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Thyroid:
Physiology:

∆ Follicular Epithelial Cells Synthesize Thyroid Hormone:

On The Surface of Thyroglobulin(A protein Secreted into colloid):
Iodine + Tyrosine --> T4 Mainly
∆ In Blood : T4 --> T3
∆ T4 Half Life = 1 week
∆ T3 Half Life = 18 hrs
∆ T3 MORE Effective in binding and activating receptors
∆ T3 and T4 BOUND in PLASMA with Thyroxine Binding Globulin (TBG)
∆ EFFECT is only of UNBOUND Thyroid Hormone
∆ Main Significance is of FREE T3 and T4 (In investigations)
∆ Significance of FREE T3 and T4:
Suppose patient is taking OCPs
OCPs have Estrogen
↑ Estrogen → ↑ TBGs → ↑ in total T3 and T4
While FREE T3 T4 remain NORMAL
∆ Hypothalamic TRH → Anterior pituitary TSH → T3 and T4
∆ TSH is the MOST IMP investigation (b/c anterior pituitary is v sensitive to levels of T4 T3)
But T4 and T3 (Free) MUST Always be considered as well

Pharmacology:
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Pathology:
i)Hyperthyroidism
a)Graves Disease
b) Multinodular Goitre
c)Toxic Adenoma
d) Thyroiditis

Clinical Features:
I)Wt Loss
ii) Inc Apetite
iii) Heat Intolerance
iv) Palpitations
v) Tremors
vi) Irritability
vii) Palmar Erythma(Vasodilation), Lid lag(Common)
viii) Graves – Diffuse Soft Goitre
ix)Irregularly enlarged MNG
Lid Lag Pathophysiology: Sympathetic Innervation of levator palpebrae ↑
x) Graves : Periorbital Edema, Conjunctival Irritation, Exophthalmos, Diplopia, Pretibial
Myxedema
Pathophysiology of eye signs:
a)Orbital fibroblasts have TSH and IGF-1 receptors, which are directly stimulated by thyroid-stimulating
immunoglobulins (TSIs). There is an enhanced
proliferation of orbital fibroblasts as a consequence, which eventually causes extensive fibrosis in the
orbit
b) TSI also mediates the differentiation of orbital fibroblasts into adipocytes and
myofibroblasts. A state of hyperproliferation of adipocytes and myofibroblasts
increases periorbital soft tissue volume
c) Also, orbital fibroblasts exhibit an exaggerated inflammatory response in the setting of TSI-TSH
receptor interaction. There is an accumulation of extracellular
matrix in the setting of this pro-inflammatory milieu, which leads to soft tissue
edema and proptosis

Upper Lid Retraction:

a)Muller’s muscle (superior tarsal muscle) under the sympathetic stimulation of excess circulating
thyroid hormones contracts and contributes to lid retraction
B)Due to extensive orbital inflammation, the levator palpebrae superioris is infiltrated by inflammatory
cells, which leads to fibrosis and contraction of the muscle
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Xi)Tachycardia
Investigations:
A) BIOCHEMICAL:
I)First Line:
Serum T3, T4 , TSH Hira_Fj'23
ii) T3 and T4 elevated
but T4 is in upper part of ref range
T3 is raised
This is in T3 Toxicosis
iii)TSH raised in sec thyrotoxicosis(Pituitary adenoma producing tsh), Not in primary
B) TSH Receptor Ab I.e TRAb
C) If Ab unavailable, go for Radio isotope Scanning or Technitium Scintigraphy scan
D) ECG Showing atrial fib or sinus tachy

Factitious Thyrotoxicosis: Consuming Levothyroxine or thyroid prep

Management: (Stepup)
I) Anti thyroid Drugs
ii) Radioactive Iodine
iii) Surgery
iv) Beta Blocker (Propranolol 160mg daily)
STEP UP:

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Methimazole preferred
THYROID STORM:
∆ Clinical:
Fever, Agitation, Delirium, tachy and atrial fib.
∆ Due to infection In patient of hyperthyroidism
∆ Or After Thyroidectomy
∆ Or after Radioactive Iodine therapy
∆ Rxn:
I)Rehydration
ii)Propranolol(80mg 4x daily)
iii)Glucocorticoids (Hydrocortisone 100mg IV every 8 hrs)
Iodine
iv)Sodium Ipodate (500mg / daily /Orally)will restore T3 levels in 48-72 hrs/ potassium iodide/
lugol soln.
v)Propylthiouracil (200mg every 4 hrs)
Propythiouracil inhibits conversion of T4 to T3 but carbimazole doesn’t

GRAVES DISEASE:
∆Women aged 30-50 yrs
∆Pathophysiology:
IgG Ab --> Against TSH receptor --> stimulate thyroid hormone production + proliferation of
follicular cells --> Goitre
∆TSH Receptor Ab = TRAb Hira_Fj'23
∆Genetic
∆Management:

∆ Start with anti thyroid drugs --> then radioactive iodine or surgery if relapse
∆Anti thyroid Drugs --> Inhibit iodination of tyrosine
∆Doses:
Carbimazole 40-60mg/ daily
Propylthiouracil 400-600mg / daily
Euthyroid after 6-8 wks
∆Prior to surgery give oral potassium iodide 60mg / 3 times daily for 10 days (To inhibit thyroid
hormone synthesis and reduce size and vascularity of gland
∆With radioactive iodine pt. Develop hypothyroidism

HYPOTHYROIDISM:
∆Hashimoto Thyroiditis
∆Thyroid Failure after radioactive iodine surgery or surgical treatment of hyperthyroidism
Clinical Features:
Accumulation of Mucopolysaccharides in Tissues
I)Low pitched Voice
ii)Poor hearing
iii) Slurred speech due to large tongue
iv)Carpal tunnel syndrome( compressed median nerve at wrist)
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v)Non pitting edema (myxedema)
vi)Periorbital puffiness
vii)Facial palor
viii) tiredness, wt gain

Investigations:
i)Low T4, elevated TSH (>20mlU/L)
ii)Thyroid Peroxidase Ab
iii)ECG – Sinus Brady
Management:
I)Levothyroxine 1.6 micro gram/ kg – Single dose daily
repeat test after 10 wks
* Suppressed TSH is a risk factor for osteoporosis and atrial fib
*In IHD pt. Introduce dose slowly and at low dose
STEP U{:

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De Quervain Thyoiriditis:
∆ Occurs after viral infection
∆Pain in thyroid region radiating to angle of jaw made worse by swallowing, coughing, neck
movement
∆20 - 40 yrs of age
∆T3 T4 increased for 4-6 wks
Then Hypothyroidism occurs(as colloid depletes)
Raised ESR
Give NSAIDs and Prednisolone (40mg daily)
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