risk for SIADH
Explain the patient’s symptoms of hypercortisolism
Early symptoms of hypercortisolism include fatigue and weakness and progress to G.I. symptoms as the patient is experiencing with nausea and vomiting. The patients hypotension is the most critical symptom of hypercortisolism as it can progress to shock with complete vascular collapse.
Explain the patient’s symptoms of hypercortisolism
These symptoms are the result of i adequate mineralocorticoid and corticosteroid synthesis and elevated ACTH levels seen in adrenal insufficiency related to the chronic use of steroids
Primary hyperthyroidism is associated with excess PTH secretion by the parathyroid glands from parathyroid adenomas, parathyroid hyperplasia, parathyroid carcinoma, or genetic causes that lead to multiple endocrine neoplasia. In
What is the role of parathyroid hormone in the development of primary hyperparathyroidism
primary hyperthyroidism, PTH is not regulated by feedback control mechanisms and hypercalcemia and hypophosphatemia present and effect various organ systems
Explain the processes involved in the formation of renal stones in patients with hyper parathyroidism
Hypercalciuria, hyperphosphaturia, and alkaline urine, associated with hyper parathyroidism lead to the formation of renal stones, as calcium phosphate salts present and alkaline urine, collecting ducts, and the renal pelvis. Calcium oxalate stones may also form
Explain how patient with hyperparathyroidism is at risk for bone fractures
In a patient with hyper parathyroidism the bones release excess calcium into the blood. Excessive osteocytic and osteoclastic activity results in bone resorption and leads to pathological fractures and compression fractures in vertebral areas of the body
What serious consequences of hypo parathyroidism occur and why
The serious consequences of hypothyroidism primarily result from hypocalcemia and hyper phosphatemia related to PTH deficiency.
What serious consequences of hypo parathyroidism occur and why
These imbalances cause a lower threshold for muscle and nerve excitation and can lead to perioral numbness, tingling, paresthesia, tetany, tonic clonic convulsions, hyperreflexia, laryngeal spasm’s, and even aphyxiation.
What serious consequences of hypo parathyroidism occur and why
Cataracts and bone deformities may also form as a result of hypocalcemia and hypo parathyroidism
The patient exhibited classic signs of type one diabetes. Explain the pathophysiology of polydipsia
Polydipsia is increased thirst and a clinical manifestation of type 1 diabetes. Polydipsia occurs when elevated blood glucose causes water to be osmotically drawn from body cells, which results in intracellular dehydration and stimulates the hypothalamic thirst response
A patient exhibited classic signs of type one diabetes. Explain the pathophysiology of polyuria
Polyuria is increased urine frequency and a clinical manifestation of type 1 diabetes. Polyuria occurs because hyper glycemia has an osmotic diuretic effect. Glucose levels filtered by the kidneys exceed what can be reabsorbed, resulting in glycosuria and large amounts of water loss
The patient exhibited classic signs of type one diabetes. Explain the pathophysiology of polyphagia
Polyphagia is increase hunger and a clinical manifestation of type one diabetes. Polyphagia occurs when cellular stores of protein, fat, and carbohydrates are depleted, causing cellular starvation and resulting in increased hunger
The patient exhibited classic signs of type one diabetes. Explain the pathophysiology of weight loss
Weight loss is a clinical manifestation of type one diabetes. Weight loss is contributed to a loss of fluid with osmotic diuresis and a loss of tissue as proteins and fats are used for energy sources when insulin is deficient
The patient exhibited classic signs of type one diabetes. Explain the pathophysiology of fatigue
Fatigue is a clinical manifestation of type one diabetes. Fatigue develops when metabolic changes causes the body to burn fat and muscle for energy, as it does not get its energy needs met through food sources. Severe nocturia also contributes to fatigue in type one diabetes
How do genetics and environmental factors contribute to the development of type one diabetes
Interactions between susceptibility genes and environmental factors may contribute to type one diabetes development.
How do genetics and environmental factors contribute to the development of type one diabetes
The major histocompatibility complex (MHC) carries the strongest genetic Association to type one diabetes. However there are multiple other gene mutations that are also associated with a risk of type one diabetes.
How do genetics and environmental factors contribute to the development of type one diabetes
Environmental factors that contribute to an elevated risk for type one diabetes include viral infections, proteins in cows milk, vitamin D deficiency, vaccinations, air pollution, gut microbial flora, family density, and stress
The hormones involved in intermediary metabolism, exclusive of insulin, that can participate in the development of diabetic ketoacidosis (DKA) are epinephrine, glucagon, cortisol, growth hormone. Describe how they participate in the development of DKA
DKA is a complication of diabetes characterized by a deficiency of insulin accompanied by an increase in insulin counter-regulatory hormones and is most common in type 1 diabetes.
The hormones involved in intermediary metabolism, exclusive of insulin, that can participate in the development of diabetic ketoacidosis (DKA) are epinephrine, glucagon, cortisol, growth hormone. Describe how they participate in the development of DKA
The counter-regulatory hormones usually antagonize insulin through glucose production and by decreasing the use of glucose in the tissues.
The hormones involved in intermediary metabolism, exclusive of insulin, that can participate in the development of diabetic ketoacidosis (DKA) are epinephrine, glucagon, cortisol, growth hormone. Describe how they participate in the development of DKA
Marked insulin deficiency causes a decrease in glucose uptake and increases fat mobilization, releasing fatty acids and accelerating glycogenesis, gluconeogenesis, and ketogenesis.
Explain the underlying processes that lead to HHNKS or HHS
HHNKS or HHS is characterized by marked elevation of glucose levels and fluid deficiency. Synergistic factors are present and include insulin deficiency, increased stress (counter-regulatory) hormones, increased glycogenolysis and gluconeogenesis, inadequate glucose use in peripheral tissues, and lack of ketosis.
Explain the underlying processes that lead to HHNKS or HHS
Pro inflammatory mediators contribute to insulin resistance and increased stress hormones that promote hyperglycemia
How would you differentiate Cushing’s disease from Cushing’s syndrome
Cushing’s disease is characterized by an excess of endogenous secretion of ACTH. Cushing syndrome, on the other hand, is characterized by chronic exposure to an excess in endogenous cortisol and mostly affects women
What is the pathogenesis of primary hyperaldosteronism
Primary hyperaldosteronism commonly results from unilateral benign aldosterone-promoting adrenal adenoma.
What is the pathogenesis of primary hyperaldosteronism
Excessive secretion of aldosterone in the absence of principal angiotensin II regulator leads to hypokalemia, insulin resistance, inflammation, endothelial damage, and cardiovascular remodeling, which affects adipose tissue function and differentiation.
What is the pathogenesis of primary hyperaldosteronism
Primary hyperaldosteronism contributes to metabolic syndrome, hypertension, dyslipidemia, obesity, insulin resistance, and hyperglycemia.
What is the basic underlying pathophysiology of type 2 diabetes
A combination of environmental and genetic factors contribute to the basic underlying pathophysiology of type two diabetes.
What is the basic underlying pathophysiology of type 2 diabetes
Several mechanisms contribute to insulin resistance in type two diabetes and include abnormal insulin molecules, excess insulin antagonists, insulin receptor down regulation, decreased post receptor kinases, and altered glucose transporter proteins.
What is the basic underlying pathophysiology of type 2 diabetes
Obesity also works through several mechanisms to contribute to insulin resistance i type two diabetes, including increased adipokine hormones, increase free fatty acids, inflammatory mediators, and ghrelin activity.
What causes diabetes insipidus
Neurogenic and central diabetes insipidus (DI) is characterized by insufficient ADH secretion that presents with lesions of the hypothalamus or pituitary dysfunction that interferes with ADH functions.
What causes diabetes insipidus
Lesions that cause DI are associated with immunologic disorders, infections, aneurysms, thrombosis, hypophysectomy, or brain tumors.
What causes diabetes insipidus
Neurogenic DI is often a complication of pregnancy, pituitary surgery, or traumatic brain injury. Other causes include hereditary disorders related to ADH genes or pituitary gland structural changes
Explain how the negative feedback loop controls thyroid levels
Thyroid hormone regulation occurs through a negative feedback loop that involves the thyroid gland, anterior pituitary, and hypothalamus.
Explain how the negative feedback loop controls thyroid levels
This negative feedback loop is initiated by thyrotropin-releasing hormone (TRH) in the hypothalamus and pituitary portal system, where it stimulates thyroid stimulating hormone (TSH) release.
Explain how the negative feedback loop controls thyroid levels
Thyroid hormones T3 and T4 are secreted by the thyroid and affect body metabolism. When concentrations of thyroid hormones in the blood rise above a certain level, TRH is inhibited to control thyroid levels
How did the patient develop thyroid storm? What were the patient factors that led to the development of thyroid storm?
Thyroid storm is associated with under treated or untreated Hyperthyroidism. Thyroid storm is characterized by an excessive production of hormones produced by the thyroid. The patient in this scenario likely developed thyroid storm from hyperthyroid with non-adherence to thyroid medication.
What causes hypothyroidism
Hypothyroidism, a condition characterized by the thyroid not producing sufficient hormones, is most commonly caused by Hashimoto’s thyroiditis, an auto immune disorder. Other possible causes may involve a response to treatment for hyperthyroidism, medications, thyroid surgery, or radiation therapy
What causes myxedema coma
Myxedema coma is caused by hypothalamus or pituitary gland failure the inhibits proper signaling of the thyroid gland. A loss of brain function results from low blood levels of thyroid hormone over an extended period of time.
What causes myxedema coma
Myxedema coma is associated with a history of hypothyroidism, thyroid disease, thyroid surgery, or radioactive iodine treatment
What is pheochromocytoma and how does it cause the classic symptoms to patient presented with
Pheochromocytomas, or chromaffin cell tumors, are rare neuroendocrine tumors that cause hyper function of the adrenal medulla with uncontrolled production of norepinephrine and epinephrine from larger tumors. In responses to stressors, including surgery, tumors may release catecholamines.
What is pheochromocytoma and how does it cause the classic symptoms to patient presented with
Pheochromocytoma symptoms are associated with effects of catecholamine release that cause the patient’s symptoms of high blood pressure, palpitations, headache, and sweating.
And what are the treatment goes for managing pheochromocytoma
Treatment goals for pheochromocytomas involve managing excess catecholamine to prevent hypertensive emergencies. This may be accomplished with alpha and beta blockers or calcium channel blocker’s, usually initiated weeks before surgery.
And what are the treatment goes for managing pheochromocytoma
Unless the tumor is large or metastasis is suspected, the tumor may be removed via laparoscopic surgery. Medication therapy is provided before, during, and after surgery. malignant tumors are typically managed with surgery and chemo therapy
Which of the following affects drug distribution throughout the body?
Protien binding
A Nurse Practitioner who provides care in a long-term care facility is documenting a new resident’s medication regimen on the resident’s intake admission. The Nurse Practitioner is documenting the generic, rather than proprietary, names of the resident’s current drugs because
there is a potential for confusion and miscommunication if proprietary names are used.
A patient is admitted to the emergency department with severe chest pain. The emergency department physician orders intravenous nitroglycerin 5 mcg/min, titrate dose by 5 mcg/min every 3 to 5 minutes per infusion pump as needed. Before administering the nitroglycerin, the nurse should prioritize which of the following assessments?
Blood pressure
A male patient is to begin treatment for pneumonia with an albuterol (Ventolin) inhaler. The nurse will advise the patient that he will most likely experience which of the following common adverse effects of the drug?
Throat irritation
A patient with type 1 diabetes has been admitted to the hospital for orthopedic surgery and the care team anticipates some disruptions to the patient’s blood glucose levels in the days following surgery. Which of the following insulin regimens is most likely to achieve adequate glycemic control?
Doses of basal insulin twice daily with regular insulin before each: meal
The APRN’s ability to prescribe controlled substances is regulated by:
A patient has been prescribed an oral drug that is known to have a high first-pass effect. Which of the following measures has the potential to increase the amount of the free drug that is available to body cells?
Administering the drug intravenously rather than orally
Federal legislation dictates a lengthy and rigorous process of testing for new drugs. What is the primary purpose of this testing process?
To ensure the safety of the public
66-year-old woman has a complex medical history that includes poorly-controlled type 1 diabetes, renal failure as a result of diabetic nephropathy and chronic heart failure (CHF). Her care provider has recently added spironolactone (Aldactone) to the woman’s medication regimen. The nurse should consequently assess for signs and symptoms of
Hyper kalemia
The lower respiratory system utilizes a number of different mechanisms that confer protection and maintain homeostasis. Which of the following physiological processes protects the lower respiratory system?
Cilia sweep foreign material and mucus upward toward the trachea and larynx where they can then be swallowed.
A 22 year old patient is transitioning from oral agents to insulin. He will be taking 20 units of lantus at bedtime and regular insulin before meals. What instructions should the NP provide about the timing and dose of regular insulin?
Nurse Practitioner who provides care on an acute medicine unit has frequently recommended the use of nicotine replacement gum for patients who express a willingness to quit smoking during their admission or following their discharge. For which of the following patients would nicotine gum be contraindicated?
A patient with a history of angina who experienced a non-ST wave myocardial infarction
Nurse Practitioner is caring for a female patient who has developed atelectasis because of thick mucus secretions. The Nurse Practitioner is monitoring IV administration of acetylcysteine (Mucomyst) and notices that the patient’s face is flushed. The appropriate nursing action would be to
slow the administration of acetylcysteine and administer diphenhydramine if ordered.
A Nurse Practitioner is caring for a 70-year-old patient who is taking desmopressin (DDAVP). The patient has a history of cardiovascular disease. The nurse will prioritize the assessment of which of the following?
Electrolyte level
Shirley, age 58, has been diabetic for 7 years. Her blood pressure for the last three office visits have been 154/100, 144/94, and 144/90. What would you prescribe today during her routine office visit?
Ace inhibitor
John is a newly diagnosed diabetic that contacts the office with complaints of severe nausea and vomiting. What instructions should the APRN provide related to his insulin doses?
Monitor your blood sugar every 4 hours and take regular insulin based on the blood sugar reading.
A patient comes to primary clinic for strep throat. A throat swab culture is sent to lab. What information is required for the nurse practitioner to disclose on lab transmittal?
National provider identification
A Nurse Practitioner is caring for a 73-year-old man who is receiving drug therapy. He is beginning to exhibit signs of decline in his renal system, yet his current serum creatinine level is normal. The Nurse Practitioner will base the patient’s plan of care on
the understanding that there is
an increase in the production of creatinine.
A Nurse Practitioner is caring for a 61-year-old man who has had a severe attack of gout while in the hospital for food poisoning. The Nurse Practitioner administers colchicine intravenously in order to
avoid aggravating the gastrointestinal tract.
A child is prescribed an inhaled corticosteroid agent to decrease respiratory inflammation related to exposure to an animal. The patient’s parent administers a higher than prescribe dose of the medication for 5 days. What should the APRN monitor the child for?
Nurse Practitioner is instructing a patient who was recently diagnosed with multiple sclerosis about dantrolene (Dantrium). The patient is a 38-year-old-male and the foreman for a construction company. In order to minimize one important adverse effect
of the drug, the nurse will give the patient which of the following instructions?
Wear appropriate clothing and sunscreen whenever he is in direct sun;ight
A Nurse Practitioner is instructing a patient concerning a newly prescribed drug. Which of the following should be included to help improve patient compliance and safety?
Measures to alleviate any discomfort associated with adverse rxn
A 47-year-old woman has been diagnosed with open-angle glaucoma. Pilocarpine drops are prescribed. The nurse’s assessment reveals that the patient has worn soft contact lenses for 15 years. The nurse will instruct the patient to
Remove contact before applying
