Case presentation

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.

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

What is your differentials diagnosis?????

Investigations

BSL- 14.8

VBG:

PH- 7.35

PCO2- 32

PO2-67

Bicarb – 17 base Excess = -7

Sodium- 140

potassium- 3.6

Chloride- 99

Creat-28

Glu- 14.6

Lactate – 1.6

HB- 147

What do you think is the diagnosis ??

Need any other investigations????

How do you manage ?????

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

ECG

What do you want to do??????

What is your differentials????

Her bloods came back : T3 >46

Cortisol serum – 1000

B HCG – negative

Calcium and rest of her bloods – WNL

What is your diagnosis???

Hyper ThyroidismMeans 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.

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.

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)

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.

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).

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.

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.

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.

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%.

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 tetra-iodothyronine (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.

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.

Thank you