Tetany can be induced in primary hypoparathyroidism by occluding flow to forearm

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..... ie: when taking blood pressure.

Why/how?


Thanks.

That is known as Trousseau sign and is a sign of hypocalcemia (secondary in this case to hypoPTH).

Hypocalcemia also manifests in Chvostek's sign, in which the mandible is tapped and elicits an ipsilateral facial spasm.

Mechanism behind Trousseau: occlude the artery, stop perfusion to the distal muscles, muscle spasm. I'm not certain about the extent to which brachial occlusion in a eucalcemic individual would eventually induce the same finding.
 
^^ Thanks, but yeah, I know about Trousseau's sign and all..... but why does it [mainly] happen in hypocalcemic states and not in eucalcemic states?

What's the mechanism?
 
Hypocalcemia leads to a resting membrane potential that is closer to -60 mV --> tetany.

Less Ca2+ in the blood, so less + charges means that the gradient between the outside and the inside is less --> higher membrane potential.

Does this make sense?
 
Yes, I knew that as well.

I guess it'd be best if I re-word my question. Why does the above ^^ happen WITHOUT occluding the blood vessel in the forearm in a hyopcalcemic patient, and why does it NOT happen in eucalcemia?

Focusing on the occlusion here.
 
Yes, I knew that as well.

I guess it'd be best if I re-word my question. Why does the above ^^ happen WITHOUT occluding the blood vessel in the forearm in a hyopcalcemic patient, and why does it NOT happen in eucalcemia?

Focusing on the occlusion here.

In the patient with hypocalcemia (before you apply the pressure cuff), the extracellular "positivity" is decreased (because there's less calcium), and so the cell membrane potential difference is reduced, leading to a cell membrane which is "hyperexcitable." When eliciting Trousseau's sign of hypocalcemia, you apply a pressure across the brachial artery above systolic so as to occlude it. This occlusion leads to ischemia distal to the site of occlusion. This results in the skeletal muscle cells receiving less oxygen tension. As the oxygen decreases, the cells lose the final electron acceptor, and thus ATP levels drop in the cell. This leads ATP-dependent processes to decrease, the most important one being the Na/K ATPase. When the pump stops working, the Na cannot be exchanged for K, and the cell becomes even more hyperexcitable, thus leading to the characteristic contractions elicited in the sign.
 
Yes, I knew that as well.

I guess it'd be best if I re-word my question. Why does the above ^^ happen WITHOUT occluding the blood vessel in the forearm in a hyopcalcemic patient, and why does it NOT happen in eucalcemia?

Focusing on the occlusion here.

The characteristic wrist flexion/finger extension spasm does not occur without occluding the vessel. The sign is elicited, by definition.

The key is hyperexcitability of the skeletal muscle cells. Whether or not this occurs in a normal individual, again, is a valid question. As a medical student with such a rich history of self-experimentation, I would encourage you to blow up a cuff on your arm to 200 for 3 minutes and find out what happens. Then, let us know.
 
In the patient with hypocalcemia (before you apply the pressure cuff), the extracellular "positivity" is decreased (because there's less calcium), and so the cell membrane potential difference is reduced, leading to a cell membrane which is "hyperexcitable." When eliciting Trousseau's sign of hypocalcemia, you apply a pressure across the brachial artery above systolic so as to occlude it. This occlusion leads to ischemia distal to the site of occlusion. This results in the skeletal muscle cells receiving less oxygen tension. As the oxygen decreases, the cells lose the final electron acceptor, and thus ATP levels drop in the cell. This leads ATP-dependent processes to decrease, the most important one being the Na/K ATPase. When the pump stops working, the Na cannot be exchanged for K, and the cell becomes even more hyperexcitable, thus leading to the characteristic contractions elicited in the sign.
Excellent, thanks.

The characteristic wrist flexion/finger extension spasm does not occur without occluding the vessel. The sign is elicited, by definition.

The key is hyperexcitability of the skeletal muscle cells. Whether or not this occurs in a normal individual, again, is a valid question. As a medical student with such a rich history of self-experimentation, I would encourage you to blow up a cuff on your arm to 200 for 3 minutes and find out what happens. Then, let us know.
lol no thanks.
 
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