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05. Andro (1569) > 15: Integrated men’s health: Androgen deficiency, cardiovascular risk, and metabolic syndrome > Flashcards

15: Integrated men’s health: Androgen deficiency, cardiovascular risk, and metabolic syndrome Flashcards

1
Q

What was the top cause of death in the United States in 2016?

A

Heart disease.

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2
Q

How many annual deaths in the United States in 2016 were attributed to heart disease?

A

633,842.

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3
Q

What was the male-to-female incidence ratio for heart disease in 2016?

A

1.12.

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4
Q

Which condition had the highest male-to-female incidence ratio in 2016?

A

Suicide, with a ratio of 3.33.

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5
Q

How many annual deaths in the United States in 2016 were attributed to dementia?

A

110,561.

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6
Q

What was the male-to-female incidence ratio for dementia in 2016?

A

0.44.

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7
Q

Which condition had an annual death toll of 49,959 in the United States in 2016?

A

Nephrological conditions.

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8
Q

What was the cause of death associated with a male-to-female incidence ratio of 0.71 in 2016?

A

Stroke.

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9
Q

How many people died due to accidents in the United States in 2016?

A

146,571.

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10
Q

Which condition had an annual death count of 57,062 in the United States in 2016?

A

Influenza or pneumonia.

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11
Q

What is the obesity/body fat distribution criteria for WHO (1999) in the context of metabolic syndrome definitions?

A

Waist/hip ratio >0.90 in men, >0.85 in women or BMI >30 kg/m^2

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12
Q

According to EGIR (Balkau and Charles, 1999), what is the waist circumference criteria for metabolic syndrome in men and women?

A

Waist circumference ≥94 cm in men, ≥80 cm in women

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13
Q

For ATP III (NCEP, 2001), at what waist circumference is metabolic syndrome defined for men and women?

A

Waist circumference >102 cm in men, >88 cm in women

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14
Q

What is the BMI criterion set by AACE (Einhorn et al., 2003) for metabolic syndrome?

A

BMI ≥25 kg/m^2

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15
Q

What conditions or measurements define insulin resistance/hyperglycemia according to WHO (1999)?

A

IGT, IFG, T2DM, or other evidence of insulin resistance

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16
Q

What is the fasting glucose level for metabolic syndrome as defined by ATP III (NCEP, 2001)?

A

Fasting glucose ≥110 mg/dL

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17
Q

According to EGIR (Balkau and Charles, 1999), what triglyceridemia level indicates metabolic syndrome?

A

≥177 mg/dL

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18
Q

What are the HDL-C level criteria for men and women as specified by IDF (Alberti et al., 2005) for metabolic syndrome?

A

HDL-C <40 mg/dL in men; <50 mg/dL in women; or on treatment

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19
Q

What is the blood pressure criterion for metabolic syndrome as defined by EGIR (Balkau and Charles, 1999)?

A

≥140/90 mm Hg or on treatment

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20
Q

According to WHO (1999), what other factor is considered in the metabolic syndrome definitions apart from the factors mentioned above?

A

Microalbuminuria

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21
Q

What is the lower limit of a normal testosterone?

A

Guideline 1: A total testosterone level below 300 ng/dL is a reasonable cut-off in support of the diagnosis of low testosterone

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22
Q

When should you measure testosterone?

A

Guideline 1: testosterone levels should be measured conducted in an early morning fashion (peak between 3-8 AM)

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23
Q

How many low testosterones should be measured to diagnose low testosterone?

A

Guideline 2: TWO total testosterone measurements that are taken on separate occasions

24
Q

How do you diagnose testosterone deficiency (not just low testosterone levels)?

A

Guideline 3: The clinical diagnosis of testosterone deficiency is only made when patients have low total testosterone levels combined with symptoms and/or signs

25
Q

In whom should you consider measuring testosterone in even in the absence of symptoms or signs associated with testosterone deficiency?

A

Guideline 4: Clinicians should consider measuring total testosterone in patients with a history of unexplained anemia, bone density loss, diabetes, exposure to chemotherapy, exposure to testicular radiation, HIV/AIDS, chronic narcotic use, male infertility, pituitary dysfunction, and chronic corticosteroid use

26
Q

Should you use a validated questionnaire to define patients who are candidates for T replacement?

A

Guideline 5: The use of validated questionnaires is not currently recommended to either define which patients are candidates for testosterone therapy or monitor symptom response in patients on testosterone therapy.

but you can still use them to supplement your thorough history. One such sample questionnaire is the Aging Male Survey (AMS)

27
Q

Once a person has a diagnosis of low testosterone, what is your next blood work?

A

Guideline 6: serum luteinizing hormone levels (LH)

28
Q

If someone has low testosterone levels combined with low or low/normal luteinizing hormone levels, what other test should you order?

A

Guideline 7: serum prolactin level

Guideline 11: (prior to starting treatment) measure hemoglobin and hematocrit (and warn men of the increased risk of polycythemia)

Guideline 12: (prior to starting treatment) PSA should be measured in men over 40 years of age

29
Q

What causes hyperprolactinemia?

A

Medications, most commonly dopamine antagonists (but also anti-psychotics, anti-emetics, proton pump inhibitors, calcium channel blockers, opiates, and selective serotonin reuptake inhibitors) may cause hyperprolactinemia.

Chronic medical conditions, such as hypothyroidism, renal failure, and cirrhosis are associated with hyperprolactinemia as well.

30
Q

Who should you refer to an endocrinologist?

A

Patients with persistently high prolactin levels of unknown etiology should undergo evaluation for endocrine disorders

31
Q

What should you measure in a testosterone deficient patients who present with breast symptoms or gynecomastia prior to the commencement of testosterone therapy

A

Guideline 9: Serum Estadiol

32
Q

What should a testosterone deficient man who is interested in fertility have done and be warned of?

A

Guideline 10: Men with testosterone deficiency who are interested in fertility should have a reproductive health evaluation performed prior to treatment.

Guideline 16: The long-term impact of exogenous testosterone on spermatogenesis should be discussed with patients who are interested in future fertility

33
Q

What should clinicians should inform testosterone deficient patients about their heart?

A

Guideline 13: That low testosterone is a risk factor for cardiovascular disease

34
Q

Patients should be informed that testosterone therapy may result in improvements in what?

A

Guideline 14: erectile function, low sex drive, anemia, bone mineral density, lean body mass, and/or depressive symptoms

35
Q

Patients should be informed that the evidence is inconclusive whether testosterone therapy does what?

A

Guideline 15: improves cognitive function, measures of diabetes, energy, fatigue, lipid profiles, and quality of life measures

36
Q

What should clinicians say about prostate cancer and testosterone therapy?

A

Guideline 17: Clinicians should inform patients of the absence of evidence linking testosterone therapy to the development of prostate cancer

Guideline 18: Patients with testosterone deficiency and a history of prostate cancer should be informed that there is inadequate evidence to quantify the risk-benefit ratio of testosterone therapy.

37
Q

What should clinicians say about venothrombolic events and testosterone therapy?

A

Guideline 19: Patients should be informed that there is no definitive evidence linking testosterone therapy to a higher incidence of venothrombolic events

38
Q

What should clinicians say about cardiovascular events and testosterone therapy?

A

Guideline 20: Prior to initiating treatment, clinicians should counsel patients that, at this time, it cannot be stated definitively whether testosterone therapy increases or decreases the risk of cardiovascular events (e.g., myocardial infarction, stroke, cardiovascular-related death, all-cause mortality)

39
Q

What is one thing all testosterone deficient men who are overweight or physically inactive should be counseled on as far as one treatment any man should do?

A

Guideline 21: All men with testosterone deficiency should be counseled regarding lifestyle modifications as a treatment strategy (weight loss and exercise will naturally boost testosterone in these men)

40
Q

When supplementing testosterone, what testosterone level should you try to achieve?

A

Guideline 22: Clinicians should adjust testosterone therapy dosing to achieve a total testosterone level in the middle tertile of the normal reference range (450-600)

41
Q

What should you not prescribe men who are currently trying to conceive?

A

Guideline 23: Exogenous testosterone therapy should not be prescribed to men who are currently trying to conceive

Guideline 27: Clinicians may use aromatase inhibitors, human chorionic gonadotropin, selective estrogen receptor modulators, or a combination thereof in men with testosterone deficiency desiring to maintain fertility

42
Q

How long should you wait to start testosterone therapy in a person with a history of cardiovascular events?

A

Guideline 24: Testosterone therapy should not be commenced for a period of three to six months in patients with a history of cardiovascular events.

43
Q

What type of testosterone should you not prescribe?

A

Guideline 25: Clinicians should not prescribe alkylated oral testosterone. (due to their liver toxicity)

You can prescribe testopils, gels, creams, liquids, sublinquial, IM, etc

44
Q

Clinicians should discuss the risk of transference with patients using testosterone gels/creams. How do you prevent this?

A

Use an alternative therapy.

Wash hands well after applying

cover the area with clothing after drying

Wash skin prior to skin to skin contact

Wash clothes that touched testosterone separately

45
Q

should you prescribe testosterone products that are compounded?

A

Guideline 28: Commercially manufactured testosterone products should be prescribed rather than compounded testosterone, when possible

46
Q

When should men measure their total testerone level after starting testosterone therapy?

A

guideline 29: Clinicians should measure an initial follow-up total testosterone level after an appropriate interval to ensure that target testosterone levels have been achieved.

generally 2-4 weeks for gels, liquids and creams
short-acting IM or short-acting SQ pellets (testosterone cypionate or enanthate) mid-cycle after ~ 4 cycles
long-acting IM testosterone (testosterone undecanoate) ~ 15 weeks
anastrozole, clomiphene citrate, and hCG > 4 weeks after starting
long-acting SQ pellets (2-4 weeks to see if number of testopels is appropriate and then 10-12 weeks)

47
Q

Once a patient is on a stable dose of testosterone therapy, how often should you check their testosterone?

A

Guideline 30 Testosterone levels should be measured every 6-12 months while on testosterone therapy. (Also check their H/H!)

48
Q

Describe testosterone regulation in the body:

A

GnRH released from hypothalamus acts on anterior pituitary to stimulate release of LH and FSH (both act on testes)

FSH → Sertoli Cells → spermatogenesis

LH → Leydig cells → testosterone

Negative feedback to hypothalamus and anterior pituitary by both testosterone and through aromatase (estradiol)

49
Q

What forms is testosterone found in the body:

A

60% bound to SHBG (not bioavailable, can measure in elderly or obese men)

Bioavailable:
1-2% free and remainder bound loosely to albumin

AR binds to testosterone and DHT (higher affinity)

50
Q

What aspects of history are important in assessment of testosterone deficiency?

A

hypothyroid (similar sxs, measure TSH)
low libido
tiredness
mood altrations (irritability)
fogginess
decreased strength/stamina
loss of muscle mass
central obesity
opioids
corticosteroids
surgeries testis or head
torsion, trauma, orchitis
chemo or radiation
HbA1C, glucose control
PSA (over 40)

51
Q

Labs to consider with low T

A

SHBG (older or obese)
TSH
PRL (severely low)
LH
HCT
PSA
HbA1C

52
Q

Types of hypogonadism:

A
  1. Hypergonadotropic hypogonadism (primary) → testicular failure; low T, elevated LH
    1. Examples: gonadotoxin (chemo, RT), congenital (UDT, Kleinfelter’s), testicular insults (torsion, trauma, testis cancer), meds (spironolactone, ketoconazole)
  2. Hypogonadotropic hypogonadism (secondary) → low LH, low T (hypothalamus or pituitary problem)
    1. Examples: genetics (Kallmann, Prader-Willi), trauma (pituitary tumor, prolactinoma, RT, infarct), substances/neg feedback (opioids, steroids, marijuana), metabolic dz (DM, OSA, ESRD, malnutrition, obesity)
  3. Mixed (compensated hypogonadism) → low T normal/borderline low LH (adult onset)
53
Q

Benefits of treating hypogonadism:

A

Sexual function (libido, erections, response to PDE5i)

Body composition (bone mineral, decreased fat, increase skeletal musc)

Psychologic (improved depression)

Cognitive (decreased memory loss, greater attention span)

Comorbidity mgmt. (improved glucose/lipid)

54
Q

Risk of T treatment:

A

Impaired spermatogenesis (decreased T production in testis)

Erythrocytosis (higher with IM), keep <54%

Gynecomastia (aromatase)

OSA worsened??

CV risk, controversial

55
Q

Contraindications to T replacement:

A

No absolute contraindications

Not ideal for fertility

recommended to avoid prostate cancer, breast cancer, severe OSA, Hct > 50%, severe LUTs, PSA . 4, male infertility

NONE of above are absolute contraindication

56
Q

Other treatment options besides T for low T:

A

Not FDA Approved

SERMs: attenuating negative feedback of estrogen on hypothalamus and pituitary → increase LH (less likely to work with testis failure)

CLOMIPHENE CITRATE

Aromatase inhibitor: inhibit conversion of T → E

ANASTRAZOLE (LETROZOLE)

HCG: stimulate Leydig cell production of T (oral and generic)

57
Q

what do you do if your patient on T therapy has Hct >54%

A

Men with significant polycythemia (Hct >54%) may require dose adjustment, periodic phlebotomy, or temporary/permanent T discontinuation.

05. Andro (1569) (16 decks)

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