Neuro - Small Groups Flashcards
Describe multiple sclerosis. How does it affect K+ permeability?
Demyelation of the CNS (and sometimes PNS) –> causes decrease in conduction velocity (increase in capacitance bigger than decrease in membrane resistance)
ALSO K+ channels are essentially absent in the nodes of Ranvier whereas they are highly concentrated in the myelin sections so demyelation will cause an increase in K+ permeability, so hyperexcitability, but very slow APs
Describe Guillain-Barre syndrome.
Autoimmune disease causing the demyelation of the PNS –> causes decrease in conduction velocity (increase in capacitance bigger than decrease in membrane resistance)
Describe Lambert-Eaton. What is the treatment? What is death caused by? Does this affect the quantal size or content? What poison has the same effect?
Autoimmune disease in which antibodies attack P-type calcium channels at the presynaptic terminals. No treatment except for plasma phoresis to take out antibodies.
Death caused by paralysis of diaphragm.
QUANTAL CONTENT DECREASED.
Funnel spider venom blocks those same channels.
Describe myasthemia gravis. What are 2 potential treatments? Does this affect the quantal size or content? What other property is affected?
Autoimmune disease where antibodies attack the ACh receptors on the postsynaptic end-plate. Can be treated with inhibitors of acetylcholinesterase (eg: tensilon) to increase time of ACh in the synaptic cleft OR poisoning of K+ VG channels.
QUANTAL SIZE DECREASED.
SAFETY FACTOR DECREASED.
Describe compression neuropathy. What test to do to confirm this?
Causes decrease in conduction velocity by decreasing the diameter of the nerves which is increasing the internal resistance (space constant goes down, time constant goes up). Intracellular recording of an AP will show it takes longer, extracellular test should be normal.
Describe polyo. What test to do to confirm this?
Nerves die which causes the extracellular recording of APs (compound AP) to have a lower amplitude.
What’s the connection between Zika and GB?
Zika sometimes causes GB.
Describe diabetes Type 1.
Autoimmune disease
Describe diabetes Type 1. What is the treatment? Reversible?
Autoimmune disease where antibodies attack the beta cells of the pancreas, which causes a lack of insulin.
Treatment: insulin administration.
Irreversible.
Describe diabetes Type 2. What is the treatment? Reversible?
Decreased sensitivity to insulin.
Treatment: less glucose intake and insulin administration OR even blocking K+/ATP channels so that cells are depolarized and secrete more insulin.
Reversible
Describe how botox works. Does this affect the quantal size or content?
Inhibiting proteins (eg: synaptotagmin) that are necessary for the fusion of the vesicles at the presynaptic neuron.
DECREASES QUANTAL CONTENT.
What are the 3 pathological disorders that cause reductions of conduction velocities?
- MS
- GB
- Compression neuropathy
How can you know that a pathology is systemic or not?
Difference between global and local
Describe poisoning by tetraethykammonium (TEA) and 2-aminopyridine. Effect on APs? Effect on EPP? How can you test for it? Is conduction velocity affected? Effect on muscle strength?
Both toxins block voltage-gated K+ channels, which means they both do not have an undershoot and take longer and the muscle one does not have the hump. NO RELATIVE REFRACTORY PERIOD.
EPP will have stronger strength (way above safety factor) but no effect because of safety factor.
You can test for it with a voltage-clamp experiment.
Conduction velocity unaffected because propagation depends on Na+ channel.
Muscle strength is increased because APs are firing at a very high frequency and are lasting longer and calcium concentration in the sarcoplasm is high.
Describe mcartles disease = glycogen storage disease type 4. 3 symptoms? Explain each. Why is there a contracture once the muscle is initially excited and why is it electrically silent? How are the calcium intracellular levels affected and what does this cause? What kind of exercises can these patients perform? How can this be tested for?
Symptoms:
1. Lactate levels are constantly low instead of increasing during exercise because patients lack the enzyme glycogen phosphorylase which breaks down glycogen into glucose for glycolysis where lactic acid is a by-product
2. White fibers are defective because of the enzyme missing.
3. Myoglobinuria because red fibers are damaged because abused since no white fibers available to do work.
The muscle can initiate the initial contraction, but there is not enough ATP (usually produced by glycolysis) to return calcium to the SR and to go through cross-bridge cycles: causing cramps that are electrically silent.
Calcium levels are constantly high meaning his muscles keep trying to contract.
Patients can only perform endurance exercises.
Test: western blot to look for the enzyme glycogen phosphorylase or genetic test
