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Biology, 18.03.2021 01:20 jameslinimk

You are a vet and today an emergency appointment is made for you to see a dalmatian named Pongo. The owner has noticed some symptoms that have gotten progressively worse over the past couple of months of which include muscle weakness and trouble breathing. After a quick physical exam, you note that Pongo also has depressed reflexes. Your plan of attack is to first run some blood work and then proceed accordingly. However, the blood test results prove to be very telling as they show that Pongo has a condition known as Lambert-Eaton Syndrome (LES), which involves an autoimmune attack directed against the voltage-gated calcium channels (VGCCs) found at the terminal end of somatic motor neurons. This results in a loss of functional VGCCS. Which of the follow best describes how this disease impacts normal skeletal muscle physiology?
A. Of the following options, choose the one that would help to properly match the above scenario. Reject all the rest. For full points you must also provide an explanation for each case, identifying all aspects that are correct or incorrect. Defend the correct choice with adequate justification. For those that are false. explain why they are incorrect. (10 pts)
1. Accept/Reject: Pongo must have excess amounts of ACh in the synaptic clefts of his neuromuscular junctions.
2. Accept/Reject: Lambert-Eaton syndrome causes a decrease in Ca2+ levels floating within the sarcoplasm of Pongo's skeletal muscle cells.
3. Accept/Reject: The pathophysiology associated with this condition causes ryanodine receptors to be open for longer periods of time and ultimately a shorter period between initial excitation and the contraction phase for Pongo's skeletal muscles.
4. Accept/Reject: Impaired VGCC function contributes to excess cross-bridge formation which gives rise to Pongo's muscle weakness.
5. Accept/Reject: The symptoms are most likely caused by decreases in action potentials traveling down somatic motor neurons, resulting in greater exposure of myosin binding sites on actin.

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