10 free Paramedic practice questions: Advanced Diabetic and Endocrine Emergencies

Treat as a postictal state and transport without glucose correction: A postictal patient can be confused and combative, and an unwitnessed seizure is always possible. A postictal state gradually clears, hypoglycemia is itself a cause of seizures, and skipping glucose correction is the one move that can turn a reversible problem into a permanent one.

Treat for hyperglycemia with fluid, since the skin findings fit either: Fluid is the right treatment for a hyperglycemic emergency and it is never harmful in small amounts, so this feels safe. The onset over 20 minutes and the pale cool moist skin are a hypoglycemic picture, and a hyperglycemic crisis does not develop while a family member watches.

Withhold sugar until a reading confirms which problem this is: Wanting a number before you treat is good discipline in almost every other situation, and it is why this answer reads as careful. Waiting is itself a decision here, and the cost of waiting through a real hypoglycemia is permanent injury while the cost of treating a high patient is close to nothing.

Intramuscular glucagon, since the patient cannot swallow: Glucagon is a legitimate rung on this ladder and the reasoning about swallowing is correct as far as it goes. It is the answer only when access has not been obtained, and choosing it here trades a drug that works in minutes for one that takes ten to twenty.

Glucose gel under the tongue, since it is absorbed without swallowing: Buccal and sublingual absorption gets taught as a workaround, so this sounds like a clever middle path. Glucose gel is absorbed poorly through the mucosa and still ends up somewhere it can be aspirated, and none of that is necessary when a line is already in place.

Oral glucose gel, since the gag reflex is intact: An intact gag reflex is genuinely reassuring and makes oral glucose look available. Protecting the airway and being able to swallow on command are two different abilities, and a patient who cannot stay awake long enough to swallow cannot take anything by mouth safely.

Fifty percent dextrose is too slow to act through a small catheter: Speed does matter with a glucose of 26, and it is true that a small catheter slows any infusion. Concentration does not change onset time in a meaningful way here, and thicker solutions are actually harder to push through a small catheter rather than slower to act.

Ten percent dextrose requires a central line to run safely: Central access does get required for some concentrated infusions, so the idea has a real basis. It applies to concentrated solutions rather than to dilute ones, and ten percent dextrose is the option specifically chosen to be gentler on peripheral veins.

Ten percent dextrose cannot raise a glucose level this low: Doubting a weaker solution feels prudent when the number is this low. Ten percent dextrose corrects hypoglycemia reliably; it simply takes a larger volume, which is why it is given as 100 to 250 mL titrated to mental status.

The newborn's kidneys spill glucose into the urine until feeding is established: Spilling glucose into the urine is a real way to lose it, and it is the mechanism behind ketoacidosis with a normal glucose in an adult on certain diabetes medications. It is not how a healthy newborn kidney behaves, and nothing here points at it.

The mother's insulin crossed the placenta and is still circulating in the newborn: This is the most understandable version of the right idea, because insulin really is at the center of what is happening. The insulin in question is the newborn's own, which ran high in response to the mother's glucose before delivery and keeps working now that the supply it was answering has been cut off.

The newborn burned through its glycogen making heat during and after the delivery: Glycogen burned for heat is a genuine mechanism and it puts cold newborns on the same risk list. This newborn was dried, covered, and feels warm, so the vignette has taken that mechanism off the table and left the maternal history standing.

Give intramuscular glucagon to hold the glucose level up: Keeping the glucose from falling again is a legitimate worry, especially with long acting agents on board. Glucagon raises a glucose that is already normal at 118, and it does not address the reason this patient is still unresponsive.

Assume a slow awakening and hold further assessment until arrival: Delayed awakening after a long period of a low glucose is real, so this is not an absurd thought. Deciding that in advance and holding further assessment turns a hypothesis into a conclusion, and any second cause goes unfound for the whole transport.

Give a second dose of dextrose and recheck in ten minutes: Giving more of something that should have worked is the most natural reflex there is, and dosing really can be inadequate. The repeat reading of 118 shows the dose was adequate, so a second one corrects a number that is already corrected and buys nothing.

Compensated hypovolemic shock, since the heart rate is holding output: Tachycardia really is the hallmark of compensation and a rate of 132 shows the body is trying. Compensated means the pressure is still being held up, and at 76 over 44 with a weak radial pulse and a falling mental status the compensation has already failed.

Decompensated distributive shock from an underlying infection: Distributive shock is worth considering because infection is a common trigger for a hyperglycemic crisis, and the staging is correct. The mechanism here is volume poured out through the kidney rather than vessels dilating and leaking, and cool mottled skin argues against a distributive picture.

Irreversible shock, since the pressure and mentation are both falling: Describing a patient this sick in the strongest terms available feels honest, and the term appears in older materials. This program stages shock as compensated or decompensated only; there is no irreversible stage to assign.

The glucose has fallen enough to slow the breathing down: The glucose does fall with fluid, so linking that to calmer breathing has a certain logic. The breathing is driven by the acid rather than by the glucose, and a falling glucose would not slow a compensatory pattern while the mental status worsens.

The acidosis is resolving as the fluid takes effect: A number heading back toward normal really does look like improvement, and fluid is the right treatment, so this is the reading most crews reach for first. Fluid does not resolve a ketoacidosis in 25 minutes, and a patient whose acidosis was clearing would be waking up rather than getting harder to rouse.

The reading has drifted because the cannula has shifted: Equipment problems are always worth ruling out and a shifted cannula does change the reading. A drifting sensor would not also drop the measured respiratory rate by fourteen and would not explain a patient who has become harder to rouse.

Thyroid storm: the same gland failing in the other direction, so a student who spots a thyroid problem still has to pick which way it went. Storm runs hot, fast, and agitated, with hyperthermia and marked tachycardia. Every vital sign here points the opposite way.

Adrenal crisis: belongs on the list for any patient who is weak and deteriorating after an illness. Its signature is hypotension that does not respond to fluid and pressors, and this blood pressure is 104/62. Adrenal crisis also does not bring hypothermia with a rising carbon dioxide.

Septic shock: A recent pneumonia makes sepsis a fair thought, and a septic patient can be hypothermic. Septic patients are typically tachycardic and hypotensive, and this patient is bradycardic with a blood pressure of 104/62. The dry scaly skin and the slow, shallow breathing point at the thyroid instead.

Opioid overdose: doesn't explain the hypothermia, bradycardia, and puffy facial appearance together. Those findings point toward a metabolic process tied to the patient's known hypothyroidism, not an opioid toxidrome.

Thyroid storm: produces the opposite picture: a hypermetabolic state with fever, tachycardia, and agitation, not the hypothermia, bradycardia, and hypoventilation seen in this patient.

Adrenal crisis: doesn't typically produce this specific combination of hypothermia, puffy dry skin, and slowed everything. That pattern is the signature of severe untreated hypothyroidism rather than adrenal insufficiency.

50% dextrose by rapid push: too concentrated for a small peripheral vein in an infant and carries an osmotic load and vein injury risk that a more dilute pediatric concentration avoids.

Oral glucose gel in the cheek: contraindicated in a limp, difficult-to-arouse infant who can't reliably swallow and protect the airway.

Glucagon by the intramuscular route: depends on liver glycogen stores to mobilize glucose, and it's a slower, less direct correction than dextrose delivered through the intravenous access this infant already has.