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obesity is defined as a BMI

>30 kg/m2

true BMI equation

weight/height2 = kg/m2

approximate BMI equation

pounds/inches2 X 704

BMI 18.5 - 24.9

normal weight

BMI 25 - 29.9


BMI 30 - 34.9

Class I obesity

BMI 35 - 39.9

Class II obesity

BMI >40

Class III obesity

for females to have regular menses they must have a minimum body fat of

13 - 17%

If a male has <3% body fat

may suffer from chronic fatigue and increased susceptibility to illness

Etiologies for obesity

High fat/high caloric intake
Increased amount of food eaten Decreased physical activity
genetic risk
- Prader-Willi syndrome

obesity is a major risk factor for what conditions

Coronary heart disease
Diabetes (type2)

obesity is a major risk factor for what other conditions

Osteoarthritis/gout, Sudden death, Congestive heart failure
All-cause mortality, Thromboembolic disease (stroke, DVT), Low HDL cholesterol, Gallstones, Sleep apnea, Restrictive lung disease, Colo-rectal cancer, Endometrial/breast cancer

a good family history for an obese patient includes

Age of onset of obesity, occupational history, previous weight loss attempts and methods, etc

what may you like to include when developing a wise food plan for your obese patient

Have the pt keep a food diary as part of the assessment of present dietary behaviors.
Refer the patient to a dietician
Exercise is a must!

your pt has: rapid weight gain without change in diet or exercise
Signs: upper body obesity, striae, easy bruising, thin skin, HTN, glucose intolerance
you suspect

Adrenal overactivity (Cushing's syndrome)

behavior modification for the obese pt

goal-directed behavior therapy. Small group therapy (Weight Watchers, individual psychotherapy) may be helpful for some patients

Consider this adjunct if there has been little or no progress after AGGRESSIVE attempts to lose excess weight AND the patient has a BMI that justifies use of


weight loss off ____lbs per week is recommended

Weight loss should be in 10 pound increments

to lose 1 lb per week

(current weight x 13) - 500 calories/day = 1 pound/week weight loss

when are low calorie diets utilized

if the BMI > 25 with co-morbidities 800-1000 calories/day (0.8 g protein per kg daily)

BMI > 35 with or without co-morbidities (patients who are at least 30% overweight)
may need a ________diet

very low calorie
High protein, no fat
Safe if monitored
600-800 calories/day

an obese pt that exercises

shows commitment
Reduces risk of developing cardiovascular disease and/or type 2 diabetes
improves their immunity

behavioral changes can help an obese pt by

influence stimulus control, provide positive reinforcement (increases self-esteem), enhance stress management, and are an integral part of the permanent cognitive restructuring that is essential if weight loss is to be permanent

many obese females may have a present or past history of physical, emotional, or sexual abuse and/or depression

SSRI therapy for these patients (Zoloft, Prozac)

androgens act on

sex-hormone responsive hair follicles
Chin, upper lip, chest, axillae, abdomen, pubic region

excessive growth of terminal hairs in androgen-dependent regions of the body in an adult female



Elevated levels of circulating androgens OR
Increased sensitivity of hair follicles to normal levels of androgens

testosterone sources in females

Ovary (60%)
Peripheral conversion of androstenedione (40%)

what is the most potent androgen


how much testosterone circulates freely


testosterone circulates in the blood for _____

30-60 minutes then becomes "fixed" to tissues or degraded and excreted

"Fixed" testosterone is converted to DHT (the active form) by

by 5-alpha-reductase in the skin
Fixed testosterone stimulates androgen-dependent hair follicles

DHT targets

external genitalia, male pattern body hair, temporal baldness, and prostate

testosterone to aromatase in fat --->


testosterone targets

wolfian duct, brain, muscle, body hair, spermatogenesis, and libido

2 main etiologies of hirsutism

adrenal or ovarian neoplasms

other causes of hirsutism

Use of non-prescription DHEA or abuse of androgenic substances

Normal androgen levels
More common in Mediterranean, Middle Eastern ethnic groups
Onset is usually in the peri-pubertal period
There is a slow progression of hair growth


Dilantin (phenytoin)
Anabolic steroids
Certain progestins in oral contraceptives

pharmacologic etiologies of hirsutism

Irregular menses since menarche
Gradual onset of hirsutism
Congenital adrenal hyperplasia (21-hydroxylase deficiency)
Cushing's syndrome
Polycystic ovary syndrome (PCOS)

Unlikely Neoplastic Etiology of hirsutism

Accounts for approximately 50% of cases of hirsutism

Polycystic Ovary Syndrome
A common functional disorder of the ovaries

Excess LH acts on thecal cells of ovaries causing excess androgen production

polycystic ovary syndrome

Signs/Symptoms: hirsutism, amenorrhea, oligomenorrhea, infertility, obesity, insulin resistance


most common cause of hyperandrogenic anovulatory infertility.
Hypofunction of FSH causes chronic anovulation


Onset of hirsutism is outside the peri-menarchal period
There is rapid progression of hair growth
The hirsutism is SEVERE
There is a recent onset of menstrual irregularity

possibility of adrenal or ovarian neoplasm

Other signs of virilization are typically present:
Temporal hair recession and crown balding
Deeping of the voice
Loss of female body contour or breast tissue
Increased muscle mass, especially upper shoulder girdle

possibility of adrenal or ovarian neoplasm

when evaluating for hirsutism what must be done first

Perform laboratory tests before proceeding to imaging studies

what labs should you order when evaluating for hirsutism

Free and total testosterone
Hcg, urinary free cortisol

Total testosterone > 200 ng/dl or free testosterone > 40 ng/dl necessitates

a pelvic exam and pelvic ultrasound

If the pelvic examination and ultrasound are negative for the presence of polycystic ovaries, what next

perform a bilateral adrenal CT scan

serum androsternedione >1000 ng/dl

indicates an ovarian or adrenal neoplasm

Serum DHEAS > 600 mcg/dl indicates

an adrenal source of androgen
Adrenal hyperplasia or adrenal carcinoma
Perform a bilateral adrenal CT scan

Elevated UFC, cortisol and a suppressed ACTH level indicate

an adrenal etiology.

Whenever the testosterone level is > 200 or the DHEAS level is > 700, suspect a


treatment for neoplastic hirsutism

Surgical/medical treatment of lesion

treatment for idiopathic hirsutism, PCOS, CAH

Oral contraceptive agents with low-androgenic progestins
Suppresses LH/FSH production
Gonadotropin-releasing hormone analogs + estrogen/progesterone
Decreases LH/FSH production - example: leuprolide (Lupron)
Weight loss

treatment of CAH hirsutism

Glucorticoids (but consider long-term side effects)
Inhibits ACTH production
Laparoscopic bilateral adrenalectomy

Glucocorticoids inhibit ACTH production

There is an increased level of ACTH in CAH that is converted to androgens because of the 21-hydroxylase deficiency

Spironolactone (Aldactone)

commonly Rx-ed w/OCPs

Presence of palpable breast tissue in the male
Glandular tissue > 4cm


Often caused by an imbalance of the estrogen-androgen ratio


Endocrine diseases
Systemic diseases

causes of gynecomastia

Idiopathic or Familial Gynecomastia

Breast tissue is extremely sensitive to estrogens OR there is excess conversion of estrogen precursors to estrogen

neonnatal gynecomastia

Reflects high level of estrogens in the maternal-fetal unit

pubertal gynecomastia affects up to

60% of normal teens
Reflects imbalance between estrogen and androgen action on the breasts
Caused by increased sex steroid production

pubertal gynecomastia

usually subsides within a year
may be unilateral or bilateral

Testosterone levels decrease + level of sex hormone binding globulin (SHBG) increase with age and this further reduces free testosterone levels

aging gynecomastia
1/3 of males 50-80

obesity related gynecomastia

Increased fat causes increased aromatase activity
More testosterone is converted to estradiol

Androgen resistance syndromes (testicular feminization)
Aromatase excess syndrome
Klinefelter's syndrome

endocrine causes of gynecomastia


prolactin diminishes the peripheral action of testosterone and suppresses LH/FSH secretion


elevated LH and FSH causes increased secretion of estradiol from Leydig and Sertoli cells in the testes

chronic liver/renal disease is an example of what type of cause of gynecomastia


Steroid-producing neoplasms (estrogen-producing neoplasms of the adrenal glands or testes)
hCG-producing neoplasms of the testes or lung

gynecomastia caused by neoplasms

Unilateral, irregular, painless, firm/hard mass that is fixed to underlying tissues

breast cancer
There is a higher incidence of breast cancer in men with Klinefelter's syndrome`

Type I and II 5-alpha-reductase inhibitors - Proscar (finasteride), Avodart (dutasteride)
Exogenous steroids and androgens

medications that can ncause gynecomastia

Laboratory Investigation of Gynecomastia
initial tests

Prolactin and beta-hCG:
Elevated levels of either indicate a testicular tumor or other malignancy (usually lung or liver) Low levels of beta-hCG indicate primary hypogonadism
LH and testosterone:
Diagnoses primary and secondary hypogonadism
Estradiol - usually normal
Increased in testicular tumors, liver disease, obesity, and with increased beta-hCG

In cases of persistent gynecomastia without an identifiable etiology

Karyotype for Klinefelter's Syndrome

Suspicious unilateral or asymmetric enlargement

needle biopsy

In unclear cases
May reveal bronchogenic or metastatic carcinoma

chest X-ray

Idiopathic or pubertal: observe and reassure

A follow-up visit at 6 months is appropriate to check for resolution

Medication-induced gynecomastia

stop offending drug if possible

Painful gynecomastia treatment

Tamoxifen (antiestrogen)
Danazol (testosterone derivative)

hypogonadism gynecomastia treatment

Not aromatized to estradiol

Persistent or severe gynecomastia


GnRH: released in a

pulsatile manner

LH: binds to specific receptors on

Leydig cells in the testes and stimulates production of testosterone

FSH: binds to receptors on

Sertoli cells of the seminiferous tubules
Necessary for spermatogenesis

Early prenatal testosterone deficiency

Ambiguous genitalia
Either testes or ovaries but not both

inEarly prenatal testosterone deficiency accessory sex organs and/or the external genitalia

are not completely developed or are inappropriate for chromosomal sex

Later prenatal testosterone deficiency

Failure of one or both testes to descend

Testosterone deficiency in puberty (delayed puberty)

Poor muscle development
Decreased strength and endurance
High-pitched voice
Sparse axillary and pubic hair
Absence of facial and body hair

Testosterone deficiency in puberty

Long bones may continue to grow under influence of GH

Eunuchoidal proportions

arm span > height
crown-pubis < pubis-floor

normal proportions

arm span = height
crown-pubis = pubis-floor length

Post-pubertal testosterone deficiency

Decrease in libido
Low energy
Fine wrinkling around eyes and mouth
Diminished facial and body hair
Testes may be small or normal in size

3 Types of Hypogonadism

Defect in androgen action

Primary hypogonadism - defect of the testes

Low testosterone, elevated LH/FSH

Secondary hypogonadism - hypothalamic-pituitary defect

Low testosterone, low LH/FSH

Defect in androgen action:

Elevated testosterone, elevated LH/FSH

when do you want to measure serum free testosterone

nonfasting morning specimen

Free testosterone

1-2% of total testosterone
It is the biologically active portion

Total testosterone

60-75% is bound to SHBG
Elderly men have increased SHBG that decreases level of free testosterone

at what age are testosterone levels the highest

20-30 years

If the LH and FSH are low

further evaluation of pituitary function is warranted

causes of primary hypogonadism

Klinefelter's syndrome
Bilateral anorchia
Acquired gonadal failure
Other etiologies:
Lymphoma, anti-tumor chemotherapy, radiation therapy, testicular trauma

The most common congenital cause of primary hypogonadism

Klinefelter's Syndrome

47 XXY genotype

Klinefelter's Syndrome
male phenotype

Puberty findings of?
low testosterone: Small, firm testes measuring < 2 cm (normal > 3.5), Testes were of a normal size during childhood
Body hair and external genitalia mature to varying degrees
Gynecomastia, impotence, infertility
Eunuchoidal proportions - tall stature

Klinefelter's Syndrome

Female habitus, poorly virilized, gynecomastia, eunuchoidism, small phallus, small testes, and sparse body hair

Klinefelter's Syndrome

Eunuchoid, normal phallus, small testes & gynecomastia

Klinefelter's Syndrome


Undescended testes
Occurs in 3% of full-term male infants
By 1 year of age 0.75% of those infants are still affected

Undescended testes may become

cancerous after several years

Bilateral Anorchia

Vanishing testicle syndrome
Testes are present during the 1st 14-16 weeks of gestation
The scrotum is empty at birth
Growth and development are normal until secondary sexual development fails to occur at puberty

no increase in testosterone after injection of hCG

bilateral anorchia

hCG stimulation is used to differentiate

between bilateral anorchia and cryptorchidism

acquired gonadal failure at the level of the seminiferous tubules

Mumps, gonorrhea, leprosy
Vascular injury
Alcohol ingestion
FSH level is usually elevated, but may be normal

acquired gonadal failure at the level of the Leydig cell level

The LH level is usually elevated

when treating for primary hypogonadism how often and how to you give testosterone

IM every 2-3 weeks
May also use the following formulations:
Transdermal patches (Testoderm, Androderm)
Used on scrotal and non-scrotal areas
Gel - 1% testosterone (Androgel)
Same areas as patch
Oral (methyltestosterone, fluoxymesterone)
Not as effective as IM therapy

what must be done before testosterone therapy is begun

Prostate cancer screening prior to testosterone therapy is appropriate for older men (DRE and PSA)

contraindications of testosterone use

Prostate hyperplasia
Prostate cancer
Should not be used in boys < 13 years old to avoid premature epiphyseal closure and short stature

side effects of testosterone

Side effects: acne, decreased HDL levels, gynecomastia

testosterone administration follow up

Check testosterone at 1 month, then every 6 months
At 3 months, lipid levels and hemoglobin/hematocrit
DRE every 6 months, PSA

Other etiologies

secondary hypogonadism

The most common form of secondary hypogonadism

Kallmann's Syndrome

Associated with the inability to discriminate odors (anosmia)

Kallmann's Syndrome

Kallmann's Syndrome

defective development of hypothalamic cells that secrete GnRH (these cells are near the olfactory bulbs
The individual will have prepubertal testes, eunuchoidal proportions, and gynecomastia

Congenital disorders
Infarction from vascular insufficiency
Autoimmune diseases

secondary hypogonadism

pituitary adenoma
Inhibits normal GnRH release
Inhibits the action of testosterone
Decreases the effectiveness of LH

secondary hypogonadism

ETOH abuse
Chronic illnesses (renal failure, CHF, others)
Obesity (BMI > 40 kg/m2)
Marijuana use
Cushing's syndrome
Cancer, AIDS

etiologies of secondary hypogonadism

Testicular feminization

complete androgen insensitivity
Testes function normally but are located intra-abdominally
Abnormal receptors in the pituitary gland do not recognize testosterone so development proceeds as if there is a lack of testosterone

Incomplete testicular feminization

incomplete androgen insensitivity
There is a mixed pattern of virilization and feminization

5-alpha-reductase deficiency

(variable degrees of gynecomastia, hypospadias, cryptorchidism) (hypospadias)

There are elevated levels of FSH/LH and testosterone
External female genitalia is observed
There is no uterus or fallopian tubes
There are no male accessory sex organs
The testes are cryptorchid
Child has appearance of a normal prepubertal girl

Testicular Feminization - Genetic Male

At puberty, the testes secrete large amounts of testosterone:
Converted by adipose tissue into estrogens
Result is a phenotypic female with well-developed breasts that never menstruates

Testicular Feminization - Genetic Male

Testicular Feminization - genetic male
Testosterone is not recognized so it is converted to estradiol by aromatase in adipose tissu

There is an abundant amount of testosterone produced by the testes. Some is converted to DHT but the vast majority is converted into estradiol.
The estradiol causes female sex characteristics to develop.

what treatment restores androgen receptors

There are no treatments that can restore androgen receptors
Phenotype and gender assignment are female
Estrogen treatment is provided to develop secondary female sexual characteristics

Intra-abdominal testes must be removed to avoid


LH, FSH, and testosterone levels are normal
Internal sex organs develop normally
There are cryptorchid (intra-abdominal) testes

5-Alpha-Reductase Deficiency (DHT Deficiency)

Dihydrotestosterone-dependent structures fail to develop

The prostate and external genitalia are poorly developed
The individual appears female or has ambiguous external genitalia at birth

At puberty, testosterone levels rise dramatically to overcome the defect:
Secondary sexual characteristics develop
The external genitalia becomes masculinized
A penis develops at this time

5-Alpha-Reductase Deficiency (DHT Deficiency)
("guevedoce" = penis at 12)

hCG increases


A rise in testosterone after hCG administration indicates

the presence of functional testicular tissue (cryptorchidism).

If there is NO rise in testosterone after hCG administration indicates

then bilateral anorchia is present

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