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
medications
weight loss off ____lbs per week is recommended
1-2 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 Consider
excessive growth of terminal hairs in androgen-dependent regions of the body in an adult female
hirsutism
hirsutism
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
testosterone
how much testosterone circulates freely
1%
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 --->
estradiol
testosterone targets
wolfian duct, brain, muscle, body hair, spermatogenesis, and libido
2 main etiologies of hirsutism
PCOS adrenal or ovarian neoplasms
other causes of hirsutism
idiopathic 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
IDIOPATHIC OR FAMILIAL HIRSUTISM
Minoxidil Cyclosporine 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
most common cause of hyperandrogenic anovulatory infertility. Hypofunction of FSH causes chronic anovulation
PCOS
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 Clitorimegaly
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 Serum DHEAS
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
neoplasm
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)
ANTI-ANDROGEN commonly Rx-ed w/OCPs
Presence of palpable breast tissue in the male Glandular tissue > 4cm
gynecomastia
Often caused by an imbalance of the estrogen-androgen ratio
prolactin diminishes the peripheral action of testosterone and suppresses LH/FSH secretion
hypogonadism
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
systemic
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`
marijuana amphetamines 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
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
Cryptorchidism
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 Irradiation Vascular injury Trauma Alcohol ingestion Chemotherapy FSH level is usually elevated, but may be normal
acquired gonadal failure at the level of the Leydig cell level
Aging 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
Kallman's Panhypopituitarism Hyperprolactinemia 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
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
malignancy
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
testosterone
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