<span>The nurse determines this patient is displaying Circulatory hypoxia.Sickle cell anemia can lead to circulatory hypoxia as the cells sickle in the blood vessels and block them. It also produces an anemic hypoxia as the sickled blood cells are removed from circulation.</span>
Answer: D
Explanation:
During embryogenesis, hematopoiesis begins in week 3 in the Yolk Sac, in Pander´s Island or Wolff´s Island, commonly known as the "blood islands". These blood islands develop from the umbilical vesicle, allantois, and chorion. In week 5, blood production starts on the fetal liver, and finally, at week 12 it begins in the bone marrow, spleen and, thymus.
Answer:
I think that "gills, which help it take in oxygen from the water, and two legs." this is the answer
Explanation:
Hope this helps<3
A neuromuscular junction (or myoneural junction) is a chemical synapse formed by the contact between a motor neuron and a muscle fiber.[1] It is at the neuromuscular junction that a motor neuron is able to transmit a signal to the muscle fiber, causing muscle contraction.
Muscles require innervation to function—and even just to maintain muscle tone, avoiding atrophy. Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage-dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor proteins (synaptotagmin) on synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. In vertebrates, motor neurons release acetylcholine (ACh), a small molecule neurotransmitter, which diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) on the cell membrane of the muscle fiber, also known as the sarcolemma. nAChRs are ionotropic receptors, meaning they serve as ligand-gated ion channels. The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade that eventually results in muscle contraction.
Neuromuscular junction diseases can be of genetic and autoimmune origin. Genetic disorders, such as Duchenne muscular dystrophy, can arise from mutated structural proteins that comprise the neuromuscular junction, whereas autoimmune diseases, such as myasthenia gravis, occur when antibodies are produced against nicotinic acetylcholine receptors on the sarcolemma.
