PAINE #PANCE Pearl – Endocrine



Question

58yo male, with DMI controlled with insulin, has blood glucose measurements in the morning of 205-272 mg/dL for the past week.  He reports that his evening blood glucose measurements before bed range from 103-127 mg/dL.  What are two potential causes of these findings?



Answer

There are two potential causes of early morning hyperglycemia in a diabetic patient on insulin.

  1. Dawn Phenomenon
    1. Due to the early morning rise of cortisol, patients can experience an early morning hyperglycemia as a result
  2. Somogyi Phenomenon
    1. (as covered by last week’s Ep-PAINE-nym) This was theorized to occur as undetectable hypoglycemia while the patient was asleep and the resultant hyperglycemia from instrinsic protective mechanisms.

Ep-PAINE-nym



Somogyi Phenomenon

 

Other Known Aliasesposthypoglycemic hyperglycemia

 

Definitionrebounding hyperglycemia in the setting of a undetected hypoglycemic event

 

Image

 

Clinical Significance It had been hypothesized that patients who had a hypoglycemic event during sleep would have rebound hyperglycemia due to the protective mechanism of the body to counteract this.  This would result in an undetectable change that would cause hyperglycemia in the morning.  This hypothesis has been proven wrong by numerous studies, but it is still a favorite among endocrinologists to pimp their students on.

 

History – Named after Michael Somogyi (1883-1971), who was a Hungarian American biochemist and received his doctorate degree from the University of Budapest in 1914.  He took a position as professor of biochemistry in 1922 at the Washington University’s Medical School in St. Louis, where later that year the first child with diabetes was treated with an insulin prepared by Somogyi himself.  His career work revolved around diabetes and theorized that insulin itself could causes unstable diabetes.  He published this paper describing the phenomenon that bears his name in 1938 in the Weekly Bulletin of the St. Louis Medical Society entitled “Insulin as a cause of extreme hyperglycemia and instability”.  He also went on to develop the test for serum amylase to help diagnose acute pancreatitis.  Dr. Somogyi died from a stroke on July 21st, 1971.

 

Michael Somogyi early portrait cropped 01.03.002.tif


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. M. Somogyi, “Insulin as a cause of extreme hyperglycemia and instability,” Weekly Bulletin of the St Louis Medical Society, 1938, 
  7. Tordjman KM, Havlin CE, Levandoski LA, White NH, Santiago JV, Cryer PE. Failure of nocturnal hypoglycemia to cause fasting hyperglycemia in patients with insulin-dependent diabetes mellitus. The New England journal of medicine. 1987; 317(25):1552-9. [pubmed]
  8. Hirsch IB, Smith LJ, Havlin CE, Shah SD, Clutter WE, Cryer PE. Failure of nocturnal hypoglycemia to cause daytime hyperglycemia in patients with IDDM. Diabetes care. 1990; 13(2):133-42. [pubmed]

PAINE #PANCE PEARL – Endocrine



Question

 

58yo male, with DMI controlled with insulin, has blood glucose measurements in the morning of 205-272 mg/dL for the past week.  He reports that his evening blood glucose measurements before bed range from 103-127 mg/dL.  What are two potential causes of these findings?

Ep-PAINE-nym



Grave’s Disease

 

Other Known AliasesAutoimmune hyperthyroidism

Definition – Hyperthyrodism caused by antibodies that stimulate T3/T4 secretion.  The most common antibodies are thyroid-secreting hormone (TSH) and thyrotropin receptor antibody (TRAb). 

Clinical SignificanceClassic clinical manifestations of hyperthyroidism include thyromegaly, ophthalmaopathy, resting tremor, palpitations, weight loss, heat intolerance.  For more in depth analysis of hyperthyroidism, see my 2017 talk at ASPA here.

History – Named after Robert James Graves (1796-1853), who was an prolific Irish physician, surgeon, and educator.  He was named Regius professor of the Institute of Medicine in Trinity College, founded the Dublin Journal of Medical and Chemical Sciences, and was a an early adopter of clinical bedside rounding and teaching with medical students. Dr. Graves wrote a routine clinical lecture series in the London Medical and Surgical Journal and first described a young female patient with ophthalmopathy and goiter in 1835.  Dr. Armand Trousseau then published the collection of these articles in 1864 entitled “Clinical Lectures on the Practice of Medicine” and gave him this eponym.  Another contribution of Dr. Graves was the creation of the second hand on watches to time pulses and the practice of providing food and water with patients with a fever, instead of the common practice of withholding nourishment.

Image result for robert james graves

 


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Graves RJ.  Newly Observed Affection of the Thyroid Gland. London Medical and Surgical Journal.  1835. Vol.7. Part 2. 512
  6. Graves RJ, Trousseau A.  Clinical Lectures on the Practice of Medicine.  1864.  Dublin.
  7. Smith TJ, Hegedüs L. Graves’ Disease. The New England journal of medicine. 2016; 375(16):1552-1565. [pubmed]

PAINE #PANCE Pearl – Endocrine



  1. What the two main sub-types of diabetes insipidus and how do you differentiate between the two?
  2. What are the two lesser known sub-types?


Answer

 

  1. The two main types of diabetes insipidus (DI) are central and nephrogenic.  The hallmark of DI is deficiency of vasopressin and you can think of central DI as an ABSOLUTE deficiency and nephrogenic as a RELATIVE deficiency.  Meaning, in central DI there is a problem with secretion of vasopressin from the posterior pituitary.  The kidneys are fine, there just isn’t any vasopressin to make the kidneys hold onto water.  In nephrogenic DI, there is plenty of circulating vasopressin (due to feedback to a normally functioning pituitary), but the kidneys are not responding to this stimulus.  Central DI is most commonly caused by head trauma, post-neurosurgery, or autoimmune issues.  Nephrogenic DI is most commonly caused by genetic defects in children, or renal problems in adults.  A simple test to differentiate between central and nephrogenic DI is a desmopressin challenge.  You can give desmopressin IN or SQ and measure urine osmolarity and volume every 30 minutes for 2 hours.  In central DI, you should see a decrease in urine volume and increase in urine osmolarity.  In nephogenic DI, nothing will change.
  2. There are 2 other sub-types of DI that you need to be aware of as well.  Gestational DI, which is considered a form of nephrogenic DI, can occur in the second/third trimester of pregnancy.  This manifests as a transient ADH resistance due to increased vasopressinase from the placenta.  The other subtype of DI is dipsogenic DI, which is a result of either a defect in the thirst center of the hypothalamus, or due to mental illness, which causes near constant polydipsia and polyuria.  This basically overpowers the circulating ADH

 


References

  1. Robertson GL. Diabetes insipidus: Differential diagnosis and management. Best practice & research. Clinical endocrinology & metabolism. 2016; 30(2):205-18. [pubmed]
  2. Aleksandrov N, Audibert F, Bedard MJ, Mahone M, Goffinet F, Kadoch IJ. Gestational diabetes insipidus: a review of an underdiagnosed condition. Journal of Obstetrics and Gynaecology Canada. 2010; 32(3):225-31. [pubmed]
  3. Perkins RM, Yuan CM, Welch PG. Dipsogenic diabetes insipidus: report of a novel treatment strategy and literature review. Clinical and experimental nephrology. 2006; 10(1):63-7. [pubmed]

Ep-PAINE-nym



Addison’s Disease

 

Other Known Aliasesprimary adrenal insufficiency

Definitionautoimmune destruction of the adrenal cortex that produces cortisol

Clinical SignificanceIn times of physiologic stress, the adrenal glands are unable to produce and secrete cortisol, which is a key hormone in the “fight-or-flight” response.  If the stress is significant (trauma, surgery, hemorrhage, etc.), then the patient can not mount a compensatory response to this stress and can have life-threatening consequences

History – Named after Thomas Addison (1795-1860), an English physician, who first wrote about the condition in a short note in the London Medical Gazette called “Anaemia – Disease of the Suprarenal Capsules”.  This was then followed up by the more well known article “On the Constitutional and Local Effects of Disease of the Suprarenal Capsule” in 1855, which is largely considered the beginning of the study of the adrenal glands.  The disease eponym was original given to Dr. Addison by the French physician, Armand Trousseau, after fierce debate among experts as to whether the disease actually existed.

Image result for thomas addison

Image result for on the constitution and local effects of disease of the suprarenal capsules

https://library.sydney.edu.au/collections/rare-books/online-exhibitions/medicine/AddisonConstitutional1855plate8.jpg


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Addison T.  On the Constitutional and Local Effects of Disease of the Suprarenal Capsules.  1855.  London: Samuel Highley.