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Visual Field Testing

Test: Automated perimetry

Use: Checks for optic chiasm compression

Important in macroadenomas, craniopharyngiomas

Classical finding: Bitemporal hemianopia

Basal Blood Hormone Levels

Taken fasting, in the morning

Can assess all anterior pituitary axes

Stress, illness, time of day can affect results

Urine Collection

24h Urine Collection

Cushing’s disease: Free cortisol

Diabetes Insipidus: Volume > 40 mL/kg, low osmolality

Practical issues: adherence, completeness

Salivary Hormone Testing

Midnight salivary cortisol

Very specific for Cushing’s syndrome

Reflects free cortisol, easy and non-invasive

Stimulation/Suppression Tests

Radiological Investigations

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Location:

In between eyes, behind nose

Brain base

Located in the pituitary fossa

Relationship to the hypothalamus (above the pituitary stalk)

Enclosed in a bony box →bony erosion when there is expansion

Surrounding Structures:

Hypothalamus: Control of pituitary function →Around the third ventricle at the base of the brain and above the pituitary stalk.

Pituitary Stalk: Pathway to the hypophyseal portal system (blood supply)

Optic Chiasm: Located immediately above the pituitary fossa; clinical importance in expansile lesions →problems with sight caused. More involved in suprasellar extensions.

Sphenoid Sinus: Located inferior to the pituitary fossa

Cavernous Sinus: Lateral extension of lesions may involve vascular and nervous structures (cranial nerves III, IV, VI). More involved in later extensions.

Temporal Lobes: Rare lateral extension can reach

Cerebral ventricles: Injuries can interrupt the flow of cerebrospinal fluid (CSF), leading to hydrocephalus

Vascularization:

Pituitary Portal System: Transport of releasing and inhibiting hormones from the hypothalamus to the anterior pituitary

Tissue:

Unique combination of primitive (foregut) tissue and neural (hindgut) tissue

Bone (Sella Turcica):

Bony structure surrounding the pituitary gland

Pituitary expansion (lateral, anterior or posterior) should cause bone erosion

Anterior Part (Adenohypophysis):

Embryological origin of Rathke's pouch (ectodermal)

Five main hormonal axes:

Gonadotropic

Growth

Prolactin

Thyroid

Adrenal

Posterior Part (Neurohypophysis):

Embryological origin of an evagination of the floor of the third ventricle (ectodermal + the Rathke’s pouch meets the an outpouching of the ventricular floor) →Genes involved in process, when mutated cause pituitary disease

Neuroanatomically connected to specific hypothalamic nuclei (supraoptic and paraventricular)

Acts as a storage organ for ADH (vasopressin) and oxytocin, synthesized in the hypothalamus

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Hypothalamus as Controller: Secretes releasing and inhibiting hormones that regulate the pituitary (Table 19.3, Figure 19.7).

Appetite, thirst, thermal regulation and sleeping/waking involved.

Combination centre of neural and endocrine functions to control the release of pituitary hormone-releasing factors.

Role in circadian rhythm, menstrual cyclicity and responses to stress/exercise/mood.

Through the portal system

VIP, neuropeptide Y and nitric oxide can also alter pituitary secretion

Anterior Pituitary:

→Positive control by the hypothalamus of AP hormones (apart from prolactin)

→5 anterior pituitary axes: gonadotropin axis, the growth axis , prolactin,   thyroid axis and the adrenal axis.

Growth Hormone (GH):

Dual control by GHRH (stimulatory) and somatostatin (inhibitory)

Stimulates the release of IGF-1 in the liver and other tissues

Thyroid Stimulating Hormone (TSH): Stimulated by TRH from the hypothalamus

Adrenocorticotropic Hormone (ACTH):

Stimulated by CRH from the hypothalamus

Vasopressin (ADH) also stimulates the secretion of ACTH

Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH):Stimulated by GnRH (LHRH) from the hypothalamus

Prolactin:

Under tonic inhibition of hypothalamic dopamine

TRH may increase prolactin secretion

Posterior Pituitary:

→Neuro-anatomically connected to specific hypothalamic nuclei

→Acts as a storage organ

Vasopressin (Antidiuretic Hormone, ADH) + Oxytocin: Synthesized by the supraoptic and paraventricular nuclei in the anterior hypothalamus →transported along the axon and stored in the posterior pituitary.

Both nonapeptides

Damage to the stalk of pituitary alone does not prevent synthesis and release of ADH and oxytocin.

Negative Feedback: Hormones from peripheral endocrine glands exert negative feedback on the hypothalamus and pituitary

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Divided into adenohypophysis & neurohypophysis, separated by the pars intermedia

Adenohypophysis (endocrine function)

Tissue Type: Glandular epithelial

Staining: Stains darker due to high cellularity

Cell types:

Chromophils (strongly staining cytoplasm):

Acidophils (red-staining):

Somatotrophs – secrete GH

Lactotrophs – secrete Prolactin

Basophils (purple-blue staining):

Corticotrophs – secrete ACTH, MSH

Thyrotrophs – secrete TSH

Gonadotrophs – secrete LH, FSH

Chromophobes (poorly staining cytoplasm):

Possibly degranulated chromophils or stem-like cells

Erythrocytes

Pars Intermedia

Located between anterior and posterior lobes

Contains colloid-filled cysts (remnants of Rathke’s pouch)

Contains basophilic cells and sometimes lymphocytes

May extend into neurohypophysis

Neurohypophysis (storage function)

Tissue Type: Neural tissue

Staining: Pale/light staining due to unmyelinated axons and low nuclei count

Components:

Unmyelinated axons: originate in the hypothalamus (supraoptic & paraventricular nuclei)

Herring bodies:

Dilated nerve terminals storing:

Oxytocin

Antidiuretic hormone (ADH) / Vasopressin

Released into nearby capillaries

Pituicytes:

Glial support cells

Highly branched; help maintain structure

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Anterior Pituitary

Prolactin:

Synthesized in lactotroph cells of the anterior pituitary

Secretion

Tonic inhibition by dopamine from the hypothalamus (major regulator)

Stimulated by:

Thyrotropin-releasing hormone (TRH)

Angiotensin II (Ang II)

Arginine vasopressin (AVP)

Estradiol:

Increases sensitivity of lactotrophs to TRH

Decreases sensitivity to dopamine inhibition

Increases during acute stress: e.g., sexual intercourse, intense exercise, myocardial infarction.

During pregnancy:

Prolactin levels increase 10-fold

Suckling reflex inhibits hypothalamic dopamine → further prolactin release

Action

Primary functions: induces and maintains lactation & promotes mammary gland development

Suppresses reproductive function: inhibits GnRH → reduces LH/FSH → decreases gonadal steroid production

Ovary: leads to hypoestrogenism and anovulation

Reduces libido and sexual drive (contributes to postpartum anorgasmia)

Growth Hormone (GH)

Produced by somatotrophs in the anterior pituitary

Sleep is very important!

Age & nutritional influences

Secretion

Stimulated by:

Growth hormone-releasing hormone (GHRH)

Ghrelin

Estrogens

Inhibited by:

Somatostatin

Insulin-like growth factor 1 (IGF-1)

Excess glucocorticoids

Pulsatile secretion, especially during sleep

Declines with age

Influenced by nutritional state (malnutrition suppresses GH)

Action

Stimulates:

Protein synthesis and nitrogen retention

Lipolysis (mobilization of fat stores)

Bone growth, especially at the epiphyseal plates

Antagonizes insulin action (reduces glucose uptake)

Stimulates IGF-1 production in liver and other tissues:

Endocrine, paracrine, and autocrine functions.

Enhances protein synthesis, bone turnover, and insulin sensitivity

Adrenocorticotropic Hormone (ACTH)

Made by corticotrophs in the anterior pituitary

Derived from POMC (pro-opiomelanocortin) gene

Secretion

Pulsatile and exhibits circadian rhythm (peaks in early morning)

Stimulated by:

Corticotropin-releasing hormone (CRH)

Stress, exercise, illness

Inhibited by:

Negative feedback from glucocorticoids on CRH, ACTH, and POMC expression

Action

Maintains metabolic homeostasis

Critical for the neuroendocrine stress response

Stimulates adrenal cortex → glucocorticoid release (mainly cortisol)

Gonadotropins: FSH & LH

Produced by gonadotrophs in the anterior pituitary

Regulation

GnRH from the hypothalamus (pulsatile release essential):

Continuous GnRH → receptor desensitization

Kisspeptin neurons stimulate GnRH secretion

Estrogen:

Acute rise → positive feedback (LH surge)

Chronic elevation → negative feedback

Progesterone:

Slows GnRH pulse frequency

Enhances FSH and LH response to GnRH

Action

In females:

FSH → follicle growth

LH → ovulation and corpus luteum formation

In males:

FSH → spermatogenesis

LH → testosterone production (Leydig cells)

Thyroid Stimulating Hormone (TSH)

Produced by thyrotrophs in the anterior pituitary

Regulation

Stimulated by:

Thyrotropin-releasing hormone (TRH)

Inhibited by:

Thyroid hormones (T3/T4) – negative feedback

Dopamine, somatostatin, glucocorticoids

Action

Pulsatile secretion (low amplitude, long half-life)

Stimulates:

Thyroid hormone synthesis and release (T3 and T4)

Thyroid gland growth

Posterior Pituitary

Vasopressin (Antidiuretic Hormone, ADH)

Synthesized by magnocellular neurons in the hypothalamus

Transported down axons and stored in the posterior pituitary (neurohypophysis)

Secretion

Stimulated by:

Increased plasma osmolality:

Detected by osmoreceptors in the hypothalamus

Even a 1% rise in osmolality (e.g., dehydration) can trigger release

Decreased blood volume or pressure:

Detected by baroreceptors in carotid sinus and aortic arch

Needs ~10% drop in blood volume for activation

Angiotensin II

Nausea, pain, hypoglycemia, and stress

Drugs: e.g., nicotine, morphine, and some SSRIs increase ADH

Inhibited by:

Ethanol (alcohol)

ANP (Atrial Natriuretic Peptide)

Low plasma osmolality

Adequate hydration or hypervolemia

Receptors

V1 receptors (Gq protein-coupled):

Located on vascular smooth muscle

Causes vasoconstriction → increases systemic blood pressure

V2 receptors (Gs protein-coupled):

Located in the renal collecting ducts (principal cells)

Promotes insertion of aquaporin-2 channels → increases water reabsorption

Reduces urine volume, concentrates urine

Acts via cAMP second messenger

V3 receptors (in anterior pituitary):

Enhance ACTH release (synergistic with CRH)

Action

Renal/Water balance:

Promotes water retention in kidneys

Helps maintain plasma osmolality and blood pressure

Produces concentrated urine

Vascular:

Vasoconstriction increases systemic vascular resistance and blood pressure

Endocrine:

Facilitates ACTH secretion via V3 receptors (enhances stress response)

Oxytocin

Synthesized in the hypothalamus (paraventricular and supraoptic nuclei)

Stored and released by the posterior pituitary

Action

Uterine contraction during labor (positive feedback loop via cervical stretch)

Milk ejection during breastfeeding (stimulated by suckling)

Emotional bonding and social behavior (“love hormone”)

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⬆️ Can Cause Hyperprolactinemia

Antidopaminergics:

Antipsychotics: Chlorpromazine, Haloperidol, Risperidone

Antiemetics: Metoclopramide, Domperidone, Prochlorperazine

⬆️ Affect Cortisol Physiology

Estrogens (e.g. OCPs): Increase CBG, elevating total cortisol

Steroids (e.g. prednisone): Chronic use → Cushingoid features, HPA axis suppression

Anabolic steroids: Suppress gonadotropin secretion

⬆️/⬇️ Affect Thyroid Axis

Levothyroxine (excessive use): Causes suppression of TSH

⬇️ Therapeutic Dopamine Agonists

Cabergoline, Bromocriptine: Inhibit PRL → treatment of hyperprolactinemia

🔄 Drugs That Affect ADH (Vasopressin)

Desmopressin is a synthetic form of the vasopressin hormone

⬆️ ADH: SSRIs, TCAs, carbamazepine, chlorpropamide → SIADH risk

⬇️ ADH: Lithium, alcohol, phenytoin → risk of DI

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Transsphenoidal resection: First-line for many adenomas (e.g. non-functioning, GH, ACTH, TSH-secreting)

Transcranial: For large/complex suprasellar tumors (e.g. craniopharyngiomas)

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Always replace cortisol before thyroxine to avoid adrenal crisis

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Important for exam!! Be able to differentiate

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Extensions from pituitary or hypothalamus can produce visual defects

Upward expansion: suprasellar extension

Lateral extension: involves vascular & nervous structures in the cavernous sinus, rarely reaches the temporal lobe

Lateral, anterior, or posterior expansion must cause bony erosion

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Tumours are the most common cause of pituitary disease.

Most are benign pituitary adenomas.

Investigations:

MRI of the pituitary →Gold standard + Shows mass right away

Problem: Sometimes incidentalomas happen, so the MRI detects a small lesion that is not a tumor.

Visual Fields →Formally by computed perimetry or Goldmann perimetry + clinical assessment confrontational using a small red pin as target

Common seen lesions: temporal quadrantanopia and bitemporal hemianopsia

Hormone levels

→The clinical presentation/complaints of the patient are related to tumor characteristics:

Local Effects: Visual field defects/visual loss (compression of the optic chiasm), cranial nerve injuries - the cavernous sinus (III, IV, VI)-, headaches, changes in appetite, thirst, sleep, precocious puberty (hypothalamic centre compression), hydrocephalus (compression of the ventricles causing interruption of the CSF), CSF rhinorrhea (sphenoid sinus invasion).

Result of inadequate production of hormone by the remaining normal pituitary (hypothyroidism)

Tumors can be able to produce more than one pituitary hormone. 3 major conditions caused by adenomas:

→Prolactin excess: Prolactinoma or Hyperprolactinemia = Chromophobe adenomas in staining appearance

→GH excess: Acromegaly or Gigantism= Somatotroph adenomas normally acidophil (sometimes due to G protein mutations) →Problems in growth

→ACTH secretion excess: Cushing’s Disease and Nelson’s Syndrome = Corticotroph adenomas normally basophil →Slow lethargic adult with pale skin

Treatment for Tumor:

1. Aimed at removal or control!

Surgery →Gold Standard if possible. Via the trans-sphenoidal route normally. For large tumors through the open transcranial route.

Radiotherapy →Only controls tumor mass, normally when surgery doesn’t fully resolve problem

Medical Therapy→Somatostatin analogues and/or dopamine agonists  can shrink tumor

2. Reduction of excess hormone secretion!

Mostly through removal of tumors but sometimes medical treatment.

Dopamine agonists = Prolactinoma

Somatostatin analogues + Growth Hormone antagonists = Acromegaly

Nothing for ACTH secretion = need for removal

3. Replacement of hormone deficiencies such as hypopituitarism.

Differential Diagnosis for Masses:

Craniopharyngioma: Usually cystic and hypothalamic tumour often calcifies arises from Rathke’s pouch →Mimics an intrinsic pituitary lesion. Most common in children

Uncommon Tumors: Meningiomas, gliomas, chondromas, germinomas, pinealomas, Primary pituitary carcinomas, Metastases (rare)

Hypophysitis: Inflammatory masses in hypothalamus and pituitary. Rare pituitary specific conditions (Autoimmune Hypophysitis, Postpartum Hypophysitis) or pituitary manifestations of more generalized disease processes(Sarcoidosis, Granulomatosis). These lesions are common in weird patterns of hypopituitarism and diabetes insipidus.

Carotid artery aneurysms: Can look like pituitary tumors

Cystic lesions can present as a pituitary mass (arachnoid cyst, Rathke's pouch cyst).

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Most common cause: prolactinoma

PRL > 200 μg/L usually suggests prolactinoma.

Microadenomas: more common in females

Macroadenomas: similar distribution in both sexes

Other causes: pregnancy, lactation, stress, dopamine antagonists, opiods, CCB, renal failure, hypothyroidism, stalk compression, trauma

Clinical features:

Women:

Amenorrhea, oligomenorrhea

Galactorrhea

Infertility

Osteopenia (chronic hypoestrogenism)

Men:

Low libido, erectile dysfunction

Infertility

Visual field defects (macroadenoma)

Galactorrhea is rare

Chronic: ↓ muscle mass, sparse beard growth

Diagnosis:

Fasting morning serum prolactin:

Normal < 20 μg/L in men, < 25 μg/L in women

Rule out secondary causes:

TSH, T4 (exclude hypothyroidism)

Renal function

Pregnancy test

Imaging: Pituitary MRI for suspected adenoma

Treatments:

First-line: Dopamine agonists (e.g. cabergoline, bromocriptine)

Address underlying causes

Surgery: Transsphenoidal resection for drug-resistant macroadenomas or acute optic compression

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Cushing's disease (ACTH-dependent Cushing’s Syndrome)

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Cushing's disease (ACTH-dependent Cushing’s Syndrome)

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Most common endogenous cause: Corticotrope pituitary adenoma

Exogenous corticosteroids = most common overall cause (iatrogenic), ectopic ACTH (small cell lung carcinoma), adrenal tumours

Clinical features:

Central obesity, moon face, buffalo hump

Purple striae

Proximal muscle weakness

Thin skin, easy bruising

Hypertension, glucose intolerance, osteoporosis

Menstrual irregularities, mood changes

Diagnosis:

Initial screening (choose ≥2):

24-hour urinary free cortisol

Overnight dexamethasone suppression test

Late-night salivary cortisol

ACTH assay:

High ACTH = ACTH-dependent

Low ACTH = ACTH-independent (suggests adrenal source)

MRI: to visualize pituitary lesion (may require inferior petrosal sinus sampling if imaging inconclusive)

Treatments:

Transsphenoidal surgery (for pituitary adenoma)

Medical therapy (when surgery not feasible or as bridge):

Steroidogenesis inhibitors: ketoconazole, metyrapone

Pituitary-directed agents: pasireotide

Radiation or bilateral adrenalectomy in refractory cases

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Most common cause: Somatotroph adenoma (GH-secreting pituitary tumor)

Rare cause: Ectopic GHRH/GH secretion (e.g. pancreatic or lung tumors)

Clinical features:

Skeletal changes:

Frontal bossing, prognathism, enlarged hands/feet, increased shoe/ring size

Widened tooth spacing, jaw malocclusion

Gigantism if onset before epiphyseal fusion (in children)

Soft tissue features:

Coarse facial features, thickened skin

Enlarged nose, lips, tongue

Heel pad thickening

Visceromegaly:

Cardiomegaly, LVH, arrhythmias

Thyroid enlargement

Metabolic:

Insulin resistance, diabetes mellitus

Diagnosis:

Serum IGF-1: screening test (elevated in acromegaly)

Oral glucose tolerance test (OGTT):

GH levels fail to suppress after glucose load

MRI of pituitary

Treatments:

Surgery: Transsphenoidal resection

Medical therapy:

Somatostatin receptor ligands (SRLs): octreotide, lanreotide

GH receptor antagonist: pegvisomant

Dopamine agonists (less effective)

Radiation: adjunctive in residual/recurrent disease

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Very rare, typically macroadenomas

Often locally invasive

Clinical features:

Features of thyrotoxicosis: weight loss, heat intolerance, palpitations, anxiety, goiter

May have mass effect (visual disturbances, headache)

Diagnosis:

TSH, Free T4, Free T3:

Inappropriate normal or elevated TSH in the setting of high free T4/T3

May measure α-subunit (elevated in TSH-omas)

MRI: confirms pituitary adenoma

Treatments:

Transsphenoidal surgical resection (first-line)

May require somatostatin analogs (octreotide) or radiotherapy if residual tumor

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Usually acquired: pituitary tumors, surgery, irradiation, trauma, infiltrative disease

Clinical features:

Body composition: ↓ Lean body mass, ↑ Fat mass (especially visceral), ↑ Waist-to-hip ratio

Metabolic: hyperlipidemia & insulin resistance

Quality of life: fatigue, depression, low self-esteem, poor concentration

Cardiovascular: ↑ Atherosclerosis risk, ↑ Blood pressure, ↓ Cardiac output

Diagnosis:

IGF-1: often low

Stimulation testing: insulin tolerance test, GHRH-arginine test

Treatments:

GH replacement:

Subcutaneous recombinant GH

Monitor IGF-1 levels, lipids, glucose, and body composition

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Most common hormonal deficiency in hypopituitarism

Causes:

Genetic disorders

Hypothalamic dysfunction: anorexia, stress, excessive exercise

Stalk compression, trauma, tumors

Clinical features:

Women:

Oligomenorrhea or amenorrhea

Infertility

↓ Vaginal secretions, ↓ libido

Breast atrophy, osteoporosis

Men:

↓ Libido and erectile function

Infertility

↓ Muscle mass, weakness

↓ Beard/body hair growth

Testicular atrophy, soft consistency

Fine facial wrinkles, osteoporosis

Diagnosis:

Sex hormone levels:

↓ Estradiol/testosterone

Low or inappropriately normal FSH/LH

MRI: assess for structural lesion

Evaluate other pituitary hormones

Treatments:

Men:

Testosterone replacement (IM/transdermal)

For fertility:

hCG + FSH injections (stimulate spermatogenesis)

Pulsatile GnRH (if hypothalamic cause)

Women:

Cyclic estrogen + progesterone (HRT)

For fertility:

Gonadotropin injections

Pulsatile GnRH (if hypothalamic)

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Ischemic infarction of the pituitary due to severe postpartum hemorrhage

Pathophysiology

During pregnancy: Pituitary enlarges and becomes more vascular

Massive blood loss leads to hypoperfusion and infarction

Results in hypopituitarism, often pan-hypopituitarism

Clinical Features

Failure to lactate (↓ prolactin)

Amenorrhea or oligomenorrhea

Fatigue, hypotension

Symptoms of hypothyroidism, adrenal insufficiency, and hypogonadism

Diagnosis

History of severe postpartum hemorrhage

Hormone panel: ↓ ACTH, TSH, FSH/LH, GH, prolactin

MRI: May show empty sella or pituitary atrophy

Treatment

Lifelong hormone replacement:

Hydrocortisone

Levothyroxine

Estrogen/progesterone or testosterone

GH (optional depending on needs)

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Craniopharyngioma is a benign, slow-growing, suprasellar tumor

Arises from epithelial remnants of Rathke’s pouch, an embryologic precursor of the anterior pituitary

Epidemiology:

Bimodal age distribution:

Common in children (5–14 years) and older adults (50–75 years)

Most cases in children present before age 15

No strong gender predilection

Pathology:

Composition: cystic & solid components, often calcified, epithelial-lined cysts filled with "machine oil"-like cholesterol-rich fluid

Histological types:

Adamantinomatous: children, calcifications, cysts, "wet keratin", and cholesterol crystals

Papillary: adults, less cystic, rare calcifications

Clinical features: due to mass effect and hypopituitarism

Headache

Vomiting (↑ intracranial pressure)

Papilledema

Visual field defects: classically bitemporal hemianopsia due to optic chiasm compression

Growth failure (in children, due to GH deficiency)

Delayed puberty

Sleep disturbances, personality changes, behavioral issues

~90% of patients develop hypopituitarism: ↓ GH, TSH, ACTH, LH/FSH

Can lead to diabetes insipidus

Diagnosis:

MRI:

Shows cystic mass, often suprasellar, with variable solid components

Can reveal relationship to optic chiasm, hypothalamus, and pituitary

CT scan:

Best for detecting calcifications, seen in ~90% of cases (especially in adamantinomatous type)

Endocrine workup:

Comprehensive pituitary hormone panel to assess for deficiencies

Treatments:

Surgical Resection:

Approach depends on tumor size and location:

Transcranial approach for large/suprasellar tumors

Transsphenoidal approach for intrasellar/accessible lesions

Goal: Maximal safe resection, though complete excision is often difficult due to tumor adherence to vital structures (optic chiasm, hypothalamus)

Radiation Therapy:

Post-operative radiotherapy (e.g., proton therapy or stereotactic radiosurgery):

Reduces risk of recurrence, which is common

Hormone Replacement Therapy:

Lifelong pituitary hormone replacement usually required:

Hydrocortisone, levothyroxine, growth hormone, sex hormones, possibly desmopressin (DDAVP) if diabetes insipidus develops

Prognosis:

Generally good long-term survival, especially with early treatment

High recurrence rate (~20–30%), especially if resection is incomplete

Requires lifelong follow-up

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Kallmann’s Syndrome: Isolated gonadotropin deficiency

→Due to mutation in KAL1 gene in short arm of X chromosome

→Anosmia due to lack of anosmin

→Anosmin has a role in the developing olfactory system and migration of GnRH secreting neurons

Septo-optic Dysplasia: Congenital and rare

→Due to mutation in HESX1 gene

→Childhood presentation

→Midline: forebrain abnormalities, hypopituitarism and hypoplasia

Pituitary Apoplexy: Tumor that enlarges fast due to hemorrhage or infarction

→ Causes double vision, headache, sudden severe visual loss

→At times followed by acute life-threatening hypopituitarism

→Treated mostly conservatively with hormone replacement.

→When there is a sudden deterioration in visual acuity and fields then surgical decompression of the optic chiasm is done.

The empty sella Syndrome: Seen on pituitary imaging. Due to sudden infarction or regression of pituitary tumor  OR defect in the diaphragma and extension of the subarachnoid space. Sella turcica is involved.

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Partial or complete deficiency of one or more anterior pituitary hormones

Progression (often sequential): GH → FSH/LH → TSH → ACTH

Causes:

Pituitary tumors or surgery

Radiation

Traumatic brain injury

Infiltrative diseases

Vascular causes (Sheehan's syndrome, apoplexy)

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- know function & physiology/secretion of each hormone and what it means if it is hyper-secreted or deficient, what symptoms it then produces!

- important diagnostics: visual field, OGT (article), basal hormone testing, dexamethasone suppression