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Yr 2 Endocrinology > Wk 1 - Symposium 2: Clinical Aspects of pituitary Function > Flashcards

Wk 1 - Symposium 2: Clinical Aspects of pituitary Function Flashcards

1
Q

List the hormones produced by the anterior pituitary.

A
  • Tropic hormones (act indirectly on other glands):
    • ACTH (adrenocorticotropic hormone)
    • TSH (thyroid-stimulating hormone)
    • FSH (follicle-stimulating hormone)
    • LH (luteinizing hormone)
  • Non-tropic hormones (act directly on tissues)
    • Prolactin
    • GH (growth hormone)
    • MSH

FLAT PiG

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2
Q

List the hormones produced by the posterior pituitary.

A

Hormones produced in the hypothalamus and stored in the pituitary

  • ADH
  • Oxytocin
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3
Q

ADH and Oxytocin and secreted by cells in the _____ and stored in the _____.

A

ADH and Oxytocin and secreted by cells in the hypothalamus and stored in the pituitary.

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4
Q

What are the diseases that could occur in the pituitary?

A
  • Structural
    • E.g. Tumours
  • Functional
    • Hypofunction – hypopituitarism
    • Hyperfunction – hormone excess
  • Often both structural & functional
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5
Q

Describe the difference between microadenoma and macroadenoma of the pituitary.

A

Size matters:

  • < 10 mm is known as microadenoma
  • > 10mm is known as macroadenoma
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6
Q

The earliest symptoms of such tumors are due to endocrine abnormalities and include…

A

Hypogonadism ie diminished functional activity of the gonads, the most frequent.

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7
Q

Primary pituitary carcinomas are…

A

very rare, usually adenoma/benign

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8
Q

What are Rathke’s cysts?

A

Rathke’s cleft cyst is an abnormal fluid-filled (cyst) sac that usually is found between the anterior and posterior pituitary glands

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9
Q

What are craniopharyngiomas?

A
  • Craniopharyngiomas are benign tumours arise within the sellar/suprasellar space.
  • Typically both cystic and solid in structure.
  • Most commonly in childhood and adolescence and in later adult life after age 50 years
  • Arise from remnants of the craniopharyngeal duct or Rathke’s pouch
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10
Q

Craniopharyngiomas usually arise from

A

Arise from remnants of the craniopharyngeal duct or Rathke’s pouch

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11
Q

What visual defect would happen as a result of a pituitary tumour?

A

Would press on optic chiasm – bitemporal hemianopsia

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12
Q

What is ‘empty sella syndrome’?

A

Empty sella syndrome is a condition where the pituitary gland appears flattened or shrunken within the sella turcica on a MRI scan. Alternatively, the sella turcica can enlarge with the pituitary gland size remaining relatively normal, giving the appearance of an ‘empty sella’.

ONLY CALLED SYNDROME WHEN THERE ARE ASSOCIATED ISSUES WITH PITUITARY

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13
Q

What is pituitary apoplexy?

A

Pituitary apoplexy is a condition in which there is a haemorrhage or infarction of the pituitary gland. This disorder usually occurs in a pre-existing pituitary adenoma. This is a medical emergency because of ACTH and the control of glucocorticoids.

Characterised by onset of:

  • Headache
  • Vomiting
  • Visual Disturbances
  • Opthalmoplegia – Cranial III most common
  • Meningism
  • Fever
  • Decreased Consciousness
  • Death
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14
Q

How are pituitary tumours treated?

A
  • Conservative: e.g non-functional and no mass effect
  • Surgical resection e.g. functioning: GH & ACTH tumours and mass effect (visual failure or risk of it)
  • Pharmacotherapy e.g. dopamine agonists (D2) for prolactinoma/somatostatin analogues for acromegaly
  • Radiotherapy e.g failure of surgery to control tumour growth or hyperfunction, often second or third-line treatment
  • Often a combination of the above
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15
Q

What is hypopituitarism?

A

Hypopituitarism is manifested by diminished or absent secretion of one or more pituitary hormones:

  • Anterior Hypopituitarism
  • Posterior Hypopituitarism
  • Panhypopituitarims – both lobes involved
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16
Q

Describe the clinical symptoms and presentations associated with a gonadotropin deficiency.

A

Women:

  • Oligomenorrhea or amenorrhea
  • Loss of libido
  • Vaginal dryness or dyspareunia
  • Loss of secondary sex characteristics (Oestrogen deficiency) – if happens at early stages

Men:

  • Loss of libido
  • Erectile dysfunction
  • Infertility
  • Loss of secondary sex characteristics (testosterone deficiency) – if happens at early stages
  • Atrophy of the testes
  • Gynaecomastia (testosterone deficiency)
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17
Q

What happens in ACTH deficiency?

A
  • Results in hypocortisolism
    • Malaise
    • Anorexia
    • Weight-loss
    • Gastrointestinal disturbances
    • Hyponatremia (low sodium) + hyperkalemia (high potassium)
  • Pale complexion
    • Unable to tan or maintain a tan
  • No features of mineralocorticoid deficiency
    • Aldosterone secretion unaffected
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18
Q

TSH deficiency results in…

A

Hypothyroidism (secondary) – low TSH and low T4

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19
Q

What happens in prolactin deficiency?

A
  • Inability to lactate postpartum
  • Often 1st manifestation of Sheehan syndrome (pituitary infarction secondary to post-partum haemorrhage)
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20
Q

What is Sheehan syndrome?

A

Sheehan syndrome which is also called post-partum pituitary necrosis refers to the necrosis of cells of the anterior pituitary gland following significant post-partum bleeding, hypovolemia, and shock. Advances in obstetrical care in developed countries has reduced the incidence of this condition.

21
Q

Describe the symptoms associated with growth hormone deficiency.

A

Adults

  • Often asymptomatic
  • May complain of Fatigue
  • Abdominal obesity
  • Loss of muscle mass
  • Loss of bone mass – osteoporosis

Children

  • Constitutional growth delay
22
Q

Diabetes insipidus is a result of ____ (decreased/increased) ADH.

A

Diabetes insipidus is a result of decreased ADH.

23
Q

What are the two types of diabetes insipidus?

A
  1. Central/cranial - damage to the hypothalamus or the pituitary
  2. Nephrogenic - defect in renal tubules, do not respond to ADH
24
Q

Decreased production od ADH leads to …

A

diabetes insipidus, which will lead to water loss and ultimately hypovolaemia and dehydration

25
Q

List the clinical manifestation of diabetes insipidus.

A
  • Polyuria ( > 3 litres/ day)
  • Urine specific gravity low
  • High plasma osmolality
  • Low urine osmolality
  • Polydipsia (excessive drinking)
  • Weight loss
  • Dry skin & mucous membranes
  • Hypotension, & hypernatraemia
26
Q

How is diabetes insipidus diagnosed?

A

Water deprivation test

27
Q

How is CRANIAL diabetes insipidus treated/managed?

A

Replace ADH – vasopressin given orally or nasally; parenterally in acute phase

if no response then likely DI is nephrogenic not cranial/central

28
Q

How is nephrogenic diabetes insipidus treated?

A
  • Dietary restriction of Na
    • < 3grams/day
  • Thiazide diuretics
    • Allows kidney to absorb more water in the loop of Henle & distal tubule
    • Increases the amount of Na excreted in the urine
  • Amiloride
29
Q

Describe how individuals with hyperprolactinemia (ie excess prolactin) present.

A
  • Women may present with oligomenorrhea, amenorrhea, galactorrhea (milk expression) or infertility- often small tumours
  • Men often have less symptoms than women (sexual dysfunction, visual problems, or headache) and are diagnosed later
  • In both sexes, tumor mass effects may cause visual-field defects or headache
30
Q

List some causes of hyperprolactinemia (ie excess prolactin).

A
  • Physiological:
    • Stress
    • Pregnancy /Lactation/Oestrogen
  • Hypothalamic Dopamine Deficiency
    • Diseases of the hypothalamus (including tumours, arterio-venous malformations, and inflammatory processes)
    • Drugs (dopamine antagonists e.g. antiemetics/ anti-depressants and anti-psychotics)
  • Defective Transport Mechanisms
    • Defect of the pituitary stalk – injury/ surgery
    • Pituitary or stalk tumours
  • Other conditions:
    • Renal failure
    • Hypothyroidism
    • Polycystic ovaries
31
Q

What are prolactinomas?

A
  • Prolactin-secreting tumours of the pituitary gland are called prolactinomas.
  • It is the most common secretory tumours of the pituitary gland accounting for up to 40% of total pituitary adenomas.
  • Prolactinomas cause a wide variety of symptoms either due to mass effect of the tumour or due to hypersecretion of prolactin.
  • Based on the size of the tumours, prolactinomas can be classified as micro prolactinoma (smaller than 10 mm), macroprolactinoma (larger than 10 mm) or giant prolactinoma (larger than 4 cm).
    • 60% men with macro vs 90% women with micro
32
Q

How are prolactinomas treated?

A

First-line treatment in prolactinoma is MEDICAL therapy

  • Dopamine agonists (act on D2 receptors)
  • Include Bromocriptine, Cabergoline & Quinagolide

Side effects include postural hypotension, dizziness, nasal stuffiness, GI side effects.

They also cause tumour shrinkage

33
Q

List the clinical manifestations of growth hormone excess.

A

GIGANTISM IN CHILDREN

  • Skeletal growth

ACROMEGALY IN ADULTS

  • enlarged feet/hands
  • thickening of bones
  • prognathism
  • HTN, wt. gain, H/A
  • visual disturbances, diabetes mellitus
  • enlargement of the heart and liver

Acrogigantism (mixed features)

34
Q

What is acromegaly?

A
  • Acromegaly is a disorder caused by excessive production of growth hormone from the anterior pituitary gland, resulting in excessive growth of body tissues and other metabolic dysfunctions.
  • Adult patients with acromegaly have the characteristic facial features of a large lower jaw, prominent forehead, and large hands and feet.
  • This takes place after the growth plates are fused, distinguishing acromegaly from gigantism which occurs before the fusion of growth plates.
35
Q

What are the symptoms of acromegaly?

A
  1. Arthralgia/arthritis
  2. Blood pressure raised
  3. Carpal tunnel syndrome
  4. Diabetes
  5. Enlarged organs
  6. Field defect
36
Q

List some complications of acromegaly.

A
  1. Cardiovascular
    1. Ischemic heart disease /Cardiomyopathy /heart failure
    2. Arrhythmias/ Hypertension
  2. Respiratory
    1. Kyphosis
    2. Obstructive sleep apnea
  3. Metabolic
    1. Diabetes mellitus/IGT
    2. Hyperlipidemia
  4. Neurologic
    1. Carpal Tunnel syndrome
    2. Stroke
  5. Neoplastic
    1. Colorectal
    2. (Breast and prostate - uncertain)
  6. Musculoskeletal
    1. Degenerative arthropathy
    2. Calcific discopathy, pyrophosphate arthropathy
37
Q

What are some causes of growth hormone excess?

A
  • Growth Hormone Secreting Tumour - most commonly macroadenoma (>10mm)
  • Rarely GHRH tumour - including ectopic secretion
38
Q

How is growth hormone excess disorder diagnosed?

A
  • Random GH – not useful because fluctuates
  • Insulin-like growth factor 1 (IGF-1) – best for screening
  • Oral glucose GH suppression testing – gold standard to confirm diagnosis - normally GH concentration falls with oral glucose; in acromegaly it does not and may paradoxically rise
  • Prolactin levels as well as other pituitary function tests
  • MRI or CT & visual field tests to determine size and position of the adenoma
39
Q

How is acromegaly treated?

A
  • *1. Surgical: First-line treatment**
    2. Medical (in those contraindicated for surgery):
  • Somatostatin analogues (octreotide) - monthly injections, reduces GH secretion (and can reduce tumour size in 20-30% of case )
  • Growth hormone receptor antagonist decreases the action of GH on target tissues (pegvisomant - injections, no effect on tumour size)
  • Dopamine agonists: Dopamine agonists work on specialist markers (dopamine receptors) on the surface of the tumour to inhibit GH release from the tumour (oral, least effective, may work in mild GH excess)
  • External Radiotherapy (conventional or focused “so-called radiosurgery”: if failed surgery or not appropriate

Often offer a combination of therapies

40
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A
  • Cushing’s syndrome is a syndrome due to excess cortisol from pituitary, adrenal or other sources (exogenous glucocorticoids, ectopic ACTH, etc.)
  • Cushing’s disease is hypercortisolism due to excess pituitary secretion of ACTH (about 80% of cases of endogenous Cushing’s syndrome)
41
Q

List the clinical manifestations of Cushing’s syndrome.

A
  • Moon facies (extra fat builds up on the sides of the face)
  • Facial plethora
  • Supraclavicular fat pads
  • Buffalo hump
  • Truncal obesity
  • Weight gain
  • Purple striae
  • Depression/psychosis
  • Proximal muscle weakness
  • Easy bruising
  • Hirsutism
  • Hypertension
  • Osteopenia
  • Diabetes mellitus- hyperglycaemia
  • Impaired immune function/poor wound healing
  • HTN/low K
42
Q

How is Cushing’s syndrome diagnosed?

A
  • Morning ACTH
    • high or normal = ACTH-driven (ATCH- dependent)
    • low/suppressed = adrenal/ exogenous (ACTH-independent)
    • 24-hour urine cortisol –> high
  • Dexamethasone suppression tests - failure to suppress cortisol
    • Overnight - screening test (1mg dexamethasone at midnight, cortisol > 50 nmol/l)
    • Low dose (0.5 mg x 4 for 48 hr); confirms if this is true hypercortisolaemia
    • High dose (2mg x 4 for 48hr)- may help differentiate pituitary from non-pituitary source ( suppresses in pituitary source)
  • Midnight salivary cortisol - failure of circadian rhythm (remain high)
43
Q

What treatments are used for Cushing’s syndrome?

A
  • Transphenoidal surgery if the condition is due to a pituitary tumuor is first line Rx
  • Where surgery is contraindicated or fails to reduce cortisol levels, adrenalectomy
  • Adrenocortical Inhibitors (eg metapyrone, ketoconazole - antifungal) are only effective short-term
  • New generation somatostatin analogues (Pasireotide - expensive)
44
Q

Syndrome of inappropriate ADH (SIADH) is…

A

a condition of inappropriate ADH production where there is EXCESS ADH

45
Q

How is SIADH diagnosed/what is found on lab investigations?

A
  • Low serum Na+ <134 mmol/l
  • Low serum osmolality <280 OSM/kg H2O
  • High urine specific gravity >1.005
  • Relatively high urine:plasma osmolality
  • Low or normal urea
46
Q

List some clinical manifestations of SIADH.

A

Mainly due to low sodium ( hyponatraemia)

  • Lethargy & weakness
  • Confusion or changes in neurological status
  • Cerebral oedema & seizures leading to death
  • Muscle cramps
  • Decreased urine output
  • Weight gain without oedema
47
Q

What are some possible causes of SIADH?

A
  • Pituitary and hypothalamic disease: post pituitary surgery
  • Malignancies
    • Carcinomas, lymphomas, sarcoma
  • Pulmonary disorders
    • Infectious, asthma, CF
    • Tumours: ectopic ADH secretion
  • CNS disorders
    • Infectious, bleeding, tumours, trauma
  • Drugs
    • Chlorpropamide, SSRIs, cyclophosphamide, ecstasy
48
Q

How is SIADH treated?

A
  • Treat the underlying cause, if known
  • Fluid Restriction:
    • commonly 750-1000ml/day
  • Correct Sodium Deficit – no more than 10mEq/L in 24 hours
    • Hypertonic saline ( 1.8% & 3%- under close monitoring HDU or ITU setting)
    • Avoid rapid correction as can result in brain stem stroke ( central pontine myelonosis)
  • ADH receptor antagonists (Tolvalptan)- under close monitoring & specialist advice
    • Demeclocycline – acts on renal tubules; can cause kidney damage

Yr 2 Endocrinology (10 decks)

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