Download File - Marian E. Thompson

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.
 https://education-portal.com/academy/lesson/male-
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 20-25 grams?
DIAGNOSES
 Diagnostics
 CBC (testosterone promotes erythropoiesis)
 Total T ( range 437-707 ng/dl)
 FSH ( range 2.0-9.2 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
https://online.epocrates.com/noFrame/
 Carnegie, C. (2004). Diagnosis of Hypogonadism: Clinical
Assessments and Laboratory Tests. Reviews in Urology, 6(6), 3-8.
Retrieved from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472884/
REFERENCES
 Carson, C. C. (2003, February 7). Prevalence, Diagnosis and Treatment of
Hypogonadism in primary care practice. Boston school of medicine . Retrieved from
http://www.bumc.bu.edu/sexualmedicine/publications/prevalence-diagnosis-andtreatment-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), 762-769. http://dx.doi.org/
10.1111/j.1742-1241.2006.00992.x
REFERENCES
 Normal Testosterone Production and Pathophysiology of Primary
and Secondary Hypogonadism. (2013). Retrieved from
http://www.hypogonadismpro.com/primary-secondaryhypogonadism
 Osteoporosis in Men. (2012). Retrieved from
http://www.niams.nih.gov/health_info/bone/osteoporosis/men.asp
#a
IMAGES
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