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Muscle Recovery and Fatigue01:24

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Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective...
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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The...
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Diphtheria is an acute, toxin-mediated infectious disease that primarily affects the upper respiratory tract. It is caused by Corynebacterium diphtheriae, a Gram-positive, pleomorphic rod that lacks spore-forming capability and exhibits a characteristic club-shaped morphology under microscopic examination. While C. diphtheriae can asymptomatically colonize mucosal surfaces, clinical disease manifests only when the bacterial strain is lysogenized by a specific β-corynephage. This phage...
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Toxic Reactions: Overview01:26

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When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
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Acute Respiratory Failure-III01:30

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Hypercapnic respiratory failure, also known as Type 2 or ventilatory respiratory failure, is a severe condition characterized by the body's inability to effectively remove carbon dioxide (CO2) from the bloodstream. It leads to an arterial CO2 pressure (PaCO2) exceeding 45 mmHg and a blood pH above 7.35. This situation indicates that the body's ventilatory demand, or the ventilation needed to maintain normal PaCO2 levels, surpasses its supply or the maximum gas flow achievable without...
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The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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Related Experiment Video

Updated: Mar 29, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

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Trauma triggering thyrotoxic crisis with lactic acidosis.

Jennifer S Prosser1, Dan K Quan1

  • 1Department of Emergency Medicine, Maricopa Medical Center, Phoenix, Arizona, USA.

Journal of Emergencies, Trauma, and Shock
|November 26, 2015
PubMed
Summary
This summary is machine-generated.

Thyrotoxic crisis (TC), a life-threatening endocrine emergency, can be triggered by trauma, leading to severe metabolic disturbances like lactic acidosis. Prompt diagnosis and treatment are crucial for patient survival.

Keywords:
Lactic acidosisthyroid stormthyrotoxic crisistrauma

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Area of Science:

  • Endocrinology
  • Emergency Medicine
  • Toxicology

Background:

  • Thyrotoxic crisis (TC) is a severe, life-threatening exacerbation of hyperthyroidism.
  • It presents with significant autonomic and metabolic disturbances, requiring urgent medical intervention.
  • Trauma is an uncommon but critical precipitant of TC.

Observation:

  • A 24-year-old male with a history of hyperthyroidism presented after a motor vehicle accident.
  • Initial presentation included tachycardia, hypertension, and importantly, severe lactic acidosis (lactic acid 7.6).
  • Laboratory results revealed suppressed thyroid-stimulating hormone (< 0.015) and elevated free T4 (5.61 ng/dL).

Findings:

  • The patient was diagnosed with thyrotoxic crisis precipitated by trauma.
  • Treatment involved intravenous fluids, propranolol, and methimazole.
  • The patient showed improvement in tachycardia and lactic acidosis following treatment.

Implications:

  • This case highlights trauma as a potential trigger for thyrotoxic crisis.
  • It underscores the importance of recognizing and managing metabolic sequelae, such as lactic acidosis, in TC.
  • Early diagnosis and aggressive management are vital for improving outcomes in thyrotoxic crisis.