Summary of Hyperthyroidism

I. Causes of Hyperthyroidism:

Graves' Disease: An autoimmune condition where the body produces antibodies that stimulate
the thyroid gland to produce excess thyroid hormones (T3 and T4).

Toxic Multinodular Goiter (Plummer's Disease): The thyroid gland develops multiple nodules
that independently produce thyroid hormones.

Toxic Adenoma: A single nodule (adenoma) in the thyroid becomes overactive, producing
excessive thyroid hormones.

Subacute Thyroiditis: An inflammatory condition of the thyroid gland often triggered by a viral
infection.

Excessive Thyroid Medication: Overuse of thyroid hormone replacement medication.

Iodine-Induced Hyperthyroidism: Excessive iodine intake from diet or medications can trigger
hyperthyroidism.

Thyroid Cancer: Rarely, thyroid cancer can lead to hyperthyroidism.

II. Clinical Features (Signs and Symptoms) of Hyperthyroidism:

 Nervousness and Irritability

 Tachycardia (Fast Heart Rate)
 Weight Loss Despite Increased Appetite
 Heat Intolerance and Increased Sweating
 Tremors
 Enlarged Thyroid (Goiter)
 Fatigue and Muscle Weakness
 Exophthalmos (Protruding or Bulging Eyes) in Graves' Disease
 Menstrual Irregularities
 Frequent Bowel Movements or Diarrhea

III. Investigations for Hyperthyroidism:

Thyroid Function Tests: Includes measurement of serum levels of thyroid hormones (T3 and T4)
and thyroid-stimulating hormone (TSH). Elevated T3 and T4 levels with low or undetectable TSH
are indicative of hyperthyroidism.

Thyroid Ultrasound: To evaluate the size, structure, and nodules within the thyroid gland.
Radioactive Iodine Uptake (RAIU) Test: Measures the thyroid's ability to take up iodine, helpful
in differentiating causes of hyperthyroidism.

Thyroid Antibody Testing: May be done to diagnose autoimmune causes like Graves' disease.

Imaging: Computed tomography (CT) or magnetic resonance imaging (MRI) may be used to
assess the thyroid gland and adjacent structures.

IV. Treatment of Hyperthyroidism:

Antithyroid Medications: Drugs like Methimazole or Propylthiouracil (PTU) to reduce thyroid

hormone production.
Radioactive Iodine Therapy: A radioactive iodine drink or capsule is used to reduce thyroid
activity.
Thyroidectomy: Surgical removal of all or part of the thyroid gland.
Beta-Blockers: Medications like Propranolol to manage symptoms like rapid heart rate and
tremors.

Case Scenario of Hyperthyroidism:

Patient Profile:
Jane, a 32-year-old woman, presents to her primary care physician with complaints of
unexplained weight loss (despite a healthy appetite), palpitations, and excessive sweating for
the past three months. She also mentions that her menstrual cycle has become irregular.

Clinical Examination:

 Rapid heart rate (tachycardia).

 Fine tremors in her hands.
 Enlarged thyroid gland (goiter).
 Elevated blood pressure.
 Protruding eyes (exophthalmos).
Investigations:

 Thyroid function tests reveal elevated levels of T3 and T4 with a significantly low TSH
level.
 Thyroid ultrasound shows a diffusely enlarged thyroid gland.
 Radioactive iodine uptake test confirms high iodine uptake, consistent with Graves'
disease.

Diagnosis:
Jane is diagnosed with hyperthyroidism, specifically Graves' disease, based on her clinical
presentation, thyroid function tests, and radioactive iodine uptake results.
Treatment:

Initially, she is prescribed Methimazole to reduce thyroid hormone production.

Her symptoms improve, and her thyroid function tests begin to normalize.
Jane continues with regular follow-up visits to monitor her thyroid function and adjust her
medication as needed.

Summary of Hypothyroidism:

I. Causes of Hypothyroidism:

Primary Hypothyroidism: Dysfunction of the thyroid gland itself.

• Autoimmune Thyroiditis (Hashimoto's Thyroiditis): The immune system attacks the
thyroid gland, leading to inflammation and decreased thyroid function.
• Iodine Deficiency: Inadequate dietary iodine can result in thyroid hormone deficiency.
• Thyroid Surgery or Radiation: Removal of the thyroid gland or exposure to radiation
can impair its function.
• Medications: Some medications, such as lithium or certain anti-thyroid drugs, can
cause hypothyroidism.
Secondary Hypothyroidism: Dysfunction of the pituitary gland or hypothalamus, leading
to reduced stimulation of the thyroid gland.
• Pituitary Tumors
• Hypothalamic Disorders
II. Clinical Features (Signs and Symptoms) of Hypothyroidism:

o Fatigue and Weakness

o Weight Gain
o Cold Intolerance
o Constipation
o Dry Skin and Hair
o Depression
o Memory Problems
o Muscle Aches and Joint Pain
o Hoarseness
o Menstrual Irregularities
o Bradycardia (Slow Heart Rate)
III. Investigations for Hypothyroidism:

Thyroid Function Tests: Measurement of serum levels of thyroid hormones (T3 and T4)
and thyroid-stimulating hormone (TSH). Elevated TSH with low T3 and T4 indicates
hypothyroidism.
 Thyroid Antibody Testing: To identify autoimmune causes like Hashimoto's Thyroiditis.
IV. Treatment of Hypothyroidism:

• Levothyroxine (Synthetic Thyroid Hormone): The standard treatment for hypothyroidism

involves daily administration of levothyroxine to replace the deficient thyroid hormones.
Case Scenario of Hypothyroidism:

Patient Profile:

John, a 45-year-old man, presents to his family physician with complaints of fatigue, weight
gain, and feeling unusually cold, despite warm weather. He has also noticed that his skin and
hair have become dry, and he's experiencing constipation. He reports a history of Hashimoto's
Thyroiditis in his family.

Clinical Examination:

• Sluggish movements.
• Coarse, dry skin.
• Slow, hoarse speech.
• Bradycardia (slow heart rate).
Investigations:

• Thyroid function tests reveal an elevated TSH level and low T3 and T4 levels.
• Thyroid antibody testing confirms the presence of autoimmune antibodies associated with
Hashimoto's Thyroiditis.
Diagnosis:

John is diagnosed with hypothyroidism, specifically Hashimoto's Thyroiditis, based on his clinical
presentation, thyroid function tests, and autoimmune antibody status.

Treatment:

• He is prescribed levothyroxine to replace the deficient thyroid hormones.

• Over time, his symptoms improve, and his thyroid function tests normalize.
• John continues with regular follow-up visits to monitor his thyroid function and adjust his
medication as needed.
Causes of Cushing's Syndrome:

Adrenal Gland Tumors:

• Adrenal adenomas or carcinomas can produce excess cortisol (a stress hormone),
leading to Cushing's syndrome.
Pituitary Tumors:
• Pituitary adenomas, specifically corticotroph adenomas, can stimulate the adrenal
glands to overproduce cortisol (Cushing's disease).
Ectopic ACTH Production:
• Tumors in other parts of the body, such as the lungs or pancreas, can produce
adrenocorticotropic hormone (ACTH), which stimulates the adrenals to release
cortisol.
Exogenous Corticosteroid Use:
• Prolonged use of corticosteroid medications can result in iatrogenic Cushing's
syndrome.
II. Clinical Features (Signs and Symptoms) of Cushing's Syndrome:

Weight Gain and Central Obesity: Accumulation of fat in the abdomen and upper back
(buffalo hump).
Skin Changes: Thinning of the skin, easy bruising, and purple stretch marks (striae).
Moon Face: Round and flushed appearance of the face.
Hypertension: Elevated blood pressure.
Muscle Weakness: Especially in the hips and shoulders.
Osteoporosis: Weak bones, leading to fractures.
Irregular Menstrual Periods in Women
Hirsutism: Excess hair growth in women.
Mood Changes: Irritability, depression, and anxiety.
Glucose Intolerance: Increased risk of diabetes.
III. Investigations for Cushing's Syndrome:

 Cortisol Levels: Measurement of cortisol levels in urine, blood, or saliva over a 24-hour
period.
 ACTH Levels: To determine if the cause is ACTH-dependent or ACTH-independent.
 Imaging: CT or MRI scans to identify tumors in the adrenal glands or pituitary.
 Dexamethasone Suppression Test: A test to see how cortisol levels respond to synthetic
cortisol (dexamethasone).
 CRH Stimulation Test: Helps differentiate between pituitary and ectopic ACTH
production.

IV. Treatment of Cushing's Syndrome

Surgery: Surgical removal of tumors causing Cushing's syndrome, such as adrenal gland tumors
or pituitary adenomas.
Radiation Therapy: Used for pituitary tumors if surgery is not possible or effective.
Medications: Drugs that reduce cortisol production, such as ketoconazole or metyrapone.
Pituitary Radiotherapy: In cases of Cushing's disease (pituitary tumor).

Case Scenario of Cushing's Syndrome:

Patient Profile:

John, a 45-year-old man, visits his endocrinologist with a history of unexplained weight gain,
muscle weakness, and worsening hypertension over the past year. He has also noticed purple
stretch marks on his abdomen and mood swings.

Clinical Examination:

• Moon face.
• Buffalo hump.
• Elevated blood pressure.
• Skin thinning and easy bruising.
Investigations:

• Urine and blood cortisol levels are significantly elevated.

• ACTH levels are normal, suggesting an ACTH-independent cause.
• An abdominal CT scan reveals a 4 cm mass on the right adrenal gland.
Diagnosis:

John is diagnosed with Cushing's syndrome caused by an adrenal adenoma.

Treatment:

• John undergoes surgical removal of the adrenal adenoma.

• Post-surgery, his symptoms gradually improve, and cortisol levels return to normal.
• Regular follow-up is scheduled to monitor his progress and adrenal function.

Summary of Conn's Syndrome (Primary Aldosteronism):

I. Causes of Conn's Syndrome:

Conn's syndrome is characterized by the overproduction of aldosterone, a hormone that

regulates sodium and potassium levels in the body. The main causes include:

Aldosterone-Producing Adenoma (APA): A non-cancerous tumor in one of the adrenal glands

that produces excess aldosterone.
Bilateral Adrenal Hyperplasia (BAH): Overactivity of both adrenal glands, leading to increased
aldosterone production.
Familial Hyperaldosteronism (FH): A genetic condition that can result in Conn's syndrome.

II. Clinical Features (Signs and Symptoms) of Conn's Syndrome:

 Hypertension (High Blood Pressure): Persistent, often resistant to antihypertensive

medications.
 Hypokalemia (Low Blood Potassium): May lead to muscle weakness, muscle cramps,
and cardiac arrhythmias.
 Polyuria (Excessive Urination): Increased urine output.
 Polydipsia (Excessive Thirst): Increased thirst.
 Muscle Weakness and Fatigue: Due to low potassium levels.
 Headache: Can be a symptom of hypertension.
 Heart Palpitations: May result from electrolyte imbalances.
 Metabolic Alkalosis: An abnormal increase in blood pH due to excess aldosterone.

III. Investigations for Conn's Syndrome:

 Blood Tests: Measure aldosterone and renin levels. A high aldosterone-to-renin ratio is
suggestive of Conn's syndrome.
 24-Hour Urine Collection: To assess urinary potassium and aldosterone levels.
 Imaging: CT or MRI scans of the adrenal glands to identify adenomas or hyperplasia.
 Adrenal Vein Sampling: A specialized test to confirm the source of excess aldosterone
production (usually done when imaging is inconclusive).
IV. Treatment of Conn's Syndrome:

Surgical Removal (Adrenalectomy):

If a single adenoma is identified, surgical removal of the affected adrenal gland is curative.
In the case of bilateral adrenal hyperplasia, targeted medications are preferred.

Medications:
Mineralocorticoid receptor antagonists (e.g., spironolactone) to block the effects of excess
aldosterone.
Potassium supplements to correct hypokalemia.
Antihypertensive medications to manage blood pressure.

Case Scenario of Conn's Syndrome:

Patient Profile:
John, a 45-year-old man, presents to his primary care physician with a history of uncontrolled
high blood pressure, fatigue, and muscle cramps. He reports increased thirst and frequent
urination. Despite taking multiple antihypertensive medications, his blood pressure remains
elevated.

Clinical Examination:

 Hypertension with no apparent secondary cause.

 Muscle weakness and fatigue.
 Low serum potassium levels (hypokalemia).

Investigations:

 Blood tests reveal elevated aldosterone levels and an elevated aldosterone-to-renin

ratio.
 24-hour urine collection shows increased urinary aldosterone levels.
 A CT scan of the adrenal glands identifies a single adenoma in one of the adrenal glands.
Diagnosis:
John is diagnosed with Conn's syndrome, specifically due to an aldosterone-producing adenoma
in one of his adrenal glands.

Treatment:

John undergoes surgical removal of the affected adrenal gland (adrenalectomy).

Following surgery, his blood pressure normalizes, and his electrolyte imbalances resolve.
He continues with regular follow-up to monitor blood pressure and electrolyte levels.