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Related Concept Videos

Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...
Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
Diabetic Ketoacidosis ll: Pathophysiology01:22

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Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
Skeletal Muscle Relaxants: Adverse Effects01:21

Skeletal Muscle Relaxants: Adverse Effects

Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
Unlike...
Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
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Swimming Induced Paralysis to Assess Dopamine Signaling in Caenorhabditis elegans
07:36

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Published on: April 3, 2019

Hyperkalemia-induced paralysis.

Nikita S Wilson1, Joanna Q Hudson, Zachary Cox

  • 1Department of Pharmacy, Methodist University Hospital, Memphis, TN 38104, USA.

Pharmacotherapy
|October 2, 2009
PubMed
Summary
This summary is machine-generated.

Hyperkalemia, a rare cause of paralysis, can lead to severe weakness. Prompt treatment of high potassium levels in patients with kidney disease can resolve paralysis symptoms.

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Area of Science:

  • Nephrology
  • Neurology
  • Internal Medicine

Background:

  • Hyperkalemia is a critical electrolyte imbalance with potentially severe health consequences.
  • Paralysis as a manifestation of hyperkalemia is exceptionally rare, with limited documented cases.

Observation:

  • A 60-year-old male presented with profound generalized weakness, indicative of paralysis.
  • His laboratory results revealed severe hyperkalemia (serum potassium >8 mEq/L) and elevated creatinine (7 mg/dL), suggesting renal impairment.
  • Electrocardiography showed abnormalities consistent with hyperkalemia.

Findings:

  • The patient's paralysis resolved following treatment for hyperkalemia.
  • The Naranjo scale suggested a probable link between the patient's paralysis and hyperkalemia (score of 5).
  • The patient was diagnosed with end-stage renal disease.

Implications:

  • Clinicians must consider hyperkalemia as a potential cause of paralysis, even in rare instances.
  • This case highlights the critical, non-cardiac toxicity of severe hyperkalemia.
  • Awareness of this association is crucial for timely diagnosis and management, particularly in patients with renal failure or those on specific medications like lisinopril and naproxen.