3. CRETINISM
▶ Inadequate thyroid hormone during foetal and neonatal
development
▶ Two types
▶ Endemic - Due to dietary iodine deficiency
▶ Sporadic - Due to either an inborn error of thyroid
metabolism or complete or partial agenesis of the
gland.
9. LAB FINDINGS
▶ Thyroid function tests
▶ Low T4 and T3 levels with a high TSH
▶ High serum levels of TPO antibodies are characteristic of
autoimmune disease.
10. TREATMENT
▶ Oral thyroxine (0.1 – 0.2 mg) as a single daily dose is curative.
▶ Triiodothyronine(20 μg three times a day) , if rapid response is
required
11. MYXOEDEMA
▶ Adult onset severe hypothyroidism
▶ The signs and symptoms of hypothyroidism
are accentuated
▶ Facial appearance is typical
Supra clavicular puffiness
Malar flush
A yellow tinge to the skin
12. ▶ Myxoedema coma -
Altered mental state
Hypothermia
Precipitating medical condition - cardiac failure or infection
High mortality rate
13. TREATMENT
▶ Thyroid replacement, either as a bolus of 0.5 mg of T4 or 10 μg of
T3 either i.v / orally every 4–6 hrs
▶ Body Temp <30oC - warmed slowly
▶ IV broad spectrum antibiotics and Hydrocotisone (divided doses)
14. DYSHORMONOGENESIS
Genetic deficiencies in the enzymes controlling the synthesis of
thyroid hormones
▶ Inherited as autosomal recessive
▶ Family history is common
▶ If biochemical effect is of moderate degree, Thyroid enlargement
may be the only manifestation
▶ Most common abnormalities affect TPO activity and thyroglobulin
synthesis.
▶ Eg: Pendred’s syndrome – goitre + severe sensorineural hearing loss
+ abnormality of bony labyrinth
18. SIMPLE GOITRE
▶ Aetiopathogenesis -
▶ Stimulation due to increased TSH Decreased level of
circulating thyroid hormones or due to inappropriate secretion
from a microadenoma in ant. Pituitary.
▶ MC factor is dietary deficiency of iodine (endemic goitre)
▶ Following are causes of such goitre:
▶ Endemic goitre -iodine deficiency
▶ Dyshormonogenesis or Enzyme deficiency
▶ Goitrogens – vegetables of brassica (cabbage)
19. Stages of goitre formation
▶ Initially Persistent growth stimulation – diffuse hyperplasia
▶ Later Fluctuating stimulation – mixed pattern with areas of active
lobules and inactive lobules
▶ Active lobules – become more vascular & hyperplastic –
hemorrhage occurs– central necrosis
▶ Necrotic lobules coalesce – nodules filled with iodine free colloid or
mass of new but inactive follicles
▶ Continual repetition of process – results in nodular goitre
20. DIFFUSE HYPERPLASTIC GOITRE
▶ Corresponds to first stage of natural history
▶ Goitre in childhood usually seen in endemic areas,
sporadic cases usually occurs in puberty
▶ Goitre is soft, diffuse, large enough to cause
discomfort
▶ Colloid goitre occurs in late stage when TSH
stimulation has fallen off
21. MULTINODULAR GOITRE
▶ C/P - Females-late 30s or 40s-multiple
palpable nodules
▶ Occasionally a solitary nodule may be
palpable but there are multiple small
nodules impalpable.
▶ Nodules may be colloid or cellular, cystic
degeneration and hemorrhage.
22. COMPLICATIONS
▶ Secondary thyrotoxicosis – in about 30% nodular goitre.
▶ Tracheal obstruction – huge goitres or substernal prolongation of
goitre
▶ Carcinoma (usually follicular)
23. Investigations
▶ Thyroid Function Tests
▶ Isotope scan-to differentiate hot and cold nodules.
▶ USG
▶ FNAC
▶ Core biopsy
▶ CT and MRI
▶ Thyroid autoantibodies
▶ Chest radiography
24. TREATMENT
▶ Most patients are asymptomatic and do not need operation
▶ Operation may be indicated on cosmetic grounds, for pressure
symptoms, or in response to patient anxiety
▶ Choice of surgery
▶ Total thyroidectomy
▶ Subtotal thyroidectomy
▶ Total lobectomy
25. SOLITARY NODULE THYROID
▶ Isolated thyroid swelling
▶ Isolated , confined to one or other lateral lobe or to
isthmus.
▶ Mostly they are SNG formed by inactive colloid or
apparently localized manifestations of simple MNG.
▶ Also include-#neoplastic - benign/malignant
#cysts
#localised chronic lymphocytic
thyroiditis.
26. THYROID CYSTS
▶ Routine FNAC shows that >30% of clinically isolated swellings
contain fluid-are cystic or partially cystic.
▶ Tense cysts – hard &mimic carcinoma
▶ Bleeding into cysts- acute painful swelling.
▶ 50% as a result of colloid degeneration or of uncertain etiology like
absence of epithelial cells in the lining.
▶ C/P- In women aged 20-40 yrs - as discrete swellings
▶ Appropriate investigation : FNAC
27. RETROSTERNAL GOITRE
▶ Arise from lower pole of nodular goitre, from ectopic thyroid tissue.
▶ If neck is short and pretracheal muscles are strong , -ve intrathoracic
pressure tends to draw the goitre into the superior mediastinum.
▶ Obstructive symptoms - dyspnea, cough and stridor, dysphagia,
engorgement of neck veins, recurrent nerve paralysis
▶ Xray- soft tissue shadow in superior mediastinum, deviation and
compression of trachea
29. CHRONIC LYMPHOCYTIC THYROIDITIS
▶ Autoimmune disease - HASHIMOTO’S DISEASE
▶ Raised titres of thyroid antibodies.
▶ C/P : diffuse or nodular with a characteristic bosselated feel or
subclinical thyroid failure.
▶ Onset may be insidious and asymptomatic or sudden and painful.
▶ Initially mild hyperthyroidism later hypothyroidism
▶ Goitre is usually lobulated ; diffuse or localised to one lobe.
▶ Large or small ; soft , rubbery or firm in consistency- depending on
cellularity and degree of fibrosis.
▶ Mc –women at menopause
▶ DIAGNOSIS- Raised serum levels of one or more thyroid antibodies,
FNAC, diagnostic lobectomy
30. SUBACUTE THYROIDITIS
▶ Granulomatous thyroiditis ; de Quervain’s thyroiditis.
▶ May follow viral infection
▶ C/F: pain in neck , fever , malaise and firm, irregular enlargement of
one or both thyroid lobes
▶ Raised inflammatory markers , absent thyroid antibodies , serum T4
is slightly raised
▶ Self limiting - a period of months of hypothyroidism may be present
before eventual recovery
▶ DIAGNOSIS - FNAC , radioactive iodine uptake and by rapid
symptomatic response to prednisolone.
▶ TREATMENT- PREDNISOLONE 10-20mg daily for 1 week & then
gradually reduced dose over next month
31. REIDEL’S THYROIDITIS
▶ Very rare - 0.5% of goitres.
▶ Thyroid tissue replaced by cellular fibrous tissue - infiltrates through
capsule into muscle and adjacent structures including parathyroid,
recurrent nerves, carotid sheath.
▶ Probably a collagen disease
▶ Goitre may be U/L or B/L - very hard and fixed
▶ TREATMENT-High dose steroid, tamoxifen, thyroxine replacement
33. HYPERTHYROIDISM
▶ Hyperthyroidism –term used for over production of thyroid
hormones
▶ Pathology is in thyroid gland itself
▶ Hyperthyroidism is one of the causes of thyrotoxicosis
▶ Thyrotoxicosis is symptom complex due to increased levels of
thyroid hormones
▶ It refers to biochemical and physiological manifestations of
excessive thyroid hormones
35. Diffuse toxic goitre (Grave’s Disease)
▶ A Diffuse vascular goitre appearing at the same time as the
hyperthyroidism, usually occurs in younger women and is frequently
associated with eye signs.
▶ The syndrome is that of primary thyrotoxicosis
▶ 50 % family history of autoimmune endocrine diseases.
▶ Thyroid stimulating immunoglobulins and long acting thyroid
stimulator are responsible for pathological changes.
▶ Whole functioning thyroid tissue is involved
▶ Hypertrophy and hyperplasia due to abnormal thyroid stimulating
antibodies (TSH-RAb) that bind to TSH receptor sites and produce a
disproportionate and prolonged effect
36. TOXIC NODULAR GOITRE
▶ Simple nodular goitre is present for a long time before the
hyperthyroidism, usually in the middle-aged or elderly, and very
infrequently associated with eye signs
▶ The syndrome is that of secondary thyrotoxicosis.
▶ In many cases- nodules are inactive
▶ Inter nodular thyroid tissue – over active
▶ However, in some toxic nodular goitres, one or more nodules are
overactive and here the hyperthyroidism is due to autonomous
thyroid tissue as in a toxic adenoma
37. TOXIC NODULE
▶ A solitary overactive nodule
▶ It may be part of a generalised nodularity or a true toxic adenoma.
▶ It is autonomous and its hypertrophy and hyperplasia are not due
to TSH-R Ab.
▶ TSH secretion is suppressed by the high level of circulating thyroid
hormones and the normal thyroid tissue surrounding the nodule is
itself suppressed and inactive.
38. Symptomatology
▶ 8 times more common in women
▶ Significant symptoms- loss of weight despite good appetite, recent
preference for cold, and palpitations
▶ Significant signs- excitability of patient, presence of goitre, exophthalmos,
tachycardia or cardiac arrhythmia
▶ Primary thyrotoxicosis- goitre is diffuse and vascular, large or small, firm or
soft, onset is abrupt, a thrill and a bruit may be present,
▶ Secondary thyrotoxicosis- goitre is nodular, onset is insidious, may present
with cardiac failure or atrial fibrillation
40. EYE SIGNS
LID RETRACTION
▶ Over activity of involuntary part of the levator palpebrae superioris
muscle.
▶ The upper eye lid is higher than normal and the lower eyelid is in its
normal position
Exophthalmos
▶ When eyeball is pushed forwards due to increase in fat or oedema
or cellular infiltration in the retro orbital space the eyelids are
retracted and sclera becomes visible below the lower edge of the
iris first followed by above the upper edge of the iris
41.
42. ▶ Von Graefe's sign.— The upper eyelid lags behind the eyeball as the
patient is asked to look downwards.
▶ Stellwag's sign — This is staring look and infrequent blinking of eyes with
widening of palpebral fissure
▶ Joffroy’s sign – absence of wrinkling on forehead when patient looks up
with head bent down.
▶ Moebius' sign — Inability or failure to converge the eyeballs.
▶ Dalrymple's sign— The upper sclera is visible due to retraction of upper
eye lid
▶ Ophthalmoplegia
▶ Chemosis, papilloedema, corneal ulcer
43. ▶ Cardiac manifestations
▶ Multiple extrasystoles, paroxysmal atrial tachycardia, paroxysmal
atrial fibrillation, persistent atrial fibrillation
▶ Myopathy
▶ Proximal muscle weakness
▶ Pretibial myxoedema
▶ Bilateral, symmetrical, shiny red, thickened dry skin with coarse
hair in feet and ankles
▶ Usually in areas of trauma , by deposition of hyaluronic acid in
dermis and subcutis
45. ▶ Radioisotope study – I123 more uptake – hot nodules
▶ TRH estimation
▶ ECG- cardiac involvement
▶ Total count and neutrophil count
▶ Thyroid antibody estimation
46. TREATMENT
▶ Relief of symptoms
▶ Beta blocker- control cardiovascular manifestation
▶ Calcium channel blocker
▶ Oral rehydration
▶ Antithyroid drugs
▶ Methimazole 20 – 40 mg OD (blocks thyroid hormone synthesis)
▶ Carbimazole 5-10 mg three times a day
▶ Propyl thiouracil 200 mg three times a day (blocks thyroid
hormone synthesis as well as blocks peripheral conversion of T4
to T3)
▶ Iodides – reduce vascularity
▶ Steroids
47. ▶ Radioactive iodine therapy – I131
▶ Destroys cells and cause complete ablation of thyroid gland
▶ Usual dose- 5 to 10 millicurie or 160 microcurie/gm of thyroid
▶ Surgery
▶ Total thyroidectomy
▶ Subtotal thyroidectomy
▶ Hemithyroidectomy
