Thread by @kidney_boy

About to see a small group session on the adrenal run by @ohamnvik and @jwilliamMD at @harvardmed

Case 1. 48 with fatigue, hx of cancer, chemo including dexamethasone. Stopped a month ago. Difficult getting out of a chair. Gained weight.

Describe the findings.

How do they help you identify what might be going on?

How would you hypothesize her use of dexamethasone impacted her hypothalamic pituitary adrenal function and physical condition?

Illustrate your hypothesis in a diagram.

The room is quiet as 43 students puzzle over the case on their own. After a few minutes the room erupts with bubbling laughter and conversation as the 4 person tables start to discuss their thoughts and collaborate on their answers.

Now the group comes together and one of the students is describing the constellation of findings: moon face, stria, weight gain. Indicate Cushings. Then patient had fatigue and nausea due to low cortisol. Two clinical syndromes.

Dexamethasone was given at high dose which caused the Cushings. And this supressed ACTH and CRH. Since ACTH is both stimulatory and trophic so loss of the latter causes atrophy of the adrenal gland leading the Addisonian sxs.

Bruising is due to dexemethasone as opposed to the high ACTH after stopping the dexamethasone as hypothesized by a student.

Question from the student: Is aldosterone (zona glomerulosa) spared?

en.wikipedia.org/wiki/Zona_glom…
en.wikipedia.org/wiki/Zona_fasc…

Notes by @ohamnvik

the blood pressure is maintained because of all the systems that work to sustain blood pressure including RAAS and the sympathetic nervous system. Adrenal crisis with hypotension is reserrved for late and severe disease.

Follow up question why does this patient have normal potassium and blood pressure. Zona glomerulosa (and so aldo is intact)

Question on whether you can see pituitary or adrenal atrophy on imaging in situations like this. Answer is no.

Case Number 2. 23 yr old with HTN. 178/98, low potassium. Why is she hypokalemic and hypertensive? What factors regulate aldo synthesis and secretion? What stimulates aldo? What supresses aldo? How would you distuinguish the potential processes you hypothesized above?

What mechanism could explain the HTN and hypokalemia?

First answer offered: high MR would increase Na resorption and K secretion in the collecting duct.

What regulated aldo synthesis and secretion: Aldo stimulated by AngII in hypovolemia and hyperkalemia. Without those two factors then Aldo should be suppressed.

What would you do to make the dx?

Check renin if high think reninoma or RAS; if low check aldo
If Aldo is high: think primary hyperaldo; if low think pseudohyperaldo

Aldo is 33 and renin 0.3, ARR is 110. Patient has a positive family history uncles, father, brother. Patient received prednisone incidentally and blood pressure improved.

First team suspects glucocorticoid remedial hypertension as a germ line mutation. The prednisone suppresses ACTH and lowers the stimulation of the fusion promoter gene decreasing aldosterone. Wow. Smart kids.

These patients need life long steroids usually paired with aldosterone antagonist. The pathology is in the zona glomerulosa.

And the video by @AnandVaidya17

update @AnandVaidya17 tells me that most of this is actually in the zona fasciculata

Next case 59 year old woman presented with weakness and headache. High blood pressure and hypokalemia. Renin and aldo are both unmeasurably low.

Hypothesize what may be causing her high blood pressure and low potassium.

Since the hypertension was new at age 59, they are thinking acquired 11-BHSD2 from licorice (and that is what the answer is). Patient drinks > 1 liter of tea sweetened with licorice root. Central European and South East Asian cultures consume a lot of licorice.