Endo-Reproductive Men Flashcards

1
Q

What is primary hypogonadism and what usually causes it?

A

Primary hypogonadism, or testicular failure, represents a decrease in testosterone or sperm production. Primary hypogonadism is uncommon and may have congenital or acquired causes.

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2
Q

Causes of primary testicular failure?

A
  1. Klinefelter (most common congenital)
  2. Exposure to chemotherapy or radiation
  3. Local injury as a result of torsion, orchitis, or trauma may result in ischemia and necrosis of testicular tissues
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3
Q

Describe the impact of Klinefelter syndrome.

A
  • Most common cause of congenital primary hypogonadism and infertility (hypergonadotropic hypergonadism)
  • 47,XXY karyotype
  • Symptoms: sexual dysfunction, generalized fatigue, tall stature, fail to achieve puberty
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4
Q

Kallman syndrome

A
  • congenital cause of secondary hypogonadism due to low GnRH production
  • Iatrogenic due to steroid abuse
  • other causes: untreated sleep apnea, hyperprolactinemia, chronic opioid use, glucocorticoid use, infiltrative disease (lymphoma or hemochromatosis)
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5
Q

When working up hypogonadism, when should testosterone be checked? When should you consider checking it?

A

Do not test it at first… look into other causes.

Measurement of testosterone levels is not recommended if a patient is having regular morning erections, does not have true gynecomastia on examination, and has a normal testicular examination, as it is highly unlikely that he has testosterone deficiency.

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6
Q

If testosterone deficiency is suspected, how is it diagnosed?

A

two early morning serum total testosterone levels below the reference range.

Note, it can be falsely lowered!:

Because illness and strenuous activity can falsely lower testosterone levels, measurement should occur in healthy men who have avoided strenuous activity for several days. Measurements of the testosterone level occurring later in the morning or in the afternoon are not useful for interpretation.

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7
Q

If two morning testosterones are low, then what?

A
  • Refer to endocrinologist

- Check LH, FSH, prolactin, and TSH

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8
Q

How does obesity impact testosterone level?

A

In morbid obesity, total testosterone may be low but free testosterone may be normal. Free testosterone assays can be unreliable, and routine measurement of free testosterone is not recommended. Free testosterone by equilibrium dialysis is the gold-standard assay.

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9
Q

What are the hormone levels for primary and secondary hypogonadism?

A

Primary testosterone deficiency (hypergonadotropic hypogonadism) is diagnosed when FSH and LH levels are frankly elevated in the presence of a simultaneously low testosterone level. Low or inappropriately normal FSH and LH levels in the presence of simultaneous low testosterone levels are diagnostic of secondary hypogonadism (hypogonadotropic hypogonadism).

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10
Q

What’s the workup if LH and FSH are found to be elevated?

A
  • karyotype if no history of gonadotoxic therapy or testicular insult is elicited
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11
Q

What’s the workup if LH and FSH are found to be low?

A
  • If a hypogonadotropic state is revealed, transferrin saturation and ferritin levels should be evaluated to exclude hemochromatosis.
  • MRI of the pituitary should be performed to evaluate for hypothalamic or pituitary masses as the cause of the hypogonadotropic state if no confounding medications or reversible secondary causes are discovered.
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12
Q

What are the adverse effects of testosterone therapy?

A

Testosterone therapy has been associated with increased hemoglobin and hematocrit levels, worsened obstructive sleep apnea, and a decrease in HDL cholesterol levels. LDL cholesterol levels do not appear to be affected. There are also adverse CV effects and can increase risk of thrombosis.

They require daily use and may incur significant cost to the patient, but the steady level of testosterone achieved within 30 minutes of application is an appealing feature. Inadvertent absorption by patient contacts may occur; users should be informed that virilization of contacts is not uncommon and premature puberty can occur in exposed children. The patient should also be counseled that decline in endogenous testosterone production and spermatogenesis may occur. If fertility is desired, testosterone therapy should be avoided, and consultation with a reproductive endocrinologist is recommended.

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13
Q

IF someone starts testosterone therapy, when should follow-up testing occur?

A

Patients requiring testosterone replacement therapy should have testosterone levels monitored at 3 and 6 months after initiation and annually thereafter; the goal total testosterone level should be in the mid-normal range.

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14
Q

What are some bad things that happen with anabolic steroid abuse?

A

Testicular testosterone production is suppressed in the presence of exogenous testosterone administration.

Excessive muscle bulk, acne, gynecomastia, and decreased testicular volume may be found on physical examination in patients using anabolic steroids. Irreversible hypogonadism may result and often presents as male infertility with oligospermia or azoospermia on sperm analysis. Permanent inability to produce endogenous testosterone may occur. Extratesticular effects may also be noted, including low HDL cholesterol level, hepatotoxicity, erythrocytosis, and increased risk of obstructive sleep apnea. Mood disorders are common in anabolic steroid users.

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15
Q

What are the lab findings of anabolic steroid use?

A

-low or normal gonadotropin levels and a low testosterone level with clinical evidence of hyperandrogenism are consistent with use of a non–testosterone-containing product, such as one containing androstenedione, or cessation of long-standing (typically greater than 1 year) anabolic steroid use, with failure to recover endogenous testosterone function.

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16
Q

what is the best way to obtain a semen analysis sample for male infertility?

A

Semen analysis obtained after 48 to 72 hours of abstinence from sexual activity is the best test to assess male fertility; if abnormal, the test should be repeated for confirmation.

17
Q

What is the vast number of causes of gynecomastia?

A

There are many causes of gynecomastia, ranging from drug-induced (marijuana, alcohol, 5α-reductase inhibitors, H2-receptor antagonists, spironolactone, digoxin, ketoconazole, calcium channel blockers, ACE inhibitors, antiretroviral agents, tricyclic antidepressants, selective serotonin reuptake inhibitors) and hypogonadism (primary, secondary) to chronic illness (hepatic cirrhosis, chronic kidney disease) and endocrine disorders (hyperprolactinemia, acromegaly, hyperthyroidism, Cushing syndrome). Obesity and aging are associated with gynecomastia owing to increased aromatase activity in the periphery. Estrogen-secreting tumors (such as Leydig or Sertoli cell tumors or adrenal cortical carcinoma) and HCG-secreting tumors (such as germ cell tumors and hepatic carcinomas) are associated with gynecomastia.