NMJ Events
Name the neurotransmitter associated with skeletal muscle contractions, the enzyme that breaks it down, and the two molecules that are left after the enzyme breakdown.
Acetylcholine, acetylcholinesterase, and acetic acid and choline
What kind of chemical is botulinus toxin and would it lead to flaccid or spastic paralysis?
Inhibitor of acetylcholine release -> flaccid paralysis
List the 3 products of aerobic glycolysis.
The hormone that stimulates osteoblast activity
Calcitonin
This region of the sarcomere contains overlapping actin and myosin filaments
A band
An action potential traveling down an axon will open these channels which will facilitate vesicle fusion to the neurolemma
Voltage gated Ca++ channels
What kind of disorder is myasthenia gravis, what is destroyed, and would it lead to flaccid or spastic paralysis?
Autoimmune disorder, ACh receptors are destroyed, and it would result in flaccid paralysis
The NADH molecules produced during the TCA cycle undergo _______ and are therefore called _____ agents at the ETC.
Oxidized, reducing agents
The enzyme that adds the last OH group to 25-cholecalciferol to make active Vitamin D
1 alpha hydroxylase
Scurvy and rickets are deficiencies of which vitamins respectively?
Scurvy - Vitamin C
Rickets - Vitamin D
Explain what must occur before voltage gated Na+ channels open
Acetylcholine must bind to receptor, ligand Na+ channels open, Na+ must flow into cell and the membrane potential must reach threshold
Would competitive acetylcholine antagonists lead to flaccid or spastic paralysis? Explain why and give 2 examples of drugs under this category.
Antagonist binds to ACh receptor site -> ACh cannot bind -> no depolarization -> flaccid paralysis. Atropine and curare are two examples (alpha-bungarotoxin is another)
The fatty acid chain of a triglyceride undergoes this metabolic process
Beta-oxidation
The hormone released during elevated blood calcium levels and the cells and gland that it is released from
Calcitonin released from the parafollicular cells of the thyroid
Electrochemical gradients for Na+, K+ Ca++ and Cl-
Na+ : +20 to +30 mV
K+ : -90 mV
Cl- : -80 mV
Ca++ : +45 mV
These channels open and these channels close once an action potential has been generated at the sarcolemma
Voltage gated Na+ channels close and voltage gated K+ channels open
Would acetylcholinesterase inhibitors cause spastic or flaccid paralysis? Explain why and give 2 examples.
Inhibition of ACh esterase -> increased ACh in synaptic cleft -> constant depolarization -> spastic paralysis. Two examples are organophosphates and neostigmine (others are tetany toxin and prostigmine)
List the number of carbons for: Glucose, pyruvate, acetyl-CoA, glycerol, and lactic acid
Glucose (6), pyruvate (3), acetyl-CoA (2), glycerol (3), lactic acid (3)
Give two names for the molecule that promotes Ca++ absorption in the GI tract and what hormone stimulates its activation.
Calcitriol, active Vitamin D3, or 1,25-dihydroxycholecalciferol and the hormone that stimulates its activation is PTH
The pH of this region of the mitochondria would be expected to drop greatly during the process of oxidative phosphorylation
Intermembrane space
List the events the lead to a muscle contraction after an action potential has been generated at the sarcolemma
AP travels into T tubule, voltage gated Ca++ channels open, Ca++ flows from SER to sarcoplasm, Ca++ binds to troponin, troponin-tropomyosin complex exposes binding site, myosin head uses ATP to attach to binding site --> contraction
Would K+ channels blockers cause spastic or flaccid paralysis? Explain why and give 2 examples.
K+ channel blocked -> K+ cannot flow out of postsynaptic cell -> no repolarization -> spastic paralysis. TEA and 4-amino pyride are examples.
Describe how a protein enters metabolism.
Protein is hydrolyzed by protease -> amino group from amino acid is removed by deaminase -> the amino group turns into urea -> amino acid enters the metabolic pathways depending on the # of carbons
RANKL is expressed on this cell and this molecule inhibits its binding to its receptor during elevated blood Ca++ levels
Expressed by osteoblasts and OPG inhibits its binding to RANK receptor during high blood Ca++ levels
List all of the steps of the production of active vitamin D starting from the skin
7-dehydrocholesterol -> cholecalciferol -> 25-hydroxycholecalciferol -> 1,25-hydroxycholecalciferol