Hypercalcemia

[@racheldmassey7129]

I sent all of your videos to my classmates, and they all thanked me repeatedly because your videos are saving us!! They match EXACTLY what we are taught, they are simplified, but give all the important details. THANK YOU

[@StrongMed]

Thank you! I'm so glad the videos have been helpful!

[@MrCabimero]

I have been in practice 30 years- where have you been? This is wonderful content and so thankful that I stumbled onto this. Thank you for your contribution to our collective knowledge.

[@StrongMed]

Great question! About 40% of patients with 1 hyperPTH have hypercalciuria, the other 60% have normal urinary Ca. What presumably happens in the 40% is the excessive PTH causes such a high concentration of Ca filtered through the glomeruli, that it overwelms the renal tubules' ability to reabsorb it, even under the influence of the additional PTH. (The diagnosis algorithm in the video is misleading - should say high OR NORMAL indicates 1 hyperPTH. I'll prob add an annotation to address this.)

[@sunving]

Nice lecture , nice music thank you Dr Strong.

[@youbetyourwrasse]

When I asked the ER Doctor last month if his diagnosis of hypercalcemia could be responsible for the confusion and anxiety that had disturbed me enough to seek advice, his reply was "maybe." Maybe AI doctors would not be such a bad idea in some cases. Because this is one Smart Video. I am Enlightened.

[@marenkuether-ulberg3311]

Thank you for the information. I have breast cancer, osteopenia and familial hypercalcemia… that’ll be possibly dicey when given anti-estrogen meds which leach calcium from the bones.

[@obeyxana34]

I actually have hypercalcemia but from too much calcium intake (90%-125%) a day not from antacids but from milk .

[@haqzahoorul]

Thanks very much for the lovely presentation 👏👏👏

[@aashritharamesh6620]

I am an intern in IM currently in the US ..very helpful. Please do more of such videos .. treatment of a fib with rvr, PE, DKA , acute limb ischemia,

[@StrongMed]

One step ahead of you (on some of those...) ;) kzbin.info/aero/PLYojB5NEEakUXq0Dr5BqJsbt3MJdb7RsZ

[@manuh6567]

I think this video will save lives. Many thanks. 👍🏻

[@StrongMed]

Thanks for pointing this out!

[@sabihhuq]

Eric, these videos are amazing. Great detail AND practicality, which is a rare combination. Thank you so much for making them! Do you have any thoughts on DENOSUMAB or CINACALCET?

[@igorsnast6694]

hello, great lectures. why would the 24 urine excretion on calcium be high in primary hyper-PTH? isnt PTH suppose to do just the opposite?

[@cyrdeh7943]

Hi, thank you Eric for this great lecture. There is a link between oestrogen and calcium / bone physiology, are there any causes of hypercalcemia caused by excess oestrogen (OC, Hepatic failure, etc.). Is it clinically relevant?

[@Malhiu]

Hello Eric, could you please tell me when to check ionized calcium in either hypo or hypercalcemia ? In both hypoalbumenic and eualbuminic patients. Thanks.

[@MrSgshields]

Interesting and accessible video. Thank you. Sorry if you did cover this and I missed it, but I don't recall you mentioning parathyroidectomy as an obvious first treatment option for primary hyperparathroidism. I thought this became particularly relevant during the section on treatments with medicines as if the cause were an adenoma, then excision of that would usually be the initial treatment, which would then require different medical intervention (such as calcium supplementation in cases of post-op 'hungry bones'). My concern was that a patient viewing this may not realise that surgery is the only known effective treatment for a parathyroid adenoma and that is what they should expect in most cases of hyperparathyroidism. I guess the same could be said of malignant parathyroid tumours, but aren't as familiar with that. Again, apologies if you covered this and I'm being dim, which is quite possible. If it was unintentionally omitted, I hope you can add in your comments (even if brief: I note your comment above on video length), as I'm sure they would be much appreciated.

[@amitpatel936]

I have borderline hypercalcaemia but there is no symptoms. Should I go and see a doctor?

[@ejestradag]

Dr. Strong: While I don’t have hypercalcemia, my three siblings and myself accumulate calcium within the heart, its valves and its internal vascular system, and very little anywhere else. No one seems to have studied this situation. Could you give some guidance for this abnormality?

[@StrongMed]

I'm afraid that I can't offer specific, individualized medical advice here, and I recommend speaking with your own physician about any personal health concerns. However, *in general*, preferential calcium accumulation on heart valves (particularly the aortic), in the coronary arteries, and in the aortic arch is relatively common - though it is a sign of atherosclerosis and warrants discussion with an internist and/or cardiologist. For most people, the reason why this preferential deposition happens (rather than calcium being deposited equally everywhere) is not known.

[@Maria-qm9cg]

Thank you Dr. This video is golden. 🌟🌟🌟🌟🌟

[@Toscalily]

I was wondering if it would be possible to get a video about FHH. I've known I have since sometime last year and showing symptoms since '13. I can never find any real info on it and my poor specialist has never diagnosed someone before me so he cant really enlighten me that much. I'd just like to understand it better :)

[@nttdahir]

if the person you use milk only for long time with out any other food, is he in risk of hypercalcemia ? where i from, there some people who use Camel milk exclusively without other food, because they do not have it.

[@hardikpatel.]

hey Mr. Eric.....you have a very good knowledge......but it would b great if u tell why signs and symptoms occurs???? reasoning is better way to learn.....right....?????

[@StrongMed]

Mr. Patel, thanks for your feedback! Yes, in general I agree that it is best to understand the mechanisms behind symptoms and signs. I chose not to explain them here for 2 reasons. First, I was really trying to keep all of my electrolyte videos under 20 min (a goal I needed to abandon when I reached sodium), and also because the mechanism behind most symptoms in hypercalcemia involves membrane potentials and action potentials. Since most students and medical professionals don't remember the basics behind action potentials, it wouldn't actually help to describe the mechanism unless I reintroduced them to membrane ion channels in detail - a diversion that some viewers would welcome, but I suspect most would prefer to skip. I hope you'll check out some of my other videos, and I think you'll find that I describe relevant mechanisms and physiology in more detail in most. For hypercalcemia, in extreme brief, most symptoms (e.g. constipation, depression, fatigue, nausea) are related to impairment of action potential generation in neurons. Most web-based resources state that hypercalcemia "hyperpolarizes" cells, which I think is not strictly true. In actuality, calcium ions inhibit the voltage-gated sodium channels in the cell membrane. Since an increase in sodium conductance is responsible for the "upswing" of the action potential, relative inhibition of the sodium channels results in it become more difficult to generate and/or propagate an action potential. My best understanding is that the cell's resting membrane potential is more or less unaffected, but I'm not able to find a source that explicitly confirms that. The mechanism of the abdominal pain is a little less clear, but with some "hand-waving", can be attributed to the decreased muscular function from poor action potential generation as above; the subsequent constipation and ileus could initiate pain through bowel distention. Finally, the mechanisms behind the renal insufficiency and other renal problems frequently seen are complex and multiple, but a large component is an increase in renal vascular resistance induced by an increase in vascular smooth muscle tone. Hope that helps!

[@hardikpatel.]

Hey Eric I really appreciate.....your effort...just didn't expect your reply.....thank u...m happy....!!!

[@StrongMed]

hardik patel No problem!

[@HaroldSchranz]

Of interest as i had HL at age 3 or so (unusual) , Co60 radiotherapy ... leading decades later to hyperparathyroidism due to parathyroid carcinoma (and thyroid carcinoma X 2) ... the psychiatric overtones are concerning ... as I suspect I had hypercalcemia for around 8 years (given the undiagnosed weight gain) and 20+ years later get diagnosed for unmasking ADHD (and ASD). Lived experience is consistent with growing ADHD symptoms since the hypercalcemia (resolved in 2005 by surgery); but long-term effects on the brain are plausible - given undiagnosed ADHD/ASD. Finding a medical specialist with knowledge across cancers/hypercalcaemia and ADHD/ASD is almost impossible. Undiagnosed amplifying ADHD is not good for relationships. (EBV from an unscreened post-natal blood transfusion seems to be a plausible initial cause). No proof but the lived experiences are compelling (and rather traumatic in the last couple of years as being blamed for having ADHD/ASD).

[@kleshtringu01]

Eric, thank you so much for your lectures! those are the first ones which I actually like to watch! The nice intro's and clear illustrations, but most importantly the way you're talking transform learning into fun! I have one question though concerning Chondrocalcinosis: Do you know in which cases of hypercalcemia it occurs, and why? For me, each form of hypercalcemia should lead to intra-articular deposits of Ca and thus leading to visible deposits in X-Rays?! Greetings from Switzerland, and sorry for my English

[@philistinezigurath1368]

why does it causes polyuria?

[@sunving]

thank you very much Dr Eric Strong !

[@dattatraybagle2207]

EXCELLENT 💯

[@sarahal-shehri8389]

this video is very helpful. thank you

[@absolutjag9]

thx for explaining hypercalcemia of malignancy workup algorithm

[@MikeBirkhead]

This is probably too late to ask, but I have to give a presentation on this tomorrow morning and your slides are 100% superior to what I've put together. Is it possible to get a copy of your powerpoint presentation (assuming that's what you're using)? Thanks for the reply? Thanks twice if you reply this evening or tomorrow!

[@StrongMed]

Mike Birkhead Sorry Mike, just seeing this now. Hope your presentation went well!

[@nystagmussumgatsyn15]

Thanks, I learned a lot but what about thyrotoxicosis?

[@StrongMed]

The hyperthyroidism that I briefly mention is a slightly more general category than thyrotoxicosis. The hypercalcemia of thyrotoxicosis is caused by increased bone resorption, is present in ~15-20% of patients with that condition, and resolves with restoration of normal thyroid hormone levels.

[@nystagmussumgatsyn15]

thanks

[@sharonasugah7462]

if at all this patient with hypercalcemia was to use intravenous fluid which intravenous fluid would you use without leading to elevated bloodpressure

[@drabhijeetchopade]

Sharon Asugah IVF to be used is 0.9% NS with careful monitoring to look for fluid overload especially in cardio-pulmonary diseasesed individuals.

[@nellyhoffman6194]

Doctor i have one question ,,, Why is alkaline phosphatase elevated in Osteitis fibrosa cystica ?

[@StrongMed]

In osteitis fibrosa cystica, excessive osteoclast activity leads to bone breakdown, and any disease with excessive bone breakdown, or excessive bone turnover, results in an elevation of alk phos.

[@nellyhoffman6194]

Thanks for your time doctor ! your work is beyond great ! :)

[@ronilata1997]

Thx you so much dr :))) you help me everyday. Big greetings from Sarajevo :))

[@TheEmperorMim]

I need the presentation as ppt plz

[@nystagmussumgatsyn15]

I know that Hypercalcemia can cause a hypercalcemia induced nephrogenic diabetes insipidus and polyuria, but can dehydration by itself and hemoconcentration cause hypercalcemia?

[@StrongMed]

Hemoconcentration could lead to excessive concentration of albumin, which would lead to high levels of total serum calcium, with a normal serum ionized calcium (i.e. patients shouldn't be symptomatic). Some very thorough sources also mention hemoconcentration in the absence of hyperalbuminemia as a potential cause, which may be the primary mechanism by which hypercalcemia can develop in adrenal crisis. I've never personally seen this, and suspect it's quite uncommon.

[@nystagmussumgatsyn15]

really great thanks so much

[@sherylhokianga3]

I’ve Bin Dynoised With Primary Hyercalcemia!!..I’m On a 3 Monthly Injection Of Prolia denosumab!...Now, I’ve Bin Called In 2 Hospital 2 Have An Injection!..Not Quite Sure Wat That Jab Entails?..Proberly 4 More Testing Most Likely!

[@muhammadnaveed6815]

Thank u so much Dr!!!

[@rosskay]

and thank you for posting this

[@sunving]

Thank you Dr Strong

[@DuvAngel1]

You missed the treatment of hyperparathyroidism with surgery.

[@ekbaldesoky1118]

VI illustrative thanks a lot

[@raudoniguzikai]

Thank you very much for this very informative video. Do you know, if it is possible to decrease production of PTHrP or somehow block it after it's been produce by malignant cells? Are there any treatment options available? (for a patient with severe hypercalcemia; triple neg.Breast Cancer..)

[@StrongMed]

Unfortunately, there are currently no therapies which can either inhibit production of PTHrP, or block its action after production. Treatment of hypercalcemia secondary to PTHrP relies on the same general options as other etiologies of hypercalcemia (e.g. hydration, furosemide, bisphosphanates, etc...), though also unfortunately, in my experience hypercalcemia from PTHrP tends to be more difficult to treat than from other causes.

[@raudoniguzikai]

Thank you very much for an answer!! I appreciate your time you spend sharing your knowledge :)

[@hemmojito]

Hello Eric, I love your videos and watch them very carefully. I have a quick question concerning this video: Here you talk about PTHrP being also physiologically produced in small amounts. I asked myself by which cells? Also by Chief Cells or cells other than that? Thanks in advance.

[@StrongMed]

Hemmojito, thanks for the feedback! The normal physiology of PTHrP is rich, complicated, and incompletely understood. It appears to be produced by cells throughout the body in response to all kinds of different stimuli, and with different effects. The most well studied sites of production include bones/teeth, smooth muscle lining blood vessels, placenta, mammillary glands (it's secreted in breast milk), and pancreatic islet cells. Sometimes, PTHrP is released by cells into the systemic circulation, and in other situations, PTHrP remains intracellular and moves back and forth between the nucleus and cytoplasm for purposes largely unknown.

[@hemmojito]

Wow, thank you very much. That is fascinating and such a fast and thorough response, too. Stunned me for a second there. That was really kind of you, Eric,

[@Teresahorner]

Strong Medicine my test said smooth muscle antibodie, i got high phosphate but i got lupus and it seems that bile duct enlarged? This i dont understand all. Have you got link sir on bile duct? Thank you

[@nellyhoffman6194]

THANKS DOCTOR

[@marialeonoramaria]

Thanks

[@bruh0-037]

I had this as a baby and I almost died

[@dr.ashraf2015]

Osborn wave

[@rosemaines8895]

Thanks