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Red colour indicates lesser value than normal

Yellow indicates Greater value
Blue indicates Normal value
Case 1
A 32-year married man presents to OPD with a complaint of infertility for>12 months
duration.He also complaints of headache, blurred vision, diplopia and weight gain. He denies any
past medical or surgical history of relevance. He is not taking any prescribed or over the counter
medications. Laboratory investigation revealed that he had oligospermia. His hormone
evaluation revealed:
FSH: 0.6 (1.4-15.4 IU/L)
LH: 0.8(1.2-7.8 IU/L)
Testosterone:<0.02 (2.8-8 ng/mL)
Prolactin:12000 (1.8-20 ng/mL)
Cortisol: 0.4 (6.2-14.4 µg/dL)
ACTH: 8.8 (7.2-63 pg/dL)
fT4:1.0ng/dL (0.8-2 ng/dL)
TSH: 2.05 (0.5-5 mIU/L)

Questions
1. What is the reason for decreased FSH, LH and testosterone level?
Prolactin has inhibitory effect(synthesis and secretion) on Gonadotropin releasing
hormone(By inhibiting pulsatile nature) so when it is increased there is less FSH and LH
and also LH is responsible for Testosterone secretion so less testosterone.
2. What is the reason for oligospermia?
FSH is responsible for spermatogenesis as there is less FSH there will be oligospermia
3. What is the difference in the synthesis of FSH and testosterone level?
● FSH stimulate spermatogenesis and LH stimulate testosterone release

● FSH secreted by Pituitary gland (Gonadotropes cells) while Testosterone is secreted by

Leydig cell
4. Why cortisol level is decreased?
Tumor compressing others cells so decreased function of Corticotropes in releasing
ACTH which stimulate Cortisol release.

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 5. What does the blood level of ACTH, T4 and TSH in lower level indicate?
Like wise other cells are also being compressed
6. What is your conclusion?
Prolactinoma(Secreting lactotropes adenoma)

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Case 2
A 43-year woman presented with a three-week history of vaginal bleeding. A vaginal mass was
seen on pelvic examination. Ultrasonography showed a thickened complex endometrial echo.
Vaginal and uterine biopsies were suggestive of choriocarcinoma. Laboratory investigations
showed,
β-hCG: 2,704,040 mIU/mL (non pregnancy< 5 mIU/mL)
TSH: 2.1 mIU/L (0.4 – 4.0 mIU/L)
fT3: 8.1 pmol/L (4-7.4 pmol/L)
fT4: 2.5 ng/dL (0.8-2 ng/dL)
Later on she was started with Methotrexate.

1. Why β-hCG was measured?

Some tumors(Choriocarcinoma) secretes HCG so to used as tumor marker we can use
beta HCG level.

2. Why her thyroid hormones levels were increased?Is there any association between
β-hCG and thyroid hormones?
Beta HCG weakly binds with TSH receptor causing more thyroid hormone release

3. Will you order β-hCG test again after the treatment? Give reason.
Yes after treatment if there is presence of any tumor which is secreting beta HCG is left
behind so I will test again.
4. What further test will you do in her vaginal and uterine biopsies to confirm
choriocarcinoma?
Microscopic examination, Biopsies, Immunohistochemistry
There may be presence of other germ cell tumor

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Case 3
A 57-year woman came to hospital with 2-day history of flu-like symptoms. The symptoms
included malaise, headache, vomiting, appetite loss, dizziness as well as neck and joint pain. She
had a history of hypothyroidism and was on adequate levothyroxine replacement.
In addition to her acute symptoms, the patient reported 20 kg of weight loss, lethargy, skin
darkening and intermittent abdominal pain over 12 months preceding the acute presentation.
Blood tests showed,

● Serum sodium level: 128 mmol/L (135–145 mmol/L),

● Serum potassium: 5.3 mmol/L (3.5–5.2 mmol/L),

● Fasting blood glucose level: 65 mg/dL (70-100 mg/dL)

● Morning cortisol: 147 nmol/L (200–700 nmol/L).

● Adrenocorticotropic hormone (ACTH): 220 pmol/L (2–11 pmol/L).

● A short ACTH stimulation test (Synacthen test) was performed; baseline cortisol was 123

nmol/L, with a response to 132 and 143 nmol/L at 30 min and 60 min.

Questions:

1. What is the relationship between cortisol and ACTH?

ACTH stimulate glucocorticoids to release Cortisol.

2. Why ACTH stimulation test is performed in this case?

To distinguish that the decreased in Cortisol is ACTH dependent or not.In normal person
there will be 2-3 fold increase in cortisol level.
So primary cause of adrenal insufficiency

3. Why her sodium decreased and potassium is increased?

As there is less action of aldosterone so less Na absorbed and less potassium is expelled.

4. Why her blood glucose level is low?

Gluco-corticoides causes glucose release by catabolic action as there is less Cortisol so
that leads to less glucose.

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 Why Weight loss in Patients?
If there is more ACTH there will be more MSH so,
MSH interact with MCR neurons in Arcuate nucleus in POMC/CART pathway so it
gives signal to inhibit food intake(Inhibits Appetite)

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Case 4
A couple was trying to conceive a baby since 1 year. To confirm the pregnancy, they were using
the pregnancy test kits. The wife used to test every month to confirm the pregnancy. Once, the
husband also thought of using the kit with his own urine sample which surprisingly came out to
be positive. They thought it was a mistake and tried with another kit. But it again came positive.
So, they went to hospital for doctor's consultation and there also the result was positive.

1. Which compound was being checked in pregnancy test?

Beta HCG

2. Why pregnancy test was positive in the husband’s urine sample?

Ectopic secretion of Beta HCG from choriocarcinoma
3. What could be the other reasons for?

In Embryonal carcinoma there is also increase in Beta HCG level

4. What other biochemical parameters would be elevated in this condition? What is the
rationale behind them?
In choriocarcinoma in male there is High Beta HCG secretion
OCT3/4, Cytokeratin, KIT can also be increased

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Case 5:

A 28‐year married male presented to an infertility clinic with complaints of fatigue and low libido.
Physical examination showed bilateral gynaecomastia and firm but small testes. His semen analysis
showed azoospermia. His blood tests reported as follows:

Test Result Reference Range

Prolactin 300 < 500 mU/L

LH 36 1.0 – 9.0 U/L

FSH 21 1.0 – 10.0 U/L

Testosterone 5 10 – 30 nmol/L

Estradiol 280 < 160 pmol/L

1. What is azoospermia? How does it occur? Which hormones are responsible for sperm production?
No sperm in semen,
Not production , autoimmune destruction, Genetic (Klinefilter’s syndrome)etc,
FSH, testestorone
2. Why was his prolactin measured? What does his prolactin level suggest?
Higher prolactin can also cause Gynaecomastia so to rule out that feature.This level suggest that
gynaecomastia, loss of libido is not due to prolactin abnormality
3. What do his high LH, FSH and Estradiol as well as low Testosterone levels suggest? What do these
results suggest as regards the cause of his infertility?
There may be problem in testis so other parameter are increased while testosterone is decreased.
4. What are the common causes of this type of infertility? What further investigation confirms the
case of this case?

● Klinefelter syndrome

● Cryptorchidism

● Orchitis

● Tumors

Karyotyping etc

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Workdev
Case 6:

A 46-year female visited the endocrine clinic with complaints of skin pigmentation, bruising, obesity,
hypertension and proximal muscle weakness. Her lab investigation results were as follow:

Serum sodium 140 mmol/L (135–145)

Serum potassium 3.0 mmol/L (3.5–5.0)

Blood Urea 25 mg/dL (10–45)

Serum Creatinine 1.1mg/dL (0.7–1.3)

Fasting blood glucose 225mg/dL (70–100)

24-hr Urinary free Cortisol 1700 nmol (100–350)

An overnight dexamethasone suppression test was performed:

Serum cortisol, 09.00 AM 969 nmol/L (180–720)

Serum cortisol 990 nmol/L (after low-dose 1 mg dexamethasone test)

ACTH 454 ng/L (20–80)

Questions:

1. Why were serum electrolytes measured? What does low potassium level suggest?
Cotisol has some mineralocorticoides activity also so low potassium.
2. Why were blood urea and serum creatinine measured?
Any kidney problem occuring
3. What is overnight dexamethasone suppression test? Why is it performed in this case?
Dexamethasone is given at night and it suppress the pituitary to secret ACTH, So there is other site
secretion (Ectopic)of ACTH
4. Why was fasting blood glucose performed and what does its high level suggest?
Fasting blood glucose high suggests high hepatic conversion to glucose.(Gluconeogenesis)
5. What is the change in protein metabolism?
Increased protein metabolism
6. Why 24-hr urinary free cortisol is preferred over serum cortisol?
The serum cortisol level is fluctuating with time so if we measure the cortisol level of whole day then
the deranged value at some time doesn’t affect the value of cortisol.
7. How do you interpret her cortisol and ACTH results?

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 .ACTH stimulates to secretes more cortisol

Case 7
A 20-year girl presented to emergency with pain abdomen and whole body weakness. Her vitals were
normal except for her blood pressure which was 90/60 mmHg. She had a short stature and her limbs
were muscular. Past medical history revealed that she had genital abnormalities such as the
hypertrophy of labia and clitoris after the birth. At the age of 5, there was pubic hair growth,
accompanied with gradually enlarged clitoris and labia, which were in rapid growth before 8. So far
there is no breast development neither any menstrual cramps. She was in full-term delivery. Her mother
had no obvious infection and no drug history of androgen during pregnancy.

Laboratory investigation revealed

Serum Sodium: 120 (135-145 mEq/L)

Serum Potassium: 5.8 (3.5-5.0 mEq/L)

Follicle-Stimulating Hormone (FSH) : 4.71 mU/L (2.5-10)

Luteinizing Hormone (LH): 8.54 mU/L (4.9-13)

Estradiol (E2): 48.05 ng/ml (19.5-144.2)

Testosterone (T): 358 ng/ml (14-76)

17-hydroxyprogesterone (17 OHP): 32.35 ng/ml (0.07-1.53)

Dehydroepiandrosterone (DHEA): 829 μg/dl (35-430)

Androstenedione: >10 ng/ml (0.3-3.5)

Adrenocorticotropic Hormone (ACTH): 252 ng/L (12-78)

Cortisol at 8 AM in the morning: 3.74 μg/dL (4.3-22.4)

Adrenal gland CT scan showed congenital bilateral adrenal hyperplasia.

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 1. What is the rationale behind adrenal hyperplasia?
Less cortisol, less inhibition ,More ACTH so stimulation to secrete more so Hyperplasia
2. Why blood pressure is low? Explanation for low sodium and high potassium

Less aldosterone release

3. What if the patient is male? What would be the difference in clinical features?
● More Masculization etc
4. What if the enzyme deficient is 11 β-hydroxylase deficiency?
● Cortisol will be less

● Overproduction of androgens causing Masculinnization and virilization

5. Why 17-hydroxyprogesterone, Dehydroepiandrosterone (DHEA) and

androstenedione are raised?

Pathway of testosterone formation is stopped so that these are increased.

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