Case problem

[ItsGavinC]

Hi all. I'm wondering if any of you brilliant med students have any thoughts on this case my professor assigned. And no, you aren't doing my homework for me, this was a case from last week. My group has already come to a conclusion, however our gripe is that the conclusion the professor desired was far too minimal for the broad (and minimal) amount of information he gave us.

Since we're dental students, I'm curious to find out what the medical students think. I'm hoping to use your responses as ammo in my argument to have him reevaluate the case.

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A 45 year-old man has suffered from occipital headaches for the last 6 months, especially in the morning. He has been feeling fatigued and weak for some weeks and has noticed difficulties assuming the upright position without using his arms. He is currently taking no medications. Physical examination showed no signs of volume depletion or of edema. Arterial blood pressure was 170/110 mm Hg, pulse rate 72, respiration 14/min.

The following laboratory data were obtained for arterial blood:

Na+ = 142 mEq/L
K+ = 2.3 mEq/L
Cl- = 98 mEq/L
HCO3- = 34 mEq/L
BUN = 10 mg/dL
Creatinine = 0.8 mg/dL
Ang II = 0.3 ng/ml/hr (low)

What do you think this patient is suffering from? How did you arrive at this conclusion? Are all the laboratory findings consistent with this conclusion? How should he be treated?
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[mongoose]

well, with a potassium that low, it's a wonder he's not dead. chloride also a bit low. bicarb high, probably a good indicator of acidosis. BUN and creatinine not too shabby. angiotensin II is low, indicating a problem with ACE i'm assuming since they make no mention of angiotensin I being low. i'm not sure how this would play into the diagnosis since it is noted he is neither hypervolemic/hypovolemic nor edematous.

so the question becomes, what would cause him to have a low potassium, low chloride, and low angiotensin 2 levels, right?

aldosterone will cause low potassium levels, low angiotensin 2 levels, but i am not sure of what it does to chloride levels.

maybe a primary hyperaldosteronism. is that the dx?

 

[nuclearrabbit77]

Originally posted by ItsGavinC
Hi all. I'm wondering if any of you brilliant med students have any thoughts on this case my professor assigned. And no, you aren't doing my homework for me, this was a case from last week. My group has already come to a conclusion, however our gripe is that the conclusion the professor desired was far too minimal for the broad (and minimal) amount of information he gave us.

Since we're dental students, I'm curious to find out what the medical students think. I'm hoping to use your responses as ammo in my argument to have him reevaluate the case.

----------------------------------------------
A 45 year-old man has suffered from occipital headaches for the last 6 months, especially in the morning. He has been feeling fatigued and weak for some weeks and has noticed difficulties assuming the upright position without using his arms. He is currently taking no medications. Physical examination showed no signs of volume depletion or of edema. Arterial blood pressure was 170/110 mm Hg, pulse rate 72, respiration 14/min.

The following laboratory data were obtained for arterial blood:

Na+ = 142 mEq/L
K+ = 2.3 mEq/L
Cl- = 98 mEq/L
HCO3- = 34 mEq/L
BUN = 10 mg/dL
Creatinine = 0.8 mg/dL
Ang II = 0.3 ng/ml/hr (low)

What do you think this patient is suffering from? How did you arrive at this conclusion? Are all the laboratory findings consistent with this conclusion? How should he be treated?
-----------------------------------------------

chloride levels can be explained due to electrostatic balance reasoning....(Chloride + HC03-) + Na = anion gap......HC03- and chloride sum is constant unless of fixed acid production changes.
aldosterone explains the metabolic alkalosis as well.
use spironolactone or equivalent drug that would block the action of aldosterone. imaging to locate probable aldosterone secreting adrenal tumor. renin secreting neoplasm is not probable due to low levels of angiotensin II. ACE inhibitors would not be very helpful due to the fact that angiotensin II is not the cause, aldosterone is. eventually include thiazide diuretics after spironolactone (with careful monitoring of potassium levels).

goals:
-decrease blood volume
-stabalize potassium
-remove tumor


must rule out: licorice ingestion, self-medication, little's syndrome

 

[EUROdocMOM]

I agree with nucleearrabbit77 it does look like a hyperaldosteronism of some cause, but mongoose, shouldn't an increased HCO3 indicate a metabolic alkalosis (unless it's a compensated resp. acidosis). Do they give a pH or a PaCo2?
I am curious why they gave this in dental school... is there a special reference to a particular anesthetic, medication, or syndrome that affects a person's oral heath, or perhaps a contraindication to a procedure?

 

[Darth Vader]

I believe that the key to this case is the lab value that was given to us that normally is not given. Most people don't order an AII level unless they are looking for something specifically. The renin angiotensin aldosterone level is sensitive to hypo and hyperkalemia along with renal perfusion, so you would expect that with a symptomatic hypokalemia (weakness), angiotensin II levels should be elevated. He also has some sort of metabolic alkalosis going on in the setting of hypertension. Given all of this information, I would suspect that he has some sort of aldosterone or mineralcorticoid secreting tumor that is causing him to be hypertensive and secrete potassium and be alkalotic while causing low levels of AII. Therapy includes determining the etiology, but you can use spirnolactone or an aldosterone antagonist in the interim. I would also replete his electrolytes as well.

 

[nuclearrabbit77]

Originally posted by EUROdocMOM
I agree with nucleearrabbit77 it does look like a hyperaldosteronism of some cause, but mongoose, shouldn't an increased HCO3 indicate a metabolic alkalosis (unless it's a compensated resp. acidosis). Do they give a pH or a PaCo2?
I am curious why they gave this in dental school... is there a special reference to a particular anesthetic, medication, or syndrome that affects a person's oral heath, or perhaps a contraindication to a procedure?

yes i believe mongoose meant to say metabolic alkalosis not acidosis.

 

[mongoose]

Originally posted by nuclearrabbit77
yes i believe mongoose meant to say metabolic alkalosis not acidosis.

d'oh! sorry for any confusion caused by my careless error.

 

[souljah1]

I agree with mongoose. The headaches, fatigue, and weakness may be related to the hypokalemia. The hypertension and metabolic alkalosis with hypokalemia and low angiotensin II point toward mineralcorticoid or apparent mineralcoriticoid excess. Primary hyperaldosteronism would lead to a decrease in serum renin, and a consequent decrease in angiotensin II. Also on the differential would be Cushing's (but doesn't really fit clinical picture), licorice, Liddle's (would have low aldosterone levels), ectopic ACTH secreting tumor (i.e small cell carcinoma of the lung). The later may present with more of the mineralcorticoid excess but initially may not show symptoms of glucocoritoid excess.

I'd get a plasma aldo, head and abdominal CT or MRI to get a look at the adrenals, pituitary/hypothal and await results. If primary hyperaldo is ruled out, I'd start searching for some ectopic ACTH tumors. I'd get a quick ECG to look for inverted T waves (i think that is right) seen with hypokalemia and treat the hypokalemia accordingly.

But if I had to make a guess I'd go with primary hyperaldosteronism based on the labs and brief/incomplete H&P. I'd treat with spironolactone to block aldosterone's ability to reasorb Na+/H2O. I'd also get a surgical consult to discuss the possibility of adrenalectomy.

 

[ItsGavinC]

Originally posted by EUROdocMOM

I am curious why they gave this in dental school... is there a special reference to a particular anesthetic, medication, or syndrome that affects a person's oral heath, or perhaps a contraindication to a procedure?

Nope, just part of our curriculum. We are systems-based at my school, and the professor who taught us this was Dr. Jackson from Univ. of Kentucky College of Medicine (maybe some of you have had him). Our professors fly in from medical schools all across the country. But that's another tale for another day...

In any event, if it were hyperaldosteronism, wouldn't we expect the sodium levels to be elevated? At 142 they are still within normal range, are they not? My group believed that the aldosterone would affect the principal cells so that greater amounts of sodium would be reabsorbed (and of course potassium secreted).

 

[babinski bob]

You can NEVER equate serum Na concentration as a true indicator of total body sodium because water always follows sodium reabsorption. High levels of sodium are ALMOST always due to volume depletion. However, in this case, the patient is normovolemic according to physical exam. That basically leaves the diagnosis of hyperaldosteronism as a very likely cause. Potassium wasting is causing the proximal muscle weakness being observed and sodium is still within normal limits.

 

[nuclearrabbit77]

Na reabsorption is invariably linked to water reabsorption. Low levels of angiotensin II would also decrease bicarbonate reabsorption at the proximal tubule as well (to help correct the metabolic alkalosis). In addition, there is a decrease in the amount of Na reabsorbed at the proximal tubule, due to a decrease in sympathetic tone (afferent/efferent arteriole vasodilation) atrial natriuretic peptide (efferent vasoconstriction), decrease in oncotic pressure (less volume reabsorption), would all contribute to increasing filtering levels to get rid of volume.

 

[Darth Vader]

hypernatremia is seen with ~80% of cases with hyperaldosteronism. It's probably the same thing that drives ADH in extreme hypovolemia, at the extremes, it's overriden. That also means that 20% of hyperaldosteronism's have normal sodium levels. Most aren't all that high either. Also, this is a strange dental question. I'm trying to think how this relates to dentistry, but I can't think of how it does.

 

[nuclearrabbit77]

Originally posted by nuclearrabbit77
Na reabsorption is invariably linked to water reabsorption. Low levels of angiotensin II would also decrease bicarbonate reabsorption at the proximal tubule as well (to help correct the metabolic alkalosis). In addition, there is a decrease in the amount of Na reabsorbed at the proximal tubule, due to a decrease in sympathetic tone (afferent/efferent arteriole vasodilation) atrial natriuretic peptide (efferent vasoconstriction), decrease in oncotic pressure (less volume reabsorption), would all contribute to increasing filtering levels to get rid of volume.

i want to clarify what i said....

(sympathetic, ANP, oncotic) attempt to alleviate the increased Na and volume by increasing net filtration, while decreasing Na reabsorption at the proximal tubule.
Increasing the flow rate, while decreasing Na reabsorption at the proximal tubule will decrease volume and Na. Physiologists refer to this as "escape" from hyperaldosteronism.

 

[ItsGavinC]

Originally posted by Darth Vader
Also, this is a strange dental question. I'm trying to think how this relates to dentistry, but I can't think of how it does.

It doesn't directly relate to dentistry at all, only to our Kidney/Urinary module. You guys would be surprised at the stuff we've had to learn this semester. Although I'm not saying it is equal to what you get put through your first years, I'm certain that my dental education would surprise many physicians just by the sheer breadth of it (Monday we begin OB/GYN).

And, of further surprise perhaps, would be that questions pertinent to this case are on our NBDE I (similar in timeline to your Step 1). But I digress...

Thanks for all the responses. I'm going to post my professors answer to the question, but I'm going to get his permission before I do so.

 

[ItsGavinC]

And I'd be amiss if I didn't mention how smart all of you are. I know these answers came as second nature to you, whereas I'm sooooo slow in forming a dx and have to methodically look things up.

I appreciate all of your responses because they often make much better sense than Guyton's or Robbins' or the other 110 textbooks I own.

Thanks again.

 

[nuclearrabbit77]

why do you need to ask him? does he have a patent on conn's syndrome? j/k

 

[nuclearrabbit77]

gavin- i highly recommend you use a physiology book called Physiology - by Costanzo. It is the most important book i used my first year. It reads like time magazine....simple, to the point, etc. how all books should be written........ she also writes the "little costanzo"= BRS physiology.

 

[mongoose]

Originally posted by ItsGavinC
Nope, just part of our curriculum. We are systems-based at my school, and the professor who taught us this was Dr. Jackson from Univ. of Kentucky College of Medicine (maybe some of you have had him). Our professors fly in from medical schools all across the country. But that's another tale for another day...

In any event, if it were hyperaldosteronism, wouldn't we expect the sodium levels to be elevated? At 142 they are still within normal range, are they not? My group believed that the aldosterone would affect the principal cells so that greater amounts of sodium would be reabsorbed (and of course potassium secreted).

I thought Dr. Jackson was an extremely good lecturer and overall was a great guy. He was our course director for Physiology. That was at the time when I had dislocated my elbow and broken a bone in my arm, and needed surgery. He was very flexible with allowing me to take tests at alternate times due to my circumstances. I thought then and still feel that Physio was our best course overall at our med school.

 

[mongoose]

Originally posted by ItsGavinC
And I'd be amiss if I didn't mention how smart all of you are. I know these answers came as second nature to you, whereas I'm sooooo slow in forming a dx and have to methodically look things up.

I appreciate all of your responses because they often make much better sense than Guyton's or Robbins' or the other 110 textbooks I own.

Thanks again.

Dude, hang in there. I remember my first year when professors would ask these types of questions all I could offer was blank stares. Now, after being exposed to the stuff multiple times I can offer (sometimes) insightful comments on the cases. Hang in there. It DOES get better.

 

[ItsGavinC]

Mongoose, I didn't even associate with the fact that you attend UK!

Dr. Jackson is the 3rd professor we've had from your school. We also had Dr. Randall and Dr. Speck come and teach us our cardio and pulmonary courses.

 

[ItsGavinC]

Originally posted by nuclearrabbit77
gavin- i highly recommend you use a physiology book called Physiology - by Costanzo. It is the most important book i used my first year. It reads like time magazine....simple, to the point, etc. how all books should be written........ she also writes the "little costanzo"= BRS physiology.

Thanks, I'll check into it. I DO use the BRS Phys. book quite extensively (as with all the BRS books).

 

[eagle26]

She was my teacher last year and does the USMLE prep course!!

 

[nuclearrabbit77]

if im ever in virginia i'll ask for an autograph. she's dope. somebody gave me some text file she wrote about USMLE I prep, that was excellent as well too.