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.

Ep-PAINE-nym



Bowman’s Capsule

 

Other Known AliasesCapsula glomeruli, glomerular capsule

DefinitionDouble walled, cup-like capsule surrounding the glomerulus

Image result for bowman's capsule

Clinical SignificanceIt is made up of two poles: a vascular pole (afferent and efferent arterioles) and a urinary pole (proximal convoluted tubule). Within the capsule, there is a parietal layer and visceral layer with a space in between.  This is where ultrafiltration takes place and urine is filtered from the blood.

History – Named after Sir William Bowman (1816-1892), who was an English ophthalmologist, histologist, and anatomist, and first identified this structure in 1841.  He published his findings at the age of 25 and was awarded The Royal Medal by the Royal Society of  London.

He was well known for his extensive use microscopes in visualizing structures of the human body and publishing two works with his mentor, Robert Bentley Todd, entitled “Physiological Anatomy and Physiology of Man” and “Cyclopaedia of Anatomy and Physiology”.

William Bowman.jpg

The Cyclopaedia Of Anatomy And Physiology


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. Bowman W.  On the Structure and Use of the Malpighian Bodies of the Kidney.  Phil Trans R Soc Lond.  1842;132:57-80
  6. Eknoyan G. Sir William Bowman: his contributions to physiology and nephrology. Kidney international. 1996; 50(6):2120-8. [pubmed]
  7. Galst JM. Sir William Bowman (1816-1892). Archives of ophthalmology (Chicago, Ill. : 1960). 2007; 125(4):459. [pubmed]

#34 – Electrolytes Q & A



***LISTEN TO THE PODCAST HERE***

 



These questions stemmed from an email I got from a former student about electrolyte questions they are getting in the clinical year.  These are a quick and basic overview of common electrolyte questions and issues students may see on clinical rotations


 

#1 – Clinical Repletion of Electrolytes and Monitoring

Not every electrolyte on the chemistry panel needs to be repleted when low…but you need to know which ones can cause problems. The problem children are:

  • Potassium
  • Calcium
  • Magnesium
  • Phosphorus

Why?  These four can all cause cardiac dysrhythmias when low and why all these should be on telemetry, or at least some basic monitoring, when repleting.

 

Your first step should ALWAYS ALWAYS ALWAYS be to make sure you know why it is low.  Yes, we can keep repleting electrolytes to normal levels, but you will be doing this in perpetuity unless you fix the problem causing it in the first place.  Let’s review the major points for each:

  • Hypokalemia
    • Major Cause – Diuretics, GI losses
    • EKG Changes – Flat T-waves, U-wave. ST-depression
    • Repletion Pearls
      • Asymptomatic
        • Oral replacement – KCl 10-40 mEq 2-4 times per day
      • Symptomatic
        • IV replacement – KCl 20-40 mEq/L at 10 mEq/hr
  • Hypocalcemia
    • Major Cause – Diuretics, Hypoparathyroidism, CKD
    • EKG Changes – Prolonged QT
    • Repletion Pearls
      • Asymptomatic
        • Oral elemental calcium 1500-2000 mg/day
      • Symptomatic
        • IV calcium gluconate 1-2g in 50mL D5W
        • IV calcium chloride 1000mg in 10mL D5W
  • Hypomagnesemia
    • Major Causes – GI losses, Diuretics
    • EKG Changes – QRS widening, peak T-wave, prolongation PR
    • Repletion Pearls
      • Asymptomatic
        • Oral magnesium salts 240-1000mg 2-4 times/day
      • Symptomatic
        • IV MgSO4 1-8g
  • Hypophosphatemia
    • Major Causes – Hyperparathyroidism, Refeeding Syndrome, Hungry Bone Syndrome
    • Major Sequelae – ATP depletion, hemolysis
    • Repletion Pearls
      • Asymptomatic
        • Oral sodium/potassium phosphate 30-80 mmol/day
      • Symptomatic
        • IV sodium/potassium phosphate 10-40 mmol/day


 

#2 – Calcium/Magnesium/Phosphorus Relationship

You must have a good understanding of this relationship when managing electrolyte deficiencies because you may not be able to make any headway on one if you don’t fix the other.

  • Magnesium and Calcium/Potassium
    • Hypomagnesemia causes functional hypoparathyroidism by inducing PTH resistance and decreasing calcium secretion and increasing calcium excretion.
    • Hypomagnesemia also causes cellular expression of ROMK channels in the nephron which increase potassium excretion
  • Calcium and Phosphorus
    • There is an inverse relationship between calcium and phosphorus because of PTH. As PTH increases (seen as a response to hypocalcemia), there is an increase in phosphorus excretion


 

#4 – Hyponatremia Pearls

Hyponatremia is actually really easy to work up.  If you find you patient has a low sodium, check a serum osmolarity, urine osmolarity, and urine sodium.



References

  1. Maday KR. Understanding electrolytes: important diagnostic clues to patient status. JAAPA. 2013; 26(1):26-31. [pubmed]
  2. Gennari FJ. Hypokalemia. NEJM. 1998; 339(7):451-8. [pubmed]
  3. Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ. 2008; 336(7656):1298-302. [pubmed]
  4. Agus ZS. Hypomagnesemia. JASN. 1999; 10(7):1616-22. [pubmed]
  5. Gaasbeek A, Meinders AE. Hypophosphatemia: an update on its etiology and treatment. AJM. 2005; 118(10):1094-101. [pubmed]
  6. Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. JASN. 2007; 18(10):2649-52. [pubmed]
  7. Blaine J, Chonchol M, Levi M. Renal control of calcium, phosphate, and magnesium homeostasis. CJASN. 2015; 10(7):1257-72. [pubmed]
  8. Adrogué HJ, Madias NE. Hyponatremia. NEJM. 2000; 342(21):1581-9. [pubmed]

Ep-PAINE-nym



Gerota’s Fascia

 

Other Known AliasesRenal fascia

DefinitionConnective tissue layers covering the kidneys and adrenal glands

Clinical Significance This connective tissue encapsulates these organs and must be excised to perform nephrectomies and adrenalectomies.  It has 4 attachments:

  • Anterior attachment – Connects the anterior layer of the renal fascia of the opposite kidney.
  • Posterior attachment – Connects the psoas fascia and the body of the vertebrae.
  • Superior attachment – The anterior and posterior layers fuse at the upper pole of the kidney and then split to enclose the adrenal gland. At the upper part of the adrenal gland they again fuse to form the suspensory ligament of the adrenal gland and fuse with the diaphragmatic fascia.
  • Inferior attachment – The posterior layer descends downwards and fuses with the iliac fascia. The anterior layer blends with the connective tissue of the iliac fossa.

History – Named after Dimitrie D. Gerota (1867-1939), who was a Romanian physician and professor of surgical anatomy and experimental surgery at the University of Bucharest.  He was also the first radiologist in Romania and developed a method for injecting lymphatic vessels known as “The Gerota Method”

13-foto1

 


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

Ep-PAINE-nym



Systemic Lupus Erythematosus

 

Other Known AliasesLupus

DefinitionAutoimmune disease that can effect the entire system…most commonly skin, joints, and constitutional.

Clinical Significance For this eponym, there is no clinical significance.  Just a cool fact I wanted to bring up….

History – You may have been wondering (or maybe not) where the “lupus” part of this disease comes from.  Having studied Latin in high school all four years, this perplexed me in PA school because “lupus” is Greek for wolf.  So why did early physicians decide on throwing “wolf” into the disease title?

Well (since you asked), it has been attributed to the 13th century Rogerius (who practiced with his friend, Stevius) who thought the characteristic erosive, dermatologic skin findings were similar to the effects of a wolf bite.

 

For those fellow PotterHeads out there, now you know the foreshadowing of (my favorite character) Remus LUPIN in the series.

Image result for lupin potter


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. Blotzer JW. Systemic lupus erythematosus I: historical aspects. Maryland State Medical Journal. 1983; 32(6):439-41. [pubmed]
  6. Bertino LS, Lu LC. The bite of a wolf: systemic lupus erythematosus. Rehabilitation nursing : the official journal of the Association of Rehabilitation Nurses. 1993; 18(3):173-8. [pubmed]