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Continuing isotonic fluids alone is not the next step when blood glucose drops to 190 mg/dL in DKA. Isotonic fluids (e.g., 0.9% saline) are used initially to restore volume, but as glucose nears 200 mg/dL, adding dextrose prevents hypoglycemia while insulin continues to resolve acidosis, making this choice less appropriate.

Discontinuing insulin infusion is incorrect, as DKA requires continuous insulin to correct acidosis and ketosis, even after glucose normalizes. Insulin suppresses ketone production by inhibiting lipolysis and gluconeogenesis, driven by glucagon excess. Stopping insulin prematurely risks worsening acidosis, making this an unsafe intervention.

Monitoring blood glucose every 4 hours is insufficient during active DKA treatment, where hourly checks are standard to titrate insulin and fluids. Glucose at 190 mg/dL requires adding dextrose to prevent hypoglycemia while continuing insulin, making frequent monitoring and intervention more critical than this choice suggests.

Decreased white blood cell (WBC) count is not expected in acute pancreatitis, which typically causes elevated WBC due to inflammation from autodigestion of pancreatic tissue by enzymes like trypsin. Leukocytosis reflects the body’s immune response to pancreatic injury, making this choice incorrect for the condition.

Decreased serum lipase is not expected in acute pancreatitis. Lipase levels rise due to pancreatic cell damage, often remaining elevated longer than amylase. This enzyme’s release into the blood is a key diagnostic marker, making this choice incorrect for the condition’s presentation.

Increased serum calcium is not typical in acute pancreatitis. Hypocalcemia may occur due to calcium binding with fat necrosis products (saponification) from enzyme leakage. Elevated calcium is unrelated to pancreatitis pathophysiology, making this choice incorrect for expected laboratory findings.

Diarrhea is not a common complication of total parenteral nutrition (TPN), which bypasses the gastrointestinal tract. Diarrhea is more associated with enteral feeding due to intestinal stimulation. TPN’s intravenous delivery avoids gut-related issues, making this an unlikely complication in this context.

Aspiration is not a complication of TPN, as it is administered intravenously, not via the respiratory or gastrointestinal tract. Aspiration is a risk with enteral feeding or impaired swallowing, not TPN, which delivers nutrients directly into the bloodstream, bypassing the airway.

Stomatitis, or oral inflammation, is not directly caused by TPN, which is delivered intravenously. It may occur in malnourished patients but is not a specific complication of TPN therapy, unlike metabolic issues like hyperglycemia, which result from high glucose content in TPN solutions.

Providing oral hygiene is important for patient comfort but not the priority in acute pancreatitis. Withholding oral intake prevents pancreatic stimulation, reducing enzyme release and autodigestion, which is critical to minimize inflammation and complications, making this a secondary intervention.

Assisting the client to a semi-prone position may reduce pressure on the pancreas, alleviating discomfort, but it is not the priority. Withholding oral intake directly addresses pancreatic inflammation by minimizing enzyme secretion, making it more critical to prevent further tissue damage.

Documenting pain assessment is necessary for continuity of care but not the priority. Withholding oral intake directly reduces pancreatic enzyme activity and inflammation, preventing worsening of acute pancreatitis, making it more urgent than documentation in the immediate management plan.

Administering desmopressin (DDAVP), a synthetic antidiuretic hormone, is contraindicated in SIADH, as it exacerbates water retention, worsening hyponatremia. Desmopressin is used for diabetes insipidus, where ADH is deficient, not SIADH, where ADH excess causes fluid overload and sodium dilution.

Maintaining an IV infusion of 5% dextrose water is inappropriate for SIADH, as it adds free water, further diluting serum sodium and worsening hyponatremia (125 mEq/L). Hypertonic saline or fluid restriction is needed to correct sodium imbalance, making this intervention incorrect.

Providing a low sodium diet is not indicated for SIADH, as the primary issue is water retention, not sodium intake. Restricting sodium could worsen hyponatremia by further reducing serum sodium availability, making fluid restriction a more effective intervention for this condition.

Moist mucous membranes are not expected in diabetes insipidus (DI), which causes excessive water loss due to deficient antidiuretic hormone, leading to dehydration and dry mucous membranes. This finding is more typical in conditions with fluid retention, like SIADH, making it incorrect.

Bradycardia is not typical in DI. Dehydration from excessive water loss increases heart rate (tachycardia) as a compensatory response to maintain cardiac output. Bradycardia may occur in other conditions but not in DI’s hypervolemic state, making this choice incorrect.

Bounding peripheral pulses are not expected in DI, where dehydration reduces blood volume, leading to weaker pulses. Bounding pulses occur in hyperdynamic states like thyrotoxicosis, not DI’s hypovolemic state, making this an incorrect finding for the condition.

PaCO2 31 mmHg (normal 35-45 mmHg) suggests respiratory alkalosis, not typical in HHS. HHS primarily causes metabolic acidosis or normal pH due to severe hyperglycemia and dehydration, not respiratory compensation, making this an incorrect finding for HHS’s acid-base profile.

HCO3 15 mEq/L (normal 21-28 mEq/L) indicates metabolic acidosis, more common in DKA than HHS. HHS typically has normal or slightly reduced HCO3 due to minimal ketone production, making this finding less consistent with HHS’s metabolic profile.

pH 7.27 indicates significant acidosis, typical of DKA, not HHS. HHS involves severe hyperglycemia and dehydration with minimal ketosis, resulting in normal or slightly acidotic pH, making this finding inconsistent with the expected acid-base balance in HHS.

Including only high protein snacks is inappropriate, as excessive protein can strain the liver in viral hepatitis, increasing ammonia production and risking encephalopathy. A balanced diet with moderate protein is preferred, making this choice incorrect for supporting liver function.

Administering acetaminophen for pain is risky in viral hepatitis, as the liver’s impaired metabolism increases toxicity risk, potentially causing hepatotoxicity. Safer analgesics or non-pharmacologic measures are preferred to manage discomfort, making this an inappropriate intervention for this condition.

Encouraging three large meals daily may overwhelm the liver’s capacity in viral hepatitis, exacerbating nausea and diarrhea. Smaller, frequent, high-carbohydrate meals are better tolerated, supporting energy needs without straining digestion, making this choice less effective for symptom management.

Administering a diuretic is contraindicated in diabetes insipidus, as it exacerbates water loss, worsening dehydration. DI requires interventions like vasopressin or fluid replacement to correct dilute urine output, making diuretics harmful and inappropriate for managing this condition’s pathophysiology.

Measuring blood glucose every 4 hours is irrelevant to DI, which involves water balance, not glucose metabolism. Glucose monitoring is key in diabetes mellitus, not DI, where polyuria results from ADH deficiency, making this intervention unrelated to the condition’s management.

Initiating fluid restrictions is inappropriate for DI, as it worsens dehydration caused by excessive water loss from low ADH. Fluid replacement or vasopressin is needed to restore water balance, making fluid restriction a harmful intervention that exacerbates DI’s hypovolemic state.