Thyroid disorders Part 1

Thyroid Disorders

1. Thyroid disorders..Part 1
Pratap Sagar Tiwari, MD
Lecturer, NMCTH

2. Anatomy
http://khalidalomari.weebly.com/blood-supply-and-venous-drainage.html

3. Vascular/Neural Anatomy
Superior thyroid artery  external carotid artery,
Inferior thyroid artery  thyrocervical trunk,
Thyroid ima artery  subclavian artery.
superior thyroid veins internal jugular vein,
Middle thyroid vein internal jugular vein
inferior thyroid veins  left brachiocephalic vein.
Lymphatic drainage : the lateral deep cervical lymph nodes and
the pre- and parathracheal lymph nodes.
Parasympathetic nerve input  superior laryngeal nerve and
recurrent laryngeal nerve.

4. Thyroid Histology
http://www.studyblue.com/notes/note/n/anatomy-lab-shit/deck/7511240

5. Histology
Follicles The thyroid is composed of spherical follicles
Inside the follicles there is follicular lumen. It is surrounded by
follicular cells and filled with colloid.
Colloid is rich in a protein called thyroglobulin.
Thyroid epithelial
cells
(or "follicular cells")
The follicles are surrounded by a single layer of thyroid
epithelial cells, which secrete T3 and T4.
Parafollicular cells
(or "C cells")
Scattered among follicular cells and in spaces between the
spherical follicles are another type of thyroid cell,
parafollicular cells, which secrete calcitonin.

6. Thyroid hormone synthesis

7. Thyroid hormone synthesis
•The thyroid secretes predominantly T
4 and only a small
amount of T
3.
•Approximately 85% of T
3
in blood is produced from T
4
by a
family of monodeiodinase enzymes which are active in
many tissues including liver, muscle, heart and kidney.
•T
4
can be regarded as a pro-hormone, since it has a longer
half-life in blood than T
3
(approx. 1 wk compared with
approx. 18 hrs).
•T4 binds and activates thyroid hormone receptors less
effectively than T
3
.
•T
4
can also be converted to the inactive metabolite, reverse
T
3
.

8. Thyroid Binding Globulin
•Most of the thyroid hormones in the blood are
attached to a protein called thyroid binding
globulin (TBG).
•If there is an excess or deficiency of this protein it
alters the T4 or T3 measurement but does not
affect the action of the hormone.
•If a patient appears to have normal thyroid
function, but an unexplained high or low T4, or
T3, it may be due to an increase or decrease of
TBG.

9. Radioactive iodine uptake (RAIU) test
•A low uptake of tracer by the thyroid gland:
hyperthyroidism is caused by inflammation of the
thyroid gland (thyroiditis) or taking too much thyroid
medicine.
•A high uptake of tracer (spread evenly in the thyroid
gland): hyperthyroidism is caused by Graves' disease.
•An uneven spread of tracer in the thyroid gland (with
either low or high areas of uptake) :hyperthyroidism is
caused by a multinodular goiter or a noncancerous
(benign) tumor called a toxic adenoma.

10. •Thyroid Ultrasound: solid vs cyctic
•Thyroid Scan: hot vs cold
•Thyroid Needle Biopsy
•Thyroid Antibodies(anti-TG, anti-TPO):
hashimoto
•TSI Test: Graves’ disease

11. Interpretation
T3 T4 TSH State
↔ ↔ ↔ Euthyroid
↑ ↑ ↓ Primary hyperthyroidism
↓ ↓ ↑ Primary hypothyroidism
↓ ↓ ↓ Secondary hypothyroidism
↑ ↑ ↑ Secondary hyperthyroidism
↔/↑ ↔/↑ ↔ Euthyroid hyperthyroxinemia
↔/↓ ↔/↓ ↔ Euthyroid hypothyroxinema
↔ ↔ ↑ Subclinical hypothyroidism
↔ ↔ ↓ Subclinical hyperthyroidism

12. Thyrotoxicosis
•Thyrotoxicosis describes a constellation of
clinical features arising from elevated
circulating levels of thyroid hormone.
•The most common causes are Graves'
disease, multinodular goitre and
autonomously functioning thyroid nodules
(toxic adenoma).

13. Interpretation

14. Thyrotoxicosis: causes
Common causes
Graves' disease Iodide-induced (amiodarone, contrast)
Multinodular goitre Extrathyroidal source
Factitious thyrotoxicosis
Struma ovarii
Solitary thyroid adenoma TSH-induced
TSH-secreting pituitary adenoma
Choriocarcinoma and hydatidiform mole
Thyroiditis (de Quervain's or
Postpartum)
Follicular carcinoma ± metastases

15. Thyrotoxicosis
Symptoms SIgns
Weight loss despite normal or increased
appetite
Weight loss
Tremor
Heat intolerance Palmar erythema
Palpitations Sinus tachycardia
Dyspnoea Lid retraction, lid lag
Irritability, emotional lability
Fatigue, Sweating, Tremor
Less common
Osteoporosis, Diarrhoea, steatorrhoeaGoitre with bruit
,
Atrial fibrillation, HF
Muscle weakness, Pruritus, Ankle swelling
Alopecia
Systolic hypertension/increased pulse
pressure
Amenorrhoea/oligomenorrhoea
Infertility, spontaneous abortion
Hyper-reflexia, Ill-sustained clonus, Proximal
myopathy

16. Jod-Basedow phenomenon
•is hyperthyroidism following administration of
iodine or iodide, either as a dietary
supplement or as contrast medium.
•This phenomenon is thus iodine-induced
hyperthyroidism, typically presenting in a
patient with endemic goiter (due to iodine
deficiency).

17. Graves' disease
•is a syndrome that may consist of hyperthyroidism,
goiter, eye disease (orbitopathy), and occasionally a
dermopathy referred to as pretibial myxedema.
•Hyperthyroidism is the mc feature of GD, affecting
nearly all patients, and is caused by autoantibodies to
the thyrotropin (TSH) receptor (TSHR-Ab)
•TSHR-Ab activate the receptor, thereby stimulating
thyroid hormone synthesis and secretion as well as
thyroid growth (causing a diffuse goiter).
•The presence of TSHR-Abs in serum and orbitopathy
on clinical examination distinguishes the disorder from
other causes of hyperthyroidism.

18. Treatment options
Therapy Advantages Disadvantages
Thionamides
Methimazole
Carbimazole
Propylthiouracil
Chance of
permanent
remission
rash, arthralgias, GI,
agranulocytosis, vasculitis
(lupus-like syndrome),
hepatitis (PTU)
Radioiodine Permanent
resolution of
hyperthyroidism
Permanent hypothyroidism
oncogenic effects of radiation
Surgery Rapid,
permanent cure
of
hyperthyroidism
Permanent hypothyroidism
Risk of hypoparathyroidism,
recurrent laryngeal nerve
damage.

19. Antithyroid drugs
1.carbimazole
2.methimazole
3.Propylthiouracil
•reduce the synthesis of new thyroid hormones
by inhibiting the iodination of tyrosine.
•Carbimazole also has an immunosuppressive
action, leading to a reduction in serum TSHRAb
concentrations.
•CI: Breastfeeding (propylthiouracil suitable)

20. B blockers
•HT is a/w an increased number of ß-adrenergic receptors . The
ensuing increase in ß-adrenergic activity is responsible for many of
the symptoms .
•It also explains the ability of ß-blockers to ameliorate rapidly many
of the symptoms, including palpitations, tachycardia,
tremulousness, anxiety, and heat intolerance .
•Propranolol in high doses (above 160 mg/day) also slowly
decreases T3 concentrations by as much as 30 % , via inhibition of
the 5'-monodeiodinase that converts T4 to T3.
•Start with atenolol 25 to 50 mg daily, and increase the dose as
needed (up to 200 mg daily) to reduce pulse to under 90 bpm if bp
allows.
•Patients should have their thyroid function assessed at 4-6 wks
intervals until stabilized on maintenance thionamide therapy.

21. Iodinated contrast agents and iodine
•The oral radiocontrast agents sodium ipodate
and iopanoic acid are potent inhibitors of the
peripheral conversion of T4 to T3.
•When given in combination
with methimazole (at doses of 500 to 1000
mg/day), they can rapidly ameliorate severe
hyperthyroidism and can also be used to
prepare a hyperthyroid patient for early
surgery.

22. Thyrotoxicosis in pregnancy
•Propylthiouracil may be preferable to
carbimazole since the latter might be
associated with a skin defect in the child,
known as aplasia cutis.
•In order to avoid fetal hypothyroidism and
goitre, it is important to use the smallest dose
of antithyroid drug (optimally < 150 mg /d)
that will maintain maternal (and presumably
fetal) free T
4
, T
3
and TSH WNR.

23. Graves' ophthalmopathy
(orbitopathy)
•The eye disease often associated with Graves' thyroid
disease is referred to as Graves' ophthalmopathy.
•This condition is immunologically mediated.
•Within the orbit (and the dermis) there is cytokine-mediated
proliferation of fibroblasts which secrete hydrophilic
glycosaminoglycans.
•The resulting increase in interstitial fluid content, combined
with a chronic inflammatory cell infiltrate, causes marked
swelling and ultimately fibrosis of the extraocular muscles
and a rise in retrobulbar pressure.
•The eye is displaced forwards (proptosis/ exophthalmos) and
in severe cases there is optic nerve compression.

24. Features
•Ptosis, pseudo ptosis, strabismus (hypotropia,
esotropia)

25. Mobius sign (poor convergence)Mobius sign (poor convergence)

26. 26
Ballet signBallet sign
–restriction of one or more extra ocular musclesrestriction of one or more extra ocular muscles
–Initially due to edema , later fibrosis Initially due to edema , later fibrosis
–All 4 recti are involved but mainly IR and MRAll 4 recti are involved but mainly IR and MR

27. 27
Restrictive myopathy
Elevation defect Abduction defect
Depression defect Adduction defect

28. 28
•Upper lid retraction (Dalrymple sign) Upper lid retraction (Dalrymple sign)
-90%-90%

29. 29
Mechanisms for upper lid retraction
Up gaze restriction Proptosis
Fibrotic contracture of LPS
Secondary over action of LPS-SR complex
Muller muscle over action

30. 30
Signs of eyelid retraction
• Bilateral lid retraction
• No associated proptosis
• Bilateral lid retraction
• Bilateral proptosis
• Lid lag in downgaze
• Unilateral lid retraction
• Unilateral proptosis

31. 31
Lid lag on down gaze
(von Graefe’s sign)

32. 32
Glabellar furrows Eyelid edema

33. 33

Stellwag sign (incomplete and infrequent blinking) Stellwag sign (incomplete and infrequent blinking)
Goffroy sign (absent creases in the forehead on superior gaze) Goffroy sign (absent creases in the forehead on superior gaze)
Enroth’s sign (eyelid fullness) Enroth’s sign (eyelid fullness)
Gifford’s signGifford’s sign
(difficulty in upper lid eversion )(difficulty in upper lid eversion )

34. 34
Minimal staining
Ulceration
perforation
Corneal signs

35. Assessment of severity
•Class 0 — No symptoms or signs
•Class I — Only signs, no symptoms (eg, lid
retraction, stare, lid lag)
•Class II — Soft tissue involvement
•Class III — Proptosis
•Class IV — Extraocular muscle involvement
•Class V — Corneal involvement
•Class VI — Sight loss (optic nerve involvement)

36. End of slides
References:
•Davidson 21
st
•Uptodate 20.3
•Medscape
•Wikipedia
•Eye signs pics taken from slides of :
THYRIOD EYE DISEASE Dr. Gyanendra
Lamichhane,Lumbini Eye Institute,Bhairahawa
,Nepal