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10 > Endocrinology I - Hypothalamic pituitary axis > Flashcards

Endocrinology I - Hypothalamic pituitary axis Flashcards

1
Q

What is the bony cup the pituitary gland sits on?

A

Sella Turcica within the spehnoid sinus
- Helps protect the pituitary gland

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2
Q

1- Where does the hypothalamus develop embryologically?

2- Where does the anterior pituitary develop from embryologically?

3- Where does the posterior pituitary develop from embryologically?

A

1- neuroectoderm of the forebrain

2- Adenohypophysis (anterior pituitary) is derived from the Rathke’s pouch (Ectodermal in origin)

3- neurohypophysis and forms from the ventral hypothalamus +3rd ventricle

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3
Q

What hormones are released from:

1- Hypothalamus
2- Anterior pituitary
3- Posterior pituitary

A

1)
GHRH- Growth hormone - releasing hormone
TRH- Thyrotropin releasing hormone
CRH- Corticotropin releasing hormone
GnRH- Gonadotropin releasing hormone
Dopamine
Somatostatin

2-
ACTH - Adrenocorticotropic
LH- Luteinising hormone
FSH- Follicular stimulating hormone
TSH- Thyroid stimulating hormone
GH- Growth hormone
PRL- Prolactin

3-
- Vasopressin (ADH)
- Oxytocin

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4
Q

What are the effects of different hypothalamic hormones on the anterior pituitary hormones?

A
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5
Q

What are the 3 different clinical presentations that are seen in pituitary tumours?

A

1- Hormone hyper-secretion
2- Space occupying lesion leads to:
- Headaches
- Visual loss (field defect) > Pressing against the optic chiasm
3- Hormone deficiency states
- Interference with surrounding normal pituitary

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6
Q

Tumours in the anterior pituitary can cause syndromes of hormone excess.
What condition is caused by an increase in:
ACTH - Adrenocorticotropic
TSH- Thyroid stimulating hormone
GH- Growth hormone
PRL- Prolactin
LH/FSH

A

> ACTH = - Cushing’s syndrome - overproduction of cortisol by adrenal glands
- Leads to increased skin bruising - fat in trunk but slim arms and legs

> TSH = Secondary thyrotoxicosis

> GH = Acromegaly (bones increase in size, including those of your hands, feet and face)

> PRL = Prolactinoma (Decreased levels of sex hormones)

> (Non-functioningpituitarytumour)

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7
Q

What are the effects of pressure of pituitary tumours?

A
  • Optic chasm takes banana shape
    = Peripheral field loss
    (slow growing nature so change in peripheral vision is not noticeable)
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8
Q

What are non-functioning pituitary tumours and their effects?

A
  • Benign tumours of the pituitary where the cells have no function. Most common and do not cause excess hormone production.

Symptoms due to space occupation = Headache / visual field defect / Interfere with rest of pituitary function .. deficiency of hormones

Treatments= Transsphenoidal surgery/ Radiotherapy

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9
Q

1- What condition is caused with growth hormone excess in childhood?
2- What condition is caused with growth hormone excess in adulthood?

A
  • Giantism
  • Acromegaly
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10
Q

Acromegaly:
(Occasionally familial in association with MENI)
M:F 1:1 > onset 40-60

1- What does it present as? (4)
2- How is It diagnosed?
3- How is it treated?

A

1-
– signs of GH excess
– pressure symptoms
– field defects
– loss of anterior pituitary function

2-
* Raised Insulin like Growth Factor 1 (IGF1) - integrated effect of growth hormone (GH) at tissue level
* Oral glucose tolerance test (GTT) with GH measurement – GH should suppress completely
* Imaging – MRI pituitary with Gadolineum contrast

3-
* Endoscopic transnasal transsphenoidal Surgery
* Radiotherapy
* Growth hormone receptor antagonist
* Dopamine Agonist therapy – Dopamine inhibits GH secretion
* Somatostatin Analogues – Somatostatin inhibits GH secretion

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11
Q

How is prolactin inhibited?

A
  • Prolactin inhibiting factors (PIFs)
  • Dopamine is the most important of these

= prolactinaemia is often drug induced = Antipsychotic medication

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12
Q

1- What are clinical manifestations of Hyperprolactinaemia in men/women?

2- How is It treated?

A

Dopamine agonists
Surgery
Radiotherapy

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13
Q

1- Define hypopituitarism
2- What are the causes of hypopituitarism?

A

1- Loss of function where pituitary gland can no longer produce 1 or more hormone

  • Pituitary tumours
  • Pituitary surgery
  • Pituitary radiotherapy
  • Pituitary infarction
  • Pituitary apoplexy: blockage in blood flow or bleeding (hemorrhage) in your pituitary gland.
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14
Q

Describe HPA axis.

A
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15
Q

What do adrenal glands produce?

A
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16
Q

Cushing syndrome vs Cushing disease.

A

Cushing’s Syndrome:
This is a medical condition characterized by an excess of the hormone cortisol in the body.

Cushing’s Disease:
Cushing’s disease is a specific form of Cushing’s syndrome.
It is primarily caused by a benign (non-cancerous) tumor in the pituitary gland, known as an adenoma.
This tumor releases excess adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands to produce more cortisol. In Cushing’s disease, the root cause is the pituitary tumor.

17
Q

1- How is Cushing syndrome diagnosed?

A
  • Screening
    – 24 hour urinary free cortisol
    – Overnight Dexamethasone suppression test
  • Confirming
    – Low dose Dexamethasone suppression
  • Source
    – ACTH measurement
    – Highdos edexamethasone -50%fallin80-90% with pituitary disease
    – CRF test-normal or exaggerated response of ACTH in Cushings disease

Tumour localisation
* Pituitary – MRI
– Petrosal sinus sampling +CRH
* Adrenal
– MRI
– Selective venous catheterisation
* Ectopic
– MRI/CT

18
Q

How is cushings syndrome treated?

A
  • Surgical-transphenoidal,adrenal
  • Medical–adrenolytic therapies may be used in preparation for surgery
  • Chemotherapy
  • Radiotherapy
19
Q

1- What is Addisons disease?
F:M 2:1

2- How does it present?

3- Describe the biochemistry.

A

1- Primary adrenocortical failure

2- Non-specific
* Weakness & fatigue
* Anorexia & weight loss
* Abdominal pain
* Postural hypotension
* Pigmentation due to ACTH hypersecretion

3-
– Serum sodium normal or reduced
– Serum potassium increased
– Urea increased (dehydration)
– May be hypoglycaemic

20
Q

1- How do we investigate Addisons disease?
2- How do we treat this?

A

1-
* Basal cortisol
* Adrenal antibodies
* Short synacthen test

2-
Emergency
– IV fluids, IV hydrocortisone 100 mg stat, then IV hydrocortisone 50 mg 6 hrly or as infusion
Replacement
– Hydrocortisone per oral 20 mg/day in divided doses
– Fludrocortisone 50 to 200 microgram/day

21
Q

Describe the HPT AXIS.

A
22
Q

1- What is hyperthyroidism?

2- What are some causes of primary hyperthyroidism?

2a- Why may you get Thyrotoxicosis without hyperthyroidism?

3- How does it present clinically?

4- What treatments are there?

A

1- Syndrome resulting from excess of free T4and/ or freeT3
* More common in women
* Indicates thyroid gland overactivity

2- Graves’ disease
* Toxic multinodular goitre
* Toxic adenoma

2a-
* Excessive T4 administration
* Thyroiditis
* New immune therapy drugs

4- Antithyroiddrugs
* Radioactive iodine therapy
* Thyroidectomy

23
Q

1- What is primary hypothyroidism?
2- Causes?
3- How does it present?
Treatment?

A

1- Low free T4 and T3 leading to stimulation of pituitary TSH levels where TSH levels are normal but thyroid gland is unable to produce T3 and T4

2- * Autoimmune thyroiditis*
* Idiopathic atrophy*
* Previous Rx history*
* Iodine deficiency
* Antithyroid drugs
* Other drugs (e.g. lithium or amiodarone)
* Subacute and silent thyroiditis

3- Could be non-specific and vague symptoms

4- Thyroxine replacement

24
Q

Describe secondary hypothyroidism.

A
  • Patients with pituitary tumour would have low TSH as the tumour compresses on pituitary, leading to low production of TSH
  • Leads to low T3 and T4
25
Q

Describe Hypothalamic-pituitary gonadal axis.

A
26
Q

Describe what happens with HPG dysfunction.

A
  • Problems with sexual maturation/ secondary characteristics – Precocious puberty
    – Short stature
    – Delayed puberty
  • Men
    – Hypogonadism
    – Infertility
    – Erectiledysfunction
  • Women
    – Infertility
    – Secondary Amenorrhoea
  • Pituitary causes
  • Gonadal causes

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