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Endocrine > Reproductive Disorders > Flashcards

Reproductive Disorders Flashcards

1
Q

What are the classifiactions of hypogonadism? And what causes each?

A

Primary: end organ failure at level of the ovary or testis

Secondary: pituitary or hypothalamus problem

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2
Q

What cells produce testosterone?

A

The Ledig cells (interstitial cells)-produce primarily testosterone and are stimulated by LH.

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3
Q

What is most of the testicular volume is made up of? What occurs here?

A

Seminiferous tubules; 90% testicular volume
Spermatogenesis occurs here

Comprised of sertoli cells and germ cells
stimulated by LH and FSH and local testosterone

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4
Q

What converts Testosterone to estradiol? Where does this occur?

A

Aromatase enzyme; In testes and adipose tissue

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5
Q

What converts Testosterone to DHT? Where does this occur?

A

5-alpha reductase; in the tissues

DHT is more potent. Both bind to androgen receptors

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6
Q

Tanner stages of male development:

A 
1.
2.
3.
4.
5.
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7
Q

What is male hypogonadism?

A

Defined as either low sperm in the semen and/or low testosterone level (<300)

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8
Q

Types of male hypogonadism

A

Primary Hypogonadism (hypergonadotropic hypogonadism)
Testicular failure
High LH,FSH, low Testosterone

Secondary Hypogonadism-(hypogonadotropic hypogonadism)
Any damage to the pituitary gland or hypothalamus
Inappropriately low LH, FSH, low testosterone

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9
Q

What are the causes of primary male hypogonadism?

A 
Genetic
Kleinfelter’s syndrome (XXY)
XX males
XYY syndrome
Y chromosome deletion
Cryptoorchidism
Orchitis
Chemotherapy and RT
Trauma
Chronic illness
Drugs/ETOH
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10
Q

What are the causes of secondary male hypogonadism?

A 
Kallmann syndrome
Idiopathic
Systemic illness
Anabolic steroids
Recreational drugs/narcotics
Anorexia
Tumors, surgery, RT
Prader willi
Hemochromatosis
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11
Q

What are the symptoms of male hypogonadism?

A

Delayed puberty, Sex dysfunction & Infertility

Non specific sx: fatigue, mood changes,weight gain

Dec libido, Dec muscle mass/body hair
Hot flashes, Gynecomastia

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12
Q

What are the post puberty signs of male hypogonadism?

A 
Testes soft, <15 ml
Normal phallus 
Normal skeletal proportions
Gynecomastia
Normal hair distribution, but reduced amount
Central fat distribution
Osteoporosis
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13
Q

What are the prepuberty signs of male hypogonadism?

A 
Testicular volume < 5 cm
Gynecomastia
Central fat deposition
Eunuchoidism
Delayed bone age
Decreased body/facial hair
High pitched voice
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14
Q

When are testosterone levels at their highest? How is testosterone stored in the body?

A

Peak testosterone levels in the AM;

Testosterone is protein bound: SHBG or albumin. Only 2-4 % of testosterone is unbound

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15
Q

Which testosterone to order?

A

Total testosterone: 300-800 ng/dl

Free levels can be done if SHBG is abnormal or calculate based on total and SHBG

Free levels should be done by equilibrium dialysis

Bioavailable testosterone –fairly reliable

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16
Q

What are causes of low SHBG?

A 
Hyperinsulinemia
Obesity
Acromegaly
Androgen replacement
Hypothyroidism
 cushings/steroids
Nephrotic syndrome
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17
Q

What are causes of high SHBG?

A 
Androgen deficiency
GH deficiency
Aging
Thyrotoxicosis
Estrogen
Liver cirrhosis
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18
Q

Additional testing for primary and secondary hypogonadism.

A
  • If primary: may require a karyotype or US of the testes
  • If secondary; may require an MRI to evaluate the pituitary gland
  • Prolactin
  • Iron saturation
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19
Q

What is Klinefelter’s Syndrome?

A

Most common congenital abnormality causing primary hypogonadism.

47XXY, behavior can be aggressive

20
Q

What are the characteristics of Klinefelter’s Syndrome?

A

Damage to all testicular cells resulting in low testosterone and high FSH/LH. Long bone abnormality causing increased length.

Small firm testes; small phallus; infertility; sparse body hair; gynecomastia; female body habitus

21
Q

What is Kallmann Syndrome?

A

Hypogonadotropic Hypogonadism – deficient hypothalamic secretion of GnRH

Associated with: anosmia, red-green color blindness, cleft palate, hearing loss, urogenital tract abnormalities

22
Q

When do we give Testosterone Replacement therapy?

A

For patients with symptoms and evidence of low testosterone

No meant for use in men with sx and normal testosterone

Goal is to restore testosterone to normal range

23
Q

What are the different types of testosterone replacement therapy?

A

Testosterone injections
Buccal tablets
Testosterone pellet (testopel)

Transdermal forms:
Patch
Gel (androgel, testim, fortesta, axiron)

24
Q

How do we monitor Testosterone?

A

Injections: check midway between injections
Should be mid normal range

Transdermal preps:
6-8 hrs post application of the patch
anytime with gel preps
Values should be in normal range

25
Q

What are the side effects of testosterone?

A 
Acne
Prostate disorders
Inc prostate volume, PSA
Worsening of underlying OSA
Erythrocytosis
Skin irritation to the patch
Suppression of sperm production (dec LH)
26
Q

What is Gynecomastia?

A

Benign proliferation of the glandular tissue of the male breast, Due to the increased ratio of estrogen: testosterone.

27
Q

What is Pseudogynecomastia?

A

Fat deposition in the breast rather than glandular proliferation. Differentiation can be determined on physical exam.

28
Q

What causes gynecomastia?

A

Normal : as an infant, puberty, and in the elderly

In adults commonly caused by :	
Drugs (spironolactone)
Persistent pubertal gynecomastia 
Idiopathic
Cirrhosis or malnutrition (inc conversion to E2)
Primary hypogonadism
hyperthyroidism
Germ cell tumors testes (Inc HCG)
29
Q

What is the treatment for gynecomastia?

A
  • Observation
  • Pre pubertal-tends to resolve spontaneously
  • Medication related; stop agent if possible, will regress spontaneously
  • Consider therapy if persists >2 years, painful, severe enlargement
  • Administer testosterone in deficient patients only
  • Tamoxifen/raloxifene (dec breast volume)
  • Aromatase inhibitors
  • Inhibit coversion T-E
  • Surgery
30
Q

Tanner Stages of Development of Secondary Sex Characteristics. Development of Pubic Hair:

A

Stage 1: Prepubertal (can see velus hair similar to abdominal wall)
Stage 2: Sparse growth of long, slightly pigmented hair, straight or curled, at base of penis or along labia
Stage 3: Darker, coarser and more curled hair, spreading sparsely over junction of pubis
Stage 4: Hair adult in type, but covering smaller area than in adult; no spread to medial surface of thighs
Stage 5: Adult in type and quantity, with horizontal distribution

31
Q

Tanner Stages of Development of Secondary Sex Characteristics. Development of Breasts:

A

Stage 1: Prepubertal
Stage 2: Breast bud stage with elevation of breast and papilla; enlargement of areola
Stage 3: Further enlargement of breast and areola; no separation of their contour
Stage 4: Areola and papilla form a secondary mound above level of breast
Stage 5: Mature stage: projection of papilla only, related to recession of areola

32
Q

What is Amenorrhea?

A

Absence of Menses in presence of normal growth and secondary sex characteristics

Primary: no menses in female > 15 yrs

Secondary: absence of menses for > 6 months in females post-menarche

Menopause: no menses for > 1 year

33
Q

What are the causes of Primary Amenorrhea?

A

Gonadal dysgenesis 2/2 chromosomal abnormalities

Hypothalamic Amenorrhea

Mullerian Agenesis (absence of vagina w/variable uterine dev)

Imperforate hymen/transverse vaginal septum

Pituitary disease/tumors

Kallmans Syndrome

46XY – Androgen Insensitivity Syndrome (resistant to testosterone), and 5-alpha-reductase Deficiency (ambig genitalia)

34
Q

How do we diagnose Amenorrhea?

A

Look at History with special Attention to Exercise, Stress, Eating Disorders.

Physical: Ht, Wt, Goiter, Galactorrhea, Tanner Staging, GYN exam.

Labs: LH, FSH, E, T, prolactin, TFTs
βHCG

35
Q

What is Turners syndrome?

A

Karyotype: 45X0. Gonadal dysgenesis – Instead of being a girl with XX you’re missing an X. The ovaries are little streaks of fibrous tissue- can be seen in a CT scan

36
Q

What are the clinical features of Turners Syndrome

A

Short stature
Distinctive facies: micrognathia (small chin/jaw), prominent low set ears, fishlike mouth, ptosis is present to varying degrees.
Shield-like, square chest
Neck is short, broad, and webbed

37
Q

How do we treat Turners Syndrome?

A

Estrogen and cyclic progesterone replacement at puberty will result in normal pubertal development

Pubic hair, breast growth, cyclic vag bleeding and maturation of external genitalia

Growth hormone sometimes used to gain max height

Pts are infertile

38
Q

What are complications of Turners Syndrome?

A

Renal abnormalities (50%) – Horseshoe Kidney

They will be infertile and wont have good female hormones, but theses associated non hormonal issues are more serious and life threatening.

Coarctation- aorta gets kinked in half and blood can’t flow through well

Cubitus valvus- arms are kinked to side so their arms point out in anatomical position

39
Q

What is the main cause of secondary amenorrhea?

A

PREGNANCY

40
Q

What is functional hypothalamic amenorrhea

A 
Disease of exclusion
Decreased release of GnRH, dec FSH/LH , anovulation and low serum estradiol
At risk for bone loss 2/2 to low estrogen
Risk factors:
Disorders of malabsorption (celiac)
Eating disorders
Exercise
Stress (emotional and illness)
41
Q

Female althlete triad:

A

Amenorrhea
Disordered eating
Osteoporosis/osteopenia

42
Q

Polycystic Ovarian Syndrome

A

A Spectrum of a Disease

Key Characteristics:
Androgen excess 
Menstrual Irregularity/Anovulation
Polycystic Ovaries
Increased Risk for: 
Infertility
Metabolic Syndrome
CVD
Type 2 Diabetes
43
Q

pos

A

Only need a couple- not all to have this disease
Girls have testosterone too, but you need less than estrogen.
More often, these people don’t have polycystic ovaries they have other characteristics
If you don’t have an egg you cant get pregnant- anovulation
Treat these people like diabetes

44
Q

pcos

A

PCOS accounts for 20% of secondary amenorrhea

is the most common endocrine abnormality in reproductive aged women

It is a dx of exclusion

45
Q

po insuff

A

Previously referred to as premature ovarian failure

Onset prior to age 40

Can have intermittent ovulation, cycles

Decreased estrogen, results in High FSH

Screen these patients for Turner’s and fragile X , consider autoimmune etiology

Require HRT for bone health

46
Q

menopause

A

No menses for 12 months

Average age of 51.4 years

Sxs: hot flashes, vaginal atrophy/dryness, sleep disturbances, mood swings

Hormone replacement:
uterus – estrogen + progesterone
no uterus - estrogen

47
Q

hormone replacement

A

Prevent hot flashes
Can help maintain BMD
Maintains GU health – can be treated with local therapy
Long term use controversial re: Breast cancer/CVD risks
Can consider use of SSRIs, clonidine for vasomotor symptoms

Endocrine (8 decks)

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