HYPOGONADISM IN MALES Marian Thompson February 15

CLIENT AND ENCOUNTER  Patient five presented to the office in the beginning of February for a routine follow-up including his DRE and review of his lab work for his secondary hypogonadism r/t idiopathic (?) pituitary dysfunction.

PRESENTATION/HPI Though P.5 was without complaint at the time of this visit, he initially presented to the office with symptoms similar to depression. Decreased sex drive Low energy Infrequent erections without ejaculation. Low total T (250), Low LH ( 5). Low FSH (1.4).

REVIEW OF SYSTEMS On day of follow up, Pt. Denies visual changes. Skin changes. Heat or cold intolerance. Appearance of breast, or abnormal testes. Pt. denies inattention, or trouble sleeping. Though present on initial visit on f/u day pt denies, Sexual dysfunction, Low energy.

PMH  Patient 5’s PMH is virtually unremarkable. On initial visit the PMH was unremarkable as well. Pt. is without medical history other than the current Hypogonadism. Immunizations are UTD. Patients family is alive and well through to grandparents, there is no reported history of hypogonadism, though his grandfather does have osteoporosis. Pt. is single, denies alcohol and drug abuse, pt exercises daily. Pt is a Fire fighter.

CURRENT MEDICATIONS  Multivitamin 1 tab PO Q day.  Testosterone 200mg/ml IM every other week.  Vitamin D 4000 units PO Q day.

DIFFERENTIAL DX  Pituitary Macroadenoma  Depression  Opioid Abuse  Steroid abuse

DIFFERENTIAL DX  Pituitary Macroadenoma- though the patient did not have physical S/S of the disease he initially presented with low hormone levels (LH, and FSH) so this must be ruled out.  Depression the presenting s/s can easily be depression until laboratory tests are ruled out.  Opioid and steroid usage can affect hormone levels and cause hypogonadism. (This was denied by patient, but there is suspicion)

PHYSICAL EXAM  EOM WNL. Visual fields intact to confrontation. Noted small testes 20g, DRE WNL Rest of exam WNL.  The patient is a healthy 30 year old. Lab results on visit after initial visit is what led to the diagnosis of Secondary Hypogonadism r/t idiopathic pituitary dysfunction.

DEFINITIVE INFORMATION  Hypogonadism is frequently misdiagnosed due to lack of patient providing pertinent information, and most commonly due to age. Older adults and obese patients are frequently misdiagnosed. Also, the disease may be asymptomatic. The appropriate testing is out there, but frequently not utilized. In my opinion, yearly testosterone levels should become a part of the yearly exam, in order to provide a thorough clinical picture. Otherwise, we are treating symptoms, and not the cause.

ANALYSIS  It is approximated that 4-5 million males are affected with hypogonadism in the U.S. (Carson, 2003).  The prevalence increases as men get older, and is often misdiagnosed. Often times elderly men with decreased libido, and osteoporosis is attributed to age.  The most common cause of osteoporosis in males, is low testosterone.

PATHOPHYSIOLOGY  In normal functioning males, the hypothalamus produces GnRH that then stimulates the pituitary gland to release FSH and LH.  LH and FSH then stimulate the testes to produce sperm and testosterone. If too much testosterone is produced negative feedback then inhibits the production of GnRH in the hypothalamus ("Hypogopro," 2013). This lovely circle of life is called the hypothalamic pituitary gonadal axis.

PATHOPHYSIOLOGY  SHOW VIDEO.  reproductive-disorders-hypogonadism.html reproductive-disorders-hypogonadism.html

ETIOLOGY Primary Hypogonadism Secondary Hypogonadism

CAUSES OF PRIMARY  In primary hypogonadism the testicles are affected. It is associated with low testosterone and elevated gonadotropins elevated FSH and LH (Athena health [hypogonadism], 2015).  Klinefelter syndrome in the most common congenital cause. Male born with one or more X chromosomes.  Cryptorchidism (undescended testes)  Testicular trauma  HIV  Excessive alcohol consumption  Drugs (Alkylating agents (Cancer drugs))

CAUSES OF SECONDARY  Secondary hypogonadism the flaw lies within the hypothalamic pituitary axis. Decreasing the release of FSH and LH.  Pituitary tumors  Opiods, steroids  Infiltrative diseases such as Sarcoidosis  Head trauma  Genetic mutations that initiate maldevelopment of GnRH neurons.  Obesity associated with decreased testosterone (often asymptomatic)  Chronic diseases  Idiopathic

DIAGNOSIS  Thorough history taking. (if it’s uncomfortable, TALK ABOUT IT) –decreased sex drive? -Depression? -Inability to father children? –hot flashes? – decrease or loss of ‘morning wood’ ? – Shrinking boys? –Have you noticed breast development? - lack of concentration? –Irritable (ask partnered person this question)? –Hair loss? –loss of strength? <~~~ important question for body builders.

DIAGNOSIS  Physical Exam -Don’t start down there, look up first! – Visual testing EOM, visual field test to confrontation. Abnormal? Consult ophthalmology A.S.A.P. (pituitary tumor can affect vision) - Body habitus (do they have a large belly?) – Normal body proportions (this one is subtle, but important) – Absence of facial Hair? –Does your male patient have breast (hard to evaluate in obese patients)? –Now touch the boys are they small, and firm (klinefelter syndrome)? Is micropenis present? –Are the boys equal grams?

DIAGNOSES  Diagnostics  CBC (testosterone promotes erythropoiesis)  Total T ( range ng/dl)  FSH ( range milliunits/L)  LH (range 7-24 units/L)  Semen analysis  MRI (if applicable)

MANAGEMENT AND EDUCATION  HRT (Gels, patches, and Shots OH MY!)  IM testosterone injections. Check T level after one week of therapy initiation. If appropriate F/U every 3 months for one year if maintained F/U every 6 months.  CBC, PSA, Total T every visit.  DRE (recommended every visit) usually done once a year.  Prostate CA is a contraindication of T therapy.

MANAGEMENT AND EDUCATION  Patient education would include medication administration. Especially with Gels!  Also, The importance of having lab levels drawn first thing in the morning.  The importance of Follow- up and DRE, and self testicular exams.

REFERENCES:  Athena health. (2015). Hypogonadism. In Epocrates (Version 15.1) [Mobile application software]. Retrieved from  Carnegie, C. (2004). Diagnosis of Hypogonadism: Clinical Assessments and Laboratory Tests. Reviews in Urology, 6(6), 3-8. Retrieved from

REFERENCES  Carson, C. C. (2003, February 7). Prevalence, Diagnosis and Treatment of Hypogonadism in primary care practice. Boston school of medicine. Retrieved from treatment-of-hypogonadism-in-primary-care-practice/  Mulligan, T., Frick, M., Zuraw, Q., Stemhagen, A., & Mcwharter, C. (2006, July 1). Prevalence of hypogonadism in males aged at least 45 years: the HIM study. International Journal of Clinical Practice, 60(7), /j x

REFERENCES  Normal Testosterone Production and Pathophysiology of Primary and Secondary Hypogonadism. (2013). Retrieved from hypogonadism  Osteoporosis in Men. (2012). Retrieved from #a

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