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Endocrinology > Pituitary > Flashcards

Pituitary Flashcards

1
Q

When are pituitary adenomas removed?

A
  • Normally asymptomatic
  • Indication for treatment if it causes mass effect (headache, visual changes, pituitary compression affecting hormone function)
  • Surgery: transphenoidal
  • Can use radiotherapy + surgery
  • Temozolamide can be used, alkylating agent
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2
Q

What is the function of ADH?

A

To reabsorb and concentrate water. Impaired ADH function causes diabetes insipidus which cause polyuria (dilute urine)

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3
Q

Difference between central and nephrogenic diabetes insipidus.

A
  • Central DI: occurs due to the posterior pituitary not producing ADH. ADH renal receptors still working.
  • With water deprivation test, urine osmolality does not improve but with desmopressin, urine osmolality improves.
  • Hypertonic saline infusion test to diagnose central - measurement of copeptin (c terminal segment of ADH) in blood, low level and fails to rise in central DI
    Causes: craniopharyngioma, sheehan syndrome, pituitary haemorrhage.
    ADH levels are low.
  • Nephrogenic DI: occurs due to defective ADH receptors in distal tubules and collecting duct. Urine osmolality does not improve with water deprivation or desmopressin administration.
    Causes: medications like lithium, demeclocycline (used for SIADH as it acts on the ADH receptors and reduce their responsiveness), renal disease. ADH levels are normal or increased to compensate for high urine output.

Symptoms: polyuria, polydypsia, nocturia, severe dehydration.

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4
Q

What is a new way to diagnose central diabetes insipidus?

A

Hypertonic saline infusion test with copeptin measurement (low levels fails to rise in central DI)

  • Being used over water deprivation as it takes a shorter time to perform
  • Involves infusion of 250mL bolus of hypertonic (3%) saline then infusion 0.15ml/kg/min with blood tests every 30 mins. Test finished when serum sodium reaches >150mmol/L. Measure of copeptin (c terminal segment of arginine vasopressin prohormone) level in blood at end of test. Failure of copeptin to rise during test to >4.9pmol/L indicates partial/total central DI

Copeptin = ADH
- If copeptin > 21.4 (without water deprivation): nephrogenic DI (as ADH is high)
- If copeptin <2.6 (with prior fluid deprivation): Complete central DI (as ADH remains low)
- Stimulated copeptin
If stimulated copeptin < 4.9: partial central DI
If stimulated copeptin >4.9: primary polydypsia

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5
Q

Treatment of central and nephrogenic DI

A
  • Central: desmopressin
    SE: hyponatremia
    Other indications of desmopressin include haemophilia A, von willebrand, sleep enuresis, chlorpropamide
  • Nephrogenic: salt restriction and water intake.
    Discontinue meds, eg: llithium
    Thiazide diuretics
    Nsaids
    Amiloride: indicated in patients with lithium associated (potassium sparing agent)
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6
Q

In adrenal insufficiency, what glucocorticoids can you use?

A
  • Pred 5mg/day
  • Hydrocortisone 20-30mg/day in divided doses
  • Cortisone acetate 25-37.5mg in divided dose
  • Dex 0.5-1mg day
  • Hydrocortisone and cortisone acetate provide the most physiological replacement.
  • Dex not usually used to treat secondary hypocortisolism as correct dose difficult
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7
Q

What happens in hypopituitarism for prolactin?

A

Unlike most pituitary hormones the hypothalamus INHIBITS prolactin secretion, through prolactin inhibitory factor (dopamine)
A lesion of the pituitary stalk leads to loss of other pituitary hormones but increases in prolactin

Hypopituitarism = everything low except prolactin is high

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8
Q

What inhibits prolactin and what inhibits growth hormone?

A

Prolactin inhibited by dopamine. Therefore in prolactinoma, you give dopamine agonists. This is also why antipsychotics which are dopamine antagonist can increase prolactin (not usually more than 2-4x increase)
- Prolactin increases with stress, oestrogen and antipsychotics

Growth hormone is inhibited by somatostatin and thus in acromegaly, you give somatosatin.

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9
Q

Clinical signs and treatment of prolactinomas.

A

Hyperprolactinemia inhibits pulsatile gonadotropin release and thus can cause hypogonadism

  • Pre-menopausal: amenorrhoea, infertility, galactorrhoea
  • Post menopausal: mass effect
  • Men: hypogonadism, reduced libido, impotence - often not diagnosed until tumour is large often with visual change

Tx: medical and then surgery.
- Dopamine receptor agonist: bromocriptine or cabergoline.
- Carbegoline: long effect, less side effects and preferred over bromcriptine who has SE including nausea, postural hypotension, nasal stiffness
- If not effective, surgery + radiotherapy
SE of dopamien receptor agonist include pulmonary and retroperitoneal fibrosis, pleural and pericardial effusion and constrictive pericarditis

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10
Q

Diagnosis of acromegaly

A
  • Elevated IGF-1: best single test and then conduct OGTT
  • OGTT with baseline GH and GH after 2 hours: most specific test
    If GH suppressed: acromegaly ruled out
    If GH not suppressed: confirmed acromegaly
  • Pituitary MRI for pituitary adenoma
    If normal for extrapitutiary cause, CT chest/abdo, measure GHRH

 If IGF1 normal- acromegaly excluded
 If IGF1 elevated, proceed to OGTT
 If normal suppression: GH <1; acromegaly excluded. Otherwise proceed to MRI pituitary
 If no pituitary mass noted, consider empty sella
 If no abnormalities noted on MRI, consider pan CT and GHRH measurement to look for malignancy and extrapituitary acromgelay

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11
Q

Treatment of Acromegaly

A

surgery –> somatostatin analogue –> pegvisomant

  • Primary Treatment: Transsphenoidal resection of pituitary tumour, success 80%
  • Can also use radiotherapy to shrink tumour

Medical Treatment:
- Octreotide: long acting analogue of somatostatin , now available as monthly depot injection
SE: cholelithiasis/ gallstones, abdominal pain and diarrhoea/steatorrhoea, restores fertility (need to use contraceptive), bradycardia, hypothyroidism, hair loss

  • Pegvisomant: GH receptor antagonist
    Effective in normalising IGF1
    Blocks peripheral production of insulin-like growth factor 1 (IGF-1)
    Does not affect size of pituitary tumour or growth hormone secretion
    Useful for resistant disease as is most potent agent for lowering IGF-1 levels
    Although it reduces IGF-1 levels, GH level increase and adenoma could grow (can be combined with somatostatin analgoues)
    SE: transaminitis, lipohypertrophy
    Pegvisomant effectively lowers IGF-1 levels, but patients on pegvisomant have risk of tumor growth because the medication works in the peripheral tissues as an antagonist to GH and does not decrease GH production by the tumor.
  • Dopamine agonists (cabergoline) useful if co-secrete prolactin mainly, reduce tumour size and GH secretion
    Used in patients with prolactin and growth hormone co-secretion
    Added to somatostatin analogue when monotherapy is not effective
    SE: restores fertility (need to use contraceptive), impulse control disorder in those with neuropsychiatric conditions, nausea, vomiting, abdominal pain, constipation, headache, dizziness, orthostatic hypotension, weakness, fatigue, nasal congestion, peripheral oedema

Radiotherapy: for failed surgery, slow effect

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12
Q

What are the causes of cushing syndrome?

A
  • Iatrogenic: exogenous glucocorticoids
  • ACTH dependent (high normal or increased ACTH); normally due to pituitary adenoma
  • ACTH independent (low): adrenal adenoma/carcinoma and require adrenal imaging
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13
Q

Clinical features of cushings

A
  • Early: weight gain (centripetal), hypertension, glucose intolerance, mood, attention and concentration change, androgen excess, back pain
  • Later: bruising, thin skin, osteoporosis with fractures, muscle weakness, infections
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14
Q

What clues indicate a TSH secreting pituitary tumour?

Treatment

A
  • Clue is presence of hyperthyroidism but TSH is not suppressed
  • A TSH-secreting pituitary adenoma should be suspected in hyperthyroid patients with diffuse goiter and no extrathyroidal manifestations of Graves’ disease, who have high serum free T4 and T3 concentrations and unsuppressed (normal or high) serum TSH concentrations, particularly in the presence of headache or clinical features of concomitant hypersecretion of other pituitary hormones (eg, symptoms of acromegaly). The subsequent finding of a pituitary macroadenoma by magnetic resonance imaging (MRI) is very strong evidence that the patient has a TSH-secreting pituitary adenoma, particularly in the presence of an elevated alpha subunit.

Surgery, radiotherapy, octreotide (somatostatin)

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15
Q

What does TRH (thyrotropin releasing hormone) secrete?

A

TSH and prolactin.

An increase in TRH levels can result in the development of galactorrhoea because it stimulates prolactin levels.

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16
Q

What inhibits TSH secretion?

A

Dopamine
Somatostatin
Glucocorticoids

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17
Q

What is the function of GNRH?

A
  • Stimulates FSH and LH secretion
    LH - triggers ovulation in females, stimulates testosterone in the Leydig cells in males
    FSH - stimulates the maturation of germ cells in both female + male
  • During breast feeding, high prolactin levels cause suppressed GNRH secretion which results in the development of lactational amenorrhea
  • Pulsatile GNRH secretion is responsible for puberty and reproductive function

During pregnancy, prolactin levels go up. After the baby is born, there is a sudden drop in estrogen and progesterone. High prolactin levels trigger the body to make milk for breastfeeding

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18
Q

What can synthetic forms of GHRH (tesamorelin) be used for?

A

Synthetic forms of GHRH (tesamorelin) can be used for abdominal fat reduction in HIV associated lipodystrophy.

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19
Q

What is the role of somatostatin?

A
  • Inhibits GH and TSH secretion

- Synthetic forms of somatostatin are used in the treatment of acromegaly, eg: octreotide

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20
Q

Function of growth hormone

A

Located in arcuate nucleus of hypothalamus.
Direct effects
- Increase lipolysis
- Decrease glucose uptake in the cells (increase insulin resistance)
- Increase protein synthesis
- Increase amino acid uptake
- Causes liver to release IGF-1 which induces cell division, protein synthesis and bone elongation.

Indirect effects

  • Growth stimulation
  • Anabolic effect on body
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21
Q

What stimulates and inhibits growth hormone levels?

A

Increases

  • hypoglycaemia, fasting, exercise, sleep, sepsis. puberty, ckd, thyroid hormone, estrogen, testosterone, short term glucocorticoid exposure, ghrelin in the stomach (hunger hormone)
  • Increased ghrelin, increased amino acids, decreased blood sugar, decreased fatty acids

Decreases

  • Glucose, somatostatin, chronic glucocorticoid therapy, leptin, obesity
  • decreased ghrelin, decreased amino acids increased blood sugar, increased fatty acid
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22
Q

What does CRH (corticotropin releasing hormone) do?

A
  • Stimulate ACTH, MSH (melanocyte stimulating hormone), B-endorphin
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23
Q

When does ACTH peak?

A

ACTH: pulsatile and exhibits a characteristic circadian rhythm. Peaks in the morning and then decreases

24
Q

What are the hormones of the anterior and posterior pituitary?

A

Anterior:

  • Prolactin (inhibited by dopamine)
  • TRH –> TSH (T3/T4)
  • CRH –> ACTH (Cortisol)
  • GH (ILF-1) (inhibited by somatostatin)
  • GnRH –> LH/FSH (androgens)

Posterior

  • Oxytocin
  • ADH
25
Q

Effects of ADH

A

Regulation of plasma osmolality

  • Mediated by V2 receptors
  • Act on renal collecting duct and DCT
  • Results in increased water reabsorption

Regulation of BP
- Mediated by v1 receptors

ACTH release

  • Acts on kidney (collecting duct and DCT) to increase water reabsorption and increase BP
  • On vascular smooth muscle causing vasoconstriction and increase BP
  • Anterior pituitary to release ACTH

Activated by:

  • increased plasma osmolality
  • increase angiotensin II
  • Decreased blood pressure
  • Decreased blood volume

Inhibited by alcohol causing diuresis

26
Q

Cause of acromegaly

A
  • In most cases would be benign growth hormone secreting pituitary adenoma (>95% of cases)
  • Rare:
    Neuroendcorine tumour: small cell lung cancer, pancreatic islet tumour found in MEN1
    Multiple endocrine neoplasia type 1 (MEN1) is a hereditary condition associated with tumors of the endocrine (hormone producing) glands. Develop tumours of parathyroid, pituitary, pancreas, duodenum, stomach
27
Q

Difference between excess GH secretion prior and after to epiphyseal plate closure.

A
  • Prior to epiphyseal plate closure: gigantism, longitudinal growth
  • After epiphyseal plate closure, acromegaly (overgrowth of face, hands feet) but not height.
    Pathological growth of internal organs
28
Q

Clinical features of acromegaly.

A
  • Tumour mass effect: Headache, bitemporal hemianopia
  • Pituitary dysfunction due to decreased secretion of other hormones: menstrual dysfunction +- galactorrhoea, hot flushes, vaginal atrophy, hyperpolactinaemia

Soft tissue overgrowth

  • Widended hands, fingers and feet
  • Coarsenign of faical features: Enlarged nose, forehead, jaw (macrognathia) with diastema (gaps in teeth)
  • Painful arthropathies
  • Hyperhydrosis (excessive sweating)
  • Deepening of voice
  • Macroglossia with fissures

Report haing had to increase hat/shoe/glove and ring sizes

Bone: hypertrophic painful arthropathy (ankles, knees, hips, spine)

Visceral enlargement: cardiomyopathy, diastolic dyfunction, htn
OSA

Metabolic: diabetes due to insulin resistance, hyperphosphatemia due to renal absoprtion

Cancers
- excess risk of colon polyps, diverticular and cancer
Melanoma

29
Q

Complications of acromegaly

A

Main cause of death is cardiovascular complications

  • Hypertension (30% of cases)
  • LVH and cardiomyopathy
  • Arrhthmia
  • Valvular disease

Impaired glucose tolerance and diabetes
Colorectal polyps and cancer
Thyroid enlargement and cancer
Cerebral aneurysm

30
Q

Causes of high prolactin levels

A
  • Pituitary adenoma causing increased prolactin production by anterior pituitary
  • Primary hypothyroidism
  • Cirrhosis, CKD
  • Dopamine antagonist, eg: metoclopramide, domperidone, haloperidol, risperidone, verapamil, methyldopa, opiates, cocaine

Other: physiologic stress, exercise, pregnancy, post partum

31
Q

Clinical feature of prolactinoma

A
  • Females: galactorrhoea, amenorrhoea, loss of libido, osteoporosis, infertility
  • Males: loss of libido, gynecomastia, erectile dysfunction

Depending on size of pituitary adenoma can also cause bitemporal heminaopia with headche

32
Q

Diagnosis of prolactinoma

A
  • Prolactin levels

Galactorrhoea –> measure prolactin –> if elevated measure:
BHCG: if elevated pregnancy
TSH: if elevated primary hypothyroidism
Creatinine: if elevated chronic renal failure

MRI pituitary

33
Q

Side effects of dopamine agonists

A

Restores fertility (need to use contraceptive), impulse control disorder in those with neuropsychiatric conditions, nausea, vomiting, abdominal pain, constipation, headache, dizziness, orthostatic hypotension, weakness, fatigue, nasal congestion, peripheral oedema

Note: Pleuropulmonary and retroperitoneal fibrosis, pleural and pericardial effusion and constrictive pericarditis

34
Q

Causes of pituitary adenoma

A
  • Most occur sporadically
  • 5% have genetic/familial association
    Multiple endocrine neoplasia (MEN) type 1
    Familial isolated pituitary adenoma syndrome - caused by mutations in AIP gene

Pituitary microadenoma < 10mm, macroademona >10mm

Secretory pituitary adenomas –> hyperpituitarism
Normally secrete one hormone, if secreting multiple pituitary hormones then atypical pituitary adenoma or pituitary carcinoma
Can also have hypopituitarism picture
Pituitary masses can compress the normal pituitary gland, causing hormone deficiencies; a large pituitary
mass may cause panhypopituitarism in which there is impaired secretion of all pituitary hormones

35
Q

Management of hyperpituitarism

A
  • Prolactinomas - medical therapy first and then surgery

- Other adenomas: surgery except prolactinomas

36
Q

Causes of hypopituitarism

A
  • Most common cause is compression of the pituitary gland by a non-secretory pituitary macroadenoma.
  • Other common causes include postpartum pituitary necrosis (Sheehan), traumatic brain injury, hypophysectomy, irradiation of the pituitary gland
    Acquired
  • Non-secretory pituitary macroadenomas >10mm causing compression of pituitary gland
  • Lesson common include meningiomas, craniopharyngiomas
  • Pituitary apoplexy: infarction of pituitary gland secondary to ischaemia and/or haemorrhage - primary affects anterior pituitary as it receives blood supply from low pressure arterial system.
    Sheehan syndrome: post-partum necrosis. During pregnancy, hypertrophy of prolactin producing regions increases the size of pituitary gland and makes it sensitive to ischaemia

Congenital

  • Infiltration of pituitary secondary to sarcoid, amyloid
  • Kallmann syndrome (GnRH deficiency)

Pituitary irradiation

37
Q

Clinical features of hypopituitarism

A
  • GH deficiency: growth retardation, decreased bone density, muscle atrophy, hypercholesterolemia
  • Prolactin deficiency: lactation failure following delivery
  • FSH/LH deficiency:
    Female: amenorrhoea, irregular menstrual cycles, infertility
    Males: loss of libido, infertility, testicular atrophy
  • TSH deficiency: secondary hypothyroidism
  • ACTH deficiency: secondary adrenal insufficiency - weight loss, weakness, hypotension, hyponatremia, hypoglycaemia
  • ADH deficiency: central diabetes insipidus
  • Oxytocin deficiency: no effect

Mass effect: headache, bitemporal hemianopia, diplopia

38
Q

Treatment for myxedema coma

A

Give IV hydrocortisone due to the risk of levothyroxine precipitating adrenal crisis through enhanced clearance of cortisol
- Replace thyroid hormones via IV levothyroxine, liothyronine

Treatment of hypothyroidism with thyroxine has been reported to precipitate addisonian crisis in patients who also have adrenal insufficiency. This may be due to an increase in metabolic rate induced by thyroid replacement therapy resulting in overt manifestations of adrenal insufficiency.

39
Q

Features of acromegaly

A

In acromegaly there is excess growth hormone secondary to a pituitary adenoma in over 95% of cases. A minority of cases are caused by ectopic GHRH or GH production by tumours e.g. pancreatic.

Features
• coarse facial appearance, spade-like hands, increase in shoe size
• large tongue, prognathism, interdental spaces
• excessive sweating and oily skin: caused by sweat gland hypertrophy
• features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
• raised prolactin in 1/3 of cases → galactorrhoea
• 6% of patients have MEN-1
Complications
• hypertension
• diabetes (>10%)
• cardiomyopathy
colorectal cancer

40
Q

What are causes of gynaecomastia?

A
  • Syndromes with androgen deficiency: kallman’s klinefelter’s
  • Testicular failure, eg: mumps
  • Testicular cancer, eg: seminoma secreting hcg
  • Hyperthyroidism
  • Haemodialysis

Drugs

  • Spironolactone (most common drug cause)
  • Digoxin
  • GnRH agonists, eg: goserelin, buserelin used in prostate cancer
41
Q

What are associated electrolyte abnormalities in addison’s disease?

A

Hyperkalaemia
Hyponatremia
Hypoglycaemia
Metabolic acidosis

42
Q

What electrolyte abnormalities are associated with Cushing’s syndrome

A

Hypokalaemia

Metabolic alkalosis

43
Q

Characteristics of multiple endocrine neoplasia (MEN) - MEN type I, IIa, IIb

A
  • MEN1: hyperparathyroid, pituitary, pancreas (insulinoma, gastrinoma which leads to recurrent peptic ulceration). Adrenal and thyroid. Most common presentation being hypercalcaemia
- MEN IIa
Medullary thyroid cancer
Pheochromocytoma 
Parathyroid 
RET oncogene
- MEN IIb
Medullary thyroid
Pheochromocytoma
Marfanoid body habitus
Neuroma 
RET oncogene
44
Q

How do you treat growth hormone deficiency?

A

Somatoptropin

45
Q

In hypopituitarism, which hormones are lost early?

A
  • GH and gonadotropin deficiencies often occur early when the pituitary gland is damaged by tumor, radiation, surgery, or
    hemorrhage because the cell lines that synthesize GH (somatotrophs) and LH and FSH (gonadotrophs) are most sensitive
    to injury.
  • Secondary hypothyroidism (TSH deficiency) and
    secondary cortisol deficiency (ACTH deficiency) often occur
    later in the disease process.
  • Pituitary adenomas can cause
    elevation in prolactin due to stalk compression, leading to a
    decrease in dopaminergic inhibition of prolactin secretion causing a prolactinoma.
46
Q

Indications for removal of a non-functional pituitary tumour.

A

Indications for surgery include mass effect,
particularly a visual field defect; tumor that abuts the optic chiasm; tumor growth; or an invasive tumor (invading the
brain or cavernous sinus). Surgery should also be considered in a patient with a tumor close to the optic chiasm who plans
to become pregnant (due to the physiologic enlargement of the
pituitary associated with pregnancy).

47
Q

Effects of thyroid hormone deficiency.

A
  • Thyroid-stimulating hormone (TSH) deficiency leads to secondary or central hypothyroidism.
  • Secondary hypothyroidism is clinically identical to primary hypothyroidism
  • Secondary hypothyroidism is diagnosed by demonstrating a simultaneously inappropriately normal or low TSH and low T4 (free or total). Patients are treated with levothyroxine replacement in the same manner as primary hypothyroidism; however, the serum TSH cannot be used to monitor and assess for adequacy of thyroid hormone replacement dosing. Instead, the levothyroxine dose is adjusted based on free T 4 levels with the goal of obtaining a value within the normal reference range.
48
Q

What are the effects of growth hormone deficiency, investigations and management.

A

GH deficiency causes fatigue, loss of muscle mass, an increased ratio of
fatty tissue to lean tissue, and increased risk for osteoporosis.

Low IGF1

Tx: Somatropin (recombinant human growth hormone)

49
Q

In patients with panhypopituitarism, what needs to be replaced?

A

Patients with panhypopituitarism require lifelong replacement of T4 , cortisol, and ADH because these deficiencies can be life-threatening. GH and sex hormones are replaced dependent on each patient’s preference coupled with a discussion of the risks and benefits of therapy. In addition to requiring exogenous gonaclotropins to conceive. a reproductive-aged woman with panhypopituitarisrn will not
go into spontaneous labor and will not lactate. These pregnancies are classified as high risk. and obstetric care should be provided by a maternal-fetal specialist.

50
Q

What the most common hormones secreted by functional pituitary tumours?

A

Most commonly GH and prolactin

51
Q

How does non-functional pituitary macroadenomas cause an increase in prolactin?

A
  • Non-functioning macroadenomas cause stalk compression usually cause prolactin rise of < 5x ULN
52
Q

Difference between psychogenic polydypsia/primary polydypsia and diabetes insipidus

A

Primary polydyspia

  • Hyponatremia
  • Plasma osmolality low-normal
  • Urine osmolality low
  • Urine osmolalilty improves after water deprivation + desmopressin

Diabetes Insipidus

  • Hypernatremia
  • Plasma osmolality high -normal
  • Urine osmolality: low
53
Q

Growth hormone deficiency

A
  • Insulin tolerance test (but need to be aware in epilepsy as hypos can further trigger epilepsy)
  • Alternative if epilepsy is glucagon stimulation test
54
Q

Acromegaly

A
  • Insulin growth factor 1

- Oral glucose tolerance test

55
Q 
What is the most common presenting
symptom of pituitary apoplexy?
A. Diplopia.
B. Headache.
C. Neck stiffness.
D. Vertigo.
E. Visual loss
A

B. Headache.

56
Q

Symptoms of pituitary apoplexy

A

Acute onset of

  • Severe headache
  • Hypopituitarism
  • Bilateral hemianopia + diplopia due to damage to CNIII
  • Sudden hypotension, possibly shock

Endocrinology (10 decks)

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