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



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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

#18 – Benign Prostatic Hyperplasia



***LISTEN TO THE PODCAST HERE***



Epidemiology

The prostate begins to enlarge in the 4th decade of life with a significant jump in the 6th decade of life.  Mean prostate weight in normal men < 30yo is around 20g and steadily increases after this.  Volume of the prostate also steadily increases after the 4th decade with symptoms typically starting to manifest once it reaches 30cc3.

picture1

Up-To-Date. 2016


Risk Factors

  • Race
    • African Americans are at higher risk of requiring surgery
    • Asians have the lowest risk of requiring surgery
  • Prostatitis
    • Associated with increased risk of BPH

Pathogenesis of BPH

The main areas of the prostate that contribute to BPH are the periurethral (transitional zone) of the prostate and the hyperplastic nodules that develop are primarily comprised of stromal cells. The specific pathogenesis of BPH is still not completely understood and only 2 variables that have been identified as essential for BPH development: age and functioning Leydig Cells of the testes.  Androgens, estrogens, inflammation, genetics, and stromal growth factors have all been studied and have variable results.

picture1

De Marzo. 2007.

 


Clinical Manifestations of BPH

The signs of symptoms of BPH can be broken down into 3 main categories:

  • Storage Symptoms
    • Urgency
    • Daytime frequency
    • Nocturia
    • Urgency incontinence
  • Voiding Symptoms
    • Slow, urinary stream
    • Splitting or spraying of the urinary stream
    • Intermittent urinary stream
    • Urinary hesitancy
    • Straining to void
    • Terminal dribbling
  • Post-micturition Symptoms
    • Incomplete bladder voiding
    • Post micturition dribble

Differential Diagnosis of BPH Symptoms

  • Urethral stricture or bladder neck contracture
    • Previous history of catheterization or instrumentation
    • Urethral trauma
    • Urethritis
  • Neurogenic bladder
    • Other signs and symptoms of neurologic disease
  • Bladder calculi
    • History of nephrolithiasis
  • Carcinoma of the bladder or prostate
    • Hematuria
    • Previous history of cancer
  • Urinary tract infection and prostatitis
    • Dysuria
    • Fever
  • Medications
    • Antcholinergics (decreases bladder function)
    • Sympathomimetics (increases outflow resistance)

International Prostate Symptom Score

The original AUA score was developed in 1992 and is used to assess the severity of symptoms of BPH, BUT NOT FOR DIFFERENTIAL DIAGNOSIS.  This is a seven-part questionnaire that evaluates symptoms on a 0-5 scale and then calculates the symptoms as mild, moderate, or severe.  An eight question was added to evaluate quality of life.

picture1

International Prostate Symptom Score


Work-Up

  • Physical Exam
    • Digital Rectal Exam (DRE) should be performed to assess size, contour, regularity, and nodularity
    •  

  • Laboratory Testing
    • Urinalysis
      • Initial test to evaluate for microscopic hematuria and infection
    • Basic Metabolic Profile
      • BUN/Creatinine
        • Evaluate baseline renal function
      • Serum Prostate Specific Antigen (PSA)
        • PSA and prostate volume have a log-linear relationship
        • DOES NOT CORRELATE WITH CANCER
        • picture1
    • Uroflowmetry Study
      • Optional testing per AUA
      • Can evaluate maximal urinary flow rate
      • Patient voids with a full bladder (> 150cc)
      • < 15ml/s = outflow obstruction
      • picture1
      • picture1
    • Post-void Residual Urine Volume
      • Bladder scan is least invasive and most common
      • Normal men have < 12mL of residual urine post-void
      • picture1

Management

BPH can be managed by PCP if the patient has mild symptoms (low IPSS ≤ 7) and no complications.

Indications for urology referral are:

  • Symptoms with autonomic or peripheral neuropathy
  • Symptoms following invasive treatment of the urethra or prostate
  • Age < 45yo
  • Abnormality of prostate on DRE
  • Presence of hematuria in the absence of infection
  • Incontinence
  • Severe symptoms (IPSS ≥ 20)

Treatment

  • Medical
    • Alpha-1-adrenergic antagonists
      • Mechanism of Action
        • Relax smooth muscle of bladder neck, prostate capsule, and prostatic urethra
      • Side effects
        • Hypotension
      • Drugs
        • Terazosin (need to titrate)
        • Doxazosin (need to titrate)
        • Tamsulosin
    • 5-alpha-reductase inhibitors
      • Used if patients can’t tolerate hypotension of alpha-1-adrenergic antagonists
      • Need 6-12 months of treatment to see effects
      • Mechanism of Action
        • Reduce prostate size by preventing the conversion of testosterone to the more potent dihydrotestosterone
      • Drugs (no difference due to EPICS trial)
        • Finasteride
        • Dutasteride
    • Combination Alpha-1/5-Alpha Therapy
      • Indications
        • Severe symptoms (IPSS ≥ 20)
        • Large prostate (> 40cc)
        • Inadequate response to maximal monotherapy
      • Drugs
        • Doxazosin/finasteride
        • Tamsulosin/dutasteride
  • Surgical
    • Indications
      • Moderate/severe symptoms (IPSS ≥ 8) with high quality of life score (≥ 4)
      • Urinary retention refractory to medical therapy
      • Renal insufficiency secondary to BPH
      • Median lobe hypertrophy
    • Transurethral Procedures

Complications of Surgery

  • Bleeding
    • Higher in traditional TURP
  • Postprostatectomy Syndrome
    • Hyponatremia as a result of the systemic absorption of the hypotonic irrigation solution
  • Sexual Dysfunction
    • Ejaculatory Dysfunction
    • Erectile Dysfunction
  • Urethral Stricture
  • Urinary Incontinence

Cottage Physician

cottage-physician


References

  1. Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with age. The Journal of Urology. 1984;132(3):474-9. [pubmed]
  2. Bosch JL, Hop WC, Kirkels WJ, Schröder FH. Natural history of benign prostatic hyperplasia: appropriate case definition and estimation of its prevalence in the community. Urology. 1995;46(3 Suppl A):34-40. [pubmed]
  3. Sidney S, Quesenberry CP, Sadler MC, Guess HA, Lydick EG, Cattolica EV. Incidence of surgically treated benign prostatic hypertrophy and of prostate cancer among blacks and whites in a prepaid health care plan. American Journal of Epidemiology. 1991;134(8):825-9. [pubmed]
  4. Kang D, Andriole GL, Van De Vooren RC. Risk behaviours and benign prostatic hyperplasia. BJU International. 2004;93(9):1241-5. [pubmed]
  5. St Sauver JL, Jacobson DJ, McGree ME, Girman CJ, Lieber MM, Jacobsen SJ. Longitudinal association between prostatitis and development of benign prostatic hyperplasia. Urology. 2008;71(3):475-9; discussion 479. [pubmed]
  6. Rohr HP, Bartsch G. Human benign prostatic hyperplasia: a stromal disease? New perspectives by quantitative morphology. Urology. 1980;16(6):625-33. [pubmed]
  7. De Marzo AM, Platz EA, Sutcliffe S. Inflammation in prostate carcinogenesis. Nature Reviews. Cancer. 2007;7(4):256-69. [pubmed]
  8. Jones C, Hill J, Chapple C, . Management of lower urinary tract symptoms in men: summary of NICE guidance. BMJ (Clinical research ed.). 2010;340:c2354. [pubmed]
  9. Barry MJ, Fowler FJ, O’Leary MP. The American Urological Association symptom index for benign prostatic hyperplasia. The Measurement Committee of the American Urological Association. The Journal of Urology. 1992;148(5):1549-57; discussion 1564. [pubmed]
  10. McVary KT, Roehrborn CG, Avins AL. Update on AUA guideline on the management of benign prostatic hyperplasia. The Journal of Urology. 2011;185(5):1793-803. [pubmed]
  11. Roehrborn CG. The utility of serum prostatic-specific antigen in the management of men with benign prostatic hyperplasia. International Journal of Impotence Research. 2008;20 Suppl 3:S19-26. [pubmed]
  12. Oelke M, Bachmann A, Descazeaud A. EAU guidelines on the treatment and follow-up of non-neurogenic male lower urinary tract symptoms including benign prostatic obstruction. European Urology. 2013;64(1):118-40. [pubmed]
  13. Chapple CR. Pharmacological therapy of benign prostatic hyperplasia/lower urinary tract symptoms: an overview for the practicing clinician. BJU International. 2004;94(5):738-44. [pubmed]
  14. McVary KT, Roehrborn CG, Avins AL. Update on AUA guideline on the management of benign prostatic hyperplasia. The Journal of Urology. 2011;185(5):1793-803. [pubmed]
  15. Nickel JC, Gilling P, Tammela TL, Morrill B, Wilson TH, Rittmaster RS. Comparison of dutasteride and finasteride for treating benign prostatic hyperplasia: the Enlarged Prostate International Comparator Study (EPICS). BJU International. 2011;108(3):388-94. [pubmed]
  16. McConnell JD, Roehrborn CG, Bautista OM. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. NEJM. 2003;349(25):2387-98. [pubmed]
  17. Roehrborn CG, Siami P, Barkin J. The effects of combination therapy with dutasteride and tamsulosin on clinical outcomes in men with symptomatic benign prostatic hyperplasia: 4-year results from the CombAT study. European Urology. 2010;57(1):123-31. [pubmed]
  18. The Urology Book. urologybook.com. Accessed September 12, 2016.
  19. Gómez Sancha F, Bachmann A, Choi BB, Tabatabaei S, Muir GH. Photoselective vaporization of the prostate (GreenLight PV): lessons learnt after 3500 procedures. Prostate Cancer and Prostatic Diseases. 2007;10(4):316-22. [pubmed]

 

Answer to Genitourinary Question

22yo male presents to emergency department with a 2-hour history of increasingly intense testicular pain.  He reports being sexually active with multiple partners and intermittent condom use.  He is a very active person and completed a triathlon the day before presentation.  He denies dysuria, urethral discharge, or flank pain, but did have an episode of vomiting prior to arrival.  He is in visible distress and can not seem to get comfortable.  Evaluation of the scrotum reveals a tender, swollen left testicle.

  1. What are some bedside maneuvers you can perform to help with the differential?
    1. Epididymitis
      1. Point tenderness over the superior aspect of the testicle
      2. (+) Prehn Sign
        1. Manual elevation of the testicle improves pain
    2. Testicular Torsion
      1. High-riding and/or horizontal lie of testicle (“Bell Clapper Deformity)
      2. PMC2791735_wjem-10-281f2
      3. Absent cremesteric reflex
        1. Normal = pinching/stroking the thigh causes ipsilateral elevation of testicle
      4. (-) Prehn Sign
    3. Torsion of Appendix Testes
      1. More common in children
      2. 5940956_m
      3. (+) Blue Dot Sign
      4. Fig-1-'Blue-dot'-sign-in-patients-with-a-left-torted-hydatid-or-Mor-gagni

 

  1. What should be the initial management of this patient?
    1. If suspected epididymitis:
      1. Urinalysis, urine culture, and gonorrhea/chlamydia testing
      2. Antibiotics are directed towards:
        1. C. trachomatis or N. gonorrhoeae
          1. Ceftriaxone 250mg IM and doxycycline 100mg PO BID x 10 days
        2. Gram-negative enteric pathogens
          1. Levofloxacin 500mg PO daily x 10 days
    2. If suspected testicular torsion:
      1. Manual detorsion may be attempted
        1. 2/3 torse medially and detorsion is performed by rotating testicle outwards laterally
      2. Ultrasound may be performed if immediately available (this should not delay surgical consult or evaluation)
        1.  

        2.  

      3.  Surgical evaluation and management is the preferred initial management of patients with suspected testicular torsion
    3. If suspected torsion of appendix testes:
      1. Ultrasound is performed to rule-out other pathologies.
      2. Management is conservative with rest, ice, and NSAIDs.
      3. Surgical removal may be required if pain does not improve with conservative management.

 

Testicular Torision


References

  1. Tracy CR, Steers WD, Costabile R. Diagnosis and management of epididymitis. The Urologic Clinics of North America. 35(1):101-8; vii. 2008. [pubmed]
  2. Galejs LE. Diagnosis and treatment of the acute scrotum. American Family Physician. 59(4):817-24. 1999. [pubmed]
  3. Workowski KA, Bolan GA, . Sexually transmitted diseases treatment guidelines, 2015. MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports / Centers for Disease Control. 64(RR-03):1-137. 2015. [pubmed]
  4. Sessions AE, Rabinowitz R, Hulbert WC, Goldstein MM, Mevorach RA. Testicular torsion: direction, degree, duration and disinformation. The Journal of Urology. 169(2):663-5. 2003. [pubmed]
  5. Palestro CJ, Manor EP, Kim CK, Goldsmith SJ. Torsion of a testicular appendage in an adult male. Clinical Nuclear Medicine. 15(7):515-6. 1990. [pubmed]

Genitourinary Question

22yo male presents to emergency department with a 2-hour history of increasingly intense testicular pain.  He reports being sexually active with multiple partners and intermittent condom use.  He is a very active person and completed a triathlon the day before presentation.  He denies dysuria, urethral discharge, or flank pain, but did have an episode of vomiting prior to arrival.  He is in visible distress and can not seem to get comfortable.  Evaluation of the scrotum reveals a tender, swollen left testicle.

 

  1. What are some bedside maneuvers you can perform to help with the differential?
  2. What should be the initial management of this patient?

 

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