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MSc Endocrinology > Lecture: Pituitary Function > Flashcards

Lecture: Pituitary Function Flashcards

1
Q

What makes up the Pituitary Gland?

A
  • Anterior Pituitary
  • Posterior Pituitary
  • Pituitary Stalk
  • Pars Intermedia
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2
Q

What is the actions of the Posterior Pituitary?

A

Secretes

  • Oxytocin
  • AVP
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3
Q

What is the action of Oxytocin?

A

Similar structure to AVP

Actions

  • Aids contraction of the pregnant uterus and assists milk ejection during lactation
  • May also aid contraction of seminal vesicles of the testis, and increase lipolysis in the adipocyte.
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4
Q

How is Ocytocin Regulated?

A
  • Physiologic regulation largely unknown but released in response to suckling and increasing to very high levels at the end of pregnancy.

AKA the ‘cuddle hormone’

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5
Q

What is the Action of AVP? (ADH)

A
  • AVP acts on V1 receptor to increase systemic vasular resistance
  • AVP acts on V2 receptor to increase blood volume through aquaporins
  • These actions come together to increase Arterial Pressure
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6
Q

What triggers AVP to be released?

A
  • Decreased Plasma Volume
  • Increased Plasma Osmolality
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7
Q

What is SIADH?

A
  • Normovolaemic hyponatraemia due to excessive AVP production.
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8
Q

What are causes of SIADH?

A
  • Drugs – opiates, NSAID, carbamazepine, valproate, MAOIs, Cisplatin, cyclophosphamide, Haloperidol, amitryptilline
  • CNS disorders – stroke, trauma, haemorrhage
  • Pulmonary disease
  • Surgery – possibly mediated by pain response
  • Malignancy – ectopic AVP from e.g. small cell lung tumour
  • Hereditary defects in AVP receptors
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9
Q

What are diagnositic Criteria for SIADH?

A
  • Diagnosis of exclusion
  • Patient must have euvolaemichyponatraemia
  • Serum osmolality <275 mosm/kg
  • Urine sodium >25 mmol/L
  • Urine osmolality >100 mosm/kg
  • No renal, adrenal or thyroid disease
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10
Q

How is SIADH treated?

A
  • Remove cause if possible
  • Water restriction (500-750 mL/day)
  • Increasing solute intake (urea)
  • Low dose loop diuretics with oralsodiumchloride
  • Vaptans – competitively bind to the V2 receptor in the kidney causing aquaresis.
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11
Q

What causes Diabetes Insipidus?

A

Causes by Lack of production of AVP or Lack of response to AVP

  • Lack of free access to fluid may lead to dehydration and hypernatraemia in patient
  • Difficult to distinguish DI and Primary Polydipsia
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12
Q

What are the symptoms of Diabetes Insipidus?

A
  • Polyuria
  • Polydipsia
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13
Q

How is the Water Depravation Test conducted?

A
  • At 0800, weigh patient. Take samples of urine and serum for osmolality. Note urine volume. Commence fluid restriction.
  • At 0900 and hourly thereafter weigh patient and take urine and serum samples for osmolality

After this

  • Carry out desmopressin test if urine osmolality rises by <30 mosm/kg in total over 3 successive urine samples or if urine osmolality still <750 mosm/kg after 8 hours fluid restriction
  • Give 2µg IM desmopressin
  • Measure urine and serum osmolality hourly for at least 3 hours.
  • Must be carried out after 8 hours fluid restriction.
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14
Q

When is fluid restriction stopped in the Water Deprivation Test?

A
  • Fall in weight >5%
  • Serum osmolality >300 mosm/kg

This means patient is becoming dangerously dehydrated.

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15
Q

What are the types of Diabetes Insipidus and their results for the tests?

A

Nephrogenic Diabetes Insipidus

  • Post Dehydration Osmolality: High Serum Osmolality and Low Urine Osmolality
  • Post Desmopressin Osmolality: Low Urine Osmolality

Cranial Diabetes Insipidus

  • Post Dehydration Osmolality: High Serum Osmolality and Low Urine Osmolality
  • Post Desmopressin Osmolality: High Urine Osmolality
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16
Q

What are the types Partial Diabetes Insipidus and their results?

A

Partial Nephrogenic Diabetes Insipidus or Primary Polydipsia

  • Post Dehydration Osmolality: High Serum Osmolality, Urine osmality (300-750)
  • Post Desmopressin Osmolality: Low Urine Osmolality

Partial Cranial Diabetes Insipidus

  • Post Dehydration Osmolality: High Serum Osmolality, Urine osmality (300-750)
  • Post Desmopressin Osmolality: High Urine Osmolality
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17
Q

What is the treatment for Cranial Diabetes Insipidus Treatment?

A

Desmopressin

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18
Q

What is the treatment for Nephrogenic Diabetes Insipidus Treatment?

A

Hydrochlorothiazide Diuretic

  • Inhibits NaCL transporter in DCT increasing Na excretion
  • ECF contraction leading to decrease in GFR
  • Increased Na and H2O reabsorption in PCT
  • Decreased urine output

Low salt diet is also used. It is important that patients have free access to water to prevent dangerous dehydration

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19
Q

Which hormones are released by Anterior Pituitary?

A
  • TSH
  • ACTH
  • FSH
  • LH
  • GH
  • Prolactin
  • Endorphins
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20
Q

What is the Hypothalamic-Pituitary-Thyroid Axis?

A
  • TRH from the hypothalamus stimulates TSH production from the anterior pituitary.
  • TSH stimulates the thyroid gland to produce T3 and T4, which have a direct inhibitory effect on TSH and TRH production, forming a negative feedback loop.
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21
Q

Aside from Thyroid homrone, what stimulates and inhibits TSH and TRH?

A
  • TRH synthesis and secretion is also stimulated by leptin,
  • TRH inhibited by the pro-inflammatory cytokines Il-1, Il-6 and TNF-α
  • TSH production is inhibited by somatostatin
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22
Q

What is the Hypothalamic-Pituitary-Adrenal Axis?

A
  • CRH from the hypothalamus and AVP from the posterior pituitary synergistically stimulate ACTH production from the anterior pituitary
  • This in turn increases cortisol production from the adrenal gland.
  • Cortisol inhibits ACTH, CRH and AVP secretion to form a negative feedback loop.
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23
Q

What is the Growth Hormone Axis?

A
  • Hypothalamus secretes GNRH to stimulate the Pituitary Gland to Produce Growth Hormone
  • Hypothalamus is stimulates by IGF-1 and Ghrelin to do this. They also act on the Pituitary Gland
  • The hypothalamus is stimulated by Growth Hormone secretion to produce somatostatin to inhibit the proudction of Growth Hormone by the Anterior Pituitary
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24
Q

What is the Hypothamic-Pituitary-Ovarian Axis?

A
  • GnRH from the hypothalamus triggers release of LH and FSH from the Anterior Pituitary
  • In females, FSH causes follicular growth in the ovary and LH triggers ovulation and formation of the corpus luteum
  • In males, FSH is critical for spermatogenesis and LH stimulates Leydig cell production of testosterone.
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25
Q

How is Prolactin Released?

A
  • Prolactin is secreted by lactotrophs in the anterior pituitary.
  • Prolactin production is controlled in an inhibitory manner by dopamine produced by the hypothalamus.
  • TRH acts as a prolactin releasing factor. Other PRFs include VIP.
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26
Q

What is the function of Prolactin?

A

The primary function of prolactin is lactogenesis

  • Molecular weight of 23000 Daltons and consists of 199 amino acids
  • 16 kDa cleavage product of prolactin has been shown to have anti-angiogenesis & anti-tumorigenic effects
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27
Q

What is Macroprolactin?

A
  • Prolactin can bind to IgG to form macroprolactin, a molecule thought to be biologically inactive.
  • Many prolactin immunoassays cross-react with macroprolactin so macroprolactin should be tested for to avoid misdiagnosis of hyperprolactinaemia
28
Q

How is Macroprolactin Tested?

A

Gel filtration chromatography is the gold standard.

PEG precipitation tends to be the test used in most labs.

  • Dilute serum sample 1:2 with 25% (w/v) PEG 6000
  • Measure prolactin on neat and diluted sample
  • Recovery = (2 x PEG precipitated prolactin x100) / Neat prolactin
  • Recovery
    • 61-110% macroprolactin not present in significant amounts
    • 40-60% macroprolactin present as minor component
    • <40% macroprolactin present in significant amounts
29
Q

What are causes of Hyperprolactinaemia?

A

Hypothalamic dopamine deficiency

  • Tumours
  • Arteriovenous malformations
  • Inflammation
  • Depletion of stores by reserpine or methyldopa

Factitious

  • Macroprolactin
  • HAMA

Physiological

  • Stress
  • Pregancy
  • Lactation

Defective dopamine transport

  • Pituitary or pituitary stalk tumours
  • Dissection of the pituitary stalk

Stimulation of lactotrophs

  • Increased TRH production in hypothyroidism
  • Oestrogens
  • Injury to chest wall

Lactotroph insensitivity to dopamine

  • Phenothiazines e.g. chlorpromazine
  • Butyrophenones e.g. haloperidol
  • Benzamides e.g. metoclopramide, sulpride, domperidone

Prolactinoma

30
Q

What are differentials to be exclude in hyperprolactinaemia?

A
  • Exclude hypothyroidism
  • Exclude ingestion of drugs that deplete dopamine or block dopamine receptors
  • Carry out pituitary imaging to look for a tumour
31
Q

What is the background for pituitary tumours?

A
  • Account for 15% of intracranial tumours
  • Can be function or non functional
  • Symptoms of functional caused by excess hormone production
  • Symptoms fo non-functional tumours tend to be due to mass effects of the tumour and may include headache, hypopituitarism, and visual field defects
32
Q

What are cell types, hormones produced and syndromes of Pituitary Adenomas?

A
  • Lactotroph: Prolactin. Leads to Hypogonadism, Galactorrhea
  • Somatotroph: Growth Hormone. Leads to Acromegaly or Gigantism
  • Combined: Growth hormone & Prolactin. Leads to Hypogonadism and Acromegaly
  • Corticotroph: ACTH. Leads to Cushing’s disease. There can also be a silent corticotroph which only has mass effects as possible symptoms
  • Thyrotroph: TSH. Hyperthyroidism
  • Non-Functioning Gonadotroph: LH, FSH, α-subunit. Mass effects &/or Pituitary failure
33
Q

What is the percentage of occurrence for Pituitary Hormones?

A
  • Lactotroph (29%)
  • Non-functioning Gonadotroph (27%)
  • Somatotroph (15%)
  • Cobined (12%)
  • Corticotroph (10%)
  • Corticotroph (6%)
  • Thyrotroph (0.9%)
34
Q

What are the types of Adenomas?

A
  • Microadenomas - <10 mm at their widest diameter
  • Macroadenomas - >10 mm at their widest diameter
35
Q

What is the amount secreted by Prolactinomas?

A
  • Microadenoma: Prolactin <4000 mU/L
  • Macroadenoma: Prolactin usually >4000 mU/L. If <4000 mU/L, it may actually be a nonfunctioning tumour that is blocking dopamine’s negative inhibition
36
Q

What are other types of Pituitary Tumours?

A
  • Rathke’s Cysts
  • Granular Cell Tumours
  • Chordomas
  • Craniopharyngiomas
  • Meningiomas
  • Gliomas
  • Mucocele
37
Q

What are Rathke’s Cysts?

A
  • Pituitary Gland is formed from Rathke’s Pouch.
  • Inadequate Pouch obliteration results in Cysts.
  • These vary in size & may cause Panhypopituitarism with or without Diabetes insipidus
38
Q

What are Pituitary Mass Effects?

A

Upward

  • Headaches
  • Hydrocephalus
  • Visual Field effects

Sideways

  • Cranial nerve palsies and temporal lobe epilepsy

Downward

  • Cerebrospinal fluid rhinorhea
39
Q

What is diagnoses of Pituitary Tumour?

A
  • Imaging is the mainstay of tumour diagnosis
  • Tumours may be suspected from the results of baseline hormone tests e.g. raised ACTH with high cortisol in Cushing’s disease, raised prolactin in Prolactinoma.
40
Q

What is the involvement of Pituitary Imaging?

A
  • CT and MRI have largely replaced conventional X-Ray as X-Ray is poor for delineating soft tissues
  • CT is computed tomography which uses computer processed X-Rays to make detailed pictures of structures within the body which is not detailed
  • Multiple 2D X-rays are taken round a single axis of rotation and used to create a 3D image.
  • Patients are exposed to radiation during the procedure
41
Q

Why is MRI preferred over CT scan?

A
  • MRI is generally preferred over CT for diagnosis of Pituitary Adenomas because of its superior definition of small lesions in Pituitary sellar.
  • CT has limited role in Pituitary imaging, with low sensitivity in detecting microadenomas but may be useful in claustrophobic patients or those who cannot have MRI due to presence of metal clips, pacemakers
42
Q

Why is a PET scan used for Microadenomas?

A
  • Positron emission tomography detects gamma rays emitted from radioactive tracer injected into patient to produce an image.
  • F18-flourodeoxyglucose used as tracer for pituitary imaging. Labelled glucose is taken up by tumour tissue and PET can be used to differentiate between residual or recurrent tumours and post-operative changes.
  • Can differentiate between scar tissue and real tumours
43
Q

What is the treatment of Pituitary Tumours?

A

Observation for small non-functioning tumours

Drug treatment

  • Cabergoline or Bromocriptine for hyperprolactinaemia
  • Somastostatin analogues, Pegvisomant for GH over secretion
  • Replacement therapy for hypopituitarism

Surgery

  • Transphenoidal or Transfrontal Routes

Radiotherapy

  • Enternal beam radiation
  • Gamma knife stereotactic surgery
44
Q

What is Hypopituitarism?

A
  • Deficiency of one or more hormones of anterior or posterior pituitary gland
  • Clinical feautres depend on whether onset is during childhood or adulthood, which hormones are affected and whther there are coexisting features of Pituitary or Extrasellar mass lesion
45
Q

What is cause of Hypopituitarism?

A
  • Tumour: Pituitary Adenoma, Craniopharyngioma, Rathke’s Pouch Cyst, Metastatic Tumour
  • Infarction: Sheehan’s syndrome, Pituitary apoplexy, CABG
  • Inflammation: Hypophysitis, TB, Meningitis, Sarcoidosis, Histiocytes
  • Autoimmune: Isolated ACTH deficiency, Lymphocytic Hypophysitis
  • Trauma
  • Radiation treatment to brain
  • Genetic
46
Q

What is the order of loss of Pituitary Hormones?

A
  • Growth Hormone
  • LH
  • FSH
  • TSH
  • ACTH
  • Prolactin

If Growth hormone is normal whereas another hormone is abnormal it is unlikely to have panhypopituitarism

47
Q

How is hypopituitarism investigatd?

A
  • Baseline assessment of Pituitary and Target gland hormones
  • Pituitary hormones are low in presence of low target gland hormone concentrations
  • Hypothyroidism, Hypogonadism & severe Hypoadrenalism due to Pituitary Insufficiency can be indentified by baseline hormone measurement.
  • Dynamic testing used as well
48
Q

What is Dynamic Function Testing done?

A
  • Direct - use hypothalamic releasing hormones e.g. TRH, GnRH, GHRH
  • Indirect - pharmalocologic stimuli that result in release of secretagogous from the hypothalamus e.g. insulin tolerance test
49
Q

Describe the principles of Insulin Tolerance Test?

A
  • Hypoglycaemia is induced
  • This leads to stress within the body
  • This stimulates Pituitary End Organ Axis
  • This leads to increased hormone production
50
Q

When should the insulin tolerance test be avoided?

A

Contra-indicated in

  • Epilepsy
  • Cardiac rhythm disturbances
  • Ischaemic heart disease
  • Previous CVA or unexplained fits or collapses
  • Severe panhypopituitarism (cortisol < 100 nmol/L at 9AM)
51
Q

How should patient prepare for an insulin tolerance test?

A
  • Oestrogen containing medications must be stopped 6 weeks prior to the test.
  • Patients should fast from midnight the night before the test.
52
Q

What are the steps to conduct the Insulin Tolerance Test?

A
  • Insert i.v. cannula into large antecubital vein and flush with 0.9% saline
  • Take blood for glucose, cortisol and growth hormone at T=0.
  • Administer 0.15 units/kg actrapid insulin i.v. (0.3 units/kg in patients with known acromegaly)
  • If patient does not become clinically hypoglycaemic or blood glucose does not fall below 2.2 mmol/L, repeat the insulin dose at 45 minutes and continue sampling at 60, 75, 90, 120 and 150 minutes
  • As soon as patient is symptomatically hypoglycaemic & this is confirmed biochemically, give oral glucose, lucozade, fruit juice or carbohydrate meal. Severe symptoms may require i.v. glucose.
  • Observe the patient for at least 2 hours after the test and give a high carbohydrate meal.
53
Q

How is the Insulin Tolerance tests assessed in diabetics?

A
  • Patients with diet or tablet controlled DM can have the test as normal.
  • Insulin-controlled diabetics should fast from midnight & omit their morning insulin dose. At 8AM they should start an insulin infusion of 0.5 units/hour. The infusion should be increased to 1 unit/hour at 9AM if blood glucose is >9 mmol/L.
  • The usual ITT protocol should then be started at 10AM.
54
Q

How is the insulin tolerance test intepreted?

A

The test cannot be interpreted unless a glucose <2.2 mmol/L is achieved

  • Cortisol at peak concentration of more than 550 nmol/L - normal response
  • Cortisol at peak concentration of less than 550 nmol/L - inadequate response
  • Growth hormone more than 6.5 mcg/L - normal response
  • Growth hormone less than 6.5 mcg/L - inadequate response
55
Q

How is Cortisol deficiency in ITT intepreted?

A
  • Patients with maximum cortisol 400-550 nmol/L may only need steroid cover for illnesses or stresses.
  • No test is perfect
  • 5-15% of normal people will show a suboptimal cortisol response
56
Q

What is the Glucagon Tolerance Test?

A
  • Alternative test of the whole hypothalamic-pituitary-end hormone axis (cortisol and growth hormone)
  • Particularly useful when the ITT is contraindicated
  • Glucagon stimulates release of GH and ACTH by a hypothalamic mechanism. Simultaneous administration of TRH and GnRH does not interfere with the effects of glucagon
  • Patient should fast from midnight but can drink water. Give 1 mg glucagon I.M at 0 and take samples for GH & Cortisol at 0, 150 and 180 minutes.
57
Q

What are limitations for Glucagon Tolerance tests?

A
  • Should not be used in patients with hypothyroidism or severe adrenal insufficiency (9AM cortisol <100 nmol/L)
  • Unreliable in patients with Diabetes Mellitus
  • Hypoglycaemia may occur in patients with phaeochromocytoma, insulinoma, after starvation for >48 hours or in patients with glycogen storage diseases.
58
Q

How is the glucagon test interpreted?

A

Blunted response may be seen in hypothyroidism and obesity. Slightly less reliable test than the ITT but very useful for patients who cannot have the ITT

  • Cortisol at peak concentration of more than 550 nmol/L - normal response
  • Cortisol at peak concentration of less than 550 nmol/L - inadequate response
  • Growth hormone more than 6.5 mcg/L - normal response
  • Growth hormone less than 6.5 mcg/L - inadequate response
59
Q

What is the Gonadotrophin releasing Hormone test?

A
  • Used to diagnose hypothalamic-pituitary disease in precocious and delayed puberty in children with low baseline gonadotrophins
  • Can be performed simultaneously with TRH and Glucagon or Insulin tolerance tests
60
Q

How is the Gonadotrophin releasing hormone test undertaken?

A
  • Give I.V. Bolus of GnRH 2.5 mcg/kg to a maximum dose of 100 mcg.
  • Take a sample for LH & FSH at 0, 20 mins and 60 mins
61
Q

How is the GnRH test interpreted?

A
  • Normal baseline level are <2IU/L for LH and FSH in pre-pubertal children. Response is normal if baseline values are within the referance range and there is doubling of LH and FSH at 20 minutes
  • Exaggerated response seen in primary and secondary gonadal failure
  • Increase <5 IU/L is seen in pre-pubertal children and in pituitary/hypothalmic disease. However, normal response does not exclude disease
  • Magnitude of LH response in proportional to mean nocturnal LH therefore evolution of puberty
62
Q

What is the TRH test used for?

A
  • Distinguish thyroid home resitance from TSHoma. Relaible TSH tests means no longer need for primary ad eondayr thryoid disorders
  • Test should not be used in pregnancy and patient should not take T4 or T3 for 3 weeks prior to test.
  • Involves 200 mcg TRH I.V as a bolus (7 mcg/kg up to maximum of 200 mch in children) and taking samples of TSH at 0 minutes, 20 minutes and 60 minutes
63
Q

What is the expected result for TRH tests?

A
  • Normal basal TRH should be 0.2-6.0 mU/L with an increment of 5-30 mU/L at 20 minutes and slight fall at 60 minutes
  • TSH response is flat in most cases of TSHoma but a brisk response is seen in thyroid hormone resistance
  • Exaggerated reponse seen in primary hypothyroidism with peak resposne <5 mU/L in primary hyperthyroidism.
  • Delayed response may be seen in hypothalamic disorders
64
Q

Which medications affect the TRH test?

A

Decreased response

  • Glucocorticoids
  • L-Dopa
  • Bromocriptine

Enhancement of response

  • Metoclopramide
  • Oestrogens
  • Dopamine Agonists (Sertraline, Theophylline)
65
Q

What is the treatment of Hypopituitarism?

A

Replace lacking hormones, find underlyin cause and treat if appropriate

  • Thyroxine replacement for TSH deficiency
  • Hydrocortisone to treat cortisol deficiency
  • Testosterone in males, Oestrogen and/or Progesterone as appropriate in females
  • GH replace in chidlren but rare in adults
  • Desmopressin given intranasally for AVP deficiency
66
Q

When do you have to be careful with thyroxine replacement?

A

Not to be given alone in hypoadrenalism as subsequent increase in metabolism can precipitate adrenal crisis. Hydrocortisone repalcement should be given first

MSc Endocrinology (16 decks)

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