NURS 510 Nursing Research Methods

Correct Answer: D) The focus of treatment is symptom management.

Explanation:

Irritable Bowel Syndrome (IBS) is a functional gastrointestinal disorder with no identifiable structural or inflammatory pathology. It is characterized by abdominal pain, bloating, and altered bowel habits (diarrhea, constipation, or both). The primary treatment approach for IBS is symptom management, including dietary modifications, stress reduction, and medications targeting specific symptoms like bowel irregularity or abdominal discomfort.

Why the other options are incorrect:

A) This disease leads to cancer of the bowel:

IBS does not increase the risk of colorectal cancer. It is a non-inflammatory, non-progressive condition.

B) The pathology for irritable bowel syndrome is the same as Crohn's disease:

IBS has no visible pathology or inflammation on imaging or biopsy, whereas Crohn’s disease is an inflammatory bowel disease with transmural inflammation, ulcers, and tissue damage.

C) The pharmacological treatment targets inflammatory disease in the bowel:

IBS is not an inflammatory disease, so medications like corticosteroids or immunosuppressants used in IBD are not indicated. Instead, treatment targets motility, pain, and bowel habit regulation.

Correct Answer: D) Cortisol

Explanation:

Cortisol, the end product of the hypothalamic-pituitary-adrenal (HPA) axis, regulates its own production through negative feedback. When cortisol levels rise, it signals the hypothalamus to decrease secretion of corticotropin-releasing hormone (CRH) and the anterior pituitary to decrease secretion of adrenocorticotropic hormone (ACTH). This, in turn, reduces further cortisol production by the adrenal cortex.

Why other options are wrong:

A) Corticotropin releasing hormone (CRH):

CRH is secreted by the hypothalamus and stimulates the anterior pituitary to release ACTH, which increases cortisol production—not inhibit it.

B) Adrenocorticotropic hormone (ACTH):

ACTH is secreted by the anterior pituitary and stimulates the adrenal cortex to produce cortisol, so it does not inhibit cortisol secretion.

C) Antidiuretic hormone (ADH):

ADH plays a role in water balance and vasoconstriction, not cortisol regulation. It is not part of the HPA axis.

Correct Answer: C) Lithium is classified as a mood stabilizer

Explanation:

Lithium is a well-established mood stabilizer used primarily in the treatment of bipolar disorder, especially for managing manic and depressive episodes. It helps regulate mood swings and is one of the most effective long-term treatments for this condition.

Why other options are wrong:

A) Regular blood levels are not needed when lithium is used:

This is false. Lithium has a narrow therapeutic index, and regular monitoring of serum lithium levels is essential to avoid toxicity, which can cause tremors, confusion, seizures, and even death.

B) Lithium is used only for anxiety:

Lithium is not typically used to treat anxiety as a primary indication. While it may indirectly reduce anxiety by stabilizing mood in bipolar disorder, its main use is not anxiety treatment.

D) Lithium has no interactions with other drugs so it is safe to use with all prescriptions:

Lithium interacts with several medications, including NSAIDs, diuretics, and ACE inhibitors, all of which can increase lithium levels and risk of toxicity. Clients must report all medications to their provider.

Correct Answer: C) Increased urine flow

Explanation:

Tamsulosin (Flomax) is an alpha-1 adrenergic blocker used primarily to treat benign prostatic hyperplasia (BPH). It works by relaxing the smooth muscle in the bladder neck and prostate, thereby reducing resistance to urinary flow and improving urinary symptoms such as hesitancy, urgency, and weak stream. The desired therapeutic effect is increased urine flow and improved bladder emptying.

Why the other options are incorrect:

A) Hypotension:

Tamsulosin may cause hypotension as a side effect, especially after the first dose, but this is not its intended therapeutic effect.

B) Syncope:

Like hypotension, syncope (fainting) is a potential adverse effect, not the goal of treatment.

D) Increased urinary obstruction:

Tamsulosin is specifically prescribed to relieve urinary obstruction, not worsen it. Increased obstruction would suggest treatment failure or a different underlying problem.

Correct Answer: A) Blocks glucose reabsorption by the kidneys and increases glucose excretion to lower blood sugar.

Explanation:

SGLT-2 inhibitors (e.g., canagliflozin, empagliflozin, dapagliflozin) work by inhibiting the sodium-glucose cotransporter 2 in the proximal renal tubules. This transporter is responsible for reabsorbing glucose from the urine back into the bloodstream. By inhibiting this transporter, glucose is excreted in the urine, which helps lower blood glucose levels independently of insulin.

Why the other options are incorrect:

B) Interacts with the transcription factor that improves insulin sensitivity in liver, muscle, and fat:

Incorrect. This describes the mechanism of thiazolidinediones (TZDs) like pioglitazone, which activate PPAR-γ receptors.

C) Inhibits hepatic glucose production and increases insulin sensitivity in peripheral tissues:

Incorrect. This is the mechanism of metformin, a biguanide, which suppresses gluconeogenesis and improves insulin sensitivity.

D) Blocks ATP-sensitive K+ channels on beta cells to promote insulin secretion:

Incorrect. This is the mechanism of sulfonylureas like glipizide and glyburide, which stimulate pancreatic insulin release.

Correct Answer: B) "This medication decreases the production of uric acid."

Explanation:

Allopurinol is a xanthine oxidase inhibitor that works by reducing the production of uric acid, which helps prevent gout attacks and uric acid-related kidney stones. It is used as a long-term management strategy to maintain lower serum uric acid levels and is not meant for acute pain relief.

Why other options are wrong:

A) "This medication will target the inflammation and pain during an acute attack.":

Allopurinol does not treat acute gout attacks. In fact, initiating it during an acute flare can sometimes worsen symptoms. NSAIDs or colchicine are typically used to manage acute inflammation and pain.

C) "Kidney function tests are not necessary when using this medication.":

This is incorrect. Allopurinol is renally excreted, and doses must be adjusted in renal impairment. Routine monitoring of BUN, creatinine, and uric acid levels is essential to ensure safe and effective use.

D) "Limit fluid intake to 1000cc per day to prevent urinary incontinence.":

Fluid intake should not be restricted. In fact, adequate hydration is important to help flush uric acid from the body and reduce the risk of renal stones or nephrotoxicity. Limiting fluids can worsen the risk of complications.

Correct Answer: C) "The bone will be more like 'normal' when bone-forming cells absorb the callus into woven bone."

Explanation:

Bone healing occurs in several stages: inflammation, soft callus formation, hard callus formation (woven bone), and remodeling. During the remodeling phase, osteoblasts (bone-forming cells) replace the immature woven bone with lamellar bone, which is structurally and functionally similar to the original bone. This final phase gradually restores the bone’s strength, structure, and function, making it more "normal."

Why the other options are incorrect:

A) "The bone will be more 'normal' when there is inflammation and hematoma..."

This is the initial stage of healing, not the phase where the bone resembles its original form. It is necessary but far from restoration.

B) "The bone will be more 'normal' when callus formation occurs."

Callus formation is an intermediate phase in healing that provides temporary stabilization but is still structurally immature and not yet like normal bone.

D) "The bone will be more normal when there is a proliferation of osteoclasts at the site."

Osteoclasts break down bone, which is part of remodeling, but they don’t form new bone. Osteoblast activity is what restores normal bone structure.

Correct Answer: D) "Taking steroids and NSAIDs can increase the risk for stomach ulcers so we need to discuss an alternate plan for pain management."

Explanation:

Prednisone (a corticosteroid) and ibuprofen (a nonsteroidal anti-inflammatory drug or NSAID) both increase the risk of gastrointestinal (GI) irritation, ulcers, and bleeding. Using these together significantly raises the risk of peptic ulcer disease due to their combined effects on gastric mucosa and prostaglandin inhibition. For patients who require both, gastroprotection (e.g., proton pump inhibitors) or alternative pain control strategies should be considered. The nurse should advocate for safer pain management options and collaborate with the provider to prevent complications.

Why the Other Options Are Wrong:

A) "Prednisone can exacerbate pain by increasing prostaglandin synthesis..."

This is inaccurate. Prednisone actually inhibits prostaglandin synthesis by blocking phospholipase A2, contributing to its anti-inflammatory and pain-relieving effects. It does not exacerbate pain through prostaglandin production.

B) "I will talk to the provider about having your prednisone switched to alternate day dosing..."

Alternate-day dosing may reduce long-term side effects but is not typically used for acute pain management. Also, pain control often requires daily anti-inflammatory coverage, especially in autoimmune diseases with chronic inflammation.

C) "Ibuprofen is not a very strong analgesic..."

Ibuprofen is actually an effective NSAID for pain and inflammation, especially at higher doses. The concern here is not its potency but the risk of GI complications when combined with corticosteroids.

Correct Answer: D) "The body is experiencing a fluid imbalance related to changing osmotic pressures."

Explanation:

Ascites is the accumulation of fluid in the peritoneal cavity, most commonly due to portal hypertension and hypoalbuminemia in liver disease (such as cirrhosis). The liver's impaired function leads to decreased production of albumin, reducing oncotic pressure, while increased hydrostatic pressure from portal hypertension pushes fluid out of the vasculature. This imbalance in osmotic and hydrostatic pressures causes fluid to shift into the abdominal cavity, resulting in ascites.

Why the other options are incorrect:

A) "Inflammatory molecules have increased the permeability of the abdominal capillaries.":

This mechanism is more typical of peritonitis or systemic inflammatory responses, not the primary process of ascites in chronic liver disease.

B) "Low aldosterone levels have caused fluid retention and peritoneal edema.":

In fact, aldosterone levels are often elevated in liver disease due to secondary hyperaldosteronism, leading to sodium and water retention, not low levels.

C) "The liver is not manufacturing clotting factors to prevent bleeding in the peritoneum.":

While liver disease does reduce clotting factor production, this contributes to bleeding risk, not directly to the formation of ascitic fluid.