ATI-AMS ATI Adult medical surgical Exam - Set 1 - Part 2

Correct Answer: Dyspnea and peripheral edema

Fluid volume excess causes dyspnea as fluid backs into the lungs and peripheral edema as excess fluid collects in tissues. Crackles, weight gain, and distended neck veins also accompany this overload. Option b is incorrect because sunken eyeballs and oliguria are classic deficit findings caused by low fluid volume. In excess the body holds extra fluid, so these signs of dehydration contradict the overloaded state. Option c is incorrect because a thready pulse and thirst signal deficit, where shrinking volume weakens the pulse and triggers thirst. Excess instead produces a strong bounding pulse, making these findings inconsistent with overload. Option d is incorrect because flattened neck veins and a dry tongue reflect inadequate volume. Fluid excess distends the neck veins and moistens tissues, so these dehydration signs belong to deficit rather than overload.

Correct Answer: Monitor for orthostatic hypotension

With dizziness on standing and borderline pressure, the nurse should monitor for orthostatic hypotension, offer fluids, and keep the client in bed because the dehydration creates a real fall risk. Option a is incorrect because restricting fluids worsens dehydration when the client actually needs rehydration. Limiting intake would deepen the volume loss driving the low pressure and confusion, moving care in the wrong direction. Option b is incorrect because encouraging independent ambulation ignores the fall risk created by dizziness and orthostatic changes. A dehydrated, confused client should be kept safe in bed rather than pushed to walk alone. Option d is incorrect because withholding IV fluid therapy denies one of the main treatments for dehydration. Oral or IV rehydration restores the lost volume, so refusing fluids leaves the underlying deficit and its troubling symptoms completely uncorrected.

Correct Answer: Administer oxygen

In hypovolemic shock, oxygen delivery to the tissues drops sharply, so administering oxygen is the priority to support oxygenation while fluid replacement and other measures follow close behind. Option b is incorrect because obtaining a daily weight tracks fluid status over time but does nothing for the immediate perfusion crisis. During active shock the client needs oxygen and volume, not a routine monitoring task. Option c is incorrect because antiembolism stockings address clot prevention, an issue unrelated to the failing perfusion of shock. They do not restore oxygen delivery, so applying them would not meet the urgent need. Option d is incorrect because a sodium-restricted diet is a measure for fluid excess, the opposite of this client's problem. Restricting sodium offers no help in a deficit emergency that calls for oxygen and fluids.

Correct Answer: Frothy pink-tinged sputum

Pulmonary edema produces frothy pink-tinged sputum along with ascending crackles and dyspnea at rest as fluid floods the alveoli. This finding signals a serious complication of fluid overload. Option a is incorrect because sunken eyeballs are a sign of fluid deficit, not the overload that causes pulmonary edema. This dehydration finding would not appear in a client whose lungs are filling with excess fluid. Option b is incorrect because poor skin turgor reflects low fluid volume and dehydration. Pulmonary edema arises from too much fluid, so diminished turgor points to the opposite imbalance and would not be expected here. Option c is incorrect because flattened neck veins appear when the circulating volume is low rather than high. In fluid overload the neck veins distend with the extra volume, so flat veins directly contradict the excess state that produces pulmonary edema.

Correct Answer: 'Report a sudden weight gain promptly.'

Clients who have fluid excess should weigh themselves daily at the same time each morning and report any sudden weight gain, since a rapid rise reflects retained fluid that needs prompt attention. Option a is incorrect because drinking all fluids in the morning ignores the instruction to divide the daily fluid allotment across the day. Front-loading intake could overload the client and does not match the prescribed restriction. Option b is incorrect because adding salt directly opposes the sodium-restricted diet these clients need. Extra sodium pulls water into the vascular space and worsens fluid retention, making this advice harmful for overload. Option d is incorrect because lying flat all day works against positioning for fluid excess, which favors semi- or high-Fowler's to ease breathing. A flat position can increase respiratory effort when fluid is overloaded.

Correct Answer: Confusion and muscle weakness

Hyponatremia causes water to shift into cells, producing cellular edema with confusion, headache, decreased reflexes, and muscle weakness. Severe cases can progress to seizures from the swelling of brain cells. Option a is incorrect because intense thirst and high fever belong to hypernatremia, where water leaves the cells and dehydrates them. These findings reflect a high sodium level rather than the low sodium of hyponatremia. Option b is incorrect because dry mucous membranes and restlessness are features of hypernatremia and cellular dehydration. In hyponatremia cells take on water, so these signs of a fluid-depleted state point to the opposite imbalance. Option c is incorrect because increased deep-tendon reflexes accompany hypernatremia, whereas hyponatremia tends to lower the reflexes instead. The depressed neuromuscular response that comes with a low sodium level makes brisk, exaggerated reflexes inconsistent with this particular finding.

Correct Answer: Encourage water intake and restrict sodium

Care for hypernatremia includes encouraging water and restricting sodium to dilute the elevated level, often with loop diuretics. Seizure precautions are also maintained because high sodium can cause seizures and coma. Option b is incorrect because rapidly giving hypertonic saline would raise sodium further and worsen the imbalance. Hypertonic saline is reserved for severe hyponatremia and is infused slowly, making it inappropriate for an already high level. Option c is incorrect because providing high-sodium foods adds the very electrolyte that is already elevated. The plan calls for sodium restriction, so increasing dietary sodium would deepen the hypernatremia rather than correct it. Option d is incorrect because limiting free water deprives the client of the dilution needed to lower sodium. Because water follows sodium, encouraging fluids helps restore balance, so restricting water moves care in the wrong direction.

Correct Answer: Tap-water enemas diluting electrolytes

Tap water is hypotonic and the GI losses from enemas are isotonic, so repeated tap-water enemas dilute the blood and flush out electrolytes, producing the low sodium and potassium described. Option a is incorrect because isotonic IV fluids match the body's tonicity and would not dilute the blood or cause this drop. Because they do not lower electrolytes, they cannot explain the low sodium and potassium values. Option b is incorrect because routine antibiotics do not characteristically deplete sodium and potassium through this mechanism. The imbalance here arises from the enemas, not from antibiotic therapy, which targets infection instead. Option c is incorrect because a high-sodium meal plan would tend to raise sodium rather than lower it. This intake works against the observed hyponatremia, so it cannot be the source of the depleted electrolytes.

Correct Answer: Cardiac rhythm on the ECG

Hyperkalemia raises the risk of dangerous dysrhythmias, so the nurse prioritizes assessing the cardiac rhythm. Peaked T waves and a widened QRS can progress to life-threatening rhythms or asystole. Option a is incorrect because polyuria and thirst are not the hallmark of high potassium, and hyperkalemia tends to cause oliguria instead. These findings do not capture the cardiac danger that makes rhythm the priority assessment. Option c is incorrect because constipation reflects hypokalemia, where slowed bowel activity occurs, rather than hyperkalemia, which often brings hyperactive bowel sounds and diarrhea. Focusing on the bowel pattern here would miss the urgent cardiac concern that dominates high potassium. Option d is incorrect because hand tremors are not a defining feature of hyperkalemia and do not signal its most lethal threat. The peaked T waves and rhythm changes of high potassium make cardiac monitoring far more important.

Correct Answer: Calcium gluconate

Calcium gluconate provides cardiac protection in hyperkalemia by stabilizing the myocardium against dysrhythmias. Insulin with dextrose or sodium bicarbonate may also be used to shift potassium back into the cells. Option a is incorrect because potassium chloride would add more potassium to an already dangerous level. Giving it would intensify the hyperkalemia and its cardiac threat, the exact opposite of the protection the client requires. Option b is incorrect because a potassium-sparing diuretic causes the body to retain potassium and is actually a cause of hyperkalemia. Using it here would worsen the elevation rather than protect the heart from rhythm disturbances. Option c is incorrect because salt substitutes are high in potassium and contribute to hyperkalemia. Rather than safeguarding the heart, this choice would raise the potassium level and heighten the risk of dysrhythmias.

Correct Answer: Infuse the potassium with an IV pump

IV potassium must be infused slowly with a pump and never bolused, because rapid administration can cause cardiac arrest. The maximum recommended rate keeps the infusion safe for the client. Option a is incorrect because giving potassium by rapid bolus risks fatal cardiac arrest, which is why it is never bolused. The drug must drip slowly within a strict rate limit rather than being delivered all at once. Option b is incorrect because the subcutaneous route is prohibited for potassium because it causes tissue necrosis. Potassium is never given subQ or IM, so this route would harm the client and is not an option. Option d is incorrect because pushing the dose to fix the level fast ignores the strict slow-infusion requirement. Speeding correction this way could trigger cardiac arrest, defeating the careful pace that potassium replacement demands.

Correct Answer: Flattened T wave, prominent U wave

Hypokalemia produces a flattened T wave, a prominent U wave, and ST depression on the ECG. These changes reflect the altered repolarization caused by a low potassium level. Option b is incorrect because peaked T waves with a widened QRS are the signature of hyperkalemia, not low potassium. These findings appear when potassium is high and can progress to asystole, the opposite imbalance. Option c is incorrect because tall narrow T waves suggest elevated potassium rather than a deficit. Hypokalemia instead flattens the T wave and adds a U wave, so this tall-T pattern points to the wrong direction. Option d is incorrect because a shortened QT interval is not the characteristic change that hypokalemia produces. Low potassium produces a flat T wave and prominent U wave, making the shortened QT an inaccurate expectation here.

Correct Answer: Diabetic ketoacidosis

Diabetic ketoacidosis is associated with hyperkalemia because the acidosis shifts potassium out of the cells and into the bloodstream, raising the measured potassium level even when total body potassium is not increased. Option a is incorrect because heart failure is linked with hyponatremia rather than high potassium. Fluid retention dilutes sodium in this condition, so it does not produce the elevated potassium seen with acidotic shifts. Option c is incorrect because the electrolyte pattern of Cushing's syndrome tends toward hypernatremia from excess corticosteroid effects, not hyperkalemia. This condition drives sodium retention rather than the potassium elevation that the acidotic shift in ketoacidosis produces. Option d is incorrect because thyroidectomy is associated with hypocalcemia when the nearby parathyroid glands are damaged or removed during the operation. The electrolyte risk it carries involves calcium, not the potassium rise tied to the acidosis of ketoacidosis.

Correct Answer: Tetany and paresthesia of the fingers

Hypocalcemia causes tetany along with paresthesia of the fingers and lips, muscle twitches, and hyperactive reflexes. Positive Chvostek's and Trousseau's signs further reflect the heightened neuromuscular excitability that a low calcium level produces. Option b is incorrect because constipation and hypoactive bowel sounds belong to hypercalcemia, where excess calcium slows smooth muscle activity. Low calcium instead heightens neuromuscular excitability, so these sluggish gastrointestinal findings reflect the opposite imbalance from the one described. Option c is incorrect because decreased reflexes directly contradict hypocalcemia, which produces hyperactive deep-tendon reflexes instead. The increased neuromuscular irritability that defines a low calcium level makes diminished or sluggish reflexes inconsistent with this particular condition. Option d is incorrect because flat or inverted T waves are linked to hypercalcemia and its dysrhythmia risk. Hypocalcemia instead prolon

Correct Answer: Tap the cheek over the facial nerve

To elicit Chvostek's sign the nurse taps the cheek over the facial nerve and watches for facial twitching, a positive response that indicates the neuromuscular irritability of hypocalcemia. Option a is incorrect because inflating a blood-pressure cuff tests for Trousseau's sign, not Chvostek's. While both detect hypocalcemia, the cuff produces hand and finger spasm rather than the facial twitch of the cheek-tap test. Option b is incorrect because dorsiflexing the foot is a maneuver for assessing other conditions and does not elicit Chvostek's sign. The facial nerve, accessed at the cheek, is the structure tested for this calcium-related response. Option c is incorrect because pressing over the carotid artery is unrelated to Chvostek's sign and could be unsafe. Chvostek's testing targets the facial nerve at the cheek, not the neck vessels, to detect low calcium.

Correct Answer: Infuse the calcium slowly using a pump

Calcium gluconate for life-threatening hypocalcemia must be given slowly through an infusion pump, because administering it too quickly can cause cardiac arrest. Careful pacing keeps the replacement safe. Option a is incorrect because a rapid IV push delivers the calcium too fast and can trigger cardiac arrest. The drug requires a slow, controlled infusion, so pushing it quickly directly violates the safety requirement. Option b is incorrect because the intramuscular route is not appropriate for emergency calcium gluconate replacement. This electrolyte requires slow IV infusion via pump, so giving it IM would not safely or effectively correct the deficit. Option d is incorrect because mixing the dose into a large bolus to run in quickly defeats the need for slow administration. Speeding the calcium this way raises the cardiac arrest risk the controlled infusion is meant to prevent.

Correct Answer: Hyperactive deep-tendon reflexes and tetany

Hypomagnesemia increases nerve impulse transmission, producing hyperactive deep-tendon reflexes, paresthesias, tetany, and seizures. Positive Chvostek's and Trousseau's signs often accompany the low magnesium level, much as they do in hypocalcemia. Option a is incorrect because decreased reflexes and flaccid paralysis suggest an excess of magnesium, which depresses neuromuscular activity. Low magnesium instead heightens excitability, so these dampened findings reflect the opposite of the deficit the client actually has. Option c is incorrect because a bounding pulse and hypertension relate to fluid excess rather than to a magnesium deficit. These cardiovascular findings do not capture the heightened neuromuscular irritability with tetany and brisk reflexes that defines low magnesium. Option d is incorrect because warm flushed skin and lethargy do not match the heightened nerve activity of hypomagnesemia. The deficit instead causes brisk reflexes and tetany, making these calm,

Correct Answer: An elevated carbon dioxide level

Respiratory acidosis results from hypoventilation, which retains carbon dioxide and raises its level. Because the lungs control carbon dioxide, the respiratory disorders are identified by an abnormal carbon dioxide value. Option a is incorrect because a low carbon dioxide level points to respiratory alkalosis from hyperventilation, the exact reverse of this disorder. Acidosis from hypoventilation builds carbon dioxide up in the blood rather than blowing it off through the lungs. Option b is incorrect because an elevated bicarbonate points to metabolic alkalosis, a problem of the kidneys rather than the lungs. Respiratory acidosis is defined by a carbon dioxide change, not a bicarbonate elevation. Option c is incorrect because a low bicarbonate level signals metabolic acidosis, which arises from bicarbonate loss through routes like diarrhea. This is a metabolic finding, whereas respiratory acidosis is identified instead by retained carbon dioxide from the lungs.

Correct Answer: Respiratory alkalosis

Hyperventilation from anxiety blows off carbon dioxide and lowers its level, producing respiratory alkalosis. Anxiety reduction and rebreathing techniques help the client retain carbon dioxide and restore balance. Option a is incorrect because respiratory acidosis comes from hypoventilation that retains carbon dioxide, which is the opposite of fast breathing. Hyperventilation from anxiety lowers carbon dioxide, so this rising-carbon-dioxide disorder does not fit the scenario described. Option c is incorrect because metabolic acidosis stems from a low bicarbonate due to causes like ketoacidosis or diarrhea. It is not produced by rapid breathing, which alters carbon dioxide rather than bicarbonate. Option d is incorrect because metabolic alkalosis results from a high bicarbonate, often from vomiting or antacids. Because hyperventilation affects carbon dioxide and not bicarbonate, this metabolic disorder does not match the anxious client.

Correct Answer: Kussmaul respirations

Diabetic ketoacidosis causes metabolic acidosis with a low bicarbonate, and the client develops Kussmaul respirations. These rapid, deep breaths are the lungs compensating by blowing off carbon dioxide to raise the falling pH. Option b is incorrect because numbness, tingling, and tetany are features of metabolic alkalosis, not metabolic acidosis. These signs reflect a high bicarbonate state, so they do not match the acidosis driven by ketoacidosis. Option c is incorrect because tinnitus and finger numbness point to respiratory alkalosis from hyperventilation. While salicylate toxicity can begin that way, the ketoacidosis here produces metabolic acidosis and its deep Kussmaul breathing. Option d is incorrect because tachycardia attributed to anxiety alone fits respiratory alkalosis rather than the acidosis of ketoacidosis. Choosing it overlooks the deep, compensatory Kussmaul respirations that truly distinguish the metabolic acidosis developing in this client.