Hirsutism Virilization and CAH (Darrow) - MT Flashcards Preview

Endocrine II - Exam 2 > Hirsutism Virilization and CAH (Darrow) - MT > Flashcards

Flashcards in Hirsutism Virilization and CAH (Darrow) - MT Deck (21):
1

Causes of Hirsuitism which usually cause decreased sex hormone binding globulin (free testosterone) include what 9 things?

1. Decreased Estrogen (prolactinoma)

2. Insulin

3. GH (acromegaly)

4. Obesity

5. Hypothyroidism

6. Glucocorticiods (cushings)

7. Androgens

8. Nephrotic syndrome (protein dumping = dec SHBGs)

9. excess activity of 5-alpha-reductase

2

Where is Sex hormone binding globulin (free testosterone) produced?

Liver (slide 3)

3

This skin condition is common in what endocrine disorder?

What causes it?

Q image thumb

- Hirsutism d/t CAH

- Excess circulating Androgens

4

The PHODDCI pneumonic for Hirsutism stands for what causes?

 

- PCOS (LH/FSH ration >2 = decrased Est/Test)

- Hypothyroidism (dec SHBG, and inc TRH--> inc prolactin)

- Ovarian/Adrenal tumors (LH/FSH inc --> Hyperthecosis = arrested follicular developent in lutenized thecal cells--> Testosterone overproduction)

 

- Drugs (steroids, penicillin, minoxidil)

- Deficient 21 hydroxylase (CAH)

- Cushing syndrome (inc sec of androgens w/ cortisol)

- Idiopathic/familial (increased skin 5 alpha reductase activity)

5

Ovarian causes of Hirsutism include what 2 conditions?

- Polycystic ovarian syndrome

- Tumors

6

You recieve that labs for a patient with known hirsutism, what will you see in the testosterone, DHEAS, and 17 hydroxy progesterone levels if the cause of the patient's  hirsutism stems from:

1. Idiopathic/hereditary

2. Polycystic ovarian syndrome

3. CAH

* give mild increase, normal, or all increased anwer for the levels

1. Idiopathic/hereditary = All normal

2. Polycystic ovarian syndrome = testosterone mild increase

3. CAH = all increased (17 OHP> 500 ng/dL)

7

Physical examination of a patient with a Virilizing condition would yield what d/t overproduction of androgens? (x5)

1. Increased muscularity

2. temporal alopecia

3. deepening voice

4. acne

5. clitoromegaly (adrenal, ovaries, CAH)

8

Lab levels of Testosterone, DHEAS (dehydroepiandrosterone), and 17 hydroxyprogesterone in a patient suffering from virilization (not hirsutism) d/t an Ovarian tumor would be?

- total testosterone greatly increased

(total testosterone > 200 ng/dL points to ovary or adrenal tumor)

 

 

- normal DHEAS and 17 OHP

9

Lab levels of Testosterone, DHEAS (dehydroepiandrosterone), and 17 hydroxyprogesterone in a patient suffering virilization d/t and Adrenl tumor would be?

- Greatly increased DHEAS > 700 ng/dL

 

 

10

Lab levels of Testosterone, DHEAS (dehydroepiandrosterone), and 17 hydroxyprogesterone in a patient suffering from virilization d/t congenital adrenal hyperplasia would be?

- Total testosterone, DHEAS, 17OHP are all increased

(17OHP > 500 ng/dL = Diagnostic)

11

Where are androgens produced?

- Increase to > 1000 ng/dL of androstenedione could indicate what?

- Increased to >700 ng/dL of DHEAS could indicate what?

- Adrenal gland reticularis layer

- Adrenal or Ovarian neoplasm

- Adrenal neoplasm or CAH

12

1 - Total testosterone > 200 ng/dL is most indicative of what condition causing hirsutism or virilization?

2 - DHEAS >700 mcg/dL is most indicative of what condition causing hirutis or virilization?

3 - 17 OHP >500 ng/dL is diagnostic for what?

1 - Ovarian neoplasm

2 - Adrenal neoplasm

3 - CAH

13

Treatment for histuitism includes use of antiandrogens like:

1. Spironolactone and flutamide

2. finasteride

3. Metformin

4. GnRH agonist

What are their respective general mechanisms of action?

1. spirnonolactone and flutamide = androgen receptor blockers

2. finasteride = 5-alpha reductase inhibitor

3. Metformin = reduces hepatic gluconeogenesis--> lowers insulin levels)

4. GnRH agonist = decreases gonadotropins by constant stimulation

14

What stimulates the zona glomerulosa to produce Aldosterone?

What stimulates the zona fasciculata to produce cortisol as well as the zona reticularis to produce androstenedione?

- Angiotensin II, K+, ANP stim ZG

- ACTH stims ZF and ZR

15

21 hydroxylase deficiency in a patient with CAH will lead to an excess of what molecule?

- Androgens

16

What are the 2 main symptoms of 21 hydroxylase deficiency in CAH?

Why do these symptoms appear?

- Masculinization (virilization) in females from excess androgen (or in males more pronounced genetalia, and oligospermia)

 

- Hypotension salt wasting from deficient production of aldosterone)

17

What is usually a diagnostic lab level of 17 OH prognenolone (androgen precursor) for CAH 21 hydroxylase deficiency? (ng/dL)

- > 500 ng/dL

18

In 11 beta hydroxylase deficiency, a build up excess of what molecule causes masculinization and hypertension?

- 11 Deoxycorticosterone (DOC)

(has aldosterone like affects and can be converted into androgen pathway)

19

How does the adrenal hyperplasia occur in CAH? (21 hydroxylase deficiency)

- lack of cortisol production eliminates negative feedback loop to hypothalamus and pituitary, thus ACTH is continuosly secreted and overstimulates the Zona fasciculata and Zona reticularis --> hyperplasia and excess androgens

20

Because there is an excess of 11 deoxycortisterone in 17 hydroxylase deficiency, ACTH stimulation causes what two predominating symptoms to occur?

1. Ambiguous genetalia from lack of androgens

2. Hypertension d/t mineralcorticoid activity and increased corticosterone w/ glucocorticoid activity

21