The pituitary gland sits in the sella turcica, directly below the optic chiasm. When a pituitary tumour grows upward (suprasellar extension), it compresses the chiasm. The fibres that cross at the chiasm are from the nasal halves of each retina — these carry the temporal visual fields. Hence compression → bitemporal hemianopia ^[1][2].

Key concept: The nasal fibres decussate; temporal fibres do not. A chiasmal lesion therefore produces a bitemporal (heteronymous) field defect, not a homonymous one. ^[1]

Localise the field defect:

The title supplies the visual clue even though this 25-slide deck contains no visual-field diagram. Compression from below may begin with superior-temporal field loss before the full bitemporal pattern becomes apparent.

The anterior pituitary has five cell types producing six hormones, regulated by hypothalamic releasing/inhibiting hormones delivered via the hypophyseal portal system:

The posterior pituitary stores and releases AVP (ADH) and oxytocin, synthesized in the hypothalamus and transported down the pituitary stalk.

• Visual loss: Bitemporal hemianopia (classic); can progress to complete blindness if untreated. May start as a subtle upper temporal quadrantanopia (chiasm compressed from below, affecting inferior nasal fibres first).
• Headache: Often non-specific and may relate to sellar pressure, dural stretch or cavernous-sinus involvement. A sudden severe headache, vomiting, reduced consciousness, meningism, ophthalmoplegia or abrupt visual loss is different: suspect pituitary apoplexy and treat as an endocrine/neurosurgical emergency. ^[8]
• Cranial nerve palsies: Large tumours with lateral extension into the cavernous sinus can compress CN III, IV, V₁, V₂, VI → diplopia, facial numbness.
• CSF rhinorrhoea: If tumour erodes through the floor of the sella into the sphenoid sinus.

These depend on whether the tumour secretes a hormone (functioning adenoma) or destroys normal pituitary tissue (causing hypopituitarism).

These are sellar or parasellar lesions discovered on imaging performed for another reason. Evaluate the clinical context, dedicated pituitary imaging, hormone hypersecretion and deficiencies; assess visual fields when the lesion approaches the optic apparatus. Observation versus surgery depends on symptoms, growth, chiasmal proximity, endocrine effects, age, functional status and patient preference—not size alone. ^[7]

6–18% of all brain tumours. Unselected autopsy series: prevalence 12–22%; most common being prolactinomas. ^[1]

Size classification:

• Microadenoma: < 10 mm
• Macroadenoma: ≥ 10 mm

Practical consideration from the slide: Usually no hypopituitarism if microadenoma (< 1 cm). ^[1]

This is a useful tendency, not a rule. Microadenomas can still cause clinically important hormone excess, while macroadenoma size alone does not mandate an operation. ^[7]

Functioning adenomas (70–80%) vs. Non-functioning adenomas (20–30%) ^[1]

Transcription factors that regulate pituitary cytogenesis ^[1]:

• TPIT (TBX19) — corticotroph differentiation
• Pit1 (POU1F1) — lactotroph, mammosomatotroph, somatotroph, thyrotroph differentiation
• SF1 (NR5A1) — gonadotroph differentiation

Why this matters:

1. Improves diagnostic accuracy: Immunohistochemical staining for transcription factors gives strong nuclear staining (vs. patchy cytoplasmic staining with hormonal stains alone) ^[1]
2. Adds prognostic context: the slide gives SF1-lineage/gonadotroph tumours as a relatively indolent example ^[1], but lineage alone does not guarantee behaviour; invasion, proliferation, residual tumour and longitudinal imaging also matter.

The term "Pituitary Neuroendocrine Tumour (PitNET)" has been proposed by pathologists as a new name, but is not widely supported by endocrinologists. ^[1]

This sentence records the lecture's terminology debate. The WHO 2022 pathological classification uses PitNET, while pituitary adenoma remains common in clinical guidance and practice; recognise both names rather than treating one as an error. ^[7]

Key features ^[1]:

• 50% have calcification present (this is a classic radiological finding — look for suprasellar calcification on CT)
• 50% present with symptoms in childhood
• 25% present between ages 20–40
• Hypopituitarism (e.g., growth retardation in children)
• Stalk compression → diabetes insipidus (because AVP travels down the stalk)
• Chiasmal compression — common
• Obstruction to 3rd ventricle → hydrocephalus

Craniopharyngiomas arise from Rathke's pouch remnants. They are histologically benign but locally aggressive. Treat the slide's percentages as historical teaching estimates; the useful recognition cluster is suprasellar lesion + calcification + growth/endocrine deficits + AVP-D + chiasmal or third-ventricular effects.

Lecture-era diagnostic pattern ^[1]:

• Prolactin usually > 10× normal (the slide gives > 5000 mU/L)
• Tumour shrinkage by > 50% in 90% of patients treated with dopamine agonists

Marked prolactin elevation proportionate to tumour size supports prolactinoma, and biochemical/radiological response to dopamine agonist adds evidence. Do not apply one universal numerical cut-off without the laboratory reference range or ignore the hook effect in a large mass. ^[6]

Diagnosis as presented in the 2023 slide ^[1]:

• Screening: Serum IGF-1 — above normal for age and gender
• Confirmation: Non-suppressible serum GH during OGTT
  • Nadir > 0.4 ng/mL (AACE 2011)
  • Nadir > 1 ng/mL (AES 2014)

Why IGF-1 and not random GH? GH is pulsatile and fluctuates throughout the day (exercise, stress, sleep all affect it). IGF-1 is produced by the liver in response to GH but has a long half-life and stable levels → better screening test.

Current interpretation: In a patient with typical clinical features, age-adjusted IGF-1 > 1.3× the upper limit of normal confirms acromegaly. Repeat IGF-1 using the same validated assay when results are equivocal or discordant; OGTT-based GH suppression is useful in selected equivocal cases, but its cut-off is assay-, sex-, BMI- and glucose-status dependent. Do not mix the slide's 0.4 and 1 ng/mL historical cut-offs as if both were universal. ^[9]

Not detailed on these slides. First establish endogenous hypercortisolism with validated testing, then determine ACTH dependence and localise with expert endocrine assessment. Pituitary MRI does not by itself prove Cushing disease, and bilateral inferior petrosal sinus sampling is reserved for biochemically confirmed ACTH-dependent Cushing syndrome when the source remains uncertain; it is not a screening test. ^[10]

MRI (magnetic resonance imaging): imaging modality of choice. ^[1]

MRI with gadolinium contrast is superior to CT for soft tissue resolution of the sella. The normal pituitary enhances brightly; microadenomas enhance less (hypoenhancing on early post-contrast images). CT is useful for craniopharyngiomas (detects calcification).

Broad indications as stated on the 2023 slide ^[1]:

• All tumours causing pituitary hyperfunction
• All macroadenomas
• For prolactinomas, medical treatment may be preferred

Transsphenoidal: route of choice

• Approach: transnasal endoscopic or sub-labial The slide lists a transfrontal route for very large suprasellar extension/severe chiasmal compression. ^[1]

Why transsphenoidal? It avoids brain retraction—the surgeon goes through the nose and sphenoid sinus directly into the sella. Modern extended endoscopic transsphenoidal approaches can reach many suprasellar lesions; a transcranial route is reserved for selected anatomy after specialist neurosurgical planning, not simply because chiasmal compression is severe.

Advantages: Rapid decrease in secretion and tumour size ^[1] Disadvantages: Residual/recurrence especially if macroadenomas; hypopituitarism; diabetes insipidus ^[1] Acute complications: Post-operative bleeding; CSF rhinorrhoea ^[1]

Conventional external irradiation ^[1] Radiosurgery: "Gamma knife"; "X-knife" — not used if suprasellar extension to within 5 mm of optic chiasm ^[1]

The slide says radiation may be primary therapy for macroprolactinomas. ^[1]

That statement should be treated as historical: dopamine agonist therapy is usually first-line for macroprolactinoma, including many tumours affecting vision, with close monitoring. Surgery is considered for resistance/intolerance, selected resectable tumours or urgent complications; radiotherapy is generally reserved for residual, recurrent or aggressive disease that is not controlled by medical and surgical treatment. ^[6]

Why delayed effect? Radiation causes DNA damage that takes months to years to fully manifest as cell death and reduced hormone production. Patients need ongoing hormonal monitoring for years post-radiation.

I. Structural damage of hypothalamus, pituitary, or pituitary stalk ^[1]:

The mnemonic is "T-I-I-I-I-I" (Tumours, Trauma, Infarction, Infiltration, Infections, Immunologic):

II. Functional disorders: isolated or multiple ^[1]:

Usually no hypopituitarism if microadenoma (< 1 cm) ^[1] (a tendency, not a guarantee) Complication of radiotherapy for head and neck tumours such as nasopharyngeal carcinoma (NPC) ^[1] — this is especially high-yield for HKU given the high prevalence of NPC in Southern China May be hypothalamic in origin — elevated prolactin and diabetes insipidus often present ^[1] ACTH deficiency — often asymptomatic and unmasked by stress ^[1]

AVP-Deficiency (AVP-D) — formerly Cranial DI: ^[1]

• Lesions of hypothalamus, pituitary stalk, or posterior pituitary
• Urine osmolality increases with DDAVP treatment

AVP-Resistance (AVP-R) — formerly Nephrogenic DI: ^[1]

• No response to AVP or DDAVP
• Genetic or acquired (e.g., lithium, hypercalcaemia, hypokalemia, chronic kidney disease)

Reason for name change: to eliminate confusion with diabetes mellitus and endorse a name that more accurately reflects the disease's aetiology ^[1]

The proposed names improve aetiological clarity and reduce dangerous confusion with diabetes mellitus, although older records, examinations and many clinicians still use central/cranial DI and nephrogenic DI. ^[13]

1. Confirm hypotonic polyuria with measured 24-hour urine volume and simultaneous serum/urine osmolality. Exclude diabetes mellitus/solute diuresis, diuretics, renal impairment, hypercalcaemia and hypokalaemia first.
2. If hypernatraemia or high plasma osmolality already coexists with inappropriately dilute urine, AVP dysfunction may be evident without deliberate dehydration.
3. A classical indirect water-deprivation test uses serial weight, urine output, urine osmolality, plasma sodium/osmolality and then desmopressin response. The slide-style thresholds (> 600, < 300 and > 50% response) best describe complete syndromes; partial AVP-D, partial AVP-R and primary polydipsia overlap.
4. Do not perform water deprivation unsupervised. Stop according to protocol for excessive weight loss, rising sodium/osmolality, hypotension or symptoms. Where available, specialist copeptin-based testing—particularly hypertonic-saline-stimulated copeptin—has substantially higher diagnostic accuracy than the indirect water-deprivation test for distinguishing AVP-D from primary polydipsia. ^[13][14]

1. Visual field defect interpretation: "A patient bumps into things on their sides. What visual field defect? Where is the lesion?" → Bitemporal hemianopia; optic chiasm compression.

2. Prolactinoma vs. stalk compression: Relate prolactin magnitude to tumour size and the laboratory range, but remember medicines, systemic causes, macroprolactin and the hook effect. The slide's > 10× versus < 3× pattern is a clue, not an absolute rule.

3. Diagnosis of acromegaly: Explain why age-adjusted IGF-1 is preferred to random GH and when repeat testing or an OGTT is needed.

4. AVP-D/AVP-R investigation: Past paper 2016 SAQ Q4 asked about biochemical confirmation and DDAVP differentiation. In clinical practice, first prove hypotonic polyuria; water deprivation is supervised, and copeptin-based testing may better separate partial AVP-D from primary polydipsia. ^[3][13][14]

5. Causes of hypopituitarism: The "T-I-I-I-I-I" mnemonic with specific examples. Sheehan's syndrome is a classic stem. Lymphocytic hypophysitis from checkpoint inhibitors is increasingly tested.

6. Hypogonadism: Differentiate central (low LH/FSH) from peripheral (high LH/FSH). Features of pre-pubertal vs. post-pubertal onset.

7. Craniopharyngioma: Calcified suprasellar tumour in a child with growth retardation and DI → classic stem.

8. Post-operative complications of transsphenoidal surgery: DI, hypopituitarism, CSF rhinorrhoea, bleeding.