Pituitary Gland and Its Disorders Flashcards
Pituitary Gland
Where does it lie? how is this in relation to the brain?
how is the anterior lobe derived?
how is the posterior lobe formed?
what important structures are around the gland? above? on the side? below it?
what disease may affect these structures?
The pituitary gland lies below the brain in the Sella Turcica, the anterior lobe (adenohypophysis) is derived from an invagination of the roof of the embryonic oropharynx known as Rathke’s pouch.
A notochordal projection forms the pituitary stalk which connects the gland to the brain and also the posterior lobe of the pituitary (neurohypophysis).
The pituitary gland is surrounded by important structures which can be affected in disease, namely in diseases such as adenomas which can press on the nearby structures.
Above the pituitary we have the optic chiasm, we have the internal carotid arteries on the side. Underneath the sella turcica is the sphenoid sinus.
Pituitary cell type was, originally classified by their staining characteristics with acidic (orange-G) and basic (aldehyde fuscin) dyes.
Pituitary Hormones
what is produced at anterior and what do they do?
what is produced at posterior and what do they do?
Anterior:
• ACTH is released which regulates the adrenal cortex
• TSH controls production of thyroid hormones from the thyroid
• GH controls growth
• LH/FSH involved in reproductive control
• Prolactin (PRL) is involved in breast milk production
Posterior:
• ADH regulates water, it retains water (anti-duiris)
• Oxytocin causes uterine contraction in delivery but also in breast milk release
Nomenclature of Pituitary and Hypothalamic Hormones
4 different names
o LH and FSH: Gonadotrophin = Hypothalamic hormone = Gonadotrophin Releasing Hormone
o Growth and Hormone: Somatotropin – Growth Hormone Releasing Hormone
o TSH: Thyrotropin = Thyrotropin Releasing hormone
o ACTH: Corticotrophin = Corticotrophin Releasing Hormone
The endocrine system is organised into layers
how many layers? And what do they correspond to?
explain the links between the layers so
where does all the info go?
why can’t hypothalamus dump all the hromones itself? where does it go and what happens next?
what is the function of hypothalamus and pituitary gland?
why is the endo system primed with little bit stored hromone?
what is the principle of the negative feedback system?
- Primary layer is end organ
- Secondary is pituitary
- Tertiary is hypothalamus
The endocrine system is slow, long and about states of being.
- The hypothalamus takes inputs of our senses and higher centres and integrates them. These signals maybe stress/threat in front of us/is there someone attractive in front of me.
- The hypothalamus then releases hormones saying stress/attraction/hunger.
- But the hypothalamus is very small, so in order to dump enough hormone into blood the neurones would have to be very large. So, it doesn’t do this. Instead it puts it into the portal vessels to the pituitary.
- The pituitary has enough hormone to enter into blood and be diluted enough that they can have their effects on the body.
Hypothalamus function is to integrate signal, function of pituitary is to amplify the signal.
It takes time to synthesise peptide hormones, so this wouldn’t be useful if it was needed straight away. So, the endocrine system is always primed with a little bit of stored hormone to get into action straight away if needed.
But of course, you also want to be able to switch it off quickly, so the peripheral hormones switch off production of the central ones. So that the moment the response starts, it is trying to be switched off again.
This is the principle of negative feedback -> allows system to be dynamic, be responsive
This principle is heavily used in the diagnosis of endocrine disorders
Clinical Presentation of Pituitary Tumours
what 3 things do we need to consider?
syndromes of hormone excess - give example of diseases for the hormones
When dealing with pituitary lesions we generally have three things to consider:
- Hormone hypersecretion (due to tumour secreting)
- Hormone deficiency status, tumour can squish the normal pituitary surrounding it leading to decreased hormone release from those parts
- Space occupying lesion, as tumour grows more can affect nearby structures -> headaches, visual loss, cavernous sinus invasion
Tumours of the anterior pituitary can cause syndromes of hormone excess
- GH = Acromegaly
o If child, bones growing so child gets big = gigantism, once older long bones can’t grow anymore this leads to soft tissue growing = acromegaly
- ACTH = Cushing’s disease
- TSH = Secondary thyrotoxicosis
- LH/FSH = Non-functioning pituitary tumour
- PRL = Prolactinoma
Growth Hormone (excess)
what does GH cause release of? frome where?
systemic effects?
metabolic changes?
other consequences?
GH causes release of IGF-1 from the liver which acts on the bones causing linear growth. To grow you need energy, lipids needs to be metabolised and protein synthesised, these metabolic effects are mediated by GH itself.
Systemic effects:
- Acral enlargement
- Increased skin thickness
- Increased sweating
- Skin tags
- Changed appearance
- Visceral enlargement (e.g. spleen enlargement)
Metabolic changes:
- Impaired fasting glucose
- Impaired glucose tolerance
- Diabetes mellitus
- Insulin resistance
- Increased TAG
Other consequences:
- Cardiomyopathy
- Hypertension
- Bowel polyps (can become malignant, because GH causing increased growth)
- Colonic cancer
- Multinodular goitre
- Hypogonadism
- Arthropathy
When a woman has acromegaly, she looks like a guy, when a guy has it he looks like a thug.
Actions of Cortisol
what happens to plasma glucose levels? how?
what happens to fat stores?
what happens to muscles?
How is bp maintained?
Other 2 effects
- Increased plasma glucose levels o Increases gluconeogenesis o Decreased glucose utilisation o Increases glycogenesis o Increases glycogen storage
- Increases lipolysis
o Provides energy - Proteins are catabolized
o Releases AA - Na+ and H2O retention
o Maintains BP - Anti-inflammatory
- Increased gastric acid production
Cushing’s Syndrome
3 key changes and their symptoms
Changes in protein and fat metabolism
- Change in body shape
- Central obesity
- Moon face
- Buffalo hump
- Diabetes
Changes in sex hormones
- Excess hair growth
- Irregular periods
- Problems conceiving
- Impotence
Salt and water retention
- High blood pressure
- Fluid retention
Prolactinomas
Why is prolactin release different to the other hormones? what stimulates production?
What is the afferent limb of the signal? what does it inhibit?
What happens when inhibitor is removed?
how do you terminate the production? what is this an example of and similar to?
what else can cause high prolactin levels?
what increases the size of lactotrophs?
what are features of PRL excess?
how do you treat excess? (name 2 drugs)
The control of prolactin release is different to the other pituitary hormones. This is because the stimulus for production is external to the body, it is mechanical stimulation of the breast.
The afferent limb of the signal is neuronal with mechanical stimulation of the nipple sending a neural signal to the brain, this inhibits dopamine.
The other cells of the anterior pituitary they wait quietly until stimulated by the hormone from hypothalamus. Prolactin is different in that the lactotrophs intrinsically has a high production rate of prolactin, but it is tonically inhibited by dopamine produced in the hypothalamus and travels down to the pituitary.
So, when dopamine production is switched off, you have an instant surge in prolactin production, allowing milk to enter breast for baby.
The way you terminate this is by removing the baby from the nipple. This is an example of positive feedback; the same thing applies to oxytocin.
High prolactin levels may not be due to pituitary tumours, there are many drugs that interfere with dopamine and PRL secretion, including antiemetics, antipsychotics, OCP (oral contraceptive pill)/HRT.
Oestrogen increases size of lactotrophs getting them to increase PRL production, to get ready to make milk at end of pregnancy.
Features of PRL excess
- Infertility (
Non – functioning pituitary tumours
what is a key feature of this and what symptoms may it cause?
what is treatment options?
what is the first defect of eyes?
These make up 30% of all pituitary tumours and when no syndrome of hormone excess is produced. Instead they cause symptoms due to space occupation such as headache, visual field defects and nerve palsies.
They may interfere with the rest of pituitary function leading to deficiency of hormones.
Treatment is surgery and or radiotherapy
Visual field defect is first visual loss on the sides, due to compression of where the where the fibres cross.
Loss of Pituitary Function with an Expanding Tumour
what is the set order of loss of pituitary hromones and what is it based on?
why may prolactin levels rise?
There is a set order in which you lose the pituitary hormones and it is based on the biological importance of them
.
1. LH/FSH go first as sex/reproduction is least priority
2. GH is then next to go, as growth not as important
3. TSH, metabolic rate goes which is important
4. ACTH is our last to go, i.e. our stress response last to go. As we need this for survival
Prolactin levels rise due to compression of the pituitary stalk, meaning that dopamine cannot reach the lactotrophs, so they will not be being inhibited.
Treatment of Pituitary Adenomas
first inital treatment method
what if its too large? (issue with this treatment)
how do we treat prolactinoma?
Surgery to remove tumour and get rid of it (through transphenoidal surgery), we don’t if prolactinoma as they respond to drug therapy.
If tumour is too big, we use radiotherapy, but this is slow.
Or we could use drugs, drugs to either block hormone production or to stop hormone release.
Causes of Pituitary Failure
other reasons for pituitary failure (4)
Problems with the pituitary gland can be caused by tumours (main reason pituitary may not work) but another reason could be:
- Trauma
- Infection
- Inflammation
- Iatrogenic -> caused by doctor
Hypopituitarism - pituitary failure
symptoms of the different deficient hormones
how can hypopituitarism be treated?
name the drugs for each hormone
When you have pituitary failure, there becomes a deficiency of hormones
Thyroid • Bradycardia • Weight gain • Cold intolerance • Hypothermia • Constipation
Sex Steroids • Oligomenorrhoea • Reduced libido • Hot flushes • Reduced body hair
Reduced cortisol • Tiredness • Weakness • Anorexia • Postural hypotension • Myalgia (muscle pain)
Reduced GH
• Tired
• Central weight gain
Hypopituitarism Treatment
- Thyroid – thyroxine
- Sex steroids – Testosterone, oestrogen
- Reduced cortisol – Hydrocortisone
- Reduced GH – Growth hormone
Vasopressin
2 functions of ADH
what detects stimulus? what stimulus? (2 stimuli)
what does adh do to collecting duct?
ADH stops you peeing and also vasoconstricts blood vessels.
A lack of water in the blood causes an increase in plasma osmolality which can be sensed by osmoreceptors in the hypothalamus.
Decreased blood pressure sensed by the baroreceptors (volume receptors in atria) as well as reduced PaO2 and increased PaCO2 and cortisol, sex steroids and ang II in the blood. All the previous are stimulating controls of ADH release.
ADH will open aquaporins in the collecting ducts which increases the permeability for water. As a result, there is increased reabsorption of water into the blood.
There is also vasoconstriction.
