Pituitary and thyroid diseases

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Here is a comprehensive medical student-level overview of both pituitary and thyroid diseases, drawn from Robbins & Kumar Basic Pathology and Textbook of Family Medicine.

Pituitary and Thyroid Diseases - Medical Student Overview

PART 1: THE PITUITARY GLAND

Anatomy & Physiology

The pituitary is a small, bean-shaped gland at the base of the brain within the sella turcica. It has two lobes:

Anterior lobe (adenohypophysis) - epithelial cells derived from the oral cavity; produces trophic hormones
Posterior lobe (neurohypophysis) - modified glial cells (pituicytes) and axonal processes from the hypothalamus

The hypothalamic-pituitary axis controls hormone release through stimulatory and inhibitory factors:

Anterior pituitary cell types and hormones:

Cell Type	Hormone(s)
Somatotrophs	GH (growth hormone)
Lactotrophs	PRL (prolactin)
Mammosomatotrophs	GH + PRL
Corticotrophs	ACTH, POMC, MSH
Thyrotrophs	TSH
Gonadotrophs	FSH, LH

Posterior pituitary stores and releases ADH (antidiuretic hormone) and oxytocin - both synthesized in the hypothalamus.

Clinical Presentations of Pituitary Disease

Pituitary disease produces symptoms in three ways:

Local mass effects - expanding lesions compress the optic chiasm -> bitemporal hemianopsia (most classic finding). Also cause headache, nausea, vomiting from raised intracranial pressure.
- Pituitary apoplexy: acute hemorrhage into a pituitary tumor -> sudden enlargement + loss of consciousness. This is a neurosurgical emergency.
Hyperpituitarism - excess secretion of trophic hormones, most often from an anterior pituitary adenoma.
Hypopituitarism - deficiency of trophic hormones from ischemic injury, surgery, radiation, inflammation, or nonfunctional adenomas.

Anterior Pituitary Adenomas (Key Exam Tumors)

Formerly called "pituitary adenomas," now officially termed pituitary neuroendocrine tumors (PitNETs) - though "adenoma" remains in common use.

Classification:

Microadenoma: <1 cm
Macroadenoma: >1 cm (more likely to cause mass effects)

Adenoma Type	Hormone	Key Clinical Features
Prolactinoma	PRL	Most common. Women: amenorrhea, galactorrhea, infertility. Men: impotence, decreased libido. Tx: dopamine agonists (cabergoline, bromocriptine)
GH-secreting	GH	Gigantism (before epiphyseal fusion) / Acromegaly (after fusion) - enlarged hands, feet, jaw (prognathism)
ACTH-secreting	ACTH	Cushing disease - central obesity, moon face, buffalo hump, striae, hypertension, hyperglycemia
TSH-secreting	TSH	Rare; causes secondary hyperthyroidism
Null cell / nonfunctional	None	Causes mass effects and hypopituitarism

Diagnosis: hormone assays + MRI of the sella turcica.

Hypopituitarism

Causes include:

Nonfunctional adenoma compressing normal gland
Sheehan syndrome (postpartum ischemic necrosis of pituitary)
Craniopharyngioma (most common pituitary tumor in children)
Radiation, surgery, inflammatory disease (sarcoidosis, TB)

Deficiencies appear in order: GH first, then FSH/LH, then TSH, then ACTH (ACTH last = most resilient).

Posterior Pituitary - Diabetes Insipidus

ADH deficiency (central DI) or renal resistance to ADH (nephrogenic DI) -> polyuria + polydipsia + dilute urine. Treated with desmopressin (DDAVP) in central DI.

PART 2: THE THYROID GLAND

Key Physiology

Hypothalamus releases TRH -> Anterior pituitary releases TSH -> Thyroid produces T4 (thyroxine) and T3 (triiodothyronine)
T3 is the active form (T4 is converted peripherally to T3)
Classic negative feedback: high T3/T4 suppresses TSH

Hyperthyroidism (Thyrotoxicosis)

Diagnosis: suppressed TSH (<0.1 mIU/L) + elevated free T4 (and/or T3).

Common causes:

Cause	Key Feature
Graves disease	Most common. TSH receptor-stimulating antibodies (TSH-RS Abs) mimic TSH. Diffuse goiter + ophthalmopathy (exophthalmos) + pretibial myxedema
Toxic multinodular goiter (Plummer disease)	Multiple autonomously functioning nodules
Toxic adenoma	Single autonomous nodule (gain-of-function mutation in TSH receptor or GNAS)
Subacute thyroiditis	Transient thyrotoxicosis followed by hypothyroidism
TSH-secreting pituitary adenoma	Rare secondary hyperthyroidism

Symptoms of hyperthyroidism (hypermetabolic state):

Tachycardia, wide pulse pressure, systolic hypertension
Weight loss, diarrhea
Anxiety, tremor, irritability
Warm, moist skin
Proximal muscle weakness (thyroid myopathy, ~50%)
Exophthalmos (Graves-specific)

Thyroid storm: acute severe hyperthyroidism - triggered by infection, surgery, or stress. Medical emergency; significant mortality from cardiac arrhythmias.

Apathetic hyperthyroidism: seen in elderly patients, where classic features are blunted - presents as unexplained weight loss or worsening heart disease.

Graves disease - long-term treatment options:

Antithyroid drugs (PTU or methimazole/MMI)
Radioactive iodine (¹³¹I) ablation
Thyroidectomy

Radioactive iodine scan findings:

Graves: diffuse uptake
Toxic adenoma: focal uptake in nodule
Thyroiditis: decreased uptake

Hypothyroidism

Diagnosis: elevated TSH (>10 mIU/L in overt hypothyroidism) + low free T4.

Causes:

Category	Examples
Primary (most common)	Hashimoto thyroiditis, iodine deficiency, surgery/radiation, drugs (lithium, amiodarone)
Secondary	Pituitary failure (low TSH + low T4)
Congenital	Thyroid dysgenesis or dyshormonogenesis

Hashimoto thyroiditis (Chronic Autoimmune Thyroiditis - CAT):

Most common cause in the developed world
Female:male ratio = 10-14:1, typically diagnosed in 5th decade
Anti-TPO antibodies (primary) and anti-thyroglobulin antibodies attack thyroid stroma -> progressive fibrosis
Treatment: L-thyroxine replacement (average dose 1.6 mcg/kg/day)
TSH monitored annually

Congenital hypothyroidism: Iodine deficiency is the most common cause worldwide (affecting ~2 billion people). If untreated, causes cretinism (severe intellectual disability + growth retardation).

Symptoms of hypothyroidism (hypometabolic state):

Fatigue, cold intolerance, weight gain
Constipation, bradycardia
Dry skin, coarse hair, hair loss
Myxedema (non-pitting edema)
Delayed deep tendon reflexes
In children: growth retardation, intellectual disability

Treatment: L-thyroxine replacement alone. Some patients may need combined T4+T3 if symptoms persist despite TSH in range.

Thyroid Nodules and Neoplasms

Multinodular goiter (MNG):

Enlarged thyroid with multiple nodules due to iodine deficiency or other factors
Follicles filled with stored colloid, lined by flattened epithelium
May become "toxic" (hyperthyroid) - called Plummer disease

Follicular adenoma:

Benign, solitary, encapsulated tumor derived from follicular epithelium
Most are nonfunctional (cold nodule on scan); a few are toxic (hot nodule)
Key hallmark: intact capsule - distinguishes it from follicular carcinoma
Mutations: TSH-receptor or GNAS gain-of-function in toxic adenomas; RAS or PTEN mutations in nonfunctioning adenomas

Thyroid Cancers (exam high-yield summary):

Type	Key Feature	Prognosis
Papillary (most common, ~85%)	Orphan Annie eye nuclei, psammoma bodies, nuclear grooves; RET/PTC and BRAF mutations	Excellent
Follicular	Capsular/vascular invasion (must check capsule); hematogenous spread	Good
Medullary	Calcitonin-secreting C-cells; amyloid stroma; associated with MEN2	Moderate
Anaplastic	Undifferentiated; most aggressive; local invasion rapid	Poor (weeks-months)

Quick Lab Reference

Condition	TSH	Free T4
Primary hyperthyroidism	Low	High
Secondary hyperthyroidism (pituitary TSHoma)	High/normal	High
Primary hypothyroidism	High	Low
Secondary hypothyroidism (pituitary failure)	Low/normal	Low
Subclinical hyperthyroidism	Low	Normal
Subclinical hypothyroidism	High	Normal

Sources: Robbins & Kumar Basic Pathology, Chapter 18 (Endocrine System); Textbook of Family Medicine 9e, Chapter 35 (Thyroid and Pituitary Diseases)

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