Bow-Tie NCLEX Practice Questions

The picture is classic for pulmonary embolism: an immobile postoperative orthopedic client with unilateral calf swelling who develops abrupt dyspnea, pleuritic chest pain, tachycardia, tachypnea, and hypoxemia with clear breath sounds. Clear lungs are the key discriminator. Asthma exacerbation produces wheezing and a prolonged expiratory phase. Pneumothorax produces absent or diminished unilateral breath sounds with possible tracheal deviation. Atelectasis develops gradually with diminished bases and crackles, and it does not typically drop the SpO2 to 86% in minutes.

Oxygen is the immediate priority because hypoxemia is life threatening; targeting an SpO2 of at least 94% follows current practice for acute hypoxemic respiratory failure. Anticoagulation is the definitive therapy that prevents clot propagation and recurrent embolization, so preparing the prescribed intravenous unfractionated heparin infusion is correct. Massaging the calf is contraindicated because it may dislodge additional thrombus. A bronchodilator treats bronchospasm, which is absent here. Trendelenburg worsens ventilation by pushing abdominal contents against the diaphragm and is not indicated.

For evaluating treatment effectiveness, oxygen saturation and respiratory rate directly reflect whether oxygenation and gas exchange are improving. The aPTT or anti-Xa level shows whether unfractionated heparin is in the therapeutic range, which is how anticoagulation is titrated. D-dimer is a diagnostic screening test with high sensitivity and poor specificity; it stays elevated after surgery and is not trended to judge response. Potassium is unrelated to this problem. The Wells score estimates pretest probability, which is an etiologic and diagnostic tool rather than an outcome measure. Parameters to monitor must be measures you trend to determine whether the interventions are working.

Hypoglycemia is defined by the American Diabetes Association as a glucose below 70 mg/dL (3.9 mmol/L); a value below 54 mg/dL (3.0 mmol/L) is clinically significant. This client took both basal and rapid-acting insulin and then missed two meals, producing the classic adrenergic symptoms of tremor, diaphoresis, pallor, and tachycardia along with the neuroglycopenic symptom of confusion. Diabetic ketoacidosis and hyperosmolar hyperglycemic state both involve hyperglycemia, not a glucose of 48 mg/dL. The dawn phenomenon is an early morning rise in glucose from counterregulatory hormones, the opposite of this presentation.

Because the client is awake and can swallow safely, the correct treatment is the rule of 15: give 15 grams of fast-acting carbohydrate such as 4 ounces of juice or glucose tablets, then recheck the glucose in 15 minutes and repeat if it remains below 70 mg/dL. Giving more insulin, whether the scheduled aspart dose or an infusion, would deepen the hypoglycemia and could cause seizures or coma. A peanut butter sandwich is inappropriate as initial treatment because fat and protein slow gastric emptying and delay glucose absorption; a protein-containing snack is given only after the glucose has normalized and the next meal is more than an hour away.

The outcome measures are the capillary glucose, which shows whether the carbohydrate corrected the deficit, and neurologic status, which shows whether the neuroglycopenic symptoms are resolving. Serum ketones and urine specific gravity relate to DKA and hydration status, not hypoglycemia correction. Hemoglobin A1C reflects average glycemia over roughly three months and cannot change in response to an acute intervention, so it is not a parameter used to evaluate this treatment.

The 6-hour trend shows a widening pulse pressure (52 to 106 mm Hg), bradycardia (78 to 52/min), and irregular respirations with apneic periods. That is Cushing triad, a late and ominous sign of severely increased intracranial pressure. Add the Glasgow Coma Scale fall from 15 to 9 (eyes open to pain 2, incomprehensible sounds 2, localizes to pain 5), the enlarged sluggish left pupil from oculomotor nerve compression on the side of impact, and vomiting without preceding nausea, and the picture is rising intracranial pressure with impending uncal herniation. Neurogenic shock follows spinal cord injury and produces bradycardia with hypotension and warm dry skin; hypovolemic shock produces tachycardia with hypotension. This client is hypertensive, so neither fits. Postconcussion syndrome causes headache, dizziness, and poor concentration days to weeks after injury, not pupillary change or a declining level of consciousness.

Head of bed at 30 degrees with the head midline and neck unflexed promotes jugular venous drainage and lowers intracranial pressure. Notifying the provider and preparing hyperosmolar therapy, mannitol or hypertonic saline, treats cerebral edema while imaging or surgical decompression is arranged. Deep suctioning sharply raises intracranial pressure; passes should be limited to 10 seconds or less with preoxygenation. Clustering care into one prolonged session causes cumulative pressure elevation, so activities are spaced to let pressure recover. Sharp hip and knee flexion raises intra-abdominal and intrathoracic pressure and impedes cerebral venous return.

Glasgow Coma Scale score and pupillary response are the direct neurologic measures of whether intracranial pressure is responding to treatment. Serum sodium and osmolality are trended during hyperosmolar therapy to confirm effect and avoid excessive hypernatremia. Troponin, lower-extremity capillary refill, and the mechanism of injury are unrelated or historical data rather than measures of treatment response.

Dehydration, exertion, and heat are classic triggers that promote hemoglobin S polymerization, red cell sickling, and microvascular occlusion. Severe bone and joint pain in the extremities and back with a hemoglobin near the client's baseline defines a vaso-occlusive pain crisis. Acute chest syndrome requires a new pulmonary infiltrate plus fever and/or chest or respiratory findings such as cough, chest pain, tachypnea, wheezing, or hypoxemia; this client has clear lungs and no chest complaints, although the borderline SpO2 makes ongoing respiratory surveillance essential. Aplastic crisis, often triggered by parvovirus B19, presents with a hemoglobin far below baseline and a low reticulocyte count. Osteomyelitis is focal with localized erythema, warmth, and high fever rather than diffuse bilateral pain.

The two priorities are aggressive analgesia and hydration. Severe crisis pain warrants scheduled parenteral opioids rather than as-needed dosing, because peaks and troughs allow pain to escalate. Isotonic fluids reduce blood viscosity and improve microvascular perfusion. Cold application causes vasoconstriction that worsens sickling; warmth is applied instead. Fluid restriction directly worsens sickling. Meperidine is avoided in sickle cell disease because its metabolite normeperidine accumulates and lowers the seizure threshold, especially with repeated dosing and renal impairment.

The outcome measures are the pain score, trended on the same scale to show analgesic effectiveness, and oxygen saturation with respiratory assessment, which detects the evolution of acute chest syndrome, the leading cause of death in this population. Hemoglobin electrophoresis confirms the diagnosis of sickle cell disease but does not change with treatment. Family history is etiologic. Potassium is unrelated unless another complication develops, and it does not measure the response to analgesia or fluids.

This client has intrinsic acute kidney injury, most consistent with acute tubular necrosis from the combination of sepsis-related hypoperfusion, an aminoglycoside, and iodinated contrast. The creatinine more than doubled since admission 3 days ago and urine output is under 0.5 mL/kg/hr, meeting standard AKI criteria. Acute urinary retention is excluded by the bladder scan showing only 25 mL. SIADH causes dilutional hyponatremia with concentrated urine and euvolemia, not a rising creatinine with a potassium of 5.9 mEq/L. Chronic kidney disease develops over months and would not show a normal admission creatinine three days earlier.

Holding nephrotoxic drugs, including the gentamicin, is the first protective action and requires provider notification for dose adjustment or substitution. A potassium of 5.9 mEq/L is a potentially life-threatening finding, so obtaining an ECG to look for peaked T waves, a widened QRS, or a flattened P wave and initiating prescribed treatment such as calcium gluconate, insulin with dextrose, or a potassium binder is the other priority. Increasing fluids to 250 mL/hr is dangerous in a client already 3 kg heavier with crackles and edema. Ketorolac is an NSAID that reduces renal prostaglandin-mediated perfusion and is contraindicated. Potassium-rich foods would worsen the hyperkalemia; potassium is restricted.

Hourly urine output and daily weight are the most sensitive bedside indicators of whether renal function and fluid balance are improving, with daily weight the most reliable measure of fluid status. Creatinine and potassium trend the severity and the response to hyperkalemia treatment. Amylase, lipase, and INR are unrelated. The number of contrast studies is an etiologic exposure, not an outcome measure.

Anaphylaxis is highly likely when there is acute onset of skin or mucosal involvement plus respiratory compromise, reduced blood pressure, or severe gastrointestinal symptoms, or when hypotension, bronchospasm, or laryngeal involvement follows exposure to a known or highly probable allergen, even without skin signs. This client has urticaria and tongue swelling with stridor, wheezing, hypoxemia, and hypotension within minutes of a first-dose beta-lactam, which meets the criteria. Vasovagal syncope produces bradycardia with pallor and diaphoresis, not urticaria or stridor. Septic shock develops over hours with fever and vasodilation and would not begin five minutes into an infusion. A panic attack does not cause urticaria, stridor, or hypotension with an SpO2 of 89%.

Stopping the infusion removes the antigen and is the first action. Intramuscular epinephrine is the only first-line treatment for anaphylaxis; the adult dose is 0.3 to 0.5 mg of the 1 mg/mL concentration given in the vastus lateralis, which achieves faster absorption than the deltoid or subcutaneous route, and it may be repeated every 5 to 15 minutes. Antihistamines such as diphenhydramine relieve itching and hives but do not reverse airway edema or hypotension and must never delay epinephrine. Slowing the infusion leaves the trigger in place and permits progression to arrest. A bronchodilator is an adjunct for persistent bronchospasm after epinephrine, and waiting 30 minutes to reassess a client with stridor is unsafe.

Blood pressure and heart rate show whether epinephrine is reversing the distributive shock. Airway patency, stridor, and oxygen saturation show whether the laryngeal edema is resolving and whether intubation is still likely. Serum tryptase is a confirmatory diagnostic test drawn within a few hours of the event, not a treatment-response measure. WBC count is unrelated. Allergy history is etiologic data collected before the event.

Alcohol withdrawal delirium, historically called delirium tremens, typically begins 48 to 96 hours after the last drink and is defined by delirium plus autonomic hyperactivity. This client has the full picture at 72 hours: disorientation, tactile and visual hallucinations, tremor, diaphoresis, fever, tachycardia, and hypertension, with a CIWA-Ar of 24, which indicates severe withdrawal. Wernicke encephalopathy presents with the triad of confusion, ophthalmoplegia or nystagmus, and ataxia rather than autonomic storm. Hepatic encephalopathy causes asterixis and lethargy progressing to coma with an elevated ammonia, not hyperadrenergic agitation. Acute intoxication would occur on admission, not three days later, and produces sedation rather than withdrawal.

Benzodiazepines are the first-line treatment because they replace the GABA-ergic tone lost with alcohol cessation and have the strongest evidence for preventing withdrawal seizures and delirium and reducing mortality. Symptom-triggered dosing guided by the CIWA-Ar delivers less total drug and shortens treatment compared with fixed schedules. Fall precautions and a calm, quiet, well-lit environment with frequent reorientation address the delirium and the very real injury risk in a client climbing out of bed. Restraints are a last resort after less restrictive measures fail, because they increase agitation and injury. Thiamine must be given before or with glucose, since a glucose load in a thiamine-deficient client can precipitate Wernicke encephalopathy. Confronting or arguing about hallucinations escalates agitation; the nurse acknowledges the client's fear without validating the content.

The CIWA-Ar score is the standardized outcome tool that drives dosing and shows whether withdrawal is being controlled, and the vital signs objectively track resolution of autonomic hyperactivity. The admission blood alcohol level and the reported daily intake are etiologic and historical. Ammonia belongs to hepatic encephalopathy.

Uterine atony causes 70 to 80 percent of early postpartum hemorrhage and is the answer here. The hallmark is a boggy, poorly contracted fundus; a fundus that has also risen above the umbilicus and deviated laterally suggests a distended bladder, which impedes contraction, so the bladder is emptied as part of management. This client has major risk factors: macrosomia at 4,100 g and prolonged oxytocin-augmented labor, both of which overstretch or fatigue the myometrium. ACOG defines postpartum hemorrhage as a cumulative blood loss of 1,000 mL or more, or any loss with signs of hypovolemia, and both are present. A cervical laceration bleeds briskly with a firm fundus, which is the distinguishing feature. Uterine inversion presents with a fundus that cannot be palpated abdominally, often with a mass at the introitus and profound shock. Postpartum infection develops over days with fever and foul-smelling lochia.

Fundal massage is the immediate action because mechanical stimulation causes the myometrium to contract and compress the open spiral arterioles at the placental site. Increasing the oxytocin infusion sustains that contraction pharmacologically. Delaying reassessment for 30 minutes in an actively hemorrhaging, hypotensive, tachycardic client is unsafe. A sitz bath applies heat that promotes vasodilation and does nothing for atony, and ambulating a hypotensive client risks syncope. Ibuprofen treats afterpains but does not address bleeding.

Fundal tone with quantified blood loss directly measures whether the uterus is contracting and bleeding is slowing; quantified measurement is now the standard because visual estimation underestimates loss. Blood pressure and heart rate track the hemodynamic response, remembering that tachycardia appears before hypotension in a healthy postpartum client. Apgar scores, blood type, and gestational age are documentation or etiologic data, not measures of treatment response.