Download Question IN BOOK Answers of Oral Contraceptive Case 1. Account

Question IN BOOK
Answers of Oral Contraceptive Case
1. Account for Heba’s high blood pressure & elevated blood glucose.
High blood pressure: Due to Na & water retention.
High blood glucose: estrogens might impair glucose tolerance.
2. Discuss the effect of COC on liver enzymes & prothrombin time.
COCs cause hepatotoxicity ►↓ prothrombin synthesis ►↑prothrmbin time.
3. If your blood pressure rises while you are using the pill, what is the best measure
to control it.
Use diuretics to treat Na & water retention.
4. Discuss the interation between OC:
- Antibiotics:
Normally estrogen is conjugated in liver
release in bile
intestine
bacterial degradation (convert conjugated estrogen into free). Free estrogen
reabsorbtion (enterohepatic circulation)
repeated cycle
Antibiotics alter liver metabolism of COCs & interfere with bacterial breakdown
of conjugated estrogen
dec reabsorbtion of estrogen
dec plasma
level
- Anticonvulsants: Coadministration with inducers of CYP450 3A4 may decrease
the plasma concentrations of estrogens and progestins.
Q4: How can you prevent the previous symptoms?
Shift to progestin only contraceptives & stop estrogen.
Q5: How estrogen & progesterone make
contraception?
1. ↓GnRH↓ FSH/LH
↓ follicle maturation/ovulation
2. Progesterone effects
3. ↑Viscosity of cervical secretion:↓sperm penetration
4. ↓ Rate of oocyte transport through oviducts
5. May also ↓GnRH & Pituitary sensitivity to it
Male sex hormones Answers
1. What is the pharmacological class of nandrolone decanoate?
Anabolic steroid.
2. Account for Khalid’s short stature knowing that his parents are of normal
length.
As nandrolone has some androgenic character & can close the epiphysis of
long bones.
3. Discuss the effect of nandrolone on liver enzymes, blood lipids & prothrombin
time.
Nandrolone cause hepatotoxicity ►↓ prothrombin synthesis ►↑prothrmbin time.
Nandrolone elevate liver enzymes & elevate lipid profile.
4. Discuss the interaction between nandrolone decanoate &:
- Warfarin: nandrolone increase the effect of warfarin by displacement from
plasma proteins.
- L-Thyroxin: Androgens induced decrease in T4 binding globulin
increase
free L-Thyroxin resulting in increasing the action of L-Thyroxin (hyperthyroidism).
5- Why this patient has no children until now?
Since Nandrolone cause negative feedback on LH & FSH which is responsible for
spermatogenesis.
Extra Case #1: Central Hypogonadism
Chief complaint:
Amenorrhea for 6 months
Case Presentation:
A 35-year-old woman presented for evaluation of amenorrhea. She described an unremarkable
menstrual history with menarche at age 12 and normal menstrual cycles (30 days in length)
since that time, with the exception of two successful pregnancies. However, in the previous 6
months, she has had no menses. Her only evaluation was a Provera (10mg×5 days) challenge
with no subsequent withdrawal bleeding. Otherwise, she had been feeling well. She denied
visual changes, hot flushes, or night sweats. She also denied heat or cold intolerance, changes in
her skin or hair texture, weight changes, or changes in her bowel habits. Interestingly, she did
describe galactorrhea during this same 6-month period. No new symptoms of acne, hirsutism, or
alopecia were present. Her past medical history was remarkable for migraine headaches, which
had recently increased in frequency and intensity.
On physical examination, she was a well-developed,well-nourishedwoman in no acute distress.
Her body mass index (BMI) was 23 kg/m2, blood pressure 110/65, and pulse 72. Skin
examination revealed no acne, hirsutism, alopecia, or vitiligo. Head and neck exam revealed full
visual fields and a normal funduscopic exam. The thyroid was 20 g and without nodule. Breast
examination revealed expressible galactorrhea bilaterally..
Medications
Her only medications were Excedrin on an as-needed basis for her migraines and a daily
multivitamin.
Family history
unremarkable for any reproductive disorders, thyroid disease, or infertility.
Laboratory evaluation
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negative human chorionic gonadotropin (HCG),
prolactin 42 ng/mL (normal 2.6–13.1),
follicle-stimulating hormone (FSH) 0.3 mIU/mL (normal 1–18),
thyroid-stimulating hormone (TSH) 3.0 mIU/L (normal 0.5–5)
insulin like growth factor I (IGF-I) level : normal
free thyroxine (T4) : normal
An overnight dexamethasone suppression test to rule out Cushing’s syndrome was
normal as well.
An MRI of the pituitary gland revealed a 5 mm pituitary mass. Mild compression of the
optic chiasm was noted.
Questions:
1) Differential diagnosis#1: What are the major possible causes for the patient’s condition?
Suggest the most likely one.
This young woman presented with a 6-month history of amenorrhea. When investigating
secondary amenorrhea, the initial differential diagnosis must be broad, including
1. pregnancy,
2. ovulatory disorders.
Pregnancy was excluded in our patient (HCG). Therefore, an ovulatory disorder seemed the
most likely etiology.
2) What is the Provera challenge? What does it indicate?
Progestin (Provera) challenge is used to assess the ability of the endometrium to respond to
steroid hormones.
Medroxyprogesterone acetate - MPA - is given at 10 mg/day p.o. for 5 days.
 If withdrawal bleeding occurs 5-7 days later then the endometrium must have been
previously exposed to adequate levels of oestrogen, and the endometrium is able to
proliferate in response to progesterone.
 Polycystic ovarian syndrome and hypothalamic dysfunction are the most likely
causes of the amenorrhoea, the former being indicated by polycystic ovaries on
ultrasound scan. (high LH/FSH ration, high testosterone, low progesterone)
 If no withdrawal bleeding occurs, give oestrogen prior to MPA. A typical regimen would be
ethinyloestradiol, 50 mcg daily for 21 days with MPA 10 mg daily on days 16-21.
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Withdrawal bleeding indicates an oestrogen deficiency state. This may be due to
ovarian failure, indicated by raised FSH, or hypothalamic-pituitary failure.
No withdrawal bleeding after the oestrogen / progesterone regime indicates a
uterine disorder.
3) Differential diagnosis#2: The patient had a negative Provera challenge. How can this lead you
further in your diagnosis?
The fact that she did not have a withdrawal bleed in response to a Provera challenge provides
an important clue to hypoestrogenism:
1. The most likely diagnosis for young women with amenorrhea and a negative
progesterone challenge test is functional hypothalamic amenorrhea. This led to further
questions about her eating patterns, exercise regimen, and stress level at home and
work. However, the patient’s responses to these questions were unremarkable.
2. Another disorder, polycystic ovary syndrome was excluded since she had a negative
progestin challenge and did not have any signs or symptoms of polycystic ovary
syndrome, such as acne and hirsutism.
4) Differential diagnosis#3: Why values of TSH, Prolactin and FSH were ordered? What do they
indicate?
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When evaluating ovulatory disorders, initial testing in all patients should include a TSH,
prolactin, and FSH to exclude thyroid disease, hyperprolactinemia, and premature ovarian
failure, respectively.
The patient had no signs or symptoms of thyroid disease (weight changes, skin or hair
texture changes, heat or cold intolerance, bowel habit changes) or premature ovarian failure
(hot flushes, night sweats), and her TSH values were in the normal ranges. Low FSH
Prolacin levels were raised, suggesting hyperprolactinemia
5) Differential diagnosis#4: Besides prolactin levels, what other findings support
hyperprolactinemia as the diagnosis for this case?
The only positive physical exam finding was galactorrhea.
6) Differential diagnosis #5: a young intern at the hospital made a final diagnosis of
prolactinoma (prolactin secreting adenoma) induced secondary amenorrhea. He mentions three
findings supporting his diagnosis.
1. Increased prolactin levels
2. The patient’s history of increasing headaches in the setting of hyperprolactinemia raises
the possibility of a prolactin-secreting adenoma.
3. An MRI of the pituitary gland revealed a 2.7-cm mass
7) Differential diagnosis #6: The expert endocrinologist suggests the young intern is mistaken.
He mentions that: [A prolactin of greater than 200 ng/mL would be expected in the presence of a
mass >10 mm if this mass were a pure prolactin secreting adenoma. A prolactin of level of 42
ng/mL, as was seen in this patient, is more consistent with a nonfunctioning adenoma]
He mentions the Mild compression of the optic chiasm as a clue to the correct diagnosis.
Could you provide the final diagnosis of this case?
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Non-functioning adenoma compressing the optic chiasm, interfering with the normal tonic
inhibition mediated by hypothalamic dopamine on prolactin secretion by lactotrophs of the
anterior pituitary, thus leading to hyperprolactinemia
Amenorrhea was mediated possibly by:
1. Interference with normal GnRH stimulation of the pituitary .
2. Hyperprolactinemia can interfere with normal LH and FSH secretion by decreasing GnRH
pulse frequency.
8) Multiple choice questions:
1. Which of the following lab tests should you order when a patient presents with secondary
amenorrhea?
A. HCG
B. Prolactin
C. TSH
D. FSH
E. All of the above
Answer: E.
2. In a patient with amenorrhea and an elevated prolactin, which of the following would be the
next appropriate step?
A. Treat with a dopamine agonist.
B. Perform a pituitary MRI.
C. Treat with an oral contraceptive pill.
D. Treat with hormone replacement therapy.
Answer: B. It is essential that a patient with a persistently elevated prolactin level have a
neuroimaging study to rule out a large hypothalamic or pituitary tumor. Treatment with a
dopamine agonist will mask the symptoms and needs to be reserved for use after the cause of
the elevated prolactin has been ascertained. Oral contraceptives and hormone replacement will
likewise obscure the problem and may mask the appropriate diagnosis.
Case 2:
Chief complaint:
Absence of menstruation, hot flushes and anxiety.
History of patient illness:
A 32 year old female was referred to the hospital Endocrinology Department
for evaluation of amenorrhoea (absent menstruation). The patient was in
good health until eight months previous, when she started noticing scanty
menstruation followed by complete cessation two months later. One year
earlier, she had started experiencing occasional episodes of hot flushes and
anxiety. This had become more pronounced in the last four months. The
patient had been married for the past eight years, and had had two successful
pregnancies in this time, but reported loss of libido in the past one year. She
had no other medical history. Physical examination revealed fine wrinkles
under the eyes, and a thin dry skin; the remainder of the examination was
normal. There was no evidence of adrenal insufficiency or diabetes mellitus.
Family history:
Unremarkable for any reproductive disorders, thyroid disease, or infertility.
Lab values:
 Serum oestradiol level of 18 pg/ml (normal >25 pg/ml)
 Serum levels of LH and FSH: 57 mlU/ml and 40 mlU/ml respectively
(normal female 4–30 mlU/ml for both LH and FSH).
 Thyroid hormone levels were normal, and she did not test positive for
thyroid antibodies.
 Serum prolactin measurement revealed a normal level.
Medications:
Captopril.
Questions:
Question 1: Based upon the patient’s history, physical examination and
laboratory data, what is the most likely diagnosis of her condition?
This case is characterized by a low oestrogen level, associated with
increased levels of gonadotrophins (hypergonadotropic hypogonadism),
suggesting the ovaries as the most likely target of dysfunction. Usually, this
hormonal pattern, coupled with amenorrhoea, hot flushes of the skin and
anxiety, is only seen at the time of the menopause.
Question 2: How may this condition arise?
The patient is most likely suffering from a premature ovarian failure (POF),
leading to secondary amenorrhoea; [this refers to individuals who once
menstruated, but subsequently stopped menstruating; primary amenorrhoea
refers to patients who have never menstruated]. In about 20% of cases of
POF, the condition is due to specific autoimmune disease, accompanied by
the presence of serum antiovarian antibodies (causing accelerated oocyte
degeneration) or it may be part of a polyglandular autoimmune syndrome,
When POF is associated with POF, other autoimmune diseases are often present such as
hypothyroidism, diabetes mellitus and Addison’s disease.
Question 3: What would be the recommended therapy for this patient?
Ovulation can sometimes be temporarily restored with oral corticosteroid
treatment
however, in general the return of normal menses (and fertility) is unlikely. In
this case, the clinical symptoms of hypogonadism and the long-term risk of
osteoporosis warrant hormone replacement therapy (HRT). Since the uterus
is intact, oestrogens should be cycled with progestogens to induce regular
withdrawal menstruation (artificial periods) and to avoid endometrial
hyperplasia.
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