After reading this note you will be able to recognise, investigate and outline the acute and definitive management of common pituitary disorders seen in Kenyan clinical rotations. Always verify drug choices, doses and local protocols against the Kenya Ministry of Health guidelines and your hospital formulary.
Definition
A pituitary disorder is any condition that impairs the normal structure or function of the pituitary gland, leading to excess or deficiency of one or more pituitary hormones. Disorders are broadly grouped into hypopituitarism, hyperpituitarism, and space‑occupying lesions (adenomas, cysts, infiltrative disease).
Anatomy and physiology you need
| Structure | Key point for clinical relevance |
|---|---|
| Anterior pituitary (adenohypophysis) | Produces ACTH, TSH, GH, PRL, LH, FSH; vulnerable to vascular compromise and compression. |
| Posterior pituitary (neurohypophysis) | Stores ADH and oxytocin; lesions here cause diabetes insipidus. |
| Stalk (infundibulum) | Conveys hypothalamic releasing/inhibiting hormones; stalk effect → hyperprolactinemia. |
| Portal circulation | Low‑pressure venous system; thrombosis → pan‑hypopituitarism. |
| Sella turcica | Bony enclosure; expansion produces headache, visual field loss (bitemporal hemianopia). |
Causes and risk factors
| Category | Common aetiologies in Kenya |
|---|---|
| Primary tumours | Pituitary adenoma (prolactinoma, GH‑secreting, ACTH‑secreting), craniopharyngioma (children). |
| Infiltrative / infectious | Tuberculosis (sellar TB), HIV‑associated opportunistic infections, malaria cerebral complications, fungal infections (Histoplasma, Cryptococcus). |
| Vascular | Pituitary apoplexy (hemorrhage/infarction), Sheehan’s syndrome (post‑partum haemorrhage). |
| Autoimmune / inflammatory | Lymphocytic hypophysitis (more common in postpartum women). |
| Traumatic / iatrogenic | Head injury, surgery, radiotherapy to brain. |
| Systemic diseases | Sickle cell disease (micro‑infarction), systemic lupus erythematosus, sarcoidosis. |
| Metabolic / endocrine | Chronic glucocorticoid therapy, severe hypothyroidism (can suppress TSH). |
Pathophysiology
- Adenoma growth → mass effect → compression of optic chiasm → bitemporal visual field loss.
- Hormone hypersecretion → autonomous release → feedback inhibition lost → clinical syndrome (e.g., prolactinoma → galactorrhoea, amenorrhoea).
- Infiltration/infection → granulomatous destruction → loss of hormone‑producing cells → pan‑hypopituitarism.
- Vascular insult (apoplexy, Sheehan’s) → sudden ischemia → necrosis of pituitary → acute ACTH, TSH, GH deficiency → adrenal crisis.
- Stalk compression → reduced dopamine delivery to lactotrophs → disinhibition → mild hyperprolactinemia.
Arrows representation:
``` Adenoma → ↑ hormone secretion → loss of negative feedback → clinical syndrome
Adenoma → ↑ size → optic chiasm compression → visual field defect
Infection/TB → granuloma → destruction of pituitary cells → hormone deficiency → adrenal, thyroid, gonadal failure
Vascular event → ischemia → necrosis → abrupt loss of ACTH → adrenal crisis
Stalk compression → ↓ dopamine → ↑ prolactin → galactorrhoea/infertility ```
Clinical features
| Aspect | Key questions for the history | Why it matters / pathophysiologic link |
|---|---|---|
| General | Weight change (gain or loss), appetite, fatigue, fever, night sweats | Weight gain suggests ACTH excess (Cushing); loss points to hypopituitarism or chronic infection (TB, HIV). Fever/night sweats raise suspicion of infectious pituitary involvement (TB, malaria‑related sepsis). |
| Headache | Onset, pattern (steady vs. sudden), radiation to eyes, aggravating/relieving factors | Pituitary macroadenoma or apoplexy compresses the dura and cavernous sinus → frontal‑temporal headache; sudden “thunderclap” headache suggests apoplexy or hemorrhage. |
| Visual symptoms | Blurred vision, loss of peripheral vision, double vision, colour changes | Enlargement of the sellar mass compresses the optic chiasm → bitemporal hemianopia; cavernous sinus invasion can affect cranial nerves III, IV, VI → diplopia. |
| Menstrual / reproductive | Cycle regularity, amenorrhoea, galactorrhoea, infertility, libido | Hyperprolactinaemia (prolactinoma) suppresses GnRH → oligomenorrhoea/amenorrhoea; galactorrhoea from prolactin excess. In men, low libido and erectile dysfunction reflect gonadotropin deficiency. |
| Sexual / adrenal | Decreased libido, erectile dysfunction, loss of axillary/pubic hair, skin hyperpigmentation, salt craving | ACTH deficiency → adrenal insufficiency (fatigue, hyperpigmentation). Low LH/FSH → loss of secondary sexual hair. |
| Metabolic | Central obesity, moon face, striae, easy bruising, hypertension, glucose intolerance | Classic Cushing’s syndrome from ACTH‑secreting adenoma or ectopic source. |
| Growth / bone | Height change (in children), joint pain, fractures, bone pain | GH excess (acromegaly) → soft‑tissue swelling, joint pain; GH deficiency → reduced bone density. |
| Infectious / systemic | Recent TB exposure, HIV status, malaria episodes, sickle‑cell crises, rheumatic fever history | TB, HIV, malaria and sickle‑cell disease can infiltrate or infarct the pituitary, leading to hypopituitarism or mass effect. |
| Medication / substance | Use of dopamine antagonists, estrogen therapy, steroids, opiates | Dopamine antagonists raise prolactin; steroids suppress ACTH → secondary adrenal insufficiency. |
Examination findings and rationale
| Finding | Why it occurs |
|---|---|
| Visual field testing (confrontation) | Detects bitemporal hemianopia from chiasmal compression. |
| Fundoscopy | May reveal papilledema if raised intracranial pressure from large adenoma or apoplexy. |
| Cranial nerve palsies (III, IV, VI) | Mass effect on cavernous sinus; explains diplopia. |
| Galactorrhoea | Prolactin excess stimulates milk production. |
| Skin changes | Purple striae, bruising, acne, hyperpigmentation reflect cortisol excess or deficiency. |
| Blood pressure & glucose | Hypertension & hyperglycaemia are common in Cushing’s; hypotension may signal adrenal crisis. |
| Body habitus | Central obesity, moon face, buffalo hump point to chronic cortisol excess. |
| Peripheral edema, loss of axillary/pubic hair | Low androgen production from gonadotropin deficiency. |
| Joint swelling, enlarged hands/feet | GH excess (acromegaly) causes soft‑tissue overgrowth. |
| Signs of chronic infection | Cervical lymphadenopathy, hepatosplenomegaly (TB, malaria) may coexist with pituitary involvement. |
Differential diagnosis
| Condition | Points toward it | What separates it from other pituitary disorders |
|---|---|---|
| Prolactinoma | Galactorrhoea, amenorrhoea, infertility, mild headache | Isolated hyperprolactinaemia; normal ACTH/cortisol; MRI shows sellar lesion without cavernous sinus invasion. |
| ACTH‑secreting adenoma (Cushing disease) | Central obesity, striae, hypertension, hyperglycaemia, facial rounding | Elevated ACTH with loss of diurnal cortisol rhythm; high‑dose dexamethasone suppression fails to suppress cortisol. |
| Non‑functioning macroadenoma | Headache, visual field loss, hypopituitarism, no hormone excess | Normal hormone panels; mass effect dominates; MRI shows large sellar mass. |
| Pituitary apoplexy | Sudden severe headache, vomiting, rapid visual loss, ophthalmoplegia | Acute hemorrhage/infarction on MRI; emergency presentation distinguishes from slower‑growing adenomas. |
| Tuberculous pituitary abscess | History of TB, HIV, constitutional symptoms, pituitary enlargement | CSF/acid‑fast bacilli positive; MRI shows rim‑enhancing lesion; often associated with basal meningitis. |
| Lymphocytic hypophysitis (autoimmune) | Peripartum women, headache, visual changes, pituitary enlargement | Autoimmune antibodies, transient enlargement, often resolves with steroids; differs from adenoma by lack of discrete tumor. |
| Metastatic pituitary lesion | Known primary cancer, rapid visual decline, pain | Rapid progression, multiple lesions, history of malignancy; imaging shows infiltrative pattern. |
Investigations
| Test | What it answers | Typical interpretation |
|---|---|---|
| Serum prolactin | Hyperprolactinaemia vs. stalk effect | Markedly raised → prolactinoma; mild rise → stalk compression. |
| Morning cortisol & ACTH | ACTH‑dependent vs. independent Cushing | High ACTH with high cortisol → pituitary source; low ACTH → adrenal source. |
| 24‑h urinary free cortisol | Overall cortisol output | Elevated in Cushing; normal excludes chronic excess. |
| Low‑dose dexamethasone suppression | Presence of cortisol excess | Failure to suppress → Cushing syndrome. |
| High‑dose dexamethasone suppression | Distinguish pituitary vs. ectopic ACTH | Suppression → pituitary; no suppression → ectopic. |
| IGF‑1 (and GH after oral glucose) | GH excess | Elevated IGF‑1; lack of GH suppression after glucose → acromegaly. |
| TSH, free T4, LH, FSH, testosterone/estradiol | Global pituitary function | Low peripheral hormones with normal pituitary hormone → hypopituitarism. |
| MRI sellar region (contrast) | Structural lesion | Microadenoma (<10 mm), macroadenoma, cyst, infiltrative pattern. |
| CT chest/abdomen (if ectopic ACTH suspected) | Search for ectopic source | Mass in lung, pancreas, thymus suggests ectopic ACTH. |
| HIV, TB (GeneXpert, sputum), malaria smear | Infectious contributors | Positive tests support infectious pituitary involvement. |
| Visual field testing (automated perimetry) | Functional impact of mass | Bitemporal hemianopia confirms chiasmal compression. |
Diagnosis and severity
- Establish the hormonal profile – Identify which pituitary axes are over‑ or under‑active using the hormone panel above.
- Correlate with imaging – MRI defines size (micro <10 mm, macro ≥10 mm), invasiveness (cavernous sinus, suprasellar extension) and lesion character (solid, cystic, hemorrhagic).
- Classify severity
- Mild – Hormone excess/deficiency without visual field loss, lesion ≤10 mm, no cavernous sinus invasion.
- Moderate – Hormonal disturbance plus visual field defect or lesion 10–20 mm, limited suprasellar extension.
- Severe – Acute apoplexy, profound hypopituitarism, visual loss >30 % of field, lesion >20 mm with cavernous sinus invasion or rapid growth.
- Assign a primary diagnosis – e.g., “Prolactinoma (micro, symptomatic)" or “Non‑functioning macroadenoma with partial hypopituitarism, moderate severity.”
- Document any co‑existing infections (TB, HIV, malaria) that modify management and prognosis.
The clinical approach proceeds from confirming the hormonal disturbance, through imaging to stage the lesion, and finally to grade severity, which guides urgency of treatment and need for multidisciplinary input (endocrinology, neurosurgery, infectious disease).
Management
| Phase | Key actions | Rationale / safety notes |
|---|---|---|
| Immediate stabilisation | • Secure airway, breathing, circulation – treat adrenal crisis with IV hydrocortisone (or equivalent) and isotonic saline. <br>• Correct severe hyponatraemia or hypoglycaemia promptly. <br>• Give high‑dose glucocorticoid before any thyroid hormone if both are deficient. | Prevent life‑threatening shock, seizures and cerebral oedema. Glucocorticoid replacement precedes thyroxine to avoid precipitating adrenal collapse. |
| Definitive endocrine therapy | • Long‑term glucocorticoid replacement (physiological dose). <br>• Mineralocorticoid replacement if primary adrenal insufficiency (fludrocortisone). <br>• Levothyroxine titrated to normal TSH once cortisol covered. <br>• Sex steroid replacement (estrogen‑progestogen or testosterone) for gonadal failure. <br>• Desmopressin for central diabetes insipidus. | Mimic normal pituitary output; avoid over‑replacement which can cause osteoporosis, hypertension or fluid overload. |
| Surgical / radiological treatment | • Trans‑sphenoidal surgery for macroadenoma causing visual loss, CSF leak or apoplexy. <br>• Radiosurgery (Gamma Knife) for residual or recurrent tumour. <br>• Dopamine agonists (e.g., cabergoline) for prolactinoma; somatostatin analogues for GH‑secreting adenoma. | Aim for tumour control while preserving pituitary function. Dopamine agonists are first‑line for prolactinoma because they shrink tumour and restore gonadal axis. |
| Monitoring | • Daily electrolytes, glucose and blood pressure in acute phase. <br>• 6‑weekly TFT, cortisol, IGF‑1, prolactin after initiating therapy. <br>• Visual field testing after surgery or when tumour enlarges. <br>• MRI at 3‑6 months post‑op, then annually if stable. | Detect under‑ or over‑replacement, tumour regrowth and complications early. |
| Contra‑indications / safety | • Do not start levothyroxine before adequate glucocorticoid cover. <br>• Avoid abrupt withdrawal of steroids – taper slowly. <br>• Dopamine agonists are contraindicated in uncontrolled hypertension or severe cardiac disease. | Prevent adrenal crisis, thyroid storm, hypertensive emergencies and cardiac arrhythmias. |
Complications and prognosis
| Complication | Typical presentation | Impact on prognosis |
|---|---|---|
| Adrenal crisis | Sudden hypotension, vomiting, abdominal pain, hypoglycaemia | High early mortality; reversible with prompt steroids and fluids |
| Permanent hypopituitarism | Need for lifelong hormone replacement | Good quality of life if replacement is adequate; risk of osteoporosis, cardiovascular disease |
| Visual field loss | Bitemporal hemianopia, decreased acuity | May improve after decompression; delayed treatment leads to permanent deficit |
| Pituitary apoplexy | Sudden severe headache, ophthalmoplegia, altered consciousness | Acute emergency; surgery within 24 h improves outcomes |
| Diabetes insipidus | Polyuria, polydipsia, hypernatremia | Managed with desmopressin; chronic cases need monitoring of fluid balance |
| Tumour recurrence | Rising hormone levels, new visual symptoms, MRI growth | Requires repeat surgery or radiotherapy; long‑term surveillance essential |
| Cardiovascular disease | From chronic cortisol excess (Cushing) or GH excess | Increases morbidity; control of hormone excess improves survival |
Overall, patients with microadenomas and isolated hormone excess have an excellent prognosis when treated appropriately. Macroadenomas with visual compromise or apoplexy carry higher morbidity but still achieve good outcomes with timely intervention.
High‑yield exam points
- “First, give steroids, then thyroxine” – the classic pitfall in combined ACTH and TSH deficiency.
- Pituitary apoplexy mimics meningitis – look for sudden headache, ophthalmoplegia, and a known adenoma.
- Prolactinoma vs. hypothyroid‑induced hyperprolactinaemia – check TSH; primary hypothyroidism raises TRH and prolactin.
- Empty‑sella syndrome – often asymptomatic; if present with headache, consider CSF leak.
- Differentiating central vs. nephrogenic DI – water deprivation test; response to desmopressin confirms central.
- Examiner bedside question: “A patient with pan‑hypopituitarism is about to start levothyroxine. What must you do first and why?”
- Common wrong first step: giving levothyroxine before glucocorticoids in adrenal insufficiency.
Clinical case
Patient: 27‑year‑old Kenyan male, HIV‑negative, presents with 3 weeks of fatigue, weight loss, decreased libido, and occasional blurry vision.
Key findings:
- BP 95/60 mmHg, pulse 88 bpm.
- Skin hyperpigmentation, loss of axillary hair.
- Visual field testing shows bitemporal hemianopia.
- Serum cortisol low, ACTH low; TSH low, free T4 low; prolactin mildly elevated.
- MRI: 1.8 cm sellar mass compressing optic chiasm.
Questions
- What is the most urgent immediate intervention?
Answer: Administer IV hydrocortisone (stress‑dose) and isotonic saline before any other therapy to treat possible adrenal crisis.
- Which long‑term endocrine replacement is required first, and why?
Answer: Glucocorticoid replacement (physiological hydrocortisone) must be started before levothyroxine to avoid precipitating adrenal collapse when metabolic rate increases.
- What definitive treatment is indicated for this patient’s tumour?
Answer: Trans‑sphenoidal surgical resection, given the size (>1 cm) and visual field compromise.
Practice questions
Question 1
A 45‑year‑old woman with known macroadenoma presents with sudden severe headache, vomiting and left‑sided ptosis. MRI shows haemorrhage into the tumour. What is the next best step?
A. High‑dose oral prednisone
B. Immediate trans‑sphenoidal surgery
C. Start levothyroxine
D. Observe and repeat MRI in 48 h
Answer: B. Immediate trans‑sphenoidal surgery – pituitary apoplexy is a neurosurgical emergency to decompress the optic apparatus and restore circulation.
Question 2
A 32‑year‑old man with infertility is found to have a 6 mm pituitary lesion and prolactin of 150 µg/L. Which medication is first‑line?
A. Somatostatin analogue
B. Cabergoline (dopamine agonist)
C. Levothyroxine
D. Fludrocortisone
Answer: B. Cabergoline – dopamine agonists are the treatment of choice for prolactinomas, shrinking the tumour and restoring gonadal function.
Question 3
A patient with central diabetes insipidus is started on desmopressin. Which laboratory change would indicate overt over‑replacement?
A. Serum sodium 130 mmol/L
B. Serum sodium 150 mmol/L
C. Serum potassium 4.5 mmol/L
D. Serum calcium 2.2 mmol/L
Answer: A. Serum sodium 130 mmol/L – hyponatraemia reflects water retention from excess desmopressin.
Question 4
A 58‑year‑old farmer with poorly controlled hypertension presents with a pituitary macroadenoma compressing the optic chiasm. Which drug class should be avoided as first‑line therapy for his tumour?
A. Dopamine agonists
B. Somatostatin analogues
C. GnRH antagonists
D. Steroidogenesis inhibitors
Answer: D. Steroidogenesis inhibitors – they are not used for pituitary adenomas and can worsen hypertension and fluid balance.
Question 5
A patient on long‑term glucocorticoid replacement complains of fatigue and joint pains. Bone density scan shows osteopenia. Which adjunctive measure is most appropriate?
A. Increase glucocorticoid dose
B. Add calcium and vitamin D supplementation
C. Start high‑dose levothyroxine
D. Begin insulin therapy
Answer: B. Add calcium and vitamin D supplementation – to mitigate glucocorticoid‑induced bone loss and reduce fracture risk.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.