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Physiology 1 > 61) The Pituitary and its disorders > Flashcards

61) The Pituitary and its disorders Flashcards

1
Q

What is the pituitary gland?

A
  • It is a bilobed gland which lies below the brain in the Sella Turcica
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2
Q

Describe the structure of the anterior lobe

A
  • The anterior lobe (called the adenohypophysis) is derived from an invagination of the roof of the embryonic oropharynx (called Rathke’s pouch)
  • This pouch breaks off and migrates upwards to form the anterior pituitary.
  • Hence it is mesodermal in origin
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3
Q

Describe the structure of the posterior lobe

A
  • The posterior lobe (called the neurohypophysis) is formed form a notochordal projection from the brain.
  • The axons from cells within the hypothalamus project down towards the pituitary.
  • When they reach the pituitary they synapse onto vessels (rather than onto other nerves).
  • This means that the posterior pituitary releases its hormones into the blood stream and not into synaptic clefts.
  • It is endodermal in origin
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4
Q

Where does the posterior pituitary produce and release hormones?

A
  • The cell bodies for the posterior pituitary are in the brain so there is no direct hormonal production in the brain (the hormones are just released there).
  • However the anterior pituitary are glandular cells as there are nuclei within the anterior pituitary
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5
Q

Describe the blood supply within the pituitary gland?

A
  • They have a dual blood supply (the long and short pituitary arteries) which bring in oxygenated blood
  • There is also a portal circulation that goes from the hypothalamus to the pituitary and is how the hypothalamus communicates with the anterior pituitary
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6
Q

How were pituitary cell types named before?

A
  • They were named based on their ability to pick up red acidic dyes or blue basic dyes
  • However there was no correlation between staining and hormone production
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7
Q

How are pituitary cell types named now?

A
  • They are named depending on the hormone they produce:
  • Gonadotrophs (secrete LH and FSH)
  • Lactotrophs (secrete Prolactin)
  • Somatotrophs (secrete GH)
  • Corticotroph (secrete ACTH)
  • Thyrotroph (secretes TSH)
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8
Q

Why is the pituitary known as the master gland?

A
  • The anterior pituitary hormone governs the rest of the hormonal systems
  • It controls the release of:
  • ACTH (which regulates the adrenal cortex)
  • TSH (which regulates thyroid hormone regulation)
  • GH (which governs growth)
  • LH and FSH (which govern reproductive function)
  • Prolactin (which is important in breast milk production)
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9
Q

What are the functions of the posterior pituitary secretions?

A
  • ADH governs the release of water from the kidneys and also governs fluid balance
  • Oxytocin is important in lactation (causes expulsion of milk from the best) and parturition/giving birth (causing contraction of the uterus which expels the foetus)
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10
Q

What do the different hormones of the pituitary hormones do?

A
  • “Trophy” means food or to grow
  • Gonadotrophin causes growth of gonads
  • Somatotrophin causes growth of the body
  • Thyrotrophin causes growth of thyroid
  • Corticotrophin causes growth of the adrenal cortex
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11
Q

How are the hypothalamic hormones named?

A
  • They are named after the hormones they modulate
  • Gonadotrophin Releasing Hormone (stimulates release of gonadotrophin)
  • Growth Hormone Releasing Hormone (stimulates release of somatotrophin)
  • Thyrotrophin Releasing Hormone (stimulates release of thyrotrophin)
  • Corticotrophin Releasing Hormone (stimulates release of corticotrophin)
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12
Q

How and why is the endocrine system organised?

A
  • It is organised into three distinct layers:
  • Primary: End/target organ
  • Secondary: Pituitary
  • Tertiary: Hypothalamus
  • This is to allow for endocrine control
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13
Q

What is the outline of endocrine action?

A
  • The hypothalamus takes input from the brainstem, from the senses, from the higher senses
  • It then changes these neuroelectric signals into a collection of corresponding hormones that elicit the specific response (e.g. a collection of hormones released during stress)
  • These pass through the hypophyseal portal blood vessel where it passes from the hypothalamus into the pituitary
  • In the pituitary there is a large amount of prestored hormones which amplifies the weak signal sent by the hypothalamus to the end organ
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14
Q

Why is the endocrine system constantly working?

A
  • The glands within the endocrine system are constantly secreting hormones at very low levels.
    This is because if hormones were to be created and secreted only when a stimuli was detected it would take too long for the end organ to react
  • Instead we find a constant supply of hormones in the system and there is a rapid rise in secretion of hormones when there is an increased stimuli
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15
Q

Why is there a negative feedback system in place in the endocrine system?

A
  • The endocrine system needs to be able to switch off quickly or else one signal will bleed into the next signal
  • The end organ in endocrine pathways have the action of switching off the production of the central hormones (from the pituitary and hypothalamus)
  • This means that whenever an endocrine response is occurring it will immediately try to switch itself off
  • This allows the system to be dynamic
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16
Q

What are the different clinical presentation of pituitary tumours?

A
  • Hormone hypersecretion: Excess secretion of hormones causing further problems and complications within the body
  • Space occupying lesion: This can compress the pituitary (to stop it working)
  • Hormone deficiency states: It can compress important structure around the pituitary (leading to vision loss, headaches and cancerous sinus invasion)
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17
Q

What is an excess production of each hormone called?

A
  • GH: Acromegaly
  • ACTH: Cushing’s disease
  • TSH: Secondary thyrotoxicosis
  • LH/FSH: (usually seen in non-functioning tumour)
  • Prolactin: Prolactinoma
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18
Q

What is the growth hormone inhibitory hormone?

A
  • Somatostatin
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19
Q

What is the mechanism of growth hormone action?

A
  • Firstly growth hormone stimulates the liver to produce Insuline-like Growth Factor 1 (IGF-1) which acts on chondrocytes in long bones to cause linear growth
  • IGF-1 also produces negative feedback to the brain to inhibit GH production
  • When growth occurs the cells have to absorb protein and energy to allow growth to happen
  • This means that IGF-1 will also work on fat tissue and muscle tissue which means that glucose will be trapped within them
  • This means there will be a decrease in glucose metabolism and an increased flux of amino acids
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20
Q

What are the effects of acromegaly?

A
  • Increased hand, shoe and tongue size
  • Increased skin thickness
  • Increased sweating
  • Metabolic changes
  • Impaired fasting glucose
  • Impaired glucose tolerance
  • Diabetes mellitus
  • Insulin resistance
  • Reduced total cholesterol
  • Cardiomyopathy (increased heart size) and hypertension
  • Bowel cancer
  • Goitre
  • Arthritis
  • Obstructive Sleep Apnoea
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21
Q

What is the main problem with acromegaly?

A
  • It is a subtle condition that is diagnosed using “coarsening of the facial features” (changes in the facial features)
  • Patients may be asked to bring pictures of themselves from 5 years ago in order to compare facial features
22
Q

What are the effects of cortisol on the body?

A
  • Increases plasma glucose levels: Due to increased gluconeogenesis, decreased glucose utilisation (in non-essential tissue), increased glycogenesis (except kidneys) and increased glycogen storage
  • Increases lipolysis: Which provides energy when glucose stores run out
  • (non-essential) Proteins are catabolised: Which releases Amino Acids to repair essential structures
  • Na+ and H2O Retention: To maintain BP if blood is lost
  • Anti inflammatory
  • Increased gastric acid production
23
Q

What causes cortisol secretion to increase?

A
  • Stress
24
Q

What are the effects of Cushing’s syndrome?

A
  • Changes in fat and protein metabolism: Causing central obesity, thin skin, easy bruising, osteoporosis and diabetes
  • Changes in sex hormones: Excess hair growth, irregular periods, problems conceiving and impotence
  • Changes in salt and water retention: High blood pressure and excess fluid retention
25
Q

What is the mechanism for the release of prolactins?

A
  • Normally the hypothalamus secretes TRH which causes the pituitary to produce dopamine (an inhibitor of prolactin).
  • The hypothalamus also produces LHRH which stimulates the release of LH from the pituitary that acts on ovaries
  • Mechanical stimulation of the nipple sends a neural signal to the brain which stops the production of TRH and hence dopamine
  • Hence there is an immediate increase in prolactin production and an immediate increase in milk production so the baby can be fed
  • Prolactin also inhibits the production of LHRH which means less LH is produced so less stimulation of ovaries
  • This ensures that energy goes into feeding the baby and is not split with making another baby
  • By taking the baby off the nipple we stop the mechanical stimulation and so dopamine secretion increases causing inhibition of prolactin production
26
Q

How does the secretion of prolactin differ from the other hormones?

A
  • It works under a positive feedback loop
  • This is because an increase in mechanical stimulation of the nipple sends a neural signal to the brain which stops the production of dopamine
  • Hence there is an immediate increase in prolactin production and an immediate increase in milk production so the baby can be fed
  • By taking the baby off the nipple we stop the mechanical stimulation and so dopamine secretion increases causing inhibition of prolactin production
27
Q

What are the effects of hypogonadism?

A
  • Infertility
  • Oligomenorrhoea
  • Amenorrhoea (period mixed up completely)
  • Galactorrhoea (milk released from the breast)
  • Reduced libido
  • Impotence
28
Q

What drugs interefere with dopamine and prolactin secretion?

A
  • Antiemetics
  • Antipsychotics
  • OCP/HRT (contraceptive pill)
29
Q

What is the treatment for prolactinoma?

A
  • Dopamine agonist: Bromocriptine and Cabergoline
30
Q

What are the effects of non-functioning pituitary tumours?

A
  • In some tumours there is no hormone production and so the primary effect of the tumour is the effect it has on primary structures
  • This includes headaches, visual field defects and interreference with the rest of the pituitary function
31
Q

What is the treatment for non-functioning pituitary tumours?

A
  • Surgery
32
Q

What is the optic chiasm?

A
  • The area in which the neurones from the retinas of two different eyes come together
  • They return to the same part of the brain and so we produce one picture in our eyes (rather than two different pictures)
33
Q

How does non-functional pituitary tumour affect vision?

A
  • The optic chiasm sits above the pituitary gland
  • Getting a tumour in this area will compress the optic chiasm and stop it from working
  • As a result there is a visual feed loss (called bitemporal hemianopia)
34
Q

What is bitemporal hemianopia?

A
  • When we loose vision in both our temporal fields
  • “Bitemporal”- Both temporal fields
  • “Hemi”- Exactly half
  • “Anopia”- Loss of vision
35
Q

What happens to the pituitary hormones when a loss of pituitary function tumour occurs?

A
  • The tumour will compress the glands and so will result in loss of pituitary hormones in a specific order of importance:
  • 1st is LH and FSH (When we are ill we should not be reproducing as we will not be there to look after the offspring so is the first to go)
  • 2nd is GH (Growth is no very important)
  • 3rd is TSH (Metabolic rate is quite important)
  • 4th is ACTH (Needed for survival and is the last that goes)
  • Prolactin is different to the other hormones as prolactin levels increase (due to positive feedback system including dopamine)
36
Q

How do we treat pituitary adnomas?

A
  • Surgery
  • Radiotherapy
  • Drugs (which will either block hormone production or stop hormone release)
37
Q

What are the causes of pituitary failure?

A
  • Tumour: Can be benign or malignant
  • Trauma
  • Infection
  • Inflammation: Histiocytosis (affecting the pituitary specifically) or sarcoidosis
  • Latrogenic (doctor induced)
38
Q

What are the effects of Hypopituitarism?

A
  • There will be a massive decrease in hormone secretion
  • Thyroid: This can cause bradycardia (low heart rate), weight gain, cold intolerance, hypothermia and constipation
  • Sex Steroids: This can cause oligomenorrhoea (periods will stop), reduced libido, hot flushes and reduced body hair
  • Reduced Cortisol: This can cause tiredness, weakness, anorexia, postural hypotension (unable to retain salt in the kidney) and myalgia
  • Reduced GH: This can cause tired and central weight gain
39
Q

How do we treat hypopituitarism?

A
  • We treat it by replacing pituitary hormones
  • Thyroid: We would use thyroxine
  • Sex Steroids: We would use either testosterone (men) or oestrogen (females)
  • Reduced Cortisol: We would use hydrocortisone
  • Reduced GH: We would use growth hormone
  • They are all normally tablets or gels except for the GH which has to be given as an injection
40
Q

What is Antidiuretic Hormone (ADH)?

A
  • ADH or vasopressin acts on collecting ducts within the kidneys and icnreases water permeability which allows water to leave the urine and return to the body
  • It also acts to vasoconstrict blood vessels
  • Overall ADH helps you to stop passing urine (i.e. stopping diuresis)
41
Q

How is ADH secretion stimulated?

A
  • ADH secretion is stimulated by dehydration and increase plasma osmolality
  • When there is a loss of water the kidney will try to retain water
  • It is also secreted in response to low blood pressure that is sensed by the baroreceptors in the arch of the aorta and the left atrium
  • Hypoxemia and hypercapnia also stimulate ADH secretion
  • There is also some control from other hormones such as sex hormones, cortisol and angiotensin II
  • Finally ADH secretion can also be stimulated by shock
42
Q

How does shock stimulate ADH release?

A
  • When we are in shock our blood pressure is low which means the blood flow is slow
  • This allows more time for oxygen extraction from the blood and carbon dioxide return into the blood from the tissues
  • This means that in shock we suffer from hypoxaemia and hypercapnia
43
Q

What is Syndrome of Inappropriate ADH (SIADH)?

A
  • When too much ADH is in circulation
44
Q

What are the causes of Syndrome of Inappropriate ADH (SIADH)?

A
  • Brain injury/infection: This irritates the brain leading to increased secretion of ADH
  • Lung cancer/infection asthma IPPV: This is because the lung is very dry (as there is very little interstitial fluid) so normally the lungs inhibits ADH secretion. However during lung infections this mechanism is inhibited.
  • Metabolic: Hypothyroidism (the expression of ADH receptors in the kidney depends on the level of thyroid hormone levels) or Addison’s (as cortisol is important in closure of aquaporin in the kidney which allows water to return from the urine)
45
Q

How do we diagnose SIADH?

A
  • Low blood volume
  • Increased plasma Na+
  • Increased plasma osmolality
  • Increased urine osmolality
  • Increased urine Sodium
46
Q

What is the treatment for SIADH?

A
  • Fluid restriction
  • Demeclocycline
  • ADH Antagonist (Tolvaptan)
47
Q

What is diabetes insipidus?

A
  • The underproduction of ADH
48
Q

What are the causes of diabetes insipidus?

A
  • Cranial: (e.g. damage to the brain) Can lead to lack of production
  • Nephrogenic: (e.g. damage to the receptor in the kidney) Can lead to receptor resistance
49
Q

How do we diagnose diabetes insipidus?

A
  • Polyuria (too much urine being produced)
  • Polydipsia (feeling of extreme thirst)
  • Increased plasma osmolality
  • Increased urine osmolality
50
Q

How do we test between nephrogenic diabetes insipidus and cranial diabetes insipidus?

A
  • We use the water deprivation test
  • In this test we deprive a patient off water and we see if they can pass urine and dehydrate
  • We can see if someone is dehydrated if they loose 3% of the body weight in the 8 hours that we test them for
  • At the end of the dehydration phase we give an injection of ADH and see what happens
51
Q

How can the results of a water deprivation test show what type of diabetes insipidus our patient has?

A
  • In a normal person after 8 hours the plasma level stays normal however the urine becomes concentrated and the osmolality of the urine is at least 3 times that of the plasma
  • In someone with diabetes insipidus they continue to pass urine and are unable to control it and hence their plasma becomes concentrated (as they loose too much water) while their urine is not very concentrated
  • If after the dehydration phase (when we give the injection of ADH) things go back to normal then this tells us that the person is able to respond to ADH and so the problem is that the person is not making enough ADH. Hence they have a cranial diabetes insipidus
  • However if after the dehydration the conditions remain worse then it tells us that the body cannot respond to ADH and so tells us it is nephrogenic diabetes insipidus
52
Q

What is the treatment for diabetes insipidus?

A
  • Giving ADH either as an injection, a tablet or a nasal spray
  • For cranial diabetes insipidus we can use low doses of medication
  • However for nephrogenic diabetes insipidus we have to use high doses of medication (due to increased resistance to ADH)

Physiology 1 (64 decks)

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