Goiter Flashcards

1
Q

What’s Goiter:?

A
  • Definition: The term goiter refers to any enlargement of the thyroid gland, regardless of the cause. It can be due to various reasons such as iodine deficiency, thyroid dysfunction, or autoimmune conditions like Graves’ disease or Hashimoto’s thyroiditis.
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2
Q
  • Normal Anatomy: A normal thyroid gland is typically impalpable. Goiter may manifest as a generalized enlargement of the entire thyroid gland or as discrete nodules (lumps) in one or both lobes of the gland.
  • Solitary Nodule: A discrete swelling in one lobe with no other abnormalities in the thyroid.
  • Dominant Nodule: A nodule that stands out in a gland with other diffuse abnormalities.
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3
Q

What’s the Anatomy of the Thyroid Gland:

BS, LD, NS?

A
  • Blood Supply:
  • Supplied by the superior and inferior thyroid arteries.
  • Drained by the superior, middle, and inferior thyroid veins.
  • Lymphatic Drainage:
  • Drains into the upper and lower deep cervical lymph nodes, as well as the pretracheal and paratracheal lymph nodes.
  • Nerve Supply:
  • Innervated by the middle cervical ganglion and the superior and inferior cervical ganglia.
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4
Q

What’s the Histology of the Thyroid:

A
  • Follicular Cells:
  • Secrete thyroid hormones (T3 and T4).
  • These hormones are stored in the follicles as thyroglobulin (colloid).
  • Parafollicular Cells (C Cells):
  • Secrete calcitonin, a hormone involved in calcium regulation.
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5
Q

Physiology of the Thyroid Gland:

  • Hormone Secretion:
  • The thyroid gland primarily secretes thyroxine (T4) and a smaller amount of triiodothyronine (T3).
  • T3 is more active than T4 but is less abundant.
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6
Q
  • what are the Functions of Thyroid Hormones:
A
  • Regulation of Basal Metabolic Rate (BMR): Thyroid hormones regulate the rate at which the body uses energy at rest.
  • Psychosomatic Growth: These hormones are essential for normal physical and mental development.
  • Cardiac Function: Thyroid hormones exert chronotropic (heart rate) and inotropic (force of contraction) effects on the heart.
  • Catecholamine Sensitivity: They increase the sensitivity of receptors to catecholamines like adrenaline and also increase the number of receptors.
  • Respiratory Function: They are essential for maintaining normal respiratory drive.
  • Hematopoiesis: Necessary for normal blood cell production.
  • Bone Metabolism: They regulate bone turnover and growth.
  • Opposite Effect to Insulin: Thyroxine increases glucose metabolism, opposing the action of insulin.
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7
Q

What are the Physiologic Effects of Calcitonin:

A
  • Bone: Calcitonin inhibits osteoclasts, reducing bone resorption and thus lowering the release of calcium and phosphorus into the blood.
  • Kidneys: Calcitonin reduces reabsorption of calcium and phosphorus in the kidney, leading to increased excretion of these minerals in the urine. This helps lower blood calcium levels.
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8
Q

Summary:

Goiter represents an enlargement of the thyroid gland due to various causes. Thyroid hormones like T3 and T4 play essential roles in regulating metabolism, growth, heart function, and bone turnover. The parafollicular cells, which secrete calcitonin, help regulate calcium levels in the body by acting on bones and kidneys. Proper testing and scanning are crucial in evaluating thyroid function and identifying conditions like hyperthyroidism, hypothyroidism, and thyroid nodules.

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9
Q

What are the Classification of Goitres?

A

Simple

Diffuse Colloid (or Hyperplastic) Goitre

Nodular Goitre
(3. Nodular Goitre:

  • Simple Nodule: A single nodule in the thyroid gland, often benign.
  • Toxic Nodular Goitre: Multiple nodules that are overactive and secrete excess thyroid hormones, causing hyperthyroidism)

Toxic Goitre

Neoplastic Goitre

Inflammatory Goitre

Simple (Non-toxic) goitre (Endemic/sporadic)

Diffuse colloid (or hyperplastic) goitre

Nodular goitre

Simple nodule

Toxic goitre

Diffuse toxic goitre (Grave’s disease)

Toxic nodular goitre

Toxic nodule

Rarely toxic malignant tumour

Neoplastic goitre

Benign

Malignant

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10
Q

Simple (Non-toxic) Goitre
Can bring divided into?

A
  1. Simple (Non-toxic) Goitre:
  • Endemic: Occurs in areas with iodine deficiency, affecting many people.
  • Sporadic: Occurs in individuals without any geographical pattern of iodine deficiency.
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11
Q

Diffuse Colloid (or Hyperplastic) Goitre
Can bring divided into?

A
  1. Diffuse Colloid (or Hyperplastic) Goitre:
  • This is characterized by a uniform enlargement of the thyroid gland with accumulation of colloid in the follicles
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12
Q

Toxic Goitre Can bring divided into?

List 5 examples of inflammatory goitre

A
  1. Toxic Goitre:
  • Diffuse Toxic Goitre (Graves’ Disease): An autoimmune condition leading to generalized thyroid enlargement and overproduction of thyroid hormones.
  • Toxic Nodule: A single nodule in the thyroid gland that produces thyroid hormones independent of TSH regulation.
  • Toxic Malignant Tumour: Rarely, a thyroid malignancy may be overactive and secrete thyroid hormones.
  1. Neoplastic Goitre:
  • Benign: Non-cancerous tumors in the thyroid.
  • Malignant: Cancerous tumors in the thyroid.
  1. Inflammatory Goitre:
  • Autoimmune Thyroiditis (Hashimoto’s Disease): An autoimmune condition causing inflammation of the thyroid and often leads to hypothyroidism.
  • Acute Suppurative Thyroiditis: Bacterial infection causing acute inflammation of the thyroid.
  • Subacute Thyroiditis: A viral infection causing inflammation of the thyroid, typically painful.
  • Riedel’s Thyroiditis: A rare chronic inflammatory condition where the thyroid becomes fibrotic and hard.
  • Specific Infective Thyroiditis: Infection of the thyroid caused by diseases like tuberculosis.
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13
Q

What are theAtiology (Causes of Goitre)

A
  1. Iodine Deficiency:
  • The most common cause of goitre, especially in endemic areas.
  1. Dyshormonogenesis:
  • A congenital condition where the thyroid cannot produce enough hormones due to enzyme defects.
  1. Goitrogens:
  • Substances that interfere with thyroid hormone production, leading to goitre (discussed in more detail below).
  1. Neoplasia:
  • Tumors (benign or malignant) in the thyroid can cause the gland to enlarge.
  1. Inflammations:
  • Infections and autoimmune conditions that cause thyroid inflammation and enlargement.
  1. Medications and Foods (Goitrogens):
  • Drugs: Anti-thyroid drugs, cough medicines, sulfonamides, lithium, phenylbutazone, PAS (para-aminosalicylic acid), iodine, and oral hypoglycemic agents can interfere with thyroid function.
  • Foods: Soybeans, millet, cassava, and cabbage can reduce thyroid hormone production.
  1. Pituitary or Hypothalamic Disease:
  • Conditions affecting the pituitary or hypothalamus can lead to abnormal TSH production, which affects the thyroid.
  1. Thyroid Destruction:
  • Radioactive iodine or surgery can destroy thyroid tissue, leading to goitre in some cases.
  1. Autoimmune Thyroiditis (Hashimoto’s Disease):
  • Chronic inflammation of the thyroid due to autoimmune attack leads to goitre formation.
  1. Lymphocytic Thyroiditis:
  • Can occur after hyperthyroidism, leading to thyroid inflammation.
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14
Q

What areGoitrogens

Drugs&food

A
  • Drugs:
  • Certain medications like anti-thyroid drugs, lithium, and iodine-containing drugs can inhibit thyroid hormone production, causing goitre.
  • Foods:
  • Foods like soybeans, cassava, millet, and cabbage contain substances that inhibit thyroid hormone synthesis, leading to goitre if consumed in large amounts.
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15
Q

What’s the Pathophysiology of Goitre

A

When T3 and T4 (thyroid hormones) levels decrease, the pituitary gland responds by increasing TSH (thyroid-stimulating hormone) secretion. The elevated TSH stimulates the thyroid gland to try to produce more hormones, leading to hypertrophy (increase in cell size) and hyperplasia (increase in cell number) of the follicular cells. This causes the thyroid to enlarge in an effort to produce more thyroid hormones, which may lead to the following changes:

  1. Diffuse Enlargement: Initially, the thyroid undergoes diffuse and homogeneous enlargement.
  2. Colloid Goitre: The thyroid may become enlarged with colloid-filled follicles, known as a colloid goitre.
  3. Nodular Goitre: Over time, different parts of the thyroid may respond unevenly to TSH, forming nodules. These nodules may eventually coalesce to form a multinodular goitre.
  4. Secondary Changes: These nodules can undergo various secondary changes, such as:
  • Central necrosis (death of tissue in the middle of the nodule),
  • Cystic degeneration (fluid-filled spaces form within the nodule),
  • Haemorrhage (bleeding into the nodule),
  • Calcification (hardening due to calcium deposits),
  • Malignant transformation (in rare cases, 3% of nodules may turn cancerous).
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16
Q

What are the Clinical Features of Goitre

A
  1. Gradual Onset: Goitres typically develop slowly over time, especially in iodine-deficient areas.
  2. Painless Anterior Neck Swelling: The most common symptom is a painless swelling in the front of the neck.
  3. Pain and Rapid Growth: Sudden pain or a rapid increase in size may indicate secondary changes like hemorrhage, inflammation, or malignancy.
  4. Compression of Neighboring Structures:
  • Airway Obstruction: Enlarged goitre can compress the trachea, leading to breathing difficulties.
  • Esophageal Obstruction: Compression of the esophagus can cause difficulty swallowing (dysphagia).
  • Laryngeal Nerve Compression: This can result in voice changes or hoarseness.
  • Neck Vein Compression: Compression of neck veins can cause venous congestion and swelling of the neck or face.
  • Superior Vena Cava Syndrome (Pemberton’s Sign): When the goitre compresses the superior vena cava, it causes a combination of facial swelling, cyanosis (bluish discoloration), and breathing difficulties.
  1. Local Compression Symptoms: Compression of local structures can cause symptoms such as:
  • Dysphagia (difficulty swallowing),
  • Dyspnea (difficulty breathing),
  • Stridor (noisy breathing),
  • Plethora (redness of the face due to venous obstruction),
  • Hoarseness (due to laryngeal nerve compression).
  1. Pain: Can occur due to hemorrhage, inflammation, necrosis, or malignant transformation within the thyroid.
  2. Signs of Hyperthyroidism or Hypothyroidism: Depending on the functional status of the thyroid, patients may exhibit symptoms of an overactive thyroid (hyperthyroidism) or underactive thyroid (hypothyroidism).
  3. Thyroid Cancer: In some cases, goitre may be associated with thyroid cancer, with or without metastases (spread to other areas).
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17
Q

Conclusion

Goitres represent a wide range of thyroid gland enlargements that can result from various causes like iodine deficiency, autoimmune diseases, inflammation, and tumors. They may be simple, toxic, neoplastic, or inflammatory in nature. Understanding the underlying pathophysiology and potential complications of goitres is essential for proper diagnosis and treatment. Early detection and management can prevent complications such as airway obstruction, nerve compression, or the development of malignancies.

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18
Q

What are the Investigations for Goitres
And why?

A
  1. Thyroid Function Tests (TFTs):
    • Thyroxine (T4): Measures the amount of T4 hormone in the blood, helping to assess the thyroid’s hormone production.
    • Triiodothyronine (T3): Measures the level of T3 hormone, the more active form of thyroid hormone.
    • Thyroid-Stimulating Hormone (TSH): Produced by the pituitary gland, TSH regulates thyroid hormone production. High levels suggest hypothyroidism, while low levels suggest hyperthyroidism.
    • Thyrotropin-Releasing Hormone (TRH): Stimulates the release of TSH from the pituitary. Testing TRH levels can help assess the function of the pituitary and hypothalamus.
    These tests help determine if the thyroid is functioning normally, overactive (hyperthyroidism), or underactive (hypothyroidism).
  1. Thyroid Scan with Radioactive Iodine (I-123 or I-131):
    • Purpose: Used to visualize the thyroid gland’s ability to take up iodine, which is necessary for hormone production.
    • Procedure: A small amount of radioactive iodine (I-123 or I-131) or Technetium is injected into the bloodstream. The thyroid gland absorbs this iodine, and a gamma camera detects the radiation emitted to create an image.
    • Findings:
      • Hot Nodules: Areas that take up more iodine than the rest of the thyroid, often indicating hyperfunction (such as in secondary hyperthyroidism).
      • Cold Nodules: Areas that do not take up iodine, potentially indicating malignancy.
    • Preference: I-123 is preferred over I-131 due to its shorter half-life and reduced radiation exposure.
  1. Anti-Thyroid Receptor Antibodies:
    • Purpose: This test detects antibodies that stimulate the thyroid to overproduce hormones, such as in Graves’ disease (primary hyperthyroidism).
    • Use: It is especially useful in diagnosing autoimmune thyroid diseases like Graves’ disease.
  1. Radiological Investigations:
    • Chest X-rays (AP and lateral views): Used to assess the presence of retrosternal extension of the goitre (when the thyroid gland extends into the chest cavity).
    • Findings: Retrosternal shadows on X-rays may indicate that the goitre is growing behind the sternum, potentially compressing nearby structures.
  1. Ultrasound (USG) of the Neck:
    • Purpose: A non-invasive imaging method to assess the size, structure, and texture of the thyroid gland.
    • Normal Findings: The thyroid gland is homogeneous and slightly hyperechoic (bright on ultrasound). It normally measures 2 cm or less in the transverse dimension and depth, with a length of 4.5-5.5 cm, and the isthmus (the part connecting the two lobes) measures about 0.5 mm.
    • Abnormal Findings: A diffusely enlarged gland with an isthmus width of 1.5 cm may indicate goitre.
  1. Fine Needle Aspiration Cytology (FNAC):
    • Purpose: A minimally invasive procedure to collect thyroid cells for examination under a microscope to rule out malignancy.
    • Results:
      • Benign: The cells are non-cancerous.
      • Malignant: The cells are cancerous.
      • Suspicious Malignant: The findings are inconclusive but raise suspicion of cancer.
      • Inconclusive or Inadequate: The sample collected may not be sufficient for a clear diagnosis.
    • Additional Steps: If a follicular pattern is seen, a lobectomy (surgical removal of a thyroid lobe) may be needed to exclude follicular carcinoma. This cancer type is diagnosed based on the presence of capsular invasion.
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19
Q

Treatment and Prevention of Simple Goitre

A
  1. Dietary Measures:
  • Iodine Supplementation: In iodine-deficient areas, iodine supplements and food fortification with iodine are highly effective preventive measures against goitre.
  1. Medical Treatment:
  • Thyroxine (T4) Supplementation: Patients with diffuse hyperplastic goitre may benefit from taking thyroxine for several months (0.1 to 0.2 mg daily) to reduce thyroid enlargement and normalize thyroid function.
  1. Surgical Indications:

Surgery is considered in specific cases, such as:

  • Obstructive Symptoms: When the goitre is large enough to cause breathing difficulties, dysphagia (difficulty swallowing), or compression of nearby structures.
  • Suspected Malignancy: Surgery is indicated if there is clinical suspicion of thyroid cancer, or if FNAC results suggest malignancy.
  • Hyperfunctioning Nodules: Surgical removal may be necessary for nodules that are overproducing thyroid hormones.
  • Cosmetic Reasons: Some patients opt for surgery to reduce the cosmetic appearance of a large goitre.
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20
Q

Conclusion

Goitres can be diagnosed through a combination of blood tests, imaging studies, and tissue sampling. Early detection and treatment are essential to prevent complications, such as airway obstruction or malignancy. Treatment varies from dietary iodine supplementation to surgery, depending on the underlying cause and severity of the condition.

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21
Q

What’s Hypothyroidism

What are the possible causes of hypothyroidism

A

Hypothyroidism is a condition where the thyroid gland fails to produce sufficient thyroid hormones (T3 and T4). These hormones play essential roles in regulating growth, development, and various cellular processes, so their deficiency leads to widespread effects on the body, impacting metabolism, energy production, and overall health.

Hashimoto thyroditis
Thyroid destruction secondary to radioactive iodine therapy
Hypothyroidism secondary to thyrodectomy
Pituitary and hypothalamus dxs(dysfunction)
Iodine deficiency

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22
Q

What’s Hashimoto’s Thyroiditis

A

Hashimoto’s thyroiditis is a common cause of hypothyroidism. It is an autoimmune disorder where the body’s immune system mistakenly attacks the thyroid gland, leading to inflammation and impaired hormone production. This condition is characterized by:

  • Goitre (Enlarged Thyroid): In Hashimoto’s thyroiditis, the thyroid gland is often enlarged but loses its ability to produce hormones effectively.
  • Autoimmune Nature: The immune system targets the thyroid tissue, particularly the enzyme thyroid peroxidase (TPO), which is essential for producing thyroid hormones.
  • Prevalence in Women: Hashimoto’s is significantly more common in women, being 5 to 10 times more frequent than in men.
  • Association with Other Autoimmune Diseases: Patients with Hashimoto’s may also have other autoimmune conditions such as diabetes or pernicious anemia.
  • Anti-TPO Antibodies: A key diagnostic marker for Hashimoto’s thyroiditis is the presence of anti-TPO antibodies in the blood, which help confirm the autoimmune nature of the disease.
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23
Q

Thyroid Destruction Secondary to Radioactive Iodine or Surgery

Hypothyroidism can develop after medical interventions, such as radioactive iodine treatment or surgery:

  • Radioactive Iodine Therapy: This treatment is used to manage hyperthyroidism or thyroid cancer by destroying overactive thyroid tissue. If the remaining thyroid function is insufficient after six months, permanent hypothyroidism is usually assumed.
  • Surgical Removal: Partial or complete removal of the thyroid gland (thyroidectomy) also leads to hypothyroidism, especially if most of the gland is removed.

The likelihood of hypothyroidism depends on the amount of thyroid tissue affected and the dose of radioactive iodine used.

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24
Q

Pituitary or Hypothalamic Disease

Hypothyroidism can also result from dysfunctions in the pituitary gland or hypothalamus, which control thyroid hormone production:

A
  • Secondary Hypothyroidism: If the pituitary gland fails to produce adequate TSH (thyroid-stimulating hormone), the thyroid gland is not signaled to produce T4 and T3, leading to hypothyroidism. This condition is called secondary hypothyroidism, as it originates from the pituitary rather than the thyroid itself.
  • Tertiary Hypothyroidism: When the hypothalamus fails to produce sufficient thyrotropin-releasing hormone (TRH), the pituitary gland does not receive signals to release TSH. This is known as tertiary hypothyroidism.
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25
Q

Pituitary Injury

Hypothyroidism can occur due to damage to the pituitary gland:

  • Causes: Injury to the pituitary may occur following brain surgery or due to decreased blood supply, which can result in inadequate TSH production.
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26
Q

Distinguish between primary and secondary hypothyroidism.

A
  • Distinguishing Feature: Unlike primary hypothyroidism (due to thyroid disease), where TSH levels are elevated as the pituitary tries to compensate, pituitary injury results in low TSH levels. This helps differentiate the cause of hypothyroidism.
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27
Q

Severe Iodine Deficiency

Iodine is essential for thyroid hormone production, so severe iodine deficiency can lead to hypothyroidism:

  • Prevalence: In regions with insufficient dietary iodine intake, up to 5-15% of the population may suffer from severe hypothyroidism.
  • Impact: Iodine deficiency leads to an inability of the thyroid to synthesize adequate T3 and T4, causing thyroid enlargement (goitre) and the clinical signs of hypothyroidism.

*Conclusion**

Hypothyroidism can result from various causes, including autoimmune conditions like Hashimoto’s thyroiditis, medical treatments (radioactive iodine or surgery), dysfunctions of the pituitary or hypothalamus, pituitary injury, and iodine deficiency. The specific cause of hypothyroidism determines the clinical presentation, diagnostic markers (like anti-TPO antibodies), and treatment approach, which may include hormone replacement therapy or addressing the underlying cause.

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28
Q

Hypothyroidism’s symptoms tend to develop gradually, making them subtle and often mistaken for other conditions or aging. For those with mild hypothyroidism, there may be little to no noticeable symptoms. However, as the condition worsens, symptoms become more pronounced, with most of the complaints tied to the body’s slowing metabolism.

What are the Symptoms of Hypothyroidism

A

Common Symptoms of Hypothyroidism:

  • Fatigue: A constant feeling of tiredness, even after adequate rest.
  • Depression: A noticeable low mood, often accompanied by feelings of sadness.
  • Modest Weight Gain: Unexplained weight gain due to the slowed metabolism.
  • Cold Intolerance: Feeling cold even in warm environments, caused by reduced body heat production.
  • Excessive Sleepiness: Increased need for sleep and difficulty staying awake during the day.
  • Dry, Coarse Hair: The hair may become brittle, dry, and break easily.
  • Constipation: Slowed digestion leading to infrequent bowel movements.
  • Dry Skin: The skin may become rough, dry, and flaky.
  • Muscle Cramps: Aching and stiffness in muscles.
  • Increased Cholesterol Levels: Hypothyroidism can lead to elevated blood cholesterol.
  • Decreased Concentration: Difficulty focusing or remembering things.
  • Vague Aches and Pains: Generalized body discomfort without an obvious cause.
  • Swelling of the Legs: Fluid retention, leading to swelling in the lower limbs.
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29
Q

Symptoms of Severe Hypothyroidism Symptoms:

A

As hypothyroidism progresses, more severe symptoms can develop:

  • Puffiness Around the Eyes: Facial puffiness, especially around the eyes.
  • Slowing of the Heart Rate: The heart rate slows down, which can contribute to fatigue and weakness.
  • Drop in Body Temperature: Hypothermia due to a significant drop in metabolic activity.
  • Heart Failure: The heart’s ability to pump blood may become impaired.
  • Myxedema Coma: This is the most severe form of hypothyroidism, a life-threatening condition characterized by profound hypothyroid symptoms. It is often triggered by serious illness, surgery, trauma, or extreme stress.
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30
Q

Diagnosis of Hypothyroidism

Hypothyroidism is suspected in patients who present with symptoms such as fatigue, cold intolerance, constipation, and dry skin. However, the definitive diagnosis is made through blood tests to measure thyroid hormone levels.

What are the Diagnostic Tests: you will like to do?

A
  • Thyroid Hormone Levels (T3 and T4): In hypothyroidism, these hormone levels are often decreased. However, in early stages, they may still be within normal limits.
  • TSH (Thyroid-Stimulating Hormone) Assay: TSH is the most sensitive test for detecting primary hypothyroidism. In hypothyroid patients, TSH levels are typically elevated as the pituitary gland tries to stimulate the thyroid to produce more hormones. A normal TSH range is 0.40 – 4.2 mIU/L. When TSH levels are high, free T4 levels are usually measured to confirm hypothyroidism.
  • Primary Hypothyroidism: Characterized by elevated TSH and low T4 levels.
  • Secondary Hypothyroidism: Due to pituitary or hypothalamic dysfunction, TSH levels do not rise appropriately in response to low T4 levels.
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31
Q

How do you treat hypothyroidism

A

Treatment of Hypothyroidism

Hypothyroidism is treated with lifelong hormone replacement therapy, typically in the form of levothyroxine (T4).

  • Dosage: Usually, 100 to 150 micrograms per day, but the dose can vary based on the patient’s age, weight, and severity of hypothyroidism.
  • Once-a-day Dosing: Levothyroxine has a longer half-life compared to T3, allowing for once-daily dosing.
  • Conversion of T4 to T3: The body naturally converts levothyroxine (T4) into the active hormone triiodothyronine (T3), which regulates metabolism.

Treatment is usually effective in normalizing thyroid hormone levels and alleviating symptoms, but monitoring is necessary to ensure the proper dose is being maintained.

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32
Q

What’s Cretinism

And it’s clinical features

A

Cretinism refers to hypothyroidism that develops during infancy or early childhood. It is particularly devastating in iodine-deficient regions of the world, such as parts of inland China, Africa, and the Himalayas, where iodine is scarce.

  • Impaired Skeletal Development: Growth may be stunted, leading to shorter stature.
  • Impaired CNS Development: The brain doesn’t develop properly, leading to severe mental retardation.
  • Maternal Thyroid Hormone Deficiency: If maternal hypothyroidism occurs before the fetal thyroid gland forms, it can result in significant neurological deficits. If the maternal deficiency occurs after fetal thyroid gland development, brain function is usually less severely affected.

Adequate maternal iodine intake during pregnancy is critical to prevent this severe form of developmental delay.

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33
Q

Differentiate between Hyperthyroidism and Thyrotoxicosis

A
  • Hyperthyroidism refers to the condition where the thyroid gland becomes overactive and produces an excess of thyroid hormones (T3 and T4), which then circulate in the blood.
  • Thyrotoxicosis, on the other hand, is a broader term that describes the toxic effects caused by excess thyroid hormones in the body. It can result from any cause, including hyperthyroidism or an excessive intake of thyroid hormone.

Hyperthyroidism can be primary (originating directly from the thyroid) or secondary (caused by another source affecting the thyroid gland).

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34
Q

What are the possible Causes of Hyperthyroidism

A

Hyperthyroidism can arise from several conditions, such as:

  1. Graves’ Disease: The most common cause, an autoimmune disorder where the immune system overstimulates the thyroid.
  2. Functioning Adenoma (Hot Nodule): A single benign thyroid nodule that produces too much thyroid hormone.
  3. Toxic Multinodular Goiter (TMNG): Multiple nodules in the thyroid that lead to overproduction of thyroid hormones.
  4. Excessive Thyroid Hormone Intake: Taking too much thyroid medication.
  5. Abnormal Secretion of TSH: Excessive stimulation of the thyroid gland due to abnormal thyroid-stimulating hormone production.
  6. Thyroiditis: Inflammation of the thyroid gland causing the release of excess hormones.
  7. Excessive Iodine Intake: Too much iodine can cause the thyroid to produce excess hormones.
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35
Q

What’s Grave’s Disease: The Main Cause of Primary Hyperthyroidism

A

Grave’s disease is an autoimmune disorder where the body mistakenly produces antibodies that target the thyroid. These antibodies, particularly Thyroid Stimulating Immunoglobulin (TSI), bind to TSH receptors on the thyroid gland, mimicking the effects of Thyroid Stimulating Hormone (TSH). This results in the overstimulation of the thyroid gland, leading to an excess production of thyroid hormones.

36
Q

What are the Antibodies Involved in Grave’s Disease:

A
  • TSI (Thyroid Stimulating Immunoglobulins): These antibodies are the main culprits, acting like TSH and causing the thyroid to release more hormones.
  • Thyroid Peroxidase (TPO) Antibodies: These antibodies target the enzyme involved in thyroid hormone production.
  • TSH Receptor Antibodies: These bind to TSH receptors and stimulate hormone production.
37
Q

What are the Key Features of Grave’s Disease:

A
  • Hereditary: The condition runs in families and is more common in women than in men, with a female-to-male ratio of 9:1.
  • Age Group: It typically affects younger women.
  • Common Cause of Hyperthyroidism: Grave’s disease accounts for about two-thirds of all hyperthyroid cases.
  • Exophthalmos (Protruding Eyeballs): The antibodies involved in Grave’s disease can also react with tissues behind the eyes, causing periorbital edema and exophthalmos (bulging eyes), a classic sign of the disease.
38
Q

Triggers of Grave’s Disease: are?

A

Grave’s disease can be triggered or worsened by:

  • Stress
  • Smoking
  • Radiation exposure to the neck
  • Certain medications
  • Viral infections
39
Q

Secondary Hyperthyroidism

Secondary hyperthyroidism occurs when there is pre-existing thyroid pathology (such as a goiter or inflammation) or when there is an extra-thyroidal source of hormone production. Unlike primary hyperthyroidism, this form is often triggered by conditions external to the thyroid.

A
  1. Multinodular Goiter: Also known as Plummer’s disease, it occurs when multiple nodules in the thyroid produce excess thyroid hormone. This is commonly seen in regions with iodine deficiency, leading to endemic goiters.
  2. Toxic Adenoma: A benign nodule within the thyroid (usually follicular in nature) that autonomously secretes thyroid hormone, leading to hyperthyroidism.
  3. Ectopic Thyroid Hormone Production: In this case, a tumor elsewhere in the body produces excess thyroid hormone or hormone-like substances. For example, a metastatic follicular thyroid carcinoma or a choriocarcinoma (which produces β-hCG, whose alpha subunit resembles TSH, leading to thyroid stimulation).
40
Q

Clinical Features of Hyperthyroidism

Regardless of the cause, excess thyroid hormones lead to the following symptoms associated with hyperthyroidism:

A
  • Increased metabolic rate: Leading to weight loss despite an increased appetite.
  • Heat intolerance: The body becomes intolerant to heat, and patients may sweat excessively.
  • Palpitations: Faster and sometimes irregular heartbeat.
  • Tremors: Fine shaking of the hands or fingers.
  • Nervousness and Anxiety: Increased nervousness and restlessness.
  • Exophthalmos: In Grave’s disease, the eyes may bulge due to tissue reactions behind the eyes.

These symptoms can significantly impact a person’s daily life, and diagnosing the underlying cause is essential for effective treatment.

41
Q

Exogenous Causes of Hyperthyroidism

Exogenous hyperthyroidism occurs when excess thyroid hormones are introduced into the body from external sources.

There are two key examples: which are?

A
  1. Thyrotoxicosis Factitia: This condition arises from excessive intake of thyroid hormone (thyroxine, T4). It may occur in individuals taking thyroid hormone medication improperly or those with access to synthetic thyroid hormones.
  2. Jod-Basedow Phenomenon: This refers to the excessive intake of iodine, typically in individuals with endemic goiters (goiters in iodine-deficient areas). The sudden increase in iodine can overstimulate the thyroid, leading to excess hormone production.
42
Q

TSH-Producing Pituitary Adenoma

Another cause of hyperthyroidism is a pituitary adenoma, which is a benign tumor in the pituitary gland. The pituitary normally regulates thyroid function by producing Thyroid Stimulating Hormone (TSH). However, in cases where there is a TSH-producing adenoma, the gland produces excess TSH, which overstimulates the thyroid to produce more T4 and T3 hormones, leading to hyperthyroidism. This form of hyperthyroidism is often secondary, as the primary issue is with the pituitary gland rather than the thyroid.

A
43
Q

Whatre the Other Causes of Hyperthyroidism

A
  1. Post-Viral Thyroiditis (Subacute De Quervain’s Thyroiditis): This condition follows a viral illness and leads to temporary hyperthyroidism. It is characterized by inflammation of the thyroid gland, which causes the release of preformed thyroid hormones. Symptoms include pain in the thyroid region, systemic symptoms like fever, and a sore throat that worsens with swallowing. This condition is typically self-limiting and resolves over time.
  2. Radiation-Induced Thyroiditis: Patients undergoing radiation therapy, particularly to the neck, may develop thyroiditis as a side effect. The radiation causes inflammation of the thyroid, leading to the release of preformed thyroid hormones into the bloodstream, resulting in hyperthyroidism.
  3. Thyroiditis (General): Inflammation of the thyroid gland can also result from autoimmune reactions, leading to lymphocytic thyroiditis. In this condition, white blood cells called lymphocytes accumulate in the gland. Symptoms may include fever, sore throat, tender thyroid, and generalized neck pain.
44
Q

Clinical Features of Hyperthyroidism

Central Nervous System

A

Patients with hyperthyroidism, particularly primary thyrotoxicosis, often exhibit various central nervous system-related symptoms:

  • Tremors: Trembling of the hands, fingers, or even the tongue.
  • Nervousness: Anxiety and restlessness.
  • Emotional Liability: Irritability and mood swings; patients can alternate between lethargy and agitation.
  • Warm and Moist Hands: Excess thyroid hormone increases the body’s metabolic rate, leading to heat intolerance and sweating.

One of the most prominent effects of hyperthyroidism is an increase in metabolism:

  • Weight Loss: Despite an increased appetite, the body burns energy rapidly, resulting in significant weight loss.
  • Heat Intolerance: Patients feel overheated easily and sweat excessively.
  • Muscle Weakness and Fatigue: Due to proteolysis (the breakdown of proteins in muscles), patients experience tiredness and muscle weakness.
45
Q

Clinical Features of Hyperthyroidism

Cardiovascular Symptoms

A

Cardiovascular issues are especially common in secondary hyperthyroidism:

  • Palpitations: Patients become highly aware of their heartbeat due to the chronic effects of excess thyroid hormones on the heart.
  • Arrhythmias: Irregular heart rhythms are often seen in hyperthyroid patients.
  • Tachycardia During Sleep: The heart beats abnormally fast, even during sleep.
  • High-Output Heart Failure: Due to increased blood flow, the heart may struggle to pump efficiently.
  • Thyroid Bruit: A “bruit” is a sound heard over the thyroid due to increased blood flow to the overactive gland.
46
Q

Clinical Features of Hyperthyroidism

Gastrointestinal (GIT) Symptoms

A

Hyperthyroidism also affects the gastrointestinal system:

  • Weight Loss: Despite a good or increased appetite, the patient loses weight.
  • Increased Bowel Motions: Patients may have frequent bowel movements or diarrhea due to the sped-up metabolism.
47
Q

Clinical Features of Hyperthyroidism

Genitourinary (GUT) Symptoms
And
ophthalmological symptoms

A

The excess thyroid hormones affect reproductive and urinary systems as well:

  • Irregular Menstrual Cycles: Menstrual periods may become irregular or infrequent.
  • Amenorrhea: The complete absence of menstruation can occur.
  • Loss of Libido: Patients may experience reduced sexual drive.
  • Erectile Dysfunction: Men may have difficulty achieving or maintaining an erection.

Eye symptoms, particularly exophthalmos (protrusion of the eyeballs), are commonly seen in Grave’s disease:

  • True Exophthalmos: This occurs due to retrobulbar cellular infiltration and the deposition of mucopolysaccharides behind the eyes, pushing them forward.
  • False Exophthalmos: This results from the elevation of the upper eyelid due to hyperactivity of the levator palpebrae superioris muscle or Muller’s muscle, which is driven by increased sympathetic tone.

These ophthalmological symptoms are classic in Grave’s disease and can lead to significant discomfort and vision problems if untreated

48
Q

*summary**

Hyperthyroidism and thyrotoxicosis are serious conditions caused by an excess of thyroid hormones, with many potential causes ranging from Grave’s disease to TSH-producing pituitary adenomas, excess hormone intake, and thyroiditis. The clinical manifestations affect multiple body systems, leading to a variety of symptoms including weight loss, heat intolerance, palpitations, tremors, and, in the case of Grave’s disease, exophthalmos. Accurate diagnosis and treatment of the underlying cause are crucial for effective management.

A
49
Q

What’s True Exophthalmos and how does it occur?

A

True exophthalmos refers to the actual protrusion of the eyeballs, which is a hallmark feature of Grave’s disease. Grave’s disease is an autoimmune condition, and in this context, the immune system attacks the tissues behind the eyes, leading to:

  • Infiltration of retrobulbar tissues: Immune cells (inflammatory cells) infiltrate the tissue behind the eye.
  • Accumulation of fluid and mucopolysaccharides: This leads to swelling and pushing of the eyeballs forward.
50
Q

What are the Eye Signs Associated with Hyperthyroidism

A

Several eye signs are associated with Grave’s disease or hyperthyroidism. These include:

  1. Stellwag’s Sign: Characterized by a staring appearance with infrequent blinking. This gives the eyes a “fixed” look.
  2. Dalrymple’s Sign: This sign shows a visible rim of sclera (the white part of the eye) between the cornea and the upper eyelid, giving the eye a wide, open appearance.
  3. Von Graefe’s Sign: The upper eyelid lags behind when the eye moves downward, causing difficulty in fully closing the eyelids.
  4. Joffroy’s Sign: The loss of forehead wrinkling when the patient looks upwards. Normally, the forehead creases when one looks up, but this doesn’t happen in patients with hyperthyroidism due to weakness of facial muscles.
  5. Moebius’ Sign: This is the lack of eye convergence, which is caused by ocular myopathy (muscle weakness). Normally, both eyes should move inward when focusing on a nearby object, but this fails in hyperthyroid patients.
51
Q

What are the Complications of Exophthalmos

A

Exophthalmos can lead to several complications due to the eyes being exposed and unprotected:

  • Exposure conjunctivitis: Inflammation of the conjunctiva (the thin membrane that covers the white part of the eye).
  • Keratitis: Ulceration or damage to the cornea (the clear front surface of the eye).
  • Perforation: In severe cases, the cornea may be damaged to the point of perforation.
  • Ophthalmoplegia: Paralysis of the eye muscles due to cellular infiltration in the eye’s soft tissues. This paralysis can be bilateral (affecting both eyes) or unilateral (affecting one eye). It may also cause diplopia (double vision).
52
Q

Grave’s Ophthalmopathy Staging

Grave’s ophthalmopathy progresses through different stages, which are categorized as:

A
  • Class 0: No symptoms or signs.
  • Class I: Signs only, such as lid retraction, staring, and lid lag, but no symptoms.
  • Class II: Soft tissue involvement, such as swelling or redness around the eyes.
  • Class III: Proptosis (forward bulging of the eyes).
  • Class IV: Extraocular muscle involvement, causing restricted eye movement.
  • Class V: Corneal involvement, with the cornea being at risk of ulceration due to exposure.
  • Class VI: Sight loss due to optic nerve involvement, which is the most severe stage.
53
Q

Comparison of Primary vs. Secondary Hyperthyroidism

A
  1. Primary Hyperthyroidism (Grave’s disease):
  • Age: Typically affects younger individuals.
  • Onset: Abrupt.
  • Course: Characterized by remissions and exacerbations.
  • Nervous Symptoms: Prominent (e.g., tremors, anxiety, emotional instability).
  • Metabolic Manifestations: Marked (e.g., weight loss, heat intolerance).
  • Eye Signs: Common and prominent (e.g., exophthalmos).
  • Cardiovascular Manifestations: Less severe.
  • Thyroid Gland: Diffusely enlarged.
  1. Secondary Hyperthyroidism (Plummer’s disease):
  • Age: More common in the elderly.
  • Onset: Gradual.
  • Course: Steady without remissions.
  • Nervous Symptoms: Mild.
  • Metabolic Manifestations: Less pronounced.
  • Eye Signs: Absent.
  • Cardiovascular Manifestations: More prominent.
  • Thyroid Gland: Nodular, rather than diffusely enlarged.
54
Q

What’s Thyroid Storm (Thyrotoxic Crisis)

It’s often triggered by stressors such as:

A

A thyroid storm is a rare but life-threatening condition that represents an extreme form of thyrotoxicosis. It occurs in patients with uncontrolled hyperthyroidism,

often triggered by stressors such as:

  • Surgery without proper preoperative control of hyperthyroidism.
  • Major trauma or severe infection.
55
Q

What are the Clinical Features of Thyroid Storm:

A
  • Hyperthermia: Extremely high body temperature.
  • Tachycardia: Very rapid heart rate.
  • Irritability: Marked agitation and nervousness.
  • Profuse Sweating: Excessive perspiration due to hypermetabolism.
  • Diarrhea: Increased bowel movements, often severe.

This condition requires urgent medical intervention to prevent severe complications or death.

56
Q

Summary

True exophthalmos is a serious condition commonly associated with Grave’s disease, characterized by the protrusion of the eyeballs due to autoimmune inflammation. The condition can lead to various complications, including eye muscle paralysis and vision problems. Grave’s ophthalmopathy has distinct stages, from no symptoms to sight-threatening involvement of the optic nerve. Understanding the clinical differences between primary (Grave’s disease) and secondary (Plummer’s disease) hyperthyroidism is crucial, as these conditions affect different age groups and have varied courses. The thyroid storm is a medical emergency that can result from poorly controlled hyperthyroidism, leading to extreme symptoms like hyperthermia and tachycardia.

A
57
Q

Treatment of Thyrotoxicosis

Thyrotoxicosis, a condition of excessive thyroid hormone production, can be treated through different approaches depending on the severity, underlying cause, and patient factors. The main treatment categories includes?

A

The main treatment categories include medical treatment, symptomatic treatment, antithyroid treatment, and surgical treatment.

58
Q

1. Medical Treatment

Medical treatment involves the use of medications that target thyroid hormones or relieve symptoms associated with thyrotoxicosis. The indications for medical management include:

A
  • Primary thyrotoxicosis in patients with a small gland.
  • Primary thyrotoxicosis in younger patients.
  • Pre-operative preparation: To stabilize the thyroid before surgery.
  • Post-operative recurrence: When the condition returns after surgery.
  • Patient refusal of surgery: For patients who opt not to undergo surgery.

These medications aim to either inhibit thyroid hormone synthesis or control the symptoms caused by excess thyroid hormones.

59
Q

2. Symptomatic Treatment

This treatment targets the central nervous system and cardiovascular symptoms of thyrotoxicosis. The primary goal is to alleviate symptoms such as

A

The primary goal is to alleviate symptoms such as tremors, anxiety, palpitations, and increased heart rate.

  • Beta-adrenergic blockers: These are the cornerstone of symptomatic therapy for thyrotoxicosis, with Propranolol being most effective. It not only relieves symptoms but also reduces the conversion of T4 to T3 (the more active thyroid hormone).
  • Propranolol dosage: 40 mg taken 2 to 3 times daily for optimal symptom control.

Other symptomatic treatments include:

  • Fever management: Using cooling measures and antipyretics (fever-reducing medications).
  • Glucocorticoids: Administered intravenously if adrenal insufficiency is suspected.
  • Aggressive hydration: Infusing 3–5 liters of crystalloid fluids per day to compensate for gastrointestinal and insensible losses due to thyrotoxicosis.
  • Charcoal hemoperfusion: This can be employed in cases of iatrogenic or intentional overdose of levothyroxine (thyroid hormone replacement).
60
Q

How does Antithyroid Treatment work? And examples of its drug

A

Antithyroid drugs work by either:

  • Blocking iodine binding to tyrosine, which reduces the synthesis of thyroid hormones.
  • Decreasing antibody levels: This is especially useful in autoimmune thyrotoxicosis (Grave’s disease).
  • Blocking peripheral conversion of T4 to T3: This is the mechanism of propylthiouracil (PTU).

These drugs are used to inhibit thyroid hormone synthesis or block hormone release:

  1. Inhibitors of hormone synthesis:
  • Propylthiouracil (PTU): The drug of choice, particularly for pregnant or breastfeeding women.
  • Methimazole (Tapazole).
  1. Blockers of hormone release:
  • Lopanoic acid.
  • Saturated solution of potassium iodide (SSKI).
  • Lugol’s solution: Used to block the release of thyroid hormones and reduce vascularity in preparation for surgery.
61
Q

Propylthiouracil (PTU) Dosage in hyperthyroidism, thyrotoxic crisis and graves dxs

A
  • Hyperthyroidism:
  • Initial dose: 300–450 mg/day divided into 3 doses every 8 hours.
  • In severe cases, up to 600–900 mg/day may be required.
  • Maintenance dose: 100–150 mg/day in 3 divided doses.
  • Thyrotoxic crisis:
  • Initial dose: 200–300 mg orally every 4–6 hours on the first day.
  • Some practitioners may start with 600–1000 mg/day and gradually taper the dose.
  • Maintenance dose: 100–150 mg/day, divided every 8–12 hours.
  • Grave’s Disease:
  • Initial dose: 50–150 mg orally.
  • Maintenance dose: 50 mg every 8–12 hours for 12–18 months. The medication can be tapered off and discontinued if TSH levels normalize.
62
Q

4. Surgical Treatment

Surgical treatment is considered when medical management is not sufficient or when there are specific indications. Thyroid surgery typically involves removing part or all of the thyroid gland.

What are the pre surgical preparations?

Ad indications for surgical intervention

A

Pre-surgical Preparation

  • Euthyroid state: All patients must be made euthyroid (normal thyroid function) before surgery. This is essential to avoid complications like thyroid storm.
  • ECG, CXR, and Echocardiogram: These tests are performed to rule out arrhythmias and heart failure.
  • Thoracic inlet X-ray: For patients with large goiters to check for tracheal deviation or compression.
  • Lugol’s iodine: Administered before surgery to reduce thyroid gland vascularity and minimize the risk of hemorrhage.

Surgery is indicated in the following scenarios:

  • Grave’s disease in younger patients.
  • Large thyroid gland or exophthalmos.
  • Multinodular goiter or solitary nodule.
  • Unresponsiveness or poor compliance to medical therapy.
  • Contraindications to medical treatment, such as drug hypersensitivity.
63
Q

Summary

The treatment of thyrotoxicosis involves a combination of medical, symptomatic, antithyroid, and surgical approaches. Medical treatment focuses on controlling hormone production, while symptomatic treatment addresses the cardiovascular and nervous system effects. Antithyroid drugs like propylthiouracil and methimazole are the mainstays of therapy for reducing hormone synthesis. Surgery is reserved for patients with large goiters, exophthalmos, or when medical therapy fails. Proper preoperative preparation, including achieving a euthyroid state, is crucial to minimize complications during thyroid surgery.

A
64
Q

What are the Types of Thyroid Surgery

Thyroid surgery is often required in cases of large goiters, thyroid cancer, or unresponsive hyperthyroidism. There are various types of thyroid surgery depending on how much of the thyroid gland needs to be removed:

Examples are?

A
  1. Subtotal Thyroidectomy:
  • This procedure leaves behind 8-10 grams of thyroid tissue.
  • The remaining tissue is either equally distributed (4-5 grams on each side) or left on one side (8-10 grams).
  1. Near-Total Thyroidectomy:
  • Nearly all the thyroid tissue is removed, leaving only about 4 grams of tissue.
  1. Lobectomy with Isthmectomy:
  • This surgery involves the removal of one lobe of the thyroid along with the isthmus.
  • It is often performed for a solitary toxic nodule.
  1. Total Thyroidectomy:
  • The entire thyroid gland is removed.
  • This is often indicated in cases like thyroid cancer or severe thyrotoxicosis that does not respond to other treatments.
65
Q

What are the possible Complications of Thyroid Surgery

Thyroid surgery, while generally safe, has several potential complications. These can occur either during surgery or in the postoperative period.

A

1. Hemorrhage (Bleeding)

  • Primary bleeding: Occurs during surgery due to accidental cutting of arteries or veins.
  • Reactionary bleeding: Happens after surgery when a patient’s blood pressure normalizes (especially after the effects of anesthetics wear off) or due to pain. It can cause a significant hematoma.
  • Secondary bleeding: Occurs 7 days to 2 weeks after surgery, often due to a wound infection.

Airway obstruction is a serious complication that may arise from several factors after thyroid surgery, including:

  • Hematoma formation: A collection of blood compresses the airway.
  • Traumatic laryngeal edema: Swelling around the larynx caused by trauma during surgery.
  • Bilateral recurrent laryngeal nerve injury: This can result in vocal cord paralysis, leading to airway obstruction and difficulty breathing, especially in cases involving large goiters or complicated surgeries.
  • Tracheomalacia: Softening of the trachea, usually in patients with large or retrosternal goiters, can lead to airway collapse postoperatively.

The recurrent laryngeal nerve is responsible for controlling the vocal cords. Injury to this nerve can result in:

  • Unilateral injury: Results in hoarseness of voice and shortness of breath on exertion.
  • Bilateral incomplete injury: May cause stridor due to irritation of the adductor fibers.
  • Bilateral complete injury: Causes aphonia (loss of voice) and severe airway obstruction, which is a surgical emergency.

In difficult thyroid surgeries, the superior laryngeal nerve can also be damaged, which leads to the inability to produce high-pitched sounds (due to paralysis of the cricopharyngeal muscle).

  • Hypothyroidism, or thyroid insufficiency, can occur after surgery, particularly in patients who have undergone total thyroidectomy.
  • This complication may take 2 to 5 years to develop post-surgery, with an incidence rate of 20-45% in total thyroidectomy cases.
  • Hypoparathyroidism occurs when the parathyroid glands (which regulate calcium levels) are accidentally damaged, traumatized, or devascularized during surgery.
  • In cases where the parathyroid glands are removed or damaged, they may need to be reimplanted into other muscles, such as the deltoid or sternocleidomastoid muscles.
  • The incidence of hypoparathyroidism is low, occurring in less than 0.5% of patients who undergo thyroidectomy.
  • Since the parathyroid hormone (PTH) plays a crucial role in maintaining calcium homeostasis, the absence of PTH leads to hypocalcemia (low blood calcium levels).
  • These are late complications of thyroid surgery that can occur years later.
  • Keloid scars: Characterized by a thick, raised mass that extends beyond the incision line.
  • Hypertrophic scars: Remain confined to the original incision and do not cross the incision line.

Both keloid and hypertrophic scars can affect the aesthetic outcome and may require further treatment.

66
Q

Summary

Thyroid surgery, whether partial or total, comes with a range of complications, including bleeding, respiratory obstruction, nerve injuries, and long-term complications like hypothyroidism and hypoparathyroidism. Understanding these risks is crucial for both patients and healthcare providers when considering surgical intervention for thyroid conditions.

A
67
Q

Management of Some Important Post-Operative Complications

Thyroid surgery carries risks of complications, and early management is crucial to avoid severe consequences. Below are some common post-operative complications and their management:

1. Hematoma and Bleeding

A

Hematoma and bleeding are among the most frequent complications after thyroid surgery. If left untreated, a hematoma can compress the airway, leading to respiratory obstruction. When suspected:

  • Immediate action: Reopen the wound and ligate any bleeding vessel (wound exploration and bleeder ligation). This is an emergency and must be addressed promptly.
  • Severe bleeding/obstruction: Perform this at the bedside if necessary.
  • IV fluids: Administer IV fluids using a large-bore cannula to maintain blood pressure and circulation.
  • Blood transfusion: Transfuse the patient if significant blood loss has occurred.
68
Q

2. Respiratory Obstruction and Recurrent Laryngeal Nerve Damage

In cases of respiratory obstruction due to recurrent laryngeal nerve damage or hematoma:

A
  • Immediate intubation: If obstruction is severe and the airway is compromised, intubate the patient.
  • Cricothyroidotomy: If intubation is not feasible or is delayed, perform a cricothyroidotomy to ensure an airway.
  • Oxygen: Provide high-flow oxygen (8 liters per second) and ventilate the patient if necessary.
  • IV fluids: Establish an intravenous line using crystalloids to maintain hydration and blood pressure.
69
Q

3. Hypoparathyroidism it’s compilation and management

A

Hypoparathyroidism is a condition where the parathyroid glands are damaged during thyroid surgery, leading to hypocalcemia (low calcium levels). Symptoms of hypocalcemia include:

  • Circumoral paraesthesia (tingling around the mouth)
  • Mental status changes
  • Tetany (involuntary muscle contractions)
  • Carpopedal spasm (spasms of the hands and feet)
  • Laryngospasm, seizures, and cardiac issues (QT prolongation on ECG, cardiac arrest)

Management:

  • IV calcium: Administer 10 mL of 10% Calcium Gluconate over 10 minutes.
  • Oral calcium: If the patient is stable, give calcium carbonate (2.5g to 5g orally) to replenish calcium levels.
70
Q

4. Thyroid Storm and it’s management

A

A thyroid storm is a life-threatening complication that can occur in hyperthyroid patients undergoing thyroid surgery. It is characterized by an extreme exacerbation of thyroid hormone effects on the body, leading to fever, tachycardia, heart failure, and altered mental status.

Supportive Measures:

  • IV fluids to prevent dehydration.
  • Ice packs and antipyretics to reduce fever.
  • Oxygen through a mask at 8 liters per second.
  • Sedatives to calm the patient.

Specific Treatment:

  • Propranolol: Give 1mg of Propranolol IV as a drip, repeat if needed to control tachycardia.
  • Carbimazole or Propylthiouracil to inhibit thyroid hormone production.
  • Digoxin if heart failure is diagnosed to manage cardiac function.
71
Q

What’s Retrosternal Goitre it’s types and xteritics

A

A retrosternal goitre (RG) is a thyroid enlargement where part of the thyroid mass extends into the mediastinum (the central compartment of the thoracic cavity).

  1. Primary Retrosternal Goitre:
  • This type arises from ectopic thyroid tissue located in the mediastinum.
  • The goitre is not connected to the cervical thyroid and receives its blood supply from mediastinal vessels.
  • Primary RGs are rare, representing less than 1% of all retrosternal goitres.
  1. Secondary Retrosternal Goitre:
  • This type originates from the normal cervical thyroid but migrates downward into the mediastinum.
  • Secondary RGs are usually continuous with the cervical portion of the thyroid and receive their blood supply from cervical vessels, particularly the inferior thyroid artery.
72
Q

What are the Factors that facilitate this migration in secondary RG

A
  • Negative intra-thoracic pressure
  • Gravity
  • Traction forces during swallowing
  • Anatomical barriers like the thyroid cartilage, vertebral bodies, and strap muscles (especially in patients with short, large necks)
73
Q

Summary

Post-operative management of thyroid surgery complications includes handling emergency situations like hematoma, bleeding, respiratory obstruction, and life-threatening conditions like thyroid storm. Hypoparathyroidism requires swift calcium replacement, and retrosternal goitres are categorized based on their origin and location. Prompt recognition and appropriate management of these complications can prevent serious outcomes and ensure patient safety.

A
74
Q

what are the Types of Retrosternal Goitre

A
  1. Plunging Goitre:
  • This type of goitre rises with deglutition (swallowing) and then descends back into the thoracic inlet. It moves during swallowing but remains tethered to the thyroid.
  1. Mediastinal Goitre:
  • This type lies mostly within the chest but maintains a connection with the cervical thyroid gland through a narrow band of tissue.
  • It is supplied by thyroid vessels.
  1. Intrathoracic Goitre:
  • This goitre is located entirely within the chest and is completely separated from the cervical thyroid.
  • It receives its blood supply from mediastinal vessels, not the thyroid vessels.
75
Q

What are the Symptoms of Retrosternal Goitre

Many retrosternal goitres can remain asymptomatic for years. However, symptoms can occur when the goitre becomes large enough to compress nearby structures, such as

A

the trachea and esophagus.

  • Dyspnoea (difficulty breathing):
  • This occurs when the goitre displaces and compresses the trachea.
  • Worsened by posture: Symptoms can become aggravated when lying down or flexing the neck, as these positions further reduce the size of the thoracic inlet.
  • Patients may prefer to sleep while sitting upright, often spending the night in a chair to ease breathing difficulties.
  • Misdiagnosis:
  • Some patients may be mistakenly diagnosed with asthma due to the dyspnoea and respiratory distress caused by tracheal compression.
  • Dysphagia (difficulty swallowing):
  • This can occur if the goitre compresses the esophagus, leading to difficulty swallowing food.
76
Q

What is the test you caaan do at bedside to check for Retrosternal Goitre

A
  • Percussion of the sternum may reveal retrosternal dullness, suggesting that part of the goitre extends behind the sternum.
77
Q

What Investigations you you like to do in a Retrosternal Goitre

A

To confirm the presence and extent of a retrosternal goitre, several imaging studies can be used:

  1. X-ray: Can reveal tracheal deviation or compression.
  2. CT scan: Provides detailed images of the goitre’s size, location, and relation to surrounding structures.
  3. Tc99m Scan: A nuclear medicine test that evaluates thyroid function and can help differentiate between different types of thyroid nodules or masses.
78
Q

What Treatment would you do and what are some special considerations during surgery

A

The only definitive treatment for retrosternal goitre is thyroidectomy, which involves surgical removal of the thyroid or goitre.

  • Cervical approach: In most cases, the surgery is performed via an incision in the neck.
  • Median sternotomy: Rarely, if the goitre extends deeply into the chest, a sternotomy (opening the sternum) may be required to access the goitre.
  • Devascularization: The blood supply to the retrosternal portion of the goitre is usually derived from vessels in the neck. During surgery, these vessels must be carefully ligated to avoid excessive bleeding.
  • Recurrent Laryngeal Nerve Injury: Care must be taken to avoid injury to the recurrent laryngeal nerve, which is responsible for controlling the vocal cords. Damage to this nerve can result in voice changes or airway obstruction.
79
Q

Summary

Retrosternal goitre can remain symptomless for a long time, but when it grows large, it can cause dyspnoea and dysphagia due to compression of the trachea and esophagus. Proper investigation using imaging studies helps in diagnosis, while surgical removal is the definitive treatment. Surgical care must be taken to avoid complications such as nerve injury.

A
80
Q

Simple (diffuse) goiter
The entire thyroid gland swells and feels smooth.

Nodular goiter
A solid or fluid-filled lump called a nodule develops within the thyroid, making it feel lumpy.

Multinodular goiter
There are many nodules within the thyroid. These nodules may be visible or only discovered through examination or scans.

Substernal goiter
The thyroid gland extends underneath the breastbone and possibly in between the lungs.

Goiters can also be classified by the levels of thyroid hormones produced:

Toxic multinodular goiter: Makes too much thyroid hormone and causes hyperthyroidism.

Non-toxic multinodular goiter: Does not make too much thyroid hormone.

Euthyroid goiter: The thyroid gland creates the typical amount of hormone.

A
81
Q

How do you manage an emergency pt with goitre?

A

Let’s start with the emergency management of goitre using the A, B, C, D, E steps, focusing on addressing any immediate life-threatening conditions. Here’s a breakdown:

  1. Assess airway patency: Goitre, especially if large, can compress the airway, causing difficulty breathing.
  2. Intervene if airway is compromised: If there’s any obstruction or signs of airway compression (stridor, difficulty breathing), consider:
    • Positioning: Elevate the patient’s head.
    • Oxygen: Provide supplemental oxygen if hypoxia is evident.
    • Secure the airway: If obstruction persists, prepare for possible intubation or tracheostomy, particularly in severe cases of airway compression.
  1. Assess breathing: Look for signs of respiratory distress, including:
    • Respiratory rate and rhythm.
    • Use of accessory muscles.
    • Cyanosis.
  2. Support breathing as needed: Administer high-flow oxygen, monitor oxygen saturation, and prepare for ventilation support if respiratory failure is imminent.
  1. Assess circulation: Check pulse, blood pressure, and capillary refill time.
  2. Manage cardiovascular status: Large goitres with vascular involvement can lead to blood flow obstruction.
    • IV Access: Establish intravenous (IV) access.
    • Fluid support: Start IV fluids if there are signs of shock or hypotension.
    • Monitor for thyrotoxicosis in patients with hyperthyroidism, as it can cause a thyroid storm, which is life-threatening.
  1. Assess mental state: Evaluate for altered consciousness or agitation, which may indicate hypoxia or thyroid storm.
  2. Check blood glucose: Correct any hypoglycemia, as it may contribute to altered mental status.
  1. Expose and examine the neck area to visualize the size, location, and any visible signs of goitre compression.
  2. Check for additional signs: Look for skin changes, signs of hypothyroidism or hyperthyroidism, or any abnormal lumps.

After these emergency steps, we can move on to the History Taking section if you’re ready.

82
Q

How do you take history for a goitre pt.

A

Great! Let’s move on to the History Taking for a patient presenting with goitre. This step is essential to gather information about the patient’s symptoms, medical history, and risk factors.

  1. Presenting Symptoms:
    • Neck swelling: Ask about the duration, onset, and any increase in size over time.
    • Symptoms of compression: Difficulty breathing, swallowing issues, hoarseness of voice, or stridor.
    • Pain: Goitre is usually painless, but sudden pain could suggest hemorrhage into a thyroid cyst or an inflammatory process.
  2. Thyroid Dysfunction Symptoms:
    • Hyperthyroid symptoms (if overactive): Palpitations, weight loss, heat intolerance, tremors, sweating, and anxiety.
    • Hypothyroid symptoms (if underactive): Weight gain, fatigue, cold intolerance, constipation, hair loss, and dry skin.
  3. Systemic Symptoms:
    • General symptoms: Unexplained weight changes, fatigue, or changes in energy levels.
    • Symptoms of thyroid storm (if hyperthyroidism is suspected and severe): Fever, rapid heart rate, confusion, and agitation.
  4. Duration and Course:
    • Onset and progression: When was the swelling first noticed, and has it grown gradually or rapidly?
    • Pattern of symptoms: Are the symptoms persistent or episodic?
  5. Past Medical and Surgical History:
    • History of thyroid issues: Previous thyroid disorders, thyroiditis, or thyroid surgery.
    • Radiation exposure: History of head or neck radiation, which is a risk factor for thyroid disease.
    • Family history: Any family history of thyroid disease, goitre, or autoimmune conditions.
  6. Medications and Allergies:
    • Current medications: Any medication that could affect thyroid function (like lithium, amiodarone).
    • Iodine intake: Whether the patient has been using iodine supplements or has had recent iodine exposure (important, as it can affect thyroid function).
  7. Lifestyle and Social History:
    • Diet: Any iodine deficiency due to diet (such as low seafood or iodized salt intake).
    • Smoking and alcohol: These can influence thyroid function.
    • Occupational exposure: Exposure to chemicals or radiation at work.

This detailed history will help narrow down the possible causes and guide further steps. Let me know if you’re ready to move on to the Physical Examination section.

For the History Taking in goitre management, we’ll structure questions with explanations for their purpose.

  1. Presenting Symptoms
    • Ask about neck swelling: When did the swelling start, and has it changed in size?
      Rationale: This helps establish the duration and progression of the goitre, which can indicate whether it’s acute or chronic. Rapid enlargement might suggest hemorrhage, cystic degeneration, or malignancy.
    • Inquire about symptoms of pressure effects: Any difficulty swallowing (dysphagia) or breathing (dyspnoea), hoarseness of voice?
      Rationale: These symptoms suggest possible compression of nearby structures (esophagus, trachea, recurrent laryngeal nerve), which may indicate a large or retrosternal goitre.
  2. Systemic Symptoms
    • Ask about symptoms of hyperthyroidism: Palpitations, heat intolerance, weight loss, increased appetite, irritability, or sweating?
      Rationale: These symptoms help assess thyroid function, especially if there’s suspicion of Graves’ disease or a toxic goitre.
    • Ask about symptoms of hypothyroidism: Fatigue, cold intolerance, weight gain, dry skin, constipation, or hair loss?
      Rationale: Hypothyroid symptoms can indicate a hypothyroid goitre or Hashimoto’s thyroiditis, both of which have implications for treatment and management.
  3. Past Medical History
    • Any history of thyroid disease?
      Rationale: Previous thyroid issues could suggest a recurrent or chronic condition. Autoimmune conditions like Hashimoto’s disease or Graves’ disease often have familial links.
    • Previous neck irradiation or cancer treatment
      Rationale: Radiation exposure is a known risk factor for thyroid malignancies, especially in childhood or adolescence.
  4. Family History
    • Family history of thyroid disease or goitre
      Rationale: Goitre and thyroid dysfunction can be familial, and a history can guide the differential diagnosis, such as familial multinodular goitre or autoimmune thyroid disorders.
  5. Medication and Dietary History
    • Current medications, particularly iodine-containing or thyroid-related drugs
      Rationale: Medications like amiodarone or lithium can influence thyroid function, contributing to goitre formation.
    • Dietary iodine intake: Any recent changes in diet or history of living in an iodine-deficient area?
      Rationale: Iodine deficiency remains one of the most common causes of goitre worldwide, and identifying it can aid in preventive and corrective measures.
  6. Social History
    • Occupational exposure to radiation or other chemicals
      Rationale: Exposure to specific environmental factors may predispose individuals to thyroid disorders.
    • Smoking history
      Rationale: Smoking has been linked to thyroid enlargement and may exacerbate thyroid dysfunction, especially in those with autoimmune thyroiditis.

Once history-taking is complete, we’ll move on to Physical Examination. Let me know if you’d like to proceed.

83
Q

Physical examination for a thyroid patient

A

2. Neck Examination

In examining a patient with a goitre, thorough evaluation focuses on determining the goitre’s characteristics, assessing thyroid function, and identifying any potential complications or compression of nearby structures.

  1. General Physical Examination
    • Vital Signs: Check pulse, blood pressure, respiratory rate, and temperature.
      Rationale: Elevated pulse and blood pressure may suggest hyperthyroidism, while hypotension could indicate severe hypothyroidism. Respiratory rate assessment is crucial to identify any breathing difficulty due to tracheal compression.
    • Signs of Thyroid Dysfunction: Look for tremors, sweating, pallor, dry skin, and swelling of the face or eyelids.
      Rationale: These features can indicate hyperthyroid (sweating, tremor) or hypothyroid (pallor, dry skin) states.
  • Inspect for Visible Swelling: Observe the neck for any visible swelling or asymmetry. Ask the patient to swallow (as the thyroid moves up with swallowing).
    Rationale: Swelling that moves with swallowing is often thyroid-related. Assessing for asymmetry can differentiate between diffuse and nodular goitre.
  • Palpate the Thyroid Gland:
    • Size: Assess the size of the gland to gauge the goitre’s extent.
    • Consistency: Determine whether it feels soft, firm, or hard. A firm or hard goitre can suggest malignancy, while a soft consistency is often benign.
    • Surface: Identify if it is smooth (suggesting diffuse goitre) or nodular (suggesting multinodular goitre).
    • Tenderness: Check for tenderness, which could indicate thyroiditis or recent hemorrhage within a nodule.
    • Mobility: Evaluate if the goitre is fixed or mobile. A fixed, immobile goitre can raise suspicion for malignancy.
  • Assess for Retro-sternal Extension: Tap on the chest to elicit dullness over the manubrium and check for any visible venous engorgement.
    Rationale: Signs of retro-sternal extension can indicate large goitres, possibly pressing on the thoracic structures.
  1. Lymph Node Examination
    - Palpate cervical lymph nodes: Check for any enlargement, especially around the thyroid region.
    Rationale: Enlarged lymph nodes may suggest malignancy or thyroiditis.
  2. Special Maneuvers
    - Pemberton’s Sign: Have the patient raise their arms above their head for 1–2 minutes to see if there’s any facial congestion or cyanosis.
    Rationale: A positive Pemberton’s sign (facial redness or cyanosis) may indicate thoracic outlet obstruction due to retrosternal goitre compression on veins.

With the physical examination complete, the next step will be Investigations to gather further diagnostic information. Let me know when you’re ready to move forward.

84
Q

Investigation

A

After completing the history and physical examination, investigations are essential for confirming the diagnosis, determining thyroid function, and assessing the need for treatment or further intervention. Here’s an approach to investigations for goitre.

  1. Thyroid Function Tests (TFTs)
    • Serum TSH (Thyroid-Stimulating Hormone): This is typically the first test to assess thyroid function.
      Rationale: Low TSH suggests hyperthyroidism, while high TSH suggests hypothyroidism. Normal TSH indicates euthyroid status, where the goitre may be due to structural causes rather than functional imbalance.
    • Free T4 and Free T3: If TSH is abnormal, free T4 (and possibly T3) levels are checked to further assess thyroid status.
      Rationale: Elevated T4 or T3 confirms hyperthyroidism, and low T4 indicates hypothyroidism, helping guide treatment.
  2. Thyroid Antibodies
    - Anti-Thyroid Peroxidase (Anti-TPO) and Anti-Thyroglobulin Antibodies: These antibodies help identify autoimmune thyroid diseases.
    Rationale: Positive anti-TPO or anti-thyroglobulin antibodies are commonly seen in Hashimoto’s thyroiditis, while TSH receptor antibodies (TRAb) are seen in Graves’ disease, both of which can cause goitre.
  3. Imaging Studies
    • Ultrasound of the Thyroid: An ultrasound is the preferred initial imaging study for goitre evaluation.
      Rationale: Ultrasound helps to determine the size, structure (solid or cystic), and presence of nodules within the thyroid gland. It also aids in identifying suspicious features such as irregular margins or microcalcifications, which may suggest malignancy.
    • Radioisotope Thyroid Scan (Scintigraphy): In cases of thyrotoxicosis, this scan helps assess the function of the thyroid.
      Rationale: A scan differentiates between diffuse uptake in Graves’ disease and focal uptake in toxic nodular goitre. A ‘cold nodule’ (no uptake) on scintigraphy can indicate a higher risk of malignancy.
  4. Fine-Needle Aspiration Cytology (FNAC)
    • FNAC is recommended if the goitre has nodules, especially if they are larger than 1 cm or show suspicious ultrasound features.
      Rationale: FNAC is crucial for differentiating benign from malignant nodules. It provides a cytological diagnosis, guiding further management if surgery is needed.
  5. Cross-Sectional Imaging (CT/MRI)
    • CT or MRI of the Neck and Chest: Ordered in cases of retrosternal goitre or when there are signs of tracheal or esophageal compression.
      Rationale: CT or MRI provides detailed images of the extent of the goitre, particularly if it extends into the chest, and helps in surgical planning if there’s compression of nearby structures.
  6. Other Relevant Tests
    - Calcium Levels: Assessed if there is suspicion of a parathyroid disorder (e.g., hyperparathyroidism) that could coexist with goitre.
    Rationale: Elevated calcium may indicate hyperparathyroidism, often associated with thyroid or parathyroid pathology.

These investigations provide a comprehensive view of the goitre’s cause, nature, and impact, guiding appropriate management and treatment decisions. Let me know if you’d like to proceed to the next phase or if there’s anything specific you’d like me to expand on!

85
Q

History taking in goitre

A

To gather comprehensive information on a patient presenting with goitre, the history-taking process focuses on key elements, including symptom analysis, etiological factors, and potential differentials. Here’s a breakdown of each aspect:

Symptom Analysis
This section explores the characteristics of neck swelling and other associated symptoms to understand the goitre’s presentation and any underlying thyroid dysfunction.

  1. Analysis of Anterior Neck Swelling
    • Duration: How long the swelling has been present.
    • Mode of Onset: Was the onset gradual or sudden?
    • How it was Noticed: Did the patient or someone else notice the swelling?
    • Progression: The rate of growth over time (rapid or slow).
    • Associated Pain: If pain is present, further details are gathered, including:
      • Onset: When did the pain begin?
      • Duration: How long has the pain been occurring?
      • Severity: Pain intensity.
      • Character/Nature: Is the pain sharp, dull, throbbing, etc.?
      • Pattern: Is it intermittent or constant?
      • Radiation: Does the pain extend to other areas?
      • Alleviating and Aggravating Factors: What reduces or worsens the pain?
      • Progression: Has the pain intensity or frequency changed over time?
  2. Pressure Symptoms
    • Dyspnea/Stridor; Snoring: Possible airway obstruction.
    • Dysphagia: Difficulty swallowing due to compression.
    • Hoarseness/Voice Change: Possible involvement of recurrent laryngeal nerve.
    • Syncope: Fainting episodes possibly due to vascular compression.
    • Horner’s Syndrome: Signs of ptosis (drooping eyelid), miosis (constricted pupil), and anhidrosis (lack of sweating) can indicate sympathetic nerve involvement.
  3. Toxic Symptoms
    • Assessing for Metabolic/Endocrine Symptoms like:
      • Heat Intolerance and Excessive Sweating: Signs of hyperthyroidism.
      • Weight Loss with Good Appetite: Suggestive of increased metabolic rate.
      • Diarrhea and Hyperdefecation: Gastrointestinal effects of thyroid hormone excess.
      • Amenorrhea/Decreased Menstruation and Gynecomastia: Hormonal imbalances.
    • Cardiovascular Symptoms:
      • Palpitations, Dyspnea on Exertion, Chest Pain, Ankle Swelling: Symptoms indicating possible congestive heart failure (CCF).
    • Neuromuscular Symptoms:
      • Nervousness, Irritability, Tremors, Muscle Weakness: Neuromuscular manifestations of thyroid imbalance.
    • Eye Symptoms:
      • Visual Disturbances, Double Vision, Difficulty Closing Eyelids, Protruding Eyeball: Can indicate Graves’ disease.
    • Symptoms of Hypothyroidism:
      • Weight Gain, Cold Intolerance, Constipation, and Hoarseness: Common signs of low thyroid function.
      • Falling Hair, Memory Issues, Slowed Thought, Speech, and Actions, Muscle Fatigue, Menstrual Irregularities: Reflects a systemic slowdown.

Analysis of Etiological Factors
1. Physiologic Factors: Conditions like puberty, menstruation, pregnancy, and lactation can influence thyroid changes.
2. Endemic Factors: Long-term residence in iodine-deficient areas like rocky or mountainous regions increases goitre risk.
3. Goitrogens (Environmental and Dietary Factors):
- Food/Diet: High intake of goitrogenic foods (e.g., cassava, cabbage).
- Excessive Calcium in Water: Common in limestone regions; assess if iodized salt is used.
- Drugs: Includes oral contraceptives, para-aminosalicylic acid, phenylbutazone, chlorpropamide, tolbutamide, and iodine-containing cough mixtures.
- Irradiation: History of neck or head irradiation can be a risk factor.

Analysis of Differentials
1. Malignancy: Recent rapid growth, bone pain, dyspnea, cough with hemoptysis, weight loss, jaundice, or scalp swellings may suggest malignancy.
2. Infective/Inflammatory Processes: Associated fever, malaise, recent trauma, or short duration of symptoms could indicate an infection or inflammation.

Physical Examination
1. General Patient Positioning: Patient should sit with the head, neck, upper chest, arms, and legs exposed for thorough assessment.
2. Examination of Anterior Neck Mass:
- Inspection: Observe the site, number of swellings (solitary or multiple), shape (globular or butterfly), skin over swelling (any color change, ulcer, sinus, scar, or dilated neck veins), and surrounding skin for changes or enlarged lymph nodes. Note movement with swallowing and protrusion with tongue movement.
- Palpation (In Front of the Patient):
- Assess temperature, tenderness, tracheal position, attachment to skin, edges, and dimensions.
- Palpation (Behind the Patient):
- Ask the patient to swallow to check for retrosternal extension.
- Examine each thyroid lobe for surface (smooth or nodular), consistency (firm or cystic), and mobility.

  • Hypothyroidism Signs: Includes dry, inelastic skin, macroglossia, masklike face, delayed ankle reflexes.
  • Malignancy Signs: Assess for pulsatile metastases on the skull (seen in follicular carcinoma), spine abnormalities, and lung sounds (for metastasis).

This structured history-taking format enables thorough assessment of patients with goitre, allowing clinicians to evaluate both the primary condition and any associated complications or underlying causes.