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Untitled Prezi

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Hannah Fleckenstein

on 6 March 2013

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Malignant Hyperthermia Part IV How do muscles contract? Case Study 1)A signal is sent from the brain or the spinal cord to the muscle via neurons Malignant hyperthermis is an inherited condition that causes a patient's muscles to become very rigid and the patient's body temperature to rise rapidly when exposed to general anesthia. What is malignant hyperthermia? 7)Ca++ bind with troponin C, causing the tropomyosin to shift and expose the myosin binding sites on actin Malignant hyperthermia only has to be carried by one parent for a child to inherit the condition. What triggers malignant hyperthermia? 2)An action potential is generated in the neuron, releasing Ca++ in the neuromuscular junction 3)The influx of calcium ions causes acetylcholine (AcH) to be released in the synaptic cleft 4)AcH binds to the AcH receptors present in the sarcolemma, increasing its permeability 5)Na++enter the sarcolemma, changing its polarity and creating an action potential 6)Ca++ are released by the sarcoplasmic reticulum, as the action potential travels down the T-tubules in the muscle fiber 8)ATP is hydrolyzed into ADP and phosphorus, releasing energy for myosin power stroke 9)Myosin binds to actin 10)Myosin head bends and actin slides over the myosin surface 11)Myosin releases the ADP molecule
As the myosin head swivels, another ATP molecule binds to myosin, breaking the actin-myosin bridge. The ATP is again hydrolyzed and last four steps of the process are repeated, making the sarcomere shorter and shorter, until adequate Ca++ and ATP are present. Many myosin heads move in the same direction and a number of times, and a single muscle is contracted. General anesthesia is the main trigger of malignant hyperthermia. The volatile gaseous inhalation anesthetics included are:
desflurane
sevoflurane
halothane
isoflurane
enflurane
methoxyflurane "The stiffening killer" What is the "metabolic storm" that develops during malignant hyperthermia? The "veritable metabolic storm" refers to the development of a rapid heart rate and breathing, abnormal muscle stiffening, blotchy blueness of the skin and a rapid rise in temperature. The muscles lose adenosine triphosphate (a muscle cell's fuel) and release a tremendous amount of acid and potassium which helps to stop their hearts after being exposed to the general anesthesia. How does malignant hyperthermia disrupt muscle physiology? In a person with malignant hyperthermia, the calcium ion release in skeletal muscle is abnormal. This abnormality interferes with the regulation of calcium in the muscle. The channel remains open causing a chemical imbalance and the muscle to continually contract. Adenosine triphosphate is loss at this time. Why does body temperature rise during malignant hyperthermia? Body temperature rises during a malignant hyperthermia reaction because of an uncontrollable increase in skeletal muscle oxidative metabolism that overwhelms the body's capacity to regulate body temperature. How can you tell if you have malignant hyperthermia? A patient can not tell if they have malignant hyperthermia. Patients often find out they have the condition after being exposed to general anesthesia. If a patient has a family history of the condition then they will be tested or a different type of anesthesia will be utilized if possible. What drug is used to treat malignant hyperthermia and what are the mechanisms of action of how this drug works? Dantrolene is used to treat malignant hyperthermia. Dantrolene has been shown to produce relaxation by affecting the contractile response of the muscle at a site beyond the myoneural junction. In skeletal muscle, dantrolene dissociates the excitation-contraction coupling, interfering with the release of Ca from the sarcoplasmic reticulum. Inhibition of calcium release from the sarcoplasmic reticulum, by dantrolene reestablishes the myoplasmic calcium equilibrium, increasing the percentage of bound calcium. Why doesn't the antidote to malignant hyperthermia impact smooth of cardiac muscle? Dantrolene doesn't affect either muscle types because both are involuntary muscles. Smooth and cardiac muscle are also not affected by the antidote because both are not triggered by the same process as skeletal muscles are (calcium channel and it's release for muscle contraction). Hannah Fleckenstein, Alexandra Morehead, Bana Hadid, Bhavana Patil
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