Diabetes Management NCLEX Practice Questions

Clients in DKA are profoundly volume depleted from osmotic diuresis, so restoring circulating volume with 0.9% normal saline is the first priority. Rehydration improves perfusion and renal clearance of glucose and begins lowering the serum glucose even before insulin is started.

Starting an IV regular insulin infusion is essential but comes AFTER fluids are underway and the potassium is known, because insulin shifts potassium into cells and can trigger dangerous hypokalemia. Giving insulin first to a dehydrated, hypokalemic client risks vascular collapse and lethal arrhythmias. IV sodium bicarbonate is not routine and is considered only for severe acidosis (pH below 7.0), because insulin therapy clears ketones and self-corrects the acidosis; unnecessary bicarbonate can cause hypokalemia and paradoxical CNS acidosis. Potassium chloride is NEVER given by IV push under any circumstance because it causes fatal cardiac arrest; potassium is diluted in IV fluids and infused slowly on a pump once the level is verified.

Clinical pearl: remember the DKA priority order as Fluids, Insulin, Potassium, Dextrose (F-I-P-D). Fluids come first to fill the tank; insulin and potassium travel together; and dextrose is added to the fluids once glucose falls to about 200-250 mg/dL so the insulin drip can keep clearing ketones without causing hypoglycemia. This reflects current ADA-aligned inpatient DKA management.

The feature that distinguishes DKA from HHS is ketosis with acidosis. Fat breakdown produces ketones (ketonuria/ketonemia) and a metabolic acidosis, and the lungs try to blow off acid through deep, rapid Kussmaul respirations, often with fruity/acetone breath. HHS characteristically has little or NO ketosis and no significant acidosis, so Kussmaul breathing is a DKA finding.

Blood glucose greater than 600 mg/dL is more typical of HHS, where glucose can climb far higher (often over 600 and sometimes above 1000 mg/dL) than in DKA, which usually runs over ~250 mg/dL. Markedly elevated serum osmolality is the hallmark of HHS (the second H in the name stands for hyperosmolar), driven by extreme hyperglycemia and dehydration. Profound dehydration with altered level of consciousness is also more prominent in HHS, which develops slowly in older type 2 adults and carries higher mortality than DKA.

Clinical pearl: DKA is the acid one (think type 1, ketones, Kussmaul, fruity breath), while HHS is the sugar-and-dehydration one (think older type 2, sky-high glucose, hyperosmolarity, mental status changes, minimal ketones). Both are treated with aggressive IV fluids, insulin, and close electrolyte/potassium monitoring, but recognizing the ketoacidosis picture is how you tell them apart on the exam.

A glucose of 58 mg/dL is hypoglycemia (under 70 mg/dL) in a client who is alert and able to swallow, so the correct response is the Rule of 15: give 15 g of fast-acting carbohydrate, such as 4 oz of fruit juice or glucose tablets, then recheck in 15 minutes and repeat the carbohydrate if the glucose is still low.

IM glucagon is reserved for clients who are unconscious or unable to swallow safely. This client is awake and can take oral carbohydrate, so glucagon is unnecessary and slower to act than juice already in the gut. Notifying the provider and withholding food is unsafe: hypoglycemia is a time-sensitive emergency that the nurse treats immediately with carbohydrate rather than delaying to make a call. A turkey sandwich provides protein and complex carbohydrate that are absorbed too slowly to correct acute hypoglycemia, and waiting an hour to recheck delays confirming that the low has resolved; a snack like that has a role only AFTER the glucose has normalized, to prevent a rebound drop.

Clinical pearl: remember 15/15 — 15 grams of fast carb, recheck in 15 minutes, repeat if needed, then follow with a longer-acting snack once you are back above 70 mg/dL. Fast simple sugar first, complex carb/protein second.

Holding metformin at the time of contrast and resuming after 48 hours once renal function is rechecked is correct for this client. Under the current ACR Manual on Contrast Media, metformin is withheld when the eGFR is below 30, when acute kidney injury is present, or for intra-arterial procedures with renal embolic risk. This client's eGFR of 26 places the client squarely in the hold category.

Contrast can precipitate acute kidney injury, and because metformin is renally cleared, impaired excretion lets it accumulate and raises the risk of lactic acidosis, a rare but potentially fatal complication. Note that contrast does not directly cause lactic acidosis; the risk comes from reduced drug clearance.

Continuing metformin as usual would be acceptable if the eGFR were 30 or greater with no AKI, but it is unsafe at this level of renal function. Increasing fluids helps protect the kidneys, yet taking an extra metformin dose compounds accumulation and is wrong. Taking metformin just before the contrast offers no protection against nausea and increases lactic-acidosis risk.

Clinical pearl: think eGFR-driven, not automatic. Hold metformin when eGFR is under 30, when AKI is present, or for arterial contrast studies, and always recheck renal function before restarting. Metformin is first-line for type 2 diabetes, commonly causes GI upset, and is not used in type 1 diabetes. Teach clients to report muscle aches, unusual fatigue, and difficulty breathing, which can signal lactic acidosis.

The correct sick-day teaching is to CONTINUE taking insulin, monitor blood glucose and ketones frequently, and stay hydrated. Illness triggers a stress response that releases counter-regulatory hormones (cortisol, epinephrine, glucagon), which RAISE blood glucose even when the client is eating little. Omitting insulin during illness is one of the most common precipitants of diabetic ketoacidosis in type 1 diabetes.

Stopping insulin until nausea resolves is dangerous precisely because glucose climbs during illness, and a type 1 client with no insulin rapidly develops ketosis and DKA. Automatically taking only half the dose is not a safe blanket rule. Insulin needs often INCREASE during illness, and any dose adjustment should be individualized and guided by frequent glucose checks and the provider's sick-day plan rather than an arbitrary cut. Using insulin only if glucose exceeds 300 mg/dL leaves the client without basal insulin coverage and invites ketoacidosis long before that threshold.

Clinical pearl: the golden sick-day rule for type 1 diabetes is 'never skip your insulin.' Check glucose every 2-4 hours, check urine or blood ketones, sip sugar-containing fluids if not eating and sugar-free fluids if glucose is high, and call the provider for persistent vomiting, rising ketones, or glucose that will not come down.

For a client who is unconscious and cannot protect the airway, the safe treatment is IM (or subcutaneous) glucagon, which mobilizes glucose from hepatic glycogen stores. Nothing should be given by mouth to an unconscious client because of the high risk of aspiration. In the hospital the equivalent action is IV dextrose 50% (D50), but at home glucagon is the go-to.

Placing glucose gel between the cheek and gum is intended for a drowsy client who still has a gag reflex and some ability to swallow. In a truly unconscious, unarousable client it can be aspirated, so it is not the best action here. Giving orange juice by mouth is contraindicated for the same reason: an unconscious client cannot swallow safely and can aspirate the fluid into the lungs. Simply waiting 15 minutes and rechecking wastes critical time. Profound hypoglycemia can cause seizures, brain injury, and death, so it must be treated immediately, not observed.

Clinical pearl: 'conscious and can swallow = oral fast carb (Rule of 15); unconscious or cannot swallow = glucagon (home) or IV D50 (hospital), and NOTHING by mouth.' After glucagon works, turn the client on their side (glucagon commonly causes vomiting) and give oral carbohydrate once they are fully awake to prevent a rebound drop.

Increased thirst, frequent urination, and increased hunger are the classic three P's of hyperglycemia (polydipsia, polyuria, and polyphagia) and are hallmark presenting symptoms of new or poorly controlled diabetes. When glucose exceeds the renal threshold, it spills into the urine and pulls water with it (osmotic diuresis), causing polyuria. The resulting dehydration drives thirst (polydipsia). Because cells cannot use glucose without adequate insulin, the body signals hunger (polyphagia), often with fatigue, blurred vision, and weight loss.

These are NOT signs of hypoglycemia, which presents acutely with shakiness, sweating, tachycardia, and confusion, not weeks of thirst and urination. They are not normal aging changes; persistent polyuria and polydipsia always warrant evaluation rather than being dismissed. While diabetes insipidus also causes marked polyuria and polydipsia, it does NOT cause polyphagia or hyperglycemia, so this trio points to diabetes mellitus, not DI alone.

Clinical pearl: memorize the three P's — Polyuria, Polydipsia, Polyphagia — as the fingerprint of hyperglycemia, and pair them with fatigue and blurred vision. Follow-up includes a fasting glucose, random glucose, or A1c; an A1c of 6.5% or higher supports the diagnosis, and the general A1c goal for many nonpregnant adults with diabetes is under 7%.

DKA management centers on fluids, insulin, potassium, and dextrose (F-I-P-D): fluids first, then insulin, with potassium watched the whole time and dextrose added as glucose falls. Administering IV 0.9% sodium chloride is correct and comes first to reverse the profound dehydration from osmotic diuresis. A continuous IV regular insulin infusion is correct: regular (short-acting) insulin given IV is titratable and is the standard for clearing ketones and lowering glucose in a controlled way. Monitoring serum potassium closely and replacing it as ordered is essential because insulin drives potassium into cells and causes hypokalemia; potassium is added to the fluids once the level is in or near the normal range, and insulin is not started on a low potassium until it is replaced. Adding dextrose to the IV fluids when glucose reaches about 200-250 mg/dL is correct: it lets the insulin drip continue clearing ketones without causing hypoglycemia.

Giving subcutaneous NPH insulin as the primary treatment is wrong. NPH is intermediate-acting with an unpredictable subcutaneous absorption in a dehydrated client and cannot be titrated; IV regular insulin is used. Withholding all potassium replacement throughout therapy is wrong and dangerous, because insulin-driven potassium shifts predictably cause hypokalemia that must be corrected.

Clinical pearl: continue the insulin infusion until the acidosis and ketosis resolve, not just until the glucose looks normal.

Correct diabetic foot-care teaching aims to prevent the ulcers and infections that stem from neuropathy and peripheral arterial disease. Inspecting the feet every day is correct, because reduced sensation means a client may not feel a developing wound and must look for it, using a mirror if needed. Drying carefully between the toes is correct, because trapped moisture promotes fungal infection and skin breakdown. Wearing well-fitting shoes and never going barefoot is correct, since neuropathy blunts protective pain sensation and an unnoticed puncture or blister can become a limb-threatening infection. Reporting any sore or blister to the provider promptly is correct because early treatment prevents progression to ulceration and amputation.

Soaking the feet in hot water for 30 minutes daily is wrong on two counts: neuropathy impairs temperature sensation so hot water can cause burns, and prolonged soaking macerates the skin and promotes breakdown. Feet should be washed with lukewarm water (checked with a thermometer or the elbow, since neuropathy can blunt hand sensation) and dried, not soaked. Going barefoot at home is wrong because it exposes insensate feet to injury from stepped-on objects and stubbed toes.

Clinical pearl: teach 'look, wash, dry, protect, report' — inspect daily, wash with lukewarm (not hot) water, dry between the toes, never go barefoot, cut nails straight across or see a podiatrist, and report any wound early. Diabetic foot ulcers are a leading cause of nontraumatic lower-limb amputation, which is why this teaching is high-yield.

Hypoglycemia (glucose under 70 mg/dL) produces two overlapping symptom groups: adrenergic (sympathetic) and neuroglycopenic. Diaphoresis with cool, clammy skin is correct: the epinephrine surge triggered by falling glucose causes sweating and cold, moist skin, a classic early warning sign. Tremors or shakiness is correct and is also adrenergic, reflecting catecholamine release. Tachycardia is correct for the same reason: the sympathetic response speeds the heart. Confusion or irritability is correct and is neuroglycopenic. The brain depends on glucose, so as it drops the client becomes confused, irritable, and eventually loses consciousness or seizes.

Polyuria (increased urine output) is wrong; it is a sign of HYPERglycemia, where glucose spills into the urine and drags water with it via osmotic diuresis. A fruity odor to the breath is wrong; it reflects ketones in diabetic ketoacidosis, a hyperglycemic emergency, not hypoglycemia.

Clinical pearl: remember hypoglycemia as 'cold and clammy, need some candy' versus hyperglycemia as 'hot and dry, sugar high.' The adrenergic signs (sweating, shakiness, tachycardia, hunger, anxiety) tend to appear first and are the body's alarm; the neuroglycopenic signs (confusion, slurred speech, seizures) signal that the brain is being starved and demand immediate treatment. Note that beta-blockers can mask the adrenergic warning signs, so those clients may present with sudden neuroglycopenic symptoms instead.