Endocrine conundrum

1. Case presentation

2. Case history
24 F presented with vomiting , diarrhea , lethargy for
the period of 6 weeks.
No travel, Nil fever, Not on any medications.
Recent history of boyfriend separation , Hx of
anxiety.
Has visited her GP 3 weeks ago was started on
antidepressant but did not take it.
Her GP died the week ago so did not visit her.

3. On examination- lean , sick looking, constant
vomiting, not settling down on the bed, rolling
around, sunken eyes, wants to drink water
Vitals- PR- 140/min, regular, BP- 110/66mmhg
Systemic exam- tachycardia, rest WNL
Rest of her examination- unremarkable
Has about 5% dehydration

4. What is your differentials diagnosis?????

5. Investigations
BSL- 14.8
VBG:
PH- 7.35
PCO2- 32
PO2-67
Bicarb – 17
Sodium- 140
potassium- 3.6
Chloride- 99
Creat-28
Glu- 14.6
Lactate – 1.6
HB- 147
base Excess = -7

6. What do you think is the diagnosis ??
Need any other investigations????
How do you manage ?????

7. After 2 hrs of treatment she settled well, but her HR was still 140/minute, she looked
more confortable, and she is more alert, and cheerful.
RPT VBG- PH-7.35
PCO2- 32
PO2 -70
Bicarb -17
sodium-134
potas- 4.1
Glu-9.3
Lact- 0.6

8. ECG

9. What do you want to do??????
What is your differentials????

10. Her bloods came back : T3 >46
Cortisol serum – 1000
B HCG – negative
Calcium and rest of her bloods – WNL
What is your diagnosis???

12. Hyper Thyroidism
Means overactive thyroid and produces free thyroid
hormones ,T3 and or T4
Grave’s disease is the most common cause of
hyperthyroidism.
This is one cause of thyrotoxicosis.
The management and therapy differ for
thyrotoxicosis from hyperthyroidism and
thyrotoxicosis caused by other conditions.

13. Explanation
• Thyroglobulin is synthesized in the rough endoplasmic reticulum and follows the secretory pathway to enter the colloid in the lumen of the thyroid follicle by
exocytosis.
• Meanwhile a sodium – iodine (Na/I) symporter pumps Iodide (I-) actively into the cell, which previously has crossed the endothelium by largely unknown
mechanisms.
• This iodide enters the follicular lumen from the cytoplasm by the transporter pendrin, in a purportedly passive manner.
• In the colloid, iodide (I-) is oxidized to iodine (I0) by an enzyme called thyroid peroxidase
• Iodine (I0) is very reactive and iodinates the thyroglobulin at tyrosyl residues in its protein chain (in total containing approximately 120 tyrosyl residues).
• In conjugation, adjacent tyrosyl residues are paired together.
• The entire complex re-enters the follicular cell by endocytosis.
• Proteolysis by various proteases liberates thyroxine and triiodothyronine molecules, which enter the blood by largely unknown mechanisms.

14. Clinical features of hyperthyroidism
Skin- sweating, heat intolerance, onycholysis ,
hyperpigmentation, Pruritus and hives
Vitiligo , alopecia areata, thinning of hair.
Eyes – Stare and lid lag, only Grave’s patients have
opthalmopathy – inflammation of the extra ocular
muscles and orbital fat and connective tissue, which
results in proptosis, impairment of eye muscle and
conjunctival edema.
CVS – Increased cardiac output, PR- high, Pulse pressure is
widened, PVR is decreased, High or normal output CCF can
occur on these patients.
AF can occur in 10-20% of people ( role of anticoagulation)

15. Metabolic/endocrine:
Serum lipids- low serum total and HDL.
Hyperglycemia – Associated with both increased
sensitivity of pancreatic beta cells to glucose,
resulting in increased insulin secretion and
antagonizing to the peripheral action of insulin.
Which will result in impaired GTT.
Adrenal Function – CBG will decrease resulting in
lower total serum cortisol concentrations.
Respiratory – Dyspnea on exertion , pulmonary
arterial systolic pressure is increased.
GIT – weight loss, hyper metabolism, and increased
gut motility, diarrhea.

16. Hematologic – RBC mass is increased , with the plasma
volume is increased too, they can be prothrombotic ( rise in
factors VIII, IX, Fibrinogen, Von willibrand factor, and
plasminogen activator, inhibitor.
Genitourinary – urinary frequency and nocturia.
Bone – stimulates bone resorption so indirectly serum
calcium level may increase.
Neuropsychiatric – may experience behavioral and
personality changes (psychosis, agitation and depression).

17. Diagnosis
Clinical features
Laboratory – Low or undetectable TSH with very high T3 and
T4.
The patient will need a 24 hr radioiodine uptake and scan.

19. If TSH is low and only serum T3 is high, then the
patient most likely has Graves disease or an
autonomously functioning thyroid adenoma.
If TSH is low , Free T4 is high, and T3 is normal –
patient may have hyperthyroidism with concurrent
nonthyroidal illness, amiodarone induced thyroid
dysfunction.
If Free T4 and T3 are elevated and serum TSH is
normal or elevated, then we need MRI as it may be a
pituitary tumor.

20. Thyroid storm
Thyrotoxic crisis (or thyroid storm) is a rare but severe
complication of hyperthyroidism, which may occur when a
thyrotoxic patient becomes very sick or physically stressed.
Its symptoms can include: an increase in body temperature to
over 40 degrees Celsius (104 degrees Fahrenheit), tachycardia,
arrhythmia, vomiting, diarrhea, dehydration, coma, and death.
Thyroid storm requires prompt treatment and hospitalization.
The main treatment is to decrease the circulating thyroid
hormone levels and decrease their formation.

21. Propylthiouracil and methimazole are two agents that decrease
thyroid hormone synthesis and are usually prescribed in fairly
high doses.
To inhibit thyroid hormone release from the thyroid gland,
sodium iodide, potassium iodide, and/or Lugol's solution can be
given.
Beta blockers such as propranolol can help to control the heart
rate, and intravenous steroids may be used to help support the
circulation.
Earlier in the 20th century the mortality of thyroid storm
approached 100%. However, now, with the use of aggressive
therapy as described above, the death rate from thyroid storm is
less than 20%.

22. Anti thyroid drugs
Thyrostatics are drugs that inhibit the production of thyroid hormones such
as CARBIMAZOLE, METHAMIZOLE and PROPYLTHIOURACIL.
Thyrostatics are believed to work by inhibiting the iodination of
thyroglobulin by thyroperoxidase, and, thus, the formation of tetraiodothyronine (T4).
Propylthiouracil also works outside the thyroid gland, preventing
conversion of (mostly inactive) T4 to the active form T3.
Thyroid tissue usually contains a substantial reserve of thyroid hormone,
thyrostatics can take weeks to become effective, and the dose often needs
to be carefully titrated over a period of months, with regular doctor visits
and blood tests to monitor results.
A very high dose is often needed early in the treatment.

23. Beta blockers
Propranolol – has two roles two different isomers
L propranolol – causes beta blockade
D propranolol – inhibits Thyroxin deiodinase there by blocking
the conversion of T4 to T3.
Food and diet – not to have food enriched in iodine
Surgery – Thyroidectomy.
Radioiodine - common outcome following radioactive iodine
therapy is a swing from hyperthyroidism to simple treatable
hypothyroidism.

24. Thank you