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This deck focuses on Endocrine And Metabolic Emergencies, giving you a quick way to review the definitions, rules, and examples that matter most for NREMT Paramedic Level.
Study Endocrine And Metabolic Emergencies in NREMT Paramedic Level with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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Which endocrine emergency is caused by acute cortisol deficiency and can present with shock?
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Adrenal crisis (acute adrenal insufficiency). Sudden cortisol lack disrupts metabolism and vascular tone, precipitating refractory shock.
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This deck focuses on Endocrine And Metabolic Emergencies, giving you a quick way to review the definitions, rules, and examples that matter most for NREMT Paramedic Level.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: Adrenal crisis (acute adrenal insufficiency). Sudden cortisol lack disrupts metabolism and vascular tone, precipitating refractory shock.
Answer: Isotonic fluids; consider dextrose and steroids per protocol. Fluids restore volume; dextrose and steroids address hypoglycemia and cortisol deficiency per guidelines.
Answer: Severe hyperglycemia and dehydration with minimal or no ketosis. HHS occurs in type 2 diabetes with enough insulin to prevent ketosis but not hyperglycemia, causing osmotic diuresis and dehydration.
Answer: Kussmaul respirations. Deep, rapid breathing compensates for metabolic acidosis by expelling CO2 to raise blood pH.
Answer: Hypoglycemia. Rapid reversal of confusion with glucose confirms low blood sugar as the etiology of neurologic symptoms.
Answer: Stabilize myocardium with calcium per protocol; treat underlying cause. Calcium antagonizes potassium's membrane effects, stabilizing cardiac rhythm while addressing root cause.
Answer: Hyperthermia, tachycardia, agitation, and altered mental status. Thyrotoxicosis causes hypermetabolic state with sympathetic overdrive, leading to these systemic effects.
Answer: Absolute insulin deficiency due to pancreatic beta-cell failure. Type 1 diabetes results from autoimmune destruction of pancreatic beta cells, leading to no insulin production.
Answer: Hypothermia, bradycardia, hypotension, and altered mental status. Severe hypothyroidism slows metabolism, resulting in decreased heat production and cardiovascular depression.
Answer: Point-of-care blood glucose. Altered mental status often stems from metabolic issues like hypo- or hyperglycemia, making rapid glucose check essential.
Answer: Tachycardia with diaphoresis and possible hypotension. Adrenergic response to low glucose causes sympathetic activation, manifesting as these signs of compensatory shock.
Answer: Glucagon IM or IN per protocol. Glucagon stimulates hepatic glycogenolysis to increase blood glucose when IV routes are inaccessible.
Answer: Blood glucose less than 60 mg/dL. Levels below this threshold impair brain function, as glucose is the primary neuronal energy source.
Answer: Older patients with type 2 diabetes mellitus. Elderly type 2 diabetics are prone to HHS due to comorbidities, reduced thirst response, and gradual onset.
Answer: Aggressive isotonic fluid resuscitation per protocol. Fluid replacement addresses profound dehydration and hypovolemia critical in both conditions to restore perfusion.
Answer: Sulfonylureas. These agents stimulate insulin release, risking prolonged hypoglycemia in elderly with reduced clearance.
Answer: Hyperosmolar hyperglycemic state (HHS). Presentation indicates severe hyperglycemia without acidosis, often with neurologic signs from hyperosmolarity.
Answer: Passive rewarming and gentle handling. Avoid active rewarming to prevent vasodilation and shock; gentle methods support gradual recovery.
Answer: Hypovolemic shock from severe dehydration. Osmotic diuresis from hyperglycemia causes massive fluid loss, leading to circulatory collapse if untreated.
Answer: Hyperglycemia, ketosis, and metabolic acidosis. DKA manifests from insulin lack causing glucose elevation, fat breakdown to ketones, and acid buildup from ketoacids.
Answer: Oral glucose (or other oral carbohydrates) if able to protect airway. Oral intake rapidly raises blood glucose without IV risks, provided airway protection ensures safety.
Answer: IV dextrose per protocol (for example, D10 or D50 depending on system). Intravenous administration provides immediate glucose delivery to reverse severe symptoms efficiently.
Answer: Insulin resistance with relative insulin deficiency. Type 2 diabetes involves peripheral tissues resisting insulin effects, combined with inadequate compensatory insulin secretion.
Answer: Diabetic ketoacidosis (DKA). Symptoms reflect insulin deficiency causing hyperglycemia, dehydration, and acidosis with compensatory breathing.
Answer: Acetone (ketone) breath odor. Ketone production in DKA leads to acetone exhalation, producing a distinctive fruity scent.