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MBBS IV - Junior Clerkship WCS > JC41 (Medicine) - Pituitary tumors and hypopituitarism > Flashcards

JC41 (Medicine) - Pituitary tumors and hypopituitarism Flashcards

1
Q

Pituitary gland

  • Location
  • Borders
  • Anatomical division and secretions
A

Site: enclosed in sella turcica (normally <0.8cm deep)

Superior → diaphragm sellae
Anterosuperior → optic chiasm
Inferior → sphenoidal sinus
Lateral → cavernous sinus

Anterior lobe secretes prolactin, LH/FSH, TSH, ACTH, GH
Posterior lobe secretes oxytocin and ADH

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2
Q

Anatomical connection between pituitary and hypothalamus

A

Connected to hypothalamus via infundibular stalk
- Portal vessel carrying blood from median
eminence of hypothalamus to anterior lobe
- Nerve fibres from PVN and SON to posterior lobe (neurohypophysis)

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3
Q

List non-functional tumors of pituitary

A

Non-functional tumours:
→ Pituitary adenoma (most common)
→ Craniopharyngioma
→ Metastatic tumours

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4
Q

List pituitary diseases with hormone excess/ deficiency

A

Hormone excess:
→ Hyperprolactinemia
→ Acromegaly
→ Cushing’s disease
→ SIADH
→ TSH-/LH-/FSH-secreting adenomas (rare)

Hormone deficiency:
→ Hypopituitarism
→ Diabetes insipidus
→ GnRH deficiency (Kallmann’s syndrome)

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5
Q

Approach to ascertain type of pituitary disease

A

Approach to pituitary diseases:

  1. Hormonal secretion: depends on mode of secretion
    → Pulsatile secretion: GH, ACTH → requires suppression/stimulation tests
    → Constant secretion: prolactin, TSH, LH/FSH → direct measurement of its level
  2. Perimetry for visual defects due to compression on optic pathways
  3. MRI pituitary if pituitary tumour suspected
  4. Intra-op biopsy for histological Dx
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6
Q

Tests for ACTH excess/ Deficiency

A

ACTH Excess:

Low-dose dexamethasone suppression test
Late-night salivary cortisol
24h urine free cortisol

ACTH Deficiency:

Low 9am serum cortisol
Short synacthen test (SST)
Insulin tolerance test (ITT)

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7
Q

Tests for Growth hormone excess/ deficiency

A

GH excess:

Oral glucose tolerance test (OGTT)
High serum IGF-1

GH deficiency:

Low serum IGF-1
Insulin tolerance test (ITT)
Glucagon stimulation test
Arginine-GHRH stimulation test

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8
Q

Tests for FSH/ LH deficiency

A

Random serum LH/FSH
Random serum testosterone in M
GnRH (LHRH) stimulation test

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9
Q

Tests for TSH excess/ deficiency

A

Random serum T4, TSH

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10
Q

Tests for prolactin excess/ deficiency

A

Random serum prolactin

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11
Q

Test for ADH excess/ deficiency

A

ADH excess - Diagnosis of exclusion

ADH deficiency - Water deprivation test

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12
Q

Outline clinical presentation of Pituitary tumor

A

Local compressive symptoms:

  • Headache, Visual field defect, Diplopia, Disconnection hyperprolactinaemia, Pituitary apoplexy

Hormonal symptoms:

  • Hypersecretion: acromegaly, Cushing’s, hyperprolactinaemia
  • Hyposecretion: hypopituitarism
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13
Q

Local compressive symptoms of pituitary tumor

A
  1. Headache (Stretching diaphragma sellae)
  2. Visual field defect (optic chiasm involvement)
  3. Diplopia (Cavernous sinus involvement)
  4. Acute infarction/ expansion (pituitary apoplexy, sudden hemorrhage)
  5. Disconnection hyperprolactinaemia
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14
Q

S/S of hypopituitarism

A
  • Growth hormone deficiency:

Growth retardation, Lethargy

  • Gonadotrophin deficiency:

Lethargy, Loss of libido, Hair loss, Amenorrhea

  • ACTH deficiency:

Lethargy, Pallor, Postural hypotension, Hair loss

  • TSH deficiency:

Hypothyroidism S/S

  • Vasopressin deficiency:

Thirst, polydipsia, polyuria

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15
Q

S/S hyperpituitarism

A

Cushing’s disease

Acromegaly

Hyperprolactinemia: Galactorrhea, Amenorrhea, Hypogonadism

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16
Q

Characteristic sign of pituitary tumor on Cranial XR?

A

Skull XR: double-flooring due to asymmetrical enlargement

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17
Q

Ddx sellar masses

A

□ Pituitary adenomas

□ Pituitary carcinomas: very rare
→ Types: germ cell tumours, chordoma, lymphoma, metastatic

□ Craniopharyngiomas: majority in children/young adulthood

□ Other tumours: meningioma, pituicytoma, lymphoma, germ cell tumour, metastatic tumours (esp CA breast, lung)

□ Non-neoplastic masses: Rathke’s cleft cyst, arachnoid cyst, pituitary abscess, carotid-cavernous fistula, hypophysitis

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18
Q

Craniopharyngioma

  • Site
  • Morphology
  • Age of onset
  • Presentation, S/S
A

Site: commonly in suprasellar region but can occur intrasellarly

Nature: often cystic, 50% calcified (visible on XR/CT)

Onset:
→ 50% present in childhood
(more common than pituitary adenoma in young people)
→ 25% presents between 20-40y
→ 25% presents >40y

Presentation:

  • Hypopituitarism, eg. growth retardation
  • Central DI due to stalk compression
  • Visual field defects due to chiasmal compression
  • ↑ICP due to 3rd ventricle compression
  • Hypothalamic damage, eg. hyperphagia, obesity, loss of thirst sensation, disturbance of temperature regulation
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19
Q

Pituitary adenoma

Site

Size cut-off

Subtypes

A

Site: usually within sella turcica
Size: microadenoma (<1cm) vs macroadenoma (>1cm)

Functional adenomas:

Prolactinoma

GH-secreting

ACTH-secreting

Glycoprotein-secreting: FSH, LH, TSH

Non-functional adenomas: Hypopituitarism

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20
Q

Clinical presentation of functioning pituitary adenomas

A
  • Prolactinoma: Galactorrhea, Hypogonadotropic hypogonadism - Amenorrhea and Impotence
  • GH-secreting adenoma: Acromegaly in adults, Gigantism in children
  • ACTH-secreting adenoma: Cushing’s disease
  • Glycoprotein-secreting tumors: Secondary hyperthyroidism, Precocious puberty, Ovarian Hyperstimulation syndrome, Hypopituitarism, Local compressive symptoms
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21
Q

Clinical presentation of non-functioning pituitary adenomas

A

Hypopituitarism (classically GH → FSH/LH → ACTH → TSH)
Local symptoms including headache and visual loss

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22
Q

Clinical diagnosis of functional pituitary adenoma

A

Dx:
Hormonal hypersecretion in functional adenomas
→ Prolactinoma: ↑serum prolactin >200ng/mol (usu >10× ULN)
→ Acromegaly: ↑serum IGF-1, non-suppressible GH on OGTT
→ Cushing’s disease: ↑ACTH + ↑cortisol (by ≥2× diagnostic tests)
→ 2o hyperthyroidism: ↑TSH, ↑fT4
→ Gonadotroph tumour: seldom hypersecretes

Radiological diagnosis:
→ Contrast MRI: modality of choice
→ CT: better for calcified tumour (meningioma, craniopharyngioma)

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23
Q

Pituitary apoplexy

S/S

Diagnosis

Management

A

□ S/S: sudden onset of excruciating headache (stretching of sella) + diplopia (pressure on CNIII) + hypopituitarism (esp adrenal crisis)

□ Dx: acute blood in pituitary seen on CT/MRI

□ Mx: steroid cover + urgent surgical decompression if
→ Signs of ↑ICP
→ Change in conscious state
→ Evidence of compression on neighbouring structures

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24
Q

Management options of pituitary tumors (functional and non-functional)

A

Non-functional microadenoma - Observe and FU

Functional adenoma and Non-functional Macroadenoma:

→ Surgical Tx: first-line for all
→ RT: usually as adjunct to surgery
→ Medical Tx: first-line only to prolactinoma

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25
Q

Surgery for pituitary tumor

  • Indication
  • Approach
  • Advantages
  • Disadvantages
  • F/U
A

□ Indication: all functioning tumours (except prolactinoma) and all macroadenomas

□ Approach:
→ Trans-sphenoidal (route of choice): transnasal endoscopic or sublabial
- Unresectable if compresses/abuts optic pathway or invades cavernous sinus → maximal debulking instead
→ Transfrontal if very large suprasellar extension or severe chiasmal compression

□ Advantages: rapid ↓secretion and ↓size → remission >85% for micro-, 40-50% for macroadenoma

□ Disadvantages:
→ Residual or recurrence esp if macroadenomas (2-8%)
→ Hypopituitarism
→ DI due to surgical injury to stalk or posterior pituitary (may be transient)

□ F/U:
→ Monitor pituitary function for 4-6w for hypopituitarism
→ Post-op imaging at 1y, 2y, 5y, 10y for any recurrence

26
Q

Radiotherapy for pituitary tumor

  • Modalities
  • Indication
  • Advantages
  • Disadvantages
A

□ Modalities: conventional EBRT or stereotactic radiosurgery (SRS) by gamma/X-knife

□ Use:
→ Usually as adjunct to surgery (for residual tumours)
→ May be primary therapy for macroprolactinoma

□ Advantages: restrains tumour growth

□ Disadvantages:
→ Delayed effect on secretion (not used in acute setting)
→ Higher incidence of hypopituitarism
→ Risk of damage to other structures (NOT used if <5mm from optic chiasma)

27
Q

Medical treatment for pituitary adenoma

  • Indication
  • Efficacy
  • Drug options
A

□ Use: 1st line for prolactinomas and as adjunct to surgery/RT in others

□ Efficacy:
→ Usually reversible on drug withdrawal
→ No reduction in size except for prolactinomas (by dopamine agonists); 50% of GH/TSH-producing tumours (by somatostatin analogues)

Options:

Dopamine agonists, eg. bromocriptine, cabergoline

Somatostatin analogues, eg. octreotide LAR, lanreotide, pasireotide

GH receptor antagonists, eg. pegvisomant

28
Q

Dopamine agonists for pituitary tumors

Efficacy

Examples

S/E

F/U

A

Dopamine agonists, eg. bromocriptine, cabergoline

Effect:

  • Prolactinoma: >90% achieve normal prolactin, tumour shrinkage
  • Acromegaly: IGF-1 normalized in 10% pt
  • FSH-producing tumours: ↓FSH but no effect on tumour size

S/E: constipation, nausea and headaches. hallucinations, peripheral edema, gastrointestinal ulcers, pulmonary fibrosis and psychosis.

F/U:

  • Monitor tumour size by serial MRI
  • Monitor prolactin level → taper off after dropping to normal
29
Q

Somatostatin analogues for pituitary tumors

Efficacy

Examples

S/E

A

Somatostatin analogues, eg. octreotide LAR, lanreotide, pasireotide

Use as adjunct to surgery/RT

Octreotide LAR/lanreotide: predominantly act on sstr
→ ↓size and secretion of GH and TSH-producing tumours
→ 60% acromegaly pt achieve normal GH/IGF-1

Pasireotide: high affinity for sstr5,
→ Effective for ACTH-producing tumours
→ more effective for some GH-producing tumours

S/E: 3Gs

  • GI side-effects: nausea/vomiting, steatorrhoea, abdominal cramps
  • Gallstones due to ↓gallbladder motility
  • ↓glucose tolerance due to ↓insulin secretion (hyperGly more common for pasireotide)
30
Q

GH receptor antagonists for pituitary tumor

Example

Efficacy

S/E

A

GH receptor antagonists, eg. pegvisomant

Effect:

  • 90% normalize IGF-1 in 12mo, 76% in long-term
  • No ↓tumour size, no ↓GH level (-ve feedback)

S/E: ↑liver transaminases (5%)

31
Q

Causes of Hyperprolactinemia

A
32
Q

Clinical presentation of hyperprolactinemia

A

Hypogonadotropic hypogonadism due to inhibition on GnRH secretion
→ Female: secondary amenorrhoea, anovulation with infertility, climacteric symptoms, ↓BMD
→ Male: ↓libido, lethargy, erectile dysfunction, infertility

Galactorrhoea due to ↑breast milk production (NOT breast development – due to oestrogen!)
→ Female: can present with milk discharge
→ Male: rarely occur unless gynaecomastia already induced (oestrogen-mediated)

33
Q

Serum prolactin levels and associated conditions at each level

Define Macroprolactin

A

Levels:

  • <500mU/L → normal
  • 500-1000mU/L → stress, drugs
  • 1000-5000mU/L → drugs, microprolactinoma, disconnection prolactinoma
  • >5000mU/L → highly suggestive of macroprolactinoma
  • >100000mU/L → potential for high-dose hook effect and thus false -ve

Macroprolactin: prolactin bound to IgG Ab

  • Cannot cross blood vessel walls → NOT physiologically active
  • May cause interference! → use assays that are known not to cross-react
34
Q

Investigations for Hyperprolactinemia

A
  1. Exclude pregnancy if female and child-bearing age
  2. Serum prolactin levels
  3. MRI/CT pituitary for pituitary adenoma
  4. Pituitary hormones: IGF-1, ACTH, FSH/LH/sex hormones
  5. T4, TSH to exclude 1o hypothyroidism
35
Q

Treatment of hyperprolactinemia

A

Dopamine agonist as 1st line, treat if symptomatic or macroadenoma
→ Efficacy: ↓prolactin secretion, ↓size of adenoma in >90%
→ Termination: taper off DA if prolactin normalized + no adenoma by MRI for ≥2y (off when pregnant)
→ S/E: nausea, postural hypotension, mental fogginess, impulse control disorders (hypersexuality, compulsion)

Surgery ± adjuvant RT if failed medical Tx or very large adenoma planning pregnancy

36
Q

Acromegaly

Cause

Clinical features

A

Cause: GH-secreting pituitary adenoma (most), GHRH-secreting hypothalamic tumours, ectopic GHRH/GH secretion by neuroendocrine tumours

Clinical features:

  1. Pituitary local compressive symptoms: headache, VF defects, CN palsies, hypopituitarism
  2. GH-excess:
  • Soft tissue overgrowth: Coarse facial features, Macroglossia, Malocclusion, OSA, Prognathism
  • Acral overgrowth: Large hands with board palms, spatulate fingers, sweaty palms; Large feet with thick heel pads
  • Skin changes: Hyperhidrosis, Hirsutism
  • Bone: Hypertrophic arthropathy, increase BMD
  • Visceromegaly: Goiter, Testiculomegaly
37
Q

Complications of Acromegaly

A

Complications: overall mortality 1.72× to general population (mainly due to CVS risk)

  • Cardiovascular: HTN, LVH, cardiomyopathy with diastolic HF, CV mortality, VHD
  • Metabolic: IGT (40%), T2DM (20%), ↑lipids, ↑Ca, ↑PO4
  • Colon: ↑risk of colon CA, polyp, diverticulosis
  • Others: ↑risk of other malignancy, renal stones (hypercalciuria)
  • hyperprolactinemia (30%) (due to interference with hypothalamic/pituitary blood flow or from cosecretion of PRL)
38
Q

Investigations for acromegaly

A

□ Serum IGF-1: elevated
□ OGTT: inadequate GH suppression
Normal → adequate suppression to <1ng/L after 2h
Acromegaly → no suppression or paradoxical increase (30%)

□ Pituitary MRI and pituitary hormone profile
□ Colonoscopy for any colonic tumours

39
Q

Treatment options for acromegaly

A

Transsphenoidal surgery (1st line)
→ Postop evaluation: IGF-1 + random GH and MRI at postop 12w
→ Residual disease: repeat OT if resectable or compresses vital structures, otherwise medical or SRS

Medical Rx if not a surgical candidate or incomplete clearance
→ Somatostatin analogues, eg. octreotide, lanreotide
→ GH receptor antagonist, eg. pegvisomant
→ Dopamine agonist if co-secrete prolactin

Stereotactic RT if refractory to medical therapy

40
Q

Structural causes of hypopituitarism

A

Structural damage involving hypothalamus, pituitary or stalk

→ Tumours: large pituitary or hypothalamic tumours
→ Trauma: surgery, RT, head injury
→ Infarction: post-partum necrosis (Sheehan’s syndrome), pituitary apoplexy
→ Infiltration: haemosiderosis/haemochromatosis, histiocytosis, sarcoidosis
→ Infection: TB, syphilis, mycosis, toxoplasmosis (in AIDS)
→ Immunological: lymphocytic hypophysitis (spontaneous or induced by cancer immunotherapy), isolated ACTH deficiency (due to anti-ACTH secreting cell Ab)

41
Q

Congenital causes of hypopituitarism

A

→ Congenital panhypopituitarism
→ Isolated GH deficiency
→ Isolated LH/FSH deficiency, eg. in Kallmann’s syndrome (may be a/w anosmia)

42
Q

Functional causes of hypopituitarism

A

→ Emotional deprivation (GH insufficiency)
→ Anorexia nervosa (LH/FSH ± TSH insufficiency)

43
Q

Panel of tests for hypopituitarism

A

GH:
- IGF-1, ITT, GST, Arginine- GHrH stimulation test

ACTH:
- Short synacthen test, ITT, 9am serum cortisol

TSH: Thyroid function test

FSH/ LH: Random serum levels

Basal non-stressed prolactin

44
Q

Treatment of Growth hormone deficiency

A

GH replacement in children ± adults

Route: SC injection of recombinant GH daily

Indications in adult: impaired QoL + severe GH deficiency → reassess symptoms at 9mo
(defined as peak GH <9mU/L during a stimulation test)

45
Q

Treatment of Gonadotropin deficiency

A

Testosterone in M

  • Route: usually long-acting IM injections every few weeks
  • S/E: CA prostate (screen before starting and at 3mo, 1y), BPH, erythrocytosis, VTE, ?↑CVD risk

Oestrogen ± progestogen in Female in the form of COCP

Gonadotropins for ovulation induction

  • Eg. human menopausal gonadotropin (HMG): mainly FSH
  • Eg. human chorionic gonadotropin (hCG): mimics LH action
  • Eg. recombinant FSH/LH, i.e. follitropin + lutropin α
46
Q

Treatment for TSH deficiency

A 
T4 replacement (start at 1.6μg/kg)
→ Should be deferred until cortisol replaced as treatment of hypothyroidism may ↑cortisol clearance
→ Should aim serum T4 in upper 1/2-2/3 of normal range
47
Q

Treatment of ACTH deficiency

A

ACTH deficiency: hydrocortisone replacement (15-25mg/d)
→ Mineralocorticoid NOT required (independent of ACTH)

48
Q

Diabetes Insipidus

Definition

2 subtypes

A

Diabetes insipidus (DI): characterized by persistent excretion of excessive quantities of dilute urine

□ Cranial DI: deficient ADH production/secretion by pituitary

□ Nephrogenic DI: renal tubules unresponsive to ADH
→ More common, often asymptomatic
→ Only presents during episodes of water deprivation (eg. solute diuresis, ↓water intake)

49
Q

Familial causes of Diabetes insipidus

A

Central DI

  • Vasopressin prohormone mutation (AD)
  • Wolfram syndrome
  • PCSK1 deficiency

Nephrogenic DI

  • V2 receptor mutation (X-linked)
  • Aquaporin 2 mutation (AR)
  • Sickle cell trait
50
Q

Acquired causes of central DI

A

Traumatic – accidental, surgical

Neoplasm causing damage to pituitary stalk

  • Primary – craniopharyngioma, dysgerminoma, meningioma, adenomal
  • Secondary – metastasis

Granulomas – TB, sarcoidosis, Langerhans’ histiocytosis, toxoplasmosis…

Infections – meningitis, encephalitis

Vascular – Sheehan’s syndrome, aneurysm, hypoxic encephalopathy

Idiopathic or congenital – Congenital hypopituitarism, septo-optic dysplasia

51
Q

Acquired causes of nephrogenic DI

A

Renal tubular damage - Chronic pyelonephritis, APCKD, obstruction…

Metabolic – hypoK, hyperCa

Drugs

  • Lithium carbonate for bipolar disorder
  • Drugs causing tubular damage – eg. cisplatin, amphotericin B
  • Others: cidofovir, foscarnet, demeclocycline, ifosfamide, ofloxacin, orlistat, didanosine

Gestational DI

52
Q

Clinical presentation of Diabetes insipidus

A

Clinical presentation:
□ Polyuria + polydipsia: suspect if >50mL/kg/d (>3000mL for 60kg female)
→ May be masked by associated cortisol deficiency (impairment of diuresis)

□ ± hyperNa: usu high-normal except in impaired thirst mechanism (eg. unconscious, hypothalamic lesion)

53
Q

Ddx of polyuria + polydipsia

A

Polyuria as primary defect: urine output > water intake, ↑plasma osmolality

  • Solute (osmotic diuresis): DM (esp if hyperGly or on SGLT-2), urea diuresis (post AKI), mannitol, sodium diuresis (post volume expansion, post-obstructive)
  • Water diuresis: diabetes insipidus
  • Early CKD
  • Diuretics

Excessive drinking as primary defect: water intake > urine output, ↓plasma osmolality
→ Primary polydipsia: excessive drinking in pt with psychiatric disease or hypothalamic lesions

54
Q

Investigations for Diabetes Insipidus

A
  1. Chart I/O to document polyuria and rule out obvious alternative causes
  2. Paired plasma/urine osmolality + plasma electrolytes
  3. Water deprivation test
55
Q

Differentiate plasma osm, urine osm, Paired urine/plasma osmolality ratio results between:

Diabetes insipidus

Primary polydipsia

Osmotic diuresis

A
56
Q

Water deprivation test

  • Indication
  • MoA
  • Procedure
  • Findings
A

Indication: Suspected* DI
(already diagnostic if Urine: Plasma osmolality ratio <1 or Na conc. >145 + Urine osmolality <300)

Principle: to induce ↑ADH by creating hyperosmolar state and to detect response to ↑ADH

Procedure:

  • No fluid intake for 8h (only dry food allowed)
  • During test, measure hourly body weight, urine volume and U/P osmolality
  • Stop when end-point reached (U/P osmo ratio ≤2 with Plasma osmo > 300) or lose 3% body weight)
  • *- Give DDAVP 2μg IM**

Findings:

  • Normal/primary polydipsia = adequate concentration of urine (U/P ratio ≥2)
  • DI = plasma osmolality >300, U/P osmo ratio still ≤1.9 (cannot concentrate urine) (i.e. U < 600)
  • Cranial DI = ↑ ≥50% urine osmo (adequate urine concentration) after DDAVP
  • Nephrogenic DI = no change in urine osmo after DDAVP
57
Q

Management of cranial DI

Route of administration

S/E

A

Cranial DI: desmopressin (DDAVP)
→ RoA: usually intranasal, PO/sublingual also available

→ S/E: excessive Tx (water intoxication, hypoNa), inadequate Tx (hyperNa)

58
Q

Management of nephrogenic DI

Route of administration

S/E

A

Nephrogenic DI:
→ Treat underlying cause, eg. stop offending medication

→ Low Na/protein diet + thiazide diuretics ± amiloride

→ NSAIDs (inhibit prostaglandin production (antagonist of ADH action) and thus increase concentrating ability)

→ Consider DDAVP if refractory

59
Q

Acute post-operative/ Traumatic DI

Clinical presentation

A

Clinical presentation: follows classical triphasic pattern

→ Polyuric phase (phase I) due to transient DI from hypothalamic dysfunction leading to inhibition of ADH release
- Time frame: begins ≤24h and lasts till 4-5d

→ Antidiuretic phase (phase II) due to release of stored ADH from degenerating posterior pituitary → SIADH
- Time frame: usually d6-11, lasts 2-14d

→ Return of DI (phase III) due to depletion of stored ADH → may be permanent

60
Q

Management of Acute post-operative/ traumatic DI

A

Monitor: Chart I/O, Body weight, serum Na, urine osmolality

  • Oral hydration or IV hydration with oral DDAVP
  • Allow some polyuria between doses and give next dose if previously urine output >200mL/h in successive hours
  • Target urine output 1-2L/ Day
  • Advise drug holiday if appropriate

MBBS IV - Junior Clerkship WCS (131 decks)

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