Give point wise description for hyperthyroidism and hypothyroidism for 10 marks each for my kayachikitsa final year paper rghus university 2026

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hyperthyroidism AND treatment

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hypothyroidism AND treatment

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American Thyroid Association hyperthyroidism hypothyroidism patient brochure diagnosis treatment

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1. Hyperthyroidism / Thyrotoxicosis - 10 marks

Definition

  • Hyperthyroidism is a state of increased synthesis and secretion of thyroid hormones by the thyroid gland.
  • Thyrotoxicosis is the clinical syndrome due to excess circulating thyroid hormones (T3/T4), whether produced by the gland or received from outside.
  • It causes a hypermetabolic, hyperadrenergic state.

Etiology

  1. Graves' disease - most common cause; autoimmune stimulation of TSH receptors.
  2. Toxic multinodular goitre.
  3. Toxic adenoma.
  4. Thyroiditis - subacute, painless, postpartum.
  5. Excess intake of thyroid hormone.
  6. Iodine-induced or amiodarone-induced thyrotoxicosis.
  7. Rarely, TSH-secreting pituitary adenoma.

Clinical features

General/metabolic
  • Weight loss despite increased appetite
  • Heat intolerance and excessive sweating
  • Weakness, fatigue and increased thirst
  • Fine tremors
Neuropsychiatric
  • Nervousness, irritability, anxiety
  • Insomnia, hyperactivity and poor concentration
  • Hyperreflexia
Cardiovascular
  • Palpitations, tachycardia
  • Systolic hypertension
  • Atrial fibrillation, especially in elderly patients
  • Heart failure in severe untreated disease
Gastrointestinal and reproductive
  • Increased bowel frequency or diarrhoea
  • Oligomenorrhoea/amenorrhoea and infertility in females
  • Reduced libido and erectile dysfunction in males
Eye and skin
  • Staring look, lid retraction and lid lag
  • Graves' orbitopathy: exophthalmos, diplopia
  • Warm, moist skin; fine hair
  • Pretibial myxoedema in Graves' disease
Thyroid examination
  • Diffuse goitre in Graves' disease, sometimes with bruit
  • Nodular goitre in toxic multinodular goitre

Investigations

  1. Serum TSH: suppressed or low, best initial screening test.
  2. Free T4 and/or T3: raised.
  3. TSH-receptor antibody: supports Graves' disease.
  4. Radioactive iodine uptake scan:
    • Diffuse increased uptake: Graves' disease
    • Focal uptake: toxic adenoma
    • Low uptake: thyroiditis or exogenous hormone intake
  5. ECG: tachycardia or atrial fibrillation.
  6. CBC and liver function tests before antithyroid medication.

Management

  1. General measures
    • Rest, avoid excess iodine and stimulants.
    • Treat precipitating factors.
  2. Symptomatic treatment
    • Beta-blocker, such as propranolol, for tremor, tachycardia and palpitations.
  3. Antithyroid drugs
    • Methimazole/carbimazole are commonly used.
    • Propylthiouracil is preferred during the first trimester of pregnancy and in thyroid storm.
    • Monitor for agranulocytosis and hepatotoxicity.
  4. Definitive treatment
    • Radioactive iodine ablation.
    • Thyroidectomy in large goitre, suspicion of malignancy, compressive symptoms, or selected Graves' disease cases.
  5. Graves' orbitopathy
    • Smoking cessation, eye protection and specialist management.
    • Severe disease may need corticosteroids or other therapy.

Complications

  • Thyroid storm
  • Atrial fibrillation and thromboembolism
  • Heart failure
  • Osteoporosis and fractures
  • Infertility and adverse pregnancy outcomes

Ayurvedic correlation and principles

  • There is no exact single classical Ayurvedic equivalent of hyperthyroidism.
  • It may be understood as a Pitta-Vata predominant condition with tikshnagni, dhatu-kshaya, kampa, daha, sweda, hrid-drava and anidra.
  • Chikitsa principles:
    • Nidana parivarjana
    • Pitta-Vata shamana
    • Mridu langhana where appropriate
    • Manasika shanti, adequate sleep and avoidance of excessive ushna, tikshna, amla and katu ahara
    • Any Ayurvedic treatment should be adjunctive and must not delay endocrine evaluation, especially in severe disease.

2. Hypothyroidism - 10 marks

Definition

  • Hypothyroidism is a clinical state caused by deficient production or action of thyroid hormones.
  • It leads to slowing of metabolic processes.
  • It may be:
    1. Primary: disease of thyroid gland
    2. Secondary: pituitary TSH deficiency
    3. Tertiary: hypothalamic TRH deficiency

Etiology

  1. Hashimoto thyroiditis - common cause in iodine-sufficient regions.
  2. Iodine deficiency.
  3. Post-thyroidectomy or post-radioactive iodine therapy.
  4. Drugs: amiodarone, lithium and some immunotherapies.
  5. Postpartum thyroiditis.
  6. Infiltrative disease of thyroid.
  7. Congenital thyroid dysgenesis or dyshormonogenesis.
  8. Pituitary or hypothalamic disease causing central hypothyroidism.

Clinical features

General/metabolic
  • Fatigue, lethargy and weakness
  • Weight gain despite poor appetite
  • Cold intolerance
  • Reduced sweating
Skin and hair
  • Dry, coarse, cold skin
  • Coarse, brittle hair and hair loss
  • Puffy face and periorbital puffiness
  • Non-pitting oedema: myxoedema
Neuromuscular and neuropsychiatric
  • Slow speech and slow mental activity
  • Poor memory, depression and drowsiness
  • Muscle cramps and proximal muscle weakness
  • Delayed relaxation of deep tendon reflexes
  • Carpal tunnel syndrome
Cardiovascular
  • Bradycardia
  • Low cardiac output
  • Diastolic hypertension
  • Pericardial effusion in severe cases
Gastrointestinal and reproductive
  • Constipation
  • Menorrhagia, infertility and recurrent miscarriage
  • Decreased libido and erectile dysfunction
Other features
  • Hoarse voice
  • Goitre may be present in Hashimoto thyroiditis or iodine deficiency
  • In children: growth retardation and delayed development

Investigations

  1. Serum TSH
    • Increased in primary hypothyroidism.
    • Low or inappropriately normal in central hypothyroidism.
  2. Free T4
    • Reduced in overt hypothyroidism.
  3. Subclinical hypothyroidism
    • Increased TSH with normal free T4.
  4. Anti-thyroid peroxidase antibodies:
    • Often positive in Hashimoto thyroiditis.
  5. Additional tests where indicated:
    • Lipid profile: hypercholesterolaemia may occur.
    • CBC: anaemia may occur.
    • ECG: sinus bradycardia.
    • Ultrasound when structural thyroid disease is suspected.

Management

  1. Levothyroxine replacement
    • Treatment of choice.
    • Usually taken once daily, preferably on an empty stomach.
    • Dose is individualized based on age, body weight, cardiac disease, pregnancy and laboratory values.
  2. Monitoring
    • Check TSH after starting or changing dose, generally after about 6-8 weeks.
    • In central hypothyroidism, monitor free T4 rather than relying only on TSH.
  3. Special situations
    • Elderly persons and patients with coronary artery disease: start with a low dose and titrate slowly.
    • Pregnancy: thyroid hormone requirement often rises, so early monitoring and dose adjustment are required.
    • Correct iodine deficiency where relevant.
  4. Avoid
    • Unsupervised use of T3 or thyroid extracts.
    • Taking levothyroxine together with iron, calcium, antacids or certain foods that impair absorption.

Complications

  • Myxoedema coma: hypothermia, bradycardia, hypotension, altered sensorium and hypoventilation
  • Hyperlipidaemia and atherosclerotic cardiovascular disease
  • Infertility and poor pregnancy outcomes
  • Pericardial effusion
  • Growth and intellectual impairment in untreated congenital hypothyroidism

Ayurvedic correlation and principles

  • Hypothyroidism also has no exact one-to-one classical Ayurvedic diagnosis.
  • It can be interpreted as a Kapha-Vata predominant state, with mandagni, meda vriddhi, shotha, gaurava, alasya, sheetata and mala-sanga.
  • Chikitsa principles:
    • Nidana parivarjana
    • Agni deepana and ama pachana according to patient assessment
    • Kapha-Meda hara ahara-vihara
    • Appropriate vyayama, pathya ahara and weight management
    • Shodhana or shamana only after proper Ayurvedic assessment
  • Levothyroxine should not be abruptly stopped or replaced by Ayurvedic medicines without endocrinology supervision.

Important laboratory comparison

FeatureHyperthyroidismPrimary hypothyroidism
TSHDecreasedIncreased
Free T4/T3IncreasedDecreased
Metabolic stateIncreasedDecreased
Body weightLossGain
Temperature intoleranceHeat intoleranceCold intolerance
PulseTachycardiaBradycardia
Bowel habitDiarrhoea/frequent stoolsConstipation
For exam wording, remember: Hyperthyroidism = Pitta-Vata, tikshnagni, kshaya, kampa, daha; Hypothyroidism = Kapha-Vata, mandagni, sthoulya, shotha, alasya, sheetata.
The biochemical distinction and treatment outline follow standard internal medicine teaching: hyperthyroidism is hormone excess with low TSH, while primary hypothyroidism is thyroid hormone deficiency with raised TSH. Recent reviews mainly address specialist treatment questions, such as thyroid eye disease, rather than changing these core examination points.
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