NCLEX Medical-Surgical: Endocrine Disorders 1 β Questions and Answers
Question 1: A patient is admitted with diabetic ketoacidosis (DKA). Which combination of lab findings confirms this diagnosis?
- Blood glucose 600 mg/dL, pH 7.39, serum osmolality 330 mOsm/kg
- Blood glucose 380 mg/dL, pH 7.24, serum ketones positive, anion gap 18 (Correct answer)
- Blood glucose 250 mg/dL, pH 7.32, bicarbonate 22 mEq/L
- Blood glucose 180 mg/dL, pH 7.42, HbA1c 9%
Correct answer: Blood glucose 380 mg/dL, pH 7.24, serum ketones positive, anion gap 18
DKA is defined by the triad: hyperglycemia (typically >250 mg/dL), metabolic acidosis (pH <7.35, bicarbonate <18 mEq/L), and positive serum ketones with elevated anion gap.
DKA diagnostic criteria: (1) Hyperglycemia: blood glucose >250 mg/dL (may be lower in euglycemic DKA with SGLT2 inhibitors); (2) Metabolic acidosis: pH <7.3 and/or bicarbonate <18 mEq/L; (3) Ketonemia/ketonuria: positive serum ketones (beta-hydroxybutyrate >3 mmol/L); (4) Elevated anion gap: >12 mEq/L. Compare with HHS (Hyperosmolar Hyperglycemic State): glucose typically >600 mg/dL, extreme hyperosmolarity (>320 mOsm/kg), minimal ketones, no significant acidosis. DKA treatment: IV fluids (0.9% NS first, then 0.45% NS), regular insulin IV infusion, electrolyte replacement (especially potassium β must be β₯3.5 before starting insulin), address precipitating cause. Monitor glucose every hour.
Question 2: A patient with hypothyroidism is started on levothyroxine (Synthroid). Which instruction should the nurse include?
- Take the medication with breakfast to prevent GI upset
- Take the medication 30β60 minutes before breakfast on an empty stomach for best absorption (Correct answer)
- Take the medication at bedtime to coincide with thyroid hormone production
- Take the medication with calcium supplements to enhance absorption
Correct answer: Take the medication 30β60 minutes before breakfast on an empty stomach for best absorption
Levothyroxine absorption is maximized on an empty stomach, 30β60 minutes before breakfast. Food, calcium, iron, and antacids significantly reduce absorption.
Levothyroxine (T4 replacement) has predictable, but highly variable, individual absorption. Key patient education: (1) Take on empty stomach, 30β60 minutes before breakfast (or 4 hours after last meal); (2) Avoid calcium supplements, iron supplements, antacids containing calcium/magnesium/aluminum, and high-fiber foods within 4 hours β all reduce absorption; (3) Take at the same time daily; (4) Consistent formulation (brand vs. generic differences can affect thyroid levels); (5) Dose titrated by TSH levels (goal: TSH 0.4β4.0 mIU/L for most patients); (6) Signs of too much (hyperthyroid): tachycardia, weight loss, heat intolerance, insomnia; (7) Therapy is lifelong; never stop abruptly.
Question 3: A patient is admitted in an Addisonian crisis. Which nursing intervention is the highest priority?
- Administer IV hydrocortisone and IV normal saline immediately (Correct answer)
- Restrict fluids until blood pressure stabilizes
- Administer mineralocorticoid replacement as the sole treatment
- Obtain cortisol level and wait for results before starting treatment
Correct answer: Administer IV hydrocortisone and IV normal saline immediately
Addisonian crisis (acute adrenal insufficiency) is life-threatening, with profound hypotension, hyponatremia, and hyperkalemia. Immediate IV hydrocortisone and aggressive IV fluid resuscitation are the priority.
Addisonian crisis (acute adrenal insufficiency) is a life-threatening emergency caused by acute deficiency of cortisol (and often aldosterone). Triggers: abrupt steroid withdrawal, physiologic stress (surgery, infection, trauma) in a patient with adrenal insufficiency, bilateral adrenal hemorrhage. Presentation: severe hypotension/shock, profound weakness, nausea/vomiting, abdominal pain, altered mental status, hyponatremia, hyperkalemia, hypoglycemia. Emergency treatment: (1) IV hydrocortisone 100 mg bolus, then 50β100 mg every 6β8 hours; (2) IV 0.9% NS with dextrose (D5NS) β aggressive fluid resuscitation; (3) Correct electrolyte abnormalities; (4) Identify and treat precipitating cause. Do NOT delay treatment for laboratory results β clinical diagnosis justifies treatment.
Question 4: A nurse is teaching a patient with type 2 diabetes about metformin. Which laboratory value requires immediate provider notification before administering metformin?
- HbA1c of 8.2%
- Fasting glucose of 185 mg/dL
- eGFR of 25 mL/min/1.73mΒ² (Correct answer)
- Triglycerides of 220 mg/dL
Correct answer: eGFR of 25 mL/min/1.73mΒ²
Metformin is contraindicated with eGFR <30 mL/min/1.73mΒ² due to risk of lactic acidosis from accumulation. An eGFR of 25 is below this threshold β metformin should be withheld and the provider notified.
Metformin is the first-line oral agent for type 2 diabetes. It decreases hepatic glucose production and increases peripheral insulin sensitivity. Primary concern: lactic acidosis β rare but potentially fatal. Risk increases with impaired renal function (metformin is renally excreted). FDA guidelines: (1) Contraindicated if eGFR <30 mL/min/1.73mΒ²; (2) Not recommended if eGFR 30β45 β use with caution; (3) Dose reduction considered at eGFR 45β60; (4) Safe at eGFR β₯60. Also hold for: IV contrast (as discussed), major surgery, conditions causing acute kidney injury, hepatic failure, or excessive alcohol intake. Check eGFR before starting and at least annually thereafter. Signs of lactic acidosis: nausea, vomiting, abdominal pain, myalgias, respiratory distress, altered consciousness.
Question 5: A patient is admitted with a serum calcium level of 13.2 mg/dL (normal 8.5β10.5 mg/dL). Which set of symptoms would the nurse expect?
- Tetany, muscle cramps, and positive Chvostek's sign
- Bone pain, constipation, polyuria, confusion, and muscle weakness (Correct answer)
- Hyperreflexia, carpopedal spasms, and laryngospasm
- Bradycardia with peaked T waves on ECG
Correct answer: Bone pain, constipation, polyuria, confusion, and muscle weakness
Hypercalcemia causes 'bones, stones, groans, and moans': bone pain, kidney stones, constipation, nausea, polyuria, confusion, muscle weakness. Tetany and positive Chvostek's are signs of hypocalcemia.
Hypercalcemia (Ca > 10.5 mg/dL) mnemonic β 'Bones, Stones, Groans, and Moans': Bones: bone pain, pathologic fractures (from hyperparathyroidism); Stones: kidney stones (calcium oxalate, calcium phosphate); Groans: constipation, nausea, vomiting, anorexia, peptic ulcers; Moans: cognitive dysfunction (confusion, depression, lethargy, coma). Also: polyuria/polydipsia (hypercalciuria), muscle weakness, shortened QT interval on ECG. Most common causes: Primary hyperparathyroidism (outpatient), malignancy (inpatient). Treatment depends on severity: mild (<12): hydration; moderateβsevere (>12 + symptoms): IV 0.9% NS (fluids), calcitonin, bisphosphonates (pamidronate), steroids, loop diuretics. Compare hypocalcemia: tetany, Chvostek's/Trousseau's signs, hyperreflexia.
Question 6: A patient undergoes a total thyroidectomy. Postoperatively, which assessment is the priority?
- Blood glucose monitoring every 2 hours
- Monitoring for hypocalcemia symptoms: perioral tingling, muscle cramps, positive Chvostek's sign (Correct answer)
- Assessing for weight gain and cold intolerance
- Monitoring for adrenal insufficiency
Correct answer: Monitoring for hypocalcemia symptoms: perioral tingling, muscle cramps, positive Chvostek's sign
Total thyroidectomy can damage the parathyroid glands (located on the posterior thyroid), causing hypoparathyroidism and hypocalcemia. Perioral tingling, muscle cramps, tetany, and positive Chvostek's/Trousseau's signs are early indicators.
Total thyroidectomy complications: (1) Hypocalcemia β most common complication; parathyroid glands may be inadvertently removed or devascularized β hypoparathyroidism β decreased PTH β hypocalcemia. Monitor for: perioral and fingertip tingling, Chvostek's sign (facial twitch with tapping CN VII), Trousseau's sign (carpal spasm with blood pressure cuff inflated), tetany, laryngospasm. Have calcium gluconate at bedside. (2) Laryngeal nerve damage β hoarseness, voice changes; bilateral damage β respiratory obstruction. (3) Hematoma β airway compression emergency. (4) Thyroid storm β rare, from manipulation during surgery. Calcium levels monitored every 4β6 hours postoperatively; oral calcium and calcitriol may be required.
Question 7: A patient with Cushing's syndrome is being assessed. Which cluster of findings is most consistent with this diagnosis?
- Weight loss, hyperpigmentation, and hypotension
- Central obesity, moon face, buffalo hump, purple striae, and hyperglycemia (Correct answer)
- Exophthalmos, heat intolerance, and tachycardia
- Myxedema, constipation, and bradycardia
Correct answer: Central obesity, moon face, buffalo hump, purple striae, and hyperglycemia
Cushing's syndrome results from excess cortisol causing central obesity, moon face, buffalo hump (cervical fat pad), purple striae (thin skin), hyperglycemia, hypertension, and osteoporosis.
Cushing's syndrome = excess cortisol (endogenous β pituitary adenoma [Cushing's disease], adrenal tumor, ectopic ACTH; exogenous β prolonged high-dose corticosteroid therapy). Classic features: (1) Weight redistribution: central obesity (truncal), moon face, buffalo hump (dorsocervical fat pad), supraclavicular fat pads; (2) Skin changes: purple/violaceous wide striae, thin skin, easy bruising, poor wound healing; (3) Metabolic: hyperglycemia (cortisol opposes insulin), hypertension, hypokalemia; (4) Musculoskeletal: proximal muscle weakness, osteoporosis; (5) Immune suppression: recurrent infections; (6) Menstrual irregularities, hirsutism; (7) Psychological: depression, anxiety, cognitive changes. Screening: 24-hour urinary free cortisol, late-night salivary cortisol, overnight dexamethasone suppression test.
Question 8: A patient with type 1 diabetes has a blood glucose of 52 mg/dL and is conscious and able to swallow. What is the priority intervention?
- Administer 1 mg glucagon IM
- Give 15 g of fast-acting carbohydrate orally and recheck glucose in 15 minutes (Rule of 15) (Correct answer)
- Start a 10% dextrose IV infusion immediately
- Administer 50 mL of 50% dextrose IV push
Correct answer: Give 15 g of fast-acting carbohydrate orally and recheck glucose in 15 minutes (Rule of 15)
The 'Rule of 15' for conscious hypoglycemia: give 15 g of fast-acting carbohydrate (4 oz juice, glucose tabs), wait 15 minutes, recheck glucose. Repeat if still <70 mg/dL. Glucagon and IV dextrose are for unconscious patients.
Hypoglycemia management ('Rule of 15'): For conscious patient able to swallow: (1) Give 15 g fast-acting carbohydrate: 4 oz (120 mL) juice/regular soda, 3β4 glucose tablets, 1 tablespoon honey, 15 jellybeans; (2) Wait 15 minutes; (3) Recheck glucose; (4) Repeat if still <70 mg/dL; (5) Once normalized, eat a snack or meal to prevent recurrence. For unconscious/unable to swallow: (1) Hospital: D50W (dextrose 50%) 25β50 mL IV push; or (2) Home: glucagon 1 mg IM/SQ (kit). Neonates/pediatrics: dextrose 10% IV. After treatment, identify and address cause: too much insulin, missed meal, unusual exercise. Document glucose before and after treatment.
Question 9: A patient with SIADH (syndrome of inappropriate antidiuretic hormone) has a serum sodium of 118 mEq/L. Which intervention should the nurse anticipate?
- Encourage liberal fluid intake to dilute the excess sodium
- Fluid restriction, monitoring neurological status, and possibly hypertonic saline (3% NaCl) (Correct answer)
- Administer IV potassium replacement as the priority
- Initiate diuretic therapy to eliminate excess fluid rapidly
Correct answer: Fluid restriction, monitoring neurological status, and possibly hypertonic saline (3% NaCl)
SIADH causes dilutional hyponatremia. With severe hyponatremia (Na < 120 mEq/L), neurological symptoms (confusion, seizures, coma) can occur. Treatment is fluid restriction and potentially hypertonic saline for severe/symptomatic cases.
SIADH: ADH causes excess water retention, diluting serum sodium (dilutional hyponatremia). Causes: CNS disorders, pulmonary disease (SCLC), medications (SSRIs, carbamazepine, cyclophosphamide). Clinical features: hyponatremia (Na <135), urine osmolality > plasma osmolality, concentrated urine sodium >20 mEq/L, euvolemia or mild hypervolemia. Management: (1) Mild-moderate (Na 125β135): fluid restriction 800β1000 mL/day; (2) Moderate (Na <125, asymptomatic): fluid restriction, salt tablets, demeclocycline or tolvaptan (ADH antagonist); (3) Severe/symptomatic (Na <120 with neurological symptoms): 3% hypertonic saline via central line, rate to raise Na no more than 8β12 mEq/L per day (prevent osmotic demyelination syndrome β rapid correction is dangerous). Monitor serum sodium every 2β4 hours during active treatment.
Question 10: A patient presents with pheochromocytoma. Which vital sign finding is most characteristic?
- Persistent low-grade fever with sinus bradycardia
- Severe paroxysmal hypertension (BP >200/120) with headache, diaphoresis, and palpitations (Correct answer)
- Orthostatic hypotension with reflex tachycardia
- Fixed hypertension without variation throughout the day
Correct answer: Severe paroxysmal hypertension (BP >200/120) with headache, diaphoresis, and palpitations
Pheochromocytoma is an adrenal medullary tumor secreting excess catecholamines. Classic triad: episodic severe hypertension, headache, and diaphoresis with palpitations. Paroxysmal episodes are triggered by tumor release of epinephrine/norepinephrine.
Pheochromocytoma is a catecholamine-secreting tumor of the adrenal medulla (90%) or extra-adrenal paraganglia. Classic '5 Ps': Pressure (severe episodic hypertension), Pain (severe headache β worst of their life), Perspiration (profuse diaphoresis), Palpitations (tachycardia), Pallor/Panic. Episodes may last minutes to hours, triggered by emotional stress, exercise, urination, tumor manipulation. Diagnosis: 24-hour urinary catecholamines/metanephrines (most sensitive), plasma metanephrines. Imaging: CT or MRI abdomen. Treatment: surgical resection (only cure) after alpha-blockade (phenoxybenzamine or phentolamine β MUST start alpha-blocker before beta-blocker to prevent hypertensive crisis). Hypertensive crisis: phentolamine IV. NEVER give beta-blockers first β causes unopposed alpha stimulation and worsens hypertension.
Question 11: A patient with diabetes insipidus (DI) is being evaluated. Which laboratory findings would the nurse expect?
- Low serum sodium, high urine specific gravity, and oliguria
- High serum sodium (hypernatremia), low urine specific gravity (<1.005), and polyuria (Correct answer)
- Low serum sodium, low urine specific gravity, and normal urine output
- Normal serum sodium, high urine osmolality, and oliguria
Correct answer: High serum sodium (hypernatremia), low urine specific gravity (<1.005), and polyuria
DI results from ADH deficiency (central) or kidney resistance to ADH (nephrogenic), causing inability to concentrate urine. This leads to massive dilute urine output, dehydration, and hypernatremia.
Diabetes Insipidus: absence or resistance to ADH β kidneys cannot concentrate urine β dilute polyuria (3β20 L/day), polydipsia. Two types: Central DI (ADH deficiency β pituitary/hypothalamus damage): low ADH, brain tumor, head trauma, neurosurgery; Nephrogenic DI (kidney resistance to ADH): caused by lithium, demeclocycline, hypercalcemia, hypokalemia, genetic. Lab findings: (1) Serum sodium: HIGH (hypernatremia) β excessive free water loss; (2) Serum osmolality: HIGH (>300 mOsm/kg); (3) Urine specific gravity: LOW (<1.005); (4) Urine osmolality: LOW (<200 mOsm/kg). Water deprivation test confirms diagnosis. Treatment: Central DI: desmopressin (DDAVP) intranasal/oral/IV; Nephrogenic DI: thiazide diuretics, NSAIDs, low-sodium diet. Differentiate from SIADH (opposite findings).
Question 12: A nurse is monitoring a patient after subtotal parathyroidectomy for hyperparathyroidism. The patient reports tingling around the lips and in the hands 12 hours postoperatively. What is the priority action?
- Administer PRN pain medication β this is expected postoperative discomfort
- Assess for positive Chvostek's and Trousseau's signs and notify the provider for possible hypocalcemia (Correct answer)
- Encourage the patient to breathe into a paper bag to correct hyperventilation
- Administer a prescribed antihypertensive for expected postoperative hypertension
Correct answer: Assess for positive Chvostek's and Trousseau's signs and notify the provider for possible hypocalcemia
Perioral and extremity tingling are classic early signs of hypocalcemia ('hungry bone syndrome') following parathyroidectomy. Chvostek's and Trousseau's signs confirm tetany risk; IV calcium is the urgent treatment.
After parathyroidectomy for hyperparathyroidism, serum calcium can drop precipitously β 'hungry bone syndrome' occurs when bones, previously depleted by excess PTH, rapidly absorb calcium from the bloodstream. Signs of hypocalcemia: perioral tingling (earliest), fingertip tingling, muscle cramps, Chvostek's sign (tap CN VII at cheek β facial muscle twitch), Trousseau's sign (BP cuff inflated above systolic for 3 min β carpal spasm), laryngospasm, generalized tetany, seizures. If confirmed: IV calcium gluconate (slow IV push, 1β2 g in 10 min); maintain IV access; PO calcium carbonate + vitamin D (calcitriol) for ongoing management. Serum calcium monitored every 4β6 hours postoperatively. Keep calcium gluconate at the bedside.
Question 13: A patient with hyperthyroidism develops fever of 104Β°F, extreme agitation, tachycardia (HR 160), and hypertension after thyroid surgery. What condition does this represent?
- Malignant hyperthermia from anesthesia
- Thyroid storm (thyrotoxic crisis) (Correct answer)
- Neuroleptic malignant syndrome
- Septic shock from surgical infection
Correct answer: Thyroid storm (thyrotoxic crisis)
Thyroid storm is a life-threatening exacerbation of hyperthyroidism characterized by extreme hyperthermia, tachycardia, hypertension, and altered mental status, triggered by surgical stress, infection, or non-compliance.
Thyroid storm (thyrotoxic crisis) is a rare, life-threatening emergency of extreme thyroid hormone excess. Triggers: thyroid surgery, infection, trauma, childbirth, radioiodine therapy, abrupt antithyroid drug discontinuation. Features (Burch-Wartofsky scoring): fever >104Β°F (38.9Β°C), tachycardia >140 bpm, hypertension, extreme agitation, tremors, vomiting, diarrhea, CHF, altered consciousness. Management (BPTIS): (1) Beta-blockers (propranolol β reduce HR and peripheral T4βT3 conversion); (2) PTU (propylthiouracil, preferred over methimazole β also blocks T4βT3 conversion); (3) Thyroid blocking iodine (Lugol's solution/SSKI β given 1 hour AFTER PTU); (4) ICU care, IV dexamethasone (inhibits T4βT3 conversion + adrenal support); (5) Supportive: cooling, IV fluids. Mortality 10β30% even with treatment.
Question 14: Which patient finding would suggest secondary rather than primary hypothyroidism?
- Elevated TSH and low T4
- Low TSH and low T4 (Correct answer)
- Elevated TSH and normal T4
- Normal TSH with low T3 only
Correct answer: Low TSH and low T4
Primary hypothyroidism (thyroid gland failure) causes low T4 with compensatory high TSH. Secondary hypothyroidism (pituitary failure) causes both low TSH and low T4 because the pituitary cannot produce TSH.
Hypothalamic-Pituitary-Thyroid (HPT) axis: Hypothalamus β TRH β Pituitary β TSH β Thyroid β T3/T4. Primary hypothyroidism: thyroid gland fails β low T4 β pituitary responds with high TSH (negative feedback lost) β TSHβ, T4β. Most common cause: Hashimoto's thyroiditis. Secondary hypothyroidism: pituitary fails β inadequate TSH β thyroid not stimulated β TSH low or inappropriately normal, T4β. Causes: pituitary adenoma, Sheehan's syndrome, pituitary surgery/radiation. Tertiary: hypothalamic failure (TRH deficiency) β same lab pattern as secondary. Clinical distinction important: treatment is the same (levothyroxine), but secondary/tertiary hypothyroidism must be evaluated for other pituitary hormone deficiencies (cortisol, GH, FSH/LH) and intracranial pathology.
Question 15: A nurse is administering insulin to a patient with type 1 diabetes. The prescription reads: 'Regular insulin 10 units IV push.' The insulin is available as 100 units/mL. How many milliliters should the nurse draw?
- 0.5 mL
- 0.1 mL (Correct answer)
- 1.0 mL
- 0.01 mL
Correct answer: 0.1 mL
Dose = 10 units. Available: 100 units/mL. Volume = 10 units Γ· 100 units/mL = 0.1 mL. Use a tuberculin syringe for accuracy with such small volumes.
Insulin calculation: Volume = Dose Γ· Concentration = 10 units Γ· 100 units/mL = 0.1 mL. Insulin safety: (1) Always use an insulin syringe (calibrated in units) to minimize errors β however, when drawing from a vial for IV administration, use a tuberculin syringe for accuracy; (2) Insulin is a HIGH-ALERT medication requiring independent double-check by two nurses in most facilities; (3) Only regular insulin can be given IV; all others (NPH, glargine, detemir, lispro, aspart, glulisine) are SQ only; (4) Regular insulin IV has a half-life of approximately 30 minutes; peaks at 15β30 minutes; (5) Verify with pharmacist or second nurse before administration; (6) Monitor glucose every 30β60 minutes during IV regular insulin infusion.
Question 16: A patient is diagnosed with primary hyperaldosteronism (Conn's syndrome). Which electrolyte abnormality is most expected?
- Hyperkalemia and hyponatremia
- Hypokalemia and hypernatremia (Correct answer)
- Hyperkalemia and hypercalcemia
- Hyponatremia and hypocalcemia
Correct answer: Hypokalemia and hypernatremia
Excess aldosterone causes sodium retention and potassium excretion by the kidneys, resulting in hypokalemia (low K+) and hypernatremia (or high normal Na+), along with hypertension and metabolic alkalosis.
Aldosterone (mineralocorticoid) acts on the principal cells of the collecting duct: promotes Na+ reabsorption (and Cl- and water follow) β volume expansion and hypertension; promotes K+ and H+ excretion β hypokalemia and metabolic alkalosis. Primary hyperaldosteronism (Conn's syndrome β usually adrenal adenoma): classic features are hypertension (often difficult to control), hypokalemia (muscle weakness, cramps, polyuria), hypernatremia or normal-high sodium, metabolic alkalosis. The hypertension is volume-dependent. Diagnosis: elevated aldosterone-to-renin ratio (ARR) β high aldosterone with suppressed renin. Treatment: adrenal adenoma β surgical resection (adrenalectomy); bilateral hyperplasia β spironolactone (aldosterone antagonist) or eplerenone.
Question 17: A patient with type 2 diabetes asks about the purpose of their newly prescribed GLP-1 receptor agonist (semaglutide/Ozempic). The nurse correctly explains that this medication:
- Increases insulin release at all times regardless of blood glucose levels
- Stimulates glucose-dependent insulin release, suppresses glucagon, slows gastric emptying, and reduces appetite (Correct answer)
- Replaces natural insulin in patients with complete beta-cell failure
- Blocks glucose reabsorption in the kidneys to lower blood sugar
Correct answer: Stimulates glucose-dependent insulin release, suppresses glucagon, slows gastric emptying, and reduces appetite
GLP-1 receptor agonists mimic incretin hormones: they stimulate insulin release only when glucose is elevated, suppress glucagon, delay gastric emptying (reducing postprandial glucose), and reduce appetite β leading to weight loss.
GLP-1 (glucagon-like peptide-1) receptor agonists (semaglutide/Ozempic/Wegovy, liraglutide/Victoza, dulaglutide/Trulicity, exenatide/Byetta) mechanisms: (1) Glucose-dependent insulin secretion β stimulate insulin release only when blood glucose is elevated, minimizing hypoglycemia risk; (2) Suppress glucagon secretion β reduces hepatic glucose production; (3) Delay gastric emptying β reduces postprandial glucose spike; (4) Central appetite suppression β significant weight loss benefit; (5) Cardiovascular benefits β reduce MACE (major adverse cardiovascular events). Side effects: nausea, vomiting, diarrhea (usually improves with time β start at low dose and titrate); risk of pancreatitis; contraindicated with personal/family history of medullary thyroid carcinoma or MEN2. SGLT2 inhibitors block renal glucose reabsorption (different mechanism).
Question 18: A patient with myxedema coma is admitted to the ICU. Which interventions are the nursing priorities?
- Administer IV thyroid hormone, maintain airway, rewarm slowly, and monitor hemodynamic status (Correct answer)
- Administer high-dose corticosteroids as the sole treatment and observe for response
- Rapidly rewarm the patient with heating blankets and administer stimulants
- Restrict fluids and administer antithyroid medications to prevent overload
Correct answer: Administer IV thyroid hormone, maintain airway, rewarm slowly, and monitor hemodynamic status
Myxedema coma is severe hypothyroidism causing coma, hypothermia, bradycardia, and respiratory failure. Treatment includes IV levothyroxine, airway management, slow passive rewarming, and IV hydrocortisone (in case of concomitant adrenal insufficiency).
Myxedema coma is the extreme manifestation of hypothyroidism, with life-threatening complications: altered consciousness/coma, hypothermia (<35Β°C), bradycardia, hypotension, hyponatremia, respiratory depression/failure, ileus. Triggers: cold exposure, infection, sedatives, surgery. Management: (1) Airway: often requires mechanical ventilation (respiratory depression); (2) IV levothyroxine (T4) 200β500 mcg loading dose, then daily; some add T3 (liothyronine) for faster peripheral action; (3) Rewarming: passive/active EXTERNAL rewarming (not core rewarming β risk of cardiovascular collapse); (4) IV hydrocortisone (100 mg every 8 hours) β hypothyroid patients may have relative adrenal insufficiency; treat until this is ruled out; (5) Treat precipitating cause; (6) Electrolyte correction; (7) ICU monitoring. Mortality 20β50%.
Question 19: A patient with diabetes mellitus has a foot wound that is not healing. The nurse notes peripheral neuropathy and reduced pedal pulses. Which nursing intervention is most important?
- Massage the foot vigorously to improve circulation
- Maintain strict glycemic control, inspect feet daily, provide wound care, and consult vascular surgery (Correct answer)
- Apply a heating pad to the foot to promote healing and circulation
- Elevate the foot high above the level of the heart at all times
Correct answer: Maintain strict glycemic control, inspect feet daily, provide wound care, and consult vascular surgery
Diabetic foot wounds require glycemic optimization (promotes healing), daily foot inspection, evidence-based wound care, and vascular surgery consultation to assess perfusion. Heating pads risk burns in neuropathic feet.
Diabetic foot disease is the leading cause of non-traumatic lower extremity amputation. Pathophysiology: peripheral neuropathy (painless injury, can't feel wounds) + peripheral arterial disease (reduced blood flow, impaired healing) + immune dysfunction (infection risk). Nursing priorities: (1) Glycemic control β hyperglycemia impairs leukocyte function, collagen synthesis, and wound healing; (2) Daily foot inspection β assess color, temperature, sensation, pulses, wounds (patient should use mirror or family help); (3) Wound care β off-loading pressure (diabetic footwear, total contact casting), moist wound healing principles, debridement; (4) Vascular assessment β ABIs (ankle-brachial index), Doppler studies; vascular surgery for revascularization if PAD significant; (5) Antibiotic therapy for infection (tissue culture); (6) Avoid heating pads, soaking feet, walking barefoot. Multidisciplinary team: endocrinology, wound care, podiatry, vascular surgery.
A patient is admitted with diabetic ketoacidosis (DKA).
Which combination of lab findings confirms this diagnosis?