HYPERTHYROIDISM

Department:-Medicine
Professor:- Dr. Pillai

Chinmay Gawade-21
Mehak Tangri-51
Vaishnavi Galange-94
LOCATION OF THYROID GLAND
• ANTERIOR PART OF NECK
• BELOW LARYNGEAL PROMINENCE
REGULATION OF THYROID HORMONES
HYPERTHYROIDISM
• It is a hypermetabolic condition associated
with elevated levels of thyroxine (T4) and/or
triiodo-thyronine (T3)
Clinical features
of
Hyperthyroidism
DIAGNOSIS
• Elevated T4 and low TSH- Hyperthyroidism
• Isolated elevation of T3 and Normal T4 and Low TSH- T3 Toxicosis
• On thyroid scan of hyperthyroid patient – if diffuse enlargement
present – GRAVES Disease
• Low TSH and Normal T3, T4 – Subclinical Hyperthroidism
• ECG- Atrial fibrillation
• Radioactive iodine uptake test
MANAGEMENT
MEDICAL MANAGEMENT-
• Drug therapy(ANTITHYROID DRUGS)
Methimazole (inhibit synthesis of thyroid hormone)
• RADIOACTIVE IODINE THERAPY- Concentrates in thyroid gland and
destroys thyroid tissue- In cases of recurrent thyrotoxicosis

Surgical Management-
• Thyroidectomy
Graves'
Disease
AN Overview
Definition and Epidemiology:-
• - Autoimmune disorder causing hyperthyroidism via TSH receptor
autoantibodies.
• - Most common cause of hyperthyroidism.
• - Affects women more than men (5:1 ratio).
• - Peak incidence between 20–40 years.
 Pathophysiology:-
• - Autoantibodies stimulate TSH receptors, mimicking TSH.
• - Leads to increased thyroid hormone (T3, T4) synthesis and release.
• - Causes systemic metabolic hyperactivity.
Clinical Features: Part 1
• 1. Thyrotoxicosis Symptoms:
• - Nervousness, irritability, heat intolerance, excessive sweating.
• - Unintentional weight loss despite increased appetite.
• - Palpitations, tachycardia, fatigue, muscle weakness, tremors.
Clinical Features: Part 2
• 2. Thyroid Enlargement (Goiter):
• - Diffuse, non-tender thyroid gland enlargement.

• 3. Ocular Manifestations:
• - Exophthalmos, periorbital edema,
• conjunctival redness, diplopia.
• - Severe cases: Corneal ulceration,
• optic nerve compression.
Clinical Features: Part 3
• 4. Dermatologic Signs:
• - Pretibial myxedema (localized shin thickening).
• - Thyroid acropachy (rare): Clubbing, soft tissue
swelling.

• 5. Other Signs:
• - Hyperreflexia, fine tremors, onycholysis.
Diagnosis: Part 1
• 1. Laboratory Tests:-
• - Elevated free T4 and/or T3.
• - Suppressed TSH.
• - Positive TSH receptor antibodies (TRAb).
Diagnosis: Part 2

• 2. Imaging:-
• - Radioactive iodine uptake (RAIU): Diffuse increased uptake.
• - Thyroid ultrasound with Doppler: Increased vascularity ('thyroid
inferno').

• 3. Orbital Imaging:-
• - MRI or CT for severe eye disease evaluation.
Management: Part 1
• 1. Medical Therapy:
• - Antithyroid drugs (Methimazole preferred; PTU for
pregnancy/thyroid storm).
• - Beta-blockers (Propranolol): Control symptoms like tachycardia,
tremors.
• - Steroids: For severe thyroid eye disease or thyrotoxic crisis.
Management: Part 2
• 2. Definitive Therapy:
• - Radioactive iodine (RAI): Destroys overactive thyroid tissue.
• - Surgery (subtotal or total thyroidectomy):
• - For large goiters, suspected malignancy, or RAI/ATD intolerance.

• 3. Adjunctive Measures:
• - Artificial tears, selenium supplements for eye disease.
Complications and Prognosis

• Complications:
• - Thyroid storm (life-threatening thyrotoxicosis).
• - Cardiac: Arrhythmias, heart failure.
• - Persistent eye symptoms, optic nerve compression.

• Prognosis:
• - Most patients achieve euthyroidism or require levothyroxine
replacement.
• - Eye symptoms may need prolonged or additional treatment.
Toxic Adenoma
Definition
• Toxic adenoma is a solitary autonomously functioning thyroid nodule
(AFTN) that secretes excessive thyroid hormones, leading to
hyperthyroidism. It is distinct from Graves' disease and multinodular
goiter and results from a somatic mutation in the TSH receptor
pathway.
Epidemiology
• • Common in iodine-deficient areas.
• • Typically occurs in adults, more frequently in middle-aged women.
• • Can occur in younger individuals.
Etiology and Pathogenesis
• • Caused by somatic mutations in the TSH receptor gene or signaling
pathways.
• • Autonomous thyroid hormone production occurs, independent of
TSH regulation.
• • TSH levels are suppressed due to negative feedback from excess
thyroid hormones.
 Clinical Features
• • Symptoms of hyperthyroidism:
• - Weight loss, heat intolerance, sweating, palpitations.
• - Anxiety, nervousness, tremors, muscle weakness.
• • Local effects of the nodule:
• - Neck swelling or palpable thyroid nodule.
• - Rarely, pressure symptoms like dysphagia or hoarseness.
Diagnosis
• • Thyroid Function Tests:
• - Elevated T3 and T4, suppressed TSH.
• • Radioactive Iodine Uptake (RAIU):
• - Solitary 'hot' nodule with suppressed surrounding thyroid uptake.
• • Ultrasound:
• - Solid or cystic nodule, increased vascularity on Doppler.
• • Fine Needle Aspiration Cytology (FNAC):
• - Typically used if malignancy is suspected.
Management
• • Medical Therapy:
• - Beta-blockers (e.g., propranolol) for symptoms.
• - Antithyroid drugs (e.g., methimazole) for temporary hormone
reduction.
• • Definitive Therapy:
• - Radioactive iodine (RAI) therapy to destroy the nodule.
• - Surgery (Hemithyroidectomy) for malignancy suspicion or
compressive symptoms.
• - Percutaneous ethanol injection therapy (PEIT) in select cases.
Prognosis
• • Most patients achieve symptom resolution with appropriate
therapy.
• • Regular follow-up is necessary to monitor for recurrence,
hypothyroidism, or complications from treatment.
 Thyroid Strom
 It also known as THYROTOXICOSIS
 It is define as a state of thyroid hormone excess in
circulation
 It is not a synonymous with hyperthyroidism
 Etiology :-
Primary Hypothyroidism
Secondary Hyperthyroidism

Graves disease  Pituitary adenoma

Toxic Multinodular goiter  Gestational thyrotoxicosis
Toxic adenoma
Activating mutation of TSH receptor
Thyrotoxicosis factitia
Jod Basedow Effect
Struma ovarii
Etiology :-

Thyrotoxicosis without hyperthyroidism

1)Subacute thyroiditis
2)silent thyroiditis
3)thyrotoxicosis factitia
4)radiation/Amiodarone/Infarction of large
tumor
 Graves disease Thyrotoxicosis factitia

Have L.A.T.S. antibody • Intake of cattle/beef meat containing

thyroid gland of animal →→ s/s of toxicity
(long acting thyroid stimulating antibody)
• High salt intake
Also known as TSI (Thyroid stimulating
immunoglobulin)
• Obesity – intake of medicine containing
Levothyroxine
Behave as TSH • Thyroid hormone excess → HR increase ,
Result in T3,T4 increase O consumption increase can lead to
& TSH reduces angina
 Pituitary • ↑synthesis of TSH
• T4↑ , T3↑
adenoma

Struma • Ovarian tumor synthesis

• Thyroid thomone
ovarii

Jod basedow • Intake of iodized salt long duration

• ↑iodine trapping ↑T3,T4
effect
Toxic multinodular
goiter
Clinical Features:-
Show symptoms of hyperthyroidism
Atrial fibrillation / palpitation, tachycardia,
nervousness, tremor, weight loss
• Radioactive Iodine Uptake
Shows areas of ↓ uptake cold nodule
TFT:- TSH↓, T4 normal/minimally ↑, T3 ↑↑↑ Defuse uptake

Treatment:- Fine Needle aspiration, SURGERY

Blood
pressure
decreases
 Treatment:-

Drug of choice:- Propylthiouracil – inhibits conversion of t4 to t3

---given by Ng tube/rectal route
To prevent HR --- beta blockers
Hydorcortisone – spike level of Cortisone – inhibits conversion of t4 to t3