Question

Samuel is a 34-year-old man. He is seeing his family doctor today because he has been feeling more and more muscle strain lately.

After several investigations, a diagnosis is made: primary hypoparathyroidism, which means that its parathyroid glands do not secrete enough PTH.

a) Explain what effect this pathology would have on Samuel's calcemia. Produce a clear, precise and detailed answer by describing all the functions and effects of PTH.

b) This disorder of calcemia causes an inhibition of neurons which explains muscle weakness. What link do you make between calcemia and the functioning of neurons? In your answer, you must explain the precise and detailed functioning of a chemical synapse.

Help please

Answer 1

a. Parathyroid hormone is secreted by the parathyroid gland that is present near the thyroid gland. It is secreted in response to low calcium levels in blood via exocytosis from membrane bound vesicles. It has a short half-life and it removed by kidneys and liver. Hypoparathyroidism is the less production of PTH by the parathyroid glands.

PTH and Calcemia: Calcemia or low calcium levels in blood activate secretion of PTH. It stimulates the release of calcium by the osteoclasts. Osteoclasts are bone cells that degrade bone. Bone matrix has calcium in combination with phosphate (hydroxyapatite). Osteoclast activity will degrade bone and release calcium in blood. PTH stimulates the production of osteoclasts from osteoblasts by increasing their expression of RANKL.

PTH acts on kidneys to increase calcium reabsorption. It acts on distal convoluted tubules and collecting duct and increases calcium absorption. It also decreases phosphate reabsorption in collecting duct. Thus, this will cause calcium to remain in ionic form.

PTH stimulates the production of 1alpha-hydroxylase in the proximal convoluted tubule, an enzyme that converts inactive vitamin D to active vitamin D. Active vitamin D, 25-hydroxycholecalciferol increases calcium reabsorption in distal convoluted tubules of kidneys. Vitamin D also increases calcium absorption from food via transcellular and paracellular pathways.

The hypoparathyrodism will cause decreased PTH levels. This will decrease calcium levels in blood, leading to calcemia.

b. Calcium is required by nerve cells for generation of action potential in nerve cells. When a nerve impulse reaches the motor neuron, there is opening of sodium channels. This results in depolarization of the neuron. When the depolarization reaches a threshold value, action potential is generated, which the travels and reaches the axon terminal of the neuron. There is causes the synaptic vesicles to fuse with the axon membrane, releasing acetylcholine in neuronal synapse. ACh bind to its receptor on the sarcoplasma of the muscle cell. This results in release of calcium from T tubules. The calcium binds to troponin, thereby causing release of myosin binding sites on actin. Actin then binds to myosin, initiating cross bridging and muscle contraction.

The release of neurotransmitter requires calcium. Calcium channels are involved in release of calcium. Depolarization causes the release of calcium via these calcium stores. Calcium promotes the exocytosis of the synaptic vesicles through the plasma membrane. Thus, there is release of neurotransmitter. Low calcium will decrease the synaptic exocytosis. As there is no neurotransmitter release, there will be no muscle contraction, causing muscle weakness. Further, as no calcium can be released even in muscle cell, no muscle contraction will occur.