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MSC - F. Surgery Answers 2025

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oGoitrogens (foods: cassava, cabbage, soy; drugs: thioureas, sulfonamides)

o Environmental toxins: lead, nitrates, organophosphates.

oGenetic factors: dyshormonogenesis (peroxidase defects, impaired iodide trapping).

oAutoimmune element: mild immune dysregulation may enhance growth, not function.

Clinical Picture:

Goiter type: Diffuse or mixed (diffuse-nodular).

Symptoms: Often asymptomatic. If large:

o Local compression: dysphagia, dyspnea, hoarseness.

oCosmetic concerns.

Thyroid function: Usually euthyroid, but subclinical or overt hypothyroidism may occur.

oLabs: ↑ TSH, ↑ T3, ↓ T4/T3 ratio, ↓ urinary iodine.

Diagnosis:

Clinical: Palpable thyroid enlargement (≥Grade II–III).

Imaging: Ultrasound, scintigraphy for structure and nodularity.

Lab: TSH, T3, T4, urinary iodine excretion.

Fine needle aspiration biopsy: for nodular/mixed goiter (rule out malignancy).

Differentiate from: Hashimoto’s thyroiditis, thyroid neoplasm, infiltrative diseases.

Treatment:

Indications: Goiter ≥ Grade II in children, ≥ Grade III in adults.

First-line: Long-term thyroid hormone suppression therapy (L-thyroxine 50–200 µg/day).

oGoal: ↓ TSH → reduce stimulation → shrink goiter.

Other options:

oNSAIDs (e.g., Indomethacin) in mild forms.

oSurgery: for compressive symptoms or nodules with suspicious features.

Prevention:

Mass prophylaxis: Universal iodized salt (≥25 mg potassium iodate/kg).

Group/individual prophylaxis:

oAntistrumin (potassium iodide 1 mg) weekly for:

Children in endemic regions.

Pregnant and lactating women.

Public health monitoring: Regular goiter surveys, iodine status evaluation.

4.Sporadic goiter. Clinical picture, diagnosis, treatment.

Non-toxic enlargement of the thyroid gland occurring outside endemic regions, in the absence of widespread iodine deficiency. Thyroid function is usually normal (euthyroid).

Etiology:

Unlike endemic goiter, sporadic goiter is caused by individual-specific factors, including:

Goitrogenic substances (e.g., cassava, soy, certain drugs like thioureas, sulfonamides, lithium).

GI and liver diseases → impaired iodine absorption/metabolism.

Iodine in poorly bioavailable forms.

Congenital thyroid enzyme deficiencies (dyshormonogenesis), especially:

oDeficient iodide transport, peroxidase activity, organification defects.

Clinical Picture:

Thyroid enlargement: Usually diffuse, sometimes nodular.

Function: Mostly euthyroid, though subclinical or overt hypothyroidism can develop.

Symptoms:

o Often asymptomatic.

o Cosmetic neck swelling.

oLarge goiter may cause compressive symptoms (dysphagia, dyspnea, hoarseness).

Diagnosis:

Clinical exam: Palpable thyroid enlargement.

Thyroid function tests:

o TSH: normal or slightly ↑

oT3/T4: normal (in euthyroid state)

Ultrasound: Evaluate size, texture, nodularity.

Fine needle aspiration biopsy (FNAB): For nodules to rule out malignancy.

Exclude: Autoimmune thyroiditis, neoplasia.

Treatment:

Indications: Cosmetic concern, compression, progressive growth, or thyroid dysfunction.

Medical:

oL-thyroxine suppression therapy (50–150 µg/day) to reduce TSH stimulation.

Surgical: Large nodular goiter or suspicion of cancer.

Radioiodine: Rarely used, more for toxic nodules.

Prevention:

No mass prophylaxis needed (non-endemic regions).

Avoid goitrogens, especially in susceptible individuals.

Ensure adequate iodine intake (WHO: 150 µg/day for adults).

5.Nodular goiter. Clinical picture, diagnosis, treatment.

A thyroid enlargement characterized by one or more palpable nodules, often due to long-standing thyroid hyperplasia and degeneration. It is the most common thyroid disorder in adults, especially women >35 years.

Etiology:

Often evolves from a longstanding diffuse goiter (e.g., untreated endemic goiter).

May involve:

o Colloid accumulation

o Cystic degeneration

o Hemorrhage

oFibrosis and calcification

TSH stimulation, oxidative stress, and local growth factors contribute.

Clinical Picture:

Symptoms:

Most are asymptomatic

Neck swelling is the most common complaint

Pressure symptoms (when large):

o Dysphagia (esophageal compression)

o Dyspnea, stridor (tracheal compression)

oJugular venous distention

Acute pain/swelling: Sudden hemorrhage into a cyst—surgical emergency

Rarely:

oRecurrent laryngeal nerve palsy

o Horner’s syndrome → Suggests malignancy

Signs:

Swelling moves with swallowing

On palpation:

o Irregular, nodular surface

o Multiple nodules usually, but may present as solitary nodule

oSoft to firm; softer than Graves’ gland

May be retrosternal in large cases

Complications:

Secondary thyrotoxicosis (autonomous hot nodules)

Compressive symptoms

Thyroid carcinoma (~5–10%)

Diagnosis:

Basic Labs:

TSH, Free T4, T3: Usually euthyroid; may show mild thyrotoxicosis

Anti-TPO/anti-Tg antibodies: To exclude thyroiditis

Imaging & Tests:

1.Ultrasound: First-line; identifies number, size, structure of nodules

2.FNAC: Key to exclude malignancy

3.Thyroid scan (radioisotope):

o Cold nodule = suspicious

oHot nodule = usually benign

4.X-ray neck/chest: Tracheal deviation, retrosternal extension, calcification

5.Barium swallow: If dysphagia present

6.CT/MRI: Rarely, for large retrosternal or substernal goiters

Treatment:

Medical:

L-thyroxine suppression therapy:

o 50% show reduction in size with 120–180 mcg/day

oHowever, nodularity persists

Goal: Suppress TSH to halt growth stimulus

Surgical:

Definitive treatment

Indications:

o Large goiter

o Suspicion of malignancy

o Pressure symptoms

oCosmetic concern

Procedures:

oTotal or subtotal thyroidectomy

oLobectomy if confined to one lobe

Always followed by:

oL-thyroxine 100 mcg/day to suppress TSH and prevent recurrence

Follow-up:

Thyroid function tests

Neck ultrasound (if nodules remain)

Lifelong L-thyroxine therapy postoperatively

6.Diffuse toxic goiter. Clinical picture, conservative and surgical treatment.

Synonym: Graves’ disease

Etiology: Autoimmune thyroid disorder caused by thyroid-stimulating immunoglobulins (TSI) that bind to the TSH receptor, leading to:

Thyroid hyperplasia

Increased thyroid hormone synthesis and secretion (T3/T4)

Diffuse gland enlargement

Pathophysiology

Strong association with HLA-B8, HLA-DR3

More common in women (female:male = 7:1)

Typical onset: 20–40 years

Clinical Features

1.Hypermetabolic Symptoms (due to ↑ T3/T4):

Weight loss despite increased appetite

Heat intolerance, sweating

Warm, moist skin

Low-grade fever

2.Cardiovascular:

Tachycardia, palpitations

Atrial fibrillation (especially in elderly)

High systolic / low diastolic BP

Development of thyrotoxic heart disease

3.Neurological:

Anxiety, tremors, restlessness

Insomnia

Reflexes exaggerated

Proximal muscle weakness

4.Gastrointestinal:

Frequent defecation/diarrhea

5.Ocular (Graves’ ophthalmopathy):

Exophthalmos

Lid lag and stare

Periorbital edema

Diplopia (due to extraocular muscle involvement)

Rare: optic neuropathy

6.Reproductive:

Menstrual irregularities

Infertility

Gynecomastia (in males)

7.Goiter Signs:

Diffuse, symmetrical thyroid enlargement

Bruit on auscultation (↑ vascularity)

Moves on swallowing

Severity Classification

 

 

Grade

Pulse

Weight loss

Complications

Mild

<100 bpm

10–15% body

None

weight

 

 

 

 

100–120

15–25% loss

Mild symptoms

Moderate bpm

Severe

>120 bpm

>25–50% loss

Thyrotoxic heart, hepatitis,

encephalopathy

 

 

 

Diagnosis

1. Thyroid Function Tests:

o ↓ TSH

o ↑ Free T4 and/or T3

oT3 toxicosis possible

2.Thyroid Autoantibodies:

oPositive TSI (Thyroid-stimulating immunoglobulins)

oAnti-TPO and Anti-Tg antibodies may also be elevated

3.Ultrasound:

oDiffuse enlargement, increased vascularity

4.Radioactive Iodine Uptake Scan (RAIU): o Diffuse, homogeneous uptake

5.ECG/Echo: Rule out cardiac complications

Management

I. Conservative (Medical) Treatment

Goal: Achieve euthyroid state

A.Antithyroid Drugs:

Methimazole (preferred): 10–30 mg/day

Propylthiouracil (PTU): preferred in 1st trimester of pregnancy or thyroid storm

B.Beta-blockers (Symptomatic control):

Propranolol 40–80 mg TID or

Metoprolol, Atenolol

C.Corticosteroids:

In severe cases with ophthalmopathy or thyroid storm

↓ Peripheral conversion of T4 to T3

D.Sedatives/Tranquilizers:

To reduce sympathetic overdrive

E.Plasmapheresis (in severe or resistant cases):

↓ Hormone levels rapidly

Helpful in thyrotoxic crisis or drug-resistant cases

II.Indications for Surgery (Subtotal or Near-total Thyroidectomy)

1. Failed medical therapy after 1.5–2 years