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Questions and Answers
Which of the following describes a direct consequence of too much calcium being released inside a sarcomere? (Select all that apply)
Which of the following describes a direct consequence of too much calcium being released inside a sarcomere? (Select all that apply)
- Excess calcium triggers increased ATP consumption, leading to the generation of large amounts of heat and COâ‚‚. (correct)
- Muscle contraction is halted as the increased calcium blocks the binding sites on actin, preventing myosin from attaching.
- Troponin is unable to bind with calcium again, preventing muscle relaxation. (correct)
- Calcium is pulled away from the sarcolemma membrane, resulting in decreased action potential transmission.
In the context of muscle contraction, what is the primary role of Ryanodine Receptor 1 (RyR1)?
In the context of muscle contraction, what is the primary role of Ryanodine Receptor 1 (RyR1)?
- RyR1 binds to troponin, triggering the conformational change that allows for muscle contraction.
- RyR1 regulates the amount of calcium released from the sarcoplasmic reticulum, impacting the extent of muscle contraction. (correct)
- RyR1 acts as a calcium pump, returning calcium into the sarcoplasmic reticulum after muscle contraction.
- RyR1 facilitates the release of calcium from the sarcolemma, triggering muscle depolarization.
Why is rhabdomyolysis a significant complication associated with excessive muscle contraction?
Why is rhabdomyolysis a significant complication associated with excessive muscle contraction?
- Rhabdomyolysis compromises the immune system by decreasing white blood cell count, increasing susceptibility to infections.
- Muscle breakdown causes the release of significant amounts of acetylcholine, leading to uncontrolled muscle spasms and neuromuscular dysfunctions.
- Rhabdomyolysis causes a massive increase in blood glucose levels, leading to hyperglycemia and diabetic complications.
- The breakdown of skeletal muscle releases potentially toxic substances into the bloodstream, which can obstruct the kidneys and lead to acute kidney injury. (correct)
Which of the following is NOT a direct physiological consequence of the excessive muscle contraction leading to hypermetabolic state?
Which of the following is NOT a direct physiological consequence of the excessive muscle contraction leading to hypermetabolic state?
Why does a decrease in blood oxygen saturation (SpOâ‚‚) occur during excessive muscle contraction?
Why does a decrease in blood oxygen saturation (SpOâ‚‚) occur during excessive muscle contraction?
Which of the following is MOST directly responsible for the development of hyperthermia in individuals experiencing excessive muscle contraction?
Which of the following is MOST directly responsible for the development of hyperthermia in individuals experiencing excessive muscle contraction?
What is the primary mechanism by which excess calcium in the sarcomere contributes to the development of metabolic acidosis?
What is the primary mechanism by which excess calcium in the sarcomere contributes to the development of metabolic acidosis?
What is the primary reason for the development of tachycardia in individuals experiencing excessive muscle contraction?
What is the primary reason for the development of tachycardia in individuals experiencing excessive muscle contraction?
Why does an increased carbon dioxide level in the blood (hypercarbia) contribute to the development of hypoxemia in individuals with excessive muscle contraction?
Why does an increased carbon dioxide level in the blood (hypercarbia) contribute to the development of hypoxemia in individuals with excessive muscle contraction?
How does excessive muscle contraction contribute to the development of rhabdomyolysis?
How does excessive muscle contraction contribute to the development of rhabdomyolysis?
Which of the following is the MOST direct consequence of the RyR1 defect in the context of excessive muscle contraction?
Which of the following is the MOST direct consequence of the RyR1 defect in the context of excessive muscle contraction?
What is the primary mechanism driving the development of hyperkalemia during rhabdomyolysis?
What is the primary mechanism driving the development of hyperkalemia during rhabdomyolysis?
Which of the following best describes the primary mechanism by which excessive calcium release during muscle contraction directly leads to hypercarbia?
Which of the following best describes the primary mechanism by which excessive calcium release during muscle contraction directly leads to hypercarbia?
Which of the following is a direct consequence of rhabdomyolysis that contributes to the development of ventricular extrasystoles?
Which of the following is a direct consequence of rhabdomyolysis that contributes to the development of ventricular extrasystoles?
Which of the following is a direct consequence of the RyR1 defect leading to excessive calcium release, EXCEPT?
Which of the following is a direct consequence of the RyR1 defect leading to excessive calcium release, EXCEPT?
How does excessive muscle contraction contribute to the development of metabolic acidosis?
How does excessive muscle contraction contribute to the development of metabolic acidosis?
What is the primary mechanism by which excessive calcium release, as a result of a defect in RyR1, contributes to a decrease in blood oxygen saturation (SpOâ‚‚)?
What is the primary mechanism by which excessive calcium release, as a result of a defect in RyR1, contributes to a decrease in blood oxygen saturation (SpOâ‚‚)?
In the context of MH, which of the following best describes the sequence of events leading to the development of hyperthermia?
In the context of MH, which of the following best describes the sequence of events leading to the development of hyperthermia?
Flashcards
Normal Contraction
Normal Contraction
Contraction involving calcium release and actin-myosin interaction.
Calcium Release
Calcium Release
Calcium released from the sarcoplasmic reticulum triggers muscle contraction.
Rhabdomyolysis
Rhabdomyolysis
Breakdown of skeletal muscle leading to renal obstruction and high potassium levels.
Hyperkalemia
Hyperkalemia
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Hyperthermia
Hyperthermia
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Hypermetabolism
Hypermetabolism
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Depolarization
Depolarization
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Troponin Function
Troponin Function
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RyR1 Defect
RyR1 Defect
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Consequences of Excess Calcium
Consequences of Excess Calcium
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Hypoxaemia
Hypoxaemia
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Tachycardia Causes
Tachycardia Causes
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Calcium's Role in Muscle Contraction
Calcium's Role in Muscle Contraction
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Excess Calcium Effects
Excess Calcium Effects
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Metabolic Acidosis
Metabolic Acidosis
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Rhabdomyolysis Consequence
Rhabdomyolysis Consequence
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Hypercarbia
Hypercarbia
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Hyperthermia Build-Up
Hyperthermia Build-Up
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Study Notes
Calcium Release and Muscle Contraction
- Depolarization releases calcium from the sarcoplasmic reticulum
- Ryanodine receptor (RyR1) controls calcium release
- Troponin binds calcium
- Troponin moves away, allowing actin and myosin to interact
- ATP and oxygen stop actin and myosin interaction
- Calcium returns to the sarcoplasmic reticulum
- RyR1 defects cause excessive calcium release, leading to excessive muscle contraction and heat
Consequences of Excessive Calcium
- Excess calcium prevents troponin from re-sheathing
- ATP and oxygen consumption increases, generating heat and carbon dioxide
- This leads to metabolic acidosis
- Rhabdomyolysis (skeletal muscle breakdown) occurs, blocking renal tubules
- Potassium moves into extracellular blood, causing hyperkalemia
- Hyperkalemia can cause ventricular extrasystoles.
- Muscle breakdown releases potassium into the blood, causing hyperkalemia.
- Hyperkalemia can lead to ventricular arrhythmias, including ventricular extrasystoles.
- Excess calcium and muscle contractions result in an increased need for oxygen and a buildup of CO2 and heat.
Other Effects
- Hypoxia (low oxygen) increases the demand for oxygen , resulting in increased CO2 production and acidosis. Reduced oxygen in red blood cells (RBCs) is indicated as a contributing factor.
- Hypermetabolism from muscle contractions
- Tachycardia (fast heart rate) can result from hypermetabolism and acidosis
- Hyperthermia (high body temperature) can occur after tachycardia and hypercarbia (high carbon dioxide) - it increases 1 degree Celsius every few minutes.
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