Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

LCRS Year 2 - Endocrinology > Hypersecretion of Anterior Pituitary Hormones > Flashcards

Hypersecretion of Anterior Pituitary Hormones Flashcards

1
Q

What is hyperpituitarism?

A

Symptoms associated with excess production of adenohypophysial (anterior pituitary) hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is hyperpituitarism usually caused by and what is the other cause?

A

Usually due to isolated pituitary tumours also producing ant. pituitary hormone
- Can also be ectopic (i.e. from non-endocrine tissue) in origin, basically an odd case where tissue elsewhere in the body somehow ends up making ant. pituitary hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What defects, signs and symptoms is hyperpituitarism often associated with?

A
  • Visual field, cranial nerve defects due to compression of optic chiasm and cranial nerves by the tumour
  • Endocrine-related signs and symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is bitemporal hemianopia and how is it caused?

A

Tunnel vision, blindness in lateral half of view in both eyes.
“Bitemporal” in both temporal (lateral) views
“Hemianopia” blindness in half the field of vision

Caused by impingement of optic chiasm where optic nerve fibres cross. Fibres crossing are the fibres that supply lateral vision so no signal is received by the brain from lateral view thus the blindness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is bitemporal hemianopia assessed and diagnosed?

A

Perimetry

  • Flash on screen which patient responds to
  • Builds an image of their vision field
  • Each eye’s field of vision will be half white (can see) and half black (can’t see)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Cushing’s syndrome - too much cortisol

Cushing’s disease - an ACTH-producing adenoma causing too much ACTH to be released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What disorder is caused by excess ACTH?

A

Cushing’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What disorder is caused by excess TSH?

A

Thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What disorder is caused by excess gonadotrophins (LH/FSH)?

A

Precocious puberty in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What disorder is caused by excess prolactin?

A

Hyperprolactinaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What disorders are caused by excess GH?

A

Gigantism, Acromegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are two physiological (normal) causes of hyperprolactinaemia?

A

Pregnancy

Breastfeeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the usual pathological cause of hyperprolactinaemia and what is special about it?

A

Prolactinoma

- Special as prolactinomas are the most common functioning type of pituitary tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does high prolactin interact with other ant. pituitary hormones?

A

High prolactin suppresses GnRH pulsatility (think about LH/FSH low levels and no spiking during pregnancy/conception)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the signs and symptoms of hyperprolactinaemia in women?

A
  • Galactorrhoea (milk production outside of when it’s needed e.g. pregnancy/birth)
  • Secondary amenorrhoea or oligomenorrhoea
  • Loss of libido
  • Infertility (usually this or amenorrhoea as presenting feature)

These are certainly tied in with the lack of GnRH pulsatility and low gonad hormone levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the signs of symptoms of hyperprolactinaemia in men?

A
  • Galactorrheoa although uncommon (requires estrogen)
  • Loss of libido
  • Erectile dysfunction
  • Infertility (usual presenting complaint)
17
Q

How is prolactin release regulated in the pituitary gland?

A

Dopamine neurones via D2 receptors

- When dopamine binds, they act as a brake on prolactin release, suppressing prolactin secretion

18
Q

How can the regulation mechanism of prolactin be manipulated pharmacologically to treat hyperprolactinaemia?

A

Dopamine receptor (D2) agonists

  • decrease prolactin secretion
  • reduce tumour size
19
Q

What are 2 examples of dopamine receptor (D2) agonist drugs and how are they administered?

A

Bromocriptine
Cabergoline
- Oral administration (tablet)

20
Q

Is medical (drugs) treatment or surgical treatment first-line for prolactinomas?

A

Medical

- Largely because the D2 agonists are so effective and also reduce tumour size

21
Q

What are the side effects of dopamine receptor agonists?

A
  • Nausea, vomiting
  • Postural hypotension
  • Dyskinesias (involuntary movement)
  • Depression
  • Pathological gambling(!)
22
Q

What is the name of GH excess during childhood/teenage years and during adulthood?

A

Childhood - gigantism

Adult - acromegaly

23
Q

What is GH excess usually due to?

A

“Benign” growth hormone secreting pituitary adenoma

“Benign” by definition as there are no cancer cells present, but not in terms of absence of disease-causing properties e.g. these GH excess disorders are being caused by it

24
Q

What is the nature of the onset of acromegaly, how do signs and symptoms progress and what happens if excess GH is left untreated?

A
  • Insidious in onset, very difficult to notice over years
  • Signs and symptoms progress gradually over a number of years
  • Untreated, excess GH is associated with increased morbidity and mortality
25
Q

What are the 3 areas of cause of death as a result of excess GH and what are their respective proportions?

A
  • CVS disease - 60%
  • Respiratory complications - 25%
  • Cancer - 15%
26
Q

What parts of the body grows in acromegaly?

A
  • Periosteal bone
  • Cartilage
  • Fibrous tissue
  • Connective tissue
  • Internal organs (cardiomegaly, splenomegaly, hepatomegaly etc.)
27
Q

What are the clinical features of acromegaly?

A
  • Excessive sweating (hyperhidrosis) (common)
  • Headache (common)
  • Enlargement of supraorbital ridges, nose, hands/feet (spade-like hands), thickening of lips and general coarseness of features
  • Enlarged tongue (macroglossia)
  • Mandible grows causing protusion of lower jaw (prognathism)
  • Carpal tunnel syndrome (connective tissue and fibrous tissue enlarged compressing median nerve)
  • Enlargement of the chest (barrel chest)
28
Q

What are the metabolic effects of excess GH?

A
  • Increased endogenous glucose production, decreased muscle glucose uptake
  • Increased insulin production thus increased insulin resistance
  • Impaired glucose tolerance

Thus predisposition to Diabetes Mellitus

29
Q

What are complications of acromegaly?

A
  • Obstructive sleep apnoea
  • Hypertension
  • Cardiomyopathy
  • Increased risk of cancer (due to exposure to high GH levels all the time)
30
Q

What can be co-secreted often in cases of acromegaly?

A

Prolactin

  • Prolactin often high in acromegaly, can indicate tumour secreting GH AND prolactin
  • Hyperprolactinaemia will cause secondary hypogonadism
31
Q

How is acromegaly diagnosed?

A
  • GH pulsatile so random tests will be unhelpful
  • Sometimes serum IGF-1 will be elevated
  • BUT gold standard test is measurement of GH following oral glucose load

Normal person - dip in GH levels (suppression) after taking the glucose load

Acromegaly patient - large jump (paradoxical rise) in GH levels following the glucose load

Cause for this unknown hence paradoxical rise

32
Q

What are the lines of treatment for acromegaly?

A 
1st line - Surgery (trans-sphenoidal)
2nd line - Medical
- Somatostatin analogue (octreotide)
- Dopamine agonists (cabergoline)
3rd line - Radiotherapy on pituitary (can result in general hypopituitarism)
33
Q

What is the purpose of giving somatostatin analogues?

A

Reduces GH secretion and tumour size

34
Q

When are somatostatin analogues given and how are they administered?

A
  • Pre-treatment before surgery may make tumour removal (resection) easier
  • Post-operatively if not cured or whilst waiting for radiotherapy to take effect

Either administered by injection (usually surgery premedicine) or monthly depot (usually post-operative)

35
Q

What are side effects of somatostatin analogues?

A

GI side effects are common

  • Nausea
  • Diarrhoea
  • Gallstones
36
Q

What is an example of a dopamine agonist and a somatostatin analogue?

A

Dopamine agonist - CABERGOLINE

Somatostatin analogue - OCTREOTIDE

LCRS Year 2 - Endocrinology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions